Abstract
walled-off pancreatic necrosis (WOPN) is one of the complications of acute pancreatitis (AP) with high mortality. A method to predict the development of WOPN in AP patients admitted to the emergency department may guide life-saving practices such as early initiation of antibiotic therapy and, when necessary, referral of the patient to a center where necrosectomy can be performed. This study is a prospective observational study. One hundred eleven AP patients who applied to the emergency department were included in the study. The mean of QT interval (QT) dispersion, systemic immune–inflammation Index (SII), multi-inflammatory index-I (MII-1), multi-inflammatory index-II (MII-2), and multi-inflammatory index-III (MII-3) were compared between patients who developed WOPN and patients who did not develop WOPN during their hospitalization. In the study, the mean of QT dispersion, SII, MII-1, MII-2, and MII-3 were significantly lower in the patient group who developed WOPN compared to those who did not develop WOPN. In the receiver operating characteristic analysis, all methods except SII were found to be successful in predicting WOPN. QT dispersion, SII, MII-1, MII-2, and MII-3 are valuable tools that provide rapid results and successfully predict the development of WOPN in AP. However, MII-2 and QT dispersion appears to be slightly more successful than the others.
Keywords: acute pancreatitis, inflammation, prediction, walled-off pancreatic necrosis
1. Introduction
Walled-off pancreatic necrosis (WOPN) is the term used for the encapsulated fluid collection that develops after acute necrotizing pancreatitis (ANP). WOPN is a heterogeneous formation of varying amounts of liquid and solid necrotic material.[1] Although it is a rare complication seen in the late stages of acute pancreatitis (AP), the mortality of WOPN is relatively high, especially when infected.[2] In addition to interventional treatments such as endoscopic and surgical necrosectomy, the use of antibiotics in the presence of infection is also indicated in patients who develop WOPN. Routine antibiotic therapy is not recommended in patients with pancreatitis.[3,4] However, when the development of WOPN can be predicted, prophylactic antibiotics administered to the patient may positively affect the prognosis. Considering that AP is one of the common reasons for admission to the emergency department (ED),[5] evaluation for the development of WOPN in the ED initiating early antibiotic treatment and, when necessary, quickly referring the cases to centers where endoscopic necrosectomy can be performed may be life-saving for these patients.
Some methods are used to predict the development of WOPN in AP. For example, a study by Fujiwara et al[6] showed that elevated CRP was associated with the development of WOPN in pancreatitis patients. However, since the maximum CRP level is seen 2 days after the diagnosis of pancreatitis, it is not a valuable method for the ED. In another study, Yamamiya et al[7] showed that pancreatic blood volume measurement with whole pancreatic perfusion CT can predict whether pancreatitis cases will progress to WOPN. However, with this method, it is possible to make this prediction within 72 hours after the pancreatitis diagnosis. Therefore, it is not very suitable for ED use. A method that can provide faster results is required to evaluate the risk of WOPN development in the ED.
Systemic immune–inflammation index (SII), multi-inflammatory index-I (MII-1), multi-inflammatory index-II (MII-2), and multi-inflammatory index-III (MII-3) calculated based on laboratory parameters are tools that measure the severity of inflammation, used to predict the prognosis of many diseases such as various cancers and tumors, infections, ischemic stroke, rheumatic diseases, and pulmonary embolism. SII is calculated by multiplying the neutrophil/lymphocyte ratio (NLR) by the platelet count. MII-1 is calculated as NLR multiplied by CRP, MII-2 is calculated as platelet/lymphocyte ratio (PLR) multiplied by CRP, and MII-3 is calculated as SII multiplied by CRP.[8–11]
QT dispersion is the difference in QT interval (QT) between different leads of the 12-lead ECG. High QT dispersion indicates that the homogeneity between leads is impaired, and there is a risk of arrhythmia.[12] Increased QT dispersion is the most common cardiac pathology in AP. The QT dispersion, which is prolonged during the pancreatitis attack, is observed to return to normal after treatment.[13] Some studies have shown that the increase in QT dispersion is associated with the severity of AP.[14,15] However, to our knowledge, no study has evaluated the relationship between QT dispersion and the development of WOPN in AP.
This study evaluated the success of QT dispersion, SII, MII-1, MII-2, and MII-3 in predicting the risk of WOPN development in acute AP patients admitted to the ED.
