MUMJ

Clinical Review 15

CLINICAL REVIEW

Intracerebral Hemorrhage: Pathophysiology, Diagnosis and

Management

Fabio Magistris, BMSc

Stephanie Bazak, BScH
Jason Martin

ABSTRACT
Stroke is one of the leading causes of death globally and in Canada. There are two major classifications of
stroke: ischemic and hemorrhagic. Intracerebral hemorrhage (ICH) a subtype of hemorrhagic stroke is as-
sociated with substantial morbidity and mortality. The varied clinical presentation of ICH, ranging from minor
neurological deficits to fatal herniation syndromes arises from parenchymal damage, elevated intracranial
pressure and cardiopulmonary instability. Diagnosis is based on clinical presentation, laboratory investiga-
tions and imaging, which include computed tomography (CT), magnetic resonance imaging (MRI) and angi-
ography. Validated clinical scoring systems for stroke, such as the ICH and FUNC scores, allow for improved
prognosis assessment. Management is comprised of surgical, endovascular and medical interventions. Surgi-
cal clipping and endovascular coiling are used as a preventative measure for cerebral aneurysms, while the
current medical therapies attempt to limit the neurological sequelae following stroke by limiting the extent of
parenchymal involvement. Currently there are no proven therapies for brain protection, although this is cur-
rently a major target for research. Thus, stratification of hemorrhagic stroke based on clinical, laboratory and
imaging findings enables appropriate treatment and assessment of patients at risk of hematoma expansion
in order to prevent clinical deterioration and adverse sequelae.

S
INTRODUCTION
troke is one of the leading causes of death in Canada,
accounting for approximately 14,000 deaths annually1
and is a significant source of morbidity. Stroke can be
classified into ischemic and hemorrhagic, with the former
representing the vast majority of cases (87%).2 In hemorrhag-
ic stroke, bleeding can occur within the cerebral parenchyma
or within the meninges. Intracerebral hemorrhage (ICH) is
defined as bleeding into the brain parenchyma. The current
review excluded epidural hematoma, subdural hematoma
and subarachnoid haemorrhage but includes intraventricular
hemorrhage. Prognoses of hemorrhagic strokes depend on
the initial clinical presentation, rapidity of diagnosis and time
to initiation of intervention. This paper is a non-systematic
review of the current literature on intracranial hemorrhage
(ICH). An overview of the epidemiology, common risk fac-
tors, pathogenesis, clinical manifestations, diagnosis and
treatment approach to ICH are presented.
EPIDEMIOLOGY
The World Health Organization (WHO) estimates that 15
million patients worldwide suffer from stroke annually. Ap-
proximately one third of these cases die, one third are left
disabled and one third have a good outcome.3 High blood
pressure is a contributing factor in more than 12.7 million
strokes annually worldwide. 3 Incidence is greater among the
elderly and those of African and Asian decent.4,5 The over-
all incidence of new or recurrent hemorrhagic strokes in the
United States is 795,000 people pear year. The majority of
these are new strokes (approximately 610,000).6 In 2000,
stroke accounted for 7% of all deaths in Canada.7 Generally,
ICH accounts for ~10% of all strokes and is associated with
a 50% case fatality rate.8 Since 1980, the incidence of hyper-
tensive ICH has declined, reflecting improved blood-pressure
control in the population.9
16 Clinical Review Volume 10 No. 1, 2013
RISK FACTORS
Modifiable
Modifiable risk factors for ICH include hypertension, anti-
coagulant therapy, thrombolytic therapy, high alcohol intake,
previous history of stroke, and illicit drug use (particularly
cocaine).10 Hypertension is by far the most common cause of
hemorrhagic stroke, accounting for up to 60% of all ICH cas-
es. Moreover, approximately two thirds of patients with ICH
have a history of hypertension. Hypertensive ICH results from
tiny aneurysms that rupture and result in intracranial hemor-
rhage.9,11 Anticoagulation therapy causes a seven to tenfold in-
crease in risk for hemorrhagic stroke.12
Intracranial aneurysms are commonly acquired lesions
found in 1-6% of postmortem autopsies.13 Most do not rupture
