Hemorrhagic stroke management Dr Ganesh.pptx

MANAGEMENT OF HEMORRHAGIC STROKE
Dr Ganeshgouda Majigoudra
Consultant Neurologist
Nanjappa Hospitals Davanagere
ganeshgoudam4@gmail.com
9380906082

INTRODUCTION
• ICH is a medical emergency
• More than 20% of patients will experience a decrease in the Glasgow Coma
Scale (GCS) of 2 or more points between the prehospital emergency medical
services (EMS) assessment and the initial evaluation in the emergency
department .
• Furthermore, another 15% to 23% of patients demonstrate continued
deterioration within the first hours after hospital arrival.

INTRODUCTION
• Spontaneous ICH is defined as intraparenchymal bleeding in the absence of
trauma or surgery.
• Spontaneous ICH can be classified as either primary or secondary depending
on the underlying cause.
• Primary ICH accounts for ∼70–80% of cases and is due to spontaneous rupture
of small vessels damaged by HTN or amyloid angiopathy.
• Secondary ICH is associated with a number of congenital and acquired
conditions such as vascular malformations, tumours, coagulation disorders, use
of anticoagulants and thrombolytic agents, cerebral vasculitis, drug abuse and
cerebral venous thrombosis.

Greenberg, S. M. 2022 AHA/ASA . Guideline for the Management of Patients with Spontaneous Intracerebral Hemorrhage. Circulation.
ICH Etiology Determines Hemorrhage Location
Deep/Posterior Fossa ICH
Etiologies
Arteriolosclerosis
• Penetrating arteriole lipohyalinosis due to
HTN, DM, Age
Macrovascular
• AVM
• Aneurysm
• Dural AVF
• Cavernous Malformation/Cavernoma
• Cerebral Venous Thrombosis
Lobar ICH Etiologies
Cerebral Amyloid Angiopathy
• Amyloid deposition in vessel walls
Arteriolosclerosis
Macrovascular
Diagnostic Reasoning: CAA typically causes only lobar (or superficial cerebellar)
hemorrhages. Arteriolosclerosis may cause both deep and lobar hemorrhages. Coexistent
pathology is possible.
Abbreviations: AVF indicates arteriovenous fistula; AVM, arteriovenous malformation; CAA, cerebral amyloid angiopathy; DM, diabetes mellitus; HTN, hypertension; and ICH, intracerebral hemorrhage.
5

MECHANISMS OF BRAIN INJURY AFTER ICH

Mechanisms of ICH Injury
8
Hematoma
Expansion
↑ ICP
Hydrocephalus
Herniation
0 - 6 hours
Primary Injury
>6 hours
Secondary Injury
Cerebral Edema
Inflammation
Toxicity from Blood Products
General Principle: Acute ICH management targets these mechanisms.
Abbreviations: ICH indicates intracerebral hemorrhage; and ICP, intracranial pressure.

Diagnosis & Assessment | Work-Up for Acute ICH Course
Time of
symptom onset
• Headache
• Focal neurologic
deficits
• Seizures
• Decreased level
of consciousness
• Ischemic Stroke
• Prior ICH
• Hypertension
• Hyperlipidemia
• Diabetes mellitus
• Metabolic syndrome
• Imaging biomarkers
o Cerebral microbleeds
• Antithrombotics:
• Anticoagulants,
thrombolytics,
antiplatelet agents,
NSAIDS
• Vasoconstrictive
Agents:
o Triptans, SSRIs,
decongestants,
stimulants, phentermine,
sympathomimetic drugs
• Antihypertensives:
• Estrogen-containing
oral contraceptives
Associated with
(but not specific
for) amyloid
angiopathy
• Smoking
• Alcohol use
• Marijuana
• Sympathomimetic
drugs
• Amphetamines,
methamphetamines
, cocaine
May be associated
with coagulopathy
9
History
Time Symptoms Vascular
Risk Factors
Medications Cognitive
Impairment or
Dementia
Substance Use Liver disease,
Uremia,
Malignancy and
Hematologic
disorders
Abbreviations: ICH indicates intracerebral hemorrhage; NSAIDS, non-steroidal anti-inflammatory drugs,
and SSRI, selective serotonin reuptake inhibitors.

