Intracerebral Hemorrhage

Resource Speaker: Roderick B. Cevallos, MD, FPCP

Moderator: Myrna Bobis, FPCP
Presentor: Giselle M. Regaspi, MD
General Objective

To present a case of Intracerebral Hemorrhage

Specific Objectives
 To discuss the clinical presentation, etiologies
and diagnostic approach of intracerebral
hemorrhage

 To present the 2015 AHA/ASA Guidelines on

the management of Intracerebral
Hemorrhage
CASE
Patient's Profile
• M.R.
• 68 year old female
• Filipino
• Roman Catholic
• Zone 2, Burabod, Lagonoy, Camarines Sur
• Admitted for the first time at Bicol Medical
Center on September 13, 2016
Chief Complaint
• right sided body weakness
History of the Present Illness
Patient is apparently well until

Three hours PTA

right sided body weakness,
slurring of speech,
no associated loss of consciousness, headache
and vomiting

Patient was brought to local hospital

BP of 220/120 mmHg, GCS 13,
Hooked to PNSS 1 L,and was given Captopril 25 mg
SL
Past Medical History
Hypertensive- unknown duration, unknown
medication

Non-asthmatic
Non-diabetic
No previous hospitalization
Family History
No family history of hypertension, diabetes, liver
disease, kidney disease and other heredofamilial
disease
Personal/Social History
• Non-smoker
• Non alcoholic beverage drinker
• No history of illicit drug use
REVIEW OF SYSTEM
Constitutional: (-) weight change, (-) fever
HEENT: (-) blurring of vision, (-) nasal obstruction, (-) sore throat
CVS: (-) chest pain, (-) palpitations, (-) easy fatigability, (-) PND,
(-) orthopnea, (-) stiffining of extremities
Respiratory: (-) cough (-) hemoptysis
GIT: (-) abdominal pain, (-) nausea and vomiting, (-) diarrhea,
(-) constipation, (-) hematemesis, (-) melena
REVIEW OF SYSTEM
Genitourinary Sys: (-) dysuria (-) urinary frequency (-) urgency
(-) polyuria (-) hematuria
Extremities: (-) edema (-) swelling of joints (-) stiffness
Nervous Sys: (-) syncope (-) syncope
Hematopoietic Sys: (-) bleeding tendencies (-) pallor (-) easy
bruising
Endocrinology: (-) intolerance to heat and cold, (-) excessive
wt. gain and loss, (-) polyuria, (-) polydipsia
PHYSICAL EXAMINATION
GENERAL SURVEY:
Drowsy, not in cardiorespiratory distress
BP: 140/100 mmHg HR: 80 bpm RR: 20 cpm
T: 36 C O2 Sat: 97%
HEENT: Pink palpebral conjunctivae, anicteric sclera, no
tonsillopharyngeal congestion, no nasoaural discharge,
no cervical lymphadenopathy, non-tender, no neck vein
engorgement
CHEST: Symmetrical chest expansion, no retraction,
clear breath sounds
PHYSICAL EXAMINATION
HEART: Adynamic precordium, normal rate regular
rhythm, apex beat at left 5th ICS MCL, (+) grade 3 systolic
murmur at the left 5th ICS 1-2 cm medial to the
midclavicular line
ABDOMEN: Flabby, soft, normoactive bowel sounds, no
organomegaly
EXTREMITIES: No gross deformities, no edema, full and
equal pulses, no cyanosis
Neurological Examination
Drowsy
GCS 10 (E4V1M5)
Cranial Nerve:
I - not assessed
II- 2-3 mm pupil ERTL
III, IV, VI- not assessed
V- (+) corneal reflex
Neurological Examination
VII - narrow nasolabial fold, right
VIII- not assessed
IX, X- not assessed
XI – not assessed
XII – not assessed
Pathological Reflexes: (+) Babinski, Right
Motor (R) Motor (L) Sensory (R) Sensory (L) Deep Tendon Deep Tendon
Reflex (R) Reflex (L)

