Hand Surgery
1st Edition

103
Hand Infections
Donald H. Lee
Randolph J. Ferlic
Robert J. Neviaser
Hand and upper extremity infections have a wide range of clinical manifestations. They vary from simple superficial infections (e.g., mild cellulitis) treatable by oral antibiotics to limb- or life-threatening infections (e.g., necrotizing fasciitis) requiring a combination of surgical débridement and intravenous antibiotics. They can also present as indolent, chronic infections (e.g., mycobacterial infection) in which the diagnosis is either delayed or missed. The hand being constantly exposed to the environment provides a wide variety of pathogens (bacteria, fungi, viruses, Mycoplasma) ample opportunity to invade it. With the rise of immunosuppression secondary to a variety of conditions—including human immunodeficiency virus (HIV) infections; use of posttransplantation immunosuppressants, chemotherapy, or chronic steroids; hematologic malignancies; chronic renal failure; diabetes; advanced age; alcohol abuse; and rheumatologic conditions—a simple hand infection can rapidly become a serious health problem (1). An understanding of infectious pathogens, the clinical conditions they produce, and the appropriate treatment helps limit these potential debilitating conditions.
GENERAL PRINCIPLES
Several factors may predispose the hand or extremity to an infection. These include local wound conditions (crush injuries, contaminated puncture wounds, chronic edema), altered immune states, or host conditions (diabetes, poor nutritional status, tobacco dependency). A careful medical history and physical examination should identify any additional infection risk factors, which may determine the need for more aggressive treatment. The successful treatment of hand and upper extremity infections requires an early recognition of the infection; the initiation of empiric and subsequent culture-directed antibiotic coverage; surgical débridement and irrigation of contaminated, devitalized tissues; and adequate follow-up care (2,3,4,5,6,7,8 and 9). Prompt recognition and initiation of treatment increase the chance of a favorable outcome (10,11 and 12). Delay in treatment, especially in conjunction with severe contamination, can lead to an increased incidence in wound infections (1).
Although diabetes mellitus has not been shown to be an independent risk factor for postoperative wound infection, it is a host risk factor for established upper extremity infections (13,14,15,16 and 17). The prevalence of diabetic comorbidities, including vasculopathy and neuropathy, increases as the duration of the disease process progresses. These poor host factors are often adversely complemented with other additional factors of poor prognostic value, including tobacco abuse and malnutrition. This combination of host factors is manifested by a higher incidence of diabetes in patients requiring inpatient admission for hand infection, ranging between 7% and 58% (9,15).
Diabetic patients presenting with an infection have predominately gram-negative or mixed cultures rather than the typical predominance of gram-positive organisms seen in nondiabetic patients. In addition, surgical outcomes and rates of reoperation, amputation, and mortality are higher (13,14,15 and 16,18,19).
PATHOPHYSIOLOGY
Pathogens are microorganisms capable of invading the body and causing disease. An infection is the disease caused by replicating pathogens, usually in the presence of tissue damage. The ability of a pathogen to produce an infection in a given host depends on the organism’s pathogenicity and virulence (20,21,22,23 and 24). The pathogenicity, or likelihood of producing a disease, is determined by several factors, including the organism’s ability to survive in the environment, to be transmitted between hosts, to attach to body surfaces, to defend itself against the host’s immunologic attack and reproduce, and to damage the host (e.g., by toxin production). Virulence is the ability of an organism to cause severe disease. Infectiousness is the ease with which a pathogen can spread within a given population.
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There are several routes of transmission of an infection. Fomites are inanimate environmental objects acting as intermediaries, transporting pathogens from source to host (e.g., towels or bedding transmitting an infection between hospital patients). Vectors are living creatures that can transmit infection from one host to another [e.g., arthropods (mosquito, flea, tick)]. Infections can also be spread through direct contact, inhalation, ingestion, and inoculation.
A pathogen can produce host damage through a variety of mechanisms, including the direct action of the microorganism or production of bacterial toxins. Endotoxins are the intracellular and cell-associated toxic components of gram-negative organisms, including the lipopolysaccharide antigen of the bacterial cell wall. It partly protects the bacteria against the bactericidal activity of serum and can also activate the complement cascade. Exotoxins are toxic substances excreted by the organism. These toxins can be classified in a variety of ways. For instance, they can be classified according to the symptoms produced (neurotoxin, enterotoxin, cytotoxin), their mode of action (extracellular or transmembrane toxins, membrane-damaging toxins, deregulating toxins), their intracellular targets, their biologic effects (hemolytic toxin, edema-producing toxins), and the producing organism (pertussis toxin, cholera toxin).
Microbes also work synergistically to help establish an infection, facilitate tissue invasion, reduce the host’s immune response, and enhance the virulence of the various pathogens. Such polymicrobial infections include necrotizing fasciitis and gangrene. HIV infections, by diminishing the host’s virulence, allow other pathogens to invade the host.
Pathogens can be classified into five main groups: bacteria, fungi, viruses, protozoa, and metazoa (20). Bacteria are grouped by four characteristics: Gram’s stain reaction (gram-positive and gram-negative), shape (cocci, bacilli, spiral), atmospheric requirements (obligate aerobes, microaerophilic, capnophiles, facultative anaerobes, obligate anaerobes), and the presence of spores. Other varying structural characteristics of bacteria include the cell wall, plasma membrane, bacterial capsule, extracellular slime, fimbriae (pili), flagella, and pathogenicity islands (genomic regions that determine pathogenicity and virulence). Fungi are classified in different ways, including the means of reproduction and morphology or the type of infection produced (superficial and subcutaneous, systemic, or fungi associated with immunocompromised patients). Viruses are classified according to the type of nucleic acid and means of transcription (DNA, RNA), the structure and symmetry of the structural proteins (capsids), and the presence or absence of an envelope. Protozoa are classified according to spore production (sporozoa), flagellate (flagellates), ameboid, and ciliate. Metazoa or helminths are classified into nematodes or roundworms, platyhelminths or flatworms, cestodes or tapeworms, and flukes.
Resistance to infection occurs through several mechanisms, including nonspecific, or innate, immunity and specific immunity (20,24,25). Nonspecific immunity includes normal mechanical and physiologic properties of the host (e.g., skin, mucosae, gastric acid, complement system, phagocytosis). Specific immunity includes a variety of defensive responses by the host to microorganisms (antigens, cell-mediated and humeral immune responses).
The manifestations of infection include fever, inflammation, and rashes (20,22). Fevers occur due to a release of cytokines and interferon-alpha by activated mononuclear phagocytes, which act on specialized endothelial cells in the hypothalamic blood vessels. The subsequent release of prostaglandins causes a resetting of the body temperature that is controlled by the hypothalamus. Inflammation occurs as a combination of several events: vasodilatation at the affected site, exudation of tissue fluid from dilated capillaries, accumulation of neutrophils and macrophages at the site, and the release of active chemicals (lysozymes, free radicals, lactoferrin, leukotrienes) from neutrophils. These events cause local heat and redness. Rashes are a particular form of inflammation or tissue affecting the skin. They may be generalized or localized. The characteristics of rashes (e.g., appearance, method of spread) are frequently typical of the organism(s) producing the infection.
CLINICAL EVALUATION
Bacterial infections usually produce the normal signs of infection, including erythema, edema, and tenderness. Dorsal, as opposed to palmar, hand swelling may be noted due to the relative pliability of the dorsal skin as compared with the thickened, glabrous palmar skin. Certain infections (e.g., pyogenic tenosynovitis) present with classic clinical findings, including fusiform digital swelling and a flexed finger position (see below). However, nonbacterial infections (e.g., mycobacterial infections) may present with innocuous swelling without significant erythema or pain. Included in the differential diagnosis of hand infections are gout, inflammatory conditions (e.g., tenosynovitis, rheumatoid arthritis), collagen vascular diseases, foreign body reactions, soft tissue calcifications, and neoplasm (26).
An appropriate history includes the location and quality of pain, the duration of the process, any systemic manifestations (fever, chills), the mechanism of injury (if applicable), any previous antibiotic or surgical treatment, and a complete medical history. The physical examination includes inspection and palpation of the involved area, evaluation of lymphadenopathy, neurovascular examination, and use of provocative maneuvers (e.g., passive finger extension for pyogenic tenosynovitis). The presence of fever should be noted.
IMAGING STUDIES
Diagnostic studies should include radiographs to rule out a fracture, foreign body, periosteal reaction, osteomyelitis, or
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implant loosening (28,29). Soft tissue shadows, indicative of edema, may be seen. Computed tomography can help determine the presence of septic arthritis and adjacent osteomyelitis. Magnetic resonance imaging is helpful in the evaluation of musculoskeletal infections, providing excellent soft tissue contrast, multiplanar capability, and improved assessment of bone marrow and joint involvement. Early changes in the bone marrow space in the early stages of acute osteomyelitis can be defined by magnetic resonance imaging scan. A decreased signal intensity in the bone marrow density is seen on T1-weighted images and increased signal intensity on T2-weighted images (21,22,24,27). These images can help define distended joint spaces and periarticular extensions of infections. Ultrasound can be used to evaluate areas of edema, fluid accumulation, abscess formation, pyarthrosis, and osteomyelitis (27). Nuclear imaging is used to detect abscesses, septic arthritis, and osteomyelitis (20,22).
