Raised Intracranial Pressure

• With only blood, brain parenchyma and CSF within the cranial vault, for there to be raised ICP one of these must have to increase

• Intracranial haemorrhage
• Increased blood flow:
• Hypercarbia
• Hypoxia

• Coughing
• Straining
• Excessive PEEP
• Impediments to jugular venous drainage e.g. central lines, tube ties, rigid collars

• Hydrocephalus
• Idiopathic intracranial hypertension

• Cerebral oedema
• Abscesses
• Contusion
• SOL
• Other inflammation

• Headache; worse in the morning and on raising ICP e.g. lying flat, leaning forward, sneezing/coughing/straining
• Vomiting, typically without nausea
• Blurred vision or diplopia

• Papilloedema
• Seizures
• Decreased conscious level
• Bulging fontanelles (paediatrics)
• Bradycardia and hypertension
• Decerebrate posturing
• Hemiparesis
• Fixed, dilated pupils
• Irregular respiration
• Death

• Control the airway
• Tape (rather than tie) ETT or use fastening systems such as anchor-fast
• Keep head in midline
• Avoid or loosen C-spine collars
• Sit up to 30-45°
• No greater than 45° as this may cause reduced CPP and paradoxical increases in ICP

• Ventilation to maintain PCO₂ 4.5 - 5.0kPa
• Oxygenation to maintain PO₂ >10 - 13kPa and SpO2 >98%
• Minimise intrathoracic pressure by keeping PEEP ∽5cmH₂O

• Increase MAP in order to keep CPP >60mmHg (e.g. if presumed ICP is 20-30mmHg then target MAP of 80-90mmHg)
• Avoid internal jugular central venous lines
• NG nimodipine to control cerebral vasospasm e.g. in SAH
• Avoid hypervolaemia


• In the presence of severe systemic hypertension, use either ɑ-blockers (clonidine) or β-blockers (labetalol) to reduce systemic BP without affecting ICP
• Avoid calcium channel blockers, which cause dilation of intracerebral vessels and therefore increase ICP

• Sedate with anaesthetic agents
• Propofol, thiopentone and etomidate all reduce CMR, CBF and thus ICP
• Propofol is felt to be the agent of choice, reserving barbiturates for refractory ICP
• Ketamine is classically thought to increase CBF and therefore ICP, so is often avoided
• This mayn't be true, and use of ketamine mayn't affect neurological outcomes, length of ICU stay or mortality
• Volatile agents and nitrous oxide are best avoided as can increase ICP through increased CBF


• Opioids do not have an intrinsic ICP-reducing effect, although reasons to still infuse them in cases of raised ICP/TBI:
• Decrease rises in ICP in response to noxious stimuli
• Ablate the cough reflex, which causes a rise in ICP
• Sedative-sparing effect to mitigate cardiovascular effects of sedatives
• Appear to reduce CMRO₂ via an additive effect
• Humanitarian considerations; trauma is painful


• Benzodiazepines also appear to have little direct effect on ICP, though midazolam is a typical 2^nd line agent in TBI/raised ICP
• Propofol-sparing effect
• Minimal effect on CMRO₂ at lower doses but modest effects at higher doses
• Midazolam (vs. propofol) does not influence duration of ICU stay nor mortality


• NMBA do not in-and-of themselves reduce ICP
• They may be used to avoid coughing and straining whilst ventilated, both of which increase ICP
• Suxamethonium can cause a transient increase in ICP


• Treat seizures with anti-epileptic agent of choice e.g. keppra, phenytoin for at least 7 days

• Options include:
• 20% (20g/100ml) mannitol
• Dose of 0.5-1g/kg (i.e. 2.5-5ml/kg)
• Typically 0.5g/kg for one pupil blown, 1g/kg for two


• Initial osmotic effect draws water from brain parenchyma into the intravascular compartment
• Secondary diuretic effect leads to loss of free water >Na⁺
• In addition to osmotic diuresis, also acts as a free radical scavenger and reduces CSF production


• Lowers ICP within 5-20mins
• Peak effect 20 - 60mins post-administration
• Duration of action up to 6hrs


• 3% saline
• Dose of 1 - 2ml/kg 3% saline


• Treats raised ICP to an equal extent as mannitol
• Advantageous as it will also treat hypotension and raised MAP, and therefore CPP

• Pyrexia is a potent vasodilator
• Increased systemic metabolism and CMRO₂ by 7% per 1°C rise in temperature
• Therefore treat pyrexia with paracetamol and active cooling


• There is not high-level evidence for therapeutic hypothermia in brain injury
• The BTF guidelines say: 'early (<2.5 hours), short-term (48 hours post-injury) prophylactic hypothermia is not recommended to improve outcomes in patients with diffuse injury'
• Landmark studies include:
• Eurotherm (2015)
• POLAR (2018)
• A detailed summary of therapeutic and prophylactic hypothermia for traumatic brain injury can be found on the Deranged Physiology site

• Steroids e.g. dexamethasone
• Useful for decreasing vasogenic cerebral oedema associated with intracerebral tumours or abscesses
• Neurological improvement occurs within hours but ICP decreases over 2 - 5 days
• No benefit in TBI or ICH

• Maintain normoglycaemia
• Adequate nutrition
• VTE prophylaxis

• Measure ICP e.g. EVD, ICP bolt

• Drain placed into ventricle via frontal lobe
• Continuous drainage (∽20ml/hr i.e. same as CSF production) felt to be better than intermittent

• Craniotomy e.g. to evacuate clot
• Tumour debulking


• Decompressive craniectomy
• May provide benefit for treatment of refractory raised ICP from:
• Malignant MCA syndrome (improves mortality but without improved disability)
• Traumatic brain injury (improves mortality but at the expense of increase disability)
• Intra-cranial haemorrhage including SAH
• Other causes of raised ICP e.g. dural sinus thrombosis, encephalitis
• Landmark trials include DECRA and RescueICP
• See the summary by LITFL