Tuberculosis of the Hand

Tuberculosis is a pulmonary disease primarily spread by inhalation, and is now commonly seen in immunocompromised patients, such as those with acquired immunodeficiency syndrome (AIDS). There also has been a recent increase in drug-resistant tuberculosis. Extrapulmonary tuberculosis is rarely seen in the hand but when it does occur, M tuberculosis is the most common causative organism. Often with tuberculosis infections of the hand, constitutional symptoms such as night sweats and weight loss are absent, and chest radiographs can be normal.

The various clinical presentations include cutaneous infections, tenosynovitis, osteomyelitis, septic arthritis, and dactylitis. Tenosynovitis of the flexor or extensor tendon sheath is most common. The tenosynovitis can extend into the carpal tunnel and cause a carpal tunnel syndrome. In these cases, rice bodies ( Fig. 1 ), which are tubercles in the synovial tissue that become detached and contain live mycobacteria that grow on culture, are seen coming from the tenosynovium walls intraoperatively. Tuberculosis can also invade the bones and joints of the hand. Distal radius osteomyelitis and radiocarpal arthritis via direct inoculation from adjacent tenosynovitis in the carpal tunnel have been reported. Tuberculosis osteomyelitis can be unifocal or multifocal, and the appearance of bony involvement can vary from cystic lesions, to a honeycomb pattern, to sclerosis. Dactylitis has been mostly reported in children and presentations range from mild soft-tissue involvement to bony destruction. The osseous destruction can present as either a cystic lesion or a tubular expansion of the bone. Usually, appropriate antibiotic treatment leads to reformation of the damaged bone. Other less common presentations of tuberculous infections in the hand include cutaneous nodules, tuberculous bursitis, and a hypersensitivity-type of reaction with aseptic arthritis and soft tissue swelling.

Rice bodies. Tubercles in the synovial tissue that become detached and contain live mycobacteria that grow on culture. They are seen coming from the tenosynovium walls intraoperatively.

Pathologic specimens usually show caseating granulomas. Tzanck smears, Ziehl-Neelsen (acid-fast) staining, and cultures are frequently negative. Cultures can take up to 3 to 6 weeks to yield a positive diagnosis. Appropriate treatment of tuberculous infections of the hand consists of multidrug therapy with isoniazid, rifampin, and pyrazinamide, with or without ethambutol. A typical treatment course consists of 2 months of treatment with this regimen; after the 2 months, the isoniazid and rifampin are continued for 4 months. However, some investigators are now recommending a longer treatment course, up to 18 months. Initiating full treatment and completing the full course is essential to preventing recurrence, as well as the formation of resistant strains.

Mycobacterium leprae

M leprae causes leprosy, or Hansen disease, which is endemic in Africa and Asia. The organism is carried by Southwestern armadillos. It typically affects the skin and peripheral nerves. The main clinical types of the disease are tuberculoid, borderline, and lepromatous. Tuberculoid disease affects patients with more competent resistance, and typically presents with a single anesthetic skin lesion, and early nerve thickening and dysfunction. Nerve abscess is also common and lepromin skin tests are strongly positive. In contrast, the lepromatous form affects patients with incompetent resistance, and is associated with multiple skin lesions with relative preservation of skin sensation and delayed nerve thickening. Lepromin skin tests in these patients are usually negative. One common issue with the lepromatous type is secondary bacterial infection of ulcers. Borderline tuberculoid disease affects those with intermediate resistance and their presentation fluctuates between tuberculoid and lepromatous types.

Diagnosis begins by recognizing 3 cardinal signs emphasized by the World Health Organization:

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  An anesthetic skin patch

  
  
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  Nerve thickening

  
  
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  A hypopigmented skin lesion.

A slit-skin smear, which uses a thin (∼3 mm) sample of tissue taken with a scalpel, confirms the diagnosis and also helps to classify the disease as paucibacillary (negative smear) versus multibacillary (positive smear). When a slit-skin smear is negative, skin and nerve biopsies can also be considered if the diagnosis is in doubt.

