Transient Hepatic Perfusion Differences (THAD/THID) What? When? Where?

Transcription

1 Transient Hepatic Perfusion Differences (THAD/THID) What? When? Where? Poster No.: C-2151 Congress: ECR 2017 Type: Educational Exhibit Authors: J. Saraiva, C. Bilreiro, J. Brito, B. M. Q. Santos; Portimão/PT Keywords: Arteriovenous malformations, Abscess, Diagnostic procedure, MR, CT, Vascular, Liver, Abdomen, Artifacts DOI: /ecr2017/C-2151 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 35

2 Learning objectives To learn the physiopathology ("What?") and the several causes ("When?) of transient hepatic perfusion differences found in dynamic CT and MR imaging studies, as well as their different imaging findings, namely their morphology and distribution pattern on the liver ("Where"?). Background In CT and MRI dynamic studies (and more recently in contrast-enhanced ultrasound studies) it's not uncommon to find liver perfusion abnormalities that are only present in one of the acquisition phases (namely either on arterial or portal venous phase). These are the so called transient hepatic attenuation differences (THAD) on CT studies, intensity differences (THID) on MRI studies and echogenicity differences (THED) on US studies. These findings have their origin in focal perfusion abnormalities of the hepatic parenchyma, and morphologically they can be either: Hypervascular (more commonly): hypervascular areas that are hyperdense/hyperintense in arterial phase and revert to isodense/isointense in the portal venous phase (although they can persist more discretely in this phase when a large area is encompassed or there is venous drainage blockage). Hypovascular (rarely): hypovascular areas can become transiently present solely in the arterial phase, show throughout the portal venous phase or even appear only on the latter. These perfusion abnormalities result from focal changes in the hepatic parenchyma normal "double" blood inflow ratio (about 30% arterial flow and 70% portal venous flow), resulting in areas of different density/intensity only present in specific phases of the contrast-enhanced (CE) studies: Imbalances due to increase in arterial flow are the most common. The arterial blood flow increase can be primary or secondary: 1. Primary increase in arterial blood inflow (Fig. 1 on page 6) Page 2 of 35

3 1.1. Hypervascular tumors 1.2. Local inflammatory changes 1.3. Vascular malformations Fig. 1: Primary increase in arterial flow: 1.1: "Syphoon" effect of the parenchyma adjacent to hypervascular lesions; 1.2: hyperemia due to local inflammatory changes in reaction to a hepatic or adjacent lesion; 1.3: arterial malformations/variants (e.g. hepatic arterial branch of the cystic artery - ramus profundus) References: José Saraiva 2. Secondary increase in arterial blood inflow (compensatory to portal flow shortage) (Fig. 2 on page 6) 2.1. Direct portal hypoperfusion # Compression / Infiltration / Portal thrombosis Page 3 of 35

4 # Cirrhosis # Biliary obstruction 2.2. Arterio-portal shunt 2.3. Anomalous venous drainage Fig. 2: Increase of arterial inflow secondary to portal hypoperfusion - 2.1: direct portal hypoperfusion (e.g. thrombosis); 2.2: arterio-portal shunting; 2.3: anomalous venous drainage (e.g. portal-systemic shunting). References: José Saraiva The more rare hypovascular imbalances (Fig. 3 on page 7) (due to reduction in proportional arterial inflow) can have the following mechanisms: a. Hepatic venous drainage reduction Page 4 of 35

5 b. "Steal phenomenon" by hypervascular tumors c. Non-portal venous blood mixture ("third inflow") - Actually more commonly presenting as a hypervascular perfusion anomaly, but they can also be a cause of hypovascular THA/I/ED due to their complex hemodynamics. Fig. 3: Hypovascular transient perfusion anomalies are caused by a proportional decrease in the arterial inflow - a: hepatic venous drainage reduction; b: "Steal phenomenon" by hypervascular tumors; c. Non-portal venous blood mixture ("third inflow"). References: José Saraiva It is also important to bear in mind that one: transient hepatic perfusion differences can change with time; and two: they are frequently related to fatty infiltration focal changes given they are within the same physiopathological spectrum: portal hypoperfusion -> transient hepatic perfusion differences -> metabolic changes leading to differences in fatty infiltration -> fibrosis -> atrophy. Page 5 of 35

