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30919664 Foot and Ankle

30919664 Foot and Ankle

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Foot & Ankle Pearls


Professor of Foot and Ankle Orthopedics

Temple University-School of Podiatric Medicine Director 01 Foot and Ankle Surgical Residency Program

and Medical Education Graduate Hospital Philadelphia,. Pennsylvania

HANLEY s, BELFUS, INC. I Philadelphia


HANLEY & BELFUS, INC. Medical Publishers

210 S. 13th Street Philadelphia, PA 19107

(215) 546-7293, 800-962-1892 FAX (215) 790-9330

Website: http://www.hanleyandbelfus.com

library 01 Congress Cataloging-in-Publication Data

Foot and ankle pearls I edited by Richard M. Jay. p. : cm.-(The pearls series)

Includes bibliogrllphicai references and Index. tSBN 1-56053-445-1 (alk, paper)

1. Fool-Diseases--Case studies. 2. AnK'le-Diseases-Case studies. I. Jay, Richard M.

II. Series

[DNLM: 1. Foot Diseases--diagnosis--Gsse Report. 2. Fool Diseases--diagnosis-Problems and Exercises. 3 Ankle Injuries-diagnosis--Gase Report. 4. Anklelnjuries--dlagnosis--Problems and Exercises, 5. Foot tnjurles--dlagnosis--Gase Report. 6. Foot Injuries-----<:liagnosis-Problems and Exercises. WE 18.2 F687 2001]

acssi ,F66 2002



Printed in Canada


I SBNl-56053-44S-1

© 2002 by Hanley & Belfus, Inc. All rights reserved. No part of this book may be reproduced, reused, republished, transmitted in any form or by any means. or stored in a database or retrieval system without written permission of the publisher.

last digit is the print number: 9 8 7 6 5 4 3 2 1


~~ ~

1. A 43-year-old woman with a painful and swollen great toe " .

2. A 43-year-old man with constant heel pain , , , 3

3. A 24-year-old man with a crushed fool 5

4. A 56-year-old woman with shooting posterior heel pain "......................... 7

5. A 63-year-old woman with insulin-dependent diabete and non-healing ulcers.... 9

6. A 46-year-old man with a cyanotic hallux. and fiftb toe 11

7. A 46-year-old woman with a hot and swollen foot................................................. 13

8. A 22-year-old man with pain in his third toe.......................................................... 15

9. A 33-year-old woman with a painful right ankle.................................................... l7

10. A 56-year-old man with a traumatic injury 10 his ankle " "...................... 20

II. A 44-year-old woman with right foot pain of insidious onset................................ 22

12. A 60-year-old woman with a continually aching arch............................................ 25

13. A 52-year-old woman with a painful bump on her foot 28

14. A 7l-year-old man with an itchy. scaly rash on his upper and lower

extremitie and a lesion on his right foot.......................................... 30

15. A 51-year-old man with chronic diabetic foot ulcerations 32

16. A 74-year-old man with nontraumaric heel pain 35

17. A 52-year-old man with an 8-month history of a foot ulcer 37

18. A 13-year-old girl wi th lateral foot pain..... 39

19. A IS-year-old girl with pain in her second toe 42

20. A 13-year-old girl with a painful foot..................................................................... 44 2 L A 14-year-old boy with severe foot pain causing him to crawl.............................. 46

22. An 8-year-old girl with nightly heel pain 48

23. A 19-month-old girl who is unable to walk............................................................ 50

24. A 6-year-old boy who walks with flat feel.............................................................. 52

25. A 58-year-old man with complications after arthroplasty 54

26. A 19-year-old man with a soccer injury to his right ankle ,........ 56

27, A 14-year-old boy with all internal rotation injury to his ankle ".. 58

28. An I I-year-old boy with arch pain 60

29. A 72-year-old diabetic woman with a plantar ulcer........................... 62

30. A 65-year-old, insulin-dependenr woman with a painful blister 65

3 I. A 23-year-old woman with excruciating foot pain after a motorcycle accident... 67 32. A 34-year-old woman with high-arched feet and ankle pain.................................. 69



An I l-year-old girl with a short loe......................... 72

A 25-y..:ur-old TmU1 v, ith pers.isrcru ankle pain 74

A. ..J.6-year-old woman with II lump on the top of her foot 76

A 26-year-old man with a painful, discolored great toenail .,. 78

A 36-year-old woman with l<!fL forefoot pain after II jog "., 80

A 61-year-.old man with son tissue masses at his ankle and heel.. _................ 82

A 29-year-uld man with a painful ankle , ,........ 84

A '21-~ear-old woman with a stiff, painful foot 86

An 84-year-old man with painful hallux ulcers 88

A S5-yeal'-old woman with II raised mass on her second toe.................................. 90

A 2-ycar-okl girl with one severely tlartenerl foo1......... 92

A I u- year-old boy with II pamfu I right arch ,... 94

A 30-yt·ar-old man with a clinically deformed left fool and ankle 96

A 25-ycW--l)ld runner with persistent ankle pain "................ 98

A SO-year-old woman with severe. recurring foot pain " 100

A lfl-year-nkl boy wilh a limp _ 102

A 3-year-oLu boy with bowed legs , _ , " , 104

A 12-year-old boy with painful. aching ankles _............................. 106

A ,-year-old boy with persistent left foot pain 108

A 6-year-oIJ girl with discomfort in her hands and feet., 110

53. A 59-ycar-old-man with a slirf hallux 112

54. A 52-yc:ar-11Id woman wub burning pain in her forefcot.. 115

55. A -IO-year-old man ,I ith ,I progressively flattened foot after a minor fall 118

56. A 14-year-old boy with persistent pain in his knee " 121

57. A 27-month-old girl who i~ unable 10 walk 123

58. A 11-ycar-old boy with a painful and swollen ankle 125

59. A 17-ycar-old boy \\ ith a red. swollen toe.................................. 1.27

60. A 41-year-old woman whh a darkened and painful toe _ 129

61. An lMl-}ear-old man with chronic foot pain , , 131

62. A ltl-year-old boy with II painful. swollen fuot. , , l34

63. A 3D-year-old man with painful, warm, ~prelltlillg cellulitis of the kg U6

64. A Srl-year-old diabetic man with a foot ulcer , lJB

65. A 55-year-old man with fever. erythema, and purulent drainage from

[he right leg ,.............. 140

66. A 3J-year-old woman with a cold Foot. _ , 143

67, A 50~year-old tennis player with acute calf pain 1-1-6



68. A 54-year-old man with painful thigh muscles 148

69. A 33-year-old woman with heel pain 150

70. A 40-year-old diabetic man with a persistent ulcer 153



Riehard M, Jay. D.P.M., FACFAS

Professor of Foot and Ankle Orthopedics, Temple University-School of Podiatric Medicine, Philadelphia: Director of Foot and Ankle Surgical Residency Program and Medical Education. Graduate Hospital, Philadelphia, Pennsylvania

The Graduate Hospital Foot and Ankle Residency Program Philadelphia, Pennsylvania

Jeffrey DeLoll. D.P.M.

Shane Hollawell, D.P.M.

Raben McCone\..ey. D.P.M.

Michael Rayno. D.P.M.

Brian Rell, D.P.M.

Thomas Landino. D.P.M.

Dawn Pfieffer. D.P.M.

Barry White. D.P.M.

Jodi Schoenhaus, D.P.M.



FOOl and Ankle Pearls is the latest volume in the highly popular Pearls Series®. This book is a compilation of interesting lind challenging cases seen at the Graduate Hospital in Philadelphia, and it provides valuable Information not readily available in standard textbooks. Each CMe is unique and illustrates one or more diagnostic or therapeutic issues confronting the clinician. It is also "interactive' in that the reader, based on rhe information represented (l1Sl1~ ally relating to a pain syndrome), is asked to make a diagnosis. The diagnosis is later revealed and discussed, and aspects that are especially important are captured and llsted at the end of each case as "Clinical Pearls."

I have availed myself of the expertise of (he Graduate Hospital Foo1 and Ankle surgical residents, as they have a keen and observant eye for interesting cases and are among the brightest and most energetic physicians [ know. It was natural to ask them for help in putting together this book. Thanks to Hanley & Belfus for allowing me to reprint a few cases from Rheumatology Pearls and Infectious Disease Pearls.




A ~3·year.old woman with a painful and swollen great toe

The patient presents with a 3·day history or pain and swelling ln the left big toe joint. She says, "It hurts to even have the sheets touch my toe" The patient denies any history of trauma to the left foot and stale, that she saw her primary doctor, who started her on indomethacin 50mg BID. Wilen relief hod not been obtained 2. days later. she carne to the emergency department for treatment, The patient i ~ without II sign i ficant past medical h istory.

Pllysical E.mmirIUUQfI: Vital signs: normal. General: mild distress. HEENT: normal. Cardiac: regular rate, no murmurs. Chest: clear breath sounds. Abdomen: soft, nonrender, Extremities: palpable pedal pulses bilaterally; a swollen. reddened, tender left lSI MTP joint of the left foot, with 1+ nonpitting edema, Neur~logic: intact.

Laboratory Findings: CBC wi th differential: WBC13.30011-"l (4000- J.O.OOO normal); lyrnphocytes 50001.fJ.III000-4500 normal). Radiograph uf left foot (see figure): erosion of the Fir.;( metatarsal head with sclerotic bone exhibiting a martel sign. Serum urinalysis: normal. ESR 45 mmlhr (increased). Arthrocentesis of lefl lSI MTP joint: increased WBC. specifically neurrophils 85 (O-::!4 normal); monosodium urate crystals (needle-shaped and display a negative birefringence tinder pelarizing light microscopy).

Questioll: What syndrome explains this patient's signs and symptoms?


Diagnosis: Acute gouty arthritis

Discussion: Gout isa disorder of purine metabolisrn characterized by hyperuricemia and the deposition of monosodium urate crystals in joints. Attacks may be precipitated by trauma, surgery, fasting, infection, and medications such as diuretics. Gout is usually monoarticular and predorninately affects the joints of the lower extremity, specifically the lsI MTP joint. This diseese is widely dispersed among many races and has a higher incidence in men vs, women typically over the age of 30. Women who are affected are usually postmenopausal. The discrepancy between [he sexes is believed to be due to [he action that estrogen plays in promoting renal excretion of line acid.

Pathoge ne sis in vo I ves u ric acid, ei the r fro m ingestion of foods eontalning purines (e.g., shellfish, beef. alcoholic beverages) or endogenous synthesis of purine nucteotides.Humans lack the enzyme uricase, which oxidizes uric acid to allantoin. Under steady-stale conditions .. renal CJl:C!1;(ion is the major route of uric acid dispos al (approximately two-thirds), and bacterial oxidization of urate into the gut account> for the remaining one-third. Two factors-either alone or in combination -contribute substantially to the hyperuricemia of gout: Increased uric acid production due to an abnormality in the metabolism (HGPRT deficiency), and diminished uric acid secretion by the kidney.

The pathology of acute gout arthritis involves urate crystallizing as a monosodium salt and oversaturating joint. tissue. Sodium urate becomes less soluble at lower temperatures, which may explain why the urate crystals predispose to deposition in areas such as the toe joints and earlobes. The urate crystal s init i ate a nd susta i n intense an acks 0 f

acute inflammation because of their ability to stimulate the release of several icflammatory mediators.

Signs and symptoms include redness, heal, swelling, and tenderness of [he affected joint, often with prodromal irritability and a sudden onset of pain in the early hours of the morning. The patient typically remarks that it hurts to even have the sheets of the bed touch the area. Serum uric acid levels may Of may nat be elevated, and often there is an increased serum WBe as well as an elevated ESR acutely, Radiographic findings are uSllaHy normal at rhls stage, but may demonstrate soft tissue swelling und jcinreffusiens. Definitive diagnosis is established by arthrocentesis of the joint and synovia! fluid analysis. The presence of monosodium urate crystals that are needle-shaped and display negative birefringence under polarizing light microscopy is definitive. Also, synovial fluid leukocytesare elevated, with a predomination of neutrophils,

Treatment consists of the oral admiaistration of NSAfDs, such as indomethacin, up to 7Smg sustained-release B rn and/or colchicine. Colchicine is a very toxic drug with GI effects such as nansea, vomiting, diarrhea, and cramping when administered orally, it has been suggested mal a prompt response to colchicine is diagnostic of gout. However, nore that other arthropathies also respond to colchicine. Also, if it is starred 24 hours after onset of an attack. the response can be variable. Other treatment options include an intraarticular injection of eortiesteroids, administration of ACfH .. rest. and elevation of affected area.

In the present patient, atreatment course of colchicine provided a marked reduction of pain after 5 hours.

CUnical Pearls

L In acute gout)' arthritis, ESR and serum WBCs are often elevated.

2, Presence of needle-shaped monosodium urate crystals with negative birefringence in synovial aspirate is diagnostic.

3. Acute gouty arthritis usually is monoarticular EIl1d. is preceded by prodromal irritability.

4. lt affects more males than females over the age of 30.


I. lssetbaeher KJ, Bnmnwn[d E, Wi[~on m .• t al teds): Harrison's Principles of lmernnl Medicine. I -lth ed, New York, McG,.w·Hill, t998.

2. Klippe[ lH. Wey In<l eM. w onmunn RL I eds I: Pri mer on the Rho" m "lit: Di,~""," I I til ed. Auun tao GA, Anhri!ls Pou ndeuon, [9Q7



A 43-year-old man with constant heel pain

A 43-year-Old rnun presents with a 2- to 3-month history of constant leftplantar and lateral heel pain, He relates that he has experienced intermittent foot and bi lateral knee pain for several years. Surgical arthroscopy was performed on his bilateral knees, with mild La moderate pain relief. However, pain in the left heel has persisted with both ambularion and nouweight-bcaring. and has become mildly progress i ve.

PhySical Examination: Temperature 98.6° F: pulse 7f!; respiration> 16; blood pressure 150180.

HEENT: normal. Lungs: clear. Cardiac: regular, Abdomen: no ntender, Skin: normal, with healed arthroscopy portals on the left and right knees .. Musculoskeletal: pain on palpation of plantar medial and lateral tubercles of left calcaneus, and on lateral compression of left calcaneus; nonrender planrar t'a"cia: manual muscle testing of lower extrem it} normal.

Laboratory Findings: CBe with di fferential: normal. Chemistry profile: normal. Lung function tests: normal, PTIP1T: normal, Cholesterol: 209 {120-199 normal). Pathology: Gf{l~' specimen -2.5 X 1.5 X I em aggregate of yellow bony tissue, Microscopic spedmen-cystic lesion with dense. hyal i nized wall contalni ng area of bony sclerosis, some hemosideri n plgrnem deposition. ami areas of increased vascularity: surrounding bone showed fatty replacement of marrow. Imaging: Radiographs of light foot-no osseous pathology: left toor (see left flgure.)-Iarge intra-calcaneal hone cyst of the body, with well-circumscribed borders. MRlof left foot tsee right figurej= intercsseous significantly lobulated calcaneal bone cyst with marked increasein signal intensity, indicative of high fluid content 011 T2-weighted image: signal intensity comparable to subcutaneous fat and adjacent intramedullary 1:-:_'!!~ 0'!! p!""0~0!! ctr:"~!~'~y-'l;'~~g..~r_~~ ~!:!!!g~_

Question: What is the most Iikely cause of the patient's hee 1 pain '?


Diagnosis: Intruosseous I ipoma of the calcaneus

Discussion: lntraosseous lipomas of the calcaneus are extremely rare. They ure mare commonly found in the lower extrernhy than the upper extremity. The bones most often affected are the metaphyseal regions of long bones such as the femur. tibia, and fibula. Irregular bones such as the spine and calcaneus, however. can be affected. The perce III age a f all bon e tu mors occ U rri n gin the foot is less than 2%. The majority of intraosseous lipomas of the calcaneus are typically found within the central portion or body. Though uncommon. tile diagnosis of calcaneal bone cyst should be considered in the differential dlagnosls of atypical heel pain.

The diagnosis of calcaneal bone cyst is based on the patient's history, clinical findings. physical exam, and radiologic evaluation. Ihere are many different etiologies of heel pain, Note that the accurate diagnosis of iiraosseous lipoma can lead to a proper and effecti ve treatment for the patient.

The present patient was taken 10 the operating room. and an excisional biopsy was performed

through II curved lateral incision over the calcaneus. A lateral cortical window was created over the underlying cystic lesion with 11 sagittal saw. The lipomatous lobular mass was removed en 1010 and sent to pathology for frozen specimen determinatlon and subsequent histologieal evaluation. The sclerotic wall of the cyst was aggressively curetted, The void was filled with "ground down" mixture of autogenic iliac bone graft and allogenic corricocancellous bone graft chips because of the large size of the iruracsseous deficit .. The cortical window was replaced and secured with an orthosorb pin. Closure was then performed in sequential fashion.

The patient was immobilized for approximately 6 weeks in a can. and then given a cam walker. Progressive weight-bearing began at approximately 8 weeks, and at the 3-month followlip the patient was almost 100% pain-free in his left foot. He returned to ful! activity without limitations, only occasional Iy experiencing discomfort in his left knee and fOOL if swelling occurred.

Clinical Pearls

I. There are several hypotheses, but the true enology of an intraosseous lipoma is nnknown.

1. The pain of intraosseous lipomas can vary from intermittent 10 constant, dull aching, Upon palpation there may be tenderness in the involved bone, and symptoms may last for years.

3. MRI and CT scan can be extremely helpful ill outlining the borders of the lesion and determining the extent of imraosseous involvement, They can also be very useful when pi anning (he surgical excision of the lesion.

4. There is a risk for pathological fracture of the calcaneus when a large tumor or intraosseous cyst is present. Therefore excislonal biopsy with curettage and bone grafting is often recommended.

5. Though the lesion is benign .. [he possibility of malignancy exists, either as a prim ary bone to mo r a r a secon dary area of metastases - es peci all y if there is cortic aI erosion or expansi ve destruction of surrounding tissues.


I. Bernstein AI.. Jacobs ,\ M: Cyst and cy,tlik" Tesion, M tho rOOL J Foot Surg ~4:3-t7. 1 Q3S.

2. Mli'grnm JW; lnrraosseous lipcmns: RadiologiC and parhotogic mnnifesrations. Rodintogy 167; 155-I(i(I, t998.

3. SChOlZ S G. Dtpaolu 10. D'Ag",UllOA el ul.Inrraosseous Ilpoma nf~l~e"\cancus. J FoO[ Ankl~ SLirg 31(-1): J8t-384. lW2.




A 24-year-old man with a crushed foot

A 24-year-old man relates a history of having his right foot crushed in a hydrolic jack-lift 2 days ago while al work. The patient had immediate pain and swelling and sought treatment through employee health. where x -rays revealed no fractures or dislocations of the right foot. As pain and numbness progressed, me patient sought additional medical advice.

Physical Examination: Vital signs: normal. General: mild distress. HEENT: normal, Cardiac: regular rate. no murmurs. Chest: clear breath sounds. Abdomen: sofe, nontcnder. Extremities: nonpalpable DP pu lse with II palpable posterior tibial pulse on right: 2 + nonpitti I1g edema to the medial forefoo; and. arch area: ecchyrnosi s extends from arch to hallux and firstinterspace. Neurological: decreased seusation {two-point discrimination, sharp and du II) dorsally. toes to ankle; all extensor tendon fimcliol1 intact, hut increased pain with passive ROM of roeextensors.

Laboratory Findings: Radiographs of right root: increased soft tissue density: 110 fractures or dislocations,

Questioll: What syndrome explains this patient's signs and symptoms?


Diagnosis: Compartment syndrome right foot

DiscItSSWII: Cornpartrnent syndromes of the upper and lower extremities are well-recognized complications of trauma. Eighty percentof compartment syndromes occur in the lower extremity. Aside trom trauma" other etiologies are fracture. musculoskeletal surgery, hematoma, and infection.

Early signs and symptoms are: pain (usually out of proportion 10 what is expected for the dinical situation); increased pain with passi ve stretch of tendons in the suspected areas of disorder-c-t he o steofasc ial compartments; the pre se nee 0 f pulses or. in severe or advanced cases, pulselessness; paresthesia, followed by hypoesthesia and anesthesia; pink (normal) capillary refill; and decreased sensation in the distribution atthe posterior tibial, deep peroneal, or superficial peroneal nerves via two-point discrimination. light touch. and pin prick. Note that the most reliable indicator of the syndrome i~ an inrrncornpartmental pressure > 30 mmHg as measured by II Wicks catheter.

Compartment syndrome begins with increased tissue pressure causing increased pressure on the vessel wal Is. Th is leads to increased venous pressure.a decreased arteriovenous gradient, and overall decreased local blood flow and llxygeoadon. After approximately 30 minutes of ischemia. paresthesia OCt:UfS. Within 2.-4 hours, functional changes occur in the involved muscles, resulting in paresis. In 4-12 hours. irreversible muscle deterioration begi ns, and in L 2 + hours. contractures [ann. After 24 hours marks the onset or rnyoglo-

biuurta, which. if unrecognized, can lead to acute renal failure.

Time is of the essence in diagnosing and treating compartment syndrome, as the late sequelae arc permanent dys functionand disfigurarion.

Treatment consists of removing all casts and dressings and keeping the limb at heart level, as elevation creates more ischemia and interferes with venous return. Hydration is also importam 10 help counteract the effects of myoglobinuria In severe. progressive compartment syndrome, surgical decompression is indicated via either a single or double incision that allows adequate decompression of the medial, interosseus, central. and lateral compartments (see figure).

ln the present patient, a surgical i ncisional release of the medial and central compartments resolved the syndrome.

Clinical Pearls

I, Remember the 7 Ps: pain. paresthesia, paralysis, pain on passi ve ROM. pulses or

pulse lessness, and pink.

2. Compartment pressures> ]0 mmHg are diagnostic of compartrnent syndrome.

3. Do [Jot elevate the I imb in question.

4. Hydrate the patiem to prevent myoglobinuria and acute renal failure,

5. The best treatment of compartment syndrome is Iascioromy.

6. Late-stage findings are drop foot, clawing of toes, and sensory and ischemic changes.


I, MrGlnml:)' E. Bnnk_, A. Dnwnoy M: Cump"'h""';"~Te~'b",,~,,[ Foa! S"r~e,.,.. 2nd eJ. Baltimore. :\oID. Wlllinm, & Wilkins. 19~2."

2. M~e""" M M.nllg<menL "f ccmpunrneru syndrornes of tho foot, elm Urtho v, Z71. lQ'II.



A 56.year-old woman with shooting posterior heel pain

A 56-year-old woman presents with J 5-mQ~tb history of posterior superior right heel pain. Initially .. she noticed sharp. shooting pain thll! was remitting. but it progressed to constant tenderness approximately 3-4 weeks mf!c.r the onset of initial. symptoms. IITi tat ing pai n, swelling. and tenderness. Me present with both arnbulaucn and nonweight-bearing. but are especially aggravated with activity. The pnrient denies any precipitating activity or history of trauma to the area. Conservative treatment CODsisted of unti- inflarnmarory medication. physical therapy, en 111 walker. and rest. with minimal relief of symptoms,

Physical Examination: Temperature 98.2," F: pulse 74: respirations 17; blood pressure 145/80.

HEENT: normal. Lungs: clear, Cardiac: regular. Abdomen: non tender. Skin: normal texnrre/rurgor/ temperature. Musculoskeletal: pain on palpution of posterior superior II~~CI of right calcaneus and Achilles tendon at its inseruon: slightly proximal, palpable osseous protuberance on superior posterior surface of right calcaneus; non render plantar fascia or plantar medial tubercle of calcaneus; no signs of crepitus on ROM of righr Addles tendon. bur positive discomfort on dorsiflexion and plantarflexion of right ankle: manual muscle resting of lower extremity =rlecreased plantarflexory power of the right ankle, all other muscle groups normal.

LaboralOry Findillg$: Radiographs of right foot/ankle: mild unhritic changes in ankle with talar neck lipping. decreased calcaneal inclination angle with mild prornineru posterior superior calcaneus {Haglund' s deformity}. prom] nent plantar calcaneal spur, M RI of right foot/ankle (see figure): lack of homogenicity with multiple intratendinous splits: intrarendinous fluid within Achilles tendon through multiple slices on ax ial view of T::!-weighted image; increased thickness of Achilles tendon Jnd decreased signal intensity within the tendon approxlrnarely 2-5 em from Achilles insertional area LIn T l-weighted image.

QU.f!stiOll: Whm is the most like! y cause of the patient's posterior superior heel pain"?


Diagnosis: Chronic Achilles tendon rupture with minor Haglund'j deformity

Discussion: Postenor superior heel pain can encorn puss many emil ies. Retrocalcaneal or retroAchilles bursitis. Haglund's deformity, Achilles tendon dysfunction or rupture. re trocalc aneal spurn ng or enthesopathy, and poss: ble fracture are some of the more commonentries in the differential diagnosis. A thorough history and physical.us well as plain-film radiography, bane scan, and 1VlRf can he Ip narrow your differential.

The diagnosis of chronic Achilles tendon tear is based on the patient'S symptoms, the physical exam, and, many rimes, rnagneric resonance imaging. There ure severn] hypotheses regarding the cause of Achilles tendon rupture. Sume of the more-recognized etiologies that have been linked. to the disorderinclude intratendinous steroid injections, mucoid degeneration and rnicrotears within the tendon. intensive physical training without proper warm-up, chronic tendinous inflammation or tenosynov his, and retrocalcaneal spurring.

When the d iagnosis of chronic Achi lies tendon ru ptu re is I he made. the ph ys ician most then irnplernent a treatment course. Conservative therapy i'~ often employed 11fSl. COil' isting of a cornbi nation of NSMDS. rest. physical therapy (such as phonophoresis. propriucepti ve exercises, U lirasound. iCI::_ whirlpool). accommodative paddlng, heel lifts, and functional orthotics. If conservati ve care is exhausted without illly signi licant relief in symptoms. then surgical intervention is usually undertaken. Surgical treatment typically involves tendon repair. recolysis. bursectomy, and excision of calcinosis and any bony prominences DS deemed appropriate. V MOllS surgical techniques and postoperative protocols that have been established and ref! ned over the years have proven effecti ve.

In the presen I patient. <I repuir of the Achilles was performed. along wirha resecuon of the rerrocalcaneal spur. She healed wei L and the pain resolved.

Clinical. Pearte

I. There are manytheories regarding rupture of the Achilles tendon. bUI the true elielegy is still unclear.

2. The Achilles tendon is different from other tendons inserting inro the Fom because il lacks a sy nov ial sheath, 1L has a paratenon instead,

3. The Achilles tendon has all area of decreased vascularity, known us the "watershed" area. This area is approximately 2-6 em proximal to the Achilles insertion and is part icu I ar Iy vu I nera b Ie to [<I ptu re.

4. MRl is very useful in determining Achilles tendon pathology, particularly in the axial and sagittal views.

5. Conservative therapy often fails to alleviate the symptorns associated with chronic Achilles tendon ruptures. Surgical intervention may be necessary.


1 Clement DB. Tauntun JE Srnar: GW: Achilles tendonitis and periiendoniris: Etiology and tn-arment. Am J Sports Mod 2.:

I ill-I t!4. 19~4.

~. M"ITulli N. Te:<10 V. Capasso G. Achill" tendon rupture in athletes: Histochemistry <lr Lh~ rnc epv "J'''' muscle, J p",,, An" kle SurIl3[Jl6J: 5211-53]. 191)\.

]. S >lX.no . .l,. Surgery r(or ch ron ic Ach illes tendon proble ms. J PQO [ Ank I ~ S" rg 34{31: ~ Q4- 300. I ~95



A 63-year-old woman with insulin-dependent diaaetes and non-healing ulcers

A 63-year-old woman presents with multiple small ulcerations on the dorsum of her right foot, The bases of the ulcers are necrotic and surrounded by periwound hyperpigmerned sclerotic plaque. The patient has :l long history of non-healing ulcers on the dorsum of her right foot. At age 61, an erythematous papule developed ill this same area. The lesion remained relatively stable for 12 months. but then began to erode and become inflamed. and she noted purulent drainage from the periphery of the lesion.

