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DR. SANKALP MOHAN
SENIOR RESIDENT, NEUROLOGY
Etiology and classification
Ischemic stroke – 1. thrombosis
2. embolism
3. systemic hypoperfusion
Hemorrhagic stoke–
1 . intracerebral
2 . subarachnoid
THREE STROKE TYPES
Intracerebral
Hemorrhage

Ischemic
Stroke

85%

Clot occluding
artery

Subarachnoid
Hemorrhage

10%

Bleeding
into brain

5%

Bleeding
around brain
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
INVESTIGATIONS AND

MANAGEMENT GUIDELINES
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
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.
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)
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
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
SURGICAL MANAGEMENT
A) endovascular interventions
 1) angioplasty and stenting
 2) mechanical clot disruption
 3) clot extraction
 B)carotid endartectomy
MANAGEMENT OF
COMPLICATIONS
 1.cerebral edema
 2. hemorrhagic transformation
 3. siezures
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
 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
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 ..
 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
BLOOD PRESSURE MANAGEMENT
Reducing
formation of brain
edema
lessening
hemorrhagic
transformation
preventing early
recurrent stroke
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
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
 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
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)
 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.
Management of complications
 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
 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
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
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.
 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
• 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.
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
 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.
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
MERCI Device

Source: St. Petersburg Times, October 2003
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.
ANTIPLATELET AGENTS
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…
VOLUME EXPANSION, INDUCED
HYPERTENSION
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
NEUROPROTECTIVE AGENTS
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
GENERAL ACUTE TREATMENT FOR
HOSPITALISED PATIENTS
INTRACEREBRAL
HEMORRHAGE
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,
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
 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.
 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)
TREATMENT
GENERAL MANAGEMENT
 Fever should be treated
 Hyperglycemia current guidelines suggest insulin
treatment for elevated serum glucose >140 to 185
mg/dL)
 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
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.
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
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)
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
 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
TREATMENT OF ACUTE
NEUROLOGIC COMPLICATIONS
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..
 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
THANK YOU

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Types, Causes, Diagnosis and Management of Strokes

  • 1. DR. SANKALP MOHAN SENIOR RESIDENT, NEUROLOGY
  • 2. Etiology and classification Ischemic stroke – 1. thrombosis 2. embolism 3. systemic hypoperfusion Hemorrhagic stoke– 1 . intracerebral 2 . subarachnoid
  • 3. THREE STROKE TYPES Intracerebral Hemorrhage Ischemic Stroke 85% Clot occluding artery Subarachnoid Hemorrhage 10% Bleeding into brain 5% Bleeding around brain
  • 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. 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.
  • 8. 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.
  • 9.
  • 10. 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)
  • 11.
  • 12.
  • 13. 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
  • 14.
  • 15.
  • 16.
  • 17. 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
  • 18. SURGICAL MANAGEMENT A) endovascular interventions  1) angioplasty and stenting  2) mechanical clot disruption  3) clot extraction  B)carotid endartectomy
  • 19. MANAGEMENT OF COMPLICATIONS  1.cerebral edema  2. hemorrhagic transformation  3. siezures
  • 20. 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
  • 21.  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
  • 22. 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 ..
  • 23.  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
  • 24. BLOOD PRESSURE MANAGEMENT Reducing formation of brain edema lessening hemorrhagic transformation preventing early recurrent stroke
  • 25. 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
  • 26. 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
  • 27.  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
  • 28. 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)
  • 29.  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.
  • 31.
  • 32.  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
  • 33.  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
  • 34. 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
  • 35. 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.
  • 36.
  • 37.
  • 38.  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
  • 39. • 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.
  • 40.
  • 41. 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
  • 42.  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.
  • 43. 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
  • 44. MERCI Device Source: St. Petersburg Times, October 2003
  • 45.
  • 46.
  • 47. 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.
  • 49.
  • 50.
  • 51.
  • 52. 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…
  • 54. 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
  • 55.
  • 56.
  • 58.
  • 59. 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
  • 60.
  • 61. GENERAL ACUTE TREATMENT FOR HOSPITALISED PATIENTS
  • 62.
  • 64. 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,
  • 65. 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
  • 66.  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.
  • 67.  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)
  • 68. TREATMENT GENERAL MANAGEMENT  Fever should be treated  Hyperglycemia current guidelines suggest insulin treatment for elevated serum glucose >140 to 185 mg/dL)
  • 69.  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
  • 70. 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.
  • 71. 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
  • 72. 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)
  • 73. 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
  • 74.  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
  • 76. 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..
  • 77.  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