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 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 (CO2 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 PCO2 PO2 Acidosis

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

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

Classification of Cerebral Edema Interstitial Vasogenic Cytotoxic

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

Vasogenic Edema

Vasogenic Edema Tumor Abscess Hemorrhage Contusion Infarction Meningitis Lead encephalopathy

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 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

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

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

Normal fundus

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

Factors That Worsen Secondary Injury ↓ BP ↓ PaO2 ↑ PaCO2

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

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

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.

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.

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.

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 2.5-3.0cm lateral to midline (green line). This puts you anterior to the coronal suture and thus the motor strip.

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

Management Definitive treatment: treat underlying patholgy To control raised ICP: Head elevation Controlled ventilation: maintain PaCO2 at 30-35 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: 0.5-1.0g/kg. monitor serum osm Hypertonic saline Barbiturate therapy: thiopentone when given as a bolus dose can be helpful in temporarily reducing ICP.

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

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