(Netter Clinical Science) Walter Greene MD-Netter's Orthopaedics, 1e-Saunders (2005) - PDFCOFFEE.COM (2024)

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Preface Netter’s Orthopaedics is an essential text on the pathophysiology, diagnosis, and treatment of musculoskeletal disorders. The need for such a book results from the commonality of these disorders, which are second only to respiratory illnesses as a reason that patients seek medical care, and their diversity, in that they comprise everything from injuries and infections to metabolic and neoplastic diseases. Patients with conditions affecting the musculoskeletal system present in many settings, requiring that virtually all health care providers be familiar with the diagnosis and treatment of these disorders. This book, therefore, is intended for use by the many clinicians who will see these patients—students in medicine, physical therapy, and osteopathy, and residents in primary care, orthopaedics, family practice, and emergency medicine. The first 12 chapters of Netter’s Orthopaedics are concerned with topics related to the entire musculoskeletal system, and provide principles that can be applied to the management of many disorders. The final 7 chapters are organized by region, and offer techniques of diagnosis and treatment specific to each region. Given the widely different backgrounds of the anticipated readers of this book, we have tried throughout to make the text as accessible as possible, presenting practical information in a clear and straightforward manner. Although the multiplicity and variety of musculoskeletal disorders may make learning this subject seem daunting, an understanding of the anatomy and basic science pertaining to the musculoskeletal system, combined with fundamental principles of evaluation and treatment, can guide most diagnostic and therapeutic interventions. Therefore, each chapter of this text begins with relevant basic science to lay the foundation for understanding the pathophysiology, diagnosis, and treatment of the clinical conditions. Because knowledge of anatomy is crucial to the evaluation and treatment of musculoskeletal conditions, this component of basic science has received particular emphasis. All of the authors owe a great debt to Frank H. Netter, MD, the medical illustrator who created the majority of the illustrations in this book. Dr. Netter’s legacy, and his importance in medical education, cannot be overstated. Through his art, Dr. Netter has been a mentor to thousands of physicians and allied health professionals. His precise and beautifully rendered depictions of the human body in health and illness communicate, as no writer can, the essential concepts of basic science and applied medicine that every student must learn. It was Dr. Netter’s belief that a medical illustration is of little value if it does not provide the student with an essential point that has application in the practice of medicine. Examination of any of Dr. Netter’s works in this book will demonstrate his dedication to that principle. Although much of Dr. Netter’s work is just as relevant today as it was when he created it, new techniques and procedures developed since his death in 1991 have caused us to call upon the talents of his successors, particularly John A. Craig, MD, and Carlos A. G. Machado, MD. As will be seen from their work, these artists, trained in the Netter tradition, faithfully uphold the high standards that Dr. Netter set. The authors and illustrators hope that Netter’s Orthopaedics will be a valuable resource for the many individuals who care for patients with these often complex and challenging conditions. Walter B. Greene, MD

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Acknowledgments I would like to acknowledge the staff at Saunders who worked on this book and, in particular, Paul Kelly and Greg Otis who coordinated the development of this project, Jennifer Surich who managed the editorial process, Jonathan Dimes who directed the art program, and Marybeth Thiel for providing assistance and support throughout all stages of the project. I would also like to thank Mary Berry, development editor. Their extraordinary patience and skills were pivotal in this publication.

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List of Contributing Authors Walter B. Greene, MD OrthoCarolina Charlotte, NC

Derrick J. Fluhme, MD Associate Partner South Hills Orthopaedic Surgical Associates St. Clair Hospital Pittsburgh, PA

Roy K. Aaron, MD Professor Department of Orthopaedics Brown University School of Medicine Providence, RI

Freddie H. Fu, MD David Silver Professor and Chairman Department of Orthopaedic Surgery University of Pittsburgh School of Medicine Pittsburgh, PA

Jeffrey O. Anglen, MD, FACS Professor and Chairman Department of Orthopaedics Indiana University Indianapolis, IN

Barry J. Gainor, MD Professor Department of Orthopaedic Surgery University of Missouri Hospital and Clinics Columbia, MO

Judith F. Baumhauer, MD Professor of Orthopaedics, Chief of Division of Foot and Ankle Surgery Department of Orthopaedics University of Rochester School of Medicine and Dentistry Rochester, NY

Lawrence C. Hurst, MD Professor and Chairman Department of Orthopaedic Surgery Stony Brook University Stony Brook, NY

Philip M. Bernini, MD Professor of Orthopaedic Surgery Department of Orthopaedics Dartmouth-Hitchcock Medical Center Lebanon, NH

Lee D. Kaplan, MD Assistant Professor Department of Orthopaedics University of Wisconsin Madison, WI

Eric M. Bluman, MD, PhD Assistant Clinical Instructor Department of Orthopaedic Surgery Brown University School of Medicine Providence, RI

Keith Kenter, MD Assistant Professor and Director of Resident Education Department of Orthopaedic Surgery University of Cincinnati Cincinnati, OH

Susan V. Bukata, MD Orthopaedic Research Fellow Department of Orthopaedics University of Rochester Medical School Rochester, NY

John D. Lubahn, MD Department Chair Program Director Department of Orthopaedics Hamot Medical Center Erie, PA

Michael G. Ehrlich, MD Vincent Zecchino Professor and Chairman Department of Orthopaedics Brown University School of Medicine Providence, RI

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List of Contributing Authors Vincent D. Pellegrini Jr., MD James L. Kernan Professor and Chair Department of Orthopaedics University of Maryland School of Medicine Baltimore, MD

Peter G. Trafton, MD, FACS Professor and Vice Chairman Department of Orthopaedic Surgery Brown University School of Medicine Providence, RI

Michael S. Pinzur, MD Professor of Orthopaedic Surgery and Rehabilitation Department of Orthopaedic Surgery and Rehabilitation Loyola University Medical Center Maywood, IL

Edward D. Wang, MD Assistant Professor Department of Orthopaedic Surgery Stony Brook University Hospital and Health Sciences Center Stony Brook, NY D. Patrick Williams, DO Clinical Professor Orthopaedic Residency Program Hamot Medical Center Erie, PA

David T. Rispler, MD Assistant Professor River Valley Orthopaedics Michigan State University Grand Rapids, MI

David J. Zaleske, MD Surgical Director, Orthopaedics Department of Orthopaedics Children’s Hospitals and Clinics Minneapolis and St. Paul, MN

Randy N. Rosier, MD, PhD Wehle Professor and Chair Department of Orthopaedics University of Rochester Medical School Rochester, NY

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one Embryology and Formation of Bone David J. Zaleske, MD

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Chapter 1

A

n understanding of embryology facilitates the study of postnatal anatomy and the treatment of patients with congenital malformations. Furthermore, as research elucidates the fascinating but complex embryologic process, it has become clear that many genes and transcription factors involved in movement from the genome to a three-dimensional organism are phylogenetically conserved. This complex and highly interactive process includes normal cytodifferentiation and morphogenesis, and it is recapitulated, at least in part, in the healing of injuries. (Note: Bone is the only tissue that regenerates completely after injury [fracture].) A better understanding of development should allow more precise treatment of many illnesses and, ultimately, tissue engineering with regeneration of specific organs. disc (gastrula). Mesoderm develops from two thickenings of ectoderm. The primitive knot (node) forms a midline cord of mesoderm, known as the notochord. This primitive streak gives rise to the rest of the mesoderm, including the cardiogenic mesoderm, which separates and is located in front of the oropharyngeal membrane. Gastrulation is complete when the mesoderm condenses into three, initially connected columns that flank the notochord: the paraxial columns (future somites), the intermediate mesoderm, and the lateral plates (Figure 1-2). Mesoderm that surrounds the columns becomes mesenchyme, the loose embryonic connective tissue that surrounds structures. Shaping of the embryo involves bending of the amnion around and under the gastrula (Figure 1-3). Concurrently, folding of the ectoderm initiates development of the nervous system, and somites in the paraxial mesoderm initiate development of the axial skeleton. The gut is formed from a tube of endoderm. The lateral plate extends and splits to form the lining of the coelomic cavities. The superior portion of the lateral plate joins with the surface ectoderm to form the ventrolateral body wall somatopleure, which ultimately develops into the skin, connective tissue, striated muscle, and bone in the limbs and some parts of the body wall. The inferior portion of the lateral plate joins with the endoderm to form the splanchnopleure, which forms the walls of visceral organs and their suspending mesenteries. The mesodermal notochord and the paraxial columns induce ectodermal tissue to form the neural plate, thus beginning the process of

CELL DIVISION AND THE MAIN EMBRYONIC PERIOD The 9 months of prenatal human development can be divided into a period of cell division (weeks 1 and 2), a main embryonic period (weeks 3 to 8), and a fetal period (encompassing the last 7 months). Approximately 60 hours after fertilization, the zygote has progressed to a morula (“little mulberry”), a ball of cells that continues cell division as it travels through the uterine tube to the uterine cavity; it transitions to the fluid-filled blastocyst at approximately day 5. The blastocyst develops an inner cell mass (embryoblast) and an outer trophoblast as it adheres and then is implanted within the posterior wall of the endometrium of the uterus. By the end of week 2, the embryo is a two-layered cell disc of endoderm and ectoderm (Figure 1-1). The embryonic period progresses from gastrulation to folding of the embryonic disc and eventual formation of the primordia of all organ systems. It is a very dynamic period of development and morphogenesis, in which masses of cells coalesce, migrate, and remodel (programmed cell death is included). Because this is the most active phase of differentiation, abnormalities of development that occur in the embryonic period usually result in major birth defects. The cardiovascular system is the first organ system to function at day 21/22. At that time, the embryo is too large for diffusion to satisfy the nutritional needs of the embryo. Gastrulation is the production of mesoderm during the third week that changes the bilaminar embryonic disc into a trilaminar

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Embryology and Formation of Bone Figure 1-1: Cell Division: The First Two Weeks Myometrium

Four-cell stage (approx. 40 hr)

Early morula (approx. 80 hr)

Two-cell stage (approx. 30 hr)

Endometrium Advanced morula (4 days)

Ovary

Blastocyst (approx. 5 days) Early implantation (approx. 61/2 days)

Fertilization (12 to 24 hr) Developing follicles

Embryoblast (inner cell mass)

Mature follicle

Discharged ovum Extraembryonic mesoderm Yolk sac Endoderm

Exocoelomic cyst

Ectoderm Amniotic cavity Connecting stalk Cytotrophoblast Syncytiotrophoblast

Extraembryonic coelom

Endometrium Approximately 15th day

neural tube and notochord into the somatopleure. Bone development of the axial skeleton begins with mesenchymal condensations in the sclerotome. Cells from the mesenchymal primordia differentiate into chondroblasts, which become the cartilaginous precursors of the axial skeleton and bones at the base of the cranium (Figure 1-4). Enchondral ossification converts these cartilage templates into various bones. Most bones of the skull and part of the clavicle develop through intramembranous (mesenchymal) ossification with direct formation of bone in mesenchyme derived from the neural crest. At each level, the somites migrate ventrally to incorporate the notochord and dorsally to

neurulation; this plate then folds and invaginates to form the neural tube. Closure of the neural tube advances cranially and caudally. As the neural tube invaginates, ectodermal neural crest cells from each side are joined together. Later, some neural crest cells migrate to form other tissues (Tables 1-1 and 1-2).

HUMAN AXIAL SKELETAL EMBRYOLOGY The axial skeleton includes the vertebrae, ribs, and sternum. Its development is initiated by paired condensations in the paraxial mesoderm—the somites. Each somite differentiates into a sclerotome and a dermomyotome. The sclerotomes separate and migrate around the

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Chapter 1 Figure 1-2: Gastrulation Formation of Intraembryonic Mesoderm from the Primitive Streak and Node (Knot) Ectoderm

Oropharyngeal membrane

Amniotic cavity Notochord Primitive knot (node) Primitive streak Extraembryonic mesoderm Endoderm Migration of cells from the primitive streak to form the intraembryonic mesoderm

Yolk sac cavity Cupola of yolk sac

Oropharyngeal membrane Spreading of intraembryonic mesoderm

Notochord Paraxial column

Cloacal membrane

Intermediate column

Appearance of the neural plate

Lateral plate

cover the neural tube. The precursors of the axial skeleton have formed by the fourth embryonic week. Somites undergo rearrangement by division into superior and inferior halves; then, adjacent superior and inferior halves join together to form single vertebral bones (Figure 1-5). Thus, the vertebral arteries are relocated to the middle of the vertebral body. Vertebral bodies, the posterior bony arch, and vertebral processes have a similar pattern of formation with various dimensions and nuances (refer to Figures 13-2 and 13-4 in Chapter 13). Development of C1 (atlas) differs from that of C2 (axis) in that the body (cen-

trum) of the atlas fuses to the C2 body and becomes the odontoid process (dens). Parts of the somites may fail to segment, migrate, or rejoin appropriately. This failure is the basis for congenital scoliosis, which may be associated with rib fusion at single or multiple levels (see Chapter 13).

Skeletal Muscle and Peripheral Nerve Embryology Similar to the somites, myotomes are paired and segmented. Each segmental myotome is innervated by a spinal nerve. The dermatomes divide into an epimere—the small dorsal segment—and a hypomere—

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Embryology and Formation of Bone Figure 1-3: Folding of the Gastrula and Early Development of the Nervous System Midsagittal section of folding gastrula Notochord in gastrula

Cross section of folding gastrula

Amnion Amnion Connecting stalk Extraembryonic mesoderm Allantois

Oropharyngeal membrane Cardiogenic mesoderm

Cloacal membrane

Yolk sac

Neural crest Neural plate forming neural tube Somite Intermediate mesoderm Intraembryonic coelom Notochord

Yolk sac

Vertebrate Body Plan after 4 Weeks Intermediate mesoderm: Embryonic endoderm Nephrogenic ridge forming gastrointestinal Nephrogenic cord (gut) tube Genital ridge Splanchnopleure Somatic mesoderm (endoderm plus of lateral plate lateral plate mesoderm) Somatopleure (ectoderm plus Amnion tucking lateral plate around the sides mesoderm) of the folding Gut tube embryo Yolk sac (stalk just out of the plane of section)

Splanchnic mesoderm of lateral plate Hepatic diverticulum Septum transversum

Yolk sac stalk and allantois within the umbilical cord

Dermomyotome of somite

Dorsal Views Somites appear (day 20)

Neural groove

Notochord Somite sclerotome surrounds the neural tube and notochord to form vertebral column Spinal nerve Dermomyotome Aorta Dorsal mesentery Ventral mesentery Umbilical cord Amnion against chorion Amniotic cavity Neural tube above notochord

Intermediate mesoderm Embryonic gut tube Yolk sac stalk compressed into umbilical cord

cord Neural plate

Intraembryonic mesoderm

Sclerotome of somite

Intraembryonic coelom Amnion surrounded by surrounding lateral plate the umbilical mesoderm

Amnion pressed against the chorion

Neural plate

Cranial neuropore

Early closure of neural tube (day 21)

Late closure of neural tube (day 22)

1.8 mm

2.0–2.1 mm

Week 3 (late)

Week 4 (early)

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Caudal neuropore

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Chapter 1 Table 1-1

Table 1-2

Ectodermal Derivatives

Mesodermal Derivatives

Primordia

Derivatives

Primordia

Derivatives

Surface ectoderm

Skin epidermis Sweat, sebaceous, and mammary glands Nails and hair Tooth enamel Lacrimal glands Conjunctiva External auditory meatus Oral and nasal epithelium Anterior pituitary Inner ear Lens of eye

Notochord

Induction of neurulation Intervetebral disc nucleus pulposus

Neural tube

Neural crest

Amnion

Paraxial column Somites Myotome Dermatome

Central nervous system, including cranial nerves Retina/optic nerves Posterior pituitary Spinal cord, including lower motor neurons and presynaptic autonomic neurons with associated axons Ganglia and sensory neurons associated with spinal dorsal root and cranial nerves Adrenal medulla cells Melanocytes Bone, muscle, and connective tissue in the head and neck

Bone and cartilage Skeletal muscle Dermis of the skin

Intermediate mesoderm

Gonads Kidneys and ureters Uterus and uterine tubes Upper vagina Ductus deferens, epididymis, and related tubules Seminal vesicles and ejaculatory ducts

Lateral plate mesoderm

Dermis (ventral) Superficial fascia and related tissues (ventral) Bones and connective tissues of limbs Pleura and mesoderm GI connective tissue stroma

Cardiogenic mesoderm

Heart and pericardium

trunk wall muscles, as well as to muscles of the limbs. Myotomes fuse to form individual muscles; therefore, most muscles are innervated by more than one spinal nerve root. Back and abdominal muscles are innervated by multiple spinal nerves, whereas the brachial and lumbosacral plexuses combine multiple spinal nerves into single peripheral nerves that innervate the limb muscles. Limb muscles are divided into (1) ventral extensor compartment muscle groups innervated by anterior division branches of the ventral rami in the brachial and lumbosacral plexus, and (2) dorsal flexor compartment muscle groups innervated by posterior division branches of the ventral rami (Figure 1-6).

Protective bag (with chorion) around the fetus

the larger ventral segment. The epimere is innervated by the dorsal ramus of a spinal nerve, and the hypomere is innervated by the ventral ramus. The epimere is the site of origin of the intrinsic back muscles (ie, splenius group, erector spinae, transversospinalis group). The hypomere gives rise to the lateral and ventral

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Embryology and Formation of Bone

Figure 1-4: Myotomes, Dermatomes, and Sclerotomes Differentiation of somites into myotomes, sclerotomes, and dermatomes Cross section of human embryos A. At 19 days Neural groove

Ectoderm of embryonic disc

Somite

Cut edge of amnion

Mesoderm

Intraembryonic coelom Endoderm (roof of yolk sac)

Notochord

B. At 22 days

Ectoderm

Neural tube

Dorsal aortas

Dermomyotome

Intraembryonic coelom

Sclerotome

Cut edge of amnion

Notochord

Endoderm of gut

Mesoderm C. At 27 days Ectoderm Dermomyotome

Sclerotome contributions

Spinal cord

to neural arch to vertebral body (centrum) to costal process

Dorsal aortas Posterior cardinal vein Mesoderm

Notochord

D. At 30 days

Coelom

Note: Sections A, B, and C are at level of future vertebral body, but section D is at level between developing bodies

Spinal cord Dorsal root ganglion Ventral root of spinal nerve Mesenchymal contribution to intervertebral disc

Ectoderm (future epidermis) Dermatome (future dermis)

Aorta

Myotome

Posterior cardinal vein Coelom

Notochord (future nucleus pulposus) Mesoderm Mesonephric kidney

Dorsal mesentery

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Chapter 1 Figure 1-5: Muscle and Vertebral Column Segmentation Progressive stages in formation of vertebral column, dermatomes, and myotomes Ectoderm

Ectoderm

Dermomyotome

Somite

Sclerotome

Myocoele Sclerotome

Primordium of vertebral body

Notochord

Notochord

Intersegmental artery

Intersegmental artery Ectoderm Vertebral body Dermatome Intervertebral fissure Myotome Intersegmental artery Nucleus pulposus forming from notochord

Segmental nerve Nucleus pulposus

Ectoderm (future epidermis)

Annulus fibrosus of intervertebral disc

Dermatome of subcutaneous tissue (dermis)

Vestige of notochord

Myotome Vertebral body (centrum) Costal process

Intersegmental artery Segmental nerve

Appendicular Skeletal Embryology

continues to progress slightly ahead of lower limb development. Blood vessels develop in the limb buds early and before the development of bone or nerves. During the sixth week of gestation, the distal portion of the limb bud becomes paddle-like, with indentations and rays that ultimately develop into the digits of the hands and feet. Mesenchymal condensations are initially continuous in the extremities. Interzonal re-

Limb development begins as outpouchings (paddle-like extensions) from the somatopleure ventrolateral body wall that appear during the early part of the fifth embryonic week. The limb somatopleure mesenchyme is capped by the apical ectodermal ridge. Upper limb bud mesenchymal condensations appear 1 to 2 days before the lower limb buds appear, and morphogenesis of the upper limb

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Embryology and Formation of Bone Figure 1-6: Development of Epimere and Hypomere Muscle Groups and Their Nerve Innervation Somatic development

Ventral root

Dorsal root

Epaxial muscles Dorsal ramus

Posterior cutaneous nerve

Ventral ramus Posterior division Anterior division

Epaxial muscles Dorsal ramus

Hypaxial muscles (extensors of limb)

Ventral ramus

Hypaxial muscles in thoracic and abdominal wall Hypaxial muscles (flexors of limb)

Lateral cutaneous nerve

Hypaxial muscles (flexors of arm and shoulder)

Anterior cutaneous nerve

genesis and cytodifferentiation. Specific portions of the limb bud direct this process. The zone of polarizing activity (ZPA), an area of mesenchymal cells located at the caudal aspect of each limb bud, directs patterning along the anteroposterior axis (anterior refers to the thumb side and posterior is the little finger) by a gradient of the gene Sonic hedgehog (Shh). Transcription molecules Wnt7a and Lmx-1 are necessary for dorsoventral patterning. Proteins such as syndecan-3, tenascin, and versican mediate the formation of the mesenchymal condensations and their transformation to cartilage. Core binding factor 1 (Cbfa1) and Indian hedgehog (Ihh) are involved in the cartilage maturation process leading to endochondral ossification.

gions form between these condensations. These interzonal regions cavitate to form joints (Figure 1-7). Articular cartilage and intraarticular structures such as ligaments and menisci are formed from interzonal tissue. The upper and lower limb buds rotate in opposite directions during development (Figure 1-8). Therefore, segmental dermatomes within the limbs also rotate and are not organized in the proximal-to-distal linear arrangement found along the trunk. Descriptive embryology at the tissue level is increasingly elucidated at the molecular level (see Figure 1-9). Interaction of transcription factors, growth and inductive factors, and adhesion molecules establishes the information blueprint for bone and joint morpho-

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Chapter 1 Figure 1-7: Joint Development Development of three types of synovial joints

Cartilage (rudiment of bone) Perichondrium

Precartilage condensation of mesenchyme

Joint capsule Circular cleft (joint cavity)

Site of future joint cavity (mesenchyme becomes rarefied)

Periosteum

Perichondrium Cartilage

Articular menisci

Articular disc

Epiphyseal cartilage growth plate Epiphyseal bone Joint capsule Synovial membrane Joint cavity Articular cartilages

Joint cavities

Joint cavity

Epiphyseal bone Interphalangeal joint

Knee joint

Bone Formation

Sternoclavicular joint

Endothelial cells invade the condensation to form a blood supply; then, osteoblasts form new bone—a process that is followed by remodeling (Figure 1-10). Most bones of the calvaria, the facial bones, and, in part, the clavicle and mandible are formed through intramembranous ossification. All other bones (ie, base of the skull, axial skeleton, appendicular skeleton with the exception of the clavicle) develop in the cartilage condensations derived from mesenchymal aggregates. Chondrocytes hyper-

The term bone has two common meanings: (1) it may refer to osseous, or bone, tissue; or (2) it may denote an organ, such as the femoral bone. At the end of the embryonic period and the beginning of the fetal period, the mesenchymal precursors of the skeleton begin to form osseous tissue through two methods. With intramembranous formation, the mesenchymal connective tissue of the neural crest condenses under the influence of specific signals.

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Embryology and Formation of Bone Figure 1-8: Limb Rotation and Dermatomes Preaxial border C7 C8

Upper limb

C6 T1

C3 C4 C5

T2

Postaxial border Preaxial border

L2 L3 L4

Lower limb

L5 S1

S2

Postaxial border At 6 weeks At 6 weeks. Limbs bend anteriorly, so elbows and knees point laterally, palms and soles face trunk

At 8 weeks. Torsion of lower limbs results in twisted or “barber pole” arrangement of their cutaneous innervation

Dorsal surface Postaxial border S1

L5

L4

L3

L2 S2

Preaxial border At 8 weeks

Big toe

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S3

S3

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Chapter 1

Figure 1-9: Growth Factors Limb buds in 6-week embryo Growth factors that influence limb morphology: Fibroblast growth factor-8 (FGF-8)—limb bud initiation Retinoic acid—limb bud initiation FGF-2, 4, and 8—outgrowth of the limbs Bone morphogenetic proteins—apoptosis of cells between digits Sonic hedgehog—establishment of craniocaudal limb axes Wnt-7a—dorsal patterning of the limbs En-1—ventral patterning of the limbs

Apical ectodermal ridge

Zone of polarizing activity Mesenchymal bone precursor

Growth factors that promote tissue development: Bone morphogenetic protein family—bone development Indian hedgehog—bone development Growth/differentiation factor 5—joint formation Transforming growth factor-␤ family—myoblast proliferation Nerve growth factor—sensory and sympathetic neurons Insulin-like growth factor-1 (IGF-1)—general proliferation of limb mesoderm Scatter factor (hepatic growth factor)—myotome cell migration in the limbs

Extensor muscle

Flexor muscle Preaxial compartment

Postaxial compartment Ant. division nerve Post. division nerve

Ventral compartment Flexor muscles Anterior division nerves

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Dorsal compartment Extensor muscles Posterior division nerves

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Embryology and Formation of Bone

Figure 1-10: Intramembranous (mesenchymal) Bone Formation Initial bone formation in mesenchyme Mesenchymal cells Reticular fibers in extracellular fluid of mesenchyme Osteoblasts (from mesenchymal cells) sending out extensions Bundles of collagen fibers laid down as organic osteoid matrix

Lacuna Mineralized bone matrix (organic osteoid and collagen fibers impregnated with hydroxyapatite crystals) Osteocytes (from osteoblasts)

Extensions of osteocytes filling canaliculi

Early stages of intramembranous bone formation Capillaries in narrow spaces

Periosteum of condensed mesenchyme Trabeculae of cancellous (woven) bone lined with osteoblasts forming in mesenchyme

Dense peripheral layer of subperiosteal bone surrounding primary cancellous bone. Both initially consist of woven bone

Bone trabeculae lined with osteoblasts Capillary Nerve fiber

Marrow spaces (primary osteons)

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Chapter 1 trophy within the cartilage anlage. Capillaries invade the central region of the anlage. Enchondral ossification ensues, and the primary ossification center is formed (see Figure 111). Primary centers of ossification most often develop at various prenatal times that are

unique to each bone. Most long-bone primary centers of ossification are present by the eighth week of gestation (Figure 1-12). Some small bones (eg, patella, wrist, midfoot) do not initiate ossification until early childhood.

Figure 1-11: Endochondral Ossification in a Long Bone Growth and ossification of long bones (humerus, midfrontal sections)

Perichondrium Periosteum

At 8 weeks

Proliferating small-cell hyaline cartilage Hypertrophic calcifying cartilage Thin collar of cancellous bone from periosteum around diaphysis

Epiphyseal capillaries

Calcified cartilage

Canals, containing capillaries, periosteal mesenchymal cells, and osteoblasts, passing through periosteal bone into calcified cartilage (primary ossification center) At 9 weeks

Epiphyseal (secondary) ossification center for head

Cancellous endochondral bone laid down on spicules of calcified cartilage

Outer part of periosteal bone beginning to transform into compact bone

Primordial marrow cavities

Central marrow (medullary) cavity Epiphyseal capillary

At 10 weeks

At birth

Greater tubercle

Proximal physis

Epiphyseal ossification centers of lateral epicondyle, medial epicondyle, trochlea, and capitulum Calcified cartilage

Articular cartilage of head

Anatomical neck

Epiphyseal ossification centers for head and greater tubercle

Sites of growth in length of bone Distal physis

Proliferating growth cartilage

Bone of proximal epiphysis

Hypertrophic calcifying cartilage

Proximal metaphysis

Enchondral bone laid down on spicules of degenerating calcified cartilage Enchondral bone laid down on spicules of degenerating calcified cartilage Hypertrophic calcifying cartilage

At 10 years

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Distal metaphysis Bone of distal epiphysis

Articular cartilage of condyles

Proliferating growth cartilage

At 5 years

Diaphysis; growth in width occurs by periosteal bone formation

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Embryology and Formation of Bone

Figure 1-12: Ossification Present in the Newborn Skeleton of full-term newborn Time of appearance of ossification centers (primary unless otherwise indicated) Anterior fonticulus (fontanelle)

Parietal bone (12th week)

Coronal suture

Sphenoid fonticulus (fontanelle)

Frontal bone (9th week)

Squamosal suture

Nasal bone (9th week)

Temporal bone (9th week)

Lacrimal bone (12th week)

Mastoid fonticulus (fontanelle)

Ethmoid bone (12th week)

Occipital bone (9th week) Styloid process

Sphenoid bone (12th week) Maxilla (9th week)

Clavicle (7th–8th weeks)

Zygomatic bone (9th week)

Secondary proximal epiphyseal center of humeral head (8th fetal–1st month postnatal)

Mandible (9th week) Center for hyoid bone (36th week)

Ribs (8th to 9th week) Scapula (8th week)

Intervertebral disc

Humerus (6th–8th weeks) Sternum (8th – 9th week) Vertebral body

Radius (6th–8th weeks)

Triradiate cartilage

Ulna (6th–8th weeks) Carpal cartilages

Large femoral head articulating with shallow acetabulum (2nd– 6th month postnatal)

Metacarpals (2nd–4th months) Phalanges (2nd–6th months)

Pubic symphysis Femur (6th–12th weeks)

Ilium (8th week) Coxal bone

Secondary distal epiphyseal center of femur (36th week)

Ischium (16th week) Pubis (16th week)

Secondary proximal center of tibia (8th fetal–1st month postnatal)

Patella (6th year) Center for talus (4th–8th months)

Tibia (6th–12th weeks)

Metatarsals (2nd–6th months)

Fibula (6th–10th weeks)

Phalanges (2nd–4th months) Center for calcaneus (4th–7th months)

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Chapter 1 The diaphysis is the shaft of a long bone (see Figure 1-11). Metaphyses are the adjacent flared-out regions. Epiphyses are the ends of a long bone. The physis or growth plate, which is located between the metaphysis and the epiphysis of long bones, provides longitudinal growth until the time of skeletal maturity. Growth of small bones and of the epiphysis is promoted by growth cartilage that surrounds these structures. Bone tissue forms within the cartilaginous ends, or chondroepiphyses, of long bones, which are called secondary centers of ossification. In humans, the only secondary center of ossification that forms before birth is the one located at the distal femur, which forms at 36 weeks’ gestation (see Figure 1-12). The appearance of various secondary centers of ossification may be used to determine the biologic or bone age of a given child.

repair, or turnover) is woven bone. At the microscopic level, the osteoid matrix of woven bone reveals an amorphous or patchwork pattern of osteoblasts, osteoid matrix, and randomly oriented collagen fibers. Woven bone remodels internally to lamellar bone. This process requires close coupling of bone formation and bone resorption. Osteoblasts form bone, osteocytes maintain bone, and osteoclasts (specialized macrophages) resorb bone. With successive resorption and formation, woven bone is remodeled into concentric lamellar bone, which is made up of collagen fibers, haversian systems, and interstial lamellae aligned for maximum strength per volume of bone. The cells that deposit newly formed bone, the osteoblasts, become surrounded by bone matrix and develop into mature osteocytes, which form cellular extensions for intercellular transport (Figure 114).

BONE STRUCTURE AND HISTOLOGY Bone Growth and Remodeling

Bone as an organ consists of trabecular and cortical bone (Figure 1-13). Both types of bone contain the same cell and matrix elements, but structural and functional differences between the two are observed. Cortical bone, sometimes called compact bone, is denser (80% to 90% of the volume is calcified) and stronger than cancellous bone. The diaphyses of long bones primarily comprise cortical bone. Thus, shafts of long bones have a relatively small cross-sectional area that can accommodate the bulk of surrounding musculature while continuing to resist lifting and weight-bearing stresses. Cancellous bone, sometimes called trabecular bone, is a network of bony trabeculae or struts that are aligned to counteract stress and support articular cartilage. Only 15% to 25% of the medullary canal is made up of cancellous bone; the remaining volume is occupied by marrow, blood vessels, fibrous tissue, and fatty tissue. The metaphysis and the epiphysis primarily comprise cancellous bone covered by a relatively thin layer of cortical bone. Growth of the entire human body involves a net accumulation of bone mass. Newly formed bone (during development, fracture

Cartilaginous growth regions throughout the skeleton are programmed to add to the size of bones as organs. Absolute and relative changes in the size and shape of bones throughout the fetal and postnatal periods cause the changes in body size and proportion that result in growth of the organism. This occurs in single bones and regions. For example, the calvaria is much larger than the facial skeleton at birth (the ratio is 8:1 in a newborn compared with 2:1 in an adult). Similarly, upper limb growth is more rapid during early gestation, and it is not until birth that the length of the lower limbs is equal to that of the upper limbs. The physis is organized to move cells along columns in a progression of cytodifferentiation (Figure 1-15). Cells at similar levels in adjacent columns resemble one another and constitute zones. Growth or movement occurs from the small cell phenotype on the epiphyseal side of the physis to hypertrophic cells on the metaphyseal side. The blood supply to the reserve and the proliferating zones is derived from the epiphyseal artery, whereas the hypertrophic zone is avascular. Metaphyseal vessels supply

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Embryology and Formation of Bone

Figure 1-13: Histology of Bone Cortical (compact) bone Subperiosteal outer circumferential lamellae Periosteum

Endosteal surface Trabeculae project into central medullary (marrow) cavity

Interstitial lamellae Capillaries in haversian canals Perforating fibers Periosteal vessels

Inner circumferential lamellae

Trabecular bone (schematic) On cut surfaces (as in sections), trabeculae may appear as discontinuous spicules Osteoid (hypomineralized matrix) Active osteoblasts produce osteoid Inactive osteoblasts (lining cells) Marrow spaces contain hematopoietic cells and fat Osteoclasts (in Howship’s lacunae) Osteocytes Trabeculae Section of trabecula (schematic) Active osteoblasts Osteoid (hypomineralized matrix) Inactive osteoblasts (lining cells) Osteocytes Osteoclast (in Howship’s lacuna)

17

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Chapter 1 Figure 1-14: Composition of Lamellar Bone Osteocytes Originate from osteoblasts

Osteoblasts (Matrix-forming cells) Originate from mesenchyme Hypomineralized matrix (osteoid) Mineralized matrix (bone)

Osteoclasts Originate from bone marrow–derived macrophage- monocyte line

which lay down bone on the calcified cartilage armatures. Osteoclasts immediately begin to remove the first-formed woven bone and cartilaginous septa, and osteoblasts produce more mature cancellous bone in the secondary spongiosa. Remodeling is disrupted in osteopetrosis, a genetic disease characterized by dysfunction of the osteoclasts. In osteopetrosis, the bones appear dense or like “marble” on radiographs because the primary spongiosa with its calcified cartilage cores persists throughout the bone as an organ. Osteopetrotic bone, however, is markedly weaker than normal bone because the deficiency in internal remodeling does not permit the production of stronger lamellar bone. The physis directs growth along the longitudinal axis. The total longitudinal growth of a bone is the height gained by a hypertrophic chondrocyte multiplied by the aggregate of all such cellular activity. Different growth plates contribute different percentages to overall longitudinal growth. For example, the distal femoral physis contributes 70% to the growth of the femur, whereas the proximal femoral physis contributes 30%. The circumferential growth of bone occurs by appositional intramembranous formation.

the area of primary spongiosa but do not enter the physis. Cells of the reserve zone participate in the production of matrix and the storage of metabolites that are required farther along the growth plate (see Figure 1-15). Stem cells for longitudinal growth reside in the upper proliferative zone. Newly formed cells progress through the proliferative zone to the hypertrophic zone, where chondrocytes enlarge and the proteoglycan matrix is degraded to disaggregated, short-chain protein polysaccharides—a process that allows the matrix to become calcified. In the upper portion of the hypertrophic zone, chondrocytes switch to anaerobic glycolysis and store calcium in the mitochondria. In the lower portion of the hypertrophic zone, the energy is depleted and calcium is discharged into the matrix, which permits hydroxyapatite crystal formation and provisional calcification. Progressive calcification forms longitudinal septa, on which enchondral ossification can occur. Because calcified cartilage matrix has more calcium per unit volume than does bone, the zone of provisional calcification is seen as a dense band on radiographs. In the primary spongiosa region of the metaphysis, blood vessels bring in osteoblasts,

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Embryology and Formation of Bone Figure 1-15: Close-up View of Epiphysis, Physis, and Adjacent Metaphysis Articular cartilage Epiphyseal growth plate (poorly organized) Secondary (epiphyseal) ossification center Reserve zone

Epiphyseal artery

Proliferative zone

Ossification groove of Ranvier

Maturation zone

Perichondral fibrous ring of La Croix

Degeneration zone

Hypertrophic zone

Zone of provisional calcification

Perichondral artery

Primary spongiosa Metaphysis

Last intact transverse cartilage septum

Secondary spongiosa

Metaphyseal artery

Periosteum

Diaphysis Cartilage Calcified cartilage Bone

Nutrient artery Peripheral fibrocartilaginous element of growth plate Load

Perichondral fibrous ring of La Croix (provides support) Ossification groove of Ranvier (provides cells for growth in width) Illustration of how perichondral fibrous ring of La Croix acts as limiting membrane and provides mechanical support to cartilaginous growth plate

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Chapter 1 Figure 1-16: Physis (Growth Plate) Zones Structures

Histology

Functions

Blood supply

PO2

Cell (chondrocyte) health

Cell respiration

Cell glycogen

Anaerobic

High concentration

Aerobic

High concentration (less than in above)

Secondary bony epiphysis Epiphyseal artery Matrix production Reserve zone Storage

Matrix production

Poor (low)

Good, active. Much endoplasmic reticulum, vacuoles, mitochondria

Excellent Excellent

Cellular proliferation (longitudinal growth)

Fair

Excellent. Much endoplasmic reticulum, ribosomes, mitochondria. Intact cell membrane

Hypertrophic zone

Degenerative zone

Zone of provisional calcification

Calcification of matrix

Metaphysis

Primary spongiosa

Vascular invasion and resorption of transverse septa Bone formation

Secondary spongiosa Branches of metaphyseal and nutrient arteries

Poor (very low)

Closed capillary loops

Poor

Good

Good

Remodeling Internal: Removal of cartilage bars, Excellent Excellent replacement of fiber bone with lamellar bone External: Funnelization

20

Progressive deterioration

Anaerobic glycolysis

Anaerobic glycolysis

Cell death

Progressive reversion to aerobic

Nil Last intact transverse septum

Still good Progressive decrease

Preparation of matrix for calcification

Progressive decrease

Maturation zone

Glycogen consumed until depleted

Poor (low)

Progressive change to anaerobic

Proliferative zone

Vessels pass through, do not supply this zone

Aerobic

Nil

?

?

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Embryology and Formation of Bone In long bones, appositional growth results from lining of the periosteum by osteoblasts and is accompanied by concomitant osteoclastic resorption of the endosteum and widening of the medullary cavity. The broad metaphysis increases the surface area of the articular surfaces, thus decreasing the unit load on the cartilage. This funnelization of the metaphysis occurs through progressive intramembranous bone formation and subsequent osteoclastic resorption at the cutback zone. Metaphyseal cancellous bone with a thin cortex gradually transitions to typical diaphyseal compact cortical bone.

Practical Applications of Physiologic Principles

cause woven bone is biomechanically inferior to lamellar bone the initial callus at the organ level compensates through its distribution around a larger radius, which can better resist bending and torsional moments. Internal remodeling, which continues for months, reconstitutes lamellar cortical bone, tubular proportions, and the intramedullary canal. Fracture repair and bone remodeling are discussed in greater detail in Chapter 9. An understanding of the scientific basis of bone growth and remodeling forms the basis for provision of good clinical care. Future discoveries that will lead to control of the molecular events that mediate bone growth and remodeling will result in better clinical care.

The unique regenerative capacity of bone at the tissue level in fracture repair is retained throughout life. The capacity of bone to regenerate shape at the organ level also exists throughout life but is especially notable in the immature skeleton. Displaced fractures treated by closed means typically heal with a surrounding collar of callus that is formed by the periosteum. This initial callus, which includes woven bone at the tissue level, is deployed broadly around the fracture site. Be-

Cochard LR. Netter’s Atlas of Human Embryology. Teterboro, NJ: Icon Learning Systems; 2002. Dietz FR, Morcuende JA. Embryology and Development of the Musculoskeletal System. In: Morrisey RT, Weinstein SL, eds. Lovell and Winter’s Pediatric Orthopaedics, 5th edition. Philadelphia, Pa: Lippincott Williams and Wilkins; 2001:1–31. Schneider RA, Miclau T, Helms JA. Embryology of Bone. In: Fitzgerald RH, Kaufer H, Malkani AL, eds. Orthopaedics. Philadelphia, Pa: Mosby; 2002:143–146.

ADDITIONAL READINGS

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two Metabolic Bone Disease and Osteonecrosis Susan V. Bukata, MD, and Randy N. Rosier, MD, PhD

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Chapter 2

E

ach individual bone has a structure that is uniquely designed for local stability and function. Bone, that is, the skeleton, is an organ that is the major storehouse for calcium and phosphorus, and it also is a site of active hematopoietic tissue. Metabolic disease can alter normal bone deposition through conditions that alter the process of bone formation or bone resorption, or through disorders that affect both formation and resorption. Bone formation may be altered during the process of osteoblastic organic matrix (osteoid) formation or during the subsequent process of osteoid mineralization. Calcium and phosphate are critical in bone formation, and during the mineralization of osteoid, calcium and phosphate are transformed from the fluid phase to hydroxyapatite crystals. Serum ionized calcium levels are crucial in cardiac and skeletal muscle function and neuronal activity. Therefore, despite daily fluctuations in calcium intake, ionized calcium concentrations are maintained at a remarkably constant level at between 4.5 and 5.0 mg/dL by input/output exchanges in the gut, kidney, and bone that are regulated by parathyroid hormone (PTH), 1,25-dihydroxyvitamin D3 (1,25-D3), and calcitonin (Figures 2-1 and 22). The initial response to hypocalcemia is an increase in PTH secretion by the parathyroid gland, and the initial response to hypercalcemia is an increase in calcitonin secretion by the thyroid gland. These changes in PTH and calcitonin are augmented by changes in 1,25D3 levels to rapidly correct ionized calcium levels. A seven-transmembrane, G-protein–coupled receptor found on many cell types is responsible for sensing extracellular ionized calcium. Therefore, an elevated calcium level also has a direct effect on inhibition of renal cell calcium resorption and osteoclast activity. The skeleton is the major reservoir of calcium. Calcium ions mobilized by bone resorption are replaced by bone formation. However, if bone formation does not equal bone resorption, the skeleton will be weakened (Figure 2-3). Metabolic bone disease affects the entire skeleton, but because certain areas of the skeleton are under increased stress, patients with metabolic bone disease frequently have symptoms such as back pain related to compression fracture of the thoracic area and lumbar spine, as well as leg pain secondary to

bowing of the femur and/or tibia and pathologic fracture of the lower limbs. Some generalized disorders of bone are influenced by the local environment; therefore, patients may develop scattered, symptomatic lesions but have normal form and function of uninvolved bones.

HYPERPARATHYROIDISM Primary hyperparathyroidism occurs when PTH is produced in excess, even with normal or elevated serum calcium levels (Figure 2-4). It is generally caused by an adenoma of the chief cells of a single parathyroid gland. A less common cause is hyperplasia of all four parathyroid glands. Patients with type I multiple endocrine neoplasia also may have parathyroid hyperplasia. Hyperparathyroidism is caused by carcinoma in less than 0.5% of cases. No specific genetic defect has been identified, but certain chromosomal alterations are associated with primary hyperparathyroidism. Some patients have inactivation of tumor suppressor genes on either chromosome 11 or chromosome 1. Other patients have a genetic rearrangement, with the PRAD 1 protooncogene placed near the genes that control PTH production. In this situation, cell growth is stimulated when normal PTH production is stimulated, leading to adenoma formation and excessive production of PTH. Primary hyperparathyroidism is relatively common, with an incidence of 1 in 1000. The disease can occur at all ages but is more common after 50 years. Women predominate at a 3:1 ratio. A 4- to 5-fold increase in incidence

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Metabolic Bone Disease and Osteonecrosis Figure 2-1: Normal Calcium and Phosphate Metabolism Ca++ and PO4 Vit. D2 in food

Sun

Parathyroid hormone (PTH)

Ultraviolet light

Parathyroid glands

Skin Vit. D3 Serum and extracellular fluid

Vit. D25hydroxylases

Inhibition

Stimulation

Liver

25-D3 Ca++

Ca +

PO

+

PO4

Ca++

1,25-D3

PO4

++

PO

Ca

1,25-D3 promotes absorption of Ca++ and PO4 from intestine

4

4

25-D3 Stimulation 1-␣-hydroxylase

Inhibition 1,25-D3 Ca++ PO4 PTH

Kidney

PTH increases production of 1,25-D3, promotes Ca++ reabsorption, inhibits PO4 reabsorption 1,25-D3 necessary for normal mineralization of bone

25

Ca++

PO4

PTH promotes osteoclastic resorption of bone (Ca++, PO4, and matrix)

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Chapter 2 Figure 2-2: Regulation of Calcium and Phosphate Metabolism Parathyroid hormone (PTH) (peptide)

1,25-D3 (steroid)

Calcitonin (peptide)

Hormone

From proximal tubule of kidney

From chief cells of parathyroid glands

Factors stimulating production

From parafollicular cells of thyroid gland

Elevated PTH Decreased serum Ca++

Decreased serum Ca++

Elevated serum Ca++

Decreased serum Pi

Factors inhibiting production

Decreased PTH

Elevated serum Ca++

Elevated serum Ca++

Elevated 1,25(OH)2D

Elevated serum Pi

No direct effect Acts indirectly on bowel by stimulating production of 1,25(OH)2D in kidney End organs for hormone action

Decreased serum Ca++

Strongly stimulates intestinal absorption of Ca++ and Pi

Intestine

Stimulates 25(OH)D-1α-OHase in mitochondria of proximal tubular cells to convert 25(OH)D to 1,25(OH)2D

Increases renal calcium excretion

Increases fractional reabsorption of filtered Ca++ Kidney

Bone

Net effect on calcium and phosphate concentrations in extracellular fluid and serum

Promotes urinary excretion of Pi Increases bone resorption indirectly by upregulating osteoblast production of autocrine cytokines such as interleukin-6, which results in increased production of paracrine cytokines that stimulate osteoclast production and activity. PTH also has an anabolic effect on osteoblasts that results in overproduction of osteoid in chronic hyperparathyroidism

Increased serum calcium Decreased serum phosphate

26

Stimulates bone resorption in a similar fashion to PTH and also other membrane receptors

Inhibits bone resorption by direct inhibition of osteoclast differentiation and activity

Increased serum calcium

Decreased serum calcium (transient)

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Metabolic Bone Disease and Osteonecrosis Figure 2-3: Dynamics of Bone Homeostasis Cortical (compact)

Trabecular

Cortical (compact)

Active osteocytes maintain bone

Periosteum

Lining cells (inactive osteocytes)

Endosteum Osteoclasts resorb bone

Osteoid (hypomineralized matrix) Osteoblasts form osteoid (bone matrix)

Lack of weight-bearing activity or decreased use of antigravity muscles

Testosterone

Pituitary

Growth hormone (normal level)

Thyroid

Thyroid hormone (normal level)

Intake Ca 800 mg/day

500 mg/day of Ca++

Testes

Promote net bone resorption (osteoclastic bone resorption > osteoblastic bone formation)

Glucocorticoids (decrease Ca++ absorption from intestine)

Thyroid

PTH Stimulated by low serum Ca++ and acidosis

Ca Ca Amino Adequate intake acids and absorption of ++ Ca needed to maintain blood and tissue-fluid levels. Levels regulated by PTH, 1,25(OH)2D, 8000 mg/day and calcitonin filtered

Parathyroids

Acidosis

Ca

Protein (urea)

Ca 500 mg/day absorbed

Ca

Adrenal cortex

Excess hormone

500 mg/day of Ca++

Estrogen Ovaries

Promote net bone formation (osteoblastic bone formation > osteoclastic bone resorption)

Vitamin C and other cofactors needed for osteoid (matrix) formation

Weight-bearing activity and use of antigravity muscles

1,25(OH)2D promotes Ca++ absorption Intestine

Ca 300 mg/day returned to intestine

Ca

7800 mg/day reabsorbed

Amino acids (adequate intake and absorption of protein needed for bone matrix formation)

Ca Renal tubule

Blood and tissue fluid 600 mg/day lost in stool

Ca

Ca 800 mg/day (loss=intake)

27

++ * All Ca are Ca

200 mg/day lost in urine

Ca

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Chapter 2 Figure 2-4: Pathologic Physiology of Primary Hyperparathyroidism Adenoma

Hyperplasia

Carcinoma

(~85% of cases)

(~15% of cases)

(rare)

Skin

Gut

Ca++ Pi

Vit. D

Liver Parathyroid hormone (PTH) elevated

25(OH)D Ca++ Pi

Serum and extracellular fluid

High 1,25(OH)2D promotes absorption of Ca++ from gut

Renal tubule

Ca++

Ca++

Ca++ filtration increased

Serum Ca++ increased; fails to suppress PTH secretion Pi Pi

Pi

Serum Pi low or normal

25(OH)D normal 1,25(OH)2D elevated PTH Ca++ Pi

Ca++ Pi

Ca++ Pi

High PTH promotes Ca++ reabsorption, inhibits Pi reabsorption. Also promotes conversion of 25(OH)D to active metabolite 1,25(OH)2D

Ca++ Pi Nephrocalcinosis

Ca++ Pi

Larger amount of Ca++ filtered into tubule exceeds its resorptive capacity and results in hypercalciuria

Compensatory increase in osteoblastic activity with variable rise in serum alkaline phosphatase

Ca++ Pi

High PTH stimulates osteoclastic resorption of bone (Ca++, Pi, and matrix)

Calculi Urine Ca++ elevated

Variable reduction in bone density. In rare, severe cases, cysts and brown tumors (due to osteitis fibrosa cystica) and subperiosteal resorption

28

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Metabolic Bone Disease and Osteonecrosis Figure 2-5: Clinical Manifestations of Primary Hyperthyroidism Moderate-to-severe, symptomatic: Uncommon (serum Ca++ often >12 mg/100 mL)

Mild, asymptomatic: Most common (serum Ca++ often 2 mm) of the head or angulated (usually >30°) of the neck.

Excision of fragment or entire radial head via posterolateral incision. Radial head should be replaced with a prosthesis in patients with certain complex fractures.

range-of-motion exercises. Type II fractures with acceptable fracture patterns should be treated with open reduction and internal fixation. In equivocal situations, particularly if the patient has a low-demand occupation, type II injuries can be treated nonoperatively, with delayed excision of the radial head if persistent pain or significant limitation of forearm rotation occurs. Uncomplicated type III fractures should be treated with excision of the radial head. When radial head fractures are associated with dislocation of the elbow and severe ligament injury or disruption of the forearm

Type III: severely comminuted fractures of the radial head and neck.

