DOI: https://doi.org/10.21203/rs.3.rs-1493337/v1
Background: Abdominal compartment syndrome (ACS) after blunt abdominal trauma is a rare complication that requires early recognition and subsequent surgical intervention for optimal outcome. We aimed to investigate how differences in injured abdominal organs affect ACS development in patients with severe blunt abdominal trauma.
Methods: This nested case-control study used a nationwide registry of trauma patients, namely, the Japan Trauma Data Bank (JTDB), and only included patients aged ≥ 18 years with blunt severe abdominal trauma, defined as an AIS score of abdomen ≥ 3, sustained between 2004 and 2017. Patients without ACS were used as control subjects and identified using propensity score (PS) matching. Characteristics and outcomes between patients with and without ACS were compared and logistic regression was used to identify specific risk factors for ACS.
Results: Among 294,274 patients in the JTDB, 11,200 were eligible for inclusion before PS matching, and 150 (1.3%) developed ACS after trauma. PS matching led to the inclusion of 131 and 655 patients with and without ACS, respectively. Compared to controls, patients with ACS had higher number of injured organs in the abdomen and displayed a greater frequency of vascular and pancreatic injuries, need for blood transfusion, and disseminated intravascular coagulopathy, a complication of ACS. In-hospital mortality was higher in patients with ACS than those without ACS (51.5% vs. 24.4%, p < 0.01). Logistic regression analysis revealed that a higher number of injured organs in the abdomen [odds ratio (OR) (95% confidence interval [CI]): 1.71 (1.22–2.40)] and pancreatic injury [OR (95% CI): 1.44 (1.03–2.03)] were independently associated with ACS.
Conclusions: Greater number of injured organs in abdomen and pancreatic injury are independent risk factors for the development of ACS; injuries to other organs were not associated.
Abdominal compartment syndrome (ACS) occurs following intraabdominal hypertension and is a rare complication that is associated with poor outcomes. Intraabdominal hypertension results in a series of pathophysiologic changes that begin with impaired regional blood flow, and these changes are associated with the systemic inflammatory response and whole-body ischemia-reperfusion secondary to blood loss and resuscitative procedures.1 As decompressive laparotomy is recommended for the management of ACS,2 early recognition and subsequent treatment are essential for achieving optimal outcomes.
Risk factors for ACS after trauma have been reported by several studies and include severe trauma,3,4 hemorrhagic shock,5,6 and positive fluid balance.7,8 Most cases of ACS appear to be related to abdominal trauma; however, ACS has also been documented in cases without abdominal trauma.7,9,10 As the pathophysiology of ACS varies with and without abdominal trauma, and categorizing all abdominal trauma as a single phenomenon may be inappropriate, it is prudent to separately assess risk factors. Therefore, based on data from a nationwide trauma registry in Japan, we aimed to investigate how differences in injured abdominal organs affect ACS development in patients with severe blunt abdominal trauma.
This nested case-control study used information available in the Japan Trauma Data Bank (JTDB) for the period between 2004 and 2017. The JTDB is a nationwide trauma registry established in 2003 by the Japanese Association for the Surgery of Trauma and the Japanese Association for Acute Medicine to improve and ensure quality of trauma care in Japan.11 A total of 272 hospitals, including more than 75% of the certified tertiary emergency medical centers in Japan, contributed to the JTDB in March 2018. Data captured in the JTDB includes patient and hospital information, such as patient demographics, Abbreviated Injury Scale (AIS) scores, Injury Severity Score, in-hospital procedures, complications, and clinical outcomes. Data collection is a part of routine clinical patient management.
Inclusion criteria were age ≥ 18 years and blunt trauma with severe abdominal injury, defined as an AIS severity score of 3 or greater for the abdomen. Patients with an AIS score of 6 (i.e., nonsurvivable injury) or those who died in the emergency department were excluded.
Primary outcome was the development of ACS, which was diagnosed based on the report of the physician in-charge; however, the database has no data on diagnostic criteria used for this purpose. The definitions of other complications included in this study concurred with those of the JTDB.11 All emergency procedures were performed during resuscitation or initial management at the emergency department.
We categorized AIS codes representing injuries in the abdomen according to major organs involved, using AIS 90 Update 98 and AIS 2005 Update 2008, and presented the data as such. Injured organs included the blood vessels, digestive tract (stomach, duodenum, small intestine, colon, and rectum), mesentery, kidney, liver, pancreas, and spleen, among others.
