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Table of Contents
LETTER TO THE EDITOR
Year : 2019  |  Volume : 10  |  Issue : 4  |  Page : 229-230

Cortical blindness in posterior reversible encephalopathy syndrome in postpartum eclampsia


1 Department of Obstetrics and Gynecology, Datta Meghe Institute of Medical Sciences (Deemed to be University), Wardha, Maharashtra, India
2 Department of Medicine, Datta Meghe Institute of Medical Sciences (Deemed to be University), Wardha, Maharashtra, India

Date of Submission23-Sep-2019
Date of Acceptance03-Oct-2019
Date of Web Publication18-Nov-2019

Correspondence Address:
Dr. Sourya Acharya
Department of Medicine, Datta Meghe Institute of Medical Sciences (Deemed to be University), Sawangi (Meghe), Wardha . 442 001, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/INJMS.INJMS_123_19

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How to cite this article:
Singhal S, Baheti A, Singh K, Acharya S, Acharya N. Cortical blindness in posterior reversible encephalopathy syndrome in postpartum eclampsia. Indian J Med Spec 2019;10:229-30

How to cite this URL:
Singhal S, Baheti A, Singh K, Acharya S, Acharya N. Cortical blindness in posterior reversible encephalopathy syndrome in postpartum eclampsia. Indian J Med Spec [serial online] 2019 [cited 2019 Dec 14];10:229-30. Available from: http://www.ijms.in/text.asp?2019/10/4/229/271219



Dear Editor,

A 21-year-old primipara was referred to this hospital on postnatal day 2 of cesarean section with complaints of recurrent seizures for 2 days. The patient underwent cesarean section in a private nursing home for eclampsia and uncontrolled hypertension. Postnatally, the seizures persisted, and the patient was refractory to anticonvulsants and was referred to this hospital.

On examination, the patient was drowsy. Glasgow Coma Scale score was 9 (E-2, M-4, and V-3). She was having intermittent seizures. Pulse was 118/min, regular; blood pressure (BP) was 178/100 mmHg; respiratory rate was 42 cycles/min; and SpO2 was 86% while the patient was breathing ambient air. Auscultation of the chest revealed crepitation in the right inter- and infrascapular regions. Cardiovascular system: S1 was loud; there were no murmurs or gallop. Central nervous system: Higher functions could not be tested. There was no obvious cranial nerve deficit; the pupils were bilateral and normal in size reacting to light; deep tendon reflexes were normal; and plantars were bilateral extensors.

Her complete blood counts and renal function tests were normal. Liver function test revealed serum bilirubin of 3.2 mg/dl, alanine aminotransferase of -400 IU, aspartate transaminase of 342 IU, alkaline phosphatase of 73 IU, international normalized ratio of 1.6, and serum albumin of 3.2 g/dl. Absolute platelet count was 3.5 lakh/mm3. Urine analysis showed 2+ proteinuria by dipstick. Chest X-ray revealed aspiration pneumonia.

In view of status eclampticus and aspiration, the patient was intubated and mechanical ventilation was initiated. For status seizures, intravenous (IV) phenytoin loading was given, but the seizures were refractory, so IV midazolam was started at a dose of 0.1–0.2 mg/kg bolus with maintenance infusion of 0.1 mg/kg/h. IV broad-spectrum antibiotics were given for pneumonia. IV labetalol was initiated for hypertension.

The seizures were controlled after 3 h. IV midazolam was gradually tapered; on the next day, the patient was conscious, opened eyes, could move limbs to commands, was able to open and close eyes, and was able to identify left or right limbs by moving them to commands. However, she complained of vision loss in both eyes through gestures. Examination showed intact pupillary reflexes but absence of reflex blinking to visual threats suggestive of cortical blindness [Video 1]. A computed tomography (CT) scan of the brain, without contrast, showed multiple, ill-defined hypodensities of the bilateral high parital and occipital white matter, which corresponded with vasogenic edema typical for posterior reversible encephalopathy syndrome (PRES) [Figure 1]. IV dexamethasone 4 mg was initiated 8 hourly for the next 3 days, which was tapered. IV labetalol was switched over to amlodipine, and her BP was controlled. The patient was extubated after 2 days. Liver enzymes came down to normal range in the next 3 days. Over the next 5 days, vision improved in both eyes.
Figure 1: Noncontrast computed tomography of brain: Multiple ill-defined hypodensities of the bilateral high parital and occipital white matter, which corresponded with vasogenic edema typical for posterior reversible encephalopathy syndrome

