11/27/2017. Stroke Management in the Neurocritical Care Unit. Conflict of interest. Karel Fuentes MD Medical Director of Neurocritical Care

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1 Stroke Management in the Neurocritical Care Unit Karel Fuentes MD Medical Director of Neurocritical Care Conflict of interest None Introduction Reperfusion therapy remains the mainstay in the treatment of acute ischemic stroke Good critical care can make a difference 1

2 Outline Airway and ventilatory support Blood pressure management Hemorrhagic conversion Ischemic brain swelling Other causes of acute neurological worsening Admission Criteria Neurologic Post-reperfusion therapy by thrombolysis or endovascular treatment Non-Neurologic Respiratory failure and mechanical ventilation Massive cerebral infarction Cerebellar and brainstem infarctions Hemorrhagic conversion Worsening neurological symptoms Persistent hypotension Severe hypertension requiring intravenous therapy Cardiac infarction or arrhythmias Severe systemic bleeding Airway and ventilatory support Prevent hypoxia and hypotension Posterior circulation strokes are at higher risk Partial airway obstruction Hypoventilation Abnormal respiratory patterns Aspiration pneumonia 2

3 Angioedema Orolingual angioedema occurs in 1.3%-5.1% of all pts receiving IV Tpa Associated with ACE inhibitors use More common with Insular and Frontal cortex infarctions Usually mild and contralateral to the ischemic hemisphere Severe cases might require fiberoptic intubation Treatment with H2 blockers, Diphenhydramine and steroids Airway and ventilatory support Need for endotracheal intubation indicates a poor prognosis Mortality of approximately of 50% at 30 days Figure 3. Survival curves for intubated patients with stroke by Glasgow Coma Score (GCS) rank. With increasing rank, the GCS is significantly correlated with 30-day survival using the multiple logistic regression model (p = 0.03, OR = 0.849, c index = 0.805). Bushnell CD et al. Survival and outcome after endotracheal intubation for acute stroke. Neurology. 1999;52: Acute Neurological Worsening Hypotension Stroke Progression Fever Hypoglycemia Acute Neurological Worsening Seizures Hydrocephalus Ischemic Brain Swelling Hemorrhagic Transformation 3

Blood pressure management No specific guidelines in optimal BP management after endovascular therapy Keep BP 185/110 after IV Tpa Hemorrhagic conversion vs.

4 Blood pressure management No specific guidelines in optimal BP management after endovascular therapy Keep BP 185/110 after IV Tpa Hemorrhagic conversion vs. decreased collateral flow Case by case approach is preferred SBP < 160 in most patients for the first 24 hours (TICI 2b/3 was achieved) Blood Pressure: Hypotension Arterial Hypotension should be avoided Systolic BP < 100 mmhg or Diastolic BP < 70 mmhg associated with poor outcome Investigate underlying cause Leonardi-Bee J et al. Blood pressure and clinical outcomes in the international stroke trial. Stroke 2002; 33: Raising BP improves Outcome? Castillo J et al. Blood pressure decrease during the acute phase of ischemic stroke is associated with brain injury and poor stroke outcome. Stroke. 2004;35:

5 Blood Pressure: Induced Hypertension Blood Pressure: Induced Hypertension Hemorrhagic Transformation Symptomatic vs. Asymptomatic Risk factors: Older age Large stroke Cardioembolic and large artery occlusion etiology Reperfusion therapy 5

6 Asymptomatic Hemorrhagic Transformation Asymptomatic hemorrhagic conversion occurs in about one third of all treated ischemic strokes. The presence of asymptomatic hemorrhagic conversion had no influence on outcomes at 3 and 6 months as measure by the MRs and the Barthel Index. Asymptomatic Hemorrhagic Transformation Head CT Timing matters Study CT scan Timing Rate of AHTI NINDS trial 24 hrs 2.9 % Desmotaplase in Acute Ischemic Stroke Trial Multicenter Acute Stroke Trial-Europe 72 hrs 18.5% 5 days 31% ECASS I-II 7 days 29.9% 36.8% Symptomatic Hemorrhagic Transformation Occurs in about 1% of all strokes patients Incidence increases to 5-6 % after IV Tpa or endovascular therapy Most common in the first hrs Hypertension usually implicated Hyperglycemia increases the risk Very high mortality 6

ECASS Classification HI-1 : Small Petechiae along along the margins of the stroke HI-2 : Confluent petechiae within the infarcted area PH-1 : Parenchymal hematoma < 30% of the infarcted area (slight

Decreased level of consciousness Headache Vomiting Hypertension /bradycardia/ apnea Worsening neurological symptoms Symptomatic Hemorrhagic transformation Stop ongoing thrombolytic infusion Stat head

