Relationship between type of injured organ and development of abdominal compartment syndrome after severe blunt abdominal trauma: a nested case-control study using nationwide trauma registry in Japan

Abstract

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. 

Background

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.

Methods

Results

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).

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.

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

Discussion

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

Conclusions

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.

List of abbreviation

ACS, abdominal compartment syndrome; AIS, Abbreviated Injury Scale; DIC, disseminated intravascular coagulopathy; ICU, intensive care unit; JTDB, Japan Trauma Data Bank; PS, propensity score

Declarations

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.

References

1. Balogh ZJ, Lumsdaine W, Moore EE, Moore FA. Postinjury abdominal compartment syndrome: from recognition to prevention. Lancet. 2014;384(9952):1466–75.
2. Kirkpatrick AW, Roberts DJ, De Waele J, Jaeschke R, Malbrain ML, De Keulenaer B, et al. Intra-abdominal hypertension and the abdominal compartment syndrome: updated consensus definitions and clinical practice guidelines from the World Society of the Abdominal Compartment Syndrome. Intensive Care Med. 2013;39(7):1190–1206.
3. Strang SG, Van Imhoff DL, Van Lieshout EM, D'Amours SK, Van Waes OJ. Identifying patients at risk for high-grade intra-abdominal hypertension following trauma laparotomy. Injury. 2015;46(5):843–8.
4. Ertel W, Oberholzer A, Platz A, Stocker R, Trentz O. Incidence and clinical pattern of the abdominal compartment syndrome after "damage-control" laparotomy in 311 patients with severe abdominal and/or pelvic trauma. Crit Care Med. 2000;28(6):1747–53.
5. Balogh ZJ. Mission to eliminate postinjury abdominal compartment syndrome. Arch Surg. 2011;146(8):938.
6. Balogh Z, McKinley BA, Cocanour CS, Kozar RA, Holcomb JB, Ware DN, et al. Secondary abdominal compartment syndrome is an elusive early complication of traumatic shock resuscitation. Am J Surg. 2002;184(6):538–43.
7. Balogh Z, McKinley BA, Holcomb JB, Miller CC, Cocanour CS, Kozar RA, et al. Both primary and secondary abdominal compartment syndrome can be predicted early and are harbingers of multiple organ failure. J Trauma. 2003;54(5):848–59; discussion 859 – 61.
8. Hwabejire JO, Nembhard CE, Oyetunji TA, Seyoum T, Siram SM, Cornwell EE. Abdominal compartment syndrome in traumatic hemorrhagic shock: is there a fluid resuscitation inflection point associated with increased risk? Am J Surg. 2016;211(4):733–8.
9. He L, Yi C, Hou Z, Hak DJ. Intraabdominal hypertension/abdominal compartment syndrome after pelvic fractures: how they occur and what can be done? Injury. 2019;50(4):919–25.
10. Macedo FI, Sciarretta JD, Otero CA, Ruiz G, Ebler DJ, Pizano LR, et al. Secondary abdominal compartment syndrome after complicated traumatic lower extremity vascular injuries. Eur J Trauma Emerg Surg. 2016;42(2):207–11.
11. Abe T, Komori A, Shiraishi A, Sugiyama T, Iriyama H, Kainoh T, et al. Trauma complications and in-hospital mortality: failure-to-rescue. Crit Care. 2020;24(1):223.
12. Kainoh T, Iriyama H, Komori A, Saitoh D, Naito T, Abe T. Risk factors of fat embolism syndrome after trauma: a nested case-control study with the use of a nationwide trauma registry in Japan. Chest. 2021;159(3):1064–71.
13. Pereira R, Buglevski M, Perdigoto R, Marcelino P, Saliba F, Blot S, et al. Intra-abdominal hypertension and abdominal compartment syndrome in the critically ill liver cirrhotic patient–prevalence and clinical outcomes. A multicentric retrospective cohort study in intensive care. PLOS ONE. 2021;16(5):e0251498.
14. Smit M, Koopman B, Dieperink W, Hulscher JBF, Hofker HS, van Meurs M, et al. Intra-abdominal hypertension and abdominal compartment syndrome in patients admitted to the ICU. Ann Intensive Care. 2020;10(1):130.
15. El-Menyar A, Abdelrahman H, Al-Hassani A, Peralta R, Abdelaziz H, Latifi R, et al. Single versus multiple solid organ injuries following blunt abdominal trauma. World J Surg. 2017;41(11):2689–96.
16. Rogers WK, Garcia L. Intraabdominal hypertension, abdominal compartment syndrome, and the open abdomen. Chest. 2018;153(1):238–50.
17. Chikhladze S, Ruess DA, Schoenberger J, Fichtner-Feigl S, Pratschke J, Hopt UT, et al. Clinical course and pancreas parenchyma sparing surgical treatment of severe pancreatic trauma. Injury. 2020;51(9):1979–86.
18. Debi U. Pancreatic trauma: a concise review. World J Gastroenterol. 2013;19(47):9003.
19. Na Q, Liu C-X, Cui H, Chen J, Liu S-S, Li Q-L. Successful treatment of two patients with postpartum disseminated intravascular coagulation complicated by abdominal compartment syndrome. Gynecol Obstet Invest. 2012;73(4):337–40.
20. Gando S, Shiraishi A, Wada T, Yamakawa K, Fujishima S, Saitoh D, et al. A multicenter prospective validation study on disseminated intravascular coagulation in trauma-induced coagulopathy. J Thromb Haemost. 2020;18(9):2232–44.
21. Johansson PI, Sørensen A, Perner A, Welling K, Wanscher M, Larsen CF, et al. Disseminated intravascular coagulation or acute coagulopathy of trauma shock early after trauma? An observational study. Crit Care. 2011;15(6):R272.
22. Brohi K, Cohen MJ, Ganter MT, Matthay MA, Mackersie RC, Pittet JF. Acute traumatic coagulopathy: initiated by hypoperfusion: modulated through the protein C pathway? Ann Surg. 2007;245(5):812–8.
23. Neal MD, Hoffman MK, Cuschieri J, Minei JP, Maier RV, Harbrecht BG, et al. Crystalloid to packed red blood cell transfusion ratio in the massively transfused patient. J Trauma Acute Care Surg. 2012;72(4):892–8.
24. Reintam Blaser A, Regli A, De Keulenaer B, Kimball EJ, Starkopf L, Davis WA, et al. Incidence, risk factors, and outcomes of intra-abdominal hypertension in critically ill patients-a prospective multicenter study (IROI study). Crit Care Med. 2019;47(4):535–42.