Abdominal imaging activities 1-6 Flashcards
1
Q
What are the three different types of aneurysms?
A
True aneurysm
Pseudoaneurysm
Dissecting aneurysm
2
Q
Define a true aneurysm
A
Focal increase in the diameter of a vessel involving all three of it’s layers (Adevntitia, media, intima)
3
Q
What are the two types of true aneurysm?
A
Commonly fusiform, occasionally saccular
4
Q
How does a pseudoaneurysm form?
A
From a defect in the intima. Blood penetrates through the defect but is contained by the media and adventitia. (different from a pseudoaneurysm in the peripheral arteries)
5
Q
Why are pseudoaneurysms concerning?
A
High risk of rupture
6
Q
Describe a classic aortic pseudoaneurysm
A
A contained rupture of the aorta in which the majority of the wall has been breached. the luminal blood is held in only by a thin rim of remaining wall or adventitia.
7
Q
What typically causes an aortic pseudoaneurysm?
A
Focal aortic transection 85% of which are the result of penetrating trauma (gun shot, stabbing) and 15% of which are from blunt trauma (MVA or fall). A non taumatic cause could be penetrating atherosclerotic ulcers
8
Q
Describe a dissecting aortic aneurysm
A
It is a result of the intima lifting from the vessel wall and allowing blood to flow through the false lumen that is created. There will be blood flow in both the true and false lumen. Chronic dissection may appear as a relatively thickened bridge of tissue through the lumen of the vessel.
9
Q
What are the two types of IVC thrombus?
A
Bland and tumour
10
Q
What may cause bland thrombus in the iVC?
A
propagation of thrombus from the iliofemoral veins, renal veins or hepatic veins
11
Q
What may cause tumour thrombus in the IVC?
A
usually arises from a renal cell carcinoma extending through the renal vein or a hepatocellular carcinoma extending through the hepatic vein
12
Q
If you examine IVC thrombus how would you extend the exam to determine the cause?
A
The examination should be extended to assess the proximal and distal extent of the thrombus and to assess which tributaries might be affected by it.
The thrombus should be interrogated with appropriately set colour Doppler to assist with the differentiation of tumour and bland thrombus.
If tumour thrombus is suspected the renal veins and hepatic veins should be examined to find the source. Once the source has been found then the tumour it originates from should be identified.
13
Q
Explain the use of a filter placed in the IVC
A
An IVC filter is used to prevent emboli arising from an iliofemoral or femoral DVT travelling to the lungs and causing a pulmonary embolus.
14
Q
Describe the criteria for classification of retroperitoneal lymph nodes based on node size.
A
in the abdomen, a node greater than 1cm is suspicious and a single node greater than 1.5cm is abnormal. Multiple nodes greater than 1cm are also abnormal
15
Q
Describe the criteria for classification of retroperitoneal lymph nodes based on node size.
A
in the abdomen, a node greater than 1cm is suspicious and a single node greater than 1.5cm is abnormal. Multiple nodes greater than 1cm are also abnormal
16
Q
Other than size, what features of retroperitoneal nodes suggest malignant change?
A
If size is the only criteria used to assess nodes then disease will be missed. Malignant nodes usually have a long/trans ratio of less than 2. A thickened cortex, or an absent or compressed hilus is suggestive of malignancy.
17
Q
What is the Couinaud liver classification system?
A
The Couinard classification divides the Liver into 8 independently functional segments. This division is based on the right and left branches of the hepatic artery and the portal vein with tributaries of bile (hepatic) ducts following.
18
Q
Name the sections and how they are divided
A
The hepatic veins run in three vertical planes radiating from the intrahepatic IVC separating the liver into 4 sections. A section is two segments on top of each other.
• Right hepatic vein is located in the right intersegmental fissure
• Middle hepatic vein lies in the main lobar fissure, divides the liver into right and left lobes. This vertical plane runs from the inferior vena cava to the gallbladder fossa and is known as Cantlie’s line.
• Left hepatic vein is located in the left intersegmental fissure
19
Q
What forms the horizontal plane?
A
A horizontal plane further divides the liver, known as the portal plane where the portal vein bifurcates and becomes horizontal, dividing each section (or sector) of the liver into superior and inferior segments.
20
Q
Briefly describe the components of each segment
A
Each segment has its own vascular inflow, outflow and biliary drainage. In the centre of each segment, there is a branch of the portal vein, hepatic artery and bile duct. In the periphery of each segment there is vascular outflow through the hepatic veins.
