Bariatric surgery encompasses surgical procedures that modify the gastrointestinal tract to induce sustained weight loss in patients with severe obesity, primarily through restrictive, malabsorptive, or combined mechanisms.

Exam domain	One-glance essentials
Definition / diagnosis	Bariatric/metabolic surgery alters GI anatomy to produce sustained weight loss and metabolic improvement after failed conservative treatment ^[1] Effects combine restriction, malabsorption and hormonal changes; sleeve gastrectomy and RYGB are key procedures ^[1]
Epidemiology / risks	Consider after failed structured lifestyle therapy ± pharmacotherapy for 6–12 months ^[1] Asian indications: BMI ≥35, or BMI ≥30 with T2DM/major comorbidity ^[1] Exclude reversible endocrine obesity, active psychiatric illness, substance abuse and inability to follow lifelong care ^[1]
Core mechanism	Sleeve gastrectomy removes the fundus, reducing ghrelin and gastric capacity ^[1] RYGB combines restriction, bypass and incretin effects, with greater T2DM remission potential ^[1] Bypass of the pylorus predisposes to rapid nutrient delivery and dumping syndrome ^[1]
Clinical picture	Early postoperative tachycardia >120 bpm is anastomotic/staple-line leak until proven otherwise ^[1] RYGB internal hernia causes intermittent or acute colicky pain, nausea and vomiting ^[1] Early dumping causes post-meal cramps, diarrhoea and vasomotor symptoms; late dumping causes reactive hypoglycaemia ^[1]
Investigations	Preoperative assessment is multidisciplinary: metabolic, nutritional, psychological and anaesthetic ^[1] OGD is recommended for bariatric candidates in East Asia; assess H. pylori, hernia, Barrett's and gastric pathology ^[1] Suspected leak: CT abdomen with oral water-soluble contrast; suspected internal hernia: CT for the swirl sign ^[1]
Management	Optimise with liver-shrinkage diet, correction of deficiencies, OSA treatment, smoking cessation and glycaemic control ^[1] Significant GORD or Barrett's favours RYGB; sleeve is simpler, while RYGB favours metabolic remission ^[1] Postoperatively use ERAS, early mobilisation, VTE prophylaxis, staged diet, medication adjustment and lifelong supplementation ^[1]
Complications	Early: leak, bleeding, VTE and respiratory failure; VTE is a leading cause of postoperative death ^[1] RYGB-specific: internal hernia, marginal ulcer, dumping, stomal stenosis and excluded-remnant surveillance difficulty ^[1] Late nutritional complications include iron, B12, folate, calcium, vitamin D and thiamine deficiency ^[1]
Prevention / follow-up	Establish and correct nutritional deficiencies before surgery; obesity does not exclude sarcopenic obesity ^[1] Close RYGB mesenteric defects to reduce internal hernia risk; provide LMWH, compression and early mobilisation for VTE prevention ^[1] Lifelong supplementation and annual nutritional surveillance are mandatory ^[1]
Exam traps	Do not operate before excluding secondary obesity, especially Cushing syndrome and hypothyroidism ^[1] Do not dismiss postoperative tachycardia, pain or vomiting as expected recovery: investigate leak or obstruction ^[1] Sleeve gastrectomy may worsen GORD; RYGB creates an excluded gastric remnant that is difficult to access endoscopically ^[1]

References

^[1] Lecture slides: GC 212. Weight loss and vomiting gastric cancer; abdominal imaging.pdf

Bariatric Surgery

Bariatric surgery (from Greek: baros = weight, iatrike = medical treatment) refers to a group of surgical procedures performed on the gastrointestinal tract to achieve sustained weight loss in patients with clinically severe obesity, typically after failure of conservative medical management. These procedures work through restriction (limiting gastric capacity → early satiety), malabsorption (bypassing segments of small bowel → reduced nutrient absorption), or a combination of both, and increasingly are recognised to exert profound metabolic/hormonal effects independent of weight loss per se — hence the modern term metabolic surgery ^[1]^[2].

Why 'Metabolic Surgery'?

The term has shifted from purely "bariatric" to "metabolic" because procedures like Roux-en-Y gastric bypass can induce Type 2 Diabetes Mellitus (T2DM) remission within days — long before significant weight loss occurs. This is driven by changes in gut hormones (especially GLP-1, PYY, ghrelin), bile acid signalling, and gut microbiome composition. The surgery treats the metabolic syndrome, not just the weight.

2. Epidemiology and the Obesity Problem

Worldwide obesity has nearly tripled since 1975 (WHO 2024). Over 1 billion people globally are now obese (BMI ≥ 30 kg/m²).
Obesity is a leading modifiable risk factor for T2DM, cardiovascular disease, obstructive sleep apnoea, non-alcoholic fatty liver disease (NAFLD/MASLD), and multiple cancers.

Prevalence of obesity (BMI ≥ 30 by WHO Asian criteria) is rising: ~30% of adults in HK are overweight/obese by Asian cut-offs.
Asian populations develop metabolic complications at lower BMI thresholds compared to Caucasians — hence lower BMI cut-offs for surgical indications (see below).
Bariatric surgery volume in HK has increased significantly, primarily laparoscopic sleeve gastrectomy (LSG), which is the most commonly performed bariatric procedure in HK and globally ^[1]^[2].

Genetic predisposition (polygenic; rarely monogenic e.g. MC4R mutations, leptin deficiency)
Sedentary lifestyle and caloric excess
Endocrine causes: hypothyroidism, Cushing syndrome, insulinoma, hypothalamic lesions
Medications: corticosteroids, atypical antipsychotics, insulin, sulfonylureas, valproate
Psychological/behavioural: binge eating disorder, depression, childhood trauma
Socioeconomic factors

3. Anatomy and Physiology Relevant to Bariatric Surgery

Understanding the stomach's anatomy is essential because bariatric procedures physically alter it:

Structure	Relevance to Bariatric Surgery
Fundus	Highly distensible; main reservoir. Removed in sleeve gastrectomy. Contains most ghrelin-producing cells
Body (Corpus)	Parietal cells (HCl) and chief cells (pepsinogen). Partially preserved in most procedures
Antrum	Gastrin-producing G cells; mixes food. Preserved in RYGB pouch but excluded from food stream
Pylorus	Controls gastric emptying. Preserved in sleeve gastrectomy (important for preventing dumping). Bypassed in RYGB
Greater curvature	Blood supply from gastroepiploic arcade; line of resection in sleeve gastrectomy
Lesser curvature	Blood supply from left/right gastric arteries; preserved as the "sleeve"
Angle of His	Gastroesophageal junction angle; maintained in sleeve to preserve anti-reflux mechanism

Relevant to malabsorptive procedures:

Duodenum: Main site of iron, calcium, folate absorption; bypassed in RYGB and BPD-DS → deficiency risk
Jejunum: Carbohydrate and protein absorption; bypassed in RYGB (alimentary limb)
Ileum: Bile salt reabsorption (terminal ileum), Vitamin B12 absorption, GLP-1/PYY secretion (L-cells concentrated distally)

Hormone	Source	Effect	Change After Bariatric Surgery
Ghrelin	Fundus of stomach (P/D1 cells)	Orexigenic (stimulates appetite); rises before meals	↓↓ after sleeve gastrectomy (fundus removed). Variable after RYGB
GLP-1 (Glucagon-Like Peptide-1)	L-cells (distal ileum/colon)	Incretin effect: stimulates insulin secretion, suppresses glucagon, slows gastric emptying, promotes satiety	↑↑ after RYGB (rapid nutrient delivery to distal gut → exaggerated incretin response) — key mechanism for T2DM remission
PYY (Peptide YY)	L-cells (distal ileum/colon)	Anorexigenic (suppresses appetite), slows GI motility	↑ after RYGB
Leptin	Adipose tissue	Signals satiety to hypothalamus; levels proportional to fat mass	↓ with weight loss (reduced fat mass)
Insulin	Pancreatic β-cells	Anabolic; promotes glucose uptake	Improved sensitivity; reduced hyperinsulinaemia
Cholecystokinin (CCK)	I-cells (duodenum/jejunum)	Stimulates satiety, gallbladder contraction, pancreatic secretion	Variable changes

The Hindgut Hypothesis

After RYGB, undigested nutrients reach the distal small bowel (hindgut) much faster than normal. This stimulates L-cells to release GLP-1 and PYY in an exaggerated fashion — the so-called "hindgut hypothesis." This explains why diabetes improves rapidly post-RYGB, even before significant weight loss. It is essentially surgically induced incretin enhancement — the same principle behind GLP-1 receptor agonist drugs like semaglutide!

4. Indications for Bariatric Surgery

Failed medical treatment (lifestyle modification ± pharmacotherapy for ≥ 6–12 months) PLUS ^[1]^[2]:

Criterion	BMI Threshold (Asian)
BMI ≥ 35 kg/m²	With or without comorbidities
BMI ≥ 30 kg/m²	With T2DM or other obesity-related comorbidities (hypertension, OSA, NAFLD, dyslipidaemia)
BMI ≥ 27.5 kg/m² (emerging)	With poorly controlled T2DM — "metabolic surgery" indication per IFSO-APC 2024 guidelines

For Caucasian populations, the traditional NIH 1991 criteria use BMI ≥ 40, or BMI ≥ 35 with comorbidities. Asian thresholds are 5 units lower because Asians develop metabolic complications at lower BMIs due to higher visceral adiposity for a given BMI.

Contraindications include:

Reversible endocrine causes of obesity (e.g. untreated hypothyroidism, Cushing syndrome) — must be excluded and treated first
Active psychiatric disorders (uncontrolled; must be stabilised)
Active substance abuse (alcohol, drugs)
Non-compliance to medical care / inability to adhere to lifelong follow-up and supplementation
Pregnancy or planning pregnancy within 12–18 months
Advanced malignancy with poor prognosis
Inability to tolerate general anaesthesia
Active peptic ulcer disease (relative; treat first)

Exam Pearl

A common exam mistake: listing obesity itself as an indication. The question is always which patients warrant surgery. You must state: (1) failed conservative management, (2) specific BMI threshold, and (3) absence of contraindications. For Asians, the thresholds are lower — this is frequently tested.

The ABCD score is a validated scoring system predicting likelihood of T2DM remission after metabolic/bariatric surgery ^[2]:

Parameter	Points
A — Age	Younger age → higher score (better β-cell reserve)
B — BMI	Higher BMI → higher score (more weight to lose → greater metabolic improvement)
C — C-peptide	Higher C-peptide → higher score (reflects residual β-cell function; if β-cells are burned out, surgery won't restore insulin secretion)
D — Duration of DM	Shorter duration → higher score (less β-cell apoptosis)

Total score = 10
Score > 6 predicts DM remission after bariatric surgery ^[2]

Why C-peptide?

C-peptide is co-secreted with insulin in a 1:1 molar ratio from β-cells. Unlike insulin, it is not cleared by the liver and has a longer half-life, making it a reliable marker of endogenous insulin production. A high C-peptide means the pancreas still has functional β-cells — the hormonal changes from surgery (↑GLP-1, improved insulin sensitivity) can "rescue" these cells. A very low C-peptide suggests near-complete β-cell destruction (as in longstanding T2DM or T1DM), and surgery will not reverse diabetes.

6. Classification and Types of Bariatric Procedures

6.2 Detailed Procedure Descriptions

A. Restrictive Procedures — Cause early satiety; overeating → upper abdominal pain [2]

Mechanism: A silicone cuff/band is placed around the proximal stomach (just below the GEJ), creating a small pouch above the band. The band is connected to a subcutaneous port through which saline can be injected to inflate/tighten the band or withdrawn to loosen it, allowing adjustable restriction ^[2].
Advantages: Reversible, adjustable, no GI anastomosis, lowest perioperative risk
Disadvantages: Poorest long-term weight loss; high reoperation rate (30–50%)
Largely fallen out of favour — rarely performed now due to high complication and failure rates

Mechanism: Approximately 75–80% of the stomach is resected along the greater curvature, leaving a narrow tubular "sleeve" along the lesser curvature, roughly the width of a bougie (32–40 Fr). The fundus is removed — this is where most ghrelin-producing cells reside.
Effects:
- Restrictive: Dramatically reduced gastric volume (from ~1000 mL to ~100–150 mL) → early satiety
- Hormonal: ↓↓ Ghrelin (fundus removed) → reduced hunger drive; also ↑ GLP-1 and PYY (though less than RYGB) due to accelerated gastric emptying and faster nutrient delivery to distal gut
- Pylorus preserved → more physiological gastric emptying than RYGB; lower risk of dumping syndrome
Advantages: Technically simpler (no anastomosis to bowel), no foreign body, no malabsorption of most nutrients, good weight loss
Disadvantages: Irreversible; risk of staple line leak; can worsen GORD (controversial but recognised)

B. Combined (Restrictive + Malabsorptive) Procedures

Mechanism:
1. A small gastric pouch (~30 mL) is created from the proximal stomach, completely divided from the gastric remnant
2. The jejunum is divided ~50–75 cm from the ligament of Treitz
3. The distal cut end of jejunum is brought up and anastomosed to the gastric pouch — this is the Roux (alimentary) limb (where food travels)
4. The proximal cut end (carrying bile and pancreatic secretions) is anastomosed further downstream to the Roux limb — this is the biliopancreatic (BP) limb
5. The point where bile/pancreatic secretions meet food is the common channel — absorption only occurs here
Effects:
- Restrictive: Tiny pouch → early satiety
- Malabsorptive: Duodenum and proximal jejunum bypassed → reduced absorption of iron, calcium, folate, fat-soluble vitamins
- Hormonal (most important): Rapid nutrient delivery to distal gut → ↑↑ GLP-1, PYY → enhanced incretin effect → T2DM remission (hindgut hypothesis); also foregut exclusion reduces anti-incretin factors (foregut hypothesis)
- Dumping syndrome can occur (see complications) — acts as negative reinforcement against simple sugar intake

Similar to RYGB but with only one anastomosis (loop gastrojejunostomy rather than Roux-en-Y configuration)
Simpler, shorter operative time
Concern: potential for bile reflux into the gastric pouch/oesophagus (theoretical carcinogenesis risk)
Gaining popularity but less long-term data than RYGB

v. Biliopancreatic Diversion ± Duodenal Switch (BPD-DS)

Mechanism: Sleeve gastrectomy PLUS bypass of a large portion of small bowel. The common channel (where food meets bile/pancreatic juice) is very short (~75–100 cm).
Effects: Greatest weight loss but highest nutritional complication rate
Rarely performed due to severe malabsorption, nutritional deficiencies, and complexity
Largely reserved for super-morbid obesity (BMI > 50)

Feature	Gastric Banding	Sleeve Gastrectomy	RYGB	BPD-DS
Mechanism	Restriction	Restriction + hormonal	Restriction + malabsorption + hormonal	Malabsorption (predominant) + restriction
Excess Weight Loss (% EWL)	40–50%	55–70%	60–80%	70–85%
T2DM remission rate	~45%	~60%	~80% (highest for RYGB)	~95%
Reversibility	Reversible	Irreversible	Technically reversible but rarely done	Irreversible
Operative complexity	Simple	Intermediate	Complex (2 anastomoses)	Most complex
Perioperative mortality	0.05%	0.1–0.3%	0.2–0.5%	0.5–1%
Nutritional deficiency risk	Low	Low–moderate	Moderate–high (Fe, Ca, B12, folate, fat-sol vitamins)	Very high
GORD	May improve	May worsen	Improves (best for GORD)	Improves
Dumping syndrome	No	Rare	Yes (common)	Yes
Popularity (2024)	Declining	Most popular globally	Second most popular	Rare

7. Preoperative Assessment and Surgical Nutrition

This section draws heavily on surgical nutrition principles ^[3].

"Feed him up before surgery" — malnourished patients have significantly worse surgical outcomes ^[3].

