Disorders of the Foot and Ankle

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Contents 1 Disorders of the Foot and Ankle 1.1 NAIL AND SKIN DISORDERS 1.1.1 Onychomycosis 1.1.2 Onychocryptosis 1.1.3 Partial and Total Nail Avulsion. 1.2 COMMON SKIN DISORDERS 1.2.1 Tinea Pedis 1.2.2 Hyperkeratotic Lesions 1.2.3 Verrucae 1.3 MUSCULOSKELETAL DISORDERS 1.3.1 Forefoot: Digital and Metatarsal Disorders 1.3.2 Hallux Valgus and Bunions. 1.3.3 Hallux Rigidus. 1.3.4 Sesamoiditis. 1.3.5 Metatarsalgia. 1.3.6 Morton's Neuroma. 1.3.7 Plantar Keratoses and Lesser Metatarsalgia. 1.3.8 Stress Fractures. 1.3.9 Bunionette. 1.3.10 Midfoot Disorders 1.3.11 Flatfoot. 1.3.12 High-arched Foot. 1.3.13 Rearfoot Disorders 1.3.14 Heel Spur and Plantar Fasciitis. 1.3.15 Posterior Tibial Tendinitis. 1.3.16 Ankle Disorders 1.3.17 Sprains. 1.4 LOCAL ANESTHESIA 1.5 THE DIABETIC FOOT 1.5.1 Treatment 1.6 REFERENCES

[edit] Disorders of the Foot and Ankle

Robert G. Frykberg

Foot problems, although usually not serious, can be a significant source of discomfort or morbidity.A simple ingrown toenail may first be only an annoyance that limits one's ability to walk comfortably and that is easily treated.When left unattended or improperly treated, however, this common malady can progress to cellulitis or osteomyelitis.In the patient with diabetes mellitus or significant peripheral vascular disease, an infected ingrown toenail can lead to gangrene and subsequent amputation.Once a lower extremity amputation has been performed in these high-risk patients, their 5-year survival rates approach only 50%.Although this is a rather dramatic scenario not common to most foot disorders, it illustrates the significance of failing to manage properly an easily treatable condition at an early stage.As with any medical problem, most foot and ankle disorders can be effectively resolved with early diagnosis and appropriate intervention.

In an attempt to quantify the incidence and prevalence of foot disorders in the civilian noninstitutionalized U.S.population, the National Center for Health Statistics designed and conducted the 1990 National Health Interview Survey (NHIS) with a special supplement dealing exclusively with the foot.^[1] From the 120,000 responses to the podiatry supplement, data were available for the first time on the magnitude and range of specific problems afflicting the general U.S.population. Incidence was defined by the number of respondents or family members who had foot trouble within the previous 12 months, and prevalence was defined by those who currently had the problem at the time of interview.The results represent age-adjusted values, using the age distribution of the U.S.population as the standard (Table 130-1).Of the estimated 43.1 million people with foot problems in the 12-month period (175 per 1000 population), toenail problems (ingrown or other), foot infections (including athlete's foot and warts), and corns or calluses each affected more than 11 million.Corns and calluses have thegreatest prevalence of all disorders, with 9.2 million people affected and a prevalence rate of 38 per 1000.The second most prevalent condition is toenail problems, which chronically affect more than 7 million people at a rate of 30 per 1000.A common and often neglected deformity, hallux valgus (bunion), affects 3.8 million people, or 16 per 1000, ranking second only to flatfeet as one of the most prevalent recognized foot deformities in the U.S.population.Table 130-2 presents the incidence of specific foot problems stratified by gender and race.Females report foot problems much more frequently than males, especially bunions, which are five times more common in women than in men.Whites report foot problems more often than blacks, although blacks report corns and calluses 30% more often than whites.Incidence of all disorders rises significantly with age (Table 130-3).In the age group under 5 years, the incidence of all foot problems combined is only 26 per 1000 but dramatically rises to 336 per 1000 in those age 75 and older.Older adults age 65 or over have foot problems almost three times more often than young adults ages 18 to 44.^[1]

Table 130-1 Incidence and Prevalence of Foot Problems in the United States, 1990

From Greenberg L, Davis H: Foot problems in the US: the 1990 National Health Interview Survey, J Am Podiatr Med Assoc 83:475, 1993.

Problem	People who reported having had this problem in the past 12 months		People who reported having this condition now
		Number (in millions)	Rate per 1000 population	Number (in millions)	Rate per 1000 population
Ingrown toenails or other toenail problems	11.3	46	7.3	30
Foot infection, including athlete's foot, other fungal infections, and warts	11.3	46	6.2	25
Corns and calluses	11.2	45	9.2	38
Foot injury (sprain, strain, fracture, or dislocation)	5.6	23	1.8	7
Flatfeet or fallen arches	4.6	19	4.4	18
Bunions	4.4	18	3.8	16
Arthritis of toes	3.9	16	3.5	14
Toe and joint deformities (hammer toe, claw toe, missing toes)	2.5	10	2.2	9
Bone spurs	0.95	4	0.67	3
Nerve damage to foot	0.23	0.9	0.17	0.7
Clubfoot	0.16	0.6	0.13	0.5
Others	2.7	11	2.2	9
Total number of conditions reported	58.8	239	41.6	170
Unduplicated number of persons involved	43.1	175	31.7	129

Table 130-2 Number of People per 1000 Who Reported Having Specific Foot Problems in the Past 12 Months, by Gender and Race, 1990

From Greenberg L, Davis H: Foot problems in the US: the 1990 National Health Interview Survey, J Am Podiatr Med Assoc 83:475, 1993.

Problem	Total US	By gender		By race
				Men	Women	White	Black
Toenail problems	46	42	49	48	33
Foot infections	46	61	31	49	28
Corns and calluses	45	30	60	45	56
Foot injuries	23	23	22	24	15
Flatfeet	19	19	18	18	25
Bunions	18	6	29	18	17
Arthritis of toes	16	10	22	17	13
Toe and joint deformities	10	6	14	11	5
All foot problems combined	175	163	186	182	144

Table 130-3 Number of People per 1000 Who Reported Having Specific Foot Problems in the Past 12 Months, by Age, 1990

From Greenberg L, Davis H: Foot problems in the US: the 1990 National Health Interview Survey, J Am Podiatr Med Assoc 83:475, 1993.

Problem	Age (years)
		Under 5	5-17	18-24	25-44	45-64	65-69	70-74	75 and older
Toenail problems	5	20	39	44	59	78	94	123
Foot infections	5	44	45	52	52	55	46	41
Corns and calluses	✢	5	23	48	72	90	105	125
Foot injuries	3	22	36	28	21	17	14	10
Flatfeet	7	14	20	20	23	25	24	23
Bunions	✢	2	8	14	29	44	47	66
Arthritis of toes	✢	1	3	7	30	47	68	68
Toe and joint deformities	2	3	4	6	16	24	39	41
All foot problems combined	26	100	148	179	229	281	316	336

✢Statistically unreliable; fewer than 10 observations in the sample.

[edit] NAIL AND SKIN DISORDERS

Nail pathology is one of the most common of all foot conditions, affecting more than 11 million annually.

[edit] Onychomycosis

Fungal infection of the toenails is undoubtedly the most prevalent of nail and skin disorders, often involving all 10 toenails in extreme cases.Although painless and fairly benign, onychomycosis (tinea unguium) causes concern and frustration because it responds poorly to most treatments.^[2][3] The mycotic nail is easily recognized by its typical yellowishwhite, opaque appearance on a thickened nail plate.On close inspection the accumulation of subungual debris is evident and often appears as a “double” nail.Most often the infection begins at the distal aspect of the nail plate and gradually spreads proximally to involve the nail matrix, nail bed, and entire nail plate.Frequently the patient had an injury in the remote past, with subungual hematoma, loss of the nail, and regrowth of the dystrophic nail.Chronic plantar and interdigital dermatophytosis is usually associated with the nail involvement.The most common infecting organisms are Trichophyton rubrum and T.mentagrophytes, although Candida albicans can often be cultured from moist subungual debris.Differential diagnoses include psoriatic nails, lichen planus, and posttraumatic nail dystrophy.Diagnosis can be confirmed by gathering nail and debris scrapings for dermatophyte culture or potassium hydroxide (KOH) examination.Placing the scrapings in a drop of KOH on a glass slide should reveal the fungal hyphae coursing through the epidermal cells.

