Section: UGI Sub-section: Bariatrics Curriculum: Curriculum, page 83
Definition
- Abnormal or excessive fat accumulation that presents a risk to health
Incidence
- Global epidemic with numbers increasing over time
- NZ (2006-2007)
- Adults
- 30% Obese (50% Māori, 70% PI, 10% Asian)
- Children
- 20% Overweight, 10% Obese
- Adults
- Causes more deaths/ year than Breast & Colorectal Cancer combined
- After tobacco use, second leading cause of preventable death
- Second most common cause of preventable cancers
- Leading cause of mortality in obese pts
- Morbid obesity is associated with a decreased life expectancy
- 4yrs (F) and 7yrs (M)
- Males have a tendency for abdominal fat distribution
- Females → Gluteal / peripheral
Measures of Obesity
- BMI
- Generally accepted measure of degree of overweight
- Easy, reliable and reproducible
- Correlates well to % body fat and body fat mass
- Better estimate of body fat than weight alone
- Beware
- May overestimate degree of adiposity in highly muscular individuals
- May underestimate adiposity in aging with loss of muscle mass
- BMI classification categories are based on risk of cardiovascular disease
- Different cut offs for different ethnicities, and have higher/lower cardiac risk at same BMI
WHO classification
| Category | BMI (kg/m2) |
|---|---|
| Underweight | < 18.5 |
| Normal weight | 18.5 – 24.9 |
| Overweight | 25.0 – 29.9 |
| Obese (Class I) | 30.0 – 34.9 |
| Obese (Class II) | 35.0 – 39.9 |
| Obese (Class III) | ≥ 40.0 |
- Waist Circumference
- Measurement with flexible tape placed on horizontal plane at the level of the iliac crest
- At the end of normal expiration
- Assessment of abdominal obesity
- Indicative of cardio/metabolic risk
- Utility lies in the BMI 25-35 range
- Above this, almost guaranteed to have waist circumference over cut-off
- Abnormal
- ≥ 102cm males
- ≥ 88cm females
- Provides independent risk information that is not accounted for by BMI
- Increased risk for
- Heart disease
- Diabetes
- HTN
- Dyslipidaemia
- NASH
- Mortality
Aetiology
- Regulation of energy homeostasis is complex and multifactorial
- Related to multiple genetic and environmental factors
- Increase in body fat requires:
- Energy intake to be increased over energy expenditure, for an extended period
- However, feedback mechanisms between energy intake and expenditure
- Weight gain promotes increased expenditure
- Weight loss associated with decreased expenditure
- Mechanism to defend against further weight loss, body “defends its fat”
- Environmental factors
- Sedentary lifestyle
- Cheap calorie dense foods
- Genetic + Hormonal control
- Lack of satiety
- ? Leptin resistance, ? Reduced Leptin production
- Ghrelin + CCK involved in increased hunger (fundus and prox small bowel)
- GLP-1 and Peptide YY induce satiety
- Incompletely understood genetic factors
- ↓ Thermogenic response to meals
- ? Abnormally high set point for body weight
- Lack of satiety
- Central melanocortin system plays a role
- Gene mutation MC4R
Pathophysiology of Gut Hormones and Obesity
Excess body weight arises from a complex interplay of signals within the gut-brain-endocrine axis, leading to a chronic imbalance between energy intake and expenditure. Contributing factors include:
- Genetic: Inherited traits influencing appetite regulation, metabolism, and fat storage
- Environmental: Availability of energy-dense foods, reduced physical activity, and sedentary lifestyle
- Sociocultural: Dietary habits, socioeconomic status, and cultural attitudes towards food and body weight
- Inflammatory: Adipose tissue, particularly in obesity, secretes pro-inflammatory adipokines (e.g. TNF-α, IL-6) and leptin in proportion to fat mass, leading to chronic low-grade inflammation and leptin resistance
- Metabolic: Inflammation-induced impairment of insulin signalling results in insulin resistance and other metabolic complications (e.g. dyslipidaemia, type 2 diabetes)
- Endothelial dysfunction: Chronic inflammation and insulin resistance contribute to impaired endothelial function, increasing cardiovascular risk
- Gut hormone dysregulation: Increased levels of orexigenic hormones such as ghrelin and neuropeptide Y (NPY) enhance hunger and food intake, while reduced levels or resistance to anorexigenic hormones like GLP-1 and CCK impair satiety and delay gastric emptying
Ghrelin
- “Hunger hormone”
- Produced by enteroendocrine cells
- Mostly stomach (fundus) and duodenum
- Also in jejunum, lungs, islet cells, adrenal, placenta, kidney
- Receptor
