An overview on the management of acute stroke with emphasis on the 2013 guidelines of the American stroke association/ American heart association .

1. MANAGEMENT OF STROKE
DR MALLUM C.B.
NEUROLOGY UNIT
DEPT OF INTERNAL MEDICINE
JUTH

2. OUTLINE
• DEFINITIONS
• TYPES OF STROKE
• EVALUATION OF STROKE
• INVESTIGATIONS
• POOR PROGNOSTIC FACTORS IN STROKE
• DEFINITION OF LEVELS OF
EVIDENCE/RECOMMENDATIONS
• MEDICAL MANAGEMENT
• PREVENTION AND MANAGEMENT OF COMPLICATIONS
• SURGICAL MANAGEMENT

3. DEFINITION
• Stroke(CVA) is defined by the World Health
Organization as a clinical syndrome consisting of
‘rapidly developing clinical signs of focal (at times
global) disturbance of cerebral function, lasting
more than 24 h or leading to death with no
apparent cause other than that of vascular origin’.
• CVD - parent term = also includes Cerebral
arteriosclerosis; cerebral angioma ; Cerebral
artero-venous malformation ; Subdural
hematoma

4. TRANSIENT ISCHEMIC ATTACK(TIA)
• Transient ischemic attack is temporary focal
neurological deficit of sudden onset caused by
ischemia of the brain, retina lasting less than
24 hours followed by complete recovery.
• New definition: No objective evidence of
acute infarction in the affected region of brain
or retina; < I hour
• Therefore, CT/MRI necessary to increase
diagnostic accuracy.

5. CLASSIFICATION OF STROKE
Stroke
Primary Hemorrhagic
(20% of Strokes)
Primary Ischemic
(80% of Strokes)
Thrombotic
50%
Embolic
30%
Intracerebral
Hemorrhage 15%
Subarachnoid
Hemorrhage 5%
5

6. STROKE
Which is an Ischaemic Stroke?

7. Causes
Destruction of brain cells and tissue

8. Types of Stroke
85%
Ischemic
15 %
hemorrhagic

9. ISCHEMIC STROKE PATHOPHYSIOLOGY
The First Few Hours
Penumbra
Core
Clot in
Artery
“TIME IS BRAIN:
SAVE THE PENUMBRA”
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

10. Cerebral Arterial territory
Anterior cerebral
Middle cerebral
Posterior cerebral
Anterior choroidal

11. Cerebral BloodFlow

12. EVALUATION OF STROKE
• 1. Determine if symptoms are due to stroke
• 2. Localize site of brain lesion
• 3. Establish the type of stroke
• 4. Ascertain the likely cause
• The clinical assessment (history, general examination,
and neurological examination) remains the cornerstone
of the evaluation.
• The use of a stroke rating scale, preferably the NIHSS, is
recommended (Class I; Level of Evidence B).
• It has been recommended that patients with acute
stroke <7 days or progressive stroke should be
admitted

13. Stroke - questions
• Is it a stroke ?
• What type of stroke ?
• Why did it happen ?
• How does it affect the patient ?
• What is the prognosis ?

14. 14
The symptoms of a stroke are dependant on what
portion of the brain is damage.
http://www.pdrhealth.com/patient_education/images/BHG01NE13F01.GIF

15. 1/18/2015 15
Pathological: WHO Criteria
C.I C.H
• L.O.C. -ve +ve
• Headache - ve +ve
• Vomiting - ve +ve
• T.I.A. +ve - ve
• Gradual onset +ve -ve
• Activity -ve + ve
• HBP mild /-ve mod/severe
• Bldy csf -ve + ve

17. EMERGENCY INVESTIGATIONS
• To establish the diagnosis of stroke
• to determine the underlying cause of the
event.

18. Immediate Diagnostic Studies: Evaluation of a
Patient With Suspected Acute Ischemic Stroke
Stroke 2007;38;1655-1711;

19. INVESTIGATIONS
• full blood count, serum electrolytes, renal function
tests, cardiac enzymes, and coagulation studies
• Blood sugar is mandatory to exclude hypoglycemia or
diagnose diabetes mellitus
• Full blood count to detect Polycythaemia,ESR for
endocarditis,
• clotting studies for Hypercoagulable States
• An electrocardiogram (ECG) : arrhythmias and
myocardial infarction. Baseline ECG is recommended in
all patients with stroke(AHA/ASA Guidelines)
• Echocardiography : valve disease and intra-cardiac clot

