Guidelines for management of acute stroke


Published on

Guidelines For Acute ischemic stroke
By Dr Sankalp Mohan ,Senior resident Neurology

under guidance of Dr Vijay Sardana (HOD Neurology)

Published in: Education, Health & Medicine
  • Be the first to comment

No Downloads
Total views
On SlideShare
From Embeds
Number of Embeds
Embeds 0
No embeds

No notes for slide

Guidelines for management of acute stroke

  2. 2. Etiology and classification Ischemic stroke – 1. thrombosis 2. embolism 3. systemic hypoperfusion Hemorrhagic stoke– 1 . intracerebral 2 . subarachnoid
  3. 3. THREE STROKE TYPES Intracerebral Hemorrhage Ischemic Stroke 85% Clot occluding artery Subarachnoid Hemorrhage 10% Bleeding into brain 5% Bleeding around brain
  4. 4. ISCHEMIC STROKE PATHOPHYSIOLOGY The First Few Hours “TIME IS BRAIN: SAVE THE PENUMBRA” Core Penumbra is zone of reversible ischemia around core of irreversible infarction—salvageable in first few hours after ischemic stroke onset Penumbra damaged by: • Hypoperfusion • Hyperglycemia • Fever • Seizure Penumbra Clot in Artery
  6. 6. Emergency evaluation and diagnosis of acute ischemic stroke Data: ER Evaluation and Management Assessment Goal: in first 10 minutes Assess ABCs, vital signs Provide oxygen by nasal cannula Obtain IV access; obtain blood samples (CBC, ’lytes, coagulation studies) Obtain 12-lead ECG, check rhythm, place on monitor Check blood sugar; treat if indicated Alert Stroke Team: neurologist, radiologist, CT technician Perform general neurologic screening assessment
  7. 7. National Institutes of Health Stroke Scale  1a. Level of Consciousness (LOC): tests stimulation. Graded from 0-3.  1b. LOC Questions: tests the patient's ability to answer questions correctly. Graded from 0-2.  1c. LOC Commands: tests the patient's ability to perform tasks correctly. Graded from 0-2.  2. Best Gaze: tests horizontal eye movements. Graded from 0-2.  3. Visual: tests visual fields. Graded from 0-3.  4. Facial Palsy: tests the patient's ability to move facial muscles. Graded from 0 5. Motor Arm: tests motor abilities of the arms. Graded from 0-4.  6. Motor Leg: tests motor abilities of the legs. Graded from 0-4.  7. Limb Ataxia: tests coordination of muscle movements. Graded from 0-2.  8. Sensory: tests sensation of the face, arms, and legs. Graded from 0-2.  9. Best Language: tests the patient's comprehension and communication. Graded from 0-3.  10. Dysarthria: tests the patient's speech. Graded from 0-2.  11. Extinction and Inattention: tests patient's recognition of self. Graded from 0-2.
  8. 8. STROKE EMERGENCY BRAIN IMAGING: NONCONTRAST CT SCAN Acute (4 hours) Infarction R L Subtle blurring of gray-white junction & sulcal effacement Subacute (4 days) Infarction L R Obvious dark changes & “mass effect” (e.g., ventricle compression)
  9. 9. MRI BRAIN IN HYPERACUTE ISCHEMIC STROKE  DWI & ADC: Early infarction visible  FLAIR: No signal changes; possible sulcal effacement in area of infarction R L DWI R L ADC R L FLAIR
  10. 10. MEDICAL MANAGEMENT 1. supportive management- airway, temperature, blood pressure, blood glucose, cardiac assessement 2. thrombolysis – intravenous / intra arterial 3. antiplatelet drugs 4. anticoagulant drugs 5. hemodilution, vasodilators and induced hypertension 6. Neuroprotective agents
  11. 11. SURGICAL MANAGEMENT A) endovascular interventions  1) angioplasty and stenting  2) mechanical clot disruption  3) clot extraction  B)carotid endartectomy
  12. 12. MANAGEMENT OF COMPLICATIONS  1.cerebral edema  2. hemorrhagic transformation  3. siezures
  13. 13. AIRWAY AND VENTILATION Patients with decreased consiousness AND or patients with brainstem stroke are at the greatest risk for airway compromise in stroke Seriously ill patients or those at risk for aspiration Elective intubation may help in the management of who have severely increases ICT
  14. 14.  SUPPLEMENTAL OXYGEN – adequate tissue oxygenation is important to prevent further brain injury  Most common causes of hypoxia are partial airway obstruction, hypoventilation. ,aspiration pneumonia,atelectasis..  Some patients develop cheynes stoke s respiration which is readily reversed by oxygen  Hyperbaric oxygen – studies done have been inconclusive or have shown that it does not improve outcome
  15. 15. TEMPERATURE  FEVER in the setting of acute stroke is associated with poor outcome possibly due to  1. increased metabolic demands  2.enhanced release of neurotransmitters  3.increased free radical production  Lowering acutely elevated body temperature might improve the prognosis in stroke pateints .. Antipyretic agents like acetaminophen and coolong devices might be used ..
