ANA 873 Obesity Baker & Leighow PP

Obesity

•Complex & multifactorial, chronic disease

•Develops from interaction between an individual’s genotype & the environment

•2^nd leading cause of preventable death in the U.S. (112K /year)

~75% of U.S. adults are overweight or obese

•Class 3 obesity (BMI >40)  Men= 5.5%    Women= 9.9%

•In U.S. obese individuals have 10-50% greater risk for death, greatest risk is cardiovascular causes.

obesity definitions- KNOW 1,2,3

•BMI= weight (kg)/height(m)²  OR
BMI = (weight lbs /height [in inches]²) x 703

•Overweight: BMI= 25-29 kg/m²

•Obesity: BMI= >30 kg/m²

•Class I : 30-34.9 kg/m²

•Class II: 35-39.9 kg/m²

•Class III: >40 kg/m²

•Use extreme obesity not morbid obesity

What is IBW used for

•Useful for calculating drug dosages

•Certain drugs if given per weight can lead to toxicity, renal damage or hemodynamic instability

LBW is 30% higher than IBW.

How to calculate IBW for men

height (cm)-100

How to calculate IBW for women

height (cm) - 105

How much does lean body mass increase in obese person

•Lean body mass increases by 30% in the obese individual d/t increased muscle development to carry extra body weight

LBW is 30% more than IBW

How to calculate LBW

IBW x 1.3

adipose tissue fxn

•Has major integrative physiological functions

•Secretes numerous protein hormones: leptin, adiponectin & resistin. (influence energy metabolism)

•Is considered an endocrine organ

•Synthesizes & secretes fatty acid substances called prostanoids (prostaglandin) which inhibits the breakdown of fat.

•Adipose cells secrete cholesterol and retinol (Vitamin A)

•Provides a reservoir of readily convertible & usable energy

•Maintains heat insulation

Liver fat metabolism & adipose tissue

•Degradation of fatty acids into usable units of energy

•Synthesis of triglycerides from carbohydrates & proteins

•Synthesis of other lipids from fatty acids (i.e.) cholesterol & phospholipids

•All cells contain some unsaturated fats synthesized by the liver

•Important in heat regulation & insulation

•Fat cells, which are modified fibroblasts enlarge & will fill with liquid triglycerides 95% capacity

•Liquid fat can be hydrolyzed &transported from the cells to be used for energy

body fat distribution

•Fat cell formation occurs rapidly in early childhood

•Overfeeding during this time accelerates fat storage & triggers hyperproliferation of fat cells

•During adolescence, the number of fat cells stabilizes and remains constant throughout adult life

•Children become obese through increase in fat cell numbers, whereas adults become obese through hypertrophy of existing fat cells. They shrink but do not decrease in number.

•Where the fat is distributed is a better indication of increased health risk.

High risk of comorbidites in obese patients

Central, android or abdominal visceral (apple shape)

waist: hip ratio >0.85 in men & >0.92in women

is correlated with a higher risk of comorbidities in obese patients.

What is associated with increased risk for ischemic heart disease, diabetes, hypertension, dyslipidemia & death

•Waist circumference > 102 cms (40 inches) in men & >88 cm (35inches) in females

What correlates with varicose vein development & joint disease

•Peripheral gynecoid, or gluteal femoral obesity (pear shape)

waist: hip ratio < 0.76

correlates with varicose veins & joint disease and a reduced incidence of non-insulin-dependent DM

Medical risk are decreased in what individuals?

individuals with gynecoid fat distribution compared to those with android fat distribution

What is the difference in morbidity between android & gynecoid fat patterns

RT metabolic characteristics of the adipose tissue & the adjacent tissues.