Diagnosis & Assessment | Work-Up in Acute ICH
Physical Examination
• Airway, Breathing & Circulation
• Vital signs
• General: Focused on the head,
heart, lungs, abdomen, and
extremities
• Focused Neurological Exam
(NIHSS, GCS)
Serum
• CBC
• BUN and Creatinine
• LFTs
• Glucose
• Inflammatory markers
• (ESR and/or CRP)
• PT (with INR)
• aPTT
• Specific tests for DOACs
Urine
• Urine toxicology screen
• Pregnancy test
Cardiac-specific
• Troponin
• ECG
Abbreviations: aPTT indicates activated partial thromboplastin time; BUN, blood urea nitrogen; CRP, C-reactive protein; DOAC, direct oral anticoagulant; ECG, electrocardiogram; ESR, erythrocyte sedimentation rate; GCS,
Glasgow coma scale; ICH, intracerebral hemorrhage; INR, international normalized ratio; LFTs, liver function tests; NIHSS, National Institutes of Health Stroke Scale; and PT, prothrombin time.
10

Diagnosis & Assessment | Work-Up in Acute ICH
Indicators of Increased Morbidity & Mortality:
• Thrombocytopenia
• Acute Kidney Injury
• Hyperglycemia
• Elevated troponin
Indicators of Increased HE:
• Anemia
• Anticoagulant-related
hemorrhages
• Identification of a spot
sign on CTA or contrast-
enhanced OR certain
imaging features on
NCCT such as
heterogeneous densities
within the hematoma or
irregularities at its
margins.
Abbreviations: CTA indicates computed tomography angiography; HE, hematoma expansion; ICH, intracerebral hemorrhage; and NCCT, noncontrast computed tomography .
11

EMERGENCY MANAGEMENT
• Stabilisation of airway, breathing and circulation (ABCs) is essential for
preventing secondary injury from hypoxaemia, HTN and haematoma
expansion.
• Intubation for airway protection is indicated in patient with GCS ≤8 or
significant respiratory distress.
• Monitoring of vital signs and neurological status.
• A baseline severity score should be performed as part of the initial evaluation
of patients with ICH (Class I; Level of Evidence B).
• A brief clinical history regarding time of onset of stroke, medical and drugs
history, recent surgery and routine blood investigations including a
coagulation profile to be send.

EMERGENCY TREATMENT
• A baseline severity score should be performed as part of the initial evaluation
of patients with ICH (Class I; Level of Evidence B).
• Standardized neurological assessment using NIHSS (baseline) or GCS if the
patient is comatose or obtunded.
• ICH score is to be calculated to see the prognosis of the patient.

NEUROIMAGING
• Rapid neuroimaging with CT or MRI is recommended to distinguish ischemic stroke from
ICH (Class I; Level of Evidence A).
• CTA and contrast-enhanced CT may be considered to help identify patients at risk for
hematoma expansion (Class IIb; Level of Evidence B).
• NCCT head and CTA( POINTS TO BE NOTED)
Location: Suratentorial /infratentorial bleed
Calculate volume of bleed
Presence of IVH
Any signs of mass effect, hydrocephalus or herniation.
Spot sign
Etiology of ICH

Calculating Volume in ICH
• Definitions:
• A = the largest cross-sectional
diameter (in cm to the nearest 0.5
cm)
• B = the largest diameter 900 to A
on the same slice(in cm to the
nearest 0.5 cm)
• C = the approximate number of 10
mm slices on which the ICH is
seen
• ABC/2 = added to approximate the
volume of an ellipsoid