- Growth Hormone Secretagogue Type 1a receptor (GHS-R)
- Hence name GHRelin
- Action
- Stimulates food intake (number of meals) and motivation to find meals
- Activates cells in Anterior Pituitary, and Arcuate Nucleus (Hypothalamus)
- Activate Growth Hormone and Neuropeptide-Y
- Increases body weight and fat mass
- Activates cells in Anterior Pituitary, and Arcuate Nucleus (Hypothalamus)
- Decreases sensitivity of Vagal afferents
- Less sensitive to Gastric Distension
- Increases motility and gastric acid secretion
- Regulates reward cognition, learning and memory, sleep/wake cycle, glucose metabolism
- Stimulates food intake (number of meals) and motivation to find meals
- Blood levels of Ghrelin highest pre-meals, low post meals
- NB: Ghrelin levels in obese individuals is low
- Higher in lean individuals
- Highest in those with anorexia nervosa, and cancer-induced cachexia
- Ghrelin may not be a driver for obesity (Except Prader-Willi syndrome)
- Sleeve gastrectomy will decrease plasma Ghrelin levels by 60%
- Unclear evidence to say if ghrelin returns to normal levels over time
Leptin
- Produced by adipose cells and small intestine enterocytes
- Regulates energy balance by inhibiting hunger
- Decreased fat storage in adipocytes
- Works on receptors in the Arcuate Nucleus, and other locations in the Hypothalamus
- Obese individuals have a decreased sensitivity to Leptin
- Leads to decreased satiety despite high energy stores and high levels of Leptin
- Similar to insulin resistance in T2DM
Glucagon-Like Peptide-1 (GLP-1)
- Produced by enteroendocrine L-cells
- Main action - Acts as an incretin
- Decreases BSL
- Glucose-dependent increased insulin secretion
- NB: Preserved in T2DM
- Decreases BSL
- GLP-1 receptors on Brainstem & Hypothalamus
- Promotes satiety
- GLP-1 Receptors in the stomach
- Decreased gastric emptying and motility
- Decreased acid secretion
Cholecystokinin (CCK)
- Peptide hormone secreted by enteroendocrine I-Cells in Duodenum + Jejunum
- Released rapidly in response to a meal
- Fatty acids and amine acids in chyme entering duodenum
- Actions
- Stimulates digestion of fat and protein
- Stimulates pancreatic acinar cells
- Release of digestive enzymes
- Increases hepatic bile production Stimulates gallbladder contraction and Sphincter of Oddi relaxation
- Decreases gastric emptying
- Via CNS, and Vagal stimulation
- Proposed mechanism for hunger suppression
- Essentially opposes the Ghrelin action on Vagus
Peptide YY (P-YY)
- Short amino acid released from Ileum and colonic cells in response to feeding
- Acts to reduce appetite
- Anorexigenic
- Inhibits gastric motility and emptying
- Increases water and electrolyte absorption in the colon
- May also inhibit pancreatic secretion
- May be used as alternative to Leptin for weight loss
- Don’t get the same resistance in obese people as you do for Leptin
Associated Co-morbidities
- NASH, Hyperlipidaemia
- DVT – hypercoagulability
- Venous stasis – ulcers
- Hormone imbalance → Dysmenorrhoea, Hirsutism, Infertility, PCOS
- Gallstones
- If present consider cholecystectomy during bariatric surgery
- If absent consider ursodeoxycholic acid treatment for 6 months post-op
- Cardiac - CM, Right HF, Pulmonary HTN
- Cancer
- Psychosocial
- Metabolic Syndrome
Hepatic steatosis
- NAFLD/MASLD
- Presence of hepatic steatosis in the absence of causes of secondary hepatic fat accumulation
- E.g Heavy EtOH
- NASH/MASH
- Hepatic steatosis with associated hepatocyte ballooning degeneration and hepatic inflammation
- Can have features of cirrhosis
- Histologically indistinguishable from EtOH cirrhosis
- Incidence high in bariatric patients
- 37% NASH, 1-7% Cirrhosis
- Bariatric surgery can potentially reverse
- But some at risk of decompensated liver failure
Association With Cancer
- Excess weight associated with increased risk of multiple cancers
- Estimated cause of up to 40% of cancers
- Can also increase the risk of dying from cancer
- Strong evidence supporting link with:
- Endometrial
- Renal
- Oesophageal and Gastric (cardia)
- Colon and Rectum
- Biliary
- Pancreas
- Breast
- Ovarian
- Multiple Myeloma
- HCC
Metabolic Syndrome
- Cluster of multiple medical conditions that may increase risk of cardiovascular disease or developing diabetes
- Need 3/5 of
- Abdominal obesity
- Hypertension
- Hyperglycaemia
- Impaired hepatic insulin uptake, systemic hyperinsulinaemia, and tissue resistance to insulin
- Hypertriglyceridaemia
- Low HDL
- Thought linked to impaired hepatic glucose uptake
- Associated with PCOS, OSA etc.
