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NEUROANESTHESIA: Edited by Keith J. Ruskin

Postoperative care of the neurosurgical patient

Siegemund, Martin; Steiner, Luzius A.

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Current Opinion in Anesthesiology: October 2015 - Volume 28 - Issue 5 - p 487-493
doi: 10.1097/ACO.0000000000000229
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Neurosurgical critical care patients can be separated in two major groups: neurosurgical emergency cases like traumatic brain injury (TBI) or subarachnoid hemorrhage (SAH) for monitoring the neurological state and early therapeutic interventions, and elective neurosurgical patients for a close-meshed observation of consciousness and neurological deficits to detect hematoma and other early postoperative complications. Particularly regarding the latter group, data are scarce.

Postoperative monitoring of neurosurgical patients undergoing elective surgery

Increased awareness of cost-effectiveness questions the necessity of intensive care admission or early computed tomography (CT) scans [1] for elective neurosurgical patients. A multivariate analysis in a recent retrospective study of 400 elective patients undergoing intradural operations revealed only diabetes and older age to be predictive for postoperative ICU admission [2]. In an accompanying editorial, Hecht et al.[3] stated that serious problems after craniotomy mostly occur within the first postoperative hours. They described the transfer of patients to a regular ward after uneventful elective craniotomy after controlling blood pressure and initiating sufficient analgesia. This approach seems feasible, although a lack of correlation in such a small cohort does not mean that these factors alone indicate the need for intensive care [4]. Other relevant factors are intraoperative bleeding, blood product administration, and duration of surgery [2]. To test coagulation sufficiency and the risk of postoperative bleeding, fibrinogen appears to be a modifiable risk factor, as levels below 2 g/l correlate with a 10-fold increase in risk of postoperative hematoma [5]. Together with the fact that delayed ICU admission was not associated with postoperative complications or prolonged length of ICU stay [6], a stepwise approach of ICU or regular ward admission after postanesthesia unit care should be considered in further trials.

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Box 1:
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The Neurocritical Care Society and the European Society of Intensive Care Medicine have recently published multimodal monitoring guidelines providing pragmatic guidance and recommendations for bedside monitoring of patients receiving neurological critical care [7▪▪]. Alongside the classical monitoring of systemic hemodynamic parameters, intracranial pressure (ICP) and cerebral perfusion pressure (CCP) are the mainstay of neurocritical care monitoring. For guidance of therapeutic interventions, either by parenchymal or intraventricular ICP measurement, the consensus statement provides a strong recommendation supported by high quality evidence [8]. ICP/CPP as a part of multimodal monitoring should be used as the prerequisite for the interpretation of other monitoring devices in protocol-driven care.

In many patients, clinical deterioration occurs before other parameters, such as ICP, alert the clinician [9]. To establish baseline conditions and detect changes in neurological status in most patients, a brief neurological assessment is sufficient. Attention has to be paid to two characteristics: changes in consciousness and focal neurological findings. The latter, for example unilateral paresis, suggests a specific lesion. A deteriorating level of consciousness, however, may signal a variety of conditions, including a rise in ICP, vasospasm after aneurismal subarachnoid hemorrhage (aSAH), or systemic complications. A depressed level of consciousness has been shown to be the most consistent clinical presentation of postoperative intracranial hematoma, with one-third of cases presenting within 12 h of surgery [10]. To facilitate repeated quantitative reporting of the neurological status, standardized scoring systems have been developed. The two most useful scores in neurosurgical patients are the Glasgow Coma Scale (GCS) [11] and the more recently developed Full Outline of UnResponsiveness score (FOUR score) [12]. The GCS, originally developed as a prognostic tool for head-injured patients, is now widely used to estimate the level of consciousness in critically ill patients. There are several shortcomings of the GCS: it may not detect subtle neurological changes, it does not consider brainstem reflexes, and in intubated patients, the verbal response cannot be examined, making the assessment of deeply comatose patients difficult [13]. Although more time-consuming and more difficult to perform than the GCS, the FOUR Score [12] offers important additional information.