1/5 5/5 NA NA ++ ++
1/5 5/5 NA NA ++ ++
 9/13/17 9/14/17 9/15/17 9/16/17 9/16/17 9/20/17

FBS 5.66
Total Chole 5.20
Triglyceride 0.62
s
HDL 1.05
LDL 3.9
INR 0.83
% Activity 113
WBC 11.52
Hgb 123
Plt ct 186
neutrophils 92.90
Na 135.27 139.72 134.60
K 2.66 3.25 3.27
Crea 64.54
BUN
12 L ECG SR, NA, LVH,
Parieto Temporal Hge, Left
Salient Features
• 68 year old female
• hypertensive
• right sided body weakness
•slurring of speech
•BP: 220/120 mmHg
•drowsy
•GCS 10 (E4v1M5)
•Motor: 1/5 at the right
•CN VII- (+) narrow nasolabial fold at the right
•(+) Babinski, the right
Differential Diagnosis
• SAH
• Ischemic Stroke
• Metabolic
Hyper/hypo glycemia
Post Arrest Ischemia
Drug Overdose
• Head and Cervical Trauma
• Intracranial Mass
Tumor
Sub/Epi dural hematoma
• Meningitis/Encephalitis
• Hypertensive Encephalopathy
Admitting Diagnosis

Cerebrovascular Disease, Left Middle Cerebral Artery

At the ER
• Drowsy, not in • PNSS 1 L x 12 Hours
cardiorespiratory distress • Mannitol 150 cc IV bolus was
• GCS 9 (E 3V1 M5) given
• BP 140/100 mmHg CR 88 bpm • NGT was inserted
• RR 26 Temp 36 O2 Sat 97% • OTF 1600 kcal divided in six
• Motor
equal feeding was started
0/5 5/5 • The following diagnostics
were done CBC Na, K, BUN,
0/5 5/5
Creatinine, FBS, Lipid profile,
CXR-PA, 12 L ECG, Plain
Cranial Ct Scan, ABG
• CBG 129 mg/dl
At the ER
• Drowsy, not in • The following
cardiorespiratory distress medications were started
• GCS 9 (E 3V1 M5) • Mannitol 150 cc IV q6,
• BP 140/100 mmHg CR 88 • Citicoline 1 g IV q12,
bpm • Lactulose 30 cc OD at HS,
• RR 26 Temp 36 O2 Sat 97%
• Omeprazole 40 mg IV
• Motor OD,
• Amlodipine 10 mg/tab
OD at PM
• Hooked to O2 support at
2 lpm via nasal cannula
Course in the Ward
• BP: 160/90 mmHg • Mannitol was decrease to q8
CR: 92 bpm RR: 18 cpm hour
• Atorvastatin was decrease
Temp 36.5 C O2 Sat 97 %,
to 40 mg/tab OD at HS
• GCS 10 (E4V1M5)
• Losartan 50 mg/tab BID
• 12 L ECG revealed Sinus
• Started on K correction,
Rhythm with Left
Ventricular Hypertrophy PNSS 1L + 40 meqs KCl to
with Non-Specific ST-T run for 12 hours for 3 cycles
Wave Changes • Foley Catheter was inserted
• Laboratory result revealed
Na 135, K 2.66 Crea 64.4
Course in the Ward (2nd HD)
• Had two episodes of • Started on Nicardipine drip:
vomiting Nicardipine 1 amp in 90 cc D5W
• BP 180/100 mmHg
at 10 ugtt/min titrate by 5
ugtt/min to attain a MAP of 126
• GCS 11 (E4V1M6)
• Discontinue Amlodipine while
• pupils 2-3 mm ERTL on Nicardipine
• Referred to Neurosurgery and
0/5 5/5
• Motor Neurology service
0/5 5/5

•
Course in the Ward (3rd HD)
• GCS 10 E3V1M5-6 • PNSS 1L was increased to 8
• had episode of fever
hours
• Omeprazole 40 mg IV OD was
• initial Ct Scan Result:
started
Bleed, no midline shift
• Nicardipine drip was titrated
• Motor to maintain systolic BP 140-
0/5 5/5 160 mmHg
0/5 5/5
Course in the Ward (4th HD)
• Omeprazole 40 mg/tablet 1 cap OD
• (+) fever
• Paracetamol 300 mg IV forTemp > 38.6 C
• no seizure
• Paracetamol 500 mg/tab q4 for temp
• no headache
> 37.8 C
• BP: 130/90 mmHg
• Mannitol was decrease to 150 cc q12
• CR: 95 bpm
• TSB as needed
• RR: 16 cpm
• Nicardipine drip was hold
• Temp. 37.8 C
• O2 Sat 99 %
Course in the Ward (4th HD)
• (+) fever • Started on Amlodipine 10 mg/tab OD
• no seizure • Ampicillin-Sulbactam 750 mg IV q8
• no headache • N-Acetylcysteine 600 mg/tab in ½
• BP: 130/90 mmHg
glass of water OD
• Seen by Neurology service
• CR: 95 bpm
• Started on Acetazolamide 250 mg/tab ,
• RR: 16 cpm TID
• Temp. 37.8 C • Transfer to regular ward

