Septic tenosynovitis is an infection of tendon sheaths that represents a serious orthopedic emergency in horses.
Overview and Clinical Importance
Septic tenosynovitis is an infection of tendon sheaths that represents a serious orthopedic emergency in horses. The condition occurs when bacteria invade the synovial structures surrounding tendons, most commonly affecting the digital flexor tendon sheath (DFTS) in the fetlock region. Due to the superficial nature of synovial structures in the equine distal limb and limited soft tissue coverage, penetrating wounds frequently result in bacterial contamination of these structures.
The clinical significance of septic tenosynovitis cannot be overstated. Without prompt recognition and aggressive treatment, infection leads to severe inflammation, fibrous adhesion formation, tendon damage, and potentially life-threatening complications including laminitis in the contralateral limb. Studies indicate that only approximately 50% of horses treated for septic digital tenosynovitis return to their previous level of athletic function, making early diagnosis and intervention critical.
High-YieldOn the NAVLE, septic tenosynovitis typically presents as a horse with an acute-onset severe lameness (grade 4-5/5), diffuse swelling of the fetlock region, heat, and pain on palpation. Look for a history of a penetrating wound to the palmar/plantar aspect of the limb. Time from injury to treatment is the most critical prognostic factor.
| Structure |
Clinical Significance |
| Manica Flexoria |
Extension of SDFT that wraps around DDFT at fetlock level; tears are a common cause of non-septic tenosynovitis |
| Palmar Annular Ligament |
Maintains flexor tendons in position; may require desmotomy if constriction occurs secondary to septic tenosynovitis |
| Vinculae (Mesotendon) |
Blood supply to tendons within sheath; present below the proximal phalanx; damage compromises tendon healing |
| Proximal Sesamoid Bones |
Can become secondarily infected (osteitis/osteomyelitis) in chronic septic tenosynovitis; worsens prognosis significantly |
Relevant Anatomy
Digital Flexor Tendon Sheath (DFTS)
The digital flexor tendon sheath is a synovial structure that extends from the distal third of the metacarpus/metatarsus to the level of the middle phalanx. It encompasses both the superficial digital flexor tendon (SDFT) and deep digital flexor tendon (DDFT) as they pass around the palmar/plantar aspect of the fetlock joint.
Key Anatomical Structures Within the DFTS
Other Commonly Affected Tendon Sheaths
| Tendon Sheath |
Location |
Contents |
| Carpal Sheath |
10 cm proximal to carpus to mid-metacarpus |
SDFT, DDFT within carpal canal |
| Tarsal Sheath |
Medial aspect of tarsus |
Lateral digital flexor tendon (LDFT) |
| Extensor Tendon Sheaths |
Dorsal carpus and tarsus |
Common digital extensor, lateral digital extensor |
Etiology and Pathophysiology
Causes of Septic Tenosynovitis
In adult horses, septic tenosynovitis most commonly results from penetrating wounds (94% of cases). The superficial location of tendon sheaths in the equine distal limb makes them particularly vulnerable to contamination. Common wound locations include heel bulb lacerations, palmar/plantar pastern wounds, and dorsal fetlock injuries.
NAVLE TipRemember the bacterial patterns: WOUNDS = Streptococcus predominates; INJECTIONS = Staphylococcus predominates; FOALS = Gram-negatives (especially E. coli). Culture-positive cases have a worse prognosis than culture-negative cases (50% vs 70.5% successful outcome).
Pathophysiology of Synovial Infection
Following bacterial inoculation, a cascade of inflammatory events occurs. Neutrophils are rapidly recruited to the synovial space, releasing proteolytic enzymes and reactive oxygen species that damage synovial structures. Fibrin deposition leads to formation of pannus (fibrinocellular conglomerates) within the tendon sheath, which can sequester bacteria and hinder treatment. Ongoing inflammation results in decreased synovial fluid viscosity due to hyaluronic acid degradation.
