FUNCTIONS OF THE

GALLBLADDER
•CONCENTRATES BILE
THROUGH THE GALLBLADDER
EPITHELIUM
•STORES CONCENTRATED BILE
•CONTRACTS TO RELEASE BILE
 GALLBLADDER
DIVISIONS
• FUNDUS
• BODY
• NECK
 GALLBLADDER LOCATION
•INTRAPERITONEAL
•LOCATED IN THE
GALLBLADDER FOSSA ON THE
POSTERIOR SURFACE OF THE
GALLBLADDER
•LATERAL TO THE INFERIOR
VENA CAVA, ANTERIOR AND
MEDIAL TO THE RIGHT KIDNEY
GALLBLADDER ANATOMICAL
VARIANTS

• HARTMANN POUCH
GALLBLADDER ANATOMICAL
VARIANTS
• JUNCTIONAL FOLD
GALLBLADDER ANATOMICAL
VARIANTS
• PHRYGIAN CAP
 GALLBLADDER SIZE
•NORMAL FASTING ADULT
GALLBLADDER MEASURES
8-10 IN LENGTH AND 3-5 CM
IN DIAMATER
SONOGRAPHIC
APPEARANCE
NORMAL FASTING
GALLBLADDER
• ELLIPSOID ANECHOIC STRUCTURE
LOCATED IN THE GALLBLADDER FOSSA
WITH POSTERIOR ACOUSTIC
ENHANCEMENT
• DEMONSTRATES SMOOTH
HYPERECHOIC WALLS 3 mm OR LESS
• LOCATED IN THE INFERIOR MEDIAL
ASPECT OF THE LIVER
ABNORMAL FASTING
GALLBLADDER
•TRANSVERSE DIAMETER ABOVE 5 CM
•THICK OR EDEMATOUS WALL 3 mm
•IRREGULAR WALL CONTOUR
•INTRALUMINAL FOCUS OR ECHOES
•ACOUSTIC SHADOWING POSTERIOR
TO THE GALLBLADDER FOSSA
 SONOGRAPHIC
APPEARANCE
• ABNORMAL FASTING GALLBLADDER
-THICK EDEMATOUS WALL
EXCEEDING 3 mm IN THICKNESS
-IRREGULAR WALL CONTOUR
-INTRALUMINAL FOCUS OR
ECHOES
-ACOUSTIC SHADOWING
POSTERIOR TO THE GALLBLADDER
FOSSA
REASONS FOR
NONVISUALIZATION OF THE
GALLBLADDER
• NON FASTING PATIENT
• SURGICALLY ABSENT
• OBLITERATION OF THE
GALLBLADDER LUMEN BY
INTESTINAL AIR OR GALLSTONE
• PATIENT BODY HABITUS
• ECTOPIC LOCATION
• AGENESIS
NONINLAMMATORY CAUSES OF
GALLBLADDER WALL
THICKENING
• NON FASTING PATIENT
• ASCITES
• CIRRHOSIS
• CONGESTIVE HEART
FAILURE
• HYPOALBUMINEMIA
• ACUTE HEPATITIS
ENLARGED(DISTENDED)
GALLBLADDER
• DEHYDRATED
• LOW FAT DIET
• INTRAVENOUS
NUTRITION
IF THERE IS NO
CONTRACTION, SEARCH FOR:
• GALLSTONE OR ANY CAUSE OF
OBSTRUCTION
• A STONE OR SOME OBSTRUCTION IN
THE COMMON BILE DUCT
• IF THE GALLBLADDER IS DISTENDED
WITH THICKENED WALLS AND FILLED
WITH FLUID, THERE MAY BE EMPYEMA
• IF THE GALLBLADDER IS DISTENDED
WITH THIN WALLS AND FILLED WITH
FLUID, THERE MAY BE MUCOCELE
•SCHEDULES ARE MADE AT THE
BEGINNING OF THE PATIENT’S
DAY:

-DECREASES THE AMOUNT

OF INTESTINAL AIR
