Multimodal Monitoring in Subarachnoid Hemorrhage

Abstract

In severely injured patients, the immediate goal of resuscitation is restoration and maintenance of adequate tissue metabolism by ensuring sufficient delivery of fuel, typically oxygen and glucose, to meet cellular metabolic demands. In neurocritical care, traditional goals of resuscitation-intracranial pressure (ICP), cerebral perfusion pressure (CPP), and the clinical examination-have been extrapolated from those of general critical care. These variables are analogous to central venous pressure, mean arterial pressure, and urine output and are similarly crude. These distant surrogates for cerebral perfusion do not account for dynamic changes in cerebral autoregulation, tissue metabolic rate, cellular fuel use, and microcirculatory dysfunction, all of which impact tissue metabolic health. Although standard, it seems intuitively obvious that a uniform approach of maintaining ICP Ͻ20 mm Hg and CPP Ͼ60 mm Hg is overly simplistic. This approach does not address either significant baseline differences in patient physiology nor the complex, dynamic, and variable pathophysiological changes that ensue after severe brain injury. A more tailored therapeutic strategy that responds to multiple simultaneously measured and more relevant physiological variables is logically appealing. Until recently, however, the requisite individual patient physiology was inaccessible at the bedside.The emergence of technology that allows for continuous real-time bedside monitoring of cerebral physiology marks a new era in neurocritical care. These monitors facilitate assessment of therapeutic efficacy and may provide more relevant physiological end points for resuscitation. Combining these monitors in a multimodal approach allows for the practice of goal-directed cerebral resuscitation that emphasizes the individual patient's unique neurological and systemic physiology.

Early Moderate Hyperoxemia Does Not Predict Outcome After Aneurysmal Subarachnoid Hemorrhage

“…Although intracranial pressure and cerebral perfusion pressure are often used as surrogates for cerebral blood flow, there is growing evidence that detrimental ischemia-related processes may be present despite adequate cerebral perfusion pressure and intracranial pressure levels. 22,23 The most efficacious way to correct low brain tissue oxygen is to increase the fraction of inspired oxygen in mechanically ventilated patients. 1 Liberal use of high fractions of oxygen in the neurocritical care setting, without robust evidence supporting its safety, is common, although only few studies are done with SAH patients.…”

Acute impairment of saccadic eye movements is associated with delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage

“…28,29 As a result, there has been increasing inter- est in the use of multimodal monitoring following aSAH to optimize the diagnosis and individualize therapeutic interventions aimed at preventing secondary neuronal injury. 26 However, the majority of techniques currently in use to objectively quantify DCI are either unsuitable for monitoring those patients with "good grade" aSAH who do not require sedation/mechanical ventilation (e.g., tissue oxygen and intracranial pressure monitoring), or have high user variability, require significant training to perform, and have a high false-positive rate (e.g., TCD). It is probable that the prolonged latencies observed in patients in the first 72 hours following aSAH are a result of acute neuronal damage caused by early brain injury.…”

Intracranial pressure monitoring, cerebral perfusion pressure estimation, and ICP/CPP-guided therapy: a standard of care or optional extra after brain injury?

“…While intracranial hypertension after ICH is associated with increased mortality, 140 there is little evidence that treating it influences outcomes. 141 The principles of utilizing an individualized approach to therapy, combined with multimodality monitoring, applies to all forms of ABI, including TBI, 142 SAH, 19 and ICH. 92 Evidence suggests that the use of PtiO 2 monitoring in comatose ICH patients can identify CPP targets for optimal brain tissue oxygenation.…”