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Surgical decision-making begins before an operation is proposed, by identifying the findings that meaningfully change diagnosis, urgency or choice of treatment. A thyroid nodule is sent first for a TSH, because a suppressed value points to an autonomous hot nodule that rarely turns malignant. A breast lump in a woman under 40 goes first to ultrasound, because dense tissue defeats mammography. The same discipline governs the abdomen: identify the indicator, sort the patient, choose the operation, and anticipate its complications.

Bariatric procedures fall into three families defined by mechanism. Sleeve gastrectomy, adjustable banding and vertical banded gastroplasty are purely restrictive. Roux-en-Y gastric bypass combines restriction with malabsorption. Biliopancreatic diversion with duodenal switch is predominantly malabsorptive; it produces the greatest weight loss and the most severe nutritional deficiency. Sleeve gastrectomy is now the most frequently performed operation worldwide, yet severe reflux disease reverses that preference, because a sleeve tends to aggravate reflux whereas bypass relieves it.

These operations are called metabolic because their effect is hormonal rather than merely mechanical. After bypass or sleeve, nutrients reach the distal small bowel earlier, so GLP-1 and PYY rise while ghrelin falls. Consequently glycaemic control often improves within days, well before meaningful weight loss. The benefit belongs to type 2 diabetes, in which beta cells survive; it cannot rescue type 1 disease, where they have been destroyed.

Eligibility rests on a BMI of 40 or more, or 35 or more with a comorbidity such as type 2 diabetes, severe sleep apnoea or resistant hypertension. Recent guidelines extend consideration to a BMI of 30 or more when diabetes remains poorly controlled. Psychological assessment is mandatory, not optional, and a family decision cannot replace it. The most serious early complication is an anastomotic or staple-line leak, announced by fever, tachycardia and pain and usually requiring reoperation. Lifelong supplementation of vitamin B12, iron, calcium, vitamin D and folate follows, and dumping after bypass brings vasomotor symptoms within thirty minutes of sugary food.

The groin offers a second axis, this time defined by blood supply. A reducible hernia is repaired electively; an incarcerated hernia is trapped but perfused; a strangulated hernia has lost its blood supply and demands immediate surgery. Indirect hernias, the commonest and congenital, pass through the deep ring lateral to the inferior epigastric vessels. Direct hernias bulge through Hesselbach's triangle medial to those vessels. Femoral hernias lie below the inguinal ligament, favour women, and strangulate most often, so they are repaired once diagnosed. The Lichtenstein tension-free mesh is the standard repair, elective surgery waits at least six months after myocardial infarction, and pain is the commonest early complication.

The central distinctions can be recalled as follows.

All bariatric operations are sorted by mechanism: sleeve, band and gastroplasty restrict, Roux-en-Y bypass also malabsorbs, and duodenal switch malabsorbs most.
Is there severe reflux disease? Then Roux-en-Y bypass replaces the sleeve, because a sleeve worsens reflux while bypass treats it.
On the hormonal axis GLP-1 and PYY rise and ghrelin falls, so type 2 diabetes improves before the weight does.
Lumps in the groin are graded by blood supply: reducible waits, incarcerated is urgent, strangulated is operated on at once, and femoral hernias strangulate most.

Colorectal carcinogenesis often unfolds over years, creating opportunities for prevention before invasive disease develops. Normal mucosa becomes an adenoma when APC is inactivated, advances when KRAS mutates, and turns malignant only after TP53 and SMAD4 fail. Accumulating these events takes five to ten years, sometimes fifteen, which is why removing adenomas at colonoscopy prevents cancer. Two faster lanes exist. The serrated pathway runs through BRAF and microsatellite instability. In Lynch syndrome, defective mismatch repair drives a few adenomas rapidly to cancer, usually right-sided and often paired with endometrial cancer. Peutz-Jeghers syndrome, from STK11, brings hamartomas and mucocutaneous pigmentation, while familial adenomatous polyposis, from APC, carpets the colon with adenomas. Obesity and inactivity increase risk rather than reduce it.

