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AJR:159,

COLOR

November1992

DOPPLER

IMAGING

OF HEPATIC

947

VASCULATURE

Fig. 7.-Recanalized umbilical vein. A, Color Doppler Image shows large tubular structure In area of falclform ligament and confirms hepatofugal flow In recanallzed umbilical veIn (U). Note small, nodular liver (L). B, High-resolution linear-array color Dopplerimage obtained by scannIng beneath anterior abdominal wall shows typical helical flow pattern of portal vein and Its collaterals. Net flow Is In one dIrection, but helical flow Is dIrected both toward and away from transducer. Such patterns can create Images with flow above and below baselIne when spectral analysis Is used alone. Use of color and spectral Doppler Imaging facilitates proper placement of Doppler sample volume.

A mortality

and morbidity.

palliative

measure,

orrhage

or intractable

portosystemic

Sclerotherapy

but patients

shunt.

ascites

is currently

with repeated may

Although

B

require

variations

tered, three main types of shunts are mesocaval, and splenorenal. Placement

used

as a

bouts of hem-

construction

of a

may be encounused: portacaval, of a transjugular

intrahepatic portosystemic stent between the right or middle hepatic vein and the portal vein is an attractive new option [23] (Fig. 8A). The walls of this type of stent are highly attenuating to the ultrasound beam, but an adequate Doppler imaging study can be obtained in most cases. Historically, the most commonly used shunt has been the end-to-side or sideto-side portacaval shunt. Both types of shunt can be easily imaged by using color Doppler technology (Fig. 8B). Occasionally, in patients who have extremely small, cirrhotic livers or those who have undergone surgical removal of the right hepatic lobe, scanning may be difficult because the usual acoustic window provided by the right lobe of the liver is absent. Portacaval shunts are now used less frequently, as orthotopic liver transplantation has become an accepted form of treatment in patients with end-stage liver disease. An intact portal vein is desirable for transplantation, and any form of disturbance,

such

as the construction

of a portacaval

shunt,

should be avoided. Selective

portosystemic

shunts

(mesocaval

and

spleno-

renal) are considered advantageous because they do not divert all blood from the portal vein and potentially worsen hepatic encephalopathy. A mesocaval shunt is typically an Htype synthetic graft between the mid superior mesenteric vein and the inferior vena cava (IVC). These shunts are usually located deep in the mid abdomen and may be difficult to detect because of overlying bowel gas and mesentery. Reports of the use of color Doppler sonography in patients who have these shunts, however, show that persistence yields good results [24]. The examination should begin with realtime scanning in an effort to detect the characteristic serrated walls of the Gortex graft. Duplex or color Doppler imaging can be used to confirm flow (Fig. 8C). Alternatively, color Doppler imaging can be used to follow the IVC either proximally or distally until flow enters from a large vessel below the level of the renal veins, which is presumptive evidence that the junction between the graft and the IVC has been

found and that the shunt is patent. Gentle pressure with the transducer will often displace bowel gas and allow at least a portion of the graft walls to be detected. Detection of flow in any portion of a synthetic mesocaval graft is sufficient to confirm patency. In those unusual patients in whom the shunt cannot be detected with certainty, detection of flow reversal in the proximal superior mesenteric vein can be taken as presumptive evidence of patency. Distal splenorenal or Warren shunts are a third alternative,

in which the distal splenic vein is severed and anastomosed to the left renal vein. Portal hypertension is reduced by diverting continues

splenic blood flow; oxygenated to reach the liver. Splenorenal

blood from the bowel shunts are often the

most difficult to image sonographically. The anastomosis usually lies deep in the left upper quadrant, and the walls of this vein-to-vein graft are invisible sonographically. In a study by Foley et al. [25], duplex sonography was unacceptable in evaluation of the patency of splenorenal shunts, and a more recent study [24] corroborated these results. However, the latter study [24] showed color Doppler imaging was quite successful in the evaluation of distal splenorenal shunts [24]. The limbs of these shunts typically lie perpendicular to each other, and Doppler signals are optimally received from two different directions. The splenic limb is often best imaged from an anterior approach, as the vessel is typically oriented vertically. The renal vein, on the other hand, runs in a horizontal plane, and reception of Doppler signals is optimized by scanfling from the left flank. The anastomosis itself may be difficult to define in one plane, but its detection is not essential to define patency. Detection of appropriately directed flow in well-defined splenic and renal limbs can be used to imply patency (Fig. 9A). When the shunt is occluded, the thrombus itself is difficult to define. Detection of multiple collaterals in the left upper quadrant instead of singular, well-defined splenic and renal limbs should suggest thrombosis or at least physiologic

compromise

left renal vein). Further The Hepatic

(possible

studies

narrowing

of the proximal

are then warranted

(Fig. 9B).