• O2 Sat 99 %
Course in the Ward (5th HD)
• No dyspnea • IM-Neurology Service
• provide bedside turning
• No fever
schedule
• Vital sign were • for referral to rehab medicine
• BP 130/80 mmHg
• CR 82 bpm
• RR 21 cpm
• Temp 36.5 C
• GCS (11) E3V2-3M5
Course in the Ward (5th HD)
Official CT Scan result:
• Acute Parenchymal Hemorrhage involving the left parieto-
temporal lobes with moderate surrounding edema, compression of
the ipsilateral lobes with moderate surrounding edema,
compression of the ipsilateral left lateral ventricle and midline shift
towards the right.
• Sub-acute infarct considered involving the head of the right
caudate nucleus, the rigth thalamo-ganglionic region and the right
corona radiata. Small subdural hygroma considered in bilateral
parietal convexities. Mild cerebral volume loss is also considered.
Course in the Ward (6-7th HD)
• BP: 120/80 mmHg • On Ampicillin Sulbactam 750 mg IV,
• CR: 96 bpm
day 4
• for repeat Cranial CT Scan
• RR: 22 cpm
• Temp 37.8 C
• GCS 11 (E4V1-2M5)
• Motor
0/5 5/5

0/5 5/5
Course in the Ward (8th HD)
• GCS 12 (E4V2M6) Seen by Neurosurgery:
 no immediate neurosurgical
intervention
 to continue medical
decompression
 for repeat of Cranial CT scan
after 1 week
Course in the Ward (8th HD)
 Patient improved, discharged with the following
medications:
Cefexime 200 mg/tab BID for 3 more days,
Amlodipine 10 mg/tab OD,
Losartan 50 mg/tab BID,
Citicoline 1 g/tab OD,
Lactulose 30cc OD at HS,
Acetazolamide 250 mg/tab x 1 week,
N-acetylcysteine 600 mg/tab OD x 10 days.
 For follow up Friday at 1 pm after 1 week with repeat Cranial CT
scan result
Final Diagnosis
• Intracerebral Hemorrhage, Left Parieto-Temporal Lobes
• Hypertensive Atherosclerotic Cardiovascular Disease
 DISCUSSION
INTRACEREBRAL HEMORRHAGE
Epidemiology
 Intracerebral hemorrhage (ICH) affects >1 million
people annually worldwide and is the deadliest and
most disabling type of stroke

 ICH accounts for ~10% of all strokes, and about 35–

45% of patients die within the first month

 The incidence of ICH is higher in Asians, partly due to

limited primary care for HTN and non-compliance

Harrison's Principles of Internal Medicine 19th Edition

Major Cause of ICH
Hypertension
Coagulopathy
Sympathomimetic drugs (cocaine, methamphetamine)
Cerebral amyloid angiopathy
Advanced age and heavy alcohol consumption
Cocaine and methamphetamine use is one of the most
important causes in the young
Classification of ICH
 Spontaneous ICH- intraparenchymal bleeding in the
absence of trauma or surgery
a. Primary ICH
i. Lobar ICH-cerebral amyloid angiopathy
ii Non-lobar or hypertensive ICH- long-standing
high blood pressure resulting in lipohyalinosis of
small perforating arteries affects mostly the
basal ganglia, especially the putamen, the most
common site for hypertensive hemorrhage,
thalamus, cerebellum, pons

BMJ Journal
Classification of ICH

• Secondary ICH
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

BMJ Journal
Pathogenesis
Hypertensive Intracerebral
Hemorrhage
ICH usually results from
spontaneous rupture of a small
penetrating artery deep in the
brain

Harrison's Principles of Internal Medicine 19th Edition

BMJ Journal
Thalamic Pontine Cerebellar Lobar Hemorrhage
hemorrhages hemorrhages hemorrhages
contralateral Deep coma with Occipital headache, Left temporal
hemiplegia quadriplegia often repeated vomiting, hemorrhage
occurs over a few and ataxia of aphasia and
sensory deficit minutes gait. delirium;

