- Email: [email protected]
Endocrine Angiography
and most often are associated with intravenous drug abuse and immune deficiency states.
Angiomyolipoma of the kidney. An angiographic review. ACTA Radiol 1973;14:561.
Arteriovenous Fistulas These lesions may be acquired after trauma and tumor erosion into the venous system. Arteriovenous fistulas after renal biopsy are common, but most resolve spontaneously. Those that persist may be treated effectively byembolotherapy.
8. Bonavita ]A, Pollack HM, Banner MP. Renal oncocytoma: Further observations and literature review. Urol Radiol 1981;2:229.
Arteriovenous Malfonnation These lesions are often congenital and present as bleeding or hypertension. Careful demonstrations of the feeding vessels is mandatory so that embolotherapy can be planned in such a fashion as to allow for obliteration of the "nidus." Emboli Larger emboli to the renal arteries may be associated with infarction. It is not unusual to have temporary loss of perfusion of the vascular bed due to associated spasm. Untreated emboli may lyse in time, leaving a diminished overall kidney size and corresponding reduction in diameter of the recanalized artery. Lysis with urokinase can be performed in selected cases. Chronic Renal Abscess Infection leading to abscess formation may be treated with antibiotics. If the collection is not drained, the granulation tissue formed in the wall of the abscess proliferates. This new blood supply may mimic tumor vessels on the angiogram.
References 1. Cuttino]T ]r, Clark RL. The normal vasculature of the genitourinary tract: Embryology, anatomy, and hemodynamics. In: Pollack's Clinical Urography. Philadelphia, PAc W.B. Saunders Co, 1990:2076-2091. 2. Mitty HA. Circumaortic renal collar: A potentially hazardous anomaly of the left renal vein. Am ] Roentgenol 1975;125:307-310. 3. Pollack HM, Popky GL. Roentgenographic manifestations of spontaneous renal hemorrhage. Radiology 1974;110:1-8. 4. Mitty HA, Shapiro RS, Parsons RB, Silberzweig ]E. Renovascular hypertension. Radiol Clin North Am 1996;34:1017-1036 5. Working Group on Renovascular Hypertension. Detection, evaluation, and treatment of renovascular hypertension-final report. Arch Intern Med 1987; 147:820-829. 6. Sos TA, Trost DE. Renal artery angioplasty and stenting. Presented at the Third Annual Symposium on Current Issues and New Techniques in Interventional Radiology, New York, New York, November 1995.
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7. Becker ]A, Kinhabwal AM, Pollack H, Bosniak M.
9. Hillman B]. Disorders of the renal arterial circulation and renal vascular hypertension. In: Pollack's Clinical Urography. Philadelphia, PAc W.B. Saunders Co, 1990:2127-2187. 10. Stanley]C, Gewertz BL, Bove EL, et al. Arterial fibrodysplasia. Arch Surg 1976;110:561-565. 11. Sharma S, Thatai D, Sapona A, et al. Renovascular hypertension resulting from nonspecific aortoarteritis in children: Midterm results of PTRA and predictors of restenosis. Am] Roentgenol 1996;166:157-162.
4:30 pm Endocrine Angiography John 1. Doppman, MD National Institute ofHealth Bethesda, Maryland Learning objectives: As a result of attending the categorical course on vascular diagnosis, specifically endocrine angiography, the attendee will: (1) Understand the indications for and techniques ofparathyroid arteriography for localization in patients with failed previous surgery; (2) Appreciate the technical problems of adrenal venous sampling and interpretation of results in patients with hyperaldosteronism; (3) Understand the most effective angiographic and sampling techniquesfor patients with functioning islet cell tumors of the pancreas; (4) Appreciate the pitfalls ofpetrosal sinus sampling in patients with functioning pituitary tumors; (5) To illustrate the limited but critical role of arteriography in the localization of endocrine tumors not visualized on cross-sectional imaging or scintigraphy; (6) To appreciate the importance of venous sampling for truly occult parathyrOid adrenal and islet cell tumors; (7) To introduce the concept of arterial stimulation and nonselective venous sampling in the localization of insulinomas, gastrinomas, and parathyroid adenomas. Adrenal Glands Pheochromocytomas Computed tomography and MIBG scanning have solved most of the localization problems of pheochromocytomas. Extra-adrenal pheos are generally in the abdomen in the vicinity of the renal hilum. Pheochromocytomas in the organ of Zuckerkandl are supplied by the inferior mesenteric artery but arteriography is rarely required preoperatively. Extra-adrenal pheochromocytomas are readily demonstrated by screening coronal MRIs by virtue of their high signal intensity on T2-weighted and Sh011 inversion time inversion recovery (STIR) images. Ectopic pheochromocytomas of the urinary bladder may be missed on MRI because of the high signal intensity of
the adjacent urine within the bladder. Arteriography is sometimes necessary.