throughout a persons lifetime and remain undiagnosed. How-
ever, 27,000 new cases of subarachnoid hemorrhage follow-
ing a ruptured aneurysm occur in the United States annually,
accounting for 5-15% of hemorrhagic stroke cases.13 The pro-
cess of aneurysm formation and their rupture is incompletely
understood. However, hypertension and smoking have been
clearly documented to be associated with ruptured cerebral
aneurysms and both evidenced to cause structural defects by
inducing endovascular changes.13, 14 The tunica media layer is
often implicated, causing focal weakness in the vessel wall that
can result in aneurysmal ballooning at arterial bifurcations.13
Common locations of aneurysms are presented in Figure 1.18
Figure 1. Common locations of cerebral aneurysms are near
the anterior communicating and anterior cerebral arteries,
at the junctions near the middle cerebral artery and at the
junction between the basilar and posterior cerebral artery.18
Non-Modifiable
Non-modifiable risk factors for hemorrhagic stroke in-
clude advanced age, negroid ethnicity, cerebral amyloido-
sis, coagulopathies, vasculitis, arteriovenous malformations
(AVMs), and intracranial neoplasms.9,10,11,15
Intracranial hemorrhage associated with hereditary cer-
ebral amyloid angiopathy (CAA) is caused by mutations in
the amyloid precursor protein (APP) or cystatin C protein
(CST3) genes inherited in an autosomal dominant pattern. 16
Although often asymptomatic, cerebral amyloid angiopathy
(CAA) is an important cause of primary lobar intracerebral
hemorrhage in the elderly.10 Coagulopathies predisposing to
excessive bleeding can be due to inherited factor deficien-
cies or due to acquired liver pathology. Acquired coagulopa-
thies causing ICH may stem from the use of anticoagulants,
platelet antagonists and natural remedies with anticoagulant
properties amongst others. Some drugs without anticoagulant
properties are known to cause intracerebral hemorrhages.
These include amphetamines Phencyclidine and Cocaine. In
children, the most common cause of ICH are vascular mal-
formations (AVMs), about tenth as frequent as cerebral aneu-
rysms in adults with spontaneous intracranial haemorrhage.
There are a number of other causes that are beyond the scope
of this paper and have been reviewed in detail elsewhere. 9,11,17
PATHOGENESIS
ICH consists of three distinct phases: (1) initial hemor-
rhage, (2) hematoma expansion, and (3) peri-hematoma ede-
ma.19 The initial hemorrhage is caused by rupture of cerebral
arteries influenced by the aforementioned risk factors. The dis-
ease outcome depends primarily on the latter two phases of
progression. Hematoma expansion, occurring hours after ini-
tial symptom onset, involves an increase in intracranial pres-
sure (ICP) that disrupts the integrity of the local tissue and the
blood-brain barrier. Additionally, obstructed venous outflow
induces the release of tissue thromboplastin, resulting in local
coagulopathy2. In over a third of patients, hematoma expan-
sion is associated with hyperglycemia,20, 21,22 hypertension,23
and anticoagulation.24-26 The initial size of the hemorrhage
and the rate of hematoma expansion are important prognos-
tic variables in predicting neurologic deterioration. Hematoma
size >30 ml is associated with greatly increased mortality.27
Following the expansion, cerebral edema forms around the
hematoma, secondary to inflammation and disruption of the
blood-brain barrier. This peri-hematoma edema is the primary
etiology for neurological deterioration and develops over days
following the initial insult.
In up to 40% of ICH cases, the hemorrhage extends into
the cerebral ventricles causing intraventricular hemorrhage
(IVH).28 This is associated with acute obstructive hydro-
cephalus and substantially worsened prognosis.2,28 ICH and
accompanying edema may also disrupt or compress adjacent
MUMJ Clinical Review 17
brain tissue, leading to neurological dysfunction. Substantial
displacement of brain parenchyma may cause elevation of in-
tracranial pressure (ICP) with the potential outcome of fatal
herniation syndromes.29
CLINICAL MANIFESTATION
Rapid recognition of ICH is crucial. Rapid clinical pro-
gression during the first several hours can quickly lead to
neurological deterioration and cardio-pulmonary instability.
