INTRACEREBRAL

HEMORRAGHE
STROKE SYMPOSIUM

Co-Ordinator: Dr.Meenakshisundaram.U
Presenter: Dr.M.Ramesh Babu
 Introduction

• Intracerebral hemorrhage is defined as an acute and spontaneous

bleeding within the brain parenchyma that may extend into the
ventricles and subarachnoid space. ( ICH, IVH, SAH)

• Third most frequent cause of stroke, following cerebral

embolism and thrombotic disease.
1.ICH occurred at a younger age than brain infarction.

General Rules of ICH

2.The major cause of ICH was hypertension, often severe.
3.Symptoms of ICH began abruptly.
4.Loss of consciousness was a nearly constant feature.
5.Headache always accompanied ICH, and was usually
severe.
6.The most common locations for ICH were the putamen,
internal capsule, lobar, thalamus, cerebellum and pons.
7.CT Brain imaging of choice , MRI helps in detecting the old
haemorrhage.
8. ICH was invariably fatal or devastating, with few, if any,
intact survivors.
 Epidemiology
• It is common: 12-15 cases per 100 000 people per
year

10%~15% of all stroke cases

• Asian countries have a higher incidence ( 20-30%) of
intracerebral hemorrhage than other regions of the world.
• A higher incidence of intracerebral hemorrhage has been
noted in Chinese, Japanese, and other Asian populations,
possibly due to environmental factors (eg,a diet rich in
fish oils) and/or genetic factors.
 Epidemiology

• Intracerebral hemorrhage has a 30-day mortality rate of ~ 50 % .

• Pontine or other brainstem intracerebral hemorrhage has a
mortality rate of 75% at 24 hours.
• Incidence of intracerebral hemorrhage increases in individuals
older than 55years and doubles with each decade until age80.
 Etiology
• Hypertensive ICH (70 -80%)
• Non-hypertensive ICH
– Vascular malformation: AVM,Aneurysm, Cavernous
hemangioma
– Bleeding disorders/anticoagulant
– Amyloid angiopathy
– Trauma
– Tumor
– Drug abuse: amphetamine, cocaine, PPA
 Tumors commonly a/w ICH
• Malignant
Glioblastoma multiforme , Lymphoma
Metastasis (melanoma, choriocarcinoma, renal cell carcinoma ,
bronchogenic carcinoma)

• Benign
Meningioma , Pituitary adenoma
Hemangioblastoma , Acoustic neuroma
Cerebellar astrocytoma
 Risk Factors for underlying Vascular
Abnormalities
• Age <65 years,

• Female sex,

• Nonsmoker,

• Lobar ICH,

• Intraventricular extension,

• Absence of a history of hypertension or coagulopathy

 History Comments
Time of symptom onset (or time the patient
was last normal)
Vascular risk factors Hypertension, diabetes, hypercholesterolemia,
and smoking
Medications Anticoagulants, antiplatelet agents,
decongestants, antihypertensive medications,
stimulants (including diet pills),
sympathomimetics
Recent trauma or surgery Carotid endarterectomy or carotid stenting in
particular, as ICH may be related to
hyperperfusion after such procedures
Dementia Associated with amyloid angiopathy
Alcohol or illicit drug use Cocaine and other sympathomimetic drugs are
associated with ICH, stimulants
Seizures
Liver disease May be associated with coagulopathy
Cancer and hematologic disorders. May be associated with coagulopathy
 Physical Examination Comments

Vital signs Fever is associated with early neurologic

deterioration.19
Higher initial blood pressure is associated with
early neurologic deterioration and increased
mortality.216

A general physical exam focusing on the head,

heart, lungs, abdomen, and extremities.
A thorough but time urgent neurologic exam A structured exam such as the National
Institutes of Health Stroke Scale (NIHSS) can
be completed in minutes and provides a
quantification that allows easy communication
of the severity of the event to other caregivers.
Glasgow Coma Score (GCS) is similarly well
known, easily computed, and the initial GCS is
a strong predictor of long term outcome. 167, 215
These can be supplemented as needed.
Hypertensive Hemorrhage
• Accounts for 60-70% of ICH
• Theory:
▪ Chronic hypertension causes degeneration,
fragmentation and fibrinoid necrosis of small
perforating arteries
▪ Predisposes to rupture

