ROTEM and von Willebrand Factor in COVID patients presenting with acute ischemic stroke: A case series: ROTEM and von Willebrand Factor in COVID-19 Related Stroke.

OBJECTIVES: SARS-CoV-2 (COVID) induces systemic thrombotic complications including acute ischemic stroke. In this case series, we report markers of inflammation, coagulation factors including von Willebrand factor antigen, and rotational thromboelastometry (ROTEM) data. MATERIALS AND METHODS: Retrospective case series of COVID patients seen at a single comprehensive stroke center between 2020-2022. For patients undergoing mechanical thrombectomy (MT), ROTEM data was collected during the procedure and analyzed on ROTEM delta system. RESULTS: Fifteen patients (33.3% female) median age 65-years-old presented with COVID and acute ischemic stroke. Thirteen had LVO. The mean NIHSS was 15 (range 0-35) on admission and 18 (0-42) at discharge. Most were cryptogenic (N=7, 46.7%), followed by cardioembolic (N=6, 40%) and large artery-to-artery embolization (N=2, 13.3%). mRS was < 3 in 8 (53%) patients at discharge. None of the patients were on anticoagulation, and five were on antiplatelet therapy pre-hospitalization. Seven received thrombolytics with alteplase (tPA), and 10 had MT. Baseline platelet count was 102 K/uL (range 102-291 K/uL). vWF was measured in 12 patients, all elevated, with seven having levels >400 (180%). ROTEM data was collected in six patients. Three who received tPA had abnormal EXTEM and FIBTEM data (CT extem > 85secs, A10 EXTEM < 45mm, and A10 FIBTEM < 10mm). Notably, INTEM (CT INTEM >208secs) was abnormal in five of the six patients, two of whom did not receive tPA. CONCLUSIONS: Elevated vWF antigen levels with abnormal ROTEM data suggests that COVID induces changes in the clotting cascade. More robust research is needed to investigate these findings. Thrombolytics, MT, and antiplatelet agents should be utilized to treat COVID-related ischemic stroke based on current clinical guidelines.

Clinical Factors Associated With Mode of Death Following Cardiac Arrest.

BACKGROUND: Death after resuscitation from cardiac arrest is common. Although associated factors have been identified, knowledge about their relationship with specific modes of death is limited. OBJECTIVE: To identify clinical factors associated with specific modes of death following cardiac arrest. METHODS: This study involved a retrospective medical record review of patients admitted to a single health care center from January 2015 to March 2020 after resuscitation from cardiac arrest who died during their index hospitalization. Mode of death was categorized as either brain death, withdrawal of life-sustaining therapies due to neurologic causes, death due to medical causes, or withdrawal of life-sustaining therapies due to patient preference. Clinical characteristics across modes of death were compared. RESULTS: The analysis included 731 patients. Death due to medical causes was the most common mode of death. Compared with the other groups of patients, those with brain death were younger, had fewer comorbidities, were more likely to have experienced unwitnessed and longer cardiac arrest, and had more severe acidosis and hyperglycemia on presentation. Patients who died owing to medical causes or withdrawal of life-sustaining therapies due to patient preference were older and had more comorbidities, fewer unfavorable cardiac arrest characteristics, and fewer days between cardiac arrest and death. CONCLUSIONS: Significant associations were found between several clinical characteristics and specific mode of death following cardiac arrest. Decision-making regarding withdrawal of care after resuscitation from cardiac arrest should be based on a multimodal approach that takes account of a variety of personal and clinical factors.

Neurocognitive Sequelae and Rehabilitation after Subarachnoid Hemorrhage: Optimizing Outcomes.

Subarachnoid hemorrhage (SAH) is a medical emergency that requires immediate intervention. The etiology varies between cases; however, rupture of an intracranial aneurysm accounts for 80% of medical emergencies. Early intervention and treatment are essential to prevent long-term complications. Over the years, treatment of SAH has drastically improved, which is responsible for the rapid rise in SAH survivors. Post-SAH, a significant number of patients exhibit impairments in memory and executive function and report high rates of depression and anxiety that ultimately affect daily living, return to work, and quality of life. Given the rise in SAH survivors, rehabilitation post-SAH to optimize patient outcomes becomes crucial. The review addresses the current rehabilitative strategies to combat the neurocognitive and behavioral issues that may arise following SAH.

Risk factors for development of cerebral edema following cardiac arrest.

