Treatment of intracranial hypertension Thomas Lescota, Lamine Abdennoura, Anne-Laure Bochb and Louis Puybasseta a

Department of Anesthesiology and Critical Care and Department of Neurosurgery, Pitie´-Salpeˆtrie`re Teaching Hospital, Assistance Publique – Hoˆpitaux de Paris and Universite´ Pierre et Marie Curie – Paris 6, Paris, France b

Correspondence to Professeur Louis Puybasset, Unite´ de Neurore´animation, De´partement d’Anesthe´sieRe´animation, Groupe Hospitalier Pitie´-Salpeˆtrie`re, 47–83 Boulevard de l’Hoˆpital, 75651 Paris, Cedex 13, France Tel: +33 142 163 371; fax: +33 142 163 390; e-mail: [email protected]

Current Opinion in Critical Care 2008, 14:129– 134

Purpose of review The review provides key points and recent advances regarding the treatments of intracranial hypertension as a consequence of traumatic brain injury. The review is based on the pathophysiology of brain edema and draws on the current literature as well as clinical bedside experience. Recent findings The review will cite baseline literature and discuss emerging data on cerebral perfusion pressure, sedation, hypothermia, osmotherapy and albumin as treatments of intracranial hypertension in traumatic brain-injured patients. Summary One of the key issues is to consider that traumatic brain injury is more likely a syndrome than a disease. In particular, the presence or absence of a high contusional volume could influence the treatments to be implemented. The use of osmotherapy and/or high cerebral perfusion pressure should be restricted to patients without major contusions. Some physiopathological, experimental and clinical data, however, show that corticosteroids and albumin – therapies that have been proven deleterious if administered systematically – are worth reconsidering for this subgroup of patients. The current Pitie´-Salpeˆtrie`re algorithm, where treatments are stratified according to their potential side effects, will be added at the end of the review as an example of an integrated strategy. Keywords cerebral perfusion pressure, intracranial pressure, osmotherapy, sedation, traumatic brain injury Curr Opin Crit Care 14:129–134 ß 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins 1070-5295

Introduction Most traumatic brain injury (TBI) patients with cerebral lesion on cerebral computed tomography (CT), such as hematomas, swelling, contusions or herniation, will develop intracranial hypertension in the days following injury [1]. A recent observational study showed that mean intracranial pressure (ICP) peaks in half of such patients during the first 3 days after injury, while 25% show highest mean ICP after 5 days [2]. An uncontrolled rise in ICP is probably the most common cause of death in TBI patients. For these reasons, intracranial pressure monitoring is strongly recommended in cases of severe TBI associated with abnormal cerebral CT [3]. Intracranial pressure monitoring allows the continuous monitoring of ICP, the management of cerebral perfusion pressure (CPP), and the withdrawal of cerebrospinal fluid (CSF) in the event that external ventricular drainage is inserted. Elevated intracranial hypertension is strongly associated with poor outcome among patients with severe TBI. Indeed, elevated ICP may lead to a decrease in CPPinduced cerebral ischemia and/or herniation. The ICP threshold above which treatment should be initiated is

still a matter of debate. A large prospectively collected database study was published in 1991 by Marmarou et al. [4]. The authors found a strong correlation between outcome and the number of hours with an ICP above 20 mmHg. Similar results have been recently reported by Balestreri et al. [5] in a retrospective analysis performed on 429 TBI patients. Does treatment aimed at decreasing ICP improve outcome in TBI? Few data exist regarding this question, and no randomized controlled trials are available. Nonetheless, it seems that patients whose ICP can be efficiently controlled have a much better outcome than those whose ICP remains uncontrolled [6,7]. More recently, two retrospective studies showed similar results, suggesting an improved outcome with aggressive ICP therapy [8,9]. Regarding the treatment of intracranial hypertension, one of the key issues is to consider that TBI is more likely a syndrome than a disease. After trauma, the traumatized brain is characterized by a huge pathophysiological heterogeneity: ischemic areas (cytotoxic edema) coexist

1070-5295 ß 2008 Wolters Kluwer Health | Lippincott Williams & Wilkins

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130 Neuroscience

with areas with blood–brain barrier disruptions (vasogenic edema), contusions and normal brain parenchyma. The proportion of each of these areas likely depends on the etiology of TBI. ICP-lowering therapies may have some systemic or cerebral differential effect according to the TBI presentation. In the case of blood–brain barrier disruption, for example, one can consider that treatment such as hypertension-induced high CPP and osmotherapy could worsen contusional areas of the traumatized brain.

