Contrast enhanced ultrasound - CEUS

“Second-generation” blood pool ultrasonographic (US) contrast media are filled with gases other than air and allow continuous real-time assessment of liver lesions at low acoustic pressure (low mechanical index).

Older Air-filled agents (first-generation US contrast media), on the other hand, can be used only with high-mechanical-index intermittent technologies because micro-bubble rupture is necessary to obtain an adequate echo signal.

1- The arterial (early) phase (15–35 seconds after injection),

2- the portal (venous) phase (35–90 seconds),

3- the sinusoidal (parenchymal or late vascular) phase (90–240 seconds).

What do we see afte injection?

Contrast medium is seen arriving in the hepatic artery and rapidly spreading through its branches. Liver parenchymal echogenicity increases consistently from the arterial to the portal phase and then decreases slightly during the sinusoidal phase. Enhancement of the branches of the hepatic artery and portal vein is readily visualized, without flow signals “bleeding” outside the vessel lumina (as happens with Doppler US). Cirrhotic liver may exhibit slightly delayed and less intense parenchymal enhancement during the portal phase.

How to describe what we see?

Echogenicity is defined with respect to the surrounding parenchymal echo levels at the same imaging time and depth. In addition, lesions can be compared with the blood pool, being hypervascular when demonstrating the same echogenicity as contrast material–enhanced vessels and hypovascular when demonstrating a lower echogenicity.

Example:

Lesion conspicuity depends on the lesion-to-parenchyma echogenicity gradient; in this case, HCC has greater conspicuity during the arterial phase and appears hyperechoic. During the portal and sinusoidal phases, the lesion is first slightly and then clearly hypoechoic relative to the surrounding parenchyma.

Enhancement may be absent (eg, cyst, small hemangioma, dysplastic nodule, or early HCC) or

may be diffuse homogeneous or diffuse heterogeneous (eg, hypervascular metastasis or atypical CCC, lymphoma, FNH).

Rim pattern manifests as peripheral, irregular but continuous arterial phase enhancement (eg, metastasis, CCC).

The globular pattern consists of discontinuous peripheral arterial phase enhancement with discrete echoic globules (eg, cavernous hemangioma). The spokelike pattern seen during the arterial phase is due to discrete arteries radiating to the periphery (eg, FNH).

The stippled pattern seen during this phase consists of discrete arteries with a chaotic distribution (eg, HCC).

The arterial phase “basket” pattern, usually seen in combination with a stippled appearance, consists of a feeding artery branching around and then within a nodule (eg, HCC).

The liver-enhancing effect of the blood pool contrast agent SonoVue (Bracco, Milan, Italy) lasts 3–5 minutes; more than 5 minutes after contrast material injection, most lesions become undetectable or have the same echogenicity as on baseline images.

Imaging techniques:

Can be divided into two main groups:(a) high-mechanical-index modalities, which allow static, intermittent imaging, and (b) low-mechanical-index modalities, which allow dynamic, continuous acquisition and require second-generation contrast media.

SonoVue: A sulfur hexafluoride–based contrast medium. This agent comes as a sterile, nonpyrogenic, lyophilized powder. A white milky suspension is obtained by adding 5 mL of 0.9% normal saline solution with an aseptic technique and vigorously shaking the mixture for 10 seconds. The reconstituted product provides 8 μL/mL of SF₆ micro-bubbles, which is then administered either in its entirety (4.8 mL) or as a half dose (2.4 mL). The half dose is usually sufficient, but injecting the entire volume may be desirable in cases of liver steatosis or chronic hepatitis.

It is usually administered as a single rapid bolus injection into an antecubital vein. US is started immediately and lasts 4–5 minutes.

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HEMANGIOMA:

Liver hemangioma is a hypervascular lesion consisting of a network of vascular spaces with slow or, less commonly, rapid flow. The distribution of small arterial branches, venous lakes, and fibrosis varies. Arterial inflow is present, whereas portal afference is absent or minimal, and there is no arteriovenous fistula.