LABORATORY STUDIES
Complete Blood Cell Count with Differential
The complete blood cell count with differential white blood cell count is frequently used to detect signs of infection. Leukocytosis (white blood cell count of more than 12,000) and a left shift showing more immature polymorphonuclear leukocytes are signs of an infectious process (22,23,27).
Acute-Phase Proteins
The concentration of several plasma proteins rises in the presence of inflammation. C-reactive protein, a commonly monitored acute-phase reactant, is produced in the liver. Its levels are rapidly elevated during the acute inflammatory phase in many bacterial and viral infections (20). Serum levels increase from 1 μg per milliliter by 100 to 1,000 times within hours due to an induction in hepatic synthesis (22,27). It is a disc-shaped pentameric molecule that readily binds a number of substances, including the C fraction of pneumococcal lysates, hence its name (20,22). In its bound form, it activates the complement cascade.
Erythrocyte Sedimentation Rate
The viscosity of plasma is altered during inflammation secondary to protein changes. The erythrocyte sedimentation rate (ESR) is the rate that red blood cells settle in anticoagulated blood left standing. The normal ESR is less than 20 mm per hour, rises to 30 to 50 mm per hour in acute infections, and can rise to 70 to 100 mm per hour in certain conditions (abscesses, immunologic diseases, atypical pneumonias) (20). It can also be elevated with recent surgery or fractures; malignancies; myocardial infarction; and gastrointestinal, thyroid, renal, and collagen vascular diseases (29). Both the ESR and C-reactive protein level are nonspecific indicators of inflammatory changes, with the ESR rising more slowly than the C-reactive protein levels.
NONOPERATIVE MANAGEMENT OF HAND INFECTIONS
Uncomplicated simple lacerations of the hand do not require the use of prophylactic antibiotic therapy (30). Cleansing these simple lacerations with povidone-iodine (Betadine) solution, followed by loose primary suture approximation, is adequate (31). The use of prophylactic antibiotic coverage for more complex (contaminated wounds or those involving bone, tendon, or neurovascular structures) lacerations or for elective hand surgery is controversial and currently is best decided at the treating surgeon’s discretion (32,33,34,35,36,37,38 and 39).
The initial medical treatment of open contaminated wounds should include the use of relatively broad-spectrum antibiotics covering the more commonly found aerobic pathogens (e.g., Staphylococcus, Streptococcus, Haemophilus) and anaerobic organisms (e.g., Eikenella, Bacteroides, Enterobacter) (26). In general, penicillin (anaerobic coverage) with nafcillin or a first-generation cephalosporin [e.g., cefazolin (Ancef) (gram-positive coverage, penicillinase resistance)] is used (26). Gentamicin is added for broader coverage for gram-negative infections (40). Table 1 includes a list of common types of infections, commonly involved pathogens, and the recommended initial antibiotic coverage until culture results and sensitivities can be obtained.
SURGICAL MANAGEMENT OF HAND INFECTIONS
A biopsy is indicated in cases of persistent signs of infections failing to respond to splinting, elevation, and antibiotics; in cases of obvious infections (e.g., abscesses); and in cases in which a definitive diagnosis is needed. The initial biopsy should include a deep wound sample of the infected area. An adequate surgical field and setup, with use of a tourniquet and appropriate anesthesia, should be used to allow for formal débridement and irrigation should an obvious infection be found. Sufficient tissue samples should be obtained for multiple cultures, including aerobic, anaerobic, mycobacterial, atypical mycobacterial, and fungal cultures. A specimen is sent for Gram’s stain, and in cases of suspected mycobacterial and Fungal Infections, appropriate stains (acid-fast bacillus stain and potassium hydroxide preparation) should also be sent.
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TABLE 1. EMPIRIC ANTIBIOTIC RECOMMENDATIONS FOR HAND INFECTIONS
Infection Organisms Antibiotic Alternative antibiotic
Paronychia/felon Staphylococcus aureus, oral anaerobes Nafcillin, cefazolin, clindamycin, dicloxacillin Cephalexin, erythromycin
Flexor tenosynovitis S. aureus, Streptococcus, gram-negative rods Cefazolin Nafcillin or vancomycin plus gentamicin, imipenem
Deep space infection S. aureus, anaerobes, gram- negative rods Cefazolin, ampicillin/sulbactam (Unasyn) Nafcillin, vancomycin plus gentamicin, imipenem
Cellulitis/lymphangitis Streptococcus, S. aureus Nafcillin, cephalexin, dicloxacillin Cephalexin, erythromycin
Human bite S. aureus, Staphylococcus epidermidis, Eikenella corrodens, Streptococcus, Bacteroides, Peptostreptococcus, anaerobes Cefazolin plus penicillin, clindamycin plus ciprofloxacin, trimethoprim-sulfamethoxazole (Bactrim/Septra), ampicillin/clavulanate (Augmentin) Nafcillin plus penicillin, amoxicillin-clavulanate (Augmentin), ampicillin/sulbactam (Unasyn), cefoxitin
Animal bite Gram-positive cocci, S. aureus, anaerobes, Pasteurella multocida Cefazolin plus penicillin, amoxicillin-clavulanate (Augmentin) Nafcillin plus penicillin, amoxicillin-clavulanate (Augmentin), ampicillin/sulbactam (Unasyn), clindamycin plus ciprofloxacin, trimethoprim-sulfamethoxazole (Bactrim/Septra)
Septic arthritis S. aureus, Streptococcus, Neisseria gonorrhoeae Cefazolin, ceftriaxone Nafcillin, vancomycin, clindamycin, doxycycline
Osteomyelitis S. aureus, Streptococcus, gram-negative rods Cefazolin plus gentamicin Nafcillin, vancomycin, clindamycin, doxycycline
Traumatic/contaminated wounds S. aureus, Streptococcus, anaerobes, gram-negative rods Imipenem Cefazolin plus gentamicin
Intravenous drug abuse–related Gram-positive, gram-negative methicillin-resistant S. aureus Nafcillin plus gentamicin Vancomycin plus gentamicin, imipenem
Diabetes-related Gram-positive cocci, gram- negative rods Cefazolin plus gentamicin Cefoxitin, ampicillin/sulbactam
Herpetic whitlow Herpes simplex virus Acyclovir Valacyclovir, famciclovir
Data from references 21, 24, 26, 27, and 97.
ALGORITHM FOR THE EVALUATION AND MANAGEMENT OF HAND INFECTIONS
Figure 1 provides an algorithm for the evaluation and management of hand infections.
INFECTIONS
Paronychia
The perionychium is defined as the paronychium (border tissue around the nail) and the nailbed (germinal and sterile matrix). A paronychia is an infection of the lateral nail fold (Fig. 2). When the infection extends to the eponychium (defined as the thin membrane distal to the nail wall at the base of the nail), it is properly termed an eponychia. When infection involves both lateral nail folds and eponychium, it is called a run-around infection (41,42).
In adults, Staphylococcus aureus is the most common pathogen (43). Infection occurs when there is violation of the seal between the nail plate and nail fold, allowing the inoculation of bacteria. Hangnails, manicures, penetrating trauma, constant exposure to a wet or moist environment, and nail biting or sucking are common inciting events for an infection (44). Initial swelling, erythema, tenderness with progression to fluctuance, and abscess formation are the typical clinical presentation. Spontaneous decompression can occur, including tracking beneath the nail plate (subungual abscess). Deeper infections can involve the nailbed, pulp space, and bone, producing nailbed destruction, felon, or osteomyelitis. In children, there is often a mix of aerobic and anaerobic organisms believed to be related to the finger-sucking and nail-biting habits of this young population (45).
Infections in the early stages can be treated with oral antibiotics, warm soaks, rest, and observation. Otherwise, surgical decompression is the treatment of choice for acute, established paronychia. With simple infections, a digital or metacarpal local anesthetic block may not be needed. Decompression is performed by carefully entering the abscess cavity between the nail plate and nail fold with a scalpel blade or hemostat (Fig. 3) (41,43,46). A small wick is placed for 24 to 48 hours to prevent the incision from closing and recurrence of the infection. The wick is removed, and saline warm soaks are begun.
Aggressive decompression is needed with more established or resistant infections. A digital or metacarpal block with local plain lidocaine (Xylocaine) is used. Depending on the extent of the infection, a partial or complete nail plate removal with or without lateral nail fold relief incision(s)
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is performed. The incision should be made perpendicular to the edge of the nail fold (Fig. 4). A single or double incision is used depending on the location of the infection. As before, the wound is packed with a wick and subsequently changed, and intermittent warm saline soaks are started.
FIGURE 1. Algorithm for the evaluation and management of hand infections. AFB, acid-fast bacillus; CBC, complete blood cell count; CRP, C-reactive protein; ESR, erythrocyte sedimentation rate; KOH, potassium hydroxide; PE, physical examination; ROM, range of motion.