Sedation as a therapy Sedatives and anesthetics are widely used to prevent agitation, minimize noxious stimuli and adapt TBI patients to mechanical ventilation. For that purpose, benzodiazepines, especially midazolam, are administered in combination with morphine or derivatives such as sufentanil. Benzodiazepines are particularly suitable in the neuro-intensive care unit, but due to their plateau effect, cannot depress brain electrical activity even at high doses. A further disadvantage is that they present a long duration of action. Propofol administration has been proposed as an alternative in TBI patients. Propofol decreases ICP through a reduction in brain metabolism [10,11], which explains its potential neuroprotective effect. Only one double-blind randomized controlled trial has been conducted to compare propofol infusion with another sedative regiment in TBI patients. Kelly et al. [12] evaluated the clinical safety of multiple clinical and radiological endpoints in 23 patients treated with low-dose propofol-morphine and 19 patients treated with morphine alone. The authors found a lower incidence of intracranial hypertension at day 3 in the propofol group without any difference in terms of adverse effects between groups. The combination midazolam-propofol allows control of intracranial hypertension with the possibility of obtaining burst-suppression at high doses. Such a combined strategy reduces the use of barbiturates. The ‘propofol infusion syndrome’ must be a constant fear when using propofol. This syndrome, characterized by multiorgan failure, has a high incidence in sepsis or septic shock, which are therefore contra-indications to propofol administration. It is mandatory to stop propofol in the event of metabolic acidosis (with or without lactates), hyperkaliemia, renal insufficiency, rhabdomyolysis or triglycerides level above 4 mmol/l [13]. A daily dosage of blood triglycerides is a common practice in our unit. Hypertriglyceridemia is a warning symptom in this context [14].

Drainage of cerebrospinal fluid Drainage of CSF is frequently performed in TBI patients. An external ventricular drain connected to an

external strain gauge allows the continuous measurement of ICP and the calculation of CPP (when the drainage line is externally clamped), or withdrawal of CSF (when the drainage line is open). In case of low cerebral compliance due to cerebral edema, the evacuation of a few milliliters of CSF may be sufficient to decrease ICP dramatically. Kerr et al. [15] showed that a 3-ml withdrawal of CSF resulted in a mean 10% decrease in ICP and a mean 2% increase in CPP, which were sustained for 10 min. This therapy is simple, cost-effective and overrides the often serious systemic complications related to drug or physical therapies, especially those induced by barbiturates and hypothermia. Drain placement might be technically difficult, and can be complicated by cerebral contusion or ventriculitis [16]. Two studies have shown that the difference in pressure gradient induced by intracranial CSF drainage facilitates the transfer of cerebral edema to the ventricles, thus improving its clearance [17,18]. Continuous drainage of CSF against a zero pressure, using the external ventricular drain, combined with the continuous monitoring of ICP with an intraparenchymal catheter is a common practice in our unit. This technique likely increases the volume of drained CSF as compared with a discontinuous drainage although there are no hard data to support this clinical observation.

