In October 2013, the Neurocritical Care Society (NCS) held its 11th annual meeting. In a little more than 10 years, neurocritical care has solidified its standing as a “bona fide” medical subspecialty. In 2005, the United Council for Neurological Subspecialties laid the groundwork for accreditation of neurocritical care training programs, and the first certification exam was offered in 2008. That same year, the Leapfrog Group recommended that neuro ICUs be staffed by specialty-trained neurointensivists.1 A growing body of research suggests reduced mortality and improved neurologic outcomes in neurologically-injured patients managed by dedicated neurointensivists.2-4 Last year, in an effort to further improve and standardize care of patients with life-threatening neurologic illness, the NCS introduced a formal, advanced cardiac life support (ACLS)-style course, the Emergency Neurologic Life Support (ENLS) program.
While the majority of neurointensivists are still neurologists, the NCS has maintained a diverse and multidisciplinary membership. Accredited fellowships are open to diplomates in neurology, neurosurgery, anesthesiology, emergency medicine, surgery, internal medicine and pediatrics. At this year’s annual meeting, a working group was formed to more formally evaluate the needs and potential challenges facing the “non-neurologist neurointensivist.”
Throughout the early development of the specialty, anesthesiologists have been a small but important minority. In a 2008 survey of the international neurocritical care physician workforce, anesthesiologists represented 9.4 percent of respondents.5 This year, James et al. published the results of a survey of anesthesiologists providing neurocritical care in the United States. One-hundred and four dedicated neuro ICUs were identified, and 22 units had staff anes-thesiologists, for a total of 41 providers. The majorityof anesthesia-based neurointensivists practice in larger aca-demic centers. Importantly, 85 percent of these providers reported supervising anesthesia residents as part of their role in the neuro ICU. Finally, 76 percent re-ported a high level of job satisfaction.6 Respondents to the survey were more likely to hold certification in general critical care or a European certification, but as of 2013, 48 anesthesiologists are also certified in neurocritical care by the UCNS. In the context of anesthesiology’s growing emphasis on perioperative medicine, our current national intensivist shortage, and the rapid development of dedicated neuro ICUs, the authors of this survey suggest that neurocritical care represents a rewarding and important growth area for the specialty in coming years.6
This year’s meeting featured research on cerebral physiology in microgravity environments, ongoing research in neuroprotection, the coagulopathy and neurohormonal effects of acute brain injury, quality improvement and systems of care, and the effects of withdrawal of care. New to the annual meeting of the NCS this year was a formal “Practice Update,” which included a series of lectures outlining recent guidelines and current evidence-based management strategies. A full discussion of these strategies is beyond the scope of this article. What follows is intended to highlight current trends and call attention to several important changes in recent guidelines.
Multi-Modality Neurophysiologic Monitoring
Current evidence emphasizes tailoring therapy to the individual patient rather than over-reliance on standardized cutoffs for intracranial pressure (ICP), cerebral perfusion pressure (CPP) or other indices. Multimodal monitoring offers the potential for more sophisticated goal-directed cerebral resuscitation.
Parenchymal brain oxygen tension (PbtO2) monitoring appears to have utility when used in conjunction with ICP and CPP monitoring to guide therapy. Elevated ICP in conjunction with low brain oxygen tension predicts worse outcome than elevation of ICP alone.7 PbtO2 has also shown promise in the determination of patient-specific optimal CPP.8-9 Finally, use of this modality may prevent excess treatment and aid prognosis. Failure of patients with high-grade subarachnoid hemorrhage to respond to therapy aimed at increasing PbtO2 was associated with worse neurologic outcome.10
Cerebral microdialysis assesses cerebral energy metabolism by measuring cerebral glucose, glutamate and lactate-to-pyruvate ratio. Despite practical limitations, this technique may be useful for serum glucose and nutrition management as well as detection of cerebral ischemia.11-13
Quantitative EEG, which analyzes the variability of α and δ power, has also shown promise in the detection of cerebral ischemia.14
Regional cerebral blood flow monitors are currently under investigation but cannot be said to be ready for widespread implementation.
Traumatic Brain Injury (TBI)
In the recent multicenter randomized BEST TRIP trial, patients with severe TBI had equivalent outcomes whether they were managed using ICP monitoring (goal ICP <20 mmHG) or an alternative strategy using serial neurologic examination and CT imaging.15 This large study was carried out in Bolivia and Ecuador and its generalizability to more resource-rich settings remains unclear. Nevertheless, clinical equipoise is suggested and further study is indicated.
To date, there is still no evidence from large, randomized, controlled trials favoring mannitol or hypertonic saline as osmotic therapy for intracranial hypertension.
