GALLBLADDER STONES

Presented by: Amer AlQaisi Faisal AlEnezi

Supervised by: Prof. Kamal Gharaibeh

OUTLINES1. Anatomy of gallbladder2. Anatomy of biliary tree3. Physiology of biliary system4. Bilirubin metabolism cycle.5. Congenital abnormalities6. Gallstones7. Complications of gallstones8. Clinical presentation & Management9. Choledocolithiasis & cholangitis10. Neoplasms

• Gallbladder is a pear-shaped sac lying on the undersurface of the live which is 7.5-12 cm long and it has a capacity of 30-50 ml.

• It is divided to : - Fundus - Body - Neck

The Hartmann's pouch : is a dilatation in the gallbladder just before the origin of cystic duct .

Anatomy of Gallbladder

Relation: Anteriorly :

the anterior abdominal wall and the inferior surface of the liver.

Posteriorly : the transverse colon(proximal)

1st and 2nd part of duodenum.

The fundus is usually projects inferiorly (at the level of the 9th costal cartilage in the midclavicular line) and the neck directed upward backward.

Blood supply:- by the cystic artery , a branch from the right hepatic artery .- cystic vein which drain directly into the portal vein.

The lymph drainage:- into the cystic lymph node of Lund which situated near the neck of the gallbladder.

Nerve supply: supplied by 3 types of innervation, The celiac plexus supplies sympathetic innervation, the vagus nerve supplies parasympathetic innervation, and the right phrenic nerve conveys sensory information.

ANATOMY OF BILIARY TREE

The ducts of biliary tree are : The common hepatic duct :

-it is about 4 cm (result from the union of Rt.& Lt hepatic duct).

Cystic duct : -it is about 3.8 cm, somewhat S shaped

which connect the neck of the gallbladder with the common hepatic duct.

The common bile duct : -it is about 8 -10 cm that is result from

the union of the common hepatic duct with the cystic duct.

• The common bile duct descends behind the duodenum and pancreas and usually joined by pancreatic duct, and together, they open into a small ampulla in the duodenal wall ( ampulla of vater ).

There are a small ducts that drain bile directly into the gallbladder from the liver, called Duct of Luschka .

• Cystohepatic triangle an anatomic space bordered by the common hepatic duct medially, the cystic duct laterally and the inferior edge of the liver superiorly.

•Calot's Triangle : cystic duct, the common hepatic duct, and the cystic artery

PHYSIOLOGY Gallbladder is under control of Cholecystokinin (CCK ) and its

functions are : Contraction of the gallbladder Relaxation of the Sphincter of Oddi Slowing gastric emptying increase pancreatic enzyme secretion

The gall bladder is a reservoir for bile. During fasting, resistance to flow through the sphincter is high, and bile excreted by the liver is diverted to the gall bladder. After feeding, the resistance to flow through the sphincter of Oddi is reduced, the gall bladder contracts, and the bile enters the duodenum. These motor responses of the biliary tract are in part effected by the hormone CCK.

PHYSIOLOGYThe second main function of the gall bladder is concentration

of bile by active absorption of water, sodium chloride and bicarbonate by the mucous membrane of the gall bladder. The hepatic bile that enters the gall bladder becomes concentrated 5–10 times, with a corresponding increase in the proportion of bile salts, bile pigments, cholesterol and calcium.

The third function of the gall bladder is the secretion of mucus– approximately 20 ml is produced per day. With total

obstructionof the cystic duct in a healthy gall bladder, a mucocele

developson account of this function of the mucosa of the gall bladder.

Bile Components of bile:

Water 95%electrolytesbile salts (like cholic acid & chenodeoxycholic acid )phospholipids ( like licithin) bilirubin (conjugated)fatty acids

The function of bile is to emulsify fat.

Absence of bile causing malabsorption of fat and fat soluble vitamins ( A , D , E , K )

95% of bile salts are reabsorbed in the terminal ileum , pass back via the portal venous drainage to the liver and once again secreted in the bile (EHC). So, resection of terminal ileum will decrease bile salts that will cause GB stones formation.

