Principals of Neurocritical Care in the Acute Stroke Patient

1. Principals of Neurocritical Carein the Acute Stroke Patient

2. DISCLOSURE Relevant Financial Relationship(s) None Off Label Usage None

3. Objectives Learning 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 edema Describe nursing care guidelines for the pre and post neurosurgical stroke patient

4. Pressing Issues in Acute Ischemic Stroke Restoring blood flow Monitoring for edema and swelling Managing risk of bleeding with tPA Preventing and minimizing secondary injury

5. General Care Principles Maximize standard medical management B/P, fever, hyperglycemia, seizure activity Neuroprotection Improve cerebral blood flow Induce HTN Recanilization with thrombolysis Large vessel intra-arterial thombolectomy/lysis Prevention of complications

6. Airway 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 function Mode of mechanical ventilation in acutely ill neurologic patient is often limited to intermittent mandatory or assist control modes Ventilator dependency is much less common

7. Airway 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.

8. Volume 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 patient Initial correction of hypovolemia should be done with crystalloids (normal saline). Glucose containing solutions may precipitate increased lactate production and secondary brain injury

9. Volume Status 200 mL/hr .9% sodium cloride Correct insensible loss GI 250 mL Skin 750 mL Fever 500 mL/degree C Sweating Fluid balance 750-1,000 mL/ day excess Maintain body weight Hematocrit < 55% Osmolality <350 mosm/L Serum sodium < 150 meq/L

11. Management 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.

15. Infections / 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).

16. The Importance of Body Temperature Fever after acute stroke is associated with worse functional outcome Preliminary evidence suggests that aggressive control of hyperthermia (and perhaps induced hypothermia in cases of massive brain infarction) may be beneficial Rigorous, larger interventional trials needed

17. Nutrition The main goal of nutrition should be to preserve muscle mass, and to provide adequate fluids, minerals and fats It 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.

18. Seizures Acute injury to the cortical structures can elicit seizures. Seizures may be focal or generalized, single or continuous Tonic�clonic status epilepticus is commonly defined as repetitive seizures without full recovery between the episodes, usually with seizure intervals of 5 to 10 minutes

19. Seizures Nonconvulsive 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.

20. Seizure Assessment Continuous clinical assessment Continuous vEEG monitorin 20 minute EEG will demonstrate 15% of seizures 60 minute EEG � 50% 24 hours monitoring � close to 90%

21. Seizure Management Benzodiazepins Ativan 4 mg IV push Antiepileptic medications Dilantin may be toxic for the acutely injured brain Depakote may cause severe platelet dysfunction and bleeding Keppra seems to avoid significant side effects and used widely in NICU

22. Seizure Management Failure 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.

23. Anticoagulation Neurological 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 stroke Subclinical DVT occurred in 28 to 73%, mostly in the paralyzed extremity 5% of the patient with ICH died of pulmonary embolism (PE) within the first 30 days.

24. Anticoagulation Only 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 practitioner One study in TBI patients demonstrated no increase risk of hemorrhage in patients treated with unfractionated heparin within 72 hours

25. Large Hemispheric Stroke Issues High risk for deterioration in first 24-72 hours Neurologic causes: edema, hemorrhagic transformation, restroke Systemic causes: fever, infection, hypotension, hypoxia, hypercarbia

26. Malignant MCA Syndrome Malignant brain edema Mortality up to 80% Starts days 1-3 Peaks days 3-5 Subsides by 2 weeks

27. Who is at Risk for Developing Malignant MCA Syndrome? Clinical Picture: hemispheric syndrome with hemiparesis, hemianesthesia eye deviation those requiring early intubation for airway protection global asphasia somnolence Radiographic Picture CT findings in 1st 6 hours Large early hypodensity Loss of gray/white matter distinction Hyperdense MCA sign CT findings at 24 hours Mass effect

28. Intracranial pressure Monro-Kelly doctrine ICP depends on the volumes of blood, cerebrospinal fluid and brain to be in the balance.

29. Intracranial 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.

30. Intracranial 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

31. Intracranial Pressure Management Head position should be neutral to reduce any possible compression of jugular veins. Head elevation of 30� is considered standard Patients should be made comfortable, avoid pain, bladder distention, and agitation, because all of them might increase ICP.