▪ The hypertensive vascular lesion that leads to arteriolar

rupture in most cases appears to arise from an arterial
wall altered by the effects of hypertension,
▪ i.e., the change referred to in a preceding section as
segmental lipohyalinosis and the false aneurysm
(microaneurysm) named for Charcot and Bouchard
• The most common cause of ICH is hypertension, but the blood
pressure does not need to be elevated to malignant ranges

• It is difficult to know how much, if any, of the blood pressure

elevation is secondary to raised ICP (the Cushing response), and
what the level of blood pressure was before the bleed.

• Acute fluctuations in blood pressure and flow, and chronic

degenerative changes are both important in the etiology of
Hypertensive ICH.

• Acute changes in blood pressure and blood flow can precipitate

rupture of penetrating arteries in the absence of prior hypertension

• It is not known whether the size, location, and clinical picture

differs in normotensive individuals who have an acute spike in
blood pressure from those who have chronic hypertension.
 Charcot - Bouchard
Aneurysm

• Discrete arteriolar
microaneurysms

• Most common in the distal

portions of medium and
small arterioles
 Amyloid Angiopathy
• Especially in the elderly

• Deposition of amyloid β peptide in small and medium sized

blood vessels

• Results in fibrinoid necrosis and microaneurysm formation

• Prevalence increases with age from ~ 9% in age 60-69 to 58% in

age >90
❑ Lobar (Occipital & Parietal) haemorrhages - Quite large & Multiple
❑ Chances of rebleed : 21% in 2 yrs
❑ Amyloid-laden arteries are most often found in the occipital and parietal
regions
• Multiple, nearly simultaneous intracerebral hemorrhages raise
the possibility of amyloid angiopathy or a bleeding diathesis
 Bleeding Diathesis
• The most consistent risk factor for intracranial or systemic bleeding is
prolongation of the INR beyond the therapeutic range.

• Features of anticoagulant-induced ICH differs from others by:

• Hemorrhage often develops gradually and insidiously during many hours, or
even days (6/14 patients with anticoagulant-related ICH had an insidious
clinical course).17

• Hematoma growth is greater in patients with oral anticoagulant-related

hemorrhage than in patients who had other spontaneous (that is non-traumatic,
not associated with vascular malformations or aneurysms) causes.

• The cerebellum and cerebral lobes are involved more frequently than in
hypertensive ICH.

• Oral anticoagulant-related hemorrhages have a high morbidity and mortality

rate.

• If a patient on anticoagulants develops neurological symptoms, the cause is

anticoagulant-related hemorrhage until proven otherwise
 Timing of re-instituting anticoagulants
• The timing of re-instituting anticoagulants must be based on the situation in
the individual patient.
• Some studies show that waiting 3 weeks or more after hemorrhage to restart
led to fewer recurrent brain infarctions than expected.
• In other patients restarting anticoagulation early (within 7–10 days) led to less
recurrent hemorrhage than anticipated.
• The treating clinician must weigh the risk of recurrent embolization (that is
the benefit from anticoagulation) versus the risk of rebleeding. When the risk
of rembolization is high and the risk of rebleeding low, then early reinstitution
is recommended.
• When the risk of embolization is small (atrial fibrillation with normal left
atrial size and no past brain infarcts) and the risk of rebleeding is substantial
(poorly controlled hypertension ) then a much longer delay, or using an
antiplatelet rather than an anticoagulant seems prudent.
• Anticoagulation of patients with lobar ICH had more risk and less potential
gain than patients with deep hemorrhages (in whom hypertension could
usually be controlled).
 Drugs Related
• A variety of commonly abused substances are known to cause ICH.
• Clinicians should always think of the possibility of drug-related
hemorrhage in young normotensive patients.
• Hemorrhage often develops within a few minutes of drug use.
• The most frequent presenting symptoms are headache, confusion,
and seizures.
• Despite large-volume ICHs, few focal signs are present in such
patients . This phenomena explained by frequent coexistence of
brain edema, infarcts, and a diffuse vasculopathy.
• Angiography - Chronic amphetamine users and other patients with
amphetamine-related ICH. Most common are segmental areas of
constriction, irregularity, and occasionally fusiform dilatation.
• The focal vascular abnormalities in superficial cortical arterial
branches and are often referred to as beading.
 Pathophysiology
• Primary immediate effect
–Hemorrhage growth
–Increase ICP
• Secondary effect
–Downstream effect
–Edema
–Ischemia
• Progression of Hematoma
 Hemorrhage Growth Predictors
• Early Presentation

