Possible Causes of Continued Severe Hypertension in This Patient
In a 57-year-old woman with no prior hypertension presenting with sudden severe headache and blood pressure of 220/118 mmHg, the most likely causes are either previously unrecognized essential hypertension with acute progression to malignant hypertension, or an identifiable secondary cause—which occurs in 20–40% of such presentations. 1
Primary Consideration: Malignant Hypertension
The majority of patients presenting with malignant hypertension have unrecognized or uncontrolled essential hypertension that has suddenly escalated, rather than a secondary cause. 1
The sudden onset in a patient with no prior hypertension history, combined with severe headache, strongly suggests hypertensive emergency with possible hypertensive encephalopathy or intracranial hemorrhage—both of which require immediate neuroimaging and ICU admission. 1, 2
The rate of blood pressure rise is often more clinically important than the absolute value; previously normotensive individuals tolerate acute severe elevations poorly compared to chronic hypertensives. 2
Secondary Causes to Investigate (20–40% of Cases)
Renal Causes (Most Common Secondary Etiologies)
Renal artery stenosis is one of the two most frequent secondary causes of malignant hypertension and should be screened with renal artery duplex ultrasound or CT angiography after stabilization. 1, 3
Renal parenchymal disease is the other leading secondary cause; check serum creatinine, urinalysis for proteinuria, and renal ultrasound. 1, 3
The incidental finding of 90% carotid blockage suggests widespread atherosclerotic disease, which increases the likelihood of concurrent renal artery stenosis in this patient. 1
Endocrine Causes
Pheochromocytoma should be considered given the sudden severe hypertension with headache; obtain plasma metanephrines or 24-hour urine catecholamines. 1, 3
Primary aldosteronism accounts for a notable proportion of secondary causes in malignant hypertension; measure plasma aldosterone-to-renin ratio. 1, 3
Endocrine causes appear relatively rare compared to renal etiologies but must not be missed. 1
Medication and Substance-Related Causes
Alcohol abuse (documented in this patient) can contribute to acute blood pressure elevations, particularly during withdrawal or binge drinking. 3
NSAIDs, steroids, or sympathomimetic agents (cocaine, methamphetamine) can precipitate hypertensive crises; obtain a detailed medication and substance use history. 3
Vascular Causes
- Acute aortic dissection must be excluded urgently given the severe hypertension and atherosclerotic risk factors (smoking, hyperlipidemia, carotid disease); obtain CT angiography of the chest if any chest or back pain is present. 3
Pathophysiologic Mechanisms Perpetuating Severe Hypertension
Marked activation of the renin-angiotensin system is frequently present in malignant hypertension and correlates with the degree of microvascular damage, creating a self-perpetuating cycle. 1, 3
Pressure-induced natriuresis leads to volume depletion, which paradoxically further activates the renin-angiotensin system and maintains elevated blood pressure. 1, 3
Acute hypertensive microangiopathy with endothelial dysfunction and thrombotic microangiopathy can develop, causing renal vasoconstriction and perpetuating the hypertensive crisis. 1, 3
Critical Immediate Assessments Required
Neurologic Evaluation
Perform urgent non-contrast head CT to exclude intracranial hemorrhage or acute stroke, as severe headache with this blood pressure mandates immediate imaging. 2
Assess for hypertensive encephalopathy (altered mental status, visual disturbances, seizures), which occurs in 10–15% of malignant hypertension cases. 1
Note that advanced hypertensive retinopathy may be absent in up to one-third of patients with hypertensive encephalopathy, so diagnosis relies on neurologic symptoms and imaging. 1
Cardiac and Renal Assessment
Obtain ECG and troponin to exclude acute coronary syndrome, as heart failure, stroke, and myocardial infarction represent the largest proportion of hypertensive emergencies. 1
Measure serum creatinine, urinalysis, and urine sediment to detect acute kidney injury or thrombotic microangiopathy. 2
Check hemoglobin, platelets, LDH, and haptoglobin to screen for microangiopathic hemolytic anemia associated with thrombotic microangiopathy. 2
Ophthalmologic Examination
- Fundoscopy is essential to look for bilateral retinal hemorrhages, cotton-wool spots, or papilledema (grade III-IV retinopathy), which define malignant hypertension. 2, 4
Post-Stabilization Workup
After achieving blood pressure control (target 20–25% reduction in MAP within first hour, then gradual normalization over 24–48 hours), systematic screening for secondary causes is mandatory given the 20–40% prevalence. 1, 2
Renal artery duplex ultrasound or CT/MR angiography should be performed to evaluate for renovascular disease. 1
Plasma aldosterone-to-renin ratio and plasma or urine metanephrines should be obtained to screen for primary aldosteronism and pheochromocytoma. 1, 3
Renal ultrasound can identify structural renal disease or asymmetric kidney size suggesting renal artery stenosis. 2
Common Pitfalls to Avoid
Do not assume this is simply "uncontrolled essential hypertension" without excluding secondary causes, as 20–40% of malignant hypertension has identifiable etiologies. 1
Do not delay neuroimaging in a patient with severe headache and this blood pressure; intracranial hemorrhage or stroke must be excluded immediately. 2
Do not overlook medication non-adherence as a contributing factor, though this patient has no prior hypertension diagnosis, making non-adherence less likely as the primary cause. 3
Do not normalize blood pressure too rapidly; excessive drops >70 mmHg systolic can precipitate cerebral, renal, or coronary ischemia, especially given her significant atherosclerotic disease. 2
Do not forget that the 90% carotid stenosis places her at extremely high risk for stroke if blood pressure is lowered too aggressively or if she has concurrent intracranial vascular disease. 2