Hypertensive retinopathy

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Hypertension may lead to multiple adverse effects to the eye. Hypertension can cause retinopathy, optic neuropathy, and choroidopathy,. This article focuses upon hypertensive retinopathy, which is the most common ocular presentation, but also includes hypertensive optic neuropathy and choroidopathy.

Contents

Disease Entity

Disease

Hypetensive retinopathy includes two disease processes. The acute effects of systemic arterial hypertension are a result of vasospasm to autoregulate perfusion[1]. The chronic effects of hypertension are caused by arteriosclerosis and predispose patients to visual loss from vascular occlusions or macroaneurysms[2].

Etiology

The arteriosclerotic changes of hypertensive retinopathy are caused by chronically elevated blood pressure, defined as systolic greater than 140 mmHg and diastolic greater than 90 mmHg[2]. Hypertension is usually essential and not secondary to another disease process. Essential hypertension is a polygenic disease with multiple modifiable environmental factors contributing to the disease. However, secondary hypertension can develop in the setting of pheochromocytoma, primary hyperaldosteronism, cushing’s syndrome, renal parenchymal disease, renal vacular disease, coarctation of the aorta, obstructive sleep apnea, hyperparathyroidism, and hyperthyroidism[3].

Risk Factors

Risk factors for essential hypertension include high salt diet, obesity, tobacco use, alcohol, family history, stress, and ethnic background. The major risk for arteriosclerotic hypertensive retinopathy is the duration of elevated blood pressure. The major risk factor for malignant hypertension is the amount of blood pressure elevation over normal.

General Pathology

Arterioles respond to elevated luminal pressure by vasoconstriction to reduce flow. Pathology develops when the increased pressure causes endothelial damage. Degeneration of the arteriolar smooth muscle leads to stretching of the endothelium, breaks, and leakage of plasma into the vessel wall. Plasma clotting within the vessel wall produces mural thickening and luminal narrowing. This process is called fibrinous necrosis[4].

Pathophysiology

Retinal hemorrhages (Figure 1-3) develop when necrotic vessels bleed into either the nerve fiber layer (flame shaped hemorrhage) or the inner retina (dot blot hemorrhage). Cotton wool spots (Figure 1 & 3) are caused by ischemia to the nerve fiber layer secondary to fibrinous necrosis and luminal narrowing. Ischemia to the nerve fibers leads to decreased axoplasmic flow, nerve swelling, and ultimately fluffy opacification. Exudates (Figure 2) occur later in the course of disease, surrounding areas of hemorrhage, as a result of lipid accumulation. Papilledema (Figure 3) is a result of both leakage and ischemia of arterioles supplying the optic disc that undergo fibrinous necrosis. Ischemia causes optic nerve swelling and blurred disc margins, while leakage causes hemorrhage and disc edema[4].


Primary prevention

Routine blood pressure monitoring and treatment will prevent hypertensive retinopathy from developing.

Diagnosis

Hypertensive retinopathy is diagnosed based upon its clinical appearance on dilated fundoscopic exam and coexistent hypertension.


History

The history should focus upon the hypertension disease history, symptoms of hypertension, and history of its complications. To gauge hypertension disease severity, patients should be asked about their severity and duration of hypertension, and about the medications taken as well as compliance. Symptoms of hypertension to ask about include headaches, eye pain, reduced visual acuity, focal neurological deficits, chest pain, shortness of breath, dyspnea on exertion, paroxysmal nocturnal dyspnea, orthopnea, and palpitations. Patients should be asked about the complications of hypertension, including history of stroke or transient ischemic attack, history of coronary or peripheral vacular disease, and history of heart failure[3].


Physical examination

The physical exam on a patient with hypertension includes vital signs, cardiovascular exam, pulmonary exam, neurological exam, and dilated fundoscopy. Vital signs should obviously focus on blood pressure. Key elements of the cardiovascular exam include heart sounds (gallops or murmurs), carotid or renal bruits, and peripheral pulses. Pulmonary exam can identify signs of heart failure if rales are present. Signs of cerebral ischemia can be detected by a good neurological exam[3]. And finally, dilated fundoscopic exam is necessary for staging of hypertensive retinopathy.

Signs

The signs of malignant hypertensive retinopathy include constricted and tortuose arterioles, retinal hemorrhage (Figure 1-3), hard exudates (Figure 2), cotton wool spots (Figure 1 & 3), retinal edema, and papilledema (Figure 3). The signs of chronic arterial hypertension in the retina include widening of the arteriole reflex, arteriovenous crossing signs, and copper (Figure 1 & 3) or silver wire arterioles (copper or silver colored arteriole light reflex)[1]. Hypertension causes choroidopathy. Poor perfusion of the choriocapillaris causes Elschnig spots, defined as hyperpigmented patches in the choroid surrounded by a ring of hypopigmentation. Siegrist streaks can also be found, defined as linear hyperpigmented lesions over choroidal arteries. Hypertensive choroidopathy can cause a focal pigment epithelium detachment, leading to exudative retinal detachment2. Hypertension may lead to optic neuropathy (Figure 3). The signs of optic neuropathy include flame shaped hemorrhages at the disc margin, blurred disc margins, congested retinal veins, papilledema, and secondary macular exudates[2].


Symptoms

Acute malignant hypertension will cause patients to complain of eye pain, headaches, or reduced visual acuity[1]. Chronic arteriosclerotic changes from hypertension will not cause any symptoms alone. However, the complications of arteriosclerotic hypertensive changes will cause patients to present with the typical symptoms of vascular occlusions or macroaneurysms.