The role and timing of decompressive craniectomy also remains unclear. The large multicenter DECRA trial found that early bifrontal decompression for diffuse TBI was effective in reducing intracranial hypertension but was associated with worse functional neurologic outcome.16
Recent experience in Iraq and Afghanistan suggests that blast injury has a high incidence of delayed cerebral vasospasm when compared with other TBI.17
Acute Ischemic Stroke
Blood pressure control in I.V. t-PA candidates should achieve systolic blood pressure <185 and diastolic <110 prior to administration and for 24 hours post-administration. Patients who are not candidates for t-PA and have blood pressure greater than 220/120 should have their blood pressured reduced by 15 percent over the first 24 hours post-stroke. Patients with other evidence of end-organ damage from malignant hypertension should be treated accordingly.18
Urgent anticoagulation is not recommended in acute ischemic stroke; its use in intracranial stenosis is not well established.18
Although FDA approved only for use up to three hours from onset of symptoms, the results of recent trials have led many centers to consider administration of IV t-PA up to 4.5 hours.
Use of IV t-PA in patients taking newer classes of anticoagulants, including direct thrombin inhibitors or factor Xa inhibitors, may be harmful and is not recommended unless specific lab testing is available to indicate normal factor levels or >2 days have elapsed since last dose.18
Endovascular management of acute ischemic stroke is evolving rapidly: patients <6 hours from symptom onset should be considered for possible endovascular management.
Aneurysmal Subarachnoid Hemorrhage (aSAH)
The efficacy and safety of endovascular versus open surgical repair is dependent on patient factors, aneurysm morphology and location, and presence of hematoma. Patients appear to be best served by referral to large centers (>35 aSAH cases/year) with both surgical and endovascular capability.19
Re-bleeding remains a significant source of mortality in aSAH. Antifibrinolytics were routinely used in the 1980s to prevent re-bleeding but were largely abandoned due to increased risk of delayed cerebral ischemia. However, in conjunction with early definitive aneurysm treatment, recent evidence has renewed interest in these drugs and consensus guidelines now suggest an early course of antifibrinolytic therapy (<72 hours) may reduce the risk of re-bleeding in patients without contraindications.19
Detection of cerebral vasospasm and delayed ischemia remains a crucial area of investigation. Transcranial Doppler is widely used despite operator dependence and potentially limited sensitivity. Numerous alternative imaging and monitoring techniques, including CT angiography and perfusion, Xenon CT, MRI perfusion, brain tissue oxygen monitoring, cerebral blood flow monitoring, cerebral microdialysis and continuous EEG are all under investigation. Thus far, none of these modalities can be considered a gold standard.
“Triple H” therapy has largely been abandoned, having failed to be of benefit in randomized, controlled trials. Hemodilution (and resulting anemia) is now thought to be potentially harmful, and hypervolemia may result in fluid overload and pulmonary complications, which remain an important source of morbidity and mortality in aSAH. Current consensus guidelines recommend maintenance of euvolemia and support the use of enforced hypertensive therapy in the setting of delayed ischemic deficits.19
Oral nimodipine remains the only well-established therapy for the prevention of cerebral vasospasm and should be administered to all patients after aSAH. Nicardipine has been used as an intravenous, intra-arterial and intra-thecal therapy, but data are lacking. Finally, animal and small observational studies have suggested a prophylactic role for I.V. magnesium, but there has been little support from phase III clinical trials.20-21
Spinal Cord Injury
The 2013 American Association of Neurological Surgeons (AANS) and Congress of Neurological Surgeons (CNS) Guidelines for the Management of Acute Cervical Spine and Spinal Cord Injuries do not recommend methylprednisolone use in acute spinal cord injury.22 This topic may be revisited in future updates as questions remain regarding the timing and duration of therapy used in older studies, and some authors have suggested that many of the potential risks of aggressive steroid use may be better ameliorated by recent developments in critical care.
As with TBI, current guidelines recommend avoidance of hypotension in acute spinal cord injury and it is recommended that mean arterial pressure (MAP) be maintained at 85-90 for seven days following injury.22
In 2012, the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS) found a significant benefit to early (<24 hours from injury) surgery for symptomatic cervical spine injuries amenable to decompression.23
Interest in therapeutic moderate hypothermia for neuroprotection in spinal cord injury has grown recently, supported by animal data and human case reports. However, robust clinical data are lacking, and this modality remains experimental.
Other promising avenues of research, particularly for subacute and chronic management, include stem cell therapies, bio-engineered prostheses and Schwann-cell transplantation.
1. The Leapfrog Hospital Survey: what’s new in the 2008 survey (Version 5.0). The Leapfrog Group website. http://www.leapfroggroup.org/media/file/WhatsNewin2008Survey.pdf. Published April 15, 2008. Accessed October 28, 2013.