20. NEUROIMAGING
• Brain CT scan: CT is sensitive to the intracranial blood
and is readily available.
Normal early CT therefore rules out haemorrhagic stroke.
CT Scan changes in ischemic stroke may take several days
to develop.
• MRI: MRI is better at detecting posterior fossa lesions
especially in posterior circulation stroke such as Pons
or cerebellum
• It is also recommended that all patients with transient
neurologic symptoms have a neuroimaging within 24
hours or as soon as possible.(Class 1,LOE B)

21. 3 types of stroke

26. POOR PROGNOSTIC FACTORS IN
STROKE
• Accompanying fever
• Hypotension and severe hypertension
• Low oxygen saturation
• Hyperglycaemia and hypoglycemia
• Total anterior circulation stroke (55% dead)
• Pontine Haemorrhage
• Low GCS score
• heart failure
• severity of hemiparesis

27. Total Ant. Cir. Syndrome
 ALL OF THESE:-
 Higher Dysfunction
 Dysphasia
 Visuospatial
 Homonymous Hemianopia
 Motor / Sensory Deficit
 >2/3 Face / Arm / Leg

28. COMMON PITFALLS IN MANAGEMENT
OF STROKE
• Aggressive early treatment of blood pressure
in stroke.
• Misdiagnosis of haemorrhagic stroke as
hypertensive encephalopathy.
• Failure of adequate hydration of patients
• Failure to diagnose and treat
hypo/hyperglycemia
• Inability to effective diagnose and manage
complications of stroke

29. Definition of Classes Used in AHA/ASA
Recommendations
• Class I Conditions for which there is evidence for
and/or general agreement that the procedure or
treatment is useful and effective.
• Class II Conditions for which there is conflicting
evidence and/or a divergence of opinion about the
usefulness/efficacy of a procedure or treatment.
• Class IIa The weight of evidence or opinion is in favor of
the procedure or treatment.
• Class IIb Usefulness/efficacy is less well established by
evidence or opinion.
• Class III Conditions for which there is evidence and/or
general agreement that the procedure or treatment is
not useful/effective and in some cases may be harmful.

30. Definition of Levels of Evidence Used in
AHA/ASA Recommendations
Therapeutic recommendations
• Level of Evidence A Data derived from multiple randomized
clinical trials or meta-analyses
• Level of Evidence B Data derived from a single randomized
trial or nonrandomized studies
• Level of Evidence C Consensus opinion of experts, case
studies, or standard of care
Diagnostic recommendations
• Level of Evidence A Data derived from multiple prospective
cohort studies using a reference standard applied by a
masked evaluator
• Level of Evidence B Data derived from a single grade A
study or 1 or more case-control studies, or studies using a
reference standard applied by an unmasked evaluator
• Level of Evidence C Consensus opinion of experts

31. Table 1 :PHASES OF CONTEMPORARY
MANAGEMENT OF STROKE
Phases Period from onset Activities Prefered location
1Acute (emergency)
care:
hyperacute / acute
1st-7th day a)Assessment
b)Early supportive
care
Hospital
2 Early sub-
acute(supportive)
care
2nd-4th week a)prevention and
treatment of
complications
Hospital
3 Late sub-
acute(maintanance)
care
2nd-6th month a)Rehabilitation
b)Psychological
support
c)Prevent recurrence
Hospital/Community
4.Long-term (chronic)
care
7th month onwards a)Rehabilitation
b)Psychological
support
c)Social support
d)Prevent recurrence
Community
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32. MEDICAL MANAGEMENT1. 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

33. PREVENTION AND MANAGEMENT OF
COMPLICATIONS
• Management of complications improves both
short-term and long-term prognosis.
• Complications of stroke can be divided into
General medical and Neurological
complications.
• They can also be divided into Acute(<7 days)
or subacute(>7days) based on time of
occurrence.

34. SURGICAL MANAGEMENT
• For Ischemic stroke:
A) endovascular interventions: angioplasty and stenting,
mechanical clot disruption,clot extraction
B)carotid endartectomy
C) EC/IC bypass surgery
• For ICH: Surgical evacuation of haematoma
• For Subarachnoid haemorrhage:Clipping and coiling of
aneurysm
• Surgical decompression of cerebellar haematoma
• Decompressive craniectomy for cerebral oedema
• Ventricular drainage: pts with intra ventricular
haemorrhage and acute hydrocephalus.