Calculating Volume in ICH
• How to Calculate C
• C: if haemorrhage area > 75% of the haemorrhage on the index slice count as 1
• C: if haemorrhage area approximately 25-75% of haemorrhage on index slice count
as 0.5
• C: if haemorrhage area approximately < 25% of haemorrhage on index slice don't
count
• C: add the "haemorrhage slice values“
• if 5mm slices are used divide by 2
• OR C = number of slides ×SLICE THICKNESS IN CENTIMETERS
• 1 if the slice thickness is 10mm or 1 cm
• 0.5 if the slice thickness is 5mm or 0.5cm
• ABC/2 gives the ICH volume in cubic centimeters

SPOT SIGN
• Spot sign: foci of enhancement
seen within the hematoma on CTA.
• Clinical implication:
Identification of contrast
extravasation and the spot sign are
potent and independent predictors of
hematoma expansion
SPOT SIGN ON CTA BRAIN

NEUROIMAGING
When to suspect underlying vascular abnormality in ICH on neuroimaging????
• Presence of subarachnoid hemorrhage
• Enlarged vessels or calcifications along the margins of the ICH
• Hyperattenuation within a dural venous sinus or cortical vein along the
presumed venous drainage path
• Inusual hematoma shape
• Presence of edema out of proportion to the time of presumed ICH,
• An unusual hemorrhage location, and
• The presence of other abnormal structures in the brain (like a mass).

DIFFERENTIATING ANTICOAGULANT INDUCED
VERSUS SPONTANEOUS ICH
• The presence of a blood-fluid
level on an acute CT scan is
specific for anticoagulant
treatment induced ICH.
BLOOF FLUID LEVEL ON NCCT HEAD IN OAC INDUCED ICH

MANAGEMENT OF HEMATOMA
EXPANSION
BP
MANAGEMENT CORRECTION OF
COAGULOPATHY
MANAGEMENT
OF RAISED ICP

Management of Increased BP
AHA RECOMMENDATION FOR BP TARGET FOR ACUTE ICH:
• For ICH patients presenting with SBP between 150 and 220 mm Hg and
without contraindication to acute BP treatment, acute lowering of SBP to 140
mm Hg is safe (Class I; Level of Evidence A).
• For ICH patients presenting with SBP >220 mm Hg, it may be reasonable to
consider aggressive reduction of BP with a continuous intravenous infusion
and frequent BP monitoring (Class IIb; Level of Evidence C).

INTRAVENOUS AGENTS FOR ACUTE ICH
Note: Nitroprusside is not recommended for acute ICH because of its tendency to increase intracranial pressure

RECENT TRIALS FOR BP MANAGEMENT
• INTENSIVE BLOOD PRESSURE REDUCTION IN ACUTE CEREBRAL
HEMORRHAGE TRIAL(INTERACT)
• 404 Chinese patients assessed, treated, and monitored within 6 hours of the onset of
ICH
• 203 patients  treated with locally available intravenous BP-lowering agents to
target SBP of 140mmHg, within 1 hour and maintained for at least the next 24 hours
• 201 patients  more modest SBP target of 180 mm Hg (as per AHA1999)
• Trend toward lower relative and absolute growth in hematoma volumes from
baseline to 24 hours in the intensive treatment group compared with the control
group
• NO EXCESS OF NEUROLOGICAL DETERIORATION OR OTHER ADVERSE
EVENTS RELATED TO INTENSIVE BP LOWERING

RECENT TRIALS FOR BP MANAGEMENT
• Antihypertensive Treatment in Acute Cerebral Hemorrhage (ATACH) trial
• Nonrandomized, open-label, uncontrolled, single-group assignment, safety study.
• evaluate the feasibility and safety of lowering BP, using Nicardipine in patients who have
acute hypertension following acute ICH.
• All patients were treated with IV Nicardipine in a stepwise fashion, with successive
systolic BP goals of 170 mm Hg to 200 mm Hg, 140 mm Hg to 170 mm Hg, and 110 mm
Hg to 140 mm Hg.
• The observed proportions of neurologic deterioration and serious adverse events were
below the prespecified safety thresholds, and the 3-month mortality rate was lower than
expected in all systolic blood pressure tiers.