21
Q
Describe segment 1
A
Segment 1 is the caudate lobe, which is easily identified immediately to the left of the IVC and has the thin echogenic line of the ligamentum venosum covering its anterior surface.
22
Q
Describe segment 2
A
Segment 2 is the lateral superior segment of the left lobe. This is the portion of liver at the tip of the left lobe, to the left of the left hepatic vein and against the diaphragm (superior to the left portal vein).
23
Q
Describe segment 3
A
Segment 3 is the lateral inferior segment of the left lobe. This is immediately inferior to segment 2, to the left of the left hepatic vein, but inferior to the left portal vein. This segment often is used as an acoustic window to image the pancreas.
24
Q
Describe segment 4
A
Segment 4 is between the middle and left hepatic veins, and to the left of the porta hepatis (but does not include the caudate lobe). It is divided into 4A, superior to the left portal vein (adjacent to the diaphragm) and 4B inferior to the left portal vein (adjacent to the free edge of the liver).
25
Describe segment 5
Segment 5 is between the middle and right hepatic veins, to the right of the porta hepatis and inferior to the right portal vein. It is adjacent to the free edge of the liver.
26
Describe segment 6
Segment 6 is to the right of the right hepatic vein, inferior to the right portal vein and adjacent to the free edge of the liver. It is often in contact with the anterior border of the right kidney.
27
Describe segment 7
Segment 7 is to the right of the right hepatic vein, superior to the right portal vein and adjacent to the diaphragm.
28
Describe segment 8
Segment 8 is between the right and middle hepatic veins and superior to the right portal vein, adjacent to the diaphragm.
29
In cases of obstructive jaundice, would the conjugated or unconjugated bilirubin be more likely to be elevated?
Conjugated bilirubin would most likely be elevated as obstructive jaundice has a post hepatic cause.
30
Can cholelithiasis cause an increase in bilirubin levels?
Cholelithiasis is the formation of gallstones. This can cause an increase in bilirubin levels if the stones move to the common bile duct and obstruct it. This is known as choledocholithiasis. Another very unusual situation where gallstones in the gallbladder could cause obstruction is Mirrizzi's syndrome.
31
List the three types of portal hypertension
- Presinusoidal extrahepatic hypertension
- Presinusoidal intrahepatic hypertension
- Intrahepatic hypertension.
32
List the common causes of intrahepatic portal hypertension
* cirrhosis;
* diffuse metastatic disease;
* Budd-Chiari Syndrome; and
* chronic right heart failure
33
What are the most common causes of intrahepatic presinusoidal portal hypertension?
result of diseases affecting the portal zones of the liver, notably schistosomiasis, primary biliary cirrhosis, congenital hepatic fibrosis, and toxic substances, such as polyvinyl chloride and methotrexate.
34
What is the most common cause of extrahepatic presinusoidal portal hypertension?
thrombosis of the portal or splenic veins. This should be suspected in any patient who presents with clinical signs of portal hypertension (ascites, splenomegaly, and varices) and a normal liver biopsy
35
List the portal hypertension collateral pathways which may be seen on ultrasound
Paraumbilical vein, Gastroesophageal junction, Gastrorenal/splenorenal varices, Intestinal, Hemorrhoidal
36
What are the sonographic findings of portal hypertension?
Sonographic findings of portal hypertension include the secondary signs of splenomegaly, ascites, and portosystemic venous collaterals.
37
How to portosystemic collaterals form?
When the resistance to blood flow in the portal vessels exceeds the resistance to flow in the small communicating channels between the portal and systemic circulations, portosystemic collaterals form.
38
Describe the paraumbilical vein collateral venous pathway
The para umbilical vein is identified in the left lobe of the liver coursing inferiorly from the left portal vein to the liver edge. In normal patients the ligamentum teres appears as an echogenic structure, and in portal hypertension the para umbilical vein is one of the collaterals that may form producing a 'bull's eye' type appearance with an echogenic rim surrounding a hypoechoic centre. Collaterals may also form adjacent to the lig teres but not within it. Demonstration of collaterals is pathognomonic for sonographic diagnosis of portal hypertension.
39
Describe gastroesophageal junction varices
The gastroesophageal junction is seen deep to the left lobe of the liver and superficial to the aorta. Varices may appear as hypoechoic tortuous veins resembling 'bunches of grapes' around the gastroesophageal junction. Gastroesophageal varices are formed when the coronary vein functions as a collateral. The coronary vein may be seen arising from the portal vein adjacent to the confluence of the splenic vein and the inferior mesenteric vein and flow can be demonstrated flowing away from the portal system.
