- Email: [email protected]
Acute Hand Infections
CURRENT CONCEPTS
Acute Hand Infections Meredith Osterman, MD, Reid Draeger, MD, Peter Stern, MD CME INFORMATION AND DISCLOSURES The Review Section of JHS will contain at least 3 clinically relevant articles selected by the editor to be offered for CME in each issue. For CME credit, the participant must read the articles in print or online and correctly answer all related questions through an online examination. The questions on the test are designed to make the reader think and will occasionally require the reader to go back and scrutinize the article for details.
Provider Information can be found at http://www.assh.org/Pages/ContactUs.aspx.
The JHS CME Activity fee of $30.00 includes the exam questions/answers only and does not include access to the JHS articles referenced.
ASSH Disclosure Policy: As a provider accredited by the ACCME, the ASSH must ensure balance, independence, objectivity, and scientific rigor in all its activities.
Statement of Need: This CME activity was developed by the JHS review section editors and review article authors as a convenient education tool to help increase or affirm reader’s knowledge. The overall goal of the activity is for participants to evaluate the appropriateness of clinical data and apply it to their practice and the provision of patient care. Accreditation: The ASSH is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. AMA PRA Credit Designation: The American Society for Surgery of the Hand designates this Journal-Based CME activity for a maximum of 2.00 “AMA PRA Category 1 Credits”. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Technical Requirements for the Online Examination can be found at http://jhandsurg. org/cme/home. Privacy Policy can be found at http://www.assh.org/pages/ASSHPrivacyPolicy.aspx.
Disclosures for this Article Editors Ghazi M. Rayan, MD, has no relevant conflicts of interest to disclose. Authors All authors of this journal-based CME activity have no relevant conflicts of interest to disclose. In the printed or PDF version of this article, author affiliations can be found at the bottom of the first page. Planners Ghazi M. Rayan, MD, has no relevant conflicts of interest to disclose. The editorial and education staff involved with this journal-based CME activity has no relevant conflicts of interest to disclose. Learning Objectives
ASSH Disclaimer: The material presented in this CME activity is made available by the ASSH for educational purposes only. This material is not intended to represent the only methods or the best procedures appropriate for the medical situation(s) discussed, but rather it is intended to present an approach, view, statement, or opinion of the authors that may be helpful, or of interest, to other practitioners. Examinees agree to participate in this medical education activity, sponsored by the ASSH, with full knowledge and awareness that they waive any claim they may have against the ASSH for reliance on any information presented. The approval of the US Food and Drug Administration is required for procedures and drugs that are considered experimental. Instrumentation systems discussed or reviewed during this educational activity may not yet have received FDA approval.
Describe the predisposing factors for acute hand infections. List the common microorganisms that cause acute hand infections. Appraise the antibiotic management and mode of administration for each acute hand infection. Offer surgical treatment strategies for various acute hand infections. Discuss treatment outcomes and complications of acute hand infections.
Deadline: Each examination purchased in 2014 must be completed by January 31, 2015, to be eligible for CME. A certificate will be issued upon completion of the activity. Estimated time to complete each month’s JHS CME activity is up to 2 hours. Copyright ª 2014 by the American Society for Surgery of the Hand. All rights reserved.
Current Concepts
The continued emergence of antibiotic-resistant bacteria and the development of only a few new classes of antibiotics over the past 50 years have made the treatment of acute hand infections problematic. Prompt diagnosis and treatment are important, because hand stiffness, contractures, and even amputation can result from missed diagnoses or delayed treatment. The most common site of hand infections is subcutaneous tissue and the most common mechanism is trauma. An immunocompromised state, intravenous drug abuse, diabetes mellitus, and steroid use all predispose to infections. (J Hand Surg Am. 2014;39(8):1628e1635. Copyright 2014 by the American Society for Surgery of the Hand. All rights reserved.) Key words Flexor tenosynovitis, infection, MRSA, necrotizing fasciitis osteomyelitis.
From Mary S. Stern Hand Fellow, Department of Orthopaedic Surgery, University of Cincinnati College of Medicine, Cincinnati, OH.
Corresponding author: Meredith Osterman, MD, Mary S. Stern Hand Fellow, 538 Oak Street, Ste. 200, Cincinnati, OH 45219; e-mail: [email protected].
Received for publication March 17, 2014; accepted in revised form March 25, 2014.
0363-5023/14/3908-0035$36.00/0 http://dx.doi.org/10.1016/j.jhsa.2014.03.031
No benefits in any form have been received or will be received related directly or indirectly to the subject of this article.
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requires the initiation of antibiotics. Increased organism resistance to antibiotics has complicated this aspect of patients’ treatment. Specimens of infected tissue should be sent for aerobic and anaerobic cultures. If chronic hand infection is suspected, fungal and atypical mycobacterium cultures should be sent in addition to staining for acid-fast bacteria. Hand infections can be superficial or deep. Superficial infections can often be treated with antibiotics alone, except in cases of necrotizing fasciitis, for which early surgical intervention is imperative. Surgical irrigation and debridement in conjunction with antibiotic treatment are usually necessary for deep or severe infections. Short-term splinting is also helpful, despite the type or severity of infection. Prompt diagnosis and early treatment are necessary, because hand function can be compromised with missed diagnoses. The most common site of hand infections is the dorsal subcutaneous tissue and the most common mechanism is trauma, such as penetrating injuries or bites.1 The virulence of the organism, the local and systemic host factors, and the anatomical location all have a role in the severity and progression of hand infections.2 An immunocompromised state, intravenous drug abuse, diabetes mellitus, and steroid use all predispose to infections.1 These patients require more operative procedures to eradicate the infection and are more likely to go on to amputation.2 Ischemia from microvascular disease or from trauma disrupts the blood supply to the tissue, preventing host factor bacterial eradication and limiting exposure to antibiotics.
close, prolonged contact with others (military recruits, prison inmates, and homeless individuals).5,6 ANTIBIOTICS The choice of antibiotic treatment depends on the type and severity of infection, host factors, clinical presentation, and regional infectious epidemiology. The high prevalence of antimicrobial-resistant organisms necessitates initial broad-spectrum antibiotic coverage. Consultation with the infectious disease team can help and is encouraged, especially in patients with antimicrobial allergies, immunocompromised states, unusual presentations, or atypical organisms. Intravenous antibiotics are recommended for bone or flexor tendon sheath infection. Septic arthritis requires between 1 and 4 weeks of intravenous antibiotics, and osteomyelitis requires 6 to 8 weeks. Oral antibiotics are appropriate for skin or other superficial soft tissue infections. The typical course is 14 to 21 days. Trimethoprimesulfamethoxazole covers 90% of community acquiredeMRSA and can be used in conjunction with rifampin. Our current recommendation is for 2 double-strength trimethoprime sulfamethoxazole tablets twice daily. Clindamycin and ciprofloxacin are also good first-line agents, especially if the patient has a sulfa allergy, but they have 50% and 40% resistance to ca-MRSA, respectively. Once cultures confirm methacilin sensitive S aureus, the oral regimen can be transitioned to cephalexin or amoxicillin (Tables 1, 2). CELLULITIS Cellulitis is an infection of the skin and subcutaneous tissue without accompanying abscess formation. Patients present with an erythematous, swollen, and painful hand. Associated lymphangitis, when present, may indicate a more severe infection. Presumptive antibiotics should cover the most common causative organisms, Streptococcus pyogenes and S aureus. Although cellulitis may occur in any area of the body, hand cellulitis has a higher likelihood of requiring hospital admission for intravenous antibiotics, to curb the infection.7
COMMON ORGANISMS Staphylococcus aureus and beta-hemolytic streptococci are the most common bacterial culprits of acute hand infections.3 Up to 60% of hand infections result from to S aureus.1 Although the infectious organism is most often a gram-positive bacteria, gram-negative, mycobacterial, or fungal organisms can also cause chronic infections. Over half are polymicrobial.4 Patients with infections caused by mixed bacterial flora, often seen in human bite wounds, have the highest complications.4 Bacteria resistance, specifically methicillin-resistant S aureus (MRSA), is becoming more prevalent both in the hospital and community setting. The incidence of MRSA infections ranges from 34% to 73% of all hand infections.3 Risk factors for the development of MRSA include prolonged hospitalization, prolonged antimicrobial therapy, previous surgical procedures, chronic illnesses, intravenous drug use, and patients who have J Hand Surg Am.