Small (<1-cm) hemangiomas are usually iso-vascular relative to the surrounding parenchyma during the arterial phase. Less commonly, a subtle, diffuse enhancement (homogeneous or heterogeneous) is seen. Larger hemangiomas (>1 cm) usually demonstrate peripheral globular pooling of contrast medium, with hyperechoic globules (nodules) becoming progressively larger and more numerous (puddle enhancement). Contrast material uptake can be fast or slow depending on intralesional circulation speed. Uncommonly, contrast material enhancement is rapid and homogeneous, simulating that of hypervascular metastases. Rarely, peripheral rimlike enhancement or diffuse homogeneous enhancement is seen (small, hypervascular hemangioma). Discrete intralesional arteries are usually not seen in hemangiomas.

(a) Baseline US image shows two homogeneously hyperechoic lesions (arrowheads) contiguous with a portal branch (arrow).

Early portal phase US image obtained 35 seconds after contrast material injection demonstrates lesion isoechogenicity. Arrow indicates an enhanced vein.

(c) Parenchymal phase US image obtained 121 seconds after injection demonstrates persistent lesion isoechogenicity.

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(a) Baseline US image shows a heterogeneously hypoechoic lesion (arrow).

(b) Arterial phase US image obtained 22 seconds after contrast material injection demonstrates peripheral globular enhancement (large arrow) and a perilesional vessel (small arrow).

(c) Portal phase US image obtained 93 seconds after injection demonstrates centripetal (albeit incomplete) lesion enhancement (large arrow), which is clearly hyperechoic relative to the surrounding parenchyma. Small arrow indicates the perilesional vessel.

(d) Portal phase computed tomographic (CT) scan shows a hyperattenuating lesion with small central areas of poor enhancement (arrow).

Isovascularity persists throughout the portal and sinusoidal phases in small hemangiomas. In contrast, larger hemangiomas show progressive centripetal enlargement of peripheral hyperechoic globules with progressive filling. As the globules enlarge, they create “bridges” to the opposite side of the lesion. Centripetal filling may be absent in smaller lesions, but real-time images usually allow identification of this finding even in small, rapidly enhancing hemangiomas. Persistent strong intralesional enhancement (hyperechogenicity) is typical, although a central area or sac of persistent poor enhancement due to fibrosis may be seen in larger hemangiomas; owing to the blood pool nature of US contrast media, incomplete centripetal filling is more common at US than at CT or magnetic resonance (MR) imaging. Rarely, hemangioma shows heterogeneous hypoechogenicity (thrombosis)

Early portal phase US image obtained 43 seconds after contrast material injection shows multiple peripheral enhancing globules (large arrows) and thin enhancing septa centrally (small arrows). Although most of the lesion is hypoechoic, and was even on delayed images (not shown), the globular pattern allowed characterization.

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HEPATOCELLULAR ADENOMA:

Adenoma is a hypervascular lesion without portal tracts. Large, subcapsular tributary arteries are typical, whereas necrotic and hemorrhagic changes are frequently seen in larger masses.

Intense, rapid or slow contrast material enhancement is seen during the arterial phase. Discrete, perilesional feeding arteries manifest as enhancement around the tumor capsule; such enhancement is never seen in HCC. Heterogeneous enhancement with perfusion defects corresponding to hemorrhagic areas is present in larger masses.

More or less rapid washout is seen during the portal and sinusoidal phases, with initial hypervascularity followed by isovascularity; a hypoechoic appearance is never seen. A heterogeneous texture is seen in larger masses, with internal hypoechoic regions.

(a) Baseline US image shows a subtle hyperechoic area (arrow).

(b) Arterial phase US image obtained 21 seconds after contrast material injection demonstrates early, marked lesion enhancement (arrow). K = kidney.

(c) Portal phase US image obtained 55 seconds after injection demonstrates subtle but persistent enhancement (arrow). K = kidney.

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Focal Nodular Hyperplasia - FNH

FNH is a hypervascular, hyperplastic lesion caused by preexisting vascular malformation. Patients are typically women with a history of oral contraception. FNH is not seen in patients with cirrhosis. There is usually a peripheral pseudo-capsule and a central or eccentric fibrous scar radiating to the periphery and containing arteries.

During the arterial phase, FNH manifests as a tortuous feeding artery and a central artery with very early centrifugal stellate branching (“wheel spoke” or “central spider” pattern). Immediately thereafter, during the full arterial phase, the lesion demonstrates homogeneous, intense, and very rapid contrast material enhancement. A hypoechoic central scar may be present.

