Acute management of Stroke By Dr Sanjay jaiswal Neurologist sept2012

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Acute management of ischaemic stroke 2012

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  • Sudden: Sudden onset out of full health DD post MI, endocarditis, vasculitis, mets Focal: intoxication, vasculitis, encephalitis, hysteria, >24 hrs: TIA, Todd’s, migraine Presumed non-traumatic vascular origin: exclude head trauma, neck trauma, whiplash, systemic vascultitis, cardiac source of emboli AF, but also endocarditis, post MI, hypotension
  • Each year, 40,000 more women than men have strokes. Stroke or heart disease in parents younger than 60 years of age. Cardiac Disease – A fib, CHF, Cardiomyopathy, Valve disease, Cardiac procedures CCL
  • Homocysteine is an amino acid in the blood. Too much of it is related to a higher risk of coronary heart disease, stroke and peripheral vascular disease (fatty deposits in peripheral arteries). Evidence suggests that homocysteine may promote atherosclerosis (fatty deposits in blood vessels) by damaging the inner lining of arteries and promoting blood clots. However, a causal link hasn't been established. Folic acid and other B vitamins help break down homocysteine in the body.
  • ER Procedure: Differential Diagnosis In stroke patients, clinical features are usually sufficient to enable at least preliminary diagnosis. CT scanning is instrumental in documenting cerebral haemorrhage, neuroinfection or brain injury, but does not help to exclude possibilities such as syncope, partial epileptic seizure with Todd’s paresis, migraine attack with aura, hypoglycaemia, hysteria, intoxication, meningitis or multiple sclerosis. In this context, it is important to remain aware that confirmatory tests should supplement – rather than replace – conventional clinical skills. In practice, the most important distinction is between ischaemic stroke and intracranial haemorrhage. The clinical features of these conditions may overlap, but their treatment is markedly different. 1 Early distinction between the various subtypes of ischaemic stroke is also becoming important (i.e. lacunar vs large artery or cardioembolic stroke), as there is evidence that these may respond differently to different treatments. This is a situation in which neuroimaging techniques such as CT scanning can be invaluable, although clinical scoring systems based on the presence or absence of specific clinical features can also be strongly predictive. One such system – the Allen score – has been found to be 90% accurate in the identification of haemorrhage. 2–4 References 1. European Ad Hoc Consensus Group. European strategies for early intervention in stroke: a report of an Ad Hoc Consensus Group meeting. Cerebrovasc Dis 1996; 6: 315–24. 2. Allen CMC. Clinical diagnosis of the acute stroke syndrome. Q J Med 1984; 208: 515–23. 3. Sandercock PAG, Allen CMC, Corston RN et al. Clinical diagnosis of intracranial haemorrhage using Guy’s hospital score. Br Med J 1985; 291: 1675–7. 4. Celani MG, Righetti E, Migliacci R et al. Comparability and validity of two clinical scores in the early differential diagnosis of acute stroke. Br Med J 1994 ; 308: 1674–6 27
  • Aspirin should be given within 24 to 48 hours of stroke onset in most patients (grade A )
  • Acute management of Stroke By Dr Sanjay jaiswal Neurologist sept2012

    1. 1. Early Management of Ischemic Stroke DR SANJAY JAISWAL, MD,DM Member world stroke organization Consultant Neurologist Jaiswal Hospital and Neuro Institute Kota ,Rajasthan.