Classification of Obesity
- Uses BMI
- Based on ranges of cardiovascular risk
Management of Obesity
Goals of Treatment
- Prevent, treat, or reverse complications of obesity AND…
- Increase quality of life
- Health benefits reported with as little as 5% of TBW
- Expected benefits
- Lifestyle measures: 5-7% TBW
- Often difficult to maintain
- Pharmacologic: 5-10% TBW
- Bariatric surgery often needed if 30% TBW wanting to be lost
- Lifestyle measures: 5-7% TBW
Identifying Candidates for Therapy
- Assess patients
- Degree of overweight (BMI and waist circumference)
- Presence of CVS risk factors (HTN, DM, Hyperlipid)
- Other comorbidities (OSA, NAFLD etc)
- Little or no risk (BMI 20-25)
- Low Risk (BMI 25-29.9 without other CVS risk factors)
- Counsel on preventing weight gain, basic dietary advice
- Moderate Risk (BMI 25-29.9 with CVS risk factor, or 30-34.5)
- Offer intensive behavioural intervention
- Can consider pharmacologic therapy
- High Risk (BMI 35-40+, especially younger patients)
- Offer intensive behavioural therapy, pharmacologic therapy, and consider bariatric surgery
- In 2022, the American Society of Metabolic and Bariatric Surgery (ASMBS) and the International Federation for the Surgery of Obesity and Metabolic Disorders (IFSO) published the following guidelines
- Body mass index (BMI) ≥35 kg/m2 (Class 2 and higher) regardless of comorbidities
- BMI between 30.0 and 34.9 kg/m2 (Class 1) and type 2 diabetes
- BMI between 30.0 and 34.9 kg/m2 who cannot achieve substantial or sustainable weight loss or comorbidity improvement with nonsurgical weight loss methods.
- NICE guideline
- BMI 40+
- BMI 35+ with complications
- BMI 30+ with poorly controlled diabetes
Initial Treatment
- Comprehensive lifestyle intervention
- Dietary therapy
- Exercise
- Behaviour modification
- Programs that include the above:
- Self-management
- Individual case managers
- Group sessions
- Individualised adherence strategies
- Networks for feedback and clinical/emotional support
- Average TBW loss is approx. 4%
- Maintaining this weight loss is difficult
Dietary Therapy
- Many types of diets
- Balanced low calorie
- Low fat/low calorie
- Moderate fat/low calorie
- Low carbohydrate
- Mediterranean diet
- Diet adherence is important predictor of weight loss, regardless of type
- Should tailor diet to what pt will tolerate
- Focus on reducing intake below expenditure, not worrying about specific composition
- Should tailor diet to what pt will tolerate
- Most adults will lose weight if calorie intake <1000 kCal/day
- Severe caloric restriction may lose weight faster, but
- 400kCal vs 800 kCal showed no difference in weight loss
- Difficult to maintain very low cal diets
- Body adapts to starvation
-
800kCal/day recommended
- Severe caloric restriction may lose weight faster, but
- Need continued monitoring for progress
- If < 5% TBW loss at 6 months, try different approach
- Difficulty with diets is maintaining weight loss and the body’s adaptation to dieting
- Generally prevents dieting alone as being a viable long term strategy
Exercise
- Less potent than dietary restriction
- But physical activity is strong predictor of long term weight loss maintenance
- Aim is 30+mins, 5-7x days per week
