Pyogenic Flexor Tenosynovitis

INTRODUCTION

Flexor tendon sheath infections are a surgical urgency because they can have devastating outcomes such as loss of motion, deformity, and loss of digit if treatment is delayed.
Kanavel originally described the physical presentation of pyogenic flexor tenosynovitis (PFT) in 1912.¹
Despite improving antibiotic and surgical treatments, it continues to be crucial to have early detection and treatment of PFT to minimize long-term complications.

ANATOMY

The flexor tendon sheath is a two-layered structure.
- Visceral layer adheres closely to the tendon, forming the epitenon.²
- Parietal layer abuts the pulley mechanism.²
These layers connect both proximally and distally to create a closed system. The portion of the tendon that is within the sheath receives its nutrients and blood supply through diffusion of the synovial fluid. The portion of the tendon outside of the sheath receives its blood supply through a direct system through the vinculae.³
Index, middle, and ring finger sheaths extend from the A1 pulley at the level of the distal palmar crease proximally to the level of the distal interphalangeal joint distally.²,⁴
Thumb tendon sheath is situated around the flexor pollicis longus tendon. This typically communicates with the radial bursa at the level of the metacarpophalangeal (MCP) joint, which then extends proximally past the transverse carpal ligament.
Small finger tendon sheath extends and typically communicates with the ulnar bursa, which extends proximal to the transverse carpal ligament as well.
Radial and ulnar bursae frequently communicate (33%-100%) through the space of Parona, which can lead to the formation of a horseshoe abscess.⁵,⁶
Anatomic variation of tendon sheath connections exists in approximately 15% to 30% of the population (Figure 44.1).⁷,⁸,⁹

FIGURE 44.1 Illustration demonstrating the anatomic variations of the flexor tendon sheath and bursa patterns of the hand as well as their relative frequency. Reproduced with permission from Doyle JR, Botte MJ. Hand. In: Doyle JR, Botte MJ, eds. Surgical Anatomy of the Hand and Upper Extremity. Philadelphia, PA: Lippincott Williams & Wilkins; 2003:605.

PATHOGENESIS

Bacteria infect the nutrient-rich synovial fluid of the tendon sheath between the visceral epitenon layer and the parietal layer.¹⁰,¹¹
Infection in this closed space leads to tendon damage through multiple pathways.
- Increased pressure within this closed space is detrimental because the tendon itself receives its nutrients through diffusion from the
  synovial fluid. If the synovial space becomes distended with purulent fluid, the tendon will be denied vital nutrients as well as blood supply. This can lead to ischemia and ultimately tendon rupture.³
- The tendon sheath itself acts like a barrier and limits the ability of the host’s immune system to defend against bacterial proliferation and invasion.¹²
- Anatomic borders of the tendon sheath compound effects of inflammatory response to the infection, leading to stiffness and adhesion formation.¹⁰
Owing to the body’s poor ability to fight this infection, it has the ability to spread to other flexor tendon sheaths or into the midpalmar, thenar, or lumbrical compartments.²

EPIDEMIOLOGY

PFT represents 2.5% to 9.4% of all hand infections.¹¹
Goal is for early antibiotic therapy directed at the likely causative organism.
Approximately 20% to 30% of cultures are negative, which is likely due to preoperative antibiotic administration.¹³

Acute Infection

Direct inoculation is the most likely etiology, which is most likely to be a puncture injury.⁴
For penetrating injury, skin flora is the likely causative organism, with Staphylococcus present in 50% to 80% of cases.⁴,¹⁴
Methicillin-resistant Staphylococcus aureus is found in up to 29% of cases.¹⁵
Diabetes mellitus and being in a rural area are risk factors for polymicrobial infections.¹³
Animal bites increase the risk of Pasteurella infection.
Human bites increase the risk of alpha hemolytic Streptococcus or Eikenella.

Chronic Infection

An indolent course/chronic infection is more consistent with mycobacterial or fungal infection.
Musculoskeletal involvement makes up 1% to 5% of extrapulmonary tuberculosis (TB).
Tuberculous tenosynovitis makes up approximately 5% of bone and joint TB.¹⁶
If there is concern for TB, then a synovial biopsy should be sent for Ziehl-Neelsen staining or intradermal tuberculin reaction test should be pursued.¹⁷

EVALUATION

Physical Examination

Kanavel signs (Table 44.1, Figure 44.2)
- Excessive tenderness to palpation over the flexor tendon sheath
- The finger rests in a flexed position.
- Excruciating pain with passive extension of the finger, which is most marked at the proximal end of the sheath
- Fusiform swelling of the digit¹
All four Kanavel signs are present in 54% of the cases.¹³
Kanavel signs are 91.4% to 97.1% sensitive but only 51.3% to 69.2% specific to PFT.¹⁸
Pain over the tendon sheath has been found to be most sensitive of the four signs, with painful passive extension of the digit being the second most sensitive.¹³,¹⁸
Flexed posture of the digit and fusiform swelling are not independent risk factors for PFT.
It has been found that tenderness along the tendon sheath, pain with passive extension of the digit, and duration of symptoms less than 5 days correlates to a 87.9% likelihood of being positive for PFT.¹⁹