ACUTE AND CHRONIC CHOLECYSTITIS

Contents:

1- Surgical anatomy of the gallbladder "GB".

2- Embryology.
3- Congenital abnormalities.
4- Cholelithiasis.
5- Bile composition and function.
6- Types of gallstones "GS".
7- Complications of GS.
8- Biliary colic.
9- Acute cholecystitis "AC", chronic cholecystitis.
10- Jaundice in AC.
11- Acute acalculous cholecystitis.
12- Chronic cholecystitis.
13- Management of cholecystitis.

Surgical Anatomy:

The gallbladder is present in the right upper quadrant of the abdomen, below the visceral surface
of the liver. GB is a pear-shaped muscular tube, with fundus, body and neck.

Right and left hepatic ducts  common hepatic duct // common hepatic duct with cystic duct 
common bile duct. The common bile duct "CBD" descends behind the duodenum and pancreas and
may be joined by main pancreatic
duct before it enters the second
part of duodenum.

CBD ends in a dilation in the wall of

the second part of duodenum called
the ampulla of vater, which opens
into the duodenum at the major
duodenal papilla. The intra-
duodenal part of the CBD is
surrounded by sphincter of oddi.

Blood supply: cystic artery 

branch of right hepatic artery.

The harmann's pouch: is a dilation

in the GB just before the origin of
cystic duct  it is a pathological
pouch not a physiological one.

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Embryology:

A diverticuum grows out from the ventral wall of foregut

"primitive duodenum"  differentiates into hepatic ducts
and liver.

A lateral bud from this diverticulum becomes GB and

cystic duct.

Congenital abnormalities: (in 10% of subjects) include:

1- Agenesis: congenital absence of GB.

2- Double GB: rare
3- Floating GB: when GB has its own mesentery that
hangs from the visceral surface of the liver, this long mesentery allows acute torsion of the
GB to occur with consequent gangrene and rupture.
4- Phrygian cap: presence of septum that incompletely divides the GB (single or multiple)

5- Biliary atresia: loss of the duct system which will be replaced by solid fibrous strands "this
atresia is most commonly extra-hepatic "it is one of the causes of neonatal jaundice.
6- Choledochal cyst: presence of cystic dilatation in the biliary tree, most commonly in CBD.
7- Along cystic duct travelling alongside the common hepatic duct to open near the duodenal
orifice, this occurs in 10% of cases.
8- Absence of the cystic duct: the GB opens directly in the side of CBD.
9- Anomalies of the arrangement of blood vessels: e.g.: right hepatic artery crosses infront of
common hepatic duct instead of behind it in 25% of subjects.

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Gallbladder Stone "cholelithiasis":

Very common  affect more than 15% of adults in USA .85% of cases are a symptomatic. It affects
females more than males "F:M  3:1".

Remember the five Fs:

1- Female  F:M 3:1
2- Forty: more common in middle age groups "in 4th decade" .
3- Fat: more common in obese people, because they secrete a bile that is supersaturated with
cholesterol.
4- Fertile: more common in multi parous women.
5- Fair: more common in Europe and North America than Africa and Asia.

But many cases don't fit any of the above criteria.

Bile:

GB works as a storage and site of concentration of bile. Bile composition:

1. Water (92%): this is after reabsorption.

2. Electrolytes: most are absorbed in the GB.
3. Bile salts (like cholic acid and chenodeoxycholic acid)
4. Phospholipids (like lecithin):
bile salts and phospholipids are used for 1- excretion of cholesterol in a micellar from "since
cholesterol alone is water insoluble" , 2- digestion and absorption of lipids .
5. Bilirubin (conjugated) .
6. Fatty acids : also secreted with cholesterol in micells .

Enterohepatic circulation : 95% of bile salts are reabsorbed in the terminal ileum , pass back via the
portal venous drainage to the liver , from where they are once again secreted in the bile  surgical
importance of this point ; that resection of terminal ileum , so decrease in bile salts that causes GS
formation .

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

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Types of GS:

3 types:

1. cholesterol stones (20%) :

it's uncommon to have pure cholesterol stones , but the vast majority of stones contain
some degree of cholesterol . it's formed when the bile become super saturated with
cholesterol , and this occurs in 3 cases :
1- Excessive cholesterol excretion like in obese people.
2- Resection of terminal ileum  decrease bile salts and lecithin.
3- Over absorption of water in the GB during concentration of bile.

* Risk factors for cholesterol stones are: contraceptive pills, pregnancy, obesity, low dietary
fibers, increase age, and family history.
* Stones: single or multiple, yellow, greasy to touch.

2. Pigment stones (5%):

*Stones: brown and black, small, irregular, multiple and fragile.
* contain bilirubin and calcium.
* occur in cases of chronic hemolytic diseases like: congenital spherocytosis and sickle cell
anemia
3. Mixed stones (75%):
*The most common
*cut surface is laminated with alternate dark and light zones of pigment and cholesterol
respectively.
You can differentiate between these types by sending samples to the lap. But this will not
affect the operation and not important nowadays.

