The hand can easily be injured during everyday activities. Any trauma to the hand, particularly a penetrating trauma, may introduce damaging pathogens. The hand's compartmentalized anatomy may contribute to the development of an infection, and if an infection is not appropriately diagnosed and treated, significant morbidity can result.

Some general wound care principles apply to all hand infections.¹ Initial nonsurgical management of superficial infections includes rest, elevation, and splint immobilization in the position of function (Figure 1).¹ Splints are indicated for rest and prevention of flexion contractures, elevation reduces edema, and warm compresses improve blood flow and antibiotic delivery.^2,3 Open wounds should be copiously irrigated with tap water or saline, and abscesses should be drained.^4–6 Surgical debridement may be necessary to remove necrotic tissue that is not adequately removed by irrigation.⁷ Several studies have failed to show that the addition of povidone-iodine or other antibacterial solutions are more beneficial than saline alone.^8,9

More severe infections, such as deep hand infections, require early surgical intervention and oral or parenteral antibiotics.^1,4 Selection of empiric antibiotics depends on the type and severity of the infection, host factors, and local antibiotic resistance patterns (Table 1).^{1,3,8,10–23} Anti-tetanus immunoglobulin, plus tetanus and diphtheria toxoids (Td) or the tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis (Tdap) vaccine, should be administered per recommendations from the Advisory Committee on Immunization Practices (i.e., administer if the patient has not had a tetanus toxoid–containing vaccine in the past five years).²⁴

Management of Specific Conditions

Acute hand infections are grouped broadly into two categories: superficial and deep infections. Table 2 lists the differential diagnosis for acute hand infections and common noninfectious mimickers.^{10,16,25–39} eTableA provides links to previous American Family Physician articles that include more details about related topics.

SUPERFICIAL HAND INFECTIONS

Superficial infections arise from the skin and subcutaneous soft tissues located superficially to the tendons in the hand.⁴⁰Superficial hand infections are more common than deep infections, with infections of the fingertip (paronychia and felon) being most common.⁸ Other superficial hand infections are listed in Table 2.^{10,16,25–39}

Acute Paronychia. Paronychia is inflammation of a nail fold, with or without abscess formation. Paronychia can be acute (typically limited to a single digit and caused by infection) or chronic (lasting at least six weeks, affecting multiple nails, or related to chemical irritants).^1,10,11,40 Acute paronychia is caused by trauma to the nail, cuticle, or nail fold that leaves it vulnerable to bacterial invasion, infection, and inflammation. Symptoms include redness, swelling, and tenderness of the nail fold with or without pallor and fluctuance suggestive of abscess (Figure 2 and Figure 3). Risk factors include artificial nails or recent manicure, manipulating a hangnail, occupational trauma (e.g., dishwashers), ingrown nails, and nail biting or thumb-sucking.¹⁰ Staphylococcal and streptococcal species are the most common pathogens, followed by polymicrobial infections including anaerobes (more common in people with diabetes mellitus or exposure to oral flora, and in injection drug users).^{1,8,10,12,40,41} Pseudomonas (suggested by a discolored green nail bed) and gram-negative bacilli are rare isolates.^12,42

Mild infections without obvious abscess should be treated with warm soaks and topical antibiotics.¹⁰ If an abscess is present, conservative measures to provoke spontaneous drainage may be tried for two to three days; however, mechanical drainage is often needed.⁸ Procedures for draining paronychia have been described in a previous American Family Physician article.¹⁰ Routine cultures for uncomplicated skin and soft tissue infections are not recommended.^26,43 Oral antibiotics typically are not needed after successful drainage, but if used, they should be limited to treatment of immunocompromised or severely ill patients, based on local community resistance patterns and established guidelines.^10,12,14,26

Felon. A felon is a subcutaneous infection within the fleshy part of the fingertip, known as the distal digital pulp (Figure 4).¹ Common causes include puncture wounds (e.g., finger stick, splinters) and spread of untreated paronychia.¹ The digital pulp is divided into compartments by numerous fibrous septae^1,16,40 (Figure 5). A felon presents with severe throbbing pain, tense swelling, and erythema of the finger pad that does not extend proximal to the distal interphalangeal joint because the infection is confined within the noncompliant septal compartments of the digital pulp. Ultrasonography can be used to evaluate for the presence of an abscess.⁴⁴

