latest guidelines in management of stroke

1. STROKE
DR HARSIMRAN WALIA
MICU

2. STROKE
• Third leading cause of death globally
• Incidence in INDIA-73/100000
• Likely to increase with risk factors- aging,
smoking, dietary habits
• DEFINED AS FOCAL NEUROLOGICAL DEFICIT
OF PRESUMED VASCULAR ONSET LASTING 24
HRS OR LONGER AS OPPOSED TO TIA(<24hrs)

3. Causes of stroke
• 87% strokes – Ischemic
• ETIOLOGY- 29% Cardioembolic (AF)
16% Large vessel stenosis
16% Lacunar
3% Migraine, malignancy,
hypercoagulable states
• 13% of them- ICH OR SAH
Petty GW, Brown RDJ, Whisnant JP et al (1999) Ischemic stroke subtypes: a
population-based study of incidence and risk factors. Stroke 30:2513–2516

4. OXFORD/BAMFORD CLASSIFICATION
• TOTAL ANTERIOR CIRCULATION(TACS)
• PARTIAL ANTERIOR CIRCULATION(PACS)
• POSTERIOR CIRCULATION(POCS)
• LACUNAR (LACS)
Bamford J, Sandercock P, Dennis M et al (1991) Classification and natural history of
clinically identifiable subtypes of cerebral infarction. Lancet 337:1521–1526

5. ARTERIAL
SUPPLY OF
BRAIN
CIRCLE OF
WILLIS

6. SYMPTOMS
CAROTID DISTRIBUTION
• HEMIPARESIS
• HEMISENSORY LOSS
• APHASIA
• RETINAL ISCHEMIA
• NEGLECT
• HOMONYMOUS HEMIANOPIA
VERTEBROBASILAR DISTRIBUTION
• MOTOR DYSFUNCTION
• SENSORY LOSS
• GAIT ATAXIA
• HOMONYMOUS HEMIANOPIA
• DIPLOPIA,DYSPHAGIA,DYSARTHRIA,
VERTIGO,HICCUPS- NONE OF THESE
ALONE CLASSIFY AS STROKE
• COMBINATIONS OF ABOVE

7. Clinical mimics of STROKE
• PSYCHOGENIC
• SEIZURES
• HYPOGLYCEMIA
• MIGRAINE
• HYPERTENSIVE ENCEPHALOPATHY
• WERNICK’S ENCEPHALOPATHY
• CNS ABSCESS
• CNS TUMOUR
• DRUG TOXICITY

8. Stroke chain of survival
• Detection - early recognition of s/s
• Dispatch - activation of 9-1-1,EMS dispatch
• Delivery - triage and transport
• Door - ED triage to high acuity area
• Data - ED evaluation, labs , imaging
• Decision - appropriate t/t, discussion with family
• Drug - appropriate drugs or other interventions
• Disposition- timely admission to stroke unit/ICU/Transf

9. ED BASED CARE
• DOOR TO PHYSICIAN ≤10 minutes
• DOOR TO STROKE TEAM ≤15 minutes
• DOOR TO CT INITIATION ≤25 minutes
• DOOR TO CT INTERPRETATION ≤45 minutes
• DOOR TO DRUG ≤60 minutes
• DOOR TO STROKE UNIT ADM ≤3 hours

10. Management based on
AHA/ASA/ESO STROKE guidelines

11. • FOUR INTERVENTIONS IN AIS SUPPORTED BY
CLASS I EVIDENCE:
1. Care on a stroke unit
2. Intravenous tissue plasminogen activator within
4.5 h of stroke onset
3. Aspirin within 48 h of stroke onset
4. Decompressive craniectomy for Supratentorial
malignant hemispheric cerebral infarction

12. MANAGEMENT
• Airway
• Breathing
• Circulation
• Assess neurological deficits
• Exclude stroke mimics

13. Patient history
• Time of symptom onset
• Defined as when the patient was at his or her
previous baseline or symptom-free state.
• For patients unable to provide this information or
who awaken with stroke symptoms, the time of
onset is defined as when the patient was last awake
and symptom-free or known to be “normal”
• Risk factors for arteriosclerosis and cardiac disease
• History of drug abuse, migraine, seizure, infection, trauma, or
pregnancy
• Historical data related to eligibility for therapeutic
interventions in acute ischemic stroke

