03/05 /12Je remy KamInternRoya l Me lbourne Hosp i ta l

RAISED INTRACRANIAL

PRESSURE

Basic Principles Review Basic Anatomy of Skull and Spinal Cord Review Basic Physiology of CSF production and flow Monro Kellie Doctrine and concepts of CBF and CPP

Conceptualising ICP Spectrum of Intracranial Pressure Causes of Raised ICP

Assessment of Raised ICP Symptoms Signs and basic examination techniques Investigating ICP

Management Monitoring Treatment

OVERVIEW AND OBJECTIVES

1. Skull is a rigid box: The volume inside the cranium is a fixed volume (nearly). 2. The cranial contents incompressible (nearly)3. The cranium and its constituents (blood, CSF, and brain tissue) create a state of volume equilibrium, such that any increase in volume of one of the cranial constituents must be compensated by a decrease in volume of another

CONTENTS OF THE SKULL AND THE MONRO KELLIE DOCTRINE

FIXED BOX: SKULL/SPACE

1. BRAIN

2. CSF

3. BLOOD

INTRACRANIAL VOLUME

ICP normal values

Age Group Normal Range (mmHg)

Adults and older children

< 10-15

Young Children 3-7

Term Infants 1.5-6

Standing 0

INTRACRANIAL PRESSURE

“Intracranial pressure (ICP) is the pressure inside the skull and thus in the brain tissue and cerebrospinal fluid (CSF).”

Constantly changing: exercise, coughing, straining, respiratory cycle

INTRACRANIAL PRESSURE VS INTRACRANIAL VOLUME

INTRACRANIAL PRESSURE VS INTRACRANIAL VOLUME

CPP = MAP – ICPCEREBRAL PERFUSION PRESSURE = MEAN ARTERIAL PRESSURE – INTRACRANIAL PRESSURE

Why do we care? 1. Brain survival depends on cerebral blood fl ow meeting

cerebral metabolic requirements2. Cerebral blood fl ow depends on Cerebral Perfusion Pressure3. CPP depends upon ICP

Normal CPP > 50 mmHg

CEREBRAL PERFUSION PRESSURE

CEREBRAL BLOOD FLOW

What happens if ICP is too high?

CPP = MAP – ICP

As ICP increases. Where MAP is constant. CPP will decrease. Ideally CPP > 70-80mmHg This is bad.

IC-HTN = ICP >20mmHg for >10 minutes

Increased ICP Decreased CPP Decreased CBF

MAP will compensate for awhile. CBF = CPP/CVR

INTRACRANIAL HYPERTENSION (FINALLY)

Why do we care?Raised ICP may CAUSE problems itself e.g

herniation, decrease in cerebral perfusion ischemia edema

Raised ICP may be a SIGN of problems being caused e.g mass eff ect; tumour, haemorrhage

INTRACRANIAL HYPERTENSION

CAUSES OF RAISED ICP

ACUTE VS CHRONICSEVERE VS MILDSYMPTOMS AND SIGNS from raised ICPSYMPTOMS AND SIGNS from CAUSE of raised ICP

E.g:Acute Traumatic Intracranial Haemhorrhage Mass Eff ectVs Neoplasm causing Mass eff ect

SPECTRUM OF RAISED ICP

CAUSES OF RAISED ICP

Subdural Hematoma

Epidural Hematoma

Intracerebral Haemorrhage

Subarachnoid Haemorrhage

Cerebral Contusion

INTRACRANIAL HAEMHORRAGES

Brain Abscess: Develop as a result of a

localized bacterial cerebritis followed by necrosis and encapsulation

Mechanisms: – Haematogenous – Extension from neighbouring

structures – Penetrating injuries Symptoms of infection may be

absent in 50% of cases

Treatment: Excision drainage

SPACE OCCUPYING LESION

1 Obstructive hydrocephalus – obstruction from lesion along ventricle system. E.g tumor, col loid cyst, primary stenosis. 2 Communicating hydrocephalus - (a) obstruction to fl ow of CSF through the basal cisterns or (b) fai lure of absorption of CSF through the arachnoid granulations over the cerebral hemispheres. The most common causes of communicating hydrocephalus are infection (especial ly bacterial and tuberculous) and subarachnoid haemorrhage (either spontaneous, traumatic or postoperative).Treatment: Ventriculoperitoneal Shunt, 3 r d Ventriculostomy

HYDROCEPHALUS

TRAUMATIC BRAIN INJURY

Middle cerebral artery occlusion causing extensive infarction with mass effect. The appearances after decompressive craniotomy are shown in the third panel.

