Prévention des séquelles de la réanimation encéphalique

Prévention des séquelles de la réanimation encéphalique

Les séquelles motrices et les limitations articulaires sont au premier plan des préoccupations. Le délai de transfert en centre de rééducation des patients souffrant d’un coma est souvent long. Il est donc très important de prévenir et de traiter, dès la réanimation, les séquelles physiques liées à ce coma. L’hypertonie de la phase de réveil des comas est difficile à traiter malgré les myorelaxants (baclofène). La kinésithérapie douce est le seul moyen de retarder les rétractions tendineuses. Il est inutile et néfaste de lutter activement contre la rétraction en maintenant un membre en extension par des attaches. Ceci ne fait qu’augmenter l’hypertonie sans modifier l’évolution. En revanche, lorsque l’hypertonie est limitée à quelques groupes musculaires, une myorelaxation à l’aide de toxine botulique peut être indiquée. L’effet est temporaire (quelques mois) et permet d’abolir la spasticité dans le muscle traité. Les para-ostéoarthropathies (POA) sont une autre cause fréquente de limitation articulaire. Elles se manifestent le plus souvent au niveau des grosses articulations par un syndrome inflammatoire local.

L’augmentation des phosphatases alcalines, voire la scintigraphie osseuse permettent de faire le diagnostic. Le traitement consiste à arrêter la mobilisation de l’articulation atteinte et à administrer des anti-inflammatoires.

Les séquelles cutanées sont actuellement assez facilement prévenues par le nursing associé à des matelas « antiescarres » permettant la répartition des pressions d’appui. Les escarres peuvent encore survenir chez les patients les plus graves et sont en général liées à l’apparition d’une dénutrition sévère.

Les atteintes oculaires sont à craindre lorsqu’il existe une paralysie faciale. L’absence d’occlusion de la paupière peut créer en 24 heures une kératite, point de départ d’une infection. En l’absence de récupération rapide, une tarsorraphie est nécessaire.

Enfin, la sonde gastrique aggrave les troubles de la déglutition et crée des lésions d’oesophagite. Lorsque la durée prévisible de la nutrition entérale est supérieure à 1 mois, une gastrostomie d’alimentation (le plus souvent pratiquée par voie endoscopique) est souhaitable.

Conclusion

Il ne fait pas de doute que la réanimation des patients ayant une atteinte neurologique ou neurochirurgicale présente des spécificités nombreuses. L’hyperspécialisation des réanimateurs pour s’occuper de ces patients n’est pas possible partout. Elle n’est sûrement pas souhaitable si elle conduit à un isolement vis-à-vis des autres aspects de la réanimation. Cependant, la réanimation encéphalique ne se limite pas à celle du traumatisé crânien. De plus en plus de patients sont adressés pour d’autres pathologies, en particulier l’AVC. Contrairement à l’attitude défaitiste du passé, de nouveaux moyens thérapeutiques médicaux et chirurgicaux ont permis d’améliorer significativement le pronostic et justifient de s’investir dans l’amélioration de nos connaissances médicales sur ces pathologies. Il n’est bien sûr pas possible de remplacer le neurologue, le neurochirurgien ou le neuroradiologue mais le fait de partager les connaissances de base sur les mécanismes de l’aggravation neurologique des patients permet d’améliorer la qualité de la coopération entre les différents acteurs. Comme dans les autres domaines de la réanimation, le travail en équipe est la clé du succès thérapeutique.

“ Points essentiels

- La meilleure évaluation neurologique initiale et le meilleur monitorage de l’aggravation neurologique restent l’examen clinique. Les avantages d’une sédation profonde sont à mettre en balance avec la perte de cet élément essentiel de la surveillance.

- Parmi les nombreux moyens de monitorage neurologique instrumental, la PIC et le Doppler transcrânien sont devenus des éléments incontournables de la réanimation des patients neurochirurgicaux.

- Les complications extracérébrales (cardiaques, pulmonaires, septiques, métaboliques) surviennent chez 40 % à 60 % des patients souffrant d’une atteinte encéphalique aiguë en réanimation.

- La correction des troubles de la coagulation est essentielle avant tout geste neurochirurgical.

- Les traitements médicaux de l’HIC ne doivent pas retarder un traitement chirurgical. Le raccourcissement des délais entre l’apparition de signes d’engagement et la décompression chirurgicale est le meilleur garant d’une évolution favorable.

- À la phase aiguë, l’objectif thérapeutique médical est de limiter au maximum la fréquence des épisodes d’ischémie cérébrale pour préserver la zone de « pénombre ischémique ».

