Morbid Obesity - Weebly

Morbid Obesity - Weebly

Morbid Obesity Presented by Erin McLean Overview Patient information Disease background Nutrition care process Conclusion Review of key points Personal impressions 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 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. 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 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 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 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: BMI Classification (kg/m2) Underweight Normal weight Overweight Obesity class I Obesity class II Obesity class III BMI BMI

24.9 BMI BMI BMI BMI 18.49 18.5 to 25 to 29.9 30 to 34.9 35-39.9 40 (Ogden, Carroll, Kit, & Flegal, 2012; Sturm & Hattori, 2013; Hurt & Frazier, 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) 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 ) 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) 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) 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) Etiology Obesogens Alter lipid metabolism and promote fat accumulation Act as endocrine disruptors Pharmaceutical obesogens Thiazolidinediones Selective serotonin reuptake inhibitors Diethylstilbestrol Industrial obesogens

Tributyltin and triphenyltin compounds Bisphenol A Perfluorooctanoic acid Diethylhexyl phthalate Dietary obesogens Monosodium glutamate Genistein Fructose (Holtcamp, 2012) Etiology Pathogens 10 infectious agents implicated in adipogenesis Bacteria Viruses Gut microflora Prions

(Mahan, Escott-Stump, & Raymond, 2012) Treatment Lifestyle modification Behavior modification Diet intervention Calorie restriction diets Meal replacement diets Commercial diet programs Physical activity Treatment Pharmaceutical management Few drugs approved by FDA BMI of 30 kg/m2 or BMI of 27-29 kg/m2 with at least one obesity-related comorbidity to qualify Available drugs Orlistat/Xenical/Alli

Lorcaserin/Belviq Phentermine-topiramate/Qsymia Prescription medications, 2013) Treatment Surgical intervention Restrictive procedures Laparoscopic adjustable gastric banding Sleeve gastrectomy Treatment Surgical intervention Malabsorptive procedures Biliopancreatic diversion Duodenal switch Jejunoileal bypass Treatment

Surgical intervention Combined restrictive and malabsorptive procedure Roux-en-Y gastric bypass 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) 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) 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)

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 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) 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) 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) 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) 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) 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 ding causes, 2013; Top 10, 2013; Stoklossa & Atwal, 2013) 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)

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/m 2, 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 normalweight patients Potential cofounders adjusted for using logistic generalized estimating equations and Cox proportional hazard methods with ICU clustering

(Martino et al. 2011) 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 nonsignificant after 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) Nutrition Care Process Assessment Anthropometric data Height: 57 Weight: 264.5 kg IBW: 67.3 kg 10% Percent IBW: 393% BMI: 91 kg/m2

UBW: 318 kg Percent UBW: 83% Assessment Biochemical labs Date Glucose (mg/dL) BUN (mg/dL) Creatinine (mg/dL) Sodium (mEq/L) Potassium (mEq/L) Chloride (mEq/L) CO2

(mEq/L) Calcium (mg/dL) GFR (mL/min/1.73 m2) Basic Metabolic Panel 01/26 02/02 372, High 205, High 02/08 280, High 02/12 124, High

Normal 44, High 28, High 59, High Normal Normal Normal 3.43, High 131, Low Normal

Normal Normal Normal Normal Normal 6.1, High 95, Low Normal Normal

Normal 23, Low 32, High 34, High Normal Normal Normal Normal Normal Normal

Normal Normal 19, Low Assessment Biochemical labs Date Glucose (mg/dL) BUN (mg/dL) Creatinine (mg/dL) Sodium (mEq/L) Potassium

(mEq/L) Chloride (mEq/L) CO2 (mEq/L) Calcium (mg/dL) Albumin (gm/dL) Phosphoru s (mg/dL) GFR (mL/min/1.73 m2 ) Renal Profile 01/30 02/12 02/14

191, 174, 137, High High High Normal 62, High 32, High Normal 02/17 215, High 74, High 133, Low 3.81,

High Normal 2.36, High Normal 3.52, High Normal Normal 5.9, High Normal 5.1, High

98, Low Normal Normal Normal Normal Normal Normal Normal Normal Normal

7.9, Low Normal 1.7, Low 1.8, Low 1.8, Low 1.7, Low 4.5, High Normal Normal

4.4, High Normal 17, Low 29, Low 18, Low Assessment Biochemical labs Complete Blood Count Date 01/25 02/01