Aphasia, Decerebrate rigidity Dizziness or vertigo Parietal hemorrhage

and “pinpoint” (1 hemisensory loss;
preserved verbal mm) pupils that react paresis of conjugate frontal hemorrhage,
repetition, to light lateral gaze toward arm weakness
the side of the
constructional (doll’s-head hemorrhage, Large hemorrhages
apraxia or mutism or oculocephalic or an ipsilateral sixth stupor or coma if
maneuver) nerve palsy they compress the
ocular disturbances thalamus or midbrain
deviation of the eyes Hyperpnea, severe Ocular bobbing, and
downward and hypertension, and skew deviation
inward hyperhidrosis are Dysarthria and
common. dysphagia may occur

Harrison's Principles
of Internal Medicine
19th Edition
Hypertensive ICH
 Most hypertensive ICHs- develop over 30–90 min

 ICH associated with anticoagulant therapy may evolved 24–48 h

 Within 48 h, macrophages begin to phagocytize the hemorrhage

at its outer surface

 After 1–6 months, the hemorrhage is generally resolved

Harrison's Principles of Internal Medicine 19th Edition

Hypertensive ICH

 clinical symptoms, maximal at onset

 focal deficit worsens over 30–90 min
 diminishing level of consciousness
 signs of increased ICP such as headache and
vomiting

Harrison's Principles of Internal Medicine 19th Edition

Cerebral amyloid angiopathy

 Amyloid angiopathy causes both single and recurrent

lobar hemorrhage in the elderly

 Present with multiple hemorrhages (and infarcts) over

several months or years or in patients with “microbleeds”
seen on brain MRI sequences sensitive for hemosiderin
(iron-sensitive imaging)

 Diagnosed by pathologic demonstration of Congo red

staining of amyloid in cerebral vessels

Harrison's Principles of Internal Medicine 19th Edition

Cocaine and Methamphetamine
 Stroke in the young (age <45 years)
 ICH, ischemic stroke, and SAH are all associated with
stimulant use
 Sympathetic activity causing acute, sometimes severe,
hypertension, and this may lead to hemorrhage
 In cases of SAH, a saccular aneurysm is usually identified

Harrison's Principles of Internal Medicine 19th Edition

Anticoagulant Therapy
 Lobar or subdural, anticoagulant related ICHs
 ICHs may continue to evolve over 24–48 h is
insufficiently reversed

Harrison's Principles of Internal Medicine 19th Edition

ICH associated with Hematologic
Disorders
 Leukemia
 Aplastic anemia
 Thrombocytopenic purpura
• can occur at any site and may present as multiple ICHs

 Skin and mucous membrane bleeding may be evident

and offers diagnostic clue

Harrison's Principles of Internal Medicine 19th Edition

Hemorrhage Into a Brain Tumor
Hemorrhage into a brain tumor may be the first
manifestation of neoplasm
Choriocarcinoma,
malignant melanoma,
renal cell carcinoma
and bronchogenic carcinoma are among the most
common metastatic tumors associated with ICH

Glioblastoma multiforme in adults and

medulloblastoma in children may also have areas of ICH

Harrison's Principles of Internal Medicine 19th Edition

Hypertensive encephalopathy
In this acute syndrome, severe hypertension is
associated with
headache,
nausea,
vomiting,
convulsions,
confusion,
stupor,
and coma

There are retinal hemorrhages, exudates, papilledema

(hypertensive retinopathy), and evidence of renal and
cardiac disease

Harrison's Principles of Internal Medicine 19th Edition

Vasculitis associated ICHs
polyarteritis nodosa or lupus erythematosus
produce hemorrhage in any region of the central
nervous system;
most hemorrhages are associated with hypertension,
arteritis
cause bleeding by disrupting the vessel wall
Nearly one-half of patients with primary intraventricular
hemorrhage have identifiable bleeding sources seen using
conventional angiography

