Advertisement

Fluid management in trauma

  • J. Boldt
Part of the Topics in Anaesthesia and Critical Care book series (TIACC)

Abstract

Trauma-related hypovolemia may be associated with flow alterations which are inadequate to fulfill the nutritive role of the circulation [1]. During this hypovolemia-related low output syndrome (LOS), the organism tries to compensate perfusion deficits by redistribution of flow to vital organs (i.e., heart and brain) resulting in an underperfusion of other organs such as splanchnic bed, kidney, muscles, and skin. Various inflammatory mediators and circulating vasoactive substances are of particular importance for impaired perfusion in trauma patients. Activation of the sympathetic nervous system and the renin-angiotensin system (RAS) are compensatory mechanisms to maintain peripheral perfusion. Although this compensatory neurohumoral activation is beneficial at first, this mechanism becomes deleterious and may be involved in the poor outcome of the critically ill [2].

Keywords

Trauma Patient Pulmonary Capillary Wedge Pressure Human Albumin Volume Replacement Volume Therapy 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Intaglietta M (1990) Objectives for the treatment of the microcirculation in ischemia, shock, and reperfusion. In: Vincent JL (ed) Update in intensive care and emergency medicine. Vol 10. Springer-Verlag, Berlin Heidelberg New York, pp 293–298.Google Scholar
  2. 2.
    Turnbull AV, Little RA (1993) Neuro-hormonal regulation after trauma. Circulating cytokines may also contribute to an activated sympathetic-adrenal control. In: Vincent JL (ed) Update in intensive care and emergency medicine. Springer-Verlag, Berlin Heidelberg New York Tokyo, pp 574–581.Google Scholar
  3. 3.
    Beards SC, Watt T, Edwards JD et al (1994) Comparison of the hemodynamic and oxygen transport responses to modified fluid gelatin and hetastarch in critically ill patients: a prospective, randomized trial. Crit Care Med 22:600–605.PubMedCrossRefGoogle Scholar
  4. 4.
    Davidson I (1989) Fluid resuscitation of shock: current controversies. Crit Care Med 17:1078–1080.CrossRefGoogle Scholar
  5. 5.
    Edwards JD, Nightingale P, Wilkins RG et al (1988) Hemodynamic and oxygen transport response to modified fluid gelatin in the critically ill patients. Crit Care Med 17:996–998.CrossRefGoogle Scholar
  6. 6.
    Prough DS, Johnston WE (1989) Fluid restoration in septic shock: no solution yet. Anesth Analg 69:699–704.PubMedCrossRefGoogle Scholar
  7. 7.
    Vincent JL (1991) The colloid-crystalloid controvery. Klin Wochensch 69(Suppl 26):104–111.Google Scholar
  8. 8.
    Lamke LO, Liljedahl SO (1976) Plasma volume changes after infusion of various plasma expanders. Resuscitation 5:93–98.PubMedCrossRefGoogle Scholar
  9. 9.
    Emmerson TE (1989) Unique features of albumin: a brief review. Crit Care Med 17:690–693.CrossRefGoogle Scholar
  10. 10.
    Laxenaire M, Charpentier C, Feldman L (1994) Reactions anaphylactoides aux subitutes colloidaux du plasma: incidence, facteurs de risque, mecanismes. Ann Fr Anest Reanim 13:301–310.CrossRefGoogle Scholar
  11. 11.
    London MJ, Ho SJ, Triedman JK et al (1989) A randomized clinical trial of 10% pen-tastarch (low molecular weight hydroxyethyl starch) versus 5% albumin for plasma volume expansion after cardiac operations. J Thorac Cardiovasc Surg 97:785–797.PubMedGoogle Scholar
  12. 12.
    Webb AR, Barclay SA, Bennett ED (1989) In vitro colloid osmotic pressure of commonly used plasma substitutes: a study of the diffusibility of colloid molecules. Intensive Care Med 15:116–120.PubMedCrossRefGoogle Scholar
  13. 13.
    Brenner BM, Troy JL, Ballermann B (1989) Endothelium-dependent vascular responses. J Clinical Invest 84:1373–1378.CrossRefGoogle Scholar