- Prevents weight gain and improves CVS health
- Multicomponent program preferred
- Aerobic and resistance exercise
- Need to take into account
- Medical conditions
- Age
- Preferences for types of exercise
Behavior Modification
- Behavioural therapy/modification is cornerstone of obesity therapy
- Goal - Help patients make long term changes in eating behaviour by
- Modifying and monitoring food intake
- Modifying physical activity
- Controlling cues and environmental stimuli that trigger eating
Pharmacologic Management
- Consider in those with BMI > 30, or 27-30 with weight related comorbidities
- Who have not met weight loss goals with comprehensive lifestyle intervention
- Single agents preferred vs combination therapy
- Choice depends on preference, adverse effects, patient comorbidities, costs etc
- Liraglutide
- Usually first line
- Orlistat
- Often second line
- Phentermine
- Also widely prescribed option
Liraglutide (Saxenda)
- Glucagon-Like Peptide-1 Receptor Agonist
- Chemically modified version of human GLP-1
- Stimulate glucose dependent insulin secretion
- Inhibits Glucagon release
- Inhibits gastric emptying
- Usually given in higher doses than for diabetes
- 3mg daily, subcut daily injection, needs to be up titrated
- Expensive ($5000 per year)
- Good for glycaemic control and weight loss
- Significant reduction in weight (2-4kg) compared to placebo
- Reduces major cardiac disease events in pts with T2DM and pre-existing CVS disease
- Adverse Effects
- GI side effects – Nausea and vomiting due to decreased emptying
- Hypoglycaemia
- Less commonly – Pancreatitis, Gallstones, Renal Impairment
- NB: Association in rodents with Medullary Thyroid Ca
- Contraindications
- Pregnancy
- Personal or Fam Hx Medullary Thyroid Ca or MEN 2A/2B
Orlistat (Xenical)
- Lipase inhibitor
- 120mg PO TDS
- Alters fat digestion by inhibiting pancreatic lipases
- Not completely hydrolysed, faecal fat excretion increased
- Weight loss 5-10kg (cf placebo 3-6kg)
- Maintained for 24-36 months of treatment
- Improves BP in hypertensive patients
- Also serum lipid values
- Adverse Effects
- GI – Borborygmi, cramps, flatus (with discharge) (15-30%)
- Severe liver injury reported (13 cases in 40 million)
- Lowers fat soluble vitamins
- Renal injury – Oxalate stones related to malabsorption
- Contraindications
- Pregnancy, Chronic malabsorption, Cholestasis, Hx of Ca Oxalate stones
Phentermine (Reductil/Duramine)
- Sympathomimetic drugs
- Stimulates noradrenaline release or inhibits reuptake
- Can increase blood pressure
- Reduce food intake by causing early satiety (seratogenic effect)
- Structurally similar to amphetamines
- Most often prescribed weight loss drug in the US
- Good efficacy (7-8kg vs 1kg placebo)
- Only approved for short term use (12 weeks)
- Potential side effects, potential for abuse, etc.
- Adverse
- Tachycardia and hypertension
- Insomnia, dry mouth, constipation, nervousness
- Contraindications
- Coronary artery disease
- Uncontrolled hypertension
- Hyperthyroidism
- History of drug abuse
Other medications
- Contrave - naltrexone/buproprion
- Semaglutide (Ozempic) - in New Zealand, it is approved by Medsafe for the treatment of type 2 diabetes. It’s not approved for weight loss.
