AP was diagnosed by the criteria based on the consensus of the international symposium on AP (Atlanta definition)[2]. The presence of IAH/ACS was defined by the criteria of the World Society of ACS (WSACS)[3]. The association between IAH and organ dysfunction characterized the ACS. IAH was defined as an IAP of 12 mmHg or higher, which often rendered many organs dysfunctional. IAH was a consistently increased IAP value of ≥ 12 mmHg recorded by at least three standardized pressure measurements during at least 8 h. ACS was diagnosed when the IAP exceeded 20 mmHg at which IAH caused severe physiologic derangements and associated with new, attributable single organ dysfunction or MODS. Septic shock was defined according to the American-European conference consensus definitions[4].

The study population included 74 patients with AP admitted to the surgical intensive care unit (SICU), Xuan Wu Hospital of Capital Medical University, from May 2002 to May 2006. General inclusion criteria for AP were defined as: (1) a time interval between onset of typical abdominal symptoms and study inclusion of 72 h and less; (2) the presence of systemic inflammatory response syndrome (SIRS) manifested by two or more of the following conditions: temperature > 38°C or < 36°C; heart rate (HR) > 90 beats/min; respiratory rate >20 breaths/min or PaCO₂ < 32 mmHg; WBC count > 12 000/mm³ or < 4000/mm³, or > 10% immature(band) forms; and (3) at least 3-fold elevated serum amylase or lipase levels, or a APACHE II score > 8, or a C-reactive protein (CRP) of ≥ 250 mg/L.

All patients were treated according to our standard management of pancreatitis protocol and the practice guidelines in AP[5]. The patients recruited in this study were divided into two groups according to IAP determined during the first week after admission. Patients (n = 44) with IAP ≥ 12 mmHg were assigned in IAH group, and the remaining patients (n = 30) with IAP < 12 mmHg in normal IAP group. Patients with IAH or ACS were treated by lowering IAP with promoting enterokinesia, and/or percutaneous abdominal decompression and drainage and/or decompressive emergency laparotomy. A silastic covering was placed to achieve a pressure-free abdominal closure when decompressive laparotomy was performed. The definitive closure was performed within 5-7 d. In the setting of gallstone pancreatitis and evidence of common bile duct obstruction, urgent endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy was indicated to remove the impacted stone.

Patients with AP admitted to SICU underwent intermittent measurement of IAP, recording of the clinical data and calculation of MODS scores by Marshall et al[6]. Since intravesical pressure (IVP) measurement had been described as a standard and validated technique of indirectly reflecting IAP and rapidly recognizing ACS[7], urinary bladder pressure (UBP) was routinely measured in all AP patients in our study. In brief, the patient was placed in complete supine position with a Foley catheter. One end of a transducer was connected to the Foley catheter through 3-way stopcocks. The monitor was zeroed with the transducer at the level of the symphysis pubis. After clamping the drainage tube of the urinary catheter, the bladder was instilled with 50 mL of sterile normal saline injected through a Foley catheter under aseptic condition, the bladder was then emptied by removing the clamp off the drainage tube. IVP was measured using a pressure transducer, and a series of reading were obtained every 4 h apart and their average calculated as one standardized measurement in mmHg (1 mmHg = 1.36 cmH₂O). Only end-expiratory values were used in an effort to avoid interference from respiratory excursion of the diaphragm into the intra-abdominal space. A sustained increase in IAP was detected based upon at least three consecutive standardized measurements during at least 8 h.