Hypoxia and hypotension have been shown to be the two most important systemic secondary insults in patients with TBI [14], and it is reasonable to assume that this also holds true for patients with other forms of brain injury and for postoperative neurosurgical patients. Therefore, oxygen saturation by pulse oximetry and blood pressure are continuously monitored. Although evidence is lacking, continuous intra-arterial blood pressure monitoring is a common practice in neurosurgical patients because even short periods of hypotension may compromise cerebral perfusion and oxygenation. The regional measurement of brain tissue oxygen pressure or jugular bulb oximetry and brain metabolism by means of microdialysis are strongly recommended by the new monitoring guidelines, despite the availability of only low-quality evidence [7▪▪]. Both techniques provide valuable information about integrity and oxygen supply of the local brain microcirculation and can be used to guide medical therapies such as blood transfusion, hyperoxia, or therapeutic hypothermia. Especially the application of high inspiratory oxygen concentrations needs more than the usual monitoring by blood gas analysis and pulse oximetry. After adjustment for different possible confounding factors, both hyperoxia and hypoxia were associated with an increased risk of mortality [15,16] or delayed cerebral ischemia [17]. Despite the clear advantage of an adequate oxygen supply to brain tissue at risk, supranormal oxygen partial pressures seem to harm brain cells through the generation of oxygen and nitrogen free radicals [18] and an increase in cerebral excitotoxicity because of glutamate [19]. In addition to local oxygen metabolism, cerebral microdialysis can be used to monitor consequences of systemic glucose variations and the concentration of local neurotoxic substances [20].

The arterial partial pressure of CO2 (PaCO2) is an important determinant of cerebral blood flow (CBF). However, the linear relationship between CBF and PaCO2 may be altered in some neurosurgical patients [21]. Nevertheless, monitoring of PaCO2 is general practice. In particular, patients with low intracranial compliance have a significant risk of developing raised ICP with rising PaCO2. There is some controversy as to the usefulness of end-tidal CO2 (ETCO2) as an indicator of PaCO2 in neurosurgical patients. Three studies specifically addressed the problem of reliability of ETCO2 in head-injured patients [22–24]. Of these three, one reported a good correlation between the two methods [22], whereas the most recent article reported that the PaCO2 and ETCO2 varied considerably, and that the PaCO2-ETCO2 gradient was not stable over time [24]. As pulmonary problems are frequent in neurosurgical patients, we suggest that PaCO2 rather than ETCO2 be monitored whenever possible.

Subarachnoidal hemorrhage

Compared with patients who underwent endovascular coiling, those who underwent surgical clipping seemed to have a significantly higher probability of death or functional dependency [25]. The unfavorable outcome in the clipping group does not seem to result from vasospasm-induced delayed cerebral ischemia (DCI) and cerebral infarction [26] because the incidence of these complications is similar after clipping or coiling of aneurysms in the anterior circulation [27,28]. Prophylaxis, detection, and therapy of cerebral vasospasms to prevent delayed neurological deficits after SAH are of great importance.

Transcranial Doppler ultrasonography (TCD) remains the most important monitoring method to estimate CBF after repair of aneurysmal bleeding, despite differing accuracy caused by operator variability [29]. High-quality evidence demonstrates that TCD can predict angiographic-confirmed vasospasm [30,31] and with less accuracy the development of delayed ischemic neurological deficits [32].

Beside the key role of TCD in the monitoring of patients with SAH, the role of other monitoring modalities is not so clear. The 2011 Neurocritical Care Society's Multidisciplinary Consensus Conference recommended no specific monitoring for cardiac function, intravascular volume status, or other regional neurophysiological monitors in patients following aSAH [33]. In a prospective, multicenter, cohort study, echocardiographic wall motion abnormalities were independent risk factors for poor clinical outcome after SAH [34]. Delayed cerebral ischemia only partially explained this relationship. Cardiac dysfunction was also associated with a poor-grade aSAH and consecutive rapid and sustained catecholamine release [35].

In poor-grade SAH patients, monitoring of ICP over a therapeutic ventricular drainage already in place or an intra-parenchymal probe seems to be valuable because increased ICP is common in these patients early after SAH [36]. A lack of reaction to therapeutic approaches aiming at a lower ICP appeared to be associated with early brain injury, poor clinical outcome, and mortality [36,37].

The incidence of DCI and early brain injury seems clearly related to the intravascular volume status, and the 2011 recommendations proposed euvolemia as a target for intravascular volume management [33]. Because classical triple-H therapy consisting of hypertension, hemodilution, and hypervolemia did not prophylactically or therapeutically prevent cerebral vasospasm and DCI [33,38], new monitoring and volume resuscitation strategies have been tested. In their recent study including 204 SAH patients, Yoneda et al.[39] showed that the cardiac index measured by transpulmonary thermodilution was significantly lower in patients with poor-grade aSAH and that patients developing DCI had a significantly lower global end-diastolic volume index (GEDI) than patients without these neurological sequelae. The same study group was able to show that the GEDI was an independent risk factor associated with the occurrence of DCI and severe pulmonary edema [40], the Scylla and Charybdis of volume therapy in aSAH. They found a lower threshold of 822 ml/m2, slightly above the normal range, correlated with an increased risk of DCI. A GEDI threshold above 921 ml/m2 was best correlated with the occurrence of severe pulmonary edema in 47 of 180 patients after aSAH [40]. The infusion of crystalloid or colloid infusion to increase the cardiac index and raise GEDI above normal values reduced DCI and improved postoperative functional outcome in poor-grade SAH patients [41]. Application of fluid boluses that increased cardiac index in parallel to GEDI was also associated with a significantly higher increase of regional brain tissue oxygen pressure in patients after SAH [42]. In a prospective randomized double-blind trial, the use of isotonic saline for fluid boluses after aSAH was associated with hyperchloremia, hyperosmolality, and a positive fluid balance, whereas patients receiving balanced crystalloid infusion did not show electrolyte disturbances or hypoosmolality [43].

