Cushing's Triad is a classic but late indicator of brainstem compression. Its presence demands immediate Tier 2 and 3 ICP management interventions.
Physiological probe
Assess the presence of the three Cushing physiological markers to identify late-stage intracranial hypertension and terminal risk status.
Guidelines & Evidence
Clinical Details
Section 1
When to Use
When to Use
Rapid assessment of patients with severe TBI, intracranial hemorrhage, or large tumors.
Monitoring for sudden decompensation in neuro-intensive care.
Section 2
Literature
Development
Harvey Cushing originally described this reflex in 1901. When ICP rises to equal MAP (Mean Arterial Pressure), cerebral perfusion ceases (CPP = 0). The brain stem becomes profoundly ischemic and triggers a massive sympathetic surge. This shoots the blood pressure up drastically to force blood into the brain (hypertension). The body's baroreceptors sense this extreme BP and command the vagus nerve to slow the heart (bradycardia). As the pressure mechanically crushes the medulla, central respiratory drive fails (irregular respirations).
Section 3
Pearls/Pitfalls
A Terminal Sign
Cushing's triad is a pre-terminal sequence. Do not rely on it as a screening tool for raised ICP. By the time the triad is fully present, brainstem herniation is actively occurring. Action must be swift—do not wait for diagnostic imaging if the triad abruptly appears post-injury.
Section 4
Evidence Appraisal
Primary Reference
Concerning a definite regulatory mechanism of the vaso-motor centre which controls blood pressure during cerebral compression
Cushing H. • Bull Johns Hopkins Hosp. 1901;12:290-292
