Iodinated Contrast and Thyrotoxicosis

The risk of iodine-induced thyrotoxicosis is low in euthyroid patients, ranging from 0% to about 2.5% depending on the study. The risk for hyperthyroid patients has not been defined, but in one study of elderly hyperthyroid patients 25% developed self-limited hyperthyroidism after nonionic contrast radiography. Prophylactic medications may be given, and include perchlorate with or without thiamazole, but there are no studies on the benefits of these medications.

References

• Fricke E, Fricke H, Esdorn E, Kammeier A, Lindner O, Kleesiek K, Horstkotte D, Burchert W. Scintigraphy for risk stratification of iodine-induced thyrotoxicosis in patients receiving contrast agent for coronary angiography: a prospective study of patients with low thyrotropin. J Clin Endocrinol Metab. 2004 Dec;89(12):6092-6.
• Martin FI, Tress BW, Colman PG, Deam DR. Iodine-induced hyperthyroidism due to nonionic contrast radiography in the elderly. Am J Med. 1993 Jul;95(1):78-82.

Venous Collateral Pathways

• Axillary or subclavian vein occlusion: Collateral flow through muscular and superficial veins of the shoulder, scapula, and chest wall into the ipsilateral internal jugular and intercostal veins, and the contralateral jugular or subclavian veins.
• Brachiocephalic vein occlusion: 1) Collateral flow through deep and superficial veins of the back, chest, and neck into the contralateral jugular, subclavian, and brachiocephalic veins. 2) Collateral flow through superficial chest wall veins such as the internal mammary and intercostal veins into the azygos (if right-sided occlusion) or hemiazygos (if left-sided) or into inferior epigastric veins.
• Superior vena cava occlusion above azygos vein: Collateral flow through the chest wall and intercostal veins into the azygos system.
• Superior vena cava occlusion below azygos vein: Collateral flow through retrograde flow in the azygos vein into the inferior vena cava.
• Superior vena cava occlusion above and below azygos vein: Collateral flow through chest wall and intercostal veins into the azygos and hemiazygos system into the inferior vena cava.
• Inferior vena cava occlusion below the renal veins: Collateral flow through ascending lumbar, paraspinal, gonadal, inferior epigastric, and abdominal wall veins.
• Inferior vena cava occlusion between renal and hepatic veins: Collateral flow through ascending lumbar, paraspinal, gonadal, inferior epigastric, and abdominal wall veins (as above) and azygos and hemiazygos veins (particularly for the renal veins)
• Inferior vena cava occlusion above hepatic veins: Collateral flow through ascending lumbar, paraspinal, gonadal, inferior epigastric, and abdominal wall veins, as well as azygos and hemiazygos veins (as above). In addition, gonadal and ureteric veins can also serve as collaterals.
• Right renal vein occlusion: Collateral flow through lumbar, ureteric and azygos veins.
• Left renal vein occlusion: Collateral flow through lumbar, hemiazygos , and left gonadal veins.
• Adrenal vein occlusion: Collateral flow through small retroperitoneal veins such as the renal capsular veins.
• Gonadal vein occlusion: Collateral flow through transpelvic, ascending lumbar, and internal iliac veins.
• Splenic vein occlusion: 1) Collateral flow through the short gastric veins into the left gastric vein. 2) Collateral flow through the omental vein to the gastroepiploic or superior mesenteric vein. Frequently submucosal collaterals prone to bleeding into the gastrointestinal tract.
• Central superior mesenteric artery occlusion: Collateral flow through mesenteric, paraduodenal, and marginal veins. Frequently submucosal collaterals prone to bleeding into the gastrointestinal tract.
• Portal vein occlusion: Collateral flow through network of small veins in the gastrohepatic ligament (cavernous transformation). Portal-to systemic varices.
• Main hepatic vein obstruction: Intrahepatic collateralization or collateral flow through capsular veins.
• External iliac and common femoral vein obstruction: 1) Collateral flow through profunda femoral veins to gluteal and other pelvic veins into the internal iliac veins. 2) Collateral flow through the ipsilateral abdominal wall veins and across the perineum to the contralateral common femoral vein.
• Internal iliac vein occlusion (unilateral): Collateral flow through contralateral internal iliac vein.
• Internal iliac vein occlusion (bilateral): Collateral flow through gonadal, ureteric, and the inferior mesenteric veins (via hemorrhoidal veins).
• Common iliac vein occlusion (unilateral): Retrograde flow through the ipsilateral internal iliac vein, across the pelvis through collaterals, into the contralateral internal iliac vein.
• Common iliac vein occlusion (bilateral): Identical to infrarenal inferior vena cava occlusion (see above).
• Common and external iliac vein occlusion: Collateral flow through pubic, inferior epigastric, and lumbar veins.

References

Kaufman JA and Lee MJ. Multiple chapters in Vascular and interventional radiology: The Requisites. Mosby 20004.

