CHAPTER 48. Bariatric Care
Kim A. Noble
OBJECTIVES
At the conclusion of this chapter, the reader will be able to:
1. Describe the normal anatomy and physiology of the gastrointestinal (GI) tract.
2. Describe the incidence and physiological impact of obesity.
3. Compare and contrast surgical options for weight loss with bariatric surgery.
4. Describe important considerations for patient selection for bariatric surgery.
5. List the potential complications and their physiological rationale(s) for bariatric surgery.
6. Describe the implications for the perianesthesia care of the bariatric surgical patient.
I. OVERVIEW
A. Parallel to the pandemic occurrence of obesity is the incidence of bariatric surgery (Table 48-1).
| Country | No. of Bariatric Procedures | No. of Bariatric Surgeons | Year Bariatrics Began |
|---|---|---|---|
| Argentina | 200 | 30 | 1988 |
| Australia (New Zealand) | 2750 | 68 | 1960 |
| Austria | 1396 | 38 | 1973 |
| Belgium | 6000 | 200 | 1970 |
| Brazil | 4000 | 510 | 1973 |
| Czech Republic | 400 | 6 | 1983 |
| Egypt | 2750 | 12 | 1996 |
| France | 12,000 | 200 | 1984 |
| Germany | 1100 | 54 | 1975 |
| Greece | 500 | 8 | 1978 |
| Hungary | 30 | 1 | 1999 |
| Israel | 1000 | 50 | 1978 |
| Italy | 3000 | 200 | 1973 |
| Japan | 20 | 20 | 1982 |
| Mexico | 2500 | 200 | 1971 |
| Netherlands | 800 | 40 | 1973 |
| Panama | 60 | 5 | 2002 |
| Poland | 145 | 14 | 1974 |
| Russia | 350 | 35 | 1969 |
| Spain | 2000 | 160 | 1977 |
| Sweden | 600 | 20 | 1970 |
| Switzerland | 800 | 90 | 1970 |
| Turkey | 150 | 5 | 1990 |
| Ukraine | 150 | 10 | 1978 |
| United Kingdom | 600 | 13 | 1955 |
| USA/Canada | 103,000 | 850 | 1953 |
| Totals | 146,301 | 2,839 |
B. Obesity is defined as a body mass index (BMI) >30.
1. Associated with an increased comorbidity risk (Box 48-1)
BOX 48-1
COMORBIDITY ASSOCIATED WITH BMI >25
Cardiovascular Comorbidity
Hypertension
Dyslipidemia
Coronary artery disease
Atherosclerosis
Angina
Sudden cardiac death
Congestive heart failure
Endocrine Comorbidity
Type 2 diabetes
Insulin resistance
Glucose intolerance
Neurological Comorbidity
Stroke
Gastrointestinal Comorbidity
Cholecystitis
Cholelithiasis
Gastroesophageal reflux disease
Respiratory Comorbidity
Obstructive sleep apnea
Asthma
Musculoskeletal Comorbidity
Osteoarthritis
Gout
Reproductive Comorbidity
Complications of pregnancy
Poor female reproductive health
Endometrial, breast, prostate cancers
Urological Comorbidity
Stress incontinence
Bladder infection
Renal calculi
Miscellaneous Comorbidity
Colon cancer
Depression
Eating disorders
Distorted body image
BMI, Body mass index.
2. Approximately 30% of the adult population in the United States and more than 300 million people worldwide considered obese
a. Crosses all demographic classifications
C. Morbid obesity is approximately twice ideal body weight with BMI >40.
D. Bariatric surgery has been shown to be the best weight loss option for obese patients.
E. Caring for patients undergoing bariatric surgery is challenging because they frequently have derangements leading to challenges for their perianesthetic management.
