Podiatry Institute Manual

PODIATRY

INSTITUTE•

THE P.I. MANUAL A Handbook of Podiatric Medicine and Surgery

2nd Edition

The Podiatry Institute Decatur, Georgia D. Scot Malay, DPM, MSCE, FACFAS, Editor

Podiatry Institute Publishing, Inc. Decatur, Georgia

©2006 by The Podiatry Institute, Inc. All rights reserved. This book is protected by copyright. No part of it may be reproduced, stored in a retrieval system or transmitted in any form or by any means electronic, mechanical, photocopy, recording, or otherwise without the prior written consent of the publisher. For information write Podiatry Institute Publishing, 2675 North Decatur Road, Suite 309, Decatur, GA 30033.

Care has been taken to confirm the accuracy of the information presented and to describe generally accepted practices. However, the editor and publisher are not responsible for errors or omissions, or for any consequences from application of the

information in this book, and make no warranty, express or implied, with respectto the contents of the publication. The reader is urged to check the package insert of all drugs for current recommendations regarding indications and dosage, and for added warnings and precautions.

20 1 em diameter Papule-slightly elevated Idue to inflammatory dermal infiltrate). well circumscribed, up to 1 em diameter Plaque-larger or coalesced papules,< 2 em diameter Nodule-well circumscribed, firm elevations,> 2 em but< 3 em diameter Tumor--well circumscribed elevation> 3 em diameter Vesicle-serous fluid-filled, elevated,< 1 em diameter Bulle-serous fluid-filled, elevated,> 1 em diameter Imay be hemorrhagic) Cyst-sterile intradermal mass of fluid or other material, contained within a defined wall, such as a mucus, epidermoid inclusion, or sebaceous cyst Burrow-intra-epidermal tunnel formed by scabies or other insect/parasite Secondary Skin Lesions Scale-thin, plate-like, cornified compact epithelial cells Excoriation---superficial loss of skin Erosion-gradual epidermal breakdown, sometimes referred to as a superficial ulcer that heals without scarring Ulcer-local excavation or surface defect created by sloughing of inflamed necrotic skin Crust-a scab, caused by surface drying of exudate or secretions

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Fissure-abnormal cleft or deep groove, usually hyperkeratotic superficially with an open or hemorrhagic dermal wound deep in the recess Scar-cicatrix, or the mark remaining after a dermal, or deeper, defect or other morbid process has healed (hypertrophic, keloid) Pustule--visible accumulation of pus within or beneath the epidermis, frequently in an eccrine duct or hair follicle (pus is a liquid inflammatory product consisting of leukocytes and serous transudate, along with bacterial and other proteins) Abscess-a collection of pus in a cavrtyformed by disintegration of surrounding tissue Furuncle-an accumulation of pus in the skin and succutaneous tissue, also known as a boil; typically caused by Staph. entering through a follicle, associated with a painful, nodular inflammation of skin with corium erythema and subcutaneous edema Carbuncle--a cluster of boils (furunc!es) affecting skin, associated with subcutaneous necrosis and multiple draining sinuses

Sinus tract-a cavity or channel connecting an abscess to the skin surface or adjacent tissue layers (a fistula generally refers to a channel or tract connecting a deeper organ to another organ or tissue layer, or the skin surface) Hyperkeratoses (HPKs) Non~mechanically induced diffuse keratoses are usually bilateral, symmetrical, plantar and palmar, and often inherited. Characteristics include 4:1 ratio of stratum (st.) corneum to st Malplghil {germinative layers of the epidermis, st. basale and st spinosumL with the granular layer, between the st. spinosum and st. lucidum of the epidermis. Common non~mechanical diffuse HPKs include: Psoriasis-maculopapulosquamous, silvery scales on erythematous base, Auspitz sign (bleeds when scale removed), elbows and knees Unna Thost disease--bilateral, symmetrical, palms and soles, dominant inheritance Mal de Maleda-torme fruste (partial expression) of Unna Thost, recessive inheritance, with nail, ocular and dental involvement. Vohwinke/'s disease (keratoma mutilans hereditarium)--diffuse, honeycombed, rippled keratosis of soles, star burst keratoma on knees. associated digital contracture and pseudo ainhum Keratosis pfantarum su/catum--status~post immersion toot with Dermatophilus congolensis Pachyderma periostosis-keratosis of soles, periosteal hyperostosis, associated with alveolar cell carcinoma Alcoholic keratosis-mosaic, honeycomb dystrophic keratosis with sympathetic component Hauxthausen's disease (keratosis climactericum)-commonly on heels, erythematous base, in postmenopausal women, associated with hypertension and hyperuricemia Moccasin foot-chronic, dry, hyperkeratotic T. rub rum dermatophytosis Hyperkeratosis traumaticum marginus os calcis (housewives heel)-secondary to prolonged weight bearing barefoot or in an open back slipper failing to support the heel (no counter) Keratoderma blenorrhagica---chronic inflammatory maculopapular and scaly dermatosis associated with Reiter's syndrome (urethritis, iritis, arthritis), usually in young males, localized to palms, soles and digits

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35

Mechanically induced diffuse keratoses can be unilateral or bilateral on the soles,

and show a 1:1 ratio of st. corneum to st. Malpighii with the granular layer intact. The underlying dermis is usually fibrous, with dilated capillaries and eccrine sweat ducts, and perineural fibrosis. There are typically about 400 eccrine ducts per cm 2 of plantar skin. This is often observed in patients with global anterior pes cavus with callus extending across the entire ball of the foot.

Non-mechanically induced punctate keratoses characteristically display increased st. corneum, a normal st. Malpighii, an intact st. granulosum, and loose underlying dermis. Genetically determined forms include keratosis punctata of Hallopeau, which is dominantly inherited, and displays hundreds of evenly distributed punctate keratoses, bilateral and symmetrical, with truncated, macular and verrucoid lesions. Acquired punctate keratoses are generally few in number, asymmetrical, and localized to skin creases. Acquired forms include: Arsenical keratoses--arsenic intoxication (Cruveiler~Baumgartener disease), affecting palms/soles, with hepatic failure; associated in past with certain asthma preparations, wines, and seen in coal miners Secondary syphilis-palms/soles, maculopapular, evolves to punctate keratoses Darier's disease-greasy, vegetative lesions, punctiform on palms/soles, external auditory meatus, cheeks Aigner's syndrome (form fruste of Albers-Schonberg disease}-----punctate keratoses of palms/soles with osteopetrosis Hanhart's syndrome-punctate keratoses of palms/soles, with multiple lipomas Basal cell nevus syndrome-pink (ham colored) pits with ice pick, punctate keratoses

Non-mechanically induced punctate keratoses of unknown etiology include heloma neurofibrosum, which displays keratinous filaments, typically about the perimeter of the heel, resembling mosaic verruca, with banana~like projections, single or multiple, and very painful. Mechanically induced punctate keratoses characteristically display a 1:1 ratio ofst corneum to st. Malpighii, a parakeratotic plug with atrophy of underlying granular layer, dilated eccrine sweat ducts, dermal fibrosis, capillary ectasia and perineural fibrosis. Included are: Parakeratosis plantaris discretum of Steinberg---translucent keratinous plug with surrounding white (macerated) rim of blocked eccrine duct Vamp disease-typically overlying EHL, or another extensor, tendon, where shoe vamp chronically irritates skin resulting in parakeratosis, loss of granular layer, and often a sinus tract due to draining bursa or tendon sheath

Dermatitides Dermatitis has many causes and forms, and is typically treated with topical or systemic corticosteroid, local care, and protection. Atopic dermatiti~a chronic pruritic eruption common in adolescents and adults, attributed to allergic, genetic and psychogenic causes; common to flexor surfaces, displaying crusts, lichenification, and excoriation Nummular (coin~like} dermatitis-of unknown etiology, affects extensor surfaces, buttocks and legs, and displays papulovesicular eruption, forming crusts Lichen simplex chronicus (focalized neurodermatitis}-----due to repeated scratching, most common in females and Asian individuals, with well~demarcated scaly erythema

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Contact dermatitis-an acute inflammation caused by contact with an allergen effecting delayed hypersensitivity, and usually well-demarcated with a raised margin Dyshidrosis--any disorder of eccrine sweat ducts, such as pompholyx. Pompholyx ("bubbles") is a skin eruption, typically on the sides of fingers and toes, palms and soles, consisting of discrete 1 to 2 mm intra-epidermal vesicles with surrounding erythema, associated with intense itching, lasting 1to 2 weeks intermittently ldreactian (id rash}-a remote rash associated with a primary lesion caused by cutaneous sensitization resulting in a distant site allergic reaction to circulating allergen, such as dermatophytid or syphilid Stasis dermatitis-affects the distal leg, ankles and hindfoot, secondary to chronic venous insufficiency (valvular incompetence due to dilation of vein) or lymphedema, with cyanosis, erythema, pruritus; progressive over years, and may eventually ulcerate Purpura and other Hemorrhagic Lesions Purpura are a group of disorders characterized by brown, red or purple subepidermal hemorrhages. Petechiae are pinpoint, macular, round, purple or red, intradermal or submucous hemorrhages. Purpura are larger than petechiae{< 1 em), but smaller than ecchymosis(> 1 em). Ecchymosis, are large hemorrhages causing black and blue marks or bruises. Purpura are caused by thrombocytopenia, amyloid, steroids (capillary fragility), rheumatic vasculitis (leukocytoclastic angiitis), polyarteritis nodosa, serum sickness, SLE, Henoch-Schonlein disease, and hemorrhagic fever (Ebola virus). Splinter hemorrhages occur in the nail bed, and may be indicative of subacute bacterial endocarditis. Papulosquamous Eruptions These are characterized by slightly elevated, erythematous and scaly lesions, and include: linea pedis---dermatophyte or other fungal or yeast infection Psoriasis---chronic, hereditary, recurrent papulosquamous eruption occurring on the scalp and extensor surfaces, displaying a red macule, papule or plaque covered with silvery scales, removal of which effects local bleeding (Auspitz sign) Secondary syphHis-maculopapular and pustular eruption caused by T. pallldum infection, a venereal disease; the primary stage being a hard chancre, from which the bacteria spread systemically via lymphatics and blood. Secondary syphilis occurs 612 weeks after initial infection, displays fever, copper-hued multiform papular skin eruptions (syphilids), iritis, alopecia, mucous patches, and severe arthritis. Tertiary syphilis is late stage generalized disease affecting the CNS, bones, joints, and parenchymal organs Lichen planus-wide, flat, violaceous, itchy skin papules with a characteristic sheen, occurring in persistent patches, of unknown etiology (viral or psychogenic are suspected). The scaling lesion of Lichen planus may demonstrate Wickham's striae (network of white lines) Pffyriasis rose.r---fine, branny, scaling pink oval maculas aligned with skin creases

Benign Pigmented Skin lesions A nevus is a well-demarcated, stable, malformation of hereditary origin, involving epidermal, skin adnexal or vascular elements. A nevus containing melanin is said to be pigmented. Pigmented nevi include: Junctional nevus---brownish, smooth, hairless, macular or slightly elevated, 1to 8 mm diameter, occurring on any skin surface, histologically displaying nests of melanocytes "dropping off" into the dermis

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Compound nevus-raised, flesh~colored to brown, often papillomatous, may contain hairs, with melanocytes in the epidermis (newly formed) and dermis (older) Intradermal nevus-similar to compound, typically more papillomatous, with hairs, and all melanocytes are in the dermis (older) Nevi evolve from epidermis to dermis, associated with elevation and involvement of skin appendages (hair). Nevus flammeus (port wine stain, or capillary hemangioma) is a diffuse, poorly demarcated area of pink/red/blue/purple capillary dilation in otherwise normal skin (not melanocytic). Livedo, or livedo reticularis, is vascular congestion causing mottled cyanosis, often caused by cold exposure but may be permanent secondarytovenular dilation.

Vesicles and Bullae

Table 3.1. CAUSES OF BULLOUS ERUPTIONS COMMON BUllOUS DISORDERS

UNCOMMON BULLOUS DISORDERS

Physical (heat, friction, cold) Excess sun or UV exposure Drug-induced photosensitivitv Systemic drug reaction Infection (bacterial, fungal, viral)

Pemphigus Epidermolysis bullosa Dermatitis herpetiform is Bullous lichen planus Toxic epidermal necrolysis Diphtheria cutis

Contact dermatitis Eccrine dysfunction (pomphylox) Erythema multiforme

Herpes infection--results in clusters of small vesicles, with H. simplex Type I occurring on skin or perioral, and Type II affecting genitalia. There is often a prodromal fever, and lesions can be recurrent Herpes zoster is caused by the same virus that causes varicella (chicken pox), which resides in the dorsal root ganglion, and erupts in a unilateral, tense vesicular, usuaHytruncal, inflammation in the dermatomal distribution of the affected spinal nerve root, frequently painful, and occasionally associated with post-herpetic neuralgia (shingles). Erythema multiforme--an urticarial eruption of immune origin, displaying red to purple, raised bullae, classically with target or iris lesions, severe forms of which are termed Stevens-Johnson syndrome, and can be fatal. Pemphigus-typically occurs in middle to older aged persons of Jewish descent, considered autoimmune or viral, with vesicles and bullae On skin and mucus membranes, treated with steroids, chronic, and often with high morbidity or death. Epidermolysis bullosa-typically occurs early in life (1 to 2 years) at sites of previous skin trauma, typically minor, can be fatal in an infant, and treated with supportivemeasures. Dermatitis herpetiformis {Duhring's disease}-a chronic, systemic vesiculobullous eruption on the extremities and torso, wrth associated enteritis, large concentrations of lgA, and considered autoimmune. Toxic epidermal necrolysis {scalded skin syndrome)-can affect all ages with epidennal necrosis and slough or peeling, often caused by staphylococci, and treated in a fashion similar to burns. Can also be a drug reaction, most notably with the use of Allopurinol, NSAIDs, Sulfonamides and measles vaccine.

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Nodular or Granulomatous Lesions Necrobiosis lipoidica diabeticorum-------disp!ays dermal edema and collagen distortion, yellow-brown pigmentation, loss of elasticity, well-circumscribed annular pretibial patches in diabetics, histologically showing palisading granuloma. Granuloma annulare---annular, hard, reddish, perimalleolar or dorsal. nodular lesion,

benign and. recurrent, occasionally related to diabetes, histologically showing palisading granuloma.

Erythema nodosum----acute inflammatory skin disease with tender red, pretibial nodules, successive patches over a few weeks, considered an allergic reaction, frequently seen with tuberculotoxin, streptococcal infection, drug reaction, coccidiomycosis and psittacosis. Sarcoidosis-chronic, progressive, systemic granulomatous disease of unknown etiology, affecting any organ system, a common cause of pulmonary hilar adenopathy, histologically showing noncaseating epithelioid cell tubercles (tuberculin negative usually). Angiolipoma-we!l vascularized, benign tumor of mature fat cells, often localized aboutthe tibial plateau and malleoli. Neurilemmoma is a peripheral nerve sheath tumor of myelin. Glomus tumor-reddish~blue nail bed lesion displaying myoepithelial cells and dilation of the Sequet-Boyer canal in the subungual papillary dermis, rarely observed beyond 25 years of age. Eccrine spiradenoma---deep, benign, solitary nodule arising from the coil of an eccrine gland, covered by normal appearing skin and associated with paroxysmal pain. Leiomyoma---benign arrector pili smooth muscle tumor (more commonly, uterine fibroid). Leprosy (Hansen's disease}--due to Mycobacterium leprae infection, causing asymmetrical, maculopapular, hypopigmented, circumscribed skin granulomas that often progress to digital ainhum and spontaneous amputation. Leprosy is diagnosed bacteriologically and histologically, and treatment entails diaminodiphenylsulfone (Dapsone or DDS) combined with rifampin, or clarithromycin and clofazimine. Ulcerative Skin lesions Hypertensive ulcers-localize to the lateral malleolar, digital, and dorsal areas,

are punched-out secondary to occlusion or spasm of arterioles, and are very painful. Treatment entails control of underlying HTN and local care. Venous stasis ulcers-localize along the saphenous vein secondary to venous hypertension caused by valvular incompetence, display stasis dermatitis with surrounding hyperpigmentation and eczematous vesicles and crusts, and are irregularly shaped with granular base and may become secondarily infected. Treatment consists of venous compression, elevation, cleansing, and protection. Decubitus ulcers-display a well-circumscribed, undermined margin; are localized to bony prominences and are associated with immobility and pressure. They are often tender, and respond well to cleansing and pressure relief. Mal perforans ulcers-punched out, nontender (insensitive), undermined and related to repetitive pressure. They respond well to supportive measures unless underlying bone infection develops. Sickle cell ulcerations-localize perimalleolar, are recurrent due to sludging of sickled RBCs and infarction. They are associated with hyperpigmentation and inflammatory infiltrate effecting induration, and are very painful.

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Skin Lesions Predisposed to Malignant Transformation or Association Actinic (solar) keratosis-sharply outlined, red or flesh colored macule, or slightly raised, verrucous or squamous growth on sun exposed surfaces. It may develop into a cutaneous horn, or evolve into squamous cell carcinoma. It is considered to be of UV mutation origin and is seen in the middle aged to elderly, usually in light

skinned individuals (also called solar or senile keratosis). Parakeratosis of Mibelli--rare chronic hereditary skin disease of the hands and feet,

with hypertrophy of the st. corneum about the eccrine sweat ducts. It may become dysplastic and effect squamous carcinoma. Xeroderma pigmentosu!TI---rare, familial recessive trait, that is often fatal, affecting skin with atrophy and pigmentation. It is associated with skin and eye photosensitivity has its onset in childhood with development of affiliates (freckles), telangiectasia, papilloma, hyperkeratoses, melanoma and carcinoma. Ataxia telangiectasia (Louis Bar syndrome)-hereditary progressive ataxia. It is associated with oculocutaneous telangiectasia, pulmonary disease and respiratory tract infection, and ocular muscle dysfunction. Malignant Skin Lesions

See selected neoplasms. Nail Disorders (Onychopathy) Congenital Defects Anonychia---------absence of one or more nail plates, associated with ichthyosis. Macronychia-anomalously large nail plate, otherwise normal in appearance (may also be acquired secondary to acromegaly, COPD or pulmonary hypertrophy [clubbing ofthe digits]). Micronychia-anomalously small nail plates, otherwise normal. Onychoheterotopia--nail growth in abnormal location, such as the dorsal or plantar skin of the toe or foot Pachyonychi&-abnormallythick, heavily striated longitudinally, occasionally lytic nail p!ates jean also be acquired secondary to repetitive microtrauma). Polyonychia-extra or supernumerary nail plate on a single toe, with one or more matrices. Synonychia-a single nail shared by two or more syndacty!ized digits.

Traumatic Conditions HangnaiJ.....-.periungual, filamentous epidermal spicule. Subungual hematoma-damage to the nail bed causes hemorrhage that fills the potential space between nail plate and bed, may be associated with simple or complex bed laceration, open phalangeal fracture, and should be drained (hand cautery perforation) if acute and painful or throbbing, or requires removal of the nail plate for repair of the bed if more than 25% ofthe visible nail plate displays hematoma or ifthe plate is substantially unstable. Onychophagi&-nail biting. Onychocryptosis-a late effect of matrix distortion due to acute trauma or repetitive microtrauma, wherein the plate grows into the adjacent nail fold, or when the nail is cut incorrectly and the adjacent fold is pushed by external forces into and over the plate. Onychophosis represents nail fold hyperkeratosis prior to dermal violation and paronychia.

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Onychogryphosis-distal plantar curvature, with thickening or clubbing of the nail plate, a late effect of matrix and/or bed disruption, either acute or chronic. Leukonychia--white spots due to chronic microtrauma effecting plate separation from the bed, with a change in the refractive index of light; to be distinguished from white superficial onychomycosis. Onychia or paronychia--nail fold inflammation, red and swollen, tender and often with drainage, usually due to onychocryptosis. Onycholysis--separation ofthe plate from the bed, can be traumatic or secondaryto bed hypertrophy or accumulation of subungual debris, as in onychomycosis.

Metabolic and Systemic Conditions That Affect the Nails Hyperthyroidism--koilonychia, onycholysis, fingernails more so than toenails. Psoriatic arthritis-------pitting and onycholysis, discoloration, subungual hyperkeratosis, splinter hemorrhages; usually treated with systemic control of arthritis, local protection and palliative care. Hypertrophic pulmonary asteodystrophy-tibia>humerus) precedes this form of osteomyelitis in 33% of cases. Acute Hematogenous Osteomyelitis (AHO)- can be effected by Streptococcal skin infection, often associated with measles or chicken pox in childhood. Similarly, otitis media due to Hemophilus, Staph.~ or pneumococcus can hematogenously spread to bone. AHO localizes in metaphyseal bone due to the paucity of phagocytes and sludging venous sinusoids. AHO in the infant (0 to 1 year) can involve the joint, as capillaries traverse the epiphysis and effusion develops in 60~70% of cases. Group B Strept, Staph. au reus, and E coli are the most common organisms in AHO in the infant. In the child, AHO usually does not involve the joint space and most commonly localizes around the hip, shoulder, and ankle (distal lateral tibial metaphysis is intra-articular, and can lead to septic arthritis with osteomyelitis). Extensive cortical damage and involucrum develop, rarely is there damage to the growth plate or joint, and Staph. epidermidis is causative in 60~90% of cases of AHO. In patients with sickle~cell anemia or Sc hemoglobinopathy, Salmonella is most common; and Hemophilus influenza is most common in children less than two years old. In the adult, AHO is usually seen in patients older than 50 years of age. Pseudomonas is common in IV drug abusers developing AHO; and in adults using IV catheters, suffering urinary tract and pulmonary infection, or within two .years following major surgery. Joint infection may accompany AHO in the adult. Cases of AHO displaying purulence upon aspiration, or failing to respond favorably within 36 hours of initiating antibiotic therapy warrant operative intervention.

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Contiguous Spread Osteomyelitis~ results from direct contamination of bone due to spread of bacteria from contiguous tissue, is the most common form of osteomyelitis observed in podiatric cases; generally involves patients over 40 years of age; and may occurfollowing puncture, laceration, ulceration, or surgical intervention. Postoperative Contiguous Spread Osteomyelitis- includes acute postoperative osteomyelitis {observed within one month of surgery), delayed postoperative osteomyelitis (observed between one month and two years of surgery), and late postoperative osteomyelitis (not observed until at least 2 years after surgery). Most commonly, postoperative osteomyelitis is ofthe delayed or late sort, usually growing Staph. or mixed flora. In all forms of contiguous spread osteomyelitis, adjacent soft tissue or bone infection must be identified. A thorough search for a nearby ulcer or sinus tract is important

Direct Inoculation Osteomyelitis~ is caused by contamination of bone without adjacent soft tissue infection, and is either traumatically or surgically induced. A distinction between postoperative contiguous spread osteomyelitis should be made. Vascular Insufficiency Osteomyelitis- occurs in patients with peripheral vascular disease, wherein associated gangrene and ulceration are usually present. May involve anaerobes, and myonecrosis should be considered. Has features similar to contiguous spread osteomyelitis, however the overriding distinguishing factor is peripheral vascular disease. The Cierny-Mader classification of OM combines anatomic and physiologic categories in an effort to direct therapy. Twelve different stages of osteomyelitis can be described by combining the different categories (Table 3-2).

TABLE 3-2. THE CIERNY-MADER CLASSIFICATION OF OSTEOMYELITIS.

Anatomical category

Physiological category

I. Medullary II. Superticial

A. intact local vascularity and systemic immune competence B. Compromised local vascularity and/ or systemic immune competence C. Host not a surgical candidate, as operative risks outweigh potential benefits

Ill. Localized IV. Diffuse

Bucholtz classified osteomyelitis using 7 categories (Table 3-2).

TABLE 3-3. THE BUCHOLTZ CLASSIFICATION OF OSTEOMYELITIS.

Category A B

c

D

E

F G

Etiology, anatomical site, and physiological type Wound induced Mechanogenic Physeal OM Ischemic limb Combination of A-D Septic arthritis with adjacent OM Chromic OM with osteitis

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Pus Periosteum Bone abscess Dead and dying bone (sequestrum)

A

B

Involucrum

c

D

Figure 3.1 Diagnostic Imaging Of Infection-radiographic signs of infection inctude increased soft tissue density and volume associated with inflammation and, in cases of OM, include osteolysis, involucrum, cloaca, and sequestration (Fig. 3.1). Osteolysis is not visible as radiolucency until 30-50% of osseous mineralization has been washed away by

inflammatory hyperemia. This generally takes 10-14 days after the onset of symptoms. Thereafter sclerosis and periosteal new bone formation, known as involucrum, surrounds necrotic and infected bone, known as sequestrum, and ultimately a channel, known as a cloaca, forms in new bone as bacteria proliferate and exudate drains. Chronic OM involves the presence of microbes living in dead bone (sequestrum), surrounded and contained within new bone (Involucrum). Eventually, after trauma or some other instigating factor, an ncute flare-up can develop with drainag·e, and signs and symptoms of acute infection. Chronic osteomyelitis can lay dormant for many years (reportedly> 50 years) before a flare-up occurs. In the presence of a chronic draining sinus due to OM (or other causes), squamous cell carcinoma (SCC) can develop in the epithelium along the sinus tract as a longterm seque!!um. Radionuclide studies can be useful in the evaluation of suspected OM, and include WB'C scans labeled with Tc-99 or 1n-111.ln most cases, bone scintigrams become positive within 48-72 hours. In patients with Charcot neuroarthropathy, or suspected fibrous nonunion, bone and joint infection may be strongly suggested with identification of a "hot" ln-111 or Tc-99 labeled WBC scan (Indium and Seratec scans, respectively). MRI may be the most useful imaging method when considering OM, however positron emission tomography {PET) scans have been shown to be even more

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Selected Diseases and Pathological Conditions

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sensitive and specific for Charcot neuroarthorpathy, in comparison to MRI scans. None of the imaging methods can be used to definitively ascertain OM, although alone and in combination, they can be very helpful. Definitive diagnosis OM is made by means of biospy, and bone gram stain and C&S. Treatment of Infection-the treatment of any infection, including OM, entails adherence to several general principles, including the 5 Ds: 1) decompression, 2) drainage,

3) debridement, 4) dressings, and 5) drugs. Decompression is achieved with incision and drainage 0&0) or removal of operatively-placed sutures, following surgical preparation. Drainage is achieved with copious lavage, debridement and excision of necrotic and/or grossly infected tissue, removal of implanted materials or foreign bodies, removal of unstable internal fixation devices, open packing with fine-mesh gauze, or partial or complete closure with drain placement, and use of an appropriate dressing. Tourniquets are generally not used when performing 1&0. The extent of infection is thoroughly explored and drained, and definitive cultures and stains are obtained from the deep tissues. In cases of OM, a small margin of apparently uninfected bone can be debrided and sent for pathological inspection. In any infection, drainage is allowed to proceed as long as necessary, usually a minimum of 48to 72 hours, with dressing changes consisting of lavage and debridement as indicated by wound appearance.lf necessary, additional debridement can be carried out by a return to the operating room, which is frequently necessary in cases involving necrotizing infection. Care should be taken to avoid performing a delayed primary closure too soon. Antibiotic Therapy-antibiotics are the primary drugs used in the treatment of infection. Consideration must be given to the spectrum of coverage, frequency of administration, toxicity, duration of treatment and cost. Prior to ascertaining the microbiological results of definitive culture specimens, empiric antibiotic therapy is initiated (Table 3-4). In cases of OM, antibiotic therapy is usually continued for 6 weeks following final debridement A Hickman, Broviac or PICC (peripherally inserted central catheter) can be used for longterm IV therapy. Monitoring the course of treatment of infection requires attention to fever, antibiotic levels, renal and hepatic function, wound appearance and pain, complete blood count(CBC) and differential, erythrocyte sedimentation rate (ESR), insulin requirement in the diabetic, and C&S results. Antibiotic impregnated calcium sulfate, or polymethylmethacrylate (PMMA), beads may be packed in the wound and used in conjunction with IV antibiotics. Antibiotic beads are usually made in the OR, using gentamycin, vancomycin, clindamycin, or another antibiotic, and packed in the debrided bone to increase local concentration of antibiotic. The wound is closed over the beads and, after 10-20 days (or sooner or later, depending upon wound appearance), the patient returns to the operating room tor bead removal, further debridement, and placement of more antibiotic beads if needed, or reconstruction and closure. A previously infected wound is ready for closure after achieving at least one negative culture, and the wound looks clean with beefy red granulations, no evidence of purulence or sinus tract, and resolution of marginal erythema. In some cases, delayed primary closure can be undertaken without first ascertaining a negative wound culture, as a wound that is clinically ready for closure usually has some degree of surface contamination. Closure may be achieved by means of secondary intention, or via delayed primary closure, skin graft, or flap. Previously infected wounds are generally closed over a drain of some sort, or only partially closed. Depending upon the specifics of the infection, use of the wound vacuum, as well as hyperbaric oxygen therapy, should also be considered.

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Diabetic Polymicrobial Infection-diabetic polymicrobial infection can be limb and life threatening. Plantar space infection may develop, with abscess dissection along fascial

planes of the plantar vault into the posterior compartment of the leg, or through an intermetatarsal space into the dorsum then into the anterior leg. The patient must be evaluated for constitutional signs and symptoms of septic shock, including incoherence or confusion, hypotension, tachycardia, and extreme hyperglycemia and ketoacidosis. Hospital admission and inpatient management are usually in order. It is useful to obtain a serum g!ucose level, CBC and differential, ESR, urinalysis, biochemical levels other than glucose, EKG, foot/leg and chest X-rays, blood cultures x3 from 3 separate sites 30 minutes apart, other labs and tests that may be warranted by the patient's individual condition, medical and anesthesia consultation and co~management, and supportive therapy in preparation 'for surgical debridement. Orders should also include NPO, wound and skin isolation, IV LR at KVO via 18~gauge IV catheter, specific medications (chronic and acute), non~weight bearing, on call to operating room for 1&0. The patient, and/or a family member, must be informed of the emergent nature of the condition, and possible consequences. Empiric antibiotic therapy should be initiated prior to identifying definitive culture results, and coverage should include anaerobic, aerobic, gram(+) and gram(~) organisms. A useful initial regimen consists of a combination of amoxicillin~clavulonate, clindamycin, and a quinolone (see Table 3-4). Intravenous antibiotics, such as ticarcillin-clavulonate, could also be used until definitive cultures are identified. It can be helpful to obtain an infectious disease consultation, as well as consultation regarding the potential benefits of hyperbaric oxygen therapy (HBOT). Incision and Drainage (I&D}-once the patient is prepared for surgery, 1&0 is performed in the operating room. The patient should be supine, without a tourniquet, and an orthopedic prep of the lower extremity performed. The wound or abscess is then probed to determine its extent and confines, after which a wide incision is made in order to allow drainage. Exploration entails inspection of all undermined or abscessed areas. In cases of diabetic plantar vault infection, decompression of the vault requires opening the deep fascia adequately enough to drain the medial, central, lateral, and deep plantar spaces, as necessary. Deep specimens are obtained for gram stain and C&S, necrotic and infected tissues are excised and biopsied, and foreign bodies are removed. IV antibiotics may be altered based upon the results ofthe gram stain, however empiric therapy usually does not change until definitive culture results are known. Copious lavage, sometimes using a pulsed, power-flushing system, is perfomed after initial sharp debridement. Close inspection is paid to all tissues prior to open packing with fine mesh gauze, then application of sterile dressing. Subsequent daily or BID dressing changes are performed with lavage and curettage of the wound, and additional specimens obtained for C&S as indicated by the appearance of the wound. If the patient and wound are not responding to the treatment, then there is either persistent abscess or the choice of antibiotic is incorrect An MRI could help detect an unrelieved abscess. A return to the operating room for additional debridement is performed whenever indicated, based on the patient's progress. The goal is to achieve a beefy red granular base, with no purulence or malodor, with decreased edema and erythema and pain, and no residual undermining or tunneling. Closure occurs thereafter via either continued secondary intention healing, or delayed primary closure, or the use of a skin graft or flap. In some cases involving aerobic infection, especially those with deep or large defects, as well as those with considerable drainage, vacuum-assisted wound closure can be helpful. The wound vacuum can also be used over skin grafts and flaps.

Ch.3

Selected Diseases and Pathological Conditions

47

Chronic Pedal Wound-when a patient presents with a chronic pedal wound, perhaps with intermittent drainage that has lasted for months, consideration should be given to the possibility of previous puncture wound or osteomyelitis. Common sites for chronic pedal wounds include the digits, metatarsal ball, 5th metatarsal base, heel, and perimaHeolar areas. Protective sensation should be determined, since chronic ulceration is very commonly associated with the insensitive foot {mal perforans ulcer). Puncture wounds that have penetrated the sole of the shoe are likely to involve Pseudomonas aeruginosa, although Staph aureus remains the most common pathogen in barefoot punctures and in children. As with a!I chronic wound, diagnostic images should be obtained, and consideration should be given to the potential benefits of wound margin biospy and surgical debridement. Radiographs are obtained, as are labs (as noted above for the diabetic infection), and consideration given to a bone scan, or aCT or MAl scan. When indicated, the patient is taken to the operating room for 1&0 and exploration. Do not dissect through the site of a chronic draining sinus tract if possible, when exploring bone that may not be infected. A dorsal approach can be useful in the case of a chronic plantar wound, as long as the nidus of infection is not obscured from inspection. If there is any concern about compromising drainage of the abscess, then simply excise the entire sinus tract The important point is to explore the involved area and obtain appropriate samples for gram stain and C&S, as well as soft tissue and bone biopsy. After obtaining specimens for C&S, then initiate IV antibiotics, lavage, pack open, and initiate daily wound care.

Fungal infection-fungal infections are extremely common in the foot and !ower extremities, and must be differentiated from other causes of papulosquamous eruption \secondary syphilis, psoriasis, pityriasis rosea, contact dermatitis) when localized to the glabrous skin. Fungi are eukaryotic and reproduce bv spore formation, grow as hyphae and form a mycelium. Some organisms, such as Candida, are dimorphic and grow as either yeast or fungal hyphae depending upon the host environment Fungi that infect humans are categorized as either dermatophytes (superficial) or deep pathogens. The most common pathogenic fungi affecting humans are the Fungi lmperfecti, although other groups can infect the compromised host. Identification of the infecting fungus is made via skin shaving or nail fragment exam for hyphae or yeast using KOH (potassium hydroxide) to dissolve keratin from skin scrapings, or periodic acid Schiffs (PAS) stain; and by means of fungal C&S using Sabouraud's dextrose agar (SDA). Superficial mycoses include tinea pedis, candidiasis (thrush), onychomycosis, tinea corporis, tinea cruris, tinea capitis, tinea axillaris, and tinea versicolor. linea pedis is usually responsive to topical antifungal cream application for 2~6 weeks, with agents such asterbinafine and econazole proving to be effective. Patients are encouraged to try oveHhe~counter antifungal preparations (tolnaftate, undecylenic acid, miconazole, c!otrimazole) for minor conditions oftinea pedis, if they have not already done so. Candida species often infectthe nail bed in compromised hosts, and cause paronychia and pseudo-clubbing due to chronic digital inflammation. Onychomycosis typically presents as either white superficial onychomycosis (WSO), which is usually caused by Trichophyton mentagrophytes or yeast and is least common; distal subungual onychomycosis (DSO), which is usually caused by T rubrum and is most common; and proximal subungual onychomycosis IPSO), which is also usually caused by T rubrum and is rare and usually associated with systemic disease or HIV. Onychomycosis must be distinguished from mechanically induced nail dystrophy, psoriatic pitting and flaking, lichen planus and pterygium, COPD induced clubbing, dystrophy due to peripheral vascular

48

Selected Diseases and Pathological Conditions

Ch. 3

disease, and subungual exostosis. Whe·n harvesting nail and nail bed fragments for fungal tissue examination and C&S, it is imperative to obtain plenty of nail bed fragments from deep to the nail plate. Palliative treatment of onychomycosis includes nail plate debridement and regular application of topical antifungal (ciclopirox 8% lacquer or miconazole 2% solution, or similar agents), however cure rates are usually< 75~80% with topical therapy, although debridement alone is known·to improve foot~related quality of life. Cure is more likely with oral administration of either terbinafine (250 mg PO QD x 3 months) or itraconazole (200 mg PO QD x 3 months), or perhaps fluconazole (as an adjunct for the treatment of yeast). it is prudent to check liver enzymes and CBC, current medications, and past medical history, prior to initiating oral antifungal therapy. Chemically induced hepatitis has been greatly diminished using the newer systemic antifungal agents, as therapy is only administered for 3-4 months, generally. Drug interactions (certain antihistamines, anti-lipid agents, and others) must also be considered prior to initiating oral antifungal therapy. The active metabolite of the agent is maintained in the substance ofthe nail for 6-9 months, and the ultimate appearance of the nail plate cannot be truly assessed until 6-12 months following initiation of oral therapy. Prevention of recurrent onychomycosis may require periodic maintenance use of topical therapy, and concurrent debridement is a crucial part of any treatment plan. Deep mycoses include mycetoma and madura foot, sporotrichosis, and blastomycosis; caused by Madurefla mycetoma, Sporothrix schenkii, and Blastomycoses, respectively. Deep fungal infections are granulomatous, with papular and nodular inflammation of the subcutaneous tissues and overlying skin, sinus tract formation, foul odor, and secondary bacterial infection may ensue. Treatment may require excision of infected tissue, including amputation, and systemic administration of amphotericin-8 (sporotrichosis), sufonamide and other oral antifungal agents (mycetoma, madura foot, blastomycosis).