Angiographic Findings of the Vasculitides

Vasculitis	Vessels	Angiography/CT	Clinical
Takayasu	Thoracic and abdominal aorta and proximal branch vessels, pulmonary and coronary arteries	Long-segment smooth stenoses of the aorta & common carotid & subclavian arteries. Stenoses of the pulmonary and coronary arteries. Aortic aneurysm. Thick, enhancing wall on CT/MR.	Young Asian woman
Polyarteritis Nodosa	Medium and small arteries of visceral organs, heart, and hands and feet.	Multiple small aneurysms of renal or visceral arteries, and digital artery occlusions.	Hep B, C, IVDA
Giant Cell	Distal subclavian, axillary, brachial, carotid branches, aorta.	Long irregular stenoses and occlusions.	Elderly woman with several weeks of fever, headache, tender temporal arteries, elevated ESR. Ophthalmic artery involvement is feared complication.
Buerger	Veins and medium and small arteries of extremities	Occlusion of small and medium vessels. Arterial and venous thrombosis	Male smoker younger than 50. Migratory thrombophlebitis
Behçet	Veins, pulmonary arteries, medium and large arteries.	Arterial and venous (more common) thrombosis. Aneurysms of aorta, pulmonary arteries, and peripheral vessels.	Recurrent oral and genital apthous ulcers.
Kawasaki	Medium and small arteries	Aneurysms of the coronary and medium-sized arteries	Infant younger than 1
SLE	Usually upper extremity medium and small arteries	Tapered stenoses on occlusions, especially of the digital arteries.	Digital ischemia and ulceration in a young woman with SLE.
RA, HLA-B27s	Thoracic aorta.	Aortic root dilatation

The patient shown here has inflammatory changes surrounding his right distal subclavian/axillary artery, consistent with giant cell arteritis.

References

Vascular and Interventional Radiology: The Requisites. 2004.

Normal Appearance of the Vaginal Cuff on Ultrasound

Normal vaginal cutoff on ultrasound (US) following hysterectomy.

The vaginal cuff is the apex of the vagina after hysterectomy where the upper walls are sutured together. It can be a site of recurrent malignancy after hysterectomy in patients with cervical or endoemtrial cancer, being more common in the former case.

The normal vaginal cuff is "small, symmetric, and homogeneously hypoechoic, with a thin central echogenic line that represents the vaginal mucosa." Bulky, nodular, or heterogeneous appearance may represent recurrent tumor or radiation fibrosis in a patient with history of cervical or endometrial cancer. The size of the normal cuff can be up to about 2 cm. There is no statistically significant difference in the size of the vaginal cuff in women with transabdominal hysterectomy compared to those with transvaginal hysterectomy.

Patients who have undergone supracervical hysterectomy have a cervical remnant and not a vaginal cuff. The cervical remnant is larger than the vaginal cuff, with mean transvaginal dimensions of about 3 cm.

Without knowing the history, a prominent soft tissue mass in the lower pelvis may be due to recurrence in a patient with abdominal or transvaginal hysterectomy or represent normal finding in a patient with a supracervical hysterectomy. Look for the vaginal mucosa to help determine if it's a vaginal remnant. Nabothian cysts will be seen in cervical remnants in patients with supracervical hysterectomy.

The image shown here is a normal vaginal cuff in a patient with a transabdominal hysterectomy for fibroids. We don't really see the echogenic vaginal mucosa, but the whole thing is within normal limits of size and is pretty homogeneous.

References

Stein MW, Grishina A, Shaw RJ, Roberts JH, Ricci ZJ, Adachi A, Freeman K, Koenigsberg M. Gray-scale and color Doppler sonographic features of the vaginal cuff and cervical remnant after hysterectomy. AJR Am J Roentgenol. 2006 Nov;187(5):1372-6.

Direct Origin of the Left Gastric Artery from the Aorta

The left gastric artery most commonly arises from the celiac trunk. In 0.5%-15% of cases, it may have a direct origin from the aorta (arrow). This can become important in angiographic treatment of gastrointestinal hemorrhage.

References

• Naidich JB, Naidich TP, Sprayregen S, Hyman RA, Pudlowski RM, Stein HL. The origin of the left gastric artery. Radiology. 1978 Mar;126(3):623-6.
• Yildirim M, Ozan H, Kutoglu T. Left gastric artery originating directly from the aorta. Surg Radiol Anat. 1998;20(4):303-5.

Pressures in Interventional Radiology

Absolute Pressures

• Normal right atrial pressure: 2-6 mm Hg
• Normal right ventricular pressure: 15-25 mm Hg (systolic)/0-8 mm Hg (Diastolic)
• Normal main pulmonary artery pressure: 22/8 mm Hg, with a mean of 13 mm Hg.
  • Pulmonary arterial hypertension: > 30 mm Hg systolic, or
  • Mean pulmonary artery pressure > 25 mm Hg at rest, or
  • Mean pulmonary artery pressure > 30 mm Hg with exercise.
• Normal left atrial pressure: Estimated by pulmonary capillary wedge pressure. Between 6-12 mm Hg.
  • Cephalization: 12-18 mm Hg.
  • Interstitial edema: 15-25 mm Hg.
  • Alveolar edema: > 25 mm Hg.
• Portal hypertension: Absolute portal venous pressure > 10 mm Hg.