1. Respiratory
2. Metabolic
3. Endocrine
F. A comprehensive understanding of bariatric surgery and the physiological challenges of caring for obese patients can lead to potential surgical complication:
1. Prevention
2. Earlier identification
3. Treatment
II. ANATOMY AND PHYSIOLOGY OF DIGESTION AND ABSORPTION
A. Stomach
1. Gastric anatomy (Figure 48-1)
a. Pouchlike reservoir for ingested food located in the upper abdomen
b. Has three anatomic areas
(1) Fundus
(a) The upper arching area immediately distal to the cardiac sphincter
(b) Location of the gastric crypts containing secretory cells
(c) Responsible for the chemical digestion of ingested food
(d) Primary area for the accommodation of the ingested meal
(2) Body
(a) Central, thick walled muscular central area of the stomach
(b) Responsible for the mechanical digestion of ingested food
(3) Antrum
(a) Funnel-like portion of the stomach between the body and pyloric sphincter
c. Contains two sphincters
(1) Cardiac sphincter at the junction of the esophagus and stomach
(2) Pyloric sphincter at the junction of the stomach and duodenum
d. Gastric wall structure
(1) Has four layers consistent with entire GI tract
(a) Gastric mucosal layer
(i) Innermost layer
[a] Made up of epithelial cells that produce the mucous barrier
[b] Rapid cellular turnover; complete replacement every 4 to 5 days
(ii) Provides protective mucous barrier
[a] A prostaglandin grid work containing mucus and bicarbonate
[b] Protects gastric cells from acid digestion and provides lubrication
(b) Gastric submucosal layer
(i) Connective tissue
(ii) Contains blood vessels, nerves, and secretory structures
(c) Gastric muscular layer
(i) Thick muscular layer arranged in longitudinal, circular, and oblique direction
(ii) Provides grinding contractions involved in the mechanical digestion
(d) Gastric serosal layer
(i) Outermost protective layer continuous with the lesser omentum
(ii) Made up of fibrous connective tissue
e. High degree of gastric accommodation (enlargement) with ingested meals
(1) Empty stomach contains approximately 50 mL of acid with a significantly low pH.
(2) Stomach can expand to almost 1000 mL without an increase in intraluminal pressure.
 |
| FIGURE 48-1 ▪ Stomach. (From McCance KL, Huether SE: Pathophysiology: The biologic basis for diseases in adults and children, ed 5, St Louis, 2006, Mosby.) |
2. Gastric physiology
a. Stomach receives ingested food from the esophagus via the cardiac sphincter.
b. Chemical digestion begins in the stomach.
(1) Gastric acid secretion amounts to 2 L of fluid daily.
(a) Control of gastric acid secretion
(i) Endocrine secretion: blood-borne hormonal control of acid secretion
[a] GI tract is the largest endocrine organ in the body.
[b] Direct hydrochloric acid (HCl) release occurs when gastrin is released by:
[1] Parasympathetic nervous system
[2] Presence of alcohol
[3] Calcium-containing foods
[4] Protein in the stomach
[c] Secretin released from duodenum upon entry of chyme with pH <4.5, causes the release of large amounts of bicarbonate and water from the pancreas and liver into the common bile duct (CBD), and enters the duodenum via the sphincter of Oddi
[d] Cholecystokinin released from duodenum upon entry of protein and fat, leading to the release of pancreatic enzymes via the CBD and contraction of the gallbladder, leading to emptying of bile into the CBD and duodenum via the sphincter of Oddi.
(ii) Paracrine secretion: local control of acid secretion
[a] Histamine secretion from cells adjacent to parietal cells (local) stimulated by the endocrine release of gastrin. Histamine causes:
[1] Parietal cell stimulation
[2] Increased release of HCl
[b] Somatostatin released locally during times of fasting (decreasing pH) and leads to inhibition of gastrin and HCl release from the parietal cells
(b) Structures responsible for chemical digestion in the stomach
(i) Parietal cells
[a] Approximately 1 billion parietal cells located in the fundus
[b] Produce HCl
[c] Produce intrinsic factor necessary for vitamin B 12 absorption
(ii) Chief cells
[a] Produce pepsinogen, an inactive substance
[b] Rapidly converted to pepsin in an acidic environment
[c] Pepsin chemically digests protein.
(iii) Gastric lipase enzymatically degrades dietary fats into fatty acids.
(2) Chemical digestion is the process of chemically dividing food items into smaller parts.
(a) Starch and fibers degraded by gastric acid
(b) Protein degraded into small particle through the action of pepsin
(c) Fats delivered to the small intestine in a nondigested state
(3) Combination of the food derivative and gastric secretions called chyme
c. Mechanical digestion begins in the mouth (teeth) and continues in the stomach.
