Treatment of Symptomatic Carotid Webs: A Single-Center Review.

BACKGROUND: Carotid webs are abnormal thin shelf-like or flap-like tissue in the carotid bulb (proximal internal carotid artery). Rarely are carotid webs detected prior to symptoms since routine carotid artery surveillance is not performed in younger individuals without traditional risk factors for carotid disease. The cause and natural history remain unknown. In general, they are not common but should be considered in the differential diagnosis of a patient who presents with ischemic neurologic symptoms. The web can create a flow disturbance, potentiating local thrombus formation, which can embolize producing resulting in cerebral ischemia. Current treatment is to reduce thrombus formation (antithrombotics and/or anticoagulation) or to alter the flow disturbance caused by the web (surgical removal or stent). METHODS: We retrospectively identified all patients presenting with acute ischemic stroke to our Comprehensive Stroke Center that were diagnosed with carotid web from January 2020 to December 2023. Patient demographics, presentation, hospital course including treatment and complications were collected and reported. RESULTS: Fifteen patients presented with carotid web and stroke from 2020 to 2023 and 13 underwent carotid artery stenting or endarterectomy with no periprocedural complications. Most (40%) carotid webs were not primarily identified by the initial radiology interpretation. CONCLUSIONS: We discuss our experience of carotid web and its management as well as review of the current literature.

Pseudo Subarachnoid Hemorrhage Sign in Bacterial Meningitis in a Patient Presenting With Acute Ischemic Stroke: A Novel Radiological Clue to Rapid Diagnosis.

Pseudo subarachnoid hemorrhage (SAH) is an entity defined when characteristic computed tomography (CT) findings of SAH are seen without evidence of hemorrhage on MRI, autopsy, or cerebrospinal fluid analysis. This imaging phenomenon has been reported in association with multiple clinical settings including diffuse cerebral edema, hypoxic-ischemic injury, post percutaneous coronary intervention, and the focus of our report, acute bacterial meningitis. The mechanisms leading to this finding are poorly understood. Current hypotheses explaining this pattern vary widely depending on the associated pathology. In this report, we present a case of pseudo SAH associated with bacterial meningitis and a literature review on the causes, neuroimaging findings, and mechanisms associated with pseudo SAH. We discuss dual energy CT as a possible tool for differentiating pseudo SAH from true SAH. We analyze the timing of imaging studies and the role timing plays in the presentation of the pseudo SAH sign. We conclude that the extravasation of iodine contrast into the subarachnoid space can mimic SAH on CT. Ultimately, our case adds to the growing body of evidence that clinicians should be aware of acute bacterial meningitis as a potential mimic of SAH on CT.

Paradoxical and Retrograde Air Embolism from Pressurized Peripheral Bolus.

INTRODUCTION: Cerebral air embolism is a rare, yet serious neurological occurrence with unclear incidence and prevalence. Here, we present a case of fatal cerebral arterial and venous cerebral gas embolism in a patient with infective endocarditis and known large right-to-left shunt and severe tricuspid regurgitation following pressurized fluid bolus administration. Case Presentation. A 32-year-old female was admitted to the medical intensive care unit from a long-term acute care facility with acute on chronic respiratory failure. Her medical history was significant for intravenous heroin and cocaine abuse, methicillin-sensitive Staphylococcus aureus tricuspid valve infective endocarditis on vancomycin, patent foramen ovale, septic pulmonary embolism with cavitation, tracheostomy with chronic ventilator dependence, multifocal cerebral infarction, hepatitis C, nephrolithiasis, anxiety, and depression. After intravenous fluid administration, she became unresponsive with roving gaze, sluggish pupils, and hypotensive requiring vasopressors. CT of the brain showed diffuse arterial and venous cerebral air embolism secondary to accidental air administration from fluid bolus. Magnetic resonance imaging of the brain showed diffuse global anoxic injury and flattening of the globe at the optic nerve insertion. Given poor prognosis, her family chose comfort measures and she died. CONCLUSIONS: Fatal cerebral air embolism can occur through peripheral intravenous routes when the lines are inadequately primed and fluids administered with pressure. Caution must be exercised in patients with right-to-left shunting as air may gain access to systemic circulation.

COVID-19 Related Acute Hemorrhagic Necrotizing Encephalitis: A Report of Two Cases and Literature Review.

Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus, has proven neurotropism and causes a multitude of neurologic manifestations. Acute hemorrhagic necrotizing encephalitis (AHNE), though rare, can be seen in patients with severe infection and is associated with devastating neurologic outcomes. The true prevalence of this syndrome is unknown due to underrecognition, difficulty in timely acquisition of neuroimaging, and high mortality in this subset of patients escaping detection. It is a distinct clinicoradiological syndrome, with patients suffering from rapidly worsening encephalopathy and coma within the first two weeks of severe illness and hemorrhagic necrotizing parenchymal changes on neuroimaging. The pathophysiology of this syndrome is unclear but hypothesized to occur due to cytokine storm, blood-brain-barrier dysfunction, and direct viral-mediated endotheliopathy. Diagnosis requires a high index of suspicion in patients who have unexplained persistent severe encephalopathy associated with COVID-19 infection. Most patients have elevated systemic inflammatory markers and severe lung disease with hypoxic respiratory failure requiring mechanical ventilation. MRI is the imaging modality of choice, with a distinct neuroimaging pattern. CSF (cerebrospinal fluid) studies have a low yield for viral particle detection with currently available testing. While long-term outcomes are unclear, early immunomodulatory treatment with intravenous immunoglobulin, plasma exchange, and steroids may portend a favorable outcome. We discuss two cases of COVID-19 related AHNE and also include a pertinent literature search of similar cases in PubMed to consolidate the AHNE clinical syndrome, neuroimaging characteristics, management strategies, and reported short-term prognosis.

COVID-19 Disease and Hypercoagulability Leading to Acute Ischemic Stroke.

INTRODUCTION: SARS-Coronavirus-2 infection leading to COVID-19 disease presents most often with respiratory failure. The systemic inflammatory response of SARS-CoV-2 along with the hypercoagulable state that the infection elicits can lead to acute thrombotic complications including ischemic stroke. We present 3 cases of patients with COVID-19 disease who presented with varying degrees of vascular thrombosis. CASES: Cases 1 and 2 presented as cerebral ischemic strokes without respiratory failure. Given their exposure risks, they were both tested for COVID-19 disease. Case 2 ultimately developed respiratory failure and pulmonary embolism. Cases 2 and 3 were found to have simultaneous arterial and venous thromboembolism (ischemic stroke and pulmonary embolism) as well as positive antiphospholipid antibodies. CONCLUSION: Our case series highlight the presence of hypercoagulability as an important mechanism in patients with COVID-19 disease with and without respiratory failure. Despite arterial and venous thromboembolic events, antiphospholipid and hypercoagulable panels in the acute phase can be difficult to interpret in the context of acute phase response and utilization of thrombolytics. SARS-CoV-2 testing in patients presenting with stroke symptoms may be useful in communities with a high case burden or patients with a history of exposure.

Ipsilateral Reversible Cerebral Vasculopathy Secondary to Carotid Artery Revascularization: A Case Report.

BACKGROUND: The emergence of neurologic symptoms after carotid revascularization is not uncommon and typically caused by perioperative ischemic stroke or hyperperfusion. Postoperative vasculopathy, including reversible cerebral vasoconstriction syndrome (RCVS) is a rare complication of carotid intervention and may be an under-identified cause of neurologic deficit after revascularization. We report a case of reversible postoperative vasculopathy following carotid revascularization as well as its management. CASE PRESENTATION: A 74 year old right-handed woman presented to the emergency department with sudden onset left arm weakness and episodic shaking while hypotensive. Computed tomography angiography revealed total occlusion of her right internal carotid artery. Transcranial Doppler monitoring demonstrated active embolic events in her right middle cerebral artery raising concern for continued stump embolization. She underwent carotid revascularization with carotid endarterectomy, mechanical thrombectomy, and carotid angioplasty and initially did well postoperatively. On postoperative day 5, she developed a fixed right gaze and left hemiparesis. Computed tomography revealed new right frontal lobe and basal ganglia infarcts, and angiography showed new right internal carotid, middle cerebral, and anterior cerebral artery vasoconstriction consistent with postoperative vasculopathy. Despite treatment with pressure augmentation and vasodilator therapy, her symptoms persisted resulting in left hemiplegia at discharge. DISCUSSION: This case highlights postoperative vasculopathy (including RCVS) as a rare potential complication after carotid revascularization that should be considered in a patient with persistent acute neurologic symptoms. Information regarding incidence and predisposing risk factors is limited. Multiple diagnostic and therapeutic modalities may be necessary in the recognition and treatment of postoperative vasculopathy.

Acute Symptomatic Seizures in Critically Ill Patients with COVID-19: Is There an Association?