If infection persists, intrathecal adhesions form between the tendons, synovial lining, and annular ligaments, restricting normal tendon gliding. Extension of infection to adjacent structures including the proximal sesamoid bones (osteitis/osteomyelitis) or adjacent joints significantly worsens prognosis and has been associated with non-survival.
| Etiology |
Common Organisms |
| Penetrating Wounds |
Streptococcus spp. (38.9%), mixed flora, Enterobacteriaceae, anaerobes |
| Iatrogenic (post-injection) |
Staphylococcus aureus (most common), coagulase-negative Staphylococci |
| Hematogenous (foals) |
Enterobacteriaceae (E. coli in greater than 27%), Salmonella, Rhodococcus equi |
Clinical Presentation
Classic Clinical Signs
| Clinical Sign |
Description and Clinical Notes |
| Severe Lameness |
Typically grade 4-5/5 (non-weight bearing to severely lame at walk); acute onset within hours to days of injury |
| Diffuse Swelling |
Marked effusion of the DFTS extending proximal and distal to fetlock; may have soft tissue cellulitis |
| Heat |
Palpable warmth over affected region; differentiates from chronic "windpuffs" |
| Pain on Palpation/Flexion |
Marked pain on firm flexion of fetlock; pain on direct palpation of tendon sheath |
| Synovial Drainage |
Presence of clear to purulent fluid draining from wound indicates communication with synovial structure |
| Systemic Signs |
Fever, depression, decreased appetite may be present; adult horses often have normal CBC |
Diagnosis
Synoviocentesis and Fluid Analysis
Synoviocentesis is the cornerstone of diagnosis. The procedure should be performed aseptically at a site distant from any wounds or potentially contaminated tissue. Collected fluid should be placed in EDTA (purple-top) for cytology, plain (red-top) for chemistry, and a blood culture bottle to improve culture sensitivity.
Synovial Fluid Analysis Parameters
High-YieldThe classic triad for diagnosing septic synovitis on the NAVLE is: (1) TNCC greater than 30 x 10^9/L, (2) greater than 90% neutrophils, and (3) TP greater than 40 g/L. Remember that bacterial culture is POSITIVE in less than 50% of confirmed septic cases - a negative culture does NOT rule out infection!
Additional Diagnostic Methods
| Parameter |
Normal |
Septic |
Clinical Significance |
| Total Nucleated Cell Count (TNCC) |
Less than 0.5 x 10^9/L |
Greater than 30 x 10^9/L |
Most useful single parameter |
| Neutrophil % |
Less than 10% |
Greater than 80-90% |
Neutrophilia is hallmark |
| Total Protein (TP) |
Less than 20 g/L |
Greater than 40 g/L |
Increased vascular permeability |
| Appearance |
Clear, light yellow |
Turbid, serosanguinous to purulent |
Gross appearance guides urgency |
| Viscosity |
High (string greater than 2.5 cm) |
Decreased |
Hyaluronic acid degradation |
| Bacterial Culture |
Negative |
Positive (37-50% sensitivity) |
Use blood culture bottles to improve yield |
Treatment
Early aggressive treatment is essential for successful outcomes. The primary goals are to eliminate infection, reduce inflammation, prevent adhesion formation, and restore normal tendon sheath function. Treatment typically involves a multimodal approach combining surgical debridement/lavage with systemic and local antimicrobial therapy.