  14. 14.
    Lewis DH (1988) The effect of multiple organ failure on the regulation of the circulation with special reference to the microcirculation. In: Manabe H, Zweifach BW, Messmer K (eds) Microcirculation in Circulatory Disorders. Springer-Verlag, Tokyo Berlin Heidelberg, pp 103–108.CrossRefGoogle Scholar
  15. 15.
    Boldt J, Müller M, Mentges D et al (1996) Influence of different volume therapy regime on regulators of circulation in the critically ill. Br J Anaesth 77:480–487.PubMedCrossRefGoogle Scholar
  16. 16.
    Boldt J, Lenz M, Kumle B et al (1998) Volume replacement strategies on intensive care units: results from a postal survey. Intensive Care Med 24:147–151.PubMedCrossRefGoogle Scholar
  17. 17.
    DeJonge E, Levi M, Berends F et al (1998) Impaired haemostasis by intravenous administration of a gelatin-based plasma expander in human subjects. Thromb Haemost 79:286–290.Google Scholar
  18. 18.
    Strauss RG (1981) Review of the effects of hydroxyethyl starch on the blood coagulation system. Transfusion 21:299–309.PubMedCrossRefGoogle Scholar
  19. 19.
    Treib J, Haass A, Pindur G et al (1996) All medium starches are not the same: influence of hydroxyethyl substitution of hydroxyethhyl starch on plasma volume, hemorrheologic conditions, and coagulation. Transfusion 36:450–455.PubMedCrossRefGoogle Scholar
  20. 20.
    Treib J, Haass A, Pindur G (1997) Coagulation disorders caused by hydroxyethyl starch. Thromb Haemost 78:974–983.PubMedGoogle Scholar
  21. 21.
    Boldt J, Zickmann B, Benson M et al (1992) Influence of 5 different priming on platelet function in patients undergoing cardiac surgery. Anesth Analg 74:219–225.PubMedCrossRefGoogle Scholar
  22. 22.
    Warren BB, Durieux ME (1996) Hydroxyethylstarch: safe or not? Anesth Analg 84:206–212.Google Scholar
  23. 23.
    Schmand J, Ayala A, Chaudry IH (1994) Effects of trauma, duration of hypotension, and resuscitation regimen on cellular immunity after hemorrhagic shock. Crit Care Med 22:1076–1083.PubMedCrossRefGoogle Scholar
  24. 24.
    Dorman T, Breslow MJ (1994) Altered immune function after trauma and hemorrhage: what does it all mean? Crit Care Med 22:1069–1070.PubMedCrossRefGoogle Scholar
  25. 25.
    Chaudry IH, Ayala A (1993) Immune consequences of hypovolemic shock and resuscitation. Curr Opin Anaesth 6:385–392.CrossRefGoogle Scholar
  26. 26.
    Mariscalco MM (1993) Leukocytes and the inflammatory response. Crit Care Med 21: S347–S348.PubMedCrossRefGoogle Scholar
  27. 27.
    Williams TJ, Hellewell PG (1992) Endothelial cell biology. Am Rev Resp Dis 146:S45–S50.PubMedGoogle Scholar
  28. 28.
    Springer TA (1990) Adhesion receptors of the immune system. Nature 346:425–434.PubMedCrossRefGoogle Scholar
  29. 29.
    Rothlein R, Mainolfi EA, Czajkowski M et al (1991) A form of circulating ICAM-1 in human serum. J Immunol 147:3788–3793.PubMedGoogle Scholar
  30. 30.
    Seth R, Raymond FD, Makgoba MW (1991) Circulating ICAM-1 isoforms: diagnostic prospects for inflammatory and immune disorders. Lancet 338:83–84.PubMedCrossRefGoogle Scholar
  31. 31.
    Jochum M, Inthorn D, Waydhas Ch et al (1994) Diagnostic relevance of PMN elastase and soluble adhesion molecules in acute inflammation. Intensive Care Med 20:S102.Google Scholar
  32. 32.
    Boldt J, Müller M, Heesen M et al (1996) Influence of different volume therapies and pentoxifylline infusion on circulating soluble adhesion molecules in critically ill patients. Crit Care Med 24:385–391PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Italia 1999

Authors and Affiliations

  • J. Boldt

There are no affiliations available

Personalised recommendations