The classic presentation in ICH is the progressive onset of
focal neurological deficits over minutes to hours with accom-
panying headache, nausea, vomiting, decreased level of con-
sciousness and elevated blood pressure.2,30 Comparatively,
in ischemic stroke and subarachnoid hemorrhage, there is
typically a more abrupt progression of focal deficits.2 Symp-
toms of headache and vomiting are also observed less often
in ischemic stroke compared with ICH.30 Symptoms of ICH
are typically due to increased ICP. This is often evidenced
through the presence of Cushings triad hypertension, brad-
ycardia and irregular respiration triggered by the Cushings
reflex.31 Dysautonomia is also frequently present in ICH,
accounting for hyperventilation, tachypnea, bradycardia, fe-
ver, hypertension and hyperglycemia.2,27
Stroke can often be confused with other neurological
conditions that mimic stroke in their clinical presentation.
The most common stroke-mimics are seizure, syncope
and sepsis. Sensory symptoms such as vertigo, dizziness
and headaches are non-discriminatory between stroke and
non-stroke.32 Furthermore, ICH is particularly difficult to
diagnose because symptoms of syncope, coma, neck stiff-
ness, seizure, diastolic blood pressure (BP) of >110 mmHg,
nausea, vomiting, and headache are typically present in
ischemic stroke but usually absent in ICH.32 As a result,
early neuroimaging becomes vital in the diagnosis of ICH.
The most common symptoms of hemorrhagic and ischemic
stroke are acute onset, limb weakness, speech disturbances
and facial weakness (Table 1).
Table 1. Common clinical stroke symptoms in order of
decreasing frequency. These symptoms are used to differentiate
stroke from neurological conditions that mimic stroke
Symptoms Cases (%)
Acute onset 96
Arm weakness 63
Leg weakness 54
Speech disturbances 53
Facial weakness 23
Limb parasthesia 20
Visual disturbances 11
Facial parasthesia 9 Visual field defect
Vertigo 6 Seizure
Impaired limb coordination 5 Loss of consciousness
Convulsive fits 1
DIAGNOSIS
Clinical
As with any medical emergency, a thorough and focused
history eliciting specific risk factors and preceding events is
critical for every patient presenting with stroke-like symp-
toms. Important risk factors include any recent trauma, hy-
pertension, prior strokes, diabetes, smoking, alcohol, over-
the-counter, prescription or recreational drugs (specifically
cocaine, warfarin, aspirin, and other anticoagulants), hemato-
logic disorders, liver disease, neoplasm, infections and AVM.33
Although risk factors and patient comorbidities have implica-
tions for clinical management and outcome, clinical presenta-
tion alone is insufficient to reliably differentiate stroke from
other clinical entities.2 The difficulty for most physicians lies
in the ability to distinguish stroke from those that mimic it
such as syncope, sepsis and seizures. To improve diagnostic
accuracy in stroke diagnosis, tools such as the ROSIER Scale
(Table 2) have been developed for use in the emergency room
to help reduce the number of unnecessary referrals for non-
stroke cases.32 The ROSIER Scale is a rapid stroke assess-
ment tool that uses clinical signs such as asymmetrical weak-
ness, speech and visual disturbances, to help rule out stroke
mimics. The ROSIER scale ranges from -2 to +5 points, with
any patient scoring greater than 0 having a 90% likelihood of
stroke. The ROSIER scale has a sensitivity of 92%, specificity
of 86%, positive predictive value (PPV) of 88%, and negative
predictive value (NPV) of 91%.32
Although tools such as the ROSIER scale have helped
to improve diagnostic accuracy for stroke in general in the
emergency department to 80-95%32, no signs or symptoms
reliably distinguish ICH from ischemic stroke. Therefore,
neurological imaging plays an increasingly important role in
the diagnosis of ICH.32-35 Laboratory investigations for diag-
nosis and prognosis assessment consist of CBC, electrolytes,
a hemostasis screen including INR and PT, a -HCG test in
women of childbearing age and a toxicology screen to test for
cocaine and other prescription drugs.33,36 Patients with an el-
evated PT or INR due to anticoagulant therapy have a greater
risk of hematoma expansion and, when possible, their antico-
agulation therapies should be, at least temporarily, reversed.