The increase of oxygen transport capacity to improve microvascular oxygenation in brain tissue at risk is also known to prevent DCI in patients after aSAH, although no critical hemoglobin concentration is known [44▪]. In general, a threshold of 7 g/l in ICU patients is standard, as higher values seem to increase mortality. Within the scope of multimodal monitoring, measurement of local brain oxygen partial pressure is a possibility to monitor the effect of red blood transfusion, especially because transfusions may increases venous thromboembolism and thrombotic events [45].

For more than a decade, intensive care support of patients after aneurysmal SAH has consisted of administration of statins and magnesium in addition to prophylactic nimodipine treatment. Recent work challenges this approach. A recent multicenter, randomized, double-blind trial showed that intravenous magnesium sulphate does not improve clinical outcome after SAH. The authors concluded that routine administration could not be recommended [46]. Nevertheless, in a recent meta-analysis, DCI was the only outcome with a statistically significant effect favoring magnesium treatment [47]. This meta-analysis also concluded that prophylactic use of magnesium is not supported by current evidence, as functional outcome was not improved.

Enhancement of CBF, anti-inflammation, and increased endothelial nitric oxide production were potential beneficial effects justifying the use of statins for prevention of cerebral artery vasospasm and consecutive DIC [44▪]. Although 80 mg of simvastatin for 2 weeks decreased the number of patients with high blood velocities in TCD and neurologic deterioration, there was no improvement in functional outcome [48]. In a double-blind randomized controlled trial of 800 patients after SAH, the application of 40 mg of simvastatin for 3 weeks did not improve functional neurological outcome after 6 months [49▪]. The authors also performed a small meta-analysis dominated by their own data, which did not show any benefit of statins on short or long-term outcome in these patients. The authors do not recommend not treating patients with simvastatin after SAH.

Several groups of direct vasodilator drugs have been tested for reduction of angiographic vasospasm and DCI. The endothelin A receptor antagonist clazosentan indeed reduced vasospasm but without a significant effect on functional outcome [44▪,50,51]. Rho-kinase inhibitors like fasudil and eicosapentaenoic acid, which reduce smooth muscle contraction, lower the incidence of angiographic vasospasm and cerebral infarction, and increase the probability of good recovery [44▪,52]. The phosphodiesterase-III inhibitor cilostazol has antithrombotic as well as cardiac and vasodilatory effects. In two recent trials, cilostazol significantly decreased angiographic vasospasm and cerebral infarction and showed an improved clinical outcome [53,54]. Antithrombotic therapy with low-dose intravenous heparin (8–10 U/kg/h), 12 h after securing the aneurysms, reduced the incidence of clinical vasospasm and delayed infarction after SAH without clinically significant hemorrhage [55]. Although applications of antiplatelet drugs also seem to reduce poor outcome, they showed a trend toward increased cranial hemorrhage [44▪]. Antithrombotic therapy warrants further clinical investigation.

Traumatic brain injury

Patients with severe TBI are usually admitted to intensive care for early clinical recognition of neurological deterioration, prevention of secondary cerebral ischemia, and monitoring and therapy of ICP or CCP [56]. Actual guidelines propose an ICP below 20 mmHg as threshold for treatment [57]. A single episode of an ICP above 20 mmHg for more than 15 min is an adequate predictor of poor outcome, whereas a CPP below 50 mmHg for the same time period did not affect survival [58]. Although the value of ICP measurement was recently questioned [59], we believe that ICP monitoring combined with continuous brain tissue oxygen measurement [60,61] provides the best information about regional microcirculatory perfusion in the brain. In contrast to acute ischemic stroke, cerebral perfusion CT cannot be performed regularly in patients with severe head injury. In a very recent study, the combination of ICP monitoring together with brain tissue oxygen pressure and cerebral microdialysis [62] was more accurate in predicting cerebral hypoperfusion measured by perfusion CT scan than ICP measurement alone [60].

