The Body and the Eye
Inside Hypertension:

The Causes and Consequences of High Blood Pressure

Though hypertension is one of the most common systemic diseases in the United States, a huge number of patients are unaware they have high blood pressure. Even among those correctly diagnosed, most have poorly controlled blood pressure. As a primary care provider, you can help reverse this trend.

Thomas J.W. Stokkermans, O.D., Ph.D.
Cleveland

As providers of the majority of primary eye care in the United States, optometrists have direct impact on their patients’ overall health. We’re often the only health-care provider a patient consults.9 In screening for systemic diseases that have ocular signs and symptoms, we may fill a life-saving role.

This is critical in hypertension, the focus of this, the first installment of our series, “The Body and the Eye.” Future articles will address multiple sclerosis, infectious and inflammatory diseases, thyroid diseases and cardiovascular disorders.

Hypertension, one of the most common systemic disorders in the United States1,2,3 has many ocular sequelae,4 and is associated with a significant risk of death.5,6,7 Diagnosis and referral of hypertensive patients offers opportunities to serve the patient better, and improve inter-professional relations and your image as a health-care provider. You should be able to monitor for ocular and systemic side effects of anti-hypertensive drugs, prescribe ocular medications with drug-interaction profiles in mind, and critically evaluate regimens instituted by other physicians.

Pathophysiology
Ninety percent of hypertensive patients have essential hypertension. The rest mostly have secondary hypertension caused by renal disease. The underlying cause of essential hypertension isn’t clear, but the mechanisms that af- fect blood pressure are known. Anti-hypertensive drugs modulate these mechanisms (see “Commonly Used Anti-hypertensives,” page 82.)

The pumping action of the heart and resistance of the peripheral vasculature determine a person’s blood pressure.11,12 Adrenergic and cholinergic stimuli modulate heart rate and strength of contraction. The action of pressor systems such as the renin-angiotensin-aldosterone system and adrenergic input determine peripheral resistance.11,12

Reduced plasma sodium stimulates the kidneys to produce renin, resulting in conversion of angiotensinogen to angiotensin I. This is in turn converted by angiotensin-converting enzyme (ACE) in the lungs to angioten- sin II, which stimulates aldosterone release from the adrenal glands.11,12 Angiotensin II is a potent vasoconstrictor and causes vascular hypertrophy when chronically elevated, while aldosterone impairs sodium excretion and leads to water retention.8,11,12
Stimulation of the sympathetic nervous system causes the release of the hormones epinephrine and norepinephrine. These hormones cause vasoconstriction, increase the heart rate and stimulate renin release, impair sodium excretion and cause vascular hypertrophy when they are chronically elevated.

Secondary hypertension can be caused by renal vascular stenosis, parenchymal renal disease, renal dysgenesis, primary aldosteronism, pheo- chromocytoma, Cushing’s syndrome, coarctation of the aorta, pregnancy and certain drugs (birth control pills and excessive alcohol consumption).8

While secondary hypertension is less common, it is more likely to result in malignant hypertension, in which hypertension and renal damage augment each other. Malignant hypertension occurs in less than 5 percent of hypertensive patients but requires rapid intervention to prevent death from uremia, cerebral hemorrhage or cardiac failure.12

Treatment
The goal of treatment is to reduce blood pressure to below 140/90mm Hg in all patients. The common approach is called “stepped care,”8 beginning with minimal treatment, followed by more intensive treatment if initial therapy fails.1,8,13 (See “Classification and Management of Blood Pressure in Adults,” page 80.)

Initial steps may entail lifestyle changes only, such as weight loss to within 15 percent of ideal weight, dietary sodium restriction to 4g of salt daily, moderation of alcohol intake to below 1 ounce daily, isotonic exercise, biofeedback/relaxation training, and potassium, calcium and magnesium supplementation.8

If the patient doesn’t make lifestyle changes or they fail to control blood pressure, the patient will likely receive drug therapy for life. Monotherapy controls mild hypertension for about 50 percent of patients; a combination of two drugs pushes this rate to 90 percent.

