Obesity Flashcards

1
Q

Stats around obeisty (unsure if really testable)

A
  • Incidence:
    • 34% US population
      • 25% of children
    • 1.9 billion overweight adults and over 650 million obese people globally
    • more than 2 out of 3 of the U.S. adult population are overweight or obese
    • one in three adults has obesity and 1 in 13 has extreme obesity with a body mass index (BMI) > 40
      • second only to smoking as a preventable cause of death
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2
Q

Definition of obesity? overweight?

A
  • Overweight
    • Defined: “increased body weight above a standard related to height”
  • Obesity
    • Defined: “excessive body weight for the patient’s age, gender and height”
      • body wt > 20% ideal weight
        • ~ disorder of energy balance
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3
Q

How do you calculate BMI? IBW?

A
  • BMI: most common categorization of weight status
    • patient’s weight (kg), divided by square of pt’s height in meters
      • BMI = kg/m2
        • 1 m = 39.3 inches
  • Ideal Body Weight: weight associated with the lowest mortality rate for a given height and gender
    • Broca’s Index:
      • IBW (kg) = height (cm)- x
        • Males: x = 100
        • Females: x = 105
    • Miller 8th:**
      • Male: 50 kg + 2.3 kg for each 2.54 cm (1 in) >152 cm (5 ft)
        Female: 45.5 kg + 2.3 kg for each 2.54 cm (1 in) > 152 cm (5 ft)
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4
Q

What are the categories for BMI?

A
  • BMI = body weight (kg)
  • Obesity = BMI of 30kg/m2
  • Morbid Obesity = BMI of 40kg/m2
  • Super Morbid Obesity = BMI of 50kg/m2
  • Super-Super Obesity= BMI of > 60kg/m2
    • BMI > 30: increased morbidity d/t
      • Stroke
      • ischemic heart disease
      • diabetes
        • W/ obesity → 3-4 X the risk in the general population
  • > BMI → risk of developing problems becomes higher
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5
Q

What are some obesity related diseases?

A
  • insulin resistance
  • type 2 diabetes mellitus
    • see chart (pic)
  • obstructive sleep apnea (OSA)
  • asthma
  • chronic obstructive pulmonary disease
  • hypoventilation
  • cardiovascular disease
  • hypertension
  • certain malignancies
  • osteoarthritis
  • liver and gall-bladder disease
    • ​overweight and obesity a/w NA fatty liver dx and NASH
    • 40% NASH pt obese and 20% have dyslipidemia
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6
Q

What is metabolic syndrome?

A
  • increased r/f cardiovascular disease events and are at increased risk for all-cause mortality
  • up to 30% middle aged people in developed countries have metabolic syndrome

Diagnosis: Need 3 present

  • Abdominal obesity
  • Elevated fasting glucose
  • HTN
  • Low HDLs
  • Hypertriglyceridemia

Metabolic syndrome:

  • Abdominal obesity
  • Atherogenic dyslipidemia
    • ↑ TGs
    • ↓ HDL-C
    • ↑ ApoB
    • ↑ small LDL particles
  • Elevated blood pressure
  • Insulin resistance ± glucose intolerance
  • Proinflammatory state (↑ hsCRP)- inflammatory resp elevated
  • Prothrombotic state (↑ PAI-1, ↓ FIB)
  • Other
    • endothelial dysfunction
    • microalbuminuria
    • polycystic ovary syndrome
    • hypoandrogenism
    • non-alcoholic fatty liver disease- 40% of NASH are obese
    • hyperuricemia
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7
Q

What is OSA?

A
  • Recurrent episodes of partial or complete upper airway collapse occurring during sleep
    • 70% pts obese
  • Obstructive apneic event:
    • complete cessation of airflow during breathing lasting > 10 seconds despite maintenance of neuromuscular ventilatory effort
  • Dx: only by polysomnography
    • Results of polysomnography are reported as the apnea-hypopnea index (AHI)
      • total number of apneas and hypopneas divided by total sleep time
      • (or) Respiratory disturbance index (RDI) → includes resp effort related arousals (RERAs)
  • Apnea = 10 seconds or more of total cessation of airflow despite continuous respiratory effort against a closed glottis with decrease in SaO2 >4% (at least 5X/hr)
  • Hypopnea = a 50% reduction in airflow that lasts at least 10 seconds or a reduction sufficient enough to cause a 4% decrease in arterial SaO2
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8
Q

What is the AHI index?

