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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
Management of Increased intracranial pressure in cerebellar stroke
Management of Increased intracranial pressure in cerebellar stroke
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.
Management of Increased intracranial pressure in cerebellar stroke
Management of Increased intracranial pressure in cerebellar stroke
Management of Increased intracranial pressure in cerebellar stroke
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.
Management of Increased intracranial pressure in cerebellar stroke
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
Management
Approach
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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Management of Increased intracranial pressure in cerebellar stroke

  • 1. 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
  • 2. 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.
  • 3. 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 )
  • 4. 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
  • 7. 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.
  • 11. Digital substraction angiography Right vertebral artery, AP view. Early phase.
  • 12. Digital substraction angiography Right vertebral artery, lateral view. Early phase.
  • 13. Digital substraction angiography Left vertebral artery, AP view. Unremarkable
  • 14. Digital substraction angiography Left vertebral artery, lateral view. Early phase. Compare the adequate vascularization in the territory of the PICA.
  • 15. Right vertebral artery, lateral view. Left vertebral artery, lateral view.
  • 17. 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
  • 18. 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).
  • 20. Cerebellar Strokes     PICA 40% SCA 36% AICA 12% Multiple vascular territories 12%
  • 21. 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
  • 22. 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
  • 24. 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.
  • 26. 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
  • 29. 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
  • 30. 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
  • 31. 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.
  • 32. 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
  • 33. 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.

Editor's Notes

  1. Three components explained by the rule of Monroe-Kellie
  2. OG = measured serum osmolality − calculated osmolality **Calculated osmolality = 2 x [Na mmol/L] + [glucose mmol/L] + [urea mmol/L]