Physical Examination: Temperature 98.90 F: pulse 82; respirations 18; blood pressure I 88f89.

Skinrotherwise normal. HEENT: normal. Lungs: clear. Cardiac: normal. Abdomen: nonteader, Lower extremity: nonpalpable dorsalis pedis pulse on the right foot, all other pulses weakly palpable; diffuse tenderness noted over entire dorsal aspect of right foot: necrotic base of u leers. fibrinous wound edges. periwcund hyperpigrnented sclerotic plaques surrounded by erythema (see figure),

Laboratory Findings: WBC 11 ,OOOlfLl. hemoglobin 10 gfdl, Het 26.9% .. platelets 300J)OOf .... J.

Urinalysis normal,

QuesliOII: Whal is the etiology of the patient's ulcers?


Diagnosis: Necrobiosis lipoidica diaberlcorurn

Discussion: Necrobiosis lipoidica, according to Muller and Winkelmann, is a degenerative diseese of derm III connecti ve tis sue ch arac rerized el inically by an in.P.tammatory, pretibial. sclerodermatous plaque that is often associated with diabetes mellitus. Necrobiosis lipoidica is not directly reI ated to hy perglycerni a. but rather is a resu I! of deposits of lmrnunoglobullns and complement in the vessel walls. Ullman and Dahl suggest that the pathogenesis of necrobiosis is an immune complex vascu li ti s. Th isis S U pported by Hunde Ism an. who believes that a glycoprotein is deposited in the blood vessel walls and bel ween the co llage n bundl us. und thartraurna often determines the site of necrobiosis,

Pathological findings of necrobiosis include illdefined areas of fibrosis associated with granulomatous infiltrate with lymphocytes and plasma cells. H istologicatly there is palisadlng or histiocytes about the necrobiotic areas, especially 'in diabetic patients, who are more likely to have intimal thickening and perivascular f brosis of the middle and lower dermal vessels close to the necrobloue areas. Deposition of fat is also seen in th e uecrob iotic areas.

Necrobiosis lipoidlca usually begins as an erythematous papule or nodule. The lesion becomes a shiny. waxy. or yellow ish-red sclerotic plaque.

The central portion of the lesion becomes sligbtly scaly .atrophic. and depressed, and ulcerarlen may develop. The most common location for necrobiotic lesions is the pretibial region. They may also be mani festsd on the thighs. popliteal areas, and dorsum of reel and arms. The lesions tend to be multiple. bilateral, and symmetrical. Misdiagno- 5:i5 can OCCUf because of variation in size. shape. location, or inflammatory degenerative changes.

The di ff erential diagnos i s of neerob i milS li poi d ic a sho u Id i ncl ude sarco i d, gran uloma an nul are, stas is dermatitis. posttraumatic Ilbrosis with hernosiderosis. rheumatoid nodules. erythema induratum, ecthyma, nodular panniculitis, and xanthoma

Treatment of the lesion is quite controversial.

However. most agree that although this lesion is commonly seen in diabetic patients, complete contra! of the diabetes does not affect the course of the lesion,

The present patient had necrobios is lipoidica diabeticnrum that was secondarily infected by rnethyci llian-resi stan! Staphylococcus aureus. The patient underwent a popliteal-dorsalis pedis bypass to increase blood How to the involved area. The wounds were debrided intraoperatively, and a full course of vancomycin was completed, The patient went 00 to heal uneventfully.

Clinical Pearls

L Necrobiosis I ipoidica occurs in both diabetic and nondiabetic patients,

2. Development is not directly related to hyperglycemia"

3. Spontaneous resolution of lesions can occur after years of persistance.

4. Necrobiosis is most commonly found in the pretibial region; however, jt can occur on the thigh, popliteal fossa, dorsum of foot Of forearm. and other areas.


Campbell OR, Diobnk vascular disease. [11 Fr~kberg T~: The ['[igh-Risk Fcc: in Diabetes McUi!U •. New York. Churrhill Liv;ng,lone. 1991. pp 33-J8,



A 46-year-old man with a cyanotic hallux and .fifth toe

A 46-year-old man preSCIl1S with a 3-day hi story of increased cyanosis of the hallux and the fifth lot' plantarly, increased swelling, und eruptions of multiple bullae. The patient has a long history of drug and alcohol abuse am] was recently living in nn unheated, abandoned house. He was brought to the hospital by his mother for exacerbation of herpes zoster with secondary bacterial infection on his buttocks and bi lateral thi ghs. The patient had lost his third and fourth toes to frostbite 3 years earlier.

PllysicaIE.ramiIIQtioll: Temperature IOO.Et F: pulse 65: respirations 15: blood pressure 100168.

Skin: large eruptions of herpes zoster effecting mult iple derrnatomes on the back, bullocks. and posterior thighs. HEENT: normal. Lungs: clear. Cardiac: normal. Abdomen: non-tender. Lower extremity: pulses palpable in dorsal is pedis and posierior tibiul arteries; h31lUA and lateral digits cold. with .. yanosis: increased pedal edema' multiple bullae with clear fluid plantarly under digits (see figure): decreased ep icri tic, sh arp-dull, lind pro lee!i ve se 11 sa 1 i 011 b i I at era U y .

Laboratory Findings: WBe 90001f.l1. hcrnoglohln II g/dl, He! 29.9%. platelets 300.0001f,t1. Urinalysis: normal.

Que~·tion; What is the etiology of the patient's pedal presentation?


DiagIlQSIS,: Frostbite

Discussion: Frostbite is an injury that results frnrn exposing [he body 10 temperatures 01' 0 degrees or colder; peripheral tissue freeze ar the cellular level. Hayes et al suggest Ihm this leads [0 inflammation, free radical-induced tissue damage, vascular dcfic rencies, platelet function abnormalities, and ischemic-reperfusion injury,

The pathophysiology of frostbite has been attributed (0 IWO distinct mechanisms according to WeaTherly-White er al: (11 cellular death that occurs mihe lime of exposure, and (2) deterioration and necrosis attributable to progress] ve dermal ischemia.

Clinical manifestations of frostbite have been categorized according [0 Murphy et al into four degrees. First-deg;ree frostbite presents with a centralized whue plaque tbal is numb and SLIfrounded by erythema, Second-degree injury has blister with a clear or milky fluid and is surrounded by erythema and edema, Thlrd-degree i nj u ry is c haracreri zed by he rnorrh ag i c b lis! ers that result i n hurd. b I ae k esc bars 2 weeks I ater. Fourth-degree injury produces complete necrosis and tissue loss. However. this staging does nOI help in predicting the extent of tissue Joss.

Radiographic imaging can aid the physician in predicting (he leve I of demarcation or tissue loss. Plain radiographs can demonstrate soft tissue swell ing in early stages. and osteoporosis and periostitis in Mer stages. Gralino suggests that arteriography can demonstrate the slowing of flow and occ lusions that OCCILT. bur does no! adequately clarify the level of injury. Bone scan. according to Ikawa. has now become the standanlimaging study in the first few days of injury and can be used to guide 3 surgeonand allow earlier debridemerit of damaged areas. However. it does not

show "dear-cut" level uf demarcation. !vlR angiography has been suggc,ted to aid 1Il the accurucy of determining the level of demarcation; however. no srudies have yet been published ..

According to Murphy et 11.1. there ure three phases of treatment tor frostbite, First. in the preihaw phase. i I is i mperati ve 10 prorect the area involved from mechanical trauma or from slowed rewarming. Ln the second phase, rewarming. it is Important to rapidly rewarm the involved areas, Placing the involved extremities tn a 40- to -+2- degree waterbath with hexachlorophene or betadine for 15 to J(] minutes is the best way to accomplish this task. Acti ve motion of the inv 01 ved part is a!J,o recommended.

McC;]uley et al have recommended a protocol for the final. pesuhaw phase. Paramount are suppression oflocal and systemic thrornboxane. adequare analgesia, mid prevention of infection, Ibuprofen [a systemic inhibitor of rhromboxane) and aloe vera (a topical unthhromboxane), rombined with penicillin llild a vasodilater such as oxpentitylline. can improve tissue survival. Debridernent of clear blisters. which represent superficial injury, can reduce further contacr with the h igb levels of prostaglandin F2 and thromboxane A2 in the exudate, Hernorrhagic blisters that represent damage 10 the dermal plexus may benefit from aspiration: however. many believe they should be left intact.

The current patiem presented several days after injury: thus the prethaw and rapid rewarming phasescould no! be i nitiated, His clear blisters were debrided, and since prevention of infectiou was a priority. he was placedon cetazolin. The patient is scheduled for ccntinued totlow-upappoinunents to watch for level of demarcation.

Clinical Pearls

I. Managemeru of injury should include:

• Protection of the involved area prior to rewarming

• Rapid rewarming in 40- 10 4:!-degree Celsius waierbath with hexachlorophene or betadine for 15 to 30 minutes

• Triple therapy with ibuprofen, aloe vern. and penicillin,

2, Bone scan cal] aid Ul early detemunation of the level of demarcation.

J, Complete demarcation of the invol ved extrerni ty should be acquired before ~ urgical debridement is unernptcd -barring signs of infection.


\\'I::I,"Iihbum B: Frostbhe: \Vhlll is u, how ro prevent it. emergencj' treatment N~w EIL.11 J Y1e:.t.1 ~i']ib.l:n<l. 19tJ~_



A 46-year-old woman with a hot and swollen foot

A 46-yeur·oh.l wurnan presents 10 the emergency department with a red. hOI, and swollen fool that 's C-811Si ng her pai n. She states that over the course of 7 days the foot became massively edematous. red. nnd very warm. She denies any history of trauma. The patient has a past medical history ~igni ficant for insulin-dependent diabetes mell irus and hypertension.

Physical Exomination: Temperature 97.9" F: pulse 63: respirations 16; blood pressure 100/55, Skin, normal. HEENT: normal. Chest: clear. Cardiac: normal. Abdomen: nornender. Lower extremity: nonpalpable dorsalis pedis and posterior tibial pulses on left fOOL secondary 10 massive edema, audible with Doppler: left foot warm in comparison with contralateral side: grade 2 pitting edema from distal left foot to middle thud of left leg, Skin: large bullae on plantar distal left foot from submetatarsals 3 ttl 5; small hyperkerruotic lesion with hemorrhagic central area at submeiatursal 2,

Laboratory FindiNgs: WSC 13.0(0/).1-1. Hg I:! I. l-kI29,3. platelet 200.0001j.l1. Urinalysis: normal.

Qllestion: What is the etiology uf rhis root disorder?


Diagnosis.' Puncture wound with foreign bod)'

Disclluiol!: A variety or foreign bodies are common following a puncture wound, Seriou .... cernplicatlons can deve lop i f proper d iagnosl« and treatment are 1I0t established. Compllcatlons may include osteomyelitis, absces .... epidermoid inclusion cysts, septic art hri lis. gas gangrene .. sepsis, and possibly loss of limb or life.

Diagnosls 01' foreign budy cun be made with careful history and phyvical exam marion, Radiographic evaluation CIlIl reveal all metal fragrnents and most glass regardless of lead content. Tandberg confirmed Ihal all glass i1> vis ible rad icgruphically because the density of the glass is greater than that of the surround ing tissue. He ~hHJied 66 types of glass and concluded that heavy metals or pigments are n 01 required for rad ioopaci ry. Xe rornd i ogrs ph Y , ultrasonography. CT. and MR imaging can oc helpful ill defining small pieces of g I ass,

Detection of wood with standard radiograph, is difficult. Studie-, by Charney and Woesner tompared the use of standard radiography and xeroradiography. The results of Charney', work centradieted thai of Wnesner, Po, ilion of the fragment was determined to be the most important factor for visualization, Wood is nest seen with MRL The inflammatory capsule produced by the body in response to the foreign wood hngmem is seen easily on T2-weighted images,

The first step in management 01 foreign bodies is removal of the offensi ve agent. This can be accomplished at beside if the wound is superficial, or in the operating room if nccessary, The puncture tract should be reopened and explored. AU devital ized tissue and foreign bod ies should be removed, If an abscess is pre,e~ I. surgical i ncision

and drninagc are required. The area should then be x-ruyed ag.ain to ,,,~ure that all foreign substances were removed. Pack [he wound to allow drainage and prevc n! prematu re closure, Cultures should be taken at the lime of surgical debridement to identi fy I he causative agent and allow for proper seleer ion of an! ibiol ic therapy.

The second step i .... selecting the appropriate antibiotics until 11llal' culture resu lrs can be obtained" The most common infective agents ill 3 puncture wound \II' i 111 ce llulitis ,11e SWplt_V/OCOt'CIIS £It/rerIS. alphu-hernolytic streptococci, Staplrylococcus epidermidis, Escherichia coli, ilnd Proteus. The most common organism found in puncture wounds with osteomyelitis is Pseudomonas ueruginosa. Cefazol i n, umpic i I [i n/su lbuctarn, ticarcillinrclavulanic a . cid, or clindarnycin for puncture wounds associated withee llul iii s are recorn mended. If os teomyelitis is suspected. cettazidirne or ciprorloxacin ure excellent choices.

In the present patient. glass embedded in the base uf the wound probed deeply (0 the dorsal surI'ac~ of ihe foot. An ab,ces, wus localed plantarly from the second merararsal to the fifth, The patient was owned on empiric antibiotics (injected cefazolln and rnetrouidazole) and taken to the operating room for immediute incision and drainage. At the lime ot surgery, a small piece of glass was removed I'rom tile wound. The area was packed open, and the parienr recei ved dressing changes twice II (jay, Her culture result, carne back posirive for coagulase-negative staphylococci (multi-drug resistant] and enterococci. The patient's antibiotics were dunged 10 vancomycin for a 2-lVeek course. She went en to heal uneventfully,

Clinical Pearls

I. Once rne diagnosis IJ F osreomyel il is w ith puncture wound is made, the Treatment must be swift.

2. Superhcial wounds CUD be treaiedwith local wound care, Deep wounds should be completed explored and debrided, When in doubt. open it up.

J. Convert the contaminated wound to a clean wound.

4. Prevent tetanus: consider one dose of tetanus immune glnbulill for all wounds that are SUSplC ious and not clean.


I. Cbnmey DB. Mn.n:iI'_j J.\I ~1 al. NUI'lIL1dJHil,.' t"OTi!'ign bL~l1;ll~ in lhl'! fnLl~: R fI_llir''w'''ph: versus '~lllrrHJjugruphy J Foot Surg

25;~9, I'JM,

2. P;<z2-"roJd R. COW"" J: Puncture ","""J, ul 11i< toot. Drthup Clm North \m b,%5-~71. 1975.

j" Inh.an5GT1 r~ Pseudomonas if! feet ton'S of (h~ fOOl folJuwin~ 1)tJJ1CLUrt: wounds. J.AMA ~~J.l: 170 11'1. I c)()8. 4, Joseph WS, Handbook 01 Lower E\<",mily !nhl"ln' !'-lev. Y",l. Churchill L"ing""ne. )<1')0.



A 22-yea.r-old man with pain in his third toe

A 22-year-old man presents with pain in his left third digit. He was jumping off a diving board when he felt a "snap" in this me. He had pain immediately following this sensation and had difficulty moving the LOC. The patient is healthy, with no past medical history.

Physical Examination: Temperature 98.6" F, pulse 65, respirations 15, blood pressure 100/68.

Lower extremity: pulses palpable b ilarerally, left third digit sl ightly edematous and erythematous; pain on palpation of distal aspect of third proximal phalanx: pain with range of motion of proximal interphalangeal joint,

Laboratory Findings: WBC 5000/ .... 1. Hg 16. He! 36.9, platelets 300.0001 .... 1. Urinal), is: normal.

Question: What i~ the etiology of the patient's pain?


Diagnosis: Enchondroma with pathologic Iracrure

Discussion: An enchondroma is u tumor that develops in the rned uUary cavity and is composed of lobules of hyaline cartilage. The neoplasm is usually discovered in the third to fourth decade of life. I! is seen equally in men and women. Solitary enchondromas are usually asymptomatic and are therefore diagnosed a" an incidental finding on radicgrapb or bone scan, Resnick suggests that pain associated with a lesion can be suggestive of malignant transformation - a complication that is more commonly noted in the long tubular bones.

According to a study by Arata er al., enchondromas represent about 3 % percent of biopsyanalyzed primary bone rumors, Resnick and Marco et al state rhat approximately 40-65% of solitary enchondromas occur in the hands or the feel. It is one of the most common tumors found in the fOOL Arata et al, suggest, however. that the most common sites of involvement in order of decreasing frequency are diaphysis, rnetadiaphysis of the femur (40%). humurus, tibia .. and shan tubular bones of the hands and feet. Less common sites inc! ude the ribs. radius. fibula, ulna. and pelv is. Some enchondromas lead to osseo us expansion renchoncroma prorube rans ) ilia! simulates till: appcarance of an osteochondroma.

&.-lJjug.ti1l1hi~ c.\.titrUutiUU/I, ~ U.~t...:l 't~ uy lVllucu et al, reveals a well-defined, medullary lesion with stippled cnleification .. a lobulated contour. and endosteal scallo pi ng. Lesions may de monstraie coni-

cal ex pans i on JIl d pathologic frac I UTe. MRJ Fe veals a well-circumscribed lesion of low signa! intensity in Tl -weighted images and of high signal intensity in T2-weighted images. Calcifications may appear as regions of low signal Imensity,

Most enchondromas consist microscopically of lobules of hyaline-type cartilage. They also conlain calcified regions in which the cell, may appear degenerative or necrotic.

Marco et al slate that enchondromas in the small tubular bones or the hands and feet rarely transform into chondrosarcomas, which are the usual result of malignancy, Malignant transformation is more likely in enchondromas in the long tubular or flat bones. lndicaticns of malignant transformation inc! ude an en larging rad iol ucent area. cortical ex puns ion. pathologic fracture. soft tissue mass. and d isappearunce of pre-ell. isti ng calc i Ii carien,

The present patient sustained a pathologic fracture ofa previously undiagnosed enchondroma, He was taken to the operating room where the dorsal cortex of the third proximal phalanx was penetrated by U CLI rene, The enc hondro rna was ~ vacua ted and sent fur frozen section. which demonstrated ~I benign cartilaginous tumor. A burr was used to re•• III V" ""}' ''''''l!i"j''g u.'IJe.:l, Llf ii.le .:urliil!l;liuuu~ iumar form the inner lining. The bone was Hu.shed and packed wi.tlt corticocanceilous bone chips. The patient went an to heul uneventfully.

Clinical Pearls

I. Enchondromas life found equally in men and women, generally in the tbird and fourth decades of life.

2. Enchondromas are most often asymptomatic.

3. These tumors are most commonly found in the bands and feet, but are also seen in the femur. tibia. and humerus.

4. Enchondromas t-hat are painful or sustain a fracture should be biopsied ro rule out malignant transformation.


I. Arata MA Peterson lA. Dahlin [)('; Pathologic Iracrurc through non-ossrfymg nbrornus. I Bone 1",", Su'll ~ 'A:\lM-9l1B.


2, Marco RA. Gilelis 5 .• 1 ul: Cartilage rumors: Evaluauon and treatment. J Am A'"ad Ortho Surg 8!~1:192-J04_ ~lJIl(].

3 Re.ni<.k c.<;. L., in" ,\M. et ;11: Case Report S 22: Concurrent odJocem csteuchoudroma WId enchondroma, Skel Rudiol lSI I 1,66-69. t 989,



A 33-)'car-old woman with 8 painful right ankle

A 33-year-old woman presents witha chief cornplairu of pain on the lateral aspect of her light ankle. The pain has been present For about :!. weeks and MJ a relatively acute onset. The patient. who is an avid runner. stated that she was in the middle of a IO-mile run when she began to experience "signiricant pain" in her outer ankle, which prevented her from finishing the run. Currently. she is unable to run because the pain is too intense during exercise, The patient's past medical history is unremark.ible, and her only medication i~ oral contraceptives.

Physical Examination: Vital signs: normal. Skin: mild localized edema at lateral right ankle; no ecchymosis or open Ie. ions present. Musculoskeletal: tenderness on palpation of right lateral malleolus and right distal fibula; tenderness on palpation of peroneal tendons. posterior to right lateral mulleolus, ROM: normal right ankle. subtalar. and midtarsal joints: tenderness on resistance against eversion of subtalnr joint. 0 gro!>~ orthopedic rnalalignment noted.

l.aboratory Findings: Radiographs: no occult fractures or other osseous lesions of distal right rihula. 1vIRI: distal third of right fibula included both II. linear decreased intensity Oil T l-weighted im- 3ge and a localized increased inrensuy on T2 in same area.

Question: What is the likely cause of the patienr's right ankle pam?


DiagllO~'is: Stress fracture of right Iibul [I

DisrIlH'!OII: Stress fractures are fairly common clinical entities encountered in podiatric medical practice. They ore generally the result of a repetitive, sub-threshold amou nt of load on a bone. Theload. which represents abnormal stress on 1I1l otherw ise normal bone. can be a re-u It of ground reactive forces or cycl ic tension from tendinous arid ligamentous artachrnenrs. Similar in outcome but different in cause are i nsufriciency fractures, which rei me to normal stresses placed upon an abnormal bone Insufficiency fractures are seen in pauenrs with osteoporosis, osreornalucia, Paget's disease, and other metabolic bone disorders.

Stress Iracru res can be see n in I he metatarsal s, calcaneus. fibula. tibia, femur. navicular. sesamoid. and other bones of the lower extrernlry and, le~~ Irequeruly, in some. bones of the upper extremity, They generally occur in the physically active. e,pecially in runners. Several factors coutribme to the development of stress fractures. The most common factor is trai ni ng error; for examp le, a sign I licaur increase in training distance- ur n decrease in iniervals between long runs, Mare intense traini ng allows little lime for the affected bone to udapt physio I ogically to the inc re ased s rres se s p laced upon i I. Other factors are rigid running surfaces, pour shoe gear, and poor physical fitness. A narorn ic malalignments such as limb length discrepancies, byperpronmicn . and rigid ell. vus feet also may lead to stress fracru res.

Diagnosis can at limes be a difficult problem. bUI several signs and symptoms are helpful. The patient'S history usually includes an insidrous onset of symptoms while training, The pain is LI,Ually relieved with cessation of activity. Further questioning of the patient may uncover recent changes in tra in ing habits. such JS higher mileage, different running surfaces.or new sneakers. Phy~" ical exam may reveal an abnormal gail, pain on palpation over the affeeu"d area, and localized warmth.

Confi rmation of stress fracture generally re-


ljui res a rad iograph, bone scan, or /viR r. Recent <tress fractures may nOI appear 00 x-ray, as osseous changes require 1-3 weeks to register 011 f Lm. Some rad io graphic s i g ns i ncl ude peri as leal reaction, a srnal] break in the bone cortex, and/or a foc'~l area of'sclernsis. Stress traetures within the cortical portion uf long bone usua lIy show a periosteal reaction: in the metaphyseal portion, which i> mnde of cancellous bone. they show 11 sclerotic li lie.

Patients wi til a suspicious cl inical presentation bur no evidence of stres fracture on conventionel x-rny require more sensiti ve and specific testing. Bone scans rernai n ;l_ good option for diagnosing a stress Iructure, They are highl y sensi ti ve for bone turnover and are positive long before an x-ray. They 11111 ,how an increased area nf 11 ptake in the ureu of the fracture. Bmw scans are sensiri ve bur not specific for fracture, and positive resulrs ~0I11d be due [0 malignancy and bone infection,

MRI has become 3 more popular modality for diagnosing '\IT~S" fracture In the present patient, M Rl waschosen because of her son tissue symproms, including peroneal tendonitis, which can be ruled out using this modality, In this case, the T2- weigh led image showed increased intens-ity within the medullary canal of the fibula, and the TI image showed a trnusverse line of nypoinren~il)' with a cortical break iD the same area,

Trearrnent of stress fractures is much easier when an early diagnosis is made, Early on. simple res! may go a long. w~y toward relieving tile symptoms. Tim, along with ice and NSAIDs. can be sufficient to allow tile bone to heal, If a later diaguosis is made. urunobilizatiou of the affected area may be required, Some bones affected by a stress fracture may require more aggressive therapy, such as surgical Ii xation, because 0 f their poor healing ability; these include the base of tile fifth me ratars a I. the na vicular, and the scaphoid in [he hand, Once the SI ress fracture is healed. it is i rnperative For the athlete 10 change the training habits thar leu to the fracture.

Clinical Pearls

I. Radiographs may be negative immediately following the injury. Two to three weeks later. a periosteal rene-lion may be visualized.

2. Bone scan is serisiti vc, bUI not specific,

3. MRI shows a linear decrease in uuensuy on Tl and increased intensity on 1'2- weighted image».


McBryde AM: Sire" fractures in IIlhlete's_l Sport Mod 3:2 T !-17. 1975.

2_ Santi M, Sartoris DJ. Resnick D: Mngneuc resunnnre imaging in [he diugnn.;, of metatarsal mess fractures. J FOOl Surg 27: 111-77,1988_

~_ Tuunton lE. et.ul: LOWl:r extremlty stress fracture in arhletes PhY' Sports Mod 9: 77-83, 1981_

4. Wil,on E. Kiln F: Stress frnerurcs An analysis of250 consecuti ve cases. Radiology 92: 4HI-86, 1969.



A 56-year-old man with a traumatic Injury to his ankle

A 56.year·old man presents to the emergency department (ED) immediately I'ollowing a traumatic incident to his right ankle. The patient was walking all the sidewalk when his right foot hila steel elevation in the sidewalk. His was body propelled forward while hi~ foci remained planted, He b currently unable to bear weight all that foot. The patient's medical history is noncontributory. but he does mention 3 right ankle sprai n 40 years earl ier.

Physical Examination: Skin: moderate swelling; no ecchymos is. M u sculoskeletal: pain on palpation to anterior aspect of ankle joint. which extended to botb malleoli; pain on attempted range of motion (ROM). Due to severity of pain. talar lilt and anterior drawer tests not performed.

Laboratory Findings: Radiographs: increased soft tissue density m anterior aspect of ankle joint; avu lsion fiecks off of lateral malleolus; i ncidental anterior ankle joi nt arthritis with spur formaLion. No overt fractures roankle, no osteochondral lesions noticed, and no oi slocauons. Ankle joint in good alignment, and medial clear space normal.

Course: The patient was placed ill 11 Jones' compression C!Il;[ and lolt.l [0 take ibuprofen for the pain and inflammation, He W:1:5 also informed about the principles of rest. ice. compression. and elevation. Finally. he was given crutches, with the direction to be nonweight-bearlng until hi~ fellow-up appointment with his podiatrist. The patient returned 1.5 weeks lnter using crutch assistance, He admined to removing the compression cast 2 days after its applicaucn due [a discomfort. At that rime. he had swelling and ecchy rnosis about the ankle joint, mostly lateral. There was continuation of pain on ROM of the ankle joint and with supination of the subralar joint. An M RI was ordered.

,'vIRJ Fir/dings: Partial rears of anterior and posterior ralofibular ligaments. with joint effusion through these defects. Calcaneal fibular ligament could not be visual ized on any of M RT cuts. and extent of pathology cou ld not be appreci ated, Deltoid ligaments intact; no abnorrnallties of tibioralar and subralar joints.

Qllfstion." What is the best treatment option for this injury?


Answer: Removal of bone flecks and rcattuchrnent of ligaments

Discussion: Ankle trauma, which displays as ankle pain. edema. and ecchymosis, is very COIllman. Studies have shown that up to ]2% of patients with lateral ankle trauma have recurrences: thus, there is a need for lateral unkle stabilization and fixation. Awareness of the angles formed by the oriental ion of the Ii gnments and their relation to the ankle and subtalar joint axes is crucial for understanding the mechanics of ankle sprains.