A
  • Most sleep centers commonly use an AHI between 5 and 10 events per hour as a normal limit
  • AHI categories:
    • Mild Disease: 5-15 events/hr
    • Moderate Disease: 15-30 events/hr
    • Severe Disease: > 30 events/hour
      • Moderate/severe disease → tx w/ continuous positive airway pressure (CPAP) during sleep
    • Additional measures:
      • weight loss
      • avoidance of ETOH
      • side sleeping
        *
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9
Q

What is STOPBANG?

A

STOPBANG Assessment:

8 question survey

Score 5-8 → identify moderate/severe disease (KNOW)

  • Snoring
  • Tired
  • Observed apnea
  • Blood Pressure
  • BMI >35
  • Age >50
  • Neck >40 cm
  • Gender: Male
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10
Q

What are some risks of OSA?

A
  • Systemic and pulmonary hypertension
  • Left ventricular hypertrophy
  • cardiac arrhythmias
  • cognitive impairment
  • persistent daytime somnolence
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11
Q

What are some characteristics of the airway in obses OSA patients?

A
  • increased amounts of adipose tissue deposited into oral and pharyngeal tissues
  • inverse relationship exists between the degree of obesity and pharyngeal area
  • Increased airway obstruction
    • more difficult to maintain airway patency during mask ventilation
    • more diff perform direct laryngoscopy
  • Neuromuscular blockade should be fully reversed prior to extubation
  • Airway obstruction following extubation is worse with use of opiate and sedative drugs
    • these drugs tend to decrease pharyngeal dilator tone and increase the likelihood of upper airway collapse
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12
Q

What is the impact of the anatomic distribution of fat?

A
  • Adipose tissue location
    • Android (central) obesity/truncal distribution (apple)
      • located predominantly in upper body (intra-abdominal fat).
        • Increased O2 consumption
        • CV disease
        • LV dysfunction
    • Gynecoid (peripheral) obesity (pear)
      • located predominately in the hips, buttocks, and thighs.
        • Less CV disease because this fat is less metabolically active
  • Waist circumference directly related to risk of pathophysiology
    • Increased risk for morbidities:
      • Men: >102 cm
      • Women: >88 cm
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13
Q

What are adverse health implications a/w obesity?

A
  • Restrictive lung disease
  • Hypertension
  • Coronary artery disease
  • Hyperlipidemia
  • Type II Diabetes Mellitus
  • Gall bladder disease (cholelithiasis)
  • Cirrhosis/Fatty Liver Disease
  • Degenerative joint/disc disease
  • Obstructive Sleep Apnea/hypoventilation syndrome
  • Psychological and socioeconomic impairment
  • Increased breast, prostate, cervical, uterine, and colorectal malignancy
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14
Q

Respiratory pathophys in obese patient?

A
  • Chest wall and lung compliance reduced
    • Fat accumulation on thorax & abdomen
    • Increased pulmonary BV
      • Needed to perfuse excess adipose tissue
      • Polycythemia from chronic hypoxemia
  • Add the supine position and anesthesia = situation worse
    • increased work of breathing
    • Increased RR with decreased Vt
    • limited maximum ventilatory capacity = decreased respiratory muscle efficiency
  • PEEP is the only ventilatory parameter that has been shown to improve respiratory function in obese patients
    • 10-12 cmH20 (watch BP)
      • Increased PEEP → decrease VR (watch hypoTN)
  • Increased oxygen consumption and carbon dioxide production
  • High minute ventilation
  • As obesity worsens you will see lung disease and pulm HTN
    • PFTs remain normal until point of pulmHTN
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15
Q

Effect of obesity on lung volumes?

A
  • ↓ decreased ERV (60% of normal)
  • ↓decreased FRC (80% of normal)
    • FRC reductions with anesthesia are exaggerated
      • 20% nml
      • 50% obese
  • ↓ decreased VC
  • ↓ decreased TLC
    • RV and CC: not changed
    • relationship between FRC and CC: adversely affected
    • FEV1 and FVC: w/in normal limits
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16
Q

What are some airway changes in obesity?

