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Transcript
A woman with abdominal pain…. Michelle Papandony Amanda Vo Veronica Mezhov Wei De Tee Patient • Mrs Wong • 65 yo • Migrated from China 5 years ago with her family HOPC • Presented to ED with – Pseudocolic • • • • RUQ pain 7/10, no radiation Started 30 mins after dinner No relieving/ aggravating factors 2-3 similar episodes over the last 2 months but each lasting 10-15 mins – Slightly nauseated, no vomiting – Relevant negatives • • • • • • • • • • • No abdominal distension Denies change in appearance of stool or urine No diarrhoea No jaundice No fever/ rigors No recent travel No sick contacts No take-away food No cough No CV or resp symptoms No urinary symptoms PHx • GORD • Hyperlipidaemia (diet control) • Salpingectomy and hysterectomy 15 years ago due to peri-menopausal dysmenorrhea and menorrhagia Medications • Omeprazole • NKDA • • • • No relevant family history No smoking history Social drinker Lives at home with her husband and two daughters • No financial/ other stressors Examination • Vital Signs (HR 90, BP 150/90, RR 18, Temp 36.9) • Mild truncal obesity • Slight scleral icterus, nil other peripheral stigmata of liver disease • Small xanthelasma bilaterally • Nil scars or distension of abdomen • • No peritonism • • Tender RUQ • • Positive Murphy’s sign• • Liver non palpable due to pain • • Liver span normal • Bowel sounds present • Kidneys not ballotable • No hernia detected PR not performed Chest clear S1S2 NAD, no murmur Peripheral examinations unremarkable FWT: NAD Ddx • • • • • • • • • Cholecystitis ?Ascending cholangitis Hepatitis Pancreatitis AMI Lower lobe pneumonia PID – not in this patient Appendicitis – anatomical variant Perforated peptic ulcer Pyelonephritis – unlikely Ix • Bloods – FBE + CRP – U&E – LFT + Coags – Lipase/ Amylase • Imaging – Abdo USS • Ix to rule out other dx if suspected eg. ECG • While in ED, Mrs Wong became febrile (38.5) and developed rigors. While her skin was not jaundiced, her scleral icterus appeared to worsen. • Mx Plan – IV Fluids – Morphine + Metaclopramide – NBM – IV antibiotics (Ceftriaxone and Metronidazole) Ix Results • • • • • • • • Mildly increased WCC Raised CRP (250) Markedly raised ALP and GGT Mildly raised ALT and AST Raised bilirubin Coags NAD Lipase NAD U/S showed: • Enlarged common bile duct of 10mm • Gallbladder wall thickened • Stones within the gallbladder and the common bile duct • Mrs Wong was diagnosed with cholecystitis with secondary ascending cholangitis (Charcot’s triad). Mx • Endoscopic Retrograde Cholangiopancreatography (ERCP) • Cholecystectomy 6 weeks after Biliary Disease Gallstone(s) Defn: Solid crystal deposits that form within biliary tract Types: 1) Mixed (80%) 2) Cholesterol 3) Pigment stones a) Black (2° haemolytic disease) b) Brown (2° infection) Normal bile Bile salts Phospholipids (lecithin) Cholesterol Protein Bilirubin Definitions • Cholestasis = Obstruction of bile flow • Cholelithiasis = Gallstone(s) within the gallbladder • Choledocholithiasis = Gallstone(s) within the CBD *CBD = common bile duct Overview of Biliary Disease • Biliary colic • Cholecystitis – Acute – Chronic • Cholangitis – Acute – Primary Sclerosing (PSC) cholangitis • Primary Biliary Cirrhosis (PBC) Overview of Biliary Disease • Biliary colic Defn: Cystic duct obstruction • Cholecystitis Features – Acute – Chronic • Cholangitis – Acute – Primary Sclerosing (PSC) • Primary Biliary Cirrhosis (PBC) – 2° gallstone • Epigastric / RUQ pain – Resolves <6hrs – Usu. constant • Otherwise: colicky – Intermittent pain 2° gallbladder contractn – Quality: • Aching • Tightness – Location: • Epigastric (usually) • RUQ ± Referred pain: shoulder / scapula Overview of Biliary Disease • Biliary colic Defn: Gallbladder inflammation • Cholecystitis Features – Acute – Chronic • Cholangitis – Acute – Primary Sclerosing (PSC) • Primary Biliary Cirrhosis (PBC) – 2° cholestasis from blocked cystic duct • Epigastric / RUQ pain – Persists >6hrs – Usu. constant • Otherwise: colicky – Intermittent pain 2° gallbladder contractn – Quality: • Aching • Tightness – Location: • Epigastric (usually) • RUQ ± Referred pain: shoulder / scapula Overview of Biliary Disease • Biliary colic • Cholecystitis – Acute – Chronic • Cholangitis – Acute – Primary Sclerosing (PSC) • Primary Biliary Cirrhosis (PBC) Defn: Infection & inflammation of CBD Features • • • RUQ pain Jaundice Fever (CHARCOT’s TRIAD) Cholecystitis Aetiology • 90% ‘Calculous cholecystitis’: gallstones obstructing of cystic duct causing inflammation of gallbladder • 10% ‘Acalculous cholecystitis’: inflammation of gallbladder without associated stones • Bile cultures are positive for bacteria in 5075% of cases but bacterial proliferation may be A RESULT of cholecystitis and not the precipitating factor Risk factors Calculous Cholecystitis: •Female sex •Obesity or rapid weight loss •Increasing age •Pregnancy (elevated progesterone levels cause biliary stasis) •Drugs- especially hormonal therapy in women Acalculous Cholecystitis: Conditions associated with biliary stasis • Critical illness • Major surgery/severe burns or trauma • Sepsis • Long-term total parenteral nutrition (TPN) • Prolonged fasting Clinical Presentation-History • Pain begins in epigastric region • Localizes to RUQ, radiating to the scapula/right shoulder • Pain described as colicky initially but usually becomes constant • Nausea and vomiting • Fever • History of biliary pain but differentiated from biliary colic by persistence of severe constant pain >6hours Clinical Presentation-Examination • Fever, tachycardia • Tenderness in RUQ often with guarding or rebound tenderness • ‘Murphy Sign’ tenderness and inspiratory pause elicited during palpation of RUQ • Palpable gallbladder in 30-40% • Jaundice in 15% Clinical Presentation • Absence of findings does not rule out cholecystitis, many present with diffuse epigastric pain without localization to RUQ • Elderly patients and patients with diabetes have often atypical presentations including absence of fever and localized tenderness with only vague symptoms Ix/Dx Lab Tests •Leukocytosis •AST/ALT may be elevated in cholecystitis or common bile duct obstruction •Bilirubin and ALP are elevated in common duct obstruction, ALP is raised in 25% of cholecystitis •Amylase/Lipase used to evaluate for pancreatitis •Urinalysis used to rule out pyelonephritis and renal calculi •All females of childbearing age should undergo pregnancy testing Ix/Dx Abdo Xray: •Gallstones visualized in 10-15% of cases Abdo US: •First line investigation •90-95% sensitive and 80% specific for cholecystitis CT/MRI: •Sensitivity and specificity are >95% •Unlike ERCP, both are non-invasive but not therapeutic Ix/Dx Hepatobiliary Scintigraphy (HBS): •Isotopes are taken up by hepatocytes and secreted into bile, delineating the biliary tree •If the cystic duct and gallbladder do not take up the isotope, it indicates acute cholecystitis Endoscopic Retrograde