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Postnatal stroke:Is it always sinister?

Monday, 24 June, 2013 - 13:00
Board 01

Postnatal stroke: Is it always sinister?

F Nizami, V Mistry, P Maharajan

Department of Obstetrics and Gynaecology, Oxford University Hospitals NHS Trust, Oxford, UK


Stroke is an important cause of severe maternal morbidity and mortality. It is widely believed that the risk of cerebrovascular events in otherwise healthy young women is significantly greater during pregnancy. However, a recent UK Obstetric Surveillance System (UKOSS) study estimated the incidence of antenatal haemorrhagic and ischaemic stroke to be 0.6 and 0.9 per 100,000 maternities respectively, which is considerably lower than previous estimates1.


Furthermore, evidence from population-based studies indicates that the risk of both haemorrhagic and ischaemic stroke is greater in the peripartum and postnatal periods than in the preceding 9 months of gestation2,3. We henceforth present a case of rapidly resolving postpartum stroke in a young mother.

Case Report:


A 26-year-old nulliparous woman with an otherwise uncomplicated pregnancy, underwent induction of labour at 34 weeks of gestation due to preterm prelabour rupture of membranes (PPROM). The baby was delivered via forceps and was admitted to the special care baby unit (SCBU) for monitoring, but was otherwise well. The immediate post-natal period was uneventful and the woman was discharged after 2 days.



The woman presented to A&E on the 6th postnatal day with sudden onset slurred speech and left-sided facial and upper arm weakness. The symptoms resolved within 30 seconds; however the dysarthria persisted. She denied headaches, neck stiffness and visual disturbance, and there was no preceding trauma. She had a history of surgical closure of two large ventricular septal defects (VSDs) at 5 months of age; her medical history was otherwise nil of note. She denied any personal or familial history of venous thromboembolism or cerebrovascular disease.



Observations on admission were stable, except for new-onset hypertension (BP 178/109mmHg), for which she was given a stat dose of nifedipine 10mg. Urine dip showed 2+ protein. Neurological examination revealed dysarthria, bilateral lower limb hyperreflexia and left ankle clonus.  Tone and power was normal. Upper limb examination was unremarkable, as were cranial nerves. There were no visual disturbances and no cerebellar signs. Systemic examination was normal.



Full blood count, clotting, renal function and liver function were normal, as were thrombophilia, pre-eclampsia and autoimmune serology. 12-lead electrocardiogram (ECG) revealed right bundle-branch block (RBBB). Unenhanced computed tomography (CT) of the head showed no haemorrhagic lesion or collection. Carotid Doppler was unremarkable. A magnetic resonance image (MRI) of the head revealed an acute cortical infarction in the territory of the right middle cerebral artery (MCA), with no haemorrhagic transformation, no mass-effect and no evidence of cerebral venous thrombosis (CVT).



A diagnosis of postnatal cerebral infarction was made and the patient was transferred to the stroke unit. She was not a candidate for thrombolysis and was thus commenced on aspirin, labetalol and simvastatin. Her dysarthria improved over the next 48hours and she was stepped-down to the post-natal ward for further monitoring. She was discharged after 4 days and advised to convert her aspirin to clopidogrel after one week.


Outcome and follow-up:

The patient was seen in stroke, cardiology and obstetric medicine clinics. An outpatient bubble study showed mild tricuspid regurgitation and an intact VSD repair, indicating no cardiac source of cerebral embolism. As of April 2013, the patient’s dysarthria had completely resolved and she had no residual deficit; she was thus discharged from stroke clinic.



The risk of both ischaemic and haemorrhagic stroke during the peripartum and postnatal periods is greatly increased compared to the risk outside of pregnancy2,3. Kittner et al calculated the relative risk (RR) of all strokes in the 6 weeks following a live or stillbirth to be 12.7 (95% confidence interval 7.8-20.7)2. The relative risk of haemorrhagic stroke was greater compared to ischaemic stroke (RR 28.3 and 8.7 respectively)2. Contrastingly, both during pregnancy and after a miscarriage or termination, the risk of stroke was not different compared to the non-pregnant state2.


Physiological changes that occur throughout pregnancy may contribute to increased stroke risk, including activated protein C resistance, reduced free protein S, increased clotting factors and enhanced heparin neutralisation3. It has been hypothesised that the increased risk specifically in the postnatal period could be due to a reduction in blood volume, or changes in hormones, coagulation or vessel walls2. None of these however have been proved. Other studies have shown that Caesarean section, gestational diabetes, migraine and acid-base disturbances are strongly linked to pregnancy-associated stroke1,3.


Most postnatal strokes are due to aeitiologies seen in non-pregnant patients, including hypertension, bleeding diatheses or disseminated intravascular coagulation (DIC)3. Nevertheless, there are causes that are specific to pregnancy, the most common being pre-eclampsia/ eclampsia3. Other rarer pregnancy-specific aeitiologies are peripartum cardiomyopathy, postpartum cerebral venous thrombosis (CVT), paradoxical embolism, postpartum cerebral angiopathy and choriocarcinoma3.


The principles of treatment for pregnancy-associated stroke should be the same as treating a stroke in a non-pregnant young adult3. The mainstay for haemorrhagic stroke is supportive care3. However, there is debate regarding management of ischaemic stroke in pregnancy3. Contentions surround the use of thrombolysis, due to the bleeding risk and lack of evidence for its use2,3.


The outcome from pregnancy-associated stroke is poor; case fatality is 20% and it has been estimated that cerebrovascular disorders account for 12% of all maternal deaths1,3. Of the survivors, 45% will have a significant disability at discharge and 30% require intensive rehabilitation (not mutually exclusive)1. In terms of prevention, there is no consensus on the use of anti-thrombotic therapy in pregnant women with a history of ischaemic stroke3. Low-dose aspirin however has been shown to be safe both antenatally and postnatally3.



The peripartum and postpartum periods are associated with a significantly increased risk of both haemorrhagic and ischaemic stroke, compared to the antenatal period and non-pregnant state.


This case report describes the symptoms, investigations and management of an ischaemic postnatal stroke of unknown aetiology, and highlights the importance of swift intervention and specialist care in leading to a favourable maternal outcome.


1. Scott CA, Bewley S, Rudd A, Spark P, Kurinczuk JJ, Brocklehurst P, Knight M. Incidence, Risk Factors, Management, and Outcomes of Stroke in Pregnancy. Obstetrics & Gynecology. 2012; 120(2 Pt1): 318-324.

2. Kittner SJ, Stern BJ, Feeser BR, et al. Pregnancy and the Risk of Stroke. The New England Journal of Medicine. 1996; 335:768-774.

3. Helms AK, Kittner SJ. Pregnancy and Stroke. CNS Spectrums. 2005; 10(7): 580-587.