Septic Arthritis (see Arthritides) Antibiotic Therapy-antibiotic therapy varies from community to community, and the clinician is encouraged to be familiar with the characteristics of the organisms in his/her own community. The local hospital's antibiotic susceptibility and causative organism prevalence report can be a useful guide to therapy, and the county health department also monitors organisms responsible for reported infections. Although it is often necessary to initiate therapy empirically, it is always adviseable to obtain a culture from the lesion if this is possible. Once again, appropriate specimens should be obtained for isolation of the causative organism and determination of its susceptibility to antibiotic therapy. Bacterial cultures are particularly important in cases of severe infection, in diabetic or compromised hosts, and for chronic or recurrent infection wherein previous culture and sensitivity has not been performed. In all cases of infection, ongoing assessment of the response to therapy must be undertaken. Therapy is generally continued for 10-14 days for soft tissue infections, and 6 weeks for OM, and the treatment should be honed to the individual patients specific local and systemic requirements. The following information is meantto serve as a general guide to antibiotic therapy for infections involving the foot. ankle and leg. Since organisms and antibiotcs evolve and change frequently, the reader is encouraged to check with appropriate updated literature, such as the drug package insert, for specific indications and dosages.

Ch. 3

Selected Diseases and Pathological Conditions

49

Methicillin-resistant Staphylococcus aureus(MRSA)-community acquired methicillinresistant Staphylococcus aureus (MRSA) represents an ever-increasing proportion of wound infections, particularly in children. MRSA resists the cidal effects of beta lactam antibiotics such as penicillin and cephalosporin, including cephalexin, ceftriaxone, and amoxicillin-clavulanate; and the organism may also resist the static effects of

erythromycin, clarithromycin, and azithromycin. Potentially useful oral agents include clindamycin, trimethoprim-sulfamethoxazole, doxycycline, and linezolid; IV agents include vancomycin or daptomycin; and mupirocin can be used topically. Rifampin can also be used, however not as a sole antibiotic. For limb- or life-threatening MRSA infection, high-dose IV antibiotic therapy using vancomycin or daptomycin, perhaps combined with gentamicin, should be considered. Some strains of MRSA display "inducible resistance" to agents such as clindamycin, and these can oftern be identified using the "D test." A positive "D test" is associated with an increased risk of antibiotic resistance, and careful clinical follow~up is important. In an effort to prevent colonization and relapsing infection, 4~6 weeks of therapy may be necessary. Postoperative Infection------overall, the prevalence of postoperative infection ranges from

1~2% of clean, elective bone surgical cases, and most of these involve Staph. aureus. In cases involving implant infection, Staph. epidermidis, with its glycocalyx, is also common. Other causative species associated with postoperative infection include Proteus, Pseudomonas, B-hemolytic Streptococcus, Klebsiella, Serratia, Enterobacter, E. coli, and Bacteroides. In general, when stable osteosynthesis implants are present in cases of acute postoperative infection, metallic fixation devices are left in place unless they are associated with loose or necrotic bone (hence, loose or unstable). Chronically infected hardware should be removed and osteomyelitis therapy instituted. Puncture Wounds-the status of the patienfs tetanus prophylaxis should be ascertained whenever a puncture wound is encountered. Appropriate diagnostic measures combined with local wound care and antibiotic therapy are basic elements in the treatment of puncture wounds. In general, antibiotic therapy should cover Staph. aureus, and other gram(+) organisms, with appropriate attention to 1&0 if edema, cellulitis, induration, pain and Hx suggest abscess. The use of cephalexin, dic!oxacillin, or amoxicillin/clavu!onate should be considered. Punctures also convey the risk of anaerobic infection, and radiographs should be inspected for the presence of subcutaneous gas, primarlly hydrogen sulfide. Gas~ forming infections are usually necrotizing and require timely 1&0, and hyperbaric oxygen therapy may also be useful (see Necrotizing Infection, above). For punctures that involve penetration through the sole of the shoe, coverage of Pseudomonas sp. should be considered, and potentially useful agents include aztreonam + clindamycln, or imipenem + ci!istatin, piperacillin +tazobactam, or ampicillin+ sulbactam (see Table 3~4). Empiric Antibiotic Therapy-the following table (Table 3.4) is meant to provide guidelines for empiric antibiotic therapy, and the reader is encouraged to obtain definitive specimens for C&S, and to be familiar with the detailed information contained in the package insert for the specific antibiotic used.

50

Selected Diseases and Pathological Conditions

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TABLE 3-4. EMPIRIC DRUGS OF CHOICE fOR PREDOMINANT BACTERIA SEEN IN ADULT FOOT AND ANKLE SURGERY.* Organism Gram(+) Staphylococcus (methicillin sensitive)

Therapy of Choice

Alternate Therapy

cephalexin 1250 mg PO OlD) cefazolin (1-2g IV q8h)

Streptococcus

clindamycin (300 mg PO OlD) vancomycin 115 mg/kg IV ql2h) dicloxacillin 1250 mg PO OlD) nafcillin 12 grams IV q4h) azithromycin 1500 mg as a single dose on day 1, followed by 250 mg daily on days 2-5) clindamycin 1300 mg PO OlD)

penicillin (penicillin V 0.25-0.5 grams PO TID-OlD, or penicillin G 1.2-20 million units IM/IV per day) cephalexin (250 mg PO OlD) vancomycin 115 mg/kg ql2h IV) cefazolin (1-2g IV q8h) vancomycin 115 mg/kg IV q12h) clindamycin (300 mg PO OlD) doxycycline (0.1 gram PO/IV q12h) minocycline 10.1 gram PO ql2h) linezolid (600 mg PO/IV q12h) TMP/SMX 11 OS tab PO BID) gentamicin 12 mg/kg load followed by 1.7 mg/kg IV q8h) [if limb- or life threatening] ampicillin (250 mgamoxiclllin-clavulonate 1 gram PO TID) l875/125mg PO q12h x 14 days) vancomycin (15 mg/kg IV q12h) gentamicin (2 mg/kg IV load Streptomycin 115 mg/kg IM q24h) followed by 1.7 mg/kg IV q8h) piperacillin/tazobactam (3.375 grams IV q6h) combination ciprof!oxacin i500750 mg PO BID), rifampin (10 mg/kg/day up to 600 mg/day PO single dose), gentamicin 12 mg/kg load fullowed by 1.7 mg/kg IV q8h) or ceftriaxone (1-2 grams IV once daily) chloramphenicol (0.25-1 gram PO/IV q6h up to 4 grams/day)

Staphylococcus \methicillin resistant)

enterococcus vancomycin resistant enterococcus

!

-

Ch. 3

Selected Diseases and Pathological Conditions

51

Gram(-)

Escherishia coli, Proteus cephalexin (250 mg PO QID) ECSM group

ciprofloxacin (500-750 mg PO BID)

Pseudomonas aeruginosis

ciprofloxacin (500-750 mg PO BID)

Anaerobic infection Bacteroides

Diabetic foot infection polymicrobial

ciproftoxacin (500-750 mg PO BID) cefazolin (1 gram IV qBh) 3rd generation cephalosporin (such as ceftriaxone 1-2 grams IV once daily) aztreonam (1 gram qBh2 gram IV q6h) TMP/SMX (1 DStab PO BID) ceftazidime (2 grams IV q8h) aztreonam (2g IV q8h) gentamicin (2 mg/kg load followed by 1.7 mg/kg IV q8h)

metronidazole (500 mg PO q6-8h)

clindamycin (300 mg PO GID)

amoxi cilli n-c Iavu Ion ate (875/125mg PO q12h x 14days) cefazolin (1-2 grams IV qBh) +metronidazole (500mg PO/IV q6-8h)

ampicillin sulbactam (1.5-3 grams IV q6h) ticarcillin clavulonate (3.1 grams IV q6h) piperacillin tazobactam (3.375 grams IV q6h) lmipenem cilistatin (500mg IV q6h)

vancomycin (15 mg/kg q12h IV)+ aztreonam (2g IV q8h) + metronidazole (500mg PO/IV q6-8h)

*Specific dosages, serum drug level monitoring, creatinine and other appropriate serum laboratory tests, culture and sensitivity, adjunct therapy, and clinical reassessments should be individualized to the specific patient The reader is encouraged to consider the factthat recommended antibiotic therapy often varies overtime and geographic area.

ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS) AIDS is caused by infection with the cytopathic human immunodeficiency virus (HIV) retrovirus (RNA virus), which causes cell death. The CD-4 surface glycoprotein is the essential molecule recognized by the retrovirus, on the surfaces ofT41ymphocytes, monocytes, and macrophages. T-helper lymphocytes also become infected and destroyed, which greatly impairs the immune system. Natural killer lymphocytes are also destroyed, which impairs immune surveillance against neoplasms and virus infected cells. Approximately 40% to 50% of patients infected with HI\/, and possessing less than 400T-helper cells, develop AIDS within 2 years of HIV infection. Eighty-five percent of patients with T-helper cells less than 200, will develop AIDS within 2 years of infection.

52

Selected Diseases and Pathological Conditions

Ch. 3

Four Stages of Hl\llnlection Stage 1- manifesting acute HIV, wherein the patient displays general malaise and "mono-like" symptoms Stage II - chronically infected wrth HIV, often asymptomatic while developing antibodies to HIV Stage Ill- persistent generalized lymphadenopathy Stage IV- serious manifestations of immunodeficiency, frequent serious infections

and debilitation Subgroups ol Manifestations of Hill Infection Subgroup A- Constitutional symptoms Subgroup B- Neurological syndromes Subgroup C- Associated with infectious diseases C(1)- Defect in cell mediated immunity (Pneumocystis pneumonia) C(2)- Less profound infections Subgroup D -Secondary cancers (e.g. Kaposi's sarcoma) Subgroup E- Chronic lymphoid interstitial pneumonitis The treatment of AIDS includes supportive measures, as well as suppressive and disease modifying agents such as AZT. Therapeutic regimens have been shown to be most effective when disease modifying agents are used in synergy. Maternal transmission of the disease to the fetus has been controlled with AZT. Treatment regimens are very expensive. Any patient suspected of being HlV positive should be counseled regarding the importance of testing to confirm the presence of antibody, then appropriately referred for infectious disease consultation. Social setvices consultation is also important as various agencies may be able to assist with therapy. Regardless of whether or not you suspect a patient of being HIV positive, univers.al precautions are the standard of care in ALL aspects of health care.

SElECTED PERIPHERAL VASCULAR DISEASES Raynaud's Phenomenon Raynaud's phenomenon is an episode of small arterial and arteriole constriction resulting in acral pallor, cyanosis, or both color changes; with subsequent rubor due to hyperemia after the vasospasm has subsided {white, blue, and red coloration pattern).ln severe cases, prolonged vasospasm can effect cutaneous digital gangrene. The condition is usually bilateral, however it may rarely be unilateral. It is more common in females. Serious organic disease (atherosclerosis) is not usually present in the vessel in Raynaud's phenomenon. When a specific cause for the vasospasm, such as trauma, connective tissue disease, or neurogenic, cannot be identified after several years of suffering, then the condition can be termed Raynaud's disease (also known as primary Raynaud's phenomenon). Secondary Raynaud's phenomenon can be attributed to trauma, either acute or repetitive microtrauma; neurogenic due to nerve entrapment such as thoracic outlet, carpal or tarsal tunnel syndromes; occlusive arterial disease such as thromboangitis obliterans, arteriosclerosis obliterans, or status-post arterial thrombosis or embolism; thermal injury such as trench foot (cold and wet); or for miscellaneous conditions such as scleroderma, lupus erythematosus, RA, dermatomyositis, Fabry's disease, cryoglobulinemia (as in multiple myeloma or chronic leukemia), hemoglobinuria, myxedema, neoplastic disease, hepatitis B, pheochromocytoma, and ergotism. Treatment consists of protection, maintaining warmth,

Ch.3

Sele~;ted

Diseases and Pathological Conditions

53

use of vasodilators (Procardia, alpha~adrenerg.ic blocking prazosin, norepinephrine

depleting methyldopa, and reserpine), topical nitroglycerine and antibiotics. Frostbite and Cold Injury Frostbite implies freezing of the skin. Superficial frostbite is also termed chilblains, and is a mild cold injury. Classifications of frostbite 1st degree (chilblains)- skin frozen, no blisters 2nd degree -skin frozen, blisters formed 3rd degree- skin frozen and necrotic, ulceration, subcutaneous exposure 4th degree- skin and subcutaneous tissue frozen and necrotic. The treatment of chilblains is re-warming in 105-108° Fwhirlpool for 30 minutes, and administer analgesic (meperidine). Blisters are left intact unless they have ruptured, wherein they are treated as burns with cleansing debridement, Silvadene and dry sterile dressing. The treatment of more advanced or deep frostbite is rapid rewarming in 108~ 110° F water, administer antibiotic (cefazolin), tetanus prophylaxis, and analgesic (meperidine). It is important to protect the frozen part until proper thaw and care can be administered, and to avoid thaw followed by refreeze. PosHreezing sequella include vasomotor instability and cold hypersensitivity, paresthesia, depigmentation, hyperhidrosis, and atrophy. Arteriosclerosis Obliterans (Atherosclerosis Obliterans, ASO~ASO is the primary cause of occlusive lower extremity vascular disease, with the main lesion being atherosclerotic plaque occlusion of the superficial femoral or femoral level arteries. It is most common in males age 50-70 years, and more likely in patients with diabetes mellitus, hypertension, cigarette smokers, and/or hyperlipidemia. Pathological findings include atheromatous plaque formation, with secondary thrombosis. Symptoms include intermittent claudication, rest pain, cold intolerance, ulceration and gangrene, ischemic neuropathy, disuse atrophy, joint stiffness and contracture. Aorta or iliac artery occlusion causes buttock, hip and thigh pain; occlusion of the femoral artery and its branches causes thigh and calf pain; and popliteal and tibial artery occlusion causes calf, ankle and foot pain. Findings include diminished peripheral pulsation, discoloration (dependent rubor, pallor, or cyanosis), exaggerated distal cooling, edema, atrophy, cutaneous compromise, intrinsic atrophy, ulceration, and gangrene. The ankle-brachial index (ABI, Table 3-51. toe pulse pressure and amplitude, and TcPO, are diminished. Healing is generally anticipated if: ABI >.5, toe pressure >40 mm Hg, TcP0,>30 mm Hg, and toe pulse amplitude >4 mm. Duplex Doppler ultrasound noninvasive vascular testing, magnetic resonance angiography, and perhaps an arteriogram if surgical care warrants, can assist in the diagnosis. Treatment includes con~ trol of associated systemic disease (HTN, hyperlipidemia, anemia, arrhythmia). avoiding cold exposure, exercise to tolerance, hemorheologic agent (pentoxifylline, cilostazol), antiplatelettherapy (aspirin, clopidogrel, ticlopidine, dipyridamole), vasodilating agents (a and ~~adrenergic blockers, calcium channel blockers), peripheral angioplasty or vascular reconstruction, or amputation. Operative intervention is warranted whenever claudication, rest pain, or non~helaing wound is present. Peripheral arterial disease is often associated with carotid, coronary, and renal vascular insufficiency.

54

Selected Diseases and Pathological Conditions

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TABlE 3-5. ANKLE-BRACHIAL INDEX (ABI) CATEGORIES.* Ratio >0.96 0.81-0.95 0.051-0.8 ,0.05

Category Normal Mild obstruction

Moderate obstruction Severe obstruction

*Misleading, elevated ratios may be observed in cases of noncompressible arteries. Thromboangiitis Obliterans (TAO, Buerger's Disease)

TAO is a segmental inflammatory, obliterative disease of medium sized arteries and veins (posterior tibial), most common in the lower extremities of males who smoke cigarettes, the cause of which is unknown. TAO results in gangrene. Treatment involves arresting

progression of the disease by avoiding tobacco products, administering anticoagulants and corticosteroids; followed by effecting vasodialation with Procardia or other agents; and surgical management of gangrenous wounds.

Monckeberg's Medial Calcific Sclerosis This is a form of non-atheromatous degenerative arterial disease observed in middle-age to elderly males. There is fine calcification of the tunica media, which may lead to a non-compressible vessel, and effect a misleadingly high ankle/arm index. This occurs in the aorta and other large vessels. Venous Thrombosis and Pulmonary Embolism-the deep veins of the lower extremity include the plantar arch, posterior tibial, peroneal, anterior tibial, sura!, popliteal, superficial femoral, and deep femoral. Venous thrombosis, particularly ofthe deep system at or above the popliteal fossa, is associated with pulmonary embolism (PE), and for this reason can be fatal or extremely morbid. Predisposing factors fOr venous thrombosis include congestive heart failure, malignancy, trauma, surgery, pregnancy, and thrombocytosis. Other risk factors include cigarette smoking, oral contraceptive use, obesity, advanced age, bed rest or confinement, and paraplegia. Deep venous thrombosis prophylaxis should be instituted in patients at risk (Tables 3-6 and 3-7). Lower extremity deep vein thrombophlebitis {OVT, also known as venous thromboembolism, or VTE) presents with deep, aching pain and tightness in the calf or thigh. Pain upon active dorsiflexion ofthe ankle, or resistance to ankle dorsiflexion is known as Homan's sign, and is a nonspecific and unreliable clinical diagnostic maneuver. Tenderness upon calf or thigh muscle compression is a more specific test for DVT, when associated with edema and local increase in skin temperature. Superficial thrombophlebitis, which conveys a lower likelihood of PE, more commonly displays local heat, edema. erythema, and a palpable cord consistent with the thrombosed vein. Application of a tourniquet above the suspected thrombosis may cause pain at the level ofthrombosis within 30~45 seconds, and is strongly suggestive of DVT. Comparison of calf circumference wiH often show enlargement of the affected side. Constitutional findings may include temperature elevation 139.5'-40.5" C), chills, and malaise. Arterial embolism is usually more painful early on, with less swelling, exaggerated distal temperature decrease, and early sensory deficit. Severe venous thrombosis effecting retrograde arterial flow decrease may result in phlegmasia cerulea dolens, which can result in pedal ischemia and gangrene. Coagulation studies are usuarty

Ch.3

Selected Diseases and Pathological Conditions

55

normal unless full blown disseminated intravascular coagulation (DIC), familial

antithrombin Ill deficiency, or lupus erythematosus clotting inhibitors exist The laboratory diagnosis of DVT hinges on venous non-invasive duplex Doppler examination, and

magnetic resonance venography or contrast venography may be employed if ultrasound is equivocal. Radioactive 125 1-fibrinogen scanning, in conjunction with occlusion impedance plethysmography is also a sensitive combination for DVT of the calf. Use of the 0-dimertest may also be useful, however combined clinical and venographic tests are more reliable. An accurate diagnosis of DVT is made upon identification of predisposing factors and clinical observation, combined with duplex Doppler ultrasound and, perhaps, magnetic resonance venogram or contrast venography. Prevention of DVT is recommended, and can be achieved in several different ways (Tables 3-6 and 3-7). Prophylactic therapy in the !ow-risk patient involves mini-dose subcutaneous administration of 5000 units of heparin every 8 or 12 hours beginning about 60 minutes preoperatively. Adjunct physical measures include support hose, intermittent sequential pneumatic compression of the lower extremity, leg elevation with the knee flexed, and out-of-bed activity at an early stage after surgery. In high-risk patients, DVT prophylaxis is administered preoperatively with mini-dose heparinization, however in the postoperative phase, the heparin dose is adjusted upward to keep the PTT within 4 seconds of high norma!. Despite statistically more postoperative hemorrhage, this form of DVT prophylaxis appears to be worthwhile in the high-risk patient A baseline platelet count is recommended prior to mini-dose heparinization, and should be monitored periodically if it is observed to be low. High-risk patients may also be prophylaxed with a combination of mini-dose heparin and dihydroergotamine, which causes venular constriction and rapid venous return. Other prophylactic combinations include heparin and antithrombin Ill administration, and the use of low molecular weight heparin administered once daily has been shown to be effective and popular (see risk stratification and ·guidelines for prophylaxis, below). Coumadin, which inhibits the vitamin ! 105 min

•

Tourniquettime >90 min Rearfoot or ankle surgery Age 40-60 years Pregnancy or postpartum 20 lbs over ideal body weight) Diabetes meHrt:us Hypertension Hyperlipidemia Smoker Polycystic ovary syndrome Immobilized in BK or AK cast for> 1 week

• • •

•

Risk factor points assigned

Patient confined to bed for >72 hours Central venous access Age >60 years Oral contraceptive use Hormone replacement therapy Inflammatory bowel disease

2

Congestive heart failure •

Ankle, pi!on or tibial fracture

•

Severe sepsis/infection

3

Mu~iple

trauma Acute spinal cord injury

Cancer treatment Currently treated or history of DVT or PE

5

Ch.3

Selected Diseases and Pathological Conditions

57

TABLE 3-7. DVT RISK STRATIFICATION AND GUIDELINES FOR PROPHYLAXIS. Risk

points 0

1-2

3-4

Risk stratum Low

Moderate

High

Very high

Clinical features •60 years old+ minor surgery+ no other risks e >40 years old+ minor surgery+ any other risk

• Patient education, early ambulation, elastic stockings •Intermittent pneumatic compression (ifNWB) ., Low dose unfractionated heparin (5000 units sq), or low molecular weight heparin (enoxaparin 30 mg sq q 12 hours or 40 mg sq qd) • Mechanical therapy starting 1-2 hours before surgery, or 12-24 hours postop if needed to achieve adequate hemostasis • Continue therapy throughout hospitalization and up to 7-14 days, then decide duration based on degree of immobilization, ROM and WB status

• > Past PE, cancer or major trauma •>40yearsoldt major surgery+ any other risk factor

• Patient education, early ambulation, elastic stockings •Intermittent pneumatic compression (ifNWB) • Low molecular weight heparin (enoxaparin 30 mg sq q 12 hours or 40 mg sq qd), or fondaparinux, or adjusted dose heparin • Warfarin (therapeutic when INR 2-3) • Start therapy 1-2 hours preop, or 12-24 hours postop if needed to achieve adequate hemostasis • Continue therapy 10-14 days or entire time of immobilization • Encourage early ROM and/or WB if indicated

stockings •Intermittent pneumatic compression (if NWB) • Low dose unfractionated heparin (5000 units sq), or low molecular weight heparin (enoxaparin 30 mg sq q 12 hours or 40 mg sq qd) • Mechanical therapy starting 1-2 hours before surgery, or 12-24 hours postop if needed to achieve adequate hemostasis • Continue therapy while inpatient or during initial recovery, then decide whether to extend 7-14 days

58

Selected Diseases and Pathological Conditions

Ch. 3

Treatment of DVT involves assessment of the PT and PTT, followed immediately by IV infusion of heparin 5000~ 10,000 units. Thereafter, heparin is infused continuously at a rate of 800-1500 units per hour, maintaining the PTI at2-2.5 times the baseline value, and the INR at 2.0-3.0. The patient is maintained at bed rest with the lower extremities elevated at 15 degrees to 20 degrees above the level of the heart. It takes approximately one week for thrombi to become firmly adherent to endothelium and thereby diminish the risk of PE. Coumadin is started as soon as longterm anticoagulation is planned, and takes 3-5 days to

become therapeutic monitoring the PT. The patient is maintained in an anticoagulated state for 4-6 weeks for the treatment of isolated calf DVT, and for 3-6 months for more proximal vein thrombosis. Clinical and/or venographic evidence of clot propagation indicates the need for vascular surgical consultation regarding the potential benefits of Greenfield filter (umbrella) placement in the inferior vena cava. Moreover, thrombolytic therapy, or phlebectomy in rare instances, may be indicated. Postphlebitic syndrome may ensue, and involves venous insufficiency, chronic venous stasis dermatitis, permanent ca!f enlargement and predisposition to recurrent superficial and deep thrombophlebitis, postphlebitic neuritis, and the need for indefinite use of support hose and perhaps other physical measures.

Chronic venous insufficiency(postphlebitic syndrome, chronic venous stasis) affects the skin and subcutaneous tissues of the legs and ankles; and may occur secondary to DVT, varicose veins, cavernous hemangioma, congenital A-V fistula, or pelvic neoplasm obstructing venous outflow from the lower extremity. Findings include edema, stasis dermatitis with hyperpigmentation, eczema, induration, pain, and ulceration. Ulcerations are usually peri-malleolar, and display sharply demarcated or "punched-out" margins (local tissue hypertension). Squamous cell carcinoma may develop. Treatment consists of elevation, application of an Unna-paste bandage, antibiotics as indicated, diuresis, and protection. Consideration should be given to the potentially beneficial effects of topical corticosteroid on inflamed, non-ulcerated skin. Atypical skin lesions should be biopsied. Skin grafting, often in combination with vein surgery wherein varicosities are ligated or sclerosed, and incompetent perforating veins are bypassed via direct connection of superticial veins to deeper veins, may also be usefuL Pulmonary Embolism IPE} PE is very common and a leading cause of death in the US. Lower extremity DVT accounts for 60-80% of PEs. Thrombi embo!ize from the lower extremities, traverse the pelvis and inferior vena cava, then enter the right side of the heart, and subsequently obstruct the pulmonary vessels. Pulmonary infarction ensues thereafter. Clinical signs and symptoms vary with the degree of pulmonary occlusion and infarction, and include crushing chest pain, dyspnea, tachypnea, tachycardia, low grade temperature elevation 138" C [101" F]}, neck vein distension, ipsilateral diaphragm elevation on standard chest X-ray, a positive ventilationperfusion lung scan ("'I or 51Cr}, S-T segment depression (cardiac hypoxia} and other EKG changes, arterial blood gas abnormalities such as decreased P02 and PC02 and Ph, increased serum LDH and bilirubin in the presence of normal SGOT. The differential includes acute Ml and pneumonia.

Treatment includes immediate anticoagulation with IV administration of 5,000-10,000 units of heparin, followed by continuous infusion of 800-1500 units/hr while monitoring the PH Supportive measures include administration of D2, bed rest, and analgesia; while

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proceeding with definitive diagnostic measures. Thrombolytic therapy, or surgical phlebectomy, may be indicated. Septic pulmonary emboli may be observed as a

complication of infected pelvic thrombosis, indwelling catheter, transvenous pacemaker, arteriovenous or ventriculovenous shunts, or in cases of IV drug abuse.

Fat embolism is most common after long bone or pelvic fracture. Cerebral infarction symptoms of restlessness, confusion, stupor and coma may accompany pulmonary symptoms of dyspnea and tachypnea; in conjunction with fever, lipuria, and the appearance of chest and conjunctival petechiae. The treatment of fat embolism includes supportive measures identified previously for PE (heparin also activates lipase), in addition to large doses of corticosteroid.

Catheter embolism is also possible when central venous catheterization is performed. Surgical excision is usually indicated in patients that can sustain operative intervention. lymphedema Lymphedema is swelling of soft tissues due to an increased quantity of lymph, which is also associated with increased tissue fluid found outside of the blood and lymphatic capillaries. Primary (idiopathic) lymphedema is noted to be present at birth (congenital), seen early in life (lymphedema praecox), or observed late in life (lymphedema forme tarde). Congenital lymphedema can be hereditary (Milroy's disease) or non-familial (simple congenital). Consideration should be given to congenital or acquired hemihypertrophy. Secondary lymphedema is of either the obstructive or inflammatorytype. Obstructive lymphedema occurs secondary to either malignant occlusion, or surgical radiation-induced disruption, of lymphatic channels and/or nodes. Nontropical inflammatory lymphedema is highlighted by recurrent lymphangitis and cellulitis, fever and chills, adenopathy, and is attributed most commonly to streptococcus infection (although trichophytosis, and other microbes may be causative). Tropical secondary lymphedema is attributed to filariasis. Chronic lymphedema may cause fibrosis, verrucous dermatitis, ulceration, elephantiasis, and/or lymphangiosarcoma (rare). The differential diagnosis for lymphedema includes hypothyroid myxedema, CHF, nephrotic syndrome, and hypoproteinemia. Clinical acumen and historical interview are the mainstays of diagnosis, and biopsy may be beneficial. Treatment should be instituted as early as possible, and is primarily medical, although surgery may be indicated rarely. Medical treatment consists of elevation of the edematous part, diuresis (furosemide), prophylactic anticoagulation with subcutaneous heparin, and observation of serum potassium. Antibiotics may also be indicated. After initial reduction of the extremity, customized support hose measured and fabricated for regular wear, and longterm diuresis may be maintained. If medical therapy fails, vascular consultation regarding surgical efforts aimed at improving lymphatic drainage or excision of edematous tissues may be entertained.

DIABETES MELLITUS Diabetes mellitus (OM) affects about 10 million people in the US. It is a leading cause of blindness, renal disease, PVD, peripheral neuropathy, lower extremity ulceration and amputation, and death. In DM, the ability to oxidize carbohydrates is diminished or lost, usually due to pancreatic dysfunction, particularly of the islets of Langerhans, with resultant disruption of insulin function. Classification includes insulin-dependent diabetes mellitus (lOOM, Type 1, juvenile-onset [although it can develop in adulthood]), and non-insulin

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dependent diabetes mellitus (NIDDM, Type 2, adult-onset}.IDDM is caused by autoimmune destruction of pancreatic beta cells, and must be treated with insulin replacement NIDDM can be divided into obese and non-obese groups, the obese group displaying the possibility of returning to euglycemia associated with weight loss and dietary control. Gestational OM is observed during pregnancy, and usually subsides postpartum. Findings include hyperglycemia, polyuria, polydipsia, polyphagia, emaciation, weakness, acidosis due to dysfunctional fat metabolism, dyspnea, ketonuria, and coma. lmmunopathy accompanies long-standing hyperglycemia. Diabetic ketoacidosis or non ketotic hyperosmolar coma may result from prolonged or severe hyperglycemia. Diabetic retinopathy and nephropathy are the result of small vessel diseases associated with long-standing hyperglycemia. Diabetic peripheral neuropathy produces pain and paresthesia, pedal insensitivity, anhidrosis, vasodialation, brittle hyperkeratosis, mal perforans ulceration, and Charcot neuroarthropathy. All patients suspected of having OM, or previously diagnosed with the disease, should undergo pedal monofilament esthesiometer testing to determine whether protective sensation is present Diabetic dermopathy creates thin, atrophlc, and friable skin in the pretibial region, wounding of which results in post-inflammatory hyperpigmentation. Necrobiosis lipoidica diabeticorum also affects the pretibial area as an atrophic plaque with telangiectasia, and microscopically displays palisading granuloma formation.·The laboratory diagnosis of DM hinges on an abnormal glucose tolerance test, and/or repetitively high fasting blood glucose measurements. C-peptide assay can be used to distinguish endogenous insulin, and Type 2 OM, from exogenous insulin (administered for therapy), since exogenous insulin doe not contain C-peptide. The GAD 65 antibody assay can also be used to distinguish Type 1from Type 2OM. Therapy includes effortsto identify the cause, after which dietary controls and exercise are instituted (as indicated). Patient education is a crucial partofthe management of DM. Oral hypoglycemic agents may be used in conjunction with dietary control, and include sulfonylureas (chlorpropamide, tolbutamide, tolazamide, and acetohexamide), as well as metformin. Insulin preparations are indicated when the blood glucose level is not adequately controlled with diet and oral medication, and in cases of Type 1 DM. Adjusting the administration of insulin requires close communication between the internist and the patient, and often entails lifestyle alteration. In the peri-operative period, a sliding scale of insulin, based on the blood glucose value, can be useful until a regular regimen is resumed. The goal of therapy in the perioperative phase is to maintain plasma glucose between 150-250 mg%. Pancreas and islet cell transplantation can also be used in an effort to cure DM.

THYROID DISEASE Hypothalamic thyrotropin-releasing hormone stimulates pituitary release of thyroid stimulating .hormone, which activates thyroidal uptake of iodine and production of thyroxine (T,} and triiodothyronine (T,}, which exert negative feedback inhibition of pituitary thyroid stimulating hormone release. Thyroid hormones regulate metabolism. Enlargement of the thyroid gland is referred to as a goiter, and may be associated with overactive or underactive function. Hypothyroidism can occur due to surgical or medical (radioactive iodine) ablation, or inflammation (Hashimoto's disease) of the thyroid gland; or secondary to hypothalamic or pituitary dysfunction (tumor, CVA, trauma, other}. Hypothyroidism effects myxedema, which specifically presents as non-pitting edema, associated with facial changes that include swelling and a thickened nose, dry or hoarse voice, dry and waxy skin, and mucinous deposition in tissues. Hypothyroid patients display fatigue, general malaise, weight gain, bradycardia, and may become comatose (myxedema coma) in severe disease. Thyroid

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supplementation with T• (Synthroid) and T, (Cytomel), or natural preparations, as well as supportive therapy are used as indicated. Hyperthyroidism, or Grave's disease, effects exophthalmos (lid lag), tachycardia, profuse diaphoresis, nervousness, restlessness, fine tremors, emaciation, and psychosis. Treatment involves supportive measures and drugs that alter hormone metabolism or the end-organ effects of the hormone. Thyroid storm is a medical emergency wherein severe hyperthyroidism effects organ damage and death. Drugs

that inhibit hormone formation and release include thiourea derivatives that block organification of iodine, iodide which blocks thyroid hormone synthesis, and lithium which blocks release of thyroid hormone. Propranolol controls the peripheral manifestations of thyroid hormone. Radioactive iodine destroys thyroid tissue, thereby decreasing thyroid function and possibly effecting hypothyroidism (which can be treated with thyroid supplementation).

HEPATITIS Inflammation of the liver can be caused by trauma, toxins, autoimmune disease, and viral infection. Liver dysfunction results in inability to detoxify a wide range of substances, failure to produce blood elements, such as platelets, and inadequate bile production, resulting in faulty digestion. Acute hepatitis lasts< 6 months, and can result from trauma, vascular insult, viral infection {cytomegalovirus, Epstein-Barr, Herpes simplex, adenovirus, hepatitis A virus [infectious jaundice, due to picornavirus], hepatitis E viruses [common during pregnancy]), bacterial or parasitic infection (Rocky Mountain spotted fever, Leptospira, toxoplasmosis, and Q fever), toxicity (alcohol, carbon tetrachloride, APAP, minocycline, isoniazide, ketoconazole, methyl-dopa, nitrofurantoin, ch!orambutol, penicillin, anesthetics, mushroom toxin), collagen vascular disease (SLE), and metabolic or inherited disorder (Wilson's disease, alpha 1-antitrypsin deficiency). Chronic hepatitis lasts > 6 months, and can result from any of the conditions that cause acute hepatitis, if the condition persists or treatment fails, or the most common forms are related to the hepatitis viruses B, C, and D. Hepatitis B, due to hepadenovirus, results in chronic disease in approximately 15% of those infected; is transmitted via blood transfusion, sexual intercourse or exchange of body fluids, tattooing, needle sharing, and mother-to-child via breast feeding; is successfully treated (remission) in about 45% of those infected, with alphainterferon, pegylated interferon adefovir, entecavir, telbivudine and lamivudine; causes cirrhosis and hepatocellular carcinoma. A vaccine exists that conveys immunity to hepatitis B virus. Hepatitis C(formerly non-A non-B), due to flavivirus, often results in chronic hepatitis that evolves to cirrhosis. Hepatitis Cis transmitted through contact with blood, and It crosses the placenta; and it may remain inactive for 10-20 years. Hepatitis C viral loads can be made undetectable with a combination of interferon and ribavarin, and the response to therapy has been shown to vary with viral genotype. There are other hepatitis viruses, as well.

ARTHRITIDES Rheumatoid Arthritis Rheumatoid Arthritis IRA) is a constitutional disease with inflammatory changes throughoutthe connective tissues. It is generally a wasting disease with muscle and bone atrophy. Chronic proliferative inflammation of the synovium exists and causes irreversible damage to joint capsule and cartilage, which are replaced by granulation tissue. Radiographically

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there is joint space narrowing, periarticular demineralization, bone erosion, "punched out" periarticular lesions, subluxation, deformity (arthritis mutilans), and osteoporosis. RA primarily affects the small joints of the hands and feet, most commonly the PIPJs and MTPJs. It can also present in the hindfoot and ankle, with progressive metatarsal joint and subtalar joint subluxation and ankle pes valgus. Frequentlythe posterosuperior process of the calcaneus is involved.

