High fibrin/fibrinogen degradation product to fibrinogen ratio is associated with 28-day mortality and massive transfusion in severe trauma

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Abstract

Purpose

There is a lack of association between coagulation biomarkers and long-term mortality in severe trauma. We aimed to investigate the association between coagulation biomarkers on admission and outcome of late stage of trauma.

Methods

This retrospective observational study included patients admitted with severe trauma between 2012 and 2015. We used the area under the receiver operating characteristic curve (AUROC) of coagulation biomarkers to determine 28-day mortality. Head Abbreviated Injury Scale scores greater than 3 were defined as traumatic brain injury (TBI). The primary outcome was 28-day mortality and the secondary outcome was massive transfusion.

Results

Of the 1266 patients included in the study, 28-day mortality rate was 19.7% (n = 249) and 7.9% (n = 100) of patients received massive transfusion. The AUROC of fibrin/fibrinogen degradation product (FDP) to fibrinogen ratio had a significantly higher prognostic performance than other markers. Multivariate analysis revealed that d-dimer level [odds ratio (OR) 1.033; 95% confidence interval (CI) 1.016–1.051] and FDP/fibrinogen ratio (OR 1.007; 95% CI 1.001–1.013) were independently associated with 28-day mortality. d-dimer (OR 1.028; 95% CI 1.003–1.055) and FDP/fibrinogen ratio (OR 1.035; 95% CI 1.012–1.058) were associated with 28-day mortality in the TBI group. In the non-TBI group, d-dimer was associated with 28-day mortality (OR 1.033; 95% CI 1.008–1.059), but the FDP/fibrinogen ratio was not. FDP/fibrinogen ratio, not d-dimer level, was an independent predictor for massive transfusion (OR 1.005; 95% CI 1.001–1.010).

Conclusions

High FDP/fibrinogen ratio on arrival is a predictor of 28-day mortality and the requirement for massive transfusion in severe trauma.

Keywords

Trauma Prognosis Massive transfusion Fibrinogen Fibrin/fibrinogen degradation products (FDP) d-dimer 

Introduction

Approximately 9–44% of hemostatic disturbance occurs in all trauma patients, although this varies according to the inclusion criteria used [1, 2, 3]. In addition to hemodilution, hypothermia, and acidosis, which have been identified as potential causative factors [4], injury itself may result in hemostatic disturbance in trauma patients [5, 6]. Among manifestations of hemostatic disturbance, disseminated intravascular coagulation (DIC) enhances the inflammatory response, sustaining the systemic inflammatory response syndrome. Subsequently, in the late stage of trauma, insufficient coagulation and decreased fibrinolysis cause microvascular thrombosis, eventually leading to organ dysfunction [7]. Therefore, identifying patients with DIC in the early stage of trauma and administering intensive care is crucial to achieve good outcomes in the late stage of trauma.

Recent studies have found that there exists an association between coagulation biomarkers on admission and early clinical outcome in trauma patients [8, 9, 10, 11]. High d-dimer levels on admission have been associated with death or massive transfusion during the first 24 h [8]. In another study, low levels of fibrinogen on admission were associated with in-hospital mortality [9]. Sawamura et al. found that low levels of fibrinogen and high levels of fibrin/fibrinogen degradation product (FDP) were independent factors for poor outcome [10]. Furthermore, a high FDP/fibrinogen ratio was associated with extravasation in patients with pelvic fracture [11].

Previous studies have examined the association between coagulation biomarkers in trauma and in-hospital mortality, as a primary outcome. However, Skaqa et al. showed that in-hospital mortality at the primary hospital was different from 1-month mortality [12]. Therefore, in-hospital mortality does not reflect actual trauma related mortality. However, the association between coagulation biomarkers on admission and long-term mortality, such as 28-day mortality, has not been examined.

This study examined the association between coagulation biomarkers on admission and outcome of the late stage of trauma.