BACKGROUND: The coronavirus disease of 2019 (COVID-19) emerged as a global pandemic. Historically, the group of human coronaviruses can also affect the central nervous system leading to neurological symptoms; however, the causative mechanisms of the neurological manifestations of COVID-19 disease are not well known. Seizures have not been directly reported as a part of COVID-19 outside of patients with previously known brain injury or epilepsy. We report two cases of acute symptomatic seizures, in non-epileptic patients, associated with severe COVID-19 disease. CASE PRESENTATIONS: Two advanced-age, non-epileptic, male patients presented to our northeast Ohio-based health system with concern for infection in Mid-March 2020. Both had a history of lung disease and during their hospitalization tested positive for SARS-CoV-2. They developed acute encephalopathy days into their hospitalization with clinical and electrographic seizures. Resolution of seizures was achieved with levetiracetam. DISCUSSION: Patients with COVID-19 disease are at an elevated risk for seizures, and the mechanism of these seizures is likely multifactorial. Clinical (motor) seizures may not be readily detected in this population due to the expansive utilization of sedatives and paralytics for respiratory optimization strategies. Many of these patients are also not electrographically monitored for seizures due to limited resources, multifactorial risk for acute encephalopathy, and the risk of cross-contamination. Previously, several neurological symptoms were seen in patients with more advanced COVID-19 disease, and these were thought to be secondary to multi-system organ failure and/or disseminated intravascular coagulopathy-related brain injury. However, these patients may also have an advanced breakdown of the blood-brain barrier precipitated by pro-inflammatory cytokine reactions. The neurotropic effect and neuroinvasiveness of SARS-Coronavirus-2 have not been directly established. CONCLUSIONS: Acute symptomatic seizures are possible in patients with COVID-19 disease. These seizures are likely multifactorial in origin, including cortical irritation due to blood-brain barrier breakdown, precipitated by the cytokine reaction as a part of the viral infection. Patients with clinical signs of seizures or otherwise unexplained encephalopathy may benefit from electroencephalography monitoring and/or empiric anti-epileptic therapy. Further studies are needed to elucidate the risk of seizures and benefit of monitoring in this population.

Fatal Brain Injury Following Carbon Dioxide Angiography.

INTRODUCTION: Carbon dioxide (CO2) as a contrast agent has been in use as early as the 1920s for visualization of retroperitoneal structures. Digital subtraction angiography (DSA) using CO2 as a contrast agent for vascular imaging was developed in the 1980s. Currently, CO2  angiography is an alternative agent in patients with chronic kidney disease (CKD) and those who are at risk of developing contrast-induced nephropathy. However, CO2 causes neurotoxicity if the gas inadvertently enters the cerebrovascular circulation leading to fatal brain injury. CASE PRESENTATION: A 71-year-old female with h/o sickle cell trait, hypertension, obesity, metastatic renal cell cancer status post nephrectomy, bone metastasis, chronic kidney disease was admitted for elective embolization of the humerus bone metastasis. Given the high probability of contrast-induced nephropathy, CO2 angiography was chosen for embolization of the metastasis. During the procedure, the patient became unresponsive. Emergent medical management with hyperventilation, 100% fraction oxygen inhalation was performed. Her neuroimaging showed global cerebral edema. An intracranial pressure monitor was placed which confirmed intracranial hypertension. Hyperosmolar therapy was administered with no improvement in clinical examination. She progressed to brain stem herniation. Given poor prognosis, the family opted for comfort measures and the patient expired. DISCUSSION AND CONCLUSIONS: Inadvertent carbon dioxide entry into cerebrovascular circulation during angiography can cause fatal brain injury. Caution must be exercised while performing CO2  angiography in blood vessels above the diaphragm.

Early detection of brainstem herniation using electroencephalography monitoring - case report.

BACKGROUND: Continuous electroencephalography (cEEG) is an important neuromonitoring tool in brain injured patients. It is commonly used for detection of seizure but can also be used to monitor changes in cerebral blood flow. One such event that can cause a change in cerebral blood flow is imminent, cerebral herniation. cEEG monitoring and quantitative electroencephalography (QEEG) can be used as neurotelemetry to detect cerebral herniation prior to onset of clinical signs. CASE PRESENTATION: We discuss two cases highlighting the use of cEEG in cerebral herniation accompanied by clinical examination changes. The first case is a patient with multiorgan failure and intracerebral hemorrhage (ICH). Given his coagulopathy status, his ICH expanded. The second case is a patient with intraventricular hemorrhage and worsening obstructive hydrocephalus. In both cases, the cEEG showed increasing regional/lateralized slowing. The Quantitative electroencephalography (QEEG) showed a decrease in frequencies, worsening asymmetry, decreasing amplitude and increasing burst suppression ratio corresponding with the ongoing herniation. Clinically, these changes on cEEG preceded the bedside neurological changes by up to 1 h. CONCLUSIONS: The use of cEEG to monitor patients at high risk for herniation syndromes may identify changes earlier than bedside clinical exam. This earlier identification may allow for an earlier opportunity to intervene.

