Causes / typical injury mechanism: Flexor tenosynovitis is an infection between the visceral and the parietal layer of the protective sheath that surrounds the flexor tendons of the hand. This infection occurs most commonly when material is introduced directly to the tendon sheath via penetrating trauma.

Contiguous spread can occur via a septic joint or deep space infection into the flexor sheath. Hematogenous spread is rare outside of disseminated gonococcal infections.

Classic history and presentation: Pain, swelling, and overriding erythema and warmth on the palmar aspect of the affected digits.

Classic findings are called Kanavel signs:

• Pain with passive extension of the affected digit
• Pain with palpation along the flexor tendon sheath of the affected digit
• Fusiform swelling of the affected digit
• Affected digit is held in flexion

Pain with passive extension and with palpation along the flexor tendon sheath are the most useful signs early in the disease presentation.

It is important to note that fever may or may not be present, and its absence does not rule out flexor tenosynovitis. The infection is typically isolated to a single digit, but the infection has the potential to spread to multiple digits or to spread proximally up the tendon sheaths into the palm, carpal tunnel, and/or forearm.

The infection may be self-limited but may evolve into compartment syndrome, osteomyelitis, tendon necrosis, skin necrosis, or necrotizing fasciitis. Flexor tendon adhesions may occur after resolution.

Prevalence: Up to 10% of all acute hand infections.

Risk factors: Neonates and elderly patients are at increased risk, as are patients with diabetes, intravenous (IV) drug use, immunocompromised status, or penetrating traumatic injuries.

Pathophysiology: Overall, the most common organisms involved are Staphylococcus aureus, including methicillin-resistant S aureus (MRSA). If the infection occurs after a simple penetrating wound, skin flora (such as Staphylococcus epidermitis, group A beta-hemolytic Streptococci, and Pseudomonas aeruginosa) are likely infectants. Spontaneous infection by mixed flora and gram-negative bacteria are more likely if the patient is immunocompromised. If the mechanism of injury is a human bite, mouth flora such as Eikenella sp. are possible infectants. If the injury is caused by an animal bite, Pasturella multocida should be suspected.

Those who are immunocompromised (ie, HIV-positive, long-term steroid use, those on immunomodulating drugs for chronic disease, or post-transplant) are at risk of spontaneous infection by mixed flora, gram-negative bacterial infection, and atypical fungal infections.

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