Morbid Obesity

1. Presented by Erin McLean Morbid Obesity

2. Overview • Patient information • Disease background • Nutrition care process • Conclusion • Review of key points • Personal impressions

3. Patient Profile • Gender: Male • Age: 51 • Ethnic background: Hispanic • Household situation: Patient bedbound at home, cared for by brother and sister, separated from wife, no children • Education: Not disclosed • Occupation: Not disclosed • Religion: Not disclosed • Admit date/discharge date: 01/25/14, 02/17/14

4. Reason for Hospital Admission • The patient was admitted for surgical debridement of an abscess that presented on his right groin. The abscess grew in size and began draining pustular fluid three weeks prior to his admission.

5. Medical/Health/Family History • Past medical history • Morbid obesity • Hypertension • Chronic lymphedema • Sleep apnea • Anxiety • Remote history of seizure disorder • Past surgical history • Cholecystectomy • Gunshot wound repairment

6. Medical/Health/Family History • Health history • Recent 91 kg weight loss PTA • Gross movement of extremities • Not using CPAP at night • No dental or swallowing issues • Some digestive issues • No eliminative issues • No history of alcohol of illicit drug abuse • Family history • Positive for diabetes mellitus

7. Medical Diagnoses • Groin abscess • Cellulitis • Morbid obesity • Diabetes mellitus • Acute respiratory failure • Urinary tract infection • Septic shock • Aspiration pneumonia • Acute kidney injury • Possible ischemic bowel

8. Morbid Obesity Defined • Morbid obesity • NHANES: 35.7% of US adults are obese • 6.6% of US adults are morbidly obese • Marked by excessive accumulation of fat in body • Associated with many comorbid conditions • BMI classification: (Ogden, Carroll, Kit, & Flegal, 2012; Sturm & Hattori, 2013; Hurt & Frazier, 2012)

9. Pathophysiology • Appetite regulation and weight management are influenced by the interplay between the CNS and hormones. • Leptin • Simulates ↓ food intake and ↑ energy expenditure • Proportional to amount of total fat mass • Leptin resistance vs. leptin deficiency in obesity development • Insulin • Involved in food intake regulation and production/storage of fat • Proportional to amount of total fat mass • Impaired insulin action → ↓ thermogenesis → ↑ adiposity (Beckman, Beckman, & Earthman, 2010; Mahan, Escott-Stump, & Raymond, 2012)

10. Pathophysiology • Ghrelin • Stimulates ↑ appetite • ↑ levels in normal-weight individuals, ↓ levels in obese individuals • Absent ↓ in post-prandial circulating levels in obese individuals • Glucagon-like peptide (GLP-1) • Stimulates ↓ appetite, imparts satiety • ↑ levels in normal-weight individuals, ↓ levels in obese individuals • Peptide YY (PYY) • Stimulates ↓ appetite, imparts satiety • ↑ levels in normal-weight individuals, ↓ levels in obese individuals (Perry & Wang, 2012; Beckman, Beckman, & Earthman, 2010 )

11. Symptoms/Clinical Manifestations • Accumulation of adipose tissue primarily in subcutaneous tissue and in abdominal region • Adipocytes increase in number and size as obesity develops. • Linked to >3o comorbidities • DM • CAD • Hypercoagulable state • Sleep apnea • NAFLD • Sex hormone disorders • Depression (Brethauer, Kashyap, & Schauer, 2013)

12. Etiology • Diet • Frequent meals high in unhealthy fats, red meats, refined grains, sugar-laden beverages • Access to energy-dense foods easier and cheaper • Disordered eating habits • Physical activity level • Sedentary lifestyle coupled with chronic overeating • Exercise replaced with sedentary activities (“Obesity causes,” n.d.; Hurt & Frazier, 2012; Mahan, Escott-Stump, & Raymond, 2012)

13. Etiology • Chronic sleep deprivation • Endocrine regulation altered • Can change composition, quantity, and timing of food intake • Heredity • Genes influence satiety, RMR, quantity and size of adipose cells, distribution of fat mass • Gene activation or deactivation (Mahan, Escott-Stump, & Raymond, 2012; Mahan, Escott-Stump, & Raymond, 2012)