Developmental Venous Anomaly Presenting with Spontaneous Intracerebral Hemorrhage, Acute Ischemic Stroke, and Seizure.

Developmental venous anomaly (DVA) is the most common, benign, congenital vascular malformation of the brain and mostly an incidental finding on imaging. The exact etiology of DVA is unknown but thought to be due to medullary vein thrombosis during embryonic venous development. DVA is generally asymptomatic although associated neurologic deficits and seizures have been described. Several reports of DVA causing neurovascular compression, obstructive hydrocephalus, venous infarction, and intracerebral hemorrhage (ICH) have been described. In this report, we discuss a patient with fluctuating neurological symptoms found to have multiple DVA, predominantly draining into the deep venous system. To the best of our knowledge, DVAs leading to simultaneous ischemic stroke, intracerebral hemorrhage, and seizures are not reported in the literature. We reviewed the relevant literature and discussed the epidemiology and clinical and radiological characteristics of DVA.

Anti-N-methyl-D-aspartate Encephalitis Concomitantly with Tall-cell Variant Papillary Thyroid Carcinoma.

Anti-N-methyl-D-aspartate (NMDA) encephalitis is an autoimmune-mediated process characterized by psychosis, seizures, dyskinetic movements, and autonomic instability. At least half of the reported cases are paraneoplastic, particularly associated with an ovarian teratoma. None have been reported to be associated with thyroid tumor. We present a case of anti-NMDA encephalitis concomitantly occurring in setting of papillary thyroid carcinoma in a woman who presented with headaches, myalgia and somnolence mimicking meningoencephalitis. A 29-year-old African female presented with fever, headache, myalgia, somnolence and behavioral changes. Initial evaluation was significant for lymphocytic pleocytosis with normal glucose and protein. She was started on broad spectrum empiric antibiotics. Despite antibiotics, she continued to have worsening encephalopathy, hallucinations, epileptic seizures, and multifocal dyskinesias involving the face and extremities with no electroencephalogram correlate. Extensive infectious workup was unremarkable. Whole-body CT with contrast and ovarian ultrasound were unremarkable for malignancy. Serum auto-antibodies to the NMDA receptor and thyroid peroxidase were detected. She was treated with high-dose intravenous steroids, plasmapheresis, intravenous immunoglobulin, and rituximab with no clinical or serological response. Fluorodeoxyglucose positron emission tomography (FDG-PET) showed a hypermetabolic thyroid nodule. Fine needle aspiration of the nodule revealed papillary thyroid carcinoma. She underwent total thyroidectomy and pathology showed two foci of tall-cell variant papillary thyroid carcinoma. Serological and clinical response followed shortly after tumor resection. The NMDA receptor stain of the papillary thyroid carcinoma was nonreactive. We describe the coincidentally co-occurrence of NMDA encephalitis in a patient with papillary thyroid carcinoma. This case highlights the importance of presumed cases of non-paraneoplastic NMDA encephalitis, FDG-PET may help in detecting occult malignancies.

Super-Refractory Status Epilepticus Treated with High Dose Perampanel: Case Series and Review of the Literature.

INTRODUCTION: Acute symptomatic seizures are frequent in the critically ill patient and can be difficult to treat. The novel anticonvulsant perampanel may be effective in the treatment of status epilepticus considering its mechanism of action of being an AMPA antagonist. We present four cases of super refractory status epilepticus treated with high dose perampanel. METHOD: Case report. CASES: Four patients were treated with perampanel for their refractory status epilepticus. One patient had new onset refractory status epilepticus of unknown etiology. Three other patients had status epilepticus as a result of their cardiac arrest. Two of the cardiac arrest patients had myoclonus. In all patients, the additional of perampanel resulted in a reduction of seizure burden without affecting hemodynamics or hepatic or renal function. CONCLUSION: Perampanel may be effective in the treatment of super-refractory status epilepticus of varying etiologies. A larger, prospective study is needed to further assess this therapy.

