Patients and methods: The retrospective study included 36 patients (27 males, 9 females; mean age: 68.9±7.2 years; range, 61 to 81 years) who presented with rAAA between May 2016 and July 2023. In all patients, data regarding demographic characteristics, type of repair (open repair or endovascular aneurysm repair [EVAR]), ACS onset, morbidity, and mortality were recorded. The diagnosis of ACS was made by clinical signs and abdominal pressure measurements.

Results: The overall mortality was 41.7% (n=15). Abdominal compartment syndrome developed in five (13.9%) patients, including two (25%) of eight patients who underwent EVAR and three (10.7%) of 28 patients who underwent open repair. In the open repair group, three (60%) of five patients who developed ACS and 12 (38.7%) of 31 patients without ACS died while one (50%) of two patients who developed ACS died in the EVAR group. No death was noted among patients without ACS in the EVAR group.

Conclusion: This study shows that ACS can develop following both EVAR and open rAAA repair. Decompression laparotomy and open abdominal treatment should not be delayed when indicated. Although intra-abdominal pressure remains high, appropriate therapy may significantly affect outcomes.

As was the case in elective endovascular interventions, novel complications have been defined with unclear treatment paradigms by improving experience in emergent endovascular repair. Intraabdominal hypertension (IAH) and abdominal compartment syndrome (ACS) are known causes off multiorgan failure (MOF) and leading causes of postoperative mortality in rAAA patients undergoing open repair.[4-6] Abdominal compartment syndrome development was observed following both open and endovascular rAAA repair.[7-9] However, unlike open surgery, endovascular repair does not allow evacuation of retroperitoneal hematoma, which theoretically may lead to increased ACS incidence. Intra-abdominal hypertension and ACS resulting from elevated intra-abdominal pressure (IAP) have long been known in patients with acute aortic pathologies.[10] However, the diagnosis of IAH and ACS is underestimated in many clinics. Although treated sufficiently, the IAH overlooked following open and endovascular rAAA repair can transform into ACS with remarkable mortality rate due to irreversible pathophysiological changes causing MOF.[10]

The term IAP refers to pressure in the intraabdominal cavity. Reference values are defined following intermittent measurements through the bladder. The measurement is performed during expiration at supine position with the abdominal muscles relaxed. It was reported to be 0-5 mmHg in healthy individuals.[11] The mean IAP was reported as 5-7 mmHg in critically ill patients.[12]

Intra-abdominal hypertension is a term used for IAP that continuously or recurrently exceeds 12 mmHg in pathological conditions.[11,12] Four grades have been defined based on pressure level (Table 1).[11] Abdominal perfusion pressure is a relative marker of abdominal blood flow, which is estimated using the following formula: abdominal perfusion pressure = mean arterial pressure-IAP.

Table 1: Stages of intra-abdominal hypertension

Intra-abdominal hypertension is often associated with bleeding or splanchnic reperfusion-related massive fluid resuscitation, resulting in profound physiological derangement affecting each organ system in either a direct or indirect manner, and can also lead ACS.[12-15] Vena cava inferior is stressed by IAP elevation, which results in decreased venous return, leading to systemic vascular resistance through decrease in end-diastolic ventricular volume, stroke volume, and cardiac output. In addition, IAP elevation also affects kidneys, leading to decreased renal flow and urine output together with unfavorable effects on cardiac function. Simultaneously, the elevated IAP compresses the diaphragm and leads to increased intrathoracic pressure by elevating the airway pressure, pulmonary artery pressure, and central venous pressure and decreasing pulmonary compliance. Individual organ perfusion dysfunction occurs at a different level of IAP. For instance, renal blood flow and renal function will manifest as oliguria at an IAP level of 15 mm and anuria at 30 mmHg. If ACS is left untreated, MOF will develop. All pathophysiological changes are potentially reversible without severe organ dysfunction if IAH is diagnosed early and treated adequately.[7-10] The management often requires decompression laparotomy and aims at reducing IAP. Failure to relieve pressure is almost always fatal and surgical decompression provides significant improvement in mortality.[7]

In the literature, there is limited data regarding ACS development following open or endovascular rAAA repair and its effects on morbidity and mortality. Hence, this study aimed to reveal the incidence, treatment, and outcomes of ACS following open or endovascular repair of rAAA.

Statistical analysis
Statistical analyses were performed using IBM SPSS version 19.0 (IBM Corp., Armonk, NY, USA). Comparisons were made by the unpaired t-test. Categorical data was compared with Fisher exact test or the Mann-Whitney U test. A p-value <0.05 was considered statistically significant.

