malignant hypertension

Malignant hypertension results from a rapid, severe rise in blood pressure that overwhelms vascular autoregulation, leading to endothelial damage, fibrinoid necrosis of arterioles, and microvascular injury. Pathologically, it is characterized by fibrinoid necrosis of the arteriolar walls and 'onion-skin' hyperplastic arteriolosclerosis, particularly evident in the kidney. Clinically, it presents with markedly elevated BP (often diastolic >120-130 mmHg) accompanied by evidence of acute end-organ damage: papilledema and retinal hemorrhages/exudates (grade IV hypertensive retinopathy), encephalopathy (headache, confusion, seizures), acute kidney injury (hematuria, proteinuria, rapidly rising creatinine), and cardiac involvement (heart failure, myocardial ischemia). Microangiopathic hemolytic anemia (schistocytes) and thrombocytopenia can occur due to mechanical shearing of red blood cells in damaged small vessels, mimicking TTP/HUS. Common causes include poorly controlled essential hypertension, renovascular disease, pheochromocytoma, and medication non-compliance. Management requires controlled, gradual reduction of BP (typically no more than 25% within the first hour, then gradual normalization over 24-48 hours) using IV agents such as labetalol, nicardipine, or nitroprusside to avoid precipitating ischemic events from too-rapid correction. This is distinguished from hypertensive urgency, where BP is severely elevated but without acute end-organ damage, and treatment can be more gradual with oral agents. Untreated, malignant hypertension carries a high risk of stroke, myocardial infarction, renal failure, and death within months.