2.3: 16. Intracranial Hemorrhage

Front 1

What is an intracranial hemorrhage?

Back 1

Intracranial bleeding when intracranial blood vessels are ruptured or leak
Can result from:
- physical trauma (as occurs in head injury)
- nontraumatic causes (as occurs in hemorrhagic stroke)
-- eg. ruptured aneurysm.

Front 2

What is the epidemiology of strokes?

Back 2

~800,000/year in the US
- 88% ischemic
- 9% intracerebral hemorrhage (ICH)
- 3% subarachnoid hemorrhage (SAH)

Non-Caucasians > Caucasians

Front 3

What is the epidemiology of intracerebral hemorrhages?

Back 3

Deep intracerebral hemorrhages are more common
The ICH rate +18% in the last decade, possibly due to:
- Longer lifespan
- Anticoag/antiplatelet use (atrial fibrillation treatment)
- Demographic changes (higher risk factor populations up)
(-lots of people have HTN)

Front 4

What is a possible risk factor for an intracerebral hemorrhage?

Back 4

Uncontrolled hypertension

Front 5

Where do intracerebral hemorrhages occur?

Back 5

Location in the brain:
- Two general categories in terms of pathophysiology:
-- Lobar (towards the periphery, typically linked to cerebral amyloid angiopathy [CAA])
-- Deep (in the deep white matter of the cerebrum, typically linked to hypertension)

Location in vessels:
- Bifurcations of small penetrating arteries from basilar, anterior, middle, or posterior cerebral arteries. (Anterior>>Posterior Circulation)
- Small arteries may be ruptured at multiple sites
- Artery walls may have layers of platelet and fibrin aggregates with breakdown of the elastic lamina; smooth muscle atrophy; wall dissection; and cell degeneration.

Front 6

What can cause intracerebral hemorrhages? (2 main categories) Where is each generally located?

Back 6

1) Hypertension (HTN) -> deep intracerebral hemorrhages
- Most common cause of ICH
- Lipid deposition, atherosclerosis, and fibrinoid necrosis in the subendothelium -> ischemic stroke (less common: formation of microaneurysms & vessel rupture)
- Recurrence risk ~2%/y if BP controlled.
2) Cerebral amyloid angiopathy (CAA) -> peripheral/lobar hemorrhage (particularly in elderly)
- Disease of small vessels
- Deposition of amyloid-β peptide and degenerative changes in non-large arteries in cortex, leptomeninges, and cerebellum
- Recurrence risk 5-15%/y
- Microbleeds can be seen as dark spots on gradient echo MRI (common and often peripheral but sometimes asymptomatic).
3) Other causes: Anticoagulants, Vascular malformations/aneurysms, Tumors (renal cell and melanoma), Infarction with hemorrhagic transformation, Venous sinus thrombosis, Drug use.

Front 7

What is the likely cause of what is shown in the CT above?

Back 7

CAA (Cerebral amyloid angiopathy) peripheral/lobar hemorrhage is mostly likely

Front 8

What is the likely cause of what is shown in the CT above?

Back 8

CAA (Cerebral amyloid angiopathy) peripheral/lobar hemorrhage is mostly likely

Front 9

What is the likely cause of what is shown in the CT above?

Back 9

This is less clear, and it could be a CAA (Cerebral amyloid angiopathy) peripheral/lobar hemorrhage or a hypertensive hemorrhage (not quite a deep hemorrhage though)

Front 10

What is the likely cause of what is shown in the CTs above (left is earlier than right)?

Back 10

The first image (to the left) shows the darker contrast, indicating a probably ischemic occlusion (right MCA infarction), but the brighter contrast in the later image (to the right) then indicates a secondary hemorrhagic transformation of the initial ischemic infarct

Front 11

What is the likely cause of what is shown in the CT above?

Back 11

Hypertension -> Deep hemorrhage is most likely

Front 12

What is the likely cause of what is shown in the CT above?

Back 12

Traumatic brain injury due to the multiple hemorrhage locations (coup/contrecoup)

Front 13

What is the pathology of an intracerebral hemorrhage?

Back 13

1) Hematoma formation after initial hemorrhage, impacting the surrounding brain tissue and causing further ischemia
2) Hematoma growth (early) -> Increased intracranial pressure, tissue shear/disruption
3) Secondary Events: triggered by the presence of blood in the brain
- Toxic effects of blood products/oxidative effects
- Inflammatory effects
- Edema

Front 14

What is the clinical presentation of a patient with a cerebral hemorrhage?

