Table of Contents  
CASE REPORT
Year : 2015  |  Volume : 8  |  Issue : 3  |  Page : 458-460

Postoperative complete amaurosis fugax in severe pre-eclampsia: a case report


Department of Anaesthesia, Mahatma Gandhi Medical College, Jaipur, Rajasthan, India

Date of Submission31-Oct-2014
Date of Acceptance16-Mar-2015
Date of Web Publication29-Jul-2015

Correspondence Address:
Mohit Somani
Department of Anaesthesia, Mahatma Gandhi Medical College, RIICO Institutional Area, Sitapura, Jaipur, Rajasthan - 302 022
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/1687-7934.161740

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  Abstract 

Introduction
One of the complications of severe preeclampsia is cortical blindness which could be reversible or permanent. It is the most disturbing symptom of reversible post encephalopathy syndrome in preeclampsia and eclampsia.
Case Discription
An 18-year-old primigravida was admitted with term pregnancy in the obstetrics department, having high arterial blood pressure with pitting edema with proteinuria, hematuria, impaired renal functions, and elevated serum transaminases. She was treated with 250 mg of methyldopa three times a day, but as hypertension persisted, the patient was admitted to ICU and was given labetolol 200 mg three times a day orally, along with oxygen by mask. Sonographic examination showed cord around the neck with an arterial blood pressure of 160/110 mmHg. Cesarean section was planned. The patient was given 500 mg of methyldopa and labetalol 200 mg orally in the morning, few hours before being taken to the operating room. Segmental epidural block with 12 ml of 0.5% ropivacaine was performed, with epidural catheter left in situ in the L2-3 space and top up dose of same 6ml drug is given later on. Lower segment cesarean section was performed and the baby was delivered with an APGAR score of 8. On the second postoperative day, she developed headache, giddiness, and blurred vision, which became progressive. Computed tomography and MRI reports confirmed posterior reversible encephalopathy syndrome. She was treated accordingly and early management helped her recover completely.
Conclusion
This case report emphasizes the need for early diagnosis and prompt treatment of PRES to avert short-term and long-term neurological sequelae. Early treatment usually results in complete reversal of deficits over few days to few weeks.

Keywords: cesarean section, epidural block, posterior reversible encephalopathy syndrome, pre-eclampsia


How to cite this article:
Somani M, Sharma P, Mathur V, Jethava D, Sachdev S. Postoperative complete amaurosis fugax in severe pre-eclampsia: a case report. Ain-Shams J Anaesthesiol 2015;8:458-60

How to cite this URL:
Somani M, Sharma P, Mathur V, Jethava D, Sachdev S. Postoperative complete amaurosis fugax in severe pre-eclampsia: a case report. Ain-Shams J Anaesthesiol [serial online] 2015 [cited 2019 Jul 16];8:458-60. Available from: http://www.asja.eg.net/text.asp?2015/8/3/458/161740


  Introduction Top


Severe pre-eclampsia can be associated with a number of perioperative complications. One of the complications of pre-eclampsia is cortical blindness, which could be reversible or permanent [1] . It is the most disturbing symptom of reversible postencephalopathy syndrome in pre-eclampsia and eclampsia. The patient and her family were informed about the case report and gave written permission to publish the report.


  Case description Top


The patient was an 18-year-old primigravida admitted with term pregnancy in the obstetrics department, having an arterial blood pressure (BP) of 150/102 mmHg with pitting edema. In blood and urine samples sent for examination, there was proteinuria ++, hematuria+, along with impaired renal functions and elevated serum transaminases in the liver function tests. Thrombocytopenia was not present.

Initial treatment was carried out with 250 mg of methyldopa three times a day, but as hypertension persisted, the patient was admitted to ICU and advised for labetolol 200 mg three times a day orally, along with oxygen by mask and strict intake output charting. Serial sonographies for fetal well-being were conducted 4 hourly.

