Transcript Gallstones
Gallstones Mrs. Kirsty Cattle MRCS SHO General Ian Aird said “Good pathology makes mighty surgeons proud.” Incidence – common (17% at time of death) Age – any age, mostly 40s Aetiology – bile constituents, infective, bile stasis Sex ratio – female>male Geography – Western diet Predisposing factors – “fat, fair, fertile, flatulant, forties” Macroscopy – cholesterol, mixed (90%), pigment Microscopy – histology of gallbladder wall Spread Prognosis Anatomy Presentation Asymptomatic (85-90%) Biliary colic Cholecystitis Obstructive jaundice Ascending cholangitis Pancreatitis Rarities: Gallstone ileus, Mucocoele, Perforation, Mirizzi’s syndrome, Carcinoma Biliary colic Definition: colicky abdominal pain due to the presence of gallstones in gall bladder Investigations Normal blood results USS: gallstones within thin-walled gall bladder, no CBD dilatation Management Symptomatic Cholecystectomy Cholecystitis Definition: constant abdominal pain and tenderness due to an infected gall bladder Investigations Raised WBC, Normal LFTs USS: gallstones within thick-walled gall bladder, no CBD dilatation Management Symptomatic Cholecystectomy Jaundice Definition: obstructive jaundice due to CBD stone Investigations Raised LFTs: Alk Phos > ALT, USS: gallstones, CBD dilatation ± CBD stone Management ERCP Cholecystectomy Ascending cholangitis Surgical emergency Definition: jaundice, rigors, RUQ tenderness Investigations Raised WBC, raised LFTs USS: gallstones, CBD dilatation ± CBD stone Management Urgent resuscitation, iv Antibiotics (e.g. Ciprofloxacin) Urgent ERCP Cholecystectomy Acute Pancreatitis Definition Presentation acute inflammation of the pancreas, primarily due to intracellular activation of trypsinogen to trypsin. Epigastric pain, radiating to back, nausea ± vomiting, dehydration, renal failure Investigations Amylase >3x normal range Scoring of severity Causes of Acute Pancreatitis Obstruction: Gallstones (30-70%) Ampullary or pancreatic tumours (3%) Congenital abnormalities (5%) Sphincter of Oddi hypertension (1-2%) Ascariasis Drugs/Toxins: Alcohol (30-70%) Azathioprine, 6mercaptopurine, some antibiotics (metronidazole, tetracycline), H2 blockers, others Iatrogenic/Trauma: Metabolic: Hypertriglyceridaemia (2%) Hypercalcaemia, hyperparathyroidism (rare) Infection: ERCP Cardiopulmonary bypass Blunt abdominal trauma AIDS, secondary infection Mumps, Coxsackie virus, hepatitis A, B and C Idiopathic (10%) Modified Glasgow Score Indication of severity of pancreatitis Factors: Age > 55 WBC > 15 Glucose > 10 Urea > 16 PaO2 < 8.0 kPa Calcium < 2 mmol/l Albumin < 32 LDH > 600 A score of 3 or more indicates severe pancreatitis and requires anaesthetic input regarding HDU care Compete score on admission and 48 hours later Management Supportive – analgesia, iv rehydration, catheterise, fluid balance, NBM (± NG tube). Consider Antibiotics. Observe for complications: Systemic: cardiovascular, pulmonary, renal, haematological, metabolic, neurological, gastrointestinal Local: fluid collections, pseudocyst, necrosis, ascites, infection, pseudoaneurysm Establish and remove cause: ERCP, Cholecystectomy Strongly advise patient to stop drinking alcohol Rarities Gallstone ileus: Large gallstone erodes through gall bladder wall into neighbouring duodenum, passes along small bowel until it lodges and causes small bowel obstruction AXR: distended loops of small bowel, typically to terminal ileum, with air in biliary tree Rarities Mucocoele: Gallstone lodges in neck of gall bladder, preventing drainage of mucous. May become infected, causing empyema Require drainage and later cholecystectomy Perforation Carcinoma Mirizzi’s syndrome: In 1948, P. L. Mirizzi described an unusual presentation of gallstones which, when lodged in either the cystic duct or the Hartmann pouch of the gallbladder, externally compressed the common hepatic duct (CHD), causing symptoms of obstructive jaundice (Mirizzi, 1948). Pathophysiology: Impaction of a large gallstone (or multiple small gallstones) in the Hartmann pouch or cystic duct results in the Mirizzi syndrome in 2 ways: (1) Chronic and/or acute inflammatory changes lead to contraction of the gallbladder, which then fuses with and causes secondary stenosis of the CHD, or (2) large impacted stones lead to cholecystocholedochal fistula formation secondary to direct pressure necrosis of the adjacent duct walls. Increasingly, these phenomena are seen not as distinct and separate steps but as part of a continuum (Pemberton, 1997; Hazzan, 1999). Laparoscopic cholecystectomy This is a case of a 42 year old male with a previous history of abdominal pain for 6 months. He was admitted to the hospital with nausea but vomiting or fever. An ultrasound study showed gallstones with some thickening of the gallbladder wall. The diagnosis of cholecystitis was made and the patient was scheduled to undergo a laparoscopic cholecystectomy. This picture shows the omentum partially covering the gallbladder in its normal position. Due to significant distention of the gallbladder, a needle is used to drain some bile so grasper clamps can be applied for dissection and manipulation. The Hartmann'a pouch is rectracted laterally and upward, exposing the triangle of Calot where the cystic artery can be identified branching off the right hepatic artery. A short cystic duct is dissected free using a "right angle" clamp. Clips are applied to the cystic duct away from the common bile duct. The cystic duct is transected using scissors. Same technique is used with the cystic artery which is dissected free using a "right angle" clamp and will be divided between clips. Hook electrocautery is used to dissect the gallbladder off the liver bed. The gallbladder is now free and will be placed into a Pleatman sac for retreival. This picture shows the body of the gallbladder, that becomes distended during removal. Caution must be used to avoid rupture while pulling. Thank you Questions?