Clinical diagnosis

The signs of malignant hypertension are well summarized by the Modified Scheie Classification of Hypertensive Retinopathy[2]: Grade 0: No changes Grade 1: Barely detectable arterial narrowing Grade 2: Obvious arterial narrowing with focal irregularities (Figure 1) Grade 3: Grade 2 plus retinal hemorrhages, exudates, cotton wool spots, or retinal edema (Figure 3) Grade 4: Grade 3 plus papilledema (Figure 4)

The signs of chronic arteriosclerotic hypertension are also summarized by the Scheie Classification[1]. Stage 1: Widening of the arteriole reflex Stage 2: Arteriovenous crossing sign (Figure 3) Stage 3: Copper-wire arteries (copper colored arteriole light reflex) Stage 4: Silver-wire arteries (silver colored arteriole light reflex)


Diagnostic procedures

Fluorescein angiography (FA) during acute malignant hypertension will demonstrate retinal capillary nonperfusion, microaneursym formation, and a dendritic pattern of choroidal filling in the early phase. In the late phase, diffuse leakage will be seen[2]. Indocyanine green angiography during malignant hypertension will show a moth eaten appearance of the choriocapillaris[2]. Fluorescein angiography can demonstrate hypertensive choroidopathy. FA will show focal choroidal hypoperfusion in the early phases and subretinal leakage in the later phases[2].


Laboratory test

Laboratory tests are not routinely helpful for the diagnosis of hypertension. Laboratory tests can be useful for risk stratification and monitoring of complications. These tests include echocardiography, electrocardiography, serum electrolytes, serum creatinine, urinalysis, fasting lipid profile, serum glucose, and hemoglobin A1C. If secondary hypertension is suspected possible workup includes chest x-ray (coarctation of the aorta), dexamethasone suppression test or urinary cortisol (cushing’s syndrome), plasma renin to aldosterone ratio (primary hyperaldosteronism), plasma and urine metanephrines (pheochromocytoma), angiography (renal vascular disease), serum creatinine and urinalysis (renal parenchymal disease), serum calcium and parathyroid hormone level (hyperparathyroidism), thyroid stimulating hormone (hyperthyroidism), and sleep study (obstructive sleep apnea)[3].

Differential diagnosis

The differential for hypertensive retinopathy with diffuse retinal hemorrhage, cotton wool spots, and hard exudates includes most notably diabetic retinopathy. Diabetic retinopathy can be distinguished from hypertensive retinopathy by evaluation for the individual systemic diseases[1]. Other conditions with diffuse retinal hemorrhage that can resemble hypertensive retinopathy include radiation retinopathy, anemia and other blood dyscrasias, ocular ischemic syndrome, and retinal vein occlusion.


Management

The treatment for hypertensive retinopathy is primarily focused upon reducing blood pressure.

General treatment

The treatment for malignant hypertensive retinopathy is to reduce the systemic blood pressure below 140/90 mmHg. This can be accomplished by any of the armamentarium of medical treatments for hypertension. Medical treatment can only treat the acute changes of hypertension from vasospasm and vascular leakage. There is no treatment for arteriosclerotic changes of chronic hypertension1.

Medical therapy

Drugs that are commonly used in the outpatient setting to reduce blood pressure include angiotensin converting enzyme inhibitors, calcium channel blockers, diuretics, and -adrenergic blockers. Other less commonly used medications include -adrenergic blockers, direct vasodilators, and central 2-adrenergic agonists.

Medical follow up

Follow up is dependent upon the degree of hypertension and resistance to medications. Close contact is essential between the ophthalmologist and the primary care physician for consistent follow up individually tailored to each patient.

Surgery

There is no surgical treatment for essential hypertension nor the ocular complications. In cases of secondary hypertension surgical treatment may be effective, depending upon the etiology.


Complications

Hypertension predisposes patients to many other retinal vascular diseases including central or branch retinal artery occlusion, central or branch retinal vein occlusion, and retinal arterial macroaneurysms. Ischemia secondary to vascular occlusions can cause neovascularization, vitreous hemorrhage, epiretinal membrane formation, and tractional retinal detachment. Hypertension also leads to more advanced diabetic retinopathy progression2. Hypertensive optic neuropathy can cause chronic papilledema, leading to optic nerve atrophy and severe loss of visual acuity[1].

Prognosis

Patients with severe hypertensive retinopathy and arteriosclerotic changes are at increased risk for coronary disease, peripheral vascular disease, and stroke. Since arteriosclerotic changes in the retina do not regress, these patients remain at increased risk for retinal artery occlusions, retinal vein occlusions, and retinal macroaneurysms. Most retinal changes secondary to malignant hypertension will improve once blood pressure is controlled. Damage to the optic nerve and macula, however, could cause long term reductions in visual acuity.


Additional Resources

http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001994/

http://en.wikipedia.org/wiki/Hypertensive_retinopathy

http://www.nlm.nih.gov/medlineplus/ency/article/000999.htm

http://emedicine.medscape.com/article/1201779-overview

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 Lang, G.K. Ophthalmology: A Pocket Textbook Atlas (Thieme, Stuttgart, 2007).
  2. 2.0 2.1 2.2 2.3 2.4 2.5 2.6 AAO. in Basic and Clinical Sciences Course (Lifelong Education for the Ophthalmologist, San Fransisco, CA, 2006).
  3. 3.0 3.1 3.2 3.3 Katakam, R., Brukamp, K. & Townsend, R.R. 2008. What is the proper workup of a patient with hypertension? Cleve Clin J Med 75: 663-72.
  4. 4.0 4.1 Garner, A. & Ashton, N. 1979. Pathogenesis of hypertensive retinopathy: a review. J R Soc Med 72: 362-5.

Grosso, A., Veglio, F., Porta, M., Grignolo, F.M. & Wong, T.Y. 2005. Hypertensive retinopathy revisited: some answers, more questions. Br J Ophthalmol 89: 1646-54.

Original article contributed by: Judy E. Kim, MD
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