BILIRUBIN PRODUCTION

Heme

Heme oxygenase

Biliverdin reductase

Hemoglobin(70 to 80%)

Heme proteinsmyoglobin, cytochromes

(20 to 25%)

Biliverdin

Bilirubinindirect

unconjugated

pre-hepatic

albumin

BILIRUBIN PROCESSINGalbumin-Bilirubin

ligandin

Bilirubin diglucuronide

ER

hepatocyte

UDP-Glucuronyl transferase

albumin

ligandin-Bilirubin

bile (gall bladder)

directconjugate

dpost-

hepatic

BILIRUBIN EXCRETION

Bilirubin diglucuronide

80% Stercobilinogen

Bacterial enzymes

Bilirubin

Bacterial enzyme2 glucuronate

Bacterial enzyme

Urobilinogen

90% liver

Urobilin10% kidneys

urine

Stercobilin feces

intestines

>--------20%

CONGENITAL ABNORMALITIES Absence of the gall bladder Occasionally, the gall bladder is absent. Failure to

visualise the gall bladder is not necessarily a pathological problem. The Phrygian cap present of septum that incompletely divides the GB.

(SINGLE OR MULTIPLE)

Floating gall bladderThe organ may hang on a mesentery, which makes it

liable to undergo torsion of GB to occur with consequent gangrene & rupture

Double gall bladderRarely, the gall bladder is duplicated. One may be

intrahepatic

Absence of the cystic ductThis is usually a pathological, the GB open directly

ino the side of common bile duct

A long cystic duct travelling alongside the common hepatic duct to open near the duodenal orifice ( occur in 10% of cases )

CHOLEDOCHAL CYST : Presence of cystic dilation in the biliary tree (most commonly in CBD)

Classification according to the site of the cyst or dilatation

Type I: Most common variety (80-90%) involving saccular or fusiform dilatation of a portion or entire common bile duct (CBD) with normal intrahepatic duct.

Type II: Isolated diverticulum protruding from the CBD. Type III or Choledochocele: Arise from dilatation of duodenal

portion of CBD or where pancreatic duct meets. Type IVa: Characterized by multiple dilatations of the intrahepatic

and extrahepatic biliary tree. Type IVb: Multiple dilatations involving only the extrahepatic bile

ducts. Type V: Cystic dilatation of intra hepatic biliary ducts.

BILLIARY ATRESIA - Biliary atresia (BA) is a progressive, idiopathic, fibro-

obliterative disease of the extrahepatic biliary tree that presents with biliary obstruction exclusively in the neonatal period.

- The extrahepatic bile ducts are progressively destroyed by an inflammatory process, which starts around the time of birth. The aetiology is unclear. The inflammatory destruction of the bile ducts has been classified into three main types :

• type I: atresia restricted to the common bile duct;• type II: atresia of the common hepatic duct;• type III: atresia of the right and left hepatic ducts.-Associated anomalies include, in about 20% of cases,

cardiac lesions, polysplenia, situs inversus, absent vena cava and a preduodenal portal vein.

COMPLICATIONS :

-Ascending cholangitisIntrahepatic changes can occur and eventually result in biliary cirrhosis and portal hypertension. Untreated, death from the consequences of liver failure occurs before the age of 3 years.

Liver transplantation is the main choice of treatment .

GALLSTONES Cholelithiasis means stones in the gallbladder. (the

most common biliary pathology) affect more than 15% of adult in USA . Asymptomatic (most common) >80 % Symptomatic (complicated) 10-20% : pain, jaundice,

pruritus, fever……etc. 10% of gallstones are radio-opaque .

Risk factors :The big 5 : “five Fs : female 3:1 , forty (>40) , fat , fertile,fair.”

less common : -Oral Contraceptives. - Rapid weight loss. -Hyperlipidemia -Gallbladder stasis. -Family history -Ileal diseases or resection

Types of GB stones :1. Cholesterol 20 %.2. Pigmented ( Black , Brown ) 5 %.3. Mixed 75 %

CHOLESTEROL STONES

Pathogenesis: →When bile is

supersaturated with cholesterol, unstable unilamelar phospholipid vesicles are formed. (Cholesterol > 80%)

→This leads to formation of cholesterol crystals.

Characteristics :Yellowish , greasy.Ovoid , firmSingle or multipleMost are radiolucent.

PIGMENTED STONES

Contains less than 30% cholesterol. Contain bilirubin and calicium

Two types : Black and Brown.

Black stones : Accompanies hemolysis (hereditary spherocytosis ,

sickle cell anemia). Brown Stones :

Form in bile duct and related to bile stasis and infected bile.

Associated with the presence of foreign bodies within the bile ducts such as stents, or parasites .

• Characteristic : Anywhere in the biliary tree. Black: in sterile GB bile ,small, numerous, friable, 50-75%

are radio-opaque

Brown: in infected intra- or extrahepatic ducts, single or few, soft & greasy, radiolucent

MIXED STONES Is the most common 75%

cut surface is laminated with alternate dark &light zones of pigment & cholesterol respectively

WHAT ARE THE COMPLICATIONS OF GALLSTONES?