A
  • Upper thoracic and low cervical fat pads →
    • Limited movement →
      • TMJ
      • atlanto-axial joint
      • cervical spine movement
  • Redundant tissue folds in the mouth and pharynx = narrowed upper airway
  • Short, thick neck: measure neck circumference
    • Neck circ strongly predictive of diff w/ int, more so than some other msrs of assessing for diff with int
      • 40 cm = 5% incidence difficult intubation
      • 60 cm= 35% incidence difficult intubation (6 x increase)
  • Fat in suprasternal, pre-sternal, posterior cervical and submental regions → diff to position
    • Use stubby laryngoscope
  • Shortened distance between mandible & sternal fat pads
  • OSA = INCREASE risk of excess pharyngeal tissue on lateral walls – why they obstruct
  • Creates difficulty maintaining mask airway
  • Creates difficult laryngoscopy and intubation
  • “Ramp patient” to align sternum with ear → improve visualization
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17
Q

Pathophysiologyc of OSA

A
  • Altered functioning during the daytime:
    • Sleepiness
    • impaired concentration
    • impaired memory
    • headaches
  • Ultimately lead to:
    • Chronic hypoxia, hypercapnia
    • pulmonary and systemic vasoconstriction (HTN)
    • secondary polycythemia
    • Chronic HPV → leads to right ventricular failure
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18
Q

What are some perioperative complications with OSA?

A
  • HTN
  • Hypoxia
  • Arrhythmias
  • MI
  • Pulmonary Edema
  • Cognitive impairment
  • Stroke
  • Difficult mask ventilation
  • Post-operative airway obstruction
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19
Q

What is pickwickian/obesity hypoventilation syndrome

A

extreme consequence of obesity

  • Extreme obesity with:
    • Hypercapnia
    • cyanosis induced polycythemia
    • somnolence
    • *right sided heart failure
    • *pulmonary HTN
  • Diagnosis:
    • Obese pt w/ PCO2 >45 mm Hg w/o sig COPD
    • Chronic daytime hypoxemia → better predictor of pulmHTN and cor pulmonale (‘pickwickian”) than the presence and severity of OSA
    • A supine room-air SpO2 < 96% or increased Hct may merit further investigation (pulm HTN)
      • Preop:
        • PFTs
        • ABGs
        • CXR
        • echo
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20
Q

CV alterations in obesity?

A
  • increase total BV –
    • blood flow to fat: 2-3ml/100g tissue
      • Obese pt: 50ml/kg
      • Normal wt pt: 70ml/kg
  • increase renal and splanchnic blood flow
  • éincrease CO
    • d/t ventricular dilation
  • increase SV
  • increase O2 consumption
  • increase renin-angiotensin system (RAAS)
  • increase SNS activity
  • HTN:
    • SBP: increase 3-4mmHg/10 kg wt gain
    • DBP: increase 2mmHg/10kg wt gain
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21
Q

CV complications of obesity?

A
  • Need ECG
    • left or right ventricular hypertrophy
    • ischemia
    • conduction defects
  • Increased left ventricular wall stress →
    • Hypertrophy
    • reduced compliance
    • impaired left ventricular filling (reflect diastolic dysfunction)
    • increase left ventricular pressures
    • increase diastolic pressure
      • → progresses to pulmonary edema
  • Eventually LV wall thickening fails to keep pace with ventricular dilation and systolic dysfunction or “obesity cardiomyopathy”
    • → results with eventual biventricular failure.
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22
Q

What are some associated postoperative comp,ications related to CV changes in obesity?

A
  • Limited mobility can mask significant cardiac disease and peri-op risk (difficult to calculate METS)
    • CAUTION:
      • Rapid IV fluids → result in ventricular failure
      • Exaggerated negative inotropy with anesthetic agents
      • Hypoxia and hypercapnia → may result in pulmonary HTN
        • Careful with acute CO2 changes
  • higher risk arrhythmias
    • D/t: hypoxia, hypercapnia, CAD, OSA, increased circulating catecholamines, myocardial structural changes (hypertrophy, fatty infiltrates)
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23
Q

Hematologic changes in obesity?

A
  • Polycythemia
  • Hypercoagulation promoted by increased
    • Fibrinogen
    • Factor VII
    • Factor VIII
    • Von Willebrand factor
    • Plasminogen activator inhibitor-1
24
Q

GI alterations in obesity?