Malnutrition screening and assessment is essential preoperatively:

Subjective Global Assessment (SGA) — gold standard bedside nutritional assessment tool:
- Combines history (weight change, dietary intake, GI symptoms, functional capacity) with physical examination (subcutaneous fat loss, muscle wasting, oedema)
- Classifies patients as: A (well-nourished), B (mildly/moderately malnourished), C (severely malnourished)
Objective nutritional markers:
- Albumin: Half-life ~20 days; reflects chronic nutritional status but also acute phase reactant (↓ in inflammation, liver disease, losses)
- Prealbumin (transthyretin): Half-life ~2 days; more sensitive to acute nutritional changes
- Transferrin: Half-life ~8 days
- BMI, weight loss trajectory
- Handgrip strength (functional measure of sarcopenia)

Important

Obese patients can be malnourished! This is called "sarcopenic obesity" — adequate or excess fat mass but depleted lean body mass. Do not assume a high BMI = adequate nutrition. Bariatric surgery candidates may have micronutrient deficiencies (iron, vitamin D, B12, folate) even before surgery due to poor dietary quality. Always screen and correct deficiencies preoperatively ^[3].

Effects of malnutrition on surgical outcomes:

System	Effect of Malnutrition
Immune function	↓ Immune function → increased infection risk (wound infections, pneumonia, sepsis)
Wound healing	Impaired collagen synthesis → poor wound healing, anastomotic dehiscence
Respiratory	Respiratory muscle weakness → difficulty weaning from ventilator, atelectasis
GI function	Gut mucosal atrophy → bacterial translocation → sepsis
Cardiac	Cardiac muscle wasting → reduced cardiac output
Psychological	Apathy, depression → poor rehabilitation

7.3 Perioperative Nutritional Support [3]

Key principles:

"If the gut works, use it" — enteral nutrition is always preferred over parenteral ^[3]
Early enteral feeding is beneficial (within 24–48 hours post-surgery when safe)
Preoperative nutritional optimisation ("prehabilitation"): aim to correct deficiencies 2–4 weeks before elective surgery

Definition: Nutrition delivered via the GI tract — orally or via feeding tube
Routes:
- Oral: First line if patient can swallow safely
- Nasogastric tube (NGT): Short-term ( < 4–6 weeks); stomach must be functional
- Nasojejunal tube (NJT): Bypasses stomach; useful if gastroparesis or post-gastric surgery
- Percutaneous Endoscopic Gastrostomy (PEG): For long-term feeding ( > 4–6 weeks); placed endoscopically through abdominal wall into stomach
- Percutaneous Endoscopic Jejunostomy (PEJ) or surgical jejunostomy: For long-term feeding bypassing the stomach
Advantages of enteral over parenteral ^[3]:
- Maintains gut mucosal integrity (prevents villous atrophy and bacterial translocation)
- Lower infection risk (no central line → no CRBSI)
- Cheaper
- More physiological (stimulates gut hormones, bile flow, immune function)
- Fewer metabolic complications
Complications of enteral feeding:
- Aspiration pneumonia (especially NGT in patients with poor GCS or GORD)
- Diarrhoea (osmotic; too rapid infusion; bacterial contamination of feed)
- Tube displacement or blockage
- Refeeding syndrome (see below)
- Abdominal distension, nausea

Definition: Intravenous delivery of nutrients (amino acids, glucose, lipids, electrolytes, vitamins, trace elements) bypassing the GI tract entirely
Indications — when the gut cannot be used or is insufficient:
- Intestinal failure (short bowel syndrome, severe Crohn's, radiation enteritis)
- Prolonged ileus or bowel obstruction
- High-output intestinal fistula
- Severe pancreatitis (if enteral not tolerated — note: modern practice favours early enteral even in pancreatitis)
- Perioperative when enteral not feasible for > 7 days
Routes:
- Peripheral PN (PPN): Lower osmolality solutions; for short-term use ( < 2 weeks); limited by peripheral vein tolerance (risk of phlebitis if osmolality > 900 mOsm/L)
- Central PN (TPN — Total Parenteral Nutrition): Via central venous catheter (subclavian, internal jugular, PICC); higher osmolality solutions can be given; for longer-term use
Complications of parenteral nutrition ^[3]:
- Line-related: Catheter-related bloodstream infection (CRBSI) (most feared), pneumothorax (insertion), thrombosis, air embolism
- Metabolic: Hyperglycaemia (commonest), electrolyte imbalance, hepatic steatosis/cholestasis (with prolonged use — "PN-associated liver disease"), hypertriglyceridaemia
- Refeeding syndrome
- Gut atrophy with prolonged use (no enteral stimulation → villous atrophy → bacterial translocation)

Refeeding Syndrome

Refeeding syndrome occurs when a chronically malnourished patient is fed too rapidly (enterally or parenterally). The shift from fat/protein catabolism to carbohydrate metabolism drives insulin secretion → intracellular shift of phosphate, potassium, and magnesium → severe hypophosphataemia (hallmark), hypokalaemia, hypomagnesaemia. This can cause cardiac arrhythmias, heart failure, seizures, respiratory failure, and death.

Prevention: Start feeding slowly ("start low, go slow"), monitor electrolytes closely (especially phosphate), and supplement prophylactically. High-risk groups: anorexia nervosa, chronic alcoholism, prolonged starvation, cancer cachexia ^[3].

8. Clinical Features — Presentation of the Obese Patient Being Considered for Bariatric Surgery

Patients presenting for bariatric surgery consultation typically have:

Symptom	Pathophysiological Basis
Excessive weight / inability to lose weight	Energy imbalance; possible leptin resistance (hypothalamus "deaf" to satiety signals); genetic predisposition
Joint pain (knees, hips, lumbar spine)	Mechanical loading on weight-bearing joints → accelerated osteoarthritis. Every 1 kg of weight = 3–5 kg extra force across the knee joint
Snoring / witnessed apnoeas / daytime somnolence	Obstructive sleep apnoea (OSA): pharyngeal fat deposition → upper airway collapse during sleep → intermittent hypoxia → daytime sleepiness, ↑ cardiovascular risk
Exertional dyspnoea	Obesity hypoventilation syndrome; ↓ lung compliance (abdominal fat restricts diaphragmatic excursion); ↑ work of breathing; may have coexistent heart failure
Heartburn / acid regurgitation	GORD: ↑ intra-abdominal pressure → incompetent LES → acid reflux; also hiatal hernia more common in obesity
Polyuria, polydipsia	T2DM: insulin resistance → hyperglycaemia → osmotic diuresis
Skin changes (acanthosis nigricans, skin tags, intertrigo)	Insulin resistance → hyperinsulinaemia → keratinocyte/fibroblast proliferation (acanthosis nigricans); skin folds → moisture trapping → fungal/bacterial infection (intertrigo)
Menstrual irregularity / subfertility	PCOS: hyperinsulinaemia → ovarian androgen excess → anovulation; also ↑ aromatisation of androgens to oestrogens in adipose tissue
Depression / low self-esteem	Psychosocial stigma; neuroinflammation from chronic low-grade inflammation; leptin/serotonin pathway dysregulation
Headaches (pseudotumour cerebri)	Idiopathic intracranial hypertension — mechanism unclear but associated with obesity, especially in young women

Sign	Pathophysiological Basis
↑ BMI, ↑ waist circumference	Central/visceral adiposity — metabolically more active and harmful than subcutaneous fat; produces inflammatory cytokines (TNF-α, IL-6)
Elevated blood pressure	Hyperinsulinaemia → Na+ retention, sympathetic activation; RAAS activation; endothelial dysfunction
Acanthosis nigricans (velvety hyperpigmentation in skin folds — neck, axillae, groin)	Hallmark of insulin resistance; insulin and IGF-1 stimulate epidermal keratinocyte and fibroblast proliferation
Skin tags (acrochordons)	Associated with insulin resistance (same mechanism)
Intertrigo (erythema in skin folds)	Maceration from moisture in deep skin folds → secondary candidal/bacterial infection
Hepatomegaly	NAFLD/MASLD — hepatic steatosis from insulin resistance → lipogenesis in liver
Striae (stretch marks)	Rapid weight gain → dermis stretching beyond elastic limit → collagen rupture
Bilateral leg oedema	Chronic venous insufficiency (obesity → ↑ venous pressure in lower limbs); may also be right heart failure, hypoalbuminaemia
Mallampati class III/IV (difficult airway)	Pharyngeal fat deposition, short thick neck → anaesthetic concern
Neck circumference > 43 cm (men), > 41 cm (women)	Strong predictor of OSA

The metabolic syndrome is a cluster of interconnected metabolic abnormalities driven by visceral obesity and insulin resistance:

Diagnostic criteria (IDF 2005 — Asian cut-offs):

Central obesity: waist circumference ≥ 90 cm (men) or ≥ 80 cm (women) in Asians
Plus ≥ 2 of:
- Triglycerides ≥ 1.7 mmol/L
- HDL < 1.03 mmol/L (men) or < 1.29 mmol/L (women)
- BP ≥ 130/85 mmHg or on treatment
- Fasting glucose ≥ 5.6 mmol/L or diagnosed T2DM

Bariatric surgery can achieve remission of metabolic syndrome components — this is the key rationale for metabolic surgery ^[1]^[2].

Comorbidity	Mechanism	Resolution Rate After Bariatric Surgery
T2DM	Insulin resistance + progressive β-cell failure	~80% remission after RYGB (via ↑GLP-1, ↑insulin sensitivity)
Hypertension	↑ SNS activity, Na+ retention, RAAS activation	~60–70% improvement
Dyslipidaemia	↑ VLDL synthesis, ↓ HDL	~70% improvement
OSA	Pharyngeal fat, central respiratory drive affected	~85% improvement
NAFLD/MASLD	Hepatic insulin resistance → steatosis → steatohepatitis	~90% improvement in steatosis
GORD	↑ IAP, hiatal hernia	Improves after RYGB; may worsen after SG

While bariatric surgery is not oncological surgery per se, the principles of surgical oncology are relevant because: ^[4]

Obesity is a risk factor for multiple cancers — endometrial, breast (post-menopausal), colorectal, oesophageal adenocarcinoma, hepatocellular, pancreatic, renal cell, gastric
Bariatric surgery has been shown to reduce cancer incidence by 33–50% (Swedish Obese Subjects study)
Preoperative nutritional optimisation principles apply equally to bariatric and cancer surgery ^[3]^[4]
Enhanced Recovery After Surgery (ERAS) protocols — originally developed for colorectal surgery — are now standard in bariatric surgery:
- Early oral feeding
- Early mobilisation
- Multimodal analgesia (opioid-sparing)
- VTE prophylaxis (obese patients are high VTE risk)

High Yield: Obesity and Cancer

Mechanism of obesity → cancer: (1) Chronic hyperinsulinaemia → ↑IGF-1 → mitogenic signalling (cell proliferation, anti-apoptosis); (2) ↑ aromatase activity in adipose tissue → ↑ oestrogen → oestrogen-dependent tumours (endometrial, breast); (3) Chronic low-grade inflammation (↑TNF-α, IL-6) → pro-tumorigenic microenvironment; (4) Altered adipokines (↓ adiponectin, ↑ leptin) ^[4].

While IBD is not directly related to bariatric surgery, the lecture slides on IBD ^[5] highlight important principles of nutritional management in surgical patients:

Crohn's disease patients may develop strictures requiring surgical resection → risk of short bowel syndrome → may require long-term PN
Nutritional deficiencies in IBD (iron, B12, folate, zinc, vitamin D) parallel those seen post-bariatric surgery
Exclusive enteral nutrition (EEN) is a first-line treatment for paediatric Crohn's disease — demonstrating the therapeutic power of nutritional management
The gut microbiome is altered in both IBD and post-bariatric surgery, contributing to metabolic changes

The lecture on gastric cancer ^[1] is relevant because:

Weight loss and vomiting in the context of gastric cancer must be distinguished from post-bariatric surgery complications
Post-gastrectomy nutritional consequences (dumping syndrome, vitamin B12 deficiency, iron deficiency) are identical to those after RYGB because both involve gastric bypass/resection
Abdominal imaging techniques (CT, US) used to assess gastric cancer are the same modalities used to assess bariatric surgery complications (e.g., CT with oral contrast for suspected anastomotic leak)
Staging of gastric cancer involves nutritional assessment — just as bariatric surgery requires preoperative nutritional optimisation ^[1]^[3]

High Yield Summary

Definition: Bariatric (metabolic) surgery = surgical procedures on the GI tract for sustained weight loss and metabolic improvement in severe obesity after failed conservative management.

Key Indications (Asian): Failed medical Rx + BMI ≥ 35 (with/without comorbidities) OR BMI ≥ 30 with T2DM.

Contraindications: Reversible endocrine causes, active psychiatric disorders, substance abuse, non-compliance.

ABCD Score: Age, BMI, C-peptide, Duration of DM. Total = 10. Score > 6 → predicts T2DM remission.

Procedures:

Restrictive: Gastric banding (declining), Sleeve gastrectomy (most popular)
Combined: RYGB (gold standard for metabolic effect, ~80% T2DM remission)
Malabsorptive: BPD-DS (rarely done)

Key Hormonal Changes: ↓ Ghrelin (especially SG — fundus removed), ↑↑ GLP-1 and PYY (especially RYGB — hindgut hypothesis) → T2DM remission.

Nutritional Principles: "If the gut works, use it" — enteral > parenteral. Correct deficiencies preoperatively. Watch for refeeding syndrome (hypophosphataemia hallmark). Obese patients can be malnourished (sarcopenic obesity).

Preoperative Assessment: Nutritional status (SGA), exclude reversible causes of obesity, assess comorbidities (OSA, T2DM, HTN, NAFLD), psychological evaluation.

Active Recall - Bariatric Surgery (Definition, Epidemiology, Anatomy, Etiology, Classification, Clinical Features)

Differential Diagnosis in the Context of Bariatric Surgery

The differential diagnosis (DDx) in bariatric surgery operates on two distinct clinical axes. First, before surgery, you must differentiate primary (idiopathic) obesity from secondary causes of obesity — because operating on a patient whose obesity is driven by a reversible endocrine or pharmacological cause is a contraindication ^[2]. Second, after surgery, you must differentiate the expected post-operative course from complications that mimic other conditions. Both are fair game in exams.

The question here is: Why is this patient obese? Most obesity (~95%) is primary/exogenous (caloric excess + sedentary lifestyle + polygenic predisposition). However, you must exclude reversible causes before committing a patient to irreversible surgery ^[2].

Think systematically using the mnemonic "COMES":

Category	Condition	Mechanism / Why it causes obesity	Key Distinguishing Features
C — Cushing syndrome	Excess cortisol (exogenous steroids, pituitary adenoma, adrenal tumour, ectopic ACTH)	Cortisol → ↑ gluconeogenesis, insulin resistance, ↑ appetite, preferential visceral fat deposition (central obesity), protein catabolism (thin limbs)	Central obesity with thin extremities, moon face, buffalo hump, striae (wide, purple — unlike simple obesity which has narrow, pale striae), proximal myopathy, easy bruising, hypertension, hyperglycaemia
O — Other endocrine	Hypothyroidism	↓ Basal metabolic rate → reduced energy expenditure; also myxoedema (mucopolysaccharide deposition → non-pitting oedema that adds weight)	Fatigue, cold intolerance, constipation, dry skin, bradycardia, delayed relaxation of ankle jerks. Weight gain is usually modest (5–10 kg), rarely causes morbid obesity alone
	Insulinoma	Excess insulin → recurrent hypoglycaemia → compensatory ↑ eating (defensive eating to prevent hypoglycaemia) + anabolic effect of insulin (lipogenesis)	Whipple's triad: symptoms of hypoglycaemia, documented low glucose ( < 2.5 mmol/L), resolution with glucose administration. Episodes often fasting-related
	Growth hormone deficiency	GH promotes lipolysis; deficiency → ↑ fat mass (especially visceral), ↓ lean mass	Central adiposity, reduced muscle mass, fatigue, ↓ bone density. Usually in context of panhypopituitarism
	Hypogonadism	Testosterone promotes lean mass and lipolysis; deficiency → ↑ visceral fat. Oestrogen excess in males → gynoid fat distribution	Males: ↓ libido, erectile dysfunction, gynaecomastia, reduced body hair. Females: amenorrhoea (but note PCOS can cause both hyperandrogenism and obesity)
M — Medications	Corticosteroids, insulin, sulfonylureas, atypical antipsychotics (olanzapine, clozapine), valproate, SSRIs/mirtazapine, β-blockers, TZDs	Various: ↑ appetite (central mechanisms), ↓ metabolic rate, insulin resistance, lipogenesis, fluid retention	Temporal relationship between drug initiation and weight gain. Always take a thorough drug history!
E — Eating disorders	Binge eating disorder (BED)	Recurrent episodes of uncontrolled large-volume eating without compensatory purging → chronic caloric excess	Eating large amounts when not hungry, eating until uncomfortably full, eating alone due to embarrassment, marked distress. Present in ~25–50% of bariatric surgery candidates — must screen
S — Syndromic/Genetic	Prader-Willi syndrome	Hypothalamic dysfunction → insatiable appetite (hyperphagia), ↓ GH → ↓ lean mass	Childhood onset, intellectual disability, short stature, hypogonadism, hypotonia in infancy
	Bardet-Biedl syndrome	Ciliopathy → hypothalamic-pituitary dysfunction	Retinitis pigmentosa, polydactyly, renal anomalies, intellectual disability
	MC4R mutations	Most common monogenic cause of obesity; melanocortin 4 receptor deficiency → disrupted hypothalamic satiety signalling	Severe early-onset obesity, hyperphagia, tall stature, hyperinsulinaemia
	Leptin/leptin receptor deficiency	Extremely rare; absent leptin signal → hypothalamus never receives "full" signal	Severe early-onset obesity, hypogonadism. Responds to exogenous leptin if leptin-deficient (not receptor-deficient)

Exam Approach: Secondary Obesity

On an exam, if a patient has features suggesting secondary obesity (e.g., striae that are wide and purple, proximal myopathy, virilisation, childhood onset with intellectual disability), name the condition and state that it must be excluded/treated before considering bariatric surgery. The key principle: reversible causes of obesity are a contraindication to bariatric surgery ^[2].

