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Saturday, 21 May 2011

Doppler of the liver made simple

Figure 1

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).

Figure 2

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

Figure 3
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°.

Figure 4

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).

Figure 5
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).

Figure 6
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.

Figure 7
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.

Figure 8
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

Figure 9
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.

Figure 10
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.

Figure 11
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.

Figure 12
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).

Figure 13

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.

Figure 14
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.

Figure 15

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.

Figure 16
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
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)

Figure 18
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.

Figure 3
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.

Figure 4a

Figure 4b

Figure 4c

Figure 4d

Figure 5e

Figure 19

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

Figure 20a
(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.

Figure 20b
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.

Figure 21
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
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.

Figure 22
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.

Figure 8

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.

Figure 23
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.

Figure 25
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.

Figure 26
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.

Figure 27
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

Figure 28
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.

Figure 29
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.

Figure 30
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.

Figure 31
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)





Abdomial x-rays

Coffee-bean sign / Sigmoid volvulus

The coffee-bean sign (also known as kidney bean sign and bent inner tube sign 4 ) is a sign on an abdominal plain film of a sigmoid volvulus although some authors have also used the term to refer to closed loop small bowel obstructions.

This thick 'inner wall' represents the double wall thickness of opposed loops of bowel, with thinner outer walls due single thickness.


This patient has undergone an ERCP, on the image you can see air in the common bile duct (ductus choledochus)

The fatty liver

-One of the most common abnormalities of the liver.
-Common patterns include diffuse fat accumulation, diffuse fat accumulation with focal sparing, and focal fat accumulation in an otherwise normal liver.
-Unusual patterns that may cause diagnostic confusion by mimicking neoplastic, inflammatory, or vascular conditions include multinodular and perivascular accumulation.


-Most common: Alcohol, insulin resistance, obesity, hyperlipidemia.
-Common: Viral infection (hep. B.,C.), drug use.
-Rare: rapid weight loss, surgery ( jejuno-ileal bypass), parenteral nutrition, starvation, radiotherapy.
-Congenital: Storage disorders(Glycogen storage disorder, 1-Antitrypsin deficiency, Wilson disease, Hemochromatosis), cystic fibrosis.

Characterized histologically by triglyceride accumulation within the cytoplasm of hepatocytes.
Hepatocytes in the center of the lobule (near the central vein) are particularly vulnerable to metabolic stress and tend to accumulate lipid earlier than those in the periphery. Therefore steatosis tends to be most pronounced histologically in the zone around the central veins and less pronounced in zones around the portal triads.

Steatosis may progress to steatohepatitis (with inflammation, cell injury, or fibrosis accompanying steatosis) and then cirrhosis. There are data that suggest that the coexistence of steatosis with other liver diseases, such as viral hepatitis, increases the risk of disease progression

The accumulation of discrete triglyceride droplets in hepatocytes and, rarely, in
other cell types. Infiltration of fat into the parenchyma does not occur. The term fatty liver is
more accurate than fatty infiltration.

The prevalence of fatty liver in the general population is about 15%, but it is higher among those
who consume large quantities ( 60 g per day) of alcohol (45%), those with hyperlipidemia (50%) or obesity (body mass index, 30 kg/m2 ) (75%), and those with both obesity and high alcohol consumption (95%).


The echogenicity of the normal liver equals or minimally exceeds that of the renal cortex or spleen. Intrahepatic vessels are sharply demarcated, and posterior aspects of the liver are well depicted. Fatty liver may be diagnosed if liver echogenicity exceeds that of renal cortex and spleen and there is attenuation of the ultrasound wave, loss of definition of the diaphragm, and poor delineation of the intrahepatic architecture. To avoid false-positive interpretations, fatty liver should not be considered present if only one or two of these criteria are fulfilled.

normal FigureFigurefatty


At unenhanced CT, the normal liver has slightly greater attenuation than the spleen and blood,and intrahepatic vessels are visible as relatively hypoattenuated structures. Fatty liver can be diagnosed if the attenuation of the liver is atleast 10 HU less than that of the spleen or if the attenuation of the liver is less than 40 HU. In severe cases of fatty liver, intrahepatic vessels may appear hyperattenuated relative to the fat-containing liver tissue.
Fatty liver can be diagnosed at contrast-enhanced CT if absolute attenuation is
less than 40 HU, but this threshold has limited sensitivity.




Chemical shift gradient-echo (GRE) imagingwith in-phase and opposed-phase acquisitions is the most widely used MR imaging technique forthe assessment of fatty liver. The signal intensityof the normal liver parenchyma is similar on in phase and opposed-phase images. Fatty liver may be present if there is a signal intensityloss on opposed-phase images in comparison within-phase images, and the amount of hepatic fat present can be quantified by assessingthe degree of signal intensity loss.


