A 60-year-old woman presented with a history of severe pain in the left shoulder joint.
The patient was diabetic and presented with two months history of severe and rapidly progressive pain in left shoulder joint. There was no history of previous trauma. On examination, the left shoulder joint had a diffuse swelling with ill defined margins. The overlying skin was tense and shiny. Movements of shoulder were painful and restricted in all directions. There was no distal neurovascular deficit. The tuberculin test was strongly positive. Chest X-Ray was normal. An anteroposterior roentegenogram of the left shoulder revealed a soft tissue swelling and a lytic lesion of the head of the humerus (fig 1). An enhanced computed tomography scan showed bony destruction of the head of humerus (fig 2-3). There was calcifications in and around the joint. Ponction and synovial biopsy of joint was removed. A cytological examination showed caseation and a granulomatous lesion strongly suggestive of tuberculosis. The patient was started on four drug antiubercular therapy initially (INH, RFP, EB, PZA) and was put on two drugs after two months. There was continued for sixteen months. The shoulder was immobilized. At final follow up she had gained weight, had no pain or swilling, but the movements were restricted.
The incidence of tuberculosis of the shoulder joint is 1- 2,8% of the skeletal tuberculosis. This is may differ clinically and pathologically from tuberculosis of other joints and can be difficult to diagnose in early stages. The dry type of lesion is commonly reported in adults, commonly known as “caries sicca” (1-2). There is usually concomittent involvement of the synovial membrane and the subchondral bone. Radiologically such a lesion may show osteoporosis, subchondral erosions, diminished joint space, relative sclerosis and progressive joint destruction (1). The acute fulminating variety of shoulder tuberculosis, as seen in our patient, is common in children but very rare in adults and may simulate acute osteomyelitis, septic arthritis or ostegenic sarcoma. Computed tomography was more helpful than plain X-rays in diagnosis as it clearly demonstrated bony destruction of the glenoid cavity and the humerus, and showed pathological fracture dislocation of the shoulder (1, 3). In MRI, T2-weighted images showed extension of abscess clearly (2, 3). The diagnosis was confirmed by synovial biopsy or fine needle aspiration cytology (1, 2). The patient responded very well to anti-tubercular therapy with rest in an immobilizer.
Fulminating shoulder joint tuberculosis
Based on the provided shoulder X-ray and CT images, the main features are as follows:
1) Bone destruction at the glenohumeral joint and the proximal humerus: The glenoid cavity (joint surface of the scapula) and the humeral head show marked bone erosion and destruction, with some areas displaying localized or diffuse lytic changes.
2) Signs of pathological fracture and subluxation/dislocation: CT images suggest a significant pathological fracture or subluxation/dislocation between the humeral head and the glenoid cavity.
3) Changes in joint space: The joint space is narrowed, accompanied by soft tissue swelling, indicating possible effusion or inflammation.
4) Possible soft tissue lesions: In certain slices, enhanced or altered density in the surrounding soft tissue is visible, raising suspicion of a perijoint abscess or granulation tissue formation.
Considering the clinical background of a 60-year-old female patient presenting with severe left shoulder pain, along with the imaging findings of bone destruction and joint involvement, the possible diagnoses include:
Based on the clinical symptoms (acute severe shoulder pain), imaging findings (marked bone destruction of the humeral head and glenoid, narrowed joint space, possible soft tissue abscess), and pathological evidence (e.g., synovial or soft tissue biopsy indicating Mycobacterium tuberculosis infection), the most likely diagnosis is “tuberculous arthritis of the shoulder (tuberculous synovitis with bone destruction).” As this is relatively uncommon in older adults and can be easily mistaken for acute pyogenic infection or tumor, further laboratory tests (joint fluid or lesion aspiration) and pathological examinations are needed to confirm the diagnosis.
1) Treatment Strategy:
• Anti-tuberculosis therapy: Once tuberculosis infection is confirmed, initiate a standard anti-tuberculosis multidrug regimen (commonly four-drug therapy or adjusted according to pathogen and drug resistance). The treatment course typically lasts 6 to 9 months or longer, depending on the extent of the lesion and therapeutic response.
• Immobilization: During the acute phase, shoulder immobilization (e.g., bracing or sling) may help alleviate pain and facilitate lesion healing. Appropriate immobilization can help control symptoms when there is active infection or severe pain.
• Surgical intervention: In cases of severe bone destruction, significant joint deformity, or large abscesses, surgical debridement or even joint reconstruction may be required. If the pathological fracture is unstable, internal fixation or joint replacement should be considered as appropriate.
2) Rehabilitation and Exercise Prescription (FITT-VP Principle):
Once the acute inflammation is effectively controlled and pain is reduced, progressive functional exercises of the shoulder joint can be introduced.
Note: Given the patient’s advanced age and potentially fragile bones, close monitoring of the shoulder and overall condition is required. Exercise intensity should be increased gradually under the supervision of physicians or rehabilitation therapists.
This report provides a preliminary analysis based on the available imaging and clinical information for reference only, and does not replace in-person consultation or professional medical advice. The final treatment plan should be determined by a specialist physician after a comprehensive assessment of the patient’s specific condition.
Fulminating shoulder joint tuberculosis