35. EARLY SUPPORTIVE CARE
• 25 %of patients may have neurological worsening
during first 24-48 hours.
• The use of stroke unit is recommended to
improve general management.
• Nurse in slight head-up tilt to improve venous
drainage from the head region.
• continuous monitoring of neurological deficit for
deterioration, including the level of
consciousness, which may herald impending
herniation.
•

36. EARLY SUPPORTIVE CARE
• Continuous cardiac monitoring, if indicated,
particularly if risk factors for coronary heart
disease are present.
• Do not feed orally if patient is unconscious or
drowsy. Swallowing test should be done in
conscious patients before oral feeding and feed in
the semi-recumbent position (450) – ensure
correct consistency of food.
• Early mobilization of less severely affected
patients
• Early physiotherapy should be initiated

37. AIRWAY AND VENTILATION
• Airway – Foreign Bodies, dentures, tongue
• Patients who exhibit a decreasing level of
consciousness or signs of brain stem dysfunction
are candidates for elective intubation .
• Indications for intubation
- hypoxia (pO2 <60 mm Hg or PCO2 >50 mm Hg) -
risk of aspiration with or without impairment of
arterial oxygenation
• elective tracheostomy should be performed after
2 weeks for prolonged coma or pulmonary
complications

38. SUPPLEMENTAL OXYGEN
• Adequate tissue oxygenation is important to
prevent further brain injury
• Current American Stroke Association
recommendations call for supplemental
oxygen to be given as needed to maintain an
oxygen saturation of more than 95% by pulse
Oximetry.

39. VOLUME STATUS
• Hypovolaemia has been associated with
worse outcome and increased mortality in
acute ischemic stroke.
• Isotonic saline, i.e. "normal" or 0.9%, should
be used for volume repletion and
maintenance, typically 3 litres per day is given.
• Do not give hypotonic solution, eg 5%
Dextrose in water, as it may worsen cerebral
oedema.

40. 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
coolIng devices might be used .
• Relevant antibiotics might also be used.

41. TEMPERATURE
• Fever worsens outcome:
• for every 1°C rise in temp, risk of poor
outcome doubles (Reith, Lancet 1996)
• Greatest effect in the first 24 hours
• Brain temp is generally higher than core
• Treat aggressively with acetaminophen

42. THROMBOLYSIS
• Thrombolysis within 1st 4.5 hrs (3-15% pts)
• rtPA, alteplase; streptokinase.
• Door to needle < 1 hr.
• Patient
- Normal CT scan
- BP <180/100 mmHg.
- No bleeding tendency
• Dose - 0.9mg /Kg. (max 90mg)
• - 10% bolus, Rest 60 min by infusion
• Risk - ICH in 6% of patients
• - Reduced morbidity by 30%

43. BLOOD PRESSURE MANAGEMENT
• Reduction of BP in acute stroke phase is
controversial
• BP Should be kept within higher normal limits
since low BP could precipitate perfusion failure
• 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

44. BLOOD PRESSURE MANAGEMENT
Reducing formation
of brain edema
lessening
hemorrhagic
transformation
preventing early
recurrent stroke

45. BLOOD PRESSURE MANAGEMENT
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

46. BLOOD PRESSURE MANAGMENT
• Some authorities believe BP should not be
actively lowered in the 1st 10 days after stroke
unless MAP > 145 (SBP > 220; DBP>120)
• Indications for lowering BP:
-dissecting aortic aneurysm
-Myocardial Ischemia or acute myocardial
infarction
-Acute pulmonary oedema.
-Rapid decline in renal function.
• Aim: MAP = 130; DBP = 105; (185/105)

47. BLOOD PRESSURE MANAGEMENT
In patients with markedly elevated blood pressure
who do not receive fibrinolysis, a reasonable goal
is to lower blood pressure by 15% during the first
24 hours after onset of stroke. The level of blood
pressure that would mandate such treatment is not
known, but consensus exists that medications should
be withheld unless the systolic blood pressure is >220
mm Hg or the diastolic blood pressure is >120 mm Hg
(Class I; Level of Evidence C).