Table 2. The ROSIER Scale is a rapid stroke assessment tool
that uses clinical signs to help rule out stroke mimics. The
scale ranges from -2 to +5 points, with any patient scoring
greater than 0 being likely to have a stroke
Components Points
Asymmetrical facial weakness 1
Asymmetrical arm weakness 1
Asymmetrical leg weakness 1
Speech disturbances 1
1
-1
-1
18 Clinical Review Volume 10 No. 1, 2013

Imaging underlying aneurysm or lesion is noted using 3D-CTA, the

The primary purpose of diagnostic imaging is to differen-
tiate between ischemic and hemorrhagic strokes and to rule
out other CNS lesions.35 Computed tomography (CT) and
magnetic resonance imaging (MRI) are both first line imag-
ing modalities, supported by level 1 evidence (RCTs).37 If an
MRI can be ordered as quickly as the CT, it should be consid-
ered first. 35 In patients with contraindications to MRI, namely
those with metallic fragments or devices in the brain, eyes
or spinal canal, a CT scan should be obtained.2 CT may be
superior at showing ventricular extension, while MRI better
detects structural lesions, edema, and herniation.2 The non-
contrast CT (NCCT) is the most readily available tool provid-
ing rapid feedback and is thus commonly used in emergency
departments. It is thought to be nearly 100% sensitive for
detecting clinically relevant acute hemorrhages. Moreover,
it may elucidate hematoma location and expansion and the
presence of edema.38 MRIs are most frequently utilized as
follow-up investigations to identify secondary causes of ICH,
such as arteriovenous malformation (AVM), amyloid angi-
opathy, or associated neoplasm.
With advances in imaging, CT angiography (CTA) has
proven to be a useful tool in predicting hematoma expansion
in patients with ICH. Wada et al. (2007) demonstrated foci
of contrast enhancement in 91% of expanded hematomas.39
CTA and contrast-enhanced CT may identify patients at risk
for hematoma expansion through this novel discovery of the
spot sign (Figure 2).38 The spot sign has helped enhance vis-
ualization of hematoma expansion with the ability to stratify
risk of hemorrhagic stroke. The literature has noted a particu-
larly high specificity (85-89%) of the spot sign for ICH, with
negative predictive values of 76-96% and a positive likeli-
hood ratio of 2.7-8.5.39-42
In the absence of CTA, it would be difficult to accurately
detect structural causes of the hemorrhage, such as bleeding
from a cerebral aneurysm or a vascular malformation. If no
peripheral enhancement on source images of 3D-CTA sup-
ports the assertion that these foci represent active hemor-
rhage from secondarily damaged or torn perforations.39 In a
study by Park et al. (2010), the mean duration of hospital ad-
mission for patients exhibiting the spot sign was 47.37 days,
whereas those lacking the sign were admitted for 37.11 days
(p < 0.001). Mortality rates between two groups also differed
significantly over the 90 days following admission (40.5%
vs.13.4%, p < 0.001).43 Thus, this association between the
spot sign and hematoma expansion may reflect the role of a
spot sign as a reliable radiologic predictor of clinical deterio-
ration and poor outcomes in spontaneous ICH.