INTENSIVE BLOOD PRESSURE REDUCTION IN ACUTE CEREBRAL HEMORRHAGE
TRIAL(INTERACT2)
• The largest randomized clinical trial evaluating the efficacy of intensive BP
lowering, a phase 3 trial undertaken in 2839 patients with SBP between 150 and 220
mm Hg within 6 hours of ICH.
• INTERACT2 study found better outcomes if blood pressure was < 140
Reduction in Death and disability
Better functional recovery
• Current AHA guidelines suggest SBP< 140 as guideline for acute ICH.(based on
INTERACT2 trial)

RCTs comparing aggressive vs standard
management of BP

Medical and Neurointensive Treatment for ICH
Acute Blood Pressure Lowering in Spontaneous ICH
To improve functional outcomes.
Medication titration to ensure continuous smooth & sustained control of BP, avoiding peaks
and large variability in SBP, can be beneficial. (2a)
Initiating tx within 2 hrs of ICH onset and reaching target within 1-hr can be beneficial to
reduce the risk of HE. (2a)
In ICH of mild to moderate severity presenting with SBP between 150 and 220 mmHg, acute lowering of
SBP to a target of 140 mmHg with the goal of maintaining in the range of 130 to 150 mmHg is safe and
may be reasonable. (2b)
If presenting with large or severe ICH or those requiring surgical decompression, the safety and efficacy
of intensive BP lowering are not well established. (2b)
If ICH is mild to moderate severity presenting with SBP >150 mmHg, acute lowering of SBP
to hrs. <130 mmHg is potentially harmful. (3:Harm)
Abbreviations: HE indicates hematoma expansion; ICH, intracerebral hemorrhage; mmHg, millimeters of mercury; SBP, systolic blood pressure; and tx, treatment.
33

REVERSAL OF COAGULOPATHIES
• Whenever ICH is diagnosed, any antithrombotic agent should be immediately
discontinued.
• The method of reversal will depend on the agent used.

VKA(Vitamin K Antagonist) induced ICH
• Administration of intravenous vitamin K in a dose of 5 to 10 mg and 3-factor
or 4-factor prothrombin complex concentrates (PCCs) should be administered
intravenously for patients with INR ≥1.4. (Class I; Level of Evidence C).
• If repeat INR 15–60 min after PCC administration shows continued INR
elevation above 1.4, consider further correction with 2–4 units FFP.
• PCCs may have fewer complications and correct the INR more rapidly than FFP
and might be considered over FFP (Class IIb; Level of Evidence B).
• rFVIIa is not recommended for VKA reversal in ICH (Class III; Level of
Evidence C).

rtPA induced ICH
• For thrombolytic (eg, recombinant tissue plasminogen activator (rtPA))
reversal:
• 10 units of cryoprecipitate may be considered.
• If the level of fibrinogen is <150 mg/dL post cryoprecipitate use, consider
additional cryoprecipitate administration.
• If cryoprecipitate is contraindicated or unavailable, an antifibrinolytic agent
(tranexamic acid 10–15 mg/kg intravenous or ε-aminocaproic acid 4–5 g
intravenous) can be considered.

ANTIPLALELETS INDUCED BLEEDING
• For patients taking antiplatelet agents (eg, aspirin, clopidogrel and abciximab),
platelet transfusion is not recommended routinely, regardless of antiplatelet
agent, platelet function testing, haemorrhage volume or neurological
examination.
• Platelet transfusion should be considered for patients with aspirin- or adenosine
diphosphate receptor (ADP) inhibitor-associated ICH who will undergo a
neurosurgical procedure.
• If platelet function is within normal limits or patient has documented
antiplatelet resistance, platelet transfusion should be avoided.
• Platelet transfusion is not recommended for non-steroidal anti-inflammatory
drugs (NSAIDs) or glycoprotein (GP) IIb/IIA inhibitor-related ICH.

