COMMENTARY

Nutrition Support for the Obese Surgical Patient

Jay M. Mirtallo, MS, RPh

Disclosures

January 14, 2008

In This Article

Consequences of Obesity Affecting Nutrition Support

It is important to elaborate on those conditions listed in Table 1 that could significantly influence nutrition support. Increased severity of obesity is associated with type 2 diabetes mellitus, characterized by decreased insulin sensitivity and secretion, which leads to glucose intolerance.[1] This may be exacerbated by the physiologic response to acute illness following surgery, or as a result of complications of surgery. Obesity is also associated with a higher prevalence of hypertriglyceridemia,[4] which may impede the tolerance to fat provided by parenteral or enteral nutrition.

Glucose intolerance and hypertriglyceridemia are components of the metabolic syndrome, which is a group of cardiovascular disease risk factors present in 24% of US adults.[6] This syndrome is also associated with increased abdominal girth (> 35 inches for women and > 40 inches for men).[2] Importantly, this syndrome has been found to be associated with increased biomarkers of chronic inflammation (eg, C-reactive protein, tumor necrosis factor) and increased nervous system activity and sodium retention.[6] These potentially could impede the success of nutrition support or contribute to complications.

In addition, the respiratory system is compromised in obesity,[2,5] with restrictive defects such as a decreased functional residual capacity (FRC) and expiratory reserve volume (ERV). These effects are likely due to the excess weight on the chest wall or displacement of the diaphragm. Further impairment may be observed in more severe degrees of obesity, leading to hypoventilation syndrome and obstructive sleep apnea. Also, increased abdominal weight is associated with an increased incidence of aspiration
pneumonia.[3]

The effects of obesity on the cardiovascular system impact the fluid volume that may be delivered via nutrition support. Increases in blood volume and cardiac output are the result of increasing stroke volume and cardiac preload, which over time lead to increased left ventricular end-diastolic volume and other effects that eventually manifest as coronary artery disease, congestive heart failure, and its associated fluid-overloaded status.[6]

Obesity is also a risk factor for nonalcoholic fatty liver disease (NAFLD). The incidence of NAFLD is especially high among obese patients with type 2 diabetes, hyperinsulinemia, hypertension, and older age.[2] NAFLD in obese patients may progress to steatosis (fatty infiltration of the liver), inflammatory nonalcoholic steatohepatitis, fibrosis, or cirrhosis.

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