Subungual abscesses are treated with removal of a portion of or the entire nail. The abscess is carefully débrided while protecting the sterile and germinal matrices. Cultures should be obtained at the time of decompression, with initiation of empiric oral antibiotic therapy. Wound care, including splinting of the distal interphalangeal joint, warm saline or Epsom salt soaks, and serial observation, should be continued until wound healing. The antibiotic coverage is adjusted based on the results of the wound cultures. The majority of these infections resolve without permanent sequelae, including nail dystrophy.
Chronic paronychia occurs more commonly in individuals constantly exposed to moist environments. Infections may be intermittent; clinically, the eponychial fold is thickened and painful. Candida albicans is a frequent offending organism (see the section Fungal Infections).
Marsupialization of the nail may be needed with chronic paronychias (47). After digital block anesthesia, a small, crescent-shaped portion of the eponychial fold is removed and made proximal to the distal edge of the eponychial fold without injuring the germinal matrix. A 5-mm wedge of skin, extending to lateral margins of the nail fold, is removed (Fig. 5). The nail plate is removed if severely deformed or if there are signs of infection. Xeroform or similar nonadhering gauze is placed under the nail fold and changed at 24 to 48 hours. Wound epithelialization gradually occurs over 2 to 3 weeks. Topical antifungal ointments are generally used 4 to 6 weeks.
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Felon
A felon is a deep space infection or abscess of the distal pulp of the finger or thumb. It differs from the superficial apical infection involving the distal portion of the pulp skin, which often responds to a small, deroofing incision (41,43,46). The hyponychium, the region of keratinized skin beneath the distal nail plate, is normally very resistant to infection.
FIGURE 2. A,B: A paronychia, or infection of the lateral and eponychial nail fold.
FIGURE 3. Decompression of a paronychia by entering the abscess cavity between the nail plate and nail fold with a scalpel blade.
The pulp is composed of multiple vertical septae extending from the skin to the palmar distal phalanx, creating multiple small enclosed compartments in the pulp. Penetrating trauma, such as that from a splinter, often, but not always, serves as the event introducing a bacterial load. The infection can progress to produce a sinus, skin sloughing, or osteomyelitis. With further progression, the infection can produce a septic arthritis of the distal interphalangeal joint or pyogenic tenosynovitis. The organism most frequently cultured from a pulp space infection is S. aureus (43,48). Clinical presentation includes throbbing pain and tense swelling localized to the pulp (Fig. 6).
FIGURE 4. A: An infected lateral and proximal nail fold can be elevated by an elevator or scalpel. B: For extensive infections, a relief incision(s) is made perpendicular to the edge of the nail fold to allow for removal of a portion or all of the nail plate. (Reprinted from Seiler JG. Essentials of hand surgery. Philadelphia: Lippincott Williams & Wilkins, 2002, with permission. Copyright American Society of Surgery of the Hand.)
Surgical decompression of a felon is performed when an obvious infection with fluctuance is noted. One of several incisions can be used, including a preferred unilateral longitudinal incision, a J-shaped or hockey-stick incision, a through-and-through incision, or a volar longitudinal incision. A fishmouth incision should be avoided (Fig. 7) (6,7,46,49,50,51,52 and 53). Although the site of maximal induration often dictates the location of the incision, a unilateral longitudinal incision is ideally performed on the noncontact surface of the involved digit. This includes the ulnar sides of the index and long fingers and the radial sides of the ring finger,
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small finger, and thumb. The incision begins dorsal and distal to the distal interphalangeal joint flexion crease and extends distally toward, but does not include, the hyponychium. This incision parallels the lateral nail fold with a 5-mm interval of separation. Sharp dissection is carried out in line with the skin incision to the volar cortex of the distal phalanx. A small hemostat is then gently spread to allow complete decompression by disrupting the vertical septae.
FIGURE 5. Eponychial marsupialization is performed by removing a small, crescent-shaped portion of the eponychial fold proximal to the distal edge of the eponychial fold. Care is taken to not injure the underlying germinal matrix. (Reprinted from Seiler JG. Essentials of hand surgery. Philadelphia: Lippincott Williams & Wilkins, 2002, with permission. Copyright American Society of Surgery of the Hand.)
FIGURE 6. A,B: A felon, or abscess of the distal finger pulp. Note the smaller, normal-sized adjacent finger. C: A unilateral longitudinal incision is used to decompress the felon.
FIGURE 7. Incisions used for decompression of a felon. A: A midlateral incision is preferred. B: A J-shaped or hockey-stick incision. C: A through-and-through incision. D,E: A volar transverse or longitudinal incision.
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A longitudinal central midline incision (43,52) is advocated in an attempt to avoid skin slough, digital nerve injury, or creation of an unstable fat pad. This incision is preferred in the presence of a sinus track, allowing incorporation of the sinus track with the incision. The hockey-stick, fishmouth, and transverse palmar incisions are to be avoided due to their potential iatrogenic morbidity. With any of these incisions, care is taken not to injure the neurovascular structures or introduce an infection into the flexor tendon sheath. A common problem is using too small an incision to adequately decompress the infection.
After appropriate lavage irrigation, a small wick is placed for 24 to 48 hours, with initiation of appropriate wound care and allowance of secondary wound closure. As with paronychias, cultures should be obtained at the time of decompression, and empiric oral antibiotics should be started. The antibiotics are adjusted according to the results of the deep wound cultures.
Deep Space Infections
The appropriate treatment of deep space infections requires careful surgical planning and drainage, acquiring intraoperative cultures to direct the antibiotic coverage needed, and allowing wound closure by secondary intention. Postoperative wound care, edema control, splinting, and motion optimization are preferably pursued with therapy supervision (54). Initial empiric antibiotic coverage with a second-generation cephalosporin, such as cefazolin, while awaiting culture identification and sensitivity is usually adequate. Addition of gram-negative coverage is recommended in an immunocompromised individual.
Web Space Infections
A web space infection, also known as a collar button abscess or hourglass abscess, involves the subfascial palmar space between the digits. The infection begins as an infected blister, an open wound, or a palmar callus or from the adjacent subcutaneous area (55). An abscess subsequently develops and extends either volarly or usually dorsally to include the contiguous subcutaneous space of the dorsal hand. The involved adjacent digits are held apart from one another in a characteristic abducted posture. This clinical presentation, combined with prominent dorsal hand swelling and a tender palmar web space, usually makes the diagnosis clear. Incisional drainage is performed with separate dorsal or volar or combined approaches (Fig. 8) (46,50,55,56,57 and 58). The type of incision(s) used depends on the location of the abscess. A combined approach is used in cases in which the infection is noted both dorsally and volarly. A transverse incision in the web space itself should be avoided to prevent possible web space scar contracture (46,57). After formal débridement and irrigation of the wound, a 16-gauge polyethylene catheter can be sutured into an open wound to allow for subsequent saline irrigation (100 mL per hour) of the wound for 24 to 48 hours (46).
FIGURE 8. Incisions used for decompression of a web space infection. A: A curved volar incision. B: A dorsal longitudinal incision.
Dorsal Subaponeurotic Space Infections
The dorsal subaponeurotic space is a potential space located deep to the extensor tendons and dorsal to the metacarpals. Penetrating trauma usually introduces bacteria to this space, which can subsequently become an abscess (55). Although it is difficult clinically to discern from subcutaneous edema with overlying cellulitis, aggressive surgical incision and débridement are recommended if in doubt. Two dorsal longitudinal incisions are preferable rather than a single central one, which may result in tendon desiccation. One incision is centered over the second metacarpal; the other is in the fourth-fifth intermetacarpal region to allow an adequate intervening skin bridge. Care is taken to protect the dorsal veins to minimize hand swelling. The wounds are allowed to heal by secondary intention, and early hand motion is instituted to minimize extensor tendon adhesions (26).
Palmar Space Infections
The deep palmar spaces are potential spaces in the hand and are divided into the midpalmar space, thenar space, hypothenar space, and posterior adductor space (Fig. 9) (26,46,57,59). The midpalmar space is located deep to the flexor tendons and lumbricals and extends dorsally to the volar fascia, investing the second and third volar interossei and the third and fourth metacarpals. Radially, it is bordered by the midpalmar or oblique fascial septum. This septum extends from the third metacarpal to the sheath, enclosing the long-finger flexor tendons
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(ulnar bursa in some people). The midpalmar space extends distally to the level of the vertical septa of the palmar fascia, ending approximately 2 cm proximal to the web spaces. Proximally, the space extends to the distal edge of the carpal canal.
FIGURE 9. Diagram of palmar spaces. (Reprinted from Seiler JG. Essentials of hand surgery. Philadelphia: Lippincott Williams & Wilkins, 2002, with permission. Copyright American Society of Surgery of the Hand.)
The thenar space is bordered ulnarly by the vertical midpalmar septum and posteriorly and radially by the adductor pollicis fascia, and it lies deep to the flexor pollicis longus. The hypothenar space is located ulnar to the midpalmar space, contains the hypothenar muscles, and is enclosed by their investing fascia. This space is bordered radially by a fibrous hypothenar septum coursing between the fifth metacarpal and palmar aponeurosis. The posterior adductor space is another potential space located dorsal to the adductor pollicis and palmar to the first dorsal interosseous.
