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Stroke Hemorragic

stroke henorragic
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0% found this document useful (0 votes)
115 views48 pages

Stroke Hemorragic

stroke henorragic
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd

ACUTE HEMORRHAGE

STROKE

Risa Puista
RS. St. Elisabeth Semarang
2017
STROKE
• Stroke is acute disorders of cerebral
circulation, rapidly developing clinical
signs of focal (at times global) disturbance
of cerebral function, lasting more than 24
hours or leading to death with no apparent
cause other then that of vascular origin
• Two major categories of Stroke:
 Ischemic strokes
 Hemorrhagic strokes
HEMORRHAGIC STROKE
Hemorrhagic strokes, caused when a cerebral
artery ruptures.
O ICH accounts for approximately 10-20% of all
strokes
O 8-15% in western countries like USA, UK and
Australia, and 18-24% in Japan12 and Korea
O A case fatality rate of ICH is approximately
40% at 1 month and 54% at 1 year.
O Only 12% to 39% of patients achieve
longterm functional independence

Journal of Stroke 2017;19(1):3-10 https://doi.org/10.5853/jos.2016.00864


HEMORRHAGIC STROKE

Types of Hemorrhage Stroke :

O Intracerebral Hemorrhagic
hemorrhage into the
parenchyma of the brain

O Subarachnoid Hemorrhagic
Bleeding in the subarachnoid
spaces surrounding the brain
INTRACEREBRAL HEMORRHAGE

O Often a sudden onset of symptoms, with


progression over minutes to hours because of on
going bleeding
O Bleeding within the brain caused by rupture of a
vessel
O Hemorrhage commonly occurs during periods of
activity

5
INTRACEREBRAL HEMORRHAGE

O Brain injury after ICH


O Thrombin and iron, released upon red blood
cell (RBC) lysis, are 2 major factors causing
brain injury after ICH.
O Thrombin at high concentrations kills neurons
and astrocytes in vitro.
O Hemoglobin degradation can result in iron
release. The iron causes marked brain
edema, even in small concentration
INTRACEREBRAL HEMORRHAGE
Causes Of ICH :
O Hypertension (40 - 60 %)
O Aneurysm and AVM ( 10 – 20 %)
O Amyloid Angiopathy ( 5 – 10 % )
O Coagulopathy ( 5 % )
O Tumor ( 2 – 10 % )
O Drug related ( 5 % )
O Hemorrhagic transformation of Ischemic Stroke
( 5 – 7 %)

7
INTRACEREBRAL HEMORRHAGE

Locations of
hypertensive ICH :
O A : Putamen
O B : thalamus
O C : subcortical white
matter
O D : pons
O E : cerebellum

• F :cerebral amyloid angiopathy drug abuse or


vascular anomaly often causes lobar haemorrhage
INTRACEREBRAL HEMORRHAGE

O IVH occurs in ≈45% of patients with


spontaneous ICH and is an independent factor
associated with poor outcome.
O Pooled analysis of 13 studies found IVH in
association with ICH increased the risk of death
from 20% without to 51% with IVH.
O IVH can be primary, confined to the ventricles, or
secondary, originating as an extension of an ICH.
Most IVH is secondary and related to
hypertensive hemorrhages involving the basal
ganglia and thalamus
INTRACEREBRAL HEMORRHAGE

Clinical diagnosis & History of :


Features O Hypertension
O Neurologic deficits O Intake of anticoagulant
O Headache
or antiplatelet
medication
O vomiting
O Smoking
O Decreased levels of O Alkohol/ drug abuse
consciousness O Blood Dyscrasias
O No definite history of
trauma before onset
simptom

10
SUBARACHNOID
HEMORRHAGE
O Intracranial bleeding into
cerebrospinal fluid–filled space
between the arachnoid and pia
mater
O Commonly caused by rupture of
a cerebral aneurysm
O An aneurysm may be saccular or
berry.
O Majority of aneurysms are in the
circle of Willis.
SUBARACHNOID
HEMORRHAGE
SUBARACHNOID HEMORRHAGE
Clinical diagnosis & Features
History of :
O Sudden severe headache
O Intake of anticoagulant or
“Worst headache of one‟s
antiplatelete medication
life”
O Blood dyscrasias
O May or may not associated
with : O Smoking
O Loss of consciousness O Hypertension
O Vomiting O Arteriosclerosis
O Decressed sensorium O No definited history before
O Focal neurologycal deficits onset symptom
O Nuchal rigidity
PREHOSPITAL MANAGEMENT