14. EXAMINATION
• VITAL SIGNS- HR,BP,TEMP,O2 SATURATION
• Detailed physical examination head to toe
• Head and face- signs of trauma or seizure activity.
• Auscultation of the neck may reveal carotid bruits
• Signs of congestive heart failure.
• Chest exam - cardiac murmurs, arrhythmias, and
rales
• Skin -stigmata of coagulopathies, platelet
disorders, signs of trauma, or embolic lesions
(Janeway lesions, Osler nodes)

15. NEUROLOGICAL ASSESSMENT

16. CINCINNATI PREHOSPITAL STROKE
SCALE(CPSS)
• FACIAL DRIFT
• ARM LIFT
• ABNORMAL SPEECH

17. National
Institutes
of Health
Stroke
Scale

19. Score grading
SCORE STROKE SEVERITY
0 NO STROKE
1-4 MILD STROKE
5-15 MODERATE STROKE
16-20 MODERATE TO SEVERE
21-42 SEVERE STROKE

21. Immediate evaluation
ALL PATIENTS
• Noncontrast brain CT or
brain MRI
• Blood glucose
• Oxygen saturation
• Serum electrolytes
• Renal function tests
• Complete blood count
• Platelet count
• Markers of cardiac ischemia
• Prothrombin time/INR
• APTT
• ECG
SELECTED PATIENTS
• TT and/or ECT if it is suspected the
patient is taking direct thrombin
inhibitors or direct factor Xa
inhibitors
• Hepatic function tests
• Toxicology screen
• Blood alcohol level
• Pregnancy test
• Arterial blood gas tests (if hypoxia is
suspected)
• CXR (if lung disease is suspected)
• Lumbar puncture (if SAH is
suspected and CT negative for
blood
• EEG(if seizures are suspected)

22. Early Diagnosis - Imaging
• NCCT - most common modality used in acute
ischemic stroke imaging.
• NCCT excludes parenchymal hemorrhage
• NCCT may demonstrate subtle visible
parenchymal damage within 3 hours.

23. EARLY SIGNS ON CT
• Loss of gray-white differentiation
• Lenticular obscuration-loss of distinction
among the nuclei of the basal ganglia
• Insular ribbon sign-blending of the densities of
the cortex and underlying white matter in the
insula and over the convexities -Cortical
ribbon sign
• Sulcal effacement

25. CT ANGIOGRAPHY
• CT angio head and neck to assess intracranial and cervical
circulation for stenoses and occlusions
• Useful
1. patients who present just outside the treatment window for I/V
thrombolysis but may be candidates for intraarterial clot lysis
(provides information as to the location and extent of the clot)
2.patients who cannot undergo MRI
• Perfusion CT measures absolute cerebral blood flow to help
identify the degree of reversibility of brain injury, but not all
vascular territories can be imaged completely
• Diff. between regions of brain infarction and ischemic penumbra
• A complete CT examination including NCCT, CT angio &perfusion
CT can be performed in approximately 10 minutes

26. MRI BRAIN
• Standard MRI sequences (T1 weighted, T2 weighted,
fluid- attenuated inversion recovery [FLAIR]) are
relatively insensitive
• Diffusion-weighted imaging (DWI) most sensitive(88%
to 100%) and specific(95% to 100%) for detecting
infarcted regions, even at very early time points, within
minutes of symptom onset
• DWI allows identification of the lesion size, site, and
age
• DWI can detect relatively small cortical lesions and
small deep or subcortical lesions, including those in the
brain stem or cerebellum, areas often poorly or not
visualized with standard MRI sequences and CT scan

27. • MR angiography evaluates the blood vessels
of the brain and neck
• MRI perfusion-weighted imaging (PWI)
measures relative blood flow in the brain
• Perfusion maps may take 5 to 40 minutes of
postprocessing time
• The use of PWI and DWI may identify patients
who would benefit from recanalization
therapy outside the established 3-hour time
window for intravenous tPA

