Learn — Gastrointestinal & hepatic

31 notes · 68 questions on the topic

Bedsores (pressure ulcer stages)

A pressure injury (bedsore, decubitus ulcer) is localised damage to skin and underlying soft tissue, usually over a bony prominence or under a medical device, caused by sustained pressure or by pressure in combination with shear. It matters because it is the classic nurse-sensitive harm — almost entirely preventable by repositioning, offloading, skin care and nutrition — and because once it reaches full thickness it takes months to heal and can end in osteomyelitis and sepsis.

The mechanism is ischaemia: capillary closing pressure is about 32 mmHg, and pressure above that for long enough occludes the capillaries, so damage is the product of the intensity and the duration of the pressure. Shear, as when a patient slides down a raised bed head, angulates and kinks the vessels and does more damage than direct pressure alone, and moisture from sweat, urine or exudate macerates the skin and lowers its tolerance.
Stage 1 is intact skin with non-blanchable erythema over a bony prominence; in darkly pigmented skin the redness cannot be seen, so look instead for a change in colour compared with the surrounding skin and for a difference in temperature, firmness, oedema or reported pain.
Stage 2 is partial-thickness loss of dermis presenting as a shallow open ulcer with a pink or red moist bed, or as an intact or ruptured serum-filled blister; there is no slough, no granulation tissue and no exposed fat, and it must not be used to describe moisture-associated skin damage, skin tears or tape injury.
Stage 3 is full-thickness loss in which subcutaneous fat is visible and slough, undermining and tunnelling may be present, but bone, tendon and muscle are not exposed; the depth varies by site, so a stage 3 injury on the bridge of the nose or the ear is shallow while one on the buttock can be very deep. Stage 4 is full-thickness loss with exposed or directly palpable fascia, muscle, tendon, ligament, cartilage or bone.
Unstageable means a full-thickness injury whose base is covered by slough or eschar so that the depth cannot be judged; stable, dry, adherent eschar on an ischaemic heel is left alone rather than debrided. A deep tissue pressure injury is persistent non-blanchable deep red, maroon or purple discolouration, or a blood-filled blister, over intact or broken skin, and it can deteriorate into a stage 4 within days. Medical device-related and mucosal membrane pressure injuries are named separately.
The commonest sites are the sacrum and coccyx and the heels; then the ischial tuberosity in the chair-bound patient, the greater trochanter in the side-lying patient, the lateral malleolus, elbow, scapula and occiput — the occiput being the commonest site in infants and small children — and under oxygen tubing, masks, catheters, casts and cervical collars.
Risk assessment on admission, on any change in condition and at least daily: the Braden scale scores six subscales (sensory perception, moisture, activity, mobility, nutrition, and friction and shear) from 6 to 23, where 15 to 18 is mild risk, 13 to 14 moderate, 10 to 12 high and 9 or less very high risk; Norton (14 or less at risk) and Waterlow (10 at risk, 15 high, 20 very high) are the other scales in use.
Prevention: reposition at least two-hourly in bed and hourly in a chair (or teach 15-minutely lifts), use a 30-degree tilt rather than 90-degree side lying, keep the head of the bed at or below 30 degrees unless contraindicated to limit shear, float the heels completely off the bed on a pillow with the knee slightly flexed, use a pressure-redistributing foam or alternating mattress for anyone at risk, keep the skin clean and dry with a barrier film, use a slide sheet rather than dragging, and give about 30 to 35 kcal/kg and 1.25 to 1.5 g/kg of protein a day. Never massage a reddened bony prominence and never use a ring or donut cushion — both make the ischaemia worse.
Management by stage: stage 1 needs the pressure removed and the skin protected; stage 2 needs moist wound healing with a hydrocolloid or foam; stages 3 and 4 need slough debrided (autolytic with a hydrogel, sharp, or enzymatic), the dead space filled with an alginate or hydrofibre if it is exuding, and consideration of negative pressure wound therapy or a flap. Every pressure ulcer is colonised, so swab only when there are clinical signs of infection, and document length, width, depth, undermining, exudate, odour, wound bed and surrounding skin at every dressing change. A healing ulcer is never reverse-staged: a healing stage 4 is a healing stage 4, not a stage 2.

Liver abscess and cancer

A liver abscess is a localised collection of pus within the hepatic parenchyma — amoebic in most Indian adults and pyogenic where there is biliary or portal sepsis — while hepatocellular carcinoma is the primary malignancy of hepatocytes, which almost always arises in a liver already damaged by hepatitis B, hepatitis C or cirrhosis. They are learned together because both present with a painful enlarged liver and both are diagnosed by imaging, but one is cured in ten days with a tablet and the other needs staging, resection or transplantation.

Amoebic liver abscess: Entamoeba histolytica trophozoites travel from the colon to the liver in the portal vein, and because superior mesenteric blood streams to the right, the abscess is usually solitary and in the right lobe. It is commonest in adult men, often with alcohol use, and presents with fever, tender hepatomegaly, intercostal tenderness over the liver and pain referred to the right shoulder tip; the aspirate is odourless, chocolate-brown anchovy-sauce necrotic liver rather than true pus, and it is sterile on ordinary culture, with amoebic serology positive in over 90%.
Treatment of an amoebic abscess is metronidazole 750 to 800 mg three times daily for 7 to 10 days (or tinidazole), and it must be FOLLOWED by a luminal amoebicide — diloxanide furoate 500 mg three times daily for 10 days or paromomycin — to clear the intestinal carrier state, or it relapses. Aspiration is added for a left lobe abscess (which can rupture into the pericardium), a large abscess or one with a thin overlying rim, failure to improve after 48 to 72 hours of metronidazole, or when a pyogenic abscess cannot be excluded.
Pyogenic liver abscess: usually polymicrobial and secondary to biliary sepsis (ascending cholangitis is now the commonest source), to portal pyaemia from appendicitis or diverticulitis, or to haematogenous spread; often multiple. Escherichia coli, Klebsiella pneumoniae (the classic organism in Asia, associated with diabetes and with metastatic endophthalmitis), Streptococcus milleri and anaerobes predominate, the patient is toxic with rigors and a raised alkaline phosphatase, and treatment is broad-spectrum antibiotics for 4 to 6 weeks with percutaneous catheter drainage and correction of the source.
Rupture is the feared complication of an amoebic abscess: into the pleural cavity most often, into the lung with expectoration of anchovy-sauce sputum, into the peritoneum with generalised peritonitis, and from the left lobe into the pericardium, which is the most lethal of all.
Hepatocellular carcinoma risk factors are chronic hepatitis B (the commonest cause worldwide and the one that does not need cirrhosis first), hepatitis C, alcoholic and non-alcoholic fatty liver cirrhosis, aflatoxin B1 from Aspergillus-contaminated groundnuts and grain, and haemochromatosis. It presents with weight loss, right upper quadrant pain, a hard irregular enlarged liver, sometimes an arterial bruit, and often as sudden decompensation — ascites, jaundice or variceal bleeding — in a previously stable cirrhotic.
Diagnosis and treatment of hepatocellular carcinoma: alpha-fetoprotein above 400 ng/mL in the right clinical setting is strongly suggestive but a normal level does not exclude it; triple-phase CT or MRI showing arterial enhancement with washout in the portal venous phase is diagnostic without biopsy. Cirrhotic patients are screened with six-monthly ultrasound. Treatment depends on tumour burden and liver function: resection for a solitary tumour with preserved function, transplantation within the Milan criteria (one lesion up to 5 cm or up to three lesions each up to 3 cm with no vascular invasion or spread), local ablation, transarterial chemoembolisation, and systemic therapy for advanced disease.
Secondary tumours are far commoner than primary liver cancer — the liver is the commonest site of blood-borne metastasis in the abdomen, most often from a colorectal primary, and resection of a limited number of colorectal liver metastases is potentially curative.
Nursing points that recur in exams: an amoebic abscess needs no surgical drainage in most cases, aspiration is diagnostic and therapeutic in selected cases, and metronidazole must never be given without warning the patient about alcohol because of the disulfiram-like reaction; and a patient with cirrhosis and a new abscess or tumour needs careful attention to coagulation, ascites, encephalopathy and nutrition.

Gallbladder stones (cholelithiasis)

Cholelithiasis is the formation of stones in the gallbladder from bile that has become supersaturated with cholesterol or overloaded with pigment, helped along by gallbladder stasis and by nucleating factors in the mucus. Most gallstones are silent and are found incidentally, so the topic is really about the complications they cause — biliary colic, acute cholecystitis, stones in the common bile duct with obstructive jaundice, ascending cholangitis, gallstone pancreatitis and, rarely, gallstone ileus.

Cholesterol and mixed stones make up about 80% of stones in Western and urban Indian practice and go with the classic profile of female sex, forty, fertile, fat and fair, together with rapid weight loss, the oral contraceptive pill, terminal ileal disease or resection and prolonged parenteral nutrition. Pigment stones are black (chronic haemolysis in sickle cell disease, thalassaemia, hereditary spherocytosis, and in cirrhosis) or brown (biliary stasis and infection, often with worms or flukes, and the commoner type in much of Asia).
Biliary colic is misnamed because the pain is constant rather than colicky: severe right upper quadrant or epigastric pain radiating to the tip of the right scapula, beginning an hour or two after a fatty meal, lasting from 30 minutes to a few hours and then settling, with no fever, no peritonism and a normal white cell count.
Acute cholecystitis is obstruction of the cystic duct with inflammation: the pain now lasts more than 6 hours, with fever, a raised white cell count and a positive Murphy's sign — arrest of inspiration when the right upper quadrant is palpated, with no equivalent arrest on the left. Ultrasound is the first investigation and shows stones, a gallbladder wall thicker than 3 mm, pericholecystic fluid and a sonographic Murphy's sign. Management is admission, nil by mouth, intravenous fluid, analgesia and antibiotics, with laparoscopic cholecystectomy ideally within 72 hours of onset or else delayed by about 6 weeks.
Choledocholithiasis gives obstructive jaundice with pale stools, dark urine and itching, a raised conjugated bilirubin and alkaline phosphatase and a common bile duct dilated beyond about 6 mm on ultrasound; MRCP confirms it and ERCP with sphincterotomy clears it. Charcot's triad of fever with rigors, right upper quadrant pain and jaundice means ascending cholangitis, and Reynolds' pentad adds hypotension and confusion — an emergency requiring resuscitation, antibiotics and urgent biliary drainage.
Eponyms that recur in papers: Courvoisier's law says that in a jaundiced patient a palpable, painless gallbladder is unlikely to be due to stones, because a stone-bearing gallbladder is fibrotic and cannot distend, so think of a periampullary or pancreatic head carcinoma. Mirizzi syndrome is obstruction of the common hepatic duct by a stone impacted in Hartmann's pouch or the cystic duct. Gallstone ileus follows a cholecysto-duodenal fistula and shows Rigler's triad on the abdominal film — small bowel obstruction, gas in the biliary tree and an ectopic radio-opaque gallstone.
Laparoscopic cholecystectomy is the standard operation, and the critical view of safety must be obtained before any structure is clipped, because bile duct injury is the serious complication. Truly asymptomatic stones are usually left alone; prophylactic cholecystectomy is offered for a porcelain (calcified) gallbladder, stones larger than 3 cm, an associated gallbladder polyp over 1 cm, and in patients with haemolytic anaemia or awaiting transplantation, because of the risk of carcinoma or of complications at a bad time.
Post-operative nursing: expect shoulder-tip pain from residual carbon dioxide and treat it with mobilisation and analgesia rather than investigation; watch the drain for bile, and for the triad of bile-stained drainage, right upper quadrant pain and fever that signals a bile leak; watch for returning jaundice from a retained duct stone; advise a normal diet reintroduced gradually with fat reduced for the first weeks.
After exploration of the common bile duct a T-tube drains about 300 to 500 mL in the first 24 hours and then less; keep the bag below the level of the abdomen, record the volume and colour, never irrigate or clamp it without an instruction, and expect a T-tube cholangiogram at about 7 to 10 days before it is removed.