Definitive treatment for onychomycosis has traditionally been disappointing, and therefore palliation with periodic debridement has most often been the treatment of choice.Only early in the course of fungal infection under the nail is topical antifungal treatment effective.Miconazole, clotrimazole, ketoconazole, and terbinafine creams may be beneficial when applied twice daily to a debrided nail for months until improvement is noted.Trials of oral ketoconazole or griseofulvin have had limited success.Liver toxicity, gastrointestinal disturbances, and blood dyscrasias frequently accompany prolonged use, with recurrence following discontinuance of the medicine.Two newer oral antifungal agents have an improved safety profile and more clinical efficacy (90%) for this recalcitrant problem.Itraconazole, a broad-spectrum agent active against dermatophytes, saprophytes, and Candida, is effectively administered with a pulsed dosing schedule of 200 mg twice daily for 7 days in each of 3 consecutive months.Plasma clearance occurs in 7 to 10 days, providing a depot effect in the skin and nails for 6 to 10 months.Although liver toxicity and other adverse events are rare, metabolism through the cytochrome P-450 enzyme pathway precludes use of itraconazole in patients taking cisapride, terfenadine, astemizole, and lovastatin.Terbinafine, an allylamine, is effective only against the dermatophytes and is administered for 90 days in single daily doses of 250 mg.Taste disturbances and agranulocytosis are reported, but liver toxicity is not a significant complication of terbinafine treatment.

Permanent surgical removal of the nail with matrixectomy remains the only certain method of eradicating the mycotic nail with severe dystrophy of the nail plate.This is not usually performed, however, unless the nail becomes symptomatic.Although untested by formal clinical trials, simple temporary removal of the nail (avulsion) followed by topical antifungal treatment generally is not clinically effective.Once the nail is completely infected into the matrix, total permanent removal (matrixectomy) will prevent reinfection.

[edit] Onychocryptosis

The most symptomatic of nail dystrophies, onychocryptosis (ingrown toenail) ranges from a simple pinching of a distal skin fold to a severely infected paronychia with granuloma formation.This painful malady is frequently self-inflicted through “bathroom surgery” on nail borders.Self-treatment of this disorder often exacerbates a relatively benign condition.Cryptotic nail borders may therefore be idiopathic, iatrogenic, or secondary to injured matrix tissue, hypertrophic nail folds, or a subungual exostosis.Tight shoes and injudicious nail care often lead to an inflamed nail fold from an offending nail border or spicule.Patients in the habit of digging out the corners of a painful nail often leave a deep portion of the nail intact, which acts as a lancet and grows forward into the distal nail groove.A paronychia then develops from the break in the skin, followed by a granuloma (“proud flesh”) from the chronic irritation and inflammation (Fig.130-1).Extremely incurvated or “tented” nails may be caused by the constant deforming pressure from a subungual exostosis on the dorsum of the distal phalanx, and exostosis must be treated as well as the nail disorder.

The primary goal of treatment for any ingrown toenail is to remove the offending nail border from the inflamed skin fold (ungualabia).Antibiotic administration and soaks may reduce inflammation and infection when present but usually are not sufficient to resolve the problem.The severity of the condition usually dictates the appropriate treatment.A simplenail debridement of the nail's distal corner usually is enough to eradicate a minor paronychia.Occasionally, packing the nail groove with cotton after trimming the nail back is helpful.In more advanced cases, especially those with granuloma formation, avulsion of the nail or nail border under local anesthesia is required to allow resolution of the process before regrowth of the nail.With chronic recurrent onychocryptosis, permanent removal of the entire nail or just the offending nail borders should be performed by a matrixectomy procedure, including phenol or sodium hydroxide chemical cauterization, surgical techniques (e.g., Zadik, Winograd, Frost), or carbon dioxide (CO₂) laser vaporization.^[4]

[edit] Partial and Total Nail Avulsion.

For immediate relief and drainage of any paronychia of one or both borders, a partial nail avulsion is sufficient.When the entire nail, both borders, or a deformed nail is involved, a total nail avulsion can temporarily remove the entire nail plate to allow resolution of the drainage.This is also an optimal procedure for traumatically loosened toenails or subungual hematomas that fail to respond to simple drainage procedures and soaks.^[4] After performing a digital block with local anesthesia (see later section), the nail folds should be freed from the nail border(s) and proximal eponychium with a Freer elevator or spatula-like instrument.Starting centrally and distally, the nail is carefully separated from the bed, working side to side and back to the matrix area under the proximal eponychium.Once the nail is adequately loosened, a straight hemostat is used to grasp the entire plate back to its origin.A rolling motion from side to side releases any remaining lateral attachments while the toe is held firmly with the other hand (Fig.130-2).Finally, the nail is rolled from proximal to distal to remove the nail plate from its attachment to the matrix under the eponychium.If only a partial avulsion of a border is required, the nail should be split with an English anvil or other appropriate straight-edge nail splitter approximately ¼ inch from the inflamed nail fold.Only this portion of nail needs to be freed and removed, using the same basic technique while leaving the remainder of the nail intact.An appropriate antiseptic (e.g., povidone-iodine, bacitracin) is then applied, followed by a dry, sterile dressing.Bathing is allowed within 24 hours, and the dressing is then changed twice daily until the wound heals.Usually these procedures allow a rapid, uneventful recovery, with complete healing within 1 week.

[edit] COMMON SKIN DISORDERS

[edit] Tinea Pedis

Tinea pedis is a very common foot problem not specific to any particular age group, race, gender, or disease status.^[2][3] Often the patient with chronic dermatophytosis also has chronic onychomycosis, which may be the source of the chronic fungal infection. T.mentagrophytes, T.rubrum, and Epidermophyton floccosum are the most frequent pathogens, with C.albicans occasionally present on fungal culture.The patient presents with an erythematous pruritic desquamating rash, usually extending up the medial and lateral borders of the foot (moccasin distribution) and frequently with maceration and peeling between the toes, which may cause secondary bacterial infection.Diagnosis is confirmed by KOH examination or culture of skin scrapings from active peripheral vesicular lesions.Dermatophytosis must be differentiated from other skin dermatoses, such as contact dermatitis, atopic dermatitis, dyshidrotic eczema, lichen planus, and psoriasis.Interdigital lesions also may be caused by simple maceration, white psoriasis, verrucae, or erythrasma (Corynebacterium minutissimum).

Treatment consists of drying the moist lesions and eradicating the dermatophyte infection by applying topical antifungal agents.Systemic therapy with itraconazole or terbinafine is rarely necessary.Effective topical medications include tolnaftate, miconazole, clotrimazole, econazole, ciclopirox, and ketoconazole, and terbinafine applied twice daily.For severely inflamed cases, a combination therapy of clotrimazole with betamethasone is available.Since “athlete's foot” is produced by a warm, moist environment, proper foot hygiene is important.The feet should be bathed daily, dried between the toes, and powder applied routinely or after antifungal application.Antifungal powders or sprays are helpful as prophylactic agents but are not sufficient to treat active cases.When hyperhidrosis is a coexisting andcontributing problem, absorbent socks should be worn and changed at least twice daily.Sneakers and other synthetic or rubber-soled shoes are also contributory; their use must be limited, especially during warmer months of the year.

[edit] Hyperkeratotic Lesions

Hyperkeratotic lesions (corns or calluses) are extremely common foot disorders because of their chronicity as well as frequency.^[1][3] Corns and calluses are pressure-induced lesions and indicate areas of high or repetitive pressure.Dorsal, medial, and lateral lesions are almost exclusively the result of shoe pressure.Contracted hammer toes abutting against the top of the shoe are typically the etiology of very painful digital corns (clavi). Plantar keratoses can be focal or diffuse callosities, usually termed intractable plantar keratoses(IPKs), and are extremely distressing for the patient who must walk on them.As always, pressure is the etiology.A plantar-flexed or long metatarsal is the most frequent underlying structural deformity giving rise to the hyperkeratosis.^[5] When palpated, the underlying bone is immediately evident, as is pain from the chronic inflammation.On debridement, no skin lines are visible coursing through the center or core of the lesion; this often represents a plugged sweat duct lesion, referred to as a porokeratosis. The opaque core may be the “corn” so often mentioned by patients but is not always present in digital clavi, which are routinely called by the same name.Diffuse plantar calluses (tylomata) are usually biomechanical and, although possibly large, are typically not as painful as IPKs because of their more superficial nature and lack of a discrete central site of pressure, even though an IPK may be found in the center of a diffuse tyloma.Discolored lesions signify capillary hemorrhage with fluid collection under the keratosis and are usually more symptomatic or acute than normal-appearing callosities.