(1) Mechanical digestion (gastric motility) grinds food into chemically digestible particles.
(2) Gastric motility
(a) Peristaltic mixing and churning contractions begin in the body of the stomach and move toward the antrum, propelling the chyme toward the antrum.
(b) Large particles return to the body of the stomach for additional mechanical digestion.
(c) Opening of the pylorus and gastric empting into the duodenum is regulated by:
(i) pH of the chyme: pH is sensed by receptors on the duodenal wall, and a low pH delays gastric empting, allowing time for buffered secretions from the liver and pancreas to normalize pH before movement into the portal circulation.
(ii) Fat content of the chyme: fat delays gastric empting.
(iii) Osmolarity of the chyme: either hyperosmotic (caloric-dense foods or high protein content) or hypoosmotic chyme will delay gastric empting.
(iv) Volume of chyme in the stomach: an increase in the volume and gastric intraluminal pressure will accelerate empting.
(d) With each peristaltic contraction, a small amount of digested chyme is propelled through the pyloric sphincter.
(3) Neural control of gastric motility
(a) Enteric nervous system
(i) Local neural control in the muscular layer of the wall of GI tract
[a] Responsible for muscular contraction along the length of GI tract
(b) Autonomic nervous control of gastric motility
(i) Sympathetic nervous system stimulation
[a] Directly decreases GI motility and secretion
(ii) Parasympathetic nervous system stimulation
[a] Directly increases motility and acid secretion
(c) Endocrine control of gastric motility
(i) Gastric inhibitory peptide is released from the duodenal mucosa in response to increased concentration of glucose and/or fat in the duodenum; this causes the inhibition of
[a] Gastric acid secretion
[b] Gastric motility
[c] Gastric emptying
B. Small intestine (Figure 48-2)
1. Anatomy
a. Contains same layers as found in the stomach; anatomical variation in layers based on function
b. Muscle fibers thin compared with gastric muscle and have a longitudinal and circular arrangement allowing for coordinated peristalsis
c. Small intestine has plica, or wrinkles, that slow chyme movement to allow additional time for absorption.
(1) Plica are most numerous in:
(a) Jejunum
(b) Ileum
d. Small intestine consists of three segments:
(1) Duodenum
(a) U-shaped connection with the pylorus; entry into the small intestine
(b) Approximately 22 cm (10 inches) long
(c) Entry point for CBD via sphincter of Oddi
(i) Entry point for pancreatic enzymes and bicarbonate from the pancreas and liver after the endocrine release of secretin
(ii) Entry point for bile stored in the gallbladder after the endocrine release of cholecystokinin
(d) Large surface area for absorption related to villi and microvilli; projections of enterocyte-covered portal capillaries
(i) Villi and microvilli decrease the distance required for the diffusion of nutrients from the GI lumen into the portal blood supply, increasing absorption.
(2) Jejunum
(a) Together with the ileum approximately 7 m (23 feet) long
(b) No clear separation from duodenum or ileum
(3) Ileum
(a) Terminates into the large intestine
(b) Separated from the large intestine by the ileocecal valve
(c) Location of the appendix
2. Physiology
a. Chyme propelled through the pylorus as a liquid containing small, undigested food particles
b. Chemical digestion continues in the segments of the small intestine.
(1) Carbohydrates break down into disaccharides and monosaccharides (single sugars).
(2) Protein breaks down into amino acids and peptides.
(3) Fats emulsified into monoglycerides and fatty acids
c. Digestive role of small intestine
(1) Duodenum
(a) Digestive role for fat with entry of bile
(b) Protein digestive role with pancreatic enzymes, which activate due to acidic pH
(c) Continued digestion of carbohydrates through the secretion of digestive enzymes from the intestinal enterocytes
(d) Intestinal secretion amounts to approximately 4 L of fluid daily.
