Abstract SNACC-51

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Noska R, Friedrich A
University of Cincinnati Medical Center, Cincinnati, Ohio, United states

Patient background:
Patient was a 38 yo female who presented to OSH 7 days after cesarean section, complicated by pre-eclampsia, in which her husband witnessed the patient collapse at home and have tonic/clonic activity.

Clinical course:
Initially at OSH, she was given a bolus of 4g magnesium, a loading dose of Dilantin and intubated for airway protection. Initial CT Head was normal, initial blood pressure was 170/100 and CSF studies at OSH were normal (repeat LP was also normal). She was transferred to UCMC NSICU where MRI Head showed bilateral, scattered infarcts in the posterior circulation. Her initial neurological exam consisted of GCS 1/t/2 with sluggishly reactive 3mm pupils, with no blink to threat and flickering extension in all 4 extremities. Angiography on HD 4 revealed Rt MCA/Rt ACA/Rt PCA/Lt proximal superior cerebellar artery constriction and IA Verapamil was injected into these fields. She went for additional IA verapamil treatments on HD 10 and 17 where there was improvement of vasoconstriction from initial imaging. Final physical exam had the patient giving thumbs up, wiggling toes bilaterally, shaking head yes/no, and mouthing words. She appeared to have persistent right pupillary dilation, could follow with all 4 extremities but had left arm spasticity (likely due to her thalamic infarcts) and chorea-like movement with the right arm being extended and abducted. She was discharged to LTAC for further rehabilitation.

Post-partum angiopathy (PPA), a variant of reversible cerebral vasoconstriction syndrome (RCVS), usually occurs within 1-3 weeks post-partum and presents with thunderclap headaches, a constellation of neurological signs based on affected regions of the brain, seizures, and ischemic stroke. Brain imaging is normal in approximately 70% of patients with RCVS while others have border-zone ischemic strokes, parenchymal hemorrhage, vasogenic edema, and non-aneurysmal SAH. Even though it is thought vasoconstriction resolves within 3 months, it was determined with this patient that intervention would need to be done to prevent further neurological complication. The decision to administer IA verapamil was based on clinical exam, TCDs, and imaging. The mechanism of action of PPA is not quite understood at this point. Recent studies have shown placental growth factor (P1GF), soluble P1GF receptor and soluble endoglin correlate with presence of eclampsia and prediction of its development but it is unsure of whether these play a true role in post-partum angiopathy. Overall, goals of management was MAP ~ 100, SBP > 160 mmHg, [Mg] > 2.5mg/dL, ASA 325 mg (spasm antiplatelet affect), and verapamil 80 mg TID. The risk with repeated angiographies and IA verapamil most significantly included hemorrhagic transformation of brainstem strokes but the risk of a disabling stroke without treatment, such as further pontine strokes which could lead to a locked in state, was deemed to outweigh the risk thus multiple doses of IA Verapamil was deemed to be the appropriate choice to give the patient a chance at a reasonable recovery.

Singhal, A.B., et al (2009) NEJM; 360:1126-1137
Chen (2010) Theory of Advanced Neurological disorders 3(3): 161-171

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