SCVIR Annual Meeting Film Panels

SCVIR Annual Meeting Film Panels

Special Communication SCVIR Annual Meeting Film Panels Authors: Robert K. Kerlan, Jr, MD, and Jeanne M. LaBerge, MD Moderator: Robert K. Kerlan, Jr, ...

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Special Communication

SCVIR Annual Meeting Film Panels Authors: Robert K. Kerlan, Jr, MD, and Jeanne M. LaBerge, MD Moderator: Robert K. Kerlan, Jr, MD Panelists: Curtis W. Bakal, MD, Matthew A. Mauro, MD, Anne C. Roberts, MD, and Robert L. Vogelzang, MD Index term:

SCVIR Annual Meeting, 2002

J Vasc Interv Radiol 2002; 13:119 –136

INTRODUCTION In this issue of JVIR, we are pleased to present eight Interventional Radiology cases selected for discussion at the 4th

From the Department of Radiology (R.K.K., J.M.L.), University of California, San Francisco, San Francisco; Department of Radiology (A.C.R.), University of California San Diego/Thornton Hospital, La Jolla, California; Department of Radiology (C.W.B.), Beth Israel Medical Center, New York, New York; and Department of Radiology (R.L.V.), Northwestern Memorial Hospital, Chicago, Illinois. Address correspondence to R.K.K., Department of Radiology, Box 0628, University of California, San Francisco, 505 Parnassus Ave., San Francisco, CA 94143-0628. © SCVIR, 2002

Annual Film Panel Session at the 2002 SCVIR Annual Meeting. These cases represent challenging diagnostic and therapeutic conundrums that will be shown to four expert panelists. We present them here so that the SCVIR Membership can preview the cases and formulate their own diagnostic and management decisions before the discussion at the Film Panel Session. Members of the SCVIR have contributed the eight cases that appear in this issue of JVIR. We thank all authors for their efforts. Their authorship will appear in subsequent issues of JVIR in which the diagnoses and management options for each case will be presented.

These cases are available at SCVIR’s web site (www.scvir.org) and will also be on display in the poster area at the meeting in Baltimore. After the Film Panel Session, the correct answers will be posted and will be available electronically on the Annual Meeting Home Page. Members are encouraged to review the cases and submit their answers to Robert K. Kerlan, Jr, MD, Department of Radiology, Box 0628, University of California, San Francisco, 505 Parnassus Ave., San Francisco, CA 94143-0628, or electronically via the SCVIR web site. Please submit one answer per case and one set of answers per member.

Readers are invited to visit the SCVIR web site at www.scvir.org and view the unknown cases and vote on the diagnosis. Case answers will be posted on the web after the SCVIR 2002 Annual Meeting and will be published in the May and June issues of JVIR.

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Case 1 History A 49-year-old woman presented with a 2-month history of rapidly progressive right leg claudication that now precluded her from ambulation. Noninvasive examination revealed diminished ankle-brachial indices bilaterally (right, 0.16; left, 0.60). Medical history is remarkable for psoriasiform dermatitis and allopecia universalis of 10 years duration and a 10-pound weight loss over the past 6 months. Physical examination revealed diffuse lympadenopathy. The patient was hospitalized for further diagnostic evaluation. Com-

plete blood count (CBC) revealed anemia, lymphopenia, and mild eosinophilia. The CD4 count was low and the sedimentation rate was elevated. Immunoglobulin (IG) levels (predominantly IGG) were elevated. Lipid profile and homocysteine levels were normal. Hepatitis B and C antibodies were negative and the rheumatoid factor was negative. On admission, laboratory values were as follows: hematocrit, 30% (normal, 36 – 460); lymphocyte count, 0.7 ⫻ 109/L (normal, 0.9 –2.9); eosinophil count, 0.5 ⫻ 109/L (normal, 0.0 – 0.4); absolute CD4, 96 ⫻ 106/L (normal, 410 –1590); sedimentation rate, 50 mm/h (normal, 0 –15);

IGG, 1,900 mg/dL (normal, 580 –1530); complement-C4, 14 mg/dL (normal, 15–58); homocysteine, 12 ␮mol/L (normal, 5–15). Abdominal aortography (Fig 1.1) and bilateral lower extremity arteriography (Figs 1.2–1.6) was performed. Right leg arteriography was repeated after the administration of intra-arterial priscoline but the images were unchanged from those shown in Figures 1.2–1.6. Question • What is your diagnosis?