Comminuted fracture of radial head with dislocation of distal radioulnar joint, proximal migration of radius, and tear of interosseous membrane (Essex-Lopresti fracture)

interosseus, the fragments should be removed and the radial head replaced by a prosthesis. Results of treatment are uniformly good for type I fractures and often satisfactory for simple type II and type III fractures. Potential complications include loss of motion, elbow instability, posttraumatic arthritis, myositis ossificans, and distal radioulnar symptoms.

Olecranon Fractures Olecranon fractures are caused by a direct blow or an indirect avulsion injury (eg, a fall on an outstretched hand with the elbow

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Elbow and Forearm Figure 15-17: Olecranon Fracture Displaced fracture of olecranon requires open reduction and internal fixation

Open reduction of olecranon fracture. Fracture secured with two Kirschner wires plus tension band wire passed around bent ends of Kirschner wires and through drill hole in ulna

type 3, and the ulnar fracture is angulated in the direction of the radial head dislocation. In a type 4 injury, the proximal radius and ulna are fractured, and the radial head is dislocated anteriorly. Type 1 and type 2 account for 70% to 90% of Monteggia injuries. Type 1, the most common, may be caused by a direct blow or a fall on the outstretched hand with the forearm in full pronation. Type 2 injuries occur most often in adults. Radial nerve injury, often isolated to the posterior interosseous branch, is relatively common in Monteggia lesions. These injuries are frequently misdiagnosed, particularly in children, in whom palpation of an anteriorly displaced radial head is more difficult. Another common mistake is to recognize the fracture of the ulna but miss the dislocated radial head, either because the radiograph did not adequately show the elbow or because the evaluator did not understand that on both anteroposterior and lateral radiographs, a line through the axis of the proximal radius and the radial head should pass through the capitellum. If recognized early, Monteggia injuries in children usually can be treated by closed reduction and cast immobilization. Adults require open reduction and internal fixation of the ulnar fracture. When the ulna is anatomically reduced, the radial head typically reduces and becomes stable without additional surgical intervention.

slightly flexed while the triceps is contracting). Avulsion injuries create a transverse or slightly oblique fracture pattern. Direct blows typically are associated with some degree of comminution. A palpable defect is present with displaced fractures. The skin should be evaluated carefully for possible open injury. Radiographs should be scrutinized for detection of associated fractures of the radial head or coronoid process. Nondisplaced fractures can be treated with a splint or cast (Figure 15-17). The elbow is positioned in approximately 45°of flexion to relax the pull of the triceps. Displaced fractures require open treatment. Tension band wiring, which transforms distraction forces into compression, is the most common form of fixation. Plate fixation is required for fractures that extend to the coronoid or ulnar shaft. Comminuted fractures can be managed by excision of the fragments and repair of the triceps tendon. If the collateral ligaments are intact, as much as 70% of the proximal olecranon can be excised without resultant instability.

Monteggia Fractures/Dislocations The Monteggia fracture/dislocation is a fracture of the ulna that is associated with dislocation of the radial head (Figure 15-18). Bado classified these injuries into four types. The radial head is dislocated anteriorly in type 1, posteriorly in type 2, and laterally in

327

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Chapter 15 Figure 15-18: Monteggia Fracture/Dislocation Type 1 Monteggia fracture/dislocation with anterior dislocation of radial head and anterior angulation of proximal or middle third ulna fracture

Less common type 2 Monteggia fracture/dislocation with ulna fracture angulated posteriorly and radial head dislocated posteriorly

Fracture of ulna treated with open reduction and internal fixation using compression plate and screws. After reduction of ulna, radial head spontaneously reduced Preoperative radiograph shows Type I Monteggia fracture/dislocation

Postoperative radiograph shows compression plate in place

with

C.A. Luce

Anconeus m.

Annular ligament (sutured)

Extensor carpi ulnaris m.

If radial head does not reduce after angulation of ulna is corrected, open reduction of radial head dislocation and repair of annular ligament are needed. Typically, this is done through a separate incision between the anconeus and extensor carpi ulnaris muscles

Radius Supinator m. (incised) Ulna

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Elbow and Forearm Fractures of the Diaphysis of the Radius and Ulna

Fractures About the Elbow in Children

In adults, motor vehicle accidents or falls from a considerable height usually cause both-bone forearm fractures. Displacement, angulation, and shortening are common when both the radius and the ulna are fractured. A direct blow usually fractures only one bone—typically the ulna, as the forearm is positioned to stop the oncoming injury (“nightstick” fracture). Because only one component of the “structural rectangle” has been disrupted, direct-blow injuries of the ulna or radius are minimally displaced and usually can be treated by nonoperative methods. However, a fall on the outstretched hand with the forearm pronated can cause a fracture at the middle/distal third junction of the radius with associated disruption of the distal radioulnar ligaments (Galeazzi fracture). In this injury, two sides of the structural rectangle are injured; therefore, the fracture of the radius is displaced and unstable. Displaced forearm fractures in adults are best treated by open reduction and internal fixation. This procedure minimizes the relatively high rates of malunion, nonunion, and loss of forearm rotation associated with management by closed techniques. Bone grafting should be considered with comminution of more than a third of the diameter of the bone or with a segmental fracture.

Fractures about the elbow are more common in children than in adults, and treatment in children often differs from treatment of injuries at similar locations in adults. Occult fractures are more common in children, particularly young children, in whom low-impact falls are common. A significant portion of the bone in young children has not ossified, so some fractures are more difficult to visualize on initial radiographs. A child who has a history of injury, tenderness about the elbow, and a positive posterior fat pad sign should be assumed to have an occult fracture and should be immobilized for 3 weeks.

Supracondylar Fractures Fracture of the supracondylar humerus is the most common elbow fracture in children. The typical age group is 2 to 12 years—a time when a child is able to hyperextend the elbow. The typical mechanism of injury is a fall on the outstretched arm with the elbow in full extension. The distal fragment is displaced posteriorly (Figure 15-19). The less common flexion injuries cause anterior displacement of the distal humerus and are more common in the adolescent years. Supracondylar fractures are associated with a relatively high incidence of neurovascular injury. Usually only one nerve is injured. The median, radial, or ulnar nerve may be

Figure 15-19: Supracondylar Fracture of the Humerus Extension type Posterior displacement of distal fragment (most common). In general, supracondylar fractures occur more frequently in children

329

Flexion type Anterior displacement of distal fragment (uncommon in children)

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Chapter 15 involved. Median nerve injury, the most common type, may be limited to the anterior interosseous branch. Compartment syndrome of the forearm may occur, and failure to treat this problem in a timely fashion may result in Volkmann ischemic contractures of the wrist and fingers. Malunion with resultant cubitus varus is another potential complication. To minimize the risk of complications, displaced fractures typically are treated with closed manipulation and percutaneous pinning. If the radial and ulnar pulses are absent, the fracture is reduced. Frequently, the pulse returns after the fracture is reduced and the proximal fragment no longer stretches the brachial vessels. If the pulse does not return but the capillary refill is normal and there are no signs of compartment syndrome, the patient may be treated with observation with careful monitoring. If the pulse does not return after the fracture has been reduced and the fingers or forearm show signs of ischemia, the vessels should be explored. Cubitus varus, the “gunstock deformity,” results from malrotation and the resultant tilt of the distal fragment. The thin, spadelike shape of the distal humerus, in combination with a swollen arm and the small size of a child’s bone, is a predisposing factor. The deformity is primarily a cosmetic rather than a functional problem.

injury in children. Lateral condyle fractures result from a fall on a varus, supinated elbow, with the condyle avulsed by attached extensor muscles. Medial condyle fractures are uncommon, but the treatment principles are the same as for lateral condyle fractures. When these fractures cross the articular surface, displacement ⬎1 mm at the joint requires reduction and pinning to minimize associated problems of nonunion, cubitus valgus, tardy ulnar nerve palsy, and traumatic arthritis.

Lateral and Medial Epicondyle Fractures Lateral epicondyle fractures are uncommon in children, but avulsion of the medial epicondyle by forceful contraction of the flexorpronator muscles with the elbow in valgus is the third most common pediatric elbow fracture. The injury typically occurs in a 10- to 15year-old child. A concomitant posterior dislocation of the elbow may occur. In this situation, open reduction should be performed if the medial epicondyle fragment is incarcerated in the joint. Otherwise, medial epicondyle fractures, even when markedly displaced, do not commonly cause residual disability and can be treated with short-term splinting.

Radial Neck Fractures In children, fracture of the proximal radius typically involves the physis, with extension into the neck of the radius (Peterson II or Salter II). The typical age group is 7 to 12 years. Associated injuries may include fracture of the olecranon or medial epicondyle, as well as dislocation of the elbow. Isolated fractures result from a fall on an extended elbow with valgus stress. Treatment depends on the age of the child and the degree of angulation. Tilt of more than 30° may result in loss of forearm rotation. With more than 30° angulation, closed reduction with or without percutaneous manipulation of the fracture should be attempted with the goal of reducing angulation to less than 30°. Open reduction may be required but has a greater risk of osteonecrosis of the radial head and synostosis between the radius and ulna. Premature fusion of the

Transphyseal Fracture Separation of the Distal Humerus Transphyseal separations of the distal humerus typically occur in infants and young children as a result of child abuse. Radiographs may be difficult to interpret because the secondary centers of ossification have not developed in children this young. Typically, the proximal forearm is displaced medially and posterior to the humeral shaft. Arthrography, MRI studies, or ultrasonography may be necessary to distinguish this lesion from an elbow dislocation or lateral condylar fracture.

Lateral and Medial Condyle Fractures Fracture of the lateral condyle of the distal humerus is the second most common elbow

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Elbow and Forearm physis usually is of little significance, because 80% of the growth of the radius occurs at the distal physis.

Dislocation of the Elbow The elbow is the most commonly dislocated joint in children and the second most common site of dislocation in adults (Figure 15-20). Posterior dislocations are most common. Anterior dislocation is rare because of the shape of the olecranon process. Divergent dislocation with separation of the radius and the ulna results from severe disruption of the soft tissues. Posterior dislocations typically occur in a fall on the outstretched hand with the shoulder abducted. Axial compression at the elbow combined with an external and valgus stress at the elbow (the body internally rotates) results in a continuum of ligamentous injury that typically starts laterally and moves

Olecranon Fractures and Diaphyseal Fractures of the Radius and Ulna Olecranon fractures are uncommon in children and are likely to be nondisplaced. Displaced fractures usually require open reduction and tension band wire and pin fixation. Most diaphyseal forearm fractures in children can be managed by closed techniques. Proximal and middle third forearm fractures account for only 15% to 20% of pediatric forearm fractures, but these injuries are more likely to develop complications such as compartment syndrome, malunion, or synostosis.

Figure 15-20: Dislocation of Elbow Joint Fracture of coronoid process of ulna with posterior dislocation of elbow. Coronoid fracture may occur occasionally without dislocation Posterior dislocation. Note prominence of olecranon posteriorly and distal humerus anteriorly

Posterior dislocation with fracture of both coronoid process and radial head. Rare but serious; poor outcome even with good treatment. May require total elbow replacement Divergent dislocation, anterior-posterior type (rare). Medial-lateral type may also occur (extremely rare)

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Chapter 15 medially. The first stage tears the ulnar portion of the lateral collateral ligament (LCL), followed by disruption of the entire LCL complex, then the anterior and posterior capsules, then the posterior band of the medial collateral ligament (MCL), and lastly, the anterior band of the MCL. Associated injuries may include avulsion of the medial and lateral epicondyles, radial head and radial neck fractures, and coronoid fractures. These additional injuries increase instability and may necessitate internal fixation. Isolated dislocation of the elbow is treated by closed reduction. Distal traction is applied with the elbow in extension and the forearm in supination. After reduction, elbow stability is assessed with the forearm in pronation. If ligament disruption involves the anterior band of the medial collateral ligament, instability is noted with the elbow in extension. This injury will need 3 to 6 weeks of protection, starting with the elbow in pronation and 90°of flexion. More stable injuries should be immobilized for a short time (1 to 2 weeks) to prevent the complications of elbow stiffness and loss of extension. Other complications, such as heterotopic ossification, brachial artery injury, ulnar nerve injury, and compartment syndrome, are associated with highenergy injuries and concomitant fractures.

distress. The extremity is held with the elbow slightly flexed and the forearm pronated. Tenderness over the radial head and resistance on attempted supination are the only consistent findings. Radiographic findings are normal. Reduction is accomplished by applying pressure over the radial head, followed by quick supination. If this maneuver fails to produce the snap of reduction, the elbow should be flexed. Resistance is perceived just before full flexion. As the elbow is pushed through that resistance, the annular ligament will reduce, and a snap will be perceived as the radial head is reseated. If the reduction is successful, the child will resume use of the extremity in a few minutes. In a child who presents for evaluation 1 to 2 days after injury, however, swelling may obscure the snap of reduction and deter the immediate resumption of normal function. If the elbow has full flexion and supination, the radial head has been reduced. Immobilization is ineffective as slings are quickly discarded.

PEDIATRIC DISORDERS Congenital Dislocation of the Radial Head Isolated congenital dislocation of the radial head, although present at birth, is usually not diagnosed until a child is 2 to 5 years of age, when the parents note mild limitation of elbow extension and an abnormal prominence (Figure 15-21). The dislocation may be bilateral or unilateral. Most dislocations are posterior or posterolateral, but they may be anterior. The limitation of motion is rarely dysfunctional, and most patients are asymptomatic. Excision of the radial head, after completion of growth, is indicated for relief of pain from joint incongruity; however, elbow motion does not improve after the procedure.

Subluxation of the Radial Head Subluxation of the radial head, also called a “pulled elbow” or “nursemaid’s elbow,” is the most common elbow injury in children younger than 5 years. Subluxation occurs with a pull on the forearm when the elbow is extended and the forearm pronated. The annular ligament (see Figure 15-13) slips proximally and becomes interposed between the radius and the ulna. This injury is associated with ligamentous laxity, a condition that is almost universal in young children and typically occurs when a young child is “helped along” or lifted by pulling on the forearm. Immediately after the injury, the child will cry, but the initial pain quickly subsides. Thereafter, the child is reluctant to use the arm but otherwise does not appear to be in great

Congenital Radioulnar Synostosis Congenital radioulnar synostosis is an uncommon congenital abnormality caused by failure of separation of the proximal radius and ulna during fetal development. As a result, forearm rotation is lost. The synostosis is frequently an isolated event but may be

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Elbow and Forearm Figure 15-21: Congenital Dislocation of Radial Head

Lateral view of upper extremity reveals posterior bulge of head of radius and inability to fully extend elbow

Anteroposterior and lateral radiographs reveal posterior dislocation of radial head, most evident on elbow flexion. Note also hypoplastic capitulum of humerus.

cally, the dominant forearm is positioned in 0° to 20°of pronation. Compartment syndrome is the most common postoperative complication.

associated with other conditions. Most cases involve some degree of fixed pronation. The degree of disability depends on the amount of fixed pronation and whether the condition is unilateral or bilateral. Patients with bilateral involvement and forearms fixed in greater than 60°of pronation have the greatest difficulty with activities such as holding a fork, dressing, and maintaining good personal hygiene after bowel movements. Patients with less fixed pronation often can substitute shoulder motion. Surgery to resect the synostosis and restore motion has not been successful. Rotational osteotomy through the synostosis to change the position of the forearm varies according to the amount of functional impairment. Typi-

Osteochondrosis of the Elbow Children involved in repetitive throwing activities or gymnastics repetitively overload the elbow into valgus with tension on the medial epicondyle and compression on the capitellum. Traction apophysitis of the medial epicondyle, better known as “little leaguer’s elbow,” may develop. The resultant pain responds well to a relatively short period of rest. Chronic lateral elbow pain in pediatric athletes usually occurs secondary to osteonecrosis of the capitellum and is more problematic.

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Chapter 15 Figure 15-22: Osteochondrosis of the Capitellum

Bone resorption seen as radiolucent areas and irregular surface of capitulum of humerus

Characteristic changes in capitulum of left humerus (arrow) compared with normal right elbow

the anterior central capitellum (Figure 15-22). Osteochondral loose bodies may be present. An MRI study often helps define the extent of osteonecrosis. Treatment for patients in this age group includes activity modification, excision of osteochondral fragments, and occasionally, drilling of the defect to stimulate a fibrocartilaginous response.

When osteonecrosis occurs in children younger than 10 years, the condition is called Panner disease and has a good prognosis for healing with a period of rest and, sometimes, immobilization. When the condition occurs during adolescence, it is called osteochondritis dissecans of the capitellum and has a more guarded prognosis. Adolescents with osteonecrosis of the capitellum report the insidious onset of lateral elbow pain that is aggravated by throwing activities. Examination shows tenderness over the lateral elbow, tenderness at the extremes of passive elbow motion, and a flexion contracture of 10° to 30°. Typical radiographic changes include lucency and fragmentation of

ADDITIONAL READINGS Chen FS, Rokito AS, Jobe FW. Medial elbow problems in the overhead-throwing athlete. J Am Acad Orthop Surg. 2001; 9:99–113. Morrey BF, ed. The Elbow and Its Disorders, 2nd edition. Philadelphia, Pa: Saunders; 2000. Staheli LT, ed. Pediatric Orthopaedic Secrets, 2nd edition. Philadelphia, Pa: Hanley and Belfus; 2003.

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sixteen The Hand and Wrist John D. Lubahn, MD D. Patrick Williams, DO

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Chapter 16

T

he human hand, as an extension of the brain, allows us to manipulate and interact with our environment and to perform activities as routine as opening a door or as intimate as caressing a loved one. The hand also functions as part of the sensory system, providing tactile sensation for complex hand movements without the necessity of constant visual guidance; this function is epitomized by blind people who read and musicians who entertain. An understanding and careful examination of hand anatomy and function is crucial for the student of medicine. carpometacarpal (CMC) joint of the thumb is saddle-shaped, a configuration that permits abduction-adduction, as well as the circumduction that permits opposition of the thumb to the fingers. The metacarpophalangeal (MP), proximal interphalangeal (PIP), and distal interphalangeal (DIP) joints basically are flexion-extension hinge joints. The skin on the dorsal surface of the hand is thin and flexible to allow full flexion of the fingers, whereas the palmar surface skin is thicker and characterized by creases. The

ANATOMY AND BIOMECHANICS The carpus, or wrist, is composed of eight carpal bones that link the forearm to the hand (Figure 16-1). The proximal carpal row (scaphoid, lunate, and triquetrum) articulates with the distal radius and ulna, as well as the distal carpal row (trapezium, trapezoid, capitate, and hamate). The pisiform, also part of the proximal row, is a sesamoid bone in the flexor carpi ulnaris tendon that articulates only with the triquetrum. The bones of the hand are the metacarpals and phalanges. The

Figure 16-1: Bones and Joints of Hand

Distal phalanges

Head Tuberosity Shafts Base Head Shafts Base

Middle phalanges

Right hand: anterior (palmar) view

Proximal phalanges

Head Shafts Base

Metacarpal bones

Head Shafts Base

Carpal bones

5

4

3

Sesamoid bones

2 1

Hamate and Hook Capitate

Trapezoid

Pisiform Triquetrum Lunate

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Trapezium and Tubercle Scaphoid and Tubercle

Carpal bones

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The Hand and Wrist distal volar crease of the wrist crosses the proximal scaphoid and the pisiform. The distal palmar crease of the hand corresponds to the MP joint, and the proximal finger crease is at the base of the proximal phalanx. The extrinsic muscles of the wrist and hand originate on the medial and lateral humeral condyles and the proximal radius and ulna (see Figure 15-2). The extrinsic extensor tendons cross the wrist and are surrounded by tendon sheaths in six compartments bounded by the extensor retinacular ligament (Figure 16-2). The extrinsic finger and thumb flexor tendons and the median nerve enter the hand through the carpal canal (Figure 16-3). The transverse carpal ligament, a thick band extending from the hamate and pisiform to the scaphoid and trapezium, forms the inelastic roof of the carpal canal. A decrease in the size of the canal or an increase in the size of its contents can cause compression of the median nerve (carpal tunnel syndrome). Intrinsic musculature includes thenar, hypothenar, and interosseous muscles (Figure 16-4; see also Figures 15-4 and 15-5). The thenar muscles are the abductor pollicis brevis, the opponens pollicis, and the superficial head of the flexor pollicis brevis. The hypothenar muscles are composed of the abductor digiti quinti, the opponens digiti quinti, and the flexor digiti quinti. The dorsal interossei, commonly referred to as dorsal intrinsics, abduct the fingers; the palmar interossei (palmar intrinsics) adduct the fingers. The DIP joint of the fingers is flexed by the flexor digitorum profundus (FDP). It has a separate muscle belly for the index finger (which therefore flexes independently) but a common muscle belly for the long, ring, and small fingers (which tend to work as a single unit). The PIP joint of the fingers is primarily flexed by the flexor digitorum superficialis (FDS). It has individual muscle bellies for each finger, thus providing the individual finger flexion at the PIP joint that is necessary for activities such as playing a musical instrument and typing. The FDS separates into two parts before its point of insertion, and the FDP passes through the split (Figure 16-5). Both finger

flexors are enclosed in a common tendon sheath. The proximity of the FDS and FDP tendon to the surrounding sheath promotes efficient movement, but adhesions from injury or infection can be problematic in this region. The interossei, along with the lumbrical muscles, flex the MP joints and extend the PIP and DIP joints. The lumbrical muscles are unique in that they originate from the profundus tendons to insert into the dorsal apparatus of the antagonistic extensor mechanism (see Figure 16-5). The interossei and the two ulnar lumbricals are innervated by the ulnar nerve, but the two radial lumbricals are innervated by the median nerve. The MP joints of the fingers are extended by the extensor digitorum longus, extensor indicis proprius, and extensor digiti quinti. When the MP joints are flexed, these muscles also can extend the PIP joints; otherwise, the intrinsic muscles extend the PIP and DIP joints. The complex arrangement of the tendons on the dorsum of the hand provides the necessary synchrony and balance between flexors and extensors during the multiple precise motions of the MP, PIP, and DIP joints working in concert. The main insertion of the extrinsic extensor muscle tendon is through the central slip at the base of the middle phalanx. The intrinsic muscles join with the extrinsic extensor through the interdigitating transverse and oblique fibers of the dorsal apparatus to extend the PIP and DIP joints. Contracture or spasticity of the intrinsic muscles creates increased tension on the dorsal hood. A swan-neck deformity develops, with PIP joint hyperextension and MP and DIP joint flexion (Figure 16-6). Laceration of the central extensor tendon proximal to its insertion into the middle phalanx allows the lateral bands to slip volarly and produces the opposite flexion, boutonnière (French from “button hole”) PIP joint deformity. The radial artery lies radial to the flexor carpi radialis tendon at the wrist (see Figure 16-3). After crossing the snuffbox (see Figure 16-2), the radial artery passes through the first intermetacarpal space to the palm as the main contributor to the deep palmar arch,

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Chapter 16 Figure 16-2: Extensor Tendons at the Wrist Posterior (dorsal) view Extensor carpi ulnaris – Compartment 6 Extensor digiti minimi – Compartment 5 Extensor digitorum Compartment 4 Extensor indicis Extensor pollicis longus – Compartment 3 Extensor carpi radialis brevis Extensor carpi radialis longus

Compartment 2

Abductor pollicis longus Compartment 1 Extensor pollicis brevis

Plane of cross section shown below Extensor retinaculum

Radial artery in anatomical snuffbox Abductor digiti minimi muscle Dorsal interosseous muscles Intertendinous connections

Transverse fibers of extensor expansions (hoods)

Cross section of most distal portion of forearm Extensor retinaculum Extensor pollicis longus – Compartment 3 Compartment 4

Compartment 5

Compartment 6

Extensor digitorum and extensor indicis

Extensor carpi radialis brevis Extensor carpi radialis longus

Extensor digiti minimi Extensor carpi ulnaris

5

4

3

6

2 1

Ulna

Radius

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Compartment 2

Extensor pollicis brevis Abductor pollicis longus

Compartment 1

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The Hand and Wrist Figure 16-3: Flexor Tendons, Arteries, and Nerves at Wrist Palmar view Median duo

Flexor digitorum superficialis tendons and Two flexor digitorum profundus tendon tendons quartets Common flexor sheath (ulnar bursa)

Palmaris longus tendon Median nerve

Radial artery Flexor carpi radialis tendon Radial trio Flexor pollicis longus tendon in tendon sheath (radial bursa) Palmar carpal ligament (reflected) (Synovial) tendon sheath

Ulnar artery Ulnar nerve Ulnar trio Flexor carpi ulnaris tendon Pisiform

Transverse carpal ligament Abductor digiti minimi muscle

Trapezium 1st metacarpal bone

Flexor digiti minimi brevis muscle

Opponens pollicis muscle Abductor pollicis brevis muscle (reflected)

Opponens digiti minimi muscle Superficial palmar (arterial) arch Lumbrical muscles

Flexor pollicis brevis muscle (reflected)

Adductor pollicis muscle

Figure 16-4: Intrinsic Muscles of Hand Dorsal view

Palmar view

Tendinous slips to hood of extensor digitorum muscle Deep transverse metacarpal ligament

Dorsal interosseous muscles

Abductor pollicis brevis muscle

Palmar interosseous muscles

Abductor digiti minimi muscle Radial artery Radius

Ulna

Radius

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Ulna

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Chapter 16 Figure 16-5: Flexor and Extensor Tendons in Fingers Dorsal Slips of long expansion extensor tendon (hood) to lateral bands

Insertion of extensor tendon to base of middle phalanx Triangular aponeurosis

Dorsal view

Long extensor tendon

Interosseous muscles

Metacarpal

Insertion of extensor tendon to base of distal phalanx

Lateral bands

Interosseous muscle slip to lateral band Lumbrical muscle

Lateral view, finger extended Insertion of extensor tendon to middle phalanx Insertion of extensor tendon to distal phalanx

Collateral ligaments

Lateral view, finger flexed

Vinculum breve

Portion of interosseous tendon passing to base of proximal phalanx and joint capsule

Dorsal expansion (hood)

Lateral band

Long extensor tendon

Metacarpal

Vincula longa Flexor digitorum superficialis tendon

Flexor digitorum profundus tendon

Interosseous muscles Lumbrical muscle

Insertion of deep portion of extensor tendon to proximal phalanx and joint capsule Attachment of interosseous muscle to base of proximal phalanx and joint capsule Palmar ligament

Lumbrical muscle

Interosseous muscles

Flexor digitorum superficialis tendon (cut) Collateral ligaments

Note: black arrows indicate pull of long extensor tendon; red arrows indicate pull of interosseous and lumbrical muscles

Flexor digitorum profundus tendon (cut)

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Lateral band relaxed in this position; correct for splinting of “mallet finger”

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The Hand and Wrist Figure 16-6

causes atrophy between the metacarpals on the dorsum of the hand. Look at the nails for evidence of pitting or signs of other systemic disorders. Palpate bony landmarks and any swelling or osteophytes. At the wrist, the radial and ulnar styloid processes are palpable; the radial styloid is approximately 1 cm distal to the ulnar styloid. The dorsal tubercle at the distal radius, commonly called Lister tubercle, is palpable. It functions as a pulley for the extensor pollicis longus and is a marker for surgical approaches. The pisiform on the volar aspect of the wrist is a landmark for the ulnar nerve and artery. The zero starting position for determining wrist motion is the forearm in pronation and the carpus aligned with the plane of the forearm. In young adults, normal wrist motion is approximately 75°of flexion, 75° of extension, 20° of radial deviation, and 35° of ulnar deviation (Figure 16-7). Finger joint motion occurs primarily in the flexion-extension plane, with flexion accounting for most of the motion. The wrist should be in the neutral position when finger or thumb flexion is measured. When the wrist is flexed, the extensor digitorum communis and thumb extensors are under tension, thereby limiting finger and thumb flexion. Flexion and extension can be measured at the MP, PIP, and DIP joints, but from a functional perspective, finger flexion is a composite movement of motion from the three finger joints. Ask the patient to touch the distal palmar crease. In young and middle-aged adults, the fingertip should touch this crease. Lack of full finger flexion can be quantified by measuring the distance from the fingertip to the distal palmar crease (see Figure 16-7). The planes of thumb motion are flexionextension, abduction-adduction, and opposition. Opposition is a composite motion at the CMC, MP, and interphalangeal (IP) joints that is critical to daily activities. In disability ratings, opposition is valued as 50% to 60% of thumb function. In normal opposition, the tip of the thumb touches the base of the little finger (see Figure 16-7). Impaired opposition can be quantified by measuring the distance from

Boutonnière deformity of index finger with swan-neck deformity of other fingers in a patient with rheumatoid arthritis

which is completed by the deep palmar branch of the ulnar artery. The ulnar artery and nerve lie radial to the flexor carpi ulnaris and pisiform as they enter Guyon canal and the palm. The ulnar artery is the main contributor to the superficial palmar arch, which is completed by a branch of the radial artery. After traversing Guyon canal, the ulnar nerve branches into a superficial cutaneous branch that provides sensation to the ulnar aspect of the palm and the ulnar one and a half fingers, and a deep motor branch that supplies the hypothenar muscles. The ulnar nerve then travels with the deep palmar arch, supplying all the interossei, the third and fourth lumbricals, the adductor pollicis, and the deep head of the flexor pollicis brevis (see Figure 15-4). The median nerve supplies the remaining thenar muscles and the first and second lumbricals, and it provides sensation to the thumb and radial two and a half fingers (see Figure 15-3).

PHYSICAL EXAMINATION Inspect the hand for atrophy of the thenar muscles (innervated by the median nerve) or hypothenar and intrinsic muscles (innervated by the ulnar nerve). Intrinsic muscle weakness

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Chapter 16 Figure 16-7: Measurement of Wrist Motion and Finger Motion, Lack of Finger Flexion, and Thumb Opposition Wrist Range of Motion Deviation 90˚ 75˚

20˚

Radial rotation

Ulnar deviation

Extension 30˚

Flexion 90˚

90˚

75˚

Range of Finger Flexion

Distal palmar crease

Range of Thumb Opposition

MP joint

CMC joint

PIP joint

MP joint IP joint

DIP joint

Distal palmar crease

90˚

Normal finger flexion is composite of flexion of MP, PIP, and DIP joints and allows fingertip to touch distal palmar crease.

Normal thumb opposition is composite of movements of CMC, MP, and IP joints. Normal range is to base of little finger.

Limitation of finger flexion may be quantified by measuring distance from fingertip to distal palmar crease.

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Limitations of thumb opposition may be quantified by measuring distance from tip of thumb to base of little finger.

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The Hand and Wrist the tip of the thumb to the base of the little finger. All thumb joints move in flexion and extension, but this range is difficult to quantify at the CMC joint. Flexion at the thumb MP joint is typically 50° to 60°. Extension is not typically observed at the thumb MP joint. Normal thumb IP motion in young adults is 55° to 75°of flexion and 5° to 10°of extension. To assess the strength of the wrist flexors, the most powerful of which is the flexor carpi ulnaris, resist the patient’s effort to flex the wrist with the elbow flexed to 90° and the thumb and fingers in the extended, neutral position (eliminates action of finger flexors). To test the wrist extensors, the most powerful of which are the extensor carpi ulnaris and the extensor carpi radialis brevis, resist the patient’s effort to extend the wrist with the elbow flexed to 90° and the fingers flexed (eliminates action of the finger extensors). To test the integrity of the FDP tendon, hold the PIP joint in extension, and ask the patient to flex the distal phalanx. To assess the flexor digitorum sublimis, neutralize the profundus tendon by holding all the fingers except the one being tested in full extension, and ask the patient to flex the finger. Median nerve paralysis above the elbow causes weak pronation, wrist flexion, and an “ape hand” with thenar atrophy and weakness of thumb opposition. Thenar muscle strength (motor branch of median nerve) can

be evaluated by asking the patient to position the thumb in abduction as you push it into adduction. Assess sensation of the median nerve at the volar tip of the thumb. Test intrinsic muscle weakness (motor branch of ulnar nerve) by asking the patient to abduct the index finger against resistance while you palpate the first dorsal interosseous muscle. In addition, ask the patient to pinch a piece of paper while you pull on it. Weakness of the adductor pollicis results in flexion of the IP joint of the thumb (positive Froment sign) (Figure 16-8). Assess ulnar nerve sensation at the volar tip of the little finger. If ulnar nerve entrapment or laceration occurs above the wrist, sensation may be lost on the dorsum of the hand. If the ulnar nerve is divided distal to the mid-forearm, all the intrinsic muscles of the hand are paralyzed except for the first and second lumbricals and the thenar muscles. Lack of intrinsic muscle function to the ring and little fingers causes an ulnar claw hand, or hand of benediction, with the fourth and fifth fingers hyperextended at the MP joints and flexed at the PIP and DIP joints (Figure 16-9). The intact lumbricals to the index and long fingers provide enough intrinsic muscle function to prevent clawing of these digits. However, if the ulnar nerve is lacerated at or proximal to the elbow, clawing of the ring and little fingers does not occur because the FDP to these fingers is also paralyzed. A distal forearm

Figure 16-8: Positive Froment Sign

When pinching a piece of paper between thumb and index finger, the thumb IP joint will flex if the adductor pollicis muscle is weak (ulnar nerve paralysis).

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Chapter 16 Figure 16-9: Hand of Benediction

joint that are exacerbated by axial pressure of the metacarpal on the trapezium (the grind test). Radiographs show narrowing of the joint and varying degrees of subluxation of the joint (Figure 16-10). Nonoperative treatment alternatives include activity modification, nonsteroidal anti-inflammatory drugs (NSAIDs), short-term full-time splinting followed by intermittent bracing, and steroid injections. Reconstructive operations are indicated in patients with persistent, disabling symptoms. Osteoarthritis of other joints in the hand and wrist is uncommon and usually is secondary to trauma. Predisposing injuries in traumatic wrist arthropathy include intra-articular fractures of the distal radius, unrecognized scaphoid fractures, and ligament disruptions that cause abnormal wrist kinematics.

Kienböck Disease

laceration of the median and ulnar nerves results in a complete claw hand because all intrinsic muscles are paralyzed, but the extrinsic flexors and extensors are intact.

Osteonecrosis of the lunate, commonly referred to as Kienböck disease, can occur at any age but most commonly affects men between the ages of 20 and 40 years. The exact cause is usually not known, but repetitive or singleepisode trauma that interrupts the blood supply to a “lunate at risk” is the most accepted theory. Risk factors include a lunate supplied by a single nutrient vessel, which occurs in 7% of the population, and ulnar negative variance (an ulna shorter than the radius). Studies have shown increased contact stress at the radiolunate in patients with negative ulnar variance; however, osteonecrosis of the lunate also occurs in patients with positive ulnar variance. Patients with Kienböck disease typically present with the insidious onset of wrist pain that is increased with activity. Examination shows variable limitation of wrist motion and mild swelling on the dorsum of the wrist. Routine radiographs are usually diagnostic (Figure 16-11). If no changes are apparent in the lunate, a bone scan or magnetic resonance imaging (MRI) may be diagnostic. Treatment is based on the stage of disease and the degree of disability. Immobilization may be successful if the lunate has not collapsed; however, the effect of immobilization on the natural history of the disease

DEGENERATIVE DISORDERS Osteoarthritis Osteoarthritis may affect any joint of the hand. It is common in the DIP and PIP joints of the fingers with normal aging—a process that usually begins earlier and is more severe in females. Heberden nodes (in the DIP joints) and Bouchard nodes (in the PIP joints) are prominences caused by osteophytes and deformation of the joints (see Figure 4-7). A degenerative cystic lesion, referred to as a mucous cyst, may be present on the dorsum of the DIP joint. The joints may be painful and stiff early in the process, but the pain usually subsides over time. Although the stiffness and nodules remain, surgical treatment (arthrodesis) of these joints is not commonly required. Osteoarthritis of the thumb CMC joint is common and affects women more often than men. Predisposing factors are ligamentous laxity and repetitive stress from pinch maneuvers that load the joint (eg, knitting or cutting). Patients report pain with pinch activities. Examination shows swelling and pain over the CMC

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The Hand and Wrist is unclear. Surgical options for patients with no collapse or with some collapse of the lunate but no degenerative changes in the adjacent joints include vascular pedicle transplantation, radial shortening osteotomy, ulna-lengthening osteotomy, and

capitate-shortening osteotomy. Surgical options for patients with arthritic changes include limited carpal arthrodesis, resection arthroplasty with interposition of tendon graft or silicone implant, proximal row carpectomy, and wrist arthrodesis.

Figure 16-10: Osteoarthritis of Thumb Carpometacarpal Joint

A

C

B (A) Lateral radiograph and (B) AP radiograph of thumb of 56-year-old male with activity-related pain at base of thumb. Radiographs show early stages of disease with narrowing of thumb CMC and mild subluxation. (C) AP radiograph of hand of 73-year-old female with severe pain at base of thumb. Exam showed swelling and tenderness to palpation at the base of the thumb. Radiographs show subluxation and degenerative changes at the thumb CMC joint with a large osteophyte between the first and second metacarpal. The joint space between the scaphotrapezial was preserved.

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Chapter 16 The finger may lock or stick with flexion of the digit (Figure 16-12). On awakening, the digit may be locked in the palm and unlocking the digit may require that the finger be pushed into extension. Patients with diabetes mellitus or rheumatoid arthritis may have multiple digit involvement. Injection of corticosteroid into the tendon sheath is often successful as an initial treatment for trigger finger; however, patients with diabetes mellitus are less likely to improve after an injection. If symptoms persist, release of the A1 pulley is indicated (see Figure 1622). De Quervain tenosynovitis, the most common cause of tendinitis on the extensor side of the wrist, involves swelling or stenosis of the first dorsal compartment tendon sheath, which surrounds the extensor pollicis brevis and the abductor pollicis longus. It most commonly occurs in patients who have (1) one or more additional anomalous tendons within the compartment, or (2) a septum within the compartment that separates and narrows the space for the extensor pollicis brevis and the abductor pollicis longus. This disorder most commonly occurs in middle-aged women and is frequently brought on by repetitive thumb motion. Tenosynovitis constricts the tendons as they glide within the sheath. Patients note pain and swelling in the region of the radial styloid that are aggravated by use of the thumb (Figure 16-13). Crepitus may be sensed as the compartment is palpated during thumb motion. The Finkelstein test is diagnostic with exacerbation of pain when the thumb is flexed and the wrist is then placed in ulnar deviation. Radiographs are typically normal and are used to exclude other possibilities, such as fracture of the scaphoid or arthritis of the wrist or thumb CMC joint. Treatment begins with immobilization of the thumb in a splint, as well as the use of NSAIDs. If this treatment fails, a corticosteroid injection into the tendon sheath is indicated. Surgical treatment to release the area of stenosis is indicated for relief of persistent symptoms. Anomalous slips of the abductor

Figure 16-11: Radiograph in Kienböck Disease

Radiograph of wrist shows characteristic sclerosis of lunate.

Tendinitis of the Hand and Wrist Tendinitis (tendinosis) of the hand and wrist is common. The most common etiology is predisposing anatomic factors such as a narrow canal for the tendon exacerbated by overuse. Fortunately, most patients respond to nonoperative treatment, including modification of activities, short-term immobilization, NSAIDs, and judicious injections of steroids. Stenosing tenosynovitis of the finger or thumb flexors, better known as trigger finger, is the most common cause of hand tendinitis. Bow stringing of the flexor tendons and its resultant mechanical disadvantage is prevented by five annular and three cruciate pulleys. The first annular pulley may become thickened, causing snapping or locking of the tendon during flexion of the finger or thumb. Predisposing factors include diabetes mellitus, rheumatoid arthritis, and aging. Patients note pain and catching when moving the finger, as well as a nodule in the distal palm that moves with flexion and extension.

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The Hand and Wrist Figure 16-12: Trigger Finger

Patient unable to extend affected finger. It can be extended passively, and extension occurs with distinct and painful snapping action. Circle indicates point of tenderness where nodular enlargement of tendons and sheath is usually palpable.

Inflammatory thickening of fibrous sheath (pulley) of flexor tendons with fusiform nodular enlargement of both tendons.

Figure 16-13: De Quervain Tenosynovitis The Finkelstein test exacerbates the pain; it is performed by flexing the thumb and then placing the wrist in ulnar deviation.

Point of exquisite tenderness over styloid process of radius and sheath of involved tendons.

Course of abductor pollicis longus and extensor pollicis brevis tendons through 1st compartment of extensor retinaculum, transverse incision, and relation of sensory branches of radial nerve and synovial sheaths.

Superficial branch of radial nerve

Extensor pollicis longus, extensor pollicis brevis, abductor pollicis longus tendons. Extensor retinaculum

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Skin incision

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Chapter 16 The disease is uncommon before 40 years of age. A typical presentation is a 40- to 65year-old patient who notices a painless nodule near the distal palmar crease on the ulnar side of the hand. The cords initially may be tender and may occur in other locations. The nodules may remain confined to the palm and cause few symptoms. However, the disease may extend into the fingers, with progressive, albeit variable, flexion contracture of one or more digits at the MP and, in more severe cases, the PIP joints (Figure 16-14). The ring finger is most often involved, followed by the little, long, thumb, and index fingers. Concomitant involvement of the plantar fascia, the fascia of the penis, or both occurs in less than 3% of individuals with Dupuytren disease. Early treatment of a nodule in the palm consists of reassurance that no surgery is needed unless the contracture progresses to functional impairment. Splinting is ineffective. Recent research on collagenase injections has shown promising results. Surgery is indicated for significant contractures that interfere with extension of the fingers and functional activities such as retrieving objects from a pocket. The goals of surgical treatment are to excise the diseased tissue and release the contractures; however, the procedure is technically

pollicis longus are commonly noted. The most dorsal tendon of the compartment should be identified as the extensor pollicis brevis; otherwise, a separate septum for this tendon may be overlooked. Complications of surgery include failure to completely decompress all tendons within the sheath, and injury to the superficial radial nerve. Other potential, but less common, areas of wrist tendinitis include the flexor carpi radialis, extensor pollicis longus (third compartment), extensor digitorum communis (fourth compartment), extensor digiti minimi (fifth compartment), and extensor carpi ulnaris (sixth compartment).

Dupuytren Disease Dupuytren disease is contracture of the palmar fascia. The pathologic process begins with a proliferation of fibroblasts and type III collagen to produce cords and nodules in the dermis and skin. Predisposing factors include male gender, alcoholism, epilepsy, diabetes mellitus, HIV infection, trauma, and possibly smoking. A genetic, autosomal dominant predisposition has been noted; penetrance is variable, however, as indicated by the fact that the family history is positive in less than 10% of affected patients.

Figure 16-14: Dupuytren Disease Flexion contracture of 4th and 5th fingers (most common). Dimpling and puckering of skin. Palpable fascial nodules near flexion crease of palm at base of involved fingers with cordlike formations extending to proximal palm.

Partial excision of palmar fascia. Proximal portion of fascia divided and freed via thenar incision, then drawn up into palmar incision, where it is further dissected with care to avoid neurovascular bundles. Dissection is then continued into fingers. Buttonholing of skin must be avoided. Nodules and cordlike fascial thickening are apparent.

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The Hand and Wrist demanding and may be complicated by nerve injury, skin slough, and recurrent contractures.

Ganglia of the Hand and Wrist The most common benign tumor of the hand and wrist is a ganglion. These cystic lesions contain a thick, yellowish, mucinous fluid with a composition similar to joint fluid. Ganglia are thought to arise from the degeneration or tearing of a joint capsule or tendon sheath, which creates a one-way valve through which synovial fluid can enter the cyst but cannot easily flow back. The most common age at presentation is 15 to 40 years, but ganglia also develop in children and older adults. Ganglia may develop at any site. The most common location is the dorsoradial aspect of the wrist over the scapholunate joint (Figure 16-15). The lump may be asymptomatic or may cause aching that is aggravated by activities requiring repetitive wrist movements. Examination reveals a firm, cystic mass that transilluminates when a penlight is pressed against its side. The second most common site of ganglia is the volar radial aspect of the wrist between the flexor carpi radialis and the

radial styloid. These ganglia originate from the capsule of the scaphotrapezial joint and may wrap around the radial artery. A volar retinacular ganglion of the flexor tendon sheath typically is just proximal to the MP flexion crease of the finger. This “seed ganglion” is a small, firm nodule that is frequently tender when gripping objects, but does not limit or move with finger flexion/extension. Mucous cysts, a type of ganglion, develop at osteoarthritic DIP joints and most commonly are located on either side of the extensor tendon. Treatment options include observation, aspiration, and surgical excision. Ganglia may spontaneously recede, and observation is appropriate for patients with minimal symptoms. Aspiration is often successful in the treatment of volar retinacular ganglia, may be useful in the treatment of dorsal wrist ganglia (although recurrence rates are high), and is used with caution in volar wrist ganglia or mucous cysts. Surgical excision includes the joint capsule attachments. The risk of recurrence after surgery is 5% to 10% if the procedure is combined with 2 weeks of immobilization. Mucous cyst excision at the DIP joint requires careful removal of the cyst and any associated osteophytes.

Figure 16-15: Ganglion of Wrist Extensor tendon retracted

Carpal ligaments and capsule

Firm, rubbery, sometimes lobulated swelling over carpus, most prominent on flexion of wrist. Broken line indicates line of skin incision.

Excision of ganglion via transverse incision

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Chapter 16 bite wounds. Other bacteria commonly found in dog and cat bite wounds include ␣-hemolytic streptococci, Staphylococcus aureus, Bacteroides species, and Fusobacterium species. Human bite wounds often occur at the fingers (a direct injury) or MP joints (an indirect, clenched fist injury). Because the circumstances of the injury are often embarrassing and the laceration is often small, patients commonly delay evaluation. As a result, many patients with human bite wounds do not present until a well-established infection has developed. Gram-negative, anaerobic organisms— particularly Eikenella corrodens—are common in human bite wounds. Examination should assess location, swelling, erythema, and purulent discharge. Evaluate possible tendon or neurovascular dysfunction. Provide appropriate tetanus prophylaxis, and débride necrotic tissue. Most bite wounds should not be closed primarily. Pending culture results, treat animal bites with oral or intravenous ampicillin-sulbactam. Penicillin and a cephalosporin are the standard initial antibiotic therapy for human bite wounds.

NERVE ENTRAPMENT SYNDROMES AT THE WRIST For signs and symptoms of nerve entrapment syndromes at the wrist, see Chapter 6. Carpal tunnel syndrome is most common in middle-aged or pregnant women. The syndrome is often idiopathic, but predisposing factors that reduce available space in the carpal tunnel or affect peripheral nerve function should be investigated. These factors include tenosynovitis of the adjacent flexor tendons due to rheumatoid arthritis or overuse syndrome; edema resulting from pregnancy or hypothyroidism; and peripheral neuropathy caused by diabetes mellitus, alcoholism, or other conditions. The differential diagnosis includes cervical radiculopathy that affects the C6 nerve root, median nerve entrapment at the elbow, ulnar entrapment at the wrist, and wrist arthritis. Ulnar nerve entrapment at the wrist in Guyon canal is less common than ulnar entrapment at the elbow. Predisposing factors include a space-occupying lesion (such as a ganglion) or repetitive trauma (such as trauma produced by operating a jackhammer, or that caused by repetitive pressure associated with extended crutch ambulation). The differential diagnosis includes cervical radiculopathy that affects the C8 nerve root, thoracic outlet syndrome, ulnar nerve entrapment at the elbow, carpal tunnel syndrome, and wrist arthritis. More proximal entrapment of the ulnar nerve or C8 nerve root typically causes numbness of the dorsum of the hand.

UNIQUE HAND INFECTIONS The flexor tendons of the fingers and thumb are surrounded by a tenosynovial sheath that extends from the distal palm to the DIP joint (Figure 16-16; also Figure 1622). Infections within this sheath usually develop from a puncture wound. Because the sheath is a closed space with limited blood supply, an infection rapidly becomes an abscess. The sheath of the thumb and little finger flexor tendons extends to the radial and ulnar bursae, so infections in these tendon sheaths have the potential for extension into the forearm. Patients with septic flexor tenosynovitis develop progressive pain and swelling of the digit 24 to 48 hours after injury. Examination reveals diffuse swelling of the finger, maximal tenderness over the tendon, a finger held in a semiflexed position, and marked increased pain on passive extension of the digit. Patients

BITE WOUNDS OF THE HAND Dog, cat, and human bites account for approximately 1% of all emergency room visits. Dog bites account for approximately 80% to 90% of animal bites, but only 10% of wounds from dog bites become infected. In contrast, approximately 30% to 50% of wounds from cat bites become infected, most likely because the sharp, needlelike teeth of cats inject bacteria deep into the tissues. The causative organisms of dog and cat bite infections are similar. Pasteurella multocida is found in 50% of wounds from cat bites and in some dog

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The Hand and Wrist Figure 16-16: Infections of the Hand Insertion of flexor digitorum profundus tendon

Annular and cruciform parts of fibrous sheath over (synovial) flexor tendon sheaths

Insertion of flexor digitorum superficialis tendon

5th finger tendinous sheath extends to ulnar bursa

1st dorsal interosseous muscle

Fascia over adductor pollicis muscle

Common flexor sheath (ulnar bursa)

Ulnar artery and nerve

Palmar view of hand

Recurrent branch of median nerve to thenar muscles

For severe and longstanding purulent flexor tenosynovitis, open drainage and débridement is done by zigzag volar incision. Tendon sheath is opened by reflecting cruciate pulleys and preserving annular pulleys. With more prompt diagnosis, closed tendon sheath irrigation provides drainage while promoting healing and return of finger motion. An incision is made in the palm proximal to the A1 pulley. A second midlateral incision is made distally in the finger and the tendon sheath incised distal to the A4 pulley. A catheter is inserted into the proximal end of the tendon sheath and a drain in the distal end. The tendon sheath is irrigated until all purulent material is removed. Postoperatively, the catheter is kept in place for approximately 48 hours to allow intermittent saline irrigation of the tendon sheath.

