Intracerebral Hemorrhage Case presentation

It is not simply bleeding in
the brain
Usama Ragab Yousif (Msc.)
Internal Medicine Department

Personal History
• 65-year old male, M.I.K., from Bordain,
married and have 6 offspring, the youngest
is 28 years old, retired (was a driver),
cigarette smoker, right handed.

Chief Complaint
• Disturbed conscious level, with right side
weakness 5 days before admission.
• The patient was brought comatose to ER.

History of present illness
• According to the statement of the relative
who brought the patient, that he was
reasonably well 6 days before. Suddenly the
night before admission, while eating dinner,
he felt weakness of the right side of the
body, followed by sudden collapse.
• Since then, he is comatose in ICU.

History of present illness
• There is no history of fever, convulsion,
trauma to the head.
• No symptoms suggest other system
affection.

History of Past illness
• He is hypertensive and diabetic on no
treatment.
• There is no history of any cardiac
abnormality.
• Chronic kidney disease on conservative
measures.

Examination
Patient is comatose, GCS
•Eye movement: Eye to pain→ 2
•Speech: no speech → 1
•Motor response: flexion to pain → 3
Vital Signs:
oBlood Pressure: on admision 200/110
oPulse: 110, regular, equal on both sided, of
average volume
oTemperature: 37.8ᵒ
c
oRespiratory rate: 25/min
HEENT: normal

Examination (cont.)
Extremities:
• Upper limbs: no clubbing, no pigmentations, no
pallor, normal muscles and nerves.
• Lower limbs: no edema, no pigmentation.
Back: no pigmentation, no swelling, no spine
deformities.

Examination (cont.)
Neurologic examination:
oLevel of responsiveness: obtunded; arousable
only with repeated and painful stim; verbal output is
unintelligible or nil; some purposeful movement to
noxious stimuli.
oPupillary responses: RRR
oEye movements
oFundoscopic examination
oCorneal reflex: intact.

Examination (cont.)
Neurologic examination (cont.):
oMotor examination:
•Muscle tone: hypotonia in 4 limbs equally
distributed.
•Reflexes: hyporeflexia in 4 limbs equally
distributed.
oMeningeal signs: no meningeal irritation signs.
oResponse to stimuli: flexion attitude.

Examination (cont.)
Cardiac examination: Normal
Chest examination: there is decrease air entry bilaterally,
harsh vesicular breathing, coarse crackles, expiratory rhon
ci allover the chest.
Abdomen: Normal.

Salient Features
Male, 65 years, smoker, Diabetic, hypertensive and CKD.
presented with sudden weakness of the right side of
the body and DCL.
He is now comatose
He is hypertensive and diabetic on no treatment.
There is no history of any cardiac abnormality.
He is a smoker for the last 40 years, used to take 30
cigarette/day. There is no family history of similar
illness.

Investigations
ControlPatient
4-119.7WBCs
11.5 – 15.510.4 (NC/NC)HB
150-450231Platelets
1.2INR
0.5 – 1.2mg/dL2.34Creatinine
6 – 20 mg/dL54BUN
3.5 – 5.5 mmol/L4.4K
3.4/7.2Albumin/TP
Up to 33 U/L19/34ALT/AST
Up to 1.1 mg/dL0.39Bilirubin
199Blood Glucose

Investigations (con.)
Patient
7.46PH
30.4PCO2
19.5HCO3
88.5%SO2
4.4K
150Na

Investigations (cont.)
Pelviabdominal US:
- Chronic parencymatous liver disease.
- Average sized spleen.
- Rt kidney : mild back pressure, no increased in
echogenicity or loss of CMD.
- Lt Kidney: sonofree.
- Otherwise normal sonographic study.

Epidemiology
• Globally, about 17
million strokes occur
every year and stroke is
the second leading
cause of death after
coronary heart disease,
and the third most
common cause of
disability.
1- Krishnamurthi RV: Lancet Glob Health. 2013;1(5):e259.
Figure: http://www.who.int/mediacentre/factsheets/fs310/en/

Epidemiology
• Globally, the incidence of stroke due to ischemia is 68
%, while the incidence of hemorrhagic stroke
(intracerebral hemorrhage and subarachnoid
hemorrhage combined) is 32 %.
• Men have a higher incidence of stroke than women at
younger but not older ages, with the incidence reversed
and higher for women by age 75 years and older.
Mikulik R: J Intern Med 2015; 278: 145–165.
Lozano R, et al: Lancet. 2012 Dec;380(9859):2095-128.

Presentation
• Sudden onset
• Focal neurological deficit
• Progresses over minutes to hours
• Depends on location
• Symptoms include:
 SUDDEN numbness or weakness of face, arm or leg
 SUDDEN confusion, trouble speaking or understanding.
 SUDDEN trouble with vison.
 SUDDEN trouble walking, dizziness, loss of balance or coordination.
 SUDDEN severe headache.