- Le respect d’objectifs généraux de pression de perfusion, de ventilation, d’oxygénation, de transfusion est certainement important. Mais des objectifs thérapeutiques individuels, basés sur les données du monitorage, doivent aussi être intégrés dans les algorithmes de traitement.

- À côté de la traumatologie crânienne, la réanimation des AVC (hémorragiques et ischémiques) a connu des avancées majeures ces dernières années. Le réanimateur qui prend en charge ces pathologies doit connaître l’ensemble des possibilités thérapeutiques médicales et chirurgicales et leurs complications.

- Une coopération permanente avec les neurochirurgiens, les neuroradiologues et les neurologues à la phase aiguë est indispensable.

- La prévention des séquelles physiques débute dès le séjour en réanimation et justifie d’établir un réseau de soins avec la rééducation fonctionnelle.

 Références

[1] Diringer M, Edwards D. Admission to a neurologic/neurosurgical intensive care unit is associated with reduced mortality rate after intracerebral hemorrhage. Crit Care Med 2001;29:635-40.

[2] Mirski MA, Chang CW, Cowan R. Impact of a neuroscience intensive care unit on neurosurgical patient outcomes and cost of care: evidencebased support for an intensivist-directed specialty ICU model of care. J Neurosurg Anesthesiol 2001;13:83-92.

[3] Barlas I, Oropello JM, Benjamin E. Neurologic complications in intensive care. Curr Opin Crit Care 2001;7:68-73.

[4] Bleck TP, Smith MC, Pierre-Louis SJ, Jares JJ, Murray J, Hansen CA. Neurologic complications of critical medical illnesses. Crit Care Med 1993;21:98-103.

[5] Clavier N. Évaluation clinique et paraclinique d’un coma. In: Conférences d’actualisation. Paris: SFAR-Elsevier; 1997. p. 417-28.

[6] Vargas F, Hilbert G, Gruson D, Valentino R, Gbikpi BG, Cardinaud J. Fulminant Guillain-Barré syndrome mimicking cerebral death: case report and literature review. Intensive Care Med 2000;26:623-7.

[7] Anonymous. Prise en charge des traumatisés crâniens graves à la phase précoce. Recommandations pour la pratique clinique. Ann Fr Anesth Reanim 1999;18:11-41.

[8] NamenA, Ely E,Tatter S, Case L, Lucia M, SmithA, et al. Predictors of successful extubation in neurosurgical patients. Am J Respir Crit Care Med 2001;163:658-64.

[9] Shibata Y, Meguro K, Narushima K, Shibuya F, Doi M, Kikuchi Y. Malignant lymphoma of the central nervous system presenting with central neurogenic hyperventilation. Case report. J Neurosurg 1992; 76:696-700.

[10] Jaeckle K, Digre K, Jones C, Bailey P, McMahill P. Central neurogenic hyperventilation: pharmacologic intervention with morphine sulfate and correlative analysis of respiratory, sleep, and ocular motor dysfunction. Neurology 1990;40:1715-20.

[11] Qureshi A, Suarez J, Parekh P, Bhardwaj A. Prediction and timing of tracheostomy in patients with infratentorial lesions requiring mechanical ventilatory support. Crit Care Med 2000;28:1383-7.

[12] Messina AV, Chernik NL. Computer tomography: the ″resolving″ intracerebral hemorrhage. Radiology 1976;118:609-13.

[13] Camboulives J, Bruder N. Anesthésie pour IRM. Paris: Elsevier; 2004.

[14] Bruder N, N’Zoghe P, Graziani N, Pelissier D, Grisoli F, Francois G.A comparison of extradural and intraparenchymatous intracranial pressures in head injured patients. Intensive Care Med 1995;21:850-2.

[15] Bruder N, Cohen B, Pellissier D, Francois G.The effect of hemodilution on cerebral blood flow velocity in anesthetized patients. Anesth Analg 1998;86:320-4.

[16] Giller C, Bowman G, Dyer H, Mootz L, KrippnerW. Cerebral arterial diameters during changes in blood pressure and carbon dioxide during craniotomy. Neurosurgery 1993;32:737-42.

[17] Ducrocq X, Braun M, Debouverie M, Junges C, Hummer M, Vespignani H. Brain death and transcranial Doppler: experience in 130 cases of brain dead patients. J Neurol Sci 1998;160:41-6.

[18] Stocchetti N, Paparella A, Bridelli F, Bacchi M, Piazza P, Zuccoli P. Cerebral venous oxygen saturation studied with bilateral samples in the internal jugular veins. Neurosurgery 1994;34:38-43.

