Endocrinology Internal Medicine

Malignant Hypertension

Malignant Hypertension

Introduction – Malignant Hypertension

Malignant hypertension is a severe form of primary, but more commonly, secondary hypertension. Patients have definite ocular abnormal findings (hypertensive retinopathy) and/or renal involvement (fibrinoid necrosis). The condition, which is now uncommon, leads to early and severe cardiac, cerebrovascular and renal complications without adequate treatment. You usually see very high blood pressure levels.

Causes

Untreated primary hypertension may be the cause, but most often malignant hypertension has secondary causes such as renal artery stenosis or other kidney diseases, primary hyperaldosteronism (eg Mb Conn) or pheochromocytoma. No uniform etiology can be identified. The renin-angiotensin-aldosterone system is extensively activated, which is thought to cause the advanced vessel damage in this condition.

The severe blood pressure causes extensive cardiovascular hypertrophy and kidney damage with proteinuria.


Symptoms and Clinical Findings – Malignant Hypertension

Symptoms

  • Many times mild symptoms in early stages
  • Visual impairments due to papillary edema, which prompts the patient to visit the ophthalmologist
  • Headache, dizziness or nausea
  • The condition is often detected in late stages, after development of heart failure or encephalopathy

Clinical findings

  • Very high blood pressure, usually diastolic >120 mmHg
  • Sometimes encephalopathy with headache, dizziness, visual disturbances, nausea, vomiting
  • Sometimes pulmonary edema, heart failure with ECG signs of left-sided hypertrophy and ischemia
  • Sometimes renal failure with anuria/oliguria, rising s-creatinine. Pathognomonic signs of the condition are retinal abnormalities with bleeding (hypertensive retinopathy 3) and/or papillary edema (hypertensive retinopathy 4)
  • Primary or secondary hyperaldosteronism often gives low potassium

Differential Diagnoses – Malignant Hypertension

  • Severe primary hypertension
  • Rapidly progressing secondary hypertension
  • Increased intracerebral pressure, eg stroke with high blood pressure
  • Intoxicated state – agitated patient
  • Abstinence phase after varying intoxications

Diagnostics 

  • History and physical examination (including eye examination!)
  • Blood pressure in both arms
  • Electrolyte status with S-creatinine, urinalysis, and monitored urine volume
  • ECG
  • S-aldosterone/peripheral renin activity (elevated levels ​​of both)
  • At a later stage, renal vascular doppler as a screening for renovascular hypertension
  • In persistent proteinuria, urography or ultrasound is performed to assess renal parenchyma and flow
  • Possibly, 24-hour catecholamine/urinary VMA

Treatment – Malignant Hypertension

  • Intensive care cases: Immediate treatment aims to moderately reduce the blood pressure within a few hours and to reasonably normal levels in 1-2 days. NOTE: Rapidly resorbable, short-acting calcium antagonists usually cause excessive blood pressure drops.
  • In renal impairment, loop diuretics eg (furosemide (Furix)) are recommended. 40-80 mg (possibly iv administration) together with orally-acting beta-blocker, e.g., metoprolol 100 mg, atenolol 100 mg, or bisoprolol 5-10 mg and orally-acting vasodilator calcium antagonist, eg felodipine 5 mg or amlodipine 5 mg. The latter medications are titrated within 2 days to recommended daily doses. Furosemide can be iterated within an hour. Urine production, as well as blood pressure, is monitored.
  • Inj. of labetalol (Trandate) 5 mg/ml 2-5 ml iv. Can be repeated at 5-minute intervals x 3.
  • ACE blockade should initially be given as a test dose eg 12.5-25 mg captopril PO, which has a short half-life. Pronounced blood pressure reduction suggests renin-dependent hypertension. In long-term treatment, enalapril is usually given 10-20 mg or ramipril 2.5-5 mg PO. Significant blood pressure drops suggest renin/angiotensin-dependent hypertension and/or renal artery stenosis.
  • In severe hypertension, spironolactone is often used in doses of 25-100 mg or eplerenone 50-100 mg as 3rd or 4th agents.
  • In normal kidney function, only beta-blockers + calcium antagonists may be given. The effect is followed. However, thiazide or loop diuretics are usually needed in these cases as well.
  • In the case of intolerance (usually coughing) of ACE blockade, angiotensin receptor antagonists, such as losartan 50-100 mg or candesartan 16-32 mg can be given.
  • Complementary treatment with eg doxazosin 4-8 mg or other alpha antagonists.
  • Often 4-5 medications are required for the chronic blood pressure maintenance of these patients. After the titration phase, fixed combinations are often found to facilitate patient compliance and reduce costs.

Follow-up – Malignant Hypertension

  • Secondary hypertension should be excluded and blood pressure treatment optimized. The prognosis has improved significantly with modern treatment.
  • The overall risk profile is mapped and the patient is motivated for lifelong treatment with pharmaceuticals or curative intervention against the etiology of hypertension.
  • Patients should at least initially be followed up by physicians with cardiovascular expertise.

Further Reading