To maintain adequate CPP, isotonic saline for fluid resuscitation and norepinephrine are usually used in patients with severe head injury. In case of arrhythmias or refractoriness to norepinephrine, vasopressin seems to be a valuable alternative for blood pressure support [63]. Isotonic saline potentially causes hyperchloremic acidosis and reduced renal blood flow. A recent study showed that balanced crystalloid infusion can be used in TBI patients without any increase in ICP or mortality, and that this type of infusion reduces hyperchloremic acidosis [64].

Increased ICP was traditionally treated with a stepwise approach [56]. After intensification of analgesia and sedation, hyperosmolar therapy, usually using mannitol, was started. Mannitol decreases ICP first by reducing CBF and after establishing an osmotic gradient by extraction of water from brain tissue [65]. After degradation and elimination of the mannitol molecules, osmotic equilibrium is re-established. In contrast, bolus administration of hypertonic saline was more effective in lowering the cumulative and daily ICP burden after severe TBI and significantly reduced ICU length of stay [66]. Effectiveness of osmotic therapy depends on an intact blood-brain barrier. In a small study, more than one-third of patients treated with hypertonic saline had an impairment of passive blood brain barrier function, a higher ICP, and a trend toward increased mortality [67]. Continuous application of half-molar sodium lactate after TBI for 48 h reduced episodes of increased ICP and reduced fluid and chloride load [68,69]. Sodium lactate may also be used as an alternative energy substrate in conditions of increased energy demand and limited glucose availability [70]. Beside the ICP-lowering effect, sodium lactate decreased brain tissue concentration of the excitotoxic neurotransmitter glutamate and increased the concentration of lactate and pyruvate after TBI [69].

Therapeutic hypothermia is another option to decrease ICP after severe head injury [56]. Until now, no clear evidence exists that hypothermia (at 32–34°C) effectively influences functional neurological outcome by decreasing ICP [71]. Currently, the large multicenter EUROtherm3235 trial has closed recruitment of patients with severe TBI [72]. This trial is investigating influence of early therapeutic hypothermia for 48 h followed by a rewarming phase, (+0.25°C/h) on mortality and functional outcome [73].

If classical intensive care procedures to lower ICP fail, surgical interventions like cerebrospinal fluid drainage and decompressive craniectomy are last resorts. Despite the persuasive concept of enlargement of possible volume for cerebral edema, a large clinical trial could not confirm the presumed benefits of decompressive craniectomy [70,74]. In patients with diffuse head injury, craniectomy within 72 h after trauma had the same mortality as patients receiving intensive medical treatment, but the rate of unfavorable neurological outcome was significantly higher. The ‘Randomised Evaluation of Surgery with Craniectomy for Uncontrollable Elevation of Intra-Cranial Pressure’ (RESCUEicp) trial has completed recruitment, and data are awaited after follow-up and data analysis has been completed [75].

Different response to TBI between sex as well as the results of small phase II trials and animal experiments has led to increased research on hormone therapy [71]. In animals, progesterone reduced cerebral edema, neuronal loss, and behavioral alterations [70]. Two large multicenter trials investigated the influence of progesterone therapy for 4–6 days on functional outcome and mortality. Although, together, both studies included nearly 2000 patients, no benefit could be found in patients treated with progesterone after TBI [76,77]. Erythropoietin also showed anti-inflammatory, antiapoptotic, and vascular neuroprotective mechanisms in experimental models. Application of 500 IU/kg of erythropoietin and a transfusion threshold of 100 g/l were tested in 200 patients [78]. Neither the administration of erythropoietin nor the maintenance of hemoglobin concentrations above 100 g/l resulted in improved functional outcome after 6 months.

In the recent consensus guidelines on multimodal monitoring, regular wake-up tests and sedation interruption are not recommended for patients at increased risk for intracranial hypertension [13]. In an average population of ventilated intensive care patients, daily interruption of sedation resulted in a higher amount of sedative use and nurse-related workload without decreased ventilation time or ICU length of stay [79]. In patients with TBI or SAH, the daily interruption of sedation has the risk of a prolonged elevation of ICP accompanied by a decrease in CPP [80] and brain tissue oxygen tension [81]. Current guidelines recommend additional monitoring for cerebral ischemia should patients with increased ICP require controlled hyperventilation to decrease CBF [61]. Patients with severe head injury and prolonged mechanical ventilation may benefit from early tracheostomy. In an observational propensity-matched cohort study, tracheostomy before day 9 decreased ventilator time, length of ICU, and hospital stay but not in-hospital mortality [82].