  16. 16.  HYPOTHERMIA –  Has been shown to be neuroprotective in experimental and focal hypoxic brain injury models..  Inspite of expermimental and clinical evidence shows that hypothermia is neuroprotective data about induced hypothermia for the treatment of stroke are not available
  17. 17. BLOOD PRESSURE MANAGEMENT Reducing formation of brain edema lessening hemorrhagic transformation preventing early recurrent stroke
  18. 18. HOWEVER ,,, aggressive treatment of blood pressure may reduce the perfusion pressure to the ischemic areas of the brain In majority of patients decline in blood pressure occurs within the first few hours of stroke even without any treatment
  19. 19. When To Lower Blood pressure the hypertension is extreme (systolic blood pressure >220 mmHg or diastolic blood pressure >120 mmHg) ischemic coronary disease, heart failure, Aortic dissection Hypertensive encephalopathy Acute renal failure or pre-eclampsia/ Eclampsia
  20. 20.  When treatment is indicated, cautious lowering of blood pressure by approximately 15 percent during the first 24 hours after stroke onset is suggested  Systolic blood pressure > 185 and diastolic > 110 is a contraindication for thrombolysis
  21. 21. BLOOD GLUCOSE LEVELS Hyperglycemia may augment brain injury by several mechanisms including  increased tissue acidosis from anaerobic metabolism  free radical generation  increased blood brain barrier permeability.  CONCLUSION – evidence suggests that persistent hyperglycemia >140 mg/dl is associated with poor outcomes within the first 24 hrs of stroke ..  The American Heart Association/American Stroke Association guidelines recommend treatment with insulin for patients who have serum glucose concentrations >140 to 185 mg/dL (>7.8 to 10.3 mmol/L)
  22. 22.  HYPOGLYCEMIA- Hypoglycemia can cause focal neurologic deficits mimicking stroke, and severe hypoglycemia alone can cause neuronal injury  Check the blood sugar and rapidly correct low serum glucose  Normoglycemia is the desired goal while avoiding marked elevation of serum glucose.
  23. 23. Management of complications
  24. 24.  INTRAVENOUS THROMBOLYSIS — Results from the NINDS trial showed that intravenous alteplase (recombinant tissue-type plasminogen activator or tPA) improves functional outcome at three months, if given within 3 hours of symptom onset  The ECASS 3 clinical trial found that intravenous alteplase is beneficial when given up to 4.5 hours after stroke onset
  25. 25.  Despite recommendations, less than 1% of potentially eligible patients are currently being treated in India  Principle behind the time dependency of thrombolysis is that of penumbra – the salvageable tissue which decreases every minute after stroke
  26. 26. CCrainCONTRAINDICATIONS The following contraindications apply in general: •significant bleeding disorder at present or within the past 6 months, known haemorrhagic diathesis •patients receiving oral anticoagulants, .g. warfarin sodium (INR> 1.7) any history of central nervous system damage (i.e. neoplasm, aneurysm, intracranial or spinal surgery) •history or evidence or suspicion of intracranial haemorrhage including sub-arachnoid haemorrhage •severe uncontrolled arterial hypertension •major surgery or significant trauma in the past 15 days (this includes any trauma associated with the current acute myocardial infarction), recent trauma to head or cranium •prolonged or traumatic cardiopulmonary resuscitation (> 2 minutes), obstetrical delivery, within the past 10 days, recent puncture of a non-compressible blood-vessel (e.g. subclavian or jugular vein puncture) •severe hepatic dysfunction, including hepatic failure, cirrhosis, portal hypertension (oesophageal varices) and active hepatitis •bacterial endocarditis, pericarditis •acute pancreatitis •documented ulcerative gastro-intestinal disease during the last 3 months •arterial aneurysms, arterial/venous malformations •hypersensitivity to the active substance alteplase or to any of the excipients
  27. 27. In the indication acute ischaemic stroke the following contraindications apply in addition: •symptoms of ischaemic attack began more than 4.5 hours prior to infusion start or when time of symptom onset is unknown •symptoms of acute ischaemic stroke that were either rapidly improving or only minor before start of infusion •severe stroke as assessed clinically (e.g. NIHSS>25) and/or by appropriate imaging techniques •seizure at the onset of stroke •history of previous stroke or serious head-trauma within three months •a combination of previous stroke and diabetes mellitus •administration of heparin within 48 hours preceding the onset of stroke with an elevated activated partial thromboplastin time (aPTT) at presentation •platelet count of less than 100,000 / mm3 •systolic blood pressure > 185 or diastolic blood pressure > 110 mmHg, or aggressive management (IV medication) necessary to reduce blood pressure to these limits •blood glucose < 50 or > 400 mg/dl ACTILYSE is not indicated for the therapy of acute stroke in children and adolescents under 18 years or adults over 80 years of age.