PROGNOSIS
Approximately half of all ICH-related mortality occurs
within the first 24 hours after the initial hemorrhage.44 Mor-
tality approaches 50% at 30 days.19,36 Factors associated with
poor outcomes include large hematoma volume (>30 mL),
posterior fossa location, older age, mean arterial blood pres-
sure (MAP) >130 mmHg at admission36,44 and a score of be-
low 4 on the Glasgow Coma Scale (GCS) on admission. The
same factors are also the most powerful predictors of mortal-
ity at 30 days. Hematoma expansion has also been shown
to be an independent predictor of diminished functional out-
comes, neurological deterioration20,21,45 and mortality.2,46 In a
study by Alvarez-Sabn et al. (2004) increased levels of ma-
trix metalloproteinase (MMP)-9 and MMP-3 at 24 hours are
associated with increased peri-hematomal edema and mortal-
ity, respectively.2,47
The ICH score and FUNC score are two clinical grad-
ing scales used to prognosticate patients with hemorrhagic
stroke. The ICH Score predicts 30-day mortality using fac-
tors including age, ICH volume, GCS score and presence of
IVH (Table 3).48 In a study by Hemphill et al. (2001), all 26
patients with an ICH score of 0 survived and all 6 patients

Figure 2. Patient with spot sign demonstrating extravasation and hematoma expansion. A. Unenhanced CT demonstrates
left posterior putaminal and internal capsule hematoma with mild surrounding edema. B. A small focus of enhancement is
seen peripherally, consistent with the spot sign (black arrow). C. Post-contrast CT demonstrates enlargement of the spot sign,
consistent with extravasation (white arrow). D. Unenhanced CT image 1 day after presentation reveals hematoma enlargement
and intraventricular hemorrhage.39
MUMJ Clinical Review 19

with an ICH Score of 5 died within the 30 days.48 The limi- Table 4. The FUNC (Functional outcome risk stratification)
tation of the ICH score is that it is solely used to prognos- score assesses the patient for risk of functional impairment
ticate survival at 30 days without accounting for functional at 90 days post-stroke. The scores range from 0 to 11 based
on ICH volume, age, ICH location, GCS score, and pre-ICH
outcome. The ICH score should thus be used in combination
cognitive impairment. A greater score is associated with a
with the FUNC score to assess functional outcome. greater chance of functional independence, defined as GCS
>4, at 90 days. Limitations include lack of predictive value
for scores in the mid-range
Table 3. The ICH Score predicts 30-day mortality using
factors including GCS score, ICH volume, presence of Component Points
intraventricular hemorrhage (IVH), and age. The scale ranges ICH volume (cm3)
from 0 to 6 points. In the original study all patients with a <30 4
score of 0 survived and all patients with a score of 5 died 30-60 2
within 30 days. The limitation of the ICH score that is does >60 0
not account for functional outcome
Age (y)
Component Points <70 2
GCS score 70-79 1
3-4 2 >80 0
5-12 1 ICH location
13-15 0 Lobar 2
ICH volume (cm3) Deep 1
>30 1 Infratentorial 0
<30 0 GCS score
IVH 9 2
Yes 1 8 0
No 0 Pre-ICH cognitive impairment
Infratentorial origin of ICH Absent 1
Yes 1 Present 0
No 0
Age (y)
>80 1 TREATMENT
<80 0 Surgical
Two surgical interventions are available for treating aneu-
rysms. The surgical approach entails placement of permanent
Another prognostic tool is the FUNC (Functional outcome alloy clips across the neck of the aneurysm through cranioto-
risk stratification) score. The patient is assessed for risk of my access. The patient is typically under general anesthesia.
functional impairment at 90 days post-stroke. The FUNC This prevents blood flow from reaching the aneurysm and
scores range from zero to eleven based on ICH volume, age, lowers the risk of rupture.14
site of ICH, GCS score and pre-ICH cognitive impairment49 The aneurysm can also be coiled through endovascular
(Table 4). A greater score is associated with a greater chance access while the patient is under general anesthesia or se-
of functional independence, defined as GCS 4 at 90 days.49 dation.14 Intra-procedural neurologic function is observed
According to Rost et al. (2008), no patient with a FUNC through neurophysiological monitoring. Using fluoroscopy
score 4 achieved functional independence and over 80% of and digital subtraction angiography, a catheter is advanced
those with a maximal FUNC score of 11 reached functional through the femoral artery, aorta, carotid artery and into the
independence at 90 days.49 The limitation, however, is that aneurysm. A sufficient number of detachable coils are then
only scores at the extreme ends seem to be clinically useful as positioned into the aneurysm to minimize the amount of
scores in the mid-range have little predictive value.49 blood filling the aneurysm.14,52-54 Systematic reviews have as-
Although these prognostic tool scores are important in the sociated the use of coils with lower rates of inpatient mortal-
hospital setting, the AHA recommends prompt and aggressive ity, shorter hospital stay and decreased treatment costs.14
full care upon ICH onset with postponement of new AND
(Allow Natural Death) orders until at least the second full Medical
day of hospitalization.50 This is because there is evidence that The patients vital signs must be immediately stabilized
a stated poor prognosis can lead to self-fulfilling prophecies according to ATLS guidelines.34 Patients with ICH are often
of early death.50 Withdrawal of care is the strongest predictor unable to protect their airway and may need endotracheal in-
of death after ICH44 and, thus, in the emergency setting new tubation (criteria for intubation, GCS <8). Rapid sequence
AND orders or withdrawal of care are not recommended.45 intubation is the preferred approach with administration of
20 Clinical Review Volume 10 No. 1, 2013
short-acting IV thiopental (1-5 mg/kg) or lidocaine (1 mg/kg)
to prevent the increase in ICP that may result from tracheal
stimulation.34,37 A chest X-ray and an EKG must be ordered to
assess cardiopulmonary function.