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Chapter 16 require prompt treatment for prevention of tendon adhesions and necrosis. If the infection is recognized early, parenteral antibiotic therapy that covers both staphylococci and streptococci may be satisfactory. Most patients, however, require surgical drainage supplemented by closed tendon sheath irrigation and appropriate intravenous antibiotics. The pulp of the fingertip has fibrous septa that provide support for pinching and grasping activities. These septa create many small compartments in which a felon (pulp space infection) may develop (Figure 16-17). A felon typically develops after a puncture wound, most commonly involves the index and long fingers, and is characterized by intense pain and swelling of the palmar tip of the finger. Untreated felons progress to osteomyelitis of the distal phalanx. Surgical drainage can be performed through a central incision that extends from the flexion crease to the fingertip when an abscess collection is identified on the pad side of the finger, or through a midaxial incision when the location of the pus is not visible. “Fish mouth incisions” that extend across the tip of the finger cause painful scars and should be avoided. The wound should be packed open for 24 to 48 hours. The usual infecting organism is S aureus. Herpetic whitlow, a herpes simplex virus infection, can affect the fingertip and may cause swelling that should be differentiated from a felon. Herpetic whitlows have vesicular lesions and typically have less erythema and swelling than occur with felons. Lesions occur in adults and children and are more common in medical personnel, who are frequently exposed to human saliva. The swelling from a herpetic whitlow resolves within 10 to 21 days. Unnecessary surgical drainage predisposes the patient to secondary infection. Paronychial infections are the most common hand infections. The paronychia is the skinfold radial and ulnar to the fingernail. The eponychium is proximal to the nail. Paronychial infections typically develop from a hangnail, an ingrown nail, or a poorly performed manicure; they also may result from fingernail biting. The infection may involve only one

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side of the nail or both sides of the nail and the eponychium (see Figure 16-17). Early-stage infections may be treated with warm soaks and oral antibiotics that cover S aureus. Laterstage infections require elevation of the skinfold or partial or complete removal of the nail.

WRIST AND HAND TRAUMA Fractures in Adults Fractures of the Distal Radius When we fall, the most common protective mechanism involves catching ourselves on an outstretched, hyperextended hand. As a result, Colles fracture of the distal radius is the most common fracture in adults. This injury is more common in women and in older adults; after age 50, the female predominance increases. Colles fracture begins on the volar aspect of the distal radius, which fails in tension. The fracture propagates dorsally, and the bone then is loaded in compression. Therefore, Colles fractures typically reveal dorsal comminution, volar angulation, and dorsal displacement of the distal radius (Figure 16-18). Smith fracture is the opposite of Colles fracture and occurs with a backward fall on a

Figure 16-17: Felon and Paronychia Infections

Felon. Line of incision indicated.

Paronychia

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The Hand and Wrist Figure 16-18: Fractures of the Distal Radius

Colles fracture Lateral view of Colles fracture demonstrates characteristic silver fork deformity with dorsal and proximal displacement of distal fragment. Note dorsal instead of normal volar slope of articular surface of distal radius.

Barton fracture Dorsal Barton more common. Note dorsal intra-articular lip fracture of distal radius and associated subluxation of the carpus.

Die-punch, comminuted Colles fracture

flexed wrist. In these injuries, the distal radius is tilted volarly. Barton fracture is a dorsal or palmar lip fracture of the distal radius with associated subluxation of the carpus (see Figure 16-18). A die-punch fracture is an intraarticular, depressed fracture of the distal radius that occurs with increased axial compression. A transverse or oblique fracture across the radial styloid (a chauffeur fracture) results from a direct blow to the lateral aspect of the forearm. Examine the patient to detect swelling and deformity of the distal forearm, and determine the circulatory and neurologic status of the hand. Inspect anteroposterior (AP) and lateral radiographs to determine the direction and magnitude of displacement and whether the fracture is extra-articular or intra-articular. Median nerve dysfunction is the most common associated injury. The degree of acceptable displacement varies according to the age of the person and

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whether the fracture is intra-articular or extraarticular. Generally, fractures with 5° to 10° of dorsal angulation, a loss of more than 10°of radial inclination, and more than 2 mm of intra-articular step-off should be reduced and stabilized with the use of sugar tong splints or external or internal immobilization devices. Elderly patients with marked osteopenia and borderline reasons for reduction often function satisfactorily and with fewer complications when treated by shortarm cast or splint immobilization.

Fractures of the Scaphoid The scaphoid spans the proximal and distal rows of the carpus. Its anatomic location makes it vulnerable to axial loading between the ground and the distal radius when the wrist is hyperflexed (Figure 16-19). Therefore, the scaphoid is the most commonly fractured carpal bone. Fractures of the scaphoid are

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Chapter 16 Figure 16-19: Fracture of Scaphoid Lunate Usually caused by fall on outstretched hand with impact on thenar eminence.

Scaphoid (fractured) Trapezium Trapezoid

Triquetrum Pisiform Hamulus (hook) of hamate

Capitate with

C.A. Luce Less common fractures Tubercle Fracture of middle third (waist) of scaphoid (most common).

Distal pole

Proximal pole

proximal pole fractures. Displaced fractures have more than 1 mm of displacement, dorsal angulation, or both. The rate of nonunion markedly increases in displaced fractures. Osteonecrosis is associated with any proximal pole fracture and with displaced waist injuries. Symptoms include pain and tenderness on the radial aspect of the wrist localized to the anatomic snuffbox, or pain and tenderness on pressure over the scaphoid tubercle on the palmar side of the wrist. In addition to routine posteroanterior and lateral radiographs of the wrist, a posteroanterior view with the wrist in ulnar deviation and an oblique view should be obtained if examination indicates the possibility of a scaphoid fracture. If the exam suggests a possible scaphoid fracture but radiographs are not diagnostic, treatment should consist of a short-arm cast that includes the thumb for 2 weeks and repeated radiographs. Treatment for acute, stable fractures is a short-arm, thumb-spica cast

more common among males; the age group most often affected is 15 to 40 years, an age at which the distal radius is relatively strong. Scaphoid fractures have an increased incidence of nonunion and osteonecrosis for two reasons. First, the diagnosis is often delayed or missed. Patients may dismiss the injury as a simple sprain and may not seek medical attention. Furthermore, the radiographic findings of an acute injury are often subtle and may not be apparent unless routine AP and lateral radiographs are supplemented with additional oblique radiographs. The second reason for nonunion and osteonecrosis is a vulnerable blood supply. Articular cartilage covers 80% of the surface of the scaphoid, and the fracture may interrupt the major blood supply, which enters the distal pole at the dorsal ridge. Tuberosity fractures and incomplete waist (middle third) fractures are stable injuries. Unstable patterns include oblique fractures of the distal pole, complete waist fractures, and

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The Hand and Wrist metacarpal neck (the distal metaphysealdiaphyseal junction) that results from a closed fist striking an object (see Figure 16-20). Because of the dorsal-palmar mobility of the fifth metacarpal, residual dorsal angulation of 40° to 50° is well tolerated. These fractures usually can be treated with an ulnar gutter splint that positions the fourth and fifth fingers in the “safe, clam-digger” position (MP joints in 80° of flexion, and PIP and DIP joints in extension). The index finger and long metacarpals have less mobility, and only 10° to 15° of angulation is acceptable for metacarpal neck fractures involving these bones. Displaced fractures of the metacarpal shaft frequently require open reduction and internal fixation to prevent extensor lag at the MP joint (caused by shortening at the fracture) or malrotation of the digit. Rotational malalignment may be difficult to appreciate with the fingers extended but will be evident as the fingers are

with the wrist in radial deviation. Nondisplaced, unstable fractures can be treated with either internal fixation or cast immobilization for 12 weeks. Reduction and internal fixation is indicated in patients with displaced fractures or delayed diagnosis.

Fractures of the Metacarpals Fractures of the base of the thumb metacarpal can be classified as Bennett or Rolando injuries (Figure 16-20). These fractures cause functional incompetence of the trapeziometacarpal ligament; therefore, the abductor pollicis longus exerts a subluxating force on the main metacarpal fragment. Displaced fractures require reduction and pinning. Fractures of the second through fifth metacarpals typically result from axial loading. The most common fracture in the hand is the boxer fracture, a fracture of the fifth

Figure 16-20: Base of Thumb Metacarpal and Metacarpal Neck Fractures

1st metacarpal

Bone fragment Trapezium Abductor pollicis longus tendon

Rolando fracture. Y-shaped intra-articular fracture that is less common than a Bennett fracture.

Bennett fracture. Oblique intra-articular fracture of base of thumb metacarpal. Small triangular fragment retains alignment with trapezium while abductor pollicis subluxates main portion of 1st metacarpal. Fractures of metacarpal neck commonly result from end-on blow of fist. Often called boxer fracture.

In fractures of metacarpal neck, volar cortex is often comminuted, resulting in instability after reduction that may necessitate pinning.

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Chapter 16 partially flexed. A malrotated metacarpal or phalangeal fracture causes the finger to overlap the adjacent digit. Nondisplaced and minimally displaced fractures are common when only the third or fourth metacarpal is injured. In these injuries, the transverse metacarpal ligament stabilizes and suspends the injured metacarpal between the adjacent ones.

Fractures in Children The distal third of the forearm is the most common location for fractures in children. Several patterns of injury may occur (Table 16-1). These injuries are relatively uncommon before age 4 years and in this age group are mostly torus or greenstick fractures. A torus fracture is the least complicated distal forearm fracture and most commonly involves the dorsal cortex of the radius (see Figure 101). A metaphyseal fracture isolated to the distal radius is typically minimally displaced. Most distal forearm fractures in children, including fractures with complete displacement and shortening, can be treated by closed means. Because the distal radial and ulnar physis contribute approximately 80% of forearm length, residual angulation typically remodels completely in 1 to 2 years. Loss of rotational alignment is the only absolute

Fractures of the Phalanges In adults, the distal phalanx is the most commonly injured finger bone, followed by the proximal and middle phalanges. Fractures of the middle and distal phalanges are often nondisplaced and may be managed by splinting or buddy-taping the injured finger to an adjacent digit. Maintenance of reduction is difficult in displaced fractures of the proximal phalanx, so these injuries typically require internal fixation (Figure 16-21).

Figure 16-21: Fracture of Proximal Phalanx

Transverse fractures of proximal phalanx tend to angulate volarly because of pull of interosseous muscles on base of proximal phalanx and collapsing action of long extensor and flexor tendons.

Reduction of fractures of phalanges or metacarpals requires correct rotational as well as longitudinal alignment. In normal hand, tips of flexed fingers point toward tuberosity of scaphoid, as in hand at left. Hand at right shows result of healing of ring finger in rotational malalignment. Rotational malalignment, usually discernible clinically, may also be evidenced on radiographs by discrepancy in cross-sectional diameter of fragments, as shown at extreme right. Discrepancy in diameter is most apparent in true lateral radiograph but is visible to some extent in anteroposterior view.

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The Hand and Wrist indication for reduction or remanipulation. The reason for reduction is to relieve pressure on adjacent soft tissues and to facilitate healing. Closed reduction generally is indicated for angulation of 10° to 15°. Fractures of the wrist and hand are uncommon in children. The most common such injury is a Peterson II (Salter II) physeal fracture of the proximal phalanx. This injury most often involves the little finger and occurs when the finger is caught on an object and is pushed in a lateral direction.

Table 16-1

Distal Forearm Fracture Patterns in Children (in order of relative severity) Torus fracture* Metaphyseal fracture, complete* Greenstick fracture of the distal radius Greenstick fracture of the distal radius and ulna Complete fracture of the distal radius and greenstick fracture of the distal ulna

Tendon Injuries Lacerations cause most tendon injuries in the hand. Examination should carefully assess which tendons are injured, as well as the status of adjacent digital nerves. Flexor tendon injuries in zone II are particularly difficult to treat (Figure 16-22). Zone II begins at the ori-

Complete fracture of the distal radius and ulna Physeal fracture Galeazzi fracture *Typically nondisplaced or minimally displaced.

Figure 16-22: Flexor Tendon Anatomy and Injuries Anatomy of finger flexor tendon sheaths and pulleys A1

C1

A2

C2

A3

C3

A4

C4

A5

Tendons of flexor digitorum superficialis and profundus muscles (Synovial) tendon sheath

Palmar ligaments (plates)

Note: Flexor digitorum superficialis and profundus tendons encased in synovial sheaths are bound to phalanges by fibrous digital sheaths made up of alternating strong annular (A) and weaker cruciform (C) pulleys. Mallet finger

Jersey finger

Usually caused by direct blow on extended distal phalanx, as in baseball, volleyball

Flexor digitorum profundus tendon may be torn directly from distal phalanx or may avulse small or large bone fragment. Tendon usually retracts to about level of proximal interphalangeal joint, where it is stopped at its passage through flexor digitorum superficialis tendon; occasionally, it retracts into palm. Early open reduction and repair of FDP tendon to insertion site is indicated.

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Chapter 16 gin of the flexor tendon sheath and extends to the insertion of the FDS. In this zone, both the FDP and the FDS are often lacerated. Laceration may involve the tendons at which the FDS splits to allow passage of the FDP. In addition, injury and repair processes violate the tendon sheath and its associated annular and cruciate pulleys that normally facilitate gliding and nutrition of the tendons. As a result, the site of injury is often complicated by peritendinous adhesions that can seriously compromise function. Extensor tendon injuries in the distal forearm or wrist often heal well, but lacerations over the metacarpal head and the dorsum of the fingers can be complicated by injury to the sagittal bands and adhesions to surrounding structures that limit flexion. Both flexor and extensor tendon injuries require meticulous operative technique and a postoperative rehabilitation protocol that minimizes adhesions, contracture, and disruption of the repaired tendon. The A2 and A4 pulleys must be repaired or preserved to prevent bow stringing and dysfunction of the flexor tendons. Avulsion injuries also may disrupt finger tendons. A mallet finger results from forced flexion of the extended finger (eg, when a ball strikes the tip of the finger) and subsequent avulsion of the extensor tendon at the distal phalanx (see Figure 16-22). A similar mechanism can result in an intra-articular fracture of the distal phalanx (bony mallet finger). Examination shows a flexion posture of the DIP joint and an inability to actively extend this joint. Splinting the DIP joint in full extension for 6 weeks if the injury is acute, and for 8 weeks if diagnosis is delayed, is often successful. Avulsion ruptures of the central slip of the extensor tendon insertion into the middle phalanx result in an inability to fully extend the PIP joint. If diagnosis is delayed, lateral bands displace below the axis of rotation, resulting in flexion of the PIP joint and hyperextension of the DIP joint (boutonnière deformity; see Figure 16-6). Acute injuries can be treated by splinting of the PIP joint in extension. Chronic injuries may require surgical reconstruction.

Avulsion of the FDP insertion into the distal phalanx usually involves the ring finger (see Figure 16-22) and occurs when the flexed finger is caught and is forcefully pulled into extension, as when a sports player is grasping the jersey of another player (“jersey finger”). Examination reveals an inability to flex the DIP joint. Treatment requires operative reinsertion of the FDP to its bony insertion point.

Ligament Injuries and Dislocations of the Hand Sprains of the hand are common and typically involve a collateral ligament and/or volar plate of the MP, PIP, or DIP joint. Patients note pain and swelling after a jamming type of injury. After obtaining radiographs to rule out a fracture, assess stability by gently stressing the adjacent ligaments. Most sprains of the hand, even those that demonstrate complete disruption, can be treated with splinting. A digit with collateral ligament injury can be buddytaped to an adjacent digit. Complete ruptures of the volar plate are initially splinted in 30°of flexion for 1 to 3 weeks, with transition to buddy-taping and motion. Disruption of the ulnar collateral ligament of the thumb MP joint results from forced abduction of the thumb. This injury requires special consideration because this ligament is an important stabilizer of the thumb, and the adductor pollicis tendon may become interposed between bone and torn ligament, thus preventing adequate healing. The term gamekeeper thumb is used because English gamekeepers sustained this injury when they killed rabbits by means of a forceful blow from their thumb web space to the back of the hare’s neck. The injury is also observed in skiers (from forced abduction of the thumb against the ski pole), in sports players (from the ball’s forcing the thumb into abduction), and in persons who have fallen (Figure 16-23). Partial injuries can be treated with cast immobilization. Complete disruption requires surgical stabilization. Finger joint dislocations are typically dorsal and result from hyperextension injuries that disrupt the volar plate. Dislocation of the PIP

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The Hand and Wrist Figure 16-23: Gamekeeper Thumb Stress test for ruptured ulnar collateral ligament of thumb (gamekeeper thumb).

joint is the most common. MP dislocations are more common in the thumb and may be simple or complex (interposition of the volar plate between the metacarpal head and the proximal phalanx). Treatment of a PIP or DIP joint dislocation consists of closed reduction after the administration of a digital block anesthetic. Distal traction is followed by appropriate volar and dorsal applied pressure. Stability should be assessed after reduction. Stable injuries can be buddy-taped. When instability is observed with the joint positioned in full extension, the finger should be immobilized with a dorsal extension block splint. Complex dorsal dislocations of the MP joint often benefit from regional block anesthesia. These injuries are reduced by pushing the proximal phalanx over the metacarpal rather than by traction. Complex dislocations of the MP joint may require open reduction.

Nail Injuries Nail bed and fingertip injuries are common. These include simple lacerations, stellate/ crushing lacerations, and avulsion injuries with loss of nail bed tissue. Associated fractures of the distal phalanx are common, as is extension of the laceration through the surrounding skin and pulp. Various levels of fingertip amputation may occur.

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The goal of treatment is to prevent hypersensitivity of the fingertip and deformity of the nail such as split, ridged, ingrown, or poorly adherent nails. Assess the extent of injury, including whether the nail bed laceration involves the sterile matrix, germinal matrix, or both. Obtain AP and lateral radiographs of the finger, and note the location and displacement of any fractures. Simple and stellate/crushing lacerations should be treated by primary repair using digital block anesthesia, a finger tourniquet, loupe magnification, 6-0 chromic suture for the nail bed, and 5-0 nylon suture for any associated skin lacerations. If the germinal matrix is avulsed and lying on top of the nail plate, the nail bed should be repositioned and secured in its anatomic position. Loss of nail bed tissue requires split-thickness or more complicated grafting procedures. Soft tissue loss without exposed bone and with a defect of ⬍1 cm heals well by secondary intention. More complicated injuries with bone exposed require the use of local or regional flaps or shortening of the digit with primary closure. Tuft fractures and nondisplaced fractures of the distal phalanx are treated with symptomatic splinting.

PEDIATRIC CONDITIONS Syndactyly Syndactyly is a congenital condition characterized by failure of normal separation of the fingers or toes. At a genetically predetermined time, production of apical ectodermal ridge maintenance factor (AERMF) ceases. If AERMF continues to be produced, apoptosis and disruption of the interdigital space do not occur. The degree of syndactyly can vary from the presence of a thin web of skin to synostosis (bony fusion) of the phalanges. The webbing may extend to the tips of the digits (complete webbing) or may involve only a variable extent of the digit (partial webbing) (Figure 16-24). Syndactyly occurs twice as often in males, is 10 times more common in whites than in blacks, and most often involves the long and ring fingers. Syndactyly may occur in association with other syndromes. Apert syndrome is an auto-

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Chapter 16 Figure 16-24: Syndactyly

Figure 16-25: Polydactyly

Postaxial

Preaxial

served in 16 syndromes and is occasionally noted in 31 associated conditions. Polydactyly of the foot usually causes difficulty with shoe wear. Even when polydactyly of the hand does not create functional difficulties, it causes a significant cosmetic deformity. Vestigial digits can be ablated with the use of a constricting, circumferential suture at the skin bridge. Otherwise, removal of accessory digits should be delayed until the child is 9 to 10 months old.

somal dominant condition that results in premature closure of the cranial sutures and complete, complex syndactyly of the hands and feet. Poland syndrome is a sporadic congenital deficiency of the pectoralis major ranging from hypoplasia to absence of the muscle that has a 3:1 male and 3:1 right-sided predominance. Hypoplasia of the distal upper extremity and varying degrees of brachydactyly and syndactyly may be present. Because fingers differ in length, angular deformity may occur, and release before age 1 year is recommended for index-thumb and ring finger–small finger syndactyly. Long finger–ring finger syndactyly release may be delayed. The results of surgery are improved with a well-designed dorsal commissural flap and liberal use of full-thickness skin grafts. Recurrent web space contracture is the most common long-term complication.

Camptodactyly Camptodactyly (bent fingers) usually occurs at the PIP joint of the little finger. The extent of the flexion deformity varies. Approximately 70% of all patients have bilateral involvement. Other fingers may be involved, but incidence decreases toward the radial side of the hand. The natural history of untreated, severe camptodactyly is no improvement or a gradual increase in deformity with growth. Camptodactyly may occur in isolation or may be associated with syndromes. Almost every conceivable structure has been implicated in the pathogenesis of isolated camptodactyly. Dynamic muscular imbalance is thought to be the primary cause in most cases. No treatment is uniformly successful, probably because it is difficult to differentiate primary and secondary contractures. Treatment begins with splinting. For the young

Polydactyly Polydactyly is the presence of extra digits on the hand or foot (Figure 16-25). The condition is usually postaxial (ulnar to the little finger or lateral to the fifth toe) or preaxial (radial to the thumb or medial to the great toe), but it may occur in a central location. Extra digits range from a vestigial digit attached by a narrow bridge of skin to a completely developed digit with its own metacarpal or metatarsal. Polydactyly may occur sporadically or as an autosomal dominant disorder. It is frequently ob-

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The Hand and Wrist viation of the hand, variable defects in the radial carpal bones, and variable presence and stiffness of the thumb and index fingers (Figure 16-26). The extent of deficiency is also variable in congenital hypoplasia/aplasia of the thumb. Both conditions may be associated with other disorders, including congenital heart disease (Holt-Oram syndrome), craniofacial abnormalities, vertebral anomalies (VATER association), and Fanconi anemia. TAR syndrome (thrombocytopenia with absent radius) is unique because in this syndrome, the thumb is normal. In other syndromes, if the radius is deficient, the thumb is also hypoplastic or absent. Operative management is based on the severity of the deficiency. Reconstructive procedures are indicated when the hypoplastic thumb is adequately sized and the CMC joint is stable. Transfer of the index finger to the position of the thumb (index pollicization) is used in the treatment of severe thumb hypoplasia/aplasia. In patients with radial hemimelia, procedures to centralize the hand are performed at approximately 1 year of age, except when a short forearm and limited elbow motion are present.

child with persistent PIP joint contractures of 40°or greater and no bony changes, soft tissue releases are useful.

Clinodactyly Clinodactyly is curvature of the finger in the radial or ulnar plane. The most common deformity is radial angulation of the little finger secondary to a delta-shaped middle phalanx. Clinodactyly is more common in males and is usually bilateral. The disorder is frequently seen in 30 syndromes and is found occasionally in 22 conditions. Isolated clinodactyly is usually simple (no rotation and less than 45° of angulation) and does not require treatment. Surgical realignment is indicated when overlap of the fingers interferes with gripping of objects.

Hypoplasia/Aplasia of the Thumb and Radial Hemimelia Radial hemimelia and hypoplasia/aplasia of the thumb are part of a spectrum of congenital deletions of the radial portion of the upper limb. Radial hemimelia, also called radial club hand, is characterized by partial or complete absence of the radius, variable shortening and bowing of the ulna, radial de-

Figure 16-26: Paraxial Radial Hemimelia Short, bowed forearm with marked radial deviation of hand. Thumb absent. Radiograph shows partial deficit of radial ray (vestige of radius present). Scaphoid, trapezium, and metacarpal and phalanges of thumb absent.

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Chapter 16 ital deformities, surgical reconstruction is not commonly required in ulnar hemimelia.

Ulnar Hemimelia Children with ulnar hemimelia have a deficiency of bone and soft tissue on the ulnar aspect of the forearm and hand. Deficiency of the ulna ranges from the presence of an ulna that is well formed but short to complete absence of the ulna, which may be associated with radiohumeral synostosis. In contrast to radial defects, ulnar hemimelia is uncommonly associated with abnormalities of other organ systems. However, patients with ulnar hemimelia are more likely to have other skeletal anomalies, including tibial hemimelia and scoliosis. Except to correct the associated dig-

ADDITIONAL READINGS Berger RA, Weiss A-PC, eds. Hand Surgery. Philadelphia, Pa: Lippincott Williams and Wilkins; 2004. Green DP, Hotchkiss RN, Pederson WC, Scott WW, eds. Green’s Operative Hand Surgery, 5th edition. New York, NY: Churchill Livingstone; 2005. Mackin EJ, Callahan AD, Osterman AL, Skirven TM, Schneider LH, Hunter JM, eds. Hunter, Mackin, and Callahan’s Rehabilitation of the Hand and Upper Extremity, 5th edition. Philadelphia, Pa: Mosby; 2002. Smith PJ, Lister G. Lister’s The Hand: Diagnosis and Indications. Smith P, ed. New York, NY: Churchill Livingstone; 2002.

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seventeen The Pelvis, Hip, and Thigh Roy K. Aaron, MD Eric M. Bluman, MD, PhD Michael G. Ehrlich, MD Peter G. Trafton, MD, FACS

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Chapter 17 anteriorly at the fibrocartilaginous symphysis pubis. The sacrum and the coccyx do not contain joints, and they function as a single unit. The posterior sacrum contains five neural foramina to allow passage of the four sacral nerve roots and a single inferior foramen for the filum terminale (Figure 17-2). The triangular sacrum is contoured into the two ilia. This interlocking shape, in addition to the very strong anterior and posterior sacroiliac ligaments, transmits the weight of the trunk to the lower extremities. The sacroiliac joints are synovial joints, but their interlocking shape permits no significant motion. Stability of the pelvis is enhanced by the sacroiliac, sacrospinous, sacrotuberous, iliolumbar, and symphyseal ligaments. The ball-and-socket shape of the hip joint provides many degrees of freedom and resultant mobility. The articular surface of the acetabulum includes a broad, horseshoe-shaped outer rim called the lunate surface, a central

ANATOMY AND BIOMECHANICS The pelvis is a basin-shaped structure that supports the spine and joins the axial skeleton to the lower extremities. At maturity, the pelvis includes two innominate bones—the sacrum and the coccyx. Each innominate bone is formed by the fusion of the ilium, ischium, and pubis at the triradiate cartilage, a trefoil-shaped growth plate that has an important role in determining the shape of the acetabulum, the congruency of the hip joint, and the propensity to osteoarthritis (Figure 17-1). The ilium is a broad, fan-shaped bone with a concave inner table that tapers inferiorly to form the roof to the acetabulum. The ischium forms the inferior border of the obturator foramen and the posterior wall of the acetabulum. Its thickened tuberous portion bears significant weight when an individual is seated. The pubis forms the anterior wall of the acetabulum and includes the superior and inferior pubic rami, which form the remainder of the obturator foramen before joining together

Figure 17-1: Hemipelvis Lateral view

Medial view

Posterior superior iliac spine

Iliac tuberosity

Anterior superior iliac spine

Posterior superior iliac spine

Ala or wing of ilium Iliac fossa Anterior inferior iliac spine Iliopubic eminence Acetabulum Acetabular notch Superior pubic ramus Pecten Pubic tubercle

Posterior inferior iliac spine Greater sciatic notch Body of ilium Spine of ischium Lesser sciatic notch Body of ischium

Iliac crest

Obturator foramen

Ischial tuberosity

Auricular surface (for sacrum)

Obturator foramen Obturator crest Symphyseal surface Inferior pubic ramus

Ramus of ischium Ilium

Ischium

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Posterior inferior iliac spine Greater sciatic notch Spine of ischium Lesser sciatic notch Arcuate line Body of ilium Body of ischium Ischial tuberosity Ramus of ischium

Pubis

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The Pelvis, Hip, and Thigh Figure 17-2: Sacrum and Coccyx Posterior superior view

Facets of superior articular processes

Sacral tuberosity Auricular surface Lateral sacral crest Median sacral crest Posterior sacral foramina Sacral cornu (horn) Coccygeal cornu (horn)

Sacral hiatus Dorsal surface

fossa that gives rise to the ligamentum teres, and an inferior notch that is bridged by the transverse acetabular ligament (Figure 17-3). The circumferential fibrocartilaginous acetabular labrum increases the effective surface area of the acetabulum by 40%, thereby reducing stress on the articular cartilage. The shape of the mature hip joint and its strong capsule

makes dislocation unlikely without significant trauma. The femur is the largest bone in the body and provides osseous support for the thigh. The proximal end includes the head, neck, and greater and lesser trochanters at the junction of the neck and femoral shaft. The neckshaft angle varies somewhat with age and

Figure 17-3: Hip Joint Joint opened: lateral view Anterior superior iliac spine Anterior inferior iliac spine Iliopubic eminence

Articular cartilage

Acetabular labrum (fibrocartilaginous) Fat in acetabular fossa

Greater trochanter

Obturator artery Anterior branch

Head of femur

Posterior branch

Neck of femur

Obturator membrane

Intertrochanteric line

Transverse acetabular ligament Ligamentum teres (cut)

Ischial tuberosity Lesser trochanter

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Chapter 17 don. Other significant flexors are the tensor fascia lata, sartorius, rectus femoris, pectineus, adductor longus, and adductor brevis. The chief extensor is the gluteus maximus. Other hip extensors are the hamstrings. The hip abductors are the gluteus medius and gluteus minimus. The hip adductors are the adductor longus, adductor brevis, adductor magnus, and gracilis. External rotators are the gluteus maximus and several small muscles that insert on or about the posterior edge of the greater trochanter. The primary internal rotators are the gluteus minimus and the tensor fascia lata. The muscles of the thigh are arranged into three compartments: anterior (quadriceps), medial (adductors), and posterior (hamstrings) (Figure 17-6). Several muscles about the hip also cross the knee. Examples include the hamstrings, rectus femoris, sartorius, tensor fascia lata, and gracilis. These two-joint muscles are important in fine-tuning movement of the two joints, particularly during forceful activities, such as running. Furthermore, the span of these muscles across two joints must be understood if they are to be accurately examined for strength and possible contracture or strain.

gender but is approximately 125° in adults— a position that places the center of the head at the level of the tip of the greater trochanter. Coxa valga is a neck-shaft angle greater than 135°; this condition places the femoral head above the trochanter and predisposes the patient to subluxation. Coxa vara is a neck-shaft angle less than 115°—a condition that decreases effective abductor muscle function and effectively shortens the thigh. The neck of the femur is anteverted, or anteriorly angled, in relationship to the femoral condyles, by about 15°. Blood to the femoral head is primarily supplied by the medial circumflex femoral artery through its subsynovial retinacular vessels (Figure 17-4). The lateral circumflex and ligamentum teres arteries provide minor contributions to the femoral head. Almost the entire surface of the pelvis and thigh is covered by muscle (Figure 17-5). As a result, the pelvis and femur have a very good vascular supply that results in consistent fracture healing (femoral neck fractures are the exception). The chief flexor of the hip is the iliopsoas, which in reality comprises two muscles that come together at the iliopsoas ten-

Figure 17-4: Blood Supply to Femoral Head Posterior view

Anterior view Retinacular arteries (subsynovial)

Superior Anterior Inferior

Acetabular branch of obturator artery (often minute)

Anastomosis between medial and lateral circumflex femoral arteries Insertion of anterior joint capsule Ascending, Transverse, Descending branches of Lateral circumflex femoral artery

Superior Retinacular Posterior arteries Inferior (subsynovial) Anastomosis

lliopsoas tendon Medial circumflex femoral artery Profunda femoris artery

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Medial circumflex femoral artery Lateral circumflex femoral artery

Insertion of posterior joint capsule

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The Pelvis, Hip, and Thigh Figure 17-5: Bony Attachments of Buttock and Thigh Muscles Anterior View Origin of psoas major m. from sides of vertebral bodies, intervertebral discs, and transverse processes (T12–L4)

Iliacus m. Sartorius m. Rectus femoris m. Obturator internus and superior and inferior gemellus mm. Piriformis m. Gluteus minimus m. Vastus lateralis m. Intertrochanteric line Vastus medialis m. Vastus intermedius m.

Origins Insertions

Piriformis m. Pectineus m. Adductor longus m. Adductor brevis m. Gracilis m. Obturator externus m. Adductor magnus m. Quadratus femoris m. Iliopsoas m. Gluteus maximus m.

Posterior View Gluteus medius m. Gluteus minimus m. Tensor fasciae latae m. Sartorius m.

Superior gemellus m. Inferior gemellus m. Quadratus femoris m.

Rectus femoris m. Obturator externus m. Gluteus medius m. Quadratus femoris m. Iliopsoas m.

Obturator internus m. Articularis genus m.

Gluteus maximus m.

Adductor magnus m. Biceps femoris (long head) and semitendinosus mm.

Adductor magnus m.

Semimembranosus m.

Vastus lateralis m. Adductor magnus m. Adductor brevis m.

Iliotibial tract

Pectineus m. Vastus medialis m.

Biceps femoris m.

Adductor longus m. Rectus femoris, vastus lateralis, vastus intermedius and vastus medialis via patellar ligament

Sartorius m. Pes Gracilis m. anserinus Semitendinosus m.

Adductor magnus m. Gastrocnemius m. (medial head)

Vastus intermedius m. Biceps femoris m. (short head) Adductor magnus m. Vastus lateralis m.

Plantaris m. Gastrocnemius m. (lateral head) Popliteus m.

Semimembranosus m. Popliteus m. Note: Width of zone of attachments to posterior aspect of femur (linea aspera) is greatly exaggerated

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Chapter 17 Figure 17-6: Muscles of Hip and Thigh Anterior, deeper dissection Anterior superior iliac spine

Anterior superior iliac spine Iliacus muscle

Sartorius muscle (origin)

Psoas major muscle

Anterior inferior iliac spine

Gluteus medius muscle Inguinal ligament

Ligaments of hip joint

Pubic tubercle Iliopsoas muscle

Pectineus muscle

Tensor fasciae latae muscle Pectineus muscle Tensor fasciae latae muscle (origin) Rectus femoris muscle (origin) Greater trochanter Iliopsoas muscle (cut) Adductor longus muscle Gracilis muscle Sartorius muscle Rectus femoris muscle* Vastus lateralis muscle* Vastus intermedius muscle* Vastus medialis muscle* Iliotibial tract Rectus femoris tendon (becoming part of quadriceps tendon) Lateral patellar retinaculum Patella Medial patellar retinaculum Patellar ligament

Anteromedial intermuscular septum

Sartorius tendon Gracilis tendon Semitendinosus tendon

Pes anserinus

Tibial tuberosity Anterior, superficial dissection

Iliotibial tract (cut) Rectus femoris tendon (cut) Quadriceps tendon Patella Lateral patellar retinaculum Medial patellar retinaculum Head of fibula

*Muscles of quadriceps femoris

Patellar ligament Tibial tuberosity

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Sartorius tendon

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The Pelvis, Hip, and Thigh Figure 17-6: Muscles of Hip and Thigh (continued) Posterior, superficial dissection

Posterior, deeper dissection Iliac crest Gluteal aponeurosis over Gluteus medius muscle Gluteus minimus muscle Gluteus maximus muscle Piriformis muscle Sciatic nerve Sacrospinous ligament Superior gemellus muscle Obturator internus muscle Inferior gemellus muscle Sacrotuberous ligament Quadratus femoris muscle Ischial tuberosity Semitendinosus muscle Greater trochanter Biceps femoris muscle (long head) Adductor minimus part of Adductor magnus muscle Semimembranosus muscle Iliotibial tract Gracilis muscle Biceps femoris muscle Short head Long head Semimembranosus muscle Semitendinosus muscle Popliteal vessels and tibial nerve Common fibular (peroneal) nerve Plantaris muscle Gastrocnemius muscle Medial head Lateral head Sartorius muscle Popliteus muscle

Plantaris tendon (cut)

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Chapter 17 Figure 17-7: Lumbar Plexus T12

Subcostal nerve (T12)

L1 Iliohypogastric nerve Ilioinguinal nerve

L2

Genitofemoral nerve

Ventral rami of spinal nerves

Lateral cutaneous nerve of thigh

L3

L4

Muscular branches to psoas and iliacus muscles Femoral nerve Accessory obturator nerve (often absent)

Anterior division Posterior division

L5 Obturator nerve

Lumbosacral trunk

short head of the biceps femoris, which is innervated by the peroneal component of the sciatic nerve. The vessels, similar to the nerves, leave the pelvis anterior and posterior to the hip joint. The buttocks are supplied primarily by the superior and inferior gluteal arteries, which are branches of the internal iliac artery. The femoral artery, a continuation of the external iliac artery, supplies most of the remainder of the lower extremity. The femoral artery exits the pelvis between the femoral vein medially and the femoral nerve laterally and thereafter gives off the profunda femoris and the medial and lateral circumflex femoral arteries before continuing down the leg with the saphenous nerve deep to the sartorius. In the distal thigh, it passes to the posterior thigh through an opening in the adductor magnus, at which time its name is changed to the popliteal artery (Figure 17-9). In quiet, two-legged standing, very minimal hip muscle force is necessary to maintain erect stance. However, during the midportion of the stance phase of gait, all the body weight is on one leg while the opposite limb is swinging through. At this time, a force of approximately 3 times body weight must be developed through the abductor muscles

The lumbar plexus is formed by L1–L4 ventral rami (Figure 17-7). The femoral nerve (posterior branches of L2–L4) enters the thigh lateral to the femoral artery. After supplying motor branches to the sartorius and quadriceps and cutaneous branches to the anterior thigh, the femoral nerve continues as the saphenous nerve, supplying sensation to the medial calf and ankle. The obturator nerve (anterior branches of L2–L4) supplies the adductor muscles and provides sensation in the medial thigh. The sacral plexus is formed by the L4–S4 ventral rami (Figure 17-8). The nerves from the sacral plexus exit the pelvis posterior to the hip joint. The superior gluteal nerve (posterior branches L4–S1) innervates the primary hip abductors (gluteus medius and gluteus minimus). The inferior gluteal nerve (posterior branches L5–S2) innervates the primary hip extensor (gluteus maximus). The sciatic nerve includes the tibial nerve (anterior branches L4–S3) and the common peroneal nerve (posterior branches L4–S2). The tibial segment of the sciatic nerve innervates the posterior muscles of the thigh (except for the short head of the biceps femoris). The tibial segment of the sciatic nerve innervates the posterior muscles of the thigh except for the

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The Pelvis, Hip, and Thigh Figure 17-8: Sacral Plexus L4 Anterior division Posterior division

Lumbosacral trunk

L5 Gray rami communicantes S1

Superior gluteal nerve

S2 Inferior gluteal nerve S3

Pelvic splanchnic nerves (parasympathetic to inferior hypogastric [pelvic] plexus)

Nerve to piriformis S4 Tibial nerve Sciatic nerve

S5 Coccygeal nerve

Common fibular (peroneal) nerve

Nerve to quadratus femoris (and inferior gemellus) Nerve to obturator internus (and superior gemellus)

Anococcygeal nerve Perineal branch of 4th sacral nerve Nerve to levator ani and (ischio-) coccygeus muscles Pudendal nerve Perforating cutaneous nerve Posterior cutaneous nerve of thigh

Note any pelvic obliquity (one iliac crest lower than the other). A leg-length discrepancy causes an apparent obliquity that can be corrected by placing blocks under the shorter limb, but fixed obliquity from a spinal deformity or hip abduction contracture cannot be corrected by this maneuver. Other palpable landmarks are the greater trochanter; the anterior superior iliac spine (ASIS); and, deep to the dimples of Venus, the posterior superior iliac spine (PSIS). Observe the patient walking. If the problem is primarily pain without significant deformity, the patient will shorten the stance phase on the affected side (coxalgic gait). If the problem is abductor muscle weakness or severe arthritis, the patient will compensate by means of Trendelenburg lurch. The hip joint allows motion in all planes. With the pelvis stabilized (preventing pelvicvertebral motion), the average range of hip flexion in adults is 120°, and extension is 15°. Abduction averages 40°, adduction averages 30°, and internal and external rotation (with the hip in extension) are both

to counteract gravity and keep the pelvis from dropping down on the non–weight-bearing side. Weakness or paralysis of the hip abductor muscles from coxa vara or neuromuscular disorders may require compensatory gait mechanics. The patient leans over the affected hip during the stance phase (abductor or Trendelenburg lurch) to decrease the moment arm of the contralateral side. Likewise, an arthritic hip may increase friction at the joint surface, which results in greater abductor force required to balance the moment of body weight and compensation by Trendelenburg lurch. Using a cane in the opposite hand counteracts some of the stance limb weight-bearing forces and can be quite helpful in relieving pain and allowing patients with osteoarthritis or hip abductor weakness to walk more efficiently (see Chapter 12).

PHYSICAL EXAMINATION With the patient standing, inspect the anterior thigh for quadriceps atrophy and overall alignment of the hip, knee, and ankle. From the posterior aspect, palpate the iliac crests.

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Chapter 17 Figure 17-9: Arteries and Nerves of Thigh Superficial dissection Lateral femoral cutaneous nerve (cut) Sartorius muscle (cut) Tensor fasciae latae muscle (retracted)

Iliopsoas muscle Femoral nerve, artery, and vein

Gluteus minimus and medius muscles

Pectineus muscle Lateral circumflex femoral artery

Deep artery of thigh Adductor longus muscle

Rectus femoris muscle

Adductor canal (opened by removal of sartorius muscle)

Vastus lateralis muscle

Saphenous nerve

Vastus medialis muscle

Nerve to vastus medialis muscle Adductor magnus muscle Anteromedial intermuscular septum covers entrance of femoral vessels to popliteal fossa (adductor hiatus)

Saphenous nerve and saphenous branch of descending genicular artery Articular branch of descending genicular artery (emerges from vastus medialis muscle)

Sartorius muscle (cut)

Patellar anastomosis

Superior medial genicular artery (from popliteal artery)

Infrapatellar branch of Saphenous nerve

Inferior medial genicular artery (from popliteal artery)

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The Pelvis, Hip, and Thigh approximately 30° to 40°. Greater degrees of rotation, particularly external rotation, are observed if the measurements are made with the hip flexed. The zero starting position for measuring hip motion is with the thigh in line with the trunk. In measuring flexion and extension, the opposite hip is held in enough flexion to prevent pelvic-vertebral motion. Avoid positioning the opposite hip in excessive flexion because this position will rock the pelvis into abnormal inclination, thereby creating a false-positive

hip flexion contracture. Instead, flex the opposite hip to a position where the lumbar spine just starts to flatten or, more precisely, to a position in which the inclination of the pelvis is similar to a normal standing posture (ASIS inferior to PSIS by approximately 3°). Maximum flexion is the point at which the pelvis begins to rotate. Now, allow the hip to extend. If the patient has a hip flexion contracture, the pelvis will start to rock before the leg reaches the examination table (positive Thomas sign) (Figure 17-10).

Figure 17-10: Measurement of Hip Flexion/Extension and Thomas Test 90˚

120˚

0˚ Zero starting position is the thigh in line with the trunk. In measuring hip extension, the contralateral limb should be held in flexion to eliminate lumbar spine motion. Hip flexion is typically measured by bringing both thighs into flexion.

120˚

0˚ Neutral

Positive Thomas test indicates a hip flexion contracture, ie, the affected hip cannot be extended to the neutral position.

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Chapter 17 Measure abduction and adduction with the pelvis level (limbs 90° to a transverse line across the ASISs). Maximum abduction is reached when the pelvis begins to tilt—a movement that you can detect by keeping one hand on the opposite ASIS while moving the leg. For adults, it is more practical to measure rotation with the hips in flexion. However, this approach should not be used in children or when femoral torsion is assessed (see Chapter 3). Assess hip flexors with the patient seated. To quantify strength, ask the patient to flex the hip, and then resist the effort. Test the gluteus maximus with the patient prone and the knee flexed 90° (to minimize concurrent hamstring activity). Hip abductor strength is measured with the patient lying on the unaffected side; ask the patient to abduct the hip while you resist the effort. Trendelenburg test is a useful maneuver for assessing hip abductor function (Figure 17-11). Place your hands on both iliac crests, and ask the patient to stand on one leg. A positive test is dropping of the pelvis on the opposite side and results from either abductor weakness or hip dysplasia and resultant abnormal abductor mechanics. FABER (flexion, abduction, and external rotation) is a stress maneuver that chiefly detects sacroiliac pathology. Place the hip in 90° of flexion and maximum abduction and external rotation. Apply a posteriorly directed force to the knee. A positive test is increased pain. A positive FABER sign, however, is not specific for sacroiliac pathology, as it may be found with hip joint pathology or may be a nonorganic finding.

Figure 17-11: Trendelenburg Test

Trendelenburg test Left: Patient demonstrates negative Trendelenburg test of normal right hip. Right: positive test of involved left hip. When patient is standing on the affected side, the pelvis on the opposite side drops, indicating either actual weakness of the gluteus medius muscle, functional weakness of the hip abductors secondary to altered alignment of the hip joint, or a painful arthritic hip joint that cannot tolerate the normal force of hip abductor contraction during single-legged stance. The trunk shifts to the left as patient attempts to decrease biomechanical stresses across involved hip and thereby maintain balance.

the pain is referred to the buttocks or distal thigh. As degeneration of the articular cartilage progresses, the duration and the frequency of the pain intensify. Pain at rest or pain that wakens the patient at night is associated with severe arthritis. The most sensitive sign of early osteoarthritis of the hip is loss of internal rotation (Figure 1712). As the disease and joint contractures progress, decreased abduction, flexion, and extension are observed. A coxalgic limp, with or without Trendelenburg lurch, is often present. Anteroposterior (AP) and lateral radiographs show joint space narrowing in the early stages and osteophytes, cyst formation, and sclerosis as the disease progresses (Figure 17-13). Osteophytes can occur in the

DEGENERATIVE DISEASES AND DISORDERS Osteoarthritis Osteoarthritis of the hip may be primary (idiopathic) or secondary to an underlying hip disorder (eg, pediatric hip disease, osteonecrosis, previous infection, or previous trauma). Typical presenting symptoms are indolent onset of anterior thigh or groin pain that is deep and activity related. Occasionally,

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The Pelvis, Hip, and Thigh Figure 17-12: Osteoarthritis of the Hip Characteristic habitus and gait

Limitations of Internal Rotation

30˚ 10˚

Internal rotation

0˚ External rotation

Loss of internal rotation with hip flexed is a sensitive and easy test of hip arthritis.

floor of the acetabulum and around the periphery of the femoral head and may cause lateralization and proximal migration of the femoral head.

The differential diagnosis includes: ✦

Osteonecrosis of the femoral head (evident on radiographs) ✦ Trochanteric bursitis (localized tenderness, normal radiographs) ✦ Lateral femoral nerve entrapment (burning pain, sensory changes, normal motion) ✦ Lumbar disc herniation or degenerative disc disease (buttock pain, distal motor and sensory changes, no restriction of hip motion) ✦ Tumors of the lumbar spine, pelvis, or upper thigh (back pain, night pain, normal motion)

Figure 17-13: Osteoarthritis of the Hip

Nonoperative treatment includes education of the patient, activity modification, optimization of any leg-length discrepancies (often with a small heel lift), and judicious use of nonsteroidal anti-inflammatory drugs (NSAIDs). Physiotherapy to improve range of motion is often unsuccessful because this type of exercise provokes joint pain. Low-impact exercises, particularly swimming, may improve muscle strength. As the disease progresses, the patient will

AP radiograph of the hip showing degeneration of cartilage and osteophytes at margins of acetabulum

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Chapter 17 benefit from the use of a cane in the opposite hand. Adolescents and young adults who have malalignment of the acetabulum, proximal femur, or both, may benefit from realignment osteotomies of the pelvis, proximal femur, or both. Arthrodesis should be considered for adolescents or young adults with unilateral end-stage arthritis and no other significant limb dysfunction. In other patients who have severe pain and joint erosions, a total hip replacement arthroplasty is indicated (see Figure 4-8). These procedures can dramatically reduce pain and improve function, but the decision for surgery should be made with an understanding of potential complications, including infection (0.5% to 1.0%), dislocation (8% to 10%), and deep venous thrombosis (40% to 60% if no prophylaxis is used). The long-term concern of total joint arthroplasty is aseptic loosening. When a joint implant is loose and has to be revised, less bone stock is available and the rates of all complications are higher, particularly the rate of recurrent loosening. The risk of needing to replace a hip arthroplasty is very low in a patient older than 65 years, who typically places moderate demands on the joint and who has a limited life expectancy, but it is virtually universal in a young adult who is in good health and places more strenuous demands on the joint. Appropriate preoperative planning and better implants have improved the results of both primary and revision arthroplasty.

to femoral head collapse and, ultimately, endstage arthritis. Common causes of femoral head osteonecrosis include trauma (hip dislocations and femoral neck fractures), corticosteroid use, sickle cell disease, systemic lupus erythematosus, and alcohol abuse. The male-tofemale ratio is approximately 4:1. Osteonecrosis is bilateral in approximately 50% of patients, but the onset of disease and symptoms is typically earlier on one side. Indolent onset of dull, activity-related pain is the usual presenting symptom, with the pain most often located in the groin or buttock. However, the onset of pain may begin suddenly if an acute collapse or shear fracture involves the articular surface. Early signs include decreased internal rotation and abduction. As incongruity of the joint progresses, the pain increases, the gait becomes antalgic, and range of motion decreases. Good-quality AP and lateral radiographs are important in making the diagnosis. Sclerosis is a typical radiographic finding early in the disease process; however, in the early stage of osteonecrosis, the radiographs may be normal, but magnetic resonance imaging (MRI) will be positive (see Figure 2-14). MRI also is useful in defining the extent of osteonecrosis and identifying early osteonecrosis in patients who are susceptible to bilateral involvement and who have normal radiographs of the contralateral hip. Treatment and prognosis depend on the extent of osteonecrosis and the degree of joint congruity. Observation is indicated if the area of osteonecrosis is small and unlikely to cause collapse of the articular surface. The optimal procedure if the area of osteonecrosis is large but the joint has not collapsed is highly debatable at this time. Options include vascularized or nonvascularized structural bone grafts, osteoinductive grafts, osteotomies, and electrical stimulation. For hips that have progressed to significant segmental collapse, total hip arthroplasty is the best salvage procedure. Because many patients are young, subsequent revision arthroplasty, with its attendant problems, is common.

Osteonecrosis The femoral head, with its vulnerable circulation (see Figure 17-4), is the most common site of osteonecrosis. The true incidence is difficult to establish, but osteonecrosis accounts for 5% to 10% of the total hip replacements done in the United States. The cause and pathophysiology of osteonecrosis are discussed in Chapter 2; in brief, some disturbance of circulation causes death of osteocytes in a variably sized segment of the femoral head. Subsequent secondary structural changes lead

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The Pelvis, Hip, and Thigh ping. If symptoms are severe, the patient feels that “the joint is coming out of the socket.” Snapping and pain are commonly noted when climbing stairs, when rising from a seated position, or when lying with the affected side up and rotating the leg. Examination typically shows no restriction of motion or abnormal gait. Snapping of the iliotibial band can be provoked if the patient stands with the leg adducted, then rotates the hip. A snap or subluxation will be perceived over the greater trochanter. Snapping of the iliopsoas tendon is caused by subluxation of the tendon over the iliopectineal eminence as the hip goes from flexion to extension. Patients perceive pain in the groin. AP and lateral radiographs of the hip are obtained to exclude other conditions such as osteoarthritis, osteonecrosis, and intra-articular loose bodies. Treatment in most patients constitutes explanation of the condition and observation. Patients with pain are managed with activity modification, judicious use of NSAIDs, and stretching exercises for associated iliotibial band contractures. Corticosteroid injections may be helpful for more resistant cases. Surgery is infrequently needed and is reserved for cases that do not respond to nonoperative management.