In the upper extremity, the ulnar nerve is usually the first major nerve affected. Treatment includes systemic multidrug therapy with dapsone and rifampin, with the addition of clofazimine for multibacillary disease. Systemic steroids are also often used, especially in the setting of lepromatous reactions in which patients present with acute onset of skin, nerve, or synovial lesions. The additional benefit of nerve decompression is a topic of controversy. A recent Cochrane review was unable to show a significant added benefit to steroid therapy. However, nerve decompression and drainage of nerve abscesses are procedures commonly done that are thought to relieve pain and preserve nerve function. Other procedures that may be of benefit in patients with leprosy affecting the upper extremity include release of contractures after long-standing ulnar nerve palsy. Tendon transfers may also be appropriate, depending on which nerves are affected and what alternative motors are available. For example, combined ulnar and median nerve paralysis is the second-most common deformity, behind the ulnar claw hand. Described tendon transfers to correct ulnar claw hand include the extensor-to-flexor 4-tailed tendon transfer and the palmaris longus 4-tailed tendon transfer.

Mycobacterium marinum

M marinum is the most common mycobacteria causing hand infections. It is seen in patients who have been injured by aquatic organisms, such as those cleaning aquarium tanks, fishing, and preparing seafood for consumption. The presentation can vary and has been classified previously into 3 types: type I consists of self-limited verrucal lesions, type II presents with single or multiple subcutaneous granulomas with or without ulceration, and type III infections are deep-tissue infections involving either tenosynovium, bursa, bone, or joints. Hurst and colleagues reported on 15 subjects with M marinum infections in the hand, and classified 6 of them as type II infections and 9 of them as type III, with most of these being tenosynovitis. Of the 27 lesions in their 14 subjects, 21 were in the fingers and 6 were in the wrist. Deep M marinum infections most commonly manifest as extensor or flexor tenosynovitis but can also present as joint infections. Flondell and colleagues describe a case of invasive M marinum hand infection that spared the extensor tendons, but led to necrotic interosseous muscles and septic metacarpophalangeal joint arthritis.

M marinum infections often present in a delayed fashion. In a recent case series on 5 subjects with chronic flexor tenosynovitis, Pang and colleagues reported an average delay of 32 days between injury and time of presentation. In the series by Hurst and colleagues, the average time between symptom onset and initial consultation was 7.7 months. This delay is due to an indolent course of illness, nonspecific presentation, and long time to positive culture results. Initial diagnoses are often erroneous. There are no pathognomonic features of the disease. In some of the described cases of M marinum flexor tenosynovitis, the subjects were afebrile, with a normal white count, absent Kanavel signs, and were initially diagnosed with cellulitis and abscess. Diffuse pain and swelling to the hand and/or digits is the most common presentation with M marinum infections, with some patients also having painful ulcers.

At the time of surgery, the tenosynovium in M marinum flexor tenosynovitis is commonly described as chronic, granulomatous inflammatory tissue. Histopathology from tissue taken intraoperatively from M marinum infections typically shows noncaseating granulomas, unlike M tuberculosis , which typically shows caseating granulomas. Only 46% of patients have positive pathologic findings. Although commonly performed, Ziehl-Neelsen staining (for acid-fast bacilli) is frequently negative. Cultures for M marinum must be performed on special medium, specifically Lowenstein-Jensen media at 30°C for at least 4 to 6 weeks. This temperature requirement explains why the organism usually infects cooler parts of the body.

Treatment depends on the type of infection and structures affected. Although verrucal lesions are typically superficial and self-limiting, deeper lesions are usually treated with a combination of surgery and antibiotics. Subcutaneous granulomas may be adequately treated with surgical excision of masses but infections that present as flexor tenosynovitis, deep abscesses, or septic arthritis require more extensive debridement ( Fig. 2 ). The optimal antibiotic regimen for M marinum has not been defined but usually includes some combination of clarithromycin, rifampin, or ethambutol. M marinum is almost always resistant to isoniazid and streptomycin.

