Intracerebral Hemorrhage

Front 1

Most common stroke type?
2nd most?
3rd most?

Back 1

Ischemic
Intracerebral hemorrhage
Subarachnoid hemorrhage

Front 2

Where in the brain, generally, does intracerebral hemorrhage occur?

Back 2

Deep structures (vessels there are vulnerable to HTN)

Front 3

ICH pathophysiology:
6

Back 3

-Rupture of a bv--> hematoma
-Later, hematoma expands
-+ ICP
-Tissue disruption/ischemia around hemorrhage
-Inflammation
-Edema/possible herniation

Front 4

Typical ICH locations:

What happens to the artery walls?

Back 4

-Small penetrating aa coming off ACA, MCA, PCA, Basilar.

-May be ruptured at multiple sites.

-Artery walls have layers of platelet and fibrin aggregates with breakdown of the elastic lamina; smooth muscle atrophy; wall dissection; and cell degeneration.

Front 5

Describe how HTN contributes to ICH:

Back 5

-Combination of lipid deposition, atherosclerosis, and fibrinoid necrosis in the subendothelium can result in ischemic stroke or, less commonly, the formation of microaneurysms & vessel rupture.

Recurrence risk ~2%/y if BP controlled.

Front 6

Cerebral Amyloid Angiopathy:

Back 6

-Hereditary or sporadic.

-Characterized by the deposition of amyloid and degenerative changes in the capillaries, arterioles, and small and medium sized arteries in cortex, leptomeninges, and cerebellum.

-Cerebral amyloid angiopathy leads to sporadic (usually lobar) ICH in the elderly.

-Recurrence risk 5-15%/y. Microbleeds can be seen as dark spots on gradient echo MRI. There are also white matter hyperintensities.

Front 7

Treatment for CAA?

Back 7

None.

Front 8

Causes of ICH: 8

Back 8

HTN
CAA
Anticoagulants
Vascular malformations/aneurysms
Tumors
Infarction with hemorrhagic transformation
Venous sinus thrombosis
Drug use

Front 9

Things you must ask about in ICH pts: 6

Back 9

History of Trauma
Hematologic abnormality (coagulopathies)
History of anticoagulant med taking
Anti-platelet med usage
Symptoms prior to the hemorrhage
Non-hypertensive site of bleeding

Front 10

ICH presentation of typical ICH patient:
BP, history, etc.

Back 10

•Blood pressure > 150/90 in 80% patients
•History of HTN, poor medication compliance, and cardiomegaly are common
•No prodromal transient symptoms
•Onset while patient is active

Front 11

Signs and symptoms of ICH: 8

Back 11

•Abrupt onset with gradual evolution over minutes to hours

•A one-time event with rare recurrence

•Headache appears in only 50%

•Neck stiffness

•Vomiting (+ICP)

•Focal seizures in approximately 10%

•Focal symptoms a function of site/size of bleed

•Symptoms and signs persist for months

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Imaging/lab options for ICH evaluation:

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CT
-Fast (secs-mins), commonly available
-Easy to read & very sensitive for acute blood (appears bright white); also may reveal hydrocephalus, edema, mass effect, and (potentially) tumor
-Inexpensive

MRI
-Not so fast (mins-hrs), not so common, not so available
-Very sensitive (acute blood); much more sensitive (chronic blood)
-Gives a more detailed look for other causes of ICH
-Expensive

Labs: CBC, Chem, Coags

Front 13

Anticoagulant use and its implications for ICH:

Back 13

-Most ICH occurs within therapeutic range of anticoagulation, but the risk of hematoma formation and expansion in ICH rises with the level of anticoagulation.

-Rapid reversal of Warfarin with FFP, vitamin K, and prothrombin complex concentrate (2,7,9,10) is recommended to resolve coagulopathy.

Front 14

Thrombolytic use and its implications for ICH:

Risk factors?

Back 14

-Makes hemorrhage more likely when used to dissolve a clot. TPA.

Risk factors:
age >70, large stroke, early ischemic changes visible on CT, serum glu > 300 mg/dL

Front 15

Discuss the significance of vascular malformations in causing ICH:

Back 15

-Accounts for 5% of ICH; more common in the young.

-Arteriovenous malformations (AVM)
-Dural A-V fistulas (dAVF)
-Cavernous malformations
-Aneurysms (berry, saccular, or infective)

Front 16

Who should get an angiogram to try to detect vascular malformations?

Back 16

-Probably only young, healthy people (some risk attached to them)
-Imaging (MRI) can serve the function of an angiogram to an extent and is non-invasive.

Front 17

Treatment for ICH:
supportive measures? 6

Back 17

-No Definitive Treatment
-Supportive care:
*Correct treatable causes of bleeding
*Treat seizures (not prophylaxis)
*Treat raised intracranial pressure
*Blood pressure management; levels are under debate.
*Surgery is controversial (Probably only helpful in avoiding catastrophic herniation or if ICH close to surface)
*ICU/hospital care & prophylaxis: DVT, GI, euthermia/ euglycemia

Front 18

Prognosis for ICH:
how does it compare to ischemic stroke?