Cholangiopancreatography (ERCP): •Endoscope passed through duodenum, catheter into ampulla of Vater and contrast medium injected •Allows direct visualization of biliary tree and pancreatic ducts and can perform therapeutic interventions including stone extraction •Better for biliary obstructive jaundice Ix/Dx Management • Gallstones that are not symptomatic do not need treatment • Some people are able to manage mild symptoms with a combination of low fat diet and painkillers Alternatives to Surgery • Dissolution Agent: Ursodeoxycholic Acid (Urdox tablets) – Medication used to dissolve the gallstones – Not effective – takes too long to dissolve gallstone and recurs post treatment cessation – Suitable gallstones • Small • Radiolucent (do not show up on xray) • Gallbladder needs to have the ability to contract • Lithotripsy: using a beam of sound energy to blast the stone – The gallbladder is diseased blasting the stone is not treating – Fragments of the shattered stone will still need to be removed by ERCP – Commonly used for kidney stones Surgery • Laparoscopic cholecystectomy – Removal of the gallbladder and gallstones together (if gallbladder left behind, likely that further stones will develop) – In under 5% of cases convert to open surgery Indications for Cholecystectomy Conditions When to perform surgery Biliary pain First open operative day Biliary dyskinesia First open operative day Calcified gallbladder First open operative day Acute cholecystitis Urgent (within 72 hours) Choledocholithiasis After the common bile duct is cleared Before discharge but after pancreatitis resolves Gallstone pancreatitis Cholecystitis • • • • Nil orally IV fluids Pain relief: Pethidine Surgery Complications of surgery • General – DVT – Anaesthetic complications • Specific – Infection of the wound – Bleeding Cystic artery – Damage to the common bile duct – Damage to abdominal visci Complications: Gallbladder • Biliary colic – Colic: intermittent pain that increases in intensity and them completely disappears – In this case, the pain is PSEUDO-Colic: pain never completely disappears • Chemical cholecystitis – Laceration of gallbladder wall by a stone – Bile to leak into the submucosa Infection • Empyema of the gallbladder Continued inflammation pus Empyema (collection of pus in organ) • Gangrene and necrosis – Inflammation swelling increase in interstitial pressure interstitial pressure = arterial pressure (Cystic artery that supplies gallbladder) stop in arterial flow gangrene and necrosis of gallbladder wall • Perforation (Peritonitis) – Gangrene and necrosis of the gallbladder wall perforation contents seep into peritoneum peritonitis Complications: Other • Obstructive jaundice (stone in common bile duct) – Bile from the liver cannot flow into duodenum – Ascending cholangitis: inflammation of common bile duct • Liver abscess – Infection spread to the liver • Pancreatitis • Gallstone ileus – Impaction of a gallstone in the terminal ileum by passing through a biliary-enteric fistula (often from duodenum) LFT’s ALT Produced by: Elevation Liver AST Liver Cardiac muscle Sk muscle Kidneys Brain Pancreas Lungs RBC and WBC Intra-hepatic pathology - Acute viral - Drug/toxins - Ischaemic liver injury ALP GGT Liver Bone Placenta Liver Biliary epithelium Biliary obstruction Bony disease Biliary obstruction EtOH abuse Warfarin Drugs Normal LFTs Alb Bilirubi n ALP GGT ALT AST >35 <20 Total serum is given. Must ask for conjugated and unconjugated. <120 Raised in post- hepatic