Pancreatitis and Whipple procedure

Acute pancreatitis is acute inflammation of the pancreas caused by premature intracellular activation of its own digestive enzymes, with a spectrum from a self-limiting illness to necrosis with multi-organ failure; the Whipple operation, or pancreaticoduodenectomy, is the resection performed for tumours of the pancreatic head and the periampullary region. They sit together because both are diseases of the same organ in which the nursing task is fluid, nutrition, drains and the early detection of a leak or of organ failure.

Gallstones and alcohol cause about 80% of acute pancreatitis; the rest are remembered as I GET SMASHED — Idiopathic, Gallstones, Ethanol, Trauma, Steroids, Mumps and other infections, Autoimmune, Scorpion sting, Hyperlipidaemia, hypercalcaemia and hypothermia, ERCP, and Drugs such as azathioprine, sodium valproate, thiazides and oestrogens.
Diagnosis under the revised Atlanta classification needs two of three: characteristic epigastric pain radiating to the back and eased by sitting forward, serum amylase or lipase at least three times the upper limit of normal, and characteristic findings on imaging. Lipase is more specific and stays raised longer; the height of the enzyme does not indicate severity, and the amylase can be normal in alcoholic and hyperlipidaemic pancreatitis.
Severity is graded as mild (no organ failure and no local complication), moderately severe (transient organ failure resolving within 48 hours, or local complications) and severe (persistent organ failure beyond 48 hours). Ranson's 11 criteria — five on admission such as age over 55 and a white count over 16,000, and six at 48 hours such as a fall in haematocrit over 10% and a calcium under 8 mg/dL — predict severe disease when three or more are present; Glasgow-Imrie, APACHE II and BISAP are used similarly, and a C-reactive protein over 150 mg/L at 48 hours is a practical marker.
Contrast-enhanced CT is best performed at 72 hours or later, because necrosis takes that long to declare and a scan on day one underestimates it; ultrasound is done early to look for gallstones and a dilated duct.
Cullen's sign (periumbilical bruising) and Grey Turner's sign (bruising in the flanks) indicate retroperitoneal haemorrhage and are late and uncommon. Hypocalcaemia from saponification of fat by released lipase is both a Ranson criterion and a marker of severity, so look for Chvostek's and Trousseau's signs and monitor the corrected calcium.
Management is aggressive early fluid resuscitation with Ringer's lactate in the first 24 to 48 hours titrated to urine output, haematocrit and urea, good analgesia, and EARLY ENTERAL FEEDING — the old regimen of pancreatic rest with nil by mouth and parenteral nutrition has been abandoned, and oral or nasogastric feeding within 24 to 72 hours as tolerated reduces infection and length of stay.
Antibiotics are not given prophylactically for sterile necrosis; they are for proven infected necrosis or another documented infection. Intervention for infected necrosis is delayed for about 4 weeks so the collection walls off, and then follows a step-up approach of percutaneous or endoscopic drainage before minimally invasive necrosectomy. Urgent ERCP within 24 to 72 hours is reserved for gallstone pancreatitis with cholangitis or persisting biliary obstruction, and cholecystectomy is done in the same admission for mild gallstone pancreatitis to prevent recurrence.
Complications: early are systemic inflammatory response, acute respiratory distress syndrome, acute kidney injury, hypocalcaemia, hyperglycaemia and disseminated intravascular coagulation; later are acute peripancreatic fluid collections, a pseudocyst (a collection with a defined wall at 4 weeks or more, treated only if symptomatic, enlarging or infected, usually by endoscopic cystogastrostomy), walled-off necrosis, splenic vein thrombosis with left-sided portal hypertension and gastric varices, pancreatic ascites and abscess.
The Whipple procedure removes the head of the pancreas, the duodenum, the proximal jejunum, the gallbladder and the distal common bile duct, together with the gastric antrum unless the pylorus-preserving variant is used, and reconstructs with three anastomoses: pancreaticojejunostomy, hepaticojejunostomy and gastrojejunostomy or duodenojejunostomy. The commonest serious complication is a leak from the pancreatic anastomosis — defined as drain amylase more than three times the serum level on or after the third post-operative day — followed by delayed gastric emptying and post-pancreatectomy haemorrhage.
Nursing after a Whipple: record the volume, colour and amylase of each drain, watch for a sentinel bleed of fresh blood in the drain which precedes catastrophic haemorrhage, monitor blood glucose because both endocrine and exocrine function fall, give pancreatic enzyme replacement with meals, follow the enhanced recovery pathway with early mobilisation and early oral intake, and expect delayed gastric emptying to need a nasogastric tube and patience rather than reoperation.

Hernia — types and complications

A hernia is the protrusion of a viscus or part of a viscus through an abnormal opening in the wall of the cavity that contains it, and it has three parts — a peritoneal sac, its coverings and its contents. It matters surgically because a hernia that stops being reducible can obstruct and then strangulate, cutting off the blood supply of its contents within hours, so a lump in the groin that becomes tense and painful is a theatre case and not an outpatient appointment.

Inguinal hernia accounts for about 75% of abdominal wall hernias: an indirect hernia enters through the deep ring lateral to the inferior epigastric vessels, follows the cord and can reach the scrotum, and is controlled by pressure over the deep ring after reduction; a direct hernia bulges forward through Hesselbach's triangle medial to those vessels, rarely reaches the scrotum and is not controlled by deep-ring pressure.
A femoral hernia passes through the femoral canal, below and lateral to the pubic tubercle and medial to the femoral vein; it is commoner in women than in men (although inguinal hernia is still the commonest hernia in women), has a narrow rigid neck, strangulates in up to 40% of cases and is therefore repaired as soon as it is diagnosed.
The bedside discriminator is the pubic tubercle: an inguinal hernia lies above and medial to it, a femoral hernia below and lateral.
Other hernias by site are umbilical and paraumbilical, epigastric, incisional (complicating 10 to 15% of laparotomy wounds, with obesity, wound infection, steroids, chronic cough and poor closure as risks), Spigelian, obturator and lumbar.
Named hernias by content are Richter's (only part of the bowel circumference is trapped, so it strangulates without obstructing), Littre's (containing a Meckel's diverticulum), Maydl's (a W-shaped loop in which the strangulated segment lies inside the abdomen) and sliding hernia (a retroperitoneal viscus such as caecum or bladder forms part of the wall of the sac).
The complications run in sequence: reducible, then irreducible or incarcerated (no ischaemia), then obstructed (colicky pain, vomiting, distension, absolute constipation), then strangulated (constant severe pain, a tense tender irreducible lump with no cough impulse, overlying redness and systemic toxicity), then infarction and perforation with peritonitis.
Never attempt to reduce a tender, red, irreducible hernia — pushing dead bowel back into the abdomen (reduction en masse) hides a perforation that will present as peritonitis; the correct action is resuscitation and emergency surgery.
Elective repair is tension-free: open Lichtenstein mesh repair or laparoscopic TEP/TAPP in adults; children have a herniotomy alone, because the defect is a patent processus vaginalis and no mesh is needed.
Discharge teaching after repair: scrotal support and ice for scrotal swelling, early walking, treat the causes of straining (cough, constipation, prostatism), no heavy lifting for about 4 to 6 weeks, and return at once with fever, wound discharge or a painful lump.

Achalasia cardia

Achalasia cardia is a primary motility disorder in which the ganglion cells of the myenteric (Auerbach's) plexus in the distal oesophagus degenerate, so the lower oesophageal sphincter fails to relax on swallowing and the body of the oesophagus loses its peristalsis. It matters because the obstruction is functional rather than mechanical: food and saliva stagnate in a progressively dilating oesophagus, causing regurgitation, night-time aspiration and weight loss, and long-standing disease carries a raised risk of squamous carcinoma.

The hallmark is dysphagia to solids and liquids from the very beginning, coming on slowly over months or years in a patient aged roughly 25 to 60 — a mechanical obstruction such as carcinoma starts with solids and only later includes liquids.
Other features are regurgitation of undigested, non-acidic food especially on lying flat, with nocturnal cough and repeated aspiration pneumonia, retrosternal chest pain, and weight loss that is usually modest for the duration of symptoms.
Barium swallow shows a smooth, tapering bird-beak or rat-tail narrowing at the cardia with a dilated body above it, absent primary peristalsis and a fluid level; the chest X-ray may show a widened mediastinum with an absent gastric air bubble.
High-resolution manometry is the gold standard and shows absent peristalsis with incomplete relaxation of the lower oesophageal sphincter (a raised integrated relaxation pressure), and it separates the three Chicago types, which predict the response to treatment.
Upper gastrointestinal endoscopy is mandatory in every case to exclude pseudoachalasia caused by a carcinoma of the cardia — suspect that when the patient is older, the history is short and the weight loss is rapid.
Treatment options: pneumatic balloon dilatation of the sphincter (effective, with perforation as its main risk, quoted at around 2%), laparoscopic Heller's cardiomyotomy combined with a partial fundoplication (Dor or Toupet) to control the reflux the myotomy creates, and peroral endoscopic myotomy; botulinum toxin injection and drugs such as nifedipine or isosorbide dinitrate are reserved for patients unfit for a procedure and last only months.
After dilatation or myotomy the patient is kept nil by mouth until a water-soluble contrast swallow excludes a leak, then progressed from fluids to a soft diet; teach eating slowly, chewing well, drinking water with meals, taking the last meal at least 3 hours before lying down, sleeping with the head end raised, and taking a proton pump inhibitor after a myotomy.
Chagas' disease from Trypanosoma cruzi produces an identical picture in South America; in India the disease is idiopathic.

Zenker diverticulum

Zenker's diverticulum is a pharyngo-oesophageal pulsion diverticulum in which mucosa and submucosa herniate backwards through Killian's dehiscence, the weak triangle between the oblique fibres of the thyropharyngeus and the transverse fibres of the cricopharyngeus, because the cricopharyngeal sphincter fails to relax as the pharynx contracts. It is therefore a false diverticulum with no muscle in its wall, and it matters because the pouch fills with food that is regurgitated undigested, causing halitosis and repeated aspiration in an elderly patient.

It is typically a disease of men over 60; the sac develops posteriorly and then deviates to the left of the midline, so a gurgling swelling may be felt in the left side of the neck and emptied by pressure (Boyce's sign).
Symptoms follow a recognisable order: intermittent dysphagia, then regurgitation of undigested food hours after a meal with no acid taste, halitosis, a gurgling neck swelling, chronic cough with recurrent aspiration pneumonia, and weight loss.
Barium swallow is the diagnostic test and outlines the pouch; endoscopy is done cautiously or avoided at first, because the scope readily enters the pouch and can perforate it.
Treatment is endoscopic stapling or laser division of the common wall between pouch and oesophagus (Dohlman's procedure) for most patients, or open diverticulectomy, diverticulopexy or inversion — and in every approach a cricopharyngeal myotomy, because dividing the sphincter treats the cause and without it the pouch recurs.
A small asymptomatic pouch can be watched, but symptomatic disease is repaired because the danger is aspiration pneumonia rather than the swelling itself; carcinoma developing in a long-standing pouch is rare but recognised.
Nursing care: nil by mouth with a contrast study before feeding after operation, observe the neck for swelling, surgical emphysema or a salivary leak, listen for a hoarse voice suggesting recurrent laryngeal nerve injury, and teach the patient to sit upright to eat, to empty the pouch before lying down and to avoid a late meal.

GERD

Gastro-oesophageal reflux disease is the flow of gastric contents back into the oesophagus in a volume or frequency that produces troublesome symptoms or mucosal injury, because the lower oesophageal sphincter and the crural diaphragm fail as a barrier — usually through transient sphincter relaxations, a hiatus hernia or raised intra-abdominal pressure. It matters because it is the commonest upper gastrointestinal complaint in surgical clinics, because years of reflux are what create Barrett's oesophagus and adenocarcinoma, and because heartburn can be the presenting symptom of a myocardial infarction.

Typical symptoms are heartburn 30 to 60 minutes after meals and on bending or lying flat, acid regurgitation and waterbrash; atypical or extra-oesophageal presentations are chronic cough, nocturnal asthma, hoarseness, globus sensation, dental erosion and non-cardiac chest pain.
Risk factors: obesity and central adiposity, hiatus hernia, pregnancy, smoking and alcohol, large or late meals, and agents that lower sphincter tone — chocolate, peppermint, caffeine, fat, calcium-channel blockers, nitrates, anticholinergics and theophylline.
Diagnosis is usually clinical and a trial of a proton pump inhibitor is both treatment and evidence; endoscopy is done for alarm features or persistent symptoms and grades oesophagitis by the Los Angeles classification A to D, ambulatory 24-hour pH or pH-impedance monitoring off therapy is the gold standard for proving acid exposure, and manometry is done before antireflux surgery to exclude achalasia and to plan the wrap.
Alarm features that make endoscopy urgent: dysphagia, odynophagia, unintentional weight loss, haematemesis or melaena, iron-deficiency anaemia, persistent vomiting, a palpable mass, and new-onset symptoms in an older patient.
Lifestyle measures worth teaching because they work: weight loss, stopping smoking, raising the head of the bed by 15 to 20 cm on blocks rather than piling up pillows, leaving 3 hours between the last meal and lying down, sleeping on the left side, and eating smaller meals.
Drug treatment: a proton pump inhibitor such as omeprazole 20 mg or pantoprazole 40 mg once daily, taken 30 to 60 minutes before breakfast, for 8 weeks and then stepped down to the lowest effective dose, with a second pre-evening-meal dose for nocturnal symptoms; H2-receptor blockers and alginate antacids are add-ons rather than substitutes.
Surgery — laparoscopic Nissen (360 degree) or partial Toupet or Dor fundoplication with crural repair — is for a large hiatus hernia, volume regurgitation, intolerance of proton pump inhibitors or well-documented refractory disease; its specific complications are dysphagia, gas-bloat with an inability to belch or vomit, and slippage of the wrap.
Complications of untreated disease: oesophagitis, peptic stricture presenting as progressive dysphagia to solids, ulceration with bleeding and iron-deficiency anaemia, Barrett's oesophagus in roughly 10 to 15% of chronic refluxers, and aspiration.
Discharge teaching after fundoplication: small soft meals for 2 to 6 weeks, chew thoroughly, avoid fizzy drinks and drinking straws, expect early fullness and difficulty belching, avoid heavy lifting and straining, and report persistent dysphagia or the return of reflux.

Oesophageal perforation

Oesophageal perforation is a full-thickness breach of the oesophageal wall that spills saliva, gastric acid, food and organisms into the mediastinum or pleural cavity, producing first a chemical and then a bacterial mediastinitis. It matters because it is the most lethal perforation of the gastrointestinal tract and because survival depends almost entirely on time — repair within the first 24 hours carries a mortality of about 10 to 20%, while delay beyond that doubles it — so the diagnosis is acted on when it is suspected, not when it is proved.

Causes in order of frequency: iatrogenic (about 60%) from endoscopy, dilatation, stenting, transoesophageal echocardiography, intubation or a nasogastric tube; spontaneous Boerhaave's syndrome (about 15%) from a violent vomit against a closed cricopharyngeus, classically after a binge of food and alcohol; swallowed foreign bodies and caustics; and penetrating or blunt trauma.
Boerhaave's tear is typically a vertical, full-thickness split in the left posterolateral wall of the lower third just above the diaphragm, so contamination enters the left pleural cavity; a Mallory–Weiss tear, by contrast, is a mucosal tear at the gastro-oesophageal junction that bleeds but does not perforate.
Mackler's triad — violent vomiting, then severe lower chest or epigastric pain, then subcutaneous emphysema — is complete in only a minority; a patient who looks septic and shocked out of proportion to the abdominal findings after vomiting has Boerhaave's until proved otherwise.
Signs: pain made worse by swallowing and by lying flat, odynophagia, tachycardia, fever, crepitus in the neck or supraclavicular fossa, Hamman's crunch (a crackle over the precordium synchronous with the heartbeat), and a pleural effusion that is usually left-sided.
Investigations: an erect chest X-ray showing mediastinal or subcutaneous emphysema, pleural effusion, hydropneumothorax or a widened mediastinum; a water-soluble (Gastrografin) contrast swallow rather than barium first, because barium in the mediastinum provokes a dense inflammatory reaction; and CT with oral contrast, now the most sensitive test. Pleural fluid with a pH below 6, a high amylase or visible food particles is diagnostic.
Immediate management: strictly nil by mouth, two wide-bore cannulae with aggressive crystalloid resuscitation, broad-spectrum intravenous antibiotics with antifungal cover, a proton pump inhibitor, analgesia, and nothing passed blindly into the oesophagus — a nasogastric tube goes in only under endoscopic or radiological guidance.
Definitive treatment depends on the delay and the degree of contamination: primary repair over a drain with a buttress and wide drainage within the first 24 hours gives the best outcome; later or septic cases need drainage, exclusion, a T-tube or oesophagectomy; and a small contained iatrogenic perforation in a stable, fasted patient may be managed with a covered stent, drainage and antibiotics.
Nursing care: nil by mouth with scrupulous mouth care and no oral drugs, chest drain observation with hourly output and air-leak checks, nutrition by the parenteral or feeding jejunostomy route, sitting the patient at 45 degrees, strict fluid balance and sepsis observations, and no oral intake until a contrast study shows the leak has sealed.

Barrett oesophagus

Barrett's oesophagus is the replacement of the normal stratified squamous lining of the distal oesophagus by metaplastic columnar epithelium containing intestinal-type goblet cells, an adaptation to years of acid and bile reflux. It matters because it is the only recognised precursor of oesophageal adenocarcinoma, and the whole clinical purpose of diagnosing it is to put the patient into an endoscopic surveillance programme that finds dysplasia while it can still be cured endoscopically.

At endoscopy it appears as salmon-pink columnar mucosa extending upwards from the gastro-oesophageal junction as tongues or as a circumferential segment; biopsy confirmation of intestinal metaplasia with goblet cells is required, because the appearance alone is not the diagnosis.
The Prague C&M classification records the circumferential (C) and maximal (M) extent in centimetres above the top of the gastric folds: 3 cm or more is long-segment, less than 3 cm is short-segment, and an irregular Z-line under 1 cm is not sampled as Barrett's.
Screening is offered to patients with chronic reflux — 5 years or more, or frequent symptoms — plus risk factors: male sex, age over 50, white ethnicity, central obesity, smoking, and a first-degree relative with Barrett's or oesophageal adenocarcinoma.
The Seattle biopsy protocol takes four-quadrant biopsies every 2 cm (every 1 cm when dysplasia is known or suspected) plus targeted biopsies of any nodule or irregularity, and it is done after 8 to 12 weeks of acid suppression so that inflammation is not misread as dysplasia; every dysplasia diagnosis is confirmed by a second expert gastrointestinal pathologist.
Surveillance intervals: no dysplasia every 3 to 5 years; indefinite for dysplasia, repeated after 3 to 6 months of optimised acid suppression; confirmed low-grade dysplasia treated by endoscopic eradication or watched at 6-monthly intervals; high-grade dysplasia and intramucosal cancer treated by endoscopic resection of visible lesions plus radiofrequency ablation of the rest of the segment rather than by oesophagectomy in most cases.
The absolute risk of progression from non-dysplastic Barrett's to adenocarcinoma is low — of the order of 0.3 to 0.5% a year — which is why surveillance is spaced out and why the patient is counselled to be watchful rather than frightened; the risk rises with the length of the segment and steeply with dysplasia.
Treatment is a once-daily proton pump inhibitor for everyone (symptom control and probable chemoprevention), weight loss and stopping smoking, with aspirin considered where there is a cardiovascular indication; antireflux surgery controls symptoms but does not remove the need for surveillance, and the metaplasia does not reliably regress.
The nursing role is continuity: making sure the patient understands that being symptom-free does not mean the Barrett's has gone, keeping them on the surveillance recall list, teaching proton pump inhibitor timing before breakfast, and preparing them for endoscopic therapy — 6 hours nil by mouth, consent, anticoagulation managed per protocol, and post-procedure observation for chest pain, bleeding and later dysphagia from a stricture after ablation.

Infantile hypertrophic pyloric stenosis (IHPS)

Infantile hypertrophic pyloric stenosis is progressive hypertrophy of the circular muscle of the pylorus that narrows the gastric outlet in an infant who fed normally at birth. It matters because the repeated vomiting produces a very specific biochemical picture — hypochloraemic, hypokalaemic metabolic alkalosis with paradoxical aciduria — and because the pyloromyotomy that cures it is never the emergency: the emergency is the dehydration and the alkalosis, which must be corrected first, since an alkalotic infant is at risk of apnoea after anaesthesia.

It presents between 3 and 6 weeks of age (range 2 to 12 weeks), is about four times commoner in boys, is more frequent in first-born infants and where there is a family history, and is associated with exposure to erythromycin or azithromycin in the infant or the breastfeeding mother.
The vomiting is projectile and non-bilious, because the obstruction is proximal to the ampulla of Vater, and it comes shortly after a feed; the baby is hungry immediately afterwards and feeds eagerly again, yet loses weight, becomes constipated and passes less urine while remaining alert until late.
Examination after a test feed shows visible gastric peristalsis running from left to right across the epigastrium and a firm, mobile, olive-shaped mass in the right upper quadrant lateral to the rectus muscle, best felt from the baby's left side while he sucks; a palpable olive is diagnostic and no imaging is then needed.
Biochemistry: loss of hydrogen and chloride in the vomit gives a hypochloraemic, hypokalaemic metabolic alkalosis, and in the later dehydrated phase the kidney excretes hydrogen ions to conserve sodium, so the urine is paradoxically acidic despite the alkalosis.
Ultrasound is the imaging test of choice: a pyloric muscle thickness of 3 mm or more and a channel length of about 15 to 17 mm or more, with the target or doughnut appearance in cross-section; a barium meal, rarely needed, shows the string sign and the shoulder sign.
Preoperative correction is the examinable answer: nil by mouth with a nasogastric tube on free drainage, intravenous rehydration with sodium chloride solution, and potassium chloride added once the baby is passing urine, continued until the chloride is above about 100 mmol/L, the bicarbonate is below about 30 mmol/L and the potassium is normal — usually 24 to 48 hours.
The operation is Ramstedt's pyloromyotomy, through a right upper quadrant or circumumbilical incision or laparoscopically: the serosa and hypertrophied muscle are split down to the intact mucosa, which is deliberately not opened, and any mucosal breach is recognised and repaired on the table.
After operation feeds restart within about 4 to 6 hours and are graded up to full feeds over 24 to 48 hours; some vomiting on the first day or two from gastric atony is expected and does not mean the myotomy has failed, and apnoea monitoring continues because residual alkalosis depresses respiratory drive.
Complications: mucosal perforation with peritonitis, incomplete myotomy with continuing vomiting, wound infection and, rarely, incisional hernia.

Peptic ulcer

A peptic ulcer is a break in the mucosa of the stomach or duodenum that penetrates the muscularis mucosae, produced when acid and pepsin overwhelm the mucosal defences — in practice almost always because of Helicobacter pylori infection or NSAID use. It matters surgically because although medical cure rates are high, the three complications — bleeding, perforation and gastric outlet obstruction — still fill emergency theatres, and perforation is one of the classic causes of the acute abdomen.

Duodenal ulcer is three to four times commoner than gastric ulcer, occurs in a younger age group, causes hunger pain 2 to 3 hours after food and at night that is relieved by food, milk or antacids, and is associated with Helicobacter pylori in about 90% of cases.
Gastric ulcer occurs in older patients, the pain comes on soon after eating so the patient avoids food and loses weight, Helicobacter pylori is found in about 70%, and every gastric ulcer must be biopsied from its edge and re-scoped after 6 to 8 weeks because it may be malignant — duodenal ulcers are not.
Other causes: NSAIDs, aspirin and steroids taken with them, smoking, severe physiological stress (Curling's ulcer after major burns, Cushing's ulcer after head injury), and Zollinger–Ellison syndrome from a gastrinoma, which gives multiple, distal, refractory ulcers with diarrhoea.
Testing for Helicobacter pylori: the urea breath test and the stool antigen test both need the proton pump inhibitor stopped for 2 weeks and antibiotics or bismuth stopped for 4 weeks beforehand, or they are falsely negative; serology stays positive after cure and can never be used to confirm eradication.
Eradication runs for 14 days: bismuth-based quadruple therapy (a proton pump inhibitor twice daily with bismuth subcitrate, tetracycline and metronidazole) is preferred where clarithromycin resistance is high, as it is in much of India, while the older triple therapy is a proton pump inhibitor twice daily with amoxicillin 1 g twice daily and clarithromycin 500 mg twice daily. Cure is confirmed by a urea breath test or stool antigen at least 4 weeks after the course finishes.
Perforation is the classic surgical presentation: sudden severe epigastric pain that becomes generalised, a silent board-like rigid abdomen, obliteration of liver dullness, and free gas under the diaphragm on an erect chest X-ray in about 70 to 80%; treatment is resuscitation, nasogastric decompression, antibiotics and laparoscopic or open omental (Graham) patch repair, followed by eradication therapy.
Bleeding is the commonest complication, classically from the gastroduodenal artery behind a posterior duodenal ulcer: resuscitate first, score the risk (Glasgow-Blatchford), then endoscopy within 24 hours — immediately after resuscitation if the patient is unstable — with adrenaline injection combined with a clip or thermal therapy, high-dose intravenous proton pump inhibitor afterwards, and angiographic embolisation or surgery if endoscopy fails.
Gastric outlet obstruction from a chronically scarred duodenal ulcer causes copious vomiting of food eaten a day or more earlier, a succussion splash, visible gastric peristalsis and a hypochloraemic hypokalaemic alkalosis; treat with nasogastric decompression and correction of fluid and electrolytes before endoscopic balloon dilatation or gastrojejunostomy.
Discharge teaching: stop NSAIDs and aspirin or cover them with a proton pump inhibitor, stop smoking because it delays healing and doubles recurrence, moderate alcohol, take the proton pump inhibitor 30 to 60 minutes before breakfast, finish all 14 days of antibiotics even after the pain settles, and return at once with vomiting of blood or coffee-ground material, black tarry stools, sudden severe pain or fainting.

Portal hypertension

Portal hypertension is a sustained rise in the pressure of the portal venous system above its normal 5 to 10 mmHg, defined haemodynamically as a hepatic venous pressure gradient greater than 5 mmHg. It matters because that gradient predicts events — varices form once it exceeds 10 mmHg (clinically significant portal hypertension) and bleed above 12 mmHg — and because variceal haemorrhage is the way portal hypertension kills.

Causes are grouped by the site of the block: prehepatic (portal or splenic vein thrombosis, which is extrahepatic portal venous obstruction and the commonest cause in Indian children), intrahepatic presinusoidal (non-cirrhotic portal fibrosis, schistosomiasis), sinusoidal (cirrhosis, the commonest cause overall) and posthepatic (Budd-Chiari syndrome, constrictive pericarditis, right heart failure).
Portosystemic anastomoses open up and become varices: oesophago-gastric (the dangerous ones), rectal (which are not true haemorrhoids), periumbilical producing caput medusae, and retroperitoneal.
Consequences besides varices: splenomegaly with hypersplenism — a platelet count below 150,000 with a big spleen is a useful bedside clue — ascites, hepatic encephalopathy, spontaneous bacterial peritonitis and hepatorenal syndrome.
Screening and primary prophylaxis: endoscopy when cirrhosis is diagnosed, then a non-selective beta-blocker (propranolol titrated to about a 25% fall in resting heart rate, or carvedilol) or endoscopic variceal band ligation for medium and large varices.
Acute variceal bleeding: two wide-bore cannulae, a restrictive transfusion strategy targeting a haemoglobin of 7 to 8 g/dL because over-transfusion raises portal pressure and restarts the bleed, a splanchnic vasoconstrictor such as terlipressin or octreotide started before endoscopy, prophylactic antibiotics (ceftriaxone for up to 7 days) which independently reduce mortality, and endoscopic band ligation within 12 hours.
When bleeding continues: balloon tamponade with a Sengstaken–Blakemore or Minnesota tube as a bridge for no more than 24 hours and only with the airway protected, a self-expanding covered oesophageal stent, or a transjugular intrahepatic portosystemic shunt — with early pre-emptive TIPSS within 72 hours in high-risk patients; surgical shunts and devascularisation are last resorts.
Encephalopathy commonly follows a bleed because blood in the gut is a protein load: give lactulose titrated to 2 or 3 soft stools a day with rifaximin, look for and correct the precipitants — infection, hypokalaemia, constipation, sedatives and dehydration — and do not restrict dietary protein.
Nursing during a bleed: position the patient on the side with suction ready because aspiration is the immediate killer, hourly observations with strict fluid balance, record every vomit and stool, watch the conscious level for encephalopathy, weigh daily and restrict salt for ascites, and teach avoidance of alcohol, NSAIDs and aspirin at discharge.

Meckel diverticulum

Meckel's diverticulum is the persistent remnant of the vitello-intestinal (omphalomesenteric) duct — a true diverticulum containing all layers of the bowel wall, arising from the antimesenteric border of the ileum. It matters because about half contain heterotopic gastric or pancreatic tissue, and acid secreted by that ectopic mucosa ulcerates the adjacent ileum, making it the commonest cause of massive painless rectal bleeding in a young child.

The rule of 2s: present in about 2% of the population, sited about 2 feet (60 cm) proximal to the ileocaecal valve, roughly 2 inches (5 cm) long, twice as common in boys, most often symptomatic within the first 2 years of life, and containing 2 types of ectopic mucosa — gastric and pancreatic.
Most are silent for life: the lifetime risk of complications is only about 4% and falls with increasing age, which is why an incidental diverticulum in an older adult is usually left alone.
It presents in four ways — brisk painless rectal bleeding, dark red or brick-red, in a toddler who otherwise looks well; intestinal obstruction from volvulus around a persistent band to the umbilicus or from intussusception with the diverticulum as the lead point; diverticulitis that mimics appendicitis exactly; and perforation with peritonitis.
Diagnosis in the bleeding child is a technetium-99m pertechnetate scan (Meckel's scan), because the isotope is taken up by gastric mucosa; pretreatment with an H2-blocker or proton pump inhibitor improves sensitivity by preventing washout of the tracer. The scan is much less useful in obstruction or diverticulitis, where the diagnosis is made on CT or at operation.
The operative rule: if the appendix looks normal at an operation for suspected appendicitis, the terminal ileum is run for about 2 feet to look for a Meckel's diverticulum before the abdomen is closed.
Treatment is diverticulectomy, or a segmental ileal resection with anastomosis when the base is broad or the adjacent ileum is ulcerated; an incidentally found diverticulum in a child or young adult with a narrow base is commonly removed.
Nursing the bleeding child: two points of intravenous access, urgent group and cross-match, hourly observations with capillary refill and urine output, nil by mouth, and an accurate record of the number and character of the stools — a normal blood pressure does not exclude major blood loss in a child, because tachycardia and poor perfusion come first and hypotension comes late.

Appendicitis

Acute appendicitis is inflammation of the vermiform appendix that begins when the lumen is obstructed by a faecolith, by lymphoid hyperplasia or, in older patients, by a tumour, so that secretions accumulate, intraluminal pressure rises and the wall becomes ischaemic and infected. It is the commonest abdominal surgical emergency, with a lifetime risk of about 7 to 8% and a peak in the second and third decades, and it matters because an appendix that is not removed perforates, typically after 48 to 72 hours of symptoms.

The classic sequence is a few hours of colicky periumbilical pain (visceral, referred to the T10 dermatome) with anorexia and nausea, after which the pain shifts and settles as constant, sharp pain in the right iliac fossa when the parietal peritoneum becomes involved — this migration is the single most useful feature in the history.
Signs: tenderness and guarding at McBurney's point (the junction of the lateral and middle thirds of a line from the right anterior superior iliac spine to the umbilicus), rebound and percussion tenderness, Rovsing's sign (pressure in the left iliac fossa produces pain on the right), the psoas sign (pain on extending the right hip, suggesting a retrocaecal appendix), the obturator sign (pain on internally rotating the flexed right hip, suggesting a pelvic appendix), and a low-grade fever of about 37.5 to 38.5°C with tachycardia.
Anorexia is almost invariable — a hungry patient rarely has appendicitis — and the order matters: in appendicitis pain comes first and vomiting follows, whereas vomiting that precedes the pain suggests gastroenteritis.
The Alvarado (MANTRELS) score out of 10 is Migration 1, Anorexia 1, Nausea or vomiting 1, Tenderness in the right iliac fossa 2, Rebound tenderness 1, Elevated temperature 1, Leucocytosis 2 and Shift to the left 1: a score of 7 or more makes appendicitis likely, 5 to 6 is equivocal and needs imaging or active observation, and 4 or less makes it unlikely.
Imaging: ultrasound first in children, thin adults, women of childbearing age and pregnancy, looking for a non-compressible appendix over 6 mm with free fluid; contrast CT is the most accurate in adults. A urine pregnancy test is mandatory in every woman of childbearing age, because ectopic pregnancy, ovarian torsion, mittelschmerz and pelvic inflammatory disease all mimic appendicitis, as do ureteric colic, mesenteric adenitis, Meckel's diverticulitis and right lower lobe pneumonia.
Treatment is appendicectomy, laparoscopic in preference to open, with a single dose of prophylactic antibiotic before the incision; antibiotics alone can be used in selected uncomplicated cases, but about a quarter of those patients recur within a year.
An appendicular mass or phlegmon presenting after 4 or 5 days is treated conservatively on the Ochsner–Sherren regimen — intravenous fluids, antibiotics, nil by mouth and careful charting of pulse, temperature and the marked outline of the mass — with an interval appendicectomy considered later, whereas an appendicular abscess is drained.
Special groups: in pregnancy the appendix is displaced upwards and laterally and the diagnosis is often late; in the elderly and the immunosuppressed the signs are muted and perforation is common; in small children the omentum is short, so peritonitis develops quickly.
Nursing care and discharge: analgesia is given and does not mask the diagnosis, but a laxative or an enema is dangerous and may cause perforation; after operation encourage early mobilisation and diet, observe the wound (infection is the commonest complication, especially after perforation), watch for a pelvic abscess presenting on day 5 to 7 as a swinging fever with diarrhoea and tenesmus, and tell the patient to return with fever, increasing pain, wound discharge or failure to pass flatus.

Haemorrhoids

Haemorrhoids are the symptomatic enlargement and downward displacement of the anal cushions, the normal vascular submucosal pads that sit at the 3, 7 and 11 o'clock positions in the lithotomy position and help to seal the anal canal. They are internal when they arise above the dentate line from the superior haemorrhoidal plexus — columnar mucosa with autonomic innervation, so they bleed but do not hurt — and external when they arise below it in somatically innervated squamous skin, so they hurt; that single line explains why one anal lump needs reassurance and another needs urgent pain relief.

Goligher grading of internal haemorrhoids decides the treatment: grade I bleed but do not prolapse, grade II prolapse on straining and reduce spontaneously, grade III prolapse and need manual reduction, and grade IV are permanently prolapsed and irreducible.
The classic symptom is painless, bright red bleeding that drips or splashes into the pan at the end of defecation and is separate from the stool, with pruritus, mucus discharge and a lump; pain means either a complication (thrombosis or strangulation) or a different diagnosis such as fissure or abscess.
Risk factors are chronic constipation and straining, a low-fibre diet, prolonged sitting on the toilet, pregnancy, obesity, chronic cough and portal hypertension.
Every patient with rectal bleeding needs a digital rectal examination and proctoscopy, and colonoscopy is arranged for patients over about 40 to 50 or with a family history, altered bowel habit, weight loss or iron-deficiency anaemia — colorectal carcinoma is the diagnosis that hides behind the label 'piles'.
First-line treatment for grades I and II is conservative: 25 to 30 g of dietary fibre and about 2 litres of fluid a day, a bulking agent or stool softener, no straining and no more than a few minutes on the toilet, warm sitz baths for 10 to 15 minutes two or three times a day, and topical local anaesthetic or steroid preparations for short courses only.
Office procedures: rubber band ligation is the most effective for grades I to III, and the band is applied above the dentate line where there is no somatic sensation — a band placed below it causes severe pain and must be removed; sclerotherapy and infrared coagulation are alternatives.
Surgery for grade III and IV, mixed or failed cases: Milligan–Morgan open or Ferguson closed haemorrhoidectomy, stapled haemorrhoidopexy, or Doppler-guided haemorrhoidal artery ligation. Postoperative pain is severe and is managed as a package — regular oral and topical analgesia, a stool softener started on day 1, metronidazole and sitz baths — because the first bowel motion is what the patient fears most.
Complications to teach and watch for: reactionary haemorrhage within the first 24 hours and secondary haemorrhage around day 7 to 10 from infection, urinary retention (very common early, especially after spinal anaesthesia), anal stenosis after over-enthusiastic excision, and incontinence if the sphincter is damaged.
A thrombosed external haemorrhoid, or perianal haematoma, is an acutely painful tense blue lump at the anal verge: it can be incised or excised under local anaesthesia within the first 48 to 72 hours, after which analgesia, stool softeners and sitz baths are enough because it resolves over about two weeks.

Anal fissure

An anal fissure is a longitudinal tear or ulcer in the anoderm — the modified squamous lining of the anal canal below the dentate line — and because that lining is somatically innervated by the inferior rectal nerve the tear produces pain out of all proportion to its size. It matters clinically because the pain drives spasm of the internal anal sphincter, the raised resting pressure strangles the already poor blood supply of the posterior commissure, and the fissure cannot heal until that pain-spasm-ischaemia cycle is broken, which is exactly what every treatment from a sitz bath to lateral sphincterotomy is designed to do.

About 90 per cent of fissures lie in the posterior midline (the 6 o'clock position with the patient in lithotomy); an anterior midline fissure is the pattern seen in women after childbirth, and a fissure that is lateral, multiple, painless, ragged or associated with a fistula is not a simple fissure and demands biopsy for Crohn's disease, tuberculosis, syphilis, HIV-related ulceration or carcinoma.
The posterior midline is a watershed with the poorest arterial supply of the anal canal, and manometry in these patients shows a raised resting anal pressure; this is why chemical or surgical relaxation of the internal sphincter, not wound care, is the treatment that heals the fissure.
An acute fissure is a clean-edged tear of under six weeks; a chronic fissure is defined by a triad of a sentinel skin tag at the outer end, transverse white fibres of the internal sphincter visible in the floor, and a hypertrophied anal papilla at the inner end.
The symptom pattern is diagnostic: knife-like or tearing pain that starts with defecation and lasts minutes to hours afterwards, with bright red blood streaking the outside of the stool or on the paper rather than mixed through it, and a patient who begins to avoid defecation, becomes constipated and so makes the fissure worse.
Diagnosis is made by gently parting the buttocks and inspecting; digital rectal examination and proctoscopy are too painful in an acute fissure and are deferred until the pain settles or done under anaesthesia, so a normal-looking perineum in a patient with classic pain never rules the diagnosis out.
First-line treatment for six to eight weeks heals roughly two-thirds of fissures: a high-fibre diet of about 25 to 30 g daily with ispaghula husk, generous fluids, a stool softener, a warm sitz bath for 10 to 15 minutes after defecation to relax the sphincter, and a topical relaxant — glyceryl trinitrate 0.2 to 0.4 per cent or diltiazem 2 per cent applied twice daily.
Glyceryl trinitrate causes headache in a large minority and is the commonest reason patients stop treatment; topical diltiazem heals at a similar rate with far less headache, and botulinum toxin injected into the internal sphincter is the chemical sphincterotomy used when ointments fail.
Lateral internal sphincterotomy is the operation of choice for a chronic fissure and heals over 90 per cent; it is placed laterally at 3 or 9 o'clock and never in the posterior midline, which would leave a keyhole deformity and faecal soiling, and its own risk is incontinence to flatus, so the surgeon must consent for it and uncontrolled anal dilatation has been abandoned for the same reason.

Haemodialysis — AV fistula care

An arteriovenous fistula is a surgically created direct connection between an artery and a vein, usually at the wrist or the elbow, which arterialises the vein so that it becomes big enough and strong enough to take two large dialysis needles three times a week. It is the access of choice because it lasts longest and has the lowest rates of infection and thrombosis, and protecting it is one of the few nursing duties in which a single careless blood pressure cuff can cost a patient their lifeline.

The order of preference is a native arteriovenous fistula first, then a synthetic arteriovenous graft, then a tunnelled central venous catheter, with a non-tunnelled catheter only for immediate short-term use; catheters carry the highest infection risk and the worst survival.
The radiocephalic or Brescia-Cimino fistula at the wrist is created first so that failure still leaves the elbow available, and the non-dominant arm is used whenever possible.
A fistula needs time to mature — at least 6 weeks and often around 3 months before first cannulation — and maturity is judged by the rule of 6s: a vein at least 6 mm in diameter, no more than 6 mm deep, with a flow of at least 600 mL/min, by about 6 weeks. A graft can be used far sooner and a catheter immediately.
Assessment every shift is look, feel and listen: look for redness, swelling, bleeding or an aneurysm; feel for a continuous THRILL, the soft buzz over the fistula; listen with a stethoscope for a low-pitched continuous BRUIT. A thrill that has disappeared, or a bruit that has become high-pitched and discontinuous, means stenosis or thrombosis and is reported immediately.
The arm carrying the fistula is protected absolutely: no blood pressure measurement, no venepuncture, no intravenous cannula, no injections, no tight sleeves, watches or bangles, no sleeping on that arm, no carrying heavy bags with it and no restraints — and a sign is placed above the bed so that every member of staff knows.
Patient teaching covers feeling for the thrill morning and evening, keeping the arm clean, doing isometric exercises such as squeezing a ball to help the fistula mature, avoiding dehydration and hypotension which promote clotting, and reporting an absent thrill, pain, coldness, numbness, bleeding or fever the same day.
Steal syndrome is diversion of arterial blood into the fistula, leaving the hand pale, cold, painful and numb with weak or absent distal pulses and worst during dialysis; it is reported urgently because a neglected steal ends in tissue loss.
Bleeding from a needle site after dialysis is controlled with firm digital pressure over the site for about 10 minutes, hard enough to stop the bleeding but never hard enough to obliterate the thrill, and the patient is not discharged until the site is dry.
Dialysis-related problems to anticipate are hypotension during the session from too rapid ultrafiltration, muscle cramps, disequilibrium syndrome with headache, nausea, restlessness and rarely seizures when urea is cleared too fast in the first sessions, and access infection; weigh the patient before and after every session against the dry weight and hold antihypertensives before the session as prescribed.

Colostomy care

A colostomy is a surgically created opening that brings a segment of colon through the abdominal wall so that faeces divert onto the skin surface into an appliance, made as an end stoma (after abdominoperineal resection or a Hartmann procedure), a loop stoma to defunction a distal anastomosis, or a double-barrel stoma. It matters at the bedside because the stoma is a piece of live bowel with a blood supply that can fail in hours, and it matters in the exam because the level of the colostomy predicts the consistency of the output and therefore the whole nursing plan.

A healthy stoma is pink to beef-red, moist and shiny, and protrudes about 1 to 2.5 cm above the skin; a pale stoma suggests anaemia, a dusky purple or black stoma means ischaemia and needs the surgeon at once, and slight oozing when the stoma is cleaned is normal because the mucosa is vascular and carries no pain fibres.
The output follows the level: an ascending colostomy gives semi-liquid enzyme-rich effluent, a transverse colostomy gives semi-formed output, and a descending or sigmoid colostomy gives formed stool once or twice a day. The stoma is sited on the left iliac fossa for a sigmoid colostomy, which is how it is told apart from the right iliac fossa ileostomy.
Function returns as peristalsis recovers, usually flatus by 24 to 48 hours and stool by the third to fifth postoperative day; a colostomy that has passed nothing at all with a distended abdomen and vomiting is obstructed, not merely slow.
Cut the skin barrier opening 2 to 3 mm larger than the measured stoma. An opening cut too large exposes skin to effluent and is the commonest cause of peristomal excoriation, while one cut too tight cuts the stoma; remeasure at every change for the first six to eight weeks because the stoma shrinks as oedema settles.
Empty the pouch when it is one-third to one-half full, because a heavier pouch drags the wafer off the skin and causes leaks; change the whole appliance every three to seven days, or immediately whenever there is leakage, burning or itching under the wafer.
Only a sigmoid or descending colostomy may be irrigated, using 500 to 1000 mL of lukewarm water through a cone tip at the same time each day to establish a routine; never irrigate an ileostomy or a transverse colostomy.
Diet is low-residue for the first six to eight weeks and then liberalised one food at a time, with thorough chewing and adequate fluid. Onion, cabbage, beans, eggs, carbonated drinks and chewing gum increase gas and odour; curd, buttermilk and parsley reduce odour; nuts, popcorn, seeds, coconut and raw fibrous vegetables can block the stoma.
Complications to look for are necrosis and retraction in the first week, and prolapse, stenosis, parastomal hernia, mucocutaneous separation and peristomal dermatitis later. Body image disturbance, fear of odour and sexual anxiety are as much part of the care plan as the appliance, and a stoma nurse referral before discharge improves both.

Acute pancreatitis

Acute pancreatitis is a sudden inflammation of the pancreas caused by premature activation of trypsinogen inside the acinar cells, so that the gland digests itself and releases enzymes and inflammatory mediators into the circulation. It matters because a mild attack settles with fluids and feeding in a week while a severe attack with persistent organ failure carries a mortality of 20 to 30 per cent, and the nurse at the bedside is the one who detects the change from one to the other.

The revised Atlanta diagnosis needs two of three features: epigastric pain boring through to the back and relieved by sitting forward, serum lipase or amylase more than three times the upper limit of normal, and characteristic findings on contrast CT, ultrasound or MRI. Only one of the three has to be missing, so a normal enzyme level does not exclude the diagnosis.
Lipase is the better test: amylase rises within 6 to 12 hours and falls again in 3 to 5 days, while lipase stays raised for 8 to 14 days and is more specific. The height of the enzyme does not grade the severity and must never be used to decide the level of care.
Gallstones and alcohol cause most cases in India; the rest come from hypertriglyceridaemia above 1000 mg/dL, endoscopic retrograde cholangiopancreatography, hypercalcaemia, trauma, drugs, scorpion sting, ascariasis and viral infection.
Severity by the revised Atlanta classification: mild means no organ failure and no local complication, moderately severe means transient organ failure resolving within 48 hours or a local complication, and severe means persistent organ failure beyond 48 hours. Organ failure is scored on the modified Marshall system for respiratory, renal and cardiovascular systems.
Fluid resuscitation uses lactated Ringer solution in preference to normal saline, given at a moderate goal-directed rate of about 5 to 10 mL/kg/h and reassessed every few hours against heart rate, blood pressure, urine output above 0.5 mL/kg/h and haematocrit; indiscriminate aggressive fluid loading causes volume overload and respiratory failure rather than benefit.
Feed early rather than resting the gut: oral low-fat feeding within 24 to 72 hours as soon as pain allows in mild disease, and nasogastric or nasojejunal enteral feeding if oral intake is not tolerated. Enteral nutrition preserves the gut barrier and reduces infected necrosis, whereas parenteral nutrition is reserved for those who cannot be fed enterally at all.
Antibiotics are not given prophylactically, however severe the attack; they are started only for infected necrosis or another proven infection, when a carbapenem or a fluoroquinolone with metronidazole is used because these penetrate necrotic pancreas.
Gallstone pancreatitis with cholangitis needs endoscopic retrograde cholangiopancreatography with sphincterotomy within 24 hours, and mild biliary pancreatitis needs cholecystectomy during the same admission because delay leads to recurrent attacks.
Complications to anticipate: acute peripancreatic fluid collection and pseudocyst (walled off after four weeks), walled-off necrosis, acute respiratory distress syndrome, acute kidney injury, hyperglycaemia, and hypocalcaemia from fat saponification that shows as Chvostek and Trousseau signs. Cullen sign around the umbilicus and Grey Turner sign in the flanks are late, uncommon signs of haemorrhagic pancreatitis.

Biliary colic

Biliary colic is the pain of a gallstone transiently impacting at the neck of the gallbladder or in the cystic duct, so that the gallbladder contracts against an obstruction that then falls back and relieves itself. Despite its name the pain is steady rather than colicky: it builds over an hour, plateaus, lasts from 30 minutes to about 6 hours and then goes completely, and it is exactly this self-limiting course with no fever and no leukocytosis that separates it from acute cholecystitis.

The pain is in the right upper quadrant or epigastrium, radiates to the right shoulder tip or the interscapular area, often begins a few hours after a fatty meal or at night, and comes with nausea and vomiting; Boas sign is an area of hyperaesthesia below the right scapula.
In simple biliary colic the temperature is normal, the white cell count is normal, Murphy sign is negative between attacks and the liver function tests are normal. Pain lasting beyond 6 hours with fever, a positive Murphy sign and leukocytosis has become acute cholecystitis.
Ultrasound is the first-line investigation and is over 95 per cent sensitive for stones, showing a mobile echogenic focus with posterior acoustic shadowing; a gallbladder wall thicker than 3 mm, pericholecystic fluid and a sonographic Murphy sign indicate cholecystitis instead.
Risk factors are summarised as the five Fs — female, fertile, forty, fat and fair — plus rapid weight loss, pregnancy, oral contraceptives, diabetes, terminal ileal disease or resection, and haemolytic anaemia, which produces pigment rather than cholesterol stones. About 80 per cent of stones in adults are cholesterol or mixed stones.
Treatment of the attack is analgesia and nil by mouth until the pain settles: a non-steroidal anti-inflammatory such as diclofenac is first line and also reduces progression to cholecystitis, with an opioid added if the pain is severe, together with an antiemetic and intravenous fluid if vomiting.
The definitive treatment for symptomatic gallstones is elective laparoscopic cholecystectomy, because roughly a third of patients have another attack within a year and the risk of cholecystitis, pancreatitis and choledocholithiasis persists; a low-fat diet and ursodeoxycholic acid only reduce symptoms and do not clear the stones.
Asymptomatic gallstones are not operated on as a rule, but cholecystectomy is offered when there is a porcelain gallbladder, a stone larger than 3 cm, a gallbladder polyp over 1 cm, or a patient from a region such as the Gangetic belt of north India where gallbladder cancer is common.
Learn the three step-ups by their signs: biliary colic is pain alone, acute cholecystitis is pain with fever and a positive Murphy sign, and ascending cholangitis is the Charcot triad of right upper quadrant pain, fever with rigors and jaundice, becoming the Reynolds pentad when hypotension and confusion are added.

Inflammatory bowel disease (UC vs Crohn)

Inflammatory bowel disease is chronic relapsing immune-mediated inflammation of the gastrointestinal tract in a genetically susceptible person, taking two forms — ulcerative colitis, which is a continuous mucosal disease of the colon starting at the rectum, and Crohn disease, which is a patchy transmural disease that can affect any part of the gut from mouth to anus. It matters because the two look alike at the bedside but differ in their complications, their drugs and whether surgery cures, and because in India the nearest confusable is not the other form of inflammatory bowel disease but intestinal tuberculosis.

Ulcerative colitis is limited to mucosa and submucosa, is continuous, always involves the rectum and extends proximally; it presents with bloody diarrhoea, mucus, urgency and tenesmus, shows crypt abscesses and goblet cell depletion on biopsy and a featureless lead-pipe colon on barium, is associated with primary sclerosing cholangitis and toxic megacolon, is made less likely by smoking, and is cured by proctocolectomy.
Crohn disease is transmural with skip lesions and a predilection for the terminal ileum; it presents with right lower quadrant pain, weight loss and non-bloody diarrhoea, shows non-caseating granulomas on biopsy, cobblestone mucosa and the string sign of Kantor on imaging, produces fistulae, strictures, fissures and perianal disease, is made worse by smoking, and recurs after surgery, so resection is never curative.
Extraintestinal manifestations that track the bowel activity are peripheral arthritis, erythema nodosum and episcleritis; those that run independently of it are ankylosing spondylitis, primary sclerosing cholangitis, pyoderma gangrenosum and uveitis.
Before starting steroids or a biologic in India, intestinal tuberculosis must be excluded, because ileocaecal tuberculosis mimics Crohn disease exactly and immunosuppression will disseminate it. Tuberculosis gives caseating granulomas, transverse ulcers, a positive GeneXpert or acid-fast bacilli and often a chest lesion, while Crohn gives non-caseating granulomas and longitudinal ulcers.
Severity of an ulcerative colitis flare is graded by the Truelove and Witts criteria: six or more bloody stools a day plus any of temperature above 37.8 degrees Celsius, pulse above 90/min, haemoglobin below 10.5 g/dL or ESR above 30 mm in the first hour marks severe disease needing admission.
Drug ladder: 5-aminosalicylates such as mesalamine and sulfasalazine induce and maintain remission in ulcerative colitis but have little role in Crohn disease; corticosteroids treat a flare and are never used for maintenance; thiopurines such as azathioprine 2 to 2.5 mg/kg/day maintain remission and need a blood count watch, with NUDT15 and TPMT testing where available because the NUDT15 variant that causes severe myelosuppression is common in Asians; anti-tumour-necrosis-factor agents, vedolizumab and ustekinumab are the biologics.
Screen and immunise before any biologic: latent tuberculosis by Mantoux or interferon-gamma release assay with a chest radiograph, hepatitis B and C serology, and inactivated vaccines given in advance, because live vaccines are contraindicated once the patient is immunosuppressed.
Long-standing colonic disease carries a colorectal cancer risk, so surveillance colonoscopy begins about 8 years after the onset of pancolitis and is then repeated at intervals set by the extent, the presence of primary sclerosing cholangitis and the family history.
Nursing care runs alongside the drugs: record the number and character of stools and the blood in them each day, weigh weekly, correct iron, B12, folate, calcium and vitamin D, watch for steroid side effects, and treat the effect on schooling, work and body image as part of the problem.

Ileostomy

An ileostomy is a surgically created opening that brings the ileum through the abdominal wall, usually in the right iliac fossa, either as an end stoma after proctocolectomy for ulcerative colitis or familial adenomatous polyposis, or as a loop stoma to defunction a distal anastomosis. It is deliberately made to protrude 2 to 3 cm as a spout, because the effluent is liquid and full of proteolytic enzymes that would digest the skin if the stoma were flush, and that same effluent is why fluid and electrolyte loss, not the appliance, is the main nursing risk.

The effluent is liquid to porridge-like and enzyme-rich; once the stoma has adapted over the first few weeks it settles to roughly 500 to 1000 mL a day. A sustained output above 1000 to 1500 mL a day is a high-output stoma and causes dehydration, hyponatraemia, hypokalaemia, hypomagnesaemia and acute kidney injury.
Site tells the two stomas apart in a picture question: an ileostomy is in the right iliac fossa, spouted, with liquid output, while a sigmoid colostomy is in the left iliac fossa, flush, with formed output.
Manage a high-output stoma by restricting hypotonic fluid, giving an oral rehydration solution rather than plain water — plain water drives further sodium loss across the small bowel — and adding loperamide 2 to 4 mg about 30 minutes before meals, with codeine and a proton pump inhibitor to cut gastric secretion when loperamide alone is not enough.
Skin protection is non-negotiable: use a skin barrier with a convex appliance if the stoma is retracted, cut the opening 2 to 3 mm larger than the stoma, empty the pouch when it is one-third full, and change the appliance every three to five days or at once if there is leakage or burning under the wafer.
Never irrigate an ileostomy, and never give it a routine enema or suppository; irrigation belongs only to a descending or sigmoid colostomy.
Diet: chew thoroughly, eat regular small meals, keep to a low-fibre diet for the first six to eight weeks, and be cautious lifelong with nuts, popcorn, seeds, coconut, mushrooms, dried fruit and raw fibrous vegetables, which are the classic causes of food blockage at the fascial opening.
Absorption changes with the loss of the colon and terminal ileum: vitamin B12 must be monitored and replaced when a long segment of terminal ileum is gone, bile-salt loss causes gallstones, and the concentrated acidic urine of chronic dehydration causes uric acid and oxalate renal stones.
Drugs are absorbed differently — enteric-coated and sustained-release tablets may appear whole in the pouch, so switch to liquid or immediate-release preparations; a woman on an oral contraceptive with a high-output ileostomy needs another method.
Expect a temporary loop ileostomy to be closed only after the distal anastomosis has been shown to be intact, and teach output measurement, appliance change and the signs of dehydration before discharge.

Oesophageal varices

Oesophageal varices are dilated submucosal collateral veins in the lower oesophagus that open up when portal pressure rises, most often in cirrhosis, and carry blood from the portal system back to the systemic circulation. They matter because they bleed without warning and without pain, a variceal bleed is the most lethal upper gastrointestinal haemorrhage a nurse will meet, and the drug, the antibiotic and the endoscopy that change survival all have to be started in the first few hours.

Portal hypertension begins above a hepatic venous pressure gradient of 5 mmHg, becomes clinically significant at 10 mmHg when varices form, and varices bleed once the gradient exceeds about 12 mmHg. Roughly half of all cirrhotics have varices, and the risk of bleeding rises with large size, red wale marks on the varix and advanced Child-Pugh class.
Presentation is painless massive haematemesis with melena, often with hypotension and tachycardia out of proportion to what is visible; a cirrhotic on a beta blocker may not mount the expected tachycardia, so judge the loss on blood pressure, urine output and mental state.
Resuscitate with two wide-bore cannulae and crystalloid, but transfuse restrictively to a haemoglobin target of about 7 to 8 g/dL, because over-transfusion raises portal pressure and provokes rebleeding. Cross-match, correct gross coagulopathy on advice, and protect the airway before endoscopy in an encephalopathic or actively vomiting patient.
Start a vasoactive drug before the endoscopy, as soon as a variceal bleed is suspected: terlipressin 2 mg intravenously every 4 hours until bleeding is controlled and then 1 mg every 4 hours, or octreotide as a 50 microgram bolus followed by a 50 microgram per hour infusion, continued for 2 to 5 days. Watch terlipressin for hyponatraemia, abdominal cramps and peripheral or myocardial ischaemia.
Give antibiotic prophylaxis to every cirrhotic with an upper gastrointestinal bleed — intravenous ceftriaxone 1 g daily for up to 7 days — because it independently reduces infection, rebleeding and mortality, and is one of the commonest omissions in a viva answer.
Endoscopy within 12 hours is the definitive step: endoscopic variceal band ligation is preferred to sclerotherapy for oesophageal varices, while gastric varices are treated with cyanoacrylate glue injection.
When endoscopy fails, balloon tamponade with a Sengstaken-Blakemore or Minnesota tube is only a bridge for up to 24 hours in an intubated patient, or a self-expanding covered oesophageal stent; the definitive rescue is a transjugular intrahepatic portosystemic shunt, which is also offered pre-emptively within 72 hours to those at highest risk of failure, with hepatic encephalopathy as its main complication.
Prevent the next bleed: a non-selective beta blocker, with carvedilol now preferred, or a banding programme repeated every 2 to 4 weeks until the varices are obliterated, and both together for secondary prophylaxis, with lactulose to clear the swallowed blood that would otherwise precipitate encephalopathy.

Perforated duodenal ulcer

A perforated duodenal ulcer is a peptic ulcer that has eroded through the full thickness of the duodenal wall, most often on the anterior wall of the first part of the duodenum, spilling acid, bile and gas into the peritoneal cavity. It matters because it produces the classic surgical abdomen of the exam — sudden agonising epigastric pain with a board-like rigid abdomen and free gas under the diaphragm — and because survival depends on how quickly resuscitation and laparotomy follow, not on any medical treatment.

The pain begins suddenly and is at its worst within moments, is felt in the epigastrium and then all over the abdomen, and may be referred to the shoulder tip because the spilled contents irritate the diaphragm; the patient lies still because any movement hurts, unlike the restless patient of renal or biliary colic.
Examination shows a board-like rigid abdomen with generalised guarding and rebound, absent bowel sounds and obliteration of liver dullness on percussion as gas collects under the diaphragm.
The illness passes through three stages: chemical peritonitis in the first 2 hours, a deceptive stage of reaction between about 2 and 12 hours when the pain eases and the patient seems better, and bacterial peritonitis with septic shock after 12 hours. The middle stage is the trap that sends patients home.
An erect chest radiograph showing free gas under the diaphragm confirms it in about 70 to 80 per cent of cases, so a normal film does not exclude perforation; computed tomography is more sensitive. Serum amylase may be modestly raised and mimic pancreatitis, but rarely rises above three times the upper limit of normal.
The risk factors are Helicobacter pylori infection, non-steroidal anti-inflammatory drugs, smoking, steroids and severe physiological stress; duodenal ulcer pain classically comes 2 to 3 hours after food and at night and is relieved by eating, while gastric ulcer pain is made worse by eating.
Resuscitation comes before the knife: nil by mouth, a wide-bore nasogastric tube on free drainage to stop further spillage, two intravenous lines with crystalloid, a urinary catheter to guide fluid, adequate analgesia, an intravenous proton pump inhibitor and broad-spectrum antibiotics covering Gram-negative and anaerobic organisms.
The operation is a laparotomy or laparoscopy with a Graham omental patch closure and thorough peritoneal lavage; definitive acid-reducing surgery is not done in the emergency setting.
After recovery, test for and eradicate Helicobacter pylori and confirm the eradication with a urea breath test or stool antigen, stop the causative non-steroidal drug, and continue a proton pump inhibitor, because the ulcer recurs otherwise.

Cirrhosis of liver

Cirrhosis is the end result of any chronic liver injury, in which diffuse fibrosis and regenerative nodules replace the normal lobular architecture, so that the liver both fails to work and obstructs portal blood flow. Clinically it is divided into compensated cirrhosis, which may be silent for years, and decompensated cirrhosis, which is defined by the appearance of ascites, variceal bleeding, hepatic encephalopathy or jaundice, and it is that transition that brings the patient to the ward.

In India the common causes are alcohol, chronic hepatitis B and C, and non-alcoholic fatty liver disease, with autoimmune hepatitis, Wilson disease and haemochromatosis in the young, and a cryptogenic group that is largely burnt-out fatty liver.
Signs of hepatocellular failure are jaundice, spider naevi, palmar erythema, gynaecomastia, testicular atrophy, loss of body hair, Dupuytren contracture, leuconychia, fetor hepaticus and asterixis; signs of portal hypertension are splenomegaly, ascites, dilated abdominal wall veins with caput medusae and oesophageal varices.
Typical laboratory picture: low serum albumin, prolonged prothrombin time and international normalised ratio, thrombocytopenia from hypersplenism, and in alcohol-related disease an aspartate to alanine aminotransferase ratio above 2. A falling platelet count is often the earliest laboratory clue to portal hypertension.
Child-Turcotte-Pugh scoring uses bilirubin, albumin, international normalised ratio, ascites and encephalopathy to give class A at 5 to 6 points, class B at 7 to 9 and class C at 10 to 15, and is used for operative risk; the MELD score, built from bilirubin, international normalised ratio and creatinine with sodium added in MELD-Na, decides transplant priority.
Ascites is managed by restricting dietary sodium to about 2 g a day (roughly 5 g of salt) and by spironolactone with furosemide in a 100 mg to 40 mg ratio, increased in steps to a maximum of 400 mg and 160 mg; aim for a weight loss of about 0.5 kg a day without oedema and up to 1 kg a day with peripheral oedema, and give intravenous albumin of 6 to 8 g for every litre removed when more than 5 litres is tapped.
Spontaneous bacterial peritonitis is diagnosed on an ascitic fluid neutrophil count of 250 cells/mm3 or more and is treated with intravenous cefotaxime plus albumin 1.5 g/kg on day 1 and 1 g/kg on day 3, which prevents hepatorenal syndrome; it can present with nothing more than a low-grade fever, mild abdominal pain or new confusion, so a diagnostic tap is done on every cirrhotic admitted with ascites.
Hepatic encephalopathy is precipitated by gastrointestinal bleeding, infection, constipation, dehydration and over-diuresis, hypokalaemia, sedatives and a large protein load; treat the precipitant and give lactulose 30 mL titrated to two or three soft stools a day, with rifaximin added as maintenance. Protein is not restricted long-term — a cirrhotic needs about 1.2 to 1.5 g/kg/day, preferably from vegetable and dairy sources.
Screen for hepatocellular carcinoma with a six-monthly ultrasound, band or beta-block varices, vaccinate against hepatitis A and B, influenza and pneumococcus, and stop alcohol absolutely.
Drugs to avoid: non-steroidal anti-inflammatory drugs and aminoglycosides precipitate hepatorenal syndrome, sedatives and opioids precipitate encephalopathy, and paracetamol up to 2 g a day is the safer analgesic in a patient who is not drinking.

GERD

Gastro-oesophageal reflux disease is the reflux of gastric contents into the oesophagus often enough to cause troublesome symptoms or visible mucosal injury, driven by transient relaxations of the lower oesophageal sphincter, a hypotensive sphincter, hiatus hernia, delayed gastric emptying or raised intra-abdominal pressure. It matters because it is extremely common and mostly benign, yet the same burning chest pain can be myocardial ischaemia, and long-standing reflux can end in Barrett oesophagus and adenocarcinoma.

The typical symptoms are heartburn beginning 30 to 60 minutes after a meal and worse on lying flat or bending forward, regurgitation of sour fluid, and water brash; the atypical presentations are chronic cough, night-time asthma, hoarseness, globus and dental erosion.
Diagnosis in a young patient with typical symptoms and no alarm features is clinical, confirmed by an 8-week trial of a proton pump inhibitor; endoscopy is done for alarm features and grades erosive oesophagitis by the Los Angeles classification from A to D. Ambulatory 24-hour pH with impedance is the reference standard when the diagnosis is in doubt or before surgery, and manometry is done before fundoplication to exclude achalasia.
Alarm features that demand endoscopy are dysphagia, odynophagia, unintentional weight loss, anaemia or overt gastrointestinal bleeding, persistent vomiting, a palpable mass, new-onset symptoms in an older patient and a family history of upper gastrointestinal cancer.
The proton pump inhibitor is taken 30 to 60 minutes before breakfast, because it only blocks proton pumps that are actively secreting; taking it with or after food, or at bedtime alone, is the commonest reason a patient is labelled a treatment failure. Treat for 8 weeks then step down to the lowest dose that controls symptoms.
Lifestyle measures with real evidence are weight reduction, raising the head end of the bed by 15 to 20 cm, and leaving 3 hours between the last meal and lying down; stopping smoking and alcohol, avoiding large fatty meals, chocolate, caffeine, peppermint, citrus and spicy food help individual patients.
Drugs that lower sphincter tone and worsen reflux include calcium channel blockers, nitrates, anticholinergics, theophylline, diazepam and progesterone, so a medication review is part of treatment.
Complications are erosive oesophagitis, peptic stricture presenting as slowly progressive dysphagia to solids, Barrett oesophagus in which squamous epithelium is replaced by intestinal columnar metaplasia and which is premalignant for adenocarcinoma, and aspiration pneumonitis.
Laparoscopic Nissen fundoplication is offered for disease refractory to or intolerant of medical treatment, or for a large hiatus hernia, after pH and manometry studies; its recognised sequelae are dysphagia and the gas-bloat syndrome with inability to belch.

Melena

Melena is the passage of black, tarry, sticky stool with a characteristic offensive smell, produced when haemoglobin is degraded to haematin by gastric acid and intestinal bacteria during transit. It signals bleeding proximal to the ligament of Treitz in most cases, needs only about 50 to 100 mL of blood and roughly 14 hours in the gut to appear, and it is a sign of an active bleed rather than a diagnosis, so the priority is always circulation before endoscopy.

True melena is black, tarry, sticky and foul-smelling; iron, bismuth and charcoal give a greenish-black, non-sticky, non-offensive stool, which is why the appearance is confirmed by inspecting the stool and, where needed, a faecal occult blood test rather than taken from the history alone.
Common causes are peptic ulcer, which accounts for most cases, oesophageal and gastric varices, Mallory-Weiss tear after retching, erosive gastritis from non-steroidal anti-inflammatory drugs or alcohol, gastric malignancy and a Dieulafoy lesion; slow bleeding from the small bowel or right colon can also turn black.
Haematochezia, the passage of bright red blood, usually means a lower gastrointestinal source, but a brisk upper bleed can present as haematochezia with shock, so red blood in a hypotensive patient is an upper bleed until an endoscopy says otherwise.
A raised blood urea with a normal creatinine supports an upper gastrointestinal source, because the blood in the gut is absorbed as a protein load; a falling haemoglobin lags behind the loss, so it must never be used to decide whether the patient is bleeding now.
Score the risk rather than guess it: the Glasgow-Blatchford score uses urea, haemoglobin, systolic pressure, pulse, melena, syncope, liver disease and cardiac failure, and a score of 0 to 1 identifies patients safe for outpatient management, while the Rockall score is completed after endoscopy to predict rebleeding and death.
Resuscitate with two wide-bore cannulae and crystalloid, cross-match, and transfuse red cells restrictively at a haemoglobin threshold of about 7 g/dL, using a higher threshold only in significant cardiovascular disease, because liberal transfusion worsens outcome in upper gastrointestinal bleeding.
Give an intravenous proton pump inhibitor while awaiting endoscopy — pantoprazole 80 mg as a bolus followed by an 8 mg/h infusion — and, in a known or suspected cirrhotic, add a vasoactive drug and intravenous ceftriaxone because the source may be variceal.
Upper gastrointestinal endoscopy is done within 24 hours, and within 12 hours if the patient is unstable or a variceal bleed is suspected; the ulcer stigmata are graded by the Forrest classification, and a spurting or oozing vessel or a visible vessel is treated endoscopically with a combination of adrenaline injection and a second modality such as a clip or thermal coagulation.
After control, test for and eradicate Helicobacter pylori, stop or reassess non-steroidal anti-inflammatory drugs, antiplatelets and anticoagulants with the medical team, and continue a proton pump inhibitor.

Kernicterus

Kernicterus is the permanent brain injury that follows acute bilirubin encephalopathy, in which unconjugated bilirubin that is not bound to albumin crosses the blood-brain barrier and stains and damages the basal ganglia, globus pallidus, subthalamic nucleus, hippocampus and cranial nerve nuclei. It matters because it is entirely preventable — every case represents a jaundiced newborn whose bilirubin was not measured, plotted and treated in time — and because the earliest signs are the ordinary ones of a baby who is sleepy and feeding poorly.

Acute bilirubin encephalopathy evolves in three phases: an early phase of lethargy, hypotonia, poor suck and a high-pitched cry; an intermediate phase of irritability, fever and hypertonia with retrocollis and opisthotonus; and an advanced phase of apnoea, seizures, coma and death.
The chronic sequelae are a recognisable tetrad: athetoid or dyskinetic cerebral palsy, sensorineural hearing loss with auditory neuropathy, paralysis of upward gaze, and dental enamel dysplasia, usually with normal or near-normal intelligence.
The danger is free unconjugated bilirubin, so the same level is more toxic when albumin is low, in prematurity, and in the presence of acidosis, sepsis, hypoxia, hypothermia or hypoglycaemia, or when a drug such as a sulphonamide or ceftriaxone displaces bilirubin from albumin — which is why ceftriaxone is avoided in the jaundiced neonate.
The high-risk causes in India are Rh and ABO incompatibility, glucose-6-phosphate dehydrogenase deficiency, sepsis, cephalhaematoma or extensive bruising, prematurity and inadequate breastfeeding; Crigler-Najjar syndrome is the rare inherited cause.
Jaundice appearing in the first 24 hours of life is always pathological, as are a rise of more than 5 mg/dL a day, jaundice reaching the palms and soles, conjugated bilirubin above 2 mg/dL or more than 20 per cent of the total, and jaundice persisting beyond 2 weeks in a term baby or 3 weeks in a preterm baby.
Kramer rule gives the bedside estimate of cephalocaudal progression: face about 5 mg/dL, upper trunk about 10, lower trunk and thighs about 12, arms and legs about 15, and palms and soles above 15 mg/dL — an estimate only, which must be confirmed by a transcutaneous or serum bilirubin.
The decision to treat is never made on a single number: the total serum bilirubin is plotted against the age in hours on the hour-specific nomogram for the baby's gestation and neurotoxicity risk factors, and phototherapy or exchange transfusion is started at the line the chart gives.
Phototherapy uses blue-green light of about 460 to 490 nm to convert bilirubin to lumirubin, a water-soluble isomer excreted without conjugation; expose the maximum skin surface, shield the eyes and genitals, keep the baby in the cot at the prescribed distance, monitor temperature and hydration, allow for the increased insensible water loss, continue breastfeeding, and never use it for conjugated hyperbilirubinaemia because of the bronze baby syndrome.
Double-volume exchange transfusion uses twice the neonatal blood volume, that is about 160 to 170 mL/kg at 80 to 85 mL/kg per volume, removes roughly 85 per cent of the circulating sensitised red cells and is done for a bilirubin at exchange level or for any sign of acute bilirubin encephalopathy at any level; watch afterwards for hypocalcaemia, hypoglycaemia, thrombocytopenia, arrhythmia, sepsis and necrotising enterocolitis. Intravenous immunoglobulin is added in isoimmune haemolysis when the level keeps rising on intensive phototherapy.

Barium enema

A barium enema is a fluoroscopic contrast study of the large bowel in which barium sulfate suspension, usually with insufflated air for a double-contrast film, is run in through a rectal catheter and the colon is screened in several positions. Colonoscopy and CT colonography have replaced it for most adult work, but it survives in Indian practice as a cheap way to answer three questions: where is the obstruction, is this Hirschsprung disease, and can this intussusception be reduced without opening the abdomen.

Single-contrast barium fills and outlines the lumen and is used for obstruction, volvulus and fistula; double-contrast barium with insufflated air or carbon dioxide coats the mucosa and is what shows polyps, early carcinoma and inflammatory change.
Preparation is a low-residue diet for 1 to 2 days, clear fluids the previous evening, the prescribed bowel purgative and nothing by mouth for 6 to 8 hours, because residual faeces mimic polyps and an unprepared colon means a second dose of radiation.
Classical appearances: an apple-core or napkin-ring stricture in carcinoma of the colon, a featureless lead-pipe colon with lost haustra in long-standing ulcerative colitis, a bird-beak tapering at the sigmoid in volvulus, a coiled-spring or claw sign in intussusception, a cone-shaped transition zone above a narrow rectum in Hirschsprung disease, and thumbprinting in ischaemic colitis.
In Hirschsprung disease the aganglionic rectum is the narrow segment and the point of the study is the reversed rectosigmoid index, with the rectum smaller than the sigmoid; the enema is done without prior bowel washouts, because washouts empty the very segment being studied.
In intussusception the enema is both test and treatment: pneumatic reduction with air under fluoroscopy or hydrostatic reduction with saline under ultrasound is now preferred to barium, succeeds in roughly 80 to 90% of cases, and carries a real risk of perforation, so a surgeon and an operating theatre must be available before it begins.
Absolute contraindications are suspected perforation, toxic megacolon and acute severe colitis; recent deep biopsy or polypectomy, peritonitis and shock also stop it, and pregnancy is asked about before any fluoroscopy.
When perforation is possible the study is done with water-soluble iodinated contrast instead of barium, because barium that leaks into the peritoneum causes a dense granulomatous barium peritonitis with high mortality.
Afterwards the patient needs the prescribed laxative and 2 to 3 litres of fluid over the next day, with a warning that stools will be chalky white for 24 to 72 hours and that failure to pass stool for two days with pain or distension means barium impaction and must be reported.
Order of investigations matters: retained barium obscures abdominal ultrasound, CT and colonoscopy for days, so the enema is booked after them, and an upper gastrointestinal barium study is never scheduled in the days before a barium enema.

Liver function tests

The liver function test panel is really three tests in one: markers of hepatocyte injury (ALT and AST), markers of cholestasis (alkaline phosphatase, gamma-glutamyl transferase and bilirubin), and the only true measures of synthetic function (serum albumin and the prothrombin time or INR). Reading the panel means deciding which of the three patterns dominates, because a hepatocellular pattern sends the nurse chasing viral serology and a drug history, while a cholestatic pattern sends the patient for an ultrasound of the biliary tree.

Usual adult reference values are ALT about 7 to 56 U/L, AST about 10 to 40 U/L, alkaline phosphatase about 40 to 130 U/L, total bilirubin 0.3 to 1.2 mg/dL with direct bilirubin under 0.3 mg/dL, albumin 3.5 to 5.0 g/dL and INR 0.8 to 1.2, with the exact range set by the local laboratory.
Jaundice becomes visible in the sclera only at a total bilirubin of about 2 to 3 mg/dL, so a patient can be significantly hyperbilirubinaemic before anyone can see it.
ALT is the more liver-specific enzyme, while AST is also found in heart, skeletal muscle, kidney and red cells — which is why a haemolysed sample, a recent intramuscular injection or a seizure raises AST falsely.
The AST:ALT ratio is a discriminator: a ratio above 2 with both enzymes under about 300 U/L points to alcoholic liver disease, while a ratio below 1 fits viral hepatitis and non-alcoholic fatty liver disease, in which a rising ratio suggests progression to fibrosis.
Aminotransferases above 1000 U/L narrow the diagnosis to three groups — acute viral hepatitis, drug or toxin injury with paracetamol at the head of the list, and ischaemic hepatitis after shock, which rises and falls very fast alongside a high LDH.
An isolated rise in alkaline phosphatase is confirmed as hepatic by a raised gamma-glutamyl transferase; a normal GGT points instead to bone (Paget disease, metastases, growing adolescents) or to the physiological placental rise of the third trimester, and GGT on its own is induced by alcohol, phenytoin, carbamazepine and rifampicin without meaning liver disease.
Jaundice sorts three ways. Prehepatic jaundice from haemolysis or Gilbert syndrome is unconjugated with no bilirubin in the urine, normal enzymes and raised LDH and reticulocytes; hepatocellular jaundice is mixed with ALT and AST dominant; post-hepatic obstruction is conjugated with a dominant alkaline phosphatase and GGT, pale clay-coloured stools, dark urine and itching.
The prothrombin time and INR are the earliest markers of acute synthetic failure because factor VII has a half-life of only a few hours, while albumin has a half-life of about 20 days and therefore reflects chronic disease; a prolonged prothrombin time that corrects after parenteral vitamin K is obstructive, and one that does not correct is hepatocellular failure.
Ammonia is not a liver function test and its level does not track the grade of encephalopathy; when it is sent, the sample goes on ice to the laboratory at once and the tourniquet is released promptly, because delay and stasis both raise it falsely.
The panel feeds the prognostic scores that decide surgery and transplant: Child-Pugh uses bilirubin, albumin, INR, ascites and encephalopathy, while MELD uses bilirubin, INR, creatinine and sodium.

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