BACKGROUND: Recent data suggests that increased intra-abdominal pressure (IAP) is one factor associated with the morbidity of morbidly obese patients, who have a BMI>35 kg/m2. IAP has been proposed to be an abdominal compartment syndrome (ACS). This study investigated the characteristics of IAP in morbidly obese patients. METHODS: 45 morbidly obese patients (mean BMI55+/-2 kg/m2) had IAP measured using urinary bladder pressure. RESULTS: The mean IAP for the morbidly obese group was 12+/-0.8 cmH2O, increased when compared to controls (IAP=0+/-2 cmH2O). The IAP correlated to the sagittal abdominal diameter, an index of the degree of central obesity (r=+0.83, P<0.02); however, it did not correlate to basal insulin, body weight, or BMI. The end-expiratory IAP did not change when measured after the laparotomy incision was made, but IAP measured in the last 15 patients increased during the first 2 postoperative days. The IAP for patients with pressure-related morbidity (gastroesophageal reflux disease, hernia, stress incontinence, diabetes, hypertension, and venous insufficiency) was 12+/-1 cmH2O, while those without these morbidities had an IAP of 9+/-0.8 cmH2O. CONCLUSION: We conclude that IAP is increased in morbid obesity. This increased IAP is a function of central obesity and is associated with increased morbidity. The degree of IAP elevation correlates with increased co-morbidities. We also conclude that elevation in IAP in morbid obesity is not a true ACS but represents a direct mass effect of the visceral obesity.
BACKGROUND: Recent data suggests that increased intra-abdominal pressure (IAP) is one factor associated with the morbidity of morbidly obesepatients, who have a BMI>35 kg/m2. IAP has been proposed to be an abdominal compartment syndrome (ACS). This study investigated the characteristics of IAP in morbidly obesepatients. METHODS: 45 morbidly obesepatients (mean BMI55+/-2 kg/m2) had IAP measured using urinary bladder pressure. RESULTS: The mean IAP for the morbidly obese group was 12+/-0.8 cmH2O, increased when compared to controls (IAP=0+/-2 cmH2O). The IAP correlated to the sagittal abdominal diameter, an index of the degree of central obesity (r=+0.83, P<0.02); however, it did not correlate to basal insulin, body weight, or BMI. The end-expiratory IAP did not change when measured after the laparotomy incision was made, but IAP measured in the last 15 patients increased during the first 2 postoperative days. The IAP for patients with pressure-related morbidity (gastroesophageal reflux disease, hernia, stress incontinence, diabetes, hypertension, and venous insufficiency) was 12+/-1 cmH2O, while those without these morbidities had an IAP of 9+/-0.8 cmH2O. CONCLUSION: We conclude that IAP is increased in morbid obesity. This increased IAP is a function of central obesity and is associated with increased morbidity. The degree of IAP elevation correlates with increased co-morbidities. We also conclude that elevation in IAP in morbid obesity is not a true ACS but represents a direct mass effect of the visceral obesity.
Authors: Kathryn A Schlosser; Sean R Maloney; Tanushree Prasad; Paul D Colavita; Vedra A Augenstein; B Todd Heniford Journal: Surg Endosc Date: 2019-06-24 Impact factor: 4.584
Authors: Yogesh N V Reddy; Masaru Obokata; Jeffrey M Testani; G Michael Felker; W H Wilson Tang; Omar F Abou-Ezzeddine; Jie-Lena Sun; Hrishikesh Chakrabothy; Steven McNulty; Sanjiv J Shah; Gregory D Lewis; Lynne W Stevenson; Margaret M Redfield; Barry A Borlaug Journal: J Card Fail Date: 2019-10-13 Impact factor: 5.712