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Advanced Anesthesia III > GI/Obesity > Flashcards

GI/Obesity Flashcards

1
Q

Define obesity

A

20% or more above IBW. Disorder of energy balance.

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2
Q

Diagnosis of metabolic syndrome

A

Diagnosed when 3 or more of the following are present

1) Abdominal Obesity
- Waist circumference > 102cm in men or 88cm in women

2) High TGs
- > 150mg/dL

3) Low HDL
- 130/85

5) FBS > 110

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3
Q

What is IBW? Definition and calculation

A

The weight associated with the LOWEST mortality rate for a given height and gender

Use Broca’s Index to calculate:
IBW (kg) = height (cm) - x

Men, x = 100
Women, x = 105

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4
Q

Calculation fro BMI

A

(weight in kg / height squared in meters)

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5
Q

Degrees of obesity based on BMI

A

Obesity > 30
Morbid Obesity > 40
Super morbid obesity > 50

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6
Q

BMI > ____ is associated with increased morbidity (3x) due to stroke, CAD, and DM

A

28

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7
Q

Implications of fat distribution

A

2 distributions

1) Android (central) obesity / truncal distribution
- Mostly intra-abdominal fat (fat is mostly upper body)
- Presents higher risk in anesthesia
- Higher incidence of CV disease b/c this fat is more metabolically active
- However, because it’s more metabolically active means it’s easier to lose

2) Gynecoid (peripheral) Obesity
- Lower risk in anesthesia
- Located mostly in hips, ass, and thighs
- Less CV disease b/c this tissue is less metabolically active

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8
Q

Respiratory patho in obesity

A
  • Reduced lung and chest wall compliance
  • Pulmonary blood volume is increased to perfuse extra adipose tissue
  • Polycythemia from chronic hypoxia
  • Difficulty breathing in the supine position
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9
Q

This is the only ventilatory parameter that has actually been shown to improve respiratory function in obese patients

A

PEEP (use 10-12 cmH2O)

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10
Q

Effects of obesity on lung volumes

A

ERV = 60% of normal
FRC is 80% normal (even worse with anesthesia, normal population, FRC will decrease by 20% with induction of anesthesia, but in the obese, it will decrease by 50%)
VC and TLC are decreased

RV and CC are unchanged. However, because FRC is decreased, TV may fall into the range of CC.

FVC and FEV1 are unchanged.

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11
Q

Metabolic rate is proportional to

A

body weight

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12
Q

Metabolic rate in obesity

A

Increased d/t increased body weight. Results in increased O2 consumption and CO2 production (excess fat tissue increases workload).
The body compensates by increasing CO and MV.

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13
Q

PaO2 is usually ___ in obese patients.

A

Less than predicted on room air. This chronic alteration can lead to pulm HTN and for pulmonale

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14
Q

OSA diagnosis

A

Involves apneic and hypopneic events.

Apnea = 10 seconds or more of TOTAL airflow cessation despite respiratory effort, resulting in SaO2 drop by 4%

Hypopnea = 10 seconds or more of a 50% or more reduction of airflow, or a reduction significant enough to cause a 4% drop in SaO2.

Apnea-hypopnea index (# events per hour)
> 30 = severe
16-30 = moderate

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15
Q

Peri-op complications associated with OSA

A 
HTN
Hypoxia
Arrhythmia
MI
Pulm edema
Cognitive impairment
Stroke
Post-op airway obstruction
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16
Q

What is Obesity Hypoventilation Syndrome

A

Also called Pickwickian Syndrome

  • OSA progression to daytime hypercapnea
  • Extreme obesity with hypercapnia, cyanosis, polycythemia, somnolence, and eventual R sided HF and pulm HTN
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17
Q

Diagnostic of obesity hypoventilation syndrome

A

PaCO2 > 45 in the absence of COPD

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18
Q

This would lead you to investigate further about obesity hypoventilation syndrome

A

SUPINE SaO2

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19
Q

CV alterations in obestity

A
  • Increased total blood volume
    (BF to fat is 2-3mL/100g tissue)
    (Overall 50mL/kg for obese person vs. 70mL/kg for normal weight)
  • Increased renal and splanchnic flow (cause they eatin’ all the time!)
  • Increase in CO (2/2 ventricular dilation from increased blood volume), increased SV, and O2 consumption
  • Increased SNS and RAAS activity
  • LVH from increased body mass to serve, resultant diastolic dysfunction, and eventually pulm edema
  • Eventually, this LVH is unable to keep up with body’s demands, resulting in “obesity cardiomyopathy,” causing biventricular failure
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20
Q

On average, BP increases this much per amount of weight gained

A

Increased of 3-4mmHg SBP and 2mmHg DBP per 10kg of weight gained

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21
Q

Why should we get an EKG in obese patients?