A CT scan must then be obtained to determine further
management and to make a final diagnosis.34 With ICH there
is often a need to transfer a patient to an intensive care unit
for ICP monitoring and potential neurosurgical intervention.
Physicians should determine whether the level of care re-
quired exceeds the capacity of their facility and if their patient
needs to be transferred to the nearest tertiary stroke centre.2
Bleeding, seizures, blood pressure, and intracranial pressure
must be monitored and actively controlled. A new AHA/ASA
guideline states that glucose should be monitored and normo-
glycemia is recommended (Class I: Level of Evidence: C).50
Special attention should be given to the risk of iatrogenic
hypoglycemia associated with increased risk of mortality.50
Antacids are administered to prevent associated gastric ul-
cers. Fever must be controlled and thromboembolic prophy-
laxis undertaken with compression stockings. Normothermia
is recommended as even mild hyperthermia can accentuate
the cellular damage in the area of ischemic penumbra post-
stroke. Following 1-2 days of treatment, heparin therapy can
be considered for further thromboembolic prophylaxis when
no increased risk of recurrent hemorrhage is suspected.27
Reversal of warfarin anticoagulation is undertaken to con-
trol bleeding and ICH. This must be accomplished as quickly
as possible to stop further hematoma expansion. Agents for
reversal therapy include intravenous vitamin K (VAK), fresh
frozen plasma (FFP), prothrombin complex concentrates
(PCC) and rFVIIa.55,56 Vitamin K should be given with either
FFP or PCC as it requires more than six hours to normalize
the INR. According to Huttner et al. (2006) the incidence of
hematoma expansion in patients receiving PCCs (19%) was
significantly lower than those receiving FFP (33%) or VAK
(50%) (2 P<0.01 for PCCs).55 Although the extent of hema-
toma growth did not significantly differ between the groups
(p=0.36), more rapid INR reversal was achieved through
treatment with PCCs as compared with FFP and VAK (2
P<0.01). This suggests that the superior effect of PCC is re-
lated to the more rapid INR reversal.55 Studies using recom-
binant factor VIIa (rFVIIa) have been disappointing and it is
not commonly used clinically to treat bleeding. This product
is currently being tested in patients with spot sign.
Blood pressure should be controlled to prevent re-bleed-
ing and hematoma expansion. A beta-blocker, such as Labet-
alol, and an ACE inhibitor, such as enalapril, are often used
to achieve blood pressure control. Nitroprusside may raise
intracranial pressure and should be avoided, except when
necessary in patients with asthma or heart failure where beta-
blocker administration is contraindicated.57 The decision to
actively pursue hypertensive control depends on the systolic
pressure, mean arterial pressure (MAP) and presence or ab-
sence of intracranial pressure on admission and is beyond the
scope of this paper but is covered by the 2010 AHA/ASA
guidelines.50
Intracranial pressure (ICP) management relies on eleva-
tion of the head of the bed to 40 degrees to improve jugular
venous outflow. More aggressive therapies, such as osmotic
therapy (mannitol, hypertonic saline) require intracranial
pressure and BP monitoring to maintain an adequate cerebral
perfusion pressure greater than 70 mmHg.2,50 These are rou-
tinely used during transfer of patients from peripheral cen-
tres. Special attention should be given to the risk of iatrogenic
hypotension caused by rapid and aggressive hypertensive
therapy, which can induce cerebral ischemia.57 For seizure
control, the 2010 AHA/ASA guidelines recommended that
patients with seizures accompanied by change in mental sta-
tus should be treated with a benzodiazepine for rapid seizure
control and Phenytoin for long-term management.50 Figure 3
represents a flowchart for the approach to ICH identifying the
various steps involved from presentation through diagnosis
to treatment.