Pressure Gradients

• A pressure gradient > 2mm Hg between the inferior vena cava and the renal vein is suggestive of renal venous hypertension due to outflow obstruction.
• A pressure gradient > 2mm Hg across the hepatic vein or inferior vena cava webs in patients with Budd-Chiari syndrome suggests that intervention may be beneficial.
• May-Thurner syndrome can be divided into three venographic stages. The first stage is asymptomatic compression of the left common iliac vein with no collaterals and a pressure gradient < 2 mmHg. Stage 2 is the presence of intraluminal webs or spurs, and stage 3 is thrombosis.
• Pressure gradient > 3 mm Hg across a lesion in the inferior vena cava is considered significant.
• The normal hepatic vein pressure gradient (also known as corrected sinusoidal pressure) is < 5 mm Hg. Portal hypertension is hepatic vein pressure gradient (see below)> 5 mm Hg. Hepatic vein pressure gradient > 12 is associated with variceal hemorrhage. Hepatic vein pressure gradient is measured as follows: Pressure in a hepatic vein is measured using an uninflated occlusion balloon catheter giving us the free hepatic venous pressure. The occlusion balloon is then inflated and the wedged hepatic venous pressure is measured. The free pressure is subtracted from the wedged pressure to give the gradient.
• Pressure gradient > 20 mm Hg between the aorta and a point distal to a renal artery narrowing suggests the diagnosis of renal artery stenosis. However, this has no physiologic foundation and has not been validated clinically. 10-15 is considered borderline under this scheme.
• Pressure gradient < 20 mm Hg across an area of apparent aortic narrowing suggests pseudocoarctation.

Augmented pressure gradients can be obtained in arteries by injecting a vasodilator (200-300 mcg of nitroglycerin, or 15-25 mg tolazoline) distal to the lesion. This will induce hyperemia and may unmask a gradient.

References

• Interventional Radiology: The Requisites.
• Drieghe B, Madaric J, Sarno G, Manoharan G, Bartunek J, Heyndrickx GR, Pijls NH, De Bruyne B. Assessment of renal artery stenosis: side-by-side comparison of angiography and duplex ultrasound with pressure gradient measurements. Eur Heart J. 2008 Feb;29(4):517-24.
• Gluecker T, Capasso P, Schnyder P, Gudinchet F, Schaller MD, Revelly JP, Chiolero R, Vock P, Wicky S. Clinical and radiologic features of pulmonary edema. Radiographics. 1999 Nov-Dec;19(6):1507-31;

Nonocclusive Mesenteric Ischemia

Nonocclusive mesenteric ischemia is an acute syndrome of low superior mesenteric flow in the absence of a fixed obstruction. It is seen most commonly in ICU patients on vasopressors or digitalis or in patients in septic or cardiogenic shock.

Angiography is the gold standard diagnostic modality and demonstrates:

• Slow flow in the superior mesenteric artery
• Diffuse narrowing of the superior mesenteric artery branches with interspersed areas of normal caliber vessels ("string of sausages" sign).
• Poor filling of the vasa recta
• Spasm of the marginal artery of Drummond and other branch points
• Persistence of contrast enhancement of intestinal branches for longer than 2 seconds after injection.

When suspected, vasodilators can be injected to counteract the spasm. And continuous intra-arterial infusion of papaverine, prostaglandin E₁, or nitroglycerine can be used for treatment.

CT will show diffuse severe narrowing of the mesenteric arteries or branches with segmental stenoses and dilations.

References

• Ofer A, Abadi S, Nitecki S, Karram T, Kogan I, Leiderman M, Shmulevsky P, Israelit S, Engel A. Multidetector CT angiography in the evaluation of acute mesenteric ischemia. Eur Radiol. 2009 Jan;19(1):24-30.
• Mitsuyoshi A, Obama K, Shinkura N, Ito T, Zaima M. Survival in nonocclusive mesenteric ischemia: early diagnosis by multidetector row computed tomography and early treatment with continuous intravenous high-dose prostaglandin E(1). Ann Surg. 2007 Aug;246(2):229-35.

Lobulated Hepatic Contour: Differential Diagnosis

Coarse hepatic lobulation

• Cirrhosis: Small liver with relative hypertrophy of the left and caudate lobes and signs of portal hypertension.
• Chronic Budd-Chiari syndrome: Look for hepatic vein thrombosis.
• Chronic portal vein thrombosis:
• Pseudomyxoma peritonei: Look for additional foci of implants.

Fine hepatic lobulation

• Cirrhosis: Small liver with relative hypertrophy of the left and caudate lobes and signs of portal hypertension.
• Pseudocirrhosis of treated breast cancer metastases to the liver: Specific to breast cancer. May also see multifocal retraction of the liver capsule, enlargement of the caudate lobe, and features of portal hypertension.
• Fulminant hepatic failure: Alternating areas of regenerative nodules and necrosis can give a nodular contour.
• Miliary metastases: Lobulated contour is a rare manifestation of miliary metastases.
• Sarcoidosis: Uncommon presentation of hepatic sarcoidosis may include diffuse granular heterogeneity and fine nodular contour.

References

Jha P, Poder L, Wang ZJ, Westphalen AC, Yeh BM, Coakley FV. Radiologic mimics of cirrhosis. AJR Am J Roentgenol. 2010 Apr;194(4):993-9.

The Fontan and Glenn Procedures

The Glenn operation is diversion of superior vena caval blood to the right pulmonary artery. The classic, or unidirectional Glenn procedure involved proximal ligation of the right pulmonary artery separate it from the main and left pulmonary arteries and to divert all superior vena caval blood into the right pulmonary artery. The bidirectional Glenn procedure skips the ligation, allowing vena caval blood to be distributed to both lungs. For the Glenn procedure to work, we need to have normal pulmonary arterial pressures, patent pulmonary arteries, and enough function in the left ventricle to handle pumping blood through the body and the lungs.

