Printer Friendly

Early Kinetics of Procalcitonin in Predicting Surgical Outcomes in Type A Aortic Dissection Patients.

Byline: Hua. Liu, Zhe. Luo, Lan. Liu, Xiao-Mei. Yang, Ya-Min. Zhuang, Ying. Zhang, Guo-Wei. Tu, Guo-Guang. Ma, Guang-Wei. Hao, Jian-Feng. Luo, Ji-Li. Zheng, Chun-Sheng. Wang

Background: In cardiac surgery, elevation of procalcitonin (PCT) could be observed postoperatively in the absence of any evidence of infection and also seems to be a prognostic marker. PCT levels measured in patients undergoing Type A aortic dissection (TAAD) were used to determine prognostic values for complications and surgical outcomes. Methods: Measurements of PCT, C-reactive protein (CRP), and leukocyte count were observed in TAAD surgery patients (n = 251; average age: 49.02 [+ or -] 12.83 years; 78.5% male) at presurgery (T0) and 24 h (T1), 48 h (T2), and 7 days (T3) postsurgery. PCT clearance (PCTc) on days 2 and 7 was calculated: (PCT[sub]day1− PCT[sub]day2/day7)/PCT[sub]day1 x 100%. Endotracheal intubation duration, length of stay (LOS) in the Intensive Care Unit (ICU)/hospital, and complications were recorded. Results: PCT peaked 24 h postsurgery (median 2.73 ng/ml) before decreasing. Correlation existed between PCT levels at T1 and duration of cardiopulmonary bypass (P = 0.001, r = 0.278). Serum PCT concentrations were significantly higher in nonsurvivor and multiple organ dysfunction syndrome groups on all postoperative days. PCT levels at T1 correlated with length of time of ventilation support and ICU/hospital LOS. Comparing PCT values of survivors versus nonsurvivors, a PCT cutoff level of 5.86 ng/ml at T2 had high sensitivity (70.6%) and specificity (74.3%) in predicting in-hospital death. PCTc-day 2 and 7 were significantly higher in survivor compared with nonsurvivor patients (38% vs. 8%, P= 0.012, 83% vs. −39%, P< 0.001). A PCTc-day 7 cutoff point of 48.7% predicted survival with high sensitivity (77.8%) and specificity (81.8%). Conclusions: PCT level and PCTc after TAAD surgery might serve as early prognostic markers to predict postoperative outcome. PCT measurement may help identify high-risk patients.


In the clinical setting, morbidity and mortality associated with the Stanford Type A aortic dissection (TAAD) remain higher than for other cardiac operations, such as valvular surgery and coronary artery surgery. The most recent International Registry of Acute Aortic Dissection report showed an 18% operative mortality.[sup][1] Although improved surgical experience and perioperative management have contributed to enhanced operative outcome of this lethal aortic disease, severe postoperative complications continue to arise. Intimal tear and crossing of blood into the artery wall leads to the formation of a false lumen and subsequent systemic inflammatory responses.[sup][2] Aortic surgery, along with greater surgical trauma, longer cardiopulmonary bypass (CPB) time, deep hypothermic circulatory arrest (DHCA), and massive transfusion aggravates this response. Presentations of TAAD, such as tamponade and malperfusion, have a major impact on clinical outcome,[sup][3] but prolonged or severe systemic inflammatory responses also negatively affect postoperative recovery and surgical outcome. Typical markers, such as white blood cells (WBCs) and C-reactive protein (CRP), may reflect this response but nonspecifically. Procalcitonin (PCT) is the calcitonin precursor protein comprising 116 amino acids. It originates from the liver upon stimulation by tumor necrosis factor or interleukin-6 arising from bacterial infection.[sup][4] PCT is usually undetectable in healthy humans and is considered a specific marker of infection.[sup][5] Studies have shown that PCT is a promising diagnostic and prognostic biomarker of severe sepsis and septic shock.[sup][6],[7] However, it is now known that PCT is elevated in several noninfectious conditions such as myocardial infarction, malaria, severe trauma, surgery, cardiogenic shock, and burns.[sup][8],[9],[10] In cardiac surgery, elevation of PCT has been observed postoperatively in the absence of any evidence of infection and also appears to be a good prognostic marker.[sup][11] A single postoperative PCT measurement predicts delayed complications in patients undergoing elective cardiac surgery.[sup][12] To our knowledge, only a few studies of small sample size have examined perioperative PCT levels in TAAD patients.[sup][13],[14] The objective of our study was to investigate the perioperative changes in PCT levels and their value in reflecting postoperative complications and mortality in TAAD patients.