Hyperaldosteronism Some investigators have presumed that CT and iodocholesterol scanning have replaced the need for venous sampling in hyperaldosteronism. As cross-sectional imaging improves with 3-mm thick, bolus-enhanced helical scans of the adrenal glands, many patients with hyperaldosteronism tend to show multiple small adrenal nodules even in the presence of a single dominant aldosteronoma. Iodocholesterol scanning fails to resolve lesions smaller than 15 mm. For these reasons, adrenal venous sampling is being resurrected as a critical study to distinguish unilateral aldosteronomas from idiopathic hyperaldosteronism resulting from hyperplasia. In our experience 0,2), over half the patients referred with a diagnosis of hyperplasia based on multiple unilateral or bilateral nodules have aldosteronomas and will respond to unilateral adrenalectomy. The role of adrenal sampling is to prove that one gland is totally suppressed because, under these circumstances, resection of the contralateral gland invariably cures hyperaldosteronism and improves control of hypertension. Adrenal venous sampling in patients with hyperaldosteronism should always be performed before and after ACTH stimulation. ACTH stimulates the release of both cortisol and aldosterone from the normal adrenal gland. Under the conditions of prolonged ACTH stimulation (Cushing's disease), aldosterone production escapes from ACTH control, but acutely, ACTH greatly enhances the sensitivity of adrenal vein sampling. Catheterization of the left adrenal vein is easily performed with an S-shaped catheter or a high flow Tracker catheter passed through a catheter with a recurved tip, such as a Simmons I. We routinely catheterize the right adrenal vein with a Mikaellson catheter having first placed an additional hole just proximal to the tip on the superior aspect. The right adrenal vein is less than 1 cm in length and the end hole of the catheter usually is occluded when the right adrenal vein is catheterized. A small hole proximal to the tip enables one to aspirate effluent from the gland. AJI patients should be anticoagulated. The principal risk of this procedure is not extravasation of contrast but adrenal venous thrombosis, the cause of the very rare adrenal infarction and, if bilateral, Addisonian crisis. Samples are obtained before and 15 minutes after a bolus injection of 250 jLg of ACTH followed by a continuous infusion of 500 ml saline containing 250 jLg of ACTH. One must calculate aldosterone/cortisol (AlC) ratios to correct for the varying dilution of samples from the right and left adrenal/veins. In the presence of an aldosteronoma, samples from the contralateral adrenal gland show an AlC ratio less than one and generally lower than the peripheral A/C ratio. At the conclusion of the study, gentle retrograde injections of contrast are performed to identify the position of the catheter in the
adrenal vein but no effort is made to perform a diagnostic adrenal venogram. Using the above-described technique, our success rate in the last 50 bilateral adrenal vein catheterizations has been 98%. In over half the patients with an imaging diagnosis of hyperplasia, the presence of an aldosteronoma has been established and confirmed by adrenalectomy (1). Rarely are aldosteronomas too small to be seen by modem cross-sectional techniques. More common is the dilemma of multiple nodules which, even in the presence of a dominant nodule, mandates a diagnosis of hyperplasia. Pancreatic Islet Cell Tumors In our experience, only 60% of insulinomas are visualized by cross-sectional imaging (CT, MRI, or ultrasound) although there may be a referral bias. Bolus-enhanced CT and fat-suppressed T2-weighted SPGR MR images are the best noninvasive localizing studies. When noninvasive studies are negative, pancreatic arteriography and portal venous sampling are performed but sampling of the portal vein has been replaced by stimulating the release of insulin with intraarterial injection of calcium at the time of arteriography (3). In our experience, arteriography visualizes about 50% of insulinomas. Immediately following each selective arteriogram (gastroduodenal, splenic, superior mesenteric), a bolus injection of 0.025 mEq of calcium per kilogram in the form of calcium gluconate diluted to a 5 ml bolus is injected and samples from the right hepatiC vein are obtained before and at 20, 40, and 60 seconds after calcium gluconate injection. When the vessel supplying the insulinoma is injected, a twofold or larger increase of insulin is measured in the right hepatic vein on the 20- or 40-second samples. Insulin levels are generaJly declining by the 60-second sample. However, patients with histories of frequent hypoglycemic attacks are at risk for a hypoglycemic episode at the time of calcium stimulation. O'Shea et al (4). have successfully reduced the dose of calcium fourfold from 0.025 mEg/kg to 0.00625 mEg/kg and obtained positive responses in five patients. It may turn out that this reduced dose is equally efficacious and safer. However, one can always control hypoglycemia at the time of angiography by a bolus of 50% glucose which should be readily at hand during calcium stimulation studies. Patients experience a mild warm sensation in the abdomen as the only side effect of intraarterial calcium injection. In our first 25 occult insuIinomas, arteriography was positive in 12 of 25 (48%), pOl1al venous sampling in six of nine (66%) (subsequently discontinued), and intraarterial calcium stimulation was positive in 22 of 25 (88%). Our series now numbers 40 patients, and calcium gluconate stimulation has been positive in 93% (37 of 40). Calcium stimulation and venous sampling should be performed in all patients with hyperinsulinism and multiple endocrine neoplasia syndromes, because such patients usually have more than one islet cell tumor, and the larger, more readily apparent tumor at the time of
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surgery may not be the adenoma responsible for the hyperinsulinism. Intraoperative ultrasound has become so sensitive that many surgeons now feel that once a diagnosis of insulinoma is established, the patient should go directly to the operating room if experienced intraoperative ultrasound is available. At the Mayo Clinic, patients are taken directly to surgery following diagnosis with no attempts of preoperative localization. I have not reached this stage of confidence in intraoperative ultrasound although its sensitivity in our last 30 patients has been 100%. A similar technique has been used extensively to localize gastrinomas. Intraarterial secretin (30 units) is injected selectively into the gastroduodenal, proximal splenic, and superior mesenteric arteries. Because over 60% of gastrinomas are malignant, one should perform secretin stimulation in the hepatic artery as well (not necessary in insulinomas because less than 10% are malignant). A 1.5-fold rise in gastrin in the right hepatic vein following interarterial injection of secretin localizes the gastrinoma to the downstream distribution of the injected artery. A positive response in the gastroduodenal artery does not distinguish between lesions in the pancreatic head and the increasingly common gastrinomas in the duodenal wall. Arterial stimulation and venous sampling is the single most successful localizing study for gastrinomas (>850/0), although octreotide scanning is proving to be a very successful noninvasive competitor. Over 75% of extrahepatic and pancreatic gastrinomas are demonstrated by octreotide scanning, better than all of the noninvasive imaging modalities combined (5).