2. Materials and methods
2.1. Study design and setting
This study is a prospective observational study. The study was carried out in the ED of a tertiary hospital with an annual patient admission of 400,000 between January 1, 2023 and January 1, 2024. The center where the study was conducted is a tertiary hospital where endoscopic or surgical necrosectomy can be performed on patients when necessary. Before initiating the study, approval was obtained from the local ethics committee with a decision number of 0495 (Approval date November 24, 2022).
2.2. Patient selection
Volunteers aged 18 and over who applied to ED and were diagnosed with pancreatitis were included in the study. Revised Atlanta criteria were used to diagnose pancreatitis. According to the revised Atlanta Classification, at least 2 of the following 3 criteria must be met for the diagnosis of AP:
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Lipase or amylase level is 3 times the upper limit of normal.
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Abdominal pain is compatible with pancreatitis.
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Abdominal imaging is compatible with AP.[16]
Pregnant patients were excluded from the study because their changing physiology could negatively affect the study results. Patients unable to give written consent were excluded for ethical reasons. Additionally, patients with cardiopulmonary arrest at the time of admission and those with missing data were also excluded from the study.
2.3. Data collection tools
Their primary physician performed all evaluations, examinations, and treatments of the patients included in the study. The demographic characteristics of the patients, the ECG, and laboratory results obtained at the first admission were recorded in the case report form (CRF) by the researchers. In addition to calculating QT dispersion using ECG, SII, MII-1, MII-2, and MII-3 were calculated according to laboratory results. Afterward, the patients were followed for developing in-hospital WOPN and in-hospital mortality, and the results were added to the CRF.
2.4. Sample size
Since there was no previous similar study, the effect value was accepted as 0.7, and the sample size calculated with a 95% confidence interval (CI), 95% power, and a 5% alpha error probability was found to be 110.
2.5. Statistical analysis
Data were analyzed using the IBM SPSS Statistics 23 program. When evaluating the study data, frequency distribution (number, percentage) is given for categorical variables, mean, and standard deviation (SD) are given for numerical variables if they show a normal distribution, and median and interquartile range (IQR) are given if they do not show a normal distribution. Shapiro–Wilk test, skewness, and kurtosis values were used to evaluate the normal distribution. When evaluating independent group averages, the Student t test was used to analyze normally distributed data, and the Mann–Whitney U test was used to analyze non-normally distributed data. ROC analysis was performed to evaluate diagnostic test success. The cutoff value was determined according to ROC analysis for tests that were found to be successful in predicting the development of WOPN. At these cutoff values, the sensitivity and specificity of the tests in predicting WOPN development were calculated. Data were presented with a 95% CI. A P value < .05 was considered statistically significant.
3. Results
A total of 111 patients, 51 women, and 60 men were included in the study. While the mean white blood cell (WBC), neutrophil, lymphocyte, and platelet count were similar between the WOPN (+) and WOPN (−) patient groups, the mean CRP was found to be higher and the mean amylase and lipase were significantly lower in the WOPN (+) group. While the mean WBC, neutrophil, lymphocyte, platelet, amylase, and lipase were found to be similar between the patient groups with and without Excitus, the mean of CRP was significantly higher in the group with Excitus (Table 1).
Table 1.
Comparison of demographic characteristics and laboratory levels of patients grouped according to walled-off pancreatic necrosis positivity and mortality development.
| WOPN | Mortality | ||||||
|---|---|---|---|---|---|---|---|
| WOPN (+) mean ± SD | WOPN (−) mean ± SD | P | Mortality (+) mean ± SD | Mortality (−) mean ± SD | P | ||
| Gender | Female | 9 (18%) | 42 (82%) | .367 | 4 (8%) | 47 (92%) | 1.000 |
| Male | 15 (25%) | 45 (75%) | 5 (8%) | 55 (92%) | |||
| Age | 67 ± 17 | 64 ± 13 | .296 | 74 ± 20 | 63 ± 13 | .057 | |
| WBC | 12 ± 7 | 11 ± 5 | .435 | 14 ± 6 | 11.5 ± 5.4 | .196 | |
| Neutrophil | 10 ± 6 | 9 ± 5 | .254 | 12 ± 5 | 9 ± 5 | .097 | |
| Lymphocyte | 1 ± 0.9 | 2.2 ± 6 | .457 | 1.2 ± 1.3 | 2 ± 6 | .664 | |
| Platelet | 271,000 ± 100,000 | 273,000 ± 118,000 | .941 | 300,000 ± 105,000 | 270,000 ± 115,000 | .465 | |
| CRP | 119 ± 119 | 47 ± 58 | <.001 | 115 ± 94 | 58 ± 78 | .042 | |
| Amylase | 682 ± 833 | 1299 ± 1426 | .024 | 1206 ± 1059 | 1172 ± 1385 | .887 | |
| Lipase | 1676 ± 2370 | 2719 ± 3398 | .027 | 2631 ± 3943 | 2496 ± 3281 | .969 | |
WOPN = walled-off pancreatic necrosis.