Review of Anatomy
• Blood reaches the brain through 2 systems:
1. The carotid system (Anterior Circulation)
2. The vertebral system (Posterior Circulation)

Emergency Diagnosis and Assessment
1. A baseline severity score should be performed as part of the initial
evaluation of patients with ICH (Class I; Level of Evidence B).
2. Rapid neuroimaging with CT or MRI is recommended to distinguish
ischemic stroke from ICH (Class I; Level of Evidence A).
3. CTA and contrast-enhanced CT may be considered to help identify patients
at risk for hematoma expansion (Class IIb; Level of Evidence B), and
CTA, CT venography, contrast-enhanced CT, contrastenhanced MRI,
magnetic resonance angiography and magnetic resonance venography, can
be useful to evaluate for underlying structural lesions including vascular
malformations and tumors when there is clinical or radiological suspicion
(Class IIa; Level of Evidence B).

• Maximum score described is 5 in which
% of mortality at 30 days is nearly 100%.
• Although an ICH Score of 6 is possible
with the scale, this is rarely observed and
is considered highly likely to be fatal.
ICH Score
JC Hemphill et al: Stroke 32:891, 2001; JC Hemphill et
al: Neurology 73:1088,2009.

Neuroimaging
 CT is very sensitive for identifying acute hemorrhage and is considered the
“gold standard”;
 Gradient echo and T2* susceptibility-weighted MRI are as sensitive as CT for
detection of acute hemorrhage and are more sensitive for identification of
prior hemorrhage.
 CT angiography (CTA) and contrast-enhanced CT may identify patients at
high risk of ICH expansion based on the presence of contrast within the
hematoma, often termed a spot sign. A larger number of contrast spots
suggests even higher risk of expansion.
 MRI, magnetic resonance angiography, magnetic resonance venography, and
CTA or CT venography can identify specific causes of hemorrhage, including
arteriovenous malformations, tumors, moyamoya, and cerebral vein
thrombosis.
Cerebrovasc Dis. 2013;35:582–589.

CT scans (without contrast enhancements):
sensitivity= 89%specificity= 100%
MRI scan:
sensitivity= 83%specificity= 98%
CT imaging is also sensitive for detecting SAH (although by itself does not rule it
out), and CTA can readily identify intracranial aneurysms.
On CT brain, hemorrhage appears as
hyperdense region, i.e. more white
Case courtesy of A.Prof Frank Gaillard, Radiopaedia.org, rID: 10598

The CT angiographic (CTA) spot sign is defined as unifocal or multifocal contrast
enhancement within an acute primary intracerebral haemorrhage (ICH) visible on
CTA source images and discontinuous from adjacent normal or abnormal blood
vessels . It should not be present on pre-contrast images. It corresponds to a site of
active, dynamic haemorrhage and is an independent predictor of ICH growth and
poor outcome
The CT angiographic (CTA) spot sign
Lancet Neurol. 2012;11 (4): 307-14.

Localization
CerebellarPontineBasal ganglia
10%10%80%

Investigations (cont.)
Modified Fisher scale on CT brain (predict risk of vasospasm):
Risk of vasospasmIVHSAH
24%-No or minimalGrade I
33%+MinimalGrade II
33%-Diffuse focal or thickGrade III
40%+Diffuse focal or thickGrade IV
Frontera, Jennifer A., et al. "Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: the Modified
Fisher Scale." Neurosurgery 59.1 (2006): 21-27.

Fisher, CM, Kistler, JP, Davis, JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by CT scanning. Neurosurgery 1980;
6:1.
Frontera, Jennifer A., et al. "Prediction of Symptomatic Vasospasmafter Subarachnoid Hemorrhage: the Modified Fisher
Scale." Neurosurgery 59.1 (2006): 21-27.

Ageing blood on MRI
The imaging characteristics of blood on MRI are variable and change with the
age of the blood.
In general, five stages of haematoma evolution are recognised:
isointense on T1
isointense to hyperintense on T2
1- Hyperacute
T2 signal intensity drops (T2 shortening)
T1 remains intermediate-to-long
2- Acute (1-2 days)
T1 signal gradually increases (T1
shortening) to become hyperintense
3- Early subacute (2-7days)
increase in T2 signal4- Late subacute (7-14days)
low on both T1 and T25- Chronic (>14-28 days)

Exapmple to Subacute ICH in MRI

Hemostasis and Coagulopathy, Antiplatelet Agents,
and DVT Prophylaxis
1. Patients with a severe coagulation factor deficiency or severe
thrombocytopenia should receive appropriate factor replacement therapy or
platelets, respectively (Class I; Level of Evidence C).
2. Patients with ICH whose INR is elevated because of VKA should have their
VKA withheld, receive therapy to replace vitamin K–dependent factors and
correct the INR, and receive intravenous vitamin K (Class I; Level of
Evidence C). 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 does not replace all clotting factors, and although the
INR may be lowered, clotting may not be restored in vivo; therefore, rFVIIa is
not recommended for VKA reversal in ICH (Class III; Level of Evidence C).