DEEP SPACE INFECTIONS OF THE HAND The deep spaces of the hand include the thenar space, hypothenar space, midpalmar space, webspaces, dorsal subaponeurotic space, and Parona space.8,9 Infections in these spaces commonly result from a puncture wound or spread from a contiguous area. The mainstays of treatment are incision and drainage in the operating room and appropriate antibiotics. r
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REATMENT OF ALL INFECTIONs
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TABLE 1.
ACUTE HAND INFECTIONS
Antibiotic Recommendations for Common Organisms Organism
Antibiotic
Methicillin-sensitive Staphylococcus aureus
Cephalexin, amoxicillin clavulanate (orally)
Methicillin-resistant S aureus
Trimethoprim/sulfamethoxazole (orally), linezolid (orally or IV) If sulfa allergy, clindamycin or doxycycline Vancomycin (IV), daptomycin (IV) Quinupristin/dalfopristin (IV) Tigecycline (IV) Ceftaroline (IV)
Vancomycin-resistant Enterococci
Daptomycin, linezolid (orally or IV), tigecycline (IV), quinupristin/dalfopristin (IV)
Gram negative
Piperacillin/tazobactam Ceftriaxone Ertapenem Quinolones/ciprofloxacin
Pseudomonas
Piperacillin/tazobactam Cefepime Meropenem
Anaerobic infections
Ampicillin/sulbactam, Piperacillin/tazobactam, Ertapenem, meropenem Metronidazole Clindamycin Tigecycline
Vibrio vulnificus
Ceftriaxone and doxycycline Imipenem and doxycycline
Nocardia
Trimethoprim/sulfamethoxazole If sulfa allergy: imipenem, ceftriaxone, amikacin
Sporothrix schenckii
Itraconazole fluconazole and voriconazole
Mycobacterium marinum
Clarithromycin/azithromycin Trimethoprim/sulfamethoxazole minocycline Ethambutol
Aeromonas hydrophilia
Ciprofloxacin Imipenem Trimethoprim/sulfamethoxazole
Cutaneous anthrax
Ciprofloxacin Doxycycline
Tularemia
Gentamicin and doxycycline
Additional Information
Linezolid: expensive, avoid in endocarditis or meningitis, weekly complete blood cell monitoring Dapto: weekly creatinine phosphokinase monitoring
6 mo of treatment in immunesuppressed patients
Treatment for 60 d to treat any remaining spores
IV, intravenously.
Current Concepts
Table 3 outlines the anatomic borders of these spaces, the clinical presentations, and surgical considerations for drainage.
introduce bacteria into the area. Patients present with swelling, erythema, tenderness, and abscess formation along the nailfold, often extending beneath the nail plate or into the pulp space. The most common organism is S aureus, followed by S pyogenes, Pseudomonas pyocyanea, and Proteus vularis.10 Acute paronychia can be treated with warm water soaks (with or without povidone or chlorhexidine) and oral antibiotics.11 If an abscess is present, incision
PARONYCHIA Acute paronychia is a soft tissue infection of the lateral nailfold. Minor trauma from nail biting, hangnails, or manicures inoculate the nailfold and J Hand Surg Am.
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TABLE 2.
Antibiotic Recommendations for Specific Clinical Scenarios
Injury/Organism
Antibiotics
Duration of Treatment
Suture line abscess
Cephalexin or sulfamethoxazole/trimethoprim
Abscess
Ampicillin/sulbactam þ vancomycin Cefazolin þ vancomycin Clindamycin if severe penicillin allergy
Cat or dog bites
Amoxicillin/clavulanic acid (orally) or ampicillin/sulbactam (intravenously) If penicillin allergic, ciprofloxacin, ceftriaxone, or doxycycline
Human bites
Cephalosporins gentamicin and penicillinase-resistant penicillin
Osteomyelitis
Vancomycin and piperacillin/tazobactam
6e8 wk
Septic arthritis
Vancomycin and piperacillin/tazobactam
3e4 wk
Tenosynovitis
Vancomycin and piperacillin/tazobactam
2e3 wk
7e10 d
7e14 d
The antibiotics listed in this chart are first-line antibiotics to be used until cultures dictate treatment.
FELON A felon is an abscess of the digital pulp. The septal compartments of the palmar pad create a closed space that can easily form an abscess when inoculated with an infectious organism. Patients present with pain, swelling, and a history of penetrating trauma. Treatment consists of oral antibiotics and surgical drainage.13 The most common organism is S aureus, with MRSA becoming more commonplace. Empiric treatment with antibiotics that cover MRSA is recommended until cultures dictate treatment.13 A longitudinal incision from the distal flexion crease to the pulp apex avoids the neurovascular bundles and permits disruption of the septal compartments. J Hand Surg Am.
HUMAN BITES A human bite (fight bite) initially appears benign but always requires surgical exploration and irrigation. The area around the metacarpophalangeal joint is most often involved and the position of the fingers at the time of impact contributes to the significance of the injury. A human tooth contacting a clenched fist usually violates the extensor tendon and joint capsule and may injure the metacarpal head, inoculating the metacarpophalangeal joint. The human bite injury wound should be surgically extended, an arthrotomy performed with debridement, r
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Current Concepts
HERPETIC WHITLOW Herpetic whitlow is a viral infection that can be mistaken for a felon, usually affecting the fingertip and caused by herpes simplex virus (HSV) 1 or 2. Herpes simplex virus 1 is the primary cause in patients under age of 10, whereas adults can be infected with either HSV-1 or HSV-2.14 Patients present within 2 weeks of viral contact with throbbing pain and vesicles or bullae containing clear fluid.9 The clinical diagnosis can be confirmed with Tzanck smear or viral cultures. The virus is self-limiting, often resolving within 3 weeks without treatment. The vesicles drain, coalesce, and ulcerate before resolution and are contagious during the first 2 weeks.14 It is paramount to prevent spreading infection during this time and a dry dressing should be worn at all times. Surgical incision and drainage are contraindicated because a superimposed bacterial infection can develop. After resolution of the finger lesions, the virus enters into a latency phase and can be retriggered by physiological or psychological stressors.14 The recurrence rate is 20%.15
and drainage are recommended in conjunction with oral antibiotics. We routinely remove all or part of the nail plate. Chronic paronychia is distinct from acute paronychia and is common when hands are constantly exposed to water, such as for dishwashers, swimmers, and medical professionals. The eponychium becomes rounded and indurated with repeated episodes of inflammation and drainage, the nailfold separates from the nail plate, and the area becomes colonized, often with polymicrobial or fungal organisms. This can lead to grooving and thickening of the nail plate. Keeping the area dry, applying antifungal topical creams, and trying oral antifungal or antibiotics is a reasonable first line of attack. Surgical treatment is often required, because topical and oral medications are often unsuccessful. Eponychial marsupialization is the mainstay of treatment. If nail deformity is present, the nail plate should be removed to help reduce recurrence.12
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Anatomy, Presentation, and Treatment of Deep Hand Space Infections
Deep Hand Space
Borders
Presentation
Surgical Points
Dorsal subaponeurotic
Dorsal: extensor tendons; volar: metacarpals and interossei
Dorsal hand swelling and fluctuans
Longitudinal incisions over index and ring metacarpals, not directly over extensor tendons
Thenar
Dorsal: adductor pollicis; volar: index flexor tendons; ulnar: septum of Legueu and Juvara; radial: adductor pollicis insertion at P1 of thumb
Thenar and first webspace swelling, thumb abduction with painful adduction or opposition, pantaloon-shaped abscess if involvement of first dorsal webspace through contiguous spread (Burkhalter)
Palmar, dorsal, or 2-incision approaches; for pantaloon, abscess may drain through dual incisions or single incision perpendicular to first webspace to minimize webspace contracture
Midpalmar/deep palmar
Dorsal: middle and ring finger metacarpals and second and third interossei; volar: flexor tendons and lumbricales; ulnar: hypothenar muscles; radial: septum of Legueu and Juvara
Loss of normal palmar concavity with marked palm tenderness, painful passive motion of middle and ring fingers; substantial dorsal swelling may be present
Transverse incision in distal palmar crease; curvilinear incision along thenar crease
Webspace
Subfascial palmar space between digits
Abducted posture of adjacent digits with accompanying dorsal swelling and volar tenderness at webspace
Must drain both dorsal and volar aspects of abscess; incisions both dorsally and volarly; avoid webspace incisions to prevent contracture
Parona
Volar: pronator quadratus; dorsal: digital flexor tendons; ulnar: flexor carpi ulnaris; radial: flexor pollicis longus
