Cortical blindness as a complication of eclampsia

CASE REPORT blindness, in pregnancy; eclampsia, blindness in; encephalopathy, hypertensive, in pregnancy; hypertension, in pregnancy; pregnancy, complication

Cortical Blindness as a C o m p l i c a t i o n of E c l a m p s i a Howard A Liebowitz, MD* Prudence E Hall, MDt Los Angeles, California From the Emergency Department, Cedars Sinai Medical Center,* and the Department of Obstetrics-Gynecology, University of Southern California Women's Hospital,t Los Angeles, California. Received for publication July 8, 1982. Revision received May 9, 1983. Accepted for publication June 20, 1983. Address for reprints: Howard A Liebowitz, MD, Lifeline Physicians, 14860 Roscoe Boulevard, Suite 211, Panorama City, California 91402.

Presented is a case of an eclamptic patient whose primary clinical presentation was cortical blindness. The patient was not known to be preeclamptic during her prenatal course, but she was lost to follow up one month prior to her presentation. Computed tomographic scan of the head was consistent with hypertensive encephalopathy. She was treated as an eclamptic patient. Her blood pressure was controlled with hydralazine, and she was given magnesiurn sulfate intravenously and intramuscularly. Labor was induced with a pitocin infusion. After delivery of a term infant, her vision returned and all other s y m p t o m s resolved without sequelae. The etiology and pathophysiology of cortical blindness as a symptom of eclampsia are discussed. ]Liebowitz HA, Hall PE: Cortical blindness as a complication of eclampsia. Ann Emerg Med May 1984;13:365-367.]

INTRODUCTION Visual disturbances are c o m m o n in patients with preeclampsia or eclampsia. Their occurrence is one of the criteria for diagnosis of severe preeclampsia. 1 Dieckmann2 found that 30% to 50% of eclamptic women had complaints of visual symptoms, including diplopia, blurry vision, scotomata, amaurosis, homonymous hemianopsia, transient color blindness, and cortical blindness. These disorders rarely are associated with severe retinopathy or permanent sequelae. 1 We present the case of an eclamptic patient with acute cortical blindness as her chief complaint.

CASE REPORT A 19-year-old gravida 1 para 0 woman was brought to the emergency department by her mother because of loss of vision and decreased level of consciousness. The patient's sister reported that the patient awakened with blindness on the day of admission, complained of a severe frontal headache, vomited five times, and was becoming gradually less alert. She was 403/7 weeks pregnant by dates. She had no history of seizure activity or any problems with the pregnancy. Her prenatal care had begun at 13 weeks and continued until 37 weeks. During this time she was never noted to be hypertensive or to have peripheral edema or proteinuria. She was lost to follow up between 37 weeks and this presentation. She had no significant medical history. Her only medications were prenatal vitamins and iron. Physical examination revealed a somnolent patient who was able to respond appropriately to questions, but who was disoriented to place and time. Her blood pressure was 138/116 m m Hg; pulse, 132 and regular; respirations, 24/rain; and rectal temperature, 37.2 C. Her eyes were able to cross the midline but rested mostly toward the right with lateral nystagmus. The pupils were round, equal, and briskly reactive to light. Her fimdi were normal. Deep tendon reflexes were 3 + in the upper extremities and knees, and 2 + at the ankles. Her sensory and motor examination was unremarkable. Her fundal height was 45 cm, with an estimated fetal weight of 4,000 g. Fetal heart tones were 150/min. She had 2 + bilateral lower extremity pitting edema. Hemoglobin was 11.2 g/dL, and hematocrit, 33.4%; platelets were 256,000/ 92/365

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Primary Ocular Changes Arteriolar spasm Central retinal artery occlusion Retinal edema, hemorrhages Retinal detachment Ocular Changes Secondary to Cerebral Disease Cortical blindness Papilledema mma, and WBC, 10,200 with normal differential. Serum electrolytes were as follows: sodium, 138; potassium, 4.4; chloride, 110; bicarbonate, 24; BUN, 8; creatinine, 0.9; calcium, 7.9; and glucose, 79. Prothrombin time was within normal limits. Proteinuria was 2 +. The patient was treated with 4 g 20% magnesium sulfate intravenously {IV) over five minutes, immediately followed by 2.5 g 50% m a g n e s i u m sulfate intramuscularly into each buttock. Her diastolic blood pressure remained at 115 m m Hg, and a test dose of 5 mg hydralazine was administered IV push. H e r blood p r e s s u r e was monitored every five minutes for 20 minutes. Because the diastolic blood pressure did not come down to between 90 and 100 m m Hg, a 10-mg dose of hydralazine was administered IV push. Her blood pressure then stabilized at a satisfactory level between 130/90 and 140/100 m m Hg. An e m e r g e n c y c o m p u t e d t o m o graphic (CT} scan of the brain obtained within 30 minutes of her arrival revealed multiple small, hypodense lesions in the basal ganglion and occipital lobe. In the labor and delivery area, internal fetal monitors were placed and a pitocin infusion was begun by continuous infusion pump. Ten units of pitocin were added to 1 L 0.9% aqueous sodium chloride solution, result13:5 May 1984

Fig. Visual manifestations of hyper-

tensive encephalopathy. 4 ing in a concentration of 10 mU/mL. The infusion was begun at an initial rate of 0.2 mL (or 2 mU) per minute through a peripheral IV site. Every 15 minutes the rate was increased by 0.2 mL/min until contractions of 60 m m Hg every three m i n u t e s were achieved. She delivered a term male infant with the aid of outlet forceps after seven hours of labor. The patient's vision began to return two and a half hours postpartum, and within six hours her vision had returned nearly completely. At this time she was alert and well oriented, with no recollection of the events of the previous 36 hours. Her blood pressure remained normal without further antihypertensive medication. A repeat CT scan performed three days p o s t p a r t u m showed decreasing size of several areas of infarction. The patient continued to do well with no further complications. She was discharged h o m e w i t h her b a b y on postpartum day 5.