Gynecoid fat- KNOW 7

1. Peripheral/ Glut-Fem/ pear-shaped

2. lower body obesity

3. primarily found in women

4. less metabolically active (inactive)

5. fxn= energy store for pregnancy/ lactation

6. Waist hip ratio <0.76

7. less medical risk but A/W varicose veins and joint dx

Android Fat- KNOW 8

1. Central/abdominal/ apple shaped

2. Upper body obesity

3. Increased visceral & retroperitoneal fat which compresses renal veins, lymph vessels, ureters and renal tissues

4. Increased pressure is linked to HTN

5. primarily found in men

6. waist hip >0.85 men; 0.92 women

7. metabolically active in free fatty acid release

8. ↑ risk of CV dz, metabolic syndrome, HTN, DM, CVA

diseases related to obesity 8

HTN (most common)

CAD

HLD
DM
Coagulopathy

Cholelithais

DJD
OSA

Liver & adipose tissue

•When increased free fatty acids (FFA) are released from adipose tissue, portal venous drainage delivers high concentrations of FFA to the liver

•This stimulates the liver to make VLDL & LDL

•Liver exposure to high levels of FFA increases gluconeogenesis & inhibits insulin uptake, which l/t non-insulin dependent diabetes

What is A/W cardiovascular & cerebrovascular disease

VDL, LDL, and hyperglycemia

slide 17

(not on leighow’s pp)

Causes of obesity

•Genetics ~40% of the variances in body mass

•Environmental factors that result in increased caloric intake & decreased physical activity

•Other factors include, socioeconomic factors, age, sex & race

•U.S “super-sizing” portions & easily available high-fat foods

•Physical activity is reduced d/t modernization (I-pads, computers, T.V.)

•Our lifestyles are more sedentary

Role of inflammation

•Several inflammatory mediators including, angiotensin, growth factor a, alpha? & interleukin 6 are elevated in morbidly obese patients

•Leads to insulin resistance 

•When these patients lose weight, the inflammatory mediators and comorbidities associated with obesity are decreased.

Leukocytes and adipose tissue inflammation.

Macrophage and lymphocyte infiltration in adipose tissue may greatly contribute to obesity-related metabolic dysfunction and chronic inflammation.

Box 48.1 Conditions A/W obesity

CV disease

•Cardiac involvement is d/t the compensatory processes that occur to meet the increased metabolic demands

•CVD is the primary cause of the M&M in obese

•Manifests as ischemic heart disease, HTN & cardiac failure

organ is maintained by formation of extra blood vessels & increased circulatory, pulmonary, central & peripheral blood volume

•For every 13.5 (30 lbs.) gained, ~ 25 miles of neovascularization is generated to provide blood flow to the fat tissues

•Increased cardiac output of 0.1 L/min for each kg of fat

•Greater stress on the heart d/t expanded blood volume through expanded vascular system which is under pressure by adipose tissue

•Increased workload l/t increased CO, increased O2 consumption & increased CO2 production

•Higher cardiac output leads to increased left-sided heart pressures and LVH

•HR unchanged= EXAM so increased CO RT increased SV

•Leads to cardiomegaly, atrial & biventricular dilation & hypertrophy which l/t HTN & CHF

•Reduced atrial filling is caused by decreased venous compliance

HTN

•SBP > 140 mmHg  & DBP > 90 mmHg or both

Incidence of HTN in obese patients compared to lean patients

•HTN in obese patients is 2x that of lean patients

How much does BP increase per body weight

•BP increases 6.5 mmHg for every 10% increase in body weight

How do severely obese patients who are not hypertensive maintain BF

decreased SVR assists to maintain blood flow through the enlarged body habitus

HTN is due to 5

•increased blood viscosity

•altered catecholamines action

•hyperinsulinemia

•increased mineralocorticoids

•abnormal sodium reabsorption

Renal induced HTN caused by 5

•Visceral compression of the kidneys from fat deposits in & around the kidneys

•Impaired sodium excretion

•Activation of the renin-angiotensin-aldosterone system

•Increased SNS

•Hypercholesterolemia > 240 mg/dl l/t to atherosclerosis & CVAs

Arrythmias may occur due to 7

1. hypoxemia

2. hypercapnia

3. electrolyte disorder

4. OSA

5. ventricular hypertrophy

6. HTN

7. CAD

What is fequent A/W obestiy

•CAD is frequently associated with obesity, but it is an independent risk factor

CAD can occur ± 5

HTN

hypercholesterolemia

DM

HLD

sedentary lifestyle

Obese patients with CAD have 4

frequent angina

CHF

acute MI

sudden death

When is ischemic heart disease more common

•in obese patients with central fat distribution

Resp system

•Compromise of the respiratory system results from the compression of fat on abdominal, diaphragmatic & thoracic structures

thoracic kyphosis/ lumbar lordosis impair rib movement and fixes thorax in the inspiratory position

l/t reduced chest wall compliance, parenchyma, lung and pulmonary system→Decreased TLC, VC & FRC