[19] Ter Minassian A, Poirier N, Pierrot M, Menei P, Granry JC, Ursino M, et al. Correlation between cerebral oxygen saturation measured by nearinfrared spectroscopy and jugular oxygen saturation in patients with severe closed head injury. Anesthesiology 1999;91:985-90.

[20] Vespa P, NenovV, Nuwer M. Continuous EEG monitoring in the intensive care unit: early findings and clinical efficacy. J Clin Neurophysiol 1999;16:1-3.

[21] Vespa P, Nuwer M, Nenov V, Ronne-Engstrom E, Hovda D, Bergsneider M, et al. Increased incidence and impact of nonconvulsive and convulsive seizures after traumatic brain injury as detected by continuous electroencephalographic monitoring. J Neurosurg 1999;91: 750-60.

[22] Solenski N, Haley E, Kassell N, Kongable G, Germanson T, Truskowski L, et al. Medical complications of aneurysmal subarachnoid hemorrhage: a report of the multicenter, cooperative aneurysm study. Participants of the Multicenter CooperativeAneurysm Study. Crit Care Med 1995;23:1007-17.

[23] Piek J, Chesnut R, Marshall L, Van BC, Klauber M, Blunt B, et al. Extracranial complications of severe head injury. J Neurosurg 1992; 77:901-7.

[24] GruberA, ReinprechtA, Illievich U, Fitzgerald R, DietrichW, CzechT, et al. Extracerebral organ dysfunction and neurologic outcome after aneurysmal subarachnoid hemorrhage. Crit Care Med 1999;27: 505-14.

[25] Johnston KC, Li JY, Lyden PD, Hanson SK, Feasby TE, Adams RJ, et al. Medical and neurological complications of ischemic stroke: experience from the RANTTAS trial. RANTTAS Investigators. Stroke 1998;29:447-53.

[26] Tong C, Konig MW, Roberts PR, Tatter SB, Li XH. Autonomic dysfunction secondary to intracerebral hemorrhage. Anesth Analg 2000;91:1450-1.

[27] Chesnut RM, Gautille T, Blunt BA, Klauber MR, Marshall LF. Neurogenic hypotension in patients with severe head injuries. J Trauma 1998;44:958-63.

[28] Yoshikawa D, Hara T, Takahashi K, Morita T, Goto F. An association between QTc prolongation and left ventricular hypokinesis during sequential episodes of subarachnoid hemorrhage. Anesth Analg 1999; 89:962-4.

[29] Zaroff JG, Rordorf GA, Ogilvy CS, Picard MH. Regional patterns of left ventricular systolic dysfunction after subarachnoid hemorrhage: evidence for neurally mediated cardiac injury. J Am Soc Echocardiogr 2000;13:774-9.

[30] Wijdicks EF, Vermeulen M, ten Haaf JA, Hijdra A, Bakker WH, van Gijn J. Volume depletion and natriuresis in patients with a ruptured intracranial aneurysm. Ann Neurol 1985;18:211-6.

[31] Oppenheimer SM, Kedem G, Martin WM. Left-insular cortex lesions perturb cardiac autonomic tone in humans. Clin Auton Res 1996;6: 131-40.

[32] Friedman JA, Pichelmann MA, Piepgras DG, McIver JI, Toussaint 3rd LG, McClelland RL, et al. Pulmonary complications of aneurysmal subarachnoid hemorrhage. Neurosurgery 2003;52: 1025-31.

[33] Schievink WI, Wijdicks EF, Parisi JE, Piepgras DG, Whisnant JP. Sudden death from aneurysmal subarachnoid hemorrhage. Neurology 1995;45:871-4.

[34] Bracco D, Favre JB, Ravussin P. Les hyponatrémies en neuroréanimation : syndrome de perte de sel et sécrétion inappropriée d’hormone antidiurétique. Ann Fr Anesth Reanim 2001;20:203-12.

[35] Qureshi AI, Suri MF, Sung GY, Straw RN, Yahia AM, Saad M, et al. Prognostic significance of hypernatremia and hyponatremia among patients with aneurysmal subarachnoid hemorrhage. Neurosurgery 2002;50:749-55.

[36] Hasan D,Wijdicks EF,Vermeulen M. Hyponatremia is associated with cerebral ischemia in patients with aneurysmal subarachnoid hemorrhage. Ann Neurol 1990;27:106-8.

[37] Boulard G. Sodium, osmolarité plasmatique et volume cérébral. Ann Fr Anesth Reanim 2001;20:196-202.

