HEPATOCELLULAR CARCINOMA (HCC)
Found in pre existing post necrotic or macro nodular cirrhosis who are hepatitis B positive and alpha fetoprotein is raised.
Sonological features are.
Multiple nodules through out the liver
Diffuse infiltration.
solitary massive tumour
Discrete echogenic/discrete echo free /isoechoic / mixed echo texture / hypo echoic
Hepatomegaly.
Tip.
Any macro nodular cirrhotic patient who suddenly shows progressively enlargement of liver or suddenly deteriotes & there is haemorrhagic ascites,one should suspect HCC.
COMMON LIVER TUMOUR PATTERN
Primary site
1 Cystic deposit Mucin secreting tumour
2 Echogenic deposit GUT/Urogenital tract
3 Calcified deposit colorectal tumour
4 Echo poor deposit any tumour
HODGEKINS LYMPHOMA
1 . Hypo echoic and Diffuse pattern of liver seen.
NON HODGEKINS LYMPHOMA 1. Hypoechoic and diffuse pattern of liver.
2. Target and echogenic pattern also may be seen.
LEUKAEMIA
1 Multiple discrete solid/anechoic masses without PAS seen in liver.
2 Bulls eye (Target lesion) also could be seen in liver parenchyma.
ACUTE PANCREATITIS
1. Focal tenderness with normal size & echo texture of Pancreas. OR
2. Enlargement may be diffuse( more than 3.5cm for head and tail) with Hypoechoic to anechoic texture or less than liver parenchyma.
3. Margin smooth / blurred with indistinct.
4. Splenic vein distinction usually lost.
5. Focal enlargement and focal loss of echotexture
CHRONIC PANCREATITIS.
1. Normal size or less.
2. Irregular Pancreatic out line.
3. Pancreatic duct dilated more than 3mm.
4. Patchy high level echoes (Fibrosis or Calcification).
5. Calculi could be seen as dense echoes with PAS giving impression of stippled appearance of gland.
PSEUDOCYST
1. Margin initially ill defined but later clear cut as it matures.
2. Mostly seen in lesser sac anterior to tail of Pancreas, but can be seen any where in abdomen.
3. Anechoic generally, sometimes it may have internal echoes/ fluid fluid level or irregular border if infected or haemorrhagic.
CARCINOMA OF PANCREAS.
1. Pancreas may or may not be enlarged.
2. Hypoechoic mass with irregular border.
3. Pancreatic duct dilated ( Either smooth or irregular dilatation).
4. CBD,IHBR dilated.
5. Nodal metastasis.
6. Hepatic metastasis.
7. Splenic vein enlarged.
8. Portal system may be involved.
9. Ascites.
10. Splenomegaly.
GALLBLADDER
1. GB is pear shaped usually 8 cm in length and 3.5cm in diameter.
2. Wall is less than 3 mm and lumen is anechoic.
3. GB is divided in fundus body and neck.
4. various folds and kink in GB are.
· Hartman pouch. It is portion of GB between junctional fold and neck.
· Phrygian cap .Fundus of GB is separated by a junctional fold from its body. It should not be confused with stone.
5. GB may be dilated in Diabetics, prostrated bed ridden patients, Pancreatitis, patients on i/v fluids and anticholinergic drugs.
COMMON BILE DUCT ( CBD)
1. Normally less than 4 mm in adult ,I mm in neonates.
2. CBD lumen with age ie. 1mm for every 10 yrs of age, but usually it should not exceed 6 mm and occasionally 8mm in older patients.
CHOLEDOCOLITHIASIS
1. Hyper echoic stones in CBD.
2. Posterior acoustic shadow (PAS) present.
TIPS.
Exclude air, mucous plug in CBD, calcification of head of Pancreas, postoperative cholecystectomy clips, air and residues in bowel.
ACUTE CHOLECYSTITIS.
a. Wall is thick more than 4mm.
b. Sonological Murphy’s sign present.( Tenderness when transducer is applied to site of GB)
c. Pericholecystic fluid.( Peri GB discrete Fluid).
d. Usually GB filled with stones,
e. PAS seen.
f. Wall echo sign ( WES) present.
g. Gas in GB also shows PAS but not as sharp as in stone filled post. Acoustic shadowing.
h. Rounded or oval GB with transverse diameter more than 5cms.
NOTE. Acalculous cholecystitis is extremely uncommon.