48. BLOOD PRESSURE MANAGMENT
• Evidence from one clinical trial indicates that initiation
of antihypertensive therapy within 24 hours of
stroke is relatively safe. Restarting antihypertensive
medications is reasonable after the first 24 hours for
patients who have preexisting hypertension and are
neurologically stable unless a specific contraindication
to restarting treatment is known (Class IIa; Level
of Evidence B).

49. BLOOD PRESSURE MANAGEMENT
• No data are available to guide selection of medications
for the lowering of blood pressure in the setting of
acute ischemic stroke
• If systolic BP >180–230 mm Hg or diastolic BP >105–
120 mm Hg:
-Labetalol 10 mg IV followed by continuous IV infusion
2–8 mg/min; or
-Nicardipine 5 mg/h IV, titrate up to desired effect by
2.5 mg/h every 5–15 minutes, maximum 15 mg/h
• If BP not controlled or diastolic BP >140 mm Hg,
consider IV sodium nitroprusside
• use oral agents (captopril, calcium channel blockers)

50. BLOOD PRESSURE MANAGEMENT
• Systolic > 220 OR Diastolic 121 to 140: treat with
goal of a 10% to 15% reduction in blood pressure
using:
1. Labetalol 10 to 20 mg intravenously over 1 to 2
minutes (may repeat or double every 10 minutes;
max dose is 300 mg) or
2. Nicardipine infusion, 5mg/hour, titrate up by
0.25 mg/hour at 5- to 15-minute intervals,
maximum dose 15 mg/hour. When desired blood
pressure is attained, reduce to 3 mg/hour

51. GUIDELINES FOR BP MGT IN
HAEMORRHAGIC STROKE
• 1. Until ongoing clinical trials of BP intervention for ICH
are completed, physicians must manage BP on the
basis of the present incomplete efficacy evidence.
Current suggested recommendations for target BP in
various situations are available and may be considered
(Class IIb; Level of Evidence: C). (Unchanged from the
previous guideline)
• 2. In patients presenting with a systolic BP of 150 to
220 mm Hg, acute lowering of systolic BP to 140 mm
Hg is probably safe (Class IIa; Level of Evidence: B).

52. GLYCAEMIC CONTROL
Hyperglycemia may augment brain injury by several
mechanisms including
• increased tissue acidosis from anaerobic metabolism
• free radical generation
• increased blood brain barrier permeability.
• Aggressive Glycaemic control utilizing a continuous insulin,
potassium, and glucose infusion(GKI) is feasible.
• For patients with blood glucose >200 mg/dl, 6 units of
insulin hrly can be given until blood sugar is <120 mg/ dl.
• GKI infusion may need to be continued in comatose
patients or those unable to swallow

53. GLYCAEMIC CONTROL
• 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
• Hypoglycemia (blood glucose <60 mg/dL) should
be treated in patients with acute ischemic stroke
(Class I; Level of Evidence C).
• The goal is to achieve normoglycemia.

54. GLYCAEMIC CONTROL
• Evidence indicates that persistent in-hospital
hyperglycemia during the first 24 hours after
stroke is associated with worse outcomes than
normoglycemia, and thus, it is reasonable to
treat hyperglycemia to achieve blood glucose
levels in a range of 140 to 180 mg/dL and to
closely monitor to prevent hypoglycemia in
patients with acute ischemic stroke (Class IIa;
Level of Evidence C).

55. ANTI COAGULANTS
• Anticoagulation in acute ischemic stroke is not
recommended for treatment of stroke.
• If hemiplegia is dense, commence subcutaneous
Heparin 5,000 units 12 hourly(or 8hrly)
• low dose subcutaneous low-molecular-weight
heparin or unfractionated heparin may be
considered for prevention of DVT in patients with
intracerebral haemorrhage after 4 days from
onset (latest AHA/ASA guidelines)

56. ANTIPLATELET AGENTS
• Aspirin –within 48hrs – reduce risk of
mortality/ disability in ischemic stroke
• Other antiplatelets: Abciximab - II B / III A
inhibitor, Cilostazol - phosphodieterase (PDE )
type 3 inhibitor, Dipyridamole ,
• Antiplatelets contraindicated in haemorrhagic
stroke

57. ANTIPLATELETS

58. Volume Expansion, Vasodilators,
and Induced Hypertension
• The administration of high-dose albumin,
Hemodilution by volume expansion, and
administration of vasodilatory agents, is not
recommended for treatment of ischemic
stroke.