[38] Zornow M, Todd M, Moore S. The acute cerebral effects of changes in plasma osmolality and oncotic pressure. Anesthesiology 1987;67: 936-41.

[39] Sviri GE, Feinsod M, Soustiel JF. Brain natriuretic peptide and cerebral vasospasm in subarachnoid hemorrhage. Clinical and TCD correlations. Stroke 2000;31:118-22.

[40] Hans P, Bonhomme V, Damas F. Les hypernatrémies en pathologie neurochirurgicale. Ann Fr Anesth Reanim 2001;20:213-8.

[41] Lanier WL, Stangland KJ, Scheithauer BW, Milde JH, Michenfelder JD. The effects of dextrose infusion and head position on neurologic outcome after complete cerebral ischemia in primates: examination of a model. Anesthesiology 1987;66:39-48.

[42] Diaz-Parejo P, Stahl N, Xu W, Reinstrup P, Ungerstedt U, Nordstrom CH. Cerebral energy metabolism during transient hyperglycemia in patients with severe brain trauma. Intensive CareMed 2003;29:544-50.

[43] Lam AM, Winn HR, Cullen BF, Sundling N. Hyperglycemia and neurological outcome in patients with head injury. J Neurosurg 1991; 75:545-51.

[44] Lanzino G, Kassell NF, Germanson T, Truskowski L, AlvesW. Plasma glucose levels and outcome after aneurysmal subarachnoid hemorrhage. J Neurosurg 1993;79:885-91.

[45] Ginsberg MD, Busto R. Combating hyperthermia in acute stroke: a significant clinical concern. Stroke 1998;29:529-34.

[46] SanoT,DrummondJ, Patel P, Grafe M,Watson J, Cole D.Acomparison of the cerebral protective effects of isoflurane and mild hypothermia in a model of incomplete forebrain ischemia in the rat. Anesthesiology 1992;76:221-8.

[47] Verlooy J, Heytens L, Veeckmans G, Selosse P. Intracerebral temperature monitoring in severely head injured patients. Acta Neurochir (Wien) 1995;134:76-8.

[48] Mellergard P. Monitoring of rectal, epidural, and intraventricular temperature in neurosurgical patients. Acta Neurochir (Wien) 1994; 60(suppl):485-7.

[49] Rossi S, Zanier ER, Mauri I, Columbo A, Stocchetti N. Brain temperature, body core temperature, and intracranial pressure in acute cerebral damage. J Neurol Neurosurg Psychiatry 2001;71:448-54.

[50] Kilpatrick MM, Lowry DW, Firlik AD, Yonas H, Marion DW. Hyperthermia in the neurosurgical intensive care unit. Neurosurgery 2000;47:850-6.

[51] Stocchetti N, Rossi S, Zanier ER, Colombo A, Beretta L, Citerio G. Pyrexia in head-injured patients admitted to intensive care. Intensive Care Med 2002;28:1555-62.

[52] Oliveira-Filho J, Ezzeddine MA, Segal AZ, Buonanno FS, Chang Y, Ogilvy CS, et al. Fever in subarachnoid hemorrhage: relationship to vasospasm and outcome. Neurology 2001;56:1299-304.

[53] Castillo J, Davalos A, Marrugat J, Noya M. Timing for fever-related brain damage in acute ischemic stroke. Stroke 1998;29:2455-60.

[54] Wang Y, Lim LL, Levi C, Heller RF, Fisher J. Influence of admission body temperature on stroke mortality. Stroke 2000;31:404-9.

[55] Gando S, Tedo I, Kubota M. Posttrauma coagulation and fibrinolysis. Crit Care Med 1992;20:594-600.

[56] Stein SC, Chen XH, Sinson GP, Smith DH. Intravascular coagulation: a major secondary insult in nonfatal traumatic brain injury. J Neurosurg 2002;97:1373-7.

[57] Fredriksson K, Norrving B, Stromblad LG. Emergency reversal of anticoagulation after intracerebral hemorrhage. Stroke 1992;23:972-7.

[58] Crawley F, Bevan D, Wren D. Management of intracranial bleeding associated with anticoagulation: balancing the risk of further bleeding against thromboembolism from prosthetic heart valves. J Neurol Neurosurg Psychiatry 2000;69:396-8.

[59] Cannegieter SC, Rosendaal FR, Briet E. Thromboembolic and bleeding complications in patients with mechanical heart valve prostheses. Circulation 1994;89:635-41.

[60] Wijdicks EF, Schievink WI, Brown RD, Mullany CJ. The dilemma of discontinuation of anticoagulation therapy for patients with intracranial hemorrhage and mechanical heart valves. Neurosurgery 1998;42: 769-73.