pathology <80 <50 Raised in intra- hepatic pathology <50 - Acute viral - Drug/ toxins - Ischaemic liver injury Interpreting LFTs 1 Alb 33 ↓ Bilirubin 90 ↑ ALP 160 ↑ GGT 120 ↑ ALT 2100 ↑↑ AST 1985 ↑↑ Jaundice, viral prodrome (lethargy, nausea, vague abdominal discomfort) Acute hepatitis Alb 33 ↓ Bilirubin 90 ↑ ALP 160 ↑ GGT 120 ↑ ALT 2100 ↑↑ AST 1985 ↑↑ Jaundice, viral prodrome (lethargy, nausea, vague abdominal discomfort) ACUTE HEPATITIS (acute inflammation) e.g. OD on paracetamol, viral hep, EBM/ CMV, autoimmune hepatitis Interpreting LFTs 2 Alb 30 ↓ Bilirubin 400 ↑ ALP 900 ↑↑ GGT 915 ↑↑ ALT 60 ↑ AST 55 ↑ Obstructive jaundice Alb 30 ↓ Bilirubin 400 ↑ ALP 900 ↑↑ GGT 915 ↑↑ ALT 60 ↑ AST 55 ↑ OBSTRUCTIVE JAUNDICE Pain cholangitis (sudden dilatation) Painless pancreatic tumour (gradual increase in pressure) Interpreting LFTs 3 Alb Bilirubin ALP GGT >35 50 250 120 + Increased WCC ↑ ↑↑ ↑↑ (variable) ALT AST 80 80 ↑ ↑ Cholangitis Alb Bilirubin ALP GGT >35 50 250 120 ↑ ↑↑ ↑↑ ALT AST 80 80 ↑ ↑ + Increased WCC CHOLANGITIS – infection of the biliary tree. Increase in ALT/ AST as there is a dilatation of tight junctions in liver due to biliary obstruction and increased intraluminal pressure. Due to stasis (blockage), the bile is often infected, and enters the blood stream risk of sepsis, thus EMERGENCY Histology: yellow because of bile Interpreting LFTs 4 Alb 30 ↓ Bilirubin 60 ↑ ALP 160 ↑↑ GGT 300 ↑↑ ALT 70 ↑ AST 150 ↑ Alcoholic hepatitis or cirrhosis Alb 30 ↓ Bilirubin 60 ↑ ALP 160 ↑↑ GGT 300 ↑↑ ALT 70 ↑ AST 150 ↑ ALCOHOLIC HEPATITIS OR CIRRHOSIS Usually ALT mirrors AST, but in alcoholic hepatitis, there is: 2:1 ratio of AST: ALT Isolated increase in GGT - Alcohol (not alcoholic hepatitis) - Phenytoin Bilirubin 1 1) Fragile RBCs phagocytosed by macrophages • Aka Reticulendothelial system • Within macrophages: • Haemoglobin split globin & heme • Heme breakdown products Biliverdin Bilirubin 2) Free bilirubin – Transported through blood plasma bound • With albumin – Transported to liver Bilirubin 2 3) Liver conjugates free bilirubin conjugated bilirubin – With glucuronic acid • Makes bilirubin H2O soluble 4) In intestines: Conjugated bilirubin urobilinogen – By bacterial action 5) Urobilinogen – Reabsorbed into plasma (5%) • Excreted by kidneys – Oxidised in intestines stercobilin • Excreted in faeces Jaundice • Definition = yellow discolouration of tissue due to increased bilirubin concentration in blood Types • Prehepatic (haemolytic) • Intrahepatic • Post-hepatic (obstructive) Pre-hepatic jaundice • Excessive haemolysis (destruction of RBC) increased bilirubin • Liver cannot conjugate the bilirubin as rapidly as it is formed • Increased free unconjugated bilirubin bound to albumin in blood plasma • ↑ urobilinogen excreted in urine Intra-hepatic jaundice • Poor hepatocyte function impaired uptake, transport and conjugation of bilirubin (unconjugated and conjugated) Conjugated bilirubin AST or ALT Prehepatic Intrahepatic Posthepatic Absent ↑ ↑ ↑ ↑ ALP Urine Bilirubin Absent Present Present Urine Urobilinogen Present Present Absent Post-hepatic jaundice • Due to cholestasis (obstruction of bile ducts) gallstones or pancreatic tumour • Causes impaired excretion of conjugated bilirubin into intestine, HENCE conjugated bilirubin reflux to blood – Increased conjugated bilirubin (H20 soluble) increased bilirubin and bilirubinuria – No conjugated bilirubin into intestine no oxidation into stercobilin • CLINICAL PICTURE= jaundice, dark urine, pale stools