Stage directs treatment. Node-positive stage III colon cancer receives adjuvant FOLFOX or CAPOX, oxaliplatin with a fluoropyrimidine, and no targeted agent. Targeted therapy belongs to metastatic stage IV disease: bevacizumab broadly, and cetuximab or panitumumab only for RAS wild-type tumours of the left colon and rectum. The rectum sits in the pelvis and recurs locally more often, so locally advanced rectal cancer receives neoadjuvant chemoradiotherapy, then total mesorectal excision, then adjuvant chemotherapy. TME follows the embryological plane of the mesorectal fascia, removing the mesorectum intact while sparing the hypogastric and pelvic splanchnic nerves. Sexual and bladder function are consequently not worsened. Laparoscopic resection matches open surgery oncologically, as the COLOR and COST trials showed, with faster recovery and unchanged mortality.

The dentate line divides the anal canal into two worlds, because endoderm meets ectoderm there. Above it the epithelium is columnar and the superior rectal artery arrives from the inferior mesenteric. Venous blood returns to the portal system, innervation is autonomic and painless, lymph drains to internal iliac nodes, and haemorrhoids are internal. Below it the epithelium is squamous and the inferior rectal artery arises from the internal pudendal. Blood returns to the inferior vena cava, the pudendal nerve from S2 to S4 makes every lesion painful, lymph drains to superficial inguinal nodes, and haemorrhoids are external. Portal hypertension distends the anastomosis between the two systems. The middle rectal artery comes from the internal iliac, not the inferior mesenteric, whose branches are the left colic, sigmoid and superior rectal arteries.

The sigmoid perforates more than any other segment, not because its wall is thin but because diverticula are common and its calibre is small. By Laplace's law wall tension equals pressure multiplied by radius, so a narrow lumen needs higher pressure to generate the same tension, and thin-walled diverticula give way first. Hinchey grades the consequences: a pericolic abscess is treated with antibiotics, a pelvic abscess with antibiotics and CT-guided drainage, and purulent or faecal peritonitis with emergency surgery. A colovesical fistula is repaired electively, and chronic anaemia is never an emergency indication.

The central distinctions can be recalled as follows.

All colorectal cancers travel the APC, KRAS and TP53 sequence over five to ten years, which is why removing adenomas prevents cancer.
Is the disease stage III or stage IV? Stage III receives FOLFOX or CAPOX alone, while stage IV adds bevacizumab, or cetuximab for RAS wild-type left-sided tumours.
On the dentate line everything changes: portal drainage, autonomic nerves and painless internal haemorrhoids above, caval drainage, the pudendal nerve and painful external haemorrhoids below.
Luminal narrowness and diverticula, not a thin wall, make the sigmoid perforate, and Hinchey III or IV peritonitis means emergency surgery.

The assessment of a vomiting newborn begins with the timing and character of the vomiting, followed by examination and appropriately selected imaging. When did the vomiting begin, and does it contain bile? Bile enters the duodenum at the ampulla of Vater, so obstruction beyond the ampulla produces bilious vomiting, whereas obstruction above it, including pyloric stenosis, does not. The plain film then counts bubbles. A double bubble with no distal gas is duodenal atresia, associated with Down syndrome in about 30 per cent and with maternal polyhydramnios. Multiple air-fluid levels indicate jejunoileal atresia, usually from a prenatal vascular accident. Dilated bowel with no anal opening is anorectal malformation, which travels with the VACTERL association.

Hypertrophic pyloric stenosis presents at three to six weeks with projectile non-bilious vomiting, a hungry infant, visible gastric peristalsis and a palpable olive. Because gastric acid is lost with every vomit, hydrogen and chloride fall, volume depletion raises aldosterone, and the kidney excretes potassium and hydrogen. The result is hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria. Ultrasound confirms the thickened, elongated pylorus. Surgery is never an emergency: chloride-containing fluid with potassium corrects the alkalosis first, and pyloromyotomy follows, splitting the muscle without breaching the mucosa.

Abdominal wall defects are separated by position and covering. Gastroschisis lies beside the cord, usually on the right, has no membrane, and is most often complicated by intestinal atresia rather than other anomalies. Omphalocele is midline, covered by peritoneum and amnion, and carries associated anomalies in about half of cases, particularly cardiac and chromosomal. Malrotation with midgut volvulus announces itself with bilious vomiting and a corkscrew duodenum, and demands Ladd's procedure: counterclockwise detorsion, division of Ladd's bands, widening of the mesenteric base and appendicectomy.