• Irregular shape

• Liver disease

• Hypertension

• Hyperglycemia

• Alcohol use ( causes platelet dysfunction, red. coagulation

factors, inc. blood pressure)

• Hypofibrinogenemia
Priorities for Clinical Research in ICH: NINDS ICH Workshop; Stroke March 2005
 Clinical Features

• Alteration in level of consciousness (~ 50%)

• Nausea and vomiting (~ 40-50%)

• Headache (~40%)

• Seizures[3](~6-7%)

• Focal neurological deficits

• Headache : was much more frequent with larger lesions,
and was often absent or minimal in patients with small
lesions.

• Most common in patients with lobar and cerebellar

hematomas, locations near the meningeal surface, and was
common in patients with meningeal signs.

• Patients with small, deep hematomas almost never develop

headache during their course of illness.

• In many patients, headache occurs as the hematoma

enlarges and is accompanied by vomiting and decreased
alertness
• Decreased level of Consciousness accompanies only
large hematomas and those found in the brainstem.

• Diminished alertness in patients with ICH is caused by

mass effect and increased ICP, or direct involvement of
the brainstem reticular activating system.

• Decreased level of consciousness has been found to be an

important adverse prognostic sign .
• Vomiting is an especially important sign in patients with
ICH.

• In ICH and SAH, vomiting is usually caused by

increased ICP or local distortion of the IVth ventricle.

• In the posterior circulation, vomiting usually reflects

dysfunction of the vestibular nuclei, or the so-called
vomiting center, in the floor of the IVth ventricle.

• Patients with cerebellar hemorrhage almost always vomit

early in their clinical course.
• Seizures : Lobar hemorrhages situated near the gray–
white junction of the cortex, and putaminal
hemorrhages that undercut the cerebral cortex are
especially epileptogenic.

• When pts. with subcortical large and expanding ICHs

are monitored using continuous EEG recordings,
electrographic seizure discharges are often found.

• May present with “non-convulsive seizures “

• Other Symptoms and Signs: Neck stiffness is uncommon in
putaminal hemorrhage, but is often found in patients with
31

caudate, thalamic, and cerebellar hemorrhages. 34,35

• Fever is relatively common, but is often related to infectious

complications, such as pulmonary and urinary tract infections.

• Subhyaloid retinal hemorrhages, common in SAH, are rare in

ICH

• Cardiac arrhythmias and pulmonary edema develop in some

patients with ICH, and are usually attributed to changes in ICP
and catecholamine release, a similar pathogenesis to that used to
explain cardiac findings in patients with SAH.
• Keys to localization of ICH are as follows:

1. Motor signs – quadriparesis, hemiparesis, or no paresis

2. Pupillary function – asymmetry, size, and light reaction

3. Extraocular movements – supranuclear, nuclear,

internuclear gaze palsies

4. Gait abnormalities – especially ataxia

• Hemorrhages of the lateral basal ganglia, putamen, and internal capsule
(Striatocapsular hemorrhage):

• Most common location of hypertensive ICH is the lateral basal

ganglionic capsular region

• This location is the most common site for putaminal hemorrhage

because it is supplied by the largest of the lateral lenticulostriate arteries

• These lesions have traditionally been referred to as putaminal

hemorrhages because they most often begin in the putamen.