Veins

The hepatic veins are anatomically separate from the portal venous system and are normally the sole route of egress of

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948

GRANT

Fig. 8.-Portosystemic shunts. A, Color Doppler image shows transjugular

intrahepatic

portosystemic

ET AL.

shunt

(arrow)

AJR:159,

is patent.

Note

reversal

of flow in upper

portal

November

1992

vein (P). Metallic

stent may be highly attenuating to ultrasound beam and make confirmation of flow challenging. B, Color Doppler image shows communication between base of portal vein (P) and inferior vena cava (I), confirming patency of portacaval shunt. C, Color Doppler image shows flow In mesocaval shunt (M). Note echogenic walls of graft, which connects superior mesenteric vein (SMV) to IVC.

Fig. 9.-Splenorenal A, Color Doppler

shunts. image of patient

with susthrombosis of splenorenal shunt shows large pancreatic pseudocyst (P). Note well-defined, patent splenic (S) and renal (R) limbs. Although anastomosis was not specifically imaged,

pected

well-defined limbs with appropriately directed flow allowed presumptive diagnosis of patency. Sonographic findings were confirmed with anglography. B, Color Doppler Image of another patient with

splenorenal

shunt and pancreatltis

shows a pan-

creatic pseudocyst (P). Spleen was enlarged and numerous collaterals (arrows) In left upper quadrant were detected. Shunt thrombosis was confirmed with celiac artery arteriogram.

blood from the liver. There are usually three main hepatic veins (left, middle, and right), although many patients have an accessory

or inferior

right

hepatic

vein

[26].

Centrally,

the

hepatic veins join the IVC immediately inferior to the diaphragm and are in open communication with the right side of the heart. Pulsations from the right atrium are reflected back in a complex,

tniphasic

flow

pattern

found

in all central

sys-

temic veins. The hepatic veins have two periods of forward flow within each cardiac cycle, corresponding to the two phases of right atrial filling. Contraction of the right side of the heart produces a period of normal, transient flow reversal. Unlike the portal circulation, in which a variety of pathologic processes may be found, abnormalities affecting the hepatic veins are almost always associated with some form of obstruction,

which

results

in Budd-Chiari

syndrome.

The signs

and symptoms include hepatomegaly, ascites, and upper abdominal pain. Factors associated with Budd-Chiari syndrome are hypercoagulable states (polycythemia rubra vera and paroxysmal nocturnal hemoglobinuria), neoplasia (HCC

and renal and adrenal carcinomas), use of oral contraceptives, trauma, pregnancy, collagen-vascular disorders, and vascular webs. In two thirds of cases, no underlying cause is found [27, 28]. Compromise of hepatic venous outflow can be caused by a lesion located anywhere between the IVC and the hepatic venules, and, as signs and symptoms are not specific, an adequate method for both screening and characterizing the blockage would be desirable. Preliminary experience with color Doppler imaging [29] has been quite encouraging, and suggests that this technique can serve as the initial radiologic examination in any patient suspected of having Budd-Chian syndrome. Several investigators [30, 31 ] have studied the use of realtime and duplex sonography in the diagnosis of Budd-Chiari syndrome. Hepatomegaly and cirrhosis, however, often compress the hepatic veins and make them invisible on neal-time sonography. In such cases, duplex sonography cannot be used to evaluate these vessels. The value of duplex sonog-

AJR:159,

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raphy

November

in the

COLOR

1992

diagnosis

of Budd-Chiani

DOPPLER

syndrome

IMAGING

is further

decreased by the propensity for pulsations from the left side of the heart to be transmitted throughout much of the left lobe of the liver, such that Doppler signals can be obtained almost anywhere in the parenchyma. These problems are decreased with colon Doppler imaging, and compressed but patent hepatic veins often can be visualized even when the veins

are

not

clearly

seen

anatomic

display

entiation

of the vessel

on

real-time

of color Doppler from

sonography.

imaging

The

also allows differ-

the background

artifact

caused

by cardiac motion. Although imaging of the hepatic veins is more difficult in patients with severely shrunken, cirrhotic livers, acute Budd-Chiani syndrome patients. Conversely, patients with

is quite cirrhosis

unusual in such associated with

long-standing Budd-Chiari syndrome should have specific and readily detectable abnormalities. In the acute phase, Budd-Chiari syndrome is diagnosed when flow in the hepatic veins cannot be detected by using color Doppler imaging. Depending on the cause, actual thrombus may or may not be seen with real-time sonography. Three hepatic veins must be detected in order diagnosis, because segmental involvement

to exclude may occur.

the The

veins of the caudate lobe drain directly into the IVC and are frequently spared when the other hepatic veins are compromised.