40
Why is it important to identify gastroesophageal junction varices
It is important to identify gastroesophageal varices because the first episode of haematemesis is fatal in a significant proportion of people.
41
Describe gastrorenal/splenorenal varices
Tortuous veins may be seen in the region of the splenic and left renal hilus, which represent collaterals between the splenic, coronary, and short gastric veins and the left adrenal or renal veins. The hilum of the left kidney and the course of the left renal vein is best seen in the RPO position using either a coronal or sagittal approach. Venous collaterals may be visualised adjacent to the renal hilum or between the splenic and left renal veins. The hilum of the spleen is usually demonstrated in the RPO position using an intercostal approach. Varices may be seen adjacent to the splenic hilum.
42
Describe Intestinal varices
Regions in which the gastrointestinal tract becomes retroperitoneal so that the veins of the ascending and descending colon, duodenum, pancreas, and liver may anastomose with the renal, phrenic, and lumbar veins (systemic tributaries).
43
Describe hemorrhoidal varices
The perianal region where the superior rectal veins, which extend from the inferior mesenteric vein, anastomose with the systemic middle and inferior rectal veins.
44
List the quantitative measurements used to assess portal hypertension using ultrasound.
* splenomegaly. Splenomegally is a soft sign. It may not be enlarged in a patient with PHT. Similarly an enlarged spleen can be a part of the disease process of many other conditions.
* portal vein diameter greater than 13mm. Remember that the portal vein diameter may return to normal when collaterals form.
* visible gastroesophageal varices. The demonstration of collaterals is pathognomic of PHT. This includes collaterals in the gastroeosophageal junction, splenic hilum, paraumbilical vein and any other site that you can identify.
* coronary vein diameter greater than 7mm with flow towards the gastroeosophageal junction.
* patent para umbilical vein with hepatofugal flow greater than 5cm/s.
45
What is the mot reliable sign of portal hypertension?
Demonstration of collaterals
46
Define cirrhosis
The World Health Organization (WHO) defines cirrhosis as a diffuse process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules.
47
Name the three major pathological processes, which combine to create cirrhosis.
cell death, fibrosis, and regeneration.
48
What are the most common causes of cirrhosis?
Alcohol consumption is the most common cause of micronodular cirrhosis, and chronic viral hepatitis is the most frequent cause of the macronodular form. Other causes are biliary cirrhosis (primary and secondary), Wilson disease, primary sclerosing cholangitis, and hemochromatosis.
49
What is the classic clinical presentation of cirrhosis?
The classic clinical presentation of cirrhosis is hepatomegaly, jaundice, and ascites. However, serious liver injury may be present without any clinical clues. In fact, only 60% of patients with cirrhosis have signs and symptoms of liver disease.
50
Briefly discuss the ultrasound characteristics of cirrhosis.
The morphologic patterns associated with cirrhosis include volume redistribution, coarse echotexture, nodular surface, nodules (regenerative and dysplastic), portal hypertension: ascites, splenomegaly, and varices.
51
Discuss the various vascular appearances that can be seen in portal hypertension. What changes may be seen in the hepatic artery?
Sonographic findings of portal hypertension include the secondary signs of splenomegaly, ascites, and portosystemic venous collaterals.
In patients with cirrhosis, hepatic artery compensation occurs when the portal venous flow is compromised . Further, the hepatic arterial flow regulation in cirrhosis patients is maintained via a mechanism called the hepatic arterial buffer response, which increases the flow in this case.
The hepatic arterial flow rate and velocity may increase as may the resistive index.
52
With what frequency do hepatic haemangiomas occur in the population?
4%
53
Which portion of the population is most commonly affected by hepatic haemangiomas?
Adult women
54
What is the typical appearance of hepatic haemangioma?
The sonographic appearance of cavernous hemangioma varies. Typically, the lesion is small (<3 cm in diameter), well defined, homogeneous, and hyperechoic. Hemangiomas are characterized by extremely slow blood flow that will not routinely be detected by either color or duplex Doppler sonography.
55
Describe the spectrum of atypical sonographic features of hepatic haemangiomas.
* heterogeneous echotexture;
* large size;
* cystic centre;
* thick echogenic rim;
* thin echogenic rim;
* hypoechoic echotexture;
* scalloped margins; and
* calcification (rare).
56
Briefly describe the life cycle of the parasite responsible for hydatid disease.
