# Neurocritical Care: ICP, SAH and Status Epilepticus > ICP and CPP targets, hyperosmolar therapy, subarachnoid haemorrhage care and status epilepticus protocols for NEET-SS Critical Care exams. - Canonical URL: https://prepelephant.com/topics/neet-ss/critical-care-medicine/neurocritical-care-dm - Exam / course: NEET-SS · Subject: Critical Care 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: "Neurocritical Care: ICP, SAH and Status Epilepticus", PrepElephant, https://prepelephant.com/topics/neet-ss/critical-care-medicine/neurocritical-care-dm ## Direct answer Secondary brain injury is preventable where the primary insult is not — so neurocritical care holds intracranial pressure below 22 mmHg, cerebral perfusion pressure between 60 and 70 mmHg, PaCO2 normal, sodium above 140 mmol/L, temperature and glucose normal, and seizures treated or pre-empted. An elevated ICP is managed in tiers from head position and sedation through hyperosmolar therapy to decompression, subarachnoid haemorrhage gets nimodipine and euvolaemia, and status epilepticus gets benzodiazepines then a second-line antiseizure drug without delay. ## What you must remember - Brain Trauma Foundation fourth edition: treat ICP above 22 mmHg; target CPP 60 to 70 mmHg — higher pressures flood the lungs, lower ones starve the brain. - Prophylactic antiseizure medication for the first seven days after traumatic brain injury; no longer-term prophylaxis. - Hyperosmolar therapy: mannitol 0.25 to 1 g per kg or 3 per cent saline bolus (about 250 mL) — hypertonic saline may edge out mannitol for ICP control, and mannitol loses effect above serum osmolality of about 320 mOsm/kg. - Therapeutic hypothermia in TBI is dead; normothermia with active pyrexia control is standard, and targeted temperature management 32 to 36 degrees Celsius applies after cardiac arrest. - Subarachnoid haemorrhage: oral nimodipine 60 mg every four hours for 21 days, euvolaemia (triple-H therapy abandoned), transcranial Doppler for vasospasm peaking days 4 to 10, and induced hypertension once delayed cerebral ischaemia appears. - Status epilepticus: lorazepam 0.1 mg per kg intravenously (or intramuscular midazolam 10 mg per RAMPART), then a second-line agent — fosphenytoin 20 mg phenytoin-equivalents per kg, levetiracetam 60 mg per kg, or valproate 40 mg per kg, equivalent per ESETT. - Non-convulsive status is found only by looking: continuous EEG for any unexplained coma, and neuroprognostication after arrest is multimodal, deferred to at least 72 hours off sedation. ## Climbing the ICP ladder A 32-year-old, day two after a severe TBI, develops anisocoria on an external ventricular drain reading 28 mmHg. Work upward in tiers and stop when the number falls. Tier zero: head at 30 degrees and midline, sedation deepened, PaCO2 held 35 to 40 mmHg, pyrexia treated, hyponatraemia corrected toward 140 to 145 mmol/L with hypertonic saline rather than waterlogged with plain saline. Tier one: drain cerebrospinal fluid via the ventriculostomy — the fastest definitive litre in medicine — and give a 3 per cent saline bolus. Tier two: if pressure stays above 22 mmHg, a short infusion of neuromuscular blockade for synchrony, CSR drainage repeated, and hyperosmolar therapy continued with sodium targeted around 145 to 150 mmol/L. Tier three: decompressive craniectomy for refractory elevation as a last-resort conversation — DECRA warned against early bifrontal surgery for moderate elevations, RESCUEicp established unilateral surgery as an ultimate option with survival bought at the cost of severe disability in a proportion of survivors. Alongside the ladder runs the search for a surgical lesion — a clot that needs the operating theatre outranks every tier above. ## Where students slip The recurring errors are physiology-shaped. Prophylactic hyperventilation to PaCO2 of 30 causes the cerebral vasoconstriction it once sought to exploit — it is a temporising manoeuvre for impending herniation only. Steroids in TBI increase mortality and are contraindicated; stating that plainly earns marks. Nimodipine is enteral, 60 mg every four hours for 21 days — intravenous nimodipine is a historical hazard, and confusing the route is a genuine fail-grade slip. CPP pushed above 70 recreates the fluid-overload ARDS of old protocols. And the modernity trap: quoting a single "72-hour unmapped EEG" as prognostication — the answer is multimodal (examination, EEG, SSEP N20, imaging, biomarkers) at 72 hours or later, off sedation. ## Frequently asked questions ### What ICP and CPP targets does the Brain Trauma Foundation set? Treat intracranial pressure above 22 mmHg; maintain cerebral perfusion pressure 60 to 70 mmHg. ### Mannitol or hypertonic saline for raised ICP? Either as bolus — mannitol 0.25 to 1 g per kg capped by osmolality near 320 mOsm/kg; 3 per cent saline about 250 mL with sodium targeted to the upper-normal range, with growing preference in many units. ### What is the nimodipine regimen after subarachnoid haemorrhage? Oral 60 mg every four hours for 21 days, started early, alongside euvolaemia and monitoring for delayed cerebral ischaemia from day 4 to 10. ### What is the second-line drug in status epilepticus? Any one of fosphenytoin 20 mg phenytoin-equivalents per kg, levetiracetam 60 mg per kg, or valproate 40 mg per kg — ESETT found them equivalent after benzodiazepines. ### Is therapeutic hypothermia used in traumatic brain injury? No — trials were negative; maintain normothermia and treat pyrexia. Targeted temperature management 32 to 36 degrees Celsius applies after cardiac arrest. ### When is neuroprognostication performed after cardiac arrest? Not before 72 hours, off sedation, using multiple modalities — examination, EEG, somatosensory evoked potentials, imaging and biomarkers together.