Decompression Hemicraniectomy for Refractory Intracranial Hypertension in Reversible Cerebral Vasoconstriction Syndrome.

Reversible cerebral vasoconstriction syndrome (RCVS) is a disorder of dysregulation of cerebrovascular tone resulting in transient segmental vasoconstriction which resolves in 1-3 months. Cerebral edema is an underrecognized complication in RCVS. It is likely multifactorial. This edema can lead to intracranial hypertension that can be refractory to medical management. Limited evidence exists regarding surgical management of intracranial hypertension in RCVS. We present a 29-year-old Caucasian right-handed female patient with a medical history of migraine, polysubstance abuse presented to the emergency department (ED) daily for 3 days with the chief complaint of recurrent thunderclap headache. She declined neuroimaging and lumbar puncture. She was treated for migraine with abortive medications with no improvement. During the third ED visit, she became lethargic with right-sided homonymous hemianopia. Computerized tomography of the brain showed left parietal intracerebral hemorrhage with intraventricular extension, cortical subarachnoid hemorrhage, and diffuse cerebral edema. Digital subtraction angiography showed multifocal moderate-to-severe segmental vasoconstriction suggestive of vasculopathy. Oral verapamil was initiated. Continuous intracranial pressure monitoring showed uncontrolled intracranial hypertension, despite maximal medical management with hyperosmolar therapy, induced coma, and hypothermia. Decompressive hemicraniectomy with duraplasty was performed for refractory intracranial hypertension. We provisionally diagnosed her with RCVS. She was discharged to inpatient rehabilitation with residual right homonymous hemianopia. Transcranial Doppler study during follow-up showed improved mean flow velocities. She continued to have residual cognitive deficits with complete resolution of headache.

False-Negative Platelet Factor 4 Antibodies and Serotonin Release Assay and the Utility of Repeat Testing in the Diagnosis of Heparin-Induced Thrombocytopenia and Thrombosis.

OBJECTIVE: To report a case of false-negative serological tests in the diagnosis of heparin-induced thrombocytopenia (HIT) followed by a brief review of the literature on this topic. CASE PRESENTATION: A 75-year-old Caucasian female patient was admitted with a traumatic right ankle fracture that required open reduction and internal fixation. Despite postoperative subcutaneous heparin chemoprophylaxis, she developed deep vein thrombosis (DVT) and pulmonary embolism (PE) on day 4 and subsequently started on continuous heparin infusion. On day 5, she suffered a stroke from a complete occlusion of the right common carotid artery with tandem occlusion of the right middle cerebral artery. She underwent successful thrombectomy of both arteries. The proposed stroke mechanism was paradoxical embolism through a patent foramen ovale. Over the next few days, thrombocytopenia was noted, the heparin drip was stopped, and HIT antibodies (antibodies targeting the complex of platelet factor 4 and heparin; PF4-H AB) and serotonin release assay (SRA) tests were sent. Because of the suspicion for HIT, she was started on bivalirudin with subsequent improvement in platelet count. Initial PF4-H AB and SRA tests were negative, bivalirudin was stopped, and heparin was restarted. Subsequently, her platelets trended down, again raising clinical suspicion of HIT. Repeat PF4-H AB and SRA testing resulted positive. CONCLUSIONS: A positive SRA in the appropriate context is considered for the diagnosis of heparin-induced thrombocytopenia. This case report highlights that false-negative serological evaluation is possible early in the course of the disease. Repeat testing is recommended in patients with high clinical suspicion.

Intracranial Calcification Masquerading as Hemorrhage in a Patient with Multiple Myeloma Presenting with Facial Neuropathy.

Multiple myeloma is an immunoglobulin-producing plasma cell neoplasm that commonly affects the bones, kidneys, the hematopoietic system, and rarely the nervous system. Peripheral nervous system involvement in the form of cranial neuropathy, radiculopathy, and polyneuropathy are common. Compressive myelopathy constitutes the majority of central nervous system disorders followed by cerebrovascular disorders, intracranial plasmacytomas, and leptomeningeal myelomatosis. Cerebrovascular complications such as acute ischemic stroke and transient ischemic attack are not uncommon. Intracerebral hemorrhage, although infrequent, can be secondary to refractory hypertension from renal failure and intratumoral hemorrhage in intracerebral plasmacytomas. Metastatic calcifications in lungs, liver, and skin with high levels of serum calcium and phosphate are seen in patients with multiple myeloma, but intracerebral calcifications are not common. We report an unusual case of intracranial calcification masquerading as acute intracerebral hemorrhage in a patient presenting with acute facial weakness.

