Intensive Care Management of Poor-grade SAH Patients. An Overview

Figure 73.1. An algorithm for decision-making in suspected vasospasm after SAH is provided.

EVD = external ventricular drain; HC = hydrocephalus; ICH = intracerebral hemorrhage; IVH = intraventricular hemorrhage; MAP = mean arterial pressure.

First choice of monitoring always includes neurological assessment if the patient is rousable without focal neurological deficit. If a patient recovers after the initial insult and is awake for several days after the treatment of the aneurysm, neurological assessment in combination with transcranial doppler sonography (TCD) may be sufficient monitoring to exclude clinically relevant vasospasm. However, as most patients with poor-grade SAH do not recover sufficiently to be monitored clinically, discussion of most further treatment issues has to be focussed on intubated patients with impaired consciousness. Despite its limited sensitivity, TCD is an established bedside tool, where flow of the intracranial vessels can be assessed non-invasively. Usually, the flow velocity within the proximal MCA is measured for the ease of accessibility from the second day after hemorrhage. Not only absolute flow values are important in the management decision (norm ~55cm/s); while an increase of more than 50cm/s from one day to the other or an absolute flow exceeding 160cm/s may already raise suspicion as to the development of vasospasm, the Lindegaard index (ratio of flow velocity within the MCA/extracranial ICA) is more sensitive and specific. An index of greater than 3 is highly suspicious of ensuing vasospasm (which should prompt further diagnostics including conventional angiography), while increased flow velocities and an index of less than 3 may indicate hyperemia. If the latter scenario coincides with refractory elevation of ICP, a quantitative measurement of CBF, such as XeCT may help to frame a therapeutic decision, such as moderate hyperventilation to minimize the effects of hyperemia and/or lower ICP.

Conventional angiography, however, is still considered the gold standard in the diagnosis of vasospasm. It should be performed routinely on day 7-9 after SAH where the risk of vasospasm is highest. Imaging may also serve as a control for clip- and coil-positioning and determine the necessity of further follow-ups (conventional angiography versus CTA or MRA). If angiography demonstrates significant vasospasm, adequacy of cerebral perfusion is the main goal of future treatment. In selected cases, spontaneous upregulation of mean arterial blood pressure and tachycardia is observed, and this might suffice to prevent critical hypoperfusion. A new deficit in an awake patient (new focal deficit, confusion/lethargy, neglect) should always prompt rigorous assessment of hemodynamics and the need of further imaging. CT scanning can exclude hydrocephalus and subacute infarction. However, if CT scanning is normal, but hypoperfusion due to impending vasospasm is suspected, mean arterial blood pressure should be increased to levels above 90 mmHg empirically until diagnostics such as angiography can be performed.

If a patient cannot be assessed clinically, as is the case in most poor-grade SAH patients, the need for further means of monitoring arises. ICP measurement is mandatory in all unconscious patients, and elevation should be treated accordingly (see above). For the treatment of vasospasm, our department has implemented a modified approach to the widely-used concept of triple-H therapy (hypertension, hypervolemia, hemodilution), a therapy concept both moderately plausible but unproven at the same time. Since complications such as pulmonary edema, myocardial infarction and electrolyte imbalance are frequent (20-30%), the widely propagated hypervolemia has been omitted since its efficacy is not proven and reduction in regional cerebral blood flow has been observed [5]. Moderate hemodilution with a hematocrit around 30-35% is usually achieved automatically when keeping patients normovolemic after surgery. While sedation sometimes is required, depending on the severity of vasospasm a mean arterial blood pressure of at least 100 mmHg (or sometimes >120 mmHg) is mandated, usually requiring the use of vasopressors. The efficacy of hypertension has to be assessed either by way of intermittent global CBF measurements (such as XeCT, to some semiquantitative extent also perfusion CT or MRI), more practical, however, are continuous measurements. Various, validated intraparenchymal probes exist to indirectly measure CBF (thermal diffusion flowmetry=TDF probe; brain tissue oxygen tension=p_tiO₂ probe) or the change in local metabolism (microdialysis). As the area of parenchyma analyzed with these probes is spatially very restricted, the application of this technique to detect distant vasospasm may be limited as well, but their usefulness to estimate efficacy of treatment has been repeatedly demonstrated. Placement of the probe is essential and should be aimed at potential areas of misery perfusion. In most cases, placement may be guided by angiography, which identifies hypoperfused territories at greatest risk for infarction. It seems plausible to guide treatment according to the results obtained within these critical regions, since they are most vulnerable and are likely to turn ischemic. Even though pathophysiology may vary significantly throughout the brain, it is suspected that “healthy” territories are less susceptible to modulation and are more robust to changes in perfusion. Different ranges of critical values have been identified for most methods. The critical threshold for p_tiO₂ (usually advocated over holohemispheric measures such as jugular venous oxygen saturation=S_jvO₂) and the thermal probe is generally considered to be around 10-15 mmHg and 15 ml/100 g x min respectively, with values below indicating impending hypoxia or ischemia. For microdialysis, a variety of metabolic markers can be analyzed. Lactate, the calculated ratio of lactate and pyruvate as well as glutamate mirror the extent of change towards anaerobic metabolism, with an increase implying ischemia. However, it has to be stated critically, that these metabolic markers usually are only obtained after a relevant change in metabolism has already occurred and therapeutic relevance remains limited.

