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Inicio Revista Colombiana de Anestesiología Trastornos de coagulación en trauma craneoencefálico
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Vol. 36. Núm. 3.
Páginas 199-206 (agosto - octubre 2008)
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Vol. 36. Núm. 3.
Páginas 199-206 (agosto - octubre 2008)
ARTÍCULO DE REVISIÓN
Open Access
Trastornos de coagulación en trauma craneoencefálico
Visitas
3760
M.C. Niño de Mejía1, M.V. Caicedo2, J.A. Torres3, J.A. Tovar4
1. Neuroanestesióloga, Hospital Universitario Fundación Santa Fe de Bogotá, Bogotá, D.C., Colombia
2. Residente de anestesia, Hospital Universitario Fundación Santa Fe de Bogotá, Bogotá, D.C., Colombia
3. Residente de anestesia, Hospital Simón Bolívar, Universidad El Bosque, Bogotá, D.C., Colombia
4. Residente de anestesia, Universidad Surcolombiana, Neiva, Colombia
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Información del artículo
RESUMEN

La comprensión del proceso de la coagulación ha progresado durante la última década, evolucionando a partir del concepto según el cual la producción del coágulo se iniciaba por acción de las plaquetas y la activación de uno de los dos sistemas separados, la vía extrínseca y la vía intrínseca, al concepto actual que hace énfasis sobre la vía común y un sistema proteolítico que da lugar a la degradación de los coágulos formados y a la prevención de la formación indeseada de coágulos.

La alteración de este equilibrio cobra especial importancia en los pacientes con trauma craneoencefálico, en quienes -a la luz de los conocimientos actuales- se pueden presentar trastornos de la coagulación que van desde lesiones procoagulantes, en un extremo, hasta lesiones anticoagulantes, en el otro extremo. La meta de los autores es brindar a los clínicos de una guía de evaluación inicial, de seguimiento y, de las posibilidades terapéuticas disponibles en el momento.

Palabras clave:
Trauma craneoencefálico
trastornos procoagulantes y anticoagulantes
evaluación incial
Key words:
Craneoencephatic trauma
procoagulant and anticoagulant injuries
clinical initial evaluation
ABSTRACT

The understanding of the coagulation process has progressed during last decade evolving from the concept according to which the production of the clot begins by means of the action of platelets and the activation of one of two separated systems, the extrinsic route and the intrinsic route, to the present concept that makes emphasis on the common route and a proteolytic system that give rise to the degradation of formed clots and to the undesired prevention of the formation of the clot. The alteration of this balance receives special importance in the patients with brain trauma in those who to the light of the present knowledge may present upheavals of the coagulation which can go from procoagulating injuries in one end to anticoagulating injuries in the other. The goal of the authors is to provide a clinical guide with initial evaluation, pursuit and therapeutic possibilities available at the moment.