CEREBRAL OEDEMA

1. Decreased LEVEL OF CONSCIOUSNESS - DROWSINESS MOST IMPORTANT never put down to simple sleepiness – measure Glasgow Coma Scale Requires serial assessment Progressive decrease in GCS = worsening ICP state

2. Altered MENTAL STATUS Confusion, restlessness, lethargy, diffi culty thinking,

3. HEADACHE Frontal, worse after lying down, Relieved by vomiting, Severe, Worse with coughing

and straining

4. NAUSEA and VOMITING Persistent

5. VISUAL CHANGES Pupillary Dysfunction Changes in Vision VI nerve Palsy – false localising sign Papilloedema - requires more than 24 hours

SYMPTOMS AND SIGNS

GLASGOW COMA SCALE

ABDUCENS PALSY

Venous engorgement (usual ly the fi rst s igns) loss of venous pulsation hemorrhages over and / or adjacent to the optic disc blurring of optic margins elevation of optic disc Paton's l ines = radial retinal l ines cascading from the optic disc

PAPILLOEDEMA

Continuous DECREASE in GCS stuporous comatose

d iffi cul ty to arouse

VISUAL CHANGES Pupi ls become uni latera l ly en larged progress ing to fi xed and d i lated – eventua l ly

b i la tera l ly fi xed and d i lated Papi l loedema

NEUROLOGICAL FUNCTION Decort icate or Decerebrate Postur ing Loss o f corneal and gag refl exes Hemiplegia – that progresses

VITAL SIGNS Bradycard ia Increas ing Hypertens ion – w i th w idening pulse pressure I rregular Respi rat ion – neurogenic Hypervent i lat ion Respi ratory arrest Cushing's Tr iad Hyperthermia

SIGNS OF BRAIN HERNIATION

PROGRESSION OF SIGNS

seen in 33% of IC-HTN

1. HYPERTENSION (Widening Pulse Pressure)

2. BRADYCARDIA3. RESPIRATORY IRREGULARITY

INDICATES IMPENDING HERNIATION

CUSHING’S TRIAD

Transtentorial:Foramen MagnumSubfalcine

BRAIN HERNIATION SYNDROMES

SEVERITY AND INDICATIONS

Indications for Treatment:ICP ≥ 20- 25 mmHg as the upper limit. Initiate Treatment for ICP > 20 mmHg – in combination with clinical exam and brain CT findings.

Herniation can still occur at ICP < 20

Higher mortality and worse outcomes among patients with ICP persistently >20 compared to < 20.

CPP Targets:Avoid CPP < 50mmHgInitiate treatment when CPP falls below 60mmHg

LUMBAR PUNCTURE IS CONTRAINDICATED

CT BrainMRI BrainBiopsyAngiographyTranscranial Doppler Flow Velocity

INVESTIGATIONS

Indications for ICP Monitoring: CT CRITERIA:

For salvageable patients with severe traumatic brain injury – GCS ≤ 8 after cardiopulmonary resuscitation

Abnormal admitting brain CT (60% risk of IC-HTN)or Normal brain CT but with ≥2 risk factors (=60% risk of IC –HTN vs 13% r.f -ve):

• Age >40 years• SBP < 90 mmHg• Decerebrate or decorticate posturing on motor exam – unilateral or bilateral

Neurological criteria – where GCS ≥ 9 – low r isk for IC-HTN – serial neurological exam

Multiple system injury – where ICP l ikely to be eff ected by interventions e.g large volume IV fl uids, PEEP