Clinical manifestations include post~static dyskinesia (pain that is worse after periods of immobility) and non-weight bearing, as well as stiffness. Post-static dyskinesia is a hallmark of any type of arthritis. Pain and stiffness often subside somewhat after motion has proceeded and the joint "warms up." Prolonged activity thereafter can lead to worsening of pain. Constitutional symptoms of weight loss, fever, coldness, numbness, tingling, fatigue and malaise are common. The cardinal objective findings are bilateral, symmetrical sma!! joint swelling (fusiform, sausage fingers and toes), tenderness to palpation (or even barometric pressure), and pain with motion. Swelling due to synovia! hypertrophy is palpably spongy or rubbery, and often crepitant. Synovitis may lead to effusion. Limited motion over a long period is associated with muscle wasting, contracture, fibrosis, and ankylosis. Subcutaneous rheumatoid nodules {palisading granulomas) may form in areas of bony prominence, weight bearing or contact. Diagnosis ofRA is based on disease characteristics overtime. Classic RA displays 7 of the fo!!owing symptoms, the first 5 presenting for at least 6 weeks: morning stiffness, painful range of motion in at least one joint, swe!!ing in at least one joint, swe!!ing of at least one other joint, symmetrical joint swelling wfth simultaneous involvement of the same joint on both sides ofthe body (except PIPJs), subcutaneous nodules, X-ray changes typical of RA {peri-articular osteopenia, joint narrowing, bone whittling), positive agglutination test (rheumatoid factor), poor mucin clot precipitate, characteristic histologic changes in synovial membrane, characteristic histologic granulomatous nodules. Five of these findings in combination represent definitive RA, 3 represents probable RA. Possible RA is represented by any 2 of the following tor3 weeks: tenderness or pain with motion, morning stiffness, history of joint swelling, subcutaneous nodules, elevated ESR or CAP, or iritis.

Exclusions to RA include: 1. Malar rash typical of systemic lupus erythematosus ISLE) 2. Rash typical of drug reaction 3. High concentration of lupus erythematosus ILEI cells 4. Histologic evidence of polyarteritis nodosa 5. Trunk or neck or pharyngeal weakness or swelling or dermatomyositis 6. Definite scleroderma 7. Rheumatic fever 8. Tophi or gout 9. Septic arthritis 10. Reiter's syndrome 11. Tubercle bacilli in joint 12. Shoulder-hand syndrome 13. Hypertrophic pulmonary osteodystrophy 14. Clinical picture characteristic of neuropathy 15. Homogentisic acid in urine 16. Histological evidence of sarcoidosis 17. Positive Kveim {sarcoid antigen) test

Selected Diseases and Pathological Conditions

Ch.3 18. 19. 20. 21.

63

Multiple myeloma Characteristic skin lesions of erythema nodosum Leukemia or lymphoma Agammaglobulinemia

Lab Testing for RA includes CBC with slight to moderate normocytic hypochromic anemia, white count decreased or, in acute cases, elevated (PMNs may be increased with left shift), chronic normal to slight decrease ESR, moderate to marked increase rheumatoid factor (RF) with this agglutination test positive 75% after several months to a year, normal uric acid, altered plasma proteins (fibrinogen and globulin increased, albumin and total protein and AJG ratio decreased), normal Ca++ and P04, and the synovial fluid is cloudy with increased WBCs and decreased viscosity. The differential diagnosis includes any po!yarthritic inflammatory disease with constitutional signs and symptoms.

Osteoarthritis Osteoarthritis (OA) can be idiopathic and defined as primary OA; or the result of repetitive mechanical strain, and defined as secondary OA. Secondary OA is also termed degenerative joint disease or "wear and tear" arthritis, and is generally not inflammatory beyond the confines of the joint Chronic subtalar joint and metatarsophalangeal joint hyperpronation is a common cause of degenerative joint disease in the foot, with resultant pes valgus, forefootsupinatus and hallux limitus/rigidus, plantar fascitis, flexor stabilization induced hammertoes, and medial Lisfranc breakdown. Any joint can be subject to degenerative joint disease, particularly when subjected to weight bearing or in the post~traumatic phase. There are three cardinal roentgen signs of OA, including joint space narrowing, subchondral sclerosis, and osteophytosis. The classic dorsal "flag" of hallux rigidus (dorsal bunion), first metatarsal-cuneiform exostosis, and the anterior tibial exostosis are examples of advanced osteophytosis. Clinical manifestations include PSD, joint pain without acute inflammation, stiffness, fine and/or coarse crepitus, and symptoms that worsen with weight-bearing activity. Although range of motion may be diminished, there is rarely ankylosis. OA usually affects middle-aged or older individuals, with history of insidious onset (unless post-traumatic), with gradual progression. The differential diagnosis includes rheumatoid arthritis, gout, and Charcot neuroarthropathy. GoutyArthritis Chronic hyperuricemia can result in monosodium urate crystal deposition in joints and soft tissues. The four main etiological forms of gout include: 1. primary metabolic gout- chronic over-production of uric acid, often dietary in origin 2. secondary metabolic gout- myeloproliferative disease with high rate of cellular turnover causing over-production of uric acid 3. primary renal gout- under-excretion of uric acid due to primary kidney disease 4. secondary renal gout- under-excretion of uric acid due to renal disease other than primary kidney lesion (certain diuretic medications). Serum uric acid levels of7 mg/dl for males and 6 mg/dl for females indicate a supersaturated state wherein crystals may precipitate In joints and the kidneys. Clinical forms ofgouty arlhritisinclude acute gouty arthritis, intercritical or quiescent, and chronic gouty arthritis. Acute gouty arthritis presents as monoarticular, sudden onset and intensely painful inflammation (red, hot, swollen, excruciating pain), stiffness and antalgic guarding, and overlying cutaneous desquamation. Chronic gouty arthritis presents

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insidiously with gradual, progressive tophus formation; intermittent acute gouty attacks; and is associated with indurated tophus formation (advanced monosodium urate

deposition) in subcutaneous and/or tendon, auricular helix, and the small joints of the hand and foot; and advanced deformity (bunion, hammertoes, nodular lesions) effecting

cutaneous compromise. A draining tophus reveals a white, chalky exudate of monosodium urate crystals. The diagnosis of gout is confirmed by the presence of strongly birefringent

monosodium urate crystals identified on joint aspiration. The presence of a phagocytosed monosodium urate crystal within a granulocyte is pathognomonic, and termed the "martini sign." Serum uric acid, which is chronically elevated in chronic gout is normally 8 mg%; however the serum value can actually be within the normal range during an acute gouty attack. Roentgen signs of acute gouty arthritis consist primarily of increased soft tissue density and volume; while chronic gouty arthritis reveals punched out or "rat bite" defects of bone at the capsular attachment. Overtime, chronic erosion and ankylosis may develop. The most common locations of gouty arthritis are the first MTPJ, posterior heel at the Achilles insertion, the plantar inferior calcaneus, other pedal articulations (lesser MTPJ, MTJ), the ankle; the hand, wrist and elbow, and knee. The differential diagnosis includes pseudogout; suppurative arthritis, acute bursitis, and rheumatoid arthritis.

Oral therapy consists of indomethacin 50 mg Q 6 hours x 24 hours, followed by 50 mg Q 8 hours x 24 hours, followed by 25 mg Q 8 hours x 24 hours. Alternatively, one may use colchicine (inhibits PMN migration) 0.5 mg Q 1 hour or 1 mg Q 2 hours until the symptoms subside, or Gl distress develops, or a total of 6 mg has been administered without relief. Colchicine can also be administered intravenously as an inltia12 mg bolus followed by 1 mg IV Q 6 hours for two additional doses. In surgical or traumatized patients with a history of acute gouty arthritis, prophylactic therapy using colchicine can be administered as 0.5 mg PO Q8 hour for one week, beginning two days preoperatively. Patients with hyperuricemia require medical evaluation, including 24 hour urine uric acid analysis, and may benefit from longterm anti-hyperuricemic therapy. ln such patients, if the uric acid excretion is less than 700 mg/24 hour period, then probenecid sulfinpyrazone is used; and if the uric acid excretion is over700 mg/24 hours, then Allopurinol is used regularly for an indefinite period oftime. 1\nkylosing Spondylitis The criteria for the diagnosis of ankylosing spondylitis include: 1. Limited motion of lumbar spine in anterior and lateral flexion and extension 2. History of pain or presence of pain in dorsolumbar junction or in lumbar spine 3. Limitation of chest expansion to one inch or less Definite ankylosing spondylitis is confirmed by the presence of bilateral sacroiliitis associated with at least one clinical criteria. Probable ankylosing spondylitis exists in the presence of bilateral sacroiliitis associated with none of the clinical criteria. Common symptoms include low back pain, prolonged back stiffness, ascending back pain, heel pain, peripheral joint pain, fatigue, and diminished vision and/or eye pain. Roentgen signs vary with duration of the disease. Early signs include sacroiliac joint blurring, joint space narrowing and widening, subchondral sclerosis, diffuse osteoporosis of spine, apophyseal joint sclerosis, and straightening of spine. Advanced ankylosing spondylitis reveals apophyseal joint erosion, squaring of vertebrae, narrowed disc space, vertebral collapse, pelvic whiskering, and pubic symphysis involvement Terminal roentgen signs include

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intervertebral disc calcification, paravertebral ligament calcification, vertical syndesmophytes, sacro-iliac joint fusion, and bamboo spine. Reiter's Syndrome This is a seronegative \no presence of rheumatoid factorL asymmetrical arthritis that presents with one or more of the following: urethritis, cervicitis, dysentery, inflammatory

eye disease (iriditis), and mucocutaneous disease consisting of balanitis or oral ulceration or keratoderma blenorrhagica. Characteristics include synovitis, symphysitis and

enthesitis; asymmetrical lower extremity arthritis with predilection for small joints of the teet and the ankle, pericalcaneal enthesitis, knee and sacroiliac disease; bone erosion with osteophytosls, and paravertebral. ossification. Diagnostic tests suggestive of Reiter's syndrome include negative rheumatoid factor, demonstration of HLA 8~27 in the serum, Pekin cells in synovial fluid and neutrophilia in prostatic fluid, and unilateral sacroiliitis. Psoriatic Arthritis Psoriatic Arthritis is an often severe polyarthropathy that is more common in females (3:2 M:F ratio), and can affect patients of any age. Patterns of psoriatic arthritis include polyarthritis with DIPJ involvement and nail disease, symmetrical seronegative polyarthritis simulating rheumatoid arthritis, monoarthritis or asymmetrical oligoarthritis, sacroiliitis and spondylitis, and arthritis mutilans. Diagnostic features include papulosquamous skin lesions and nail dystrophy (pitting, onycholysis, flaking, hypertrophy, nonsuppurative paronychia); DIPJ arthritis, fusiform digital swelling (sausage toes), unilateral sacroiliitis, simultaneous exacerbation of cutaneous psoriasis and arthritis, absence of subcutaneous nodules, and serum negative for rheumatoid factor. Roentgen signs include bone resorption with "pencil-in~cup" IPJ osteolysis and mineral resorption (DIPJ involvement with erosion and expansion of base of distal phalanx with proximal osteolysis), oligoarthritis, sacroiliitis, and spinal column involvement.

Charcot Neuroarthropathy (Neuropathic Arthropathy) Causes of Charcotneuroarthropathy include central nervous system defect, such as syphilis (check fluorescent Treponema! antibody if suspect this with charcot foot), syringomyelia, meningomyelocele, post-traumatic degeneration, multiple sclerosis, and spinal cord compression. Peripheral nervous system disorders such as Charcot-Marie-Tooth disease, diabetic peripheral neuropathy, alcoholic peripheral neuropathy, tuberculous or lepromatous infection, amyloidosis, pernicious anemia, and steroid-induced neuropathy. An unusual disorder known as congenital indifference to pain can also effect neuroarthropathic joint disease. Pathologically, Charcot joints have been attributed to, primarily, autonomic denervation with loss of vasomotor tone, hyperemia, increased bone perfusion and loss of bone mineralization. The loss of proprioception, joint relaxation and hypotonia, recurrent microtrauma, possible major injury, resultant malallgnment, cartilage fibrillation, and subchondral plate fragmentation have also been sited as components of the development of Charcot joint disease. Ankle equinus is a primary deforming influence in many cases of pedal Charcot degeneration. The foot is usually warm, dry, and swollen. Other effects of peripheral neuropathy, such as increased hyperkeratosis and keratin stiffness, loss of sudomotortone (anhydrosis), protective touch-pressure sensation (5.1 0 or red West-Foot monofilament esthesiometer), and intrinsic muscle atrophy (intrinsic minus foot), also contribute to pedal breakdown. Increased blood flow results in abnormal venous pooling and edema.

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TABLE 3-8. HARRIS AND BRAND ClASSIFICATION OF INSENSITIVE FOOT DEFORMITY.

Pattern I II Ill IV

v

Anatomical apex of pedal breakdown Calcaneal Talar Midtarsal Lateral hindfoot(calcaneocuboid) Usfranc (tarsometatarsal)

Harris and Brand have divided tarsal destruction in the insensitive foot into five patterns. Pattern 1- Calcaneal, Pattern II - Talar, Pattern Ill - Midtarsal, Pattern IV- Lateral hindfoot, and Pattern V - Lisfranc. As degeneration progresses, cartilage debris is

imbedded in synovium and detritic synovitis develops from deposition of cartilage and bone fragments, and shards of bone and cartilage can migrate into soft tissue along

the extremity. Other causes of detritic synovitis include silicone polymer degradation, osteonecrosis, calcium pyrophosphate deposition {pseudogout), psoriatic arthritis, and osteoarthritis. Microscopic evidence of shards of cartilage and bone in synovium is diagnostic of Charcot joints. Extreme angular deformation of the joint leads to ligamentous and capsular rupture, gross fracture, and progressive deformation. Treatment must encompass systemic medical management in conjunction with local care. Nonwweight bearing using bedrest, patellar tendon bearing bracing, and total contact casting; as well as antibiotic prophylaxis or therapy, and surgical management of cutaneous wounds and bone and joint deformity, are all components in the coordinated treatment of Charcot neuroarthropathy. Prior to surgery for stabilization of deformed joints and fractured bone, it is necessary to achieve a state of quiescence. Equinus deformity is addressed, and the mainstay of surgical reconstruction is arthrodesis in conjunction with electrical bone growth stimulation. Fixation methods for neuroarthropathic bone include internal fixation, external fixation, and intramedullary nailing of the tibia. Careful perioperative management is critical. Septic Arthritis Septic arthritis usually presents as a monoarticu!ar, erythematous (unless vascular compromised), lower extremity disease with the knee as the primary site of involvement. Etiologies include contiguous spread, direct implantation, hematogenous sources, or surgical contamination. Contiguous spread septic arthritis occurs when osteomyelitis is present in metaphyseal or epiphyseal bone, with resultant bacterial spread into subchondral bone leading to eventual joint infection. Hematogenous spread is common in children, and often the result of otitis media or upper respiratory tract infections. Direct implantation of bacteria into the joint may occur due to puncture wound. Postsurgical joint infection is most likely when endoprosthesis are used. Common infecting organisms include S. aureus, H. influenza, and others. Septic arthritis correlates with patient age as follows: S. au reus is the most common organism in all patient populations; Streptococcus and gram negative organisms are most common in neonates, Hemophilus influenza is most common in children 6 months to 5 years of age, Neisseria is most common in teenagers; and in adults, less than 5% of cases are caused by E coli, Proteus mirabilis, and P aeruginosa. (P aeruginosa is common after puncture injuries); while sickle cell anemia patients are predisposed to Salmonella; and the compromised host (burn wounds, drug addict, HIV positive, chemotherapy, steroid therapy) is susceptible to Serratia marcescens. Patients with pyarthrosis present with an

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extremely painful, hot, and swollen joint that they will antalgically guard. The patient may also exhibit varying signs of septicemia. The onset of symptoms and joint destruction are

frequently rapid and, therefore, timely diagnosis and treatment are necessary in order to salvage the joint The differential diagnosis in children includes acute rheumatic fever and/or a flare up of juvenile rheumatoid arthritis. In adults consideration should be given to the possibility of joint trauma, gout, pseudogout, or foreign body synovitis. Useful clinical lab findings include neutrophilia with left shift, elevated ESR, positive CRP; and blood cultures are positive in 50% of cases. Roentgen signs include increased soft tissue density and volume, effusion and juxta~articular osteopenia. A Tc-99 bone scan, in combination with a Ga-67 scan, may be helpful in making an early diagnosis, despite the lack of specificity. An ln-111 labeled leukocytes scan is both specific and sensitive for infection, and may be used instead of Ga-67. Joint aspiration should be performed when septic arthritis is considered, however care should be taken to avoid aspiration through an area of distinct overlying cellulitis or infection, as this technique may actually inoculate a sterile arthritic joint with bacteria. A sterile surgical prep of the overlying skin is mandatory before joint aspiration is performed. In order of importance, aspirate should undergo the following studies: C&S (aerobic and anaerobic, and fungal), gram stain and acid-fast stain, examination for crystals, WBC count and differential, glucose concentration. In a septic joint the WBC will usually be higher than 100,000, with the exception of gonococcal arthritis wherein the WBC count is usually less than 50,000. In septic arthritis, the differential cell count consists of 90-95% neutrophils. In additional to lab analysis, the aspirate is grossly inspected for color, consistency, and clarity. In septic arthritis, the clarity and color will vary from cloudy yellow to creamy white or gray. The treatment of septic arthritis is much the same as that for an abscess, wherein incision and drainage, foreign body removal and debridement are performed. Controversy exists as to whether or not adequate drainage and cleansing can be performed via multiple repeated needle aspirations and lavage. This technique has also been criticized for potential cartilage damage due to needle trauma as well as pain and anxiety related to multiple aspirations (particularly in young patients). Open surgical joint drainage and debridement allows for direct visualization, lysis of adhesion or scar tissue, removal of necrotic and infected tissue, placement of drain tube, placement of antibiotic impregnated PMMA beads if osteomyelitis is present, and thorough inspection of the joint confines. The criticism of open drainage and debridement is that it promotes arthrofibrosis and dysfunction due to scar formation. In a child, arthrotomy may be reserved in case of failed drainage using multiple needle aspirations and lavage. Arthrotomy should be performed in patients with suspected osteomyelitis, infected endoprosthesis, long-standing infection or resistance to previous aspiration/lavage, or in the septicemic or endotoxic patient. Following arthrotomy the wound is initially immobilized and packed open. It is important to avoid dessication of the joint tissues, and BID wound lavage and fresh dressing applications are used until the acute inflammatory episode subsides (24 to 48 hoursLafter which gentle passive range of motion should be initiated. Early motion is critical in preventing significant arthrofibrosis and limited motion. Presumptive antibiotic therapy should cover S. au reus (intravenous cefazo!in or nafcillin, or cl!ndamycin in patients sensitive to PCN), and any other suspected organisms based on clinical history. Antibiotic therapy is adjusted in accordance with definitive C&S results, and should be continued IV for a minimum of two weeks. If the patient is responding well, then conversion to oral antibiotics is made at approximately two weeks, and continued until a full antibiotic course of four weeks is completed (oral antibiotic being administered from the second through fourth weeks).

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SELECTED NEUROLOGICAL DISORDERS

Familial Sensorimotor Polyneuropathy (CharcotwMarie-Tooth Disease) Familial Sensorimotor Polyneuropathy is also know as Gharcot-Marie-Tooth Disease (GMT) and Peroneal Muscular Atrophy. GMT disease is a progressive, familial, symmetrical, peripheral polyneuropathy that affects males five times more often than females, and presents in varying degrees from mild to severe. Severe cases may display significant cardiac dysrhythmia, Friedreich's Ataxia, and often do not survive beyond adolescence. GMT involves distal muscle atrophy that begins in the feet and hands then legs and arms. Lower extremity involvement is often more pronounced, and observed earlier, than is upper extremity involvement Classically, the peronii, tibialis anterior, long extensors, pedal lumbricals and interossei are gradually denervated as the disease progresses, leading to muscular atrophy and the "stork leg" or "wine goblet" appearance of the legs. Muscle wasting effects drop foot, pes cavus \more specifically, cavo-adductovarus), steppage gait, recurrent lateral ankle ligamentous sprains that eventually develop into chronic instability, claw toes and MTPJ subluxations, and mechanically induced cutaneous compromise. Peripheral touch-pressure sensation, deep tendon reflexes, and voluntary muscle function are diminished. Electroneurodiagnostic testing will show markedly slowed conduction velocity (normal conduction 45 to 55 m/sec), while EMG reveals increased fibrillation potentials. Muscle biopsy reveals atrophy. Neurological consultation and genetic counseling are in order. Conservative treatment is aimed at increasing stability, and includes cavus-mold orthoses, digital retainers, ankle sleeve, drop foot bracing (MAFO or similar device), and palliative skin and nail care. ReconstrucTive surgical intervention addresses the pes cavus, digits, and drop foot; and usually combines stabilization arthrodesis, or sometimes osteotomy, with tendon transfer. Arthrodesis is generally preferred whenever progressive neuromuscular disease is treated. Arthrodesis yields a stable bone mass upon which the transferred tendons can function. When heel varus is mild, the Dwyer osteotomy combined with heel cord lengthening and Ste!nd!er stripping \release of plantar intrinsics and fascia from calcaneus) may be adequate; however triple arthrodesis and tendon transfer from the posterior or medial leg compartment to the dorsum of the foot (tibialis posterior through the interosseous membrane) offers more correction and longterm improvement Digftal stabilization, in the form of lesser toe PIPJ and hallux IPJ arthrodesis, in conjunction with MTPJ relocation, is also very usefuL Consideration may also be given to first metatarsal dorsiflexory base osteotomy. Dejerine Sottas Disease (Hypertrophic Interstitial Polyneuropathy) Clinically .this disease is similar to CMT, with distal muscle weakness of the lower extremities with associated sensory deficit, and decreased deep tendon reflexes. Pedal deformities include pes cavus and claw toes, and the patient may display kyphoscoliosis. The most distinctive feature ofthis disorder is palpable and sometimes visible enlargement of the peripheral nerves. Nerve biopsy (usually sural nerve) will confirm the diagnosis. Roussy-Levy Syndrome Patients with this disease have been compared to patients with CMT disease, with the addition of an essential tremor that is most prominently expressed in the hands. This is a familial, slowly progressive, symmetrical neuromuscular disease. Clinical findings include areflexia, intrinsic pedal muscle atrophy, pes cavus and claw toes, clumsy gait and poor equilibrium, and the presence of the previously noted essential tremor.

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Refsum's Disease This disease is the result of abnormal lipid metabolism wherein phytanic acid accumulates in the serum, which results in elevation of serum phytanic acid to levels up to 50 times greater than normal. Associated findings include ichthyosis, night blindness, and a

preceding febrile illness. Peripheral muscle paresis, areflexia, dropfoot, pes cavus, and

claw toes are also observed. Friedreich's Ataxia This is typically a more severe and disabling disease than CMT disease, and the onset is noted early in life (childhood) and progresses until the patient is essentially incapacitated by

middle-age. Hallmarks ofthe disease are ataxia, unstable gait, and pes cavus with clawtoes. Muscular Dystrophy I MDI Muscle fibers atrophy and become necrotic, resulting in weakness, clinically evident muscle atrophy (decreased girth), areflexia, and secondary muscle contracture. Mental impairment may also be present There are three types of MD: 1. Duchenne's pseudohypertrophic MD- most common, muscles appear large and firm because of fatty conversion, affects only males, and the onset is between 1-3 years of age with subsequent rapid progression 2. Facioscapulohumeral MD 3. Limb girdle MD -Ankle equinus and equinovarus deformities are common foot conditions seen in patients with MD, although pes valgus may also appear. Classically individuals with MD display Gauer's sign when they raise themselves from seated or recumbent position, where in they "climb up themselves" by pushing their hands/arms against their knees and thighs, thereby pushing the torso upward. Myelodysplasia(Spina Bilida) These disorders comprise a group of developmental deformities of the spinal cord and vertebrae that most commonly affect the lumbar and sacral levels, and include: 1. spinal bifid a with meningocele The meningeal sac protrudes through an open neural arch vertebral defect and extends to the subcutaneous layer. 2. spina bifid a with myelomeningocele Other elements ofthe spinal cord and nerve roots have also protruded 3. myelocele Even the skin fails to enclose the cord protrusion, resulting in the most severe form of spina bifida. 4. spina bifida occulta The neural arches of the vertebra have not completely closed, however all of the neural elements remain within the spinal canal. Pathologically, the spinal cord defect effects motor, sensory and autonomic functional deficits observed in the lower extremities. The dynamic muscle imbalance tends to worsen over time, resulting in equinus, equinovarus, and equinovalgus, and marked rotary deformities of the lower extremities. Associated findings include urinary bladder paralysis

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(which requires catheterization during operative intervention) which may be associated with chronic urinary tract infection; and profound anesthesia and lack of protective

sensation, often with mal perforans ulceration.

Poliomyelitis The polio virus affects the anterior horn cells (!ower motor neuron) of the spinal cord, resulting in some degree of lower extremity flaccid paralysis (areflexia, hypotonia, and weakness). The central neJVous system defect in poliomyelitis is non~progressive,

however the disease can lead to contracture that changes overtime. Common deformities include equinovalgus, and others, and tibiocalcaneal and pantalarfusion can be useful. Cerebral Palsy (CP) Classically, a congenital neuromuscular disorder caused by an intracranial brain lesion,

and identified early on in the patients life. Three types of CP 1. Spastic CP Upper motor neuron disease effects hyperreflexia, clonus, and extensor plantar response, typically anterior leg compartment weakness, dropfoot, pes cavus, clawtoes, and steppage gait with circumduction. This is the most common form of spastic CP, and affects approximately 65% of CP patients.

2.

Athetoid CP This form affects approximately 20% of patients with CP, and is associated with a slow, worm-like hypertonia due to upper motor neuron disease.

3.

Ataxic CP Ataxic affects about 15% of CP patients, and is associated with tremor and atonia.

UMN disease causes more spasticity in muscles that cross more than one joint, such as gastrocnemius. Muscles of flexion, adduction, and internal rotation tend to overpower those of extens·lon, abduction, and external rotation. Talipes equinova!gus, or equinovarus, is common. Complex regional pain syndrome (CRPS)-This is a serious chronic pain condition, the hallmark symptom being unrelenting, progressively worsening, intense pain out of proportion to the severity of the injury or inciting event Patients with CRPS often display allodynia, wherein they relate pain caused by what would have otherwise been a nonoxious stimulus, and hyperpathia, wherein a stimulus that would typically be considered painful is much more painful. CRPS usually affects an arm, leg, foot or hand, and the pain may evolve to include the entire, dystonic extremity. Although CRPS affects men and women, it is more common in young females. CRPS is thought to be the result of peripheral and central nervous system dysfunction. CRPS I, often referred to as reflex sympathetic

dystrophy syndrome (RSDS), occurs with tissue injury that does not involve direct, underlying nerve trauma. CRPS IJ, often referred to as causalgia, is associated with known trauma involving a known anatomical nerve trunk. The clinical signs and symptoms of CRPS 1and II are the same. Characteristic signs and symptoms include color and teperature changes involving the skin, associated with sharp and burning pain, swelling, and sweating. Associated with these symptoms are exquisite skin sensitivity, vasomotor instability that causes the affected part to be colder or warmer than the contralateral limb, discoloration that includes mottled blue, pallor, purple; textural changes that include thin,

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shiny skin; hypertrophy or atrophy of digital hair and nail growth; fusiform digital swelling and stiffness, dystonia that affects the ipsilateral extremity and may extend to other extremities; symptoms may be heightened by emotional stress, and depression secondary to chronic pain is common. Although there is no definite cutoff between symptoms and signs that define distinct stages of CRPS, many clinicians categorize Stage 1 as lasting from 1-3 months and characterized by sharp, burning pain, myalgia and dystonia, temperature and color changes, and increased hair growth. Stage 2 extends from 3-6 months and is associated with worsening pain, edema, nail dystrophy and diminished hair growth, muscle atrophy and weakness. Stage 3 extends beyond 6 months and entails irrevesible skin and bone atrophy (Sudek's atrophy of bone), and permanent pain and limb contracture. The pathophysiology of CRPS is notfully understood, although it is believed that the sympathetic nervous system plays an important role in maintianing the pain, as pain receptors in the affected limb become sensitive to catecholamines. It has also been theorized that CRPS represents disruption of the healing process secondary to an abnormal immune response to injury. Due to the complexity of symptoms and similarities with other conditions, the diagnosis of CRPS can be difficult to make, especially early in the course of the disease. There is no single diagnostic test for CAPS, and it is important to rule out other conditions so that the diagnosis can be made by exclusion. A triphasic bone scan may be useful, and often shows a splotchy uptake of radiotracer in cases of CAPS. Supportive therapies include the use of topical analgesics, anticonvulsant and antidepressant medications, corticosteroids and opiate analgesics. Physical therapy and movement are encouraged. Sympathetic nerve blockade, using phentoloamine or local anesthetic; sugical sympathectomy, only if blockade afforded prolonged and marked relief; spinal cord stimulation, using an implantable generator with a stimulating electrode along the spinal cord; and spinal intrathecal local anesthetic and/or analgesic pumps, may be usefuL The prognosis tor patients with CAPS varies from person to person, and outcomes range from permanent pain and disability to spontaneous remision and revovery.

NEOPLASMS Any enlargement oftissue, whether edematous, hypertrophic or neoplastic, can be referred to as a tumor. Whenever dealing with neoplasm, a high index of suspicion should be maintained tor potential malignancy. Malignancy of epidermal germ eel! origin is termed carcinoma, whereas those of mesenchymal origin are referred to as sarcoma. Any lesion, even what is thought to be persistent pyogenic granuloma, chronic onychocryptosis, resistant verruca, or a diffuse subcutaneous mass that does not respond to reasonable therapy should be more closely inspected. Closer inspection may involve radiographs or MRI, lab testing, or biopsy. Consultation may also be helpful. In general, any lesion suspected of being malignant warrants oncologkal consultation and systemic evaluation for lymph node, lung, Gl, bone, and other sites of potential metastasis or regional dissemination. Proper biopsy technique is crucial. General considerations in the assessment of a neoplasm include coloration, change in appearance, presence of symptoms such as pain or pruritus, hemorrhage, location superticial(freely moveable below or within the skin) or deep (fixed) to the deep fascial (muscle fascia), sensory or motor disturbance, vascularity or pulsatile nature of the lesion, status of the popliteal and inguinal lymph nodes (tender and/or enlarged), and the presence of metastatic disease elsewhere in the body. Diagnostic imaging, such as standard radiographs, MRI and CT scans may be helpful, and a chest X-ray should be obtained whenever cancer is considered, as the lungs are the

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primary site of sarcoma (and many carcinoma) metastasis. Clinical lab testing, including CBC and differential, biochemical profile, tumor antigen testing, and ESR may be helpfuL Needle biopsy (not fine needle) can be helpful if multiple core specimens are obtained from different sites within the lesion, and incisional biopsy through the mid portion of the soft tissue mass is routinely performed. Whenever performing an incisiona! biopsy for suspected sarcoma (or carcinoma), the biopsy channel to the lesion should be oriented longitudinally in line with the suspicious mass and within a region to be fully excised with subsequent definitive surgical excision of the lesion. Moreover, it is important to avoid dissection into adjacent fascial compartments, in an effort to maintain natural anatomical barriers to spread of malignant cells. The oncological surgeon can, in many cases of sarcoma, preserve adjacent intact muscle compartments protected by intact deep fascia, when appropriate biopsy technique has been used. Attention to such detail may be the difference between muscle compartment resection from the foot into the leg, versus BK or AK amputation. Selected Neoplasms Epidermal (epidermoid)inclusion cyst~ precipitated by skin trauma, wherein e-pidermis is forced into underlying dermis and continues to desquamate and build up degenerating keratin within the dermis. This leads to slow development of a firm, round, subcutaneous nodule that is often seen on the sole or toes. Pilar and sebaceous cysts are inclusion cysts around the hair follicle. Eccrine poroma ~ a sweat gland tumor that is nodular and may drain serous fluid.

Squamous cell carcinoma {SCC)- a malignant epithelial neoplasm with predilection for skin and mucous membranes. The lesions display erythematous margin, nodules or shallow ulceration. There are several variations, including verrucous carcinoma, prickle cell carcinoma, epidermoid carcinoma, and epithelioma cuniculatum. SCC is more common in light-skinned individuals than in African-Americans, usually localizes to sun-exposed surface or previously scarred, burned, or irradiated skin; is usually seen in patients over the age of 40 years, 5% affect the foot and leg, rarely invade deep to bone and rarely metastasize, and there is a 95% cure rate with adequate excision. sec can develop in a chronic, non-healing wound or ulcer, Oncological consultation and possibly adjunct radiation or chemotherapy may be in order. Basal cell carcinoma (BCC)- the most common skin cancer, usually observed on sunexposed surfaces in the 30to 50 year-old patient, more common in women, lighter- skinned individuals, involving basal cells of the epidermis, very slow growing and unlikely to metastasize unless ignored or neglected.lt is also referred to as basal cell epithelioma due to its failure to metastasize. Four types include superficial, pigmented, nodular, and morpheaform. BCC has been known to form in scar tissue. Appears as a shiny nodule with surface telangiectasia. There is a 99% cure rate with adequate excision or ablation via cryogen, electrodesiccation, or radiotherapy. Routine follow~up is required after eradication, and there is a 35% recurrence rate within 5 years. Bowen's Disease (carcinoma in situ)- an in situ squamous cell carcinoma involving skin and mucocutaneous junctions; appearing as a crusty, nodular looking plaque. When the superficial crust is curettaged, the lesion appears dull red and moist It may appear as a

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keratotic lesion on the plantar surface, and pathologically the basement membrane is intact (CAin situ). Proper excision is curative. Bowen's disease is often associated with internal malignancy, and oncological consultation is in order. Dermatofibroma·

this fibrous skin tumor rarely occurs in the foot, appears flesh-colored,

and may be observed as a periungual angiofibroma which is also referred to as Koenen's fibroma and associated with tuberous sclerosis, cafe au !a it spots and mental retardation.

Plantar fibromatosis- this is a benign and reactive lesion of fibrous tissue (plantar fascia) affecting the plantar aspect of the foot. The lesions are firm and nodular, and may resemble a low grade fibrosarcoma due to its fixed nature. Isolated excision is associated with a 65% recurrence rate, and total excision of the affected band of plantar fascia is indicated if padding and accommodative insole has failed to yield pain relief when weight bearing. There is no distinct benefit to injection therapy. Plantar fibromatosis is also known as Lederhaus disease, and associated with people of a Germanic heritage. These individuals may also have Dupuytren's palmar contracture or Peronies penile fibromatosis.

Fibrosarcoma- these are firm, fixed small nodular to expansive irregular lesions that may occur in the lower extremity. Fibrosarcoma may metastasize, and radical excision, amputation, and oncological management are required. Lipoma- these are composed of mature fat cells with thin capsular structures, and may lead to adjacent nerve entrapment They are commOnly observed about the malleoli and knee, and are amenable to excision. Liposarcoma- a malignant lesion, often with vascular infiltration and termed angiolipoma. Treatment is excision and oncological management Ganglion cyst- the most frequently encountered tumor affecting jointtissue, and may also affect the tendon sheath or nerve connective tissue (usually epineurium). These are generally of traumatic etiology (perhaps distant incidental trauma), with myxoid degeneration of connective tissue effecting gelatinous fluid that gels over time. A history consistent with size change and aggravation by activity is common. The ganglion may entrap adjacent vital structures and tendon. When in the popliteal fossa, a ganglion is referred to as a Baker's cyst Conservative treatment consists of padding and gentle compression, aspiration of cyst contents and local infiltration of acetate corticosteroid. Lesion may recur after reduction in size and symptoms, and additional injection therapy or surgical excision may be effective. Ganglions are seen in a!l age groups, even in the very young. Digital mucous cysts~ a small cystic lesion overlying a digitaiiPJ, resembling a ganglion cyst, and observed in the 30 to 80 year age group Inot typical in young individuals). The lesion stems from myxoid degeneration of the underlying joint capsule, and treatment may require IP arthroplasty. Leiomyoma- a well-encapsulated, firm, rubbery-textured smooth muscle tumor arising from erector pili or vascular smooth muscle. The treatment is usually excision or obseJVation overtime.

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Rhabdomyoma- a benign tumor of skeletal muscle that occurs usually in young patients. The treatment is excision. Rhabdomyosarcoma- a malignant tumor of skeletal muscle that occurs usually in the 5th to 6th decade of life. The treatment is oncological consultation, adjunct radiation and/or chemotherapy, and appropriate excision or amputation. Giant cell tumor of tendon sheath- a true benign neoplasm of synovial structure which is actually a variation of pigmented villonodular synovitis (PVS). It is usually seen in the 30 to 50 year age group, and is the second most common tumor oftendon after the ganglion cyst. Observation or excision is the recommended treatmen~ and it is importantto note thatthere is a high rate (25%) of recurrence following excision. Synovial sarcoma- this malignancy arises from joint capsule, tendon, or bursa; and is usually seen in youngsters and adolescents, aged 10 to 40 years. The knee and ankle predominate, and radical excision, or perhaps amputation, is indicated after oncological consultation and consideration to adjunct radiation and/or chemotherapy. The ankle is frequently involved with a periarticular synovial sarcoma in the periarticular soft tissues. Unlike piezogenic papules, synovial sarcoma is present as a subcutaneous nodule even in the non-weight bearing attitude. The tumor can be of a fibroblastic (spindle cell) or epithelioid cell type, and tissue specific antigens can aid the pathological diagnosis. Wide excision, sometimes in conjunction with radiation or chemotherapy, is usually indicated after biological staging is determined.