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REFERENCIAS
[1.]
J.R. Hees, J.H. Laeson.
The coagulopathy of trauma versus disseminated intravascular coagulation.
[2.]
Ratnoff Davie.
Coagulopatía del paciente quirúrgico.
Revista Mexicana de Anestesiología, 27 (2004), pp. 219-230
[3.]
H. Rott, H. Trobisch, E. Kretzschmar.
Use of recombinant factor VIIa in the manegement of acute haemorrhage.
Cur Opin Anaesthesiol, 17 (2004), pp. 159-163
[4.]
N. Cosgriff, E.E. Monroe, A. Sauaia, M. Kenny-Moynihan, J.M. Burch, B. Galloway.
predicting life-threatening coagulophaty in the massively transfused trauma patient: hypothermia and acidosis revisited.
J Trauma, 42 (1997), pp. 857-862
[5.]
Z.H. Meng, A.S. Wolberg, D.O. Monroe III, M. Hoffman.
The effect of temperature and ph on the activity of factor VIIa: implications for trhe efficacy of high-dose factor VIIa in hypothermic and acidotic patients.
[6.]
J.C. Kermode, Q. Zheng, E.P. Milner.
Marked temperature dependence of the platelet calcium signal induced by human von Willebrand factor.
Blood, 94 (1999), pp. 199-207
[7.]
S.P. Baker, B. O'Neill, W. Haddon, W.B. Long.
The injury severity score: A method for describing patients with multiple injuries and evaluating emergency care.
J Trauma, 14 (1974), pp. 187-196
[8.]
B.S. Harhangi, E.J.O. Kompanje, F.W.G. Leebeek, A.I.R. Maas.
Coagulation disorders after traumatic brain injury.
Acta Neurochir (Wien), 150 (2008), pp. 165-175
[9.]
F. Hulka, R.J. Mullins, E.H. Frank.
Blunt brain injury activates the coagulation process.
Arch Surg, 131 (1996), pp. 923-927
[10.]
J. Piek, R.M. Chesnut, L.F. Marshall, M. van Berkum-Clark, M.R. Klauber, B.A. Blunt.
Extracranial complications of severe head injury.
J Neurosurg, 77 (1992), pp. 901-907
[11.]
P.L. Giesen, Y. Nemerson.
Tissue factor on the loose.
Semen Thromb Hemost, 26 (2000), pp. 379-384
[12.]
R.U. Scherer, P. Spangenberg.
Procoagulant activity in patients with isolated severe head trauma.
Crit Care Med, 26 (1998), pp. 149-156
[13.]
J.H. Lawson, M. Kalafatis, S. Stram, K.G. Mann.
A model for the tissue factor pathway to thrombin. I. An empirical study.
J Biol Chem, 269 (1994), pp. 357-366
[14.]
R.M. Keimowitz, B.L. Annis.
Disseminated intravascular coagulation associated with massive brain injury.
J Neurosurg, 39 (1973), pp. 178-180
[15.]
T. Astrup.
Assay and content of tissue thromboplastin in different organs.
Thromb Diath Haemorrh, 14 (1965), pp. 401-406
[16.]
S.H. Goodnight, G. Kenoyer, S.I. Rapaport, M.J. Patch, J.A. Lee, T. Kurze.
Defibrination after brain-tissue destruction: a serious complication of head injury.
N Engl J Med, 290 (1974), pp. 1043-1047
[17.]
S. Gando.
Disseminated intravascular coagulation in trauma patients.
Semin Thromb Hemost, 27 (2001), pp. 585-592
[18.]
A. Pathak, S. Dutta, N. Marwaha, D. Singh, N. Varma, S.N. Mathuriya.
Change in tissue thromboplastin content of brain following trauma.
Neurol India, 53 (2005), pp. 178-182
[19.]
K.G. Mann, S. Butenas, K. Brummel.
The dynamics of thrombin formation.
Arterioscler Thromb Vasc Biol, 23 (2003), pp. 17-25
[20.]
H.H. Kaufman, K.S. Hui, J.C. Mattson, A. Borit, T.L. Childs, W.K. Hoots.
Clinicopathological correlations of disseminated intravascular coagulation in patients with head injury.
Neurosurgery, 15 (1984), pp. 34-42
[21.]
M. Levi.
Disseminated intravascular coagulation: what's new?.
Crit Care Clin, 21 (2005), pp. 449-467
[22.]
M. Levi, H. Ten Cate.
Disseminated intravascular coagulation.
N Engl J Med, 341 (1999), pp. 586-592
[23.]
M.E. Miner, H.H. Kaufman, S.H. Graham, F.H. Haar, P.L. Gildenberg.
Disseminated intravascular coagulation fibrinolytic syndrome following head injury in children: frequency and prognostic implications.
J Pediatr, 100 (1982), pp. 687-691
[24.]
M. Nekludov, B.M. Bellander, M. Blomback, H.N. Wallen.
Platelet dysfunction in patients with severe traumatic brain injury.
J. Neurotrauma, 24 (2008), pp. 1699-1706
[25.]
S.C. Stein, D.H. Smith.
Coagulopathy in traumatic brain injury.
Neurocrit Care, 1 (2004), pp. 479-488
[26.]
S. Gando, S. Nanzaki, O. Kemmotsu.
Coagulofibrinolytic changes after isolated head injury are not different from those in trauma patients without head injury.
J Trauma, 46 (1999), pp. 1070-1077
[27.]
J.R. Hess, J.H. Lawson.
The coagulopathy of trauma versus disseminated intravascular coagulation.
[28.]
R.C. Jacoby, J.T. Owings, J. Holmes, F.D. Battistella, R.C. Gosselin, T.G. Paglieroni.
Platelet activation and function after trauma.
J Trauma, 51 (2001), pp. 639-647
