Join now to get access to this content and more.
Become a SOAP member and have access to our benefits.
- 2020 SOAP Virtual Meeting Series Videos
- For Review: SOAP Consensus Statement on Neuraxial Procedures in Thrombocytopenic Parturients
- Sample Centers of Excellence Applications
- ASA Corner
- SOAP Policy and Procedure Manual (P&P Manual)
- SOAP Expert Opinions
- SOAP's Learning Modules
- 2019 Annual Meeting Lecture Videos
- December 2018 - SOAP Unofficial Guide to ASA Committees Webinar
- Submit a Position
- View Job Postings
- Previous Meeting Archives
- Previous Meeting Abstract Search
- CMS Guidelines
- Member Benefits
- Newsletter Clinical Articles
- ACOG Documents
- Search our Patient Safety Archive
- Ask SOAP a Question
- Global Health Opportunities
- And more…
The Perfect Storm: IVH due to postpartum HELLP in a patient with antithrombin III (ATIII) deficiency and an undiagnosed Arteriovenous Malformation (AVM)
Abstract Number: SAT-04
Abstract Type: Case Report/Case Series
The prevalence of AVM is estimated to be 0.01-0.5% and usually presents between 20-40 y/o, corresponding with childbearing age(1,2). While some AVMs have symptoms allowing for prompt diagnosis, others have a hemorrhagic presentation in peripartum resulting in increased maternal mortality(1,2). This is a case of a 30 y/o pt who had a hemorrhagic presentation of an undiagnosed AVM in the postpartum period. Due to confounding factors, including the concurrent development of HELLP in an anticoagulated patient, she was at a particularly high risk for complications.
A 30 y/o G1P0 with an IUP at 39 weeks EGA presented for induction of labor. Her history was significant for ATIII deficiency and PE. Patient was on Lovenox and then transitioned to heparin. She was started on Pitocin, had an epidural placed and delivered after 30 minutes of pushing.
Postpartum, she was restarted on Lovenox. 8 hrs after, she began complaining of a HA, abdominal pain, chest pain, SOB and N/V. Her SBP was in the 150-190 range. She was started on magnesium and given labetalol. CTA chest was negative for PE. Platelets were 170 K/uL. AST and ALT had increased. 6 hrs later, the patient became unresponsive with minimal response to sternal rub and SBP in the 180’s. CT revealed a large IVH with non-communicating hydrocephalus. She was taken to the ICU where an arterial line was placed and patient was intubated.
Platelets then decreased to 38 K/uL while AST and ALT increased to 1665 and 1170 respectively. A left frontal craniotomy was performed revealing a ruptured AVM. This was resected requiring multiple blood products. She was weaned to extubation and discharged to rehab on POD 27 with aphasia and right hemiplegia.
Coagulopathies, HTN, and eclampsia are well known causes of hemorrhagic strokes during pregnancy(3,4). However, in a survey conducted by Takhashi et al., over 50% of hemorrhagic strokes were the result of underlying cerebrovascular disease. Of those, 87% of the lesions were undiagnosed until the onset of stroke with AVMs being the most frequent(3). Although there have been numerous studies on the hemorrhagic risk of AVM during pregnancy, they provide insufficient evidence on whether pregnancy increases the risk of rupture(2). While MRI and cerebral angiography can help identify the characteristics of an AVM, in the case of an acute hemorrhage with worsening neurologic status, quick imaging with CT and emergency neurosurgical intervention is warranted(2). In our case, the pt had multiple factors increasing her risk for ICH. She was being anticoagulated, became hypertensive and developed HELLP resulting in a severe coagulopathy. While these factors alone have been responsible for ICH occurring in some pregnant patients, they further complicated the management of our patient whose ICH occurred due to the rupture of a previously undiagnosed AVM.
1. Lv 2016
2. Lv 2015
3. Takahashi 2014
4. Khan 2013