The gall bladder and bile ducts - PowerPoint Presentation

Slide1

The gall bladder and bile ducts

Haneen

Omar Abu Hani

Slide2

Anatomy

The gallbladder lies on the underside of the liver

at

the junction of the right and left lobes of the liver. It is intraperitoneal, pear-shaped sac, 7.5–12cm long, with a normal capacity of about 25–30mL.The anatomical divisions are a fundus, a body and a neck that terminates in a narrow infundibulum. The mucous membrane contains indentations of the mucosa, called the crypts of Luschka.The mucosa of the cystic duct is arranged in spiral folds known as the valves of Heister and the wall is surrounded by a sphincteric structure called the sphincter of Lütkens.

Slide3

Calot’s triangle

(Hepatobiliary triangle)

:

space bordered by :1-Cystic duct inferiorly2-Common hepatic duct medially3-Cystic artery superiorlyContents: Calot’s nodeIt is an important surgical landmark as the cystic artery usually can be found within it.

Slide4

The Biliary Tree

The

biliary tree is a series of gastrointestinal ducts allowing newly

synthesised bile from the liver to be concentrated and stored in the gallbladder (prior to release into the duodenum).Bile is initially secreted from hepatocytes and drains from both lobes of the liver via canaliculi, intralobular ducts and collecting ducts into the left and right hepatic ducts. These ducts amalgamate to form the common hepatic duct, which runs alongside the hepatic vein.

Slide5

As the common hepatic duct descends, it is joined by the

cystic duct

– which allows bile to flow in and out of the gallbladder for storage and release. At this point, the common hepatic duct and cystic duct combine to form the

common bile duct.The common bile duct descends and passes posteriorly to the first part of the duodenum and head of the pancreas. Here, it is joined by the main pancreatic duct, forming the hepatopancreatic ampulla (commonly known as the ampulla of Vater) – which then empties into the 2nd part of the duodenum via the major duodenal papilla. This papilla is regulated by a muscular valve, the sphincter of Oddi.

Slide6

Functions of the gallbladder:

It is

a reservoir for bile.

Concentration of bile by active absorption of water, sodium chloride and bicarbonate via the mucous membrane of the gallbladder. It becomes concentrated 5–10 times.secretion of mucus – approximately 20mL is produced per day. a mucocoele may develop as a result of ongoing mucus secretion by the gallbladder mucosa.

Slide7

Surgical

physiology

Bile

is produced by the liver and stored in the gallbladder,from which it is released into the duodenum. As it leaves the liver it is composed of 97% water, bile salts,phospholipids, cholesterol and bilirubin. The liver excretes bile at a rate estimated to be approximately 40mL/hour.About 95% of bile salts are reabsorbed in the terminal ileum (enterohepatic circulation).

Slide8

The

arterial supply to the gallbladder is via the

cystic artery

– a branch of the right hepatic artery (which itself is derived from the common hepatic artery, one of the three major branches of the coeliac trunk).Venous drainage of the neck of the gallbladder is via the cystic veins, which drain directly into the portal vein. Venous drainage of the fundus and body of the gallbladder flows into the hepatic sinusoids.The gallbladder receives parasympathetic (vagus nerve), sympathetic and sensory innervation (coeliac plexus).

Slide9

The

lymphatic vessels of the gallbladder (

subserosal

and submucosal) drain into cystic lymph nodes of Lund, situated at the junction of the cystic and common hepatic ducts, then emptying into the hepatic lymph nodes, and ultimately, the coeliac lymph nodes.The subserosal lymphatic vessels of the gallbladder also connect with the subcapsular lymph channels of the liver, and this accounts for the frequent spread of carcinoma of the gallbladder to the liver.

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Cholelithiasis

Slide11

- Cholelithiasis refers to the

presence of abnormal concretions (gallstones) in the gallbladder

.

Gallstones are the most common biliary pathology. It is estimated that gallstones affect 10–15% of the population in Western societies. They are asymptomatic in the majority of cases (>80%). Approximately 1–2% of asymptomatic patients will develop symptoms requiring surgery per year, making cholecystectomy one of the most common operations performed by general surgeons

Slide12

Gallstones form as a result of

supersaturation

of the bile.

