Fulminant Postpartum Weil’s Syndrome Presenting with Refractory Seizures and Multiorgan Failure: A Case Report and Critical Care Management.

Abstract

Leptospirosis is a globally prevalent zoonotic infection with protean manifestations, while severe disease (Weil’s syndrome) is uncommon and rarely reported in the postpartum period, where it can closely mimic obstetric emergencies. We report a rare case of severe postpartum leptospirosis complicated by sudden-onset seizures and multiorgan failure. A 32-year-old woman developed generalized tonic–clonic seizures two hours after vaginal delivery, followed by septic shock, hyperpyrexia, refractory seizures, acute liver failure, acute kidney injury, coagulopathy, and stress-induced cardiomyopathy. Initial differentials included obstetric catastrophes such as eclampsia, acute fatty liver of pregnancy, and amniotic fluid embolism.

Diagnosis was supported by a positive Leptospira IgM ELISA in the appropriate clinical context; however, confirmatory testing with the microscopic agglutination test (MAT) or polymerase chain reaction (PCR) could not be performed, which remains a limitation of this report. Magnetic resonance imaging (MRI) of the brain revealed features of cerebral hyperperfusion, a finding not previously reported in postpartum Weil’s disease. Prompt institution of targeted antimicrobial therapy, aggressive critical care support, and multimodal monitoring resulted in gradual recovery. Cerebral oxygenation and response to therapy were continuously monitored using bilateral near-infrared spectroscopy (NIRS), representing a novel neuromonitoring strategy in this setting.

This case highlights leptospirosis as an important differential in postpartum seizures with multiorgan failure in endemic regions. It expands the spectrum of postpartum Weil’s disease by demonstrating cerebral hyperperfusion on MRI, novel use of NIRS monitoring, and associated stress-induced cardiomyopathy, with important implications for critical care management.

Introduction

Leptospirosis is a globally prevalent zoonotic infection caused by Leptospira interrogans, with rising incidence in tropical and urban settings. Although most infections are mild and self-limiting, approximately 5–10% progress to severe disease, classically termed Weil’s syndrome, characterized by jaundice, acute kidney injury, coagulopathy, hemorrhagic manifestations, and multiorgan dysfunction. Neurological involvement, though uncommon, may present with seizures, altered sensorium, or encephalopathy. ^1-3

Leptospirosis in pregnancy and the postpartum period is uncommon and poorly described in the literature. Physiological adaptations of pregnancy, such as immune modulation, increased plasma volume, and endothelial vulnerability, can obscure early clinical manifestations, leading to delayed diagnosis and fulminant disease. ^4-6 In the postpartum period, these changes may precipitate rapid clinical deterioration, mimicking obstetric catastrophes such as eclampsia, acute fatty liver of pregnancy (AFLP), amniotic fluid embolism (AFE), and postpartum neurovascular syndromes. ^7-9

For anaesthesiologists and intensivists, postpartum collapse with seizures and multiorgan failure presents a unique diagnostic and therapeutic challenge, requiring rapid airway control, hemodynamic stabilization, and broad etiological evaluation. We report a rare case of severe postpartum leptospirosis complicated by septic shock, hyperpyrexia, refractory seizures, acute liver failure, acute kidney injury, coagulopathy, and stress-induced cardiomyopathy, highlighting key peri-anesthetic and critical care considerations.

Case Description

A 32-year-old woman (G3P1), a booked antenatal case with hypothyroidism on regular treatment and documented euthyroid status, from a rural background, presented at 39 weeks and 2 days of gestation with complaints of decreased fetal movements. The symptoms resolved spontaneously; however, labour was induced in view of borderline oligohydramnios using a transcervical Foley catheter. After 24 hours, she delivered vaginally with forceps assistance and mediolateral episiotomy due to maternal exhaustion and fetal bradycardia with a heart rate (HR) of 75-80 beats/min. The neonate had Apgar scores of 2 and 6 at 1 and 5 minutes, respectively.