Ethical approval

This study was approved by the Ethics Committee of this hospital. And all patients provided informed consents.

Patient selection

Patients who underwent TAAD surgery from April 2013 to November 2015 were included in the study. All procedures involved a median sternotomy and total CPB. CPB was instituted using right axillary artery or femoral artery perfusion and right atrial venous drainage. Core cooling was carried out to an esophageal temperature of 20–25[degrees]C. Antegrade selective cerebral perfusion was applied during circulatory arrest.

Definitions and experimental protocol

Blood samples were obtained preoperatively (T0) and at 24 h (T1), 48 h (T2), and 7 days (T3) postoperation. Serum concentrations of CRP, leukocyte counts, and PCT were measured. PCT clearance (PCTc) on days 2 and 7 was calculated using the following formula: PCTc[sub]day2/day7 (%) = (PCT[sub]day1 − PCT[sub]day2/day7)/PCT[sub]day1 x 100%. Body temperature measurements, microbiologic culture, and radiologic examinations were performed postoperation. Duration of endotracheal intubation, duration of stay in the Intensive Care Unit (ICU) and hospital, and complications were recorded.

Asides from clinical examination, infection was diagnosed by chest radiography, leukocyte count, blood culture, sputum culture, and drainage culture. The final diagnosis of infection was determined by two independent experts in regard to the complete medical chart. Mortality was defined as death occurring within 30 days of operation during the initial hospital stay. Organ dysfunctions included respiratory dysfunction (PaO[sub]2/FiO[sub]2<200 or the need for ventilator support for >72 h), cardiac dysfunction (low cardiac output syndrome or continuous infusion of inotropic agents or vasopressor in absence of hypovolemia), renal dysfunction (an increase in serum creatinine of 44 [micro]mol/L over baseline value or the need for hemodialysis), and nervous system complications (including persistent paraparesis or paraplegia due to impairment of blood supply to the spinal cord and brain or signs of central neurological damage after cerebral hypoperfusion). Multiple organ dysfunction syndrome (MODS) was defined when two or more organ dysfunctions were present.

Statistical analysis

Quantitative variables were expressed numerically as the mean [+ or -] standard deviation or medians (25–75%), depending on the nature of the distribution. Qualitative variables were expressed as frequencies. Student's t -test or the Mann–Whitney U -test was used to evaluate differences between groups. Categorical variables were analyzed by the Pearson's Chi-square test. To explore the relationship between serum PCT concentration and duration of CPB and aortic clamping, linear regression analysis was performed. To identify factors affecting 30-day mortality, we performed binary logistic regression analysis using death as a dependent variable. Differences were considered statistically significant when the P < 0.05. The optimum cutoff points were determined with a receiver operating characteristics (ROC) curve. Statistical analysis was performed using SPSS Statistics 17.0 (SPSS Inc., Chicago, USA).


Demographics of patients

Two patients were excluded from the study due to death on the 1[sup]st postoperative day. A total of 251 patients were included in the study, of which 197 patients (78.5%) were male and 54 were female. The average age was 49.02 [+ or -] 12.83 years. Two hundred and twenty-five patients (89.6%) were admitted with acute aortic dissection (chest pain or other related symptoms which presented less than 14 days before the operation). The preoperative characteristics and comorbidities of the patients are shown in [Table 1], and there was no difference between survivor and nonsurvivor groups. Mean pump time, cross-clamp time, and DHCA time were 165.54 [+ or -] 37.80 min, 101.23 [+ or -] 28.69 min, and 29.11 [+ or -] 9.50 min, respectively. The surgical procedures are shown in [Table 1]. Concomitant procedures included coronary artery bypass grafting (CABG) in 13 patients, aortic-femoral artery bypass in nine patients, mitral valve replacement in one patient, and atrial septal defect repair in two patients.{Table 1}

Of the 251 patients, 56 (22.3%) developed cardiac dysfunction, 69 (27.5%) developed severe renal dysfunction requiring dialysis therapy, 98 (39%) developed respiratory dysfunction, 50 (19.9%) developed infections, and 47 (18.7%) developed nervous complications. Twenty-seven patients (10.8%) died within 30 days of operation and 79 patients (31.5%) developed MODS.