29. REPERFUSION THERAPY
• Intention of reperfusion therapy is to restore
impaired blood flow to the ischemic penumbra
before irreversible neuronal death occurs.
• Use of intravenous rt-PA as soon as possible but
within 4.5 h of stroke onset, following exclusion
of a hemorrhagic stroke by NCCT
• Intraarterial thrombolysis can be done within 6 h
and mechanical embolectomy within 8 h of
symptom onset in those who are not candidates
for rt-PA or who fail to improve after full rt-PA
therapy

30. I/V Thrombolysis
• NINDS rtPA STROKE study- 1996
• Two parts- part 1 – rate of neurogical recovery
at 24 hrs- no sig diff observed
• Part 2 – rate of complete recovery at 90 days
and the results were significant
• ECASS, ECASSII , ATLANTIS- No benefit
• Diff between NINDS AND these studies was
time of intervention and dose used

31. CRITERIA(0-3hrs)
INCLUSION CRITERIA
• Ischemic stroke with clearly defined time of onset
• Onset of symptoms<3hrs before start of t/t
• Neurologic deficit measurable using the NIH
stroke scale
• Age >18yrs
• CT scan of the brain without evidence of ICH

32. Exclusion criteria(Absolute C/I)
• Head trauma or prior stroke within past 3 mths
• Symptoms s/o SAH
• Prior H/O Intracranial hemorrhage
• BP>185/110 not responding to antihypertensive t/t
• Arterial puncture at non compressible site within last 7 days
• Evidence of active internal bleeding
• Intracranial neoplasm, aneurysm, AV malformation
• Recent intracranial/intraspinal surgery
• Blood glucose <50 mg/dl
• CT – MULTILOBAR infarction(>1/3rd)
• Acute bleeding diathesis
plat count<100000
Heparin received within 48hrs- Elevated APTT
Current use of anticoagulant with INR>1.7
Current use of DTI or Direct factor Xa inhibitors with elevated
tests

33. Relative exclusion criteria
• Only minor or rapidly improving stroke symptoms
• Pregnancy
• Seizure at onset with postictal residual
neurological impairments
• Major surgery or serious trauma within previous
14 days
• GI or Urinary tract hemorrhage within previous
21 days
• Acute MI within previous 3 months

34. CRITERIA FOR EXTENDED PERIOD
(UPTO4.5HRS)
Inclusion criteria
• Age 18-80yrs
• Diagnosis of ischemic stroke causing measurable
neurological deficit(sym for atleast 30 mins)
• Onset within3-4.5hrs
Relative exclusion criteria
• Age>80yrs
• Severe stroke(NIHSS>25)
• Taking anticoagulant regardless of INR
• H/O both DM and prior ischemic stroke

35. • FDA approved dose of rtPA-0.9mg/kg(max 90mg)
• Bolus of 10%dose over 1 min with rest over 60 mins
• Close monitoring of patients for first 24 hrs
• BP every 15 mins for first 2 hrs, every 30 mins for next 6hrs
and then every hour for 16hrs
• Should be maintained below 185/110mmHg
• Neurological assessment using NIHSS – If change noted
stop infusion and do CT SCAN .
• Arterial punctures, nasogastric tubes, and catheterization
avoided in order to minimize the risk of bleeding.
• Subjects who have been on antiplatelet agents before their
event may receive t-PA
• NO Anticoagulant/antiplatelet for first 24 hrs
• CT at 24hrs –no hemorrhage- start antithrombotic

36. ENDOVASCULAR THERAPY
• INTRA ARTERIAL THROMBOLYSIS
• MECHANICAL CLOT EXTRACTION
• CAROTID ENDARTERECTOMY
• CAROTID ANGIOPLASTY/STENTING

37. INTRA ARTERIAL THROMBOLYSIS
• Direct administration of intra-arterial thrombolytic
agents into the clot –
• ADV- lower tPA dose and a decreased risk of
systemic hemorrhagic complications.
• DISADV- time and expertise required for
catheterization.