Materials and methods

Study design and population

We performed a retrospective observational study including patients with severe trauma at Chonnam National University Hospital, Gwangju, South Korea admitted between January 2012 and December 2015. Severe trauma was defined as an injury severity score (ISS) greater than 16 [13]. The following exclusion criteria were applied: age under 18 years; lack of fibrinogen, FDP, or d-dimer measurements within 1 h of admission; trauma mechanisms, such as drowning or hanging; cardiac arrest following trauma; conditions resulting in coagulation abnormalities, such as hematologic malignancy, pregnancy, severe hepatic dysfunction, and current use of anticoagulant agents; and missing data. The study was approved by the Institutional Review Board at Chonnam National University Hospital.

Data collection

The following variables were obtained for each patient: age, sex, time interval from accident to arrival at our emergency department (ED), vital signs on admission [systolic arterial blood pressure (mmHg), heart rate, and respiratory rate], initial Glasgow Coma Scale (GCS), laboratory data on admission [pH, PaCO2, HCO3 , white blood cell count, hemoglobin, platelet count, activated partial thromboplastin time (APTT), international normalized ratio of prothrombin time (PT-INR), fibrinogen level, FDP level and d-dimer level], FDP/fibrinogen ratio, amounts of transfusion packed red blood cells (PRC), fresh frozen plasma (FFP), and platelet concentrates (PC) during the first 24 h after trauma, and 28-day mortality. The revised trauma score (RTS) was calculated based on vital signs and GCS. The Abbreviated Injury Scale (AIS) score and ISS were calculated on arrival. Massive transfusion was defined as transfusion of ≥ 10 units PRC from initial presentation in the ED to 24 h after arrival. Patients with head AIS scores greater than 3 were defined as traumatic brain injury (TBI) patients [14]. The primary outcome was the 28-day mortality and the secondary outcome was massive transfusion.

Hemoglobin and platelet count were measured with fluoro-flow cytometry using XE-2100 (Sysmex Corporation, Kobe, Hyogo, Japan). PT-INR, aPTT, and fibrinogen, FDP, and d-dimer levels were measured using the immunoturbidimetric method with the CA-7000 and CS-5100 systems (Sysmex Corporation., Kakogawa, Hyogo, Japan).

Statistical analysis

Continuous variables did not satisfy the normality test and are presented as median values with interquartile ranges (IQR). Categorical variables are presented as frequencies and percentages. Differences between the two groups were tested using the Mann–Whitney U test for continuous variables. The Fisher’s exact test or Chi-square test was used for comparison of categorical variables, as appropriate. ROC analysis was performed to examine the prognostic performance of PT, aPTT, fibrinogen level, FDP level, d-dimer level, and FDP/fibrinogen ratio for 28-day mortality. The comparison of dependent ROC curves was performed using the method of DeLong et al. [15]. Optimum cutoff values were provided by using Youden’s index.

Logistic regression analysis was used to identify independent risk factors for 28-day mortality or massive transfusion, after adjusting for relevant covariates. Then, patients were divided into the TBI and non-TBI groups and logistic regression analysis was performed for each group. All variables with a p value less than 0.1 on univariate analysis were included in the logistic regression. Backward selection was used to achieve the final model. Data were analyzed using PASW/SPSS™ software, version 18 (IBM Inc., Chicago, IL, USA). The ROC curves were calculated and compared using MedCalc version 16.1 (MedCalc Software, bvba, Ostend, Belgium). A two-sided significance level of 0.05 was used for statistical significance.

Results

Patient selection and characteristics

A total of 2165 severe trauma patients were identified during the study period. Following the exclusion of 899 patients, 1266 patients were included in this study (Fig. 1).

Fig. 1

Schematic diagram showing the number of patients with severe trauma included in the present study. ISS Injury Severity Score, FDP fibrin degradation product

Table 1 shows the baseline and clinical characteristics of the patients. There were 914 (72.2%) male patients and the median age was 57.0 years (45.0–70.0 years). Blunt trauma was the predominant form of injury. RTS and ISS were 7.84 (5.97–7.84) and 22(17–26), respectively. The median time from accident to ED arrival was 180.0 min (60.0–300.0 min). The 28-day mortality was 19.7% (n = 0.249). Massive transfusion was performed on 100 (7.9%) patients.