6 Images for this section: Fig. 1: Primary increase in arterial flow: 1.1: "Syphoon" effect of the parenchyma adjacent to hypervascular lesions; 1.2: hyperemia due to local inflammatory changes in reaction to a hepatic or adjacent lesion; 1.3: arterial malformations/variants (e.g. hepatic arterial branch of the cystic artery - ramus profundus) José Saraiva Page 6 of 35

7 Fig. 2: Increase of arterial inflow secondary to portal hypoperfusion - 2.1: direct portal hypoperfusion (e.g. thrombosis); 2.2: arterio-portal shunting; 2.3: anomalous venous drainage (e.g. portal-systemic shunting). José Saraiva Page 7 of 35

8 Fig. 3: Hypovascular transient perfusion anomalies are caused by a proportional decrease in the arterial inflow - a: hepatic venous drainage reduction; b: "Steal phenomenon" by hypervascular tumors; c. Non-portal venous blood mixture ("third inflow"). José Saraiva Page 8 of 35

9 Findings and procedure details As previously explained, several entities can be associated with transient hepatic perfusion differences and their physiopathology is diverse: Table 1: Entities that can present with ("When?") hypervascular THAD/THID/THED (and their respective physiopathology mechanisms - "What?"). References: José Saraiva Page 9 of 35

10 Fig. 4: Hepatic abscess (CE-CT study before (PRE) and after contrast administration in arterial (A), portal venous (P) and late (L) enhancement phases): typical hypervascular THAD with polymorphous pattern (see ahead), mainly visible in the arterial phase (A), almost imperceptible in the portal venous phase (P) and absent in the late acquisition (L) and before iodine injection (PRE). The physiopathology is thought to be related to immune-mediated arterialization phenomena of the parenchyma surrounding the abscess (primary arterial flow increase) and/or due to the parenchymal edema and consequent portal obstruction (secondary arterial flow increase). References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 10 of 35

11 Fig. 5: Hepatic abscesses (same patient CE-CT in upper row and CE-MR T1 VIBE in the lower row, both before (PRE) iodine/gadolinium injection and after in the arterial (A), portal venous (P) and late (L) phases): hypervascular THAD and THID is seen in both the CT and MR studies, only in their respective arterial (A) phases. There is some movement artifact on the portal venous MR image, not to be confused with THID persistence. Also one should be able to diferentiate between the late peripheral abscess enhancement here shown and the THAD/THID of the surrounding hepatic parenchyma. References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 11 of 35

12 Fig. 6: Multiple renal cell carcinoma metastasis (axial CE-CT before (PRE) and after iodine injection in the arterial (A), portal venous (P) and late (L) enhancement phases): several THAD areas surrounding the metastasis, presenting as hyperenhancing areas only seen in the arterial phase (A). References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 12 of 35

13 Fig. 7: Multiple portal vein branch thrombosis (axial CE-CT before (PRE) and after iodine injection in the arterial (A), portal venous (P) and late (L) enhancement phases): two hyperenhancing areas surrounding different portal vein branch thrombosis in the same patient. These are clearly seen during arterial phase (A), almost disappear in the portal venous phase (P) and don't present in the remaining phases. This is an example of a hypervascular THAD due to secondary arterial flow increase (compensatory to the portal flow reduction). References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 13 of 35

14 Fig. 8: Superior vena cava (SVC) obstruction (axial and coronal CE-CT before (PRE) and after iodine injection in the arterial (A) and late (L) enhancement phases): segment IV THAD only seen in the arterial phase (A) due to the portal-systemic shunting of internal thoracic collateral vessels (not shown here) compensatory to the obstruction of the SVC caused by a small-cell lung carcinoma (coronal image on the left). References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT As stated, although most transient hepatic perfusion differences are of the hypervascular type, there are rare instances where hepatic perfusion abnormalities manifest as Page 14 of 35

15 hypodense/hypointense areas (sometimes persisting during the portal venous phase). Their etiology is also diverse: Table 2: Entities that can present with ("When"?) hypovascular THAD/THID/THED (and their respective physiopathology mechanisms - "What?"). References: José Saraiva Page 15 of 35