38. Inclusion criteria
• Patient must be between 18 and 85 years of age
• National Institutes of Health stroke scale score between 11 and 30
• Angiographic complete occlusion (TIMI 0) or penetration with
minimal perfusion (TIMI 1) of the apparent symptom-related M1 or
M2 segment of the MCA or of the basilar artery
• Diagnosis of ischemic stroke causing measurable neurological deficit
characterized by the sudden onset of acute focal neurologic deficit
presumed to be due to cerebral ischemia after exclusion of
hemorrhage by CT scan.
• Onset of symptoms within 6 hours of IA t-PA administration.
(Consider if patient presents within 4.5 hours of stroke.) In event of
basilar thrombosis, the time window is 12 hours.

39. Mechanical clot disruption/extraction
• Considered as both primary perfusion therapy
and in conjunction with pharmacological
fibrinolysis for recanalization
• 4 devices have FDA approval
1. MERCI RETRIEVAL SYSTEM(2004)
2. THE PENUMBRA SYSTEM(2007)
3. SOLITAIRE FLOW RESTORATION DEVICE(2012)
4. TREVO RETREIVER(2012)

40. MECHANICAL THROMBOLYSIS
• Patients who are ineligible for or who failed I/V
rtPA treatment
• The Mechanical Embolus Removal in Cerebral
Ischemia (MERCI) retrieval device has been
studied most extensively (FDA approved)
• The Multi-MERCI trial tested a newer device (L5)
and allowed pretreatment with intravenous tPA
• Further studies of the MERCI device are
forthcoming in the MR- Rescue and the IMS III
trials.

43. STUDY DESIGN
• Phase 3 multicentre clinical trial
• randomized clinical group assignment
• open label treatment
• blinded end point evaluation

45. MR CLEAN STUDY CONCLUSION
• In patients with acute ischemic stroke caused by a
large arterial occlusion of anterior circulation,
intra arterial treatment within six hours were
effective and safe
• IA treatment leads to a clinically significant
increase in the functional independence in daily
life by 3 months, without any increase in
mortality
• Triggered stoppage of mutilpe other trials:
ESCAPE, SWIFT, PRIME, EXTEND1A and REVASCAT

51. Management in ICU
• Airway and ventilation management
• Hemodynamic and fluid optimization
• Fever and Glycemic control
• Anticoagulation, Antiplatelet and
thromboprophylaxis therapy
• Control of seizures
• Surgical interventions for malignant middle
cerebral artery and cerebellar infarction

52. Airway and Ventilation
• Causes of hypoxemia following stroke
Respiratory infections
Aspiration
ARDS
Pulmonary embolus
Pulmonary edema (neurogenic or cardiogenic)
Respiratory muscle weakness
• All patients should undergo swallow assessment on admission
• Continuous monitoring of oxygenation with pulse oximetry
• Oxygen supplementation reserved for those with SpO2 <94 %.
• Regular ABG monitoring - to maintain normocapnea-target PaCO2
35–45 mmHg (higher in those with COPD and CO2 retention).

53. INDICATIONS FOR INTUBATION AND MECHANICAL VENTILATION
• Decreased conscious level (GCS <8)
• evidence of brainstem dysfunction
• To prevent aspiration pneumonia
• Adjuvant therapy for intracranial hypertension or significant
cerebral edema
Acute respiratory failure,
• Generalized tonic–clonic seizures or status epilepticus
If endotracheal intubation required-RAPID SEQUENCE
INTUBATION
• Short-acting sedatives should be used
• Minimise hemodynamic changes
• Tracheostomy should be considered after 1 week of
mechanical ventilation if a reasonable outcome is predicted

54. Hemodynamics and fluid management
• 80 % - hypertensive at presentation (chronic hypertension,
stress, raised ICP or neuroendocrine response)
• Severe hypertension contributes to cardiorespiratory
complications and promotes cytotoxic edema and hemorrhagic
transformation within infarcted tissue
• Conversely, severe hypotension will compromise cerebral
perfusion and potentially increase infarct volume
• Regular noninvasive BP monitoring in all AIS patients on the ICU
& continuous BP monitoring in patients with cardiovascular
instability and those who are mechanically ventilated
• Fluid balance should be carefully monitored and managed to
maintain euvolemia
• 0.9 % saline to be used for fluid replacement and dextrose-
containing fluids should always be avoided