Complications of GS :

A) Silent stones: asymptomatic, if the stone is lying free in the lumen.

B) Complication in the GB:

1. Biliary colic.
2. Acute cholecystitis.
3. Chronic cholecystitis.
4. Gangrene.
5. Perforation.
6. Empyema.
7. Mucocele.
8. Carcinoma.

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Note: if the GS obstructs the GB  water is absorbed from the contained bile, which becomes
concentrated and produces a chemical cholecystitis. This is first sterile, but may then become
secondarily infected from organisms secreted from the liver into the bile stream.

Note: if the stone impact in the outlet of an empty GB, the walls of the organ may continue to
secrete mucous and the GB distended to form mucocele.

C) Complications in the bile duct:

1. Obstructive jaundice.
2. Cholangitis.
3. Acute pancreatitis.
4. GS ileus: this occurs when there is ulceration through the wall of the GB into the duodenum
or colon, the large GS may pass per rectum or produce GS ileus – so it is mechanical
obstruction.
Classic findings of pneumobilia "air in the gallbladder", small bowel obstruction, and
radiolucent gallstone on abdominal plain films is known as Rigler's Triad.

Biliary colic:

 Caused by transient obstruction of the gall bladder by a stone in Hartman's pouch or cystic
duct, which leads to spasm in the wall of gall bladder.
 It produces a sudden onset of sever, gripping pain over the upper abdomen (maximally over
the right hypochondrium but may be epigastric or spread as a band across the upper
abdomen).
 The pain radiated to the back (T9, T10 dermatomes).
 Referred to the tip of right scapular, because the gall bladder is supplied by the same nerve
roots that supply the shoulder.
 The pain increases in intensity, then reaches a plateau, then decreases but never disappear
 so it's not a true colic.
 Pain is precipitated by a fatty meal.
 Associated symptoms: nausea, vomiting, sweating.
 It ends because of passage of stone through cystic duct or return back to gall bladder.
 Duration of pain is less than six hours.
 Patient is restless and keeps rolling in his /her bed.
 If it continues  then its acute cholecystitis.
 Sometimes there will be an accessory duct, if you didn't notice it and you made your
operation either open or by laparoscope, there will be accumulation of bile.

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Acute cholecystitis:

 Pathogenesis: obstruction of Hartmann's pouch or cystic duct by a stone

 Duration of pain more than 6 hours.
 Initially chemical irritation to mucosa  damage  inflammatory response in the wall of
gall bladder.
 This will lead to edema and distention in the wall  increase in intraluminal pressure
compromise blood flow.
 Decrease in blood flow with infection lead to gangrene that cause softness of the wall of gall
bladder.
 Gangrene can cause perforation which will cause either abscess (because of localization of
perforation) or chemical peritonitis which is very sever type of peritonitis.
 Unrelieved obstruction without superimposed infection will lead to mucocele (because of
absorption of bile and continuous secretion of clear mucous).
 Unrelieved obstruction with superimposed infection and pus production will lead to
empyema.
 Source of infection either from the bile (20 – 30%) or ascending from the liver.
 Cholecystenteric fistula: with duodenum lead to ileus.
 History in acute cholecystitis:
o The patient came with sudden onset of severe pain in the right hypochondrium,
radiating to the back and referred to the tip of right scapula.
o More than 6 hours duration.
o Associated symptoms: nausea, vomiting, pyrexia.
o Because it is an inflammatory process and one of the cardinal signs of inflammation
is tenderness, movement and breathing causes movement of gall bladder 
stimulation  pain.
o The patient may have a history of previous biliary colic that ends spontaneously.
o The patient may have paresthesia.
o In biliary colic  beginning of inflammatory process.
 Examination in acute cholecystitis:
o General : patient is distressed of pain , tachycardia , high fever ( > 38.5 c ) , shallow
breathing because the in trying to minimize his movement as much as possible.
o Abdomen : tenderness and guarding over right hypochondrium .
o Murphy's sign : catching of breath at height of inspiration when the patient takes a
deep breath because the inflamed gall bladder strikes the palpating hand.

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o Murphy's point: the tip of 9th rib, the junction between lateral rectus and costal
margin.
o We can find a palpable mass in cases of empyema or mucocele.
o By auscultation sounds are present normally except in peritonitis.
 Investigation:
o Blood test: it will show leukocytosis, but you have to check for bilirubin (for bile duct
stones and obstructive jaundice) and amylase (for acute pancreatitis).
o Ultrasonography: it can show us any stone in the gall bladder, the size of the gall
bladder, thickness of the wall and the presence of inflammation around the gall
bladder.
o X-ray: only 15 % of stones can be observed.
o MRCP (magnatic resonance cholangiopancreatograohy) and ERCP (endoscopic
retrograde cholangiopancreatography): both are used for diagnosis and ERCP for
therapy of common bile duct stones.
o Others: oral cholecystography, Intravenous cholangiography and percutanous
transhepatic cholangiography  all of them are not commonly used now, they tell us
about intra hepatic and extra hepatic biliary tree.
 Jaundice and acute cholecystitis :
Few patient with acute cholecystitis will have jaundice and this occurs by 2 mechanisms:
1- Stone passed to common bile duct leading to obstructive jaundice.
2- Mirrizi syndrome : 3 types , occurs when the cystic duct is densely adherent to the
common bile duct and because of inflammation a stone may ulcerate to the common
bile dust or the common bile duct is obstructed by edema.
 Differential diagnosis :
1- Perforated peptic ulcer = since the pain starts suddenly in the epigastric region.
2- High appendicitis = right sided pain.
3- Acute pancreatitis = exclude by amylase.
4- Acute pyelonephritis = the tenderness will be more confined to the loin, with urinary
symptoms.
5- Right lobe pneumonia = can be diagnosis by chest X – ray
6- MI = MI in the inferior wall of the heart can produce epigastric pain.