In gallbladder :- Acute cholecystitis.

- Chronic cholecystitis - Biliary Colic- Empyema.- Mucocele.- Perforation - Carcinoma (0.08%)

In the Bile Ducts: - Obstructive jaundice - Ascending cholangitis - Acute pancreatitis

In the intestine - Gallstone ileus (intestinal obstruction)

BILIARY COLIC It is a misnomer because the pain increases in

intensity then reaches a plateau then decreases but never disappears . So not a true colic

Caused by:- Transient obstruction of the GB by a stone in Hartmann’s pouch or cystic duct , which leads to spasm in the wall of GB

Presentation:

pain:S:Right upper quadrant.O: suddenly after fatty mealsC: gripping pain, dull.R: referred to the tip of the right shoulder and radiate to the backA: Associated with - Nausea, vomiting, flatulence, dyspepsia .T: Less than 6 hours, if more then it is acute cholecystitis.

ACUTE CHOLECYSTITIS 1-acute calculous cholecystitis –

95% 2-acute Acalculous cholecysitis –

5%

ACUTE CALCULOUS CHOLECYSTITIS Definition: Inflammation of the gallbladder that

develops over hours, usually resulting from a cystic duct obstruction by a gallstone.

This form of gallbladder disease usually subsides within 1 to 7 days with a conservative plan of treatment .

Not everyone who has gallstones will go on to develop cholecystitis .

Pathophysiology

1 •- A stone obstructing the gallbladder neck (Hartmann’s pouch) or anywhere in cystic duct.

2 •- Stasis and Concentrated bile , with superimposed bacterial infection

3•inflammation of the mucosa by the

congested bile salt. This will lead to edema and distention in the wall causing increased intraluminal pressure and compromises blood flow to mucosa.

4 •- Decrease blood flow with infection lead to gangrene that cause softness of GB wall

5 •- Gangrene may cause perforation (causing abscess and chemical peritonitis )

6

•Unrelieved obstruction , without infection and continuous mucus secretion >> Mucocele

•Unrelieved obstruction with infection and pus formation >> Empyema

CLINICAL PRESENTATION(ACUTE CHOLECYSTITIS)Age : Typically 30-60 year old.

Presentation in younger patients, may be due to congenital hemolytic anemia(sickle-cell disease often form pigment stones, which may precipitate an attack of acute cholecystitis).

Gender : Females are more commonly affected

Analysis of Pain:S: RUQ O: sudden onsetC: sharpR: radiates to the back (close to the inferior angle of right scapula)A: associated with nausea , vomiting and feverT: continuous , Duration of pain usually >6 hoursE: aggravated by movements and breathingS: severe

*The patient May have previous history of flatulent dyspepsia or biliary colic .

PHYSICAL EXAMINATION

General Examination :

_ Patient appears ill _ shallow breathing _ Tachycardia +ve, Pyrexia +ve

** few patients with AC have jaundice by two

mechanisms :1- stone passed to the CBD “obstuctive jaundice”2- Mirrizi syndrome : occur when the cystic duct is densely adhered to the CBD . the stone in the cystic duct cause compression of the CBD .

PHYSICAL EXAMINATION

Abdominal Examination :RHC mass and tenderness, guarding/rigidity

Zackary-cope's sign : RHC fullness

Boas Sign : hyperaesthesia (increased or altered sensitivity) below the right scapula.

Murphy's sign : Cessation of breath at deep inspiration during

the deep palpation at the tip of 9th rib

Bowel sounds are normally present except in biliary peritonitis(GB has infarcted/ruptured ) rare complication

What are the differences in the clinical presentation between biliary colic

and Acute cholecystitis ??? Biliary colic :

pain duration < 6 hrs Afebrile patient vomiting once or twice mild tenderness Acute cholecystitis : pain duration > 6 hrs febrile patient repeated vomiting severe tenderness

INVESTIGATION

1. Full blood count - reveals leukocytosis2. KFT3. LFT – bilirubin (to detect bile duct obstuction) 4. Amylase and lipase level ( for acute pancreatitis) 5. US abdomen ( THE GOLD STANDARD)6. HIDA scan ( if US is not diagnostic)7. X-ray (not useful,only10-15% of stones are

visible)8. MRCP9. ERCP

What are the ultrasonic features of Acute Cholecystitis??