    2. 2. Reference Guidelines for the Early Management of Adults With Ischemic Stroke Stroke 2007;38;1655-1711 Acute ischemic stroke N Engl J Med 2007; 357:572-579, Aug 9, 2007
    3. 3. Brain Attack!  Acute stroke = ‘brain attack’  Every minute matters: ‘time is brain’  Combat therapeutic nihilism
    4. 4. Time is Brain…why?The typical patient loses 1.9 million neurons each minute in which stroke is untreated The ischaemic penumbra
    5. 5. WHO DEFINITION OF STROKEA NEUROLOGICAL DEFICIT OF Sudden onset With focal rather than global dysfunction In which, after adequate investigations, symptoms are presumed to be of non-traumatic vascular origin and last for >24 hours
    6. 6. New definition of TIA A brief episode of neurological dysfunction caused by focal brain or retinal ischaemia with clinical symptoms lasting less than one hour without evidence of infarction
    7. 7. Types of Stroke 85% 15 %Ischemic hemorrhagic
    8. 8. Left MCA Syndrome •Language loss (aphasia) •Right hemiparesis •Right hemisensory loss •Right visual field cut •Left gaze preference
    9. 9. Right MCA Syndrome •Left hemi-neglect visual,spatial, •Left hemiparesis •Left hemisensory loss •Left visual field cut •Neglect of deficits “anasgnosia”
    10. 10. Stroke is due to sudden vascular occlusion ACA MCA
    11. 11. Vascular occlusion causes stroke symptoms •50-70% of all stroke is due to embolism (cardiogenic and artery-to-artery) •80 % of acute strokes are due to MCA territory ischemia • Arterial occlusion is seen in 80-90% within 6-24° of symptom onset • Spontaneous recanalization seen in ~ 20% within 6 ° of symptoms
    12. 12. Stroke Risk Factors Non-modifiable AGE Gender -male Race – Blacks > Asians or Hispanics> Whites Family Hx. Coagulation Disorders Cardiac Disease
    13. 13. Stroke Risk Factors Modifiable Hypertension  Alcohol Abuse  Oral Contraceptives Diabetes mellitus  Pregnancy Hypercholesterolemia  Migraine Headaches Elevated LDL or Low  Obesity HDL  Sleep apnea Elevated homocystein  Carotid stenosis Smoking A combination of these risk Drug abuse factors will increase risk of stroke!
    14. 14. Many Causes of Stroke
    15. 15. THE BURDEN OF STROKE Anually more than 15 million people world wide suffer a stroke, 5.5 million die and 5 million are left with permanent disability. Stroke is 2nd most common cause of death(9.7%). Incidence of stroke is on the increase in India and other developing countries. More than 80% of stroke occurs in underdeveloped and developing countries. Cruide annual incidence rate for first ever stroke (FES) is 145 per 100,000 Persons.
    16. 16.  Case fatality rate at 28 days after FES was 29.8%.Of the surviving patients 38.5% had moderate to severe disability. Hypertension (BP>140/90 alone or in various combination) was present in 82.8% cases. (dalal et al, Mumbai stroke registry,2005- 2006). WHO estimated that in 1990 ,out of a total 9.4 million deaths in India , 619,000 deaths were due to stroke. This gives stroke mortality rate of 73 per 100,000 population. 1880 people die every day in India due to stroke. In 1990 the estimated no of death due to stroke were 22 times that due to malaria,1.4 times that due to tuberculosis,4 times that due to RHD, and almost equal to IHD. Stroke mortality rate is declining in USA and other developed countries it is likely to increase in India.
    17. 17. Stroke is a treatable condition. IV tPA is approved for use within 3 hours ( 4.5 hours) . (NINDS) Intra-arterial therapy has proven to be safe and effective within 6 hours (PROACT II) Combined IV/IA may be more effective than IV t-PA (Interventional Management of Stroke -IMS) Mechanical and laser catheter technologies are showing great promise (Angio-Jet)
    18. 18. Stroke: The Challenge Only 1-3% of all stroke victims receive treatment with tPA in the US . 25% of Acute MI patients receive treatment (lytics or PTCA) in the US . Mean time to presentation  AMI: 3hrs  Acute Stroke: 4-10hrs.
    19. 19. Reasons for lack of treatment:1. Patient’s inability to recognize stroke symptoms  40% of stroke patients can’t name a single sign or symptom of stroke or stroke risk factor.  75% of stroke patients misinterpret their symptoms  86% of patients believe that their symptoms aren’t serious enough to seek urgent care2. Physician’s lack of experience with stroke treatment and therefore reluctance to “risk” treatment3. Lack of organized delivery of care in many medical centers throughout the country.
    20. 20. Current Status of Specific Treatment for Acute Ischemic StrokeYes 1. Tissue plasminogen activator within 3-4.5 hrs. 2. Aspirin within 48 hrs. 3. Management in SCUMay Be 1. NeuroprotectionNo ? 1. Heparin, Heparinoids 2. Hemodilution 3. Steroids
    21. 21. Acute Stroke Treatments % patients Prevention Prevention that can death/dependency per death/dependency per benefit 100 treated 100 admitted Stroke Unit 90% 5 4.5 10% Thrombolysis ischaemic 12 1 0-3hr strokes 65% Aspirin ischaemic 1 0.5 0-48hr strokes 0.5%Hemicraniectomy Ischaemic 22 0.1 0-48hr strokes Slide by Prof G Ford, presented at UKCRN 21.11.2007 ,adapted from Gilligan et al 2005
    22. 22. Pre of hospital recognition of stoke. FAST Facial Weakness  Stroke Association campaign to  Can person smile raise awareness  Has mouth dropped  Practice staff should be trained Arm Weakness to inform doctor immediately if  Can person raise both arms patient calls with symptoms Speech problems identifiable  Can person speak clearly and understand what you say  Ambulance crews now trained to use FAST score to prioritise Test all three symptoms Calls and dispatch.  Act FAST call 108 ambulance.