Despite the lack of high-grade evidence for most interventions in the care of emergency neurosurgical patients, there is a broad consensus on how to monitor and treat intensive care patients after neurological emergencies. The results of ongoing prospective, randomized, multicenter trials will shed some light on the future therapy of neurointensive care patients [73,75]. Although evidence from the above-mentioned studies is very much appreciated, preliminary research focusing on solid evidence regarding monitoring and therapy is urgently needed.


The authors thank Allison Dwileski, Department for Anesthesia, Surgical Intensive Care, Prehospital Emergency Medicine and Pain Therapy, University Hospital Basel, Basel, Switzerland, for editorial assistance.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.


Papers of particular interest, published within the annual period of review, have been highlighted as:

  • ▪ of special interest
  • ▪▪ of outstanding interest


1. Fontes RB, Smith AP, Munoz LF, et al. Relevance of early head CT scans following neurosurgical procedures: an analysis of 892 intracranial procedures at Rush University Medical Center. J Neurosurg 2014; 121:307–312.
2. Hanak BW, Walcott BP, Nahed BV, et al. Postoperative intensive care unit requirements after elective craniotomy. World Neurosurg 2014; 81:165–172.
3. Hecht N, Spies C, Vajkoczy P. Routine intensive care unit-level care after elective craniotomy: time to rethink. World Neurosurg 2014; 81:66–68.
4. Awad IA. Intensive care after elective craniotomy: ‘all politics is local’. World Neurosurg 2014; 81:64–65.
5. Adelmann D, Klaus DA, Illievich UM, et al. Fibrinogen but not factor XIII deficiency is associated with bleeding after craniotomy. Br J Anaesth 2014; 113:628–633.
6. Zhou JC, Pan KH, Huang X, et al. Delayed admission to ICU does not increase the mortality of patients post neurosurgery. Int J Neurosci 2015; 125:402–408.
7▪▪. Le Roux P, Menon DK, Citerio G, et al. Consensus summary statement of the International Multidisciplinary Consensus Conference on Multimodality Monitoring in Neurocritical Care: a statement for healthcare professionals from the Neurocritical Care Society and the European Society of Intensive Care Medicine. Intensive Care Med 2014; 40:1189–1209.

This consensus statement gives a comprehensive overview about all monitoring techniques for mutlimodal monitoring in neurocrticial care and reviews the current evidence for their use.