A

Probably have L or R ventricular hypertrophy, may have CAD, and conduction defects

Risk for arrhythmia 2/2 hypoxia, hypercapnia, CAD, OSA, increased circulating catecholamines, and changes int he myocardium (hypertrophy, etc)

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22
Q

Hematologic changes in obesity

A 
Polycythemia
Hyper coagulable state (from increased)
- Fibrinogen
- Factors 7, 9, and vWF
- Plasminogen activator inhibitor-1
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23
Q

GI changes in obesity

A
  • Higher incidence of GERD and hiatal hernia
  • Delayed gastric emptying
  • Increased gastric residual volume after fasting
  • Risk risk of pneumonitis if aspiration occurs
  • Normal fasting guidelines can be followed as long as no other GI patho
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24
Q

After fasting, gastric volume and pH are typically

A

> 25mL

ph

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25
Q

Liver alterations in the obese patient

A
  • Fatty infiltrates (high incidence of non-alcoholic fatty liver disease)
  • Liver inflammation
  • Focal necrosis
  • Cirrhosis (from chronic inflammation)
  • Normal clearance despite altered histology and LFTs
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26
Q

Renal alterations in obesity

A
  • RBF and GFR 2/2 increased total blood volume
  • SNS and RAAS activation leads to sodium retention
  • Eventually nephron function can be lost
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27
Q

Endocrine alterations in obesity

A
  • Fatty tissues become resistant to insulin (causes glucose intolerance and DM II)
  • High lipid panels, leading to CAD
  • Hypothyroidism is common
  • Increased SNS and RAAS
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28
Q

Neck circumference and difficult intubation incidence

A

> 40cm = 5% incidence difficult intubation

> 60cm = 25% incidence difficult intubation

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29
Q

The obese patient should be ramped so that ____ aligns with ____

A

The ear aligns with the sternum

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30
Q

Pharm alterations in obesity

A
  • Increased adipose and lean tissue
  • Central compartment is unchanged
  • Absolute TBW is decreased
  • Blood volume and CO are increased
  • Increased a-1 glycoprotein and fats leading to decreased free drug
  • Organomegaly
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31
Q

Drug metabolism in obesity

A

Phase I reactions unaffected
- Oxidation, reduction, hydrolysis

Phase II reactions enhanced
- Glucuronidation, sulfation, etc.

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32
Q

Drug clearance in obesity

A
  • Hepatic clearanced unchanged despite histologic and LFT alterations
  • Renal clearance is increased (d/t increased RBF, GFR, and tubular secretion)
  • Lipophilic drugs (lots of our anesthetics) have increased e1/2 life d/t increased Vd
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33
Q

Drug dosing of drugs with low lipophilicity in obesity

A
  • Drugs with weak or moderate lipophilicity should be based on IBW or LBM (lean body mass)
  • Makes sense, because central circulating volume doesn’t change
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34
Q

How to calculate LBM (lean body mass) in obese patients

A

Add 20% to IBW

35
Q

TPL in obesity

A
  • Highly lipophilic, so prolonged DOA
  • Dose on LBW
  • Induction dose should be increased (d/t increased TBV, CO, and muscle mass)
36
Q

Propofol in obesity

A
  • Induction dose based on IBW (no difference in initial Vd between obese and non-obese patients)
  • Maintenance dose based on TBW
  • Increased Vd at steady state parallels increase in clearance, so overall no change in elimination 1/2 life
37
Q

Benzos in obesity

A
  • Initial doses based on TBW
  • Highly lipophilic, so need higher doses to reach adequate serum concentrations
  • Prolonged DOA d/t high Vd and need for larger initial doses
38
Q

NMBs in obesity

A
  • All based on LBW except sux
  • Sux is based on TBW (this is because weight and ECF increase leads to an increase in pseudocholinesterase activity)

Overall, there is a slower recovery from NMBs.

