A woman with abdominal pain….
Michelle PapandonyAmanda Vo
Veronica MezhovWei 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
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)
Definitions
• Cholestasis =
• Cholelithiasis =
• Choledocholithiasis =
Obstruction of bile flow
Gallstone(s) within the gallbladder
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 DiseaseDefn: Cystic duct obstruction
– 2° gallstone
Features•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
• Biliary colic
• Cholecystitis– Acute– Chronic
• Cholangitis– Acute– Primary Sclerosing (PSC)
• Primary Biliary Cirrhosis (PBC)
Overview of Biliary DiseaseDefn: Gallbladder inflammation
– 2° cholestasis from blocked cystic duct
Features•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
• Biliary colic
• Cholecystitis– Acute– Chronic
• Cholangitis– Acute– Primary Sclerosing (PSC)
• Primary Biliary Cirrhosis (PBC)
Overview of Biliary DiseaseDefn: Infection & inflammation of CBD
Features (CHARCOT’s TRIAD)•RUQ pain •Jaundice•Fever
• Biliary colic
• Cholecystitis– Acute– Chronic
• Cholangitis– Acute– Primary Sclerosing (PSC)
• Primary Biliary Cirrhosis (PBC)
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 50-75% of cases but bacterial proliferation may be A RESULT of cholecystitis and not the precipitating factor
Risk factorsCalculous 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/DxLab 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/DxAbdo 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/DxHepatobiliary 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
Gallstone pancreatitis Before discharge but after pancreatitis resolves
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 gallbladderContinued 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 AST ALP GGT
Produced by:
Liver Liver Cardiac muscleSk muscle KidneysBrainPancreasLungsRBC and WBC
LiverBone Placenta
Liver Biliary epithelium
Elevation Intra-hepatic pathology -Acute viral -Drug/toxins -Ischaemic liver injury
Biliary obstruction Bony disease
Biliary obstruction EtOH abuse WarfarinDrugs
Normal LFTs
Alb >35
Bilirubin
<20 Total serum is given. Must ask for conjugated and unconjugated.
ALP <120 Raised in post- hepatic pathology
GGT <80
ALT <50 Raised in intra- hepatic pathology-Acute viral-Drug/ toxins-Ischaemic liver injury
AST <50
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 jaundiceAlb 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 3Alb >35 -Bilirubin 50 ↑ALP 250 ↑↑GGT 120 ↑↑ (variable)
ALT 80 ↑AST 80 ↑
+ Increased WCC
Cholangitis Alb >35 -
Bilirubin 50 ↑
ALP 250 ↑↑
GGT 120 ↑↑
ALT 80 ↑
AST 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 ↑
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
ALCOHOLIC HEPATITIS OR CIRRHOSIS
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 1
Bilirubin 23) 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)
Prehepatic Intrahepatic Posthepatic
Conjugated bilirubin
Absent ↑ ↑
AST or ALT ↑
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