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Vol. 56. Núm. 2.
Páginas 99-103 (Febrero 2002)
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Vol. 56. Núm. 2.
Páginas 99-103 (Febrero 2002)
Acceso a texto completo
Alteraciones del sistema de la coagulación y la fibrinólisis en el shock séptico asociado a púrpura
Abnormalities in coagulation and fibrinolysis in septic shock with purpura
Visitas
11277
A. Sánchez Mirallesa, R. Reig Sáenza,
Autor para correspondencia
reig_rob@gva.es

Correspondencia: Unidad de Cuidados Intensivos. Hospital General Universitario de Alicante. Maestro Alonso, 109. 03010 Alicante.
, P. Marco Verab, F. Muñoz Péreza, B. Álvarez Sáncheza, I. Sebastián Muñoza
a Unidad de Cuidados Intensivos Pediátricos. Servicio de Medicina Intensiva
b Servicio de Hematología. Hospital General Universitario de Alicante
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Información del artículo
Objetivos

Describir las alteraciones en el sistema de la coagulación y la fibrinólisis en el shock séptico asociado a púrpura y analizar la relación entre concentración plasmática de inhibidor del activador del plasminógeno tipo 1 (PAI-1) y la presencia de fracaso multiorgánico (FMO).

Métodos

Estudio observacional en la Unidad de Cuidados Intensivos Pediátricos (UCIP) de un hospital universitario de tercer nivel. Se analizó en 15 niños ingresados de forma consecutiva con shock séptico y púrpura la presencia de FMO en el momento del ingreso. Se obtuvieron muestras sanguíneas para estudiar los parámetros del sistema de coagulación y la fibrinólisis.

Resultados

En el momento del ingreso 7 pacientes (46,7 %) presentaban FMO; 6 pacientes (40 %), síndrome de distrés respiratorio agudo (SDRA); 7 pacientes (46,7 %), coagulopatía de consumo, y 1 paciente (6,7 %), fracaso renal agudo. La mortalidad observada fue de 40 %. Los parámetros del sistema de la coagulación analizados estaban en general alterados, aunque sólo se observaron diferencias estadísticamente significativas en las concentraciones plasmáticas de fibrinógeno y antitrombina III que fueron menores en el grupo con FMO que en los pacientes sin disfunción de órganos. Los parámetros de la fibrinólisis estaban aumentados en todos los pacientes pero sólo se observaron concentraciones plasmáticas de PAI-1 significativamente elevadas en el grupo con FMO y en aquellos con SDRA.

Conclusiones

Los resultados sugieren que las alteraciones del sistema fibrinolítico pueden tener un papel importante en el desarrollo de FMO en niños con shock séptico y púrpura.

Palabras clave:
Shock séptico
Fracaso multiorgánico
Síndrome de distrés respiratorio agudo
Coagulación intravascular diseminada
Púrpura
Inhibidor del activador del plasminógeno tipo 1
Niños
Objective

To describe abnormalities in coagulation and fibrinolysis in septic shock with purpura and to assess the relationship between plasma plasminogen activator inhibitor-1 (PAI-1) concentrations and multiple organ system failure (MOSF).

Methods

Observational study in the pediatric intensive care unit of a tertiary care hospital. The presence of early MOSF was assessed at admission in 15 children with septic shock and purpura consecutively admitted to the pediatric intensive care unit. Blood samples were taken to determine coagulation and fibrinolysis parameters.

Results

At admission, MOSF was diagnosed in 7 patients (46.7%), acute respiratory distress syndrome (ARDS) in 6 (40 %), consumption coagulopathy in 7 (46.7 %) and acute renal failure in 1 (6.7 %). The overall mortality rate was 40 %. Coagulation parameters were generally affected but statistically significant differences were found only in concentrations of fibrinogen and antithrombin III, which were lower in patients with MOSF than in those without organ dysfunction. Fibrinolysis parameters were increased in all patients but plasma PAI-1 concentrations were significantly elevated only in patients with MOSF and in those with ARDS.

Conclusions

These data indicate that impaired fibrinolysis could play a major role in the development of MOSF in children with septic shock and purpura.

