Postpartum Atypical Posterior Reversible Encephalopathy Syndrome in a COVID-19 Patient - An Obstetric Emergency.

Encephalopathy in COVID-19 has been widely reported with several reports of posterior reversible encephalopathy syndrome (PRES) speculated to be due to an abrupt surge in blood pressure caused by coronavirus disease. Though peripartum posterior reversible encephalopathy syndrome is well recognized, its atypical variant with hemorrhage is uncommon. Peripartum atypical posterior reversible encephalopathy syndrome with COVID-19 requires early recognition and warrants dedicated inter-disciplinary management. We present a case of postpartum atypical posterior reversible encephalopathy syndrome with good maternal and fetal outcome. Our clinical and treatment approach with differential diagnosis are discussed in this hitherto unreported obstetric emergency with COVID-19.

Case report

A 25 year old primigravida with unremarkable antenatal period went into spontaneous labor at term and delivered a healthy baby weighing 3.2 kg. She had an unremarkable hemogram (hemoglobin: 12.4 g/dL, total leucocyte count: 5500/cu.mm with 65% neutrophils and 35% lymphocytes, platelets: 2.7 lacs/cu.mm), renal function test (urea 23 mg/dL, creatinine 0.7 mg/dL), liver function tests(AST 34 U/L, ALT 36 U/L) and a normal urinalysis at admission. Twelve hours after delivery she started spiking high grade fever and developed cough. Her blood work up showed neutrophilic leucocytosis (absolute neutrophil count:12,500/cu.mm), platelets(2.8 lacs/cu.mm), creatinine (0.7 mg/dL), mildly raised transaminases(AST 56, ALT 58), elevated C-reactive protein(40 mg/L), raised D-dimer (1.8 mg/L) with normal prothrombin and activated partial thromboplatin time and no proteinuria. Reverse transcriptase based nasopharyngeal swab testing for coronavirus disease came positive. High resolution computed tomography of chest showed symmetrical ground glass opacities concerning less than 50% of lung parenchyma (Fig. 1G). Hydroxychloroquine,oseltamivir,piperacillin-tazobactum and azithromycin were started. A day later she complained of headache and had blood pressure fluctuations with maximal blood pressure of 190/120 mm of Hg. Subsequently, she had a cluster of generalized tonic-clonic seizures,became drowsy and was placed on mechanical ventilation. She was treated with benzodiazepines, labetalol and levetiracetam with stringent blood pressure control. Scalp electroencephalogram showed left occipital sharp waves with no electrographic seizures. Differential diagnosis of PRES, cerebral venous thrombosis, encephalitis, cerebral vasculitis were considered. Non contrast CT head showed symmetrical parieto-occipital hypodensities, likely vasogenic edema with small hemorrhages noted bilaterally and concurrent CT angio-venogram were normal (Fig. 1D,1E,1F). Intermittent pneumatic compression device was applied to reduce the risk of venous thromboembolism. Pharmacological prophylaxis with anticoagulant for venous thromboembolism was avoided in view of bilateral parieto-occipital small hemorrhages on neuroimaging. Repeat blood work up on day 4 of hospitalization showed declining neutrophilia, creatinine and transaminases with sterile blood, urine, endotracheal cultures and no proteinuria. Autoimmune panel for APLA, SLE, rheumatoid arthritis, Sjogren's,c-ANCA, p-ANCA were negative. Cerebrospinal fluid analysis was normal except for mildly elevated protein (50 mg/dL), gram stain, culture and encephalitis PCR panels were negative. She had no further seizures, became conscious and was extubated six days later. MRI brain confirmed bilateral posterior predominant subcortical vasogenic edema with bilateral small hemorrhages suggestive of atypical PRES (Fig. 1A,1B,1C ). There was no vertical transmission of COVID-19. At time of discharge on hospital day 12, she was alert, independently ambulating and was on single antihypertensive.

Figure 1

MRI Brain A–C (A)Fluid Attenuated Inversion Recovery – Bilateral parieto-occipital hyperintensities (B and C) Diffusion Weighted Imaging and Apparent Diffusion Coefficient in same areas as in (A), high signal on b-1000 with no corresponding ADC fall suggestive of vasogenic edema (D) CT head- Bilateral parieto-occipital hypodensities with small hemorrhages noted on both sides (E and F) Normal contrast enhanced CT venogram and angiogram of brain, respectively (G)High Resolution Computed Tomography of thorax shows bilateral sub-pleural lower zone ground glass opacities with areas of consolidation.

Discussion

This sudden surge of blood pressure was unexpected as our patient was normotensive during pregnancy, had an uneventful normal delivery and had no suggestion of preeclampsia. SARS CoV-2 can bind directly to angiotensin-converting enzyme 2 receptors causing endothelial disruption, an abrupt rise in blood pressure and failure of cerebral blood flow autoregulation. We speculate a peripartum infection with COVID-19 could have triggered cerebral autoregulatory dysfunction leading to blood-brain barrier breakdown and consequent vasogenic edema. Presence of hemorrhage, diffusion restriction and contrast enhancement with symmetrical or asymmetrical posterior predominant vasogenic edema constitute atypical PRES, these findings are known to be uncommon in postpartum PRES. , While there are several reports of PRES with COVID-19, the atypical variant has only been rarely reported and none in pregnancy. To our knowledge this is the first case report on postpartum atypical PRES with COVID-19.

Declaration of Competing Interest

Nil.