Hemodynamics and other physiologic parameters, including HR, mean arterial pressure (MAP), central venous pressure (CVP), urine output (UO), peak airway pressure (PAP), arterial carbon dioxide partial pressure (PaCO₂), modified respiratory index (MRI) expressed as the arterial oxygen partial pressure (PaO₂) to fraction of inspired oxygen (FiO₂) ratio (PaO₂/FiO₂), arterial pH, arterial base deficits (BE) and arterial lactic acid, were registered before and after decompression of ACS. The worst Acute Physiology and Chronic Health Evaluation (APACHE) II score and Ranson scoring system during the first 24 or 48 h of SICU stay were recorded respectively in the identification of the severity of pancreatitis. In this study, we applied a Marshall subscore of 2 or more in any of the 6 organs (respiratory, cardiovascular, coagulation, central nervous system, hepatic, and renal) to indicate organ dysfunction associated with IAH (IAP > 20 mmHg), and defined the presence of ACS. MODS was defined as two or more organs having persistently 2 or more Marshall subscores for more than 24 h despite aggressive resuscitation and organ support. Total Marshall scores were computed daily and for the entire duration of the intensive care stay.

All 74 patients with AP were detected using contrast enhanced computed tomography (CT) on admission. The contrast-enhanced CT scan severity index (CT-SI) developed by Balthazar and coworkers was used for evaluating severity of pancreatitis[8]. CT-SI was measured for all patients on admission in this study. The incidences of pancreatic infection, septic shock, MODS, and the in-hospital mortality were also recorded. Pancreatic infection included infected necrosis and pancreatic abscess. Necrosis formation of the pancreas was assessed by contrast-enhanced CT. Patients with pancreatic necrosis or large peripancreatic fluid collections who manifested clinical signs of sepsis with a non-improving or deteriorating clinical course despite a reasonable time of medical therapy underwent fine-needle aspiration (FNA) of the necrotic areas or fluid collections under CT or ultrasound guidance to determine the presence of bacterial contamination or pancreatic infection.

Patients’ clinical records were retrospectively reviewed. Data were analyzed using the software package SPSS version 11.5. Continuous data are presented as mean ± SD. Categorical variables are expressed as numbers and percentages for the group from which they were derived. The comparisons of age, gender, APACHE II score and CT-SI on admission, Ranson score within 48 h after admission, incidences of pancreatic infection and MODS, and the in-hospital mortality between the two groups were analyzed using the independent sample t test or χ² test as appropriate. Comparison of clinical parameters between before decompression and after decompression of ACS was performed by paired samples t test. Bivariate correlations were analyzed by Pearson test between the mean IAP in any 24-h period within the first week after admission and the Marshall score at the same time interval, or, between the IAP on admission and the APACHE II score on admission or Ranson score within 48 h after admission. Difference was defined as statistically significant if P < 0.05. P` (corrected P) < 0.017 indicated statistically significant difference in multiple comparisons of complications and outcome between patients with and without ACS in χ² test.

Seventy-four patients (39 men and 35 women) were included in the study; the mean age was 63.00 ± 9.79 years (range, 42-87 years). The mean time interval between onset of AP and admission was 34.97 ± 30.16 h. IAH developed in 44 (59.46%) of 74 patients with AP. The etiologic causes of their AP are detailed in Table 1. The difference in etiologic causes between the two groups was not statistically significant, P = 0.803 (Fisher two-tail exact probability test). The differences in age, gender, APACHE II score, Ranson score and CT-SI on admission were also not statistically significant between IAH group and group with normal IAP (Table 2). Neither age nor gender was correlated with IAH development. Similarly, APACHE II score and CT-SI on admission, and Ranson score within 48 h after admission, contrary to accepted belief, were not found predictive of early IAH development.

During any 24-h period of the first week after admission, the recorded mean IAP was correlated significantly with the Marshall score calculated at the same time interval in IAH group (r = 0.635, P < 0.001), but IAP on admission had no significant correlation with APACHE II score on admission and Ranson score within 48 h after admission (r = 0.127, P = 0.248, and r = 0.145, P = 0.263, respectively).

