Transcript Intracranial Hemorrhage & Emergency Management of elevated

INTRACRANIAL HEMORRHAGE &
EMERGENCY MANAGEMENT OF
ELEVATED ICP.
Najwa Al-Bustani
Neurology PGY-3
INTRACEREBRAL HEMORRHAGE:

Bleeding into the parenchyma of the brain that
may extend into the ventricles and, in rare cases,
the subarachnoid space.
Subcortical/lo
bar:
20 %
LOCATIO
NS
Thalamus
15 %
Pons
8%
Putamen
40-50 %
Cerebellum
8%
PATHOPHYSIOLOGY:

1.
1.
2 main concepts:
Haemorrhages continue to grow and expand over
several hours after onset of symptoms—a process
known as early haematoma growth.
Brain injury and swelling that happens in the
days after ICH is the result of inflammation
caused by thrombin and other coagulation endproducts.
Lancet Neurol 2005; 4: 662–72
INCIDENCE &
MORTALITY:

Each year, approximately 37,000 to 52,400 people
in the United States.

The case-fatality rate 34.6% at 7 days.

50.3% at 30 days.

59.0% at 1 year.
(Stroke. 2009;40:00-00)
RISK FACTORS:

Hypertension- 60-70 %.

Cerebral Amyloid Angiopathy- 15 %.
Heavy alcohol consumption.
 Hypercholesterolemia.
 Anemia.
 Smoking/anti-platelet agents >> merging
evidence.

PREDICTORS OF
OUTCOME:

GCS score.

ICH volume.
Modifiable

IVH.

Systolic BP.

Location: Supra/Infratentorial origin.

Age->65 years.
(Stroke. 2009;40:00-00)
MANAGEMENT:
4.
Medical:
Supportive care.
BP control.
Prevention of Hematoma growth.
ICP

Surgical options.

1.
2.
3.
BP MANAGEMENT:

Hypertension theoretically could contribute to
hydrostatic expansion of the hematoma, perihematoma edema, and rebleeding, all of which
may contribute to adverse outcomes in ICH.
Assessed 76 consecutive patients with
hypertensive ICH retrospectively.
 Attempted to lower SBP below targets of 140,
150, or 160 mm Hg.
 Recordings of serial BP from admission until the
second CT scan were assessed.
 Hematoma enlargement was defined as an
increase in volume of 140% or 12.5 cm3.

RESULT
S:




Hematoma enlargement occurred in 16 patients.
Maximum SBP was significantly associated with
hematoma enlargement.
After adjustment for other factors, maximum
SBP was independently associated with
hematoma enlargement.
Target SBPs of 160 mm Hg were significantly
associated with hematoma enlargement
compared with those of 150 mm Hg.
(Stroke. 2004;35:1364-1367.)
CONCLUSION:

Findings suggest that elevated BP increases the
risk of hematoma enlargement.
Efforts to lower SBP below 150 mm Hg may
prevent this risk.
(Stroke. 2004;35:1364-1367.)
INTERACT:



Open-label, randomized, controlled trial
undertaken in 404 mainly Chinese patients.
203 randomized to lower BP to target a low
systolic BP goal of 140 mm Hg within 1 hour and
maintained for at least the next 24 hours.
201 randomized to a more modest systolic BP
target of 180 mm Hg, as recommended in an
earlier AHA guideline.
INTERCT:


There was trend toward lower relative and absolute
growth in hematoma volumes from baseline to 24
hours in the intensive treatment group compared
with the control group.
There was no excess of neurological deterioration or
other adverse events related to intensive BP
lowering, nor were there any differences across
several measures of clinical outcome.
ANTIHYPERTENSIVE AGENTS:
Lancet Neurol 2005; 4: 662–72
HAEMOSTATIC THERAPY:

Use of anticoagulation.

Reversal of anticoagulation.
N.ENGL.J MED. 358;20, may 15, 2008
AIM:

Phase 3 trial to confirm a previous study in
which recombinant activated factor VII (rFVIIa)
reduced growth of the hematoma and improved
survival and functional outcomes.
N.ENGL.J MED. 358;20, may 15, 2008
METHODS:



Randomly assigned 841 patients with ICH to receive
placebo (268 patients), 20 μg of rFVIIa per kilogram
of body weight (276 patients), or 80 μg of rFVIIa
(297 patients) within 4 hours after the onset of
stroke.
The primary end point was poor outcome, defined as
severe disability or death according to the modified
Rankin scale 90 days after the stroke.
Exclusion criteria: secondary ICH, anticoagulation use,
GCS <5, pregnancy, previous disability.
N.ENGL.J MED. 358;20, may 15, 2008
RESULTS:


The mean estimated increase in volume of the ICH at
24 hours was 26% in the placebo group, as compared
with 18% in the group receiving 20 μg of rFVIIa/Kg
and 11% in the group receiving 80 μg.
Growth in volume of ICH was reduced by 2.6 ml in
the group receiving 20 μg of rFVIIa/Kg and by 3.8 ml
in the group receiving 80 μg, as compared with the
placebo group.
N.ENGL.J MED. 358;20, may 15, 2008
RESULTS:


Despite the reduction in bleeding, there was no
significant difference among the three groups in
the proportion of patients with poor clinical
outcome (24% in the placebo group, 26% in the
group receiving 20 μg of rFVIIa/Kg, and 29% in
the group receiving 80 μg).
Overall frequency of thromboembolic serious
adverse events was similar in the three groups;
however, arterial events were more frequent in
the group receiving 80 μg of rFVIIa than in the
placebo group.
N.ENGL.J MED. 358;20, may 15, 2008
CONCLUSIO
N:

Haemostatic therapy with rFVIIa reduced
growth of the hematoma but did not improve
survival or functional outcome after intracerebral
hemorrhage.
WARFARIN ASSOCIATED ICH:




7- to 10-fold higher than in patients not receiving
warfarin therapy.
Risk reaches 1% to 2% per year, and increases to
4.2% in patients older than 75 years.
Mortality - 60%.
INR <1.2, there was no difference in hematoma
size for patients with INR 1.2–2.0 or INR 2.1–3.0,
but patients with INR >3.0 had greater hematoma
volume.
Neurology 2008;71;1084-1089
REVERSAL OF
ANTICOAGULATION:

Therapy within 1.5 hours, early reversal by 2
hours.

No randomized trials.

Management Varies.
(Stroke. 2006;37:1465-1470.)
REVERSAL OF
ANTICOAGULATION:
Therapy chosen:
Time to OAC reversal:
Discontinuation of
warfarin


FFP
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
PCC
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
VIIa
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5-14 days
3 - 6h for infusion & 12 - 36h
for reversal
10 - 50 min infusion & 15
min for reversal
15 min post bolus IV
PROTHROMBIN COMPLEX
CONCENTRATE (PCC):
Octaplex:
 Factors II, VII, IX, X, Protein C,S, Heparin.

Dose:
 Initial dose is 40 mL (1000 IU Factor IX activity)
and 10 mg vitamin K intravenously.
 If the INR is greater than 1.5 after initial or
subsequent doses and the patient continues to bleed,
consider administering an additional dose of 20 mL
(500 IU Factor IX activity).
 The rate of infusion should not exceed 2-3 mL/min.

OCTAPLEX IN MNI:

60ml/hr over 5 minutes.

If no interaction >> 120-180ml/hr.

Vitamin K to be given.

Octaplex lasts 6 hours, vitamin K starts within 8
hours, lasts 24-48 hours.
FFP:


Volume of 1 Unit Plasma: 200-250 mL.
1 mL plasma contains 1 unit of coagulation
factors.

Unit contains 220 unit coagulation factors.

Dose: 10-15 ml/Kg.

Volume overload: infusion rate 1 ml/Kg/hour.


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Hold Warfarin.
PCCs have not shown improved outcome
compared with FFP but may have fewer
complications compared with FFP and are
reasonable to consider as an alternative to FFP
(Class IIa; Level of Evidence: B).
rFVIIa is not routinely recommended as a sole
agent for OAC reversal in ICH (Class III; Level of
Evidence: C).


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 in unselected
patients. (Class III; Level of Evidence: A)


Usefulness of platelet transfusions in ICH patients
with a history of antiplatelet use is unclear and is
considered investigational (Class IIb; Level of
Evidence: B).
Patients with ICH should have intermittent
pneumatic compression for prevention of venous
thromboembolism in addition to elastic stockings
(Class I; Level of Evidence: B).

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).
RESTARTING WARFARIN:


All experts favored resumption of warfarin therapy
within 3 to 10 days of ICH in stable patients in whom
subsequent anticoagulation is mandatory.
No general agreement occurred regarding subsequent anticoagulation of patients with atrial
fibrillation who survived warfarin-associated ICH.
Mayo Clin Proc. 2007;82(1):82-92
SURGICAL OPTIONS:



The usefulness of surgery is uncertain (Class IIb; Level of
Evidence: C).
Cerebellar hemorrhage, brainstem compression/hydrocephalus
>> should undergo surgical removal of the hemorrhage as soon
as possible (Class I; Level of Evidence: B), ventricular drainage
alone rather than surgical evacuation is not recommended.
Patients presenting with lobar clots >30 mL and within 1 cm of
the surface, evacuation of supratentorial ICH by standard
craniotomy might be considered (Class IIb; Level of Evidence: B).
(Stroke. 2010;41:00-00.)
SURGICAL OPTIONS:


No clear evidence at present indicates that ultra-early removal
of supratentorial ICH improves functional outcome or mortality
rate. Very early craniotomy may be harmful due to increased
risk of recurrent bleeding (Class III; Level of Evidence: B).
Intraventricular administration of recombinant tissue-type
plasminogen activator in IVH appears to have a fairly low
complication rate, efficacy and safety of this treatment is
uncertain and is considered investigational (Class IIb; Level of
Evidence: B).
(Stroke. 2010;41:00-00.)
IN
SUMMARY:

Be aware of early hematoma growth.