Figure 1.1. Abdominal aortogram.

Figure 1.2. Bilateral pelvic arteriogram (LAO projection).

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Figures 1.3–1.6. (1.3) Bilateral arteriogram of proximal thigh, anteroposterior projection. (1.4) Bilateral arteriogram of distal thigh, anteroposterior projection. (1.5) Bilateral arteriogram of knees, anteroposterior projection. (1.6) Bilateral arteriogram of calves, anteroposterior projection.

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Case 2 History A 21-year-old man with a history of bleeding esophageal varices treated by endoscopic sclerotherapy presented with recurrent upper gastrointestinal bleeding. Esophagogastroduodenoscopy revealed grade 1 distal esophageal varices (improved from grade 3), varices in the gastric cardia and congestive gastropathy. His medical history was remarkable for recurrent respiratory tract infections leading to brochiectasis and

Figure dome.

episodes of hemoptysis that were managed by embolization. Physical examination revealed a thin, somewhat cachetic appearing man in no acute distress. Examination of the abdomen disclosed marked splenomegaly but no ascites. The liver edge felt irregular without a focal, dominant mass. Admission laboratories included: international normalized ratio, 1.8 (normal, 0.6 –1.2), albumin, 3.4 g/dL (normal, 3.4 – 4.7); total bilirubin, 2.4 mg/dL (normal, 0.3–1.3); hemoglobin, 11.9 g/dL (normal, 12.0 –15.5); platelets, 42 ⫻ 109 per L (normal, 140 – 450);

2.1. Non-contrast abdominal CT through the hepatic

and a normal serum creatinine, calcium, and phosphorus. A computed tomographic (CT) examination of the abdomen was performed without intravenous contrast material (Figs 2.1–2.3). Subsequently, a hepatic venogram (Fig 2.4) was obtained. Questions 1. What is the most likely etiology of this patient’s liver disease? 2. How should this patient be treated?

Figure 2.2. Non-contrast abdominal CT through the hepatic hilum.

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Figure 2.3. Noncontrast abdominal CT through the upper abdomen.

Figure 2.4. Right hepatic venogram.



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Case 3 History A 42-year-old woman presented with mild abdominal pain and bilateral lower extremity claudication. She had been asymptomatic until 2 months before admission. Since that time, her symptoms had progressively increased. Medical history was remarkable only for oral contraceptives. No surgeries had been performed.

Physical examination was remarkable for absent femoral, popliteal, posterior tibial, and dorsalis pedis pulses bilaterally. The neurologic examination of both lower extremities was normal. Laboratory evaluation was as follows: blood urea nitrogen, 19 mg/dL (normal, 8 –23), serum creatinine, 1.8 mg/dL (normal, 0.6 –1.2); aspartate aminotransferase, 145 U/L (normal, 16 – 41). Prothrombin time, fibrinogen, D-

dimers, anti-thrombin III, protein C & S, and antiphospholipid antibodies were all within normal limits or negative. Contrast enhanced computed tomography (CT) of the chest, abdomen and pelvis was obtained (Figs 3.1–3.5). Question • What is your diagnosis?

Figures 3.1–3.3. (3.1) CT image through the transverse aorta. (3.2) CT image through the upper abdomen. (3.3) CT image through the upper abdomen, slightly caudal to Figure 3.2.

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Figures 3.4, 3.5. (3.4) CT image through the mid-abdomen (3.4) and the pelvis.

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Case 4 History An 85-year-old woman presented with a 2-week history of dyspnea on exertion and sharp left-sided chest pain. Her medical history was significant for polymyalgia rheumatica treated with steroids, diverticulitis, and low back pain. Chest CT on admission revealed bilateral pulmonary

emboli and the patient was treated with anticoagulation. The patient was initially heparinized and then was started on Coumadin. While in the hospital, she became acutely unresponsive and was noted to be hypotensive and tachycardic. Her hematocrit dropped from the admission value of 35% to 20%. International normalized ratio (INR) was 4.3 (normal: 0.9-1.2).