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If there is increase in amylase but you still suspect acute cholecystitis , make laparscopy and
look at the pancreas and see if it affected or normal.

Acute acalculous cholecystitis:

 It occur in 5 % of patients with acute cholecystitis.
 Occurs in seriously ill patients : -
1- Post operative.
2- Traumatic
3- Sepsis
4- Burns
 It occurs because of dehydration and vascular compromise and gallbladder stasis and bacterial
infection.
 In all the above cases we will have hypotension and ischemia so blood will be shifted to the vital
organs and because gall bladder is supplied by end artery it will deprived of blood with stasis 
so inflammation will develop.
 Acute acalculous cholecystitis carries a higher mortality rate because 1- the pre disposing
condition, 2- the diagnosis usually delayed.

Chronic cholecystitis:

 Caused by repeated attakacks of acute cholecystitis or biliary colic which lead to chronic
inflammatory changes in the gall bladder like thickening and fibrosis of the wall.
 The patient chief complaint is repeated attacks of flatulent dyspepsia (( indigestion + belching +
right upper abdominal pain especially after fatty meals )) .
 May be associated with heart burn.
 Differential diagnosis :-
1- Duodenal ulcer = because of repeated attacks
2- Hiatus hernia : reflex esophagitis  because of repeated attacks.
3- Myocardial ischemia.
4- Chronic pancreatitis = because of repeated attacks
5- Neoplasm in GI.
6- Irritable bowel syndrome.
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Management:
 Conservative treatment which includes :
1- NPO.
2- IV fluid.
3- Analgesia.
4- Antibiotics  3rd generation cephalosporin because they work on gram –ve bacteria.
5- Nasogastric aspiration  if vomiting  not used commonly nowadays.
 90% of patients subside within few days , then we have 2 options :
1- A delayed cholecystectomy (after 2-3 months).
2- Early cholecystectomy (within 72 hours of the onset of symptoms  operation in the 1st
available list.
But now the routine in the whole world to do an early cholecystectomy. If it is done properly
then it carries no increase risk but has a benefit of decreasing the duration of illness.
 Emergency cholecystectomy: done only when the pyrexia and tachycardia don’t subside in the first
few hours and the patient develops rigors  because this may indicate the formation of empyema
and increase the risk of perforation.
 Sometimes in cases of empyema we may do cholecystostomy which means drainage of the gall
bladder, with removal of stones ... why? because the surrounding inflammation obscure the
structure and increase the risk of inflammation.
 After cholecystectomy we admit the patient for elective cholecystectomy 2 months later.
 In cases of chronic cholecystitis we do elective surgery.
 Cholecystectomy  open (old fashion) or laparoscopic;
- Open cholecystectomy is done by right subcostal transverse incision.
- In both open and laparoscopic cholecystectomy you have to cut the cystic duct and artery and
ligate them, then gall bladder in cut in cut and removed.
- Conversion from laparoscopic to open surgery is done for safety in the following cases:-
1- Not well defined anatomy= in this situation is more common in empyema which needs
emergency operation.
2- Uncontrolled bleeding.
3- Bile duct injury.

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Postoperative complication:
1- Hemorrhage: from cystic artery for instance.
2- Wound infection: more in open surgery.
3- Bile leakage :
1- From accessory duct.
2- Slippage of ligature of cystic duct  may lead to peritonitis.
3- Injury of common bile duct.
4- Bile duct strictures: the most common dangerous complication, caused by damage during
surgery and this may lead to cholengitis and obstructive jaundice, secondary biliary cirrhosis
and hepatic failure.
5- Post cholecystectomy syndrome: the symptoms are not relieved, so the patient complains of
right hypochondrial pain, fat intolerance and heart burn.
The cause as the dr said that you removed the gall bladder because you think that the
gallstones are the cause of the problem but it wasn't here the symptoms was because bile
duct, hiatus hernia, irritable bowel syndrome.

Not mentioned in the lec :

- Biliary colic : < 6 hours , vomiting once or twice , patient afebrile ,
minimal tenderness .
- Acute cholecystitis : > 6 hours , repeated nausea , vomiting ,
febrile , sever tenderness , guarding.

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