Signs and Symptoms of Significant Intracranial Pressure (ICP)

Clinical Presentation

Changes in behavior with minimal change in level of consciousness (Grade I encephalopathy) are associated with elevated ICP, as defined by the American Association for the Study of Liver Diseases 1
Gross disorientation, drowsiness, possibly asterixis, inappropriate behavior (Grade II encephalopathy) are indicative of progressing intracranial hypertension, according to the American Association for the Study of Liver Diseases 1
Marked confusion, incoherent speech, sleeping most of the time but arousable to vocal stimuli (Grade III encephalopathy) is a sign of severe ICP, as reported by the American Association for the Study of Liver Diseases 1
Comatose state, unresponsive to pain (Grade IV encephalopathy) indicates severe intracranial hypertension, as defined by the American Association for the Study of Liver Diseases 1

Pupillary changes - including anisocoria (unequal pupils) or bilateral mydriasis (dilated pupils) are associated with elevated ICP, as noted by the American Society of Anesthesiologists 2, 3
Hypertension - often with widened pulse pressure, bradycardia - irregular heart rate, and irregular respirations - abnormal breathing patterns are components of Cushing's triad, which is a late sign of elevated ICP, according to the American Association for the Study of Liver Diseases 2
Disappearance of cerebral ventricles on CT scan, brain midline shift over 5 mm, intracerebral hematoma volume over 25 mL, and compression of basal cisterns are imaging findings associated with elevated ICP, as reported by the Society of Neurointerventional Surgery 4, 5
Absence of basal cisterns is associated with ICP higher than 30 mmHg in more than 70% of cases, according to the Society of Neurointerventional Surgery 4, 5

An ICP of 20-40 mmHg is associated with a 3.95 times higher risk of mortality and poor neurological outcome, as reported by the Society of Critical Care Medicine 5
Above an ICP of 40 mmHg, mortality risk increases 6.9-fold, according to the Society of Critical Care Medicine 5
Traumatic subarachnoid hemorrhage is associated with a higher risk of intracranial hypertension, as noted by the Brain Injury Foundation 4, 5

Relying solely on CT findings can be misleading, as visibility of basal cisterns does not completely exclude intracranial hypertension, according to the American Society of Neuroradiology 4, 5
Waiting for the full Cushing's triad to appear before intervention may result in delayed treatment, as these signs typically manifest late in the course, as reported by the American Association for the Study of Liver Diseases 2
Transcranial Doppler findings (such as increased pulsatility index) require confirmation by other means to reliably indicate intracranial hypertension, as noted by the American Heart Association 6, 7