E. granulosus tapeworm 3 to 6 mm lives in the intestine of the definitive host, usually the dog. Eggs are excreted in its feces and eaten by the intermediate host (sheep, cattle, goats, humans). Embryos are freed in the duodenum and pass through the mucosa into the liver through the portal vein system. Surviving embryos form slow growing cysts. When hydatid cysts within the organs of an herbivore are eaten, the scolices attach to the intestine and grow to adult tapeworms, thus completing the life cycle.
57
Describe the spectrum of sonographic features of hydatid disease.
The cyst wall consists of an external membrane that is approximately 1 mm thick, which may calcify (ectocyst).
Four groups for hydatid cysts
- Simple cysts containing no internal architecture except sand
- Cysts with detached endocyst secondary to rupture.
- Cysts with daughter cyst matrix (echogenic material between daughter cysts)
- Densely calcified masses
58
Briefly describe the spectrum of sonographic features of a liver abscess.
The ultrasound features of pyogenic abscesses are varied. Frankly, purulent abscesses appear cystic, with the fluid ranging from echo free to highly echogenic. Regions of early suppuration may appear solid with altered echogenicity, usually hypoechoic, related to the presence of necrotic hepatocytes. Occasionally, gas producing organisms give rise to echogenic foci with a posterior reverberation artifact. The abscess wall can vary from well-defined to irregular and thick.
The spectrum of sonographic features of a liver abscess is:
• cystic area with fluid ranging from echo free to echogenic;
• solid elements;
• echogenic gas;
• fluid-fluid interfaces;
• septations;
• well defined thick wall;
• well defined thin wall; and
• poorly defined wall.
59
What are the major predisposing factors to hepatocellular carcinoma (HCC)?
HCC occurs predominantly in men, with a male-to-female ratio of approximately 5:1. The major predisposing factors to hepatocellular carcinoma (HCC) are:
• alcoholic cirrhosis; and
• cirrhosis due to chronic hepatitis
Fatty liver with the development of steatohepatitis is increasingly important as an antecedent to the development of cirrhosis and HCC.
60
Name the three forms of HCC.
Solitary tumor
Multiple nodules
Diffuse infiltration (Fibrolamellar form- Typically occurs in younger patients and does not have an association with cirrhosis)
61
Are there any features of an HCC that might allow you to diagnose its nature?
Studies evaluating focal liver lesions with duplex Doppler and CDFI suggest HCC has characteristic high-velocity signals. Doppler sonography is excellent for detecting neovascularity within tumor thrombi within the portal veins, diagnostic of HCC even without demonstration of the parenchymal lesion.
62
Describe the appearance of post traumatic hepatic haematoma and changes seen over time.
Acute (<24 hours)- fresh haemorrhage is echogenic
Sub-acute (first week)- hepatic laceration becomes more hypoechoic as a result of resorption of tissue and interstitial fluid
Chronic (2-3 weeks)- becomes isoechoic due to fluid resorption and filling with granular tissue
63
List the common causes of moderate, and marked, splenomegaly.
The causes of splenomegaly are varied, and can be thought of under a number of headings:
- hematological disease
- hemodynamic
- infectious
- storage diseases/metabolic/infiltrative disorders
- neoplastic (non-hematologic)
- traumatic
- connective tissue disorders
64
Describe the sonographic appearance of the normal gallbladder in a fasted patient.
The wall of a normally distended gallbladder should appear as a thin pencil line around the anechoic bile.
o variable shape and location of the fundus with the neck having a fixed relationship to the main lobar fissure adjacent to the porta hepatis;
o maximum transverse diameter 2-5cm;
o pencil thin gallbladder wall not exceeding 3mm in thickness; and
o internal lumen free of echoes.
65
The measurements you perform and document pertaining to the gallbladder in your department
Gallbladder wall with the gallbladder in transverse, measured perpendicular to the probe. If gallbladder appears large a longitudinal measurement and volume.
66
The sonographic criteria used for normality of the gallbladder in your department.
The sonographic criteria used for normality of the gallbladder in your department.
The sonographic criteria used for normality of the gallbladder in the reading are as follows:
• maximum transverse diameter 2-5cm;
• pencil thin gallbladder wall not exceeding 3mm in thickness; and
• internal lumen free of echoes.
67
Briefly describe the sonographic criteria used to diagnose cholelithiasis.
Cholelithiasis will have an echogenic appearance with strong posterior shadowing due to the large difference in acoustic appearance between it and the surrounding bile. If a stone is small (<5mm) it may not demonstrate shadowing but will still appear echogenic.