Appropriate management is critical because felons can cause tissue necrosis of the finger pad, osteomyelitis, or pyogenic flexor tenosynovitis if untreated.¹⁶ Treatment of an early felon in which no abscess is present should include warm soaks, elevation, and empiric oral antibiotics directed at staphylococcal and streptococcal infections.^12,15 Surgical drainage is required if an abscess is present; a high lateral incision should be made for a deep abscess, and a volar longitudinal incision should be made for a superficial abscess.^1,16 Methods of performing these incisions, risks of the incisions (anesthetic fingertip, neuroma, and unstable finger pad), and postoperative care recommendations have been described in a previous American Family Physician article.¹ Surgical drainage of a felon with abscess is the mainstay of treatment; antibiotics do not provide additional benefit once appropriate drainage has been performed.⁴¹

Herpetic Whitlow. Herpetic whitlow is a viral infection of the distal finger caused by inoculation of herpes simplex virus through broken skin. Vesicles of clear fluid on an erythematous base appear within three to four days of exposure to the virus, often coalescing into bullae (Figure 6). Fluid may become turbid or opaque over time. In the absence of other symptoms, this does not signify bacterial superinfection and should not be routinely drained.⁴⁵ The diagnosis of herpetic whitlow is clinical. In uncertain cases, Tzanck testing, viral culture, or polymerase chain reaction testing of fluid from an unroofed vesicle can confirm the diagnosis. Recurrence occurs in 20% to 50% of cases.^17,46 A prodrome of mild burning, itching, and discomfort at a site of prior eruption may occur two to three days before a recurrent outbreak, similar to other herpes simplex virus infections.

Mainstays of therapy for herpetic whitlow include reducing the risk of transmission, pain control, and consideration of antiviral medications. Primary herpetic whitlow is typically self-limited, with complete resolution within 21 days. However, off-label use of oral antivirals should be considered for patients with recurrent lesions or symptoms present for less than 48 hours, or for immunocompromised patients, who may develop disseminated disease requiring intravenous antiviral treatment and critical care.^1,18,47 It is important to keep dressings over active lesions dry and to refrain from incision and drainage, which increases the likelihood of bacterial superinfection.¹⁷

DEEP HAND INFECTIONS

The anatomy of the hand allows infections to easily spread from the point of inoculation to deep structures, including tendon sheaths, adjacent anatomic compartments, deep fascial planes, bursae, joint spaces, and bones.⁴⁰ Penetrating trauma often results in severe or rapidly progressing infections within deep structures of the hand. These infections are associated with significant morbidity and dysfunction if not recognized and treated early with surgical management and antibiotics.^1,40 Two of the most common deep hand infections are pyogenic flexor tenosynovitis and clenched-fist bite wounds.

Pyogenic Flexor Tenosynovitis. Pyogenic flexor tenosynovitis is a closed-space infection of the flexor tendon sheath. It is most commonly caused by a penetrating injury to the finger. The flexor tendon sheaths in the hand typically span from the neck of the metacarpal to the distal interphalangeal joint, although there are many anatomic variations. Flexor tendon sheaths have a poor vascular supply and are filled with synovial fluid, which is a good medium for bacterial growth.³ Inoculation of bacteria into the synovial fluid causes increased pressure within the sheath, leading to impaired vascular flow, tendon necrosis, and ultimately, tendon rupture.¹⁶ Staphylococcus species, including methicillin-resistant S. aureus, and Streptococcus species are the most commonly identified pathogens,¹² although approximately one-third of wound cultures show no growth, and gram-negative organisms are present in 10% of cases.² Hematogenous spread to the tendon sheaths is less common and typically occurs only in immunocompromised patients.⁴⁰

Pyogenic flexor tenosynovitis is a clinical diagnosis (Figures 7A and 7B) and is classically characterized by the four Kanavel signs: pain with passive extension, tenderness to palpation of the tendon sheath, flexed position, and fusiform swelling^1,48 (Table 3^49–51). Surgical consultation within 72 hours of symptom onset and early treatment with systemic antibiotics improve outcomes.⁵² Early pyogenic flexor tenosynovitis can be managed nonoperatively, although no specific protocol exists.⁵² If a nonoperative approach is chosen, surgery should be considered if there is no improvement within 12 to 24 hours.^2,52 Minimal incision with catheter irrigation is the mainstay of surgical treatment and results in improved range of motion and fewer infectious complications compared with open surgery⁵³ (Figure 7C). Tobacco use (greater than five-pack-year history) is a newly identified risk factor for more serious infections and delayed wound healing.⁵⁴

