Maternal collapse can occur during any stage of pregnancy and up to 6 weeks after delivery. It usually involves the cardiorespiratory/central nervous system resulting in reduced or absent consciousness and may even result in death. Acute pituitary hemorrhage associated with maternal collapse secondary to drug toxicity is rare.

Prior informed consent was taken from the patient with approval from the hospital ethics committee to publish this case report. A 24-year-old primigravida at 27 weeks and 4 days of gestational age, with a body mass index (BMI) of 22.5 kg/m2, was referred to our tertiary care center with severe preeclampsia.

The patient’s blood pressure was poorly controlled on oral labetalol. Investigations revealed massive proteinuria (urine albumin 4 +) with features of HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count). Serum lactate dehydrogenase (LDH)-574 IU/l, serum (aspartate transaminase/alanine transaminase) AST/ALT-171/184 IU/l, and platelets were 70,000/mm3, respectively.

An emergency lower segment cesarean section (LSCS) was done under general anesthesia (GA) at 28-week POG for hypertensive crisis and a non-reassuring fetal nonstress test (NST) with an impending abruption of the placenta. Her blood pressure remained high (180/130 mmHg–190/138 mmHg with a heart rate of 90–100/min) during the perioperative period, and there was a blood loss of 450 ml during the surgery. A female child weighing 657 g was delivered. Intravenous labetalol infusion at 30 mg/h was started during the intraoperative period for optimizing the blood pressure, and the mother was successfully extubated uneventfully in the postoperative period and was transferred to maternal HDU (high-dependency unit). Magnesium sulfate infusion was started as per the Zuspan regimen (4-g i.v. in 100-ml NS over 20 min) along with labetalol infusion with continuous electrocardiogram (ECG) and urine output monitoring. Twenty minutes post-magnesium sulfate infusion, the patient became unresponsive, with an absent carotid pulse and asystole.

The code blue team was activated, and the patient was resuscitated with cardiopulmonary resuscitation (CPR) as per the advanced cardiac life support (ACLS) protocol with chest compressions and i.v. adrenaline boluses repeated every 3 min, and the trachea was intubated. Eclampsia/intracerebral hemorrhage/drug toxicity (β-blocker and hypermagnesemia) was suspected as the likely etiology of cardiac arrest. Intravenous calcium gluconate 3 g was given for suspected magnesium toxicity. A return of spontaneous circulation (ROSC) was achieved after 15 min of resuscitation.

A point-of-care ultrasound (POCUS) was done for evaluation of sudden collapse. 2D echocardiography showed normal left ventricular function with no RA/RV (right atrium/right ventricular dilation) or pericardial collection. A lung scan ruled out pneumothorax. There was no evidence of deep vein thrombosis in the lower limbs, and abdominal scanning showed a minimal fluid collection in the pouch of Douglas. There was no obvious bleeding from the operated site or per vagina. Pupils were dilated and unresponsive initially but were responding after 12-h post-resuscitation. Targeted temperature management (TTM) at 36 °C was done by external cooling measures. The patient was placed on mechanical ventilation with sedation and muscle relaxation for 24 h. Post-ROSC, the patient had stable hemodynamics with ECG showing persistent bradycardia (HR: 30–35/min) with prolonged QTc interval (526 ms) (see Fig. 1) which responded transiently to i.v. atropine.

ECG showing prolonged QTc interval

Drug toxicity with magnesium and labetalol overdose was suspected, and both infusions were stopped. Serum magnesium level after 1-h post-ROSC was 7.1 mg/dl. Acute hemodialysis (HD) was done to reduce the magnesium levels (3.4 mg/dL post 3 h of dialysis) following which the heart rate (70/min) and the QTc (480 ms) were stabilized. A temporary pacemaker though kept standby was not contemplated as the heart rate had remained normal post-dialysis. She had recurrent hypoglycemic episodes which were managed with an intravenous infusion of 50% dextrose.

Clinical investigations included a complete endocrine workup that was done after ICU admission are shown in Table 1.

The serum cortisol, LH, and FSH were low, with elevated insulin levels. A primary adrenal failure (secondary to hemorrhage) with the involvement of the HPA (hypothalamic–pituitary–adrenal) axis was suspected. The patient was started on i.v. hydrocortisone which corrected her hypoglycemic episodes. Non-contrast computed tomography (CT) imaging of the brain and abdomen was done which showed pituitary hemorrhage with a normal CT abdomen (Fig. 2). Magnetic resonance imaging (MRI) T1-weighted images (Fig. 2) of the brain confirmed the findings.

NCCT and MRI T1 sagittal images of the brain

A diagnosis of pituitary hemorrhage with atypical features of Sheehan’s syndrome was made as there was no lactation failure. The neonate delivered had developed sepsis with acute respiratory distress syndrome (ARDS) and necrotizing enterocolitis (NEC) which was managed with surfactant, antibiotics, continuous-positive pressure ventilation (CPAP), and intra-abdominal drain.

The patient was successfully extubated after 36 h on mechanical ventilation without any residual neurological deficits and was followed up for 3-month duration during the above period the neonate was in the neonatal intensive care unit (NICU). Steroids were tapered and stopped after 3 months. Currently, both the mother and child were discharged with regular follow-ups.