[61] Wijdicks EF, Schievink WI, Brown RD, Mullany CY. Early anticoagulation in patients with prosthetic heart valves and intracerebral hematoma. Neurology 1999;52:676-7.

[62] Sirvent J, Torres A, Vidaur L, Armengol JdB, Bonet A. Tracheal colonisation within 24 h of intubation in patients with head trauma: risk factor for developing early-onset ventilator-associated pneumonia. Intensive Care Med 2000;26:1369-72.

[63] Akca O, Koltka K, Uzel S, Cakar N, Pembeci K, Sayan M, et al. Risk factors for early-onset, ventilator-associated pneumonia in critical care patients: selected multiresistant versus nonresistant bacteria. Anesthesiology 2000;93:638-45.

[64] CoplinW, Pierson D, Cooley K, Newell D, Rubenfeld G. Implications of extubation delay in brain-injured patients meeting standard weaning criteria. Am J Respir Crit Care Med 2000;161:1530-6.

[65] De Jonghe B, Cook D, Appere-De-Vecchi C, Guyatt G, Meade M, Outin H. Using and understanding sedation scoring systems: a systematic review. Intensive Care Med 2000;26:275-85.

[66] Riker R, Picard J, Fraser G. Prospective evaluation of the Sedation- Agitation Scale for adult critically ill patients. Crit Care Med 1999;27: 1325-9.

[67] Albanese J, Viviand X, Potie F, Rey M, Alliez B, Martin C. Sufentanil, fentanyl, and alfentanil in head trauma patients: a study on cerebral hemodynamics. Crit Care Med 1999;27:407-11.

[68] Carrasco G, Molina R, Costa J. Propofol vs midazolam in short-, medium-, and long-term sedation of critically ill patients: a cost benefit analysis. Chest 1993;103:557-64.

[69] Cannon ML, Glazier SS, Bauman LA. Metabolic acidosis, rhabdomyolysis, and cardiovascular collapse after prolonged propofol infusion. J Neurosurg 2001;95:1053-6.

[70] Cray SH, Robinson BH, Cox PN. Lactic acidemia and bradyarrythmia in a child sedated with propofol. Crit Care Med 1998;26:2087-92.

[71] Cremer OL, Moons KG, Bouman EA, Kruijswijk JE, de Smet AM, Kalkman CJ. Long-term propofol infusion and cardiac failure in adult head-injured patients. Lancet 2001;357:117-8.

[72] Anonymous. Sédation, analgésie, curarisation en réanimation. Recommandations pour la pratique clinique. Paris: SFAR-Elsevier; 2000.

[73] Cammarano W, Pittet J, Weitz S, Schlobohm R, Marks J. Acute withdrawal syndrome related to the administration of analgesic and sedative medications in adult intensive care unit patients. Crit Care Med 1998;26:676-84.

[74] Katz R, Kelly H, Hsi A. Prospective study on the occurrence of withdrawal in critically ill children who receive fentanyl by continuous infusion. Crit Care Med 1994;22:763-7.

[75] Bruder N, Raynal M, Pellissier D, Courtinat C, Francois G. Influence of body temperature, with or without sedation, on energy expenditure in severe head-injured patients. Crit Care Med 1998;26:568-72.

[76] Rapp R, Young B, Twyman D, Bivins B, Haack D, Tibbs P, et al. The favorable effect of early parenteral feeding on survival in head-injured patients. J Neurosurg 1983;58:906-12.

[77] Bruder N, Dumont JC. Nutrition artificielle du traumatisé crânien. Ann Fr Anesth Reanim 1998;17:186-91.

[78] Bruder N, Dumont JC, Francois G. Evolution of energy expenditure and nitrogen excretion in severe head-injured patients. Crit Care Med 1991;19:43-8.

[79] Kudsk K, Croce M, FabianT, Minard G,Tolley E, Poret H, et al. Enteral versus parenteral feeding. Effects on septic morbidity after blunt and penetrating abdominal trauma. Ann Surg 1992;215:503-11.

[80] Moore F, Feliciano D, Andrassy R, McArdle A, Booth F, MorgensteinWT, et al. Early enteral feeding, compared with parenteral, reduces postoperative septic complications. The results of a metaanalysis. Ann Surg 1992;216:172-83.

[81] Ott L, Young B, Phillips R, McClain C, Adams L, Dempsey R, et al. Altered gastric emptying in the head-injured patient: relationship to feeding intolerance. J Neurosurg 1991;74:738-42.