Traumatic IC Mass – EDH, SDH, depressed skul l fracture Post Op – may elect Non-traumatic Contraindications to ICP monitoring: “awake” patient, coagulopathy

MANAGEMENT - MONITORING

Intraventricular Catheter – IVC Most accurate, allows therapeutic CSF drainage May be diffi cult to insert into compressed or displaced ventricles,

may obstruct Intraparenchymal monitor Subarachnoid Screw (bolt)

INVASIVE ICP MONITORING

1. MAINTAIN CEREBRAL PERFUSION PRESSURE by LOWERING ICP Reduce size of brain VOLUME by decreasing cerebral volume, CSF fl uid

volume, or blood volume whi le maintaining cerebral perfusion Make more SPACE – e.g surgical decompression GOAL ICP <20 mmHg and CPP > 50mmHg

2.DECREASE METABOLIC DEMANDS

3. PREVENT COMPLICATIONS GI r isk of develop ing Cushing stress ulcers and GI b leeding. Give PPIs and H2 antag. Flu id and e lectrolytes – d iabetes insp idus - desmopress in. C lose moni tor ing of

e lectro lytes . Hematolog ical – DIC can occur after severe head in jury. Coagulopathies aggress ive ly

t reated FFP and Vi t K 10mg a dai ly. Nutr i t ion

4. IDENTIFY CAUSE – TREAT e.g remove space occupying lesions, insert VP shunt

MANAGEMENT

↓ ICP via ↑ Venous Outflow Elevation of Head of Bed 30-45 degrees

optimised trade off between promoting Venous Outfl ow vs Reducing MAP

Keep Neck Straight Midline , avoid t ight t rach tape

Maintain CPP with NormotensionAvoid Hypotension (SBP < 90 mm Hg) Achieved v ia normal is ing intravascular volume. Use of pressors i f needed.

Contro l hypertension i f present , Ni t ropruss ide i f n i l tachy vs beta blocker i f tachy

HyperventilationMay be necessary for br ief per iods when acute neurologic deter iorat ion. Do not use prophylact ical ly. Short term.

Venti late to NORMOcarbia PaCO 2 = 35-40mmHg)

Avoid Hypoxia (PaO 2 < 60mmHg or sat 90%) – maintain airway and oxygenation ↓O 2 = bad

BLOOD VOLUME

OSMOTIC AGENTS Mannitol - Eff ects occur within 20 minutes; does not cross

intact blood-brain barrier; observe for rebound ICP; 0.25-1 gm/kg IV over 24h

Frusemide 10-20mg IV q6 hours. PRN ICP > 20. Hypertonic Saline - When refractory to mannitol – 3% saline

infusion or bolus – if serum osmolarity greater than 320 – hold no more benefi t

EUVOLEMIA

CORTICOSTEROIDS Decreases cerebral edema in brain tumors Reduce CSF production, stabil ize blood-brain barrier and cell

membranes -> overall improvement of neuronal function Dexamethasone

BRAIN VOLUME

Drain CSF Ventriculostomy – Pliable catheter inserted into lateral

ventricle on nondominant side Can remove CSF intermittently or continuously Removal of even small amount will dramatically decrease

ICP Shunts

CSF VOLUME

TEMPERATURE CONTROL Antipyretic medications, cooling blanket

SEIZURE CONTROL Phenytoin: 15-18 mg/kg; not to exceed 50 mg/min Diazepam: 5-10 mg bolus at 2 mg/min Barbiturates (Pentobarbital & thiopental) when not responsive to

conventional therapy

SEDATION Paralyzing agents; CV monitoring; endotracheal intubation;

mechanical ventilation; ICP monitoring; arterial pressure monitoring Reduce sympathetic tone

ENVIRONMENT dark room – free from noise minimise stimulus.

DECREASING METABOLIC DEMAND

Decompressive Craniectomy Considered for IC-HTN refractory to medical treatment.

Surgical Mx of subdural, epidural or intraparenchymal hematoma.

SURGICAL MANAGEMENT