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 Table of Contents  
CASE REPORT
Year : 2022  |  Volume : 12  |  Issue : 1  |  Page : 59-61

Spontaneous postpartum intracranial haemorrhage: A case report


Department of Anesthesiology, The University of Kansas School of Medicine, Wichita, Kansas, United States

Date of Submission31-Aug-2021
Date of Acceptance12-Sep-2021
Date of Web Publication14-Mar-2022

Correspondence Address:
Dr. Felecia A Newton
Department of Anesthesiology, Room 8074, The University of Kansas School of Medicine – Wichita, 929 N. Saint Francis St. Wichita, KS - 67214
United States
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/JOACC.JOACC_81_21

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  Abstract 


Pregnancy-associated strokes are rare but can have detrimental effects on both mother and baby. A young female patient, 6 days postpartum, suffered a spontaneous intraparenchymal haemorrhage (IPH) and subarachnoid haemorrhage (SAH). The patient exhibited aphasia, right facial droop and right hemiparesis. Serial imaging showed no vascular malformation or other cause of her haemorrhages. Our pregnant patient presented with concurrent IPH and SAH. Given the timing of her stroke and the absence of underlying vascular lesion, it is possible her stroke was a case of IPH and SAH due to reversible cerebral vasoconstriction syndrome (RCVS). More specifically, it may reflect postpartum angiopathy, a subtype of RCVS presenting around 5 days postpartum. Alternatively, this could simply be a subarachnoid extension of a primary IPH.

Keywords: Case report, haemorrhagic stroke in pregnancy, postpartum angiopathy, pregnancy-associated stroke, reversible cerebral vasoconstriction syndrome


How to cite this article:
Smith MD, Walker JL, Pradhan S, Newton FA. Spontaneous postpartum intracranial haemorrhage: A case report. J Obstet Anaesth Crit Care 2022;12:59-61

How to cite this URL:
Smith MD, Walker JL, Pradhan S, Newton FA. Spontaneous postpartum intracranial haemorrhage: A case report. J Obstet Anaesth Crit Care [serial online] 2022 [cited 2022 Jul 2];12:59-61. Available from: https://www.joacc.com/text.asp?2022/12/1/59/339551




  Introduction Top


Pregnancy-associated stroke (PAS) occurs in approximately 10.3–34.2/100,000 deliveries (mortality rate of 1.4/100,000).[1] While some research claims that ischemic strokes are more common,[2] recent reviews state haemorrhagic stroke is more common.[3] Previous studies have shown pregnancy is a risk factor for stroke, although pregnant women typically lack the common risk factors seen in the general population.[2] This suggests some poorly understood pathological processes may be induced by pregnancy leading to increased stroke risk.


  Case Report Top


Informed consent was obtained. A 32-year-old smoker presented 6 days postpartum with 24hr headache, intermittent chest pain, and breathlessness. While her pregnancy was uncomplicated, she suffered from postpartum uterine haemorrhage. Initially, in the emergency department, she was hypertensive though neurologically intact. Head computed tomography (CT) revealed a large left parietal intraparenchymal haemorrhage (IPH) and subarachnoid haemorrhage (SAH) overlying the left cerebral hemisphere and anterior right frontal lobe [Figure 1]. After the CT scan, she developed neurological deficits. A nicardipine drip was initiated to maintain systolic blood pressure <140 mmHg and she was admitted to the neurocritical care unit.
Figure 1: Two slices of noncontrast computed tomography of the head on day of admission exhibiting (a) 3.6 cm × 3.0 cm IPH of the left parietal lobe and left hemispheric SAH and (b) further caudal extension of the SAH. IPH, intraparenchymal haemorrhage; SAH, subarachnoid haemorrhage

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Exam revealed severe aphasia and right-sided facial droop, upper extremity weakness, and sensory deficit. She underwent CT angiography that showed patent dural venous sinuses without evidence of cerebral aneurysm or arteriovenous malformation (AVM). The following morning, she underwent four-vessel digital subtraction cerebral angiography that showed some spasm of the distal left M3 and A2 segments near the involved regions of the haemorrhage, again without vascular malformation or aneurysm. A repeat four-vessel angiogram 8 days post-bleed showed some interval improvement in the “luminal irregularity” of the middle cerebral artery, and an area of diminished vascularity suspected secondary to the presence of the IPH, but otherwise remained negative for aneurysm, AVM, or thrombosis. The patient was discharged to a rehabilitation facility and eventually regained all function barring mild residual right leg weakness.


  Discussion Top


PAS can be categorised as ischemic or haemorrhagic with haemorrhagic being either IPH or SAH. Miller et al. (2018)[4] subcategorises IPH as primary IPH (no vascular lesion), secondary (vascular lesion) or due to reversible cerebral vasoconstriction syndrome (RCVS), whereas SAH is subcategorised into aneurysmal, non-aneurysmal due to RCVS, or other. PAS increases the morbidity of both mother and baby. Pregnancy induces a hypercoagulable state[5] which could lead to an increased risk of ischemic strokes but does not explain the relationship between pregnancy and increased incidence of haemorrhagic stroke.