MISCELLANEOUS AND SPECIAL CONDITIONS Trochanteric Bursitis Inflammation of the greater trochanteric bursae, known as trochanteric bursitis, is the most common cause of bursitis about the hip. This problem is more common in females and middle-aged to older patients. The problem may be isolated or associated with lumbar spine disorders, hip conditions, leg-length discrepancy, rheumatoid arthritis, previous surgery about the hip, and ipsilateral quadriceps weakness and knee conditions. Sometimes, it is difficult to distinguish whether the pain over the greater trochanter is referred pain or a concomitant bursitis. Tendinosis of the gluteus medius and minimus tendons is also difficult to distinguish. Typical symptoms include pain and tenderness in the region of the greater trochanter that may radiate to the lateral thigh. Symptoms may be increased in the morning on initiation of walking, after extended walking, or on rising after sitting for a period of time. Patients note discomfort when lying on the affected side. Examination demonstrates tenderness over the lateral aspect of the greater trochanter that is exacerbated at the extremes of adduction and internal rotation. Treatment includes activity modifications, use of a cane, and NSAIDs. Injection of the bursa with corticosteroids and a local anesthetic can be diagnostic and therapeutic. Surgery is rarely needed.

Meralgia Paresthetica Meralgia paresthetica is entrapment of the lateral femoral cutaneous nerve, usually between the inguinal ligament and the medial edge of the sartorius. This syndrome is associated with obesity, direct compression from tight clothing or straps around the waist (eg, tool belts or backpacks), scar tissue from previous operations, or repetitive trauma over the nerve. Infrequently, an intrapelvic mass causes compression of the nerve. Typical symptoms include pain and dysesthesia that radiate to the lateral aspect of the thigh. Examination typically shows decreased sensation in the distribution of the lateral femoral cutaneous nerve and positive Tinel sign medial to the ASIS. Muscle strength, hip motion, and the abdominal examination

Snapping Hip Snapping or popping sensations about the hip are usually caused by tendons sliding over bony prominences, but occasionally may be symptoms of uncommon problems such as acetabular labral tears or intra-articular loose bodies. In most patients, the snapping is mild clicking that is not painful and resolves without treatment. A few patients have pain that is persistent and limiting. The iliotibial band moving over the greater trochanter is the most common site of snap-

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Chapter 17 Pelvic ring injuries can be classified as stable or unstable. Stable injuries involve only one side of the ring. Examples include directimpact fracture of the sacrum, coccyx, or iliac wing and isolated pubic ramus fractures associated with low-energy falls in osteoporotic elderly individuals (Figure 17-14). Stable injuries can be treated symptomatically with crutch- or walker-assisted ambulation. Unstable pelvic fractures include fracture and/or ligamentous disruption in two parts of the ring. Examples include straddle injuries with bilateral superior and inferior pubic rami fractures, lateral compression injuries with overlapping pelvis, open book fractures with disruption of symphysis pubis and anterior sacroiliac ligaments, and vertical shear fractures with ipsilateral disruption of the anterior and posterior ring (Figures 17-15 and 17-16). Some unstable pelvic fractures can be treated nonoperatively with a period of bed rest to

are normal unless a concomitant disorder is present. Treatment includes avoidance of clothes or activities that compress the nerve. Weight reduction can alleviate symptoms in obese patients. A corticosteroid and local anesthetic injection can be diagnostic and occasionally therapeutic. Surgical release is indicated for persistent and severe symptoms.

TRAUMATIC DISORDERS Fractures of the Pelvis Although the acetabulum is part of the pelvis, the term pelvic fractures is typically restricted to fractures of the pelvic ring. These fractures range from low-impact injuries that are simple to treat to high-impact injuries that cause hemodynamic instability, may be life threatening, and result in a very unstable pelvis.

Figure 17-14: Stable Pelvic Ring Fractures

Fracture usually requires no treatment other than care in sitting; inflatable ring helpful. Pain may persist for a long time. Transverse fracture of the sacrum that is minimally displaced

Fracture of iliac wing from direct blow

Fracture of ipsilateral pubic and ischial ramus requires only symptomatic treatment with shortterm bed rest and limited activity with walker- or crutch-assisted ambulation for 4 to 6 weeks.

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The Pelvis, Hip, and Thigh Figure 17-15: Unstable Pelvic Fractures

Radiograph shows open book fracture.

Open book fracture. Disruption of symphysis pubis with wide anterior separation of pelvic ring. Anterior sacroiliac ligaments are torn, with slight opening of sacroiliac joints. Intact posterior sacroiliac ligaments prevent vertical migration of the pelvis.

Caused by forceful impact to knee or foot transmitted to pelvis or by direct blow to pelvis.

Straddle fracture. Double break in continuity of anterior pelvic ring causes instability but usually little displacement. Visceral (especially genitourinary) injury likely.

Vertical shear fracture. Upward and posterior dislocation of sacroiliac joint and fracture of both pubic rami on same side result in upward shift of hemipelvis. Note also fracture of transverse process of 5th lumbar vertebra (L5), avulsion of ischial spine, and stretching of sacral nerves.

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Chapter 17 Figure 17-16: Internal Fixation for Type of Vertical Shear Fracture

Vertical shear fracture with disruption of symphysis pubis and sacroiliac joint

Reduction and internal fixation with percutaneous screw fixation of the sacroiliac joint and open reduction and plate fixation of the symphysis pubis disruption

The peroneal segment of the sciatic nerve is at greatest risk. Radiographic evaluation includes AP radiographs of the pelvis, and internal and external Judet views (AP radiographs centered on the hip with the pelvis rotated 45° internally and externally). A CT scan further characterizes the injury. The Judet and Letournel classification of acetabular fractures is most commonly used (Figure 17-17). If the injury involves a significant portion of the weight-bearing dome and the articular surface is displaced more than 2 mm, open reduction and internal fixation are required to minimize the risk of traumatic arthritis (Figure 17-18).

allow initial healing, followed by progression to assisted ambulation. Other injuries require reduction and internal fixation of one or both sides of the ring to avoid or minimize the risk of pelvic deformity and associated pain and dysfunction. Examination shows tenderness on compression and possible instability of the pelvis. Evaluation should include assessment for all potential associated injuries. Most injuries are obvious on an AP radiograph of the pelvis; however, special views and computed tomographic (CT) scans are frequently required to delineate the full extent of injury.

Acetabular Fractures Hip Dislocation

Acetabular fractures often result from highimpact falls or motor vehicle accidents that transmit force most commonly from an impact to the greater trochanter or the flexed knee. These intra-articular fractures may result in a disabling, traumatic arthropathy. Associated injuries such as posterior dislocation of the hip and fracture of the femoral head complicate treatment and results. Examination should include assessment of sciatic, femoral, and obturator nerve function.

Approximately 90% of hip dislocations are posterior and are caused by a highenergy impact on the knee of a person sitting with the hip flexed and adducted (Figure 17-19). Less adduction of the hip at injury makes an associated posterior acetabular wall fracture more likely. These injuries typically occur to unbelted automobile occupants and would be rare if seat belt use were more prevalent. Fracture of the acetabulum,

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The Pelvis, Hip, and Thigh Figure 17-17: Acetabular Fractures

Posterior wall fracture

Transverse fracture

Posterior column fracture

Anterior wall fracture

Anterior column fracture

Associated posterior column Associated transverse and and posterior wall fractures posterior wall fractures

Associated anterior and posterior hemitransverse fractures

T-shaped fracture

Fracture of both columns

shear fracture of the medial femoral head, or both, may be present. The vascular supply to the femoral head and the sciatic nerve are vulnerable. Anterior dislocations often occur in sporting events. A forceful abduction and external rotation movement ruptures the stout anterior capsule, with the femoral head typically displaced to an inferior obturator position (Figure 17-20). Impaction fractures of the posterior femoral head may occur. The femoral nerve and artery are vulnerable.

Patients with posterior dislocations present with the hip held in flexion, adduction, and internal rotation and have apparent shortening of the limb. Persons with anterior dislocations present with the leg in marked abduction and external rotation. An AP radiograph of the pelvis and a cross-table lateral view confirm the diagnosis. Prompt treatment of posterior dislocations is mandated because the incidence of osteonecrosis of the femoral head progressively increases when reduction is delayed. Most

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Chapter 17 Figure 17-18: Acetabular Fracture Fixation

Representative fixation for both-column fracture with associated iliac wing fractures

ery 6 years of age. Factors that increase the risk of fracture are those that exacerbate osteoporosis and those that increase the likelihood of a fall. Therefore, associated risk factors include age, gender, race, alcoholism, rheumatoid arthritis, sedentary lifestyle, cerebral dysfunction, dementia, cerebrovascular disease, use of psychotropic medications, and peripheral neuropathies. The goals of treatment are to reduce mortality (10% to 30% in elderly patients at 6 months after hip fracture) and return patients to their preoperative functional status. Increased mortality is associated with male gender, advanced age, poorly controlled systemic disease, cerebral dysfunction, institutionalization, internal fixation before optimization or correction of medical problems, and postoperative complications. Factors associated with return to independent function include absence of mental impairment,

hip dislocations can be reduced by closed means using either conscious sedation or general anesthesia. Principles of reducing a posterior dislocation include traction with the hip in a position of 90° flexion and slight adduction. As the femoral head reenters the acetabulum, there is a palpable clunk. Postreduction radiographs are critically assessed to confirm a congruent reduction and no evidence of osteochondral fragments in the joint. Subsequent management depends on associated injuries and stability of the joint. Uncomplicated dislocations can be managed with activity modifications and crutchassisted ambulation.

Fractures of the Proximal Femur Fractures of the proximal femur, often called hip fractures, are very common in the elderly population. After the age of 50 years, the incidence of hip fractures doubles for ev-

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The Pelvis, Hip, and Thigh Figure 17-19: Posterior Dislocation of Hip

Typical deformity. Injured limb adducted, internally rotated, and flexed at hip and knee, with knee resting on opposite thigh. Mechanism of injury often by impact with dashboard, which drives femoral head backward, out of acetabulum.

Dislocated femoral head lies posterior and superior to acetabulum. Femur adducted and internally rotated; hip flexed. Sciatic nerve may be stretched.

AP radiograph shows superior position of femoral head and no apparent fracture of the acetabulum.

Figure 17-20: Anterior Dislocation of Hip, Obturator Type

Characteristic position of affected limb. Hip flexed, thigh abducted and externally rotated.

Femoral head in obturator foramen of pelvis; hip flexed and femur widely abducted and externally rotated.

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Chapter 17 independent community ambulation prior to injury (as opposed to walking only in therapy sessions or around the house), the presence of another person in the home, and interdisciplinary management. Most hip fractures are caused by a fall from a standing position with a direct blow over the greater trochanter. The two patterns of injury are femoral neck and intertrochanteric fractures (Figures 17-21 and 17-22). Osteonecrosis of the femoral head and nonunion may complicate femoral neck fractures; however, patients with intertrochanteric fractures have an overall poorer prognosis because, on average, they are older and typically have more limited preoperative ambulation function. Presenting symptoms include an inability to walk after a fall and pain in the groin or buttock. Patients with a displaced fracture lie with the extremity shortened and with the hip in external rotation and slight abduction. Patients with nondisplaced fracture may have no obvious deformity but a positive log-roll test (pain on internal and external rotation of the limb). AP and cross-table lateral radiographs of the hip demonstrate most fractures. MRI is the most sensitive test for identifying an occult fracture. Treatment and complications are determined by whether the fracture is in the

femoral neck or the intertrochanteric region. Femoral neck fractures that are impacted or nondisplaced have a low rate of nonunion (⬍5%) and avascular necrosis (⬍10%); however, in displaced femoral neck fractures, the incidence of avascular necrosis (AVN) is approximately 40%, and the nonunion rate is 10% or greater. Nondisplaced femoral neck fractures are best treated by multiple-screw fixation. Displaced femoral neck fractures in active, healthy elderly patients are best treated by reduction and screw fixation, but this injury in older, sedentary individuals is better managed by a hemiarthroplasty prosthetic replacement. Fractures of the femoral neck occurring in young adults are usually secondary to highimpact motor vehicle accidents. The degree of soft tissue damage is greater, and therefore, the incidence of AVN is much higher (approximately 80% in persons 20–40 years of age). This is a “vascular emergency,” and urgent reduction is required. In the elderly population, the timing of surgery is less urgent; however, unless there are comorbidities that must be corrected, patients do better if the hip fracture is reduced and fixed within 24 to 48 hours. Although technically a femoral neck injury, a cervicotrochanteric fracture, or fracture at the base of the femoral neck, has a low

Figure 17-21: Fracture of Femoral Neck and Intertrochanteric Fracture of Femur

Nondisplaced femoral neck fracture

Two-part, minimally displaced intertrochanteric femur fracture

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Comminuted four-part intertrochanteric femur fracture

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The Pelvis, Hip, and Thigh incidence of osteonecrosis. Furthermore, these fractures cannot be adequately fixed with multiple pins and should be managed with techniques used for intertrochanteric fractures. Intertrochanteric fractures of the femur occur in a region of ample blood supply. Therefore, fracture hemorrhage may be a problem, but the incidences of osteonecrosis and nonunion are low. Stable intertrochanteric fractures are two-part fractures without significant posteromedial comminution in the posterior medial aspect of the region. Unstable fractures have posteromedial comminution and frequently are three- or four-part injuries with separate fractures of the lesser trochanter, greater trochanter, or both. Intertrochanteric fractures of the femur are best managed by reduction and internal fixation with the use of a device that stabilizes the head and neck to the shaft while the intertrochanteric fracture heals. The development of compression sliding hip screws has significantly reduced the complication of the fixation device cutting out of the osteopenic femoral head during the healing process (Figure 17-22).

Figure 17-22: Intertrochanteric Fracture of Femur

Fractures of the Femoral Shaft

Fractures of the Femur in Children

Femoral shaft fractures in adults are usually the result of high-energy trauma in younger patients with normal bone. Consequently, these fractures usually are displaced and have obvious swelling and pain. AP and lateral radiographs confirm the diagnosis. Over the past 30 years, treatment of femoral shaft fractures has evolved from several weeks of skeletal traction followed by several weeks of cast immobilization to early reduction and intramedullary rod fixation (Figure 17-23). This change has greatly reduced the morbidity associated with prolonged immobilization, as well as the incidences of malunion, limb shortening, and nonunion. Furthermore, in multiply injured patients, early stabilization of femoral shaft fractures greatly reduces the risks of pulmonary and other systemic complications.

As in adults, fractures of the femur in children may occur anywhere (femoral neck, intertrochanteric, femoral shaft, etc.), but in children, most injuries involve the femoral shaft. In young children, child abuse should be considered. The incidence of abuse is particularly high in children younger than 1 year; at this age it is approximately 50% in those who present with an apparent isolated fracture of the femur. Treatment of femoral fractures in children varies according to fracture location, age of the child, and degree of displacement. Nondisplaced femoral neck and intertrochanteric fractures can be treated in a spica cast. Displaced fractures in these locations should be treated with reduction and internal fixation, often supplemented by spica casting in a young child.

Sliding compression screw and plate. As fracture settles, screw can slide in plate, thus preventing penetration of articular surface of femoral head.

Intertrochanteric fracture reduced and fixated with sliding compression screw system.

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Chapter 17 Femoral shaft fractures in children up to 6 years of age are most often treated by immediate reduction and spica cast immobilization. If the fracture is significantly displaced, children are placed in skeletal traction until enough callus has formed to allow maintenance of alignment in a cast. Older children may be candidates for fixation of femoral shaft fractures. Flexible intramedullary rods are often used in the 6- to 12-year-old child. Older adolescents and younger obese children often require intramedullary rod fixation, but the insertion point should be through the greater trochanter to diminish the risk of osteonecrosis that has a small but greater prevalence when the proximal femoral physis is still open and the standard entry site is used (slightly posterior to the pyriformis fossa).

clude evaluation for a compartment syndrome, and radiographs may be required to exclude a femoral fracture. To enhance rehabilitation and minimize the risk of myositis ossificans, the treatment of a quadriceps contusion should include immobilization of the knee for the first 48 hours, followed by exercises that decrease thigh atrophy and increase knee flexion. Myositis ossificans may complicate a direct blow to the thigh (see Figure 8-16). The incidence correlates with the severity of the associated contusion. The development of this complication is probably related to concomitant injury of the periosteum and the subsequent reparative process, which initiates a metaplastic chondroid and osseous response. The firm mass interferes with knee flexion and may be confused with a neoplastic process. Function can usually be regained with rangeof-motion and strengthening exercises, but occasionally, excision of a persistently large mass is necessary once osteogenesis has ceased and the bone is mature.

Strains and Contusions of the Pelvis and Thigh Strains of thigh muscles typically occur in a sporting event or fall when a muscle forcefully contracts while it is in a relatively lengthened position (on stretch). In addition to the history, the key to diagnosis is location of the pain and exacerbation of the pain on muscle contraction against resistance and on passive stretch of the muscle. The latter is a more sensitive test. For example, a strain of the hip adductors is indicated by groin pain that is increased by contraction of the adductors and by movement of the hip into abduction. The position of the knee and hip must be controlled when two-joint muscles are assessed. For example, a strain of the semitendinous muscle is indicated by pain in the posteromedial thigh that is exacerbated by flexing the hip to 90°, then extending the knee. For most patients, modification of activities, followed by simple home exercises and progressive resumption to full activity, is adequate. Rehabilitation of elite athletes usually includes a more aggressive and costly regimen. A direct blow to the anterior thigh can cause a painful and disabling hemorrhage into the quadriceps. Examination should ex-

PEDIATRIC HIP DISORDERS Developmental Dysplasia of the Hip Developmental dysplasia of the hip (DDH) includes the typical dislocatable hips present at birth; rigid dislocations at the time of birth from conditions such as arthrogryposis; and hip dysplasia that develops during early childhood, usually from conditions that cause severe ligamentous laxity or neuromuscular dysfunction. Typical DDH usually is detectable at birth. Associated factors in these patients include an increased incidence in females (5:1 ratio), breech presentation (20% for frank breech position), left hip predominance (3:1 ratio), and greater incidence in individuals of northern European and American Indian ancestry. In addition to normal perinatal laxity, additional ligamentous laxity is the cause for the greater incidence in females and the greater incidence in some families. The acetabulum is relatively shallow in all babies, and breech presentation probably increases the likelihood of DDH by altering the shape of the acetabulum. In the center of the

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The Pelvis, Hip, and Thigh Figure 17-23: Femoral Shaft Fracture

A AP radiograph of femur on date of injury

C

B AP radiograph of femur 2 months after retrograde intramedullary nailing

Lateral radiograph of femur 2 months after retrograde intramedullary nailing

20-year-old female who was unrestrained passenger in a motor vehicle accident. The patient sustained multiple fractures including a closed fracture of the right femoral shaft (A), an open grade IIIA comminuted fracture of the junction of the middle third-distal third right tibia and fibula (see Figure 18-19), a closed, comminuted fracture of the middle third of the left tibia and fibula, and comminuted fracture of the right calcaneus (Figure 18-19). On the date of injury, the patient underwent débridement of the right tibia with application of an external fixator, retrograde nailing of the right femur, and intramedullary nailing of the left tibia. Radiographs of the femur 2 months after injury (B and C) show good alignment and interval healing of the fracture.

acetabulum is a growth plate, the triradiate cartilage. Like all growth plates, it responds to pressure. If the femoral head is hyperflexed and adducted (i.e., in a breech position), the pressure will flatten the outer rim of the socket, and the resultant insufficient acetabulum predisposes the hip to dislocate or become dislocatable. Physical examination is the key to early diagnosis. The examination should be done on a firm surface, with the infant calm and relaxed. Hip instability may not be detected when the infant is upset. Two provocative maneuvers should be performed during the newborn examination (Fig-

ure 17-24). The Barlow test, a “sign of exit,” is done first. A positive test is a clunk as the dislocatable femoral head slides over the posterior rim of the acetabulum. The Ortolani maneuver is a “sign of relocation” as the dislocated femoral head is manipulated back into the acetabulum. Again, a clunk and sudden give are perceived as the femoral head slides over the posterior lip of the acetabulum into the socket. If the acetabulum is very shallow, the sense of relocation may be soft compared with the typical clunk, making the diagnosis questionable. To increase the sensitivity of this test, push the femoral head toward the acetabulum when performing this maneuver.

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Chapter 17 Figure 17-24: Developmental Dysplasia of the Hip Ortolani (reduction) test With baby relaxed and content on firm surface, hips and knees fixed to 90˚. Hips examined one at a time. Examiner grasps baby's thigh with middle finger over greater trochanter and lifts thigh to bring femoral head from its dislocated posterior position to opposite the acetabulum. Simultaneously, thigh gently abducted, reducing femoral head into acetabulum. In positive finding, examiner senses reduction by palpable, nearly audible "clunk."

“clunk”

Barlow (dislocatable) test Reverse of Ortolani test. If femoral head is in acetabulum at time of examination, Barlow test is performed to discover any hip instability. Baby's thigh grasped as in image to the left and adducted with gentle downward pressure. Dislocation is palpable as femoral head slips out of acetabulum. Diagnosis confirmed with Ortolani test

After the neonatal period, perinatal laxity wears off, and with the femoral head in a dislocated position, the joint capsule and hip adductors contract. As a result, by 2 weeks to 3 months of age or older, the hip cannot be relocated by the Ortolani maneuver. Other signs, however, are present. A unilateral dislocation is more obvious because the affected thigh appears shortened (positive Galeazzi sign), and decreased abduction of the affected hip causes obvious asymmetry when both hips are abducted (Figure 17-25). Furthermore, a toddler with one hip dislocated will stand bending the knee on the normal limb and will walk up on the toes on the affected side to make the leg longer. Bilateral DDH is more difficult to diagnose. Thigh lengths are equal, and abduction is symmetric. Bilateral DDH is suggested by hip abduction of less than 45° to 50°.

Radiographs are not very useful until the femoral head ossifies (3 to 5 months of age in girls and 5 to 7 months of age in boys). When the newborn examination is equivocal, ultrasonographic examination can be helpful. This study also can help confirm reduction as treatment proceeds. AP radiographs of the pelvis are helpful in older children. Treatment of DDH should begin as soon as possible. The longer a hip is dislocated, the less likely it is that closed reduction will be possible. Untreated DDH causes a dysfunctional gait and a secondary osteoarthritis that may become painful in the adolescent or young adult years. The goals of treatment are to concentrically reduce the femoral head into the acetabulum without causing excessive tension on the contracted vascular supply to the femoral head, and to maintain the reduction until the hip

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The Pelvis, Hip, and Thigh Figure 17-25: Clinical Signs in Older Infant with Developmental Dysplasia of the Hip

Limitation of abduction due to shortened and contracted adductor muscles of hip

Galeazzi sign With hips flexed, the knee on the dislocated side is lower, because the femoral head lies posterior and superior to the acetabulum

limp is usually more noticeable at the end of the day). Pain is often insignificant or mild; therefore, the limp has usually been present for 4 to 8 weeks before the initial visit. Examination reveals limitation of hip motion, mostly in abduction and internal rotation. Abduction is particularly restricted and usually measures 30° to 40° less on the involved side (60° to 70° abduction normally is present at this age). Good-quality AP and frog-leg lateral radiographs of the pelvis should be obtained. Increased density of the femoral head is an early sign of LCP. The crescent sign indicates that a shear collapse has occurred in the subchondral bone (Figure 1727). In the early stages of LCP, plain radiographs may be normal, and MRI may be necessary to document the osteonecrosis. In a child with bilateral LCP, AP radiographs of the hand and knee should be obtained to screen for a possible epiphyseal dysplasia or hypothyroidism. The healing process in LCP involves revascularization of the femoral head, removal of necrotic bone, replacement with viable bone that is initially weak (woven bone), and remodeling of woven bone to normal lamellar bone. Although this physiologic process occurs more rapidly and with greater consis-

joint stabilizes. For a dislocatable hip, the treatment of choice in a child up to 6 months of age is a Pavlik harness, a dynamic positioning splint that holds the hips in flexion and abduction, thus promoting normal growth of the acetabulum and stabilization of the somewhat lax and stretched-out hip capsule (Figure 1726). Consistent, full-time wearing of the splint for 2 to 3 months is necessary for treatment of an unstable hip. If reduction does not occur in the harness, or if the child is older than 6 months at diagnosis, an examination and arthrogram under anesthesia, along with a closed or open reduction with application of a spica cast, will be necessary.

Legg-Calvé-Perthes Disease Legg-Calvé-Perthes (LCP) disease is idiopathic osteonecrosis of the femoral head in children. LCP typically affects children between the ages of 4 and 8 years, but it can occur anytime between 2 and 12 years of age. It is unilateral in 90% of cases, more frequent in boys (4:1 ratio), and uncommon in blacks. The prognosis is worse in older children and in those with severe involvement (osteonecrosis of all or most of the femoral head). Typical symptoms include the indolent onset of a limp that is activity related (i.e., the

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Chapter 17 note, none of these treatment modalities completely contains the femoral head during all phases of gait. As a general rule, osteotomy is reserved for older children. The abduction brace is used until the lateral portion of the femoral head has reossified, a process that generally takes 12 to 24 months. With a lateral buttress present, the remaining portion of the femoral head is shielded from weightbearing stresses during the remainder of the reossification process.

Figure 17-26: Pavlik Harness

Slipped Capital Femoral Epiphysis Slipped capital femoral epiphysis (SCFE) is displacement of the femoral head (epiphysis) through the physis, which typically occurs during the adolescent growth spurt. During adolescence, the physis of the proximal femur becomes more vertical. That orientation, coupled with increased body size and activity, may cause intolerable shear at the relatively weak physis. The result is microscopic fractures and gradual slippage of the femoral head posteriorly, and usually also medially. Occasionally, an acute event causes sudden displacement of the femoral head—in essence, a fracture or unstable slip. Obesity, male gender, and heavy involvement with sports activities are predisposing factors. A high degree of femoral retroversion also is a risk factor, which probably explains the greater incidence of SCFE in blacks. Bilateral involvement is eventually found in 40% to 50% of cases. A small percentage of patients with SCFE have an endocrine disorder that alters the strength or growth of the physis. Hypothyroidism and growth hormone deficiency are most common. In children with hypothyroidism, SCFE often occurs before the endocrine abnormality has been diagnosed. The mean age at presentation is 12 years for girls (typical range, 10 to 14 years) and 13 years for boys (typical range, 11 to 16 years). Onset before or after the typical range is associated with an increased incidence of some type of endocrine disorder. Proximal thigh pain exacerbated by activity is the most common presenting symptom.

Harness adjusted to allow comfortable abduction within safe zone. Forced abduction beyond this limit may lead to avascular necrosis of femoral head.

tency in children, it still requires many (24 to 84) months, and no current interventions accelerate reossification. Furthermore, no treatment modality consistently produces good outcomes or prevents the deformity of the femoral head that occurs when the bone structure is relatively weak (i.e., during revascularization and woven bone formation). The goal of treatment is to minimize deformity and lateralization of the femoral head. Before any treatment is initiated, motion must be regained. A short period of bed rest and traction is commonly required. Observation is acceptable for children who are unlikely to develop significant deformity. Therefore, observation may be used for children younger than 6 years who do not have significant subluxation of the femoral head and who maintain satisfactory abduction (approximately 40° to 45°). To facilitate early healing, a short period (6 to 8 weeks) of abduction casting may be used at the start of observation. The principle of active intervention is to “contain” the femoral head within the depth of the acetabulum and thereby maintain, as well as possible, the spherical shape of the femoral head. Options include an abduction brace that extends below the knees or an osteotomy of the femoral head or pelvis. Of

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The Pelvis, Hip, and Thigh Figure 17-27: Legg-Calvé-Perthes Disease

C A

A. At initial evaluationradiographs radiographs demonstrate At initial evaluation demonstrate crescent sign and flattening/mild sclerosis of the right femoral head.

B

C. Fourteen monthslater, later,radiographs radiographs show Fourteen months showlateral lateral and maintained on AP andmedial medialbuttress buttress maintained on radiographs. AP Areas of radiolucency areradiolucencey indicative of resorption of radiographs. Areas of are the osteonecrotic segments woven bone indicative of resorption ofand thenew osteonecrotic formation. segments and new woven bone formation.

D

D. years afteronset onsetof ofpresentation, presentation, bone FiveFive years after boneformation is almost complete. Right femoral head formation is almost compete. Right femoral shows mild coax magna. Hip function minimally impaired.

B. Three months later, increased sclerosis is evident as woven bone formation is deposited on necrotic trabeculae. In each group, top image is an AP radiograph and bottom is a “frog leg” position.

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Chapter 17 1 to 3 cm shorter, with the degree of shortening dependent on the severity of the slip. AP and frog-leg lateral radiographs of the pelvis confirm the diagnosis. No displacement is evident in a few patients, but in this pre-slip phase, the physis is widened. The severity of displacement is measured by the degree of posterior displacement as mild (less than 30°displacement), moderate (30° to 50°), and severe (more than 50°). Severe displacement is more likely with long duration of symptoms or an acute, unstable slip. The severity of the slip correlates with the subsequent development of osteoarthritis. Most patients with mild or moderate SCFE remain asymptomatic or do not develop significant arthritis until the older adult years. The goals of treatment are to prevent further slippage of the femoral head and to promote closure of the physis, an event that

Parents may note that the child walks with the foot turned out. In one third of patients, pain is referred to the distal thigh and may be mistaken for a knee problem. Clinical examination is easy and virtually diagnostic. Loss of hip internal rotation is the most sensitive finding on examination. This limitation is more severe when the hip is flexed and is readily apparent even with minimal displacement of the femoral head (Figure 17-28). Furthermore, SCFE is the only pediatric hip disorder that causes greater loss of internal rotation when the hip is flexed. Assessment of internal rotation with the hip flexed to 90° is a useful screening maneuver for all adolescents who have lower extremity pain. Other findings on clinical examination include mild limitation of hip abduction and extension. Patients typically walk with the leg externally rotated. The affected extremity is

Figure 17-28: Slipped Capital Femoral Epiphysis

Clinical finding that is virtually diagnostic of SCFE is greater loss of internal rotation as the hip is brought into flexion.With patient supine, as thigh is flexed, it rolls into external rotation and abduction. Frog-leg radiograph demonstrating posterior displacement of the epiphysis.

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The Pelvis, Hip, and Thigh

Figure 17-29: Proximal Femoral Focal Deficiency

Type A PFFD with associated coxa vara

Girl with Type A PFFD Type C PFFD. Femoral head absent or not ossified; acetabulum dysplastic. Femoral shaft very short and displaced laterally and superiorly

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Type B PFFD with associated fibular hemimelia. Foot lies opposite contralateral knee.

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Chapter 17 sedimentation rate, blood cultures, radiographs, and sometimes aspiration of the hip joint under anesthesia. Transient synovitis resolves without therapy or sequelae. With a short period of bed rest, symptoms and limping typically resolve within 3 to 14 days.

ensures that no further displacement will occur. Most patients are treated by in situ stabilization with a single cannulated screw. This procedure is associated with the lowest risks of osteonecrosis and chondrolysis. A patient with severe deformity may require a realignment osteotomy. Patients with an unstable SCFE experience severe pain after a fall, are unable to walk, and have severe displacement of the femoral head. They are at increased risk for AVN and require urgent reduction and stabilization.

Proximal Femoral Focal Deficiency Proximal femoral focal deficiency (PFFD) is an uncommon, sporadic congenital deformity characterized by dysgenesis of the proximal femur. Shortening of the femur is marked. Coxa vara is common, and pseudarthrosis of the femoral neck may be present. Associated abnormalities in the extremity include hip dysplasia, absence of the anterior cruciate ligament, and mild fibular hemimelia. Other organ systems are uncommonly involved in PFFD. The classification system described by Torode and Gillespie is most useful. In type A, the foot lies opposite the midpoint of the contralateral tibia. These children can be treated by limb equalization procedures and correction of associated coxa vara. In type B, the foot lies opposite the contralateral knee, and the femoral head and neck are absent or have a pseudarthrosis. In type C, the foot lies proximal to the knee joint. Both types B and C require some type of amputation to equalize the limb-length discrepancy (Figure 17-29).

Transient Synovitis Transient synovitis of the hip is an aseptic effusion that is a common cause of limping or refusal to walk. Children 2 to 5 years of age are most commonly affected, and the incidence is 2 to 3 times greater in boys. The cause is unknown, but mild trauma or overuse at an age when the acetabulum is not fully developed seems to be the best explanation. Numerous studies have failed to identify a bacterial or viral origin. Typically, the child awakens with a limp or refusal to walk. Later, the limp may improve but will again worsen toward the end of the day. Children old enough to communicate typically localize their pain to the anterior proximal thigh. Examination reveals mild restriction of hip motion. Abduction is most sensitive and typically is 20° to 40° on the affected side. Transient synovitis is a diagnosis of exclusion. How much evaluation is performed varies according to the degree and duration of symptoms. Septic arthritis of the hip is the primary disorder to exclude. If the child has very limited motion and a temperature higher than 37.5°C, diagnostic studies should include complete blood count (CBC), erythrocyte

ADDITIONAL READINGS Callaghan JJ, Rosenberg AG, Rubash HE, eds. The Adult Hip. Philadelphia, Pa: Lippincott, Williams and Wilkins; 1997. Chapman MW, ed. Chapman’s Orthopaedic Surgery, 3rd edition. Philadelphia, Pa: Lippincott Williams and Wilkins; 2001.

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eighteen The Knee and Leg Derrick J. Fluhme, MD Lee D. Kaplan, MD Freddie H. Fu, MD

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Chapter 18 plateaus. The medial condyle is narrower in the anteroposterior (AP) plane and extends farther distally. The articular surfaces of the femoral condyles join anteriorly to articulate with the patella. Posteriorly, they remain separate to form the intercondylar notch. The proximal tibia is composed of medial and lateral condyles (often called medial and lateral plateaus), which are separated by an intercondylar eminence that has medial and lateral intercondylar tubercles (spines). The intercondylar eminence has no ligament attachments, but the anterior and posterior areas receive the cruciate ligaments and horns

ANATOMY Compared to the hip and ankle, the intrinsic bony configuration of the knee provides limited support for the weight-bearing demands of walking and running (Figure 18-1). Knee stability is created primarily through a complex interplay of passive (collateral ligaments, cruciate ligaments, menisci, and joint capsule) and active stabilizers (quadriceps, hamstrings, and popliteus muscles). The distal femoral metaphysis expands into a medial and a lateral condyle, each of which is convex and articulates with the corresponding, slightly concave medial and lateral tibial

Figure 18-1 Anterior view of knee

Patellar surface Adductor tubercle

Lateral condyle Lateral tibial space Lateral condyle Gerdy tubercle (insertion of iliotibial tract)

Neck of fibula

Medial condyle Medial condyle Medial tibial space Anterior intercondylar area Tibial tuberosity

Femoral mechanical axis 87˚

87˚ Tibial mechanical axis

Oblique line Lateral surface Line of attachment of synovium (edge of articular cartilage) to distal femur Line of reflection of synovial membrane Hip-Knee-Ankle Mechanical Axis Mechanical axis of the lower extremity is the angle from the center of the femoral head to the center of the knee (usually, anterior tubercle of the tibia) to the center of the ankle. Normal is 1° of varus. Femoral mechanical axis is the femoral mechanical axis and a line tangential to the joint line. Normal is 87°. Tibial mechanical axis is tibial mechanical axis line and line tangential to the joint. Normal is 87°.

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The Knee and Leg of the menisci. Palpable insertion sites are the tibial tubercle (patellar tendon) and Gerdy tubercle (iliotibial band). Abnormal alignment predisposes the joint to osteoarthritis. Normal alignment parameters include the following: both femoral condyles form a horizontal plane parallel to the ground, the plane of the femoral condyles relative to the femoral shaft (the anatomic

axis) is 5° to 7° valgus, the mechanical hipknee-ankle axis (center of the femoral head–center of the knee–center of the distal tibia) is approximately 1° varus, and the tibial articular surface is sloped posteriorly 7° to 10° (see Figure 18-1). The patella, the largest sesamoid bone in the body, lies within the substance of the quadriceps tendon (Figure 18-2). The proxi-

Figure 18-2: Medial and Lateral Views of the Knee Lateral view Vastus lateralis m.

lliotibial tract Biceps head femoris Long Short head m. Bursa deep to iliotibial tract Fibular collateral lig. and bursa deep to it

Quadriceps femoris tendon

Sagittal section (lateral to midline of knee)

Patella

Femur

Lateral patellar retinaculum

Biceps femoris tendon and its inferior subtendinous bursa Common peroneal n. Head of fibula Gastrocnemius m. Soleus m.

Articularis genus m. Quadriceps femoris tendon Suprapatellar fat body

Joint capsule of knee Patellar lig.

Suprapatellar (synovial) bursa Patella Subcutaneous prepatellar bursa Articular cavity Synovial membrane

Tibial tuberosity

Peroneus longus m.

Medial view

Tibialis anterior m. Synovial membrane

Patellar lig. Infrapatellar fat pad Subcutaneous infrapatellar bursa Deep (subtendinous) infrapatellar bursa

Sartorius m. Vastus medialis m. Quadriceps tendon

Patella Medial patellar retinaculum Joint capsule Patellar lig. Tibial tuberosity

Gracilis m. Tendon of semitendinosus m. Semimembranosus m. and tendon Adductor magnus tendon

Lateral meniscus Tibia

Parallel fibers Tibial collateral Oblique fibers lig. Semimembranosus bursa Anserine bursa deep to Semitendinosus, Pes Gracilis and Sartorius tendons anserinus Gastrocnemius m. Soleus m.

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Tibial tuberosity

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Chapter 18 Figure 18-3: Axial View of Meniscus Oblique popliteal ligament Superior view Semimembranosus tendon

Posterior meniscofemoral ligament Arcuate popliteal ligament

Posterior cruciate ligament

Fibular collateral ligament

Tibial collateral ligament (deep part bound to medial meniscus) Medial meniscus

Bursa Popliteus tendon Subpopliteal recess

Synovial membrane

Lateral meniscus

Superior articular surface of tibia (medial facet) Joint capsule

Superior articular surface of tibia (lateral facet) lliotibial tract blended into capsule Infrapatellar fat pad

Anterior cruciate ligament Patellar ligament Anterior aspect

mal two thirds of the patella’s undersurface articulates with the anterior surface of the femoral condyles and is divided by a longitudinal ridge into medial and lateral facets. The distal third provides attachment for the patellar tendon; this tendon is more precisely called the patellar ligament because it extends from bone to bone (from the patella to the tibial tuberosity). The quadriceps tendon inserts into the superior border of the patella, and retinacular expansions of the vastus medialis and vastus lateralis occupy the corresponding border of the patella. The medial and lateral menisci are triangular wedge–shaped rims of fibrocartilaginous tissue that line the periphery of the tibial plateaus (see Figures 18-2 and 18-3). The menisci aid in load transmission, reduce articular surface stresses, deepen articular surfaces of the tibial plateau, and contribute to joint stability. The medial meniscus is C-shaped, whereas the lateral meniscus forms an incomplete circle. The collagen fibers of the menisci are arranged radially and circumferentially. The circumferential (longitudinal) fibers dissipate “hoop” stresses and allow meniscal expansion under compressive loads. The broad, flat medial collateral ligament (MCL) is the primary restraint to valgus stress (Figure 18-4). The superficial portion of the

MCL originates at the medial femoral epicondyle and inserts distally into the proximal tibia, deep to the pes anserinus tendons. The deep portion of the MCL is a thickening of the knee capsule that blends with the fibers of the superficial MCL at its insertion on the tibia. The lateral (fibular) collateral ligament (LCL) is the primary restraint to varus stress. It originates on the lateral femoral condyle, posterior and superior to the popliteus tendon, and inserts on the lateral aspect of the fibular head. The anterior cruciate ligament (ACL) is the primary restraint (85%) to anterior translation of the tibia relative to the femur. It originates on the posteromedial aspect of the lateral femoral condyle and inserts at the anterior intercondylar area of the tibia. The ACL includes two functional bundles: the anteromedial bundle, which tightens in flexion, and the posterolateral bundle, which tightens in extension. Thus, the ACL maintains some tension throughout the full arc of knee motion. Mechanoreceptors in the ACL provide protective proprioception against abnormal joint translations. The posterior cruciate ligament (PCL) is the primary restraint (95%) against posterior translation. It originates on the posterolateral aspect of the medial femoral condyle and in-

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The Knee and Leg Figure 18-4: Collateral and Cruciate Ligaments of the Knee

Adductor tubercle on medial epicondyle of femur Anterior cruciate ligament Lateral condyle of femur (articular surface) Popliteus tendon Fibular collateral ligament Lateral meniscus Transverse ligament of knee Head of fibula Gerdy tubercle

Posterior cruciate ligament Medial condyle of femur (articular surface) Medial meniscus Tibial collateral ligament Medial condyle of tibia

Tibial tuberosity

Posterior cruciate ligament Anterior cruciate ligament Posterior meniscofemoral ligament Lateral condyle of femur (articular surface) Popliteus tendon Fibular collateral ligament Lateral meniscus Head of fibula

Right knee in extension: posterior view

Right knee in flexion: anterior view

serts in the posterior intercondylar area of the tibia. The PCL also is made up of two functional bundles. The anterior meniscofemoral (ligament of Humphrey) and the posterior meniscofemoral ligament (ligament of Wrisberg) originate from the posterior horn of the lateral meniscus and contribute to the function of the PCL. The extensors of the knee are the five components of the quadriceps muscle. Knee flexors include the three hamstrings, as well as the sartorius, gracilis, and popliteus muscles. The pes anserinus (goose foot) is the convergence of the sartorius, gracilis, and semitendinosus tendons where they insert on the anteromedial aspect of the proximal tibia (see Figure 18-2). The tibia and the fibula are connected by an interosseous membrane. The slender fibula has limited weight-bearing function. The muscles of the legs are separated into four compartments (Figure 18-5). Anterior compartment muscles (tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius) dorsiflex the ankle and

399

extend the toes. Lateral compartment muscles (peroneus longus and peroneus brevis) originate from the fibula and primarily function as evertors of the foot. Posterior compartment muscles are separated into superficial (gastrocnemius and soleus) and deep posterior compartments (tibialis posterior, flexor hallucis longus, and flexor digitorum longus). The two components of the sciatic nerve separate within the proximal aspect of the popliteal fossa (Figure 18-6). The common peroneal nerve travels across the lateral gastrocnemius; becomes subcutaneous and vulnerable to injury as it goes around the neck of the fibula; and, after penetrating the posterior intermuscular septum, divides into the superficial and deep peroneal nerves. The deep peroneal nerve supplies the anterior compartment muscles, and the superficial peroneal nerve provides motor branches to the lateral compartment. The tibial nerve continues its posterior course and innervates the posterior compartment muscles. Proximal to the knee, the femoral artery separates from the saphenous nerve, passing

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Chapter 18 Figure 18-5: Fascial Compartments of the Leg Deep fascia of leg Anterior compartment Extensor muscles Tibialis anterior Extensor digitorum longus Extensor hallucis longus Peroneus tertius Anterior tibial artery and veins Deep peroneal nerve Anterior intermuscular septum

Interosseous membrane Tibia Deep posterior compartment Deep flexor muscles Flexor digitorum longus Tibialis posterior Flexor hallucis longus Popliteus Posterior tibial artery and veins Tibial nerve Peroneal artery and veins Transverse intermuscular septum

Lateral compartment Peroneus longus muscle Peroneus brevis muscle Superficial peroneal nerve Posterior intermuscular septum Fibula Deep fascia of leg

Superficial posterior compartment Superficial flexor muscles Soleus Gastrocnemius Plantaris (tendon) Cross section just above middle of leg Anterior tibial artery and veins and Tibialis anterior muscle deep peroneal nerve Extensor hallucis longus muscle Tibia Extensor digitorum longus muscle Interosseous membrane Peroneal nerve Great saphenous vein and saphenous nerve Tibialis posterior muscle

Anterior intermuscular septum Deep fascia of leg

Flexor digitorum longus muscle Peroneal artery and veins Posterior tibial artery and veins and tibial nerve Flexor hallucis longus muscle Deep fascia of leg

Peroneus longus muscle Peroneus brevis muscle Posterior intermuscular septum Fibula Transverse intermuscular septum

Plantaris tendon

Soleus muscle

Gastrocnemius muscle (medial head)

Gastrocnemius muscle (lateral head)

Sural cutaneous nerve Small saphenous vein

from the anterior compartment of the thigh through an opening in the adductor magnus tendon to enter the popliteal space as the popliteal artery. The popliteal artery provides five geniculate and two sural branches before it divides into the anterior and posterior tibial arteries. The anterior tibial artery passes directly forward above the upper end of the interosseous membrane to enter the anterior compartment. The posterior tibial artery continues down the leg, accompanied by the tibial nerve. Its largest branch, the peroneal

artery, supplies the muscles of the lateral side of the leg and arises 2 to 3 cm distal to the origin of the posterior tibial artery.

BIOMECHANICS The primary plane of knee motion is flexion and extension, but small degrees of rotation, adduction/abduction, and anterior/posterior translation occur as well. Maximum stability is needed when the limb is in the midstance phase of walking or running, and several factors enhance stability in this phase (refer to

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The Knee and Leg Figure 18-6: Tibial Nerve and Cutaneous Innervation of Sole Common fibular (peroneal) nerve Tibial nerve (L4, 5, S1, 2, 3)

Articular branch Lateral sural cutaneous nerve (cut)

Medial sural cutaneous nerve (cut) Articular branches

From tibial nerve

Plantaris muscle

Gastrocnemius muscle (cut)

Saphenous nerve (L3, 4) Sural nerve (S1, 2) via lateral calcaneal and lateral dorsal cutaneous branches

Nerve to popliteus muscle Popliteus muscle Interosseous nerve of leg Soleus muscle (cut and partly retracted) Flexor digitorum longus muscle Tibialis posterior muscle Flexor hallucis longus muscle

Sural nerve (cut)

Lateral calcaneal branch sural nerve Medial calcaneal branch tibial nerve Lateral dorsal cutaneous nerve

Medial calcaneal branches (S1, 2) Medial plantar nerve (L4, 5) Lateral plantar nerve (S1, 2)

Cutaneous innervation of sole

Tibial nerve Medial calcaneal branch Medial plantar nerve Flexor digitorum brevis muscle and nerve Abductor hallucis muscle Flexor hallucis brevis muscle 1st lumbrical muscle Common plantar digital nerves Proper plantar digital nerves

Lateral calcaneal branch of sural nerve Lateral plantar nerve Nerve to abductor digiti minimi muscle Quadratus plantae muscle Abductor digiti minimi muscle Deep branch to interosseous muscles, 2nd, 3rd, and 4th lumbrical muscles and Adductor hallucis muscle Superficial branch to 4th interosseous muscle and Flexor digiti minimi brevis muscle

Note: Articular branches not shown

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Chapter 18 Chapter 19, section on phases of gait). Especially important is that the knee is in almost full extension during midstance. In extension, medial rotation of the femur achieves the close-packed, stable position. The femoral condyles have larger articular surfaces than the tibial condyles. Therefore, knee movement has a component of rolling and gliding of the femoral condyles. As the knee is extended, the shorter, more highly curved lateral condyle reaches its limit sooner. The lateral meniscus is displaced forward on the tibia and becomes firmly seated in a position that blocks further motion of the lateral femoral condyle. However, the medial femoral condyle continues to glide backward, thus bringing its flatter, anterior surface into full contact with the tibia. Medial rotation of the femur also brings the cruciate and collateral ligaments into maximum tension. The tension of the ligaments and the close approximation of the flatter parts of the condyles also make standing in the erect position relatively easy to maintain. Flexion of the extended knee is initiated by lateral rotation of the femur, a process facilitated by contraction of the popliteus muscle. Lateral rotation relaxes the taut ligaments enough to allow flexion. An important function of the patella is to reduce the force requirements of the quadriceps muscle by use of a variable-lever arm. As the knee goes into extension, the patella rides up in the femoral notch, thereby increasing the moment arm and extension torque. Less torque is required when the knee is flexed, and the patella sinks into the femoral notch, thereby reducing the quadriceps lever arm. Patellectomy reduces the lever arm and increases, by 15% to 20%, the force required by the quadriceps to bring the knee into full extension.

due to overuse or degenerative problems. Contact injuries may involve single or multiple knee ligaments; in noncontact injuries, often the ACL is the only ligament torn. The sensation of feeling or hearing a pop is associated with ACL tears. An effusion that develops within hours suggests an ACL injury, whereas an effusion that develops overnight suggests a meniscal injury. Buckling of the knee, a transient sensation of the knee’s giving way, may arise from meniscal tears, ligamentous instability, patellar instability (subluxation/dislocation), or weakness of the quadriceps. Locking of the knee, a transient or sometimes longer lasting sensation of the knee being stuck in a semiflexed position, is associated with displacement of a meniscal tear into and out of its normal alignment. Difficulty with cutting maneuvers suggests ACL or patellar instability. Difficulty climbing or descending stairs is associated with patellofemoral problems. Observe the patient as he or she walks, to detect antalgic movements. Inspect the knee for swelling, ecchymosis, and malalignment. Examine the knee with the patient first in the supine position, then seated. With the patient supine, inspect, then palpate the knee for effusion by placing one hand above and one hand below the patella. Any fluid in the knee can then be displaced and palpated proximally and distally. Have the patient point to, then palpate, the site of maximum tenderness. Tenderness at the medial joint line suggests a tear of the medial meniscus or medial compartment arthritis. A history of an acute valgus injury and tenderness anywhere over the MCL suggests MCL sprain. Pain at the medial aspect of the proximal tibia suggests pes anserinus bursitis. Lateral joint line tenderness is associated with a tear of the lateral meniscus, sprain of the LCL, or tendinitis of the popliteal tendon or iliotibial band. Tenderness at the medial-superior border of the patella suggests acute patellar subluxation/dislocation. When the patient is seated, observe the patella while the patient moves the knee. Note abnormal crepitation and excessive lat-

HISTORY AND PHYSICAL EXAMINATION A history of acute knee pain typically indicates an injury to ligamentous, meniscal, or bony tissue or a combination of these injuries. Chronic pain without specific cause usually is

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The Knee and Leg eral movement. With the quadriceps relaxed and the knee in extension, push the patella laterally, then flex the knee. In a patient who has patellar instability, this test displaces the patella to an abnormal position that creates pain and apprehension as the knee is flexed. Knee motion is primarily flexion and extension. The zero starting position is a straight knee. Normal knee flexion is 135° to 145° (Figure 18-7). Extension beyond the zero starting position is seen more often in young children; adults commonly have a 5° knee flexion contracture. Test the strength of the quadriceps with the patient seated. Ask the patient to keep the knee extended while you resist the effort by pushing against the tibia. Measure hamstring strength with the patient prone and the knee in 90° of flexion. Ask the patient to extend the hip as you resist the effort by pushing against the thigh.

improve as the knee “warms up” (see Figure 4-6). Swelling caused by an effusion and mild synovitis may be present. A knee flexion contracture of 10° to 20° and limitation of knee flexion are common. Catching or locking of the incongruent joint may be noted as the knee moves. In addition to displaying the typical shortened stance phase of an antalgic gait, a patient with varus malalignment and resultant stretching of the LCL may demonstrate a lateral thrust during midstance. Similarly, a patient with a valgus knee may demonstrate a varus thrust caused by weight-bearing forces and instability of the MCL. AP and lateral weight-bearing radiographs show narrowing of the joint space, as well as osteophyte formation, cortical sclerosis, and subchondral cysts. With varus malalignment, the medial aspect of the joint becomes more involved. With valgus deformities, greater narrowing is noted on the lateral side of the joint. Radiographs also should be inspected for concomitant patellofemoral arthritis. An AP standing radiograph with the knee flexed 45° is required if only the posterior aspect of the joint is involved. Nonoperative management of knee osteoarthritis includes observation, weight re-

DEGENERATIVE DISORDERS Osteoarthritis of the Knee Osteoarthritis of the knee may be primary but often is secondary to predisposing conditions. Presenting symptoms include activityrelated pain and stiffness that characteristically

Figure 18-7: Zero Starting Position and Arc of Flexion Knee motion is primarily flexion and extension. The zero starting position is with the knee straight. Normal knee flexion is 135˚ to 145˚. Extension beyond the zero starting position is more often seen in young children. Adults commonly have a 5˚ knee flexion contracture.