The Glenn procedure is now considered the first stage of a complete systemic venous to pulmonary arterial anastomosis, also known as a Fontan procedure. The Fontan procedure is basically a Glenn procedure combined with a right atrium–to–left pulmonary artery connection. Different connections may be used to the left pulmonary artery. The Hancock conduit is a porcine aortic valve sutured into the center of a woven fabric conduit.

Acquired arteriovenous malformations can occur following Glenn or modified Fontan procedures. This is of unknown etiology. One idea is that they develop as a result of loss of "hepatic factor," with blood reaching the right lung through the superior vena cava absent of this mysterious humour, leading to pulmonary arteriovenous malformations on the right. It is also known that the Glenn shunt favors flow to the lower lobes, leading some to suggest this maldistribution of pulmonary blood flow to the lower lobes as a causative factor.

The patient shown here had tricuspid atresia, for which he had a unidirectional Glenn procedure when he was 2 and a modified Fontan when he was 13, followed by a stent of the Hancock conduit in his 20s. The unidirectional Glenn can be seen in the top pair of images, showing a direct connection between the superior vena cava and the right pulmonary artery. The bottom image pair shows the second stage of the procedure, with diversion of inferior vena caval blood into the left pulmonary artery via a Hancock conduit. Multiple clipped pulmonary arteriovenous malformations are seen.

References

Pike NA, Vricella LA, Feinstein JA, Black MD, Reitz BA. Regression of severe pulmonary arteriovenous malformations after Fontan revision and "hepatic factor" rerouting. Ann Thorac Surg. 2004 Aug;78(2):697-9.

Types of Surgical Portosystemic Shunts

• Side-to-side portacaval shunt: Nonselective surgical shunt that diverts portal flow away from the liver. Used for treatment of Budd-Chiari syndrome.
• Side-to-side mesocaval shunt: Nonselective surgical shunt that diverts portal flow away from the liver.
• Mesoatrial shunt: Nonselective surgical shunt that diverts all portal flow away from the liver.
• Distal splenorenal (Warren) shunt: Selective surgical shunt from gastroesophageal varices that preserves portal blood flow through the liver while lowering variceal pressure. Effectively prevents rebleeding, but still carries a risk of hyperammonemia.

References

Yoshida H, Mamada Y, Taniai N, Tajiri T. New trends in surgical treatment for portal hypertension. Hepatol Res. 2009 Oct;39(10):1044-51.

Radiographic Patterns of Pulmonary Edema

Different patterns of pulmonary edema can be seen on chest radiographs depending on the cause. The table below summarizes principal (bold) and ancillary (italic) variables that should be evaluated. The vascular pedicle width was described previously (normal: 38-58 mm). Pulmonary blood volume is assessed as the size of the azygos vein (normal: 7-11 mm) and the degree of peripheral branching.

	Cardiogenic	Volume overload/Renal failure	Permeability
Distribution of pulmonary flow	Inverted (cephalization)	Balanced	Normal
Distribution of pulmonary edema	Basal and homogeneous from heart to chest wall ± perihilar	Central	Peripheral
Width of the vascular pedicle	Normal (acute heart failure) or widened (chronic heart failure)	Widedned	Normal or narrowed
Pulmonary blood volume	Normal or increased	Increased	Normal or decreased
Peribronchial cuffing	+	+	Uncommon
Septal lines	±	±	-
Pleural effusions	±	±	Rare
Air bronchograms	Rare	Rare	Present
Lung volumes	Decreased	Normal or increased	Normal
Cardiac size	Enlarged	Enlarged	Normal

References

Milne EN, Pistolesi M, Miniati M, Giuntini C. The radiologic distinction of cardiogenic and noncardiogenic edema. AJR Am J Roentgenol. 1985 May;144(5):879-94.

The Vascular Pedicle

The vascular pedicle is bordered on the right by venous structures (right brachiocephalic vein above and superior vena cava) and on the left by an arterial structure (the left subclavian artery origin). The azygos vein (black oval) is seen en face above the right main bronchus.

The vascular pedicle width (VPW) is the distance between parallel lines drawn from the point at which the superior vena cava intersects the right main bronchus an a line drawn at the takeoff of the left subclavian artery from the aorta. The mean vascular pedicle width is 38-58 mm on posteroanterior chest radiographs.

The vascular pedicle width correlates well with systemic blood volume and can help differentiate different forms of pulmonary edema. It is usually normal in acute cardiac failure and wide in overhydration/renal failure pulmonary edema and chronic heart failure. In can be normal or narrowed in capillary permeability pulmonary edema.

References

• Milne EN, Pistolesi M, Miniati M, Giuntini C. The vascular pedicle of the heart and the vena azygos. Part I: The normal subject. Radiology. 1984 Jul;152(1):1-8.
• Milne EN, Pistolesi M, Miniati M, Giuntini C. The radiologic distinction of cardiogenic and noncardiogenic edema. AJR Am J Roentgenol. 1985 May;144(5):879-94.

Pulmonary Arteriovenous Malformations

Pulmonary arteriovenous malformations are most commonly seen in patients with hereditary hemorrhagic telangiectasias (Osler-Weber-Rendu syndrome). Pulmonary arteriovenous malformations may be simple (90%) or complex (10%). Simple arteriovenous malformations have a single segmental arterial supply and a single draining vein, while complex arteriovenous malformations have multiple segmental arterial supply and multiple draining veins.