Clenched-Fist Bite Wounds. Human bite wounds most often result from direct contact of the fist on incisor teeth, and are known as clenched-fist bite wounds, “fight bite,” or tooth-knuckle injuries. These injuries are more common in younger males and often occur during physical altercations. Clenched-fist bite wounds are usually characterized by a 3- to 5-mm laceration, most often over the metacarpophalangeal joint, followed by the proximal interphalangeal joint.²⁹ Because these injuries do not initially appear severe, many patients do not seek medical attention until infections are advanced.

Because the fist is clenched during injury, teeth may damage deeper structures within the hand, resulting in fracture, joint capsule penetration, or extensor tendon damage^29,55 (Figure 8). Older studies have shown that up to 75% of clenched-fist bite wounds result in tendon, bone, joint, or cartilage damage, whereas newer studies suggest that the incidence of joint capsule penetration may be higher, with 100% proximal interphalangeal joint involvement and 95% metacarpophalangeal joint involvement.^55,56 Because of the high level of tendon, bone, and joint involvement, it is important that physicians recognize the potential for serious complications when managing clenched-fist bite wounds. Radiography should be obtained to evaluate for fracture, foreign bodies, and early signs of osteomyelitis.¹⁹ Neurovascular and musculoskeletal examinations should be performed, and Elson testing should be performed on each digit to evaluate extensor tendon function (https://www.youtube.com/watch?v=wyHSKgAZ1eA).¹⁹

Initial wound management should include hemostasis, copious irrigation, removal of any foreign bodies, and debridement of necrotic tissue.^19,29 The wound should be extended to inspect the joint capsule and extensor tendon mechanism.^19,55 A tetanus booster and immunoglobulin should be administered, if indicated.^19,24,29 Before initiation of empiric antibiotics, tissue should be obtained for Gram staining and aerobic and anaerobic cultures. Tissue cultures are preferred over wound cultures because of their improved accuracy.¹⁹ Wounds should be allowed to heal by secondary intent,^19,20 and the hand should be splinted in a position of function and elevated.¹

Human saliva is bacteria rich; as a result, clenched-fist bite wounds are often polymicrobial.^1,12 A single prospective randomized controlled trial supports empiric antibiotic use in all patients.²¹ This trial compared mechanical wound care alone (n = 15) with wound care plus oral cefaclor (n = 16), or intravenous cefazolin plus penicillin G (n = 17). Patients with joint capsule penetration, tendon injury, or bites older than 24 hours were excluded.²⁰ The trial was terminated because of high rates of infection with wound care alone (47%).²⁰ None of the patients who were treated with antibiotics developed infection.^20,21 Oral and intravenous antibiotics were equally effective.^20,21

Patients presenting with clenched-fist bite wounds within 24 hours after injury may be treated as outpatients if there are no signs of infection. They should be instructed to follow up within 24 hours after initial treatment.¹⁹ Hospitalization should be considered for patients with delayed presentation (more than 24 hours since injury); immunocompromised patients; and those with established infection, systemic manifestations, or evidence of joint capsule penetration.^19,22,23,55 Empiric broad-spectrum antibiotics and urgent surgical consultation are indicated for inpatient management.^19,22,23,55

This article updates a previous article on this topic by Clark.¹

Data Sources: A PubMed search was conducted using the key terms acute hand infection, paronychia, felon, herpetic whitlow, flexor tendon synovitis, pyogenic tenosynovitis, human bite injury, clenched fist injury. The search included systematic and clinical reviews, meta-analyses, reviews of clinical trials and other primary sources, and evidence-based guidelines. Also searched were the Cochrane database, the National Institute for Health and Care Excellence guidelines, the Choosing Wisely Campaign, Essential Evidence Plus, Google Scholar, and UpToDate. References from these sources were consulted to clarify the statements made in publications. Search dates: November 2017 to November 2018.

Figure 1 provided by David Klemm. Figure 4 provided by Anthony J. Viera, LCDR, MC, USNR.

The opinions and assertions contained herein are the private views of the authors and are not to be construed as the official policy or position of the Department of Defense or the U.S. government.