Liver Function Tests explained for Radiologists

LIVER FUNCTION TESTS

Albumin (plasma or serum) 32-45 g/L. Varies with age.

Assessment of hydration, nutritional status, protein-losing disorders and liver disease.

ALP (alkaline Phosphatase)

Neonate: 50-300 U/L

Growing child: 70-350 U/L

Adult, non-pregnant: 25-100 U/L

Higher levels are seen in the third trimester of pregnancy and in individuals over 50 years of age.

Investigation of hepatobiliary or bone disease.

AST <40 U/L. (<80 U/L in neonates).

Detection and monitoring of liver cell damage.

Bilirubin

Bilirubin (total): <20 µmol/L

Bilirubin (direct): <7 µmol/L

Investigation and monitoring of hepatobiliary disease and haemolysis.

In most circumstances total bilirubin is sufficient.

GGT

Male: <50 U/L

Female: <30 U/L

Assessment of liver disease.

Increased levels are found in cholestatic liver disease and in hepatocellular disease when there is an element of cholestasis.

Levels are increased in diabetes, with chronic intake of excess alcohol and with certain drugs (especially phenytoin) as a result of enzyme induction.

Pancreatitis and prostatitis may also be associated with increased levels.

Levels may be normal early in the course of acute hepatocellular damage eg, acute viral hepatitis,

paracetamol hepatotoxicity.

Globulins

Calculated: globulin = total protein - albumin.

Neonate: 12-36 g/L

Adult: 25-35 g/L.

Identification of hypo- and hyper-gammaglobulinaemia.

Paraproteinaemias are not reliably detected by calculation of total globulin.

Specific measurement of immunoglobulins and protein electrophoresis is preferred.

Reference values may differ between racial groups.

Levels are increased with chronic inflammation, infection, autoimmune disease, liver disease, and paraproteinaemia.

Levels are decreased in protein-losing enteropathy, humoral immunodeficiency and sometimes in the nephrotic syndrome.

LD 110-230 U/L (method and age dependent).

It is occasionally useful in the assessment of patients with liver disease or malignancy (especially lymphoma, seminoma, hepatic metastases); anaemia when haemolysis or ineffective erythropoiesis suspected.

Although it may be elevated in patients with skeletal muscle damage it is not a useful in this

situation.

ALT

Adult: <35 U/L

Neonate: <50 U/L

Detection and monitoring of liver cell damage.

Increased ALT levels are associated with hepatocellular damage.

ALT is more specific for hepatocellular damage than is AST or LD and remains elevated for longer, due to its longer half-life.

The AST/ALT ratio is typically >1 in alcoholic liver disease and <1 in non-alcoholic liver disease.

PT

Reagent dependent; prothrombin time generally 11-15 seconds.

More sensitive than the APTT for the detection of coagulation factor deficiencies due to

vitamin K deficiency, liver disease.

Screen for deficiency of factor VII and, with APTT, factors X, V, II, I.

An abnormal result is most often due to liver disease, vitamin K deficiency or oral anticoagulant therapy.

REFERENCE: http://www.rcpamanual.edu.au/default.asp

ultrasoundpaedia.com

CT evaluation of Parenchymal Liver Disease

STUDY PROTOCOLS:

Pt. preparation

-Oral contrast:

water as a neutral contrast to distend the stomach- to be able to better define the varicies in chirrosis, to eliminate pseudotumours of the stomach.

oral iohexol (Omnipaque) for positive agent

-IV contrast

100-120ml of iohexol 350

100-120ml of iodixanol 320

Phases of acquisition

- non-contrast scanb

- Arterial ph.

-early- 15 sec

-late - 25-30 sec

- Venous ph. - 60 sec

- Late or excretory ph. - 3-4 min

In most of the cases there is no need for non-contrast CT, it might be useful in chirrotic pts to differentiate between regenerating nodules which look denser in native scans than hepatomas.

If you want to diagnose a fatty liver then the most accurate way is do a native scan, with one or two slices and there is no need to scan the whole organ.

Arterial phase imaging is done in cases of hepatomas (liver cc.), of which 30% or more will only be seen in arterial ph. imaging. The late arterial ph (30 sec) is usually applied for the liver.

Early arterial ph. (15 sec) would be good for vessel mapping, but its just too early for tumours to light up.

Routinely the second ph. (60-70 sec) is the venous ph.

Occasionaly like with tumor imaging we make a delayed ph imaging (3-4 min), like when you are looking for delayed ph enhancement of mets like that of cholangiocarcinomas, hemangiomas, but routinely its not done.

Injection rate: 4-5 ml/sec, a total of 100-120ml is used (3ml/sec if IV access is poor)

slice thickness is around 0.6-0.75 mm

FATTY INFILTRATION OF THE LIVER:

Insults to liver (dietary, trauma, ischemia). Diffuse or focal. When focal can simulate tumor or mass like process.

10% undergoing liver biopsy have steatosis. Obesity is the biggest risk factor for steatosis

15-30% of obese pts have steatosis.

Clinical presentation: DM, hyperlipidemia, severe hepatitis, parenteral hyperlimentation, malabsorption, corticosteroids, trauma.

How does it look like on CT?

liver attenuation lower than the spleen or paraspinal muscles, vessels are seen through the zone of fatty liver without distortion or invasion.

LIVER ATTENUATION <40 HU

Others: liver attenuation less than or equal to spleen minus 10HU, liver attenuation equal to or less than the spleen, liver attenuation less than or equal to spleen plus 5 HU, liver splenic attenuation ratio <1.1

The presence of fatty liver is a strong predictor of coronary artery disease.

With fatty infiltartion the vessels become well defined.

LIVER CIRRHOSIS

Fibrosis and necrosis of the liver parenchyma. Alcohol is the most common cause, followed by HCV, HBV, billiary cirrhosis, Primary sclerosing cholangitis, drugs.

Ct findings:

Nodular liver with increase in size of the left lobe with decrease in size of the right lobe.

Increased distance between abdominal wall and liver surface.

Nodularity of the liver will vary with nodules often seen on non contrast CT as high density nodules.

Hypervascular nodules on arterial phase are usually hepatomas, but also can be regenerating nodules.

Commonly occures with varicies, therefore check the venous phase.

High risk of GI bleeding.

Extensive ascites.

Wet bowel due to hypoproteinemia,

-> thickening of bowel wall especially of colon - no need for colonoscopy

Distended vessels of the mesentery

Recanalisation of umbilical veins in abdominal wall.

Regenerating nodules: potentially confusable with hepatomas.

It can be extreemly difficult to differentiate a hepatoma in such livers.

If you don`t do native scan and only do the arterial ph then be careful before calling it a fatty liver as the spleen can enhance very quickly in arterial ph and case a large density difference.

In early phase imaging don`t confuse varicies with lymphnodes.