Back 14

Typical Presentation:
- BP > 150/90 (80% of patients)
- History of HTN
- Poor medication compliance
- Cardiomegaly
- No prodromal transient symptoms
- Onset while patient is active.

Red Flags:
- Head trauma (distinguish between a spontaneous or traumatic hematoma)
- Hematologic abnormality
- *History of anticoagulants, aspirin
- Symptoms prior to hemorrhage (ie. establishing if there was an underlying lesion if a patient had a symptom that went back months it could theoretically be a tumor whereas just days it could be an ICA)
- Non-hypertensive site of bleeding.

Symptoms:
- Abrupt onset with gradual evolution over minutes to hours
- A one-time event with rare recurrence (intracerebral hem = 1x event, in contrast to ischemic stroke)
- Headache appears in only 50%
- Neck stiffness
- Vomiting
- Focal seizures in approximately 10%
- Focal symptoms a function of site/size of bleed
- Symptoms and signs persist for months

Front 15

What is the significance of hematoma growth in intracranial hemorrhage?

Back 15

It happens early and correlates with mortality and function.
The first 24 hours are the most important -> 10% increase in hematoma size = 5% increase in mortality + 18% increase in functional shift (independent -> assisted -> poor)

Front 16

What are the diagnosis methods for intracranial hemorrhage?

Back 16

CT
- Fast (secs-mins), common (almost all ED) & available
- Easy to read & very sensitive for acute blood (appears bright white); also may reveal secondary symptoms of ICH → hydrocephalus, edema, mass effect, and (potentially) tumor
- Inexpensive (relative to MRI)
MRI
- Slower then CT (mins-hrs) → bad for unstable patients, less common/available
- Also very sensitive (acute blood); much more sensitive (chronic blood)
- More detailed look for other causes of ICH
- Expensive
Labs: CBC, Chem, Coags

Front 17

What can worsen prognosis of intracranial hemorrhage?

Back 17

1) Anticoagulant use [eg. warfarin]
- Increased use of anticoagulant (atrial fibrillation treatment, venous thromboembolism, valve replacements) increases the risk of hematoma
- Data has been produced to show higher deterioration in anticoagulated patients, but causation not established
- Rapid reversal (fresh frozen plasma, VitK, prothrombin complex concentration [2,7,9,10]) recommended to resolve coagulopathy

2) Thrombolytics
- tPA (tissue plasminogen activator) administration in the case of CNS ischemic infarction can increase the risk for hemorrhage
- 20% of hemorrhages in these cases are distant from stroke site, but the other 80% is at the stroke site (secondary hemorrhage) due to leaky/weak vasculature
- Risk factors:
-- Age > 70
-- Stroke is large
-- Early ischemic changes are visible on CT
-- Serum glucose > 300 mg/dL

3) Vascular Malformation (cause of 5% of intracranial hemorrhages)
- Arteriovenous malformations (AVM)
- Dural A-V fistulas (dAVF)
- Cavernous malformations
- Aneurysms (berry, saccular, or infective)
- May get an angiogram to distinguish between the above, generally up to physician's judgment

Front 18

What is the treatment for intracranial hemorrhage?

Back 18

No definite treatment
Mostly supportive:
- Seizure treatment (non-prophylactic)
- Lowering BP may be helpful
- Surgery is controversial, may save life at the cost of function
- Skin breakdown, pneumonia, UTIs, DVT prevention due to disability of patients

Front 19

What is the outcome of intracerebral hemorrhage? How does it compare to ischemic stroke?

Back 19

6 month mortality is 30-50%, with < 20% being independent
After 1 year, 50% patients undergo functional recovery
$125,000 lifetime cost per person (1990)

Compared to ischemic stroke, the outcome is much worse with ICH, with higher mortality and higher loss of function

Front 20

What determines the prognosis of intracerebral hemorrhage?

Back 20

1) Size (hematoma volume):
- 35-50% overall mortality
- ~75% mortality from massive ICH
2) Site:
- worse prognosis for midline, infratentorial (higher risk for brain stem compression, little room to expand elsewhere)
3) Other factors:
- age, presence of IVH (intraventricular hemorrhage, presence of blood in the ventricles), edema (probably as a marker for a midline shift), exam on presentation
4) Early withdrawal of care (careful of self-fulfilling prophecy: pts do poorly after we offer poor prognosis despite incomplete prognosis data): current recommendations are to hold off DNR for 24 h

Front 21

What are ways to predict intracerebral hemorrhage outcome?

