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

Contents



Brain – 80%



Blood – 10%



CSF – 10%

Components of the Brain

Components of the Brain

Fig. 55-

1

Intracranial Pressure

•

Normal ICP = 4 -15 mmHg

•

Factors that influence ICP

–

Arterial pressure

–

Venous pressure

–

Intraabdominal and intrathoracic pressure

–

Posture

–

Temperature

–

Blood gases (CO

2

levels)

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

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

Intracranial Pressure:

Regulatory Mechanisms of

Cerebral Blood Flow

•

Autoregulation of cerebral blood
flow

•

Metabolic Regulation of cerebral
blood flow

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

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

Intracranial Pressure:

Regulatory

Mechanisms

of

Cerebral Blood

Flow

•

Metabolic Regulation of

cerebral blood flow

Factors affecting cerebral blood

flow

–

PCO

2

–

PO

2

–

Acidosis

Cerebral Blood Flow

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

Autoregulation

Autoregulation



CBF is regulated over a wide range of MAP



Range of 60-150 mmHg



Regulated by the tone of small arteries
and arterioles and by Blood Brain Barrier
(BBB)

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

PATHOPHYSIOLOGY

PATHOPHYSIOLOGY



Primary injury

- parenchymal injury



Secondary injury

-

reaction of neural tissue to primary injury

 edema
 cell death

Pathophysiology

Pathophysiology



Cerebral Edema

 increase in brain volume

 increase in Na+ and H

2

O

Classification of

Classification of

Cerebral Edema

Cerebral Edema



Interstitial



Vasogenic



Cytotoxic

Interstitial Edema

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

Vasogenic Edema

Vasogenic Edema



Increased permeability of brain capillary

endothelial cells to macromolecules.



Neurons are not primarily injured

Vasogenic

Edema

Vasogenic Edema

Vasogenic Edema



Tumor



Abscess



Hemorrhage



Contusion



Infarction



Meningitis



Lead encephalopathy

Cytotoxic Edema

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

Cytotoxic Edema

Symptoms/signs



DROWSINESS



Headache



Nausea/vomiting



Papilloedema



Cushing’s triad



Altered mental status



Altered mental status

Cushing

Cushing

Reflex

Reflex



Bradycardia



Hypertension



Altered respiratory status

OFTEN A VERY LATE CLINICAL

FINDING!

Symptoms of

Symptoms of

Increased ICP

Increased ICP



Altered mental status



Neurological deficit

- common is 3rd or 6-th nerve palsy
- dilated pupil(s)

Normal fundus

Papilloedema

Factors That Worsen

Factors That Worsen

Secondary Injury

Secondary Injury



↓ BP



↓ PaO2



↑ PaCO2

Cerebral herniation



Can occur depending on cause of raised
ICP



3 major types:

–

Transtentotial

–

Foramen magnum

–

subfalcine

Herniation

Herniation

Syndromes

Syndromes

Critically important herniation

Critically important herniation

syndromes:

syndromes:



Uncal Herniation

Uncal Herniation

:

:

-

-

occurs when a lateral expanding mass

occurs when a lateral expanding mass

lesions pushes the uncus and hippocampal

lesions pushes the uncus and hippocampal

gyrus over the lateral edge of the tentorium

gyrus over the lateral edge of the tentorium

- Unilateral dilated pupil

- Unilateral dilated pupil





progresses to

progresses to

brain stem dysfunction

brain stem dysfunction

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

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.

Subfalcine



Cingulate gyrus herniates under falx.



Usually asymptomatic unless ACA kinks
and occludes causing bifrontal
infarction.

ICP monitoring



Indications:

–

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

INCREASED ICP

INCREASED ICP

General Care

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

Management



Definitive treatment: treat underlying patholgy



To control raised ICP:

1.

Head elevation

2.

Controlled ventilation: maintain PaCO2 at 30-35 mmHg.

Reduction of CO2 will reduce cerebral vasodilatation

3.

Sedation/paralysis: decrease metabolic demand

4.

If ventricular catheter in situ, drain CSF

5.

Diuretic therapy: mannitol – osmotic diuretic, increases

serum osm and draws water out of the brain. Usual dose:

0.5-1.0g/kg. monitor serum osm

6.

Hypertonic saline

7.

Barbiturate therapy: thiopentone when given as a bolus

dose can be helpful in temporarily reducing ICP.

Manipulation of

Manipulation of

ICP

ICP

Brain

Brain



Mannitol
- dehydrates the brain, not the
patient
- monitor osmolality



Hypertonic saline

Manipulation of ICP

Manipulation of ICP

Blood

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