Regenerating nodule types:

Monoacinar regenerative nodules

- Diffuse noduler hyperplasia

- Nodular regenerative hyperplasia

Multiacinar regenerative nodules

Lobar or segmental hyperplasia

Cirrhotic nodule

FNH

A vascular leasion is a hepatoma until proven otherwise!

If leasion become larger in late phases then its a regenerating nodule, hepatoma don`t get larger in later phases, they stay the same or become smaller or stay isodense.

Small nodules are less likely to be non malignant.

PASSIVE CONGESTION

Facts: due to cardiac disease (RHF, constrictive pericarditis, tricuspid insufficiency).

What do we see?

Retrograde flow in IVC and hepatic veins

Mottled (tarka) enhancement of the liver due to hepatic congestion

Hepatomegaly

Ascites

Periportal edema

BUDD-CHIARI SYNDROME:

Facts: aka hepatic veno-occlusive disease, acute or chronic, regenerating nodules are very common and these can simulate hepatomas.

Acute phase:

- Early enhancement of caudate lobe and central portion of liver around IVC, with decreased enhancement of the rest of the liver.

- Delayed enhancement of peripheral portios of the liver and central portion of low density ( called flip-flop appearance).

- Narrow hypodense hepatic veins and IVC with dense walls.

Chronic phase:

- Non visualization of IVC and hepatic veins.

- Hyperdense nodules or regenerating nodules.

Primary: membranous obstruction of heparic venous outflow

Secondary: thrombosis, tu.

LIVER ABSCESS:

Facts: pyogenic, fungal or amoebic in nature. 90% are pyogenic and E. coli most common in adults as etiology.

Can simulate mets or malignancy therefore history is important!

Right lobe is more commonly involved.

There is a regulra wall with enhancement.

Air fluid level is diagnostic, present in 15%.

Cluster sign is classic on CT.

Can be single or multiple.

Fungal abscess is associated with immunosuppresion.

Amebic and parasitic abscess is frequent amongst travelers.

Pyogenic abscess: Hematogenous spread from GIT, ascending cholangitis or superinfection of necrotic tissue. Clinical presentation: fever, right-sided abdominal pain, weight loss, elevated LFTs. Single or multiple, few mm-s to several cm-s, rim enhancement may occure, may contain gas within the abscess.

Parasitic Abscess-Hydatid: Echinococcus granulosus- hydatid disease or echinococcus cyst - endemic to mediterranean basin and other sheap raising areas.

Humans acquire disease from eating contaminated food.

Many times calcification on the rim of the abscess.

Eosinophilia is common.

Amebic abscess: contaminated water, multiple cluster like cysts, very sick with high fever, travel history is critical.

CT findings: enhancing rim, cystic leasion, zone of edema around border of the leasion, usually solitary but may be multiple.

Candidiasis: immunosuppressed pts, hypodense liver leasions.

HEPATIC INFARCTS

Can simulate an abscess, periphery and wedge shape!

Septic emboli, post biopsy, post transplant,

Infart can turn into abcess.

WHAT CAN SIMULATE A HEPATIC TUMOR?

Abscess, sarcoidosis, angiomyolipoma, hepatic infarct, regenerating nodule, AVM.

SARCOIDOSIS

Up to 94% have liver involvement, most patients areassymptomatic, most common CT finding is hepatomegaly, lesion may be solitary but multiple is more common.

Diff dg: lymphoma, mets.

Mostly accompanied by sarcoid of the spleen.

They are hypovascular lesions, best seen on venous phase.

PORTAL VEIN THROMBOSIS

Partial or occlusive. Acute or chronic. Due to a range of conditions ranging from pancreatitis to hepatoma, abscess, trauma

Arterial phase: perfusion changes in adjacent liver (usually increased).

Portal venous phase imaging: thrombus defined, collateral vessels well seen.

Perfusion changes in liver.

Adjacent zones have hyperemia.

MIP can be tricky and you can easily overlook a thrombus if its no totally occlusive in MIP!

PORTAL VEIN ANEURYSMS:

Rare, assymptomatic, main portal vein mostly, >20mm.

SPLANCHNIC ARTERY ANEURYSMS:

Rare, most common in splenic artery, hepatic artery is second most common.

Rupture is associated with high mortality.

HEREDETARY HEMORRHAGIC TELANGIECTASIA:

RENDU-OSLER-WEBER DISEASE

Telangiectases and AVMs.

Many times assymptomatic.

SOURCE:

CTISUS:

Part1: http://www.youtube.com/watch?v=mPd2Oe6w3BQ&feature=relmfu

Part2: http://www.youtube.com/watch?v=W3HNDbiMIjY&NR=1

Part3: http://www.youtube.com/watch?v=0a_ZxENDRCw

Bowel wall US

The typical sonographic appearance of the normal bowel wall consists of five concentric, alternately echogenic and hypoechoic layers that we describe from the lumen outward.

1- a small echogenic layer is seen that reflects the superficial mucosal interface.

2- The deep mucosa, including the muscularis mucosa, is seen as a second hyperechoic layer.

3- A third hyperechoic layer is produced by the submucosa and the muscularis propria interface.

4- The muscularis propria is seen as a fourth hypoechoic layer.

5- Finally, the marginal interface to the serosa is seen as the fifth small hyperechoic layer.

The average thickness of the normal gut wall is 2-4 mm.

IBD:

The classic sonographic feature of Crohn's disease is the "target" sign.
which means a strong echogenic center surrounded by a relatively sonolucent rim of more than 5 mm. This transmural inflammation or fibrosis can lead to complete circumferential loss of the typical gut wall layers, which results in a thick hypoechoic rim on axial images. Strictures are shown as marked thickening of the gut wall with a fixed hyperechoic narrowed lumen, dilatation, and hyperperistalsis of the proximal gut. Peri-intestinal inflammation leads to the "creeping fat" sign, which appears as a uniform hyperechoic mass typically seen around the ileum and cecum. Mesenteric lymphadenopathy is seen as multiple oval hypoechoic masses, usually in the right lower quadrant. In contrast to other forms of colitis, Crohn's disease is suggested by skip areas and involvement of the distal ileum. Possible complications of Crohn's disease comprise fistulas, abscess formation, mechanical bowel obstruction, and perforation. Abscesses are seen as poorly defined, mostly hypoechoic focal masses that can contain hyperechoic gas. Fistulas are a hallmark of Crohn's disease and are seen in as many as one third of patients with advanced disease as hypoechoic tracts with gas inclusions connecting bowel loops or adjacent structures (bladder, abdominal wall, vagina, psoas muscle). Detection of gas bubbles in abnormal locations raises the possibility of fistulous communication.


Target sign


Circular hypoechoic wall thickening and loss of stratification


"thumbprinting" and narrowing of jejunal lumen in left lower abdomen. Crohn's disease

Transverse sonogram of ileum (arrows) shows severe narrowing of small hyperechoic central lumen caused by excessively echolucent wall thickening and loss of stratification, indicating scarring of entire bowel wall.

Large-bowel enema with fine granularity of mucosa reflecting hyperemia and edema confirms suspected sonographic diagnosis of early changes in ulcerative colitis.



