What Is Infectious Tenosynovitis?
Tenosynovitis is an inflammation of the fluid-filled synovium, which is present inside the tendon sheath. The condition commonly manifests as pain, swelling, and stiffness. Infective tenosynovitis is caused due to infiltration and proliferation of infective pathogens within the tendon sheath. The pathogens reach the sheath either through direct inoculation or spread from local or distant foci of infection.
Who Is Susceptible to Infectious Tenosynovitis?
The stenosing form of tenosynovitis is found in about 1.7 to 2.6 percent of the general population, which increases to 10 to 20 percent in patients with diabetes mellitus. About 2.5 to 9.4 percent of the patients who develop some kind of hand infection will go on to develop infectious tenosynovitis. Patients with predisposing rheumatoid arthritis are at the highest risk of tenosynovitis, with 55 percent incidence reporting an average of 3.1 number of tendon inflammations.
What Causes Infectious Tenosynovitis?
Infectious tenosynovitis is caused by inoculation, spread, and growth of pathogens in the tendon sheaths. The most common organisms causing infectious tenosynovitis are Staphylococcus aureus (40 to 75 percent of the cases), MRSA - Methicillin-resistant Staphylococcus aureus (29 percent of the cases), other common skin commensal bacteria like Staphylococcus epidermidis, beta-hemolytic streptococcus, Pseudomonas aeruginosa, Eikenella in human bites, and Pasturella multocida in animal bites.
What Is the Pathophysiology of Infectious Tenosynovitis?
The mechanism of tenosynovitis is similar to the findings in inflammation within the tendon sheath. Various etiological pathways affect the tendon synovium or the tendon itself, which results in inflammation and thickening of the tendon, which comprises the natural gliding ability of the tendon sheath. Not all tendons are capsulated within a sheath like the Achilles tendon. The progression of infectious tenosynovitis is through a series of surgically significant steps. The first step demonstrates exudative distension of the tendon sheath apparatus. The second stage demonstrates purulent filling, and the final stage results in necrosis and destruction of the sheath, tendon, and adjacent structures.
What Are the Signs and Symptoms of Infectious Tenosynovitis?
Infectious tenosynovitis presents with a history of injury, fever, ulceration, or purulence with acute digit contracture or pain upon flexion or extension.
To diagnose infectious flexor tenosynovitis, the criteria to be satisfied are:
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Pain in the flexor sheath.
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Symmetric enlargement of the affected tendon.
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Baseline contracture of the infected tendon.
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Passive straightening of the tendon with tenderness.
What Are the Evaluation Methods for Infectious Tenosynovitis?
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Laboratory Studies: Elevated WBC (white blood cells), bacteremia, and culture studies.
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Microscopic examination to distinguish infectious pathology from crystalline pathology.
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Radiographic shreds of evidence are not always useful.
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CT (computed tomography) scan can detect bony abnormalities but soft tissue sensitivity for synovitis and tenosynovitis is low.
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Ultrasound may show echotexture changes in tendons and blurring of tendon margins. Additionally, tendon thickening, sheath cysts, and further abnormalities of the metacarpophalangeal joints may also be observed.
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MRI (magnetic resonance imaging) may reveal peritendinous edema and increased thickening of the extensor brevis longus (EBL) and abductor pollicis longus (APL) tendons.
How to Treat Infectious Tenosynovitis?
Various pathogens involved in infectious tenosynovitis are:
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Methicillin-susceptible Staphylococcus aureus.
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Methicillin-resistant Staphylococcus aureus (MRSA).
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Streptococcus species.
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Pseudomonas aeruginosa.
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Neisseria gonorrhoeae.
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Pasteurella multocida.
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Mycobacterium marinum.
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Sporothrix schenckii.
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Coccidioides species.
Treatment regimens against methicillin-susceptible Staphylococcus aureus:
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Penicillin G (4 million units Intravenous (IV) every four hours).
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Nafcillin (2 g (grams) IV every four hours).
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Oxacillin (2 g IV every four hours).
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Cefazolin (2 g IV every eight hours).
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Cephalexin (250 to 1000 mg (milligram) every six hours).
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Duration of therapy: 7 to 14 days (uncomplicated infection) or 14 to 21 days (complicated infections).
Treatment regimens against methicillin-resistant Staphylococcus aureus (MRSA):
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Doxycycline (100 mg twice a day).