Axis 2: Differential Diagnosis of Post-Bariatric Surgery Symptoms

After bariatric surgery, patients may present with symptoms that could represent normal post-operative changes, expected physiological consequences, or serious complications. The DDx here is symptom-driven.

Differential	Mechanism	Distinguishing Features
Anastomotic leak	Disruption of staple line (SG) or surgical anastomosis (RYGB) → peritoneal contamination	Most feared early complication. Tachycardia (often the earliest and most reliable sign — even before fever or pain), fever, peritonism, sepsis. CT with oral contrast: extravasation of contrast. Tachycardia > 120 bpm in the first 48 hours post-op = leak until proven otherwise
Staple line bleed	Bleeding from the long staple line (especially SG)	Tachycardia, hypotension, dropping Hb, blood per drain. Usually within first 24–48 hours
Internal hernia	Mesenteric defects created during RYGB allow bowel to herniate through → closed-loop obstruction → strangulation	Specific to RYGB. Colicky abdominal pain, vomiting, signs of SBO. Can present months to years post-op, especially after significant weight loss (mesenteric fat loss widens defects). CT: "swirl sign" (mesenteric vascular rotation)
Bowel obstruction (adhesive)	Post-surgical adhesions (any abdominal surgery)	Colicky pain, distension, vomiting, absolute constipation. AXR/CT: dilated bowel with transition point
Marginal ulcer	Ulcer at the gastrojejunal anastomosis (RYGB) — due to acid exposure on unprotected jejunal mucosa, NSAIDs, smoking, H. pylori	Epigastric pain, GI bleeding (haematemesis/melaena). Risk factors: smoking, NSAIDs, H. pylori — all should be addressed preoperatively. Diagnosed by OGD
Band slippage/erosion (gastric banding)	Band slips → gastric prolapse through band → obstruction. Band erosion → penetration into gastric lumen	Acute dysphagia, vomiting, pain. X-ray: "O-sign" (horizontal band = slipped from normal oblique position)
Cholelithiasis / cholecystitis	Rapid weight loss → ↑ cholesterol saturation of bile (liver mobilises cholesterol from adipose stores) + ↓ gallbladder motility → gallstone formation	Right upper quadrant pain, Murphy's sign positive. Very common (up to 30% develop gallstones in first 6–12 months post-bariatric surgery). Some centres offer prophylactic ursodeoxycholic acid or concurrent cholecystectomy
Acute pancreatitis	Gallstone migration → ampullary obstruction; or hypertriglyceridaemia	Epigastric pain radiating to back, ↑ amylase/lipase

Differential	Mechanism	Distinguishing Features
Overeating (most common)	Restrictive mechanism — eating more than the small pouch/sleeve can accommodate	Upper abdominal pain and vomiting immediately after eating too much or too fast ^[2]. Self-limited. Patient education is key
Stomal stenosis	Scarring/narrowing at the gastrojejunal anastomosis (RYGB) or sleeve narrowing (usually at incisura angularis)	Progressive dysphagia, intolerance to solids > liquids. Usually 4–8 weeks post-op. Diagnosed by OGD/barium swallow. Treated by endoscopic balloon dilation
Marginal ulcer	As above	Epigastric pain ± bleeding
Internal hernia	As above	Intermittent colicky pain + vomiting (SBO pattern)
GORD (especially post-SG)	SG may worsen GORD: ↑ intragastric pressure in a narrow sleeve, disruption of angle of His, altered LES pressure	Heartburn, regurgitation, especially nocturnal. Chronic GORD post-SG may require conversion to RYGB
Gastrogastric fistula (RYGB)	Communication between the small gastric pouch and the excluded gastric remnant → food enters remnant → pain, GORD, weight regain	Weight regain + GORD symptoms post-RYGB. Diagnosed by upper GI series or OGD

Differential	Mechanism
Dietary non-compliance	Most common cause — snacking, high-calorie liquids (smoothies, sugary drinks) that bypass restriction
Pouch/sleeve dilation	Over time, pouch/sleeve stretches → accommodates more food → reduced restrictive effect
Gastrogastric fistula (RYGB)	Food enters excluded stomach → absorption from larger surface area
Psychological/eating disorder	Unaddressed binge eating disorder; emotional eating returns
Inadequate initial procedure	Pouch too large, limb lengths too short (RYGB)

Dumping syndrome deserves special attention because it is very commonly tested ^[1]^[2]:

Early dumping (15–30 minutes after eating):
- Mechanism: After RYGB, food bypasses the pylorus → rapid delivery of hyperosmolar chyme into the jejunum → osmotic fluid shift into the gut lumen → intravascular volume depletion + gut distension
- Symptoms: Nausea, cramping, diarrhoea, bloating, tachycardia, flushing, diaphoresis, dizziness (vasomotor symptoms from hypovolaemia and autonomic response)
Late dumping (1–3 hours after eating):
- Mechanism: Rapid glucose absorption → exaggerated insulin release → reactive hypoglycaemia
- Symptoms: Diaphoresis, tremor, weakness, confusion, palpitations (adrenergic counter-regulatory response to hypoglycaemia)

Why Dumping Syndrome Can Be 'Therapeutic'

Interestingly, dumping syndrome after RYGB acts as a form of negative reinforcement — patients quickly learn to avoid simple sugars and high-glycaemic-index foods because they cause unpleasant symptoms. This contributes to long-term dietary modification and weight maintenance. It is a "feature, not a bug" of the RYGB design.

This is particularly relevant given the gastric cancer lecture ^[1]. A patient with a history of bariatric surgery presenting with weight loss and vomiting can be diagnostically challenging:

Feature	Post-Bariatric Surgery (Expected/Complication)	Gastric Cancer
Weight loss	Expected in first 12–18 months; concern if excessive or after plateau	Progressive, unintentional weight loss; often with anorexia and early satiety
Vomiting	Usually related to overeating, stomal stenosis, or dumping	Persistent, may contain food eaten hours/days ago (gastric outlet obstruction); may have haematemesis
Timing	Early post-op period or related to eating patterns	Insidious onset, progressive
Red flags	Tachycardia (leak), peritonism, fever	Dysphagia (proximal tumour), palpable epigastric mass, left supraclavicular lymphadenopathy (Virchow's node), iron deficiency anaemia, acanthosis nigricans (paraneoplastic — malignant type)
Investigation	CT with oral contrast (leak), OGD (stenosis, ulcer)	OGD with biopsy (gold standard for diagnosis), CT TAP for staging

Critical Exam Point

Never assume that weight loss and vomiting in a bariatric surgery patient is simply from the surgery. Always consider the possibility of de novo pathology, including gastric cancer — especially if the gastric remnant (in RYGB) is not easily accessible by standard OGD. The excluded gastric remnant in RYGB is a "blind spot" — cancers arising here may present late. Some centres advocate preoperative OGD ± H. pylori eradication in all bariatric surgery candidates, especially in high-prevalence regions like East Asia ^[1]^[2].

Timing	Key Differentials	Approach
Pre-operative	Cushing syndrome, hypothyroidism, insulinoma, medication-induced obesity, genetic syndromes (Prader-Willi, MC4R), eating disorders	Endocrine workup (cortisol, TSH, glucose/insulin), drug history, psychological assessment, genetic testing if early-onset
Early post-operative ( < 30 days)	Anastomotic leak, staple line bleed, PE/DVT, bowel obstruction, rhabdomyolysis	CT with oral contrast, Hb monitoring, CTPA, CK levels
Late post-operative ( > 30 days)	Internal hernia, marginal ulcer, stomal stenosis, cholelithiasis, dumping syndrome, nutritional deficiencies, GORD (post-SG), weight regain	CT (swirl sign), OGD, barium swallow, RUQ USS, dietary assessment, micronutrient levels

High Yield Summary — Differential Diagnosis in Bariatric Surgery

Always exclude secondary/reversible causes of obesity before bariatric surgery — especially Cushing syndrome and hypothyroidism.
Tachycardia > 120 bpm in first 48 hours post-bariatric surgery = anastomotic leak until proven otherwise.
Internal hernia is specific to RYGB (mesenteric defects) — look for "swirl sign" on CT.
Dumping syndrome = early (osmotic, vasomotor) vs late (reactive hypoglycaemia). More common after RYGB because pylorus is bypassed.
Gallstones are very common after rapid weight loss — up to 30% incidence in first year.
The excluded gastric remnant in RYGB is a "blind spot" for gastric cancer surveillance.

Active Recall - Bariatric Surgery Differential Diagnosis

References

^[1] Lecture slides: GC 212. Weight loss and vomiting gastric cancer; abdominal imaging.pdf ^[2] Senior notes: maxim.md (section 3.8 Bariatric surgery)

Bariatric surgery is unique in that the "diagnosis" is not of a single disease but of a clinical state — severe obesity with or without comorbidities — that meets specific criteria for surgical intervention. The diagnostic workup therefore serves three purposes: (1) confirming eligibility (meeting indications, excluding contraindications), (2) preoperative risk stratification and optimisation, and (3) postoperative surveillance and complication detection. We will cover all three systematically.

1. Diagnostic Criteria for Bariatric Surgery Candidacy

All of the following must be met:

Criterion	Detail
Failed conservative management	Documented failure of structured lifestyle intervention (diet + exercise + behavioural therapy) ± pharmacotherapy for at least 6–12 months
BMI threshold (Asian cut-offs) ^[2]	BMI ≥ 35 kg/m² — with or without comorbidities OR BMI ≥ 30 kg/m² with T2DM or other major obesity-related comorbidities (hypertension, OSA, NAFLD, dyslipidaemia, PCOS) OR BMI ≥ 27.5 kg/m² with poorly controlled T2DM (emerging indication per IFSO-APC 2024 — "primary metabolic surgery")
Absence of contraindications ^[2]	No reversible endocrine causes (Cushing syndrome, hypothyroidism, insulinoma excluded), no active psychiatric disorders, no active substance abuse, patient capable of compliance with lifelong follow-up and supplementation
Multidisciplinary team assessment	Evaluated by surgeon, endocrinologist/physician, dietitian, psychologist/psychiatrist, anaesthetist
Informed consent	Patient understands risks, benefits, lifelong dietary changes, and need for supplementation

When the primary indication is metabolic surgery for T2DM, the ABCD score helps predict likelihood of diabetes remission and guides patient selection:

Component	Scoring	Rationale
A — Age	0–4 points (younger → higher)	Younger patients have better β-cell reserve and regenerative capacity
B — BMI	0–3 points (higher → higher)	Greater BMI = more weight to lose = greater metabolic improvement; also correlates with insulin resistance (which is reversible) rather than β-cell failure
C — C-peptide	0–2 points (higher → higher)	C-peptide reflects endogenous insulin production. High C-peptide = functioning β-cells that can respond to improved incretin signalling post-surgery. Low C-peptide = burned-out β-cells = poor chance of remission
D — Duration of DM	0–1 point (shorter → higher)	Shorter duration = less cumulative glucotoxicity and lipotoxicity = more β-cells still alive

Total score = 10
Score > 6 → predicts T2DM remission after bariatric surgery ^[2]
Score ≤ 2 → very low chance of remission; surgery still beneficial for weight loss but patient should not expect diabetes cure

Clinical Pearl: C-peptide Interpretation

C-peptide is the connecting peptide cleaved from proinsulin when insulin is processed in β-cells. It is secreted in a 1:1 molar ratio with insulin. Unlike insulin, C-peptide is not extracted by the liver and has a longer half-life (~30 min vs ~5 min for insulin), making it a far more reliable marker of endogenous insulin secretion. A fasting C-peptide > 1.0 ng/mL (or stimulated C-peptide > 2.0 ng/mL) generally indicates adequate β-cell reserve for metabolic surgery to have a meaningful effect on diabetes.

The preoperative workup is structured as a multidisciplinary assessment across several domains. Think of it as asking: Is this patient safe for surgery? What comorbidities need optimisation? Which procedure is best? What is the baseline for postoperative monitoring?