Table 1

Comparison of baseline characteristics according to 28-day mortality

Variables

All patients (N = 1266)

Survivor (N = 1017)

Non-survivor (N = 249)

p value

Age, years

57 (45–70)

55 (44–68)

67 (53–76)

< 0.001

Male, n (%)

914 (72.2%)

735 (72.3%)

179 (71.9%)

0.904

Mechanism of trauma

   

0.326

 Blunt

1234 (97.5%)

990 (97.3%)

244 (98.0%)

 

 Penetrating

22 (1.7%)

20 (2.0%)

2 (0.8%)

 

 Burns

10 (0.8%)

7 (0.7%)

3 (1.2%)

 

Injury Severity Score

22 (17–26)

20 (17–25)

25 (22–34)

< 0.001

 Head/neck AIS

2 (0–4)

2 (0–4)

4 (0–5)

< 0.001

 Face AIS

0 (0–0)

0 (0–0)

0 (0-0.5)

0.366

 Chest AIS

2 (0–3)

2 (0–3)

0 (0–3)

0.322

 Abdomen AIS

0 (0–3)

0 (0–2)

0 (0–2)

0.308

 Extremity/pelvic AIS

2 (0–2)

2 (0–3)

0 (0–2)

0.154

 External AIS

0 (0–0)

0 (0–0)

0 (0–0)

0.009

Revised Trauma Score

7.841 (5.967–7.841)

7.841 (6.904–7.841)

4.944 (4.094–6.376)

< 0.001

Glasgow Coma Scale

15 (9–15)

15 (14–15)

5 (3–11)

< 0.001

Systolic BP, mmHg

110 (80–130)

110 (90–130)

100 (70–130)

< 0.001

Respiratory rate, /min

20 (20–22)

20 (20–22)

20 (20–22)

0.060

Time from accident to ED visit

180 (60–300)

180 (120–300)

120 (60–180)

< 0.001

Arterial blood gas analyses

    

 pH

7.39 (7.34–7.43)

7.40 (7.35–7.43)

7.36 (7.25–7.42)

< 0.001

 PaCO2, mmHg

35.6 (31.9–39.2)

36.0 (32.3–39.2)

34.0 (29.0–39.0)

< 0.001

 HCO3 , mmol/L

21.5 (18.1–23.9)

22.1 (19.0–24.3)

18.6 (13.9–21.5)

< 0.001

Laboratory tests

    

 White blood cell count, ×109/L

13.7 (10.2–18.2)

13.5 (10.2–18.0)

14.4 (9.8–19.7)

0.189

 Hemoglobin, g/dL

11.8 (10.0–13.5)

12.2 (10.4–13.6)

11.0 (8.6–12.3)

< 0.001

 Platelet count, ×109/L

189 (149–231)

193 (155–238)

165 (128–212)

< 0.001

 APTT, s

31.6 (27.9–37.3)

30.6 (27.4–35.0)

39.6 (32.0-55.2)

< 0.001

 PT-INR

1.11 (1.03–1.25)

1.09 (1.02–1.19)

1.28 (1.12–1.59)

< 0.001

 Fibrinogen, mg/dL

188 (134–239)

197 (152–244)

126 (83–192)

< 0.001

 FDP, mg/L

72.7 (26.7–158.0)

58.7 (22.1–129.5)

161.5 (99.6–338.8)

< 0.001

 d-dimer, mg/L

24.1 (6.1–35.2)

18.3 (4.8–35.2)

35.2 (29.2–35.2)

< 0.001

 FDP/fibrinogen ratio

3.91 (1.20–11.23)

2.86 (0.99–7.52)

13.79 (6.56–34.44)