7 ECASS Classification HI-1 : Small Petechiae along along the margins of the stroke HI-2 : Confluent petechiae within the infarcted area PH-1 : Parenchymal hematoma < 30% of the infarcted area (slight space occupying effect) PH-2 : Parenchymal hematoma > 30% of the infarcted area with substantial mass effect or any hemorrhage outside the infarcted area Symptomatic Hemorrhagic Transformation Decreased level of consciousness Headache Vomiting Hypertension /bradycardia/ apnea Worsening neurological symptoms Symptomatic Hemorrhagic transformation Stop ongoing thrombolytic infusion Stat head CT w/o contrast (ABC) Send for HH, PT, PTT, INR, platelet count, fibrinogen and type and cross-match Hemorrhagic Transformation Reversal of coagulopathy should be attempted: 4 units Fresh Frozen Plasma 10 units of Cryoprecipitate Consider recombinant Factor VIIa or Prothrombin complex concentrate (PCC) Consult Neurosurgery for evacuation of hematoma once the coagulopathy is corrected 7

Ischemic brain swelling Associated with astrocytic ischemia Cytotoxic edema Peak swelling usually day 2-3

Emphasis on pressure gradient causing horizontal shift diencephalon midbrain pons Force vector displacing

Young age History of hypertension NIH stroke scale > 18 Heart failure Elevated WBC?

8 Ischemic brain swelling Associated with astrocytic ischemia Cytotoxic edema Peak swelling usually day 2-3 Resolution starts by day 5-6 Life threatening in MCA and Cerebellar strokes 20 mm Hg Focal Model 25 mm Hg Emphasis on pressure gradient causing horizontal shift diencephalon midbrain pons Force vector displacing diencephalon laterally DeGeorgia M Malignant MCA territory infarction Risk factors for clinical deterioration Young age History of hypertension NIH stroke scale > 18 Heart failure Elevated WBC? SIRS Involvement of non dominant hemisphere Kasner SE et al. Predictors of fatal brain edema in massive hemispheric ischemic stroke. Stroke. 2001;32:

9 Malignant MCA territory infarction Risk factors for clinical deterioration CT findings Early CT hypodensity (within 5 hours) More the 50% of the MCA territory affected Dense MCA sign More than one territory involved Kasner SE et al. Predictors of fatal brain edema in massive hemispheric ischemic stroke. Stroke. 2001;32: Malignant MCA territory infarction Protect the airway (ABC) Intubation should occur in a controlled setting by an experience practitioner (RSI) Corticosteroids do not work for cerebral edema caused by ischemia and might cause harm Prevent factors that worsen cerebral edema: Hypoxia, hypercapnia, hyponatremia and fever Global ICP measurements can be deceiving Treatment HOB at 30 degrees Osmotherapy (mannitol, hypertonic saline) Drainage of CSF (Ventriculostomy) Mild Hypothermia (33 degrees) Barbiturate coma Neuromuscular paralysis Hyperventilation only as a temporary measure Decompressive hemicraniectomy 9

Acute neurological worsening Seizures occur in 10% of patients with acute stroke Incidence higher in patients with hemorrhagic

conversion and cerebral edema ( Keep blood glucose 140-180 mg/dl ) Hyponatremia worsens cerebral edema and increase the risk of

acute ischemic stroke Patients undergoing chemical or mechanical reperfusion therapy are at higher risk for hemorrhagic conversion

10 Acute neurological worsening Seizures occur in 10% of patients with acute stroke Incidence higher in patients with hemorrhagic transformation No data to support the administration of prophylactic antiepileptics Hyperglycemia increases the risk of hemorrhagic conversion and cerebral edema ( Keep blood glucose mg/dl ) Hyponatremia worsens cerebral edema and increase the risk of seizures Fever is associated with a twofold increased risk in short term mortality Conclusions Hypotension should be avoided after acute ischemic stroke Patients undergoing chemical or mechanical reperfusion therapy are at higher risk for hemorrhagic conversion Screen every patient for possible development of ischemic brain swelling Maintain normothermia, normal Na levels and normoglycemia to optimize outcomes 10

11 Thank you 11

11/23/2015. Disclosures. Stroke Management in the Neurocritical Care Unit. Karel Fuentes MD Medical Director of Neurocritical Care.

11/23/2015. Disclosures. Stroke Management in the Neurocritical Care Unit. Karel Fuentes MD Medical Director of Neurocritical Care. Stroke Management in the Neurocritical Care Unit Karel Fuentes MD Medical Director of Neurocritical Care Disclosures I have no relevant commercial relationships to disclose, and my presentations will not