As the foot moves through its rnnge of motion during gait. the anterior talofibular ligament is mostly used 10 resisl inversion when the ankle is plantarflexed and the ligament is parallel to the fibula, The calcaneofibular ligament. being the only lateralcollateral llgament to pass the ankle joim and subtalar joi Ill, lies nearl y parall el toth e s u btal ar joi n 1 axis and allows unrestricted motion in the subtalar

jo i n L The more the lie Ii g am e nrs are spra i ned" th e weaker they become. and they will not bt:Jble to resist the forces coming across the unkle and subialar joints. Intraoperative repair i~ required for both recurrence of ankle sprains and a single traumatic event obliterming the ankle joint ligaments.

In the present pauem, arthroscopy showed ucute synovitis between the inferior tibial surface and the lateral malleolus LInd cartilage damage within the rigtu ankle joint. The anterior ru lofibular llgament of the lateral ankle joint was partially tom, lind the calcaneal fibular and posterior fibular I igaments could no! be \' isual ized, There were avulsion frnClllres off ofboth the anterior talofibular and calcaneal fibular ligamerus. The avulsed pieces Of bone were removed. and the ligaments were. reattached using PEBA anchors.

Clinical Pearls

1_ When examining patients with ankle injuries. take extru time 10 carefully scrurimze t.he ankle joint for ligament tears and fractures. Also perform a complete examinaLion to rule out any fractu res Of dislocations.

2. Radiographic evidence of bone flecks inferior La the lateral malleolus is highly suggestive of avulsion fractures in the Iigarnerus about the ankle joint.

3. \\liRl studies are 1101 always completely accurate and should not be the unly mudaliry used for diagnosis. Take into account the mechanism of injury. the clinical ~nding,. and the radiographic stud ies to help corroborate your Ii ndi ngs,

4. If surgery is needed. intraoperative visualization of the injury is the best way 10 make your final diagnosis.


Harniltnn W: The moJifi .. -d Bronstrnrn procedure f~" lateral unkle instability, Fno, An).!. 1+111: 1-7 19'101.

1. Perlman M- Inversion lateral ,nkle trauma Differennul diagnosis. review "rille llterruure, "nd ~""p<!C(j ve -rudy, J Foot Surg 16(2): 95-129. 1987_



A 44-yeur-old woman with rlght fool pain of insidious onset

A 44-year-old woman presents 10 the office with a cornplaint of pain in the dorsal aspecr of her right 1'001 for" period of 2 rnoruhs. She relates a somewhat insidious onset. as well as radiation of pain and some occasional nngl ing into her third and fourth toes. The pain is generally present while the palien! is ambulating, and it feels better when "he rests. She was seen at an emergency department approximately 2 weeks prior. with severe pain in the same fcot, Radiographs taken at thm lime revealed no osseous deformity Past medical history is ,ignilkant for depression. Her only medication Is Prozac, The patient IS allergic to codeine, penicillin, and sulfa drugs. She denies tobacco and alcohol use,

Physical Examination: General: no apparent distress. Lower extremities: bilateral palpable pedal pulses: normal capillary refill lime: no edema of the right foot, Skin: no open lesions; normal color/tu rgOT/lex ture: no erythema .. Museu loskeletal palpation of right tOOl caused pain between 2nd unci 3rcl metatarsals just proxunul to metatarsal heads, radiating into ::'nd and 3rd toes: lateral cumpression ofmedial and lateral Ioot caused pain in second interspace: palpation at base uf2nd. metatarsal and plantarflex ion of Lisfranc" s joint alsocaused pain. Neurologic: decreased sensation to light touch and pain along lateral aspect of 2nd digit and medial a ... peer of 3nl digit..

Laboratory Findings: Radiograph I see I1gmeJ and MRI of right foot: bone defect at base of second metatarsal: false motion when put through ROM under fluoroscopy: sclerosed bone ends developing at base of second metatarsal.

Question: What is the cause or causes of the patient' s pain?


Diagnosls: Neuroma ami fracture non union or 2nd metatarsal

Distus s iOIl: The initi aI impress ion on first exarninmg !his parient led the physician [0 lean toward n diagnosis of neuroma of the 2nd interspace, However, palpation of the 2nd metatarsal directly reveal ed pain that was more cons i s tent wi th a stress or occult fracture of the 2nd metatarsal. The x-ray of the foot demonstrated a sclerotic area and II periosteal reaction at the base of the 2nd metatarsal. Because of the possibility of a concomitant neuroma, it was decided that MR1 would be the best choice to visualize both the neuroma and the metatarsal fracture, The MRI showed increased signal intensity within the marrow of the 2nd metatarsal base on the T2-weighte.d image and an enlarged interdigital nerve in the 2nd interspace,

With over 2 million bone fractures in tbe U.S. each year, there is about 5% incidence of nonunions and even more delayed unions. There is not a distinct line Clinically and radiographically that delin[',31CS a nonunion from a delayed union. Generally. the diagnosis of a delayed union is made when a fracture bas not advanced at an average rate of healin g for a particular type and location 0 f fracture, This time frame is usually J-6 months, but is variable depending on the bone and type of fracture. A nenunlen diagnosis requires evidence either clinically or OD x·ray that healing has ceased and union across the fracture site is highly unlikely. The FDA has further class i fied II nonunion as a fracture th at has failed to completely heal after a minimum of 9 months. and healing has nOI progressed radiographically for a period of 3 months.

Delayed union and nonunion can be due to both local and systemic factors. Systemic factors inelude the patient's nutritional status, activity level. and even tobacco use, which has been shown ro have a very detrimental effeci on bone healing. Local factors include motion at the fracture site, inadequate fixation, open fractures. cornminuted fractures, and impaired blood supply.

Nonunions have been divided into two types

based on the viabili ty of the fracture ends. First is the hypervascular (or hypertrophic) type, in which the bone end is viable and capable of healing. This is eli lferent from the avascular (or atrophic) type, which has a nonviable bone end and 00 chance of biologic reaction. Hypertrophic nnnunions can be further eli vided into the elephant foot, horsehoof, and oligotrophic types. and avascular nommions are separated into the comminuted, torsion-wedge, defect, and atrophic types. These subdivisions are based on the blood supply-or lack thereof-supplying the bone ends.

Treatment of delayed unions in most cases can be as simple as jmmobillzarion of the fracture fragments. Electrical stimulation to accelerate the union has become popular when immobilization ts insufficient to complete the consolidation. The placement of II bone stimulator causes a steadystate potential around the bone fragments, with the electronegative side stimulating osteogenesis.

Nonunions require II more aggressive treatment proroco I because rh e y have 1 i ttie or no ch anee of healing due !O a rlysvascular state. Such treatment is generally surgical in nature. Because the hone ends are dysvascular, they must be resectedand then rigid Iy fixated 10 have any chance of healing. The repair generally requires some type of bone grafting to maintain the length of the repaired bone. Bone grafting techniques vary greatly (e.g., in lay bone grafts. onlay bone grafts). Once the procedure is completed, the repaired bone must be completely immobilized. and II bone stimulator is used to hasten cnnsolldation. This procedure can lake up to 4-6 months for complete healing.

The present patient underwent SUrgical reseclion of the dysvascular bone ends; a bone graft was placed between the two ends; and the area. was immobilized with internal fixation. Sbe was placed in II below-knee cast and was instructed to remain non-weight bearing for a total of 6 weeks. The patient went on [0 heal uneventfully.


Clinical Pearls

I. A nonunion i. chara terized by:

A bone defect False motion

Sclerosis of bone ends

Rounding und mushrooming (If bone ends Sell I ing of bone ~ nds w ith com pact bone.

2. Ccntruindicauons 10 the use of electrostl I1lU larion in the rreatment of nonun ions arc:

Synov iul pseudoarthrosis

BOlle gap greater than half [he dia meier of the bone Bone gap greater than I em

Uncontrollable morlon


Bri1\hlon C'f' Principl e of tracture heulinj:. lnsrr Courve L",·t JN~I. 1')8~



A 60-year-old woman with a continually aching arch

A 60-yeaN)ld woman presents with a complaint of increasing tenderness in the medial' aspect of her right ankle for a period of 3 months. The painoccasionally radiates distally into her foot, and generaJly increases while ambulating and during prolonged periods of acti viry, She relates no antecedent WIU rna thai led to the onset of the pain. Further quest ioning reveals that she noticed a progressive .tlontening of the arch over the past several months. There has been no treatment to dale. except for acetaminophen for the pain, wh ich 'provided I i HII' rel ie r, Past medical history i riel UdC1 hypertens len and acid r-eflux; medications included metoprolol and orneprazole, She has no known drug allergies. and her only previous surgery was right foot bunionectorny without complication.

Physical Examination: General: no apparent distress. Lower Extremities: patpable pedal pulses hilarerall y: normal capi llary fill time, with some mild edema along medial uspecr of right ank le. Sk in: no ecchymosis: no open lesions; color, turgor, and texture normal. Musculoskeletul: .:om,i,kmble tenderness along course of posterior from just behind medial rnalleolous to its insertion nr navicular: normal ROM at ankle joint and subtalar and midtarsal joints; manualmuscle testing revealed all groups full strength.except some weakness of foot and pain on resistance against inversion: a bducted forefoot on rearfooi, especially on right foot: positive heel rise test with obvious inability to rise up on toes, Neurologic: all sensation grossly intact: negative Tinel's sign in tarsal tunnel.

Loboratory Findings: MR1: thickening of tibialis posterior tendon: increased signal circumferenrially, with tendon sheath effusion; increased inrratendinous signal. Radiographs (lateral view, see ligure): loss in tcngjtudinal arch, with 11rsl ray elevatus and break in cyrna line: en plaruarflexion of talus, calcaneal inc! ination approached parallel weight-bearing surface: no osreoarthn tic f no..! ings,

Qlle.stioll: What is causing the medial. ankle pain?


Diagnosis: Posienor tibial tendon dysfunction

Discu ssion: Posterior tibial I 1'1'\ tendon dysfunction hi.l~ been clingnu,eJ more frequently over the past several years, Previously, it was commonly misdiagnosed ,11" at least under-diagnosed, A recent surge in published 'lI1i(.·j,.!.> about this disorder has led 10 more ready recogniuori uf its signs and symptoms.

The tendon's main function is help resist and s low rearfoot eversion upon hce 1 stri ke duri ng the stance phase of gait, As the fOOL progresses into mill-stance, the tendon hel ps lock the 111 idtursal Joint and begins contract i I'Ig to cause su bralar joi nt i nversion. Finally. I n I he propu bi ve phase of gail the tendon acce lerates subtul nr joi nt i nversion ends in heel lift. So, simply rUI, the posterior lih~ ial tendon is the mum inverter of the rom and is largely respnnsible I'm muintaiuing arch heig.ht.

There has been -ome controversy as 10 the cause of IT tendon dysfuncrlcn II generally involves a degenerm ionuithe tendon from ~ multirude of causes, each of II hich is usually mulrlfactorial in nature Some structural abnormaliries. 310nc or in combinntinn, which may lead 10 PT tendon dysfunction inrl ude <111 accessory n;\ v leular, rigid or ltexible flatfoot. and equinus, These dlsorders. along with a possible lone nf relative dysvascu laruy with 111 the tendon bet w een the medi al malleolus und the tendon insertion, lead LO degeneration within the london. As the tendon degenerates it begin. to slowly elongate and eventually lost', mechanical advantage. This los, or rnechan real advnrnage allows the peroneus brevis to gain advantage and causes loss of arch height and midtarsal joint break,

Various classi fications and SI aging s ysterns have been proposed for the progression of the deformity, Stage 1 is mnsidcrell an asymptomatic period. during which the pauem has nething more than an underlying s true rura I or anatomic ahnorrnality that predisposes him or her 10 the development of PT tendon dys fun ct ion. As the patient progresses into slage 2. symptoms develop that bring I hem [0 your office. S yrnptorns include 11:11- dinitis, some effusion behind the medial malleolus. and progression ot ;1 flat fOOl deformity. The


patient will have tenderness along the course of rhe tendon. abduction of the lorefoot, and failure to successfully rise up on the toes on one side. Stage 3 is similar to stage 2. bUI with more disnbling symptoms and greater degeneration within the tendon [e.g .. longitudinal tears or partial ruptures), Finally, in stage 4, the patient begins to experience join! adaptation nnd functional disability.

Diagnosis can generally be made from the patient's history nml a good clinical exam. Radingmphs can be useful to assess joint adaptations in later stages of dysfuncticn u nd are useful in surgical pi ann ing. The Iv! RI has become a useful [001 10 assess the pathology within lile tendon, determining whether II simple tenosynovitis oxists or whether the dysfunction has progressed [0 mid~lIbsI31K·e tears and partial ruptures. MRI also may aid in surgical plann ing.

Treatment is generally based on the stage of dysfunction. Mild stage I dysfunction in some patients Gill be treated conservatively. The underlying blorncchanicnl abnormality mUSI be controlled to prevent further progression of the deformity. This is generally accomplished with some type of orthotic device with a high degree of varus posting. NSAIDs iUld physical therapy may have some benefit as well. Once the dysfunction progresses into the later Singes, surgery becomes the only viable option. Surgicalintervention (see f g II re 1 SUI rt ~ w i th direct tendon re pair and pmgresses to tendon transfers and finally to bony reconstruction. inc Iudi ng calcaneal osteotomies and subtalar arthroereisis procedures. with the last step being a triple arthrodesis,

Early and accurate diagnosis is paramount to prevent progression of deformity into the later stages of posterior tibial tendon dysfunction. The present patient had direct surgical repair or the tendon. A synovectomy was performed along with repair of the longitudinal fears that were found intraoperarively. The patient was immobilized in 3 short leg cast for :l. period of 4 weeks. lIpon removal of [he cast. she was provided cuslorn-molded orthoses, and healed uneventfully.

Clinical Pear.ls

I. [0 the early stages of posterior tibial tendon dysfunction, patients describe an ache along the inner side of the foot, with a moderate amount of warmth between the malleolus and the navicular.

2. When looking directly at the foot from behind, you wi!! note the too-many-toes sigll-lhe foot is abducted, and the toes are seen laterally.

3. The patient has difficulty standing on the toes and usually is surprised not 10 have noticed i L earl ier,

4. Simply resisting active inversion in the rronweight-bearing position uSllally elicits pain along the PT tendon.

5. MRI can show inrrasubstance tears even in the early stages.


t. Rosenberg Zs. Cheung Y: Rupture of the postericr tibial iendcn: CT and MRI With surgical onrrelanon, Radiology 169:219~2J5. 19B8.

1. S;:OIlOriS OJ. R",nick 0: Magn"lic resonance Imaglng of tendons in the foot and ankle, J FOOl Surg 28:310-377, 1989.



A 52-year-old woman with a painful bump on her foot

A 52-yeur-old woman presents with a painful bump on the dorsomedial aspect of her right root. It has been present for many years and has grown slightly during this time, but has never been painful. It is now especially uncomfortable in tight shoe gear. There has been no trauma to the Foot thai could ha VI' led \0 development of the bump. The patiem has changed shoe gear in an uuernpt to accommodate the lesion. She denies the presence of other soft-tissue masses elsewhere on her body. There is no !;igni Iicant past medical history; the patient is not laking tiDy medications: and she has no known drug allergies, Reviewof systems is negative for fever/chills/night sweats, recent weight loss. cough and shortness of breath .. nausea/vorniring. and diarrhea or consti parion.

Physical Examination: Pedal pulses: bilateral palpable. Vascular: capillary refill time normal.

Skin: no edema, normal temperature. Palpation: firm and freely movable mass. approxirnarely 3 em X I em, on dorsomedial aspect of right fooi: location just lateral to tibia lis anterior tendon (no! within tendon). Aspiration: no fluid within mass.

Labora.tory Findings: Radiograph (right lootj: soft-tissue swelling over dcrsomedial aspect: cortex of first metatarsal and medial cuneiform intact .. will] no periosteal reaction or invasion; no ossitication within lesion.

Question: Considering the histolngic findings. what is your diagnosis?


Diagnosis: Benign fibrous hisriocytcrna

Discussion: This is a common soft-tissue les ion Lll at has a lso been re t·c rred loa S 11 dermuto r1- broma or sclerosing hemangioma. It is most commonly found all the lower extremity and has a higher incidence in women, 11 usually comes about o.Ifter some type of innocuous trauma: some have proposed that an insect bite is causative. Thelesion generally is a firm papule or nodule varying in size from 3 [0 10 em. The color is quite variable.

A somewhat pathognomonic sign of a dermatofibroma i~ the so-called dimple slgn. When the lesion is squeezed between - the forefinger and thumb. a. chamcteristic dimple is produced

in the center of the lesion, This dimple is caused by tile tethering of the lesion to the overlying epidermis.

Generally. the leslon causes no symptoms that would require it, excision. and it frequently regresses in size. In those raw cases when pain is persistent. the lesion can be excised.

The present patient underwent an excisional biopsy. The lesion WIJ:.> excised in toto and sent to pathology. where it was revealed to be a fibrous histiocytoma. This lesion's large size required a skin Rap closure after exci sion, due to the redundant skin that remained follow ing its removal.

Clinical Pearls

l. Histiocytomas can be confused with melanomas because of the change in skin color,

2. Histiocytornas are ,1 variety of dermatofibromas, which are rare ly mal ignant.

3. The treatment is simple excision.


1 McGllunry ED. or "I; Ccmprehenslve Texrbook of Foot SUIgery.1nded. Eloltimme. W,lliam, & Wilkms.It/92_ 1 Pearson A. W~II'ord R. Mamlgemenl of Skin Trmnnu, Prlm Care 17,2\: 2lliJO.

1 1'{lIl<>rm(. Wam K,\: Tumors. In McGbmry ED. Blink-AS. Dow<ley M~ le<hr Comprehensrve Textbook of F~o' SUrgtlr;'. ""d ed. Boinmore. William, /I< W,lkin,_ Balnrnore. I ~92.



A 71-year-old man with an itchy, scaly rash on his upper and lower extremities and a lesion on his right foot

A 71-year-old man with a past medical history significant for chronic Iymphagenous lymphoma presents with 11 dry. scaly. red rash all both his upper and lower extremities. face and trunk The patient recalls the rash beginning :3 years riga. but then disappearing il.l the end or the summer, 11 returned L year ago.

Physical Examination: Vital signs: normal, General: no distress. HEENT: coarsening of facial features. Cardiac: regu lar rate, no murmurs, Chest: clear breath sounds. Abdomen: soft. non lender; red. raised, scaly plaques. Extremities: more plaques: bullous lesion at right medial arch. Neurological: inlac t; no focal de Ii c its,

Laboratory Findings: WBC 12.800111-1 (normal 5OOO-IO.UOO)_ Buffy coal (abnormal circularing T -cells), Serum chemistry: increased LDH isoenzy rnes 1,2,3. Chest x-ray: hilar lymphadenopathy. Positive for human T-Iymphotropic virus (- 1)_

Question: What syndrome explains [his patient's signs and symptoms?


Diagnosis: Mycosis fungoide, (cutaneous Tvcel! lymphoma I(,TeLi)

Discussion: Mycosis fungoides or Cl'Cl, is a malignancy of CD4 helper Tvcells that usually Ilrs! manifests in the skin, The neoplast ic process involves the entire lyrnphoreiicular system. and the lymph node, and internal organ~ become invalved in the course of the disease, Epidcrniologlcally, [his disorder has a 2: I male 10 female ratio, and the age range is 5-70 years with typical onset in the 6th or 7th decade of life. The causati vc agent is believed [0 be the human Tvlyrnphotropic virus (HTL V). which often is not easily detected initially.

The patient typically reports onset of large. pruritic. red. and scaly plaques perhaps as recently as 1 month, but also as long as several year", ago. These plaqaes, which are round or arciformshaped. 'can be random Iy distributed over the enlite body. Peripheral lymphadenopathy is of len pre sen t. and many ti rn es the patie nt has preced i n g diagnoses such us psoriasis, contact dermariris, and nummular dermatitis, Chest x-ray reveals a hilar lymphadenopathy. and hematologic exam shows eosinophilia, Tvcclls, anti increased WBC (20.000 rnl), Serumchemistry demonstrates increased lactate dehydrogenase iseenzymes 1.2,:1,

CT scans are helpful with more advanced stages of the disease and may aid ill discovering retroperitoneal nodes in patients with extensive skin involvement. lymphadenopathy, or tumors

of the skin, Diagnosis in the early stages is often problematic. and hi'lolngic confirrnatlon may not be possi ble for years despi Ie repeated biopsics.

Dermatopathology of this disorder includes: ( I) mycosis cells, which are Tvcells with hyperchromatic. irregular-shaped nucle i, in the epidermis a~t.l dermis skin layers: (2) rnicroabscesses in the epidermis with mycosis cells; and (3) bandlike and patchy infiltrrue in the upper dermis CX~ tending into skin appendages. Monoclonal antibody techniques are useful, l\~ mycosis cells are activated CD4 Tvhelper cells.

The course and prognosis of the disease is unpredictable. but the survival rate generally decreases if tumors and lyrnphadenoparhy are present and more than to"'" of the skin surface is involved.

Trearmcnt for mycosis f'ungoides is stagedependent. In the pre-CTCL stage, with an establixhed histologic dlagnosis, PUV A photochemetherapy is the most effective treatment. In the histologically proven plaque stage whhout lyrnphadernoparhy. PUVA photochcmotherapy is also the method of Choice. For the extensive plaque stage with mil ltipic tumors or in the presence of lyrnphcdenoparhy or abnormal eirculering T -cells, electron beam plus chemotherapy is probably the best current combination.

Clinical Pearls

1. Biopsy wi th histologic- eval uation may ur may not give the diagnm;is of cutaneous Tvcell lymphoma initially,

1. Look for hilar lymphadernopathy on chest x-ray.

3. Dn physical exam. look [or peripheral lymphadenopathy w ith red, raised, round to arciform-shaped, pruritic plaques .

.+ Histo logic exam wi II reveal mycosis ce lis (T -eells with hyperchromatic. irregularly shaped nuclei],


L Fitzpatne T: Cot", Alh, and Syn"p''' 01 ("1;",""1 De m111 IOloIl'Y. ·\,,1 «I "lew York. MeG".", HIll. I'lln ~. Glusac E. et 01: Curnneous T -cell l~mpf1olll". Dermmel CI in 171 JI. 1m



A 51-year-old man with chronic diabetic foot ulcerations

A 5 l-yeur-old man preserns with a 3-month history of ulceration at the :!nd submetararsal. The patie nt recall- that utter weari ng an old pair of shoes. a call us formed and prugressi ve ly increased to an ulcer. The pauen: saw his primary tare physician. who then referred him to the wound care center. Past medical h i . .'. (01) is ~ igni ficaru for diabetes me llirus,

Physical Examination: Vital signs: normal. General: no distress. FfEENT: NCA T. Cardiac; regu I ar rare '" uhout murmurs, Chest: clear breath sounds. Abdomen: soft and nontender. Extremities: small. probing ulcerarion of 2nd subrnetatarsal, with yellow. foul-smelling drainage. mostly fibrous base, and hyperkeratotic rim; palpable pedal pulses bilaterally: decreased protective sensation to Semmes-Weinstein 5.07 rnonotilament from roes 10 mid foot.

Loboratory Findings: WBe l-1'.200/j-L1. Radiographs of right foot (see figure): increased seelerosis and I} ,i, of I.'! and 2nd metatarsal heads, with bony erosions and toss of architecture: probing soft I issue u leer below ~nd metatarsal head on lateral view; no sort tissue emphysema ev ident,

Qnestion: What are some treatment options for this patient?


Diagnosis: Osteomyelitis or the 2 nd metatarsal

Discussion: Osteomyelitis 01" the diabetic foot is often ~ challenge to treat und eradicate, because peripheral vascular disease is usuany coexisting, With compromised circulation, delivery of systemic antibiotics (A BXj to the afffected area may he null, Therefore, alremutive methods of delivery must be employed, In F170. Buchholz and Engelbrecht ~Tst described the \lSI.' of ABXrmpregnnred cement for the treatment of infected total hip arthroplasties. This technique was modifled by Calhoun C! al in 1994 to the form of A BX polymethylrnethacrylare I PM MA) beads on SUl"" grcal wife for the treatment of osteomyelitis in the ischemic foot.

Commercially prepared ABX-impregnnted PMMA bend, are not available in the U.S. mainly because of the lack of completed clinical trialx, However. most surgeons prepare their own ABXirnpregnared beadsInrraoperatively. PMMA is :I compound used 10 cement the components in place during arthoplasty surgery, The ABX beads are fabricated by implanting antibiotic powder Into PMMA cement m a rutin of 5: I. Typically. PMMA cement is distributed in -WS packets, and to avoid excess waste. halt' of the package can be mixed wirh the appropriate rnrio of ABX. Too much AEX prevents the beads from hardening, whereas too linle ABX limits the effectiveness of the beads.

Choice of ABX depends upon the type of microbial infection suspected. Arninoglycosides such as gentamicin. vancomycin. and tobrarnycin are the most wide I Y used, J ue to the ex tensi ve research available on these ABX.low incidence ofreacrion, broad spec tru III of ac ri v i ty, and hca; stab iii ry . PM:MA cement hardens via 311 exothermic renerion; therefore. the ABX must be hen! stable and water soluble, When possible. choice of ABXImpregnated bends should be directed per culture

and sensitivity, Other ABX choices include cefazolin, ticarcillin, pipercillin and doxycycline ..

An ri b i 0 rio beads are fabri cared in traope rat i vel y by mixing pharmaceutical-grade, powdered antibiotic and liquid rnerhtyrnethacrylare into II putty-like conslsrency. Next. while the PI\.1MA mixture is still soft, small beads or pelletsapproxirnately 3-7mm in diameter are roiled. The beads are then placed on stainless-steel surgical wire or non absorbab I e s u tu re r n o. 10- 1 5). The beads harden in roughly 5-10 minutes via an exothermic reacuon-ctherefcre. the surgeon must work efficiently. Following debridement and excision of all dev ital ized son tissue and bone, the string of beads is placed loosely into the void of the wound, either completely buried or left with one bead exposed (see figure). The skill is then dosed primarily.

Typically the string of beads is left in for 2 weeks. However. if the needexists to fill a dead spac e or if Ii s It of it seco nd p roce du re toremov e thee beads is not advisable, the beads can remain permanently Without causing adverse effects. Two weeks h, the period within which the beads cun be removed with minimal granulation tissue overgrowth. Note that the beads can be removed In toto, or inched OUI one at II time as the granulelion tissue fi iis {he wound. If the wound caDDO! be pri rnarily closed. an occ lusi VI.' fi I m dressing can be employed to form an ABX bead pouch.

The benefit of this procedure is Ihe ability \0 ach ieve high levels of ABX concentration at a local site white avoiding systemic toxicity. The closed space is a requirement to obtain a high. 10- cal concentration of the ABX. The ABX is then released into [he wound by diffusion. Elution of the ABX is greatest within the first 48 hours ilJId then tapers down over the next couple of months. Detectable levels of ABX have been recorded in beads implanted over 4 years.


Small-sized beads \3-7 mm drarneter) are ideal because increased surface area allows a large pertentage of A B X to be released ala quicker rare, ABX-impregna~ed pt\.!MA heads avoid adverse side effects and systemic toxicity .. They areespedally useful when managing patients in whom

achieving therapeutic tissue levels of A BX in the foot is rJ i fficu It.. sucn as those with diabetes rnelliIUS or infrapopliteal occlusive artery.

In the present patient, resection, biopsy, and insertion of antibiotic- impregnated beads were used to eradicate th is osteomyeli tic process.

Clinical Pearls

l. Use heat-stable, powdered ABX and liquid PMMA cement to prepare antibiotic heads. Mix ABX with cement 5: I respectively.

2. Make small-diameter beads and use Slain less-steel surgical wire or nonabsorbable suture,

]. Close the wound primarily. or use occlusive film dressing over u,

4. Beads can remain permanently without adverse effects, or can be removed.


L Henry 51..! ABX·impregn","d bends. Pnn I Ortho Rev 20(3): "42-247. 19<)[

]. Henry 51..; L""ill'\BX treatment for rnarmgemem of orthotic infections. Clin Pharmoklnetics 29[ tl' 35-15. 1995.