Harrison's Principles of Internal Medicine 19th Edition

Other Causes of ICHs
Sepsis can cause small petechial hemorrhages throughout the
cerebral white matter
Moyamoya disease, mainly an occlusive arterial disease
that causes ischemic symptoms, produce ICH particularly in the
young
Hemorrhages into the spinal cord are usually the result of an AVM,
cavernous malformation, or metastatic tumor
Epidural spinal hemorrhage produces a rapidly evolving syndrome
of spinal cord or nerve root compression
Spinal hemorrhages usually present with sudden back pain and
some manifestation of myelopathy

Harrison's Principles of Internal Medicine 19th Edition

Laboratory and Imaging
Evaluation
PT/PTT/INR is important to identify coagulopathy
CT imaging, detects acute focal hemorrhages in the
supratentorial space
Images of flowing blood on MRI scan may identify AVMs as
the cause of the hemorrhage
MRI, CT angiography (CTA), and conventional x-ray
angiography are used when the cause of intracranial
hemorrhage is uncertain, if the patient is young or not
hypertensive and the hematoma is not in one of the usual
sites for hypertensive hemorrhage

Harrison's Principles of Internal Medicine 19th Edition

Laboratory and Imaging
Evaluation
Haematoma volume can be estimated on head CT
ABC/2 method
 A is maximal haematoma diameter on the axial slice with largest
haematoma area,
 B is maximal haematoma diameter perpendicular to A and
 C is the number of CT slices with haematoma multiplied by slice
thickness (ignoring slices with <25% of haematoma area compared
with the reference slice)

Harrison's Principles of Internal Medicine 19th Edition

Harrison's Principles of Internal Medicine 19th Edition
ICH MANAGEMENT
AHA/ASA ICH Guideline, 2015
Safety of Early Intensive BP-Lowering
Treatment
No significant ischemic penumbra in ICH
A randomized clinical trial using CT perfusion in primarily
small and medium ICH found no clinically significant
reduction in cerebral blood flow within the perihematomal
region related to early intensive BP lowering to an SBP target
of <140 mm Hg within several hours of ICH

AHA/ASA ICH Guideline, 2015

Safety of Early Intensive BP-
Lowering Treatment
Compared with ischemic stroke, in which consistent U-
or J-shaped associations between SBP nadir of 140 and
150 mm Hg and poor outcome have been shown
Only 1 study of ICH has shown a poor outcome at low
SBP levels (<140 mm Hg)

• AHA/ASA ICH Guideline, 2015

 Safety of Early Intensive BP-
Lowering Treatment
• AHA/ASA ICH Guideline, 2015
• AHA/ASA ICH Guideline, 2015
In a clinical cohort of 211 patients who received a standard
protocol of nicardipine-based BP lowering to reach an SBP target
of <160 mm Hg at a mean of 30 minutes (range, 15–45 minutes)
within 3 hours of the onset of ICH, the best outcomes were seen
in the group with the lowest achieved SBP (<135 mm Hg)

AHA/ASA ICH Guideline, 2015

Seizure Management

 Clinical seizures should be treated with antiseizure drugs

 Patients with a change in mental status who are found to
have electrographic seizures on EEG should be treated
with antiseizure drugs
 Continuous EEG monitoring is probably indicated in ICH
patients with depressed mental status that is out of
proportion to the degree of brain injury
 Prophylactic antiseizure medication is not recommended

AHA/ASA ICH Guideline, 2015

Temperature Management

 Treatment of fever after ICH may be reasonable

 common in intraventricular hemorrhage associated with
hematoma growth
 therapeutic cooling may reduce perihematomal edema

AHA/ASA ICH Guideline, 2015

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

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 PCCs may have
fewer complications and correct the INR more rapidly
than FFP

AHA/ASA ICH Guideline, 2015

Hemostasis and Coagulopathy, Antiplatelet
Agents, and DVT Prophylaxis
3. For patients with ICH who are taking dabigatran,
rivaroxaban, or apixaban, treatment with FEIBA, 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
4. Protamine sulfate may be considered to reverse
heparin in patients with acute ICH

AHA/ASA ICH Guideline, 2015

Glucose Management
 Both hyperglycemia and hypoglycemia should be avoided

 High blood glucose on admission predicts an increased

risk of mortality and poor outcome in patients with ICH,
independent of the presence of diabetes mellitus

 A randomized trial showing improved outcomes with tight

glucose control (range, 80–110 mg/dL) using insulin
infusions in mainly surgical critical care patients

