for neurocritical care experts
Pathophysiology of cardiopulmonary complications in SAH. SAH leads to catecholamine surge, which activates alpha, alpha + beta, and beta receptors. This leads to pulmonary and myocardial dysfunction as well as platelet aggregation. Patients then develop neurogenic pulmonary edema, LV dysfunction and shock.
Muehlschlegel, S. (2018). Subarachnoid Hemorrhage. CONTINUUM: Lifelong Learning In Neurology, 24(6), 1623-1657. doi: 10.1212/con.0000000000000679
Historically, DCI thought to be caused by cerebral vasospasm. Recent studies now indicates DCI may be caused by several factors, including early brain injury, microthrombosis, cortical spreading depolarizations and related ischemia, in addition to cerebral vasospasm.
Cerebral vasospasm may be an epiphenomenon, and underlying biochemical and biophysical changes that lead to DCI occur as early as SAH onset.
Supporting evidence? Endothelin 1 is strongest vasoconstrictor mediator in SAH. Administration of clazosentan (potent endothelin 1 receptor inhibitor) resulted in less angiographic vasospasm but did not decrease DCI nor lead to improvement in 90-day outcomes.
Muehlschlegel, S. (2018). Subarachnoid Hemorrhage. CONTINUUM: Lifelong Learning In Neurology, 24(6), 1623-1657. doi: 10.1212/con.0000000000000679
AHA/ASA
Continuum (2020)
Powers, W., Rabinstein, A., Ackerson, T., Adeoye, O., Bambakidis, N., Becker, K., Biller, J., Brown, M., Demaerschalk, B., Hoh, B., Jauch, E., Kidwell, C., Leslie-Mazwi, T., Ovbiagele, B., Scott, P., Sheth, K., Southerland, A., Summers, D. and Tirschwell, D., 2019. Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke, 50(12).
Hurford, R., Sekhar, A., Hughes, T. and Muir, K., 2020. Diagnosis and management of acute ischaemic stroke. Practical Neurology, pp.practneurol-2020-002557.
Rabinstein, A. (2020). Update on Treatment of Acute Ischemic Stroke. CONTINUUM: Lifelong Learning In Neurology, 26(2), 268-286. doi: 10.1212/con.0000000000000840
Common and Uncommon Etiologies of Hypoglycorrhachia in the Literature
ETIOLOGIES COMMONLY ASSOCIATED WITH HYPOGLYCORRHACHIA
ETIOLOGIES UNCOMMONLY ASSOCIATED WITH HYPOGLYCORRHACHIA
Etiologies reported to cause severe hypoglycorrhachia, (CSF glu ≤10 mg/dL)
Frequency of Different Known Diagnoses Seen in Patients with Hypoglycorrhachia
2. HIV-Infected Patients
3. Patients with History of Neurosurgery
4. Patients without HIV or Neurosurgical History
Chow, E., & Troy, S. (2014). The Differential Diagnosis of Hypoglycorrhachia in Adult Patients. The American Journal Of The Medical Sciences, 348(3), 186-190. doi: 10.1097/maj.0000000000000217
Case report: COVID-19 associated acute necrotizine hemorrhagic encephalopathy – ANE – associated iwth other viral infections. Female, late 50s, 3-day cough, fever, altered mental status.
Work-up NEG for influenza, nasopharyngeal swab (+) coronavirus, CSF limited – traumatic LP, CSF bacterial culture NG, HSV HSV 1 and 2, varicella, WNV NEG; unable to test CSF for SARSCoV-2.
CT head: symmetric hypoattenuation within the bilateral medial thalami with a normal CT angiogram and CT venogram
MRI: hemorrhagic rim enhancing lesions within the bilateral thalami, medial temporal lobes, and subinsular regions
Acute necrotizing encephalopathy
Imaging Features
Image from noncontrast head CT demonstrates symmetric hypoattenuation within the bilateral medial thalami (arrows). B, Axial CT venogram demonstrates patency of the cerebral venous vasculature, including the internal cerebral veins (arrows). C, Coronal reformat of aCT angiogram demonstrates normal appearance of the basilar artery and proximal posterior cerebral arteries.
MRI images demonstrate T2 FLAIR hyperintensity within the bilateral medial
temporal lobes and thalami (A, B, E, F) with evidence of hemorrhage indicated by hypointense signal intensity on susceptibility-weighted images (C, G) and rim enhancement on postcontrast
images (D, H).
Poyiadji, N., Shahin, G., Noujaim, D., Stone, M., Patel, S., & Griffith, B. (2020). COVID-19–associated Acute Hemorrhagic Necrotizing Encephalopathy: CT and MRI Features. Radiology, 201187. doi: 10.1148/radiol.2020201187
HIMALAIA Study – Netherlands. The only RCT looking at efficacy of BP augmentation in DCI in increasing cerebral blood flow (via CT perfusion). Small n, negative study.
Tey article – XeCt to measure regional CBF, at onset of DCI suspicion, 5 days of induced HTN, hypervolemia, hemodilution. Compared XeCT before and after treatment and showed increase in regional CBF in worst vascular territories from 19 to 227ml/100g/min, significant reduction of regions with CBF <20ml/100g/min from 26 to 10%.