3. Roeder B, et al: Antlbiotic bNLd~ m the treutment (If OM pedal ,,>re"'nytlili~. J Fe"'! Ankle Surg 39(2).124-13(\. 1000_



A 74-year-old man witb nontraumatie heel pain

A 74-year-Ll!d man presents with a J-week history uf rigbt heel pain. He relates receiving a steroid injection from his primary cure physician 2 weeks ago, which did offer some relief, The patient describes severe pain over the last couple of days, increased with activity and when he wears his dress shoes. He has obtained on Iy minimal relief from anti-inflammntories. He den ies nny trauma to the area.

Physical Examination: Vila] signs: stable, HEENT: normal. Cardiac. regular rate and rhythm.

Chest: clear. Abdomen: benign. Skin; normal. Neurologico'l: motor und sensory intuct. Lower exrremit}": palpable pedal pulses: mild tenderness with palpation of plantar medial tubercle 0]' right heel, negative discomfort along plu ntar fasc ia, sign i ficant pain with rned in 1 and lateral compression of'calcaneus, no tenderness noted In insertion of Achilles tendon, negative Tine I· s sign, no evidence of erythema, ecchymosis, or edema.

Laboratory Findings: CBe: normal. Uric acid: j rngnll. Rheumatoid factor: negmive. Radiographs: small plantar calcaneal spur of right loot: negati ve cortical or bony di sn: ption, Tc99 bone scan (see figure): intensely increased activity all all three phase, within [he right heel,

Qrusriolls: Whm IS [he cause of this paticru's heel pain? Describe the recommended treatment.


Diagnosis: Stress rrurture nght calcaneus

Disc Fusion: Stress fractures of the fOOL are m,li n I v locahzed to the 2nd metatarsal and calcnneus, The mcchan i 'In ,>[ i nju ry, wh ich is common to all .Lre" fra .. .rures. i~ excess! ve repetitive force that cnuses fal iguc und eventually fractu re, The body responds 10 thl~ repetitive stre ... ~ by laying down I1~W IXJnC' rrabeculations along the lines of increased stress, w h ich can rake up lU 2. weeks, Lf rhe repeiluve terce continues during this process. the b()(ly doe, not have a chance io lay down new trabeculae .• ind fnilure ensues. The primarily caneellous calcaneus reacts w ith a compression-type fracture usually perpendicular 10 the trabeculatiuns I'll the junction of rile hody and tuberosity. This doe, not become apparent on radiographs unli.!:! weeks from date of injury,

Consider the d: O!!.rIOS1S of stress fracture in any patient that presents w uh heel pain. Patients usually present with pciru tenderness to the plantar .: a Ie uneu s, lind d e scri be pa i n th at i nc reases throughout the day ami i~ often aggravated by lack of cushioning in shoe genr. Occasionally, patients relate 11 recent h isrcry [1 r beginni ng a running rouLine or weight gain. A variety of metabolic diseuses including osteoma lac ia, osteogenesis imperfecia, hj perpararnyroldism. scurvy. Pagers disease. fiim)ll,< dysplasia. and even rheumatoid arrhri ns pred lspose a patient to develop stress fractures.

Fi nd ing, <Ire often ~ imilar tu plantar fasciitis, hut patients do not complai 11 of post suuic dy,kinesia-c-rather, pain increases with continued activity, The i;I:1);SIL- clinical finding is severe pain

with lateral compression of the calcaneus and m inirnaltenderness of the plantar medial tubercle,

Plain radiographs appear normal DI the onset of sy rnptoms, The most useful diagnostic modality is a three-phase Tc99 bone scan. which shows focal uptake withi n me calcaneus as early as 2 days following fracture, An MRl may also be helpful. showing signs of marrow ede rna (decreased signal intensity on T'l-weighted image).

The earlier the patient presents for treatment, the better he or she responds, An injection for plantar faseiius should be avoided if there is any sus p ici 0 11 u f stress frac I.U re due to de la y ed healing or avascu lar necrosis of the calcaneus, If diagnosed early enough .. a stress reaction may be all i hat is prese n L. These pari en rs res po ndq uickl y to 1-2 weeks of nonweight-bearing with crutches, soft cast, and gradual return to acti viry, Once a definitive fatigue fracture has been diagnosedvarnpie lime must be given to allow for complete healing, Ideally. a short kg cast and removal of weight-bearing until the fracture is nontender (usually 4-6 weeks) i~ me treatment of choice. A earn walker and an ACE bandage may be. used for immobilization if the pariemis not able [0 mainrain non-weigh! bearing.

The present patient was placed in a below-knee cast for a total of 6 weeks. He was instructed to remain non-weight bearing for this lime with the aid of a roll ing wal ker, A lter the cast was removed, rhe patient slowly increased physical activity He remained asymptomatic and was able LO return to normal daily activities ..

Clinical Pearls

I. A calcaneal stress fracture may present similarly to plantar Iaclius, but the patient is srenincuntly more tender on lateral compression

1: If there is any suspicion of fracture. a corticosteroid Injection should be avoided, 3. Obtain a bone scan or MRI if the patient states that pain increases throughout [he Jay. ;1111.1 rhere i~ point tenderness and pain with compression of the calcaneus.

.. ,'I, three-pbase T~99 bone scan shows i ncreased uptake in all three phases with 3 posiuv ~ Sin::" fracture,

_:; Trentmenr of calcuneal stress fractures includes immobilization with 11 short leg CIM und nonwerght-hearing for at least 4--6 weeks.


B[i~hm" CT Pnnclples 01 iracrure "".\[i"~ lnstr CO""~ l.ect 33,(,0. I ~84.



A 52-year-old man with an 8-monlh history ora foot ulcer

A 52-ye~-olli man is adrnitted to the hospital becuuseof an ulcer under the 2nd metatarsal head of the right Ieot, The ulcer has been present for approximately B months. It is approximately 10 mm in depth witb :; nUI1 of undermining. ~J1d the wound is 7 X 9 rnrn. The patient received weekly treatments in a wound-cure fac il iry Treatment consisted of a variety of wound-care products. sharp debridement. :Imi.lceommolhuil'c and uffioading shoes. All ofthese measures were unsuccessful in healing the ulcer.

He IS H type 2 diabetic wjrh ::I JD-year hi Story of di nhetes. H istory i ncludes alcohol abuse and a 3- pack-a-day smoking addictinn. He is allergic to penici II ill, Current medications include glyburide, 2 j rng/day: ciprofloxacin. 7j(J mg by rnnuth, twice daily; clindamycin, 300 mg by mouth, every 6 hours.

Physical Examination: General: well-developed, well-nourished. in no distress. Temperature ()!I$' F. pulse ~8. respirurions 18. blood pressure I 10170 in the supine position. Skin; ulcer under 2nd metatarsal head of ngfn foot: hone exposed; no ~igns of cellulitis and minimal serous drainage. Musculoskeletal: strength 5/5 in all extremities; deep tendon reflexes: normal. Neurological: IOI.jJ sensory 1L.l'" of rigl'H foot when I<,,,(ed with a 507 Sernmes-Weinsteiu monufilament.

Laboratory Findings: WBC 49001j.l.1, glucose 180 rng/dl, ESR 52 rnm/hr, hemoglobin 13. I gldl, her 37 _6"k. lmunin g: Radiographs of right toor=Ioss of distal portion of 2mJ metatarsal head: periosteal new bene formal;, III (;;ct' f gure l. Three-phase technetium-99m bone scan - increased uptake in delayed phase of 2nd and 3rd metatarsals: no other uptake noted wi thin foot or ankle. Noninvasi ve arterial blood now studies= rriphasic wave lorrns al dorsnlls pedis, posterior tibial, and popliteal arteries: pressures nDa mmHg at second [O~ nnd 110 rnrnl+g at rransmetararsal level: ankle-brachial index 0.9.

Que.'i/ions: Describe your diagnostic impression. How would you proceed?


Diagnosis: Osteomyel itis of the 2nd metatarsal

Discussion: Certainly a bone biopsy and culture is the gold standard in [he diagnosjs of osteomyelitis, giving the absolute information needed for further treatment. In the present patient, the pathology report revealed multiple areas of plasma cells, osteonecrosis. and inflammatory responses. consistent with osteornycli tis. The dern ineralization process confirmed the presence of osteomyelitis microscopically. The microbiology results of the bone specimen revealed Stopliylococcus aureus. which was rnerhicillin-resistant.

The patient underwent a proxima] rransmetatarsal amputation and received a 6· week course of IV vancomycin through H Hickman. He was kept offioaded during the emi re postoperative course, and upon complete closure of the wound Sill'. he was fined with a molded shoe and toe filler.

This fonn of osteomyelitis tends to be chronic.

The patiem did nor fit the systemic illness pattern, bu t father had a I DC alized disease process. Pe rsistent drainage may be the only finding from a small

sinus I ract, All too often. the patient igno-res [his n!ld ing, or the practitioner ignores the potential danger. Rarely does the patient feel pain oreven see red ness u nlil the are a beco rnes <;upe rficiall Y inleered. It is 110t until the radiographs reveal the rypical findings of thickened. irregular-shaped sclerotic bone with are as of tad io I ucency and areas of periosriurn elevution that the alurm is sounded,

A radical approach is cri tical. aslocal antibiotic or IV therapy is usually unsuccessful. Inadequate treatment leaves a low-grade infection rhar persists and may explode into an infective processwhich agaln is treated inapproptiarery. In the patient described here. the 2nd metatarsal bead is ill a destructive radiolucenr phase: if this follows its chronic nature, a III yering of eburnated pericstiu m w ill develop, resulting in II shorten ing of [he ::':nd met a tarsa I with II shift and transfer of weigh! to me ad j aCCnL me tar ars a 1 hea d. Th i:" area w ill then break open into another ulcer, turther complicating this diabetic patient's ambulatory 5WtUS.

Clinical Pearls

1_ As important !I~ it ls to recognize and diagnose osteomyelitis early. it is more important 10 isolate the orgnnisms nearing the infection early in the process.

2. Bone cultures via an adjacent site or excisionof the bone in question i~ imperative for a complete diagnosis.

J. In a diabetic patient. if bone is exposed for any period of lime. osteomyelitis should be III the top of your di fferential diagnosis 1 ist,


MoGlamry E. Banks A. Do"ney M: Cornp",,,,",iwTc.iNnK of Foru Surgery, 2nd ed. Baltimore. ~lD. Williams & Wilkin,. 1992_

2_ MtJ<i!lrid. LS. Mc!{jmick JB. Risley TS: Trunarneunarsal urnpututions for mfection or gn"grt"ne in patients wi,h diube .. mellitus. Ann Surg lJO: 816, 1'14Q_



A L3-year·uld girl with latera] fool pain

The patient presents with complaint. of left foot pain of approximately 2-yeaT duration. There is no specific history of a traumatic event. The pain is primarily at the lateral aspect of the foot. i, WOThC at the end oi the day, and i, somewhat relieved by rest. The child relates that over the past 3 months the pain has increased .• md it not relieved by NSAID~. She is unable La participate in school sports and cannot walk for any long distances.

Physico! Examination: Genera]: no swelling of left foot: lender at nnterolatcral aspect. Musculoskeletal: exquisite pain on ankle pluntarflexlon; subtalar motion limited; eversion present; peroneal tendons no! in spasm: no lateral leg pain: midtarsal joint ROM unattainable. Gait analysis: gastrocnemius equinus, demonstrated by limitation (If dorsiflexion at ankle when leg is extended Oil thigh (illcreased dorsiflexion when leg is fl~xeJ on thigh); longitudinal medial arch decreased with abduction 01 forefoot.

Laharatory Findings." Radiographs; AP and lateral=beaking of talus anll narrowing of subtalar i,"m: "anteater ~ign:· Medial oblique-e calcaneonavicular bony bridge. Harris-Beaihe-c rniddle and poxrcricr facets of suhtalar joi n rs parallel to one another. CT scan I see figure): bony bridge between calcaneus ami navicular. with no changes in subtnlar joints.

Questioll s: What type of coa I itinn i'i present? Whot wall Id be an acceprab le conservati V~ coarse \ If irea tmen t?


Diagnosis: Calcaneonavicu lar coal il ion lind secondary gastrocnern ius equi nus

Discussio»: In young children. the most comrnonshe fur fibrocartilaginous unions is the pesterior region of the subralar joint. Moblllzarion of the coalesced joint, rather than II fusion, is common practice in the therapy of this disorder. The release of the fibrous tissue can restore motion to the rearFoot. Only when the foot matures (16-18 years of age) does one consider any type of single or multiple joint fusions. Conservative treatment usually fails in the treatment of calcaneonavicu lar (CoN) bridges. Success is reported when resecting this bridge in the you ng, acu ve chi Id. Subtalar fusion is not necessary even in rhe presence of talar beaking in a child with caleaneonavicu lar coa lition,

However, in the adult. the prognosis is worse if ialar beakin.!: is present. Simple resect ion of the CN bar in the adult and replacement with wax or sl 1- icone, or interposing the belly of the extensor digitorurn brevis. does not guarantee mobilization. The young child is more active and itIs possible that this explains tile higher success rate of resecI ion in children,

The difficulty and the usual complication that arises with the young child and their complaint of pain in the rearfoot is misdiagnosis and inappropriate treatmern. Without proper visualization of the rearfoot, you cannot treat this condition, CT has certainly helped in the diagnosis of osseous or narrow coalitions. but wi tn the aid of MHI you can isolate the exact position, thickness. and length of the fibrous bond in any of the joints. When the subialar joint is restricted and the midtarsal joint loses its gl iding motion. the talus starts to override the navicular and talar beaking results.

W111:n the coal i ti on is prese m in a ch il d 's early tlevdopil'lg stages. the adjacent joint changesas well. Besi des the future art:hri lie chan ges and Dd a ptive changes (Iipping and jamming of joints). another phenomenon occurs: a ball and socket ankle develops as a compensatory response to the restricted motion of the subialar joint. The tibial plafond becomes concave. and the dome appears to be con vex and ball-shaped: thejoirn now accepts full R:OM tn dorsiflexion, plantarflexion, inversion. and


eversion. Ankle ~tab)lity b ru risk. however, vince the fom is In a valgus position I t\{11~: After lusion, thb is the position 10 strive r"f- [he instability is not pronounced.) If rhe pain is extreme. cast we fOOl in ~Hght pmnat ron - do not invert, A period of immobilization O~6 weeks) may be arternpted using this ~h011 leg wal king cast. Rest. ice. and antiin tl umrna tories 1113 y have a pes I t i v e effect

In the aging child arul the child who develops the coalition late, the result will not be the ball and Socket ankle but an ank le w ith deuenerari VI' joi 111 changes, In t l1i,; situutiun. a pant;lar Fu~ion is required, A, with many childhood comlitions. early recognu ion reduces the need for radical, complication-prone procedures .. The hrst course of treatment is h} conserv ~li ve means, A s·pOJ1 orthotic would be well tolerated and allow the foot to pronate slightly. Omit forefoot posting so as 1'I0t to drive the fin;t I'ay higher. affectlng the midtarsal joint. Do not post the footi 11. rearfoor varus, as this will allow too much motion to bring the Fort!foot down. It" I he In idmr,.ll mol iOI1 is increased. pain will be increased, Stabilize the heel to decrease the 'ilre%e~ across a xtiff subtalar joint, When subralar joint motion is restricted and the midtarsal jo int l[l~ses its gl id in'S motion, the tal IlS starts to override the navies lur, ami talar be-ak ing results.

When all conservative steps fail. consider surgery. S igni Ikanl relief can be obtained by re~ section of I he coali rion. Place a layer 0 r materia! in the calcanconavicular space to uvold 11 recurrence. Resect the bur. and imerpose the extensor dieirorurn brevis.

The present patien I fai led all conservative meaSUf(~S. S he underwent su rgical resec rion of the calcaneona v iculur \.'(>~l i tion. with lruerposi rion of the extensor !l igitornm brevis muscle, A gastrocm::mius lengthening Wi,S 31~o performed. A short leg cast was applied postoperatively for a period of 6 weeks. After removal of the cast the patient was placed in custom-molded orthoses. She nnw enjoys an 3c'l ive chi ldhonrl and partici pates in .1''11- ernl sc hoo I spo ns.

Clinical Pearls

("] in 1 col (]iagnn<;is ,I s qu lte nnporta rtt. If al i mi rarion of m idtarsul joint motion is noted ill light flf an acceptable .unouru of reartoot 1ll01iQI1, then Slrongly consider calcaneona vic ulur coalin on.

::'., Arter clinical impression. 111,;: medial oblique radiograph is key, It allows parallel observation of rile jo inr and easy idcnti ticsuon of signs.

3. If ill doubt, an MRI will nicely demonstrate fibrous ~m.l osseous unions.

4. The CT is most useful when the child is older and an osseous union is suspected uver .1 tibrous.

j, If D secondary gastrocnemius equinus develops because of [he abducted position, consirler a heel-raised orthotic. If the equinus is significant. perhapslengthen the tendon at rhe lime Df resection,


Gonzalez P Jt~Yl.lIo.L1mLLf S CJ.lk~m-C'on.:..I\·lLHId[' ~(MIUlOfl trented by rC~:>d IWl and unerposuion or the 1!':U~I1~or t_hgitorum brevi< mu .• cle. J B,,,,~ j, ""1 ~"r~ 72" '11 77. I'J'KI

Herzenberg JE. uldl1<r J L. M~rrl"'" S. Silverman PM: Computerrzed l.omogJ'aphy "r IJloe"lc""~"I",,,,"1 c,,,,lil;,,n. fool An~I" ()\51."73--co~. I'!~~,

J. Ma,ier KM .. 'I,he[)'1 T"".JI ,'"01111",,, .,,1<1 penmen! 'pic'ii'· nlll roo I. J BOlle Joint Surg b('A:976-9sa. I Q8~.



A IS-year-old girl with pain in her second toe

A 15-y~ar-old girl presents with lefr fOOL pain near the second toe. The pain has been present for I year. She has no history or trauma. and describes the pain as a constant, dull ache that has been getting progressively worse. She also reveals that the pain increases when she wears high-heeled shoes.

Physical Examination: Musculoskeletal: exquisite tenderness at metatarsal with flexion and extension of left second [De: tenderness on palpation over dorsum of 2nd metatarscphalangeal joi m: exireme pain on forcible compression of phalanx base against 2nd metatarsal head, Gai t analys is: patient places majority of her weight on lateral aspect: forefoot inverted.

Laboraiory Findings': Radiographs: AP view (sec Iigl1rel-fhm~ning of metatarsal head and joint space widening with <I central depression: lateral view-deft in dorsal bead/neck region with slight beaking, and small osrecphytic fragment near joint level.

Qu.estions.: \Nllat is your first impress ion? What are your surgical options?


Diagnosis: Freiberg', infraction

Discussion: .1\ pi ausi ble theory for the Iailure (If this an icular epiphys is \0 heal i~~<HL'I<I nt cernpression. Delayed union and poor endochondral nssification are the result. Consranr trau rna to an immature epiphysis changes the mechanical ettorts exerted hy the joint, The normal rotmion about the articular surface LeaS~5 and is replaced by direct compressu m, 1[' lel: unchecked UVCf the j <lars, rhe joint IV i 11 hecorne rigid. pni ntu I. and osteoarthritic.

Radiographically, the most obvious finding is widening of the joint space. This widening occurs by the sixth week after symptom onset, With progressioll of the condition, the density of the subehondrel bone ; ncreases, and the rnetararsal head fI arrens.l n the ad v anced stage ill the u ldcr chi 10.1. the I~ c hemic epiphyseal bone and an icular cartilage weaken and collapse. The collapsed bone cremes fracturing withi n the jni nt, and loose bod ieo. appear. wuh resultant pain. It is not unusual to see these fragments in the dorsal aspect III the jni nr space,

The least traurnauc and certainly the most amhulatory surgery e ntui b removal uf the fragment Resecting the dorsal aspect of the metatarsal head ..!i!llWS for increased dorsal range of motion, Re-ection of the proximal phalanx base decem-

presses the metatarsal head and usually reduces the sy rnproms, Ln lime. hUW<:VoOT, weight as well as pressure on the surrounding: rneuuarsal heads will i ncrease, creari ng a transfer lesion.

Perfornrlng the 5U bchond ral surface by drilling is an option i r considered early in the development of Freiberg's, Penetration through the metatarsal head. epiphysis, and metatarsal shaft causes increased blood to be de.l lvered to the distal aspect. It may be advisable to consider an osteotomy to real ign the metatarsal head. This would eliminate the direct compressionon the head from the plantar weight-bearing surface, III addi tion, rotating the head effects a decrease in the retrograde force from the phalanx ••

Joint destructlve procedures should be avoided in children: however. if the pain is significant. and the damage to the articular portion is extensive, yuu may be led !O resect tbe metatarsophalangeal juint completely or partially. Implants arc not contraindicated. Pain with this deformity is exhausting [0 the child and to the parents: il' all else has failed. then this rudica: approach is recommended.

In the present patient, the rreutmcnt WJS radical due to the ex tensi ve damage to the u rticular surface.

Clinical Pearls

Early recognition of Fr~ih<;rg', infraction i, puramount. Ofllonding the joint with decumpression hll~ proved successful,

2. An orthotic cunstructcd to maintain (I lorefoot V~IUS as well as forefoctextension. with a cut-out to allow the 2nu rnetatarsalm drop. decreases jamming of the second too.

J. Consider 0.11 <:arl y dorsi flexory osteotomy on the neck of the metatarsal to increase dorsl tlexion. This i~ sirru lar to a Waterman procedure. and will increase motion.


I Il'" .. k R."' u]; Freiberg', di", .. se "uml'li~~li"g unrelated tr-mma. Orrh"p"d,", I 1;5:753-757. 19~8. ~. c,m;,t. S. B~'lV I Operative Itdi,uri, Onlu'r"'ui<:,. 2nd <d. ~r. I_<>ui" ro.-IO. Mo,b" ] (Iq'.

,. Drennun J: Th~ Cluld« FUUI .• nd A nkle, New York, R.lI en Pre-s, I Q'r'.. .

oJ Hettil B. Gibb P: I'",irerg.·' di'e:" e, Font Ankle ~'I4-t02 .• 1987

"!:. Kinmnd FI, l.irene R. Dr"Ir~ifie'(wn L~ ... H~Utunly in Frclberg" ... rJiwn...,~_ FI'OT vnkle 9216----111. 1989 ~. Meehan P: 1.","" ."''' Wml.,,,. P«Ii"rric Onll,,~a<"ic,. lrel "J. Phlludclphiu. Lippineen, 1Q<m .

., Spmul J. 01 .,1. Su'~i,·"I[I<.Jln ... nr of I',,;b<rg"> 1"[,,,,[;,," i11 .nhILle, ,\'IJ J Spnrr-, M"~ 2113): 181-1S4. I~Q3



A 13-year-old girl witb a painful foot

A 13~year-old gi rl has been complaining of pain in her left fOOl for 3 mont hs. Conservari VI' home remedies did nOI provide any ,igoi licant relief. Her chief campi aim j~ acute pain localized wi thin the sinus tarsi and pain corresponding to the course of the peroneal tendons along the hnerat uspect of her left foot, The left foot is more symptomatic than right. Playing sports especially aggrnvarcs the problem. She experiences greatest pain when walking barefoot. The patient's past medical history IS unremarkable. Family history includes maternal talonavicular synostosis and symptomatic subtalar coalition.

PhJ,sit:al Examination: Pedal pulses: steady and palpable. Skin: normal. Neurologic: normal.

General: rear foot valgus bi laterally. wiih forefoot perpendicular to rearfoot: gastrocne mius eq u inus bilaterally: mild hallux abducto valgus IV ith valgus rotation of interphalangeal joint and contracted digits two through five bilaterally. Musculoskeletal: hip. knee. and ankle joint ROM normal: subtalar and midtarsal joint ROM restricted bilaterally; muscle strength normal and symmetrical, Gall analysis: antalgic apropulsive cycle.

Laboratory Findings: Radiographs: talonavicular synostosis and subtalar coalition; talar beuking: narrowing of posterior rulocalcaneal space; rounding or lateral process of talus: middle subtalar joint obliteration on lateral view: asy rnrnetry or anterior facet of subralar join! in lateral oblique: halo effect (continuous sclerotic rim around sustentaculu mrali 1: irregular and hazy cortical surface surrounding coalition; no distinct cortical margins: secondary degenerative joint disease and ball-andsocket ankle (BASA 1 joint (see figure),

Course: Initially she W3S given a peroneal nerve block with 2% lidocaine. which relieved a p.!roneal spasm, Subsequently a sinus tarsi injection was ndrnlnistered with 2% Lidocaine. methylprednisolone --1-0 mglm1. lind dexamethasone 4 mglml. and a Unna bum was applied. Tile patient was instructed to walk wiih crutches, ncnwelghr-bearing. After J months of conservative therapy, she is still experiencing significant pain while walking,

Qllestion: Why is the patient sti II experienc ing pain after 3 mouths of conservative therapy?

Diagllo£is: J ulonav icu lar coati I ion and subralar coalition

DiSClIssiOH: Most of the present patient's discomfort was relieved by a limitation of motion. The most common presen tuiinn of I alonavicul ar ~yno;;losis is local tenderness over the coalition .,i te, enhanced by acti v ity and rei ieved by imrnobilizauun or rest, However, the pain is referred 10 J proximal joint. In this case it was the suhtalar joint, Pain is usually deep withi n the sinus tarsi, und a restrict ion of subtal ar ini 1]1 and midtarsal Joint runge of motion is characteristic.

Peroneal spasm may be present, but not neees-urily, Pe ro Ileal spasm is frequently found in medrul ralocalcsneul coalitions. the most common

IIlTS.aJ coal ilion. in wh ich there is a restriction of monon on the medial aspect of the joim, but not laterally. This ultimately leads to a calcaneovalgus deformity, with a decrease iA the medial longitudinal arch and abduction of the forefoot.

With most coalitions. motion is transferred 10 [he adjacerujointIn this patient.the motion was picked up by the ankle. Since this was an early-onset synostesis, the Mar dome began rounding to create 3 ball-and-socket ankle. This development increased inversion and eversion, The solution to the patient'S persistent pain was a deep-seated heel seal to prevent the increased frontal plane motion of the ankle.

Clinical Pearls

Early identlficatlon of a synostosis with protection of the prux irnal jo ints decreases the chance or ja int arthrit is as the chi ld grows.

2. III early fusing of joint" the restriction of motion only increases proximal joint motion. Always evaluate the ankle for the pctential development of a ball-and-socket joint (I i 111 11111 ion of moll on distally. with 3 resultant increase Illation proximally).


Cow,,11 HR_ Elener V' Rigid p:"nfut ~",fl\"1 !e~"mlary to tarsal coalition. Cllu O'1hop 177'54. 19113.

2 D","[l<-~ MS Tn",,, I eOl,lili,'" In Curnprehensive Textbook or FOOl Surgery. Vnl I . Baltirnore. Willi"Tm & Wilki",. 1992, pr K'IR--Q3(I.

I,,",.,bs ,\M. S"U""ilo v OloFf lM. Klein N, TIL,,".I "0"111;0"'. An instrucrinnal review. J FOQI Surg 20(4), I QS I.



A 14-year-uld boy with severe foot paln causing him to crawl

The patient usually i~ a very active child. Until recently. he played sports all year round. Over (he past 3 months h~ has been complaining of increasing pain over the lateral aspect of his right FOOL He CHIl no longer play My "port. When he hll~ been wal king for 3 long period I he pai n i~ ,0 i nrense that he begms to crawl. Upon questioning. he points directly to rbe area of tile' ,inLis tarsi. The lise of icc and ·11 nonsteroidal anti-inflammatory drug has offered him some relief, An nver-the-couruer insert he purchased also has somewhat mirigated the pain.

Plly.~ical Examination: General: overall health V<;:fY guod, Lower exrremuy: limitation of midlar~al and subtalar motion; moderate swelling of righl fUOI compared LO kl1,. Neurovascular: normal, Gail analysis: stance= right root abducted with loss M medial longitudinal urcb ~I1O.J everted heel [0 ground position. galr=-eurly heel-off with murked abduction 01- footto leg.

