Hypertension Blog

The signs and symptoms of hypertensive encephalopathy result from a rapid increase in diastolic blood pressure to more than 140 mm Hg and the abrupt onset of hypertension in a patient with no history of hypertension or in one with well-controlled hypertension.

Initially, your patient may complain of a severe, generalized headache and restlessness. This may progress to nausea and projectile vomiting. His neurologic signs and symptoms may include confusion, drowsiness, stupor, and generalized tonic­clonic or focal seizures. Because the encephalopathy results from emergency hypertension, he also may exhibit signs of impaired cardiovascular and renal function, such as myocardial ischemia and a decreased glomerular filtration rate.

Retinal damage also can result from hypertensive encephalopathy. An ophthalmic examination may reveal retinal hemorrhages, exudates, and papilledema-a condition known as grade I.V. hypertensive retinopathy.

Only 5% or fewer hypertensive patients have secondary hypertension. If a patient over age 50 suddenly develops hypertension, especially if it’s severe, suspect a secondary cause, such as a disease that increases cardiac output (CO) or peripheral vascular resistance. After the cause has been identified and treated, generally with surgery or drug therapy, the patient’s blood pressure should return to normal.

To identify the cause of secondary hypertension, a physician will order a basic workup that evaluates a patient’s cardiac system. Abnormalities in these systems commonly cause hypertension in young hypertensive patients, severely hypertensive patients, and hypertensive patients who don’t respond to standard antihypertensive therapy.

Cardiovascular Disorders

Coarctation of the aorta, a localized narrowing or constriction of the lumen of the aorta, is a vascular defect that commonly causes hypertension. Generally, the disorder is diagnosed in children.

Coarctation may occur anywhere along the aorta, but it most commonly occurs just beyond the origin of the left subclavian artery. When the condition is severe, the constriction of the lumen produces absent or markedly diminished femoral pulses as well as bruits heard throughout the posterior thorax.

Coarctation of the aorta can be detected by carefully timing the appearance of the patient’s femoral pulse with his radial or brachial pulse to determine if a substantial delay exists between pulses. If so, the patient’s blood pressure should be taken in both arms and his legs. The blood pressure of a patient with coarctation of the aorta will be elevated in the arms and reduced in the legs.

Surgical repair is usually required to correct coarctation of the aorta. Following surgical repair, only 5% to 10% of patients still have hypertension.

Subclavian artery stenosis also causes hypertension. If a patient has subclavian artery stenosis, his pulse in one arm will be absent or significantly diminished, and his blood pressure in that arm will be significantly lower than in his other arm.

Renal Disorders

Renovascular stenosis is the most common cause of hypertension that can be reversed by surgery or percutaneous trans luminal angioplasty. Stenosis of one or both renal arteries can produce severe hypertension and a loss of kidney function. Arterial fibromuscular dysplasia, fibrosis of the muscular layer of the artery wall, is the most common cause of renovascular hypertension in patients under age 40; atherosclerosis is the most common cause of renovascular hypertension in older patients.

Systolic bruits in the upper abdominal quadrants may indicate renovascular stenosis or renal arteriovenous malformation. If the bruit is continuous and extends into diastole, the stenosis is severe.

Hypertension can also result from renal parenchymatous disease, a consequence of acute and chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney disease, collagen vascular disorder, intercapillary glomerulosclerosis, and interstitial nephritis. Many hypertensive patients with renal parenchymatous disease develop chronic renal failure. Generally, the treatment of choice for their condition is a diuretic and a diet limiting them to a daily intake of 2 grams of sodium and 40 to 50 grams of protein. Eventually, these patients may also need dialysis.

Though rare, renin-producing tumors also cause hypertension. These tumors, includingWilms’ tumor found in infants and children, arise from either the cortex or pelvis of the kidney and may be benign or malignant. The malignant form is more common, and the treatment is usually radical nephrectomy and, possibly, radiation therapy.

Neurologic Disorders

A patient who has sustained a spinal cord injury above the T7 level is at risk for hypertension because of autonomic hyperreflexia, a potentially life-threatening complication resulting from the sympathetic neurons’ loss of control over their sympathetic outflow. Stimulation of nerves below the injury, such as from fecal impaction, urine retention, or tactile stimulation, can cause reflex sympathetic activity along the spinal cord resulting in hypertension, bradycardia, severe headache, sweating, blurred vision, a flushed feeling, and nasal congestion. Any quadriplegic who complains of a headache should have his blood pressure promptly checked to determine if hypertension exists as a possible result of autonomic hyperreflexia.

When a patient with a spinal cord injury develops hypertension, his systolic blood pressure may rise to 300 mm Hg, and if the condition is left untreated, he may have a CVA or die. Treatment of autonomic hyperreflexia consists of immediately removing the source of the nerve stimulation, such as bladder distention. If the patient’s hypertension persists, his physician may prescribe antihypertensive drugs.

Patients with brain injuries are also at risk for hypertension. When a patient’s brain is injured, his intracranial pressure increases, and the blood volume and flow to his brain becomes passively controlled by the pressure in his systemic circulation. So a patient who sustains a brain injury has an elevated blood pressure because of the autoregulatory and compensatory mechanisms within the brain trying to maintain optimal cerebral perfusion pressure.