Tom 15, Nr 3 (2019)
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Opublikowany online: 2019-10-22

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Eksport do Mediów Społecznościowych

Eksport do Mediów Społecznościowych

Obrzęk mózgu u chorych po urazach czaszkowo-mózgowych

Karol Wiśniewski1, Bartłomiej J. Posmyk1, Maciej Bryl1, Ernest J. Bobeff1, Rafał Wójcik1, Patrycja Kowalczyk2, Dariusz J. Jaskólski1
Pol. Przegl. Neurol 2019;15(3):151-160.

Streszczenie

Pourazowy obrzęk mózgu jest jedną z najczęstszych przyczyn wzmożonego ciśnienia śródczaszkowego oraz wtórnego niedokrwienia mózgu u chorych po ciężkim urazie czaszkowo-mózgowym (TBI, traumatic brain injury). Wyróżnia się obrzęk cytotoksyczny, czyli dotyczący komórek, i naczyniopochodny, będący następstwem zaburzeń w przepuszczalności bariery krew–mózg (BBB, bloodbrain barrier), w wyniku których woda gromadzi się w przestrzeni pozakomórkowej. Czynnościowo i anatomiczne zmiany w BBB spowodowane niedokrwieniem dzieli się na trzy etapy: jonowy, obrzęk naczynioruchowy i tak zwaną konwersję krwotoczną (prowadzącą do powstania ogniska krwotocznego, często występującą w letalnym TBI). Szybkie wdrożenie leczenia przeciwobrzękowego po urazie czaszkowo-mózgowym ma zasadnicze znaczenie dla rokowania, zwiększając szanse przeżycia chorych.