[29.]
M.M. Carrick, A.H. Tyroch, C.A. Youens, T. Handley.
Subsequent development of thrombocytopenia and coagulopathy in moderate and severe head injury: support for serial laboratory examination.
J Trauma, 58 (2005), pp. 725-730
[30.]
M. Engstrom, B. Romner, W. Schalen, P. Reinstrup.
Thrombocytopenia predicts progressive hemorrhage after head trauma.
J Neurotrauma, 22 (2005), pp. 291-296
[31.]
B.L. Parry-Jones, F.L. Vaughan, W. Miles Cox.
Traumatic brain injury and substance misuse: a systematic review of prevalence and outcomes research (1994–2004).
Neuropsychol Rehabil, 16 (2006), pp. 537-560
[32.]
A. Bell.
The Ivy bleeding time.
Am J Med Technol, 24 (1958), pp. 264-270
[33.]
A.J. Singer, C.J. Mynster, B.J. Mcmahon.
The effect of IM ketorolac tromethamine on bleeding time: a prospective, interventional, controlled study.
Am J Emerg Med, 21 (2003), pp. 441-443
[34.]
F. Raffán, F.J. Ramírez, J.A. Cuervo, L.F. Sánchez.
Tromboelastografía.
Rev Col Anes, 33 (2005), pp. 181-186
[35.]
T. Maeda, Y. Katayama, T. Kawamata, N. Aoyama, T. Mori.
Hemodynamic depression and microthrombosis in the peripheral areas of cortical contusion in the rat: role of platelet activating factor.
Acta Neurochir, 70 (1997), pp. 102-105
[36.]
S. Schwarzmaier, S.W. Kim, R. Trabold, N. Plesnila.
Intravascular leukocytes and secondary brain damage after experimental TBI.
Presented at the 8th International NeuroTrauma Society (INTS) Meeting, (2006),
[37.]
L. Auer.
Disturbances of the coagulatory system in patients with severe cerebral trauma. I.
Acta Neurochir (Wien), 43 (1978), pp. 51-59
[38.]
M. Cortiana, G. Zagara, S. Fava, M. Seveso.
Coagulation abnormalities in patients with head injury.
J Neurosurg Sci, 30 (1986), pp. 133-138
[39.]
D.B. Hoyt.
A clinical review of bleeding dilemmas in trauma.
Semin Hematol, 41 (2004), pp. 40-43
[40.]
P.A. Gómez, R.D. Lobato, J.M. Ortega, J. De La Cruz.
Mild head injury: differences in prognosis among patients with a Glasgow Coma Scale score of 13 to 15 and analysis of factors associated with abnormal CT findings.
Br J Neurosurg, 10 (1996), pp. 453-460
[41.]
E. Kumura, M. Sato, A. Fukuda, Y. Takemoto, S. Tanaka, A. Kohama.
Coagulation disorders following acute head injury.
Acta Neurochir (Wien), 85 (1987), pp. 23-28
[42.]
M.A. Schreiber, J. Differding, P. Thorborg, J.C. Mayberry, R.J. Mullins.
Hypercoagulability is most prevalent early after injury and in female patients.
J Trauma, 58 (2005), pp. 475-480
[43.]
M.S. Keller, D.G. Fendya, T.R. Weber.
Glasgow Coma Scale predicts coagulopathy in pediatric trauma patients.
Semin Pediatr Surg, 10 (2001), pp. 12-16
[44.]
S.C. Stein, C. Spettell, G. Young, S.E. Ross.
Delayed and progressive brain injury in closed-head trauma: radiological demonstration.
Neurosurgery, 32 (1993), pp. 25-30
[45.]
J.D. Olson, H.H. Kaufman, J. Moake, T.W. O'Gorman, K. Hoots, K. Wagner, C.K. Brown, P.L. Gildenberg.
The incidence and significance of haemostatic abnormalities in patients with head injuries.
Neurosurgery, 24 (1989), pp. 825-832
[46.]
B.M. Selladurai, M. Vickneswaran, S. Duraisamy, M. Atan.
Coagulopathy in acute head injury – a study of its role as a prognostic indicator.
Br J Neurosurg, 11 (1997), pp. 398-404
[47.]
S. Kushimoto, Y. Shibata, Y. Yamamoto.
Implications of fibrinogenolysis in patients with closed head injury.
J Neurotraum, 20 (2003), pp. 357-363
[48.]
G.D. Murray, I. Butcher, G.S. McHugh, J. Lu, N.A. Mushkudiani, I. Maas, A. Marmarou, E.W. Steyerberg.
Multivariable prognostic analysis in traumatic brain injury: results from the IMPACT study.
J Neurotraum, 24 (2007), pp. 329-337
[49.]
S.C. Stein, D.H. Smith.
Coagulopathy in traumatic brain injury.
Neurocrit Care, 1 (2004), pp. 479-488
[50.]
A.K. May, J.S. Young, K. Butler, D. Bassam, W. Brady.
Coagulopathy in severe closed head injury: is empiric therapy warranted?.
Am Surg, 63 (1997), pp. 233-236
[51.]
G.R. Bernard, J.L. Vincent, P.F. Laterre, S.P. LaRosa, J.F. Dhainaut, A. López-Rodríguez.
Efficacy and safety of recombinant human activated protein C for severe sepsis.
N Engl J Med, 344 (2001), pp. 699-709
[52.]
I. Roberts.
The CRASH-2 trial of an antifibrinolytic agent in traumatic haemorrhage: an international collaboration.
Indian J Med Res, 125 (2007), pp. 5-7
[53.]
S.A. Mayer, N.C. Brun, K. Begtrup, J. Broderick, S. Davis, M.N. Diringer.
Recombinant activated factor VII for acute intracerebral haemorrhage.
N Engl J Med, 352 (2005), pp. 777-785
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