Pathology

Granulomas are composed of epithelioid cells (macrophages with abundant pink cytoplasm) with surrounding multinucleated giant cells and lymphocytes. Th1 cells secrete IFN-γ, activating macrophages. TNF-α from macrophages induces and maintains granuloma function. Anti-TNF drugs can cause sequestering granulomas to break down, leading to disseminated → always test for latent TB before starting anti-TNF therapy. - Associated with hypercalcemia due to calcitriol production. - Caseous necrosis is more common with an infectious etiology (eg, TB). Diagnosis of sarcoidosis requires noncaseating granulomas on biopsy.

Cardiac: Cardiac arrest, arrhythmias Neurologic: Peripheral nerve damage, seizures, confusion, respiratory arrest, autonomic dysfunction Dermatologic: Lichtenberg figures (erythematous cutaneous marks in a fern-leaf pattern, pathognomonic of lightning strike), burns Musculoskeletal: Rhabdomyolysis, bone fractures, compartment syndrome Other: Cataracts (late sequelae), ruptured tympanic membranes, curling ulcers

Pathogenesis: Valvular endothelial injury caused by inflammatory cytokines, which triggers platelet deposition in the presence of an underlying hypercoagulable state. Associated with:- Advanced malignancy (especially mucinous adenocarcinoma)- Systemic lupus erythematosus (Libman-Sacks endocarditis)- Less commonly: antiphospholipid syndrome, DIC, extensive burns Histology: Sterile, platelet-rich thrombus with strands of fibrin, immune complexes, mononuclear cells.  Most common presentation is systemic embolization (eg, stroke, acute limb ischemia).