2. Josephson SA, Douglas VC, Lawton MT, English JD, Smith WS, Ko NU. Improvement in intensive care unit outcomes in patients with subarachnoid hemorrhage after initiation of neurointensivist co-management. J Neurosurg. 2010;112(3):626–630.
3. Knopf L, Staff I, Gomes J, McCullough L. Impact of a neurointensivist on outcomes in critically ill stroke patients. Neurocrit Care. 2012;16(1):63–71.
4. Varelas PN, Eastwood D, Yun HJ, et al. Impact of a neurointensivist on outcomes in patients with head trauma treated in a neurosciences intensive care unit. J Neurosurg. 2006;104(5):713–719.
5. Markandaya M, Thomas KP, Jahromi B, et al. The role of neurocritical care: a brief report on the survey results of neurosciences and critical care specialists. Neurocrit Care. 2012;16(1):72–81.
6. James ML, Dority J, Gray MC, Bellows ST, McDonagh DL, Brambrink AM. Survey of anesthesiologists practicing in American neurointensive care units as neurointensivists [published online ahead of print July 24, 2013]. J Neurosurg Anesthesiol. doi: 10.1097/ANA.0b013e31829e705e.
7. Oddo M, Levine JM, Mackenzie L, et al. Brain hypoxia is associated with short-term outcome after severe traumatic brain injury independent of intracranial hypertension and low cerebral perfusion pressure. Neurosurgery. 2011; 69(5):1037-1045
8. Jaeger M, Dengl M, Meixensberger J, Schuhmann MU. Effects of cerebrovascular pressure reactivity-guided optimization of cerebral perfusion pressure on brain tissue oxygenation after traumatic brain injury. Crit Care Med. 2010;38(5):1343-1347.
9. Jaeger M, Soehle M, Schuhmann MU, Meixensberger J. Clinical significance of impaired cerebrovascular autoregulation after severe aneurysmal subarachnoid hemorrhage. Stroke. 2012;43(8):2097-2101.
10. Bohman LE, Pisapia JM, Sanborn MR, et al. Response of brain oxygen to therapy correlates with long-term outcome after subarachnoid hemorrhage [published online ahead of print August 15, 2013]. Neurocrit Care. doi: 10.1007/s12028-013-9890-6.
11. Vespa P, McArthur DL, Stein N, et al. Tight glycemic control increases metabolic distress in traumatic brain injury: a randomized controlled within-subjects trial. Crit Care Med. 2012;40(6):1923-1929.
12. Schmidt JM, Ko SB, Helbok R, et al. Cerebral perfusion pressure thresholds for brain tissue hypoxia and metabolic crisis after poor-grade subarachnoid hemorrhage. Stroke. 2011;42(5):1351-1356.
13. Timofeev I, Carpenter KL, Nortje J, et al. Cerebral extracellular chemistry and outcome following traumatic brain injury: a microdialysis study of 223 patients. Brain. 2011;134(pt 2):484-494.
14. Foreman B, Claassen J. Quantitative EEG for the detection of brain ischemia. Crit Care. 2012;16(2):216
15. Chesnut RM, Temkin N, Carney N, et al. A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med. 2012;367(26):2471-2481.
16. Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011;364(16):1493-1502.
17. Magnuson J, Leonessa F, Ling G. Neuropathology of explosive blast traumatic brain injury. Current Neurol and Neurosci Rep. 2012;12(5):570-579.
18. Jauch EC, Saver JL, Adams HP, Jr., et al. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2013;44(3):870-947.
19. Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2012;43(6):1711-1737.
20. Dorhout-Mees SM, Algra A, Vandertop WP, van Kooten F, Kuijsten HAJM, Boiten J, et al. Magnesium for aneurysmal subarachnoid haemorrhage (MASH-2): a randomised placebo-controlled trial. Lancet. 2012;380(9836):44-49.
21. Wong GK, Poon WS, Chan MT, et al.; IMASH Investigators. Intravenous magnesium sulphate for aneurysmal subarachnoid hemorrhage (IMASH): a randomized, doubleblinded, placebo-controlled, multicenter phase III trial. Stroke. 2010;41(5):921-926.
22. Guidelines for the management of acute cervical spine and spinal cord injuries. Neurosurgery. 2013;72(suppl 2):1-259.
23. Fehlings MG, Vaccaro A, Wilson JR, et al. Early versus delayed decompression for traumatic cervical spinal cord injury: results of the Surgical Timing in Acute Spinal Cord Injury Study (STASCIS). PLoS One. 2012;7(2):e32037. doi:10.1371/journal.pone.0032037.