O Prehospital management for ICH is similar to that for


ischemic stroke
O The primary objective is to provide airway, cardiovascular
support, and transport patient
O Secondary priorities for providers include obtaining a focused
history regarding the timing of symptom onset; information
about medical history, medication, and drug use; and contact
information for family
O the crucial resources necessary to manage patients with ICH
include neurology, neuroradiology, neurosurgery, and critical
care facilities that include adequately trained nurses and
physicians
EMERGENCY DIAGNOSIS AND ASSESMENT

History :
O Time of symptom
O Vascular risk factors
O Hypertension, diabetes, hypercholesterolemia, and
smoking
O Medications
O Anticoagulants, antiplatelet agents, decongestants,
antihypertensive medications, stimulants (including diet
pills), sympathomimetics
O Recent trauma or surgery
O Carotid endarterectomy or carotid stenting in particular, as
ICH may be related to hyperperfusion after such
procedures
EMERGENCY DIAGNOSIS AND ASSESMENT

History
O Dementia (Associated with amyloid angiopathy)
O Alcohol or illicit drug use
O Cocaine and other sympathomimetic drugs are
associated with ICH, stimulants
O Seizures
O Liver disease (May be associated with
coagulopathy)
O Cancer and hematologic disorders. (May be
associated with coagulopathy)
EMERGENCY DIAGNOSIS AND ASSESMENT

Physical Examination
O Vital signs
O Fever is associated with early neurologic deterioration.
O Higher initial blood pressure is associated with early
neurologic deterioration and increased mortality.
O A general physical exam focusing on the head, heart, lungs,
abdomen, and extremities.
O A thorough but time urgent neurologic exam
O A structured exam such as the National Institutes of
Health Stroke Scale (NIHSS) Glasgow Coma Score (GCS),
ICH Score
EMERGENCY DIAGNOSIS AND ASSESMENT

O Serum and Urine Tests


O Complete blood count, electrolytes, blood urea nitrogen and
creatinine, and Glucose
O Prothrombin time (PT) or international normalized ratio (INR) and
an activated partial thromboplastin time (aPTT)
O Warfarin-related hemorrhages are associated with an
increased hematoma volume, greater risk of expansion, and
increased morbidity and mortality
EMERGENCY DIAGNOSIS AND ASSESMENT

O Serum and Urine Tests


O Toxicology screen in young or middle-aged patients to detect
cocaine and other sympathomimetic drugs of abuse
O Urinalysis and urine culture and a pregnancy test in a woman of
childbearing age.
O EKG
To assess for active coronary ischemia or prior cardiac injury
O Chest radiograph
O Neuroimaging
CT or MRI; consider contrast-enhanced or vascular imaging
MEDICAL TREATMENT
O Hemostasis and Coagulopathy, Antiplatelets, and Deep Vein
Thrombosis Prophylaxis
O BP-Lowering Treatment
O Prevention of Secondary Brain Injury
O Glucose Management
O Temperature Management
O Antiseizure Drugs
O Management of Medical Complications

American and Best practice canadian guidelines for stroke management


REVERSING COAGULOPATHIES
O Check Coagulation and platelets
O Correct thrombocytopenia below 100, some references say
below 75.
O If on ASA or clopidogrel, should be held and transfused
platelets
O Warfarin should be stopped and treated with prothrombin
complex concentrate (PCC) (contains factor 2, 7, 9, 10,
protein c and protein s) and Vitamin K 10 mg IV. Fresh-
frozen plasma 2-6 units and Vitamin K could be used as
alternative if PCC is not available

American and Best practice canadian guidelines for stroke management


REVERSING COAGULOPATHIES
O If on heparin best reversed with protamine
sulfate (1.0 to 1.5 mg/1000 U heparin
O Dabigatran reversal may benefit from PCC but
the evidence is weak and efforts should be
directed toward improving renal clearance with
consideration of hemodialysis in emergency
situations.
O Rivaroxaban and apixaban are more likely to
benefit from PCC administration than dabigatran
but are unlikely to benefit from hemodialysis.