•Greater WOB

•Increases in CO2 production & retention with decreased ventilation L/T reduced respiratory muscle efficiency

•Lung inflation is inhibited—> decreased FRC< than CC

•Premature airway closures increases dead space, and causes CO2 retention, V/Q mismatch, shunting & hypoxemia

•Extreme obesity A/W reduced FRC, ERV, TLC

•FRC declines as BMI increases

•Extreme obese patients will have major reductions in lung function even if asymptomatic

Rapid shallow breathing is from decreases in 4

VC

TLC
ERV
IC

are demonstrated by rapid shallow breathing

characteristics of restrictive lung disease

Decreased VC, TLC, ERV, and IC

•Eventual hypoventilation, hypercarbia and acidosis result from the depression of the CNS’s responsiveness to hypoxia

•Hypoxemia l/t polycythemia & increases rx of CAD CVA

Resp muscule dysfunction results from

•inefficiency d/t changes in chest wall compliance & lower lung volumes which can lead to respiratory failure

Obesity linked to what resp disease

•linked to asthma-like symptoms such as dyspnea, systemic inflammation and increased work of breathing

•Weight loss will result in improvement of these symptoms

Obstructive lung disease

characterized by reduction in airflow. so SOB—> in exhaling air

Air remains inside lung after full expiration

Ex COPD, asthma, Bronchiectasis

Restrictive lung disease

Reduction in lung volume (difficult taking in air in lungs)

RT stiffness inside the lung tissue or chest wall cavity

Ex. ILD, scoliosis, neuromuscular cause, marked obesity

32

OSA

•Patients with OSA have a BMI > 30kg/m², abdominal fat distribution and neck girth >17 inches in men & 16 inches in women

•Characterized by excessive episodes of apnea (>10 seconds) and hypopnea caused by complete or partial airway obstruction

•OSA is present in 25% of surgical patients

•Apnea is considered obstructive if there is continued respiratory effort despite airflow cessation

•Hypopnea is a 50% reduction in airflow for 10 seconds that occurs 15 or more times per hour & is associated with snoring and low SaO2 readings

•Is diagnosed by10 episodes of apnea-hypopnea per hour of sleep plus daytime sleepiness

•Obese patients have more adipose tissue in the airway & relaxation of muscle tone during sleep leads to collapse of the upper airway

mild OSA as an AHI 5 and 15; moderate 15-30, and severe >30.

•More than 30 episodes per night results in hypoxia, systemic & pulmonary hypertension and arrhythmias

•OSA patients have higher incidences of comorbidities

Mallampati score

Class I: no limitation

Class II: Loss of pillars

Class 3: loss of pillars and fauces

Class 4: Hard palate only

STOP- BANG

STOP

Do you SNORE loudly

do feel TIRED, fatigued, sleepy during day

has anyone OBSERVED you stop breathing

do you have high blood PRESSURE

BANG
BMI >35

Age >50

Neck >40cm

Gender: Male

0-2=low risk

3-4 intermediate

>5 high risk

OSA outpt vs inaptient basis consdierations

•Sleep apnea status

•Anatomic & physiologic abnormalities

•Coexisting diseases

•What surgery is being performed

Type of anesthesia

•Need for post op opioids

•Patient’s age

•Postop observation

•Capabilities of outpt facility: difficult airway equipment, Xray avail, etc.

day sx with OSA

What are the 7 anesthetic concerns

Premedication

Potential difficult airway, difficult mask ventilation, and tracheal intubation

GERD
Opioid resp depression

Carry over sedative effects from longer acting IV and VA

Excessive sedation in MAC
post extubation airway obstruction

Premedication principles of management 2

avoid sedation premedication

consider A2 agonists (clonidine, Dex)