Surgical Treatment Options
Antimicrobial Therapy
Supportive Care
- NSAIDs: Phenylbutazone (2.2-4.4 mg/kg PO BID) or Flunixin meglumine (1.1 mg/kg IV BID) to reduce pain and inflammation
- Bandaging: Sterile, padded bandages to protect wound and reduce swelling
- Hyaluronic acid: Intrathecal administration after infection controlled may reduce adhesion formation
- Controlled exercise: Early passive motion and handwalking after infection resolves to prevent adhesion formation
- Heel elevation: Often improves weight bearing and comfort during treatment
| Diagnostic |
Application and Findings |
| Distension Test |
Inject sterile saline into sheath distant from wound; fluid egress from wound confirms communication (positive test) |
| Ultrasonography |
Marked effusion in 81% of cases; echogenic fluid (54%); fibrinous loculations (64%); synovial thickening; assess for concurrent tendon damage |
| Radiography |
Evaluate for foreign bodies, gas within soft tissues, bone involvement (osteitis/osteomyelitis); soft tissue swelling |
| Contrast Tenography |
Inject contrast into wound tract to confirm communication with synovial structure |
| Serum Amyloid A (SAA) |
Elevated in systemic inflammation; can be measured in synovial fluid as adjunct biomarker |
| Tenoscopy |
Gold standard for visualization; allows assessment of tendon integrity, adhesions, pannus; combined diagnostic and therapeutic |
Prognosis
Prognosis for septic tenosynovitis is guarded overall, but significantly improves with early diagnosis and aggressive treatment. Studies report the following outcomes:
Negative Prognostic Factors
- Concurrent complications (present in 80% of cases): adhesions, tendonitis, tendon rupture, adjacent joint sepsis
- Bone involvement (osteitis or osteomyelitis of sesamoid bones)
- Severe pannus formation
- Positive bacterial culture (especially S. aureus or gram-negative multidrug-resistant organisms)
- Delay in treatment initiation
- Need for multiple surgical procedures
NAVLE TipFor NAVLE prognosis questions, remember: approximately 50% of horses with septic tenosynovitis return to previous athletic function. Key negative factors are S. aureus isolation (only 30% return to function), bone involvement, and severe pannus. Early, aggressive treatment is the most important prognostic factor under our control.
Long-Term Complications
- Intrathecal adhesions: Restrict tendon gliding, causing mechanical lameness and reduced range of motion
- Chronic tenosynovitis: Persistent effusion and synovial thickening
- Annular ligament constriction: May require desmotomy
- Tendon damage: Tendonitis or rupture from direct infection or adhesions
- Contralateral limb laminitis: Due to weight shifting during prolonged lameness
| Technique |
Description |
Indications/Notes |
| Through-and-Through Needle Lavage |
Insert large-bore needles at proximal and distal ends of sheath; flush with several liters of sterile polyionic fluid |
Most common initial treatment (51%); can be performed standing; limited visualization; less effective at removing fibrin clots |
| Tenoscopy |
Endoscopic examination and lavage of tendon sheath under general anesthesia; allows debridement of fibrin, pannus, adhesions |
Gold standard for diagnosis and treatment; used in 39% of cases; allows synovial resection; can perform PAL desmotomy if needed |
| Open Tenosynoviotomy |
Surgical incision into tendon sheath for direct access, debridement, and open drainage |
Reserved for severe or chronic cases; allows excellent debridement; risk of adhesion formation; used in 10% of cases |
| Route |
Common Drugs/Doses |
Notes |
| Systemic |
Procaine penicillin (22,000 IU/kg IM BID) + Gentamicin (6.6 mg/kg IV SID); or Ceftiofur; or Trimethoprim-sulfa |
Broad-spectrum empirical coverage; adjust based on culture and sensitivity; duration typically 10-14 days |
| Intrathecal |
Amikacin (250-500 mg) most common; Gentamicin (100-200 mg) |
Achieves very high local concentrations; administered after lavage; may repeat daily or every other day |
| Regional Limb Perfusion (RLP) |
Amikacin (1-2 g in 60 mL saline); Gentamicin (1 g); Tourniquet proximal to lesion |
Achieves 10-100x systemic levels; can perform via IV (cephalic/saphenous) or intraosseous route; repeat every 24-48 hours |
| Outcome Measure |
Percentage |
| Survival to hospital discharge |
78-88% |
| Survival at 1 year post-treatment |
73% |
| Return to previous athletic function |
50-57% |
| Culture-negative cases: Long-term success |
70.5% |
| Culture-positive cases: Long-term success |
50% |
| S. aureus isolation: Return to function |
30.4% (significantly worse) |