A
  • increase incidence hiatal hernia & GERD
  • Gastric emptying delays
    • d/t
      • éincrease abdominal mass with antral distention
      • increase gastrin release
  • Pneumonitis risk – same fasting guidelines
    • *If aspiration occurs:
      • after fasting morbidly obese patient’s gastric volumes > 25ml & pH< 2.5 (increased parietal cell secretion)
    • However, in obese patient with no GI/GE patho follow normal fasting guidelines
25
Q

Liver alterations in obese pt

A
  • Fatty infiltration (high prevalence of nonalcoholic fatty liver disease)
  • Inflammation
  • Focal necrosis
  • Cirrhosis
  • Normal clearance despite often altered histology and LFT’s
26
Q

Renal alteration in obese pt?

A
  • increase renal plasma flow
  • increase GFR
  • increase renal tubular resorption
  • impaired naturesis secondary to SNS and renin-angiotensin system activation (also physical compression of the kidney)
    • Eventually nephron function can be lost
27
Q

What are some metabolic alterations in obesity?

A
  • Metabolic rate → proportional to body weight
  • Increased oxygen consumption and carbon dioxide production (excess fat increases workload)
  • Compensation via increased C.O. and increased minute ventilation
  • Arterial oxygen tension in morbidly obese patients breathing room air is lower than predicted
  • These chronic alterations can result in:
    • pulmonary HTN
    • cor pulmonale
28
Q

Endocrine alteration in obesity?

A
  • Fatty tissues are resistant to insulin = glucose intolerance and DM type II
  • Abnormal serum lipid panels = high prevalence of CAD
  • Hypothyroid common
  • increase renin-angio and SNS systems
29
Q

What are some alterations in the pharmacology of obese patients?

A
  • Volume of Distribution
    • Central compartment is unchanged
    • decrease Absolute total body water
    • increase Adipose and lean tissues
      • Most altered VOD:
        • Lipophilic
        • polar drug
          • Ex: barbiturates and benzos.
    • increase Blood volume and CO
    • Blood concentration of free fatty acids, triglycerides, cholesterol, and alpha 1 glycoprotein increased= decreased free drug concentration
    • Organomegaly
30
Q

What are some alterations in drug metabolism in obese pt?

A
  • Phase I (oxidation, reduction, hydrolysis)
    • unaffected
  • Phase II (glucuronidation, sulfation)
    • enhanced
31
Q

Affect of obesity on drug clearance?

A
  • Hepatic clearance - unchanged
    • despite histological and LFT alterations
  • Renal clearance of drugs - increased
    • (increased GFR, RBF, and tubular secretion)
  • Lipophilic drugs have an increased elimination half-life because of increased Vd but have normal clearance
32
Q

Generic principles for dosing of meds in obese patients?

A
  • Weak or Moderate Lipophilicity dose on IBW or LBM (lean body mass)
    • Adding 20% to IBW with hydrophilic medications (i.e. muscle relaxants) will include the extra LBM associated with obesity
    • Miller 8th provides this formula for LBM- do not need to know
      • Male: 1.1 × TBW − 128 × (TBW ÷ Ht) 2
      • Female: 1.07 × TBW − 148 × (TBW ÷ Ht) 2
  • Loading dose
    • ​drug distributed to lean tissue dose on LBW
    • Drug even distribution b/w adipose and lean- use TBW
  • Maintenance
    • ​drug similar clearance in obses and nonobese, use LBW
    • Drug has clearance increased with obesity should have maintenance dose based on TBW
33
Q

Considerations for propofol dosing in obese pt

A
  • Induction dose
    • *LBW (no difference in initial VD between obese and non-obese patients)
  • Maintenance dose
    • *TBW
  • Increased Vd (high affinity for fat and other well perfused organs) at steady state parallels increased clearance (high hepatic extraction and conjugation rate) = no change in E ½ life
34
Q

Benzodiazepine dosing in obese pt?

A
  • Highly lipophilic drugs with larger Vd in obese patients
    • Initial doses → LBW – may titrate to TBW (need larger doses to reach adequate serum concentrations)
    • Infusions → LBW
  • Prolonged duration of action though secondary to larger Vd and need higher loading doses
35
Q

Considerations of NMB drugs in obesity?

A
  • Pseudocholinesterase activity increases as weight and ECF increases (linear relationship)
    • Dose: Succinylcholine → TBW
    • Vecuronium and Rocuronium –LBW
    • Atracurium and Cisatracurium –LBW (Miller 8th TBW)
      • General trend= exhibit prolonged DOA and recovery
36
Q

Sugammadex dosing in obesity?