Pulmonary arteriovenous malformations are important in that they provide a right-to-left shunt, which may lead to cerebral infarction or brain abscess. Other common presenting symptoms include hemoptysis, as well as consequences of return of deoxygenated blood to the heart (dyspnea, and fatigue).

Chest radiographs show well-defined nodules that are often lobulated and most commonly seen in the lower lobes and medial third of the lungs. Dynamic contrast-enhance CT can be used for evaluation, but thrombosis may sometimes lead to lack of opacification. CT will show a dilated pulmonary artery feeding directly into a dilated vein that drains into the left atrium. Angiography shows dilated segmental arteries feeding a dilated sac with rapid venous outflow.

Embolotherapy with coils or detachable balloons (for smaller feeding arteries) is the treatment of choice and has a > 90% success rate. Fever and pleuritic chest pain are common post-procedure symptoms.

References

• McCloud. Chapter 2. in Chest Radiology: The Requisites. Mosby 1998.
• Valji K. Chapter 12. in Vascular and interventional radiology. Saunders, 1999.

Posterior Fossa Tumors

italic=rare

Hiatt Classification of Hepatic Artery Variants

• Type I: Normal configuration.
• Type II: Replaced or accessory left hepatic artery arising from the left gastric artery.
• Type III: Replaced or accessory right hepatic artery arising from the superior mesenteric artery.
• Type IV: Combination of replaced types II and III (double-replaced pattern).
• Type V: Common hepatic artery arising from the superior mesenteric artery.
• Type VI: Common hepatic artery arising from the aorta (case shown here, arrows).

This classification is not all-inclusive, and many other variants can exist. A replaced hepatic artery is the sole such arterial trunk. For example a person with a replaced right hepatic artery will not have another right hepatic arterial supply arising from the celiac axis. An accessory hepatic artery, on the other hand, will be just what its name suggests: an extra arterial supply. For example a patient with an accessory right hepatic artery will also have a normal right hepatic arterial supply.

References

Hiatt JR, Gabbay J, Busuttil RW. Surgical anatomy of the hepatic arteries in 1000 cases. Ann Surg. 1994 Jul;220(1):50-2.

Popliteal Artery Entrapment

Popliteal artery entrapment is due to compression of the popliteal artery by adjacent muscle, tendinous structures, or neural structures. Extrinsic arterial compression causes chronic vascular microtrauma, early arteriosclerosis, and thrombus formation and can lead to limb ischemia.

Popliteal artery entrapment can be classified into 6 types, with the caveat that not all causes are included in this classification.

• Type 1: Most common type. Normal medial head of the gastrocnemius muscle but abnormal medial course of the popliteal artery.
• Type 2: Abnormally lateral origin of the medial head of the gastrocnemius muscle.
• Type 3: Compression by an accessory strip of the medial head of the gastrocnemius muscle.
• Type 4: Compression by the popliteus muscle or branch of tibial nerve.
• Type 5: Any type with involvement of the popliteal vein.
• Type 6: Normal anatomy, but with functional compression of the popliteal artery due to hypertrophic muscles. Usually seen in well-conditioned athletes.

On angiography there is smooth narrowing of the popliteal artery. Medial deviation may also be seen. The contralateral leg must also be evaluated, as the anatomic abnormality may be bilateral in one third of cases.

Some patients have symptoms of popliteal artery entrapment without anatomic abnormality (type 6). In these patients, passive dorsiflexion or active plantar flexion of the ankle can induce narrowing of the popliteal artery due to hypertrophic muscles (usually the medial head of the gastrocnemius muscle). It must be noted that narrowing of the popliteal artery with passive dorsiflexion or active plantar flexion of the ankle can also be seen in asymptomatic patients with normal anatomy.

References

Elias DA, White LM, Rubenstein JD, Christakis M, Merchant N. Clinical evaluation and MR imaging features of popliteal artery entrapment and cystic adventitial disease. AJR Am J Roentgenol. 2003 Mar;180(3):627-32.

Left Ventricular Aneurysms

A left ventricular aneurysm is a focal outpouching from the diastolic contour of the heart associated with akinetic or dyskinetic wall motion. The usual trabeculations are absent, and the wall of the aneurysm is usually smooth. Left ventricular aneurysm are present in about 10% of patients with coronary artery disease, usually associated with severe disease involving more than one vessel.

Left ventricular aneurysms can be classified as functional, true (anatomic), or false. Unique findings of each are underlined.

• Functional: Also known as a forme fruste of the true aneurysm. The contour is normal during diastole, but bulges out during systole. Occurs because of spasm, ischemia, or infarction and may be reversed following revascularization. The wall of the aneurysm is left ventricle with scar with or without myocardial fibers. Thrombus formation is rare. Calcification is never seen. Rupture is rare.
• True (anatomic): A bulge is seen during both systole and diastole. Location is typically anterolateral, apical, or septal. The mouth of the aneurysm is as wide as or wider than its maximal diameter. The wall of the aneurysm is left ventricle with scar with or without myocardial fibers. Thrombus and calcification are common. Rupture is rare (less than 5% of cases).
• False: A bulge is seen during both systole and diastole. Typically occurs along the inferior and anterolateral walls. The mouth of the aneurysm is typically less than 50% of its maximal width. The wall of the aneurysm is the pericardium. Thrombus and calcification are uncommon. It has a propensity to expand and rupture (45% of cases). Contrast material may not fill the aneurysm until late in systole and opacification of the sac may persist after contrast has left the left ventricle. Differential considerations include congenital diverticula (smaller and occur at the apex), African cardiomyopathies (different clinical course and lack of coronary artery disease).