< 0.001

Massive transfusion

100 (7.9%)

55 (5.4%)

45 (18.1%)

< 0.001

 PRC, unit

2 (0–4)

0 (0–4)

4 (0–8)

< 0.001

 FFP, unit

0 (0–2)

0 (0–2)

2 (0–4)

< 0.001

 PC, unit

0 (0–0)

0 (0–0)

0 (0–8)

< 0.001

AIS Abbreviated Injury Scale, BP blood pressure, ED emergency department, aPTT activated partial thromboplastin time, PT-INR international normalized ratio of prothrombin time, FDP fibrin/fibrinogen degradation product, PRC packed red blood cell, FFP fresh frozen plasma, PC platelet concentrates

There were significant differences between the survivor and non-survivor groups (defined by 28-day mortality) in RTS and ISS values. Patients in the survivor group were younger, had higher levels of hemoglobin and bicarbonate, and had arrived at our ED significantly later after accident than non-survivor group. The fibrinogen level was significantly lower, while FDP, d-dimer levels and FDP/fibrinogen ratio were significantly higher in the non-survivor group. The proportion of massive transfusion and transfused blood products were significantly higher in non-survivors than survivors.

Prognostic performance of coagulation biomarkers for 28-day mortality

Figure 2 shows the area under the receiver operating characteristic (AUROC) curve of coagulation biomarkers. Table 2 shows the results of ROC analysis of coagulation biomarkers in predicting mortality. The AUROC curve for the FDP/fibrinogen ratio was significantly different from the AUROC curve for platelet count, aPTT, PT-INR, fibrinogen level, FDP level, and d-dimer level.

Fig. 2

Area under the receiver operating characteristic (AUROC) analyses of coagulation biomarkers. The AUROC for fibrin/fibrinogen degradation product (FDP) to fibrinogen ratio was significantly different from that for platelet count, activated partial thromboplastin time, prothrombin time, fibrinogen level, FDP level, and d-dimer level

Table 2

Performance of coagulation biomarker in predicting poor outcomes

 

Cutoff

Sensitivity

Specificity

PPV

NPV

AUC (95% CI)

p value

FDP/fibrinogen

6.59

75.1

71.9

39.5

92.2

0.780 (0.756–0.802)

< 0.001

Fibrinogen, mg/dL

148.8

61.4

76.8

39.3

89.1

0.712 (0.687–0.737)

< 0.001

FDP, mg/L

105.7

74.7

67.9

36.3

91.6

0.755 (0.731–0.779)

< 0.001

d-dimer, mg/L

34.53

71.9

68.8

36.1

90.9

0.721 (0.695–0.745)

< 0.001

PT-INR

1.22

59.8

79.6

41.9

89.0

0.738 (0.713–0.762)

< 0.001

APTT, s

34.5

67.5

73.5

38.4

90.2

0.748 (0.724–0.772)

< 0.001

Platelet, ×109/L

163

49.8

70.3

29.1

85.1

0.618 (0.590–0.645)

< 0.001

PPV positive predictive values, NPV negative predictive values, FDP fibrin/fibrinogen degradation product, PT-INR international normalized ratio of prothrombin time, aPTT activated partial thromboplastin time

Association between coagulation biomarkers and 28-day mortality

Table 3 shows the association between variables and 28-day mortality. After adjustment for confounders, we found that d-dimer level [odds ratio (OR) 1.033; 95% CI 1.016–1.051] and FDP/fibrinogen ratio (OR 1.007; 95% CI 1.001–1.013) were associated with 28-day mortality. Supplemental Tables 1 and 2 show univariate analyses between survivors and non-survivors in the TBI and non-TBI groups. Table 4 shows the independent factors for 28-day mortality in both TBI and non-TBI groups. d-dimer (OR 1.028; 95% CI 1.003–1.055) and FDP/fibrinogen ratio (OR 1.035; 95% CI 1.012–1.058) were associated with 28-day mortality in the TBI group (Table 4). In the non-TBI group, d-dimer was associated with 28-day mortality (OR 1.033; 95% CI 1.008–1.059), but the FDP/fibrinogen ratio was not.