16 Fig. 10: Hemangioma (Dynamic FS-T1-VIBE study before (PRE) and after gadolinium administration in arterial (A), portal venous (P) and late (L) enhancement phases): hypovascular THID due to "steal phenomenon" by the hypervascular tumor presents as hyperenhancing areas only seen in the arterial phase (A), during the remaining enhancement phases and before gadolinium injection the surrounding hepatic parenchyma is homogenous. References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT "Third inflow" anomalies (Fig. 9 on page 32) are very complex and they can either present as hypovascular or hypervascular perfusion differences (the latter without presenting the typical arterial flow increase, either primary or secondary, but instead having a third aberrant inflow from accessory veins that drain in the liver). However, most commonly, the contamination of additional systemic blood during late arterial phase produces a focal blood pool with more contrast than the remaining areas which have a higher ratio of portal blood (yet to have contrast in the arterial phase), thus leading to a hypervascular THA/I/ED. Page 16 of 35

17 Fig. 9: "Third inflow" example due to an aberrant right gastric vein (Dynamic FS-T1VIBE study before (PRE) and after gadolinium administration in arterial (A), portal venous (P) and late (L) enhancement phases): a hypovascular THID is seen only in the portal venous phase. One can see the aberrant right gastric vein (arrow) in the precise center of the hypoenhancing area. It's origin can be traced back to the gastric antrum by carefully following it in different slices (lower images). The exclusive portal venous hypoenhancing happens because the drainage of systemic gastric blood into the hepatic parenchyma produces a "mixture" of venous blood with different gadolinium concentrations (owing to the different kinetic profiles in portal and systemic circulation). References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Given their etiology, all transient hepatic perfusion differences have some common imaging findings: Relatively homogenous areas Most have sharp distinct borders ("straight border sign") Vessels run without disturbance through these areas, indicating no mass effect ("vessel penetration sign") Some present specific morphology (Fig. 11 on page 26) according to their mechanism of origin (e.g. triangular, wedge or fan shaped) Page 17 of 35

18 Are only apparent in multi-phase studies, and for instance don't produce any changes in T2 weighted images. There is a small exception: perfusion abnormalities with marked increase of hepatic arterialization can be slightly hyperintense in T2 due to the increase in water content (doesn't reflect the difference in arterial vs portal ratio). Fig. 11: There are different morphologic patterns of THA/I/ED: 1. multi-segmental lobar; 2. Sectorial (2.1. wedge-shaped; 2.2. fan-shaped); 3. polymorphous; 4. diffuse. References: José Saraiva 1. Lobar multisegmentar morphology (Fig. 12 on page 26) typically occur with hypervascular lesions due to the "syphoon effect" that increases the arterial flow of the surrounding parenchyma not triangular may (or may not) have a "straight border sign" the size of the lesion relates to the involvement of a main branch of the hepatic artery (giving rise to a lobar pattern) or just a smaller branch (giving rise to smaller segmental anomalies) a variant exists where the involvement of one of the main branches of the hepatic artery produces hypoperfusion of the contralateral branch ("steal mechanism") Page 18 of 35

19 Fig. 12: Axial CE-CT before (PRE) and after iodine injection in the late arterial phase (A): hepatic abscess due to a fish bone (arrow) giving rise to a hypervascular THAD with left lobar pattern (in these slices Couinaud's segments IVb and III are clearly delimited). References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT 2. Sectorial morphology (Fig. 13 on page 27, Fig. 14 on page 28, Fig. 15 on page 28) appears when a portal territory is delimited by the perfusion abnormality usually it's either due to arterio-portal shunting or portal vein branch thrombosis (both more commonly secundary to hypervascular tumors, abscesses, chirrhosis, iathrogeny) triangular shaped areas delimited by the hypoperfused portal veins area can be either (2.1) wedge-shaped (Fig. 13 on page 27, Fig. 14 on page 28) if the lesion is central or lateral to arterialization site or (2.2) fanshaped (Fig. 15 on page 28) if the lesion is exactly at the point where the shunt is produced the THA/I/ED area size is directly related to the distance of the lesion to the Gleason's capsule there is no relationship between the lesion size and the perfusion abnormality area size Page 19 of 35

20 Fig. 13: Multiple hemangiomas with arterio-portal shunting (T1WI before (PRE) and after administration of gadolinium in arterial (A), portal venous (P) and late (L) enhancement phases): two hypervascular THID are seen only in the arterial phase. Both present sectorial wedge-shaped morphology. References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 20 of 35

21 Fig. 14: Gastric carcinoma metastasis (axial/coronal CE-CT before (PRE) and after iodine injection in the arterial (A) and portal venous (P) enhancement phases): hyperenhancing area only seen during arterial phase (A) depicting hypervascular THAD due to hypervascular tumor related arterio-portal shunting. This is an example of wedge-shaped morphology, and it's possible to confirm that the lesion is not at the base of the affected portal territory (otherwise a "fan-shaped" morphology would ensue: see figure 9). References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 21 of 35