-PATIENT IS FASTING
LABORATORY VALUES
 ALKALINE
PHOSPHATASE
• NORMAL ADULT RANGE 35-150
U/L
• ENZYME PRODUCED PRIMARILY
BY THE LIVER, BONE AND
PLACENTA
• EXCRETED THROUGH THE BILE
DUCTS
• OBSTRUCTIVE JAUNDICE
ALANINE AMINOTRANSFERASE
• NORMAL RANGE 1-45 U/L
• ENZYME FOUND IN HIGH
CONCENTRATION IN THE
LIVER
• REMAINS ELEVATED LONGER
THAN AST
• CIRRHOSIS, HEPATITIS,
BILIARY OBSTRUCTION
• LIVER METASTASIS
ASPARTATE
AMINOTRANSFERASE
•NORMAL RANGE 1-36 U/L
•ENZYME PRESENT IN
MANY TYPES OF TISSUE
THAT IS RELEASED WHEN
CELLS ARE DAMAGED
•CIRRHOSIS, HEPATITIS
AND MONONUCLEOSIS
 BILIRUBIN
• A PRODUCT FROM THE BREAKDOWN
OF HEMOGLOBIN IN OLD RED BLOOD
CELLS
• LEAKAGE INTO TISSUES GIVES THE
SKIN A YELLOW APPEARANCE
• NORMAL TOTAL BILIRUBIN 0.3-1.1 mg/Dl
• NORMAL DIRECT BILIRUBIN 0.1-0.4 mg/dL
 BILIRUBIN
• ELEVATION OF DIRECT OR
CONJUGATED BILIRUBIN
-OBSTRUCTION, HEPATITIS,
CIRRHOSIS AND LIVER
METASTASIS
• ELEVATION OF INDIRECT OR
UNCONJUGATED BILIRUBIN
-NON OBSTRUCTIVE
CONDITIONS
PATHOLOGY
 PNEUMOBILIA
•PRESENCE OF GAS IN THE BILIARY
SYSTEM
•ETIOLOGY: SURGICAL PROCEDURE,
TRAUMA, INFECTION
•CLINICAL FINDINGS:
ASYMPTOMATIC, RUQ PAIN
 PNEUMOBILIA
•SONOGRAPHIC APPEARANCE:
-HYPERECHOIC FOCUS IN THE
INTRAHEPATIC BILE DUCTS
-COMET TAIL ARTIFACT OFTEN
CENTRALLY LOCATED
PNEUMOBILIA
BILIARY ASCARIASIS
• WORMS THAT COLONIZE THE INTESTINAL TRACT
MAY FIND THEIR WAY INTO THE BILIARY TREE
AND GALLBLADDER. LIVING WORMS MAY
OBSTRUCT THE BILIARY TREE AND
GALLBLADDER AND CAUSE CHOLANGITIS,
CHOLECYSTITIS, AND PANCREATITIS, WITH A
HIGH ASSOCIATED MORTALITY.
• WORMS ARE SEEN BY US AS MOVING TUBULAR
ECHOGENIC STRUCTURES WITH AN
ECHOLUCENT CORE.
 BILIARY ASCARIASIS
•ETIOLOGY: INGESTION OF
CONTAMINATED WATER OR
FOOD
•CLINICAL FINDINGS: RUQ
PAIN, FEVER, LEUKOCYTOSIS
BILIARY ASCARIASIS
•SONOGRAPHIC APPEARANCE:
-SPAGHETTI LIKE ECHOGENIC
STRUCTURE WITHIN A BILE DUCT
-NON SHADOWING
-POSTERIOR ACOUSTIC
ENHANCEMENT
BILIARY ASCARIASIS
 GALLBLADDER POLYP
• APPEAR AS ECHOGENIC
NONSHADOWING NODULES THAT
EXTEND FROM THE GALLBLADDER
WALL MOST ARE CHOLESTEROL
POLYPS, WHICH ARE SMALLER THAN
1 CM AND ARE COMMONLY MULTIPLE.
• ADENOMATOUS POLYPS ARE RARE
AND INDISTINGUISHABLE FROM
CHOLESTEROL POLYPS.
