Sunday, November 15, 2009

Musculoskeletal Manifestations of HIV infection

MUSCULOSKELTAL MANIFESTATIONS OF HIV INFECTION

• The etiologic agent of AIDS is HIV, which belongs to the family of human retroviruses (Retroviridae) and the subfamily of lentiviruses
• The most common signs and symptoms are fever, fatigue, and a maculopapular skin rash and seen in 90 % patients with acute infection
• Around 50% to 70% also complain of myalgias, arthralgias, and paresthesias, which may be the only symptoms of the acute infection.
• Acute HIV infection should be included in the differential diagnosis of sudden onset of arthralgias and myalgias with a compatible history of exposure.





Myopathies
a) Pyomyositis :maybe misdiagnosed as muscle strain, contusion, hematoma, cellulitis, deep vein thrombosis, osteomyelitis, septic arthritis, or neoplasm
• Staphylococcus aureus is the most common pathogen (90% of cases) but Streptococcus pyogenes, Mycobacterium tuberculosis, Nocardia asteroides, and Cryptococcus neoformans is also found.
• Pyomyositis develops in patients with preexisting muscle damage who experience transient bacteremia.
• Muscle injury maybe due to nutritional deficiencies, azidothymidine (AZT)-induced mitochondrial injury, opportunistic infections, or direct viral invasion of muscle tissue in HIV-infected patients.
• Aggressive management with i.v antibiotics and surgical drainage should be done.

b) Polymyositis:
- bilateral, symmetrical proximal muscle weakness associated with elevated
serum CK levels.
• Cause: direct muscle injury by the virus or immunogenic reaction
• MRI, EMG or muscle biopsy will confirm the diagnosis.
• In MRI, Unlike pyomyositis, rim enhancement is not present
• NSAIDs, oral prednisolone(upto 60mg/day)

c) AZT Myopathy• Reversible toxic mitochondrial myopathy that mimics polymyositis clinically.
• Patients usually present with myalgia, fatigue, proximal muscle weakness, and elevated serum CK levels.
• EMG shows myopathy
• Treatment is withdrawal of AZT and institution of another antiviral agent.

Infections

a) Tuberculous Osteomyelitis
• Commonly affects the spine
• The thoracic and lumbar (especially L1) regions are most commonly affected;
• Infection usually begins in the vertebral body and spreads to adjacent disc.
• The duration of antibiotic tuberculosis therapy usually is longer in HIV-infected patients(1 year)

b) Bacillary Angiomatosis
• Caused by bartonella henselae(formerly Rochalimaea henselae)
• Cat bite and cat scratch are strong risk factors.
• Multiorgan involvement may include adenitis, intracerebral mass lesions, aseptic meningitis, peliosis hepatis, and osteomyelitis.
• Cutaneous lesions are characterised by friable angiomatous papules, which resemble Kaposi’s sarcoma lesions.
• The presence of osseous lesions, which are not typically seen with Kaposi’s sarcoma, may help differentiate this disease
• Osseous lesions are lytic and can be associated with periostitis and a soft-tissue mass
• Extensive cortical damage and medullary permeation are seen, often preceding the cutaneous lesions by many months.
• The overlying skin changes mimic cellulitis.
• Increased uptake on technetium 99m bone scan; MRI shows the nonspecific changes of osteomyelitis.
• Warthin- Starry silver staining is used to identify the bacillary organism.
• Early treatment with erythromycin should be instituted when an osteolytic lesion in present

Neoplasms

a) Non-Hodgkin’s Lymphoma
• It is the second most common type of tumor in HIV-infected persons after Kaposi’s sarcoma
• Extranodal involvement, including the central nervous system, bone marrow, abdominal organs, and mucocutaneous sites, is common
• Patients may present with pain, fever, weight loss and pathologic fracture.
• On X-rays it is commonly osteolytic with cortical destruction and permeation. Sclerotic and mixed appearance may also be seen. DD includes osteomyelitis
• Treatment is by chemotherapy, radiotherapy and surgical debulking in selected patients

b) Kaposi’s sarcoma
• Is seen in 20% of patients with HIV
• Osseous lesions range from erosions to discrete osteopenia or cortical destruction
• Treatment consists of chemotherapy and radiation

