1) The document discusses raised intracranial pressure (ICP), including the definition of ICP, physiology of cerebral circulation, causes of raised ICP, clinical presentation, imaging, and management. 2) Causes of raised ICP include brain edema, increased cerebral blood flow, increased CSF volume, and pathological masses. Clinical manifestations range from non-specific signs to neurological deficits and herniation syndromes. 3) Management involves first-tier approaches like positioning, ventilation, hyperventilation, and hyperosmolar therapy as well as second-tier options of barbiturate coma, hypothermia, and decompressive craniectomy for refractory cases.

1. Raised Intracranial
pressure
By
Wafaa Laimon
Resident in Pediatrics
MUCH

2. 2

3. OUTLINES:
 Definition of intracranial pressure(ICP).
 Physiology of cerebral circulation.
 Causes of raised ICP.
 Clinical presentation of raised ICP.
 Measurement of ICP.
 Management of raised ICP.

4. INTRACRANIAL PRESSURE
(ICP)
is the pressure
exerted by cranial
contents on the dural
envelope.
 It comprises the partial pressures of brain, blood and
cerebrospinal fluid (CSF).
 ICP= P cerebrum +P blood +P csf
 Intracranial volume=brain volume+cerebral blood
volume+csf volume
(Monro –Kellie hypothesis)
 Normal intracranial pressure is
below 10 mmHg.

5. Compliance:
is the ability to tolerate an increase
in volume without a corresponding
increase in Pressure.
Relationship of intracranial volume to intracranial pressure
(ICP). At normal brain compliance ICP increases only slightly as
intracranial volume increases . A further increase in volume
results in a steep rise in ICP.

6. Cerebral autoregulation:
(A) In the normal
situation, cerebral blood flow remains
constant over a wide range of cerebral
perfusion pressure.
(B) in acute
head injury, the autoregulatory curve is
shifted to the
Right.
(C) in some cases of acute head
injury, autoregulation
is lost and cerebral blood flow becomes
pressure
dependent.

7. Regulation of cerebral blood
flow:
Pressure
Autoregulation
Metabolic
Autoregulation

8. Pressure autoregulation
CPP=MAP-ICP
 CPP= effective pressure that results in blood flow to
the brain.
 MAP=Mean Arterial Blood Pressure.
•CBF remains constant with variations in MAP in the range(50-150
mmHg).
• Beyond these limits or with acute brain insult this autoregulation is
disturbed.

9. CPP=MAP-ICP
 Arterial hypotension--
-- reduced CBF--
 Increased ICP--
reduced CPP
cerebral ischemia.
reduced CPP
-- reduced CBF-- cerebral ischemia.

10. Metabolic autoregulation
 CBF is sensitive to changes in PaCO2 and PaO2.
Metabolic autoregulation is resistant to acute brain injury.
 Hypoventilation--
increase PaCO2-increase CBF-- increase ICP.
 Hyperventilation-- reduce PaCO2-- reduce CBF
-- decrease ICP.
 Arterial hypoxemia--- increase in CBF and ICP.
 Increase in PaO2-- cerebral vasoconstriction.

11. PATHOLOGY
 When to say intracranial hypertension??
If ICP more than 20 mmHg more than 5 minutes.
Degrees
 Mild:20-29 mmHg.
 Moderate:30-40 mmHg.
 Severe:more than 4o mmHg.

12. Causes of raised ICP according to mechanism:
 Brain edema:
• Cytotoxic
• Vasogenic
• Interstitial
 Increased cerebral blood flow:
•
•
•
•
•
Hypoxemia
Hypercarbia
Hyperpyrexia
Convulsion
Hypertension
 Increased CSF volume(obstruction-excess
production).
 Pathological volume(mass-hemorrage).

13. Clinical manifestations of increased ICP
 What is the outcome of raised ICP??

14. Clinical manifestations of increased ICP
Non specific
manifestations
Neurological
manifestations
Complications

15. Clinical presentation of raised ICP
1
2
Non specific
manifestations
Neurological
manifestations
•Headache
and
vomiting.
•Cushing response.
•Disturbed conscious
level.
•Sluggish
pupillary
reaction to light and
may be dilatation.
•Increased Muscle tone
and exaggerated deep
tendon reflexes.
•Hyperventilation with
deep inspiration and
expiration.
3
Complications
•Ischemia.
•Tonic convulsions.
•Herniation
syndromes.

