Feline Systemic Hypertension-A Hidden Killer
Andrew H. Sparkes, BVetMed, PhD, DECVIM-CA, MRCVS
The Feline Unit, Animal Health Trust Lanwades Park
Kentford, Suffolk, UK

Hypertension is now recognised with increasing frequency as a feline problem, particularly in association with other diseases such as hyperthyroidism and chronic renal failure, although primary hypertension may also be seen occasionally.

Clinical findings

Affected cats may present with signs referable to underlying systemic disease such as polyuria, polydipsia, inappetence, polyphagia and weight loss. Specific clinical signs associated with hypertension include visual deficits and blindness, neurological signs, left ventricular hypertrophy, and potentially impaired renal function. Early recognition of hypertension is important in order to minimise these effects.

Pathogenesis of ocular signs

The most pressure sensitive structure in the vascular system is the capillary. Mechanisms involved in the response to systemic hypertension are therefore designed to defend the capillary from raised pressure for as long as possible.

In response to raised intra-luminal pressure, arterioles initially undergo constriction due to contraction of the smooth muscle in their walls, resulting in the maintenance of normal tissue perfusion. In the face of severe and prolonged arteriolar contraction, the tissue beds supplied by the affected arteriole may become ischaemic. Furthermore, persistent contraction may also lead to degeneration and necrosis of the smooth muscle in the arteriole itself. As the necrotic muscle can no longer maintain constriction, the arteriole undergoes relaxation and dilation. The unprotected vessel is thus now exposed to the full force of raised intraluminal pressure. Endothelial damage results and exudation through the vessel wall occurs. Leakage of plasma and fibrinogen into the vessel wall may follow, leading to thickening of the wall and even occlusion of the lumen. Fibrinogen is converted to fibrin in the wall. Where necrosis accompanies this fibrinoid change it is referred to as fibrinoid necrosis, the hallmark of malignant hypertension. Arteriolar incompetence and fibrinoid necrosis may lead to ischaemia, exudation and haemorrhage in the retina.

Similar changes can occur in the choroid. Where terminal choroidal arterioles are affected there is secondary ischaemia of the choriocapillaris and the retinal pigment epithelium (RPE). Severe RPE damage leads to subretinal fluid accumulation and retinal detachment.

Early ocular changes

Perhaps the earliest ophthalmoscopic change observable in systemic hypertension is bullous retinopathy. Animals examined at this time are likely to still be visual. Most of the fundus may appear normal, but small circular "doughnut" lesions are observable in varying numbers throughout the fundus. Such lesions are more clearly seen in the tapetal fundus, appearing as hypo-reflective grey circles. These lesions represent the accumulation of fluid either within or beneath the retina, forming small focal areas of retinal oedema or detachment. Increased vascular tortuosity may accompany this change, representing smooth muscle necrosis and localised dilatation, leading to vessel wall permeability and plasma leakage.

In the earliest cases, gross retinal haemorrhage may not be present. Although vision is likely to be affected, only the most observant of owners will detect partial blindness. It is only by recognising the need to perform funduscopy as a routine part of an examination that such lesions will be discovered.

More severe ocular changes

Most cases are presented when a more extreme event has taken place. This usually takes the form of hyphaema or sudden onset blindness. Although the anterior chamber may be completely filled with blood, hyphaema is usually seen as a small haemorrhage. Gross haemorrhages at various depths in the retina may be seen, and an associated retinal detachment is often present. Severe cases will be blind. Where fundus examination is precluded ocular ultrasound can be beneficial. In some cases the presentation is of blindness with serous retinal detachment.

Sequelae of previous haemorrhage or detachment

Occasionally cats may be presented with long standing abnormalities without ever being seen in the acute phase of disease. Various presentations are possible in such situations. common finding may be fibrous tissue tags in the anterior chamber, often running from the iris to the anterior lens capsule. In other cases distortion of the pupil margin occurs, following posterior synechiae of iris to lens. In other cases, a detached retina may reattach, leaving wrinkles observable over its surface.

Ancillary diagnostic tests

Ancillary diagnostic procedures will often need to be employed in order to reach a definitive diagnosis. Haematology and biochemistry profiles should be routinely performed, including thyroid hormone assays where indicated. Echocardiography may be useful to assess for concurrent cardiac disease. In cases where fundus examination is not possible, ocular ultrasound should be performed in order to detect the possibilities of detachments or tumours.