[82] Qureshi AI, Geocadin RG, Suarez JI, Ulatowski JA. Long-term outcome after medical reversal of transtentorial herniation in patients with supratentorial mass lesions. Crit Care Med 2000;28:1556-64.

[83] Krieger DW, De Georgia MA, Abou-Chebl A, Andrefsky JC, Sila CA, Katzan IL, et al. Cooling for acute ischemic brain damage (cool aid): an open pilot study of induced hypothermia in acute ischemic stroke. Stroke 2001;32:1847-54.

[84] Marion D, Penrod L, Kelsey S, ObristW, Kochanek P, Palmer A, et al. Treatment of traumatic brain injury with moderate hypothermia.NEngl J Med 1997;336:540-6.

[85] Polderman KH, Tjong Tjin Joe R, Peerdeman SM, Vandertop WP, GirbesAR. Effects of therapeutic hypothermia on intracranial pressure and outcome in patients with severe head injury. Intensive Care Med 2002;28:1563-73.

[86] Shiozaki T, Sugimoto H, Taneda M, Yoshida H, Iwai A, Yoshioka T, et al. Effect of mild hypothermia on uncontrollable intracranial hypertension after severe head injury. J Neurosurg 1993;79:363-8.

[87] Bernard SA, GrayTW, BuistMD,JonesBM,SilvesterW, Gutteridge G, et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 2002;346:557-63.

[88] Group THACAS. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest. N Engl J Med 2002;346: 549-56.

[89] Cruz J, Minoja G, Okuchi K. Improving clinical outcomes from acute subdural hematomas with the emergency preoperative administration of high-doses of mannitol: a randomized trial. Neurosurgery 2001;49: 864-71.

[90] Cruz J, Minoja G, Okuchi K. Major clinical and physiological benefits of early high-doses of mannitol for intraparenchymal temporal lobe hemorrhages with abnormal pupillary widening: a randomized trial. Neurosurgery 2002;51:628-37.

[91] Polderman KH, Van De Kraats G, Dixon JM, Vandertop WP, Girbes AR. Increases in spinal fluid osmolarity induced by mannitol. Crit Care Med 2003;31:584-90.

[92] Zornow M, Oh Y, Scheller M. A comparison of the cerebral and haemodynamic effects of mannitol and hypertonic saline in an animal model of brain injury. Acta Neurochir (Wien) 1990;51(suppl):324-5.

[93] QureshiAI, Suarez JI. Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension. Crit Care Med 2000;28: 3301-13.

[94] Qureshi AI, Suarez JI, Bhardwaj A. Malignant cerebral edema in patients with hypertensive intracerebral hemorrhage associated with hypertonic saline infusion: a rebound phenomenon? J Neurosurg Anesthesiol 1998;10:188-92.

[95] Mayhall CG,Archer NH,LambVA, SpadoraAC, BaggettJW,Ward JD, et al. Ventriculostomy-related infections.Aprospective epidemiologic study. N Engl J Med 1984;310:553-9.

[96] KorinekAM.Risque infectieux des dérivations ventriculaires externes. Ann Fr Anesth Reanim 1999;18:554-7.

[97] Piek J. Decompressive surgery in the treatment of traumatic brain injury. Curr Opin Crit Care 2002;8:134-8.

[98] ZiaiWC, Port JD, Cowan JA, Garonzik IM, BhardwajA, Rigamonti D. Decompressive craniectomy for intractable cerebral edema: experience of a single center. J Neurosurg Anesthesiol 2003;15:25-32.

[99] Hornig CR, Rust DS, Busse O, Jauss M, Laun A. Space-occupying cerebellar infarction. Clinical course and prognosis. Stroke 1994;25: 372-4.

[100] Mathew P, Teasdale G, Bannan A, Oluoch-Olunya D. Neurosurgical management of cerebellar haematoma and infarct. J Neurol Neurosurg Psychiatry 1995;59:287-92.

[101] Litofsky NS, Chin LS, Tang G, Baker S, Giannotta SL, Apuzzo ML. The use of lobectomy in the management of severe closed-head trauma. Neurosurgery 1994;34:628-32.

[102] Bruder N.Awakening management after neurosurgery for intracranial tumours. Curr Opin Anaesthesiol 2002;15:477-82.

[103] Grillo P, Bruder N, Auquier P, Pellissier D, Gouin F. Esmolol blunts the cerebral blood flow velocity increase during emergence from anesthesia in neurosurgical patients. Anesth Analg 2003;96:1145-9.

[104] Anonymous. Recommandations pour la pratique clinique. Anévrysmes intracrâniens rompus : occlusion par voie endovasculaire versus exclusion par microchirurgie. Paris: ANAES; 2000.