Between three months and three years, intussusception brings colicky pain, redcurrant-jelly stool, a sausage-shaped mass and a target sign on ultrasound. Air or contrast enema reduces 70 to 90 per cent of cases; surgery is reserved for perforation, peritonitis or failed reduction. Necrotising enterocolitis follows prematurity, ischaemia, bacterial colonisation and feeding, producing pneumatosis intestinalis, portal venous gas in severe disease and thrombocytopenia. Most infants are managed with bowel rest, decompression, antibiotics and fluids; pneumoperitoneum is the absolute indication for surgery.

Persistent conjugated jaundice in a newborn raises the question of biliary atresia. A hepatobiliary scan showing no excretion into the bowel supports it, but liver biopsy is the diagnostic gold standard. The Kasai portoenterostomy restores drainage and succeeds most often when performed within 60 days of birth.

The central distinctions can be recalled as follows.

All bilious vomiting in a newborn means obstruction beyond the ampulla of Vater, while pyloric stenosis vomits milk without bile.
Is the biochemistry hypochloraemic, hypokalaemic metabolic alkalosis? Then correct chloride and potassium with saline before pyloromyotomy, because the operation is never an emergency.
On the abdominal wall, a midline membrane with anomalies in half the cases is omphalocele, and exposed bowel beside the cord is gastroschisis.
Luminal telescoping in intussusception is reduced by enema in most children, necrotising enterocolitis is operated on only for pneumoperitoneum, and Kasai must happen within 60 days.

Appendicitis can progress from local inflammation to ischaemia and perforation, although its clinical course is variable rather than governed by a fixed timetable. Luminal obstruction, by a faecolith in adults, lymphoid hyperplasia in children and tumour in the elderly, raises intraluminal pressure and obstructs venous return. Ischaemia, bacterial overgrowth, necrosis and finally perforation follow. In the first twelve hours visceral afferents at T10 report only vague periumbilical pain and nausea. Between twelve and twenty-four hours the parietal peritoneum becomes involved, somatic nerves localise the pain to McBurney's point and fever begins. Beyond twenty-four to seventy-two hours perforation brings rebound tenderness, guarding and a mass. Migration of pain from the umbilicus to the right iliac fossa is the most valuable feature in the history.

Signs map the position of the appendix. Rovsing's sign, right-sided pain on left-sided palpation, indicates peritoneal irritation. A positive psoas sign points to a retrocaecal appendix lying on the iliopsoas, and a positive obturator sign to a pelvic appendix. Children, pregnant women and young women are imaged first with ultrasound, which seeks a non-compressible blind-ending tube over 6 mm with a target sign and simultaneously examines the ovaries. Adults are best served by CT, whereas a plain radiograph offers only indirect signs.

Laparoscopic appendicectomy is the standard treatment for uncomplicated disease. Antibiotics alone are feasible in selected cases, yet 25 to 40 per cent of patients require surgery within a year. A periappendiceal abscess or phlegmon is treated with antibiotics and drainage, with interval appendicectomy considered after six to eight weeks. Perforation demands urgent surgery, antibiotics and peritoneal lavage. Surgical site infection is the commonest complication, affecting 10 to 20 per cent after perforation. In the elderly the surgeon must think of tumour, because carcinoid and adenocarcinoma often present as appendicitis.

Infection prevention follows fixed rules. A single prophylactic dose is given within 60 minutes before incision, or 120 minutes for vancomycin and fluoroquinolones. It is repeated when the operation exceeds two half-lives of the drug or blood loss exceeds 1500 millilitres, and it stops within 24 hours. Hair is clipped rather than shaved, skin is prepared with chlorhexidine in alcohol, and normothermia and a glucose below 200 mg/dL are maintained. A clean wound carries a 1 to 5 per cent infection rate, whereas a dirty wound exceeds 27 per cent and is left for delayed primary closure.