Laboratory Findings; Radiographs (see f gll res): hueral v jew - elongated anterosuperior process or calcaneus. known as anteater sign; mediul oblique view-ecnlcaneus and navicular in close proximity: bones appear Hattened with irregular, indistinct corticnl suriucex, MRI' rhanged ,ignais on the T2-w~ighred image

Qlle.dinn; What is the like! ihonoJ thui r h is deform ity wi II <"\ enrua II y reuu ire "llrgicaJ interventicn?


,.inSlI'l'r: Thirty- tive percent of soft tissue calcaneonavicular coalitions eventually require surgery.

D in: ussion: Pain i~ a common finding in lhi~ condition. und IS usually insidious in onset following some recent activity or trauma. Limitation of suhtnlar and midtarsal joint motion is anobvi«us L~I inical lindi ng. The subuilar joint ib usually I im ited in the direction or in version, with greater Ii rnitntion if peroneal muse le spasm is present. Parients may present with 11 valgus deformity due to intense tonic peroneus brevis spasm. which is simply a reflex mechanism to limit painful inver,iun. r nversion ami eversion or the midtarsal jolm induce pain. With. lime. the vulgus defurmity becurnes more rigid. There are, however. several reported cases of spasriciry of muscles other than the peroneus brevis and of a varus pes: lion of the heel in patients with calcaneona v irular coalitions,

Pain is usually isolated to the midtarsal joint reg.i(lIl, and the child point, directly to the area of the xutus tarsi. With limitation of midtarsal and subtulur joints, the foot begins to compensate in the d I r ecuon of abduction and eversion. The per"Ileal]; shonen up due ro this compensated posl[JOn. Any attempt to invert or plantnrtlex the foot creates extreme pain. Unfortunately. a peroneal spastic flmfuut often b d iagnosed inappropriately.

Calcaneonavicular coalitions are usually idenufiable on the rnedial obl ique view. This coal it-ion typically appears as a J -crn wide bar bridging the gctp normally found between thecalcaneus and ItaVICU.l!!.L A "pseudocoalitlon" due (0 bony over- 1.1(1 can gi ve the false impression of 11 calcaneonavicular bar. making it necessary to obtain several medial obi ique v iews at di ffe rent angles to di ffercntiate between positional artifact and true coalition. In the case of a fibrous or carrilagi nous calraneonavicular coalition. the diagllo,~is will be more difficult. On the lateral view. an elongated amerosuperior process of the calcaneus, known as

the anteater sign, may be seen. The calcaneus and navicular are closer than normal on the medial oblique view. and the bones appear flattened with irregu lar, indistinct conical surfaces.

MRI virtually eliminates the difficulty in diagnosis of soft tissue, and provides the physician with an advantage when he or she suspects nonosseous coal itions, Although relatively invisible on conventional radiography, fibrous or -cartilaginous unions can be confirmed with the use of MRL Radiographs and cr have not proven reliable in the Identification of fibrous tnrsal coalitiuns. MRI accurately and reliably indicates fibrous. cartilaginous, and osseous coalitions of the talocalcaneal an d cal can eonav ie u I ar jo i n IS, and is useful for detecting the presence of coex isting bars. MRJ is recornmended with suspected tarsal coalitions when radiography and CT are negative,

Early intervention is paramount Young children Ihat present witb talar beaking secondary to compensation respond favorably to resection of the calcaneonavlcular soft tissue coalition. When tal ar beaking is present in the older child or young aduh, response is less favorable, and a triple arthrodesis is generally necessary.

Conservati ve treatment is aimed at resrricticn or subtalar and m idtarsul joint motion [0 reduce pain. This may be accomplished throughthe use of shoe mod ificarions, orthoses. padding. or casting. Physical therapy. anti-inflamrrrarory medicauons, and local steroid injection inro the area of the coalition may be used as adjuncts. Although the symptoms may resolve for a time. (hey may recur in the future, requ iring repealed casting or even surgical intervention.

In the present patient, a resection was inev irable. and the child was then maintained in an orthosis In minimize midtarsal motion.

Clinical Pearls

l , lsolate the midtarsal joint by stabilizing the heel with your hand, maintaining >I neutral posi ion, Abduct-dorsiflex the foot and then repeal In a plantarflexory adducted position. Two lhings bappen with a coalition: pain is elicited over the sinus torsi, and a lirnitaricn of motion is noted.

2. MRI is recommend D5 the best diagnostic aid for a suspected coalition.


I. Downey ~ts: Tarxal cnallrluns: A ,ufgic"t cla"ifiNlim,. J Am rl,di~!r Mod A,,,,,,, S l: I ~7. 1991

C. Pa..:JmJa Nl\t Lasday SD,Joy RM: TH".I conllnnn: El,iQt"SY, ~iugn<l<;" and treaunenr, J Poot SUf£ 29:474. 1900. 3. Penman MD. Wmheime, SJ: T""".! coalitions, J FOOl SOfg l5·198~.



An 8-year-old girl with nightly heel pain

A healthy. athletic I iule girl complains of severe right fooL pai n al the end of the day <1nu ill the middle of the night. Her parent, slate thai she awakes in tears as the cnri re 1'001 is pam lul. 111C pain has been present r ur over 9 months and has been i nereas ing in seve ri ty. It renters around the lower ankle and heel. The family doctor auributedthe pain to increased activity and "growing pains." The girl's pediatrician ndvlsed ihe parents to take her to a podiatrist for orthotic devices. The devices afforded her no relief, and she W3S referred for ~ second opin ion,

The patient's past medical history is uneventful. with no history of trauma, She experience, ,j decrease in pal 11 when aspirin ls adrnin isrered,

Ph)'sical Examination: General: sil ffuess and guarrf ng around subtalar joint. phI" decrease in total ROM: riglu calf muscle atmph) (thinner than opposite extremity by I ern), Musculoskeletal: pain localized (0 right arch and hee I area both medi ally und laterall y: 110 pa i 11 IJ pon posterior compression of calcaneus .. nor upon acti VI! dorsi flex ion of ank le. Ski n: 110 ~ igl1s of i nflarnmution or edema: \'llSCU lar supply 10 foot excellent,

Laboratory Findings: Radiographs r see Ii gure): lateral v iell - Op,lq ue, ha 10-1 iJ..~ 'lI\:U I em in d i· arnerer, res! ing i nferior and posterior to the sustentaculum tHI i; ax ial v rew (of calcaneus, directed 0 degrees to superior surfacej= similar hndings, with halo locate'! approximately 1 r rn from ltueral wall of the calcaneus, Fechnetiutn 99 three-phase bone scan: focal area \11' increased perfusion in region of right cal cuneus; immed iate and posrinjection image, - focal area of increased vascularity in region of midright calcaneus; static images- increased acu v ity in t.h is region. CT: density ill vupcrior margin of right ("nle::!!lelJ.S body a_rllj nidus lu("~nry in. inferior ~~..l!rgH'i_

Questions.' What is your differential diagnosis'! What is the probable diagnosis?

Diagnosis: O~t"uio.l osteoma

Discussion: Ovteuchondruis. stress fracture, hone islands len\J,[U,;;).lIml Bru;Jie~', abscess lire suggested by [he '<Idiographic modalities. Radioi,'gi~ studies have pru ved IO be the most valuable dragnostic tool. btl! the hazy. trabecular pattern of c.mcellous bone in ItU: young child makes the leS](l11 difficult to locate. There. should be II dense, ,c:krnuc rim surrounding the lesion. This. lOO. is not easily sported 111 the very young child with an euriy developrng lesion. The dense rim L1oe~ not appear umillme in the lesion's maturation. when it I' being vascularly cornpre ... sed, 1 r located in the 'I,ollgy bone layer. the lesion i ncreases in size with referring pai 11. but does not consolidate a sclerotic rim about the central c lear 11 idus.

Additional studies are recommended in young .:11 i ldren present i ng w iLtt til i~ vague bu L cluss ic purn, 10 dearly .dentify " suspected lesion. NUTrnuily, children do not have pain. If pain i~ pres" ~1l1. it mU~1 be seriously considered until a ~rm diagnosis is attained, A lexion may he located in the cortical, cancellous, or subperosteul bone. While

All will dernonstrme a radiolucent nidus with D sclerotic ri I'll, cance llous and subperiosteal bone lesions are more d ifficult to diagnose as these fealures are less pronounced.

In the atypical situation. the nidus is not surrounded by sclerotic bone. which makes it especi ully difficu It to identify within tile complex radiological anatomy of the joints. This scenario uften leads to misdiagnosis and delayed definitive treatment. Misdiagnoses include post-traumatic synovitis, rheumatoid arthritis, and even hysteria. In many cases, patients undergo unnecessary treatment, such as immobilization with plaster. use or crutches for an extended period of time. joint injections. arthroscopy. and even psychoanalysis.

In the present patient. a CT was obtained, and the osteoid osteoma was identified and surgically resecte d. A bo ne gra ft was p Inc ed in the defect. Thepatient was placed in II below-knee cast for a period of 6 weeks. She well! on to heal uneventfully,

Clinical Pearls

I. Pain i~ the most important clue; cbiklren do /1(1/ huve pain III/Ie,,;' there is a disorder ImJ~"III. When in doubt. cheek if OUI. Do nut aSSLIme hysteria.

1, If [here is suspicioo of an osteoid osteoma in a young patient with persistent. undiagnosed joint pain. radiological examination. bone scan, and CT should be repeated I year after the onset of vyrnpioms. since the initial negative findings may be positive at II later date. BOlle ,cj ntigraphy and CT aid in the diagnosis. Scintigraphy ldernifies rhe affected [oi nt, and CT [t.,.'>bt~ in I ocal izing the precise tumor site.


UU\lq;-, .-\G ,~d'· BiH1c" Tumor-s. 1J~:3g.JIO:O;h_ T~aJm~TlI. and Prognosis. 2nd ed, PhUtJ.J~tphla1 W B. Seunders. 11)90. 2, In)' RM S"'.g,",,1 rrcounem "I rcteonl ~"e"m" in the adolescent. J F"QI Sure' 29:495-498. t99O.

1-. Kenzn nl I.E Problem ~ II! ni.-' ian terc din ! he d I,agnn~i~ I mel rren I rneru o r osteoid os reorna -of the t [\1 us. Fool A nk 11; ::!: 17 2-J7 g.

I"~ I.

-l. Resnick D 1~!lI' DUl~no>i, "I' Buoe urul Iuim Disorders, 41], ed. Philadelphia, W,B. Saunders, 2001



A 19-monlh-oId girl who is unable to walk

A \9-m<ll,th-old girl h presenred for e val ual ion of an u nstuble grrillipon urnbulation, The parent,' primary concern is a falling tendency that has been evident since the child began 10 walk at <;) months of age.

Physical Examination: Gail analysis: abnormal cquinus gail: heels elevated Juring enrlre gail cycle: when c~[alionur .... heels came JO~~fI to supporting surface and kn.ec, weru inlLl genu recurvatum, Neurologic: no delay in development, no deficit; normal for age: equinus congenital. I10t related to any neuromuscular d isease,

Treatmeru Course: Serial dorsiflexing casts were employed in <111 attempt to reduce the bilateral equinus and geuu recurvatum. The casts were applied in knee extension, from the l,)e~ W !.he proximal thigh. and changed weekly for a -l-week period, Gradually Jllrsillexing the foot 10 decrease the plantarftexion III the ankle reduced tbe equ mus. Fullowi ng cast removal. reduct ion OJ!" the equinus deform il)' was rnaintained. Ankle dorsiflexion W;lS increased to 15 degrees, arid the child had u remarkable abilil}' (0 amhulute.

A pproximatcly (] weeks after rhecasts had been removed. tilt' parent. observed the ch ild 10 have some difficulty walking. and within a few weeks she had 10.'( all ability (0 sturul straight. The genu recurvatum returned in compensation of the equinus. The chihl ev enrually ~tar(ed leaning so tar forward in an effort to rnuintam balance that she wOl.IlIJ fall, In" short lime ~hc W,L' unable to stand or walk. CaRling wag rei nstnted and the possible need for an Achilles iendnn-lengthening procedure wus discussed,

After I month of casting no Improvement of the equinus was observed. and casting was disconrinued, A COllSU lmtlon with the ch ilds pedi auicia n revealed ihut he too had riot detected any neurologic abnormalities or deve loprnental delay. With this con fusi Ilg picture of con ti nua] contracture of un known origin, additional studies were perf ormed prior 10 the tendo Achil ie'i lengt hell ing.

LaboraJ.o!J' Findings: EMG Herve conduction velocities: no sural nerve sensory response: motor nerve velocities in upper and lower extremities slowed; sensory action potentials diminished in ampllrnde. with prolonged latency to peak, MRL of brain tTl-weighted images): ahuorrnal mcreased signal intensity in supratentorial while matter bilaterally, occipital region greater than frontal Enzyme analysis: arylsulfarase A deficiency.

Question: Whar i~ your diagnosis?


DiagrlO,~is: Metachromatic leukodystrophy (MLD)

Discussion: The late infantile form of MLD hegins insidiously between the first and second year. II is transrni ned il~ an autosomal recessi VI' trait, Patients homozygous for th is allele have a .;umplete absence of arylsulfarase A acriviry. With the absence of th i~ enzyme. cerebroside su 1- lute accumulates in the lysosomes of different tissues. including the liver, kidney, gall bladder. and white matter. Deficiency in the activity of this enI} me. the heat-labile component of cerebroside sulfatase. nas been established as the primary enzyrnatic abnormality ill 1V1LD.

The deficiency I"; most frequently demonstrated In urine. peripheral I eukocy tes, and cultured skin fth rob I asts, bUI is also see n in se rum. kidney ti ssue, ,1111.1 bone marrow cells, Not all of these tissues are affected by the abnormal amount. of [his sui fatide, hut the white maner of the nervous system does lend IU be damaged. In faci. it ls the abnormal accurnulacon of sulfande within the oligodendrogliai and \chwann cells (two cell types t'ulilld in the myelin <heath) and [he metabolic fail t1IC of these cells that precede and trigger the events that cause dernyelinlzation. Myelin breakdown resu lis From . .:1 defective

resorption of cerebroside sulfate. which is necessary for the axon to grow. Additionally. even after maturity . enzymatic failure to metabolize this lipid can prevent normal restrucmring uF the myelin sheath.

Early on. most patient s appear normal clinically and neurologically, Then progressive menta! regression. loss of speech, ataxia. and muscle weakness become evident. Genu recurvaturn secondary to equinus deformity is often present, and a child who has al ready learned to Walk, similar to the one presented, becomes unsteady in gait.

The child with the late infantile form usually does not survi ve beyond the first decade, Central ani.! peripheral nervous system demyelinization and degradation often lead to a very debilitating ex isren ceo and must uf I hese child ron con tract fatal respi ratory infect ions,

In Ih~ present patient. EMG findings were considered to be consistent with 11 demyeJ ineting neuropathy. MRI findings were consistent with leukodystrophy. These findings. coupled with the discovery of'arylsutfatase A deficiency. pointed to the diagnosis, This final stage of metachromatic leukodystrophy proved to be fatal.

Clinical Pearls

L A complete neurologic examination is imperative when considering any tendon pathology thar exh ibirs ei ther a spasticity or ~accidity,

1. Any change in gait. stance, or position afterthe child has begun to walk is a cardinal sign of some type or degradation of motor function. A complete exam is required.


I Jay RJI..1: Meruchrntruulc leukodystrophy: A ,UNe report or" child wrth on e quinus deformity, J Foot Ankle Surg 34:206-207. 1995,

]. Kclodny EH: )vkWchwIIL"iLl' leukodystrophy and multiple ,,,In,,,,. deticiency: Sulfuude lipidosis. ln Scnver CR, Beaudet AL. S[ Y WS" v ill I" 0, et at I ~dsJ: Men bolic und Mol eo" tor Buses of lnhe rlted 0 t se ase, ~ lh ed. New York. McGraw-Hit 1. zco:

], Kcivil W Treatment o] late mfuntile metuchromunc leukodystrophy by bone marrow rransplnnrmlon. New Engl I Mod J!21 [):"3-31. I ~y{).



A 6-Yi!ar-old boywho waJks with flat feet

A 6-yellr-olll boy is seen for evaluation of iruueing. He has been previouvly Jiugnu","u with bilateral metatarsus adductus, Prior treatment consisted of serial ea-ting for 8 wed" begun shortly after birth. followed by correcu ve shoes unri) age 12 months. H is parents feel (ha~ the metatarsus udductus has improved since birth: however, they still have concerns about the residual dcforruity They deny thai. their child had any luncucnal problems.Muternul famlly hisrory i, r",ilive for InIl1dng:. which was treat ed wit h II De nis Brow n e bar an d c orrect j ve :; hoes.

Physical ExaminatiOIl: Gait analysis: bilateral dcfbrmitiev-c-rcurtoot -rnnre position 20° evened (valgus): forefoot adductcd. on reartoor, General (see figure): large prominence ar base of 5th metatarsal, prominence 01' talar head; medial arch thickened with callus over bony prominence. Musculoskeletal: limitation of dorsiflexion III ankle in both knee extension ami flexion,

Laboratory Findings: Radiographs: talocalcaneal angle > Jj degrees 1111hl' weighl-bemng position; lateral subluxation/dislocation of navicular from talar head: adduction III' metatarsals at Lisfranc's joint with [alar-Is! metatarsal angle divergent medially: ·incfea~ed larerul tHloc:aicsneai angle with talus planiarfiexed on calcaneus.celcaneal lnclinauon parallel to suppnrting surface

QueSUQn: What is your cunc c rn ill a child with recurrent rneunlductus"


Diagnosis: Residual metatarsus adductus and secondary cquinus

Discussion: The position of the navicular on Ihe talar head should be taken into consideration when determining It surgical versus conservative dpproach. A laterally posirioned navicular demonsrrates subralar pronation, while a medially posiriuned navicular on the ralar head is seen with talIpes equinovarus and cavus foot deformities. This type of supinated position has to be addressed separately and is usually seen with a forefoot adLiucrus deformity. The radiograph will reveal the navicular position on the talar head .. When reducmg the metatarsus adduct us angle with transverse plane abduction, an abductory force may be exerred at Chopart's articulation. If 11 lateral devialion of the navicular occurs during this cast reduction, cas! therapy should cease. With continued transverse force and midtarsal joint abduction. the result will be a rectus foot at theexpense of a pronated flatfoot.

The calcaneal cuboid relationship is studied to

determine the presence or absence of forefoot adductus. Forefoot adducrus is a ,on tissue. deformity produced by midtarsal joint -upinatlcn around the oblique axis, resulting in plnntarflexicn. adduction. and inversion of the forefoot, Forefoot adducrus is evident with an adducted position of the cuboid on the calca ne us. On the radi ograp h "f an add uc led forefoot. a line from the calcaneus through the Imeral surface of the cuboid deviates in the direction of adduction. Normally.these tWO lines do not converge. An adducting line demonstrares ubi ique ax is supination; an abducting lint' demonstrates mid" tarsal joint oblique axis pronation .. In the presence of abduction of the cuboid t rn idtarsal joint pronalion), II metatarsus adductus deformity will need 10 be addressed more radically and rrggrcbslvely.

In the present patient, a conserv at i VI? treauneru was planned with the use of a dynamic. stabilizing shoe insert. This orthotic managed his problem successfu lly by limi ti ng prouaiory changes.

Clinical Pearls

I. Total reduction of the rnetadductus deformity means not just the reduction of the forefoot at Lisfrane' s. but also prevention of pronat ion .and the development of an equinus, Always reduce the deformity early and maintain in a high flange insert to prevent transverse plane.

2. Equiuus is the great deforrner of the fool. Consider lengthen ing procedures. if neeessary, 10 i nerease dorsiflexion and thus prevent secondary pronat ion.


1. J~y RM. Johnson M: Recurrent metatarsus adductus. Current P,l<iinlry 33:33-12. 1 q84.

2. Kite JH: C"ngenilal metatarsus varus. J Bnne Joiru Surg·49A:388-397. 1957.



A 58.~'car-old man wilh complications after arthroplasty

A 58-ycltr-old man was ,1dll1iIL~d In [he hospital with D chief complaint {If a stiff, painful 6rsi rnetararsophulangea I. (M1'Pl· jn rru of [he right foot, This condition had been present for many years, but recently The puin become more intense, The patient underwent an arthroplasty of the .lirSI MTP joint, with a totul sillcon-type large implant, He tolerated the surgery. nnd did nOI develop any posroperative cornplicatiens He W:C, then followed weekly for observation and dressing changes: no complications oecurred during this period.

Two months after the surgery, the patient returned with [he complaint that the operated MTP joint had become progressi. ely swollen. Warm water soaks were prescribed, along with ampicillin for a 10- day period. Following (hi,. therapy, the inflarnrnarinn decreased, However, a month later, the patient returned [(1 the emergen.:y dcpurtrneru with a red, hut. swollen first MTP joint und celiulitis extending proximally to the ankle. The patient IHIS directly admrued to the hospital.

Physica! Examinations: lnitiat-« MlI~cultl~kdetal: MTP joint approximately 10° range of molion: stiff on both planmrfiex inn and dol'S i tle~ inn. Palpation: dorsal promi nence; joint painful at rest and upon increas e tI motion (..<H(' Pnstoperutive-: Skin: ~Iighl edema. Palpation: tenderness along MTP joint at surgical site: drairnng soft-tissue mass on medial aspect or firSI M'IP JOInt of right foot

Luboratory Findings: /Ililiul-Radillgraphs I right foot'): narrowing and sclerosis of first MTP joint. with rruld hn 1111,\ abducto \ algus detorrni [)': small ostecphyres and large dorsal ledge on luteral view. ulll' Postuperntive= Radiographs (righl foot): marked resorption a! proxima: phalangeal shaft; marked periosteal reaction ru first metatarsal shaft and head: radiolucency within shaft and bone at area uf total implant.

Questions: What i~ the most likely diagnosis? What other conditinn can present withthe above findings'!


Diagnosis: Osteomyelitis of the first metatarsophalangenl joint with foreign body reaction

Discussion: Silicon is virtually inert: however, there is 01 ways the poss ibi I it}" of lnreign rnarerials adhering to the implant after nutoclaving. The particular matter on the i mpJant- possibly Ii 111 (rom drapes or powder from gloves-is then trapped in the rned 1.111 ary cana I all d can con cei vably touch off a Foreign body reaction. When the rrnplam is in place, there is a diminution of the vascular supply to the area in contact with [he implant.

With the decrease in blood volume. it is under'[a nda b I e th at there will be a decrease in the to tal phagocytic action in that un it area, A long the same lines, we mUM consider why there is a predilection of bacteria at the implant site or metaphysis. In the metaphysis, there is a normal slowing down of blood at the juxtarnetaphysenl hairpin turn. This slowing predisposes il, bacterial emboli w seule in the veins and cause thrombosis. with a retrograde occlusion of the capi llaries, then transudation. and n nul j y marro IV neeros i s.

There is also tile pnss i b ili ty 1)[ a v llSCUJ ar necroSIS. because capillary loops adjacent to the epiphy,eal growth ptaie are nonunasrornising branches of the nutrient artery, Understanding this, we can appredate the great nsk of an insidious contam inm ion or un predi c tab lei n feet ion.

In most noncontaminated surgical wounds, rhe acute inflammatory reaction subsides. and recognimble tissue repair commences in 3 10 5 days, Surgical wounds that have become comaminated.

or those that contain a foreign material noteliminated by the acute inflammatory process, manifest a chronic inflammatory reaction.

Mononuclear cells are the predominant cells of the chronic inflammatory reaction. They phagecyuze the remaining foreign material that the eozymes of the granulocytes were unable to make soluble. If the foreign rnateri al persists. II chronic inllummatory reaction is set up in which the mononuclear cells undergo a prol i fe rari on. These rnacrophages are responsible For the chronicity of the influmruarory response. They remain in close proximity to the foreign substance for as long as it takes \0 eliminate it,

The magnitude of a chronic inflammatory reaction depends on boththe chemical and physical re(lclivil) of the causative material. Every foreign substance. no maner how inert. evokes an immune response, A relati ve Iy inert substance such as silicone, upon removal from the body. might appear as if no reac tic n had (lee 1.I rred, Howe ver, on microscopic examination, (I layer of mononuclear cells covered by ,I thin fibrous capsule is discernible,

[1:1 regard to the physical properties of a foreign substance that affect its reactivhy, both surface quality and mohility are important, A SUbSLilJWe that is smooth and immobile produces much less horous proli Ieration than one thai is rough and subjected [0 motion.

Clinical Pearls

J, Tin}' silicone particles can breakoff un impl am with wear or shear w ithin a joint. :!, MRI is mos: useful to determine the presence of shards within the surrounding joint.

J_ Complete removal u]' the implant should be performed and antibiotics adrninistered prophylactically,


Shiel we Grunularmuous lngumul Jymphedeuopathy "1'1« b,IOIcro! mcrutarxuphalungecl iOlnl uihcone Arthropl as ty. FooLAn~k 6-~I6-cIS. 1986,



A 19-year-old man witb a soccer injury to bis right ankle

A ! 9-yem--o!d man sustained ;J rapid dorsiflexlon injury of the right ankle ..... hile playing soccer, He was unable to continue pi ayi ng because of pain and swell ing. which developed rapidly over the next hour. The immediate physical and radiogmphic examination yielded a diagno,i> of a moderate grade 1I ligamentous sprain of the right ankle. The patient was placed in compressive dressing with a posterior splint, and gi vencrutches w il h instruc lions for non-weight bearing. The pain continued for approximately 2 weeks. and the pencnr felt no better rhan at the lime of original treatment. f-Ie now presents for nddirional assistance.

Physical Examination: Pulses: no! palpable due ro massive edema. Doppler study: dorsalis pedis and posterior ti bial vessels patent. Museu loskeletal: ROM li mi ted and painful in all planes of motion; no pain nt medial and lateral malleoli: severe pain upon grasping tibia and fibula malleoli between heels uf both hands DnJ squeezi ug. Pain was greater with subtalar in version than unkle i 11 version,

Laboratory Finding»: Radiographs: linear. nondisplaced fracture of talar body extending from ankle joint uno posterior tacet uf subtalar jnim,

Qllestion: What complication must be ruled out in a patient with a ralar fracture?


Answer: Avascular necrosis

Discussion; Talar fractures are relatively uncommon, but they can lead to potentially serious complications. Since the talus has no tendinous atracbments. and 70% of its surface is covered by .uticlilar cartilage, the blood supply is extremely tenuous. As a result, avascular necrosis (A VN) of tne talar body is a commoncomplication.

Although there are a number of classification ~ ystems for talar frac lures, Can al e and Kelly recumrnend the Hawkins classification. This system describes the fracture pattern and predicts the likelihood of future complications, such as A VN and post-traumatic arthritis. There are fOUT types of fracture with an increasingfrequency of A VN: type J bas iii 0-13% chance of developing AVN; type J] is worse, at 20-40%. Type III has a 8Q.-100% chance, and type IV win go onto A VN 100% ofthe lime. The mechanism of injury involves a rapid, forceful dorsiflexion of the foot against a stationary tibia, causing impingement of the talar neck on the tibial plafond, Continued force results in medial and dorsal comminution. along with disruption of

the talocalcaneal ligaments and ankle and subtalar capsules, As II result of this disruption. ihe already tenuous blood supply to the. talar body can be sig~ifica[Jtly disrupted, and A VN occurs.

The diagnosis of A VN can be made on plain radiographic eval uat ion by the absence of the socalled Hawkins sign. This sign. which Hawkins described as subchondral bony atrophy found in the body of the talus, indicates a normal reacti ve hyperemic stare at 6--8 weeks l'ollowi ng these fractures. Additional methods ofcvaluarlng AVN lnelude scintigraphy and MRf.

Once A VN has been diagnosed, the goal is to prevent talar dome collapse. According to Penny and Davis, it takes 2 years for a scleroticralus to revascularize. With this in mind. patients should he kept non-weight bearing on that side for an extended period with the use of a pall'!lar tendon beari n g brace.

In the present patient, A VN was ruled Out by absence of the Hawkins sign on x-ray. The talar fracture was treated with a below-knee cast, nonweight bearing. for 6--8 weeks.