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Parathyroid Localization The most common localization problem in endocrinology involves the parathyroid gland. There is an epidemic of low-grade hyperparathyroidism in middle-aged and elderly females, many of whom do not require surgery as the hypercalcemia is detected incidentally and does not threaten their well-being. Patients without previous surgery require no localization studies, because an experienced parathyroid surgeon 00-12 operations/year) has a cure rate at the initial operation of over 95%. After a failed operation, all patients should undergo noninvasive imaging studies--ultrasound, CT, MRl, and sestamibi imaging. If any two procedures are positive at the same site, angiography is not indicated. In our experience (6,7) about 60% of reoperative patients have successful localization by the noninvasive workup. If localization is not provided by noninvasive studies, parathyroid arteriography and venous sampling are performed. Arteriography is positive in about 50% of the cases and provides a road map of venous drainage that has often been altered by previous unsuccessful surgery. One should selectively inject both internal mammalY and both inferior thyroid arteries and, if negative, both superior thyroid arteries. Parathyroid adenomas are
demonstrated as areas of diffuse opacification. When arteriography is negative, venous sampling will provide a localized gradient in over 90%) of patients (8). However, this study provides regionalization, not precise localization, of abnormal parathyroid tissue, because the adenoma is not visualized. We have recently applied a technique involving stimulation of release of parathyroid hormone at the time of arteriography to replace parathyroid venous sampling. This technique is based on the same principle as the use of intraarterial calcium for localiZing insulinomas and intraarterial secretin for localiZing gastrinomas. Initially, we performed a prolonged infusion of normal saline into the selectively catheterized artery to provide a hypocalcemic stimulus which is responsible for the release of parathyroid hormone. However, we discovered that the nonionic contrast material used for arteriography is also a stimulant for releasing PTH. A catheter is placed in the superior vena cava at the time of parathyroid arteriography. Because the inferior thyroid veins, right and left vertebral veins, and the thymic veins drain into the innominate veins, the catheter in the SVC just below the junction of the right and left innominate vein samples the entire effluent from the neck and anterior mediastinum. A baseline 5-rnl sample is obtained immediately before each selective arteriogram and then at 20, 40, and 60 seconds following the arteriogram. A l.4-fold elevation of parathyroid hormone in the samples following arteriography localizes the adenoma to the distribution of the injected artery. Our experience with this technique is evolving but it has proved successful in 13% of our last 20 (65%) cases and obviated the need for the more tedious and difficult parathyroid venous sampling. In at least one third of these cases, arterial stimulation with venous sampling was positive when the arteriogram failed to demonstrate the adenoma (9). The two most likely sites for overlooked parathyroid adenomas are in the tracheoesophageal groove and in the anterior mediastinum. Recently, we have seen an increasing number of glands in an undescended location at the level of the carotid bifurcation (0). These glands are usually supplied by the superior thyroid artery and often cannot be reached from a standard collar incision. A less common site for ectopic glands is in the space between the aorta and pulmonary artery (aortopulmonary window). We have seen 10 patients with glands at this site in the past year (11). Blood supply is from the bronchial artery. These glands can reacWy be detected on CT and sestamibi scanning if the aortopulmonary window is appreciated as a site for ectopic glands. There are two nonsurgical techniques for treating enlarged parathyroid glands. Adenomas can be stained by injecting contrast material forcefully into the feeding artery. We have stained over 50 mediastinal adenomas, in fact, we rarely perform sternotomy to remove mediastinal adenomas (2). The thymic branch from the internal mammary artelY can usually be catheterized with
a Tracker catheter. A high-flow Tracker is preferred because one must inject contrast material rapidly enough to produce an intense stain of the adenoma. Staining is generally associated with mid-substernal burning that the patients will suggest is cardiac in origin. They should be forewarned of this sensation. We repeatedly stain adenomas until a persistent stain is obtained that does not fade for 15 minutes. One often stains the adjacent thymic tissue as well. A CT scan should be performed at 24 hours to document persistent contrast in the adenoma, a finding that indicates permanent ablation in our experience. We have, however, returned to stain a recurrent adenoma, a technique not available with embolization because the feeding artery is blocked. We originally used embolic material but found that staining with contrast media was more effective. We do not stain adenomas of the neck because the surgery is generally simple. The second technique for treating enlarged parathyroid glands is the direct injection of alcohol under CT or ultrasound control (13). I do not think that this is acceptable treatment for cervical adenomas because the risk to the recurrent laryngeal nerve and other vitaJ structures is significant. Local alcohol injection often renders subsequent surgical extirpation extraordinarily difficult. The intralesional injection of alcohol for well-localized cervical adenomas in patients with no previous surgery is never indicated as the potential complications are serious and the surgery is simple and extraordinarily effective. However, in patients with chronic renal failure and secondalY hyperparathyroidism, one can often control hypercalcemia by injecting hyperplastic glands. This technique rarely cures patients but will often control hypercalcemia, a satisfactory outcome in patients with chronic renal failure but not in patients with adenomas.
Petrosal Sinus Sampling Petrosal sinus sampling in patients with ACTH-dependent Cushing's syndrome is the most reliable technique for distinguishing pituitary from ectopic ACTH production and for lateralizing the microadenoma when MRl of the pituitary gland is negative (14). Neuroradiologists claim petrosal sinuses as their territory but drainage actually occurs into the internal jugular vein below the bulb and, therefore, outside the base of the skull (15). In many hospitals, petrosal sinus sampling is performed by general angiographers. It should always be performed bilaterally with simultaneous sampling before and after the administration of corticotropin releasing hormone (CRH) (16) which has recently been approved by the FDA. We perform the study with 4 French polyethylene catheters having a 20° hockey stick terminal curvature. In most instances, inferior petrosal sinuses drain into the anteromedial aspect of the internal jugular vein below the base of the skull. If the patient complains of ear pain, one is searching too high. In 95% of the patients the procedure is quite simple. III 5% the petrosal sinuses are replaced either by a plexiform network of vessels (4%)
or do not connect at all with the internal jugular vein on one side (1%) (17). Tracker catheters may also fail under such circumstances. One can use a Tracker to cross from the available petrosal sinus to the contralateral cavernous sinus to obtain bilateral samples. Tracker catheters are not necessary for successful petrosal sinus sampling and add significantly to the cost of the procedure. Neuroradiologists are addicted to such microcatheters and some insist that sampling be performed in the cavernous sinuses (18). Placing Tracker catheters in the cavernous sinuses is not difficult technically but we have published data (19) showing that it is unnecessary, expensive, and if widely applied would probably be associated with more serious consequences (cavernous sinus thrombosis) than have been associated with petrosal sinus sampling. We have performed over 1,000 petrosal sinus samples with only a single serious complication (20). We have recently demonstrated that bilateral jugular vein sampling combined with CRH administration is 80% sensitive for distingUishing Cushing's disease from ectopic ACTH syndrome (21). Because specifiCity is 100% (no false positive), it can be used as a simple screening test in institutions with little petrosal experience.