A large,

patent

caudate

vein

should

not be confused

with a patent middle hepatic vein. In patients with acute hepatic vein thrombosis who are having thrombolytic therapy, color Doppler imaging is useful for monitoring the effect of treatment. Color Doppler imaging has also been used to guide angioplasty and in follow-up studies of patients with IVC webs [32]. After an acute thrombotic episode, or in patients with longstanding obstruction associated with a web on extrinsic mass, collateral pathways develop. Many of these pathways are unique

to Budd-Chiari

syndrome

and provide

definitive

fea-

tunes for diagnosis based on color Doppler imaging [29]. A “bicolored” hepatic vein is pathognomic and indicates a proximal blockage. In this situation, two adjacent branches of a hepatic vein are assigned different colors. Flow is normally directed

toward

directed

toward

the

diaphragm

the periphery

Fig. 10.-Intrahepatic

in one

collaterals

In Budd-Chlari shows classic bicolor hepatic vein In a patient with chronic BuddChiari syndrome. Note appropriately directed flow in superior hepatic vein branch (shown in blue) and reversed flow (shown in red) In other branch.

syndrome. Color Doppler Image

Fig. 11.-Budd-Chiari syndrome. Color Doppler image shows Inferior vena cava (I) Is occluded. Flow is reversed and shown In red. Portal vein (arrow) Is patent, but flow is hepatopetal, suggesting occlusion of mesoatrial shunt. Occlusion of proximal IVC and patient’s mesoatrial shunt were confirmed with angiography. Occluded shunt Is consistent

with

hepatopetal

and

reversed

of the liver in the other

flow in portal

vein.

and

(Fig.

OF HEPATIC

10). Any intrahepatic bilical

vein)

949

VASCULATURE

should

collateral suggest

(except

for a necanalized

Budd-Chiari

syndrome;

umportal

hypertension, on the other hand, almost invariably diverts blood around but not through the liver. In patients with evidence of Budd-Chiari syndrome, the portal vein should be evaluated for concurrent thrombosis, which occurs in about 20% of patients [28]. A unique group of patients with a propensity for venous outflow obstruction are those who have undergone bone marrow transplantation. In this population, conditioning regimens (chemotherapy and radiation) cause an inflammatory reaction that leads to nonthrombotic obliteration of the hepatic venules. Although obstruction is at the microscopic level, signs and symptoms of Budd-Chiari syndrome are similar to those caused by macroscopic obstruction. This phenomenon is specifically termed hepatic venoocclusive disease. The diagnosis of hepatic venoocclusive disease is difficult to establish with radiologic methods, because the main, central hepatic veins remain patent and appear normal with most imaging techniques; transvenous biopsy may be necessary. In a recent study, Brown et al. [33], however, found color Doppler imaging useful in detecting hepatic venoocclusive disease because portal vein flow may be reversed. Although this feature is present in a minority of patients with the disease, it is, nonetheless, sufficiently specific to eliminate the need for further evaluation. A decrease in portal vein velocity is also suggestive of venous occlusion. Unfortunately, portal vein velocities

are normally

so variable

that

a baseline

scan

would have to be available before a true reduction in flow could be determined. For this reason, it has been suggested that all patients have duplex sonography of the portal vein before they begin conditioning for bone marrow transplantation [33]. Contrary to the work of Brown et al. [33], the recent study of Hommeyer et al. [34] found no correlation between sonographic abnormalities (when real-time and color Doppler imaging were used) and venoocclusive disease. Further investigations are necessary to define the role of Doppler imaging in this unusual entity. In patients with Budd-Chiari syndrome, conversion of the portal vein to an outflow tract by construction of a portacaval shunt can adequately reduce hepatic congestion and actually

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950

GRANT

halt the progression of parenchymal damage. Unfortunately, compromise of the IVC is often present in Budd-Chiari syndrome and may result from either a primary (extension of thrombus or neoplasm from IVC, congenital web) or a secondary (extrinsic compression from an enlarged caudate or hepatic mass) process (Fig. 1 1). Evaluation of the IVC is, therefore, essential in patients who are being considered for surgical decompression. Caval compromise precludes the simple decompression of the portal vein via the IVC and necessitates the construction of the far more complex mesoatrial shunt. In these shunts, a synthetic (Gortex) interposition graft diverts blood from the mid superior mesenteric vein to the right atrium [35]. PVT makes construction of either a portacaval or mesoatnial shunt impossible. Mesoatrial shunts have a high propensity for thrombosis and may require frequent imaging. Reported experience with color and duplex Doppler imaging of these shunts has been excellent [23, 29]. Patency can be implied when reversed flow is detected in the portal vein, but the shunt itself is usually easily visualized directly beneath the skin in the right upper quadrant. As with mesocaval grafts, appropriately directed flow in any part of the mesoatnial shunt implies patency. Scans of the shunt obtained within several days of surgical implantation may not be diagnostic, as air within the walls can produce posterior acoustic shadowing and obscure the Doppler image.