Simple debridement of a hyperkeratotic lesion provides immediate relief in most patients but cannot be expected to eradicate the problem, which involves correcting the under lying source (e.g., bony prominence, structural deformity, tight shoe, biomechanical imbalance).In patients unwilling or unable to undergo corrective surgery, conservative measures (e.g., shoes, orthotic therapy) combined with regular palliative care can achieve pain-free ambulation.Sneakers and cushioned walking shoes with generous toe room are advised for daily use in most patients.When necessary, cushioned insoles and prefabricated or custom-made orthoses are beneficial in relieving pressure on the sole.Although generally not successful in eradicating IPKs, such devices can provide comfort and extended periods between necessary debridements.If conservative measures fail, elective reconstructive surgery should be considered on the underlying structural deformity in the appropriate patient,^[5][4] usually performed on an outpatient basis under local anesthesia (see later discussion).

[edit] Verrucae

Verruca plantaris is a common skin lesion, especially in children and adolescents, who are not particularly prone to callus development.This lesion is different from other hyperkeratotic disorders because of its viral etiology, human papillomavirus (HPV).A verruca can be distinguished from a callus by its typical pinpoint bleeding on debridement and well-defined borders.The patient may relate a history of a minor puncture wound at the site that allowed entrance of the virus.These lesions enlarge over time and frequently develop small satellites near the primary wart.HPV is ubiquitous and causes skin lesions ranging from genital warts to planar warts on the dorsum of the hand.On the foot, HPV causes several warts with distinct morphologies, probably due to different strains of the virus.The simple plantar verruca is the most common.This singular verruca can also occur on the dorsum of the foot, on the toes, adjacent to or under the toenails, or in the interdigital areas.A difficult type to manage involves multiple, small, disseminated warts across the entire sole of the foot.The most challenging verruca is the mosaic plantar verruca.This lesion with a mosaic pattern can consist of literally hundreds of confluent individual verrucae.Such lesions, usually evolving from longstanding or ineffectively treated single warts, can grow to several centimeters in diameter (Fig.130-3).

Treatments for verrucae are numerous because no therapy is superior to the others or is successful on all patients for all warts.^[2][3] Large clinical trials have not been performed contrasting the multiple therapies currently in use.Salicylic acids (40% or 60%) are the mainstay of treatment and are applied either once or twice a day in a paste form or as a plaster on an adhesive-backed dressing.Combinations of lactic and salicylic acids are also available over the counter in a liquid or gel form and are similarly applied by the patient each day.Such acid treatments can be effective but might require many months to show improvement.Other topical therapies include acetic acids, cantharidin, injection of sclerosing agents, formalin, and retinoic acid preparations.Care must be taken with aggressive blistering agents because of violent skin reactions and attendant pain.Dermatologists often use cryotherapy with liquid nitrogen or liquid CO₂, especially for singular lesions.Usually applied without local anesthesia, cryotherapy is uncomfortable and produces a painful blister.Repeated applications are frequently required,as with most modalities.Surgical treatments include electrocautery, blunt dissection, curettage, excision, and CO₂laser vaporization.Although perhaps most effective on smaller, untreated verrucae, such methods are most frequently used on lesions recalcitrant to other, more conservative therapies.I prefer laser vaporization of recurrent or large mosaic verrucae, but success rates only approach 80% for multiple recurrent lesions.Frequently this treatment must be repeated to eradicate recurrent lesions.

These common lesions are difficult to eradicate permanently, and success can take months to years to achieve.Persistence and patience are mandatory in their management.Early recurrence or recalcitrance to therapy typically occurs, so long-term follow-up is required to assess adequacy of treatment.Recurrent lesions should be treated early to prevent regrowth.Combinations of therapies or successive changes in therapy should also be considered for unresponsive lesions.^[2]

[edit] MUSCULOSKELETAL DISORDERS

Musculoskeletal problems within the foot and ankle are diagnostically challenging.Structural deformities are usually self-evident either clinically or radiographically, but soft tissue, joint, and functional abnormalities are difficult to specify and manage.Fortunately, specific diagnoses of related disorders (e.g., tendinitis, bursitis, capsulitis) are not as important as general management, since treatment regimens for the related disorders are the same.When the etiology of a problem is overuse, regardless of the specific source of pain, rest and immobilization are generally effective.Diagnostic acumen is still essential in distinguishing among infectious, metabolic, and traumatic etiologies, however, since the management of each is different (Fig.130-4).

[edit] Forefoot: Digital and Metatarsal Disorders

Digital disorders become symptomatic primarily because of shoe pressure abutting on dorsal surfaces or squeezing the toes together.The digital deformity causing most distress is the hammer toe, which can affect children and adults alike.Although this term is generally used to denote any toe with a dorsal contracture, hammer toe is distinct from claw toe and mallet toe.A hammer toe has a dorsal (extensor) contraction at the metatarsophalangeal (MTP) joint and a flexion contracture at the proximal interphalangeal (PIP) joint (Fig.130-5, A).The contractures can result from dynamic imbalances of tendinous structures around the joints secondary to hypermobility or neuropathy, as well as from traumatic or arthritic processes.A claw toe, in addition to the MTP and PIP contractures, also has a flexion contracture at the distal interphalangeal (DIP) joint (Fig.130-5, B).A mallet toe is characterized by a single flexion contracture at the DIP joint, with weight on the tip of the toe (Fig.130-5, C).In all these conditions, abnormal pressures are applied on dorsal digital surfaces from shoes and on distal toe surfaces directly.Since these sites are not protected by a fat pad, painful digital keratoses often develop.Contracted toes also can lie under or over adjacent digits, causing painful interdigital corns.Since these deformities progressively worsen over time, patients need to consider corrective surgery when conservative measures fail to provide long-term relief.A simple arthroplasty with resection of the proximal phalangeal head can permanently correct these conditions, generally with a rapid recovery.^[4]

[edit] Hallux Valgus and Bunions.

Metatarsal problems are often categorized into first metatarsal and lesser metatarsal disorders because of the separate axes of motion and distinguishing pathologic entities.First ray deformities comprise the most significant metatarsal complaints, with bunion deformities affecting an estimated 3.8 million people annually. Hallux valgus, as bunions are more properly called, refers not only to the medial prominence of the first metatarsal head, but also to the lateral drifting (abduction) and valgus rotation of the great toe.^[6] The etiology of this condition, besides its strong familial predisposition, is a hypermobility of the first metatarsal, which allows it to drift progressively and medially.Hypermobility routinely accompanies a pronated foot (flatfoot) but is not specific to it.Concurrent with the adduction of the metatarsal is a lateral contracture of the hallux caused by a compensatory bow stringing effect of the long and short flexor (with sesamoids) and extensor tendons inserting into the great toe.In severe cases the great toe crowds the second toe, eventually causing a hammer toe of this digit.Progressive deformity results in not only a large bunion and abducted hallux, but a second toe that overlaps it as well (Fig.130-6).

Although hallux valgus can be the sequela of rheumatoid, psoriatic, or gouty arthritis, degenerative joint disease eventually develops as the joint slowly becomes subluxed.Bunions are not characteristic of only an elderly population.Juvenile and adolescent hallux valgus may occur and, when left unattended, may progress to the severe deformities seen so often in geriatric patients.Bunions are not always painful, and thus patients and physicians tend to ignore them as long as a shoe can fit over them.They insidiously worsen, however, and both patient and physician should consider correcting the deformity before severe degeneration of the joint.