Pre-Surgical Considerations
- Indications for Offering Bariatric Surgery
- 18-65 years old
- BMI > 35 or
- BMI > 30 + Obesity-related complications
- Failed other measures with previous serious attempts at weight loss
- Pt well informed, compliant (understands post-op requirements) & motivated
- Commits to long term follow up
- Fit for anaesthesia
- Contraindications to Bariatric Surgery
- Untreated mental health disorder / drug & alcohol abuse
- Inability to comply with follow-up and vitamin replacement
- Prohibitive anaesthetic risk
- Unstable CAD
- Uncontrolled OSA + Pulmonary HTN
- Systolic pressure > 50mmHg
- Cancer within the last 2 years / Active Ca
- Portal HTN – Absolute
- Crohn’s – relative
- Connective tissue disease
- Prader-Willi Syndrome
- Concerns re: Pregnancy after bariatric surgery (due to nutritional deficiencies)
- Should wait 2 yrs Post-op
Pre-operative Workup
- Always an MDT approach
- Dietician, psychiatrist, physician, surgeon, nurse educator, anaesthetist, GP
- History and Exam
- Cardiovascular testing
- Pulmonary assessment
- Consider endocrine testing if Cushing’s/Hypothyroid suspected
- USS of Gallbladder
- Endoscopy – probably not routine, do if symptomatic
MDT Involvement
- Dietician
- Assess nutritional status and aid in patient education about what to expect after surgery:
- Up to 1/3 may have variable difficulty with eating
- May result in regular vomiting or regurgitation of some food & limitation of the type of food
- Small no. on pureed food for life
- Will probably need to avoid bread, rice, pasta, red meat initially
- Reduced alcohol tolerance
- Bypass – B12, Iron, Folate
- Monthly injection of B12
- Use the gluconate form of iron as better absorbed in non-acid environment
- Multivites for all
- Calcium 2g/ day and possibly vitamin D
- For malabsorptive think about fat soluble vitamins
- Assess nutritional status and aid in patient education about what to expect after surgery:
- Psychologist
- High prevalence of depression, anxiety, binge eating, night eating syndrome, PTSD, body dysmorphic disorder
- 50% on psychotropic medications
- Assess readiness for change
- Realistic expectations
- Surgeon
- Exercise physiologist/trainer
- Anaesthetist
- Nurse educator
- GP
History and Exam
- Obesity history
- Duration
- What attempts at weight loss
- Implications of obesity on life
- Hx of cardio/resp function
- PMHx
- ? Obesity related comorbidities
- ? Previous surgery
Cardiovascular Testing
- Simple – Exercise tolerance
- Walk 4 blocks or up 2 flights of stairs
- CPEX if borderline
- If symptomatic consider dobutamine stress ECHO and further cardiac workup
- Usually guided by anaesthetist
Pulmonary Assessment
- Look for OSA
- Routine pre-op sleep questionnaire
- +/- Sleep study
- May need pre-op CPAP
- Reduce hypercarbia, hypoxemia & pulmonary artery vasoconstriction
- May be a significant cause of mortality
- Apnoea → Hypoxemia → Sympathetic discharge → Lethal arrhythmias
- Reactive asthma
- Obesity Hypoventilation Syndrome (Pickwickian Syndrome)
- Awake alveolar hypoventilation, with daytime hypercapnoea as a result of diminished respiratory drive and capacity, related to obesity
- Super-obese
- May appear cyanotic
- PaCO2 > PaO2
- Book to ICU
- Awake alveolar hypoventilation, with daytime hypercapnoea as a result of diminished respiratory drive and capacity, related to obesity
Gallbladder USS
- Not routinely recommended
- If has gallstones, could consider taking out gallbladder at same time
- Esp. if duodenal switch or RYGB
- Recognised that weight loss predisposes to gallstones
- Incidence post-bypass = 30%
- Some surgeons say take GB if doing malabsorptive procedure but not needed if doing restrictive
- Treating with Ursodeoxycholic acid post-operative may reduce stone formation
- Ursodiol 300mg po BD
Gastroscopy
- Recommended
- Mandatory if symptoms, reflux etc
- Main reason is if significant Barrett’s present, then would recommend against a sleeve and towards RYGB
Planning/Interventions to Prevent Peri-operative Risk
- Obesity Surgery Mortality Risk Score
- Optifast
- Glycaemic Control – Aim BSL < 15, HbA1c < 53
- Smoking Cessation – Minimum 8/52 prior
- DVT prophylaxis
- Anaesthetic issues
- Pneumoperitoneum
- Equipment planning, special beds, positioning, special instruments/ports
- Peripheral Nerve Injuries
- ICU post-op
Obesity Surgery Mortality Risk Score
- Prospectively validated scoring system to evaluate mortality risk after bariatric surgery