Perioperative level of procalcitonin and other inflammatory markers

[Table 2] shows the postoperative course of the inflammatory markers in different groups. The concentrations of PCT, CRP, and WBC increased significantly compared to the basal value from T1 to T3 ( P < 0.01). The peak level of PCT was reached at T1 (2.73 ng/ml). Peak serum CRP concentrations and leukocyte counts occurred at T2, and decreased slowly thereafter, but had not returned to normal by T3.{Table 2}

Correlation existed between PCT levels at T1 and duration of CPB ( P = 0.001, r = 0.278), but no significant correlation was found between PCT levels and time of aortic clamping ( P = 0.687) or DHCA time ( P = 0.692) [Table 3].{Table 3}

Serum procalcitonin level and surgical outcomes

As shown in [Table 2], the serum PCT concentrations were significantly higher in the nonsurvivor group than in the survivor group on all postoperative days, with a peak value of 19.11 pg/ml at T2. Furthermore, serum PCT concentration increased significantly in MODS compared with non-MODS patients from T1 to T3.

Correlation existed between serum PCT concentration at T1 and the duration of endotracheal intubation ( P < 0.001, r = 0.390), duration of stay in the ICU ( P < 0.001, r = 0.371), and duration of stay in the hospital ( P = 0.008, r = 0.182) [Table 3].

[Table 4] shows intragroup analysis of survivors and nonsurvivors within the infected and noninfected groups. We found significantly higher serum PCT levels at T2 and T3 in the nonsurvivors.{Table 4}

When comparing PCT values of survivors versus nonsurvivors, the area under the ROC curve was 0.646 ( P = 0.131) at T0, 0.727 ( P = 0.003) at T1, and 0.782 ( P < 0.001) at T2 [Figure 1]. For a cutoff of 5.86 ng/ml measured at T2, PCT had a sensitivity of 70.6% and a specificity of 74.3% in predicting in-hospital death.{Figure 1}

PCTc was associated with survival prediction. Both PCTc-day 2 and PCTc-day 7 were significantly higher in survivors versus nonsurvivors ( P = 0.012, P < 0.001). The area under ROC curve of PCTc-day 7 for survival prediction was 0.870 ( P < 0.001). A cutoff point of 48.7% had a sensitivity of 77.8% and a specificity of 81.8% [Figure 2].{Figure 2}

To determine factors associated with 30-day mortality after surgery, binary logistic regression analysis was carried out using age, sex, PCT >6 ng/ml at T2, duration of CPB, respiratory dysfunction, renal dysfunction, and infection as independent variables. Serum PCT level >6 ng/ml at T2 (odds ratio [ OR ] = 7.473, 95% confidence interval [ CI ] = 1.061–32.885, P = 0.043) and infection ( OR = 5.908, 95% CI = 1.684–33.168, P = 0.008) were associated with 30-day mortality [Table 5].{Table 5}

A cutoff point of 6 ng/ml at T2 was used to stratify patients into the PCT <6 ng/ml group and PCT ≥6 ng/ml group [Table 6]. Patients with elevated levels of PCT after aortic dissection surgery had a longer duration of endotracheal intubation (296.54 [+ or -] 321.57 min vs. 140.28 [+ or -] 274.45 min, P = 0.01) and longer ICU stay (9.71 [+ or -] 12.77 min vs. 15.88 [+ or -] 13.90 min, P = 0.013) and a greater probability of cardiac dysfunction ( P < 0.001), renal dysfunction ( P < 0.001), nervous complication ( P = 0.002), infection ( P = 0.034), and death in hospital ( P = 0.002).{Table 6}


When measuring PCT in TAAD patients, we found that the early kinetics of PCT might show a better prognostic value compared to other classic markers. The finding of this study had verified the prior hypothesis. First, serum PCT concentrations and PCTc were significantly higher in the nonsurvivor group and MODS group. ROC analyses revealed that PCT levels and PCTc had a highly predictive accuracy to detect in-hospital death. Second, increased PCT levels were related to complications and poor outcomes after TAAD surgery.