Step 1
Patient must be assessed and stabilized if necessary according to ATLS
guidelines.
Patients with a GCS score under 9 require endotracheal intubation.33
Step 2
Clinical History Questions should be asked about any recent trauma,
hypertension, prior strokes, diabetes, smoking, alcohol, over-the-counter,
prescription or recreational drugs (specifically cocaine, warfarin, aspirin,
other anticoagulants), hematologic disorders, liver disease, neoplasm,
infections, or AVM.33
Step 3
Assess symptoms using the ROSIER Scale32 (scores >0, 90% chance of
stroke) to diagnose, and the ICH48 (the greater the score, the poorer the
outcome) and FUNC Scores49 (the greater the score, the greater the chance
of functional independence) to prognosticate.
Step 4
Lab test should be performed to guide diagnosis, assess risk factors for
ICH and discover potential underlying causes. Sample tests include a CBC,
electrolytes, a hemostasis screen including INR and PT, a pregnancy test, a
toxicology screen, matrix metalloproteinase, chest X-ray and an ECG.2
Step 5
Diagnostic Imaging2,35 CT and MRI are both first-choice imaging modalities
(both level 1evidence). Using CTA the spot sign can indicate risk for
hematoma expansion is a warning for poorer outcomes unless treated
quickly.
Step 6
Treatment 2 (Note: this step may occur prior to other steps)
Potential treatments in ICH: stopping or slowing initial bleed during the
initial hours after onset (pharmacotherapy, surgical clipping, endovascular
coiling)
Management of symptoms, signs and complications such as elevated ICP,
decreased cerebral perfusion and supportive management of patients with
severe brain injury is required.
Figure 3. Flowchart for the approach to stroke, specifically
intracerebral hemorrhage (ICH), in the acute care setting
starting with a focused history, lab testing, diagnostic imaging
and acute treatment.
MUMJ Clinical Review 21
CONCLUSION
Given the high mortality rate of ICH, early recognition
and correct diagnosis is vital. While making the diagnosis,
one must distinguish stroke mimics from actual stroke signs
and identify common signs such as acute onset, limb weak-
ness or speech disturbances. Among their diagnostic arsenals
and prognostic tools, ICH can be assessed through the Rosier
scale (diagnostic) and the ICH and FUNC scores (prognos-
tic). However, such tools are limited in their interpretation of
mid-range scores. Neurological imaging techniques, such as
CT and MRI are playing an increasingly central role in the
early diagnosis of ICH. The spot sign has been suggested as
a marker of hematoma expansion as identified on CTA.
A major limitation in stroke management is that no effec-
tive targeted therapy for hemorrhagic stroke yet exists.
Rather, symptoms and complications are individually
managed, with increased ICP and neurological deterioration
being particularly important. The recent advent of endovas-
cular coiling of aneurysms as a preventative measure against
ICH has improved clinical outcomes in appropriately select-
ed patient populations.
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Author Biographies
Fabio Magistris graduated from the University of Western Ontario with a degree in Medical Sciences before attending
McMaster University. He is currently in his first year of the MD program.
Stephanie Bazak graduated from Acadia University with a Bachelor of Science in Psychology. She is currently in her
second year of medicine at McMaster University
Jason Martin completed three years of the Medical Sciences program at the University of Western Ontario before attending
McMaster University. He is currently in his second year of the MD program. He has an active interest in neuroradiology.