Cocaine Induced Bilateral Posterior Inferior Cerebellar Artery and Hippocampal Infarction.

Cocaine is one of the most commonly abused recreational drugs, second only to marijuana. It blocks the reuptake of neurotransmitters such as norepinephrine and dopamine, that leads to persistent post-synaptic stimulation responsible for its excitatory effects. Cocaine-related strokes, both ischemic and hemorrhagic, have been well described in the literature and cerebral vasospasm is hypothesized as one of the major mechanisms responsible for the presentation. Although cases of posterior circulation infarction were previously reported, we herein report a rare presentation of a cocaine-induced bilateral posterior inferior cerebellar artery and hippocampal infarction in a middle-aged female.

Dihydroergotamine Complicating Reversible Cerebral Vasoconstriction Syndrome in Status Migrainosus.

Reversible cerebral vasoconstriction syndrome (RCVS) is a clinicoradiological syndrome that occurs due to dysfunction of cerebrovascular autoregulation. It is characterized by recurrent thunderclap headache from cerebral vasoconstriction which can cause ischemic infarction, spontaneous intraparenchymal and subarachnoid hemorrhage. This syndrome can be triggered by a variety of etiologies including medications, infectious, and inflammatory conditions. The diagnosis is often delayed due to unawareness among the health-care providers and delayed neuroimaging evidence of vasoconstriction with or without ischemic and/or hemorrhagic infarction. Status migrainosus is a prevalent condition requiring emergency room visits and inpatient admission. Thus, patients with RCVS can be easily misdiagnosed with migraine. We report a patient with RCVS misdiagnosed as status migrainosus with visual aura, treated with intravenous dihydroergotamine with worsening of cerebral vasoconstriction and lead to ischemic and hemorrhagic complications. We discuss this complication and provide guidance on differentiating between migraine and RCVS.

Wernekink commissure syndrome with palatal myoclonus at onset: a case report and review of the literature.

BACKGROUND: Wernekink commissure syndrome causes a peculiar combination of internuclear ophthalmoplegia, dysarthria, and delayed-onset palatal myoclonus. Palatal myoclonus is thought to be secondary to delayed hypertrophic degeneration of the bilateral inferior olivary nuclei secondary to involvement of bilateral dentatoolivary tract. We describe a case of a patient with early-onset palatal myoclonus. CASE PRESENTATION: A 53-year-old Caucasian man with several vascular risk factors presented to our emergency room with slurred speech, double vision, difficulty with swallowing and walking, and rhythmic contractions of the soft palate. Brain magnetic resonance imaging showed an acute infarct of the right caudal midbrain and an old infarct of the right medulla. We hypothesize that the cause of early palatal myoclonus in our patient was a two-hit mechanism with degeneration of the right olivary nucleus resulting from prior right medullary lacunar stroke with the new infarct affecting the dentato-rubro-olivary tract on the left side, causing bilateral dysfunction initiating palatal myoclonus. CONCLUSIONS: Wernekink commissure syndrome with palatal myoclonus at onset suggests the presence of a prior ischemic insult in the medulla. Careful examination is important to identification of this presentation.

Trans-cranial Doppler as an Ancillary Study Supporting Irreversible Brain Injury in a Post Cardiac Arrest Patient on Extracorporeal Membrane Oxygenation.

Obtaining neuroimaging in patients on cardiopulmonary support devices such as extracorporeal membrane oxygenation (ECMO) can be challenging, given the complexities in monitoring, instrumentation, and associated hemodynamic lability. Transcranial Doppler (TCD) is used as an ancillary test for the assessment of cerebral circulatory arrest, but its use in non-pulsatile blood flow in venoarterial (VA) ECMO is not well described. We report the use of TCD in a patient on VA ECMO post-cardiac arrest for evaluation of death by neurological criteria. A 72-year-old female was admitted for elective trans-catheter aortic valve replacement. Her postoperative course was complicated by hemo-pericardium evolving into pulseless electrical activity causing cardiac arrest. She was resuscitated with return of spontaneous circulation and initiated on VA ECMO and intra-aortic balloon pump for cardiogenic shock. Over the next few days, serial evaluations persistently showed a poor neurological examination. She was too unstable to transport for neuroimaging. Evaluation for death by neurological criteria was performed with a clinical examination, apnea testing, and TCD as an ancillary study. TCD showed systolic spikes supporting an impression of cerebral circulatory arrest consistent with an irreversible brain injury.