55. Approach to elevated BP
A.NOT ELIGIBLE FOR THROMBOLYTIC THERAPY
1.SBP<220 mmHg or DBP<120
• Observe unless other end-organ involvement (e.g., aortic dissection, acute
myocardial infarction, pulmonary edema, hypertensive encephalopathy)
• Treat other symptoms of stroke (e.g., headache, pain, agitation, nausea,
vomiting)
2.SBP>220 or DBP>121-140
• Labetalol 10-20 mg IV over 1-2 min
May repeat or double every 10 min (maximum dose 300 mg)
OR
• Nicardipine 5 mg/hr IV infusion as initial dose; titrate to desired effect by
increasing 2.5 mg/hr every 5 min to maximum of 15 mg/hr
Aim for a 10-15% reduction
3.DBP>140
• Nitroprusside 0.5 μg/kg/min IV
• Aim for 10-15% reduction

56. B. ELIGIBLE for thrombolytic therapy
Pretreatment
• Systolic >185 mm Hg OR diastolic >110 mm Hg
• Labetalol 10 to 20 mg IV over 1 to 2 min, may repeat OR
• Nicardipine infusion 5 mg/hr, titrate up by 2.5 mg/hr at 5- 15min
intervals
• If BP does not decline and remains >185/110 mm Hg, do not
administer rtPA
During/after Treatment
1. Diastolic >140 mm Hg
Sodium nitroprusside 0.5 μg/kg/min IV infusion as initial dose and
titrate to desired blood pressure
2. Systolic >230 mm Hg OR diastolic 121-140 mm Hg
• Labetalol 10 mg IV over 1-2 min (UPTO300MG) or give initial
labetalol dose, then start labetalol drip at 2-8 mg/min OR
• Nicardipine 5 mg/hr IV infusion as initial dose and titrate to desired
effect if not controlled , consider sodium nitroprusside
3. Systolic 180-230 mm Hg OR diastolic 105-120 mm Hg
• Labetalol 10 mg IV over 1-2 min May repeat or double labetalol
every 10-20 min

57. • Cardiac problems commonly coexist with AIS, either as
a trigger for the disease (e.g., cardioembolic stroke) or
as a result of the stroke itself
• Dysrhythmias ( 57 % ) elevated cardiac troponin levels (
17.5 %) and at least 12 % have abnormal left
ventricular function on ECHO
• All AIS patients on ICU should undergo continous ECG
monitoring
• ECHO at least once during the course of their
admission (repeated if abnormal ventricular function
identified).
• Cardiac troponin should be measured in patients with
ECG changes and echocardiographic evidence of
impaired ventricular function.

58. Hyperglycemia
• Hyperglycemia occurs in more than 40 % of AIS patients
• Marker of illness severity, associated with deleterious
effects, including increased cortical toxicity, larger infarct
volumes and susceptibility to infection.
• Poststroke hyperglycemia is independently associated with
increased mortality and morbidity at 90 days and
postthrombolysis ICH
• Regular blood glucose monitoring is essential.
• Treatment with continuous insulin infusion to maintain
serum glucose between 140 and 180 mg/dl is preferred in
the ICU.

59. FEVER
• Pyrexia affects up to 50 % of patients after AIS and
is independently associated with poor outcome
• Avoid pyrexia (T >37.5 °C).
• Investigate for and treat infectious causes of fever
• Regular paracetamol (acetaminophen) therapy as
a first- line therapy in those with temperatures
>37.5 °C,
• Second-line therapy includes intravenous
metamizole, rapid infusion of cold saline (4 °C) and
the use of automatic cooling systems.
• Role of therapeutic hypothermia is controversial

60. Antiplatelet agents
• For patients who are not eligible for tPA, aspirin is
the only antiplatelet drug that has been
evaluated in the acute treatment of stroke.
• Oral administration of aspirin (initial dose is 325
mg) within 48 hours after stroke onset is
recommended (Class I A).
• In patients who receive tPA, antiplatelet therapy
should start 24 hours after thrombolytic therapy
• The usefulness of clopidogrel for the treatment of
acute ischemic stroke is not well established
(Class IIb C).

