The ACS is an increasingly recognized complication of both medical and surgical patients. This syndrome has been described in a wide variety of clinical scenarios and results from a persistent elevation in IAP characterized by graded organ system dysfunction. The definitions and diagnosis of IAH or ACS depend greatly on the accuracy and reproducibility of the IAP measurement technique. As a result, IAP must be measured with an accurate, reproducible, and reliable tool. The diagnosis of ACS requires a high level of clinical suspicion combined with an increased IAP, usually obtained via UBP measurement. UBP measurement as an estimation of IAP is simple, reliable and widely accepted.
The bladder gold standard measurement techniques reported are not uniform[9
]. The volume instilled in the bladder is important. This was shown by Fusco et al[7
], who compared direct laparoscopic insufflation pressure with IVP measured with different bladder volumes. They found that a bladder volume of 50 mL revealed the least bias in measuring elevated IAP. The current standard of IAP measurement in our study via
the urinary catheter is labor intensive, and its intermittent nature could prevent timely recognition of significant changes in IAP. The continuous IAP measurement proposed by Balogh et al[10
] can be accurately measured via the irrigation port of a three-way catheter and has good agreement with the standard intermittent IAP. Recently, a fully automated IAP measurement technique was described that it can minimize the pitfalls that may alter the accuracy and reproducibility of intermittent IAP measurements (such as volume instilled, zero reference level, air bubbles, over- or underdamping). The IAP catheter is introduced like a nasogastric tube and is equipped with an air pouch at the tip. Automated IAP measurement had good correlation with the standard IVP method[11
]. Schachtrupp et al[12
] compared different direct and indirect IAP measurement methods in a porcine model and found a very good correlation between the above-mentioned air pouch system and direct insufflator pressure. However, the air pouch system was not available for use in our study.
IAH was defined in our study as a mean IAP ≥ 12 mmHg, whereas ACS was defined as a gradually and consistently increased IAP value of > 20 mmHg associated with at least one organ dysfunction or failure that was not previously present. This study confirms that IAH and ACS are frequent occurrences in patients with AP because these conditions were observed in 59.46% and 27.03% of the studied patients, respectively.
Although ideally the diagnosis of ACS should be made based on the clinical picture and confirmed by measurements of bladder pressure or equivalent, Pickhardt and others[13
] described the CT findings in four patients with confirmed ACS. They reported that the anteroposterior to transverse abdominal ratio was increased (round belly sign) in patients with ACS. The ACS patients had a ratio of 0.85 compared with 0.70 in controls. Al-Bahrani et al[14
] concluded in their prospective evaluation of CT features that the presence of round belly sign and bowel wall thickening with enhancement on CT images should alert clinicians to the possibility of presence of IAH and ACS, and to prompt measurement of the IAP and consideration of suitable interventions. The radiological data of CT scans that paralleled with the development of ACS in any course of the disease were deficient in our clinical information, so, we could not analyze the CT findings in ACS patients with SAP in our study.
Patients with AP are at risk for IAH/ACS because of the large volume of intra-abdominal and peripancreatic inflammatory fluid collection, capillary leakage caused by increased permeability, bowel and splanchnic edema, resuscitation fluid, and other factors. Gastrointestinal ileus or distension is a common risk factor for IAH among patients with AP. Both air and fluid within the hollow viscera can raise IAP and lead to IAH. IAH also leads to intestinal edema and visceral swelling triggering a vicious cycle. IAH impairs organ perfusion and leads to organ dysfunction. Manifestations of ACS include cardiovascular, pulmonary, renal, splanchnic and neurologic impairment. Hypoperfusion of the gastrointestinal tract was reported at IAP of 12 mmHg[15
]. Oliguria and marked reduction in cardiac output have been shown to develop at an IAP greater than 20 mmHg[16,17
]. The relationship among rise in IAP, greater organ dysfunction and, subsequently, higher disease mortality was well illustrated in our study. A positive significant correlation was observed between IAP and Marshall organ dysfunction score. We also observed significant improvement in Marshall score and MODS of patients with resolution of IAH. The overall mortality rate in our study of approximately 23% is comparable to the 10%-50% reported in AP patients by others[18–21
]. The mortality in ACS patients in our study (75%), however, was much higher than that in patients without ACS which is not acceptable for us, although post-injury ACS has been consistently reported to have a high mortality ranging from 25%-75%. We then compared the early onset of organ dysfunction (within 7 d of admission with AP) and risk of the disease.
While non-operative medical management strategies are now recognized as playing a vital role in both the prevention and treatment of physiologic compromise and organ dysfunction due to elevated IAP, surgical decompression is commonly considered the only treatment for aggravated ACS. All patients with IAH/ACS in our study were initially managed with noninvasive measures. In an attempt to decrease the elevated IAP, nasogastric decompression, prokinetic motility agents, bowel care, sedation, analgesia and pharmacologic paralysis were administered. Those patients who failed to improve rapidly after institution of these conservative measures underwent percutaneous abdominal decompressive drainage or operative abdominal compartment release. Although the obvious amelioration in physiological variables within 24 h after decompression have been observed in ACS patients, the clinical relevance of ACS in patients with AP in our study was illustrated, in part, by the greater probability of pancreatic infection, MODS and mortality. For this reason, a high index of suspicion and low threshold for decompressive procedure appear appropriate in patients with AP. Patients at risk for ACS warrant close monitoring and we recommend prompt abdominal decompression following documentation of increased IAP in the setting of physiologic compromise, despite in the absence of organ dysfunction/failure.