The normal range of serum PCT concentration after cardiac surgery is undefined. Serum PCT levels peak within 24 h postoperatively and return to normal values in the days following an uncomplicated cardiac surgery. Peak values of PCT range from 0.5 to 7.0 ng/ml.[sup][15] Specific surgical techniques may influence the evolution of serum PCT concentration after cardiac surgery in the absence of postoperative complications. Patients are reported to have higher PCT levels after CABG than after off-pump coronary artery bypass [sup][16] and higher PCT levels after valvular and thoracic aortic surgeries than after CABG.[sup][17] Other investigators have not found a difference in PCT levels between different types of operations.[sup][18],[19] Intraoperative factors such as aortic cross-clamping time, duration of CPB, and duration of surgery influence serum PCT levels.[sup][20],[21] Our research shows that median PCT levels peaked (2.73 ng/ml) at 24 h postoperation. Patients may have higher PCT levels after aortic surgery than after CABG or valve surgery because they have a longer duration of operation and CPB.

PCT levels are higher in patients with a poor outcome and are increased in patients who develop later postoperative complications. Several studies have reported higher PCT levels in nonsurvivors compared with survivors after cardiac surgery. Dorge et al .[sup][22] found that PCT levels >10 ng/ml 24 h after operation could discriminate nonsurvivors in a high-risk group of patients with a sensitivity of 72% and a specificity of 51%. They also reported higher PCT levels in patients who developed postoperative organ failure than in those who did not. Adamik et al . reported that PCT concentrations were significantly elevated in patients with complications.[sup][23] Loebe et al . investigated 722 patients after routine cardiac operations and found that an elevated PCT level of >5 ng/ml 24 h after CPB was predictive of outcome.[sup][17] CRP does not represent a useful prognostic marker likely because of its prolonged elevation after an uncomplicated course. On the other hand, PCT yields an elevated negative predictive value of complications after cardiac surgery. A study by Kerbaul et al . suggests that PCT concentrations of <5 ng/ml are not associated with any postoperative complication.[sup][24] Our results showed that serum PCT concentrations were significantly higher in the nonsurvivor group on all postoperative days than in the survivor group. For a cutoff of 5.86 ng/ml at T2, PCT had a sensitivity of 70.6% and specificity of 74.3% in predicting in-hospital death. Patients with PCT ≥6 ng/ml 48 h after aortic dissection surgery had a longer duration of endotracheal intubation, a longer stay in the ICU, and greater probability of cardiac dysfunction, renal dysfunction, nervous complication, infection, and death in hospital. Correlation existed between serum concentration of PCT at 24 h postoperation and the duration of endotracheal intubation and duration of stay in the ICU/hospital. This finding supports the prognostic value of PCT.

The prognostic value based on the evolution of PCT levels may be more useful than the individual evaluation of initial PCT levels. When serum PCT levels were measured over several days, we observed that patients whose PCT levels remained elevated were at much greater risk of developing severe complications and death than those whose levels dropped in response to therapy. PCTc is an innovative concept that reflects PCT dynamics.[sup][25] In our study, PCTc increased progressively in survivors but decreased in nonsurvivors with significant differences at PCTc-day 2 and 7. Reduction in PCT concentration above 48.7% between days 1 and 7 was considered a good predictor of survival. The dynamics of PCT level, better than the absolute values, could therefore be important in identifying patients who will survive.

The mechanism by which PCT levels are elevated after cardiac surgery is unclear. The use of CPB leads to varying degrees of tissue inflammation and cytokine liberation, triggering a systemic inflammatory response. On the other hand, during cross-clamp and DHCA in aortic dissection surgery, decreased blood flow affects the intestinal mucosa and enterocytes, reducing permeability of the intestinal wall. The endogenous bacteria proliferate and generate endotoxins that ultimately promote the release of PCT into the bloodstream.[sup][26] A study by Klingele et al . hypothesized that increased mortality in patients with high PCT after cardiac surgery could, at least partially, be accounted for by undiagnosed nonocclusive mesenteric ischemia (NOMI).[sup][27] However, identification of patients with NOMI remains clinically challenging due to its nonspecific symptoms, and its definitive diagnosis requires angiography which is both time- and cost-intensive.