14. Etiology • Obesogens • Alter lipid metabolism and promote fat accumulation • Act as endocrine disruptors • Pharmaceutical obesogens • Thiazolidinediones • Selective serotonin reuptake inhibitors • Diethylstilbestrol • Industrial obesogens • Tributyltinand triphenyltincompounds • Bisphenol A • Perfluorooctanoic acid • Diethylhexyl phthalate • Dietary obesogens • Monosodium glutamate • Genistein • Fructose (Holtcamp, 2012)

15. Etiology • Pathogens • 10 infectious agents implicated in adipogenesis • Bacteria • Viruses • Gut microflora • Prions (Mahan, Escott-Stump, & Raymond, 2012)

16. Treatment • Lifestyle modification • Behavior modification • Diet intervention • Calorie restriction diets • Meal replacement diets • Commercial diet programs • Physical activity

17. Treatment • Pharmaceutical management • Few drugs approved by FDA • BMI of ≥30 kg/m2orBMI of 27-29 kg/m2with at least one obesity-related comorbidity to qualify • Available drugs • Orlistat/Xenical®/Alli® • Lorcaserin/Belviq® • Phentermine-topiramate/Qsymia® (“Prescription medications,” 2013)

18. Treatment • Surgical intervention • Restrictive procedures • Laparoscopic adjustable gastric banding • Sleeve gastrectomy

19. Treatment • Surgical intervention • Malabsorptive procedures • Biliopancreatic diversion • Duodenal switch • Jejunoileal bypass

20. Treatment • Surgical intervention • Combined restrictive and malabsorptiveprocedure • Roux-en-Y gastric bypass

21. The Comparative Effectiveness of Sleeve Gastrectomy, Gastric Bypass, and Adjustable Gastric Banding Procedures for the Treatment of Morbid Obesity • Purpose • Analyze comparative effectiveness of SG, RYGB, and LAGB • Methods • 2,949 SG patients matched to same number of patients who underwent RYGB and LAGB • Matched based on 23 characteristics • Data obtained from externally audited, statewide clinical registry • Outcomes included weight loss, complications arising within 30 days of procedure, and quality of life (Carlin et al., 2013)

22. The Comparative Effectiveness of Sleeve Gastrectomy, Gastric Bypass, and Adjustable Gastric Banding Procedures for the Treatment of Morbid Obesity • Results • Weight loss at 1 year for SG was 13% lower compared to RYGB (p < 0.0001) and 77% higher compared to LAGB (p < 0.0001) • Weight loss in patients plateaued or rebounded in all three procedure groups at years 2 and 3 • Overall complication rates in patients who underwent SG were lower compared to RYGB (p < 0.0001) and higher compared to those who underwent LAGB (p < 0.0001) • Severe complication rates for SG were similar to RYGB (p = 0.736) but higher compared to LAGB (p < 0.0001) • Remission rates for comorbidities in patients who underwent SG were similar to those who underwent RYGB and higher compared to LAGB patients (Carlin et al., 2013)

23. The Comparative Effectiveness of Sleeve Gastrectomy, Gastric Bypass, and Adjustable Gastric Banding Procedures for the Treatment of Morbid Obesity • Conclusion • Due to the greater weight loss observed after SG compared to LAGB as well as the decreased complication rates compared to RYGB, insurance carriers should provide routine coverage for this bariatric procedure. (Carlin et al., 2013)

24. Treatment • Treatment specific to patient • Surgical debridement of groin abscess • Cystoscopy with Foley catheter placement • Tracheostomy placement/PEG tube placement • Dialysis catheter placement for CRRT treatment • Restricted caloric intake • Medications • Propofol • Norepinephrine • Fentanyl • Lorazepam • Insulin lispro • Nebivolol • Pantoprazole • Furosemide • Bisacodyl • Heparin • Vancomycin