A
  • Dose → TBW
  • Some have hypothesized that low Vd at steady state (estimated at 0.16 L/kg) indicates we should consider dosing on the lean/ideal body weight
  • Studies indicate that this might not be adequate
  • Controversial… follow drug insert for now
37
Q

Dosing of opioids in obesity?

A
  • Fentanyl and Sufentanil = both are highly lipid soluble so – increased Vd and elimination ½ life
    • Fentanyl → LBW (Miller 8th says TBW)
    • Sufentanil → TBW
      • then decrease maintenance to LBM
    • Remifentanil → LBW
      • pharmacokinetics are similar in obese and non-obese patients.
  • High risk bc OSA → reducing dose anyway
  • Barash 6th says dose sufentanil on TBW in text and LBW in chart 1237. Increased body fat increases the VOD of sufentanil and slows its elimination. Miller 8th presents very complex modeling that is very difficult to follow and remember for dosing in the obese pts. It also involves the definition of multiple “scaling” formulas… better summary in chapter p. 2212 but some contradiction with barash.
38
Q

Dexmedetomidine dose in obesity?

A
  • Nice adjunct to consider when respiratory depression avoidance is priority
  • Dose: 0.2-0.7 mcg/kg/hr
    • reduce analgesic and anesthetic requirements
  • Dose: TBW
39
Q

VA effect in obesity?

A
  • Metabolism is greater in obese patients = greater increase in inorganic fluoride
  • Greater incidence of halothane hepatitis
  • Some evidence suggests recovery more reliable after desflurane (i.e. fat:blood partition coefficient) compared to sevo or iso ; other evidence contradicts this???
  • N20 often avoided to maximize PaO2*
  • Even though obese pts have a greater increase in inorganic fluoride there is no significant differences in post op liver or renal function comparing obese and non-obese individuals with Sevo. Greater incidence of halothane hepatitis because obese pts use a hepatotoxic metabolic pathway to metabolize halothane.
  • VA distribute so slowly to lipid stores that increasing the fat reservoir has little clinical effect on wake-up time even w/ long sx
40
Q

Medical therapy for obesity?

A
  • Life style modifications tried 1st
  • Indications
  1. BMI > 30kg/m2 or
  2. BMI 27-29.9 kg/m2 + obesity related medical complication
41
Q

What are some medications to treat obesity?

A
  • Serotonin reuptake inhibitors/Sympathomimetics (Phen-fen= fenfluramine and phentermine) – appetite suppressants - unacceptable side effects (primary pulmonary HTN and valvular heart disease)
    • Phentermine currently approved (approved only _<_3 mo. use, hypertension, tachycardia, abuse & W/D)
      • an adrenergic reuptake inhibitor, augments adrenergic signaling within the central nervous system and peripheral tissues.
        • Phentermine decreases appetite and food intake and increases the resting metabolic rate to promote weight loss.
        • SE: tachycardia and HTN.
  • Lipase inhibitors (orlistat)
    • blocking absorption and digestion of dietary fat and binding lipases in GI tract
      • improve CF risk factors (BP, waist circum., GTT, lipid profile, cholesterol)
    • impact absorption of Vit A, D E, K.
      • ​impact VIT K absorption can affect factors II, VII, IX, X
      • resulting coagulopathy corrected 6-24 hours before sx with vit K such as phytonadione and FFP
    • sig GI s/e- diarrhea, steatorrhea, flatulence, fecal incontinence
  • Sibutramine is an adrenergic and serotoninergic agent that suppresses appetite and increases thermogenesis.
    • Common SE: HTN, tachycardia, insomnia, and dry mouth.
42
Q

What are some various forms of bariatric surgery?

A

Bariatric surgery: surgical alteration of small intestine or stomach to promote weight loss (3 types)

  • Malabsorptive procedures (jejuno-ileal bypass and biliopancreatic diversion)
  • Restrictive procedures (gastroplasty (VBG) and the adjustable gastric banding (ABG))
  • Combined restrictive and minimal malabsorptive roux-en Y gastric bypass (RYGB))

GREATEST COMPLICATION:

  • Pulmonary emboli
    • greatest cause of perioperative 30-day mortality
43
Q

Considerations with laparoscopic bariatric surgery? Benefits?