  28. 28.  HEMORRHAGE IN CLINICAL PRACTICE —  In clinical trials of IV alteplase, the rates of symptomatic intracerebral hemorrhage were 5 to 6 percent  Early CT changes — Brain edema or mass effect on the pretreatment CT scan was one of two major variables associated with an increased risk of intracerebral hemorrhage in patients treated with IV alteplase  Stroke severity — In addition to CT changes, the severity of neurologic deficit as measured on the NIHSS score) was the second major variable associated with intracerebral hemorrhage
  29. 29. • Perform neurological assessments every 15 minutes during the infusion and every 30 minutes thereafter for the next 6 hours, then hourly until 24 hours after treatment. • If the patient develops severe headache, acute hypertension, nausea, vomiting, discontinue the infusion (if rtPA is being administered) and obtain an emergency CT scan.
  30. 30. INTRA ARTERIAL THROMBOLYSIS Intra-arterial thrombolysis —The dose of thrombolytic drugs can be limited to that needed for recanalization, since the procedure is done under direct visualization. Intra arterial thrombolysis is an option of selected patients who have a major stroke < 6 hrs duration due to occlusion of MCA and who are not candidates for intravenous thrombolysis Treatment requires the patient to be at an experienced stroke center with immediate excess to cerebral angiography
  31. 31.  Combined intravenous and intra-arterial thrombolysis — The rationale for combined thrombolytic therapy is to unite the advantages of each:  the wide availability of early rapid IV thrombolysis and  potentially higher recanalization rates and therefore better outcomes of IA thrombolysis.
  32. 32. Mechanical/Endovascular methods Endovascular methods — New catheter-based therapies are being developed for angioplasty, stenting, and mechanical clot disruption .Such approaches may decrease the risk of hemorrhage that is inherent with the use of thrombolytic drugs Mechanical clot disruption — Endovascular embolectomy and clot disruption is undergoing study for acute treatment of ischemic stroke They offer the possibility of faster recanalization, higher recanalization rates, reduced total thrombolytic dose, and ultimately improved outcome
  33. 33. MERCI Device Source: St. Petersburg Times, October 2003
  34. 34. Conclusion Contraindications — Early anticoagulation should be avoided when potential contraindications to anticoagulation are present, such as a large infarction It is recommended NOT using full-dose anticoagulation for treatment acute ischemic stroke because of limited efficacy an increased risk of bleeding complications.
  36. 36. CONCLUSION Early aspirin therapy (initial dose 325 mg, thereafter 150 to 325 mg/day) be given to patients with ischemic stroke. The development of secondary hemorrhagic transformation of an ischemic infarct (ie, scattered and punctate). does not preclude the early use of aspirin, INTRAVENOUS ANTIPLATELET AGENTSGP II b III A INHIBITORS –more research is needed to determine whether these agents have a role in stroke…
  38. 38. Volume expansion and hemodilution were tried but it does not reduce case fatality or improve functional outcome in survivors VASODILATORS IN STROKE- methyl xanthine derivatives like pentoxyphylline have been tried but they do not have any role in acute stroke
  40. 40. SURGICAL INTERVENTIONS  INDICATIONS — Carotid endarterectomy (CEA) is most commonly performed for symptomatic or asymptomatic high-grade (>60 or 70 percent) internal carotid artery stenosis  HOWEVER , emergency carotid endartectomy efficacy is not established
  43. 43. ETIOLOGY Hypertensive vasculopathy is the most common etiology of spontaneous ICH. Hemorrhagic infarction (including venous sinus thrombosis) Cerebral amyloid angiopathy mycotic aneurysm Brain tumor Bleeding disorders, anticoagulants, thrombolytic therapy Central nervous system (CNS) infection (eg, herpes simplex encephalitis) Vasculitis Drugs (cocaine, amphetamines) Phenylpropanolamine in appetite suppressants,
  44. 44. INTRACEREBRAL HEMORRHAGE PROGNOSIS Initial ICH volume and level of consciousness — The ICH volume on initial head CT scan and level of consciousness on admission may be particularly important prognostic indicators  Hematoma growth — Hematoma growth is also an independent predictor of mortality and poor outcome
  45. 45.  Intraventricular extension —Independent predictor of poor outcome in patients with spontaneous ICH  Preceding antithrombotic use —Preceding use of anticoagulants or antiplatelet agents might be expected to have larger initial hematoma volumes or greater hemorrhage enlargement  Early neurologic deterioration — Early neurologic deterioration within 48 hours after ICH is associated with a poor prognosis.