- Risk Factors
- Age > 45
- Hypertension
- Male
- BMI > 50
- Risk factors for PE
- Prev VTE, Pulmonary HTN, IVC filter, Obesity hypoventilation
- Risk Factors
Optifast
- 3 sachets per day + very low calorie diet
- Aim 450-800kCal/day
- Can reverse NAFLD or NASH
- Obese individuals have 30-100% NAFLD
- Trials have shown 6/52 course of optifast reduces liver volume by 15% and liver fat content by 43%
- Helps intra-operative liver pliability
- Especially for gastric bands
DVT Prophylaxis
- Obesity is an independent risk factor for VTE
- Risk accentuated by pneumoperitoneum & peri-op hypercoagulability
- Increased fibrinogen, factor VIII & vWF
- Risk accentuated by pneumoperitoneum & peri-op hypercoagulability
- Mitigate this by
- Early ambulation
- Pneumatic compression stockings
- Clexane or heparin
- In high risk (previous DVT/PE, predisposition to hypercoagulable state) may need IVC filter
Anaesthetic Considerations
- Endotracheal intubation & airway management can be difficult – large neck circumference
- Sometimes use head up position initially as this optimises pre-oxygenation
- No benefit once paralysed
- May need large BP cuffs
- May need arterial monitoring if not working
- Venous access can be challenging
- May require larger doses of lipophilic substances
- Barbiturates, benzodiazepines
Pneumoperitoneum Factors
- Increased Systemic Vascular Resistance
- Decreased cardiac index
- Transiently increased MABP
- Can get
- Bradycardic
- Vagal response to peritoneal stretch
- Hypotensive
- Reduced venous return & relative hypovolemic from steep reverse-Trendelenburg response
- Bradycardic
- May cause transient oliguria from pressure on renal cortex & IVC
- Has no long term consequence for kidney
Peripheral Nerve Injuries
- Must always consider
- Stretch injuries of brachial plexus
- Ulnar nerve compression from excessive abduction of arm
- NB: If polyneuropathy
- Need to consider malnutrition
Consider ICU
- Risk factors for complicated stay
- Male
- BMI > 60
- DM
- OSA
- Intra-op complications
Surgery
Expected Results
- More effective and durable than conventional weight loss management (Cochrane 2005)
- Swedish obese subject (SOS) study – 10yr cohort
- 32% RR decreased of death at 10 yrs (mostly cardiovascular + ↓ co-morbidities)
- Cost effective after 3-5 years
- Better QOL, higher employment rate
Effects on Co-morbidities of Obesity
- T2DM
- 80-90% remission with BPD/DS
- 50-70% remission with bypass
- 10-20% with banding
- Attributed to decreased weight and change in GI hormones reaching the duodenum
- HTN
- 60% cured, 25% improved
- Dyslipidaemia
- 35% cured, 40% improved
- Metabolic syndrome
- Cured in > 60% after bypass; NNT = 2.1
- Cardiovascular risk improved after bypass
- Improved fertility rate
Mechanism of Weight Loss
- Metabolic surgery results in anatomical alterations that produce physiological interactions involving signaling between the gut and brain.
- It works by
- Changing hormonal signalling
- Changing neural signalling
- Anatomical restiction
- Malabsorption
- Change in guit microbiome
- It works by
Pathophysiology of obesity-related diseases
Gut brain-axis
- Enteroendocrine cells sense luminal factors, such as nutrients.
- EEC’s secrete gut hormones such as oxyntomodulin (OXM), and glucagon-like peptide 1 (GLP-1), which alert the CNS that nutrients are in the gut.
- Paracrine mechanisms (vagal, spinal afferents) also alert the CNS.
- This signaling acts on the hindbrain and hypothalamus to reduce food intake, increased energy expenditure, slow GI motility, and increase nutrient utilisation.
- Adipose tissue acts as an endocrine and immune organ.
- An increase in the adipose mass results in adipose tissue dysfunction.
- White adipose tissue produces immune factors such as leptin, adiponectin, growth factors, cytokines such as IL-6 an TNF - some of which are pro-inflammatory mediators and contribute to the obesity related complications.
Mechanism of weight loss post bariatric surgery
Hormonal signaling
- Patients have reduced food intake with decreased pre-meal hunger and increased satiety.
- Metabolic surgery increases the amount of post-prandial gut secretion of entero-endocrine hormones (GLP-1, GLP-2)
- Changes in nutrient concentrations, and higher nutrient loads to distal gut segments result in higher levels of peptides secreted by EEC’s which increase satiety.
- GLP-1 slows gastric emptying, inhibits glucagon release, and promotes insulin secretion from the pancreas.