Cardiac surgery is a sterile operation and the infection was ruled out before the operation. In a study by Chakravarthy et al ., PCT elevation was not associated with bacterial load and was proposed to be due to one or more of the following factors encountered in cardiac surgery: stress of surgery, anesthesia, inotropic and/or vasoconstrictor agent use, hemorrhage, hemodynamic changes, and inflammatory mediator release due to CPB.[sup][11] In a meta-analysis on PCT utility in surgical patients, Uzzan et al . suggested that elevated PCT alone should not be used as a criterion for diagnosing sepsis.[sup][28] However, some studies have reported the diagnostic and predictive value of PCT levels for late infection. Aouifi et al . reported that PCT was superior to CRP in predicting an infection and that PCT had a sensitivity of 85% and specificity of 95% at a concentration of 1 ng/ml.[sup][29] Comparably, Sharma et al . found that PCT >7 ng/ml had 95% sensitivity and 80% specificity to identify bacterial infection after cardiac surgery.[sup][30] The early postoperative increase in serum PCT in the absence of infection after cardiac surgery shows that PCT is influenced by the postoperative inflammatory process related to CPB. Therefore, this increase may interfere with the diagnosis of infection during the immediate postoperative period. We focused on whether infection could influence the prognostic value of PCT in mortality. We compared survivors and nonsurvivors stratified into infected and noninfected groups and used multiple logistic regression analysis to predict mortality. This showed that PCT could predict mortality excluding the influence of infection.

Our study selected TAAD surgery patients as one single disease to evaluate PCT value in predicting surgical outcomes. It may provide new insights into this "infectious marker" and stimulate further investigations in the course of TAAD surgery. This study has several limitations. First, this is a single-center observational study, and a large sample size is needed to obtain more accurate prognostic information. Second, a series of PCT measurements during all hospitalization may be more valuable. Therefore, a prospective, large-scale multicenter study is required to confirm our results.

These results provide evidence that PCT and PCTc might serve as early prognostic markers in TAAD patients undergoing surgery. Measurement of PCT can be easily integrated into clinical practice, then help identify patients at high risk, and thereby improve prognosis of this population. In the future, we will try to elucidate the underlying mechanisms of PCT elevation and the relationship between PCT and other inflammatory markers such as cytokines in further study.

Financial support and sponsorship

This study was supported by a grant from Youth Foundation of Zhongshan Hospital (No. 2014ZSQN54).

Conflicts of interest

There are no conflicts of interest.


1. Pape LA, Awais M, Woznicki EM, Suzuki T, Trimarchi S, Evangelista A, et al. Presentation, diagnosis, and outcomes of acute aortic dissection: 17-Year trends from the international registry of acute aortic dissection. J Am Coll Cardiol 2015;66:350-8. doi: 10.1016/j.jacc.2015.05.029.

2. Parolari A, Tremoli E, Songia P, Pilozzi A, Di Bartolomeo R, Alamanni F, et al. Biological features of thoracic aortic diseases. Where are we now, where are we heading to: Established and emerging biomarkers and molecular pathways. Eur J Cardiothorac Surg 2013;44:9-23. doi: 10.1093/ejcts/ezs647.

3. Kimura N, Ohnuma T, Itoh S, Sasabuchi Y, Asaka K, Shiotsuka J, et al. Utility of the Penn classification in predicting outcomes of surgery for acute type a aortic dissection. Am J Cardiol 2014;113:724-30. doi: 10.1016/j.amjcard.2013.11.017.

4. Nijsten MW, Olinga P, The TH, de Vries EG, Koops HS, Groothuis GM, et al. Procalcitonin behaves as a fast responding acute phase protein in vivo and in vitro . Crit Care Med 2000;28:458-61. doi: 10.1097/00003246-200002000-00028.

5. Wang T, Cui YL, Lin ZF, Chen DC. Comparative study of plasma endotoxin with procalcitonin levels in diagnosis of bacteremia in Intensive Care Unit Patients. Chin Med J (Engl) 2016;129:417-23. doi: 10.4103/0366-6999.176064.