However, 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. Evidence of significant organ dysfunction has been demonstrated at an IAP of 10 mmHg[22
]. It partially explains why the outcome of ACS patients in our study is poor even though invasive decompression appeared to be effective in reducing IAP and potentially ameliorating IAH-induced physiologic compromise. One of the most important determinants of mortality is the time interval between occurrence of IAH and sustained reduction in IAP of < 12 mmHg by decompression. As shown above, hypoperfusion and acidosis start occurring at pressures from 10 to 12 mmHg, an IAP near 10 mmHg is thus gaining acceptance as a cut-off value in our institution.
Some papers have demonstrated that a persistent splanchnic hypoperfusion may induce irreversible damage in organ function and death[23–25
]. We speculate that a global mechanism of ischemia and reperfusion may explain these findings. Increased IAP resulted in a decrease of mucosal blood flow to 63% of baseline despite maintaining normal mean arterial blood pressure[17
]. In addition, elevated IAP could significantly reduce bowel tissue oxygenation due to bowel ischemia[26
]. In the 1990s, several authors observed a positive correlation between bacterial translocation and IAP in animal models, even when IAP was raised for less than 1 h. This result was caused by increased gut permeability induced by splanchnic ischemia with and without reperfusion[27,28
]. The mechanism by which the necrotic pancreas becomes infected is unclear, but experimental and clinical data suggest that the gastrointestinal tract is the likely source of organisms, since intestinal colonization by pathogens often precedes pancreatic infection[29–33
]. The gut clearly plays a major role in the development of MODS. IAH has been shown to be associated with increased bacterial translocation to pancreas and probability of pancreatic infection followed by MODS and death. This increase may be more pronounced when the rise in IAP is followed by splanchnic ischemia/reperfusion after decompression because of ACS. Moreover, ACS decompression showed to provoke and amplify proinflammatory cytokine release that served as a second insult for the induction of severe organ dysfunction in the two-hit model of MODS[34
]. Time interval effect of decompression is consistent with the “vulnerable window” of inflammatory mediators cascade priming. As a result, abdominal decompression of established ACS probably causes a fulminant reperfusion syndrome. The mean time interval between diagnosis of ACS and initiation of invasive decompressive procedure in our study was 28.38 ± 2.29 h. The relatively long time for persistence of ACS before invasive decompression might be enough to induce the higher pre-decompression IAP (36.69 ± 5.33 mmHg) and occurrence of splanchnic ischemia/reperfusion, and soon thereafter, to trigger the bacteria residing within the gastrointestinal lumen to cross the intact intestine into pancreas[35
]. The sequential effects might mainly contribute to pancreatic infection, MODS and the higher mortality of ACS patients in our study. We therefore advocate performing invasive decompression for an acute IAP of 20-25 mmHg rather than 30-40 mmHg. We also should keep firmly in mind that the earlier treatment is instituted, the more likely a progression to irreversible damage is prevented. The key to managing IAH and ACS is the early recognition of the harmful effects. It is better to prevent ACS than to allow it to occur, and manage the sequelae. However, the timing, indications and threshold value for surgical decompression are controversial with very few large trials available to give firm guidance. Decompression must be strongly considered if the IAP continues to rise or if clinical deterioration occurs. We agree with the concept that IAH is a part of a continuum leading to ACS; therefore, early detection and treatment are preferable to treating the overt clinical manifestations of ACS.
The widely disparate patient populations who may develop IAH/ACS make a standardized therapeutic approach to this syndrome difficult. Thus a single threshold value of IAP cannot be globally applied to the decision making of all patients. No one management strategy can be uniformly applied to every patient with IAH/ACS. Several fundamental management concepts, however, remain appropriate among all patients with AP. While initial conservative measures are implemented and the patient nonetheless proceeds to develop IAPs by greater than 20 mmHg, invasive abdominal decompression should be performed immediately, particularly in the presence of general trend of signs towards overt ACS, including a tendency towards high airway pressures or oliguria refractory to aggressive resuscitation. In AP patients, decompression can be accomplished either by percutaneous decompression with a large-bore catheter inserted or by formal laparotomy. Failure of catheter decompression invariably leads to formal laparotomy. With an increased awareness of the signs of ACS, early conservative treatment of IAH and rapid abdominal decompression when the trend towards the syndrome manifests, clinicians can expect a lower mortality in severe AP patients. In our experience with 74 patients with AP, the following clinical features may predispose ACS in early stage of the disease: gastrointestinal ileus or distension, a large volume of intra-abdominal and peripancreatic inflammatory fluid collection, massive fluid resuscitation and oliguria.
Indeed, the data presented from our retrospective study raise more questions than answers. Further prospective multi-center studies involving a large number of AP patients are necessary to identify subgroups that might benefit from a therapeutic intervention. The outcome of ACS remains very poor in present study. This result suggests that efforts at prevention may be as fruitful as the efforts directed at early recognition and decompression. Further efforts should focus on prevention of the syndrome. For better prevention of ACS, further studies are essential to identify the independent risk factors for ACS in AP patients and build prediction models for the syndrome to identify high-risk patients with early signs and symptoms of ACS, so as to permit prevention or timely modified treatment before organ failure occurs.
In summary, we conclude that ACS is one of the most important causes of significant morbidity and mortality in AP patients. Early detection and rapid treatment of IAH via abdominal decompression should be essential to preventing the subsequent development of pressure induced organ dysfunction in AP patients.