We selected eligible patients without ACS as controls to identify risk factors for ACS. First, we used propensity score (PS) matching to ensure that the ACS and control groups were balanced with respect to baseline characteristics and severity of trauma. PS calculations used the following variables that were selected based on clinical relevance and previous research, namely, age, sex, vital signs in the emergency department (Glasgow Coma Scale, systolic blood pressure, heart rate, and respiratory rate), and Injury Severity Score.11,12 Nearest neighbor propensity matching was performed at a 1:5 ratio and was based on averaged PS with a caliper of 0.2. The standardized mean difference of variables was used to evaluate balance after PS matching, and a standardized mean difference of > 0.1 defined as meaningful imbalance.
Next, we compared injury regions, injured organs in the abdomen, comorbidities, emergency procedures or interventions, concomitant complications, and outcomes between the ACS and control groups. Continuous variables are presented as median and interquartile range and were compared using the Mann–Whitney U test because none of the variables were normally distributed. Categorical variables are presented as numbers and percentages and were compared using the Chi-square test.
After comparison of baseline characteristics, logistic regression was employed to identify risk factors for developing ACS. We assessed the multicollinearity of variables using the variance inflation factor with the tolerance value set at less than 5. We also carefully examined clinically plausible interactions; however, no meaningful interactions were found among the variables tested. We included type of injured organs in the abdomen with an AIS severity score ≥ 3 as candidate risk factors in model 1. In model 2, we included the number of injured organs in the abdomen with an AIS severity score ≥ 3 as candidate risk factor. In model 3, we used both type and number of injured organs, and added complications of coagulopathy, as disseminated intravascular coagulopathy (DIC) and thrombocytopenia, in models 4. All models were adjusted for variables such as transfusion within 24 h after arrival at the emergency department and chronic hepatic conditions, including liver cirrhosis and chronic hepatitis, as they are known to be associated with ACS.7,13 All probability values were two-sided, and p < 0.05 was considered statistically significant. We performed statistical analyses using the Stata software, version 15.1 (Stata Corp., TX, USA).
Among 294,274 trauma patients registered in the JTDB between 2004 and 2017, 11,200 patients were eligible for inclusion in this study (Fig. 1). Of these, 150 (1.3%) patients developed ACS after trauma, and after PS matching, data from 131 patients with ACS was compared with that from 655 patients without ACS. Median age of the study participants was 55 years (interquartile range, 36–70), 635 (80.8%) were male, and median Injury Severity Score was 32 (interquartile range, 20–43). PS matching did not reveal any meaningful imbalance of variables between patients with and without ACS (Table 1).
ACS |
No ACS |
||||
---|---|---|---|---|---|
N = 131 |
N = 655 |
SMD |
P - value |
||
Age |
54 (34–70) |
55 (36–70) |
0.017 |
0.86 |
|
Gender (male) |
105 (80.1) |
530 (80.9) |
0.019 |
0.84 |
|
Vital signs at emergency department |
GCS |
13 (9–15) |
13 (7–15) |
0.026 |
0.29 |
SBP |
92 (74–123) |
97 (72–121) |
0.002 |
0.94 |
|
HR |
103 (84–127) |
105 (86–124) |
0.012 |
0.99 |
|
RR |
25 (20–30) |
24 (20–30) |
0.084 |
0.42 |
|
Injury Severity Score |
27 (17–45) |
32 (21–42) |
0.004 |
0.69 |
|
Injured body region (AIS ≥ 3) |
Head |
29 (21.4) |
193 (29.5) |
0.06 |
|
Thorax |
59 (45.0) |
374 (57.1) |
0.01 |
||
Spine |
8 (6.1) |
44 (6.7) |
0.90 |
||
Upper extremity |
7 (5.3) |
43 (6.6) |
0.60 |
||
Lower extremity including the pelvis |
45 (34.4) |
226 (34.5) |
0.97 |
||
Injured organ in abdomen (AIS ≥ 3) |