Infections that present as flexor tenosynovitis, deep abscesses, or septic arthritis require extensive debridement.

Other Mycobacterial Species

M avium intracellulare (MAI) is the second-most common mycobacteria to infect the upper extremity. In immunocompromised patients, it can cause systemic illness, but it can also affect immunocompetent hosts by causing infection of the deep tissues. In their series of atypical Mycobacterium infections of the upper extremity, Kozin and Bishop found that MAC was responsible for the second-most infections overall, behind M marinum , but it accounted for the most deep infections. Granulomatous tenosynovitis is the typical presentation. As with other mycobacterial tenosynovitis, histopathology of the synovial tissue can show caseating granulomas. Ziehl-Neelsen staining is often performed but can commonly be negative.

Akahane and colleagues described a case of chronic recurrent MAC granulomatous tenosynovitis and emphasized that confirming the microbiological diagnosis can be difficult. In their case, the patient underwent an initial debridement for finger and wrist tenosynovitis, in which they noted cystic masses; synovial tissue cultures taken from these were negative. Four months later, the patient had a recurrence of swelling in the wrist and underwent another debridement. Again, tissue cultures were negative but this time synovial fluid from the cysts were positive for MAC on Lowenstein-Jensen culture at 37°C and with polymerase chain reaction (PCR).

Other nontuberculous mycobacterial organisms that have been implicated in upper extremity infections include M kansasii , M malmoense , M chelonei , M terrae , M fortuitum , and M ulcerans . Tenosynovitis of the fingers and wrist is a common presentation. Chronic flexor tenosynovitis has been reported to present as carpal tunnel syndrome due to mass effect of the inflamed flexor tenosynovium in the carpal tunnel. Other deep hand infections are possible as well, including bony involvement. M kansasii has been documented to cause osteomyelitis in the scaphoid, in an immunocompetent patient who sustained an injury from a meat hook. This patient also presented initially with carpal tunnel syndrome, and had a carpal tunnel release and subsequent steroid injections before finally being diagnosed 3 years after the initial injury. This story of an indolent disease course, misdiagnosis, misguided treatment with steroid injections, and delayed diagnosis is common in mycobacterial infections. On presentation, disabling pain, fever, and elevated inflammatory markers are typically absent.

Any suspicion for mycobacterial infection in the upper extremity should prompt an acid-fast stain of the involved tissues. Almost 30% of patients will have positive acid-fast stains. Histologic examination of tissue is also important, often showing granulomas. Maximizing results of tissue cultures requires using the right culture media and temperature. Egg-based media (Lowenstein-Jensen) is most commonly used for mycobacteria and samples are incubated at both 37° and 30°C. Organisms such as M marinum and M chelonae may grow only at 30°C, whereas others such as M tuberculosis grow at 37°C. The rate of growth on cultures also varies between species because some will grow in 7 to 10 days on culture, whereas others such as M malmoense can take up to 12 weeks.

Treatment of these mycobacterial infections is similar to that mentioned previously for M marinum . When the infection is deep, most investigators believe that the combination of surgery and antibiotic therapy is warranted. Excision of infected tissue, such as tenosynovectomy, is thought to decrease the overall disease load, even if it does not remove all infected tissue. However, there is no absolute consensus in the literature on treatment protocols. Successful treatment with medications alone has been reported in infectious tenosynovitis caused by M marinum , M kansasii , and M chelonae . Cases of mycobacterial tenosynovitis treated with tenosynovectomy alone, without medications, have also been documented. Antimicrobial therapy is typically with rifampin, isoniazid, and ethambutol, except for M marinum , which is less sensitive to isoniazid, as previously mentioned. Treatment should be for at least 9 months, with some investigators suggesting duration of up to 18 months.