But half of hypertensives discontinue their medications within the first year of diagnosis.8 Non-compliance is often due to undesired side effects, so we must be alert for patients’ comments regarding these.

Drugs usually used first for controlling hypertension are diuretics, beta-blockers, calcium channel blockers and ACE inhibitors. The direct vasodilators and central alpha agonists are only recommended in combination with other drugs, because they are associated with pseudotolerance (induction of sympathet- ic nervous system and of fluid retention with long-term use).1,2,8,13 Some first-line drugs may be contraindicated. Others may be preferred with specific health conditions. For example in a type I diabetic patient, both beta-blockers and diuretics have undesired side effects, so ACE inhibitors are often used as first-line medications (Table 2).5,8 It often takes more medication to bring blood pressure under control initially than to maintain long-term control, so the number and dosage of drugs may be les- sened as time goes on. This is called “step-down therapy.”8

Ocular Signs and Symptoms
Hypertension can be the direct cause or a risk factor for a wide variety of ocular problems. Hypertension can directly cause angiopathy, retinopathy, choroidopathy and neuropathy. (figure 1) The Keith-Wage- ner-Barker grading system, probably the most common, describes hypertension-induced angiopathy, retinopathy and neuropathy (but not choroidopathy). This system designates four grades of hypertensive fundus presentations:

• Grade 1, hypertensive retinopathy with mild arteriolar attenuation.
• Grade 2, severe attenuation with focal constriction.
• Grade 3, all the signs of grade 2 plus the presence of hemes (generally flame-shaped), and soft and hard exudates.
• Grade 4, all the signs of grade 3 with optic nerve edema.14

Occasionally optic nerve edema occurs in the absence of other hypertensive fundus changes.15 Hypertensive fundus changes are interpreted separately from changes caused by arteriolosclerosis, which has its own grading scales.

Measurement of the artery-to-vein ratio is widely used as an indicator of hypertension and arteriolosclerosis, but this is not an accurate method. The venous column can vary widely in thickness, and in the elderly arteriolosclerosis resists and masks hypertensive arteriolar constriction.

When interpresting retinopathy, remember that hypertension primarily affects the superficial capillaries and cause flame-shaped hemorrhages and soft exudates. In the presence of longstanding, severe hypertension the deeper retinal vascular layers also become involved and changes such as dot-blot hemorrhages and venous stasis are evident.(Figure 2)

Other retinal changes from hypertension are focal intraretinal periarteriolar transudates (FIPT). Focal vessel permeability causes these dull white, round to oval areas of exudate in the deep retinal layers of the posterior pole.9

Characteristic presentations of hypertension-induced fundus changes include:
Hypertensive choroidopathy. This typically presents in patients with an acute rise in blood pressure. Possible causes: eclampsia, renal diseases, pheochromocytoma, connective tissue disease, and accelerated essential hypertension. Manifestations include Elschnig spots, Siegrist streaks, macula stars and focal serous retinal detachments.

Elschnig spots and Siegrist streaks are infarcts of the choroidal vasculature. The former are pale white or reddish areas of outer retina overlying an ischemic lobule of the choriocapillaris, and often develop a pig- mented center with chronicity. Siegrist streaks appear in equatorial regions, radiate out from the optic nerve and consist of pigmentation arranged along the course of a choroidal vessel. Elschnig spots provide evi- dence of acute episodes of hypertension; Siegrist streaks indicate chronic disease and may carry a poorer prognosis for life.

A macula star is a ring of exudate in Henle’s nerve fiber layer that forms secondary to blood-vessel leakage. A partial macula star generally forms in the presence of focal leakage of plasma, as can occur with Coat’s syndrome, macroaneurysm, optic neuritis and optic neuropathy.

