Transient blindness in pregnancy induced hypertension

Znt.J. Gynecol. O&et..

249

1989,29: 249-251

lntemational Federationof Gynecology andObstetrics

Transient blindness in pregnancy induced hypertension

Sivalingam

Nalliah and A.S. Thavarashah

Department of Obstetrics and Gynecology, University Haspital, University Science Malaysia, 15990 Kota Bharu (iiialaysia) (Received March 30th. 1988) (Revised and accepted July 12th. 1988)

Abstract Transient blindness associated with pregnancy induced hypertension without neurological symptoms is a rare phenomenon. The blindness in these cases is postulated to be of “Cortical blindness”. Two such cases occurring immediately after childbirth are presented. The ophthalmic manifestations of this complication of pregnancy induced hypertension and the importance of an urgent evaluation are discussed. Keywords: Pregnancy induced hypertension; Transient blindness; Preeclampsia. Introduction Transient blindness in pregnancy induced hypertension (PIH) without neurological symptoms has been reported in the literature as a rare phenomenon [4]. The altered hemodynamic, coagulative and hormonal changes associated with PIH could produce ocular changes such as focal retinal spasm and hypertensive retinopathy but transient blindness is rare. There were two cases of transient blindness in PIH during the period 1986-1987 at the University Hospital, Kelantan. The total number of deliveries during this period was 14,130 and the 002CL7292/89/$03.50

0 1989 International Federation of Gynecology and Obstetrics Published and Printed in Ireland

incidence of hypertensive disorders of pregnancy was 9.2% and that of eclampsia, 0.27%. Case report 1 Mrs. M.B.Z., a 17-year-old nullipara was admitted with severe PIH on October 17th, 1987 at 41 weeks of gestation. Her blood pressure was 170/ 110 mmHg and gross edema of the lower limbs was noted. The urine showed massive proteinuria (500 g/l). She was conscious and alert but the tendon reflexes were brisk. The eye ground examination revealed normal eye movements and pupillary reflexes. A bolus dose of Diazepam 10 mg (Valium, Roche) was administered followed by Dihydralazine (Nepresol, CibaGeigy, Switzerland) infusion of 50 mg in 500 ml 5% dextrose in titrating dose until the blood pressure settled to 140/90 mmHg. Labor was induced by a low amniotomy and oxytocin (Syntocinon, Sandoz, Switzerland) infusion. A live healthy baby boy was delivered by outlet forcepts 6 h later; the third stage was uncomplicated. Following the delivery her blood pressure settled to 130/90 mmHg and the Dihydralazine infusion was stopped. Nine hours after delivery, she complained of blindness of both eyes and could only recognize bright light within a distance of 15 cm. A neurological examination showed no abnormalities. The conjuncCase Report

250

Nalliah and Thavarasah

tiva, cornea and optic disc were normal. There was no evidence of hemorrhage or retinal detachment and the pupils were normal in size and reacted to light. An ophthalmologist confirmed the findings. Normal vision returned spontaneously 4.5 h later. Ophthalmic examination at this stage did not reveal any abnormalities. The visual fields and acuity (VR 6/S, VL 6/5) were normal. She remained asymptomatic when reviewed at the end of 6 weeks and 3 months.

eye. A visual evoked potential was noted to be poorly formed with delayed P 100 on the right eye. When the patient was reviewed on February 27th, 1986, both eyes were normal except for residual myopia which was presumed to be present before the present ailment. Color vision was normal. She remained asymptomatic when reviewed 3 months later. Her vision was good (VR 6/5,VL 615) with corrective lenses. Discussion

Case report 2 R.B.A. a 29-year-old nullipara was admitted at 36 weeks of pregnancy with a blood pressure of 170/l 15 mmHg, proteinuria and gross edema of both her feet. She did not complain of headache or visual disturbances. She was initially given Methyldopa (Aldomet, Merck, Sharpe & Dohme, FRG) 750 mg daily. Dihydralazine infusion of 50 mg in 500 ml 5% dextrose was commenced on the fourth day because of the persistently high blood pressure and an increase of protein in the urine. The blood pressure was maintained at 140-150/85-90 mmHg. In spite of the anticonvulsive therapy, she had a seizure and an emergency lower segment cesarean section was performed on Februry llth, 1986. She had another seizure during the immediate postoperative period. Her blood pressure was 160/100 mmHg on the second postoperative day and she was started on Labetalol (Trandate, Glaxo Getz Corp., W. Malaysia) 200 mg eight hourly. The Diazepam infusion was stopped on February 13th, 1986. At this stage, she complained of loss of vision in both eyes and could not perceive light at a distance of 15 cm. The pupils were equal in size and reacted to light. The optic disc was clearly defined and there were no papilledema, hemorrhage or exudates. Her vision improved over the next few days. On February 22nd,1986 she could read at a distance of 20 cm and her visual acuity was VR6/36 (-1.50, 6/5 and VL 6/24 (1.25, 6/5). However, there were some defects of color vision in the right Int JGynecol Obstet 29