Master Diagnostic Algorithm

3. Investigation Modalities — Detailed Breakdown

Measurement	Method	Key Findings and Interpretation
BMI	Weight (kg) / Height² (m²)	Defines eligibility. Asian cut-offs: ≥ 30 with T2DM, ≥ 35 without ^[2]. Remember BMI does not distinguish fat vs lean mass (can be misleading in muscular individuals or those with oedema)
Waist circumference	Measured at midpoint between lowest rib and iliac crest	Asian cut-offs: ≥ 90 cm (men), ≥ 80 cm (women) = central obesity. Central adiposity is the strongest correlate of metabolic risk (visceral fat is metabolically active, producing IL-6, TNF-α, resistin)
Neck circumference	At the level of the cricothyroid membrane	> 43 cm (men), > 41 cm (women) → strong predictor of OSA and difficult intubation

3.2 Blood Investigations

Test	Target Condition	Key Findings
TSH ± free T4	Hypothyroidism	↑ TSH, ↓ fT4 = primary hypothyroidism. Treat with levothyroxine before considering surgery. Note: hypothyroidism alone rarely causes morbid obesity (usually 5–10 kg gain) but must be optimised
Overnight 1 mg dexamethasone suppression test (DST)	Cushing syndrome	Give 1 mg dexamethasone at 11 pm → measure 8 am cortisol. Normal: cortisol < 50 nmol/L (suppressed). Failure to suppress → Cushing syndrome. Confirm with 24-hour urinary free cortisol or late-night salivary cortisol
Fasting glucose + fasting insulin (± 72-hour supervised fast)	Insulinoma	Inappropriately elevated insulin ( > 3 µU/mL) and C-peptide ( > 0.6 ng/mL) during documented hypoglycaemia ( < 2.5 mmol/L) = endogenous hyperinsulinism. 72-hour fast is gold standard but only if clinically suspected

Test	Purpose	Key Findings and Interpretation
Fasting glucose	Screen/diagnose T2DM	≥ 7.0 mmol/L = diabetes; 5.6–6.9 mmol/L = impaired fasting glucose
HbA1c	Assess glycaemic control over prior 2–3 months	≥ 6.5% = diabetes; 5.7–6.4% = prediabetes. Target preoperatively: < 8% (reduce perioperative infection risk). HbA1c also used to monitor T2DM remission post-surgery
Fasting C-peptide	Assess β-cell reserve → ABCD score ^[2]	> 1.0 ng/mL (fasting) suggests adequate reserve. < 0.5 ng/mL suggests near-complete β-cell failure — surgery unlikely to achieve DM remission but still beneficial for weight
Fasting lipid profile (TC, LDL, HDL, TG)	Assess dyslipidaemia as comorbidity	↑ TG, ↓ HDL = metabolic syndrome pattern. Baseline for monitoring improvement post-surgery
LFTs (ALT, AST, ALP, GGT, bilirubin, albumin)	Screen for NAFLD/MASLD	↑ ALT/AST (typically ALT > AST; ratio reverses in cirrhosis or alcohol). Albumin also serves as nutritional marker (half-life ~20 days) ^[3] — but is confounded by inflammation and liver synthetic function
Fasting insulin (± HOMA-IR calculation)	Quantify insulin resistance	HOMA-IR = (fasting insulin × fasting glucose) / 22.5. Values > 2.5 suggest insulin resistance. Not routinely required but useful in research/borderline cases

This is essential because obese patients can be malnourished ("sarcopenic obesity") ^[3], and bariatric surgery will worsen absorption of certain nutrients (especially after RYGB):

Test	Deficiency Screened	Why This Deficiency Matters in Bariatric Surgery
Iron studies (serum iron, ferritin, TIBC, transferrin saturation)	Iron deficiency	Iron is primarily absorbed in the duodenum (via DMT1 and ferroportin in enterocytes). RYGB bypasses the duodenum → high risk of iron deficiency anaemia post-op. Pre-existing deficiency common in menstruating women and those with poor dietary quality
Vitamin B12	B12 deficiency	B12 absorption requires: (1) gastric acid to release B12 from food, (2) intrinsic factor from parietal cells, (3) absorption in the terminal ileum. After SG: reduced acid and intrinsic factor production. After RYGB: both reduced gastric acid AND bypassed duodenum (where B12-IF complex begins its journey). Deficiency → megaloblastic anaemia, peripheral neuropathy, subacute combined degeneration of the cord
Folate (serum and/or RBC folate)	Folate deficiency	Absorbed in the proximal jejunum — bypassed in RYGB. Deficiency → megaloblastic anaemia. Especially important in women of childbearing age (neural tube defect prevention)
Vitamin D + Calcium + PTH	Vitamin D deficiency, secondary hyperparathyroidism, osteoporosis risk	Vitamin D (fat-soluble) absorption depends on bile salts + jejunal absorptive surface. Calcium absorbed in the duodenum (active, vitamin D-dependent) and jejunum (passive). Both bypassed in RYGB → chronic low Ca²⁺ → secondary hyperparathyroidism (↑ PTH) → bone resorption → metabolic bone disease/osteoporosis. Obese patients often have baseline vitamin D deficiency (sequestration in adipose tissue)
Thiamine (Vitamin B1)	Thiamine deficiency	Risk of Wernicke encephalopathy (confusion, ophthalmoplegia, ataxia) in the early postoperative period if patient has prolonged vomiting and is not supplemented. Thiamine is absorbed in the jejunum. Rapidly depleted in starvation states
Zinc, copper	Micronutrient deficiency	Absorbed in the duodenum/proximal jejunum. Deficiency → impaired wound healing (zinc), anaemia/neutropaenia/myelopathy (copper)
Prealbumin (transthyretin)	Acute nutritional status	Half-life ~2 days → more sensitive to acute nutritional changes than albumin ^[3]. Useful for monitoring response to preoperative nutritional optimisation

Why Check Nutrients BEFORE Surgery?

Many students assume nutritional deficiencies are only a post-operative concern. In reality, up to 50% of bariatric surgery candidates have pre-existing micronutrient deficiencies (especially iron, vitamin D, B12, and folate) due to poor dietary quality — eating calorie-dense but nutrient-poor foods. If you don't correct these deficiencies preoperatively, the patient enters surgery in a compromised state, and the surgery will only make absorption worse. This is why preoperative nutritional baseline and correction is mandatory ^[3].

Test	Purpose	Interpretation
FBC (Full Blood Count)	Screen for anaemia (iron, B12, folate deficiency), polycythaemia (OSA-related chronic hypoxia), thrombocytosis	Microcytic anaemia → iron deficiency; macrocytic → B12/folate; polycythaemia → consider OSA/Pickwickian syndrome
Coagulation (PT/APTT/INR)	Preoperative haemostasis screen; also assess liver synthetic function (NAFLD)	Prolonged PT/INR → consider coagulopathy (liver disease, vitamin K deficiency)
Group and screen	Standard preoperative	In case of intraoperative/postoperative haemorrhage

Investigation	Purpose	Key Findings
ECG	Baseline; screen for arrhythmias, LVH, ischaemia	LVH (from chronic hypertension); AF (common in obese patients); Q waves or ST changes suggesting IHD
CXR	Baseline; assess cardiomegaly, pulmonary congestion, atelectasis	Cardiomegaly (HTN), elevated hemidiaphragm (abdominal obesity restricting diaphragmatic excursion), basal atelectasis
Polysomnography (or STOP-BANG questionnaire for screening)	Diagnose and grade OSA	OSA is present in 60–80% of bariatric surgery candidates. AHI (apnoea-hypopnoea index): 5–15 = mild, 15–30 = moderate, > 30 = severe. Severe OSA → initiate CPAP preoperatively (reduces perioperative risk of arrhythmia, desaturation, difficult intubation, post-operative respiratory failure)
Echocardiography	If clinical suspicion of heart failure, pulmonary hypertension, or significant cardiac disease	Assess LVEF, diastolic function, RV function, pulmonary artery pressure (obesity → pulmonary hypertension from chronic hypoxia/OSA)
Spirometry / PFTs	If respiratory symptoms or morbid obesity	Restrictive pattern common (↓ FVC, normal FEV1/FVC ratio) due to reduced chest wall compliance from abdominal and thoracic fat

STOP-BANG Screening for OSA

S = Snoring; T = Tired (daytime sleepiness); O = Observed apnoeas; P = Pressure (treated hypertension); B = BMI > 35; A = Age > 50; N = Neck circumference > 40 cm; G = Gender (male). Score ≥ 3 = intermediate-high risk → formal polysomnography indicated.

Investigation	Purpose	Key Findings
Upper GI Endoscopy (OGD)	Preoperative OGD is recommended for all bariatric surgery candidates, especially in regions with high H. pylori and gastric cancer prevalence (East Asia, including HK) ^[1]	Screen for: (1) H. pylori — eradicate before surgery (reduces marginal ulcer risk post-RYGB; reduces gastric cancer risk in excluded remnant). (2) Hiatal hernia — may need concurrent repair; influences procedure choice (large hiatal hernia favours RYGB over SG). (3) Barrett's oesophagus — indicates chronic GORD; SG may worsen GORD → favour RYGB. (4) Gastric pathology — polyps, dysplasia, early cancer in the body/fundus (would be removed in SG anyway, but changes surgical planning). (5) Peptic ulcer disease — treat before surgery
Abdominal ultrasound (USS)	Screen for gallstones and hepatic steatosis ^[1]	Gallstones: Present in ~20% preoperatively (obesity is a risk factor for cholesterol stones — "fat, female, forty, fertile, fair"). If symptomatic → consider concurrent cholecystectomy. Hepatic steatosis: Echogenic liver on USS; may indicate NAFLD/NASH. Severe steatosis → enlarged left lobe of liver which obscures the GEJ → makes laparoscopic surgery technically difficult → preoperative liver shrinkage diet (low-calorie, high-protein for 2–4 weeks) to reduce liver volume
Barium swallow / upper GI series	Occasionally used to assess anatomy, hiatal hernia, or post-operative complications	Preoperatively: assess hiatal hernia size, oesophageal motility. Postoperatively: assess for anastomotic leak (water-soluble contrast), stomal stenosis, pouch size

Assessment	Purpose	Key Findings
Structured psychiatric/psychological evaluation	Mandatory in all bariatric surgery programmes	Screen for: (1) Binge eating disorder (BED) — present in 25–50% of candidates; needs treatment (CBT ± pharmacotherapy) before surgery or outcomes are poor. (2) Depression/anxiety — if severe/uncontrolled, must stabilise first; post-operative mood disorders common. (3) Active substance abuse — alcohol use disorder especially (contraindication ^[2]); after RYGB, alcohol absorption is faster and more potent → risk of "addiction transfer". (4) Unrealistic expectations — patients expecting surgery alone to solve all problems without lifestyle change. (5) Capacity for compliance — lifelong vitamin supplementation, follow-up, dietary modification

Addiction Transfer

After RYGB, alcohol bypasses the stomach (reduced first-pass metabolism) and is absorbed rapidly in the jejunum → higher peak blood alcohol levels from the same amount of alcohol. Combined with the loss of food as an emotional coping mechanism, some patients "transfer" their food addiction to alcohol or other substances. This is called addiction transfer and is a real long-term concern. It is one reason why pre-operative psychological screening is so important.

Assessment	Purpose	Key Findings
Airway assessment	Obese patients have high rates of difficult airway	Mallampati class III/IV, short thick neck, limited neck extension, ↑ neck circumference → anticipate difficult intubation; may require fibreoptic intubation or awake intubation
VTE risk	Obese patients are high risk for DVT/PE (obesity is an independent VTE risk factor; immobility; venous stasis; hypercoagulable state from chronic inflammation)	All bariatric surgery patients should receive VTE prophylaxis: LMWH (weight-adjusted dosing) + pneumatic compression devices + early mobilisation. Some programmes extend chemoprophylaxis for 2–4 weeks post-discharge
Vascular access	Difficult peripheral IV access in obese patients	May require ultrasound-guided IV placement or central line
Drug dosing	Altered pharmacokinetics in obesity	Many drugs need dosing based on adjusted body weight or ideal body weight rather than total body weight. Lipophilic drugs (e.g., benzodiazepines) have ↑ volume of distribution

4. Postoperative Investigation and Surveillance Protocol

The primary concern is detecting anastomotic leak and staple line bleeding:

Investigation	Timing	Key Findings
Clinical monitoring (HR, BP, temp, urine output, drain output)	Continuous	Tachycardia > 120 bpm is the single most important early sign of anastomotic leak — often precedes fever, pain, and peritonism. Falling BP, oliguria, rising lactate = evolving sepsis/haemorrhage
CT abdomen with oral water-soluble contrast	If leak suspected (tachycardia, fever, peritonism)	Extravasation of contrast from staple line or anastomosis = confirmed leak. Also assess for free fluid, abscess, pneumoperitoneum. Gold standard for postoperative leak detection
FBC, CRP, lactate	Daily for first 2–3 days	Rising WCC and CRP trend + ↑ lactate → concerning for leak/sepsis. Dropping Hb → staple line bleed
Upper GI contrast study (water-soluble)	Some centres perform routinely on POD 1–2; others only if symptomatic	Alternative to CT for leak detection — patient swallows gastrografin under fluoroscopy; look for contrast extravasation. Less sensitive than CT but quicker and avoids radiation from CT

Investigation	Frequency	Purpose
Weight tracking	Every visit (monthly for first 6 months)	Monitor weight loss trajectory; expected: 50–70% excess weight loss at 12 months for SG; 60–80% for RYGB
Nutritional bloods (iron, B12, folate, vitamin D, calcium, PTH, zinc, copper, thiamine, albumin)	3 months, 6 months post-op	Early detection of deficiencies — especially iron and B12. Start lifelong supplementation regimen immediately post-op
HbA1c, fasting glucose	3 months post-op	Assess T2DM response — many patients can reduce or stop diabetic medications within weeks
Lipid profile, LFTs	6 months post-op	Monitor metabolic improvement
OGD	If symptomatic (dysphagia, pain, GORD, suspected marginal ulcer)	Assess stomal stenosis, marginal ulcer, GORD, band erosion
RUQ USS	If RUQ pain	Screen for new gallstones (up to 30% incidence in first year)

Investigation	Rationale
Annual nutritional blood panel (iron, B12, folate, vitamin D, calcium, PTH, zinc, copper, albumin)	Lifelong malabsorption risk (especially RYGB). Late-onset deficiencies can develop years later. Secondary hyperparathyroidism (↑ PTH with low Ca²⁺/vitamin D) → metabolic bone disease if untreated
HbA1c	Monitor for DM relapse (occurs in ~20–30% within 5 years; risk factors: longer DM duration, lower ABCD score)
DEXA scan	Every 2 years post-RYGB
Psychological review	Annually
Dietary/lifestyle review	Every visit

Suspected Complication	Best Investigation	Key Finding
Anastomotic / staple line leak	CT abdomen with oral water-soluble contrast	Contrast extravasation, pneumoperitoneum, free fluid, abscess collection
Staple line bleed	CT angiography (if haemodynamically stable); OR direct to theatre if unstable	Active contrast blush adjacent to staple line; haemoperitoneum
Internal hernia (RYGB-specific)	CT abdomen	"Swirl sign" (mesenteric vascular rotation around a central point), clustered small bowel, closed-loop obstruction
Stomal stenosis	OGD + barium swallow	Inability to pass endoscope through anastomosis; narrowing on barium swallow. OGD allows therapeutic balloon dilation simultaneously
Marginal ulcer	OGD	Ulcer at gastrojejunal anastomosis (RYGB); test for H. pylori; biopsy to exclude malignancy
Gastrogastric fistula (RYGB)	Upper GI contrast study or CT with oral contrast	Contrast passing from pouch into excluded gastric remnant
GORD worsening (post-SG)	OGD + 24-hour pH/impedance study	Oesophagitis on OGD; DeMeester score > 14.7 on pH study; presence of Barrett's oesophagus on biopsy
Gallstones	RUQ USS	Echogenic foci with posterior acoustic shadowing in gallbladder
Nutritional deficiency (late)	Blood tests as above	Microcytic anaemia (iron), macrocytic anaemia (B12/folate), ↑ PTH with low Ca²⁺/vitamin D (secondary hyperparathyroidism), ↓ albumin/prealbumin (protein malnutrition)
Dumping syndrome	Clinical diagnosis; can confirm with oral glucose tolerance test	Early dumping: symptoms 15–30 min post-meal. Late dumping: confirm with reactive hypoglycaemia ( < 3.3 mmol/L) on OGTT at 1–3 hours
Band slip/erosion (gastric banding)	AXR + OGD	"O-sign" on AXR: band rotated from oblique to horizontal position = slip. OGD: band visible eroding into gastric lumen

High Yield Summary — Diagnosis of Bariatric Surgery

Preoperative workup is multidisciplinary — not just surgical but medical, nutritional, psychological, and anaesthetic.
OGD is recommended for all bariatric candidates in East Asia — to screen for H. pylori, hiatal hernia, Barrett's, and gastric pathology (high prevalence region) ^[1].
Tachycardia is the sentinel sign of anastomotic leak — CT with oral contrast is the gold standard investigation.
Nutritional baseline must be established before surgery because obese patients are frequently micronutrient-deficient ^[3].
Lifelong annual nutritional surveillance is mandatory — deficiencies can appear years after surgery.
The ABCD score (Age, BMI, C-peptide, Duration) with total = 10 and threshold > 6 guides metabolic surgery patient selection for T2DM ^[2].

Active Recall - Bariatric Surgery: Diagnostics and Investigations

The management of bariatric surgery is not simply "the operation." It is a lifelong continuum spanning preoperative optimisation, intraoperative surgical technique, and decades of postoperative care. Think of the operation itself as the midpoint, not the endpoint. The best bariatric outcomes come from multidisciplinary programmes where surgeon, physician/endocrinologist, dietitian, psychologist, exercise physiologist, and nursing specialist work in concert.

2. Conservative Management (Non-Surgical)

Every bariatric surgery candidate must have failed conservative management before qualifying for surgery ^[2]. Understanding what constitutes conservative management — and why it fails — is essential.