Potential difficult airway, difficult mask ventilation, and tracheal intubation principles of management

optimal positioning (Head Elevated Laryngoscopy Position) if patient obese

Adequate preoxygenate

consider CPAP preoxygenation

2 handed triple airway maneuvers

Anticipated difficult airway. personnel familiar with difficult airway algo

GERD principles of management

Consider PPI, antacids, RSI with cric pressure

Opioid resp depression principles of management

Minimize opioid use

Use short acting agents (remifent)

multimodal analgesia (NSAIDs, tylenol, tramadol, ketamine, gabapentin, pregabalin, dex, clonidine, dexamethasone, melatonin)

consider local and regional anesthesia

Carry over sedative effects from long acting IV and VA agents principles of management

Use prop, remifent for maintence of anesthesia

Use of insoluble potent anesthetic agents (desflurane)

use regional blocks as sole anesthetic technquies

Excessive sedation in MAC principles of management

use intraop capno for monitoring of ventilation

Post extubation airway obstruction principles of management

verify full reversal of NMB
only extubate when fully conscious and cooperative

non-supine posture for extubation and recovery

Resume use of Positive airway pressure device after surgery

Obesity hypoventilation(Pickwickian) syndrome (OHS) characteristics

OSA

•BMI > 30 kg/m²

•Chronic hypercapnia- partial pressure of PcO2> 45 mmHg

•Daytime hypersomnolence

•Arterial hypoxemia PO2 <70

•Cyanosis-induced polycythemia

•Respiratory acidosis

•PHTN —> R HF

Extreme OHS

•patients develop nocturnal episodes of central apnea without respiratory effort

•This reflects the progressive desensitization of the respiratory centers to nocturnal hypercarbia

90% of patients with OHS have OSA

•Alveolar hypoventilation is the main impairment of OHS= EXAM

•Decreased TV, inadequate inspiratory strength & inadequate diaphragm movement

OHS & CNS

decreases central respiratory drive

OHS & airway

potential difficult airway

OSA

OHS & CV

CAD

CHF

OHS & resp

restrictive chest physiology

PHTN
Hypoxemia/hypercapnia

OHS & other

difficult vascular access

difficult positioning

GI system changes with obesity

•High risk for regurgitation & aspiration

•Increased gastric volume & acidity

•Delayed gastric emptying, even if fasted will still have high gastric volume

•Increased incidence of hiatal hernia

•Prone to GERD & esophageal strictures

Give bicitra to

GI disease

•Increased incidence of GERD, gallstones & pancreatitis

•At risk for developing esophageal varices, liver failure & liver cancer

•Nonalcoholic fatty liver disease (NAFLD) includes

• Steatosis

• Fibrosis

• Cirrhosis

• Hepatomegaly

• Abnormal liver enzymes

Non alcoholic fatty liver disease (NAFLD)

•Most common liver condition in the world

•Frequently found in patients with central obesity or diabetes

•Insulin resistance and obesity are associated with increased lipid influx into the liver and increased triglyceride accumulation

•Clinically, NAFLD is asymptomatic

•Increased risk of cardiovascular disease and diabetes

Gallstones

•Higher concentrations of cholesterol in the bile

•Increased ratio of bile salts to lecithin (fatty substance) causes gallstones

•Jaundice if the bile duct is obstructed

•Laparoscopic cholecystectomy

Endocrine and metabolic diseases

•Obesity is rarely the result of primary endocrine dysfunction
•Thyroid, adrenocortical and pituitary function should be investigated in obese patients

•In women, menstrual problems (oligomenorrhea, amenorrhea, menorrhagia) & hirsutism may be a sign of hypothalamic-pituitary abnormalities

•In men, decreased libido or impotence may be a sign of hypogonadism with low levels of follicle stimulating hormone and testosterone

•80% of individuals with type 2 diabetes are obese

Metabolic syndrome

Central (android) fat is strongly linked to metabolic syndrome

•Metabolic syndrome consists of an array of conditions including glucose intolerance &/or type 2 diabetes, HTN, dyslipidemia, and cardiovascular disease

