GENERAL

SURGERY
Dr. Laith Nawafleh
 Blood supply
Anatomy of GB and biliary tree
 Cystic artery (branch of right hepatic
Gall bladder artery) divides into anterior and
 present in the right upper quadrant of the posterior divisions.
abdomen  Venous drainage is usually through
 pear-shaped muscular tube, with fundus, small cystic veins then directly into
body and neck the liver
 The Hartmann’s pouch (Infundibulum): is a Calot’s triangle “hepato-cystic triangle”
dilation in the GB just before the origin of
cystic duct (it is a pathological pouch not a  It is an important surgical landmark as the Cystic artery usually
physiological one) can be found within it.
 In the gallbladder wall, the muscle layer is muscularis propria  Boundaries
 Inferior : Cystic duct & cystic artery
 Medial: common hepatic duct
Biliary tree  Superior: inferior surface of the
 Intrahepatic ducts converge to become the right and left hepatic liver
ducts Anomalies of GB (‫)قراءة‬
 Right and left hepatic ducts converge, forming the common hepatic
duct  Agenesis (absence of GB)
 Cystic duct comes off the gallbladder and joins the common  Double GB
hepatic duct to become the common bile duct  Floating GB (when GB has its own mesentery that hangs from the
 CBD joins the pancreatic duct then empties into the ampulla of visceral surface of the liver)
Vater (dilation in the wall of the second part of duodenum)  Phrygian cap (Presence of septum that incompletely divides the
 which opens into the duodenum at the major duodenal papilla GB)
(controlled by sphincter of oddi)  Anomalies of the Arrangement of Blood vessels (Right hepatic artery
Crosses in front of common hepatic duct instead of behind it)

Anomalies of biliary duct (‫)قراءة‬

 Biliary atresia
 Choledochal cyst (cystic dilatation in the biliary tree)
 Classical Triad: Abdominal pain, Jaundice, Palpable RUQ
abdominal mass
 Type 1 is the Most common type
 Treatment: Excision and reconstruction of
the biliary tree with Hepaticojejunostomy
 Long cystic duct (Travelling alongside the CHD
to open near the duodenal orifice)
 Agenesis of cystic duct

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  Other Risk factor of gallstones (PYQ)
Physiology  DM - Familial tendency. - Pregnancy - Cystic fibrosis
 Bile is the greenish-yellow fluid  component of the stones: (cholesterol +lecithin +bile salt )
 Made in the liver  type of the stones:
 Stored & concentrated in gallbladder (normal capacity 25-30ml) Cholesterol Mixed Pigmented
(NOT production). Incidence 20% 75% 5%
 Bile acids are derived from cholesterol (PYQ) Structure Pure Cholesterol + Bilirubin+ Ca
 Contents of bile: cholesterol Ca
Number Single or Multiple Multiple
Multiple
Shape oval Faceted Irregular
Color Yellow Yellowish Brown, black
brown
Cut Radiating laminated Amorphous
 Functions of bile Section with alternate
 Digestion of fat. darkened
 Absorption of fat and fat-soluble vitamins (A-K-E-D) light zones of
 Bilirubin and cholesterol excretion pigment and
Cholesterol
respectively.
 Enterohepatic circulation:
 95% of bile salts are reabsorbed in the
terminal ileum, back via the portal
venous drainage to the liver.

etiology 1- Disturbance in bile salts to brown due to : -Infections with E.

GALLBLADDER STONE (Cholelithiasis) cholesterol ratio coli +foreign body
(25-1) -mainly seen in the bile duct
 most common biliary pathology 2- Bile stasis black stones :
 risk factors  5F ’s -due to hemolytic anemia
 Female- ↑ estrogen → ↓ contractility of GB → stasis of (Excess of unconjugated bilirubin)
bile → stones formation or cirrhosis (Decrease bile acid)
 Above Forty x-ray Radiolucent Mostly Radio opaque
 Fat- more common in obese people, because they secrete radiolucent
a bile that is super saturated with cholesterol
 Fertile- more common in multiparous women.
 Fair- more common in Europe and North America than
Africa and Asia.

