Neurocritical Care Basics
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Direct answer
Four numbers organise most of neurocritical care: intracranial pressure held below 22 mmHg, cerebral perfusion pressure maintained at 60-70 mmHg, PaCO2 kept in the 35-40 mmHg range, and serum sodium defended in the high-normal band when oedema threatens. Management follows the Monro-Kellie doctrine — reduce intracranial contents through CSF drainage, hyperosmolar therapy and head-up venous positioning, while supporting mean arterial pressure and treating the primary insult. Decompressive hemicraniectomy within 48 hours rescues selected malignant middle cerebral artery infarcts and refractory traumatic hypertension; normothermia, euglycaemia (roughly 140-180 mg/dL) and short-term seizure prophylaxis complete the frame.
What you must remember
- ICP threshold: the Brain Trauma Foundation fourth edition lowered the treatment trigger to 22 mmHg (third edition said 20) — a favourite viva distinction; mortality rises once ICP sustains above this.
- CPP target 60-70 mmHg: falling below 60 risks ischaemia, while aggressive pushing above 70 with fluids and vasopressors adds adult respiratory distress syndrome without benefit.
- Hyperosmolar therapy: mannitol 0.25-1 g per kg (serum osmolality below 320, osmolar gap under about 20) or hypertonic saline boluses aiming sodium around 145-155 mEq/L; mannitol risks hypovolaemia and the rebound of interrupted infusions.
- ICP monitor indications: GCS 8 or less with an abnormal CT, or a normal CT with two of age over 40, hypotension, or motor posturing; an external ventricular drain both measures and drains.
- Decompressive hemicraniectomy: pooled DECIMAL, DESTINY and HAMLET data support surgery within 48 hours for malignant MCA infarction in patients under about 60 with infarct volume over 145 mL (DESTINY II tempered enthusiasm above 60).
- Seizure prophylaxis: seven days of levetiracetam or phenytoin after severe traumatic brain injury prevents early seizures only — prophylaxis does not improve outcome and must stop.
- Paroxysmal sympathetic hyperactivity: storming after TBI (tachycardia, hypertension, diaphoresis, extension posturing) responds to morphine, propranolol and baclofen — treat it, do not chase the "seizures".
The first 72 hours after a severe head injury
Walk a 25-year-old with an extradural haematoma evacuated in the night. Hour zero is about the ABCs with one difference: a single episode of hypotension or hypoxia doubles mortality, so intubation with normocapnia and mean arterial pressure above 80 mmHg precedes everything. She arrives sedated on propofol and fentanyl, head elevated 30 degrees and neck midline so venous outflow is unobstructed. The ICP bolt reads 19 mmHg; CPP computes at 71, so nothing is escalated yet. On day one she develops plateau waves — ICP 28 with a falling CPP. The sequence is rehearsed: sedation deepened, a 2 mL/kg bolus of 3% saline, CSF diverted through the newly placed ventricular catheter, and a repeat CT, which shows reassessment-worthy contusion growth rather than a surgical lesion. Had the CT shown a compressive lesion, the operating theatre, not the infusion pump, is the answer — no hyperosmolar agent substitutes for decompression of a mass. By day two the ICP again climbs despite tiered measures; second-tier options open up: continuous hypertonic saline infusion, briefly hyperoxia... and, if refractory, barbiturate coma with SSEP/EEG monitoring or hemicraniectomy. Temperature is checked four-hourly because fever independently worses outcome; paracetamol and surface cooling hold 36-37 °C, since the TTM trial found no benefit from prophylactic hypothermia in traumatic coma. Glucose runs in the 140-180 mg/dL lane — neither hypoglycaemia nor the oxidative stress of hyperglycaemia.
Where candidates slip
The classic error is treating the number and forgetting the doctrine: escalating hyperosmolar therapy for a high ICP caused by hyponatraemia, airway obstruction or a kinked neck — all correctable without a single bolus. The second slip is CPP arithmetic: cerebral perfusion pressure equals mean arterial pressure minus intracranial pressure, and an exam vignette will deliberately give you a systolic/diastolic pair so you must compute MAP yourself (diastolic plus one-third of pulse pressure). In Indian practice, add honesty about access: continuous ICP monitoring is confined to tertiary centres, so in most district ICUs management rides on pupillary checks, trauma CT and clinical herniation signs — which is exactly why the examiner expects you to state the Cushing response (hypertension, bradycardia, irregular respiration) and the threshold numbers unprompted.
Frequently asked questions
At what intracranial pressure should treatment be initiated after traumatic brain injury?
The Brain Trauma Foundation fourth edition recommends treating sustained ICP above 22 mmHg, since values higher than this are associated with increased mortality.
What is the target cerebral perfusion pressure and how is it calculated?
CPP equals mean arterial pressure minus intracranial pressure, and the recommended target is 60-70 mmHg; dropping below 60 risks ischaemia while over-aggressive elevation adds pulmonary complications.
Which patients qualify for ICP monitoring when the CT is normal?
A comatose patient with a normal scan qualifies with two of three features: age above 40 years, episodes of hypotension, or extensor posturing.
Is therapeutic hypothermia recommended after traumatic brain injury?
No — randomised evidence found no outcome benefit from prophylactic hypothermia in TBI; only pyrexia control to normothermia is standard.
How long should seizure prophylaxis continue after severe head trauma?
Seven days only; levetiracetam or phenytoin prevents early post-traumatic seizures but does not alter long-term outcome and is discontinued after a week.