Multiple literature reviews have identified risk factors for pregnancy-associated haemorrhagic stroke (PAHS) [Table 1]. While pregnancy increased the risk of stroke in younger women (<35 years old), the overall risk of stroke in older women was relatively unchanged compared to nonpregnant women.[6] Another study showed a bimodal distribution of PAHS in the second trimester and the postpartum period, with all of the second-trimester strokes being secondary to underlying vascular lesion while none of the postpartum strokes were related to the vascular lesion.[4] This suggests a difference in pathophysiology of postpartum haemorrhagic strokes compared to haemorrhagic occurring earlier in pregnancy. Takahashi et al.[7] found that 'cerebrovascular diseases' consisting primarily of AVMs, aneurysms and Moya Moya disease were responsible for approximately 70% of antepartum, less than 25% of intrapartum and about 33% of postpartum haemorrhagic strokes. These findings led to 'pregnancy-related angiopathy' or postpartum angiopathy (PPA), signifying a unique vascular pathology that has not yet been completely described but is thought to produce an endothelial dysfunction via pro-inflammatory cytokines such as TNF-α. This can be seen by angiography as multiple sections of arterial narrowing and may be related to migraines, RCVS, posterior reversible encephalopathy syndrome, Hemolysis, Elevated Liver enzymes and Low Platelets (HELLP) syndrome, and preeclampsia/eclampsia.[4],[8]
Table 1: Risk factors for pregnancy-associated stroke vs. stroke in the general population*

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Our case exemplifies a few interesting points discussed in the literature. Despite few risk factors and presence with SAH, multiple cerebrovascular imaging studies failed to reveal any underlying vascular abnormality besides two small areas of vasospasm in the distal M3 and A2 segments in the first angiogram report. Furthermore, our patient presented with concurrent IPH and SAH. Given the timing of her haemorrhagic stroke and the absence of underlying vascular lesion, this may represent IPH and SAH due to PPA. IPH is the most common vascular complication in hospitalized RCVS patients.[9] Although a general population study, investigators concluded that females were associated with higher odds of a haemorrhagic RCVS.[9] Alternatively, this could be a subarachnoid extension of a primary IPH. Maas et al.[10] (2003) found 39% of primary IPH patients in the general population exhibited SAH extension; however, this was usually associated with larger hematomas, anti-platelet or anti-coagulant use or lower platelet activity, poorer functional outcomes and an independent risk for death by day 14. These associations were not evident in our patient.

Our patient was managed adequately with intensive care unit admission, aggressive blood pressure control, diagnostic neuroimaging, treatment of her urinary tract infection, and consultation with the obstetrician regarding her postpartum haemorrhage. Though treated appropriately, the infection and postpartum haemorrhage were not identified as risk factors for haemorrhagic stroke. As a result, there was a delay in her presentation to obtaining a head CT identifying the stroke. Overall, she appeared low risk for stroke according to risk factors in the general population. However, no identified algorithm exists to separate pregnant or postpartum patients who have some risk factors for PAS into 'low-risk' or 'high-risk' categories, either for diagnostic/pretest probability before explicit stroke-like symptoms present or for any possible primary prevention strategies.[5] This contrasts with risk stratification and prevention strategies described for secondary prevention in nonpregnant patients who have suffered a stroke. Obstetric anaesthesiologists are best suited to recognize PAS, and early warning signs in newly postpartum women, and should promote prompt initiation of a 'code stroke' alert.[3]

Our patient presented with two simultaneous subtypes of PAHS, both appearing to be spontaneous and unrelated to a defined vascular abnormality. This supports the theory of unique pathophysiology related to vascular or endothelial changes during pregnancy that may contribute to increased risk and incidence of PAS. Further research is needed to identify and explain the pathophysiology of PPA and haemorrhagic strokes unrelated to vascular malformations to aid in risk stratifying patients and determining how best to prevent PAHS.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ascanio LC, Maragkos GA, Young BC, Boone MD, Kasper EM. Spontaneous intracranial hemorrhage in pregnancy: A systematic review of the literature. Neurocrit Care 2019;30:5-15.  Back to cited text no. 1
    
2.
Leffert LR, Clancy CR, Bateman BT, Cox M, Schulte PJ, Smith EE, et al. Patient characteristics and outcomes after hemorrhagic stroke in pregnancy. Circ Cardiovasc Qual Outcomes 2015;8(6 Suppl 3):S170-8.  Back to cited text no. 2
    
3.
Miller EC, Leffert L. Stroke in pregnancy: A focused update. Anesth Analg 2020;130:1085-96.  Back to cited text no. 3
    
4.
Miller EC, Sundheim KM, Willey JZ, Boehme AK, Agalliu D, Marshall RS. The impact of pregnancy on hemorrhagic stroke in young women. Cerebrovasc Dis 2018;46:10-5.  Back to cited text no. 4
    
5.
Barghouthi T, Bushnell C. Prevention and management of stroke in obstetrics and gynecology. Clin Obstet Gynecol 2018;61:235-42.  Back to cited text no. 5
    
6.
Miller EC, Gatollari HJ, Too G, Boehme AK, Leffert L, Elkind MS, et al. Risk of pregnancy-associated stroke across age groups in New York state. JAMA Neurol 2016;73:1461-7.  Back to cited text no. 6
    
7.
Takahashi JC, Iihara K, Ishii A, Watanabe E, Ikeda T, Miyamoto S. Pregnancy-associated intracranial hemorrhage: Results of a survey of neurosurgical institutes across Japan. J Stroke Cerebrovasc Dis 2014;23:e65-71.  Back to cited text no. 7
    
8.
Miller EC, Yaghi S, Boehme AK, Willey JZ, Elkind MS, Marshall RS. Mechanisms and outcomes of stroke during pregnancy and the postpartum period: A cross-sectional study. Neurol Clin Pract 2016;6:29-39.  Back to cited text no. 8
    
9.
Patel SD, Topiwala K, Saini V, Patel N, Pervez M, Al-Mufti F, et al. Hemorrhagic reversible cerebral vasoconstriction syndrome: A retrospective observational study. J Neurol 2021;268:632-9.  Back to cited text no. 9
    
10.
Maas MB, Nemeth AJ, Rosenberg NF, Kosteva AR, Guth JC, Liotta EM, et al. Subarachnoid extension of primary intracerebral hemorrhage is associated with poor outcomes. Stroke 2013;44:653-7.  Back to cited text no. 10
    


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