Combining Serum Procalcitonin Level, Thromboelastography, and Platelet Count to Predict Short-term Development of Septic Shock in Intensive Care Unit

Abstract

Objective

Despite the recent advances in diagnosis and treatment, sepsis continues to lead to high morbidity and mortality. Early diagnosis and prompt treatment are essential to save lives. However, most biomarkers can only help to diagnose sepsis, but cannot predict the development of septic shock in high-risk patients. The present study determined whether the combined measurement of procalcitonin (PCT), thromboelastography (TEG) and platelet (PLT) count can predict the development of septic shock.

Methods

A retrospective study was conducted on 175 septic patients who were admitted to the intensive care unit between January 2017 and February 2021. These patients were divided into two groups: 73 patients who developed septic shock were assigned to the septic shock group, while the remaining 102 patients were assigned to the sepsis group. Then, the demographic, clinical and laboratory data were recorded, and the predictive values of PCT, TEG and PLT count for the development of septic shock were analyzed.

Results

Compared to the sepsis group, the septic shock group had statistically lower PLT count and TEG measurements in the R value, K value, α angle, maximum amplitude, and coagulation index, but had longer prothrombin time (DT), longer activated partial thromboplastin time (APTT), and higher PCT levels. Furthermore, the Sequential Organ Failure Assessment (SOFA) score was higher in the septic shock group. The multivariate logistic regression analysis revealed that PCT, TEG and PLT count were associated with the development of septic shock. The area under the curve analysis revealed that the combined measurement of PCT, TEG and PLT count can be used to predict the development of septic shock with higher accuracy, when compared to individual measurements.

Conclusion

The combined measurement of PCT, TEG and PLT count is a novel approach to predict the development of septic shock in high-risk patients.

Keywords

sepsis / shock / thromboelastography / procalcitonin; platelet

References

[1] KumarS, TripathyS, JyotiA, et al.. Recent advances in biosensors for diagnosis and detection of sepsis: A comprehensive review. Biosens Bioelectron, 2019, 124–125: 205-215

[2] KerriganSW, DevineT, FitzpatrickG, et al.. Early Host Interactions That Drive the Dysregulated Response in Sepsis. Front Immunol, 2019, 10: 1748

[3] CaraballoC, JaimesF. Organ Dysfunction in Sepsis: An Ominous Trajectory From Infection To Death. Yale J Biol Med, 2019, 92(4): 629-640

[4] DugarS, ChoudharyC, DuggalA. Sepsis and septic shock: Guideline-based management. Cleve Clin J Med, 2020, 87(1): 53-64

[5] LevinsonAT, CasserlyBP, LevyMM. Reducing mortality in severe sepsis and septic shock. Semin Respir Crit Care Med, 2011, 32(2): 195-205

[6] HuntonR. Seeking a balanced approach to implementing sepsis guidelines. JAAPA, 2020, 33(7): 13-17

[7] GauerRL. Early recognition and management of sepsis in adults: the first six hours. Am Fam Physician, 2013, 88(1): 44-53

[8] HotchkissRS, MoldawerLL, OpalSM, et al.. Sepsis and septic shock. Nat Rev Dis Primers, 2016, 2: 16045

[9] BlancoJ, Muriel-BombinA, SagredoV, et al.. Incidence, organ dysfunction and mortality in severe sepsis: a Spanish multicentre study. Crit Care, 2008, 12(6): R158

[10] MartinGS, ManninoDM, EatonS, et al.. The epidemiology of sepsis in the United States from 1979 through 2000. N Engl J Med, 2003, 348(16): 1546-1554

[11] AngusDC, Linde-ZwirbleWT, LidickerJ, et al.. Epidemiology of severe sepsis in the United States: analysis of incidence, outcome, and associated costs of care. Crit Care Med, 2001, 29(7): 1303-1310

[12] HungSK, LanHM, HanST, et al.. Current Evidence and Limitation of Biomarkers for Detecting Sepsis and Systemic Infection. Biomedicines, 2020, 8(11): 494

