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Etiology and clinical relevance of elevated platelet count in ICU patients

A retrospective analysis

Ätiologie und klinische Bedeutung erhöhter Thrombozytenzahlen bei Intensivpatienten

Retrospektive Studie

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Abstract

Background

Thrombocytosis is a common phenomenon in critically ill patients. Although thrombocytosis is an independent risk factor for complications, it does not seem to influence mortality in intensive care (ICU) patients.

Objectives

Our investigation aimed to evaluate the etiological and clinical relevance of a platelet count greater than 450 × 109/l in ICU patients.

Materials and methods

Patients admitted for a minimum of 4 days to an interdisciplinary ICU during a 45-month period were enrolled in this retrospective observational study. Thrombocytopenic patients (platelet count <150 × 109/l in at least one measurement) were excluded. The study patients were divided into two groups: thrombocytosis group (thrombocytes >450 × 109/l in at least one measurement) and control group (thrombocytes = 150 − 450 × 109/l during ICU stay). Univariate and multiple regression analysis were used to determine the influence of severe co-morbidities on the development of thrombocytosis and the association of elevated platelet count with thrombotic embolism, length of stay (LOS) in ICU, and mortality.

Results

A total of 307 patients were analyzed, of whom thrombocytosis was observed in 119 cases. Independent risk factors for the development of thrombocytosis included SIRS, mechanical ventilation, and acute bleeding. Increasing age reduced the risk of thrombocytosis. Thromboembolism occurred in 16 patients (13.4%) with an elevated platelet count and only in nine patients (4.7%) with physiological platelet values (OR: 3.1; 95% CI: 1.3–7.2; p = 0.009). Mean duration of LOS was significantly longer in patients with thrombocytosis (25.2 vs.11.7 days, p < 0.0001). Elevated platelet count showed a negative correlation with ICU mortality (OR: 0.32; 95%-CI: 0.12–0.83; p = 0.019).

Conclusion

In our retrospective analysis the occurrence of thrombocytosis in a cohort of interdisciplinary ICU patients was associated with a higher rate of complications and longer LOS in the ICU. Despite these findings, thrombocytosis seems to reduce mortality in critical ill patients.

Zusammenfassung

Hintergrund

Eine erhöhte Thrombozytenzahl tritt häufig bei kritisch kranken Patienten auf. Obwohl diese als ein Risikofaktor für schwere Komplikationen betrachtet wird, scheint sie die Prognose der Intensivpatienten nicht zu verschlechtern.

Fragestellung

Ziel dieser Studie war es, die Ätiologie und klinische Relevanz einer Thrombozytenzahl über 450 × 109/l in einem intensivmedizinischen Patientenkollektiv zu untersuchen.

Material und Methoden

In diese retrospektive Beobachtungsstudie wurden für einen 45-monatigen Zeitraum alle Intensivpatienten mit einer Verweildauer von mindestens 4 Tagen eingeschlossen. Die Patienten mit einer Thrombozytenzahl unter 150 × 109/l wurden aus der weiteren Analyse ausgeschlossen. Die evaluierten Patienten wurden in 2 Gruppen geteilt: Thrombozytosegruppe (Thrombozyten >450 × 109/l in mindestens einer Untersuchung) und Kontrollgruppe (Thrombozyten: 150 × 109/l bis 450 × 109/l). Mit univarianten und multiplen Regressionsanalysen wurden Komorbiditäten auf das Auftreten einer Thrombozytose hin untersucht. Darüber hinaus wurde die Assoziation einer erhöhten Thrombozytenzahl in Bezug auf eine Thromboembolie, die intensivmedizinische Verweildauer und Mortalität evaluiert.