    23. 23. Section 1 Slide30Onset to Entry (By referral method) 70 60 50 999 Pt Numbers 40 GP Other 30 GP+999 20 10 0 0-<1 1-<2 2-<3 3-<4 4-<5 5-<6 6-<9 9-<12 12-<24 >=24 HoursASIST data 1999
    24. 24. Pre Hospital care Ambulance services ,health care professionals and general public should receive education concerning the importance of early recognition of stroke, emphasing stroke is a medical emergency. Stroke patients should be given a high priority by ambulance service. Ambulance services should be trained to identify stroke by various tools and protocols. Ambulance services should transfer suspected patients to hospital with stoke unit care.
    25. 25. EMS response to 108 call:WILL QUESTION: Time of onset of stroke symptoms. Determine nature of neurological symptoms (F.A.S.T.). NIH Stroke Scale or Glasgow Coma Scale (language/motor response/eye movement). Hx: recent illness, surgery or trauma. Recent use of medication/illicit drugs. Notify receiving hospital that patient appears to be an acute stroke and gives time window.
    26. 26. Guidelines for EMS management of patients with suspected strokeRecommended Not recommended Manage ABCs  Dextrose containg fluid in Cardiac monitoring non hypoglycemic patients Intravenous access  Hypotension/excessive BP O2(if spo2,92%) reduction  Excess IV fluids Assess for hypoglycemia NBM Alert receiving ED Rapid transfer to closest stroke centre
    27. 27. Stroke units: State of the ArtAdmission to a unit that is dedicated tothe care of stroke patients helps toreduce mortality and morbidity.
    28. 28. Stroke: Differential Diagnosis Syncope  Subarachnoid Partial epileptic seizure haemorrhage with Todd’s paresis  Neuroinfection Migraine attack (aura)  Neoplasm Hypoglycaemia  Brain injury Hysteria  Multiple sclerosis Intoxication  Peripheral vertigo
    29. 29. PHYSICAL EXAM GPE,ABCs, Pulse Oximetry,temp. Carotid Bruits, JVP, Irregular Rhythm Head and Neck, Chest, Abdomen Skin –Jaundice, Purpura, Petechia
    30. 30. Early diagnostic testsALL PATIENTS SELECTED PATIENTS Non contrast brain CT or  LFT brain MRI  Toxicology screen Blood glucose  Blood alcohol level RFT,S. electrolytes  Pregnancy test ECG  ABG  Chest radiography Markers of cardiac ischemia  LP-if SAH is suspected and CT CBC, Plat count* is negative PT,INR,*APTT*  EEG –if seizures are suspected. O2 Saturation
    31. 31. EARLY DIAGNOSIS: NON CONTRAST CT SCAN OF BRAIN Initial imaging modality in hyper ac stroke Widely available, quick, easy to perform Accurately identifies ICH,SAH EARLY SIGNS OF CEREBRAL ISCHAEMIA Hyper dense MCA artery sign Hyper dense dot sign Hypo density of insular ribbon Hypoensity of basal ganglia loss of grey white matter differentiation in cortical ribbon sulcal effacement EARLY SIGNS ARE ASSOCIATED WITH POORER OUTCOMES
    32. 32. Early Hypodensity Hypodensity
    33. 33. Hyperdense middle cerebral artery Hyperdense middle cerebral artery
    34. 34. BRAIN IMAGING (CONTD)MULTI MODEL CT (A) Perfusion CT- more sensitive and specific to detect ischaemia. (b) CT Angio-for intra and extra cranial vasculatureMULTIMODEL MRI T1,T2,PD DWI-Early visualization of ischaemic regions within minutes of stroke. PWI,MRA,FLAIR,MRI MORE SENSITIVE THAN CT(26%CT VS 83 %MRI) FOR AC ISCHAEMIC STROKE VASCULAR IMAGING TCD USG,CAROTID DUPLEX SONO,CATHETER ANGIO.