FIGURE 10. Incisions used for decompression of palmar (A–D), thenar (E,F), and hypothenar space infections (G). A: A curvilinear longitudinal approach. B: A transverse incision through the distal palmar crease. C: A distal palmar incision approach through the lumbrical canal. D: A combined transverse and longitudinal incision. E: A volar curvilinear thenar crease incision. F: A dorsal first web space incision. G: A volar longitudinal incision. (Reprinted from Seiler JG. Essentials of hand surgery. Philadelphia: Lippincott Williams & Wilkins, 2002, with permission. Copyright American Society of Surgery of the Hand.)
The clinical presentation of palmar space infections typically includes pain, erythema, swelling, and guarding with tenderness at the focus of abscess. It is not unusual for a patient to present 48 to 72 hours after a penetrating injury with signs of infection.
Several possible surgical incisions can be used for midpalmar space infections (Fig. 10A–D) (6,50,55,58,60,61 and 62).
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These options include a preferred curvilinear longitudinal approach, a transverse incision through the distal palmar crease, a distal palmar incision approach through the lumbrical canal, and a combined transverse and longitudinal incision.
A thenar space infection may require a volar and a separate dorsal first web space incision if dorsal extension has occurred around the adductor pollicis and first dorsal interosseous muscles (Fig. 10E,F). This is the so-called dumbbell, or pantaloon, abscess. Hypothenar space infections can be drained using a volar longitudinal incision along the medial aspect of the hypothenar eminence (Fig. 10G). Alternately, an incision along the medial aspect of the hypothenar eminence can be used. Continuous or intermittent irrigation of the infected space can also be used (46,63).
Pyogenic Flexor Tenosynovitis
Pyogenic flexor tenosynovitis, or suppurative flexor teno-synovitis, is a bacterial infection of the digital flexor sheath. The majority of these infections are secondary to traumatic penetrating injuries; therefore, skin flora, including S. aureus, is the source of the most common infecting organisms (46,64,65,66 and 67).
The flexor sheath is an intricate continuous synovial sheath originating at the level of the metacarpal neck and ending at the insertion of the flexor digitorum profundus. It separates into an outer parietal and an inner visceral layer. The parietal layer thickens at different intervals, consistently forming discrete annular and cruciform pulleys. The visceral layer is the epitenon. Between the two layers is the synovial space, which is essentially a closed space.
The flexor sheath of the little finger flexor digitorum profundus tendon (and, on occasion, the ring, long, and index fingers) communicates with the ulnar bursa, which extends proximal to the wrist level. The flexor sheath of the flexor pollicis longus communicates with the radial bursa, which extends proximal to the wrist level as well. The radial and ulnar bursa can communicate at the level of the transverse carpal ligament through Parona’s space (57,67), producing a horseshoe abscess. Parona’s space is a potential space in the distal forearm located between the pronator quadratus muscle and the flexor digitorum profundus tendons.
The clinical findings of pyogenic tenosynovitis include Kanavel’s four cardinal signs: pain with passive extension of the digit (the most reproducible clinical sign), symmetric digital swelling (sausage digit), tenderness along the flexor sheath, and a semiflexed resting posture of the involved digit (Fig. 11) (62).
Nonoperative treatment may be possible if the infection is detected and treated early (e.g., within 24 to 48 hours) (46). Treatment includes the use of intravenous antibiotics (Table 1), splint immobilization of the hand, elevation, and serial observations for 48 hours. With continued signs of infection, surgery should be performed.
FIGURE 11. A,B: A digit with pyogenic flexor tenosynovitis showing symmetric digital swelling and a flexed resting posture. C: Palmar incision revealing purulent drainage from the flexor sheath.
Surgery is the mainstay of treatment for pyogenic teno-synovitis. Several surgical techniques can be used, including the preferred two-incision, closed–tendon sheath, irrigation method (Fig. 12) (46,64,66,67,68,69,70,71,72 and 73); open drainage of the tendon sheath (60,61,74,75); single palmar incision for antibiotic instillation (76); distal digital drainage with proximal
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antibiotic instillation with a needle (77); and a through-and-through (two-incision) intermittent irrigation (68,73).
Pyogenic flexor tenosynovitis has been classified into three stages (Table 2) (64,69,78). The type of surgical treatment varies with the clinical stage of the infection. Stages I and II can be effectively treated with the preferred two-incision, closed–tendon sheath, irrigation technique (Fig. 12). With this technique, the A1 pulley is approached proximally through a preferred transverse, versus a longitudinal or zigzag palmar, incision at the level of the metacarpal head. After entrance into the flexor sheath, cloudy fluid or pus should be identified and cultured. A No. 5 French pediatric feeding tube is inserted into the incised sheath and advanced distally. Alternatively, a 16-gauge polyethylene catheter can be used. A separate midlateral incision is made distal to the A4 pulley, where a small section of the sheath is resected. An alternate palmar incision can be used. This incision allows a through-and-through irrigation of sterile saline solution. The sheath is irrigated with 500 to 1,000 mL of saline. A small drain can be sutured in the distal incision to keep the wound patent. Postoperatively, the hand is dressed in a bulky dressing and elevated. The catheter is either manually flushed with 50 mL of sterile saline solution every 2 hours or attached to a continuous infusion pump infusing sterile saline at approximately 25 to 30 mL per hour. Care must be taken to avoid direct extravasation of fluid into the adjacent tissue. This is ensured by having the tube visibly exit the distal sheath or placing a small, separate Penrose drain in the distal incision.
FIGURE 12. A: Diagram of incisions used for decompression of flexor sheath infections. (Reprinted from Seiler JG. Essentials of hand surgery. Philadelphia: Lippincott Williams & Wilkins, 2002, with permission. Copyright American Society of Surgery of the Hand.) B: Intraoperative photograph of irrigation fluid being flushed through a pediatric feeding tube. The tube has been passed from the proximal palmar incision through the flexor sheath and out distally through a midlateral incision. The distal end of the tube is withdrawn into the sheath to irrigate the flexor sheath.
TABLE 2. THREE STAGES OF PYOGENIC FLEXOR TENOSYNOVITIS
Intraoperative stage Characteristic findings Treatment
Stage I Increased fluid in sheath, primarily a serous exudate Minimal invasive drainage and catheter irrigation
Stage II Cloudy/purulent fluid, granulomatous synovium Minimal invasive drainage with or without indwelling catheter irrigation
Stage III Septic necrosis of the tendon, pulleys, or tendon sheath Extensile open débridement, possible amputation
The radial and ulnar bursas can be drained and irrigated through the use of an open technique (50) or the through-and-through irrigation technique (46,72). The distal end of the radial bursa is exposed at the level of the proximal end of the flexor sheath near the metacarpophalangeal flexion
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sheath or, more proximally, at the level of the thenar flexion crease. The proximal end of the bursa is approached with an incision just radial to the flexor carpi radialis tendon. The ulnar bursa is exposed with a distal incision at the distal palmar flexion crease and a proximal incision ulnar to the flexor carpi ulnaris. The tendon and ulnar neurovascular bundle are retracted ulnarly during the exposure. With the open technique, after irrigation of the bursa, Penrose drains are left in wounds and removed in 24 to 48 hours. With the irrigation technique, a 16-gauge polyethylene catheter or pediatric feeding tube is used in a similar fashion for the digital sheath infections. A horseshoe abscess requires simultaneous drainage of both the radial and ulnar bursas.
To minimize the most common complication of digital stiffness, early active digit range of motion is initiated postoperatively as soon as the catheter is removed. Initial empiric parenteral antibiotic is administered, usually a second-generation cephalosporin, such as cefazolin. Patients typically can leave the hospital after 48 hours on culture-directed oral antibiotic therapy for a total of 7 to 14 days.
Stage III infections with tissue necrosis require a more aggressive regimen, including an extensile surgical approach with surgical débridement versus ultimate salvage amputation. A midaxial incision, made dorsal to the neurovascular bundle, may be preferred in an effort to limit tendon and tendon sheath exposure and desiccation (79). A synovectomy is performed, leaving the annular ligaments intact. A separate palmar incision is made to complete the synovectomy proximally. A prolonged parenteral (4 to 6 weeks) antibiotic course is not unusual. Initial broad-spectrum antibiotic coverage is preferable until culture identification, especially if the patient is immunocompromised (64).
Septic Arthritis
Septic arthritis is infection of a joint space that, if left untreated, progresses to joint destruction and osteomyelitis (80,81). The most common infecting organism is S. aureus, whereas Streptococcus species are the second most prevalent bacterial isolates in the hand and wrist (81). Organisms can gain entry to a joint either by a penetrating event or by hematogenous seeding (80).
Patients present with a painfully swollen joint with guarded limited motion. The ESR and C-reactive protein level are sensitive laboratory indicators of inflammation, although they are not specific for infection. The white blood cell count is elevated in less than one-half of these patients (81). The definitive diagnosis is made with a joint aspiration. The aspirate typically has a white blood cell count of more than 100,000, with polymorphonuclear leukocytes comprising more than 75% of the total field (27). The specimen should also be evaluated (a) for the presence of crystals; (b) for glucose and uric acid levels; and (c) with Gram’s stain, aerobic, anaerobic, fungal, and mycobacterial cultures. Local anesthetic often has an antiseptic preservative; therefore, the aspirate should be obtained with a separate syringe. A wrist aspirate is performed 1 cm distal to Lister’s tubercle at the 3-4 (between the third and fourth extensor compartments) arthroscopic portal. The small joints of the hand are typically aspirated dorsally as well.