[105] Qureshi AI, Sung GY, Razumovsky AY, Lane K, Straw RN, Ulatowski JA. Early identification of patients at risk for symptomatic vasospasm after aneurysmal subarachnoid hemorrhage. Crit Care Med 2000;28:984-90.

[106] Lysakowski C, Walder B, Costanza MC, Tramer MR. Transcranial Doppler versus angiography in patients with vasospasm due to a ruptured cerebral aneurysm: a systematic review. Stroke 2001;32: 2292-8.

[107] Suarez JI, Qureshi AI, Yahia AB, Parekh PD, Tamargo RJ, Williams MA, 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;30:1348-55.

[108] Stordeur JM, Bruder N, Cantais E, Pellissier D, Levrier O, Gouin F. Monitorage de la saturation veineuse jugulaire en oxygène au cours d’un vasospasme cérébral sévère après hémorragie sousarachnoïdienne. Ann Fr Anesth Reanim 2000;19:111-4.

[109] Rinkel GJ, Feigin VL, Algra A, Vermeulen M, Van Gijn J. Calcium antagonists for aneurysmal subarachnoid haemorrhage. Cochrane Database Syst Rev 2002(4) (CD000277).

[110] Treggiari MM,Walder B, Suter PM, Romand JA. Systematic review of the prevention of delayed ischemic neurological deficits with hypertension, hypervolemia, and hemodilution therapy following subarachnoid hemorrhage. J Neurosurg 2003;98:978-84.

[111] Shimoda M, Oda S, Tsugane R, Sato O. Intracranial complications of hypervolemic therapy in patients with a delayed ischemic deficit attributed to vasospasm. J Neurosurg 1993;78:423-9.

[112] Amin-Hanjani S, Schwartz RB, Sathi S, Stieg PE. Hypertensive encephalopathy as a complication of hyperdynamic therapy for vasospasm: report of two cases. Neurosurgery 1999;44:1113-6.

[113] Polin RS, CoenenVA, Hansen CA, Shin P, BaskayaMK,NandaA, et al. Efficacy of transluminal angioplasty for the management of symptomatic cerebral vasospasm following aneurysmal subarachnoid hemorrhage. J Neurosurg 2000;92:284-90.

[114] Rosenwasser RH, Armonda RA, Thomas JE, Benitez RP, Gannon PM, Harrop J. Therapeutic modalities for the management of cerebral vasospasm: timing of endovascular options. Neurosurgery 1999;44: 975-9.

[115] Broderick JP, Adams Jr. HP, Barsan W, Feinberg W, Feldmann E, Grotta J, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke 1999;30:905-15.

[116] Brott T, Broderick J, Kothari R, Barsan W, Tomsick T, Sauerbeck L, et al. Early hemorrhage growth in patients with intracerebral hemorrhage. Stroke 1997;28:1-5.

[117] Ohwaki K, Yano E, Nagashima H, Hirata M, Nakagomi T, Tamura A. Blood pressure management in acute intracerebral hemorrhage: relationship between elevated blood pressure and hematoma enlargement. Stroke 2004;35:1364-7.

[118] Qureshi AI, Bliwise DL, Bliwise NG,Akbar MS, Uzen G, Frankel MR. Rate of 24-hour blood pressure decline and mortality after spontaneous intracerebral hemorrhage: a retrospective analysis with a random effects regression model. Crit Care Med 1999;27:480-5.

[119] Kothari RU, Brott T, Broderick JP, Barsan WG, Sauerbeck LR, Zuccarello M, et al. The ABCs of measuring intracerebral hemorrhage volumes. Stroke 1996;27:1304-5.

[120] Mendelow AD, Gregson BA, Fernandes HM, Murray GD, Teasdale GM, Hope DT, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial. Lancet 2005;365:387-97.

[121] Mayer SA, Brun NC, Broderick J, Davis S, Diringer MN, Skolnick BE, et al. Safety and feasibility of recombinant factor VIIa for acute intracerebral hemorrhage. Stroke 2005;36:74-9.

[122] Daverat P, Castel JP, Dartigues JF, Orgogozo JM. Death and functional outcome after spontaneous intracerebral hemorrhage. A prospective study of 166 cases using multivariate analysis. Stroke 1991;22:1-6.

[123] CoplinW,Vinas F, Agris J, Buciuc R, Michael D, Diaz F, et al.Acohort study of the safety and feasibility of intraventricular urokinase for nonaneurysmal spontaneous intraventricular hemorrhage. Stroke 1998; 29:1573-9.