Pain with passive finger flexion; acute carpal tunnel syndrome may be present
Avoid placing incisions directly over flexor tendons or median nerve to avoid desiccation
Current Concepts
and appropriate cultures obtained. The wound is left open. Up to 50 species of bacteria reside in the human mouth; S aureus and beta-hemolytic streptococci are the most common.1 Broad-spectrum antibiotics such as cephalosporins or a combination of gentamicin and a penicillinase-resistant penicillin are the first-line antibiotic regimen.16 Complications such as osteomyelitis, septic arthritis, deep space infections, and stiffness are common. Factors contributing to human bite infections include a delay in initial treatment, inadequate initial debridement, and initial wound closure.17 Patients presenting with bite infections more than 8 days after the initial injury have an 18% change of requiring amputation.16
common organism found in animal bites, but Staphylococcus, Streptococcus, and anaerobes are also found.9 Pasteurella species are isolated in 50% of dog bites and 75% of cat bites, but the average bite wound yields 5 variations of bacterial species, with 60% yielding mixed aerobic and anaerobic organisms.18 Tetanus prophylaxis should be administered when indicated. Animal bite wounds should be treated with irrigation and oral amoxicillineclavulanate or intravenous ampicillinesulbactam. If patients are allergic to penicillin, they can be treated with doxycycline, sulfamethoxazoleetrimethoprim, or a fluoroquinolone plus clindamycin.18
ANIMAL BITES Most commonly, animal bites are from dogs, cats, or rodents.18 Eighty percent are from dog bites, but these rarely result in infections.18 In contrast, cat bites have a 50% infection rate, often requiring admission and intravenous antibiotics.19 The difference results from the mechanism of the bite; cats have sharp, penetrating teeth compared with the crushing, tearing bite of a dog. Pasteurella multocida is the most
PYOGENIC FLEXOR TENOSYNOVITIS In pyogenic flexor tenosynovitis (PFT), bacteria infect the flexor tendon sheath, between the visceral epitenon layer and the outer parietal layer, which is reinforced by the retinacular pulley system. The synovial space between the 2 layers becomes distended under pressure and advanced infection can lead to the breakdown of adjacent anatomic barriers. This can lead to the spread of infection to nearby flexor
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sheaths and bursae, and into the forearm through the Parona space. Purulent fluid in the synovial space surrounding the tendon denies the tendon vital nutrition, and increased pressure in the infected sheath can inhibit blood flow to the tendon, causing necrosis.20 Flexor sheath anatomy explains the spread of infection from the little finger to the thumb (or vice versa), through the contiguous palmar radial and ulnar bursae, causing a horseshoe abscess. Usually, there is a history of penetrating trauma to the digit before presentation. Although no studies have validated their sensitivity and specificity, Kanavel’s 4 cardinal signs remain helpful in diagnosing PFT. These signs, listed in descending frequency, include fusiform digital swelling (usually associated with erythema), pain with passive digital extension, semiflexed digital posture, and tenderness along the flexor tendon sheath with frequent extension into the palm.21 The presence of all 4 Kanavel signs occurred in only 54% of PFT patients in 1 series.22 Laboratory values such as white blood cell count, erythrocyte sedimentation rate, and C-reactive protein can be helpful in confirming the diagnosis of PFT.23 Elevation of at least 1 of these markers, in combination with clinical evaluation, was 100% specific in identifying cases of PFT. However, sensitivities of these markers were low (white blood cell, 39%; erythrocyte sedimentation rate, 41%; and C-reactive protein, 76%), indicating that markers were not always elevated in the setting of PFT.23 Treatment for PFT is surgical irrigation of the flexor sheath and intravenous antibiotic therapy. The most common organisms include S aureus and Streptococcus species; thus, antibiotics before culture data should cover these bacteria.22e24 For severe infections with subcutaneous purulence or necrotic tendon, open exposure of the sheath and irrigation of the sheath through windows sparing the A2 and A4 pulleys is necessary. A midaxial approach is preferred over a Bruner incision, which can lead to postoperative tendon exposure or peri-incisional skin loss.25 Limited exposure of the sheath with closed catheter irrigation is favored in the absence of loculated purulence. It allows for minimization of trauma to the digit and pulley system and has been shown to result in equivalent outcomes to open irrigation of the sheath.22,26 Factors responsible for a poor outcome or risk of amputation include age greater than 43 years, certain comorbidities (diabetes mellitus, renal failure, or peripheral vascular disease), subcutaneous purulence, and ischemic changes upon presentation.22 Digits without subcutaneous purulence or ischemic changes regain more total active motion (TAM) with J Hand Surg Am.
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NECROTIZING FASCIITIS Necrotizing fasciitis is a medical emergency. Aggressive, urgent surgical intervention is of utmost importance. Delay in diagnosis can lead to loss of life or limb. The infection involves the fascia and subcutaneous tissue, sparing underlying tissues. Two types have been described. Type 1 is most common, caused by mixed aerobic and anaerobic organisms and frequent in immunocompromised hosts.28,29 Type 2 results from group A Streptococcus and/or Staphylococcus organisms and more typically affects the extremities.28 Risk factors include immunosuppression, peripheral vascular disease, diabetes mellitus, chronic liver disease, and intravenous drug abuse.28,29 Initially, these infections can appear as low-grade cellulitis. Clinical signs more indicative of necrotizing fasciitis include crepitus, fluctuans, nonpitting edema, tenderness beyond areas of erythema, hypotension, fever, and tachycardia.29 Vascular thrombosis leads to skin sloughing, blistering, ischemia, and resultant necrosis.28 Upon surgical debridement, the fat appears gray and liquefied with a “dishwater pus” appearance. Frank pus is uncommon. Malodorous tissue is common with anaerobic organism involvement.28 Characteristically, the skin and subcutaneous tissue are elevated from the fascia, necessitating extensive debridement to healthy tissue.28 Operative cultures are taken, the wounds are left open, and debridement is repeated every 24 to 48 hours as needed. Initial treatment includes broad-spectrum intravenous antibiotics that cover aerobes and anaerobes and often require multiple drugs simultaneously. A reasonable combination includes ampicillinesulbactam, clindamycin, and ciprofloxacin.18 Amputation may be necessary to control the infection but does not reduce mortality rates.29 Mortality rates range from 23% to 76%; organ failure and sepsis are the major causes of death.30 Delay in diagnosis and delay in surgical debridement are significantly associated with increased mortality.29 Advanced age and 2 or more comorbidities further increase mortality rates.29 r
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Current Concepts
a lower incidence of amputation (average, 80% normal TAM; 0% amputation rate)21,27 than those with subcutaneous purulence (average, 72% normal TAM; 8% amputation) and or with both subcutaneous purulence and ischemic changes (average, 49% normal TAM; 59% amputation).21 In addition, delayed treatment increases the probability of a poor functional outcome.22
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Current Concepts