Focal retinal detachments can also occur in conjunction with choroidopathy and are usually associated with an underlying choroidal infarct. A serous macular detachment can occur when diffuse choroidal ischemia exists, causing acute visual loss. Many of these changes are reversible with successful blood-pressure control.9,14

Hypertensive neuropathy. A form of anterior ischemic optic neuropathy, this is always bilateral and can present either with mild swelling or with severe swelling and peripapillary hemes. (Figure 3) Accelerated hypertension describes cases in which grade 3 hypertensive fundus changes are found.
Malignant hypertension. This is where grade 4 changes are found. It was once thought that the presence of optic nerve swelling (malignant hypertension) predicts poor survival as compared to grade 3 hypertensive retinopathy (accelerated hypertension). It is now generally accepted that patients with accelerated and malignant hypertension have an equal prognosis.

In severe malignant hypertension, cerebral ischemia and edema (hypertensive encephalopathy) may occur, leading to papilledema from raised intracranial pressure. These patients are in mortal danger and not likely to see an optometrist. Acute and severe headaches, nausea and vomiting are rapidly followed by loss of consciousness.9,14 Doctors often reduce their blood pressure rapidly to avoid end organ damage. This rapid drop carries a high risk of ischemic infarcts of the brain and optic nerve.

Related Conditions
Low vision specialists may be sought out when a hypertensive stroke causes a visual deficit such as a homonymous hemianopia or visual neglect. Treatment with optical devices can be effective.16 However, the patient with homonymous hemianopia may respond differently than one with visual neglect, because the latter ignores images in real space projected from the neglected field even when they are projected into the “seeing” field. Hemianopic patients won’t have this problem.17
Patients with hypertension have a higher risk of developing a central retinal vein occlusion and/or branch retinal vein occlusions, depending on the severity of hypertension.

Patients with a CRVO have a higher chance of ischemia and of the second eye having a CRVO in their lifetimes.18,19,20 However, patients with hypertension and a CRVO have no higher mortality rate than those with hypertension alone.21

There is also evidence that amount and type of arteriovenous crossing puts an eye at risk for BRVO.23,24 As both hypertension and arteriolosclerosis induce arteriovenous crossing changes, direct compression of the vein by the artery may predispose the vein to occlusion.

Hypertensive patients are at 2.6 times higher risk than non-hypertensives for hemiretinal vein occlusions.25 Hypertension also increases the risk for retinal macroaneurysm threefold, while the presence of a vein occlusion increases the risk 12-fold.26 (Figure 5)

Non-arteritic anterior ischemic optic neuropathy may be related to atherosclerotic changes of optic nerve head circulation in association with hypoperfusion. Many sources correlate hypertension with NAION, and hypertensive optic neuropathy is thought to be a form of NAION, but there’s no evidence that hypertension is a risk for NAION. Diabetes, but not hypertension, is a risk factor for NAION.27 However, hypotension at night and early in the morning may play a role in NAION, and may put patients who are over-treated for hypertension at increased risk.28

Ischemic palsies of cranial nerves 3, 4 and 6 have been reported to be more prevalent in hypertensive patients.29,30 (Figure 8) One study found that along with diabetes, left ventricular hypertrophy (but not hypertension) was an independent risk factor for cranial nerve palsies.31 Since left ventricular hypertrophy is a sign of hypertensive end organ damage, hypertension may play a role in ischemic cranial nerve palsy. Most ischemic palsies recover within three months. While incidence of sinister etiologies (e.g. aneurysm, tumor) is low, rule these out first.

We play an important role in the management of our hypertensive patients. We are able to look in the eyes of these patients and directly observe evidence of hypertension. We can also easily incorporate sphygmomanometry and questions pertinent to hypertension into our exam. The toll from inadequate blood pressure control reinforces the need for all providers to do their part and be especially attentive to this silent systemic disease.

Dr. Stokkermans is a staff optometrist with Uni- versity Ophthalmologists Inc. and on faculty at the Case Western Reserve University School of Medicine. He acknowledges expert assis- tance of Sonia Sharma in preparation of the manuscript.

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