There are three main types of gallstones:Cholesterol stones – composed purely of cholesterol, from excess cholesterol productionThere is a well recognised link between poor diet, obesity, and cholesterol stonesPigment stones – composed purely of bile pigments, from excess bile pigments production, There are two types: black and brown.Black stones are largely composed of an insoluble bilirubin pigment polymer mixed with calcium phosphate and calcium bicarbonate. The incidence is 20–30% & it rises with age. They are associated with haemolysis & cirrhosis.Brown pigment stones contain calcium bilirubinate, calcium palmitate and calcium stearate, as well as cholesterol

. They are rare.

Mixed stones

– comprised of both cholesterol and bile pigments.

In the USA

and Europe

80% are cholesterol or mixed stones, whereas in

Asia 80

% are pigment stones.

Slide13

Risk Factors

Classically the common risk factors for gallstone disease are colloquially described as the “

5 F’s

”: Fat, Female, Fertile, Forty, and Family history.Other recognised risk factors include pregnancy and oral contraceptives*, haemolytic anaemia (specifically for pigment stones), and malabsorption such as: previous ileal resection; (which diminishes the enterohepatic circulation, will deplete the bile acid pool and result in cholesterol supersaturation) or Crohn’s disease.*Oestrogen causes more cholesterol to be secreted into bile

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Clinical Features

80% of patients are

asymptomatic, being

detected incidentally as imaging is performed for other symptoms.Biliary colic is typically present in 10–25% of patients.Gallstone found incidentally on an ultrasound scan in an asymptomatic patient

Slide16

Biliary Colic

Biliary colic occurs when the gallbladder neck becomes impacted by a gallstone. There is no inflammatory response, yet the contraction of the gallbladder against the occluded neck will result in pain.

The pain is typically sudden, dull, and colicky in nature which

ebbs and flows. It is often focused in the right upper quadrant although it may radiate to the epigastrium,chest and/or back. The pain may be precipitated by the consumption of fatty foods* and the patient often complains of nausea / vomiting. In general, once pain relief has been started, symptoms often settle quickly.Other symptoms include dyspepsia, flatulence, food intolerance*Fatty acids stimulate the duodenum endocrine cells to release cholecystokinin (CCK), which in turn stimulates contraction of the gallbladder.

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Slide18

Cholecystitis

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Acute cholecystitis refers to

the acute inflammation of the gallbladder

, which is typically due to

cystic duct obstruction by a gallstone (acute calculous cholecystitis). Acalculous cholecystitis is less common and is seen predominantly in critically ill patients and those recovering from major surgery, trauma and burns.

Slide20

Etiology

Acute calculous cholecystitis

:

most common form, 90%Cause: obstructing cholelithiasisPathophysiology- Cholelithiasis → passage of gallstones into the cystic duct → cystic duct obstruction → distention and inflammation of the gallbladder - Secondary bacterial infection may also be present (E. coli, Klebsiella, Enterobacter, Enterococcus spp. most common) but is not necessary for the development of cholecystitis. Acalculous cholecystitis: 5–10% of acute cholecystitisAcute

and chronic inflammation of the gallbladder can

occur in

the absence of stones

The diagnosis

is often missed and the mortality rate is high

. Treatment is drainage

Slide21

Clinical features

Patients with acute cholecystitis will report:

Constant pain in the RUQ

or epigastriumTypically more severe and prolonged (> 6 hours) than in biliary colicPostprandialRadiation to the right scapula (due to referred pain from phrenic nerve irritation)- Signs of inflammation, such as fever or lethargy.positive Murphy’s signguarding (may suggest a gallbladder perforation) and for features of sepsis.Boas’ sign: referred right subscapular painAcute cholecystitis should always be suspected in a patient with a history of gallstones who presents with RUQ pain, fever, and leukocytosis

Slide22

Murphy’s Sign

Sudden pausing during inspiration upon deep palpation of the RUQ due to pain.

*Murphy sign may be falsely negative in patients > 60 years

*This can be achieved more accurately with an ultrasound, namely the sonographic Murphy sign.

Slide23

Differential Diagnosis

There are a wide variety of pathologies that can present with RUQ pain. However, differentials to consider include:

gastro-

oesophageal reflux disease peptic ulcer disease acute pancreatitis, or Inflammatory bowel disease.# Dr note: acute pyelonephritis is more common differential than perforated peptic ulcer.