Clinical Pearls

L Complications of talar neck fractures include: avascular necrosis iAVN1. nonunion. subtalar and ankle joint post-traumatic arthritis, skin necrosis, and csteornyelitis.

2. The first clinical sign of AVN is intractable pain.

3. Evaluate for Hawkins sign !J-:g weeks post-injury.

4. Once A VN is diagnosed, the goal is to prevent talar dome col lapse,

s. Rev asc 1I larization is enhanced by accurate. stable reduction of I he fracture fragments.

6. It takes approximately 2 years for II. sclerotic talus to rcvascularize.


I Ghoi"n P. et at: Treatrneat of taw neck fractures: Clinical results of 50 pnrieuts. J FOOl Ankle S",,£ 3')16): 3M-n5. XIOO. 2. Penny IN. Davis LA: Fractures and dislncatlons ofrl1e neck of the lotus_ J Trauma 20: 1029- t037. 198;0.

J. Thordarson D' Tnlo, r ra en.res FOOl Ankle Clin 4{3):555-570. t 9Q9.



A l.l-Jt!flr-old hoy with am internal rotation injury to his ankle

\ l-l-year-cld buy i, .. cen in rhe emergency department after sustaining an internal rotation injury to the right ankle :i hours U,!!". Inhial rreatment consj'1etl of x-rays, ice. elevation, compression bandage, and crutches, Fhe patieru was told he had SUSTained a severe ankle sprain and should remain nonweight bearing for I wed.

Phy . sical EXil/tliJl(ui011: Genal! I: -wollen right ankle, Musculoske feral: pain on pal pation of anterolateral ~~pec'l of ankle: neurovascular '1~IUI~ intacl ami syrnmerncal, bilaterally; ankle ROM markedly decreased; rai 11 upon plnnlarfle~ ion and eversion.

Laboratory Findings: Radiographs. avulsion fracture of tibia un nnteroposterior and lateral views, CT ~~·<IIl: intra-urtlculur lrucrure 01 epiphysls extending 10 pbysis, exhing laterally through open physls. and producing recumgular-shaped lrncrure. Evnluauon revealed I! displaced Salter-Harris rype III fruu Lire ur a juveiule 1 ractu re ul Tlilaux.

QlleSliflflS: Whlll j, rhe innial trenunent of this type of injury? Wbat is the indication for surgery?


Answers: T reatment depends on [be amount or d lsplaccmenr. Tf> 2 mm. surgery is indicated.

Di.~C!lSS;Q/I: The rnechan ism of lilt: JU veni I.:

I nu;ture of Ti llaux is either a latera I rotarian of the f"ut (abduction) or u medial rotation ell' the leg on the fixed 1'001, The fracture fragment is avulsed ['10m the anierolateral aspect uf the distn I tibial ~rtphysb by the unteroi nferior ubiof bular I igamerit, when an exre rnal rotational Fol'{'c is app! ied h) me foor and reduced by me opposite mechanism. The fracture tragrnem produced is roughly quadri latera) because the fracture I inc runs verticully LO the physis and exits an rerolurerully. producing a Salter-Harris type III fracture of rhe distal tibial epiphysis.

I'rearrnent i.'. based on the amount of displacement of the articular surface after closed reduction techniques are auempred. I f (he separation is greater than two millimeters, (hall arthruscopic.,~sisted or upen reduction with internal fixation is r.::commended. The prognosis usually is good if matornic reducuon of the art icular surface is ubrained The most serious complication reported has been pain and stl ffness secondary to articular joint mcongruiry follow i ng inadequate c losed reduction.

Initial treatment of a nondisplaced or mildly displaced juven i Ie fracture of Tilluux should con;'1:;1 of an attempt at closed reduction and placemerit In a oerow-knee Cal! WI[h the 1001 m I nternar rorarion. In the acute injury, a hemarorna block. with aspiration of the unkle joint is performed afrer appropriate skin preparation, The foot is ]1lc\ce.d in full dorsillexion and abdncted, The mechanism is then reversed with your contrulut<::r,11 thumb app] ying pressure 10 the anterolateral

tibial physis and fracture fragment. While internally rotnting the foot \.10 the leg. maintain axial traction, A natorn ical reduction of the fracture fragment i, rna ndaiory. lf the fracture i, displaced mure (han 2 millimeters. perform open reduction and internal fixation. When the fracture fragment is rotated, closed reduction can be difficult due to iruerposiuon of the periosteum and ankle joint capsule.

Su rg ical reduction requ i res an anterolateral approach to me ankle JOU!! between and parallel to the extensor digitorum longus tendon and the fi bula, Take special care to identify and avoid injury to the lateral cutaneous branch of tbe superficial peroneal nerve. TIu: superior extensor retinacul urn is rhe f rst dense structure encountered. W he n the pc ro neus tc rt i 1.1'> is presen t, the same surgical interval can be used with medial rCLTaClion of the tendon. Usually the anterolateral ankle joint capsule is tom along with the syndesmosis, which can lead to insrabl I ity between me distal tibia and fibula. Inspect me ankle joint to remove any debris. AI so check (he i nlegri Iy of the dome of the, talus ..

With open anatomic reduction of the articular surface. internal fixation is then used to maintain the correc t10 II. It IS rec 0 In menGCIJ tnatme In tern aJ fi xation be placed parallel to the physeal plate, but if il is necessary to cross the physis, smooth Kirschner wires are advi sed.

In the present pat ient, open red uction was necessary to red uce the fracture. as d i sp I ace rn e n I was more tha n 2 millimeters.

Clinical Pearls

I. Attempt closed reduct ion wi lh compression of the fragmen L Take care not to produce !I pressu re necrosis after the cast has been applied.

2. In form tile patient and rami Iy that surgical interven lion is usually indicated if the dosed reduction has failed idoes not appear rudiographically).

J. Post-reduction films are indicated 10 check [be reduction. If doubt remains. order CT scans,


I Kleiger B Mm'km Hl: Frncture "I' the loterul pcnlon 01 the d",,,,llih,al epiphysis J Bnne J(O;n' 5urg -t~A:15.1 %4_

Simon WH. Flcrns R. Schoenhuux H. lay RM- Juveni le frncmre ot Tjllau x: A distal nbral epiphyseal fracture. J Am Podlarr \.led """0, 7~'2~5. t98'1

1 <;,danic:h RJ. Lozmun l Ille juvernle fracrure M Till"u, ('I [II 1),,11,,1' 11[J;21 g. I <j~~



An Ll-year-nld boy with arch pain

An l l-year-old boy com plains of painful arches and increas ing discomfort wh i Ie weari ng shoes.

His mother observes that his walki ng l1a~ changed, and he cannot run well. He experienced occasional turning in of his ankles over the past year with increasing frequency. The patient's father and paternal uncle had similar problems when they were boys, The child is now seen in the emergency department with a fractured 5th metatarsal base. He states that he was only walking when he felt hi" foot "give way."

Phy~·icfl.l Examination: General Isee tigllre)· cavovurus deformities of both feet, w itb limitation of ankle dorsiflexion: all toes contracted and clawed. Gait analysis: patient unable to walk on heels without balancing himself against w~11. Musculoskeletal: muscle strength of tibialis anterior and peroneals weak bilaterally. Neurologic: sensution, pnnicularly vibratory and positional, reduced distally; ankle reflex not cliched.

Laboratory Findings: Electromyograph ie study: .. lowed conduction vc locities: reduced number of motor unit action potentials and fibrillauon potentials; increased proportion of polyphasic potentials and fascic It lat ion poiernials,

QIIl'S.liOflS: What is the di agnes is of this hereditary poll' neuropathy? What altemaih es are a vailable to allow gail stabi luy !


Diagnosis; Charcot-Mai ie- Tooth disease

Dlscussiou: The prognosis For progression varies with the speci lie inherited subtype of this pulynellmp~lhy. 111e inheritance pattern in this case seems to be dominant, implying a better prognosisrhan if it were recessive,

The first step is 10 control the rearfoot in version, Placing the forefoot in vulgus minimizes the supinatory rock that 'Will throw the rearfoot into further inversion. The rearfoor can be stabilized IV irh a neutral 0" post to Jock the heel: the addition of a high-heeled seat w ill insure tile stabi llry,

r n the p resen [ parie n r, a con serv J li VI' app roac h WJ~ rnitially taken to mllnage the progression of'the

deformity, However. he did not tolerate the orI horics. and surgical options were explored, The surgical procedure consisted of plantar fusciotomv Dwyer calcaneal osteororny, rendoachilles length~ ening, and posterior tibial transfer through the interosseous space to the dorsu m of the foot. The nell I stu ge cons isted u f a J one s procedure to the great toe. prox i m aJ Ii rst meta tarsal os teotom y. and trans~'er, of the e xrensor tendons into the metatarsal necks. The combination of these procedures reduced the cavus detormiry and provided a pain- free gn it, The h ee I v arus wa s red 11 red, and the ankle spraining W<lS eliminated.

Clinical Pearls

I. A high-flanged, .. leep heel seat control s the fool and can I i mil inversion-type illjuries.

1, Care must be observed when rreaung conservatively. as an overposred rearfoot will induce further sprains in the cavus foot.

J. The las] resort in children with Ch3fCOI-M;;lJie-TMth diseuse is a triple anhrodesis: with early recogn i t ion, this can be avoided.


I. Fishmun M: Pediatric Neu",Togy, Orland", Gruneann Strauon. 1')86.

1. ~kOWnry E. Bunks A, O""',, e y M. Cornprehenove Textbook ,,1 POOl Surgery. 2nd «I. Baltrmore, ~1D. Wil'l;o",.'" Wilkins, J'l9~.

1 Quin N. Jenner J>: OI>OL-.Jef'; ot l.1M<menl: Cluncu], Ph:\nnalXLtog,,-u]. and Physioto!llC.1 A,pecI" Sill' Diego. Academic Pre" ]98Q.



A 72-year-old diabetic woman with a plantar ulcer

A 72-year-old woman is admitted (0 the hospital with a plantar ulceration of the left foot, located below the 2nd and 3rd metatarsals. Cellulitis on the great roe extend; proximally \0 the 3rd metatarsal. The patient has been diabetic for 15 years. and her diabetes has been controlled with 3S units of insulin NPH. She rei ales bavmg a bunionectomy 25 years earlier,

Phssica! Examination.- Lower extremity: femoral, popliteal, and dorsalis pedis pulses easily palpable: no redness or swelling: calloused periwound with serous discharge at ulcer site; wound base firm and pink, with granular consistency. Neurologic: no response to Semmes- Weinstein probe.

Laboratory Findings: Chemistries and complete blood counts (including controlled blood sugar): normal. Temperature: 98.6° F. Culture and sensitivity tests of ulcer: 110 growth on three consecutive samplings. Radiographs (see 'igure): grossly abnormal left foor=rnerararsals tapered absence; lrst metatarsal neck absent: derninemlizauon and destruction of 2nd metatarsal bone: l rst metatarsal head and shaft appeared "moth-eaten," with atypical configuration LO trabecular structures,

Questions: What is the most likely diagnosis based all the radiographic findings? What methods are used to confirm the diagnosis? Describe the treatment SlHging that may prevent recurrence of the ulcer.


Diagnosis: Osteomyelitis

Discussion: Osteomyelitis associated with peripheral vascular disease, r ound frequently in diabetics or pauents w ith nrterlosclerosis, is a Ji.'ease of the elderly. The patient with vascular in~ sufficiencycfthe lower extremity is most likely [0 develop osteomyelitis lrorn 3 focus of conriguous infection. Small hones of the feet are most [requently affected, with mi xed infection of Stlll/lly. /(lCOCCrtS alm?ll, and enterococci .. 'I.~ would he expeered, systemic manifestations are few. ami local signs predominate.

Light touch is the primary sense that allows rhe patient to be aware of and prevent areas uf irnpending breakdown. When this sense is lost. ulcerarion is i nevitable, There Core. quantifying the pressure sense in a patient's foot is cruc ial to the exam, The optimal piece of i nstrumeniation 10 quantify light-touch sensation in 3 pinpoi ru distribution adequate for awareness of impending breakdown is the Semmes- Weinstein filament. ~ This is a ny Ion probe, smaller thana ball-point pen, th B I is cali b rated \0 b uckle at 10 grams o f I in ear pressure against the patient' 5 skln -lhe amouru of pressure necessary for protective sensmion. If the patient cannot feel the probe buckling agaim;\ the skin, then he or she is at signi ficant risk for the develcprnern of neuropathic wounds.

Biopsies and cui iures are 110/ taken .J irectly [rum the wound cavity. Wounus are conmrnlnated, Biopsies (boneculrure and bone specimen) should be taken from an adjacent, uninfected area v ia a separate incision.

At the completion of the biopsy. the wound is then addressed by surgical excision. Too often we perform local debridement in the office, removing only the obvious fibrin and necrotic tissue. but leaving devitalized deeper structures. Deep excision of tile devitalized tissue to include ~kjll. tendon. muscle. and bone is mandatory, Sharp dissection with a scalpel or with roungeurs of various sizes is helpful in isolating necrotic from healthy tissue, The roungeur is placed undernemh the wound edge, lind the hyperkeratotic and devitalized tissue is removed,

The lrsr metatarsal head is the rnnsr common area for breakdown. The normal Foot has all <:V~11 pattern or motion. with nice, graduul heel contnct=-a gentle rolling (not excessive) from the outside to the inside or the 1'00t as the foot prenares through, with one bone bearing weight that gradually shifts to another bone.

Contact casting is a way 10 reduce plantar pre~-

"The Sernmes-Wemsrein hlurnent can be obralued from the Hansen's Diseuse Center In Cnrville. Louisiana, 11 should be in the nrmarnentarluru of nil wound-cure protewionul s.


SUII' peaks or the ground reucti ve pressures, but it does nOI address shear force. Note that while the cas! may be reduce ulceration, upon removul the patient resumes his or her disordered gait pattern, and the shear forces return to create another ulceration in the sameor adjacent area.

Osteom yel i lis a f the I ISI meratars al head must be nddressed with foresight. Understand that the 1101 metatarsal head hears the rnajority of weigh! at propulsion. and 3 resecuon of the metatarsal will uans fer all of i he we i gh l to the ad] ace nt metatarsals. The new peak pressure on the 2nd metatarsal head plus the increased shear will lead to I'Lllun: calluses and the potential for plantar ulceration. Carry out a lo~oi~a_] sequence when planning metatarsal resections, and consider the deformity in stages:

Stage L The mfected metatarsal is resected as far prox imol us needed, thus decreasing the peak pressure that was the initialing cause of the ulcer. The ulcer is cornplerely and surgically excised, and the patient i~ placed on appropriate anubiorics determined by bone cu ltures,

Stage 2.111(" patient remains 100% off-loaded.

Sal i ne dressings. wet-to-dry, arc changed twice a day. The dressings should be placed (jeep into the excised wound eav ity,

Stage ), When tile plantar wound has completely closed, the forefoot is addressed with rega rd ro "u rg ic a I rebalanci ng. The fu nell on a I a oct structural integrity of the forefoot h paramount in reducing the risk or future peak pressure and shear force" related co ulcerations. Rebalancing is performed by pan metatarsal resections, rather than a transmetatarsal or isolated mel a tarsal resection. The fore fOOL mechun ics are redistributed equally. The weight-bearing surface is spread Oil! transversely over all five metatarsal shafts. With rhe rernoval 0 f on e met awn 0 l. i nc reases IV ill occ U r on adjacent metatarsals.

Stage 4_ With the fOOL now structurally balanced and able to function with equal weight distribution, orthoses can be used. A triple-laminate orthoses not only uccornrnodares me foot by molding and cushioning the abnormal bony prornleuces, bur also supports the fOOL in a neutral position.

I n the present pauent, an nlgorith III,ic treatment pklO was taken III prevent advancement ol'osteomyeliric progression, The. plan invol ved surgical debridement uf the i nrected bone and soft tisvue, The ulcer was surgicallyexcised. The patient was placed on a 6-weck ('OLlJS~ of the o pprop ri ate IV amibimics uleterrnined by the bone cultures).

We! tll dry dressing changes were performed Twice dally. and she remained non-weight bearing on the affected extremity. Once the wound granulated. the fOOL was rebalanced with the use of an

orthosis to accomodate the abnormal bony prominences and support the foot in a neutral position. The patient has now returned to normal daily activities.

Clinical Pearls

L. Never perform swab cu ltures of a wound; they are all contaminated. but not all are infected.

:'.. Bone biopsies and bone cultures are the gold standard in the diagnosls, and mandatory in seni ng up the proper course of antibiotic and surgical treatment.


Ddt J.'\, Li['.l.Ll-LOU,·h, deep-pressure '~'l'ng u,jng Semmes-Weinstein mcnohlerneats, In Mackin Ei. Callaben AD, Osterman -\ L. ~I .J \ ~(_b I: RenclbilJ 1-"1; an <If the H on". 5 [h ed. 51. LDUi •• Mo.by. 200 I .

Waldv,,~d FA. M"doffG. Swan> M'N' Osreornyelitis Clinic"! Fc'lIure£. Therapeutic Considerauons, and Unusual Aspects, Springfield, 1 L. C"hnrl." C" Thomas, 1<)7 t.

Wcing"n<h MS, The \4''''"gomen! Df Th~ (·h,.(!",~ Non-H ea hng Wound Philndelphia, Graduate Hospital Wound C.we Cenkrl" educ .. iHI .... d_l rn.mual. 1 ~Y.!.



A 65.year·old, insulin-dependent woman with a painful blister

A 65-year-old insulin-dependent woman presents with a painful "blister' on her right foot. She ,tales thai it appeared very rupidly, and has not responded to oral antibiotics und local wound care. It IS quite painful upon pressure. The woman is weari ng sneakers and socks, There is no history of lengthy walks or running rhar may have caused the blister.

Plzysical Examinanon: Tcrnperururc 99.6° F: vital signs sruble. General: alert and well oriented toJ surrounding s. Lower extremity: dorsalis pedis and posterior tibial pubes steady and palpable. Skin Isee figure): no trophic changes other than a 2.5-cm erythematous ring with 11 l-cm central bullous eruplion. located centrally on dorsum of right root. Musculoskeletal: area surrounding raised mass quite tender upon palpation.

Laboratory Findings: \VBC 16.200/fLl; ESR 160 rnrn/hr: fasting glucose J 80 mg/i.l1. Culture (WID bullae: negative for aerobe. anaerobe. lungal, and AFS.

QIII'IriOII: Whm is your clinical impression?


Diagnosis: Pyoderma gangrenosum

Discussion: Pyoderma gangrenosum (PG) was first described by Brusting. Goekerman, and O'Leary in 1930 as a rare. destructive. reactive neutrophilic dermatosis. PO begins as tender papules or vesicle. which develop inlo painful ulcerations surrounded by induration and erythema.

Pyoderma gangrencsurn ulcers may exhihit pathergy, which is an exaggerated response to a minor trauma and can lead to expansion of the u 1- ceration, PG can be iatrogenically induced from vaccination. injection . and surgery. Therefore. surgical debridement 15 II direct contraindication in this condition.

PG most commonly affects the lower extremities; however. there i an atypical form of the disease that is more prevalent in the upper extremities, head. and neck. PG primarily affects young to middle-aged adults and is seen more frequently in women then men.

Diagnosis of PG. according to Bennett 1;1 al., i~ a diagnoais of exclusion. and there is rIO specific laboratory Of histopathologic test. Biopsy of the ulceration will likely show epidermal ulceration with adjacent epidermal hyperplasia. Dermal inflammatory infiltrates and vessel walls with fibrinoid necrosis are also seen hi tologically.

PG can be associated with several systemic diseases. The literature slates rha: inflammatory bowel disease and arthritis are the most commonly reported disease associations. followed by hematologic malignancy. PG has 1I1so been asso-

elated with diabetes. SLE. lIIV. and many other conditions

The treatment of PG has been extensively debated, Topical therapy for mild conditions can include corticosteroid agents to the borders of the lesion, hydrocolloid dressings. antibacterial agents. and compression and elevation of the affected limb. Nonirnrnunosuppressive agents such as Dapsone and clofnzimine have also been used in the treatment of PG. The most commonly used and successful therapy is oral corticosteroids in large dose. Prednisone (1-1 mg/kg) is used for moderate to severe PG. However. high doses of prednisone can be accompanied by hyperten ion, hyperglycemia, osteoporosis. and increased su - ceptibility to infection.

The present parientv blister eventually ruplured and developed into an ulceration with surrounding erythema. Cultures revealed no growth. A biopsy of the lesion revealed dermal inflammatory infiltrates with fibrinoid necrosis of vessel walls and epidermal ulceration with adjacent hyperplasia. A course of loca I wound care and topical corticosteroids to the borders of the lesion was initialed. The lesion began to respond quickly to therapy. An Api igraft allogenic skin graft was applied to the base of the wound to increase healing lime and decrease wound contracture. The patient had immediate relief of painful symptoms. After a I month course of therapy. the wound was 100% epithelialized. She has had no recurrence of ulcerutions.

Clinical Pearls

I. Initial presentation of a painful. sterile nodule that eventually ulcerates is a key in the diagnosis of pyoderma gangrenosum,

2. When performing the aspirate. it is wise to collect a tissue sample at the same time.

Try to include the inner surface of the bullae or the base.

3. The hemorrhagic appearance is the salient feature of the disease.

4. Appearance is II severe destructive Slate.


l , Benne" M'L. 1[lJCA><1Il 1M. 1(1[11-1.0 JI." et "1. Pyndcrmu gllllgrtn~~um. A comparison of [}'p,eu[ nnd nrypicul forms with an ernphnsis (In lime [L' remissiun. C= ","je'" ('! 86 patients from two insurutinns. Medicine 701 [I' .l7--16. X>f1O

2. Burr BS; "11", "!i"lugy rmd treatment 01 log ulcers, J SC Mod Assoc S9·b7-70. 199,'

,. Imus G. Golomb C. Wllket C. _I ul Accelerated healing of pyodermn ~Ilngren"'"m 1"'"1«1 with binengrru-cred skm and conCnmi11l1l1 immun('lsnppre~~lcm . J Arn Acad Dermuuil -l4;bl....tJ, ::!OOl.



A 23-year-old woman with excruciating foot pain after a motorcycle aceident

A 23-year-old woman arri ves ut the emergency department via ambulance complaining of cxcruelating fight foot pain .. She has just been in a motorcycle ace idem, She was hi! head-on by another vehicle and sustained a severe dorsiflexion injury to her right ankle. She ,.tho has a minor laceration to the face, but denies any other pain.

Physical Excminatio»: Vital signs: stable. HEENT: normal. Cardiac: regular rate and rhythm; mild tachycardia. Chest: clear. Abdomen: benign. Skill: normal; noattenuation or breakdown, Neurologic: motor and sensory intact. Lower extremity: right ankle and font iii guarded position of slight plantarfiexion: dorsal is pedis and posterior tibial pulses strong, Musculoskeletal: gross swell in!.!: of midfllot and ankle, with ecchymosis; marked tenderness about ankle joint and subtalar Joint, with decreased ROM and crepitus,

Laboratorj' Findings: eBC: normal, Radiographs: skull, spine, and chest-> no abnormalities.

Ankle lateral view (see figurej=-talus posteriorly displaced. with verricel fracture through neck; dislocation of subtalar joint: ankle and talona vicular joint intact, Uri nalysis, normal,

QI1€stiorrs.: How is this fracture classified? What is the most common complicatlon'l


Diagnosis: Talur neck fracture. Hawkins type U

Discussion: The tlliu bone is pnrnarily cancellous. with no muscular origins or insertions, and rwo-rhrrds of the surface area is covered with articular cartilage. Therefore. a high percentage of talus fractures are intra-articular, and, due to me tenuous blood supply, avascular necrosis is II common complication,

Three main branches supply blood 10 the tal us: the pcsteri or ti bial, anterior Ii bial, and peroneal arteries, The posterior ti bial artery is further divided into the calcaneal, supplying the posterior tubercle: artery of the tarsal canal, supplying the body: and deltoid, supplying the medial side of the talu , The anterior tibial artery branches lruo the medial tarsal. supplying the superior medial neck; lateral tarsal, supplylng the talar head, 1l.I1U urterv of the ~illw, tarsi, which supplies the taler neck and body and is fnmled by anastomosis between the lateral tarsal and perforating peroneal.

111e typicul uilar neck fracture is vertical from l.I1e dorsal neck and exits the tarsal canal, which is the weakest portion of the talus, There an: two theories as 10 the mechanism of injury: a hyperdorsiflexion causes the ned. to impact against the anterior edge of the distal tib-a, or the talus acts 3S a cantilever and the neck breaks due to bending forces, The most widely used classification system for ralar neck fractures is the one developed by Hawkins in 1970:

Group I-undisplaced vertical neck fractures Group II -di,placed fractures with subtalar joint


Group ill-displaced fractures with subtalar joi III a nd ankle dislocation

Group IV -displaced fractures with subtalar joint, ankle, and talonavicular dislocation.

Most talar neck fractures, except nond isplaced,

require open reduction with anatomic alignment and insertion of a lag screw,

Avascular necrosis (A VN) is likely (0 occur if two-thirds of the blood supply is disrupted, causing weakening of the talar trochlea, which is subject (0 collapse if full weight-bearing is allowed, The incidence of A VN is around 40% for a type IT injury and 90-100% for type ill and TV fractures, Radiographic presentation may occur at I~ months, appearing as a relati ve increase in bone density due to loss of blood supply and no bone resorption, The surrounding bone becomes osteoporotic as a result of reactive hyperemia from trauma; disuse is also a factor, The pre ence of subchondral atrophy (lucency) in the dome of the talus on an AP radiograph (Hawkins' sign) is indicative of healing and viability, The atrophy. which usually occurs at 6-8 weeks, results from disuse osteopenia and vascular congestion. suggesting continuity of blood supply.

Treatment of A VN inc ludes non weight-bearing cast immobilization with anatomic union for up to 2 years or arthrodesis, such as subtalar, triple, pantalar, or ribiocalcaneal (Blair fusion).

In the present patient, an extremely conservalive approach was taken, She was cast for 12 weeks, and then used II Cam walker for 3 months, She was kept nonweight-bearing the eruire time, No radiographic changes were noted, and the parient continued with the Cam walker for an additional 3 months, Her talus did not collapse. and a treatment of external filiation of the ankle along with pulsed electromagnetic field stimulation was attempted. Evidence of revascularization was noted. and the patient underwent a pantalar fusion us ing an iliac graft to maintain loss of the extremIty length. These procedures were successful in returning her to MI mobility,

Clinical Pearls

I. eck fractures are the second most common talar fracture and occur from either a hyperdorsiflexion or the talus acting as a cantilever.

2, The blood supply to the talus, which is very rich but extremely delicate, comes from three main sources: posterior tibial, anterior ribial, and peroneal arteries,

], Huwkins' classfication of talar neck fractures comprises four groups, based on increas i ng d islocar ion of surroundi ng joints,

4. 0\ vascular necrosis is the most eomrnon compiical ion, It appears radiographically as 11 relative increase In bone density.

5, Hawkins ,ign is indicative of viability. Ii presents at 6-8 weeks and appears radiographrcally as a subchondral lucency,


I -"".J. T'S, Kcllv FB Fracture uf the neck u r u.., talus lung-Ic<rm evaluation of 71 co.", J Bone Joint Surg 60,0., I-B-I.56,

1<l7R, '

2, "'.!Llle, M r T.lI:], nee], fructures und nU", of nvavcular necrosis. J POOl Ankle Surg 38(2): 154-162, 1'l9'),



A )4-)'em··old woman wlth high-arebed feel and ankle pain

A .14-yeur-IIIJ WOlTILlI1 presents with bilateral ankle pain. She relate" aching pain in her lateral an. kles thar worsens wirh incre.rsed acri viiy. und complains of frequent ankle sprains. She stales that she ha~ ill ways huil v t:l"y high-arched fc·el nnd has di fficulry wearing certain shoe gear. The patient denies . . my If<W mao She has [ned prefubricated orthotics with lillie rel ief

PhYljt·a.l Exumination: Viral 'ign~ stable. H EENT: 1100111al. Canliac: regular rate and rhythm.