The sonographic criteria used to diagnose cholelithiasis are:
o highly reflective echo arising from the anterior surface of the calculi;
o posterior acoustic shadowing;
o may or may not be mobile; and
o very small calculi may not produce acoustic shadowing.
68
What sonographic features of sludge balls and polyps allow them to be differentiated from cholelithiasis?
o Sludge balls are usually less echogenic than calculi.
o Sludge balls do not create posterior shadowing.
o Sludge balls tend to move very slowly with changes in the patient's position as their density is similar to that of bile.
o Polyps appear as a soft tissue mass which is less echogenic than a calculus.
o Polyps do not create posterior shadowing.
o Polyps are fixed to the wall and do not move dependently with gravity.
. Differentiating between sludge balls and cholelithiasis can be difficult as sludge may also be mobile and mimic the appearance of cholelithiasis
69
What sonographic features of sludge balls and polyps allow them to be differentiated from cholelithiasis?
o Sludge balls are usually less echogenic than calculi.
o Sludge balls do not create posterior shadowing.
o Sludge balls tend to move very slowly with changes in the patient's position as their density is similar to that of bile.
o Polyps appear as a soft tissue mass which is less echogenic than a calculus.
o Polyps do not create posterior shadowing.
o Polyps are fixed to the wall and do not move dependently with gravity.
. Differentiating between sludge balls and cholelithiasis can be difficult as sludge may also be mobile and mimic the appearance of cholelithiasis
70
Briefly define the WES triad
The wall echo shadow sign is indicative of a gallbladder that is contracted around a stone. No bile is visualised.
With stones the gallbladder wall is first visualized in the near field, followed by the bright echo of the stone, followed by the acoustic shadowing, called the wall-echo-shadow complex.
71
when is the WES triad useful?
When air or calcification is present, the normal gallbladder wall is not seen, and only the bright echo and the posterior dirty shadowing are seen. This sonographic sign is useful to diagnose a contracted gallbladder full of calculi. The sign consists of two parallel curved echogenic lines followed by posterior acoustic shadowing. The first line is the gallbladder wall and the second is the anterior surface of the calculi. A thin hypoechoic space may separate the wall from the calculi if bile is present in the gallbladder.
72
Describe the method you would use to differentiate polyp, adenomyomatosis and adenocarcinoma.
Move the patient to demonstrate mobility. Using write zoom optimise the bmode settings to interrogate the area. If the situation is appropriate use a linear array to maximise resolution. Interogate with colour Doppler ensuring the parameters are very carefully set to detect flow in very small vessels.
73
How does a polyp appear?
Adenomatous polyps are commonly sessile (That is they are not attached by a stalk). If the size of the polyp is >1cm there is an increased risk of malignancy. The presence of hypoechoic foci centrally within the polyp and the presence of a central vessel within the polyp (vascular core) and hypoechoic appearance my indicate malignancy.
Polyps appear as a soft tissue mass which is less echogenic than a calculus.
Polyps do not create posterior shadowing.
Polyps are fixed to the wall and do not move dependently with gravity.
74
How does adenomyomatosis appear?
may be diffuse, segmental or focal in nature and often affects only the fundus of the gallbladder. Small cholesterol crystals form inside the sinuses and this gives rise to a characteristic ultrasound appearance
- Focal or diffuse gallbladder wall thickening
- Anechoic cystic spaces-Rokitanski-Aschoff sinuses
- Echogenic foci
- Comet tail artefact
The most common appearance on sonography is tiny, echogenic foci in the gallbladder wall that create comet-tail artifacts, presumably caused by either the cystic space itself or the internal debris. Prominent masslike focal areas of adenomyomatosis, called adenomyomas, are the next most common manifestation.
75
How does adenocarcinoma appear?
Can be varied
1 - irregular intraluminal vascular mass
2 - extraluminal mass continuous with the liver
3 - trapped stone sign where a mass is seen replacing the gallbladder with a stone in the center
if seen it is important to demonstrate its extension into the adjacent liver, effect on surrounding vessels and the biliary tree
76
Describe common extrahepatic duct anatomical variations.
There are three main variations of the cystic duct :
- low cystic duct insertion: into the distal-third of the CHD (~10%)
- medial cystic duct insertion: into the left, not the right, side of the CHD (~15%)
- parallel cystic duct course: courses parallel to the CHD for at least 2 cm (~10%)
77
Discuss the importance of localising the site and cause of biliary obstruction.