Table 3

Logistic regression analysis for 28-day mortality

Variables

28-day mortality, OR (95% CI)

p value

Age

1.053 (1.039–1.067)

< 0.001

Time from accident to ED visit

1.000 (0.999–1.000)

0.282

Injury Severity Score

1.032 (1.008–1.056)

0.008

Revised Trauma Score

0.446 (0.391–0.508)

< 0.001

pH

1.228 (0.444–3.396)

0.692

PaCO2

1.010 (0.978–1.043)

0.550

HCO3

0.906 (0.866–0.949)

< 0.001

Hemoglobin

1.035 (0.948–1.129)

0.440

Platelet count

1.003 (1.000-1.006)

0.095

APTT

1.004 (0.993–1.015)

0.504

PT-INR

1.309 (1.041–1.645)

0.021

d-dimer

1.033 (1.016–1.051)

< 0.001

FDP/fibrinogen ratio

1.007 (1.001–1.013)

0.031

OR odds ratio, CI confidence interval, aPTT activated partial thromboplastin time, PT-INR international normalized ratio of prothrombin time, FDP fibrin/fibrinogen degradation product

Table 4

Logistic regression analysis for 28-day mortality in the TBI and non-TBI groups

Variables

TBI group

Non-TBI group

28-day mortality, OR (95% CI)

p value

28-day mortality, OR (95% CI)

p value

Age

1.037 (1.018–1.057)

< 0.001

1.068 (1.046–1.090)

< 0.001

Revised Trauma Score

0.397 (0.316–0.499)

< 0.001

0.572 (0.473–0.691)

< 0.001

PaCO2

1.007 (0.972–1.043)

0.698

1.040 (1.001–1.081)

0.045

HCO3

0.921 (0.847–1.002)

0.055

0.810 (0.751–0.873)

< 0.001

d-dimer

1.028 (1.003–1.055)

0.028

1.033 (1.008–1.059)

0.011

FDP/fibrinogen ratio

1.035 (1.012–1.058)

0.003

0.996 (0.986–1.006)

0.457

TBI traumatic brain injury, OR odds ratio, CI confidence interval, FDP fibrin/fibrinogen degradation product

Association between coagulation biomarkers and massive transfusion

In the massive transfusion group, 94 (94%) injuries were blunt and 6 (6%) injuries were penetrating. The ISS value for the massive transfusion group [27, (20–34)] was significantly higher than the ISS value for the non-massive transfusion group [22 (17–25)]. There were significant differences in the abdomen AIS and extremity/pelvic AIS between the massive transfusion group and non-massive transfusion group. The mean number of units of PRC, FFP, and PC transfused to patients in the massive transfusion group were 13 (11–17), 7.5 (5–10), and 10 (5–10), respectively. In the present study, the FDP/fibrinogen ratio was significantly higher in the massive transfusion group than in the non-massive transfusion group [14.88 (4.41–35.79) vs. 3.59 (1.13–10.13)]. Table 5 shows that the FDP/fibrinogen ratio, and not d-dimer level, is an independent predictor for massive transfusion (OR 1.005; 95% CI 1.001–1.010).

Table 5

Multiple logistic regression model with massive transfusion as the dependent variable

Variable

Massive transfusion, OR (95% CI)

p value

Injury Severity Score

1.023 (1.004–1.043)

0.017

Hemoglobin

0.820 (0.752–0.894)

< 0.001

HCO3

0.878 (0.837–0.921)

< 0.001

FDP/fibrinogen ratio

1.005 (1.001–1.010)

0.029

OR odds ratio, CI confidence interval, FDP fibrin/fibrinogen degradation product

Discussion

In this retrospective observational study, the AUROC of the FDP/fibrinogen ratio was 0.78 (95% CI 0.75–0.81) for 28-day mortality in patients with severe trauma and the FDP/fibrinogen ratio had greater discriminatory power than other biomarkers. The FDP/fibrinogen ratio and d-dimer were independently associated with 28-day mortality. d-dimer was associated with 28-day mortality, irrespective of TBI, and the FDP/fibrinogen ratio remained the only significant predictor in the TBI group. Furthermore, the FDP/fibrinogen ratio was independently associated with massive transfusion.