Medical cost of ischemic stroke:

Back 18

Mortality
6-month, 30%-50%
1-year, 50% Functional recovery
*much worse than ischemic stroke

Medical Cost
< 20% of ICH patients are independent at 6 months vs 60% of ischemic stroke patients
$125,000 lifetime cost per person (1990)

Front 19

What does prognosis of ICH depend on?

other factors at play?

Back 19

-Prognosis depends on Size and Site of ICH
-Size (hematoma volume):
35-50% overall mortality
~75% mortality from massive ICH

-Site: worse prognosis for midline, infratentorial (higher risk for brainstem compression)

-Other factors: age, presence of IVH, edema (probably as a marker for shift), exam on presentation

-Early withdrawal of care (careful of self-fulfilling prophecy: pts do poorly after we offer poor prognoses despite incomplete prognosis data): current reccomendations are to hold off DNR for 24h.

Front 20

ICH scores for predicting mortality take what into account? 5

Back 20

-Glasgow coma scale score
-ICH volume
-Presence of IVH
-Infratentorial origin
-Age of pt

Front 21

Data on Subarachnoid Hemorrhage:
prevalance
mortality
what causes them
M/F
genetic involvement?
risk factors

Back 21

-1-7% of all strokes (dep on location), 26,000/y; unruptured aneurysms seen in 2% of routine autopsies

-Mortality approx 45%

-Vast majority of non-traumatic SAH are aneurysmal, then other vascular causes such as AVM, also trauma.

-More common in women

-There's a genetic component.

-Smoking is a risk factor.

Front 22

Mortality date on SAH:

Back 22

25-35% 0-30d mortality
~40-45% overall mortality

Despite its relatively low incidence, SAH impact is comparable to that of ischemic stroke

Front 23

Has SAH prevalance decreased with smoking cessation and HTN control over the years?

Back 23

No. hasn't helped.

Front 24

Typical pt comment upon presenting with a SAH?

Back 24

"Worst headache of my life."
-Sudden onset, high intensity
-May have had a previous, lower intensity headache due to "sentinel bleeds" (leakage from the aneurysm)

Front 25

Physical findings in SAH pts:

Back 25

-diminished LOC
-Papilledema or retinal hemorrhage
-IIId palsy
-VIth palsy

Front 26

Predictors of prognosis for SAH:

Back 26

-Hunt/Hess scale links neurological status to outcome.
-LOC is the best predictor!

Front 27

Is surgery a good call to fix a subarachnoid aneurysm?

Back 27

Endovascular coiling is better.

Front 28

What testing do you do to identify subarachnoid hemorrhage?

Back 28

-CT works really well- subtle brightness paraventricularly

-LP will tell you--presence of RBCs, high opening pressure, xanthochromia

-Angiogram (or MRA, CT)

Front 29

The immediate steps in the evaluation of SAH include:

Back 29

-Airway, breathing, and circulation, routine monitoring, labs

-Blood pressure control (usually <140 mm Hg systolic)

-Evaluation of hydrocephalus and the need for management with extraventricular drainage (EVD);

-Rapid evaluation of the intracranial vasculature and early surgery or endovascular coiling as indicated.

-Seizure prophylaxis until the source of the hemorrhage has been identified/controlled;

-Bedrest and stool softeners.

-Nimodipine, a calcium channel blocker, was originally considered as prophylaxis against vasospasm; though it had no effect on vasospasm, it did have a measurable, as-yet-unspecified neuroprotective effect which improved 6-month outcomes markedly.

Front 30

Describe hydrocephalus in SAH:

Back 30

-Blood in the CSF can cause either a non-communicating or a communicating hydrocephalus.

-Common symptoms: initial confusion and decreased level of alertness, upgaze paresis, somnolence, coma

-Patients in whom hydrocephalus is suspected are rapidly re-imaged and, if necessary, given external drainage (EVD)

-Resolution of hydrocephalus and clearance of blood from the CSF may take days; if EVD weaning is not possible, a shunt may be placed.

Front 31

Describe vasospasm in SAH:
how do you monitor it and treat it?

Back 31

-Leads to 2˚ ischemic injury and strokes (as high as 40%)

-Peaks between days 3-13 after rupture; Pts monitored with serial neuro exams and transcranial doppler evaluation of blood flow velocity through major intracerebral vessels (surrogate marker for vessel diameter)

-Occurs more often if thick clots seen on CT

-Can be treated by hemodynamic augmentation

-Classically HHH therapy (hypertension, hypervolemia, hemodilution)

-Now more typically hypertension and euvolemia

-Can also be treated with Intra-arterial therapies
Vasodilators (commonly calcium channel blockers)
Angioplasty

Front 32

What are two common complications of SAH?

Back 32

hydrocephalus

vasospasm

Front 33

Why do complications occur with SAH?

Back 33

Immediately after subarachnoid hemorrhage, a progressive decrease in cerebral blood flow occurs.

This may result from a sudden massive increase in intracranial pressure or from a transient acute vasospasm.

The net result is a decrease in cerebral perfusion pressure and, depending on its degree and duration, results in various levels of impaired consciousness or even death.

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