Inflammatory arthropathy

a) Reiter’s syndrome
• Is 100 to 200 times more frequent in the HIV infected population than in the noninfected.
• Commonly oligoarticular, predominantly involving the lower extremities.
• Enthesopathy is common, which frequently involves the Achilles tendon, plantar fascia, and extensor tendons, as well as anterior and posterior tibial tendons.
– This is called AIDS foot and presents as a broad-based gait with weight bearing through the lateral margins of the feet to protect the painful heel.
• It can be extremely disabling, some patients become wheelchair bound, and may mimic a peripheral neuropathy.
• Upper extremity enthesopathy may include medial or lateral epicondylitis, rotator cuff tendinitis, de Quervain’s tenosynovitis, or flexor tendinitis.
• Associated with HLA- B27
• Is usually refractory to treatment with NSAIDs, but possibly responds to second line drugs like phenyl butazone and sulphasalazine
• Cyclosporine and prednisone may be used in refractory cases
• But methotrexate is contraindicated since it may precipitate full blown AIDS and Kaposi’s sarcoma

b. Psoriatic Arthritis
• Typical cutaneous manifestations include circumscribed, discrete, and confluent red, silvery scaled maculopapules that occur predominantly on the elbow, knee, scalp, and trunk.
• Treatment is similar to Reiter’s syndrome

c. HIV associated arthritis
- Usually involves the knees and ankle
- X-rays show non specific changes
- Synovial biopsy shows a chronic process with a predominantly mononuclear
cell infiltrate.
- Rheumatoid factor and HLA B 27 are characteristically negative
- Treatment is by administering intra articular steroid injections

d. Painful articular syndrome
• The hallmark of this arthritis is a sharp, severe arthralgia of acute onset that often simulates a septic joint
• MC site: knee> elbow> shoulder
• Differentiated from a septic joint by its intermittent pain pattern and lack of effusion or synovitis on physical examination.
• X-rays are non specific
• This self-limited condition lasts from 2 to 24 hours and responds well to narcotics and anti-inflammatory medications.

e. Acute symmetric polyarthritis
. is unique to HIV-infected patients and resembles rheumatoid arthritis both clinically and radiographically
• Rheumatoid factor is usually negative
• Gold is used for treatment

f. Hypertrophic Osteo arthropathy:
- Severe pain in the lower extremity is typical, and
clinical manifestations include arthralgias, nonpitting edema, digital clubbing, and periarticular soft-tissue involvement of the ankle, knee, and elbow
• Extensive periosteal reaction and subperiosteal proliferative changes of the long bones
• Surgical or chemical vagotomy or radiation therapy has been used to relieve bone pain in refractory cases

g. Osteonecrosis:
• Embolic phenomena secondary to the formation of antiphospholipid antibodies and immune complexes, protein S deficiency, and hypergammaglobulinemia also have been proposed as etiologies
• There is a strong correlation between protease inhibitor use and osteonecrosis of the femoral head.

Ref:
1. Rodgers WB, Yodlowski ML, Mintzer CM: Pyomyositis in patients who have the human immunodeficiency virus: Case report and review of the literature. J Bone Joint Surg Am 1993;75:588-592.
2. Luck JV Jr, Logan LR, Benson DR, Glasser DB: Human immunodeficiency virus infection: Complications and outcome of orthopaedic surgery. J Am Acad Orthop Surg 1996;4:297-304.
3. Paiement GD, Hymes RA, LaDouceur MS, Gosselin RA, Green HD: Postoperative infections in asymptomatic HIV-seropositive orthopedic trauma patients. J Trauma 1994;37:545-551.
4. Ragni MV, Crossett LS, Herndon JH: Postoperative infection following orthopaedic surgery in human immunodeficiency virus-infected hemophiliacs with CD4 counts < or = 200/mm3. J Arthroplasty 1995;10:716-721.
5. Ayaz A. Biviji,, Guy D. Paiement, Lynne S. Steinbach : ‘Musculoskeletal Manifestations of Human Immunodeficiency Virus Infection’ J Am Acad Orthop Surg 2002;10:312-320

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