Blindness after treatment for malignant hypertension.

Abstract

245attacks. Oestrogens may increase the plasma concentrations of some of the coagulation factors with shortening of the prothrombin time. Toy et al2 found this effect with synthetic oestrogens but not with "natural" oestrogen (oestriol succinate). Thus it is improbable that this mechanism was responsible for thromboembolic episodes in our patient. The oestrogen preparation she was taking was a naturally occurring one (conjugated equine oestrogen), and the patient's prothrombin times remained within the therapeutic range, at levels similar to those maintained in the past without embolic symptoms.An increase in platelet adhesiveness, which can be shown during oestrogen therapy,3 was probably responsible for the appearance of embolic phenomena in our patient. The importance of platelets in the genesis of emboli from prosthetic heart valves is further illustrated by reports that patients being treated with dipyridamole in addition to oral anticoagulants derive greater protection from nonfatal thromboembolism than those taking anticoagulants alone.4In an extensive review of reports on oestrogen treatment in postmenopausal women, Shoemaker et a15 concluded that there was no proved risk of thromboembolic disease on such treatment. While this may be true for most women, it does not necessarily apply in those with an additional predisposing factor, such as a prosthetic heart valve. Our case illustrates the potential risks of oestrogen therapy in patients with valve prostheses. Anticoagulation with warfarin or phenindione alone should not be considered to protect these patients adequately against thromboembolic complications of oestrogen treatment. Non-essential oestrogen administration should be avoided in all patients with prosthetic heart valves.We are grateful to Dr J P Lee-Potter for providing haematological data, and to Mrs B Davies for her help in preparing this paper. Case reportsCase 1-A 30-year-old Caucasian housewife presented with a three-week history of blurring of vision of the left eye, two weeks' morning nausea and vomiting, and three days' haematuria. She had no history of hypertension and was taking no medication. She smoked five cigarettes daily. She had a sinus tachycardia of 124/min, blood pressure of 270/175 mm Hg, and clinical and electrocardiographic features of left ventricular hypertrophy. Fundoscopy showed grade IV hypertensive retinopathy, and visual acuity was decreased in the left eye. After admission to hospital she received methyldopa 500 mg by mouth six-hourly (figure). The next day she was confused and drowsy but there were no new focal neurological signs. Methyldopa was withdrawn and propranolol 80 mg eight-hourly and Moduretic two tablets daily given. Thirty-six hours after admission her conscious level was normal but she complained of total loss of vision and hallucinations. The pupils were bilaterally dilated and unresponsive to light. Fundal appearances were unchanged. Dexamethasone 4 mg six-hourly was given from the fourth day without measurable benefit. The only other neurological...

Slow release nifedipine and atenolol as initial treatment in blacks with malignant hypertension.

“…It must be a balance between the risks of uncontrolled malignant hypertension and too rapid reduction of blood pressure. Since precipitous falls in pressure in patients with severe hypertension may lead to neurological complications (Graham, 1975;Ledingham & Rajagopalan, 1979;Cove et al, 1979) it has been recommended that parenteral therapy be avoided, with few exceptions, and that initial treatment should be with one or two drugs given orally instead (Ledingham, 1983).…”

Optic Nerve Head Infarction

“…In this subgroup of patients, small-artery dis ease may have involved the posterior ciliary network supplying the circle of Zinn or small branches of the cen tral retinal artery to the optic nerve head, as the optic nerve head may receive its supply from both systems [18] . We must emphasize that in none of these patients, ONHI appeared to have been triggered by a hemody namic phenomenon, although such a factor has been mentioned previously [19][20][21],…”

Amaurosis Following Blood Loss

“…Hayreh [13] has suggested the importance of the imbalance between the perfusion pressures and the intraocular pressure compounded by systemic hypotension in the genesis of ischemic optic neuropathy. There have been described several cases of blindness in the treatment of malignant hypertension when the arterial tension became stable [14]. Tay lor et al [15] record 4 cases of children with accelerated hypertension who developed an ischemic optic neuropathy when tension came back to the normal level.…”