Slide24

Investigations

1. Laboratory Test

Certain blood tests can help in the initial evaluation of suspected cases:

FBC and CRP – assess for the presence of any inflammatory response, which will be raised in cholecystitisLFTs – biliary colic and acute cholecystitis are likely to show a raised ALP (indicating ductal occlusion), yet ALT and bilirubin should remain within normal limits (unless a Mirizzi syndrome, discussed later on)Amylase (or lipase) – to check for any evidence of pancreatitisA urinalysis, including a pregnancy test if relevant, should be performed to exclude any renal or tubo-ovarian pathology.

Slide25

2. Imaging

A trans-abdominal ultrasound is one of

the most sensitive modalities

for visualising gallstone disease and is typically used first line to investigate suspected gallstone pathology.Characteristic findings:Gallbladder wall thickening > 3–5 mm Gallbladder distension (8–10 x 4 cm)Gallbladder wall edema (double-wall sign): The innermost and outermost layers appear hyperechoic; edematous tissue appears as a hypoechoic layer in between.Sonographic Murphy signPericholecystic free fluid Presence of gallstones and/or biliary sludge (the start of gallstone formation)In emphysematous cholecystitis, mural air appears as hyperechoic shadows within the gallbladder wall.

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If results from US scans are inconclusive, further imaging options are available. The gold standard investigation* for gallstones is Magnetic Resonance

Cholangiopancreatography

(

MRCP), largely replacing ERCP for diagnostic purposes (Fig. 3). MRCP can show potential defects in the biliary tree caused by gallstone disease, with a sensitivity approaching 100%.*Any patient with symptoms suggestive of gallstones with inconclusive US (or CT scans) should undergo a MRCP

Slide27

Hepatoiminodiacetic acid scintigraphy (HIDA scan

):

Indications

: preferred confirmatory test for suspected uncomplicated acute cholecystitis if ultrasound findings are inconclusive.It can differentiate between acute and chronic cholecystitis.

Slide28

Management

Biliary Colic

Patients with biliary colic should be prescribed analgesia (regular paracetamol +/- NSAIDs +/- opiates analgesia).

The patient should be advised about lifestyle factors that may help control symptoms (and help with future surgery), such as a low fat diet, weight loss, and increasing exercise.Following first presentation of biliary colic, there is a high chance of symptom recurrence or the development of complications of gallstones, therefore an elective laparoscopic cholecystectomy* is warranted and should be offered within 6 weeks of first presentation.*The laparoscopic route is preferred for cholecystectomy but is not always possible

Slide29

Management

A

cute cholecystitis:

patients with should be started on appropriate intravenous antibiotics (such as co-amoxiclav +/- metronidazole). Concurrent analgesia and antiemetics should also be prescribed.A laparoscopic cholecystectomy is indicated within 1 week of presentation, as per NICE guidance, however this ideally should be done within 72hrs of presentation for a likely simpler procedure*.For those not fit for surgery and not responding to antibiotics, a percutaneous cholecystostomy can be performed to drain the infection (although as the gallstones remain in-situ, the risk of recurring disease remains).*In high-risk patients with severe cholecystitis, a temporizing gallbladder drainage procedure (e.g., percutaneous cholecystostomy) should be performed and elective interval cholecystectomy scheduled after the resolution of acute symptoms.Any patient readmitted with RUQ pain post-cholecystectomy, it is important to exclude a retained CBD stone post-operatively. US abdomen scan may be useful, yet if this is unremarkable, then further investigation via MRCP imaging is warranted.

Slide30

Complications

Mirizzi

Syndrome

A stone located in Hartmanns pouch (an out-pouching of the gallbladder wall at the junction with the cystic duct) or in the cystic duct itself can cause compression on the adjacent common hepatic duct.This results in an obstructive jaundice, even without stones being present within the lumen of the common hepatic or common bile ducts. Diagnosis is confirmed by MRCP and management is usually with laparoscopic cholecystectomy. Figure 5 – Mirizzi syndrome causes by a stone lodged in Hartmann’s pouch, compressing the common hepatic duct

Slide31

Gallbladder Empyema

It occurs when the gallbladder becomes filled with pus.

Patients will become unwell, often septic, presenting with a similar clinical picture to acute cholecystitis.

They are associated with significant morbidity and mortality.The condition is diagnosed by either US scan or CT scan. Treatment is via laparoscopic cholecystectomy* (may require intra-operative drainage if tense gallbladder) or percutaneous cholecystostomy (if unsuitable for surgery).*There is a higher rate of conversion to open cholecystectomy with emypema than with uncomplicated acute cholecystitis

Slide32

Chronic Cholecystitis

Patients with chronic cholecystitis will typically have a history of recurrent or untreated cholecystitis, which has led to a persistent inflammation of the gallbladder wall.