Blood vessel |
38 (29.0) |
104 (15.9) |
< 0.01 |
|
Digestive duct |
21 (16.0) |
100 (15.3) |
0.83 |
||
Mesentery |
15 (11.5) |
85 (13.0) |
0.63 |
||
Kidney |
23 (17.6) |
75 (11.5) |
0.05 |
||
Liver |
43 (32.8) |
167 (25.5) |
0.08 |
||
Pancreas |
12 (9.2) |
12 (1.8) |
< 0.01 |
||
Spleen |
22 (16.8) |
129 (19.7) |
0.44 |
||
Others |
13 (9.9) |
108 (16.5) |
0.06 |
||
Number of injured organs in the abdomen (AIS ≥ 3) |
1 |
59 (45.0) |
426 (65.0) |
< 0.01 |
|
2 |
35 (26.7) |
156 (23.8) |
|||
≥ 3 |
37 (28.2) |
73 (11.2) |
|||
Comorbidities |
Ischemic heart diseases |
2 (1.5) |
13 (2.0) |
0.73 |
|
Heart failure |
1 (0.8) |
10 (1.5) |
0.50 |
||
Hypertension |
18 (13.7) |
110 (16.8) |
0.39 |
||
Asthma |
1 (0.8) |
19 (2.9) |
0.16 |
||
COPD |
2 (1.5) |
8 (1.2) |
0.78 |
||
Liver cirrhosis |
7 (5.3) |
8 (1.2) |
< 0.01 |
||
Chronic hepatitis |
4 (3.1) |
7 (1.1) |
0.08 |
||
Peptic ulcer |
1 (0.8) |
16 (2.4) |
0.23 |
||
Inflammatory bowel diseases |
1 (0.8) |
4 (0.6) |
0.84 |
||
DM |
12 (9.2) |
48 (7.3) |
0.47 |
||
Obesity |
1 (0.8) |
3 (0.5) |
0.65 |
||
Stroke |
1 (0.8) |
14 (2.1) |
0.29 |
||
Dementia |
1 (0.8) |
10 (1.5) |
0.50 |
||
Malignancies |
2 (1.5) |
8 (1.2) |
0.78 |
||
Anticoagulant use |
1 (0.8) |
0 |
0.03 |
||
Hemodialysis |
3 (2.3) |
5 (0.8) |
0.11 |
||
Emergency procedures |
Oral intubation |
92 (70.2) |
334 (51.0) |
< 0.01 |
|
Ventilator use |
69 (52.7) |
221 (32.2) |
< 0.01 |
||
Aortic cross-clamping |
3 (2.3) |
26 (4.0) |
0.35 |
||
REBOA |
23 (17.6) |
52 (7.9) |
< 0.01 |
||
Thoracentesis |
2 (1.5) |
7 (1.1) |
0.65 |
||
Chest drainage |
27 (20.6) |
144 (22.0) |
0.73 |
||
Blood transfusion within 24 h |
96 (73.3) |
367 (56.0) |
< 0.01 |
||
Vasopressor use |
45 (34.4) |
102 (15.6) |
< 0.01 |
||
Open bone traction |
4 (3.1) |
28 (4.3) |
0.52 |
||
External skeletal fixation |
11 (8.4) |
56 (8.6) |
0.95 |
||
Other emergency bone fixation |
4 (3.1) |
21 (3.2) |
0.93 |
||
Primary surgeries |
Craniotomy |
2 (1.5) |
12 (1.8) |
0.81 |
|
Thoracotomy |
6 (4.6) |
41 (6.3) |
0.46 |
||
Celiotomy |
81 (61.8) |
278 (42.5) |
< 0.01 |
||
Bone reduction and fixation |
8 (6.1) |
73 (11.2) |
0.08 |
||
Propensity matched by age, gender, vital signs at emergency department (GCS, SBP, HR, RR), and Injury Severity Score. Continuous variables were compared using the Mann–Whitney U test. Categorical variables were compared using the Chi-square test. Missing: primary surgeries = 1. ACS, abdominal compartment syndrome; SMD, standardized mean difference; GCS, Glasgow coma scale; SBP, systolic blood pressure; HR, heart rate; RR, respiratory rate; AIS, Abbreviated Injury Scale score; COPD, chronic obstructive pulmonary disease; DM, diabetes mellitus; REBOA, resuscitative endovascular balloon occlusion of the aorta |
Vascular and pancreatic injuries were more common in patients with ACS than in those without ACS [29.0% vs. 15.9%; p < 0.01 for vascular injury, and 9.2% vs. 1.8%; p < 0.01 for pancreatic injury, respectively]. Compared to those without ACS, number of injured organs in the abdomen was higher and liver cirrhosis was more frequent in patients with ACS (5.3% vs. 1.2%, p < 0.01). Only one patient with ACS was prescribed an anticoagulant; none in the without ACS group used this medication. There were no significant differences in other comorbidities between patients with and without ACS.
Next, patients with ACS were more frequently provided blood transfusion than those without ACS (73.3% vs. 56.0%, p < 0.01). Celiotomy was the most commonly performed primary surgery in both groups, and it was more frequently indicated in patients with ACS than in those without ACS (61.8% vs. 42.5%, p < 0.01).
Concomitant complications that were more common in ACS patients than in those without ACS are listed in the Additional file: Table S1. DIC and coagulation disorders (38.9% vs. 9.0%, p < 0.01) and thrombocytopenia (26.7% vs. 3.8%, p < 0.01) were more frequent in patients with ACS than in those without ACS.