Osmotherapy In TBI, the ICP rise is mostly due to cerebral edema. Hyperosmolar agents are widely used to control edema formation after TBI. There is abundant literature supporting the use of Mannitol to decrease ICP, increase CPP, and enhance cerebral blood flow [19] without affecting cerebral oxygenation [20]. Hypertonic saline used at various concentrations (from 3% to 23.4%) has been consistently shown to decrease ICP and cerebral water content in human TBI [21,22]. Hyperosmolar agents were shown to decrease water content in nontraumatized brain tissue by osmotic mobilization of water across the intact blood–brain barrier. There is, however, the possibility of an opposed effect of osmotic agent in the areas of disrupted blood–brain barrier. Such a result was observed by Saltarini et al. [23] in a patient with refractory intracranial hypertension using magnetic resonance spectroscopy to assess cerebral water content. One recent CT-based analysis showed an increase in contusion volume after hypertonic saline infusion, suggesting a leak of electrolyte and plasma from the extracellular compartment into the contused area through a disrupted blood–brain barrier [24]. These results argue for differential effects of hypertonic saline according to the state of the blood–brain barrier in various brain areas. As a result, it could be proposed to restrict the use of osmotic agents to patients presenting with a small volume of contusion.

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Treatment of intracranial hypertension Lescot et al. 131

Cerebral perfusion pressure Management of CPP in TBI is still the subject of debate. In 1995, Rosner et al. [25] developed a management paradigm focused on maintaining CPP above 70 mmHg. This strategy, based on the integrity of the blood–brain barrier and a preserved cerebral autoregulation, seemed to improve outcome in an uncontrolled series of TBI patients. An alternative approach has been described and popularized by the Lund group [26]. Lund theory hypothesizes that the blood–brain barrier is mainly disrupted after head trauma and that cerebral autoregulation is lost. Increasing CPP or using an osmotic agent are therefore considered as potentially dangerous therapies that risk increasing edema formation. The Lund protocol therapy has two main goals: to reduce or prevent an increase in ICP (ICP-targeted goal) and to improve perfusion and oxygenation around contusions (perfusion-targeted goal) [27]. Current evidence exists to support the concept that hypotension is deleterious for the traumatized brain. Increasing CPP up to 70 mmHg, however, was associated with an increased incidence of pulmonary failure [28]. A recent prospective observational study compared the 6-month outcome of two groups of TBI patients: one group of 67 treated in Sweden with the aim of keeping ICP below 20 mmHg and CPP above 60 mmHg; and a second group of 64 treated in Scotland with a Rosnerderived strategy protocol in which the goal was to reach a CPP of at least 70 mmHg while keeping ICP below 25 mmHg [29]. The authors noted that CPP management therapy seemed to be more efficient in patients with intact cerebral autoregulation. Patients with loss of cerebral autoregulation, however, appeared to benefit from Lund CPP management. This could be linked to the presence of contusions: preserved autoregulation is known to be more frequently observed in patients with few contusions [30]. Taken together, these results suggest that patients with a large amount of contusion (blood–brain barrier mainly disrupted and loss of autoregulation) would benefit from Lund-based therapy. In contrast, this pathophysiological perspective suggests that a CPP target therapy associated with osmotherapy would be logical for patients presenting with only a few contused areas.

Hypothermia Prophylactic hypothermia is effective in improving outcome in cardiac arrest [31] although it remains controversial in other indications such as brain injury. Nevertheless, the results of different studies and meta-analyses [32–35] have not demonstrated hypothermia to be associated with reduction of mortality in TBI. The fact that hypothermia was implemented systematically in every

patient independently of ICP level, however, may imply that the usefulness of this therapy has been underestimated. Polderman et al. [33] assessed the efficacy of hypothermia therapy (32–34 8C) as part of a step-up protocol with great attention to detecting and treating side effects. The authors found that artificial cooling could improve survival and neurological outcome especially in the group with low Glasgow Coma Score. According to these results, it seems logical to restrict the use of hypothermia to patients showing an increased ICP. Indications and techniques for implementation, as well as management procedures and enforcement are all considerations in optimizing the performance of hypothermia. A rigorous and effective application cannot be conceived outside specialized units with experienced teams. After a minimum duration of 24 h and after ICP is under control, a very gradual warming can be started, allowing for possible interruption should ICP increase again [36,37]. A decrease in brain metabolism associated with anti-inflammatory effects is the main mechanism of action attributed to hypothermia. Kaliemia must be strictly controlled during the ascending and descending changes in body temperature. It is noteworthy that the implementation of hypothermia has been recently facilitated by automatic cooling blankets and specially designed catheters. Metabolism of barbiturates is profoundly modified in hypothermia with frequent overdosages.