A

Benefits:

  • Less post-op pain
  • lower morbidity
  • faster recovery
  • less third-spacing of fluid
  • lower wound infection

Requirements:

  • Complete NM relaxation**
    • Decreased mechanical retraction and smaller incision - 5-6 small abdominal incisions while pneumoperitonem is used to create a working space and gravity displacement of abdominal viscera. NMB is a must to facilitate adequate/safe working space for surgeon and controlled ventilation.
  • Positioning req → make patient high fall risk from OR table
  • right main-stem intubation risk
    • because of cephalad displacement of the carina and diaphragm from a pneumoperitoneum.
  • May need to facilitate the proper placement intragastric balloon, etc.
    • for gastric pouch sizing and leak tests with NS or methylene blue need a tight seal around ETT cuff ensure no aspiration occurs.
  • Prior to gastric diversion ensure all endogastric devices removed (avoid stapling in place or transection)
  • After gastric pouch in place → avoid blind NG insertion - watch on laparoscopic monitor so that you do not disrupt anastomosis.
  • Incidence of rhabdomyolysis in obese patients is more common than with open procedures
    • increased serum creatinine, CPK, or buttock, hip or shoulder pain indicate potential for complication
    • dx and treat to avoid myoglobinuric acute renal failure (30% with CPK >5000IU/L)
44
Q

What is an implantable gastric stimulator? Anesthetic considerations?

A
  • Laparoscopic placement
    • 2 lead electrodes on greater curvature of stomach
    • SQ electric pulse generator implanted on abdominal wall
    • Simulate gastric smooth muscle, decrease peristalsis (in theory patient feels less hungry)
  • Anesthetic considerations
    • Avoid N&V (valsalva may dislodge electrodes)
    • ECG interference
45
Q

Preop considerations of obese pt?

A
  • Population w/ High incidence of:
    • HTN, pulmonary HTN, right/left ventricular failure, CAD
      • Excess adipose tissue may hide signs of cardiac failure
      • Pulmonary HTN signs = dyspnea, fatigue, syncope, tricuspid regurgitation on echo, ECG (RVH, tall precordial R waves, right axis deviation), prominent pulmonary artery on CXR
  • Nutritional deficiencies in repeat bariatric surgery patients:
    • B12, iron, calcium, folate deficiencies
  • Severe vitamin deficiencies can lead to acute postgastric reduction surgery neuropathy (APGARS)
    • APGARS → S/S:
      • protracted N&V
      • hyporeflexia
      • muscle weakness
        • → careful dosing of NMB if s/s present
  • Chronic vitamin K deficiency – coagulation studies
  • Pre-medications:
    • Anxiolysis- small doses (bc lead to resp depression)
    • Tx as full stomach → aspiration pneumonitis precautions
      • Ex: H1/2, nonparticulate, reglan
  • IM injections unreliable – thickness overlying adipose tissue
  • DVT prophylaxis
    • Morbid obesity is a major independent risk factor for sudden death from PE. SQ heparin 5000u before surgery and repeated Q8-12hours, early mobilization
  • OSA/OHS increased risk difficult airway – pre-op ABG
  • Airway assessment = neck circumference most important factor!
46
Q

Positioning considerations in obese patients

A
  • Regular OR tables max weight ~ 200kg
    • Newer tables can hold up to 300-455 kg, with greater width or side accessories
  • High incidence of pressure sores and nerve injuries in this group
    • A documented association between ulnar neuropathy and increasing BMI – 33% incidence of ulnar neuropathy in patients with a BMI of > or + 38kg/m2 compared with 1% control group
  • “Stacking” or ramped position for intubation to align ear with sternum
  • Supine- decreased FRC, oxygenation, and ICV/aorta compression
  • Reverse Trendelenburg- longest safe apnea period VS decreased cardiac output
  • Prone- – free abdomen essential, increased intra-abdominal pressure
  • Lateral Decubitus- better than supine if possible – improved diaphragmatic excursion.
47
Q

What are some considerations of monitoring in the obese patient?

A
  • Monitors – appropriate sized BP cuff
    • Cuffs with bladders that encircle a minimum of 75% of the upper arm circumference or preferably the entire arm should be used. Forearm measurements with a standard cuff overestimate both SBP and DBP in obese patients.
  • IV/arterial line access may be challenging
  • Consider CVP or PAP catheter
  1. Significant CV or pulmonary disease
  2. When large fluid shifts expected
48
Q

Prevention of thromboembolism in obese pt?