Indications:
Baseline echo: cardiomyopathy is a contraindication
Drug of choice: Induce HTN with norepinephrine? based on reference below (we usually use phenylephrine)
End points:
Risks of Induced HTN:
Literature does not support the use of induced HTN, but how can we ignore bedside observations of patients who clinically improve with induced HTN?
Critique:
Dr. Diringer’s Advice: use induced HTN in a thoughtful and individualized manner. Trial of induced HTN at onset of DCI. If patient improves, continue. If no change, back off and explore alternative treatments. If patient exam is poor (no followable exam), answer less clear but prolonged extreme elevations should be avoided.
Another way of doing it (Continuum article on SAH)
Onset of DCI / symptomatic vasospasm – induced hypertension indicated. Standard treatment is now hypertensive and mild hpyervolemic therapy (HHT), and not Triple H therapy.
Initiate IV bolus, maintain fluids for euvolemia or mild hypervolemia.
Induce hypertension using Alpha 1 receptor agonists by infusion (norepinephrine or phenylephrine). Vasopressors of choice as brain vessels lack alpha 1 receptors. Stepwise progression of BP augmentation. Neuro assessment at each step.
Follow MAP. MAP about 20 mm Hg above baseline set as first goal, (often MAP>90).
Follow SBP: some institutions use SBP goals. No evidence exists which parameter is better to follow. Goal should be ~20-40mm Hg above baseline SBP. Commonly SBP goal >180 or >200 mm Hg.
If clinical exam returns to baseline – no further BP elevations. If exam deteriorates at this BP goal, attempt further increases. No optimal max BP goal known, but adverse effects (cardiopulmo, brain autoregulation, PRES) should be considered.
Inotropic agents (milrinone, dobutamine) reserved for patients with poor CO from acute or chronic CMP.
If neuro deficits persist despite induced HTN, perform CT/CTA ffd by DSA with endovascular therapy if VSP confirmed. NCCT prior to DSA to rule out HCP / determine pre-existing stroke prior to endovascular treatment.
References:
Gathier, C., Dankbaar, J., van der Jagt, M., Verweij, B., Oldenbeuving, A., Rinkel, G., van den Bergh, W. and Slooter, A. (2015). Effects of Induced Hypertension on Cerebral Perfusion in Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage. Stroke, 46(11), pp.3277-3281.
Diringer, M. Editorial. Hemodynamic Therapy for Delayed Cerebral Ischemia in SAH. Neurocritical Care Journal. Pre-print.
Muehlschlegel, S. (2018). Subarachnoid Hemorrhage. CONTINUUM: Lifelong Learning In Neurology, 24(6), 1623-1657. doi: 10.1212/con.0000000000000679
Criner, G., Barnette, R. and D’Alonzo, G. (2010). Critical Care Study Guide. Dordrecht: Springer.
Garvin, R. and Mangat, H. (2017). Emergency Neurological Life Support: Severe Traumatic Brain Injury. Neurocritical Care, 27(S1), pp.159-169.
Low-risk TIA
High-Risk TIA:
Gross, H. and Grose, N. (2017). Emergency Neurological Life Support: Acute Ischemic Stroke. Neurocritical Care, 27(S1), pp.102-115.
Patients eligible for intravenous alteplase should receive intravenous alteplase even if endovascular treatments are being considered
Patients should receive endovascular therapy with a stent retriever if they meet all the following criteria:
As with intravenous alteplase, reduced time from symptom onset to reperfusion with endovascular therapies is highly associated with better clinical outcomes
When treatment is initiated beyond 6 h from symptom onset, the effectiveness of endovascular therapy is uncertain for patients with acute ischemic stroke who havecausative occlusion of the internal carotid artery or proximal MCA (M1)
In carefully selected patients with anterior circulation occlusion who have contraindications to intravenous alteplase, endovascular therapy with stent retrievers completed within 6 h of stroke onset is reasonable
Although the benefits are uncertain, use of endovascular therapy with stent retrievers may be reasonable for carefully selected patients with acute ischemic stroke in whom treatment can be initiated (groin puncture) within 6 h of symptom onset and who have causative occlusion of the M2 or M3 portion of the MCAs, anterior cerebral arteries, vertebral arteries, basilar artery, or posterior cerebral arteries
Endovascular therapy with stent retrievers may be reasonable for some patients <18 years of age with acute ischemic stroke who have demonstrated large vessel occlusion in whom treatment can be initiated (groin puncture) within 6 h of symptom onset, but the benefits are not established in this age group
Observing patients after intravenous alteplase to assess for clinical response before pursuing endovascular therapy is not required to achieve beneficial outcomes and is not recommended
Endovascular therapy with stent retrievers is recommended over intra-arterial fibrinolysis as first-line therapy
It might be reasonable to favor conscious sedation over general anesthesia during endovascular therapy for acute ischemic stroke. However, the ultimate selection of anesthetic technique during endovascular therapy for acute ischemic stroke should be individualized based on patient risk factors, tolerance of the procedure, and other clinical characteristics
Continuum (2020):
Gross, H. and Grose, N. (2017). Emergency Neurological Life Support: Acute Ischemic Stroke. Neurocritical Care, 27(S1), pp.102-115.
Rabinstein, A. (2020). Update on Treatment of Acute Ischemic Stroke. CONTINUUM: Lifelong Learning In Neurology, 26(2), 268-286. doi: 10.1212/con.0000000000000840
Peripheral Brain 