22 Fig. 15: Hyperdynamic hemangioma (axial CE-CT before (PRE) and after iodine injection in arterial (A), portal venous (P) and late (L) enhancement phases): fanshaped hypervascular THAD only seen in the arterial phase, most probably due to arterio-portal shunting related to the hyperdynamic hemangioma. References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT 3. Polymorphous morphology (Fig. 16 on page 29, Fig. 17 on page 30) irregular areas with diverse morphology (according to the portal branches affected) typically centered or lateral to the lesions responsible for them may be caused by anomalous vascular flow, inflammatory changes and chemical/physical parenchymal lesions (contusion, compression (e.g. by ribs or diaphragmatic crura), percutaneous biopsy, thermoablation, ethanol injection...) Page 22 of 35

23 Fig. 16: Hepatic abscess (axial CE-CT before (PRE) and after iodine injection in arterial (A) and portal venous (P) enhancement phases): hypervascular THAD with polymorphous morphology. References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Fig. 17: Acute cholecystitis (axial CE-CT before (PRE) and after iodine injection in arterial (A) and portal venous (P) enhancement phases): hypervascular THAD with polymorphous morphology making more conspicuous the acute cholecystitis diagnosis. References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 23 of 35

24 4. Diffuse morphology (Fig. 18 on page 30, Fig. 19 on page 31) caused by portal hypoperfusion due to obstruction before, after or at the sinusoidal level there are some specific presentations related to the level of the obstruction: post-sinusoidal - centrilobular hyperenhancement ("marble liver" - Fig. 18 on page 30); pre- or intra-sinusoidal - peripheral hyperenhancement with normal central enhancement (Fig. 19 on page 31); exclusive obstruction of the peri-biliary venous plexus - hyperenhancement adjacent to the biliary ducts. Fig. 18: Budd-Chiari syndrome (axial CE-CT in arterial (A) and late (L) enhancement phases): hypervascular THAD presenting diffuse morphology with centrilobular pattern ("marble liver") due to the post-sinusoidal obstruction. References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 24 of 35

25 Fig. 19: Cavernous transformation of the portal vein (axial CE-CT before (PRE) and after iodine injection in arterial (A), portal venous (P) and late (L) enhancement phases): hypervascular THAD presenting diffuse morphology with marked peripheral pattern clearly sparing the central liver. References: Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 25 of 35

26 Table 3: Entities associated ("When?") with the different known morphologies and distribution patterns ("Where?") of THA/I/ED. References: José Saraiva Images for this section: Fig. 11: There are different morphologic patterns of THA/I/ED: 1. multi-segmental lobar; 2. Sectorial (2.1. wedge-shaped; 2.2. fan-shaped); 3. polymorphous; 4. diffuse. José Saraiva Page 26 of 35

27 Fig. 12: Axial CE-CT before (PRE) and after iodine injection in the late arterial phase (A): hepatic abscess due to a fish bone (arrow) giving rise to a hypervascular THAD with left lobar pattern (in these slices Couinaud's segments IVb and III are clearly delimited). Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 27 of 35

28 Fig. 13: Multiple hemangiomas with arterio-portal shunting (T1WI before (PRE) and after administration of gadolinium in arterial (A), portal venous (P) and late (L) enhancement phases): two hypervascular THID are seen only in the arterial phase. Both present sectorial wedge-shaped morphology. Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Fig. 14: Gastric carcinoma metastasis (axial/coronal CE-CT before (PRE) and after iodine injection in the arterial (A) and portal venous (P) enhancement phases): hyperenhancing area only seen during arterial phase (A) depicting hypervascular THAD due to hypervascular tumor related arterio-portal shunting. This is an example of wedgeshaped morphology, and it's possible to confirm that the lesion is not at the base of the affected portal territory (otherwise a "fan-shaped" morphology would ensue: see figure 9). Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 28 of 35

29 Fig. 15: Hyperdynamic hemangioma (axial CE-CT before (PRE) and after iodine injection in arterial (A), portal venous (P) and late (L) enhancement phases): fan-shaped hypervascular THAD only seen in the arterial phase, most probably due to arterio-portal shunting related to the hyperdynamic hemangioma. Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 29 of 35