A
  • Most mortality in the 30-day perioperative period after bariatric surgery is due to PE (at least 3 X more frequent than anastomotic leak with subsequent sepsis)
  • LMW heparin (limit postop pain tx options)
  • Pre-op aspirin and subsequent warfarin to INR= 2.3
  • Decrease the risk : preoperative exercise, antithrombotic drugs, stocking prophylaxis, nonpolycythemic HCT, increased CO, and early ambulation
49
Q

Induction considerations of obese patient?

A
  • Pre-oxygenation = most important step!
    • 30 degree RT position
  1. Decreased FRC
  2. Increased O2 consumption
  3. +/- Higher incidence of difficult airway
  • Induction drug dosing altered
  • Consider awake intubation with minimal sedative – hypnotics
  • RSI? Aspiration concerns
  • May need two handed mask – extra help!
  • Breath sounds difficult → Diff confirming ETT placement to hear
  • PEEP 10 cm H20 can be helpful intra-op (if BP tolerates…)
50
Q

Intraoperative fluid balance in obese patient?

A
  • Diff to assess peripheral perfusion
  • Greater blood loss compared with non-obese secondary to technical difficulties/need for more extensive dissection
  • Less compensation for BL
    • early threshold for replacement with colloids/blood products
  • In bariatric surgery → risk of acute tubular necrosis with inadequate fluid replacement
51
Q

Emergence of obese patient?

A
  • Respiratory failure # 1 problem
    • Prompt extubation
      • fully awake
      • NMB fully reversed
      • adequate MV confirmed
  • Semirecumbent position with 100% O2
  • CPAP and Bi-PAP to combat post-operative atelectasis/ airway obstruction
  • Analgesia to promote pulmonary toilet
    • But caution
  • Pulse oximetry and arterial blood gas monitoring often indicated
52
Q

Regional anesthesia in obese patient

A
  • Avoidance of intubation challenges VS technically challenging landmark identification
  • Central neuraxial blockade easier in the lumbar region
  • Longer needles may be required
  • Ultrasound and fluoroscopy have been used to place catheter in epidural space
  • Local anesthetic doses reduced 20-25% in obese patients
    • epidural vascular engorgement and fatty infiltrates decrease volume of epidural space*
  • Subarachnoid block height can be unpredictablehigh spinal possible
    • Hypotension common in this population IVC compression etc.
53
Q

Postop pain control considerations in obesity?

A
  • Epidural anesthesia
    • prevent DVT, improved analgesia, GI motility, decreased O2 consumption, decreased LV stroke work
  • PCA with opioid
    • (multi-modal opioid sparing should be attempted)
  • Local anesthetic infusion to incision site
  • Non-opioid analgesics and adjuvants
  • Obesity significant risk factor for postop hypoxemia
    • partially remedied by placing the patient in the semirecumbent (rather than the supine) position for 1st 48 - 72 hrs post-op
  • Consider monitored bed/ICU + CPAP post-op
    • POD #1, 75% obese pt have PaO2 <60
54
Q

ACLS in obese patients?

A
  • Adequate chest compressions difficult
    • may need mechanical compression device
  • Use 400 joules of energy on defibrillator and be prepared to complete several attempts to overcome higher transthroacic impedence
  • LMA and Combitube useful emergency supraglottic airway devices
55
Q

What is a gastroplasty (from notes, not covered in lecture in detail)

A
  • Gastroplasty creates a small upper pouch (15-30ml) in the stomach, which restricts food intake and communicates with the remainder of the stomach through a narrow channel or stoma.
  • Restrictive procedure
56
Q

What is a roux en Y gastric bypass?

A
  • Most common bariatric sx in US
    • combined restrictive and minimal malabsorptive sx
  • anastomizing the proximal gastric pouch to segment of proximal jejunum
    • bypasses most of stomach and entire duodenum
  • most effective bariatric procedure to produce safe short and long term weight loss
  • lose 50-60% excess body weight
    • BMI decrease 10 in first 12-24 months
    • T2DM resovles in most patients
57
Q

What is gastric banding?

A
  • Restrictive procedure
  • lapasroscopic
  • band placed around stomach to limit capacity
    • can be made tighter or less by adding/removing saline