8. Chesnut R, Videtta W, Vespa P, et al. Intracranial pressure monitoring: fundamental considerations and rationale for monitoring. Neurocrit Care 2014; 21 (Suppl 2):S64–S84.
9. Bullock R, Hanemann CO, Murray L, Teasdale GM. Recurrent hematomas following craniotomy for traumatic intracranial mass. J Neurosurg 1990; 72:9–14.
10. Kalfas IH, Little JR. Postoperative hemorrhage: a survey of 4992 intracranial procedures. Neurosurgery 1988; 23:343–347.
11. Teasdale G, Jennett B. Assessment of coma and impaired consciousness. A practical scale Lancet 1974; 2:81–84.
12. Wijdicks EF, Bamlet WR, Maramattom BV, et al. Validation of a new coma scale: The FOUR score. Ann Neurol 2005; 58:585–593.
13. Riker RR, Fugate JE. and Participants in the International Multidisciplinary Consensus Conference on Multimodality M. Clinical monitoring scales in acute brain injury: assessment of coma, pain, agitation, and delirium. Neurocrit Care 2014; 21 (Suppl 2):27–37.
14. Chesnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determining outcome from severe head injury. J Trauma 1993; 34:216–222.
15. Rincon F, Kang J, Vibbert M, et al. Significance of arterial hyperoxia and relationship with case fatality in traumatic brain injury: a multicentre cohort study. J Neurol Neurosurg Psychiatry 2014; 85:799–805.
16. Rincon F, Kang J, Maltenfort M, et al. Association between hyperoxia and mortality after stroke: a multicenter cohort study. Crit Care Med 2014; 42:387–396.
17. Jeon SB, Choi HA, Badjatia N, et al. Hyperoxia may be related to delayed cerebral ischemia and poor outcome after subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 2014; 85:1301–1307.
18. Budohoski KP, Guilfoyle M, Helmy A, et al. The pathophysiology and treatment of delayed cerebral ischaemia following subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 2014; 85:1343–1353.
19. Quintard H, Patet C, Suys T, et al. Normobaric hyperoxia is associated with increased cerebral excitotoxicity after severe traumatic brain injury. Neurocrit Care 2015; 22:243–250.
20. Kurtz P, Claassen J, Helbok R, et al. Systemic glucose variability predicts cerebral metabolic distress and mortality after subarachnoid hemorrhage: a retrospective observational study. Crit Care 2014; 18:R89.
21. Lee JH, Kelly DF, Oertel M, et al. Carbon dioxide reactivity, pressure autoregulation, and metabolic suppression reactivity after head injury: a transcranial Doppler study. J Neurosurg 2001; 95:222–232.
22. Mackersie RC, Karagianes TG. Use of end-tidal carbon dioxide tension for monitoring induced hypocapnia in head-injured patients. Crit Care Med 1990; 18:764–765.
23. Kerr ME, Zempsky J, Sereika S, et al. Relationship between arterial carbon dioxide and end-tidal carbon dioxide in mechanically ventilated adults with severe head trauma. Crit Care Med 1996; 24:785–790.
24. Seguin P, Bleichner JP, Branger B, et al. [The measurement of end-tidal carbon dioxide (PETCO2) is not a significant parameter to monitor in patients with severe traumatic brain injury]. Can J Anaesth 2001; 48:396–400.
25. Molyneux AJ, Birks J, Clarke A, et al. The durability of endovascular coiling versus neurosurgical clipping of ruptured cerebral aneurysms: 18 year follow-up of the UK cohort of the International Subarachnoid Aneurysm Trial (ISAT). Lancet 2015; 385:691–697.
26. Kanamaru K, Suzuki H, Taki W. Risk factors for vasospasm-induced cerebral infarct when both clipping and coiling are equally available. Acta Neurochir Suppl 2015; 120:291–295.
27. Spetzler RF, McDougall CG, Albuquerque FC, et al. The Barrow Ruptured Aneurysm Trial: 3-year results. J Neurosurg 2013; 119:146–157.
28. Suzuki H. Taki W and Prospective Registry of Subarachnoid Aneurysms Treatment G.. Effect of aneurysm treatment modalities on cerebral vasospasm after aneurysmal subarachnoid hemorrhage. Acta Neurochir Suppl 2013; 115:99–105.
29. Miller C. Armonda R and Participants in the International Multidisciplinary Consensus Conference on Multimodality M.. Monitoring of cerebral blood flow and ischemia in the critically ill. Neurocrit Care 2014; 21 (Suppl 2):121–128.
30. Kincaid MS, Souter MJ, Treggiari MM, et al. Accuracy of transcranial Doppler ultrasonography and single-photon emission computed tomography in the diagnosis of angiographically demonstrated cerebral vasospasm. J Neurosurg 2009; 110:67–72.
31. Turek G, Kochanowicz J, Rutkowski R, et al. Accuracy of transcranial colour-coded sonography in the diagnosis of anterior cerebral artery vasospasm. Neurol Neurochir Pol 2012; 46:233–238.
32. Suarez JI, Qureshi AI, Yahia AB, et al. Symptomatic vasospasm diagnosis after subarachnoid hemorrhage: evaluation of transcranial Doppler ultrasound and cerebral angiography as related to compromised vascular distribution. Crit Care Med 2002; 30:1348–1355.
33. Diringer MN, Bleck TP, Claude Hemphill J r 3rd, et al. Critical care management of patients following aneurysmal subarachnoid hemorrhage: recommendations from the Neurocritical Care Society's Multidisciplinary Consensus Conference. Neurocrit Care 2011; 15:211–240.
34. van der Bilt I, Hasan D, van den Brink R, et al. Cardiac dysfunction after aneurysmal subarachnoid hemorrhage: relationship with outcome. Neurology 2014; 82:351–358.
35. Salem R, Vallee F, Depret F, et al. Subarachnoid hemorrhage induces an early and reversible cardiac injury associated with catecholamine release: one-week follow-up study. Crit Care 2014; 18:558.
36. Zoerle T, Lombardo A, Colombo A, et al. Intracranial pressure after subarachnoid hemorrhage. Crit Care Med 2015; 43:168–176.
37. Smith M, Citerio G. What's new in subarachnoid hemorrhage. Intensive Care Med 2015; 41:123–126.
38. Tagami T, Kuwamoto K, Watanabe A, et al. Effect of triple-h prophylaxis on global end-diastolic volume and clinical outcomes in patients with aneurysmal subarachnoid hemorrhage. Neurocrit Care 2014; 21:462–469.
39. Yoneda H, Nakamura T, Shirao S, et al. Multicenter prospective cohort study on volume management after subarachnoid hemorrhage: hemodynamic changes according to severity of subarachnoid hemorrhage and cerebral vasospasm. Stroke 2013; 44:2155–2161.
40. Tagami T, Kuwamoto K, Watanabe A, et al. Optimal range of global end-diastolic volume for fluid management after aneurysmal subarachnoid hemorrhage: a multicenter prospective cohort study. Crit Care Med 2014; 42:1348–1356.
41. Mutoh T, Kazumata K, Terasaka S, et al. Early intensive versus minimally invasive approach to postoperative hemodynamic management after subarachnoid hemorrhage. Stroke 2014; 45:1280–1284.
42. Kurtz P, Helbok R, Ko SB, et al. Fluid responsiveness and brain tissue oxygen augmentation after subarachnoid hemorrhage. Neurocrit Care 2014; 20:247–254.
43. Lehmann L, Bendel S, Uehlinger DE, et al. Randomized, double-blind trial of the effect of fluid composition on electrolyte, acid-base, and fluid homeostasis in patients early after subarachnoid hemorrhage. Neurocrit Care 2013; 18:5–12.
44▪. Macdonald RL. Delayed neurological deterioration after subarachnoid haemorrhage. Nat Rev Neurol 2014; 10:44–58.

