Many acute hand and upper extremity infections should be treated as surgical emergencies to avoid stiffness, contracture, pain, and amputation. Proper treatment requires understanding of anatomy and how this influences the behavior of certain infections, common offending organisms, antibiotic treatment, management of host factors, and surgical intervention. This article reviews the microbiology, antibiotic coverage, and surgical treatment of the most common infections in the hand: paronychia, felon, herpetic whitlow, flexor tenosynovitis, deep space infections, septic arthritis, bites from humans and animals, necrotizing fasciitis, mycobacterium infections, and fungal infections. Recommendations are based on the most recent available evidence.
Key points
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Acute hand infections are most commonly caused by Staphylococcus spp and Streptococcus spp, with an increasing prevalence of methicillin-resistant Staphylococcus aureus (MRSA).
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Empiric antibiotic coverage should be withheld until cultures have been obtained. Then it should begin with broad-spectrum treatment directed by the injury environment and mechanism, including strong consideration for coverage of MRSA.
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The cornerstone of surgical treatment includes incision, drainage, debridement, and irrigation followed by daily dressing changes.
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Herpetic whitlow is a viral infection that may mimic acute bacterial infections and typically resolves spontaneously without treatment.
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Flexor tenosynovitis can be diagnosed by the classic signs of fusiform swelling, flexed resting posture, flexor sheath tenderness, and pain with passive extension.
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Septic arthritis of the wrist is typically diagnosed by a joint aspirate white blood cell count greater than 50,000 with 75% polymorphonuclear lymphocytes. It should be treated as soon as possible.
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Bite injuries should always be explored for involvement of an underlying joint or tendon, especially human bite clenched fist injuries over the metacarpal head.
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Necrotizing fasciitis is a life-threatening condition with a mortality rate of 33% that requires emergent surgical debridement.
Introduction
Infections of the hand are present in all communities, but prevalence is dependent on patient factors such as immunodeficiency (HIV, diabetes, malnutrition) and exposure (occupation, intravenous drug use). The epidemiology of cultured organisms has demonstrated a trend toward increasing rates of methicillin-resistant Staphylococcus aureus (MRSA) species, although many infections are polymicrobial or culture-negative. Rapid treatment of these infections with appropriate surgical decompression, debridement, and antibiotics, followed by wound care and hand therapy is required to minimize or prevent lasting sequelae.
Introduction
Infections of the hand are present in all communities, but prevalence is dependent on patient factors such as immunodeficiency (HIV, diabetes, malnutrition) and exposure (occupation, intravenous drug use). The epidemiology of cultured organisms has demonstrated a trend toward increasing rates of methicillin-resistant Staphylococcus aureus (MRSA) species, although many infections are polymicrobial or culture-negative. Rapid treatment of these infections with appropriate surgical decompression, debridement, and antibiotics, followed by wound care and hand therapy is required to minimize or prevent lasting sequelae.
Microbiology
The most common hand pathogens are S aureus, Streptococcus spp, and gram-negative species. Staphylococcus is the primary organism in 50% to 80% of infections. MRSA species are becoming more prevalent both in community and hospital settings with current rates as high as 78%. Industrial and home-acquired infections routinely involve a single gram-positive organism, whereas infections from intravenous drug use, bites, mutilating farm injuries, and those associated with diabetes mellitus are generally polymicrobial with gram-positive, gram-negative, and anaerobic species. Some of the most common risk factors for various bacteria include the following:
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MRSA infections are more common in patients with diabetes mellitus, immunocompromised patients, intravenous drug abusers, prisoners, and homeless individuals
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Alpha-hemolytic streptococcus and S aureus are the most common pathogens in human bite infections
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Eikenella corrodens is isolated in approximately one-third of human bite wounds
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Pasteurella multocida commonly infects animal bite and scratch wounds
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Necrotizing fasciitis can be caused by group A streptococcus alone or infections can be polymicrobial, involving alpha-hemolytic and beta-hemolytic streptococci, Staphylococcus spp, and anaerobes
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Fungi and atypical mycobacterium cause chronic indolent infections.
Antibiotics
Empiric antibiotics should be administered after performing cultures and Gram stain. Initial antibiotics should be aimed only at suspected organisms because overly broad coverage can select for resistant organisms, is costly, and needlessly exposes patients to side effects. However, increasing rates of MRSA suggest that empiric treatment to cover methicillin-resistant organisms is routinely advised, particularly in urban regions. Box 1 serves as a guide for the selection of appropriate antibiotic treatment.
