Transcript of "Management of Increased intracranial pressure in cerebellar stroke"
Department of Neurosugery, Jan. 21 2014
Management of increased intracranial pressure and
cerebral edema in ischemic stroke
Amre Nouh, MD. Neurovascular fellow
Daniel Vela, MD. PGY-3
(History of present illness)
52-year-old man, right-handed, presented with 2-days
history of headache in the right upper aspect of the neck,
radiated to the right orbital area. The pain reached its
maximum intensity while he was driving, followed by
difficulties with balance and tendency to right
lateropulsion, nausea and vomiting.
Review of systems:
Headache 2 days prior to presentation, retroocular, radiated to
the back of the head down the right neck.
No previous history of headaches.
BP 175/101 | Pulse 74 | Temp 36.7 ° C | Resp 16 | SpO2 100%
Wt 75.7 kg (166 lb 14.2 oz)
Cranial nerves intact, no nystagmus
Neck: supple, tenderness on the right side to palpation
Right sided hemiataxia
Right sided truncal lateropulsion
Wide based gait.
Remainder examination unrermarkable
NIHSS: 1 (Limb ataxia )
- LV Ejection fraction: 50% | PASP 20 mm Hg
- Low-normal left ventricular systolic function
-Otherwise, normal study.
Lipid Panel: Chol: 227 | Trigl: 149 | HDL: 43| LDL: 160 |
BMP normal, glucose: 324mg/dl | CBC: normal
EKG: Normal sinus rhythm, Left anterior fascicular block
Telemetry monitoring without remarkable events
Day # 2, Follow-up non-contrast CT head
EVD placement ~72 hrs
after onset of symptoms
Replacement of nonfunctioning right frontal
EVD, tract hemorrhage.
Right vertebral artery, AP view.
Right vertebral artery, lateral
view. Early phase.
Left vertebral artery, AP view.
Left vertebral artery, lateral
view. Early phase.
Compare the adequate
vascularization in the
territory of the PICA.
Right vertebral artery, lateral view.
Left vertebral artery, lateral view.
Pt. continued with moderate-to-severe headache, relieved after placement of
EVD. Insertion complicated by tract hemorrhage precluding antiplatelet
Initial ICP: 22cm H20
Osmotherapy: Loading dose of Mannitol, followed by regular dose every
6hrs with target Osm 300-320
Continued having frequent episodes of hiccups and vomiting
Started on Depakote
EVD subsequently clamped; however, the patient continued with headache,
ICP as high as 30s with hypertension, Systolic 180s
Cerebellum blood supply.
The PICA arises from the
vertebral Art. and courses
transversely and downward
along the medulla. The
common trunk gives rise to
the medial branch
(medPICA) and the lateral
What increases the ICP ?
When evidence of tonsilar herniation, the withdrawal of CSF will decrease the pressure
below the foramen magnum, allowing further herniation inferiorly.
This can increase compression upon the brain stem suddenly, often resulting in death
due to cardiorespiratory center compromise.
Brain parenchyma: 80%
An expansion of any of these
compartments occurs at expenses of
As no large, randomized controlled trial of
ICP treatment thresholds exist, the Brain
Trauma Foundation guidelines currently
recommend that ICP lowering therapy
should be initiated when the ICP rises
above 20–25 mm Hg in monitored
Journal of intensive care medicine, Vol 17 No 2 March/April 2002
Osmotic therapy: Mannitol / Hypertonic saline
Mannitol does not cross the BBB, creates a gradient to cause
water to move out the parenchyma, ultimately, reducing the
The osmolar gap:
estimates the actual concentration of mannitol.
It provides information whether previously administered mannitol
has been cleared by the kidneys or not.
If osmolarity > 320 mOsm/L AND osmolar Gap < 20 mOsm/L.
Safe to be given.
Curr Treat Options Neurol (2014) 16:272
barbiturate-induced coma effectively lowers ICP, it has not been shown to improve
CO2 constriction of vasculature
Vasoconstriction leads to less intravascular volume, lowering ICP
Goal: PaCO2 (30–35 mmHg)
Avoid Hypercarbia (PaCO2 945): It could induce hyperemia and sudden ICP
Allows venous drainage and minimize vascular congestion that may contribute to elevated ICP
DECIMAL, DESTINY, and HAMLET (European trials)
Ventriculostomy (EVD) or craniectomy
Early decompressive hemicraniectomy increased survival and
improved functional recovery in patients up to 60 years of age
when performed within 48 hours of stroke onset
Reduce ICP and increase CPP in patients refractory to medical
therapy and ventricular drainage alone.
Feasible only if the basal cisterns open on CT.
Jüttler, et al. Case series, 56 patients (J Neurol
No significant differences in survival between
space-occupying cerebellar infarct treated by EVD and
SODC, Kudo, et al. 25 patients J Stroke Cerebrovasc Dis
Significantly better prognosis in group of patients treated
by SODC and EVD
German–Austrian infarction study ( J Clin Neursci 1994;1:251-6 )
36 patients were medically treated
Surgical treatment for Massive cerebellar ischemic infarct was not
found to be superior to medical treatment in awake/drowsy or
Recommend Suboccipital decompressive craniectomy in
comatose patients only in cases where ICP cannot be controlled by