Favorable outcomes are directly dependent on early diagnosis and prompt surgical drainage (80,81 and 82). Wrist arthrotomy is performed through the third dorsal extensor compartment. The metacarpophalangeal joint is approached dorsally as well, often requiring splitting of the proximal extensor hood for exposure. The sagittal band is incised, and a capsulotomy is performed. The interphalangeal joints are best approached through midaxial incisions, with release of the accessory collateral ligament(s), thereby avoiding dorsal disruption of the central slip (83). Alternately, the joint can be exposed through a dorsal incision between the central slip and lateral band, preserving the collateral ligament. The wounds are then packed open with a drain, which is removed in 24 to 48 hours. Alternatively, an 18- or 20-gauge angiocatheter is sutured into the wound with a drain sutured into the opposite end of the wound. The catheter is used postoperatively to irrigate the joint for 24 to 48 hours (46). Intraoperative cultures are obtained, and the wounds are frequently left open to heal by secondary intention. Conversely, loose closure over suction drains can be performed if adequate joint débridement can be obtained. Supervised early motion improves ultimate composite digit flexion.
Osteomyelitis
Osteomyelitis infections occur secondary to an infection from an adjacent wound abscess, penetrating trauma (e.g., bites), septic arthritis, pyogenic tenosynovitis, hematogenous seeding, or open fractures or after open treatment of closed fractures (26,46,80,84). The hematogenous spread of an infection is uncommon (46). Osteomyelitis secondary to open fractures occurs in 1% to 11%, with a higher rate of infection occurring with severe contamination and soft tissue injury (80,85). The infection can involve any of the bones in the hand. The most common pathogens are S. aureus and Streptococcus (20,26,46).
Clinically, signs of infection, including pain, erythema, swelling, and warmth, are usually present. Fever and elevated white blood cell count, C-reactive protein level, and ESR are variably present. Radiographs, depending on the stage of the infection, may reveal lucencies, periosteal reaction or bone formation, osteolysis, or sequestrum formation. Computed tomography and magnetic resonance imaging can help determine the extent of the infection (21,22,27). Nuclear imaging is helpful in detecting the infection earlier than in plain radiographs.
Treatment includes performing a biopsy to identify the pathogens, using antibiotics empirically until culture sensitivities have been obtained, and surgically draining the
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infection (26,46,84). The surgical incision(s) depends on the location of the infection and the bone involved. A midaxial incision is used for phalangeal infections, and a dorsal incision is used for metacarpal and carpal infections. Distal radius infections can be approached dorsally or volarly. Surgery should include removal of all of the infected bone and sequestra. A cortical window may be needed to access the area of infection. After irrigation of the area of infection, the wound can be left open and treated with wet-to-dry or whirlpool dressing changes or closed over a drain. Repeat surgical débridement and antibiotic impregnated cement spacers may be needed. Severe infections may require an amputation. Late reconstruction may require flap coverage or skin grafting.
Animal Bites
Animal bites are common, requiring more than 1 million medical visits per year, or approximately 1% of all emergency room visits, and $30 million in health care costs annually. Eighty percent to 90% of these bites are dog bites, and cat bites comprise another 5% (1,26,86,87). The dominant hand is the most frequently involved, and children are susceptible to animal bites (86,88).
Animal bites are similar to human bites in the polymicrobial aerobic-anaerobic nature of the wounds. However, the normal animal oral flora is less pathogenic than human flora (86). This is reflected by the higher number of isolates per wound in human bites, which is subsequently reflected by a higher incidence of infections and complications in human bite wounds. Anaerobes still outnumber aerobes 10:1 in both floras (86).
Wound cultures of dog and cat bites usually consist of multiple aerobic or facultative anaerobic [Pasteurella (multocida and canis), Streptococcus, Staphylococcus (aureus and epidermidis), Moraxella, Neisseria, Bacillus, Haemophilus, Proteus, Pseudomonas, Eikenella] and anaerobic (Peptostreptococcus, Bacteroides, Fusobacterium, Porphyromonas, Prevotella, Propionibacterium, Veillonella, Actinomyces) organisms (26,27,86,88,89,90,91,92,93 and 94). P. multocida, a member of gram-negative cocci, is isolated in approximately 16% to 26% of dog bites (86,92).
Cat-scratch disease can follow a cat, dog, or monkey bite or scratch. An erythematous lesion and primary papule form 3 to 5 days postinjury, with adenopathy developing 5 to 50 days later. Afipia felis and Rochalimaea or Bartonella henselae, both gram-negative bacteria, have been implicated as causative pathogens (1,20,95,96). The disease is generally self-limiting but has been treated with ciprofloxacin, azithromycin, and trimethoprim-sulfamethoxazole (95,97).
Most animal bites have a high infection potential due to the nature of the penetrating injury, inoculation of a high number of bacterial flora, and local tissue devitalization secondary to the crushing nature of the injury. Risk factors for infection include a delay in treatment (more than 12 hours), advanced patient age, and more severe and deeper wounds. Cat scratches and bites are more likely to become infected than dog bites due to their needle-sharp teeth creating a deep-seated puncture, rather than avulsion, wound (98). Insect, snake, and arthropod bites are less likely to become infected than are cat and dog bites (87). Snake venom is sterile, although snake oral flora reflects the fecal flora of its prey. Venom is inhibitory to aerobic, but not anaerobic, flora.
Clinically, animal bite infections produce cellulitis, lymphangitis, and subsequently purulent drainage. The estimated cumulative incidence of infection after a dog bite without medical treatment is 16%. The incidence decreases to 9% in a patient population treated with prophylactic antibiotic use (99). Broad-spectrum antibiotic coverage is initially used and subsequently tailored according to culture sensitivities. A puncture wound secondary to an animal bite in the hand should be cleansed topically with an antiseptic solution and evaluated clinically and radiographically. In general, the antibiotics used should include a beta-lactam antibiotic and a beta-lactamase inhibitor, a second-generation cephalosporin with anaerobic activity, or combination therapy with penicillin and a first-generation cephalosporin or clindamycin and a fluoroquinolone (94). Penicillin is used for Pasteurella infections. Tetracycline and cephalosporin can be alternately used. Augmentin (combination of amoxicillin and clavulanate, a beta-lactamase inhibitor) is commonly used.
Surgical débridement and irrigation are indicated in those cases with an obvious infection, purulent drainage, joint (pyarthrosis) or tendon (pyogenic tenosynovitis) involvement, or osteomyelitis. Cultures for both aerobic and anaerobic organisms should be obtained. The wounds should be left open and allowed to heal by secondary intention.
Rabies prophylaxis may be indicated with wild animal bites. Emergency rooms should have a protocol in place to notify the Humane Society to verify animal identification versus capture and help assess the need for rabies immunization.
Human Bites
Human bite injuries can be classified into four different types: self-inflicted, traumatic amputations, full-thickness bite wounds to the hand or digits, and clenched-fist (e.g., blow to the mouth producing a knuckle-tooth wound) injuries (Fig. 13A) (100). They have a higher number of different bacterial, especially anaerobic (e.g., Peptostreptococcus and Bacteroides species), isolates than do animal bites (1,86,88,90,93,101,102). The most common pathogens found in human bite infections include Streptococcus and Staphylococcus (aureus and epidermidis) (1,46,86,88,90,93,103). Other isolated aerobic or facultative anaerobic organisms include Neisseria, Corynebacterium, Eikenella, and Haemophilus. The incidence of Eikenella corrodens, an anaerobic gram-negative rod, as a pathogen varies from 2% to 29% (104). It is more commonly cultured from
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dental scrapings than saliva, which may explain the higher incidence of this organism in clenched-fist injuries (91,100,105,106). Anaerobic organisms include Bacteroides, Peptostreptococcus, Propionibacterium, Fusobacterium, Eubacterium, Veillonella, and Clostridium. The presence of anaerobic spirochetes and fusiform bacilli correlates with a worse prognosis (1). Penicillin-resistant gram-negative rods have been reported in approximately one-third of bite wound cultures. Additionally, infectious diseases can be transmitted via human bites, including hepatitis B infection, tuberculosis, scarlet fever, actinomycosis (107,108,109,110,111,112,113,114,115 and 116).
FIGURE 13. A: Typical example of a human bite wound (knuckle-tooth wound). B: The wound extends to the metacarpophalangeal joint, requiring open irrigation and débridement of the wound.
The treatment of human bites depends on several factors, including the time from the occurrence of the bite, the wound location, and the presence or absence of an infection. A history is taken and physical examination performed. The mechanism and timing of the injury and any previous treatment should be known. With clenched-fist injuries, the penetrating tooth track is effectively sealed with digital extension, creating a closed-space environment. Three potential spaces may be entered: the dorsal subcutaneous space between the skin and extensor mechanism, the subtendinous space between the extensor mechanism and joint capsule, and the joint space itself (100).