61. Anticoagulation
• Use of anticoagulation in the first 24 h following
I/V rt-PA is currently contraindicated.
• Urgent anticoagulation for the management of
noncerebrovascular conditions not
recommended for patients with moderate-to-
severe strokes because of an increased risk of
serious intracranial hemorrhagic complications
(Class IIIA)

62. INDICATIONS FOR
ANTICOAGULATION
Atrial fibrillation with or without
RHD
Prosthetic heart valve
DVT
Hypercoagulable state
Venous sinus thrombosis
Arterial dissection
CHADS2 SCORE
• CONGESSTIVE HEART FAILURE
• HYPERTENSION(>140/90)
• AGE>75YRS
• DIABETES MELLITUS
• PRIOR STROKE OR TIA
• NOACS
• Dabigatran,Rivaroxaban,Api
xaban
• Efficacy equivalent to
warfarin in preventing
stroke and less likely to
produce ICH but higher
chances of GI bleed
Anticoagulants

63. Thromboprophylaxis
• Early mobilization reduces the risk of
thromboembolic complications of AIS.
• All immobilized AIS patients on ICU should be
treated with prophylactic-dose subcutaneous
LMWH to prevent DVT and mechanical
intermittent calf compression.
• Treatment should be started early, but LMWH
should not be started until 24 h following
thrombolysis.

64. Seizures
• Convulsive and nonconvulsive seizures are
uncommon after AIS
• No role for prophylactic anticonvulsants
• Seizures should be treated aggressively and a
long-acting anticonvulsant considered
• First-line anticonvulsant is phenytoin
• LEVETIRACETAM being used widely nowadays

65. NEUROPROTECTIVE AGENTS
• Among patients already taking statins at the time of
onset of ischemic stroke, continuation of statin therapy
during the acute period is reasonable (Class IIaB)
• The utility of induced hypothermia for the treatment of
patients with ischemic stroke is not well
established(Class IIbB)
• At present, transcranial near-infrared laser therapy is
not well established for the treatment of acute
ischemic stroke (Class IIbB)
• At present, no pharmacological agents with putative
neuroprotective actions have demonstrated efficacy in
improving outcomes after ischemic stroke, and
therefore, other neuroprotective agents are not
recommended (Class IIIA)

66. Complications of stroke
• Hemorrhagic transformation
• Cerebral edema
• Hyperthermia
• Hyperglycemia
• Deep venous thrombosis

67. HEMORRHAGIC TRANSFORMATION
Symptomatic intracerebral hemorrhage occurs in about 6% of patients
receiving intravenous rtPA & has been associated with high morbidity
and mortality
Risk factors include
• symptom severity
• early infarct signs on admission brain CT
• older age, elevated systolic blood pressure,
• low platelet count
• elevated serum glucose
• history of diabetes
Most tPA-related intracranial hemorrhages occur in the first few hours
after treatment.
• Hemorrhagic transformation can also occur in the absence of
reperfusion therapy

68. ICH-S/S
• New neurological deficit
• worsening of existing neurological deficits
• Headache
• Nausea, vomiting
• Decreased level of consciousness
• Marked hypertension
• Bradycardia

69. T/T-
• Discontinue infusion
• Obtain CT stat
• Order PT, APTT, fibrinogen
• Type and cross match blood
• Neurosurgery opinion
• Administer FFP OR Cryoppt
• The role of surgery is unclear, but decompressive
surgery/hematoma evacuation may be indicated
in large superficial hematomas and/or those
causing significant mass effect.

70. NEUROMONITORING
• Clinical and radiological monitoring are the
cornerstones of identifying deterioration after AIS.
• Routine ICP monitoring is not recommended but can
be considered in those with large infarct volumes or
hemorrhagic conversion with mass effect.
• However, ICP values are often normal even in the
presence of large infarct volumes.
• Optic nerve ultrasonography
• Transcranial Doppler (TCD) ultrasonography is a
noninvasive monitor that is able to assess cerebral
blood flow velocity in basal cerebral vessels and is
perhaps the most promising neuromonitor after AIS.