NON-HODGKIN LYMPHOMA IN THE GIT:

The gut is the most commonly involved extranodal site of lymphoma. The most common sites, in order of descending frequency, are stomach, small intestine, and colon, especially cecum. Eighty percent of gastrointestinal lymphomas are of B-cell origin.
Sonography classically shows transmural circumferential, profoundly hypoechoic wall thickening up to 4 cm in diameter, with loss of normal stratification. This pattern, also known as the "pseudokidney" sign in longitudinal views. The pseudokidney sign is often seen in lymphoma because of extensive hypoechoic bowel wall thickening, but it can be seen in any bowel disorder leading to marked bowel wall thickening. Other findings include nodular or bulky tumor spread caused by extraluminal involvement. Sonographic patterns favoring the diagnosis of a non-Hodgkin's lymphoma over adenocarcinoma are transmural circumferential, profoundly hypoechoic wall thickening with preserved peristalsis; lack of intestinal obstruction, because narrowing of the lumen is uncommon; involvement of a long stretch of the gut; and the presence of multiple prominent regional lymph nodes.

Other findings include nodular or bulky tumor spread caused by extraluminal involvement. Mesenteric tumor spread and bulky tumor growth need biopsy for definite diagnosis because they cannot be reliably differentiated from other diseases such as primary bowel tumors or metastases. Isolated mucosal involvement is rare and leads to hyperechoic thickening of the mucosa. Sonographic patterns favoring the diagnosis of a non-Hodgkin's lymphoma over adenocarcinoma are transmural circumferential, profoundly hypoechoic wall thickening with preserved peristalsis; lack of intestinal obstruction, because narrowing of the lumen is uncommon; involvement of a long stretch of the gut; and the presence of multiple prominent regional lymph nodes.

Profound hypoechoic wall thickening. Non-Hodgkin lymphoma


"Pseudokidney" sign in ileocecal region: marked hypoechoic thickening of bowel wall resembling form of kidney in longitudinal sonogram of cecum. Non-Hodgkin lymphoma



ACUTE TERMINAL ILEITIS

The clinical symptoms of acute ileitis are right-sided lower abdominal pain, diarrhea, and nausea, with an accelerated erythrocyte sedimentation rate, positive C-reactive protein, and leukocytosis. Caused by Yersinia species but Campylobacter and Salmonella species may also be cultured. Reported sonographic features include hypoechogenic mural thickening of the terminal ileum and cecum between 6 and 10 mm with hypoechoic swollen ileal folds in the edematous mucosa. Hypoechoic enlarged mesenteric lymph nodes are frequently seen. Color Doppler sonography in patients with infectious ileitis shows increased flow centrally rather than peripherally (as in appendicitis).
Tuberculous enteritis and Behçet's syndrome also predominantly affect the ileocecal region



APPENDICITIS

The typical finding of acute appendicitis in transverse sonograms is the target sign with a hypoechoic center, an inner hyperechoic ring, and an external thicker hypoechoic ring. In sagittal images, the inflamed appendix is seen as a blind-ending noncompressible tubular structure. Focal or circumferential loss of the inner layer of echoes usually indicates gangrenous inflammation and ulceration of the submucosa.
The diagnosis can be established with confidence if the appendix is noncompressible, shows no peristalsis, and measures more than 6 mm in diameter on axial images, and if compression leads to a localized pain response. The surrounding mesentery is often inflamed, which can be seen as a hyperechoic diffuse halo sign around the appendix. If an appendicolith is identified in an appendix of any size, the findings of the examination are always considered positive. A simple additional color Doppler examination may be helpful in the diagnosis of early acute appendicitis. The presence of visible hyperemia or increased flow in the hypoechoic muscular layer of the bowel wall may be a marker of appendicitis, whereas increased flow in the mucosal layer most likely represents enteritis. Increased flow in the fat surrounding the appendix is indicative of transmural extension of the inflammation with mesenteric response. An inflamed appendix rarely measures more than 15 mm in transverse diameter, which usually allows differentiation from ileitis. A markedly enlarged or perforating appendix or dilated fallopian tubes may lead to interpretive pitfalls.


"Target" sign (curved arrows) in acute appendicitis. On transverse image, inflamed appendix is seen with hypoechoic center, inner hyperechoic ring, and outer hypoechoic ring. Note hyperechoic circular area (straight arrows) of inflamed mesentery ("halo" sign).

Longitudinal sonogram of inflamed appendix in same patient shows blind-ending tubular structure (arrow) of at least 6 mm in diameter.


Longitudinal section of inflamed appendix reveals five round hyperechoic appendicoliths with acoustic shadows.


Complications:
A statistically significant association exists between perforation and two sonographic findings: loculated pericecal fluid and loss of the echogenic submucosa. Abscess formation is the major complication of perforating appendicitis. Abscesses may extend into the pelvis or into the peritoneal spaces of the upper abdomen. They may be sonolucent or appear as a complex mass.



SMALL BOWEL DISEASES:

Mesenteric infarction in its late stages leads to small-bowel wall thickening. In the early stages, however, no bowel wall thickening may be seen. Doppler sonography can aid in differentiating ischemic and inflammatory bowel wall thickening.
In approximately 90% of cases, small-bowel infarctions are due to arterial hypoperfusion; only 10% are caused by mesenteric vein occlusion. Acute intramural intestinal hematoma leads typically to a homogeneous hypoechoic symmetric thickening of a long stretch of the affected bowel segment, with reduced or absent peristalsis and marked luminal narrowing. In the subacute stage, strong internal echoes caused by thrombi may mimic an abscess.

OTHER TU'S

Peritoneal carcinomatosis is the most frequent malignant lesion of the small bowel and may lead to irregular wall thickening with the typical contraction of several bowel loops to a conglomerate.
Lipomas are the second most common tumors of the small intestine and occur with greatest frequency in the distal ileum and at the ileocecal valve. The location of these tumors is submucosal, or, less frequently, is subserosal. Adenocarcinoma is the second most common small intestine malignancy and the peak incidence is in the seventh decade of life.


COLITIS

Striking thickening of the colonic wall with a wide inner circle of heterogeneous medium echogenicity surrounded by a narrow hypoechoic muscularis propria is found in all patients, reflecting the gross submucosal edema. The lumen of the colon is almost completely effaced by the mural edema, and 64-77% of the patients have ascites. Pseudomembranous colitis shows typically a strong folding or gyral pattern of the swollen submucosa.