30 Fig. 16: Hepatic abscess (axial CE-CT before (PRE) and after iodine injection in arterial (A) and portal venous (P) enhancement phases): hypervascular THAD with polymorphous morphology. Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Fig. 17: Acute cholecystitis (axial CE-CT before (PRE) and after iodine injection in arterial (A) and portal venous (P) enhancement phases): hypervascular THAD with polymorphous morphology making more conspicuous the acute cholecystitis diagnosis. Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 30 of 35

31 Fig. 18: Budd-Chiari syndrome (axial CE-CT in arterial (A) and late (L) enhancement phases): hypervascular THAD presenting diffuse morphology with centrilobular pattern ("marble liver") due to the post-sinusoidal obstruction. Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 31 of 35

32 Fig. 19: Cavernous transformation of the portal vein (axial CE-CT before (PRE) and after iodine injection in arterial (A), portal venous (P) and late (L) enhancement phases): hypervascular THAD presenting diffuse morphology with marked peripheral pattern clearly sparing the central liver. Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 32 of 35

33 Fig. 9: "Third inflow" example due to an aberrant right gastric vein (Dynamic FS-T1-VIBE study before (PRE) and after gadolinium administration in arterial (A), portal venous (P) and late (L) enhancement phases): a hypovascular THID is seen only in the portal venous phase. One can see the aberrant right gastric vein (arrow) in the precise center of the hypoenhancing area. It's origin can be traced back to the gastric antrum by carefully following it in different slices (lower images). The exclusive portal venous hypoenhancing happens because the drainage of systemic gastric blood into the hepatic parenchyma produces a "mixture" of venous blood with different gadolinium concentrations (owing to the different kinetic profiles in portal and systemic circulation). Imagiologia / Radiologia, Unidade Hospitalar de Portimão, Centro Hospitalar do Algarve - Portimão/PT Page 33 of 35

34 Conclusion The correct identification of transient hepatic perfusion differences and their adequate interpretation is essential not only to elaborate a more precise differential diagnosis of several liver entities, but also because in many cases it can be the only clue allowing a final diagnosis. Figuring out the pathological mechanism responsible for any given THA/I/ED ("What?") and recognizing its morphological distribution ("Where?") at the very least enables the Radiologist to narrow down the differential diagnosis for the possible underlying diseases that give rise to this common finding ("When?"). Personal information J. Saraiva, C. Bilreiro, J. Brito, B. M. Q. Santos 1 Serviço de Radiologia Centro Hospitalar do Algarve Unidade Hospitalar de Portimão PORTUGAL References Colagrande S, Centi N, Galdiero R, et al: Transient hepatic intensity differences. Part 1, Those associated with focal lesions. AJR Am J Roentgenol 188: , Colagrande S, Centi N, Galdiero R, et al: Transient hepatic intensity differences. Part 2, Those not associated with focal lesions. AJR Am J Roentgenol 188: , Colagrande S, Centi N, La Villa G, et al: Transient hepatic attenuation differences. AJR Am J Roentgenol 183: , Ravikumar H, Singh J, Kalyanpur A. Transient hepatic attenuation difference (thad) - a case report. Indian J Radiol Imaging 2006;16:441-4 Page 34 of 35

35 5. Quiroga S, Sebastià C, Pallisa E, Castellà E, Pérez-Lafuente M, AlvarezCastells A. Improved diagnosis of hepatic perfusion disorders: value of hepatic arterial phase imaging during helical CT. Radiographics JanFeb;21(1):65-81; questionnaire Review. PubMed PMID: Torabi M, Hosseinzadeh K, Federle MP. CT of nonneoplastic hepatic vascular and perfusion disorders. Radiographics NovDec;28(7): doi: /rg Review. PubMed PMID: Lee JW, Kim S, Kwack SW, Kim CW, Moon TY, Lee SH, Cho M, Kang DH, Kim GH. Hepatic capsular and subcapsular pathologic conditions: demonstration with CT and MR imaging. Radiographics SepOct;28(5): doi: /rg Review. PubMed PMID: Kim HJ, Kim AY, Kim TK, et al. Transient hepatic attenuation differences in focal hepatic lesions: dynamic CT features. AJR 2005;184: Gabata T, Kadoya M, Matsui O, et al. Dynamic CT of hepatic abscess: significance of transient segmental enhancement. AJR 2001; 176: ChenWP, Chen JH, Hwang JI, et al. Spectrum of transient hepatic attenuation differences in biphasic helical CT. AJR Am J Roentgenol 1999; 172: Page 35 of 35