Raised intracranial pressure — CT interpretation, Cushing triad and emergency management viva

Interpretation

The examiner presents a non-contrast CT showing a high-density lentiform extra-axial collection with midline shift and effacement of the basal cisterns, and asks: "What do you see, what is happening to this patient, and how would you manage them?"^[1]

• Radiograph: an acute extradural (or subdural) haematoma with mass effect — midline shift and compressed cisterns are conventional CT danger signs of raised ICP and impending herniation (do not treat 5 mm of midline shift as a BTF 4th-edition definition of raised ICP).^[1]
• Clinical correlation: this is a surgical emergency — the classic clinical picture is a lucid interval followed by deteriorating consciousness, a fixed dilated pupil on the side of the lesion (uncal herniation compressing the third nerve), and the Cushing triad (hypertension, bradycardia, irregular respiration).
• Never do a lumbar puncture first — imaging is mandatory before any LP in a possible mass lesion, because of the risk of coning.

Key points

The examiner will probe each of these; be ready to defend them at viva depth:

1. Monro-Kellie doctrine and normal values — Benson: combined volume of neuronal tissue, blood and CSF is constant; the textbook 80/10/10 split is conventional teaching, not a fetched proportion. Typical adult ICP 5 to 15 mmHg (Kareemi); treat a sustained ICP above 22 mmHg in TBI (BTF 4th edition, Carney 2016/2017 — Hawryluk 2020 is the decompressive-craniectomy chapter only).^[8][1][3]
2. CPP equation reproduced verbatim — CPP = MAP minus ICP; target CPP 60 to 70 mmHg. BTF SBP floors are age-stratified: ≥100 mmHg (age 50 to 69) and ≥110 mmHg (age 15 to 49 or over 70). Explain that the Cushing hypertension is the brain's attempt to preserve CPP — so never blunt it with an antihypertensive.^[3]
3. Cushing triad mechanism — sympathetic surge raises BP (with widened pulse pressure), baroreceptors cause reflex vagal bradycardia, and direct brainstem compression causes irregular breathing. It is a late, pre-terminal sign and is poorly sensitive; its absence never excludes raised ICP.
4. Tiered management reproduced — Tier 0 (head up 30 degrees, neck midline, sedation, Godoy oxygenation SpO2 ≥95 percent or PaO2 ≥80 mmHg, PaCO2 35 to 40 mmHg, treat fever; prophylactic hypothermia is not recommended for diffuse TBI); Tier 1 (emergency mannitol 0.5 to 1 g/kg IV, or Kim 0.25–1 gm/kg slowly over 15 min if stable, or 3 percent / 23.4 percent 30 to 60 mL HTS — a 250 mL 3 percent bolus is unit practice); Tier 2 (barbiturate coma or decompressive craniectomy). Then treat the cause (evacuate, shunt, resect, antibiotics).^[3][4][5][9]
5. Normocapnia, not hypocapnia — Godoy: PaCO2 35 to 40 mmHg; brief 15 to 30 min hyperventilation to 30 to 35 mmHg only as a bridge in acute deterioration. Do not quote PaCO2 4.0 to 4.5 kPa as the resting target.^[4]
6. Herniation syndromes — uncal (ipsilateral fixed dilated pupil, contralateral hemiparesis; occasionally ipsilateral hemiparesis via Kernohan's notch); central (pinpoint pupils, coma, diabetes insipidus); tonsillar/coning (respiratory arrest, death).
7. Steroid pitfall — corticosteroids are harmful in traumatic raised ICP (CRASH trial); use them only for vasogenic oedema (tumour, abscess).
8. IIH contrast — young obese women, normal MRI/MRV, elevated LP opening pressure (exam teaching often quotes over 25 cmH2O in adults — that millimetre figure is not in the Wang or IIHTT abstracts); Avery: CSFOP ≤28 cm H2O can be considered normal for most children. Treat with low-sodium weight-reduction diet plus acetazolamide (IIHTT, up to 4 g/day) — do not quote an unsourced 5 to 10 percent body-weight figure as a trial result; surgery if vision threatened.^[2][6][7]

References

1. Kareemi H, et al. Initial diagnosis and management of acutely elevated intracranial pressure. J Intensive Care Med 2023.^[1]
2. Wang MTM, et al. Idiopathic intracranial hypertension: pathophysiology, diagnosis and management. J Clin Neurosci 2022.^[2]
3. Kim H. Anesthetic management of the traumatic brain injury patients undergoing non-neurosurgery. Anesth Pain Med (Seoul) 2023.^[3]
4. Godoy DA, et al. Hyperventilation therapy for control of posttraumatic intracranial hypertension. Front Neurol 2017.^[4]

References9ShowHide

1. [1]Kareemi H, Pratte M, English S, Hendin A. Initial Diagnosis and Management of Acutely Elevated Intracranial Pressure J Intensive Care Med, 2023.PMID 36802976
2. [2]Wang MTM, Bhatti MT, Danesh-Meyer HV. Idiopathic intracranial hypertension: Pathophysiology, diagnosis and management J Clin Neurosci, 2022.PMID 34929642
3. [3]Kim H. Anesthetic management of the traumatic brain injury patients undergoing non-neurosurgery Anesth Pain Med (Seoul), 2023.PMID 37183278
4. [4]Godoy DA, Seifi A, Garza D, Lubillo-Montenegro S, Murillo-Cabezas F. Hyperventilation Therapy for Control of Posttraumatic Intracranial Hypertension Front Neurol, 2017.PMID 28769857
5. [5]Ramesh Kumar R, Singhi SC, Singhi P. Raised intracranial pressure (ICP): management in emergency department Indian J Pediatr, 2012.PMID 22218806
6. [6]Avery RA. Interpretation of lumbar puncture opening pressure measurements in children J Neuroophthalmol, 2014.PMID 25133882
7. [7]Wall M, McDermott MP, Kieburtz KD, et al. Effect of acetazolamide on visual function in patients with idiopathic intracranial hypertension and mild visual loss: the idiopathic intracranial hypertension treatment trial JAMA, 2014.PMID 24756514
8. [8]Benson JC, Madhavan AA, Cutsforth-Gregory JK, et al. The Monro-Kellie doctrine: a review and call for revision AJNR Am J Neuroradiol, 2023.PMID 36456084
9. [9]Koenig MA, Bryan M, Lewin JL 3rd, Mirski MA, Geocadin RG, Stevens RD. Reversal of transtentorial herniation with hypertonic saline Neurology, 2008.PMID 18272864