Ergebnisse

Ausgewertet wurden die Daten von 307 Patienten: 119 in der Thrombozytosegruppe und 188 in der Kontrollgruppe. Die unabhängige Risikofaktoren einer Thrombozytose waren: SIRS („systemic inflammatory response syndrome“), Beatmungstherapie, akute Hämorrhagie und geringeres Alter. Eine venöse Thromboembolie trat bei 13,4 % der Patienten mit Thrombozytose und bei 4,7 % der Kontrollgruppe auf (Odds Ratio, OR: 3,1; 95 %-Konfidenzintervall, 95 %-KI: 1,3-7,2; p = 0,009). Die durchschnittliche Verweildauer auf der Intensivstation war in der Thrombozytosegruppe signifikant länger als in der Kontrollgruppe (25,2 ± 17,7 vs. 11,7 ± 10,4 Tage; p < 0,0001). Die Mortalität lag bei 11,7 % in der Thrombozytosegruppe, verglichen mit 14,9 % in der Kontrollgruppe, wobei die Patienten mit Thrombozytose einen wesentlich höheren initialen Schwergrad der Erkrankung aufwiesen (Simplified Acute Physiology Score II, SAPS II: 55 vs. 49 Punkte; p < 0,001). In der multifaktoriellen Regressionsanalyse war die Thrombozytose signifikant mit einer Risikosenkung der intensivstationären Mortalität assoziiert (OR: 0,32; 95%-KI: 0,12–0,83; p = 0,019).

Schlussfolgerung

Thrombozytose bei intensivmedizinischen Patienten ist mit einem Auftreten schwerer Komorbiditäten und einem erhöhten Risiko venöser Thromboembolien assoziiert, woraus sich eine verlängerte intensivmedizinische Verweildauer ableiten lässt. Hingegen reduziert eine Thrombozytose bei intensivmedizinischen Patienten das Mortalitätsrisiko und kann somit als Zusatzparameter in der Abschätzung des Verlaufs dienen.

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References

  1. Agrawal S, Sachdev A, Gupta D et al (2008) Platelet counts and outcome in the pediatric intensive care unit. Indian J Crit Care Med 12:102–108

    Article  PubMed  PubMed Central  Google Scholar 

  2. Akca S, Haji-Michael P, De Mendonca A et al (2002) Time course of platelet counts in critically ill patients. Crit Care Med 30:753–756

    Article  PubMed  Google Scholar 

  3. Akinosoglou K, Alexopoulos D (2014) Use of antiplatelet agents in sepsis: a glimpse into the future. Thromb Res 133:131–138

    Article  CAS  PubMed  Google Scholar 

  4. American Thoracic Society, Infectious Diseases Society Of A (2005) Guidelines for the management of adults with hospital-acquired, ventilator-associated, and healthcare-associated pneumonia. Am J Respir Crit Care Med 171:388–416

    Article  Google Scholar 

  5. Bone RC, Balk RA, Cerra FB et al (1992) Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. The ACCP/SCCM Consensus Conference Committee. American College of Chest Physicians/Society of Critical Care Medicine. Chest 101:1644–1655

    Article  CAS  PubMed  Google Scholar 

  6. Brun-Buisson C (2000) The epidemiology of the systemic inflammatory response. Intensive Care Med 26(Suppl 1):S64–S74

    Article  PubMed  Google Scholar 

  7. Buss DH, Cashell AW, O’connor ML et al (1994) Occurrence, etiology, and clinical significance of extreme thrombocytosis: a study of 280 cases. Am J Med 96:247–253

    Article  CAS  PubMed  Google Scholar 

  8. De Backer D, Orbegozo Cortes D, Donadello K et al (2014) Pathophysiology of microcirculatory dysfunction and the pathogenesis of septic shock. Virulence 5:73–79

    Article  PubMed  Google Scholar 

  9. Folman CC, Ooms M, Kuenen BB et al (2001) The role of thrombopoietin in post-operative thrombocytosis. Br J Haematol 114:126–133

    Article  CAS  PubMed  Google Scholar 

  10. Gofrit ON, Shapiro A, Rund D et al (2006) Postoperative thrombocytosis as a marker for complications after urologic surgery. Scand J Urol Nephrol 40:161–165

    Article  PubMed  Google Scholar 

  11. Griesshammer M, Bangerter M, Sauer T et al (1999) Aetiology and clinical significance of thrombocytosis: analysis of 732 patients with an elevated platelet count. J Intern Med 245:295–300

