Morbid Obesity - PowerPoint Presentation

Slide1

Morbid Obesity

Presented by Erin McLeanSlide2

Overview

Patient informationDisease backgroundNutrition care process

Conclusion

Review of key points

Personal impressionsSlide3

Patient Profile

Gender: MaleAge: 51Ethnic 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, 02/17/14Slide4

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. Slide5

Medical/Health/Family History

Past medical historyMorbid obesity

Hypertension

Chronic lymphedema

Sleep apnea

Anxiety

Remote history of seizure disorder

Past surgical history

Cholecystectomy

Gunshot wound

repairmentSlide6

Medical/Health/Family History

Health historyRecent 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 mellitusSlide7

Medical Diagnoses

Groin abscessCellulitis

Morbid obesity

Diabetes mellitus

Acute respiratory failure

Urinary tract infection

Septic shock

Aspiration pneumonia

Acute kidney injury

Possible ischemic bowel Slide8

Morbid Obesity Defined

Morbid obesityNHANES: 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/m

2

)

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 IIIBMI ≥ 40

(

Ogden, Carroll, Kit, &

Flegal

, 2012; Sturm & Hattori, 2013; Hurt & Frazier, 2012)Slide9

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)Slide10

Pathophysiology

GhrelinStimulates ↑

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 )Slide11

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)Slide12

Etiology

DietFrequent 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)Slide13

Etiology

Chronic sleep deprivationEndocrine regulation alteredCan 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)Slide14

Etiology

ObesogensAlter lipid metabolism and promote fat accumulation

Act as endocrine disruptors

Pharmaceutical obesogens

Thiazolidinediones

Selective serotonin reuptake inhibitors

Diethylstilbestrol

Industrial obesogens

T

ributyltin

and

triphenyltin

compounds

B

isphenol

A

P

erfluorooctanoic acidDiethylhexyl phthalateDietary obesogensMonosodium glutamateGenisteinFructose (Holtcamp, 2012) Slide15

Etiology

Pathogens10 infectious agents implicated in adipogenesis

Bacteria

Viruses

Gut

microflora

Prions

(Mahan,

Escott

-Stump, & Raymond, 2012)Slide16

Treatment

Lifestyle modificationBehavior modification

Diet intervention

Calorie restriction

diets

Meal replacement diets

Commercial diet programs

Physical activitySlide17

Treatment

Pharmaceutical managementFew drugs approved by FDABMI of ≥30 kg/m

2

or

BMI of 27-29 kg/m

2

with at least one obesity-related comorbidity to qualify

Available drugs

Orlistat

/

Xenical

®/

Alli

®

Lorcaserin

/

Belviq

®Phentermine-topiramate/Qsymia®(“Prescription medications,” 2013)Slide18

Treatment

Surgical interventionRestrictive procedures

Laparoscopic adjustable gastric banding

Sleeve

gastrectomySlide19

Treatment

Surgical interventionMalabsorptive procedures

Biliopancreatic

diversion

Duodenal switch

Jejunoileal

bypassSlide20

Treatment

Surgical interventionCombined restrictive and malabsorptive

procedure

Roux-en-Y gastric bypassSlide21

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)Slide22

The Comparative Effectiveness of Sleeve Gastrectomy

, Gastric Bypass, and Adjustable Gastric Banding Procedures for the Treatment of Morbid Obesity

Results

W

eight

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

)

S

evere 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)Slide23

ConclusionD

ue 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 ObesitySlide24

Treatment

Treatment specific to patientSurgical 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

F

entanyl

L

orazepam

I

nsulin

lispro

N

ebivolol

P

antoprazoleFurosemideBisacodylHeparinVancomycinSlide25

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)Slide26

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)Slide27

Nutrition Intervention

Calorie per kilogram methodUsed for critically ill, mechanically ventilated, obese patientsUsed 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)Slide28

Prediction of Resting Metabolic Rate in Critically Ill Patients at the Extremes of Body Mass Index