Several studies have demonstrated that low levels of fibrinogen are associated with outcome in severe trauma [8, 9, 10, 11]. Hayakawa et al. found that low levels of fibrinogen were associated with poor outcome, such as massive transfusion or mortality, during the first 24 h [8]. Zoe et al. showed that fibrinogen levels on admission were associated with massive transfusion, intensive care unit stay, hospital stay, 24-h mortality, and in-hospital mortality [9]. The development of DIC is also associated with outcome in patients with cardiac arrest and global ischemia [16]. However, fibrinogen levels were not associated with neurologic outcome in out-of-hospital cardiac arrest patients, who generally did not experience bleeding [17]. We postulated that fibrinogen level reflects the characteristics of trauma, including bleeding, as well as ischemia.

Many studies also reported the usefulness of d-dimer levels for trauma related coagulopathy. Hayakawa et al. reported that high d-dimer levels (≥ 38 mg/L) on arrival were significantly associated with death or the requirement for massive transfusion in patients with severe trauma [8]. FDP level is a more appropriate marker for hyperfibrinolysis, as it reflects both fibrinolysis and fibrinogenolysis, while d-dimer levels reflect only fibrinolysis [18]. Hayakawa et al. demonstrated that high levels of FDP at the early stage of trauma were associated with the occurrence of DIC [19]. In the present study, FDP level also showed reasonable prognostic performance for 28-day mortality, consistent with previous studies [10].

There was a significant difference in fibrinolytic activity between DIC groups and non-DIC groups, and the presence of DIC on arrival was associated with increased mortality in trauma [20]. This suggests that the fibrinolytic phenotype of DIC, rather than the anti-fibrinolytic phenotype, plays a major role in determining the outcomes at the early stage of trauma. Sawamura et al. showed that levels of fibrinogen and FDP on arrival were significantly associated with massive bleeding and death in patients with trauma, and these two factors were robust factors for fibrinolytic phenotype in the early stage of trauma [10]. Lower levels of fibrinogen and higher levels of FDP reflect the fibrinolytic phenotype at the early stage of trauma; therefore, we hypothesized that the ratio between these two biomarkers may reflect fibrinolytic phenotype better than FDP or fibrinogen alone. In the present study, the FDP/fibrinogen ratio was an independent predictor for 28-day mortality and showed the greatest discriminatory power compared to other coagulation biomarkers, using AUROC analysis.

In severe trauma, the occurrence of DIC does not occur only by exsanguination. Several studies have shown that TBI patients are also prone to coagulation abnormalities [21, 22]. In the present study, non-survivors were more likely to have coagulation abnormalities than survivors in the TBI group, and likewise in the non-TBI group. Consistent with previous studies that demonstrated the association between DIC and mortality in patients with TBI [21, 22], d-dimer and FDP/fibrinogen were associated with mortality in the TBI group in the present study. FDP/fibrinogen remained a significant predictor in the TBI group, while it was insignificant in the non-TBI group. Although we cannot be sure as to why there is a difference in the association between TBI and non-TBI groups, one possible explanation is that causes and times of death are different between TBI and non-TBI [23]. Another possible explanation is that TBI itself might affect the development of coagulation abnormalities. A review article suggested that local release of tissue factors, platelet dysfunction, shock or hypoperfusion, and posttraumatic inflammatory responses cause coagulation abnormalities in patients with TBI [24].

