1. Monro-Kellie Doctrine
Cranial cavity is a rigid sphere
Filled to capacity with non compressible contents
Increase in the volume of one of the constituents will lead to a rise in pressure

2. Contents
Brain – 80%
Blood – 10%
CSF – 10%

3. Components of the Brain
Fig. 55-1

4. Intracranial Pressure
Normal ICP = mmHg
Factors that influence ICP
Arterial pressure
Venous pressure
Intraabdominal and intrathoracic pressure
Posture
Temperature
Blood gases (CO2 levels)

5. Intracranial Pressure Importance of ICP to BP and CPP
Brain needs constant supply O2 and Glucose
BP: heart delivers blood to brain at an average BP of 120/80 (Mean BP = 100); this mean arterial pressure (MAP) must be higher than ICP
CPP (Cerebral Perfusion Pressure): is the pressure needed to overcome ICP in order to deliver O2 & nutrients

6. Intracranial Pressure Importance of ICP to BP and CPP
MAP is the DRIVING FORCE
ICP is the RESISTENCE
CPP = MAP – ICP
= 100 mmHg – 15 mmHg
= 85 mmHg (Normal)
CPP < 50 mmHg→ cerebral ischemia
CPP < 30 mmHg → brain death

7. Intracranial Pressure: Regulatory Mechanisms of Cerebral Blood Flow
Autoregulation of cerebral blood flow
Metabolic Regulation of cerebral blood flow

8. Intracranial Pressure: Regulatory Mechanisms of Cerebral Blood Flow
Autoregulation
The automatic alteration in the diameter of the cerebral blood vessels to maintain a constant blood flow to the brain
Maintains CPP regardless of changes in BP

9. Intracranial Pressure: Regulatory Mechanisms of Cerebral Blood Flow
Problem: Autoregulation is limited
If BP and/or ICP rises: Autoregulation fails
When autoregulation fails, blood flow to brain increases or deceases → poor perfusion and cellular ischemia or death

10. Intracranial Pressure: Regulatory Mechanisms of Cerebral Blood Flow
Metabolic Regulation of cerebral blood flow
Factors affecting cerebral blood flow
PCO2
PO2
Acidosis

12. Cerebral Blood Flow Blood supply matches metabolic needs Regulated:
- Mechanically – metabolic by-products which alter blood vessel caliber
- By sensitivity to CO2 and O2
- By adenosine and oxygenases
- Perfusion pressure

13. Autoregulation CBF is regulated over a wide range of MAP
Range of mmHg
Regulated by the tone of small arteries and arterioles and by Blood Brain Barrier (BBB)

14. Causes of raised ICP Increased volume of normal contents
Brain: oedema, benign intracranial HTN
CSF: hydrocephalus
Blood: vasodilatation, venous thrombosis
Space occupying lesions
Tumour
Abscess
Intracranial heamorrhage

16. PATHOPHYSIOLOGY Primary injury - parenchymal injury Secondary injury
- reaction of neural tissue to primary injury
 edema
 cell death

17. Pathophysiology Cerebral Edema  increase in brain volume
 increase in Na+ and H2O

18. Classification of Cerebral Edema
Interstitial
Vasogenic
Cytotoxic

19. Interstitial Edema Increased CSF hydrostatic pressures
Altered absorption of CSF
Increased edema of periventricular white matter due to CSF movement across ventricles.
Prototype
- obstructive hydrocephalus

20. Vasogenic Edema Increased permeability of brain capillary
endothelial cells to macromolecules.
Neurons are not primarily injured

21. Vasogenic Edema

22. Vasogenic Edema Tumor Abscess Hemorrhage Contusion Infarction
Meningitis
Lead encephalopathy

23. Cytotoxic Edema Cellular swelling due to cell injury
- neuronal, glial, and endothelial
Failure of ATPase dependant Na exchange
Edema is a reflection of cell death rather than a contributing factor

24. Cytotoxic Edema

25. Symptoms/signs DROWSINESS Headache Nausea/vomiting Papilloedema
Cushing’s triad
Altered mental status
Altered mental status
Headache: worse in the morning, relieved by vomiting. Intracranial pressure increases during sleep probably from vascular dilatation due to carbon dioxide retention. The cause of headache is probably traction on the pain-sensitive blood vesselsand compression of the pain sensitive dura at the base of the cranium.
N+V: worse in am
Drowsiness: most important clinical feature
Papilloedema: definitive sign. Due to transmission of raised pressure along subarrachnoid sheath of optic nerve. Initial changes: filling in of the optic cup, dilatation of retinal veins with congestion and absence of pulsations. As the pressure rises: disc margins become blurred, flame shaped hemorrhages develop around the disc margin. Severe papilloedema: blob heamorrahge, exudate. Long standing: optic atrophy.
Cushing reflex: hypertension, bradycardia