  46. 46.  ICH score — A simple six-point clinical grading scale called the ICH score has been devised to predict mortality after ICH  The ICH score is determined by adding the score from each component as follows:  Glasgow Coma Scale (GCS) score 3 to 4 (= 2 points); GCS 5 to     12 (= 1 point) and GCS 13 to 15 (= 0 points) ICH volume ≥30 cm3 (= 1 point), ICH volume <30 cm3 (= 0 points) Intraventricular extension of hemorrhage present (= 1 point); absent (= 0 points) Infratentorial origin yes (= 1 point); no (= 0 points) Age ≥80 (= 1 point); <80 (= 0 points)
  47. 47. TREATMENT GENERAL MANAGEMENT  Fever should be treated  Hyperglycemia current guidelines suggest insulin treatment for elevated serum glucose >140 to 185 mg/dL)
  48. 48.  Reversal of anticoagulation- Aggressive use of intravenous vitamin K, unactivated prothrombin complex concentrate (also called factor IX complex), and other factors may be necessary in patients who suffer an ICH while taking warfarin.  Intracranial pressure control Elevation of the head of the bed to 30 degrees, once hypovolemia is excluded Analgesia and sedation, particularly in unstable, intubated patients  — Monitoring and treatment of ICP should be considered for patients with GCS <8, those with clinical evidence of transtentorial herniation, or those with significant IVH or hydrocephalus
  49. 49. TREATMENT OF RAISED ICT Intravenous mannitol is the treatment of choice to lower ICP. It is administered as an initial bolus of 1 g/kg, followed by infusions of 0.25 to 0.5 g/kg every six hours. The goal of therapy is to achieve plasma hyperosmolality (300 to 310 mosmol/kg) while maintaining an adequate plasma volume.. Barbiturate anesthesia can be used if mannitol fails to lower ICP to an acceptable range. Barbiturate coma acts by reducing cerebral metabolism, which results in a lowering of cerebral blood flow and thus decreases ICP . Continuous electroencephalogram monitoring is suggested The ICP lowering effect of hyperventilation to a PaCO2 of 25 to 30 mmHg is dramatic and rapid. However, the effect only lasts for minutes to a few hours.
  50. 50. Neuromuscular blockade is sometimes employed to reduce ICP in patients who are not responsive to analgesia and sedation alone, as muscle activity can contribute to increased ICP by raising intrathoracic pressure, thereby reducing cerebral venous outflow Ventriculostomy is often used in the setting of obstructive hydrocephalus Ventriculostomy allows a means of both monitoring ICP and relieving hydrocephalus
  51. 51. BLOOD PRESSURE MANAGEMENT  Limited prospective data are available regarding blood pressure management in ICH.  In a randomized controlled trial (INTERACT) intensive blood pressure lowering treatment (target systolic blood pressure 140 mmHg) compared with traditional management (target systolic blood pressure 180 mmHg) was associated with a reduction in hematoma growth at 24 hours (14 versus 26 percent)
  52. 52. BLOOD PRESSURE REDUCTION  For patients with SBP >180 mmHg or MAP >130 mmHg and evidence or suspicion of elevated ICP, consider monitoring ICP and reducing blood pressure using intermittent or continuous intravenous medication to keep cerebral perfusion pressure in the range of 61 to 80 mmHg  For patients with SBP >180 mmHg or MAP >130 mmHg and no evidence or suspicion of elevated ICP, consider a modest reduction of blood pressure (eg, target MAP of 110 mmHg or target blood pressure of 160/90 mmHg) using intermittent or continuous intravenous medication, and clinically reexamine the patient every 15 minutes
  53. 53.  Seizure prophylaxis and treatment —  Appropriate intravenous antiepileptic drug (AED) treatment should be used to quickly control seizures for patients with ICH. Current guidelines suggest lorazepam or diazepam followed directly by intravenous fosphenytoin or phenytoin  Guidelines recommend against prophylactic use of AEDs
  55. 55. SURGICAL TREATMENT  Surgical removal of hemorrhage with cerebellar decompression should be performed for patients with cerebellar hemorrhages greater than 3 cm in diameter who are deteriorating, or who have brainstem compression and/or hydrocephalus due to ventricular obstruction  For patients with supratentorial ICH, current guidelines suggest consideration of standard craniotomy only for those who have lobar clots >30 mL within 1 cm of the surface..
  56. 56.  Resumption of antiplatelet therapy -Timing and dose — The AHA/ASA guidelines state that antiplatelets should be discontinued for at least one to two weeks  Resumption of anticoagulation — AHA/ASA guidelines conclude that intravenous heparin may be safer than oral anticoagulation
  57. 57. THANK YOU