Computed tomography (CT) of the abdomen (Figs 4.1, 4.2) was followed by visceral arteriography (Figs 4.3– 4.5). Questions • What is your diagnosis? • How should this patient be treated?

Figures 4.1, 4.2. Contrast-enhanced abdominal CT. (4.1) Upper hepatic image. (4.2) Mid-hepatic image.

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Figures 4.3– 4.5. Celiac arteriogram. (4.3) Arterial phase image. (4.4) Portal venous phase image. (4.5) Selective hepatic arteriogram, mid-arterial phase.

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Case 5 History A 30-year-old right-handed minor league baseball pitcher noticed slight numbness and tingling in his right hand for several months. Then while pitching, his right arm became cold, painful and numb. Right arm arteriography was performed (Figs 5.1–5.4) which revealed thrombus in the radial

and ulnar arteries. Fibrinolytic infusion was initiated with resolution of the majority of the thrombus. The patient underwent anticoagulation with use of warfarin and was referred to our institution for further evaluation. His medical history was unremarkable. On admission, his coagulation profile was normal. Physical examination revealed a normal right

radial pulse and an absent right ulnar pulse. Electrocardiogram and transesophageal echocardiogram were normal. A right arm arteriogram with stress views was performed (Figs 5.1– 5.8). Question • What is your diagnosis?

Figures 5.1–5.4. Initial right arm arteriogram. Selected images are shown. (5.1) Subclavian-axillary arteries. (5.2) Axillary-brachial arteries. (5.3) Brachial artery bifurcation. (5.4) Hand arteriogram demonstrating a filling defect and occlusion (arrows) of the arch vessels.

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Figures 5.5–5.8. Repeat arteriogram after fibrinolysis. Selected images are shown. (5.5) Right subclavian-axillary arteries, neutral. (5.6) Right subclavian-axillary arteries, maximal abduction. (5.7) Right axillary-brachial arteries. (5.8) Right brachial artery to bifurcation.

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Case 6 History A 60-year-old woman presented with gross hematuria from a nephrostomy tube placed 1 month previously into her left upper urinary tract. Her medical history was remarkable for chronic stricture of the left ureter that had been managed previously with a retrograde left ureteral stent. In addition, the patient suffered from atherosclerotic peripheral vascular disease which had been treated 3 years before admission with an aorto-

bifemoral bypass graft (AFBG). One month before admission the graft became infected with Staphylococcus epidermidis. The graft infection was managed by surgical placement of a left axillary to left profunda synthetic graft coupled with the placement of a left femoral to right femoral cryopreserved vein graft. The infected synthetic AFBG was then excised. As the patient had experienced continued claudication with a patent AFBG, the surgeon was concerned that the left axillary to left profunda bypass

graft would not provide adequate inflow to support both lower extremities. Therefore, it was elected to place an in-line aorto-left common femoral cryopreserved vein graft at the time of infected prosthetic graft explantation. Postoperatively, the patient developed left flank pain. Ultrasonography showed left hydronephrosis. Attempted retrograde replacement of the left-sided ureteral stent was unsuccessful, and a left-sided percutaneous nephrostomy was performed. The pa-

Figures 6.1– 6.3. Contrast-enhanced abdominal and pelvic computed tomography (CT). (6.1) Image through mid-left kidney. (6.2) Image through lower abdomen. (6.3) Image through mid-pelvis.

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Figures 6.4 – 6.7. (6.4) Nephrostogram performed through left nephrostomy tube. (6.5, 6.6) Abdominal aortogram, posteroanterior (PA) projection. (6.5) Early arterial phase. (6.6) Mid-arterial phase. (6.7) Pelvic arteriogram, posteroanterior (PA) view.

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tient was discharged home in stable condition, but returned 1 month later with gross bloody urine draining from her nephrostomy tube. Physical examination revealed a chronically ill-appearing woman in no acute distress. She was afebrile and mildly tachycardic to 100 bpm with a blood pressure of 104/60 mm Hg. Laboratory evaluation results were

as follows: hematocrit, 34% (normal, 36 – 46); WBC, 8.3 ⫻ 109/L (normal, 3.4 –10); platelets, 250 ⫻ 109/L (normal, 140 – 450); creatinine, 1.2 mg/dL (normal, 0.6 –1.2); prothrombin time, 12.8 seconds (normal, 11.0 –14.5); and international normalized ratio, 1.1 (normal, 0.8 –1.2). To evaluate the source of bleeding, the patient underwent abdominal and

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pelvic computed tomography (CT) (Figs 6.1– 6.3), left nephrostogram (Fig 6.4), and angiography (Figs 6.5– 6.9). Questions: 1. What is the most likely cause of this patient’s hematuria? 2. What are the options for management of this patient?