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Trimethoprim-sulfamethoxazole (160 mg or 800 mg twice a day).
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Clindamycin (300 to 600 mg thrice a day).
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Vancomycin (15 to 20 mg/kg (milligram per kilogram) two to three times a day).
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Linezolid (600 mg twice a day).
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Daptomycin (four to six mg/kg IV one time per day).
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Vancomycin is the first-line drug of choice against MRSA in hospitalized patients.
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Duration of therapy: 7 to 14 days (uncomplicated infection) or 14 to 21 days (complicated infections).
Treatment regimens against Streptococcus species:
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Penicillin G (4 million units IV every 4 hours).
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Clindamycin (300 to 600 mg thrice a day).
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Ceftriaxone (1 g IV once a day).
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Amoxicillin-Clavulanate (875 mg or 125 mg twice a day).
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Ampicillin-Sulbactam (one to two g IV four times per day).
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Duration of therapy: 7 to 14 days (uncomplicated infection) or 14 to 21 days (complicated infections).
Treatment regimens against Neisseria gonorrhoeae:
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Ceftriaxone (1 g IM (intramuscular) or IV once a day) plus single-dose Azithromycin 1 g.
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Cefotaxime (1 g IV thrice a day) plus single-dose Azithromycin 1 g.
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Ceftizoxime (1 g IV thrice a day) plus single-dose Azithromycin 1 g.
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Duration of therapy: 24 to 48 hours and transition to Cefixime 400 mg (twice a day) for at least one week.
Treatment regimens against Pasteurella multocida:
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Amoxicillin-clavulanate (875 mg or 125 mg twice a day).
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Ampicillin-sulbactam one to two g IV (four times per day).
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Doxycycline 100 mg (twice a day).
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Duration of therapy: 7 to 14 days (uncomplicated infection) or 14 to 21 days (complicated infections).
Treatment regimens against Mycobacterium marinum:
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Clarithromycin (500 mg twice a day) plus Rifampin (600 mg once daily).
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Clarithromycin (500 mg twice a day) plus Ethambutol (15 mg/kg once daily).
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Minocycline (100 mg twice a day).
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Doxycycline (100 mg twice a day).
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Duration of therapy: four to six weeks after symptoms subside with three months minimum duration.
Treatment regimens against Sporothrix schenckii:
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Itraconazole (200 mg twice a day).
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Amphotericin B (three to five mg/kg/day IV per day) until resolution, then continue with Itraconazole (200 mg twice a day).
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Deoxycholate Amphotericin B (0.7 to 1 mg/kg/day) until resolution, then continue with Itraconazole (200 mg twice a day).
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Duration of therapy: at least 12 months.
Treatment regimens against Coccidioides species:
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Itraconazole (200 mg twice a day).
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Fluconazole (400 to 800 mg once a day).
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Lipid amphotericin B (three to five mg/kg IV once daily) until improving, then continue with Itraconazole (200 mg twice a day).
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Duration of therapy: at least 6 to 12 months.
What Is the Prognosis of Infectious Tenosynovitis?
The best outcomes of infectious tenosynovitis are related to early empiric antibiotic therapy and early irrigation or debridement when necessary. The poor prognosis of infectious tenosynovitis is due to superinfection by Streptococcus pyogenes, delayed antibiotic therapy and surgical intervention, purulence of the tissue, diabetes mellitus, renal failure, and peripheral vascular disease. Stage III disease involving necrosis and destruction offers the worst outcomes, with a high amputation rate.
What Are the Complications of Infectious Tenosynovitis?
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Long-term stiffness of fingers.
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Deformation of underlying bones or tendons.
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Deep space infections of the hand.
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Tendon necrosis (death of the tendons).
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Adhesions (scar tissue between two surfaces that fuse them).
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Amputation (surgical removal of a body part).
Conclusion
Tenosynovitis requires an inter-departmental approach to treatment, including physicians, infection specialists, nurses, and surgeons, all collaborating across disciplines to achieve optimal patient results. The consultation of an infectious disease specialist is a must in infectious tenosynovitis, which will prompt early diagnosis and empirical antibiotic treatment. Early detection of pain, contracture, enlargement, or any such changes to the extremities of the patient is important in establishing an early diagnosis and treatment regime.