Disclosures: Viswanath M. Aluru, MD: No financial relationships or conflicts of interest
Case Description: 68 year old Hispanic male with hypertension, hyperlipidemia and atrial fibrillation presented with chest pain. He was admitted for inferior-wall STEMI complicated by high grade AV-block and cardiogenic shock requiring pressors. He underwent PCI with stenting of the RCA without successful restoration of flow. The procedure was complicated by V-fib requiring defibrillation and Amiodarone. Later that day he had altered mental status with left sided weakness that progressed to loss-of-consciousness requiring intubation. Initial non-contrast head CT was negative. Follow-up head CT showed loss of gray-white differentiation in multiple vascular territories suspicious for global hypoperfusion injury. Repeat imaging showed widespread bilateral infarcts in the cerebral cortex with possible early hemorrhagic conversion. He was extubated after a week. His mental status remained poor.
Setting: Community teaching hospital
Patient: 68-year old male with hypoxic ischemic encephalopathy secondary to STEMI Assessment/
Results: Upon admission to TBI unit, he was agitated and anxious. Initial medications – Benzatropine and Risperidone were held. Zyprexa, Seroquel and Amantadine were started. He further developed myoclonus that was treated with Klonopin. Medications were adjusted as he was lethargic, not participating in therapy. Zyprexa was discontinued; Seroquel administered only at night and Amantadine dose was reduced. He was more alert and non-agitated.
Discussion: Patient demonstrated improvement with initial pharmacotherapeutics in areas of agitation, arousal and memory but showed restlessness and insomnia. Management was complicated by addition of Klonopin to treat myoclonus resulting in cognitive suppression, poor arousal and increased agitation. Further titration of his medications demonstrated some improvements in terms of agitation and arousal.
Conclusion: This case highlights complexity of neuropharmacological management of patients with hypoxic-ischemic encephalopathy complicated by post-hypoxic myoclonus and bilateral widespread ischemic cortical infarcts. It is prudent to understand basic pathophysiologic mechanisms of various disease processes, their direct interactions and disease manifestations to formulate appropriate neurotherapeutic interventions to minimize medication interactions and unwarranted adverse effects.
Level of Evidence: Level V
To cite this abstract in AMA style:
Aluru VM, Patel M, Ross M. Neurotherapeutic Considerations in a Case of Hypoxic Ischemic Encephalopathy Secondary to STEMI Complicated by Post-Anoxic Myoclonus and Wide Spread Ischemic Infarcts in Bilateral Cerebral Cortex [abstract]. PM R. 2020; 12(S1)(suppl 1). https://pmrjabstracts.org/abstract/neurotherapeutic-considerations-in-a-case-of-hypoxic-ischemic-encephalopathy-secondary-to-stemi-complicated-by-post-anoxic-myoclonus-and-wide-spread-ischemic-infarcts-in-bilateral-cerebral-cortex/. Accessed December 11, 2024.« Back to AAPM&R Annual Assembly 2020
PM&R Meeting Abstracts - https://pmrjabstracts.org/abstract/neurotherapeutic-considerations-in-a-case-of-hypoxic-ischemic-encephalopathy-secondary-to-stemi-complicated-by-post-anoxic-myoclonus-and-wide-spread-ischemic-infarcts-in-bilateral-cerebral-cortex/