Conservative treatment has not been found effective in arresting the progression of hallux valgus, although orthotic therapy has been advocated.Footwear should have adequate width and depth to prevent compression of the widened forefoot.When the deformity becomes symptomatic or progresses beyond a mild stage, reconstructive surgery is indicated.Many procedures have been described for this deformity, ranging from simple excision of the medial eminence to fusion or prosthetic implantation of the first MTP joint.^[6][4] The specific procedure performed should not be a matter of routine but based on the degree of deformity, presence of arthritis, age, and activity level of the patient.The goals of surgery are relief of pain and restoration of normal alignment of the first metatarsal and great toe.Rarely is a simple bunionectomy (e.g., Silver, McBride) advisable, since it does not correct the adduction of the first metatarsal.When bunionectomy is combined with a resection of the proximal phalangeal base (Keller arthroplasty), however, an excellent correction can be obtained in geriatric patients.Furthermore, most bunionectomies are easily performed under local anesthesia without the need for casts, crutches, or inpatient hospital stays.^[6] With much of the morbidity previously associated with these procedures obviated by current techniques, physicians should be less reluctant to advise reconstruction of moderate or severe deformities.

[edit] Hallux Rigidus.

Sometimes referred to as hallux limitus, hallux rigidus is a similar yet distinct condition of the first MTP joint.It implies a rigid great toe at the MTP joint,whereas hallux limitus indicates only a limitation of motion at this joint.^[3] The bunion in these patients lies dorsal to the metatarsal head and represents dorsal osteophytic proliferation secondary to abnormal function and degenerative changes within the first MTP joint (Fig.130-7).A prior history of injury to the great toe is a common inciting event.This disorder is frequently painful, especially on range of motion, and can significantly restrict normal activity.It also can progress from a mild limitation of dorsiflexion to a severe degeneration of the joint with attendant loss of motion.Conservative care in early stages consists of wearing nonconstricting, rigid-soled footwear with low heels and a trial of orthoses.As the condition progresses, surgery is frequently required to provide relief.^[3][4] Relatively mild arthrosis of the joint can be treated with cheilectomy, a debridement of the joint osteophytes.When an elevated first metatarsal is a principal component of the hallux limitus, cheilectomy is often combined with a plantar flexion osteotomy to increase the range of dorsiflexion.If severe arthritic changes are present, Keller bunionectomy, totalprosthetic implantation, or arthrodesis procedures should be considered.^[4]

[edit] Sesamoiditis.

Sesamoiditis of either the tibial or the fibular sesamoid or of both can be a very painful malady with an insidious onset and a chronic course if not diagnosed and treated early.The periosteal inflammation is usually the result of minor repetitive trauma, such as aerobic exercises or extended walking in thin-soled dress shoes or high heels.The inflammation may also involve the long flexor tendon, when the pain also extends along the central plantar aspect of the great toe.When acute trauma has occurred, sesamoid fracture or stress fracture must be ruled out.The diagnosis of sesamoiditis is made by eliciting maximal tenderness to direct palpation of the sesamoid in question.The patient usually has no swelling, erythema, or ecchymosis.Radiographs are negative, but bone scans may show signs of hyperemia and therefore may be falsely read as positive for fracture.

Treatment is based on protecting the injured part to avoid exacerbation of the inflammation.Since each step is essentially further trauma to the sesamoids, weight bearing must be limited or modified.Although crutches are rarelynecessary, accommodative padding with rest strapping (taping) of the foot frequently provides relief.Nonsteroidal antiinflammatory drugs (NSAIDs) should be prescribed to help resolve the inflammation.The patient should wear shoes with cushioned soles and low heels and avoid activities that aggravate the condition.Frequently, soft orthoses are fabricated that can off-load the sesamoid area during gait.These should be worn on a long-term basis to prevent recurrence once the sesamoiditis has resolved.Unresolved sesamoiditis may require sesamoid excision in selected patients.

[edit] Metatarsalgia.

Metatarsalgia is a nonspecific term that refers to pain in the ball of the foot around the lesser metatarsal heads.^[5] This problem can be caused by bone, joint, musculotendinous, neurologic, vascular, or dermatologic pathology.The examination must therefore focus on specific sites, signs, symptoms, and history to differentiate possible causes of discomfort in the lesser metatarsal region.

[edit] Morton's Neuroma.

Morton's neuroma is a classic cause of metatarsalgia that is usually centered in the third intermetatarsal and web space, between the third and fourth toes.^[5] It is actually a benign enlargement of the third common digital branch of the medial plantar nerve as it passes plantar to the deep intermetatarsal ligament and between the metatarsal heads.Compression within this compartment during walking in tight shoes is considered the etiology of this painful neuralgia.Women are affected much more often than men, but no specific age ranges are predisposed in the adult population.Symptoms include burning, tingling, sharp, or shooting pains into the third or fourth toe, especially when wearing shoes or on direct compression of the interspace.Removing the shoe and rubbing the foot provide temporary relief.Symptoms are progressive, increasing in intensity and frequency over months to years.Diagnosis involves exclud ing osseous or other pathology in the region, as confirmed by negative radiographic findings.Magnetic resonance imaging (MRI), ultrasound, or electrophysiologic examination is usually not necessary in establishing the diagnosis.

Initial treatment of Morton's neuroma consists of a change to comfortable footwear and occasionally orthoses.Local corticosteroid injections and a course of NSAID therapy may provide additional relief in acute cases, but these measures are usually only temporizing.In time, most patients require excision of the neuroma when symptoms become too severe to enable normal daily activities.Surgery usually provides immediate relief, with a fairly benign postoperative recovery.

[edit] Plantar Keratoses and Lesser Metatarsalgia.

Underlying IPKs, the physician can usually palpate the plantar surface of a prominent metatarsal head.Because of plantar displacement, excessive length (or shortened adjacent metatarsal), abnormal plantar prominence, or altered biomechanics, the metatarsal head bears more weight than adjacent bones during stance and gait.This creates excessive plantar pressure, and the IPK develops.These lesions are intractable unless the underlying bony deformity is addressed.Painful lesser metatarsal problems can be found even in the absence of a keratosis but are usually more acute in nature.^[5] As with sesamoiditis, repetitive moderate stress can result in a capsulitis, tendinitis, or osteitis on the plantar surface of the metatarsal head.On occasion, stress fracture or aseptic necrosis of a lesser metatarsal (Freiberg's infraction) needs to be considered and the diagnoses differentiated through appropriate radiographic techniques.

When aberrant functioning of the metatarsal is the cause of this type of metatarsalgia, treatment should begin with custom orthoses to redistribute the weight-bearing forces properly under the foot.^[2] This therapy is recommended in concert with footwear modification for almost any metatarsal problem.External bars and similar shoe alterations are employed less often than orthoses because patients generally resist such corrections.In recalcitrant cases, however, a metatarsal osteotomy can often be performed to realign or reconstruct the offending metatarsal such that all the metatarsals lie on the same transverse plane.Care must be taken, however, to prevent excessive shortening or dorsal displacement of the metatarsal head, since such errors can lead to transfer lesions on adjacent metatarsals.Although a variety of techniques are currently practiced, osteotomies are usually performed on the metatarsal neck through a dorsal approach to facilitate postoperative ambulation in a sur gical shoe.^[5][4]

[edit] Stress Fractures.

Stress fractures of the lesser metatarsals are fairly common, especially in younger persons engaging in new activities such as running or aerobics.Older patients are equally subject to these types of fatigue fractures from common activities such as missed steps or long walks in uncushioned dress footwear.The patient presents with a mildto moderate swelling of the forefoot, perhaps with some erythema but minimal ecchymosis.Usually the pain is localized to one or two metatarsal shafts dorsally.Typically, early radiographs are negative because the bone has no complete fracture.Bone scans are positive, however, making this the diagnostic modality of choice when early stress fracture is suspected.Plain films become positive approximately 2 weeks after the injury, with evidence of periosteal proliferation at the site of maximal tenderness (Fig.130-8).The physician can palpate a painful bony prominence, usually on the dorsum of the affected metatarsal.In some cases the relatively minor stress fracture can propagate to a complete transverse fracture of the metatarsal, especially when treatment is delayed or inadequate.In suspected cases, therefore, treatment should begin with a discontinuance of recreational activities or extended periods of walking.A standard postoperative shoe should be prescribed for exclusive use until symptoms have resolved.Usually, an Unna boot, rest strapping, or an elastic bandage is applied to provide further support and reduce swelling.Ice, rest, and elevation are warranted as well.Crutches are usually not required, and the patient can return to work if walking can be limited.Stress fractures respond quickly to these measures, with symptoms resolving within a few weeks.Strenuous activities are generally avoided for 4 to 6 weeks and then only after proper conditioning and footwear have been prescribed.

