Presentation on theme: "Principals of Neurocritical Care in the Acute Stroke Patient"— Presentation transcript:
1Principals of Neurocritical Care in the Acute Stroke Patient Alexander Y. Zubkov, MD, PhD, FAHAClinical Associate Professor of NeurologyDirector of Stroke CenterFairview Southdale HospitalMinneapolis Clinic of NeurologyKari Olson, RN, BSN, CNRNNeuroscience Nurse Clinician
3ObjectivesLearning Objectives: Upon completion of this call, participants will be able to:Describe Neuro Critical Care management of acute stroke patients.Explain advances in neurosurgery for the stroke patient including decompressive hemicraniectomy for malignant cerebral edemaDescribe nursing care guidelines for the pre and post neurosurgical stroke patient
4Pressing Issues in Acute Ischemic Stroke Restoring blood flowMonitoring for edema and swellingManaging risk of bleeding with tPAPreventing and minimizing secondary injury
5General Care Principles Maximize standard medical managementB/P, fever, hyperglycemia, seizure activityNeuroprotectionImprove cerebral blood flowInduce HTNRecanilization with thrombolysisLarge vessel intra-arterial thombolectomy/lysisPrevention of complications
6Airway and Mechanical Ventilation Management of the airway and mechanical ventilator is different in neurologic critically ill patients.Many patients admitted to NICU have normal baseline pulmonary functionMode of mechanical ventilation in acutely ill neurologic patient is often limited to intermittent mandatory or assist control modesVentilator dependency is much less common
7Airway and Mechanical Ventilation Any amount of hypoxia of the injured brain will add a significant damage to the brain.Thus, intubation should be preferably performed in the controlled settings, and sometimes it is safest to perform in the anticipation of the respiratory problems rather than when the respiratory failure will occur.
8Volume Status and Blood Pressure Very few patients admitted to NICU are euvolemic and correction of volume status is one the first steps in the management of critically ill neurological or neurosurgical patientInitial correction of hypovolemia should be done with crystalloids (normal saline). Glucose containing solutions may precipitate increased lactate production and secondary brain injury
9Volume Status 200 mL/hr .9% sodium cloride Correct insensible loss GI 250 mLSkin 750 mLFever 500 mL/degree CSweatingFluid balance 750-1,000 mL/ day excessMaintain body weightHematocrit < 55%Osmolality <350 mosm/LSerum sodium < 150 meq/L
10The Importance of Blood Pressure Hypertension is a physiological response in strokeBP reduction is associated with worse outcomeBP fluctuations are associated with worse outcomeBP augmentation may be safe and effective at least in selected cases
11Management of Blood pressure Current recommendations include cutoff point in treatment of hypertension if systolic pressure is above 230 mm Hg, or diastolic pressure is above 125 mm Hg, or mean pressure above 130 mm Hg.It is reasonable to gradually decrease blood pressure with rapid-acting antihypertensive medications if mean pressure is getting above 130 mm Hg.
12Hypertension: a physiological response to brain hypoperfusion 149 pts monitored for 12 hr after IA thrombolysisSBP, DBP and MAP similar before thrombolysis12 hr after thrombolysis, SBP/MAP/DBP lowerin pts with adequate recanalizationWhen recanalization failed, BP remained elevatedlongerMattle et al. Stroke 2005;36:264-8
13Detrimental effect of BP reduction in first 24 hours after stroke onset: Prospective assessment of 115 pts evaluated within24 hr of stroke onsetMean NIHSS 4.5Most common mechanism: cardioembolism (30%)Predictors of poor outcome at 3 mo on multivariableanalysis: - Higher NIHSS(OR 1.55 per 1 point increase in score)- Degree of SBP reduction in first 24 hr(OR 1.89 per 10% SBP decrease)Oliveira-Filho et al. Neurology 2003;61:
14The Importance of Blood Glucose Hyperglycemia in acute stroke is associated with:Worse functional outcomeLower rates of recanalizationHigher rates of hemorrhagic complicationsTrials of acute intensive glycemic control ongoing
15Infections / Fever Fever develops in 25-50% of NICU patients. 52% percent of fevers were explained by infectious etiology with most predominant pulmonary pathology.Non-infectious etiologies of fever may occur and include reaction to blood products, deep vein thrombosis, drug fever, postsurgical local tissue injury, pulmonary embolism and central fever with its extreme autonomic storms (episodes of profuse sweating, tachycardia, tachypnea, bronchial hypersecretion).