References 1. Doppman JL, Gill JG, Miller DL, et al. Distinction
between hyperaldosteronism due to bilateral hyperplasia and unilateral aldosteronoma: reliability of CT. Radiology 1992; 184:677-682. 2. Doppman JL. The dilemma of bilateral adrenocortical nodularity in Conn's and Cushing's syndromes. Radiol Clin North Am 1993; 31:1039-1050. 3. Doppman JL, Chang R, Fraker DL, et al. Localization of insulinomas to regions of the pancreas by intraatterial stimulation with calcium. Ann Intern Med 1995; 123:269-273. 4. O'Shea D, Rohrer-Theus AW, Lynn A, Jackson JE, Bloom SH. Localization of insulinomas by selective intraarterial calcium injection. J Clin Endocrino] Metab 81:1623-1627. 5. Gibril F, Reynolds JC, Doppman JL, et al. Somatostatic receptor scintigraphy; its sensitivity compared with that of other imaging methods in detecting primary and metastatic gastrinomas. Ann Intern Med 1996; 125:26-34. 6. Doppman JL, Miller DL. Localization of parathyroid tumors in patients with asymptomatic hyperparathyroidism and no previous surgery. J Bone Miner Res 1991; 6:S153-S158. 7. Miller DL, DoppmanJL, Krudy AG, et al. Localization of parathyrOid adenomas in patients who have undergone surgery. Part II. Invasive procedures. Radiology 1987; 162:138-141. 8. Sugg SL, Fraker DL, Alexander R, et al. Prospective evaluation of selective venous sampling for parathy-
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roid hormone concentration in patients undergoing reoperations for primary hyperparathyroidism. Surgery 1993; 114:1004-1010. 9. Doppman )L, Skarulis MC, Chang R, et al. Hypocalcemic stimulation and nonselective venous sampling for localizing parathyroid adenomas. Radiology 1998; 208:145-151. 10. Doppman)L, ShawkerTH, Kmdy AG, et al. Parathymic parathyroid. CT, US, and angiographic findings. Radiology 1985; 157:419-423. 11. Doppman )L, Skarulis, Chen CC, et al. Parathyroid adenomas in the aortopulmonary window. Radiology 1996; 224:308-322. 12. Doheny GM, Doppman)L, Miller DL, et al. Results of multidisciplinary strategy for management of mediastinal parathyroid adenomas as a cause of persistent primary hyperparathyroidism. Ann Surg 1992; 215:10]-106. 13. Karstrup S, Transbal I, Holm HH, et al. Ultrasound guided chemical parathyroidectomy in patients with primary hyperparathyroidism. Brit) Radiol 1989; 62: 1037-1042. 14. Oldfield EH, Doppman)L, Nieman LK, et al. Bilateral inferior petrosal vein sampling with and without corticotropin releasing hormone for the differential diagnosis of Cushing's syndrome. N Engl ) Med 1991; 325:897-905. 15. Miller DL, Doppman )L. Petrosal sinus sampling. Technique and rationale. Radiology 1991; 178:3747. 16. Doppman )L, Oldfield E, Kmdy AG, et al. Anatomical and technical considerations of inferior petrosal sinus sampling for Cushing's disease. Radiology 1984; 150:99-103. 17. Miller DL, Doppman )L, Chang R. Anatomy of the junction of the inferior petrosal sinus and the internal jugular vein. A)NR 1993; 14:1075-1083. 18. Teramoto A, Nemato S, Takakura K, et al. Selective venous sampling directly from cavernous sinus and Cushing's syndrome. ) Clin Endocrinol Metab 1993; 76:630-641. 19. Doppman )L, Nieman LK, Chang R, et al. Selective venous sampling from the cavernous sinuses is not a more reliable technique than sampling from the inferior petrosal sinuses in Cushing's syndrome. ) Clin Endocrinol Metab 80:2485-3489. 20. Miller DL, Doppman )L, Peterman SB, Nieman LK, Oldfield EH, Chang R. Neurologic complications of petrosal sinus sampling. Radiology 1992; 185:143147.
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21. Doppman)L, Oldfield EH, Nieman LK. Bilateral sampling of the internal jugular vein to distinguish between mechanism of adrenocorticotropic hormone-
dependent Cushing's syndrome. Ann Intern Med -1998; 128:33-36. 5:00 pm Pelvic Angiography: What You Need to Know in the Era of Gynecologic Intervention Siobhan A. Dumbleton, MD University of Pennsylvania Philadelphia, Pennsylvania Learning objectives: As a result of attending this session, the attendee should be able to: 1) Understand pelvic angiographic anatomy as it pertains to embolization of gynecologic abnormalities; and 2) Have an understanding of the management and treatment of gynecologic entities, in particular, uterine fibroids, pelvic hemorrhage (postpartum bleeding, cervical ectopic pregnancy), and ovarian vein varices. Anatomy In brief, the internal iliac artery divides into anterior and posterior divisions in most (60%) people (1). The superior gluteal, iliolumbar, and lateral sacral arteries arise from the posterior division, with the superior gluteal artery forming the terminal branch. In general, the anterior division gives rise to the obturator, inferior gluteal, and internal pudendal arteries. It also gives rise to the superior and inferior vesical arteries and the internal genital arteries. In the female, the internal genital arteries are the uterine arteries. The terminal branch of the anterior division is the internal pudendal artery. The uterine arteries terminate in extremely tortuous end arteries within the uterine musculature. The uterine arteries also supply branches to the fallopian tubes, ovaries, cervix, and vagina (2). Gynecologic Disorders Uterine Fibroids In women older than 35 years of age, uterine leiomyomata or fibroids are the most common pelvic tumors, with an estimated prevalence of 20-40%. Symptoms include menorrhagia as well as symptoms related to bulk. To date, treatment has included hysterectomy, myomectomy, and hormonal therapy. All these treatments are associated with significant disadvantages. Twenty percent to twenty-five percent of women undergoing myomectomy will require another intervention. Hormonal therapy results in symptomatic improvement and decrease in tumor size, but once stopped, there is a rapid regrowth of the tumor. Although hysterectomy is curative, it eliminates fertility. Recently, catheter-directed means of managing leiomyomata are being explored. Results are promising. Goodwin et al (3) described a series of 11 patients, age 27-55 years, in whom prior treatments had failed. Ten patients underwent bilateral uterine artery embolization, and one patient underwent unilateral uterine artery embolization. On ultrasound examination, 10 of the 11
Angiomyolipoma of the kidney. An angiographic review. ACTA Radiol 1973;14:561.