59. NEUROPROTECTIVE AGENTS
• Protect Neurones from adverse milleu created by the
biochemical changes triggered by ischaemia:
attenuate neuronal injury
• Examples are free radical scavengers – Vit C ; E
encephabol (piritinol)
• 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 III; Level of Evidence A).

60. NEUROPROTECTIVE AGENTS
• In addition to their low-density lipoprotein
cholesterol–lowering effects, statins, or HMG-CoA
reductase inhibitors, exert acute neuroprotective
properties, including beneficial effects on
endothelial function, cerebral blood flow, and
inflammation.
• Among patients already taking statins at the time
of onset of ischemic stroke, continuation of statin
therapy during the acute period is reasonable
(Class IIa;Level of Evidence B).

61. MEDICAL COMPLICATIONS OF STROKE
• Medical complications of stroke have been reported to
occur in as high as 85% of patients with stroke
(Langhorne et al, 2000).
• Medical complications account for at least 50% of
mortality after the first week of stroke.
• The most commonly encountered complications are
those related to immobility and infection.
• However, the most important causes of mortality in the
early period following a stroke are cardiac
(arrhythmias, myocardial infarction), infections
(pneumonia, urosepsis), and venous thrombo-
embolism (pulmonary embolus)

62. Medical Complications in Hospitalized
Patients With Stroke
Complications of Immobility
• Deep vein thrombosis/pulmonary embolism
• Falls
• Pressure sores or ulceration
Infections
• Chest infection- aspiration pneumonia
• Urinary tract infection
• Other infections
Malnutrition
• Dysphagia
• Dehydration

63. Medical Complications in Hospitalized
Patients With Stroke
Pain
• Shoulder pain (subluxation in the paretic limb)
• Miscellaneous pain (headache, musculoskeletal)
• Central post-stroke pain
Neuropsychiatric Disturbances
• Depression, anxiety ,Emotional incontinence
• Acute confusional states (delirium)
Miscellaneous
• Cardiac complications (arrhythmia, myocardial ischemia)
• Gastrointestinal bleed
• Constipation
• Arthritis
• Sleep apnea
• Nutritional deficiencies

64. Deep Venous Thrombosis
and Pulmonary Embolism
• The highest incidence occurs between the second
and seventh day poststroke.(continuum)
• Estimates of early deaths attributable to PE range
from 13% to 25% and occur most frequently
between the second and fourth week.
• Measures to prevent DVT should be routine for
all patients with ischemic stroke admitted to the
hospital.

65. DVT PROPHYLAXIS
• Tight fitting knee-high or thigh-high antiembolic
stockings reduce venous stasis in the leg.
• Pneumatic compression devices can be applied to
the lower extremities of nonambulatory patients.
• The use of low-intensity anticoagulation for DVT
prophylaxis is recommended for all immobilized
patients with stroke. (Adams et al, 2007).
• In patients with primary intracerebral
hemorrhage, initiation of anticoagulation for DVT
prophylaxis is often delayed for 3 to 4 days.

66. DVT PROPHYLAXIS
• Early mobilization
• Mechanical compressive devices
Antiembolic stockings
Sequential pneumatic compression devices
• Subcutaneous unfractionated heparin
• Low-molecular-weight heparins
• patients with embolic infarction should not be
treated with heparin or with any form of
anticoagulant in the first 30 days.

67. 2013 AHA/ASA GUIDELINES ON DVT
PROPHYLAXIS
• The PREVAIL showed superiority of LMWH
(Low Molecular weight Heparin)over UFH
(Unfractionated Heparin)
• Early administration of Heparin for the
prevention of early recurrent stroke,for
improving outcome after ischemic stroke, in
patients with severe stenosis of internal
carotid artery is not recommended

68. Malnutrition and aspiration
• Malnutrition and aspiration:
- A preserved gag reflex may not indicate safety
with swallowing.
-Swallowing evaluation should be performed in all
patients with dysarthria, aphasia, or facial, buccal,
or lingual weakness.
-Inability to swallow safely should precipitate early
placement of a naso-gastric tube in order to assure
gastrointestinal access for nutrition and
medications.