16The Importance of Body Temperature Fever after acute stroke is associated with worse functional outcomePreliminary evidence suggests that aggressive control of hyperthermia (and perhaps induced hypothermia in cases of massive brain infarction) may be beneficialRigorous, larger interventional trials needed
17NutritionThe main goal of nutrition should be to preserve muscle mass, and to provide adequate fluids, minerals and fatsIt is prudent to consider postpyloric feeding in patient with neurological catastrophies, because gastric atony increases the risk of aspiration.Enteral feeding should be preferably done by continuous infusion with a volumetric pump.
18Seizures Acute injury to the cortical structures can elicit seizures. Seizures may be focal or generalized, single or continuousTonic–clonic status epilepticus is commonly defined as repetitive seizures without full recovery between the episodes, usually with seizure intervals of 5 to 10 minutes
19SeizuresNonconvulsive status epilepticus is much difficult to diagnose and likely is less common.Clinical hallmarks are decrease in the level of consciousness or fluctuation in responsiveness.Patient may have fluttering of the eyelids or eye deviation as only signs of nonconvulsive status epilepticus.
20Seizure Assessment Continuous clinical assessment Continuous vEEG monitorin20 minute EEG will demonstrate 15% of seizures60 minute EEG – 50%24 hours monitoring – close to 90%
21Seizure Management Benzodiazepins Antiepileptic medications Ativan 4 mg IV pushAntiepileptic medicationsDilantin may be toxic for the acutely injured brainDepakote may cause severe platelet dysfunction and bleedingKeppra seems to avoid significant side effects and used widely in NICU
22Seizure ManagementFailure of lorazepam and fosphenytoin in adequate doses to control seizures indicates transition to refractory status epilepticus.At this point either increasing doses of barbiturates or midazolam should be used for treatment.Propofol is another alternative but high dosis are needed. Propofol infusion syndrome – sudden cardiovascular collapse with metabolic acidosis-is a serious complication that limits the routine use of this otherwise very effective medication.
23AnticoagulationNeurological patients has a higher incidence of DVT due to lack of mobility in the affected limbs, associated with neurological injury.Clinically apparent DVT was reported in 1.7% to 5% of patients with ischemic strokeSubclinical DVT occurred in 28 to 73%, mostly in the paralyzed extremity5% of the patient with ICH died of pulmonary embolism (PE) within the first 30 days.
24AnticoagulationOnly mechanical methods (intermittent pneumatic compression with or without elastic stockings) should the standard of care.The use of unfractionated heparin was left on the discretion of the practitionerOne study in TBI patients demonstrated no increase risk of hemorrhage in patients treated with unfractionated heparin within 72 hours
25Large Hemispheric Stroke Issues High risk for deterioration in first hoursNeurologic causes: edema, hemorrhagic transformation, restrokeSystemic causes: fever, infection, hypotension, hypoxia, hypercarbia
26Malignant MCA Syndrome Malignant brain edemaMortality up to 80%Starts days 1-3Peaks days 3-5Subsides by 2 weeks
27Who is at Risk for Developing Malignant MCA Syndrome? Clinical Picture:hemispheric syndrome with hemiparesis, hemianesthesiaeye deviationthose requiring early intubation for airway protectionglobal asphasiasomnolenceRadiographic PictureCT findings in 1st 6 hoursLarge early hypodensityLoss of gray/white matter distinctionHyperdense MCA signCT findings at 24 hoursMass effect
28Intracranial pressure Monro-Kelly doctrineICP depends on the volumes of blood, cerebrospinal fluid and brain to be in the balance.
29Intracranial pressure CSF shift from ventricular or subarachnoid space into spinal compartment.Reduction of intracranial blood volume achieved by collapsing of veins and dural sinuses and by changes in the diameter of cerebral vessels.If the limits of compensatory mechanisms are exceeded, minimal increase in the intracranial volume will lead to precipitous rise of ICP.
