11/23/2015. Disclosures. Stroke Management in the Neurocritical Care Unit. 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 Disclosures I have no relevant commercial relationships to disclose, and my presentations will not include discussion of off-label or unapproved usage. 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 Malignant MCA territory infarction - Identify the patients at risk - Treatment of ischemic cerebral edema Hemorrhagic transformation - Risk factors - Practical guide to treatment Worsening neurological symptoms - Role of induced hypertension 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 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: Case # 1 56 year old man is admitted to the ED after walking up aphasic and hemiparetic. NIHSS 21 and head CT 6 hours after admission shows a dense MCA sign and hypodensityin > 50% of Left MCA territory Ischemic Brain Swelling Associated with astrocytic ischemia Cytotoxic edema Peak swelling usually day 2-3 Resolution starts by day 5-6 3
4 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: 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:
5 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 Hyperglycemia increases the risk of cerebral edema and hemorrhagic conversion Prevent factors that worsen cerebral edema: Hypoxia, hypercapnia, hyponatremia and fever Global ICP measurements can be deceiving Treat edema and elevated ICP 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 Malignant MCA territory infarction Use 23.4 % hypertonic saline Reversal of transtentorial herniation occurred in 57/76 events (75%) (only 8 stroke patients) Conclusions Infusion of 75 ml hypertonic (10%) saline decreases elevated ICP and increases cerebral perfusion pressure in stroke patients in whom mannitol had failed. The effect on the ICP and cerebral perfusion pressure reaches its maximum after the end of infusion and is seen for 4 hours 5
6 Malignant MCA territory infarction 25 patients with severe ischemic stroke in the middle cerebral artery (MCA) 33 C body-core temperature for 48 to 72 hours Decompressive Hemicraniectomy Improvement of cerebral perfusion Diminish ischemic damage Mitigate mechanical compression Decreases 1 year mortality by 50% (HAMLET, DESTINY, DECIMAL) Decompressive Hemicraniectomy Age Patient selection Timing of surgery Dominant hemisphere Social factors Functional state more important than age Co morbidities Do it early (first 48 hours) Dominant and non-dominant hemisphere Social support and access to rehabilitation Subramanian, S, Hill, M. The Neurologist 15:No. 4, July
7 Decompressive Hemicraniectomy Decompressive surgical evacuation of a space-occupying cerebellar infarction is a potentially life- saving measure, and clinical recovery may be very good Decompressivesurgery for malignant edema of the cerebral hemisphere may be life-saving, but the impact of morbidity is unknown Case # 2 67 year old arrives to the ED two hours after acute onset of right homonymous hemianopsia. IV Tpa is given and the patient is transferred to the NeuroICU. During the initial evaluation a new right sided hemiparesis is found. ED records indicate sustained BP 210/110 despite repeated doses of IV Labetalol Hemorrhagic Transformation Asymptomatic hemorrhagic conversion occurs in about one third of all treated ischemic strokes. The risk is higher on strokes cause by large vessel occlusion and cardioembolic etiology. 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. 7
8 Hemorrhagic Transformation Biologic half-life of IV TPaat the site of the thrombus is 45 minutes Bleeding usually occurs in the first hours after Tpa Hypertension usually implicated Risk higher after heparin, thrombolytics or clot retrieval Hyperglycemia increases the risk Hemorrhagic Transformation Clinical signs include: Decreased level of consciousness Headache Vomiting Increased BP /bradycardia/ apnea Worsening Neurological symptoms Hemorrhagic Transformation Stop ongoing thrombolytic infusion Stat head CT w/o contrast (ABC) Send Hemorrhagic for HH, PT, PTT, INR, platelet Transformation count, fibrinogen and type and cross-match Reversal of coagulopathy should be attempted: 4 units Fresh Frozen Plasma 10 units of Cryoprecipitate Consider recombinant Factor VIIa or Prothrombincomplex concentrate (PCC) Consult Neurosurgery for evacuation of hematoma once the coagulopathy is corrected 8
9 Case # 3 72 year old woman comes to the ED with complains of dysarthria and gait instability for last 4 hours. Pt is slertfollows commands and has 5/5 strength in all 4 extremities. The next morning the patient is found obtunded and quadriparetic with a BP is 85/43 Upon further inquiry she has been re-started her home oral metoprololearly that morning for rate control of her A fib. However her symptoms improved after administration of 1 L of NS and repeated doses of Neosynephrine. Worsening Neurological Symptoms Hypotension Fever Hypoglycemia Worsening Neurological Symptoms Seizures Hydrocephalus Hemorrhage 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:
10 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: Blood Pressure: Induced Hypertension Blood Pressure: Induced Hypertension Blood Pressure: Induced Hypertension 10
11 Blood Pressure: Induced Hypertension Good preliminary results in retrospective and small prospective clinical trials Onset <12 hours NIHSS score 11.7 Phenylephrine to target SBP 160 mmhg (or 20% above baseline) 7/13 clinically improved Blood Pressure: Induced Hypertension Who qualifies? Early acute ischemic stroke < 12hr Mismatch on functional imaging (CTP or MR perfusion diffusion) Flow limiting vessel stenosis Patients with fluctuating symptoms that are flow related Blood Pressure: Induced Hypertension What target? Clinical exam Physiology (CPP, CBF) Empirical target (SBP mmhg or % above baseline) 11
12 Blood Pressure: Induced Hypertension How? Head of bed flat Volume Vasopressors Kroppenstedt et al. Acta Neurochir 2002;81: Blood Pressure: Induced Hypertension Conclusions Screen every patient for possible development of malignant MCA territory edema Patients undergoing chemical or mechanical reperfusion therapy are at higher risk for hemorrhagic conversion Hypotension should be avoided after acute ischemic stroke Induced hypertension may be consider in a selected group of patients 12
13 Thank you 13
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