Two hours postpartum, the patient suddenly developed one episode of generalized tonic-clonic seizures. Intravenous midazolam (3 mg) and levetiracetam (1 g over 15 mins) were administered. Rapid sequence intubation was performed using succinylcholine (100 mg), and the airway was secured with a 6.5-mm internal diameter endotracheal tube. Airway management was uneventful with no difficulty encountered during laryngoscopy or intubation. Immediately following intubation, she developed supraventricular tachycardia with a HR of approximately 200 beats/min and unrecordable blood pressure (BP). Synchronized electrical cardioversion was performed, restoring sinus rhythm (HR:159 beats/min; BP: 92/50 mmHg). The patient was immediately shifted to the intensive care unit (ICU) with intermittent boluses of phenylephrine (100 μg). Once in the ICU, she was put on mechanical ventilation. Noradrenaline infusion (0.08 μg/kg/min) was initiated through the central venous catheter. On further examination, Glasgow Coma Scale (GCS) was E1VTM1, both pupils were 1.5 mm in size and sluggishly reactive, and core temperature was 106.7°F. Transthoracic echocardiography revealed stress-induced cardiomyopathy with global hypokinesia and a reduced left ventricular ejection fraction of 40%. In view of suspected sepsis, empirical broad-spectrum antibiotics (piperacillin–tazobactam 4.5 g i.v. thrice daily and metronidazole 500 mg i.v. thrice daily) were initiated after obtaining blood, urine and sputum samples for Gram staining and culture. Initial fluid resuscitation was performed with 20 ml/kg of crystalloid solution, followed by a goal-directed approach guided by dynamic hemodynamic indices (systolic pressure variation and pulse pressure variation) and lung ultrasound. Approximately 6 hours after ICU admission, the patient developed recurrent seizures, treated with an intravenous midazolam bolus. Levetiracetam 750 mg i.v, twice daily, was initiated. Non-contrast computed tomography (NCCT) of the brain (day 2) was done, which showed mild cerebral edema without features of hemorrhage or infarction. Over the next 24 hours, the patient again developed recurrent seizures along with acute liver failure with rapidly rising transaminases (>2000 IU/L), conjugated hyperbilirubinemia (6.8 mg/dl), coagulopathy (aPTT: 45 s, INR: 2.3), and mild hyperammonaemia (98 μg/dl), acute kidney injury (peak creatinine: 3.8 mg/dl) with nephrotic-range proteinuria, severe thrombocytopenia (nadir 37,000/mm³), hyperuricemia (11mg/dl), and elevated NT-proBNP (8500 pg/ml). Lacosamide 200 mg i.v. loading followed by 100 mg i.v, twice daily was added to levetiracetam for refractory seizures. Platelet transfusions, vitamin K, hepatoprotective (rifaximin, lactulose, L-ornithine-L-aspartate, and ursodeoxycholic acid) were administered. Dosages of the drugs were adjusted as per creatinine clearance. A comprehensive evaluation for tropical infections and viral hepatitis was performed. Leptospira IgM ELISA was found positive, confirming severe leptospirosis (Weil’s disease). Doxycycline (100 mg i.v. twice daily) and azithromycin (500 mg i.v. once daily) were commenced. Blood cultures remained sterile. Other infectious and autoimmune aetiologies were excluded. Magnetic resonance imaging (MRI) of the brain (day 3) demonstrated left cerebral and cerebellar hyperperfusion with mild cerebral edema (Figure 1A & 1B). Cerebral oxygenation and response to therapy were continuously monitored using bilateral near-infrared spectroscopy (NIRS). Left-sided NIRS (rSO₂) values remained consistently above 80% during the initial hyperperfusion stage, while right-sided rSO₂ values remained between 60% and 65%. Enteral feeding was initiated once the patient stabilised hemodynamically.

Figure 1:

Magnetic Resonance Imaging (MRI) T2*perfusion image shows left cerebral hemispheric hyperperfusion (bright red) (Fig 1A), left cerebellar hemispheric hyperperfusion (Fig. 1B), resolving left cerebral hemispheric hyperperfusion (green) (Fig 1C), and resolving left cerebellar hemispheric hyperperfusion (Fig 1D).