DIVERTICULITIS

Sonographic features of diverticulitis include visualization of diverticula, thickening of the bowel wall, inflammatory changes in the pericolic fat (typically on the mesenteric side of the colonic wall) , intramural or periocolic abscess , and (usually) severe local tenderness induced by graded compression. Diverticula are round or oval echogenic foci seen in or right next to the gut wall, mostly with internal acoustic shadowing. Thickening of the bowel wall is usually considered present when the distance from the echogenic lumen interface to the hyperechogenic serosa and pericolic fat exceeds 4 mm. Inflammatory changes in the pericolic fat are seen as ill-defined echogenic areas surrounding the thickened colon segment.
Pericolic abscesses typically present as hypoechoic masses adjacent to the inflamed bowel. The major sonographic finding in patients with uncomplicated acute diverticulitis of the right colon has been found to be a hypoechoic round or oval focus protruding from the segmentally thickened colonic wall and representing small abscesses in the pericolic fat.

Massive hyperechoic inflammatory infiltration seen on mesenteric side of sigmoid colon.

Echolucent fistula is seen in mesentery with small, hyperechoic, gas-containing abscess (arrow).

Diverticulum of sigmoid colon seen as focal hyperechoic intramural structure with acoustic shadow
.

COLONIC CARCINOMAS

Colonic carcinomas have two typical sonographic appearances. The first type is seen as a localized hypoechoic mass up to 10 cm or more with an irregular shape and a lobulated contour. The intraluminal gas, seen as a cluster of high amplitude, is usually eccentrically located around the mass. The second type shows segmental eccentric or circumferential thickening of the colonic wall. The mural thickening may be irregular but not as severe as in the first type. The central echo clusters are small because the diseased lumen is usually narrow. This type leads frequently to colonic obstruction. Rectum carcinomas are seen only when the bladder is well-filled.

Other features: localized irregular thickening of the colonic wall with heterogeneous low echogenicity; irregular contour; lack of movement or change in configuration on real-time scanning; and absence of a layered appearance of the colonic wall. Other findings include lymphadenopathy in most patients and abscess formation in 10% of patients.


INTUSSUSCEPTION

Only 5-10% of all intussusceptions occur in adults. The clinical symptoms may suggest partial obstruction of the intestine, but diagnosis may be difficult because symptoms are often nonspecific. The ileocecal region is the most commonly affected area in children, whereas there is no clearly preferred anatomic site in adults. Most intussusceptions in children are idiopathic and are presumed to be the result of enlarged lymphoid follicles in the terminal ileum. An organic cause can be shown in as many as 90% of cases in adults. The leading mass is nearly always a tumor of the intestinal wall, usually malignant in intussusceptions of the colon and benign in intussusceptions of the small intestine. The sonographic hallmark of intussusception has been described as the target, "doughnut," or "bull's-eye" sign. Typically, one finds two hypoechoic rings separated by a hyperechoic ring or crescent on axial images. On longitudinal images, a pseudokidney structure or layering of hypoechoic lines with hyperechoic areas is observed. The outer hypoechoic ring is formed by the intussuscipiens and the everted returning limb of the intussusceptum, with their mucosal surfaces face to face. The center of the intussusception varies with the scan level. At the apex, the center is hypoechoic because of the entering limb of the intussusceptum. At the base, the entering bowel wall forms a hypoechoic center that is surrounded by the hyperechoic mesentery. In a case of surgically proven triple jejunojejunocolonic intussusception, three hypoechoic rings separated by two hyperechoic rings were found on sonography.

SOURCE:
http://www.ajronline.org/cgi/content/full/174/1/107?ijkey=803ac7b5dd2197a30a358b5a696cd4e6a2652d4c&keytype2=tf_ipsecsha

Rheumatoid arthritis

early signs:

• fusiform periarticular soft tissue swelling (result of effusion)
• regional osteoporosis (disuse and local hyperemia)
• widened joint space
• marginal + central bone erosion (base of 4th proximal phalanx most common)
• change in ulnar styloid (erosions) and distal radioulnar joint
• atlantoaxial dislocation
• giant synovial cysts

late signs:
• flexion/extension contractures with ulnar subluxation/dislocation
• destruction/fusion of joints
• elevation of humeral heads (tear/atrophy of rotator cuff)
• resorption of distal clavicle
• erosion of superior margins of posterior portions of 3-5th ribs
• destruction/narrowing of disc spaces
• destruction of zygapophyseal joints without osteophyte formation
• resorption of spinous process
• protrusio acetabuli (from osteoporosis)

The radiographic hallmarks of rheumatoid arthritis are:

• soft tissue swelling : fusiform and periarticular. It represents a combination of joint effusion, oedema and tenosynovitis . This can be an early/only radiographic finding.
• osteoporosis that is initially juxta-articular, and later generalised. It is compounded by corticosteroid therapy and disuse.
• joint space narrowing : symmetrical or concentric.
• marginal erosions : due to erosion by pannus of the bony “bare areas”.

Hands and wrists

Diagnosis and follow-up of patients with RA commonly involves imaging of the hands and wrists. The disease tends to involve the proximal joints in a bilaterally symmetrical distribution.

There is predilection for:

• PIP and MCP joints (especially 2^nd and 3^rd MCP)
• ulnar styloid
• triquetrum

As a rule, the DIP joints are spared.

Late changes include :

• subchondral cyst formation : destruction of cartilage presses synovial fluid into the bone
• subluxation causing
  • ulnar deviation of the MCP joints
  • boutonierre and swan neck deformities
• hitchhiker’s thumb deformity
• carpal instability : scapholunate dissociation, ulnar translocation
• ankylosis

Feet

• similar to the hands, there is a predilection for the DIP and MTP joints
• involvement of subtalar joint
• calcaneal erosions

Shoulder

• erosion of the distal clavicle
• marginal erosions of the humeral head
• reduction in the acromiohumeral distance : "high-riding shoulder"

Hip

• concentric loss of joint space (cf osteoarthritis where there is tendency for superior loss of joint space)
• acetabular protrusio

Knee

• joint effusion
• loss of joint space involving all three compartments
• lack of subchondral sclerosis and osteophytes (cf OA)

Spine

The cervical spine is frequently involved in RA, whereas thoracic and lumbar involvement is rare.

Findings include :

• erosion of the dens
• atlanto-axial subluxation with cephalad migration of C2
• erosion and fusion of apophyseal joints
• erosion of spinous processes
• destruction of intervertebral disks
• osteoporosis and osteoporotic fractures

LINKS:

http://radiopaedia.org/articles/rheumatoid-arthritis

http://radiopaedia.org/articles/musculoskeletal-manifestations-of-rheumatoid-arthritis

Images: google images, www.radiopedia.org

Calcaneal apophysitis - Sever`s disease

osteochondrosis of the apophysis of the os calcis

• apopohysis becomes dense and sclerotic and undergoes fragmentation

• difficult to differentiate from normal finding on plain films
• apophysis normally varies greatly and may ossify from several centers

This is a condition that affects the cartilage growth plate and the separate island of growing bone on the back of the heel bone. This growth plate is called the physeal plate. The island of growing bone is called the apophysis. It has the insertion attachment of the achilles tendon, and it has the attachment of the plantar fascia. This island of bone is under traction from both of these soft tissue tendon and tendon-like attachments.

Sever disease is painful irritation and inflammation of the apophysis (growth plate) at the back of the calcaneus (heel bone), where the Achilles tendon inserts.