Flexion

135˚–145˚

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Chapter 18 duction, activity modification, and lowimpact exercises such as swimming or cycling, and isometric or closed-chain strengthening exercises. NSAIDs, intra-articular steroid or viscosupplement injections, and force reduction devices such as a cane or unloader braces also may be helpful. Surgical options for treating disabling arthritis are based on the age and activity of the patient, as well as the type of deformity. Arthrodesis can provide excellent pain relief and allows the patient to withstand the demands of heavy labor; however, it is uncommonly desired because sitting is compromised. It remains the best choice for a young, active adult with unilateral arthritis. Fusion in 15° of flexion is the optimal position for both walking and sitting. Varus deformity and medial compartment arthritis in a patient younger than 60 years may be treated with a valgus osteotomy of the proximal tibia by the removal of a triangular wedge of bone (a lateral closing wedge) or the medial insertion of a triangular wedge of bone (a medial opening wedge). The goal is to normalize weight-bearing forces so that pain is decreased, activity is maintained, and progression of arthritis is slowed. Results are better with correction to ⱖ8° valgus. Contraindications include grossly obese patients or those who have either ⬎10° varus, ⬍75° flexion, ⬎15° flexion contracture, and/or gross instability. The indications for a unicompartmental knee arthroplasty (UKA) are less clear. This procedure, which replaces only the medial or lateral side of the joint, is associated with less postoperative morbidity than a total knee arthroplasty (TKA); however, the long-term functional outcome of UKA is unclear. Most experts agree that both osteotomy and UKA delay the need for TKA. At present, the guidelines for UKA include isolated medial or lateral compartment arthritis, patients ⬎60 years of age who are relatively sedentary, no significant varus/valgus malalignment, and no significant instability or restriction of motion (Figure 18-8). TKA is preferred for older patients with endstage arthritis because the procedure pro-

duces more predictable pain relief and durability (Figure 18-9). This procedure is also indicated for younger patients with bicondylar or tricompartmental disease (medial, lateral, and patellofemoral). A young or middle-aged active adult who undergoes TKA will require future revision surgery. To prevent or delay the complications that incrementally increase with each revision replacement, TKA should be delayed as long as possible in these patients by the use of nonoperative or alternative operative methods. The goals of TKA include restoring normal hip-knee-ankle alignment, preserving (or restoring) a normal joint line, and balancing the collateral ligaments (joint stability). Possible complications include loosening (aseptic and septic), infection, osteolysis with subsequent aseptic loosening resulting from a macro-phage response to particulate metal and polyethylene wear debris, settling of the prosthesis into the cancellous bone and subsequent accelerated wear, peroneal nerve palsy (more likely in a patient with a preoperative valgus deformity and flexion contracture), abnormal patellar tracking, and stress fracture of the patella. Loosening and settling can be corrected by revision TKA. Infection is particularly difficult to treat because the implants act as foreign bodies in the knee, making antibiotic treatment and drainage alone unpredictable and riddled with failure. The infection can be treated definitively by removal of the prosthesis and cement with complete débridement of all infected tissue, implantation of an antibiotic-coated cement spacer, and a 6-week course of intravenous antibiotics followed by reimplantation of a new TKA.

Osteochondritis Dissecans Osteochondritis dissecans (OCD) is focal osteonecrosis at an articular surface. In the knee, OCD typically begins during the adolescent years, although symptoms may not occur until the young adult years. The cause is unclear, but the condition most likely occurs secondary to repetitive shear trauma that disrupts the blood supply to surrounding bone.

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The Knee and Leg Figure 18-8: Unicondylar Knee Arthroplasty

A

B

58-year-old male with severe bilateral knee pain on the medial aspect of the joint. Preoperative radiograph (A) showed similar findings in both knees with marked degenerative changes on the medial aspect of the knee and maintenance of joint cartilage on the lateral aspect of the joint. Patient underwent unicompartmental arthroplasty with good relief of pain. (B) Postoperative standing AP radiograph.

Positive findings are increased pain as the knee is extended to approximately 30° and reduced pain when the maneuver is repeated with the tibia externally rotated (the abutting tibial spine is now rotated away from the medial condyle). Small lesions may be missed on standard AP and lateral radiographs but may be seen on an AP tunnel view (knee held in 30° flexion). The prognosis for OCD varies according to the size of the lesion and the age of the patient. If the distal femoral physis has closed, the OCD lesion is unlikely to heal. Younger children have greater potential for osteonecrotic bone repair before the cartilage starts to separate. Activity modification to a level that diminishes shear stresses and eliminates symptoms is paramount. Lesions smaller than 1 cm in diameter

The most common location is the lateral aspect of the medial femoral condyle, but any area of the medial or lateral femoral condyle may be involved. Gradual buckling of the articular surface causes the indolent onset of activity-related pain. With buckling or disruption (dissecans) of the articular surface, patients note effusions and catching or locking symptoms. Eventually, the osteonecrotic fragment may become a loose body (Figure 18-10). Examination may demonstrate tenderness on the involved site. Assess the medial femoral condyle by flexing the patient’s knee to 90° and applying pressure just medial to the inferior pole of the patella. Perform the Wilson test with the patient’s hip and knee flexed to 90° and the tibia internally rotated.

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Chapter 18 Figure 18-9: Total Knee Arthroplasty

A

B

77-year-old male with progressive pain and difficulty walking despite intra-articular injections, NSAIDs, and using a cane. Gait antalgic with varus thrust. AP (A) and lateral (B) standing preoperative radiographs show varus malalignment, marked narrowing of the joint space, and patellofemoral involvement.

Radiographs courtesy of Dr. Thomas K. Fehring

C

D

E Postoperative radiographs demonstrating total knee arthroplasty with resurfacing of patella. Alignment of limb improved. Patient walking without pain and without a cane. AP (C) and lateral (D) standing and Merchant view (E).

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The Knee and Leg Figure 18-10: Progression of Osteochondritis Dissecans Circles indicate arthroscopic view

Stage 1. Bulge on medial femoral condyle due to partial separation of bone fragment. Articular cartilage intact, but defect evident on radiographs.

Stage 2. Fragment demarcated by separation of articular cartilage

Stage 3. Fragment of cartilage and bone completely separated as loose body. This often migrates to medial or lateral gutter.

Tunnel view radiographs of small OCD lesion involving medial femoral condyle treated with activity modification. Complete healing occurred

Stage 2 lesion

do well, whereas lesions larger than 2 cm carry a poor prognosis for healing without operative intervention (see Figure 18-10). Indications for surgical intervention include a loose body, an unstable lesion, or persistent symptoms despite nonoperative therapy. Drilling the lesion may promote revascularization. However, when partial separation of the articular surface has occurred, treatment should include not only drilling the base of the lesion but also stabilizing the fragment through temporary internal fixation. Surgical options for lesions that have completely separated and are not reparable include removal of loose bodies, drilling the defect to promote fibrocartilate replacement, grafting of the defect by osteochondral autograft (osteochondral autograft transfer system, or OATS, procedure), allograft transplantation and autologous chondrocyte implantation.

Osteonecrosis Osteonecrosis is similar to OCD, but in the knee, the diagnosis of osteonecrosis indicates a large lesion that typically occurs in a female patient older than 60 years (the female-tomale ratio is 3:1), occasionally in a younger patient with predisposing factors, such as long-term steroid therapy or sickle cell anemia. These patients often present with acute onset of pain secondary to a subchondral fracture and collapse of the articular surface. The medial femoral condyle is most commonly involved, but osteonecrosis also may occur in the lateral femoral condyle and the tibial plateau (usually medial). Initial radiographs may be normal, but eventually show flattening of the articular surface, subchondral radiolucency, and sclerosis of surrounding bone. Smaller lesions (less than 5 cm2) typically have a better clinical prognosis, and may be

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Chapter 18 satisfactorily treated with activity modification and assistive devices (ie, cane). Progressive symptoms necessitate drilling of the lesion, realignment osteotomy, or total knee replacement.

itive buckling and locking; and (2) retain as much of the meniscus as possible. Tears involving the avascular inner two thirds of the meniscus are treated with arthroscopic débridement and partial meniscectomy. The peripheral third of the meniscus has sufficient vascularity that repair should be attempted for all peripheral longitudinal tears in young patients. Meniscal repair is enhanced by placement of a fibrin clot in the tear before the sutures are tightened. The fibrin clot provides a scaffold that facilitates healing. The saphenous nerve is vulnerable in medial meniscus repairs, and the peroneal nerve, in lateral meniscus repairs (Figure 18-11).

Meniscal Tears The function of knee menisci is to dissipate stress; therefore, they are susceptible to injury from abnormal strain. The common age for traumatic tears is from late adolescence to the late forties. These injuries often occur with a twisting injury while the knee is under stress, that is, the foot planted. Degenerative tears are observed in older patients. These patients uncommonly associate onset of symptoms with significant injury. The medial meniscus is less mobile and therefore is torn approximately 4 to 5 times more frequently than the lateral meniscus. Tears may be isolated or associated with other knee injuries; lateral meniscus tears are more frequent with acute ACL injuries, whereas medial meniscus injuries are more common with chronic ACL tears. The torn portion may be unstable and intermittently displaces and interferes with the normal gliding motion of the knee. Symptoms of a torn meniscus include pain and intermittent catching, buckling, or locking. Examination frequently shows tenderness at the medial or lateral joint line. Positive McMurray test results indicate a tear of the posterior horn of the meniscus (most common site of tearing). To assess the medial meniscus, position the knee in maximum flexion and external rotation. Gradually extend the knee while keeping the leg in external rotation. Positive test findings include pain and a popping sensation. Use a similar maneuver with the knee internally rotated to assess the posterior horn of the lateral meniscus. Small tears that are causing only limited symptoms do not require treatment. Meniscal tears causing persistent symptoms should be treated by excision of the torn portion or repair of the meniscus. The goals include (1) prevent progression of arthritis from erosion of adjacent articular cartilage from repet-

Discoid Meniscus A discoid meniscus is a congenital anomaly in which the meniscus is enlarged and shaped like a disc. The lateral meniscus is mostly involved. The three types are complete, which covers the lateral tibial plateau; incomplete, and the Wrisberg variant with absence of posterior meniscotibial attachment (Figure 18-12). Patients typically present during childhood or adolescence with symptoms of pain and popping. Examination may show a palpable clunk as the knee is moved into extension. MRI can be helpful in showing the abnormal meniscus and any associated meniscal tears. Treatment options include observation, partial meniscectomy, and meniscal repair.

Bursitis The prepatellar bursa is anterior to the patella and may become inflamed by prolonged kneeling (see Figure 18-2). In bursitis, the overlying skin is erythematous. The joint appears swollen, but close inspection demonstrates the absence of a knee effusion. Pain is increased by flexing the knee. The primary differential diagnosis is cellulitis. Treatment includes aspiration and culture, short-term splinting of the knee in extension, activity modification, and other modalities that reduce inflammation. If culture is negative, a steroid injection may be considered. Excision of the bursa is seldom necessary and

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The Knee and Leg .Figure 18-11: Types of Meniscal Tears

Vertical longitudinal tear

Horizontal (cleavage) tear

Radial tear

Oblique ("Parrot-beak") tear

Complex, degenerative tear

Torn discoid meniscus

Oblique tears are most commonly seen and are best treated by arthroscopic partial meniscectomy (APM). Vertical-longitudinal tears involving the peripheral third are best managed by repair. Radial split tears are usually secondary to trauma, and when the split extends to the capsular rim, repair should be attempted in young people if at all possible. Bucket-handle tears are more likely to cause locking of the knee. Horizontal (cleavage) and symptomatic degenerative tears are best treated by APM.

Figure 18-12: Discoid Meniscus Variations

Normal

Partial discoid

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Complete discoid

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Chapter 18 should be avoided due to its subcutaneous position. The pes anserinus bursa is located between the insertion of the pes anserinus tendon and the underlying medial flare of the tibia (see Figure 18-2). Pes anserinus bursitis may be secondary to overuse or may be an early manifestation of medial compartment osteoarthritis. Examination shows mild swelling and tenderness over the bursa. Patients with osteoarthritis may have decreased motion and an antalgic gait. A torn medial meniscus should be excluded. Treatment modalities such as ultrasonography and phonophoresis are often required for patients with this overuse bursitis.

low-riding patella and other unknown factors. The result is anterior knee pain that may progress to recurrent patellar subluxation/dislocation or patellofemoral arthritis. Swelling is seldom noted. With instability, increased lateral translation of the patella and a positive apprehension sign (displacing the patella laterally, then flexing the knee with resultant pain and anxiety). Symptoms may be reproduced when the knee is flexed to 40° (patella now constrained) and then moving the patella proximally and distally. Tracking of the patella should be observed as the knee is flexed and extended. Patellar crepitation may be noted with flexion and extension. Radiographs that include Merchant views should be examined to determine the position of the patella, abnormal subluxation or tilt, and arthritic changes. Most patients respond to nonoperative management that emphasizes strengthening of the quadriceps, particularly the vastus medialis, and stretching of any tightness of the hamstrings, iliotibial band, or gastrocnemius. With persistent symptoms and instability, patients may benefit from procedures that alter the alignment of the patellofemoral joint.

Patellofemoral Pain Syndrome Anterior knee pain is a common complaint in adolescents, especially females and athletes, particularly runners. The cause is often difficult to identify but probably is a combination of instability/malalignment and overuse. The former is usually more pertinent in adolescents, and the latter makes a greater contribution in athletes. These patients note peripatellar aching that is increased by extended walking or running activities. Pain is often increased when ascending or descending stairs or sitting with the knee flexed for a prolonged time (theater sign). The knee may give way during running or climbing—activities that create forces of several times the body weight across the patellofemoral joint. Constraint of the patella in the femoral sulcus and forces acting across the patellofemoral joint are increased in the 20° to 60° arc of flexion (Figure 18-13). Factors that decrease constraint include generalized ligamentous laxity, a high-riding patella, a shallow angle/depth of the femoral sulcus, and an increased Q angle (angle formed by the quadriceps/patellar tendon alignment) that is increased with genu valgum or increased femoral anteversion and external tibial torsion. Decreased constraint of the patella causes instability and abnormal lateral translation of the patella during knee flexion/extension. Abnormal stress across the patella can occur with a

Bipartite Patella A bipartite patella results from incomplete fusion of secondary centers of ossification. The superolateral corner is involved more than 75% of the time (Figure 18-14). These lesions rarely cause symptoms and are typically incidental findings on radiographs. However, a bipartite patella may become painful with overuse or injury. Examination shows localized tenderness that may be increased on maximum flexion. Symptoms typically resolve with rest and short-term immobilization.

Plica Injury A plica is a normal fold in the synovium. The knee joint has three distinct plicae (Figure 1815). The suprapatellar plica extends from the posterior surface of the quadriceps tendon to the medial or lateral capsule of the knee. The medial plica extends from the medial joint capsule to the infrapatellar fat pad. The infrapatel-

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The Knee and Leg Figure 18-13: Subluxation and Dislocation of Patella Lateral retinaculum

Medial retinaculum

Skyline view. Normally, patella rides in groove between medial and lateral femoral condyles

Q

Medial retinaculum stretched

In subluxation, patella deviates laterally because of weakness of vastus medialis muscle, tightness of lateral retinaculum, and high Q angle

Medial retinaculum torn

In dislocation, patella displaced completely out of intercondylar groove

Apprehension test Displace patella laterally and move the knee into flexion. Unstable patella will displace laterally and pain (apprehension) is noted at approximately 20˚ to 40˚ of flexion when the patella is compressed against the edge of the lateral condyle. Q angle formed by intersection of lines from anterior superior iliac spine and from tibial tuberosity through midpoint of patella. Large Q angle predisposes to patellar subluxation. Surgical procedures for recurrent patellar subluxation or dislocation

Q Q

Lateral release. Lateral retinaculum incised, decreasing lateral pull on patella. Torn medial retinaculum sutured or tightened by plication.

Transfer of tibial tuberosity. Tuberosity osteotomized along with attached patellar ligament. Tuberosity shifted to more medial position and fixed with screw, reducing Q angle.

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Chapter 18 Figure 18-14: Bipartite Patella

AP radiograph of knee in a 13-year-old boy who presented with pain at superolateral aspect of patella after a fall. Radiographs show bipartite patella. Patient treated with 4 weeks of immobilization for suspected quadriceps strain/slight avulsion of bipartite fragment. Symptoms resolved and patient resumed full activity.

lar plica, also called the ligamentum mucosa, can overlap the ACL as it extends from the intercondylar notch to the infrapatellar fat pad. The medial plica is most likely to become symptomatic. Direct trauma to the anteriormedial aspect of the knee, often combined with repetitive flexion-extension sports, may cause inflammation and subsequent fibrosis and thickening of the plica. The thickened plica snaps across the medial femoral condyle. Patients report activity-related anterior-medial aching pain and occasionally note mild buckling of the knee. Examination shows tenderness on the medial aspect of the patella. The thickened plica may be palpated with the knee flexed. A snap is noted at 60° to 70° as the knee moves from flexion into extension. Nonoperative management includes activity modification and NSAIDs. Injection of steroids into the plica may reduce inflammation and resolve symptoms. If pain persists and there is no evidence of other disorders, resection of the plica should be considered.

Popliteal cyst in children typically presents with a painless swelling without an apparent precipitating event. Spontaneous resolution is common. A popliteal cyst in an adult is nearly always secondary to pathologic conditions within the knee, such as a tear of the medial meniscus or synovitis secondary to an inflammatory arthritis. Symptoms in adults include activityrelated posterior knee pain and the presence of a mass. Large cysts may rupture, spilling synovial fluid into the surrounding tissues with a resultant acute pain and swelling that simulates deep venous thrombosis in the calf. Initial treatment is directed at the underlying pathologic condition. The popliteal cyst commonly resolves after excision of a torn medial meniscus.

Chronic Exertional Compartment Syndrome of the Leg Chronic compartment syndrome most often occurs in the leg. These patients have a thicker, less compliant fascia that does not accommodate the increased blood and muscle volume that develops during exertion and exercise. As a result there is abnormally in-

Popliteal Cyst A popliteal (Baker) cyst is typically located between the semimembranosus tendon and the medial head of the gastrocnemius.

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The Knee and Leg Figure 18-15: Synovial Plica Patella (turned up)

Medial femoral condyle

Opening to suprapatellar pouch Suprapatellar plica (usually asymptomatic) Lateral gutter

Lateral plica (asymptomatic) Lateral femoral condyle Anterior cruciate ligament Medial (shelf) plica (symptomatic)

Infrapatellar plica Tibia

30° With flexion, plica sweeps across condyle. If thickened, it may cause pain and condylar erosion.

Fibula

After resection, preexisting condylar erosion (due to irritation by plica) can be seen

Arthrosopic resection of medial plica using motorized instrument

sent. After exercise, the involved compartment is tender, and muscle weakness and paresthesia may be present. The diagnosis is confirmed through measurement of compartment pressures before and after exercise. These patients develop pressures ⬎40 mm Hg with exercise, and the pressure typically remains elevated for a prolonged period (30 minutes or longer). Nonoperative management includes a period of exercise cessation and sometimes a

creased tissue pressure in one or more of the four leg compartments (see Figure 18-5). Patients complain of achy leg pain and sometimes paresthesia radiating into the foot after running or other exercise activities that resolves with rest. The anterior compartment is most often involved. The examination may be normal or there may be mild discomfort over the involved compartment. A fascial defect allowing muscle herniation during exertion may be pre-

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Chapter 18 Figure 18-16: Fracture of Distal Femur

Transverse supra-condylar fracture

Intercondylar (T or Y) fracture

Comminuted fracture extending into shaft

continued reduction in exercise intensity. Fasciotomy is indicated for the management of persistent symptoms.

Fracture of single condyle (may occur in frontal or oblique plane)

Fractures of the tibial plateau in young adults may occur with sports play or motor vehicle accidents (Figure 18-17). The lateral plateau is injured from a valgus, axial-loading force. More than 2 mm displacement of the articular surface necessitates operative reduction and internal fixation. Larger amounts of displacement can be accepted in a patient with osteoporosis and reduced activity. Fractures of the patella usually are caused by a direct blow, but a powerful quadriceps contraction with the knee partially flexed can cause a transverse avulsion fracture. Direct trauma typically causes variable degrees of comminution. Displaced fractures require open reduction to restore articular congruity and the extensor mechanism (Figure 18-18). Markedly comminuted fractures may require partial or complete patellectomy, although the latter should be avoided if at all possible. Fractures of the tibial shaft are common in adults, and open fractures are more common in the tibia than in any other long bone. Fractures of the tibial shaft also are more likely to be complicated by nonunion, malunion, and infection. Closed treatment is primarily used in closed, minimally displaced, and axially stable injuries.

Shin Splints Shin splints are a common, but poorly understood, condition. The primary symptom is the indolent onset of posteromedial pain in the middle to distal third of the leg, most often after running. The best explanation is inflammation of the periosteum caused by repetitive muscle contraction. Stress fracture of the tibia should be excluded.

TRAUMATIC CONDITIONS Fractures in Adults Distal femur fractures may be classified as supracondylar fractures, supracondylar fractures with intra-articular extension, or isolated fractures of the medial or lateral condyle (Figure 18-16). In young adults, these injuries typically result from high-energy axial loading of the flexed knee (eg, dashboard impact in a car crash). Concomitant injuries are common. In the elderly, the trauma that causes the injury may be trivial. Most fractures are displaced and require open reduction.

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The Knee and Leg Figure 18-17: Tibial Plateau Fractures

Split fracture of lateral tibial plateau. Repair with long cancellous screws

Comminuted split fracture of medial tibial plateau and tibial spine. Repair with buttress plate

Split fracture of lateral condyle plus depression of tibial plateau. Repair by elevation of depressed segment plus bone graft and buttress plate

Bicondylar fracture involving both tibial plateaus with widening. Repair with two buttress plates and lag screws or with single locking plate

Split depression fracture of lateral tibial plateau

Fracture of lateral tibial plateau and tibial shaft at the metaphyseal-diaphyseal junction. Repair with locking plate

Repair by elevation of depressed segment plus bone graft and buttress plate

Intramedullary nailing is preferred for most open and unstable closed tibial shaft fractures.

mon in children and are treated similar to adult injuries. Proximal tibia fractures in children occur in the adolescent years. The exception is a metaphyseal fracture, which is typically seen in the 2to 8-year-old child. These fractures may cause genu valgum secondary to overgrowth of the medial aspect of the proximal tibial physis. Fractures of the tibial tubercle occur during adolescence (Figure 18-19). Type I injuries

Fractures in Children Displaced distal femoral supracondylar and growth plate fractures can be difficult to reduce or to maintain reduction in casts. Open treatment with pin fixation and supplemental cast immobilization is commonly used for these injuries. Patellar fractures are uncom-

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Chapter 18 Figure 18-18: Fracture of the Patella

Nondisplaced transverse fracture with intact retinacula

Displaced transverse fracture with tears in retinacula

Transverse fracture with comminution of distal pole

Displaced transverse or slightly comminuted fractures fixed with Steinmann pins through vertical drill holes plus figure-of-8 tension band wire and suture of retinacula.

Complete excision of lower pole plus reattachment of patellar ligament to remainder of patella with wire through drill holes. Retinacula repaired.

Severely comminuted fracture

In badly comminuted fractures, patella removed, quadriceps femoris tendon sutured to patellar ligament with nonabsorbable sutures, and retinacula repaired.

cm of shortening. Grade III open fractures usually are treated with external fixation.

may be treated by casting in extension, while type II and type III injuries require open reduction and screw fixation. Tibial spine fractures affect the attachment of the ACL. Type I and type II injuries can be treated by casting in extension. Type III injuries require open or arthroscopic reduction with suture or screw fixation. Tibial shaft fractures in children can usually be treated by closed methods. A toddler’s fracture occurs in a 1- to 3-year-old whose foot catches on an object while running or falling. The result is a rotational injury of the distal tibia that may be difficult to visualize on initial radiographs (occult fracture). The goal of reduction for displaced fractures is coronal angulation ⬍10° in children and 5° in adolescents, ⬍10° of sagittal angulation, and ⬍1.5

Dislocation/Subluxation of the Patella Lateral subluxation/dislocation of the patella can result from a direct blow but most often occurs with the foot planted, the knee flexed 20° to 40°, and a valgus external rotation stress on the knee. These traumatic injuries merge with and have similar predisposing factors as observed in patients with instability and the patellofemoral pain syndrome. Patients report severe pain and that their knee popped out of place. The patella frequently reduces spontaneously, but closed reduction may be required. Dislocation of the patella causes tearing of the medial retinacular tissues. Examination shows swelling, decreased

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The Knee and Leg Figure 18-19 Fracture of Tibial Tubercle and Tibial Spine Tibial spine (eminence) fracture

Type I. Incomplete fracture of tibial spine

Type II. Complete fracture, nondisplaced

The terms tibial spine, tibial eminence, and intercondylar eminence are used interchangeably to designate the nonarticular portion of the adjacent medial and lateral tibial plateaus to which the anterior cruciate ligament is attached anteriorly. Injuries that typically cause ruptures of the anterior cruciate ligament in adults often cause a fracture of the tibial spine in children 7 to 14 years of age 20-year-old female who was unrestrained passenger in a motor vehicle accident. The patient sustained multiple fractures including a closed fracture of the right femoral shaft (A), an open grade IIIA comminuted fracture at the junction of the middle third-distal third right tibia and a closed, comminuted fracture of the middle third of the left tibia and fibula, and a comminuted fracture of the right calcaneus. On the date of injury, the patient underwent débridement of the right tibia with application of an external fixator, and retrograde nailing of the right femur, and intramedullary nailing of the left tibia. Nine days after injury, intramedullary nailing of the right tibia and open reduction and plating of the right calcaneus were done. AP (B) and lateral (C) radiographs of the tibia 2 months after intramedullary nailing show good alignment but limited healing of the fracture, which is not unusual in open tibia fractures at this location.

Type IIIA. Complete fracture, displaced

Type I

Type I tibial spine fracture

Type II

Type III

Fracture of the Tibial Shaft

A

B

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C

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Chapter 18 Figure 18-20: Dislocation of the Knee Circulation and nerve function must be carefully evaluated before and after reduction

Prompt reduction important and can usually be readily accomplished using manual traction, with or without pressure over prominence of dislocated bone. Tear or thrombosis of popliteal artery is frequent complication, requiring immediate repair or replacement. Tibial and common peroneal nerve function may be absent secondary to stretch or avulsion injury.

motion, and tenderness medial to the patella. AP, lateral, and sunrise radiographs should be reviewed for possible avulsion fractures. Patients who have sustained one dislocation of the patella are likely to experience additional episodes, particularly if they have predisposing factors. Recurrent episodes tend to occur with less trauma and milder symptoms than the initial episode. The principles of treatment are to reduce pain and approximate the torn medial structures so that the vastus medialis heals in a normal instead of a lengthened position, which would enhance the possibility of recurrent instability. Initial treatment includes a compressive dressing and protective splint with the knee in extension. Aspiration of the hemarthrosis should be considered when there is a significant effusion. Isometric quadriceps exercises initially are done with the splint on. Reevaluate the patient every 2 weeks, and when medial tenderness resolves, institute motion and more vigorous strengthening exercises. Associated osteochondral avulsion fractures that are intra-articular are uncommon but should be removed. Recurrent instability that does not respond to nonoperative treatment necessitates proximal and/or distal realignment of the extensor mechanism.

Dislocation of the Knee Dislocation of the knee occurs secondary to multiple ligament injuries, usually of the ACL, the PCL, and one of the collaterals. Dislocation can occur in a high-energy trauma or it can occur as an isolated sports accident, that initially may be perceived as a relatively trivial injury. Dislocation of the knee can be a serious, limb-threatening injury because popliteal vessel tears occur in approximately one third. Anterior dislocations are the most common type. The patient should be examined carefully for possible nerve or vascular injury. The dislocation should be reduced in an expedient manner (Figure 18-20). Any vascular injury requires emergency repair. Most studies recommend ACL and PCL reconstruction in 3 to 4 weeks.

Ligament Injuries Collateral Ligament Injuries An isolated MCL sprain results from an impact on the lateral aspect of the limb that causes a valgus force without rotation, such as occurs in football (see Figure 5-6). Isolated LCL sprains are less common and occur with a varus force.

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The Knee and Leg Figure 18-21: Rupture of the Anterior Cruciate Ligament Posterior cruciate ligament Anterior cruciate ligament (ruptured)

Arthroscopic view

Usual cause is twisting of hyperextended knee, as in landing after basketball jump shot

lated collateral ligament injury. For example, pain on varus stress with less than 10 mm opening in full extension and more than 10 mm opening in 25° of flexion suggests an isolated complete LCL tear. Evaluate the knee for other injuries, particularly an associated meniscal or cruciate ligament tear. Nonoperative treatment of isolated collateral ligament injury is satisfactory. Initial pain, swelling, and muscle spasm may mask the degree of injury. Management of MCL and LCL sprains requires ongoing evaluation for possible associated meniscal and cruciate injuries.

Most patients note tenderness on the involved side but are able to walk. The site of maximum tenderness varies, as the ligament may be partially or completely torn at any site. Isolated MCL or LCL sprains cause swelling of the adjacent tissues but do not create the significant joint effusion commonly observed in meniscal or cruciate ligament injuries. Evaluate ligament stability in the following sequence. Assess collateral ligament stability by applying varus and valgus stress with the knee in full extension and 25°of flexion. In full extension, the posterior capsule and cruciate ligaments contribute to varus/valgus stability. Therefore, laxity in full extension indicates greater disruption of ligamentous structures. Laxity is based on joint opening: grade 1 (0 to 5 mm), grade 2 (5 to 10 mm), and grade 3 (⬎10 mm). Grade 3 valgus laxity in full extension indicates that the MCL and the posteromedial capsule are torn. Grade 3 varus laxity in full extension indicates tearing of the LCL and posterolateral capsular complex. Concomitant ACL or PCL tears also are more likely if grade 3 varus or valgus laxity is present at full extension. With the knee in flexion, the posterior capsule and cruciate ligaments are relaxed; therefore, instability that is observed only in this position indicates iso-

Anterior Cruciate Ligament Tears The ACL is the primary restraint to anterior translation of the tibia; it also contributes to internal rotation and varus/valgus instability with the knee in extension. The anatomic configuration of its two bundles ensures functional tautness throughout the arc of motion, with the anteromedial bundle taut in flexion and the posterolateral component taut in extension. Although it may be torn by a contact injury, the ACL is most commonly injured without contact by a decelerating valgus angulation and external rotation force. In basketball, the ACL is commonly torn when a player lands from jumping with the knee in hy-

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Chapter 18 Isolated PCL injuries usually occur with the knee in flexion, but may be secondary to a hyperextension injury (Figure 18-22). With severe extension/valgus/internal rotation contact injuries, the ACL is torn first, then the PCL is disrupted. An effusion develops within 24 hours but is not as large as that observed in ACL tears. Assess PCL stability with the thumb sign and posterior drawer test. Place the leg in 90°of flexion. Usually, the tibial plateau is anterior to the femoral condyles, which permits the thumbs to rest on top of the tibial plateaus. With a disrupted PCL, the tibia falls back, and there is less space for the thumb. If the PCL is completely torn, the tibial plateaus are in line with the femoral condyles. Perform the posterior drawer test by applying a posteriorly directed force to the proximal tibia (see Figure 18-22). Increased posterior translation and a soft end point indicate PCL injury. Isolated PCL injuries should be treated in a rehabilitation program that emphasizes increasing range of motion and quadriceps strengthening. Persistent or recurrent instability suggests concomitant meniscal tears. These patients may need reconstructive procedures.

perextension and the tibia in internal rotation (Figure 18-21). Examination shows a marked effusion, and most patients with an acute knee hemarthrosis have a torn ACL. The Lachman test is the most sensitive maneuver for detecting ACL tears. It is performed with the knee flexed to 20°. One hand placed laterally stabilizes the distal femur, and the other hand grasps the proximal tibia medially. The proximal tibia is pulled forward. With an intact ligament, minimal translation is felt and a firm end point is noted. With a torn ligament, more translation is noted, and the end point is soft. The hamstrings must be relaxed during the test to prevent false-negative findings. Although not as sensitive as the Lachman maneuver, the anterior drawer test is easier to perform. It is performed with the patient supine, with the hamstrings relaxed, and the knee in 90°of flexion. The proximal tibia is grasped with both hands and pulled forward. Displacement ⬎5 mm compared with the uninvolved side indicates an ACL tear. Radiographs mostly rule out other injuries, but a lateral avulsion fracture (Segond fracture) indicating an associated lateral capsular tear may be present. If surgical reconstruction is planned, MRI is usually obtained to confirm diagnosis and to delineate associated injuries. Cruciate ligaments do not heal with nonoperative treatment. With no treatment, the resultant recurrent instability makes return to previous level of sports participation unlikely and predisposes the patient to subsequent meniscal tears. Direct repair does not work. Intra-articular midpatellar bone-tendon-bone or hamstring tendon autograft reconstructive procedures provide the most consistent results, but allograft or extra-articular procedures are also used in selected cases. Possible complications include arthrofibrosis, repeat ACL tear, and patellar symptoms.

Tendon Ruptures A fall on a flexed knee can cause excessive eccentric loading of the extensor mechanism and rupture of the quadriceps or patellar tendon. A similar mechanism of injury can cause a patellar fracture. Quadriceps tendon ruptures generally occur in patients over 40 years old, while patellar tendon ruptures are more likely to occur in patients under 40 years of age. Predisposing factors to patellar tendon ruptures include diabetes mellitus, chronic renal failure, hyperthyroidism, gout, and multiple cortisone injections. A large effusion and a palpable defect are usually present. The patient cannot actively extend the knee against gravity. With rupture of the patellar tendon, lateral radiographs show a patella that is higher than normal. Surgical repair is the treatment of choice for both quadriceps and patellar tendon rupture.

Posterior Cruciate Ligament Tears The PCL provides primary restraint to posterior translation of the tibia. The PCL is the strongest knee ligament, and isolated PCL injuries are much less common than ACL tears.

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The Knee and Leg Figure 18-22: Rupture of Posterior Cruciate Ligament Usual causes include hyperextension injury, as occurs from stepping into hole, and direct blow to flexed knee

Posterior drawer test: Procedure same as for anterior drawer test, except that pressure on tibia is backward instead of forward.

PEDIATRIC CONDITIONS Congenital Disorders of the Knee and Leg Congenital dislocation of the knee causes striking hyperextension of the knee (Figure 18-23). The disorder ranges from a position-

ing deformity that readily responds to shortterm splinting to a resistant deformity that does not respond to serial casting and requires surgery. Associated hip dislocation and clubfoot commonly accompany true dislocation of the knee. Congenital dislocation of the patella is often

Figure 18-23: Congenital Dislocation of the Knee

Infant with characteristic hyperextension deformity of both legs.

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Chapter 18 Fibular hemimelia is a sporadic congenital deletion. Leg-length discrepancy is universal, is less severe if the fibula is partially present, and ranges from 2 to 16 cm at skeletal maturity. The deletion often includes the lateral aspect of the foot with the absence of one or more lateral rays and abnormalities of the tarsal bones causing valgus alignment of the hindfoot and equinus contracture of the ankle. The tibia may be bowed anteriorly. Mild shortening of the femur and mild hypoplasia of the lateral femoral condyle with subsequent genu valgum often are observed with complete absence of the fibula. Treatment depends on the severity of the condition. If the anticipated limb-length discrepancy is large (8 to 16 cm), if the foot is dysfunctional, or if both occur, the best treatment is disarticulation at the ankle and prosthetic fitting during the first 2 years of life. In a patient with a functional foot and anticipated shortening of less than 30% of the opposite side, other modalities to equalize leg lengths may be considered. Tibia hemimelia is partial or complete absence of the fibula. Associated deletions of one or more of the medial rays and equinovarus foot deformity are common. Tibia hemimelia may be sporadic or be an autosomal dominant inherited disorder. Familial disorders are often bilateral and have upper extremity deletions. With unilateral involvement, the anticipated leg-length discrepancy

overlooked at birth because the infant’s patella is small and often cannot be palpated in its lateral dislocated position. A persistent flexion contracture and external rotation of the tibia suggest the presence of this condition. Because the patella does not ossify until 3 to 5 years of age, ultrasonography is helpful in confirming the diagnosis. Operative treatment is necessary and requires an extensive lateral release and medial imbrication/realignment. Posteromedial bowing of the tibia is usually obvious at birth; however, because the bowing causes the foot to be in apparent dorsiflexion and valgus, the disorder initially may be misdiagnosed as a calcaneovalgus foot (Figure 18-24). The condition is idiopathic, unilateral, and causes the affected limb to be short. The bowing gradually is corrected with growth, so realignment osteotomy is not necessary. Variable degrees of leg-length discrepancy persist and may require a shoe lift and possibly a contralateral epiphysiodesis. Anterolateral bowing of the tibia may not be obvious at birth, is associated with neurofibromatosis, and frequently progresses to congenital pseudarthrosis of the tibia, a condition that results in an unstable extremity and requires complicated operations that have a high failure rate (Figure 18-25). In infants with anterolateral bowing of the tibia, bracing may prevent progression to pseudarthrosis.

Figure 18-24: Posteromedial Bowing of the Tibia

Posteromedial bowing. Convexity of bow in distal third of tibia and fibula directed posteriorly and medially. Spontaneous correction usually obviates need for realignment osteotomy, but leg-length discrepancy often persistent.

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The Knee and Leg Figure 18-25: Anterolateral Bowing of Tibia and Congenital Pseudarthrosis of Tibia Congenital Pseudoarthrosis of the Tibia. Angulation of right leg. Café au lait spots on thigh and abdomen suggest relationship to neurofibromatosis.

Anterolateral bowing. In infancy it may be difficult to predict if anterolateral bowing will correct spontaneously or if bone will progress to fracture and congenital pseudarthrosis. Progression to pseudarthrosis is more likely if the medullary canal is narrow and has sclerotic changes.

Anterolateral bowing. Medullary canal present but narrow with sclerotic changes; cyst apparent. Prone to spontaneous fracture and pseudarthrosis

is large. If the proximal tibia is present and the quadriceps can actively extend the knee, disarticulation of the ankle and prosthetic fitting before age 2 years is the best treatment option. If the proximal tibia is absent or the quadriceps muscle is dysfunctional, a knee disarticulation and appropriate prosthetic fitting provide the best function.

Tibia Vara Children with infantile tibia vara have persistent and progressive genu varum (see Chapter 3). Infantile tibia vara develops from excessive loading and subsequent deficient growth of the medial aspect of the proximal tibial physis. Associated factors are obesity and walking at an early age, when the knee is

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Chapter 18 Figure 18-26: Infantile Tibia Vara Stage I

Stage II

Unilateral Bilateral

Stage III

Stage IV

Stage V

Stage VI

Radiographs demonstrate stages of Infantile Tibia Vara: progressive deformity of medial side of proximal tibial epiphysis and development of metaphyseal beak

at an older age, but measurement of the tibial metaphyseal-diaphyseal angle can help differentiate physiologic genu varum from infantile tibia vara. Bracing may correct the genu varum in children younger than 3 years. Realignment osteotomy is required for older children. Adolescent tibia vara is progressive genu varum that insidiously develops, usually after

in greater varus and walking may abnormally load the medial side of the physis. Children with infantile tibia vara typically present for evaluation at between 18 and 36 months. In addition to genu varum, the disorder is associated with internal tibial torsion (Figure 18-26). Radiographs at this age usually do not demonstrate the diagnostic inferior sloping of the metaphysis that is present

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The Knee and Leg 9 years of age. This disorder results from excessive compression and subsequent deficient growth of the medial aspect of the proximal tibial physis. Risk factors include morbid obesity, male sex, and African American race. If the physis is open, hemiepiphysiodesis should be performed on the lateral aspect of the physis. After skeletal maturity, realignment osteotomy should be performed to correct any residual deformity.

Examination shows swelling and tenderness at the tibial tubercle but no restriction of motion (see Figure 10-6). Radiographs may be normal or may show heterotopic ossification and fragmentation of the tibial tubercle. Treatment consists of activity modification to allow healing of microscopic avulsion fractures. Short-term immobilization for 4 to 8 weeks may benefit patients with severe or recalcitrant symptoms. If the patient is a highly competitive athlete, the parents and patient must understand that return to full sports activity often is not possible for 6 to 10 months.

Osgood-Schlatter Disease Osgood-Schlatter disease results from repetitive microtrauma at the insertion of the patellar tendon into the secondary ossification center of the tibial tuberosity. Onset of the condition is during early adolescence and coincides with the development of this ossification center, which is a weak link to repetitive quadriceps contraction. Overuse explains the 4 times greater incidence in athletic versus sedentary children. Patients present with a painful prominence of the anterior tibial tubercle.

ADDITIONAL READINGS DeLee JC, Dres D Jr, Millder MD, eds. DeLee and Drez’s Orthopaedic Sports Medicine: Principles and Practice, 2nd edition. Philadelphia, Pa: WB Saunders; 2003. Harner CD, Vince KG, Fu FH. Techniques in Knee Surgery. Philadelphia, Pa: Lippincott, Williams and Wilkins; 2000. Insall JN, Scott WN. Surgery of the Knee; 3rd edition. Philadelphia, Pa: Churchill Livingstone; 2001. Sculco TP, Martucci EA, eds. Knee Arthroplasty. New York, NY: Springer; 2001.

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nineteen The Foot and Ankle Judith F. Baumhauer, MD

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Chapter 19 lating sides of the mortise. As is typical with hinge joints, the capsule is thin in the plane of motion but supported by collateral ligaments. The thick deltoid ligament has four components that extend from the medial malleolus to the talus, calcaneus, and navicular (Figure 19-3). The lateral ligament complex includes the anterior and posterior talofibular ligaments and the calcaneofibular ligament. The foot is commonly divided into the forefoot, midfoot, and hindfoot. The forefoot contains 5 metatarsals and 14 phalanges and is separated from the midfoot by the tarsometatarsal joint (of Lisfranc). The midfoot includes the 3 cuneiforms, the navicular, and the cuboid and is separated from the hindfoot by the transverse midtarsal joint (of Chopart).

ANATOMY AND BIOMECHANICS The foot is composed of 26 bones with multiple articulations held together by strong ligaments (Figure 19-1). It provides a stable mobile platform for standing, walking, and running through a complex balance of muscle contractions and sensory feedback. Power for motion comes from 10 extrinsic tendons crossing the ankle joint and many intrinsic muscles with origins in the foot (Figure 19-2). The ankle is a hinge joint with articulations between the tibia, fibula, and talus. The weight-bearing surface of the tibia articulates with the spool-shaped surface of the talus. The ankle has a mortise and tenon configuration, with the talus being the tenon articulation and the medial malleolus and distal fibula (lateral malleolus) forming the articu-

Figure 19-1: Bones of Foot Lateral view

Transverse tarsal joint (Chopart)

Head Talus

Navicular

Neck

Intermediate Cuneiform Lateral

Trochlea Lateral process

Tarsometatarsal joint (Lisfranc)

Posterior process

Metatarsal bones

Tarsal sinus Body Calcaneus Peroneal trochlea Tuberosity

Phalanges

2 3 4 5 Cuboid Tuberosity

Tuberosity of 5th metatarsal

Medial view Transverse tarsal joint (Chopart) Navicular Neck Talus Tuberosity Head Intermediate Cuneiform Medial Trochlea Tarsometatarsal joint Posterior (Lisfranc) process Metatarsal bone

Groove for peroneus longus tendon

2

Phalanges 1

Sesamoid bone

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Tuberosity Groove for tendon of Calcaneus flexor hallucis longus Sustentaculum tali

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The Foot and Ankle Figure 19-1: Bones of Foot (continued) Calcaneus Body Peroneal trochlea Tarsal sinus Transverse tarsal joint Cuboid Tuberosity of 5th metatarsal

Metatarsals 5 Phalanges Proximal Middle Distal

Dorsal view

4

3

2

Lateral tubercle Medial tubercle Posterior Groove for process tendon of flexor Talus hallucis longus Trochlea Neck Head Navicular Tuberosity Lateral Intermediate Cuneiforms Medial Plantar view Tarsometatarsal sterior jointocess Lateral Base Talus Cuneiformtubercle 1 Shaft (body) Medial Talus Tars tubercle Head jo Posterior process Base Head Transverse Ses tarsal joint Head uneiforms (Chopart) Base Navicular sal Tuberosity Tuberosity Lateral Cuneiforms Intermediate Pha Medial Tarsometatarsal joint (Lisfranc) Metatarsals

1

Sesamoid Medial bones Lateral

Calcaneus Tuberosity Medial process Sustentaculum tali Lateral process Groove for tendon of flexor hallucis longus Peroneal trochlea Cuboid Tuberosity Groove for peroneus longus tendon

2

3

4

5

Tuberosity of 5th metatarsal bone Base Shaft (body) Head Base Shaft (body)

Proximal Phalanges Middle Distal e tarsal joint (Chopart) vicular Intermediate Cuneiform Lateral Tarsometatarsal joint (Lisfranc)

The hindfoot contains 2 bones—the talus and the calcaneus. The plantar fascia originates from the calcaneal tubercle, inserts on the base of the proximal phalanges, and acts as a windlass to support the longitudinal arch of the foot during the midstance phase of gait (Figure 19-4). As the weight-bearing stresses are shifted to

the foot and the toes are dorsiflexed, the plantar fascia is stiffened and pulled forward under the metatarsal heads. This elevates the longitudinal arch and plantarflexes the metatarsals. The major plane of ankle motion is dorsiflexion and plantarflexion. Inversion and eversion of the foot, as well as the ability to

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Chapter 19 Figure 19-2: Bony Attachments of Muscles of Foot Peroneus tertius muscle Plantaris muscle

Tibialis posterior muscle Peroneus brevis muscle

Tibialis anterior muscle

Peroneus tertius muscle

Extensor digitorum longus muscles

Soleus and gastrocnemius muscles via calcaneal (Achilles) tendon

Peroneus longus muscle

Flexor digitorum longus muscle

Flexor hallucis longus muscle Extensor hallucis longus muscle

accommodate to uneven ground, occur primarily at the subtalar (talocalcaneal) joint. Limited abduction and adduction of the forefoot occur at the transverse midtarsal joints (i.e., the ball-and-socket talonavicular joint and the calcaneocuboid joint). Very little motion occurs in the midfoot joints (the 3 cuneiform-navicular joints and the 5 tarsometatarsal joints). Flexibility in the fourth and fifth tarsometatarsal joints, however, does provide accommodation to uneven ground. The plane of motion at the toe joints is dorsiflexion and plantarflexion. Composite motions are supination, which includes forefoot adduction, hindfoot inversion, and ankle plantarflexion, and the opposite pronation, which includes forefoot abduction, hindfoot eversion, and ankle dorsiflexion.

Muscles posterior to the axis of the ankle joint—gastrocnemius-soleus, tibialis posterior, flexor hallucis longus, flexor digitorum longus, peroneus longus, and peroneus brevis— plantarflex the ankle joint (see Figures 19-2 and 19-4). Musculotendinous structures that pass anterior to the ankle axis—tibialis anterior, extensor hallucis longus, extensor digitorum longus, and peroneus tertius—dorsiflex the ankle (Figure 19-5). Muscles passing medial to the axis of the subtalar joint—tibialis posterior, flexor hallucis longus, flexor digitorum longus, and tibialis anterior—provide inversion motion. Structures lateral to this axis—extensor hallucis longus, extensor digitorum longus, peroneus longus, peroneus brevis, and peroneus tertius— produce eversion motion. In all, 6 nerves and 3 vessels supply the foot.