F Robert „The role of anticoagulats, antiplatelets, and their reversal strategies in the management of intracerebral
hemorrhage‟ Neurosurg focus 34 (5): 2013
Reversal of Anticoagulation in ICH patients
Patients with a severe coagulation factor deficiency or Class I, Level of
severe thrombocytopenia should receive appropriate Evidence C
factor replacement therapy or platelets, respectively
Patients with ICH whose INR is elevated due to OAC‟s Class I, Level of
should have their warfarin withheld, receive therapy to Evidence C
replace vitamin K-dependent factors and correct the
INR, and receive intravenous vitamin K
PCCs have not shown improved outcome compared Class IIa, Level
with FFP but may have fewer complications compared of Evidence B
with FFP and are reasonable to consider as an
alternative to FFP
The usefulness of platelet transfusions in ICH patients Class IIb, Level
with a history of antiplatelet use is unclear and is of Evidence B
considered investigational

© 2010 American Heart Association, Inc. All rights reserved.


Unauthorized use prohibited.
BLOOD PRESSURE MANAGEMENT

O Elevated BP is very common in acute ICH


because of a variety of factors, including
stress, pain, increased ICP, and premorbid
acute or persistent elevations in BP.
O High SBP is associated with greater
hematoma expansion, neurological
deterioration, and death and dependency
after ICH
BLOOD PRESSURE MANAGEMENT
O Maintain SBP ≤ 180 mmHg or MAP < 130 mmHg
O If SBP is >200 mmHg or MAP is >150 mm Hg, treat the BP
frequent monitoring every 5 minutes.
O If SBP is >180 – 200 mmHg or MAP is >130 - 150 mm Hg
and there is the possibility of elevated ICP, then consider
monitoring ICP and treat BP but keep cerebral perfusion
pressure > 60 mmHg. ( CPP = MAP – ICP)
O If SBP is >180 mmHg or MAP is >130 mm Hg and there is
not evidence of elevated ICP, target modest reduction of BP
of about 160/90 mm Hg or MAP of 110 mm Hg. reexamine
the patient every 15 minutes.

© 2010 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.
BLOOD PRESSURE MANAGEMENT
Drug IV Bolus Infusion
Labetalol 5-20 mg every 15 min 2-8 mg (max 300 mg/d)
Nikardipin - 5-15 mg/h
Esmolol 250 µg/kg loading 25-300 µk/kg/min
dose
Enalapril 0.625 – 5 mg every 6 -
h
Hydralazyne 5-20 mg every 30 min 1.5 – 5 µg/kg/min
Sodium - 0.1 – 10 µg/kg/min
Nitroprusside
Nitroglycerin - 20 – 400 µg/min
BLOOD PRESSURE MANAGEMENT

O Avoid drug that may precipitously drop the


BP and have prolonged effect, such as
sublingual Calcium Chaannel Antagonists.
O Monitor BP and neurologycal status every 15
min during antihypertensive therapy.
Observe for hypotension.
O Treat the BP that substantially lower than
expected (e.g SBP < 90 mmHg)
Blood Pressure Recommendations
Until ongoing clinical trials of BP intervention Class IIb, Level
for ICH are completed, physicians must of Evidence C
manage BP on the basis of the present
incomplete efficacy evidence.

In patients presenting with a systolic BP of 150- Class IIa, Level


220 mmHg, acute lowering of systolic BP to of Evidence B
140 mmHg is probably safe

© 2010 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.
Inpatient Management:
Medical Considerations
Initial monitoring and management of ICH patients Class I, Level of
should take place in an intensive care unit with Evidence B
physician and nursing neuroscience intensive care
expertise
Glucose should be monitored and normoglycemia is Class I, level of
recommended Evidence
Patients with ICH should have intermittent pneumatic Class I, Level of
compression for prevention of venous Evidence B
thromboembolism in addition to elastic stockings
After documentation of cessation of bleeding, low- Class IIb, Level
dose subcutaneous low-molecular-weight heparin or of Evidence B
unfractionated heparin may be considered for
prevention of venous thromboembolism in patients
with lack of mobility after 1 to 4 days from onset

© 2010 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.
Inpatient Management of Prevention of Secondary
Brain Injury: Medical Considerations
Seizures and Antiepileptic Drugs
Clinical seizures should be treated with Class I, Level of
anti-epileptic drugs Evidence A (