DISCUSSION Eclampsia is one of the entities in which hypertensive encephalopathy is reported m o s t frequently.3 Encephalopathy should be suspected in any patient with hypertension out of control or of recent onset who complains of severe headache, drowsiness, vomiting, and failure of vision.3 The visual d i s t u r b a n c e s of p r e e c l a m p s i a and eclampsia can be explained by the vascular abnormalities found in hypertensive encephalopathy, and have been categorized according to whether they are found solely in the eye or are secondary to cerebral disease (Figure). 4 The CT scan findings in our patient are indicative of the pathophysiology of hypertensive encephalopathy. ByAnnals of Emergency Medicine

r o m s d e m o n s t r a t e d three stages of vascular abnormalities in the brains of animals with hypertensive encephalopathy. The first stage of vasoconstriction evolved to a second stage of increased capillary permeability with d e v e l o p m e n t of generalized brain edema. The third stage, necrosis of arterioles, which is the characteristic feature of malignant hypertension, results in hemorrhage or exudation into surrounding tissues. Cortical blindness in hypertensive encephalopathy is due to multiple microinfarcts and microhemorrhages in occipital gray matter of the brain.4 Settings other than hypertension in which cortical blindness can occur include thrombotic or inflammatory lesions of posterior cerebral arteries, and s p a c e - o c c u p y i n g lesions t h a t m a y compress these vessels or directly involve the visual cortex. Less common causes are migraine, hysteria, trauma, and lead or carbon monoxide intoxication. Cortical blindness in a preeclamptic has the same clinical significance as does a seizure and, therefore, cate~ gorizes her as eclamptic. 4 It often may be associated with such other cortical dysfunctions as focal epilepsy, hallucinations, or bizarre verbal or motor activity.3 The rightward gaze preference and nystagmus in our patient actually may have been due to focal seizure activity. Although our patient did not seem preeclamptic at 37 weeks gestation, she probably developed some suggestive signs during the three and a half weeks she was lost to follow up prior to her presentation in the emergency department. However, there do not seem to be any reliable parameters to determine which patients will become encephalopathic. Jellinek 3 reported three interesting cases of hypertensive encephalopathy with normal blood pressures, and stated that 366/93

CORTICAL BLINDNESS Liebowitz & Halt

there may not necessarily be any correlation between the development of encephalopathy and the level of the blood pressure. Dexter and Weiss in 1941 made the same observation regarding blood pressures in eclampsia. 3 Eye ground changes often are undetectable in preeclampsia and eclampsia unless the blood pressure is higher than 150/100 m m Hg. However, progressive retinal arteriolar narrowing would be an indication to induce delivery. 1 Resolution of symptoms and return of vision within six hours of delivery in our patient was dramatic but consistent with the resolution of symp-

toms seen in eclampsia without blindness. Blindness due to p r i m a r i l y ocular changes also has a generally favorable outcome after delivery 6 Eclampsia is an obstetrical emergency. If a pregnant patient presenting with acute loss of vision is suspected of being eclamptic, there should be no delay in initiating evaluation and treatment. REFERENCES 1. Chesley LC: Hypertensive Disorders in Pregnancy. New York, Appleton-CenturyCrofts, 1977, p 364-367. 2. Dieckrnann WJ: The Toxemias of Pregnancy, ed 2. St Louis, Mo, CV Mosby Co,

1952, p 240. 3. Jellinek EH, Painter M, Prineas J, et al: Hypertensive encephalopathy with cortical disorders of vision. Q J Med 1964;33: 239-256. 4. Donaldson J: Neurology of Pregnancy. Major Problems in Neurology, Philadelphia, WB Saunders Co, 1978, vol 7, p 219. 5. Byrom FB: Pathogenesis of hypertensive encephalopathy and its relation to the malignant phase of hypertension; experimental evidence from hypertensive rats. Lancet 1954;2:201-211. 6. Carpenter F, Kava HL, Plotkin D: The development of total blindness as a complication of pregnancy. Am J Obstet GyneeoI 1953;66:641-647.

American Board of Emergency Medicine Notice On June 30, 1988, the practice option will terminate for those physicians wishing to meet the credential requirements of the American Board of Emergency Medicine's certification examination. Practice, teaching, or CME accumulated after the above date may not be used to satisfy the practice requirements. Questions should be directed to ABEM, 200 Woodland Pass, Suite D, East Lansing, MI 48823; 517/332-4800. Application materials for the 1984 cycle of the American Board of Emergency Medicine certifying examination will be distributed in April 1984. Applications for the 1984 cycle will be accepted with postmark dates of May 1 through July 15, 1984. For further information, contact ABEM. 94/367

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