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The Foot and Ankle Figure 19-3: Ligaments of the Ankle and Foot Right foot: medial view Medial (deltoid) ligament of ankle

Tibia

Posterior tibiotalar part Tibiocalcaneal part Tibionavicular part Anterior tibiotalar part Medial talocalcaneal ligament

Dorsal talonavicular ligament Navicular

Posterior process of talus

Dorsal cuneonavicular ligaments

Posterior talocalcaneal ligament

Medial cuneiform Dorsal intercuneiform ligament

Calcaneal (Achilles) tendon (cut)

Dorsal tarsometatarsal ligaments 1st metatarsal

Tibialis anterior tendon Tibialis posterior tendon

Right foot: lateral view

Sustentaculum tali Plantar calcaneonavicular (spring) ligament

Long plantar ligament

Tibia Posterior talofibular ligament Components of lateral Calcaneofibular ligament (collateral) ligament Anterior talofibular ligament of ankle

Fibula

Interosseous talocalcaneal ligament Dorsal talonavicular ligament Calcaneonavicular ligament Bifurcate ligament Calcaneocuboid ligament Dorsal cuboideonavicular ligament Dorsal cuneonavicular ligaments Dorsal intercuneiform ligaments Dorsal tarsometatarsal ligaments

Anterior and Posterior tibiofibular ligaments Superior peroneal retinaculum Calcaneal (Achilles) tendon (cut)

Inferior peroneal retinaculum

Dorsal metatarsal ligaments

Lateral talocalcaneal ligament

Dorsal cuneocuboid ligament

Long plantar ligament

Cuboid

Peroneus longus tendon

Dorsal calcaneocuboid ligament

Peroneus brevis tendon

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Chapter 19 Figure 19-4: Muscles, Arteries, and Nerves of Sole of Foot Superficial transverse metatarsal ligaments Proper plantar digital arteries and nerves Superficial branch of medial plantar artery Transverse fasciculi Digital slips of plantar fascia

Cutaneous branches of lateral plantar artery and nerve Lateral band of plantar fascia (calcaneometatarsal ligament) Medial calcaneal branches of tibial nerve and posterior tibial artery

Cutaneous branches of medial plantar artery and nerve Plantar fascia

Proper digital branches of medial plantar nerve Proper digital branches of lateral plantar nerve

Tuberosity of calcaneus with overlying fat pad (partially cut away)

Proper plantar digital arteries Common plantar digital arteries from plantar metatarsal arteries

Fibrous sheaths of flexor tendons Tendons of flexor digitorum brevis muscle overlying tendons of flexor digitorum longus muscle Metatarsal branch of lateral plantar artery Flexor digiti minimi brevis muscle Abductor digiti minimi muscle Plantar fascia (cut) Tuberosity of calcaneus

432

Lumbrical muscles Lateral and medial head of flexor hallucis brevis muscle Flexor hallucis longus tendon Abductor hallucis muscle and tendon

Flexor digitorm brevis muscle

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The Foot and Ankle Figure 19-5: Common Peroneal Nerve Common peroneal nerve (in phantom)

Lateral sural cutaneous nerve (in phantom)

Tendon of biceps femoris

Articular branches Common peroneal nerve

Anterior tibial recurrent branch

Head of fibula

Extensor digitorum longus muscle

Peroneus longus muscle

Deep peroneal nerve Superficial peroneal nerve

Tibialis anterior muscle

Cutaneous innervation

Branches of lateral sural cutaneous nerve Peroneus longus muscle Peroneus brevis muscle

Medial dorsal cutaneous nerve Intermediate dorsal cutaneous nerve Superior extensor retinaculum Inferior extensor retinaculum (cut) Lateral dorsal cutaneous nerve (branch of sural nerve)

Extensor digitorum longus muscle Extensor hallucis longus muscle Lateral sural cutaneous nerve Lateral branch of deep peroneal nerve to Extensor hallucis brevis muscle and Extensor digitorum brevis muscle Medial branch of deep peroneal nerve Proper dorsal digital nerves

Proper dorsal digital nerves

433

Superficial peroneal nerve

Deep peroneal nerve Sural nerve

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Chapter 19 Terminal branches of the saphenous nerve provide cutaneous sensation on the medial side of the foot, and the sural nerve innervates the lateral side. The deep peroneal nerve provides sensation to the dorsum of the first interspace, whereas the superficial peroneal nerve provides sensation to the remainder of the dorsum of the foot (Figures 19-5 and 19-6). The tibial nerve divides into medial and lateral plantar nerves that supply the numerous small plantar muscles and the bottom of the foot (see Figure 19-4). The posterior tibial artery accompanies the tibial nerve and likewise divides into medial and lateral plantar branches. The anterior tibial artery continues on the dorsal aspect of the foot as the dorsalis pedis artery, gives off medial and lateral tarsal branches, and ends by dividing into the arcuate artery and the deep plantar artery (see Figure 19-6). The perforating branch of the peroneal artery is typically small, but it may be the principal source of the blood supply to the dorsum of the foot when the dorsalis pedis is absent. The gait cycle during walking and running consists of stance and swing phases (Figure 19-7). In normal walking, the stance phase goes from ipsilateral heel-strike to ipsilateral toe-off and occupies 62% of the gait cycle. Swing is from toe-off to ipsilateral heel-strike and is the remaining 38% of the gait cycle. The stance phase includes an initial period of double-limb support, an intermediate phase of single-limb support, and a terminal stance phase of double-limb support. The initial period of double-limb support, also called the loading response, starts with heel-strike, ends with opposite toe-off, and occupies 12% of the gait cycle. Normal heel-strike occurs on the lateral aspect of the heel, with the ankle in the neutral position and the foot positioned into supination. As the foot progresses to foot flat, the ankle goes into plantarflexion, and the hindfoot progresses into valgus and pronation. This permits shock absorption and allows the foot to accommodate to uneven ground. Single-limb support (midstance) corresponds to the swing phase of the contralateral limb and marks a reversal from stance limb

absorption to stance limb propulsion. For momentum to advance the body over a stationary foot, the foot must move to a rigid lever. This is accomplished by inversion of the heel and locking of the subtalar and Chopart joints as the ankle goes into dorsiflexion. During the second phase of double support, the ipsilateral foot goes from heel-off to toe-off, with the ankle demonstrating progressive plantarflexion.

PHYSICAL EXAMINATION Inspect the foot and ankle from all four sides with the patient standing, then supine. Assess heel alignment from the back. The normal finding is slight valgus with no lateral toes visualized. With pes planovalgus (flatfoot), the lateral toes are visible from the posterior view. From the anterior view, look at the alignment of the toes and the relationship of the forefoot to the hindfoot. Inspect the foot on the medial side for a high arch (cavus foot), flatfoot, or asymmetry of the foot. On the lateral side, look for prominence of the posterior calcaneus and abnormal swelling. Inspect the plantar aspect of the foot for callosities, prominence of the metatarsals, or ulceration. Assess the alignment of the foot during the different phases of gait. Palpate the foot and ankle for abnormal tenderness or swelling. This finding might indicate synovitis, tenosynovitis, plantar fasciitis, or degenerative arthritis. To measure ankle motion, the zero starting position is with the foot perpendicular to the tibia. Dorsiflexion is movement of the foot toward the anterior surface of the tibia; plantarflexion is movement of the foot in the opposite direction (Figure 19-8). Normal ankle dorsiflexion is 10⬚ to 20⬚, and plantarflexion is 35⬚ to 50⬚. Inversion (inward turning of the heel) and eversion (outward turning of the heel) are estimated visually (Figure 19-9). The zero starting position is with the ankle in slight dorsiflexion, which limits side-to-side motion from the ankle and therefore allows better assessment of talocalcaneal mobility. Supination and pronation are difficult to quantify. Comparison with the unaffected

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The Foot and Ankle Figure 19-6: Muscles, Arteries, and Nerves of Front of Ankle and Dorsum of Foot Superficial peroneal nerve (cut)

Soleus muscle Tibialis anterior muscle and tendon

Peroneus longus tendon Peroneus brevis muscle

Tibia Anterior tibial artery and deep peroneal nerve

Extensor digitorum longus muscle

Extensor hallucis longus muscle and tendon

Fibula Perforating branch of peroneal artery

Medial malleolus Dorsalis pedis artery

Lateral malleolus Medial branch of deep peroneal nerve

Peroneus longus tendon (cut)

Tuberosity of navicular bone

Extensor digitorum brevis and extensor hallucis brevis muscles (cut)

Arcuate artery

Peroneus brevis tendon (cut)

Posterior perforating branches from deep plantar arch

Peroneus tertius tendon (cut)

Deep plantar artery to deep plantar arch

Abductor digiti minimi muscle

Abductor hallucis muscle

Dorsal metatarsal arteries Extensor hallucis longus tendon Dorsal interosseous muscles

Extensor hallucis brevis tendon (cut) Extensor digitorum brevis tendons (cut)

Sural nerve

Extensor digitorum longus tendons (cut) Dorsal digital arteries Dorsal digital branches of deep peroneal nerve

Dorsal branches of proper plantar digital arteries and nerves

Dorsal digital branches of superficial peroneal nerve

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Chapter 19 Figure 19-7: Phases of Gait 1

2

Heel strike

Foot flat

3

Midstance

4

5

Opposite heel strike

foot provides the best assessment of these composite motions. Grading muscle strength starts by placement of the muscle in a contracted position and the other muscles that have similar function in positions that eliminate or lessen their activity during the test. Therefore, when testing

Pre-swing

6

Initial swing

7

Terminal swing

Dorsiflexion 20˚

50˚ 90˚

436

Heel strike

the anterior tibialis muscle, place the foot in dorsiflexion and inversion and ask the patient to pull the foot into more dorsiflexion and at the same time flex the toes (which eliminates the activity of the toe extensors) while you provide resistance in the opposite direction (see section on muscle testing in Chapter 12).

Figure 19-8: Ankle Dorsiflexion/Plantarflexion Plantarflexion

8

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The Foot and Ankle Figure 19-9: Inversion and Eversion

Swelling and osteophytes are obvious with arthropathy of superficial joints and motion is restricted in joints that have substantial movement. Nonoperative treatment includes shoe modification or the use of supportive orthotics. For hallux rigidus or midfoot arthritis, a stiff-soled shoe may alleviate symptoms. For end-stage arthritis in the foot, arthrodesis is the most common surgical procedure (Figure 19-11). Dorsal cheilectomy or resection arthroplasty may be used to treat patients with hallux rigidus, and total joint arthroplasty may be indicated for patients with ankle arthritis.

Plantar Fasciitis Inversion 0˚

Eversion

Most precise clinical measurement performed with patient prone and knee flexed. Place ankle in slight dorsiflexion to limit side-to-side motion at the ankle; therefore, providing better isolation of talocalcaneal mobility.

DEGENERATIVE DISORDERS Arthritis of the Foot and Ankle Osteoarthritis and traumatic arthropathy are the most common types of arthritis of the foot and ankle. Common sites include the first metatarsophalangeal (MTP) joint, midfoot (Lisfranc joints), talonavicular joint, talocalcaneal joint, and ankle joint (Figure 19-10). Hallux rigidus is the term for degenerative arthritis of the great toe MTP joint. Patients report activity-related pain and swelling in the region of the affected joint. With ankle arthritis, pain frequently is localized to the anterior aspect of the joint. With talocalcaneal arthritis, pain typically is localized to the lateral aspect of the hindfoot.

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Plantar fasciitis, the most common cause of heel pain in adults, results from periostitis of the calcaneus at the origin of the plantar fascia. Plantar fasciitis is more common in females and in obese persons, but it is not associated with any particular foot type. Patients relate the insidious onset of pain that is particularly severe with first steps in the morning or when rising from a sitting position at the end of the day. Palpation with pressure demonstrates tenderness at the medial process of the calcaneal tuberosity. Radiographs show an osteophyte (heel spur) in 50% of patients; however, this spur is not the source of pain and is noted in 20% of asymptomatic adults. Differential diagnosis includes tarsal tunnel syndrome (tibial nerve compression at the ankle with resultant plantar foot paresthesias), traumatic rupture of the plantar fascia (marked pain in the middle portion of the plantar fascia and swelling), seronegative spondyloarthropathy (enthesitis that is typically bilateral, and with other sites involved), and stress fracture of the calcaneus (medial and lateral heel pain that is activity related but not severe on awakening). Most patients can be managed nonoperatively, but they should be counseled that it commonly takes 6 to 12 months for symptoms to resolve. Effective modalities include orthotics that unload the heel, exercises to

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Chapter 19 Figure 19-10: Radiographs Depicting Arthritis in Various Sites of the Foot Radiographs courtesy of Dr. James Sebold

A Arthritis of midfoot. Lateral radiograph (A) and standing AP radiograph (B) of the foot of a 61-year-old female with narrowing and degenerative changes in the tarsometatarsal and naviculocunieform joints. Arthritis secondary to transfer of stress following triple arthrodesis several years previously for foot deformity related to Charcot-Marie-Tooth disease. Obesity is a secondary factor. Toes demonstrate Charcot fragmentation secondary to the peripheral neuropathy.

B

D

C

Hallux rigidus: arthritis of great toe metatarsophalangeal joint. Standing AP radiograph (C) and standing lateral radiograph (D) of a 42-year-old male with 10 year history of progressive pain in great toe and enlargement of dorsum of the toe. Pain increased with walking and especially aggravated with walking on inclines. No history of injury. Examination showed bony osteophytes and marked restriction of great toe metatarsophalangeal motion with only 10⬚ of extension and 5⬚ of flexion. Radiographs show narrowing of the joint and marked osteophyte formation, particularly on the lateral and dorsal aspects of the metatarsal.

stretch the Achilles tendon, night splints to keep the Achilles tendon on stretch, and steroid injections. Recalcitrant symptoms may require partial release of the plantar fascia.

Posterior Tibial Tendon Dysfunction The posterior tibialis muscle is a major supporting structure of the midfoot during

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single-limb support. Not only does the posterior tibialis muscle actively contract during this phase of gait, but its tendon insertion extends beyond the navicular to all of the midfoot tarsal bones. Thus, this muscle provides an active supporting sling to counterbalance weight-bearing stresses. Dysfunction of the posterior tibialis tendon (PTT) is the most common cause of acquired

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The Foot and Ankle Figure 19-11: Triple Arthrodesis

Triple arthrodesis. Bone, including articular surfaces, removed at talocalcaneal, talonavicular, and calcaneocuboid joint.

Lateral radiograph showing triple arthrodesis with internal fixation of talocalcaneal joint with 7.3 mm screw, cross 4.5 mm screw fixation of talonavicular joint, and staple fixation of calcaneocuboid joint.

flatfoot in adults (Figure 19-12). The cause is multifactorial. Associated factors include female gender; obesity; preexisting flatfoot or accessory navicular; rheumatoid arthritis, or other inflammatory arthropathy; steroid use; and, in younger patients, elevated levels of CW6 human leukocyte antigens. The site of dysfunction correlates with the blood supply to the PTT, which includes a 14-mm zone of hypovascularity beginning 40 mm proximal to the tendon insertion at the navicular tubercle. This hypovascular zone is further challenged by mechanical stress on the PTT as it makes a sharp turn behind the medial malleolus. PTT dysfunction may result from tenosynovitis (inflammatory cell proliferation) or tendinosis (collagen degeneration with areas of focal necrosis). The latter is more common and in this situation the excursion and function of the tendon are lost. Increased stress is placed on surrounding ligamentous structures, which gradually elongate. As a result, pes planovalgus develops. Initially, the deformity is flexible, but over time, it becomes rigid and ultimately may cause a secondary valgus ankle arthropathy. Early symptoms include pain on the medial aspect of the ankle and longitudinal arch. Swelling is noted over the PTT. In the standing position, increased heel valgus and “too

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many lateral toes” may be observed on the posterior view. Standing on the toes is difficult, painful, and abnormal. Normally, when a person stands on the toes, the heel is pulled into varus by action of the PTT, but in PTT dysfunction, the heel remains in valgus or has only limited inversion on this test. With the development of fixed deformity, passive inversion is limited, and the longitudinal arch remains flattened in a non–weight-bearing position. If only tenosynovitis is present, casting or bracing to limit the excursion of PTT may eliminate the inflammatory response. If symptoms persist after 3 months, tenosynovectomy or tendon transfer—most commonly, flexor digitorum longus to the posterior tibial tendon, which is often combined with a medial displacement osteotomy of the calcaneus—is indicated. In the patient who has tendinosis, nonoperative options include a medial heel wedge, foot orthotic, or an ankle-foot orthosis (AFO). Surgical treatment yields better results in earlier stages of PTT dysfunction. If the deformity is not fixed, options include a tendon transfer combined with Achilles tendon lengthening and realignment procedures such as medial displacement osteotomy and/or lateral col-

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Chapter 19 Figure 19-12: Posterior Tibial Dysfunction Dysfunction of posterior tibial tendon may result from tenosynovitis of tendinosis. Symptoms include pain and swelling over course of tendon and loss of tendon function results in loss of longitudinal arch

Posterior tibial tendon (PTT) Navicular

Pain and swelling

Midfoot tarsal bones

Loss of longitudinal arch

Normal arch Medial view of pronated foot reveals flattened longitudinal arch

Insertion of posterior tibial tendon extends beyond navicular to all midtarsal bones of foot and is the major supporting structure of midfoot

Posterior view reveals hyperpronation in left foot. In normal foot, midlines of calcaneus and leg are aligned or deviate less than 2°. Normal varus

PTT dysfunction

Normal

Standing. In the standing position, increased heel valgus and "too many lateral toes" may be observed on posterior view

Normal PTT dysfunction Heel rise. On toe standing, normal PTT function pulls heel into varus. PTT dysfunction allows heel to remain in valgus poisition

umn lengthening of the calcaneus. With a fixed deformity, arthrodesis of the hindfoot joint is required.

shoe wear (Figure 19-13). Extreme angulation can cause lesser toe deformities, particularly the second toe overlapping the great toe with a subsequent hammertoe deformity. The site of maximum tenderness is usually over the medial eminence and its hypertrophic bursa. Assess first MTP motion (which is usually normal), flexibility of the deformity, pronation of the hallux, and any lesser toe, first metatarsocuneiform joint, or hindfoot abnormalities.

DEFORMITIES OF THE FOOT Hallux Valgus (Bunion Deformity) Hallux valgus is lateral deviation of the great toe at the MTP joint. The medial aspect of the metatarsal head becomes prominent (bunion) and may be irritated and painful secondary to

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The Foot and Ankle

Figure 19-13: Hallux Valgus Adductor hallucis m.

Transverse head

Lateral head of flexor hallucis brevis muscle

Advanced bunion. Wide (splayed) forefoot with inflamed prominence over 1st metatarsal head. Great toe is deviated laterally (hallux valgus), overlaps 2nd toe, and is internally rotated. Other toes are also deviated laterally in conformity with great toe. Laterally displaced extensor hallucis longus tendon is apparent.

Oblique head

Hallux valgus Subluxation Conjoined tendon Laterally displaced lateral sesamoid (medial sesamoid under metatarsal) Exostosis Metatarsus primus varus

> 10%

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Chapter 19 An anteroposterior (AP) radiograph is used to measure the hallux valgus angle and the intermetatarsal (IM) angle between the first and second metatarsals. Normal hallux valgus is less than 15⬚, and the normal IM angle is less than 11⬚. Radiographs are also assessed for sesamoid displacement, congruity and erosion of the MTP joint, shape of the metatarsal head, and any valgus deviation at the interphalangeal joint. Nonoperative treatment includes shoes with adequate width at the forefoot, occasional stretching of the shoe at the deformity, and/or a longitudinal arch support to decrease pronation. High heels increase pressure on the great toe and should be avoided. The indication for surgery is persistent pain. Asymptomatic feet, no matter how severe the deformity, should be managed nonoperatively. The choice of numerous surgical options is based on the degree of deformity, the IM angle, and the degree of joint congruity and erosion.

terphalangeal (DIP) joint. The MTP joint may appear hyperextended when the patient is standing, but it is flexible with the foot at rest. Shoewear causes pain and callus formation on the dorsum of the PIP joint. A mallet toe has a flexion deformity at the DIP joint with or without hyperextension at the MTP joint. Pain and callus develop at the tip of the toe. Hammertoes and mallet toes are often secondary to improperly fitting shoes, particularly highheeled and pointed-toe shoes. These deformities may be isolated to a single toe, with the second toe most commonly involved. Nonoperative management includes wearing of shoes with adequate space in the toebox and avoidance of high-heeled shoes. Metatarsal pads or orthotics, often combined with extra-depth shoes, may be helpful in alleviating abnormal pressure. Cushions for the corns may be helpful with hammertoes and mallet toes. Refractory cases may benefit from surgical intervention to correct the soft tissue and bony deformities.

Lesser Toe Deformities

Pes Cavus

Lesser toe deformities include claw toes, hammertoes, and mallet toes (Figure 19-14). A claw toe has hyperextension at the MTP joint and flexion at the proximal interphalangeal and distal interphalangeal joints. Claw toes are similar to claw finger deformities (see Chapter 16) and most commonly are secondary to a peripheral neuropathy that causes weakness of the intrinsic muscles or an inflammatory arthropathy such as rheumatoid arthritis or an idiopathic synovitis that causes laxity of the MTP joint and secondary mechanical dysfunction of the intrinsic muscles. Neurologic disorders that most often cause claw toes are diabetes mellitus and Charcot-Marie-Tooth disease. In patients with claw toes, all lesser toes are commonly involved. Pain and calluses develop on the dorsum of the proximal interphalangeal (PIP) joint, on the toe tips, and on the plantar surface of the foot beneath the depressed metatarsal head. Hammertoe is a flexion deformity of the PIP without contracture of the MTP or distal in-

A cavus foot has a high arch with the forefoot in plantarflexion relative to the hindfoot. The hindfoot is usually in varus (ie, a cavovarus foot) (Figure 19-15). Other components associated with a cavus foot include a plantarflexed first metatarsal and claw toes. The condition may be congenital or may develop during childhood or in the adult years. The cause is usually an underlying neuromuscular disorder, but the condition may be idiopathic or may occur secondary to incomplete correction of a clubfoot disorder (Table 19-1). Cavus foot secondary to neurologic conditions typically involves relative weakness of the intrinsic muscles of the foot and variable muscle imbalance of the extrinsic muscles. Examination of a patient with no previous diagnosis includes evaluation for a possible neurologic or spinal disorder. Standing radiographs of the foot and lumbar spine should be obtained. Nerve conduction studies, electromyography, and magnetic resonance imaging (MRI) of the spine may be indicated. The Coleman block test is helpful in differentiating a

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The Foot and Ankle Figure 19-14: Lesser Toe Deformities (Claw Toe, Hammertoe, and Mallet Toe) Corn

Fixed flexion of PIP joint

Callosity Hammertoe deformity Flexion deformity of DIP joint

Corn Fixed hyperextension of MTP joint

Flexion of PIP and DIP joints

Callus Callosity

Mallet toe deformity

Claw toe deformity

Painful plantar callosities over metatarsal heads greatly impair walking. Typical deformities are marked hallux valgus with bunions and hammertoes with corns caused by pressure.

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Chapter 19 Figure 19-15: Cavovarus Foot

Cavovarus foot with characteristic high arch extending upward from ball of foot and cock-up deformity of toes.

Radiograph of foot shown above reveals fixed bony configuration, dorsiflexion of hindfoot, and sharp plantarflexion of forefoot.

Posterior view clearly shows varus deformity of affected right foot. Coleman Block Test

Flexible Cavovarus

Fixed Cavovarus

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The Foot and Ankle dorsal closing wedge osteotomy of the first metatarsal to correct a plantarflexed first metatarsal, and claw toe realignment. Arthrodesis is required for patients with hindfoot arthritis and a fixed cavus malalignment.

Table 19-1

Disorders Associated With Cavus Foot Neurologic conditions Spinocerebellar degenerative conditions Friedreich ataxia Anterior horn cell deficiency Spinal muscular atrophy Poliomyelitis Arthrogryposis Spinal cord abnormalities Diastematomyelia Lipomyelomeningocele Myelomeningocele Spinal cord tumors Tethered spinal cord Peripheral neuropathies Hereditary sensory motor neuropathies (Charcot-Marie-Tooth disease) Diabetic neuropathy Clubfoot, incomplete correction Idiopathic conditions Trauma Compartment syndrome, foot/leg

MISCELLANEOUS CONDITIONS Morton Neuroma

flexible from a fixed hindfoot varus and in determining treatment. A 1-inch wooden block is placed under the patient’s hindfoot and lateral forefoot, with the first metatarsal head off the block. With a flexible deformity, the hindfoot will evert into valgus when the plantarflexed first metatarsal is not bearing weight. Nonoperative treatment includes shoe modifications, orthotics, and bracewear. Surgical treatment of any spinal pathology may stop, slow, or reverse the foot deformity. Cavus deformities are likely to progress in children, and surgical treatment is often needed in this age group. In adolescents and adults, secondary changes often require surgical reconstruction that addresses the multiple components of the deformity, including plantar fascia release, selected tendon transfers to improve muscle balance, Achilles tendon lengthening to treat equinus contracture, lateral closing wedge osteotomy of the calcaneus to correct heel varus,

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Morton neuroma is not a true neuroma but entrapment of an interdigital plantar sensory nerve in the forefoot by the transverse metatarsal ligament and the underlying plantar fascia. Perineural fibrosis and thickening of the nerve develop. Morton neuroma most frequently occurs in the third web space, perhaps because this interdigital nerve is relatively tethered by its formation from both the medial and lateral plantar nerves. Morton neuroma occurs less frequently in the second web space and is very uncommon in the first and fourth web spaces. The condition is more frequently found in females, probably because high-heeled shoes keep the MTP joints in extension—a position that increases pressure from the transverse metatarsal ligament. Patients note burning pain in the forefoot that radiates to the toes. This pain is activity related and is aggravated by shoes with high heels and a narrow toe box. Examination may demonstrate decreased sensation in the involved web space. The pain may be reproduced by application of upward pressure on the plantar surface of the foot with one hand (which puts the nerve between the metatarsal heads), followed by compression of the forefoot with the other hand. A palpable click during this maneuver is a positive Mulder click. Nonoperative treatment involves wearing of shoes with wide toe boxes and low heels. A metatarsal pad may be helpful. An injection with lidocaine and steroid may be both diagnostic and therapeutic. Excision of the affected nerve is the usual treatment for persistent symptoms. The pain relief can be immediate and striking. The “physiologic neuroma” that develops at the cut end of the nerve can cause recurrent pain if the excision is not proximal enough.

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Chapter 19 distal fibula combined with tearing of the deltoid ligament, and uncommon fractures of the medial malleolus combined with disruption of the lateral ankle ligaments. Trimalleolar fractures include fractures of the posterior malleolus. Posterior dislocation of the ankle may accompany an unstable injury, particularly a trimalleolar fracture. Evaluation should include palpation for sites of increased tenderness. Radiographs should include AP, mortise (15° internally rotated AP), and lateral views of the ankle. A stable fracture is an isolated fracture without ligamentous disruption on the contralateral side of the ankle. Functional bimalleolar injuries (eg, fracture of the distal fibula and disruption of the deltoid ligament) usually show displacement of the talus in the ankle joint. However, an isolated fracture of the distal fibula or medial malleolus with significant tenderness over the contralateral ligaments but without radiographic displacement of the talus should be treated as an unstable injury unless stress radiographs show that the joint is stable. Most stable ankle fractures can be treated symptomatically, with commencement of weight bearing in a short leg cast or clamshell walking boot as tolerated. The most common stable ankle fracture is a supination–external rotation injury limited to the lateral malleolus. Most unstable ankle fractures are treated surgically because even 1 mm of lateral displacement of the talus reduces the contact

Ingrown Toenail An ingrown toenail occurs when the distal margin of a nail grows into the adjacent skin (nailfold), causing inflammation and sometimes secondary infection. The condition is most often limited to the great toe. Predisposing factors include improper trimming of the nail; a curved shape of the nail; and environmental factors such as tight shoes, humidity, and direct trauma. An ingrown toenail is characterized initially by pain, inflammation, and swelling (Figure 19-16). Purulent drainage may develop, along with increased erythema and swelling. Treatment in the early phases of the condition includes warm soaks, placement of dental floss under the nail to direct its growth away from the skin, wearing of open-toe shoes, modification of activities, and education on proper nail trimming. Antibiotics and partial or complete excision of the nail are necessary if the pain is severe or the condition is persistent.

TRAUMATIC CONDITIONS Ankle Fractures Fractures of the ankle occur through a variety of mechanisms (Figure 19-17) and may injure the lateral malleolus (distal fibula), the medial malleolus, the posterior malleolus (posterior distal tibia), and the collateral ligaments. Bimalleolar injuries include fractures of the distal fibula and medial malleolus, fractures of the

Figure 19-16: Ingrown Toenail

Broken lines show lines of incision for excision of lateral 1/4 of toenail, nail bed, and matrix Ingrowing skinfold

Inflamed and infected ingrown toenail

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The Foot and Ankle because concomitant fracture of the lumbar spine is relatively common. Other associated injuries include fracture of the femoral neck, tibial plateau, and ankle. Calcaneus fractures are classified as extraarticular or intra-articular. Most commonly, the axial load is transmitted through the talus, which is wedged into the calcaneus, causing an intra-articular fracture of the posterior facet of the subtalar joint (Figure 19-18). The primary fracture line divides the posterior facet joint into anteromedial and posterolateral fragments. Secondary fracture lines are frequent, with resultant marked comminution and depression of the posterior facet. Assess function of the superficial and deep peroneal, medial, and lateral plantar nerves and sural nerves distal to the fracture. Pulses, capillary refill, and temperature of the toes should be assessed. Distal paresthesias and increased swelling in the midfoot suggest a possible compartment syndrome of the foot. In addition to AP, lateral, and oblique radiographs of the foot, obtain radiographs of the spine or other areas (selected on the basis of tenderness). Special views of the hindfoot

Table 19-2

Types of Ankle Fracture Stable injuries Lateral malleolus Medial malleolus Posterior malleolus Unstable injuries Bimalleolar fracture Trimalleolar fracture Trimalleolar fracture-dislocation

area of the talus by 42%, which may lead to traumatic arthropathy. Concomitant dislocation requires urgent reduction to reduce tension on compromised soft tissue.

Calcaneus Fractures The calcaneus is the most commonly fractured tarsal bone. Most calcaneus fractures occur after a significant axial load, such as a fall from a height or a head-on motor vehicle accident. Pain and swelling of the hindfoot are usually obvious. Tenderness should be sought in other areas—particularly the back—

Figure 19-17: Lauge-Hansen Classification of Ankle Fracture* III II

IV

II

II

I IV

II

I

I

Supination–external rotation (SER).

III

Pronation–external rotation (PER).

Pronation– abduction (PA).

I

Supination– adduction (SA).

*Classification based on position of planted foot at time of injury (supinated or pronated) and direction of injuring force. Numbers are the order of fracture or ligament tear. For example, with a SER fracture, the anterior talofibular ligament is the first structure torn, followed by an oblique/spiral fracture of the distal fibula (stage II), followed by fracture of the posterior lip of the tibia (stage III), followed by either transverse fracture of the medial malleolus or tear of the deltoid ligament (stage IV). SER injury may only include stage I and II.

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Chapter 19 and computed tomographic (CT) scanning may be indicated. Most extra-articular fractures are treated nonoperatively with casting or bracing for immobilization, avoidance of weight bearing, and early motion. Intra-articular fractures are usually treated operatively if the displacement is significant or joint depression makes the subtalar joint incongruent. Older adults and smokers may do better with nonoperative management, including avoidance of weight bearing and early motion. Operative intervention is delayed for up to 3 weeks to allow adequate reduction of swelling and reduced risk of wound necrosis. Because of frequent marked comminution, common sequelae of intra-articular calcaneus fractures include traumatic arthropathy and loss of subtalar motion.

Fracture of the Talus Fracture of the talus is relatively uncommon (accounts for approximately 1% of all foot fractures). The neck of the talus is the most common site of injury (Figure 19-19). A talar neck fracture usually results from a motor vehicle accident or a fall from a height. The mechanism of injury is high-velocity axial load from the anterior cortical lip of the distal tibia with the ankle in dorsiflexion. With continued energy, the surrounding soft tissues are disrupted and the joints become incongruous; with extreme injury, the body of the talus is dislocated posteromedially. Potential complications include delayed union, nonunion, osteonecrosis of the body of the talus, and secondary traumatic arthropathy of the ankle and/or subtalar joint, and avascular necrosis of the body of the talus with subsequent arthropathy of the ankle and/or subtalar joint. Greater displacement of the fracture is associated with increased risk of complications, but because of the vulnerability of the blood supply to the talus, even type I fractures may develop osteonecrosis. Principles of examination, initial radiographs, and the need for special views and CT scanning are similar to calcaneus fractures. Type I talar neck fractures are initially treated

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in a non–weight-bearing cast with the foot in slight plantarflexion. Displaced talar neck fractures require early reduction and internal fixation to minimize the risk of complications.

Tarsometatarsal (Lisfranc) Fracture-Dislocations Injuries to the tarsometatarsal (Lisfranc) joint complex can range from isolated ligamentous injuries with minimal or no joint displacement to ligamentous injuries with severe displacement with or without associated fractures. Usually, a high-energy injury causes abduction or adduction of the forefoot, with some rotational component to the tarsometatarsal joints—for example, horseback riders who have a foot caught in a stirrup when they are thrown from their horses. However, the injury may result from a relatively trivial event, such as stepping into a hole with axial compression and abduction force at the Lisfranc joint. Lisfranc fracture-dislocation has three typical patterns: (1) homolateral injury—all five rays displaced laterally; (2) isolated dislocation—the first medial ray is dislocated medially; and (3) divergent pattern—first ray deviated medially and the lateral 2 to 5 rays move laterally (Figure 19-20). A common associated injury is “nutcracker” fracture of the cuboid due to an abduction force of the lateral rays on the cuboid. Examination reveals swelling and tenderness at the midfoot. A trivial foot sprain may be the initial impression, and the true extent of injury may be missed. Radiographs should be carefully examined for discontinuity of the following radiographic lines: (1) the medial cortex of the base of the second metatarsal base should line up with the medial cortex of the middle cuneiform on the AP view, and (2) the medial cortex of the fourth metatarsal should line up with the medial cortex of the cuboid on the oblique view. Other signs of injury include increased diastasis between the first and second metatarsals on the AP or oblique view, and dorsal displacement of the metatarsals in relation to their respective tarsal bones on the lateral view. When radiographic findings are

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The Foot and Ankle Figure 19-18: Intra-articular Fracture of the Calcaneus

10˚

Primary fracture line runs across posterior facet, forming anteromedial and posterolateral fragments.

Primary fracture line Talus driven down into calcaneus, usually by fall and landing on heel. Böhler angle narrowed. 25˚–40˚

Böhler angle Formed by line through anterior process and highest point on posterior facet of calcaneus and line parallel to superior cortex of tuberosity of calcaneus. Normally 25˚to 40˚ A 20-year-old female involved in motor vehicle accident sustaining multiple fractures (see Figures 17-23 and 18-19). Open reduction and internal fixation of calcaneus performed 9 days after injury. Wound complications are decreased by waiting until the marked swelling associated with these injuries begins to subside. Lateral radiograph (top, left) of heel showing depression of posterior talocalcanel facet joint. CT scan (top, right) showing depression and comminution of talocalcaneal facet joint. CT scan (bottom, left) demonstrating typical comminution present in these fractures. Lateral radiograph (bottom, right) of heel 1 month after operation. Joint surface contour and height has been restored. Disuse osteopenia at this time is typical for this severe injury.

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Chapter 19 Figure 19-19: Fracture of Talar Neck Usual cause is impact on anterior margin of tibia due to forceful dorsiflexion.

Type I. No displacement

Type II. Fracture of talar neck with subluxation or dislocation of subtalar joint.

normal but the examination indicates possible injury, a simulated weight-bearing view of the foot, CT scan, or MRI can denote the injury complex. Nondisplaced fractures may be treated with cast immobilization and avoidance of weight bearing for 3 months. Fractures with any degree of displacement are treated with open reduction and internal fixation. Although the midtarsal joints have limited motion, their stability is critical for normal walking. Therefore, even 1 to 2 mm of residual displacement may cause traumatic arthropathy.

metaphyseal-diaphyseal junction (zone 3). This area has a tenuous blood supply, and bone healing is often delayed. Treatment options include non–weight-bearing immobilization for up to 3 months or screw fixation supplemented with a weight-bearing cast or brace.

Fractures of the Phalanges Fractures of the phalanx result from either an axial load to the toe tip (“stub toe”) or a crush injury from heavy objects that land on the toes. These fractures are acutely painful. Most are treated nonoperatively with a stiffsoled shoe, elevation, weight bearing as tolerated, and buddy-taping to the adjacent toe. Dislocations of the metacarpophalangeal (MP), PIP, or DIP joints require immediate reduction and subsequent buddy-taping. Displaced intra-articular fractures of the MTP joints of all toes and of the interphalangeal (IP) joint of the great toe may require reduction and pinning.

Fractures of the Metatarsals Metatarsal fractures are common and occur secondary to trauma or repetitive stress (Figure 19-21). Most isolated metatarsal fractures can be treated nonoperatively by wearing of a stiff-soled, open-toed shoe. Displacement in the sagittal plane, intra-articular fracture, and multiple metatarsal fractures with shortening require surgical intervention to prevent altered pressure at the dorsum of the foot or abnormal MTP mechanics. A common problematic metatarsal fracture is a fracture of the fifth metatarsal that occurs at the

Fractures in Children Fractures of the foot and ankle are relatively uncommon in children. Most injuries are min-

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The Foot and Ankle Figure 19-20: Injury to Tarsometatarsal (Lisfranc) Joint Complex Radiographs courtesy of Dr. Robert Anderson

A

B

C

D (A) AP radiograph of foot at injury; (B) radiograph of foot at injury. Postoperative AP (C), oblique (D), and lateral (E) radiographs of foot. 26-year-old male who fell while participating in sports sustaining an axial compression of the plantarflexed foot. Injury radiographs (A and B) demonstrate Lisfranc fracture-dislocation with disruption of the tarsometatarsal joints with associated fracture of base of 2nd metatarsal and subluxation of the medial cuneiform– navicular joint. Patient was treated with reduction and internal fixation (C to E). Medial column, which has no significant motion, was treated with screws to provide the rigid immobilization required for these joints. Lateral column has some flexibility and, therefore, was fixed with a smooth pin that was later removed. Patient returned to competitive sports activities.

E

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Chapter 19 Figure 19-20: Injury to Tarsometatarsal (Lisfranc) Joint Complex (continued)

Homolateral dislocation. All five metatarsals displaced in same direction. Fracture of base of 2nd metatarsal

Isolated dislocation. One or two metatarsals displaced; others in normal position

Divergent dislocation. 1st metatarsal displaced medially, others superolaterally Injury may occur from seemingly trivial event, eg, misstep into a hole with axial compression and abduction force on plantarflexed foot.

Dorsolateral dislocation often best seen in lateral view

imally displaced and can be treated by cast immobilization. Exceptions include intraarticular fractures of the distal tibia and open fractures (Figure 19-22). Lawnmower accidents are the most common cause of open foot and ankle injuries in children. These highvelocity, contaminated injuries require meticulous débridement and frequently necessitate partial amputation of the foot, as well as reconstructive skin coverage operations. Intraarticular fractures of the distal tibia are most often physeal fractures. These injuries require open reduction and internal fixation if the joint displacement is 2 mm or greater.

TENDON AND LIGAMENT INJURIES Achilles Tendon Rupture Rupture of the Achilles tendon typically occurs in middle-aged males who are participating in sports activities, especially basketball. The rupture typically occurs in a relatively avascular area 4 to 6 cm proximal to the tendon’s insertion. A typical patient reports, “I was starting to jump and felt a sudden onset of severe pain, like a gunshot went through my calf.” However, the severe pain resolves, the patient can walk with a limp, and the injury may be mislabeled as a sprain. Examination shows

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The Foot and Ankle Figure 19-21: Injury to Metatarsals

Ankle Sprain Ankle sprains are usually inversion injuries that involve the anterior talofibular and/or lateral calcaneofibular ligaments. Although very common, ankle sprains are not always simple injuries, and they may include injury of the syndesmosis (“high” ankle sprain) and/or the deltoid ligament. Patients typically report an inversion injury with a “pop” and the acute onset of swelling and difficulty walking. Examination should include palpation of different ankle ligaments for increased tenderness and elsewhere on the foot to exclude other possible inversion injuries, such as a fracture of the fifth metatarsal. Injury to the syndesmosis is suggested by pain on compression of the tibia and fibula 4 cm above the ankle (the squeeze test). The anterior drawer test is performed with the ankle in 10⬚ to 20⬚ of plantarflexion. Steady the tibia with one hand while pulling the heel anteriorly. Increased translation of the foot indicates injury of the anterior talofibular ligament. To decrease the risk of chronic ankle instability, severe ankle sprains should be protected from reinjury, and functional rehabilitation then begins.

B C D A

E F

Types of fracture of metatarsal. A. Comminuted fracture. B. Displaced neck fracture. C. Oblique fracture. D. Displaced transverse fracture. E. Fracture of base of 5th metatarsal. F. Avulsion of tuberosity of 5th metatarsal.

First Metatarsophalangeal Joint Sprain

tenderness in the area of the rupture. A palpable defect may be appreciated. The most sensitive and reliable sign is a positive Thompson test (Figure 19-23). A delay in the diagnosis causes contraction of the muscle, difficulty in approximating the tendon, and compromised results. The advantages of nonoperative versus surgical repair are debatable. Nonoperative treatment starts with casting or bracing of the ankle in plantarflexion that is followed by gradual transition to the neutral position. The ruptured tendon is somewhat like a shredded mop, and operative repair does not achieve the tight approximation that is possible with a lacerated tendon. Decreased strength of the gastrocsoleus muscle and the possibility of re-rupture accompany each modality.

First MTP joint sprain usually results from hyperextension. This injury is commonly called a “turf toe” because of its high incidence among persons playing sports on artificial turf. Grade III complete tears have marked swelling and tenderness. Radiographs are obtained to exclude other injuries. Nonoperative treatment includes compression wraps and a stiff-soled shoe worn for 1 to 3 weeks. Return to sports is possible in 4 to 8 weeks.

PEDIATRIC CONDITIONS Clubfoot Clubfoot (talipes equinovarus) is a common congenital deformity that includes ankle plantarflexion, hindfoot varus, midfoot cavus,

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Chapter 19 Figure 19-22: Fracture of Tibia in Children Tillaux (Salter-Harris type III) fracture of distal tibia. Fracture line extends partially across growth plate and vertically through epiphysis. Medial portion of growth plate and epiphysis remain intact.

and forefoot adduction (Figure 19-24). The deformity may be unilateral or bilateral, is twice as common in males, and varies in severity. Children with clubfoot typically are otherwise normal unless they have an underlying disorder such as arthrogryposis, myelomeningocele, congenital construction band syndrome, or chromosomal abnormality. Autosomal dominant inheritance with variable penetrance plays a role in some patients. The genetic association is more prevalent in the Polynesian population. The goal of treatment is a plantigrade foot

that will function well in walking activities throughout the adult years. This goal is best achieved with corrective manipulation and serial casting implemented shortly after birth, as described by Ponsetti. An Achilles tenotomy may be necessary to facilitate cast correction. With incomplete correction, surgical release of tight structures to allow repositioning of the foot may be required. Complete medial, posterior, and lateral release should be delayed until the child is 8 to 10 months of age. Even with an excellent result, ankle and subtalar motion is less than

Figure 19-23: Thompson Test Disruption of Achilles tendon results in absence of minimal plantarflexion of ankle when calf squeezed

Achilles tendon

Normal: Squeezing calf results in gastrocnemius and soleus contraction causing plantarflexion of ankle joint if Achilles tendon is intact

Plantarflexion

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The Foot and Ankle Figure 19-24: Congenital Clubfoot

Metatarsus Adductus Metatarsus adductus is a common congenital deformity characterized by medial deviation of the forefoot (Figure 19-25). Examination shows convexity at the lateral border of the midfoot-forefoot junction. The deformity may resolve spontaneously; this is more likely in patients with a flexible deformity (a foot that can be abducted beyond or to the line bisecting the heel). Serial casting is usually successful if persistent deformity is noted at 6 months of age.

Clinical appearance of clubfoot in infant

Polydactyly Polydactyly may be preaxial or postaxial (Figure 19-26). The accessory toe may be a partial toe or an entire toe, or it may include the metatarsal. Polydactyly causes problems with shoe wear. Amputation of the accessory digit with reconstruction of collateral ligaments and tendons is best performed around 8 to 10 months of age—a time when anesthetic problems are less likely but before the child begins to walk.

normal, and the affected foot and calf are smaller than normal (obvious with unilateral involvement).

Calcaneovalgus Syndactyly

Calcaneovalgus, a postural anomaly secondary to intrauterine crowding, is very common in neonates. The ankle is markedly dorsiflexed (the foot may be pressed against the anterior surface of the tibia), and the heel is in valgus. The differential diagnosis includes congenital vertical talus and lipomyelomeningocele. Unless neuromuscular disorders are present, spontaneous correction occurs.

Syndactyly in the toes occurs alone or in association with multiple other congenital abnormalities and syndromes (see Figure 19-26). Three types of syndactyly have been described that may be inherited as an autosomal dominant condition. Type I is most common and involves partial or complete webbing of the second and third toes. The fingers may similarly be involved. Type II is char-

Figure 19-25: Metatarsus Adductus Corrective stretching maneuver. Pressure applied to lateral side of hindfoot with thumb as forefoot is drawn laterally. Resistant cases may require serial casting.

Bilateral metatarsus adductus

View of sole shows medial deviation of forefoot

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Chapter 19 Figure 19-26: Polydactyly, Syndactyly, Congenital Curly Toe, and Overlapping Fifth Toe

Overlapping 5th toe

Congenital curly toes

Syndactyly (2nd and 3rd toes) Polydactyly

acterized by syndactylization of the fourth and fifth toes, and duplication of the fifth toe is common. Type III involves syndactylization of the toes with a metatarsal fusion. Syndactyly of the toes rarely causes functional problems, and surgical treatment is unnecessary unless growth causes angular malalignment.

volved. Overgrowth of forefoot soft tissues and metatarsals may be present. Surgery is indicated when shoe fit and foot function are compromised. Procedures include reduction and syndactylization to maintain toe alignment, soft tissue debulking combined with ostectomies or epiphysiodesis, toe amputation, and ray amputation. Ray amputation often provides the best long-term results.

Macrodactyly Macrodactyly occurs when one or more digits are significantly larger than the adjacent toes. Common associated conditions are neurofibromatosis and hemangiomatosis. The static form of macrodactyly is evident when the infant is born, and subsequent growth of the enlarged digit occurs in proportion to the remaining digits. In the progressive type of macrodactyly, growth is more rapid in the affected area than in the rest of the foot. The second and third toes are more commonly in-

Congenital Curly Toe Curly toe is characterized by flexion and medial rotation of the toe (see Figure 19-26). The lateral three toes are most often affected. The condition is usually idiopathic, but curly toe may be an inherited trait. Most children are asymptomatic. Strapping is ineffective. If problems develop with shoe wear, tenotomy of the toe flexors is usually successful in a young child.

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The Foot and Ankle Overlapping Fifth Toe An overlapping fifth toe is a common familial condition that consists of contracture of the dorsal and medial capsules of the metatarsophalangeal joint and short extensor tendons (see Figure 19-26). The proximal phalanx is dorsally displaced, adducted, and rotated. The condition is commonly bilateral. When other toes are involved, congenital shortening of the associated metatarsal is common. Approximately 50% of patients have shoefitting problems that warrant surgical treatment. Options include syndactylization of the fifth and fourth toes; proximal hemiphalangectomy; or a reconstructive procedure that involves a relaxing dorsal incision, lengthening of the extensor tendons, release of the contracted portion of the MTP joint capsule, and temporary pinning of the toe. Amputa-

tion of the toe is used to treat severe deformity or recurrent overlapping.

Flatfoot Pes planus, more commonly called flatfoot, is a low or absent longitudinal arch that is commonly associated with increased heel valgus (pes planovalgus). It is useful to classify the disorder as a flexible or rigid deformity. Flexible flatfoot is more common and in many people, particularly young children, is a variation of normal foot posture (Figure 19-27). Patients with a flexible flatfoot have a visible arch when they are sitting and no restriction of subtalar motion (inversion and eversion). A rigid flatfoot is revealed by persistent flattening of the longitudinal arch in non–weightbearing positions and restriction of subtalar motion. Flexible flatfoot is almost always bi-

Figure 19-27: Flexible Flatfeet

Bilateral flexible pes planovalgus in a 2-year-old child. Condition more apparent when patient stands. Flexible nature of condition determined by (1) normal range of inversion-eversion and Calcaneovalgus in 2-year-old child. Right (2) reconstitution of arch in sitting (non–weightfoot more severely affected. Condition bearing position). more apparent when patient stands.

Bilateral flexible flatfeet in adolescent Anterio boy. Valgus posterioof heels more s position of bilate in posterior view. In apparent planovato flatfeet from contrast adolesc tibial dysfunction, y. posterior Valgus n these patients have normal of heels inversion apparen of heels on toe rise. posterio

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Chapter 19 lateral, but rigid flatfoot may be bilateral or unilateral. Patients with flexible flatfeet are often asymptomatic. This is almost universal in early childhood. During the second decade, activity-related aching pain may be noted in the region of the longitudinal arch. Adolescents with symptomatic flatfeet often have an associated contracture of the Achilles tendon and limited ankle dorsiflexion. Flatfoot that initially is flexible may progress to a rigid deformity. In children, this progression is more likely to occur with neuromuscular conditions that cause hypotonia or conditions associated with abnormal ligamentous laxity (eg, Marfan syndrome and Ehlers-Danlos syndrome). Severe idiopathic flatfeet may become rigid in obese adolescents or older adults. Standing radiographs of the foot are indicated in patients with rigid flatfoot or symptomatic flexible flatfoot. Typical findings include medial deviation of the talus on the AP radiograph and plantarflexion of the talus on the lateral view. Parents of young children with asymptomatic flexible flatfeet should be counseled that the degree of flattening of the longitudinal arch often improves, that orthotics or special shoes have not been shown to enhance the development of the arch, and that most adults with flatfeet are asymptomatic. Older patients with symptomatic flexible flatfeet can usually be managed nonoperatively with orthotics and heel cord–stretching exercises. For persistent and disabling symptoms, osteotomy to lengthen the lateral column, combined with lengthening of a contracted gastrocsoleus muscle, is indicated. Arthrodesis is necessary if joint deterioration has occurred. In infancy, a rigid flatfoot most often occurs secondary to congenital vertical talus. This condition is uncommon and may be idiopathic or associated with myelomeningocele, arthrogryposis, or chromosomal abnormalities such as trisomy 18. Patients have a rigid, rockerbottom foot secondary to a markedly plantarflexed (vertical) and medially deviated talus. Most patients require surgical realignment.