[124] Naff NJ, Carhuapoma JR, Williams MA, Bhardwaj A, Ulatowski JA, Bederson J, et al. Treatment of intraventricular hemorrhage with urokinase: effects on 30-Day survival. Stroke 2000;31:841-7.

[125] Schellinger P, Fiebach J, Mohr A, Ringleb P, Jansen O, Hacke W. Thrombolytic therapy for ischemic stroke-A review. Part II-Intraarterial thrombolysis, vertebrobasilar stroke, phase IV trials, and stroke imaging. Crit Care Med 2001;29(In Process Citation):1819-25.

[126] Group TNIoNDaSr-PSS. Tissue plasminogen activator for acute ischemic stroke. N Engl J Med 1995;333:1581-7.

[127]Wardlaw J,Warlow C, Counsell C. Systematic review of evidence on thrombolytic therapy for acute ischaemic stroke. Lancet 1997;350: 607-14.

[128] HackeW, Brott T, Caplan L, Meier D, Fieschi C, von Kummer R, et al. Thrombolysis in acute ischemic stroke: controlled trials and clinical experience. Neurology 1999;53(7suppl4):S3-S14.

[129] Norris JW, Hachinski VC. Misdiagnosis of stroke. Lancet 1982;1: 328-31.

[130] Furlan A, Higashida R,Wechsler L, Gent M, Rowley H, Kase C, et al. Intra-arterial prourokinase for acute ischemic stroke. The PROACT II study: a randomized controlled trial. Prolyse in Acute Cerebral Thromboembolism. JAMA 1999;282:2003-11.

[131] LeeKY, Heo JH, Lee SI,Yoon PH. Rescue treatment with abciximab in acute ischemic stroke. Neurology 2001;56:1585-7.

[132] Fiorella D, Albuquerque FC, Han P, McDougall CG. Strategies for the management of intraprocedural thromboembolic complications with abciximab (ReoPro). Neurosurgery 2004;54:1089-97.

[133] HeinsiusT, Bogousslavsky J,Van Melle G. Large infarcts in the middle cerebral artery territory. Etiology and outcome patterns. Neurology 1998;50:341-50.

[134] Qureshi AI, Suarez JI, Yahia AM, Mohammad Y, Uzun G, Suri MF, et al. Timing of neurologic deterioration in massive middle cerebral artery infarction: a multicenter review. Crit Care Med 2003;31:272-7.

[135] Berrouschot J, Sterker M, Bettin S, Koster J, Schneider D. Mortality of space-occupying (’malignant’) middle cerebral artery infarction under conservative intensive care. Intensive Care Med 1998;24:620-3.

[136] Hacke W, Schwab S, Horn M, Spranger M, De Georgia M, von Kummer R. ’Malignant’ middle cerebral artery territory infarction: clinical course and prognostic signs. Arch Neurol 1996;53:309-15.

[137] Oppenheim C, SamsonY, Manai R, Lalam T,Vandamme X, Crozier S, et al. Prediction of malignant middle cerebral artery infarction by diffusion-weighted imaging. Stroke 2000;31:2175-81.

[138] Schwab S, SteinerT,AschoffA, Schwarz S, Steiner HH, Jansen O, et al. Early hemicraniectomy in patients with complete middle cerebral artery infarction. Stroke 1998;29:1888-93.

[139] Pranesh MB, Dinesh Nayak S, Mathew V, Prakash B, Natarajan M, Rajmohan V, et al. Hemicraniectomy for large middle cerebral artery territory infarction: outcome in 19 patients. J Neurol Neurosurg Psychiatry 2003;74:800-2.

[140] Carter BS, Ogilvy CS, Candia GJ, Rosas HD, Buonanno F. One-year outcome after decompressive surgery for massive nondominant hemispheric infarction. Neurosurgery 1997;40:1168-75.

[141] Schwab S, Schwarz S, Spranger M, Keller E, Bertram M, Hacke W. Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction. Stroke 1998;29:2461-6.

[142] Azoulay E, Pochard F, Chevret S, Vinsonneau C, Garrouste M, Cohen Y, et al. Compliance with triage to intensive care recommendations. Crit Care Med 2001;29:2132-6.

[143] Joynt GM, Gomersall CD, Tan P, Lee A, Cheng CA, Wong EL. Prospective evaluation of patients refused admission to an intensive care unit: triage, futility and outcome. Intensive Care Med 2001;27: 1459-65.

[144] Sprung CL, Geber D, Eidelman LA, Baras M, Pizov R, NimrodA, et al. Evaluation of triage decisions for intensive care admission. Crit Care Med 1999;27:1073-9.