References

Miller SW and Boxt LM. Chapter 7: Ischemic heart disease. in Cardiac Imaging, the Requisites Third edition, Miller SW, Boxt LM, and Abbara S, eds. Mosby 2009.

Pulmonary Artery Dissection

Pulmonary artery dissection is an uncommon cause of chest pain. Pulmonary arterial hypertension (either primary or due to collagen vascular diseases, chronic obstructive pulmonary disease, congenital heart diseases, etc.) is the most common cause, but less common etiologies like Marfan syndrome (our patient), instrumentation, tuberculosis, syphilis, pregnancy, idiopathic cystic medial necrosis, and amyloidosis have also been described.

CT, MRA and echocardiography will demonstrate the intimal flap. A potential pitfall is a pseudoflap due to motion artifact from aortic and cardiac motion. A similar pseudoflap in the aorta or superior vena cava can suggest that what you're seeing is artifact. Cardiac gating (as seen in our case) would be ideal; however, this is not standard in pulmonary embolism protocol CTAs.

In this patient we see an intimal flap on a cardiac-gated CTA (pink arrow), a large left subclavian artery aneurysm (blue arrow) and a stent-graft (yellow arrow) within an aortic aneurysm in a patient with Marfan syndrome.

References

• Neimatallah MA, Hassan W, Moursi M, Al Kadhi Y. CT findings of pulmonary artery dissection. Br J Radiol. 2007 Mar;80(951):e61-3.
• Pua U, Tan CH. CT diagnosis of pulmonary artery dissection--potential pitfall of multidetector CT. Br J Radiol. 2009 Jan;82(973):82-3.
• Sehdev A, Dhoble A. Pulmonary artery dissection (PAD): A very unusual cause of chest pain. J Hosp Med. 2010 Jun 9;5(5):313-316.

Post-Embolization and Post-Ablation Syndromes

Postembolization syndrome is a transient phenomenon that usually occurs within 24 hours of tumor embolization, peaks on days 3 and 5, and resolves within 7 days. Patients have low-grade fever and flulike symptoms, such as malaise, myalgia, and nausea and/or vomiting, felt to be due to cytokine production in response to necrotic tumor tissue. A similar phenomenon has been seen following radiofrequency (RF) ablation.

These symptoms must be differentiated from those of infection (e.g., pneumonia, abscess) or intestinal perforation. Suspicion is raised in patients with delayed onset of fever or persistent symptoms.

References

Wah TM, Arellano RS, Gervais DA, Saltalamacchia CA, Martino J, Halpern EF, Maher M, Mueller PR. Image-guided percutaneous radiofrequency ablation and incidence of post-radiofrequency ablation syndrome: prospective survey. Radiology. 2005 Dec;237(3):1097-102.

Prophylactic Antibiotics in IR

• Biliary procedures: Mandatory before all biliary interventions. Ampicillin 1 g IV and gentamicin 80 mg IV immediately before procedure. Alternatively, a single dose of piperacillin/tazobactam (Zosyn) 4.5 g IV can be used before percutaneous transhepatic cholangiography. For biliary drainage, antibiotic coverage can be extended to two days following the procedure.
• Embolization (TAE, TACE) and ablation (RFA): Unproven to be of benefit in RFA, but may be given in some institutions. Patients with biliary abnormalities (e.g., bilioenteric anastomosis), immunosuppression, concomitant infection, or severe cirrhosis are at higher risk for abscess formation following RFA, but I haven't been able to find any solid recommendations for prophylactic antibiotics. We use Unasyn IV the day of and the day after, and discharge the patient on 5 days of Augmentin.
• Genitourinary: We use Cipro prior to urinary procedures. Some of our referring urologists prefer ampicillin and gentamicin immediately before the procedure.
• Line placement: Coverage may be given for skin flora per institutional protocols: cephazolin 1 g, clindamycin 300 mg, or vancomycin 500 mg.
• Diagnostic angiography: Only in asplenic and severely neutropenic patients. Use coverage for skin flora: cephazolin 1 g, clindamycin 300 mg, or vancomycin 500 mg. Patients with heart valves don't need antiobiotic prophylaxis.

References

• Choi D, Lim HK, Kim MJ, Kim SJ, Kim SH, Lee WJ, Lim JH, Paik SW, Yoo BC, Choi MS, Kim S. Liver abscess after percutaneous radiofrequency ablation for hepatocellular carcinomas: frequency and risk factors. AJR Am J Roentgenol. 2005 Jun;184(6):1860-7.
• Kaufman JA and Lee MJ. Multiple chapters in Vascular and interventional radiology: The Requisites. Mosby 20004.
• Sato S, Mishiro T, Miyake T, Okamoto E, Furuta K, Azumi T, Oshima N, Takahashi Y, Ishihara S, Adachi K, Amano Y, Kinoshita Y. Prophylactic administration of antibiotics unnecessary following ultrasound-guided biopsy and ablation therapy for liver tumors: Open-labeled randomized prospective study. Hepatol Res. 2009 Jan;39(1):40-6.
• Spies JB, Rosen RJ, Lebowitz AS. Antibiotic prophylaxis in vascular and interventional radiology: a rational approach. Radiology. 1988 Feb;166(2):381-7.