In-hospital mortality was higher in patients with ACS than in those without ACS (51.5% vs. 24.4%, p < 0.01, Table 2), and while all patients with ACS were admitted to intensive care units (ICU), only 93.2% patients without ACS were admitted to the ICU. There were no significant differences in length of hospital stay or ICU stay between patients with and without ACS.
ACS |
No ACS |
||||
---|---|---|---|---|---|
N = 131 |
N = 655 |
P - value |
|||
Disposition at discharge |
Died (in-hospital mortality) |
67 (51.5) |
159 (24.4) |
< 0.01 |
|
Transfer |
33 (25.4) |
268 (41.0) |
|||
Home |
28 (21.5) |
224 (34.3) |
|||
Others |
2 (1.5) |
2 (0.3) |
|||
ICU admission |
131(100.0) |
603 (93.2) |
0.02 |
||
Length of hospital stay |
24 (3–60) |
26 (7–53) |
0.64 |
||
ICU stay |
12 (2–47) |
14 (2–39) |
0.74 |
||
Continuous variables were compared using the Mann–Whitney U test. Categorical variables were compared using the Chi-square test. Missing: disposition at discharge: 5, length of hospital stay: 4, ICU stay: 90. ACS, abdominal compartment syndrome; ICU, intensive care unit. |
Table 3 shows the results of logistic regression models to identify risk factors for developing ACS. Number of injured organs in the abdomen was consistently associated with ACS in models 2, 3, and 4. Finally, only injury to the pancreas was consistently associated with ACS, while vascular, kidney, and liver injury were not associated with ACS models 3 and 4, although an association was seen in model 1. Injury to the mesentery, spleen, and digestive tract were not associated with ACS. DIC and coagulation disorders [odds ratio (95% confidence interval): 2.85 (1.48–5.50), p < 0.01] and thrombocytopenia [3.28 (1.47–7.33), p < 0.01] were associated with ACS
N |
786 |
786 |
786 |
786 |
|
---|---|---|---|---|---|
OR (95% CI) |
|||||
Model |
1 |
2 |
3 |
4 |
|
Injured organ in the abdomen (AIS ≥ 3) |
Blood vessel |
1.40 (1.17–1.66) |
1.17 (0.96–1.43) |
1.15 (0.93–1.43) |
|
Kidney |
1.34 (1.10–1.63) |
1.13 (0.91–1.41) |
1.15 (0.92–1.44) |
||
Liver |
1.27 (1.07–1.50) |
1.10 (0.91–1.32) |
1.09 (0.89–1.33) |
||
Mesentery |
1.05 (0.84–1.32) |
0.87 (0.67–1.11) |
0.91 (0.70–1.19) |
||
Pancreas |
1.75 (1.30–2.37) |
1.52 (1.11–2.08) |
1.44 (1.03–2.03) |
||
Spleen |
1.09 (0.90–1.32) |
0.94 (0.76–1.16) |
0.97 (0.78–1.21) |
||
Digestive tract |
1.12 (0.92–1.36) |
0.96 (0.78–1.19) |
0.95 (0.75–1.19) |
||
Others |
0.98 (0.78–1.23) |
0.84 (0.66–1.07) |
0.81 (0.62–1.05) |
||
Number of injured organs in the abdomen (AIS ≥ 3) |
1.89 (1.48–2.41) |
1.78 (1.28–2.46) |
1.71 (1.22–2.40) |
||
DIC and coagulopathy |
2.85 (1.48–5.50) |
||||
Thrombocytopenia |
3.28 (1.47–7.33) |
||||
All models are adjusted by transfusion < 24 h on arrival at emergency department and hepatic diseases (liver cirrhosis and chronic hepatitis). OR, odds ratio; CI, confidential interval; AIS, Abbreviated Injury Scale score; DIC, disseminated intravascular coagulopathy |
Abdominal trauma is a major cause of ACS, and using data from a large database, we show that the prevalence of ACS among patients with severe blunt abdominal trauma was low (at 1.3%) in the Japanese national trauma registry. Further, interestingly, ACS development was associated with the number of organs injured in the abdomen rather than the type of organ injured, and injury to most organs in the abdomen, except for the pancreas, was not associated with ACS. Coagulopathy, including DIC, was also associated with ACS, and it is possible that these complications represent a cause-and-effect phenomenon. Thus, focusing on the number of abdominal organs injured may help clinicians stratify patients based on risk of ACS development during the early stages of trauma care.