Arteriovenous Fistulas These lesions may be acquired after trauma and tumor erosion into the venous system. Arteriovenous fistulas after renal biopsy are common, but most resolve spontaneously. Those that persist may be treated effectively byembolotherapy.
8. Bonavita ]A, Pollack HM, Banner MP. Renal oncocytoma: Further observations and literature review. Urol Radiol 1981;2:229.
Arteriovenous Malfonnation These lesions are often congenital and present as bleeding or hypertension. Careful demonstrations of the feeding vessels is mandatory so that embolotherapy can be planned in such a fashion as to allow for obliteration of the "nidus." Emboli Larger emboli to the renal arteries may be associated with infarction. It is not unusual to have temporary loss of perfusion of the vascular bed due to associated spasm. Untreated emboli may lyse in time, leaving a diminished overall kidney size and corresponding reduction in diameter of the recanalized artery. Lysis with urokinase can be performed in selected cases. Chronic Renal Abscess Infection leading to abscess formation may be treated with antibiotics. If the collection is not drained, the granulation tissue formed in the wall of the abscess proliferates. This new blood supply may mimic tumor vessels on the angiogram.
References 1. Cuttino]T ]r, Clark RL. The normal vasculature of the genitourinary tract: Embryology, anatomy, and hemodynamics. In: Pollack's Clinical Urography. Philadelphia, PAc W.B. Saunders Co, 1990:2076-2091. 2. Mitty HA. Circumaortic renal collar: A potentially hazardous anomaly of the left renal vein. Am ] Roentgenol 1975;125:307-310. 3. Pollack HM, Popky GL. Roentgenographic manifestations of spontaneous renal hemorrhage. Radiology 1974;110:1-8. 4. Mitty HA, Shapiro RS, Parsons RB, Silberzweig ]E. Renovascular hypertension. Radiol Clin North Am 1996;34:1017-1036 5. Working Group on Renovascular Hypertension. Detection, evaluation, and treatment of renovascular hypertension-final report. Arch Intern Med 1987; 147:820-829. 6. Sos TA, Trost DE. Renal artery angioplasty and stenting. Presented at the Third Annual Symposium on Current Issues and New Techniques in Interventional Radiology, New York, New York, November 1995.
430
7. Becker ]A, Kinhabwal AM, Pollack H, Bosniak M.
9. Hillman B]. Disorders of the renal arterial circulation and renal vascular hypertension. In: Pollack's Clinical Urography. Philadelphia, PAc W.B. Saunders Co, 1990:2127-2187. 10. Stanley]C, Gewertz BL, Bove EL, et al. Arterial fibrodysplasia. Arch Surg 1976;110:561-565. 11. Sharma S, Thatai D, Sapona A, et al. Renovascular hypertension resulting from nonspecific aortoarteritis in children: Midterm results of PTRA and predictors of restenosis. Am] Roentgenol 1996;166:157-162.
4:30 pm Endocrine Angiography John 1. Doppman, MD National Institute ofHealth Bethesda, Maryland Learning objectives: As a result of attending the categorical course on vascular diagnosis, specifically endocrine angiography, the attendee will: (1) Understand the indications for and techniques ofparathyroid arteriography for localization in patients with failed previous surgery; (2) Appreciate the technical problems of adrenal venous sampling and interpretation of results in patients with hyperaldosteronism; (3) Understand the most effective angiographic and sampling techniquesfor patients with functioning islet cell tumors of the pancreas; (4) Appreciate the pitfalls ofpetrosal sinus sampling in patients with functioning pituitary tumors; (5) To illustrate the limited but critical role of arteriography in the localization of endocrine tumors not visualized on cross-sectional imaging or scintigraphy; (6) To appreciate the importance of venous sampling for truly occult parathyrOid adrenal and islet cell tumors; (7) To introduce the concept of arterial stimulation and nonselective venous sampling in the localization of insulinomas, gastrinomas, and parathyroid adenomas. Adrenal Glands Pheochromocytomas Computed tomography and MIBG scanning have solved most of the localization problems of pheochromocytomas. Extra-adrenal pheos are generally in the abdomen in the vicinity of the renal hilum. Pheochromocytomas in the organ of Zuckerkandl are supplied by the inferior mesenteric artery but arteriography is rarely required preoperatively. Extra-adrenal pheochromocytomas are readily demonstrated by screening coronal MRIs by virtue of their high signal intensity on T2-weighted and Sh011 inversion time inversion recovery (STIR) images. Ectopic pheochromocytomas of the urinary bladder may be missed on MRI because of the high signal intensity of
the adjacent urine within the bladder. Arteriography is sometimes necessary.