and DVT Prophylaxis
3. For patients with ICH who are taking dabigatran, rivaroxaban, or apixaban,
treatment with FEIBA (factor eight inhibitor bypassing activity), other PCCs, or
rFVIIa might be considered on an
individual basis. Activated charcoal might be used if the most recent dose of
dabigatran, apixaban, or rivaroxaban was taken <2 hours earlier. Hemodialysis
might be considered for dabigatran (Class IIb; Level of Evidence C).
4. Protamine sulfate may be considered to reverse heparin in patients with acute
ICH (Class IIb; Level of Evidence C).
5. The usefulness of platelet transfusions in ICH patients with a history of
antiplatelet use is uncertain (Class IIb; Level of Evidence C).
6. Although rFVIIa can limit the extent of hematoma expansion in noncoagulopathic
ICH patients, there is an increase in thromboembolic risk with rFVIIa and no
clear clinical benefit in unselected patients. Thus, rFVIIa is not recommended
(Class III; Level of Evidence A). It was also not recommended by ESO, 2010
Stroke. 2015; 46: 3020-3035 International journal of stroke 9.7 (2014): 840-855.

and DVT Prophylaxis
7. 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). Graduated compression
stockings are not beneficial to reduce DVT or improve outcome (Class III;
Level of Evidence A).
8. After documentation of cessation of bleeding, low dose subcutaneous low-
molecular-weight heparin or unfractionated heparin 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).
9. Systemic anticoagulation or IVC filter placement is probably indicated in ICH
patients with symptomatic DVT or PE (Class IIa; Level of Evidence C).
The decision between these 2 options should take into account several factors,
including time from hemorrhage onset, hematoma stability, cause of
hemorrhage, and overall patient condition (Class IIa; Level of Evidence C).

and DVT Prophylaxis

Hypertension in acute stroke a
management dilemma
Hemorrhagic stroke
The conflict1
:
(1) Severe elevations in BP may worsen ICH.
(2) Enlargement of the hematoma is associated with neurologic deterioration and
worse outcomes. These observations indicate that significant improvements in
patient outcome from ICH can be achieved by minimizing hematoma
enlargement.
1- Stroke 2007; 38:1072–1075.

management dilemma (cont.)
The guidelines:
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) and can be effective for improving functional
outcome (Class IIa; Level of Evidence B).
For ICH patients presenting with SBP >220 mmHg, 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).
This is also supported by European Stroke Organisation (ESO) guidelines in 2014
who recommends In acute ICH within 6 h of onset, intensive blood pressure
reduction (systolic target <140 mmHg in <1 h) is safe and may be superior to a
systolic target <180 mmHg. No specific agent can be recommended.
Stroke. 2015; 46: 3020-3035 International journal of stroke 9.7 (2014): 840-855.

Studies have been carried out in that respect:
(1) In a randomized controlled trial [INTensive Blood Pressure Reduction in Acute
Cerebral Hemorrhage trial (INTERACT1)]1 on 404 patients with acute
spontaneous ICH, intensive BP lowering treatment (target SBP 140 mmHg),
compared with traditional management (target SBP 180 mmHg), was associated
with a reduction in hematoma growth at 24 h (14 vs. 26%; p = 0.04).
(2) Most recently, the main phase [(INTERACT2)]2 trial has shown no increase in
death or serious adverse events from early intensive BP lowering in eligible
patients with elevated SBP.
1- Stroke. 2012;43:2236–2238. AND Lancet Neurol. 2008 May;7(5):391-9. 2- N Engl J Med. 2013;368:2355–2365.

Studies have been carried out in that respect:
(3) Antihypertensive Treatment of Acute Cerebral Hemorrhage II (ATACH-2) trial,
involved 1000 patient, 500 were assigned to intensive treatment and 500 to
standard treatment.
•mean systolic blood pressure of 200.6 mmHg at baseline.
•Results showed that; the treatment of participants with intracerebral
hemorrhage to achieve a target systolic blood pressure of 110 to 139 mmHg
did not result in a lower rate of death or disability than standard reduction to
a target of 140 to 179 mm Hg.
3- N Engl J Med 2016; 375:1033-1043