Abdominal compartment syndrome developed in five (13.9%) patients, including two (25%) of eight patients who underwent endovascular repair and three (10.7%) of 28 patients who underwent open repair. No difference was observed in patient characteristics between patients with or without ACS in the endovascular repair and open repair groups. In the open repair group, three (60%) of five patients who developed ACS and 12 (38.7%) of 31 patients without ACS died, while one (50%) of two patients who developed ACS died in the endovascular repair group. No death was noted among six patients without ACS in the endovascular repair group (Table 2).

Table 2: Patient characteristics and patient outcomes

Abdominal compartment syndrome may develop both in patients treated with endograft repair and open repair. In our study, ACS was observed in both groups. The incidence of ACS is unclear; however, it was reported to develop in 10% of patients.[21] In a systematic review, it was reported that ACS developed in 5.5% of patients treated with endovascular repair. In a recent meta-analysis, it was estimated as 8%; however, authors proposed that actual incidence may be >20% with awareness and close monitoring.[4] In our series, ACS rate was 25% in patients treated with endovascular repair, whereas it was 10.7% in patients treated with open repair.

Following open repair, it has been suggested that the ACS-related mortality rate is generally over 50%, reaching up to 100%.[22,23] In our study, ACS-related mortality was 60%. In previous studies, mortality rate up to 57% was reported in patients who developed ACS following endovascular repair.[24] In agreement with the literature, mortality rate was found as 50% in patients who developed ACS following endovascular repair.

The mechanism underlying ACS development following endovascular or open repair of rAAA is not limited to a single mechanism and may be multifactorial in certain patients. There are several factors that may be involved in ACS development. For instance, patients who underwent endovascular repair may need substantial fluid after surgery due to effects of shock, while mass effect may be present due to retroperitoneal hematoma, or coagulopathy may exist. Similarly, patients who underwent open repair may require transfusion of blood and blood products due to coagulopathy or surgical bleeding in addition to retroperitoneal mass effect and intestinal edema caused by resuscitation. Blood transfusion need at an early phase after endovascular repair may be suggestive of ongoing bleeding related to surgical type 2 endoleak. This may warrant opening the aneurysmal sac. Early onset of ACS following open repair may result from ongoing hemorrhage due to coagulopathy or surgical bleeding. All efforts should be made to correct coagulopathy and achieve normothermia before decompression laparotomy.[7]

Abdominal compartment syndrome can lead to progressive organ dysfunction and even death if not diagnosed early and treated appropriately.[1,4,7,10,25] Thus, early diagnosis and treatment are of importance. It is widely accepted that treatment should include IAP reduction and abdominal decompression in patients with persistent IAP elevation above 20-25 mmHg.[10,26-28] In our series, IAP measurements were performed periodically, and laparotomy was performed for abdominal decompression when IAP was >20 mmHg (Figure 1).

Figure 1: Algorithm for IAP monitorization and postoperative follow-up after repair of ruptured abdominal aortic aneurysm.[28]
IAP: Intraabdominal pressure; IAH: Intraabdominal hypertension; ACS: Abdominal compartment syndrome.

Intra-abdominal hypertension and ACS are severe complications with high incidence following rAAA repair. Abdominal decompression is deemed a life-saving intervention in patients who develop ACS. In the case of ACS, a successful outcome depends on the early recognition of ACS, medical therapy directing to lower IAP, and decompression laparotomy at an early phase.[28]

This study has some limitations. First, significant changes may have occurred in diagnostic and therapeutic procedures due to differences in healthcare providers and approaches over the lengthy duration of the study. Second, this is a retrospective, nonrandomized study with a relatively limited number of patients. In addition, there was no prespecified standard for IAP measurement or ACS indication.

In conclusion, intra-abdominal hypertension and ACS are commonly seen in patients treated for rAAA and are associated with a high risk for morbidity and mortality. However, IAH/ACS are overlooked by many clinicians; in addition, the diagnosis is generally delayed, and treatment often fails. All healthcare providers involved in the treatment of rAAA via open surgery or endovascular repair should understand the pathophysiology, risk factors, and presentation. This study shows that ACS can develop following both endovascular repair and open rAAA repair. Early decompression laparotomy should be performed in patients with ACS at an early phase after endovascular repair and signs suggestive of ongoing bleeding. Nonsurgical and surgical treatment, as well as a timely diagnosis, are of importance. Decompression laparotomy and open abdominal treatment should not be delayed when indicated. Although IAP remains high, appropriate therapy may significantly affect outcomes.