26. Cushing Reflex Bradycardia Hypertension Altered respiratory status
OFTEN A VERY LATE CLINICAL FINDING!

27. Symptoms of Increased ICP
Altered mental status
Neurological deficit
- common is 3rd or 6-th nerve palsy
- dilated pupil(s)

28. Normal fundus

29. Papilloedema
Papilledema, characterized by blurring of the optic disc margins, loss of physiologic cupping, hyperemia, and fullness of the veins

31. Factors That Worsen Secondary Injury
↓ BP
↓ PaO2
↑ PaCO2

32. Cerebral herniation Can occur depending on cause of raised ICP
3 major types:
Transtentotial
Foramen magnum
subfalcine

33. Herniation Syndromes Critically important herniation syndromes:
Uncal Herniation:
- occurs when a lateral expanding mass lesions pushes the uncus and hippocampal gyrus over the lateral edge of the tentorium
- Unilateral dilated pupil  progresses to brain stem dysfunction

34. Transtentorial
Displacement of brain and herniation of uncus of temporal lobe through the tentorial hiatus
Causes compression of:
midbrain : contralateral hemiparesis (usually), Cushing response, , respiratory failure (cheyne- stokes)
CN III: dilatation of ipsilateral pupil initially
Posterior cerebral artery: hemianopia
Lateral displacement of the brainstem may result in the opposite crus cerebri being compressed against the sharp rigid tentorial edge and causeing ipsilateral hemiparesis.
Increased pressure within the posterior fossa will result in herniation of the cerebellar tonsils into the foramen magnum and compression of the medulla.

35. Foramen magnum (coning)
Progressively increasing ICP causes further downward herniation of the cerebellar tonsils into foramen magnum or coning.
With progressive herniation pupils change from dilated and fixed to midsize and unreactive.
Signifying irreversible events leading to brainstem death.

36. Subfalcine Cingulate gyrus herniates under falx.
Usually asymptomatic unless ACA kinks and occludes causing bifrontal infarction.

37. Subfalcine Herniation: (1)The cingulate gyrus is pushed laterally away from the expanding mass and herniates beneath the falx cerebri.
Transtentorial (Uncal) Herniation: (3) Due to the cerebral edema, the uncus of the temporal lobe (medial temporal lobe) herniates downward into the posterior fossa. Central herniation (2) occurs when there is downward pressure centrally and can result in bilateral uncal herniation.
Tonsillar Herniation: (4)If there is also edema or hemorrhage causing swelling in the cerebellum, the tonsil (or tonsils) of the cerebellum herniates downward into the foramen magnum.

38. ICP monitoring Indications: Normal ICP: 10-15mmHg
Head injury
Following major intracranial surgery
Assessment of benign intracranial HTN
Normal ICP: 10-15mmHg
Can be recorded from ventricle, brain substance, subdural or extradural space
Risks: CNS infection and intracranial haemorrhage
Although CT scans may suggest elevated ICP based on the presence of mass lesions, midline shift, or effacement of the basilar cisterns (picture 2), patients without these findings on initial CT may have elevated ICP.
Check coags, platelets. Position patient – head up. Prep and drape. Incision and burr hole usually on right side (non dominant), place monitor lead and close skin.
Kocher's point (Blue)- Located 10cm posterior to the nasion (black line) and cm lateral to midline (green line). This puts you anterior to the coronal suture and thus the motor strip.

39. INCREASED ICP General Care
HOB elevated 30° ↑ venous drainage
Head midline ↑ venous drainage
No jugular catheters  prevent venous obstruction
Normothermia avoid ↑ metabolism
↓ Pleural pressures (zero peep)  ↑ venous drainage

40. Management Definitive treatment: treat underlying patholgy
To control raised ICP:
Head elevation
Controlled ventilation: maintain PaCO2 at mmHg. Reduction of CO2 will reduce cerebral vasodilatation
Sedation/paralysis: decrease metabolic demand
If ventricular catheter in situ, drain CSF
Diuretic therapy: mannitol – osmotic diuretic, increases serum osm and draws water out of the brain. Usual dose: g/kg. monitor serum osm
Hypertonic saline
Barbiturate therapy: thiopentone when given as a bolus dose can be helpful in temporarily reducing ICP.

41. Manipulation of ICP Brain
Mannitol
- dehydrates the brain, not the patient
- monitor osmolality
Hypertonic saline

42. Manipulation of ICP Blood
Decrease cerebral metabolic demands
- sedation, analgesia, barbiturates
- avoid hyperthermia
- avoid seizures
Hyperventilation
- decreases blood flow to the brain
- only acutely for impending Herniation.
Mannitol