Component	Detail	Why It Often Fails
Dietary modification	Caloric deficit of 500–750 kcal/day; structured meal plans; Mediterranean or DASH-type diets; reduce processed foods	Metabolic adaptation: as weight is lost, basal metabolic rate drops (the body "defends" its set point); hunger hormones (↑ ghrelin, ↓ leptin, ↓ PYY) increase — biology fights against sustained weight loss
Physical activity	150–300 min/week moderate-intensity aerobic exercise + resistance training	Difficult in severe obesity due to joint pain, breathlessness, embarrassment; exercise alone produces modest weight loss (~2–3 kg) without dietary change
Behavioural therapy	CBT for eating behaviours; stimulus control; self-monitoring (food diary, weighing); stress management	Requires long-term engagement; relapse rates high without ongoing support

The fundamental problem: lifestyle modification alone achieves ~3–5% body weight loss on average, and most patients regain weight within 2–5 years. For a patient with BMI 45, this is clinically insignificant. This is precisely why surgery exists — it is the only intervention that produces durable, sustained weight loss of 20–35% total body weight.

Anti-obesity medications are increasingly important — some newer agents approach surgical levels of weight loss:

Drug	Mechanism	Expected Weight Loss	Key Points
Semaglutide (Wegovy, 2.4 mg/week SC)	GLP-1 receptor agonist — mimics the incretin effect. Slows gastric emptying → early satiety. Acts on hypothalamic appetite centres → reduced hunger. ↑ Insulin secretion, ↓ glucagon	~15–17% total body weight (STEP trials)	Game-changing drug; also has cardiovascular benefit. Common side effects: nausea, vomiting (usually self-limited). CI: personal/family history of medullary thyroid cancer, MEN2 (GLP-1RA → C-cell hyperplasia in animal models)
Tirzepatide (Mounjaro/Zepbound, SC weekly)	Dual GIP + GLP-1 receptor agonist — combines two incretin pathways	~20–22% total body weight (SURMOUNT trials) — approaches surgical weight loss	Newest agent; even more effective than semaglutide for weight loss. Similar side effect profile
Liraglutide (Saxenda, 3.0 mg/day SC)	GLP-1 receptor agonist (shorter-acting than semaglutide)	~8% total body weight	Older GLP-1RA; largely superseded by semaglutide for obesity indication
Orlistat (Xenical)	Pancreatic lipase inhibitor → blocks ~30% of dietary fat absorption in the gut	~3–4% total body weight	Side effects: steatorrhoea, faecal urgency, fat-soluble vitamin malabsorption. Poor tolerability limits use
Naltrexone-bupropion (Contrave)	Naltrexone (opioid antagonist) + bupropion (noradrenaline-dopamine reuptake inhibitor) → synergistic effect on hypothalamic POMC neurons to reduce appetite	~5–6% total body weight	CI: uncontrolled hypertension, seizure history, eating disorders (bupropion lowers seizure threshold)
Phentermine-topiramate (Qsymia)	Phentermine (sympathomimetic → noradrenaline release → appetite suppression) + topiramate (GABA enhancement, carbonic anhydrase inhibition → reduces appetite through multiple pathways)	~10% total body weight	Not widely available outside USA. CI: cardiovascular disease, pregnancy (topiramate is teratogenic — cleft palate)

GLP-1 Receptor Agonists and Bariatric Surgery

The GLP-1RA revolution has changed the bariatric landscape. Semaglutide and tirzepatide achieve weight loss that was previously only possible with surgery. However, key differences remain: (1) Weight is regained when the drug is stopped (surgery is permanent). (2) Surgery still produces superior T2DM remission (mechanical + hormonal changes > pharmacological GLP-1 alone). (3) Surgery is a one-time intervention vs lifelong medication (cost and compliance). (4) Some patients may use GLP-1RA as a bridge to surgery (preoperative weight loss → safer operation) or as adjunct post-surgery if weight loss is inadequate. The interplay between pharmacotherapy and surgery is the frontier of obesity medicine.

3. Preoperative Optimisation — "Feed Him Up Before Surgery"

Drawing directly from surgical nutrition principles ^[3], preoperative preparation is critical:

Very Low Calorie Diet (VLCD) — typically 800–1000 kcal/day, high protein, low carbohydrate — for 2–4 weeks before surgery
Why?: In morbid obesity, the left lobe of the liver is massively enlarged with fatty infiltration (steatosis). This enlarged liver sits directly over the gastro-oesophageal junction and proximal stomach — the operative field. An enlarged liver makes laparoscopic access extremely difficult and increases risk of intraoperative liver injury.
The VLCD depletes hepatic glycogen stores (within 24–48 hours) and then mobilises hepatic triglycerides → liver shrinks by 10–20% in volume within 2 weeks. This provides critical operative space.
Also initiates weight loss, improves glycaemic control, and psychologically prepares the patient for post-operative dietary changes.

Correct all identified micronutrient deficiencies before surgery — especially iron, vitamin D, B12, folate, thiamine
Protein optimisation: Aim for 60–80 g protein/day preoperatively to preserve lean mass
If severely malnourished (SGA Class C): Consider delaying surgery for 2–4 weeks of intensive nutritional support ^[3]

Comorbidity	Preoperative Target	Rationale
T2DM	HbA1c < 8% (ideally < 7.5%)	Hyperglycaemia → impaired wound healing (glycosylation of structural proteins, impaired neutrophil function, endothelial dysfunction) → increased surgical site infection
Hypertension	BP < 140/90 mmHg	Reduce perioperative cardiovascular risk
OSA	Initiate CPAP if AHI > 15	Untreated OSA → perioperative respiratory failure risk (desaturation during induction, post-extubation obstruction, opioid sensitivity); CPAP improves upper airway patency and oxygenation
Smoking	Cessation ≥ 4–6 weeks preoperatively	Smoking → impaired wound healing (nicotine causes vasoconstriction → tissue ischaemia), increased marginal ulcer risk post-RYGB, increased respiratory complications. Active smoking is a relative contraindication to RYGB
H. pylori	Eradicate if positive on preoperative OGD	Post-RYGB, the excluded gastric remnant is inaccessible to standard OGD → H. pylori in the remnant → risk of peptic ulcer, gastric cancer in a "blind" area. Also reduces marginal ulcer risk at the gastrojejunal anastomosis
VTE risk	Plan prophylaxis	All bariatric patients are high VTE risk (obesity + surgery + immobility). Plan: LMWH (enoxaparin 40 mg SC or weight-adjusted higher dose), pneumatic compression devices, early mobilisation

Set realistic expectations: Average excess weight loss is 50–70% (not 100%). Weight loss plateaus at 12–18 months. Some weight regain (5–10%) is normal at 2–5 years.
Dietary counselling: Post-operative diet progression (liquid → puree → soft → regular over 4–6 weeks). Lifelong small meals, high protein, low simple carbohydrate. No drinking with meals (fills the small pouch with liquid instead of nutrient-dense food).
Support groups: Peer support improves long-term adherence.

4. Surgical Management — Procedure Details and Selection

The choice of procedure is individualised based on:

Factor	Influence on Procedure Choice
GORD	If significant GORD or Barrett's oesophagus → RYGB (SG may worsen GORD by increasing intragastric pressure and disrupting the angle of His)
BMI	BMI 30–45: SG or RYGB both excellent. BMI > 50 ("super-morbid"): RYGB or BPD-DS (greater weight loss needed); or staged approach (SG first → conversion to RYGB later if inadequate)
T2DM severity / ABCD score	Higher ABCD score → RYGB preferred (superior T2DM remission rates ~80% vs ~60% for SG) ^[2]. If primary goal is metabolic surgery, RYGB has the best evidence
Surgeon expertise and centre volume	High-volume bariatric centres have lower complication rates. Surgeon comfort with RYGB (technically more demanding) matters
Patient preference	After full informed consent discussing pros/cons of each procedure
Need for endoscopic access to stomach	RYGB creates an excluded gastric remnant that is difficult to access. If patient has known gastric pathology needing surveillance, SG preserves access. If in a region with high gastric cancer risk (East Asia), some argue for SG to maintain surveillance ability — though preoperative OGD with H. pylori eradication mitigates this ^[1]
Revision surgery	Failed SG → convert to RYGB (most common revision). Failed RYGB → lengthening of limbs, or conversion to BPD-DS

4.2 Detailed Surgical Technique and Principles

Technique:

Laparoscopic approach (standard; open rare)
Patient in reverse Trendelenburg position (head up) → gravity pulls abdominal contents caudally, improving exposure
Mobilise greater curvature: divide gastrocolic ligament and short gastric vessels using energy device (LigaSure/Harmonic scalpel) from ~5 cm proximal to the pylorus up to the angle of His
Insert calibration bougie (32–40 Fr) along the lesser curvature — this determines sleeve width
Sequential stapled division of the stomach along the bougie using endoscopic linear staplers — from antrum to angle of His
The resected greater curvature (containing the fundus) is removed as specimen → sent to pathology
Staple line reinforcement: Oversewing, buttress material, or fibrin sealant — reduces bleed and leak risk (technique varies by surgeon)
No anastomosis — this is a purely resective procedure
Test for leak intraoperatively: air insufflation via NGT with the staple line submerged in saline (look for bubbles) or methylene blue test

Key technical points:

Starting point 5 cm from pylorus preserves the antral pump → maintained gastric emptying → lower dumping risk
Bougie size matters: too narrow (< 32 Fr) → higher stenosis and leak risk; too wide (> 40 Fr) → less restriction → reduced weight loss
The angle of His must be included in the resection to avoid a functional fundus remnant (which would dilate and reduce restriction)

Technique:

Laparoscopic approach (standard)
Create gastric pouch: Divide the stomach using endoscopic linear staplers to create a small pouch (~30 mL) from the cardia/proximal lesser curvature, completely separated from the gastric remnant
Identify ligament of Treitz: Trace small bowel distally from Treitz for ~50–75 cm → divide jejunum here
Create the Roux (alimentary) limb: Bring the distal cut end of jejunum up (antecolic or retrocolic route) and anastomose to the gastric pouch → gastrojejunostomy (using linear or circular stapler, or hand-sewn). This is where food enters the small bowel.
Create the biliopancreatic (BP) limb reconnection: Anastomose the proximal cut end of jejunum (carrying bile and pancreatic juice) to the Roux limb ~75–150 cm downstream from the gastrojejunostomy → jejunojejunostomy
Close mesenteric defects: Peterson's space (between Roux limb mesentery and transverse mesocolon) and the jejunojejunostomy mesenteric defect → critical to prevent internal hernia ^[2]
Test gastrojejunostomy for integrity: methylene blue or air leak test

Limb length terminology (frequently tested):

Limb	Definition	Clinical Significance
Biliopancreatic (BP) limb	From ligament of Treitz to the jejunojejunostomy — carries bile and pancreatic juice but no food	Length determines degree of malabsorption. Longer BP limb = more malabsorption
Roux (Alimentary) limb	From gastrojejunostomy to jejunojejunostomy — carries food but no digestive enzymes	Food travels through this limb undigested. Typical length: 75–150 cm
Common channel	From jejunojejunostomy to ileocaecal valve — where food meets bile/pancreatic juice and absorption occurs	Shorter common channel = more malabsorption. In standard RYGB, the common channel is long (most of the ileum) → moderate malabsorption. In BPD-DS, common channel is very short → severe malabsorption

Technique: Silicone band placed around the proximal stomach via pars flaccida technique (through the lesser omentum), creating a small pouch above the band. Band is connected to a subcutaneous port (usually on the anterior rectus sheath) via silicone tubing. Saline is injected into the port to inflate/tighten the band (more restriction) or withdrawn to loosen it ^[2].

Why it has fallen out of favour:

Poorest long-term weight loss (~40% EWL)
High reoperation/removal rate (30–50% within 10 years)
Complications: band slippage, band erosion into gastric wall, port-site infection, oesophageal dilation, reflux
Entirely replaced by SG and RYGB in modern practice

Technique: SG + division of duodenum just beyond the pylorus + bypass of most of the small bowel, leaving only ~75–100 cm common channel.

Indication: Super-morbid obesity (BMI > 50) where maximum weight loss is needed. Rarely performed due to severe nutritional complications.

Principle	Detail	Rationale
Laparoscopic approach	Standard for all bariatric procedures	Lower wound complications (SSI, hernia) in obese patients; faster recovery; less pain; earlier mobilisation. Open approach reserved for complex revisions or conversions
Pneumoperitoneum	CO₂ insufflation to 15 mmHg	Higher pressures may be needed in obese patients for adequate working space but increase risk of haemodynamic compromise (↓ venous return, ↑ airway pressures)
Patient positioning	Reverse Trendelenburg + legs apart (French position) or supine split-leg	Improves exposure; reduces diaphragmatic splinting
VTE prophylaxis	Pneumatic compression devices applied pre-induction; LMWH given 2–12 hours preop or postop (varies by protocol)	Bariatric patients are among the highest-risk groups for VTE. Enoxaparin dose: 40 mg BD (some protocols use weight-adjusted 0.5 mg/kg BD)
Antibiotic prophylaxis	Single dose IV at induction (cefazolin 2–3 g — higher dose for BMI > 40)	Prevent SSI; dose must be weight-adjusted in obesity (standard 1 g dose is subtherapeutic)
Leak testing	Intraoperative air or methylene blue test of staple line/anastomosis	Early detection prevents missed leaks presenting as sepsis on the ward

6. Postoperative Management

Domain	Management	Rationale
Monitoring	Hourly vitals — especially HR (tachycardia > 120 bpm = concern for leak/bleed) ^[2]	Anastomotic leak is the most feared early complication. Tachycardia is the sentinel sign
Pain management	Multimodal analgesia — paracetamol + NSAIDs (if no contraindication) + local anaesthetic wound infiltration ± PCA opioid (minimize opioid use)	ERAS protocol: opioid-sparing approach reduces ileus, respiratory depression (especially dangerous in OSA patients), nausea. Avoid NSAIDs if RYGB (marginal ulcer risk) — some centres avoid, others allow short courses
VTE prophylaxis	LMWH (enoxaparin 40 mg BD or weight-adjusted) + pneumatic compression + early mobilisation (day 0 — same day as surgery)	Obese patients are at very high VTE risk. Early ambulation is the single most important non-pharmacological measure
Diet	Clear liquids on day 0–1 (sips of water once fully awake) → progress as tolerated	Early oral feeding is part of ERAS; maintains gut mucosal integrity ^[3]. Some centres perform routine upper GI contrast study on POD 1 before advancing diet
Glucose monitoring	Finger-prick glucose QID	Diabetic patients often have dramatic reduction in glucose within hours of surgery (especially RYGB — incretin effect). Must reduce or stop insulin/sulfonylureas immediately to avoid hypoglycaemia. Metformin usually stopped perioperatively (AKI risk) and cautiously restarted
Respiratory care	Incentive spirometry, chest physiotherapy, semi-upright positioning, CPAP if known OSA	Obese patients are at high risk of atelectasis, hypoventilation, and desaturation. OSA patients who stop CPAP postoperatively can develop life-threatening respiratory failure

This is one of the most practically important aspects of management, directly from nutritional principles ^[3]:

Phase	Timing	Content	Rationale
Phase 1: Clear liquids	Day 0–1	Water, clear broth, sugar-free jelly, diluted juice	Test tolerance; minimal stress on staple lines/anastomosis
Phase 2: Full liquids	Day 2 to Week 1–2	Protein shakes, milk, smooth soups, yoghurt (strained)	Deliver protein (aim 60–80 g/day via supplements) while allowing surgical healing
Phase 3: Puree	Week 2–4	Blended meats, hummus, pureed vegetables, cottage cheese	Gradual reintroduction of solid texture; still low volume (60–120 mL per meal)
Phase 4: Soft solids	Week 4–6	Soft fish, scrambled eggs, soft cooked vegetables, ground meat	Test mechanical tolerance of the new gastric anatomy
Phase 5: Regular diet	Week 6+	Small, protein-first meals; avoid simple sugars, carbonated drinks, tough meats	Lifelong dietary principles: eat slowly, chew thoroughly, protein with every meal, stop when full, no drinking with meals (displaces food from tiny pouch)

Why 'Protein First'?

After bariatric surgery, total food volume is drastically reduced. If the patient fills their small pouch/sleeve with carbohydrates or fats first, they will not have room for protein — leading to muscle wasting, hair loss, and poor wound healing. The rule of "protein first" ensures adequate protein intake (~60–80 g/day) within the limited volume. This is why every bariatric programme employs a dedicated dietitian.

