Morbid ObesityPresented 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 BMI ≤ 18.49

Normal weight BMI ≥ 18.5 to 24.9

Overweight BMI ≥ 25 to 29.9

Obesity class I BMI ≥ 30 to 34.9

Obesity class II BMI ≥ 35-39.9

Obesity class III BMI ≥ 40

(Ogden, Carroll, Kit, & Flegal, 2012; Sturm & Hattori, 2013; Hurt & Frazier, 2012)

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)

• 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)

The Comparative Effectiveness of Sleeve Gastrectomy, Gastric Bypass, and Adjustable

Gastric Banding Procedures for the Treatment of Morbid Obesity

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

(“Leading causes,” 2013; “Top 10,” 2013; Stoklossa & Atwal, 2013)

• 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

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)

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: 5’7”• 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

Basic Metabolic Panel Date 01/26 02/02 02/08 02/12Glucose(mg/dL)

372, High 205, High 280, High 124, High

BUN(mg/dL)

Normal 44, High 28, High 59, High

Creatinine (mg/dL)

Normal Normal Normal 3.43, High

Sodium(mEq/L)

131, Low Normal Normal Normal

Potassium(mEq/L)

Normal Normal Normal 6.1, High

Chloride(mEq/L)

95, Low Normal Normal Normal

CO2(mEq/L)

23, Low 32, High 34, High Normal

Calcium (mg/dL)

Normal Normal Normal Normal

GFR (mL/min/1.73 m2)

Normal Normal Normal 19, Low

Assessment• Biochemical labs

Renal ProfileDate 01/30 02/12 02/14 02/17Glucose (mg/dL)

191, High

174, High

137, High

215, High

BUN(mg/dL)

Normal 62, High 32, High 74, High

Creatinine (mg/dL)

Normal 3.81, High

2.36, High

3.52, High

Sodium (mEq/L)

133, Low Normal Normal Normal

Potassium (mEq/L)

Normal 5.9, High Normal 5.1, High

Chloride (mEq/L)

98, Low Normal Normal Normal

CO2(mEq/L)

Normal Normal Normal Normal

Calcium (mg/dL)

Normal Normal 7.9, Low Normal

Albumin (gm/dL)

1.7, Low 1.8, Low 1.8, Low 1.7, Low

Phosphorus (mg/dL)

4.5, High Normal Normal 4.4, High

GFR (mL/min/1.73 m2)

Normal 17, Low 29, Low 18, Low

Assessment• Biochemical labs

Other Labs

Date 01/26 02/13

Triglycerides (mg/dL)

228, High No lab drawn

Lactate(mmol/L )

No lab drawn 5.5, High

Complete Blood Count

Date 01/25 02/01 02/08 02/15 02/17

White Blood Cell (K/uL)

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

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 2º 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 2º 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)

Personal Impressions

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