REFERENCES 1 . Linberg 2. 3. 4. 5.

6.

7.

B. Diagnosis

of portal

hypertension

by duplex

sonography

(abstr).

J Ultrasound Med 1991;10:S25 Michels NA. Blood supply and anatomy of the upper abdominal organs. Philadelphia: Lippincott, 1955: 152-1 55 Shenk WG, McDonald JC, McDonald K, Drapanas T. Direct measurement of hepatic blood flow in surgical patients. Ann Surg 1962;i56:463-467 RaIls PW. Color Doppler sonography of the hepatic artery and portal venous system. AJA 1990:155:522-526 Wing vw, Laing FC, Jeffrey RB, Guyon J. Sonographic differentiation of enlarged hepatic arteries from dilated intrahepatic bile ducts. AiR 1985;145:57-61 RaIls PW, Mayekawa DS, Lee KP, Johnson MB, Halls J. The use of color Doppler sonography to distinguish dilated intrahepatic ducts from vascular structures. AiR 1989;152:291-292 Taylor KJW, Ramos I, Morse SS, Fortune KL, Hammers L, Taylor CR. Focal liver masses: differential diagnosis with pulsed Doppler US. Radio!-

ogy 1987:164:643-647 8. Tanaka S, Kitamura T, Fujita M. Nakanishi K, Okuda S. Color Doppler flow imaging of liver tumors. AiR 1990:154:509-514 9. Mam CS, Ruber JM, Plaft JF, Adler AS, Francis IA, Merion AM. Arteriovenous shunts in cirrhosis: pitfalls in the Doppler evaluation of focal hepatic lesions (abstr).J Ultrasound Med 1991:10:S24 10. RaIls PW. Focal hepatic and pancreatic disease. In Aifkin MD, Charboneau JW, Laing FC, eds. Ultrasound 1991 syllabus: special course. Oak Brook, IL.: Radiological Society of North America, 1991:293-306 11. Falkoff GE, Taylor KJW, Morse S. Hepatic artery pseudoaneurysm: diagnosis with real-time and pulsed Doppler US. Radiology 1986:158:55-56

ET AL.

AJR:159,

November

1992

12. vine HS, Sequeira JC, Widrich WC, et al. Portal vein aneurysm. AiR 1979:132:557-558 13. Huey H, Cooperberg PL, Bogoch A. Diagnosis ofgiant varix ofthe coronary vein by pulsed-Doppler sonography. AJR 1984:143:77-78 14. Bezzi M, Mitchell DG, Needleman L, Goldberg BB. latrogenic aneurysmal portal-hepatic venous flstula: diagnosis by color Doppler imaging. J Ultrasound Med 1988;7:457-459 15. Endress C, King GA, Medrazo BL. Diagnosis of hepatic artery aneurysm with portal vein flstula using image-directed Doppler ultrasound. JCU J Clin Ultrasound 1989:17:206-208 16. Middleton WD, Erickson 5, Melson GL. Perivascular color artifact: pathologic significance and appearance on color Doppler US images. Radiology 1989:171:647-652 17. Duerinckx A, Grant E, Perrella R, Szeto A, Tessler FN. The pulsatile portal vein: correlation of duplex Doppler with right atrial pressures. Radiology 1990:176:655-658 18. Abu-Yousef MM, Milam SG, Famer AM. Pulsatile portal vein flow: a sign of tricuspid regurgitation on duplex Doppler sonography. AiR 1990:155:785-788 19. Tessler FT. Gehring BJ, Gomes A, et ci. Diagnosis of portal vein thrombosis: value of color Doppler imaging. AiR 1991:157:293-296 20. Weltin G, Taylor KJW, Carter AR, Taylor CR. Duplex Doppler: identifiCatiOn of cavemous transformation of the portal vein. AiR 1985:144:999-1001 21 . Patriquin H, Lafortune M, Bums P, Dauzat M. The duplex Doppler examination in portal hypertension: technique and anatomy. AiR 1987:149: 71-76 22. Nelson AC, Lovett KE, Chezmar JL, et al. Comparison of pulsed Doppler sonography and angiography in patients with portal hypertension. AiR 1987:149:77-81 23. Ring EJ, Lake JR, Roberts JP, et al. Using transjugular intrahepatic portosystemic shunts to control vanceal bleeding before liver transpiantation. Ann Intern Med 1992:116:304-308 24. Grant EG, Tessler FN, Gomes AS, et al. Color Doppler imaging of portosystemic shunts. AiR 1990:154:393-397 25. Foley WD, GleysteenJJ, Lawson TL, et al. Dynamic computed tomography and pulsed Doppler ultrasonography in the evaluation of splenorenal shunt patency. J ComputAssist Tomogr 1983;7:106-109 26. Makunchi M, Hasegawa H, Yamazaki 5, Bandal Y, Watanabe G, Ito T. The inferior right hepatic vein: ultrasonic demonstration. Radiology 1983;148:213-217 27. Clam D, Freston J, Kreel L, Sherlock S. Clinical diagnosis of the BuddChiasi syndrome. Am J Med 1967:43:544-554 28. Parker RGF. Occlusion of the hepatic veins in man. Medicine (Baltimore) 1959;38:369-402 29. Grant EG, Perrella A, Tessler FN, Lois J, Busuttil A. Budd-Chiari syndrome: the results of duplex and color Doppler imaging. AiR 1989:152:377-381 30. Hosoki T, Kuroda C, Tokunaga K, Marukawa T, Masuike M, Kozuka T. Hepatic venous outflow obstruction: evaluation with pulsed duplex sonography. Radiology 1989:170:733-737 31 . Sukigara M, Kimura 5, Adachi H. Primary Budd-Chian syndrome: demonstration by real-time two dimensional Doppler echography. JCU J Clln Ultrasound 1989:17:615-618 32. Lois JF, Hartzman 5, McGlade C, et al. Budd-Chiari syndrome: treatment with percutaneous transhepatic recanalization and dilation. Radiology 1989:170:791-793 33. Brown BP, Abu-Yousef MM, Famer A, LaBrecque B, Gingrich A. Doppler sonography: a new noninvasive method for evaluation of hepatic venooclusive disease. AiR 1990:154:721-724 34. Hommeyer SC, Teefey SA, Higano CS, Bianco JA, MCDOnald GB, Colacurcio CJ. Venocclusive disease of the liver: evaluation with US (abstr). Radiology 1991;181(P): 154 35. Cameron JL, Kadir 5, Pierce WS. Mesoatrial shunt: a prosthesis modification. Surgery 1984:96:114-116