All bariatric surgery patients require lifelong vitamin and mineral supplementation — the specific regimen depends on the procedure:

Supplement	Sleeve Gastrectomy	RYGB	Rationale
Multivitamin (bariatric-specific)	1 daily	2 daily	Covers multiple micronutrients; higher dose for RYGB due to malabsorption
Vitamin B12	1000 µg/day sublingual or 1000 µg IM monthly	1000 µg/day sublingual or 1000 µg IM monthly	Reduced intrinsic factor production (SG: less gastric acid; RYGB: less acid + bypassed duodenum). Sublingual/IM bypasses GI absorption
Iron (with vitamin C)	45–60 mg elemental iron/day	45–60 mg elemental iron/day (may need IV iron if oral not tolerated/absorbed)	Duodenum bypassed in RYGB; reduced acid impairs Fe³⁺ → Fe²⁺ conversion. Vitamin C co-administration enhances non-haem iron absorption (reduces Fe³⁺ to Fe²⁺)
Calcium citrate (not carbonate)	1200–1500 mg/day in divided doses	1200–1500 mg/day in divided doses	Calcium citrate is preferred over carbonate because citrate does NOT require gastric acid for absorption — critical after SG/RYGB where acid is reduced. Calcium carbonate requires acid environment for ionisation and absorption
Vitamin D3	3000 IU/day (titrate to 25-OH-D > 75 nmol/L)	3000 IU/day (titrate to levels)	Fat-soluble vitamin; absorption impaired with fat malabsorption. Synergistic with calcium for bone health. Deficiency → secondary hyperparathyroidism → osteoporosis
Folate	400–800 µg/day	800–1000 µg/day	Absorbed in proximal jejunum (bypassed in RYGB). Essential for women of childbearing age (neural tube defect prevention — advise contraception for 12–18 months post-surgery)
Thiamine (B1)	As needed	As needed (especially if prolonged vomiting)	Rapidly depleted in starvation/vomiting. Deficiency → Wernicke encephalopathy (confusion, ophthalmoplegia, ataxia) — a surgical emergency. Supplement empirically if any prolonged vomiting post-bariatric surgery
Zinc, copper	Included in bariatric multivitamin	Included; may need additional supplementation	Zinc and copper compete for absorption (excess zinc → copper deficiency). Monitor levels annually

Calcium Citrate vs Calcium Carbonate

This is a commonly tested pharmacology point. Calcium carbonate requires an acidic environment for dissolution and absorption. After bariatric surgery (especially RYGB), gastric acid production is markedly reduced → calcium carbonate is poorly absorbed. Calcium citrate is soluble in any pH and does not require acid → it is the preferred calcium supplement in all bariatric surgery patients. This same principle applies to iron — ferrous fumarate or bisglycinate may be better tolerated and absorbed than ferrous sulfate in the achlorhydric post-bariatric stomach.

Medication	Adjustment	Rationale
Insulin / Sulfonylureas	Reduce dose immediately (often by 50% or stop) on POD 0	Rapid improvement in insulin sensitivity post-surgery (especially RYGB). Continuing pre-op doses → severe hypoglycaemia. Monitor glucose closely and titrate
Metformin	Stop perioperatively; restart when renal function confirmed normal and oral intake established	AKI risk perioperatively. After restart, may eventually discontinue if DM in remission
Antihypertensives	Reduce/stop as BP normalises	Weight loss → ↓ SNS activity, ↓ Na⁺ retention, ↓ RAAS activation → BP drops. Continuing unchanged doses → hypotension
Statins	Continue initially; reassess at 3–6 months when lipids improve	Many patients can reduce or stop statins as weight loss improves lipid profile
CPAP	Continue until OSA resolution confirmed by repeat polysomnography	OSA improves with weight loss but may take months; premature discontinuation → recurrence of apnoeas
NSAIDs	Avoid lifelong after RYGB	NSAIDs → prostaglandin inhibition → reduced mucosal blood flow → marginal ulcer at the unprotected gastrojejunal anastomosis. Use paracetamol or COX-2 inhibitors with caution instead
Oral contraceptive pill	Switch to non-oral contraception (IUD, implant, injection) post-RYGB	Malabsorption after RYGB may reduce OCP efficacy → unplanned pregnancy risk (pregnancy should be avoided for 12–18 months post-surgery due to rapid nutritional flux and teratogenicity concerns of deficiencies)
Crushed/liquid formulations	All oral medications should be crushed or given in liquid form for the first 2–4 weeks post-surgery	SG/RYGB → small gastric volume cannot accommodate large tablets; also, enteric-coated or extended-release formulations may not be properly absorbed. Transition back to whole tablets when tolerating solid food

7. Management of Specific Postoperative Complications

Aspect	Management
Clinical suspicion	Tachycardia > 120 bpm (earliest sign), fever, peritonism, raised WCC/CRP, tachypnoea
Investigation	CT abdomen with oral water-soluble contrast → extravasation confirms leak
Management — depends on clinical stability and timing
Stable, contained leak, early detection	Nil by mouth + IV antibiotics + percutaneous drainage of any collection (interventional radiology). Consider endoscopic stent placement across the leak site. Start TPN if prolonged NPO anticipated ^[3]
Unstable, free leak, peritonitis	Emergency return to theatre → laparoscopic/open washout, attempt primary repair or drainage, wide drainage, +/- feeding jejunostomy for enteral nutrition distal to the leak ^[3]
Nutritional support	"If the gut works, use it" — if a feeding jejunostomy can be placed distal to the leak, enteral feeding is preferred over TPN ^[3]. If gut cannot be used → TPN via central line ^[3]

Aspect	Management
Presentation	Colicky abdominal pain, vomiting, signs of SBO. Can present months to years post-RYGB
Investigation	CT: swirl sign
Management	Urgent surgical exploration (laparoscopic) — reduce hernia, assess bowel viability (if strangulated → resect necrotic segment), close all mesenteric defects

Aspect	Management
Prevention	Avoid NSAIDs lifelong. Eradicate H. pylori preoperatively. Smoking cessation. PPI for 3–6 months post-RYGB (some programmes use lifelong PPI)
Treatment	High-dose PPI (omeprazole 40 mg BD). Check and treat H. pylori. Stop NSAIDs and smoking. If refractory → surgical revision (excision of ulcer, revision of gastrojejunostomy)

Type	Management
Early dumping	Dietary modification (first-line): avoid simple sugars, eat small frequent meals, separate solids and liquids (drink 30 min before or after meals, not during), increase fibre and protein. Lie down after meals if symptomatic
Late dumping	Dietary modification as above. If persistent → acarbose (alpha-glucosidase inhibitor — slows carbohydrate digestion → reduces rapid glucose absorption → blunts the insulin spike → prevents reactive hypoglycaemia). Dose: 50–100 mg with meals
Refractory	Consider octreotide (somatostatin analogue — inhibits insulin/GLP-1 release, slows GI motility). Rarely needed

Deficiency	Management
Iron deficiency anaemia	Oral ferrous fumarate with vitamin C; if oral not absorbed/tolerated → IV iron infusion (ferric carboxymaltose — single dose, rapid, well-tolerated)
Vitamin B12 deficiency	IM hydroxocobalamin 1000 µg every 3 months; or high-dose sublingual B12 daily
Vitamin D deficiency / secondary hyperparathyroidism	High-dose vitamin D3 (50,000 IU/week for 8–12 weeks loading → maintenance 3000–5000 IU/day). Calcium citrate. Monitor PTH — goal to normalise
Thiamine deficiency / Wernicke	IV thiamine 500 mg TDS for 3–5 days (Pabrinex) → switch to oral 100 mg daily. This is a medical emergency — treat empirically if suspected before waiting for levels
Protein malnutrition	Dietary protein optimisation; protein supplements. If severe with hypoalbuminaemia and oedema → may need short-term PN support ^[3]

Aspect	Management
Mild	PPI (lifelong if needed), dietary/lifestyle modification (elevate head of bed, avoid late meals)
Severe / refractory / Barrett's developing	Conversion from SG to RYGB — the definitive treatment for intractable GORD post-SG. RYGB diverts bile away from the oesophagus and reduces acid exposure

Cause	Management
Dietary non-compliance	Re-engagement with dietitian and psychologist; support groups; consider GLP-1 RA adjunct therapy
Pouch/sleeve dilation	Endoscopic revision (transoral outlet reduction — TORe — for dilated RYGB pouch outlet; endoscopic sleeve gastroplasty for dilated SG)
Gastrogastric fistula (RYGB)	Surgical repair of fistula
Inadequate initial procedure	Surgical revision: SG → RYGB conversion; RYGB → limb lengthening (distal RYGB) or conversion to BPD-DS

Timepoint	Assessment
2 weeks	Wound check, dietary progression, hydration status
1 month	Weight, dietary compliance, medication adjustment, psychological check-in
3 months	Weight, nutritional bloods, HbA1c, medication adjustment
6 months	Weight, nutritional bloods, lipids, LFTs, comorbidity reassessment
12 months	Comprehensive review — all of above + body composition assessment
Annually thereafter (lifelong)	Nutritional blood panel (iron, B12, folate, VitD, Ca, PTH, zinc, copper, albumin); HbA1c; weight; psychological review; DEXA every 2 years post-RYGB; dietary review

High Yield Summary — Management of Bariatric Surgery

Conservative management must be attempted and documented as failed before surgery ^[2].
Preoperative optimisation is not optional — liver shrinkage diet, nutritional correction, CPAP for OSA, smoking cessation, H. pylori eradication, glycaemic control ^[3].
Procedure selection is individualised — GORD favours RYGB; simplicity favours SG; T2DM remission favours RYGB; super-morbid obesity may favour BPD-DS.
Postoperative care = ERAS protocol + dietary progression + medication adjustment + lifelong supplementation.
Avoid NSAIDs lifelong after RYGB (marginal ulcer). Use calcium citrate not carbonate (acid-independent absorption). Crush medications for first 2–4 weeks.
Lifelong follow-up is mandatory — nutritional deficiencies can present years later.

Active Recall - Bariatric Surgery: Management

Complications of bariatric surgery are best understood by organising them along two axes: (1) timing — early vs late, and (2) procedure-specific vs general. Every complication has a mechanistic explanation rooted in what the surgery actually does to the anatomy and physiology. If you understand the anatomy of each procedure, you can predict its complications from first principles.

Timing	Definition	Key Complications
Immediate ( < 24 hours)	Related to the operative insult itself	Intra-abdominal bleeding (staple line / mesenteric vessels), anaesthetic complications, rhabdomyolysis
Early (24 hours – 30 days)	Related to healing and the acute postoperative state	Anastomotic / staple line leak, PE/DVT, wound infection, acute kidney injury, respiratory failure
Late ( > 30 days)	Related to altered anatomy, chronic nutritional changes, and long-term sequelae	Internal hernia, marginal ulcer, nutritional deficiencies (Fe, B12, Ca, VitD), dumping syndrome, gallstones, GORD, stomal stenosis, weight regain, psychological complications

2. Early Complications (Perioperative)

This is the most feared early complication of bariatric surgery ^[2]^[6].

Incidence: 1–5% overall. Highest for SG at the angle of His (the most proximal point of the staple line — where blood supply is most tenuous and intraluminal pressure is highest). For RYGB, leak most commonly occurs at the gastrojejunal anastomosis ^[2].

Why does it happen?

Technical factors: Stapler misfires, tissue ischaemia at staple line, excessive tension on anastomosis
Patient factors: Chronic tissue hypoxia (diabetes, smoking, obesity), chronic steroid use (impaired healing), malnutrition
At the angle of His (SG): This is where the oesophagogastric junction meets the staple line. The blood supply here relies on small branches from the left gastric and left inferior phrenic arteries — a relative watershed zone. The intraluminal pressure is highest at this point (narrow lumen, angle). Hence, leaks at the angle of His are notoriously slow to heal ^[2]

Clinical features:

Tachycardia > 120 bpm — often the earliest and most reliable sign, appearing even before fever, pain, or peritonism ^[2]^[6]
Fever, rising WCC/CRP, tachypnoea
Peritonism (diffuse if free leak; localised if contained)
Drain output: turbid, bilious, or resembling oral intake
If missed → intra-abdominal abscess → sepsis → multi-organ failure

Investigation: CT abdomen with oral water-soluble contrast — gold standard. Look for contrast extravasation, extraluminal air, free fluid, abscess ^[1]

Management (depends on clinical stability and containment) ^[3]^[6]:

Stable, contained: NPO + IV antibiotics + percutaneous drainage (interventional radiology) ± endoscopic stenting over the defect. Nutritional support: TPN or enteral feeding via jejunostomy distal to the leak ^[3]
Unstable, free peritonitis: Emergency return to theatre — washout, attempt repair or drainage, +/- feeding jejunostomy. Wide drainage.
Leaks at the angle of His (SG) take a long time to heal — may require weeks of NPO with nutritional support, endoscopic interventions (stents, endoscopic vacuum therapy/EndoSponge), and patience ^[2]

The Golden Rule

Tachycardia after bariatric surgery = leak until proven otherwise. Do not be reassured by the absence of fever or peritonism in the first 24–48 hours — these are late signs. In an obese patient, peritonism can be masked by the thick abdominal wall, and fever may be delayed by the immunosuppressive effect of obesity. The heart rate does not lie.

Incidence: 1–4%. Usually within first 24–48 hours.

Sources ^[2]^[6]:

Staple line bleeding — the long staple line in SG (from antrum to angle of His) has many small vessels. Even with staple line reinforcement (oversewing/buttress), oozing can occur
Mesenteric vessel injury during dissection
Reactionary haemorrhage — bleeding that occurs as the stress-response vasoconstriction wears off (within 24 hours), unmasking a bleeding vessel ^[6]
Splenic injury (rare, during mobilisation of the greater curvature near splenic hilum)

Clinical features: Tachycardia, hypotension, dropping Hb, blood in drain, melaena (intraluminal bleed) or abdominal distension (extraluminal haemoperitoneum)

Management:

Mild, self-limiting: Monitor, transfuse if needed, correct coagulopathy
Significant / haemodynamically unstable: Return to theatre → laparoscopic exploration → oversew bleeding point, washout. If intraluminal (blood per rectum), OGD may localise and treat the source

Why bariatric patients are at extremely high risk:

Virchow's triad is perfectly fulfilled:
1. Stasis: Obesity → venous compression → immobility → perioperative bed rest
2. Hypercoagulability: Obesity is a chronic inflammatory state → elevated fibrinogen, PAI-1, factor VIII; also pneumoperitoneum during laparoscopy reduces venous return
3. Endothelial injury: Surgical trauma, patient positioning (pressure points)

Incidence: Clinically significant PE: 0.3–2%. VTE is a leading cause of death after bariatric surgery.

Prevention ^[6]:

LMWH (enoxaparin 40 mg BD or weight-adjusted dosing — standard 40 mg OD is often subtherapeutic in morbidly obese patients)
Pneumatic compression devices — applied before induction, continued until fully mobile
Early mobilisation — same day as surgery (ERAS principle)
Some centres extend chemoprophylaxis for 2–4 weeks post-discharge (especially if BMI > 50 or prior VTE history)

Presentation: Sudden dyspnoea, pleuritic chest pain, tachycardia, hypoxia, haemoptysis (PE); calf pain and swelling (DVT). In an obese patient, distinguish from expected post-op breathlessness by: sudden onset, unilateral leg swelling, pleuritic quality of pain.