Hemostasis & Coagulopathy
Antiplatelet-Related Hemorrhage in Spontaneous ICH
If the patient is being treated
with aspirin, platelet
transfusion might be
considered to reduce
postoperative bleeding and
mortality.
(2b)
If the patient is being
treated with ASA,
platelet transfusions
are potentially harmful
and should not be
administered.
(3:Harm)
Does the
patient require
emergent
neurosurgery?
Patients with Spontaneous ICH
YES
NO
Abbreviations: ASA indicates aspirin; and ICH, intracerebral hemorrhage.
40
If the patient is being treated
with antiplatelet agents, the
effectiveness of desmopressin
with or without platelet
transfusions to reduce the
expansion of the hematoma is
uncertain.
(2b)

STEPWISE APPROACH TO TREATMENT OF
ELEVATED ICP
1. Insert ICP monitor: ventriculostomy vs parenchymal device.
Indications of ICP monitoring:
• Primarily neurologic disease with high risk of secondary brain injury
• Large supratentorial bleed with midline shift
• Hydrocephalus in SAH, intraventricular hemorrhage or posterior fossa stroke.
2. General Goal: maintain ICP<20 mm of hg and CPP> 60 mm of Hg.
CPP (Cerebral Perfusion Pressure)= MAP(mean arterial pressure)-ICP(intracranial pressure)

ELEVATED ICP
• For ICP > 20-25 mm of Hg for > 5 minutes:
1. Elevate the head end of the bed.
2. Drain CSF via ventriculostomy (if in place)
3. Osmotherapy :
Mannitol is used for 24 to 48 h, with an initial intravenous dose of 1 to 1.5
g/kg, followed by boluses of 0.25 to 1 g/kg, most often every 4 to 6 h (the
target serum osmolarity is 300 to 320mOsm/L).
HTS( Hypertonic Saline) should be administered via central line as
continuous infusion (3%) or 30 ml bolus (23.4%) (serum sodium level at 140–
150 mEq/L).

ELEVATED ICP
4. Glucocorticoids: are to be avoided in hemorrhagic strokes.
5. Intubate and mechanical ventilation: sedation with propofol, midazolam aqnd
add neuromuscular paralysis.
6. Hyperventilation : to PaCO2 30-35 mmHg.
7. Pressor therapy: dopamine, norepinephrine to maintain adequate MAP to
ensure CPP> 60 mm Hg( maintain euvolemia to avoid deleterious effects of
pressors).
8. Second tier therapies for refractory elevated ICP:
Decompressive hemiocraniectomy
Pentobarbitone coma

MANAGEMENT OF PERIHEMATOMA OEDEMA
• Patients with asymptomatic PHE require no specific treatment except
maintaining a normal sodium goal.
• Mannitol and HTS are the first-line medical therapies for patients with
symptomatic cerebral oedema and elevated ICP.
• Patients with large ICH (volume > 30 ml) or symptomatic peri haematoma
oedema, it may be beneficial to keep serum sodium level at 140–150 mEq/L
for 7–10 days to minimise oedema expansion and mass effect.
• Mannitol and HTS can be used emergently for worsening cerebral oedema,
elevated intracranial pressure (ICP) or pending herniation.

CONSIDERATION FOR SURGICAL
INTERVENTION

SURGICAL MANAGEMENT IN ICH
International Trial in Intracerebral Hemorrhage (STITCH).
• Aim: STICH was undertaken to determine whether early surgery reduces mortality and
improves neurological outcome compared with conservative management for
supratentorial ICH.
• In this trial, 1033 patients were randomized to early surgery (<24 hours of randomization)
or initial conservative treatment.
• A favorable outcome on the 8-point extended Glasgow Outcome Scale at 6 months was
used as the primary end point.
• STICH found no overall statistically significant difference in mortality or functional
outcome between treatment groups.
• Subgroup analysis suggested that patients with lobar hemorrhages within 1 cm of the
cortical surface might benefit from surgery.
• Additional subgroup analysis suggested that the risk for a poor outcome was increased for
patients who presented as comatose (GCS score ≤8).