This review provides the reader with all currently discussed pathopyhsiolgic mechannisms for delayed cerebral ischemia and the possible therapeutic interventions.

45. Kumar MA, Boland TA, Baiou M, et al. Red blood cell transfusion increases the risk of thrombotic events in patients with subarachnoid hemorrhage. Neurocrit Care 2014; 20:84–90.
46. Dorhout Mees SM, Algra A, Vandertop WP, et al. Magnesium for aneurysmal subarachnoid haemorrhage (MASH-2): a randomised placebo-controlled trial. Lancet 2012; 380:44–49.
47. Reddy D, Fallah A, Petropoulos JA, et al. Prophylactic magnesium sulfate for aneurysmal subarachnoid hemorrhage: a systematic review and meta-analysis. Neurocrit Care 2014; 21:356–364.
48. Garg K, Sinha S, Kale SS, et al. Role of simvastatin in prevention of vasospasm and improving functional outcome after aneurysmal sub-arachnoid hemorrhage: a prospective, randomized, double-blind, placebo-controlled pilot trial. Br J Neurosurg 2013; 27:181–186.
49▪. Kirkpatrick PJ, Turner CL, Smith C, et al. Simvastatin in aneurysmal subarachnoid haemorrhage (STASH): a multicentre randomised phase 3 trial. Lancet Neurol 2014; 13:666–675.

This randomized, controlled multicenter study could not show a decrease in mortality or functional neurological deficits after prophylactic application of simvastatin.