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951

MR

Imaging of the Lungs: Value of Short TE Spin-Echo Pulse Sequences

John Alex

Nestor

R. Mayo1 Mackay

L. MUller

OBJECTIVE. An experimental short echo delay (TE = 7 msec) TI-weighted spin-echo sequence was compared with a conventional (TE = 20 msec) TI-weighted spin-echo sequence In the assessment of normal and abnormal lung parenchyma. Comparison was also made

with

high-resolution

CT

of abnormal

lung

parenchyma.

SUBJECTS AND METHODS. At 1.5 T, an experimental short echo delay TI-weighted multislice spin-echo sequence (TR = RR interval, TE = 7 msec) was compared with an optimal

20 msec, The mean signal Intensity and signal-to-noise ratios were calculated in lung parenchyma for both sequences. Two radiologists compared the visualization of normal lung parenchymal structures with the two techniques. In 24 patients with diffuse lung disease, results with both MR sequences and with high-resolution CT were compared. RESULTS. The signal intensity was significantly greater (p < .001) with the TE of 7 meec than with the TE of 20 msec, resulting in a 3.5-fold improvement in the signal-tonoise ratio. The 7-msec TE improved visualization of lung parenchymal structures, including peripheral vessels, interlobular septa or veins, and centrilobular arteries. In the patients with diftuse lung disease, pulmonary parenchymal abnormalities were better visualized on the images with TEs of 7 msec than on images with TEs of 20 msec. When compared with high-resolution CT, the sequence with a TE of 7 msec provided comparable assessment of air-space opacification and dense consolidation, but it was inferior to high-resolution CT in the anatomic assessment of lung parenchyma. CONCLUSION. This experimental spin-echo sequence with a TE of 7 msec significantly improves the signal-to-noise ratio, allowing improved visualization of normal and abnormal pulmonary parenchyma when compared with conventional spin-echo images with a TE of 20 msec. Although anatomic detail remainsinferior to that seen with high-resolution CT, the improved image quality with a TE of 7 msec suggests that assessment and follow-up of parenchymal lung disease might be possible with MR, thereby avoiding spatial

ionizing AJR

Received

March

23, 1992:

accepted

after revi-

sion AprIl 28, 1992. This work was supported by a B.C. Health Research Foundation grant. J. A. Mayo is supported by a Sterling-Winthrop Imaging Research Foundation grant. All authors: Department of Radiology, lhversity of British Columbia and Vancouver General Hospital, 855W. 12th Ave., vancouver, B.C., Canada V5Z 1 M9. Address reprint requests to J. A. Mayo. 0361 -803X/92/1 595-0951 © American Roentgen Ray Society

conventional

presaturation).

Tl-weighted Ten

healthy

spin-echo volunteers

sequence were

(TR

examined

=

RR interval, TE with

both

=

sequences.

radiation.