Chest: clear Abdomen: benign, Skin: normal. Neurologic: diminished ueep tendon reflex, decreased ,i bratory xcnsauon. ;Vlllsnllo ... ~dew I: Rc~ i ble, bilateral ell vovarus deformity with plantarflexion of I Sl ray: evidence of weuk ness with resisti ve ROM of Ii Ilia I is anterior; contract ure of lesser digits with hyperkeratorle 1e'lOn, ar .1,,1";;\1 PIP joint: no instability of ankles; no tenderness along lateral ligaments: atrophy of posterior leg muscles,

l.abora/(}ry Findings: CBC with differential: normal, Nerve conducticn velocities: 50% dec rease in motor ami -cnsory velocily.;5· rn/scc, lIiSlll] latencies delayed. Radiographs (see figure): n iarked cak~lle:l1 i nd in.n i 1111. with divergence of talar neck in pluntarftex ion: talocalcaneal angle 0" on -\f' VI~W

Qw!slil)I!.~: Whar is till' diagnosis? What nre some treatment options?


Diagnusis: Cnarcm-Marie-Tonrh (CMT) diM!UM:

Discussion: CMT disease is II hereditary melor and 5C nsory peripheral neuropathy resu Iting from an abnormality of rnyclination. 11 accounts for 90'l!- of all hereditary neuropath ies, Charcot and Marie of France and Tooth of England described it sl mu I taneous ly in I 1186. Origi nally the disease was described as a peroneal muscle atroph)'. but it was determi ned later thar the peroneals maintain most of their strength until the late stages of the diseuse.

There are two types of CMT" Type I or hyperrrophlc CMT is the classic presentation It is usuall y autoso mal do m i nan! and begins i n the third decade of life. Type I progresses slowly, with demyelination and atrophy of nerve fiber causing moderate impairment of muscle function. Type II or nonhypertrophic is the neuronal form, with symptoms less pronounced find occurring later in life. The pathophysiology of the hypertrophic form invul ves abnormal enzymes and molecules along the nerve causing premature airophy, There is a rernyelinauon and onion bulb effect that causes enlargement of the nerve. The nonhypertrophic form. shows neuronal atrophy with "110 evidence of demyelination.

eli nical rnani festarions include distal muscle atrophy and weakness c-usually bilateral and symmetrical-c-of the llpper and lower extremities. Muscle degeneration ['allows a specific pattern. The muscles suppli.ell by the longest axons of the sciatic nerve arc affected f rst, and the smallest muscles are the lim to atrophy. Cornman presentation also incl udes ca vovarus and cqu inovarus foot type, contractu re of lesser digits, drop foot. and/or a steppage gait. The cuvovarus deformity is due 10 weakness of the tibial is anterior and peroneus brevis, causing the peroneus longus to plantarflex the I rst ray. resulting in a forefoot valgus. The remaining metatarsals may also be pi antarflexed, causing soft tissue contracture at the metmarsophalangcal joint and dorsal subluxation of the digits. The unopposed pull of the posterior tibial is exaggerates the hindfoot varus. There is also some level of scnsorv loss; vibraiorv sense

and proprioception are nlfed<:d first. .

The Coleman block test b used to determine the Hex ibil i ly of the reartoot with a plantarflexed I rst


my. A wooden block b placed underneath the 181- eral bonier. and heel and reurfoot pronation is evaluated. If the rearfoorcorrects ro neutral OJ valgU5. then a I rst ray procedure will reduce the hind fool deform ity, I f the rearfoot f~ils to move. a mid fool or hindfoo: procedure is warranted,

Diagnostic studies include nerve conduction velocities. EMG, DNA analysts, and nerve biopsy. Nerve conduction velocities are often 50% reduced in motor and sensory conduction. and distal latencies are two [0 three rimes mure than normal,

Conservative rreatrneru consists of extra-depth shoes. aceornmod arl VI' onhotics, arul strengtheni ng and stretching exercises. SUrgical trearment can be very complex: three questions should be answered before a procedure is done.

I. What is the motor 'UlI.I~ of the muse II'S around the fOOl and nil k le?

2. Is the deformity flexible or fixed?

3. How extensive is los, of sensation?

The selection of surgical procedure depends on your answers fa these questions. the patient sage. and the en ief cornpla into Su rg lculcurrection indudes arthroplasty or arthrodesis of lesser digits; dorsi flexory osteotomies of metatarsals: peroneus longus or posterior tibial tendon trans fer: rnidfoot osteotomies (Cole or Japas), calcaneal slide osteotomy: or. For a severe varus, a Dwyer osreotomy, Tri pie arthrodesis shou It! be used as a sal vuge procedure for a long-standing, ~ xed deforrnity with signs of hindfoor degenerative changes. The key to a successful procedure is reloeati ng the calcaneus beneath the talus. causing valgus of the hindfoot arid allowing the talus to plantarflex.

1 n the present pat ient, conservative therapy was attempted. Custom-molded orthoses were constructed with deep heel cups to maintain control of the reurfoor. The forefoot was rebalanced to accommodate the Iorefoot valgus. The patient had a slgnificant decrease in lateral ankle pain and denied 311y further ankle sprai ns at aS-month follow-up appointment, Continuous monitoring for evaluation or the progression of the disease is dune monthly. At this time, vhe is ~1l1J functioning wuhou I drfficu lry.

Clinical . Pearls

1. Charcot-Marie-Tooth disease is a hereditary, progressive motor and sensory neuropathy that comprises a hypertrophic type lind a nonhypertrnphic type.

2. CMT usually presents with a cavovarus deformity. sensory loss, contracture of

digits, and atrophy of lower extremity muscles ("slork leg" appearance).

3. Both motor and sensory conduction velocities are 50% reduced,

4. Use the Coleman block test to determine the flexibility of the rearfoot.

5. Surgical principles include correcting fixed deformities. restoring muscle balance, and pre venting recurrence.

6. Radiographic features include dorsiflexion and abduction of lhe talus on the calcaneus ("'bullet-hole sinus tarsi"], increased calcaneal inclination, and plantarflexion of the Ist ray.


Pi shman M: red uurle Neurolog y. Orlan ')0. Grune • nd Stratton. I QS6.

2 Quin N. knn~r P Dlsorders o r M ove me ne CJ inical, Pharm 000 I ogk<ll aml Ph y s lolo ... io.1 Aspects. Son Di "go. "'0 ude rnic Press, 1989



'\ II 11- year-old girl with H s:hort toe

A n I: l-yearold gl rl presents w rth cuncern about abnormal roes and. rIIOI"~ ~peL' i Ill',111 v. pain ill her rig hr fou rth lOX'. The mother suucs that her daughter hus been (om pl.iini ng u I -Ii ,(;( I iii flll r, IN h ich i~ tggravnted hy wearing sneakers. I'm upproximatcly : weeks. MD!n o] her [',-lin I, IlIca\~cI 111 the center of the f\WefOCI. In addition. the child's activity level is norably decreased. A[lIIIII<.I the :~" ui' -t ur 5. the glrls .j.lh 10",$ were 1l00",d to be short and deformed. There" isuo hisrorv llt IIlJlIrv (II" rraurnu. l'a,1 medicul hislory is III\i"em~rk"I;1I~. w hh 110 hno\\ n drug allergies. F~JPnil: Ilhl"l~ i, [" "iii lit.' 1m 11) f1<'n~n,iun und diabetes mel titus.

Physical EX(tlllilloJiQII: Vitul signs: normal. Pulses: PJlp~hk ,J"i",:Jii, 1)~,Ii~ .lllu J'''sl~ri"r ubial bilaterally. :X~U rolog i.: \ lower cxtrcrn ity I' norma]. D ... rm.uolngic: []\ 1 ,I:. in I ... ,,,)n,: ,I.. J II !C'\IU J ~ anti turgnr normnl. Musculnskeletal: bil.ueral-lth toe dorsal .lisloc.uion. with ,1l(l11~lIill& ,,~- .1111 roe: rnihl bilateru] halluv abducto YlIlgu, uefnmlity wub flexible pes planus: limiiecl plum.rr llexum RO\j of ~Ih rnerararsophalangeal joi 11[, bilaterally.

I.ahart/tory Findings: Radiograph I,ee figlll"O::; I: ,l1or! -lth llI<"tal tu-,..al PI horh t eet: no) joint changes ill 41h rncramrsophalangenl joint.

QUesriufl; -WI1~H IS rhl> anomaly commonly referred to us?


DiSCI/.Hi/lII: HI :tt:h_Vlnclmar'lil i .. l h:m,h.letI '"d I'>y LlIl.lhnl'rf1l;.llly .. holllllt'lal"lI,al bone. Ihe ',nJi1l"n IS pnrinu ill' 11..: I'cd II ,II V in n.uure anti tirllollgh II prcJlllllill.Lnll~ :ln~..:t, the fourth I IdlllIlP;;ll b"I1~. II may .trfcctmuluple metaurrsnl-, I he ,h'''h:nll1g fll" the' ruetut.uval i-, due to prernalute closure uf the cpiphy-eul hnc at the disral porinn of the lIleI"ldr"tI ,-\ I rholJg h the CI io IlJl:!Y is unknown, bl;lcllymt"t.ll.1r~IJ h.r- bc~n J~,(]C'iated ,"1,1\ Dowus syndrome. p"",uul1hypnparurhy,uulbm. p'~UI](" pscudoh Y pup:lrarhYI oidisrn .• -\ 1- ,'d~hr''' ,vl1dr"me. Fm ncr'< svudn 1111". (Ii(l~uophu dwnrnsm. ,111.1 other vvvtcmic di-orders. Ilradwllld,llar,ia ,., !TI1l1t: common in females I=' 5'[1 und mos: "tll'l1 '1\.'~'Hr~ h!lme-rally, R adi'hi aphic cvalu uion i-, used 10 ,'on linn .111 (l~~eUIJ' h.uternne "I the 111,'I.lt.I".11

I n (he I.:ally ~t.tge, of dl'\I.'I()pmeTII, puuerus are usually ,)_;Yll1ptonL:lIIL Th~]11 irnury complaint in I Ie: Y"tll'lg~r r:lr icru h ,\rten UNlldic .• 1I1L1 many 1II11~S rhese paucnr-, ;I' c ,t'I tconsc ious .ihou I the i r I['~:[mllc~ Old,,! f',lllelll, Ill;.) expenence ,} mp-

tumx nt pam due III excessive pressure under nd[ucenr rnerararval he-ads; chnically one may see cullu« turmauon 111 these .neus, Skin, ~Ofl ti~sue arid tendon contructions lend to additional discorruon with u-e til' shoes.

Treutrnent uf hrachyrncratarsia Inay include conservaii ve cure. such ,]. ... nn orthotic device 10 rcdistribute pressure :lW3Y rrml1 adjacent metatarsal heads Shoe gear may he modified 10 ace omm 0- dute [be uur~ally located digit: Definitive treatment requires surgical correction to address the '011 ussue cuntrnctions w, well a, the shortened metatarsal. Numerous .. urgrcal procedures exist 10 correct bruchyrnetaurrsia. including bone grafts. metatarsal osrcorornies. disrruction osteogenesis with external fiv.uion devices. .ind tendon lengthening und "kin pl.:Lst) techruques I,) uddress the ,,1ft tissue contrucuons

In rhe pres ... nt patient. ~;IIILl~ de-traction (calI LJ I tl.., i . ., ) wus pel t,ll tiled hy graJmt1ly lengthening the merataiarsal, crcaung oM~ogt'ne,i~ between the two bone lragments.

Clinical Pearls

Bnlchymd.,I,Lf",1 i, .1Il anomaly, often congenital, thaI 1.'1111, e , .1 vhorteucd I11Ct3t:1r,.1l ind tloaun.; lot'.

~. BI,I, hvrner.n.rrvu: prcdorninuntly m curs in females. wuh a ~,-". I (<'Illarl' [0 male rauo.

1 {'''''l1~lk Jild p,y~h"I"gical corupl.unts may prcseru early. [nlluwed hy puinlul cnl 11I'~, ,IIIU djlh~lllt:, v. caring shoes as the defnrmuy progres-cs.

-t ("II'c'rV;IIII'~ trearmern 111<l_V 00;: more appropriate in certain pntients but -urgical CllJ'l'~L'l1"f1 j, Ihl dcumuve rre.umem


J Pull.lIi'H. I Hlh\'j' 11'1 ~'idIIW. It)llo)

K!tI:'JIi The C luhl-1I11 f'IUI!~ ,JlIU SIJ jt{uH N~\+,I1Dr~ 1')h..l



A 25.year-old man with persistent ankle pain

A 2S-year-<.lld man presents with n chief complaint of persistent left ankle pain of 9-monlh duration. He states that the pain developed while he was participating in U recreational f{lothali game. He denies any history of directtrauma to Ihe area, Treatment with ice, aspirin. and compressive ACE bandages has offered mi nimal rei ief of symptoms,

Physica! Examinatiun: Viwl sign,,: normal. Vascular: :U .. dorsalis pedis and posterior tibial urteries hi laterally; irnmedl ate capi llary re Ii 11. Neurologic: epicritic sensation in lower extrerni ty intact bilaterally; negative Tinels ~ign on percussion of tibial nerve, Skin: texture and turgor normal: no edema or erythema. Musculoskeletal: normal ankle, subrular, and midtarsal ROM; no evidence of pain on passive joint mobility; positive pain with active plantarflexion and eversion: mild puin on pulpation of left Achilles tendon: moderate 10 severe pain on palpauon between Achilles and peroneal remlons. peste rolaieral to the s u b ta 1 nr j 0 i nl.

Laboratory Findings: Radiographs: 3cce~sory bone posternlatcrui to talus on lateral view of left rcor.

Que.~tion; What is rhe Likely diagnosis of this patient's persistent ankle pain?


Diagnosis: Os trigonum syndrome

Dlscussian: Numerous accessory bones may be located throughout the foor, The os trigonum is an accessory bone posrerolareral [Q the talus, The talus has two posterior tubercles. medial lind lateral. II) some cases. the lateral process may he elongated. i n which case i tis te rmed S tc ida' s proces s, Will, severe ankle plantarfiexion, the Intern! Lubercle may ;111;0 fracture when impacted between the tibia and calcaneus, and thereby imitate an os trigonum. Differentiation of an os trigonum and a fractured lateral talar process can be di fficulL A fracture is usually more irregular in shape and has \hlO:lll edges: un os trigonum generally h3S smoother borders, Typically the os trigonum ossifies between ages 8 and II and may be seen on ,:1 lateral ankle radiograph.

Clinically. a painful os trigonum may present us diffuse posterior ankle pain, which increases

with. activity. The flexor hallucis longus tendon courses between the posterior talar tubercles. and when the hallux is dorsifiexed, the patient's pain may be reproduced. Ligamentous attachments may also pi <ICC stress on the area. creating pain with ankle dorsiflexion. B iomechanlcally. both supinated and hyperpronated feel can cause os trigonum syndrome. MRls and CT scans are aids to diagnosis.

Treatment may be conservative. consisting of nonsteroidal auti-infiarnrnatory drugs, local corticos te ro it! ill j ec tic n. ank le su p ports/braces. orthot i c devices. and/or immobilization with a below-knee c a~t. [f co nserv ati ve rreatm en t fai I 5 to iii II ev i ale symptoms. surgical. exc ision of the os trigonum may be necessary,

ln the present patient. the 0$ trigonum was surgically excised via a medial approach,

Clinical Pearls

I. Os trigonutn syndrome is a condi tion of painexperienced upon irritation of ,In accessory bone posterolateral to the talus,

2. Clinically an 05 trigonum may lead to similar symptoms 11), that of a fractured posterulateral talar tubercle.

3. Ccnservative treatment should be employed initially. If symptoms persist, surgical excision of the bone should relieve symptoms.


1 M"GI"mry ED. 01'1. Cornprehensrve Te"OOo~ or FOOL Surgery.1nd ed. Baltlrnore. Williams & Wilkins. 1992. L Mrn:U e r FA. The o trigonum syndrome. J Am Podinir Assoc 63:491-501. 1973



A .:a6-year-old woman with a lump OIl the top of her foot

A ~6-year-{]tu. otherwise he,ll!h) woman presents, with rhe chief complaint ~,r;, painful, -on 11';sue lump on the LOp of her right fool. She Slates thar thc mass appeured apprnxirnntely :; wcek-, ago and h,IS progre~sively become larger. Wearing shoes C(UISoJS increased pain aml dixcmnfun, with ')<'c~it1nal numbness fe It around her lateral digua. The putle nt denies ~ history "rl rau 111~.

Physical Examination: Vital signs: normal. Pulses: }/4 dorsalls peul~ urnl pU,l<:flllr tibi.i! b1131 erally. with irnrnediare capillary refill Neurologic (1,)wIOr extremity I: ~pi.::II!I~ ;"';:Il~<.illl.m inLad hiluterally: positive Tinels sign with percussion 01 intermediate dorsal cutaneous nerve. Skm: texture and turgor normal; no erythema or edema: 2-cm diurneier. ra ised .. ,ut"1 [I,~tI<: Inas~ (In dllr, ... rl lateral aspect of right rrudfoot, underlying extensor brevis muscle: mass freely movable nnd 11~.ut,11l111Ilwte, light. Musculoskeletal: ankle, suhtalar. midtarsal. and rnetntatsophulangeul jninb ROll.I normal. mild p~, planus deformity bilarerally.: muscle strength 5i5 bilaterally

LQ/mF(l(Qr,Y Findings: MRI tseehgure): ~ignal changes under extensor d igi rontrn brevi, und travels into subralar joint Radiographs: no ["l.~'iCOLIS cha ngcs.

Qlleslioll" What is your diagnosis?


DisCII",'!'iIJII: cr"mdi~ .uc relativclv common ,,,(II ",ut> lcs 1,111 ,. Th-",y .rre deli ned ,b ('y\t, l'011- 1'Ilnin,g l~u<,opnl)"~lCl'h,-,riclc- rich fluid within r1- 11j"()U~ ti~'>llC <11_ (l~~'I,iu~ully, muscle. hone. or <1 semi lunar '':;It'(II;lt'~ The ~y~\ u~uaJly occurs udjacent to ;1.lUII,1 nr i ntcndon ,11o!JI h~ ,1IlU most nltcn i [I repei il i vely traurnuti 7cd . 'r~:IS. Ganglia ha ve .rlso been referred II 1 ;l~ In) XlllU ~y~t." peritendiniI i, -crosn, or ,'yl1n~ iii I cysts, The- dorsal aspect of the Iont is u cunnuon locution [,)1 development of .1 ganglion, and light .. hoe g~ar may pluy an importunr rule.

Treturneut "I g.lIl~liu includes Mellie aspirelion. infiltmtion "I corticosteroid. padding and nuhl cumpre-e.iun, ami Imgit'nl excision. Ganglia

con recur, and may require su rgic ,11 excision if ~y rnpmrns persist.

ln the present patient. needle biopsy confirmed the diagnosis, The ganglion was situated directly LInder the extensor d igiioru III brevis (see figure. 11'1'). with the staLk leading into the subtalar Joint (see figure. bottom), The lesion continued 10 recur despite numerous aspirations. When excised. the ganglion was located around the medial dorsal cutaneous nerve. which was dissected free and protected. The hypertrophic bone al the lsi metatarsalell n eifo rm j 0 i n twa, resec led to furl her red lice irritation ofthe area postoperatively, The patient W:iS asymptomatic at 6 months. with a negative Tine! 's sign.

Clinical Pearls

A gangli, In ofrt'n rnrrns on an :1",,[ 0[' irritation. overlying a joint or connected [0 a ternlun <heath.

~ ,\ corn 111011 loc.u ion is the dorsu [J I of 111.: fool. bu I gang I ions may occur anyw here (In the I""t

J N.:~dl~ a"pirilliml, p~dulng. and cnmpressirm may relieve symptoms, bUI if [he ~Jn~li(\11 p<'T,j'l> and cremes puin and discomfort. perform Surgical excision .

..jl G,In.g,I;"", lire well-defined masses ttun translurninate within the scft ussue, 3 Avpirunon "I a n.mglion reveals a straw- lJf amber-colored liquid.


L B . .JI1k"i .\S. Du,~nr' ~1'S. \I.mlll DF, MIII~., SJ MI...Gr,urn.I1".!S Comprehensi v e Texrbnuk tlfFn.o1 ~LlILJ Ankle Surgery, 1.rd ed Plul.rdelpluu. llp~~LI~lo.:ttn_ WillitllTl.'Io & \1\ rlkms. ~oo r.

~ Ste~J.llr~lh \1~.;.H~dl Dldlt~II.L'" l~ll"l~.j Plulndclplna. Ltppincon, Willlams & v,..·.H:juS-. ~Jt.l



A 26-year-old man with a painful, discolored great toenail

A 26-year-old man presents with a complaint of'pain in his right great roe. Yesterday he played in a long ten oi s match, during which he had considerable discern fort. He also relates that he was wearing a new pair of tennis sneakers, Following the match. he noticed discoloration of his grenc toenail along with a localized. throbbing pain. The pain became progressi vely worse over the next TI hours despite ice and ibuprofen. It was local i zed 10 the media 1 aspect of the great [De. and was aggra vatec w ith shoe gear and simple ambulauon. The patient' s past medical history is unremarkable, and he denies previQUS injuries 10 h is feet.

Physical Examination: General: no acute distress; well developed. well nourished. Cardiac: normal. Chest: clear bilaterally. Neurologic: normal. Lower extremity: right hallux nai I discoloreo medially; mild erythema along pro)(imal/media.1 nail margin. Skin: no open lesions, Vascular: Status intact. Orthopedic: no gross deformity. Musculoskeletll.l: considerable pain with palpation, especially along proximal medial border of nail.

Laboratory Findings: Radiographs: no evidence of distal tuft fracture or associated fractures.

Question: What is your diagnosls based on this clinical presentation')


Diagnosis: Subungual hematoma

DiscU5y!rm: Subungual hematomas resul; I rom rcpetiri ve digitul m lcrotraurna. Corn pression L.II" rhe ria ilbed bet ween (he nairplate and the underlying distal phalanx can damage nailbcd arteries. There is u potential L1end spuce between the nail plate and the underlying nail bed and matrix. which then fill, with blood. Subungual. pressure secondary to rhis hemorrhage can damage matrix cells 1U1d the -urroundi ng heal thy nail bed. and often causes extreme pain.

Patients typically present with ,\ swollen tue .md ccrnplainu nfthrubbing pain following a digrral injury. The two most common mechanisms .ire repetitive microtrauma lrorn sport, sucn a~ tennis, and 1'1 crush-type injury. The hemorrhagic nail plate discoloration U!\U~lIy cnnfirms tho: ding- 110'IS. lt IS important. however, 10 obtain radiographs of the digit since approx irnutel y 20---25o/r 01· subungual herntuomas are associated with an underlying phalangeal fructure.

Treatment III vel yes drainage of the blood to reduce subungual pressure, Hematomas involving less than ~5% of the noi I plate are usually drained

with trephination, Commonly used techniques inc lude a heated papefe lip. aol8-gauge needle. and a hand-held electrocautery device. Once the plate is penetrated. [he blood collection is expressed w ith slight pressure, The urea shou Id then be cleansed and dressed with a dry sterile dressing.

When the hematoma involves more than 25% of the nai I plate, there is an increased ri sk of nail bt!d laceration. In fact, 600/< of hematomas covering rnure than 50% of the nail plate arc associated w ith nailbed lacerations thai require repair, As a result. complete avulsion to evaluate the entire nailbed is recommended in these instances.

Decompression 01' a subungual hematoma is quick, easy, and painless. Patients feel immediate relief nnd generally huve no complications following prompt dramage. Auiornaric nail avulsion rypically occurs within 6 weeks. and a new nail 'has usually regrown by 6 mouths without dystrophy.

1n the present pal lent, a no. 11 scalpel blade was used in a drilling fashion to drain the hematoma from beneath the nail, The patient immediately had relief of the pain.

Clini.cal Pearls

I. Fractures are associated with 20-25% of subungual hematomas,

1. Nail bed lacerations TIlU,( beconsidered when the hematoma involves :> 25% ef

the nai I' plate,

3. Subungual hematomas are caused by microtrauma and by crush injuries. -I. Hand-held cautery is ideal for trephination.

S. Prompt decompression is important.

6. Hutchinson's sign must be ruled out.


I Malay S. Truurna w Ih< Mil and nssoclared snucrure-. I" M~-GT""D ED, B;",,,, A. Downe) M I e -d_q: CGn'lpr"hcn,i"" Textbook of Focr .on,1 An.l. "ur~.ry. 21ld ed. 8"lt;11111"'. Wlltiam and Wilkin,. I Q9:c.

2 Pearson A, W"IJoni R. Man"gemom nf 'kin trnurrm. Prim Care 2712). ,rJ(~I,



A 36-year-old woman with left forefoot pain after a jog

A 36-year-old 'Woman presen ts IV ith cornpkt ims of pai n in Inc urea of her Idl fordom. She ~N had discomfort in this aren ~ weeks ago following 0 jog wilh II friend. The pain W~~ inilially more of II generalized ache 111m would come and go 'With her 'Workouts. but it gradually became more intense wlth activity, despite rest, Persistent discomfort began affecting simple nmbulurion. The patient was seen in a local emergency department 2. weeks ago, where x-ruys were read as negativc Since 111~n she has tried ice and hear, as we 11 as aspirin for pain. without re lief.

The patient has jugged IWli lU t hree limes a week for the pnst 1 years, She "l~o relutes u recent increase in her mi leuge. Her past medical history is signi Meant for hy perrension and ga~tric ulrerations. She has no other cornplnints III this time and. besides the aspirin, is tllt..ing only Toprnl XL.

Physical Examination: General: normal appearance. no recent weigfu change. Cardiac: normal.

Chest: CTA bilaterally, Neurologic no focal deicers. eN 2-1::! lnracr. Lower extremity: flexible pescavus foot type with mild gastrocnemius soleus cquinus bilaterally. Va-culnr: normal. Skin; left [oreloot edema arnl ecchyrnosu: no open lesions. Musculoskeletal: no pain wuh dorsitlexion and plantarflexion al the :>nd :yj TP joint: no pain with lvITP joint compression/d i stracrion: negative Mulder' s sign: pain on palpation of dl,I(11 aspect of 2nd metatarsal shaft and .11 ~rd merururvil head with plantar to dorsal pressure No pain with vi bratory ~1 i 111 111 at ion of thi rd metatarsal. ;-"0 obv ions din i<.:<11 deferrnity noted,

LabQra.lOry Findings: Radiograph (see figure]: exuberunt bone ~all"u~ proxunul to anatomical neck tit 2nd metatarsal: intraconical lucency medinlly: alignment ucceptab]e.

Quits/ian; What IS your diagnosis?


Diagnosis: Second metatarsal stress fracture

Discussion: Briethuupr was the Iirst to describe 1l1~1 .. lar;dl stress fractures, in I H55. They were com" rnonly seen 111 young military recruits whkh led 10 the Term "march 1'1':l('JU res." Ted lIy. I hese Fractures usually result from uveruse and lire seen most commonly in the femule .nhletic population.

Women are less able [0 absorb shock due' 10 a wider pelvis (('O~" vera/genu valgum) and 15% less muscle rnnxs. They nl-,n have 11 lower bone mineral dens] I y. especial! y posi-menopouse. The "female nth lete !ri ad" for stress lractures includes: ".H mg disorderx. :1111e nnorhen, and 1I,!eopen ia,

Structurally, while II cevus foot is more likely to lend LQ [I tibial Slre~~ fracture, planus feel. are. more prone to metutarsal ... tress fractures. Add iiionally, those with metatarsus primus elevaius. Morton's foot, Dr leg length discrepancy are also .u increased ri sk. H yperprcmulon a~ we II H!\ condi!jon~ sueb lh 11aUllX limitns/rigidu» can increase rhe stress lin the 1'1 and 2nd metatarsals, While equinus ha~ not been found to be .i signi licant risk faCIOL most feel I hill u rear fout inversion greater than J3 lkgrees i ncrenses rhe r.sk of developing metatarsal ~tTC~S lracturev, Extrinsic risk factors in c] ude rral n i n g I' rro 1"" footwear. 1 h e s u rface or terrain, and individual tirnesslevels.