SEPTIC ARTHRITIS Septic arthritis of the joints of the hand is commonly caused by penetrating trauma or the spread of infection from contiguous structures. Like other closed space infections, bacterial toxins and local inflammatory response result in the majority of damage to the joint.31,32 The most common organisms are betahemolytic Streptococcus and S aureus. Neisseria gonorrhoeae should be considered in sexually active patients, whereas Haemophilus influenza should be considered in unvaccinated children. Examination reveals fusiform joint erythema and swelling and pain with active or passive motion. Joint aspiration allows for definitive diagnosis, and in addition to cultures and cell count, crystal analysis should be performed because crystalline arthropathies, particularly gout, can present with a similar picture. Classically, a cell count of 50,000 with greater than 75% polymorphonuclear leukocytes and glucose of 40 mg% less than fasting blood glucose level was consistent with a diagnosis of septic arthritis. More recent studies have demonstrated that lowering the cell count threshold to 17,500 increases the sensitivity of the diagnosis of septic arthritis to 83%, with an acceptable specificity of 67%.33,34 Treatment of septic arthritis involves irrigation and debridement of the joint and systemic antibiotics. A recent study found that after surgical drainage, a short course of intravenous antibiotics of less than 1 week supplemented with oral antibiotics for 2 to 3 additional weeks successfully treated septic arthritis of the hand and wrist in most cases.35 Open drainage of the wrist is through a longitudinal incision between the third and fourth dorsal compartments. Alternatively, arthroscopic irrigation and debridement without closure of arthroscopic portals can produce similar outcomes compared with open procedures.36 Metacarpophalangeal joints should be entered through a longitudinal, dorsal incision, with at least partial preservation of the sagittal bands to avoid postoperative extensor tendon subluxation. Interphalangeal joints should be approached through a midaxial incision between the volar plate and the accessory collateral ligament, or between the lateral slip of the extensor mechanism and cordlike portion of the collateral ligament, to avoid postoperative finger deformities.37
the severity of contamination contribute to its development. Staphylococcus aureus and Streptococcus are the most common causative organisms. Gramnegative bacteria, anaerobes and atypical and fungal organisms can also lead to osteomyelitis, and a mixed bacterial etiology is common in patients with vascular insufficiency or an immunocompromised state.38 Mixed bacterial infection predisposes the patient to the high likelihood of amputation.38 Hardware and other devitalized tissue are a nidus for bacterial inoculation, most commonly S epidermis, and must be removed to eradicate infection. The distal phalanx is the most commonly affected in the hand.38 Osteolysis and soft tissue swelling are the most common radiographic findings. Periosteal new bone formation, involucrum, and sequestrum are less common in the tubular bones of the hand. A definitive diagnosis requires a bone biopsy and cultures. Treatment consists of intravenous antibiotics and operative debridement. Intravenous antibiotics are instituted for a minimum of 4 to 6 weeks.39 REFERENCES 1. Houshian S, Seyedipour S, Wedderkopp N. Epidemiology of bacterial hand infections. Int J Infect Dis. 2006;10(4):315e319. 2. Ong Y, Levin LS. Hand infections. Plast Reconstr Surg. 2009; 124(4):225e233. 3. Tosti R, Ilyas A. Empiric antibiotics for acute infections of the hand. J Hand Surg Am. 2010;35(1):125e128. 4. Stern P, Staneck J, McDonough J, Neale H, Tyler G. Established hand infections: a controlled, prospective study. J Hand Surg Am. 1983;8(5):553e559. 5. Salgado CD, Farr BN, Calfee DP. Community-acquired methicillinresistant Staphylococcus aureus: a meta-analysis of prevalence and risk factors. Clin Infect Dis. 2003;36(2):131e139. 6. O’Malley M, Fowler J, Ilyas AM. Community-acquired methicillinresistant Staphylococcus aureus infections of the hand: prevalence and timeliness of treatment. J Hand Surg Am. 2009;34(3):504e508. 7. Volz KA, Canham L, Kaplan E, Sanchez LD, Shapiro NI, Grossman SA. Identifying patients with cellulitis who are likely to require inpatient admission after a stay in an ED observation unit. Am J Emerg Med. 2013;31(2):360e364. 8. Burkhalter WE. Deep space infections. Hand Clin. 1989;5(4):53e59. 9. Franko O, Abrams R. Hand infections. Orthop Clin N Am. 2013; 44(4):625e634. 10. Rockwell PG. Acute and chronic paronychia. Am Fam Physician. 2001;63(6):1113e1116. 11. Ritting AW, O’Malley MP, Rodner CM. Acute paronychia. J Hand Surg Am. 2012;37(5):1068e1070. 12. Bednar M, Lane L. Eponychial marsupialization and nail removal for surgical treatment of chronic paronychia. J Hand Surg Am. 1991;16(2):314e317. 13. Tannan S, Deal DN. Diagnosis and management of the acute felon: evidence-based review. J Hand Surg Am. 2012;37(12):2603e2604. 14. Rubright J, Shafritz A. The herpetic whitlow. J Hand Surg Am. 2011;36(2):340e342. 15. Wu I, Schwartz R. Herpetic whitlow. Cutis. 2007;79(3):193e196. 16. Shoji K, Cavanaugh Z, Rodner C. Acute fight bite. J Hand Surg Am. 2013;18(8):1612e1614. 17. Gonzalez M, Papierski P, Hall R. Osteomyelitis of the hand after a human bite. J Hand Surg Am. 1993;18(3):520e522.
OSTEOMYELITIS Osteomyelitis is often a sequelae of septic arthritis, soft tissue infection, or an open fracture. The degree of soft tissue injury or tissue devascularization, and J Hand Surg Am.
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29. Wong C, Chang H, Pasupathy S, et al. Necrotizing fasciitis: clinical presentation, microbiology, and determinants of mortality. J Bone Joint Surg Am. 2003;84(8):1454e1460. 30. Fontes R, Ogilvie C, Miclau T. Necrotizing soft-tissue infections. J Am Acad Orthop Surg. 2000;8(3):151e158. 31. Odio CM, Ramierez T, Arias G, et al. Double blind, randomized, placebo-controlled study of dexamethasone therapy for hematogenous septic arthritis in children. Pediatr Infect Dis J. 2003;22(10): 883e888. 32. Josefsson E, Tarkowski A. Staphylococcus aureus-induced inflammation and bone destruction in experimental models of septic arthritis. J Periodontal Res. 1999;34(7):387e392. 33. Li SF, Cassidy C, Chang C, et al. Diagnostic utility of laboratory tests in septic arthritis. Emerg Med J. 2007;42(2):75e77. 34. McGillicuddy DC, Shah KH, Friedberg RP, Nathanson LA, Edlow JA. How sensitive is the synovial fluid white blood cell count in diagnosing septic arthritis? Am J Emerg Med. 2007;25(7): 749e752. 35. Kowalski TJ, Thompson La, Gundrum JD. Antimicrobial management of septic arthritis of the hand and wrist. Infection. 2014;42(2): 379e384. 36. Sammer DM, Shin AY. Comparison of arthroscopic and open treatment of septic arthritis of the wrist. J Bone Joint Surg Am. 2009;91(6):1387e1393. 37. Freeland AE, Senter BS. Septic arthritis and osteomyelitis. Hand Clin. 1989;5(4):533e552. 38. Reilly K, Linz J, Stern P, Giza E, Wyrick J. Osteomyelitis of the tubular bones of the hand. J Hand Surg Am. 1997;22(4): 644e649. 39. Honda H, McDonald J. Current recommendations in the management of osteomyelitis of the hand and wrist. J Hand Surg Am. 2009;34(6): 1135e1136.
18. Stevens D, Bisno A, Chambers H, et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41(10):1373e1406. 19. Aghababian R, Conte JE. Mammalian bite wounds. Ann Emerg Med. 1980;9(2):79e83. 20. Schnall SB, Vu-Rose T, Holtom PD, Doyle B, Stevanovic M. Tissue pressures in pyogenic flexor tenosynovitis of the finger: compartment syndrome and its management. J Bone Joint Surg Br. 1996;78(5): 792e795. 21. Pang HN, Teoh LC, Yam AK, Lee JY, Punhaindram ME, Tan AB. Factors affecting the prognosis of pyogenic flexor tenosynovitis. J Bone Joint Surg Am. 2007;89(8):1742e1748. 22. Dailiana ZH, Rigopoulos N, Varitimidis S, Hantes M, Bargiotas K, Malizos KN. Purulent flexor tenosynovitis: factors influencing the functional outcome. J Hand Surg Eur Vol. 2008;33(3):280e285. 23. Bishop GB, Born T, Kakar S, Jawa A. The diagnostic accuracy of inflammatory blood markers for purulent flexor tenosynovitis. J Hand Surg Am. 2013;38(11):2201e2211. 24. Karagergou E, Rao K, Harper RD. Parameters affecting the severity and outcome of pyogenic digital flexor tenosynovitis. J Hand Surg Eur Vol. 2014 Jan 8. [Epub ahead of print]. 25. Draeger RW, Bynum DK Jr. Flexor tendon sheath infections of the hand. J Am Acad Orthop Surg. 2012;20(6):373e382. 26. Gutowski KA, Ochoa O, Adams WP Jr. Closed-catheter irrigation is as effective as open drainage for treatment of pyogenic flexor tenosynovitis. Ann Plast Surg. 2002;49(4):350e354. 27. Lille S, Hayakawa T, Neumeister MW, Brown RE, Zook EG, Murray K. Continuous postoperative catheter irrigation is not necessary for the treatment of suppurative flexor tenosynovitis. J Hand Surg Br. 2000;25(3):304e307. 28. Gonzalez M. Necrotizing fasciitis and gangrene of the upper extremity. Hand Clin. 1998;14(4):635e645.
JOURNAL CME QUESTIONS What percentages of Pasteurella species are isolated from dog and cat bites? a. 10% of dog bites and 35% of cat bites b. 20% of dog bites and 45% of cat bites c. 30% of dog bites and 55% of cat bites d. 40% of dog bites and 65% of cat bites e. 50% of dog bites and 75% of cat bites
Acute Hand Infections Which of the following microorganisms are most sensitive to ciprofloxacin? a. Anthrax and Aeromonas hydrophilia b. Norcardia and tularemia c. Mycobacterium and Vibrio d. Pseudomonas and Sporothrix e. MRSA and all viruses
Current Concepts
To take the online test and receive CME credit, go to http://www.jhandsurg.org/CME/home.
