# Raised Intracranial Pressure > Raised intracranial pressure for NEET-PG Medicine: Monro-Kellie doctrine, Cushing triad, CPP targets, mannitol or hypertonic saline and the steroids exception. - Canonical URL: https://prepelephant.com/topics/neet-pg/medicine/raised-intracranial-pressure - Exam / course: NEET-PG · Subject: Medicine - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Raised Intracranial Pressure", PrepElephant, https://prepelephant.com/topics/neet-pg/medicine/raised-intracranial-pressure ## Direct answer Raised intracranial pressure — above the normal supine range of about 5–15 mmHg, with treatment generally begun beyond 20–22 mmHg — threatens herniation and cerebral perfusion, and its management is a stacked ladder: head elevation to 30 degrees, sedation and normocapnia (hyperventilation only as a brief temporising measure), osmotherapy with mannitol 0.25–1 g per kg or hypertonic saline, maintenance of cerebral perfusion pressure roughly 60–70 mmHg, CSF drainage, and definitive surgery. Corticosteroids belong only to vasogenic oedema around tumours and abscesses — never to trauma or haemorrhage, where trials showed harm. ## What you must remember - Monro-Kellie doctrine: brain, blood and CSF share a fixed cranial vault; volume expansion in one must be offset by the others or pressure climbs — the physiology behind every management step. - Clinical signs: headache worse in the morning, coughing or bending, vomiting without preceding nausea, transient visual obscurations, papilloedema, sixth nerve palsy (a false-localising sign), and late Cushings triad — hypertension with bradycardia and irregular respiration, a pre-terminal event. - Monitoring and thresholds: intracranial pressure above about 20–22 mmHg generally triggers therapy; cerebral perfusion pressure (mean arterial pressure minus intracranial pressure) is maintained roughly 60–70 mmHg — do not drop blood pressure reflexively. - First-tier measures: head-up 30 degrees with the neck midline, controlled sedation and analgesia, normothermia, euglycaemia, normonatraemia, seizure control, and avoiding hypoxia and hypotension. - Ventilation: normocapnia (PaCO2 about 35–40 mmHg); hyperventilation to PaCO2 30–35 mmHg is reserved for minutes-to-hours while definitive therapy is arranged, because sustained hypocapnia causes cerebral ischaemia. - Osmotherapy: mannitol 0.25–1 g per kg intravenously (serum osmolality held below about 320 mOsm, watching renal function) or 3 per cent hypertonic saline boluses, which some protocols favour for haemodynamic stability. - Corticosteroids: dexamethasone reduces vasogenic oedema around tumours and abscesses — but is harmful and contraindicated in traumatic brain injury and intracerebral haemorrhage (CRASH trial evidence). - Second-tier and definitive: external ventricular drain for hydrocephalus (also monitors pressure), decompressive craniectomy for refractory intracranial pressure and malignant middle cerebral artery infarction, barbiturate coma in selected refractory cases, and resection or evacuation of the causative mass. - Specific scenario worth separating: idiopathic intracranial hypertension — obese young women, papilloedema with normal imaging apart from slit ventricles, visual field threat driving treatment (weight loss, acetazolamide, shunting for visual decline). ## Running the ladder in one traumatic brain injury A 22-year-old cricketer, hit on the temporal region, deteriorates from GCS 13 to 8 over an hour; the right pupil is drifting wide. The ladder runs in order, without skipping. Simultaneous first moves: intubation with sedation (avoiding coughing and spikes), head elevated 30 degrees, neck midline, ventilation set to normocapnia — and the scanner prepared, because the suspicion (an extradural haematoma under a fractured squamous temporal bone) is a surgical disease with a surgical clock. While transferring, hyperventilation to a PaCO2 of about 32 mmHg is a legitimate minutes-only bridge given the lateralising signs, and a mannitol bolus at 0.5–1 g per kg buys the same window. Blood pressure is supported, not lowered — perfusion pressure must survive the transport. The CT confirms the lens-shaped clot; the definitive therapy is craniotomy and evacuation, and every lower rung of the ladder exists only to deliver this patient to theatre with neurons intact. Had the same pressure problem instead arisen diffusely three days after a severe closed injury, the sequence would reorder: intracranial pressure monitor, external ventricular drain, hypertonic saline or mannitol by protocol, sedation deepened, and decompressive craniectomy held ready for refractory elevation — with steroids explicitly absent from the plan, the CRASH evidence having removed them. ## Where students slip The steroid exception is the single most examined error: dexamethasone for tumour and abscess oedema, never for trauma or intracerebral haemorrhage — stems offering steroids in head injury contain the planted wrong answer. The second slip is sustained hyperventilation as a routine measure, ignoring its ischaemic cost; it is a bridge, not a therapy. The third is the perfusion arithmetic — dropping the blood pressure of a hypertensive head-injured patient collapses cerebral perfusion pressure; the target is 60–70 mmHg maintained from the mean arterial side. And Cushing's triad, when it appears in a stem, means imminent herniation, not a stable observation to monitor overnight. ## Frequently asked questions ### What is the normal intracranial pressure and the treatment threshold? About 5–15 mmHg supine in adults; therapy is generally initiated when sustained pressure exceeds about 20–22 mmHg. ### What is the target cerebral perfusion pressure and how is it calculated? Mean arterial pressure minus intracranial pressure, maintained roughly 60–70 mmHg — supporting blood pressure rather than lowering it reflexively. ### When are corticosteroids indicated in raised intracranial pressure? Only for vasogenic oedema surrounding tumours and cerebral abscesses (dexamethasone); they are contraindicated in traumatic brain injury and intracerebral haemorrhage. ### How is osmotherapy given and monitored? Mannitol 0.25–1 g per kg intravenously with serum osmolality kept below about 320 mOsm and renal function watched, or 3 per cent hypertonic saline boluses per protocol. ### What is the role of hyperventilation? A temporising bridge only: PaCO2 of about 30–35 mmHg for minutes to hours during acutely lateralising deterioration, awaiting definitive treatment, because sustained hypocapnia causes cerebral vasoconstriction and ischaemia.