Acute Cholecystitis Flashcards
Define Acute Cholecystitis
What are the 2 main types?
Briefly explain the pathogenesis of acute cholecystitis
Inflammation of the gallbladder most commonly due to obstruction of the outlet of the gallbladder (cholelithiasis)
90% Calculous cholecystitis: caused by gallstones
10% Acalculous cholecystitis: caused by dysfunction in emptying
Obstruction => distension => compromise of blood supply and lymphatics => ischemia of walls of gallbladder => infection => eventual necrosis
A patient presents with RUQ pain. Quickly top 5 differentials
Top 5: Acute cholecystitis, billiary colic, ascending cholangitis, perforated duodenal ulcer, acute pancreatitis
Others: Acute hepatitis, trauma. AAA, Mesenteric Ischemia, Gastritis, retrocecal appendicitis, nephrolithiasis
What is the difference between acute cholecystitis and obstructive jaundice
This is to clarify an important concept
Acute cholecystitis refers to the gallstone in the neck or cystic duct of the gallbladder => not obstructing common bile duct. => mild jaundice, mild rise in ALP
Obstructive jaundice refers to the obstruction of the common bile duct which would affect everything distal to it including the common hepatic duct => severe jaundice and dramatic rise in ALP.
It can even go further and affect the pancreatic duct leading to acute pancreatitis => why we always check amylase
The gallbladder stores up to 50ml of bile.
What are the components of bile?
How is bile secretion stimulated?
Explain the path of bile from stimulation.
Bile is composed of bilirubin, cholesterol, bile salts, and water
When food is enters the duodenum, it activates stretch receptors and chemoreceptors leading to the secretion of cholecystokinin (produced in brain) which causes contraction of GB and relaxation of sphincter of Oddi
Bile goes through cystic duct where it then meets with common hepatic duct to form the common bile duct. The pancreatic duct also empties here. Then it reaches the sphincter of oddi at the ampulla of vater in the 2nd part of the duodenum
A patient in ICU complains of severe pain in RUQ, developed mild pyrexia, and positive sonographic murphy’s sign. They have been NPO since admission What is the most likely diagnosis?
Acalculous cholecystitis. This is because ICU patients may be on TPN and this patient is already NPO. With TPN the gallbladder is not stimulated since TPN bypasses the GIT => buildup of bile =>dilatation, obstruction….
Why? No food in duodenum => no stimulation for cholecystokinin => no emptying
Give 3 RFs for acalculous cholecystitis
Elderly patients
TPN/ICU patients
surgery
long-term starvation
CMV
With any history concerning the gallbladder, what is an important non-medical question to always ask?
Are certain heavy foods or fatty foods like burger or steak etc… cause the symptoms to become worse?
Describe the typical presentation/clinical features and exam findings of acute cholecystitis
Presentation: RUQ pain => nausea, vomiting, anorexia, weight loss, tachycardia, tachypnea + Pyrexia, worse with fatty foods
Exam: RUQ tenderness +/- guarding
Murphy’s sign (could later be elicited sonographically)
Jaundice (ONLY IN CBD OBSTRUCTION or Mirizzi syndrome)
State 4 complications of acute cholecystitis
1) Sepsis -> ascending choloangitis
2) Perforation -> Peritonitis
3) Empyema/Abscess in gallbladder -> drain
4) Gangrenous gallbladder (negative murphy’s sign)
What is Mirizzi Syndrome
What lab results will be seen with this?
State the curative management?
large stone in Hartmann’s pouch or in the cystic duct, compresses the adjacent common hepatic duct.
Causes obstructive jaundice (rarer cause than CBD obstruction)
WCC >12
LFT very very raised especially ALP and gamma GT
SBR high (=> clinical jaundice >40mmol/L)
Managed as acute surgical emergency. Removal of stone laparoscopically or via open laparotomy if needed.
What are normal levels of SBR?
What level of SBR is considered clinical jaundice?
3-17 mmol/L
Clinical jaundice => visually can see jaundice => 40mmol/L
How would you diagnose a patient with acute cholecystitis?
1) Full Hx and Exam
2) Labs: FBC w/ differentials (WCC>12), CRP (very high), SBR and LFTs (mild increase in SBR, ALP, GGT unless obstructive jaundice), ALWAYS CHECK AMYLASE, U&E. + above
3) US and MRCP looking for calculous
A patient presents with RUQ pain, nausea, vomiting, and pyrexia. You bring in an US probe. Suspecting Acute cholecystitis, what findings are you looking for?
Assume findings were present but you were unable to figure out the cause. What is your next step and what findings are you looking for?
Sonographic Murphy’s sign
Thickening of gallbladder wall
Enlarged gallbladder
Pericholecystic fluid (oedema around gallbladder)
Calculous
Honours: Check neck for Mirizzi
MRCP of the billiary tree looking for calculous and dilatation proximal to obstruction.
Define Sonographic Murphy’s Sign
Honor’s Question:
What would it mean if a patient is presenting with abdominal pain and sonographic findings of cholecystitis in the absence of the sonographic Murphy’s sign?
The abrupt cessation of inspiration due to presence of maximal tenderness elicited by direct pressure of the transducer over a sonographically localized gallbladder
The sonographic murphy’s sign is prevalent in 99% of cases with extremely high accuracy. The absence of it, based on study, indicates gangrenous cholecystitis as it has passed the stage of vitality.
You find a calculous in the CBD. What lab results will be seen here?
State the curative management?
WCC >12
LFT very very raised especially ALP and gamma GT
SBR high (=> clinical jaundice >40mmol/L)
Removal of stone via ERCP -> laparoscopy -> open laparotomy (one extra step from mirizzi)