The physical examination should determine the presence and location of erythema and swelling, purulent discharge, joint or tendon involvement (e.g., septic arthritis and pyogenic tenosynovitis), and lymph node enlargement. Radiographs are taken to rule out fractures, foreign bodies, the presence of subcutaneous gas, retained tooth remnant, or osteomyelitis (28).
Bites that are seen early, within 24 hours and without an obvious infection, and those not involving a joint or tendon may be treated with local wound care and oral antibiotics (117). Gram’s stain and cultures are obtained before antibiotic administration. Local irrigation and débridement of open wounds should be performed and the wound left open to heal secondarily. Oral antibiotics and tetanus prophylaxis are given and the hand appropriately splinted. Repeat examination should be performed in 12 to 24 hours, with follow-up therapy if needed (e.g., whirlpool and range-of-motion exercises).
Formal surgical débridement under tourniquet hemostasis is indicated in cases of obvious infection, joint involvement, or tendon and nerve injury (86,101,118,119 and 120). Clenched-fist injuries demand surgical exploration to document depth of entry and to perform a thorough irrigation and débridement (Fig. 13) (11,121). Associated structures, including the extensor mechanism and chondral surfaces, can be assessed and addressed primarily or secondarily, depending on the cleanliness of the wound. The wound is left open to heal by secondary intention, including the capsular rent if present.
Hospitalization is indicated in cases in which formal surgical débridement is indicated, as well as in those cases involving sepsis, extensive cellulitis, and patient noncompliance. Serial débridements may be needed to obtain control of the infection. The type of antibiotic used is ultimately determined by the results of culture and sensitivities. With the presence of beta-lactamase–producing isolates (e.g., P. multocida, E. corrodens) and anaerobes, antibiotics should include a beta-lactamase inhibitor and penicillin. Tetracycline may be used in patients with a penicillin allergy. E. corrodens is resistant to oxacillin, methicillin, nafcillin, most aminoglycosides, and clindamycin. It is usually sensitive to penicillin G, ampicillin, carbenicillin, and tetracycline (100). Empiric initial coverage must take this into consideration while also providing coverage for gram-positive aerobes, such as Staphylococcus and Streptococcus, as well as anaerobes.
Necrotizing Fasciitis
Necrotizing fasciitis is a severe limb- and life-threatening infection caused by a variety of organisms. A combination
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of aerobic and anaerobic bacteria spreads rapidly along fascial planes (1,27,40,122,123 and 124). The most common pathogens are streptococcal and staphylococcal organisms, but these infections can also be caused by a mixture of facultative and anaerobic organisms.
Two types of necrotizing fasciitis have been described based on the pathogens involved (125). The more common type I infections are caused by a combination of pathogens, including anaerobic bacteria and facultative anaerobic bacteria (e.g., Enterobacter and non–group A streptococci), whereas type II infections include group A streptococci combined with S. aureus or S. epidermidis. Others have reported a single pathogen (group A beta-hemolytic streptococci), instead of multiple pathogens, as the cause of the infection. The mechanism of infection appears to be the production of bacterial enzymes (e.g., hyaluronidase, lipase), which facilitates tissue necrosis (124,126).
Predisposing factors include diabetes mellitus; advanced age; obesity; arteriosclerosis; poor nutrition; peripheral vascular disease; alcoholism; malignancy; compromised immune system; polymyositis; intravenous drug use; postpartum state; and infections of the chest, trunk, or perineum (1,26,122,124,127,128,129 and 130). Infections may result from minor abrasions and lacerations, insect bites, hypodermic needle injections, or surgical incisions.
The clinical findings are variable and include some combination of pain, fever, cellulitis, soft tissue edema, crepitus, skin bullae, skin necrosis, and rapidly expanding margins of infection that are nonresponsive to antibiotic therapy if initially misdiagnosed as cellulitis. Lymphangitis and lymphedema are limited (131). Leukocytosis may be present (40). Sepsis may occur with progression to acute respiratory distress syndrome, hemodynamic instability, and multiple organ system failure (122,128,132). Reported mortality rates vary from 8.7% to 73.0%, with a mean rate of 32.2% (1,122,130).
The surgical findings can include fascial necrosis, possible underlying myositis, and myonecrosis. Treatment includes radical surgical débridement of all necrotic structures (40,122,124). A fasciotomy should be performed. The fascia appears gray or grayish-green; a watery, thin exudate may be encountered, known as dishwater pus. Multiple surgical débridements and secondary wound closure or reconstruction are usually required. Amputation may be required in severe cases.
Broad-spectrum antibiotics, including penicillin, clindamycin, or metronidazole, and an aminoglycoside are used initially and adjusted pending cultures. Fluid resuscitation and hemodynamic monitoring are required. Mortality rates are increased with older age, peripheral vascular disease, and diabetes (1).
Gas Gangrene
Gas gangrene is a rare, although potentially deadly, infectious process that can arise not only after open fractures and farm injuries, but it has also been reported after minor medical procedures, such as injection or venipuncture. Clostridium perfringens is cultured in 50% to 100% of all gas gangrene infections, although more than 150 species exist (20,27,123,124,133). Clostridia are gram-positive, anaerobic, spore-forming, encapsulated bacilli and are soil contaminants. When cultured, they often require 48 to 72 hours for growth (133).
Exotoxins produced by Clostridium cause muscle necrosis and hemolysis. The wound typically is edematous and has a gray discoloration. A brown, watery discharge occurs, with expanding marginal erythema and hemorrhagic bullae. Palpable crepitance is a late finding. Systemically, the patient may be hypotensive and tachycardic, with multiple system organ failure progressing to death if left untreated. Early recognition with aggressive serial surgical débridements, antibiotic coverage (penicillin remains the antibiotic of choice, or metronidazole), and consideration for hyperbaric oxygen therapy optimize potential results (20,134,135).
Fungal Infections
Fungal infections of the hand can occur in normal hosts or in immunocompromised patients, such as transplant patients, patients taking immunosuppressive agents, diabetics, HIV patients, chronic renal failure patients, and patients with myeloproliferative disorders (136,137). These infections can occur as cutaneous, subcutaneous, or deep wound or systemic infections (137,138,139,140 and 141). Cutaneous infections occur in three anatomic areas: the paronychium, nail, and skin (140). These infections include chronic paronychia, onychomycosis (fingernail infection), tinea manuum (palmar interdigital area infection), and tinea corporis (glabrous skin infection).
Chronic Paronychia
Chronic paronychia is usually caused most commonly by C. albicans infections (142,143,144 and 145) of the nail and usually presents with a chronically indurated eponychium, nail thickening, and episodes of inflammation and drainage (42,143,146,147). A secondary bacterial infection can occur, resulting in the appearance of acute infection. There is often a history of frequent exposure to water or moisture (e.g., as with housekeeping personnel) (144). Potassium hydroxide smears help identify spores, branching mycelia, hyphae, or budding yeast. Fungal (Sabouraud’s medium), aerobic, and anaerobic cultures should be taken to identify fungal and bacterial infections. Treatment of chronic paronychia consists of the use of topical antifungal agents (e.g., tolnaftate or clotrimazole) (Table 3) with or without nail removal or nail removal and marsupialization (42,47,140,148) of the nail fold (see the section Paronychia).
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Onychomycosis
Onychomycosis, or tinea unguium, is caused by a fungal infection of the nail plate resulting in destruction of the nail. The most common pathogens include dermatophytes, especially Trichophyton rubrum. The infection can also be caused by C. albicans (138,141,149,150 and 151). The infection can start in the hyponychium, in the eponychium, or on the nail plate surface (152). The infection can begin with localized white or yellowish discoloration of the nail, progressing to involve the entire nail and gradual nail thickening. Further nail discoloration (green, black, brown) occurs with subsequent bacterial colonization of the nail (Fig. 14) (152).
The infection can be treated with topical agents [e.g., nystatin, imidazoles (miconazole, clotrimazole, econazole, ketoconazole), tolnaftate] or oral agents [e.g., the triazoles (fluconazole, itraconazole), terbinafine, or griseofulvin] (Table 3) (141,150,151,153,154,155,156,157 and 158). These systemic medications should be used with caution due to potential liver, renal, and bone marrow toxicity.
Extensively involved nails are removed using digital block anesthesia. Care is taken to protect the germinal and sterile matrix, which are gently scraped with a curette or scalpel. Scrapings should be sent for a potassium hydroxide smear and fungal, aerobic, and anaerobic cultures. Topical antifungal agents are applied to the nailbed once or twice per day until a new nail grows (approximately 120 to 160 days) (140,150).
FIGURE 14. An example of onychomycosis. Note the discoloration and deformity of the nail compared with the adjacent nail.