Figures 6.8, 6.9. Selective left renal arteriogram. (6.8) Early arterial phase. (6.9) Late arterial phase.

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Case 7 History A 51-year-old woman presented with a 2-month history of painless jaundice. She denied fever, chills, or significant weight loss. There was no history of hepatobiliary disease, nor was there a history of abdominal surgery. Physical examination was remarkable for jaundice; however, no masses were palpable and there was no evidence of ascites.

Laboratory evaluation was remarkable for a total serum bilirubin level of 7.5 mg/dL (normal, 0.3–1.3), alkaline phosphatase level of 422 U/L (normal, 29 –111), albumin level of 3.5 g/dL (normal, 3.4 – 4.7), hemoglobin level of 13.2 g/dL (normal, 12.0 –15.5), and hematocrit level of 39.5% (normal, 36%– 46%). Ultrasound at the referral institution showed the presence of biliary ductal dilation and the patient was re-

ferred for further diagnostic evaluation and therapy. A transhepatic cholangiogram and biliary drainage (Figs 7.1, 7.2) were performed. After this, abdominal computed tomography (Fig 7.3) and portal venography (Fig 7.4) were performed.

Question • What is your diagnosis?

Figures 7.1, 7.2. (7.1) Catheter cholangiogram, right anterior oblique projection. (7.2) Catheter cholangiogram, postero-anterior projection.

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Figure 7.3. Contrast-enhanced CT image through the region of the hepatic hilum.

Figure 7.4. Transhepatic portal venogram, posteroanterior projection.

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Case 8

Figure 8.1. Contrast-enhanced thoracic CT.

History A 66-year-old man presented with massive hemoptysis. He had been in his usual state of health until 3 years before admission, when he developed shortness of breath. Subsequently, the diagnosis of usual interstitial pneumonitis (UIP) was made. Six months before admission, the patient began to experience intermittent hemoptysis. Three days before admission, the hemoptysis increased until the day of admission when he expectorated massive amounts of blood. The patient denied having chest pain, chills, or fever. Medical history was unremarkable for trauma, cardiac disease, immunosuppression, or coagulation disorder. He did not smoke, nor was he taking anticoagulant medication. Physical examination revealed a cachectic-appearing male in mild respiratory distress. He was mildly hypotensive and tachycardic. Auscultation of the chest disclosed course breath sounds with rhonchi bilaterally. Laboratory evaluation revealed a moderate anemia with a hematocrit of 31%, but was otherwise unremarkable. The renal function and coagulation profiles were within normal limits. Fiberoptic bronchoscopy was performed which revealed active bleeding from the right upper lobe. Contrastenhanced computed tomography (CT) (Fig 8.1) was then

Figures 8.2, 8.3. (8.2) Selective right subclavian arteriography, arterial phase. (8.3) Superselective right costocervical arteriogram.

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Figure 8.4. Right costocervical arteriogram following catheterinduced dissection.

Figures 8.6, 8.7. Repeat thoracic CT at time of second admission for massive hemoptysis. (8.6) Axial image through the upper thorax. (8.7) Oblique reconstruction through the right hemithorax. Figure 8.5. Contrast-enhanced thoracic CT following the arteriogram.

performed, followed by selective right subclavian and costocervical arteriography (Figs 8.2, 8.3). Attempts to embolize a branch of the costocervical trunk were thwarted by catheter induced dissection (Fig 8.4). Following the arteriogram, the patient’s hemoptysis ceased. A CT scan

(Fig 8.5) was repeated and after 3 days of in hospital observation and antibiotic therapy, the patient was discharged home. Two weeks later, the massive hemoptysis recurred. The CT scan was repeated (Figs 8.6, 8.7).

Questions 1. What is the cause of this patient’s hemoptysis? 2. How should this patient be managed?