Accelerated Hypertension ( Hypertensive Emergency /Malignant Hypertension)
BP>180/120 + End Organ Damage
What is considered end-organ damage? *Not an exhaustive list!
Cardiac-ACS/Aortic Dissection/CHF
Neuro-Stroke/Encephalopathy/Bleeding/Retinopathy/Papilledema
Renal-AKI/hematuria/proteinuria/MAHA/preclampsia/scleroderma renal crisis
Goal of Treatment Lower MAP with IV agents (eg: Labetalol/Esmolol/NTG/Nitroprusside/Nicardipine) by 10-20 % in minutes-2 hours, and then lower additional 5-15 % in next 23 hours.
Recommendations vary including lowering DBP<110 within 2-6 hours as tolerated
Compare to hypertensive urgency (no end-organ damage) where BP is lowered with oral medications and goal is to decrease BP in hours using PO agents with goal normal BP in 1-2 days
SPECIAL INSTANCE:
1)CHF and Accelerated HTN
-Treat with Diuretics and Nitroglycerin or Nitroprusside (watch for cyanide toxicity) –Avoid drugs that decrease contractility (eg: beta blockers), or increase cardiac work (Hydralazine)
–Avoid Labetalol in cases of unopposed alpha states (eg: Pheochromocytoma/cocaine/methamphetamine)
EXCEPTIONS
1)Acute ischemic stroke-generally allow permissive hypertension unless BP>220/110 and not tPA candidate or >185/110 and tPa candidate
2)Aortic dissection-goal of 100-120 SBP to decrease wall stress (especially Type B aortic dissections which are medically managed)
Secondary Hypertension Etiologies and Workup
1)Renovascular HTN-90 % of cases due to atherosclerosis, but 10 % due to FBD, MRA superior to ultrasound in diagnosis
2)CKD-Check GFR, normocytic anemia, hx of DMII, PCKD, renal ultrasound
3)Primary Hyperaldosteronism-Check Renin/Aldo levels, only 50 % have hypokalemia and metabolic alkalosis-need to confirm that patient is off anti-hypertensives and aldosterone is suppressed with saline infusion challenge
4)OSA-based on history and sleep study
5)Drugs (eg: OCP/sympathomimetics/cocaine/METH)
6)Pheochromocytoma (24 hour urine metanephrines and catecholamines-sensitive and specific, serum metanephrines easier to test but lower specificity)
7)Cushing syndrome-Dexamethasone supression test
8)Coarctation of Aorta– Associated condition (eg: Turners), Radiofemoral delay
9)Primary Hyperparathyroidism-check PTH
10)Hypo or Hyperthyroidism-Check TFT
Causes of PAINLESS loss of vision is related to either RETINA or OPTIC nerve involvement
RETINA
1)Central Retinal Artery Occlusion (CRAO)-ischemic retina, see cherry red fovea (has its own blood supply)
2)Central Retinal Vein Occlusion (CRVO)-“blood and thunder” appearance
3)Retinal detachment-new onset floaters/black dots, can be related to trauma
OPTIC NERVE involvement
1)Ischemic optic neuropathy (rule out GCA!)
2)Optic neuritis (Multiple Sclerosis commonly)-(+) RAPD but not specific
3)Papilledema (any increase in ICP)
4)Compression of optic chiasm (eg: pituitary adenoma)
See examples below (courtesy of UpToDate)