• The usual findings include C/L hemiparesis, C/L hemisensory loss, and
conjugate deviation of the eyes toward lesion.

• The pupils are generally normal and gait is hemiparetic. Patients with a

• Left putaminal hemorrhage usually have a non-fluent aphasia.

• Right-sided lesions are a/w left visual neglect, motor impersistence, and
constructional dyspraxia.
• Large putaminal hemorrhages -

• Stupor increases as the lesion enlarges

• I/L pupil at first becomes smaller, and later, larger than the
opposite pupil;

• Ipsilateral plantar response becomes extensor

• B/L horizontal gaze palsy develops

• The presence of any of these signs – ipsilateral Babinski’s sign,

abnormal ipsilateral pupil, or ipsilateral gaze paresis – has a grim
prognosis.

• These additional findings are caused by midline shift or

compression of the rostral brain stem by the expanding hematoma.
shows necropsy brain specimens of large putaminal hemorrhages
• Lesions affecting the anterior limb of the internal capsule and
anterior putamen and produce a milder, more transient
hemiparesis without sensory abnormalities.

• Posterior third of the internal capsule and at the far posterior

extreme of the putamen, sensory abnormalities predominate,
with little or no hemiparesis. An inferior quadrantanopia or
hemianopia may be present.

• Patients with lesions in the far posterior left putamen mayhave

fluent Wernicke-like aphasia because of undercutting of the
temporal lobe

• The most common and largest lesions affecting the anterior part
of the posterior limb of the internal capsule are often referred to
as the middle type, whereas the others are termed anterior or
posterior types of putaminal hematomas.
• Caudate Hemorrhage accounts for ~ 7% of ICH.

• Hematomas at this site frequently discharge quickly into the

adjacent lateral ventricle, or may spread laterally toward the
internal capsule or inferiorly toward the hypothalamus.

• Early ventricular dilatation by blood probably accounts for the

most common symptoms of caudate hemorrhage (headache,
vomiting, decreased alertness, and stiff neck).

• Some patients also are confused, disoriented, and have poor

memory.

• The larger parenchymatous hematomas cause a C/L

hemiparesis, conjugate deviation of the eyes to the side of the
lesion, conjugate gaze palsy to the opposite side, and an I/L
small pupil or Horner’s syndrome.
• Sensory findings are usually absent or minimal.

• The usual cause of caudate hemorrhage is hypertension, but

AVMs are also common, especially in the young.

• Caudate hematomas have a better prognosis than comparable-

sized putaminal hemorrhages.

• Symptoms and signs of caudate hemorrhage closely mimic

SAH, but the CT appearance of blood in the caudate and lateral
ventricles is distinctive.
• Thalamic Hemorrhage:

• It occurs secondary to rupture of the Thalamoperforating

artery.

• severe sensory loss on the entire contralateral body.

• If large or moderate in size, thalamic

hemorrhage also produces a hemiplegia or hemiparesis by
compression or destruction of the adjacent internal capsule.

• The sensory deficit involves all of the opposite side

including the trunk and may exceed the motor weakness.
• Fluent Aphasia - Lesions of the dominant side
• C/L Neglect - lesions of the nondominant side.

• Thalamic hemorrhage, by virtue of its extension into

the subthalamus and high midbrain, may also cause a series of
ocular disturbances- pseudoabducens palsies with one or both
eyes turned asymmetrically inward and slightly downward,
palsies of vertical and lateral gaze forced deviation of the eyes
downward
⦿ inequality of pupils
⦿ absence of light reaction,
⦿ skew deviation with the eye ipsilateral to the hemorrhage
assuming a higher position than the contralateral eye,
⦿ ipsilateral ptosis and miosis (Horner syndrome)
⦿ Compression of the adjacent third ventricle leads to
enlargement of the lateral ventricles that may require
temporary drainage.
⦿ early hydrocephalus is common
 Pontine Hemorrhage