MII-1, MII-2, MII-3, and QT dispersion, tools to determine clinical severity, were significantly higher in the WOPN (+) patient group. SII was similar between groups (Table 2). When the patients were grouped according to the development of mortality, MII-1, MII-2, MII-3, SII, and QT dispersion were significantly higher in the group with mortality (Table 3).
Table 2.
Comparison of clinical severity determination tools between patients who developed walled-off pancreatic necrosis and those who did not.
| WOPN (+) median (IQR) | WOPN (−) median (IQR) | P | |
|---|---|---|---|
| MII-1 | 515 (2899) | 134 (353) | .009 |
| MII-2 | 23,110 (57,348) | 4365 (10,035) | .002 |
| MII-3 | 126,407 (816,689) | 23,718 (82,283) | .009 |
| SII | 2020 (2966) | 1394 (1999) | .296 |
| QT dispersion | 80 (70) | 40 (40) | <.001 |
MII = multi-inflammatory index, SII = systemic inflammatory index, WOPN = walled-off pancreatic necrosis.
Table 3.
Comparison of clinical severity assessment tools between patients with and without mortality
| Mortality (+) median (IQR) | Mortality (−) median (IQR) | P | |
|---|---|---|---|
| MII-1 | 1620 (3358) | 150 (453) | .038 |
| MII-2 | 51,902 (80,794) | 4601 (12,509) | .022 |
| MII-3 | 498,960 (899,866) | 29,083 (111,090) | .023 |
| SII | 3080 (4760) | 1394 (1990) | .023 |
| QT dispersion | 120 (40) | 60 (40) | <.001 |
MII = multi-inflammatory index, SII = systemic inflammatory index.
In the ROC analysis performed to evaluate the success of MII-1, MII-2, MII-3, SII, and QT dispersion in predicting WOPN, when looking at the areas under the curve, it was seen that the most successful was QT dispersion (AUC: 0.741 and P < .001). While SII was found unsuccessful (AUC: 0.570 and P = .313) MII-1 (AUC: 0.676 and P = .010), MII-2 (AUC: 0.706 and P = .001), and MII-3 (AUC: 0.674 and P = .011) were found to be successful (Table 4). ROC curves regarding the success of MII-1, MII-2, MII-3, SII, and QT dispersion in predicting WOPN are given in Figure 1.
Table 4.
Comparison of severity assessment tools in predicting walled-off pancreatic necrosis.
| Variable | Area | P | Asymptotic 95% confidence interval | Cutoff | Sensitivity | Specificity | |
|---|---|---|---|---|---|---|---|
| Lower bound | Upper bound | ||||||
| MII-1 | 0.676 | .010 | 0.543 | 0.809 | 213 | 0.667 | 0.665 |
| MII-2 | 0.706 | .001 | 0.579 | 0.833 | 1076 | 0.667 | 0.747 |
| MII-3 | 0.674 | .011 | 0.539 | 0.809 | 72,030 | 0.667 | 0.713 |
| SII | 0.570 | .313 | 0.434 | 0.706 | NA | NA | NA |
| QT dispersion | 0.741 | .000 | 0.624 | 0.857 | 70 | 0.583 | 0.747 |
AUC = area under the curve.
Figure 1.
Roc curve for WOPN. WOPN = walled-off pancreatic necrosis.