Hyperaldosteronism Some investigators have presumed that CT and iodocholesterol scanning have replaced the need for venous sampling in hyperaldosteronism. As cross-sectional imaging improves with 3-mm thick, bolus-enhanced helical scans of the adrenal glands, many patients with hyperaldosteronism tend to show multiple small adrenal nodules even in the presence of a single dominant aldosteronoma. Iodocholesterol scanning fails to resolve lesions smaller than 15 mm. For these reasons, adrenal venous sampling is being resurrected as a critical study to distinguish unilateral aldosteronomas from idiopathic hyperaldosteronism resulting from hyperplasia. In our experience 0,2), over half the patients referred with a diagnosis of hyperplasia based on multiple unilateral or bilateral nodules have aldosteronomas and will respond to unilateral adrenalectomy. The role of adrenal sampling is to prove that one gland is totally suppressed because, under these circumstances, resection of the contralateral gland invariably cures hyperaldosteronism and improves control of hypertension. Adrenal venous sampling in patients with hyperaldosteronism should always be performed before and after ACTH stimulation. ACTH stimulates the release of both cortisol and aldosterone from the normal adrenal gland. Under the conditions of prolonged ACTH stimulation (Cushing's disease), aldosterone production escapes from ACTH control, but acutely, ACTH greatly enhances the sensitivity of adrenal vein sampling. Catheterization of the left adrenal vein is easily performed with an S-shaped catheter or a high flow Tracker catheter passed through a catheter with a recurved tip, such as a Simmons I. We routinely catheterize the right adrenal vein with a Mikaellson catheter having first placed an additional hole just proximal to the tip on the superior aspect. The right adrenal vein is less than 1 cm in length and the end hole of the catheter usually is occluded when the right adrenal vein is catheterized. A small hole proximal to the tip enables one to aspirate effluent from the gland. AJI patients should be anticoagulated. The principal risk of this procedure is not extravasation of contrast but adrenal venous thrombosis, the cause of the very rare adrenal infarction and, if bilateral, Addisonian crisis. Samples are obtained before and 15 minutes after a bolus injection of 250 jLg of ACTH followed by a continuous infusion of 500 ml saline containing 250 jLg of ACTH. One must calculate aldosterone/cortisol (AlC) ratios to correct for the varying dilution of samples from the right and left adrenal/veins. In the presence of an aldosteronoma, samples from the contralateral adrenal gland show an AlC ratio less than one and generally lower than the peripheral A/C ratio. At the conclusion of the study, gentle retrograde injections of contrast are performed to identify the position of the catheter in the
adrenal vein but no effort is made to perform a diagnostic adrenal venogram. Using the above-described technique, our success rate in the last 50 bilateral adrenal vein catheterizations has been 98%. In over half the patients with an imaging diagnosis of hyperplasia, the presence of an aldosteronoma has been established and confirmed by adrenalectomy (1). Rarely are aldosteronomas too small to be seen by modem cross-sectional techniques. More common is the dilemma of multiple nodules which, even in the presence of a dominant nodule, mandates a diagnosis of hyperplasia. Pancreatic Islet Cell Tumors In our experience, only 60% of insulinomas are visualized by cross-sectional imaging (CT, MRI, or ultrasound) although there may be a referral bias. Bolus-enhanced CT and fat-suppressed T2-weighted SPGR MR images are the best noninvasive localizing studies. When noninvasive studies are negative, pancreatic arteriography and portal venous sampling are performed but sampling of the portal vein has been replaced by stimulating the release of insulin with intraarterial injection of calcium at the time of arteriography (3). In our experience, arteriography visualizes about 50% of insulinomas. Immediately following each selective arteriogram (gastroduodenal, splenic, superior mesenteric), a bolus injection of 0.025 mEq of calcium per kilogram in the form of calcium gluconate diluted to a 5 ml bolus is injected and samples from the right hepatiC vein are obtained before and at 20, 40, and 60 seconds after calcium gluconate injection. When the vessel supplying the insulinoma is injected, a twofold or larger increase of insulin is measured in the right hepatic vein on the 20- or 40-second samples. Insulin levels are generaJly declining by the 60-second sample. However, patients with histories of frequent hypoglycemic attacks are at risk for a hypoglycemic episode at the time of calcium stimulation. O'Shea et al (4). have successfully reduced the dose of calcium fourfold from 0.025 mEg/kg to 0.00625 mEg/kg and obtained positive responses in five patients. It may turn out that this reduced dose is equally efficacious and safer. However, one can always control hypoglycemia at the time of angiography by a bolus of 50% glucose which should be readily at hand during calcium stimulation studies. Patients experience a mild warm sensation in the abdomen as the only side effect of intraarterial calcium injection. In our first 25 occult insuIinomas, arteriography was positive in 12 of 25 (48%), pOl1al venous sampling in six of nine (66%) (subsequently discontinued), and intraarterial calcium stimulation was positive in 22 of 25 (88%). Our series now numbers 40 patients, and calcium gluconate stimulation has been positive in 93% (37 of 40). Calcium stimulation and venous sampling should be performed in all patients with hyperinsulinism and multiple endocrine neoplasia syndromes, because such patients usually have more than one islet cell tumor, and the larger, more readily apparent tumor at the time of
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surgery may not be the adenoma responsible for the hyperinsulinism. Intraoperative ultrasound has become so sensitive that many surgeons now feel that once a diagnosis of insulinoma is established, the patient should go directly to the operating room if experienced intraoperative ultrasound is available. At the Mayo Clinic, patients are taken directly to surgery following diagnosis with no attempts of preoperative localization. I have not reached this stage of confidence in intraoperative ultrasound although its sensitivity in our last 30 patients has been 100%. A similar technique has been used extensively to localize gastrinomas. Intraarterial secretin (30 units) is injected selectively into the gastroduodenal, proximal splenic, and superior mesenteric arteries. Because over 60% of gastrinomas are malignant, one should perform secretin stimulation in the hepatic artery as well (not necessary in insulinomas because less than 10% are malignant). A 1.5-fold rise in gastrin in the right hepatic vein following interarterial injection of secretin localizes the gastrinoma to the downstream distribution of the injected artery. A positive response in the gastroduodenal artery does not distinguish between lesions in the pancreatic head and the increasingly common gastrinomas in the duodenal wall. Arterial stimulation and venous sampling is the single most successful localizing study for gastrinomas (>850/0), although octreotide scanning is proving to be a very successful noninvasive competitor. Over 75% of extrahepatic and pancreatic gastrinomas are demonstrated by octreotide scanning, better than all of the noninvasive imaging modalities combined (5).