TABLE 3. DRUGS USED TO TREAT FUNGAL INFECTIONS
Infection Organisms Drug Alternative drug
Chronic paronychia Candida albicans Nystatin, imidazoles, tolnaftate Ketoconazole, fluconazole, itraconazole, griseofulvin
Onychomycosis Dermatophytes, Candida albicans Nystatin, imidazoles, terbinafine Fluconazole, itraconazole, griseofulvin
Tinea manuum Dermatophytes, Candida albicans Nystatin, imidazoles Ketoconazole, fluconazole
Sporotrichosis Sporothrix schenckii Amphotericin B, itraconazole, potassium iodide Ketoconazole, fluconazole
Histoplasmosis Histoplasma capsulatum Amphotericin B, itraconazole Ketoconazole, fluconazole
Blastomycosis Blastomyces dermatitidis Amphotericin B, itraconazole Ketoconazole, fluconazole
Coccidioidomycosis Coccidioidomycosis immitis Amphotericin B, fluconazole Ketoconazole, itraconazole
Aspergillosis Aspergillus fumigatus Amphotericin B Itraconazole
Data from references 21–24.
Skin Infections
Tinea manuum and tinea corporis are fungal infections of the interdigital areas of the palm and the glabrous skin of the hand, respectively. All dermatophytes (Epidermophyton, Microsporum, and especially T. rubrum) and C. albicans are the usual pathogens. The fungal infection usually occurs between the digits and varies from scalelike, hyperkeratotic lesions to areas of acute inflammation and vesicles. Infections frequently occur in patients with spasticity with moist palms and fingers due to a clenched-fist posture (140).
Treatment includes addressing the cause of the cutaneous infection (e.g., decrease exposure to moisture, correct finger flexion contractures) and the use of keratolytic agents (e.g., Whitfield’s ointment), topical imidazoles, and antifungal agents (Table 3) (31,156).
Subcutaneous Infections
Subcutaneous infections include sporotrichosis caused by Sporothrix schenckii, commonly involving the lymphocutaneous system, although deep wound infections, including septic arthritis, can occur (138,159,160,161,162,163 and 164). The organism is commonly found in North America in soil and plants. The infection is noted in farmers, gardeners, florists, and forest and nursery workers. The infection commonly involves the upper extremity (160). A history of a penetrating injury (rose thorn scratch, animal bite, foreign body) is frequently noted. The infection appears as a papule at the site of the initial infection and the spreads along the lymphatic system. Secondary lesions form, appearing indurated and cordlike, and occasionally form seropurulent draining abscesses. Cultures (Sabouraud’s agar) may take days to weeks to become positive. A saturated solution of potassium iodide has been used
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to treat cutaneous sporotrichosis. Itraconazole is used to treat lymphocutaneous sporotrichosis (Table 3).
Deep Infections
Deep infections can present as chronic tenosynovial infections, septic arthritis, or osteomyelitis and are secondary to histoplasmosis, blastomycosis, sporotrichosis, coccidioidomycosis, and paracoccidioidomycosis. Infections in immunocompromised individuals can be caused by aspergillosis, candidiasis, mucormycosis, and cryptococcosis.
FIGURE 15. Systemic blastomycosis infection involving the index finger distal interphalangeal joint (A,B) and ankle joint (C,D). Cutaneous lesions are noted on the nose (E) and leg (F).
Histoplasmosis is caused by Histoplasma capsulatum, found commonly in the Mississippi-Ohio River valley. It commonly produces pulmonary infections but is also found as tenosynovial infections or septic arthritis (165,166 and 167). Blastomycosis, caused by Blastomyces dermatitidis and found in the same region, produces cutaneous lesions, subcutaneous draining abscesses, septic arthritis, and systemic infections. It can produce infections of the hand (Fig. 15) (168,169,170,171,172,173,174 and 175). Lymphangitis and lymphadenitis and skin ulcerations can occur. Coccidioidomycosis, caused by Coccidioidomycosis immitis, is endemic to the southwestern United States and northern Mexico. It commonly produces pulmonary infections that can spread hematogenously to the upper extremity. It can cause osteomyelitis, septic arthritis, and especially tenosynovitis (176,177,178,179 and 180). Dorsal or volar hand and wrist swelling secondary to synovial thickening is frequently noted. Aspergillosis, caused by Aspergillus fumigatus, is found in immunocompromised patients, producing hemorrhagic vesicles, blebs, and ulcerations of the hand and upper extremity (181,182,183,184 and 185).
In general, the treatment of deep fungal infections includes surgical débridement and antifungal agents (e.g., amphotericin B) (Table 3) (137,138 and 139). Systemic medications include griseofulvin, amphotericin B, various azole derivatives, and flucytosine (e.g., ketoconazole) (cryptococcosis, disseminated candidiasis, aspergillosis), fluconazole (cryptococcal, coccidioidal infections), itraconazole (sporotrichosis, histoplasmosis, blastomycosis, paracoccidioidomycosis, chromomycosis), or terbinafine, can be used with caution due to potential liver, renal, and bone marrow toxicity.
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Mycobacterial Infections
Mycobacterial infections involve the skin, subcutaneous tissues, tenosynovium, joints, bone, or a combination of these structures. These infections have a predilection for synovium and produce caseating and noncaseating granulomas (140). Although mycobacterial infections can simulate the appearance of rheumatoid tenosynovitis, the other clinical findings of rheumatoid arthritis are absent. The infections produced by typical and atypical mycobacterial infections are clinically similar. The diagnosis is confirmed by biopsy for histopathologic examination and cultures. Cutaneous infections are generally caused by inoculation and produce nodular or pustular lesions and abscesses draining clear liquid. Lymphangitis is commonly present, but erythema, swelling, and cellulitis are less common.
Tuberculous tenosynovitis involving the hand and forearm is the most common tuberculous infection of the hand and has the similar appearance of chronic tenosynovitis seen with rheumatoid tenosynovitis. The flexor tendons are more commonly involved than the extensor tendons. Constitutional symptoms and local inflammatory signs (erythema, warmth, and pain) are frequently absent. Coexisting pulmonary or extrapulmonary tuberculosis is uncommon. Rice bodies or melon seeds are noted within the synovial mass. A chronic draining sinus may occur. Tendon rupture or fraying occurs in long-standing infections. Osteomyelitis or septic arthritis can occur as the infection spreads.
Tuberculous arthritis most frequently involves the wrist joint. The infection can occur primarily or as the result of untreated tenosynovitis. Infections of the finger joints and elbow can also occur. Painless joint swelling and limited range of motion are noted. Periarticular tenosynovitis or osteomyelitis may be noted. Chronic joint infections can result in joint deformities (dislocation, ankylosis).
Tuberculous osteomyelitis most commonly involves the phalanges and metacarpals. Concurrent pulmonary tuberculosis is uncommon. Painless digital or hand swelling without local inflammatory signs is noted. Pathologic fractures can occur. In chronic cases, abscesses and draining sinuses can occur. Adjacent soft tissue infections can occur.
FIGURE 16. Typical example of atypical mycobacterial infection involving the forearm with encasement of the flexor tendons by the infection.
Mycobacterium tuberculosis Infections
Mycobacterium tuberculosis infection is a slow, insidious process involving the hand and upper extremity (186,187,188,189,190,191,192,193,194,195,196,197,198,199,200,201,202,203,204,205,206,207,208 and 209). The infections present as cutaneous infections (194,203,204 and 205), chronic tenosynovitis (Fig. 16) (186,188,189,190 and 191,196,197,200,206,207,210), digital infections (dactylitis) (192,198), or septic arthritis (189,190,193,201,202). Acute inflammatory signs (e.g., warmth and erythema) are usually not present. Radiographs are usually unremarkable except for soft tissue swelling. In cases of tuberculous arthritis or osteomyelitis, radiographic findings of osteopenia and bone and joint destruction may be noted. The Mantoux (tuberculosis) skin test is variably positive, and the ESR may be slightly elevated. Regional lymphadenopathy is usually absent (26,140).
Risk factors for a mycobacterial infection include immunosuppression, malnutrition, advanced age, alcohol abuse, and history of pulmonary tuberculosis (21,23,24,25,97,195). Acid-fast bacilli can be seen on smears. Histologically, caseating granulomas are noted. Cultures using Löwenstein-Jensen medium may take up to 10 weeks to become positive (23,140).
Cutaneous infections are treated with chemotherapy (199,203,204 and 205). The treatment of tuberculous tenosynovitis includes culture confirmation of the infection, complete teno-synovectomy (especially if the synovium is heavily affected), and use of antituberculous combination chemotherapy (21,22,23 and 24,26,97,140,200,210). The most commonly used first-line
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agents include ethambutol, isoniazid, pyrazinamide, rifampin, and streptomycin. Second-line agents include amikacin, capreomycin sulfate, ciprofloxacin, clofazimine, cycloserine, ethionamide, kanamycin, ofloxacin, para-aminosalicylic acid, and ributin (21,23,24 and 25,97,140). Tuberculous arthritis and osteomyelitis are treated with combination chemotherapy with or without surgical débridement (187).