(2) Jejunum
(a) Additional intestinal length for digestion and absorption as needed
(3) Ileum
(a) Additional intestinal length for digestion and absorption as needed
d. Small intestine nutrient absorption based on anatomic location
(1) Duodenum
(a) Primary site of absorption of iron, calcium, sugars, and proteins
(b) Primary site of absorption of water and water-soluble vitamins
(c) Primary site of energy-dependent absorption of magnesium and sodium
(2) Jejunum
(a) Upper jejunum is the major site of absorption of:
(i) Bile salts
(ii) Fatty acids
(iii) Fat-soluble vitamins (A, D, E, K)
(b) Additional surface area for sugar and protein absorption
(3) Ileum
(a) Primary site for absorption of:
(i) Bile salts
(ii) Vitamin B 12 (intrinsic factor)
(iii) Chloride
e. Intestinal motility
(1) Stimulated by the arrival of chyme to mix secretions
(a) Pancreatic
(b) Gallbladder
(c) Hepatic
(2) Segmentation
(a) Produced by the contraction of circular muscle fibers
(b) More common in proximal small intestine (duodenum)
(c) Divides and mixes chyme and increases contact with absorptive surfaces
(3) Peristalsis
(a) Produced by the contraction of longitudinal muscle fibers
(b) Slow wave of contraction to propel chyme through the small intestine
 |
| FIGURE 48-2 ▪ Intestine. (From McCance KL, Huether SE: Pathophysiology: The biologic basis for diseases in adults and children, ed 5, St Louis, 2006, Mosby.) |
III. OBESITY
A. Overview
1. Obesity is a syndrome of increased percentage of body fat that is correlated with increased comorbidities and decreased life expectancy (see Box 48-1).
2. Definition of obesity
a. BMI in kilograms per meter squared (kg/m 2) (Table 48-2)
(1) A ratio of weight, adjusted for height, expressed as weight in kilograms (kg) divided by height in meters squared (m 2)
(2) Important to incorporate age- and gender-related differences, especially in children (Figure 48-3)
 |
| FIGURE 48-3 ▪ Sample growth chart for boys up to 36 months of age. (From the Centers for Disease Control and Prevention.) |
(3) Abdominal circumference should also be measured, since athletes with increased muscle mass would have high BMI without obesity.
| BMI | 19 | 20 | 21 | 22 | 23 | 24 | 25 | 26 | 27 | 28 | 29 | 30 | 31 | 32 | 33 | 34 | 35 |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Height (inches) | Body Weight (lb) | ||||||||||||||||
| 58 | 91 | 96 | 100 | 105 | 110 | 115 | 119 | 124 | 129 | 134 | 138 | 143 | 148 | 153 | 158 | 162 | 167 |
| 59 | 94 | 99 | 104 | 109 | 114 | 119 | 124 | 128 | 133 | 138 | 143 | 148 | 153 | 158 | 163 | 168 | 173 |
| 60 | 97 | 102 | 107 | 112 | 118 | 123 | 128 | 133 | 138 | 143 | 148 | 153 | 158 | 163 | 168 | 174 | 179 |
| 61 | 100 | 106 | 111 | 116 | 122 | 127 | 132 | 137 | 143 | 148 | 153 | 158 | 164 | 169 | 174 | 180 | 185 |
| 62 | 104 | 109 | 115 | 120 | 126 | 131 | 136 | 142 | 147 | 153 | 158 | 164 | 169 | 175 | 180 | 186 | 191 |
| 63 | 107 | 113 | 118 | 124 | 130 | 135 | 141 | 146 | 152 | 158 | 163 | 169 | 175 | 180 | 186 | 191 | 197 |
| 64 | 110 | 116 | 122 | 128 | 134 | 140 | 145 | 151 | 157 | 163 | 169 | 174 | 180 | 186 | 192 | 197 | 204 |
| 65 | 114 | 120 | 126 | 132 | 138 | 144 | 150 | 156 | 162 | 168 | 174 | 180 | 186 | 192 | 198 | 204 | 210 |
| 66 | 118 | 124 | 130 | 136 | 142 | 148 | 155 | 161 | 167 | 173 | 179 | 186 | 192 | 198 | 204 | 210 | 216 |
| 67 | 121 | 127 | 134 | 140 | 146 | 153 | 159 | 166 | 172 | 178 | 185 | 191 | 198 | 204 | 211 | 217 | 223 |