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 Complications of Gallbladder Stones  Biliary colic: ‫كتيرر مهم‬
 Asymptomatic  Caused by transient obstruction of the gallbladder by a stone In
 Biliary colic. Hartmaan's pouch or cystic duct, which leads to spasm in the
 Acute cholecystitis and its complications wall of gallbladder
(Mucocele, empyema, gangrene, & perforation)  Site of the pain: maximally over the right hypochondrium
 Chronic cholecystitis and its complications  Onset: sudden onset, increases in intensity, then reaches a
(Squamous Cell Carcinoma (Irritation)) plateau, then decreases but never disappear (so it's not a true
 Mirrizi syndrome: stone in the Hartmann’s pouch compress on colic)
CHD and lead to → obstructive jaundice  Character: gripping pain (cramping)
 Stone migration  Radiation: epigastric or spread as a band across the upper
A. To the CBD → Obstructive jaundice→ dilatation proximal to abdomen and the back (T9,T10)dermatomes
the obstruction → Ascending cholangitis  Referred to: the tip of right scapula (due to irritation of the
B. To ampulla of Vater → acute pancreatitis. phrenic nerve )
C. To the intestine → intestinal obstruction “Gallstone ileus”  Associated symptom : nausea, vomiting, sweating
 Cause: Perforation of GB makes a
fistula between GB and duodenum or Acute Cholecystitis
colon, allow a large Gallstone to pass
and causing intestinal obstruction. Etiology
 Most common site: is Iliocecal valve  Predisposing factors
 Rigler's triad  Stones of gall bladder (most common)
 triad that describes the findings on abdominal X-ray ,  Chronic cholecystitis → recurrent acute attacks.
Associated with gallbladder perforation & gallbladder  Organisms
ileus :  E-coli (most common)
1. Small bowel obstruction  typhoid bacilli (rare)
2. Gallstone outside the gallbladder (mainly in the  clostridium perfringens → emphysymatus cholecystitis in DM
RIF) patients
3. Air in the bile ducts or GB (pneumobilia)  Route of infections
 calcular cholecystitis → Along the lumen of GB
 Non-calcular cholecystitis → Lymphatic or blood spread.
Pathology: There are two types
 acute calcular cholecystitis (98%) stones→ stasis +infections
 Catarrhal inflammation
o the GB edematous + distended by mucous and called →
mucocele of GB
 Suppurative inflammation
o More severe than catarrhal phase characterized by Multiple
micro-abscesses in the wall of gall bladder → pus
accumulation → empyema of GB

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  Gangrenous inflammation: (rare)  Ultrasound (Gold standard )
o Its rare due to rich blood supply from the cystic artery and  Reveals inflammation of the gallbladder wall
arteries from the under surface of the liver (> 4 mm)
o It occur in fundus because it’s the farthest from the blood  pericholecystic fluid
supply.  stones in the gallbladder
 Emphysematous cholecystitis (special and rare type ):  Will also see dilation of the CBD if the stone
o seen in DM patients by : clostridium perfringens (gas has passed
gangrene)
Complications
 Acute non-calcular cholecystitis  chronic cholecystitis (most common)
 more dangerous than calcular cholecystitis because occurs in  local spread :→ cholangitis , cholangiohepatitis , pancreatitis , liver
ICU patients suffering from major burn, major trauma , severe abscess
shock →→ so Its unsuspected and diagnosis is delayed  gangrene +perforation → peritonitis
 Ultrasound is diagnostic & treatment is urgent  fistulae → Cholecystoduodenal fistula mainly that can cause → GB
cholecystectomy. ileus lead to →IO
Investigation Clinical picture
 Blood tests (CBC/ LFT /KFT /Amylase and lipase/FBS)  Biliary pain: colic in nature, radiated to the right shoulder,
 CBC: Shows leukocytosis epigastrium & back below the scapula.
 LFT: Check for bilirubin.  fat- intolerance
 Amylase and lipase: for acute pancreatitis  (FAHM) Fever+ anorexia +Headache + Malaise
 KFT: for hepatorenal syndrome  N&V
 FBS: For DM ,Any patient above 25 years have diabetes until During the physical-exam
proven otherwise so do FBS
Note: Any patient has jaundice order hepatitis-test at least to  tenderness+ rigidity + rebound tenderness in the RHR
protect our self (Viral hepatitis is the commonest cause in our  murphy sign + boas sign (increased or altered sensitivity in the
countries) right Subscapular region (between 9-11ribs) ).
 Limitation of abdominal mobility with respiration in the right
 Urinalysis: To exclude renal caliculi and pyelonephritis hypochondrium.
 Plain X-ray: calcified porcelain gallbladder DDx of pain in the right hypochondrium
 HIDA scan (most sensitive): Non filing of the gallbladder
even when the small bowel is visualized is  Hepatobiliary diseases
characteristic of acute cholecystitis  Chronic cholecystitis
 MRCP (magnetic resonanc  Hepatitis and liver abscess
Cholangio-pancreatography): non-Invasive  Acute pancreatitis
 ERCP (endoscopic retrograde  Subhepatic acute appendicitis.
cholangiopancreatography): invasive & Therapeutic  IO
 Complications:,Acute pancreatitis (MC),  Perforated duodenal ulcer or perforated peptic ulcer
Hemorrhage, Perforation, CBD injury  Pneumonia
 Right acute pyelitis, right renal colic
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Treatment Pathogenesis
 depend on the time of diagnosis  Stones in GB →repeated attacks of biliary colic that lead to chronic
 within 3 days of the onset → lab cholecystectomy inflammation in the GB (thickening and fibrosis of the wall).
 after 3 days → conservative treatment (due to adhesions and friable
tissue ) Symptoms
 after 6 weeks elective cholecystectomy  Fatty dyspepsia (ingestion + blenching)-MC
 When failure of conservative treatment
 Right upper abdominal pain especially after fatty food
 In fit patient : urgent cholecystectomy
 May be associated with heart burn
 In unfit patient : cholecystostomy ( the fundus of gall bladder is
opened , remove of stones and drainage of gallbladder by a tube for Treatment
one week )
 Postoperative complication  Elective laparoscopic cholecystectomy (best choice )
 Hemorrhage: from cystic artery.  Open cholecystectomy (If complications occur during laparoscopic
 Wound infection: more in open surgery. cholecystectomy like bleeding )
 Bile leakage
 Bile duct strictures
o The most common dangerous complication caused by damage
during surgery.
Choledocholithiasis (CBD stones)
o Lead to cholangitis , obstructive jaundice Etiology
Secondary biliary cirrhosis and hepatic failure
 Post cholecystectomy syndrome  GB-Stones (commonest one)
o The symptoms have not relieved  15 % of patients of gall bladder (GB ) stones have stones in the
o Patient complains of right hypochondrial pain common bile duct ( CBD )
o Fat intolerance  brown pigment stones (primary Stones) → rare
o Heartburn.
Complications
Chronic Cholecystitis  Obstructions
 Calcular Obstructive Jaundice
Risk factors  Dilatation of extrahepatic & intrahepatict ducts
 G.B. stones  Acute pancreatitis if the stones impact in the ampulla of vater
 Bad management of acute cholecystitis or lower CBD.
 Stasis and infection leading to → Ascending cholangitis ,
Characteristics of GB cholangio-hepatitis & liver abscesses, Acute pancreatitis
 deformity in shape  Biliary cirrhosis + Bleeding tendency
 Palpable stones in the G.B
 Subserous fatty deposition
 Enlarged cystic L.N + Enlargement of
gall bladder ( mucocele or empyema)
 Wall is thickened by fibrosis and
surrounded by adhesion

