The fundus exam offers a unique opportunity to assess the state of a patient’s blood vessels.
Systemic hypertension results in chronic changes, known as arteriosclerosis, which vary in severity according to long-term blood pressure control. A fundus examination is therefore an important exam for risk stratification of a patient’s overall vascular risk profile.
Hypertensive retinopathy is the most common ocular presentation of systemic hypertension. Retinal arterioles and capillaries have auto-regulatory mechanisms and tight junctions to maintain the blood ocular barrier. Arterioles respond to elevate luminal pressure (in systemic hypertension) by vascoconstriction in order to reduce intraluminal flow. Sustained raised pressure leads to thickening of the vessel walls with sclerosis and hyalinization. This leads to increased optical density of the retinal blood vessel walls, which on fundus exam appears as sheathing of the vessels (silver-wiring, Figures 1 and 2).
At areas where the arterioles and peripheral veins cross in the retina, the two structures share a common adventitial sheath. The thickening of the arterial wall reduces volume within the adventitial sheath and directly compresses on the vein. This causes the vein to have an hourglass-like constriction at the site of crossing with aneurysm-like dilatation on either side of the crossing (arterio-venous nipping, Figure 3).
Continued chronically elevated intraluminal pressure or sudden and severely elevated intraluminal pressure (as seen in malignant hypertension) eventually causes degeneration of the arteriolar smooth muscles leading to stretching of the endothelium, which eventually breaks, causing haemorrhage and leakage of plasma into the vessel wall. The haemorrhage tends to outline the superficial horizontal nerve fibre layer travelling across the retina, producing flamed-shape haemorrhages (Figure 4). Dot and blot haemorrhages are haemorrhages occurring from smaller arterioles deep within the vertically arranged outer plexiform layer of the retina. Dot and blot haemorrhages predominate in conditions that give predominantly microvascular complications, like diabetes mellitus. Flamed-shape haemorrhages predominate in hypertensive retinopathy. Leaked lipoproteins are often visible on direct fundoscopy as well-demarcated, yellow, shiny deposits known as hard exudates. Haemorrhages and exudates are both signs of extravascular signs of hypertensive retinopathy. Another sign of severe retinopathy is cotton wool spots (Figure 4). These are fluffy, white lesions again found at the superficial horizontal nerve fibre layer. Cotton wool spots reflect swelling of nerve endings due to ischaemia-related dysfunction and thus reduction in their axoplasmic flow. In very severe cases, there is breakdown of the endothelia of the arterioles supplying the optic discs, with leakage and nerve ischaemia. This results in optic disc swelling with peri-papillary haemorrhage and cotton wool spots. If bilateral, this is called papilloedema. A ‘macular star’ (Figure 5) may also be seen in patients with severe hypertensive retinopathy. This is again is due to damage to the retinal artery endothelial wall and subsequent exudation appears in the shape of a star at the macula, owing to its unique distribution of retinal nerve fibres (Henle’s fibres).
There are several methods of grading hypertensive retinopathy, of which the Modified Scheie Classification of Hypertensive Retinopathy is most commonly used:
- Grade 0 – No changes
- Grade 1 – Barely detectable arterial narrowing (silver wiring, Figures 1 and 2)
- Grade 2 – Obvious arterial narrowing with focal irregularities (arterio-venous nipping, Figure 3)
- Grade 3 – Grade 2 plus retinal haemorrhages and/or exudates (Figure 4)
- Grade 4 – Grade 3 plus disc swelling
A diagnosis of malignant hypertension requires evidence of end-organ damage. Retinal findings of end organ damage require at least Grade 3 hypertensive retinopathy.