Sowpari R*, Warke HS**.
(* Second year resident, ** Associate Professor, Department of Obstetrics and Gynecology, Seth GS Medical college and KEM Hospital, Mumbai, India.)
Preeclampsia is an insidious disease occurring in 4-7% of all pregnancies. It can develop anytime during pregnancy, delivery or postpartum. Posterior reversible encephalopathy syndrome (PRES) is a cliniconeuroradiological diagnosis. It rarely occurs without seizures or after delivery. Here we present a case of a patient with history of severe preeclampsia with term pregnancy, complicated by posterior reversible encephalopathy syndrome (PRES) with seizures seven days after delivery in her postpartum period. Clinical improvement with complete resolution without any complications was observed within one week.
Preeclampsia can affect multiple systems, including the central nervous system. Posterior reversible leukoencephalopathy syndrome is a clinical and radiological syndrome. It is also called as reversible posterior cerebral edema syndrome, brain capillary leak syndrome or hyper perfusion syndrome. PRES can clinically associated with a number of medical conditions such as preeclampsia, eclampsia, hypertensive encephalopathy, acute renal diseases, hemolytic uremic syndrome, cytotoxic drugs and immunosuppressant drugs, blood transfusion and electrolyte imbalance.
Clinically patient may present with headache, confusion, visual disturbances, blindness, photophobia or seizures. Parieto-occipital white matter changes are observed on imaging studies due to vasogenic edema.
If early diagnosis is established and appropriate treatment is started without delay, clinical symptoms of PRES can reverse.
A 25-year-old married since 2 years P1L1 day7 of emergency caesarean was admitted in the emergency medical ward in view of post partum eclampsia. Patients’ antenatal registration was at seven months of gestation at a primary health centre and had 8 antenatal visits. Throughout her antenatal period her Blood Pressure was within the normal range and urine albumin was nil. There was no past history of any seizure disorder or any medical or surgical high risk. Patient was not compliant with hematinics. The patient was admitted at a private hospital in view of pain abdomen at 40.3 weeks of gestation. On examination, high BP of 150/100 mm of hg was recorded. There were no premonitory symptoms and urine albumin was nil. Patient was started on tablet Labetalol 100mg OD and tablet Atenlol 50 mg OD. Patient’s hemoglobin was 7.8mg% and one unit packed cell transfusion was given. Emergency LSCS was done in view of cephalopelvic disproportion in labor under spinal anesthesia. Patient delivered a healthy female child of 3.5kg. Post LSCS patient was stable. There were no premonitory symptoms or seizures observed and urine albumin was nil. Patient was discharged on antihypertensives(labetalol and atenolol) and BP was controlled at 130/80 mm of hg. Patient was not compliant with her antihypertensive medications. On day 7 after delivery, patient complained of headache and vomiting followed by one episode of generalized tonic clonic convulsions followed by unconsciousness for 30 minutes. After regaining consciousness patient was drowsy. Patient came to the emergency medical ward at our tertiary care centre. On admission patient had generalized headache with drowsiness. General condition was moderate, pulse was 96/min, BP was 180/130 mm of Hg, on auscultation chest was clear and heart sounds were normal Labetalol 20mg was given intravenously . Repeat BP was 160/110 mm of Hg. On per abdominal examination uterus was well contracted and on per vaginal examination there was no bleeding. Bilateral knee jerks were normal and urine albumin was +1. CT scan done was suggestive of PRES (posterior reversible encephalopathy syndrome). Patient was started on intravenous mannitol and levitiracetam. Labetalol 100mg thrice daily and nifedepine 10mg four times daily was started. Complete blood count revealed a hemoglobin of 11.4g/dL, platelet count of 162.000/mm3. Renal and liver function tests, serum electrolytes and electrocardiogram were normal. On day 8, post LSCS patient had second episode of convulsion followed by post ictal confusion and drowsiness. Injection Magnesium sulphate was given as per Pritchard regimen. Mannitol, levitiracetam and labetalol were continued. MRI brain was done which was suggestive of PRES. Neurology evaluation was done and injection eptoin was added. Patient was continued with these medications. No further convulsions were observed. Four days after starting treatment, her blood pressure was controlled. Meanwhile the patient had no episodes of seizures and on day 18 postpartum, there was complete recovery and was discharged without any recurrent symptoms.
PRES is a rare and serious clinical entity of central nervous system. It can present with headache, altered mental status, seizures and visual loss. The most common presentation is with generalized tonic clonic seizures. In our case PRES occurred with seizures one week after LSCS in a preeclamptic woman with no history of visual complaints. We are reporting this case as this was a delayed presentation of PRES.
Possibility of PRES must be kept in mind when a postpartum patient presenting with headache, mental confusion after seizures with high blood pressure with history of severe preeclampsia antenatally. The possibilities that must be kept in mind include eclampsia, cerebrovascular hemorrhage and PRES. If patient presents with visual complains, then ophthalmological examination must be done to rule out hypertensive retinopathy, exudative retinal detachment and cortical blindness must be ruled out as these can occur in preeclampsia and eclampsia.
The pathophysiological mechanism underlying PRES is still not clear. Two different theories have been considered. The first is the hyper perfusion or the vasogenic theory. It can be due to disordered cerebral autoregulation and endothelial dysfunction. The combination of acute hypertension and endothelial damage can lead to vasogenic edema elicited by the capillary leak of serum into the brain interstitium. The reason for the primary involvement of the posterior brain regions (parietoccipital lobes) is not well understood. It can be due to the regional heterogenicity of sympathetic innervations of intracranial arterioles. This is due to better auto regulation of the anterior circulation due to better sympathetic innervations as compared to the posterior circulation. Acute hypertension can cause hyper perfusion and edema in posterior circulation in PRES. The second theory is the hypoperfusion-ischemic theory or the cytotoxic theory in which the toxic cytokines playing a role is still uncertain.
It is thought that patients with chronic hypertension have hypertrophic arterial walls, including the central nervous system causing reduced permeability of blood brain barrier. Patients with preeclampsia do not have this compensatory effect and even a small increase in blood pressure can lead to increased permeability of the blood-brain barrier.[4,5]
Neuroimaging is impotant for the diagnosis of PRES and radiological abnormalities encountered in PRES are best demonstrated by magnetic resonance imaging (MRI). MRI shows symmetrical white matter edema in the posterior cerebellar hemispheres that particularly involves the parieto-occipital regions bilaterally. T2- weighted MRI shows areas of hyper intense signal.
The goal of therapy is to rapidly lower the blood pressure. Once the blood pressure is controlled, neurological symptoms and cerebral lesions disappear completely within days to weeks. Magnesium therapy should be started if eclampsia or PRES in pregnancy is suspected.
The prognosis of PRES is usually benign. Clinical improvement always follows the treatment of elevated blood pressure and it is important to avoid irreversible damage to the central nervous system.
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Sowpari R, Warke HS. Posterior Reversible Encephalopathy Syndrome Postpartum. JPGO 2017. Volume 4 No. 6. Available from: http://www.jpgo.org/2017/06/posterior-reversible-encephalopathy.html