- Ghrelin production (hunger hormone) is reduced.
Neural signaling
- Vagal nerve signaling increased which reduces food intake and hunger.
Gut microbiota
- After bariatric surgery, there is a change in gut microbiota which changes the energy utilisation of these microbes which may contribute to weight loss.
Bile acids
- Plasma bile acid levels a higher in patients after bariatric surgery.
- High bile acids correlate with lower post-prandial BSL.
- BA also promote other peptides including GLP-1 (which stimulates satiety)
- BA usually stay high for 3-4 years after surgery, and promote intestinal hypertrophy.
Behavioral
-
Because of the above mechanisms, behavioural changes occur - with regards to food-reward pathway which further reduce weight loss.
-
Restrictive Procedures
- Limit calorie intake by reducing stomach reservoir capacity
- Absorptive function of small intestine remains intact
- Sleeve gastrectomy most commonly used
- Success probably lies in neuro-hormonal effects on hunger control also
- Others: VBG and Lap Gastric Bands
-
Malabsorptive Procedures
- Decrease the effectiveness of nutrient absorption by shortening the absorptive length of the small intestine
- Either by bypass of small bowel absorptive area, or bypass of biliary/pancreatic secretions that facilitate absorption
- E.g. Jejunoileal bypass and BPD
- Often give profound weight loss, but offset by significant metabolic complications
-
Combined Procedures
- Roux-en-Y Gastric Bypass
- BPD (Biliopancreatic Diversion) with Duodenal Switch
- Also One-anastomosis Gastric Bypass and SADI (Single Anastomosis Duodenal-Ileal Switch)
Short Notes
Bariatric Surgery
- Indications
- From ASMBS & IFSO (American Society for Metabolic and Bariatric Surgery & International Federation for the Surgery of Obesity and Metabolic Disorders
- Anyone BMI >35
- Metabolic disease BMI >30
- Asians + metabolic disease BMI >25
- Bridge to other treatment
- Joint surgery >40
- Ventral wall repair
- Transplant
- From ASMBS & IFSO (American Society for Metabolic and Bariatric Surgery & International Federation for the Surgery of Obesity and Metabolic Disorders
- Preoperative Considerations
- Service is offered through a specialised bariatric unit with availability of MDT
- Dietician
- Psychologist
- Specialist Nurse
- Anaesthetist
- Endocrinologist, Respiratory
- Surgeon
- Patient Selection
- All appropriate non-surgical measures have been tried and failed to achieve or maintain adequate weight loss for at least 6 months
- No Surgical or Anaesthetic contraindications
- Person willing to commit to long term follow up
- Choice of Operations
- Weight of patient / required weight loss
- Previous operations
- Bariatric
- Non Bariatric
- Reflux
- Gastroscopy
- Comorbidities
- Nutritional assessment
- Thiamine, B12, Folate, Iron
- Vitamin D, Calcium
- Vitamins ADEK
- Zinc, Copper
- Optimisation
- Optimisation of comorbidities
- Patient to institute changes that will be required post operatively
- Stop smoking
- Change to diet
- Exercise
- Optifast
- For 2 weeks before operation
- VTE prophylaxis
- Service is offered through a specialised bariatric unit with availability of MDT
- Non Surgical
- Medical
- Orlistat
- Amphetamine derivatives
- Opioid antagonists
- GLP-1 agonists
- Endoscopic
- Intragastric Balloon
- Duodeno-jejunal sleeve
- Gastric plication
- Medical
- Surgical
- Restrictive
- Gastric Band
- Operation
- An inflatable silicon band fitted around the proximal stomach to create a pouch of 30mls
- Lies 45o in the 8 to 2 o’clock position (Phi angle)
- 10 to 60 degrees from vertebrae
- Secured by sutures
- Band is connected to a subcutaneous insulation port
- Complications
- Early
- Intraoperative
- Gastric perforation or splenic Injury
- Band too tight
- Pain, vomiting, dysphagia
- Mx: Decompress band with Huber needle, there will be 4-11mls
- Intraoperative
- Medium