ACS was recorded during the first week after admission in 20 patients (27.03%) in whom IAH (IAP > 20 mmHg) was associated with organ dysfunction or failure. In 14 of these patients, IAH and organ dysfunction were present on admission, 2 patients had IAH on admission and developed organ dysfunction 24-48 h later, whereas 4 patients had respiratory failure on admission without IAH but went on to develop IAH and ACS 3-5 d after admission. Medicine and physical therapy were applied in all IAH patients to promote enterokinesia for recovery of IAH/ACS. The administration of prokinetic motility agents such as erythromycin, metoclopramide, or neostigmine appeared to hold promise in evacuating the intraluminal contents and decreasing the size of the viscera. Moreover, sedation and muscle relaxant (only for mechanical ventilated patients) were also used properly to lower IAP. Seven ACS patients had restoration of organ function with their UBP lowering less than 12 mmHg via non-invasive intervention mentioned above. The remaining 13 ACS patients had progressive deterioration of organ function and increases in IAP despite active persistent non-invasive decompression management for 24 h. Therefore, these patients had abdominal decompression procedure very soon. The mean time interval between diagnosis of ACS and initiation of invasive decompressive procedure was 28.38 ± 2.29 h (range, 26-33 h). Prior to invasive decompression, aggressive attempts should be made to correct coagulation deficits, acidosis and hypovolemia.

The invasive decompressive procedure included two ways: abdominal percutaneous decompression drainage and decompressive laparotomy with temporary closure. IAP was reduced in one of the two ways. The insertion of abdominal drains was performed in 8 patients under CT or ultrasound guidance in the presence of large intra-abdominal collections more than 800 mL. These patients had their abdomens decompressed by percutaneous placement of a large-bore hemodialysis catheter into the intra-abdominal space, with drainage of intra-abdominal fluid. Percutaneous drainage was a continual process with fluid draining for several days. Once the drainage stopped, the catheter was removed. No complication related to the procedure occurred in our study. Decompressive drainage reduced the IAP by less than 20 mmHg and then further resulted in relief of the IAH in 5 patients. Decompressive laparotomy was performed in the remaining 5 patients with ACS and 3 patients of failure in previous percutaneous abdominal decompressive drainage for the reduction in IAP. The typical open abdomen operation was performed with a temporary silastic covering obtained from the sterilized inner surface of an intravenous bag sewn to the fascia to protect the underlying abdominal contents from injury and desiccation, and to prevent excessive amounts of fluid from leaking onto surrounding bandages. Removal of silastic covering and scheduled closure of abdominal wall should be subsequently attempted as soon as possible after the acute episode resolved and the edema and/or inflammatory fluid collections reduced significantly. No complication directly related to decompressive laparotomy itself occurred in our study.

All patients with bladder pressure of more than 20 mmHg immediately benefited from the alternative of invasive decompression methods. Emergency invasive decompressive procedure resulted in statistically significant improvement in physiologic parameters, with the exception of the CVP, within 24 h after decompression (Table 3). Pre-decompression bladder pressure was significantly elevated, with a mean pressure of 36.69 ± 5.33 mmHg. Abdominal compartment release resulted in a dramatic decrease of IAP to 18.31 ± 3.25 mmHg (P < 0.001). The high PAP improved significantly from 41.23 ± 12.90 cmH₂O pre-decompression to 24.46 ± 5.41 cmH₂O post-decompression (P = 0.001). Other general physiologic condition also improved significantly with decompression, as evidenced by a significant improvement in serum pH, BE, PaO₂/PaCO₂, arterial lactic acid, MAP and UO. Only one parameter registered in this study, e.g. CVP, was not affected by decompression for ACS (P = 0.072).

Seventeen of 74 patients died with a mortality rate of 22.97%. It appeared that the incidences of pancreatic infection and MODS in patients with ACS in early stage were considerably higher than other patients without ACS. Subsequently, the unacceptably high mortality rate in patients with ACS during their first week after admission was much higher than that in patients without ACS in the course of their attack of AP (75% vs 3.33% and 4.17%) (Table 4).