SURGICAL MANAGEMENT IN ICH
• STICH II trial was undertaken to address the question of whether early surgery would be
beneficial for
conscious patients(GCS>8)
superficial lobar hemorrhage of 10 to 100 mm3 within 1 cm of the cortical surface and
without IVH
who were admitted within 48 hours of ictus??
• Conclusion: 41% of patients in the early surgery group had a favorable outcome compared with
38% in the medical arm; this difference was not statistically significant.
• For most patients with supratentorial ICH, the usefulness of surgery is not well established (Class
IIb; Level of Evidence A).
• Supratentorial hematoma evacuation in deteriorating patients might be considered as a life-saving
measure (Class IIb; Level of Evidence C).

Surgical Interventions
Minimally Invasive Surgical Evacuation of ICH
Intervention
Patient Selection
MIS for ICH
Supratentorial ICH, hematoma volume
>20-30 mL, GCS 5-12
MIS ± hematoma
thrombolysis to improve
mortality can be useful (2a)
MIS ± hematoma
thrombolysis to improve
functional outcome is of
uncertain effectiveness (2b)
Choosing MIS rather than
craniotomy to improve
functional outcomes may be
reasonable
(2b)
Supratentorial ICH, hematoma volume >20-30 mL, GCS 5-12
Abbreviations: GCS indicates Glasgow Coma Scale; ICH, intracerebral hemorrhage; and MIS, minimally invasive surgery.
48

Craniotomy for Supratentorial Hemorrhage
Supratentorial ICH of moderate or greater severity*
Craniotomy for hemorrhage
evacuation to improve mortality or
functional outcomes is of uncertain
usefulness
(2b)
Craniotomy for hemorrhage
evacuation may be considered as a
life-saving measure in patients who
are deteriorating
(2b)
Note: * >10 cc with a significant neurologic deficit
Abbreviations: ICH indicates intracerebral hemorrhage.
49

Craniotomy for Posterior Fossa Hemorrhage
• Patients with cerebellar haemorrhage who are
deteriorating neurologically or
who have brainstem compression and/or
hydrocephalus from ventricular obstruction
should undergo surgical removal of the haemorrhage as soon as possible (Class I; Level
of Evidence B).
• Initial treatment of these patients with ventricular drainage rather than surgical
evacuation is not recommended (Class III; Level of Evidence C).

DECOMPRESSIVE CRANIECTOMY FOR ICH
Decompressive Craniectomy with or without hematoma evacuation might
reduce mortality for patients with supratentorial ICH
• who are in a coma(GCS<8)
• have large hematomas with significant midline shift, or
• have elevated ICP refractory to medical management
(Class IIb; Level of Evidence C).

MEDICAL VERSUS SURGICAL IN ICH
MEDICAL
• Minimally symptomatic (GCS >10)
• Hemorrhage in the brainstem
• Little chance of good outcome
High ICH score
dominant hemisphere
GCS< 5
Age over 75
• Basal Ganglia or thalamus: surgery is
no better than medical management
SURGICAL
• Lesions with MLS, herniation
• brainstem compression
• Volume: moderate (10-30cc)
• Favorable location
lobar
cerebellar* (class I level B)
• Young patient

Management of intraventricular haemorrhage and
hydrocephalus
• IVH is associated with lower GCS and an independent predictor of poor outcome.
• External ventricular drain (EVD) placement should be considered in any patient with GCS
≤ 8, significant IVH, presence of hydrocephalus or evidence of transtentorial herniation.
AHA recommendation:
• Patients with a GCS score of ≤8, those with clinical evidence of transtentorial herniation,
or those with significant IVH or hydrocephalus might be considered for ICP monitoring
and treatment.
• A CPP of 50 to 70 mm Hg may be reasonable to maintain depending on the status of
cerebral autoregulation (Class IIb; Level of Evidence C).
• Ventricular drainage as treatment for hydrocephalus is reasonable, especially in patients
with decreased level of consciousness (Class IIa; Level of Evidence B).