Steroids Steroids are particularly effective for treating intracranial hypertension secondary to cerebral tumoral process [38] and bacterial meningitis [39]. The majority of available evidence indicates that steroids do not improve outcome or decrease ICP in TBI patients. In a randomized controlled trial with 10 008 patients, the CRASH study [40] showed no effect of corticosteroids on ICP, with higher mortality observed in the steroids groups. This study demonstrates that the systematic use of corticosteroids is detrimental to TBI patients. Inclusion criteria were very broad, however, and the population of TBI patients was extremely heterogeneous. Clinical experience suggests that the use of steroids among TBI patients with severe contusions could be effective on intracranial hypertension by acting on pericontusional edema, which usually markedly increases ICP some 24–72 h post trauma. Steroid use is possible under these conditions should all other conventional therapies fail to reduce ICP. Treatment duration of 2–4 days is often enough in these circumstances. In the event that ICP increases in a patient with major brain contusions despite maximal medical therapy and temperature control, our unit uses 120 mg methylprednisolone twice daily for 3 days.

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132 Neuroscience

Albumin There are some experimental arguments showing that albumin reduces pericontusional edema [41,42]. In a model of ischemia-reperfusion in an isolated guinea pig heart model, albumin more effectively prevented fluid extravasation than crystalloid or artificial colloid. This effect may be attributable to an interaction of albumin with the endothelial glycocalyx [43] also present on the endothelial layer of the blood–brain barrier [44].

In human studies, results of systematic albumin administration are disappointing. A posthoc analysis of the SAFE study showed deleterious effects of the systematic albumin administration [45]. The main flaw of this study relies on the a posteriori analysis and on the slight imbalance between the two groups. In a small series, Tomita et al. [46] showed that albumin markedly decreased pericontusional edema assessed on CT. As with steroids, albumin use could be restricted to this subpopulation of severe TBI patients.

Table 1 Algorithm for intracranial hypertension treatment at the Department of Neuro-intensive Care, Pitie´-Salpeˆtrie`re Hospital, Paris, France Emergency care 1. Mannitol 20% (0.7–1.4 g/kg) or hypertonic saline (20%, 40 ml) if pulsatility index on transcranial Doppler above 1.4 and/or mydriasis 2. Immediate correction of hemostasis disorders Fresh frozen plasma if prothrobin time below 70% and platelets if below 70 000/mm3 Prothrombin concentrate complex if patient treated by oral anticoagulant 3. Surgical treatment 3.1 Categorical indications Extradural hematoma above 10 mm on CT Temporal polar hematoma with an ipsilateral anisocory and erasement of the basal cistern on the same side Open skull fractures 3.2 To be discussed on an individual basis Subdural hematoma with a midline shift above 5 mm if: Mydriasis duration below 30 min or reversibility with Mannitol whatever its duration Parenchymal lesions compatible with short term survival and long term relational life Closed skull fractures Drainage of an intraparenchymal hematoma Contusectomy 4. Delay all nonvital surgery Contra-indication to volatile anesthetics Surgery will be performed only after stabilization and under strict monitoring of intracranial pressure Level 1: Mandatory in every patient Homeostasis control (all items must be controlled) Head 308, rectiligne neck without venous return obstacle CPP between 65 and 75 mmHg Normovolemia Normalization of left ventricular function Sedation for adaptation to mechanical ventilation (combining sufentanil þ midazolam) PaCO2 35–40 mmHg SaO2 above 97% Temperature between 36.5 and 37.5 8C by paracetamol  automatic cooling blanket Glycemia between 5.5 and 7.5 mmol/l Natremia between 140 and155 mmol/l Diagnostic and treatment of a cerebral salt wasting Prevention of seizure (levetiracetam 500 mg every 8 h) Transfusion to maintain the hemoglobin level above 8 g/dl External ventricular drainage for cerebrospinal fluid drainage and ICP measurement Level 2: If ICP above 20–25 mmHg and/or pulsatility index on transcranial Doppler above 1.4 after level 1 completion Go to the next item if ICP is not controlled with the previous one Cerebral CT-scan will be performed to exclude new surgical lesion 2.1 Nursing without mobilization 2.2. Intraparenchymal catheter for ICP monitoring and continuous CSF drainage by the external ventricular drain 2.3. Increase sedation and add propofol (measure pH daily and triglycerides serum every 48 h – stop propofol infusion if metabolic acidosis, hyperkaliemia, renal insufficiency, rhabdomyolysis or triglycerides level above 4 mmol/l). 2.4a. Contusion volume below 20 ml: hypertonic saline and/or increase PPC above 70 mmHg 2.4b. Contusion volume above 20 ml: Methylprednisolone 120 mg every 12 h (3 days) Consider albumin administration 2.5. Hypothermia at 35–36.5 8C 2.6. Transfusion to maintain the hemoglobin level above 10 g/dl Level 3: If ICP not controlled at level 2 Decrease temperature step by step according to ICP response (control kaliemia every 6 h) Pharmacologic coma with barbiturates (low doses in addition to midazolam and propofol, and mandatory EEG monitoring) Consider surgical therapy (lobectomy, decompressive hemicraniectomy) CPP, cerebral perfusion pressure; ICP, intracranial pressure; CSF, cerebrospinal fluid