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 Treatment
Ascending cholangitis  Antibiotics + IV fluids
Definition  Cholecystectomy
 Acute infection of bile duct caused by intestinal bacteria ascending
from duodenum Summery
 Gallstones form in gallbladder → slip out → travel through cystic
bile duct, lodge in common bile duct → obstruction of normal bile
flow → bacteria ascend from duodenum to bile duct → infect
stagnant bile, surrounding tissue
 Common bacteria: E. coli, Klebsiella, Enterobacter, Enterococcus
 Medical emergency
Signs and symptoms

OBSTRUCTIVE JAUNDICE
Diagnosis How the bilirubin form (‫ احفظوها كقصة‬,‫)مهم جداااا باسئله الراوندات‬
 After 120 days the RBCs breaks in the spleen into → globin + heme
 Labs
 Then heme by the heme-oxidase → biliverdin and by the biliverdin
 Increased WBC
reductase → bilirubin (unconjugated)
 Increased serum C-reactive protein (CRP)
 Unconjugated bilirubin bind to albumin and transport to liver for
 Elevated LFTs: ALP, GGT, ALT, AST
conjugation.
 Ultrasound, ERCP
 In the liver the unconjugated bilirubin bind to glucoronic acid and
 Biliary dilation
becomes conjugated bilirubin →CBD→ Intestine
 Bile duct wall thickening
 by the colonic bacteria the conjugated bilirubin convert to →
 Evidence of etiology (stricture/stone/stent)
urobilinogin
 Urobilirugin
 80% → convert to stericobilin (responsible for stool color
(brown ))
 5%→ Reabsorbed into Blood where it is eventually filtered by
the kidneys and convert into → urobilin (responsible for
yellowish color of the urine )
 15%→ enterohepatic –circulation

