Cholangitis Flashcards

1
Q

What is acute cholangitis?

A

infection and inflammation in the bile ducts.

It is a surgical emergency and has a high mortality due to sepsis and septicaemia.

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2
Q

2 main causes of acute cholangitis

A

1.Obstruction in the bile ducts stopping bile flow (i.e. gallstones in the common bile duct)

2.Infection introduced during an ERCP procedure

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3
Q

Epidemiology of Acute (ascending) cholangitis

A

Age >50
M=F
Rare
White, hispanics and Native americans

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4
Q

Aetiology of Acute cholangitis

A
  • Choledocholithiasis, stones in the bile duct, is the most common cause of acute cholangitis.
  • Benign stricture: leading to obstruction, may occur in the biliary tree for numerous reasons
  • Malignant stricture: e.g. cholangiocarcinoma, pancreatic cancer and gallbladder cancer.
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5
Q

RFs for acute cholangitis

A
  • Gallstones:the most common predisposing factor
  • Stricture of the biliary tree:benign or malignant
  • Post-procedure injuryof the bile ducts e.g. post-ERCP
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6
Q

Pathophysiology of Acute cholangitis

A
  • Due to bacterial infection secondary to biliary obstruction
  • Bilary obstruction due to gallstones in bililary tree
  • Obstruction > cholestasis and growth of bacteria - gram negative
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7
Q

Most common organisms that cause acute cholangitis?

A

Escherichia coli
Klebsiella species
Enterococcus species

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8
Q

What is Charcot’s Triad?

A

Acute cholangitis presents with Charcot’s triad:

Right upper quadrant pain
Fever
Jaundice (raised bilirubin)

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9
Q

What is the management for acute cholangitis

A

need emergency admission for investigations and management.
Patients need acute management of sepsis and acute abdomen, including:

Nil by mouth
IV fluids
Blood cultures
IV antibiotics (as per local guidelines)
Involvement of seniors and potentially HDU or ICU

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10
Q

First line investigation for acute cholangitis

A
  • FBC:leukocytosis with neutrophilia
  • LFTs:obstructive jaundice with raised ALP > ALT, and bilirubin
  • U&Es: pre-renal acute kidney injury in sepsis
  • CRP: acute-phase protein and marker of inflammation
  • ## VBG: assess for acidosis and lactate if suspecting sepsis
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11
Q

What imaging do we use to diagnose common bile duct (CBD) stones and cholangitis?

A

Abdominal ultrasound scan
CT scan with IV contrast
Magnetic resonance cholangio-pancreatography (MRCP) - GS
Endoscopic ultrasound

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12
Q

DDs for ascending acute cholangitis

A
  • Acute cholecystitis
  • Peptic ulcer disease
  • Pancreatitis
  • Appendicitis
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13
Q

What procedure is done to remove stones blocking the bile duct?

A

endoscopic retrograde cholangio-pancreatography (ERCP)

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14
Q

What happens during an ERCP?

A

involves inserting an endoscope down the oesophagus, past the stomach, to the duodenum and the opening of the common bile duct (the sphincter of Oddi). This gives the operator access to the biliary system.

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15
Q

What is a Percutaneous transhepatic cholangiogram (PTC)?

A

involves radiologically guided insertion of a drain through the skin and liver, into the bile ducts.

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16
Q

What does a PTC do?

A

drain relieves the immediate obstruction.

A stent can be inserted to give longer-lasting relief of obstruction.

This is an option for patients that are less suitable for ERCP, or where ERCP has failed.

17
Q

What is primary sclerosing cholangitis? (PSC)

A

immune mediated chronic liver disease where the intrahepatic or extrahepatic bile ducts become inflammed, fibrotic and destroyed.

18
Q

What does PSC cause?

A

causes an obstruction to the flow of bile out of the liver and into the intestines.

Sclerosis refers to the stiffening and hardening of the bile ducts, and cholangitis is inflammation of the bile ducts.