39
Q

Opioids in obesity

A
  • Fentanyl and sufenta are highly lipid soluble
    • -> Increased Vd and elimination 1/2l
  • Fentanyl –> LBW
  • Sufenta –> TBW
  • Remifentanil –> LBW
40
Q

Precedex in obesity

A
  • Dose on TBW
  • Nice adjunct when trying to avoid respiratory depression
  • 0.2 - 0.7 mcg/kg/hr to reduce analgesic and anesthetic requirements
41
Q

Volatile anesthetics in obesity

A
  • Higher metabolism in obese pts
    • -> higher increase in inorganic fluoride
  • Higher incidence of halothane hepatitis (think about how they already have liver damage 2/2 inflammation and non-alcoholic fatty liver disease)
42
Q

Use of nitrous in obesity

A

Usually avoided to maximize FiO2

43
Q

When is medical therapy for obesity indicated?

A

BMI > 30
OR
BMI 27-29.9 with an obesity related medical complication

44
Q

Medications used to treat obesity

A

1) SSRIs
- Phen-fen (medication name)
- Appetite suppressant, but had unacceptable SEs like pulm HTN and valvular heart disease

2) SSRI and NE reuptake inhibitors
- Sibutramine

3) Lipase Inhibitors
- Orlistat
- Blocks digestion and absorption of dietary fat by binding lipase in the GI tract

4) Selective Cannabinoid 1 Receptor Antagonists
- Rimonabant
- Acts as an appetite suppressant, but caused nausea, anxiety, and depression

45
Q

This is the greatest cause of peri-op mortality in bariatric surgery

A

PE

Important to control pain and encourage ambulation after bariatric surgery!!

46
Q

Anesthesia for implantable gastric stimulator

A
  • Stimulates gastric smooth muscle to decrease peristalsis (supposed to make the pt feel less hungry)
  • Avoid NV (valsalva could dislodge the electrodes)
  • Impulses can interfere with EKG reading
47
Q

Signs of pulm HTN in obese patients

A

Dyspnea, fatigue, syncope
TR on ECHO
EKG changes (RVH, tall precordial R waves, R axis deviation)
Prominent pulmonary artery on CXR

48
Q

Nutritional deficiencies post bariatric surgery

A
  • Keep these in mind if pt is having repeat bariatric surgery
  • Often lack B12, iron, calcium, and folate
  • Chronic vitamin K deficiency can result in coagulopathies
  • Severe vitamin deficiencies can lead to acute post-gastric reduction surgery neuropathy (APGARS)
    • -> See protracted N&V, hyporeflexia, muscle weakness (if this is the case, be careful with NMB dosing)
49
Q

What is the most important factor in the obese airway assessment

A

Neck circumference

50
Q

What is the max weight of normal OR tables?

A

200kg

51
Q

Realize that there is a high incidence of ___ and ___ when positioning obese patients

A

nerve injuries and pressure sores

52
Q

BP cuff bladder should encompass ___ of the circumference of the arm

A

75%

53
Q

DVT prevention in bariatric surgery

A
  • Pre-op ASA
  • Pre-op coumadin therapy to INR of 2.3
  • LMWH
  • TEDS and SCDs, early ambulation
54
Q

Considerations for induction of obese pts

A
  • ADEQUATE PREOXYGENATION!!
  • -> Decreased FRC and increased O2 consumption
  • Higher incidence of difficult airway
  • Consider alterations of induction drug dosing
  • Need RSI? Aspiration concerns
  • May need 2 hand mask with OA
  • Breath sounds may be difficult to hear
55
Q

Blood loss in obesity

A

Usually higher due to technical difficulties of getting exposure and need more a more extensive dissection
- Pt is less able to compensate for blood loss –> lower threshold for replacement with colloids and blood products

56
Q

Emergence in obesity

A
  • # 1 concern in resp failure
  • HOB up (semi-recumbent)
  • CPAP and BiPAP
  • Analgesia to promote deep breathing and pulmonary toilet
  • SaO2 monitoring and possible ABG monitoring (consider if pt has OHS or severe OSA)
57
Q