Investigation: CTPA (PE), lower limb Doppler USS (DVT)

Complication	Mechanism	Prevention/Management
Atelectasis	Reduced FRC in obesity (abdominal fat → ↓ diaphragmatic excursion); general anaesthesia → surfactant dysfunction; hypoventilation from pain	Incentive spirometry, chest physiotherapy, early mobilisation, semi-upright positioning ^[6]
Pneumonia	Atelectasis → mucus plugging → infection; aspiration risk (GORD, post-extubation)	As above + prophylactic antibiotics if high risk
Respiratory failure / Obesity Hypoventilation Syndrome	OSA patients on opioids → central and obstructive apnoeas → hypoxia, hypercapnia	CPAP post-operatively for all OSA patients. Opioid-sparing analgesia (ERAS). Avoid benzodiazepines

A uniquely bariatric complication that is often overlooked:

Mechanism: Prolonged operative time (2–4+ hours) + morbid obesity → extreme pressure on muscles (especially gluteal and posterior thigh from positioning on the operating table) → crush injury to muscle tissue → myoglobin release → myoglobinaemia → renal tubular obstruction → acute kidney injury

Risk factors: BMI > 55, operative time > 3 hours, male sex, peripheral vascular disease

Clinical features: Muscle pain (especially buttocks/thighs — out of proportion to the surgical site), dark "cola-coloured" urine, rising CK (often > 5,000 U/L), rising creatinine, hyperkalaemia

Investigation: Serum CK (markedly elevated), urine myoglobin, renal function

Management: Aggressive IV fluid resuscitation (target UO > 200 mL/hr initially), alkalinise urine (IV sodium bicarbonate — keeps myoglobin soluble and prevents tubular precipitation), monitor and treat hyperkalaemia. Avoid nephrotoxins. Rarely requires haemodialysis.

Prevention: Adequate padding during positioning, minimise operative time, use intermittent position changes during long cases

Complication	Mechanism	Notes
Surgical site infection (SSI)	Obesity → ↓ tissue oxygenation (poor microvascular perfusion through fat), hyperglycaemia (impaired neutrophil function), large wound surface area if open	Laparoscopic approach dramatically reduces SSI risk (small port sites vs large laparotomy). Weight-adjusted antibiotic prophylaxis essential (cefazolin 2–3 g, not standard 1 g) ^[6]
Port-site hernia	Fascial defect at trocar insertion sites ( > 10 mm)	Close all fascial defects > 10 mm. More common in obesity due to raised intra-abdominal pressure
Access port infection (gastric banding specific)	Subcutaneous port acts as foreign body → biofilm formation	One of the reasons gastric banding has been largely abandoned ^[2]

3. Late Complications

Internal hernia is the most important late surgical emergency specific to RYGB ^[2]^[6].

Mechanism: During RYGB construction, the Roux limb is passed through or alongside the transverse mesocolon, creating mesenteric defects — potential spaces through which bowel loops can herniate:

Petersen's space — between the Roux limb mesentery and the transverse mesocolon (most common)
Jejunojejunostomy mesenteric defect — at the site where the two limbs of jejunum are joined
Transverse mesocolon defect — if retrocolic Roux limb route used

Why does it present late? As patients lose significant weight (months to years post-surgery), the mesenteric fat shrinks, widening these defects and allowing bowel to herniate through them. This is a complication of successful weight loss, paradoxically.

Clinical features: Intermittent or acute colicky abdominal pain, nausea, vomiting (symptoms of small bowel obstruction). Can cause closed-loop obstruction → bowel strangulation → ischaemia → necrosis → perforation → peritonitis. This can be catastrophic if delayed.

Investigation: CT abdomen — "swirl sign" (mesenteric vascular rotation), clustered small bowel loops, closed-loop configuration, mesenteric oedema ^[2]

Management: Urgent laparoscopic surgical exploration → reduce hernia, assess bowel viability (pink and peristalsing = viable; dusky/black/non-peristalsing = non-viable → resect), close all mesenteric defects with non-absorbable suture ^[2]

Prevention: Routine closure of all mesenteric defects at the time of index RYGB — this is now standard practice but was not always done historically

Exam Pearl

Internal hernia is the diagnosis you must always consider when a post-RYGB patient presents with abdominal pain — even years after surgery. The CT "swirl sign" is pathognomonic. A normal CT does not fully exclude intermittent internal hernia (bowel may spontaneously reduce). If clinical suspicion is high despite normal imaging, diagnostic laparoscopy is warranted.

3.2 Dumping Syndrome

Dumping syndrome is a constellation of vasomotor and GI symptoms caused by rapid transit of hyperosmolar gastric contents into the small intestine after loss of the pyloric sphincter mechanism ^[2]^[5]^[6].

Primarily affects RYGB (pylorus completely bypassed). Rare after SG (pylorus preserved). Also occurs after any gastrectomy (Billroth I/II) — the pathophysiology is identical ^[5]^[6].

Pathophysiology:

Hyperosmolar chyme (especially concentrated sugars) rushes into the jejunum
Osmotic fluid shift from plasma into the intestinal lumen (the gut acts like a dialysis membrane — water follows the osmotic gradient)
Intravascular volume depletion → tachycardia, hypotension, dizziness, flushing, diaphoresis
Intestinal distension → cramping, nausea, bloating, explosive diarrhoea
Release of vasoactive gut hormones (serotonin, VIP, bradykinin, neurotensin) → further vasodilation and flushing

Symptoms: Abdominal cramps, diarrhoea, nausea, bloating, vasomotor symptoms (tachycardia, flushing, diaphoresis, dizziness, weakness) ^[5]^[6]

Pathophysiology:

Rapid carbohydrate absorption in the jejunum → exaggerated glucose spike
Exaggerated insulin release (both from the glucose spike and from enhanced GLP-1 secretion in the RYGB anatomy)
Reactive hypoglycaemia — insulin overshoots, glucose crashes
Counter-regulatory hormone release (adrenaline, glucagon, cortisol, GH) → adrenergic symptoms

Symptoms: Post-prandial hyperinsulinaemic hypoglycaemia ^[5] — diaphoresis, tremor, palpitations, confusion, weakness, syncope. Can be severe enough to cause seizures.

Line	Intervention	Mechanism
1st line	Dietary modification: small frequent meals; avoid simple carbohydrates/refined sugars; separate solids and liquids; increase protein and fibre; lie down after meals	Slows gastric emptying of what remains of the pouch, reduces osmotic load, reduces glucose spike
2nd line	Acarbose (alpha-glucosidase inhibitor) — for late dumping specifically	Inhibits brush-border enzymes that break down complex carbohydrates into glucose → slows glucose absorption → blunts insulin spike → prevents reactive hypoglycaemia
3rd line	Octreotide (somatostatin analogue) — SC injection	Inhibits multiple gut hormones (insulin, GLP-1, VIP, serotonin) → reduces both vasomotor symptoms and hypoglycaemia. Delays GI transit. Reserved for refractory cases

Dumping Syndrome as 'Therapeutic'

As mentioned in the management section, dumping actually reinforces good dietary behaviour post-RYGB. Patients who eat sweets or high-GI foods feel terrible → they learn to avoid them. This conditioned aversion contributes to long-term weight maintenance. Some surgeons consider mild dumping a beneficial "side effect" rather than a true complication.

Anastomotic stricture is a narrowing; marginal ulcer is an ulceration — both occur at the gastrojejunal anastomosis of RYGB ^[2]^[5].

Pathophysiology: The gastrojejunal anastomosis exposes jejunal mucosa to gastric acid. Unlike gastric/duodenal mucosa, jejunal mucosa has no protective mucus-bicarbonate barrier and is not adapted to acidic pH → ulceration at the margin ("marginal ulcer").

Risk factors (modifiable):

NSAIDs — inhibit prostaglandin synthesis → reduce mucosal blood flow and bicarbonate secretion → universal NSAID avoidance lifelong after RYGB
Smoking — nicotine causes mucosal vasoconstriction → tissue ischaemia
H. pylori — if present in the gastric pouch or remnant → acid hypersecretion → ulceration
Ischaemia at the anastomosis — surgical technique
Corticosteroid use

Incidence: 1–16% (varies widely by series and risk factor profile)

Clinical features: Epigastric pain, GI bleeding (haematemesis, melaena), nausea, anaemia

Investigation: OGD — direct visualisation and biopsy (rule out malignancy, test for H. pylori). Seen as an ulcer crater at the jejunal side of the gastrojejunostomy.

Management: High-dose PPI (omeprazole 40 mg BD), stop NSAIDs, smoking cessation, eradicate H. pylori, sucralfate. If refractory → surgical revision (excision of ulcer, revision of gastrojejunostomy, or vagotomy) ^[5]

Incidence: 3–12% after RYGB (at the gastrojejunostomy); can also occur in SG (narrowing at the incisura angularis — the natural bend of the lesser curvature)

Pathophysiology: Healing of the anastomosis/staple line → fibrosis → cicatricial narrowing. Also ischaemia, marginal ulceration, and technical factors contribute.

Timing: Typically 4–8 weeks post-op

Clinical features: Progressive dysphagia (solids > liquids), nausea, vomiting, intolerance of solid food, weight loss (beyond expected)

Investigation: OGD (therapeutic and diagnostic) or barium swallow (shows narrowing)

Management: Endoscopic balloon dilation — first-line treatment. Usually requires 1–3 sessions. Rarely requires surgical revision ^[2]

This is the most common long-term complication category and the reason lifelong follow-up and supplementation are mandatory ^[2]^[5]^[6]^[7].

Deficiency	Mechanism (First Principles)	Clinical Manifestation	Procedure Most Affected
Iron deficiency	↓ Gastric acid (needed to convert Fe³⁺ → Fe²⁺, the absorbable form) + bypassed duodenum (main iron absorption site — DMT1 transporters) + GI bleeding from anastomotic ulcers ^[5]^[7]	Microcytic hypochromic anaemia, fatigue, koilonychia, glossitis, pica	RYGB > SG > banding
Vitamin B12 deficiency	↓ Intrinsic factor (from reduced parietal cell mass in SG; or bypassed gastric remnant in RYGB) + ↓ gastric acid (needed to cleave B12 from food proteins) ^[5]	Megaloblastic anaemia, peripheral neuropathy, subacute combined degeneration of the cord (posterior and lateral column demyelination → ataxia, loss of vibration/proprioception, spasticity), cognitive impairment	RYGB > SG
Folate deficiency	Absorbed in proximal jejunum — bypassed in RYGB. Also dietary inadequacy (reduced food variety post-surgery)	Megaloblastic anaemia, neural tube defects in pregnancy	RYGB >> SG
Calcium deficiency	Bypassed duodenum (site of active, vitamin D-dependent calcium absorption via TRPV6 channels) + fat malabsorption (calcium binds to unabsorbed fatty acids → excreted as calcium soaps) ^[7]	Hypocalcaemia → perioral paraesthesia, carpopedal spasm (Trousseau sign), Chvostek sign. Chronic: osteomalacia, osteopenia, osteoporosis	RYGB > BPD-DS >> SG
Vitamin D deficiency	Fat-soluble vitamin → impaired absorption with fat malabsorption (shorter common channel in RYGB/BPD-DS). Also: obese patients have baseline deficiency (vitamin D sequestered in adipose tissue — ↓ bioavailability)	Osteomalacia (adults), secondary hyperparathyroidism (↓ Ca²⁺ → ↑ PTH → bone resorption → metabolic bone disease), proximal myopathy, bone pain	RYGB > SG
Thiamine (B1) deficiency	Thiamine stores are depleted within 2–3 weeks of inadequate intake. Prolonged postoperative vomiting (from stenosis, overeating, or any cause) rapidly depletes thiamine. Absorbed in jejunum — bypassed in RYGB	Wernicke encephalopathy — the triad: confusion, ophthalmoplegia (lateral rectus palsy → diplopia, nystagmus), ataxia. If untreated → Korsakoff syndrome (irreversible confabulation and anterograde amnesia)	RYGB = SG (any procedure with prolonged vomiting)
Zinc deficiency	Absorbed in duodenum/proximal jejunum (bypassed). Zinc binds to unabsorbed fatty acids ^[7]	Impaired wound healing, alopecia, dysgeusia (altered taste), immune dysfunction, growth retardation (paediatric)	RYGB > SG
Copper deficiency	Absorbed in duodenum/proximal jejunum. Excess zinc supplementation competes for absorption (shared transporter — ZIP4/DMT1) → iatrogenic copper deficiency	Anaemia (refractory to iron), neutropaenia, myelopathy (mimics B12 deficiency — posterior column demyelination)	RYGB (especially if over-supplementing zinc)
Protein-calorie malnutrition	Severe restriction (too small a pouch/sleeve) + malabsorption (RYGB/BPD-DS) + dietary non-compliance (avoiding protein-rich foods)	Hypoalbuminaemia → oedema, hair loss, muscle wasting, impaired immunity, poor wound healing	BPD-DS >> RYGB > SG

Follow-up nutritional monitoring ^[2]:

After banding: CBC, RFT, HbA1c, FBG, lipids
After bypass / sleeve gastrectomy: Above + LFT, B12/folate, Fe profile, bone profile (Ca, PO₄, vitamin D, PTH), Zn, Cu

Metabolic Bone Disease — The Silent Complication

Metabolic bone disease is the most underappreciated long-term complication ^[7]. The cascade: fat malabsorption → ↓ vitamin D absorption → ↓ intestinal calcium absorption → chronic hypocalcaemia → secondary hyperparathyroidism → PTH drives osteoclastic bone resorption → osteopenia → osteoporosis → fragility fractures. This process is insidious — patients are asymptomatic until they fracture a hip. Prevention requires lifelong calcium citrate + vitamin D supplementation + annual monitoring of Ca, vitamin D, and PTH + DEXA scan every 2 years post-RYGB ^[7].

Incidence: Up to 30% of bariatric surgery patients develop gallstones within the first 6–12 months

Pathophysiology ^[7]:

Rapid weight loss → liver mobilises large amounts of cholesterol from adipose stores → supersaturation of bile with cholesterol
Decreased gallbladder motility — reduced meal volume post-surgery → less CCK release → less gallbladder contraction → bile stasis → sludge → stones
Both mechanisms favour cholesterol gallstones

Prevention: Ursodeoxycholic acid (UDCA) 300 mg BD for 6 months post-surgery — reduces bile cholesterol saturation. Some centres perform concurrent cholecystectomy if gallstones found preoperatively.

