Defining a Taxonomy of Intracranial Hypertension

Abstract

Intracranial pressure (ICP) monitoring and control is a cornerstone of neuroanesthesia and neurocritical care. However, because elevated ICP can be due to multiple pathophysiological processes, its interpretation is not straightforward. We propose a formal taxonomy of intracranial hypertension, which defines ICP elevations into 3 major pathophysiological subsets: increased cerebral blood volume, masses and edema, and hydrocephalus. (1) Increased cerebral blood volume increases ICP and arises secondary to arterial or venous hypervolemia. Arterial hypervolemia is produced by autoregulated or dysregulated vasodilation, both of which are importantly and disparately affected by systemic blood pressure. Dysregulated vasodilation tends to be worsened by arterial hypertension. In contrast, autoregulated vasodilation contributes to intracranial hypertension during decreases in cerebral perfusion pressure that occur within the normal range of cerebral autoregulation. Venous hypervolemia is produced by Starling resistor outflow obstruction, venous occlusion, and very high extracranial venous pressure. Starling resistor outflow obstruction tends to arise when cerebrospinal fluid pressure causes venous compression to thus increase tissue pressure and worsen tissue edema (and ICP elevation), producing a positive feedback ICP cycle. (2) Masses and edema are conditions that increase brain tissue volume and ICP, causing both vascular compression and decrease in cerebral perfusion pressure leading to oligemia. Brain edema is either vasogenic or cytotoxic, each with disparate causes and often linked to cerebral blood flow or blood volume abnormalities. Masses may arise from hematoma or neoplasia. (3) Hydrocephalus can also increase ICP, and is either communicating or noncommunicating. Further research is warranted to ascertain whether ICP therapy should be tailored to these physiological subsets of intracranial hypertension.

Simultaneous cardio‐cerebral infarction in a dog

“…This might be suggestive of a secondary compensatory vasodilation, where cerebral blood expansion might follow the release of vasodilators and allow preservation of cerebral perfusion to the right side of the brain that had sustained ischaemic stroke. This has been suggested to account for raised intracranial pressure observed in people after ischaemic stroke 9 . It is interesting to note that this was associated histologically with perivascular oedema, and that clinically the dog displayed signs consistent with increased intracranial pressure and responded remarkably well to osmotherapy using intravenous mannitol.…”

“…This has been suggested to account for raised intracranial pressure observed in people after ischaemic stroke. 9 It is interesting to note that this was associated histologically with perivascular oedema, and that clinically the dog displayed signs consistent with increased intracranial pressure and responded remarkably well to osmotherapy using intravenous mannitol. The left side of the thalamus, brain stem, together with the cerebellum including the cerebellar peduncles on both sides was without other significant pathological findings.…”

Actualización en el tratamiento del síndrome de hipertensión intracraneana

“…La PPC se encuentra determinada por la diferencia entre la presión arterial media (PAM) y la presión intracraneana (PIC); expresada en la fórmula: PPC = PAM -PIC. Se considera normal: PIC ≤ 15 mmHg y PPC > 50 mmHg [5][6][7] .…”

“…Clásicamente, fuera del rango 50-150 mmHg el mecanismo de autorregulación es incompetente, lo que conduce a que el FSC se vea comprometido y dependa directamente de la PAM. Además, frente a una lesión cerebral aguda, dos tercios o más de los enfermos pueden perder estos mecanismos de autorregulación, de modo que el FSC se vuelve dependiente de la PAM, de ahí que la hipotensión sea tan nociva [7][8][9] (Figura 2).…”

Optimal Hemodynamic Parameters for Brain-injured Patients in the Clinical Setting: A Narrative Review of the Evidence

“…Finally, cerebral autoregulation, while prone to impairment in an injured brain region, may remain largely intact in nonimpaired areas. In this regard, “optimizing” global cerebral perfusion may in fact be harmful to injured brain regions because of heterogenous dysautoregulation in injured areas and intact autoregulation in uninjured areas 11…”