Patients present with ongoing RUQ or epigastric pain with associated nausea and vomiting.

It can be diagnosed typically by CT imaging (or often noted on histology post-cholecystectomy). Management in uncomplicated cases is via elective cholecystectomy. Its main complications are gallbladder carcinoma and biliary-enteric fistula.

Slide33

Bouveret’s

Syndrome and Gallstone Ileus

Inflammation of the gallbladder (typically if recurrent) can cause a fistula to form between the gallbladder wall and the small bowel, termed a

cholecystoduodenal fistula, allowing gallstones to pass directly into the small bowel (typically at the duodenum)As a consequence, bowel obstruction can occur:Bouveret’s Syndrome – a stone impacts in the proximal duodenum, causing a gastric outlet obstructionGallstone Ileus*– a stone impacts at the terminal ileum (the narrowest part of the small bowel), causing a small bowel obstruction*The term ileus is misleading, as it is actually a bowel obstructionFigure 7 – A Cholecystoduodenal Fistula, resulting in a gallstone entering the small bowel

Slide34

Emphysematous cholecystitis (EC)

a rare but life-threatening form of acute cholecystitis characterized by air within the gallbladder wall that is caused by gas-forming bacteria (e.g., Clostridium spp., E.coli)

It is most commonly seen in elderly diabetic men (esp. 50–70 years of age) It is often results in perforation of gallbladder. Clinical features: Similar to acute calculous cholecystitis: fever, RUQ pain, referred pain , Symptoms progress rapidly. Associated with early gangrene and gallbladder perforation DiagnosticsImaging: The characteristic feature of EC on imaging is air within the gallbladder wall or lumenRUQ ultrasound : hyperechoic air shadows within the gallbladder wall, and within bile in the gallbladder lumen Abdominal x-ray : radiolucent rim outlining the gallbladder (pear-shaped radiolucency)If gas is present in:- Biliary tree > Think of fistula.- In gallbladder wall >think of emphysematous GB.

Slide35

Xanthogranulomatous cholecystitis

A

rare inflammatory disease of the gallbladder characterized by a focal or diffuse destructive inflammatory

process that leads to formation and accumulation of xanthoma cells.➢ Its importance lies in the fact that it is a benign condition that may be confused with carcinoma of the gallbladder.

Slide36

Choledocholithiasis

Slide37

Choledocholithiasis

It refers to the

presence of gallstones in the common bile duct.

Slide38

Etiology

Secondary

choledocholithiasis

(most common): cholelithiasis → passage of gallstones into the common bile duct → common bile duct obstruction → spasm of the biliary tractsRisk factor: a history of cholelithiasis Primary choledocholithiasis (less common): conditions predisposing to bile stasis → intraductal stone formationRisk factors:- Cystic fibrosis- Prolonged total parenteral nutritionPostcholecystectomy choledocholithiasis Residual choledocholithiasis: CBD stones missed during cholecystectomy; typically becomes symptomatic within 2 years of surgery

Recurrent

choledocholithiasis

: CBD stones that developed after cholecystectomy, typically detected after 2 years of surgery

Risk factors for recurrent stones:

periampullary

duodenal diverticulum, dilated CBD, CBD stricture, chronic cholangitis, sickle cell anemia, and rapid weight loss (e.g., after bariatric surgery)

Slide39

Clinical features

RUQ pain

- More severe and prolonged (may last > 6 hours) than in

cholelithiasis- Postprandial- May radiate to the epigastrium, right shoulder, and back (referred pain) Nausea, vomiting, anorexiaSigns of extrahepatic cholestasis (e.g., jaundice, pale stool, dark urine, pruritus) may be present Features of complications

Slide40

Diagnosis

Laboratory studies

LFTs

Characteristic findings: evidence of cholestasis, i.e., ↑ ALP, ↑ GGT, ↑ total and ↑ direct bilirubin *Tests to rule out related biliary comorbidities CBC: Leukocytosis is seen in cholecystitis or cholangitis. Amylase, lipase: elevated in biliary pancreatitis

Slide41

Imaging

1.Transabdominal RUQ ultrasound

Indications: preferred first-line imaging modality in patients presenting with RUQ pain and/or jaundice