Arc of Buhler

Arc of Buhler is a direct arterial anastomosis between the superior mesenteric artery and the celiac trunk. The arc of Buhler results from failure of regression of an anastomotic vessel between the 10th and 13th ventral segmental arteries off the aorta (the future celiac trunk and superior mesenteric artery, respectively). It is found in less than 5% of the population and has a diameter of less than 2.5 mm.

References

Saad WE, Davies MG, Sahler L, Lee D, Patel N, Kitanosono T, Sasson T, Waldman D. Arc of buhler: incidence and diameter in asymptomatic individuals. Vasc Endovascular Surg. 2005 Jul-Aug;39(4):347-9.

Blue Toe Syndrome

Blue toe syndrome is the acute rupture of atheromatous plaque causing digital ischemia or infarction with intact peripheral pulses. The toes assume a blue-red color that may be interspersed with normal skin, causing a lacy appearance (livedo reticularis). The emboli may come from the aorta or other proximal vessels and may be spontaneous or caused by vascular intervention.

A source should be sought and treated. Unilateral involvement points to a common iliac source. Bilateral involvement points to an aortic source. Bilateral involvement with synchronous renal failure points to a thoracic aortic source. 90% of untreated patients will have recurrent embolization in five years.

References

• Kaufman JA and Lee MJ. Chapter 15. in Vascular and interventional radiology: The Requisites. Mosby 20004.
• Kronzon I, Tunick PA. Aortic atherosclerotic disease and stroke. Circulation. 2006 Jul 4;114(1):63-75.

Renal Vein Renin Sampling

Renal vein renin sampling can be performed in the evaluation of renovascular hypertension in children. Blood samples are taken from the infrarenal inferior vena cava, the main renal veins, and from upper, middle, and lower renal vein tributaries, taking care to avoid tributaries of the renal veins to capsular or lumbar veins or the left gonadal vein. Renal vein renin sampling can help guide treatment to the side that has clinically important lesions and selective sampling from segmental veins can provide more precise localization of the hypertensive focus.

A ratio of > 1.5 between the two main renal veins is considered significant, with the side with the higher renin being abnormal. A ratio of greater than 1.3 between the suspected normal kidney and the infrarenal inferior vena cava is considered supportive. A positive result has been suggested as a good predictor of favorable outcome following angioplasty or surgery.

Renal vein renin sampling a more useful diagnostic tool in children than in adults, because renal artery abnormalities in children are usually bilateral and involve small arterial branches.

References

• Dillon MJ. The diagnosis of renovascular disease. Pediatr Nephrol. 1997 Jun;11(3):366-72.
• McLaren CA, Roebuck DJ. Interventional radiology for renovascular hypertension in children. Tech Vasc Interv Radiol. 2003 Dec;6(4):150-7. Review.

Paget-Schroetter Syndrome

Paget-Schroetter syndrome, also known as effort-induced axillary-subclavian vein thrombosis, is characterized by acute-onset swelling in the upper extremity, typically in young, active individuals (usually men). It is often precipitated by trauma or strenuous exercise involving arm abduction, cervical extension, and shoulder depression. The effects of such movements are magnified in the presence of a mechanical abnormality at the thoracic inlet, resulting in compression of the axillary-subclavian vein between a hypertrophied anterior scalene muscle or subclavius tendon and the first rib or a cervical rib.

Venography may show patent axillary and subclavian veins with no evidence of thrombus; however, venous collaterals may be seen. Venography during Adson maneuver (neck extension, head away from affected side, and a deep breath) can reveal dynamic obstruction of the axillary or subclavian veins.

Conservative management with rest, arm elevation, and anticoagulation have unacceptably high complication rates: pulmonary embolism (12%), venous distention (18%), and residual symptoms of swelling, pain, and superficial thrombophlebitis (70%). Therefore, thrombolysis with surgical decompression (e.g., resection of a cervical or first rib) is the favored treatment.

References

• Shah AD, Bajakian DR, Olin JW, Lookstein RA. Power-pulse spray thrombectomy for treatment of Paget-Schroetter syndrome. AJR Am J Roentgenol. 2007 May;188(5):1215-7.
• Yan BP, Kiernan TJ, Gupta V, Schainfeld RM, Garasic JM. Images in cardiovascular medicine. Over rehearsed: a cellist with Paget-Schroëtter. Circulation. 2008 Sep 16;118(12):e160-1.

Selective Catheter-Directed Thrombolysis: Contraindications

Enzymatic thrombolysis is indicated when the anticipated outcome is similar to that of surgical intervention and can be done quickly enough to avoid irreversible ischemic damage. Regarding the latter, only patients with sufficient collateral vessels to maintain limb viability for 12 hours should be considered for thrombolytic therapy.