159:951-956,

November

1992

The evaluation of lung parenchyma with MR imaging has been limited by the low signal intensity caused by the low proton density and the short T2 and T2* of inflated lung [1 -4]. As a result, minimal signal remains after the echo delay (TE) with conventional gradient-echo (TE = 15 msec) or spin-echo (TE = 20 msec) sequences on current large-bore scanners. Previous studies with a small-bore animal imager [5] have shown increased lung parenchymal signal with very short TE spin-echo sequences. In human subjects it has been shown that the lung parenchymal signal intensity can be increased by using an ultrashort TE gradient-echo sequence [6]. As a result of the very short gradient-echo delay, this sequence requires use of a projection reconstruction algorithm to calculate the image, instead of the more commonly used two-dimensional Fourier transform. The projection reconstruction algorithm can be augmented with image deblurring techniques to compensate for the

MAYO

952

distorted magnetic environment of the lung [7]. We have developed a cardiac-gated Ti -weighted sequence with a short TE (7 msec) that increases

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acquired

from

lung and

improves

visualization

modifications.

We assessed

with various

The

region

in the

in 10

pulmonary

and Methods

years) release, General Electric Medical Systems, Milwaukee, WI). Three imaging sequences were performed in all subjects. First, a coronal cardiacgated Ti -weighted localizer scan was obtained (TR = AR interval, TE = 20 msec) with one excitation per view. This was followed by a Ten

healthy

volunteers

(mean

age,

35 years; range, 28-47

were imaged with a 1 .5-1 imager (Signa, 3.3.9 software

transverse

cardiac-gated

Ti -weighted

conventional

spin-echo

se-

(TA

above

=

compensation

was used.

Sections

5 mm thick with 5-mm

weighted

images

with minimal

cardiac

motion

the

subject

on

the

scanner

table

the

TEs

bronchus

of

20

and

intermedius.

7 msec A circular

in the region

right

lung of interest

at

the (mean

-

session,

level

of

area,

deviation

of interest

from

each

(mean

area,

data.

The difference

in signal

intensity

between

t test.

The

images

were

assessed

for visualization

of central

artifacts

with

idiopathic

techniques. with lung parenchymal

the two

patients

pulmonary

fibrosis

hemorrhage,

abnormalities,

(four); sarcoidosis,

and extrinsic

includ-

cystic

fibrosis,

lipoid

syndrome

pneumonia (two each); with progressive massive (one each); single-lung trans-

transplant

and

asbestosis, talcosis, emphysema, silicosis

after the scan with TE = 20 msec, and after the scan with TE = 7 msec. The images with TEs of 20 and 7 macc were photographed at similar window widths and levels, which were appropriate for visualization of the lung parenchyma. The section thickness for both the 20- and 7-msec TE sequences were verified to be the same by using an axial-slice-thickness analysis phantom (GE model 46-287379G1). Lung parenchymal signal intensity was measured on the scans with

used.

fibrosis, plant

imaging

standard

region

and peripheral vessels; lobar, segmental and subsegmental bronchi; interlobular septa or veins; and centnlobular arterioles. The observers noted the sequences in which these structures were visualized and which sequence provided the best visualization. In addition, the observers recorded the relative seventy of cardiac and respiratory

pulmonary

artifact.

before

Student’s

factors

ing

The third imaging sequence consisted of the experimental short echo delay, transverse cardiac-gated Ti -weighted spin-echo sequence (TR = RR interval, TE = 7 msec). This sequence used a sliceselective 90#{176} pulse (2.4 msec) truncated at the first zero crossing after the peak and a slice-selective 180#{176} pulse (1 .6 msec). A single slice-select refocus gradient lobe was located after the 180#{176} pulse, and all slice-select and read gradient ramp-up and ramp-down times were 0.25 msec. The echo was acquired asymmetrically with the echo peak centered 25% into the readout window. The readout window was narrowed to 6.35 msec. The image bandwidth was ± 20.2 kHz and the low-pass filter bandwidth was ±16 kHz, resulting in attenuation of image signal intensity at the edges of the field of view in the frequency-encoding direction. However, this region of signal attenuation did not impinge on either hemithorax in any volunteer. The data were reconstructed with a standard two-dimensional Fourier transform without correction for the echo asymmetry. Spatial presaturation, flow compensation, and respiratory compensation were not used. Sections of the same thickness and gap were obtained at identical locations as used for the series with the 20-msec TE, prescribed caudad to craniad, with a 36-cm field of view and four averages. The heart rates of the subjects ranged from 53 to 87 beats per minute (TA = 690-i 1 32 msec). To monitor RF power deposition, oral temperatures were taken with

and

The 20- and 7-msec TE scans of the 10 healthy volunteers were interpreted by two chest radiologists who did not know the technical

Twenty-four

gaps were

obtained in a caudad to craniad direction [8] by using a 36-cm field of view and four averages. The phase-encoding direction was anterior to posterior. In our experience, this sequence provided optimal Ti

intensity

A larger circular

image

scanner

motion

AR interval, TE = 20 msec) with spatial presaturation and below the region imaged. Neither flow nor respiratory

quence

signal

1992

the 20- and 7-msec TE techniques was then calculated for each region sampled in the 1 0 subjects. The signal-to-noise ratio was calculated for both sequences by using the mean signal obtained in the mid lung (region 4) and the standard deviation from the air over the right side of the chest (region 7). Correction was made for the Rayleigh distribution of noise in the air by multiplying the standard deviation in air by 1 .53 [9]. Statistical analysis was performed by using

Subjects

mean

were recorded.