Ni nery percent of 1!H~I:.II~r,ul ,In''', fractures affeet metararsuls Z----4,lYPJ(;:illy occurring in the distal 111 ird of the ,h~fl ...... 11 exception (0 this rule is lound in ballet dance rs who sustai n proximal fractures near the tursomer.uarsal joi nt (secondary to "en poi me" postures), There is also a high incidence 01 2111.J metatarsal stress fractures ruler I st ray surgery respecially Keller's procedure),

Radiographically, 30-70% of metatarsal stress fractures. initially appear normal. Positive fi ndings typically become apparent by 3 weeks. but may take up to 6 weeks. A I ineurcortical lucent region associated with periosteal and endosteal thickening is seen in diaphyseal bone. A focal sclerosis tband-l ike condensaucn of trabeculae) is seen in me tD ph Y sea I bon e. The gtlld standard fa r dii\gll 0- sis is a triple-phase bone scan. Although nonspeei fie, this test is very sensitive and is usually posirive within 24---48 hours of the injury.

The differential d iagnosis includes: metatarsalgia, neuroma. neuritis, pre-dislocation syndrome. capsulitis, and bone tumor. A complete clinical history and. thorough physical exam will usually lead to an appropriate diagnosis, Most patients relate an ins idious onset of pain. with gradual pro-gression or symptoms. Often. there is an associated recent increase in activit)' level, On physical exam the hallmark i.~ pinpoim tenderness. Forefoot edema. pain with passive dorsiflexion, !IS well as an inability to hop on the affected foot are classic findings.

Once II diagnosis has been made, treatment LlSUally begin" with RICE principles. Conservative care w ith j rnmobilizarlon (~u[g_icaJ shoe). and partial weight bearing is of len effective, A gradual return 10 activity ill very important. and swimming is often an excellent start. Remember. as with any fracture, complete healing will take 4---8 weeks.

In the present patient a wedge shoe was dispensed to off-load the forefoot. This approach combined with the other conservative principles mentioned above led to uneventful healing.

Clinical Pearls

I. Ninety-five percent of stress fractures occur ill the lowerextremity, 2. TIl~ risk of stress tracru re in women is 2-!o times the risk in men.

J. Patients relate an insidious onset of pain with gradual progression, On physical exaruiu.uicn. the hallmark is pinpoint tenderness.

4 hi itial rudiographs frequently do no! reveal (he fracture; 30-70% are normal, Repeat radlugruph ... during \1 eeks 1-3 Will reveal a bone cal I us ar the site of the stress frac-


5. rile d iJgnustlc gold standard IS n tri ple-phase bone SO:21n.

6. A grrnlu LLI I eru rn rn acuv iry ls a I11lL$I!


I Ka.ufm.UI KR.clILI. nlt' I.::flt."lL ,1 1~'Hj! ,Tnh.Hlr~ ...LmJ rw']~£' of mution un mu, -, culo .. 1:.l!!let>I1 nveruse injuries. Am J Sporr- ~f~d I'NQ, 27~~1

~ M,Hlct~lb.ltml HR_ Cl ill ~tre"'", tra; I LJT~" Clin SpiJrt.3 M~tI I Q(J7: I ("C L



A. 61-year-old man with soft tissue masses at his ankle and heel

A 61 -year-old man presents with relatively painless soft tissue masses on the posterior aspect of h is left heel and ankle. He has a long-standing history of seropeshive rheumatoid arthri tis (RA). Although these nodules initially appeared over '1 years ago, they have grown ~onslderably during the past 3 months. The patient was diagnosed with RA 15 years previous. He was effectively treated with NSAJ Ds for most of thai time. until an acute rbeu matoid flare prompted the addition of methotrexate. He has been maintained on a low dose of methotrexate (7.5 mg/week), along with various NSAIDs (currently Celebrex), The patient also relates recent worsening of hi, generalized morning stiffness,

Phy.~ical Examination: General: well developed, well nourished: ambulatory. HEENT: negati ve for scleritis. ural lesions, and thyromegaly: neck supple. Cardiac: nOlIDlI.L Chest: clear bilaterally. Neurologic: no focal defects. CN }... [:2 intact, Skin: no rashes. Upper extremity: MCP swelling, mild boutonniere deformities digits 2 and 5 bilaterally. Lower extrerniry: soft (issue nodules on posterior aspect of left heel and ankle measuring 3.5 x 2 X I em and 2 x I X .5 em. respectively; no lesser digital contractures; mild bilateral hallux abducto valgus deformity. Vascular: normal.

Laboratory Findings: ESR 32 rnm/hr, rheumatoid factor 704. Radiographs: soh tissue densities; no evidence of calcaneal erosion: mild joint space narrowing without erosions.

Quesdon;' WhOI is your diagnosis, based 011 this clinical presentation?


Diagnosis: Rheumatoid nodules

Discussion: Rheumatoid arthritis is a chronic. polylllticular, symmetric. inflammatory disease with a predilection for small proximal joints. Currently affecting 2.5 million Americans, this uisease strikes women three rime, more often than men. A lthough the characreristic feature of RA is inflammatory synovitis. multiple extra-articular organ systems can be affected, In general. the number of these comp lications increases \.\ ith disease severity,

The most frequently recognized skin lesion in RA is the rheumatoid nodule. These nodules usually develop during an active phase of the disease and have been reported to occur in 20-30% of pa- 1!eIlIS with RA. Patients who develop rheumatoid nodules commonly have severe RA, and almost III vari ably are seropositive 1 +RF}.

Rneumatoid nodules are usually located in superficial subcutaneous tissue. but can OCCUI in deeper s true III res ~ uch u-" b U IS 11, jo i n ts, te ndons, or ligament. 111ey :MC found on periarticular structure s, ex tensor su rfuces, and O! her areas su b j eeted rc mechanical pressure. Common locations include the olecranon bursa. the sacrum, the occiput, and the Achilles te 0 don . They us uall y present eli nicall y as tirm, flesh-colored. nontender, and freely moveable masses. Histologically. rheumatoid nodu les ure granulomatous lesions cbaracterized by areas of central necrosis. The periphery is composed of palisading B broblasts and histioeytes with chronic inflammatory infiltration.

The pllrhophy,iology behind rheumatoid nodules is not completely understood, but a few theo-

ries ha ve been postulated: (I) vascular inliammawry changes followed by necrosis. (2) repetitive microtraurna, and (3) genetic factors. specifically the fiLA-DR B! 04 alleles. Additionally, it is well accepted [hat methotrexate. which has become the guld standard or RA therapy, can cause an accelerated nodules is.

The differential diagnosis includes ganglions, gouty to ph i, abscess. and xaruh omarosis, If after a careful history and cl inical examination there is still a question [1$ to the diagnosis, an excisional biopsy can be perf armed. Th i ~ ho we ver, is rare I y necessary. Although these nodules are most commonly seen with RA.they can 3100 be seen ill other chronic inflammatory disorders such as systemic lupus, granuloma annulare, and necrobiosis lipoidica diabericorurn, In these cases the history becomes extremely irnportam in making a correct diagnosis.

Rheumatoid nodules are usually nontender and of Len regress completely with time. However, they can become sources of continued irritation. Cornpl ications. such as overlyi 11g skin breakdown with secondary infection and/or underlying bony erosion. can also occur. Conservative measures of treatment include aperture padding. intralesional steroid injections. and cclchici ne. With the ability to inhi bit giant cell formation. colchicine has been found to gradually reduce rheumatoid nodules. If these con serv at i ve me a s u res fa il, s urg i cal excision becomes necessary,

! n the present patient. the nodules became quite large and created pain with all shoe gear. It was decided 10 surgically excise thern,


I. Only I % of all rheumatoid nodules occur in the feet. Common locations are the

olecranon bursa. sacrum, and Achilles tendon.

I. Rheumatoid nodules usually indicate an advanced disease Slate.

3. Histologic features i nclude a <x'111m! necrosis ri mrned by pal isading fibroblasts. 4, Local trauma can be a preclpltatlngeveru. Methotrexate may accelerate nodulosis. 5. Nodules often regress or involute spontaneously,

6, Cnlehicine may help reverse these growths.


t AnJ"""n R: RI1<urnn("iJ .. rtbritis. Prim", L1n the Rheumatic Di!~[lSe'.1 \ th ed • Atlanta. GA, Arthritis Foundation. 1997.

2. Parton 1. et "I, Rb~um"t"iJ artlrrttic f.,,,,. 1 Am Podlatr M~-tl Assoc 83(5):2711--275. t 093.

3. ~,Lnder', T101ulh). Rn~(]lllJlu;d Nodule of tile Foot: MRI uppeuranees mimicking an lndeierrninate "of! tissue mass. Skel Radillt 27: H 7-11',(J_ 19Q9,

.... \l.'illiums F~ et ul. .... ecelermed cutuneous 119dLJlo~i"" iJLJrFng M~lhO'lre."(i.JL~ therapy ill iJ plUr~rH with rheuutaroid arthritis. 1 Am A~"J Derrnurol NI!t J59-J~". 19Q9.



:\ 29-year-old man with a painful ankle

1\ 2lJ-ye~r-old I n,1)1 pre-en IS to the emergency department \ F D I ~ fter b..: i ng ,[1 uc], hy .1 inou« vehicle, He i, ,: .... pericncing pain and swelling of the right foot lind ankle. lInJ I' un.ihie; Itl heur w~il,!hl' 011 (he right. He ueni e , any other curuplaint or area Ill" tenderness. The putient rcl"k'~ Ih.ll ,\ hiie he was crossing the ,,(f~,·t and stepping onto the curb, a passing cur trawling ,II "l'pf('Xlnl.ll~l} ..:'(1 111ph struck the ourside nr' hi" nght leg.ankle. He arternpred [0 walk, bill W", unable ILL pin an.1 pL'~"ILr~ on his nght foot/ankle, He wa~ ilnnl~I]j,nel) taken III lh~ ED for evaluation,

Physical Examination: Temperature: afebrile. Vital signs: stable. I HcENT: riLl! mul.Thesr: clear, Cardiac: regu I:JJ", ,\ bdorne-n: ncntender. Ski n: superfici 11.1 ahras ion 110 I rue I"~ I .ISI1!;'( r "i' I"i gil I leg, with mi Id ecchyrnox IS 0 t medial heel and unkle Neumvascul ur stu! us: I iliac l. Musculoskeletal: p;u n un p31~ pauon 1(1 '1 uteral leg und rued i,~ ,mk Ie, wi LM mild ;!$soci, 11,~Ll edernu. pai II rul de II ve .uul I':I~ ,i \'<'" R OM of right ankle: Lao pam on palpation (0 right fum: abo nu pain al ankle level un 1.ll~I,,1 compression of fibula,

Laboratory Findings: Radiographs: RighI (,)",- no o"equ -; p'lIi1<lh'g~ : [J\J Ir:Ld u I ~ or dixlocatiun. Righi ankle hee figure I-tral'\sy"r,~ proxirnul/midshalt ribula (mL'ture 'I uhour Ji~rla"<'lIleTii. emgula(iOIl, ur shorten ing: eli >I..J obi ique medial rnul leola! Fr;]~lllr~ of I ib: a, wirh lT1~d i:,1 ,IIlJ pl.rn tar mlgration or JI,I.iI (r~gfl1i;'Ii!; increase in medial clear space.

QuestiorH: Wh~1 l' the mechanism of injury"! l low would you treat the i'm,·!lIle.'

D.iagllosis; The mechanism was trauma (a di reel blow I wuhour any rotational forces.

Discussien: Ankle injuries are one of the most common injuries seen in the ED. Whether the injury is diagnosed as an ankle sprain, strain, fractW'e,or fracture/dislocation,a thorough understanding of the mechenisrnof injury wi ll allow the clinician to properly treat the disorder. Some difference of opinion exists as to whether ankle injuries should be x-rayed in the ED. If there is a possibility of a fracture or if the patient is unable to bear weight on the extremity, thana radiograph should be obtained.

When evaluating an ankle fracture. the physician must evaluate both soft tissue and osseous derangement. Having a working knowledge of the pathological forces that caused the fracture wi II fac i li La te accura te anatomi e aI jo int restorati on. In the present patient, displacement of the medial malleolar fracture and an increase in the medial dear space led 10 the decision to perform an open reduction with rigid internal fixation (ORIF). The ORlF was performed to regain srabil ity of the ankle joint and to anatomically reduce rhe fracture, while at [he same time providing the patient with the best long-term outcome.

The ORIF was done to his medial malleolar fracture only, The decision to conservatively manage his high fibula fracture was based on the already near-perfect alignment of the fibular fracture r ragrnents and the nondisrup!ion of the Interosseous membrane and anterior inferior tibiofibular ligament. This injury resulted from a direct trauma!

blow to the right leg and ankle, 111<': high fibular fracture did not resu It from a pronation or eversion injury: therefore, a transsyndesrnotic screw or repair of the anterior inferior tibiofibular ligament was not indicated or necessary,

The medial malleolar fracture was tixated with two d x 0.10 mm. parallel. partially threaded. and cannu lared screws through :J curvi linear inci sian over the distal aspect of the ribiu tinder C-ann direction (see I1gure). Once the medial malleolar fmc lure was properly reduced. the an k le mortise and libulur fracture were again evaluated under fluoroscopy. The medial clear space was reduced: no tibiofibular diastssis was noted on ankle ROM; and the lihular Iructure remained in excellent alignment. The patient was then immobilized in a below-the-kneecast. Weight bearing and physical therapy were initiated after the cast was removed. a1 approx irnately 6 weeks.

Clinical Pearls

I. A high fibular fracture is usually associated with an eversion or pronation tYI)C of movement of the foot upon the leg.

2. Proximal fibula fractures typically have an associated anterior in ferior ti biofibular ligament and interosseous membrane rupture. which are usually primarily repaired and fixated with a transsyndesmouc. fuUy threaded cortical screw.

3. Medial malleolar fractures can be repaired percutaneously under flUllnJSCOPY guidance or opened and reduced with two parallel cancellous or partially threaded cannulated screws 10 anatomically align the fracture and 10 prevent rotation,

4. The focus on surgical correction of ankle fractures is tIJ restore me length of the fibula, assure syndesmotic stability. and accurately realign the ankle rnortise.

5. Osteochondral defects of the talus often occur with fracn: re-d islocation injuries about the ank le.


t. ann Irs AS. Downey MS. Mnr! i n DE. Miller 51 : M cGI am'}" S C" rrrprehenvi ve T e~ tbook of P"nl nn d Ank le Surgerv .. ~rd ed, Philndejphia, Lippincott. Willinm" & Wilk;ns.l(}(ll

2. Mitchell M. Howard B. Sartoris D, Ru,nick D; Rndiol'ogie review: Diagnostic imnging of trauma 10 the lIn. le ;lnd Ioor: I.

Fractures about the a nkle. J 1'001 Surg 28: 174--179. 1989.

J. Reinherz R. Granoff 5. Henning K. Roo, B: Cnaructcrtstics of operative management 01 supmarlon external rorauon: Ankle fracture s. J FOOl Ankle Surg 30(4): 356-36). t99t.



A 21-year-old woman with a stiff, paiatul root

A 21-year-Old. ciherwise healthy woman presents wuh a -l-rnonth history of acute len rearfom pain. The patient also relates a chronic discomfort in her left foot since early childhood: this discomfort was remitting in nature and nonprogressive until recently. She describes her symptoms as a dull ache with occasional periods of sharp. shooting pain. which limit her weight-bearing activities. She denics any history of trauma, bUI has been more ncti ve due to nurs i ng school rotations and wairressing duties the pa,t several months. PI"E'V ious treatment consisted 0 f plantar heel injections, stretching and strengthening exercises. custom-molded orthotics. and NSArD therapy without any major relief in symptoms. Her condition is pm titularly aggravated after strenuous activity, and i~ relieved only with lung periods of rest.

Physical Examination: HEENT: normal. Chest: clear. Cardiac: regular. Abdomen: nontender.

Skin: normal rex turc/turgor/rernpenuu re: no ecchymosis: mi ld pirti ng edema of left lateral rearfoot lind ankle. Musculoskeletal: pain on palpation to 1e!'1 lateral rnidfoot, rearfoor, and ankle: ROM of left ankle normal: ROM of left subtalur joinrr S'I'J) signilkantly decreased and extremely painful on both inversion and eversion: ROM ef left midunsnl joint mildly decreased, but wirhoin discomfort: left foreFoot normal.

Laboratory Findings: Radiographs: mode Me degenerative changes in ST1. with joint space narrowing and surround ing i ncreased sclerosis: ja.ggcd appearance of sustentaculum Lal i; midtarsal joi nt congruent and IV ithout arthritic degeneration. MR I [See figure): increased signal intensity on T2- weighted image in area of sinus tars i, must I ikety related [0 bone morrow edema defusing out from adjacent talus and calcaneus: irregularity at art icu I Ilrin.g aspect of ST1. particularly III middle facet. representing predominarely cartlluglnous communication with some interposed osseous fcrmation on T l-welghted image.

Question.: What is the most like tycause of the patient" s decreased ROM and pain in the rearroof)


Diagnosis: Subtalar joint coalition (middle lacei)

Discussion: Generalized pain. disco m fort, and ,riffne.ss in the h indfoot and ankle area has many ~ auses, and tbe d i fferen ti al di agnos is can be ex, tensive. A thorough history and physical exam, as well as the use of radiographic modalities such as plain-film radiography, MRl, cr scan, and even a three-phase bone scan, can help narrow your lli fferen ti al,

Tarsal coalition is .6 foot condition in which a bridge or bar across two or more tarsal bones limits or eliminates motion between the involved hones or joint The etiology of is still unclear, but the disorder may be acquired or congenital. A coalition can be a syndesmosis (a fibrous union), a synchondrosis (0 cartilaginous union), a syncstosis (an osseous union), or any combination of me three.

Tarsal coalition is sometimes accidernally found onrourine radiographs. and the patient may be completely asymptomatic. However, if symptoms are present they usually consist of diffuse

pain, muscle spasm. and limitation of joint motion, The pain onset is typically insidious, or it can occur abruprly as a resu It of minor trauma. Symptoms are usually aggravated by activity and reIieved with rest. The symptoms of a middle facet talocalcaneal coalition prese-nt as pain localized to the s in us tars i Late rall y and the susten t3.C u I um tal i medially. and as a significantly decreased STJ range of motion,

Conservative treatment usually consists of NSAIDs, physical therapy, injections, belowknee casti ng, and orthotics, particularly those that restrict subtalar and midtarsal motion. Orthotics are most effective when manufactured to hold the rearfoot in a neutral or valgus position. If conservative therapy fails, then surgical intervention is necessary to relieve symptoms. Surgicel treatment essential I y i nvol ves fusion of the involved joint complex or resection of the bar with or without performing an adjunctive procedure.

Clinical Pearls

I. A middle subtalar joint (STJ) coalition is considered to be the 11105t common tarsal coal ilion found in the fool.

l. MRI and CT scan are extremely useful imaging modalities if there is a high suspicion of a tarsal coalition. especially when x-rays are inconclusive.

2. The symptoms of an STI or midtarsal joint coalition are aching and stiffness, particularly ill the region of the sinus tarsi or deep in the STJ.

). Peroneal spastic flat foot can be a sequela of a tarsal coalition, in which the rearfoot becomes fixed ina rigid valgus position.

4. The results of bar resection are poor when degenerative adaptations have occurred in the area ofcoalition or surrounding. joinss of the rearfoot. A primary fusion of the STJ or midtarsal joint may be necessary to relieve symptoms.


I Alter S. M~Carthy BE, MeodicioQ S. OiSwziu J: C.k.n.Q"~vicutar b"r "'~.<lloo' II retrospective study, J FOOl Ankle Surg 30(4): 383-389, 1'19 t.

2. Stoller M[: Tarsal o;ooIitiQfl-A study of surgica] results. JAm Podietr Assoc 64: tOO4-IOJ5, Ig'7~.

3. SWiOOlkoWIKl MF" Scromo" PE, Hnnsen S, Tarsal conliuons: Long-tern. results "f surgical irearrneru. J Pediatr Orthop 3:

ZI!7 -292, 1983.



An 84-year-old man with painful hallux ulcers

An elderly gentleman presents with extremely painful ulcers on hi~ hallux ~nd toes, They have developed over 6 months. and are not responding 10 conservative rrearrnent. The patient has a history of noninsul in-dependent diabetes, periphera 1 vascu lar d isense, coronary artery disease, congestl V~ heart failure. and atrial fihrillnrion.

Physical Examination: General: w~11 appearing; no appareru disiress. Temperature 98.2'.'blood pressure 140165, pulse 64, respirations 12. Skin (see figure): ulcers of righ: second roe Clnd hallux; erytherna of entire forefoot: ulcers dry with 11 pale-colored granu' arion tissue. I 0091- ~ brin covering on These wounds. which measure I 8 mm l( 12 mm X 3 rnm: tip of right hall u x gangrenous. no drainage. HEENT: pupils .3 mm equal aniJ reactive; muist mucous rnernbr .. mes without lesions; dentuion poor; neck without bruits or ly rnphadcnopathy. Chest: clear. Cardiac: no jugular venous distention: regular rate and rhythm: systolic ejection murmur. Abdomen: positive bowel sounds, without ilisteruion or lenderness: no organornegaly. Rectum: negative. without polyp, or prostate abnormality. Extremities: bilaternl femoral and popliteal pulses without distal pulses.

Laburatory Findings: Dipyridamole t-.llBl test: anteroseptal defect with partia) perfusion cons isteru with myocardial in Farel. Nnn invasi VI": vascular testing: no left dorsal is pedis Doppler wave Iorm. Left ankle/arm index 0.56. Rndiogrnphs (of digits): no any evidence of osteolysis or osteornyelitis. Arteriogram. stenosis at distal femoral artery ,mu blockage just proximal 10 trifurcation; good flow to dorsalis pedis, but no flow to digits,

QUf!st/nR: Wl1at i~ your dinic::Li diagnosis?


Diagfl OS ls: Arteri al occl us i v e di sease

Discussion: Obviously, a bypass of the blockage should be considered. The question is what to do with the fool in light of the patient's age and medical status. The patient was determined 10 be an Anesthesia Class ill according to ASA physical status clas si tication reported by S akladin in t 94 1. Card i a~ c ath eterizarion prior to any plan ned surgery was recommended. A femoral distal popliteal reversed saphenous vein bypass graft,

under spinal anesthesia. is recommended. This proccd u re 1,11 III inc tease pre SHire s to the fool. bu L will nor revascu larize the digits. A plan [or II Lisfranc's proximal amputation should be considered at the same time as the bypass. This willcaprure the best time for a patent vessel and minimize the risks of anesthesia, TIle patency ct'the distal Meries within the foot wi!! dictate whether the Lisfranc amputation site should be distal or prox irnal,

Clinical Pearls

I. Decide 1:1.1 the lime of revascularizauon whether to close or lea ve I he amputation site open.

2. All too often, the distal How is [JOL Strong enough, and necrosis of the rlap clusing the site leads to an abscess. When in doubt, leave the amputation site open.

3. Leaving a wound open for delayed closure is a viable option. for the surgeon. Wet to dry saline packing is advisable. Once the bed has granulated sufficierul y. (he wound can be closed: if complete closure does not Occur. consider growth factors LO accelerate healing.


!. Campbell DR: Diabetic vascular disease. In Frykberg: The High·Ris. FOVI in Duibetes Mellltus. Nrw York, CI1UfOhJII Livi".~s{one., 1991. pp 33-38.

!. Pinzur M: Amputanon l"vel selection in the diabetic foot. Clln Orthop 2%:b8-iO. 1993.



A 55-year-old woman with a raised mass on her second toe

A 55-jear-uld woman presents with a swollen lesion .tlTOW1d her right second we. It has been illcreasing in size over the past 6 months. Over the previous 4 weeks, the rTI£lSS became painful with ambulaiion. The patient cannot recall any history or trauma or stepping on an object, Her past medical history is unrernarkablevexccpr for ~ light obesity, She denies taki ng any medications. and is in good physical health.

Physical Examinatio»: General: raised mass on plantar aspect of second metatarsophalangeal jol nt, measuring 25 rnm diameter and 13 mm height: firm and fluctuant: nOI painful upon compression between examiner's thumb and forefinger: no redness.

Laboratory Findings: Radiographs: soft-tissue swelling wilh no osseous involvement.

Histopathology. bulbous, lobular. grny soft-tissue mass excised lrorn plantar nspeet of right foot was demonstrated to be a C)-51 with numerous giant cells arul abundant keratin.

Qlwsrion: How did this lesion develop?


Diagllf}ri~: Epidermal inclusion cyst with foreign-body giant-cell reaction

Discussion; Epidermal inclusion cysts usually occur secondary 10 traumatic implantation of epidemliJl cells into dermal tissue. Once in the deeper subcutaneous tissues. the epidermal cells gmw, producing a lipid- and keratin-filled cyst that can enlarge and become quite painful and sometimes infected. Epidermal inclusion cysts create a foreign-body giant-cell reaction; this inflammation may lead to the formation of a sinus tract, When squeezed, a sinus tract yields a cheesy exudate consisting mainly of keratin.

Treatment of this lesion is excision of the cyst

and sinus tract. Left untreated, a rare occurrence of malignant transformation of epidermal cells may OCCUI_

In the present patient, an epidermal inclusion cyst developed despite the absence of a history of stepping on a sharp object. Oftentimes these lesions develop from repetitive trauma, such as with ill-fitting shoe gear, as was the case in this patient, Radiographs are helpful in determining osseous extent. In the present patient, because there was no osseous involvement, thecyst was excised, lind she ma.de a full recovery.

Clinical Pearls

L_ Epidermal inclusion cysts usually eccur secondary to trauma; w ithout this history, rule OUt ill-fitting shoes as etiology,

2. Excise the lesion, as it is possible for these masses to become malignant.


I_ Delacreraz J: Kera10tic basal-eel! ca.d"omo "filling trorn an epidermoid ",>I. J Derm Surg Oncol 3: 310-11,1\177.

2. Poll"" GK_ Ward Ki\: TUMQn;. In McGI"-mry ED. Bank. AS. Dowm:y MS f.ods): Cornprenenslve T"'lbook. or FOOl Surgery, 2nd ed, Baltimore. Willi""" and Wilkill!l. 1992. ppl 139-1 140.



A 2-year-old girl with one severely flattened font

A :!-yt:ar-oh.l girl is brought in by her mother for all evaluation of her riglu foot. The mother is coocerned because "il looks di fferent than the other fOOL" The chilJ was del i vered FuB term in a small hospital hy the local family doctor. This is her very firsr physical exam. She is the rnorhers third chilJ: the l wo other children ha ve 110 lower extrern ity parho logy and are qul te healthy, The remainder of the girl' s hisrory is normal, except for rhe lark of recent and required vuccinurions.

Physical Examination: General: right IOOL appears shorter I hun lert, and is posrnoned up and outward in reference lO leg (see ligure l. Large prominence on inner aspect of fool. C01l1e~ deformity of plantar aspect of foot with heel in valgus. Musculoskeletal: limitation 01 dorslflexion at ankle, Ieaving foot in equ inus: talur head fel I 1)11 medial plarnar ~~pe~1 or foot: forefoor abducted and dorsi ~exed at midtarsal joint

Labof(l/ory Findings: RmJiographs {standing AP and lateral. lateral planrarflexion, lateral dorsiflexionj: increased talocalcaneal angle with fcrefoot ubducrion; calcaneus ill cquinus with vertical position of talus; dorsul displacement or lorefoot LID talus, line bisecu ng talus Jid 'out pass through longi tudinal axis of metatarsals - was rnalaligned in bot II lateral and lateral plantarflexion \ iews (see tigure).

Qlleslic)//s: Whai i ~ your diagnosis '! Wh~l are some treatrneru ,.ptions 7

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