Sever disease is caused by repetitive tension and/or pressure on the growth center. Running and jumping generate a large amount of pressure on the heels.

as is shown below, however, fragmentation of the apophysis is a normal finding;

Normal heal of a child

Normal heal 2

LINKS:

http://radiopaedia.org/articles/sever-disease

http://web.me.com/radrep/Radiographers_Reporting/The_Paediatric_Leg..html

Doppler of the liver made simple

The term duplex Doppler can be confusing due to its dual usage. Sometimes, the term is used to refer to color Doppler examinations; at other times, to spectral Doppler examinations. A spectral Doppler examination includes color Doppler US; a color Doppler examination includes gray-scale US (Bmode imaging).

Doppler angle (Θ), which should be less than 60°; and sample volume or “gate” (yellow).

Cardiac phasicity creates a phasic cycle, which is composed of phases as determined by the number of times blood flows in each direction. The baseline (x = 0) separates one direction from another. Moving from left to right along the x-axis corresponds to moving forward in time. Moving away from the baseline vertically along the y-axis in either direction corresponds to increasing velocities. Any given point on the waveform corresponds to a specific velocity. The slope of the curve corresponds to acceleration (ie, a change in velocity per unit time). A bend in the curve, or inflection point, corresponds to a change in acceleration. When these turns are abrupt, they generate audible sounds at Doppler US.

strictly speaking, the term duplex Doppler refers to an examination consisting of two levels (gray-scale and color Doppler US). However, the term is commonly used by referring physicians when ordering an examination with spectral Doppler, which technically would be more accurately termed triplex Doppler. To avoid confusion, it is probably better to use terms that describe the examination more precisely. Such terms include gray-scale, color Doppler, and spectral Doppler.

Ideally, the sample volume should be placed in the midportion of the lumen, rather than toward the periphery, for optimal estimation of laminar flow. An angle indicator line is subjectively placed parallel to the vessel; however, this placement can introduce error into the final velocity calculation, especially when the Doppler angle (Θ)—the angle between the actual Doppler beam and the Doppler interrogation line—is greater than 60°.

The terms antegrade and retrograde are used to describe flow in this context. The second is to describe flow with respect to the US transducer. In this context, flow is described as moving either toward or away from the transducer. Color Doppler arbitrarily displays blood flow toward the transducer as red and blood flow away from the transducer as blue. At spectral Doppler, blood flow toward the transducer is displayed above the baseline and blood flow away from the transducer is displayed below the baseline.

Antegrade flow may be either toward or away from the transducer, depending on the spatial relationship of the transducer to the vessel; therefore, antegrade flow may be displayed above

or below the baseline, depending on the vessel being interrogated.

Retrograde flow may be seen in severe portal hypertension, in which portal venous flow reverses direction (hepatofugal flow).

Diagrams illustrate the various waveforms. The terms used to describe the degree of waveform undulation empirically describe the velocity and acceleration features of the waveform. Note that pulsatile, phasic, and nonphasic flow waveforms all have phasicity. Pulsatile flow is exaggerated phasicity, which is normally seen in arteries but can also be seen in diseased veins. Nonphasic flow does in fact have a phase (of 1); however, the phase has no velocity variation (nonphasic could be thought of as meaning “nonvariation”). The term aphasic literally means “without phase,” which is the case when there is no flow. . Phasic

is another word for cyclic.

Phasic blood flow has velocity and acceleration fluctuations that are generated by cyclic (phasic)

pressure fluctuations, which are in turn generated by the cardiac cycle (cardiac phasicity).

Differences in interpretations: D.A.M. interprets a phase as a component of the waveform on either side of the baseline; M.M.A.Y. interprets a phase as an inflection.

When phase is defined as a component of phasic flow direction, waveforms may be described in terms of the number of phases. All monophasic waveforms are unidirectional; bidirectional waveforms may be either biphasic, triphasic, or tetraphasic.

Inflection quantification. Schematics illustrate waveforms, which can be characterized on the basis of the number of inflections. Inflections occur in pairs. It is not possible to have an odd number of inflections; otherwise, a cycle would never repeat. Nonetheless, some sonologists (including M.M.A.Y.) may call the waveform on the left monophasic, based on the fact that it has only one flow velocity. M.M.A.Y. calls the waveform in the middle biphasic, based on the number of inflection points (two) per wave.

The presence or absence of phasicity can be qualified with various descriptors: pulsatile flow (arteries), phasic flow (veins), nonphasic flow (diseased veins), and aphasic flow (diseased vessels without flow).

Low-Resistance Arteries (Normal RI = 0.55–0.7)

Internal carotid arteries

Hepatic arteries

Renal arteries

Testicular arteries

illustrate that a high-resistance artery (left) allows less blood flow during end diastole (the trough is lower) than does a low-resistance artery (right). These visual findings are confirmed by calculating an RI. High-resistance arteries normally have RIs over 0.7, whereas low-resistance arteries have RIs ranging from 0.55 to 0.7. The hepatic artery is a low-resistance artery.

In the physiologic state, arteries have the capacity to change their resistance to divert flow toward the organs that need it most. In general, when an organ needs to be “on,” its arteriolar bed relaxes, the waveform takes on low resistance, and the organ is appropriately perfused. When an organ goes to “power save” mode, its arterioles constrict, the waveform switches to high resistance, and flow is diverted to other organs.

Arteries that normally have low resistance in resting (ie, nonexercising) patients include the internal carotid arteries (brain is always on), hepatic arteries (liver is on), renal arteries (kidneys are on), and testicular arteries. The postprandial (nonfasting) mesenteric vessels (superior and inferior mesenteric arteries) also have low resistance.

If the lowest point (trough) of the waveform at end diastole is high, there is relatively more flow during diastole, a finding that indicates a low-resistance vessel. If the trough is low, there is relatively less

flow during diastole, a finding that indicates a high-resistance vessel.

In general, low-resistance arteries normally have an RI of 0.55–0.7. The hepatic artery is a low-resistance vessel.

High-Resistance Arteries (Normal RI >0.7)

External carotid arteries

Extremity arteries (eg, external iliac arteries,

axillary arteries)

Fasting mesenteric arteries (superior and inferior

mesenteric arteries)

1. A high RI is not specific for liver disease;

therefore, it is less meaningful as an isolated finding than is a low RI.

2. An RI that is too high may be the result of

the postprandial state, advanced patient age, or

diffuse distal microvascular disease, which has a

wide variety of causes including chronic liver disease due to cirrhosis or chronic hepatitis.

3. An RI that is too low may be the result of

proximal stenosis or distal vascular shunting

(arteriovenous or arterioportal fistulas), as seen

in severe cirrhosis; trauma (including iatrogenic

injury); or Osler-Weber-Rendu syndrome.

n the proximal aorta (top left), plug flow results in a thin waveform and a clear spectral window (top right). Note the actual windows (yellow) superimposed on the first two spectral windows. In vessels smaller than the aorta, blood flow is laminar. In large and medium-sized vessels (left, second from top), the waveform is thick, but there is still a spectral window (middle right). In small or compressed vessels (left, second from bottom), there is significant spectral broadening, which obscures the spectral window (bottom right). Diseased vessels with turbulent flow (bottom left) also cause spectral broadening (bottom right).