Multiple comparisons of complications and outcome were made between ACS patients (IAP > 20 mmHg), IAH patients without ACS(12 mmHg ≤ IAP ≤ 20 mmHg) and normal IAP patients(IAP < 12 mmHg). The incidences of pancreatic infection, septic shock, MODS and in-hospital mortality in patients with ACS were significantly higher than those in IAH patients without ACS and normal IAP patients, respectively (pancreatic infection: χ² = 13.42, P < 0.001; χ² = 16.93, P < 0.001, septic shock: χ² = 12.84, P < 0.001; χ² = 22.12, P < 0.001, MODS: χ² = 11.01, P = 0.001; χ² = 21.33, P < 0.001, in-hospital mortality: χ² = 23.65, P < 0.001; χ² = 28.32, P < 0.001, respectively). However, the difference in incidences of pancreatic infection, septic shock, MODS and in-hospital mortality was not statistically significant between IAH patients without ACS and normal IAP patients (pancreatic infection: P = 1.000, Fisher two-tail exact probability test; septic shock: χ² = 0.527, P = 0.468; MODS: χ² = 2.078, P = 0.149; in-hospital mortality: P = 1.000, Fisher two-tail exact probability test).

Intra-abdominal hypertension (IAH) contributes to organ failure in patients with abdominal trauma and sepsis and leads to the development of abdominal compartment syndrome (ACS). ACS has also been described in patients with severe acute pancreatitis (SAP). Significant visceral edema associated with massive fluid resuscitation, paralytic ileus and formation of pancreatic ascites in patients with SAP can lead to ACS which may cause the early development of multiple organ dysfunction syndrome (MODS), especially in the early stages of the disease. Despite recent advances in the management of patients, SAP remains a disease with an unpredictable clinical course and significant morbidity and mortality. Pancreatic infection and the presence of organ dysfunction still remain the most fearing complications and are increasingly recognized as important risk factors for mortality in patients with SAP. The development of ACS in patients with SAP seems to be associated with increased mortality. The clinical impact of IAH/ACS on pancreatic infection and organ failure in SAP patients is needed to investigate.

Only recently has the important role of ACS been recognized as a contributing factor for the multiple organ failure commonly seen in SAP. Percutaneous drainage of ascites and surgical decompression are the preferred methods of treatment for ACS. However, some studies, including this study, show that although decompression has a significant effect in lowering IAP, mortality still remains high in SAP patients with ACS. The poor response might be due to an intervention performed too late. Although the 2004 international ACS conference consensus definitions committee has proposed the evidence-based treatment guidelines to assist clinicians in the management of IAH and ACS, there is no clear consensus on the critical level of IAP at which decompression is necessary. The critical level of IAP requiring decompression thus has not been established for AP patients. Because of the close correlation between ACS and death in SAP patients as suggested by this study, there is a great need for well-designed, prospective clinical trials to clarify the questions and issues that remain unanswered with respect to IAH and ACS.

The notion that patients with SAP may develop ACS, which necessitates emergency abdominal decompression, has been ignored by some current literatures. The currently prevailing paradigm calls for non-operative management of SAP as long as there is no evidence of infection. The authors of this study proposed that there is a subset of patients who may necessitate an emergency abdominal decompression or laparotomy in the absence of infection in order to decompress a clinically significant ACS, which is associated with the acute pancreatitis (AP).

The present study implicated that the timing of surgical decompression may play a crucial role in improving poor survival rates of SAP patients with ACS. Increased awareness of the syndrome of IAH/ACS in AP and transvesical measurement of intra-abdominal pressure (IAP) will reveal its prevalence and significance. This experience with the 74 patients may reinforce the enthusiasm for prevention of ACS and decompression in SAP patients with IAH. This study also gave proof of necessity for establishing a critical IAP level at which abdominal decompression or laparotomy should be performed for SAP patients.

IAP is the steady-state pressure concealed within the abdominal cavity. IAH is a sustained or repeated pathological elevation in IAP ≥ 12 mmHg. ACS is a sustained IAP > 20 mmHg associated with new organ dysfunction/failure.

Although the IAP was described by Etienne-Jules Marey in 1863 and ACS described in details by Korn et al in 1984 and more information is appearing recently in the literature, it is still important to gather more knowledge about ACS complicating severe pancreatitis. This article constitutes a fairly good number of patients with ACS.