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A rare case of antepartum posterior reversible encephalopathy syndrome.

Pre-eclampsia and eclampsia are wellknown causative factors of posterior reversible encephalopathy syndrome (PRES). As the name suggests, manifestations of PRES are usually transient and complete recovery is the rule. Most cases of PRES reported in the obstetric literature involve postpartum patients, with only a few cases of antepartum PRES (1-4). We report a primigravid woman who presented with an abrupt onset of eclampsia and PRES. She was managed with supportive care, labour was induced and maternal and neonatal outcomes were good. The challenges posed by PRES occurring in the antepartum period, as opposed to non-obstetric or postpartum PRES, are discussed.

CASE HISTORY

A 25-year-old primigravid woman with eight months of amenorrhoea presented with history of a fall at home, six hours before admission to the emergency department of our hospital. Her husband gave the history of five episodes of generalised tonic-clonic convulsions over a period of three hours and three episodes of vomiting. She had received regular antenatal checkups and her examination during the last visit (one month before the episode) had not revealed any abnormalities.

On examination in the emergency department, she was conscious, disoriented and restless. Both her pupils were 3 mm in size and reacting to light. There was a lacerated wound of the scalp over the occipital area. She was afebrile, pulse rate was 90 bpm, blood pressure 184/140 mmHg, respiratory rate 38 breaths/minute and arterial oxygen saturation (SpO2) 99% on room air. There was no pedal oedema and central cardiovascular system and respiratory system findings were normal. An urgent non-contrast computed tomography (CT) scan of the head, performed under sedation (total dose of propofol 60 mg), showed ill-defined hypodense areas in both parieto-occipital lobes and the right temporal lobe, involving the cortex and subcortical white matter (Figure 1). There was no intracranial haemorrhage. Based on these findings, PRES and superior sagittal sinus thrombosis were considered the differential diagnosis.

The patient was transferred to the surgical intensive care unit, where on admission she was restless, with pulse rate 84 bpm and blood pressure of 196/124 mmHg. She was administered intravenous fentanyl 100 [micro]g, midazolam 1 mg and labetalol 20 mg. The right radial artery was cannulated and intra-arterial blood pressure monitoring initiated. Magnesium sulphate 5 g was administered intravenously over 10 minutes, followed by an infusion at 1 g/hour. The blood pressure reduced to 166/110 mmHg. Intravenous betamethasone 12 mg was administered and repeated after 12 hours to accelerate foetal lung maturity (5).

[FIGURE 1 OMITTED]

Her baseline investigations were haemoglobin 128 g/l, leucocyte count 13,830 /[mm.sup.3] (neutrophils 88%, lymphocytes 6%), platelet count 131,000 /[mm.sup.3], blood sugar 5.1 mmol/l, serum [Na.sup.+] 134 mmol/l, serum [K.sup.+] 4.3 mmol/l, blood urea 7.8 mmol/l, serum creatinine 97.2 [micro]mol/l, uric acid 0.5 mmol/l, urinary protein [4.sup.+], prothrombin time 12.8 seconds (control 12.2 seconds), international normalised ratio 1.04, activated partial thromboplastin time 28 seconds (control 30 seconds) and liver function tests were normal. A bedside obstetric ultrasound showed a live foetus with estimated gestational age of 31 weeks and body weight of 1.1 kg (<5th percentile of the expected weight, representing severe intrauterine growth retardation). On vaginal examination, the cervix was 50% effaced, 2 cm dilated and membranes were intact. Her blood pressure remained in the range of 152/106 to 170/118 mmHg and pulse rate 70 to 85 /minute over the next three hours. An ophthalmic evaluation showed a normal fundus.

While preparations for caesarean section were made, her sensorium improved and four hours after admission to the surgical intensive care unit she started obeying commands. At review, it was decided to induce labour, in view of the severe intrauterine growth retardation and prematurity, good Bishop Score, adequate control of blood pressure and no signs of maternal deterioration. Induction of labour was with misoprostol 50 [micro]g vaginally. She had spontaneous rupture of membranes four hours later and contractions were augmented with an oxytocin infusion. The labour progressed smoothly, the foetus being monitored continuously by cardiotocograph. The woman was delivered of a male baby (weight 950 g) vaginally, 14 hours after induction. The baby cried soon after the birth and in the neonatal intensive care unit was managed with oxygen administered via hood, antibiotics and intravenous fluids. He developed sepsis on the third day but was treated successfully and discharged on the 25th day with a weight of 1.35 kg.