November

25.1 cm2; SD, 2.9 cm2) was measured in air anterior to the right chest wall. All signal intensities were corrected for the 1024 offset present

of peripheral

this new sequence

healthy volunteers and in 24 patients parenchymal abnormalities.

AJR:159,

bronchi.

spin-echo the signal

vessels and lung parenchyma. This imaging sequence uses the standard two-dimensional Fourier transform reconstruction and has been implemented on a 1 .5-T scanner with minimal

ET AL.

the 1.8

cm2; SD, 0.3 cm2) was placed at six locations along an arc in the middle third of the right lung on both images. These regions were chosen to sample lung parenchyma, avoiding visible vessels and

and Churg-Strauss

(five);

and

double-lung

heart-double

lung

trans-

plants (one each), were imaged with the 20- and 7-msec TE soquences. The parenchymal abnormalities in the native lung of the single-lung transplants included panacinar emphysema due to aantitrypsin deficiency (four) and severe pulmonary arterial hypertension as a result of portal-systemic shunting (one). The double-lung transplant was performed for cystic fibrosis and the heart-double

lung transplant for congenital heart disease and resultant pulmonary arterial hypertension. Five of the transplanted lungs showed no evidence of rejection and two showed grade 3 or 4 rejection. The scans and

were

interpreted

diagnostic

In all 24 patients, mation,

intervals

through

nary

knowledge

high-resolution

factors

used

the chest

CT (HRCT) scans (1 .5-mm colli-

reconstruction

algorithm)

also were obtained.

the MR images for dense consolidation,

parenchymal

of technical

recorded.

high-spatial-frequency

with opacification, made

without

preference

visualization and normal

at 1 0-mm

Comparison

was

of diffuse air-space and abnormal pulmo-

structures.

Results

In all six lung parenchymal regions measured, the sequence with a TE of 7 msec yielded significantly increased signal intensity (p < .001) when compared with the sequence with a TE of 20 msec (Table 1). As a result, the signal-to-noise ratio on the images with the 7-msec TE was 3.5 times greater (mean, 5.89; SE, 0.56) than that on the images with the 20msec TE (mean, 1 .70; SE, 0.1 9; p < .001). This increased signal on the image with a TE of 7 msec allowed appreciation of the gradient in lung signal intensity from the most dependent region (region 1) to the most nondependent region (region 6) in all healthy subjects (Fig. 1). In contrast, the gradient in lung signal intensity was not visualized on the image with a 20-msec TE, except for increased signal in the most dependent region of the lung.

AJR:159,

November

SHORT

1992

TABLE

1: Lung Parenchymal

Signal

953

TE MR OF LUNGS

Intensity Lun g Parenc hyma Region

Air

TE Value

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7 msec 20msec

Signal difference

1

2

3

4

5

6

52 22

41 14

36 14

33 13

31 ii

29 12

30

27

22

20

20

17

(Region7) 8 9

-1

Note-Lung intervals intensity

parenchymal signal intensity was measured with six circular regions of interest placed at equal from the most dependent to the most anterior aspects of the right lung (regions 1-6, respectively). Air signal was measured with a large circular region of interest located anterior to the right chest wall.

.

TABLE

TEl

S

2: Lung Structure

Visualization

in 10 Healthy Volunteers

TESS

Visualized with TE of:

G

Structure(s)

Best Visualized with TE of:

20 msec 7 msec 20 msec 7 msec E P420 S

LUNG

Fig. 1.-Graph

comparing

PARENCHYMALGON

signal

intensity

at each of six locations

in

right mid lung zone for MR sequences with TEs of 7 (TE 7) and 20 (TE 20) msec in 10 healthy volunteers. A gradient in signal intensity from the most dependent lung region (1) to the most anterlorlung region (6) can be seen with TE = 7 msec sequence. However, both absolute signal intensity and gradient In signal Intensity are decreased with 20-msec TE sequence.