Sonographic examination on the third day of admission showed cord around the neck. The patient's arterial BP was 160/110 mmHg. Hence, cesarean section was planned. The patient was given 500 mg of methyldopa and labetalol 200 mg orally in the morning. Segmental epidueal block with 12 ml of 0.5% ropivacaine was performed with epidural catheter left in situat L2, L3 space with top up with 6 ml after an hour. Lower segment cesarean section was performed and the baby was delivered with an APGAR score of 8.

The patient was shifted to postoperative high dependency unit, and because of poor control of BP, labetolol 20 mg intravenous was added (to a maximum dose of 80 mg/day). On the second postoperative day she developed headache, giddiness, and blurred vision, which became progressive.

On ophthalmic examination, pupils were bilaterally dilated and nonreacting, and fundus, retina and optic disc were normal.

On neurological examination, except for bilateral amaurosis no sensory or motor deficit, seizure activity, or change in consciousness was found.

Computed tomography scan demonstrated bilateral hypodensities in the occipital and posterior parietal lobes. There were no abnormalities of the ventricular system and no evidence of midline shift or mass effect with diagnosis of posterior reversible encephalopathy syndrome (PRES).

MRI was diagnostic of PRES with diffuse cytotoxic, vasogenic edema of cortex and subcortical white matter.

The patient was shifted to intensive care unit where an infusion of labetolol and nitroglycerine was started intravenously, in addition to earlier treatment. MgSO 4 4 mg through intramuscular route 8 hourly, epsolin 1 ampule 8 hourly intravenously, and methylprednisolone 100 mg 12 hourly intravenously were given. Nootropil 1 g/day and frusemide 40 mg and injectable mannitol 100 ml were administered intravenously as per need to treat brain edema. Blood pressure was controlled within 12 h, and the patient recovered her eyesight within 72 h of ICU duration. Pupils showed sluggish reaction to light, cornea was clear, and extraocular muscle functions were intact. Fundus examination showed a normal optic disc.


  Discussion Top


Pre-eclampsia is a multisystem disease characterized by increased arterial BP (>140/90 mmHg) and proteinuria (>2 g/day) and generalized edema occurring after 20 weeks of gestation and is a leading cause of maternal and foetal morbidity and mortality, having three times higher incidence in developing countries [1] .

Despite its importance for public health, the etiology of this disorder is unknown. It is a multisystem disorder with various forms, which are believed to result from a failure of the normal invasion of trophoblast cells, leading to maladaptation of maternal spiral arterioles [2] . It can also be associated with hyperplacentation disorders such as diabetes, hydatiform mole, and multiple pregnancies. However, geographical, social, economical, and racial differences are also attributed [2] .

Severe pre-eclampsia is present when arterial BP exceeds 160/110 mmHg and protein loss is greater than 5 g/day. These patients are likely to complain of headache, visual disturbances, and epigastric pain, and they may exhibit altered consciousness. The patient may develop congestive heart failure, decreased colloid osmotic pressure, pulmonary edema, arterial hypoxemia, laryngeal edema, grand mal seizures, cerebral hemorrhage, HELLP syndrome, or acute tubular necrosis. This may result in intrauterine growth retardation, abruption of the placentae, and premature delivery [3] .

PRES is a diagnosis consisting of headache, seizures, altered mental status, and a spectrum of visual deficits ranging from visual neglect to cortical blindness. There is often an acute increase in arterial BP, which is clinically indistinguishable from hypertensive encephalopathy, and has been associated with pre-eclampsia, renal failure, immunosuppressive drugs, chemotherapeutic drugs, and hypercalcemia [4] .

Computed tomography scan in PRES shows hypodensities of the posterior white and gray matter. Lesions are generally bilateral and parieto-occipital, which may or may not involve temporal or frontal lobes, brainstem, or cerebellum. T2-weighted MRI shows areas of hyperintense signal [5] .

Perioperative loss of vision is a rare but devastating complication that occurs due to retinal vascular occlusion, ischemic optic neuropathy, and hypertensive breakthrough in the autoregulation of posterior cerebral arterioles, followed by extravasation of the fluid into the brain tissue leading to vasogenic edema [6] .

