This study shows a wide range in IAP in patients undergoing elective cardiothoracic surgery, between 0 and 26 mmHg. A single IAP measurement was elevated ≥12 mmHg in more than 26 % of patients. Furthermore, an IAP > 20 mmHg was measured in 4 patients. We found a correlation between BMI and IAP. We did not find that other definitions of body shape correlated better with IAP than BMI. We did not find a correlation between CRP or serum creatinine and IAP. However, postoperative CRP and postoperative serum creatinine are correlated with BMI, WC and WHR.
The large variation in IAP shows that a single measurement of IAP should be interpreted with caution. Ultimately, the clinical context gives meaning to an increased IAP and repeated measurements should be performed before a diagnosis of IAH or ACS can be made.
Most patients were either overweight or obese. The high proportion of obesity in this cardiothoracic surgery population is not surprising, considering obesity is a risk factor for cardiovascular conditions. Mean IAP in the obese group was significantly higher than in the non-obese group. However, despite reaching statistical significance, the actual difference in mean scores between the groups was small. Furthermore, BMI is a better predictor of IAP than WHR, but BMI and WHR together explained only 5 % of the variance in IAP. This means that in an obese patient with clinical symptoms of ACS an increased IAP should never be attributed to obesity only. There is no evidence that an obesity-related elevation in IAP is not a true ACS, but only a direct mass effect of the visceral obesity .
At least 50 % of patients in this study have central obesity. The exact number of patients with central obesity varies according to which definition is used. Although there was a trend toward a higher mean IAP in central obesity according to these definitions, this was not statistically significant. Even though there seemed to be a positive correlation between IAP and WC and between IAP and WHR, this was not statistically significant. Hence, this study does not match with findings from previous studies in the morbidly obese [13, 14]. We believe that this study may have been underpowered to show these relations. We did not find a correlation between IAP and inflammation or between IAP and renal function in this population. Future studies should consider using more sensitive biomarkers for determination of both systemic inflammation and renal function and take into account that larger datasets may be required to find relations.
We did find a correlation between postoperative CRP and postoperative serum creatinine and BMI, WC and WHR. This matches with findings in a larger group of otherwise healthy persons, where the correlation between renal function and body shape was also shown .
A subgroup analysis shows that in males with central obesity, defined by WHR, IAP was significantly higher than in males without central obesity. This difference was not found in females. This matches with findings in the morbidly obese, where WHR was correlated with transvesical IAP in men but not in women . A possible explanation may be the difference in abdominal compliance between males and females. In patients with a decreased abdominal compliance, the same change in intra-abdominal volume will result in a greater change in IAP. Central obesity usually results in increased visceral fat and a sphere-like baseline shape of the abdominal cavity with poor stretching capacity, whereas in peripheral obesity the internal abdominal diameter is shaped as an ellipse and has a huge stretching capacity (and thus higher abdominal compliance) . Factors associated with decreased abdominal compliance include male gender and (central) obesity. Factors associated with increased abdominal compliance include female gender, peripheral obesity, previous pregnancy and previous abdominal surgery .
We assumed that the patients in this study did not have an increased risk for development of IAH or ACS. However, there is one study in 25 patients which concludes that the CABG procedure with extracorporeal circulation may result in increased intra-abdominal pressure due to the invoked inflammatory response by the extracorporeal circulation . Operating time, perfusion time and aorta occlusion time were not correlated with IAP in the present study. Furthermore, there was no difference in mean IAP in patients with and without extracorporeal circulation. Therefore, the findings in our study do not corroborate Dabrowski’s conclusions.
These results raise the question whether the elevations in IAP measured in this study are pathological. Since IAP was measured only once, a diagnosis of IAH or ACS could by definition not be made. Furthermore, only 3 patients developed abdominal symptoms during their stay in the ICU; none of these patients had an IAP ≥ 12 mmHg upon admission. However, higher IAP values were found in obese patients and we have to consider that the IAP in obese patients is chronically increased. Even slight elevations in IAP are associated with increased systemic inflammation, and signs of acute kidney injury  and weight excess and/or central body fat distribution are associated with increased long-term renal risk . Obesity is associated with acute kidney injury in critically ill patients , and this study shows a correlation between postoperative serum creatinine and BMI, WC and WHR. IAP is probably only one of many contributing factors to renal function, and it will be hard to dissect consequences of a slight chronic increase in IAP from other factors related to renal function loss . In contrast to acute models of ACS, there are no models of small long-term increases in IAP.
Since IAP > 12 independently predicts organ failure and mortality in a mixed population of critically ill patients [1, 2], perhaps we should monitor IAP more closely in overweight and obese patients when they are critically ill, in order to avoid any further increase in IAP.
Limitations of this study
This study was performed in a selected population of elective cardiothoracic surgery patients. Moreover, other anthropomorphic parameters like sagittal abdominal diameter were not measured in this study.
IAP was measured only once per patient; therefore, a diagnosis of IAH (sustained or repeated IAP ≥ 12 mmHg) or ACS (sustained or repeated IAP > 20 with new organ failure) could not be made. Furthermore, IAP was measured postoperatively and this measurement could have been influenced by perioperative fluid management.
CRP was measured as a marker of inflammation, and serum creatinine was measured as a marker of renal function; however, these markers lack specificity and sensitivity to determine subtle differences in inflammation and renal function. This study may have been underpowered to show a relation between body shape and IAP, CRP and serum creatinine. Sensitive AKI biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C, may reveal the relation between IAP and renal function in future studies with larger datasets.