•Are at increased risk of developing CAD, stroke, PVD, DM2

•Pts have proinflammatory and prothrombotic conditions

Metabolic syndrome diagnostic criteria

Need to have 3/5

1. central obesity (increased waist circumference >102cm (40”) males; >88cm (35”) females

2. TG >150

3. HDL <40 males; <50 females

4. HTN >130/85 or use of antiHTN meds

5. fasting BG >100 or meds for hyperglycemia

Orthopedic and joint disease

OA from continued mechanical stress on weight-bearing joints
•Ankles, hips, knees and L-spine= most affected

•Because of limited physical activity, patients may have reduced bone density, may lead to stress fractures

•Bones need to become heavier to support increased weight

Obestiy effects on bone

increases skeletal loading

cushioning affect of fat during falls

increased leptin & estrogen from fat tissue

Less physical activity

poor diet or low nutrient density

Co morbidies (DM)

degenerative joint disease

inflammation

lower vitamin D status

low bone mass relative to weight

poor balance

greater force during falls

Every lb of body weight

adds 5 pounds of force on your knee joints

pediatric obestiy

•~31% of Americans between ages 2-19 are considered overweight or obese

•Obese adolescents have a 70-80% chance of being obese adults

•Childhood obesity has increased risk of premature death and disability in adulthood

•Obese children are 3-5x more likely to suffer a heart attack or stroke before age 65

•Pediatric obesity is more common than diabetes, HIV, cystic fibrosis and all childhood cancers combined

•Prevalence of metabolic syndrome is high due to abdominal obesity, insulin resistance, high triglycerides, HTN, proinflammatory and prothrombic states 

maternal obestiy

•Maternal obesity, not diabetes, is the most important link to the nation’s increase in mean birth weights
•Prepregnancy obesity significantly increases the risk for C-Section(40%)

•Both 1^st & 2^nd stages of labor are longer in obese women

•Increased risk for developing gestational diabetes, HTN, hydramnios, preeclampsia, preterm labor, postpartum hemorrhage & infection

•Risk of miscarriage in first 6 weeks is doubled

•Large for age infants (>4000 g/ 8.8 lbs.) have greater incidence of adolescent metabolic syndrome

•Difficult epidural & I.V. placement

maternal obesity during pregnancy 9

1. insulin resistance/ DM

2. induced labor/ C-section

3. coagulopathies/ DVT

4. difficulties in anestheic administration

5. pre-e/ HTN

6. fetal and neonatal complications

7. LT AE on mother and baby health

8. PP complications

9. Resp complications

FDA approved drugs for LT tx of obesity

surgerical tx

•Roux-en-Y gastric bypass- largely restrictive/mildly malabsorptive

•Laparoscopic sleeve gastrectomy- restrictive

•Post op N&V common due to suture line & pressure on stomach. Manage aggressively! 

f•If pt has GERD, do RSI, cricoid pressure, H2 blocker, proton-pump inhibitors

Indications for bariatric surgery

Obesity related diseases requiring surgery

which is the best weight loss surgery

gastric sleeve vs gastric bypass vs lap band

complications following surgery

•Rhabdomyolysis is more common in morbidly obese following laparoscopic procedures

•Careful positioning & padding of pressure points

•Adequate hydration

•Use of mannitol to stimulate diuresis  

•Unexplained increase in creatinine phosphokinase (CPK)

•Complaints of buttock, hip or shoulder pain

•Myoglobinuric acute renal failure with CPK> 500 u/L

Pharm considerations with pharmcokinetics/dynamics

•Consider VOD for the loading dose

•Consider clearance for maintenance dose

•Give water soluble drugs according to IBW

•Give lipid soluble drugs according to TBW

•Volume of the central compartment where drugs are first distributed= unchanged

•Absolute body water content is decreased

•Lean body mass & adipose tissue are increased

Pharm considerations

Avoid post op resp depression

use short acting narcotics and adjuncts (tyleol, toradol, gapapentin)

des and sevo are good choice RT low BG coeff

N20 is safe and you use less VA

2nd gas effect N2O with induction and emergence will accelerate uptake and elimination of the VA

