Patients in the acute phase after aneurysmal SAH are at increased risk for rebleeding. The highest rates of rebleeding occur in the first 3 days after SAH, and surgical clipping or endovascular coiling of the ruptured aneurysm should be pursued as soon as possible after admission. Although the aneurysm is unsecure, systemic hypertension should be avoided; however, hemodynamic stability is crucial to avoid cerebral hypoperfusion, acute ictal infarcts, and cerebral circulatory arrest.^1–4

Liberal fluid resuscitation with crystalloids is commonly necessary in patients with poor-grade SAH before securing the aneurysm. Although frequently hypertensive, patients are admitted with relative intravascular volume depletion—due to natriuresis and the systemic inflammatory response associated with severe brain injury—and 2 L of normal saline is acutely administered to maintain organ perfusion. On arrival to the ICU, the patient should receive a central venous access and an invasive arterial line. If a mean arterial pressure (MAP) goal of 70 mm Hg is not achieved, norepinephrine should be initiated. If, instead, the MAP is > 110 mm Hg or systolic blood pressure is > 160 mm Hg, continuous infusion of nicardipine should be started to avoid unsafe BP levels. At this point, urine output, central venous pressure, arterial lactate levels, and central venous oxygen saturation (Scvo₂) are assessed to refine the evaluation of hemodynamic stability. Urine output < 0.5 mL/kg/h, lactate levels > 2 mmol/L and Scvo₂ < 65% generally represent systemic hypoperfusion and further fluid resuscitation should target CVP > 8 mm Hg, Scvo₂ > 70%, and the reduction of arterial lactate.^1,4–8

The patient is submitted to cerebral angiography that reveals an aneurysm in the intracranial part of the right internal carotid artery. Endovascular coiling is undertaken with successful occlusion of the aneurysm sac.

A comprehensive approach to goal-directed interventions requires that organ function is assessed to indicate the need and evaluate the response to specific treatments. The ideal monitoring tools in the ICU should be continuous, noninvasive (when possible), and accurate measurements of the end-organ function of interest. In order to monitor cerebral function parameters there are no good substitutes for intracranial probes that measure intracranial pressure (ICP), partial pressure of brain tissue oxygen (Pbto₂)_, and aerobic metabolic activity. Our approach to multimodal monitoring focuses on systemic and cerebral parameters and the interrelation between them, as shown in Table 17-1.

Hemodynamic monitoring is a cornerstone of the management of critically ill neurologic patients. We use either Vigileo (Edwards Lifesciences, Irvine, CA) or PiCCO (Marqet Cardiovascular, Wayne, NJ) devices to monitor MAP and pulse-contour analysis of the arterial waveform to generate continuous cardiac output.^{7–9,11–23} Both technologies also offer continuous measurement of stroke volume variation (SVV), which is used as an estimate of fluid responsiveness in mechanically ventilated patients. The PICCO^TM further calculates extravascular lung water (EVLW) and global end-diastolic volumes based on a transpulmonary thermodilution curve.^10,23 Through a central venous line, preferably on the subclavian site, CVP and Scvo₂ are continuously monitored. Arterial lactate and arterial-venous delta CO₂ (a-v ΔCO₂) allow estimation of tissue hypoperfusion and inadequate systemic CO₂ washout, an indication of inappropriate cardiac output.^5,24–27

Multimodal monitoring parameters of brain function are shown in Table 17-1. Multimodal monitoring is composed of intracranial measurements of ICP, partial pressure of brain tissue oxygen (Pbto₂), microdialysis, regional cerebral blood flow (rCBF; HemedexTM), and cortical depth continuous electroencephalography (cEEG).^28–35 In addition to the intracranial monitoring, surface, cEEG and jugular bulb oxymetry complete the armamentarium of tools available. The intracranial modalities are usually used as a bundle, inserted into a multilumen bolt, and/or tunneled in, as necessary. Pbto₂ is a measure of tissue oxygen tension and is believed to reflect the balance between delivery, consumption, and tissue diffusion of oxygen.^8,36–41 Microdialysis allows measurement of glucose, lactate, and pyruvate in a small volume of tissue around the catheter. A high lactate to pyruvate ratio (LPR) indicates anaerobic metabolism and if associated with low brain glucose, suggest tissue metabolic crisis.^42–44 Tissue perfusion (rCBF) around the area of the probe is estimated through a thermodilution method between two thermistors along the probe (Hemedex, Cambridge, MA).³⁴

Multimodal cerebral monitoring was placed in the right hemisphere. It included a triple lumen bolt with ICP, Pbto₂, and microdialysis probes and a double lumen bolt with a depth EEG electrode and a rCBF probe. A PICCO^TM catheter was placed in the femoral artery to allow for continuous monitoring of cardiac index (CI) and SVV, as well as intermittent assessment of global end diastolic volume index (GEDVI) and EVLW.