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Parathyroid Localization The most common localization problem in endocrinology involves the parathyroid gland. There is an epidemic of low-grade hyperparathyroidism in middle-aged and elderly females, many of whom do not require surgery as the hypercalcemia is detected incidentally and does not threaten their well-being. Patients without previous surgery require no localization studies, because an experienced parathyroid surgeon 00-12 operations/year) has a cure rate at the initial operation of over 95%. After a failed operation, all patients should undergo noninvasive imaging studies--ultrasound, CT, MRl, and sestamibi imaging. If any two procedures are positive at the same site, angiography is not indicated. In our experience (6,7) about 60% of reoperative patients have successful localization by the noninvasive workup. If localization is not provided by noninvasive studies, parathyroid arteriography and venous sampling are performed. Arteriography is positive in about 50% of the cases and provides a road map of venous drainage that has often been altered by previous unsuccessful surgery. One should selectively inject both internal mammalY and both inferior thyroid arteries and, if negative, both superior thyroid arteries. Parathyroid adenomas are
demonstrated as areas of diffuse opacification. When arteriography is negative, venous sampling will provide a localized gradient in over 90%) of patients (8). However, this study provides regionalization, not precise localization, of abnormal parathyroid tissue, because the adenoma is not visualized. We have recently applied a technique involving stimulation of release of parathyroid hormone at the time of arteriography to replace parathyroid venous sampling. This technique is based on the same principle as the use of intraarterial calcium for localiZing insulinomas and intraarterial secretin for localiZing gastrinomas. Initially, we performed a prolonged infusion of normal saline into the selectively catheterized artery to provide a hypocalcemic stimulus which is responsible for the release of parathyroid hormone. However, we discovered that the nonionic contrast material used for arteriography is also a stimulant for releasing PTH. A catheter is placed in the superior vena cava at the time of parathyroid arteriography. Because the inferior thyroid veins, right and left vertebral veins, and the thymic veins drain into the innominate veins, the catheter in the SVC just below the junction of the right and left innominate vein samples the entire effluent from the neck and anterior mediastinum. A baseline 5-rnl sample is obtained immediately before each selective arteriogram and then at 20, 40, and 60 seconds following the arteriogram. A l.4-fold elevation of parathyroid hormone in the samples following arteriography localizes the adenoma to the distribution of the injected artery. Our experience with this technique is evolving but it has proved successful in 13% of our last 20 (65%) cases and obviated the need for the more tedious and difficult parathyroid venous sampling. In at least one third of these cases, arterial stimulation with venous sampling was positive when the arteriogram failed to demonstrate the adenoma (9). The two most likely sites for overlooked parathyroid adenomas are in the tracheoesophageal groove and in the anterior mediastinum. Recently, we have seen an increasing number of glands in an undescended location at the level of the carotid bifurcation (0). These glands are usually supplied by the superior thyroid artery and often cannot be reached from a standard collar incision. A less common site for ectopic glands is in the space between the aorta and pulmonary artery (aortopulmonary window). We have seen 10 patients with glands at this site in the past year (11). Blood supply is from the bronchial artery. These glands can reacWy be detected on CT and sestamibi scanning if the aortopulmonary window is appreciated as a site for ectopic glands. There are two nonsurgical techniques for treating enlarged parathyroid glands. Adenomas can be stained by injecting contrast material forcefully into the feeding artery. We have stained over 50 mediastinal adenomas, in fact, we rarely perform sternotomy to remove mediastinal adenomas (2). The thymic branch from the internal mammary artelY can usually be catheterized with
a Tracker catheter. A high-flow Tracker is preferred because one must inject contrast material rapidly enough to produce an intense stain of the adenoma. Staining is generally associated with mid-substernal burning that the patients will suggest is cardiac in origin. They should be forewarned of this sensation. We repeatedly stain adenomas until a persistent stain is obtained that does not fade for 15 minutes. One often stains the adjacent thymic tissue as well. A CT scan should be performed at 24 hours to document persistent contrast in the adenoma, a finding that indicates permanent ablation in our experience. We have, however, returned to stain a recurrent adenoma, a technique not available with embolization because the feeding artery is blocked. We originally used embolic material but found that staining with contrast media was more effective. We do not stain adenomas of the neck because the surgery is generally simple. The second technique for treating enlarged parathyroid glands is the direct injection of alcohol under CT or ultrasound control (13). I do not think that this is acceptable treatment for cervical adenomas because the risk to the recurrent laryngeal nerve and other vitaJ structures is significant. Local alcohol injection often renders subsequent surgical extirpation extraordinarily difficult. The intralesional injection of alcohol for well-localized cervical adenomas in patients with no previous surgery is never indicated as the potential complications are serious and the surgery is simple and extraordinarily effective. However, in patients with chronic renal failure and secondalY hyperparathyroidism, one can often control hypercalcemia by injecting hyperplastic glands. This technique rarely cures patients but will often control hypercalcemia, a satisfactory outcome in patients with chronic renal failure but not in patients with adenomas.
Petrosal Sinus Sampling Petrosal sinus sampling in patients with ACTH-dependent Cushing's syndrome is the most reliable technique for distinguishing pituitary from ectopic ACTH production and for lateralizing the microadenoma when MRl of the pituitary gland is negative (14). Neuroradiologists claim petrosal sinuses as their territory but drainage actually occurs into the internal jugular vein below the bulb and, therefore, outside the base of the skull (15). In many hospitals, petrosal sinus sampling is performed by general angiographers. It should always be performed bilaterally with simultaneous sampling before and after the administration of corticotropin releasing hormone (CRH) (16) which has recently been approved by the FDA. We perform the study with 4 French polyethylene catheters having a 20° hockey stick terminal curvature. In most instances, inferior petrosal sinuses drain into the anteromedial aspect of the internal jugular vein below the base of the skull. If the patient complains of ear pain, one is searching too high. In 95% of the patients the procedure is quite simple. III 5% the petrosal sinuses are replaced either by a plexiform network of vessels (4%)
or do not connect at all with the internal jugular vein on one side (1%) (17). Tracker catheters may also fail under such circumstances. One can use a Tracker to cross from the available petrosal sinus to the contralateral cavernous sinus to obtain bilateral samples. Tracker catheters are not necessary for successful petrosal sinus sampling and add significantly to the cost of the procedure. Neuroradiologists are addicted to such microcatheters and some insist that sampling be performed in the cavernous sinuses (18). Placing Tracker catheters in the cavernous sinuses is not difficult technically but we have published data (19) showing that it is unnecessary, expensive, and if widely applied would probably be associated with more serious consequences (cavernous sinus thrombosis) than have been associated with petrosal sinus sampling. We have performed over 1,000 petrosal sinus samples with only a single serious complication (20). We have recently demonstrated that bilateral jugular vein sampling combined with CRH administration is 80% sensitive for distingUishing Cushing's disease from ectopic ACTH syndrome (21). Because specifiCity is 100% (no false positive), it can be used as a simple screening test in institutions with little petrosal experience.