The prevalence of ACS associated with trauma widely varies among reports and ranges from 0 to 14%.5,7–9,14 This variation may be due to the diversity in the study populations and advances in trauma care, including damage-control surgery.5
Our analysis of a national trauma registry identified an independent association between the number of injured organs in the abdomen and development of ACS. This result is as expected because hemorrhage is the main pathology in trauma, and multiple organ injuries, as well as severity of injury, are related to greater hemorrhage.15 In addition, hemorrhaging ascites directly increase intraabdominal pressure. Thus, copious fluid resuscitation to counter massive hemorrhage induces capillary leak and intestinal edema,16 both of which are risk factors for ACS secondary to increased intraabdominal pressure.2 Therefore, clinicians should be aware of the risk of developing ACS when patients present with multiple organ injuries in the abdomen.
Anatomical features of the injured organ may be important for the development of ACS, and in our cohort, only pancreatic injury was associated with the development of ACS. The pancreas is located in the retroperitoneum and is typically present near the great vessels, i.e., the inferior vena cava, portal vein, and abdominal aorta, which not only make surgical repair of the pancreatic injury challenging 17,18 but also, thereby, delay hemorrhage control. Moreover, physiological and biochemical features of pancreatic trauma, such as leakage of pancreatic enzymes, can contribute to the development of both ACS and pancreatitis.
In our study, coagulopathy, including DIC, was associated with ACS, but a cause-and-effect relationship, i.e., whether DIC associated with trauma precedes ACS, could not be established because the JTDB does not capture data about the timing complication onset. It is rational to expect that, pathophysiologically, DIC may have preceded ACS, with subsequent trauma not only exacerbating hemorrhage but also contributing to the increased intraabdominal pressure and resulting in the development of ACS. Nevertheless, it must be noted that the reverse could also be true. Very few previous studies have discussed the association between DIC and development of ACS; specifically, a single case series showed that two patients developed ACS following DIC.19 Although trauma-induced coagulopathy might be present in the early phase after trauma,20 it is unknown whether coagulopathy in the early phase progresses to DIC.21,22
Preventing complications will undoubtedly improve mortality,11 and we confirm that ACS is one of the most severe complications of severe abdominal trauma because more than half of the patients who developed ACS died. Although primary injury of the abdominal organs or DIC induced by trauma may be unmodifiable, clinicians should pay attention when patients present with these risk factors as it can help to potentially retard or stop the development of ACS, consider open abdomen procedures, and avoid excessive positive fluid balance.5,6,23
Our study has some limitations. First, unmeasured potential confounders could have affected the results, and although the amount of fluid or blood transfused are risk factors for developing ACS,6,23 our database did not contain this data. Nonetheless, we adjusted the logistic regression models using a related variable, i.e., blood transfusion within 24 h of admission. Second, celiotomy may be a potential risk factor because a few previous studies have reported abdominal surgery to be a risk factor for ACS.5,8 However, we did not include celiotomy in the logistic regression analysis because time elapsed between celiotomy and ACS was unknown. In addition, ACS rapidly develops after injury and can present early, often within 3–6 h of admission to the emergency department;1,6,7,24 hence, presumably, ACS could have developed before primary surgery in some cases. Third, potential information bias, due to the ACS diagnosis being based on the reports of the physician in-charge, along with possible underdiagnosis, cannot be ruled out. However, as most of the institutions participating in the JTDB were nationally certified emergency centers, we believe that most of the patients received appropriate trauma care.
We investigated the role of abdominal organ injury in the development of ACS in patients with severe blunt abdominal trauma and show that greater number of injured organs is an independent risk factor for ACS. In addition, injury to most other organs in the abdomen, except the pancreas, was not associated with the development of ACS.
ACS, abdominal compartment syndrome; AIS, Abbreviated Injury Scale; DIC, disseminated intravascular coagulopathy; ICU, intensive care unit; JTDB, Japan Trauma Data Bank; PS, propensity score
Ethical Approval and consent to participate
The study protocol was reviewed and approved by the Research Ethics Committee of the Tsukuba Memorial Hospital (IRB No. R03-09-05). Given the retrospective and anonymized nature of this study, the Research Ethics Committee waived the need to obtain informed consent from the study participants. JTDB administrators also provided permission to use their database.
Consent for publication
Not applicable.
Availability of data and materials
The datasets used and/or analysed during the current study are available from the corresponding author on reasonable request.
Competing interest
The authors declare that they have no competing interests
Funding
No specific funding for this study was obtained.
Author contributions
AK, HI, TK, MA, and TA conceived the study. AK and TA performed analyses for the study. AK wrote the first draft of the manuscript. AK and TA revised the manuscript for important intellectual content. All authors provided critical input into manuscript drafting and revisions.
Acknowledgments
The authors would like to thank Enago (www.enago.jp) for the English language review.