AHA/ASA ICH Guideline, 2015

Management of Medical
Complications
The most common complications were
pneumonia (5.6%),
aspiration (2.6%),
respiratory failure/distress (2%),
PE (1.3%),
and sepsis 1.7%
Approximately 50% of deaths after stroke are attributed to
medical complications, usually after 7 days of hospitalization
Dysphagia and aspiration are major risk factors for the
development
AHA/ASA ICH Guideline, 2015
ICP Monitoring and Treatment
Usual causes of elevated ICP
hydrocephalus from IVH
mass effect from the hematoma
(or surrounding edema)
Increased ICP also may be more common in younger
patients and those with supratentorial ICH
current guidelines recommend placement of an ICP
monitor in patients with a GCS score of 3 to 8 and
maintenance of an ICP <20 mm Hg and a CPP of 50 to 70
mm Hg

AHA/ASA ICH Guideline, 2015

ICP Monitoring and Treatment

Elevation of the head of the bed to 30°

The use of mild sedation
Avoidance of collar-endotracheal tube ties that might
constrict cervical veins
Mannitol or hypertonic saline may be used to treat acute
ICP elevations
Hypertonic saline may be more effective

AHA/ASA ICH Guideline, 2015

ICP Monitoring and Treatment

 CSF drainage should be considered in patients with CSF

outflow obstruction caused by hydrocephalus or a trapped
ventricle
 Hematoma evacuation and decompressive craniectomy
(DC) are options for treating elevated ICP
 Corticosteroids should not be administered for treatment of
elevated ICP in ICH

AHA/ASA ICH Guideline, 2015

ICH Surgical Indications
 Cerebellar Hemorrhage >3 cm who are deteriorating or
with brain stem coompression and hydrocephalus from
ventricular obstruction
 Vascular malformation if lesion is surgically accessible and
has chance for good outcome
 Young patients with moderate or large lobar hemorrhage
who are clinically deteriorating

 AHA/ASA ICH Guideline, 2015

Non- surgical ICH patients
 Small Hemorrhages (10 cm )
 Minimal neurological deficits
 GCS <4 excluding cerebellar hemorrhage with brain
stem compression

AHA/ASA ICH Guideline, 2015

Medical Therapy
Mannitol
• Usual Adult Dose for Cerebral Edema
• 0.5–1 g/kg 20% solution IV over at least 30 min
administered not more frequently than every 6 to 8 hrs
• In small &/or debilitated patients 500 mg/kg may be
sufficient
Medical Therapy
Mannitol
• Urine output should be monitored during mannitol infusion
• Mannitol therapy should be discontinued if
progression in renal damage or dysfunction,
heart failure,
pulmonary congestion occurs
• For patient with oliguria, treatment dose 300 to 400 mg/kg (21 to 28
g for a 70 kg patient) or up to 100 g of 15% to 20% solution IV once
• Treatment should not be repeated in patients with persistent
oliguria
Medical Therapy
Citicoline Sodium
• CNS Stimulant or a Nootropics
• It acts by increasing the blood flow and O2 consumption of the
brain and involved in the biosynthesis action
• Citicoline promotes brain metabolism
• Citicoline is indicated in CVD in acute recovery phase in severe s/sx
of cerebrovascular insufficiency and in-cranial traumatism and their
sequellae
Comparisons of Mannitol vs Hypertonic
Solutions in the Treatment of Acute
Cerebral Edema
In the Mannitol plus hypertonic saline, patients GCS escalated from
baseline to sixt hour, then noted a trending down from the sixth hour
to the third day. At around the fifth day, this has seen to increase
again until discharge.

In the Mannitol + hypertonic sodium lactate roup, the GCS score has
been shown to be consistently improving from baseline until the first
day, further increasing to the third day.

Remarkedly, the rsults obtained from Mannitol + hypertonic Sodium

Lactate group with regard the improvement of GCS was a consistent
escalation from baseline to discharge
Hypertonic Sodium Lactate
(Totilac)
For ICP Control
Load 1.5 -3 cc/kg in 15-20 minutes then continue to infuse
at 0.5 cc/kg/hr until desired sodium and serum osmolality are
achieved (145-155 meq/L and 310-320 mOsm/L rspectively)
Hypertonic Sodium Lactate
(Totilac)
• Precaution:
• Hypertensive patients because of risk of solute overload causing
congested states with pheripheral and pulmonary edema
• Do not administer Totilac if the patient has the following:
• Hypovolemia
• Hypernatremia
• Metabolic Alkalosis
Statins
• There are conflicting reports regarding use of statins in ICH
• Stroke Prevention with Aggressive Reduction in Cholesterol Levels
• (SPARCL) study
• Benefit of high dose atorvastatin was offset by increased risk of ICH
• Later ICH recurrence associated with:
• Statin treatment
• Increasing age