Schwannoma- a slow-growing benign, encapsulated tumor that develops within the nerve sheath, often of traumatic origin. The tumor causes axon compression and nerve fiber dysfunction. Microsurgical excision under Ioupe magnification is the indicated treatment Neurofibroma- a benign, circumscribed, but not encapsulated neoplasm originating in the nerve trunk, also of Schwann cell origin. The lesions are often multiple, pedunculated, and nontender. Consideration must be given to von Recklinghausen's disease. Neurofibromas may undergo malignant transformation.

Hemangioma- the most common benign vascular tumor observed in the feet There are several distinct types of hemangioma. As with most vascular lesions, they are diascopy positive (blanch when pressure is applied to the skin surface encompassing the lesion). The capillary, or strawberry, hemangioma is the most common form. It is observed in the newborn and may resolve as the child matures. The cavernous hemangioma is a large lesion consisting of a thick, extensive proliferation of vessels which may involve a large portion of the foot, and thereby pose serious surgical problems relative to excision. Arteriography is useful in the evaluation of a suspected hemangioma. Kaposi's sarcoma~ is a vascular malignancy comprised of a proliferation of capillaries and connective tissue, seen traditionally in males over the age of 50 years, and of Mediterranean descent There is also a high incidence in patients suffering with AIDS. The lesions are bluish, or purple nodules or plaques. Treatment is observation (pending general medical status) or excision.

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Glomus Tumor- a benign, neuro-arterial neoplasm that is usually localized to the periungual (nail bed) region, the hallmark of which is extreme pain, and a reddish or bluish color. Treatment is excision.

Malignant Melanoma Melanocytes have dendritic processes and are of epidermal germ cell origin. They function to produce "sun~protective" melanin pigmentthatguardsthe underlying living cells of the basal layer of the epidermis from the mutagenic effects of UV radiation. Lower extremity melanoma is more common in women, while men more commonly display melanoma on the torso. Melanoma is most commonly seen in the 30 to 60 year age group. Sun exposed surfaces are most susceptible, however the palms and soles, particularly in individuals with dark skin, can be affected. Anatomic sites prone to sun exposure include: "BANS" (back, arms, neck, scalp). Diagnostic signs focus.on the size, shape, color, location, and duration of the pigmented lesion. Benign pigmented skin lesions of the lower extremity should be less than 5 mm in diameter, homogenous in color, smooth or regular in contour, and present for as long as the patient can remember. Plantar and periungual pigmented lesions warrant an especially high index of suspicion. Any lesion on the foot that is greater than 5 mm in diameter, heterogenous in color, or displaying an irregular or notched border should be biopsied if it has not been present since birth. Melanoma grows in a radial phase and an invasive or vertical phase. The vertical growth phase correlates with metastasis. Melanoma in the horizontal or radial growth phase appear macular, while the vertical growth phase is associated with a more aggressive tumor. Poor prognostic indicators include lesions displaying a whitish or amelanotic co! or, tumor regression (notched border), progressive nodu!arity (consistent with deeper invasion of the dermis), change in size or shape, ulceration, hemorrhage, pain, or pruritus, should be considered malignant and treated after accurate identification.

Four Main Clincohisto/gic Types 1.

2.

3.

4.

Superticial spreading melanoma (SSM) may develop on any portion ofthe body with peak incidence around the 5th decade. Comprises about 70% of cutaneous melanomas. Classic SSM displays the "red, white, and blue" of advanced malignancy showing tumor regression. These are very common on the trunk of males. Lentigo mallgna malignant melanoma (LMM) is the slowest growing lesion, seen on sun exposed surfaces. LMM comprises about 15% of MM, and is most common in the elderly (mean age 70 years). The lesion is macular with color variegation. Nodular melanoma (NM) is highly malignantwith primarily a vertical growth phase only. NM comprises about 12% of cutaneous melanoma, and is seen most commonly in males approximately 50 years of age. The appearance is uniformly blue, black, or dark brown, with a nodular appearance. Ulceration is rare with NM. Acrallentiginous melanoma (ALM) shows predilection for plantar, palmar, and nail bed or grooves. Hutchinson's sign (pigment changes in the eponychium of subungual melanomas), whereas melanotic whitlow involves subungual melanoma. The peak incidence of ALM is the 7th decade. ALM accounts for about 3.5% of cutaneous melanomas.

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Staging Stage I Stage II

malignant melanoma involves a primary lesion, or one with local satellite within 5 em malignant melanoma entails in transit metastasis and regional lymph node involvement (identified by palpable adenopathy or node biopsy)

Stage Ill malignant melanoma entails distant metastasis. Melanoma can go anywhere in the body including the choroid of the eye and internal parenchyma. The most important determinant of survival rate for malignant melanoma is clinical staging. Survival of a clinical Stage !lesion is far more likely than survival of a clinical Stage II lesion, whereas clinical Stage Ill lesions are usually lethaL

Clark's Levels and Breslow's Thickness Pathological staging systems of malignant melanoma include Clark's levels and Breslow's thickness (Tables 3-9 and 3-10). The deeper the level, or thicker the lesion, the more likely is there to be metastasis, and therefore the prognosis worsens as the lesion thickens or progresses deeper into or through the skin.

Identification of the Breslow thickness has been shown to correlate better with survival rate. TABLE 3-9. CLARK'S LEVELS. level I

Microscopic appearance of melanoma Involvement of epidermis with no involvement deep to the basement membrane

II

Penetrates the basement membrane

Ill

and enters the papillary dermis Fills the papi!lary dermis and cancer cells line up against, but do not penetrate into the reticular dermis

·

IV

v

Penetrates into the reticular dermis Fills the reticular dermis and enters the subcutaneous fat layer

TABLE 3-10. BRESLOW MELANOMA THICKNESS AND CORRESPONDING SURVIVAL Thickness (mm)

5-year survival rate(%)

0-0.75 0.76-1.5 1.51-2.25 2.26-3.0 >3.0

83-100 37-90 37-83 44-72

9-55

The most important service the podiatrist can provide in regard to malignant melanoma

is timely and accurate recognition and biopsy, thereafter followed by appropriate consultation and/or definitive surgery or referral to an oncological surgeon. Clinical Stage I lesions can be definitively excised by the podiatric surgeon, whereas Clinical Stage II lesions, with regional lymph node involvement, require node dissection and the expertise of a general or vascular surgeon familiar with melanoma.

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Biopsy of a suspected malignant melanoma should be performed, when possible, using an excisional technique that provides 1to 3 mm of norma! appearing skin about the lesion, and the biopsy must include subcutaneous fat (full-thickness skin). For small lesions, local anesthesia is infiltrated in a proximal V-b!ock fashion in normal appearing tissue. Two semi-elliptical incisions are made about the lesion from proximal to distal, the resultant dimension of the lesion being about 3:1 length:width. The proximal normal margin of skin should be marked with a suture for pathological orientation. For larger lesions, where complete excision is not possible without creating a large defect, incisional or punch biopsy should be employed. The incisional or punch biopsy should be oriented in a faShion that will allow the biopsy wound to be excised in toto when subsequent definitive surgery is performed. The incision a! or punch biopsy must still be ful!~thickness skin and include underlying subcutaneous fat. Select the most clinically malignant appearing site of the lesion, and get enough of the lesion for pathological inspection. As with any biopsy of suspected malignancy, timely diagnosis and appropriate follow-up are mandatory. It is proper to perform an incisional biopsy when indicated, as long as definitive care is subsequently administered. Definitive treatment, based on clinical and pathological assessment, always includes oncological consultation prior to definitive surgical ablation of the lesion. Malignant melanoma can be a systemic disease, therefore chest X-ray and constitutional evaluation are needed. In many cases, it is best to administer chemotherapy prior to definitive surgical excision, in an effort to decrease the tumor and minimize the risk of metastasis. Survival rates may increase with adjunct preoperative radiation or chemotherapy. Guidelines for definitive excision are depicted in Table 3-11.

TABLE 3-11. GUIDELINES FOR DEFINITIVE EXCISION OF MELANOMA.* Melanoma depth (mm)

Recommended margin of normal appearing skin {em) about definitive excision

< 0.76 0.76- 4.0 >4.0

2 3 5 (with excision of underlying deep fascia)

*Closure may require use of a skin flap or graft

The definitive treatment of a subungual melanoma is digital amputation at the level of the metatarsophalangeal joint Therapeutic lymph node dissection remains somewt"lat controversial for clinical Stage II melanoma, particularly with lesions of Clark's Levell! and Ill, however it has been recommended for lesions of Clark's Ieveii I - V, and the decision has to be made by the oncological surgeon after discussion of adjunct chemotherapy, prognosis and morbidity related to inguinal node dissection. Bone Tumors

Radiographic Characteristics Three common radiographic patterns of bone destruction 1. Geographic bone destruction represents the least destructive, slowly developing and usually benign process. There is a zone oftransition that separates the lesion from normal appearing bone.

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78 2.

3.

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Moth-eaten bone destruction represents a more rapidly destructive, malignant process such as sarcoma or osteomyelitis. The transition between the lesion and normal bone is wide and less well-defined.

Permeative bone destruction represents the most aggressive and rapidly progressive, malignant process. The zone of transition between tumor and normal bone .is very wide and almost imperceptible radiographically.

Other important radiographic characteristics of bone tumors include the type of trabecular pattern, the periosteal reaction, position of the lesion both relative to anatomic location as well as.the transverse plane (cross sectional) location within the bone.

Trabecular patterns of some bone tumors giant cell tumor of bone~ delicate, and thin trabeculae chondromyxoid fibroma- coarse, and thick trabeculae aneurysmal bone cyst~ delicate, and horizontal, parallel trabeculae non~assifying fibroma- loculated trabeculae intramedu!fary hemangioma~ striated, or radiating trabeculae Periosteal patterns of new bone formation solitary bone cyst- a monolayer of new bone formation adjacent to the tumor and separated from pre-existing cortex osteogenic and Ewing's sarcoma- multiple, concentric layers ("onion skin") of new bone growth, sometimes creating a Cadman's triangle wherein periosteal elevation adjacent to pre~existing cortex radiographically depicts an angle with the apex pointing in the direction of normal bone (also seen in other expansile lesions of bone cortex, such as osteomyelitis) osteogenic sarcoma~ radiating spicules, or star burst pattern of new bone growth multiple myeloma and Ewing's sarcoma~ hair~on-end radiating spicules of new bone growth.

Transverse plane locations within the bone enchondroma and solitary bone cyst- centrally located giant cell tumor of bone, osteogenic sarcoma, chondrosarcoma, fibrosarcoma, and chondromyxoid fibroma- eccentrically located within the medullary canal, arising to one side of the central axis of a long bone; non-ossifying fibroma and osteoid osteoma -located in the cortex periosteal sarcoma osteochondroma~ lesions located in the periosteal region Characteristic anatomic sites of tumor development diaphyseal lesions- solitary and aneurysmal bone cysts, giant cell tumor of bone, Ewing's sarcoma, enchondroma, non-ossifying fibroma, osteoblastoma, eosinophilic granuloma, and fibrous dysplasia metaphyseal lesions~ solitary bone cyst, osteogenic sarcoma, osteochondroma, chondrosarcoma, non~ossitying fibroma, and chondromyxoid fibroma epiphyseal lesions- chondroblastoma, intra osseous ganglion cyst, giant cell tumor after epiphyseal plate closure, and hemangioma.

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In general, malignant bone tumors radiographically display moth eaten or permeative cortical destruction, periosteal new bone formation, and adjacent soft tissue swelling

(increased density and volume). CT scans and MRis can also be helpful in determining the location, confines, and type of tissue involved in bone tumors. Arteriography can be useful in determining vascular involvement, and aids in limb salvage planning when compartment resection or amputation is considered. Laboratory findings consistent with bone tumor formation and destruction include leukocytosis and anemia, elevated ESR, elevated serum Cat+, elevated alkaline phosphatase (osteoblastic activity), and increased total serum protein (multiple myeloma). Definitive diagnosis is made with appropriate bone biopsy, which may involve fine needle aspiration or, more reliably trephine plug(s) or en bloc excision of representative bone.

Treatment of benign bone tumors varies from observation to surgical resection and repair, depending upon symptomatology, the presence of pathological fracture, and prognosis. The treatment of malignant bone tumors always involves oncological consultation and management, as adjunct radiation or chemotherapy may be used in conjunction with appropriate resection or amputation. Longterm (life~long) follow-up is a required part ofthe management of malignancy, regardless of tissue type. Cartilaginous Tumors of Bone Enchondroma· usually a well-defined, asymptomatic, centrally located medullary lesion, seen in the 3rd to 4th decade. This tumor often appears as a lytic lesion in fingers and toes, and pathologic fracture may occur. If pain develops, consider chondrosarcoma. Multiple enchondromatoses are associated with Oilier's disease.

Periosteal (juxtacortical) chondroma - usually observed in children, wherein the juxtacortical soft tissue mass erodes or saucerizes the bony cortex. Chondroblastoma ~ usually observed in 15 to 30 year-old age group, commonly localized to the calcaneus or epiphysis of a long bone, with a well~defined osteolytic appearance. Chondromyxoid fibroma- usually observed in 2nd to 3rd decade, this lesion appears as a sharply-outlined, coarsely trabeculated, round, lytic lesion of the metaphysis. Osteochondroma~ the most common benign growth of bone occurring anywhere in the skeleton, typically in the 2nd to 4th decade, originating in the metaphysis, displaying a cartilaginous cap over new bone proliferation, and rarely associated with malignant transformation. Chondrosarcoma~ a malignant cartilaginous tumor of bone. It can arise from malignant transformation of an enchondroma, periosteal chondroma, or osteochondroma. It is rare in children, and is usually observed in the 5th to 6th decade. lt is the second most common malignant tumor of bone, following osteogenic sarcoma. Bone destruction appears moth eaten, with speckled medullary and soft tissue calcification (in general, soft tissue calcification in the presence of suspected tumor is an ominous radiographic sign), and metastasis to the lungs is common. Treatment of this lesion involves oncological management for radiation and/or chemotherapy, as well as appropriate resection or amputation.

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Bone Forming Tumors Osteoid osteoma- usually observed in children and young adults, marked by nocturnal pain alleviated with aspirin, displaying a round osteolytic defect surrounding a central

radiodense (sometimes lucent) nidus that is usually no larger than 1 em in diameter. This lesion is common in the foot.

Osteoblastoma- usually observed in 2nd to 3rd decade, larger than osteoid osteoma, more common in males, rapidly growing, metaphyseal or diaphyseal lesion the pain of which is not responsive to aspirin. Osteogenic sarcoma- the most common malignant bone lesion, usually appearing in the 2nd to 3rd decade, often affecting the metaphysis of the femur (40%) or tibia (16%). It is rapidly expansile with a star burst pattern of periosteal new bone formation, cortical erosion, and formation of Cod man's triangle. It can develop from Paget's disease of bone, which involves haphazard new bone formation and bone resorption, effecting a "woven bone" appearance, usually in males over the age of40 years, and is of unknown etiology (perhaps viral). Very high levels of serum alkaline phosphatase and urinary hydroxyproline are observed in Paget's disease. Connective Tissue Tumors Non-ossifying fibroma- usually observed in the lstto 2nd decade, eccentrically located in the metaphysis, with a sharply demarcated, lobulated osteolytic lesion displaying a sclerotic border.

Fibrosarcoma- usually observed in the medullary canal (67%) of a long bone in a young male, displaying osteolysis with minimal new bone formation. Speckled soft tissue calcification may be present

locally Aggressive Tumor Giant cell tumor- usually obse!Ved in the 3rd to 4th decade well after growth plates have closed (skeletally mature), localized to the diaphysis as well as metaphysis and epiphysis Displays thin, delicate trabeculae that have a "soap bubble" appearance, expanding into adjacent cortex, and known to undergo malignant transformation. Tumors of Vascular Origin Hemangioma- usually observed in the 4th to 5th decade, occurring in any bone. Displays a cystic lesion surrounded by a "spoke wheel" appearance of periosteal new bone formation. Glomus tumor- usually obse!Ved in the 4th-5th decade, often very painful, localized to the distal phalanx, and may require IPJ disarticulation. Tumor and Tumor-like Bone Lesions of Unknown Origin Solitary bone cyst- these are simple, or unicameral; cystic lesions of bone, often observed in the calcaneus or metaphyseal bone, in the 1st to 2nd decade, and contain a pinkish fluid upon aspiration. This is the most common fluid filled cystic lesion of bone.

Epidennoid cyst- usually obse!Ved in the 2nd to 4th decade, it is an isolated lytic lesion, usually of the distal phalanx.

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Aneurysmal bone cyst· a benign, blood-filled lesion that is usually observed in the 1stto 3rd decade. It is expansile, with horizontal, parallel trabeculae that are readily observed on MRI. The lesion is difficult to distinguish from malignancy.

Ewing's Sarcoma- usually observed in age group 5 to 25 years. It is a highly destructive lesion of cortical bone, with both "onion skin" and "hair-on-end" appearance. It displays a high rate of metastasis. It is the 4th most common malignant tumor of bone, and is rare in African-Americans. Pathological fracture is common. Metastatic Bone Disease Breast and prostate cancer often metastasize to bone, including the bones of the feet. Any musculoskeletal pain in an individual with history of previous malignancy warrants a high index of suspicion and careful examination. Leukemia, although rarely arising primarily in the foot, may effect secondary pedal osteolytic lesions, and is associated with leukocytosis, anemia, fatigue and malaise, adenopathy and splenomegaly.

SELECTED EMERGENCY SITUATIONS If a life-threatening event occurs in the office setting, the local emergency medical service (EMS) should be notified (911) immediately so thattransportto the hospital can be achieved in a timely fashion. The patient's vital signs should be monitored and recorded throughout the event, and medications administered during the event should be recorded. Following emergency treatment of any medical crisis, the patient must undergo immediate systemic medical evaluation and ongoing treatment should be provided as indicated. Medical emergencies occur, and the best treatment is prevention and preparation. Syncope Syncope is caused by temporary cerebral anoxia, often caused by bradycardia secondary to parasympathetic overtone. lt is related to emotional stress and pain, often associated with injection therapy. Trendelenburg positioning usually serves as adequate prevention. Signs and symptoms include pallor, hypotension, tachycardia, mydriasis, and diaphoresis (cool and clammy skin). Treatment consists of Trendelenburg positioning, loosening tight clothing, cool compress to forehead, aromatic spirits of ammonia, oxygen administered at 4 to 6 !/min, and monitor vital signs.

Hypersensitivity Reactions Hypersensitivity (allergic) reactions are caused by release of histamine, with resultant vasodilatation and increased vascular permeability, and bronchospasm. If the reaction progresses, airway constriction, hypotension and shock may ensue. There are four major types urticarial rash, angioneurotic edema, asthma attack and anaphylaxis.

Utticarial rash presents with wheals, hives and pruritus. Treatment involves removal of the allergen, and administration of 50-75 mg diphenhydramine (Benadryl) IM, followed by 50 mg PO q 6 h PRN. Angioneurotic edema presents with marked mucous membrane edema resulting in swelling of the eyelids, cheeks, lips, pharynx, and larynx. As the upper airway swetls, hoarseness and stridor (laryngospasm), wheezing (bronchospasm) and cyanosis develop. Treatment involves withdrawal ofthe allergen, and administration of 0.2-0.5 cc epinephrine SC q 15 min

Selected Diseases and Pathological Conditions

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Ch. 3

as needed, in addition to 50-75 mg diphenhydramine IM, and 8 mg dexamethasone (Decadron) IM for late effects. Asthma attack presents with wheezing due to bronchospasm, effecting dyspnea, and initial flush then cyanosis. Treatment involves administration of 2 puffs of aerosol

bronchodilator (Ventolln, Proventil), which asthmatic patients often carry themselves, or 0.3-0.5 cc epinephrine 1:1,000 SC q 15 min x3, in conjunction with aerosol bronchodilator.

Anaphylaxis results in rapid respiratory and cardiovascular collapse, and requires rapid administration of epinephrine in order to avoid a severely morbid or fatal reaction. Signs and symptoms include laryngospasm, bronchospasm, hypotension, nausea, diaphoresis, pruritus, urticaria and angioedema, and unconsciousness. Treatment involves withdrawal of the allergen, Trendelenburg position, maintain airway, 02, and administer epinephrine 1:1,000 SC or sublingual 0.3- 0.5 cc and repeated q 5-15 minutes until an adequate response is observed, try to establish IV access. The sublingual route of administration is acceptable when lV access is not attainable {inject into posterior ventral portion ofthe tongue where it is vascularized with larger vessels). Inject .25 cc 1:1,000 epinephrine about site of previous injection of allergen, or apply BP cuff proximal to site of allergen injection (release every 10 to 15 minutes). If hypotension does not respond to epinephrine, administer metaraminol (Aramine) 0.5- 5 mg IV. If bronchospasm persists, administer aminophylline 250 mg IV over 10 min.lf convulsion occurs, administer diazepam (Valium) up to 10 mg slow IV infusion titrated until the seizure is controlled, or administer short-acting barbiturate pentobarbitallOO mg IV. Be prepared to support and maintain respiration whenever IV diazepam or pentobarbital are administered.

Toxic Reactions to Local Anesthetics Toxic reaction to a local anesthetic involves initial central nervous system {CNS) stimulation due to inhibition of inhibitory neurons, resulting hypertension, tachycardia, and skeletal muscle twitching that may progress to convulsion. Treatment consists of administration of Oz to counter hypoxia and resist convulsion, maintain airway and, in the office, give diazepam (Valium) 10 mg slow IV titration. Following initial CNS excitation, CNS depression may develop as the toxic level of local anesthetic proceeds to suppress CNS function. Pathologic findings include hypotension, weak and rapid pulse, shallow, slow respiration, loss of speech, confusion, delirium, and coma. Treatment involves airway maintenance and administration of 02, ephedrine 0.5 cc IV or lM.Ifthe reaction proceeds to cardiovascular collapse also administer atropine 0.4 mg IV, and commence BCLS and/or ACLS.It is lmportantto know the toxic dose of the local anesthetic being administered. The maximum allowable dose of local anesthetic varies with epinephrine co-administration \Table 3-12), and readers are encouraged to be familiar with the toxic dosages of the agents thatthey use.

TABLE 3-12. MAXIMUM LOCAL ANESTHETIC DOSAGES.* Maximum dose (mg)

local anesthetic

Plain Lidocaine Bupivacaine

W~h

epinephrine

300

500

175

225

"In order to calculate the proper volume of local anestheitc for injection, the following mass per volume proportions are helpful: there are 2.5 mg/ml in a0.25% solution, 5 mg/ml in a 0.5% solution, 10 mg/ml in a 1% solution, and 20 mg/ml in a 2% solution_

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Hypertensive Crisis Hypertensive crisis can develop as a result of progressive, neglected hypertension, head injury or encephalitis, drug induced, pheochromocytoma, dissecting aortic aneurysm {will rapidly drop if aneurysm ruptures), or associated with renal and/or heart failure. Diastolic pressures of 130~140 mm Hg are considered emergent and require immediate treatment with diazoxide (Hyperstat) 300 mg IV infused rapidly over 10 seconds. The patient is

transported to the hospital as soon as possible. Hyperventilation Hyperventilation is cased by anxiety and emotional stress, perhaps related to anticipation of pain or injury, and results in blowing off C02 and development of respiratory alkalosis. Signs and symptoms include rapid, shallow breathing, vertigo, confusion, paresthesia (often affecting the forearms and hands), and carpopedal spasm. Treatment is to reassure and have the patient rebreathe into a brown paper bag so that C02 is elevated. Sedation with 510 mg of diazepam PO (or slow IV infusion) may be helpful in a prolonged event.

Seizure Seizure can result from pre-existing seizure disorder, head trauma, encephalitis, or toxic effect of medication, such as a local anesthetic. Signs and symptoms include aura, CNS stimulation, and grand mal epilepsy with tonic-clonic spasms, coma, post-ictal aphasia, and somnolence. Treatment focuses on protecting the patient from injury during the seizure and allowing the seizure to run its course. Avoiding head injury as the patient convulses or falls is important. If easily achieved, a padded tongue depressor may be placed in the mouth to prevent laceration of the tongue due to jaw compression, however it is not advisable to force anything into the mouth for fear of inducing injury (dental damage). If the patient becomes cyanotic or the seizure fails to subside, or status epilepticus occurs (one seizure is immediately followed by another), then administer diazepam 5-15 mg IV via slow infusion with attention to respiratory support as indicated. Alternatively, 50 mg (2 ml of 2.5% solution) of IV sodium thiopental may be administered. Phenytoin (Dilantin)300 mg IV slow push may also be administered. 02should also be administered. The patient should thereafter be transported to the hospital for neurological evaluation. It is important to know how well-controlled your patients with epilepsy are, and when the patienfs last seizure took place. Insulin (Hypoglycemic) Shock Insulin shock is caused by an acute episode of hypoglycemia or hyperinsulinism. Signs and symptoms include anxiety, confusion, diaphoresis, tachycardia, nausea, convulsion, and coma. Treatment consists of administration of oral glucose either as an instant glucose preparation or via fruit juice or a candy bar. An ampule of 050 may also be administered IV if oral administration has not resolved the crisis. Most experienced diabetic individuals know the warning signs of hypoglycemia, and take counter-actions in a timely fashion. Hypoglycemia may occur in a patient who was running late for a morning appointment and failed to eat breakfast after taking their insulin. Acute Adrenal Crisis

Acute adrenal crisis can occur as a manifestation of insufficient corticosteroid administration in a patient who regularly takes steroids for treatment of a steroid-responsive disease, or as the initial presentation of previously undiagnosed adrenal insufficiency {Addison's disease). Patients on chronic, regular corticosteroid supplementation or replacement therapy require

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administration of exogenous corticosteroid in the perioperative period. These patients have suppression or inadequate function of their hypothalamic-pituitary axis for any of a variety of reasons, often due to the therapeutic use of corticosteroids for the treatment of rheumatoid arthritis and other auto-immune diseases, asthma and other forms of COPD, or malignancy. The body's own production of corticosteroid is suppressed after exogenous administration of just 7.5 mg/day of prednisone over a 7 day period. Symptoms of adrenal insufficiency include hypotension, syncope, nausea and

vomiting. Cardiovascular collapse can develop if corticosteroid is not administered in a timely fashion. Serum cortisol level should be drawn as soon as possible, without delaying administration of 100 mg hydrocortisone IV, followed by 100 mg, or 15 mg/kg, IV every 8 hours. The most common complicating effects of steroid therapy, in particular chronic steroid use, are related to inhibition ofWBC function and diminished fibroplasia, both of which negatively impact soft tissue and bone healing. In the acute postoperative period, steroid supplementation can decrease the white count and mask infection, and also diminish epithelialization and wound contraction. Consideration can be given to supplementing with vitamin A to try to counter some of the detrimental affects of corticosteroids on wound healing. All patients requiring daily maintenance corticosteroid administration should continue on their regular maintenance dose, and receive supplemental corticosteroid during the peri operative period. For cases involving local anesthesia with or without lV sedation, IV administration of 100 mg hydrocortisone 30 to 60 minutes preoperative, then again postoperative in the recovery room for cases lasting greater than one hour, is generally adequate. Alternatively, 15 mg prednisone can be administered orally at 0600 the day of surgery, then again at 1600the day of surgery, and a final supplemental dose of 15 mg orally at 1600 on postoperative day number one. For patients undergoing general anesthesia, 100 mg hydrocortisone can be administered HS the evening before surgery, then again preoperative prior to starting the case, and then Q 8 hours over the first 24 hours postoperative, and continued on a Q 8 hour basis up to the second -fourth postoperative day, depending upon the physical and mental stress of the surgery. Steroid supplementation should be tapered down to the regular maintenance level if supplemental steroid has been administered for more than 3 days. Other supplementation regimens may be better suited for an individual patient, and consultation with the patient's internist is helpful. Alcohol Withdrawal Alcohol withdrawal can occur in individuals of all walks of life, and is precipitated by Illness or injury that precludes access to ethanol. Signs and symptoms include tremulousness, irritability, nausea, anorexia, hallucination, and seizure. These can develop as early as 3~5 hours or up to 48 hours after the last drink. Delirium tremens is characterized by autonomic hyperactivity resulting in hyperpyrexia, diaphoresis, and tachycardia; in conjunction with tremulousness, hallucination, agitation, and confusion. Delirium tremens conveys serious risk of injury and/or death. Treatment of alcohol withdrawal consists of chlordiazepoxide llibrium)25-100 mg PO q 6h or diazepam {Valium) 5~20 mg PO q6h; observation, protection, and reassurance. Adjuncttherapyfor malnutrition and social service intervention is also indicated.

Airway Obstruction Airway obstruction is caused by a foreign body in the airway, or angioedema- induced oropharyngeal occlusion. Signs and symptoms include choking, gagging, violent inspiratory

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effort, suprasternal notch retraction, cyanosis, respiratory arrest, and cardiac arrest.

Treatment involves establishing an airway via inspection and sweeping the oropharynx, performance of the Heimlich maneuver, placement of an oral airway or endotracheal intubation, or emergency cricothyrotomy. Once an airway is established, BCLS and/or ACLS

may be indicated. The patient is transported to the hospital as soon as possible. Respiratory Arrest Respiratory arrest is caused by airway obstruction or drug toxicity. Signs and symptoms include apnea, cyanosis, and coma. The so-called "cardinal triad" of barbiturate toxicity or narcotic overdose consists of apnea, miosis and coma (the patient is usually cyanotic as well). Respiratory arrest that is not rapidly alleviated will be rapidly followed by cardiac arrest Even a brief period of airway obstruction or respiratory arrest in an individual with coronary artery disease can effect angina pectoris, myocardia! infarction, and/or cardiac arrest Respiratory arrest is treated with BCLS wherein the airway is established and artificial respiration (rescue breathing) administered. Transport the patient to the hospital as soon as possible. Pulmonary Embolism (PEl PEcan cause acute, crushing chest pain and a sense of impending doom. See Venous Thrombosis and PulmonaJY Embolism Malignant Hyperthermia Malignant hyperthermia is a severe, adverse reaction to general anesthesia (intra-

operative) that occurs in approximately 1:20,000 patients, and displays a familial tendency. lfthere is a family history, the CPK should be assessed preoperatively for elevation (almost 80% correlation). Amide local anesthetics should be avoided in patients with a history of malignant hyperthermia. The reaction occurs upon exposure to inhalant anesthetic agents, and results in hypertonicity and skeletal muscle fasciculation, jaw clenching and rigidity, hyperpyrexia, tachycardia, tachypnea, variable blood pressure, cardiac dysrhythmia, hyperhidrosis, cyanotic mottling of the chest and extremities, and dark blood observed in the surgical wound. Treatment consists of immediate cessation of anesthetic agent, hyperventilation with 100% 02 at 8·10 liters per minute, and IV bolus administration of Dantrolene sodium at 1 mg/kg up to a maximum of 10 mg/kg. The EKG is monitored and procainamide may be administered to stabilize the myocardium. Physical measures to cool the body are instituted to counter brain·injuring hyperpyrexia. Cooling efforts include IV administration of cool saline, application of ice to the groin and axillae, ice water lavage of the stomach, rectum, and bladder. Administration of sodium bicarbonate may be indicated to counter acidosis and hyperkalemia. Kidney function is maintained at 2 ml/kg/hr using IV furosemide or mannitoL Insulin may be administered to assist in providing the cells with glucose for on·going metabolism. Following control of the acute crisis, Dantrolene sodium is administered orally over the next 2·3 days. Angina Pectoris

Angina pectoris is caused by coronary artery disease or obstruction. The patient usually has a family as well as personal history of such crushing chest pain, and may already be medicated for their disease. Anxiety, emotional or physical stress usually precipitate angina pectoris, and the characteristic crushing chest pain that lasts 3 to 5 minutes in the presence

86

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of stable vital signs. The pain may radiate to the left arm and wrist The patient may also display diaphoresis, dyspnea, nausea, and weakness. Treatment consists of administration of 100% at 61iters/minute, sublingual nitroglycerine INTG)1/150 tablets every 10 minutes as needed. Loosen tight clothing, sitthe patient in semi-Fowler's position, and transport the

o,

patient to the hospital as soon as possible. Myocardiallnlarction IMI) Ml is caused by respiratory arrest or coronary artery disease, and is usually preceded by 3to 5 minutes of angina pectoris with its associated signs and symptoms, as well as a sense of impending doom. Cardiac dysrhythmia may also develop. Treatment consists of

administration of 100%02 at61iters/minute, morphine sulfate 5-10 mg IV push, or 10-15 mg

IM, while monitoring the BP and securing IV access and initiating infusion of 05W at KVO IB hour) rate. Preparation is made to administer BCLS or ACLS, and to transportthe patient to the hospital. Cardiac Arrest Cardiac arrest is caused by myocardial infarction and/or respiratory arrest. Signs and symptoms include unresponsiveness, apnea, and absence of carotid artery pulse, and clinical death with the pupils fixed and dilated, and facial, acral and chest cyanosis. Treatment involves BCLS, ACLS, and transportation to the hospital as soon as the patient is ready. The treatment protocol involves all of the interventions defined previously for MI.

BASIC CARDIAC LIFE SUPPORT Basic Cardiac Life Support IBCLS) consists of establishment of the airway, rescue breathing, and circulatory support with external chest compression (cardiopulmonary resuscitation CPR).Table 3-13).

TABLE 3-13. CARDIOPULMONARY RESUSCITATION I CPR) PROTOCOLS.

Age of victim Adult Adult Child Infant

Number of rescuers 1 2

2 2

Compression-to-ventilation ratio 15:2 5:1 5:1 5:1

If the required equipment and medications are available, additional support can be administered based on the recuers' level of training and experience. The EKG is observed in a "quick-look" fashion via the defibrillator paddles, or an Automatic External Defibrillator reads the rhythm without visual display, and identification of a lethal dysrhythmia warrants defibrillation in the adult at200-360 joules delivered 12 joules /kg in a child) for ventricular fibrillation.

ADVANCED CARDIAC LIFE SUPPORT Advanced Cardiac Life Support IACLS) entails application of algorithms with a degree of automaticity, however permutations of the algorithms may be helpful on an individualized basis.