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Acute Hand Infections Meredith Osterman, MD, Reid Draeger, MD, Peter Stern, MD CME INFORMATION AND DISCLOSURES The Review Section of JHS will contain at least 3 clinically relevant articles selected by the editor to be offered for CME in each issue. For CME credit, the participant must read the articles in print or online and correctly answer all related questions through an online examination. The questions on the test are designed to make the reader think and will occasionally require the reader to go back and scrutinize the article for details.
Provider Information can be found at http://www.assh.org/Pages/ContactUs.aspx.
The JHS CME Activity fee of $30.00 includes the exam questions/answers only and does not include access to the JHS articles referenced.
ASSH Disclosure Policy: As a provider accredited by the ACCME, the ASSH must ensure balance, independence, objectivity, and scientific rigor in all its activities.
Statement of Need: This CME activity was developed by the JHS review section editors and review article authors as a convenient education tool to help increase or affirm reader’s knowledge. The overall goal of the activity is for participants to evaluate the appropriateness of clinical data and apply it to their practice and the provision of patient care. Accreditation: The ASSH is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. AMA PRA Credit Designation: The American Society for Surgery of the Hand designates this Journal-Based CME activity for a maximum of 2.00 “AMA PRA Category 1 Credits”. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
Technical Requirements for the Online Examination can be found at http://jhandsurg. org/cme/home. Privacy Policy can be found at http://www.assh.org/pages/ASSHPrivacyPolicy.aspx.
Disclosures for this Article Editors Ghazi M. Rayan, MD, has no relevant conflicts of interest to disclose. Authors All authors of this journal-based CME activity have no relevant conflicts of interest to disclose. In the printed or PDF version of this article, author affiliations can be found at the bottom of the first page. Planners Ghazi M. Rayan, MD, has no relevant conflicts of interest to disclose. The editorial and education staff involved with this journal-based CME activity has no relevant conflicts of interest to disclose. Learning Objectives
ASSH Disclaimer: The material presented in this CME activity is made available by the ASSH for educational purposes only. This material is not intended to represent the only methods or the best procedures appropriate for the medical situation(s) discussed, but rather it is intended to present an approach, view, statement, or opinion of the authors that may be helpful, or of interest, to other practitioners. Examinees agree to participate in this medical education activity, sponsored by the ASSH, with full knowledge and awareness that they waive any claim they may have against the ASSH for reliance on any information presented. The approval of the US Food and Drug Administration is required for procedures and drugs that are considered experimental. Instrumentation systems discussed or reviewed during this educational activity may not yet have received FDA approval.
Describe the predisposing factors for acute hand infections. List the common microorganisms that cause acute hand infections. Appraise the antibiotic management and mode of administration for each acute hand infection. Offer surgical treatment strategies for various acute hand infections. Discuss treatment outcomes and complications of acute hand infections.
Deadline: Each examination purchased in 2014 must be completed by January 31, 2015, to be eligible for CME. A certificate will be issued upon completion of the activity. Estimated time to complete each month’s JHS CME activity is up to 2 hours. Copyright ª 2014 by the American Society for Surgery of the Hand. All rights reserved.
Current Concepts
The continued emergence of antibiotic-resistant bacteria and the development of only a few new classes of antibiotics over the past 50 years have made the treatment of acute hand infections problematic. Prompt diagnosis and treatment are important, because hand stiffness, contractures, and even amputation can result from missed diagnoses or delayed treatment. The most common site of hand infections is subcutaneous tissue and the most common mechanism is trauma. An immunocompromised state, intravenous drug abuse, diabetes mellitus, and steroid use all predispose to infections. (J Hand Surg Am. 2014;39(8):1628e1635. Copyright 2014 by the American Society for Surgery of the Hand. All rights reserved.) Key words Flexor tenosynovitis, infection, MRSA, necrotizing fasciitis osteomyelitis.
From Mary S. Stern Hand Fellow, Department of Orthopaedic Surgery, University of Cincinnati College of Medicine, Cincinnati, OH.
Corresponding author: Meredith Osterman, MD, Mary S. Stern Hand Fellow, 538 Oak Street, Ste. 200, Cincinnati, OH 45219; e-mail: [email protected].
Received for publication March 17, 2014; accepted in revised form March 25, 2014.
0363-5023/14/3908-0035$36.00/0 http://dx.doi.org/10.1016/j.jhsa.2014.03.031
No benefits in any form have been received or will be received related directly or indirectly to the subject of this article.
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requires the initiation of antibiotics. Increased organism resistance to antibiotics has complicated this aspect of patients’ treatment. Specimens of infected tissue should be sent for aerobic and anaerobic cultures. If chronic hand infection is suspected, fungal and atypical mycobacterium cultures should be sent in addition to staining for acid-fast bacteria. Hand infections can be superficial or deep. Superficial infections can often be treated with antibiotics alone, except in cases of necrotizing fasciitis, for which early surgical intervention is imperative. Surgical irrigation and debridement in conjunction with antibiotic treatment are usually necessary for deep or severe infections. Short-term splinting is also helpful, despite the type or severity of infection. Prompt diagnosis and early treatment are necessary, because hand function can be compromised with missed diagnoses. The most common site of hand infections is the dorsal subcutaneous tissue and the most common mechanism is trauma, such as penetrating injuries or bites.1 The virulence of the organism, the local and systemic host factors, and the anatomical location all have a role in the severity and progression of hand infections.2 An immunocompromised state, intravenous drug abuse, diabetes mellitus, and steroid use all predispose to infections.1 These patients require more operative procedures to eradicate the infection and are more likely to go on to amputation.2 Ischemia from microvascular disease or from trauma disrupts the blood supply to the tissue, preventing host factor bacterial eradication and limiting exposure to antibiotics.
close, prolonged contact with others (military recruits, prison inmates, and homeless individuals).5,6 ANTIBIOTICS The choice of antibiotic treatment depends on the type and severity of infection, host factors, clinical presentation, and regional infectious epidemiology. The high prevalence of antimicrobial-resistant organisms necessitates initial broad-spectrum antibiotic coverage. Consultation with the infectious disease team can help and is encouraged, especially in patients with antimicrobial allergies, immunocompromised states, unusual presentations, or atypical organisms. Intravenous antibiotics are recommended for bone or flexor tendon sheath infection. Septic arthritis requires between 1 and 4 weeks of intravenous antibiotics, and osteomyelitis requires 6 to 8 weeks. Oral antibiotics are appropriate for skin or other superficial soft tissue infections. The typical course is 14 to 21 days. Trimethoprimesulfamethoxazole covers 90% of community acquiredeMRSA and can be used in conjunction with rifampin. Our current recommendation is for 2 double-strength trimethoprime sulfamethoxazole tablets twice daily. Clindamycin and ciprofloxacin are also good first-line agents, especially if the patient has a sulfa allergy, but they have 50% and 40% resistance to ca-MRSA, respectively. Once cultures confirm methacilin sensitive S aureus, the oral regimen can be transitioned to cephalexin or amoxicillin (Tables 1, 2). CELLULITIS Cellulitis is an infection of the skin and subcutaneous tissue without accompanying abscess formation. Patients present with an erythematous, swollen, and painful hand. Associated lymphangitis, when present, may indicate a more severe infection. Presumptive antibiotics should cover the most common causative organisms, Streptococcus pyogenes and S aureus. Although cellulitis may occur in any area of the body, hand cellulitis has a higher likelihood of requiring hospital admission for intravenous antibiotics, to curb the infection.7
COMMON ORGANISMS Staphylococcus aureus and beta-hemolytic streptococci are the most common bacterial culprits of acute hand infections.3 Up to 60% of hand infections result from to S aureus.1 Although the infectious organism is most often a gram-positive bacteria, gram-negative, mycobacterial, or fungal organisms can also cause chronic infections. Over half are polymicrobial.4 Patients with infections caused by mixed bacterial flora, often seen in human bite wounds, have the highest complications.4 Bacteria resistance, specifically methicillin-resistant S aureus (MRSA), is becoming more prevalent both in the hospital and community setting. The incidence of MRSA infections ranges from 34% to 73% of all hand infections.3 Risk factors for the development of MRSA include prolonged hospitalization, prolonged antimicrobial therapy, previous surgical procedures, chronic illnesses, intravenous drug use, and patients who have J Hand Surg Am.