| 68 | 125 | 131 | 138 | 144 | 151 | 158 | 164 | 171 | 177 | 184 | 190 | 197 | 203 | 210 | 216 | 223 | 230 |
| 69 | 128 | 135 | 142 | 149 | 155 | 162 | 169 | 176 | 182 | 189 | 196 | 203 | 209 | 216 | 223 | 230 | 236 |
| 70 | 132 | 139 | 146 | 153 | 160 | 167 | 174 | 181 | 188 | 195 | 202 | 209 | 216 | 222 | 229 | 236 | 243 |
| 71 | 136 | 143 | 150 | 157 | 165 | 172 | 179 | 186 | 193 | 200 | 208 | 215 | 222 | 229 | 236 | 243 | 250 |
| 72 | 140 | 147 | 154 | 162 | 169 | 177 | 184 | 191 | 199 | 206 | 213 | 221 | 228 | 235 | 242 | 250 | 258 |
| 73 | 144 | 151 | 159 | 166 | 174 | 182 | 189 | 197 | 204 | 212 | 219 | 227 | 235 | 242 | 250 | 257 | 265 |
| 74 | 148 | 155 | 163 | 171 | 179 | 186 | 194 | 202 | 210 | 218 | 225 | 233 | 241 | 249 | 256 | 264 | 272 |
| 75 | 152 | 160 | 168 | 176 | 184 | 192 | 200 | 208 | 216 | 224 | 232 | 240 | 248 | 256 | 264 | 272 | 279 |
| 76 | 156 | 164 | 172 | 180 | 189 | 197 | 205 | 213 | 221 | 230 | 238 | 246 | 254 | 263 | 271 | 279 | 287 |
B. Epidemiology
1. World Health Organization estimates 300 million people are obese worldwide.
2. Adult obesity
a. In the United States, the incidence of obesity nearly doubled over the past 25 years.
(1) 12.8% in 1962
(2) 22.5% in 1994
(3) 27% in 2000
b. Obesity at higher incidence in racial and ethnic minority populations (African Americans and Hispanic Americans) as compared with white ethnic groups
3. Childhood obesity
a. Reached when child’s weight exceeds the 95th percentile
b. Almost a 400% increase in incidence of obesity in children aged 6 to 11 years between 1963 and 2000 (from 4% to 15%)
c. For adolescents (12–19 years of age) during the same time frame (from 1963 to 2000), incidence increased 300% (from 5% to 15%)
C. Pathophysiology
1. Overview
a. Obesity is complex and multifactorial in nature.
b. Obesity follows a positive energy balance, where energy expenditure exceeds energy output.
c. Obesity carries a strong genetic predisposition with a familial pattern for excess weight.
2. Theory of ectopic fat deposition
a. When adipose tissue can no longer expand to store excess calories, fat is deposited in body tissues.
(1) Liver
(2) Skeletal muscle
(3) Pancreas
(4) Heart
b. Excess circulating fatty acids promote insulin resistance and type 2 diabetes mellitus.
c. Adipose tissue is an endocrine tissue and secretes:
(1) Hormones
(2) Inflammatory substances
3. Comorbidities of obesity affect virtually every organ system (see Box 48-1).
Get Clinical Tree app for offline access
a. Hypertension
(1) Approximately 50% of obese individuals (BMI >30 kg/m 2) have hypertension.
(2) Hypertension is seen in overweight individuals across all demographics.
(3) Hypertension is a primary risk factor for the development of atherosclerosis.
(4) Surgical treatment of obesity improves both hypertension and cardiac function.
b. Dyslipidemia
(1) Forty percent to 50% of obese individuals have dyslipidemia with:
(a) Increased low-density lipoprotein (LDL: “bad cholesterol”)
(b) Decreased high-density lipoprotein (HDL: “good cholesterol”)
(2) Hyperlipidemia is a primary risk factor for the development of atherosclerosis.
(3) Gastric bypass has been shown to be very effective in:
(a) Lowering triglycerides and LDL
(b) Increasing HDL
c. Diabetes and impaired glucose tolerance
(1) Obesity is the primary risk factor for diabetes and 90% of type 2 diabetics are obese.
