INTRACRANIAL

HEMORRHAGE
 HEMMORAGIC STROKE
location and underlying vascular pathology
1.subdural
2.epidural
3.intraparenchymal:
4.intraventricular
5.SAH
20 % of strokes - hemorrhagic,
SAH & ICH each accounting for 10 %
 Intracerebral hemorrhage
• the third most common cause of stroke
• 10 % of all strokes ( Framingham study )
• 10% of all strokes & 25% in Japan (Asian and Africa)
• incidence :increases with age, doubling q 10 yrs after 35
• highest in Asians > blacks > whites
• 50% case fatality
 Risk factors

• HTN : the most impt

• d/c of anti HTN Rx, smoking ,age < 55 yrs
• deep > lobar ICH
• Cerebral amyloid angiopathy
elderly,recurrent,microbleeds
• Hgic infarction : venous sinus thrombosis
• septic embolism : bacterial endocarditis
• brain tumor, bleeding disorders,
 Risk9
• Hypocholesterolemia - ?statins
• anticoagulants, thrombolytic therapy,
• CNSinfection :eg, herpes simplex encephalitis
• mycotic aneurysm, moyamoya, vasculitis,
• drugs :cocaine, amphetamines
 Mechanisms of brain injury
• Primary direct mechanical injury
expanding clot
• Increased intracranial pressure (ICP)
• Herniation secondary to mass effect
• Thrombin-induced activation of the
inflammatory cascade &
• overexpression of MMPs
– breakdown of the BBB &
– edema formation in ICH
• MMP-9 9 an increased volume of
peripheral edema
 Hemorrhage enlargement
• first six hours
• the clot expands, surrounding vessels 9
stretched - new sites of vessel rupture
• ass. with neurologic deterioration
• Sign, improvements in pt outcome
– by minimizing both secondary brain ischemia and
– hematoma enlargement.
• relationship of systemic BP to hematoma
enlargement = not clear
• c-Fn IL-6 9 ICH enlargement
• clinical utility of MMP, c-Fn, or IL-6 blood
levels 9 not yet clear.
 CLINICAL PRESENTATION
• exertion /intense emotional activity
• most : during routine activity
• neurologic sxs usu. increase gradually
over mins - few hrs (30-90min)
• Headache, vomiting,
• a decreased level of consciousness
most common with cerebellar and lobar
hemorrhages
 CLINICAL9
• Seizures ( 7 - 9 %)
in lobar hemorrhages
• a stiff neck & meningismus
• Stupor / coma - an ominous sign
exception - thalamic hemorrhage
 Neurologic signs
Location Frquency

putamen 35%

subcortex 30%

cerebellum 16%

thalamus 15%

pons 5-12%
 Location Neurologic signs
Putamen hemiplegia, hemisensory loss,
homonymous hemianopsia, gaze palsy,
stupor, and coma.
Cerebellar imbalance, vomiting, headache neck
stiffness, gaze palsy,facial weakness, no
hemiparesis
Thalamic hemiparesis, hemisensory loss,
occ.transient homonymous hemianopsia
"wrong way eyes",aphasia , neglect
Lobar vary with location, most : parietal &occipital
lobes, higher incidence of seizures

Pontine deep coma over the first few minutes, by

total paralysis, pupils are pinpoint, react to
a strong light source
 DIAGNOSIS
• clinical
• neuroimaging : CT or MRI
evident almost immediately
• Differential diagnosis :
Amyloid angiopathy, bleeding into a tumor &
vascular malformations -lobar / atypical in
appearance.
 TREATMENT
• medical & surgical interventions
Intracranial pressure control

• ICP monitoring
CPP maintained >60 -70 mmHg
• Medical therapies for increased ICP
mannitol,
an initial bolus of 1 g/kg, followed by
infusions of 0.25 to 0.5 g/kg every six hours
goal of therapy : plasma hyperosmolality
300 to 310 mosmol/kg
• barbiturate coma, and hyperventilation
• Steroids should not generally be used
• Hydrocephalus
thalamic & cerebellar hemorrhage
Ventriculostomies
ventriculoperitoneal shunt
 Blood pressure control
• MAP - often elevated in pts with ICH
• lowering BP - ischemia
• severe elevations - worsen ICH
• ?Local cerebral autoregulation -appears
to be intact
• gently lowering the MAP appears to be
reasonable (15-17 % )
• In the absence of intracranial monitoring
IV nitroprusside, nicardipine, or labetalol
SBP > 170 mmHg
goal : SBP 140 -160 mmHg
 Surgery
• Suboccipital craniectomy with cerebellar
decompression
for all cerebellar h’ges >3 cm diameter
• supratentorial ICH : more controversial
- open craniotomy, CT guided stereotaxic
aspiration, & newer endoscopic methods
- refractory increases in ICP
• Hemostatic therapy
• activated recombinant factor VIIa (rFVIIa)