PurposeTo

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/m

2

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 measurementsAccuracy determined when energy expenditure estimations from equations fell within 10% of IC measurement(Frankenfield, Ashcraft, & Galvan, 2013) Slide29

Prediction of Resting Metabolic Rate in Critically Ill Patients at the Extremes of Body Mass Index

ResultsPenn 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

F

or

critically ill, morbidly obese patients, Penn State equation is valid for estimating RMRFor critically ill, underweight patients, modification to Penn State equation necessary to improve accuracy rate (Frankenfield, Ashcraft, & Galvan, 2013) Slide30

Prognosis

Not a leading cause of death in US or worldDoes 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

)Slide31

PurposeResearch 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/m

2 has not been conducted and was the focus of this study.

(Martino et al. 2011)

Extreme

Obesity and Outcomes in Critically Ill PatientsSlide32

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 greaterComparison of 60-day mortality rate, DMV, LOS in ICU, and hospital LOS conducted between morbidly obese and normal-weight patientsPotential cofounders adjusted for using logistic generalized estimating equations and Cox proportional hazard methods with ICU clustering(Martino et al. 2011)Slide33

Extreme Obesity and Outcomes in Critically Ill Patients

ResultsCritically

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

ConclusionMorbid 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)Slide34

Nutrition Care ProcessSlide35

Assessment

Anthropometric dataHeight: 5’7”Weight: 264.5 kg

IBW: 67.3 kg ± 10%

Percent IBW: 393%

BMI: 91 kg/m

2

UBW: 318 kg

Percent UBW: 83%Slide36

Assessment

Biochemical labs

Basic Metabolic Panel

Date

01/26

02/02

02/08

02/12

Glucose

(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 m

2

)

Normal

Normal

Normal

19, LowSlide37

Assessment

Biochemical labs

Renal Profile

Date

01/30

02/12

02/14

02/17

Glucose (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 m

2

)

Normal

17, Low

29, Low

18, LowSlide38

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, LowSlide39

Assessment

Diet historyLost weight PTA

Consumed small, more frequent meals

Consumed mostly fruits and vegetables

Food shopping and preparation done by brother and sisterSlide40

Assessment

Initial dietary assessmentConsult sent by MD for tube feeding recommendations

Patient receiving 81 mL/

hr

of Diprivan, providing 2,138 kcal from fatSlide41

Assessment

Calculated needsCalories3,229 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 compromiseSlide42

Nutrition Diagnosis

PES statementExcessive 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. Slide43

Nutrition Intervention/

Monitoring & EvaluationNutrition 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 Slide44

Assessment

2nd assessmentFollow-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 orderSlide45

Nutrition Diagnosis

PES statementInadequate

energy intake related to current tube feeding order as evidenced by intake

record.Slide46

Nutrition Intervention/Monitoring & Evaluation

Nutrition interventionGlucerna

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

healingSlide47

Assessment

3rd, 4

th

, and 5

th 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 Slide48

Assessment

6th assessment

Follow-up

Patient NPO for 2 days 2º excessive gastric residuals and vomitingSlide49

Nutrition Diagnosis

PES statementAltered 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.Slide50

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

overhydrationSlide51

Assessment

7th and final assessment

Consult sent by MD for TPN recommendations

R

enal MD decided to manage TPN

Patient NPO for

4

days

2º possible ischemic bowelSlide52

Nutrition Diagnosis

PES StatementAltered GI function related to possible ischemic bowel disease as evidenced by a high lactate level.Slide53

Nutrition Intervention/Monitoring & Evaluation

Nutrition interventionTPN 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

.

M

onitor 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 needsPromote trend of acid-base, electrolyte, and glucose profile toward normal limitsPromote surgical wound healing Slide54

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 Slide55

Review of Key Points

Affects 6.6% of adult AmericansPhysiological 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) Slide56

Personal ImpressionsSlide57

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