ICP is normally 7–15 mm Hg; at 20–25 mm Hg, the upper limit of normal, treatment to reduce ICP may be needed.
Cerebral venous sinus stenosis has been reported in up to 90% of patients with IIH.
Repeat studies after normalization of the intracranial pressure demonstrated normalization of this finding.
The cerebral sinus narrowing might be a consequence of the increased intracranial pressure. However, venous sinus narrowing/thrombosis could cause increased intracranial pressure as well. This situation could represent the chicken or egg debate as to which occurs first 1).
Patients suffering from uncontrollable intracranial hypertension due to posttraumatic brain swelling.
An MRI or CT scan of the head can usually determine the cause of increased intracranial pressure and confirm the diagnosis.
Intracranial pressure may be measured during a spinal tap (lumbar puncture). It can also be measured directly by using a device that is drilled through the skull or a tube (catheter) that is inserted into a hollow area in the brain called the ventricle.
The diagnosis of raised intracranial pressure (ICP) is important in many critically ill patients. The optic nerve sheath is contiguous with the subarachnoid space; thus, an increase in ICP results in a corresponding increase in the optic nerve sheath diameter.
Ocular sonography shows good diagnostic test accuracy for detecting raised ICP compared to CT: specifically, high sensitivity for ruling out raised ICP in a low-risk group and high specificity for ruling in raised ICP in a high-risk group. This noninvasive point-of-care method could lead to rapid interventions for raised ICP, assist centers without CT, and monitor patients during transport or as part of a protocol to reduce CT use 2).
Autonomic impairment after acute traumatic brain injury has been associated independently with both increased morbidity and mortality. Links between autonomic impairment and increased intracranial pressure or impaired cerebral autoregulation have been described as well. However, relationships between autonomic impairment, intracranial pressure, impaired cerebral autoregulation, and outcome remain poorly explored.
If intracranial pressure gets too high, it can lead to deadly brain herniation, in which parts of the brain are squeezed past structures in the skull.
ICP-lowering therapies are usually administered in a stepwise manner, starting with safer first-line interventions, while reserving higher-risk options for patients with intractable intracranial hypertension.
In a review, LeRoux will examine the implications of the Benchmark Evidence from South American Trials: Treatment of Intracranial Pressure (BEST TRIP) trial, evidence for an influence of ICP care on outcome, and a need for greater understanding of the pathophysiology than just ICP through multimodal monitoring (MMM) to enhance the outcome.
ICP-based monitoring and treatment alone may not be enough to enhance TBI outcome, but ICP and cerebral perfusion pressure therapy remain important in TBI care. Although high-quality evidence for MMM is limited, it should be more widely adapted to better understand the complex pathophysiology after TBI, better target care, and identify new therapeutic opportunities 4).