*Supportive findingsDilated common bile duct (CBD): Normal CBD diameter varies according to patient age and whether the gallbladder is intact or has been surgically removed. Gallbladder in situ, age < 50 years: CBD diameter > 6 mm Gallbladder in situ, age > 50 years: CBD diameter > 8 mmPostcholecystectomy patients: CBD diameter > 10 mmIntrahepatic biliary dilatation may be seen.Visualization of an occluding CBD stone Stone(s) within the gallbladder2. CT abdomen with IV contrast: not routinely recommended

Slide42

Confirmatory imaging and further management

Endoscopic retrograde

cholangiopancreatography

(ERCP)Contraindication (for urgent ERCP): acute biliary pancreatitis without evidence of cholangitis or biliary obstruction.Characteristic findings- Smooth-walled, well-defined, intraluminal filling defect(s) within the CBD, which may be dilated.- Dilation of the intrahepatic biliary tree- Cholelithiasis: mobile filling defect(s) within the gallbladder lumen 2. Magnetic resonance cholangiopancreatography (MRCP)

Slide43

Differential diagnosis

* Differential diagnosis of jaundice with dilated biliary duct

- Biliary stricture

- Pancreatic carcinoma (head of pancreas)- Cholangiocarcinoma- Mirizzi syndrome- Extrinsic compression of the bile duct (e.g., lymphadenopathy at the porta hepatis)

Slide44

Treatment

* Treatment is recommended in all patients with

choledocholithiasis

, even if asymptomatic. The mainstay of treatment is the removal of the obstruction.Approach 1. Provide supportive therapy for patients with acute symptoms; analgesics, spasmolytics, and antiemetics.2. NPO in patients with acute pain 3. Identify and manage any complications (e.g., acute pancreatitis, cholangitis, cholecystitis).4. Removal of choledocholithiasis; endoscopically (ERCP) or surgically (LCBDE; Laparoscopic bile duct exploration).5. Elective cholecystectomy to prevent recurrence

Slide45

Complications

1.

Gallstone ileus

: mechanical bowel obstruction due to obstructive gallstones * Pathophysiology: gallbladder perforation or Mirizzi syndrome → biliary-enteric fistula formation (most commonly cholecystoenteric fistula) between the inflamed gallbladder and bowel → gallstones passing down into bowel lumen* Sites of obstruction- Terminal ileum, at ileocecal valve (most common) - Gastric pylorus or duodenum* Symptoms depend on the site of obstruction.- Distal bowel obstruction: features of mechanical bowel obstruction (abdominal pain and distention, nausea, vomiting)- Gastroduodenal obstruction (rare): features of gastric outlet obstruction (Bouveret syndrome).

Slide46

* Diagnosis is based on the

Rigler

triad

: imaging findings of small bowel obstruction, gallstone (most commonly in iliac fossa), and pneumobilia. * Treatment - Initial supportive therapy- NPO, IV fluid resuscitation, analgesics, antiemetics, nasogastric tube insertion- Empiric antibiotic therapy for intra-abdominal infections - Enterolithotomy: emergency surgery to remove the obstructing stone - Consider cholecystectomy and closure of the biliary-enteric fistula.

Slide47

Complications

2.

Gallstone pancreatitis

3. Acute cholangitis4. Acute cholecystitis5. Biliary stricture6. Pyogenic liver abscess

Slide48

Cholangitis

Slide49

Introduction

Cholangitis

refers to infection of the biliary tract. It is associated with high morbidity and mortality when left untreated, and therefore is an important condition to

recognise and manage.It is caused by a combination of biliary outflow obstruction* and biliary infection. During an obstruction, stasis of fluid allows the bacterial colonisation of the biliary tree to become pathological.*In patients without outflow obstruction, a bacterial colonisation is unlikely to cause cholangitis

Slide50

Causes

Any condition which causes occlusion of the biliary tree has the potential to cause cholangitis.

The most common causes are

gallstones, ERCP (iatrogenic), and cholangiocarcinoma. Rarer causes include pancreatitis, primary sclerosing cholangitis, ischaemic cholangiopathy, and parasitic infections.The most common infective organisms implicated in cholangitis are Escherichia Coli (27%), Klebsiella species (16%), and

Enterococcus

(15%).