DEEP SPACE INFECTIONS OF THE HAND The deep spaces of the hand include the thenar space, hypothenar space, midpalmar space, webspaces, dorsal subaponeurotic space, and Parona space.8,9 Infections in these spaces commonly result from a puncture wound or spread from a contiguous area. The mainstays of treatment are incision and drainage in the operating room and appropriate antibiotics. r
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REATMENT OF ALL INFECTIONs
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Antibiotic Recommendations for Common Organisms Organism
Antibiotic
Methicillin-sensitive Staphylococcus aureus
Cephalexin, amoxicillin clavulanate (orally)
Methicillin-resistant S aureus
Trimethoprim/sulfamethoxazole (orally), linezolid (orally or IV) If sulfa allergy, clindamycin or doxycycline Vancomycin (IV), daptomycin (IV) Quinupristin/dalfopristin (IV) Tigecycline (IV) Ceftaroline (IV)
Vancomycin-resistant Enterococci
Daptomycin, linezolid (orally or IV), tigecycline (IV), quinupristin/dalfopristin (IV)
Gram negative
Piperacillin/tazobactam Ceftriaxone Ertapenem Quinolones/ciprofloxacin
Pseudomonas
Piperacillin/tazobactam Cefepime Meropenem
Anaerobic infections
Ampicillin/sulbactam, Piperacillin/tazobactam, Ertapenem, meropenem Metronidazole Clindamycin Tigecycline
Vibrio vulnificus
Ceftriaxone and doxycycline Imipenem and doxycycline
Nocardia
Trimethoprim/sulfamethoxazole If sulfa allergy: imipenem, ceftriaxone, amikacin
Sporothrix schenckii
Itraconazole fluconazole and voriconazole
Mycobacterium marinum
Clarithromycin/azithromycin Trimethoprim/sulfamethoxazole minocycline Ethambutol
Aeromonas hydrophilia
Ciprofloxacin Imipenem Trimethoprim/sulfamethoxazole
Cutaneous anthrax
Ciprofloxacin Doxycycline
Tularemia
Gentamicin and doxycycline
Additional Information
Linezolid: expensive, avoid in endocarditis or meningitis, weekly complete blood cell monitoring Dapto: weekly creatinine phosphokinase monitoring
6 mo of treatment in immunesuppressed patients
Treatment for 60 d to treat any remaining spores
IV, intravenously.
Current Concepts
Table 3 outlines the anatomic borders of these spaces, the clinical presentations, and surgical considerations for drainage.
introduce bacteria into the area. Patients present with swelling, erythema, tenderness, and abscess formation along the nailfold, often extending beneath the nail plate or into the pulp space. The most common organism is S aureus, followed by S pyogenes, Pseudomonas pyocyanea, and Proteus vularis.10 Acute paronychia can be treated with warm water soaks (with or without povidone or chlorhexidine) and oral antibiotics.11 If an abscess is present, incision
PARONYCHIA Acute paronychia is a soft tissue infection of the lateral nailfold. Minor trauma from nail biting, hangnails, or manicures inoculate the nailfold and J Hand Surg Am.
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TABLE 2.
Antibiotic Recommendations for Specific Clinical Scenarios
Injury/Organism
Antibiotics
Duration of Treatment
Suture line abscess
Cephalexin or sulfamethoxazole/trimethoprim
Abscess
Ampicillin/sulbactam þ vancomycin Cefazolin þ vancomycin Clindamycin if severe penicillin allergy
Cat or dog bites
Amoxicillin/clavulanic acid (orally) or ampicillin/sulbactam (intravenously) If penicillin allergic, ciprofloxacin, ceftriaxone, or doxycycline
Human bites
Cephalosporins gentamicin and penicillinase-resistant penicillin
Osteomyelitis
Vancomycin and piperacillin/tazobactam
6e8 wk
Septic arthritis
Vancomycin and piperacillin/tazobactam
3e4 wk
Tenosynovitis
Vancomycin and piperacillin/tazobactam
2e3 wk
7e10 d
7e14 d
The antibiotics listed in this chart are first-line antibiotics to be used until cultures dictate treatment.
FELON A felon is an abscess of the digital pulp. The septal compartments of the palmar pad create a closed space that can easily form an abscess when inoculated with an infectious organism. Patients present with pain, swelling, and a history of penetrating trauma. Treatment consists of oral antibiotics and surgical drainage.13 The most common organism is S aureus, with MRSA becoming more commonplace. Empiric treatment with antibiotics that cover MRSA is recommended until cultures dictate treatment.13 A longitudinal incision from the distal flexion crease to the pulp apex avoids the neurovascular bundles and permits disruption of the septal compartments. J Hand Surg Am.
HUMAN BITES A human bite (fight bite) initially appears benign but always requires surgical exploration and irrigation. The area around the metacarpophalangeal joint is most often involved and the position of the fingers at the time of impact contributes to the significance of the injury. A human tooth contacting a clenched fist usually violates the extensor tendon and joint capsule and may injure the metacarpal head, inoculating the metacarpophalangeal joint. The human bite injury wound should be surgically extended, an arthrotomy performed with debridement, r
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Current Concepts
HERPETIC WHITLOW Herpetic whitlow is a viral infection that can be mistaken for a felon, usually affecting the fingertip and caused by herpes simplex virus (HSV) 1 or 2. Herpes simplex virus 1 is the primary cause in patients under age of 10, whereas adults can be infected with either HSV-1 or HSV-2.14 Patients present within 2 weeks of viral contact with throbbing pain and vesicles or bullae containing clear fluid.9 The clinical diagnosis can be confirmed with Tzanck smear or viral cultures. The virus is self-limiting, often resolving within 3 weeks without treatment. The vesicles drain, coalesce, and ulcerate before resolution and are contagious during the first 2 weeks.14 It is paramount to prevent spreading infection during this time and a dry dressing should be worn at all times. Surgical incision and drainage are contraindicated because a superimposed bacterial infection can develop. After resolution of the finger lesions, the virus enters into a latency phase and can be retriggered by physiological or psychological stressors.14 The recurrence rate is 20%.15
and drainage are recommended in conjunction with oral antibiotics. We routinely remove all or part of the nail plate. Chronic paronychia is distinct from acute paronychia and is common when hands are constantly exposed to water, such as for dishwashers, swimmers, and medical professionals. The eponychium becomes rounded and indurated with repeated episodes of inflammation and drainage, the nailfold separates from the nail plate, and the area becomes colonized, often with polymicrobial or fungal organisms. This can lead to grooving and thickening of the nail plate. Keeping the area dry, applying antifungal topical creams, and trying oral antifungal or antibiotics is a reasonable first line of attack. Surgical treatment is often required, because topical and oral medications are often unsuccessful. Eponychial marsupialization is the mainstay of treatment. If nail deformity is present, the nail plate should be removed to help reduce recurrence.12
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Anatomy, Presentation, and Treatment of Deep Hand Space Infections
Deep Hand Space
Borders
Presentation
Surgical Points
Dorsal subaponeurotic
Dorsal: extensor tendons; volar: metacarpals and interossei
Dorsal hand swelling and fluctuans
Longitudinal incisions over index and ring metacarpals, not directly over extensor tendons
Thenar
Dorsal: adductor pollicis; volar: index flexor tendons; ulnar: septum of Legueu and Juvara; radial: adductor pollicis insertion at P1 of thumb
Thenar and first webspace swelling, thumb abduction with painful adduction or opposition, pantaloon-shaped abscess if involvement of first dorsal webspace through contiguous spread (Burkhalter)
Palmar, dorsal, or 2-incision approaches; for pantaloon, abscess may drain through dual incisions or single incision perpendicular to first webspace to minimize webspace contracture
Midpalmar/deep palmar
Dorsal: middle and ring finger metacarpals and second and third interossei; volar: flexor tendons and lumbricales; ulnar: hypothenar muscles; radial: septum of Legueu and Juvara
Loss of normal palmar concavity with marked palm tenderness, painful passive motion of middle and ring fingers; substantial dorsal swelling may be present
Transverse incision in distal palmar crease; curvilinear incision along thenar crease
Webspace
Subfascial palmar space between digits
Abducted posture of adjacent digits with accompanying dorsal swelling and volar tenderness at webspace
Must drain both dorsal and volar aspects of abscess; incisions both dorsally and volarly; avoid webspace incisions to prevent contracture
Parona
Volar: pronator quadratus; dorsal: digital flexor tendons; ulnar: flexor carpi ulnaris; radial: flexor pollicis longus