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Treatment of intracranial hypertension Lescot et al. 133

Conclusion One of the key issues is to consider that TBI is more likely a syndrome than a disease. After trauma, the traumatized brain is characterized by a huge pathophysiological heterogeneity. A single, unique therapy cannot be efficient for all the different types of brain trauma. This could partly explain why systematic use of an increased CPP approach, hypothermia, corticosteroids and albumin all failed to demonstrate any positive effect in large multicenter trials. Indeed, the volume of contused brain seems to reflect the state of the blood–brain barrier and the preservation of the cerebral autoregulation which determine the choice of therapy. The algorithm in Table 1, used in our institution, reflects the use of a therapeutic stratification according both to the therapy side effects and the presence (or otherwise) of a high contusional volume.

15 Kerr ME, Weber BB, Sereika SM, et al. Dose response to cerebrospinal fluid drainage on cerebral perfusion in traumatic brain-injured adults. Neurosurg Focus 2001; 11:E1. 16 Korinek AM, Reina M, Boch AL, et al. Prevention of external ventricular drain– related ventriculitis. Acta Neurochir (Wien) 2005; 147:39–45; discussion 45–6. 17 Cao M, Lisheng H, Shouzheng S. Resolution of brain edema in severe brain injury at controlled high and low intracranial pressures. J Neurosurg 1984; 61:707–712. 18 Reulen HJ, Tsuyumu M, Tack A, et al. Clearance of edema fluid into cerebrospinal fluid. A mechanism for resolution of vasogenic brain edema. J Neurosurg 1978; 48:754–764. 19 Mendelow AD, Teasdale GM, Russell T, et al. Effect of mannitol on cerebral blood flow and cerebral perfusion pressure in human head injury. J Neurosurg 1985; 63:43–48. 20 Sakowitz OW, Stover JF, Sarrafzadeh AS, et al. Effects of mannitol bolus  administration on intracranial pressure, cerebral extracellular metabolites, and tissue oxygenation in severely head-injured patients. J Trauma 2007; 62:292– 298. This prospective observational study confirms that Mannitol efficiently reduces increased ICP but does not affect cerebral oxygenation. 21 Hartl R, Ghajar J, Hochleuthner H, Mauritz W. Hypertonic/hyperoncotic saline reliably reduces ICP in severely head-injured patients with intracranial hypertension. Acta Neurochir Suppl (Wien) 1997; 70:126–129. 22 Suarez JI, Qureshi AI, Bhardwaj A, et al. Treatment of refractory intracranial hypertension with 23.4% saline. Crit Care Med 1998; 26:1118–1122.