Tarsal Coalition Tarsal coalition is an abnormal connection between two tarsal bones; it is the most common cause of a rigid flatfoot. The coalition may be fibrous or cartilaginous but often ossifies during adolescence—the time when symptoms typically develop. The two most common sites of tarsal coalition are between the calcaneus and the navicular and between the medial facet of the talus and the calcaneus. Patients with calcaneonavicular coalitions typically become symptomatic between the ages of 9 and 13 years, whereas patients with talocalcaneal coalitions generally develop symptoms later, between the ages of 12 and 16 years. Of note, some patients are asymptomatic, with their coalition discovered as an incidental radiographic finding. Patients with tarsal coalition typically present with the insidious onset of activityrelated hindfoot pain. In addition to pes planovalgus, the patient walks with the leg externally rotated (Figure 19-28). Peroneal spasticity is noted on attempted inversion. An oblique radiograph of the foot readily demonstrates a calcaneonavicular coalition; however, CT scanning is often required to confirm the presence of a talocalcaneal coalition. Orthotics may control mild symptoms, and short-term cast immobilization can be helpful in treating patients with more severe pain. With persistent symptoms, excision of the coalition, along with interposition of fat or muscle tissue to minimize the risk of reossification, is indicated for a calcaneonavicular coalition and a talocalcaneal coalition that involves less than 50% of the facet. Arthrodesis is required for larger talocalcaneal coalitions or recurrent symptoms after excision.

Calcaneal Apophysitis Calcaneal apophysitis, also called Sever disease, is most commonly seen in prepubertal active children. Affected children note activity-related posterior heel pain. The condition results from repetitive stress and microfracture of the calcaneal apophysis. This weak link is obliterated when the apophysis fuses to the main body of the calcaneus.

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The Foot and Ankle Figure 19-28: Tarsal Coalition

Rigid, painful flatfoot (pes planus) with hind part of foot in valgus position, characteristic of tarsal coalition Solid, bony calcaneonavicular coalition evident on oblique radiograph

Navicular Calcaneonavicular bar Head

Postoperative radiograph

Talus Body Calcaneus

Calcaneonavicular coalition

Extensor digitorum brevis muscle interposed after resection to minimize risk of recurrence

Medial facet talocalcaneal coalition. CT scan of foot in a 7-year-old male with several month history of activity-related, medial hindfoot pain. Examination demonstrated restricted inversion and eversion, peroneal spasticity on “quick” inversion, and a rigid pes planovalgus foot deformity. Radiographs, as is often the case with this site of coalition, did not demonstrate the bony abnormality. CT scan shows a narrowing of the medial talocalcaneal facet joint consistent with fibrocartilaginous coalition.

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Chapter 19 Positive examination findings are limited to tenderness at the posterior aspect of the heel. Furthermore, routine radiographs are not diagnostic because sclerosis of the calcaneal apophysis is normal. Nonoperative treatment modalities include activity modification, heel cushion inserts, and, for resistant cases, shortterm cast immobilization. Operative treatment is not necessary.

Accessory Navicular An accessory navicular is a secondary ossification center at the primary attachment site of the posterior tibialis tendon into the navicular that does not unite (Figure 19-29). It is often associated with flatfoot deformity. Patients may be asymptomatic or have varying degrees of discomfort and swelling that are activity related or caused by pressure from shoes on the bony prominence. The activity-related symptoms are probably caused by an inefficient

transfer of stress at the bone-tendon interface. Examination reveals prominence and focal tenderness over the medial aspect of the navicular. Pes planus may be present. An oblique radiograph of the foot confirms the diagnosis. Treatment is directed toward relief of symptoms. Shoe modifications may alleviate pressure from the bony prominence, and casting for 4 to 6 weeks may relieve symptoms of repetitive microfracture at a synchondrosis. Resection of the accessory navicular, with reattachment of the posterior tibial tendon, is the treatment of choice for persistent symptoms. Alternatively, in some patients, fusion of the accessory bone to the navicular may be a better option.

Köhler Disease Köhler disease is osteonecrosis of the navicular. This uncommon condition is usually seen in children between the ages of 2 and 9

Figure 19-29: Accessory Navicular

Radiograph reveals excessively large navicular with separate ossification center on medial aspect

Tender, inflamed bony prominence on medial aspect of foot over navicular

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The Foot and Ankle Figure 19-30: Köhler Disease

Radiographs reveal characteristic changes in navicular of involved right foot.

Anteroposterior radiograph shows sclerotic, wafer-shaped navicular in right foot.

years. An insidious onset of a limp and tenderness in the area of the navicular are the most common symptoms. Bilateral changes occur in 20% of cases. Radiographs demonstrate a thin, wafer-shaped navicular with patchy areas of sclerosis and rarefaction and loss of the normal trabecular pattern (Figure 19-30). Short-term casting followed by orthotic support enhances the healing process. Even without treatment, the osteonecrosis will resolve without sequelae.

Freiberg Infraction Freiberg infraction is osteonecrosis of the metatarsal head. This disorder is most likely a result of axial loading trauma; therefore, the second metatarsal is almost always involved. Symptoms usually appear during the adolescent years with the insidious onset of forefoot pain that is activity related. The discomfort is aggravated by the wearing of high-heeled shoes. MTP motion may be limited, and pain is noted at extremes of MTP flexion and

extension. Mild dorsal swelling may be observed at the MTP joint. Early in the disease process, radiographs may be normal. Subsequent findings include flattening of the metatarsal head, fragmentation, and progressive degeneration of the joint. Treatment in the early phase of the disease process is designed to limit weight-bearing stress and includes activity modification, metatarsal pads, and a stiff-soled shoe. For patients with persistent symptoms, operative intervention to remove loose bodies and realign the metatarsal head may be necessary. With late arthritis, resection of the base of the proximal phalanx has produced good results.

ADDITIONAL READINGS Coughlin MJ, Mann RA, eds. Surgery of the Foot and Ankle, 7th edition. Philadelphia, PA: Mosby; 1999. Myerson MS. Reconstructive Foot and Ankle Surgery. Philadelphia, Pa: W.B. Saunders; 2005. Thordarson DB, ed. Foot and Ankle. Philadelphia, Pa: Lippincott Williams and Wilkins; 2004.

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Glossary of Common Orthopaedic Terms Contracture: Fixed shortening of a muscle, ligament, and/or joint capsule that results from injury, disease, or prolonged immobilization (pathologic). Cox-, Coxa: Hip. Cubitus: Elbow. Cubitus varus is adduction deformity of the elbow. Cubitus valgus is the opposite deformity. Delayed union: A delay in normal fracture healing. A delayed union may progress to an established pseudarthrosis, or continued repair may produce a solid bony union. Diaphysis: The shaft of a long bone. Dislocation: Complete disruption in the normal relationship of two bones that form a joint (ie, no contact of the articular surfaces). The direction of the dislocation is described by the position of the distal bone. For example, with an anterior dislocation of the shoulder, the humerus is displaced anterior to the scapula. Epiphysis: The end of a long bone in a child that develops from one or more secondary ossification centers. Equinus: Plantarflexed position of the ankle. Fracture: A traumatic break in the integrity of a bone. Fracture-dislocation: Fracture of the bone associated with dislocation of its adjacent joint. Genu: Knee. Greenstick: An incomplete fracture that disrupts only one side of the bone. This type of fracture is seen more often in children because of the greater plasticity of their bones. The disrupted cortex is on the tension side of the injury. Hallux: Great toe. Impacted: A fracture in which one fragment is driven into the other, conferring a degree of stability.

Abduction: Movement of a body part away from the midline. Adduction: Movement of a body part toward the midline. Ankylosis: Marked stiffness of a joint secondary to bridging bone, cartilage, or connective tissue. Typically observed in a joint affected by endstage arthritis. Antalgic: Avoiding pain. “Antalgic gait” is a commonly used term that describes walking affected by lower extremity injury or arthritic condition. The affected side has a shortened stance phase. Anteversion: Abnormal internal torsion of a bone (usually the femur). Arthrodesis: Operative procedure to fuse a joint. The essence of the procedure is excision of remaining articular cartilage followed by positioning and fixing the bones so that bone growth is promoted across the joint. A successful arthrodesis eliminates motion, provides pain relief, and stabilizes the joint. Arthroplasty: Operative procedure to mobilize a joint. Total joint arthroplasty is typically performed by removing the arthritic surfaces on both sides of the joint and replacing them with implants. Cavus: Excessive height of the longitudinal arch of the foot. Closed fracture: A fracture that does not disrupt the skin. Closed reduction: Manipulation of a fracture or dislocation to restore acceptable alignment. No incision is made. Comminuted: Fracture that has more than two fragments. Condyle: A rounded process at the end of a long bone. Contraction: Shortening of a muscle to provide joint motion (physiologic).

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Glossary of Common Orthopaedic Terms Joint capsule: Fibrous tissue that encloses a joint. Kyphosis: Posterior curvature of the spine. Ligament: Specialized collagenous tissue that spans two bones. Ligaments function to stabilize joints. Lordosis: Anterior curvature of the spine. Malunion: Healing of a fracture in an unacceptable position. Meniscus: A fibrocartilaginous structure interposed between articular cartilage to serve as a protective buffer. In the knee, the medial and lateral menisci are semicircular, wedge-shaped structures on the periphery of the joint that diminish walking and running stresses across the articular surface of the knee. Metaphysis: The broad portion of a long bone. In adults, the metaphysis is adjacent to a joint. In children, the broad portion of the bone includes the epiphysis, the physis, and the metaphysis. Myelopathy: A diseased state of the spinal cord caused by compression or a disease process. Neuropathy: An abnormal condition involving a peripheral nerve. Nonunion: Failure of a fracture or an osteotomy to unite. Open fracture: A fracture that disrupts the skin. Open reduction: An open surgical procedure in which normal relationships are restored to a fractured bone or dislocated joint. Osteomyelitis: Infection of bone. Osteotomy: Operative procedure in which a bone is cut and realigned. Pes: Foot. Pes planus: Flattening of the longitudinal arch of the foot. Pes planovalgus is a flat foot with associated heel valgus. Physis: The growth plate. Specialized cartilaginous tissue between the metaphysis and the epiphysis in long

bones of children. Provides growth in length of the bone. Plantar: Pertaining to the sole of the foot. Pseudarthrosis: A false joint produced when a fracture or arthrodesis fails to heal. Retroversion: Abnormal external torsion in a bone (usually the femur or humerus). Scoliosis: Lateral curvature of the spine. Spondylolisthesis: A slippage or subluxation of one vertebral body in relationship to the one below. The slippage may be anterior, posterior, or lateral. Spondylolysis: Unilateral or bilateral defect in the pars interarticularis. If bilateral, spondylolisthesis may develop. Sprain: Partial or complete tear of a ligament. Strain: Partial tear of a muscle, usually at the musculotendinous junction. Subluxation: An incomplete disruption in the relationship of two bones that form a joint. Synovium: The thin membrane of tissue that lines a joint capsule. It attaches to bone at the juncture of articular cartilage and bone. Tendon: A cord of specialized collagenous tissue that connects muscle to bone. Tenosynovium: Sheath around a tendon. Tenotomy: Operative division of a tendon. Torus: A fracture, seen most commonly in children, that buckles only one side of the cortex. Tuberosity: A bony elevation or protuberance that is commonly the site of muscle or tendon attachment. The greater tuberosity of the femur is the insertion site for gluteus medius and minimus tendons. Valgus: Angulation of a distal bone away from the midline in relation to its proximal partner. Genu valgum is a knock-knee deformity. Varus: Angulation of a distal bone toward the midline in relation to its proximal partner. Genu varum is a bowleg deformity.

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Frank H. Netter, MD Frank H. Netter was born in 1906, in New York City. He studied art at the Art Student's League and the National Academy of Design before entering medical school at New York University, where he received his MD degree in 1931. During his student years, Dr. Netter's notebook sketches attracted the attention of the medical faculty and other physicians, allowing him to augment his income by illustrating articles and textbooks. He continued illustrating as a sideline after establishing a surgical practice in 1933, but he ultimately opted to give up his practice in favor of a full-time commitment to art. After service in the United States Army during World War II, Dr. Netter began his long collaboration with the CIBA Pharmaceutical Company (now Novartis Pharmaceuticals). This 45-year partnership resulted in the production of the extraordinary collection of medical art so familiar to physicians and other medical professionals worldwide. Icon Learning Systems acquired the Netter Collection in July 2000 and continued to update Dr. Netter's original paintings and to add newly commissioned paintings by artists trained in the style of Dr. Netter. In 2005, Elsevier, Inc. purchased the Netter Collection and all publications from Icon Learning Systems. There are now over 50 publications featuring the art of Dr. Netter available through Elsevier, Inc. Dr. Netter's works are among the finest examples of the use of illustration in the teaching of medical concepts. The 13-book Netter Collection of Medical Illustrations, which includes the greater part of the more than 20,000 paintings created by Dr. Netter, became and remains one of the most famous medical works ever published. The Netter Atlas of Human Anatomy, first published in 1989, presents the anatomical paintings from the Netter Collection. Now translated into 16 languages, it is the anatomy atlas of choice among medical and health professions students the world over. The Netter illustrations are appreciated not only for their aesthetic qualities but, more importantly, for their intellectual content. As Dr. Netter wrote in 1949, ". . . clarification of a subject is the aim and goal of illustration. No matter how beautifully painted, how delicately and subtly rendered a subject may be, it is of little value as a medical illustration if it does not serve to make clear some medical point." Dr. Netter's planning, conception, point of view, and approach are what inform his paintings and what make them so intellectually valuable. Frank H. Netter, MD, physician and artist, died in 1991.

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Index Alkaptonuria, 95–97, 98f Alveolar rhabdomyosarcoma, 188–189 Ambulation. See also Gait. biomechanics of, 370–371 observation of, 371, 434 Ambulatory aids, 247–249, 248f, 249t Amnion, 6t Amputation, 227–249 bony overgrowth after, 229–231, 231f complications of, 233–238, 238f congenital, 228–231, 228f–230f disarticulation, in children, 229, 229f for bone tumors, 169–170 forearm, in children, 229, 229f in children, 228–231, 228f–231f in diabetes mellitus, 231–232 in peripheral vascular disease, 231–232 lower extremity, 233, 234f–238f prostheses for, 230f, 231 Syme, 233, 235f traumatic, 231 upper extremity, 230f, 232–233 Anal reflex, assessment of, 259f Anatomic snuffbox, 337, 338f Angiolipoma, 185 Ankle anatomy of, 428–434, 428f–432f disorders of degenerative, 437–440 in children, 455, 460–461 dorsiflexion of, 429–430, 434, 436f eversion of, 434, 437f examination of, 434–436 fractures of, 446–447, 447f in children, 450–452, 454f injuries of, 446–452 inversion of, 434, 437f mechanical axis of, 296f motion of, 429–430, 434, 437f muscles of anatomy of, 430, 430f, 435f grading of, 436 osteoarthritis of, 437, 439f plantarflexion of, 429–430, 434, 436f range of motion of, 436, 436f sprains of, 453 tendinitis of, posterior tibial tendon dysfunction and, 439, 440f

Abdominal reflexes, assessment of, 261 Abductor digiti quinti, 337, 339f Abductor lurch, 371 Abductor pollicis brevis, 337, 339f Abscess, subperiosteal, 145, 147f, 151 Abuse, child, 220–223, 222f Accessory navicular, 460, 460f Acetabulum anatomy of, 364, 364f fractures of, 380, 381f, 382f Achilles tendon inflammation of, 111, 111f rupture of, 109, 452–453, 454f Achondroplasia, 52–54, 53f Acquired immunodeficiency syndrome, myopathy in, 112 Acromioclavicular joint. See also Shoulder. anatomy of, 284, 285f–287f dislocation of, 302–303, 303f osteoarthritis of, 293 Acromion, 284, 285f Acromioplasty, 291, 291f Actin filaments, 100, 103f Active exercises, in rehabilitation, 240 Active-assisted exercises, 240, 242f Acute respiratory distress syndrome, in multitrauma patients, 194, 195f Adamantinoma, 184–185 Adductor brevis, 366, 367f, 368f Adductor longus, 366, 367f, 368f Adductor magnus, 366, 368f, 369f Adductor pollicis, examination of, 343, 343f Adhesive capsulitis, of shoulder, 293, 294f Adolescent(s). See also Children. strength training for, 107 Adolescent idiopathic scoliosis, 270, 279, 279t. See also Scoliosis. Adult respiratory distress syndrome, in multitrauma patients, 194, 195f Aerobic training, 107 AIDS, myopathy in, 112 Albright’s hereditary osteodystrophy, 30, 31f Alendronate for osteoporosis, 37–38 for Paget’s disease, 40 Note: Page numbers followed by f indicate figures; t indicates tables.

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Index Arthrogryposis multiplex congenita, 129, 130f Arthroplasty, resection ulnohumeral, 314–315 Aspiration. See also Biopsy. joint, in septic arthritis, 157, 158, 158f, 159f of bone tumors, 167, 168f Athletes elbow pain/instability in, 320–322 in children, 333–334 muscle injuries in, 108–109 tendon injuries in, 108–111 ulnar collateral ligament injury in, 358, 359f Atlanto-axial subluxation, 276–277, 276f Atlas, 252f, 253, 255f fractures of, 271, 272f Atrophy, muscle after nerve injury, 138 age-related, 107–108 from immobilization, 106 Avascular necrosis of bone, 40–44, 42f, 43f Avulsion fractures, 109 metaphyseal, in child abuse, 221, 222f of patella, 414 Avulsion injuries of finger, 357f, 358 of nail, 359 Axial skeleton, embryology of, 3–4, 6t, 7f Axillary artery, 284, 287f Axis, 252f, 253, 255f Axonotmesis, 137, 138f

Ankle disarticulation, 233, 235f. See also Amputation. Ankle-brachial index, 232 Ankle-foot orthosis, 247, 247f Ankylosing spondylitis, 87, 88f treatment of, 90–91 Annulus fibrosus, 256, 258f. See also Intervertebral discs. Anterior cruciate ligament anatomy of, 398, 399f healing of, 110–111 injuries of, 419–420, 419f Anterior drawer test for ankle sprains, 453 for anterior cruciate ligament tears, 420 Anterior humeral circumflex artery, 284, 287f Anterior interosseous nerve, 309, 311f Anterior interosseous syndrome, 319f Anterior tibial artery, 434, 435f Anteroposterior patterning, 9 Anteversion, femoral, 46, 47f patellofemoral malalignment and, 50, 50f Antibiotics, for osteomyelitis, 150–151, 152 Apical ectodermal ridge, 8 Apophysitis, calcaneal, 458–460 Appendicular skeleton, embryology of, 8–9, 10f–12f Apprehension test, 403 Arachnodactyly, congenital contractural, 65 ARDS (adult respiratory distress syndrome), in multitrauma patients, 194, 195f Arteries. See specific arteries. Arthodesis, elbow, 315 Arthritis cartilage in, 71–73 crystal, 91–97 degenerative, 73–79. See also Osteoarthritis. hemophilic, 95, 95f in inflammatory bowel disease, 90–91 psoriatic, 87–89, 89f treatment of, 90–91 reactive, 90–91 rheumatoid, 79–86. See also Rheumatoid arthritis. septic, 154–158. See also Septic arthritis. synovial fluid in, 73 Arthritis mutilans, 89 Arthrodesis for osteoarthritis, 79 of knee, 404 triple, 437, 439f

Back pain cervical, 261–263 in disc herniation, 254f, 261, 266 in isthmic spondylolisthesis, 280 in scoliosis, 270 low, 263–264, 264t Bacteremia, osteomyelitis and, 144 Baker’s cyst, 412 Bamboo spine, in ankylosing spondylitis, 87, 88f Bankart lesion, 301 Barlow test, 387, 388f Barton fracture, 353, 353f Baths, therapeutic, 245–246 Beevor sign, 259f Bend test, in ulnar nerve entrapment, 135 Bennett fracture, 355, 355f Biceps tendon distal, rupture of, 322–323 proximal, rupture of, 304, 304f Biopsy of bone tumors, 167, 168f of soft tissue tumors, 187

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Index Bone scan, in osteomyelitis, 148–149, 149f Bone tumors, 164–185 amputation for, 227–238. See also Amputation. benign, 170–179 aneurysmal bone cyst, 177–179 chondroblastoma, 174–175 enchondroma, 174 fibrous dysplasia, 176 giant cell tumor of bone, 177, 178f Langerhans cell histocytosis, 176–177 nonossifying fibroma, 175–176, 175f osteoblastoma, 173 osteochondroma, 173–174, 173f osteoid osteoma, 170–172, 170f, 171f solitary bone cyst, 177, 179f biopsy of, 167, 168f clinical features of, 166 diagnosis of, 166–167 grading of, 167 location of, 166 malignant, 179–185 adamantinoma, 184–185 chondrosarcoma, 181, 182f Ewing sarcoma, 181–184, 184f–185f fibrosarcoma, 181, 183f malignant fibrous histiocytoma, 181, 183f osteosarcoma, 179–181, 180f metastatic, 190–191, 190f pathogenesis of, 165–166, 166f radiographic features of, 165–166, 166f staging of, 167, 167t treatment of, 167–170 amputation vs. limb salvage in, 169–170 surgical margins in, 169, 169f Botryoid rhabdomyosarcoma, 188 Boutonnière deformity, 337, 341f, 358 Bowlegs, 50–51, 51f, 51t Boxer fracture, 355, 355f Braces for scoliosis, 279 limb, 247, 247f Brachalgia, 261 Brachial artery, 309 Brachial plexus, 284, 287f anatomy of, 295, 296f injuries of, 295–297 neonatal paralysis of, 304–305 Brain, traumatic injury of, 124–126 Brown tumors, in hyperparathyroidism, 29, 31f

Bipartite patella, 410, 412f Bisphosphonates for osteogenesis imperfecta, 54 for osteoporosis, 37–38 for Paget’s disease, 40 Bite wounds, of hand, 350 Blastocyst, 2, 3f Bleeding in quadriceps, 386 joint, in hemophilia, 94–95, 95f Blood culture in osteomyelitis, 148 in septic arthritis, 157–158 Blue sclerae, in osteogenesis imperfecta, 54, 55f Böhler angle, 449f Bone avascular necrosis of, 40–44, 42f, 43f blood supply of, 16–18, 19f brown tumors of, in hyperparathyroidism, 29, 31f cancellous (trabecular), 16, 17f, 195 cortical (compact), 16, 17f, 195 definition of, 10 formation of, 10–16, 13f–15f. See also Ossification. appositional intramembranous, 18–20 growth and remodeling of, 16–21, 19f, 20f healing of, 21, 195–198 homeostasis of, 24, 25f–27f hypertrophic zone of, 16, 18, 19f, 20f infections of, 144–153. See also Osteomyelitis. lamellar, 16, 18f marble, in osteopetrosis, 18 mechanical properties of, 195 metastases to, 190–191, 190f proliferating zone of, 16, 18, 19f, 20f regenerative capacity of, 21 remodeling of in children, 216, 218, 218f in fracture healing, 21, 196, 197f reserve zone of, 16, 18, 19f, 20f structure of, 14f, 16, 17f–20f trabecular, 16, 17f woven, 16, 21 Bone cement, for vertebral body augmentation, 38 Bone cysts aneurysmal, 177–179 solitary, 177, 179f

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Index Carpal tunnel syndrome, 122f, 132–135, 134f–136f, 337, 350 Carpometacarpal joint. See also Finger(s); Hand; Thumb. osteoarthritis of, 344, 345f Cartilage anatomy and physiology of, 70–71, 70f, 72f, 73f articular, 70, 72f, 73f calcification of, 18 formation of, 9, 10f hyaline, 70–71 in arthritis, 71–73, 156, 156f Cartilage oligomeric matrix protein disorders, 57–59 Cartilage-hair hypoplasia, 63, 64f Cascading spine, 268 Casts, 200, 202f, 204. See also Immobilization. compartment syndrome and, 207–209, 210f Cat bites, of hand, 350 Cauda equina, 253 Cauda equina syndrome, 266–267 Causalgia, 213–214, 214f contrast baths for, 246 Cavernous hemangiomas, 187 Cavovarus foot, 442–445, 444f Cell division, in embryonic period, 2–3, 3f–5f, 6t Cellulitis, vs. osteomyelitis, 149–150 Cement, for vertebral body augmentation, 38 Cerebral palsy, 121–124, 125f, 125t Cerebrovascular accident, 124–126 Cervical myelopathy, 263 Cervical radiculopathy, 261–263, 262f Cervical spine. See also Neck; Spine; Vertebrae. anatomy of, 252f, 253–256, 254f, 255f compression-flexion injuries of, 273 degenerative disease of, 261–263, 263f disc herniation in, 261–263, 262f distraction-flexion injuries of, 272–273 fractures of, 271–273, 271f, 272f instability of, 271–273, 271f motion of, 253–256 evaluation of, 262, 262f restriction of, 262, 262f sprains of, 274–275 whiplash injuries of, 275 Cervical spondylosis, with myelopathy, 263, 263f Chance fractures, 274 Charcot arthropathy, 138–140, 139f

Bunion, 440–442, 441f hammertoe and, 442, 443f Bursitis olecranon, 323 pes anserinus, 410 prepatellar, 408–410 subacromial, 290 trochanteric, 377 Buttress plates, 201, 203f Café au lait spots in fibrous dysplasia, 176 in neurofibromatosis, 133f, 176 Calcaneal apophysitis, 458–460 Calcaneovalgus deformity, 455 Calcaneus, fractures of, 447–448, 449f stress, 209–213 Calcification, of cartilage matrix, 18 Calcitonin for osteoporosis, 38 for Paget’s disease, 40 in calcium regulation, 24, 25f, 26f in phosphate regulation, 24, 25f, 26f Calcium in bone homeostasis, 24, 27f metabolism of normal, 24, 25f parathyroid hormone in, 24, 26f regulation of, 24, 26f vitamin D in, 33 supplemental, for osteoporosis, 37 Calcium pyrophosphate dihydrate crystal deposition disease, 93–94, 94f Callus, in fracture healing, 21, 196, 197f Camptodactyly, 360, 360f Cancellous bone, 16, 17f, 195 Cancer bone, 179–185. See also Bone tumors, malignant. bone metastases in, 190–191, 190f hypercalcemia in, 30 Canes, 247, 248f Capillary hemangiomas, 187 Capitellum, osteochondritis dissecans of, 334, 334f Carcinoma. See Cancer. Cardiogenic mesoderm, 6t Carpal(s). See also Wrist. anatomy of, 336, 336f fractures of, 353–355, 354f in children, 357

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Index Cleidocranial dysostosis, 305–306 Clinodactyly, 361 Clubfoot, 453–455, 455f Cobb angle, in spinal curvature, 278f, 279 Coccygeal plexus, 370, 371f Coccyx, 252f, 364, 365f. See also Pelvis; Spine; Vertebrae. Codman triangle, 166, 181, 184 Colchicine, for gout, 93 Cold therapy, 245, 246 Coleman block test, 442 Collagen in intervertebral discs, 258 type I, 104–106 disorders of, 54–55, 55t type II, disorders of, 55–57 Collateral ligaments. See Lateral collateral ligament; Medial collateral ligament. Colles fracture, 352, 353f Common peroneal nerve, 370, 371f, 433f, 434 anatomy of, 399, 400f Compact bone, 16, 17f, 195 Compartment syndrome, 207–209, 209f–211f in supracondylar humeral fractures, 330 of leg, 412–414 Complex regional pain syndrome, 213–214, 214f contrast baths for, 246 Compression fractures, vertebral in osteoporosis, 34, 36f treatment of, 38, 39f Compression plates, 201, 203f Compression syndromes. See also Nerve entrapment syndromes. in fractures, 207–209, 209f, 210f peripheral nerve, 122f, 132–137, 134f–136f in diabetes mellitus, 140–141, 140f spinal nerve, 266–267 Congenital amputations, 228–231, 228f–230f Congenital contractural arachnodactyly, 65 Congenital muscular torticollis, 275, 275f Congenital myopathies, 118, 118f Congenital pseudarthrosis, of clavicle, 306 Congenital radioulnar synostosis, 332–333 Congenital scoliosis, 4, 277, 277f, 279t Contracture(s) after amputation, 234, 238f Dupuytren, 348–349, 348f external rotation, of hip, 49, 49f of fingers, 337, 341f of palmar fascia, 348–349, 348f Volkmann, 330

Charcot-Marie Tooth disease, 129–131, 131f, 131t claw toe in, 442, 443f Chauffeur fracture, 353 Children abuse of, 220–223, 222f amputations in, 228–231, 228f–231f ankle disorders in, 455, 460–461 bone tumors in. See Bone tumors. discitis in, 158–159 dislocations in, of elbow, 331–332, 331f foot disorders in, 453–461 fractures in, 216–225. See also Fracture(s). of ankle, 450–452, 454f of clavicle, 298–299 of distal humerus, 330 of distal radius, 356–357, 357f of femur, 385 of foot, 450–452 of proximal humerus, 299, 299f of tibia, 415–416, 417f of ulna, 327 of vertebrae, 274 of wrist, 357 hand abnormalities in, 359–361, 360f hemangiomas in, 187 Langerhans cell histocytosis in, 176–177 myopathic disorders in, 112–118 osteochondrosis syndromes in, 223–225, 224f, 225t, 425 osteomyelitis in, 144–153. See also Osteomyelitis. spinal disorders in, 275–281 spinal injuries in, 274 sprains in, 223 strains in, 223 strength training for, 107 Chondroblastoma, 174–175 Chondroblasts, 3, 7f Chondrocalcinosis, 93–94, 94f Chondrocytes, 16, 18, 19f, 20f, 73 Chondrosarcoma, 181, 182f in Paget’s disease, 40 Chophart joint, 428, 428f Claudication, in spinal stenosis, 268 Clavicle congenital pseudarthrosis of, 306 fractures of, 297–298, 298f in children, 298–299 Claw hand, 343–344, 344f Claw toe, 442, 443f

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Index Debridement in amputation, 233–234 in chronic osteomyelitis, 152, 155f in septic arthritis, 158 Deep palmar arch, 337–341 Deep peroneal nerve, 433f, 434 anatomy of, 399, 401f Degenerative joint disease. See Osteoarthritis. Deltoid, 284, 285f, 286f examination of, 290 Deltoid ligament, 428, 431f Dens, 253 Dental abnormalities, in osteogenesis imperfecta, 54, 55f, 56f Dermatomes, 6t, 7f, 8f in limb development, 9, 11f Dermatomyositis, 112, 113f Dermomyotome, 3, 7f Developmental hip dysplasia, 386–389, 388f–389f Developmental milestones, screening for, 48, 49t DEXA measurement, for osteoporosis, 34 Diabetes mellitus amputations in, 231–232 Charcot arthropathy in, 138–140, 139f foot problems in, 141, 152, 155f, 231–232, 442, 443f amputation for, 231–232 neuropathy in, 138–141, 139t, 140f, 141t, 231–232 osteomyelitis in, 152, 155f Diaphysis, 14f, 16 Diastematomyelia, 277 Diastrophic dysplasia, 59–60, 62f–64f Diathermy, 246–247 Die-punch fracture, 353, 353f Digits. See Finger(s); Toe(s). 1,25-Dihydroxyvitamin D. See also Vitamin D. in calcium regulation, 24, 25f, 26f Discoid meniscus, 408, 409f Diskectomy, 266, 267f Diskitis, 158–159 Dislocation. See also Fracture-dislocations; Subluxation. in Monteggia fractures, 327, 328f of elbow, 331–332, 331f of finger, 358–359, 359f of hip congenital, 386–389, 388f–389f traumatic, 380–382, 383f

Contrast baths, 246 Contusions muscle, 108 quadriceps, 386 Conus medullaris, 253 Coracoacromial ligament, 284, 285f Coracoclavicular ligament, 284, 285f Coracoid process, 284, 285f Core decompression, for osteonecrosis of femoral head, 44 Core needle biopsy. See also Biopsy. of bone tumors, 167, 168f Corner metaphyseal fractures, in child abuse, 221, 222f Cortical bone, 16, 17f, 195 Coxa valga, 366 Coxa vara, 366 in polyostotic fibrous dysplasia, 176 Crescent sign, in osteonecrosis, 42 Crohn disease, arthritis in, 90–91 Crossed straight leg raising test, 259f Cruciate ligaments. See Anterior cruciate ligament; Posterior cruciate ligament. Crutches, 248–249, 248f, 249t Cryotherapy, 245, 246 Crystalline arthropathy, 91–97 Cubital tunnel syndrome, 122f, 135–136, 135f, 136f, 317, 318f Cubitus varus, 330 Culture blood in osteomyelitis, 148 in septic arthritis, 157–158 synovial fluid, 74f in septic arthritis, 157–158, 158f Curly toe, 456, 456f Cysts Baker’s, 412 bone aneurysmal, 177–179 solitary, 177, 179f ganglion of hand, 349 of wrist, 349, 349f popliteal, 412 Dactylitis in psoriatic arthritis, 87 in sickle cell disease, 67, 161 De Quervain tenosynovitis, 346–348, 347f

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Index Little Leaguer, 333 nerve entrapment syndromes of, 135–136, 136f, 317–320 nursemaid’s, 332 osteochondrosis of, 333–334, 334f physical examination of, 309–314 pulled, 332 range of motion of, 511–514, 514f, 515f sprains of, 320, 322f tennis, 315–316, 316f total arthroplasty of, 315, 316f Elbow flexion test, 318f Elderly, strength training for, 107 Electrical stimulation, 247 Electromyography, 121, 122f Elevated arm stress test, 137 Embryology, 2–9. See also Bone, formation of. cell division in, 2–3, 3f–5f, 6t limb development in, 8–9, 10f–12f molecular biology of, 9 of appendicular skeleton, 8–9, 10f–12f of axial skeleton, 3–4, 6t, 7f of gut, 2 of joints, 8–9, 10f of muscle, 4–6, 7f–9f of nervous system, 2–3, 5f Embryonal rhabdomyosarcoma, 188 Enchondral ossification, 3, 7f, 14, 14f Enchondroma, 174 Endoderm, 2, 3f Endurance training, 107 Enneking staging system, for bone tumors, 167, 167f Entrapment of femoral nerve, 377–378 of interdigital plantar sensory nerve, 445 of median nerve at elbow, 317–320, 319f at wrist, 122f, 132–135, 134f–136f, 337, 350 of musculocutaneous nerve, 296 of peripheral nerves, 122f, 132–137, 134f–136f of radial nerve, 135f, 136, 136f, 320, 321f of suprascapular nerve, 295–296 of ulnar nerve, 122f, 135–136, 135f, 136f Epicondylitis lateral, 315–316, 317f medial, 316–317 Epimere, 4–6, 9f

of knee congenital, 421, 421f traumatic, 418, 418f of patella congenital, 421–422 traumatic, 411f, 416–418 of radial head, congenital, 332, 333f of vertebrae, 270–275 Distal interphalangeal joints of foot. See also Foot; Toe(s). flexion deformity of, 442, 443f of hand. See also Finger(s); Hand. anatomy of, 336–337, 336f dislocation of, 358–359 osteoarthritis of, 75, 77f, 344, 345f Dog bites, of hand, 350 Doppler ultrasonography, in peripheral vascular disease, 232 Dorsal intrinsic muscles, 337, 339f Dorsal root ganglion, 120, 120f Dorsalis pedis artery, 434, 435f Dorsoventral patterning, 9 Dowager’s hump, 34, 36f Drainage, in septic arthritis, 158, 159f Dual-energy x-ray absorptiometry (DEXA), for osteoporosis, 34 Duchenne muscular dystrophy, 112–116, 115f Dupuytren disease, 348–349, 348f Dura mater, spinal, 253 Dwarfism, 52–54, 53f diastrophic, 59–60, 62f–64f Ectoderm, 2, 3f derivatives of, 6t Elbow anatomy of, 308–309, 308f arthritis of, 314–315 arthrodesis of, 315 bursitis of, 323 chronic pain in, 320–321 degenerative disorders of, 314–317 dislocations of, 331–332, 331f fat pads of, traumatic elevation of, 323, 324f fractures about, 323–331, 325f–329f in children, 327, 329–331 golfer’s, 316–317 instability of, 320–322 posterolateral rotatory, 322 ligaments of anatomy of, 320, 322f injuries of, 320–322, 331–332, 331f

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Index Femoral epiphysis, slipped, 390–394, 392f Femoral nerve anatomy of, 370, 370f entrapment of, 137, 377–378 Femur anteversion of, 46, 47f patellofemoral malalignment and, 50, 50f congenital deformity of, 393f, 394 distal anatomy of, 396, 396f fractures of, 414 fractures of distal, 414, 415 head, 384 in children, 385–386, 415 intertrochanteric, 384f, 385, 385f neck, 384–385, 384f, 385f proximal, 382, 384f shaft, 385, 387f head of anatomy of, 365–366, 366f fractures of, 384 osteonecrosis of, 40–44, 42f, 43f, 376, 389–390, 391f slipped, 390–394, 392f neck of anatomy of, 365–366, 366f fractures of, 384–385, 384f, 385f osteonecrosis of, 40, 42f, 43f proximal. See also Hip. anatomy of, 365–366, 366f realignment osteotomy of, 376 retroversion of, 46, 47f torsion of, 46, 47f, 50, 50f Fibrin clot, in meniscal repair, 408 Fibroma, nonossifying, 175–176, 175f Fibrosarcoma, 181, 183f in Paget’s disease, 40 Fibrous dysplasia, 176 Fibrous histiocytoma, 185–187 Fibula anatomy of, 399 hemimelic, 393f, 394, 422 Filum terminale, 253, 254f Fine-needle aspiration. See also Biopsy. of bone tumors, 167, 168f Finger(s). See also Hand. anatomy of, 336–337, 336f avulsion injuries of, 357f, 358 boutonnière deformity of, 337, 341f, 358 congenital deformities of, 359–361, 360f

Epiphysis, 14f, 16–18, 19f Estrogen, for osteoporosis, 37 Ewing sarcoma, 181–184, 184f–185f Exercise programs for fitness, 106–107 in rehabilitation, 240–249. See also Rehabilitation. Exercises active, 240 active-assisted, 240, 242f in rehabilitation, 240–249. See also Rehabilitation. in strength training, 106–107, 242–243, 242f isokinetic, 243 isometric, 242, 244f isotonic, 242–243 passive, 240, 242f Exostosis, hereditary multiple, 65, 173 Extensor carpi radialis brevis, examination of, 343 Extensor digiti quinti, 337, 338f Extensor digitorum longus, 337, 338f, 399, 400f, 430, 430f, 435f Extensor hallucis longus, 399, 400f, 430, 430f, 435f Extensor indicis proprius, 337, 338f Extensor retinacular carpal ligament, 337, 338f External fixation, 199, 201, 203f. See also specific fractures. Eye, abnormalities of, in juvenile rheumatoid arthritis, 85–86, 86f FABER sign, 374 Facet joints, 253 Facies, in achondroplasia, 52, 53f Falling-leaf sign, 177 Familial precocious osteoarthritis, 57 Fanconi syndrome, rickets in, 33 Fascia palmar, contracture of, 348–349, 348f plantar, 429, 432f inflammation of, 437–438 Fasciotomy, for compartment syndrome, 209, 211f Fast-twitch fibers, 103–104, 105f Fat pads, elbow, traumatic elevation of, 323, 324f Fatigue fractures, 209–213, 212f of pars interarticularis, 280–281 Felon, 352, 352f Femoral artery, 370, 372f, 400

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Index diabetic, 141, 152, 155f, 231–232 amputation of, 231–232 claw toes in, 442, 443f disorders of congenital, 453–460 degenerative, 437–440 in children, 453–461 examination of, 434–436 flat in children, 457–458, 457f posterior tibial tendon dysfunction and, 438–439, 440f tarsal coalition and, 458, 459f fractures of, 447–452 in children, 450–452 injuries of, 446–452 innervation of, 399, 401f, 430–434, 432f, 433f lawnmower injuries of, 452 Morton neuroma of, 445 motion of, 430 osteoarthritis of, 437, 438f puncture wounds of, 161 sole of, 399, 401f, 430–434, 432f triple arthrodesis of, 437, 439f Forearm. See also Elbow; Radius; Ulna; Wrist. anatomy of, 308–309, 310f–313f fractures of, 323–330, 352–353, 353f in children, 329–331, 356–357, 357f Forward bending test, for scoliosis, 278f, 279 Fracture(s), 194–214 angulation in, 200, 201f avulsion, 109 metaphyseal, in child abuse, 221, 222f patellar, 414 Barton, 353, 353f Bennet, 355, 355f boxer, 355, 355f casting of, 200, 202f, 204. See also Immobilization. compartment syndrome and, 207–209, 210f casts in, 200, 202f, 204 Chance, 274 chauffeur, 353 Colles, 352, 353f compartment syndrome and, 207–209, 209f–211f diagnosis of, 199–200 die-punch, 353, 353f displacement in, 200, 201f

contractures of, 337, 341f degenerative disorders of, 344 dislocation of, 358–359, 359f felon of, 352, 352f fractures of, 356, 356f in children, 357 jersey, 357f, 358 lacerations of, 357–358 mallet, 357f, 358 nails of infections of, 352, 352f ingrown, 446, 446f injuries of, 359 osteoarthritis of, 75, 77f, 344, 345f range of motion of, 341–343, 342f septic tenosynovitis of, 350–352, 351f supernumerary, 360, 360f swan-neck deformity of, 337, 341f trigger, 345, 347f Finkelstein test, 346, 347f Fitness training, 106–107 Flatfoot in children, 457–458, 457f posterior tibial tendon dysfunction and, 438–439, 440f tarsal coalition and, 458, 459f Flexor carpi radialis, examination of, 343 Flexor digiti quinti, 337, 339f Flexor digitorum longus, 399, 400f, 430, 430f Flexor digitorum profundus anatomy of, 337, 340f, 357f examination of, 343 injuries of, 357–358 Flexor digitorum sublimis, 343 Flexor digitorum superficialis anatomy of, 337, 340f, 357f injuries of, 357–358 Flexor hallucis longus, 399, 400f, 430, 430f Flexor pollicis brevis, 337, 339f Flexor tenosynovitis, septic, 350–352, 351f Floating shoulder, 298 Fluidotherapy, 246 Foot amputation of, 233, 234f. See also Amputation. anatomy of, 428–434, 428f–432f biomechanics of, 428, 429 cavus, 442–445, 444f, 445t club, 453–455, 455f deformities of, 440–445 congenital, 453–460

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Index shaft, 385, 387f of finger, 356, 356f in children, 357 of foot, 447–452 in children, 450–452 of forearm, 323–329 in children, 329–331 of growth plate, 216, 217f, 218–220, 219f of hand, 355–356, 355f, 356f in children, 357 of humerus distal, 330 in children, 299, 299f, 330 lateral condylar/epicondylar, 330 medial condylar/epicondylar, 330 proximal, 297, 297f shaft, 298, 299f supracondylar, 329–330, 329f transphyseal separation, 330 of metacarpal, 355–356, 355f of metatarsal, 450, 453f of odontoid, 271–272, 272f of olecranon, 326–327, 327f in children, 331 of patella, 414, 416f of pelvis, 378–380, 378f–382f of radius diaphyseal, 329, 331 distal, 352–353, 353f of head, 324–326, 326f of neck, 330–331 of scaphoid, 353–355, 354f of scapula, 298 of talus, 448, 450f of thumb base, 355–356, 355f of tibia distal, 452, 454f in children, 415–416, 417f, 452, 454f plateau, 414 proximal, 414–416 shaft, 414–415 spine (eminence), 416, 417f tubercle, 415–416, 417f of toe, 450 of ulna diaphyseal, 329, 331 Monteggia, 327, 328f of vertebrae, 270–274 cervical, 271–273, 271f, 272f compression, 34, 36f, 38, 39f in children, 274

Fracture(s), (cont’d) Galeazzi, 329 greenstick, 216, 217f hangman, 272, 272f healing of, 21, 195–198, 197f, 198f failure of, 206–207, 208f, 212f in children, 216–225 from abuse, 220–222, 221f healing of, 216, 218, 218f of ankle, 450–452, 454f of clavicle, 298–299 of distal humerus, 330 of distal radius, 356–357, 357f of elbow, 327, 329–331 of femur, 385, 415 of foot, 450–452 of forearm, 327–331 of hand, 357 of proximal humerus, 299, 299f of tibia, 415–416, 417f of ulna, 327 of vertebrae, 274 of wrist, 357 patterns of, 216, 217f treatment of, 216–218 in multitrauma patients, 194, 195f Jefferson, 271, 272f mechanics of, 195, 199 metaphyseal, in child abuse, 221, 222f Monteggia, 327, 328f neurologic complications in, 207–209, 209f, 210f nightstick, 329 nonunion of, 206–207, 208f in stress fractures, 212f of acetabulum, 380, 381f, 382f of ankle, 446–447, 447f in children, 450–452, 454f of atlas, 271, 272f of calcaneus, 447–448, 449f of clavicle, 297–298, 298f in children, 298–299 of elbow, 323–331, 325f–329f in children, 329–331 of femur distal, 414, 415 head, 384 in children, 385–386, 415 intertrochanteric, 384f, 385, 385f neck, 384–385, 384f, 385f proximal, 382, 384f

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Index tension band wiring in, 203 traction in, 200, 203f vascular complications in, 207, 208f Fracture-dislocations Lisfranc, 448–450, 451f–452f Monteggia, 327, 328f vertebral, 270–275 Frieberg infarction, 461 Friedrich ataxia, 126–128 Froment sign, 343, 343f Frozen shoulder, 293, 294f

in osteoporosis, 34, 36f in Paget’s disease, 39–40 thoracolumbar, 273–274, 273f treatment of, 38, 39f of wrist Barton, 353, 353f Colles, 352, 353f in children, 357 of scaphoid, 353–355, 354f Smith, 352–353 open, 205–206 osteonecrosis after, 40, 42f pathologic, 213 bone metastases and, 190f, 191 in osteogenesis imperfecta, 54 in osteomyelitis, 151 in osteoporosis, 34, 36f, 38 in Paget disease, 39–40, 41f in solitary bone cyst, 179f patterns of, 195, 196f, 200 physeal, 216, 217f, 218–220, 219f physical examination of, 199–200 primary union of, 196, 198f reduction of closed, 200, 202f open, 200–203, 203f, 204–205 reflex sympathetic dystrophy and, 213–214, 214f rehabilitation for, 204 Rolando, 355, 355f Segond, 420 Smith, 352–353 spiral, 222f, 223 stress, 209–213, 212f of pars interarticularis, 280–281 teardrop, 273 Tillaux, 452, 454f toddler’s, 416 torus, 216, 217f treatment of, 198–205 casts in, 207–209, 210f compartment syndrome and, 207–209, 210f evaluation in, 199–200 external fixation in, 199, 201, 203f for nonunion, 206–207, 208f historical perspective on, 198–199 internal fixation in, 199, 201–203, 203f, 204f principles of, 200–203 surgery in, 204–205

Gait assessment of, in spinal disorders, 259f, 263 biomechanics of, 370–371 crutch/walker, 249, 249t in hip osteoarthritis, 375f knee motion in, 400–402 myelopathic, 263 observation of, 371, 434, 436f phases of, 434, 436f Galeazzi fracture, 329 Galeazzi sign, 388 Gamekeeper’s thumb, 358, 359f Ganglion dorsal root, 120, 120f of hand and wrist, 349, 349f Gastrocnemius, 399, 400f, 430, 430f Gastrulation, 2, 4f, 5f Gaucher disease, 67–68, 68f Genetics, developmental, 9 Genu valgum, 51–52, 51f, 52t Genu varum, 50–51, 51f, 51t with tibia vara, 424–425, 424f Giant cell tumor of bone, 177, 178f Glenohumeral joint. See also Shoulder. anatomy of, 284, 285f–287f dislocation of, 300f, 301–302, 302f Glenohumeral osteoarthritis, 291–293 Glenoid labrum, 284, 287f tears of, 195 Gluteal arteries, 370, 372f Gluteal nerve, 370, 371f Gluteus maximus, 366, 367f, 368f Gluteus medius, 366, 367f–369f Gluteus minimus, 366, 367f–369f Golfer’s elbow, 316–317 Goniometer, 242, 243f Gout, 91–93, 92f Gower sign, 114, 115f Gracilis, 366, 367f–369f

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Index Heberden nodes, 77f, 344 Hemangioma, 187 Hemarthrosis, in hemophilia, 94–95, 95f Hematogenous osteomyelitis. See Osteomyelitis. Hematopoietic disease, skeletal dysplasias in, 65–68 Hemimelia fibular, 393f, 394, 422 radial, 361, 361f tibial, 422–423 ulnar, 362 Hemophilic arthropathy, 94–95, 95f Hemorrhage, in quadriceps, 386 Hereditary arthro-ophthalmopathy, 57 Hereditary multiple exostosis, 65, 173 Hereditary sensory motor neuropathies, 129–131, 131f, 131t Hereditary spinocerebellar ataxia, 126–128 Herniated discs. See Intervertebral discs, herniated. Herpetic whitlow, 352 Hill-Sachs lesion, 301 Hip. See also Femur; Pelvis. anatomy of, 364–371, 366f–369f blood supply of, 370, 372f developmental dysplasia of, 386–389, 388f–389f dislocation of congenital, 386–389, 388f–389f traumatic, 380–382, 383f disorders of degenerative, 374–376 in children, 386–394 examination of, 371–374 external rotation contracture of, 49, 49f innervation of, 370, 370f–372f mechanical axis of, 296f muscles of, 366, 367f–369f examination of, 374 osteoarthritis of, 374–376, 375f osteonecrosis of, 376 in children, 389–390, 391f range of motion of, 371–374, 373f rotation of measurement of, 46, 47f out-toeing and, 49, 49f septic arthritis of, in neonate, 158 snapping, 377 thigh, 386 total arthroplasty of, 376 transient synovitis of, 394

Great toe. See also Foot. amputation of, 233. See also Amputation. lateral deviation of, 440–442, 441f hammertoe and, 442, 443f osteoarthritis of, 437, 438f Greenstick fractures, 216, 217f Growth arrest, after physeal fractures, 220, 221f Growth factors, 9, 12f Growth plate, 14f, 16–18 in osteomyelitis, 151 injuries of, 216, 218–220, 219f, 221f growth arrest after, 220 Gunstock deformity, 330 Gustilo-Anderson classification, of open fractures, 205–206, 205f Gut, embryology of, 2 Hallux, amputation of, 233. See also Amputation. Hallux rigidus, 437, 438f Hallux valgus, 440–442, 441f, 442, 443f Hammertoe, 442, 443f Hamstring, 366 Hand. See also Finger(s); Thumb; Wrist. anatomy of, 312f, 313f, 336–341, 336f–340f, 357f bite wounds of, 350 claw, 343–344, 344f congenital deformities of, 359–361, 360f degenerative disorders of, 344, 345f dislocations of, 358–359, 359f Dupuytren disease of, 348–349, 348f examination of, 341–344, 342f, 343f fractures of, 355–356, 355f, 356f in children, 357 ganglion of, 349 infections of, 350–352, 351f injuries of, 352–358 lacerations of, 357–358 of benediction, 343–344, 344f osteoarthritis of, 75, 77f, 344, 345f radial club, 361, 361f sprains of, 358–359 tendinitis of, 346, 347f tendon injuries of, 357–358, 357f trident, 52, 53f Hand-foot syndrome, in sickle cell disease, 67 Hangman fracture, 272, 272f Head trauma, 124–126 Heat therapy, 245–246