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Cefazolin and penicillin G: intravenous antibiotic coverage for aerobic and anaerobic pathogens in serious infections requiring incision and drainage and hospitalization
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Gentamicin (gram-negative coverage): if intravenous drug abuse is involved or the patient is diabetic
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Vancomycin: the drug of choice for cases of methicillin resistant MRSA. Occasionally MRSA is sensitive to Septra, quinolones, tetracyclines, or rifampin; however, rifampin should never be used as a single agent
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Penicillin G (parenteral) or first-generation cephalosporin: empiric coverage for human bites; however, some investigators also recommend aminoglycoside coverage
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Piperacillin-tazobactam or ampicillin-sulbactam: good initial coverage for human and animal bites
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High doses penicillin G and aminoglycoside: empiric coverage for necrotizing faciitis
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Clindamycin: used for both anaerobic coverage and, in the case of hemolytic streptococcal infection, to stop toxin production
Patient factors
Immunosuppressive drugs, acquired AIDS, and diabetes mellitus predispose patients to hand infections. In diabetic hand infection, treatment is often delayed, resolution slowed, repeated debridement is often necessary, and amputations are frequent (20%–63%) to control infection or because of poor function. Hand infections in AIDS patients are typically from routine pathogens with atypical presentations and unusually virulent courses. Herpetic lesions are unusually dire and often require antiviral treatment. Diabetes, alcohol, and intravenous drug abuse are risk factors for necrotizing fasciitis.
Incision and wound management
Successful management of hand infections predates antibiotics. Incision and drainage remains the basis of treatment. Straight incisions are preferred to avoid flap necrosis. Placement over tendons or neurovascular structures is discouraged. Highly contaminated wounds should be left open and dressed with moist gauze and a splint, immobilizing digits in the intrinsic-plus posture and maintaining the breadth of the first web space. Sometimes repeated debridement is necessary until the wound is clean enough for delayed closure or healing by secondary intention. Wound closure over irrigation or suction drainage is sometimes feasible. Vacuum-assisted closure therapy (also known as negative pressure wound therapy) has transformed the management of large open wounds arising from extensive debridement, such as in necrotizing fasciitis. Wounds should be reexamined at 24 to 48 hours. Dressings are changed daily thereafter. Incorporating whirlpools or soaks can help encourage continued drainage. Hand therapy is initiated after inflammation and swelling have begun to resolve, usually before the wound has healed.
Management of infections unique to the hand
Paronychia
An acute paronychia is an abscess beneath the eponychial fold. It can remain superficial to the nail plate, localized to the radial or ulnar side, or the infection can spread transversely around the entire nail fold. The abscess can track proximally around and deep to the nail plate between the nail and matrix. Manicures, artificial nails, nail biting, or hangnails are common causes. Eponychial swelling, tenderness, erythema, and drainage are characteristic. S aureus is the most common pathogen, followed by Streptococcus pyogenes , Pseudomonas pyocyanea , and Proteus vulgaris .
Although early infections can be treated with oral antibiotics alone, the safest approach is drainage whenever an abscess is present under a digital block. When possible, the nail should be elevated and retained; however, if necessary, it should be removed fully or partially to achieve adequate decompression. An incision across the eponychial fold should be avoided to prevent late nail fold deformity. Soaks can be started immediately and antibiotics should be administered for at least 5 to 7 days, or until resolution of the infection.
If an abscess is not present, nonoperative treatment with antibiotics is performed in conjunction with warm soaks 3 to 4 times per day. One study examined the use of topical antibiotics in a retrospective fashion and concluded that gentamicin antibiotic alone was superior to a combined steroid-antibiotic ointment. When oral antibiotics are selected, options include amoxicillin with clavulanic acid (Augmentin); however, in areas with high rates of MRSA infections, clindamycin or trimethoprim-sulfamethoxazole (Bactrim, Septra) may be first-line agents.
Chronic paronychias can result from excessive exposure to moisture; they are characterized by intermittent periods of inflammation around the eponychium. Eventually there is separation of the nail fold from the underlying nail plate. A cheese-like drainage may exude from beneath the eponychium. Candida albicans , atypical mycobacteria, and gram-negative bacteria have all been implicated. Treatment is challenging. The most successful interventions are marsupialization or total nail removal. Adjunctive topical steroid-antifungal ointment (3% Vioform in Mycolog) or oral antifungal medications have been recommended (itraconazole, fluconazole).