References and recommended reading Papers of particular interest, published within the annual period of review, have been highlighted as:  of special interest  of outstanding interest Additional references related to this topic can also be found in the Current World Literature section in this issue (pp. 218–219). 1

Narayan RK, Kishore PR, Becker DP, et al. Intracranial pressure: to monitor or not to monitor? A review of our experience with severe head injury. J Neurosurg 1982; 56:650–659.

Stocchetti N, Colombo A, Ortolano F, et al. Time course of intracranial hypertension after traumatic brain injury. J Neurotrauma 2007; 24:1339– 1346. This retrospective analysis reports that half of the patients had their highest mean ICP during the first 3 days after TBI while 25% had highest mean ICP after day 5.



Brain Trauma Foundation, American Association of Neurological Surgeons, Congress of Neurological Surgeons, Joint Section on Neurotrauma and Critical Care and AANS/CNS. Guidelines for the management of severe traumatic brain injury. VI. Indications for intracranial pressure monitoring. J Neurotrauma 2007; 24 Suppl 1:S37–S44.


Marmarou A, Anderson R, Ward JD. Impact of ICP instability and hypotension an outcome in patients with severe head trauma. J Neurosurg 1991; 75:s59–s66.


Balestreri M, Czosnyka M, Hutchinson P, et al. Impact of intracranial pressure and cerebral perfusion pressure on severe disability and mortality after head injury. Neurocrit Care 2006; 4:8–13.


Eisenberg HM, Frankowski RF, Contant CF, et al. High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury. J Neurosurg 1988; 69:15–23.


Saul TG, Ducker TB. Effect of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury. J Neurosurg 1982; 56:498–503.


Timofeev I, Hutchinson PJ. Outcome after surgical decompression of severe traumatic brain injury. Injury 2006; 37:1125–1132.


Patel HC, Menon DK, Tebbs S, et al. Specialist neurocritical care and outcome from head injury. Intensive Care Med 2002; 28:547–553.

10 Pinaud M, Lelausque JN, Chetanneau A, et al. Effects of propofol on cerebral hemodynamics and metabolism in patients with brain trauma. Anesthesiology 1990; 73:404–409. 11 Wijdicks EF, Nyberg SL. Propofol to control intracranial pressure in fulminant hepatic failure. Transplant Proc 2002; 34:1220–1222. 12 Kelly DF, Goodale DB, Williams J, et al. Propofol in the treatment of moderate and severe head injury: a randomized, prospective double-blinded pilot trial. J Neurosurg 1999; 90:1042–1052. 13 Cremer OL, Moons KG, Bouman EA, et al. Long-term propofol infusion and cardiac failure in adult head-injured patients. Lancet 2001; 357:117–118. 14 Devlin JW, Lau AK, Tanios MA. Propofol-associated hypertriglyceridemia and pancreatitis in the intensive care unit: an analysis of frequency and risk factors. Pharmacotherapy 2005; 25:1348–1352.