50. Macdonald RL, Higashida RT, Keller E, et al. Randomized trial of clazosentan in patients with aneurysmal subarachnoid hemorrhage undergoing endovascular coiling. Stroke 2012; 43:1463–1469.
51. Macdonald RL, Higashida RT, Keller E, et al. Clazosentan, an endothelin receptor antagonist, in patients with aneurysmal subarachnoid haemorrhage undergoing surgical clipping: a randomised, double-blind, placebo-controlled phase 3 trial (CONSCIOUS-2). Lancet Neurol 2011; 10:618–625.
52. Yoneda H, Shirao S, Nakagawara J, et al. A prospective, multicenter, randomized study of the efficacy of eicosapentaenoic acid for cerebral vasospasm: the EVAS study. World Neurosurg 2014; 81:309–315.
53. Kimura H, Okamura Y, Chiba Y, et al. Cilostazol administration with combination enteral and parenteral nutrition therapy remarkably improves outcome after subarachnoid hemorrhage. Acta Neurochir Suppl 2015; 120:147–152.
54. Senbokuya N, Kinouchi H, Kanemaru K, et al. Effects of cilostazol on cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a multicenter prospective, randomized, open-label blinded end point trial. J Neurosurg 2013; 118:121–130.
55. Simard JM, Aldrich EF, Schreibman D, et al. Low-dose intravenous heparin infusion in patients with aneurysmal subarachnoid hemorrhage: a preliminary assessment. J Neurosurg 2013; 119:1611–1619.
56. Stocchetti N, Maas AI. Traumatic intracranial hypertension. N Engl J Med 2014; 370:2121–2130.
57. Brain Trauma Foundation. Guidelines for the management of severe traumatic brain injury. Guidelines for the management of severe traumatic brain injury. 3rd edNew York: Mary Ann Lieber Inc; 2007.
58. Karamanos E, Teixeira PG, Sivrikoz E, et al. Intracranial pressure versus cerebral perfusion pressure as a marker of outcomes in severe head injury: a prospective evaluation. Am J Surg 2014; 208:363–371.
59. Chesnut RM, Temkin N, Carney N, et al. A trial of intracranial-pressure monitoring in traumatic brain injury. N Engl J Med 2012; 367:2471–2481.
60. Bouzat P, Marques-Vidal P, Zerlauth JB, et al. Accuracy of brain multimodal monitoring to detect cerebral hypoperfusion after traumatic brain injury. Crit Care Med 2015; 43:445–452.
61. Oddo M. Bosel J and Participants in the International Multidisciplinary Consensus Conference on Multimodality M. Monitoring of brain and systemic oxygenation in neurocritical care patients. Neurocrit Care 2014; 21 (Suppl 2):S103–S120.
62. de Lima Oliveira M, Kairalla AC, Fonoff ET, et al. Cerebral microdialysis in traumatic brain injury and subarachnoid hemorrhage: state of the art. Neurocrit Care 2014; 21:152–162.
63. Van Haren RM, Thorson CM, Ogilvie MP, et al. Vasopressin for cerebral perfusion pressure management in patients with severe traumatic brain injury: preliminary results of a randomized controlled trial. J Trauma Acute Care Surg 2013; 75:1024–1030.
64. Roquilly A, Loutrel O, Cinotti R, et al. Balanced versus chloride-rich solutions for fluid resuscitation in brain-injured patients: a randomised double-blind pilot study. Crit Care 2013; 17:R77.
65. Ropper AH. Hyperosmolar therapy for raised intracranial pressure. N Engl J Med 2012; 367:746–752.
66. Mangat HS, Chiu YL, Gerber LM, et al. Hypertonic saline reduces cumulative and daily intracranial pressure burdens after severe traumatic brain injury. J Neurosurg 2015; 122:202–210.
67. Saw MM, Chamberlain J, Barr M, et al. Differential disruption of blood-brain barrier in severe traumatic brain injury. Neurocrit Care 2014; 20:209–216.
68. Ichai C, Payen JF, Orban JC, et al. Half-molar sodium lactate infusion to prevent intracranial hypertensive episodes in severe traumatic brain injured patients: a randomized controlled trial. Intensive Care Med 2013; 39:1413–1422.
69. Bouzat P, Sala N, Suys T, et al. Cerebral metabolic effects of exogenous lactate supplementation on the injured human brain. Intensive Care Med 2014; 40:412–421.
70. Stocchetti N, Taccone FS, Citerio G, et al. Neuroprotection in acute brain injury: an up-to-date review. Crit Care 2015; 19:186.
71. Rosenfeld JV, Maas AI, Bragge P, et al. Early management of severe traumatic brain injury. Lancet 2012; 380:1088–1098.
72. Andrews PJ, Sinclair LH, Harris B, et al. Study of therapeutic hypothermia (32 to 35 degrees C) for intracranial pressure reduction after traumatic brain injury (the Eurotherm3235Trial): outcome of the pilot phase of the trial. Trials 2013; 14:277.
73. Andrews PJ. European study of therapeutic hypothermia (32–35(C) for ICP reduction after traumatic brain injury. 2012; [Accessed 5 May 2015].
74. Cooper DJ, Rosenfeld JV, Murray L, et al. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med 2011; 364:1493–1502.
75. 2009; Hutchinson P, Kirkpatrick PJ. Randomised evaluation of surgery with craniectomy for uncontrollable elevation of intra-cranial pressure. http:// (Last updated: 2014.10.10). [Accessed 5 May 2015].
76. Wright DW, et al. Very early administration of progesterone for acute traumatic brain injury. N Engl J Med 2014; 371:2457–2466.
77. Skolnick BE, Maas AI, Narayan RK, et al. A clinical trial of progesterone for severe traumatic brain injury. N Engl J Med 2014; 371:2467–2476.
78. Robertson CS, Hannay HJd, Yamal JM, et al. Effect of erythropoietin and transfusion threshold on neurological recovery after traumatic brain injury: a randomized clinical trial. JAMA 2014; 312:36–47.
79. Mehta S, Burry L, Cook D, et al. Daily sedation interruption in mechanically ventilated critically ill patients cared for with a sedation protocol: a randomized controlled trial. JAMA 2012; 308:1985–1992.
80. Skoglund K, Enblad P, Marklund N. Effects of the neurological wake-up test on intracranial pressure and cerebral perfusion pressure in brain-injured patients. Neurocrit Care 2009; 11:135–142.
81. Helbok R, Kurtz P, Schmidt MJ, et al. Effects of the neurological wake-up test on clinical examination, intracranial pressure, brain metabolism and brain tissue oxygenation in severely brain-injured patients. Crit Care 2012; 16:R226.
82. Alali AS, Scales DC, Fowler RA, et al. Tracheostomy timing in traumatic brain injury: a propensity-matched cohort study. J Trauma Acute Care Surg 2014; 76:70–76.

elective intradural operation; hyperoxia; multimodal monitoring; subarachnoidal hemorrhage; traumatic brain injury

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