BACKGROUND: Cerebral edema following cardiac arrest is a well-known complication of resuscitation and portends a poor outcome. We identified predictors of post-cardiac arrest cerebral edema and tested the association of cerebral edema with discharge outcome. METHODS: We performed a retrospective chart review including patients admitted at a single center between January 2015-March 2020 following resuscitation from in-hospital and out-of-hospital cardiac arrest who had head computed tomography imaging. Our primary outcome was moderate-to-severe cerebral edema, which we defined as loss of grey-white differentiation with effacement of the basal and ambient cisterns and radiographic evidence of uncal herniation. We used logistic regression to test associations of demographic information, clinical predictors and comorbidities with moderate-severe cerebral edema. RESULTS: We identified 727 patients who met the inclusion criteria, of whom 102 had moderate-to-severe cerebral edema. We identified six independent predictors of moderate-to-severe cerebral edema: younger age, prolonged arrest duration, pulseless electrical activity/asystole as initial rhythm, unwitnessed cardiac arrest, hyperglycemia on admission, and lower Glasgow coma score on presentation. Of patients with moderate-to-severe cerebral edema, 2% survived to discharge, 56% had withdrawal of life-sustaining therapies and 42% progressed to death by neurological criteria. CONCLUSIONS: Our study identified several risk factors associated with the development of cerebral edema following cardiac arrest. Further studies are needed to determine the benefits of early interventions in these high-risk patients.

Cardio-cerebral infarction in left MCA strokes: a case series and literature review.

The objective of this manuscript is to describe the challenges of Cardio-Cerebral Infarction (CCI) treatment and to highlight the variable approaches in management. CCI is a rare clinical presentation of simultaneous acute ischemic stroke (AIS) and acute myocardial infarction (AMI) and poses a therapeutic challenge for practitioners. Each disease requires timely intervention to prevent irreversible damage; however, optimal management remains unclear. We describe three cases of CCI. All three patients presented with symptomatic left MCA (M1) occlusion, with ST elevation myocardial infarction (STEMI) and left ventricular apical thrombus. Fibrinolysis and mechanical thrombectomy (MT) were discussed in all cases, but only one patient received alteplase (0.9 mg/kg) and none underwent MT. Percutaneous intervention (PCI) was done in only one case. The two patients that did not receive thrombolysis were treated with modified therapeutic heparin (no bolus), and all received antiplatelet therapy. Ultimately, all three patients passed away. CCI poses a clinical challenge for physicians including (1) optimal strategies to enable swift mechanical reperfusion to both the brain and myocardium; (2) difference in dosage of thrombolytics for AIS versus AMI; (3) risk of symptomatic intracerebral hemorrhage following administration of anticoagulation and/or antiplatelet therapy; and (4) caution with use of thrombolytics in the setting of acute STEMI due to the risk of myocardial rupture. In the absence of high quality evidence and clinical guidelines, treatment of CCI is highly individualized.

Abducens Nerve Palsy as Initial Presentation of Multiple Myeloma and Intracranial Plasmacytoma.

Central Nervous System (CNS) involvement in multiple myeloma and/or multifocal solitary plasmacytoma is rare. Although they are unique entities, multiple myeloma (MM) and plasmacytoma represent a spectrum of plasma cell neoplastic diseases that can sometimes occur concurrently. Plasmacytomas very often present as late-stage sequelae of MM. In this case report, we report a 53-year-old female presenting with right abducens cranial nerve (CN) VI palsy as an initial presentation secondary to lesion of the right clivus.

Metabolic Alterations in Cancer Cells and the Emerging Role of Oncometabolites as Drivers of Neoplastic Change.

The mitochondrion is an important organelle and provides energy for a plethora of intracellular reactions. Metabolic dysregulation has dire consequences for the cell, and alteration in metabolism has been identified in multiple disease states-cancer being one. Otto Warburg demonstrated that cancer cells, in the presence of oxygen, undergo glycolysis by reprogramming their metabolism-termed "aerobic glycolysis". Alterations in metabolism enable cancer cells to gain a growth advantage by obtaining precursors for macromolecule biosynthesis, such as nucleic acids and lipids. To date, several molecules, termed "oncometabolites", have been identified to be elevated in cancer cells and arise from mutations in nuclear encoded mitochondrial enzymes. Furthermore, there is evidence that oncometabolites can affect mitochondrial dynamics. It is believed that oncometabolites can assist in reprogramming enzymatic pathways and providing cancer cells with selective advantages. In this review, we will touch upon the effects of normal and aberrant mitochondrial metabolism in normal and cancer cells, the advantages of metabolic reprogramming, effects of oncometabolites on metabolism and mitochondrial dynamics and therapies aimed at targeting oncometabolites and metabolic aberrations.