Pain with passive finger flexion; acute carpal tunnel syndrome may be present
Avoid placing incisions directly over flexor tendons or median nerve to avoid desiccation
Current Concepts
and appropriate cultures obtained. The wound is left open. Up to 50 species of bacteria reside in the human mouth; S aureus and beta-hemolytic streptococci are the most common.1 Broad-spectrum antibiotics such as cephalosporins or a combination of gentamicin and a penicillinase-resistant penicillin are the first-line antibiotic regimen.16 Complications such as osteomyelitis, septic arthritis, deep space infections, and stiffness are common. Factors contributing to human bite infections include a delay in initial treatment, inadequate initial debridement, and initial wound closure.17 Patients presenting with bite infections more than 8 days after the initial injury have an 18% change of requiring amputation.16
common organism found in animal bites, but Staphylococcus, Streptococcus, and anaerobes are also found.9 Pasteurella species are isolated in 50% of dog bites and 75% of cat bites, but the average bite wound yields 5 variations of bacterial species, with 60% yielding mixed aerobic and anaerobic organisms.18 Tetanus prophylaxis should be administered when indicated. Animal bite wounds should be treated with irrigation and oral amoxicillineclavulanate or intravenous ampicillinesulbactam. If patients are allergic to penicillin, they can be treated with doxycycline, sulfamethoxazoleetrimethoprim, or a fluoroquinolone plus clindamycin.18
ANIMAL BITES Most commonly, animal bites are from dogs, cats, or rodents.18 Eighty percent are from dog bites, but these rarely result in infections.18 In contrast, cat bites have a 50% infection rate, often requiring admission and intravenous antibiotics.19 The difference results from the mechanism of the bite; cats have sharp, penetrating teeth compared with the crushing, tearing bite of a dog. Pasteurella multocida is the most
PYOGENIC FLEXOR TENOSYNOVITIS In pyogenic flexor tenosynovitis (PFT), bacteria infect the flexor tendon sheath, between the visceral epitenon layer and the outer parietal layer, which is reinforced by the retinacular pulley system. The synovial space between the 2 layers becomes distended under pressure and advanced infection can lead to the breakdown of adjacent anatomic barriers. This can lead to the spread of infection to nearby flexor
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sheaths and bursae, and into the forearm through the Parona space. Purulent fluid in the synovial space surrounding the tendon denies the tendon vital nutrition, and increased pressure in the infected sheath can inhibit blood flow to the tendon, causing necrosis.20 Flexor sheath anatomy explains the spread of infection from the little finger to the thumb (or vice versa), through the contiguous palmar radial and ulnar bursae, causing a horseshoe abscess. Usually, there is a history of penetrating trauma to the digit before presentation. Although no studies have validated their sensitivity and specificity, Kanavel’s 4 cardinal signs remain helpful in diagnosing PFT. These signs, listed in descending frequency, include fusiform digital swelling (usually associated with erythema), pain with passive digital extension, semiflexed digital posture, and tenderness along the flexor tendon sheath with frequent extension into the palm.21 The presence of all 4 Kanavel signs occurred in only 54% of PFT patients in 1 series.22 Laboratory values such as white blood cell count, erythrocyte sedimentation rate, and C-reactive protein can be helpful in confirming the diagnosis of PFT.23 Elevation of at least 1 of these markers, in combination with clinical evaluation, was 100% specific in identifying cases of PFT. However, sensitivities of these markers were low (white blood cell, 39%; erythrocyte sedimentation rate, 41%; and C-reactive protein, 76%), indicating that markers were not always elevated in the setting of PFT.23 Treatment for PFT is surgical irrigation of the flexor sheath and intravenous antibiotic therapy. The most common organisms include S aureus and Streptococcus species; thus, antibiotics before culture data should cover these bacteria.22e24 For severe infections with subcutaneous purulence or necrotic tendon, open exposure of the sheath and irrigation of the sheath through windows sparing the A2 and A4 pulleys is necessary. A midaxial approach is preferred over a Bruner incision, which can lead to postoperative tendon exposure or peri-incisional skin loss.25 Limited exposure of the sheath with closed catheter irrigation is favored in the absence of loculated purulence. It allows for minimization of trauma to the digit and pulley system and has been shown to result in equivalent outcomes to open irrigation of the sheath.22,26 Factors responsible for a poor outcome or risk of amputation include age greater than 43 years, certain comorbidities (diabetes mellitus, renal failure, or peripheral vascular disease), subcutaneous purulence, and ischemic changes upon presentation.22 Digits without subcutaneous purulence or ischemic changes regain more total active motion (TAM) with J Hand Surg Am.
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NECROTIZING FASCIITIS Necrotizing fasciitis is a medical emergency. Aggressive, urgent surgical intervention is of utmost importance. Delay in diagnosis can lead to loss of life or limb. The infection involves the fascia and subcutaneous tissue, sparing underlying tissues. Two types have been described. Type 1 is most common, caused by mixed aerobic and anaerobic organisms and frequent in immunocompromised hosts.28,29 Type 2 results from group A Streptococcus and/or Staphylococcus organisms and more typically affects the extremities.28 Risk factors include immunosuppression, peripheral vascular disease, diabetes mellitus, chronic liver disease, and intravenous drug abuse.28,29 Initially, these infections can appear as low-grade cellulitis. Clinical signs more indicative of necrotizing fasciitis include crepitus, fluctuans, nonpitting edema, tenderness beyond areas of erythema, hypotension, fever, and tachycardia.29 Vascular thrombosis leads to skin sloughing, blistering, ischemia, and resultant necrosis.28 Upon surgical debridement, the fat appears gray and liquefied with a “dishwater pus” appearance. Frank pus is uncommon. Malodorous tissue is common with anaerobic organism involvement.28 Characteristically, the skin and subcutaneous tissue are elevated from the fascia, necessitating extensive debridement to healthy tissue.28 Operative cultures are taken, the wounds are left open, and debridement is repeated every 24 to 48 hours as needed. Initial treatment includes broad-spectrum intravenous antibiotics that cover aerobes and anaerobes and often require multiple drugs simultaneously. A reasonable combination includes ampicillinesulbactam, clindamycin, and ciprofloxacin.18 Amputation may be necessary to control the infection but does not reduce mortality rates.29 Mortality rates range from 23% to 76%; organ failure and sepsis are the major causes of death.30 Delay in diagnosis and delay in surgical debridement are significantly associated with increased mortality.29 Advanced age and 2 or more comorbidities further increase mortality rates.29 r
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a lower incidence of amputation (average, 80% normal TAM; 0% amputation rate)21,27 than those with subcutaneous purulence (average, 72% normal TAM; 8% amputation) and or with both subcutaneous purulence and ischemic changes (average, 49% normal TAM; 59% amputation).21 In addition, delayed treatment increases the probability of a poor functional outcome.22
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Current Concepts