Chronic bile obstruction eventually leads to liver inflammation (hepatitis), fibrosis and cirrhosis.

19
Q

What causes PSC?

A

Combo of genetic, autoimmune, intestinal microbiome and environmental factors

Established association with ulcerative colitis -70% of cases associated with this.

20
Q

Epidemiology of PSC

A
  • It is more common in Northern Europe and North America.
  • Male sex:two-fold more common in males than females
  • Age 40-50 years:
21
Q

PSC risk factors

A

Male
Aged 40-50
Ulcerative Colitis
Family History
HLA-A1, B8 and DR3

22
Q

Presentation of PSC

A

Jaundice
Chronic right upper quadrant pain
Pruritus
Fatigue
Hepatomegaly

23
Q

Pathophysiology of PSC

A

AI trigger > intra + extrahepatic bile duct damage > bile duct strictures + Bile and toxins in liver= cirrhosis> Retained toxic bile acids in liver > Liver fibrosis, cirrhosis and end-stage liver disease

24
Q

Primary investigations of PSC

A
  • LFTs - raised ALP and raised bilirubin, raised GGT, raised ALT and AST if liver damage present, decreased albumin.
  • Viral hepatitis screen:screen for HBsAg and anti-HCV in all patients
  • Antibodies screening:
    • pANCA Anti-neutrophil cytoplasmic antibodies: positive in 33-88% of PSC patients, however is not specific
  • MRCP
25
Q

What is the gold standard investigation for diagnosis of PSC?

A

MRCP - magnetic resonance cholangiopancreatography

involves an MRI scan of the liver, bile ducts and pancreas.

In primary sclerosis cholangitis it may show bile duct lesions or strictures.

26
Q

Associations and complications of PSC?

A

Acute bacterial cholangitis
Cholangiocarcinoma develops in 10-20% of cases
Colorectal cancer
Cirrhosis and liver failure
Biliary strictures
Fat soluble vitamin deficiencies

27
Q

Management of PSC

A

ERCP can be used to dilate and stent any strictures

Colestyramine is a bile acid sequestrate in that it binds to bile acids to prevent absorption in the gut and can help with pruritus due to raised bile acids

Healthy life + Fat soluble vitamin supplementation

28
Q

What happens when the cells in the bile ducts become inflamed in PSC?

A
  • Cells die and harden due to fibrosis
  • get this tightening of the ducts in some areas where there’s been serious fibrosis and then dilation in other areas that aren’t as affected, and this leads to the classic PSC finding of this sort of “beaded” appearance of the bile ducts.
29
Q

What is PSC most likely to be and caused by?

A

Certain genetic factors have been linked to developing PSC; studies have shown that patients with PSC tend to have in common specific human leukocyte antigens, or HLAs.

most patients with PSC have elevated IgM antibody levels in the serum, as well as an antibody called p-ANCA.

30
Q

What are the symptoms of PSC similar to?

A

obstructive jaundice, since these “beads” or pinched areas are obstructing the flow of bile.

as these epithelial cells lining the ducts die off, bile can now be allowed to leak out past the cells into the interstitial space, where it can access the bloodstream.

31
Q

How does PSC cause portal hypertension

A
  • Inside the liver, the intra-hepatic bile ducts are in close proximity to portal veins
  • So as fibrosis builds up around the bile ducts, it constricts the portal veins as well and higher pressures develop in the veins, leading to a condition called portal hypertension.
32
Q

How can it cause hepatosplenomegaly?

A

Portal hypertension cause backup of fluid in the spleen and liver and therefore cause enlargement of both, also known as hepatosplenomegaly.

33
Q

How can cirrhosis occur in PSC?

A

Over time, as fibrosis and scar tissue progress in the intrahepatic bile ducts, patients can develop cirrhosis, where the liver stops functioning right from this damage.

34
Q

Cholangiocarcinoma and PSC:

A

due to the constant damage to bile ducts, patients often have a higher risk of cholangiocarcinoma.