    Article  CAS  PubMed  Google Scholar 

  12. Gurung AM, Carr B, Smith I (2001) Thrombocytosis in intensive care. Br J Anaesth 87:926–928

    Article  CAS  PubMed  Google Scholar 

  13. Ho KM, Chavan S (2013) Prevalence of thrombocytosis in critically ill patients and its association with symptomatic acute pulmonary embolism. A multicentre registry study. Thromb Haemost 109:272–279

    Article  CAS  PubMed  Google Scholar 

  14. Ho KM, Yip CB, Duff O (2012) Reactive thrombocytosis and risk of subsequent venous thromboembolism: a cohort study. J Thromb Haemost 10:1768–1774

    Article  CAS  PubMed  Google Scholar 

  15. Kaser A, Brandacher G, Steurer W et al (2001) Interleukin-6 stimulates thrombopoiesis through thrombopoietin: role in inflammatory thrombocytosis. Blood 98:2720–2725

    Article  CAS  PubMed  Google Scholar 

  16. Kashuk JL, Moore EE, Johnson JL et al (2010) Progressive postinjury thrombocytosis is associated with thromboembolic complications. Surgery 148:667–674 (discussion 674–665)

    Article  PubMed  Google Scholar 

  17. Kaushansky K (2005) The molecular mechanisms that control thrombopoiesis. J Clin Invest 115:3339–3347

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  18. Le Gall JR, Lemeshow S, Saulnier F (1993) A new Simplified Acute Physiology Score (SAPS II) based on a European/North American multicenter study. JAMA 270:2957–2963

    Article  PubMed  Google Scholar 

  19. Moher D, Hopewell S, Schulz KF et al (2010) CONSORT 2010 explanation and elaboration: updated guidelines for reporting parallel group randomised trials. J Clin Epidemiol 63:e1–e37

    Article  PubMed  Google Scholar 

  20. Muehlstedt SG, Richardson CJ, Lyte M et al (2002) Systemic and pulmonary effector cell function after injury. Crit Care Med 30:1322–1326

    Article  PubMed  Google Scholar 

  21. Nijsten MW, Ten Duis HJ, Zijlstra JG et al (2000) Blunted rise in platelet count in critically ill patients is associated with worse outcome. Crit Care Med 28:3843–3846

    Article  CAS  PubMed  Google Scholar 

  22. Pate A, Baltazar GA, Labana S et al (2015) Systemic inflammatory response syndrome and platelet count 〉/=250x10(9) are associated with venous thromboembolic disease. Int J Gen Med 8:37–40

    PubMed  PubMed Central  Google Scholar 

  23. Powner DJ, Hoots WK (2008) Thrombocytosis in the NICU. Neurocrit Care 8:471–475

    Article  PubMed  Google Scholar 

  24. Reid VL, Webster NR (2012) Role of microparticles in sepsis. Br J Anaesth 109:503–513

    Article  CAS  PubMed  Google Scholar 

  25. Russwurm S, Vickers J, Meier-Hellmann A et al (2002) Platelet and leukocyte activation correlate with the severity of septic organ dysfunction. Shock 17:263–268

    Article  PubMed  Google Scholar 

  26. Salim A, Hadjizacharia P, Dubose J et al (2009) What is the significance of thrombocytosis in patients with trauma? J Trauma 66:1349–1354

    Article  PubMed  Google Scholar 

  27. Schafer AI (2004) Thrombocytosis. N Engl J Med 350:1211–1219

    Article  CAS  PubMed  Google Scholar 

  28. Schmuziger M, Christenson JT, Maurice J et al (1995) Reactive thrombocytosis after coronary bypass surgery. An important risk factor. Eur J Cardiothorac Surg 9:393–397 (discussion 397–398)

    Article  CAS  PubMed  Google Scholar 

  29. Stamou KM, Toutouzas KG, Kekis PB et al (2006) Prospective study of the incidence and risk factors of postsplenectomy thrombosis of the portal, mesenteric, and splenic veins. Arch Surg 141:663–669