6. Huang MY, Chen CY, Chien JH, Wu KH, Chang YJ, Wu KH, et al. Serum Procalcitonin and Procalcitonin Clearance as a Prognostic Biomarker in patients with severe sepsis and septic shock. Biomed Res Int 2016;2016:1758501. doi: 10.1155/2016/1758501.

7. Mat Nor MB, Md Ralib A. Procalcitonin clearance for early prediction of survival in critically ill patients with severe sepsis. Crit Care Res Pract 2014;2014:819034. doi: 10.1155/2014/819034.

8. Picariello C, Lazzeri C, Valente S, Chiostri M, Gensini GF. Procalcitonin in acute cardiac patients. Intern Emerg Med 2011;6:245-52. doi: 10.1007/s11739-010-0462-x.

9. Chiwakata CB, Manegold C, Bonicke L, Waase I, Julch C, Dietrich M. Procalcitonin as a parameter of disease severity and risk of mortality in patients with Plasmodium falciparum malaria. J Infect Dis 2001;183:1161-4. doi: 10.1086/319283.

10. Meisner M, Adina H, Schmidt J. Correlation of procalcitonin and C-reactive protein to inflammation, complications, and outcome during the Intensive Care Unit course of multiple-trauma patients. Crit Care 2006;10:R1. doi: 10.1186/cc3910.

11. Chakravarthy M, Kavaraganahalli D, Pargaonkar S, Hosur R, Harivelam C, Bharadwaj A, et al. Elevated postoperative serum procalcitonin is not indicative of bacterial infection in cardiac surgical patients. Ann Card Anaesth 2015;18:210-4. doi: 10.4103/0971-9784.154480.

12. Klingele M, Bomberg H, Schuster S, Schafers HJ, Groesdonk HV. Prognostic value of procalcitonin in patients after elective cardiac surgery: A prospective cohort study. Ann Intensive Care 2016;6:116. doi: 10.1186/s13613-016-0215-8.

13. Liu N, Sun LZ, Xing XY. Analyzing variations and clinical significance of perioperative serum inflammatory indicators in patients undergoing acute aortic dissection repair. Zhonghua Wai Ke Za Zhi 2012;50:1104-7. doi: 10.3760/cma.j.issn.0529-5815.2012.12.011.

14. Kin H, Kawazoe K, Nakajima T, Niinuma H, Kataoka T, Endo S, et al. Perioperative serum procalcitonin concentrations in patients with acute aortic dissection. Eur Surg Res 2003;35:451-4. doi: 10.1159/000072231.

15. Sponholz C, Sakr Y, Reinhart K, Brunkhorst F. Diagnostic value and prognostic implications of serum procalcitonin after cardiac surgery: A systematic review of the literature. Crit Care 2008;10:R145. doi: 10.1186/cc5067.

16. Franke A, Lante W, Fackeldey V, Becker HP, Kurig E, Zoller LG, et al. Pro-inflammatory cytokines after different kinds of cardio-thoracic surgical procedures: Is what we see what we know? Eur J Cardiothorac Surg 2005;28:569-75. doi: 10.1016/j.ejcts.2005.07.007.

17. Loebe M, Locziewski S, Brunkhorst FM, Harke C, Hetzer R. Procalcitonin in patients undergoing cardiopulmonary bypass in open heart surgery- first results of the Procalcitonin in Heart Surgery study (ProHearts). Intensive Care Med 2000;26 Suppl 2:S193-8. doi: 10.1007/BF02900737.

18. Aouifi A, Piriou V, Blanc P, Bouvier H, Bastien O, Chiari P, et al. Effect of cardiopulmonary bypass on serum procalcitonin and C-reactive protein concentrations. Br J Anaesth 1999;83:602-7. doi: 10.1093/bja/83.4.602.

19. Kallel S, Abid M, Jarraya A, Abdenadher M, Mnif E, Frikha I, et al. Kinetics, diagnostic and prognostic value of procalcitonin after cardiac surgery. Ann Biol Clin (Paris) 2012;70:567-80. doi: 10.1684/abc.2012.0745.