- Slippage * Pain, vomiting, dysphagia * Can develop ischaemia of prolapsed fundus * CXR shows loss of Phi angle * Mx: Decompress then laparoscopic removal. * Deflate band * Adhesiolysis from left lobe of h * Pseudo capsule of scar tissue * Cut buckle with disposable scissors. * Release gastrogastropexy * cu and remove tubing * Leak test stomach with air or meth blue
- Late
- Erosion
- Cellulitis around the port
- Infection tracks from the stomach
- No gastric perforation just band eroded through creating phlegmon
- Diagnosis is endoscopic
- Mx: Endoscopic cut the tubing and remove band. Remove tubing and port percutaneously
- Do not need to need to manage fistula as so long
- Mega-oesophagus
- Erosion
- Early
- Operation
- Gastric Sleeve
- MOA
- Restrictive and hormonal as removing fundus removes production of Ghrelin
- Pros:
- Easy to preform in super obese
- No anastomosis risk
- Normal intestinal absorption
- Pylorus preserved so prevention of dumping
- Cons:
- Irreversible
- Subsequent weight gain
- Operation
- Using a 34Fr bougie the Greater Curve side is stapled off to be removed
- Ensure not too narrow at incisura
- Complications
- Early
- Intraoperative
- Oesophageal, splenic injury
- Staple line leak
- Staple line bleed
- Intra-abdominal bleed
- VTE
- Intraoperative
- Medium
- Sleeve too narrow or twists
- Stricture
- Late
- GORD
- Weight Gain
- Early
- MOA
- Gastric Band
- Malabsorptive
- Single Anastomosis Bypass
- MOA
- Restrictive, malabsorptive and hormonal
- Operation
- Create a longer gastric pouch
- Create Gastrojejunostomy
- Pro
- Fewer anastomosis
- Fewer internal hernias
- Cons
- Bile reflux
- Malabsorption
- MOA
- Roux-en Y Gastric Bypass
- MOA
- Restrictive, malabsorptive and hormonal
- Operation
- 30ml gastric pouch
- Roux limb 75-150cm in length
- Then the Biliopancreatic limb and common channel
- Both gastrojejunostomy and jejujejunostomy anastomosis
- Close mesenteric defects
- Complications
- Early
- Intraoperative injury
- Leak
- Obstruction
- Medium
- BP or Roux limb obstruction
- Dumping Syndrome @
- Blind End Syndrome
- Late
- Marginal Ulcer
- Adhesional SBO
- Internal Hernia
- Where
- Peterson’s Space
- Between the Roux limb mesentery and transverse colon mesentery
- Mesenteric defect at the enteroenterostomy
- And if Roux limb is retrocolic then through the defect made in the transverse mesocolon
- Peterson’s Space
- ↑ risk
- Patient looses weight
- Laparoscopic surgery
- Spaces not initially closed
- Retrocolic jejunostomy
- Dissoluble suturres
- Where
- Nutritional
- Weight gain
- Early
- MOA
- Duodenal Switch
- MOA
- Malabsorptive, Restrictive, Hormonal
- Operation
- Gastric Sleeve
- Divide stomach just distal to pylorus
- Divide distal jejunum and this distal part anastomose with pylorus
- Anastomose the proximal length of the jejunum to ileum 1m from ileocaecal value
- Cons
- Extreme Malabsorption
- MOA
- Single Anastomosis Bypass
- Restrictive
- Intra-operative Considerations
- Positioning
- Non slip mat and strap
- Pressure area concern
- Head up
- Legs apart
- Ports
- Need long ports
- Ports far away to help with angles
- Positioning
- Post operative Considerations
- Observe for complications
- Bleeding
- Perforation
- Dysphagia
- VTE
- Incentive spirometry
- Clexane until mobile
- PPI
- Ensure managing fluid
- Supported regime for building up diet
- Supplementation
- Nutritional observation and support
- At least annual bloods
- FBC
- Thiamine, B12, folate, Iron
- Calcium, Vit D, PTH
- Education that need 30mins exercise
- Observe for complications
Operative: Internal Hernia
- Start Laparoscopically
- Start at IC Valve and run bowel proximally to find the JJ anastomosis
- Then go to the GJ and run distally to find the JJ anastomosis
- This will enable appreciation of where the mesentery of roux limb is relative to the transverse colon (Peterson’s)
- Then from the JJ to the DJ along the BP limb
- This should have allowed inspection of the JJ mesenteric defect and unraveled all hernias
- If Identify a Gangrenous length of bowel
- Call for help or staple off and remove
- Must decompress the remnant stomach
- NJT for roux limb decompression