Management if symptomatic: Laparoscopic cholecystectomy

Pathophysiology (especially after RYGB/BPD-DS with significant malabsorption) ^[7]:

Fat malabsorption → unabsorbed fatty acids in the gut lumen bind to calcium (forming calcium soaps) → less free calcium available to bind oxalate
Unbound oxalate is absorbed in the colon → hyperoxaluria → filtered by kidneys → calcium oxalate nephrolithiasis

Prevention: Adequate hydration, low-oxalate diet (avoid spinach, rhubarb, chocolate, tea, nuts), calcium supplementation (paradoxically — more calcium binds oxalate in the gut, reducing absorption), potassium citrate (alkalinises urine, reduces stone formation)

Pathophysiology ^[2]:

SG creates a high-pressure tube from the narrow sleeve → increased intragastric pressure
Disruption of the angle of His (natural anti-reflux mechanism) during fundus resection
Possible LES injury during dissection near the GEJ
Hiatal hernia may be unmasked or worsened

Incidence: De novo GORD in 10–30% of SG patients; worsening of pre-existing GORD in up to 50%

Clinical features: Heartburn, acid regurgitation, nocturnal cough, oesophagitis on OGD, Barrett's oesophagus (long-term)

Management: PPI (first-line); if refractory → conversion from SG to RYGB (definitive — RYGB is the best anti-reflux bariatric procedure) ^[2]

Incidence: ~20–30% of patients experience clinically significant weight regain (defined as regain of > 25% of lost weight) by 5 years

Causes:

Dietary non-compliance — most common (snacking, calorie-dense liquids, emotional eating)
Pouch/sleeve dilation — gradual stretching of the gastric pouch or sleeve over years → accommodates more food → reduced restrictive effect
Gastrogastric fistula (RYGB) — fistula between pouch and excluded remnant → food enters the large remnant → reduced restriction and malabsorption
Metabolic adaptation — some hormonal changes partially revert over time (ghrelin may increase, GLP-1 effect may diminish)
Psychological — untreated binge eating disorder, depression, addiction transfer

Management: Multidisciplinary re-engagement (dietitian, psychologist); pharmacotherapy adjunct (GLP-1 RA); endoscopic revision (TORe for RYGB, endoscopic sleeve gastroplasty); surgical revision (SG → RYGB conversion, RYGB limb lengthening, conversion to BPD-DS)

Complication	Mechanism
Depression	Body image issues (excess skin), unmet expectations, loss of food as coping mechanism, neurochemical changes
Addiction transfer	Loss of food reward → substitution with alcohol, gambling, compulsive shopping. RYGB patients are especially vulnerable to alcohol (reduced first-pass metabolism → higher blood alcohol levels from same amount)
Suicide	Risk of suicide is increased post-bariatric surgery (multiple studies). Multifactorial: pre-existing psychiatric comorbidity, persistent body image dissatisfaction, relationship changes, ongoing depression. Emphasises importance of preoperative screening and lifelong psychological support
Binge eating disorder relapse	If untreated pre-operatively, BED often recurs → weight regain, psychological distress

Complication	Gastric Banding	Sleeve Gastrectomy	RYGB	BPD-DS
Staple line/anastomotic leak	N/A (no staples)	Leak at angle of His (slow to heal) ^[2]	Leak at gastrojejunostomy	Leak at anastomosis
Bleeding	Rare	Staple line bleed	Staple line + anastomotic bleed	Staple line bleed
Band slip/erosion	Yes (band migrates or erodes into stomach) ^[2]	N/A	N/A	N/A
Access port infection	Yes ^[2]	N/A	N/A	N/A
Tubing leak	Yes ^[2]	N/A	N/A	N/A
GORD	May improve	Worsening (↑ intragastric pressure, loss of angle of His, LES injury) ^[2]	Improves (best for GORD)	Improves
Internal hernia	No	No	Yes (Petersen's defect, JJ mesenteric defect) ^[2]	Yes
Marginal ulcer	No	No	Yes (jejunal mucosa exposed to acid)	Possible
Anastomotic stricture	No (but band can cause narrowing)	Narrowing at incisura angularis	Yes (gastrojejunostomy) ^[2]	Yes
Dumping syndrome	No	Rare (pylorus preserved)	Yes (pylorus bypassed) ^[2]	Yes
Nutritional deficiency	Low	Moderate (B12, iron, VitD)	High (Fe, B12, folate, Ca, VitD, fat-soluble vitamins) ^[2]	Very high
Weight regain	High (30–50% failure) ^[2]	Moderate	Lower (but still 20–30%)	Lowest
Malnutrition	Rare	Uncommon	Moderate risk ^[2]	High risk ^[2]

When bariatric surgery patients require prolonged NPO (e.g., leak management, severe stricture, fistula), TPN becomes necessary ^[3]^[6]^[7]:

Complication	Mechanism
Catheter-related bloodstream infection (CRBSI)	Biofilm formation on central line → bacteraemia. Most feared PN complication. Prevent with aseptic insertion technique, daily line care, prompt removal when no longer needed ^[3]
TPN-associated cholestasis / hepatic steatosis	Lack of enteral stimulation → ↓ CCK release → gallbladder stasis → biliary sludge → cholestasis. Also: excess glucose/lipid in TPN → hepatic lipogenesis → steatosis ^[3]^[6]
Refeeding syndrome	When transitioning from NPO/TPN back to enteral feeding (or initiating TPN in a malnourished patient): sudden carbohydrate load → insulin surge → intracellular shift of PO₄ (first and most important), K⁺, Mg²⁺, thiamine → cardiac arrhythmias, heart failure, respiratory failure, seizures ^[3]^[6]
Catheter thrombosis	Foreign body in central vein → thrombosis → SVC syndrome, loss of access
Metabolic derangements	Hyperglycaemia (most common), hypertriglyceridaemia, electrolyte imbalances
Gut mucosal atrophy	No enteral stimulation → villous atrophy → bacterial translocation (gut bacteria cross into portal circulation → sepsis) — this is why "if the gut works, use it" ^[3]

Refeeding Syndrome — Key Details

Electrolyte disturbance priority ^[6]: ↓PO₄ (first — phosphate is consumed to produce ATP during the metabolic shift from fat to carbohydrate oxidation) > ↓K⁺ > ↓Mg²⁺ > ↓thiamine.

Prevention: Start feeding at 10 kcal/kg/day ("start low, go slow"), increase gradually over 4–7 days. Monitor electrolytes (especially phosphate) BD for the first week. Supplement prophylactically: IV Pabrinex (thiamine), oral/IV phosphate, potassium, magnesium. High-risk patients: BMI < 18.5, > 10% weight loss in 3–6 months, little/no intake for > 5 days, low baseline PO₄/K⁺/Mg²⁺, alcohol misuse, cancer cachexia ^[3]^[6].

Procedure	30-Day Mortality	Main Causes of Death
Gastric banding	~0.05%	PE, anaesthetic complications
Sleeve gastrectomy	~0.1–0.3%	Staple line leak → sepsis, PE
RYGB	~0.2–0.5%	Anastomotic leak → sepsis, PE, cardiac events
BPD-DS	~0.5–1%	Leak, PE, malnutrition-related complications

Overall bariatric surgery mortality is very low — comparable to laparoscopic cholecystectomy. The long-term survival benefit of bariatric surgery (reduction in cardiovascular death, cancer death, and all-cause mortality by 30–40% over 10–20 years, per the Swedish Obese Subjects study) far outweighs the perioperative risk.

Key Complications Principles — Summary

Tachycardia = leak until proven otherwise — CT with oral contrast is the investigation of choice.
VTE is a leading cause of perioperative death — aggressive prophylaxis mandatory (LMWH + compression + early mobilisation).
Internal hernia is RYGB-specific — presents late as weight loss widens mesenteric defects. CT swirl sign. Urgent surgery.
Dumping syndrome — early (osmotic, vasomotor) vs late (reactive hypoglycaemia). Dietary modification first; acarbose for late; octreotide for refractory.
Nutritional deficiencies are lifelong — iron, B12, folate, calcium, vitamin D, thiamine, zinc, copper. RYGB > SG. Annual monitoring mandatory.
Metabolic bone disease is the silent killer — secondary hyperparathyroidism from Ca/VitD malabsorption → osteoporosis → fragility fractures.
GORD may worsen after SG — if intractable, convert to RYGB.
Gallstones in 30% within first year — ursodeoxycholic acid prophylaxis.
Avoid NSAIDs lifelong after RYGB — marginal ulcer risk.
Psychological complications including addiction transfer and increased suicide risk — lifelong support essential.

High Yield Summary — Complications of Bariatric Surgery

Early: Leak (tachycardia — sentinel sign; CT with oral contrast), staple line bleed, VTE (leading cause of death), respiratory complications (atelectasis, OSA exacerbation), rhabdomyolysis, wound infection.

Late: Internal hernia (RYGB — swirl sign on CT), marginal ulcer (RYGB — avoid NSAIDs), dumping syndrome (early = osmotic/vasomotor; late = reactive hypoglycaemia), stomal stenosis, nutritional deficiencies (Fe, B12, folate, Ca, VitD, thiamine, Zn, Cu — lifelong monitoring), gallstones (30% in year 1 — UDCA prophylaxis), GORD worsening (SG — may need conversion to RYGB), nephrolithiasis (oxalate), weight regain, psychological complications (addiction transfer, depression, suicide).

Procedure-specific: Banding → slip/erosion/port infection; SG → leak at angle of His (slow to heal), GORD; RYGB → internal hernia, marginal ulcer, dumping, nutritional deficiency; BPD-DS → severe malnutrition.

Follow-up monitoring: After banding: CBC, RFT, HbA1c, FBG, lipids. After bypass/SG: add LFT, B12/folate, Fe profile, bone profile (Ca, PO₄, VitD, PTH), Zn, Cu.

Active Recall - Bariatric Surgery: Complications

^[1] Lecture slides: GC 212. Weight loss and vomiting gastric cancer; abdominal imaging.pdf ^[2] Senior notes: maxim.md (section 3.8 Bariatric surgery) ^[3] Lecture slides: GC 185. Feed him up before surgery Surgical nutrition, Enteral and parenteral feeding.pdf ^[5] Senior notes: felixlai.md (gastrectomy complications, post-gastrectomy syndromes) ^[6] Senior notes: maxim.md (section 1.6 Post-op complications; section on enteral vs parenteral nutrition; post-gastrectomy syndromes) ^[7] Senior notes: felixlai.md (nutritional deficiencies, metabolic bone disease, gallstones, nephrolithiasis, TPN-associated conditions)

High Yield Summary

Definition: Bariatric (metabolic) surgery = surgical procedures on the GI tract for sustained weight loss and metabolic improvement in severe obesity after failed conservative management.

Key Indications (Asian): Failed medical Rx + BMI ≥ 35 (with/without comorbidities) OR BMI ≥ 30 with T2DM.

Contraindications: Reversible endocrine causes, active psychiatric disorders, substance abuse, non-compliance.

ABCD Score: Age, BMI, C-peptide, Duration of DM. Total = 10. Score > 6 → predicts T2DM remission.

Procedures:

Restrictive: Gastric banding (declining), Sleeve gastrectomy (most popular)
Combined: RYGB (gold standard for metabolic effect, ~80% T2DM remission)
Malabsorptive: BPD-DS (rarely done)

Key Hormonal Changes: ↓ Ghrelin (especially SG — fundus removed), ↑↑ GLP-1 and PYY (especially RYGB — hindgut hypothesis) → T2DM remission.

Preoperative Assessment: Nutritional status (SGA), exclude reversible causes of obesity, assess comorbidities (OSA, T2DM, HTN, NAFLD), psychological evaluation.

High Yield Summary — Differential Diagnosis in Bariatric Surgery

Always exclude secondary/reversible causes of obesity before bariatric surgery — especially Cushing syndrome and hypothyroidism.
Tachycardia > 120 bpm in first 48 hours post-bariatric surgery = anastomotic leak until proven otherwise.
Internal hernia is specific to RYGB (mesenteric defects) — look for "swirl sign" on CT.
Dumping syndrome = early (osmotic, vasomotor) vs late (reactive hypoglycaemia). More common after RYGB because pylorus is bypassed.
Gallstones are very common after rapid weight loss — up to 30% incidence in first year.
The excluded gastric remnant in RYGB is a "blind spot" for gastric cancer surveillance.

High Yield Summary — Diagnosis of Bariatric Surgery

Preoperative workup is multidisciplinary — not just surgical but medical, nutritional, psychological, and anaesthetic.
OGD is recommended for all bariatric candidates in East Asia — to screen for H. pylori, hiatal hernia, Barrett's, and gastric pathology (high prevalence region) ^[1].
Tachycardia is the sentinel sign of anastomotic leak — CT with oral contrast is the gold standard investigation.
Nutritional baseline must be established before surgery because obese patients are frequently micronutrient-deficient ^[3].
Lifelong annual nutritional surveillance is mandatory — deficiencies can appear years after surgery.
The ABCD score (Age, BMI, C-peptide, Duration) with total = 10 and threshold > 6 guides metabolic surgery patient selection for T2DM ^[2].

High Yield Summary — Management of Bariatric Surgery

Conservative management must be attempted and documented as failed before surgery ^[2].
Preoperative optimisation is not optional — liver shrinkage diet, nutritional correction, CPAP for OSA, smoking cessation, H. pylori eradication, glycaemic control ^[3].
Procedure selection is individualised — GORD favours RYGB; simplicity favours SG; T2DM remission favours RYGB; super-morbid obesity may favour BPD-DS.
Postoperative care = ERAS protocol + dietary progression + medication adjustment + lifelong supplementation.
Avoid NSAIDs lifelong after RYGB (marginal ulcer). Use calcium citrate not carbonate (acid-independent absorption). Crush medications for first 2–4 weeks.
Lifelong follow-up is mandatory — nutritional deficiencies can present years later.

High Yield Summary — Complications of Bariatric Surgery

Follow-up monitoring: After banding: CBC, RFT, HbA1c, FBG, lipids. After bypass/SG: add LFT, B12/folate, Fe profile, bone profile (Ca, PO₄, VitD, PTH), Zn, Cu.

Bariatric Surgery

References

Bariatric Surgery

1. Definition

2. Epidemiology and the Obesity Problem

Global Context

Hong Kong Context

Risk Factors for Severe Obesity (requiring surgical consideration)

3. Anatomy and Physiology Relevant to Bariatric Surgery

3.1 Gastric Anatomy

3.2 Small Bowel Anatomy

3.3 Key Hormones in Appetite and Metabolism

4. Indications for Bariatric Surgery

4.1 Standard Indications (Asian Cut-offs)

4.2 Contraindications [2]

5. ABCD Score — Predicting T2DM Remission After Bariatric Surgery

6. Classification and Types of Bariatric Procedures

6.1 Overview by Mechanism [2]

6.2 Detailed Procedure Descriptions

A. Restrictive Procedures — Cause early satiety; overeating → upper abdominal pain [2]

i. Adjustable Gastric Banding (AGB) (Lap-Band)

ii. Sleeve Gastrectomy (SG) — Most commonly performed bariatric procedure worldwide and in HK

B. Combined (Restrictive + Malabsorptive) Procedures

iii. Roux-en-Y Gastric Bypass (RYGB) — Gold standard; best long-term data

iv. One-Anastomosis Gastric Bypass (OAGB / Mini Gastric Bypass)

C. Predominantly Malabsorptive Procedures

v. Biliopancreatic Diversion ± Duodenal Switch (BPD-DS)

6.3 Comparison Table of Major Procedures

7. Preoperative Assessment and Surgical Nutrition

7.1 Nutritional Assessment Before Surgery

7.2 Consequences of Malnutrition in Surgical Patients [3]

7.3 Perioperative Nutritional Support [3]

Enteral Nutrition [3]

Parenteral Nutrition (PN) [3]

8. Clinical Features — Presentation of the Obese Patient Being Considered for Bariatric Surgery

8.1 Symptoms (with pathophysiological basis)

8.2 Signs (with pathophysiological basis)

9. Obesity-Related Comorbidities (The Metabolic Syndrome)

10. Relevance of Surgical Oncology Principles

11. Connection to Inflammatory Bowel Disease (IBD)

12. Gastric Cancer Context

Active Recall - Bariatric Surgery (Definition, Epidemiology, Anatomy, Etiology, Classification, Clinical Features)

References

Differential Diagnosis in the Context of Bariatric Surgery

Axis 1: Differential Diagnosis of Obesity — Before Bariatric Surgery

Axis 2: Differential Diagnosis of Post-Bariatric Surgery Symptoms

A. Post-Bariatric Surgery: Acute Abdomen / Abdominal Pain

B. Post-Bariatric Surgery: Nausea and Vomiting

C. Post-Bariatric Surgery: Weight Loss Failure or Weight Regain

D. Post-Bariatric Surgery: Dumping Syndrome

Differential Diagnosis Algorithm — Systematic Approach

Special DDx: Vomiting and Weight Loss — Gastric Cancer vs Post-Bariatric Surgery

Summary Table: Key Differentials to Exclude Before and After Bariatric Surgery

Active Recall - Bariatric Surgery Differential Diagnosis

References

Diagnostic Criteria, Algorithm, and Investigations for Bariatric Surgery

1. Diagnostic Criteria for Bariatric Surgery Candidacy

1.1 Eligibility Criteria (Asian Populations — IFSO-APC / ASMBS 2022-2024 Guidelines)

1.2 ABCD Score for Predicting T2DM Remission [2]

2. Preoperative Investigation Algorithm

Master Diagnostic Algorithm

3. Investigation Modalities — Detailed Breakdown

3.1 Anthropometric Assessment

3.2 Blood Investigations

A. Excluding Secondary Causes of Obesity

B. Metabolic and Diabetes Assessment

C. Nutritional Baseline

D. Haematological and Coagulation

3.3 Cardiorespiratory Investigations

3.4 Gastrointestinal Investigations

3.5 Psychological Assessment

3.6 Anaesthetic Assessment

4. Postoperative Investigation and Surveillance Protocol

4.1 Immediate Postoperative (First 48–72 Hours)

4.2 Short-Term Follow-up (1–6 Months)

4.3 Long-Term Surveillance (Annually, Lifelong)

5. Postoperative Complication Detection — Specific Imaging and Investigation Findings

Active Recall - Bariatric Surgery: Diagnostics and Investigations

References

Management of Bariatric Surgery — Algorithm and Treatment Modalities