Procalcitonin and C-reactive protein during the early posttraumatic systemic inflammatory response syndrome
Objectives: To describe the initial evolution of serum procalcitonin (PCT) and C-reactive protein (CRP) in previously healthy adult trauma patients and to compare the relationship of the expression of these two proteins with indicators of trauma severity. Design: Prospective, descriptive, longitudinal study.
Setting: Surgical ICU in an university hospital.
Patients: Twenty-one patients admitted during the first posttraumatic 3 h exhibiting an Injury Severity Score (ISS) between 16 and 50 were enrolled.
Measurements: Blood sampling was performed on admission and on posttraumatic days 0.5,1, 2 and 3 to assess serum levels of PCT and CRP. Total creatine kinase (CKtot) and lactate dehydrogenase (LDHtot) activities in the serum were used as tissue damage indicators.
Results: PCT exhibited an early and transient increase in serum levels similar to a more delayed change of CRP levels. Peak PCT and peak CRP were related to the ISS, the extent of tissue damage and the amount of fluid replacement during the first day. During the first 3 posttraumatic days, 90 % of the patients exhibited a generalized inflammatory syndrome without infection.
Conclusions: An early and transient release of PCT into the circulation was observed after severe trauma and the amount of circulating PCT seemed proportional to the severity of tissue injury and hypovolemia, yet unrelated to infection. The predictive value of both PCT and CRP for a forthcoming multiple organ failure still remains to be clarified.
Key wordsC-reactive protein Hypovolemia Infection Organ failure Procalcitonin Trauma
Pittet D, Rangel-Fausto S, Li N, Tarara D, Costigan M, Rempe L, Jebson P, Wenzel RP (1995) Systemic inflammatory response syndrome, sepsis, severe sepsis and septic shock: incidence, morbidities and outcomes in surgical ICU patients. Intensive Care Med 21: 302–309PubMedCrossRefGoogle Scholar
Assicot M, Gendrel D, Carsin H, Raymond J, Guilbaud J, Bohuon C (1993) High serum procalcitonin concentrations in patients with sepsis and infection. Lancet 341: 515–518PubMedCrossRefGoogle Scholar
Moore FA, Moore EE (1995) Evolving concepts in the pathogenesis of postin-jury multiple organ failure. Surg Clin North Am 75: 257–277PubMedGoogle Scholar
Fisher CL, Gill Forrester MG, Nakamura R (1976) Quantitation of ‘acute phase proteins’ postoperatively. Value in detection and monitoring complications. Am J Clin Pathol 66: 840- 846Google Scholar
Waydhas C, Nast-Kolb D, Jochum M, Trupka A, Lenk S, Fritz Ff, Duswald KH, Schweiberer L (1992) Inflammatory mediators, infection, sepsis and multiple organ failure after severe trauma. Arch Surg 127: 460–467PubMedGoogle Scholar
Baker SP, O’Neill B, Haddon W, Long WB (1974) The Injury Severity Score: a method for describing patients with multiple injuries and evaluating emergency care. J Trauma 14:187–196PubMedCrossRefGoogle Scholar
Le Gall JR, Lerneshow S, Saulnier F (1993) A new Simplified Acute Physiology Score (SAPS II) based on a European/North American multicenter study. JAMA 270: 2957–2963PubMedCrossRefGoogle Scholar
American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference (1992) Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med 20: 864–874CrossRefGoogle Scholar
Garner JS, Jarvis WR, Emori TG, Horan TC, Hughes JM (1988) CDC definitions for nosocomial infections. Am J Infect Control 16:128–140PubMedCrossRefGoogle Scholar
Shahangian S, Ash KO, Wahlstrom NO, Warden GD, Saffle JR, Taylor A, Green LS (1984) Creatine kinase and lactate dehydrogenase isoenzymes in serum of patients suffering burns, blunt trauma or myocardial infarction. Clin Chem 30:1332–1338PubMedGoogle Scholar
Waydhas C, Nast-Kolb D, Trupka A, Zettl R, Kick M, Wiesholler M, Schweiberer L, Jochum M (1996) Posttraumatic inflammatory response, secondary operations and late multiple organ failure. J Trauma 40: 624–631PubMedCrossRefGoogle Scholar
Hoch RC, Rodriguez R, Manning T, Bishop M, Mead P, Shoemaker WC, Abraham E (1993) Effects of accidental trauma on cytokine and endotoxin production. Crit Care Med 21: 839–845PubMedCrossRefGoogle Scholar
Nast-Kolb D, Waydhas C, Gippner-Steppert C, Schneider I, Trupka A, Ruchholttz S, Zettl R, Scweiberer L, Jochum M (1997) Indicators of the posttraumatic inflammatory response correlate with organ failure in patients with multiple injuries. J Trauma 42: 446–454PubMedCrossRefGoogle Scholar
Fassbender K, Pargger H, Müller W, Zimmerli W (1993) Interleukin-6 and acute-phase protein concentrations in surgical intensive care unit patients: diagnostic signs in nosocomial infection. Crit Care Med 21:1175–1180PubMedCrossRefGoogle Scholar
Dandona P, Nix D, Wilson MF, Aljada A, Love J, Assicot M, Bohuon C (1994) Procalcitonin increase after endotoxin injection in normal subjects. J Clin Endocrinol Metab 79: 1605–1608PubMedCrossRefGoogle Scholar
De Bastiani G, Mosconi F, Spagnol G, Nicolato A, Ferrari S, Aprili F (1992) High calcitonin levels in unconscious polytrauma patients. J Bone Joint Surg Br 74-B: 101–104Google Scholar
Koch SM, Melhorn U, Baggstrom E, Donovan D, Allen J (1996) Hypercalcitoninemia and inappropriate calciuria in the acute trauma patient. J Crit Care 11:117–121PubMedCrossRefGoogle Scholar