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87

Statistics show that: the majority of cardiac arrests occur in patients wfth pre~existing coronary artery

disease 20% of cardiac arrests are the first and last manifestation of the disease 30% of victims have a second arrest within one year if they survive resuscitation but do not follow-up with treatment 50% suffer another arrest within the second year if left untreated the most common cause of arrest is ventricular fibrillation {V-fib)

1-2% of all hospital admissions suffer cardiac arrest and 50% are resuscitated 33% survive at least 24 hours, but only 15% survive to leave the hospital 95% die if the resuscitation extends longer than 15 minutes most codes are called \terminated) after 30 minutes if no significant positive response is noted 56% of out-of-hospital arrest victims survive if ACLS is administered within 4 minutes the prognosis for survival worsens in ascending order as follows: V-tachycardia > V-fib. >bradycardia/asystole; CPR without appropriate drugs, such as epinephrine, is inadequate to sustain adequate perfusion of the brain and heart. The ABCs (Airway, Breathe, Circulate) of cardiopulmonary resuscitation (CPR): 1. Identify unresponsiveness 2. Call for help 3. Position and establish airway 4. Check breathing 5. Begin rescue breathing with 2 full breaths 6. Check circulation by palpa~ng the carotid pulse 7. Activate emergency medical service (EMS) 8. Begin chest compressions according to victim's size/age 9. Continue basic cardiac life support or implement advanced cardiac life support (ACLS) and/or transport

Airway and ventilation protocol: 1. Heimlich maneuver--if obstruction is suspected, implement the Heimlich maneuver 2. Head back-jaw thrust-this is the standard approach to establish unobstructed airway patency 3. Rescue breathing-"mouth-to-mouth" ventilation, using appropriate protective shield \Pocket-mask or similar device) 4. Supplemental oxygen-administer 90% 02 at 10 liters/minute via line to mask or nasal cannula 5. Ventilation-use an Ambu bag-valve-mask if airway remains patent 6. Endotracheal intubation or laryngeal mask airway (LMA) insertion-resortto more secure airway management if head back-jaw thrust is insufficient; consider a nasotracheal intubation if cases involving oral trauma 7. Spontaneous ventilation-if spontaneously ventilating, reduce to 20-40% 02 via nasal cannula

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Selected Diseases and Pathological Conditions

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Emergency IV access:

Line size-attempt to obtain z16 gauge access to facilitate administration of emergency medications Srte-a central line is preferable to peripheral access Number of lines-as a rule, 2 sites may be useful, especially in a prolonged resuscitation effort Vein options-dorsal hand or antecubital, subclavian or internal jugular vein, and femoral vein (keep in mind, during CPR there is decreased flow inferior to the diaphragm) Catheter methods-Seldinger guide wire and sheath dilator, typically the easiest; catheter-over-needle (Angiocath®), catheter-through-needle (lntracath•) Cut down-as a last resort, sharp dissection to expose and catheterize either the saphenous or axillary vein can be undertaken The EKG and cardiac dysrhythmia: Conduction system-sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, left and right bundle branches Electrocardiogram-P wave= atrial depolarization, PR interval= time between atrial and ventricular depolarization, ORS complex= ventricular depolarization EKG and cardiac rate-each small grid square= 0.04 seconds, there are 5 large squares/second, 31arge squares approximates 90 beats per minute EKG tracing-monitor quick-look paddles or lead-2to determine rate, rhythm, and axis of the dominant pacer Dysrhythmias and cardiac life support: Normal sinus rhythm (NSR)----range 60-100 regular beats per minute Sinus tachycardia-response to exercise, hypovolemia, fever, anxiety, hyperthyroidism, sympathomimetic, etc. Sinus bradycardia-response to vagal overtone or atropine, sinoatrial node defect hypotension, ventricular ectopy, local anesthetic toxicity, etc. Premature atrial contractions {PACs)-ectopic atrial pacer cause irregular rate; response to sympathomimetic stimulant or a-agonist hypoxia, etc. Atrial tachycardia and fibrillation-atrium fails to effectively contract at 400-700 beats per minute, as does ventricle at 150-200 beats per minute; due to myocardial infarct or other disease; requires digitalis and/or cardioversion Junctional rhythm-AV node acts as latent pacer after 1-1.5 second delay, typically effects rate of 40~60 beats per minute Premature ventricular contraction {PVC)-due to ectopic ventricular focus or foci, runs of PVCs are ominous Ventricular tachycardia-3 or more ventricular beats, rate> 100 beats per minute Ventricular fibrillation-this results in no cardiac output and is lethal; coarse waveform represents recent fibrillation, whereas fine waveform indicates late fibrillation Ventricular asystole-flat line waveform due to cessation of ventricular contraction. Atrioventricular block~conduction blockade between the AV node and the bundle of His, effecting wide ORS segment and decreased cardiac output)

Selected Diagnostic Techniques

Ch.4

89

SELECTED !JIAGNOSTIC TECHNIQUES HISTORY AND PHYSICAL EXAMINATION The most importanttool in making an accurate diagnosis is a properly executed history and physical examination (H&P). The astute practitioner listens to the patient See Oral Exam Test Taking Format for a useful H&P form.

DIAGNOSTIC IMAGING Radiation Safety Radiation safety procedures and an understanding of the effects of ionizing radiation are

important matters tor all office personnel participating in preparation of diagnostic images. X-rays are high energy electromagnetic radiation that can effect mutation of cellular genetic material. There is no safe dose of ionizing radiation, and therefore exposure must be limited while maximizing the diagnostic benefit of the image. Pregnant women should not electively be radiographed, and alf subjects should wear protective lead apron, and the examiner should use a similar apron, thyroid shield, cornea protection, and lead gloves when manipulating the extremity under examination. Variable factors in the imaging process include: kV (kilovoltage), mS (milliseconds), collimation, distance between the foot (part), the film, and the X-ray source. Scatter radiation must be minimized to reduce environmental radiation not used for creation of diagnostic images. Fluorescent film screens are used with blue or green light sensitive films to further decrease the amount of ionizing radiation required to obtain a useful diagnostic image. Automatic or manual film processing requires exposure of the exposed film to developer, fixer, and then a water rinse followed by drying. Poor quality images are unacceptable practice, as useful diagnostic information is compromised at the expense of patient and environmental radiation exposure. Use of a radiation dosimetry service enables one to accurately monitor environmental and personal exposure. Radiographic Views

Standard pedal radiographic views are taken with the patient weight bearing, with the feet in the angle and base of gait. This allows reproducible and reliable images, from which standard angles and relationships can be assessed. Variations can be useful, depending upon specific needs. The primary views of the ankle include the mortise and lateral projections. Ankle views do not necessitate positioning the foot in the angle and base of gait. Contralateral radiographs can be obtained for comparison, particularly when evaluating the skeletally immature, or when concerned about secondary centers of ossification. Dorsoplantarfoot~ the patient standing on film cassette, beam angled 15° from vertical and aimed atthe navicular.

Lateral foot~ the foot is posrtioned beside (against) the film cassette, which is vertical to the substrate, beam angled 90° from vertical and aimed at the midfoot. Lateral oblique foot- the patient standing on film cassette, beam angled 45° from vertical

and aimed at the lateral aspect of the foot. Useful in assessment of the calcaneus, cuboid, fifth metatarsal and little toe.

90

Selected Diagnostic Techniques

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Medial oblique foot- the patient standing on film cassette, beam angled 45° from vertical

and aimed at the medial aspect of the foot. An unconventional view, useful in assessment

of the medial aspect of the foot, the first metatarsal and hallux and, in particular, the plantar medial border of the foot. It is also useful in evaluation of the tuberosity of the calcaneus, as in the case of suspected plantar heel spur.

Calcaneal axial- the patient standing on film cassette, beam angled 45° to vertical and aimed at posterior aspect of the heeL Modifications include Harris and Beath projections, wherein the beam angle ranges from 10° above and 10c below the lateral view declination angle ofthe posterior facet of the STJ las determined by a scout lateral view) or, more simply, 30°, 45° and 60° from vertical. Useful in assessment of the posterior aspect of the calcaneus, suspected calcaneal fracture or inspection of the posterior facet of the STJ or the sustentaculum.

Sesamoidal or metatarsal axial- the patient standing on orthoposer with the film vertical to the substrate, and the toes dorsiflexed against the film. The hindfoot is supported with enough radiolucent foam to elevate the heel above the substrate, with the beam angled from posterior-to-anterior parallel to the substrate and aimed at the metatarsal heads. Positioning devices are available to aid in stabilizing the patient for these views.

Isherwood views- a rarely used set of three non-weight-bearing views that display the STJs. The lateral oblique view shows the anteriorfacet, the medial oblique view shows the middle and posterior facets, and the lateral oblique axial view shows the posterior facet. CT and linear tomography are more typically used, as positioning for Isherwood views is difficult and time consuming. Other sets of radiographic views used to image the STJs, and generally superseded by linear and axial tomography, include Anthansen and Broden projections.

Mortise ankle- the heel is backed against the vertical film cassette, with the foot medially rotated 15", the beam angled parallel to the substrate and aimed at the ankle. This is the standard view for assessment of the tibiotalar and tibiofibular joints, and the dome of the talus and tibial bearing surtace.

lateral ankle- the medial aspect of the foot is positioned against the vertical film, the beam angled parallel to the substrate and aimed at the ankle.

Anterior-posterior ankle- the heel is backed against the vertical film cassette, with the toes pointing straight ahead, the beam angled parallel to the substrate and aimed at the ankle. The lateral malleolus is rotated posterior to and superimposed behind the tibia in this view, and the distal tibiofibular syndesmosis is obscured. The mortise view is much more useful for evaluation of the tibiotalar and tibiofibular joints.

Medial oblique ankle- oriented the same as in the AP or mortise of the ankle, however the foot is medially rotated 45a, thereby further opening the tibiofibular syndesmosis. Lateral oblique ankle- oriented the same as the AP or mortise of the ankle, however the foot is laterally rotated 45°. May be used to assess the medial malleolar cortex and the media! aspect of the talus.

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Stress Radiography Stress radiography can be performed with static radiographs, or dynamically under fluoroscopic image intensification. Stress radiographs are used to identify occult fractures and ligamentous instability, and can be used to evaluate any bone or joint in the leg, foot or ankle. The examiner should wear protective gloves, thyroid shield, and body apron whenever stress fllms are made. Anteriardrawerofthe ankle- with the patient supine, the lateral aspect of the foot is placed against the film cassette and the heel is cupped with one hand while the opposite hand stabilizes the anterior aspect of the tibia. The foot is rotated medially about 15°, thereby allowing visualization of the talar dome, while the talus is pulled forward out of the mortise. The distance between the nearest point on the posterior aspect ofthe dome of the talus and the most posterior margin of the distal tibial bearing surface is measured, and a distance of > 4 mm is indicative of disruption of the anteriortalofibular ligament. A Telos apparatus can be useful for applying anterior drawer in a reproducible fashion.

Inversion ankle stress (talartilt)~ with the patient supine, the ankle is oriented in a fashion similar to that used in the mortise view, while the tibia is stabilized medially and the talus lhindfoot with the STJ stabilized) forced into the tibial malleolus in an effort to stress the lateral collateral ligaments. The angle created between the plane of the distal tibial bearing surface and the dome ofthe talus is measured. Angles< 5° are considered normal, between 5-20° may be normal or abnormal, and larger angles are suggestive of lateral collateral ligament disruption. Loose bodies may be identified between the tibia and talus. Stress ankle dorsiflexion (charger)- a weight-bearing lateral view of the ankle is taken with the ipsilateral knee flexed and the ankle relatively dorsiflexed, This is used to depict osseous ankle equinus. Fluoroscopy Fluoroscopy (image intensification) is used to obtain quick radiographic images of operative maneuvers and stress manipulation, fracture reduction, fixation placement, foreign body localization, and trocar or pin placement The C-arm must be used with a radiolucent segment in the OR table. Computerized Axial Tomography (CT) And Magnetic Resonance Imaging (MRI) CT and MRI are useful imaging techniques following review of standard radiographs. Linear tomography {non-axial linear slices) can also be useful, however it is not readily available currently. Computerized tomography (CT) or computerized axial tomography (CAT scan) use high-energy ionizing radiation (X-rays), multiple projections, and a computer to generate images, and is best suited to cortical bone imaging. Magnetic resonance imaging (MRI) uses low energy radio waves traversing the body within a magnetic field, and a computer to generate images. T1 ~weighted \fat) images are dependent on the fat content of the tissue, while T2-weighted \water, inflammation) images are dependent on the water content of the tissue and are especially useful in the presence of pathological inflammation or fluid accumulation. Both CT and MRI can be enhanced when combined with contrast medium.

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Comparison of CT and MRI for Selected Pathological Conditions

Tarsal coalition- MRI is best, as not all coalitions are cortical bone Arthritis, tendinitis, and other inflammatory processes- MRI is best, as it allows early visualization of peri-articular and soft tissue changes Avascular Necrosis- MRI is preferred, and the hallmark MRI sign is a well-defined region of decreased intensity within medullary bone on both T1- and T2-weighted images. CT could be used to show advanced AVN wherein joint space has collapsed

with cortical bone defect Infection- MRI is sensitive, but not specific, tor imaging soft tissue abscess and osteomyelitis (medullary). MRI does not image subcutaneous gas. CT is useful for ·Imaging cortical defects, sequestrum, cloaca, involucrum, and intraosseous or subcutaneous gas. Neoplasm- MRI is superior for evaluating bone marrow and soft tissue; while CT is best for cortical bone, calcification, endosteal thinning, and fine periosteal reactions. Trauma- MRI is preferred for imaging soft tissue injury, in particular tendon, ligament and cartilage. CT is superior for imaging cortical bone, especially when comminution or growth plate (physeal) injury is suspected. Osteochondral lesions may warrant both CT and MRI. When in doubt as to the preferred imaging technique, simply consult with the radiologist.

Contrast Jmaging Contrast imaging using radiopaque contrast dye injected into a joint space or tendon sheath can be used to assess surface defects such as osteochondral fracture or tendon and sheath disruption. Hypersensitivity (to the contrast medium), possible sepsis, and the invasive nature of the procedure, the need for ionizing radiation and limitations related to patient positioning, are all potential disadvantages of both arthrography and tenography. MRI as well as CT scanning, despite their cost, offer excellent diagnostic images and have almost replaced contrast imaging of the ankle and peroneal sheath. Arthroscopy and endoscopy also offer diagnostic, and therapeutic, modalities applicable in the management of the foot and ankle. Ultrasonography Ultrasonography can be used for localization of foreign bodies following puncture wound, as well as identification of fluid or solid mass in the subcutaneous tissues. Radionuclide Scans Radionuclide scans are used to image bone physiology, and are usually performed using technetlum-99, ga!lium-67, or indium-111. Most scans show increased scintigraphy within 48-72 hours after the infection or other osteitis has begun. Tc-99 has a half-life of about 6 hours. Only the technetium scan labels hydroxyapatite crystals in living bone, and is therefore termed "a bone scan." Ga-67 is used to label white blood cells and plasma proteins, and is used to identifyWBC accumulation (pus, infection) in bone or other tissues. Gallium is not used as an isolated study, and is usually combined with a Tc-99 scan performed about 24-72 hours earlier. An increased uptake of Tc-99 without increased uptake of Ga-67, correlates 85% with the absence of osteomyelitis. If both Tc-99 and Ga-67 scans show increased uptake, then there is about a 70% correlation with osteomyelitis being present. ln-111 is used to tag the patienfs neutrophils, after first drawing blood and separating the PMNs. The labeled neutrophils are then infused back into the patient, and

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93

the scan performed 18 to 24 hours later. ln-111 scans are positive in cases of osteomyelitis and .negative in cases of osteoarthropathy. Since ln-111 is tagged to neutrophils chronic osteomyelitis, which is primarily an accumulation of lymphocytes, may present as a false negative indium scan (infection present despite a negative scan). An ln-111 scan may be useful in trying to distinguish postoperative infection from pseudoarthrosis or nonunion.

Bone Scans Bone scans (Tc-99) are imaged in atriphasic fashion, wherein a scintigram is made atthree specified times following administration of the radioisotope. The radio angiogram (first or immediate phase, blood flow images), is measured immediately following infusion of radionuclide and shows dynamic flow to the area. The blood pool image (second phase) is measured about 20 minutes after infusion, and shows increased scintigraphy in the presence of hyperemia. The first two phases are "hot" in both bone and soft tissue infection, or other causes of inflammation and hyperemia. The blood flow image correlates with perfusion of the part, and would not show uptake of radionuclide in the presence of ischemia. The delayed image (third phase) is measured about three hours after infusion of radionuc!ide, and correlates with skeletal uptake of the isotope. The delayed image often identifies activity related to infection or other persistent bone pathology, such as pseudoarthrosis or hypertrophic nonunion. Moreover, longer term delayed TC-99 bone scans, imaged at 24 hours !fourth phase), may be used to image infection in patients with PVD, diabetes mellitus and Charcot neuroarthropathy. Neuroarthropathy may present "hot" scans in all four phases. Soft tissue infections are usually "hot" in only the first two phases. Furthermore, a Tc-99labeled WBC scan (Seratec) can also be used to image bone infection, particularly in patients with diabetes mellitus or suffering postoperative infection. In any case, a scan is a sensitive but nonspecific imaging technique that must be combined with other diagnostic imaging techniques and clinical, as well as surgical, diagnostic measures.

Standard Radionuclide Bone Imaging Combinations

Acute Osteomyelitis Tc - 99m Scan

Ga- 67 Scan In -111 Scan

Phase I + Phase II ++ Phase Ill +++ Positive focal uptake Positive focal uptake

Inactive Chronic Osteomyelitis Tc - 99m Scan

Ga- 67 Scan In- 111 Scan

Phase I +/Phase II + Phase Ill +++!persists in longer delayed imaging)

Negative Negative

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Acute Cellulitis Tc- 99m Scan

Ga- 67 Scan In -111 Scan

Phase I +++ Phase II ++ Phase Ill + Positive diffuse uptake Positive

Septic Arthritis Tc- 99m Scan

Ga- 67 Scan ln-111Scan

Phase I +++ Phase II +++ Phase Ill +/Positive focal uptake Positive

CARTILAGE IMAGING Contrast arthrography-contrast agent (iodine for X-ray or CT, or gadopentetate dimeglumine for MRI); direct, pseudo-direct (via peroneal sheath to ankle joint), indirect methods; enhances visualization of articular cartilage margins and small cortical abnormalities; entails need trauma, possible infection and hypersensitivity to local anesthetic and contrast agent. High resolution delayed gadolinium~enhanced MRI of cartilage (HR-MRI-dGEMRIC) with fat suppression is currently the best method of cartilage imaging short of arthroscopy. The following methods are under development for clinical use, and are currently experimental research tools that show superb cartilage detail: high frequency ultrasound, diffraction enhanced imaging (MRI), gradient MRI, T1 rho time relaxation MRI, T2 time relaxation MRI, optical coherence IR tomography, and positron emission tomography (PET).

CliNICAl lABORATORY TESTING Complete Blood Count Complete blood count (CBC) with differential cell count is a general screening for a variety of conditions. CBC includes: Hemoglobin (Hgb)- normal range is 13.5-17 gm/1 00 ml for males and 12.5-16 gm/100 ml for females. Values below 11 gm/100 ml are considered to represent anemia, and should be evaluated. Elevation above 18 gm/100 ml may represent polycythemia, and increases blood viscosity and increases risk of thrombosis. Hematocrit(Hct)- normal range is 40-54% for males and 37-47% for females. Varies with the

Hgb. fled blood cell count- normal range is 5.4± 0.8x 106 /mm 3 for males and 4.8 ± 0.6 x 106/mm' for females. The RBC count increases in individuals living at high altitudes, in environmentally hot work places, and in athletically fit individuals.

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Selected Diagnostic Techniques

Corpuscular indices and anemia normocytic

macrocytic

microcytic/

hypochromic Mean corpuscular volume

82-92

95-150

50-80

Mean corpuscular Hgb

25-30

30-50

12-25

Mean corpuscular Hgb concentration

32-36

32-36

25-30

Remember the phrase "90, 30, 30," for normal MCV, MCH, and MCHC values. Normocytic anemia can be observed with acute hemorrhage, hemolytic anemia, and abnormal hemopoiesis. Macrocytic anemia occurs with pernicious anemia, sprue,

pregnancy, antimetabolic therapy, and other megaloblastic conditions. Microcytic anemia occurs with iron deficiency or malabsorption, hemorrhage, and increased iron metabolism.

White blood cell count- normal range 5,000 -10,000/ mm3. Causes of leukocytosis include: acute infection, metabolic acidosis, gout, uremia, heavy metal toxicity, tissue necrosis or injury (burns, gangrene, tumor, myocardial infarction, pulmonary embolism), secondary to hemorrhage or menstruation, and myeloproliferative diseases. Causes of leukopenia include: adverse drug reactions to Thorazine, phenylbutazone, various antifungals and antibiotics; pernicious anemia, aplastic anemia, and certain severe infections (septic shock). Differential white cell count- segmented neutrophils 40-60%, band neutrophils 0-5%, lymphocytes 20-40%, monocytes 4-8%, eosinophils 1-5%, basophils 0-1%. Some causes of neutrophilia include acute infection, necrosis, pain, exercise or post-convulsion, anoxia, hemorrhage, sunburn. Some causes of neutropenia include overwhelming infection, marrow depression, antimetabolite therapy, and autoimmunity. Lymphocytosis may indicate viral syndrome, hepatitis, chronic TB, and measles. Monocytosis occurs with leukemia, Hodgkin's disease, collagen vascular diseases and arthritides, sarcoidosis, subacute bacterial endocarditis, and other infections and wounds. Eosinophilia is indicative of allergy, asthma, eczema and urticaria; parasitic infection; scarlet fever; pemphigus and dermatitis herpetiformis; leukemia and pernicious anemia. Eosinopenia is seen in Cushing's disease, excess ACTH, chronic steroid therapy, postoperative state, shock, and labor. Basophilia occurs in polycythemia, chronic myelogenous leukemia, chicken-pox, small-pox, hypothyroid myxedema, and renal disease.

Platelet count- normal range is 140,000-340,000/ mm1 Platelets are elevated in collagen vascular disease, iron deficiency anemia, acute infection or injury, hepatic disease, cardiac disease, malignancy and polycythemia Vera. Important Labs in Rheumatoid Disease

Erythrocyte sedimentation rate (ESR)- normal anticoagulated blood shows very little settling, however, elevated globulin and fibrinogen associated with inflammation leads to Rouleaux formation and the clumped red cells settle rapidly. An elevated ESR is indicative of a measurably higher column of red cells settled at the bottom of the tube wrthin a set time. The ESR can be used to distinguish inflammatory from non-inflammatory conditions, and is used to monitor resolution of inflammation during the course of therapy.

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The ESR is very sensitive, however, nonspecific. The ESR is elevated in acute infection, rheumatoid arthritis, polyarteritis, ankylosing spondylitis, septic arthritis, acute

gout, metastasis, and other connective tissue diseases. C~reactive protein {CRP)- is a glycoprotein that reacts with C-mucopolysaccharide of many pneumococci. It is commonly produced during the acute phase of inflammation. It rises before the ESR, and normalizes in the presence of NSAIDs, aspirin and steroids. It rises in

acute flare of rheumatoid arthrftis, Strep. infection, in the last half of pregnancy, and in females using an IUD and/or oral contraceptives. Antinuclear antibody (ANA)- appears months after onset of connective tissue disease,

and may have its greatest value in monitoring SLE. It is more accurate than the LE cell test because it is unaffected by steroids. The significance of ANA titers less than 16 is uncertain, as healthy persons may display titers in this range. Elevated ANA titers suggest connective tissue disease, while absent or low titers do not rule out connective tissue disorders. High titers are common in SLE, scleroderma, and mixed connective tissue disorders, and Raynaud's phenomenon.

Pattern

Associated Antigens

Clinical Conditions

Homogenous

Deoxyribonucleoprotein

Collagen-Vascular OS

?articulated

Extractable Nuclear Antigen

Mixed C.T. OS., scleroderma, SLE, Malignancy

Peripheral

Native DNA and Histones

Active SLE with Nephritis

Nucleolar

Nucleolar RNA

Scleroderma, Raynaud's

Positive ANA is found in the following percentages in the following diseases

Systemic lupus erythematosus Rheumatoid arthritis Sjogren syndrome Systemic sclerosis Liver cirrhosis Polymyositis Dermatomyositis Malignancy Bullous pemphigus Polyarteritis nodosa or ulcerative colitis Waldenstrom's macroglobulinemia Drug reaction Myasthenia gravis

(100%, high titer) I< 60%, very low titer) (75%, low titer) 138%, low titer) (45%, low titer) 120%, low titer) (20%, low titer) (18%, low titer) (rare, low titer) (rare, low titer) (rare, low titer) (rare, low to high titer) (rare, very low titer)

Rheumatoid factor (RF)- lgM or lgG auto-antibodies that react with the Fe portion of denatured human lgG. There are two methods of measurement: latex fixation {75% sensitive and 75% specific for RA at 1:80 dilution), and sheep cell agglutination (75% sensitive and 95% specific for RA at 1:160 dilution). RF is found in the following

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percentages: Sjogren syndrome (75-100%), adult RA (70-80%), juvenile RA (10%), SLE (20-40%), scleroderma 15-10%1, polyarteritis nodosa and dermatomyositis I0-5%). Lupus erythematosus (LEI cell - mature polymorphonuclear neutrophil that has phagocytosed a spherical, homogenous inclusion derived from another neutrophil.

Characteristic of SLE, and observed in the following percentages : SLE (70-80%), Sjogren syndrome 110-20%), RA 15-10%1, scleroderma and polyarteritis nodosa and dermatomyositis I0-5%).

Serum complement series of enzymatic proteins that combine with antigen-antibody w

complexes and effect lysis when the antigen is an intact cell. Complement remains normal in Sjogren syndrome, scleroderma, polyarteritis nodosa, and dermatomyositis; is normal or decreased in SLE; and normal or slightly elevated in acute phase of RA. Anti-streptolysin 0 (ASO)- antibody against streptolysin "0" of group A streptococci {Strept. pyogenes). It is present in 80-85% of patients with acute rheumatic fever or other streptococcal infection. HL-A 827- histocompatability antigen found in the following percentages in the following diseases: ankylosing spondylitis (90%), Reiter's syndrome (75%), psoriatic arthritis and juvenile RA (high concentration). HL-A 815- histocompatability antigen found in 33% of patients with SLE.

Uric acid (UA)- elevated in gout, malignancy, renal disease, and familial hyperuricemia. Normal is 7-9 mg% in males, and slightly less in females. UA may be normal in the acute stage (first 10 days) of gouty arthritis, as much has precipitated out ofthe serum into the affected joint. Monosodium urate (gouty) crystals are needle-shaped, and form the "martini sign" when phagocytosed by a neutrophil.

Calcium pyrophosphate~ crystals are rhomboid, and observed in pseudogout Joint Fluid Analysis Joint Fluid Volume

Normal

Group-1 Increase

Group-11 Increase

Group-Ill Increase

Clarity

Clear

Clear

Cloudy

Opaque

Color

Clear

Yellow Opalescent

Yellow Green

Yellow

Viscosity

High

High

Low

Variable

WBC/mm3<

200

200-2000

2000-100,000

> 100,000

% PMNs

75%

Culture

1-1

1-)

1-1

1+1

Mucin Clot

Firm

Firm

Friable

Friable

Glucose lmg%)

=Serum

=Serum

0.75 and forefoo1/arm index> 0.65, then check Doppler flow of digital arteries. Hallux:

If ankle/arm index> 0.75, and toe/arm or forefoo1/arm index> 0.65 and two of four digital arteries identified with Doppler, then Qenerally may operate.

Lesser Toe: If ankle/arm index> 0.75 and toe/arm or forefoo1/arm index> 0.65 and either both dorsal arteries and one plantar or both plantar arteries identified with

Doppler, then generally may operate.

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Invasive arterial testing, in the form of angiography with radiopaque contrast media, is usually obtained only if reconstructive vascular surgery is being entertained. Infusion of contrast medium is not a risk-free undertaking, and conveys the risk of hypersensitivity reaction, as well as renal failure in dehydrated or predisposed individuals. Digital subtraction angiography can further enhance identification of patent and occluded vessels. Although noninvasive, MRI can also be used to evaluate blood vessels and yields considerably accurate images. Venous non-invasive Doppler assessment is used when deep vein thrombophlebitis is suspected, and a venogram may further enhance identification of a thrombosis, particularly one that is propagating or associated with embolism and consideration is given to surgical intervention.

BIOMECHANICS Biomechanics is the study of mechanical laws as they pertain to the human musculoskeletal system and, in particular, bipedal locomotion. Basic terms include: 1. Cardinal body planes sagittal (SP), frontal (FP), and transverse (TP) 2. Axes-

frontotransverse, allowing motion in the SP frontosagiltal, allowing motion in the TP sagittotransverse, allowing motion in the FP

3. Motions-

pronation and supin8.tion (triplanar) inversion and eversion (FP) adduction and abduction (TPI internal rotation and external rotation (TP) dorsiflexion and plantarflexion (SP) flexion and extension (SP)

4. Positions-

pronated, supinated, inverted, everted, abducted, adducted, externally rotated, internally rotated, dorsiflexed, plantarflexed. When a position is fixed, it is referred to as flexion, extensus or extension, adductus, abductus, varus, valgus, elevatus, supinatus, equinus, calcaneus.

Motion is described as occurring in the cardinal planes of the body or foot, in a plane 90° to the axis of motion. Single plane motion occurs in the plane perpendicular to the axis that lies at the intersection of the remaining two planes. Triplanar motion occurs in a plane perpendicular to an axis that courses through all three cardinal planes (oblique to all planes). Triplanar motion of the foot is said to be pronatory/supinatory (pronatory), and the axis is directed from posterior-lateral-plantar to anterior-medial-dorsa!. Pure SP motions include dorsiflexion and plantarflexion, while pure transverse plane motions include adduction and abduction, and pure frontal plane motions include inversion and eversion.

Biomechanical Examination The examination begins with open chain visual inspection, then patient active motion, followed by manipulation and palpation, followed by gait analysis. Special testing, such as

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pedobarographic, kinematic, and other motion analysis methods may also be used. Visual inspection is used to identify gross positional and structural features. Examination may proceed as follows: hip, knee, ankle, subtalar joint, metatarsal joint, 1st ray, 1st metatarsophalangeal joint, forefoot-to-hindfoot relationship, then on to other assessments of specific concern.

Hip -is a diarthrosis that allows enarthrous gliding, rotation, angulation, and circumduction. Motion occurs in all three body planes: TP (sagittal-frontal axis): Internal and external ROM FP (sagittal-transverse axis): Abduction/adduction ROM SP (frontal-transverse axis): Flexion/extension ROM (including hyperextension).

The mechanical axis of the hip runs from the center of hip to knee, with the mechanical axis of the femoral shaft running from a line between greater and lesser trochanters, relative to the plane of femoral condyles. Examination of the hip should reveal the following:

Adult Hip Range of Motion - Int. Rot. " Ext. Rot., with hip flexed or extended. The neutral hip should align femoral condyles on the FP. Normal SP hip flex./ ext. at birth is 150°, and about 100° after puberty. If limited in extension, then hamstrings are likely tight; if limited in flexion, then Iliopsoas is likely tight; excessive internal to external range of motion indicates tight adductors; excessive external to internal range of motion indicates tight abductors; and asymmetrical limitation of motion may indicate congenital or neglected hip dysplasia or limb length inequity. Total range of motion decreases with age.

,j

Knee- motion occurs aboutthls ginglymus jo.mtwith only two degrees of freedom \axes) of motion: SP flexion-extension, and TP internal and external rotation. 5-6o of TP motion occurs with SP flexion-extension of the knee. Motion occurs predominantly in the SP about a frontal- transverse axis, and to a lesser degree about the frontal-sagittal. FP motion is indicative of collateral ligament damage. The patella enhances quadriceps leverage. In non-weight bearing (open kinetic chain) rotation of the knee, the tibia rotates on the femur. In weight bearing \closed kinetic chain), the femur rotates on the tibia. The lateral femoral condyle rotates around the medial condyle, with motion occurring between the tibia and meniscus. Therefore, for internal rotation, the lateral tibial condyle moves anteriorly on the lateral meniscus. For external rotation, the lateral tibial condyle moves posteriorly on the lateral meniscus. The greatest degree of rotation is available when the knee is flexed at 90°. Examination of the knee should reveal the following: 1. Knee position on the FP when hip and STJ neutral, with end range of motion 180', and fixed 2. Flexion or hyperextension may indicate compensation for ankle equinus. 3. Genu valgum may effect compensatory hindfoot supination, but generally over time acts as 4. A strong pronatory influence on the hindfoot 5. Genu varum must be distinguished from tibial varum, and pro nates the hindfoot. 6. Genu recurvatum may be due to cruciate ligamentous laxity or compensation for ankle equinus. Thigh hamstrings or gastrocnemius can effect genu flexion deformity.

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Ankle- range of motion occurs about a pronatory axis running from the latera! to medial malleolus, normal range being 20°-30° dorsiflexion OF and 30°-50° PF. The axis is primarily at the junction ofthe FP and TP. deviated in the TP by about 12'-15" of malleolartorsion, thereby allowing primarily SP OF Iflexion) and PF !extension). The articulation represents a mortise (medial malleolus, distal tibial bearing surface, lateral malleolus) and tenon (talar body) joint. Range of motion is assessed by asking the patient to actively take the ankle joint through OF/PF range of motion in the sagittal plane, followed by circumduction of the ankle or figure-of-eight motion. Examination of the ankle should reveal the following: Ankle range of motion should allow 25-30° PF, and lOa or more dorsiflexion with the knee extended. Increased ankle dorsiflexion when the knee is flexed is indicative of limitation by gastrocnemius (equinus if < 10°). The Silfverskiold test is then performed, and the presence or absence of gastrocnemius or gastro soleus equinus, or bony (talotibial exostosis) equinus, is determined. Pseudo equinus, due to plantarflexed forefoot results in functional ankle equinus due to retrograde ankle dorsiflexion in weight bearing. Compensation for ankle equinus may result in normal heel-off due to adequate subtalar joint/metatarsal joint hyperpronation, early heel-off if only partially compensated by hindfoot pronation, or no heel-off whatsoever (no heel contact) if uncompensated in the foot (usually associated with genu recurvatum or fixed flexion).

Subtalar Joint- range of motion occurs about a pronatory axis deviated 42° from the TP I nearly equidistant from the horizontal TP and the vertical FP), and 16o from the SP. STJ is minimal in the SP, as the axis almost lies in this plane. Inversion/eversion and adduction/ abduction motion is greatest and almost equidistant in both the FP and TP, respectively. A higher pitched subtalar joint axis would allow more TP motion, while a lower pitched subtalar joint would allow more FP motion. The subtalar joint is an oblique hinge diarthrosis with trip!anar motion. Motion from maximum pronation to maximum supination defines an arc, with 2/3 of the arc supinated from the neutral position, and 1/3 pronated from the neutral position. Normal subtalar joint range of motion is 30°-35°, with about 10°-15° eversion and 20°- 30° inversion. Pronation of the subtalar joint in open kinetic chain (non-weight bearing) entails abduction, eversion, and dorsiflexion of the calcaneus on the talus; whereas pronation in the closed kinetic chain (weight bearing) attitude entails adduction, inversion, and plantarflexion of the talus on the calcaneus. Range of motion is assessed by observing normal excursion of 2/3 inversion to 18 years, straight> 60 years genu valgum.1ibial varum is a FP inverted angulation of the lower leg to the ground in static stance. Tibial valgum is a FP everted angulation of the lower leg to the ground in static stance. The malleoli- form a 0" angular relation to the FP at birth, followed by an external growth torque of 18-23°true tibial torsion or 13~18° of malleolar position, malleolar position being about 5° less than true tibial torsion, occurring in the transverse plane. We measure malleolar position because we can not actually measure tibial torsion clinically. As a guide, external malleolar position should be as follows 0-10" from birth to 1 year, 8-13" frorn 1-5 years, and 13-18" from 6 years to adulthood. The hindfoot relationship~ of talus to the calcaneus during fetal development reveals a FP movement of the talus over the calcaneus from a parallel position (clubfoot TEV represents cessation or limitation of the movement away from parallel). The talar head becomes less plantatflexed relative to body of calcaneus, which is importantfor development of normal TP TCA, cyma line, talar declination angle, CIA, and MTJ position.

Growth in length and width of metatarsals and phalanges- is ongoing from fetal to adult stages, and includes FP eversion torsion of metatarsals lw5, and TP abduction of 1st metatarsal to lesser metatarsals: fetal- 1st metatarsal adducted 50°, birth~ adducted 6°, by 4 years to adult~ 7-9° (if> 7~9°, get metatarsal prim us adductus or varus with juvenile HAV). The TP relation of the lesser metatarsals to the tarsus reveals: birth ~ 25° adducted, adult -15-18" adducted. Metatarsus adductus is 15-35" at birth, and 15-22" in the adult. Structural and Positional Deformities of the Lower Extremities Forefoot varus ~ is a structural deformity of the forefoot in which the plantar plane of the forefoot is inverted relative to the supporting sutface and the vertical posterior bisector of the calcaneus when the subtalarjointls neutral and the metatarsal joint maximally pronated and locked. It is associated with compensatory hyperpronation of the STJ/MTJ; submetatarsal 2~5, especially 4~5, hyperkeratosis; tailor's bunionette, flexor stabilization induced hammertoes, adductovarus 4th and 5th toes, HAV, metatarsus primus elevatus, plantar fascitis, and heel spur syndrome, and hallux limitus, medial knee strain and internal rotation secondary to compensatory hyperpronation of the hindfoot. Biomechanical treatment generally entails supporting the deformity, thereby nullifying the need for compensation in the foot, while posting the reatfootto allow 2~4° of motion. Flexible forefoot valgus~ is a structural deformity wherein the plantar plane of the forefoot is everted relative to the supporting sutface and the vertical posterior bisector of the calcaneus when the subtalar joint is neutral and the MTJ maximally pronated and locked. It is associated with compensation via supination about the LMTJ axis (forefoot supinatus); sub~

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metatarsal1 and 5 hyperkeratosis; tibial sesamoiditis, flexor stabilization hammertoes, and adductovarus 4th and 5th toes. Biomechanical treatment generally entails supporting the deformity, thereby nullifying the need for compensation in the foot, while posting the rearfoot to allow 2 to 4n of motion.