Indirect blood pressure measurement is an easily performed procedure in the cat and should be performed routinely in cases where hypertension is suspected.

Other adverse effects

The three other major target organs for hypertensive damage are the CNS (spontaneous haemorrhage and sudden onset neurological signs), the heart (left ventricular hypertrophy) and the kidneys (where hypertension is likely to be a major factor promoting progression of chronic renal failure.

Diagnosis

Hypertension should be suspected as a possibility in any cat presented with chronic renal failure, hyperthyroidism, hypertrophic cardiomyopathy, acute onset blindness or other signs of hypertensive retinopathy. A detailed ophthalmic examination is also essential both in diagnosis and assessment of the extent of ocular disease. Ideally, diagnostic evaluation should include systolic blood pressure measurement. The Doppler technique has been shown to be the most accurate and reliable technique for indirect measurement of systolic blood pressure (SBP) in conscious cats. We have demonstrated that in a typical ward or consulting room situation, an absolute upper limit of 200 mmHg should be taken using the Doppler technique. In cats with a more borderline systolic blood pressure of between 180 and 200 mmHg, it may be prudent to repeat the blood pressure after a period of acclimatisation in order to rule out anxiety related sympathetic stimulation.

Management of hypertensive cats

Potential underlying diseases should be ruled out as far as possible. This should include serum thyroxine evaluation, blood urea and creatinine levels, urinalysis and a cardiac investigation where indicated following clinical examination. A degree of left ventricular hypertrophy is a common echocardiographic finding in the hypertensive patient as a sequela of this condition. Therapy of hypertension should also be initiated. There are currently several drugs that may be used including diuretics (e.g., frusemide), beta-blockers (e.g., atenolol), ACE inhibitors (e.g., enalapril) and calcium channel blockers (e.g., amlodipine).

There is a great degree of individual variation in response to therapy, but in cats monotherapy with amlodipine is generally regarded as the treatment of choice for systemic hypertension. Other classes of drugs, when used alone, are frequently ineffective in this species. Response to therapy should ideally be monitored closely in the first two weeks of treatment by measuring systolic blood pressure and monitoring ocular abnormalities. In successfully treated cases, the blood pressure should drop into the normal range within one to two weeks of initiating therapy (ideally blood pressure between 130 and 170 mmHg). Treatment is commenced at 0.625 mg per cat daily, increasing to twice daily if response is inadequate. Occasionally a combination of two or three agents may be required to achieve an adequate response. In patients with renal failure, it is particularly important to monitor renal function, as all of the above agents are capable of reducing renal blood flow. However, deterioration in renal function is uncommon in cats treated with ACE inhibitors or Ca-channel blockers, and their use may have specific beneficial effects in many animals with renal failure.

Once blood pressure is stable, patients should be assessed every one to two months. Dietary sodium restriction may also be of value although it is unlikely to be sufficient as a sole treatment of hypertension.

Drugs useful for management of hypertension

Diuretics

 Frusemide (1-2 mg/kg q12-48hr)

 Hydrochlorothiazide (2-4 mg/kg q12hr) Not effective as single agents in cats, and may be contra-indicated (e.g., CRF). Possibly helpful acutely with retinal detachment

Beta-blockers

 Propranolol (2.5-5 mg/cat q8-12hr)

 Atenolol (6.25-12.5 mg/cat q24hr)Often not successful alone

Alpha-blockers (vasodilators)

 Phenoxybenzamine (0.5 mg/kg q12hr)

 Reflex tachycardia, hypotension, and sodium retention all significant side-effects. Not useful for long-term management of hypertension

ACE inhibitors (vasodilators)

 Enalapril (0.25-0.5 mg/kg q12-24hr)

 Benazepril (0.5-1.0 mg/kg q24hr)

 Appear to be more effective in dogs than cats, may have other benefits in renal failure making them valuable as adjunctive therapy.

Ca-channel blockers (vasodilators)

 Amlodipine besylate (0.625-1.25 mg/cat q24hr) Drug of choice, and often successful as a single drug in cats. Can be combined with ACEI, beta-blocker or diuretic if needed. Maximum effect seen within 7 days

 

Speaker Information
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Andrew H. Sparkes, BVetMed, PhD, DECVIM-CA, MRCVS
The Feline Unit, Animal Health Trust Lanwades Park
Kentford, Suffolk, UK


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