Obesity surgery · 2005
Intra-abdominal pressure in the morbidly obese.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Ошибки и ограничения
История · было → стало
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Lambert David M, Marceau Simon, Forse R Armour
Аннотация
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.
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.