32. Intracranial Pressure Management Hyperventilation Aggressive 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

33. Intracranial Pressure Management Osmotic diuresis � mainstay of the therapy Mannitol is not only facilitates movement of extracellular water, but also might be increasing CSF absorption The effect is apparent within 15 minutes and failure to respond to mannitol is usually a bad prognostic sign 100 grams IV over 30 minutes 50 grams IV q6h with osmolality monitoring. Hypertonic Saline 3% NaCl - continuous infusion 7.5% NaCl - mostly used in trauma centers 23.4% saline

34. 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%).

35. Hypertonic 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).

36. Intracranial Pressure Management Hypothermia Need to continue the study of safety and effectiveness in the Neuro ICU. Guidelines needed for best practice temperature thresholds and rates of rewarming.

38. Decompressive Hemicraniectomy Allows for the expansion of edematous tissue outside the cranial vault Decreases mortality and disability Issues: Patient Selection Timing of surgery Dominant vs. non-dominant hemisphere strokes

40. Outcome at 1 year by treatment group for all three studies combined

41. Subarachnoid 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

42. 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. Subarachnoid hemorrhage

43. Subarachnoid 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 patients Deep vein thrombosis prophylaxis should utilize mechanical means only. Gastric ulcer prophylaxis is important in all patients due to high incidence of stress ulcers.

44. Subarachnoid 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.

45. Subarachnoid hemorrhage Deterioration in patients with SAH can be delayed and related to rebleeding, hydrocephalus, vasospasm, or enlargement of frontal or temporal intraparenchymal hematoma.

46. Intracerebral 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 ischemia Comatose 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

47. AAICH Anticoagulation-associated intracerebral hemorrhages should be immediately reversed with fresh frozen plasma and vitamin K. Factor VIIa - works within 10 minutes It is short lived factor. Treatment should be followed by administration of FFP and Vitamin K INR should be monitored for at least 72 hours

49. Nursing management of Acute Stroke Airway management/ventilator management Assessment and evaluation of neurologic status to detect patient deterioration Blood pressure management General 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.

50. Nursing Management of Acute Stroke Coordination of interdisciplinary team and plan of care Support and counsel for patient & family

51. Intensive Nursing Management Monitor for bleeding complications after tPA ICH-Hemorrhagic transformation retroperitoneal bleed, genitourinary and gastrointestinal hemorrhages Patients over age of 80 with higher NIHSS score at greater risk of ICH

52. Intensive Nursing Management Management of suspected ICH after tPA Notify physician, possible neurosurgery consult Stop tPA infusion Prepare for stat brain imaging, lab, type and cross Prepare to administer platelets, cryoprecipitate, FFP Increase frequency of nursing assessment

53. Intensive Nursing ManagementCerebral Edema after stroke Usually peaks 3-5 days after stroke Can be an issue in first 24 hours in cerebellar infarct and younger stroke patients If not detected and treated can lead to increased intracranial pressure, brain herniation and death

54. Recognizing Increased ICP Early signs: Decreased LOC Deterioration in motor function Headache Changes in vital signs Late signs Pupillary abnormalities Changes in respiratory pattern Changes in ABG�s

55. Nursing Care of the Decompressive Hemicraniectomy Patient Airway management adequate O2 saturation Preventing increased ICP and providing supportive care. Hourly vitals/neuros including ICP, CPP, CVP. Maintaining BP to ensure adequate CPP Seizure precautions Antibiotic prophylaxis

56. Nursing Care of the Decompressive Hemicraniectomy Patient Place a sign on bed to alerting care providers which side of the skull is missing the bone flap Do not turn patients onto side of missing flap Monitor hemicraniectomy site for changes in appearance- bulging, inflammation, CSF leakage Fit with head gear to protect surgical site when up

57. Decompressive 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.

58. Team Work Key to the care of the NICU patient Stabilization Prevention of complications Monitoring neuro status Family support and education

59. Resources Adams, H. et al (2007). Guidelines for the Early Management of Adults with Acute Ischemic Stroke. Stroke 38, 1655-1711. 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.2004. Philadelphia, PA Summers, et al. (2009) Comprehensive Overview of Nursing and Interdisciplinary Care of the Acute Ischemic Stroke Patient. Stroke 40, 2911-2944. 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 2005. 37(4). Wojner Alexandrof, A. W., Hyperacute Ischemic Stroke Management:Reperfusion and Evolving Therapies. Critical Care Nurse Clinician North America. 21(2009) 451-470.