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Index Inferior gluteal nerve, 370, 371f Inflammation, in fracture healing, 195–196, 197f Inflammatory bowel disease, arthritis in, 90–91 Infraspinatus. See also Rotator cuff. anatomy of, 284, 285f, 286f nerve impingement and, 295–296 Ingrown toenail, 446, 446f Intermediate mesoderm, 2, 4f Internal fixation, 199, 201–203, 203f, 204f. See also specific fractures. for pathologic fractures, from bone metastases, 190f, 191 Interosseous muscles, 312f, 313f, 337 Interphalangeal joints of foot. See also Foot; Toe(s). anatomy of, 336–337, 336f embryology of, 8–9, 10f flexion deformities of, 442, 443f of hand. See also Finger(s); Hand. anatomy of, 336–337, 336f dislocation of, 358–359 osteoarthritis of, 75, 77f, 344, 345f Intervertebral discs. See also Spine; Vertebrae. age-related changes in, 258 cervical, disorders of, 261–263, 262f herniated cauda equina syndrome and, 266–267 examination in, 259f excision of, 266, 267f in cervical spine, 261–262 in lumbar spine, 265–267, 265f lumbar, disorders of, 254f, 263–267, 265f structure and function of, 254f, 256–257, 258f In-toeing, 46–50, 47f Intramedullary nails/rods, 201–203, 204f Intramembranous ossification, 3, 7f, 10, 13f Iridocyclitis, in juvenile rheumatoid arthritis, 85–86, 86f Ischium, anatomy of, 364, 364f Isokinetic exercises, 243 Isometric exercises, 242, 244f Isotonic exercises, 242–243 Isthmic spondylolisthesis, 268, 270t, 280–281, 280f

Hip-knee-angle mechanical axis, 296f Hoffmann sign, 261 Homogentisic acid oxidase deficiency, 95–97, 96f Hot packs, 245 Human immunodeficiency virus infection, myopathy in, 112 Humerus distal. See also Elbow. anatomy of, 322f fractures of, 323–324, 325f, 330 fractures of distal, 323–324, 325f, 330 in children, 299, 299f, 330 lateral condylar/epicondylar, 330 medial condylar/epicondylar, 330 proximal, 297 shaft, 298, 299f supracondylar, 329–330, 329f transphyseal separation, 330 osteonecrosis of, 40, 44 proximal. See also Shoulder. anatomy of, 284, 285f, 286f fractures of, 297, 297f Hydrotherapy, 245, 246 Hydroxyapatite crystals, formation of, 18 Hypercalcemia, in cancer, 30 Hyperparathyroidism, 24–30, 28f–30f Hyperuricemia, in gout, 91–93, 92f Hypochondroplasia, 54 Hypomere, 4–6, 9f Hypoparathyroidism, 30, 31f Hypophosphatasia, osteomalacia and, 30 Hypophosphatemic rickets/osteomalacia, 33, 63–64 Hypothenar muscles, 312f, 313f, 337 Iliopsoas, 366, 367f, 368f snapping of, 377 Ilium, anatomy of, 364, 364f Immobilization casts in, 200, 202f compartment syndrome and, 207–209, 210f for soft tissue injuries, 106, 111 local and systemic effects of, 106, 111, 240, 241f rehabilitation after, 240–249. See also Rehabilitation. traction in, 200, 202f Inferior gluteal artery, 370, 372f

Jansen metaphyseal dysplasia, 63 Jefferson fracture, 271, 272f Jersey finger, 357f, 358

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Index muscles of, 397f, 399, 400f osteoarthritis of, 75, 403–404 osteonecrosis of, 44 physical examination of, 402–403 plica injury of, 410–412, 413f prosthetic, 78f, 79 range of motion of, 403, 403f sprains of, 110f, 418–420, 419f tendon ruptures of, 420 valgus angulation in, 51–52, 51f, 52t varus angulation in, 50–51, 51f, 51t varus angulation of, with tibia vara, 424–425, 424f Knee disarticulation, 233, 237f. See also Amputation. Knock-knees, 50–51, 51f, 52f Köhler disease, 460–461, 461f Kozlowski metaphyseal dysplasia, 63 Kugelberg-Welander disease, 129 Kyphoplasty, for compression fractures, 38, 39f Kyphosis, 279–280. See also Spine, curvature of. in achondroplasia, 52, 53f in Scheuermann disease, 280, 280f postural, 280, 280f

Joint(s). See also specific joints and disorders. anatomy and physiology of, 70–73, 70f, 72f–74f bleeding in, in hemophilia, 94–95, 95f Charcot, 138–140, 139f contractures of after amputation, 234, 238f external rotation, of hip, 49, 49f of fingers, 337, 341f embryology of, 8–9, 10f immobilization of. See Immobilization. infection of, 154–158. See also Septic arthritis. range of motion of, measurement of, 240–242, 243f stiffness of, from immobilization, 106 Joint aspiration, in septic arthritis in diagnosis, 157, 158f in treatment, 158, 159f Juvenile rheumatoid arthritis, 85–86, 85f Kienböck disease, 44, 344–345, 346f Kinetic energy transfer, in fractures, 199 Klippel-Feil syndrome, 275–276, 276f Klumpke paralysis, 304 Knee anatomy of, 396–400, 396f–401f arthrodesis of, 79, 404 arthroplasty of total, 404, 406f unicompartmental, 404, 405f biomechanics of, 400–402 blood supply of, 399–400, 400f bursitis of, 408–410 cartilage of, 398, 398f congenital deformities of, 421–426 dislocation of, 418, 418f congenital, 421, 421f disorders of degenerative, 404–414 history in, 402 in children, 421–426 traumatic, 414–420 embryology of, 8–9, 10f injuries of, 414–420 innervation of, 399, 400f ligaments of, 398–399, 398f, 399f injuries of, 418–420, 419f malalignment of, 397 mechanical axis of, 296f motion of, 400–402

Lacerations of hand, tendon injuries in, 357–358 of muscle, 108, 109 of nail, 359 Lachman test, 420 Lamellar bone, 16, 18f Langerhans cell histiocytosis, 176–177 Lateral circumflex artery, 370, 372f Lateral collateral ligament of elbow anatomy of, 320, 322f injuries of, 320, 322f, 331f, 332 of knee anatomy of, 398, 399f injuries of, 418–419 Lateral epicondyle, of humerus fractures of, 330 inflammation of, 315–316, 317f Lateral epicondylitis, 315–316, 317f Lateral femoral cutaneous nerve entrapment, 137, 377–378 Lateral ligament, 428, 431f Lateral plantar nerve, 433f, 434 Lateral plates, 2, 4f, 6t Lateral retinacular release, for patellar instability, 411f

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Index disc herniation in, 265–267, 265f, 267f fractures of, 273–274, 273f sprains of, 274 stenosis of, 267–268, 269f Lumbar spondylolisthesis, 268 Lumbosacral plexus, 370, 371f Lumbosacral spine. See also Spine; Vertebrae. anatomy of, 252f, 253f, 256, 257f movement, 256 Lumbrical muscles, 337, 340f Lunate. See also Wrist. anatomy of, 336, 336f osteonecrosis of, 44, 344–345, 346f

Latissimus dorsi, 284, 287f Lauge-Hansen classification, of ankle fractures, 447f Lawnmower injuries, of foot, 452 Leg. See Lower extremity. Legg-Calvé-Perthes disease, 389–390, 391f Leukemia, vs. osteomyelitis, 150 Ligaments. See also specific ligaments and joints. age-related changes in, 108, 109 anatomy of, 104–106 healing of, 109–111 injuries of, 109–111, 110f. See also Sprains. in children, 223 Ligamentum mucosa, 412 Ligamentum teres, 365, 365f Limb. See also Lower extremity; Upper extremity. amputation of, 230f, 232–233, 234f–238f. See also Amputation. congenital absence of, 228–229 development of, 6, 8–9, 10f–12f phantom, 233–238 prosthesis for, 230f, 232–233 Limb salvage, for bone tumors, 169–170 Lipoma, 185, 186f Liposarcoma, 187, 188f Lisfranc joint, 428, 428f fracture-dislocations of, 448–450, 451f–452f Lister tubercle, 341 Little Leaguer elbow, 333 Log-roll test, for hip fractures, 384 Low back pain, 263–264, 264t. See also Back pain. Lower extremity. See also Limb and constituent parts. amputation of, 233, 234f–238f. See also Amputation. compartment syndrome of, 412–414 congenital absence of, 228–229 deformities of, 46–52 genu valgum, 51–52, 51f, 52t genu varum, 50–51, 51f, 51t in-toeing, 46–50, 47f out-toeing, 46–50 development of, 6, 8–9, 10f–12f muscles of, 366, 367f Lower motor neuron disease, 128–129 Lumbar plexus, 30, 370f Lumbar spine. See also Spine; Vertebrae. degenerative disease of, 263–265, 264f

Macrodactyly, 456 Malignant fibrous histiocytoma of bone, 181, 183f of soft tissue, 189, 189f Malignant peripheral nerve sheath tumors, in neurofibromatosis, 131–135 Mallet finger, 357f, 358 Mallet toe, 442, 443f Marble bones, in osteopetrosis, 18 Marfan syndrome, 64–65, 66f McCardle disease, 114f McCune-Albright syndrome, 176 McKusick metaphyseal chondrodysplasia, 63, 64f McMurray test, 408 Medial circumflex femoral artery, 366, 366f, 370, 372f Medial collateral ligament of elbow anatomy of, 320, 322f injuries of, 320, 322f, 331f, 332 of knee anatomy of, 398, 399f injuries of, 418–419 Medial epicondyle, of humerus fractures of, 330 inflammation of, 316–317 traction apophysitis of, 333 Medial epicondylitis, 316–317 Medial plantar nerve, 433f, 434 Median nerve anatomy of, 309, 311f, 341 entrapment of at elbow, 317–320, 319f at wrist, 122f, 132–135, 134f–136f, 337, 350 Meningocele, 126, 127f

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Index Multiple epiphyseal dysplasia, 59, 61f Multiple trauma fractures in, 194, 195f. See also Fracture(s). systemic response to, 194, 195f Muscle(s). See also specific muscles. age-related changes in, 107 anatomy and physiology of, 100–104, 101f–105f atrophy of after nerve injury, 138 age-related, 107–108 from immobilization, 106 contraction of, 100–101, 102f contusions of, 108, 386 disorders of, 111–118. See also Myopathic disorders. embryology of, 4–6, 7f–9f fiber types in, 100, 101f, 103–104, 105f injuries of, 108–109 innervation of, 6, 9f length-tension relationship in, 101, 104f metabolism in, 102–103 strains of, 108 in children, 223 thigh, 386 strength of, 102, 104f exercises for, 106–107, 242–243, 244f grading of, 243–244, 245f Muscular dystrophy Duchenne, 112–116, 115f fascioscapulohumeral, 116, 116f Musculocutaneous nerve entrapment, 296 Musculoskeletal tumors. See Bone tumors; Soft tissue tumors. Myelin sheath, 120–121, 120f Myelomeningocele, 126, 127f Myofibers, 100, 101f, 103–104, 105f Myopathic disorders, 111–118 congenital, 118, 118f Duchenne muscular dystrophy, 112–116, 115f fascioscapulohumeral muscular dystrophy, 116, 116f HIV-related, 112 in children, 112–118 inflammatory, 112 McCardle disease, 114f metabolic, 112 myotonic disorders, 116–118, 117f Myosin, 100, 103f Myosin filaments, 100, 103f

Meniscus anatomy of, 398, 398f discoid, 408, 409f tears of, 408, 409f Meralgia paresthetica, 137, 377–378 Mesenchymal condensations, 8–9, 10, 10f Mesenchymal ossification, 3, 7f, 10, 13f Mesoderm, 2, 4f cardiogenic, 6t derivatives of, 6t intermediate, 6t lateral plate, 6t Metabolic bone disease, 24–40 calcium metabolism and, 24, 25f in hyperparathyroidism, 24–30, 28f–30f in hypoparathyroidism, 30, 31f osteomalacia, 30–33, 31t, 32f osteoporosis, 33–38, 33f, 34f Paget disease, 38–40, 39f phosphate metabolism and, 24, 25f rickets, 30–33, 31t, 32f, 63–64 Metabolic myopathies, 112 Metacarpals anatomy of, 336f fractures of, 355–356, 355f Metacarpophalangeal joints anatomy of, 336–337, 336f dislocation of, 358–359 Metaphyseal chondrodysplasias, 60–64 Metaphyseal corner fractures, in child abuse, 221, 222f Metaphysis, 14f, 16, 19f, 20f, 21 Metastases, bone, 190–191, 190f Metatarsals fractures of, 450, 453f stress, 209–213, 212f osteonecrosis of, 461 Metatarsophalangeal sprains, 453 Metatarsus adductus, 455, 455f Milkman syndrome, 31 Miserable malalignment syndrome, 50, 50f Monteggia fracture-dislocation, 327, 328f Morton neuroma, 445 Morula, 2, 3f Motor development, delays in, screening for, 48, 49t Motor examination, 121, 122f. See also Neurologic examination. in spinal disorders, 259f, 260–261, 260t Mower injuries, of foot, 452 Mulder click, 445

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Index of wrist, 122f, 132–135, 134f–136f, 337, 350 Nervous system, embryology of, 2–3, 5f Neural crest, formation of, 3, 5f, 6t Neural plate, formation of, 2–3 Neural tube, formation of, 3, 5f, 6t Neural tube defects, 126, 127f Neurapraxia, 137, 138f Neurofibromatosis, 131–132, 132t, 133f café au lait spots in, 133f, 176 Neurologic disorders Charcot arthropathy in, 138–140, 139t compressive, 132–137. See also Nerve entrapment syndromes. hereditary, 129–132 in diabetes, 138–141, 139t, 140f, 141t lower motor neuron, 128–129 spinal cord, 126–128 traumatic, 137–138 upper motor neuron, 121–126 Neurologic examination, 121, 122f, 122t in spinal disorders, 259f, 260–261, 260t Neuromas, 138 Morton, 445 Neuropathic arthropathy, 138–140, 139f Neuropathy, diabetic, 138–141, 139t, 140f, 141t, 231–232 ankle-brachial index in, 232 Charcot arthropathy and, 138–140, 139f Neurotmesis, 137–138, 138f Neurulation, 2–3, 5f, 6t Newborn. See Neonate. Nightstick fracture, 329 Nonossifying fibroma, 175–176, 175f Notochord, 2, 4f, 6t Nucleus pulposus, 256, 258, 258f. See also Intervertebral discs. Nursemaid’s elbow, 332

Myositis ossificans, 185, 186f of thigh, 186f, 386 Myotomes, 4–6, 6t, 7f, 8f Myotonia congenita, 116–117, 117f Myotonic disorders, 116–118, 117f Myotonic dystrophies, 117–118, 117f Nail infections of, 352, 352f ingrown, 446, 446f injuries of, 359 intramedullary, 201–203, 204f psoriatic, 89, 89f Nail puncture wounds, of foot, 161 Navicular, of foot accessory, 460, 460f osteonecrosis of, 460–461, 461f Neck. See also under Cervical. pain in, in degenerative disorders, 261–263 webbed, in Klippel-Feil syndrome, 275–276, 276f Needle biopsy. See also Biopsy. of bone tumors, 167, 168f of soft tissue tumors, 187 Nemaline myopathy, 118, 118f Neonate, 304–305 brachial plexus palsy in, 304–305 ossification in, 14, 15f Nerve(s) anatomy and physiology of, 120–121, 120f examination of, 121, 122f peripheral, 120, 120f anatomy of, 120–121, 120f compression syndromes of, 122f, 132–137, 134f–136f. See also Nerve entrapment syndromes. examination of, 121, 122f, 123t hereditary disorders of, 129–131, 131t injuries of, 137–138, 138f repair of, 138 spinal, 120, 254f examination of, 121, 122f, 124t, 259f, 260–261, 260t Nerve conduction, 120–121 Nerve conduction studies, 121, 122f, 138 Nerve entrapment syndromes, 122f, 132–137, 134f–136f in diabetes mellitus, 140–141, 140f of elbow, 135–136, 136f, 317–320 of foot, 445 of shoulder, 295–298

Obturator nerve, 370, 370f Ochronosis, 95–97, 98f Odontoid, fractures of, 271–272, 272f Older adults, strength training for, 107 Olecranon, fractures of, 326–327, 327f in children, 331 Olecranon bursitis, 323 Onion skin appearance, of bone tumors, 166, 166f, 184 Open biopsy. See Biopsy. Open book fracture, pelvic, 378, 379f Opponens digiti quinti, 337, 339f Opponens pollicis, 337, 339f

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Index Osteoclasts, 16, 18, 18f in fracture healing, 197f, 198f Osteocytes, 16, 18, 18f Osteogenesis imperfecta, 54–55, 55f–57f vs. child abuse, 223 Osteoid osteoma, 170–172, 170f, 171f Osteomalacia, 30–33, 31t, 32f hypophosphatemic, 33, 63–64 Osteomyelitis, 144–153 acute, 146–151 clinical manifestations of, 146–148, 148f diagnosis of, 148–150, 149f, 150f differential diagnosis of, 149–150 early, 146 late, 146–148 treatment of, 150–151 causes of, 144, 144f, 145f cavitary lesions in, 152, 154f chronic, 152, 155f classification of, 146 complications of, 151 in diabetes mellitus, 152, 155f in sickle cell disease, 161 involucrum in, 145–146 multifocal, 148 of distal phalanx, 352 pathogenesis of, 144–146, 146f recurrent, 151 septic arthritis with, 146, 147f. See also Septic arthritis. sequestrum in, 146 spread of, 144–145, 146f subacute, 151–152, 153f–154f subperiosteal abscess in, 145, 147f, 151 vertebral, 159–161 Osteonecrosis, 40–44, 42f, 43f in sickle cell disease, 67 of hip, 376 in children, 389–390, 391f of knee, 407–408 of metatarsal head, 461 of navicular, 460–461, 461f Osteopenia, clinical definition of, 34 Osteopetrosis, 18 Osteoporosis, 33–38 clinical definition of, 34 diagnosis of, 34–37 pathophysiology of, 34 risk factors for, 34, 35f treatment of, 37–38

Orthotics, 247, 247f Ortolani test, 387, 388f Osgood-Schlatter disease, 224f, 225, 425 Ossification, 10–16, 13f–15f enchondral, 3, 7f, 14, 14f in neonate, 14, 15f intramembranous (mesenchymal), 3, 7f, 10, 13f of long bones, 14, 14f of small bones, 14 secondary centers of, 15f, 16 Osteitis fibrosa cystica, 30 Osteoarthritis, 73–79 aging and, 74 cartilage changes in, 71–73 clinical manifestations of, 75, 77f definition of, 73–74 disability in, 75 familial precocious, 57 histopathology of, 75, 76f management of, 75–79 arthrodesis in, 79 osteotomy in, 78f, 79 resection arthroplasty in, 79 total joint arthroplasty in. See Total joint arthroplasty. of ankle, 437, 439f of elbow, 314–315 of foot, 437, 438f of great toe, 437, 438f of hip, 374–376, 375f of interphalangeal joints, 75, 77f, 344, 345f of knee, 75, 403–404 of shoulder, 291–293, 292f of wrist, 344, 345f pathophysiology of, 75 premature primary, 74 primary idiopathic, 74 secondary, 74 sites of, 74 traumatic, 74 Osteoblastoma, 173 Osteoblasts, 16, 18, 18f in fracture healing, 197f, 198f Osteochondritis dissecans, 404–407, 407f of capitellum, 334, 334f Osteochondroma, 173–173, 173f Osteochondrosis in children, 223–225, 224f, 225t, 425 in Osgood-Schlatter disease, 224f, 225, 425 of elbow, 333–334, 334f

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Index Paraxial columns, 2, 4f, 6t Paronychia, 352, 352f Pars interarticularis, stress fracture of, isthmic spondylolisthesis and, 280–281 Passive exercises, in rehabilitation, 240, 242f Patella anatomy of, 397–398 bipartite, 410, 412f dislocation of, 411f, 416–418 congenital, 421–422 fractures of, 414, 416f function of, 402 malalignment of, 397 in patellofemoral pain syndrome, 410 subluxation of, 411f, 416–418 Patellar ligament, anatomy of, 398 Patellar tendon, rupture of, 420 Patellofemoral instability, 411f, 416–418 Patellofemoral pain syndrome, 410 Patellofemoral tracking abnormal, 50, 50f, 411f Q angle and, 410, 411f Pathologic fractures, 213. See also Fracture(s). bone metastases and, 190f, 191 in osteogenesis imperfecta, 54 in osteomyelitis, 151 in osteoporosis, 34, 36f, 38 in Paget disease, 39–40, 41f in solitary bone cyst, 179f Patterning anteroposterior, 9 dorsoventral, 9 Pavlik harness, 389, 390f Pectineus, 366, 367f, 368f Pectoralis major, 284, 287f Pelvis anatomic landmarks for, 371 anatomy and biomechanics of, 364, 364f examination of, 371 fractures of, 378–380, 378f–382f realignment osteotomy of, 376 Peripheral nerves. See also Nerve(s). anatomy of, 120–121, 120f disorders of Charcot arthropathy in, 138–140, 139f compressive, 122f, 132–137, 134f–136f, 141f. See also Nerve entrapment syndromes. hereditary, 129–131, 131t in diabetes mellitus, 138–141, 140f, 141t examination of, 121, 122f, 123t, 138

Osteosarcoma, 179–181, 180f in Paget’s disease, 40 Osteotomy for osteoarthritis, 78f, 79 valgus, for arthritic knee, 404 Out-toeing, 46–50, 49f Overhead athletes elbow pain/instability in, 320–322 pediatric, osteochondrosis of elbow in, 333–334, 334f Overlapping fifth toe, 456f, 457 Overuse injuries in athletes. See Sports injuries. nerve entrapment, 122f, 132–137, 134f–136f. See also Nerve entrapment syndromes. stress fractures as, 209–213, 212f Oximetry, transcutaneous, in peripheral vascular disease, 232 Paget disease, 38–40, 40f Pain back cervical, 261–263, 271 in disc herniation, 254f, 261, 266 in isthmic spondylolisthesis, 280 in scoliosis, 270 low, 263–264, 264t from bone metastases, 191 in compartment syndrome, 207 in reflex sympathetic dystrophy, 213–214, 214f in rotator cuff disease, 290–291 neck in degenerative disorders, 261–263 in whiplash, 275 patellofemoral, 410 postamputation, 233–238 shoulder, 290 in overhead athletes, 293–295 Palmar arch deep, 341 superficial, 341 Palmar fascia, contracture of, 348–349, 348f Palmar intrinsic muscles, 337, 339f Pan plexus palsy, 304–305 Panner disease, 334 Paraffin baths, 245 Parathyroid hormone deficiency of, 30 excess of, 24–30, 28f–30f in calcium regulation, 24, 26f in phosphate regulation, 24, 26f

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Index Plica injury, 410–412, 413f Poliomyelitis, 128–129 Polydactyly of foot, 455, 455f of hand, 360, 360f Polymethylmethacrylate, for vertebral body augmentation, 38 Polymyositis, 112, 113f Polyostotic fibrous dysplasia, 176 Popliteal artery, 370, 372f Popliteal cyst, 412 Posterior cruciate ligament anatomy of, 398–399, 399f injuries of, 420, 421f Posterior drawer test, 420, 421f Posterior tibial artery, 434 Posterior tibial tendon dysfunction, 438–440, 440f Posterior tibialis, function of, 438 Postpoliomyelitis syndrome, 128–129 Pott disease, 160f, 161 Prepatellar bursitis, 408–410 Primary spongiosa, 18, 20f Primitive streak, 2, 4f Profunda femoris artery, 370, 372f Pronator syndrome, 317–320, 319f Prone rectus femoris test, 261, 266 Proprioceptive neuromuscular facilitation, 106–107 Prosthesis in total joint arthroplasty. See Total joint arthroplasty. limb, 230f, 231 for children, 230f Proximal femoral focal deficiency, 394 Proximal interphalangeal joints of foot. See also Foot; Toe(s). flexion deformities of, 442, 443f of hand. See also Finger(s); Hand. anatomy of, 336–337, 336f dislocation of, 358–359 osteoarthritis of, 75, 77f, 344, 345f Pseudarthrosis, congenital clavicular, 306 Pseudoachondroplasia, 59, 60f Pseudofractures, in osteomalacia, 31 Pseudogout, 93–94, 94f Pseudohypoparathyroidism, 30 Psoriatic arthritis, 87–89, 89f treatment of, 90–91 Pubis, anatomy of, 364, 364f Pulled elbow, 332

Peripheral nerves, (cont’d) injuries of, 137, 138f repair of, 137, 138f Peripheral vascular disease amputations in, 231–232 ankle-brachial index in, 232 Peroneal artery, 434, 435f Peroneal nerve, 370, 371f, 433f anatomy of, 399, 400f Peroneus brevis, 399, 400f, 430, 430f, 433f, 435f Peroneus longus, 399, 400f, 430, 430f, 435f Peroneus tertius, 399, 400f, 430, 430f, 435f Pes anserinus bursitis, 410 Pes cavus, 442–445, 444f, 445t Pes planus in children, 457–458, 457f posterior tibial tendon dysfunction and, 438–439, 440f tarsal coalition and, 458, 459f Peterson classification, of physeal fractures, 218, 219f Phalanges. See Finger(s); Toe(s). Phalen test, in carpal tunnel syndrome, 132–135 Phantom limb sensation, 233–238 Phonophoresis, 246 Phosphate in bone homeostasis, 24, 27f metabolism of normal, 24, 25f regulation of, 24, 25f Physeal bar, 220, 221f Physeal fractures, 216, 218–220, 219f Physical therapy, 244–247. See also Rehabilitation. Physis, 14f, 16–18, 19f in osteomyelitis, 151 injuries of, 216, 218–220, 219f, 221f growth arrest after, 220 Pitchers elbow osteochondrosis in, 333–334, 334f elbow pain/instability in, 320–322 shoulder pain in, 293–295 Plantar fascia, 429, 432f Plantar fasciitis, 437–438 Plantar nerve, 433f, 434 Plate fixation, 201, 203f Pleomorphic rhabdomyosarcoma, 189 Plexiform neurofibromas, 131, 133f Plexus, 120

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Index Rehabilitation, 240–249 active exercises in, 240 ambulatory aids in, 247–249, 248f, 249t cryotherapy in, 245 diathermy in, 246–247 electrical stimulation in, 247 heat therapy in, 245–246 muscle testing in, 243–244 orthotics in, 247, 247f passive exercises in, 240 physical therapy in, 244–247 range-of-motion measurement in, 240–242, 243f strength training in, 106–107, 242–243 therapeutic modalities in, 244–249 Reiter syndrome, 90, 90f Renal osteodystrophy, 30, 30f Resection arthroplasty, 79 ulnohumeral, 314–315 Reverse straight leg raising test, 261, 266 Rhabdomyosarcoma, 188–189 Rheumatoid arthritis, 79–86 clinical manifestations of, 80–84, 82f, 83f diagnosis of, 80, 80t disability in, 85 epidemiology of, 79 immunogenetics of, 79, 79f immunopathogenesis of, 79–80, 81f juvenile, 85–86, 85f of elbow, 314–315 presentation of, 80, 82f radiographic features of, 84, 84f Rickets, 30–33, 31t, 32f hypophosphatemic, 33, 63–64 Risedronate for osteoporosis, 37–38 for Paget’s disease, 40 Rods, intramedullary, 201–203, 204f Rolando fracture, 355, 355f Rotator cuff anatomy of, 284, 285f, 286f disorders of, 290–291, 291f osteoarthritis due to, 291–292, 292f, 293

Puncture wounds, of foot, 161 Pyrosphosphate arthropathy, 94, 94f Q angle, 410, 411f Quadrangular space, 284, 288f Quadriceps muscle anatomy of, 366 contusion of, 386 Quadriceps tendon anatomy of, 397f, 398 rupture of, 420 Radial artery, anatomy of, 337, 338f, 339f Radial club hand, 361, 361f Radial hemimelia, 361, 361f Radial nerve anatomy of, 309, 313f entrapment of, 135f, 136, 136f, 320, 321f Radial tunnel syndrome, 135f, 136, 136f, 320, 321f Radiculopathy, cervical, 261–263 Radionuclide scanning, in osteomyelitis, 148–149, 149f Radioulnar synostosis, congenital, 332–333 Radius congenital abnormalities of, 361, 361f distal anatomy of, 308–309, 308f fractures of, 352–353, 353f, 356–357, 357f fractures of diaphyseal, 329, 331 distal, 352–353, 353f, 356–357, 357f in children, 330–331, 356–357, 357f of head, 324–326, 326f of neck, 324–326, 326f, 330–331 head of congenital dislocation of, 332, 333f fractures of, 324–326, 326f subluxation of, 332 neck of, fractures of, 324–326, 326f, 330–331 Range of motion measurement of, 240–242, 243f restoration of. See Rehabilitation. Reactive arthritis, 90–91 Rectus femoris, 366, 367f, 368f Reflex(es) anal, assessment of, 259f assessment of, 121, 122f, 122t, 261 in spinal disorders, 259f, 260–261, 260t Reflex sympathetic dystrophy, 213–214, 214f contrast baths for, 246

Sacral plexus, 370, 371f Sacroiliac joint, 364, 365f stress test for, 374 Sacroiliitis, in ankylosing spondylitis, 87, 88f Sacrum, 252f, 257f. See also Pelvis; Spine; Vertebrae. anatomy of, 364, 365f

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Index Septic arthritis, 154–158 cartilage destruction in, 156, 156f causative organisms in, 154, 157 clinical features of, 156, 157f diagnosis of, 156–158 differential diagnosis of, 157t etiology of, 154 osteomyelitis with, 146, 147f, 151 pathogenesis and pathophysiology of, 154–156, 156f sites of, 156 treatment of, 158 vs. osteomyelitis, 150 Septic bursitis, olecranon, 323 Seronegative spondyloarthropathies, 86–91 Serratus anterior, 284, 287f paralysis of, 296–297 Sever disease, 458–460 Shepherd crook deformity, in polyostotic fibrous dysplasia, 176 Shin splints, 414 Shortwave diathermy, 246–247 Shoulder adhesive capsulitis of, 293, 294f anatomy of, 284, 285f–288f arthritis of, 291–293, 292f brachial plexus injuries in, 295–297 dislocations of of acromioclavicular joint, 302–303, 303f of glenohumeral joint, 300f, 301–302, 302f of sternoclavicular joint, 303–304 disorders of degenerative, 290–297 in children, 304–306 examination of, 286–290, 289f floating, 298 frozen, 293, 294f impingement in in overhead athletes, 295 tests for, 290 injuries of, 297–304 in children, 298–299 nerve entrapment syndromes in, 296–298 osteoarthritis of, 291–293, 292f painful, in overhead athletes, 293–295 range of motion of, 286–290, 289f rotator cuff disease in, 290–291, 291f tendon ruptures in, 304, 304f total arthroplasty of, 292–293, 292f Shoulder separation, 302–303

Saphenous nerve, 370, 370f, 433f, 434 Sarcolemma, 100, 101f Sarcoma. See also Cancer. in Paget’s disease, 40, 41f of bone, 179–184. See also Bone tumors, malignant. of soft tissue, 187–189 Sarcomere, 100, 101f Sarcoplasmic reticulum, 100, 102f Sartorius, 366, 367f, 368f Scaphoid. See also Wrist. anatomy of, 336, 336f fractures of, 353–355, 354f osteonecrosis of, 44 Scapula. See also Shoulder. anatomy of, 284, 285f, 286f congenital elevation of, 305, 305f fractures of, 298 winging of, 296–297 Scheuermann disease, 280, 280f Schmid metaphyseal chondrodysplasia, 60–61, 63f Sciatic nerve, 370, 371f anatomy of, 399, 400f Sciatica, 254f, 265–266 examination in, 254f Sclerae, blue, in osteogenesis imperfecta, 54, 55f Sclerotomes, 3, 7f Scoliosis, 277–279, 278f. See also Spine, curvature of. congenital, 4, 277, 277f, 279t idiopathic, 270, 279, 279t in adults, 268–270 in Marfan syndrome, 65, 66f in muscular dystrophy, 114, 115f in neurofibromatosis, 131, 133f in osteogenesis imperfecta, 55, 56f in spinal muscular atrophy, 129 myelomeningocele and, 127f Scottie dog sign, in spondylolysis, 281f Screening, for motor development delays, 48, 49t Screw fixation, 201, 203f Secondary spongiosa, 18, 20f Segond fracture, 420 Selective estrogen receptor modulators (SERMs), for osteoporosis, 37 Sensory examination, 121, 122f. See also Neurologic examination. in spinal disorders, 259f, 260–261, 260t

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Index innervation of, 399, 401f, 430–434, 432f Soleus, 399, 400f, 430, 430f Somatopleure, 2 Somatopleure ventrolateral body wall, 8 Somites, 2, 3–4, 5f, 6t, 7f Spasticity, in cerebral palsy, 121–123 Spina bifida, 126, 127f Spinal canal, 253, 253f Spinal cord anatomy of, 253, 254f congenital anomalies of, 126–128, 127f disorders of in cervical spondylosis, 263, 263f physical examination in, 258–261, 259f, 260t injuries of, 128 in children, 274 without radiographic abnormality, 274 tethered, 277 Spinal fusion, 268, 269f for scoliosis, 279 in isthmic spondylolisthesis, 280 Spinal muscular atrophy, 129 Spinal nerves, 120, 253, 254f. See also Nerve(s). examination of, 121, 122f, 124t, 259f, 260–261, 260t Spinal stenosis cervical, 263, 263f in achondroplasia, 52, 53f, 267 lumbar, 267–268, 269f Spine. See also Vertebrae. anatomy of, 252–258, 252f–255f, 257f, 258f ankylosing spondylitis of, 87, 88f bamboo, 87, 88f cascading, 268 cervical. See also Cervical spine. anatomy of, 252f, 253–256, 254f, 255f degenerative disease of, 261–263 injuries of, 270–273, 271f, 272f congenital deformities of, 277, 277f curvature of abnormal, 277–280, 278f. See also Kyphosis; Scoliosis. measurement of, 278f, 279 normal, 252f development of, 253 disorders of, 261–281 degenerative, 261–263 in children, 275–281 embryology of, 253

Sickle cell disease, 65–67 dactylitis in, 161 osteomyelitis in, 161 Skeletal dysplasias, 52–65 achondroplasia, 52–54, 53f cartilage oligomeric matrix protein disorders, 57–59, 60f, 61t congenital contractural arachnodactyly, 65 hereditary multiple exostosis, 65 hypophosphatemic rickets, 33, 63–64 in Gaucher disease, 67–68, 68f in hematopoietic disease, 65–68 in hemophilia, 68 in Marfan syndrome, 64–65, 66f in monocyte/macrophage disorders, 67–68 in sickle cell disease, 65–67 metaphyseal chondrodysplasias, 60–63, 63f, 64f osteogenesis imperfecta, 54–55, 55f type I collagen disorders, 54–55, 55t type II collagen disorders, 55–57, 58f Skeletal muscle. See Muscle(s). Skeletal traction, 200, 202f Skeleton. See also Bone. appendicular, embryology of, 8–9, 10f–12f axial, embryology of, 3–4, 6t, 7f SLAP lesions, 295 Slipped capital femoral epiphysis, 390–394, 392f Slit catheter technique, for compartment syndrome, 207–209, 210f Slow-twitch fibers, 103–104, 105f Smith fracture, 352–353 Snapping hip, 377 Soft tissue. See also Ligaments; Muscle(s); Tendons. healing of, 198 injuries of, 108–111, 110f in children, 223–225, 224f, 225t Soft tissue tumors, 165t, 185–189 benign, 185–187 fibrous histiocytoma, 185–187 hemangioma, 187 lipoma, 185, 186f myositis ossificans, 185, 186f malignant, 187–189 liposarcoma, 187, 188f malignant fibrous histiocytoma, 189, 189f rhabdomyosarcoma, 188–189 synovial cell sarcoma, 187–188, 188f Sole. See also Foot.

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Index Sprains, 109–111, 110f. See also specific ligaments. in children, 223 of ankle, 453 of elbow, 320, 322f of hand, 358 of knee, 110f, 418–420, 419f of spine, 274–275 Sprengel deformity, 305, 305f Spurling test, 262, 262f Staphylococcus aureus, in osteomyelitis, 151, 152 Static encephalopathies, 121–126 Sternoclavicular joint. See also Shoulder. anatomy of, 284, 285f–287f dislocation of, 303–304 embryology of, 8–9, 10f Sternocleidomastoid contracture, in torticollis, 275 Stickler syndrome, 57 Stimson maneuver, 300f, 301 Stingers, 295 Straddle fracture, pelvic, 378, 379f Straight leg raising test, 259f, 260–261, 266 Strains, 108 in children, 223 thigh, 386 Strength grading of, 243–244, 245f muscle, 102, 104f exercises for, 106–107, 242–243, 244f grading of, 243–244, 245f Strength training, 106–107 in rehabilitation, 242–243 Stress fractures, 209–213, 212f of pars interarticularis, isthmic spondylolisthesis and, 280–281 Stroke, 124–126 Subacromial bursitis, 290 Subacromial impingement, tests for, 290 Subclavian artery, 284, 287f Subluxation. See also Dislocation. atlanto-axial, 276–277, 276f of cervical vertebrae, 270–277, 271f, 276f of patella, 411f, 416–418 of radial head, 332 Subperiosteal abscess, 145, 147f, 151 Subscapularis. See also Rotator cuff. anatomy of, 284, 285f, 286f Superficial palmar arch, 341 Superficial peroneal nerve, anatomy of, 399, 401f

Spine, (cont’d) injuries of, 270–275. See also Vertebrae, fractures of. in children, 274 intervertebral discs of, 253–257, 254f. See also Intervertebral discs. lumbar degenerative disease of, 263–265, 264f disc herniation in, 265–267, 265f, 267f fractures of, 273–274, 273f sprains of, 274 stenosis of, 267–268, 269f mechanics of, 258 metastases to, 190–191 motion of, 253–256 evaluation of, 259f, 260 osteomyelitis of, 159–161 Paget disease of, 38–40, 40f physical examination of, 258–261, 259f, 260f thoracic anatomy of, 252f, 256. See also Spine; Vertebrae. fractures of, 273–274, 273f movement of, 256 sprains of, 274 tuberculosis of, 160f, 161 Spinous process, vertebral, 253, 253f Spiral fractures, 222f, 223 Splanchnopleure, 2 Splints, 247, 247f Spondylitis ankylosing, 87, 88f ochronotic, 95–97, 98f Spondyloepiphyseal dysplasia congenita, 55–56, 58f Spondyloepiphyseal dysplasia tarda, 57, 58f Spondylolisthesis, 268, 270t degenerative, 268, 270t isthmic, 268, 270t, 280–281, 280f lumbar, 268, 270t Spondylolysis, without spondylolisthesis, 281f Spongiosa primary, 18, 20f secondary, 18, 20f Sports injuries of elbow, 320–322 in children, 333–334 of hand, 357f, 358 of muscles, 108–109 of tendons, 108–111 of ulnar collateral ligament, 358, 359f

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Index of wrist, 346–348, 347f septic flexor, 350–352, 351f Tendinopathy, 111 Achilles, 111, 111f Tendinosis, 111 of ankle, 439 posterior tibial tendon dysfunction and, 439–440, 440f Tendons. See also specific tendons and joints. age-related changes in, 107, 109 anatomy of, 104–106 chronic disorders of, 111 healing of, 109–110 injuries of, 109–111 in children, 223 in shoulder, 304, 304f Tennis elbow, 315–316, 316f Tenosynovitis. See Tendinitis (tenosynovitis). Tension band wiring, 203 Tensor fascia lata, 366, 367f, 368f Teres minor. See also Rotator cuff. anatomy of, 284, 285f, 286f Terminal filum, 253, 254f Tethered cord, 277 Thenar muscles, 312f, 313f, 337 examination of, 343 Thick filaments, 100, 101f Thigh. See also Lower extremity. blood supply of, 370, 372f innervation of, 370, 370f–372f muscles of, 366, 367f–369f myositis ossificans of, 186f, 386 strain of, 386 Thigh-foot angle, measurement of, 47, 48f Thin filaments, 100, 101f Thomas test, 375, 375f Thompson test, 453, 455f Thomsen disease, 117, 117f Thoracic outlet syndrome, 122f, 135f, 136–137, 297 Thoracic spine. See also Spine; Vertebrae. anatomy of, 252f, 256 fractures of, 273–274, 273f movement of, 256 sprains of, 274 Throwing athletes elbow osteochondrosis in, 333–334, 334f elbow pain/instability in, 320–322 shoulder pain in, 293–295 Thumb. See also Hand. degenerative disorders of, 344, 345f

Superior gluteal artery, 370, 372f Superior gluteal nerve, 370, 371f Superior labrum anteroposterior lesions, 295 Supracondylar fractures, of humerus, 329–330, 329f Suprascapular nerve entrapment, 295–296 Supraspinatus. See also Rotator cuff. anatomy of, 284, 285f, 286f nerve impingement and, 295–296 Sural nerve, 433f, 434 Surgical biopsy. See Biopsy. Surgical margins, for bone tumors, 169, 169f Swan-neck deformity, 337, 341f Syme amputation, 233, 235f Syndactyly of foot, 455–456, 456f of hand, 359–360, 360f Synostosis, congenital radioulnar, 332–333 Synovial cell sarcoma, 187–188, 188f Synovial fluid characteristics of, 71–73 examination of, 74f in septic arthritis, 156 Synovial joints. See also Joint(s). embryology of, 8–9, 10f Synovial plica injury, 410–412, 413f Synovitis, of hip, 394 Syphilis, Charcot arthropathy in, 138, 139f Syringomyelia, 277 Charcot arthropathy in, 138, 139f Systemic inflammatory response syndrome, in multitrauma patients, 194, 195f Talipes equinovarus, 453–455, 455f Talus fractures of, 448, 450f osteonecrosis of, 40, 42f, 44 TAR syndrome, 361 Tarsal coalition, 458, 459f Tarsal tunnel syndrome, 122f, 135f, 137 Tarsometatarsal (Lisfranc) joint, 428, 428f fracture-dislocations of, 448–450, 451f–452f Teardrop fractures, 273 Teeth, abnormalities of, in osteogenesis imperfecta, 54, 55f, 56f Tendinitis (tenosynovitis), 111, 111f De Quervain, 346–348, 347f of ankle, posterior tibial tendon dysfunction and, 439, 440f of elbow, 315–317, 317f of hand, 346, 347f

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Index great amputation of, 233. See also Amputation. lateral deviation of, 440–442, 441f osteoarthritis of, 437, 438f hammer, 442, 443f ingrown nail of, 446, 446f lesser, deformities of, 442 nails of infections of, 352, 352f ingrown, 446, 446f injuries of, 359 sprains of, 453 supernumerary, 455, 456f turf, 453 Toeing in, 46–50, 48f Toeing out, 46–50, 49f Toenail. See Toe(s), nails of. Tophi, in gout, 92f, 93 Torsion femoral, 46, 47f patellofemoral malalignment and, 50, 50f tibial, 46–47, 48f Torticollis, congenital, 275, 275f Torus fractures, 216, 217f Total joint arthroplasty for rheumatoid arthritis, 85 of elbow, 315, 316f of hip, 376 of knee, 404, 406f of shoulder, 78f, 79 Trabecular bone, 16, 17f, 195 Traction, 200, 202f Traction apophysitis, of medial epicondyle, 333 Transcutaneous oximetry, in peripheral vascular disease, 232 Transfemoral amputation, 233, 237f. See also Amputation. Transphyseal fracture separation, of distal humerus, 330 Transtibial amputation, 233, 236f. See also Amputation. Transverse acetabular ligament, 365, 365f Transverse carpal ligament, 337, 339f Transverse tarsal (Chophart) joint, 428, 428f Trapezius, 284, 287f Trauma. See also specific sites and types. fractures in. See Fracture(s). multiple, 194, 195f pediatric, 216–225 fractures in, 216–220 intentionally inflicted, 220–222, 221f

Thumb, (cont’d) fractures of, 355–356, 355f gamekeeper’s, 358, 359f hypoplasia/aplasia of, 361 osteoarthritis of, 344, 345f range of motion of, 341–343, 342f Tibia bowing of, 422, 422f congenital pseudoarthrosis of, 422, 423f distal, fractures of, 452, 454f fractures of. See also Fracture(s). distal, 452, 454f in children, 415–416, 417f, 452, 454f nonunion of, 208f of tubercle, 415–416, 417f plateau, 414, 415f proximal, 414–416 shaft, 414–415, 417f spine (eminence), 416, 417f stress, 209–213 hemimelic, 422–423 proximal anatomy of, 396–397, 396f fractures of, 414–416 torsion of, 46–47, 48f patellofemoral malalignment and, 50, 50f valgus osteotomy of, 404 Tibia vara, 423–425, 424f Tibial artery, 434, 435f Tibial nerve, 399, 401f, 433f, 434 Tibial tuberosity transfer, for patellar instability, 411f Tibialis anterior, 399, 400f, 430, 430f, 433f, 435f strength testing for, 244 Tibialis posterior, 399, 400f, 430, 430f Tibiofemoral angle, developmental changes in, 50, 51f Tillaux fracture, 452, 454f Tiludronate, for Paget’s disease, 40 Tinel sign in carpal tunnel syndrome, 132 in tarsal tunnel syndrome, 135f, 137 Toddler’s fracture, 223, 416 Toe(s). See also Foot. claw, 442, 443f congenital deformities of, 455–457, 456f curly, 456, 456f fifth, overlapping, 456f, 457 flexion deformities of, 442, 443f fractures of, 450

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Index Upper extremity. See also Limb and constituent parts. amputation of, 230f, 232–233. See also Amputation. Upper limb congenital absence of, 228–229 development of, 6, 8–9, 10f–12f prosthesis for, 230f, 232–233 Upper motor neuron disease, 121–126 Uric acid, in gout, 91–93, 92f Uveitis, in juvenile rheumatoid arthritis, 85–86, 86f

rehabilitation after, 240–249. See also Rehabilitation. soft tissue, 108–111, 110f in children, 223–225, 224f, 225t spinal, 270–275 Traumatic amputations, 231. See also Amputation. Traumatic brain injury, 124–126 Trendelenburg lurch, 371 Trendelenburg test, 374, 374f Triangular interval, 284, 288f Trident hand, 52, 53f Trigger finger, 345, 347f Triple arthrodesis, 437, 439f Triradiate cartilage, 364, 364f Trochanteric bursitis, 377 Tropomyosin, 100, 103f Troponin, 100, 103f T-score, in osteoporosis, 34 Tuberculosis, musculoskeletal involvement in, 160f, 161 Tumors amputation for, 227–238. See also Amputation. bone, 164–185, 164t. See also Bone tumors. soft tissue, 165t. See also Soft tissue tumors. Turf toe, 453

Valgus angulation in fractures, 200, 201f of knee, 51–52, 51f, 52t Valgus osteotomy, for arthritic knee, 404 Varus angulation in fractures, 200, 201f of knee, 50–51, 51f, 51t Vertebra plana, in Langerhans cell histocytosis in, 177 Vertebrae. See also under Spinal; Spine. anatomy of, 252–256, 252f–255f body of, 252–253, 253f cervical, 252f, 253–256, 255f fractures of, 271–273, 271f, 272f formation of, 4, 8f fractures of, 270–274 cervical, 271–273, 271f, 272f compression, 34, 36f, 38, 39f in children, 274 in osteoporosis, 34, 36f, 38, 39f in Paget’s disease, 39–40 thoracolumbar, 273–274, 273f treatment of, 38, 39f intervertebral discs of, 254f, 256–257, 258f. See also Intervertebral discs. lumbar, 252f, 253f fractures of, 273–274, 273f metastases to, 190–191 osteomyelitis of, 159–161 Paget disease of, 38–40, 40f sacral, 252f thoracic, 252f, 256 fractures of, 273–274, 273f Vertebroplasty, for compression fractures, 38 Vertical shear fracture, pelvic, 378, 379f, 380f Vitamin D in calcium regulation, 24, 25f, 26f

Ulcerative colitis, arthritis in, 90–91 Ulna congenital abnormalities of, 362 distal, anatomy of, 308–309, 308f fractures of diaphyseal, 329, 331 Monteggia, 327, 328f Ulnar artery, anatomy of, 337–341, 339f Ulnar collateral ligament, rupture of, 358, 359f Ulnar hemimelia, 362 Ulnar nerve anatomy of, 309, 312f entrapment of, 122f, 135–136, 135f, 136f, 317, 318f, 350 examination of, 343–344, 343f injuries of, hand deformities and, 343–344, 344f transposition of, 314–315, 318f Ultrasonography, Doppler, in peripheral vascular disease, 232 Ultrasound diathermy, 246–247 Unicompartmental knee arthroplasty, 404, 405f

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Index Wound necrosis, in amputation, 233–234, 235f Woven bone, 16, 21 Wrist anatomy of, 312f, 313f, 336–341, 336f–340f compartments of, 337, 338f degenerative disorders of, 344 examination of, 341–344, 342f, 343f fractures of Barton, 353, 353f Colles, 352, 353f in children, 357 of scaphoid, 353–355, 354f Smith, 352–353 ganglion of, 349, 349f injuries of, 352–358 Kienböck disease of, 44, 344–345, 346f nerve entrapment syndromes of, 350 osteoarthritis of, 344, 345f osteonecrosis of, 44 range of motion of, 341–343, 342f tendinitis of, 346–348, 347f Wryneck, 275, 275f

Vitamin D (cont’d) supplemental for osteomalacia/rickets, 33 for osteoporosis, 37 Vitamin D–deficiency osteomalacia, 33 Vitamin D–dependent rickets, 33, 63–64 Volkmann contracture, 330 Walker-Murdoch wrist sign, 66f Walkers, 248f, 249, 249t Walking. See also Gait. biomechanics of, 370–371 observation of, 371, 434 Wallerian degeneration, 137–138 Webbed neck, in Klippel-Feil syndrome, 275–276, 276f Weight lifting, 106–107 Werdnig-Hoffmann disease, 129 Whiplash injuries, 275 Whitlow, herpetic, 352 Winging, scapular, 296–297 Wound care in amputation, 233–234 in chronic osteomyelitis, 152, 155f in septic arthritis, 158 Wound healing in diabetes mellitus, 231–232 in peripheral vascular disease, 231–232

X-linked hypophosphatemic rickets, 33, 63–64 Zone of polarizing activity, 9 Zygote, 2, 3f

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