• Deep coma within a few minutes

• Locked in Syndrome
⦿Total paralysis with bilateral Babinski signs,
⦿Decerebrate rigidity,
⦿Small (1-mm) pupils that react to light.
⦿Lateral eye movements, evoked by head turning or
caloric testing, are impaired or absent.
 Cerebellar Hemorrhage
• Bleeding occurs from the distal branches of superior
cerebellar or PICA vessels.
• Loss of consciousness at the onset is unusual.
• Repeated vomiting is a prominent feature
• Occipital headache, vertigo, and inability to sit, stand, or
walk.
• A mild ipsilateral facial weakness, diminished corneal
reflex, paresis of conjugate lateral gaze to the side of the
hemorrhage, or an ipsilateral sixth-nerve weakness occur
with larger hemorrhages.or extend into the cerebellar
peduncle.
• Dysarthria and dysphagia may be prominent in some
cases but usually are absent.
• Infrequent ocular signs :blepharospasm, involuntary
closure of one eye, skew deviation, "ocular bobbing," and
small, often unequal pupils that continue to react.
• C/L hemiplegia and ipsilateral facial weakness occur if there is
marked displacement and compression of the medulla against
the clivus.

• The plantar reflexes are flexor in the early stages but extensor
later. When these signs occur, hydrocephalus is usually found
and may require drainage.

• Cerebellar hemorrhage is the most amenable to surgical

evacuation with good results.
 Lobar Hemorrhage
• Bleeding in areas specifically in the subcortical white
matter of one of the lobes of the cerebral hemisphere
• Not associated strictly with hypertension.
• Causes: anticoagulation or thrombolytic therapy;
acquired coagulopathies, cranial trauma, arteriovenous,
trauma, and, in the elderly, amyloidosis of the cerebral
vessels.
• Most lobar hemorrhages are spherical or ovoid, but a few
follow the contour of the subcortical white matter tracts
and take the form of a slit (subcortical slit hemorrhage).
• Many of these are the result of a bleeding diathesis, such
as thrombocytopenia.
 Lab Tests
Serum and Urine Tests Comments

Complete blood count, electrolytes, blood urea Higher creatinine is associated with hematoma
nitrogen and creatinine, and Glucose expansion. Higher serum glucose is associated
with hematoma expansion and worse outcome
(although there are no data to suggest that
normalization improves outcome).
Prothrombin time (PT) or international Warfarin-related hemorrhages are associated
normalized ratio (INR) and an activated partial with an increased hematoma volume, greater
thromboplastin time (aPTT) risk of expansion, and increased morbidity and
mortality. 17, 197, 218
Toxicology screen in young or middle-aged Cocaine and other sympathomimetic drugs are
patients to detect cocaine and other associated with ICH
sympathomimetic drugs of abuse
Urinalysis and urine culture and a pregnancy
test in a woman of childbearing age.
 Other Routine Tests Comments

EKG To assess for active coronary ischemia or prior

cardiac injury that may indicate poor cardiac
function, and to obtain a baseline in the event of
cardiopulmonary issues during hospitalization.

Chest radiograph

Neuroimaging • CT/ CECT/ CTA/CTV, MRI with

gadolinium, MRA/MRV can all be useful to
evaluate for underlying structural lesions,
including vascular malformations and/or
tumors
– When there is clinical or radiologic
suspicion
 Imaging
CT MRI
• Superior to MRI in acutely ill /
• Superior in detecting underlying
stuporous pt.
structural lesions ( AVM etc. )
• Faster , Can detect early Hemorrhage
• Gradient Echo MRI -as accurate
• CT good for 3 B’s (Blood, Brain, Bone)
as CT for identification of acute
• IVH hemorrhage within hours of
onset as regions of marked
• CECT – AVM/Aneurysm/Tumor signal loss due to susceptibility
effects & more accurate for
• CT Angio, CECT may be considered to
help identify patients at risk for identification of Chronic
hematoma expansion hemorrhage

• A newer technique for determining

haematoma expansion, the ‘leakage
sign’, has higher sensitivity and
specificity for presence & haematoma
expansion than the spot sign
 Stages of ICH in CT
• Hyper acute (0-24 hrs) :Hyperdense
• Acute (1-2 days) :Hyperdense
• Sub acute (3-28 days) : Isodense
• Chronic (> month) :Hypodense
• Chronic : Encephalomalacia