    Article  PubMed  Google Scholar 

  30. Strauss R, Wehler M, Mehler K et al (2002) Thrombocytopenia in patients in the medical intensive care unit: bleeding prevalence, transfusion requirements, and outcome. Crit Care Med 30:1765–1771

    Article  PubMed  Google Scholar 

  31. Tchebiner JZ, Nutman A, Boursi B et al (2011) Diagnostic and prognostic value of thrombocytosis in admitted medical patients. Am J Med Sci 342:395–401

    Article  PubMed  Google Scholar 

  32. Tefferi A, Thiele J, Orazi A et al (2007) Proposals and rationale for revision of the World Health Organization diagnostic criteria for polycythemia vera, essential thrombocythemia, and primary myelofibrosis: recommendations from an ad hoc international expert panel. Blood 110:1092–1097

    Article  CAS  PubMed  Google Scholar 

  33. Valade N, Decailliot F, Rebufat Y et al (2005) Thrombocytosis after trauma: incidence, aetiology, and clinical significance. Br J Anaesth 94:18–23

    Article  CAS  PubMed  Google Scholar 

  34. Van Wessem KJ, Hennus MP, Heeres M et al (2013) Mechanical ventilation is the determining factor in inducing an inflammatory response in a hemorrhagic shock model. J Surg Res 180:125–132

    Article  PubMed  Google Scholar 

  35. Van Wessem KJ, Hennus MP, Van Wagenberg L et al (2013) Mechanical ventilation increases the inflammatory response induced by lung contusion. J Surg Res 183:377–384

    Article  PubMed  Google Scholar 

  36. Vanderschueren S, De Weerdt A, Malbrain M et al (2000) Thrombocytopenia and prognosis in intensive care. Crit Care Med 28:1871–1876

    Article  CAS  PubMed  Google Scholar 

  37. Wolber EM, Fandrey J, Frackowski U et al (2001) Hepatic thrombopoietin mRNA is increased in acute inflammation. Thromb Haemost 86:1421–1424

    CAS  PubMed  Google Scholar 

  38. Zarbock A, Polanowska-Grabowska RK, Ley K (2007) Platelet-neutrophil-interactions: linking hemostasis and inflammation. Blood Rev 21:99–111

    Article  CAS  PubMed  Google Scholar 

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Acknowledgements

The authors thank Carmen Hennig and Annett Christel for the help in preparing the patients’ database.

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Authors and Affiliations

  1. Department of Anaesthesiology and Intensive Care Medicine, Martin-Luther-University, Halle-Wittenberg, Ernst-Grube-Straße 40, 06120, Halle (Saale), Germany

    M. Banach,  P. Kellner & J. Soukup

  2. Institute of Medical Epidemiology, Biostatistics and Informatics, Martin-Luther-University Halle-Wittenberg, Magdeburger-Straße 8, 06112, Halle (Saale), Germany

    C. Lautenschläger

  3. Klinik für Anästhesiologie und Intensivmedizin, Universitätsklinikum Schleswig-Holstein, Campus Lübeck, Ratzeburger Allee 16, 23538, Lübeck, Germany

    P. Kellner

  4. Department of Anaesthesiology, Intensive Care and Palliative Medicine, Carl-Thiem-Hospital, Thiemstraße 111, 03048, Cottbus, Germany

    J. Soukup

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  1. M. Banach
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Correspondence to P. Kellner.

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Conflict of interest

M. Banach, C. Lautenschläger, P. Kellner, and J. Soukup declare that they have no competing interests.

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. Informed consent was obtained from all individual participants included in the study.

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M. Buerke, Siegen

P. Kellner and J. Soukup contributed equally to this study.

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Banach, M., Lautenschläger, C., Kellner, P. et al. Etiology and clinical relevance of elevated platelet count in ICU patients. Med Klin Intensivmed Notfmed 113, 101–107 (2018). https://doi.org/10.1007/s00063-017-0276-y

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  • DOI: https://doi.org/10.1007/s00063-017-0276-y

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