Rigid forefoot valgus~ is a structural deformity wherein the plantar plane of the forefoot is

everted relative to the supporting surface and the vertical posterior bisector of the calcaneus when the subtalar joint is neutral and the MTJ maximally pronated and locked. lt is associated with compensation via supination about the OMTJ axis and subtalar joint axis; hallux malleus, tibial sesamoiditis, lateral ankle and knee strain, symptomatic Haglund's deformity (pump bump), and children may display an intoe gait Biomechanical treatment generally entails supporting the deformity and using a 1st ray cut out, thereby nullifying the need for compensation in the foot, while posting the rearfootto allow 2-4° of motion. Reatfoot varus- is a structural deformity wherein the calcaneus is inverted relative to the substrate when the subtalar joint is neutral and the MTJ maximally pronated and locked. It is associated with lateral ankle sprain, compensatory pronation of the hindfoot only to vertical (not a profound degree of pronation), submetatarsal 4-5 hyperkeratosis, adductovarus 4th and 5th toes, tailor's bunionette, Haglund's deformity, and HAV. Reatfootvalgus- is a structural deformity wherein the calcaneus is everted relative to the substrate when the subtalar joint is neutral and the MTJ maximally pronated and locked. It is associated with submetatarsal2 hyperkeratosis, HAV, plantarfascitis, flexor stabilization. Metatarsus prim us elevatus- is a structural deformity wherein the 1st metatarsal displays a resting position dorsal to the 2nd metatarsal and plane of the lesser metatarsals. It is associated with hallux limitus/rigidus, hallux equinus, dorsal bunion, lateral dumping of late midstance and propulsive phase weight bearing and sub-second metatarsalgia and hyperkeratosis, as well as 5th toe dorsolateral HD and perhaps 4th interspace HM or HO. Forefoot supinatus- is a fixed position of supination of the forefoot about the LMTJ axis, when the subtalar joint is neutral and the MTJ maximally pronated and locked. It is associated with plantar fascitis, and limited MTJ available range of motion.

Ankle equinus- is the condition of inadequate dorsiflexion range of motion ofthe foot on the leg. It is considered present when < 10° of ankle dorsiflexion is available, and the Si!fverskiold test is used to determine the influence of the Achilles tendon as a whole and the gastrocnemius muscle and aponeurosis separately. Osseous talotibial blockade may also be present Equinus deformity is associated with early heel off, knee flexion throughout stance (unless damaging hyperextension-genu recurvatum occurs), compensatory hyperpronation of the hindfoot with plantar fascitis, flexor stabilization, adductovarus 4th and 5th toes, HAV, and extensor substitution ifthe equinus persists as a dropfootthrough swing phase. Tibial torsion- is measured as malleolar position with the malleoli forming< 13-18° of external malleolar position, malleolar position being about 5° leSs than true tibial torsion, in the transverse plane. External malleolar position is as follows 0-1 0" from birth to 1 year, 8-13° from 1-5 years, and 13~ 18° from 6 years to adulthood. Internal tibial torsion often affects the left lower extremity (in utero pressure from maternal vertebral column) in males,

114

Selected Diagnostic Techniques

Ch. 4

and treatment involves serial casting to above the knee, taking care to stabilize the hindfoot

and ankle in neutral position. Genu valgum (knock knee)- is an angular deformity of the knee usually observed in obese female children, and may be associated with coxa vara or uncompensated medial or compensated lateral femoral torsion, tibial torsion, pes valgus, deformation (depression) of the lateral tibial plateau with hamstring or quadriceps or calf pain and DJD in the adult. Genu varum (bowleg)- is an angular deformity of the knee usually observed in cases of

Rickets due to vita min-D deficiency and abnormal Ca and Ph metabolism, or due to Blount's osteochondrosis deformans wherein the medial tibial condyle is flattened and fragmented (present at birth to 24-30 months).

Femoral anteversion- refers to positioning of the femur such that the condyles of the femur are internally rotated relative to the frontal plane and the head and neck of the femur. The angle between the head and neck of the femur and the femoral condyles is normally 30- 40" of anteversion at birth and 8-12° in the adult, representing a gradual retrotorsion as the femur untwists with maturation. Delayed de rotation can effect in-toe, and is often seen in the older female child with the clinical presentation of the "reverse tailor's" sitting position, increased medial femoral range of motion, and knock-knee. Treatment includes proper sitting habits, Ganley femoral derotation splint (4 to 8 years), and femoral derotation osteotomy in the older child. Knee flexion diminishes the therapeutic influence of any pedal splinting directed at the femur, and appropriate pediatric orthopedic consultation is in order whenever significant deformity exists. Unequal limb length- may be structural within the thigh, leg or both femoral and tibial/ fibular segments; or functional secondary to scoliosis induced pelvic tilt with lower side of pelvis effecting functionally longer limb, unilateral supination or pronation of the foot. Compensation for limb inequity involves pedal pronation on the longer side, along with ipsilateral inferior pelvic tilt (tilts downward) due to hyperpronating hindfoot, ipsilateral shoulder tilt downward, scoliosis, ipsilateral head tilt toward longer limb, increased stance phase on the longer side. On the short side, the hindfoot supinates, pelvis rises, shoulder rises, and there is less stance phase weight bearing. Radiographic Findings Related to Biomechanics Radiographic signs of hyperpronation of the foot include: increased TP and SP talocalcaneal angles, increased talar declination, decreased calcaneal inclination, decreased forefoot adductus and increased abductus due to unlocked MTJ, anterior break in the midtarsal cyma line, decreased ( 38.5° C) involves administration of antipyretic such as acetaminophen or aspirin (600 mg PO Q 6 h PRN), and use of a cooling blanket If the patient remains hyperpyrexic and symptomatic, then consider discontinuing all medication, consult infectious disease specialist, and re-evaluate the patient.

Chronological Sequence of Postoperative Temperature Alteration Intraoperative & first 12 to 24 hours postop

Elevated temperature due to malignant hyperthermia, or typically postoperative hypothermia.

1st postop day

Postoperative hypothermia, postanesthesia overshoot, atelectasis I pneumonitis

2nd postop day

Benign postoperative fever, urinary tract infection, pulmonary, DVT

3rd postop day

Wound infection, benign postoperative fever, and constipation.

Any time in the postop phase

Drug fever, catheter sepsis, transfusion reaction, cold, or flu.

Ch. 6

Fundamental Techniques and Procedures

123

FUNDAMENTAL TECHNIIJ.UES AND PROCEDURES SUTURE MATERIALS and WOUND CLOSURE Sutures are used to reapproximate sectioned tissue, whether it is skin, superficial or deep fascia, muscle, tendon or ligament, nerve sheath, blood vessel, or bone (stainless steel wire [SSW]). The ideal suture material is strong enough to resist disruptive tensile forces, nonallergenic and non-toxic, pliable enough to handle easily and to stay fixed once tied. Sutures that communicate between the external surface of the skin, and the subcutaneous and/or intradermal layers should also be inert, non-wicking, and easily removable after the tissues have healed. The decision to use an absorbable or nonabsorbable suture material varies with the specific requirements of the operative procedure.

Absorbable sutures-these are made of materials that break down in the tissues over varying time periods, ranging from 1~ 10 weeks. Since most soft tissues, excepttendon, heal in 3~4 weeks, sutures that degrade at a rate that provides tensile strength up to 3~4 weeks are commonly used in foot and ankle surgery. Classically, absorbable sutures were made from sheep or beef intestine, and known as catgut. Plain gut can be strengthened by the addition of chromium salts that slow down degradation by collagenase, or it can be heat~treated to Increase the rate of degradation (rapid gut). Although it is not likely, disease transmission, such as bovine spongiform encephalopathy (mad cow disease), is possible with catgut, which is a xenogeneic materiaL Although many surgeons prefer the behavior of gut suture, monofilament or braided multifilament synthetic polymers comprise the majority of absorbable sutures used nowadays. Synthetic polymers, such as polyglycolic acid, lactic acid and caprolactone, are relatively inexpensive, non~reactive due to hydrolysis rather than collagenase degradation, nontoxic and nonallergenic, and they handle very well. Immunological reaction to synthetic absorbable suture is rare, however when it occurs a sterile abscess can form, and the material may not rapidly orfu!ly absorb. Monofilament absorbable sutures are often used in the deep tissues during delayed primary closure of previously infected or contaminated tissues. Sutures range in size (gauge), as defined by the US Pharmacopeia (USP), from #11-0 (smallest) monofilament nylon used for ophthalmologic and neurosurgery, to #5 (largest) braided polyester used for ligament repair. Some suture materials are also coated or impregnated with antimicrobial agents, to minimize risk of infection. Non-absorbable sutures-these are made of materials that are not degraded by the body, such as silk, polypropylene, polyester and nylon, and are often used for skin closure (where they can readily be removed after the skin has healed), or in tissues where prolonged strength is require, such as tendon or ligament, or myocardium and blood vessel. Due to the inert nature of many of these materials, there is less inflammation and less scar formation, so they are often preferred for skin closure. Stainless steel wire can be used for intra osseous suture, cerclage, and tension banding. Suture needles-needles used for suturing are available in a number of shapes, namely: half curved, quarter circle, 3/8 circle, 5/8 circle, compound curvature, and straight (Keith needle). Separate needles with eyelets for threading suture are known as traumatic needles. Atraumatic needles have the suture material swaged to the needle by the manufacturer. Needles can also be smooth and round or oval, or they may have a cutting edge on the concave surface ofthe curve, or on the convex surface of the curve (reverse

124

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cutting needle). The body of the needle maytapertoward the tip, or retain the dimension of the body and form a blunt tip (forfriable tissue). The tip ofthe needle can be round, oval, or diamond-shaped. Generally, a non-cutting, atraumatic needle is used for reapproximation of friable tissues, whereas a cutting needle is often used for dense and durable tissues such as fascia and joint capsule.

Suture (stitching) techniques and remova~some of the most common suture techniques include the simple interrupted stitch (almost always applicable). horizontal and vertical mattress stitches {excellent margin eversion, however can strangulate), running and

running lock stitches, figure-of-8 stitch, baseball stitch, and the running subcuticular stitch. Running subcuticular skin closures are usually reinforced with adhesive skin strips. Skin sutures that are designed to be removed, are generally taken out according to the following schedule: face 3-5 days, scalp or trunk 7-10 days, limbs 10-14 days, over a joint 14-20 days, plantar 20-22 days. Care of the operative site varies with anatomical location, and wound healing progress. Stitch maneuvers suitable for tendon include the Bunnell, Kessler, and other lateral trapping methods. Nonabsorbable multifilament sutures are often used to reap proximate tendon to bone, and a variety of tendon anchors are available forth is (see section on tendon transfers). Tissue adhesive---cyanoacrylate ("liquid suture" or tissue glue) can be used as an alternative. to suture material for wound margin reapproximation where there is minimal tendency toward margin disruption. Cyanoacrylate polymerizes when it comes in contact with tissue fluid, forming a flexible adhesive bond between the wound margins. When used for skin closure, cyanoacrylate is reinforced with adhesive skin strips.

BIOPSY TECHNIQUES

lncisional Biopsy---incisional biopsy removes only a selected portion of the lesion in question, while an excisional biopsy removes the entire lesion (theoretically). Obviously, a margin of supposedly "normal" tissue is excised around the lesion in question when an excisional biopsy is performed. Actual pathological assessment of the margins of the biopsy is necessary to determine whether a "clean" margin was created. When performing an incisional biopsy, it is important to select representative portions of the lesion, and more than one sample may be harvested. It is important to accurately identify the samples relative to position about the lesion, and a diagram is helpful in this regard. The pathologist would also benefit from review of the diagram when dealing with a difficult lesion. The surgeon should not struggle to procure a margin of normal appearing tissue in the incisional specimen at the risk of missing representative lesion. Scabs, crusts, and vesicles should be preserved in the specimen, and not destroyed in the surgical preparation of the skin. Most skin biopsies can be performed under !a cal anesthesia, and dilute epinephrine (1:100,000 or 1:200,000 dilution) may aid hemostasis, if it is not contraindicated in the particular patient. The local anesthesia should not be infiltrated directly into the lesion, for fear of spreading potential malignancy or infection, although it has been shown that direct injection below or through a lesion appears to cause no significant microscopic alteration. The area is then prepped and draped in the usual s terile fashion, priOr to biopsy.

Ch.6

Fundamental Techniques and Procedures

125

Punch Biopsy--the punch biopsy is a convenient and effective method of tissue extraction and may be either incisiona! (usually), or excisional when dealing with a large punch and a smaller lesion. In the lower extremity, the 4-mm punch is typically employed, and standard punch sets include punches ranging from 2-8 mm. It should be noted that removal of a specimen 25 YEARS OF AGE, 70 KG MALE OR 60 KG FEMALE).

Duration of action

Class

name

Procaine

Novocaine®

0.75-1 hour

1000

Ponto caine®

2·3 hours

Ester Ester

750

Tetracaine

75

100

Local anesthetic

Proprietary

Maximum single dose (mg) Plain With epinephrine

Lidocaine

Xylocaine®

1-Zhours

Amide

300-350

500

Mepivacaine

Carbocaine®

1-3hours

Amide

400

500

Bupivacaine

Marcaine®

3-12 hours

Amide

175

225

General Anesthesia

General anesthesia causes reversible unconsciousness via CNS depression starting at the cerebral cortex, and proceeding through the basal ganglia, cerebellum, medulla oblongata, and finally, the spinal cord. The anesthesiologist must look for several potentially complicating factors in patients anticipating general or IV sedation anesthetics, in particular cardiovascular disease such as hypertension, coronary artery disease, valve dysfunction or arrhythmia; endocrine disorders such as diabetes me!litus, adrenal insufficiency, or thyroid disease; pulmonary disorders such as COPD, regular cigarette smoking, or chronic cough; Gl concerns such as the last time the patient ate or drank, or whether or not denture plates are present; history of hepatitis; and history of personal or familia! neuromuscular disorder or anesthesia-related adverse reactions, such as malignant hyperthermia. The stages of anesthesia are depicted in Table 6-9.

TABLE6-9. STAGES OF ANESTHESIA. Stage 1-amnesia and analgesia 2-delerium

Plane 1

2 3 1

3-surgical anesthesia

2 3 4 4-medullary paralysis

2

Physiological effects Preanalgesia, memory and sensation intact Partial amnesia and analgesia Total amnesia and analgesia Unconscious, mydriasis, irregular breathing, involuntary skeletal muscle movement Sleeping, residual lid reflex, eyes fixed centrally, regular breathing Pupils dilating, full analgesia, heart rate and BP stable Partial intercostal paralysis, tachycardia and hy potension, hypotonia Complete intercostal paralysis and respiratory arrest, requires artificial ventilation Reversible respiratory paralysis Irreversible cardiovascular and respiratory arrest

Anesthetic agents are used with such frequency that they are improved upon regularly, and new agents become available with regularity. lnhalational agents used to

Fundamental Techniques and Procedures

Ch. 6

159

achieve general anesthesia historically include diethylether, methoxyflurane, and chloroform. More recently, the following agents have been used: Enflurane-supports the cardiovascular system, can be used with epinephrine, does not induce emesis, however can be hepatotoxic.

lsoflurane----maintains heart rate, allows rapid induction and emergence, can be used with epinephrine, does not induce emesis, may be hepatotoxic, however often induces shivering. Halothane--allows rapid induction, acts as a bronchodilator, is nonemetic, however

can be negative inotropic, arrhythmogenic and it sensitizes the myocardium to catecholamines, can be hepatotoxic, often induces postoperative shivering, and is associated with malignant hyperthermia. Sevoflurane---very fast onset and offset, minimal mucus membrane irritation,

excellent cardiovascular stability, an agentthat replacing isoflurane and halothane in everyday general anesthesia. Desflurane--extreme!y fast onset and offset due to very high volatility, however may

be associated with tachycardia, limited potency, and relatively high cost. Nitrous oxide--a low-potency inhalant gaseous anesthetic that has little effect on the heart, liver, kidneys, and lungs, as long as hypoxia does not develop. Nitrous oxide provides profound analgesia, without sensitizing the myocardium, and allows rapid induction and emergence. There is, however, no muscle relaxation and nitrous oxide has been associated with fatal agranulocytosis and spontaneous abortion after prolonged administration. The patient receiving nitrous oxide should be ventilated with 100% 02 during emergence, in order to prevent postanesthetic delayed-diffusion hypoxia. Sedative and hypnotic agents are usually administered as induction and maintenance agents before or in addition to an inhalational anesthetic, in an effort to diminish anxiety, initiate, and maintain CNS depression. Traditionally used agents include barbiturates, benzodiazepines, and narcotics. Neuroleptanalgesia effects somnolence, psychological indifference, amnesia, analgesia, and loss of voluntary movement. As with all IV sedativehypnotic agents, careful assessment at the patient's respiration is mandatory, and supportive measures are often necessary. fentanyl-a short-acting narcotic that depresses respiration, effects analgesia, and is reversed by naloxone. Fentanyl is administered 0.05-0.1 mg IM 30-60 minutes pre-procedure, then titrated as indicated.

sedative-tranquilizer that effects peripheral vasodilatation, somnolence, mental dissociation (perhaps dysphoria), and serves as a strong antiemetic. The sedative dose of droperidol is 2.5-10 mg IM 30-60 minutes preprocedure. The combination of droperidol and fentanyl combines the analgesic effects of fentanyl wiTh the tranquilizing and antiemetic effects of droperidol in a 1:50 (fentanyl: droperidol) ratio. Droperidol-a

Fundamental Techniques and Procedures

160

Ch. 6

Propofo~an IV· sedative hypnotic agent used for induction and maintenance of anesthesia or sedation, and can be used in conjunction with local anesthesia. Midazola~a

short-acting benzodiazepine CNS depressant often used in

conjunction with analgesia to achieve IV conscious sedation. Midazolam is titrated

IV starting with 1 mg, then increasing up to 2.5 mg over at least two minutes, then via small increments (not to exceed 5 mg) while monitoring the degree of sedation. Other medications used in a balanced anesthesia protocol may include phenothiazine tranquilizers such as promethazine and prochlorperazine. Atropine (atropa belladonna) and scopolamine are premedications used to minimize respiratory secretions and to counter parasympathetic overtone by blocking the vagus nerve whenever a positive chronotropic cardiac effect is desired. Ondansetron is a selective 5-HT3 receptor antagonist with strong antiemetic properties, originally used in patients undergoing cancer chemotherapy, and now regularly used following general anesthesia. Ondansetron is administered 4 mg IV slow infusion over 3-5 minutes, in the treatment of postoperative nausea and vomiting. Paralytic agents such as succinylcholine are used to paralyze the body and facilitate endotracheal intubation, cause a fast onset and short duration depolarizing skeletal muscle blockade. Depolarization can be associated with marked increase intragastric and intraocular pressures, and a rise in serum K+. The rise in K+ can be arrhythmogenic in patients predisposed to high serum K+, such as patients with burn, tetanus, trauma, uremia, or lower motor neuron disease (paraplegia, quadriplegia, and muscular dystrophy, Landry-GuillainBarre syndrome). Depolarization may be associated with rhabdomyolysis, masseter spasm, malignant hyperthermia, and dysrhythmia. Atracurium-besylate is a non-depolarizing neuromuscular blocker that competitively binds with the cholinergic receptor sites on the motor end plate, and is often used when depolarization is contraindicated. Muscle relaxants not only facilitate intubation of the trachea, but aid in ventilation and abdominal dissection by diminishing muscle tone. Skeletal muscle paralysis does not cause amnesia or analgesia, and these conditions must first be achieved via administration of rapid onset IV agents before paralyzing the patient.

Spinal and Epidural Anesthesia--these methods should be considered whenever general anesthesia poses greater risk. Spinal anesthesia should not be attempted in the presence of hypovolemia, anticoagulanttherapy or bleeding diathesis (peridural hematoma and spinal compression), asthma or other GOPD, obesity, pre-existing neuromuscular disease (MS, myasthenia gravis, poliomyelitis, spinal metastasist pre-existing lumbosacral disk disease or DJD, local or systemic sepsis, or in the debilitated host Lumbar epidural anesthesia is achieved by injecting local anesthesia into the spinal epidural space, usually below b. Epidural anesthesia prevents spinal headache, can be maintained 24-48 hours for ongoing anesthesia, rapidly resolves after discontinuing anesthetic, is not associated with hypotension and allows segmental blockade. Spinal anesthesia may propagate proximally and effect spinal headache or anesthetize a broader-than-desired area; however the technique uses less local anesthetic than does an epidural block, and is generally easierto perform than an epidural block. The most common acute complication of spinal anesthesia is hypotension caused by sympathectomy. Late complications include postural headache, lumbago, meningitis, spinal neuralgia, cauda equina syndrome (very rare and due to fibrosis), and epidural hematoma.

Ch.6

Fundamental Techniques and Procedures

161

Intravenous Block (Bier Block}-Bier block is commonly used for hand surgery, however it is applicable to the lower extremity, as long as the surgeon and anesthesiologist are prepared to handle a possible toxic reaction to local anesthesia. Two pneumatic

tourniquets are placed side-by-side proximal to the operative site after obtaining IV access in the upper extremity. A butterfly needle is then introduced to the dorsal venous arch, secured, and connected to a 10 ml syringe. The extremity is exsanguinated to the distal tourniquet, and the proximal cuff inflated. Lidocaine, or carbocaine, is then infused using 3 ml/kg of body weight of a 0.5% solution 15 mg/ml), through the butterfly catheter. This effects surgical anesthesia regionally in about 5 minutes, and lasts for 60~90 minutes. When the patient begins to complain of proximal cuff tenderness, inflate the distal cuff over the now anesthetized portion of the extremity, and deflate the proximal cuff only after the distal cuff is inflated. Do not deflate both cuffs at the same time. At about 30~40 minutes after infusion of the local anesthetic agent, slow deflation of the tourniquets can be safely performed as enough of the anesthetic has been bound by local tissues and metabolized to avoid a toxic dose in the systemic circulation. Even if the surgical procedure is finished before 30-40 minutes of elapsed time, the tourniquet must remain inflated at least this long before deflation. Patient positioning and safety in the OR are the responsibility of the anesthesia!~ agist and surgeon, and care must be taken to avoid traction nerve palsy, neuropraxia, injury secondary to pinching or crushing small parts (fingers, skin and other appendages) in equipment and the operating room table.

PADDING, STRAPING, BRACING AND PROSTHESES Padding with the use of felt, rolled cotton, felted-foam, various foams and sponge materials, can be very useful whenever mechanical pressure is associated with pain or skin compromise Hichenification, hyperkeratosis, or wound). Standard pads include the metatarsal projection, toe crest medial longitudinal arch pad, heel cobra pad, heel counter pad, heel lift, aperture or pontoon pads, and bunion and bunionette flange padding. Strapping can be used to support musculoskeletal and ligamentous structures, and include standard applications such as the low Dye strap, digital sling-down strap, the Gibney ankle boot, and variations that combine different methods. A number of arch binders, and bunion and hammertoe shields can be customized or obtained commercially. Similarly, a variety of ankle and Achilles braces (McDavid-type lace~up, AircasfM stirrup, Malleotrain® and Achllliotrain®) can be obtained from surgical supply services or via online services. A wide range of braces is available for support and substitution of lost function. The use of accommodative foot orthoses, an extra depth shoe that is anatomically fitted with a roller sole or metatarsal bar can be used for many conditions, in particular the rheumatoid or insensitive foot Simple adjustments for limb length and gait imbalance can be readily applied. Reverse, adduction and straight shoe last, and custom~made shoes are also available. Surgical shoes, forefoot~relief and heel~relief orthoses, healing sandals, removable cast boots (fixed and adjustable, low- and high-top), ankle-foot orthoses IAFOs), Charcot Restraining Orthotic Walkers (CROW), and total contact casts can be used in the post-traumatic, postoperative and chronic settings. Of particular use in cases of dropfoot are molded ankle foot orthoses that fit into the shoes, and the heavier double upright brace with metal stays that are affixed directly to the shoe. The double upright (contoured aluminum) brace is preferable when ankle edema or deformation prohibits the use of a hinged AFO !Richie brace®, or similar device), a gauntlet-style brace (Arizona AFO"'), or a polypropylene molded AFO. The patellar tendon bearing brace, usually of a clamshell

162

Fundamental Techniques and Procedures

Ch.6

design, can also be used to diminish weight-bearing load transfer through the foot Of course, off~loading can be achieved using appropriately fitted crutches or a walker to aid ambulation. Off-loading of the lower extremity can be enhanced with the use of a wheelchair, a Roi!-A-BoufiD or Turning Leg Caddy"'', or, as a last resort, bed rest Braces and

shoe gear need to be periodically inspected, along with the patienfs lower extremities, in order to monitor for the possibility of cutaneous compromise, especially in those with neuropathy and/or vasculopathy, immunocompromise or steroid dependence, and

collagen disorders.

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities

163

RECONSTRUCTIVE SURGERY: BASIC CONDITIONS AND DEFORMITIES NAIL SURGERY The ingrown toenail (onychocryptosis) involves nail pathology wherein the nail plate has

grown into the ungual labia, with or without concomitant infection. Paronychia (also termed whitlow or run-around) consists of nail fold erythema, edema, and pain. Ingrown toenails are commonly classified as self-inflicted or iatrogenic. Self-inflicted is where the patient chronically cuts the nail too short or incorrectly angulates the nail nipper deep to the nail fold. Other causes of ingrown toenails include congenital abnormalities where the matrix is maligned and produces an incutvated plate; primary soft tissue hypertrophy wherein the primary pathology involves the adjacent nail fold, which is enlarged and overlaps the plate; and combinations of incurvated nail plate and nail fold hypertrophy. Nail fold hypertrophy can also develop secondary to chronic plate incurvation and repetitive wound irritation with the formation of a pyogenic granuloma. Treatment options include: Avulsion~ treatment should

involve education as to proper nail trimming technique, as well as acute intervention to alleviate paronychia and allow the wound to heal. No amount of antibiotic will cure an infected ingrown toenail until the offending nail border is satisfactorily removed. The mainstay of treatment for onychocryptosis is avulsion of the offending nail border. This effects temporary removal of the margin, and allows subsequent regeneration over the ensuing months. Avulsion can be performed with, or without, local anesthetic digital blockade, depending upon the extent of plate removal necessary to alleviate the condition and other factors, such as peripheral sensory status. Avulsion is followed by local wound care, perhaps concomitant use of oral antibiotics if paronychia and/or systemic factors warrant doing so. Re~evaluation should be performed between 2 and 3 weeks after avulsion, at which time proper nail trimming technique is reviewed with the patient Temporary removal of the offending border is generally recommended in a firsHime case of ingrown toenail, whereas recurrent onychocryptosis may be best treated with permanent matrix ablation via either chemical or surgical matrixectomy. Phenol and Alcohol (P & A) and Sodium Hydroxide (NaOH) matrix ablatiot>-these techniques of permanent partial or total nail matrix ablation are rather simple, and inflict minimal pain. The P & A involves three 30Hsecond applications (causing the nail bed and matrix to appear ashen gray) of 90% phenol followed by rinsing with alcohol (70-90% isopropyl or ethyl), then copious saline lavage and application of silver sulfadiazine cream and a sterile bandage. The NaOH procedure involves application of 10% NaOH until the matrix and nail bed tissues appear ashen gray-brown (about 20-30 seconds); followed by acetic acid (vinegar) rinse, then copious saline lavage, silver sulfadiazine cream, and a sterile bandage. It is important to avoid excessive hemorrhage during application of either chemical cauterant, as dilution could inactivate the chemical agent. A digital tourniquet can be useful in this regard, and must be removed after applying the chemical. The main disadvantage to both the P&A and NaOH procedures is the creation of a chemical injury that denatures proteins much as a thermal burn would do. The wound remains open and draining for 3-4 weeks. Chemical matrixectomy is generally not performed in the presence of advanced paronychia, and it is recommended that the patient undergo avulsion of the offending border/s followed by local wound care, and perhaps oral antibiotic therapy

164

Reconstructive Surgery of Basic Conditions and Deformities

Ch. 7

(cephalexin), with planned matrix ablation to be performed anytime after resolution of the paronychia and before recurrence of onychocryptosis. It is also advisable to have the patient initiate oral antibiotic therapy 24 hours before the planned matrixectomy.

Matrixectomy techniques (true "open" matrix excisions) employing eponychial and nail fold incision are numerous, and include: Modified Steindler Matrixectomy-a useful technique for incurvated or iatrogenic chronically ingrown toenails. This is often employed afterfai!ed chemical matricectomy, or when an "open" excision is desired. The procedure is used to excise the matrix, and does not address nail fold hypertrophy. Frost Partial MatnXectomy-employs a right angle incision into the nail fold allowing reflection of the fold and exposure of the underlying corner of the matrix, following nail plate avulsion (Figure 7-1. The involved area of nail bed is also excised. The right angle incision is actually rounded gently to avoid slough of the apex. Winograd Partial Matricectomy--uses 2 incisions, one longitudinal through the nail bed, and a second semi-elliptical incision through the adjacent nail fold, to create a wedge of nail fold and bed that are excised after avulsion of the nail plate (Figure 7-2). Hypertrophic ungual labium is readily excised. Ungual Labioplasty-involves a wedge-shaped excision ofthe hypertrophic labium, and is useful only for reduction of nail fold hypertrophy. Suppan Panhypertrophy Matrixectomy-uses a fish mouth incision through the nail folds surrounding the entire nail plate, allowing excision of surrounding hypertrophic folds and underlying matrix and bed.

I~

( Figure 7.1

Figure 7.2

I

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities

165

D

( ''~--J..'

:·~·~

Figure 7.3 Zadik (Quenu) Matrixectomy-an H-shaped incision is made with the two vertical arms through the nail medial and lateral folds, and the transverse arm through the proximal nail fold (Figure 7-3). The proximal nail fold is then reflected proximally and the underlying matrix and proximal bed excised. The exposure a!lows removal of subungual exostosis if necessary. Closure involves proximal advance of the distal nail bed flap, allowing closure without shortening of the distal phalanx.

SUBUNGUAL EXOSTOSIS Dorsal proliferation of the distal phalanx into the overlying nail plate can effect plate deformation, often described as a pincer nail, with or without associated onychocryptosis (Figure 7-4). Subungual exostosis can be of traumatic origin or, when capped with fibrocartilage, congenital due to osteochondroma. Osteochondroma is usually observed early in life, between 10-25 years of age, onset on or before puberty, and most commonly is observed in females (F: M ratio 2:1 ). Eradication of a symptomatic subungual exostosis or osteochondroma is via nail plate avulsion, and exposure of the phalangeal lesion with a distal fish mouth incision, or via longitudinal or semi-elliptical nail bed incision or excision, respectively. The semi-elliptical incisions are used to create a wedge excision of associated nail bed, when the pathology has caused nailed scar or other lesion. It may not be necessary to perform nail plate avulsion when the exostosis is small, however exposure of the exostosis should not be compromised by trying to preserve nail plate attachment. Osteotripsy may be a useful method for reduction of the osseous prominence. The excised lesion should be submitted en bloc for pathological inspection, and specimens should be obtained for bacterial C&S, as well.

Figure 7.4

166

Reconstructive Surgery of Basic Conditions and Deformities

Ch. 7

HAMMERTOES

Digital contraction deformities include hammertoes, clawtoes, and mallet toes. The deformities can be flexible or rigid, and the Kelikian push-up test is used to assess the degree of flexibility. Anatomic considerations include extrinsic and intrinsic muscufature, with emphasis on the MTPJ extensor hood expansion (Figure 7-5).

Extensor sling Metatarsal head

Capsule

Plantar interosseous

Dorsal interosseous

~ransverse metatarsal

. Lumbncal~ ~

ligament

Flexor tendons

Figure 7.5

Dynamic etiologies of digital contracture include:

Flexor Stabilization-the most common cause of pathological digital contracture (>70%}, itself caused by late stance and propulsion phase hyperpronation; the FDL and FOB fire earlier and longer to stabilize the hypermobile forefoot, thereby overpowering the interossei with resultant dorsal subluxation of the MTPJ; associated with adductovarus fourth and fifth digital deformities.

Extensor Substitution-this is associated with pes cavus, foot drop, and anterior compartmentweakness, wherein the EDL overpowers the lumbricales during swing phase, and causes dorsiflexion of the MTPJs; results in a high degree of MTPJ subluxation and retrograde plantar buckling ofthe metatarsus. Flexor Substitution-this is the least common cause of digital contracture, and occurs due to weakness of the triceps surae wherein the deep posterior leg muscles compensate and thereby overpower the interossei during stance phase, particularly during propulsion; the digits are seen primarily in the sagittal plane, with minimal varus rotation; a calcaneus gait may develop and this may be observed following over-lengthening (TAL) of the heel cord. A mallettoe involves sagittal plane plantarflexion of the DIPJ, and may be associated with a long toe. A congenital curly (varus) toe involves adduction contracture and varus rotation of the DIPJ, usually toes 3-5, and radiographs (upon reaching skeletal maturity) may show a delta-shaped middle phalanx. Hammertoes involve dorsiflexion of the proximal phalanx and plantartlexion of the middle phalanx, perhaps with transverse plane deviation in the direction of flexor plate subluxation. The clawtoe involves plantarflexion of both the PIPJ and the DIPJ, and is often seen in cases of extensor substitution (Figure 7-6).

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities MPJ extension

167

MPJ extension

DIPJ flexion

Figure 7.6 Symptoms associated with advanced digital contracture deformity include painful PIPJ motion, painful hyperkeratotic lesion(s), inability to wear regular shoes, contracted painful toe that is short and possibly dorsiflexion deformity of the DIPJ. Radiographic findings include joint narrowing and superimposition at the contracted joint levels, gun-barrel sign on the AP view due to long axis imaging of the phalanx in either dorsiflexion (proximal) or plantarflexion (middle), shortened contracted toe, DJD of the PIPJ and MTPJ, and periarticular osteoporosis. Biomechanica! signs of digital contraction deformity include the presence of hypermobile first ray and other hyperpronation findings (flexor stabilization), or Stage I pes cavus as seen in anterior cavus and dropfoot related extensor substitution. Postoperative management involves the use of a wooden or stiff-soled surgical shoe, perhaps with build-up when the pins cross the MTPJ, and may involve casting depending upon other procedures performed. A variety of nonsurgical options are availablefortreatmentof symptomatic digital contractu res, including the use of larger shoes with an extra-depth toe box, digital retainers such as dorsal (early, flexible deformity) and/or plantar (advanced, rigid deformities) toe crests, sling-down toe-MTPJ splints (Budin splint), sling-down or predislocation taping, pads and shields, and periodic debridement of hyperkeratoses. The use of a supportive insole with a metatarsal projection pad can also help to realign the MTPJs, and enhance nonsurgical treatment of hammertoes. When nonsurgical efforts fail to effect satisfactory relief, then a variety of surgical Interventions can be considered. Like the nonsurgical interventions, operative measures also take into consideration the alignment of the MTPJ as well as that of the IPJs. Surgical procedures for repair of contracted digital deformities include:

Flexor tenotomy-operative procedures for correction of digital deformities will vary depending on the degree of toe and MTPJ flexibility. The reducible lesser digital deformity may be responsive to flexor tenotomy, both long and short (flexor set), however the use of this as an isolated procedure is rarely indicated and does not provide a long lasting correction in most cases. Indications include plantarilexion deformity at the PIPJ or DIPJ that is completely reducible with manipulation. Attention may

168

Reconstructive Surgery of Basic Conditions and Deformities

Ch. 7

only be required at the long flexor and the IPJ capsule proximally and distally. Generally a plantar stab incision is indicated, however a mild contracture may be approachable through a medial or lateral exposure. This procedure can be useful in conjunction with PIPJ arthrodesis in the presence of persistent mallet toe, when the toe is pin-stabilized in a position ofslightDIPJ dorsiflexion.

Extensor tenotomy and capsulotomy--these are also rarely indicated as isolated procedures, and are commonly useful in conjunction with PIPJ stabilization and MTPJ relocation (see sequential release).

Resection arthroplasty--a variety of hammertoe procedures can be used, including the Post arthroplasty wherein the head of the proximal phalanx is resected transversely at the level of the metaphyseal flare. Resection of the base of the proximal phalanx (Gotch and Kreuz) is wrought with complications due to destruction of the intrinsic muscle attachments to the base, and must be combined with adjacent digital stabilization and syndactyly in order to avoid floating or flail toe. Digital stabilization---in general, multiple digital stabilizations, consisting of PIPJ fusion and MTPJ relocation, are indicated for correction of advanced, dynamically induced digital deformities. Such deformities are usually associated with lesser metatarsalgia, concomitant plantar hyperkeratosis (intractable plantar keratoma [IPK] or diffuse plantar tyloma), dorsal PIPJ and distal digital tip and hyponychium hyperkeratosis, mechanical onycholysis and nail dystrophy that predisposes to fugal infection, and rigidity or incomplete relocation with push-up loading. Transverse plane deformity may also be present, in particular when the second toe crosses over or, less commonly, under the hallux in the presence of associated HAV and bunion deformity. The crossover second toe is particularly hard to completely realign. Isolated interphalangeal arthroplasty can be useful in the presence of an unusually long digit that is contracted secondary to shoe crowding, however it is rarely indicated for the treatment of multiple, dynamically-induced hammertoes. Moreover, multiple adjacent PIPJ arthroplasty may IBBd to digital instability and recurrent deformity, in the postoperative phase. It can be useful to approach the deformity by means of sequential release. The sequential release for advanced hammertoe deformity (Figure 7-7) includes the following steps: 1. Long extensor hood recession, 2. Long extensor tenotomy (open Z-tenotomy or transverse), 3. PIPJ capsulotomy and arthroplasty or arthrodesis, 4. MTPJ capsulotomy, and 5. MTPJ flexor plate release (made easy using the McGiamry metatarsal elevator) and repair. The Kelikian push-up test (apply a dorsally-directed force to the plantar surface of the metatarsal head, to simulate ground reactive force) is performed between each step in the sequential release, and progression to the next level of release is not necessary if the digit and MTPJ properly align in a relaxed attitude with simple push-up loading. Full sequential release is used in the correction of advanced clawtoe or hammertoe deformities. It is necessary to perform the Z-tenotomy when advanced dorsal contracture is corrected, otherwise it may be difficult to reapproximate the tendon upon closure. Medial or lateral

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities EDL

8 A Phalangeal head

~cted

c

D

F

G

Figure 7.7

Figure 7.8

169

170

Reconstructive Surgery of Basic Conditions and Deformities

Ch. 7

dislocation of the flexor plate will cause a medial or lateral deviation of the digit upon push-up loading, and is usually related to chronic synovitis and subluxation of the flexor plate to the side of deviation. Flexor plate subluxation must be addressed at the time of sequential release, and an anchor suture may be necessary in order to maintain correct, balance alignment. In some cases, persistent deformity may require MTPJ capsulorrhaphy

with wedge excision of redundant capsule, or metatarsal osteotomy lmedia! or lateral transpositional and/or shortening) for satisfactory correction.

