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8.5 Fundus Signs ofArteriolosclerosis andHypertension

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Fig. 8.1 Luminal surface of human abdominal aorta stained with Sudan IV (fat stain) showing patchy atherosclerotic lesions. Red staining indicates fatty streaks and atherosclerotic plaques, and shiny whitish patches are calcied plaques. (Image courtesy of Prof Anjali Agarwal, Department of Anatomy, Postgraduate Institute of Medical Education and Research, Chandigarh and Prof Daisy Sahni, Ex-Professor, Department of Anatomy, Postgraduate Institute of Medical Education and Research, Chandigarh)

up to 2/3 of people above the age of 65years. Nearly 90% of the patients with hypertension are due to arteriolosclerosis changes in the arterioles. The retinal arteries and arterioles also become increasingly non-compliant to the variations in blood pressure [20]. Once patients develop chronically elevated blood pressure (Primary or essential hypertension), the process gets accelerated, retinal arteriolar walls thicken, lose transparency, and show an increasing wall-to-lumen

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ratio. Apart from ageing and hypertension, there are several other preventable risk factors, such as diabetes, smoking, obesity, and sedentary life, that accelerate all types of arteriolosclerosis.

8.5 Fundus Signs ofArteriolosclerosis andHypertension

Since the retinal vessels could have been seen with the direct ophthalmoscope more than 160 years ago, the retinal arterioles have fascinated physicians to see if the retinal arterioles reected the changes due to elevated blood pressure among other systemic vascular diseases. There is strong evidence that in patients with long-standing hypertension, the retinal arterioles undergo similar arteriolosclerotic changes as elsewhere in the body and the brain. Before effective pharmacotherapy for hypertension, retinal changes in high uncontrolled hypertension were used as a prognostic tool for the survival of the patients [21, 22]. See Box 8.4. To date, arteriolosclerosis is clinically best studied in the retinal arterioles. Using various digital fundus imaging tools, it is now possible to objectively record and document the retinal arteriolar changes and blood ow non-invasively and repetitively over the long term. Semiautomatic soft wares and articial intelligence-based microvascular analysis tools

Box 8.4 Keith, Wagener, and Barker Classication of Hypertensive Retinopathy

Grade of retinopathy Fundus signs

1 Mild to moderate diffuse

arteriolar narrowing

2 Denitive focal arteriolar

narrowing and AV nicking

3 Signs in grade 2 with retinal

haemorrhages, cotton wool spots, hard exudates

4 All the signs in grade 3 with

papilloedema±retinal detachment

Reference: Chen etal. [24]

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8 Retinal Arteriolar Changes inHypertension andArteriolosclerosis

have been developed to measure with great accuracy the changes reected in the eye that, in the near future, could predict the end-organ damage before it manifests clinically and gets incorporated into the algorithms for cardiovascular risk assessment [23]. See Box 8.5.

Box 8.5 Systemic Consequences of Uncontrolled Hypertension

Classication of hypertension

Wong and Mitchell

Mild 1–2 Microalbuminuria;

Moderate 3 Aortic arch calcication

Severe 4 Acute renal failure,

KeithWagnerBarker

Target organ damage

increased media to lumen ratio in arterioles; TIA; LVH; RAM; BRVO; RAO Carotid stiffness and carotid wall thickness in <55years of age Untreated ve-year survival 70% in grade 1 and 50% in

grade 2 Seven-year incident chronic heart failure 8%

Lunar infarcts, chronic/

ESRD

Stroke Increased carotid intimamedia thickness in <60years Untreated 5-year survival

20% Seven-year incident chronic heart failure 18%

encephalopathy, blindness, death Untreated ve-year survival

***

8.5.1 Enhanced Central Light Reex

Arteriolosclerosis is visible on ophthalmoscopy as a widening of the light reex on the retinal arterioles. The increased central light reex on ophthalmoscopy is a simple clinical clue to the possible underlying hypertension. In a Japanese non-diabetic population above the age of 35years, the enhanced arterial reex was seen in