RA considerations in obesity

A
  • Allows you to avoid intubation
  • May be difficult to find landmarks
  • Epidurals easier to get in lumber area
  • May need longer needles
  • Epidural doses can be reduced by 20-25% d/t decreased volume of epidural space
  • Block heigh for spinal can be unpredictable, risk for high spinal
58
Q

ACLS in the obese patient

A
  • May be hard to give adequate chest compressions, may need mechanical compression device
  • Use 400J on defib and may need several attempts to overcome the higher transthoracic impedance
  • LMA or combitube for emergency in difficult airway
59
Q

Pre-op considerations for GI disease

A
  • Fluid and electrolyte status (has pt been vomiting, shitting, how long NPO, etc.)
  • Pt may ave GERD, bowel obstruction, vomiting, hyperacid secretion, etc.
  • May have vit K deficit and thus be coagulopathic (Factors 2, 7, 9, 10)
  • B12 deficiency can result in megaloblastic anemia
60
Q

Factors that reduce LES tone

A
  • Obesity
  • VAs, TPL, propofol
  • Opioids
  • Cricoid pressure
  • Hiatal hernia
  • Pregnancy
  • B-agonists
  • TCAs
  • Glucagon
  • Anticholinergics
61
Q

Factors that INCREASE LES tone

A
  • Ach
  • Anticholinesterases
  • Sux
  • A-agonists
  • Reglan
  • BBs
  • Antacids
  • Serotonin
  • Histamine
62
Q

Aspiration precautions for hiatal hernia

A

Only indicated if the patient is symptomatic
Most pts with this are not symptomatic. The biggest factor in being symptomatic is the integrity of the LES
If symptomatic, can give antacids, reglan, ranitidine, etc.

63
Q

Patho of SBO

A

Progressive dilation and edema of bowel proximal to obstruction may lead to impaired bowel supply –> potential for necrosis and perforation

If perforation occurs, there is rapid fluid loss and pt is at high risk of bacterial toxemia or septicemia

64
Q

LARGE bowel obstruction

A
  • Slower and less dramatic presentation than SBO. Probably cause it’s larger and has more space to compensate for backup
  • Often due to an incompetent ileocecal valve
    • -> In this case, the bowel contents reflux into the small bowel and ultimately can cause feculent vomiting (AKA shitting out your mouth, AKA Anne Coulter syndrome)
65
Q

Goals in bowel obstruction

A
  • Protect the airway (RSI, placing NG pre-op)
  • Restore volume
  • Correct pH and electrolyte imbalances
  • Normalize SVR
  • Correct deficit with combo of crystalloid and colloid
  • Consider maintenance with D51/2NS with 20-40 mEq K/L
66
Q

PSNS and GI surgery

A
  • PSNS stimulation results in peristalsis
  • Cholinesterase inhibitors (like neostigmine and edrophonium) increase the frequency and magnitude of pressure waves in the colon (especially in the diseased bowel)
  • Anticholinergics like glycol and atropine help reduce this effect
  • Anectdotal evidence of bowel anastomosis disruption with neostigmine, but has never been verified experimentally
67
Q

Basics of acute pancreatitis

A
  • Associated with ETOH abuse and gallstones
  • Pancreas begins to autosuggest itself
  • Hallmark is increased serum amylase
  • Ileus often develops
  • Hyperglycemia (d/t decreased insulin production)
  • Hypocalcemia with tetany
  • Pleural effusions and ascites with dyspnea
  • Fever and shock (50%) - some DIC
  • ARDS (20%)
  • Renal failure (25%)
68
Q

The hallmark of pancreatitis is increased serum

A

Amylase

69
Q

Considerations for acute pancreatitis

A
  • AGGRESSIVE fluid administration (up to 10 L!!!)
  • NPO to rest the pancreas is now bing rethought. If pt is on tube feeds, ask when they were turned off.
  • Opioids for severe pain
  • ERCP within the first 24-72 hours to remove gallstones
70
Q

Considerations for Crohn’s disease

A
  • Dehydrated malnourished
  • Loss of fluid and nutrients through fistula
  • Often very ill and on steroids and immunosuppressive therapy
71
Q