Continuous EEG monitoring is probably Class IIa, Level of


indicated in ICH patients with depressed Evidence B
mental status out of proportion to the
degree of brain injury
Patients with a change in mental status Class I, Level of
who are found to have electrographic Evidence C
seizures on EEG should be treated with
anti-epileptic drugs
Prophylactic anticonvulsant medication Class III, Level of
should not be used Evidence B

© 2010 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.
Intracranial Pressure control
O Elevate the HOB to 30 degrees
O Analgesia and sedation, particularly in unstable, intubated
patients
O ICP monitor should be considered for patients with GCS <8,
those with clinical evidence of transtentorial herniation, or
those with significant IVH or hydrocephalus.
O Osmotic diuretics (eg, mannitol and hypertonic saline
solution)
O neuromuscular blockade
O Goal of maintaining cerebral perfusion pressure (CPP) of 50
to 70 mmHg

American and Best practice canadian guidelines for stroke


management
Intracranial Pressure control
O 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.
O Glucocorticoids should not generally be
used to lower the ICP in patients with ICH.
No improvement in outcome

American and Best practice canadian guidelines for stroke


management
ICP Monitoring and Ventriculostomy
Patients with a GCS score of 8 or less, those with clinical Class IIb, Level
evidence of transtentorial herniation, or those with of Evidence C
significant IVH or hydrocephalus might be considered for
ICP monitoring and treatment. A CPP of 50-70 mmHg
may be reasonable to maintain depending on the status
of cerebral autoregulation
Ventricular drainage as treatment for hydrocephalus is Class IIa, Level
reasonable in patients with decreased level of of Evidence B
consciousness
Although intraventricular administration of rt-PA in IVH Class IIb, Level
appears to have a fairly low complication rate, efficacy of Evidence B
and safety of this treatment is uncertain and is
considered investigational

© 2010 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.
SUBARACHNOID HEMORRHAGE
MANAGEMENT
O Stop antiplatelete or anticoagulation treatment. Reverse the
antithrombotic effect and correct coagulopathy if necessary.
O Assses Clinical severity SAH (GCS, Hunt & Hess grading)
O Reduce risk of rebleeding
O Complete bed rest
O Analgesia, mild sedation
O Maintan MAP < 110 mmHg
O Prophylatic anticonvulsant
O Prevent vasospasm and/or infarction
O Serial TCD
O Maintain normovolumia, normothermia, normal oxygenation
O Start nimodipine 60 mg every 4 h orally
SUBARACHNOID HEMORRHAGE
MANAGEMENT
O Suspect symptomatic Vasospasm :
O Transfer patient to the ICU
O Insert Swan Ganz catheter & arterial line
O Start Triple H (Hypertension, Hypervolemia,
Hemodilution) therapy
O Monitor the neurological status,
O cardiopulmonary status,
O electrolyte,
O osmolality
O status of vasospasm (by daily TCD)
Surgical Recommendations
For patients presenting with lobar clots >30 cc and Class IIb, Level
within 1 cm of the surface, evacuation of supratentorial of Evidence B
ICH by standard craniotomy might be considered

The effectiveness of minimally invasive clot evacuation Class IIb, Level


utilizing either stereotactic or endoscopic aspiration with of Evidence B
or without thrombolytic usage is uncertain and is
considered investigational
While theoretically attractive, no clear evidence at Class III, Level of
present indicates that ultra-early removal of Evidence B
supratentorial ICH improves functional outcome or
mortality rate. Very early craniotomy may be harmful due
to increased risk of recurrent bleeding

© 2010 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited.
ICH : Surgical Indications
O GCS < 13
O Clinical evidence of neurological deterioration
O Brain CT Scan :
O Supratentorial ICH :
O Hematoma volume > 30 ml
O Intraventricular extension of hemorrhage
O Hydrocephalus
OMidline shift
O Infratentorial ICH
O Cerebellar hematoma > 3 cm in diameter
O Brain stem compression
O Obstructive Hydrocephalus
Surgical Recommendations
For most patients with ICH, the usefulness of Class IIb, Level
surgery is uncertain of Evidence
Patients with cerebellar hemorrhage who are Class I, Level of
deteriorating neurologically or who have brain Evidence B
stem compression and/or hydrocephalus from
ventricular obstruction should undergo surgical
removal of the hemorrhage as soon as possible
Initial treatment of these cerebellar hemorrhage Class III, Level
patients with ventricular drainage alone rather of Evidence C).
than surgical evacuation is not recommended

© 2010 American Heart Association, Inc. All rights


reserved. Unauthorized use prohibited.
Surgical and Endovascular
Management of SAH
O Occluding aneurysms using endovascular coils was
described in 1991
O Improved outcomes have been linked to hospitals that
provide endovascular services
O Use of endovascular versus surgical techniques varies
greatly across centers
O Coil embolization is associated with a 2.4% risk of
aneurysmal perforation and an 8.5% risk of ischemic
complications

7/13/2017© 2009, American Heart Association. All rights reserved.