Spectral broadening occurs in small blood vessels, such as the hepatic or vertebral arteries. In general, the smaller the vessel, the more spectral broadening can be expected, since a wider range of velocities is sampled from the center to the periphery of the vessel. Another cause of physiologic spectral broadening is turbulent flow at bifurcations, such as in the carotid arteries.

Diagrams illustrate how normal waveforms can be systematically characterized on the basis of direction (D), phasicity (P), phase quantification number (Q), and inflection quantification (I). Arteries can be further characterized on the basis of their level of resistance (high or low). The femoral artery has truly triphasic flow. Normal hepatic venous flow has historically been called triphasic; in reality, however, it is biphasic with predominantly antegrade flow and four inflection points.

Waveform nomenclature (abnormal waveforms). Diagrams illustrate how abnormal waveforms, like normal waveforms, can be systematically characterized on the basis of direction (D), phasicity(P), phase quantification number (Q), and inflection quantification (I).

Subjective evidence of an upstream stenosis is commonly seen as a tardus-parvus waveform.

This description is based on empirical observations of the peak of the waveform; specifically, it

refers to the late (Latin, tardus, “slow” or “late”) and low (Latin, parvus, “small”) appearance of

the peak.

The effect of stenosis on the contour of spectral waveforms and the measured parameters, such as peak systolic velocity (PSV), end-diastolic velocity (EDV), and RI. Blue = normal vessel and waveform contour, yellow = prestenotic and poststenotic vessels and waveform contours, green = in-stenosis vessel and waveform contour. Note that velocities are increased within a stenotic portion of a vessel, and that the RI is increased when the stenosis is downstream but decreased when the stenosis is upstream. A waveform whose contour is affected by an upstream stenosis is often described as a tardus-parvus waveform.

The term tardus-parvus is most commonly applied in cases of aortic stenosis and renal artery stenosis; however, this finding may be observed in the poststenotic downstream portion of any vascular territory.

Diagram illustrates upstream stenosis (tardus-parvus waveform). Use of the term tardus-parvus requires no measurement or calculation; rather, it is based on subjective observations of the peak of a waveform. When it is apparent that the peak is too late (tardus) and too low (parvus), use of the term is appropriate. This finding occurs only downstream from a stenosis (ie, due to upstream stenosis). It is commonly seen in the setting of renal artery stenosis or aortic stenosis. However, it may also be seen in the setting of hepatic artery stenosis (upstream stenosis). PSV = peak systolic velocity, TTP = time to peak.

Liver Doppler Waveforms

The term waveform signature is often used in liver Doppler US because the waveform of each major vessel is so specific that it can be used to identify the vessel, even when the gray-scale or color Doppler US appearance is ambiguous.

Hepatic arteries

The normal hepatic arterial waveform is the easiest to understand. the normal hepatic arterial waveform may be described as pulsatile.

Its peak height corresponds to peak systolic velocity (V1), and its trough corresponds to enddiastolic velocity (V2). The flow is antegrade throughout the entire cardiac cycle and

is displayed above the baseline. Because the liver requires continuous blood flow, the hepatic artery is a low-resistance vessel, with an expected RI ranging from 0.55 to 0.7. In summary, the hepatic arterial waveform is normally pulsatile with low resistance. Liver disease may manifest in the hepatic artery as abnormally elevated (RI >0.7) or decreased (RI <0.55) resistance.

High resistance is a nonspecific finding that may be seen in the postprandial state, patients of advanced age, and diffuse peripheral microvascular (arteriolar) compression or disease, as seen in chronic hepatocellular disease (including cirrhosis), hepatic venous congestion, cold ischemia

(posttransplantation), and any stage of transplant rejection.

Normal hepatic arterial flow direction and waveform. The direction of flow in any patent hepatic artery is antegrade (left), which corresponds to a waveform above the baseline at spectral Doppler US (right). The hepatic artery is normally a low-resistance vessel, meaning it should have an RI ranging from 0.55 to 0.7.

Schematics show a spectrum of increasing hepatic arterial resistance (bottom to top). The hepatic artery normally has low resistance (RI = 0.55–0.7) (middle). Resistance below this range (bottom) is abnormal. Similarly, any resistance above this range (top) may also be abnormal. High resistance is less specific for disease than is low resistance.

Low hepatic arterial resistance is more specific for disease and has a more limited differential

diagnosis, including conditions associated with proximal arterial narrowing (transplant hepatic

artery stenosis [anastomosis], atherosclerotic disease [celiac or hepatic], arcuate ligament syndrome) and distal (peripheral) vascular shunts (posttraumatic or iatrogenic arteriovenous fistulas, cirrhosis with portal hypertension and associated arteriovenous or arterioportal shunts, Osler-Weber-Rendu syndrome with arteriovenous fistulas). Arterial resistance has been shown to be decreased, normal, or increased in cirrhotic patients.

Causes of Elevated Hepatic Arterial Resistance (RI >0.7)

Pathologic (microvascular compression or disease)

Chronic hepatocellular disease (including cirrhosis)

Hepatic venous congestion

Acute congestion -> diffuse peripheral vasoconstriction

Chronic congestion -> fibrosis with diffuse peripheral compression

(cardiac cirrhosis)

Transplant rejection (any stage)

Any other disease that causes diffuse compression or narrowing of

peripheral arterioles

Physiologic

Postprandial state

Advanced patient age

Causes of Decreased Hepatic Arterial Resistance (RI <0.55)

Proximal arterial narrowing

Transplant stenosis (anastomosis)

Atherosclerotic disease (celiac or hepatic)

Arcuate ligament syndrome (relatively less common than transplant

stenosis or atherosclerotic disease)

Distal (peripheral) vascular shunts (arteriovenous or arterioportal fistulas)

Cirrhosis with portal hypertension

Posttraumatic or iatrogenic causes

Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)

Diagram illustrates normal hepatic venous flow direction and waveform. The direction of normal flow is predominantly antegrade, which corresponds to a waveform that is mostly below the baseline at spectral Doppler US. The term triphasic, which refers to the a, S, and D inflection points, is commonly used to describe the shape of this waveform; according to D.A.M., however, this term is a misnomer, and the term tetrainflectional is more accurate, since it includes the vwave and avoids inaccurate phase quantification. Normal hepatic venous waveforms may be biphasic (bottom left) or tetraphasic (bottom right).

Hepatic Veins

The hepatic venous waveform, is much more difficult to understand than the hepatic arterial waveform, owing to its many components generated by complex alternating antegrade-retrograde pressure or flow variations, which are in turn created by pressure variations related to the cardiac cycle .