The patient's urine output was 800 ml in the first 12 hours and her blood pressure was between 150/106 and 170/118 mmHg during the active phase of labour. She did not receive analgesia during the course of labour as she was unable to give adequate feedback regarding the pain. Her blood pressure gradually reduced to 140/100 mmHg while remaining on the magnesium sulphate infusion and also receiving intravenous labetalol 20 mg six hourly. Serum magnesium level was 1.5 mmol/l. Magnesium sulphate and labetalol were stopped 24 hours after delivery and oral nifedipine 10 mg twice daily was started. She was transferred to the ward on the third day. A magnetic resonance imaging (MRI) scan performed on the eighth day (Figure 2) showed nearcomplete resolution of the lesions seen on CT at admission and also excluded superior sagittal sinus thrombosis. The patient was discharged on day 10, showing complete neurological recovery. She gave consent for publication of this report.

[FIGURE 2 OMITTED]

DISCUSSION

PRES has been reported in a wide variety of clinical settings. Presentation is varied but the most common feature has been hypertension. Precipitating factors (6) include abrupt hypertension, immunosuppressant drug use, infection, pre-eclampsia, eclampsia and renal disease. Rarely, intrathecal morphine (7) and intravenous caffeine therapy for post lumbar puncture headache (8) have also been implicated as causative factors.

Other presenting symptoms include seizures, encephalopathy, visual symptoms and headache (6). Although most patients recover completely, a 27-year-old woman in the 38th week of pregnancy who developed persistent hypertension, complicated by fatal subarachnoid haemorrhage, has been reported (1). PRES may also be associated with intracerebral haemorrhage, which is generally considered an atypical finding. The clinical outcome of PRES with associated intracerebral haemorrhage appears more variable (9).

Although PRES classically manifests in parieto-occipital white or grey matter, the temporal lobes, frontal lobes, brainstem and cerebellum may be involved (10). The posterior cerebral circulation is thought to be more susceptible, possibly because of lower sympathetic innervation than that of the internal carotid artery territory, with a consequent reduction in autoregulation of already impaired areas of circulation (11). The exact pathogenesis of PRES remains incompletely understood and is likely multifactorial. The most likely mechanism in an eclamptic patient is vasogenic oedema secondary to an acute increase in arterial blood pressure, which overwhelms the autoregulatory capacity of the cerebral vasculature causing arteriolar vasodilation, endothelial dysfunction and interstitial extravasation of fluid (2,10). In a retrospective analysis of 120 patients, Fugate et al (12) reported a high prevalence of autoimmune and inflammatory conditions in PRES patients, suggesting that endothelial dysfunction may lie at the core of its pathophysiology.

PRES is a clinical and radiological diagnosis. Clinical findings are not sufficiently specific but neuroimaging is often characteristic (13). It is important to distinguish PRES from acute stroke, to guide treatment (14). Even though MRI is considered the investigation of choice to diagnose PRES (15,16), this would have required either deep sedation or general anaesthesia during the procedure, thus exposing our patient to the risks of aspiration, haemodynamic fluctuation and the direct and indirect effects of maternally administered medications on the foetus. It might also have led to a significant delay in instituting treatment. The CT scan ruled out trauma and intracranial haemorrhage as the causes, confirming the history of a seizure first and then the fall. Clinical and radiological findings were more in favour of PRES rather than superior sagittal sinus thrombosis and subsequent MRI confirmed resolution of the pathology.

We opted in favour of induction of labour and vaginal delivery for the following reasons: the patient did not have intracranial haemorrhage and showed rapid neurological improvement; this avoided the short- and long-term maternal risks of caesarean delivery (10) and the neonatal outcome was not expected to be favourable (preterm with severe intrauterine growth retardation).

The main significance of this report lies in the antepartum presentation of PRES. Antepartum PRES poses different challenges to PRES in non-obstetric or postpartum patients because of the additional management aspects to ensure foetal wellbeing. We were posed with a difficult decision when balancing the disadvantages of caesarean section versus the risks of vaginal delivery and the rapid neurological improvement of the patient influenced our decision. This case supports others in suggesting that the outcome for obstetric patients with PRES is favourable and that timely supportive therapy is the single most important aspect of management. Magnesium sulphate was effective in stabilising this patient. Labour pain might have contributed to the slightly higher than recommended blood pressure because we did not provide analgesia during labour, other than fentanyl at admission to the surgical intensive care unit. In addition, an infusion of labetalol (rather than the intermittent dosing) would probably have avoided fluctuations in blood pressure.

Although PRES was first described in 1996 (17) and is considered a rare clinical syndrome, a single search term of "posterior reversible encephalopathy syndrome" yielded nearly 450 articles in PubMed, with more than 200 articles (mostly case reports and a few case series) published in the last two years. This indicates increased awareness about PRES among clinicians and the impact of widespread availability of imaging modalities like CT and MRI. One obstetric textbook states that the radiological and clinical features of PRES are almost universally present in eclamptic patients (10). This questions whether PRES should still be considered a rare syndrome, especially amongst obstetric patients, and whether all eclamptic patients should undergo neuroimaging. A study of PRES in severe preeclampsia and eclampsia may help. Early recognition of PRES is important for timely institution of therapy, which typically consists of gradual blood pressure control and removal or management of precipitating factors.