Consent binds all of this together. It is valid only when capacity, adequate disclosure of risks, benefits and alternatives, and voluntariness free of manipulation coexist. A competent adult may refuse even life-saving treatment; the correct response is neither detention nor silent discharge but documented counselling, a signed refusal and a clear safety net. When a patient cannot communicate, no proxy is available and delay threatens life, emergency implied consent applies. A previous refusal of an elective operation does not extend to an unforeseen emergency.

The central distinctions can be recalled as follows.

All appendicitis follows one chain, obstruction, ischaemia, infection and perforation, and the pain migrates because visceral T10 afferents give way to somatic peritoneal nerves.
Is the patient a child, pregnant or a young woman? Then ultrasound comes first, seeking a non-compressible tube over 6 mm, while adults proceed to CT.
On prophylaxis the clock rules: one dose within 60 minutes of incision, repeated after two half-lives or 1500 millilitres of blood loss, stopped within 24 hours.
Lucid, informed and voluntary refusal by a competent adult is respected and documented, yet an unforeseen emergency in an unconscious patient restores implied consent.

Gastric mucosal integrity depends on a balance between injurious factors and the mechanisms that protect and repair the epithelial surface. Acid, pepsin, Helicobacter pylori and non-steroidal anti-inflammatory drugs erode the surface, whereas the mucus-bicarbonate layer, prostaglandins and mucosal blood flow repair it. An ulcer forms when the balance tips, and its site tells the story. Duodenal ulcers wake patients at night and ease with food; almost all are Helicobacter-driven and rarely become malignant. Gastric ulcers hurt after meals, follow Helicobacter or NSAID injury, and must be biopsied to exclude carcinoma. Bleeding ulcers receive endoscopic therapy and a 72-hour proton pump inhibitor infusion. On the Forrest scale, active spurting rebleeds in about 55 per cent, a visible vessel in about 43 per cent, and a clean base in 2 to 5 per cent.

Eradication is a matter of timing. A urea breath test performed on acid suppression is falsely negative, so the proton pump inhibitor is withheld for at least two weeks beforehand. Cure is confirmed at least four weeks after the antibiotics finish. Where clarithromycin resistance is common, bismuth quadruple therapy for fourteen days is preferred. Reflux, by contrast, is not a Helicobacter disease; it follows a lax lower oesophageal sphincter, and Barrett's columnar metaplasia is the precursor of adenocarcinoma. Sliding hiatus hernias are 95 per cent of the total; the para-oesophageal type can strangulate.

Gastric surgery leaves two signatures. Afferent loop syndrome brings post-prandial fullness relieved by bilious vomiting; bacteria in the stagnant limb consume B12 yet synthesise folate. Dumping syndrome reflects the lost pylorus: early symptoms follow hyperosmolar chyme drawing fluid into the jejunum; late symptoms are reactive hypoglycaemia one to three hours after carbohydrate. Type A gastritis is autoimmune, destroys parietal cells in the body and causes B12 deficiency; type B is bacterial, antral and linked to ulcer and cancer.

Obstruction is sorted by level first. Small bowel obstruction is usually adhesive, vomits early and profusely, and shows stepladder fluid levels with valvulae conniventes crossing the lumen. Large bowel obstruction is usually carcinoma, vomits late and distends more; a caecum beyond nine centimetres threatens perforation. Serum amylase stays normal in simple obstruction, so a rise signals strangulation or pancreatitis. Uncomplicated cases receive nil by mouth, nasogastric decompression and intravenous fluid; persistent pain, fever, leucocytosis, lactate or peritonism mandates surgery. Appendicitis migrates from the umbilicus to McBurney's point, and Rovsing's sign is right-sided pain on left-sided pressure.

One bowel hosts two inflammations. Crohn's disease is transmural, skips segments, favours the terminal ileum and produces granulomas, fistulae and strictures; ulcerative colitis is mucosal, continuous from the rectum and bleeds. Smoking worsens Crohn's disease yet protects against colitis, as does appendicectomy. Corticosteroids induce remission but never maintain it. Aminosalicylates maintain colitis, anti-TNF antibodies heal fistulae and spare surgery, and bowel rest with parenteral nutrition rivals steroids in active Crohn's disease. Toxic megacolon means a transverse colon wider than six centimetres with systemic toxicity, and anticholinergics and antidiarrhoeals are forbidden.