16. What are herniation syndromes?

18. Central herniation
 Increased pressure in both cerebral hemispheres→downward
displacement of the diencephalon through the tentorium →
brainstem compression.
 Stages:
Diencephalic stage:




withdraws to noxious stimuli, increased rigidity or decorticate posturing.
small, reactive pupils.
preserved oculocephalic and oculovestibular reflexes.
yawns, sighs, or Cheyne-Stokes breathing.
Midbrain-upper pons stage:
•
•
•
•
decerebrate posturing or no movement.
mid-position pupils that may become irregular and unreactive.
abnormal or absent oculocephalic and oculovestibular reflexes.
hyperventilation.

19. Lower pons-medullary stage:
• no spontaneous motor activity.
• lower extremities may withdraw to plantar stimulation.
• mid-position fixed pupils.
• absent oculocephalic and oculovestibular reflexes.
• ataxic respirations.
Medullary stage:
• generalized flaccidity.
• absent pupillary reflexes and ocular movements.
• slow irregular respirations.
• death.

20. Uncal herniation
 Uncus of the temporal lobe is displaced medially over
the free edge of the tentorium.
 Ipsilateral third-nerve palsy (ptosis, pupil fixed and
dilated, eye deviated down and out).
 Ipsilateral hemiparesis from compression of the
contralateral cerebral peduncle (Kernohan notch).
 posterior cerebral artery compression.

21. Subfalcine (Cingulate) herniation
 Increased pressure in one cerebral hemisphere leads to
herniation of cingulated gyrus underneath falx cerebri.
 Compression of anterior cerebral artery leads to
paraparesis.

22. Tonsillar herniation
 Increased pressure in the posterior fossa leads to
brainstem compression.
 Loss of consciousness (RAS).
 Focal lower cranial nerve dysfunction.
 Respiratory and cardiovascular dysfunction with
relative preservation of upper brainstem
function, such as pupillary light reflexes and vertical
eye movements.

23. a) Subfalcial (cingulate) herniation ;
b) uncal herniation
c) downward (central, transtentorial) herniation
d) external herniation
e) tonsillar herniation.

24. Tonsillar heniation

26. IMAGING
CT BRAIN
sensitive in detecting extrabrain pathology.
Exclude secondary cause e.g tumor-mass.
Brain edema.
HOWEVER
Inferior resolution compared with MRI.
Missed pathology such as small bleeds.

27.  Diffuse Injury Type I
 no CT visible intracranial pathology
 Diffuse Injury Type II
 cisterns present with midline shift 0-5 mm
 no high- or mixed-density lesion > 25 cc
 Diffuse Injury Type III(swelling)
 cisterns compressed or absent with midline shift 0-5 mm
 no high- or mixed-density lesion > 25 cc
 Diffuse Injury Type IV (shift)
 midline shift > 5 mm
 no high- or mixed-density lesion > 25 cc
 Evacuated Mass Lesion
 any lesion surgically evacuated
 Non-Evacuated Mass Lesion
 high- or mixed-density lesion > 25 cc

28. 





Which patient will present
with raised ICP?
Patient(a)
OR
Patient(b)
?

29. MRI
More sensitive in detecting nonhemorrhagic and brain
stem lesions.
Detection of diffuse axonal injury.
Distinguishing subdural blood from subdural
hygromas and pathologic collections of CSF.
PET -SPECT
NIRS
TRANSCRANIAL DOPPLER

30. ICP MONITORING
Sites of ICP measurement:
Extradural.
Subdural.
Intraparenchymal.
Intraventricular.
Lumbar subarachnoid.

31. Intraparenchymal ICT monitoring

32. External ventricular drainage

33. LUMBAR
PUNCTURE???

34. Management of raised ICP
Decompressive
craniectomy
Forced
hyperventilation
Barbiturate coma
Tris buffer
Hypothermia
Positioning
Hyperventilation
Hyperosmolar therapy
Induced
hypertension
arterial

35. First tire
Positioning:
 Moderate head elevation at an angle 15-30.
 This enhances cerebral venous return
decreases ICP.
 Higher angle will decrease cerebral blood flow.
 Neutral position as turning head to one side will
reduce cerebral venous return.

36. Adequate ventilatory support:
 Evidence based medicine has not identified
perfect ventilation but adapted to your patient.
 Avoid fighting of the patient with ventilator.
 Effect of PEEP on MAP should be taken in
consideration.
 Hyperventilation.