69. INFECTIONS
• Urinary tract infection:
this is common as a result of catheterization.
Frequent urine culture and antibiotic treatment is
required. To avoid pseudomonas infection, acidify
urine by giving patient 2.4 g of vitamin C daily.
• Some specialists favour the use of parenteral
Vitamin C for this purpose
• If possible the placement of indwelling bladder
catheters should be avoided because of
associated risk of UTI

70. 1/18/2015 70
TABLE 2: ACUTE AND SUB-ACUTE COMPLICATIONS OF STROKE
Neurological Systemic
ACUTE (<7 days) 1.Cerebral oedema
2.Increased ICP
3.Hydrocephalous
4.Haemorrhagic
transformation
5.Seizures
6.Transtentorial herniation
1.Hypoxia
2.Hypertension
3.Hyperglycemia
4.Aspiration
5.Cardiac arrythmias
6.Inappropriate ADH secretion
SUB-ACUTE (>7 DAYS) 1.Seizures
2. Depression
1.D.V.T & Pulmonary
embolism
2.Bronchopneumonia
3.Urinary tract infections
4.Septicaemia
5.Decubitus ulcers
6.Joint stiffness

71. ACUTE NEUROLOGIC COMPLICATIONS
OF STROKE
• This is the most common cause of deterioration
in neurologic status in patients hospitalized for
stroke.
• The most common neurologic complications
Cerebral edema
-Mass effect and herniation
- Hemorrhagic transformation
- Seizures
-Progressing ischemia (33%)
- Recurrent stroke(11%) (Weimar et al, 2002).

72. TREATMENT OF RAISED ICP AND
CEREBRAL OEDEMA
• Usually occurs between 3-5 days of stroke
• Clinical features include deteriorating levels of
consciousness, ipsilateral pupillary
enlargement,worsening neurological status
• Patients may also have evidence of cushing’s
reflex – elevated BP with bradycardia.
• Patients with intracerebral haemorrhage and
large hemispheric infarcts are prone to raised
intracranial pressure.
• Brain CT scan may show features of oedema or
hydrocephalus(dilatation of ventricles)

73. TREATMENT OF RAISED ICP AND
CEREBRAL OEDEMA
• Elevation of head of the bed to 30 degrees
• Pain relief and sedation
• Normothermia
• Hyperventilation
• Administration of osmotic agents like mannitol,
hypertonic saline, glycerol,
• Use of barbiturates
• Surgical treatment like decompressive
craniectomy and placement of a ventricular drain
in cases of hydrocephalus

74. TREATMENT OF RAISED ICP AND
CEREBRAL OEDEMA
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.

75. Hemorrhagic transformation
• occurs in about 40%.
• Occurs in first 2 weeks.
• 10% of patients worsen.
• Increased risk with antithrombotics,
anticoagulants, and thrombolytic therapy.
• Size (>1/3rd) of the vascular territory and elderly
are more prone for hemorrhagic transformation.
• Managed conservatively with short-term
discontinuation of antithrombotic agents and
careful control of arterial blood pressure.

76. Seizures
• Protect patient from injury during ictus
• Maintain airway
• Benzodiazepines:
– lorazepam (1-2 mg IV)
– diazepam (5-10 mg IV)
• Phenytoin:
– 15 mg/kg loading dose, at 25-50 mg/min infusion with
cardiac monitor
• No need for prophylaxis

77. 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.
• Mortality at 30 days in general compared with
conservative management is not different.

78. MANAGEMENT OF SAH
• Bed rest Analgesic
• Blood pressure control
• TRIPLE – H therapy(hypervolemia , induced
hypertension, hemodilution )
• Oral nimodipine 60mg q6hx21 days
• Angiography for localization of bleeding
• If aneurysm
• Immediate surgical clipping for
• Grade 1-3 patient without contraindication
• Grade 4-5 with intracerebral clot and deterioratio

79. Secondary prevention of stroke
• Management of hypertension (goal <140/85 mm Hg)
• Diabetes control (goal<126 mg/dL)
• Lipid management: Statins (goal cholesterol<200 mg/dL,
LDL<100 mg/dL)
• Anticoagulants: Warfarin (target INR 2 to 3); esp.
recommended in patients with cardioembolic stroke
• Appropriate life style modification (cessation of smoking,
exercise, diet etc)
• Antiplatelet agents:Antiplatelet agents such as
aspirin(300mg) reduce the risk of recurence of all ischaemic
stroke & for patients with TIAs.
• Aspirin is not useful for preventing a first stroke in persons
at low risk (Class III; Level of Evidence A).