• ICH as the qualifying stroke for enrollment

• Meta-analysis of 31 RCTs found no significant association between
• statin use and ICH
• Continued statin use after ICH has been associated with early
neurologic improvement and improved 6 month mortality in small
study. There is no data on effect of statin discontinuation after ICH
THANK YOU
Medical Therapy
• Euvolemia
• Isotonic crystalloid solutions

• Electrolyte abnormalities
• correct deficits

• Acid/base disorders
• correct them if present

• Steroids-no benefit
Hypertonic Sodium Lactate
(Totilac)
Totilac
• made up of hypertonic saline and lactate

• hypertonic saline solution is an osmotic agent similar to

mannitol that creates an osmotic gradient between the
intravascular and intracelllular/interstitial compartments
through addition of solute to the circulation rather than
diuresis leading to vascular compartment expansion
instead of contracted as it is with Mannitol use
Fever Management
• Elevated temperatures can increase the degree of ischemic injury,
• Etiologies include infection, neuronal injury, SIRS
• Studies have demostrated increased morbidity and mortality in
paatients with sustained temperature elevation.
• Treat temperature >38.5 C
• Acetaminophen or a coolong blanket best options.
Paralytics
• Recommended in order to prevent increasing inthrathoracic and
venous pressures associated with coughing, suctioning, and
bucking on ETT, all of which may cause ICP spikes
• ICP spikes associated with poorer outcome, especially in setting of
elevated ICP
Endotracheal Intubation
• Intubation- not required, but airway protection and adequate
ventilation are necessary
• relay on clinical suspicion, not GCS
• Hyperventilation decreases ICP
• pCO2 should be kept around 30-35
• Beneficial effect of sustained hyperventilation is not proven
HOB Elevation
• Elevate head of bed-decrease ICP
• Mechanical-helps drain blood by gravity
• Does not allow blood to pool in cranium, which may occur if patient
is left laying flat
Osmotherapy
• Osmotherapy
• Cerebellar hemorrhage
• Occipital headache
• Repeated vomiting
• Ataxia
• Dizziness and Vertigo may be prominent
Localization of Hemorrhage
• Pontine Hemorrhage
• Deep coma with quadriplegia over few minutes
• Pin point pupil reacting to ligth
• Impaired reflex horizontal eye movements
• Hyperpnoea, hyperhydrosis, hypertension are common
Localization of Hemorrhage
• Putamen Hemorrhage
• Contralateral Hemiparesis, contralateral sensory loss,
contralateral conjugate gaze paresis, homonymous hemianopia,
aphasia, neglect, or apraxia
Localization of Hemorrhage
• Thalamic Hemorrhage
• Contralateral sensory loss, contralateral hemiparesis, gaze
paresis, homonymous hemianopia, miosis, aphasia or confusion
• Lobar Hemorrahge
• Contralateral hemiparesis or sensory loss, contralateral
Differential Diagnosis

Subarachnoid hemorrhage Excruciating headache “ the worst headache of life”

Sudden transient loss of consciousness
Focal neurological deficit (neuropathies/hemiparesis)
Signs/sudden coma
Meningeal signs (nuchal rigidity)

Ruptured Aortic Aneurysm Headache

Seizures
Focal deficit (which may be progressive)
Intractable headaches

Tumor Headcahe,nausea/ vomiting, coma,

seizures, progressive neurological deficit
Pathogenesis

• When hemorrhages occur in other brain areas or in non-

hypertensive patients, greater consideration should be
given to other causes such as
• hemorrhagic disorders
• neoplasms
• vascular malformations
• and cerebral amyloid angiopathy
ICP Monitoring and Treatment
1.drainage as treatment for hydrocephalus is reasonable, especially
in patients with decreased level of consciousness

2. 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 mmHg may be reasonable to maintain depending

on the status of cerebral autoregulation

3. Corticosteroids should not be administered for treatment of

elevated ICP in ICH