20. Meisner M, Rauschmayer C, Schmidt J, Feyrer R, Cesnjevar R, Bredle D, et al. Early increase of procalcitonin after cardiovascular surgery in patients with postoperative complications. Intensive Care Med 2002;28:1094-102. doi: 10.1007/s00134-002-1392-5.

21. Celebi S, Koner O, Menda F, Balci H, Hatemi A, Korkut K, et al. Procalcitonin kinetics in pediatric patients with systemic inflammatory response after open heart surgery. Intensive Care Med 2006;32:881-7. doi: 10.1007/s00134-006-0180-z.

22. Dorge H, Schondube FA, Dorge P, Seipelt R, Voss M, Messmer BJ. Procalcitonin is a valuable prognostic marker in cardiac surgery but not specific for infection. Thorac Cardiovasc Surg 2003;51:322-6. doi: 10.1055/s-2003-45425.

23. Adamik B, Kubler-Kielb J, Golebiowska B, Gamian A, Kubler A. Effect of sepsis and cardiac surgery with cardiopulmonary bypass on plasma level of nitric oxide metabolites, neopterin, and procalcitonin: Correlation with mortality and postoperative complications. Intensive Care Med 2000;26:1259-67. doi: 10.1007/s001340000610.

24. Kerbaul F, Guidon C, Lejeune PJ, Mollo M, Mesana T, Gouin F. Hyperprocalcitonemia is related to noninfectious postoperative severe systemic inflammatory response syndrome associated with cardiovascular dysfunction after coronary artery bypass graft surgery. J Cardiothorac Vasc Anesth 2002;16:47-53. doi: 10.1053/jcan.2002.29672.

25. de Azevedo JR, Torres OJ, Beraldi RA, Ribas CA, Malafaia O. Prognostic evaluation of severe sepsis and septic shock: Procalcitonin clearance vs. ? Sequential Organ Failure Assessment. J Crit Care 2015;30:219.e9-12. doi: 10.1016/j.jcrc.2014.08.018.

26. Cosse C, Sabbagh C, Kamel S, Galmiche A, Regimbeau JM. Procalcitonin and intestinal ischemia: A review of the literature. World J Gastroenterol 2014;20:17773-8. doi: 10.3748/wjg.v20.i47.17773.

27. Klingele M, Bomberg H, Poppleton A, Minko P, Speer T, Schafers HJ, et al. Elevated procalcitonin in patients after cardiac surgery: A hint to nonocclusive mesenteric ischemia. Ann Thorac Surg 2015;99:1306-12. doi: 10.1016/j.athoracsur.2014.10.064.

28. Uzzan B, Cohen R, Nicolas P, Cucherat M, Perret GY. Procalcitonin as a diagnostic test for sepsis in critically ill adults and after surgery or trauma: A systematic review and meta-analysis. Crit Care Med 2006;34:1996-2003. doi: 10.1097/01.CCM.0000226413.54364.36.

29. Aouifi A, Piriou V, Bastien O, Blanc P, Bouvier H, Evans R, et al. Usefulness of procalcitonin for diagnosis of infection in cardiac surgical patients. Crit Care Med 2000;28:3171-6. doi: 10.1097/00003246-200009000-00008.

30. Sharma P, Patel K, Baria K, Lakhia K, Malhotra A, Shah K, et al. Procalcitonin level for prediction of postoperative infection in cardiac surgery. Asian Cardiovasc Thorac Ann 2016;24:344-9. doi: 10.1177/0218492316640953.
COPYRIGHT 2017 Medknow Publications and Media Pvt. Ltd.
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2017 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:Original Article
Author:Liu, Hua; Luo, Zhe; Liu, Lan; Yang, Xiao-Mei; Zhuang, Ya-Min; Zhang, Ying; Tu, Guo-Wei; Ma, Guo-Guan
Publication:Chinese Medical Journal
Article Type:Report
Date:Jul 27, 2017
Previous Article:Left Ventricular Longitudinal Systolic Function in Septic Shock Patients with Normal Ejection Fraction: A Case-control Study.
Next Article:A National Multicenter Survey on Management of Pain, Agitation, and Delirium in Intensive Care Units in China.

Terms of use | Privacy policy | Copyright © 2021 Farlex, Inc. | Feedback | For webmasters