Treatment (cont.)
Factors Recommendation
General
Monitoring and
Nursing
Initial monitoring and management of ICH patients should take
place in an intensive care unit or dedicated stroke unit with physician
and nursing neuroscience acute care expertise (Class I; Level of
Evidence B).
Airway
&Breathing
Supplemental oxygen should be provided to maintain
oxygen saturation >94% (Class I; Level of Evidence C).
Supplemental oxygen is not recommended in nonhypoxic patients
with acute ischemic stroke (Class III; Level of Evidence B).
Mobilization Early mobilization of less severely affected patients and measures
to prevent subacute complications of stroke are recommended
(Class I; Level of Evidence C).
Nutrition A formal screening procedure for dysphagia should be performed
in all patients before the initiation of oral intake to reduce the risk of
pneumonia (Class I; Level of Evidence B).
Insert a nasogastric tube if the patient fails the swallow test.
Consider PEG only if prolonged enteral feeding is required (Class
I; Level of Evidence B).
Stroke. 2015; 46: 3020-3035

Infection and
fever
Treatment of fever after ICH may be reasonable (Class IIb; Level of
Evidence C).
Sources of hyperthermia (temperature >38°C) should be identified and
treated, and antipyretic medications should be administered to lower
temperature in hyperthermic patients with stroke (Class I; Level of
Evidence C).
Routine use of prophylactic antibiotics has not been shown to be
beneficial (Class III; Level of Evidence B).
Patients with suspected pneumonia or urinary tract infections should be
treated with appropriate antibiotics (Class I; Level of Evidence A).
Seizures Clinical as well as EEG documented seizures should be treated with
antiseizure drugs (Class I; Level of Evidence A).
Prophylactic antiseizure medication is not recommended (Class III;
Level of Evidence B).
Blood
Glucose
Glucose should be monitored. Both hyperglycemia and hypoglycemia
should be avoided (Class I; Level of Evidence C).
Treatment (cont.)

Prolonged
recumbency
As regard ICH, After documentation of cessation of bleeding, lowdose
subcutaneous low-molecular-weight heparin or unfractionated heparin
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).
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).
Brain
dehydratin
measures
Corticosteroids should not be administered for treatment of elevated
ICP in ICH (Class III; Level of Evidence B). In agreement with
International stroke foundation guidelines, 2010 (A)
Treatment (cont.)
National Stroke Foundation – Australia (2010)

Prevention of Recurrent ICH
1. BP should be controlled in all ICH patients (Class I; Level of Evidence
A). Measures to control BP should begin immediately after ICH onset
(Class I; Level of Evidence A). A long-term goal of BP <130 mmHg
systolic and 80 mmHg diastolic is reasonable (Class IIa; Level of
Evidence B).
2. Lifestyle modifications, including avoidance of alcohol use greater than 2
drinks per day, tobacco use, and illicit drug use, as well as treatment of
obstructive sleep apnea, are probably beneficial (Class IIa; Level of
Evidence B).
3. Avoidance of long-term anticoagulation with warfarin as a treatment for
nonvalvular atrial fibrillation is probably recommended after warfarin-
associated spontaneous lobar ICH because of the relatively high risk of
recurrence (Class IIa; Level of Evidence B).

Prevention of Recurrent ICH
4. The optimal timing to resume oral anticoagulation after anticoagulant-
related ICH is uncertain. Avoidance of oral anticoagulation for at least 4
weeks, in patients without mechanical heart valves, might decrease the
risk of ICH recurrence (Class IIb; Level of Evidence B). If indicated,
aspirin monotherapy can probably be restarted in the days after ICH,
although the optimal timing is uncertain (Class IIa; Level of Evidence B).
5. The usefulness of dabigatran, rivaroxaban, or apixaban in patients with
atrial fibrillation and past ICH to decrease the risk of recurrence is
uncertain (Class IIb; Level of Evidence C).
6. There are insufficient data to recommend restrictions on the use of statins
in ICH patients (Class IIb; Level of Evidence C).

Statins and ICH
There are conflicting reports regarding the use of statins in patients with ICH.
Stroke Prevention With Aggressive Reduction in Cholesterol Levels (SPARCL)
study, the benefit of high-dose atorvastatin in reducing recurrent ischemic stroke
was offset in part by an increased risk of ICH. However it was non significant.
Also a study in 2012 over 163 patients with ICH 40 was on statin treatment,
published in Stroke journal concluded that Statin use in patients with ICH is
independently associated with microbleeds
However another metanalysis in 2013, studied 31 randomized controlled trials
that included 91 588 statin-treated patients found no significant association
between statin use and ICH (OR, 1.08; 95% CI, 0.88–1.32; P=0.47).
It remains unclear whether statins should be continued or discontinued in ICH
patients.
Stroke. 2012;43:2677-2681
Neurology. 2008;70(24 Pt 2):2364–2370.
Stroke.2012;43:2149–2156.

By the year 2000 the commonest killers such
as coronary heart disease, stroke, respiratory,
diseases and many cancers will be wiped out.
Anonymous
Irish Times (24 Apr 1987)
I think this was a joke

Intracerebral Hemorrhage Case presentation

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