Ethics Committee Approval: The study protocol was approved by the Izmir Bakırçay University Non-Invasive Ethics Committee (date: 13.09.2023, no: 1192/1172). The study was conducted in accordance with the principles of the Declaration of Helsinki.

Patient Consent for Publication: A written informed consent was obtained from each patient.

Data Sharing Statement: The data that support the findings of this study are available from the corresponding author upon reasonable request.

Author Contributions: Idea, design, data collection, literature review, crtitical review, wrting the article: İ.K.; Control, literature review, references and fundings, data collection, materials: A.D.

Conflict of Interest: The authors declared no conflicts of interest with respect to the authorship and/or publication of this article.

Funding: The authors received no financial support for the research and/or authorship of this article.

1) Akkaya İ, Ersoy Ö, Umaroğlu Öztürk S, Akay HT, Sezgin A. Rüptüre abdominal aort anevrizmalarında endovasküler onarım sonrası abdominal kompartman sendromunun tedavi stratejileri: Olgu sunumu. Damar Cer Derg 2018;27:159-165. doi: 10.9739/uvcd.2016-53332.

2) Güneş T, Yılık L, Yetkin U, Yürekli İ, Özcem B, Yazman S. A comparison of open conventional and endovascular surgical therapies in abdominal aortic aneurysm repair. Turk Gogus Kalp Dama 2012;20:515-23. doi: 10.5606/tgkdc. dergisi.2012.099.

3) Ünal EU, Akkaya BB, Karahan M, Tümer NB, Civelek İ, Çelikten E, et al. What has changed in our endovascular practice at abdominal aortic aneurysms? Cardiovasc Surg Int 2020;7:51-6. doi: 10.5606/e-cvsi.2020.820.

4) Karkos CD, Menexes GC, Patelis N, Kalogirou TE, Giagtzidis IT, Harkin DW. A systematic review and meta-analysis of abdominal compartment syndrome after endovascular repair of ruptured abdominal aortic aneurysms. J Vasc Surg 2014;59:829-42. doi: 10.1016/j.jvs.2013.11.085.

5) Akansel S, Bayer Erdoğan S, Sargın M, Sokullu O, Kurç E, Aykut Aka S. Late surgical conversion after failed endovascular aortic repair: Our single-institutional experience. Cardiovasc Surg Int 2023;10:79-88. doi: 10.5606/e-cvsi.2023.1493.

6) Djavani Gidlund K, Wanhainen A, Björck M. Intra-abdominal hypertension and abdominal compartment syndrome after endovascular repair of ruptured abdominal aortic aneurysm. Eur J Vasc Endovasc Surg 2011;41:742-7. doi: 10.1016/j. ejvs.2011.02.021.

7) Rubenstein C, Bietz G, Davenport DL, Winkler M, Endean ED. Abdominal compartment syndrome associated with endovascular and open repair of ruptured abdominal aortic aneurysms. J Vasc Surg 2015;61:648-54. doi: 10.1016/j. jvs.2014.10.011.

8) Patelis N, Moris D, Karaolanis G, Georgopoulos S. Endovascular vs. open repair for ruptured abdominal aortic aneurysm. Med Sci Monit Basic Res 2016;22:34-44. doi:10.12659/MSMBR.897601.

9) Nedeau AE, Pomposelli FB, Hamdan AD, Wyers MC, Hsu R, Sachs T, et al. Endovascular vs open repair for ruptured abdominal aortic aneurysm. J Vasc Surg 2012;56:15-20. doi:10.1016/j.jvs.2011.12.067.

10) Mayer D, Rancic Z, Veith FJ, Pecoraro F, Pfammatter T, Lachat M. How to diagnose and treat abdominal compartment syndrome after endovascular and open repair of ruptured abdominal aortic aneurysms. J Cardiovasc Surg (Torino) 2014;55:179-92.

11) Muckart DJJ, Ivatury RR, Leppaniemi A, Smith RS. Definitions. In: Ivatury RR, Cheatham ML,. Malbrain M, Sugrue M, editors. Abdominal com-partment syndrome. Georgetown, TX: Landis Bioscience. Landis Bioscience; 2006. p. 19-68.

