2. Definitions

IAH has been defined as an intra-abdominal pressure (IAP) of 12mm Hg or higher (19); this is the threshold at which organ dysfunction may set in, although it is often undetectable unless specifically sought for. Oxygen exchange for instance may be impaired but compensatory mechanisms may be effective and oxygen saturation may not be changed.

In case of ACS, the IAP is 20 mmHg or higher with clinically evident new organ dysfunction; acute kidney injury, cardiovascular instability and respiratory insufficient are the most often encountered organ dysfunctions in ACS. A complete review of IAH and ACS and how it affects organ function (11) falls beyond the scope of this chapter.

3. Pathophysiology

IAH and ACS are typically an early phenomenon in SAP and in most reports IAH develops in the first 3-5 days after hospital admission (12). Several mechanisms lead to increased intra-abdominal pressure (IAP) in these patients (Table 1) with pancreatic and peripancreatic inflammation probably only of minor importance as the increase in intra-abdominal volume from the local edema is often minimal (14). The ileus that often accompanies this disease process as well as the development of ascites may further increase the intra-abdominal volume but a major contributor is undoubtedly the fluid resuscitation that is often initiated in patients with severe pancreatitis to compensate for central hypovolemia due to third spacing. Early aggressive fluid resuscitation is still considered the standard of care in many guidelines; however, fluid overload (although variably defined) has been found to be a major risk factor in several studies and different patient categories (23). Also in studies that specifically looked into ACS in pancreatitis fluid resuscitation was consistently reported as contributing to both increased intra-abdominal volume and reduced abdominal wall compliance (6).

In the context of acute pancreatitis, the effects of IAH may have an important impact, not only on organ function as a whole, but also on pancreatic perfusion in particular. Animal studies have found that pancreatic perfusion is decreased in IAH (15), which may further increase the risk of pancreatic necrosis. Also bacterial translocation – the presumed pathway for pancreatic infection in SAP – is frequent in IAH; there is a dose dependent relationship with the extent of bacterial infection. As a result, IAH may impact both pancreatic necrosis as well as subsequent infection.

4. Epidemiology

SAP is one of the conditions where IAH and ACS are consistently reported. Using the original Atlanta criteria, the incidence of IAH was between 60 and 80 percent, and ACS developed in roughly 25-50 percent of the patients, according to one study (14). Using the new criteria, the incidence in severe disease may be even higher as some patients with what is now considered moderate pancreatitis were in the original severe category. Acute pancreatitis itself has been identified as a risk factor for IAH in a recent systematic review, but also several other factors are often present in patients with SAP (16).

IAH and especially ACS has been associated with a worse outcome in all reports on this problem (2, 5, 7, 12, 17). Rosas et al. have even proposed to use IAP as a marker of severity in SAP; in their analysis, using a cut-off of 14mmHg, the Receiver Operating Characteristics curve of IAP was higher compared to the Ranson and Imrie score which could make IAP measurement a simple tool (30); unfortunately no other studies have evaluated IAP for this purpose.

5. Diagnosis of IAH

Diagnosing IAH and ACS in SAP is simple. Clinical examination is notoriously unreliable in diagnosing IAH and ACS, but IAP measurement should be now in the armamentarium of all contemporary ICUs. The bladder is used as a window to the abdomen, and several methods for reproducible IAP measurement are now available. Several reviews describing the techniques for IAP measurement have been published (31). In brief: 25 ml of sterile saline is instilled in the urinary bladder and subsequently the hydrostatic pressure is measured in mmHg (>12mmHg IAH, >20mmHg ACS) IAH grade I 12-15mmHg, grade II 16-20mmHg, grade III (ACS) 21-25, grade IV >25mmHg [34]. Small studies have investigated CT features of ACS patients and found that signs as narrowing of the vena cava, an increased in anteroposterior diameter and bowel wall thickening were associated with ACS (3). These are late signs and IAP measurement should be implemented before these occur.

6. Prevention of IAH in SAP

Now that the contributors to IAH have been better described, several options for prevention can be devised. As in other critically ill patients, fluid resuscitation has been coined as one of the key iatrogenic contributors to IAH and ACS, and in many of these conditions the concept of vigorous fluid resuscitation should be urgently reevaluated.  Several studies have linked overly positive fluid balances to worse outcomes, including ACS (17). In this context, studies have found that patients who were resuscitated less aggressively had lower incidences of ACS and better clinical outcomes. Whether the type of resuscitation fluid impacts this phenomenon remains unclear and given the ban on starches in many countries, crystalloids remain the primary resuscitation fluid. However, Zhao et al. found that patients who were resuscitated with normal saline only had higher intra-abdominal pressure (IAP) and ACS more oftenthan patients treated with a combination of colloids and crystalloids (35).