SEPTIC ARTHRITIS Septic arthritis of the joints of the hand is commonly caused by penetrating trauma or the spread of infection from contiguous structures. Like other closed space infections, bacterial toxins and local inflammatory response result in the majority of damage to the joint.31,32 The most common organisms are betahemolytic Streptococcus and S aureus. Neisseria gonorrhoeae should be considered in sexually active patients, whereas Haemophilus influenza should be considered in unvaccinated children. Examination reveals fusiform joint erythema and swelling and pain with active or passive motion. Joint aspiration allows for definitive diagnosis, and in addition to cultures and cell count, crystal analysis should be performed because crystalline arthropathies, particularly gout, can present with a similar picture. Classically, a cell count of 50,000 with greater than 75% polymorphonuclear leukocytes and glucose of 40 mg% less than fasting blood glucose level was consistent with a diagnosis of septic arthritis. More recent studies have demonstrated that lowering the cell count threshold to 17,500 increases the sensitivity of the diagnosis of septic arthritis to 83%, with an acceptable specificity of 67%.33,34 Treatment of septic arthritis involves irrigation and debridement of the joint and systemic antibiotics. A recent study found that after surgical drainage, a short course of intravenous antibiotics of less than 1 week supplemented with oral antibiotics for 2 to 3 additional weeks successfully treated septic arthritis of the hand and wrist in most cases.35 Open drainage of the wrist is through a longitudinal incision between the third and fourth dorsal compartments. Alternatively, arthroscopic irrigation and debridement without closure of arthroscopic portals can produce similar outcomes compared with open procedures.36 Metacarpophalangeal joints should be entered through a longitudinal, dorsal incision, with at least partial preservation of the sagittal bands to avoid postoperative extensor tendon subluxation. Interphalangeal joints should be approached through a midaxial incision between the volar plate and the accessory collateral ligament, or between the lateral slip of the extensor mechanism and cordlike portion of the collateral ligament, to avoid postoperative finger deformities.37
the severity of contamination contribute to its development. Staphylococcus aureus and Streptococcus are the most common causative organisms. Gramnegative bacteria, anaerobes and atypical and fungal organisms can also lead to osteomyelitis, and a mixed bacterial etiology is common in patients with vascular insufficiency or an immunocompromised state.38 Mixed bacterial infection predisposes the patient to the high likelihood of amputation.38 Hardware and other devitalized tissue are a nidus for bacterial inoculation, most commonly S epidermis, and must be removed to eradicate infection. The distal phalanx is the most commonly affected in the hand.38 Osteolysis and soft tissue swelling are the most common radiographic findings. Periosteal new bone formation, involucrum, and sequestrum are less common in the tubular bones of the hand. A definitive diagnosis requires a bone biopsy and cultures. Treatment consists of intravenous antibiotics and operative debridement. Intravenous antibiotics are instituted for a minimum of 4 to 6 weeks.39 REFERENCES 1. Houshian S, Seyedipour S, Wedderkopp N. Epidemiology of bacterial hand infections. Int J Infect Dis. 2006;10(4):315e319. 2. Ong Y, Levin LS. Hand infections. Plast Reconstr Surg. 2009; 124(4):225e233. 3. Tosti R, Ilyas A. Empiric antibiotics for acute infections of the hand. J Hand Surg Am. 2010;35(1):125e128. 4. Stern P, Staneck J, McDonough J, Neale H, Tyler G. Established hand infections: a controlled, prospective study. J Hand Surg Am. 1983;8(5):553e559. 5. Salgado CD, Farr BN, Calfee DP. Community-acquired methicillinresistant Staphylococcus aureus: a meta-analysis of prevalence and risk factors. Clin Infect Dis. 2003;36(2):131e139. 6. O’Malley M, Fowler J, Ilyas AM. Community-acquired methicillinresistant Staphylococcus aureus infections of the hand: prevalence and timeliness of treatment. J Hand Surg Am. 2009;34(3):504e508. 7. Volz KA, Canham L, Kaplan E, Sanchez LD, Shapiro NI, Grossman SA. Identifying patients with cellulitis who are likely to require inpatient admission after a stay in an ED observation unit. Am J Emerg Med. 2013;31(2):360e364. 8. Burkhalter WE. Deep space infections. Hand Clin. 1989;5(4):53e59. 9. Franko O, Abrams R. Hand infections. Orthop Clin N Am. 2013; 44(4):625e634. 10. Rockwell PG. Acute and chronic paronychia. Am Fam Physician. 2001;63(6):1113e1116. 11. Ritting AW, O’Malley MP, Rodner CM. Acute paronychia. J Hand Surg Am. 2012;37(5):1068e1070. 12. Bednar M, Lane L. Eponychial marsupialization and nail removal for surgical treatment of chronic paronychia. J Hand Surg Am. 1991;16(2):314e317. 13. Tannan S, Deal DN. Diagnosis and management of the acute felon: evidence-based review. J Hand Surg Am. 2012;37(12):2603e2604. 14. Rubright J, Shafritz A. The herpetic whitlow. J Hand Surg Am. 2011;36(2):340e342. 15. Wu I, Schwartz R. Herpetic whitlow. Cutis. 2007;79(3):193e196. 16. Shoji K, Cavanaugh Z, Rodner C. Acute fight bite. J Hand Surg Am. 2013;18(8):1612e1614. 17. Gonzalez M, Papierski P, Hall R. Osteomyelitis of the hand after a human bite. J Hand Surg Am. 1993;18(3):520e522.
OSTEOMYELITIS Osteomyelitis is often a sequelae of septic arthritis, soft tissue infection, or an open fracture. The degree of soft tissue injury or tissue devascularization, and J Hand Surg Am.
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29. Wong C, Chang H, Pasupathy S, et al. Necrotizing fasciitis: clinical presentation, microbiology, and determinants of mortality. J Bone Joint Surg Am. 2003;84(8):1454e1460. 30. Fontes R, Ogilvie C, Miclau T. Necrotizing soft-tissue infections. J Am Acad Orthop Surg. 2000;8(3):151e158. 31. Odio CM, Ramierez T, Arias G, et al. Double blind, randomized, placebo-controlled study of dexamethasone therapy for hematogenous septic arthritis in children. Pediatr Infect Dis J. 2003;22(10): 883e888. 32. Josefsson E, Tarkowski A. Staphylococcus aureus-induced inflammation and bone destruction in experimental models of septic arthritis. J Periodontal Res. 1999;34(7):387e392. 33. Li SF, Cassidy C, Chang C, et al. Diagnostic utility of laboratory tests in septic arthritis. Emerg Med J. 2007;42(2):75e77. 34. McGillicuddy DC, Shah KH, Friedberg RP, Nathanson LA, Edlow JA. How sensitive is the synovial fluid white blood cell count in diagnosing septic arthritis? Am J Emerg Med. 2007;25(7): 749e752. 35. Kowalski TJ, Thompson La, Gundrum JD. Antimicrobial management of septic arthritis of the hand and wrist. Infection. 2014;42(2): 379e384. 36. Sammer DM, Shin AY. Comparison of arthroscopic and open treatment of septic arthritis of the wrist. J Bone Joint Surg Am. 2009;91(6):1387e1393. 37. Freeland AE, Senter BS. Septic arthritis and osteomyelitis. Hand Clin. 1989;5(4):533e552. 38. Reilly K, Linz J, Stern P, Giza E, Wyrick J. Osteomyelitis of the tubular bones of the hand. J Hand Surg Am. 1997;22(4): 644e649. 39. Honda H, McDonald J. Current recommendations in the management of osteomyelitis of the hand and wrist. J Hand Surg Am. 2009;34(6): 1135e1136.
18. Stevens D, Bisno A, Chambers H, et al. Practice guidelines for the diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41(10):1373e1406. 19. Aghababian R, Conte JE. Mammalian bite wounds. Ann Emerg Med. 1980;9(2):79e83. 20. Schnall SB, Vu-Rose T, Holtom PD, Doyle B, Stevanovic M. Tissue pressures in pyogenic flexor tenosynovitis of the finger: compartment syndrome and its management. J Bone Joint Surg Br. 1996;78(5): 792e795. 21. Pang HN, Teoh LC, Yam AK, Lee JY, Punhaindram ME, Tan AB. Factors affecting the prognosis of pyogenic flexor tenosynovitis. J Bone Joint Surg Am. 2007;89(8):1742e1748. 22. Dailiana ZH, Rigopoulos N, Varitimidis S, Hantes M, Bargiotas K, Malizos KN. Purulent flexor tenosynovitis: factors influencing the functional outcome. J Hand Surg Eur Vol. 2008;33(3):280e285. 23. Bishop GB, Born T, Kakar S, Jawa A. The diagnostic accuracy of inflammatory blood markers for purulent flexor tenosynovitis. J Hand Surg Am. 2013;38(11):2201e2211. 24. Karagergou E, Rao K, Harper RD. Parameters affecting the severity and outcome of pyogenic digital flexor tenosynovitis. J Hand Surg Eur Vol. 2014 Jan 8. [Epub ahead of print]. 25. Draeger RW, Bynum DK Jr. Flexor tendon sheath infections of the hand. J Am Acad Orthop Surg. 2012;20(6):373e382. 26. Gutowski KA, Ochoa O, Adams WP Jr. Closed-catheter irrigation is as effective as open drainage for treatment of pyogenic flexor tenosynovitis. Ann Plast Surg. 2002;49(4):350e354. 27. Lille S, Hayakawa T, Neumeister MW, Brown RE, Zook EG, Murray K. Continuous postoperative catheter irrigation is not necessary for the treatment of suppurative flexor tenosynovitis. J Hand Surg Br. 2000;25(3):304e307. 28. Gonzalez M. Necrotizing fasciitis and gangrene of the upper extremity. Hand Clin. 1998;14(4):635e645.
JOURNAL CME QUESTIONS What percentages of Pasteurella species are isolated from dog and cat bites? a. 10% of dog bites and 35% of cat bites b. 20% of dog bites and 45% of cat bites c. 30% of dog bites and 55% of cat bites d. 40% of dog bites and 65% of cat bites e. 50% of dog bites and 75% of cat bites
Acute Hand Infections Which of the following microorganisms are most sensitive to ciprofloxacin? a. Anthrax and Aeromonas hydrophilia b. Norcardia and tularemia c. Mycobacterium and Vibrio d. Pseudomonas and Sporothrix e. MRSA and all viruses
Current Concepts
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