🚨 Hypertensive retinopathy… for the nephrologist

Manifestations of hypertensive retinopathy may be caused by either an acute rise in blood pressure or chronically elevated blood pressure, which may be the result of essential or secondary hypertension. The primary response of the retinal arterioles to systemic hypertension is vasoconstriction; this is less marked in older individuals due to involutional sclerosis conferring increased rigidity.

Markers of preclinical systemic disease.

  • Reduced retinal arteriolar calibre is an early pre-hypertensive sign and if identified should prompt BP monitoring.
  • Wider venular calibre is also relatively specific for impaired glucose metabolism.
  • Increased venular tortuosity can be associated with chronic hypertension and pre-hypertension, though evidence on arteriolar tortuosity is conflicting — straightening of arterioles has been reported in some studies. Numerous other causes of retinal vascular tortuosity have been described, notably conditions associated with high and low vascular flow.
A variety of grading systems have been proposed for hypertensive retinopathy in an attempt to classify its severity.

Keith, Wagener, and Barker (Am J Med Sci 1974) developed a grading system of increasing severity. Unfortunately under this classification system, the early stages of hypertensive retinopathy were not well delineated.

Wong & Mitchell (NEJM 2004) evaluated population-based data and developed a simplified prognosis-based classification of different clinical signs.

Chronic HTN: Arteriovenous crossing changes (“AV nicking”), retinal arteriolar sclerosis (“copper” or “silver” wiring), cotton-wool spots, flame-shaped hemorrhages, arterial macroaneurysms, central or branch occlusion of an artery or vein. Rarely, neovascular complications can develop.

Acute (“malignant”) HTN: Is tipically seen in patients with BP>200/100mmHg causing direct damage to retinal and choroidal vasculature (fibrinoid necrosis) and subsequently ischemic necrosis. This manifests as hard exudates often in a “macular star” configuration, papilledema (leakage from arterioles supplying optic disk), cotton-wool spots (ischemia to nerve fibers), flame-shaped hemorrhages (necrosis, bleeding), optic nerve head edema. Rarely serous retinal detachment (damage/exudation in choroid/retinal pigment epithelium) or vitreous hemorrhage. Areas of focal chorioretinal atrophy [from previous choroidal infarcts (Elschnig spots)] are a sign of past episodes of acute HTN.

Hypertension as a risk factor in ocular disease

Retinal vein occlusion, Retinal emboli, Retinal artery occlusion, Retinal macro aneurysm, Ischemic optic neuropathy, Diabetic retinopathy.

Ocular diseases where hypertension is a potential risk factor

Age-related macular degeneration, Glaucoma.

Prognostic Value of Change

No data are available whether treatment-induced regression of retinal alterations is related with reduction of other target-organ damages (e.g., left ventricular hypertrophy) or incident CV outcomes. So far, only epidemiological studies uniformly found that qualitative retinal signs of hypertensive retinopathy are related with incidence of CV disease.

Risk assessment by retinal examination

Thanks to @swissnephro to point out this chapter from Sapira’s Art and Science of Bedside Diagnosis, based on the findings of the paper “An internist looks at the fundus oculi”, here the abstract link, https://www.ncbi.nlm.nih.gov/pubmed/6389065