The true incidence of transient blindness in PIH is not known. Arulkumaran et al. [l] reported three cases among 30,867 deliveries in Singapore. Transient peripheral blindness is said to occur in 1% of women with preeclampsia, where arteriolar spasm, hemorrhage and exudate are generally seen at fundoscopy [6]. In an excellent review on maternal ocular adaptations during pregnancy, Weinab et al. [lo] listed hypertensive retinopathy, anterior ischemic optic neuropathy, exudative retinal detachment, retrobulbar neuritis, vasospasm of the conjunctival vessels and cortical blindness as the ophthalmic manifestations of pregnancy induced hypertension. Choroidal infarction with consequent extravasation of serous fluid into the subretinal space has also been reported [7]. Among these, cortical blindness is a rare phenomenon [3] usually associated with hypertensive encephalopathy or postpartum cerebral thrombosis. In both the patients reported, the pupillary reflexes and ocular movements remained intact and fundoscopic examination excluded other conditions such as retinal detachment or an anterior ischemic optic neuropathy. In view of the rapid recovery in case 1 and a complete recovery in case 2, vascular spasm could be postulated as the cause of the blindness. The clinical features and the complete recovery seen in both the patients fit into the category of “cortical blindness”. The term indicates selective involvement of the visual occipital cortex, where there is a complete loss of visual

Transient blindnew in preeclampsia

sensation with retention of reflex constriction of the pupils to illumination, convergent movements, a normal structure of the retina and the extraocular movements of the eye. Vascular spasm involving the calcrine branches of the posterior cerebral artery [9] is postulated. Sudden retinal artery occlusion [8] and bilateral arteriolar occlusion following amniotic fluid embolism [2] are other rare manifestations that should be borne in mind. When sudden blindness occurs in pregnancy, urgent evaluation is essential as a pathological cause may occur anywhere from the retina to the visual cortex. The opinion of the ophthalmologist, radiologist and neurologist are valuable. Objective evidence of abnormality in the occipital cortex on the CT scan in transient blindness with induced associated pregnancy hypertension in the presence of normal ophthalmological findings and intact pupillary refelexes was reported by Grimes et al. [S]. Although it is recommended that should be termination of pregnancy considered, blindness in both our patients occurred after delivery, hence it is not convincing enough to say that the process is necessarily preventable by immediate delivery

PI. References 1 Arulkumaran S, Gibb DMF, Rauf M, Kek LP, Ratnam SS: Transient blindness associated with pregnancy

251

induced hypertension: case reports. Br J Obstet Gynaecol 92: 841,1985. 2 Chang M, Herbert WNP: Retinal arteriolar occlusions following amniotic fluid embolism. Ophthalmology 91: 1634.1984. 3 Drymalski WG: Cortical blindness: changing incidence and shifting etiology. Postgrad Med 67: 149,198O. 4 Gandhi J, Ghosh S, Pillari VT: Blindness and retinal changes with preeclamptic toxemia. NY State Med 78: 1930,1978. 5 Grimes AD, Ekbladh LE, McCarthy HW: Cortical blindness in preeclampsia. Int J Gynecol Obstet 17: 601, 1980. 6 Hanoch L, Alexander N, Joseph Z, Jacob S, Jardena 0: Pre-eclampsia, HELLP Syndrome and postictal cortical blindness. Acta Obstet Gynecol Stand 66: 91,1987. 7 Klein BA: Ischemic infarcts of the choroid (Elsching spots). Am J Ophthalmol66: 1069, 1%8. 8 LaMonica CB, Gerard JF, Siberman L: A case of sudden retinal artery occlusion and blindness in pregnancy. Obsta Gynecol69: 433.1987. 9 Miller NR: Cortical blindness and cerebral blindness. In Walsh and Hoyt’s Clinical Neuro-Ophthalmology, p 142 -145. Williams and Wilkins, Baltimore and London, 1982. 10 Weinab RN, Arthur L, Tom K: Maternal ocular adaptations during pregnancy. Obstet Gynecol Surv 42: 471, 1987.

Address for reprints: N. Sivaam

Deputwat of Obatetries and Gynecology HospitaluxliveMiti !&insMalaysia 16150 Knbang Keriaa Kelantao west Malaysir

Case Report