It is difficult to recommend an appropriate resuscitation endpoint in SAP; conventional parameters such as central venous pressure are not recommended, as they are not predictive of fluid responsiveness, especially in IAH. Urinary output also has drawbacks as it is a typical early indicator of IAH and further fluid loading as a response to oliguria may aggravate rather than solve the problem. Dynamic indices such as stroke volume variation may be better tools (33) but can also be affected by IAH so judicious use of any parameter is advisable, and at all points, the requirement for fluids should be balanced against its side effects.

7. Treatment

WSACS – The Abdominal Compartment Society has recently updated the guidelines for managing IAH and ACS, which suggests a stepwise approach to decreasing IAP in patients (Figure 1) (19). In the context of SAP, a number of interventions are specifically relevant and these are discussed below. It is very important to realize that there are different non-surgical strategies available and although surgical intervention remains one of the definite treatment modalities, this should only be reserved for therapy resistant ACS.

Figure 1. Medical management of IAH and ACS (19).

In most patients medical therapy is the first step, and when applied consistently, this will dramatically reduce the need for decompressive laparotomy. In any case, early and repeated IAP measurement is the first step towards recognition of the problem and therapy as well.

Nasogastric Decompression

As ileus and gastroparesis are often present, reducing the intraluminal volume of the gastrointestinal tract is a logical first step. In case of gastric dilatation, nasogastric decompression can easily be done, and may have an important impact on IAP. The role of prokinetic drugs remains unclear.

Percutaneous Drainage

More frequently however, percutaneous drainage of ascites is a more useful, minimally invasive treatment option, that can be done at the bedside under ultrasound guidance. In the largest study to date in acute pancreatitis, Sun et al. describe a decrease in IAP from 29 to 14 mmHg after draining a median of 1800mL of ascites (32).

Also percutaneous drainage of retroperitoneal fluid collections or pseudocysts may reduce IAP and improve organ function (26).

Neuromuscular Blockers (NMB)

As in other conditions associated with IAH, improving abdominal wall compliance through NMB may be used (9). Although often used as a bridge to abdominal decompression, this may be continued for a short time (2-3 days) when necessary.

Fluid Removal and Hemofiltration

Small studies have focused on extracorporeal techniques to remove fluid overload. In a retrospective analysis Pupelis et al. found that hemofiltration was effective in removing fluid overload and reducing IAH, and was associated with improved outcomes (28). Also Oda et al. claimed improved outcomes after early hemofiltration to prevent IAH (25), but its exact role remains to be defined. Diuretics may be ineffective as patients often suffer from acute kidney injury with oligo- or anuria.

Surgical Decompression and Open Abdomen Therapy

Surgical decompression – usually through a full midline laparotomy - may be required in deteriorating patients with ACS who do not respond to medical therapy. Decompressive laparotomy is very effective in reducing the IAP in patients with ACS irrespective of the underlying cause (13), and also in SAP this has been documented. The role of decompressive laparotomy remains controversial and many surgeons are reluctant to operate in patients with SAP early in the course of the disease as many studies have found that early surgery in SAP was harmful. It is crucial that the pancreas not be touched during a decompressive laparotomy.

Alternatives to median laparotomy have been described for patients with SAP. Leppaniemi et al. have introduce the subcutaneous linea alba fasciotomy through small skin incisions on the anterior abdominal wall (22). Although effective to avoid median laparotomy in many patients (20), the resulting giant hernia is definitely a downside of the technique. Fascial closure rates after open laparotomy are increasing because of improved temporary abdominal closure techniques. In the context of SAP, some surgeons may prefer a transverse incision to facilitate access to the pancreas later (21).

Timing of surgical decompression is a particular interesting topic. In a series of patients treated with decompression in Finland, the authors reported a 100% mortality rate in patients who were decompressed later than 5 days after the start of symptoms (24). It should not be surprising that in cases of prolonged exposure to high IAP, organ dysfunction is irreversibly damaged. But the exact time frame within which decompressive laparotomy can be successful is difficult to determine. Ke et al. found in an animal study that early intervention (as early as 6 hours after onset of ACS) was more effective (18).

The resulting open abdomen should be managed appropriately. Whereas this once used to be the surgeons nightmare, negative pressure therapy has become the standard of care for the open abdomen, with the lowest complications and the highest primary fascial closure rates (4). Also in patients with SAP this method has been used successfully (27, 29). Using a mesh-based technique has been found the most successful method in achieving early abdominal closure (1) and can also be applied in SAP (29).

8. Conclusions

IAH and ACS are frequent findings in patients with SAP, and as in other settings, relevant contributors to organ dysfunction. IAP monitoring allows early detection of IAH and is recommended in all patients with severe disease. As fluid overload is an important risk factor for IAH this should be avoided. When IAH develops, percutaneous drainage of fluid collections is an effective strategy to reduce IAP, but other medical treatment options can be considered and should be used selectively. If medical therapy fails, decompressive laparotomy may be an appropriate option to reduce IAP and restore organ function.