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  Discussion Top


PRES is characterized by headache, nausea and vomiting, altered sensorium, visual disturbances, seizures, and coma.[1] Cortical blindness being the most common visual abnormality, homonymous hemianopia, visual neglect, and blurred vision can also occur. These symptoms are thought to develop secondary to cerebral edema. PRES is typically seen in patients with preeclampsia, transplantation, infection/sepsis/shock, autoimmune diseases, cancer chemotherapy, hypertensive crisis complicated with seizure, and in the case of multisystem mitochondrial disorder. The exact mechanism behind the development of angiogenic edema and CT and magnetic resonance imaging findings of PRES are not clear. Possible hypotheses include (a) severe hypertension causing defective autoregulation and hyperperfusion, thereby leading to endothelial injury and vasogenic edema, and (b) vasoconstriction and hypoperfusion leading to brain infarctions and subsequent vasogenic edema.[2] The characteristic localization of the edema in the parieto-occipital white matter has also been poorly understood. It probably reflects the sympathetic innervations of the brain that cause vasoconstriction which is weaker in the posterior circulation.[3]

Cortical blindness is among the most-documented complications of eclampsia/PRES. Neurological site of involvement is considered to be a dysfunction in the visual pathway which carries visual information from the lateral geniculate nucleus of the thalamus to the cerebral visual cortex, thereby not affecting the pupillary reflexes and ocular motility as demonstrated in our patient [Video 1]. It would appear that the primary visual cortex in the occipital lobes is more susceptible to vasogenic edema than other regions, leading to the development of cortical blindness.[4]

Early diagnosis of PRES is must for the timely initiation of therapy to control hypertension, vasogenic edema, and tonic-clonic convulsions. With early diagnosis and prompt treatment, patients usually recover within a few weeks. While in cases of delayed and/or inadequate treatment of PRES, secondary complications such as intracranial hemorrhage, cerebral ischemia, and status epilepticus can develop.[5]

We conclude that the cortical visual loss in patients with PRES associated with postpartum eclampsia is not so a rare identity. If detected early with prompt treatment, the condition is reversible. Simple bedside ophthalmic evaluation should be done routinely in patients complaining of visual abnormalities before going for neuroimaging. Both obstetricians and physicians should be aware of this clinical scenario because it is reversible and readily treated.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

None.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Marcoccia E, Piccioni MG, Schiavi MC, Colagiovanni V, Zannini I, Musella A, et al. Postpartum posterior reversible encephalopathy syndrome (PRES): Three case reports and literature review. Case Rep Obstet Gynecol 2019;2019:9527632.  Back to cited text no. 1
    
2.
Bandyopadhyay S, Mondal KK, Das S, Gupta A, Biswas J, Bhattacharyya SK, et al. Reversible cortical blindness: Posterior reversible encephalopathy syndrome. J Indian Med Assoc 2010;108:778-80.  Back to cited text no. 2
    
3.
Mitas L, Rogulski L. Acute cortical blindness in preeclampsia – A case of reversible posterior encephalopathy syndrome. Ginekol Pol 2012;83:469-72.  Back to cited text no. 3
    
4.
Kahana A, Rowley HA, Weinstein JM. Cortical blindness: Clinical and radiologic findings in reversible posterior leukoencephalopathy syndrome: Case report and review of the literature. Ophthalmology 2005;112:e7-11.  Back to cited text no. 4
    
5.
Sesar A, Cavar I, Sesar AP, Sesar I. Transient cortical blindness in posterior reversible encephalopathy syndrome after postpartum eclampsia. Taiwan J Ophthalmol 2018;8:111-4.  Back to cited text no. 5
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