Ulcerative Colitis consdierations

A
  • Fluid and electrolyte imbalances
  • B12 and folate deficiencies
  • Assess for arthritis, iritis, and hepatitis
  • Often present to OR for removal of precancerous lesions, hemorrhage, bowel perf, bowel obstruction, or toxic megacolon.
  • May be extensive surgeries for total colectomy or proctocolectomy
  • Often on steroids and immunosuppressants
72
Q

Carcinoid tumors are derived from ___ cells

A

Enterochromaffin cells

– can be found in any tissue derived from endoderm (from the esophagus to the rectum)

73
Q

Most frequent site for carcinoid tumor is

A

Appendix. BUT, tumors at this spot rarely metastasize or produce carcinoid syndrome.

74
Q

Carcinoid tumors from this region have the highest incidence of mets

A

Ileocecal region

75
Q

S/S of carcinoid tumors

A
  • Usually asymptomatic, but may have vague symptoms like abdominal pain, diarrhea, intestinal obstruction, or GIB
  • Most symptoms are related to hormones secreted into the GI tract and systemic circulation
  • Non-metastatic tumors secrete things that enter the portal vein and are destroyed by liver. Mets may cause systemic release of things.
76
Q

What do carcinoid tumors secrete?

A 
- LARGE AMOUNT OF SEROTONIN
  (platelet serotonin and metabolite 5-HIAA)
- Histamine
- Substance P
- Catecholamines
- Bradykinin
- Tachykinin
- Motilin
- Corticotropin
- Prostaglandins
- Kallikrein
77
Q

Carcinoid Syndrome

A
  • Only 7-20% of those with carcinoid tumor actually get carcinoid syndrome –> usually d/t liver or lung mets
  • Specific symptoms depend on tumor location and what exactly is being secreted

1) Cutaneous flushing of head, neck, and upper thorax
- Kinins and histamine

2) Bronchoconstriction
- 5HT
- Bradykinin
- Supstance P

3) Hyperglycemia
- 5HT

4) Hypotension
- Kinins or histamine (same as flushing)

5) HTN
- 5HT

6) Diarrhea
- 5HT and prostaglandins

7) Carcinoid heart disease
- 5HT

Takehome –> is that serotonin causes a lot of shit

78
Q

Carcinoid heart disease

A
  • 60% of pts with carcinoid syndrome will get this
  • See flushing, diarrhea, and cardiac dysfunction
  • Usually R sided heart failure
  • Intramyocardial mets and arrhythmias also seen
79
Q

Pre-op management of carcinoid tumor patients

A
  • Surgical excision is most effective tx
  • Octreotide
  • Anxiolytics
  • H1 and 2 antagonists
  • Nebulized ipratropium bromide
  • Steroids
  • BG monitoring (insulin gatt if needed)
  • A-line needed 2/2 rapid hemodynamic changes from tumor manipulation
  • Consider CVP, PAC, or TEE in carcinoid heart disease
80
Q

Anesthetic Management of carcinoid heart disease

A
  • Prevent carcinoid crisis with vasoactive and bronchoconstrictive conseuences
  • Get the patient DEEP for DVL and intubation
  • Avoid histamine releasing drugs (Sux, TPL, morphine, meperidine)
  • Any VA is ok
  • Epidural over spinal (to avoid hypotension)
  • Zofran is great choice (5HT antagonist)
  • Treat hypotension with fluids and octreotide (if this doesn’t work, vasopressin is next step)
  • Aprotinin (kallikrein inhibitor) is second line for hypotension
  • Treat HTN with labetalol or VA
  • Avoid drugs known to precipitate a crisis
81
Q

Octreotide dosing in carcinoid syndrome

A

Preventatie infusion = 50-100mcg/hr

For acute carcinoid crisis = 25-100 mug IVP

82
Q

Drugs known to precipitate carcinoid crisis

A

Histamine, Epi, NE, DA, and ephedrine

83
Q

Post-op carcinoid management

A
  • Residual tumor can still release things in emotional or physical stress

1) Effective analgesia
2) Invasive hemodynamic monitoring
3) Continue octreotide

Advanced Anesthesia III (6 decks)

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