(a) Baseline US image shows a slightly hypoechoic lesion (arrows).

(b) Very early arterial phase US image obtained 15 seconds after contrast material injection demonstrates rapid lesion enhancement (arrows) with discrete intralesional and perilesional arteries.

(c) Later arterial phase US image obtained 29 seconds after injection demonstrates marked homogeneous lesion enhancement (arrows).

(d) Portal phase US image obtained 49 seconds after injection demonstrates lesion isoechogenicity (arrows).

During the portal and sinusoidal phases, there is slow or, less commonly, rapid washout, with initial hypervascularity followed by isovascularity (isoechoic or hyperechoic appearance). A homogeneous texture with possible central stellate hypoechogenicity is characteristic.

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(a) Baseline US image shows a homogeneous, well-defined mass (arrows) depending from the right hepatic lobe.

(b) Arterial phase US image obtained 22 seconds after contrast material injection demonstrates multiple radiating arteries within the mass (arrows).

(c) Portal phase US image obtained 56 seconds after injection demonstrates marked enhancement of the mass (white arrows), with a hypoechoic central scar (black arrow).

(d) Late arterial phase CT scan shows a markedly enhancing mass (white arrows) with central scarring (black arrow) (cf c).

The overall appearance of FNH usually allows differentiation from fibrolamellar HCC, an uncommon lesion that also contains a central scar. Fibrolamellar HCC is usually heterogeneous because of necrosis, shows internal calcification, and is hypoechoic on portal phase images.

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Dysplastic Nodules and Early HCC

Dysplastic nodules are premalignant lesions within a cirrhotic liver that develop small arteries and exhibit portal tracts. Early HCC is usually a small, well-differentiated nodule with increased arterialization and gradual loss of portal vessels.

During the arterial phase, dysplastic nodules and early HCC are usually substantially isovascular with no arterial enhancement. Nevertheless, high-grade dysplastic nodules can sometimes demonstrate marked enhancement.

Dysplastic nodules and early HCC have an isoechoic or subtly hypoechogenic appearance throughout the portal and sinusoidal phases.

(a) Baseline US image shows a small, hypoechoic nodule (arrow).

(b) Arterial phase US image obtained 25 seconds after contrast material injection fails to depict any lesion.

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Advanced HCC

Small to medium-sized HCC (1–5 cm) is a hypervascular lesion, with neoangiogenesis. There is little or no portal supply.
In arterial phase, advanced HCC demonstrates hyperperfusion starting immediately after enhancement of the hepatic artery. Smaller HCCs usually enhance slightly faster than larger ones.

(nem másoltam ki a képeket)

One or more hypertrophic feeding arteries are seen reaching lesion poles and branching intralesionally (basket pattern).

Discrete peri- and intranodular vessels are also recognizable at US, usually being dysmorphic, chaotic, and randomly stippled and having a corkscrew-shaped distribution.

Uncommon hypovascular HCC demonstrates isoperfusion or even hypoperfusion relative to the surrounding parenchyma and hence is difficult to characterize.

Areas of fatty degeneration with increased echogenicity, within the HCC do not show enhancement. Large lesions (“big” HCC) demonstrate peripheral enhancement, central hypovascular necrotic areas, and vascular lakes with hyperechoic contrast agent pooling.

During the portal and sinusoidal phases, advanced HCC demonstrates rapid washout (faster than with FNH or adenoma) and has an isovascular or, less commonly, hypovascular appearance. Transient isoechogenicity is seen on full portal phase images, eventually followed by moderate hypoechogenicity on delayed images.

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Cholangiocellular Carcinoma

CCC can be hypovascular or, less commonly, hypervascular on arterial phase images, with portal phase vascularity usually being limited.

CCC demonstrates peripheral rimlike enhancement or heterogeneous enhancement during the arterial phase. Poor heterogeneous enhancement is possible, with an overall isoechoic or hypoechoic appearance.

CCC usually has a hypoechoic appearance on portal and sinusoidal phase images. Persistent subtle rim enhancement is possible. Conspicuity increases progressively, and necrotic areas with more marked hypoechogenicity may be seen. Satellite lesions may also be encountered.