REFERENCES

(1.) 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.

(2.) Powell ES, Goldman MJ. Posterior reversible encephalopathy syndrome (PRES) in a thirty-six-week gestation eclamptic. J Emerg Med 2007; 33:377-379.

(3.) Gasco J, Rangel-Castilla L, Clark S, Franklin B, Satchithanandam L, Salinas P. Hemorrhagic stroke with intra-ventricular extension in the setting of acute posterior reversible encephalopathy syndrome (PRES): case report. Neurocirugia (Astur) 2009; 20:57-61.

(4.) Morelli N, Gori S, Michelassi MC, Falorni M, Cafforio G, Bianchi MC et al. Atypical posterior reversible encephalopathy syndrome in puerperium. Eur Neurol 2008; 59:195-197.

(5.) Brownfoot FC, Crowther CA, Middleton P. Different corticosteroids and regimens for accelerating fetal lung maturation for women at risk of preterm birth. Cochrane Database Syst Rev 2008; 4:CD006764.

(6.) Lee VH, Wijdicks EF, Manno EM, Rabinstein AA. Clinical spectrum of reversible posterior leukoencephalopathy syndrome. Arch Neurol 2008; 65:205-210.

(7.) Eran A, Barak M. Posterior reversible encephalopathy syndrome after combined general and spinal anesthesia with intrathecal morphine. Anesth Analg 2009; 108:609-612.

(8.) Ortiz GA, Bianchi NA, Tiede MP, Bhatia RG. Posterior reversible encephalopathy syndrome after intravenous caffeine for post-lumbar puncture headaches. AJNR Am J Neuroradiol 2009; 30:586-587.

(9.) Aranas RM, Prabhakaran S, Lee VH. Posterior reversible encephalopathy syndrome associated with hemorrhage. Neurocrit Care 2009; 10:306-312.

(10.) Pregnancy Hypertension. In: Cunningham FG, ed. Williams Obstetrics, 23rd ed. New York, NY: McGraw-Hill 2010. p. 706-756.

(11.) Witlin AG, Friedman SA, Egerman RS, Frangieh AY, Sibai BM. Cerebrovascular disorders complicating pregnancy--beyond eclampsia. Am J Obstet Gynecol 1997; 176:1139-1148.

(12.) Fugate JE, Claassen DO, Cloft HJ, Kallmes DF, Kozak OS, Rabinstein AA. Posterior reversible encephalopathy syndrome: associated clinical and radiologic findings. Mayo Clin Proc 2010; 85:427-432.

(13.) Moratalla MB. Posterior reversible encephalopathy syndrome. Emerg Med J 2010; 27: 547.

(14.) Stott VL, Hurrell MA, Anderson TJ. Reversible posterior leukoencephalopathy syndrome: a misnomer reviewed. Intern Med J 2005; 35:83-90.

(15.) 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.

(16.) Covarrubias DJ, Luetmer PH, Campeau NG. Posterior reversible encephalopathy syndrome: prognostic utility of quantitative diffusion-weighted MR images. Am J Neuroradiol 2002; 23:1038-1048.

(17.) 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.

H. V. HEGDE *, P. B. PATIL ([dagger]), R. RAMESHKUMAR ([double dagger]), T. H. SUNITA ([section]), M. T. BHAT *, R. M. DESAI **, P. R. RAO ([dagger])([dagger])

Departments of Anaesthesiology, Radiodiagnosis, Obstetrics and Gynaecology, Shri Dharmasthala Manjunatheshwara College of Medical Sciences and Hospital, Dharwad, Karnataka, India

* M.D., Assistant Professor, Department of Anaesthesiology.

([dagger]) D.M.R.D., D.N.B., Assistant Professor, Department of Radiodiagnosis.

([double dagger]) M.D., Assistant Professor, Department of Obstetrics and Gynaecology.

([section]) M.D., D.N.B., Assistant Professor, Department of Obstetrics and Gynaecology.

** M.D., Professor and Head, Department of Obstetrics and Gynaecology.

([dagger])([dagger]) M.D., Professor and Head, Department of Anaesthesiology.

Address for correspondence: Dr H. V. Hegde, Department of Anaesthesiology, Shri Dharmasthala Manjunatheshwara College of Medical Sciences and Hospital, Dharwad, Karnataka 580 009, India. Email: drharryhegde@yahoo.co.in

Accepted for publication on December 9, 2010.
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Article Details
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Author:Hegde, H.V.; Patil, P.B.; Rameshkumar, R.; Sunita, T.H.; Bhat, M.T.; Desai, R.M.; Rao, P.R.
Publication:Anaesthesia and Intensive Care
Article Type:Clinical report
Geographic Code:9INDI
Date:May 1, 2011
Words:2261
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