02/08 02/15 02/17 23.71, High 17.47, High Normal 13.22, High 17.29, High Red Blood Cell

(m/ul) 4.22, Low 3.99, Low 2.56, Low 2.57, Low 2.66, Low Hemoglobin (gm/dL) 13.0, Low 12.6, Low

7.9, Low 8.0, Low 8.4, Low Hematocrit (%) Normal Normal 27.5, Low 26.5, Low 28.2, Low

White Blood Cell (K/uL) Other Labs Date Triglycerides (mg/dL) Lactate (mmol/L ) 01/26 02/13 228, High No lab drawn No lab drawn

5.5, High 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 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 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 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. Nutrition Intervention/ Monitoring & Evaluation Nutrition intervention Once weaned from Diprivan, Glucerna 1.5 Cal tube feeing at goal rate of 80 ml/hr to 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

Assessment 2nd assessment Follow-up Patient receiving Jevity 1.5 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 Nutrition Diagnosis PES statement Inadequate energy intake related to current tube feeding order as evidenced by intake record. Nutrition Intervention/ Monitoring & Evaluation Nutrition intervention Glucerna 1.5 Cal at 80 mL/hr to 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 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 Assessment 6th assessment Follow-up Patient NPO for 2 days 2 excessive gastric residuals and vomiting 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. Nutrition Intervention/ Monitoring & Evaluation Nutrition intervention

Bowel rest Initiation of PPN if medically appropriate Clinimix 2.75/5 at 100 mL/hr If Levophed dose 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 Assessment 7th and final assessment Consult sent by MD for TPN recommendations Renal MD decided to manage TPN Patient NPO for 4 days 2 possible ischemic bowel Nutrition Diagnosis

PES Statement Altered GI function related to possible ischemic bowel disease as evidenced by a high lactate level. Nutrition Intervention/ Monitoring & Evaluation Nutrition intervention TPN to provide at least 70 to 80% of estimated energy needs TPN goal of 170 g amino acids, 350 g dextrose, and 50 g intralipids. Monitor patient for refeeding syndrome since he had been NPO for four days and had, before that, been underfed with tube feedings Monitoring and evaluation TPN to meet at least 70% of goal nutritional needs Promote trend of acid-base, electrolyte, and glucose profile toward normal limits

Promote surgical wound healing Conclusion Admitted for surgical debridement of groin abscess Developed multiple conditions Nutrition diagnoses Excessive fat intake Inadequate energy intake Altered GI function Nutrition interventions Tube feeding recommendations Phosphate binder Initiation of PPN

Initiation of TPN Withdrawal of care Discharge to hospice Review of Key Points Affects 6.6% of adult Americans Physiological changes occur in relation to appetite regulation and weight management hormones Associated with many comorbid conditions Multiple factors contribute to etiology Penn State University equations to determine RMR Not a leading cause of death but comorbidities are (Sturm & Hattori, 2013)

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Charney, P., & Malone, A. (2009). ADA pocket guide to nutrition assessment (2nd ed.). Chicago, IL: American Dietetic Association. Cross section of abscess [Digital image]. (n.d.). Retrieved April 1, 2014, from http://medicaldictionary.thefreedictionary.com/_/viewer.aspx?path=dorland&name=abscess.jpg Dugdale, D. C., III, & Lin, H. Y. (2012, September 5). Acute kidney failure: MedlinePlus medical encyclopedia. Retrieved March 15, 2014, from http://www.nlm.nih. gov/medlineplus/ency/article/000501.htm Dugdale, D. C., III. (2012, August 30). Obesity hypoventilation syndrome (OHS): MedlinePlus medical encyclopedia. Retrieved March 15, 2014, from http://www.nlm.nih.gov/medlineplus/ency/article/000085.htm Dugdale, D. C., III. (2012, September 2). Abscess: MedlinePlus medical encyclopedia. Retrieved March 15, 2014, from http://www.nlm.nih.gov/medlineplus/ency /article/001353.htm [Duodenal switch]. (n.d.). Retrieved April 1, 2014, from http://www.bariatricsurgery- source.com/duodenal-switch.html Frankenfield, D. C., Ashcraft, C. M., & Galvan, D. A. (2013). Prediction of resting metabolic rate in critically ill patients at the extremes of body mass index.

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