    35. 35. Multimodal CT Imaging CT PCT CTATissue Status Perfusion Status Vessel StatusBioenergetic Hemodynamic Occlusions orCompromise Compromise Stenoses
    36. 36. Acute Stroke: CT vs. MRI
    37. 37. Multimodal Diffusion-Perfusion MRI DWI PWI MRATissue Status Perfusion Status Vessel StatusBioenergetic Hemodynamic Occlusions orCompromise Compromise Stenoses
    38. 38. Arterial Hypertension Management of hypertension is controversial. Data are inconclusive,or conflicing. Elevations of BP >160 mm of hg are detected in >60 % patients. Many patients have spontaneous decline in BP during first 24 hours onset of stroke. Both elevated and low bp are associated with poor prognosis.
    39. 39.  A reasonable goal is to lower BP by 15% during first 24 hours after onset of stroke. It is generally agreed that antihypertensive medicines can be restricted 24 hours after the stroke, in patients who have pre existing hypertension and are neurologically stable.DO NOT USE SUB LINGUAL NIFEDIPINE.IT
    40. 40. Treatment of Arterial Hypertension (for patients who are not candidates for r TPA) The consensus is that antihypertensive agents should be withheld unless the diastolic blood pressure is >120 mm Hg or unless the systolic blood pressure is >220 mm Hg (level V)
    41. 41. ARTERIAL HYPOTENSION SBP<100 and DBP <70 is associated with higher mobidity and mortality. Causes of hypotension should be sought. Potential causes are aortic dissection, volume depletion, blood loss, decreased cardiac output sec to MI or cardiac arrhythmia. hypovolemia should be corrected with normal saline.
    42. 42. T-PA for Acute Ischemic Stroke NEJM 95:333,1581-87  624 patients randomized  3 hour window  at three month. 30% less likely to have minimal or no disability  6.4% risk of hemorrhage  No change in mortality at 6 mos
    43. 43. Cerebral infarct <3hrs Onset Infarct Ischaemic penumbra
    44. 44. Cerebral infarct 6hrs Infarct Ischaemic penumbra
    45. 45. Cerebral infarct 24hrs Infarct Ischaemic penumbra
    46. 46. Intravenous thrombolysis The US FDA approved the use of r tpa in 1996 on the basis of the results of the NINDS r TPA stroke Study. Patients treated with tpa were 30 % more likely to have minimal or no disability at 3 months compared with placebo treated patients. Treatment with tpa resulted in 11 to 13 % absolute increase in the number of patients with excellent outcomes. Mortality rate at 3 months was 17 % in tpa group and 21 % in placebo treated group. Symptomatic intracerebral haemorrhage occurred in 6.4% of pts receiving tpa vs 0.6% of the palcebo group.
    47. 47. CRITERIA FOR THROMBOLYSIS WITH rTPAINCLUSION CRITERIA Clinical signs and symptoms consistent with ischaenic stroke. MEASURABLE NEUROLOGIC DEFICIT NEUROLOGICAL SIGNS SHOULD NOT BE CLEARING SPONTANEOUSLY. Neurological signs should not be minor or isolated. Onset of symptoms <3 hour before beginning treatment Caution should be exercised in treating a patient with a major deficit. Symptoms of stroke should not be s/o SAH. No head trauma or prior stroke in previous 3 months. No MI in previous 3 months. No GI OR urinary tract haemorrhage in previous 21 days.
    48. 48. Cont.. No major surgery in previous 14 days. No arterial puncture at a noncompressible site in previous 7 days. NO H/O previous intra cranial haemorrhage. Systolic BP<185 and diastolic <110 No evidence of active bleeding or ac trauma on examn Not taking oral anticoagulant or if being taken INR <1.7 If receiving HEPARIN in previous 48 hours A PTT must be normal range. Platelet count <1 lac mm3 Blood glucose >50 mg % No seizure with postictal residual neurol impairements. CT does not show a multilobar infarction (hypodensity >1/3 cerebral hemisphere) The patient or family understands the potential risks and benefits of treatment.