The increased tion

signal-to-noise

of peripheral

centrilobular

vessels,

arteries

throughout the with a 20-msec

ratio also provided

interlobular

septa

visualiza-

or veins,

on the image with a 7-msec

and

TE (Fig. 2)

lung (Table 2). In contrast to the sequence TE, signal arising from aerated lung paren-

chyma was always greater than the signal from air surrounding the patient on the image with a 7-msec TE. As a result, normal lung could be differentiated lung. Lobar and segmental airways with both TEs. However, identification

tated on the image with the 7-msec airway

was

of lower

from surrounding

signal

aerated

not seen with either

intensity

from emphysematous were visible on images of airways was facili-

TE because than

lung. Subsegmental

technique.

The course

air within the

the signal

airways

arising

were

and size of central

pulmonary vessels were equivalent with both techniques. However, contrast between flowing blood and the vessel walls was greater with the 20-msec TE than with the 7-msec TE. Visualization of chest wall and mediastinal structures was equivalent

with

was equivalent cardiac

motion

decreased

both

techniques. Respiratory the two techniques. artifact in the phase-encoding

with

motion artifact The intensity of direction was

with the TE of 7 msec in comparison

of 20 msec. In all 24 patients with pulmonary parenchymal ties, visualization of lung parenchymal structures

with the TE abnormaliwas im-

proved with the TE of 7 msec. In particular, diffuse groundglass infiltrates were more visible on the image with the 7msec TE (Fig. 3) and were more easily differentiated from

Vessels Central Peripheral Airways Lobar

10 8

10 10

10 0

0 10

10

10

0

10

Segmental

10

10

0

10

7

9 8

0 0

9 8

Secondary Interlobular

pulmonary

Centnlobular

septum

artery

lobule or vein

3

surrounding normal and abnormal lung. In patients with lung transplants, the extent of diffuse infiltrate associated with rejection was better appreciated on the image with a 7-msec TE (Fig. 4) than on the image with a 20-msec TE. In lung transplant patients with no biopsy evidence of rejection, confident identification of normal lung parenchymal structures could be made only on the image with a TE of 7 msec (Fig. 5). Densely infiltrated lung (hemorrhage, inflammation) and extensive fibrosis were visualized equally well with both techniques (Fig. 6). However, partially infiltrated and normal lung adjacent to dense infiltrates was better visualized with the TE of 7 msec. When MR images with a 7-msec TE were compared with HRCT images, the presence and extent of diffuse air-space opacification and densely infiltrated lung were comparable. While normal pulmonary parenchymal, bronchial, and vascular structures were visualized on the images with 7-msec TEs, they were identified more clearly on the HRCT images. In comparison with the oral temperature taken before the imaging session, no significant temperature difference was recorded after the scan with a 20-msec TE (0.3#{176}C; standard error, 0.2#{176}C; p > .1 0) nor after the scan with a 7-msec TE (0.09#{176}C; standard error, 0.07#{176}C; p > .10). Discussion

Previous authors have noted that normal adult lung shows no more MR signal than does background air when conventional MR gradient- and spin-echo sequences are used [1]. The lack of signal is due to both the low proton density and the difference in the diamagnetic susceptibility of air and soft

MAYO

954

ET AL.

AJR:159,

Fig. 2.-comparison with TEs of 7 (top) msec

November

1992

of MR images and 20 (bottom) at identical win-

photographed

Downloaded from www.ajronline.org by 137.30.242.61 on 06/07/14 from IP address 137.30.242.61. Copyright ARRS. For personal use only; all rights reserved

dows and levels in a healthy volunteer. A and B, Both lower (A) and upper (B) lung sections show intensity arising from with TE = 7 msec. In zation of peripheral proved on 7-msec TE

increased signal lung parenchyma addition, visualivessels is imimage.

B Fig. 3.-Patient

with asbestosis

a desquamative

reaction. trates from

interstitial

Diffuse

are more surrounding

and

pneumonia

ground-glass

infil-

easily distinguished retractile emphy-

sema on MR image with 7-msec

TE

(top) than on MR image with 20-msec TE (bottom). Peripheral vessels are more visible with TE of 7 msec because of improved signal-to-noise ratio.

Fig. 4.-MR

with TEs of 7 msec (identical windows and levels) in a patient with a right-sided lung transplant and biopsy(top)

images

and 20 (bottom)

proved grade 3 rejection. sequence with 7-msec TE provides better visualization of diffuse increase in signal in right lung than does sequence with 20msec TE. Minimal signal is seen in emphysematous left lung on both sequences. Focal nodules (arrows) seen on both sequences are due to pulmo-

nary hemorrhage

from transbronchial

biopsy.

tissue in inflated lung, which causes magnetic field gradients at each air-tissue interface [1 0]. The difference in magnetic susceptibility causes large gradient magnetic fields (up to 9 ppm) [11] in the normally homogeneous main magnetic field

present in modem superconducting MR imagers (0.5 ppm) [1 2]. In the absence of motion of the water molecules, a spinecho sequence would completely compensate for the inhomogeneity

of the

magnetic

field

in the

lung

parenchyma.