There are multiple pathological processes which may cause obstruction and every effort should be made to determine the exact level and cause of obstruction.
The clinical presentation may also give clues to the cause of obstruction, as painful obstruction is most commonly associated with choledocholithiasis.
Conversely, painless obstruction is most commonly associated with non-calculus causes, for example, pancreatic head mass.
Gallbladder dilatation and sludge formation also gives clues to the level of the obstruction.
Obstruction distal to the insertion of the cystic duct into the common bile duct will result in an obstructed gallbladder.
Obstruction proximal to this level will result in intrahepatic bile duct dilatation without a distended gallbladder.
78
Discuss the importance of localising the site and cause of biliary obstruction.
There are multiple pathological processes which may cause obstruction and every effort should be made to determine the exact level and cause of obstruction.
The clinical presentation may also give clues to the cause of obstruction, as painful obstruction is most commonly associated with choledocholithiasis.
Conversely, painless obstruction is most commonly associated with non-calculus causes, for example, pancreatic head mass.
Gallbladder dilatation and sludge formation also gives clues to the level of the obstruction.
Obstruction distal to the insertion of the cystic duct into the common bile duct will result in an obstructed gallbladder.
Obstruction proximal to this level will result in intrahepatic bile duct dilatation without a distended gallbladder.
79
List the processes that may lead to biliary obstruction
```
Benign Miscellaneous
• Choledocholithiasis
• Hemobilia
• Congenital biliary diseases (Caroli disease, Choledochal cysts)
• Cholangitis
• Biliary parasites
Neoplasms
• Cholangiocarcinoma
• Gallbladder carcinoma
• Locally invasive tumors (esp. pancreatic adenocarcinoma)
• Ampullary tumors
• Metastases
Extrinsic Compression
• Mirizzi syndrome
• Pancreatitis
• Adenopathy
```
80
Describe the sonographic appearance of choledocholithiasis
If the stone is causing biliary dilatation then the obstructing stone is easier to identify. The sonographic appearance of a calculus is an echogenic focus with acoustic shadowing. the calculus should be seen in the longitudinal and transverse plane within the bile duct lumen. A calculus may be seen to move freely within the bile duct, or may be impacted.
81
Describe the sonographic appearance of cholangiocarcinoma
Cholangiocarcinoma is unusual and due to the small lumen diameter of the biliary system; the patient often presents with a small soft tissue mass causing obstruction.
82
Describe a neoplasm vs choledocholithiasis
Neoplasm vs choledocolithiasis
Differentiating a calculus from a primary biliary neoplasm may be difficult. A few criteria to consider are listed below. Unfortunately most of the criteria are not mutually exclusive.
```
Calculus
• echogenic
• acoustic shadow
• may be mobile
• pain and jaundice
```
```
Neoplasm
• soft tissue mass
• fixed position
• painless jaundice
• evidence of metastatic spread or direct invasion
```
83
Describe the sonographic appearance of cholangitis
Cholangitis should be considered if;
biliary obstruction is seen in conjunction with concentric thickening of the intrahepatic and extrahepatic bile duct walls.
Periportal fibrosis may also be present, resulting in echogenic appearing portal triad radicles set against the background of normal liver parenchyma. Intrahepatic biliary calculi may also form as a result of chronic cholangitis.
84
Describe the sonographic appearance of bacterial cholangitis
* Dilation of the biliary tree
* Choledocholithiasis and possibly sludge
* Bile duct wall thickening
* Hepatic abscesses
85
What is a klatskin tumour?
A Klatskin tumour is a specific type of cholangiocarcinoma that occurs at the level of the confluence of the right and left hepatic ducts. The tumour may not be visualised as a separate entity but intrahepatic duct dilatation with non-union of the left and right hepatic duct is enough to suggest a Klatskin.
86
Describe the sonographic appearance of a klatskin tumour
The presence of a hilar mass with obstruction would raise concern on ultrasound. The reported echotexture according to one study 5:
• increased echogenicity relative to surrounding liver ~80%
• reduced echogenicity ~20%
• mixed echogenicity ~2%
Ultrasound may also show an intraluminal mass extending into the bile duct and in a small proportion of cases (4%), there may also be evidence of bile duct wall thickening.
87
Define Mirizzi syndrome.