Acknowledgements and disclosures

Financial support and sponsorship: Jan J. De Waele is a Senior Clinical Researcher with the Research Foundation Flanders (Belgium).

Conflicts of interest: Jan De Waele has served as a consultant to Smith&Nephew, and Kinetic Concepts Inc.

9. References 

1. Acosta S, Bjarnason T, Petersson U, Palsson B, Wanhainen A, Svensson M,  et al. Multicentre prospective study of fascial closure rate after open abdomen with vacuum and mesh-mediated fascial traction. Br J Surg 98:735-743, 2011. PMID: 21462176.
2. Aitken E, Gough V, Jones A, Macdonald A. Observational study of intra-abdominal pressure monitoring in acute pancreatitis. Surgery 155(5):910-8,2013. PMID: 24630146.
3. Al-Bahrani AZ, Abid GH, Sahgal E, O’shea S, Lee S, Ammori BJ. A prospective evaluation of CT features predictive of intra-abdominal hypertension and abdominal compartment syndrome in critically ill surgical patients. Clin Radiol 62:676-682, 2007. PMID: 17556037.
4. Atema JJ, Gans SL, Boermeester MA. Systematic Review and Meta-analysis of the Open Abdomen and Temporary Abdominal Closure Techniques in Non-trauma Patients. World J Surg 39(4):912-25,2014. PMID: 25446477.
5. Bhandari V, Jaipuria J, Singh M, Chawla AS. Intra-abdominal pressure in the early phase of severe acute pancreatitis: canary in a coal mine? Results from a rigorous validation protocol. Gut Liver 7:731-738, 2013. PMID: 24312716.
6. Blaser AR, Björck M, De Keulenaer B, Regli A. Abdominal compliance: A bench-to-bedside review. J Trauma Acute Care Surg 78:1044-1053, 2015. PMID: 25909429.
7. Chen H, Li F, Sun JB, Jia JG. Abdominal compartment syndrome in patients with severe acute pancreatitis in early stage. World J Gastroenterol 14:3541-3548, 2008. PMID: 18567084.
8. De Keulenaer B, Regli A, De Laet I, Roberts D, Malbrain ML. What’s new in medical management strategies for raised intra-abdominal pressure: evacuating intra-abdominal contents, improving abdominal wall compliance, pharmacotherapy, and continuous negative extra-abdominal pressure. Anaesthesiol Intensive Ther 47(1):54-62, 2015. PMID: 25421926.
9. De Laet I, Hoste E, Verholen E, De Waele JJ. The effect of neuromuscular blockers in patients with intra-abdominal hypertension. Intensive Care Med 33:1811-1814, 2007. PMID: 17594072.
10. De Waele JJ. Acute pancreatitis. Curr Opin Crit Care 20:189-195, 2014. PMID: 24553339.
11. De Waele JJ, De Laet I, Kirkpatrick AW, Hoste E. Intra-abdominal Hypertension and Abdominal Compartment Syndrome. Am J Kidney Dis 57:159-169, 2011. PMID: 21184922.
12. De Waele JJ, Hoste E, Blot SI, Decruyenaere J, Colardyn F. Intra-abdominal hypertension in patients with severe acute pancreatitis. Crit Care 9:R452-R457, 2005. PMID: 16137360.
13. De Waele JJ, Hoste EA, Malbrain ML. Decompressive laparotomy for abdominal compartment syndrome--a critical analysis. Crit Care 10:R51, 2006. PMID: 16569255.
14. De Waele JJ, Leppaniemi AK. Intra-abdominal hypertension in acute pancreatitis. World J Surg 33:1128-1133, 2009. PMID: 19350318.
15. Endo K, Sasaki T, Sata N, Hishikawa S, Sugimoto H, Lefor AT, et al. Elevation of intra-abdominal pressure by pneumoperitoneum decreases pancreatic perfusion in an in vivo porcine model. Surg Laparosc Endosc Percutan Tech 24:221-225, 2014. PMID: 24710250.
16. Holodinsky JK, Roberts DJ, Ball CG, Blaser AR, Starkopf J, Zygun DA, et al. Risk factors for intra-abdominal hypertension and abdominal compartment syndrome among adult intensive care unit patients: a systematic review and meta-analysis. Crit Care 17:R249, 2013. PMID: 24144138.
17. Ke L, Ni HB, Sun JK, Tong ZH, Li WQ, Li N, et al. Risk factors and outcome of intra-abdominal hypertension in patients with severe acute pancreatitis. World J Surg 36:171-178, 2012. PMID: 21964817.
18. Ke L, Ni HB, Sun JK, Tong ZH, Li WQ, Li N, et al. The importance of timing of decompression in severe acute pancreatitis combined with abdominal compartment syndrome. J Trauma Acute Care Surg 74:1060-1066, 2013. PMID: 23511145.