18.7% [33]. Interestingly, the prevalence of the

enhanced central light reex was seen to decrease with increasing age, from 36% in the youngest (<60 years) to ~19% in the oldest (>80 years); however, the markedly increased light reex when noted was associated with higher mean blood pressure, glucose, and alcohol intake, all well-known risk factors for arteriolosclerosis [34]. Compared to the retinal veins, the central light reex is of higher intensity in the retinal arterioles and more intense in the larger than, the smaller arterioles [35]. In the late nineteenth century, much debate and experimentation centred on the possible mechanisms involved in this phenomenon, concluding that the light reected from the vessel walls is responsible for the central light reex in both the retinal arteries and the veins [36]. More recently, Adaptive optics scanning laser ophthalmoscopy has revealed the arterial light reex to arise from three components, namely, the peripheral smooth plasma ow, the structural irregularity of the arterial wall, and the irregularities of the RBCs owing in the centre of the blood column [37]. Semiautomatic software has been developed to reliably measure the ratio of retinal arteriolar diameter and central light reex to study the associations of retinal arterioles with systemic diseases [38].

TIA transient ischaemic attacks, LVH left ventricular hypertrophy, RAM retinal artery macroaneurysms, BRVO branch retinal vein occlusion, RAO retinal artery occlusion, ESRD end-stage renal disease

Source of information: * Unger etal. [25,

26], ** Cuspidi et al. [27],

[28], ! Aissopou etal. [29], # Adar etal. [30],

Wong and Mitchell [31], $ Zhang etal. [32]

***

Wong et al.

8.5.2 Arterial Wall-to-Lumen Ratio

As stated above, hypertension leads to vascular remodelling resulting in hypertrophy of the tunica media’s bromuscular layer, increasing the width of the arterial wall, thus increasing the wall-to-lumen ratio of the arterioles (Fig. 8.2). Small decreases in the lumen of the peripheral arteries are responsible for the increased periph-

8.5 Fundus Signs ofArteriolosclerosis andHypertension

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Fig. 8.2 Fundus of the right eye of a patient with hypertension, showing an increased wall-to-lumen ratio in the arteries (black arrows), tapering of blood column on either side of the crossing (Gunn’s sign, blue arrows), copper wiring (arterioles appear ‘orange or yellow’ instead of ‘red’) (black arrows) due to increased reectance of light caused by wall thickening, and silver wiring (arterioles appear white as they become occluded) (yellow arrows)

eral resistance and have long-term cardiovascular consequences. Antihypertensive therapy may reverse some of these changes in small arteries and arterioles [39]. Using Doppler scanning owmeter and automatic full-eld perfusion image analysis, patients with a history of past cerebrovascular events showed the highest wallto- lumen ratio (0.46±0.08), followed by patients with poor blood pressure control (0.40 ± 0.13) that was signicantly higher than the normal controls (0.35 ± 0.12) and successfully controlled hypertensive patients (0.31 ± 0.13). Measuring the wall-to-lumen ratio is thus emerging as an interesting tool to see the efcacy of antihypertensive treatment and predict the long-term consequences of continued or inadequately treated hypertension [40].

8.5.3 Arteriovenous Nicking (AVN)

In the retina, the retinal arterioles cross the retinal veins and share a common adventitial sheath at the crossing site. These crossings are most common in the temporal retina and are more frequent in the

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superior than the inferior retina. As the vessel walls are transparent in healthy young persons, the arterioles do not obscure the venous blood column. However, as the retinal arterioles start developing arteriolosclerosis due to chronically elevated blood pressure, the arteriolar walls progressively lose their transparency, get opacied, and may be seen as a copper or a silver wire (Figs.8.2 and 8.3). In chronic hypertension, the hardened arterioles progressively compress the underlying vein, which may show tapering of the blood column on either side of the crossing (Gunn’s sign) (Figs.8.2 and

8.4). In more severe cases, the arterioles show an

‘S-shaped’ deection in their course (Salus sign) (Figs.8.2, 8.4, and 8.5). The AVN and opacication of the arterioles have been long predictors of terminal organ damage and cardiovascular disease [41]. Notably, the AVN and opacication of the retinal arterioles are a legacy of past elevated blood pressure and represent the cumulative damage sustained over a long time. These changes do not regress with the control of hypertension and do not refer to the current control status [41, 42].