Understanding it requires accepting two pieces of information. First, the bulk of hepatic venous flow is antegrade. Although there are moments of retrograde flow, the majority of blood

flow must be antegrade to get back to the heart. Antegrade flow is away from the liver and toward the heart; thus, it will also be away from the transducer and, therefore, displayed below

the baseline. Second, just as pressure changes in the left ventricle are transmitted to the systemic arteries, pressure changes in the right atrium will be transmitted directly to the hepatic veins.

Anything that increases right atrial pressure (atrial contraction toward end diastole, late systolic atrial filling against a closed tricuspid valve) will cause the wave to slope upward. Anything

that decreases right atrial pressure (downward early systolic atrioventricular septal motion, early diastolic right ventricular filling) will cause the wave to slope downward.

The normal hepatic vein waveform, despite commonly being described as triphasic, has four

components: a retrograde A wave, an antegrade S wave, a transitional V wave (which may be antegrade, retrograde, or neutral), and an antegrade D wave.

Normal triphasic Doppler waveform. Diagram shows the four waves in the normal spectral Doppler waveform. The A wave (blue), which is above the baseline, has a retrograde component of flow toward the liver. The S (red) and D (green) waves are below the baseline with flow antegrade toward the heart. The V wave (yellow) is a transitional wave, which in the normal patient may peak below, at, or above the baseline.

The a wave is the first wave encountered on the waveform. It is generated by increased right

atrial pressure resulting from atrial contraction, which occurs toward end diastole. The a wave

is an upward-pointing wave with a peak that corresponds to maximal retrograde hepatic venous flow. In physiologic states, the peak of the a wave is above the baseline, and the a wave is

wider and taller than the v wave (the other potentially retrograde wave).

Even in pathologic states, the a wave remains wider than the v wave, which represents the best way to initially orient oneself on the waveform. The only time this rule breaks down is in cases of severe tricuspid regurgitation, when the S wave becomes retrograde and merges with the a and v waves to form one large retrograde a-S-v complex.

The S wave is the next wave encountered on the waveform. Its initial downward-sloping

portion is generated by decreasing right atrial pressure, as a result of the “sucking” effect created by the downward motion of the atrioventricular septum as it descends toward the cardiac apex during early to midsystole. Note that the tricuspid valve remains closed. If it were open (tricuspid regurgitation), the result would be pathologic retrograde flow. The S wave corresponds to antegrade hepatic venous flow and is the largest downward-pointing wave in the cycle. The lowest point occurs in midsystole and is the point at which negative pressure is minimally opposed and antegrade velocity is maximal. After this low point, the wave rises again as pressure in the right atrium builds due to ongoing systemic venous return.

The v wave is the third wave encountered on the waveform. The upward-sloping portion

is generated by increasing right atrial pressure resulting from continued systemic venous return against the still-closed tricuspid valve, all of which occurs toward the end of systole. The peak of the wave marks the opening of the tricuspid valve and the transition from systole to diastole. Thereafter, the wave slopes downward because right atrial pressure is relieved during rapid early diastolic right ventricular filling. The position of the peak of the v wave varies from above to below the baseline in normal states. It should be remembered that if the v wave never rises above the baseline, it cannot be called retrograde, since the baseline marks the transition from antegrade to retrograde.

The D wave is the fourth and last wave encountered on the waveform. Its initial downward-sloping portion is generated by decreasing right atrial pressure resulting from rapid early diastolic right ventricular filling. The D wave corresponds to antegrade hepatic venous flow

and is the smaller of the two downward-pointing waves. The lowest point occurs when the antegrade diastolic velocity is maximal. The subsequent rising portion results from increasing right atrial pressure generated by the increasing right ventricular blood volume.It is almost unheard of to describe flow in the hepatic veins as hepatofugal, since the term is reserved for describing the state of pathologic flow in the portal veins. However, it is important to remember that physiologic flow in the hepatic veins is hepatofugal (ie, away from the liver and toward the heart).

In summary, the hepatic venous waveform is normally phasic and predominantly antegrade.

Causes of Pulsatile Hepatic Venous Waveform

Tricuspid regurgitation

Decreased or reversed S wave

Tall a and v waves

Right-sided CHF

Maintained S wave/D wave relationship

Tall a and v waves

(a) Tricuspid regurgitation. Spectral Doppler image clearly depicts increased pulsatility (ie, wide variation between peaks and troughs). Careful observation shows a pattern that is specific for tricuspid regurgitation. The v wave is very tall, and the S wave is not as deep as the D wave. The latter finding may also be referred to as the “decreased S wave” and is specific for tricuspid regurgitation. When tricuspid regurgitation becomes severe, the S wave will no longer dip below the baseline, and there will be one large retrograde a-S-vcomplex, or “reversed S wave”; when this occurs, the D wave is the only manifestation of antegrade flow. (b) Reversed S wave. Spectral Doppler image shows a pulsatile waveform with a reversed S wave.

Tricuspid regurgitation. Spectral Doppler image clearly depicts increased pulsatility (ie, wide variation between peaks and troughs). Careful observation shows a pattern that is specific for tricuspid regurgitation. The v wave is very tall, and the S wave is not as deep as the D wave. The latter finding may also be referred to as the “decreased S wave” and is specific for tricuspid regurgitation. When tricuspid regurgitation becomes severe, the S wave will no longer dip below the baseline, and there will be one large retrograde a-S-vcomplex, or “reversed S wave”; when this occurs, the D wave is the only manifestation of antegrade flow. (b) Reversed S wave. Spectral Doppler image shows a pulsatile waveform with a reversed S wave.

Right-sided CHF without tricuspid regurgitation. Spectral Doppler image clearly shows increased pulsatility. Careful observation shows a pattern that is specific to right-sided CHF without tricuspid regurgitation. The a wave is very tall, and the normal relationship between the S and D waves is maintained (S [systole] is deeper than D[diastole]).

Causes of Decreased Hepatic Venous Phasicity

Cirrhosis

Hepatic vein thrombosis (Budd-Chiari syndrome)

Hepatic veno-occlusive disease

Hepatic venous outflow obstruction from any cause

Overall, hepatic vein thrombosis is much less common than portal vein thrombosis. Malignant

hepatic vein thrombosis (ie, tumor thrombus) is usually the result of direct invasion from an adjacent parenchymal hepatocellular carcinoma; however, any other malignant vena cava thrombosis, such as renal cell carcinoma, adrenal cortical carcinoma, or primary inferior vena cava (IVC) leiomyosarcoma, may also cause Budd-Chiari syndrome. Similar to portal vein thrombosis, both benign and malignant hepatic vein thrombosis may manifest at gray-scale US as an echogenic intraluminal filling defect. In addition, like portal vein thrombosis, tumor thrombus classically enlarges the involved hepatic vein; however, acute bland thrombus can also cause this enlargement. Therefore, vein enlargement is not a reliable discriminating feature.