25. Nutrition Intervention • Decreasing caloric intake creates a negative energy balance, thereby causing a person to lose weight. • 10% ↓ in initial body weight over 6 month period for ambulatory, morbidly obese patients • For critically ill, morbidly obese patients, RMR critical to ↓ under- and overfeeding • Indirect calorimetry vs. predictive equations (Hurt & Frazier, 2012)

26. Nutrition Intervention • Penn State Equation [PSU(2003b)] • Used for critically ill, mechanically ventilated, obese adults ≤ 60 years of age • PSU(2003b): RMR (kcal/d) = Mifflin (0.96) + VE (31) + Tmax (167) – 6212 • Modified Penn State Equation [PSU(2010)] • Used for critically ill, mechanically ventilated, obese adults > 60 years of age • PSU(2010): RMR (kcal/d) = Mifflin (0.71) + VE (64) + Tmax(85) – 3085 (“Critical illness,” 2013)

27. Nutrition Intervention • Calorie per kilogram method • Used for critically ill, mechanically ventilated, obese patients • Used to determine high protein, hypocaloric feedings • 22 to 25 kcal/kg IBW per day • Provides 60 to 70% of estimated energy requirements • Incorrect estimated energy requirements 54% of the time • Protein requirements • 2.5 g protein/kg IBW per day for obesity class III patients (Hurt & Frazier, 2012; Wooley & Frankenfield, 2012)

28. Prediction of Resting Metabolic Rate in Critically Ill Patients at the Extremes of Body Mass Index • Purpose • To provide validation data on the accuracy of predictive equations since little data currently exists • Methods • RMR of critically ill, mechanically ventilated patients with a BMI of ≤ 21.0 or ≥ 45.0 kg/m2 was assessed using IC • Penn State equation, Ireton-Jones equation, Faisy equation, Harris-Benedict equation, Mifflin-St Jeor equation, and ACCP standard compared to IC measurements • Accuracy determined when energy expenditure estimations from equations fell within 10% of IC measurement (Frankenfield, Ashcraft, & Galvan, 2013)

29. Prediction of Resting Metabolic Rate in Critically Ill Patients at the Extremes of Body Mass Index • Results • Penn State equation had highest accuracy rate (76%) in morbidly obese patients while ACCP standard had lowest accuracy rate when actual body weight was utilized (0%) • Penn State equation had highest accuracy rate (63%) in underweight patients, but when BMI dropped below 20.5, accuracy rate fell to 58% • Conclusion • For critically ill, morbidly obese patients, Penn State equation is valid for estimating RMR • For critically ill, underweight patients, modification to Penn State equation necessary to improve accuracy rate (Frankenfield, Ashcraft, & Galvan, 2013)

30. Prognosis • Not a leading cause of death in US or world • Does increase risk for development of related comorbidities, some of which are leading causes of death • Weight loss decreases risk of developing comorbidities – all interventions, however, pose risk for weight regain • Surgical interventions provide greatest results (“Leading causes,” 2013; “Top 10,” 2013; Stoklossa & Atwal, 2013)

31. Extreme Obesity and Outcomes in Critically Ill Patients • Purpose • Research on critically ill, obese adults has found that outcomes in this patient group are not worse than in normal-weight adults. Research examining outcomes in those with morbid obesity with a BMI ≥ 40 kg/m2 has not been conducted and was the focus of this study. (Martino et al. 2011)

32. Extreme Obesity and Outcomes in Critically Ill Patients • Methods • Data gathered and evaluated from multicenter international observational study which examined nutrition practices in ICU • Observational study took place in 355 ICU units in 33 different countries and included data from 2007 to 2009 • Patients included in study were mechanically ventilated adults ≥ 18 years of age who received treatment in ICU for > 72 hours • 8,813 patients included in the study of which 3,490 had normal weight while 348 had BMI of 40 to 49.9 kg/m2, 118 had BMI of 50 to 59.9 kg/m2, and 58 had BMI of 60 kg/m2 or greater • Comparison of 60-day mortality rate, DMV, LOS in ICU, and hospital LOS conducted between morbidly obese and normal-weight patients • Potential cofounders adjusted for using logistic generalized estimating equations and Cox proportional hazard methods with ICU clustering (Martino et al. 2011)