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Metastasis

Liver metastasis can be hypo- or, less commonly, hypervascular on arterial phase images depending on the organ of origin. All metastases show some degree of arterial neoangiogenesis (peripheral macrovessels and central microvessels) and lack at least a portion of the portal supply.

During the arterial phase, liver metastasis shows peripheral rimlike enhancement of varying thickness and uniformity, with an eventual target-like appearance.

There is always some kind of arterial inflow peripherally, even if subtle and heterogeneous, whereas most of the lesion is isoechoic relative to the surrounding parenchyma. Perilesional hyperemia with arterial phase–dependent enhancement of normal tissue is possible, and few discrete perilesional arteries can be found. Macroscopic arteries are usually not seen within the lesion.

There is no centripetal filling during the portal and sinusoidal phases. Subtle rim enhancement may persist. Washout is rapid; lesions are seen as filling defects that progressively increase in conspicuity relative to normal parenchymal enhancement (black holes on a bright background).

Metastases have a heterogeneously hypoechoic appearance with internal echo pollution due to microbubbles and haphazard movement within abnormal small tumor vessels (microcirculation).

Markedly hypoechoic areas within larger lesions are due to necrosis. Less commonly, hypervascular metastases may become isoechoic (undetectable) during this phase.

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Lymphoma

Primary and secondary liver lymphomas are hypercellular lesions with some degree of arterial neoangiogenesis and a poor portal supply.

Like metastasis, lymphoma demonstrates peripheral rimlike enhancement of varying thickness and uniformity during the arterial phase, with an eventual targetlike appearance. Intense, diffuse heterogeneous enhancement is rarely noted.

Like metastasis, lymphoma demonstrates no centripetal filling during the portal and sinusoidal phase. Washout is rapid, and lymphoma has a heterogeneous hypoechoic appearance with internal echo pollution (microcirculation) that progressively increases in conspicuity.

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Abscess

Pyogenic and amoebic liver abscesses have a variable degree of liquefaction and loculation. Their vascularity depends on the evolution stage.

Liver abscesses, especially pyogenic abscesses, have an overall coalescent appearance with a sharply defined necrotic cavity. Rim enhancement is typical. Discrete arteries are noted running along lesion margins and internal septa, with persistent enhancement of the septa. Internal enhancement is absent, and there is no microcirculation within fluid or necrotic components. Perilesional hyperemia with arterial phase–dependent enhancement of normal tissue can be seen.

During the portal and sinusoidal phases, abscesses demonstrate rapid (or sometimes slower) washout, an overall hypoechoic appearance, and marked necrotic and fluid areas internally.

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Peliosis Hepatis

Peliosis hepatis is characterized by multiple blood-filled spaces ranging from 1 mm to 4–5 cm within the hepatic parenchyma.

During the arterial phase, peliosis hepatis shows a transient “fast surge” central echo enhancement that is synchronous with vessel enhancement.

During the portal and sinusoidal phases, peliosis hepatis demonstrates isoechogenicity or hypoechogenicity with no contrast material pooling or centripetal filling, allowing differentiation of this entity from hemangiomatosis.

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Focal Steatosis

Focal areas of fatty infiltration may have a round, lesionlike appearance and are hyperechoic on conventional US images. Vascularity is normal.

During the arterial phase, focal steatosis demonstrates substantial isovascularity but no arterial enhancement, with normal vessels traversing the pseudolesion without mass effect.

Isovascularity persists during the portal and sinusoidal phases, with normal vessels still traversing the pseudolesion without mass effect.

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Skip Area in Fatty Liver

Focal regions of spared normal parenchyma within a heterogeneously distributed steatosis may have a round, pseudolesional appearance and are hypoechoic at baseline US. The vascularity of these spared areas is normal.