Minimally Invasive Surgical Evacuation of Intraventricular Hemorrhage
IVH
Surgical Management
Spontaneous IVH +
Obstructive Hydrocephalus
Spontaneous ICH < 30 mL
GCS >3
IVH requiring EVD
Spontaneous ICH <30 mL
IVH requiring EVD
EVD EVD + thrombolytic
Neuroendoscopy
+ EVD
+/- thrombolytic
Functional
Outcome
Benefit
(2b*)
Mortality
Reduction
(I)
Functional
Outcome
Benefit
(2b†)
Functional
Outcome
Benefit
(2b†)
Reduced
Permanent
Shunt
Dependence
(2b†)
Note: *Not well established. †Uncertain
Abbreviations: EVD indicates external ventricular drain; GCS, Glasgow coma scale; ICH, Intracerebral hemorrhage, and IVH, intraventricular hemorrhage.
54
Mortality
Reduction
(2a)

PREVENTION OF SECONDARY BRAIN INJURY
Glucose management:
• Tight glucose control with target glucose 80–110 mg/dL increases
hypoglycaemia and the risk of morbidity and mortality.
• It is reasonable to target glucose level at 100–150 mg/dL for patients with
ICH.
• Glucose should be monitored. Both hyperglycemia and hypoglycemia
should be avoided (Class I; Level of Evidence C).
Temperature control:
• Therapeutic hypothermia and normothemia has no effect.
• Treatment of fever after ICH may be reasonable.

PREVENTION OF SECONDARY BRAIN INJURY
SEIZURES AND AED IN ICH:
• Clinical seizures should be treated with antiseizure drugs (Class I; Level of
Evidence A).
• Patients with a change in mental status who are found to have electrographic
seizures on EEG should be treated with antiseizure drugs (Class I; Level of
Evidence C).
• Continuous EEG monitoring is probably indicated in ICH patients with
depressed mental status that is out of proportion to the degree of brain injury
(Class IIa; Level of Evidence C).
• Prophylactic antiseizure medication is not recommended (Class III; Level
of Evidence B).

Seizures and Antiseizure Drugs
New onset seizures in sICH are relatively common (2.8-28%) and occur within the first 24 hrs of hemorrhage
Confirmed clinical or electrographic
seizures
Administer ASD
(1)
sICH patients without suspicion of
seizure
Unexplained abnormal or fluctuating mental
status, or suspicious of seizures, cEEG is
reasonable to
diagnose electrographic seizures and
epileptiform discharges
(24 hours or longer)
(2a)
Avoid ASD
(3: No Benefit)
Abbreviation: ASD indicates antiseizure drugs; cEEG, continuous electroencephalography; hrs, hours; and sICH, spontaneous intracerebral hemorrhage.
57

DVT PROPHYLAXIS AND MANAGEMENT
• Patients with ICH should have intermittent pneumatic compression for
prevention of venous thromboembolism beginning the day of hospital admission
(Class I; Level of Evidence A).
• After documentation of cessation of bleeding, low dose subcutaneous LMWH
may be considered for prevention of venous thromboembolism in patients with
lack of mobility after 1 to 4 days from onset (Class IIb; Level of Evidence B).