Marked systemic hypertension causes sclerosis of retinal arterioles, splinter hemorrhage, focal infarcts of the nerve fiber layer (cotton wool spots), and leakage of lipid and fluid (hard exudates) into the macula. In hypertensive crisis, sudden visual loss can result from vasospasm of retinal arterioles and retinal ischemia, along with optic disc swelling [7] .

The aim of the treatment of a pre-eclampsia patient is to minimize organ damage and maximize fetal viability. Management of the patient who developed the cortical blindness is as that of patient without any visual complication. Corticosteroid administration before 34 weeks in pre-eclamptic patient improves neonatal outcome [7] .

If antihypertensives are given in severe pre-eclampsia, they prevent cerebrovascular complications; however, the course of disease remains unchanged in women with mild pre-eclampsia [8] .

Acute and severe hypertension in women with pre-eclampsia is treated with hydralazine, labetolol, and nifedipine. In some women with severe pre-eclampsia and in all patients with eclampsia, magnesium sulphate prophylaxis is given before and after delivery as it is effective in treating both seizures and hypertension [8] .

Signs and symptomps of pre-eclampsia resolve with delivery, but in exceptional cases it may worsen within 48 h of delivery. In such cases, timely detection and intervention with aggressive antihypertensive management leads to resolution of encephalopathy within 4 h to 8 days [4] .

Complete cortical blindness is a bilateral visual loss with absence of optokinetic nystagmus and lid reflex response to threat. The papillary response, eye motility, retina, and optic nerve are normal [7] .

PRES is usually limited to the occipital lobe of the cerebral cortex, present with new onset seizure, encephalopathy, headache and visual disturbances, development of hemianopia, visual neglect, and cortical blindness. This may or may not be completely reversible. Reversibility of PRES may be clinically and radiologically incomplete, complicated by ischemic and hemorrhagic stroke leading to chronic seizure disorder and death [5] .

Arterial hypoxemia in pre-eclamptic patients should be treated efficiently and promptly to avoid multiple organ damage. Early treatment usually results in complete reversal of deficits over few days to few weeks. Thus, this case report emphasizes the need for early diagnosis and prompt treatment of PRES to avert short-term and long-term neurological sequelae.


  Acknowledgements Top


Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Mueller-Mang C, Mang T, Pirker A, Klein K, Prchla C, Prayer D. Posterior reversible encephalopathy syndrome: do predisposing risk factors make a difference in MRI appearance?. Neuroradiology 2009; 51:373-383.  Back to cited text no. 1
    
2.
Hinchey J, Chaves C, Appignani B, Breen J, Pao L, Wang A, et al. A reversible posterior leukoencephalopathy syndrome. N Engl J Med 1996; 334:494-500.  Back to cited text no. 2
    
3.
Long TR, Hein BD, Brown MJ, Rydberg CH, Wass CT. Posterior reversible encephalopathy syndrome during pregnancy: seizures in a previously healthy parturient. J Clin Anesth 2007; 19:145-148.  Back to cited text no. 3
    
4.
Casey SO, Sampaio RC, Michel E, Truwit CL. Posterior reversible encephalopathy syndrome: utility of fluid-attenuated inversion recovery MR imaging in the detection of cortical and subcortical lesions. Am J Neuroradiol 2000; 21:1199-1206.  Back to cited text no. 4
    
5.
Pratap JN, Down JF. Posterior reversible encephalopathy syndrome: a report of a case with atypical features. Anaesthesia 2008; 63:1245-1248.  Back to cited text no. 5
    
6.
Kur JK, Esdaile JM. Posterior reversible encephalopathy syndrome - an underrecognized manifestation of systemic lupus erythematosus. J Rheumatol 2006; 33:2178-2183.  Back to cited text no. 6
    
7.
Servillo G, Striano P, Striano S, Tortora F, Boccella P, De Robertis E, et al. Posterior reversible encephalopathy syndrome (PRES) in critically ill obstetric patients. Intensive Care Med 2003; 29:2323-2326.  Back to cited text no. 7
    
8.
Kastrup O, Maschke M, Wanke I, Diener HC. Posterior reversible encephalopathy syndrome due to severe hypercalcemia. J Neurol 2002; 249:1563-1566.  Back to cited text no. 8
    




 

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