Surgical and Endovascular
Management of SAH
O Combined morbidity and mortality was significantly
greater in surgically treated patients than in those
treated with endovascular techniques (30.9% vs.
23.5%; absolute risk reduction 7.4%, P = 0.0001)
O During the short follow-up period in ISAT the re-
bleeding rate for coiling was 2.9% versus 0.9% for
surgery
O There have been no randomized comparisons of
coiling versus clipping for unruptured aneurysms

7/13/2017© 2009, American Heart Association. All rights reserved.


The ED
algorithm for
early
diagnosis
and
emergent
intervention.

Cyrus K Dastur, and Wengui Yu Stroke Vasc Neurol 2017;svn-2016-000047


References
O J. Claude Hemphill III, MD, MAS, FAHA, Steven M. Greenberg,
MD, PhD, Craig S. Anderson, MD, PhD:Guidelines for the
Management of Spontaneous Intracerebral Hemorrhage.
Stroke. 2015;46:000-000 available at
http://stroke.ahajournals.org
O Ya Hua, “Intracerebral hemorrhage: introduction brain injury
afteriIntracerebral hemorrhage, ther role of Thrombin and Iron”
Stroke.2007; 38: 759-762
O Cyrus K Dastur, and Wengui Yu Stroke Vasc Neurol 2017;svn-
2016-000047
O Sang Joon An, Tae Jung Kim, Byung-Woo Yoon Epidemiology
and Risk Factors of ICH Journal of Stroke 2017;19(1):3-10
available at https://doi.org/10.5853/jos.2016.00864
TERIMA KASIH
Definition of Classes and Levels of Evidence Used in AHA Stroke
Council Recommendations
C lass I C onditions for which there is evidence for and/or general
agreement that the procedure or treatment is useful and effective.
C lass II C onditions for which there is conflicting evidence and/or a
divergence of opinion about the usefulness/efficacy of a procedure
or treatment.
C lass IIa The w eight of evidence or opinion is in favor of the procedure or
treatment.

C lass IIb Usefulness/efficacy is less well established by


evidence or opinion.
C lass III C onditions 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.

Therapeutic recommendations
Level of Evidence A Data derived from multiple randomized clinical trials or
metaanalyses
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 one or more
case-control studies, or studies using a reference
standard applied by an unmasked evaluator
Level of Evidence C Consensus opinion of experts
Glasgow Coma Scale
Eye Opening Best Motor Best Verbal

4 spontaneous 6 obeys commands 5 oriented

3 to speech 5 localizes pain 4 confused

2 to pain 4 withdraws to pain 3 inappropriate

1 none 3 abnl flexion to pain 2 incomprehensible

2 extension to pain 1 none

1 none
Hunt and Hess Scale
O Grade I: asymptomatic; or minimal
headache and slight nuchal rigidity
O Grade II: moderate-to-severe headache;
nuchal rigidity; no neuro deficit except cranial
nerve palsy
O Grade III: drowsiness; minimal neurologycal
deficit
O Grade IV: stupor; moderate-to-severe
hemiparesis ; possibly early decerebrate rigidity
and vegetative disturbances
O Grade V: deep coma; decerebrate rigidity
World Federation
Fischer grading
Neurosurgeons

How are SAH graded?


GCS 15, only CN Grade 1 No blood
deficit if any
GCS 13-14, no Grade 2 Diffuse blood, no
deficit clots & <1mm

GCS 13-14, with Grade 3 Clots & blood 1mm


deficit or more
GCS 7-12, +/- Grade 4 ICH or
deficit intraventricular
clots
GCS 3-6 +/- deficit Grade 5
ICH Score
Component ICH score points
GCS
3-4 2
5 - 12 1
13 - 15 0
ICH volume
≥ 30 ml 1
≤ 30 ml 0
IVH
yes 1
no 0
Infratentorial 1
Age > 80 1

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