Raised intracranial pressure

Surgical approach (where applicable)

• Raised ICP is a physiological problem rather than a single operation; surgical interventions aim to remove mass effect, restore CSF drainage, or decompress the brain.
• External ventricular drain (EVD) insertion
  • Burr hole → ventricular catheter → connected to transducer/drainage system; allows ICP monitoring and CSF drainage
  • Set drainage level relative to tragus (foramen of Monro reference); intermittent or continuous drainage per unit protocol
• Decompressive craniectomy
  • Large bone flap removed ± duraplasty to allow swollen brain to expand and reduce ICP
  • Indications: refractory intracranial hypertension (e.g., malignant MCA infarct, severe TBI) after maximal medical therapy
• Evacuation of mass lesion
  • Craniotomy for extradural/subdural haematoma, tumour debulking, abscess drainage
• Posterior fossa decompression / CSF diversion
  • For obstructive hydrocephalus/tonsillar crowding: EVD, endoscopic third ventriculostomy, VP shunt (usually elective once stabilised)

Anaesthetic management (typical for emergency neurosurgery in raised ICP)

• Type of anaesthesia: General anaesthesia with controlled ventilation
• Airway: Cuffed ETT (RSI often required); avoid SGA in unstable raised ICP / aspiration risk
  • Aim to blunt pressor response to laryngoscopy (opioid, lidocaine, short-acting beta-blocker, adequate hypnotic) while maintaining CPP
• Duration: variable (EVD 30–60 min; craniotomy 2–6+ h; decompressive craniectomy often 2–4 h)
• Pain: moderate–severe for craniotomy/craniectomy; EVD insertion mild–moderate
• Core goals: prevent secondary brain injury (avoid hypoxia, hypotension, hypercapnia, fever, hypo-/hyperglycaemia); maintain CPP; facilitate surgical brain relaxation
• Monitoring: invasive arterial BP early; large-bore IV access; consider CVC if vasoactive infusions/poor access; temperature; urine output; capnography; neuromonitoring per case
• Induction/maintenance: avoid large swings in MAP/PaCO2; commonly propofol + opioid + rocuronium; maintenance TIVA (propofol/remifentanil) or low-dose volatile (≤1 MAC) with opioid
• Ventilation: target normocapnia (PaCO2 ~4.5–5.0 kPa); brief hyperventilation (PaCO2 ~4.0–4.5 kPa) only as a temporising measure for impending herniation
  • Avoid prolonged aggressive hyperventilation (risk cerebral ischaemia due to vasoconstriction)
• Osmotherapy: mannitol 0.25–1 g/kg or hypertonic saline (e.g., 3% 2–5 mL/kg or bolus per local protocol) when indicated; coordinate with neurosurgeon/ICU
  • Monitor serum sodium/osmolality, haemodynamics and urine output; avoid hypotension after mannitol
• Positioning: head-up ~15–30°, neutral neck, avoid venous obstruction (tight ETT ties, extreme rotation), avoid high PEEP if it impairs venous return/CPP
• Emergence: decide early—wake for neuro exam vs postoperative ventilation (common if severe TBI, ongoing swelling, poor GCS, massive transfusion, unstable physiology)
  • If waking: smooth emergence (avoid coughing/straining): opioid titration, lidocaine, consider short-acting antihypertensives; treat PONV aggressively

Definitions and key numbers

• ICP: pressure within the cranial vault (adult normal ~5–15 mmHg). Sustained ICP >20–22 mmHg is commonly treated in severe TBI pathways.
• CPP = MAP − ICP (or MAP − CVP if CVP > ICP). Typical target CPP in severe TBI often ~60–70 mmHg (individualise; avoid excessive vasopressors causing ARDS/brain oedema).
• Monro–Kellie doctrine: fixed cranial volume; increases in brain tissue, blood, or CSF must be compensated by decreases in another component until compliance exhausted.
• Pressure–volume curve: initially flat (compensation), then steep rise in ICP with small volume increases once compensatory reserve is lost.

Aetiology of raised ICP

• Mass lesions: intracranial haemorrhage (EDH/SDH/ICH), tumour, abscess.
• Diffuse brain swelling/oedema: traumatic brain injury, hypoxic-ischaemic injury, hepatic encephalopathy, hyponatraemia, DKA/cerebral oedema, high altitude cerebral oedema.
• Hydrocephalus/CSF obstruction: intraventricular haemorrhage, posterior fossa lesions, meningitis, SAH-related hydrocephalus.
• Increased cerebral blood volume: hypercapnia, hypoxia, seizures, fever, high volatile concentration, venous outflow obstruction (neck position, raised intrathoracic pressure, SVC obstruction).
• Idiopathic intracranial hypertension (IIH): raised ICP with normal imaging (except signs) and normal CSF composition; associated with obesity, female sex, tetracyclines, vitamin A derivatives.

