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