Critical ICP in Subarachnoid Hemorrhage: How High and How Long?

  
By Andreas H. Kramer
First Online: 02 March 2021

There are numerous reasons why intracranial pressure (ICP) may be elevated in patients with aneurysmal subarachnoid hemorrhage (SAH):

When an aneurysm ruptures, it precipitates a cascade of events that may result in global cerebral edema. Contributing factors include diffuse ischemic injury and sequelae of blood degradation products in the subarachnoid space, including inflammation, oxidative stress, and blood–brain barrier disruption [1]. Global edema is more likely to occur in the presence of high-grade SAH and larger volumes of cisternal blood and is strongly associated with poor outcomes [2].

SAH is often complicated by acute hydrocephalus.

Intracerebral hemorrhage, extra-axial hematomas, and infarcts may function as space-occupying lesions.

Impaired cerebral blood flow (CBF) autoregulation makes patients vulnerable to both ischemia and relative hyperemia [3].

Observational studies demonstrate that raised ICP (conventionally, but somewhat arbitrarily, defined as ≥ 20 mmHg) is relatively common, especially among patients with high-grade SAH [4,5,6,7,8]. In most studies, raised ICP was strongly associated with poor outcomes, although this relationship usually did not persist in multivariable analyses [8]. Thus, it remains unresolved to what degree raised ICP is truly injurious rather than simply an epiphenomenon of more severe brain injury. Nevertheless, studies do suggest that incrementally higher ICP is more strongly associated with poor outcomes and that failure to respond to therapy is particularly ominous [4, 6, 7].

Existing international guidelines do not provide specific recommendations regarding ICP monitoring and treatment in SAH [9,10,11]. However, there are multiple reasons to measure ICP in selected patients:

Placement of an external ventricular drain (EVD) may be needed to treat hydrocephalus, irrespective of ICP. Attachment of the EVD to a transducer makes intermittent ICP measurements readily available.

Measurement of ICP serves as a surrogate for intracranial volume. Increasing cerebral edema and mass effect is reflected by a rising pressure, influenced by the degree of intracranial compliance.

Cerebral perfusion pressure (CPP) is defined by the difference between mean arterial pressure (MAP) and ICP (surrogate for venous pressure). Knowing ICP is necessary for clinicians to ensure that CPP levels exceed lower limits of CBF autoregulation (≥ 50–60 mmHg), thereby protecting against ischemia.

Measuring ICP offers more than a number. The relationship between MAP and ICP enables calculation of the pressure reactivity index (PRx) and assessment of CBF autoregulation. Patients with impaired autoregulation may require higher than usual CPP levels [3, 7, 12]. The morphology and amplitude of the waveform and its association with mean ICP (RAP Index) provide information about intracranial compliance. These derived measures may predict outcome more accurately than ICP alone [8]. A small randomized controlled trial suggested benefit to treatment aimed at limiting ICP wave amplitude [13].

Given the heterogeneous pathophysiology of raised ICP in SAH, optimal treatment may differ from one patient to another. Although clinicians often manage intracranial hypertension similarly to traumatic brain injury (TBI), it remains unclear whether the same therapeutic thresholds are appropriate [14].

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