Felon
Felons are painful abscesses in the digital pulp, typically following a puncture wound. Tense distension can compromise soft tissue and distal phalanx vascularity. The most common organism is S aureus . Expeditious drainage is necessary to prevent digital pad necrosis, distal phalanx osteomyelitis, or flexor tenosynovitis. Fish-mouth incisions should be avoided because they can compromise pulp vascularity. The point of maximal tenderness guides incision placement with high lateral (made just below the fingernail) and midvolar configurations preferred. Proximal probing can inoculate the flexor sheath and should be avoided. The wound should be dressed with loose gauze packing, which is removed in 24 to 48 hours, followed by warm daily soaks and gauze dressing changes until healing by secondary intention.
Herpetic Whitlow
Herpetic whitlow is a viral infection of the digital tip caused by herpes simplex virus (HSV), resulting from exposure to genital (HSV-2) or oral (HSV-1) lesions. A painful cytolytic infection occurs 2 to 14 days after contact, usually maturing in 14 days. Viral shedding, and the risk of infecting others, persists until lesion epithelialization is complete. As the infection subsides, the virus becomes latent, retreating to the sensory ganglia, avoiding immune clearance. The natural history of the infection results in complete resolution without treatment, usually in 3 weeks. The diagnosis of herpetic whitlow is made based on history and clinical examination. Patients may present with flu-like prodromal symptoms before the lesion appears. The lesion is often preceded with throbbing pain, tingling, or numbness at the lesion site. A single vesicle and/or additional vesicles may coalesce as a single larger bulla with clear vesicular fluids that can be often mistaken for a pustule. Unlike a felon, herpetic whitlow vesicles do not appear on the pulp of the digit. Non-operative treatment is the best option because, typically, the vesicles unroof, form ulcers, crust, and flake off over 2 to 3 weeks.
The disease demonstrates a bimodal age distribution that usually effects children less than 10 years of age (HSV-1) or young adults between 20 and 30 years (HSV-1 or 2). Although diagnosis is typically by history and physical examination, it can be confirmed with cultures of the vesicular fluid, Tzanck smear, direct fluorescent antibody testing, or a rise in serum antibody titers. Superinfections can follow unnecessary incision and drainage and, for this reason, it is important not to mistake the clear vesicular fluid for pus. Acyclovir, famciclovir, or valacyclovir may benefit patients troubled by frequent recurrences, to abort recurrent infections in patients who have a prodrome, decrease the clinical course in particularly protracted cases, and they are usually necessary to induce remission in patients with AIDS.
Flexor Tenosynovitis
Pyogenic flexor tenosynovitis results when a puncture wound inoculates the flexor sheath. The sheath is a mesothelium-lined closed space, extending from the proximal end of the A1 pulley to the distal interphalangeal joint. The thumb sheath is contiguous with the radial bursa and the small finger sheath is contiguous with the ulnar bursa. The radial and ulna bursae extend proximal to the carpal tunnel. In 50% to 80% of individuals, the radial and ulnar bursae communicate ( Fig. 1 ). S aureus, Streptococcus spp, and gram-negative organisms are the most common pathogens. Less often, chronic indolent infections, characterized by abundant tenosynovitis, can be caused by fungi and atypical mycobacterium. The classic clinical symptoms of a septic or pyogenic flexor tenosynovitis was described by Kanavel and includes fusiform swelling, sheath tenderness, flexed resting posture, and pain on passive extension of the involved digit. Typically, patients with a pyogenic flexor tenosynovitis will have most, but not necessarily all, of these signs ( Box 2 ).
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Flexed resting posture of the involved digit
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Flexor sheath tenderness
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Digital fusiform swelling
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Pain on passive digital extension
Treatment should be instituted expeditiously because a delay can result in tendon vascular compromise and necrosis, adhesions, or extension into adjoining deep spaces ( Box 3 ).
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Horseshoe abscess: infection of the thumb flexor sheath can spread through communication of the radial and ulnar bursae extending into the small finger sheath
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Parona space: extensive proximal spread from any digit can lead to involvement of Parona space
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Thenar space: proximal spread from the index finger flexor sheath can cause infection of the thenar space
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Midpalmar space: proximal extension from the long or ring finger sheaths
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