• CT contrast - Spot sign

Formula for Estimating ICH
Hematoma Volume
 Role of DSA
• SAH

• Abnormal calcification

• Obvious vascular malformation

• Blood in unusual location, such as sylvian fissure

• No obvious cause of bleeding such as isolated IVH

 ICH Score

Hemphill et al. Stroke 2001, 32:891-97

 Secondary Deterioration

• 25% pts. deterioration in the level of consciousness

within the first 24 hrs

▪ Expansion of the Hematoma : first 3 hrs

▪ Worsening cerebral edema : 24 ~ 48 hrs

▪ Late progression of edema: 2 ~ 3 weeks

 Outcome
• Mortality rate : 23% ~ 58% in 6 months
• GCS score on admission
• Hematoma volume & its progression
• Location of bleed
• Presence of IVH
• Use of anticoagulants

• Broderick et al: mortality rate at 1 month

• GCS < 9 , volume > 60 ml ~ 90%
• GCS ≥ 9 , volume < 30 ml ~ 17%
• Putaminal hemorrhages, lesions larger than 140 mm in one slice,
2
In
thalamic hemorrhage, lesions larger than 3.3 cm in maximal diameter,
cerebellar lesions larger than 3 cm had a poor prognosis
 Management of ICH

Blood Pressure Anti oedema

reduction measures

Surgical Reversal of
Interventions Coagulopathy
Medical Management

Journal of Stroke 2017;19(1):28-39

• A spontaneous cerebral hemorrhage presents two problems that require the
Surgical Management
involvement of the Neurosurgeon:

1. Preventing or treating any secondary damage caused by the bleed itself, due
to intracranial hypertension
2. Identifying a possible vascular origin of the bleed and treating it to prevent
subsequent bleeding
• Approach to surgical consideration is still important. Candidates must be
selected carefully
Can be divided into 3 groups:
1. Massive, rapidly developing lesions that effectively kill or devastate
patients before they reach the hospital. For these lesions, little can or should
be done. Surgery is not indicated.
2. Small hematomas, from which the patient will make an excellent
spontaneous recovery. Treatment consists of controlling the etiological
factors, such as hypertension, to prevent recurrences. Surgery is not
indicated.
3. Medium-sized hematomas (hematoma volumes between the two extremes),
• Size: Hematomas larger than 3 cm in their widest diameter
have a higher mortality and a more delayed recovery

• Location: Cerebellar, lobar, and right putaminal

hemorrhages are most accessible to surgical drainage. For
deeper hemorrhages stereotactic drainage would be
preferred.

• Mass effect and drainage: Size of the hematoma does not, by

itself, solely determine mass effect. Older patients may have
sufficient pre-existing atrophy to be able to accommodate a
sizable hematoma without a critical rise in ICP or shift

• Surgical drainage would be indicated more strongly for

lesions with greater mass effect and no spontaneous
decompression.
• Too early surgery can promote rebleeding which adversely
affects outcome.

• The ideal time to operate is unknown.

• After 7–10 days, blood begins to be absorbed, and the lesion

becomes softer again.

• Ideally, drainage should occur either early or after 7–10 days

for technical reasons.

• In general, if the patient has survived the first week,

improvement occurs as edema subsides.
• The general criteria that lead the neurosurgeon to evacuate an
intracranial space-occupying process are:
• Deterioration of consciousness
Shift of the median line exceeding 5 mm.
Unilateral disappearance of basal cisterns
•
These general criteria are less reliable in the case of spontaneous
intraparenchymal hematomas because extensive literature has
demonstrated the usefulness of surgical treatment when the clinical
condition of a patient with spontaneous deep hematoma is
compromised .

• A multicentre trial (STITCH I) which was concluded in 2005 did not

show any difference between the advantages derived from surgery and
from conservative treatment of hematomas deeper than one centimetre
from the cortical surface.