Decreased hepatic venous phasicity. Diagrams illustrate varying degrees of severity of decreased phasicity in the hepatic vein. Farrant and Meire (5) first described a subjective scale for quantifying abnormally decreased phasicity in the hepatic veins, a finding that is most commonly seen in cirrhosis. The key to understanding this scale lies in observing the position of the a wave relative to the baseline and peak negative S wave excursion. As the distance between the a wave and peak negative excursion decreases, phasicity is more severely decreased.

Portal Veins

In terms of complexity, the portal venous waveform is somewhere between those of the hepatic artery and hepatic veins. A model for understanding portal venous flow requires accepting two pieces of information. First, physiologic flow should always be antegrade, which is toward the transducer and therefore creates a waveform that is above the baseline. Second, hepatic venous pulsatility is partially transmitted to the portal veins through the hepatic sinusoids, which accounts for the cardiac variability seen in this waveform. It should also be kept in mind that the flow velocity in this vessel is relatively low (16–40 cm/sec) compared with that in the vessel coursing next to it, namely, the hepatic artery.

Normal portal venous flow direction and waveform. Drawing at top illustrates that the direction of flow in normal portal veins is antegrade, or hepatopetal, which corresponds to a waveform above the baseline at spectral Doppler US. Normal phasicity may range from low (bottom left) to high (bottom right). Abnormally low phasicity results in a nonphasic waveform, whereas abnormally high phasicity results in a pulsatile waveform. The PI is used to quantify pulsatility. Normal phasicity results in a PI greater than 0.5.

The normal portal venous waveform should gently undulate and always remain above the baseline. The peak portal velocity (V1) corresponds to systole, and the trough velocity (V2) corresponds to end diastole. . Atrial contraction, toward end diastole, transmits back pressure, first through the hepatic veins, then to the hepatic sinusoids, and ultimately to the portal circulation, where forward portal venous flow (velocity) is consequently decreased (the trough).

In summary, the portal venous waveform is normally antegrade and phasic.

Normal and abnormal portal venous phasicity. Images show a spectrum of increasing pulsatility (bottom to top). Note that increasing pulsatility corresponds to a decrease in the calculated PI. Although normal phasicity ranges widely in the portal veins, the PI should be greater than 0.5 (middle and bottom). When the PI is less than 0.5 (top), the waveform may be called pulsatile; this is an abnormal finding.

Spectral Doppler US image shows a pulsatile waveform with flow reversal in the right portal vein. The waveform may be systematically characterized as predominantly antegrade, pulsatile, biphasic-bidirectional, and di-inflectional.

Slow portal venous flow. Spectral Doppler US image shows slow flow in the main portal vein. Slow portal venous flow is a consequence of portal hypertension. In this case, the peak velocity is 9.0 cm/sec, which is well below the lower limit of normal (16–40 cm/sec). Although portal hypertension may cause a pulsatile-appearing waveform as seen in this case, the slow flow helps differentiate this condition from hyperpulsatile high-velocity states such as CHF and tricuspid regurgitation.

Hepatofugal portal venous flow. Spectral Doppler US image shows retrograde (hepatofugal) flow in the main portal vein, a finding that appears blue on the color Doppler US image and is displayed below the baseline on the spectral waveform. Hepatofugal flow is due to severe portal hypertension from any cause.

Causes of Pulsatile Portal Venous Waveform

Tricuspid regurgitation

Right-sided CHF

Cirrhosis with vascular arterioportal shunting

Hereditary hemorrhagic telangiectasia–arteriovenous fistulas

Findings that are Diagnostic for Portal Hypertension

Low portal venous velocity (<16 cm/sec)

Hepatofugal portal venous flow

Portosystemic shunts (including a recanalized umbilical vein)

Dilated portal vein

Causes of absent Portal Venous Flow

Stagnant flow (severe portal hypertension)

Portal vein thrombosis (bland thrombus)

Tumor invasion

Portal vein thrombosis (acute bland thrombus). On a spectral Doppler US image, the interrogation zone shows no color flow in the main portal vein. The spectral waveform is aphasic, which indicates absence of flow. An aphasic waveform may be produced by either obstructive or nonobstructive disease.

Portal vein thrombosis (malignant tumor thrombus). On a spectral Doppler US image, the color Doppler image shows echogenic material in a distended main portal vein without color flow. Tumor thrombus tends to enlarge veins; however, acute thrombus may do this as well. The spectral waveform is pulsatile, a finding that is abnormal in the portal vein. In fact, the pulsatility of this waveform resembles that seen in arteries; hence the term arterialization (of the portal venous waveform). This finding is specific for malignant tumor thrombus.

TIPS anatomy. Drawings at top illustrate the most common positions of a TIPS relative to the native vascular anatomy. Color Doppler US image at bottom shows the appearance of a TIPS. Note that the shunt is best seen in the long view, and that normal flow starts toward the transducer (red, above the baseline) in the caudal portion of the shunt and then moves away from the transducer (blue, below the baseline) in the cephalic part. HV = hepatic vein.

TIPS flow pattern. Drawing at top illustrates the expected flow pattern within a TIPS and the surrounding vessels when the TIPS is in the most common position. Note that any segment of the portal vein between the caudal portion of the TIPS and the portal bifurcation will have hepatopetal flow. Diagrams at bottom illustrate the appearance of normal flow in the cephalic (left) and caudal (right) parts of the TIPS.

TIPS are most commonly used for the treatment of severe portal hypertension with refractory variceal bleeding or ascites. Other indications include hepatorenal syndrome, hepatic hydrothorax, and hepatic vein occlusion (Budd-Chiari syndrome). Doppler US has a long track record of reliably helping detect TIPS malfunction.

Signs of tIPS Malfunction

Direct evidence

Shunt velocity <90 cm/sec or ≥190 cm/sec

Temporal increase or decrease in shunt velocity >50 cm/sec

Indirect evidence

Main portal venous velocity <30 cm/sec

Collateral vessels (recurrent, new, or increased)

Ascites (recurrent, new, or increased)

Right-left portal venous flow reversal (ie, hepatofugal to hepatopetal)

FOR A MORE DETAILED REVIEW OF THE TOPIC PLEASE VISIT THE SITE OF THE MAIN ARTICLE, THE LINK IS IN THE LINKS SECTION OF THIS PAGE.

THIS PAGE IS INTENDED TO BE A SUMMERY OF THE ORIGIONAL ARTICLE PUBLISHED IN THE RADIOGRAPHICS MAGAZINE.

SOURCE:

http://radiographics.rsna.org/content/31/1/161.full.pdf

http://radiographics.rsna.org/content/31/1/161.figures-only

LINKS:

http://giyabradiology.blogspot.com/2011/05/portal-vein-inferior-vena-cava.html

http://giyabradiology.blogspot.com/2011/05/fatty-liver.html

http://radiographics.rsna.org/content/29/7/2081.full.pdf

http://radiographics.rsna.org/content/24/2/497.full.pdf

http://radiographics.rsna.org/content/23/5/1315.full.pdf