Management of Increased intracranial pressure in cerebellar stroke

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Information about Management of Increased intracranial pressure in cerebellar stroke
Health & Medicine

Published on January 23, 2014

Author: danielveladuartemd



Brief presentation of medical and surgical treatment options for massive cerebellar stroke. Discussion between placement of an extraventricular drain or suboccipital decompressive craniectomy.

Vascular conference 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

Case (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.

Neurological exam  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 )

Ancillary data  Echocardiogram          - 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 | HgbA1c: 11.4 BMP normal, glucose: 324mg/dl | CBC: normal INR: 1.1 EKG: Normal sinus rhythm, Left anterior fascicular block Telemetry monitoring without remarkable events

Day # 2, Follow-up non-contrast CT head Developing hydrocephalus EVD placement ~72 hrs after onset of symptoms Replacement of nonfunctioning right frontal EVD, tract hemorrhage.

Digital substraction angiography Right vertebral artery, AP view. Early phase.

Digital substraction angiography Right vertebral artery, lateral view. Early phase.

Digital substraction angiography Left vertebral artery, AP view. Unremarkable

Digital substraction angiography 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.

Patient’s progress   Pt. continued with moderate-to-severe headache, relieved after placement of EVD. Insertion complicated by tract hemorrhage precluding antiplatelet therapy 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 branch (latPICA).

Distribution of blood supply.

Cerebellar Strokes     PICA 40% SCA 36% AICA 12% Multiple vascular territories 12%

PICA infarcts Structures affected       Inferior surface of cerebellar hemisphere/inferior cerebellar peduncle Spinothalamic tract Descending sympathetic pathway Descending tract of V nerve Vestibular nuclei Nucleus ambiguous Clinical manifestations • Ipsilateral • Horner’s syndrome • Facial hypesthesia & thermoanesthesia • Hemiataxia • Palatal asymmetry • Contralateral • Hemibody hypesthesia & thermoanesthesia • • • Vertigo Hoarseness Dysphagia

AICA infarcts Structures affected        Brachium pontis Spinothalamic tract Descending sympathetic pathway VII nerve intra-axial fascicular portion Descending tract of Vth nerve Vestibular nuclei Cochlear nucleus Clinical manifestations • Ipsilateral • Horner’s syndrome • Facial weakness • Facial hypesthesia & thermoanesthesia • Hemiataxia • Deafness • Contralateral • Hemibody hypesthesia & thermoanesthesia • Vertigo • Nystagmus

Increased intracranial pressure

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.

Clinical manifestations of  ICP

Intracranial compliance    Brain parenchyma: 80% CSF: 10% Blood: 10%  An expansion of any of these compartments occurs at expenses of another  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 patients Journal of intensive care medicine, Vol 17 No 2 March/April 2002



Strategies 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 volume.  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

Strategies  Barbiturates    Hyperventilation      Metabolic suppression barbiturate-induced coma effectively lowers ICP, it has not been shown to improve overall survival  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 elevations Head positioning  Allows venous drainage and minimize vascular congestion that may contribute to elevated ICP

Strategies  Decompressive surgery:   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 Lumbar drainage   Reduce ICP and increase CPP in patients refractory to medical therapy and ventricular drainage alone. Feasible only if the basal cisterns open on CT.

Evidence ?  Jüttler, et al. Case series, 56 patients (J Neurol 1999;246:257-64)   No significant differences in survival between space-occupying cerebellar infarct treated by EVD and SODC. SODC, Kudo, et al. 25 patients J Stroke Cerebrovasc Dis 2007;16:259-62.  Significantly better prognosis in group of patients treated by SODC and EVD

Evidence ?  German–Austrian infarction study ( J Clin Neursci 1994;1:251-6 )  84 patients.    34 craniotomies, 14 ventriculostomies 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 somnolent/stupor patients  Recommend Suboccipital decompressive craniectomy in comatose patients only in cases where ICP cannot be controlled by EVD.

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