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Contrast-enhanced US has an 89% sensitivity and a 100% specificity in the diagnosis of hemangioma. The capability of this modality to characterize hemangiomas is approximately equal to that of MR imaging, even in small lesions. Peripheral globular enhancement with centripetal filling indicates a hemangioma, even if central enhancement is subtle or absent on portal and sinusoidal phase images. Centripetal filling is not seen in malignancies. Peripheral enhancement followed by centripetal enhancement has a 100% specificity but only an 18% sensitivity for hemangioma. Globular peripheral enhancement is found in 70%–92% of hemangiomas, rimlike peripheral enhancement in 10%–25%, and diffuse homogeneous enhancement in 5% . Peripheral nodular enhancement with contrast material filling and absence of intralesional arteries has showed an 88% sensitivity and a 99% specificity for hemangioma. Peripheral or diffuse contrast material pooling is typical for hemangioma, with a 76.5% sensitivity and a 100% specificity.

Contrast-enhanced US has a 94% sensitivity and a 93% specificity in the diagnosis of HCC and has proved sensitive in demonstrating HCC vascularity. In one series, contrast-enhanced US demonstrated vascularity in 91% of HCC nodules, CT in 93%, and angiography in 88%. Contrast-enhanced US is more sensitive than Doppler US in this setting. In one study, color Doppler US demonstrated blood flow in 87% of HCC nodules that were hypervascular at contrast-enhanced US; in another series, power Doppler US demonstrated vascularity in 69% of HCC nodules that were identified at angiography-assisted CT, whereas contrast-enhanced US showed vascularity in 96%.

HCC is typically hypervascular on arterial phase images but never exhibits rim or globular enhancement. Enhancement is homogeneous in 50% of cases and heterogeneous in 50%. Diffuse lesion enhancement on early arterial phase images indicates HCC, especially when followed by rapid washout. If a diffuse or mosaic-like arterial phase enhancement pattern or a reticular parenchymal phase enhancement pattern is regarded as indicating HCC, contrast-enhanced US has a 92% sensitivity and a 96% specificity for this entity. The presence of intratumoral vessels on arterial phase images combined with homogeneous or heterogeneous enhancement on portal phase images has a 95% sensitivity and a 94% specificity for HCC. The presence of arteries spreading into the lesion together with homogeneous hyperechoic tumor enhancement has an 83% sensitivity and a 94% specificity for HCC.

Arterial phase enhancement with slow deenhancement suggests adenoma or FNH instead of HCC. HCC and FNH can be distinguished on the basis of several distinctive morphologic features. FNH is homogeneous, even when large, whereas HCC tends to develop necrotic areas. Moreover, FNH is usually hyperechoic during the portal phase of enhancement, whereas HCC becomes iso- or hypoechoic. Central stellate enhancement has a specificity of 100% but a sensitivity of only 67% for FNH.

Contrast-enhanced US has a sensitivity of 77% and a specificity of 93% in the diagnosis of metastases. This modality is more sensitive than conventional US in detecting liver metastasis and almost as sensitive as CT or MR imaging. In one series, conventional US helped detect 59% of liver metastases seen at CT, whereas contrast-enhanced US helped detect 97%. In another study, the number of lesions detected rose from nine to 19 when contrast-enhanced US was used in addition to conventional US; contrast-enhanced US in particular allowed detection of small metastases. Contrast-enhanced US has been shown to help detect 90% of liver metastases that are visualized at ferumoxides-enhanced MR imaging.

Peripheral rim enhancement strongly suggests metastasis, especially if it is not followed by lesion filling and is not combined with a finding of intralesional vessels. Rim enhancement has been observed in 48%–70% of liver metastases. Rim enhancement, a clear parenchymal phase defect, or both can be used to diagnose metastasis or CCC with a 90% sensitivity and a 95% specificity. Of course, hypervascular metastases overlap with other benign and especially malignant hypervascular lesions, although general context and a clearly hypoechoic appearance during the portal phase generally allow differentiation.

Aside from its arterial phase appearance, a homogeneously hypoechoic lesion on portal or sinusoidal phase images should be considered malignant until proved otherwise, since benign lesions are iso- or hyperechoic during these phases. A clearly hypoechoic lesion on portal or sinusoidal phase images is usually considered to represent metastasis. The differential diagnosis of enhancement defects includes lesions such as lymphoma, CCC, HCC, dysplastic nodules in chronic liver disease (rarely), and abscess. The constellation of contrast-enhanced US findings in pyogenic abscess has been shown to be effective in differentiating this benign entity from metastasis.

