Gastroenterology: Gastroenterology Emergencies (Complete)

• Overview: At a Glance | The Acute Abdomen
• GI bleeding: Upper GI Bleeding: Assessment | Peptic Ulcer Bleeding | Variceal Bleeding | Lower GI Bleeding | Anticoagulants and GI Bleeding
• Liver: Acute Liver Failure | Paracetamol Overdose | Decompensated Cirrhosis | Hepatic Encephalopathy | Spontaneous Bacterial Peritonitis | Hepatorenal Syndrome | Alcohol-related Hepatitis | Alcohol Withdrawal and Wernicke's
• Pancreas and biliary: Acute Pancreatitis | Biliary Colic and Acute Cholecystitis | Acute Cholangitis
• Bowel: Acute Severe Ulcerative Colitis | Crohn's Disease Emergencies | Severe C. difficile Infection | Acute Mesenteric Ischaemia | Bowel Obstruction | Volvulus and Pseudo-obstruction | Perforated Viscus
• Oesophagus: Food Bolus and Swallowed Objects | Oesophageal Perforation | Caustic Ingestion
• Revision: Drug Reference Table | Spot the Emergency | Exam-style Scenarios | Key Points | Guidelines and Further Reading

🩸 Gastroenterology emergencies range from the dramatic (a vomiting patient with variceal bleeding) to the deceptively quiet (an older person with mesenteric ischaemia and a soft abdomen). Many need teamwork across medicine, surgery, endoscopy and radiology. This chapter is a practical guide to the first hours of care.
Your four questions for every patient: Is the patient shocked or bleeding? Is there liver disease, and is it decompensating? Is this a surgical abdomen (peritonitis, obstruction, ischaemia)? Who needs to come now - endoscopist, surgeon, interventional radiologist, liver unit?

At a Glance

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The Acute Abdomen

Start with ABCDE. Shock with abdominal pain means bleeding (ruptured AAA, ectopic pregnancy, GI bleed), sepsis (perforation, cholangitis, ischaemia) or severe pancreatitis until proven otherwise.

Patterns of pain:

• Sudden, severe, generalised pain - perforation, ruptured AAA, mesenteric ischaemia.
• Colicky pain with vomiting and distension - bowel obstruction.
• Constant localised pain with fever - appendicitis, cholecystitis, diverticulitis.
• Pain out of proportion to examination - mesenteric ischaemia.
• Peritonitis (rigid abdomen, guarding, rebound, patient lying still) - a surgical emergency.

Medical causes to remember ("surgical-looking" abdomens that need medical treatment):

• DKA; adrenal crisis; hypercalcaemia.
• Inferior MI; lower lobe pneumonia.
• Sickle cell crisis; acute porphyria.
• Herpes zoster (before the rash); IgA vasculitis.
• Lead poisoning; familial Mediterranean fever.

Initial tests:

• FBC, U&E, LFTs, amylase or lipase, CRP, calcium, glucose.
• Venous blood gas with lactate.
• Group and save.
• Pregnancy test in anyone who could be pregnant.
• Urine dipstick; ECG.
• Erect chest X-ray (free air).
• CT abdomen and pelvis - the key test for most surgical causes.

💡 Clinical Pearl: Older people, people on steroids and people with diabetes can have catastrophic intra-abdominal disease with very few signs. A raised lactate, unexplained tachycardia or confusion with abdominal pain needs a CT.

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Upper GI Bleeding: Assessment

Presentation: Haematemesis (fresh blood or "coffee grounds"), melaena (black, tarry, offensive stool), or collapse. A brisk upper GI bleed can cause fresh red rectal bleeding with shock.

Common causes:

• Peptic ulcer - the commonest.
• Oesophageal or gastric varices (liver disease).
• Oesophagitis, gastritis.
• Mallory–Weiss tear (after retching).
• Upper GI cancer.
• Angiodysplasia; Dieulafoy lesion.

Resuscitation:

• Two large-bore cannulas.
• FBC, U&E (a high urea relative to creatinine suggests an upper GI source), LFTs, clotting, crossmatch.
• Activate the major haemorrhage protocol if bleeding is massive.
• Transfusion: Restrictive - transfuse if Hb is below 70 g/L, aiming for 70–100 g/L. Use a higher threshold (about 80 g/L) in significant cardiovascular disease.
• Platelets if below 50 × 10⁹/L and actively bleeding.
• Fresh frozen plasma if INR or APTT is above 1.5 times normal.
• Correct anticoagulation (see Anticoagulants and GI Bleeding).

Risk scores:

• Glasgow–Blatchford score (before endoscopy): Uses urea, Hb, systolic BP, pulse, melaena, syncope, liver disease and heart failure. A score of 0–1 means the patient can usually go home with outpatient endoscopy.
• Rockall score (after endoscopy): Predicts rebleeding and death.

Endoscopy (NICE CG141):

• Immediately after resuscitation if the patient is unstable with severe bleeding.
• Within 24 hours of admission for everyone else.

Drugs:

• Do not give a PPI before endoscopy. Give it afterwards if there is high-risk ulcer disease.
• Tranexamic acid is not recommended - the HALT-IT trial showed no benefit and more VTE.
• Aspirin for secondary prevention can usually be continued once haemostasis is achieved. Stop other antiplatelets and anticoagulants and plan restarting with the relevant specialists.

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Peptic Ulcer Bleeding

Causes: Helicobacter pylori and NSAIDs (including aspirin), made worse by anticoagulants, SSRIs and steroids, and by physiological stress in critical illness.

Endoscopy findings (Forrest classification) predict rebleeding:

• High risk - needs endoscopic treatment:
  • Active spurting or oozing.
  • Visible vessel.
  • Adherent clot.
• Low risk: Flat pigmented spot, clean base.

Management:

• Endoscopic haemostasis: Adrenaline injection combined with a second method - clips, thermal coagulation or haemostatic powder. Adrenaline alone is not enough.
• After treatment: High-dose PPI (e.g. IV or oral, per local protocol) for 72 hours, then oral PPI.
• Test for H. pylori and eradicate if positive.
• Stop NSAIDs.
• Rebleeding:
  • Repeat endoscopy.
  • If it fails or the patient is unstable: interventional radiology embolisation, or surgery.

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Variceal Bleeding

Mechanism: In cirrhosis, scarring raises pressure in the portal vein (portal hypertension). Blood diverts through fragile collateral veins (varices) in the oesophagus and stomach, which can rupture and bleed torrentially. Mortality is about 15% per episode.

Suspect it in anyone with known or suspected liver disease (stigmata of chronic liver disease, ascites, alcohol history) who has an upper GI bleed. Treat as variceal until endoscopy proves otherwise.

Management:

• Resuscitate - but with restrictive transfusion (Hb about 70–80 g/L). Over-transfusion raises portal pressure and worsens bleeding.
• Terlipressin (lowers portal pressure): e.g. 2 mg IV every 4–6 hours (follow local protocol; reduce once bleeding is controlled), usually continued for 2–5 days.
  • Caution in ischaemic heart disease and peripheral vascular disease.
  • Watch for hyponatraemia.
• IV antibiotics - infection is common and increases rebleeding and death. For example, co-amoxiclav 1.2 g IV three times daily, or ciprofloxacin or ceftriaxone, per local policy.
• Urgent endoscopy (within 12 hours, sooner if unstable) with band ligation for oesophageal varices. Cyanoacrylate glue for gastric varices.
• Uncontrolled bleeding: Balloon tamponade (Sengstaken–Blakemore tube, usually after intubation) or a self-expanding oesophageal stent as a bridge, then TIPSS (transjugular intrahepatic portosystemic shunt).
• Pre-emptive TIPSS within 72 hours in selected high-risk patients (e.g. Child–Pugh C 10–13) - liver unit decision.
• Airway: Intubate if the patient is drowsy (encephalopathy) or vomiting large volumes.
• Prevent decompensation: Lactulose (encephalopathy), monitor glucose and kidneys, start alcohol withdrawal care.
• Afterwards: Non-selective beta-blocker (carvedilol or propranolol) plus a band ligation programme to prevent rebleeding.

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Lower GI Bleeding

Causes:

• Diverticular disease - the commonest cause of major bleeding; painless.
• Haemorrhoids, anal fissure.
• Angiodysplasia - older people, aortic stenosis, CKD.
• Ischaemic colitis - pain and bloody diarrhoea in older people.
• Inflammatory bowel disease, infective colitis.
• Colorectal cancer and polyps; bleeding after polypectomy.
• Radiation proctitis.
• Remember: About 1 in 7 apparently "lower" bleeds with shock are from the upper GI tract.

Assessment (BSG 2019):

• Shock index (heart rate ÷ systolic BP) above 1 means unstable.
• Stable patients: The Oakland score (age, sex, previous LGIB admission, rectal examination, heart rate, systolic BP, Hb). A score of 8 or less means a minor bleed - consider discharge with outpatient investigation.
• Major stable bleeds: Admit for colonoscopy on the next available list.
• Unstable (shock index above 1 after resuscitation):
  • CT angiography to find the bleeding point.
  • Interventional radiology embolisation if a blush is seen.
  • If CT angiography is negative: upper GI endoscopy to look for an upper source.
  • Surgery is a last resort when the source is known.
• Transfusion: Restrictive - Hb threshold 70 g/L (target 70–90 g/L), or 80 g/L (target 100 g/L) with cardiovascular disease.

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Anticoagulants and GI Bleeding

• Warfarin with major bleeding:
  • Vitamin K 5 mg IV.
  • Prothrombin complex concentrate (PCC), dosed by weight and INR.
• Apixaban or rivaroxaban:
  • Stop the drug.
  • Andexanet alfa is recommended by NICE (TA697) for adults with life-threatening or uncontrolled GI bleeding on apixaban or rivaroxaban.
  • PCC is used off-label where andexanet is not used.
• Dabigatran: Idarucizumab 5 g IV. Dabigatran can also be removed by dialysis.
• Heparin: Protamine (fully reverses unfractionated heparin; partly reverses LMWH).
• Antiplatelets:
  • Continue aspirin for secondary prevention once bleeding is controlled.
  • Discuss stopping clopidogrel, prasugrel or ticagrelor with cardiology - especially after recent coronary stents, where stopping risks stent thrombosis.
  • Platelet transfusion is not routinely helpful.
• Restarting: Plan restarting anticoagulation once haemostasis is secure - often within about 7 days for patients with a strong indication (e.g. mechanical valve, recent VTE).

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Acute Liver Failure

Definition: Rapid loss of liver function in someone without pre-existing liver disease, defined by:

• Coagulopathy - INR 1.5 or more.
• Encephalopathy.
• Illness of less than 26 weeks.

"Hyperacute" cases (jaundice to encephalopathy within 7 days, typical of paracetamol) have more cerebral oedema but better spontaneous survival.

Causes:

• Paracetamol - the commonest in the UK.
• Drugs - antituberculosis drugs, anticonvulsants, antibiotics, herbal remedies, ecstasy.
• Viral hepatitis - A, B, E (especially in pregnancy); herpes simplex.
• Autoimmune hepatitis; Wilson's disease.
• Ischaemic hepatitis (shock liver); Budd–Chiari syndrome.
• Pregnancy-related - acute fatty liver of pregnancy, HELLP syndrome.
• Mushroom poisoning (Amanita); malignant infiltration.

Clinical pattern: Jaundice (may be absent early in paracetamol), confusion progressing to coma, bleeding, hypoglycaemia, AKI, lactic acidosis, infection and cerebral oedema.

Management:

• Discuss early with a liver transplant unit - before the patient deteriorates.
• Monitor glucose 1–2-hourly; give IV glucose to prevent hypoglycaemia.
• Acetylcysteine for paracetamol, and often for other causes of early acute liver failure.
• Do not routinely correct the INR with FFP unless bleeding or before a procedure - the INR is a key prognostic marker.
• Avoid sedatives; protect the airway when encephalopathy is grade 3–4 (intubate).
• Treat infection early; renal support; manage cerebral oedema in ICU.
• Transplant assessment - the King's College criteria for paracetamol cases:
  • Arterial pH below 7.3 (or lactate above 3.0 mmol/L) after fluid resuscitation, or
  • All three of: INR above 6.5, creatinine above 300 µmol/L, and grade 3–4 encephalopathy.

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Paracetamol Overdose

Mechanism: In overdose, the normal liver pathways are overwhelmed. Paracetamol is converted into a toxic metabolite (NAPQI), which is normally detoxified by glutathione. When glutathione runs out, NAPQI destroys liver cells. Acetylcysteine (NAC) replenishes glutathione - it is almost 100% effective if started within 8 hours.

Early clinical pattern: Often no symptoms or only nausea in the first 24 hours. Liver injury (raised ALT, INR) peaks at 72–96 hours, with right upper quadrant pain, jaundice and encephalopathy in severe cases.

Assessment - always use TOXBASE:

• Establish the dose (mg/kg), time and whether it was a single ingestion or staggered (over more than 1 hour).
• Single acute ingestion: Take a paracetamol level at 4 hours or later after ingestion (levels before 4 hours cannot be interpreted). Plot it on the UK nomogram - the treatment line starts at 100 mg/L at 4 hours.
• Also check U&E, LFTs, INR, glucose and a venous gas.

Start acetylcysteine immediately - without waiting for the level - if:

• The patient presents 8 hours or more after a potentially toxic overdose.
• The overdose was staggered, or the timing is uncertain.
• There are signs of liver injury or encephalopathy.

Acetylcysteine regimen: Most UK hospitals now use the 12-hour SNAP regimen (endorsed by RCEM), which causes fewer reactions than the older 21-hour regimen:

• Bag 1: 100 mg/kg over 2 hours.
• Bag 2: 200 mg/kg over 10 hours.
• Bloods (INR, ALT, paracetamol level) about 10 hours into the infusion.
• Stop at 12 hours if INR is 1.3 or less, ALT is normal, paracetamol is below 10 mg/L and there are no symptoms of liver injury. Otherwise continue (further bags) and discuss with NPIS and the liver unit.

Adverse reactions: Flushing, itch, wheeze or (rarely) hypotension - usually an anaphylactoid reaction, not true allergy. Pause the infusion, give an antihistamine, and restart at a slower rate once settled.

Refer to a liver unit if any of the following:

• INR above 3.0 at 48 hours (or above 4.5 at any time).
• Rising creatinine (above 200 µmol/L) or oliguria.
• pH below 7.3 or a raised lactate.
• Hypotension.
• Encephalopathy.
• Hypoglycaemia.

Psychiatric assessment for everyone after intentional overdose - this need not wait until treatment is finished.

💡 Clinical Pearl: A normal ALT and INR soon after a large overdose do not mean the patient is safe - the liver injury has not happened yet. Decisions are based on the dose, the timing and the paracetamol level.

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Decompensated Cirrhosis

Mechanism: Cirrhosis is "compensated" while the liver copes. Decompensation means the onset of one or more of:

• Jaundice.
• Ascites.
• Hepatic encephalopathy.
• Variceal bleeding.

Survival falls sharply once decompensation occurs.

Common triggers - always look for them:

• Infection - SBP, pneumonia, UTI, cellulitis.
• GI bleeding.
• Alcohol (alcohol-related hepatitis).
• Dehydration, over-diuresis, AKI.
• Constipation.
• Drugs - sedatives, opioids, NSAIDs.
• Portal vein thrombosis; hepatocellular carcinoma.

Acute-on-chronic liver failure (ACLF): Decompensation with failure of other organs (kidneys, brain, circulation, lungs). It has a very high short-term mortality - involve ICU and the liver unit early.

Admission care bundle (BSG/BASL decompensated cirrhosis bundle):

• Bloods: FBC, U&E, LFTs, INR, glucose, CRP, blood cultures.
• Diagnostic ascitic tap for everyone with ascites on admission - to exclude SBP.
• Alcohol: Assess withdrawal; give thiamine (IV Pabrinex if at risk).
• Look for infection and treat promptly.
• Stop or hold: Diuretics if AKI or hyponatraemia; nephrotoxins; NSAIDs.
• Encephalopathy: Lactulose.
• VTE prophylaxis - cirrhosis does not protect against clots despite a raised INR.
• Nutrition: Late-evening snack; avoid protein restriction.
• Prognosis: Child–Pugh and MELD scores; discuss goals of care and transplant referral.

Tense ascites: Large-volume paracentesis, with IV human albumin to prevent circulatory dysfunction - about 8 g of albumin per litre drained when more than 5 L are removed (e.g. 100 mL of 20% albumin per 2.5–3 L).

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Hepatic Encephalopathy

Mechanism: The failing liver (and blood bypassing it through shunts) cannot clear gut-derived toxins such as ammonia. These affect brain function, causing confusion and drowsiness.

West Haven grades:

• Grade 1: Mild confusion, poor attention, sleep reversal.
• Grade 2: Lethargy, disorientation, asterixis (liver flap).
• Grade 3: Very drowsy but rousable, marked confusion.
• Grade 4: Coma.

Management:

• Find and treat the precipitant:
  • Infection (including SBP).
  • GI bleeding.
  • Constipation.
  • Dehydration, hypokalaemia, hyponatraemia, AKI.
  • Sedatives and opioids.
  • Alcohol.
  • Hypoglycaemia.
  • TIPSS.
• Exclude other causes of confusion - hypoglycaemia, Wernicke's, subdural haematoma (falls, coagulopathy), alcohol withdrawal, sepsis.
• Lactulose (e.g. 15–30 mL two to three times daily), titrated to 2–3 soft stools a day. Phosphate enemas if the patient cannot swallow.
• Rifaximin 550 mg twice daily - added to prevent recurrence (NICE TA337).
• Protect the airway in grade 3–4 - consider intubation in ICU.
• Avoid protein restriction.

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Spontaneous Bacterial Peritonitis

Mechanism: Infection of ascitic fluid without an obvious surgical source, usually by gut bacteria (E. coli, Klebsiella, streptococci) crossing the bowel wall.

Clinical pattern: May be subtle - fever, abdominal pain or tenderness, worsening encephalopathy, AKI, or no symptoms at all. This is why every patient with ascites admitted to hospital needs a diagnostic tap.

Diagnosis: Ascitic fluid neutrophil count above 250 cells/mm³. Inoculate blood culture bottles with ascitic fluid at the bedside.

Management:

• IV antibiotics per local policy - e.g. a third-generation cephalosporin or piperacillin-tazobactam (wider cover if hospital-acquired).
• IV albumin - 1.5 g/kg at diagnosis and 1 g/kg on day 3. This reduces hepatorenal syndrome and death.
• Stop diuretics and nephrotoxins.
• Repeat tap at 48 hours - the neutrophil count should fall by at least 25%.
• Suspect secondary (surgical) peritonitis if there are multiple organisms, very high protein, low glucose, or no response. Get a CT for perforation.
• Prophylaxis: Long-term oral antibiotics (e.g. ciprofloxacin or co-trimoxazole) after an episode of SBP, and for people with low ascitic protein (NICE NG50).

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Hepatorenal Syndrome

Mechanism: In advanced cirrhosis, blood vessels in the gut dilate, so the effective blood volume falls. The kidneys respond with intense vasoconstriction, and kidney function fails - even though the kidneys are structurally normal.

Diagnosis (HRS-AKI, International Club of Ascites) - all of:

• Cirrhosis with ascites, and AKI by standard criteria.
• No improvement after 48 hours of stopping diuretics and giving IV albumin 1 g/kg.
• No shock.
• No recent nephrotoxic drugs (NSAIDs, contrast, aminoglycosides).
• No signs of structural kidney disease (proteinuria above 0.5 g/day, haematuria, abnormal ultrasound).

Management:

• Stop diuretics, nephrotoxins and beta-blockers if hypotensive.
• Treat triggers - infection (SBP), bleeding, over-diuresis.
• Terlipressin plus albumin (specialist).
  • Watch carefully for fluid overload and respiratory failure - avoid in hypoxia or volume overload.
  • Watch for ischaemic side effects.
• Noradrenaline with albumin is an alternative in ICU.
• Liver transplant assessment - the definitive treatment. Renal replacement therapy may be a bridge.

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Alcohol-related Hepatitis

Clinical pattern: Rapid-onset jaundice in a heavy drinker (usually within 8 weeks of drinking heavily). Other features:

• Fever.
• Tender hepatomegaly.
• Raised neutrophil count.
• Ascites, encephalopathy, coagulopathy.
• AST typically raised more than ALT (ratio above 1.5), but both are usually below 400 U/L.

Severity:

• Maddrey discriminant function - 32 or more means severe.
• Glasgow alcoholic hepatitis score - 9 or more means poor prognosis.
• MELD score.

Management:

• Stop alcohol - the most important treatment; manage withdrawal.
• Thiamine (IV Pabrinex).
• Nutrition - high calorie and protein; NG feeding if needed.
• Screen for infection - blood, urine and ascitic cultures; chest X-ray.
• Prednisolone 40 mg daily for 28 days can be considered in severe disease once infection and GI bleeding are excluded. It improves short-term (28-day) survival but not longer-term survival (STOPAH).
  • Use the Lille score at day 7 to decide whether to continue (stop if non-responder).
• Long-term: Alcohol care team, psychosocial support, relapse prevention medicines.

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Alcohol Withdrawal and Wernicke's

Alcohol withdrawal:

• Timing: Starts 6–24 hours after the last drink.
• Symptoms: Tremor, sweating, anxiety, tachycardia, nausea, insomnia.
• Seizures: Usually within 12–48 hours.
• Delirium tremens (24–72 hours or more): Confusion, hallucinations, fever, autonomic instability. Mortality is significant if untreated.

Management (NICE CG100):

• Benzodiazepine: Usually chlordiazepoxide, symptom-triggered using a validated scale (e.g. CIWA-Ar), or a fixed reducing regimen. In liver failure, a shorter-acting drug (e.g. lorazepam or oxazepam) at lower doses may be safer.
• Seizures: A quick-acting benzodiazepine (e.g. lorazepam).
• Delirium tremens: Oral lorazepam first-line. Parenteral lorazepam, haloperidol or olanzapine if symptoms persist. Treat in a safe environment, often HDU.
• Correct fluids, glucose, potassium, magnesium and phosphate.
• Look for head injury, infection, GI bleeding and hepatic encephalopathy.

Wernicke's encephalopathy:

• Mechanism: Acute brain injury from thiamine (vitamin B1) deficiency - alcohol misuse, malnutrition, hyperemesis, after bariatric surgery.
• Classic triad: Confusion, ataxia and eye signs (nystagmus, ophthalmoplegia). Only a minority have all three - treat on suspicion.
• Treatment: High-dose IV thiamine (e.g. Pabrinex 2 pairs three times daily for 3–5 days, per BNF and local protocol).
• Give thiamine before or with glucose in at-risk patients - glucose alone can precipitate Wernicke's.
• Untreated, it can progress to Korsakoff syndrome - permanent memory loss with confabulation.

⚠️ Safety Pearl: Any confused, unsteady or drowsy patient with alcohol dependence or malnutrition should get IV thiamine immediately. It is cheap and safe - missing Wernicke's leaves permanent brain damage.

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Acute Pancreatitis

Mechanism: Digestive enzymes are activated inside the pancreas, which starts to digest itself. Inflammation can spread throughout the body, causing organ failure.

Causes:

• Gallstones and alcohol - about 80%.
• Post-ERCP.
• Hypertriglyceridaemia (usually above 10 mmol/L).
• Hypercalcaemia.
• Drugs - azathioprine, valproate, thiazides, GLP-1 receptor agonists, steroids, oestrogens.
• Trauma; infection (mumps, CMV); autoimmune; pancreatic tumours; idiopathic.

Diagnosis - 2 of 3:

• Typical severe epigastric pain, often radiating to the back.
• Amylase or lipase more than 3 times the upper limit of normal.
• Typical findings on imaging.

Severity (revised Atlanta):

• Mild: No organ failure, no local complications.
• Moderately severe: Transient organ failure (under 48 hours) and/or local complications.
• Severe: Persistent organ failure (over 48 hours) - mortality around 30%.
• Early warning: Glasgow-Imrie score of 3 or more, CRP above 150 mg/L at 48 hours, SIRS, rising urea, older age, obesity.

Management:

• Fluids: Moderate, goal-directed IV fluid (e.g. Hartmann's or Ringer's lactate), guided by heart rate, BP, urine output and urea. Aggressive high-volume fluids cause fluid overload without benefit (WATERFALL trial).
• Analgesia - opioids are appropriate.
• Early feeding: Oral diet as tolerated. If unable to eat, enteral feeding (NG or nasojejunal) is preferred over parenteral.
• No prophylactic antibiotics (NICE NG104). Give antibiotics for proven infection - cholangitis, infected necrosis, or other sources.
• Gallstone pancreatitis:
  • Urgent ERCP if there is cholangitis or persistent biliary obstruction.
  • Cholecystectomy during the same admission (or within 2 weeks) for mild disease, to prevent recurrence (NICE NG104).
• CT is not needed for diagnosis in typical cases. Do it at 72 hours or later if the patient is not improving - to look for necrosis or collections.
• Severe disease: HDU or ICU; monitor for ARDS, AKI, abdominal compartment syndrome and hypocalcaemia.
• Infected necrosis: Antibiotics, then a "step-up" approach - delay drainage if possible (ideally around 4 weeks), then endoscopic or percutaneous drainage, and necrosectomy if needed. Specialist pancreatic centre.

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Biliary Colic and Acute Cholecystitis

• Biliary colic:
  • A gallstone temporarily blocks the gallbladder outlet.
  • Severe right upper quadrant or epigastric pain lasting under 6 hours, often after fatty food.
  • No fever, normal inflammatory markers.
  • Analgesia (NSAIDs are effective); elective cholecystectomy.
• Acute cholecystitis:
  • Mechanism: Persistent blockage causes gallbladder wall inflammation and infection.
  • Signs: Constant right upper quadrant pain, fever, raised WCC and CRP, and Murphy's sign (catching the breath on deep inspiration when pressing the right upper quadrant).
  • Ultrasound: Thickened gallbladder wall, pericholecystic fluid, stones.
  • Treatment: IV antibiotics, analgesia, fluids.
  • Early laparoscopic cholecystectomy - within 1 week of diagnosis (NICE CG188).
  • Percutaneous cholecystostomy if too unwell for surgery.
• Complications: Empyema, gangrene, perforation, Mirizzi syndrome, gallstone ileus.
• Acalculous cholecystitis: Occurs in critically ill patients (ICU, burns, TPN) - high mortality.

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Acute Cholangitis

Mechanism: Infection in a blocked bile duct - usually from a common bile duct stone, sometimes a tumour, stricture or blocked stent. Pus under pressure in the biliary tree rapidly causes sepsis.

Clinical pattern:

• Charcot's triad: Fever (often with rigors), jaundice and right upper quadrant pain.
• Reynolds' pentad adds hypotension and confusion - severe cholangitis.

Tests:

• Blood cultures.
• LFTs - obstructive pattern: raised bilirubin, ALP and GGT.
• FBC, CRP, U&E, lactate, clotting.
• Ultrasound - dilated ducts, stones. MRCP or CT if unclear.

Management (Tokyo guidelines):

• Sepsis care: IV fluids, oxygen, monitoring.
• IV antibiotics per local policy (e.g. piperacillin-tazobactam).
• Biliary drainage - usually ERCP:
  • Urgent (as soon as possible, after resuscitation) in severe cholangitis or if not responding to antibiotics.
  • Early (within about 24–48 hours) in moderate disease.
  • Percutaneous transhepatic drainage if ERCP fails or is not possible.
• Correct clotting before sphincterotomy.
• Then: Cholecystectomy if gallstones are the cause.

💡 Clinical Pearl: Antibiotics alone do not cure cholangitis - the pus must be drained. A septic, jaundiced patient with dilated ducts needs the endoscopist that day.

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Acute Severe Ulcerative Colitis

Why it matters: A medical emergency with a risk of toxic megacolon, perforation and death. About a third of patients still need colectomy despite treatment.

Definition (Truelove and Witts): 6 or more bloody stools a day, plus at least one sign of systemic illness:

• Heart rate above 90.
• Temperature above 37.8°C.
• Hb below 105 g/L.
• ESR above 30 mm/hour (or CRP above 30 mg/L).

On admission:

• Stool culture and C. difficile testing.
• Bloods: FBC, CRP, U&E, LFTs, albumin, magnesium; screen for TB, hepatitis B and C, HIV and VZV in advance of rescue therapy.
• Abdominal X-ray - toxic megacolon if the transverse colon is above 5.5–6 cm; mucosal islands.
• Flexible sigmoidoscopy with biopsies - confirms severity and excludes CMV colitis.

Treatment:

• IV hydrocortisone 100 mg four times daily (or methylprednisolone 60 mg daily).
• VTE prophylaxis with LMWH - even with rectal bleeding. IBD flares carry a high clot risk.
• IV fluids; correct potassium and magnesium (low levels encourage megacolon); nutrition.
• Avoid opioids, anticholinergics, antidiarrhoeals and NSAIDs - they can precipitate toxic megacolon.
• Involve colorectal surgeons from admission. Daily joint review; stool chart; daily CRP.

Day 3 review: Predict steroid failure (Oxford or Travis criteria):

• More than 8 stools a day, or
• 3–8 stools a day with CRP above 45 mg/L.

About 85% of these patients will need colectomy without rescue therapy.

Next steps:

• Rescue therapy: Infliximab (e.g. 5 mg/kg; some centres use higher or accelerated dosing) or ciclosporin.
• Colectomy (subtotal colectomy with ileostomy) if:
  • No response to rescue therapy within 4–7 days.
  • Toxic megacolon not improving.
  • Perforation or massive bleeding.
  Delaying surgery increases mortality.

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Crohn's Disease Emergencies

• Severe flare: Pain, diarrhoea, fever, weight loss. Exclude infection (stool tests, C. difficile) and abscess before giving steroids.
• Abscess (often in the right iliac fossa or perianal):
  • Fever, mass, tenderness.
  • CT or MRI.
  • Antibiotics plus drainage (radiological or surgical).
  • Avoid starting biologics until the sepsis is controlled.
• Bowel obstruction:
  • Inflammatory stricture - may respond to steroids.
  • Fibrotic stricture - needs surgery or endoscopic dilatation.
  • MR enterography helps tell them apart.
• Perforation and fistula: Surgical review.
• Perianal Crohn's with sepsis: MRI pelvis; examination under anaesthesia; drainage and setons.
• Treatment of a severe flare once sepsis is excluded:
  • IV hydrocortisone.
  • Exclusive enteral nutrition.
  • Biologics (anti-TNF, ustekinumab, vedolizumab) under the IBD team.
• Smoking cessation - smoking worsens Crohn's.