TABLE 4. RUNYON CLASSIFICATION OF MYCOBACTERIUM SPECIES
Type Characteristic Natural habitat Common diseases in humans
Group I Photochromogens (cream-colored colonies turning yellow on exposure to light)
   M. marinum   Water, fish Skin, soft tissue
   M. kansasii   Water, cattle Skeletal
Group II Scotochromogens (produce orange pigment independent of light)
   M. gordonae   Water Pulmonary (rare)
   M. szulgai   Unknown Bronchopulmonary
Group III Nonchromogens (white colonies that do not develop pigment)
   M. avium-intracellulare Ubiquitous (soil, water, swine, cattle, birds) Pulmonary, lymphadenitis, disseminated
   M. terrae Water, soil Pulmonary (rare)
Group IV Rapid growers (form cream-colored colonies in ≥1 wk vs. 10–28 d for other groups); resistant to most antituberculous drugs but often susceptible to amikacin, doxycycline, erythromycin, kanamycin
   M. fortuitum   Water, soil, animals, marine life Skin, soft tissue, disseminated
   M. chelonae   Water, soil, animals, marine life Skin, soft tissue, disseminated, skeletal
Others
   M. tuberculosis   Humans Bronchopulmonary, soft tissue
   M. bovis   Humans, cattle Soft tissue, gastrointestinal
   M. leprae   Humans, armadillos Skin, soft tissue, disseminated (rare)
Data from Schulman ST, Phair JP, Peterson LR, et al. The biological and clinical basis of infectious diseases, 5th ed. Philadelphia: WB Saunders, 1997; and Resnick D, Pineda CJ, Weisman MH, et al. Osteomyelitis and septic arthritis of the hand following human bites. Skeletal Radiol 1985;14:263–266.
Atypical Mycobacterial Infections
Atypical Mycobacterium infections frequently involve the hand, wrist, and upper extremity (67, 139, 195, 209, 210, 211, 212, 213, 214, 215, 216, 217, 218, 219, 220, 221, 222, 223, 224, 225, 226, 227, 228, 229, 230, 231, 232, 233, 234, 235, 236, 237, 238, 239, 240, 241, 242, 243, 244, 245, 246, 247, 248, 249, 250, 251, 252, 253, 254, 255, 256, 257, 258, 259, 260, 261, 262, 263, 264, 265, 266, 267, 268, 269, 270, 271, 272, 273, 274, 275, 276, 277, 278, 279, 280, 281, 282, 283, 284, 285, 286 and 287). Hand and upper extremity infections are more commonly produced by atypical mycobacteria rather than Mycobacterium tuberculosis. The most common pathogen is Mycobacterium avium, but others include Mycobacterium marinum, Mycobacterium kansasii, Mycobacterium bovis, Mycobacterium chelonae, Mycobacterium fortuitum, among others.
The various types of atypical mycobacteria have been classified according to their growth and pigmentation characteristics (Table 4) (24, 288). These organisms are found widely in nature and usually occur as an infection after a puncture wound or trauma and in immunocompromised individuals (23, 24, 97, 190, 210, 214). The infection frequently involves the flexor tendon, producing a flexor tenosynovitis that inhibits finger motion. Pain may be present, but most patients do not develop systemic symptoms. Skin infections are often associated with subdermal or dermal granulomas (245). Fistulae may be present, and bone and joint infections can also occur (139, 212, 223, 224, 226, 229, 247, 254). Tuberculin skin testing is usually not positive with these infections (140).
Mycobacterium avium-intracellulare is an organism found in soil, water, and domestic poultry. The clinical presentation of this infection can also vary from skin and subcutaneous infections, pulmonary disease, arthritis, osteomyelitis, and sepsis (256, 257, 275, 279, 282). It is frequently noted in patients with acquired immune deficiency syndrome. Risk factors include puncture wounds, closed trauma, treatment with oral corticosteroids, local steroid injections, and immunodeficiency. The organism is resistant to multiple drugs and is difficult to eradicate.
M. marinum is found in both fresh and salt water fish, snails, crabs, and shrimp. The organism can be found in fish tanks, aquariums, and fish farms. M. marinum infections can have a variable presentation, including subcutaneous granulomas with sinus tracks, sporotrichinlike nodules, chronic teno-synovitis, bursitis, arthritis, and osteomyelitis (210, 218, 223, 224, 225 and 226, 245, 251, 253, 260, 284, 285). A history of a puncture wound or some form of trauma within a few months is typical. Most patients are healthy and are not immunocompromised. Patients may present with carpal tunnel–like symptoms in the presence of flexor tendon involvement.
The diagnosis of an atypical mycobacterial infection requires a biopsy for histopathologic examination and cultures (23, 24, 140, 195). Cultures should be taken for aerobic, anaerobic, fungal, mycobacterial, and atypical mycobacterial infections. Histology should show evidence of inflammatory changes, noncaseating granulomas, fibrous exudates, and acid-fast bacilli (Ziehl-Neelsen stain). Findings of epithelioid histiocytes cells, multinucleated giant cells, and granulomas may be seen with synovial biopsies. Special media are frequently required to culture atypical mycobacterium (e.g.,
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Löwenstein-Jensen medium for 4 to 6 weeks at 20°C for M. fortuitum and at 30° to 32°C for M. marinum). Cultures frequently take several weeks to become positive.
In general, the treatment of atypical mycobacterial infections requires biopsy confirmation of the infection and antituberculous medications, with or without surgical débridement (26, 140, 185, 209, 210, 215, 222, 223, 242, 256, 260, 286). Subcutaneous lesions and abscesses may require drainage; joint and tendon involvement requires débridement and synovectomy (140, 210, 227). An infectious disease consultation is generally used for appropriate antibiotic and dosing regimens. In general, two antibiotic agents (e.g., isoniazid, ethambutol, and rifampin) are used for several months (see above). Clarithromycin and azithromycin in addition to first- or second-line agents have been used for M. avium infections. Minocycline, doxycycline, and trimethoprim-sulfamethoxazole, also in addition to first- and second-line agents, have been used for M. marinum infections (97, 140, 248).
Viral Infections
Herpes Infections and Herpetic Whitlow
Herpetic whitlow is a cutaneous viral infection of the digital tip caused by herpes simplex virus type 1 or type 2 (20). Herpes simplex virus type 2 typically presents in patients older than 20 years, whereas patients younger than 20 years tend to have herpes simplex virus type 1. Health workers, such as dental and medical personnel, are at particular risk (289, 290). Adults with genital herpes, all age groups with gingivostomatitis, and immunocompromised patients are also at-risk populations (291, 292 and 293).
Clinically, the digit becomes painful and erythematous. Cutaneous clear vesicular lesions occur and can coalesce and form bullae. A Tzanck test, if pursued, may support the diagnosis, although it may be falsely negative (294). The definitive diagnosis is made by direct viral culture of the vesicular fluid, although it is not usually necessary (290, 293).
The treatment of herpetic whitlow is nonoperative; therefore, distinction from paronychia or felon is important (289, 290, 294). Deep surgical drainage has the potential for secondary bacterial superinfection and the theoretical risk of viral encephalitis. Limited deroofing of the vesicles may provide pain relief, although it does not shorten the duration of involvement. Herpetic whitlow is self-limiting, resolving over a course of 3 to 4 weeks. Antibiotics are given in the rare presence of secondary infection, which tends to be cellulitic (293). In the unusual circumstance of a coinciding bacterial abscess, surgical decompression should be considered in conjunction with administration of either oral or intravenous acyclovir (293).
Human Immunodeficiency Virus
HIV can be transmitted via inoculation (e.g., intravenous drug abusers using contaminated needles), blood transfusions, open wound contact, or mucous membranes. The estimated risk of disease transmission via a contaminated needle stick is 0.4% to 0.5% (approximately 1 in 200). The estimated risk of infection for a surgeon over a 30-year career in New York is 1% to 2% and 4% for a surgeon in San Francisco (295). Universal surgical precautions include double gloves; masks; face shields; hourly check of gloves, masks, and gowns for penetration; and minimizing the number of personnel involved in high-risk patients. A minimum number of instruments should be used, with scalpels passed between the nurse and surgeon using a basin (296).
The risk of HIV transmission via blood transmission varies from 1 in 140,000 to 1 in 250,000. The risk of disease transmission with bone allograft use is approximately 1 in 10,000. There is minimal risk when using fibrin glue due to its processing. There is only one reported case of disease transmission from a health care worker (dentist) to five patients (1).
Hand and upper extremity infections are common in HIV-infected patients and include bacterial, viral infections (herpes simplex and cytomegalovirus), fungal infections (candidiasis, cryptococcosis, histoplasmosis, aspergillosis), protozoal infections, or mycobacterial infections (140, 297, 298, 299, 300 and 301). Infections include pulmonary, gastrointestinal, and disseminated infections, as well as cellulitis and osteomyelitis. The treatment for hand infections is similar to other forms of infection (e.g., débridement and intravenous antibiotics) (298). HIV-infected patients with a reduced CD4 lymphocyte count are at a higher risk for postoperative infections (302, 303).
COMPLICATIONS
Complications arising from the treatment of infections include surgical complications and complications related to antibiotic use (26). Surgical complications include inadequate drainage of the infection resulting in continued infection or spread of the infection, complications related to the poor selection of incisions (skin flap necrosis, scar contractures), and unnecessary surgery producing a secondary infection (herpetic whitlow). Complications related to the use of antibiotics include inadequate antibiotic coverage resulting in residual infection and toxicity secondary to use of the antibiotics (e.g., renal and ototoxicity with aminoglycosides). Joint stiffness, loss of motion, and deformity occur with long-standing bone, joint, or soft tissue infections. Prolonged immobilization or inadequate therapy can also contribute to the loss of hand function.
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