Back 21

MORTALITY
- Glascow Coma Scale (lower on the scale is a more severe coma, worse)
- ICH volume (cc) (larger is worse)
- Intraventricular hemorrhage (present is worse)
- Infratentorial hemorrhage (present is worse)
- Age (higher worse)
FUNCTION → functional outcome instead of just mortality. Can they eat? move? etc.
Glascow Coma Scale
ICH volume (cc)
pre-ICH cognitive impairment
Age

Front 22

What is a subarachnoid hemorrhage?

Back 22

Bleeding into the subarachnoid space (the area between the arachnoid membrane and the pia mater surrounding the brain)
May occur spontaneously, usually from a ruptured cerebral aneurysm, or may result from head injury.

Front 23

What is the epidemiology of subarachnoid hemorrhages?

Back 23

1-7% of all strokes (region-dependent) -> 26,000/yr
Unruptured aneurysms seen in 2% of routine autopsies
45% mortality rate
Majority caused by ruptured aneurysms, less commonly caused by arteriovenous malformations, other causes being trauma or ICH extension into the subarachnoid space

F:M::1.6:1
45-65 age group most susceptible
Japan and Finland have especially high rates

Front 24

What are risk factors for subarachnoid hemorrhages?

Back 24

Modifiable:
- Smoking, hypertension, heavy alcohol use, sympathomimetic (eg. cocaine) use
Non-modifiable:
- Genetics (AD PCKD, Familial Intracranial Aneurysm Syndrome, Ehler-Danlos Syndrome [Type 4])

Front 25

What is the clinical presentation of subarachnoid hemorrhages?

Back 25

1) "Worst headache of life" [WHOL]
- Sudden onset and intensity, no history of migraines (which would also have a more gradual onset)
2) Neck stiffness due to meningeal irritation
3) May have vision changes
4) Possibly previous headache days before the WHOL (1/3-1/2 of survivors) -> possibly "sentinel bleeds" - leakage of subarachnoid blood from aneurysm
5) Mass effect
- Diminished consciousness, papilledema, retinal/subhyaloid hemorrhage, cranial nerve palsies, size-dependent focal neurological symptoms

Front 26

What are predictors for subarachnoid hemorrhage?

Back 26

The Hunt and Hess scale uses a calculated score to predict a value from 1-5 (asymptomatic to coma) - these are also correlated with survival levels (lower H/H is better)

Front 27

What are tests for subarachnoid hemorrhage?

Back 27

CT - Check for blood (and possibly hydrocephalus), generally around the vessels themselves
Lumbar puncture (rare done now due to sensitivity of CT) - Higher RBC count in CSF (103-106 RBC/mm^3), with xanthochromia (persistent pigment even after centrifuging)
Angiogram - Vascular imaging in general can help visualize aneurysm

Front 28

What are the steps in treatment for subarachnoid hemorrhage?

Back 28

1) Monitoring and control breathing, circulation
2) Blood pressure control (usually <140 mm Hg systolic) to prevent recurrent hemorrhage
3) Evaluation of hydrocephalus (common complication) and the need for management with extraventricular drainage (EVD) → to alleviate pressure.
4) Rapid evaluation of the intracranial vasculature and early surgery or endovascular coiling as indicated (avoids re-rupture)
5) Seizure prophylaxis until the source of the hemorrhage has been identified/controlled
6) Bedrest and stool softeners.
7) 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 29

What are the complications of subarachnoid hemorrhage?

Back 29

Hydrocephalus
- Can be communicating (no obstruction in flow, but obstructed resorption) or non-communicating (obstructed CSF flow)
- Confusion, alertness decrease, upgaze paralysis, somnolence, eventually coma
- Can be given an external drainage if worsened (EVD), or a ventriculoperitoneal shunt for long term if necessary
- Can be protected against with monitoring and frequent imaging

Vasospasm (vessel spasm leading to vasoconstriction)
- Leads to secondary ischemic injury and strokes (as high as 40%)
- Peaks between days 3-13 after rupture; Pts monitored with serial neuro exams and transcranial doppler (ultrasound of cranial vessels that can identify vasopasm before it even becomes a problem) evaluation of blood flow velocity through major intracerebral vessels (surrogate marker for vessel diameter). If velocities increase, they are then sent to get a traditional angiogram.
- Occurs more often if thick clots seen on CT.
- Can be treated by hemodynamic augmentation
-- Classically HHH therapy (hypertension, hypervolemia, hemodilution) -> elevate BP, increase volume, and thin the blood to allow for perfusion
-- Now more typically hypertension and euvolemia (normal volume)
--- Can also be treated with Intra-arterial therapies
---- Vasodilators (commonly calcium channel blockers)
---- Angioplasty