2018, Number 4
<< Back Next >>
Med Crit 2018; 32 (4)
Correlation of leukocytosis and intracranial injury in patients with traumatic brain injury
Morán GE, Tamariz BA, Ruiz CJI, Cisneros CM
Language: Spanish
References: 30
Page: 208-216
PDF size: 173.84 Kb.
ABSTRACT
Diffuse microvascular damage is associated with loss of cerebral vascular self-regulation and loss of integrity of the blood-brain barrier. Traumatic brain injury is associated with an increase in serum levels of catecholamines. Catecholamines are responsible for neutrophil deposits. Catecholamines increase the leukocyte count by introducing the marginal cells into the circulating pool. The acute phase response is also characterized by leukocytosis on admission. Therefore, the white cell count is likely to serve as an additional indicator to the diagnosis and prognosis of TBI.
Material and methods: Longitudinal prospective cohort study. Patients treated in the emergency room with TBI were included, blood test and imaging studies were collected.
Results: Of the patients treated with subarachnoid hemorrhage (SAH), a mean of leukocytes on entry of 17,718 10∧3/μl on admission and 13,970 10∧3/μl on 24 hours of trauma, with p = 0.000 and 0.001. In patients with subdural hematoma, a mean number of leukocytes was found at 18,212 10∧3/μl and 13,319 10∧3/μl at 24 hours, with p = 0.000 and 0.003. For patients with hemorrhagic contusion, leukocytes were found on admission on average 13,225 10∧3/μl and at 12,501 10∧3/μl at 24 hours, a p = 0.091 and 0.027. In patients with epidural hematoma, a mean of 16,527 10∧3/μl leukocytes was found on admission, at 24 hours 13,240 10∧3/μl, with p = 0.000 and 0.019.
REFERENCES
Peden M, Scurfield R, Sleet D, Mohan D, Hyder AA, Jarawan E, et al. World report on road traffic injury prevention. 2004.
Kraus JF. Epidemiology of head injury. 1993.
Suleiman GH. Trauma craneoencefálico severo: Parte I. Medicrit. 2005;2(7):107-148.
Toescu EC. Hypoxia sensing and pathways of cytosolic Ca2+ increases. Cell Calcium. 2004;36(3-4):187-199.
Bárcena-Orbe A, Rodríguez-Arias CA, Rivero-Martín B, Cañizal-García JM, Mestre-Moreiro C, CalvoPérez JC y cols. Revisión del traumatismo craneoencefálico. Neurocirugía. 2006;17:495-518.
Stahel PF, Morganti-Kossmann MC, Kossmann T. The role of the complement system in traumatic brain injury. Brain Res Brain Res Rev. 1998;27(3):243-256.
Cabrera RA, Martínez OO, Ibarra GA, Morales SR, Laguna HG, Sánchez PM. Traumatismo craneoencefalico severo. Rev Asoc Mex Med Crit y Ter Int. 2009;23(2):94-101.
Lin Y, Wen L. Inflammatory response following diffuse axonal injury. Int J Med Sci. 2013;10(5):515-521.
Bouma GJ, Muizelaar JP, Choi SC, Newlon PG, Young HF. Cerebral circulation and metabolism after severe traumatic brain injury: the elusive role of ischemia. J Neurosurg. 1991;75(5):865-893.
Morganti-Kossmann MC, Satgunaseelan L, Bye N, Kossmann T. Modulation of inmune response to brain injury. Injury. 2007;38(12):1392-1400.
Pagowsta I. Isolated head injury in children affects the neutrophil function and lymphocyte count. J Trauma. 2007;63(1):179-186.
Hohl A, Gullo Jda S, Silva CC, Bertotti MM, Felisberto F, Nunes JC, et al. Plasma levels of oxidative stress biomarkers and hospital mortality in severe head injury. J Crit Care. 2012;27(5):523.e11-9.
Wagner AK, McCullough EH, Niyonkuru C, Ozawa H, Loucks TL, Dobos JA, et al. Acute serum hormone levels: characterization and prognosis after severe traumatic brain injury. J Neurotrauma. 2011;28(6):871-888.
Kayyali US, Donaldson C, Huang H, Abdelnour R, Hassoun PM. Phosphorylation of xanthine dehydrogenase/oxidase in hypoxia. J Biol Chem. 2001;276(17):14359-65.
Paolin A, Nardin L, Gaetani P, Rodriguez y Baena R, Pansarasa O, Marzatico F. Oxidative damage after severe head injury and its relationship to neurological outcome. Neurosurgery. 2002;51(4):949-54.
Padilla CN, Monge MJ. Traumatismo craneoencefálico. Trauma. 2002;5(3):92-96.
Godoy D. Intensive care in neurology and neurosurgery. Buenos Aires, Argentina: SEED, 2013.
Kakarieka A, Braakman R, Schakel, et al. Subarachnoid haemorrhage after head injury. Cerebrovasc Dis. 1995;5:403-406.
Choksey M, Crockard HA, Sandilands M. Acute traumatic in-tracerebral haematomas: determinants of outcome in a retros-pective series of 202 cases. Br J Neurosurg. 1993;7(6):611-622.
Gürkanlar D, Lakadamyali H, Ergun T, Yilmaz C, Yücel E, Altinörs N. Predictive value of leucocytosis in head trauma. Turk Neurosurg. 2009;19(3):211-215.
Rovlias A, Kotsou S. The blood leukocyte count and its prognostic significance in severe head injury. 2001;55(4):190-196.
Rovlias A, Kotsou S. Classification and regression tree for prediction of outcome after severe head injury using simple clinical and laboratory variables. J Neurotrauma. 2004;21(7):886-893.
Deibener-Kaminsky J, Lesesve JF, Grosset S, Pruna L, Schmall-Laurain MC, Benetos A, et al. Clinical relevance of leukocyte differential in patients with marked leukocytosis in the emergency room. Rev Med Interne. 2011;32(7):406-410.
Malone DL, Kuhls D, Napolitano LM, McCarter R, Scalea T. Back to basics: validation of the admission systemic inflammatory response syndrome score in predicting outcome in trauma. J Trauma. 2001;51(3):458-463.
Härtl R, Medary MB, Ruge M, Arfors KE, Ghajar J. Early white blood cell dynamics after traumatic brain injury. J Cereb Blood Flow Metab. 1997;17(11):1210-1220.
Asadollahi K, Beeching NJ, Gill GV. Leukocytosis as a predictor for non-infective mortality and morbility. QJM. 2010;103(5):285-292.
Kolias AG, Guilfoyle MR, Helmy A, Allanson J, Hutchinson PJ. Traumatic brain injury in adults. Pract Neurol. 2013;13(4):228-235.
Sistema Nacional de Vigilancia Epidemiológica. Aspectos Epidemiológicos del Trauma de Cráneo. Epidemiología. 2008. p. 26.
Ramírez MS, Ramón GI, Domínguez MA, Barba FC. Respuesta metabólica al trauma. MEDICRIT. 2008;5(4):130-133.
Cancelliere C, Cassidy JD, Côté P, Hincapié CA, Hartvigsen J, Carroll LJ, et al. Protocol for a systematic review of prognosis after mild traumatic brain injury. Syst Rev. 2012;1:17.