GALLBLADDER FILLED WITH STONES
1 Stones moves with posture of patient.
2. WES ( Wall echo sign ) present.
3 Posterior acoustic shadowing ( PAS ) present.
SLUDGE ( VISCID BILE )
1. Low level echoes seen in dependent portion of GB.
2. No PAS .
3. Moves with posture of patient but slowly in comparison to stone.
4. Indicator abnormal biliary dynamics.
5. Precursor of Cholecystitis ( Probably).
Causes.
1. Seen occasionally in normal individual.
2. Extra hepatic obstruction
3. Acute or chronic cholecystitis.
4. Starvation/fasting
5. Hyperalimentation.
6. Sepsis.
7. Liver disease.
TIP.
Exclude.
· Blunt injury abdomen.
· Rupture of hepatic artery aneurysm.
· Hematobilia.
CONTRACTED OR NON VISUALISATION OF GALLBLADDER
1. Patient not fasting.
2. GB full of stones casting many strong echoes.
3. Obstructed biliary tract proximal to cystic duct.
4. Technical error.
5. Floating stone containing gases.
6. Congenital absence of GB.
TIP.
· If many stones are filled in GB ,see for WES ,which is 2 parallel arcuate echogenic line separated by thin anechoic space with PAS.
· Confirm cholecystectomy in the past.
MIRIZZI SYNDROME
1. Recurrent jaundice / cholangitis .
2. Partial mechanical obstruction of common hepatic duct due to inflammatory reaction of impacted stones.
3. Presence of impacted stone in cystic duct or neck of GB.
4. Two parallel tubular structure seen in the position of comm0n bile duct (CBD).
TIP.
1 Exclude GB carcinoma, Hepatoma,tumour of duct, metastatic
adenopathy in porta hepatis and focal sclerosing cholangitis.
GALL BLADDER WALL THICKENING ( More than 3.5mm)
Causes.
1. Acute Cholecystitis.
2. Ascites.
3. Hypoproteinemia.
4. Pericholecystic abscess.
5. Alcoholic hepatitis..
6. Debilitated disease.
7. Acute Hepatitis ( Type E)
8. Recent Meal.
9. Congestive cardiac failure.
10. Gall Bladder tumour.
11. Portal hypertension varices
12. Systemic Venous hypertension.
13. Adenomyomatosis.
14. Multiple myeloma.
15. Renal diseases.
16. AIDS.
17. Anti miototic drugs.
ADENOMYOMATOSIS
Type.
· Diffuse .Whole GB is involved.
· Segmental .Proximal, middle or distal portion of GB is involved in circular fashion.
· Localised. E.g. Fundus of GB is involved.
Sonological Findings.
· Multiple “comet effects” due to reverberation artifacts from multiple stones formed in GB Wall.
· Diffuse or segmental thickening of GB Wall.
· Multiple septae within the GB.
· Multiple polyps in GB seen as anechoic/echogenic foci with or without PAS depending upon what is filled in polyps ,bile, sludge or stones.
· Hyperechoic mass arising from fundus of GB..
JAUNDICE
A . Hemolytic Jaundice.
Spleen enlarged,
B . Hepatocellular Jaundice.
· Alcoholic hepatitis.
· Cirrhosis of liver.
· Intrahepatic Cholestasis.
C . Obstructive jaundice.
· Carcinoma head of pancreas.
· Carcinoma Gallbladder.
· Periampullary carcinoma.
· Benign biliary structure.
· Cholangiocarcinoma.
· Hepatic tumors.
· Gall bladder Stones.
· CBD Stones.
LOW BLOCK.
1. IHBR Dilated.
2. GB dilated.
3. CBD dilated.
Causes.
· Periampullary Carcinoma.
1 CBD dilated.
2 pancreatic duct dilated.
3 No mass in Pancreas.
· Carcinoma Head of Pancreas.
A mass in Pancreas .
MID LEVEL BLOCK.
CBD block.
HIGH LEVEL BLOCK( At Porta Hepatis)
1. IHBR dilated.
2. GB not dilated (Collapsed)
3. CBD can not be traced up to head of Pancreas.
Causes.
Carcinoma Head of Pancreas.
TIP
A. IHBR dilated but no jaundice.
Think of 1. Unilateral biliary obstruction resulting one half of biliary system dilated other half being normal.(KLATSKIN TUMOUR) Here serum bilirubin will be Normal while Alkaline Phosphatase will be raised.