References 1. Doppman JL, Gill JG, Miller DL, et al. Distinction
between hyperaldosteronism due to bilateral hyperplasia and unilateral aldosteronoma: reliability of CT. Radiology 1992; 184:677-682. 2. Doppman JL. The dilemma of bilateral adrenocortical nodularity in Conn's and Cushing's syndromes. Radiol Clin North Am 1993; 31:1039-1050. 3. Doppman JL, Chang R, Fraker DL, et al. Localization of insulinomas to regions of the pancreas by intraatterial stimulation with calcium. Ann Intern Med 1995; 123:269-273. 4. O'Shea D, Rohrer-Theus AW, Lynn A, Jackson JE, Bloom SH. Localization of insulinomas by selective intraarterial calcium injection. J Clin Endocrino] Metab 81:1623-1627. 5. Gibril F, Reynolds JC, Doppman JL, et al. Somatostatic receptor scintigraphy; its sensitivity compared with that of other imaging methods in detecting primary and metastatic gastrinomas. Ann Intern Med 1996; 125:26-34. 6. Doppman JL, Miller DL. Localization of parathyroid tumors in patients with asymptomatic hyperparathyroidism and no previous surgery. J Bone Miner Res 1991; 6:S153-S158. 7. Miller DL, DoppmanJL, Krudy AG, et al. Localization of parathyrOid adenomas in patients who have undergone surgery. Part II. Invasive procedures. Radiology 1987; 162:138-141. 8. Sugg SL, Fraker DL, Alexander R, et al. Prospective evaluation of selective venous sampling for parathy-
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roid hormone concentration in patients undergoing reoperations for primary hyperparathyroidism. Surgery 1993; 114:1004-1010. 9. Doppman )L, Skarulis MC, Chang R, et al. Hypocalcemic stimulation and nonselective venous sampling for localizing parathyroid adenomas. Radiology 1998; 208:145-151. 10. Doppman)L, ShawkerTH, Kmdy AG, et al. Parathymic parathyroid. CT, US, and angiographic findings. Radiology 1985; 157:419-423. 11. Doppman )L, Skarulis, Chen CC, et al. Parathyroid adenomas in the aortopulmonary window. Radiology 1996; 224:308-322. 12. Doheny GM, Doppman)L, Miller DL, et al. Results of multidisciplinary strategy for management of mediastinal parathyroid adenomas as a cause of persistent primary hyperparathyroidism. Ann Surg 1992; 215:10]-106. 13. Karstrup S, Transbal I, Holm HH, et al. Ultrasound guided chemical parathyroidectomy in patients with primary hyperparathyroidism. Brit) Radiol 1989; 62: 1037-1042. 14. Oldfield EH, Doppman)L, Nieman LK, et al. Bilateral inferior petrosal vein sampling with and without corticotropin releasing hormone for the differential diagnosis of Cushing's syndrome. N Engl ) Med 1991; 325:897-905. 15. Miller DL, Doppman )L. Petrosal sinus sampling. Technique and rationale. Radiology 1991; 178:3747. 16. Doppman )L, Oldfield E, Kmdy AG, et al. Anatomical and technical considerations of inferior petrosal sinus sampling for Cushing's disease. Radiology 1984; 150:99-103. 17. Miller DL, Doppman )L, Chang R. Anatomy of the junction of the inferior petrosal sinus and the internal jugular vein. A)NR 1993; 14:1075-1083. 18. Teramoto A, Nemato S, Takakura K, et al. Selective venous sampling directly from cavernous sinus and Cushing's syndrome. ) Clin Endocrinol Metab 1993; 76:630-641. 19. Doppman )L, Nieman LK, Chang R, et al. Selective venous sampling from the cavernous sinuses is not a more reliable technique than sampling from the inferior petrosal sinuses in Cushing's syndrome. ) Clin Endocrinol Metab 80:2485-3489. 20. Miller DL, Doppman )L, Peterman SB, Nieman LK, Oldfield EH, Chang R. Neurologic complications of petrosal sinus sampling. Radiology 1992; 185:143147.
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21. Doppman)L, Oldfield EH, Nieman LK. Bilateral sampling of the internal jugular vein to distinguish between mechanism of adrenocorticotropic hormone-
dependent Cushing's syndrome. Ann Intern Med -1998; 128:33-36. 5:00 pm Pelvic Angiography: What You Need to Know in the Era of Gynecologic Intervention Siobhan A. Dumbleton, MD University of Pennsylvania Philadelphia, Pennsylvania Learning objectives: As a result of attending this session, the attendee should be able to: 1) Understand pelvic angiographic anatomy as it pertains to embolization of gynecologic abnormalities; and 2) Have an understanding of the management and treatment of gynecologic entities, in particular, uterine fibroids, pelvic hemorrhage (postpartum bleeding, cervical ectopic pregnancy), and ovarian vein varices. Anatomy In brief, the internal iliac artery divides into anterior and posterior divisions in most (60%) people (1). The superior gluteal, iliolumbar, and lateral sacral arteries arise from the posterior division, with the superior gluteal artery forming the terminal branch. In general, the anterior division gives rise to the obturator, inferior gluteal, and internal pudendal arteries. It also gives rise to the superior and inferior vesical arteries and the internal genital arteries. In the female, the internal genital arteries are the uterine arteries. The terminal branch of the anterior division is the internal pudendal artery. The uterine arteries terminate in extremely tortuous end arteries within the uterine musculature. The uterine arteries also supply branches to the fallopian tubes, ovaries, cervix, and vagina (2). Gynecologic Disorders Uterine Fibroids In women older than 35 years of age, uterine leiomyomata or fibroids are the most common pelvic tumors, with an estimated prevalence of 20-40%. Symptoms include menorrhagia as well as symptoms related to bulk. To date, treatment has included hysterectomy, myomectomy, and hormonal therapy. All these treatments are associated with significant disadvantages. Twenty percent to twenty-five percent of women undergoing myomectomy will require another intervention. Hormonal therapy results in symptomatic improvement and decrease in tumor size, but once stopped, there is a rapid regrowth of the tumor. Although hysterectomy is curative, it eliminates fertility. Recently, catheter-directed means of managing leiomyomata are being explored. Results are promising. Goodwin et al (3) described a series of 11 patients, age 27-55 years, in whom prior treatments had failed. Ten patients underwent bilateral uterine artery embolization, and one patient underwent unilateral uterine artery embolization. On ultrasound examination, 10 of the 11