Interphalangeal arthrodesis-this entails several modifications, including end-to-end (non-fixated, described by Soule; K-wire stabilization, described by Taylor and Selig); and peg-in-hole (pike, described by Higgs; or rounded, described by Young) techniques. Arthrodesis is generally indicated in cases of multiple lesser digital deformities, which is the typical presentation when treating dynamically induced (flexor stabilization, extensor substitution, or flexor substitution) contractu res of the toes and MTPJs. Either peg-in-hole or end-to-end fusion can be used, based on surgeon's preference. If shortening is a concern, then the end-to-end fusion may be used, as less shortening is encountered. The peg-in hole may more reliably achieve radiographic fusion mass consolidation, however, the functional result of a fibrous pseudoarthrosis of an end-to-end arthrodesis has been shown to function as well as the radiographically solid fusion in many cases. After resection of the articular surfaces, arthrodesis is completed with pin stabilization, starting the 0.045" (or 0.062" if desired) K-wire at the base of, or hole in, the middle phalanx and driving it distally across the dorsiflexed and straightened DIPJ, then out the tip of the digit centrally. Care is taken to avoid perforation of the nail bed. The K-wire is then retrograded proximally across the PIPJ to the base of the proximal phalanx, then across the realigned MTPJ if indicated by persistent upon push-up loading. Stabilization of the MTPJ is performed with the toe situated half way between the horizontal substrate (parallel to the bottom of the foot), and in line with the metatarsal declination angle. Digital alignment is slightly over-corrected in plantartlexion, and the pin crossing the MTPJ maintained for 3-6 weeks. The PIPJ fusion is stabilized for 5-6 weeks, or until radiographic and clinical evidence of fusion is observed. Placing the pin across the MTPJ requires use of a built-up surgical shoe postoperatively, in order to avoid repetitive mechanical flexure and pin breakage in the MTPJ (Figure 7-8). Interphalangeal arthrodesis can also be achieved using bioabsorbable fixation pins or screws, and other devices made to press-fit or snap-fit once seated in either the proxima! and/or middle phalanges. It is important to keep in mind that if absorbable fixation, or a device that is limited to just the interphalangeal joint/s, is used to achieve digital fusion, attention to the alignment of the corresponding MTPJ may require separate fixation or metatarsal osteotomy, if the push-up test fails to display satisfactory MTPJ realignment After realignment of the toe and MTPJ, the long extensor tendon is re-approximated in corrected alignment, followed by subcutaneous and then skin closure. Flexor tendon transfer (Girdlestone, Foerster and Brown)-can also be useful for the correction of hammertoes and clawtoes, however care must be taken to transfer the sectioned flexor tendon slips from plantar to dorsal on the phalanx in a subperiosteal fashion (to avoid constriction of digftal vessels), or through a drill hole in the phalanx, and it is possible to effect a PIPJ rocker-bottom deformity unless arthrodesis is performed (obviating the need for flexor tendon transfer). Sgarlato's modification of the Girdlestone procedure can be used for the correction of hammertoes and clavvtoes with MTPJ

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities

171

subluxation, and serves to redirect the long extensor tendon's pull to that of a stabilizing

influence on the toe and MTPJ. Two incisions are used, 1 medial or lateral aspect at the proximal phalanx, and an adjunct dorsal incision more to the side opposfte the medial or lateral incision. The long flexor tendon is split and transferred dorsally in a subfascial fashion and sutured to itself and the dorsal hood expansion as a sling dorsally atthe level of the proximal phalangeal shaft. Care must be taken to transfer the splittendon segments in a subfascial (deep fascia) fashion, in order to avoid circumferential constriction of the subcutaneous neurovascular elements coursing to the toe tip. The transfer results in decreased PIPJ range of motion. Dockery and Kuwada modified the transfer by use of a dorsal-to-plantar drill hole in the anatomic neck ofthe proximal phalanx. Moreover, a rocker bottom PIPJ or swan-neck deformity can be created if too much tension is placed within the transferred long flexor. PIPJ arthrodesis is generally considered a more effective and lasting method to stabilize the digit and convert the long flexor to a stabilizing influence on the MTPJ, particularly for the intermediate lesser digits. A flexor tendon transfer may be applicable to the fifth toe, or in the presence of congenital absence of the middle phalanx.

BUNION DEFORMITY AND HALLUX ABDUCTO VALGUS First metatarsal anatomy pertinentto the bunion deformity and hallux abductovalgus (HAV, hallux valgus) surgery includes the proximal physeal plate, which closes at about 15-18 years of age, the primary nutrient artery situated laterally about 2 em proximal to the articular surface, and the peri-articular soft tissue sleeve and sesamoid apparatus. When the hallux abducts and the first metatarsal adducts (metatarsus prlmus varus), the dorsomedial eminence of the first metatarsal head becomes clinically prominent, and is termed a "bunion." The term bunion basically refers to a bump, traditionally, from the old French buignon, from buigne or "bump on the head." (Similarly, a prominent fifth metatarsal head is often referred to as a bunionette.) Radiographic Angular and Anatomic Relationships Related to HAV~there are a number of angular relationships useful in the assessment of HAV, including:

HalluxAbductusAngle(HAA}--me angle formed by the intersection of the bisection ofthe shaft of proximal phalanx and the bisection of the shaft of first metatarsal, normally 15°, and representative of the relative position of the hallux to the first metatarsal (Fig 7-9). Distal Articular Set Angle (OASA}--the angle formed by the intersection of a line perpendicular to the effective cartilage of the base of the proximal phalanx and the bisection of the shaft of the proximal phalanx, normally 7.5°, and representative of the relative position of the effective cartilage to the shaft of the proximal phalanx. An increase in DASA may indicate lateral deviation in me shaft of the proximal phalanx (Fig 7-10). Proximal Articular Sol Angle (PASA}--the angle formed by the intersection of a line perpendicular to the effective articular cartilage of the metatarsal head and the bisection of the shaft of the first metatarsal, normally 7.5°, and representative of the relative position of the effective cartilage to the shaft of the metatarsaL An increase in PASA indicates lateral deviation (adaptation) ofthe cartilage surface (Fig 7-11).

172

Figure 7.9

Reconstructive Surgery of Basic Conditions and Deformities

Figure 7.10

Figure 7.11

Ch. 7

Figure 7.12

Metatarsus Primus Adductus or First lntennetatarsal Angle (first IMA)--the angle formed by the intersection of the bisection of the shaft of the first metatarsal and the bisection of the shaft of the second metatarsal, normally 8°, and representative of the angular relationship between the first and second metatarsals. An increase in the first IMA makes the head of the first metatarsal more prominent medially, and predisposes to HAV (Rg 7-12).

Hallux lnterphalangeusAngle (HIA)--the angle formed by the intersection of the bisection of the shaft of the proximal phalanx and the bisection of the distal phalanx, normally 10", and representative of hallux interphalangeal joint (HIPJ) or phalangeal deformily (Fig 7-13). Metatarsal Protrusion Distance-the distance between two arcs which, respectively, represent the lengths of the first and second metatarsals. A line representing the bisection of the first metatarsal is extended to intersect with a line representing the bisection of the second metatarsaL A compass is placed at the point of intersection and an arc drawn from the distal portion of the first metatarsal and another arc is drawn from the distal portion ofthe second metatarsaL A positive millimeter distance is used to indicate a longer first metatarsal. A negative distance is used to indicate the second metatarsal being longer than the first Normal is± 2 mm, and represents the relative length between the first and second metatarsals. A longer first metatarsal may be associated with hallux limitus, whi!e shortening may correlate with lesser metatarsalgia (Fig 7-14).

Metatarsus Adductus Angle (MAA)--the angle formed by the intersection of the bisection of the lesser tarsus and the bisection of the second metatarsaL The lesser tarsus is bisected by obtaining the midpoint between the anterior-medial corner of the first cuneiform and the posterior-medial corner of the navicular, and the midpoint between the anterior-lateral corner ofthe cuboid and the posterior-lateral corner ofthe cuboid. The midpoints are then connected and a perpendicular is drawn to this line. The MAA is normally 10-20"; and represents the degree of adduction of the metatarsus. As the MAA increases, the foot becomes more adducted and there is greater chance for development of HAV. Moreover, the first IMA becomes pathologically significant at a lower degree in the presence of increased MAA (Fig 7-15).

Tibial Sesamoid Position (TSP)--the position the tibial sesamoid is compared to the bisection of the first metatarsal shaft, and designated as position 1-7; normally 1-3, and traditionally representative of the need to remove the fibular sesamoid. TSP 4 predicts erosion of the tibial sesamoid against the plantar central crista of the metatarsal

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities

~\ dl

173

,,1\ ,fJ •2 ,, '

''I

l-

(!.1, "'

Figure 7.13

Figure 7.15

Figure 7.14

Figure 7.16

head, and relative deviation of the metatarsal head medially so that the fibular sesamoid is positioned in the first intermetatarsal space. When the first metatarsal plantarflexes, a relative distal position of the sesamoids may appear, whereas dorsiflexion causes relative proximal positioning (Fig 7-16). Shape ollhe Metatarsal Head-the intrinsic stability ofthe MTPJ varies with the shape of the metatarsal head. A round head is theoretically most unstable and likely to deviate into HAV; a square head is considered stable, and a square head with a central ridge is considered most stable and may be seen in cases of hallux rigidus (Fig 7-17). First MTPJ Position (Congruous, Deviated or Subluxated)-first MTPJ alignment can be congruous, deviated or subluxated. In the congruous joint, a parallel relationship exists between the effective articular cartilage of the metatarsal head and the phalangeal base. The deviated joint displays extra-articular intersection of the lines representing the effective articular surfaces of the metatarsal head and phalangeal base. The sub luxated (subluxed) joint displays intra-articular intersection of the lines representing the effective articular suliaces of the metatarsal head and phalangeal base (Fig 7-18).

~ j

./Ji

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I

I; I

Figure 7.17

I

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Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities

174

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II Figure 7.17

Figure 7.18

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Congruous

II\~

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Subluxated

Structural, Positional, and Combined HAV Delormilies-HAV can be classified as to whether or not the first MTPJ deformity is structural, positional, or a combined deformity based on the formulae depicted in Table 7·1.

Table 7-1. FORMULAE FOR STRUCTURAl, POSITIONAl, AND COMBINED FIRST MTPJ DEFORMITIES. TYPE OF DEFORMITY

FORMULA

PASAAND/ ORDASA

FIRSTMTPJ ALIGNMENT

Structural Positional

PASA + DASA ~ HAA PASA + DASA < HAA

PASAorDASA PASA and DASA

Abnormal, congruent Normal, deviated or subluxed

Combined

PASA + DASA < HAA

PASAorDASA

Abnormal, deviated or subluxed

ANGLE

Example 1: HAA ~ 35", DASA ~ 3", PASA ~ 5" (3 + 5 < 35, so MTPJ displays positional deviation or subluxation, as PASA and DASA are normal). Example 2: HAA ~ 35", DASA ~ 7", PASA ~ 28" (7 + 28 ~ 35, so MTPJ displays a congruous structural deformity, and PASA is abnormal). Example 3: HAA ~ 35", DASA ~ 1", PASA ~ 18" (1 + 18 8° is consistent with splayfoot deformity, and the tailor's bunion is often the primary area of patient concern. Surgical goals in the treatment of tailor's bunion focus on elimination of prominent lateral exostosis, either dorsal or plantar; along with correction of structural deviations such as excessive fourth IMA and/or lateral bowing. Adjunct procedures may include correction of an adductovarusflfth hammertoe. Specific procedures for correction oftailor's bunion deformity include:

Lateralexostectomy-this procedure (Fig 7-48), performed performed on mild tailor's bunions as an isolated procedure, or in conjunction with other structural corrections and a variety of fifth metatarsal osteotomies. If an over-aggressive lateral exostectomy is performed (staking the metatarsal head) in the presence of structural bowing or a high fourth IMA, excessive fifth MTPJ laxity will lead to adductovarus fifth toe contracture and retrograde MTPJ buckling with recurrence and worsening of deformity. fifth metatarsal head excisiotr-a radical procedure that involves head resection at the

anatomic neck and usually well tolerated in less ambulatory individuals due to the fifth ray's independent axis of motion; it may be indicated too, in cases of fifth metatarsal head osteomyelitis, tumor or avascular necrosis.

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities

Hohmann

Reverse Wilson

Figure 7.49

Figure 7.48

Mitchell

Figure 7.51A

197

Figure 7.50

Thomasen's

Figure 7.51 B

Hohmann osteotom~a transverse through-and-through osteotomy at the anatomic neck, usually stabilized with a K-wire (Fig 7-49).

Reverse Wilson osteotomy---an oblique osteotomy from distal-lateral to proximalmedial often floated but better to be stabilized with a K-wire (Fig 7-50).

Mitchell osteotomy---a variation of the first metatarsal osteotomy that may be limited by a narrow fifth metatarsal neck; this osteotomy is at risk for dorsiflexion if subjected to early weight bearing (Figure 7-51A).

Thomasen's osteotomy--a peg-in-hole variation of the Hohmann osteotomy, usually stabilized with a K-wire (Fig 7-51 B).

198

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities j

Figure 7.52

Figure 7.53

Figure 7.54

Reverse Austin osteotomy-a sagittal plane chevron limited by the width of the metatarsal neck and stabilized with a K-wire or absorbable pin (Fig 7-52).

Closing adductory osteotomy at neck (MercadoHistal transverse plane medially based wedge osteotomy with an intact lateral cortical hinge, stabilized wH:h either a K-wire or stainless steel wire suture, or both (Fig 7-53).

Closing adductory base wedge osteotomy (Gerbett}-a transverse plane medially based wedge osteotomy with an intact lateral cortical hinge, fixated with a K-wire and or stainless steel wire suture, or made oblique to facilitate lag screw fixation

Oblique wedge osteotomy-located at the apex of the bowing deformity, fixated with a Kwire and or stainless steel wire suture, or lag screws (Fig 7-54). HEEl SURGERY Approximately 15% of all adult foot complaints are related to disorders of the heel. The circulation to the heel entails the medial calcaneal branches of posterior tibial artery medially, the communicating branches of the peroneal and lateral malleolar arteries laterally and plantarly, and communicating branches posteriorly. The neutral or vascular triangle, of the calcaneus is the radiolucent area observed in the lateral radiograph, inferior to the sustentaculum tali within the body of the calcaneus, where the subtalar pressure trabeculae combine with traction trabeculae formed in response to the pull ofthe plantar fascia and Achilles tendon are seen under sustentaculum tali.

Plantar Fascitis and Heel Spur Syndrome---this condition results tram prolonged, excessive tension in the plantar fascia, usual!ysecondaryto hyperpronation of the STJ/MTJ, and eventually leads to fasciosis at or near the attachment of the plantar fascia to the calcaneus. Overtime, an elongated plantar spur may also develop atthe attachment of the fascia. Stress fracture may lead to development of a prominent plantar protrusion. Chronic inflammation of the fascia, with or without spur formation, may also be associated with distal tarsal (calcanea!) tunnel syndrome. The diagnosis is made based on localization of

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities

199

focal, deep tenderness to the fascial attachment to the calcaneus, the presence of similar pain upon activation of the plantar windlass (simultaneous dorsiflexion of the MTPJs and ankle, with the knee extended); post-static dyskinesia, and radiographic evidence of a plantar spur in about 75% of cases. A distinct plantar spur need not be ·present to effect pain. Differential diagnostic considerations for plantar heel pain include lumbosacral radiculopathy, systemic arthritis, tarsal tunnel syndrome, subcalcaneal bursitis, contusion

or local trauma, stress fracture, entrapment neuropathy of the lateral plantar nerve and its muscular branch, diffuse idiopathic skeletal hyperostosis (DISH) syndrome, Paget's disease, and heel neuroma. A bone scan may be helpful in resistant cases when stress

fracture is suspected. Conservative treatment combines biomechanical, pharmacological, physical, and surgical therapies (Table 7-4).

TABLE 7-4. TREATMENT HIERARCHY FOR PLANTAR FASCIITIS AND HEEL SPUR SYNDROME. Intervention

Slagel

Stage II

Pharmacological

NSAID Local steroid Oral steroid

NSAID

Biomechanical

Low Dye strap Custom orthotic Prefabricated Roller sole

Stage Ill

Stage IV

Immobilization

orthotic Physical Surgical

Ice Flexibility

Iontophoresis

Night splint Dynamic splint ESWT

Cold ablation

microdebridement, fa scioto my, spur resection;

bursectomy fxtracorporeal Shockwave Therapy(ESWT}-shockwaves consist of high amplitude, fast rising, asymmetrical, low frequency (>500 bar in 33 nanoseconds) sound energy that imparts intense pressure to the target tissues, namely the plantar fascia. Shockwaves can be generated by means of piezoelectric crystals or ceramics, electromagnetic energy, and electrohydraulic vaporization of water. Shockwaves have been used in the treatment of tendinosis calcarea (shoulder), lateral epicondylitis (tennis elbow), cedial epicondylitis (golf elbow), chronic calcifications (thigh, apophysis), patellar tendinitis, ossoue nonunions and pseudarthrosis, nephrolithiasis, and microscopic studies into the potential use in the treatment of cancer and CNS lesions are alos underway. In order to treat plantar fasciitis, shockwaves must deliver 0.26·0.32 mJ/mm2 of energy to the target fascia. This causes physical alteration of small axons, inhibiting impulse conduction, chemical alteration of pain receptor neurotransmitter, and hyperstimulation analgesia (gate control); as well as neovascularization. Resultant tissue absorption and deformation create a wound healing response that, in 3-6 weeks, may relieve chronic pain related to plantar fasciitis. Weight bearing is immediate following ESWT. Potential complications of ESWT include subcutaneous hematoma, skin erosion, swelling, petecchial hemorrhage, pain and

200

Reconstructive Surgery of Basic Conditions and Deformities

Ch. 7

paresthesia, and vasovagal syncope. Contraindications to ESWT include pregnancy, children, nerve damage, tarsal tunnel syndrome, tarsal tunnel syndrome, osteoporosis, rheumatoid arthritis, peripheral vascular disease, infection or tumor, bleeding diasthesis,

cardiac pacemaker, and healing fracture. Radiofrequency cold ablation (Coblationm} microdebridement-the plantar fascia can be debrided in an open fashion by means of a small incision over the proximal portion of the fascia, and application of 15-20 high voltage radiofrequency impulses in a saline medium that creates a plasma layer between the concentric electrodes at the tip of the probe, and disrupt the molecular bonds in the target tissue, thereby effecting localized fascia debridement with minimal collateral tissue destruction. Non~weight bearing, or partial weight bearing is employed following cold ablation debridement of the plantar fascia, varying with the nature of the plantar skin incision, surgeon's preference, and the amount of debridement undertaken.

Plantar Fasciotomy and Calcaneal Spur Resection---exposure of the attachment of the plantar fascia to the calcaneus, and the plantar spur, can be achieved through a plantar transverse, longitudinal, or oblique incision. Of historical .interest is the distally-based U~shaped pedicle flap Griffith incision, which can be used to expose the entire plantar aspect of the calcaneus. The medial DuVries approach can also be used, however this incision makes the medial calcanean nerves vulnerable to post-incisional entrapment. The deep plantar fascia is identified and sectioned from the calcaneal tuberosity, and the plantar spur resected. A small segment of the most proximal fibers of the plantar fascia is retained for pathological inspection. It is important to re-establish a normal cortical contour when the spur involves prominent plantar protrusion, even if fascitis has been essentially resolved with conservative measures. Care must be taken to avoid injury to the lateral plantar nerve and its branches, and over~aggressive resection of bone as this could weaken the calcaneus and predispose it to fracture. Other complications include recurrence, hematoma, scar pain, and chronic plantar enthesitis. A compressive dressing is applied, and early ankle range of motion and 3 weeks non-weight bearing ensue. Non~weight bearing is necessary in order to allow the plantar skin wound to heal. A wide range of techniques have been used over the years for the treatment of recalcitrant plantar heel pain, some of which are of historical interest only while others show useful application. Variations on the general theme of fasciotomy and spur resection include minimal incision or semi-closed approaches wherein the fascia is released and the spur remodeled under fluoroscopic guidance, or via topographical guidance and identification of palpable landmarks. Instep plantarfasciotomy, localized to the mid portion ofthe medial band of the plantar fascia, and not addressing the calcaneus, can also be useful in some cases. Historically, spur reduction has been addressed with a countersinking osteotomy, or a rotational osteotomy combined with tendoAchillis lengthening. Endoscopic Plantar Fasciotomy (EPF}-endoscopic plantar fasciotomy has been shown to be a useful option for releasing the fascia, and is based on the theory that the spur need not be remodeled in order to alleviate plantar heel pain. The procedure is performed under local or general anesthesia, and uses a blunt obturator to channel from medial to lateral across the heel after initially making an incision through which the obturator is passed. The deep fascia is visualized by passing a slotted cannula with obturator from medial to lateral and rotating the slot toward the fascia. An L~shaped blade is then inserted from lateral to

Ch. 7

Reconstructive Surgery of Basic Conditions and Deformities

201

medial while viewing through the endoscope, which is inserted from medial to lateral. The blade is turned dorsally at the medial margin of the fascia, and then pulled laterally. Fasciotomy is directly viewed, and several passes of the blade are usually necessary to adequately section the fascia. Care is taken when inserting and removing the L-shaped blade through the lateral incision. The wound is Javaged and skin closure performed, followed by application of a compressive dressing. It is also possible to reduce bony prominence endoscopically with the rota-osteotome and shaver, however this is generally

not done. External Neurolysis-if the cause of plantar heel pain is thought to be entrapment neuropathy of the lateral plantar nerve and/or its muscular branch (inferior calcaneal nerve and calcaneal tunnel syndromeL then external neurolysis of the nerve trunks may be in order. External neurolysis, however, is usually performed in conjunction with fasciotomy and spur reduction. External neurolysis is best performed with the use of fine-tipped instrumentation and Ioupe magnification.

Calcaneal Decompression-decompression of calcaneal intramedullary pressure, via multiple small drill or K-wire holes aligned obliquely from posterior-proximal to anteriordistal (dorsal cortex to plantar cortex) through the cortex of the calcaneal body, has also been espoused as a treatment for plantar calcaneal pain. Currently, this procedure is primarily of historical interest only, although there is some basis to its use. In essence, the decompression holes result in cortical fracture when subjected to the pull of the Achilles tendon and plantarfascia, thereby reducing tension in these soft tissues after resumption of weight bearing. Calcaneal joint depression fracture is an obvious risk of the decompression technique. Haglund's Deformity-this deformity consists of prominence of the posterosuperior aspect (bursal projection) of the calcaneus. It can be structural or positional, or a combination of both. A variety of radiographic observations (Figure 7-55) are used to assess the posterior aspect of the calcaneus. The Fowler and Philip angle (FPA) normally ranges from 44"-69", and an FPA >75° will often present with posterior swelling, cutaneous compromise and prominence just superior to Achilles insertion. Prominence of the posterior aspect of the calcaneus predisposes to the development of retrocalcaneal bursitis, as the constant pre-Achilles bursa becomes repetitively irritated with anl 90° correlates highly with retrocalcanea! bursitis and Haglund's deformity. Parallel pitch lines IPPL) have also been used to assess the prominence of the posterosuperior prominence of the body of the calcaneus. An adventitious superficial calcaneal bursa may develop superficial to the Achilles tendon secondary to repetitive mechanical irritation. Kager's triangle is demarcated by the long flexor tendons anteriorly, the Achilles tendon posteriorly, and the superior surface of the calcaneus inferiorly, and Is visualized in the lateral radiograph as a dark, radiolucent triangle with apex pointed dorsally. Kager's triangle represents the pre-Achilles fat pad. Thickening of the Achilles, which is usually about 9 mm wide in the lateral radiograph, due to retrocalcaneal bursitis and/or tendinitis will encroach on Kager's triangle and blur the usually sharp interface with the pre-Achilles fat pad. The calcaneal apophysis usually closes at 14-16 years of age. Biomechanical foot types associated with increased motion between the posterior aspect of the heel and the shoe counter, thereby aggravated by Haglund's deformity, include compensated reatfootvarus, compensated forefoot valgus, and rigid plantatflexed first ray. Symptomatic Haglund's deformity is most commonly observed in young to middleaged females; with pain and cutaneous irritation at the posterior aspect of the heel, radiographic evidence of a cortically intact bursal projection, loss of the pre-Achilles recess indicative of retrocalcaneal bursitis, Achilles tendon widening > 9 mm indicative of tendinitis, and loss of distinction of the posterior margin of Kager's triangle. A tender superficial Achilles bursitis may be present, and causes the classic "pump bump" aggravated by shoes with a tight counter and elevated heel height. Treatment of the symptomatic Haglund's deformity, due either to a prominent bursal projection, a normal posterior contour with a high CIA, or a combination of both, involves initial use of a heel lift inside the shoe and a heel counter pad to shield the tender posterior aspect of the heel. The use of NSAIDs, calf and arch flexibility exercises, orthotic control of hyperpronation, and local infiltration of corticosteroid combined with gel-cast or similar immobilization can be useful for persistent cases. Recalcitrant cases may warrant surgical intervention for excision of chronic superficial and/or retrocalcaneal bursitis, and remodeling of the prominent bursal projection. The treatment of Haglund's deformity and posterior calcaneal spur are summarized in Table7-5.

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203

TABLE 7-5. TREATMENT HIERARCHY FOR HAGLUND'S DEFORMITY OR POSTERIOR CALCANEAL EXOSTOSIS.

Intervention

Stage I

Stage II

NSAID Local steroid* Oral steroid

NSAID

Pharmacological

Heel lift Custom orthotic Biomechanical Heel counter pad Roller sole

Prefabricated orthotic Physical Surgical

Ice Flexibility

Stage IV

Stage Ill

Continued immobilization

Immobilization Iontophoresis

Night splint Dynamic splint Remodel posterosuperior process or spur resection; preserve Achilles or detach; bursectomy

*Support of the ankfe and partial immobilization (gel cast and surgical shoe, cast boot (cam walker}, BK cast} with

weight bearing are ad'Jised whenever corticosteroid is infiltrated about the Achilles tendon.

Surgical repair of Haglund's deformity of the heel involves a lateral paratendinous incision with the patient prone or in the contralateral decubitus position. The procedure is readily performed under local anesthesia with IV sedation, and anatomic dissection yields adequate hemostasis. The sural nerve must be protected within its subcutaneous bed. The deep fascia is incised in a paratendinous fashion, in line with the overlying skin incision. Care should be taken to avoid excessive reflection of the fibrous expansion of the Achilles tendon at its insertion. Plantarflexion ofthe ankle enhances retraction ofthe Achilles. The prominent posterosuperolateral process is resected with an osteotome and mallet and the remaining calcaneal surface is then rasped. "Chasing the bump" prevents creation of a new prominence dUe to over aggressive resection. It is possible to remodel the entire posterior aspect from the lateral approach, however a second medial paratendinous incision can be used if necessary, however a distance of at least 2.5 em should be maintained between the two parallel incisions. A curvilinear or lazy-S incision could also be used. Generally, with Haglund's deformity the single lateral incision will suffice. In the symptomatic, structural cavus foot with a pathologically high CIA, in the presence of a normal posterior contour and bursal projection, the Kelly and Keck osteotomy may be used to resect a dorsally based wedge from the calcaneal body. This procedure brings the posterosuperior aspect of calcaneus anteriorly. The osteotomy is fixated with Steinmann pins, staples or lag screws.

Retrocalcaneal Exostosis with Calcification in the Achilles--the retrocalcaneal exostosis differs from the Haglund's deformity in that it is usually seen in older individuals, is situated distal to the posterosuperior process, and it generally traverses the entire posterior aspect from lateral to medial. The patient should be positioned prone or in the contralateral decubitus position, and the procedure can be performed under local

204

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Ch. 7

anesthesia if desired. lncisional approaches are variable, including two paratendinous incisions, a central longitudinal posterior or an oblique curvilinear (Dickinson) incision, and it is often necessary to create a central longitudinal tendon-splitting incision in order to remove intratendinous calcification {Figure 7-57). The tendon splitting incision enables the surgeon to expose the posterior surtace of the calcaneus while preserving distal attachments medially and laterally. After remodeling the posterior surface of the calcaneus

and debriding the Achilles, the tendon is reattached with multiple intraosseous tendon anchors and nonabsorbable sutures. Following layered closure, a compressive dressing and short leg cast are applied. The patient is maintained non-weight bearing for 2-4 weeks, and immobiHzation is discontinued at 5-6 weeks followed by gradual rehabilitation. The duration of non-weight bearing and immobilization is determined by individual factors and the extent of tendon reflection. Downey has advocated the use of an inverted V-tenotomy for debridement ofthe Achilles tendon and removal of a posterior calcaneal spur, noting that this method enables the surgeon to readily access the calcaneus and easily reap proximate the tendon.

52% Anterior

Medial@:::> Lateral Posterior

35%

Medial~ Lateral

13%

Medial

€ ) lateral

Calcaneus

Figure 7.57

Figure 7.58

ANKlE EOUINUS The triceps surae consist of the medial and lateral heads of gastrocnemius, plantaris, and soleus. The medial head of gastrocnemius is thicker and broader than the lateral head, and

it extends further distally and attaches to the lateral aspect of the tendoAchillis. Soleus attaches to the medial2/3 ofthe deep surface of the tendoAchillis (Fig 7-58). Plantaris arises from the lateral femoral condyle, and Is absent 7% of the time. Plantaris attaches medially along the Achilles. The tendoAchillis averages 15 em in length and originates near the middle of the leg. Gastrocnemius traverses three joints: knee, ankle, and STJ; while soleus traverses two joints: ankle, and ST.J. The gastrosoleus complex functions in late contact through midstance and into early propulsion, and causes knee flexion and heel lift via

ankle plantarflexion.

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205

Muscular Forms of Ankle Equinus-the muscular forms are caused by skeletal muscle spasm, congenital shortness, and acquired conditions. Spastic equinus is the oldest recognized form of ankle equinus, and is caused by upper motor neuron disease such as cerebral palsy, CVA, and head and spinal trauma. Spastic equinus presents with

hypertonicity, hyperreflexia, and steppage gait Congenital equinus usually presents with toe walking until about 15·18 months of age !usually the first3·6 months after initial walking), and thereafter the equinus subsides. Acquired ankle equinus may develop in response to prolonged casting in plantarflexion, such as following Achilles tendon repair, or due to chronic use of high~heeled shoes. Chronic equinus contracture results in tightness of the deep flexors and peroneal tendons, posterior ankle and subtalar ligaments and capsule. The Silverskio!d test indicates gastrocnemius equinus if ankle dorsiflexion is 10° with superimposition of the metatarsals on the

Figure 8.1

Reconstructive Foot and Ankle Surgery

216

Ch.8

lateral radiograph. This procedure can also be used in adults with CPVP, and is often used in conjunction with other reconstructive procedures addressing the medial columnn and triceps sura e. Arthroereisis uses synthetic polymer or metallic implant, rather than bone graft, to block STJ pronation by impinging on the anterior margin of the leading edge of posterior talar facet The implanted blocking plug is usually removed after the child has achieved skeletal maturity and avoided the destructive, adaptive changes related to pathological STJ/MTJ hyperpronation during the formative years. Specific techniques include:

Lelevre------si!icone polymer (SIIastic®) plug positioned from_lateral to medial in the sinus tarsi, thereby elevating the floor of the sinus (calcaneal sulcus) and blocking talar adduction~plantarflexion. The polymeric plug has been criticized for instability, displacement, and implant degradation. StaPeg"-polyethylene plug positioned in the sinus tarsi, and noted to be more stable and durable in comparison to the LeLevre procedure.

Villadot-an hour glass-shaped Sllastic3 years of age. Fixation of calcaneal osteotomies, both with and without bone graft, can be achieved with staples, interfragmental compression screws, or absorbable pins (preferably without bone graft); and postoperative non-weight bearing and immobilization are cruciaL Lateral approaches

to the calcaneus require that attention be paid to the course of the sural nerve, lesser saphenous vein, and the peroneal tendons .. Specific procedures include:

Gleich--an oblique calcaneal osteotomy anterior to the posterior cortex that allows medial shift of the posterior segment and relative adduction of the tuberosity and posterior os cal cis.

Dwyer-a lateral opening wedge oriented obliquely from the dorsal-to-plantar margins of the calcaneus, midway between the posterior margin of the posterior STJ facet and the Achilles attachment, incorporating allogeneic or autogenous corticocance!lous bone graft insertion. It has also been described as a medial closing calcaneal osteotomy, however the contents of the tarsal tunnel can complfcate Figure 8.4 the dissection, and the procedure is not commonly done in this fashion. The lateral closing Dwyer osteotomy is a mainstay of pes cavus reconstruction \Figure 8-4). Silver-an opening wedge bone graft pertormed via a lateral approach, wherein the posterior aspect of the calcaneus and tuberosity are shifted plantarly, and medially. Koutsogiannis-a versatile, frontal plane osteotomythrough the body of the calcaneus midway between the posterior lip of the STJ and the Achilles insertion, allowing triplanar correction ofthe posterior calcaneus and tuberosity via primarily medial and plantar displacement.

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219

Pes Cavus-the etiology of pes cavus includes: 1. 2.

3. 4.

Muscular diseases such as muscular dystrophy, Peripheral or spinal nerve lesions, such as Dejerine Sottas, Charcot Marie Tooth \familial sensorimotor neuropathy, peroneal muscular atrophy), and polyneuritis and/or trauma to peripheral nerves, Spinal cord defects such as poliomyelitis (often effects paralytic flatfoot, also). spina bifid a with myelomeningocele, diastematomyelia, and spinal tumors, Spino-cerebellar defects, which are usually hereditary, including Roussy-Levy

syndrome, and Friedreich's ataxia,

5.

Pyramidal and extrapyramidal tract lesions effecting spastic and athetoid cerebral palsy,

6.

Supratentorial conditions such as hysteria,

7. 8.

Congenital defects such as talipes equinovarus, and Idiopathic pes cavus.

Etiopathogenesis hinges on muscle imbalances, often with spastic triceps surae and deep posterior musculature, and anterior and peroneal compartment weakness causing dropfoot. The first ray is usually plantarflexed as peroneus longus is unopposed. Extensor substituion results chronic MTPJ subluxation, clawtoes, metatarsalgia, and inability to get the heel to the ground. It is postulated that the extrinsic digital extensors overpower the lumbricales. TP overpowers and supinates the foot and plantarflexes the ankle. Classification of Pes Cavus-the classification of pes cavus can be confusing and cumbersome, and several systems exist, including:

Apex of the Cavus Deformity--a common classification involves identification of the apex of the cavus deformity. Anterior pes cavus can be described by the Sagittal Plane (SP) shape of the foot as it relates to the dorsal apex of the deformity, as follows: metatarsal, tarsometatarsal. lesser tarsal, and forefoot or midtarsal cavus. Subcategories of anterior cavus include isolated medial or lateral column cavus, first and fifth ray respectively, or global cavus wherein all of the metatarsal rays bear weight more or less equally due to transverse plane symmetry of the plantarly declined structures distal to the apex. Combinations of anterior cavus can also exist. Lower extremity compensation for anterior cavus includes digital and MTPJ contraction, effecting hammer and clawtoes and associated subluxation of the MTPJs; dropfoot that often catches or scuffs across the substrate, and metatarsalgia with or without plantar keratoma forma1ion. If the deformity is flexible, then loading the forefoot results in a certain degree of metatarsal and tarsal dorsiflexion that, over time, can become degenerative. Moreover, a certain degree of ankle joint dorsiflexion will also be used to compensate for residual anterior cavus, thereby limiting available dorsiflexion required for late stance propulsion. This relative limitation of ankle dorsiflexion is referred to as pseudoequlnus, and functions to further load pedal structures and lead to symptomatology. Pseudoequinus is more pronounced in rigid forms of anterior cavus. Posterior pes cavus results from structural increase in the calcaneal inclination angle, usuallywith adduction and varus of the hindtoot. Combined pes cavus typically entails fixed frontal plane varus and a non-reducible rearfoot.