For each test that was successful in predicting WOPN, the cutoff value was determined at the values where sensitivity and specificity were highest together. Accordingly, MII-1 over 213 was considered to be associated with the development of WOPN, and its sensitivity was found to be 0.667 and specificity was 0.655. MII-2 over 1076 was found to be associated with the development of WOPN, and its sensitivity was 0.667 and specificity was 0.747. MII-3 over 72.030 is associated with the development of WOPN, its sensitivity was found to be 0.667 and its specificity was 713. QT dispersion over 70 was found to be associated with the development of WOPN and had a sensitivity of 0.583 and specificity of 0.747 (Table 4).
4. Discussion
This study evaluated whether the development of WOPN could be predicted in pancreatitis cases admitted to the ED. MII-1, MII-2, MII-3, and QT dispersion are flourishing among the tools that can be used for this purpose.
To our knowledge, there is no study evaluating the role of WBC, neutrophil, lymphocyte, amylase, and lipase, which are laboratory tests obtained during the first admission to the ED, in predicting development of WOPN. However, in a study conducted only with severe pancreatitis patients, it was reported that WBC, platelets and amylase had no effect on the development of WOPN.[6] In this study, it was seen that the development of WOPN was unrelated to the laboratory results obtained at admission, such as WBC, neutrophils, lymphocytes, and platelets. Elevated CRP level was found to be associated with WOPN development, while a positive relationship was observed between low amylase and lipase and the development of WOPN. Relatively low amylase and lipase in pancreatitis may herald the onset of necrosis in the cells that produce these enzymes. Perhaps in these patients, necrosis may have started at the micro level and is not yet reflected in radiological images. Therefore, relatively low amylase and lipase levels at the time of initial presentation may be an indication that WOPN will develop. If the relationship of amylase and lipase with the development of WOPN is confirmed in future studies, perhaps low amylase and lipase levels can be included in the scoring tools and the power of these tools can be increased.
In a previous study, Ateş et al[14] found that acute biliary pancreatitis is associated with prolonged QT dispersion and may even indicate disease severity. In another study conducted by Sakagami et al[15], higher QT dispersion was detected in cases of acute alcoholic pancreatitis compared to both healthy individuals and alcohol addicts. This study observed that the prolonged QT dispersion calculated according to the ECG obtained at the admission of patients diagnosed with AP in the ED successfully predicted the development of WOPN and mortality.
A study by Liu et al[17] showed that SII can predict the severity of pancreatitis and is even more successful than PLR and NLR. Biyik et al,[18] in their study, showed that SII could predict the severity of AP and the risk of developing acute kidney injury in patients diagnosed with AP. To our knowledge, this is the first study to evaluate the success of SII in predicting the development of WOPN, specifically in AP. The study found that SII could not predict the development of WOPN in AP patients presenting to the ED but could predict the mortality of these patients. According to studies, while high NLR indicates poor prognosis in AP,[19] high platelet count and elevated mean platelet volume are associated with good prognosis.[20,21] Therefore, it is understandable why SII, obtained by multiplying NLR by platelet count, fails to predict WOPN.
To our knowledge, no study has yet evaluated the success of MII-1, MII-2, and MII-3 in predicting the severity of AP and the development of WOPN. This study showed that MII-1, MII-2, and MII-3 calculated in patients diagnosed with AP in the ED could predict the development of WOPN and mortality. Fujiwara et al suggested in their study that the maximum CRP level could predict the development of WOPN.[6] Unlike SII, which we found unsuccessful in predicting WOPN development, MII-1, MII-1, and MII-3 are all calculated using CRP. This suggests that CRP is indeed effective in the development of WOPN. However, in the study by Fujiwara et al., CRP is unsuitable for use in the ED because it reaches its maximum level about 2 days after diagnosis.[6] However, in our study, MII-1, MII-2, and MII-3, calculated according to the first laboratory results obtained in the ED, successfully predicted the development of WOPN in AP patients.
When we compare the sensitivity and specificity of the tests found to be successful in predicting the development of WOPN at the cutoff value we determined, it is seen that the specificity of all of them is higher than the sensitivity. In this case, we can comment that these tests may be diagnostic tests rather than screening test at the determined cutoff values. However, these values need to be confirmed with further clinical studies on this subject.
The study has some limitations. The most important of these is that there is no information on whether the patients were administered antibiotic treatment in ED, and the results regarding other treatment options are not included. The relatively small number of patients is another limitation. Future studies with larger patient groups, including treatment results, are needed.