37. Hyperventilation:
 It is a rescue maneuver in impending or frank
herniation.
 Keep PaCo2 between 30-35 mmHg.
 Lowering paCO2 by 1 mmHg reduces CBF by 4%.

38. CPP=MAP-ICP
CPP Concept:
 In case of intra-Cranial hypertension,autoregulation is
triggered by pharmacologically increasing MAP.
 Drugs of choice are norepinephrine(0.1 mic/kg/min)or
dopamine(4–10 mic/kg/min).
 Goal in TBI is MAP level of >70mmHg.

39. CPP CONCEPT
↑ICP
Text
CPP=MAP-ICP
↑CBV
↓CVR
Text
↓CPP

40. Drugs:
Lidocaine(1.5 mg/kg IV bolus) before intubation
and to reduce ICP.
Thiopental(1-2 mg/kg) IV bolus.
Midazolam.
Fentanyl.
WHY??

41. Hyperosmolar treatment
 Mannitol
 Hypertonic saline
Effective in few minutes
How does it act???
Dosage??

42. MANNITOL
Mechanism:
1)Osmotic diuresis(Intact BBB).
2)Decrease blood viscosity----cerebral vasoconstriction.
3)Free radicle scavenger.
Precautions:
1)Serum osmolalrity.
2)CVP.
3)Renal functions.
4)Hyperglycemia.
5)Rebound brain edema.

43. Hypertonic saline
It can be given till serum osmolarity 36o mosmol.
It acts also as volume expander.
It maintains MAP.

44. Second-tier treatment
 Forced hyperventilation:
 Hyperventilation down to a paCO2 of 25-30mmHg
 Carries the risk of cerebral ischemia.
 Barbiturate coma:
 Suppress the cerebral metabolic rate for oxygen(CMRO2).
 Terminate convulsions.
 Scavenge free oxygen radicals.
 Decrease a cerebral hyperthermic response to ischemia.

45.  Hypothermia
 Tris buffer:
 Acidosis removes the Mg lock from the NMDA receptor—
facilitating excitotoxicity.
 High pH protects energy-dependent glutamate porter
sytems and thus delays onset of excitotoxicity.
 Tris buffer corrects intracellular acidosis and increases the
buffering capacity of CSF.
 Tham(trishydroxymethylaminomethane) (1 mg/kg
intravenously)

46.  Steroids:
• in vasogenic brain edema around brain
tumors,hematoma or postoperative.
• Dexamethasone .25 mg/kg every 6 h IV.
• Methyl predinsolone 1-2 mg/kg every 6 h

47.  Indomethacin:
The non-selective cyclooxygenase inhibitor--Reduce ICP following TBI or intracranial surgery.

48. Hyperoncotic treatment
 The concept assumes importance of vasogenic edema
and colloid-osmotic pressure
 Aim is to reduce capillary pressure----precapilary
arterioles are constricted with
dihydroergotamine(DHE)
 (DHE) also constrict cerebral veins---reducingCBF
 Dose:4 mic/kg intravenously.

49. Hepatic Encephalopathy
 Hyperammoniemia is the key via
 Glutamine accumulation .
 free radicle release.
 Osmolar therapy:Mannitol-HS
 Hyperventilation
 Maitainance of MAP.
 Ornithine-L-Aspartate.
 Hypothermia.

50. Diabetic Ketoacidosis
Brain Edema
Cytogenic or
vasogenic???

51. Hypoxic–Ischemic Brain Injury
 Hypothermia is strongly tried especially in neonates.
 Cytogenic brain edema.
 Reperfusion injury----Vasogenic brain edema.

53. Infectious Causes
 Types of brain edema.
 What is the role of fluid restriction??
 Lumbar puncture.To do OR not to do??
 What is the role of steroids??

54. Mass Lesions: Tumors and
Hydrocephalus

55. Thanks….
But it’s not the end !!!

56. Always remember:
 Patient with raised ICP is critically ill patient.
So
Don not forget A,B,C,D.
 Papilledema is a late sign,
And
Pupilary dilatation deprive you
from precious sign

57. Always remember:
 Whatever the cause of raised ICP the initial
management will be the same.
 Don not rush to lumbar puncture or even CT brain
until you stabilize your patient.
 CT brain is important to diagnose some secondary
causes of raised ICP.
 Monitoring of ICP is valuable esp. in cases of TBI.

58. Thank You for Being
Patient Till the End