BP control crucial >> 150-160mmHg.

Reversal of anticoagulation.

rFVIIa controversial.


PCC coming into action, may replace FFP >> less
volume overload.
Surgical options = ??
MANAGEMENT OF RAISED
ICP
RAISED ICP TREATMENT:



Limited evidence for the monitoring and
management of ICP after ICH.
Majority of the evidence base and consensus
guidance for the treatment of intracranial
hypertension relates to traumatic brain injury.
Limited studies for stroke.
(Anesth Analg 2010;110:1419–27)
RAISED ICP TREATMENT:

Osmotic therapy.

Hyperventilation.

Surgery.

?? Controversial.
HEAD ELEVATION:

May reduce ICP by promoting venous outflow.

Helps in TBI patients >> 30° head elevation.

Cannot be easily translated to patients with
acute ischemic stroke, as head elevation may also
result in reduced cerebral perfusion pressure
(CPP).
Postgrad Med J 2010 86: 235-242
OSMOTHERAPY:


Create an osmotic gradient across the BBB,
drawing water from the interstitial and
intracellular space within the brain.
Agents which produce a more favorable osmotic
gradient are those which are excluded by the
intact BBB to a greater degree.
Postgrad Med J 2010 86: 235-242
OSMOTHERAPY:


Problems may arise in areas where the BBB is
disrupted, resulting in reversal of the osmotic
gradient and rebound cerebral edema, especially
on treatment withdrawal.
Relevant in acute stroke where large areas of the
BBB may be disrupted, and may also cause
preferential effects on the normal hemisphere
where BBB remains intact, thus worsening tissue
shifts.
Postgrad Med J 2010 86: 235-242
MANNITOL:



Cochrane review: 3 randomized trials, 226
patients.
Insufficient evidence to guide the routine use of
mannitol in acute stroke.
Effect on stroke outcome unclear, use based on
expert opinion/non-randomized trials.
Postgrad Med J 2010 86: 235-242
MANNITOL:



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20% solution, given as a bolus of 1-1.5 g/Kg.
Repeat dosing 0.25 to 0.5 g/Kg as needed, Q.16H/4-8H.
Target serum osmolality of 310-320 mOsm/l.
Effects: within minutes, peak at about one hour,
and last 4 to 24 hours.
J.Intensive Care Med 2002 17: 55
HYPERTONIC SALINE:




Limited data surrounding the use of hypertonic
saline for stroke related edema in clinical
practice.
Excluded from the BBB > Mannitol  more
potent osmotic agent.
Complications: severe hype-Na, rebound hypo-Na
on withdrawal, CHF, cardiac arrhythmia.
Dose: 0.5 to 2.0 ml/kg 23.4% hypertonic saline,
repeat 1-6H PRN.
HYPERVENTILATION:


Hypoxia & hypercarbia >> potent cerebral
vasodilators.
Hyperventilation lowers ICP by inducing hypocarbia
>> vasoconstriction.

Demonstrated in TBI patients, outcome data lacking.

Use for acute ICHT, temporizing measure

pCO2 30 – 35 mm Hg >> no response >> 25-30mmHg.

pCO2 < 25 mmHg >> vasoconstriction
HYPERVENTILATION IN STROKE:



Potential worsening of the hypoxic injury due to
vasoconstriction.
Possibility of rebound vasodilatation after
treatment discontinuation resulting in further
ICP elevation.
Generally not recommended, may be considered
as a holding measure until more definitive
treatment is initiated.
Stroke 2007;38;3084-3094
Stroke 2007;38;3084-3094
DECOMPRESSIVE SURGERY:


DECIMAL, DESTINY, HAMLET >> increase in
favorable outcome in the surgery group.
Significantly reduced mortality, at the expense of
an increase in moderate disability.
DECOMPRESSIVE
SURGERY:
Patients should be referred within 24 h of symptom onset, and
treated within a maximum of 48 h.
TAKE HOME MESSAGE:




ICPT- more data for TBI.
Osmotherapy: limited information in stroke >>
could be useful, ? Outcome change.
Hyperventilation >> temporizing solution.
Surgery >> to be considered in certain
population.
THANK YOU