antihypertensive treatment can be dangerous

1
adverse reactions/interactions ANTIHYPERTENSIVE TREATMENT CAN BE DANGEROUS Tw o cases of blindness after treatment for malignant hypertension Two young. active :=:aucasian women became blind after treatment [or malignant hypertension. No other published reports of such cases could be found . Although both patients presented with visual impairment. they bad none of the usual features of hypertensive encephalopathy. The main neurological damage was confined to the visuaJ pathways and was probably localised in the optic nerves. The only other neu rological defect in both cases was urinary retention. Ischaemia presumably resulted from a fall in perfusion pressure in tissue with a high interstitial pressure due to oedema. Case I - A 30-year-old woman presenl ed with a 3-week history of blurr ing vision of the left eye, 2 weeks ' morning nausea and vomit ing and 3 days' haematuria. She had no hi story of hypertension and was nolan medi cation. She had sinus tachycardia of 124 /m in, SP 270/175mm Hg and features ofl eft ventri cu lar hypertrophy. She had grade IV hypertensi ve retinopathy and decreased visual acuity in the left eye. She was given oral methyldopa 500mg 6-bourly, wbich was replaced the next day by propranolol80mg 8-hourly and 'Moduretic' (hy.drochlomthiazide 50mg + amiloride hydrochloride 5mg), 2 tablets/day. 36 hours after admission her conscious level was normal, but she had total loss of v isio n and hallucinations. The pupils were bilaterally dilated and unresponsive to light. She has remained blind despite good SP control and bilateral optic atrophy has developed. CQse 1- A 32-year-old woman presented with 2 weeks' blurring of vision. She had had mild hypertension (untreated) 4 years previously. She had sinus tachycardia( 120/min), SP 250/ 170mm Hg , signs orlen ventricular hypertrophy and cardiac enlargement. She bad grade IV hypertens i ve retinopathy and visual acuity slightly decreased in both eyes. She was given an IV bolus of diawxide (3 00mg), fru se mide (fu rosemi de) 80mg IV and atenolol I OOmg oraUy. SP fe ll to 90/70m m Hg within 10 mi nutes. but rose to 120 /70 mm Hg after IV sali ne. She co mplained of bli ndness in both eyes and devel oped dilat ed pupils unresponsive to lig ht. She is still bl ind, despite good SP control, and has bilateral optic atrophy . Cove, D.H. e\ al .: British Medical Journal 2: (28 Jul 1979). Although it is .known severe sy mptom s may be induced in elderly patients treated for mild hypertension . anOlher type of hazard .ous, treatment has received less attention. In 197 S, IWO cases of ischaemic brain damage after rapid BP reduction III malignant hypertensives were reported and another 10 examples of severe and often fatal side effects have been To these are added 2 cases above. Qearly, rapid IV injections of diazoxide are dangerous, and previously accepted VieWS on emergency BP reduction need to be amended. In many cases, oral preparations can be equally effective and less hazardous in severe hypertensi ve:; . Case I is particularly alanning, as the patient's BP was only reduced from 290/ 1 75to I 20/S0mm Hg over 36 hours Q rQI drugs. Eve n more gradual red u ct ion may be preferable a nd diastolic pressures should not be red uced bel ow 1 IOmm Hg. 'Injec ted antihype rt e ns ive drugs should be u sed o nl y in s evere hy pert ensive le ft ve ntricular failure or in fra nk en c ep ha lo pat hy with fluctuat ing neur ologi cal signs. We should no longe r regard s eve re or mali gnant hypertens ion by it se lf as an in. dicati on for pare nt eral t rea tment .' EdilOrial : British Me4ica1 Joum.aJ 2: 228 (28 Jill 19 79) 4 INPHARMA ISAug 1919 0156-2103 /1 9/081 8-0004 SO .SO/O O ADIS Press

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adverse reactions/interactions

ANTIHYPERTENSIVE TREATMENT CAN BE DANGEROUS

Tw o cases of blindness after treatment for malignant hypertension Two young. active :=:aucasian women became blind after treatment [or malignant hypertension. No other published reports of such cases could be found. Although both patients presented with visual impairment. they bad none of the usual features of hypertensive encephalopathy. The main neurological damage was confined to the visuaJ pathways and was probably localised in the optic nerves. The only other neurological defect in both cases was urinary retention. Ischaemia presumably resulted from a fall in perfusion pressure in tissue with a high interstitial pressure due to oedema. Case I - A 30-year-old woman presenled with a 3-week history of blurring vision of the left eye, 2 weeks' morning nausea and vomiting and 3 days' haematuria. She had no history of hypertension and was nol an medication. She had sinus tachycardia of 124/min, SP 270/175mm Hg and features ofl eft ventricular hypertrophy. She had grade IV hypertensive retinopathy and decreased visual acuity in the left eye. She was given oral methyldopa 500mg 6-bourly, wbich was replaced the next day by propranolol80mg 8-hourly and 'Moduretic' (hy.drochlomthiazide 50mg + amiloride hydrochloride 5mg), 2 tablets/day. 36 hours after admission her conscious level was normal, but she had total loss of vision and hallucinations. The pupils were bilaterally dilated and unresponsive to light. She has remained blind despite good SP control and bilateral optic atrophy has developed. CQse 1-A 32-year-old woman presented with 2 weeks' blurring of vision. She had had mild hypertension (untreated) 4 years previously. She had sinus tachycardia( 120/min), SP 250/ 170mm Hg , signs orlen ventricular hypertrophy and cardiac enlargement. She bad grade IV hypertensive retinopathy and visual acuity slightly decreased in both eyes. She was given an IV bolus of diawxide (300mg), frusemide (furosemide) 80mg IV and atenolol I OOmg oraUy. SP fe ll to 90/70m m Hg within 10 minutes. but rose to 120/70mm Hg after IV saline. She complained of blindness in both eyes and developed dilated pupils unresponsive to light. She is still blind, despite good SP control, and has bilateral optic atrophy . Cove, D.H. e\ al .: British Medical Journal 2: 24~ (28 Jul 1979).

Although it is.known th~t severe symptoms may be induced in elderly patients treated for mild hypertension . anOlher type of hazard.ous, antih~pertenslve treatment has received less attention. In 197 S, IWO cases of ischaemic brain damage after rapid BP reduction III malignant hypertensives were reported and another 10 examples of severe and often fatal side effects have been ~ported , To these are added th~ 2 cases above. Qearly, rapid IV injections of diazoxide are dangerous, and previously accepted VieWS on emergency BP reduction need to be amended. In many cases, oral preparations can be equally effective and less hazardous in severe hypertensive:;. Case I is particularly alanning, as the patient's BP was only reduced from 290/ 175to I 20/S0mm Hg over 36 hours ~ith QrQI drugs. Even more gradual reduction may be preferable and diastolic pressures should not be reduced below 1 IOmm Hg.

' Injected antihyperte nsive drugs should be used only in severe hypertens ive left ve ntricular fa ilure or in fra nk encephalopathy with fluctuat ing neurological s igns. We should no longe r regard seve re or malignant hypertens ion by itself as an in. dication for pare nte ral t rea tment .'

EdilOrial: British Me4ica1 Joum.aJ 2: 228 (28 Jill 1979)

4 INPHARMA ISAug 1919 0156-2103/19/081 8-0004 SO .SO/ O O ADIS Press