    49. 49. New England Journal, 1995 NINDS tPA Stroke Trial 30 Hemorrhage30 p < .05 2020 31 9 20 20 1010 8 0 0 1 tPA Placebo tPA Placebo NIHSS Excellent Total Death Recovery (%) Rate (%)
    50. 50. IV administration of tpa. Infuse 0.9mg/kg(max 90 mg ) over 60 mnts with 10 % of the dose given as bolus over 1 mnt. Admit pt in neuro ICU or stroke unit. Perform neurological assessment every 15 mnts during the infusion and every 30 mnts thereafter for next 6 hours then hourly until 24 hours after treatment. If pt develop severe head ache,ac HTN, nausea,or vomitting discontinue infusion and obtain emergency CT scan.
    51. 51.  Besides bleeding complications r tpa have potential side effect of angioedema that may cause partial air way obstruction. A patient with seizure at the time of onset of stroke may be eligible for tpa if physician is convinced that residual impairements are secondary to stroke not a postictal phenomenon. IV streptokinase is not recommended . IV ancrod, tenecteplase,reteplase,desmoteplase,urokinase outside the setting of clinical trial is not recommended
    52. 52. Time is Brain“The typical patient loses 1.9 million neurons each minute in which stroke is untreated” 4.0 Upper 95% CI favourable Outcome 3.5 Mean 3.0 Lower 95% CI 2.5Odds Ratio 2.0 1.5 (corrected; 95% CI) 1.0 NNT: NNT: NNT: NNT: 0.5 3.5* 7* 9* 11* (11)** (13)** (>30)** 0.0 60 90 120 150 180 210 240 270 300 330 360 Symptom-to-needle time in minutes * NNT at absolute point of time ** NNT for each 90 min interval Slide by Prof G Ford, presented at UKCRN 21.11.2007 based on Saver, Stroke 2006
    53. 53. Time is brain: benefit from rt-PA declines with increasing delay from onset to treatment time Benefit Upper and lower 95% confidence limits Line of no effect HarmIST-3 protocol 3 hours 6 hours
    54. 54. rt-PA for stroke per million popn Thrombolysis in Europe 60 Finland Austria 50 Sweden Norway 40 Belgium Spain Germany 30 Netherlands Denmark 20 Italy UK 10 Greece France Portugal 0 Slide donated by P. Sandercock, IST-3 trialists meeting, Brussels 2006
    55. 55. Intra arterial Thrombolysis PROACT II  Intra arterial Prourokinase  6 Hour time window  Relative risk reduction of 15% in functional outcome  No difference in mortality  Procedural complication 9%  Early Intra cerebral haemorrhage 10%  INTRA ARTERIAL THROMBOLYS IS REASONABLE IN PATIENTS WHO HAVE C/I TO USE OF IV TPA LIKE RECENT SURGERY.
    56. 56. Guidelines for Anticoagulant TherapyUrgent administration of anticoagulants has not yet beenassociated with lessening the risk of early recurrent stroke orimproving outcomes. Because it can increase the risk of brainhemorrhage, routine use cannot be recommended. American Heart Association, 2003
    57. 57. Guidelines for Anticoagulant TherapyAnticoagulants are not recommended for any subgroupof patients with acute stroke based on any presumedmechanism or location (e.g., cardioembolic, largevessel atherosclerotic, vertebrobasilar, or “progressing”stroke) because data are insufficient.American Academy of Neurology / AHA, 2003
    58. 58. Acute Treatment with Antiplatelet Agents Aspirin (initial dose is 325 mg) should be given within 24 to 48 hours of stroke onset in most patients (Class 1, level A). The administration of aspirin as an adjunctive therapy, within 24 hours of the use of thrombolytic agents, is not recommended (Class 3,level A). Aspirin should not be used as a substitute for other acute interventions, especially intravenous administration of rtPA, for the treatment of acute ischemic stroke (Class 3,level B). No recommendation can be made about the urgent administration of other antiplatelet aggregating agents alone or in combination with aspirin (Class 3,level C). Outside the setting of clinical trials IV administration of antiplatelet agents that inhibit the glycoprotein 2b/3a ptor is not recommended. (Class 3,level B).
    59. 59. Benefit of Early Aspirin Treatment in Acute Ischemic Stroke 9 patients benefit per 1000 treated (p<0.001) 2000 Aspirin, n=20,207 Control, n=20,190 1843 1662 1500 1327 1231 1000 636 496 500 205 168 0 Recurrent Hemorrhagic Death Death or Nonfatal Ischemic Stroke Stroke Stroke Combined Data from IST, CAST, MAST-I
    60. 60. Hemodilution,Vasodialators,and induced hypertension Hemodilution with or without venesection and volume expansion is not recommended for treatment of ac ischaemic stroke.(Class 3,level A) Vasodialators like pentoxifyline is not recommended for treatment of ac stroke.(Class 3 ,level A) Drug induced hypertension outside the setting of clinical trials is not recommended .)