19. 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 39:1190-1206, 2013. PMID: 23673399.
20. Leppaniemi A, Hienonen P, Mentula P, Kemppainen E. Subcutaneous linea alba fasciotomy, does it really work? Am Surg 77:99-102, 2011. PMID: 21396315.
21. Leppaniemi A, Mentula P, Hienonen P, Kemppainen E. Transverse laparostomy is feasible and effective in the treatment of abdominal compartment syndrome in severe acute pancreatitis. World J Emerg Surg 3:6, 2008.
22. Leppaniemi AK, Hienonen PA, Siren JE, Kuitunen AH, Lindstrom OK, Kemppainen EA. Treatment of abdominal compartment syndrome with subcutaneous anterior abdominal fasciotomy in severe acute pancreatitis. World J Surg 30:1922-1924, 2006. PMID: 16983467.
23. Malbrain ML, Marik PE, Witters I, Cordemans C, Kirkpatrick AW, Roberts DJ, et al. Fluid overload, de-resuscitation, and outcomes in critically ill or injured patients: a systematic review with suggestions for clinical practice. Anaesthesiol Intensive Ther 46:361-380, 2014. PMID: 25432556.
24. Mentula P, Hienonen P, Kemppainen E, Puolakkainen P, Leppaniemi A. Surgical decompression for abdominal compartment syndrome in severe acute pancreatitis. Arch Surg 145:764-769, 2010. PMID: 20713929.
25. Oda S, Hirasawa H, Shiga H, Matsuda K, Nakamura M, Watanabe E, et al. Management of intra-abdominal hypertension in patients with severe acute pancreatitis with continuous hemodiafiltration using a polymethyl methacrylate membrane hemofilter. Ther Apher Dial 9:355-361, 2005. PMID: 16076382.
26. Papavramidis TS, Duros V, Michalopoulos A, Papadopoulos VN, Paramythiotis D, Harlaftis N. Intra-abdominal pressure alterations after large pancreatic pseudocyst transcutaneous drainage. BMC Gastroenterol 9:42, 2009. PMID: 19500396.
27. Plaudis H, Rudzats A, Melberga L, Kazaka I, Suba O, Pupelis G. Abdominal negative-pressure therapy: a new method in countering abdominal compartment and peritonitis - prospective study and critical review of literature. Ann Intensive Care 2 Suppl 1:S23, 2012. PMID: 23281649.
28. Pupelis G, Plaudis H, Zeiza K, Drozdova N, Mukans M, Kazaka I. Early continuous veno-venous haemofiltration in the management of severe acute pancreatitis complicated with intra-abdominal hypertension: retrospective review of 10 years’ experience. Ann Intensive Care 2 Suppl 1:S21, 2012. PMID: 23281603.
29. Rasilainen SK, Mentula PJ, Leppäniemi AK. Vacuum and mesh-mediated fascial traction for primary closure of the open abdomen in critically ill surgical patients. Br J Surg 99:1725-1732, 2012. PMID: 23034811.
30. Rosas JM, Soto SN, Aracil JS, Cladera PR, Borlan RH, Sanchez AV, et al. Intra-abdominal pressure as a marker of severity in acute pancreatitis. Surgery 141:173-178, 2007. PMID: 17263972.
31. Sugrue M, De Waele JJ, De Keulenaer BL, Roberts DJ, Malbrain ML. A user’s guide to intra-abdominal pressure measurement. Anaesthesiol Intensive Ther 47(3):241-512015. PMID: 25973661.
32. Sun ZX, Huang HR, Zhou H. Indwelling catheter and conservative measures in the treatment of abdominal compartment syndrome in fulminant acute pancreatitis. World J Gastroenterol 12:5068-5070, 2006. PMID: 16937509.
33. Trepte CJ, Bachmann KA, Stork JH, Friedheim YJ, Hinsch A, Goepfert MS, et al. The impact of early goal-directed fluid management on survival in an experimental model of severe acute pancreatitis. Intensive Care Med 39:717-726, 2013. PMID: 23287870.
34. Working Group IAP/APA Acute Pancreatitis Guidelines. IAP/APA evidence-based guidelines for the management of acute pancreatitis. Pancreatology 13(4 Suppl 2):e1-e15, 2013. PMID: 24054878.
35. Zhao G, Zhang JG, Wu HS, Tao J, Qin Q, Deng SC, et al. Effects of different resuscitation fluid on severe acute pancreatitis. World J Gastroenterol 19:2044-2052, 2013. PMID: 23599623.