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Referencje

  1. Starling EH. On the absorption of fluids from the connective tissue spaces. J Physiol. 1896; 19(4): 312–326.
  2. Go KG. The normal and pathological physiology of brain water. Adv Tech Stand Neurosurg. 1997; 23: 47–142.
  3. Simard JM, Kent T, Chen M, et al. Brain oedema in focal ischaemia: molecular pathophysiology and theoretical implications. Lancet Neurol. 2007; 6(3): 258–268.
  4. Hawkins BT, Davis TP. The blood-brain barrier/neurovascular unit in health and disease. Pharmacol Rev. 2005; 57(2): 173–185.
  5. Marmarou A. A review of progress in understanding the pathophysiology and treatment of brain edema. Neurosurg Focus. 2007; 22(5): E1.
  6. Yang GY, Chen SF, Kinouchi H, et al. Edema, cation content, and ATPase activity after middle cerebral artery occlusion in rats. Stroke. 1992; 23(9): 1331–1336.
  7. Chen M, Dong Y, Simard JM. Functional coupling between sulfonylurea receptor type 1 and a nonselective cation channel in reactive astrocytes from adult rat brain. J Neurosci. 2003; 23(24): 8568–8577.
  8. Chen M, Simard J. Cell swelling and a nonselective cation channel regulated by internal Ca2+ and ATP in native reactive astrocytes from adult rat brain. J Neurosci. 2001; 21(17): 6512–6521.
  9. Simard JM, Chen M, Tarasov KV, et al. Newly expressed SUR1-regulated NC(Ca-ATP) channel mediates cerebral edema after ischemic stroke. Nat Med. 2006; 12(4): 433–440.
  10. Stiefel MF, Marmarou A. Cation dysfunction associated with cerebral ischemia followed by reperfusion: a comparison of microdialysis and ion-selective electrode methods. J Neurosurg. 2002; 97(1): 97–103.
  11. Betz AL, Ennis SR, Schielke GP, et al. Blood-to-brain sodium transport in ischemic brain edema. Adv Neurol. 1990; 52: 73–80.
  12. Young W, Rappaport ZH, Chalif DJ, et al. Regional brain sodium, potassium, and water changes in the rat middle cerebral artery occlusion model of ischemia. Stroke. 1987; 18(4): 751–759.
  13. Klatzo I. Pathophysiological aspects of brain edema. Acta Neuropathol. 1987; 72(3): 236–239.
  14. Jaillard A, Cornu C, Durieux A, et al. Hemorrhagic transformation in acute ischemic stroke. The MAST-E study. MAST-E Group. Stroke. 1999; 30(7): 1326–1332.
  15. Bouma GJ, Muizelaar JP. Cerebral blood flow, cerebral blood volume, and cerebrovascular reactivity after severe head injury. J Neurotrauma. 1992; 9(Suppl 1): 333–348.
  16. Roh D, Soojin P. Brain multimodality monitoring: updated perspectives. Curr Neurol Neurosci Rep. 2016; 16(6): 56.
  17. Thrane AS, Rangroo Thrane V, Nedergaard M. Drowning stars: reassessing the role of astrocytes in brain edema. Trends Neurosci. 2014; 37(11): 620–628.
  18. Iliff JJ, Nedergaard M. Is there a cerebral lymphatic system? Stroke. 2013; 44(6 Suppl 1): S93–S95.
  19. Xie L, Kang H, Xu Q, et al. Sleep drives metabolite clearance from the adult brain. Science. 2013; 342(6156): 373–377.
  20. Yang L, Kress BT, Weber HJ, et al. Evaluating glymphatic pathway function utilizing clinically relevant intrathecal infusion of CSF tracer. J Transl Med. 2013; 11: 107.
  21. Iliff JJ, Wang M, Liao Y, et al. A paravascular pathway facilitates CSF flow through the brain parenchyma and the clearance of interstitial solutes, including amyloid β. Sci Transl Med. 2012; 4(147): 147ra111.
  22. Cherian I, Beltran M, Kasper EM, et al. Exploring the Virchow-Robin spaces function: a unified theory of brain diseases. Surg Neurol Int. 2016; 7(Suppl 26): S711–S714.
  23. Iliff JJ, Chen M, Plog B, et al. Impairment of glymphatic pathway function promotes tau pathology after traumatic brain injury. J Neurosci. 2014; 34(49): 16180–16193.
  24. Scallan J, Huxley VH, Korthuis RJ. Capillary fluid exchange: regulation, functions, and pathology. Morgan & Claypool life sciences. San Rafael, 2010. indexed in Pubmed: 21452435.
  25. Raslan A, Bhardwaj A. Medical management of cerebral edema. Neurosurgical Focus. 2007; 22(5): 1–12.
  26. Rabinstein AA. Treatment of cerebral edema. Neurologist. 2006; 12(2): 59–73.
  27. Feldman Z, Kanter MJ, Robertson CS, et al. Effect of head elevation on intracranial pressure, cerebral perfusion pressure, and cerebral blood flow in head-injured patients. J Neurosurg. 1992; 76(2): 207–211.
  28. Carney N, Totten AM, O'Reilly C, et al. Guidelines for the management of severe traumatic brain injury, fourth edition. Neurosurgery. 2017; 80(1): 6–15.
  29. Unterberg AW, Kienning KL, Härtl R, et al. Multimodal monitoring in patients with head injury: evaluation of the effects of treatment on cerebral oxygenation. J Trauma. 1997; 42(5 Suppl): 32–37.
  30. Juul N, Morris GF, Marshall SB, et al. Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury. The Executive Committee of the International Selfotel Trial. J Neurosurg. 2000; 92(1): 1–6.
  31. Myburgh JA. Intracranial pressure thresholds in severe traumatic brain injury: pro. Intensive Care Med. 2018; 44(8): 1315–1317.
  32. Sorrentino E, Diedler J, Kasprowicz M, et al. Critical thresholds for cerebrovascular reactivity after traumatic brain injury. Neurocrit Care. 2012; 16(2): 258–266.