71. CEREBRAL EDEMA
• Patients with ischemic stroke with cerebral
edema and mass effect are at risk for brain
herniation, brainstem compression, coma, and
death.
• Mass effect caused by ischemic infarcts typically
peaks 3 to 5 days after symptom onset.
• Clinical examination more sensitive in detecting
worsening cerebral edema than ICP monitoring

72. • If suspected elevated ICP maintain ABC
• Keep head end elevated to 30 degrees
• Hyperosmolar therapy- Mannitol/hypertonic
saline
• MANNITOL-0.5 to 1 g/kg loading dose and can be
followed by boluses of 0.25 g/kg every 6 hours
• Monitor serum osm. <320 mosm
• Hypertonic saline(3%/7.5%) can be used
• 2ml/kg bolus can be given and then repeated
• Monitor serum osm and serum sodium

73. SURGERY
• Decompressive craniectomy is a controversial therapy
for malignant middle cerebral artery (MCA) stroke
Malignant MCA stroke is indicated by:
• MCA territory stroke of >50% on CT
• Perfusion deficit of >66% on CT
• Infarct volume >82 mL within 6 hours of onset (on MRI)
• Infarct volume of >145mL within 14 hours of onset (on
MRI)
• National Institutes of Health Stroke Scale score is often
>20 with dominant hemispheric infarction and >15
with nondominant hemispheric infarction

74. • There are 3 important trials that have studied
decompressive hemicraniectomy for malignant
MCA strokes in patients <60 years of age
• DESTINY trial (2007)
• Prospective, MC RCT from Germany
• Outcome: 88% vs 47% survival in favour of
decompressive craniectomy
• DECIMAL trial (2007)
• Prospective, MC RCT from France
• Outcome: ARR 52.8% in mortality favouring the
decompressive craniectomy group (75% vs 22%
survival)

76. • HAMLET trial (2009)
• Prospective, MC RCT from the Netherlands
• Outcome: ARR 38% in mortality favouring the
decompressive craniectomy group
• Pooled analysis of DESTINY, DECIMAL and HAMLET
• Patients aged <60y with supratentorial infarctions treated
with decompressive craniectomy, usually within 48 hours of
stroke onset
• Hemicraniectomy compared with medical management
• Reduced mortality (22% versus 71%)
• No individual study showed an improvement in the
percentage of survivors with good outcomes (mRS score, 0–
3)
– Only shown in a pooled analysis (43% versus 21%).
– Only 14% of surgical survivors could look after their own affairs
without assistance (mRS score, 2)
•

78. • Subsequently, the DESTINY II Trial (2014) studied
patients aged >60 years:
• n = 112 patients >60 years of age (median age was 70)
• Primary outcome measure was survival without severe
disability
• 38% in the hemicraniectomy group vs 18% in the
control group
• Secondary outcomes:
• Overall mortality was lower in the surgery group (33%
vs 70%)
• Almost none of the survivors has an outcome as good
as an mRS score of 3; almost all post-operative
survivors were severely disabled

79. END OF LIFE
• Despite early aggressive treatment some patients
do not have a satisfactory degree of clinical
recovery, and withdrawal of life-sustaining
therapies and a shift to end- of-life care is
appropriate.
• Documented early discussion with patients and
relatives to ascertain previous wishes is vital.
• An outcome that is acceptable to an individual
patient, rather than to the clinical team, should
drive decision-making regarding ‘‘do not attempt
resuscitation’’ orders and other limitations of
care.

81. Long term airway management
Close fluid status monitoring
Monitor cardiac function
Blood glucose Monitoring
Control temperature
Anticoagulant and antiplatelet
use

82. TAKE HOME MESSAGES
• Intravenous tPA should be administered to all
patients of AIS who present within 3 hours of
stroke onset and meet the NINDS inclusion and
exclusion criteria.
• The risk of symptomatic intracranial hemorrhage
with intravenous tPA is approximately 6%.
• Intra-arterial tPA and mechanical thrombectomy
are alternative treatment strategies for acute
stroke patients who are ineligible for or fail
intravenous tPA treatment .

83. • Patients with acute ischemic stroke should be
maintained euglycemic, euvolemic, and
normothermic.
• Permissive hypertension may be beneficial,
but in patients receiving tPA blood pressures
should be maintained at or less than 185/110
mm Hg.
• Patients with life-threatening cerebral edema
from hemispheric infarctions require
hyperosmolar therapy and may benefit from
early surgical decompression

84. 84