Four sentences hold the chapter together.

All duodenal ulcers point to Helicobacter and rarely turn malignant, whereas every gastric ulcer is biopsied to exclude carcinoma.
Is the breath test trustworthy? Only after two weeks without a proton pump inhibitor and four weeks after the antibiotics.
On the obstruction axis, adhesions block the small bowel and carcinoma the large, and amylase stays normal unless the loop strangulates.
Lumen-to-serosa inflammation that skips and fistulises is Crohn's disease; mucosal, continuous, bleeding inflammation is ulcerative colitis, and steroids never maintain either.

Cholesterol gallstone formation reflects three interacting processes: biliary supersaturation, crystal nucleation and impaired gallbladder emptying. Cholesterol stones make up about three quarters and are radiolucent. Ursodeoxycholic acid dissolves only small radiolucent cholesterol stones in patients too frail for surgery. Once formed, a stone is named by where it lodges.

Held in the gallbladder, it causes colic under six hours without fever. Wedged in the cystic duct, it causes cholecystitis: pain beyond six hours, fever and Murphy's sign. The inspiratory arrest occurs as the descending diaphragm presses the inflamed gallbladder onto the examiner's fingers. Ultrasound comes first, showing a wall over three millimetres and pericholecystic fluid; HIDA is most specific, and laparoscopic cholecystectomy follows within 72 hours. Acalculous cholecystitis, from stasis and ischaemia, stalks the ventilated patient on parenteral nutrition. Lodged in the common duct, the stone raises alkaline phosphatase and GGT and yellows the skin. Add bacteria and cholangitis follows: Charcot's triad is pain, fever and jaundice, never a palpable gallbladder. Shock and confusion complete Reynolds' pentad; antibiotics and fluid merely bridge to urgent endoscopic drainage. Morphine tightens the sphincter of Oddi, so an anti-inflammatory eases biliary pain.

Lodged at the ampulla, the stone triggers pancreatitis: trypsinogen activates within the gland, autodigestion follows, and cytokines produce systemic inflammation and third-space fluid loss. Diagnosis needs two of three: typical pain, lipase above three times the upper limit, and consistent imaging; stones and alcohol cause about 80 per cent. BISAP counts urea over 25, impaired mentation, SIRS, age over 60 and pleural effusion; a haematocrit above 44 per cent betrays haemoconcentration. Fluid comes first, antibiotics wait for infected necrosis, and ERCP is reserved for cholangitis or persistent obstruction. Saponification of fat consumes calcium. When the gland burns out, insulin and glucagon fail together, so type 3c diabetes fears hypoglycaemia, not ketoacidosis.

Fat and amino acids in the duodenum release cholecystokinin from I cells, which contracts the gallbladder and relaxes the sphincter of Oddi. Acid releases secretin from S cells, summoning bicarbonate and inhibiting gastric acid. Embryology adds a trap: the gallbladder is foregut endoderm from the hepatic diverticulum, whereas the spleen is dorsal mesogastric mesenchyme. The pancreatic head drains to the superior mesenteric vein, which joins the splenic vein to form the portal vein.

That portal vein is the hub of cirrhosis. Injury turns stellate cells into myofibroblasts under TGF-beta; collagen and regenerating nodules squeeze the sinusoids and resistance climbs. Varices open along the left gastric to azygos route. Ascites with a serum-ascites albumin gradient of at least 1.1 g/dL is portal; an ascitic neutrophil count of 250 or more declares peritonitis. Primary prophylaxis needs a non-selective beta-blocker: beta-1 blockade lowers output while beta-2 blockade constricts the splanchnic bed. Hepatitis C becomes chronic in 75 to 85 per cent; hepatitis B in over 90 per cent of neonates yet under 5 per cent of adults. Primary sclerosing cholangitis carries a 10 to 15 per cent lifetime risk of cholangiocarcinoma.

The central distinctions can be recalled as follows.