Diffuse fat deposition:
Its the most frequently encountered pattern. Liver involvement usually is homogeneous.

Focal Deposition and Focal Sparing:
Slightly less common patterns are focal fat deposition and diffuse fat deposition with focal sparing. In these patterns, focal fat deposition or focal at sparing characteristically occurs in specific areas (eg, adjacent to the falciform ligament or
ligamentum venosum, in the porta hepatis, and in the gallbladder fossa). This distribution is
not yet fully understood but has been attributed to variant venous circulation, such as anomalous gastric venous drainage. Focal fat deposition adjacent to insulinoma metastases also has been reported and is thought to be due to local insulin effects on hepatocyte triglyceride synthesis and accumulation.

focal deposite

Imaging findings suggestive of fatty pseudolesions rather than true masses include the following: fat content, location in areas characteristic of fat deposition or sparing, absence of a mass effect on vessels and other liver structures, a geographic configuration rather than a round or oval shape, poorly delineated margins, and contrast enhancement that is similar to or less than that of the normal liver parenchyma.

focal deposite

Involved areas usually are relatively small, but occasionally there may be confluent
heterogeneous regions of focal deposition and sparing that span large areas of the liver.

Multifocal Deposition:
An uncommon pattern is multifocal fat deposition. In this pattern, multiple fat foci are scattered
in atypical locations throughout the liver. The foci may be round or oval and closely mimic true nodules. For this purpose, chemical shift GRE imaging (MRI) is more reliable than
CT or US.

Perivascular Deposition:
This pattern is characterized by halos of fat that surround the hepatic veins, the portal veins, or both hepatic and portal veins. The configuration is tramlike or tubular for vessels with a course in the imaging plane and ringlike or round for vessels with a course perpendicular to the imaging plane. The pathogenesis of perivascular fat deposition in the liver is unknown.

perivenous fat accumulation

periportal fat accumulation

Subcapsular Deposition:
In patients with renal failure and insulin-dependent diabetes, insulin may be added to the peritoneal dialysate during kidney dialysis. This route of insulin administration exposes subcapsular hepatocytes to a higher concentration of insulin than that to which the remainder of the liver is exposed. Since insulin promotes the esterification of free fatty acids into triglycerides, the peritoneal administration of insulin results in a subcapsular pattern of fat deposition, which may be manifested as discrete fat nodules or a confluent peripheral region of fat.

Primary Lesions and Hypervascular Metastases
In general, the differentiation of focal or multifocal fat accumulations from primary hepatic lesions (eg, hepatocellular carcinoma, hepatic adenoma, and focal nodular hyperplasia) or from
hypervascular metastases in the liver is not problematic because these lesions exert a mass effect, tend to show vivid or heterogeneous enhancement after contrast agent administration, and may contain areas of necrosis or hemorrhage. Infiltrative hepatocellular carcinoma is a notable exception; on CT images, this tumor may exert a minimal mass effect, show
little evidence of necrosis, show the same degree of enhancement as the normal liver parenchyma, and closely resemble heterogeneous fat deposition. The correct diagnosis is usually possible with MR imaging.

infiltrative HCC native

infiltrative HCC portal phase

Hypovascular Metastases and Lymphoma
The clinical manifestations and imaging features such as lesion morphology, location, and microscopic fat content usually permit a correct diagnosis. Chemical shift GRE imaging may be necessary to assess the amount of intralesional fat.

Perfusion Anomalies
Are visible only during the arterial and portal venous phases after contrast agent administration. They are not detectable on unenhanced images or equilibrium phase images.

Periportal Abnormalities
The US- and CT-based differential diagnosis of periportal fat deposition is broad and includes
edema, inflammation, hemorrhage, and lymphatic dilatation. Edema, inflammation, and lymphatic dilatation tend to affect the portal triads symmetrically. Hemorrhage characteristically involves the portal triads asymmetrically and may be associated with laceration or other signs of injury.

Fatty liver is a common imaging finding, with a prevalence of 15%–95%, depending on the population. The most common imaging pattern is diffuse and relatively homogeneous fat deposition. Less common patterns include focal deposition, diffuse deposition with focal sparing, multifocal deposition, perivascular deposition, and subcapsular deposition. These patterns may
mimic neoplastic, inflammatory, or vascular conditions. Assessment of the lesion fat content, location, morphologic features, contrast enhancement, and mass effect usually permits a correct diagnosis. Chemical shift GRE imaging is more reliable than US or CT for assessing intralesional fat and may be necessary when findings are equivocal.