Pathophysiology and consequences

• Raised ICP reduces CPP → cerebral ischaemia → cytotoxic oedema → further ICP rise (vicious cycle).
• Autoregulation may be impaired (common in TBI/SAH): cerebral blood flow becomes pressure-passive; hypotension is particularly harmful.
• Herniation syndromes (conceptual): subfalcine (ACA compression), uncal/transtentorial (CN III palsy, PCA infarct, brainstem compression), tonsillar (respiratory/cardiac arrest).
  • Cushing response: hypertension + bradycardia ± irregular respiration (late sign).

Clinical features and assessment

• Symptoms/signs: headache (worse lying/AM), vomiting, reduced consciousness, papilloedema, seizures, focal neurology, pupillary changes.
• Bedside priorities: ABCDE, GCS trend, pupils, glucose, temperature; treat seizures; avoid hypoxia/hypotension.
• Investigations: CT head (mass, hydrocephalus, midline shift); consider CT angiography in SAH; labs (Na, osmolality, ABG, coagulation).

ICP monitoring (overview)

• EVD: gold standard accuracy; allows CSF drainage; infection/haemorrhage risk; requires levelling/zeroing.
• Intraparenchymal fibreoptic/strain gauge: easier insertion, lower infection risk; cannot drain CSF; drift over time.
• Indications (typical): severe TBI with GCS ≤8 and abnormal CT; or normal CT with risk factors (age >40, SBP <90, motor posturing) depending on guideline.

Acute management of raised ICP (stepwise)

• Immediate: optimise oxygenation and perfusion
  • Airway/ventilation: avoid hypoxia; target normocapnia; intubate if low GCS/airway risk
  • Circulation: treat hypotension aggressively (fluids, blood, vasopressors); aim CPP adequate
• Reduce venous congestion
  • Head-up 15–30°, neutral neck, loosen tight collars/ties, avoid jugular compression
  • Avoid high intrathoracic pressure: minimise excessive PEEP, treat coughing/straining
• Reduce cerebral metabolic demand
  • Analgesia + sedation (e.g., propofol/opioid); treat agitation and ventilator dyssynchrony
  • Treat seizures promptly (benzodiazepine → levetiracetam/phenytoin per protocol)
  • Maintain normothermia; treat fever aggressively
• Osmotherapy (temporising) and CSF drainage
  • Hypertonic saline or mannitol as above; consider EVD drainage if present
• Ventilation strategy
  • Short-term mild hyperventilation only for impending herniation while definitive therapy arranged
• Definitive management
  • Urgent neurosurgical intervention for mass lesion/hydrocephalus; reverse anticoagulation/coagulopathy; treat underlying cause (e.g., antibiotics for abscess/meningitis)
• Refractory intracranial hypertension (ICU-level therapies)
  • Deep sedation ± neuromuscular blockade; optimise CPP; consider barbiturate coma in selected cases
  • Decompressive craniectomy for refractory cases (patient selection critical)

Anaesthetic considerations: drugs and techniques

• Induction agents
  • Propofol/thiopentone reduce CMRO2 and CBF → lower ICP; risk hypotension (harmful to CPP)
  • Etomidate: haemodynamic stability, reduces CBF/CMRO2; consider adrenal suppression with repeated dosing/infusions
  • Ketamine: historically avoided; evidence suggests it does not necessarily increase ICP when ventilation controlled and sedation adequate; still consider haemodynamic effects and local practice
• Volatile agents
  • Dose-dependent cerebral vasodilation → ↑CBF/ICP; keep ≤1 MAC and avoid hypercapnia; TIVA often preferred when ICP critical
  • Nitrous oxide increases CBF/ICP and expands air; generally avoid in raised ICP and intracranial air risk
• Opioids and muscle relaxants
  • Opioids blunt sympathetic response; avoid hypoventilation/hypercapnia in spontaneously breathing patients
  • Avoid suxamethonium if possible in markedly raised ICP (transient ICP rise); if RSI required, mitigate with adequate induction and consider rocuronium
• Fluids and haemodynamics
  • Use isotonic fluids (0.9% saline, balanced isotonic solutions per local policy); avoid hypotonic fluids and free water (worsen cerebral oedema)
  • Glucose: avoid hypo- and marked hyperglycaemia; treat hypoglycaemia promptly
• Steroids
  • Useful for vasogenic oedema around tumours (e.g., dexamethasone); not beneficial and potentially harmful in TBI-related raised ICP

Special situations

• Lumbar puncture: contraindicated in suspected raised ICP due to mass lesion/obstructive hydrocephalus (risk of herniation).
• Pregnancy: maintain maternal oxygenation and BP; left uterine displacement; avoid aortocaval compression; coordinate neuro/obstetrics; consider fetal considerations if viable gestation.
• IIH: anaesthesia usually safe if no mass lesion; avoid large swings in CO2; neuraxial techniques may be acceptable in IIH (unlike mass lesions), but assess carefully and follow local guidance.