33. Extreme Obesity and Outcomes in Critically Ill Patients • Results • Critically ill, morbidly obese patients had improved 60-day mortality rate compared to normal-weight individuals (p = 0.04), but this was considered nonsignificantafter cofounders adjusted for • Morbidly obese patients had longer DMV (p = 0.0013), ICU LOS (p = 0.0016), and trend toward decreased hospital LOS (p = 0.17) compared to normal-weight individuals after adjustment of cofounders • Conclusion • Morbid obesity not associated with decreased survival rate compared to normal-weight patients during critical illness but is associated with increased DMV and ICU LOS. (Martino et al. 2011)

34. Nutrition Care Process

35. Assessment • Anthropometric data • Height: 5’7” • Weight: 264.5 kg • IBW: 67.3 kg ± 10% • Percent IBW: 393% • BMI: 91 kg/m2 • UBW: 318 kg • Percent UBW: 83%

36. Assessment • Biochemical labs

37. Assessment • Biochemical labs

38. Assessment • Biochemical labs

39. Assessment • Diet history • Lost weight PTA • Consumed small, more frequent meals • Consumed mostly fruits and vegetables • Food shopping and preparation done by brother and sister

40. Assessment • Initial dietary assessment • Consult sent by MD for tube feeding recommendations • Patient receiving 81 mL/hr of Diprivan, providing 2,138 kcal from fat

41. Assessment • Calculated needs • Calories • 3,229 kcal/d [PSU(2010)] • PSU(2003b) should have been utilized • Protein • 170 g/d (2.5 g/kg IBW) • Fluid • 3,300 mL/d (1 mL/kcal) • Level 3 nutritional compromise

42. Nutrition Diagnosis • PES statement • Excessive fat intake related to current dose of lipids from Diprivan as evidenced by parenteral intake of greater than 200 g/d of lipids and a high triglyceride level.

43. Nutrition Intervention/Monitoring & Evaluation • Nutrition intervention • Once weaned from Diprivan, Glucerna1.5 Cal® tube feeing at goal rate of 80 ml/hrto provide 2,880 kcal, 158 g protein, and 1,457 mL fluid • Monitoring and evaluation • Monitor tube feeding tolerance • Promote weight loss • Promote trend of blood glucose and triglyceride levels toward normal limits • Promote surgical wound healing

44. Assessment • 2nd assessment • Follow-up • Patient receiving Jevity1.5 Cal® at 50 mL/hr which provided 1,800 kcal, 77 g protein, and 912 mL fluid • 56% of estimated energy needs met with diet order

45. Nutrition Diagnosis • PES statement • Inadequate energy intake related to current tube feeding order as evidenced by intake record.

46. Nutrition Intervention/Monitoring & Evaluation • Nutrition intervention • Glucerna1.5 Cal® at 80 mL/hrto provide adequate nutrition and better control for blood glucose levels • Phosphate binder to better control blood phosphate levels • Monitoring and evaluation • Maintain lean body mass while promoting weight loss • Promote trend of blood glucose and electrolyte levels toward normal limits • Promote surgical wound healing

47. Assessment • 3rd, 4th, and 5th assessment • Patient still receiving Jevity 1.5 Cal® at 50 mL/hr • Later made NPO for gastrograph study • No new dietary interventions • Monitoring and evaluation of interventions remained the same

48. Assessment • 6th assessment • Follow-up • Patient NPO for 2 days 2º excessive gastric residuals and vomiting

49. Nutrition Diagnosis • PES statement • Altered GI function related to lack of GI motility due to physical inactivity, possible inadequate head of bed elevation, and maximum dose of Levophed as evidenced by vomiting, excessive residuals, and a NPO diet.

50. Nutrition Intervention/Monitoring & Evaluation • Nutrition intervention • Bowel rest • Initiation of PPN if medically appropriate • Clinimix2.75/5 at 100 mL/hr • If Levopheddose began trending below 20 mcg/min consistently, then enteral nutrition with a fiber-free formula recommended to be initiated • Monitoring and evaluation • Remained same with addition of ensuring proper hydration to prevent dehydration or overhydration