Key words:
Septic shock
Multiple organ system failure
Acute respiratory distress syndrome
Intravascular coagulation
Purpura
Plasminogen activator inhibitor type 1
Children
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Bibliografía
[1.]
American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference.
Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis.
Crit Care Med, 20 (1992), pp. 864-874
[2.]
F. Leclerc, R. Beuscart, B. Guillois, J.K. Diependaele, G. Krim, D. Devictor, et al.
Prognostic factors of severe infectious purpura in children.
Intensive Care Med, 11 (1985), pp. 140-143
[3.]
E. Girardin, G.E. Grau, J.M. Dayer, P. Roux-Lombard, P.H. Lambert.
Tumor necrosis factor and interleukin-1 in the serum of children with severe infectious purpura.
N Engl J Med, 319 (1988), pp. 397-400
[4.]
E.D. De Kleijn, J.A. Hazelze, R.F. Kornelisse, R. De Groot.
Pathophysiology of meningococcal sepsis in children.
Eur J Pediatr, 157 (1998), pp. 869-880
[5.]
R.F. Kornelisse, J.A. Hazelzet, H.F.J. Savelkoul, W.C.J. Hop, M.H. Suur, A.N.J. Borsboom, et al.
The relationship between plasminogen activator inhibitor-1 and proinflammatory and counterinflammatory mediators in children with meningococcal septic shock.
J Infect Dis, 173 (1996), pp. 1148-1156
[6.]
J.D. Wilkinson, M.M. Pollack, U.E. Ruttimann, N.L. Glass, T.S. Yeh.
Outcome of pediatric patients with multiple organ system failure.
Crit Care Med, 14 (1986), pp. 271-274
[7.]
P.W.M. Hermans, M.L. Hibberd, R. Booy, O. Daramola, J.A. Hazelzet, R. De Groot.
and the Meningococcal Research Group. 4G/5G promoter polymorphism in the plasminogen-activator-inhibitor-1 gene and outcome of meningococcal disease.
Lancet, 354 (1999), pp. 556-560
[8.]
J.T. Algren, S. Lal, S.A. Cutliff, B.J. Richman.
Predictors of outcome in acute meningococcal infection in children.
Crit Care Med, 21 (1993), pp. 447-452
[9.]
G.R. Bernard, A. Artigas, K.L. Brigham, J. Carlet, K. Falke, L. Hudson, et al.
Report of the American-European consensus conference on ARDS: Definitions, mechanisms, relevant outcomes and clinical trial coordination.
Intensive Care Med, 20 (1994), pp. 225-232
[10.]
M.B. Salzman, L.G. Rubin.
Meningococcemia.
Infect Dis Clin North Am, 10 (1996), pp. 709-725
[11.]
E. Kirsch, P.H. Barton, L. Kitchen, B. Giroir.
Pathophysiology, treatment and outcome of meningococcemia: A review and recent experience.
Pediatr Infect Dis, 15 (1996), pp. 967-979
[12.]
F. Fourrier, P. Lestavel, C. Chopin, A. Marey, J. Goudeman, A. Rime, et al.
Meningococcemia and purpura fulminans in adults: Acute deficiencies of protein C and S and early treatment with antithrombin III concentrates.
Intensive Care Med, 16 (1990), pp. 121-124
[13.]
F. Leclerc, J. Hazelzet, B. Jude, W. Hofhuis, V. Hue, A. Martinot, et al.
Protein C and S deficiency in severe infectious purpura of children: Collaborative study of 40 cases.
Intensive Care Med, 18 (1992), pp. 202-205
[14.]
K. Fijnvandraat, B. Derkx, M. Peters, R. Bijlmer, A. Sturk, M.H. Prins, et al.
Coagulation activation and tissue necrosis in meningococcal septic shock: Severely reduced protein C levels predict a high mortality.
Thromb Haemost, 73 (1995), pp. 15-20
[15.]
J.A. Hazelzet, I.M. Risseeuw-Appel, R.F. Kornelisse, W.C.J. Hop, I. Dekker, K.F.M. Joosten, et al.
Age-related differences in outcome and severity of DIC in children with septic shock and purpura.
Thromb Haemost, 76 (1996), pp. 932-938
[16.]
D. Powars, R. Larsen, J. Johnson, T. Hulbert, T. Sun, M.J. Patch, et al.
Epidemic meningococcemia and purpura fulminans with induced protein C deficiency.
Clin Infect Dis, 17 (1993), pp. 254-261
[17.]
S. Gando, T. Kameue, S. Nanzaki, T. Hayakawa, Y. Nakanishi.
Increased neutrophil elastase, persistent intravascular coagulation, and decreased fibrinolytic activity in patients with posttraumatic acute respiratory distress syndrome.
J Trauma, 42 (1997), pp. 1068-1072
[18.]
S. Gando, Y. Nakanishi, I. Tedo.
Cytokines and plasminogen activator inhibitor-1 in posttrauma disseminated intravascular coagulation: Relationship to multiple organ dysfunction syndrome.
Crit Care Med, 23 (1995), pp. 1835-1842
[19.]
G.E. Grau, P. De Moerloose, O. Bulla, J. Lou, Z. Lei, G. Reber, et al.
Haemostatic properties of human pulmonary and cerebral microvascular endothelial cells.
Thromb Haemost, 77 (1997), pp. 585-590
[20.]
G. Pralong, T. Calandra, M.P. Glauser, J. Schellekens, J. Verhoef, F. Bachmann, et al.
Plasminogen activator inhibitor 1: A new prognostic marker in septic shock.
Thromb Haemost, 61 (1989), pp. 459-462
[21.]
P. Brandtzaeg, G.B. Joo, B. Brusletto, P. Kierulf.
Plasminogen activator inhibitor 1 and 2, alpha-2-antiplasmin, plasminogen, and endotoxin levels in systemic meningococcal disease.
Thromb Res, 57 (1990), pp. 271-278
[22.]
M. Colucci, J.A. Paramo, D. Collen.
Generation in plasma of fast-acting inhibitor of plasminogen activator in response to endotoxin stimulation.
J Clin Invest, 75 (1985), pp. 818-824
[23.]
R.M. Mesters, N. Flörke, H. Ostermann, J. Kienast.
Increase of plasminogen activator inhibitor levels predicts outcome of leukocytopenic patients with sepsis.
Throm Haemost, 75 (1996), pp. 902-907
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