8.5.4 Focal andDiuse Narrowing oftheRetinal Arterioles

Whenever there is an elevation of blood pressure, the autoregulatory response of the retinal arterioles dictates the narrowing of the retinal arterioles by the contraction of the circumferentially oriented smooth muscle cells in the tunica media. Clinically, the diffuse narrowing of the arterioles is compared with the neighbouring retinal veins, which, lacking a robust tunica media, do not show any alterations in their calibre in patients with hypertension (Figs.8.4 and 8.5). The normal retinal arteriole to the corresponding vein ratio is 2:3. More discernible is the focal narrowing of the arterioles. Once the hypertension is controlled, focal narrowing may show a reversal in more than 40% of the patients [42]. The compensated arteriolar wall changes, such as diffuse and focal narrowing of arterioles, AV nicking, and copper wire appearances, are classied as ‘Mild hypertensive retinopathy’ [43].

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Fig. 8.3 Silver wiring of arteries (yellow arrows) as they appear occluded in hypertensive retinopathy (a, b)

8 Retinal Arteriolar Changes inHypertension andArteriolosclerosis

Fig. 8.4 Generalized arterial attenuation, cotton wool spots, Gunn’s sign (blue arrow) and Salus sign (red arrow) seen in right (a) and left (b) eyes of a patient with hypertension

8.5.5 Retinal Haemorrhages, Cotton Wool Spots, andMicroaneurysms

retinal arterioles and AVN may be associated with lacunar infarcts, and retinal haemorrhages and microangiopathy due to diabetes mellitus are associated with cerebral haemorrhage [44]. The

Retinal arterioles in acute hypertension may get overwhelmed, resulting in occlusion of the precapillary arterioles manifesting as supercial ame-shaped and dot and blot haemorrhages, exudation, and cotton wool spots (Figs.8.2 and

8.5). This is classied as ‘Moderate hypertensive

retinopathy’ [43]. Hypertensive retinopathy is a hallmark of decompensated acute hypertension. It is signicantly associated with damage to the kidneys, heart, and brain. The narrowing of the

exudative uid collects in the Henle’s layer, and the lipid deposits form a macular fan (Fig.8.6). Once the blood pressure is controlled, the retinopathy lesions regress over some time (Fig.8.7). Current imaging tools such as optical coherence tomography (OCT) angiography have revealed a state of chronic paracentral acute middle maculopathy (PAMM) by demonstrating a thinner inner nuclear layer and disruption of the outer plexiform layer even before the appearance of

8.5 Fundus Signs ofArteriolosclerosis andHypertension

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Fig. 8.5 Arterial attenuation (black arrows) in both eyes (a, b), cotton wool spots (blue arrows) in right eye (a), and Salus sign (yellow arrow) in left eye (b)

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Fig. 8.6 Macular star (blue arrows) formed by the shape taken by lipid deposits in the Henle’s layer due to collection of exudative uid on this layer in both eyes (a, b)

overt clinical signs of retinopathy or capillary closure in nearly 90% of a small set of patients with mild hypertension [45].

illoedema (optic disc oedema) are labelled as malignant hypertension (Fig. 8.8). Malignant hypertension may occur in poorly controlled patients with primary hypertension or de novo in nearly half of the patients. Hypertension

8.5.6 Optic Neuropathy

The patients who develop an acute and severe rise in blood pressure (accelerated hypertension) (Systolic BP ≥180mm of Hg or diastolic BP of >110mm of Hg or, by some denitions, diastolic BP ≥130mm of Hg) who in addition to extensive retinopathy changes also develop pap-

andChoroidopathy inMalignant Hypertension

complicates nearly 10% of pregnancies, and less than 2% may get complicated by pre-eclampsia/ eclampsia characterized by albuminuria and seizures. These patients have a lower blood pressure threshold for developing malignant hypertension than non- pregnant women. Eclampsia during pregnancy is a leading cause of maternal mortality [46]. Although papilloedema’s exact cause is unknown, ischaemia of the optic nerve head, raised intracranial pres-

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8 Retinal Arteriolar Changes inHypertension andArteriolosclerosis