Systemic hemodynamic resuscitation should always precede brain-targeted interventions. Comatose patients with severe brain injury are likely to be mechanically ventilated and should be monitored with an invasive arterial line, a central venous catheter, and an ICP probe. Semi-invasive continuous monitoring of cardiac output and SVV are possible through pulse contour analysis of the arterial waveform. GEDVI is used as a volumetric static measure of preload and EVLW measurements as an indicator of pulmonary edema. CVP and Scvo₂ complement this comprehensive list of hemodynamic monitoring parameters.

Markers of end-organ hypoperfusion, such as high lactate and low Scvo₂, indicate inadequate oxygen delivery and should prompt interventions in order to achieve optimal MAP and cardiac output.^5,27,45 Assessment of fluid responsiveness should follow based on GEDVI and SVV. SVV > 10% and GEDVI < 600 mL/m² generally indicate that the patient will respond to a fluid challenge with either 500 mL of crystalloid or 250 mL of colloid solution.^8,40,41,46 An increase in cardiac output confirms the response to the fluid challenge. After optimal preload is achieved, MAP should be maintained > 70 mm Hg with norepinephrine, and CI should be kept above 2.5 L/min/m² with dobutamine or milrinone, if necessary.

After hemodynamic stabilization, end-organ perfusion parameters should be reassessed. Urine output > 0.5 mL/kg/h, clearance of arterial lactate, Scvo₂ > 70%, and an a-v ΔCO₂ < 6 are good indicators of effective systemic resuscitation.

The goal of advanced neuromonitoring in patients with severe brain injury is to allow early detection of complications and ensure adequate delivery of oxygen and nutrients to the brain in order to avoid permanent damage. After the primary event, a number of processes can lead to secondary brain injury. Nonconvulsive seizures after traumatic brain injury, vasospasm after SAH, expansion of the hematoma after intracerebral hemorrhage, and increased ICP after cardiac arrest are examples of detectable complications that progress in the ICU and can be captured by comprehensive monitoring of brain function. Early detection and prompt intervention can potentially prevent irreversible damage.

Continuous multimodality neuromonitoring includes ICP, Pbto₂, microdialysis, cEEG (surface and depth), and tissue perfusion. These probes are introduced at the bedside through a multilumen bolt and/or are tunneled in subcutaneously. All the data are continuously displayed and stored at the bedside along with systemic monitoring parameters. An integrative approach to brain oxygenation, metabolism, electrical activity, and perfusion allows the clinician to understand the pathophysiology of events and to individualize clinical therapy. Small elevations in ICP below traditional thresholds may compromise perfusion and lead to brain tissue hypoxia and metabolic crisis. Early treatment to optimize perfusion may reverse these alterations and avoid a vasodilatory cascade that leads to refractory intracranial hypertension.⁴⁷ Similarly, a reduction in regional blood flow to ischemic levels may cause reduced alpha to delta ratios, elevated LPRs, and low Pbto₂.^{8,37,40,41,43,48–58} Early CPP optimization and balloon angioplasty may also reverse ischemia and avoid permanent deficits.

CPP is the primary determinant of CBF and oxygen delivery to the brain.^41,59–61 It is thus a powerful and practical tool at the bedside to achieve adequate balance between oxygen and nutrient delivery and the brain’s metabolic demand. Instead of relying on arbitrary thresholds to target CPP, functional assessment of the brain permits goal-directed management of cerebral hemodynamics and individualized targets of optimal CPP. The main goals used to optimize CPP are to maintain Pbto₂ > 15 to 20 mm Hg, jugular venous oxygen saturation (Sjvo₂) > 65%, LPR < 40, and rCBF > 20 mL/100 g/min.^43,62 The first step is usually to optimize cardiac preload with fluids in patients who are fluid responsive. Once adequate preload and an SVV > 10% are achieved, MAP and cardiac output can be improved with vasopressors and inotropes, respectively. CI and CPP should initially be kept above 2.5 L/min/m² and above 60 to 70 mm Hg, respectively.

CPP and cardiac output, though critically important, are only 2 pieces of the homeostatic puzzle where factors such as blood rheology, serum osmotic pressure, glucose, and Pao₂ (partial pressure of oxygen, arterial) influence ongoing neuronal injury. Taking into account the complexity and interactions between these variables, efforts are undertaken to adjust sedation, serum osmolarity, and blood glucose control and exclude surgical complications through neuroimaging while hemodynamics are optimized.

If brain physiological targets are not yet achieved, further efforts to increment CPP and cardiac output are undertaken. Supranormal goals are defined as optimal if they correlate with improvements in the cerebral oxygenation and metabolic profile.