5. Conclusion
WOPN is a complication with high mortality in AP patients presenting to the ED. Comparing the success of predicting development of WOPN, the weakest tool is SII (AUC: 0.570), while MII-1 (AUC: 0.676), MII-2 (AUC: 0.676), and MII-3 (AUC: 0.674), especially QT dispersion (AUC: 0.741) are promising methods in predicting the development of WOPN in ED.
Author contributions
Conceptualization: Osman Sezer Çinaroğlu, Hakan Çamyar, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Güner Yurtsever, Efe Kanter.
Data curation: Osman Sezer Çinaroğlu, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan.
Formal analysis: Osman Sezer Çinaroğlu, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Uğur Bayram Korkmaz, Güner Yurtsever, Efe Kanter.
Funding acquisition: Osman Sezer Çinaroğlu, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Güner Yurtsever, Efe Kanter.
Investigation: Osman Sezer Çinaroğlu, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Uğur Bayram Korkmaz.
Methodology: Osman Sezer Çinaroğlu, Hakan Çamyar, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan.
Project administration: Osman Sezer Çinaroğlu, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Güner Yurtsever.
Resources: Osman Sezer Çinaroğlu, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Uğur Bayram Korkmaz, Efe Kanter.
Software: Osman Sezer Çinaroğlu, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Uğur Bayram Korkmaz, Güner Yurtsever, Efe Kanter.
Supervision: Osman Sezer Çinaroğlu, Hakan Çamyar, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Uğur Bayram Korkmaz, Güner Yurtsever, Efe Kanter.
Validation: Osman Sezer Çinaroğlu, Hakan Çamyar, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Uğur Bayram Korkmaz, Güner Yurtsever.
Visualization: Osman Sezer Çinaroğlu, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Uğur Bayram Korkmaz, Güner Yurtsever, Efe Kanter.
Writing – original draft: Osman Sezer Çinaroğlu, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Uğur Bayram Korkmaz.
Writing – review & editing: Osman Sezer Çinaroğlu, Hakan Çamyar, Hüseyin Acar, Ejder Saylav Bora, Mehmet Göktuğ Efgan, Güner Yurtsever, Efe Kanter.
Abbreviations:
- ALT
- alanine transaminase
- ANP
- acute necrotizing pancreatitis
- AP
- acute pancreatitis
- AST
- aspartate transaminase
- AUC
- area under the curve
- CI
- confidence interval
- CRF
- case report form
- CRP
- C-reactive protein
- CT
- computed tomography
- ECG
- electrocardiogram
- ED
- emergency department
- GGT
- gamma-glutamyl transferase
- Hb
- hemoglobin
- IBM
- International Business Machines Corporation
- ICU
- intensive care unit
- IQR
- interquartile range
- MII-1
- multi-inflammatory index-I
- MII-2
- multi-inflammatory index-II
- MII-3
- multi-inflammatory index-III
- N/A
- not applicable
- NHANES
- National Health and Nutrition Examination Survey
- NIH
- National Institutes of Health
- NLR
- neutrophil/lymphocyte ratio
- PCT
- procalcitonin
- PLR
- platelet/lymphocyte ratio
- QT
- QT interval
- ROC
- receiver operating characteristic
- SD
- standard deviation
- SII
- systemic immune–inflammation Index
- SPSS
- Statistical Package for the Social Sciences
- WBC
- white blood cell
- WOPN
- walled-off pancreatic necrosis.
The authors have no funding and conflicts of interest to disclose.
The datasets generated during and/or analyzed during the current study are not publicly available, but are available from the corresponding author on reasonable request.
How to cite this article: Çinaroğlu OS, Acar H, Çamyar H, Bora ES, Efgan MG, Korkmaz UB, Yurtsever G, Kanter E. The success of SII, MII-1, MII-2, MII-3, and QT dispersion in predicting the walled-off pancreatic necrosis development in acute pancreatitis in the emergency department: An observational study. Medicine 2024;103:25(e38599).
Contributor Information
Osman Sezer Çinaroğlu, Email: drsezer@hotmail.com.
Ejeder Saylav Bora, Email: ejdersaylav.bora@ikc.edu.tr.
Mehet Göktuğ Efgan, Email: goktugefgan@gmail.com.
Uğur Bayram Korkmaz, Email: ugurbk07@gmail.com.
Güner Yurtsever, Email: guneryurtsever@gmail.com.
Efe Kanter, Email: efekanter@hotmail.com.
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