Mirizzi syndrome is a clinical syndrome of jaundice with pain and fever resulting from obstruction of the CHD caused by a stone impacted in the cystic duct. It occurs most often when the cystic duct and CHD run a parallel course. The stone is often impacted in the distal cystic duct, and the accompanying inflammation and edema result in the obstruction of the adjacent CHD. The obstruction of the cystic duct causes recurrent bouts of cholecystitis, and the impacted stone may erode into the CHD, resulting in a cholecystocholedochal fistula and biliary obstruction.
88
Define a choledochal cyst.
Choledochal cysts represent a heterogeneous group of congenital diseases that may manifest as focal or diffuse cystic dilation of the biliary tree.
89
What are the four types of choledochal cyst according to Todani Classification System for Choledochal Cysts.
Type I cyst: diffuse dilation of the extrahepatic bile duct; this is the most common type (80%).
Type II cyst: true diverticulum of the bile duct; very rare.
Type III cyst: also called choledochocele; diffuse dilation of the very distal (intraduodenal) common bile duct.
Type IV cyst: multifocal dilations of the intrahepatic and extrahepatic bile ducts. Type V cyst, Caroli disease, is omitted because it is not a true choledochal cyst.
90
List three parasites which may inhabit the biliary system.
Fascioliasis, Clonorchiasis and Opisthorchiasis
91
Briefly describe the sonographic appearance of Carolis disease
The disease may be diffuse, lobar or segmental. Dilatation is most frequently saccular rather than fusiform, a feature that might help in the differential diagnosis.
May show dilated intrahepatic bile ducts (IHBD)
Intraductal bridging: echogenic septa traversing the Dilated bile duct lumen
Small portal venous branches partially or completely surrounded by dilated bile ducts
(the intraluminal portal vein sign: dilated ducts surrounding the portal vein)
Intraductal calculi and sludge due to biliary stasis.
May cause bouts of cholangitis and sepsis
92
Briefly describe the sonographic appearance of biliary tree obstruction
the bile ducts in the left lobe are usually the first to demonstrate dilatation on ultrasound. Dilated intrahepatic ducts produce a distinctive ultrasound appearance of 'too many tubes' in the liver: rather than just portal vein radicles being visualised
When scanning along the length of the portal veins these produce an appearance of parallel tubular structures. In a plane transverse to the portal vein they produce the 'shot gun sign' with two circular lumens sitting adjacent to each other. Acoustic enhancement may be noted deep to the dilated bile duct and colour Doppler may be used to differentiate the portal vein from the bile duct. In the presence of portal hypertension the hepatic artery may become prominent. The application of colour Doppler will allow differentiation in these circumstances.
93
Describe type 1 pancreatic duct variation
Type 1: A bifid configuration with the main pancreatic duct (MPD) draining into the duodenum at the major papilla, communicating with a well-defined accessory pancreatic duct (APD), which drains into the duodenum at the minor papilla.
94
Describe type 2 pancreatic duct variation
Type 2: A bifid configuration with the APD as the dominant drainage. APD and MPD drains into the minor and major papilla, respectively.
95
Describe type 3 pancreatic duct variation
Type 3: Absent or rudimentary APD.
96
Describe type 4 pancreatic duct variation
Type 4: A pancreas divisum, characterized by non-fusion of the ventral and dorsal pancreatic ducts with the MPD draining into the minor papilla and APD into major papilla. There are three subtypes: (a) absent communication between the ventral and dorsal duct, (b) no ventral duct and (c) small communication between the ducts.
97
Describe type 5 pancreatic duct variation
Type 5: Ansa pancreatica in which the proximal APD at its junction with MPD is obliterated, and replaced by an S-shaped duct arising from the MPD which terminate in or around the minor papilla.
98
List the structures which may be mistaken for the pancreas or pancreatic pathology.
* Lymph nodes
* Intrapancreatic collateral veins secondary to portal hypertension, mimicking cysts
* Hypoechoic (relative to rest of pancreas) pancreatic head and/uncinate process, mimicking a mass
* Variations in shape of the head (pseudomass)
* Bulge in the anterior body where the liver touches the pancreas
99
List structures which may mimic the pancreatic duct.
* posterior wall of stomach and splenic vein
* jejunal branch of SMA surrounded by fat can mimick pancreatic tissue
* Averaging of tortuous splenic artery in pancreatic tissue
* Marked pancreatic atrophy
* Intrapancreatic collaterals
* Air in the duct mistaken for calculi
100
List structures which may mimic the pancreatic duct.