[13] TeggertA, DattaH, AliZ. Biomarkers for Point-of-Care Diagnosis of Sepsis. Micromachines (Basel), 2020, 11(3): 286

[14] BozzaFA, SalluhJI, JapiassuAM, et al.. Cytokine profiles as markers of disease severity in sepsis: a multiplex analysis. Crit Care, 2007, 11(2): R49

[15] LiuD, SuL, HanG, et al.. Prognostic Value of Procalcitonin in Adult Patients with Sepsis: A Systematic Review and Meta-Analysis. PLoS One, 2015, 10(6): e0129450

[16] GregorianoC, HeilmannE, MolitorA, et al.. Role of procalcitonin use in the management of sepsis. J Thorac Dis, 2020, 12(Suppl1): S5-S15

[17] BeckerKL, SniderR, NylenES. Procalcitonin in sepsis and systemic inflammation: a harmful biomarker and a therapeutic target. Br J Pharmacol, 2010, 159(2): 253-264

[18] FontMD, ThyagarajanB, KhannaAK. Sepsis and Septic Shock — Basics of diagnosis, pathophysiology and clinical decision making. Medi Clin North Am, 2020, 104(4): 573-585

[19] SimmonsJ, PittetJF. The coagulopathy of acute sepsis. Curr Opin Anaesthesiol, 2015, 28(2): 227-236

[20] DingR, MengY, MaX. The Central Role of the Inflammatory Response in Understanding the Heterogeneity of Sepsis-3. Biomed Res Int, 2018, 2018: 5086516

[21] BosmannM, WardPA. The inflammatory response in sepsis. Trends Immunol, 2013, 34(3): 129-136

[22] TsaoCM, HoST, WuCC. Coagulation abnormalities in sepsis. Acta Anaesthesiol Taiwan, 2015, 53(1): 16-22

[23] MullerMC, MeijersJC, VroomMB, et al.. Utility of thromboelastography and/or thromboelastometry in adults with sepsis: a systematic review. Crit Care, 2014, 18(1): R30

[24] MuzaffarSN, BaroniaAK, AzimA, et al.. Thromboelastography for Evaluation of Coagulopathy in Nonbleeding Patients with Sepsis at Intensive Care Unit Admission. Indian J Crit Care Med, 2017, 21(5): 268-273

[25] GucluE, DurmazY, KarabayO. Effect of severe sepsis on platelet count and their indices. Afr Health Sci, 2013, 13(2): 333-338

[26] Vardon-BounesF, RuizS, GratacapMP, et al.. Platelets Are Critical Key Players in Sepsis. Int J Mol Sci, 2019, 20(14): 3494

[27] GibotS, BeneMC, NoelR, et al.. Combination biomarkers to diagnose sepsis in the critically ill patient. Am J Respir Crit Care Med, 2012, 186(1): 65-71

[28] Shankar-HariM, PhillipsGS, LevyML, et al.. Developing a New Definition and Assessing New Clinical Criteria for Septic Shock: For the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA, 2016, 315(8): 775-787

[29] DewitteA, LepreuxS, VilleneuveJ, et al.. Blood platelets and sepsis pathophysiology: A new therapeutic prospect in critically [corrected] ill patients?. Ann Intensive Care, 2017, 7(1): 115

[30] IbaT, LevyJH. Inflammation and thrombosis: roles of neutrophils, platelets and endothelial cells and their interactions in thrombus formation during sepsis. J Thromb Haemost, 2018, 16(2): 231-241

[31] ChangJC. Sepsis and septic shock: endothelial molecular pathogenesis associated with vascular microthrombotic disease. Thromb J, 2019, 17: 10

[32] StiefTW, IjaghaO, WeisteB, et al.. Analysis of hemostasis alterations in sepsis. Blood Coagul Fibrinolysis, 2007, 18(2): 179-186