220

Reconstructive Foot and Ankle Surgery

Three~Stage

Ch.B

Classification of Pes Cavus-perhaps the most useful classification involves

3 stages of pes cavus, and focuses on options for surgical repair after failed non-surgical efforts. The system includes: Stage I Pes Cavus-entails claV\1oes and subluxated or dislocated MTPJs. Repair evolves around digital stabilization with PIPJ arthrodesis and MTPJ relocation with pin fixation. Adjunct procedures involve the Hibbs and Jones tendosuspensions, and perhaps tendon transfer (STATI) to enhance ankle dorsiflexion.

Stage II Pes Cavus---entails those deformities of Stage I cavus, as well as heel varus

and more significantcavoadductovarus localized primarily to the distal to the midfoot Reconstructive options are determined by the degree of flexibility, as determined by the Coleman block testfor heel varus and plantarflexed first ray. Failure to establish a perpendicular relationship of the posterior bisector of the heel to the ground when the lateral column is elevated on a block, to eliminate the varus influence of a rigid plantarflexed first ray on the hindfoot, indicates the presence affixed heel varus that will require corrective osteotomy. Corrective procedures include the Dwyer closing lateral wedge osteotomy of the calcaneus, dorsiflexory wedge o::.teotomy (DFVVO) of the first ray, Jones and/or Hibbs suspension, and tendon transfer to the dorsum of the footto enhance straight ankle dorsiflexion.

Stage Ill Pes Cavus-entalls marked, rigid, cavoadductovarus deformation, often of neurological etiology, associated with adaptive arthrosis and serious dropfoot, and typically requires Cole midfoot osteotomy or triple arthrodesis for correction. The Cole procedure involves a through-and-through, dorsally based wedge resection of bone positioned through the tarsal navicular and cuneiforms, and the cuboid, thereby elevating the forefoot out of an equinus alignment The osteotomy, after reduction, is stabilized with Steinmann pins or staples, and maintained non-weight bearing for up to three months. The triple arthrodesis is a versatile procedure for correction of the most severe cavus deformities. Assessment ofthe Patient with Pes Cavus-assessment of the patient with pes cavus requires a thorough family history that includes inquiry about parents, siblings, and other blood relatives. Neurological examination, typically with neurology consultation prior to surgery, should identify the presence or absence of spasticity, flaccidity, muscular dystrophy, spinal and other CNS defects; as well as familial diseases that may require genetic and social counseling. Nerve conduction velocity and EMG may be in order. Pedal and ankle, as well as spinal radiographs if spina bifida or other defect is suspected, should be obtained. Radiographically, the apex of the cavus deformity should be identified and the deformity classified in this regard. The radiographic evaluation of pes cavus should be performed weight bearing, and include AP, lateral and lateral oblique projections, with consideration given to ankle films. The lateral radiograph will show increases CIA >30°, norma! to posterior break in the SP cyma line, accentuated or bullet-hole sinus tarsi, SP long axis of the neck of the talus passes superior to the long axis of the first metatarsal, and dorsally based wedge shaped cuneiform& An axial view of the calcaneus at 45° should be obtained to rule out a structural heel varus.

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221

Surgical Procedures for Correction of Pes Cavus~procedures for the correction of pes cavus vary depending upon the degree of flexibility. Flexible Pes Cavus-procedures useful for correction of flexible pes cavus include the Steindler stripping, wherein the plantar fascia and intrinsic musculature is reflected from the plantar calcaneal cortex, and may be useful only if the deformity is flexible and not of bony rigidity. A Hibbs suspension may also be combined with the Steindler stripping in a flexible deformity. Tendon transfers such as the STAn and PLH or TPH are often used to balance inverter/everter imbalance in flexible deformity. Digital fusion and MTPJ relocation are crucial to the treatment of both flexible and rigid pes cavus.

Rigid Pes Cavus-for rigid deformity, where the Coleman block test failed to eliminate heel varus or the medial column is rigidly plantarflexed, a first metatarsal base DFWO combined with a Dwyer lateral closing osteotomy of the calcaneus, perhaps with the STATT, is a useful combination (Stage II pes cavus). It may also be useful to transfer TA dorsally into the base of first metatarsal and perform a plantar opening wedge osteotomy with bone graft of the medial cuneiform, along with a Jones suspension of the first ray. If fixed bony equinus is localized to the lesser tarsus and midfoot, the Cole osteotomy is indicated (Figure 8-5). The Cole osteotomy is performed as a dorsally based wedge resection of bone and joint through the navicular-cuneiform and cuboid level. A first metatarsal OFWO may also be necessary, and adductovarus deformity can be addressed by manipulating the forefoot on the hindfoot at the level of the osteotomy. The Cole should only be performed on a skeletally mature foot, as shortening will ensue. The Japas osteotomy can be used for less severe, rigid pes cavus, and involves a transverse plane V-osteotomywith the apex in the navicular and the wings diverging distally through the cuneiforms and cuboid on the medial and lateral aspects, respectively {Figure 8-6). The Japas causes less shortening than does the Cole, however it is difficult to address adducto varus deformity. In youngsters with open growth physes, in the presence of pan metatarsal global equinus, first metatarsakuneiform dorsal opening wedge osteotomy with bone graft, along with pan-lesser metatarsal DFWD may be used.ln the adult, pan metatarsal DFWOs may be considered. The triple arthrodesis remains the most versatile and powerful reconstructive procedure for repair of severe pes cavus, which is often of neurological etiology (Figure 8-7). Charcot Foot Reconstruction-Charcot deformity and treatment are described in Chapter 3. Rheumatoid Foot Reconstruction and Panmetatarsal Head Resection---when treating the patient with rheumatoid arthritis, it is necessary to consider the patient's physiologic age, general medical status, immunocompromise status, bone stock, wound healing capacity, systemic corticosteroid supplementation, and current as well as anticipated weightbearing activity level. The combination of deformities caused by rheumatoid arthritis mutilans is generally referred to as the rheumatoid foot The rheumatoid foot will usually be symptomatic in either the forefoot or hfndfoot/ankle. The majority of symptomatic presentations involve the forefoot, which displays claw or hammertoes, subluxated to dislocated MTPJs, plantar metatarsalgia with or without IPK and/or rheumatoid nodules. Excessive mechanical overload can effect ulceration and underlying bone infection. Hindfoot and ankle involvement usually entails TP synovitis and chronic dysfunction, rheumatoid nodules of the plantar and posterior heel, retrocalcaneal enthesitis, and severe pes and ankle valgus deformity. The patient often adapts a pedestal gait with antalgic

Reconstructive Foot and Ankle Surgery

222

A

c Figure 8.5 Figure 8.6

A

E~

Figure 8.7

Ch. 8

Ch. 8

Reconstructive Foot and Ankle Surgery

guarding. Fundamental

non~surgical

223

treatments include periodic, palliative skin and nail

care, accommodative foot orthoses, extra-depth shoes with an external roller sole, and other supportive measures that hinge upon adequate systemic disease modulation under a rheumatologist's guidance. Rheumatoid Foot Reconstructive Surgical Techniques-techniques useful for repair of the rheumatoid foot include: synovectomy, excision of rheumatoid nodules, digital stabilization, Keller arthroplasty, pan metatarsal head excision, first MTPJ fusion along with lesser metatarsal head excision, MTPJ and/or IPJ endoprosthesis, and arthrodesis of the greater and/or lesser tarsus and ankle. Systemic corticosteroid supplementation and prophylactic antibiotics are in order. Postoperative non-weight bearing can be difficult, and immobilization can be detrimental to subsequent joint movement. Occupational and physical therapy should also be considered.(Note: digital arthrodesis, Keller arthroplasty, endoprosthesis implantation, and first MTPJ fusion have been described elsewhere in this manua!). In regard to the use of first MTPJ endoprosthesis in rheumatoid patients, multicomponent total joint replacement is common, although the use of silicone polymer total hinged implants can also be useful. In these patients, however, endoprosthesis probably offers little more in comparison to Keller arthroplasty. Importantly, implantation requires the presence of adequate bone stock, and perhaps metatarsal osteotomy to correct angular deformity. Other useful procedures include: Panmetatarsal Head Resection-this is performed to eliminate pain and cutaneous compromise, and maintain a pedestal gait Hoffman described excision of all five metatarsal heads, while Clayton recommended excison of a portion if not all ofthe proximal phalangeal bases 1f they were large or osteophytic. Proximal phalangeal base resection is wrought with subsequent digital instability and may require syndactylization to effect stability. lncisional options include transverse plantar, orfive or three dorsal longitudinal incisions. The more severely dislocated MTPJs and clavvtoes invite a transverse plantar incision with an elliptical excision of redundant plantar skin and postoperative non-weight bearing. The subcutaneous fat layer should remain attached to the skin, and intermetatarsal dissection should be avoided. The five incision approach includes a wound over each metatarsal, while three dorsal incisions are localized to the first ray, between the second and third and between the fourth and fifth toes respectively. Separate dorsal incisions are used to perform PIPJ arthrodesis of the second through fourth and arthroplasty of the fifth. The preferred length pattern after metatarsal head resection is: 2 = 1> 3 >4 > 5. The metatarsals are transacted distally from dorsal to plantar and the plantar cortex rasped smooth. The first metatarsal is also angulated from distal lateral to proximal medial, while the third-fifth metatarsals are angulated from distal medial to proximal lateraL Most commonly, fusion of the PIPJs 2 through 4 and arthroplasty of the fifth toe are performed along with the metatarsal head excision, and for added stability a K~wire is directed through the PlPJ fusion and into the metatarsals. The combination of first MTPJ fusion with lesser panmetatarsal head excisions can be very usefuL Postoperatively, a protective cast boot works well. Some shortening of the foot can be expected, but the patient should maintain an apropulsive gait lislranc Arthrodesis-arthrodesis of all or part ofthe tarsometatarsal joint(TMJ, Lisfranc's joint) is useful in the treatment of post-traumatic or degenerative arthritis, Charcot foot associated with ankle equinus, and other maladies localized to this level (Figure 8-8).

Reconstructive Foot and Ankle Surgery

224

Ch. 8

Isolated first metatarsal-medial cuneiform arthrodesis (Lapidus procedure), as previously noted, can be used to stabilize the medial column and may be used to correct severe HAV deformity with associated metatarsal-cuneiform instability, hypermobility of the first ray and long-standing forefoot supinatus. Arthrodesis of Lisfranc's joint complex usually involves 3 dorsal incisions, the first medially over the medial column, the second and third between the second and third, and fourth and fifth metatarsals, respectively. Fixation is achieved with a

plate and interfragmental compression screw pia cement across the first metatarsal-medial cuneiform fusion site, Steinmann pins or crossed K-wires or single interfragmental screws across the lesser metatarsal-cuneiform and cuboid fusion, or perhaps a plate and screws across the fifth metatarsal-cuboid site. Specialized locking plates may also be used at this site. Furthermore, achieving primary rigid internal compression fixation of the medial column, in conjunction with splintage ofthe lesserTMJs, is an example of the vassal rule of internal fixation and serves as a common approach to Usfranc arthrodesis. Triple Arthrodesis-this is a versatile procedure that is applicable in cases that include collapsing pes val go planus, tarsal coalition, convex pes valgus, tarsal arthritis, pes cavus, residual clubfoot, neuromuscular disease, and others. Triple arthrodesis enables the surgeon to orientthe foot in relation to the leg and ankle, and to manipulate the relationship of the forefoot to the hindfoot. It also affords a stable hindfoot upon which the tendons of the extrinsic pedal musculature can function. The classic Oilier incision can be used for the triple arthrodesis, and courses from the tip of the fibular malleolus, across the sinus tarsi then on to the dorsal aspect of the talonavicular joint The Oilier incision is applicable in the cavus foot, however predisposes to difficulty exposing the TNJ in the valgus foot In the valgus foot, a 2-incision approach is preferred, and most surgeons use the 2-incision approach even for pes valgus correction. The lateral incision extends from the tip of the lateral malleolus to the dorsum of the junction between the fourth and fifth metatarsal bases, and provides excellent exposure of the STJ and CCJ. The medial incision extends from the anterior margin. of the medial malleolus longitudinally to the first metatarsal-medial cuneiform joint, and provides excellent exposure of the TNJ and neck of the talus. The lateral dissection proceeds through the superficial fascia to the deep fascia, which is incised longitudinally between EDB and the PB tendon Care is taken to preserve the peroneal sheath. EDB is reflected away from the CCJ, and the intertarsal talocalcaneal ligament and sinus tarsi are evacuated. The lateral aspect ofthe head and neck of the talus are exposed, and the peroneal tendons are retracted plantarly to expose the posterior facet of the STJ. Medially the dissection should avoid the medial marginal vein, and the deep fascial incision is made medial to the tendon ofTA. A medial periosteal and capsular incision exposes both the TNJ and the anterior margin of the ankle. The technique of osseous resection is crucial

A

Figure 8.8

B

Ch. 8

Reconstructive Foot and Ankle Surgery

225

when performing the triple arthrodesis {Figure 8~9). Preoperative assessment of the

relationship between the foot and leg enables the surgeon to take into consideration knee and ankle positions so that proper placement of the hindfoot can be achieved. The hindfoot should be positioned in slight valgus, and varus should be avoided at all costs. A varus hindfoot fusion is destined to marked weight bearing difficulties, pain, and ankle instability postoperatively. The foot should be positioned in about 12-15° of pes abductus, when the knee is on the frontal plane. Less pes abductus is needed if the knee is externally rotated, and more may be useful in the presence of medial knee position or tibial torsion. Resection proceeds from the MTJs to the STJs, as MTJ resection enables easier access to the STJ. The foot is held in a reduced attitude and the CCJ and TNJ are resected with the blade parallel to the articulations in most cases. Severe adductus or abductus may warrant transverse plane wedging, however a flush resection preserves bone mass and correction can usually be satisfactorily achieved via translocation of the forefoot on the hindfoot without the need for specific wedge resection. Similarly, a near~para!lel resection ofthe STJs (posterior, medial and anterior facets) is usually adequate, as only slight valgus positioning will suffice. STJ wedging may be more pronounced if the frontal plane deformity is severe. The calcaneus is translocated medially for correction of pes valgus, and laterally for correction of pes cavus. Sagittal plane correction is also corrected primarily via translocation of the forefoot on the hindfoot, after achieving the desired talocalcaneal alignment The calcaneus can also be shifted posteriorly to increase the lever arm for the tendoAchillis and to increase sagittal plane talar declination and thereby increase arch height. Contrari!y, sliding the calcaneus anteriorly relative to the talus dorsiflexes the talus and decreases arch heightAchilles function. The desired alignment is temporarily stabilized with cannulated screw guide pins, and intraoperative radiographs in the AP, lateral, and calcaneal axial projections are obtained and reviewed. The order of stabilization generally

proceeds from STJ to TNJ to CCJ, and is usually achieved with three 6.5-7.0 mm interfragmental compression screws (Figure 8-10). The TC fusion is achieved with a !ag screw directed from the neck of the talus dorsally, into the body of the calcaneus. In a similar fashion, the TNJ and CCJ are stabilized with distal to proximal lag screws. Care is taken to avoid the following fixation hazards: violation of the medial cortex of the body of the calcaneus and entrance of the fixation device into the tarsal tunnel when fixating the TC interface, entrance of the TN fixation into the ankle, and fracture of the dorsolateral cortex of the cuboid with the screw head. Additional intraoperative radiographs should be used to reassess final fixation if any questions exist. The TC lag screw can also be directed from the apex of the calcaneus posteroMplantarly into the body and neck of the talus. The MTJs can also be satisfactorily stabilized, each with two staples oriented 90° to each other. Closure proceeds in layers following placement of drains medially and laterally, and the foot is secured in a BK Jones compression immobilizing dressing. Aftercare involves drain removal after 24 to 72 hours, redressing between 3 to 5 days, and BK cast immobilization without weight bearing for up to 3to 4 months. Mobilization of the ankle and MTPJs can be undertaken in a non-weight-bearing attitude as soon as desired, and immobilized partial weight bearing can be initiated by 10 to 12 weeks pending clinical and radiographic findings. Full weight bearing ensues thereafter, as does conversion to desired shoes. Ankle and Pantalar Fusion-the most common indication for ankle fusion is post-traumatic

arthrosis following ankle fracture, wherein a small proximal and lateral shift of the lateral malleolus has produced mortise incongruity resulting in articular cartilage degeneration. It

226

Reconstructive Foot and Ankle Surgery

Ch. 8

Figure 8.9

Figure 8.10

has been shown that a 1 mm shift can result in greater than a 40% decrease in tibiotalar congruity. The most common predisposing causes of the need for pantalarfusion is severe cava adducto varus deformity with chronic ankle instability, and avascular necrosis of the talus for whatever reason. Other indications for ankle and pantalar fusion include destructive bone tumors, infection, and failed ankle endoprosthesis. Evaluation of the patient requires inspection ofthe knee, leg, ankle, STJ and MTJ, and the relationship of the forefoot to the hindfoot and leg. The ideal position of fusion is 90' of the foot relative to the leg, with slight ankle and/or hindfoot valgus, and approximately 10-12' of pes abductus. If tibial varum is present, increase the amount of valgus to adjust for the added varus deformity. The surgical approaches to ankle fusion include Charnley's transverse anterior incision, extending from one malleolus to the other, which is rarely used currently because of risk of injury to anterior neurovascular and tendinous structures. The lateral transmalleolar hockey stick incision is most commonly used, and begins over the junction of the middle and distal thirds of the fibula, then curves distally toward the sinus tarsi for the ankle fusion, and onward toward the junction of the bases of the fourth and fifth metatarsals for pantalarfusion. This approach yields anterior, lateral, and posterior exposure forfibufar osteotomy. An accessory medial incision over the anterior margin of the medial malleolus is usually combined with the transfibular incision to provide anteromedial exposure for resection of the cartilage of the medial malleolus and enables hardware placement through the tibial pilon. When performing ankle fusion, we are looking to position the large cancellous mass of the tibial metaphysis in rigid apposition to the trabecular bone of the body ofthe talus.

Ch. 8

Reconstructive Foot and Ankle Surgery

227

Techniques to Achieve Ankle Fusion

1.

Curettage of cartilage with interposition aI bone graft;

2.

Sliding inlay graft from the anterior surface of the tibial metaphysis into the talar

neck/body; 3. 4.

Modified Ga!lie fusion wherein allogeneic graft is inserted anterolaterally and stabilized with a staple; Transmalleolar (either fibular or tibial) with osteotomy to enhance visualization of

5.

the tibiotalar interface; The subtotal fusion for debilitated patients that cannot sustain extensive bone

6.

7.

resection and trephine plug joint resection with dowel graft fusion will suffice; Compression arthrodesis using any of a variety of external fixation devices or interfragmentallag screws; and The Blair tibiocalcaneal fusion which can be useful post*polio or after collapse

of the talus. As with all fusion procedures, Glissane's criteria must be met for successful arthrodesis: 1. 2. 3. 4.

Removal of cartilage, fibrous tissue, or other material hindering raw bone contact; Accurate and close fitting of surfaces; Optimal position of fusion; and Maintenance of apposition in undisturbed fashion until fusion is complete.

The Podiatry Institute technique of ankle and pantarlarfusions entail the use of: 1. 2. 3.

A lateral hockey stick incision; Preservation of the fibula (avoid osteotomy); Cartilage resection with preservation of as much ofthe talar body as possible;

4.

Ancillary medial approach for removal of medial malleolar and talar body

5.

cartilage; Temporary stabilization with cannulated screw guide pins;

6. 7.

Fusion alignment of 90" of the foot to the leg; 10-12" pes abductus and slight ankle/hindfoot valgus;

8. 9.

Intraoperative radiographs in the AP, lateral, and calcaneal axial views; lnterfragmental compression fixation wrth crossing 6.5~7.0 mm cancellous screws; Placement of the fibular on lay graft with interfragmenta! compression screws purchasing the tibia and talus (and calcaneus in pantalar fusion); Be sure to allow a gap between the proximal and distal segments of the osteotomized fibula in order to avoid pseudoarthrosis or nonunion; Repeat intraoperative radiographs to ascertain fixation and bone alignment; Place and activate closed suction drains, bandage and immobilize; Plan to leave hardware in indefinitely or at least6 to 12 months; and Be sure not to penetrate the STJ with fixators if only ankle fusion is performed.

10. 11. 12. 13. 14. 15.

228

Reconstructive Foot and Ankle Surgery

Ch.B

Complications of ankle and pantalar fusion include infection (reported as high as 20% in the literature); nonunion, malunion, and pseudoarthrosis; malposition due

to operative

misadventure (most often varus or calcaneus); stress transfer to MTJ and STJ (may need triple later if only ankle fusion originally performed); and limb shortening if bone graft is

not used. Total Ankle Replacement (TAR) Arthroplasty-chronic ankle pain that is not responsive to

other treatments, as well as the potential complications related to ankle arthrodesis, have prompted the quest for a total ankle replacement (TAR) that is reliable and effective. Severe ankle pain, deformity and dysfunction that serves as a constant impediment to weight

bearing ambulation, often due to arthritis secondary to rheumatoid disease, trauma, joint sepsis, or osteoarthritis, can be treated by means of TAR. There are basically 2 types of ankle endoprostheses: 1) 2-part prostheses that are either constrained, semiconstrained or nonconstrained; and 2) multi-axial 3-part prostheses that include a free gliding interposition aI core. These devices have been under development since the 1970s and have yet to be perfected, and the long term results have not be promising for any particular device, so far. Earlier models were secured with cement, however most surgeons prefer cementless models. Common complications of TAR include loosening without the presence of infection, and postoperative dehiscence. Ankle geometry and soft tibial metaphyseal bone contribute to aseptic loosening, and this complication is most common when a constrained system is used. Unconstrained systems, on the other hand, are associated with instability, ankle deformation and subsequent loosening. Difficulties mimicking ankle geometry stem from the factthatthe ankle is not a true ginglymus (hinge) joint, and the path of the center of motion evolves as the ankle goes through its range of motion. Current goals of ankle en do prosthesis design focus attention on the normal contours of the talar dome and the distal tibial bearing surface, and minimization of the amount of bone resection required to secure the implant. A number of options exist for TAR, including the Scandinavian Total Ankle Replacement (STAR) (Waldemar Link GmbH & Co., Hamburg, Germany), a 3-component device; the Agility'" Total Ankle System (DePuy, Inc., Warsaw, IN), a 2-component device; the TNK Ankle (Kyocera Corporation, Kyoto, Japan), a 2-component device; and the Buechel-Pappas Ultra Total Ankle Replacement (Endotec, South Orange, New Jersey), a 3-component device. The main alternative to TAR is ankle fusion, and both procedures aim to alleviate pain while TAR also aims to improve function. While both procedures are designed to reduce pain, TAR is also intended to improve function. If TAR fails, then consideration is given to arthrodesis, the standard therapy option for ankle arthrosis and the mainstay of salvage following failed TAR. Salvage after failed TAR often requires the use of substantia! amounts of bone grafting. To date, unlike the results of hip and knee arthroplasty, the long-term results of TAR have not been as successful. Although there are many case series describing the benefits and shortcomings of different types of TAR, further investigation is necessary to determine the best options for patients with recalcitrant anlde arthrosis.

Congenital Deformities and Juvenile Surgery

Ch.9

229

COIIIGEI\IITAL DEFORMITIES AN II JUVENILE SURGERY Congenital deformities can be familial, inherited traits, or they may present without a known family history. The condition may be idiopathic; or a known etiology such as an identified

genetic defect, intrauterine or birth trauma, hypoxia, teratogenic drug or toxin exposure, tumor or other cause may exist Some defects present as a component of a known

syndrome and other defects, both physical and mental, may be identified. Macrodactyly (Localized Gigantism)--this idiopathic, rare, usually unilateral, congenital defect displays abnormal largeness of a single or multiple adjacent toes. It may be related to or caused by hyperplastic lymphatiC or vascular elements, or neurofibromatosis; and usually occurs as an isolated defect without familial inheritance. In static macrodactyly, the giant digit(s) display a growth rate proportional to the remaining norma! parts. In progressive macrodactyly, the giant digit(s) display a more rapid growth rate than normal tissues. Treatment consists either of partial or total amputation of the giant part, or sequential operations to reduce excess soft tissue and bone in a staged fashion (Figure 9·1 ). Reconstructive efforts can be difficult and convey a high rate of complication.

A~~v {) B

~ D~

c~

Figure 9.1

Syndactyly-this is· the most common congenital deformity of the foot and hand, and is marked by partial or complete persistence of the interdigital web. The condition is familial, and can occur unilaterally or bilaterally. The defect occurs during the sixth to eighth intrauterine week, and most commonly localizes to the second-third toes. Simple syndactyly involves only fusion of the skin and soft tissues of the adjacent toes, while complex syndactyly involves fusion of the soft tissues, nails, and bone. Single syndactyly involves two toes and one web, double syndactyly involves three toes and two webs, and triple syndactyly involves four toes and three webs. Treatment is usually based not on physical dysfunction, but rather on psychological or emotional concerns ofthe older child or adult Surgical desyndactylization can be difficult, and techniques involve creation of dorsal and plantar skin flaps or use of dorsal and plantar W-plasties (Figure 9-2A), or application of a FTSG (Figure 9-28) after incislonal separation. Osteotomy may be necessary in cases of complex syndactyly.

230 _ _ _ ___':C:C,oll\ngl"ellin''ttaa".'lD~e'!'fo~rmm1ilti•'e_s_an_d_J_u_ve~n~ile~S~u~rg~e~rv _ _ _ _ _~~ , Ch. 8

c

B

A

D

Figure 9.2A

B

A

D

c Figure 9.28

Ch. 9

Congenital Deformities and Juvenile Surgery

231

Polydactyly-this is a common congenital anomaly consisting of an accessory (supernumerary) digit or digits. The condition is idiopathic and an irregular autosomal dominant inheritance has been suggested. Preaxial polydactyly involves duplication of the hallux, while postaxial polydactyly involves duplication of the fifth toe. Postaxial polydactyly occurs in approximately 80% of cases, preaxial in about 15% of cases, and central ray duplication occurs in about 5% of cases. Mixed polydactyly involves pre- and postaxial duplication, and is observed most often in black individuals. Duplication can be either of an entire extra digit complete with bone (Type A), or of a rudimentary or vestigial toe (Type B). Polydactyly occurs bilaterally in about 50% of cases. Six radiographic patterns are seen with extra digits, including the short block metatarsal, Y-shaped metatarsal, T-shaped metatarsal, normal metatarsal shaft with wide head, partial or complete ray duplication, and normal metatarsal with distal phalangeal duplication (Figure 9-3). Syndactyly can occur in addition to polydactyly (synpolydactyly). Surgical treatment entails identification of the digit that has the most potential for normal growth and function, as duplication can involve bone, tendon, vessels, and nerves. Amputation should allow the foot to assume the most normal contour and facilitate wearing a shoe. Usually, the most medial digit is amputated in preaxial polydactyly while the most lateral digit is amputated in the postaxial state. Amputation for preaxial polydactyly, involving disarticulation of the extra medial toe is associated with the development of postoperative hallux varus, and K-wire stabilization across the MTPJ with recession of abductor hallucis are recommended. In cases of postaxial polydactyly, preserve robust skin (usually plantar) for coverage and closure over the lateral aspect of the new fifth ray. In case of an abnormal metatarsal configuration (Y or T), the prominent portion of bone should be osteotomized flush with the metatarsal shaft, and a wide metatarsal head should be made more narrow with osteotomy perpendicular to the growth physis in an effort to avoid growth disturbance. Central ray duplication can be managed with a dorsal racquet shaped incision at the base of the toe, and disarticulation and/or osteotomy at the appropriate level

Block met

., 1

i~

Nocmal mel w/ J1 digital duplication

Figure 9.3

Congenital Deformities and Juvenile Surgery

232

Ch.B

Congenital Hallux Varus-this deformity involves an adductus and/or varus deviation of the hallux at the first MTPJ, and is usually observed as a complication of hallux valgus surgery. Congenital hallux varus can be observed as a consequence of neuromuscular disease, and often accompanies metatarsus primus adductus/varus. The Thompson procedure involves abductor halluc.is recession and tendon lengthening, or actual excision of the muscle, and may be used in the infant or juvenile with congenital hallux varus due to non-spastic contracture of this muscle. This technique conveys risk of overcorrection and hallux valgus. Congenital Hallux Abductus lnterphalangeus (Ungual Phalanx Valgusl-this rare congenital anomaly displays abduction and valgus positioning of the hallux, with the apex of the deformity at the hallux IPJ. Radiographically, the phalangeal primary centers appear at birth, and the secondary center between 2-3 years. By 2-3 years of age, enlargement of the medial aspect ofthe distal phalangeal base can be observed. Surgical treatment entails excision of the medial aspect of the distal phalangeal base and growth p!ate arrest, or Akin osteotomy. Congenital Curly (Underlapping) Toe-this familial, idiopathic anomaly can involve any of the lesser toes and occurs uni~ or bilaterally. Adductovarus underlapping of a lateral toe beneath its medial neighbor is most common, however abduction and vaiQus can also occur. Treatment entails interphalangeal arthroplasty and derotational skin wedge plasty (Figure 9-4 A, B, and Cl. Congenital Overlapping Filth Toe-this anomaly usually affects the fifth toe overriding the fourth, with adduction and varus, and dorsal soft tissue contracture in a proximal and medial direction. The second toe overriding the first is the next most common form of congenital overlapping toe. As the individual matures, IPJ plantar contracture and hammer or claw toe ensues. Nonsurgical treatment includes taping or use of a digital retainer to try to redirect the digit in the infant or youngster. Surgical options include amputation, (which

Figure 9.4A

A

w ~

A Figure 9.48

) B

B '' Figure 9.4C

'

Ch.9

Congenital Deformities and Juvenile Surgery

A

233

c~

B Figure 9.5 is a rather undesirable approach), as well as sequential release of the deformity and reconstruction. The Butler procedure entails use of racquet-shaped incision, EDL

lengthening, MTPJ capsulotomy (Figure 9-5). The McFarland procedure involves excision of skin of the web between the fourth and fifth toes, EDL lengthening, MTPJ and PIPJ capsulotomy, and syndactyly of the fifth-to-fourth toe. The Podiatry Institute technique involves a dorsal Z-plasty, EDL lengthening, MTPJ capsulotomy, PIPJ arthroplasty, excision of redundant plantar skin wedge, and K-wire stabilization. Cleft Foot (lobster Foot , Claw Foot)-this rare, familial, congenital anomaly displays

absence of part or all of the central rays, effecting a claw-like foot The defect can present either unilaterally or bilaterally. Associated defects include syndactyly, polydactyly, cleft palate, deafness, and many others. Surgical treatment focuses on establishing a functional

limb, and a footthat can be shod. Each case is unique and no specific procedure is always applicable. Surgery usually combines soft tissue and bone surgery, such as skin and bone grafting, arthrodesis and osteotomy. Brachyrnetatarsia-this hereditary anomaly is characterized by premature closure of the epiphyseal plate of one or more metatarsals, and most commonly affects the fourth metatarsal although any or multiple metatarsals can be affected. Associated maladies include Down's syndrome, pseudohypoparathyroidism, and poliomyelitis. The defect is usually not recognized at birth, however becomes evident between 4~15 years of age. Although usually unilateral, brachymetatarsia can occur bilaterally. Surgical treatment has traditionally hinged on one-stage autogenous bone graft elongation of the affected metatarsaL This technique, as well as elongating osteotomy such as the Giannestras step-down, and other sliding shaft designs, are limited by skin and neurovascular compromise secondary to excess lengthening. Skin plasty and Z-lengthening of tendon, as well as staging and soft tissue expansion techniques can be useful in this regard. More recently, bone transport with the mini external fixation has proven to be most effective and very safe as the soft tissues can gradually elongate along with the bone. Postoperative nonweight bearing is used for up to 2~3 months pending radiographic evidence of bone healing.

Congenital Deformities and Juvenile Surgery

234

Ch.B

Metatarsus Adductus-this transverse plane deformity displays medial deviation of the metatarsals with the apex of the deformity at Usfranc's articulation. Metatarsus adductus IMAdd) occurs in 1 out of every 1,000 live births, is familial, and the presence of the deformity conveys a 1 in 20 chance that a sibling will also have the anomaly, and it occurs bilaterally in 55% of cases. Clinical findings include a C-shaped foot with convex latera! and concave medial borders in the transverse plane, adducted metatarsals with the more medial metatarsals being more adducted (1>2>3>4>51. a high arch if there is no STJ compensatory pronation, a skewfoot (toes abducted, metatarsals adducted, tarsus abducted) with heel valgus if compensatory STJ pronation is available, separation between the first and second digits, inability to abduct the metatarsals past midline of the foot, hypertonicfty and spasm of tibialis anterior in gait or upon striking in open chain, and possible hyperactivity of abductor hal!ucis.lfthe hindfoot is in rigid equinus and varus, rule out clubfoot. Total MAdd involves all five metatarsals, whereas atavistic MAdd localizes to the first ray, and is termed congenital metatarsus prim us adductus or varus. MPV displays a first intermetatarsal angle of 10° or greater. Radiographic assessment of MAdd is necessary to quantify the degree of deformity. The AP view is used, and the long axis of the lesser tarsus or that of the second cuneiform can be compared to the long axis of the second metatarsai(Fig 9-6). Using the long axis of the lesser tarsus, the normal met-add angle is 15-21°, and 25° when using the middle cuneiform reference. The Podiatry Institute radiographic classification system employs the long axis of the lesser tarsus, and defines met-add as follows: normal(rectus foot) 0-15", mild 16-25', moderate 26-35", and severe >35°. Jn the AP view, long-term compensation will show moderate~severe hallux abductus, cuboid abduction, and digital abductus as toes align with reatfoot, and increased Kite's talocalcaneal angle as the talus adducts medial to the navicular. ln the lateral view of the compensated deformity, an anterior break in the cyma line indicates hyperpronation and is usually associated with a decreased CIA. The uncompensated toot will display characteristics of pes cavus. LTAx

Points plotted for deremination of logitudinal bisection of lesser tarsus.

Figure 9.6

Lesser tarsal axis {LTAx) represents perpendicular to bisector of lesser tarsus. Line "EF" is bisector of lesser tarsus. Line "G" is bisection of second cuneiform.

Ch. 9

Congenital Deformities and Juvenile Surgery

235

Conservative treatment can be effective if instituted in a timely fashion. For patients 6 hours) wounds. The nail bed is bandaged with nonadherent gauze preserving· the cui de sac nature of the proximal nail fold, and appropriate supportive measures are used. Nail bed tissue loss injuries are defined by the Rosenthal classification system, which describes the level of tissue loss as either distalto.the bony phalanx (zone 1), distal to the lunule (zone 2), or proximal to the distal margin of the !unula (zone 3); and according to the direction of tissue loss as either dorsal oblique, plantar oblique, transverse guillotine, tibial or fibular axial, or central gouging (Fig 10-1). Treatment includes cleansing debridement, and coveragewith local transport of adjacent skin by means ofthe Atasoy flap (plantar-to-tip V-Y flap) or Kutler flap (medial and lateral V-Y plasties) after reduction of any prominent distal phalanx. Split- and full-thickness skin grafts can also be used to cover broad defects. Lesions proximal to the DIPJ may require disarticulation. Complications of nail bed injury include delayed nail regeneration; matrix disturbance with Beau's transverse line or ridge,

II

Ill

~c~

A

D

B

c figure 10.1

E

Ch. 10

Management of Foot and Ankle Trauma

247

onychocryptosis, and nail dystrophy with onycholysis and secondary fungal infection, canaliformis or split~nail deformity, and an unstable nail. Burns and Frostbite--burns are caused bythermal injury, both hot and cold, and chemical and electrical injury. The severity of a burn depends upon the extent of surface area and depth of skin penetration. Tissue damage is caused by protein denaturation, fluid

extravasation, and edema. The extent of a burn is designated as a percent of total body surface area (TBSA). and the rule of nines is applicable. The body is divided into multiples of 9% (Fig. 10-2). Partial-thickness burns include first and second degree wounds. Full-thickness burns are designated as third degree. First-degree burns involve only the epidermis, show erythema and no blisters, and are painfuL The most common form is sunburn. Second-degree burns are either superficial or deep. A superficial second-degree burn involves injury to the epidermis and a portion of the dermis; and they are erythematous, moist with blister formation and serous drainage, and are very painfuL A deep second-degree burn injures the epidermis and most of the dermis, leaving skin appendages intact It may or may not show blister formation and can be dry and it might display scattered anesthesia. A third degree burn involves full-thickness skin and a portion of the subcutaneous layer, destroying all skin appendages, thrombosing vessels, and appearing dry, anesthetic, whitish and leathery (eschar). A third degree burn can extend to bone. Fourth degree burns are caused by low voltage (