By Day 7, vasopressors were weaned off. Gradual improvement was noted in renal function, liver enzymes, coagulation profile, and mental status (E4VtM6). Left-sided NIRS (rSO₂) values also returned to the normal cerebral oxygenation range of 65%–70%. The patient was gradually weaned off the mechanical ventilator, and the trachea was extubated on Day 10 and transitioned to supplemental oxygen with incentive spirometry. Physiotherapy and neuro-rehabilitation were initiated. A brief episode of hospital-acquired pneumonia was treated successfully. She was transferred to the ward on day 19. The patient experienced a transient ICU readmission on day 28 for a breakthrough seizure, which resolved with antiepileptic dose escalation. She was discharged home on day 36 on oral levetiracetam 1 g twice daily and lacosamide 100 mg twice daily. At 2-month follow-up, clinical examination revealed near-complete recovery, and brain MRI demonstrated resolving cerebral and cerebellar hyperperfusion (Figure 1c & 1D).

Discussion

Leptospirosis is an important yet under-recognized cause of acute febrile illness and multiorgan dysfunction in tropical regions. Severe leptospirosis (Weil’s disease) occurs in a minority of patients but is associated with high morbidity and mortality due to hepatic failure, acute kidney injury, coagulopathy, myocarditis, and septic shock. Neurological involvement, although uncommon, may manifest as seizures, encephalopathy, aseptic meningitis, or cerebellitis and is an indicator of severe systemic disease. ^1,2 In a study from Nigeria, male gender, young adult age (21–40 years), and occupational exposure (particularly crop farming with animal and contaminated water contact) were identified as significant risk factors for leptospirosis. Poor disease awareness and exposure to potentially contaminated animal water sources further increased the risk of infection. ¹⁰

Leptospirosis in pregnancy and the immediate postpartum period is exceedingly rare, with limited case descriptions. In a recent systematic review, the first of its kind on leptospirosis in pregnancy, the reported incidence was 1.3 per 10,000 among pregnant women presenting with fever or jaundice, with potentially higher rates in endemic areas. ¹¹ Physiological immune modulation, increased plasma volume, and altered endothelial permeability during pregnancy can blunt early symptoms and delay diagnosis. In the postpartum state, abrupt hemodynamic and inflammatory shifts may precipitate rapid clinical deterioration. ^4-6 In the present case, postpartum onset of seizures with hyperpyrexia, shock, hepatic dysfunction, thrombocytopenia, and cardiomyopathy initially raised a strong suspicion of obstetric emergencies such as eclampsia, AFLP, AFE, or catastrophic intracranial events. The overlap in clinical and laboratory features underscores the diagnostic complexity faced by anesthesiologists and intensivists.

Neurological manifestations in leptospirosis are thought to arise from a combination of direct leptospiral invasion, immune-mediated endothelial injury, cytokine storm, and blood–brain barrier disruption. ^{12, 13} Refractory seizures and cerebral edema, as seen in this patient, reflect severe neuroleptospirosis. MRI findings of focal hyperperfusion and cerebral edema support an inflammatory and immune-mediated mechanism rather than primary ischemic or hemorrhagic pathology. Stress-induced cardiomyopathy, another recognized but infrequent complication, likely resulted from systemic inflammation, catecholamine surge, and septic shock, further complicating peri-intubation and hemodynamic management.

From an anesthetic and critical care perspective, this case highlights several key considerations. Early airway protection and seizure control are paramount in postpartum collapse. Hemodynamic instability following intubation may be exacerbated by underlying myocarditis or cardiomyopathy in leptospirosis, necessitating cautious induction, invasive monitoring, and prompt vasopressor–inotrope support. Multiorgan failure requires meticulous drug dosing, avoidance of hepatotoxic agents, and renal-adjusted antiepileptic therapy. Importantly, early consideration of tropical infections in endemic regions and timely serological testing facilitated definitive diagnosis and targeted antimicrobial therapy, which is crucial for recovery.

Conclusion

This case emphasizes that leptospirosis should be included in the differential diagnosis of postpartum seizures with multiorgan dysfunction in endemic areas. A high index of suspicion, aggressive supportive care, and multidisciplinary management are key to preventing rapid clinical deterioration and ensuring favorable outcomes. NIRS is an effective non-invasive tool for monitoring cerebral oxygenation in neuroleptospirosis and may help in assessing response to therapy.

Patient consent

Written informed consent for the procedure and future publishing was obtained from the patient.

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Conflicts of interest

There are no conflicts of interest.