Fig. 8.7 (a–d) A 48-year-old male with BP 200/120 mmHg presented with bilateral cotton wool spots, retinal haemorrhages, and arterial changes (a, b). At 2 weeks, following control of hypertension (BP 160/90 mmHg), there was partial reversal of fundus changes as seen by a decrease in the cotton wool spots, and exudative subretinal uid leading to macular star for-

sure, and hypertensive encephalopathy may all be contributory factors. It is a life-threatening condition and needs emergency care as untreated. It leads to multiple organ failures, including the kidneys, the heart, and the brain, ultimately leading to death. The blood pressure

mation (c, d). Optical coherence tomography (OCT) images of the same 48-year-old male patient (as in a–d) with BP 200/120 mmHg showing subretinal uid (blue arrows) in right (e) and left (f) eyes at initial presentation. At 2 weeks, following control of hypertension (BP 160/90mmHg), the OCT showed resolution of subretinal uid (yellow arrows; g, h)

must be lowered slowly under direct supervision in the emergency ward (lower BP by 10–20% in the rst hour and 5–15% in the next 24 h) as sudden lowering may lead to infarction of the optic nerve head and lead to ischaemiareperfusion injury in the target end organs.

8.5 Fundus Signs ofArteriolosclerosis andHypertension

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Fig. 8.8 A patient with malignant hypertension presented with extensive retinopathy changes along with optic disc oedema (papilloedema, blue arrows) in both eyes (a, b)

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The term malignant hypertension was coined by Dr. Norman Keith almost 100years ago, who, besides ‘terminal renal insufciency’, also noted on autopsy, diffuse involvement of the arterioles practically in all the organs [47]. For the rst time, he dened the critical role of fundus examination in detecting optic disc oedema in diagnosing malignant hypertension. Despite the availability of effective pharmacotherapy to control hypertension, malignant hypertension incidence is not showing a downward trend in certain underdeveloped regions where access to care may be limited [48]. Several events occur during the malignant phase of hypertension, some of which contribute to and others the consequences of malignant hypertension. These include remarkable activation of the renin-angiotensin system, platelet activation, and elevation of brinogen levels, endothelial dysfunction, brinoid necrosis of arterioles, thrombocytopenia, haemolytic anaemia, cerebral encephalopathy, heart failure [48]. In the eye, malignant hypertension leads to acute ischaemic events due to arteriolar broid necrosis in the retinal arterioles

(Cotton wool spots) and choroidal arteries (infarction of the choriocapillaris and overlying RPE), resulting in the breakdown of the outer blood-retinal barrier [49]. These ischaemic infarcts in the choriocapillaris are seen primarily on the temporal macula and appear as pale focal areas deep into the retina. These are called acute Elschnig’s spots. Fluid leakage from these spots results in the subretinal uid collection as multiloculated or more extensive as exudative retinal detachment (Fig.8.9a, b). On FFA, these appear hypouorescent in the early frames that show late staining. Most retinopathy changes reverse quickly once the blood pressure is controlled (Fig.8.9c, d). However, pigmented target lesions (central pigmentation with a clear halo) called chronic Elschnig’s spots and Linear pigmented lines oriented along the choroidal arteries, the Siegrist’s streaks are left behind as a legacy of the past hypertensive choroidopathy. Diabetes mellitus is often a comorbidity in patients with hypertension and requires careful management and monitoring for blood pressure control. See Box 8.6.

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8 Retinal Arteriolar Changes inHypertension andArteriolosclerosis

Fig. 8.9 Exudative retinal detachment (a, b) in a patient with malignant hypertension. After 4days, with control of hypertension, there was reversal of retinal detachment (c, d)

Box 8.6 Screening and Targets for Blood

Pressure Control in Patients with

Hypertension and Diabetes Mellitus

Blood pressure if ≥140/90mmHg, repeat measurements on same/separate day. Single reading BP≥180/110 with CVD treat the same day BP recording at each visit Home monitoring of BP for all

Target BP<130/80mmHg

Existing ASCVD or 10-year ASCVD risk ≥15%

Ten-year ASCVD risk <15%

BP>120/80mmHg Weight control

BP>140/90mmHg Lifestyle changes

Target

BP<130/80mmHg if attainable safely

Target BP<140/90mmHg

Reduce sodium, increase potassium Alcohol intake moderation Physical activity

Pharmacotherapy

References

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Ofce recorded BP≥160/100mmHg, patient has CAD

In addition to lifestyle changes, prompt 2-drug pharmacotherapy, including an ACE inhibitor/ARB Annual eGFR and serum K

Reference: American Diabetes

Association [50]

Abbreviations: CVD cardiovascular dis- ease, CAD coronary artery disease, ASCVD atherosclerotic cardiovascular disease

tools.acc.org/ASCVD-Risk-Estimator-

Plus

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