23 Saltarini M, Massarutti D, Baldassarre M, et al. Determination of cerebral water content by magnetic resonance imaging after small volume infusion of 18% hypertonic saline solution in a patient with refractory intracranial hypertension. Eur J Emerg Med 2002; 9:262–265. 24 Lescot T, Degos V, Zouaoui A, et al. Opposed effects of hypertonic saline on contusions and noncontused brain tissue in patients with severe traumatic brain injury. Crit Care Med 2006; 34:3029–3033. 25 Rosner MJ, Rosner SD, Johnson AH. Cerebral perfusion pressure: management protocol and clinical results [see comments]. J Neurosurg 1995; 83:949–962. 26 Grande PO, Asgeirsson B, Nordstrom CH. Physiologic principles for volume regulation of a tissue enclosed in a rigid shell with application for the injured brain. J Trauma 1997; 42:S23–S31. 27 Grande PO. The ‘Lund Concept’ for the treatment of severe head trauma – physiological principles and clinical application. Intensive Care Med 2006; 32:1475–1484. 28 Robertson CS. Management of cerebral perfusion pressure after traumatic brain injury. Anesthesiology 2001; 95:1513–1517. 29 Howells T, Elf K, Jones PA, et al. Pressure reactivity as a guide in the treatment of cerebral perfusion pressure in patients with brain trauma. J Neurosurg 2005; 102:311–317. 30 Muller M, Bianchi O, Erulku S, et al. Brain lesion size and phase shift as an index of cerebral autoregulation in patients with severe head injury. Acta Neurochir (Wien) 2003; 145:643–647; discussion 647–648. 31 Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002; 346:549–556. 32 Clifton GL, Miller ER, Choi SC, et al. Lack of effect of induction of hypothermia after acute brain injury. N Engl J Med 2001; 344:556–563. 33 Polderman KH, Tjong Tjin Joe R, Peerdeman SM, et al. Effects of therapeutic hypothermia on intracranial pressure and outcome in patients with severe head injury. Intensive Care Med 2002; 28:1563–1573. 34 McIntyre LA, Fergusson DA, Hebert PC, et al. Prolonged therapeutic hypothermia after traumatic brain injury in adults: a systematic review. Jama 2003; 289:2992–2999. 35 Henderson WR, Dhingra VK, Chittock DR, et al. Hypothermia in the management of traumatic brain injury. A systematic review and meta-analysis. Intensive Care Med 2003; 29:1637–1644. 36 Polderman KH. Application of therapeutic hypothermia in the ICU: opportunities and pitfalls of a promising treatment modality. Part 1: Indications and evidence. Intensive Care Med 2004; 30:556–575. 37 Polderman KH. Application of therapeutic hypothermia in the intensive care unit. Opportunities and pitfalls of a promising treatment modality – Part 2: Practical aspects and side effects. Intensive Care Med 2004; 30:757–769. 38 Kaal EC, Vecht CJ. The management of brain edema in brain tumors. Curr Opin Oncol 2004; 16:593–600.

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134 Neuroscience 39 De Gans J, van de Beek D. Dexamethasone in adults with bacterial meningitis. N Engl J Med 2002; 347:1549–1556. 40 Roberts I, Yates D, Sandercock P, et al. Effect of intravenous corticosteroids on death within 14 days in 10008 adults with clinically significant head injury (MRC CRASH trial): randomised placebo-controlled trial. Lancet 2004; 364:1321–1328. 41 Elliott MB, Jallo JJ, Gaughan JP, Tuma RF. Effects of crystalloid-colloid solutions on traumatic brain injury. J Neurotrauma 2007; 24:195–202. 42 Belayev L, Alonso OF, Huh PW, et al. Posttreatment with high-dose albumin reduces histopathological damage and improves neurological deficit following fluid percussion brain injury in rats. J Neurotrauma 1999; 16:445–453.

43 Jacob M, Bruegger D, Rehm M, et al. Contrasting effects of colloid and crystalloid resuscitation fluids on cardiac vascular permeability. Anesthesiology 2006; 104:1223–1231. 44 Vogel J, Sperandio M, Pries AR, et al. Influence of the endothelial glycocalyx on cerebral blood flow in mice. J Cereb Blood Flow Metab 2000; 20:1571– 1578. 45 Myburgh J, Cooper J, Finfer S, et al. Saline or albumin for fluid resuscitation in patients with traumatic brain injury. N Engl J Med 2007; 357:874– 884. 46 Tomita H, Ito U, Tone O, et al. High colloid oncotic therapy for contusional brain edema. Acta Neurochir Suppl (Wien) 1994; 60:547–549.

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Treatment of intracranial hypertension

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