    61. 61. MERCI TRIAL Anterior circ strokes only Treatment <8 hours 151 patients entered
    62. 62. MERCI RESULTS Recanalization in 46%  Historical 18% Complication rate 7% (SAH, device fx, embolization) With recanalization, good outcome (46% vs. 10%) and mortality improved (32% vs. 54%) ICH rate 7.8%
    63. 63. Thrombolysis Augmentation Ultrasound  With or without micro-bubbles  Micro-bubbles containing TPA Combination with G2B3A inhibitors
    64. 64. Neuroprotective agents At present no neuroprotective agent is found to be effective in improving outcomes after stroke,and therefore none currently can be recommended(class 3,level A)
    65. 65. General Ac treatment after Hospitalization 25 %of patients may have neurological worsening during first 24-48 hours. The use of stroke unit is recommended to improve general management. Early mobilization of less severely affected patients is recommended. Assessment of swallowing before staring eating or drinking is recommended. Patients with suspected pneumonia,UTI should be treated with antibiotics.
    66. 66.  Sub cut anticoagulants are recommended for treatment of immobilized patients to prevent DVT.Ideal timing for starting these medications is not known. The use of intermittent external compression devices is recommended for treatment of patients who can not receive antcoagulants.(Class 2a ,level B) Pulmonary embolism accounts for 10% of deaths after stroke,and complicaton may be detected in 1%of patients who have had a stroke.
    67. 67.  Patients who cannot take food and fluids orally should receive nasogastric,nasodudenal or PEG feedings to maintain hydration and nutrition.The timing of PEG is uncertain. Nutritional supplements are not needed. Prophylactic administration antibiotic is not recommended. If possible the placement of indwelling bladder catheters should be avoided because of associated risk of UTI.(class3 ,level C)
    68. 68. Treatment of ac neurological ComplicationsBrain EdemaDevelopment of brain edema is gradual and occurs most frequently 3- 5 days after stroke.Brain edema is most frequent neurological cause of death in patients with stroke.Early CTscan hypodensity,defined as <12 hours after onset ,of >50 %of the MCA territory and presence of hyperdense MCA signs are independent predictors of neurological deterioration.Large hypodensity>2/3 of MCA terrority on CT and large hypoperfusion on CT perfusion maps predicted development of malignant MCA infarct.
    69. 69. Management of brain edema and increased ICP Modest fluid restriction Avoidence of hypo osmolar fluids like GDW. Control of fever,hypoxia,hypercapnia. Elevation of head end of bed by 30 degree. Hyperventilation to a partial co2 pressure of 28- 30 mm of hg.
    70. 70.  Administration of mannitol 0.25-0.50gm /kg IV over 30 mnts every 6 hours. Diuresis(furosemide 40 mg IV). Drainage of CSF. Resection of infarcted tissue./decompressive surgery. Antihypertensive agents particularly those causing cerebral vasodilation should be avoided.
    71. 71. Contd…… Patients with ac hydrocephalus in ischaemic stroke most commonly affecting cerebellum can be treated with placement of a ventricular drain.(class 1 level B) Decompressive craniectomy is indicated for treatment of large cerebellar infarcts in patients with clinical deterioration and evidence of early brain stem compression or hydrocephalus.This is potentially life saving measure and clinical recovery may be very good.(class 1 ,level B) Decompressive surgery for malignant brain edema may be life saving in selected patients with complete MCA infarction who are significant risk for developing trans tentorial herniation.Timing of surgery is poorly defined,with some opting for early surgery (in 24 hours) Suboccipital craniotomy is the treatment to relieve both hydrocephalus and brain stem compression caused by large cerebellar infarctions.
    72. 72.  No specific recommendation is made for treatment of patients with asymptomatic haemorrhagic transformation after ischaemic stroke. Corticosteroids are not recommended for treatment of cerebral edema and increased ICP(class 3,level A) Prophylactic administration of anticonvulsants in patients of stroke who have not had seizures is not recommended(class 3 ,level C)
    73. 73. Thank you ! ! !

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