In itself, the arrival time of contrast medium cannot be used to distinguish between benign and malignant lesions; early arrival is only 67% sensitive and 60% specific for malignancy.

SOURCE:

http://radiographics.rsna.org/content/25/2/333.full?sid=a5f65a78-bbc3-4ca0-940c-b27759b02d24

Links:

http://radiographics.rsna.org/content/25/2/333.full?sid=a5f65a78-bbc3-4ca0-940c-b27759b02d24

http://radiographics.rsna.org/content/24/4/921.full?sid=a5f65a78-bbc3-4ca0-940c-b27759b02d24
* http://www.ceusinfo.com/

Delivery of CT contrast media

IV contrast travels from the veins at the injection site to the right heart -> pulmonary arteries -> pulmonary veins -> left heart -> arterial system (first pass).

After the contrast is distributed throught the body it reenters the right heart (equilibrium phase).

Injection duration affects the cummulative arterial enhancement and peak enhancement. Both will be smaller if the injection duration is smaller. The maximal arterial enhancement response is also directly propotional to the iodine administration rate (iodine flux). and can be controlled by increasing the injection rate and / or the iodine concentration.

The bolus method involves a small test injection and multiple low dose scans performed over the artery of interest until the contrast is visualised.

The bolus triggering method involves eliminating the test injection and scan only begins when contrast density in a preselected artery exceeds a pre-set limit.

USUALLY 200 HU IS THE TRIGGERING DENSITY

There is an additional 4-8 sec delay built in to the system for table movement time in the test bolus method.

Either the Aorta, or the Pulmonary artery is selected for monitoring contrast density.

Flow in the lower limb can be assymetric and very variable. With the current 16-slice scanners it is possible to outrun the contrast bolus to the lower limbs. But it is also possible to over delay and end up with venous contamination. One trick is to use a slightly slower injection rate of 3 ml/sec and to trigger the scanner from the common femoral vein.

At 2 ml/sec injection rate, a 45-50 sec scan delay time for the chest and a 70 sec delay time for the abdomen is used.

At 3 ml/sec injection rate, a 40-4 sec scan delay, and for the abdomen a 55-60 sec scan delay time is applied.

LIVER:

Some studies like dual phase liver scan requires images in both arterial and venous phase, in these cases it is important to add 10-15 sec delay after the contrast appears in the aorta, because our goal is to image the liver in the late arterial phase, which usually occures bw 25-30 sec at 4-5 ml/sec injection rate.

The second scan can be performed at 70 sec after the start of the injection.

Summary:

25-30 s at 4-5 ml/min OR AO+10 s

Portal phase: 70s

PANCREAS:

Pancreatic phase occures at approximately 40 sec, or at 20-25 sec after the contrast appears in the aorta.

Summary:

AO + 20-25 s

Contrast amount and density:

To maximise arterial enhancement for vascular CTA studies, high-density contrast >350 mgI/ml is recommended, and should be paired with rapid injection rate of 4-5ml/sec.

Lower density contrast can be used but then it should be paired with higher injection rate of 5-6 ml/sec.

A good rule of thumb for MDCT is that the contrast time should last for the duration of the scan plus a small delay factor, which is usually 4-10 sec and may correspond to the triggering delay.

Injection duration = scan duration + delay factor

Total scan time = (Total length covered x rotation time)/(Pitch x slice thickness)

Contrast volume (mL) = Injection duration x Injection rate (mL/sec)

Injection rate:

Standard injection rate for CTA is 3-6ml/sec. The faster the contrast is injected the higher the peak aortic enhancement. The peak enhancement is also related to the injection duration.

Biphasic contrast injection could produce a more uniform plateau.

Saline flush:

25-50 ml of saline is injeted. It will clear the residual contrast from the IV tubing and accelerate washout from the arm veins. This can provide an effective 10mL of additional usable contrast .

This will decrease the risk of contrast nephrotoxicity. Saline flush also reduces the very dense contrast seen in the subclavian vein, brachiocephalice vein, and superior vena cava. This helps to reduce streak artifacts.

LINKS:
http://www.ctisus.com/media/2011/06/13/ct-evaluation-of-the-aorta

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