[edit] Bunionette.

Bunionette, or tailor's bunion, is a lateral prominence or enlargement of the fifth metatarsal head not restricted to any gender or age group.The pathology includes enlargement of the metatarsal head, lateral bowing of the fifth metatarsal, or both.^[3][4] Painful bunionettes can also arise from chronic shoe irritation over a normal fifth metatarsal head, causing only a soft tissue inflammation (adventitious bursitis).Similarly, a painful keratosis can develop over the lateral side of the fifth metatarsal head, indicating the role of footwear in the symptomatology of this disorder.Treatment therefore must initially be directed at providing relief from lateral shoe pressure, and when acutely inflamed, corticosteroid or NSAID therapy may be of benefit.Orthotic therapy is generally not successful.For patients with significant deformity or who are unresponsive to conservative measures, a partial metatarsal head resection or adductory fifth metatarsal osteotomy will correct the structural deformity (Fig.130-9).

[edit] Midfoot Disorders

Disorders of the midfoot do not present as frequently as those of the forefoot but still cause considerable discomfort and contribute to deformities of the forefoot.In most patients, midfoot structural disorders are related to problems of the rearfoot or leg and represent biomechanical disturbances that can significantly affect normal gait and propulsion.

[edit] Flatfoot.

Also called pes planovalgus or pes planus, flatfoot is the most significant of all midfoot disorders, affecting more than 4 million people at a rate of 18 per 1000 in the 1990 NHIS.Although this chronic structural deformityinfrequently originates in the midfoot in the absence of trauma, flatfoot usually results from more proximal disturbances of function.For example, a tight Achilles tendon (gastrocnemius equinus) restricts ankle joint dorsiflexion, and excessive pronation (including dorsiflexion) of the subtalar joint compensates for this during gait.The pronated subtalar joint allows an unlocking of the midtarsal joint (talonavicular and calcaneocuboid joints), which also results in excessive pronation.^[3] This general instability is translated into a hypermobility, which refers to the foot's excessive motion when it should be a stable, propulsive organ.The hyper mobility contributes to weakness of the foot, fatigue, hallux valgus with hammer toe formation, and inefficient forward propulsion in gait.Besides symptoms within the foot, excessive pronation frequently contributes to anterior shin splints or tendinitis, chondromalacia patellae, and chronic low back pain.These problems are particularly relevant in athletes or people in exercise programs because the forces sustained by the weakened feet are exaggerated.Overuse injuries of the lower extremities are therefore more prevalent and more difficult to resolve in patients with flatfeet.

A flatfoot is not a simple deformity and can have multiple etiologies and specific sites of involvement.^[3] It can be congenital or acquired, rigid or flexible, and primary or secondary.Pes planovalgus may result from a neuromuscular disease, stroke, trauma, arthritis, primary structural deformity, or a peroneal spasm secondary to a fractured tarsal coalition.Peripheral neuropathies and other acquired or congenital disorders resulting in weakness, contracture, or paralysis of leg musculature and affecting the normal mechanics of the foot can produce a flatfoot deformity.Generally, spasticity of the gastrocnemius-soleus complex results in flatfoot, whereas flaccidity results in a high-arched foot.Weakness of the posterior tibial muscle also leads to flatfoot, whereas spasticity of the long flexors leads to a high arch.Neuromuscular disorders must be evaluated to determine muscle groups affected and the qualitative impact on foot mechanics.Congenital flatfoot results from developmental aberrations such as clubfoot (talipes equinovalgus), congenital convex pes valgus, talipes calcaneovalgus, fore foot varus, torsional disturbances of the lower extremities, or ligamentous laxity.These deformities must be properly evaluated for rigidity or flexibility, since nonreducible rigid deformities portend a poor prognosis and require surgical intervention.Minor structural or functional deviations from the norm, such as forefoot varus, accessory navicular with altered insertion of the posterior tibial tendon, flexible calcaneovalgus, or tightened heel cords, are generally con sidered nonpathologic or idiopathic causes of flexible pes planovalgus.Acquired flatfoot is usually the result of neurologic disorder or trauma to the foot or leg.The most common cause of acquired adult flatfoot is a rupture of the posterior tibial tendon, frequently seen in elderly rheumatic patients.This is marked by a unilateral deformity in a patient with a prior history of injury or prodromal symptoms of chronic posterior tibial tendinitis (Fig.130-10).

Once potential pathologic causes of flatfoot have been addressed, treatment of symptomatic hypermobile pes planusshould always begin with orthotic therapy.^[3] In children with nonpathologic deformities, orthotic treatment should be initiated by age 5, even without symptoms.Early support of the flat foot in the growing child can promote better structural development and fewer symptoms within the feet and legs.It cannot be presumed, however, that orthoses will correct the structural deformity in either the child or the adult patient.The purpose of the orthosis is generally to relieve symptoms by providing structural support under the weakened foot, by limiting the amount of abnormal pronation, and by allowing more efficient locomotion.

Foot orthoses include prefabricated “customizable” devices and others custom made by laboratories or health care professionals.Since treatment for pes planus is aimed at functional improvement of the pronated foot, custom-fabricated functional orthoses should be used.Custom orthoses are usually categorized as flexible, semirigid, or rigid designs depending on the materials used in fabrication.The specific type used depends on the patient's age, weight, and activity level as well as the deformity's severity and symptoms.Flexible orthoses, often fabricated from softer materials (e.g., Plastazote, microcellular rubbers) can provide gentle support as well as cushioning.They are useful in sports medicine and for geriatric or diabetic patients.Semirigid orthoses are traditionally fabricated from leather composites, although newer synthetic materials are less bulky and more durable.A compromise between flexible and rigid designs, semirigid devices provide good support with a degree of flexibility.Many sport orthoses fabricated in commercial laboratories fall in this category.Rigid orthoses are the gold standard of orthotic devices and provide the greatest control over foot function and abnormal pronation (or supination).Although previously made from stainless steel, rigid orthoses are currently fabricated from very durable materials such as polypropylenes and thermoplastics.Often guaranteed against fatigue and breakage, these low-profile “high-tech” devices can be computer manufactured from digital scanning of plaster cast impressions of the feet.Advances in fabrication technology have also resulted in thinner, easier-to-fit designs that are extremely comfortable and more exacting in their correction of abnormal function.

Since orthoses can control function and ameliorate symp toms in flatfeet, only the most severe of deformities usually require reconstruction.These more pathologic entities include congenital vertical talus, tarsal coalitions, and neurologic or traumatic conditions.Excessive ankle equinus secondary to triceps surae contractures often requires Achilles tendon lengthening in concert with any localized foot procedure.^[4] The Kidner procedure removes the accessory navicular and tightens the pull of the posterior tibial tendon.Variations of this procedure are also performed in cases of partial or complete rupture of the posterior tibial tendon.^[7]

[edit] High-arched Foot.

Also known as pes cavus, a high-arched foot is not as common as flatfoot (pes planus) but is more difficult to treat.Classically seen with neurologic disorders such as polio or peroneal muscular atrophy, pes cavus is generally characterized by a lack of flexibility, an anterior equinus (plantar flexion) of the forefoot, and claw toes.^[3] Although underlying neurologic disturbances should always be considered in evaluating such patients, idiopathic or nonpathologic pes cavus of a moderate degree is the most frequent presentation (Fig.130-11).Cavus feet are marked by excessive supination of the rearfoot and forefoot whereby the plantar-flexed first ray (medial column) causes abnormal inversion (supination) of the forefoot to bring the lateral column (fourth and fifth rays) to the ground in stance and gait.Because of the forefoot equinus and attendant exag geration of metatarsal declination, the toes are usually clawed due to a loss of the normal stabilizing mechanism of the intrinsic muscles around the MTP and interphalangeal joints.Hyperactivity of the peroneus longus, posterior tibial, and long flexors or weakness of the triceps surae, peroneus brevis, anterior crural, and intrinsic foot muscles can all contribute to high-arched foot in varying degrees.Multiple imbalances between agonist and antagonist muscle groups often coexist, especially in patients with documented neuromuscular diseases.Therefore detailed neuromuscular, biomechanical, and gait evaluations are required to assess both the etiology and the specific pathomechanical attributes.