N2O has analgesic properties

Make sure to pretreat with antiemtics

DRUG	DOSE	COMMENT
Propofol	Induction dose based on IBW. Maintenance dose based on TBW	Increased fat mass doesn’t affect initial distribution/redistribution during induction. Cardiac depression at higher doses
Succinylcholine	Intubating dose based on TBW	Increased volume of distribution & increased pseudocholinesterase levels require higher doses
Rocuronium Vecuronium Cisatricurium	Doses based on IBW	Hydrophilic drugs, IBW doses ensure shorter duration & more predictable recovery
Fentanyl Sufentanil	Loading dose - TBW Maintenance - IBW	Increased vol of distributionà increased loading dose
Remifentanil	Infusion rate - IBW	Fast off- plan for postop analgesia
Dexmedetomidine	Infusion rate – 0.2 mcg/kg/min	Use lower than usual rate to minimize cardiac s/e
Sugammadex	Reverse -TBW	Regular dose/ # of twitches

Pharmacokinetic changes INCREASED 8

1. •fat mass

2. •cardiac output

3. •blood volume

4. •lean body weight

5. alpha-1-acid glycoprotein (AAG)

6. •free fatty acids

7. •lipophilicity of the drug

8. •Renal clearance d/t increased renal blood flow

Pharmacokinetic changes DECREASED 3

TBW
Liver function

Pulmonary function

Pharmacokinetic changes

Increased distribution of a drug prolongs elimination ½ life (benzos)

•Hyperlipidemia & ↑ AAG-1 reduces free drug concentration

•No significant changes in absorption & bioavailability

•Drug clearance is not affected by the liver

•Drugs that undergo phase I metabolism (oxidation, reduction hydrolysis) are not affected by obesity

•Drugs that undergo phase II reactions (glucuronidation, sulfation) are enhanced

•Renal clearance is increased d/t increased RBF & GFR

Preanesthetic management

•Discuss anticipated events: multiple I.V. sticks (use US), awake intubation, central line, arterial line, difficult spinal or epidural
•Discuss postop pain plan (if failed spinal or epidural)

•Medications: OTC meds for weight loss?  Diet pills can cause ↑ QT-Interval

•Continue usual medications up to surgery, except diabetic meds/insulin

•Prophylaxis against aspiration (Bicitra)

•Prophylaxis against DVT’s (Heparin SQ, check with surgeon)

•Antibiotics given prior to incision, prone to wound infection

•CPAP? OSA?

Lab tests

•CBC, BMP

•Chemistry: K+, Na+

•Blood sugar, what is their A1C?  Well managed?

•BUN & creatinine

•Liver enzymes usually elevated

•Coagulation studies if pt. is on anticoagulants

cardiac assessment

•Prior MI?  Angina? Added heart sounds?

•Heart failure(hepatomegaly, peripheral edema, elevated jugular venous pressure)

•HTN

•Peripheral vascular disease

•Exercise tolerance: Can you walk up a flight of stairs?

•Continue all cardiac meds up to morning of surgery, except ACE-Is

•12 lead ECG: rate, rhythm, ventricular hypertrophy, axis deviation, QT interval, low voltage reading may underestimate ventricular hypertrophy

•Axis deviation & atrial tachycardia are common

•Sudden cardiac death with morbid obese & refractory dysrhythmias

•ECHO will show LVEDP’s, valvular disease & wall motion abnormalities

•If TR present, think pulmonary HTN

•Cardiomegaly, pulmonary congestion, elevated diaphragm and tortuous aorta can be seen with chest X-ray

•Portable X-rays may not be sufficient to visualize structures on morbidly obese

resp eval

•OSA

•Orthopnea

•Wheezing

•Sputum, recent URI?

•Smoking 

•Airway management: beard, edentulous?

•Room air pulse ox reading

airway eval

•Atlantoaxial joint & cervical spine movement d/t cervical fat pads

•Thyromental distance, mouth opening, Mallampati class

•History of difficult airway?

•Mouth has extra tissue, how wide can they open, missing or decayed teeth

•Short thick neck

•Submental fat pad (double chin)

•BMI per se is not a factor in potential difficult airway