GALLBLADDER POLYP
•BENIGN EPITHELIAL TUMOR
•CLINICAL FINDINGS:
ASYMPTOMATIC, DULL RUQ
PAIN, INTOLERANCE TO FATTY
FOODS
GALLBLADDER POLYP
•SONOGRAPHIC APPEARANCE:
-ECHOGENIC INTRALUMINAL
FOCUS
-IMMOBILE
-NON SHADOWING
-THICKENING OF THE
GALLBLADDER WALL
GALLBLADDER POLYP
ADENOMYOMATOSIS
•HYPERPLASIA OF THE EPITHELIAL
AND MUSCLE LAYERS OF THE
GALLBLADDER WALL
•CLINICAL FINDINGS:
ASYMPTOMATIC, DULL RUQ PAIN,
INTOLERANCE TO FATTY FOODS
ADENOMYOMATOSIS
•SONOGRAPHIC APPEARANCE:
-ECHOGENIC
INTRALUMINAL FOCUS
-DIFFUSE COMET TAIL
ARTIFACT
-IMMOBILE
ADENOMYOMATOSIS
ECHOGENIC BILE
• BILE BECOMES ECHOGENIC WHEN IT IS
HIGHLY CONCENTRATED AND
CHOLESTEROL CRYSTALS AND CALCIUM
BILIRUBINATE GRANULES PRECIPITATE AS
SLUDGE. SLUDGE COMMONLY LAYERS IN
THE GALLBLADDER AND MAY BECOME
QUITE VISCOUS AND FORM SLUDGE
BALLS OR TUMEFACTIVE SLUDGE.
SLUDGE BALLS USUALLY MOVE WITHIN
THE GALLBLADDER BUT DO NOT CAST
ACOUSTIC SHADOWS.
 ECHOGENIC BILE
•MIXTURE OF PARTICULATE SOLIDS
THAT HAVE PRECIPITATED FROM
BILE
•ETIOLOGY: PROLONGED FASTING,
BILIARY STASIS, BILIARY
OBSTRUCTION, CHOLECYSTITIS,
SICKLE CELL ANEMIA
 ECHOGENIC BILE
• CLINICAL FINDINGS: ASYMPTOMATIC,
RUQ PAIN, NAUSEA, VOMITING
• SONOGRAPHIC APPEARANCE: NON
SHADOWING LOW AMPLITUDE ECHOES
LAYERING IN THE DEPENDENT PORTION
OF THE GALLBLADDER, ECHOES MOVE
SLOWLY WITH POSITION CHANGE, MAY
FILL THE ENTIRE ORGAN
ECHOGENIC BILE
CHOLELITHIASIS
two major types: 1. cholesterol stones and 2. pigment stones
Cholesterol- formed in bile that supersaturated with cholesterol and decreased amounts
of bile acids and lecithin
Pigmentary- composed of calcium bilirubinate (black or brown)
black stones - bilirubin, polymers, calcium phosphate and carbonate
-common in patients with chronic hemolytic anemia, cirrhosis
brown stones - often laminated and consist of alternating layers of calcium bilirubinate
and cholesterol admixed with calcium soaps
- Common in patients with biliary infections or liver flukes infestation
Shadowing Hyperechoic/echogenic foci
CHOLELITHIASIS
• ULTRASOUND IS THE IMAGING METHOD
OF CHOICE FOR DETECTION OF
GALLSTONES WITH ITS SENSITIVITY OF
GREATER THAN 90%. GALLSTONES
APPEAR WITHIN THE GALLBLADDER
LUMEN AS ECHOGENIC OBJECTS THAT
CAST ACOUSTIC SHADOWS AND MOVE
WITH CHANGES IN PATIENT POSITION
 CHOLELITHIASIS
• ETIOLOGY: ABNORMAL BILE COMPOSITION,
BILE STASIS, INFECTION
• RISK FACTORS: FAMILY HISTORY, OBESITY,
PREGNANCY, DIABETES, FEMALE PREVALENCE
4:1
• CLINICAL FINDINGS: ASYMPTOMATIC, RUQ
PAIN, EPIGASTRIC PAIN, CHEST/SHOULDER
PAIN, ELEVATED LIVER FUNCTION TESTS,
NAUSEA, POST PRANDIAL PAIN, FATTY FOOD
INTOLERANCE
 CHOLELITHIASIS
•SONOGRAPHIC APPEARANCE
-HYPERECHOIC INTRALUMINAL
FOCUS
-POSTERIOR ACOUSTIC