In the absence of trauma or recent neurologic disease, most patients adapt well to their longstanding cavus foot deformities, except for repeated ankle sprains (“weak ankles”), persistent plantar calluses, or painful dorsal digital corns.Periodic debridement and cushioned insoles in shoes with adequate depth for the toes are usually adequate initial measures for relief of hyperkeratotic lesions.Patients with complaints of lateral or postural instability or painful meta tarsalgia, however, are best treated with custom functional orthoses to limit supinatory motion during gait.In severe cases unresponsive to these measures, surgery can be performed to realign the forefoot, stabilize lateral ankles, or correct digital deformities.^[3]

[edit] Rearfoot Disorders

[edit] Heel Spur and Plantar Fasciitis.

Heel spur syndrome and its soft tissue analog, plantar fasciitis, are the most common disorders of the hindfoot.The painful heel can be attributed to rheumatic diseases such as rheumatoid arthritis, gout, Reiter's disease, ankylosing spondylitis, or other seronegative spondyloarthropathies (see Chapter 137 ).^[2][3]These arthritic entities are distinguished more by erosive changes to the heel than by spur formation.Heel spurs and plantar fasciitis, however, are generally considered to be pathomechanical.With each step the plantar fascia is drawn taut as it resists collapse of the arch, a function analogous to a windlass mechanism.Concurrently, there is a rather constant traction on the periosteal insertion point on the calcaneus.Over time or with overuse, this constant traction results in a spur formation at the anteroinferior aspect of the calcaneus.This enthesopathy is an insidious process in many cases, since patients often have rather large, asymptomatic calcaneal spurs as incidental findings on radiographs.Conversely, patients with acutely painful heels in the absence of trauma can have negative radiographs.These patients would then be considered to have a heel “bursitis” or localized plantar fasciitis at the insertion of the aponeurosis.Typical plantar fasciitis, as seen in overuse injuries to athletes, usually extends more distal along the medial band of the fascia.Excessive pronation is the underlying etiology of heel spur syndrome, except when a cavus foot type is subjected to repetitive heel trauma.Radiographs confirm a spur or rule out other causes of heel pain when plantar fasciitis is suspected.Differential diagnoses in patients with heel pain include stress fracture or bone contusion, subtalar joint pathology, tumor, rheumatic disease, nerve entrapment, plantar fascial tear, Achilles tendinitis, calcaneal apophysitis, or Sever's disease (calcaneal avascular necrosis).

Treatment for heel spur syndrome, including patients with plantar fasciitis only, initially requires attenuation of activities, NSAIDs, and rest strapping of the foot to limit pronation.Heel cups or prefabricated orthoses can be useful, as can simple heel cushions or cutouts.Night splints may provide symptomatic relief by maintaining a stretch on the fascia and preventing nocturnal contracture.Corticosteroid injection is reserved for recalcitrant cases and is usually limited to three injections from a medial approach.Athletic or cushioned walking shoes with slight heel elevation are also beneficial.When improvement is noted, a soft orthosis is usually fabricated to provide support and cushioning for the heel.This should be used on a long-term basis to improve foot function and prevent relapse.Once comfortable, patients can gradually discontinue NSAID therapy while continuing with orthotic therapy.Physical therapy modalities such as ultrasound are prescribed when these prior measures fail to provide relief.Below-knee casting or immobilization in ambulatory cast braces with or without crutches must also be considered in severe cases.Inferior calcaneal heel pain usually resolves in about 6 months.Patients who do not improve for 12 months or longer despite exhaustive efforts may consider heel spur surgery or plantar fasciotomy.Medial calcaneal nerve entrapment should also be evaluated at this stage and released as necessary.Since the great majority of patients eventually recover with conservative therapy alone, surgery should not be the initial treatment.

[edit] Posterior Tibial Tendinitis.

Posterior tibial tendinitis is a very painful condition of the rearfoot often mimicking a medial ankle sprain or sometimes medial arch pain.It most frequently affects people beyond middle age who are moderately active and may have a history of other rheumatic complaints.It is also a common overuse injury in younger individuals or in people with significant degrees of foot pronation.Since the posterior tibial muscle is the major antagonist to the peroneus brevis tendon, it is the major supinator of the foot and primarily functions to resist pronation of the subtalar and midtarsal joints during gait.^[3] The pronated foot alters normal anatomic relationships and vectors of force, resulting in inefficiency of the posterior tibial muscle.This insufficiency causes overuse compensation, and the muscle functions beyond its usual phasic activity, leading to both fatigue and chronic tendinitis.Chronic posterior tibial tendinitis can then lead to partial tearing, internal degeneration, or complete rupture, which is a classic cause of adult acquired flatfoot deformity.Symptoms include pain and mild swelling just below the medial malleolus as the tendon courses below this structure to insert on the navicular and plantar midfoot.Pain is exacerbated by active inversion and plantar flexion of the foot, especially when standing on the ball of the foot and toes.In cases of complete rupture the pain is usually gone, but in addition to the unilateral flatfoot, toe stance demonstrates a lack of heel and arch inversion.During stance the forefoot is greatly abducted, and when viewed from behind, the “too many toes” sign is evident.The pain from the chronic tendinitis is usually related to activity but is persistent from day to day, progressive, and almost disabling in its most severe forms.

Treatment of posterior tibial tendinitis is based on preventing pronation of the foot, resting, and reducing inflammation of the tendon and tendon sheath.Although rest strapping and resistive ankle taping are often effective, cast or cast bracing with or without crutches may be necessary to provide relief.A prolonged course of NSAID therapy is also necessary, frequently in conjunction with physical therapy.Corticosteroid injections are usually not recommended because of the risk of subsequent tendon atrophy and rupture.Custom orthotic therapy is always required to support the foot and reduce tension on the posterior tibial tendon.Rigid orthoses are preferable, but semiflexible or flexible orthoses should be fabricated as an alternative in patients who are unable to tolerate rigid support.Debridement of the degenerated tendon or repair and augmentation of the ruptured posterior tibial tendon should be reserved for patients who complain of chronic severe pain or instability.^[7] Surgery in elderly patients requires prolonged immobilization without weight bearing, making such procedures inadvisable except in the most severe circumstances.

[edit] Ankle Disorders

[edit] Sprains.

Ankle sprains are the most common ankle problem presented to primary care physicians.Lateral ankle sprains of the lateral collateral ligaments are the usual presentation of such disorders, since medial sprains of the deltoid ligament are frequently accompanied by lateral ankle fractures.^[7] Three separate collateral ligaments of the anterolateral talocrural joint are subject to tear or partial tear on inversion injury (Fig.130-12).The most anterior and most frequently torn of the three is the anterior talofibular ligament (ATFL).This intracapsular, fan-shaped ligament extends from the anteroinferior end of the fibular malleolus and inserts into the lateral surface of the body of the talus.Primarily resisting ankle inversion during plantar flexion, the ATFL is usually the first to be ruptured during inversion injuries because the ankle is least stable when plantar flexed.The extracapsular, cordlike calcaneofibular ligament (CFL) courses from the inferior tip of the fibula to the lateral surface of the calcaneus under the peroneal tendon sheath.The CFL primarily resists inversion during ankle dorsiflexion and usually ruptures only second to the ATFL in severe inversion injuries.The intracapsular posterior talofibular ligament(PTFL), the strongest of the three, runs posteriorly from the fibular malleolus to the posterior lateral surface of the talus.The PTFL is infrequently ruptured except in cases of severe trauma with associated osseous injury to the ankle.Diagnosis of a lateral ankle sprain should be obvious by the history and signs of acute edema, ecchymosis, and pain at the anterolateral aspect of the ankle.Radiographs are taken to rule out associated lateral ankle or talar fracture.The examiner must also palpate the base of the fifth metatarsal in such injuries, since ankle sprains can often be accompanied by fracture of the styloid process or proximal fifth metatarsal shaft (Jones fracture).When present, such fractures require prolonged cast immobilization or open reduction with internal fixation.