Prophylaxis
… , intermittent pneumatic compression starting on the day of diagnosis is recommended for VTE (DVT and PE)
prophylaxis. (1)
… low-dose UFH or LMWH can be useful to reduce risk of PE (2a)
… temporary use of retrievable filter as bridge until anticoagulation initiated. (2a)
… low-dose UFH or LMWH prophylaxis at 24 to 48 hrs from ICH onset may be reasonable to optimize the benefits of
preventing thrombosis relative to the risk of HE. 2b)
… graduated compression stockings of knee-high or thigh-high length alone are not beneficial for VTE prophylaxis. (3: No
Benefit)
Treatment
… and proximal DVT who are not yet candidates for anticoagulation, temporary use of retrievable filter is reasonable as a
bridge until anticoagulation initiated. (2a)
… and proximal DVT or PE, delaying treatment with UFH or LMWH 1 to 2 weeks after onset of ICH might be considered.
(2b)
Inpatient Care Checklist
In Non-Ambulatory Spontaneous ICH…
Thromboprophylaxis & Tx of Thrombosis
Abbreviations: DVT indicates deep vein thrombosis; HE, hematoma expansion; hrs, hours; ICH, intracerebral hemorrhage; LMWH, low molecular weight heparin;
PE, pulmonary embolism; Tx, treatment; UFH, unfractionated heparin; and VTE, venous thromboembolism.
59

PREVENTION OF RECURRENT ICH
• RISK FACTORS TO BE CONSIDERED FOR RECURRENT ICH
1. lobar location of the initial ICH
2. Older age
3. presence and number of microbleeds on gradient echo MRI
4. ongoing anticoagulation
5. presence of apolipoprotein E ε2 or ε4 alleles

BP management
• Measures to control BP should begin immediately after ICH onset .(Target
BP < 140mm of Hg)
• A long-term goal of BP <130 mm Hg systolic and 80 mm Hg diastolic is
reasonable (Class IIa; Level of Evidence B).

Secondary Prevention
Management of Antithrombotic Agents and Other Medications
HIGH RISK of
thrombotic events
ex. Patient with mechanical
valve, LVAD
Early resumption of
anticoagulation is
reasonable (2a)
Nonvalvular AF
WEIGH RISKS vs BENEFITS of
restarting anticoagulation
Risk<beneft
Resumption of
anticoagulation
may be reasonable (2b)
Consider initiation of
anticoagulation 7-8 weeks
after ICH ( 2b)
Resumption of antiplatelet
therapy may be reasonable
based on consideration of
benefit and risk (2b)
Benefit<risk
LAA closure may
be considered
( 2b)
Statins
Risks and benefits of statins on ICH
outcomes and recurrence are
uncertain (2b)
NSAIDs
Regular long-term use of NSAIDs is
potentially harmful because of the
increased risk of ICH (3: Harm)
Abbreviations: AF indicates atrial fibrillation; ICH, intracerebral hemorrhage; LAA, left atrial appendage; LVAD, left ventricular assist device; and NSAID, non-steroidal anti-inflammatory drugs.
63

Rehabilitation and Recovery
In patients with spontaneous ICH
Multidisciplinary rehabilitation
with regular team meetings
and discharge planning is
recommended (1)
Mild-moderate ICH severity:
Early supported discharge is
beneficial (1)
Moderate ICH severity:
Early rehabilitation
(24-48 hours after onset)
may be considered (2b)
ICH without
depression, fluoxetine
therapy is not effective
to enhance poststroke
functional status.
(3: No Benefit)
Very early and intense
mobilization < 24 hours:
potentially harmful
(3: Harm)
Abbreviations: ICH indicates intracerebral hemorrhage; and SSRIs, selective serotonin reuptake inhibitors.
64

Secondary Prevention
Blood Pressure Management
65
Abbreviations: BP indicates blood pressure; HTN, hypertension; ICH, intracerebral hemorrhage; and mmHg, millimeters of mercury.
Uncontrolled HTN accounts for
74% of global population-
attributable risk for ICH.
In patients with spontaneous ICH, it is reasonable to lower BP to 130/80 mmHg for long-
term management to prevent hemorrhage recurrence (2a).
Guiding Principle

SUMMARY
• Common causes of spontaneous non-traumatic ICH include hypertension,
amyloid and coagulopathy
• Goals of treatment of ICH
controlling ICP
reducing mass effect
and preventing secondary injury (i.e expansion of hemorrhage)
• The role for surgery in supratentorial spontaneous ICH is not clearly
beneficial, but may be useful in patients with superficial lobar bleeds with
higher GCS on admission

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