* posterior wall of stomach and splenic vein
* jejunal branch of SMA surrounded by fat can mimick pancreatic tissue
* Averaging of tortuous splenic artery in pancreatic tissue
* Marked pancreatic atrophy
* Intrapancreatic collaterals
* Air in the duct mistaken for calculi
101
Briefly describe the process of pseudocyst formation.
Pseudocysts occur from disruption of pancreatic duct structure with resulting leakage and accumulation of pancreatic juice resulting in haemorrhagic fat necrosis. They are not lined by epithelium (thus, “pseudocysts”), rather a severe inflammatory reaction results in encapsulation of the cyst by fibrosed granulation tissue. This usually takes 4-6 weeks. In approximately 50% of cases, the cyst retains a communication with the pancreatic duct. Such cysts are more problematic to treat, and are more likely to recur.
102
List the common possible sites of pseudocyst formation.
• Pancreatic bed
• Lesser sac between the stomach and the pancreas
They can be multiple and are most commonly located in the pancreatic bed. However, they can be found anywhere from the groin to the mediastinum and even in the neck, having ascended in the retroperitoneum via the diaphragmatic hiatuses into the mediastinum.
103
List serious complications of acute pancreatitis
Pancreatic fluid collections
(Acute pancreatic fluid collection {in 1st 4 week}, Pseudocyst {after 1st 4 week} , acute necrotic collection {in 1st 4 weeks}, walled off necrosis {after 1st 4 weeks}
Necrotising pancreatitis
Vascular complications (haemorrhage, pseudoaneurysm, splenic vein thrombosis, portal vein thrombosis)
Fistula formation with pancreatic ascites
104
Briefly describe acute pancreatic fluid collection
Fluid collections, when they contain debris or necrosis or may be infected, cannot always be categorized. Approximately 40% of patients with acute pancreatitis develop acute fluid collections. About half of these appear to resolve spontaneously, with almost 70% resolving in patients with nonnecrotizing pancreatitis.
105
Briefly describe pancreatic pseudocysts
Pseudocysts can range in appearance from almost purely cystic to collections with considerable mural irregularity, septations, and internal echogenicity because of debris from necrosis, hemorrhage, or infection.
Pseudocysts comprise 75% to 90% of all cystic lesions of the pancreas. The “wall” of pancreatic pseudocysts consists of fibrous and granulation tissue. Thus unlike true cysts or cystic neoplasms, pseudocysts do not have an epithelial lining. Pseudocysts are more common in patients with chronic than acute pancreatitis.
The most important issue in diagnosing pseudocysts on images is avoiding confusion with cystic neoplasm, a mistake that can lead to adverse clinical outcomes. Unfortunately, this distinction may be difficult. The major criterion for diagnosing a pseudocyst is a clinical history or imaging evidence of acute or chronic pancreatitis.
106
Briefly describe acute necrotic collections and walled off necrosis in the pancreas
fluid collections in necrotising pancreatitis
acute necrotic collections (ANCs): in the first 4 weeks; non-encapsulated heterogeneous non-liquefied material
walled-off necrosis (WON or WOPN): develop after 4 weeks; encapsulated heterogeneous non-liquefied material
107
Briefly describe pancreatitis vascular complication
Vascular complications occur in both acute and chronic pancreatitis. Pseudoaneurysms and venous thrombosis are the most important vascular complications. Most cases of clinically insignificant hemorrhagic pancreatitis are related to venous and small vessel disease, whereas potentially fatal hemorrhage is usually related to enzymatic digestion or pseudoaneurysm of major vessels, including the splenic, gastroduodenal , and superior pancreaticoduodenal arteries.
Thrombosis of the portal venous system may occur in both acute and chronic pancreatitis; splenic vein thrombosis is most common
108
Briefly describe the aetiology of chronic calcifying pancreatitis
Pancreatic fibrosis may progress to be so severe that strictures form in the main pancreatic duct with consequent upstream dilatation resulting in intraductal calcifications. Inflammation can extend to the surrounding retroperitoneal structures. Extensive calcification and advancing fibrosis may be noted in cases of chronic alcohol abuse.
109
Briefly describe the aetiology of chronic obstructing pancreatitis
Obstructive pancreatopathy may be due to partial or complete obstruction of the main pancreatic duct, resulting in pancreatic fibrosis and atrophy of the pancreatic parenchyma. Incomplete drainage due to congenital abnormalities, for example, pancreas divisum or an intraductal lesion, can also be the cause of pancreatitis. An annular pancreas may result in poor drainage and thus the subsequent fibrosis can cause duodenal stenosis