For isolated ligamentous sprains, ice, rest, elevation, and some form of immobilization are required.Crutches should be used in acute cases when symptoms and examination warrant no weight bearing.Immobilization can be a simple elastic bandage or rest strapping in minor sprains or below-knee casting, ambulatory cast bracing, or ankle stirrup braces for more severe injuries (Fig.130-13).For chronic ankle instability resulting from repeated sprains, an ankle stirrup or taping is recommended when patients engage in athletic activities.Severe instability, especially in competitive athletes, can be corrected with a variety of lateral ankle stabilization procedures.^[4][7] Such operations attempt to restore ligamentous integrity with direct repair or by augmentation with tendon transfer.In patients with chronic ankle pain and a history of previous sprain in the absence of severe instability, the physician must consider a talar dome osteochondral lesion (osteochondritis dissecans), which can usually be detected only by computed tomography (CT) scan or MRI and which rarely heals without intervention.Arthroscopic procedures can remove or repair these osteochondral fragments and are an alternative to open ankle arthrotomy procedures.

[edit] LOCAL ANESTHESIA

The primary care physician may frequently need to treat an acute paronychia or toenail injury, remove a foreign body, or fulgurate a plantar verruca.Local anesthetic injection techniques augment the physician's ability to handle such foot maladies and provide comfort to patients.The injection technique used in the foot depends on the condition and its location.Techniques include local infiltration, digital block, specific nerve block, or regional anesthesia (ankle block).The basic premise is that the afferent sensory nerves must be blocked proximal to the site of the lesion being treated.For example, when treating a paronychia, it is always advisable to perform a digital block at the base of the toe and never to inject at the distal pulp of the toe or adjacent to the nail border.Distal toe injections are simply too painful because of the tautness of the subcutaneous tissues.Conversely, when removing a simple plantar wart, it is often easier to infiltrate under and around the lesion than to perform a nerve block.With the patient's comfort always in mind, the excision of multiple plantar lesions is best approached with a posterior tibial nerve block at the medial ankle rather than repeated injections on the sole of the foot.

Lidocaine (0.5% or 1%) is the most frequently used of the local agents because of its rapid onset.Bupivacaine (0.5%) is usually mixed with the lidocaine to provide lasting anesthesia for 8 to 12 hours.Epinephrine in combination with the anesthetic agent provides not only increased duration of activity through a delay of absorption but also vasoconstriction and intraoperative hemostasis.The use of epinephrine in digits is still controversial, although many digital blocks have employed this agent without adverse sequelae.Discretion and proper patient selection are required, however, when using epinephrine in any foot procedure.

Digital blocks are simple to perform and can be used in any patient who requires anesthesia of any part of a toe.Most digital operations should be done under local anesthesia unless a specific indication requires general or spinal anesthesia.Usually, all four digital nerves must be infiltrated to produce an adequate block of the entire toe.Either a ring block technique (Fig.130-14) or an inverted-V block (Fig.130-15) can be employed using a 25-gauge 1½-inch needle on a 3-ml syringe.A total of 3 ml for the great toe and 2 ml for the lesser toes is usually sufficient to provide complete digital anesthesia after about 5 minutes.When the metatarsal head or MTP joint must be anesthetized, a more proximal V block around the metatarsal neck should be used.Bunionectomy procedures usually require a digital block in combination with a circumferential segmental block of the first metatarsal proximal to the metatarsal neck.

Ankle blocks are extremely useful in providing anesthesia to the entire foot when multiple sites must be approached.The primary care physician rarely needs to perform this technique, but a general knowledge of the anatomic location and distributions of the nerves crossing the ankle is beneficialwhen an isolated nerve block is required.The two deep nerves that cross the ankle, the deep peroneal (anterior tibial) and the posterior tibial, run adjacent to the dorsalis pedis and posterior tibial arteries, respectively.The other four nerves are all superficial and, from lateral to anterior to medial, are the sural, intermediate dorsal cutaneous, medial dorsal cutaneous, and saphenous nerves.The sural nerve lies just behind and inferior to the lateral malleolus and innervates the lateral border of the foot and fifth metatarsal.The two branches of the superficial peroneal nerve can often be seen or palpated directly under the skin on the ankle's anterior surface; they provide sensation to the dorsum of the foot and toes.The saphenous nerve lies anterior to the medial malleolus and runs with the greater saphenous vein, providing sensation to the medial border of the foot.These four superficial nerves are easily blocked with simple subcutaneous infiltration around the nerves.The deep peroneal nerve is blocked by palpating the dorsalis pedis artery and injecting around it deep to the fascia, taking care to aspirate before injection.The large posterior tibial nerve lies deep to the flexor retinaculum and runs adjacent to the posterior tibial artery and veins.The three branches—medial calcaneal, medial plantar, and lateral plantar nerves—supply the medial and plantar heel, medial plantar sole and toes, and lateral plantar sole and toes, respectively.Anesthesia of these sites is best obtained concurrently with a block of the posterior tibial nerve behind, deep to, and just above the tip of the medial malleolus.Once again, the artery should be palpated and the needle inserted so that infiltration will occur around the vessel and nerve without penetrating either structure.Aspiration should always be performed to prevent intraarterial injection.If significant pain and paresthesias occur during the injection, the needle should be slightly withdrawn to avoid injection directly into the nerve.Approximately 6 to 10 ml is required for this difficult injection, delivered with a 25-gauge needle on a 10-ml syringe.

[edit] THE DIABETIC FOOT

Of the 16 million diabetic patients in the United States, an estimated 15% to 20% will develop serious foot lesions.^[8] With a 15-to 40-fold greater risk of lower extremity amputation than for those without diabetes, one half of all nontraumatic amputations in the United States are performed on diabetic patients.^[9] In 1994 more than 67,000 diabetes-related amputations were performed, not including data from military, Veterans Administration, or Indian Health Service hospitals.Typically, 80% to 85% of these amputations can be attributed to a nonhealing foot ulceration.Since the 5-year survival rate only approaches 50% after a major amputation, prevention or aggressive treatment at an early stage is essential.Many feet and limbs can be salvaged through a better understanding of the peculiarities of such disorders in diabetic patients.

The most characteristic of all diabetic foot lesions is the plantar ulceration, often termed a mal perforans ulcer or trophic ulcer. The underlying pathophysiology is a sum of the systemic alterations occurring in diabetes with manifestations in the lower extremities.^[8][10] Most diabetic foot ulcers can broadly be categorized into neuropathic, ischemic, or neuroischemic etiologies.Further grading scales use depth of penetration, presence of infection, or degree of tissue loss, but no consensus exists on a universal classification system.The most widely used grading system is the Wagner scale,consisting of grades 0 to 5, each representing progressively deeper or more extensive loss of tissue.^[8] As might be expected, higher grades portend a worse prognosis and necessitate more aggressive surgical interventions or amputations.

A triad of intrinsic systemic disorders frequently cited as contributing to diabetic foot disease includes peripheral neuropathy, peripheral vascular disease, and impaired resistance to infection.This “triopathy” does not necessarily need to coexist in order to complete a causal chain to ulceration.Some form of trauma, when applied to the high-risk diabetic foot, can result in ulceration even in the presence of a single risk factor when such injuries are neglected or undetected.Evidence indicates that neuropathy, minor precipitating trauma, and structural foot deformity (e.g., hammer toes, Charcot's foot) are the three most common causes implicated in diabetic foot ulceration.Usually, however, interactions occur among multiple contributory factors in the etiology of diabetic foot ulceration^[10](Fig.130-16).

