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A severe postpartum headache status post wet tap, does not necessarily equal PDPH
Abstract Number: SA-72
Abstract Type: Case Report/Case Series
A 25 year-old G1P0 with a history of Crohn’s disease presented in labor, requesting an epidural. Placement was complicated by accidental dural puncture (ADP). On postpartum day (PPD) 1, she developed a bilateral frontal headache, aggravated when upright and alleviated when recumbent. Conservative therapy for suspected post-dural puncture headache (PDPH) included caffeine, acetaminophen and increased fluid intake. On PPD 2, she was discharged home, but returned complaining of unresolved headache and photophobia on PPD 8. She received a therapeutic epidural blood patch (EBP) and tolerated 9 ml of autologous blood due to lower back pressure. Vital signs remained stable for 2 hours, and she was discharged home. On PPD 11, she returned to the ED, complaining of different headache, bilateral at temples with the addition of chills, nausea, and emesis. She received IV fluids, metoclopramide, magnesium, and caffeine with relief of her symptoms, so she was discharged without further workup. On PPD 15, she developed difficulty ambulating with a right-sided headache that radiated to the right eye. A CT angiogram revealed a dural venous sinus thrombosis with complete occlusion of the superior sagittal sinus. MR venogram revealed a subacute thrombosis of the superior sagittal sinus, with extension of abnormal signal into several cortical veins. She was admitted to the neurology service and started on a heparin infusion. She was discharged on warfarin with complete resolution of all symptoms, without any residual deficits.
Headaches are common in the postpartum period due to stress, dehydration and exhaustion. The differential for other etiologies (beyond PDPH and pre-eclampsia/eclampsia) include subdural hematoma, intracranial hemorrhage, and cerebral venous sinus thrombosis (CVST). The incidence of intracranial venous thrombosis in parturients is increased 50% from baseline (1). The risk of all venous thromboembolism (VTE) is highest within 6 weeks postpartum, and declines to baseline by 12 -18 weeks.
This patient was at an increased risk for thrombosis both from pregnancy and Crohn’s disease. Pregnancy is associated with an increase in coagulation factors and a decrease in protein S (2). As an inflammatory state, Crohn’s disease increases the risk of VTE and leads to hypercoagulability and coagulation cascade abnormalities(3).
CVST may be life threatening, but is treatable if recognized early. It should be considered, among other neurologic conditions in any woman presenting with persistent neurologic deficits in the postpartum period irrespective of whether or not they also sustained an ADP.
Lanska DJ, et al. Stroke and intracranial venous thrombosis during pregnancy and puerperium. Neurology. 1998;51:1622–1628.
Bates SM, et al. Venous thromboembolism, thrombophilia, antithrombotic therapy, and pregnancy. Chest. 2008;133:844S-886S.
Craig A Solem MD, et al. Venous Thromboembolism in IBD. The American Journal of Gastroenterology. 2003;99:97-101