Fatal Stroke in Pregnancy and the Puerperium: Case Series

NCIS is a database of coronial information provided by Australian coroners’ courts. A complete NCIS case file includes demographic information, police autopsy and toxicology reports, and the coronial finding. Cause of death is noted by a forensic pathologist on the autopsy and coroner’s report. These cases were all deceased and the ethical approval to retrospectively inspect the NCIS case files of the deceased was received from the NCIS and University of New South Wales Human Research Ethics Committees and was in accordance with institutional guidelines.

This series includes all cases of fatal stroke occurring as an event or consequent to an initial event occurring during pregnancy or 6-weeks postpartum over the period January 1, 2009 to December 31, 2016.

Information was collected on maternal age, gestational age, obstetric history, including parity, gestational age at time of delivery, clinical presentation, maternal comorbidities, history of chronic hypertension (increased blood pressure before the 20th week gestation),⁴ or pregnancy-related hypertension, including gestational hypertension (newly increased blood pressure after 20th week gestation), preeclampsia-eclampsia, or hemolysis, elevated liver enzymes and low platelet count syndrome (HELLP).⁴ Obstetric management was categorized as normal delivery, cesarean section, or expectant (no obstetric intervention at time of stroke onset).⁴ Fetal outcomes were categorized as term delivery (liveborn neonate delivered 37 to 41 weeks gestation), preterm birth (liveborn neonate delivered between 20 and 36 weeks and 6 days gestation), and abortion/stillbirth.⁴

Data were collected on type of stroke (hemorrhagic, ischemic), location, extension beyond rupture site, presence of aneurysm/arteriovenous malformation. Data relating to known traditional stroke risk factors included: obesity (≥30.0 body mass index); diabetes mellitus; previous stroke; alcoholism; tobacco smoking; other drug use; cardiomyopathy; hypertension; vasculitis; and endocarditis. Diagnoses were those recorded in the findings and cause of death as reported by the coroner.

Fourteen cases were identified, of which 1 was excluded as detailed information was not available. One fatal stroke occurred in the third trimester, the remaining 12 in the puerperium (Table 1). Six deaths occurred in the first week postpartum. The mean age was 32.8 (SD=4.5); 5 were aged ≥35 years. Obstetric management comprised normal vaginal delivery (n=6), planned cesarean section (n=5), or emergency cesarean section (n=2).

All fatal strokes were hemorrhagic in origin, though in 1 woman (case 13) the fatal subarachnoid hemorrhage was preceded by an earlier nonfatal mycotic brain infarct. Among the 3 subarachnoid hemorrhages, a saccular/berry aneurysm was identified in one (case 10), not in another (case 11), and a mycotic aneurysm in the third (case 13). Neurosurgical management was not indicated in 2 women found dead, and was supportive in 5 deemed not candidates for surgery. Surgical management entailed extraventricular drain insertion in 3, and craniotomy and evacuation in 3.

In cases 1 to 5, fatal stroke occurred in the context of chronic hypertension or pregnancy-related hypertension (Table 2). In 2 cases (cases 3,4) hemolysis, elevated liver enzymes and low platelet count syndrome (HELLP) were identified at autopsy. While case 3 was reported to have had mild preeclampsia antenatally, no signs of pregnancy-related hypertension had been reported in case 4. Finally, hypertension was noted to be transiently present 1 week before delivery in an otherwise unremarkable pregnancy (case 5). The hypertension resolved spontaneously without treatment and was next reported during delivery with the emergence of an extensive intracerebral hemorrhage postpartum. This case was considered clinically as gestational hypertension, though autopsy revealed previously undiagnosed Takayasu arteritis.

In cases 6 to 8, deaths occurred secondary to posterior reversible encephalopathy syndrome and reversible cerebral vasoconstriction syndrome, disorders known to be related to preeclampsia-eclampsia. Case 6 had no antenatal signs of pregnancy-induced hypertension, but 8 days postpartum there was hypertension, proteinuria, lower leg edema, and abnormal liver function tests. Posterior reversible encephalopathy syndrome was diagnosed at autopsy after a massive left frontal hemorrhage. Reversible cerebral vasoconstriction syndrome was the cause of death in cases 7 and 8. Autopsy findings in both cases reported absence of vasculopathic changes to suggest eclampsia/preeclampsia.

An arteriovenous malformation was suggested by magnetic resonance imaging in case 9, but not identified at autopsy because of extensive disruption to brain tissue. A ruptured aneurysm was identified at autopsy in one (case 10) but not in another (case 11) case of subarachnoid hemorrhage.

None of the women had history of previous stroke, congenital heart disease, atrial fibrillation, sickle cell anemia, smoking, diabetes mellitus, or alcoholism. One was morbidly obese (body mass index=43.9; case 1). Two were found at autopsy to have previously undiagnosed risk factors: Takayasu arteritis (case 5) and cardiomyopathy (case 12).

Case 13 experienced a middle cerebral artery infarct with occlusion of the internal carotid artery suggestive of dissection. This was deemed secondary to infection with mycotic aneurysm formation of the intracranial internal carotid artery in the context of healing mitral valve endocarditis. The subsequent extensive fatal subarachnoid hemorrhage was reported at autopsy to have arisen from the mycotic aneurysm.