Peripheral neuropathy is an extremely common complication of diabetes mellitus, affecting about 50% of patients with longstanding disease.^[9] Approximately 70% of diabetic foot ulcerations can be attributed primarily to this underlying permissive factor.Neuropathy can be further categorized into motor, sensory, or autonomic components, with combinations present in many patients.Motor neuropathy results in muscle weakness, atrophy, dysfunction, and gait disturbance.Clinical manifestations include footdrop from anterior crural muscle atrophy or characteristic hammer toes from intrinsic muscle atrophy (intrinsic minus foot). Sensory neuropathy presents in the classic “glove and stocking” distribution, symmetrically affecting the toes first and gradually moving proximally.Losses in deep tendon reflexes, proprioception, vibratory, pain, and light touch sensation are the most common findings, collectively called “negative” symptoms.Conversely, painful neuropathy is a distressing manifestation of peripheral neuropathy consisting primarily of “positive” symptoms, such as burning, gnawing, or lancinating pains that worsen at night.The painful-painless leg is a descriptive term used to identify patients with positive symptoms of painful neuropathy in concert with negative symptoms characteristic of the insensate foot and limb. Autonomic neuropathy has gained attention in recent years as an early manifestation of neuropathy and a significant factor in foot ulceration.^[8][9][10] Autonomic dysfunction of thermoregulatory mechanisms in the foot results in decreased vascular tone and increased skin blood flow.Arteriovenous shunting is widespread and diverts blood flow from the nutrient capillary beds.There is also a concomitant impairment of normal hyperemic responses to injury, putatively related to insufficient endothelial cell production of nitric oxide.Sudomotor dysfunction, manifested by anhidrosis, produces dry skin that is extremely susceptible to cracking and fissuring.These are common precursors to ulceration and infection in the diabetic population.

Peripheral vascular disease, long thought to be the primary etiology of diabetic foot ulcerations, plays a dominant role in only a third of such lesions and often coexists with neuropathy.Large-vessel atherosclerotic lesions affecting the tibioperoneal trunk of the lower leg are the hallmark of diabetic macrovascular disease, although occlusions of the aortic bifurcation, iliac, and femoral systems are also common.^[9] In the typical scenario, therefore, a diabetic patient can present with a gangrenous foot in the presence of a palpable popliteal artery.A relative absence of atherosclerotic disease in the foot makes distal vascular reconstruction to the dorsalis pedis or posterior tibial arteries the limb-salvaging procedures of choice in most patients. Diabetic microangiopathy refers to disease of the capillaries, the hallmark being a thickening of the capillary basement membrane and a resulting impairment of leukocyte diapedesis and nutrient exchange.There is no intravascular occlusion of these vessels, a longstanding misconception that gave rise to the term “small-vessel disease,” which should be abandoned.

Susceptibility to infection and an impairment in the ability to fight established infections have long been recognized as significant factors in the etiology of diabetic foot infections, ulceration, and gangrene.^[10] Although infection is infrequently a direct cause of ulceration, ulcers can be infected and often place the limb at risk of amputation.The diabetic patients' “immunopathy” is caused by a deficiency in the phagocytic activity of leukocytes, impaired intracellular bacterial killing, and a defect in normal chemotactic mechanisms.Even common pathogens can result in overwhelming infections, especially in the presence of neuropathy and ischemia.Usually “benign” bacteria such as Staphylococcus epidermidis or enterococci assume extremely pathogenic roles in the diabetic milieu.Anaerobic infections with Bacteroides species are characteristic of diabetic foot infections, although they rarely cause infection as isolated organisms.Polymicrobial infection is the rule in most severe diabetic foot infections, with gram-positive cocci, gram-negative rods, and anaerobes being cultured simultaneously from deep specimens.Empiric antibiotic therapy for limb-threatening infections should always attempt to cover a broad spectrum of organisms until final specification and sensitivities are received.Osteomyelitis is an ever-present complication of such infections and must be suspected in deeply probing, longstanding, or recalcitrant ulcerations.Although ulcerations will not completely heal when underlying bone or joint infection exists, local bone debridement and culture-specific antibiotic therapy, with vascular reconstruction as necessary, are successful in eradicating such infections and preserving limb integrity.

Trauma is usually the precipitating event in the development of diabetic foot infections or ulcerations.^[8][9][10] Although such trauma can be acute (sharp, mechanical, thermal, chemical), most foot lesions in the diabetic patient are caused by the minor repetitive trauma of walking and moderate pressures, the high pressures of a tight shoe, or any degree of abnormal pressure against a structural deformity.Altered biomechanics, including increased plantar pressures, bony abnormalities (e.g., hammer toes, bunions), and limited joint mobility have been associated with an increased risk of ulceration and amputation in the diabetic population.^[9] Thus, the etiology of any lesion must be investigated with the assumption that some trauma has a role in its development.In the absence of acute trauma, dorsal, medial, and lateral lesions are usually caused by tight shoes, whereas plantar lesions are the result of repetitive moderate stress or neglected preexisting hyperkeratoses.Burns are common precursors to ulceration, especially in the insensate foot, and most often result from hot foot soaks or walking barefooted on hot sand or pavement.Acute trauma in the presence of neuropathy and abundant vascular supply can also leadto the onset of another characteristic diabetic foot disorder, Charcot's foot or osteoarthropathy.The ensuing foot deformity creates abnormally high pressures during walking and frequently leads to chronic plantar ulceration (Fig.130-17).

[edit] Treatment

Treatment of foot ulcerations must focus on the contributory factors and must be appropriately assessed at the onset.Acute infections are treated by culture-directed antibiotic therapy.Ischemic lesions must be recognized by their atrophic appearance and lack of pedal pulsations and referred for vascular consultation.Such lesions infrequently heal without restoration of pulsatile blood flow.Above all, non–weight bearing or attenuation of weight bearing is essential for the resolution of any ulceration.^[8] The neuropathic individual, for example, will continue to walk on the ulcerated foot because of absent pain sensation or denial of the ulceration.Sincewalking (trauma) is a usual causative factor in ulceration, healing will not commence until walking has ceased.Although total non–weight bearing is the ideal situation, pressure-attenuating methods include foam pressure-dispersion dressings, healing sandals, surgical shoes, total contact casting, and removable cast braces.Local wound care consists of daily or twice-daily dressing changes with a topical agent of choice (e.g., quarter-strength povidone-iodine solution, saline, silver sulfadiazine cream).Topically applied growth factors (e.g., becaplermin gel, Regranex) facilitate healing of uncomplicated foot ulcerations compared with saline alone.Clinical trials are also being conducted to assess the efficacy of tissue-engineered dermal replacements.Even when proven beneficial, however, any topical agent, graft, or dressing cannot supplant the need for pressure reduction, treatment of infection, and abundant blood flow.^[8]

Recurrent ulcers usually indicate a persistent bony structural deformity, shoe problem, or biomechanical foot disorder that needs attention to allow final resolution of the problem.Recalcitrant ulcers may indicate this same problem but also may suggest inadequate treatment, noncompliance, or an unrecognized infection and osteomyelitis.Overall treatment of foot ulcers therefore requires immediate attention not only to infection, circulation, and pressure reduction, but to long-term prevention as well.Prevention encompasses proper foot care, patient education, periodic examination, appropriate footwear, and prophylactic foot surgery as necessary to correct structural deformities.^[8] Multiple studies from the United States and abroad indicate that more than a 50% reduction in ulcer recidivism and subsequent amputation can be realized through appropriate education, regular podiatric care, and appropriate footwear.Education can consist of simple talks or handouts regarding potential diabetic foot problems and how to recognize and avoid them.Provider education is also necessary to ensure that appropriate screening and examination techniques are reinforced as highly effective measures to detect early lesions or patients at risk of ulceration.Regular podiatric care involves bimonthly visits for examination and routine care of toenails and calluses.While serving as forums for constant patient education, such visits also provide a mechanism for early detection of potential problems and appropriate intervention.Therapeutic footwear ranges from simple molded insoles in athletic shoes to extra-depth shoes to custom-molded shoes, depending on the severity of foot lesions and the magnitude of foot deformity.When shoe therapy alone is not effective, corrective surgery is recommended in the appropriate patient and may be the best chance for permanent resolution of a recurrent problem.

As with most complex medical disorders, management of the diabetic foot should ideally be accomplished through a multidisciplinary approach.^[8] The primary care physician or the podiatrist who regularly attends the patient should serve as the gatekeeper and overseer of the patient's foot health.When problems arise, an organized plan should commence for referral to the appropriate service or consultant.The emphasis is on early aggressive care and concomitant limb preservation.With such an organized approach to the high-risk foot in diabetes mellitus, the worldwide goal of a 50% reduction in lower extremity amputation can be met or exceeded within the next decade.

[edit] REFERENCES