30Intracranial Pressure Intracranial pressure monitoring is an integral part of NICU.The indications for placement of ICP monitors include GCS < 8, severe traumatic brain injury, massive cerebral edema from infarction
31Intracranial Pressure Management Head position should be neutral to reduce any possible compression of jugular veins.Head elevation of 30º is considered standardPatients should be made comfortable, avoid pain, bladder distention, and agitation, because all of them might increase ICP.
32Intracranial Pressure Management HyperventilationAggressive hyperventilation might decrease cerebral blood flow to the levels approaching ischemia.Hyperventilation should only be used as a bridge measure while other means of ICP control are instituted
33Intracranial Pressure Management Osmotic diuresis – mainstay of the therapyMannitol is not only facilitates movement of extracellular water, but also might be increasing CSF absorptionThe effect is apparent within 15 minutes and failure to respond to mannitol is usually a bad prognostic sign100 grams IV over 30 minutes50 grams IV q6h with osmolality monitoring.Hypertonic Saline3% NaCl - continuous infusion7.5% NaCl - mostly used in trauma centers23.4% saline
34Sixty-eight patients met criteria for TTH and received 23 Sixty-eight patients met criteria for TTH and received 23.4% saline, and there were a total of 76 TTH events in these patients.The 23.4% saline was administered as a bolus of 30 mL in 65 events (85.5%) and 60 mL in 11 events (14.5%).Neurology, Mar 2008; 70:
35Hypertonic Saline Effect Clinical reversal of TTH occurred in 57/76 events (75.0%).Median (IQR) GCS increased from 4(3-5) at the time of herniation to 6(4-7) (p<0.01) 1 hour and 7(5-9) 24 hours following TTH (p<0.001).Neurology, Mar 2008; 70:
36Intracranial Pressure Management HypothermiaNeed to continue the study of safety and effectiveness in the Neuro ICU.Guidelines needed for best practice temperature thresholds and rates of rewarming.
38Decompressive Hemicraniectomy Allows for the expansion of edematous tissue outside the cranial vaultDecreases mortality and disabilityIssues:Patient SelectionTiming of surgeryDominant vs. non-dominant hemisphere strokes
40Outcome at 1 year by treatment group for all three studies combined Lancet Neurology, 8( 7); , 2009
41Subarachnoid hemorrhage Hydration with normal saline should be started immediately and patient should receive at least 2-3L of fluids in the first 24 hours.Attention should be paid to possible neurogenic pulmonary edema and fluid management should be adjusted accordingly.Cardiac stunning might occur in the poor grade SAH and might contribute to pulmonary edema
42Subarachnoid hemorrhage Management of hypertension depends on the stage of the treatment.In the patients with unsecured aneurysm we tend to keep mean arterial pressure below 100 mm Hg.In patients who underwent aneurysmal repair, mean blood pressure should be liberalized up to 130 mm Hg.
43Subarachnoid hemorrhage Nutrition usually delays to the second day. Nausea and vomiting are common on the first day, in addition to gastroparesis in more severely impaired patientsDeep vein thrombosis prophylaxis should utilize mechanical means only.Gastric ulcer prophylaxis is important in all patients due to high incidence of stress ulcers.
44Subarachnoid hemorrhage Stool softeners should be used in all patients to prevent straining, which may lead to rerupture of the aneurysm.Indwelling catheters should be used to close monitoring in outputs due to potential of the development of SIADH.Headache may be relieved by acetaminophen with codeine or tramadol.Vomiting should be aggressively treated.
45Subarachnoid hemorrhage Deterioration in patients with SAH can be delayed and related to rebleeding, hydrocephalus, vasospasm, or enlargement of frontal or temporal intraparenchymal hematoma.