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Causes of OJ INVESTIGATIONS
 Causes at the level of lumen LAB
 stones (the commonest cause)
 LFT
o GB-stones
 Serum bilirubin
o primary stones (brown)→ form in the CBD
o normally the normal bilirubin less than 1 mg/100ml
 parasite
o Jaundice is clinically recognizable when conjugated bilirubin
 causes at the level of wall reaches 2-3 mg/100 ml or unconjugated bilirubin reaches 3-4
 stricture of the bile duct due to: mg/100ml
o Post-operation 80% o When the bilirubin reach 3 mg we can see jaundice in the
o Inflammatory 20% ) primary sclerosing cholangitis( sclera and mucus membrane , and when it becomes more
o Malignant stricture due to cholangiocarcinoma. than 5 we can see jaundice in the palm
 congenital atresia  Alkaline phosphatase (ALP), gamma glutamyl transferase (GGT)
 causes outside the wall   in OJ
 malignant cause  ALT , AST   IN hepatocellular jaundice
o pancreatic head carcinoma (most common in elderly)  Albumin  decreased
o periampullary carcinoma.  Prothrombin time & concentration  prothrombin time and 
Clinical picture prothrombin concentration seen in both obstructive and
hepatocellular jaundice and To differentiate between them 
 because the bilirubin can’t pass Vitamin -k (IV)
 OJ o IF the prothrombin parameters improve : this is OJ
 stool : pale o IF not : this is hepatocellular jaundice (intrinsic liver damage)
 urine : dark ( coca cola or tea like urine )  urine + stool
 Pruritus : so give the patients Cholestyramine  Urine: dark (tea like or coca cola) + frothy
 because the bile salt can’t pass  Pale stool and Steatorrhaea
 Steatorrhaea (× fat digestion)  CBC
 bleeding tendency (× absorption of fat-soluble vitamins)  To exclude hemolytic anemia
 Endotoxic shock leading to hepato-renal failure  To detect leukocytosis
 frothy urine
 If cholangitis occur , there are attacks of : Radiological Investigations
 Charcot’s triad : Pain - Jaundice - Fever & rigors  Ultrasound
 Reynold’s pentad : Charcot’s triad – Shock (hypotension) –  CT (For malignances)
confusions  MRCP (diagnostic but not therapeutic)
 Courvoisier signs (or law) PYQ  ERCP
 painless, palpable gallbladder in a patient with jaundice (A/W  diagnostic : to detect the site of obstruction + for biopsy
weight loss)  therapeutic:
 It suggests that the jaundice is due to an extrahepatic obstruction o Papilotomy → for stricture of ampula of Vater or to remove a
of the biliary tract (malignancy): stone from lower part of C.B.D
-pancreatic head tumors (MC), tumors of the biliary tree o biliary stent
Note: In Choledocholithiasis, the GB is usually not palpable (not enlarge) o Drainage
 Complications: cholangitis and pancreatitis (5%)
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  PTC (Percutaneous Transhepatic Cholangiography)
 Needle is introduced into the right 8 th . intercostal space with
Notes
continuous suction until bile is aspirated 1. Some different between
 Complication : Biliary peritonitis .+ Bleeding acute appendicitis and
cholecystitis:
Treatment (Aim: remove the CBD –stone + remove the GB (source))
 treatment of the calcular OJ
 Pre-operative preparation (symptoms correction )
o gives the patients V-k to correct coagulation defect
o Cholestyramine to treat pruritus
o IV fluid and IV mannitol +Neomycin orally to prevent
endotoxic shock & hepato-renal failure
 Definitive treatment 2. classification of jaundice
o papillotomy followed by elective lab chole
o if the papillotomy failed →laparoscopic or open surgery is
indicated
 Treatment of stricture OJ
 Dilatation and insertion of stent BY PTC or ERCP
 IF failed we need to by-pass the obstruction by one of the
following:
o Choledocho-duodenostomy
o Choledocho-jejunostomy
o Cholecysto-jejunostomy 3. if the patients had lab- cholecystectomy :
 Treatment of Malignant OJ  before 2 years :→ risk of GB stones still present
 Before more than 2 years :→ no a risk of GB stones
‫يعني اذ بيشنت كان شايل المراره و صار عنده مثال (حصوة في القناه الصفراويه ) ما بصير نحكي فورا‬
: ‫انه المصدر ليس من المراره اال بعد التاكد من المده التي اجرى خالالها العمليه‬
‫فاذا كانت العمليه قبل اكثر من سنتين فالمراره ليست مصدر لهذه الحصوه ابدا‬ 
‫ولكن اذا كانت العمليه قبل اقل من سنتين فيبقى عامل الخطر قائما بان تكون هذه المراره‬ 
‫هي المصدر‬

4. indication for urgent lab cholecystectomy

 elderly DM
 complications
 suggest perforation
 non calcular cholecystitis
 if Deterioration happened