• Rehabilitation
 Subarachnoid hemorrage
ruptured saccular aneurysms: most
Other causes :
trauma, AVM/F, vasculitides,
intracranial arterial dissections,
amyloid angiopathy, bleeding diatheses
illicit drug use :cocaine and amphetamines
• intracranial saccular aneurysms
• radiographic and autopsy series is 5
percent
• 20 - 30 % of pts - multiple aneurysms
• mean age at onset is 55 years
• most aneurysms do not rupture
• risk of rupture : size
 RISK FACTORS
• Cigarette smoking
• Hypertension,alcohol,family hx (OR 4.0)
genetics
• Phenylpropanolamine, antithrombotic
therapy , estrogen deficiency
CLINICAL MANIFESTATIONS
• rapidly increasing intracranial pressure
• bleeding usu. lasts only a few secs,
• rebleeding is common,more often within
the first day
• the sxs of SAH typically begin abruptly
• occurring at night in 30 %
• Severe headache (97%), lateralized in
30%
• onset : brief loss of consciousness,
seizure, nausea, vomiting, or meningismus
• 30 - 50 % - a minor hemorrhage /"warning
leak “
• precedes a major SAH by 6 - 20 days
• Physical exertion may be an acute trigger
for SAH
 COMPLICATIONS

• high mortality rate

~10 % die prior to reaching the hospital,
25 % die within 24 hours
45 % die within 30 days
Rebleeding Vasospasm
Hydrocephalus Increased ICP
Seizures Hyponatremia
Cardiac abnormalities
 DIAGNOSIS
• Sudden "thunderclap" headache,
regardless of severity or prior headache
history
• Noncontrast CT
• with or without lumbar puncture :mainstay
of diagnosis of SAH
• Clearing of blood,xanthochromia= at least
two hour
DDx :
• increased CSF conc. of pr (150 mg/dL),
• systemic hyperbilirubinemia (>10 to 15
mg/dL), and
• traumatic LP > 100,000 RBCs/µL.

• Brain MRI
IDENTIFYING THE ETIOLOGY
• No angiographic : 14 - 22 % of cases
• repeat the angiogram in 4 - 14 days
• Cerebral angiography
• CT and MR angiography : > 3 to 5 mm
 Grading & Px

• Rx partly dependent on severety

• Most impt Pxic factors
– Level of consciousness
– Pt age
– Amt of blood on initial CT

• A number of grading systems

– Hunt and Hess,WFNS,
– The Fisher grade,Claasen grding system
 General Mx
• ICU,hemdynamic monitoring
• Stool softners
• Bed rest
• Headache/ neck pain is severe,
• mild sedation & analgesia
– Dec. hemodynamic fluctuation
& risk of rebleeding
• Adequate hydration
 ICP & BP
ICP secondary to
• SA blood, parenchymal hematoma,
• acute hydrocephalus, or loss of vascular
autoregulation.
• stuporous = emergent ventriculostomy to
prevent cerebral ischemia
• Medical Rx : mild hyperventilation, mannitol, &
sedation can also be used as needed
• ICP refractory to Rx is a poor pxic sn.
• Occasionally an intracranial hematoma causing
neurologic deterioration = removal.
 ICP & BP
• Ventriculostomy =CPP
• Pt cognitive status : useful guide
• Pt alert = CPP is adeq. = lowering BP dec.
risk of rebleeding
• SBP < 140 mmHg
– Avoid vasodilator: nitroprusside,NG
– Prefered : labetalol
• Severly impaired consciousness : hold
antiHTN
 ICP & BP9.
Nimdipine :CCB
• Initially used in pts with SAH to prevent
vasospasm
• ?angiographic or sxic vasospasm
• Demonstrated improved out come =
standard of care in these pts
– Mech. Of benefit : UK
– Ideally adminstered with in 4 days
– Dose : 60 mg q 4 hrs( PO)
 Physiologic derangements
• Hypoxia,metabolic acidosis
• Hyperglycemia,CV instability
999..ass .with high risk of death
• Infectious and non infectious fever
– Rx suggested
• Seizure prophylaxis
– Recommended in standard texts
– ? Controversies : worse neurologic and
cognitive outcomes
• Antifibrinolytic Rx
– Dec. rebleeding
– No dec. in poor outcomes
Glucocorticoid Rx
• reduce the head & neck ache
• no good evidence :reduce cerebral edema, are
neuroprotective, or reduce vascular injury,
• their routine use therefore is not recommended.
 Prevention of vasospasm
• Clinically sign. VS ; 20-30 %
• No earlier than D3 ,Peak D7 -8
– Deterioration in neurologic status,onset of
focal neurologic abns
– Leading cause of death and disability after
aneurismal rupture
• Rx : difficult
• Prevention impt :
 vasospasm
Triple H – Rx
Some benefit on sxic VS and mortality

Surgical approaches
Investigational approaches
Endithelin receptor antagonists,Mg
sulfate,statins
 Rx of aneurysms

• Surgery : “clipped” by a neurosurgeon

• Endovascular Rx : “coiled” by a
neurointerventional radiologist
 Mx of complications
• Vasospasm ; triple H Rx
• Hydrocephalus ; shunt
• Hyponatremia
– SIADH / cerebral salt wasting
– Physiologically Dt
– Divergent Rx
Cerebral salt wasting
– Volume depletion..release of ADH
– Rx : isotonic saline
– Restoration of euvolemia9dec. ADH
 Complications9
SIADH
– Euvolemic
– Rx isotonic /hypertonic saline
• Rebleeding
Ass with poor out come
– Lowering HTN,Antifibrinolytic Rx
– Unsuccessful
– Only aneurismal Rx is effective