Malignant Hypertension
Pathophysiology
- Rapid increase in BP leading to severe HTN causing disruption of vascular endothelium which narrows/obliterates vascular lumen
- RAAS activation
- Autoregulation of BP lost
Clinical Features
- Retinal hemorrhage and exudates, papilledema
- Malignant nephrosclerosis causes AKI, proteinuria, hematuria
- Neurologic sx due to hypertensive encephalopathy, SAH, lacunar infarcts
- Hypertensive encephalopathy = cerebral edema secondary to breakthrough hyperperfusion from severe/sudden rise in BP (CPP autoregulation lost)
- Can cause microangiopathic hemolytic anemia (MAHA)
Diagnosis
- BP, physical exam, Cr, UA, +/- CT Head or MRI Brain
Treatment
- IV BP meds: nitroprusside, nicardipine, labetalol, fenoldopam
- If no IV meds: sublingual nifedipine or sublingual captopril; these can rapidly decrease BP in 10-30 min, beware of MI/stroke
- Goal: Lower BP by 25% over 2-6hr, goal DBP 100-105