  33. Cooper DJ, Rosenfeld JV, Murray L, et al. DECRA Trial Investigators, Australian and New Zealand Intensive Care Society Clinical Trials Group. Decompressive craniectomy in diffuse traumatic brain injury. N Engl J Med. 2011; 364(16): 1493–1502.
  34. Hutchinson PJ, Kolias AG, Timofeev IS, et al. RESCUEicp Trial Collaborators. Trial of decompressive craniectomy for traumatic intracranial hypertension. N Engl J Med. 2016; 375(12): 1119–1130.
  35. Burke AM, Quest DO, Chien S, et al. The effects of mannitol on blood viscosity. J Neurosurg. 1981; 55(4): 550–553.
  36. Boone MD, Oren-Grinberg A, Robinson TM, et al. Mannitol or hypertonic saline in the setting of traumatic brain injury: what have we learned? Surg Neurol Int. 2015; 6: 177.
  37. Rangel-Castilla L, Rangel-Castillo L, Gopinath S, et al. Management of intracranial hypertension. Neurol Clin. 2008; 26(2): 521–541, x.
  38. Shawkat H, Westwood MM, Mortimer A. Mannitol: a review of its clinical uses. Continuing Education in Anaesthesia Critical Care & Pain. 2012; 12(2): 82–85.
  39. André P, Villain F. Free radical scavenging properties of mannitol and its role as a constituent of hyaluronic acid fillers: a literature review. Int J Cosmet Sci. 2017; 39(4): 355–360.
  40. Bentsen G, Breivik H, Lundar T, et al. Hypertonic saline (7.2%) in 6% hydroxyethyl starch reduces intracranial pressure and improves hemodynamics in a placebo-controlled study involving stable patients with subarachnoid hemorrhage. Crit Care Med. 2006; 34(12): 2912–2917.
  41. Bentsen G, Stubhaug A, Eide PK. Differential effects of osmotherapy on static and pulsatile intracranial pressure. Crit Care Med. 2008; 36(8): 2414–2419.
  42. Al-Rawi PG, Zygun D, Tseng MY, et al. Cerebral blood flow augmentation in patients with severe subarachnoid haemorrhage. Acta Neurochir Suppl. 2005; 95: 123–127.
  43. 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(1): 202–210.
  44. Asehnoune K, Lasocki S, Seguin P, et al. ATLANREA group, COBI group. Association between continuous hyperosmolar therapy and survival in patients with traumatic brain injury - a multicentre prospective cohort study and systematic review. Crit Care. 2017; 21(1): 328.
  45. Roquilly A, Lasocki S, Moyer JD, et al. COBI group. COBI (COntinuous hyperosmolar therapy for traumatic Brain-Injured patients) trial protocol: a multicentre randomised open-label trial with blinded adjudication of primary outcome. BMJ Open. 2017; 7(9): e018035.
  46. Edwards P, Arango M, Balica L, et al. CRASH trial collaborators. Final results of MRC CRASH, a randomised placebo-controlled trial of intravenous corticosteroid in adults with head injury-outcomes at 6 months. Lancet. 2005; 365(9475): 1957–1959.
  47. Murayi R, Chittiboina P. Glucocorticoids in the management of peritumoral brain edema: a review of molecular mechanisms. Childs Nerv Syst. 2016; 32(12): 2293–2302.
  48. Jooma R. Dexamethasone and the serious head injury. Br J Neurosurg. 1987; 1(4): 400–403.
  49. Kolias AG, Viaroli E, Rubiano AM, et al. The current status of decompressive craniectomy in traumatic brain injury. Curr Trauma Rep. 2018; 4(4): 326–332.
  50. Hutchinson PJ, Kolias A, Tajsic T, et al. Consensus statement from the International Consensus Meeting on the Role of Decompressive Craniectomy in the Management of Traumatic Brain Injury. Acta Neurochirur. 2019; 161(7): 1261–1274.
  51. Jiang JiY, Xu W, Li WP, et al. Efficacy of standard trauma craniectomy for refractory intracranial hypertension with severe traumatic brain injury: a multicenter, prospective, randomized controlled study. J Neurotrauma. 2005; 22(6): 623–628.
  52. Plog BA, Nedergaard M. The glymphatic system in central nervous system health and disease: past, present, and future. Annu Rev Pathol. 2018; 13: 379–394.
  53. Giammattei L, Messerer M, Cherian I, et al. Current perspectives in the surgical treatment of severe traumatic brain injury. World Neurosurg. 2018; 116: 322–328.
  54. Cherian I, Yi G, Munakomi S. Cisternostomy: replacing the age old decompressive hemicraniectomy? Asian J Neurosurg. 2013; 8(3): 132–138.
  55. Masoudi MS, Rezaee E, Hakiminejad H, et al. Cisternostomy for management of intracranial hypertension in severe traumatic brain injury; case report and literature review. Bull Emerg Trauma. 2016; 4(3): 161–164.
  56. Cherian I, Bernardo A, Grasso G. Cisternostomy for traumatic brain injury: pathophysiologic mechanisms and surgical technical notes. World Neurosurg. 2016; 89: 51–57.
  57. Grasso G. Surgical treatment for traumatic brain injury: is it time for reappraisal? World Neurosurg. 2015; 84(2): 594.
  58. Asgeirsson B, Grände PO, Nordström CH. A new therapy of post-trauma brain oedema based on haemodynamic principles for brain volume regulation. Intensive Care Med. 1994; 20(4): 260–267.
  59. Eker C, Asgeirsson B, Grände PO, et al. Improved outcome after severe head injury with a new therapy based on principles for brain volume regulation and preserved microcirculation. Crit Care Med. 1998; 26(11): 1881–1886.
  60. Naredi S, Edén E, Zäll S, et al. A standardized neurosurgical neurointensive therapy directed toward vasogenic edema after severe traumatic brain injury: clinical results. Intensive Care Med. 1998; 24(5): 446–451.