• A second trial (STICH II) [59], which ended in 2013, seemed to

suggest a modest advantage derived from the surgical evacuation of
lobar hematomas, but not for deep ones.
• A multicentre trial (MISTIE III) is currently being carried out:
the data seems promising, although it is not at the moment
conclusive.

• The assessment of a Neurosurgeon is therefore necessary if the

patient’s clinical condition deteriorates or if the CT scan shows
a shift of the midline.

• However, the criteria are not standardized and coded clinical

deterioration is still a parameter that requires clinical assessment
regarding the possibility of surgical evacuation.
Surgical Management

Journal of Stroke 2017;19(1):28-39

 Timing of Surgery
• Cerebellar hemorrhage

• Brainstem compression

• Hydrocephalus from ventricular obstruction Intraventricular

hemorrhage

• For patients presenting with lobar clots >30 mL

• For most patients with ICH, the usefulness of surgery is

uncertain
 Stereotactic ICH Aspiration

• Many techniques
• Ultrasonic aspiration
• High pressure fluid irrigation
• Endoscopic aspiration
• Modified nucleotome
• Catheter aspiration with injection of thrombolytic agent (UK
or tPA)
• Potential advantages
• Deep putaminal or thalamic haemorrhages may be
accessible

• Less damage to overlying brain

• 77% reduction in ICH volume at 48 hours, with no

bleeding
- Saline irrigationand aspiration after 1 mg rtPA
q8h
• Indication for monitoring ICP - by means of intraparenchymal
catheter or ventricular shunt is linked to the patient’s clinical
condition (GCS <8), mass effect of the bleed and evidence of
cerebral oedema on brain CT scan

• There are no randomized studies on the monitoring - thresholds

of intracranial pressure (ICP <20 mmHg) and cerebral perfusion
pressure (CPP 50– 70 mmHg) are taken from studies carried out
on traumatic brain injury (TBI) patients.
 Coagulopathy Reversal
• INR greater than 1.4 caused by warfarin

• Fresh- frozen plasma (FFP)

• Vitamin K

• Prothrombin complex concentrates ( PCC )

• Recombinant activated factor 7 (rFVIIa)

 Risk factors for Recurrent ICH

• Lobar ICH
• Older age
• Anticoagulation
• Apo E e2 or e4 alleles
• Increased number of “microbleeds” on MRI
 Take Home Message
• ICH is the 3 rd most cause of stroke after embolic and thrombotic

• Asian population , age >55 yrs, female gender have high incidence of ICH

• Hypertension is the major cause and Putamen is most common site for H. ICH

• Early clinical diagnosis and CT imaging helps in prompt treatment and better
outcome

• GCS <9 and Hemorrhage > 3 cms have poor prognosis

• Recent large-scale clinical trials have reported that early intensive blood
pressure reduction can be a safe and feasible strategy for ICH, and have
suggested a safe target range for systolic blood pressure.

• New medical therapies associated with warfarin and non-vitamin K antagonist

oral anticoagulants have been developed to treat ICH

• Aggressive medical management and selection of patient with medium sized

Hematomas and timing of surgery are potentially helpful in saving lifes.
 References
• Caplan's Stroke, A Clinical Approach.2016.5th ed., Chapter 14:
Intracerebral hemorrhage.

• Bradley's Neurology in Clinical Practice. 7th ed, Chapter No. 66

Intracerebral hemorrhage

• Adams & Victor's Principles of Neurology, 10E.

• AHA/ASA Guidelines 2015,Guidelines for the Management of

Spontaneous Intracerebral Hemorrhage.

• Emergency Management in Neurology, Hemorrhagic Stroke, Series Editor ,

Elio Agostoni Milano, Italy

• Journal of Stroke 2017, Spontaneous Intracerebral Hemorrhage:

Management, Jun Yup Kim, Hee-Joon Bae , Department of Neurology, Stroke Center, Seoul National University
Bundang Hospital, College of Medicine, Seoul National University, Seongnam, Korea ,;19(1):28-39 .
Thank you