1) Distended gall bladder2) Fluid surrounding the gall

bladder3) Gall bladder wall thickening

(>3mm)4) Dilated cystic duct5) Stones in the gall bladder

MRCP : magnetic resonance cholangiopancreatography

ERCP : endoscopic retrograde cholangiopancreatography

Both are used for diagnosis . ERCP used also for therapy of CBD stones .

HIDA scan : reveal non-opacification of the gallbladder from obstruction of the cystic duct.

Inflammation of the gallbladder in the absence of gall stone , usually seen in seriously ill patients after :

major surgeries, trauma, burns, sepsis

It occurs because of : 1) Dehydration2) GB stasis 3) Vascular compromise4) Bacterial contamination

( mostly Gram –ve: E-coli , Klebsiella , Enterobacter )

ACUTE ACALCULOUS CHOLECYSTITIS

CHRONIC CHOLECYSTITIS

Chronic inflammation of the gall bladder because of recurrent attacks of acute cholecystitis or biliary colic ending in thickening and fibrosis of its wall.

Stones are almost always present. Supersaturation of bile predisposes to

chronic inflammation & stone formation. Bacteria are isolated in 1/3 of the cases.

PRESENTATION

-Upper abdominal pain after eating. ((begins 15 to 30 mins after a meal, and last for 30 to 90 mins)) (most common complaint).

- flatulent dyspepsia(post-prandial belching) - Heartburn

PHYSICAL EXAMINATION Signs of jaundice Abdomen looks normal RHC mass and tenderness Percussion and auscultation should be

normal

DDX OF RUQ PAIN : Common:1. Perforated peptic ulcer2. High appendicitis3. Acute pancreatitis

Uncommon:4. Acute pyelonephritis5. Right lower lobe pneumonia 6. MI(inferior)

MANAGEMENT

Conservative management : ( >90% of cases will respond)

1) Nil by mouth [NPO]2) Gain IV access, give IV fluids 3) Administration of antibiotics 4)Administration of analgesics 5) Monitoring of vital signs6) If symptoms subsided, initially oral fluid intake is allowed, then followed by fat-free diet, and lastly regular diet7) US - to evaluate whether there's any local complications8) Plan for cholecystectomy ( open or laparoscopic )A) Early (within 72 hours).B) Late ( after 2-3 months). *Sometimes we do Cholecystostomy in case of empyema

Usually we do it by laparoscopy, but in the following cases we do it by

Laparotomy :

1. not well defined anatomy2. uncontrolled bleeding3. bile duct injury

CHOLECYSTECTOMY

1- hemorrhage**usually the source is from cystic artery.** the patient complains of persistent abdominal pain, or features of hypovolemic shock

2- wound infection3- bile leak4-bile duct stricture **the most dangerous complication , leads to : cholangitis , obstructive jaundice , secondary biliary cirrhosis and hepatic failure.5-post cholecystectomy syndrome

POST – OPERATIVE COMPICATIONS

NEOPLASMS Benign tumors of the GB:

papilloma , myxoma , fibroma , adenomyoma , lipoma , carcinoid .

Malignant tumors of the GB : 80 % of the tumors are adenocarcinoma 90 % of pts have cholelithiasis Porcelain GB Carry a risk of 50 % of

malignancy (calcification of GB due to excessive

stones).

PORCELAIN GB

CHOLEDOCOLITHIASIS

- Stones present within the biliary tree.

- Stones may be:1) derived from gallbladder2) primary ductal & intrahepatic stone formation

- Asymptomatic in 10% - Symptoms due to:

1) cholangitis (Charcot’s triad), biliary obstruction (Obstructive Jaundice , Dark urine , Pale stool ,itching)2) pancreatitis3) Liver abscess4) chronic liver disease with secondary biliary cirrhosis5) acute cholecystitis

CHOLEDOCHOLITHIASIS CAN BE PRIMARY OR SECONDARY

u/s , ERCP are the diagnostic modalities

Liver function test are consistent with obstructive jaundice

Surgical TT : Cholecystectomy , choledocotomy

, CBD exploration , T tube placement & operative cholangiogram .

CHOLANGITIS : INFECTION OF THE BILLIARY TREE

- Etiology :1. CBD stones.2. post.op stricture.3. Neoplasm4. sclerosing cholangitis.5. billiary contrast studies .

Treatment : NPO , IV antibiotics ,

relief of the obstruction

CHOLANGIOCARCINOMA Malignant tumors of the bile duct may be

associated with : 1- Sclerosing cholangitis.

2- chronic parasitic infection of the bile duct. 3- Gall stones.

The tumor may be located in : distal CBD , common hepatic duct , cystic duct ,

left or right hepatic duct (most common site)

Treatment by : Whipple procedure.