(2) Thirty-six percent of individuals with impaired glucose tolerance will progress to type 2 diabetes within 10 years.
(3) Diabetes is a risk factor for the development of:
(a) Atherosclerosis
(b) Vascular disease
(c) Obesity
(d) Combined risk factors predict lethal health consequences.
(4) Weight loss in obese type 2 diabetic patients can restore blood glucose and insulin sensitivity to near-normal levels.
d. Cardiac and peripheral vascular disease
(1) Obesity is a primary risk factor for the development of atherosclerotic cardiac and peripheral vascular disease.
(2) Obesity leads to large vessel disease.
(a) Coronary artery disease
(b) Cerebrovascular accident
(c) Carotid occlusive disease
(d) Subclavian steal syndrome
(e) Aneurysmal disease
(f) Vascular occlusive disease
(g) Vascular insufficiency
(3) Obesity and diabetes lead to small vessel disease.
(a) Retinopathy
(b) Nephropathy
e. Obstructive sleep apnea (OSA)
(1) Approximately 50% of obese individuals have OSA, with increased abdominal girth the single most important risk factor for OSA.
(2) Diagnosis of OSA is made when there are the following three findings:
(a) Individuals have breathing cessation exceeding 10 seconds during sleep.
(b) Apneic episodes occur more than five times per hour.
(c) Apneic episodes have a concurrent 4% decrease in oxygen saturation.
(3) Nocturnal OSA has been associated with cardiac dysrhythmias and sudden cardiac death.
(4) OSA may carry over into the daylight hours, leading to:
(a) Drowsiness
(b) Inattentiveness
(c) Impaired job performance
(d) Decrease in cognitive functioning
(5) OSA is categorized as:
(a) Central
(b) Oropharyngeal obstructive
(c) Combined form
(6) Marked weight loss (secondary to bariatric surgery) has been nearly 100% effective in managing OSA.
f. Asthma
(1) Asthma is a prevalent comorbidity for obesity, thought to be due to decreased lung volumes (from increased abdominal girth) sensitizing the airway and leading to reactive airways.
(2) The following contribute to asthma:
(a) OSA
(b) Respiratory stasis
(c) Gastroesophageal reflux disease (GERD)
(3) Obese children have three times greater risk for asthma (30%).
(4) Obese adults have a 25% increased risk for the development of asthma.
g. Obesity hypoventilation syndrome (OHS) or Pickwickian syndrome
(1) OHS present in 30% of patients with morbid obesity, but less common than OSA
(2) OHS caused by decreased lung volumes (increased abdominal pressure), which causes:
(a) Chronic shortness of breath
(b) Decreased expiratory reserve volume
(c) Increased oxygen consumption
(d) Increased circulating partial pressure of carbon dioxide (P co2)
(3) Long-term effects of obesity are:
(a) Pulmonary hypertension
(b) Right-sided heart failure
(c) Polycythemia
(d) Ultimately death
(4) The following is seen after bariatric surgery:
(a) Marked improvement in symptoms associated with pulmonary hypertension
(b) Improved blood oxygenation
(c) Reduced hypercarbia
h. Peripheral osteoarthritis
(1) Weight-bearing destruction (osteoarthritis) found at an accelerated rate in the obese patient’s:
(a) Knees
(b) Hips
(c) Ankles
(d) Feet
(2) Obesity increases the necessity of surgical intervention.
i. Gastroesophageal Reflux Disease (GERD)
(1) GERD is a relatively common finding in the general population.
(a) Incidence in general population: 20%
(b) Incidence in obese patients: up to 50%
(2) GERD is the retrograde movement of acidic chyme into the esophagus, leading to a chronic inflammation and the potential for precancerous lesions (Barrett esophagus).
(3) Correlation of GERD and obesity most probably related to increased abdominal pressure
j. Back and disk disease
(1) Chronic lower back pain is the most common orthopedic complaint of obese persons.
(2) With increasing age, the incidence of lower back pain in obese individuals is 100%.
(3) Decreased mobility and the use of assistive devices are common findings with obesity.
k. Nonalcoholic steatohepatitis (NASH)
(1) Fatty infiltration of the liver, or NASH, present in 100% of the morbidly obese population
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree