Abdominal Pain - 3

Upper Abdominal Pain
16.10.06

Peptic ulcer disease
• Defects in mucosa as result of acid-peptic juices.
• Causes:
-H. pylori (80%).
-NSAIDs.
-Pancreatic duct blockage.
-Zollinger-Ellison syndrome.
• Males 4X>females.
• Duodenal ulcers 2-3X>gastric ulcers.

Causes
• Early 20th Century - stress and diet.
• 1950s - acid.
• 1970s - H2 receptor antagonists - ulcers chronic incurable.
• 1980s - PPIs; H. pylori.

Symptoms
DUODENAL ULCER
• Burning/gnawing in epigastrium.
• Occurs 2-3 hours after meal.
• Relieved by ingestion of food/antacids.
• 2/3 pain wakes in middle of night.
• Anorexia and weight loss unusual - can put on weight.

GASTRIC ULCER
• Burning/gnawing in epigastrium.
• Sooner after meals than duodenal ulcer.
• Not relieved/worsened by food and antacids.
• 1/3 wake from sleep with pain.

Complications
• Haemorrhage.
• Perforation, leading to peritonitis.
• Scar tissue build-up, leading to obstruction.

All gastric ulcers must be biopsied to exclude gastric cancer.
Duodenal ulcers are never malignant.

Treatment
• If H. pylori positive: H. pylori eradication triple therapy - PPI + 2 antibiotics.
• If H. pylori negative: PPI.
• Perforation needs urgent surgery.
• Haemorrhage: endoscopic therapy.

Acute cholecystitis
• Usually caused by gallstones.
• Gallstone affect 10% in West.
• 80% asymptomatic.
• Helminthic infection (ascariasis) major cause of biliary disease in developing countries.
• Obstruction of cystic duct → inflammation → acute cholecystitis.

Risk factors for gallstones
• Age >40 years.
• Bile salt loss (ileal disease/resection).
• Female sex (twice risk than men).
• DM.
• Genetic/ethnic variation.
• CF.
• High fat, low fibre diet.
• Obesity.
• Gall bladder dysmotility.
• Pregnancy.
• Etc.

Pathophysiology of cholecystitis
• 90% acute cholecystitis caused by obstruction of cystic duct by gallstones/sludge.
• Increase in intraluminal pressure and cholesterol supersaturates bile.

Clinical presentation
• Sudden onset pain in epigastrium.
• Can radiate round to back in intrascapular region.
• Pain often does not fluctuate, but persists 15 minutes - 24 hours.
• Nausea or vomiting common.
• Peritonitis localised to RUQ.

Investigations
• USS investigation of choice.
• Pericholecystic fluid.
• Distended gall bladder.

Management
• Fasting, IV fluids and analgesia.
• 20% need emergency surgery.
• Cholecystectomy.

Complications
• Gangrenous cholecystitis.
• Gall bladder perforation.
• Cholecystoenteric fistulas.

Jaundice and gall stones
• Most commonly occurs when stone migrates from gall bladder into common bile duct.
• LFT cholestatin pattern.

Acute pancreatitis
• >80% with alcohol/gallstones.
• Proteolytic enzymes activated → local and systemic inflammatory cell response.
• Often self-limiting.
• 5-20% fulminating course - pancreatic necrosis and cytokine activation → multiple organ dysfunction syndrome.

Symptoms
• Presentation variable.
• Alcohol-induced - symptoms 6-12 hours after binge drinking.
• Pain in epigastrium radiates to back.
• Associated with nausea and vomiting.
• Severe attacks mimic perforation/ischaemic bowel and "ruptured" aortic aneurysm.
• Abdominal distension.

Diagnosis
• Appropriate clinical features.
• Serum amylase activity over 3X normal.

Clinical course
• Self-limiting in 80% cases.
• Severe cases have 3 phases.

Assessing severity - initial predictors
• 1st attack alcohol induced.
• Obesity.
• Haemodynamic instability.
• Severe signs.

Severe pancreatitis
• Adequate resuscitation of hypovalaemic shock.
• Monitor urine output.
• Antibiotics - minor benefit.
• May need ventilation/dialysis.

Prognosis
• Overall mortality 10-15%.
• Not changed in past 20 years.

Abdominal aortic aneurysm
• True arterial aneurysms >50% increase in normal diameter of vessel.
• 90% mortality from ruptured abdominal aortic aneurysm, 80% die before reaching hospital and 50% die during surgery.
• Complications: rupture, thrombosis.

Presentation
• ¾ asymptomatic.
• Symptoms usually result from embolisation/rupture of aneurysm.
• Triad of hypovolaemic shock, pulsatile abdominal mass and abdominal/back pain in minority.

Factors predisposing to ruptured abdominal aortic aneurysm
• Diameter of aneurysm.
• Diastolic BP.
• COPD.
• Smoking.
• FH of ruptured aneurysm.
• Expansion rate.
• Etc.

Diagnosis
• Can usually palpate pulsatile mass.
• CT best test.

Treatment
• All should be considered for emergency surgical repair.
• Patients with symptomatic aneurysms need urgent aneurysm repair.

Non-abdominal causes of abdominal pain
• MI.
• Pneumonia, PE.
• New-onset DM.
• Addison's disease.
• Porphyria.
• Lead poisoning.

Conclusions
• Symptoms and signs often lead to correct diagnosis of acute upper abdominal pain.
• Remember non-abdominal causes of upper and mid-abdominal pain.
• USS early if atypical pain and aortic aneurysm suspected.