We can only identify the association, not the causation, between coagulation biomarkers and mortality in the present study due to the nature of study design. Therefore, it is uncertain whether correction of DIC following severe trauma can reduce mortality. Nevertheless, we can use the coagulation biomarkers as guides that reflect the severity of trauma and responsiveness of resuscitation, since coagulation biomarkers were associated with long-term mortality and those changes according to the patient’s status while ISS was fixed at ED arrival.

Massive transfusion during the first 24 h is associated with DIC at the early stage of trauma [8, 25]; therefore, we investigated factors associated with massive transfusion in trauma. Hayakawa et al. suggested that high d-dimer levels on arrival were associated with the need for massive transfusion [8]. In the present study, d-dimer level was associated with massive transfusion in univariate analysis, but not in multivariable analysis, consistent with a previous study [10]. However, as the FDP/fibrinogen ratio was independently associated with massive transfusion, we postulated that the FDP/fibrinogen ratio can serve as an indicator for blood transfusion, by predicting the requirement for massive transfusion. In a study on the prediction of extravasation in pelvic fracture, in which massive bleeding may occur [11], the FDP/fibrinogen ratio was significantly higher in the extravasation group than in the non-extravasation group, consistent with the findings of the present study.

The present study has several limitations. First, it was retrospective and single-centered study; therefore, further studies with a larger sample size, and prospective design, and involving multiple centers are necessary. Second, 630 patients (29.1%) with severe trauma were excluded because fibrinolytic biomarkers were not measured within 1 h of admission, which could have led to selection bias. Reasons for this included delayed blood sampling due to resuscitation, re-sampling due to hemolysis, relative high cost of coagulation biomarkers, and insurance issues. Third, ED arrival was significantly later for the survivor group than the non-survivor group. This may be due to the fact that patients with more severe conditions are transferred more promptly to the ED. This finding was comparable to the observations made by Hayakawa et al. [8]. Fourth, temperature was not investigated as an important factor related to hemostasis. We did not include temperature in our analysis because a considerable proportion of data on patient temperature on admission were inaccurate. Fifth, the maximum hospital d-dimer value was 35.2 mg/L fibrinogen-equivalent units. Therefore, the predicted value of the d-dimer was not sufficiently analyzed. However, there was a significant difference in d-dimer levels between the 28-day survivor and the non-survivor group. Furthermore, d-dimer level was an independent predictor in the logistic regression and Cox proportional hazard regression models for 28-day mortality. Finally, we did not investigate the effects on mortality of procedures for hemostasis, such as transfusion, intervention, and operation. It is important that future prospective studies address this point.

In conclusion, the FDP/fibrinogen ratio showed better discriminatory power than aPTT, PT-INR, fibrinogen level, FDP level, and d-dimer level. A high FDP/fibrinogen ratio on arrival is a predictor for the requirement for massive transfusion and 28-day mortality in patients with severe trauma.

Notes

Compliance with ethical standards

Conflict of interest

All authors (Dong Hun Lee, Byung Kook Lee, Sang Mi Noh, Yong Soo Cho) report no conflicts of interest relevant to this article. No funds were received by any of the authors in support of this study.

Ethical approval

The present study protocol was reviewed and approved by the institutional review board of Chonnam National University College of Medicine (Reg. No. CNUH-2017-076).

Informed consent

Informed consent was waived due to the retrospective nature of the study by the institutional review board.

Supplementary material

68_2017_844_MOESM1_ESM.docx (30 kb)
Supplementary material 1 (DOCX 33 KB)
68_2017_844_MOESM2_ESM.docx (34 kb)
Supplementary material 2 (DOCX 29 KB)

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Copyright information

© Springer-Verlag GmbH Germany 2017

Authors and Affiliations

  • D. H. Lee
    • 1
  • B. K. Lee
    • 1
  • S. M. Noh
    • 2
  • Y. S. Cho
    • 1
  1. 1.Department of Emergency MedicineChonnam National University HospitalGwangjuRepublic of Korea
  2. 2.Department of Trauma CenterChonnam National University HospitalGwangjuRepublic of Korea

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