SHADOWING
-MOBILE
-WES
CHOLELITHIASIS
CHOLELITHIASES
CHRONIC CHOLECYSTITIS
• RECURRENT INFLAMMATION SECONDARY TO
INFECTION, OBSTRUCTION OR METABOLIC
DISORDERS
• CLINICAL FINDINGS: ASYMPTOMATIC, VAGUE
RUQ PAIN, HEARTBURN, FATTY FOOD
INTOLERANCE, INTERMITTENT NAUSEA, MILD
INCREASE IN ASPARTATE
AMINOTRANSFERASE AND ALANINE
AMINOTRANSFERASE, POSSIBLE INCREASE IN
ALKALINE PHOSPHATASE AND BILIRUBIN
CHRONIC CHOLECYSTITIS
• SONOGRAPHIC APPEARANCE:
-SMALL CONTRACTED GALLBLADDER
-THICK HYPERECHOIC WALLS
-CHOLELITHIASIS, 90% OF CASES
-POSTERIOR ACOUSTIC SHADOWING
-SLUDGE
CHRONIC CHOLECYSTITIS
ACUTE
CHOLECYSTITIS
• ETIOLOGY: OBSTRUCTION OF THE CYSTIC
DUCT, INFECTION, IDIOPATHIC
• CLINICAL FINDINGS: SEVERE EPIGASTRIC
PAIN, RUQ PAIN, BILIARY COLIC, POSITIVE
MURPHY SIGN, NAUSEA, VOMITING,
JAUNDICE, ELEVATED AST, BILIRUBIN,
AND ALKALINE PHOSPHATASE
ACUTE CHOLECYSTITIS
• SONOGRAPHIC APPEARANCE
-THICK EDEMATOUS GB WALL
-IMPACTED STONE IN THE CYSTIC
DUCT
-CHOLELITHIASIS, 90%
-PERICHOLECYSTIC FLUID
-POSITIVE MURPHY SIGN
-SLUDGE
 MIRRIZI SYNDROME
•ETIOLOGY: IMPACTED STONE IN THE
GALLBLADDER NECK OR CYSTIC DUCT,
OBSTRUCTION OF THE CHD,
JAUNDICE
•CLINICAL FINDINGS: RUQ PAIN,
JAUNDICE, ELEVATED BILIRUBIN,
ALKALINE PHOSPHATASE, INCREASE
IN ALT AND AST,
 MIRRIZI SYNDROME
•SONOGRAPHIC APPEARANCE:
IMMOBILE CALCULUS IN THE CYSTIC
DUCT OR NECK OF THE
GALLBLADDER, DILATATION OF THE
INTRAHEPATIC AND CHD, NORMAL
CBD
MIRRIZI SYNDROME
MIRRIZI SYNDROME
MIRRIZI SYNDROME
PORCELAIN
GALLBLADDER
• DECREASE IN THE VASCULAR SUPPLY TO
THE GALLBLADDER
• CLINICAL FINDINGS: ASYMTOMATIC,
VAGUE RUQ PAIN
• SONOGRAPHIC APPEARANCE:
GALLSTONES 95%, HYPERCHOIC WALL,
MARKED POSTERIOR ACOUSTIC
SHADOWING
PORCELAIN GALLBLADDER
• REFERS TO CALCIFICATION OF
THE GALLBLADDER WALL
COMPLICATING CHRONIC
CHOLECYSTITIS. US
DEMONSTRATES A HIGHLY
ECHOGENIC WALL WITH
ACOUSTIC SHADOWING.
• PORCELAIN GALLBLADDER IS A
PREDISPOSING CONDITION TO
GALLBLADDER CARCINOMA.
PORCELAIN GALLBLADDER
extensive mural
calcification around the perimeter of the
gallbladder
 Wall-echo-shadow
• When the gallbladder is completely filled
with gallstones, a confident diagnosis
becomes more difficult because the
gallbladder resembles an air-filled loop of
bowel. The WES sign is definitive evidence
of a stone-filled gallbladder
• Gallstones produce a clean dark shadow,
and air in the bowel produces a dirty•
brighter shadow.
WES SIGN
GALLBLADDER HYDROPS
• ETIOLOGY: OBSTRUCTION OF CYSTIC
DUCT, PROLONG BILIARY STASIS,
SURGERY, HEPATITIS, GASTROENTERITIS,
DIABETES
• CLINICAL FINDINGS: ASYMTOMATIC, RUQ
PAIN, EPIGASTRIC PAIN, PALPABLE MASS
• SONOGRAPHIC APPEARANCE:
ENLARGMENT, GB DIAMETER EXCEEDING
5 CM, THIN HYPERECHOIC WALLS