12) Malbrain ML, Cheatham ML, Kirkpatrick A, Sugrue M, Parr M, De Waele J, et al. Results from the international conference of experts on intra-abdominal hypertension and abdominal compartment syndrome. I. definitions. Intensive Care Med 2006;32:1722-32. doi: 10.1007/s00134-006-0349-5.

13) 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;39:1190-206. doi: 10.1007/s00134-013-2906-z.

14) Vegar-Brozovic V, Stoic-Brezak J. Pathophysiology of abdominal compartment syndrome. Transplant Proc 2006;38:833-5. doi: 10.1016/j.transproceed.2006.01.077.

15) Cheatham ML. Abdominal compartment syndrome: Pathophysiology and definitions. Scand J Trauma Resusc Emerg Med 2009;17:10. doi: 10.1186/1757-7241-17-10.

16) Starnes BW, Quiroga E, Hutter C, Tran NT, Hatsukami T, Meissner M, et al. Management of ruptured abdominal aortic aneurysm in the endovascular era. J Vasc Surg 2010;51:9-18. doi: 10.1016/j.jvs.2009.08.038.

17) Karkos CD, Sutton AJ, Bown MJ, Sayers RD. A metaanalysis and metaregression analysis of factors influencing mortality after endovascular repair of ruptured abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 2011;42:775-86. doi: 10.1016/j.ejvs.2011.07.028.

18) Rayt HS, Sutton AJ, London NJ, Sayers RD, Bown MJ. A systematic review and meta-analysis of endovascular repair (EVAR) for ruptured abdominal aortic aneurysm. Eur J Vasc Endovasc Surg 2008;36:536-44. doi: 10.1016/j.ejvs.2008.08.008.

19) Antonopoulos CN, Kakisis JD, Andrikopoulos V, Dervisis K, Georgopoulos S, Giannoukas A, et al. Predictors affecting in-hospital mortality of ruptured abdominal aortic aneurysms: A Greek multicenter study. Ann Vasc Surg 2014;28:1384-90. doi: 10.1016/j.avsg.2013.12.028.

20) Mehta M, Byrne J, Darling RC 3rd, Paty PS, Roddy SP, Kreienberg PB, et al. Endovascular repair of ruptured infrarenal abdominal aortic aneurysm is associated with lower 30-day mortality and better 5-year survival rates than open surgical repair. J Vasc Surg 2013;57:368-75. doi:10.1016/j.jvs.2012.09.003.

21) Ricotta JJ 2nd, Malgor RD, Oderich GS. Ruptured endovascular abdominal aortic aneurysm repair: Part II. Ann Vasc Surg 2010;24:269-77. doi: 10.1016/j.avsg.2009.08.009.

22) Rasmussen TE, Hallett JW Jr, Noel AA, Jenkins G, Bower TC, Cherry KJ Jr, et al. Early abdominal closure with mesh reduces multiple organ failure after ruptured abdominal aortic aneurysm repair: Guidelines from a 10-year casecontrol study. J Vasc Surg 2002;35:246-53. doi: 10.1067/ mva.2002.120384.

23) Loftus IM, Thompson MM. The abdominal compartment syndrome following aortic surgery. Eur J Vasc Endovasc Surg 2003;25:97-109. doi: 10.1053/ejvs.2002.1828.

24) Mehta M, Darling RC 3rd, Roddy SP, Fecteau S, Ozsvath KJ, Kreienberg PB, et al. Factors associated with abdominal compartment syndrome complicating endovascular repair of ruptured abdominal aortic aneurysms. J Vasc Surg 2005;42:1047-51. doi: 10.1016/j.jvs.2005.08.033.

25) Acosta S, Lindblad B, Zdanowski Z. Predictors for outcome after open and endovascular repair of ruptured abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 2007;33:277-84. doi: 10.1016/j.ejvs.2006.09.017.

26) Ivatury RR, Diebel L, Porter JM, Simon RJ. Intra-abdominal hypertension and the abdominal compartment syndrome. Surg Clin North Am 1997;77:783-800. doi: 10.1016/s0039- 6109(05)70584-3.

27) Björck M. Management of the tense abdomen or difficult abdominal closure after operation for ruptured abdominal aortic aneurysms. Semin Vasc Surg 2012;25:35-8. doi:10.1053/j.semvascsurg.2012.03.002.

28) Björck M, Wanhainen A. Management of abdominal compartment syndrome and the open abdomen. Eur J Vasc Endovasc Surg 2014;47:279-87. doi: 10.1016/j. ejvs.2013.12.014.