There is continuous effort to prevent the development of vasospasm, and an abundance of studies is available regarding its etiology and possible treatment options. Inflammation as well as scavenging of nitric oxide by oxyhemoglobine and liberation of ET-1 are only some of the major pathways currently open for discussion as to the development of vasospasm. At present, therapy mostly consists of minimizing the effects of vasoconstriction. One of the most widely used and most extensively studied prophylactic treatment involves calcium antagonists such as nimodipine, the only FDA approved medication. Interestingly, however, only oral nimodipine was found to effectively reduce neurological deficits and improve overall outcome (doses usually starting at 60 mg/q4h, than tapering after 8-14 days) [6] with no apparent effect on angiographic vasospasm; neuroprotective effects or improvement of collateral circulation are assumed. Contrarily, intravenous calcium antagonists are prone to cause hypotension due to their vasodilatatory function. The use of IV nimodipine in poor-grade patients who cannot take oral medications (crunched tablets have shown to have significantly lower efficacy) and have a high risk of impaired autoregulation, has to be viewed critically. Application of magnesium sulphate might be useful, as hypomagnesemia occurs in up to 50% of cases and is also associated with the occurrence of delayed ischemic deficits and poor outcome, convincing evidence, however, is lacking as well.

CPP-monitoring is essential to avoid the risk of critical hypoperfusion. Angiography followed by either mechanical dilatation (transluminal balloon angioplasty=TBA) or application of intraarterial vasoactive substances such as papaverine (usually 200-300 mg applied over 30 mins) or calcium antagonists are other treatment options at institutions where an experienced neurointerventionalist is available. Their effectiveness, however, is usually limited to cases with localized, preferably single-vessel narrowing, and a preceding CT scan without signs of infarction. In those selected cases, repetitive treatment may be necessary, and generalized or diffuse multi-vessel vasospasm is mostly less susceptible to this kind of intervention. TBA in poor-grade patients is associated with worsening in outcome. An ongoing multicenter investigation is looking into the benefits of emergency angiography followed by vasodilatatory measures versus conventional, conservative treatment in those patients who develop new focal deficits without signs of infarction on recent CT scan.

One recent study has analyzed the effect of clazosentan, an ET-A receptor antagonist that experimentally has been shown to ameliorate the deleterious effects of ET-1 in particular [7]. While angiographic vasospasm and incidence of ischemia was influenced favorably, overall clinical outcome did not change significantly. Other multicenter trials are concerned with the role of NO-donors, statins and magnesium sulfate in ameliorating cerebral vasospasm. The application of slow release pellets of nicardipine, deposited intraoperatively in close proximity of larger vessels has gained substantial interest as of late, as the occurrence of vasospasm and subsequent infarction is significantly lower in those patients [8]. It will be the aim of future investigations, if treatment with nicardipine pellets remains equally effective when applied intraventricularly only, a treatment option tailored specifically for patients treated interventionally, as is suggested in many poor-grade SAH patients.

73.8 Conclusion

The treatment of subarachnoid hemorrhage is particularly challenging in poor-grade SAH patients, as morbidity and mortality increase exponentially. After successful treatment of the offending aneurysm, close neurological and multimodal monitoring are essential to anticipate potentially treatable complications such as refractory ICP elevation and delayed vasospasm in order to improve overall outcome.

References

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6. Dorhout Mees SM, Rinkel GJ, Feigin VL, et al. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev 2007; CD000277

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8. Barth M, Capelle HH, Weidauer S, et al. Effect of nicardipine prolonged-release implants on cerebral vasospasm and clinical outcome after severe aneurysmal subarachnoid hemorrhage: a prospective, randomized, double-blind phase IIa study. Stroke 2007; 38: 330-6

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