All gallstone disease is named by where the stone lodges: cystic duct cholecystitis, common duct jaundice, infected duct cholangitis, ampulla pancreatitis.
Is it pain, fever and jaundice with shock and confusion? Then Reynolds' pentad demands antibiotics, fluid and endoscopic drainage within hours.
On pancreatitis, fluid comes first; antibiotics wait for infected necrosis and ERCP waits for cholangitis or persistent obstruction.
Luminal pressure in the portal vein drives every complication of cirrhosis, and only a non-selective beta-blocker lowers it for prophylaxis.

Acute liver failure is characterised by coagulopathy, typically an INR of at least 1.5, together with hepatic encephalopathy developing within 26 weeks in a patient without pre-existing cirrhosis. Without encephalopathy it is acute liver injury, not failure. The jaundice-to-encephalopathy interval sorts the syndrome. Hyperacute failure, under seven days, follows paracetamol, ischaemia and hepatitis A or E, and carries the highest risk of cerebral oedema. Acute failure, seven to 28 days, is typically hepatitis B. Subacute failure, 28 days to 26 weeks, follows idiosyncratic drugs, Wilson's disease and autoimmune hepatitis; it swells the brain less but has the worst prognosis.

Two laboratory values deceive. Alanine aminotransferase leaks from hepatocytes dying now and says nothing about how many remain; when necrosis is nearly complete, the enzyme falls while the patient worsens. Ammonia does not track the grade of encephalopathy, though a level above 150 micromol/L raises the risk of intracranial hypertension. Severity is read instead from what the liver still does: synthesis by the INR, excretion by bilirubin, and the grade of encephalopathy. Fresh frozen plasma is therefore withheld unless the patient bleeds; it hides the INR.

Gluconeogenesis is hepatic, because muscle lacks glucose-6-phosphatase and can only return lactate and alanine to the liver through the Cori cycle. When hepatocytes are exhausted, glucose falls and lactate accumulates, which is why hypoglycaemia is watched hourly and a lactate above 3.0 mmol/L after resuscitation is a transplant criterion. Ethanol oxidation floods the cell with NADH and diverts pyruvate to lactate, so the fasting drinker becomes hypoglycaemic and acidotic.

Paracetamol is the commonest cause worldwide, hepatitis B in Taiwan. N-acetylcysteine, 200 mg/kg over four hours then 100 mg/kg over sixteen, starts without delay and improves survival even in non-paracetamol failure. Cerebral oedema is the leading killer, so the head is raised, sodium held at 140 to 145 mmol/L, and hypertonic saline or mannitol treats surges. The King's College criteria for paracetamol are an arterial pH below 7.30 after resuscitation, or an INR above 6.5 with creatinine above 300 micromol/L and grade III or IV encephalopathy. Once they are met, only transplantation changes the outcome.

A mutation in ATP7B stops copper entering ceruloplasmin and bile, so copper accumulates in liver, lentiform nuclei and cornea. Ceruloplasmin is low while free serum copper and urinary copper are high, a direction examiners reverse. Kayser-Fleischer rings and Coombs-negative haemolysis complete the picture, and fulminant disease needs a new liver.

Mechanism before sequence governs bleeding too. Shock kills before the lesion does, so the airway is secured, two large cannulae placed and volume restored before any endoscope. Early haemoglobin may be normal, because whole blood is lost before dilution. Suspected variceal bleeding receives terlipressin or octreotide and intravenous ceftriaxone at once, then band ligation within twelve hours; balloon tamponade bridges to TIPS. Propranolol belongs to prophylaxis and is withheld during the bleed. In mesenteric ischaemia, flow is restored with fluid and revascularisation; vasoconstrictors are forbidden.

The central distinctions can be recalled as follows.

All acute liver failure requires an INR of at least 1.5 plus encephalopathy in a previously healthy liver, within 26 weeks.
Is the ALT falling while the INR rises? Then hepatocytes are exhausted, not recovering, and the transplant unit must be called.
On a bleeding cirrhotic, airway and volume come before endoscopy, terlipressin and ceftriaxone before banding, and propranolol never in the acute phase.
Lucid or drowsy, the patient's ammonia does not grade the failure; bilirubin, INR and encephalopathy do.