Slide51

Clinical Features

The common presenting symptoms of cholangitis are

right upper quadrant pain,

fever,and jaundice (when bilirubin >50 μmol/L). The patient may also complain of pruritus (itching), as a result of bile accumulation, and pale stool with dark urine, from the obstructive jaundice.The patient’s past medical history may include gallstones, recent biliary tract instrumentation (i.e. ERCP/cholecystectomy), or previous cholangitis. Medication including oral contraceptive pill and fibrates can increase the risk, and a lipid-rich diet may be indicative of gallstones (as a potential underlying cause).On examination, patients may have pyrexia (in 90% of cases), rigors, jaundice, right upper quadrant tenderness, confusion, hypotension, and tachycardia may be present.

Slide52

Two common eponymous syndromes associated with cholangitis are:

Charcots

Triad

: Jaundice, Fever, and RUQ PainReynold’s Pentad: Jaundice, Fever, and RUQ Pain, Hypotension, and ConfusionFigure –The clinical features of Charcot’s Triad: Jaundice, Fever, and Abdominal Pain

Slide53

Differential Diagnosis

Cholangitis is

not a complete diagnosis

, as there is nearly always an underlying cause that should be identified and treated.The clinical features of cholangitis are very similar to other biliary pathologies. A biliary colic will present with a colicky RUQ pain yet without fever, leucocytosis, or jaundice. Cholecystitis will present with RUQ pain and fever yet jaundice will be absent.

Slide54

Investigations

Laboratory Tests

FBC

(leucocytosis is found in the vast majority of patients) and LFTs (showing a raised ALP ± GGT with a raised bilirubin).Blood cultures should always be taken in suspected cases, despite only being positive in 20% of cases. The best opportunity to obtain a positive blood culture is early, before the start of broad spectrum antibiotics.

Slide55

Imaging

An

ultrasound

scan of the biliary tract will show: bile duct dilation. The common bile duct is usually less than 6mm in size (it may be greater in the elderly and those who have had previous cholecystectomy), so any diameter larger than this suggests dilatation. It may also demonstrate the presence an underlying cause (e.g. gallstones).The gold standard investigation for cholangitis is ERCP, as it is both diagnostic and therapeutic. Many endoscopists may require an MRCP prior to intervention, however to obtain detailed imaging of the biliary system prior to scoping.Figure 3 – ERCP showing an obstruction in the biliary tree, resulting in cholangitis.

Slide56

Management

Immediate Management

Patients with cholangitis may present with sepsis, so should be managed promptly, appropriately and often in a higher level of care.

IV accesssufficient fluid resuscitation, routine bloods, and blood cultures taken early, with broad spectrum IV antibiotic therapy instigated (e.g. co-amoxiclav + metronidazole).

Slide57

Definitive Management

Endoscopic

biliary decompression: it is the definitive management of cholangitis is via, removing the cause of the blocked biliary tree. For patients who are deteriorating, this may need to be done earlier than those who are responding well to antibiotic therapy. ERCP, with or without a sphincterotomy and stenting, should clear any obstruction.It is important to remember that there are significant complications of ERCP, including repeated cholangitis, pancreatitis (in 3-5% of patients), bleeding (more common when a sphincterotomy is performed), and perforation (a rare complication yet requires urgent surgical intervention if present) Percutaneous transhepatic cholangiograpy (PTC) is the second line intervention, in

patients who may be too sick to tolerate ERCP

In the long-term, patients may require a

cholecystectomy

if gallstones were the underlying cause. Any other cause for the cholangitis identified should also be managed as appropriate.

Slide58

Prognosis

The mortality of cholangitis is around 5-10% in those who are given antibiotic therapy. Early ERCP and early antibiotic therapy have both been found to improve patient outcomes.

Factors which increase the mortality rate include

delayed diagnosis, liver failure, cirrhosis, CKD, hypotension, female gender, and >50yrs

Slide59

Porcelain gallbladder

It is

a calcification of the gallbladder

caused by excessive gallstones, although the exact cause is not clear. This condition occurs predominantly in overweight female patients of middle age. It is usually found incidentally on plain abdominal x-rays or other imaging because most patients are asymptomatic. It is a morphological variant of chronic cholecystitis.Inflammatory scarring of the wall, combined with dystrophic calcification transforms the gallbladder into a porcelain-like vessel. Removal of the gallbladder (cholecystectomy) is the recommended treatment.The risk of cancer in a porcelain gallbladder is 15%.

Slide60

Thank you