CEREBELLAR
HEMATOMA
Hemorrhages
into structure of the posterior fossa pose unique risks due to limited space in
this compartment and risk of hydrocephalus from compression of fourth ventricle
/ CSF pathways
- most
are neurosurgical emergencies requiring close monitoring and/or
immediate evacuation
-
deterioration can be rapid and better outcomes if caught early
History:
- Acute
onset of symptoms
- usually
during sleep or at rest
-
Headache (may be thunderclap or build over minutes); holocephalic or occipital
- may
lose consciousness transiently or remain obtunded after onset
- ataxia
prominent in most with sense of vertigo and usually dysarthria
- nausea
& vomiting
Past
medical history:
- hypertension
(responsible for most cerebellar hemorrhages)
- drug
use (eg. cocaine, amphetamines)
-
malignancy (risk of metastases)
- Hx of
vascular malformations
- anticoagulation
or coagulation disorders
Examination:
1. ABCs
- some
patients (eg. comatose, respiratory apnea) may require airway protection and
ventilation
-
patients often very hypertensive due to medullary irritation (SBP > 200 mm
Hg poor sign); not usually require or warrant aggressive treatment unless
malignant with end-organ failure
-
respiratory abnormalities incl. hyperventilation, shallow breathing, or apnea
- cardiac
arrhythmias especiallybradycardia (Cushing reflex) may be seen
2. Level
of consciousness
-
critical prognostic factor and impt in deciding acuity of intervention
-
decreased LOC due to brainstem compression and/or acute hydrocephalus with
raised ICP
3.
Cranial Nerves
-
deficits usually present from brainstem compression
- check
pupils (CN III palsy with unilateral mydriasis from midbrain compression and
may suggest upward transtentorial herniation)
-
nystagmus, may be secondary to cerebellar dysfunction in isolation (horizontal,
rotatory)
- gaze
palsy to side of lesion is most common EOM problem (+/- CN VI palsy)
- if
hydrocephalus, vertical gaze (upgaze) palsy may occur
- ocular
bobbing and skew may also be seen (former more common with pontine hemorrhages)
-
ipsilateral CN VII (LMN) palsy common
-
corneals may be reduced or absent (especiallyon same side) and oculocephalic /
caloric response may be impaired
* Classic
triad of ipsilateral facial palsy, gaze preference and limb ataxia (but
uncommon) *
4. Motor
exam:
- limited
by level of consciousness in many cases
-
posturing / failure to obey is poor sign suggesting immediate treatment is
required
-
plantars may be upgoing
Diagnosis:
-
suspicion of acute cerebellar event mandates urgent CT scan to r/o
hematoma
-
bleeding localized either to cerebellar hemisphere or vermis (less common)
- imaging
helps classify urgency by showing size of clot (> 3 cm worse) and
compression of adjacent structrures (brainstem, but especially fourth
ventricle); can assess for hydrocephalus
-
effacement of fourth ventricle with dilatation of temporal horns suggests
obstructive hydrocephalus requiring either immediate decompression or at least ventriculostomy
with drainage
- look at
basal cisterns; if effaced, suggests upward transtentorial herniation
NB:
patient may require MRI at later stage (if not evacuated) to assess for
underlying vascular malformation or tumor (esp metastasis)
Labs to
evaluate for coagulopathy including platelets and INR / PTT
+/-
toxicology (cocaine, amphetamines), neoplastic screen (esp CXR)
Management:
in many
cases (with altered LOC, significant mass effect, cranial nerve signs) hematoma
requires immediate evacuation (at least 40% of cases)
- in
others, admission to neuro-observation / ICU is mandatory
-
deterioration monitored for very closely (especially LOC)
ABCs (as
above) need to be secured first
- may
give mannitol if waiting for OR and signs of mass effect
- reverse
any anticoagulation with vitamin K (10 mg IV - works in 2-6 hrs) and FFP
(immediate but transient effect)
- some
use dexamethasone (if going to OR) to reduce edema in tight compartment
- avoid
treating hypertension unless persistent and causing organ dysfunction
-
atropine may be used for bradycardia if symptomatic / low BP associated
Decompressive
suboccipital craniectomy required for evacuation of clot
-
especially if there are any signs of mass effect with brainstem compression
- most
operate on any ICH > 3 cm in cerebellum but this is arbitrary
- may
defer surgery and even totally manage medically if small (< 3 cm) with open
basal cisterns and no hydrocephalus
-
isolated hydrocephalus without brainstem findings can be managed with
ventriculostomy
(only
successful in 10%, others still require decompression as well)
NB:
theoretical concern that with imminent upward hernation, placement of EVD for
ventricular drainage may precipitate pressure gradient that causes further
herniation
- not
borne out in most real-life cases but caution if very tight posterior fossa
(decompress first !)
Prognosis:
Poor
prognostic signs:
- Size of
hematoma (> 3 cm)
- Absent
corneal reflexes (almost 80% died, OR 26 !)
- Delayed
presentation / diagnosis (advanced brainstem compression with damage)
- Low GCS
/ LOC on presentation (especiallynot localizing to pain)
- Acute
hydrocephalus
- Age
(especially> 70 yrs)
- SBP
> 200 mm Hg on admission
- Absent
oculocephalic response
If can
avoid mortality or severe brainstem compromise, people with even large
cerebellar hematomas can make meaningful and gratifying recoveries
- even
comatose patients with some brainstem function may warrant attempt at
decompression to see reversibility once space available
References:
Wijdicks
EFM. The clinical practice of critical
care neurology, 2e. 2003; Oxford
University Press.
St. Louis
E, Wijdicks EFM, et al. Predictors of
poor outcome in patients with spontaneous cerebellar hematoma. Can J Neurol Sci 2000; 27: 32-6.
Last
update: March 2004
Reviewed
by: pending
Neurological
Medicine Pocketbook
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UWO Neurology Residents
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