.
2.Sub total biliary obstruction by a Tumour.
3. Surgical relief.
B .IHBR NOT DILATED THOUGH THERE IS OBSTRUCTION.
Causes.
1. Inexperienced sonographer
2. Sclerosing cholangitis.
3. Intermittent obstruction.
4. Early Obstruction.
HOW TO APPROACH A CASE OF BILIARY OBSTRUCTION
BILIARY OBSTRUCTION
1. Intra and extra hepatic biliary radicle dilated.
2. GB distended / collapsed.
If above present search site of obstruction it will be.
High block i.e. at porta hepatic as in Carcinoma Gall Bladder.
OR
Low Block which may be Carcinoma of Pancreas or Periampullary carcinoma.
Mid block .it will be at level of CBD.
If high block confirm Rt and left hepatic duct communicating .
If low block confirm pancreas normal or not.
Causes of Biliary obstruction could be stone ,Tumour etc.
PORTAL HYPERTENSION
Causes of PH are.
A.EXTRAHEPATIC.
1. Portal vein thrombosis
2. Compression to portal vein from out side.eg,Tumour
3. Splenic vein thrombosis.
4. splanchnic AV fistula.
5. Congenital atresia or Portal vein stenosis.
B INTRAHEPATIC.
· PRESINUSOIDAL
1. Polycystic disease.
2. Hepatic metastasis
3. Schistosomiasis (Early cases)
4. Myeloproliferative disease.
5. Early cases of Biliary cirrhosis and Idiopathic Portal hypertension
· SINUSOIDAL/POST SINUSOIDAL.
1. Portal cirrhosis
2. Idiopathic Portal hypertension (ADVANCE STAGE)
3. Acute alcoholic hepatitis
4. Congenital hepatic fibrosis
5. Advanced stage of Schistosomiasis and biliary cirrhosis.
6. Buddchiari syndrome.
C. POST HEPATIC.
1 Tricuspid regurgitation
2 Inferior Vena caval obstruction.
3 Rt sided heart failure
4 Constrictive pericarditis
5 Buddchiari syndrome.
6 Increase splenic and portal vein flow.
PORTAL HYPERTENSION
Sonological features are.
1. Portal veins are dilated. more than 15mm.
2. Splenic/superior mesenteric vein are dilated. More than 10mm in inspiration.
3. Splenic vein + Superior mesenteric vein more than 18mm in expiration.
4. Left gastric vein dilated more than 3.3mm.
5. Umbilical vein dilated more than 4mm( Bulls Eye pattern).
6. Ascites present
7. Splenomegaly.
8. Evidence of cirrhosis in liver.
9. Evidence of Intra/Extra portal vein obstruction eg Thrombosis in extra hepatic portal vein,/sclerosis of portal and splenic vein in non cirrhotic patient.
Tip.
If any doubt doppler evaluation of portal,splenic,superior mesenteric and left gastric vein could be done.
ASCITES
It is of transudate or exudate type.
Transudate Type.
· Protein less than 2.5gms.%
· Cell count less than 5 cells/cumm(Lymphocyte)
· Serum ascites albumin gradient (SAAG) more than 1.1
Causes.
· Congestive cardiac failure.
· Cirrhosis of liver with portal hypertension.
· Nephrotic syndrome.
· Anaemia with hypoproteinemia.
· Buddchiari syndrome.
Exudate Type.
· Protein more than 2.5gm %
· Cell count more than 5 cells/cu mm (Polymorph).
· Serum ascites albumin gradient (SAAG) less than 1.1.
Causes.
· Malignancy
· Tuberculosis
· Pyogenic.
· Traumatic.
· Peritonitis.
· Pancreatitis.
· Vasculitis.
SPLENOMEGALY.
Massive splenomegaly.
· Chronic malaria.
· Chronic myeloid leukaemia.
· Tropical splenomegaly.
· Ka lazar.
· Portal hypertension.
· Myelofibrosis.
Other causes.
· Typhoid.
· SABE
· Abdominal Tuberculosis
· Septicaemia.
· Splenic vein Thrombosis.
· Hodgkin’s non Hodgkin’s lymphoma..
· Leukaemia.
· Rheumatoid arthritis.
.
· Lymph sarcoma
· Sickle cell anaemia.
· Hereditary spherocytosis.
· Hemolytic Anaemia.
· Tumour and cysts of spleen.
· Disseminated lupus erythromatus.