46Intracerebral hemorrhage Hemorrhages have a potential of enlargement in about a third of the patients and management should be directed towards supportive measures.Very aggressive decrease of blood pressure may precipitate ischemiaComatose patients could benefit from the monitoring in intracranial pressure.Intracranial pressure should remain below 20 mm Hg and cerebral perfusion pressure must remain in the range of 60 to 80 mm Hg to provide adequate cerebral blood flow
47AAICHAnticoagulation-associated intracerebral hemorrhages should be immediately reversed with fresh frozen plasma and vitamin K.Factor VIIa - works within 10 minutesIt is short lived factor.Treatment should be followed by administration of FFP and Vitamin KINR should be monitored for at least 72 hours
48Time is Brain For every minute’s delay, the brain loses: 1.9 million neurons;14 billion synapses;7.5 miles of myelinated fibers.If a stroke runs its full course – an estimated 10 hours on average – the brain loses:1.2 billion neurons;8.3 trillion synapses;4,470 miles of myelinated fibers.Stroke 2006;37:
49Nursing management of Acute Stroke Airway management/ventilator managementAssessment and evaluation of neurologic status to detect patient deteriorationBlood pressure managementGeneral supportive care and prevention of complications associated with:Dysphagia, HTN, hyperglycemia, dehydration, malnourishment, fever, cerebral edema, infection, and DVT, immobility, falls, skin care, bowel and bladder dysfunction.
50Nursing Management of Acute Stroke Coordination of interdisciplinary team and plan of careSupport and counsel for patient & family
51Intensive Nursing Management Monitor for bleeding complications after tPAICH-Hemorrhagic transformationretroperitoneal bleed, genitourinary and gastrointestinal hemorrhagesPatients over age of 80 with higher NIHSS score at greater risk of ICH
52Intensive Nursing Management Management of suspected ICH after tPANotify physician, possible neurosurgery consultStop tPA infusionPrepare for stat brain imaging, lab, type and crossPrepare to administer platelets, cryoprecipitate, FFPIncrease frequency of nursing assessment
53Intensive Nursing Management Cerebral Edema after stroke Usually peaks 3-5 days after strokeCan be an issue in first 24 hours in cerebellar infarct and younger stroke patientsIf not detected and treated can lead to increased intracranial pressure, brain herniation and death
54Recognizing Increased ICP Early signs:Decreased LOCDeterioration in motor functionHeadacheChanges in vital signsLate signsPupillary abnormalitiesChanges in respiratory patternChanges in ABG’s
55Nursing Care of the Decompressive Hemicraniectomy Patient Airway management adequate O2 saturationPreventing increased ICP and providing supportive care.Hourly vitals/neuros including ICP, CPP, CVP.Maintaining BP to ensure adequate CPPSeizure precautionsAntibiotic prophylaxis
56Nursing Care of the Decompressive Hemicraniectomy Patient Place a sign on bed to alerting care providers which side of the skull is missing the bone flapDo not turn patients onto side of missing flapMonitor hemicraniectomy site for changes in appearance- bulging, inflammation, CSF leakageFit with head gear to protect surgical site when up
57Decompressive Hemicraniectomy Bone flap stored in a Bone Bank or sewn into a pouch in patient’s abdomen.Bone replaced at around 3 months from the time of the infarction.
58Team Work Key to the care of the NICU patient Stabilization Prevention of complicationsMonitoring neuro statusFamily support and education
59ResourcesAdams, H. et al (2007). Guidelines for the Early Management of Adults with Acute Ischemic Stroke. Stroke 38,Ropper, A.H., Gress, D.R., Diringer, M.N., Green, D.M. , Mayer, S.A. , Bleck, T.P. Neurological and Neurosurgical Intensive Care. Fourth edition. Lippincott Williams & Wilkins Philadelphia, PASummers, et al. (2009) Comprehensive Overview of Nursing and Interdisciplinary Care of the Acute Ischemic Stroke Patient. Stroke 40,Tazbir, J., Marthaler, M.T., Moredich, C., Keresztes, P. Decompressive Hemicraniectomy with Duraplasty: A treatment for Large-Volume Ischemic Stroke. Journal of Neuroscience Nursing. August (4).Wojner Alexandrof, A. W., Hyperacute Ischemic Stroke Management:Reperfusion and Evolving Therapies. Critical Care Nurse Clinician North America. 21(2009)