Absolute contraindications:

• Irreversible ischemia: Due to reperfusion syndrome and the fact that opening a vessel that has no run off is pointless, as it will quickly thrombose again.
• Recent (> 3 hours and <3 months) ischemic stroke: Patients with ischemic stroke < 3 hours may be eligible for thrombolysis.
• Recent (2 months) intracranial surgery
• Recent (3 months) major blunt head or facial trauma
• History of hemorrhagic stroke
• History of spontaneous intracranial hemorrhage
• Intracranial neoplasm (primary or metastatic) or vascular malformation
• Suspected aortic dissection
• Active bleeding
• Bleeding diathesis

Major relative contraindications:

• Remote (> 3 months) ischemic stroke
• Recent (3 weeks) major thoracic or abdominal surgery
• Recent major trauma
• Recent (1 month) internal bleeding
• Recent (3 months) gastrointestinal hemorrhage
• Uncontrolled hypertension: Increased risk of intracranial hemorrhage.
• Prolonged (> 10 minutes) or traumatic CPR
• Current use of anticoagulants

Minor relative contraindications:

• Pregnancy
• Infected thrombus
• Renal or hepatic insufficiency: Due to increased risk of coagulopathy in these states
• Diabetic retinopathy

References

• Antman EM, Anbe DT, Armstrong PW, Bates ER, Green LA, Hand M, Hochman JS, Krumholz HM, Kushner FG, Lamas GA, Mullany CJ, Ornato JP, Pearle DL, Sloan MA, Smith SC Jr, Alpert JS, Anderson JL, Faxon DP, Fuster V, Gibbons RJ, Gregoratos G, Halperin JL, Hiratzka LF, Hunt SA, Jacobs AK, Ornato JP. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction; A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of patients with acute myocardial infarction). J Am Coll Cardiol. 2004 Aug 4;44(3):E1-E211.
• Kaufman JA and Lee MJ. Chapter 4: Vascular Interventions. in Vascular and interventional radiology: The Requisites. Mosby 20004.
• Schmittling ZC, Hodgson KJ. Thrombolysis and mechanical thrombectomy for arterial disease. Surg Clin North Am. 2004 Oct;84(5):1237-66, v-vi.
• Valji K. Chapter 2: Standard angiographic and interventional techniques. in Vascular and interventional radiology. Saunders, 1999.

Transjugular Intrahepatic Portosystemic Shunt Malfunction

Doppler can be used to determine the status of a transjugular intrahepatic portosystemic shunt (TIPS). A normal TIPS study is shown above. The following are bad prognostic signs:

• Absent flow in shunt.
• Hepatopetal flow in the intrahepatic portal veins. Flow in the left and right portal veins should become hepatofugal after TIPS placement, that is out of the liver and toward the shunt. Hepatopetal flow in either the right or the left portal vein has an 85% positive predictive value for shunt stenosis, but hepatofugal flow has only a 60% negative predictive value. A change in flow direction from hepatofugal to hepatopetal, on the other hand, is a strong indication of shunt malfunction with approximately 90% positive predictive value, but is not very sensitive.
• Low mean main portal vein velocity (<30 cm/s) has 80% sensitivity and 75% specificity for detection of shunt stenosis.
• Peak shunt velocity that is too low (<90 cm/s) or too high (>190 cm/s). The velocity is usually slower near the portal venous end and fastest in the middle segment of the shunt. Flow is usually turbulent.
  
  
• >50 cm/s change in shunt velocity compared with the immediate postprocedural study. This has a reported 90% sensitivity and 75% specificity for detection of shunt stenosis. A decrease of greater than 40 cm/sec or an increase of greater than 60 cm/sec had 75% sensitivity and 85% specificity in another report. 50 seems like a nice round number, so let's stick with that.
• Decrease (>20%) in main portal vein velocity compared compared with the immediate postprocedural study has 80% sensitivity and 75% specificity for detection of shunt stenosis.

Note: Sensitivity, specificity, and positive and negative predictive values rounded to the nearest 5 to ease memorization and better reflect the actual precision of numbers in medicine.

References

• Kanterman RY, Darcy MD, Middleton WD, Sterling KM, Teefey SA, Pilgram TK. Doppler sonography findings associated with transjugular intrahepatic portosystemic shunt malfunction. AJR Am J Roentgenol. 1997 Feb;168(2):467-72.
• Pozniak MA and Henesler KP. T.I.P.S. Imaging. GE Ultrasound.

Calcinosis Cutis

Calcinosis cutis refers to calcium deposits in the skin seen in many different conditions. The image shown here is from a patient with dermatomyositis. The typical sheet-like calcifications, though pathognomonic, are uncommon and not seen here. What we do see are multiple subcutaneous calcifications, many of which have lucent centers (think mammo). Patients with juvenile dermatomyositis are 3 times more likely to develop calcifications compared to the adult-onset form. Calcifications tend to occur over joints and spare the digits.

Calcinosis cutis can be seen in the setting of:

• Normal serum calcium and phosphate levels (dystrophic calcinosis): Trauma, inflammation, varicose veins, infections (e.g., onchocerciasis, cysticercosis, histoplasmosis, cryptococcosis, and intrauterine herpes), tumors, connective tissue diseases (dermatomyositis, lupus erythematosus [rare], systemic sclerosis), panniculitis (e.g., pancreatitis or pancreatic malignancy), and congenital (Ehlers-Danlos syndrome, Werner syndrome, pseudoxanthoma elasticum, and Rothmund-Thompson syndrome).
• Abnormal calcium or phosphate metabolism (metastatic calcinosis): Primary or secondary hyperparathyroidism, paraneoplastic (bone metastases or abnormal hormone production), milk-alkali syndrome, vitamin D overconsumption, and sarcoidosis (1,25-vitamin D produced by sarcoid granuloma).
• No known tissue injury or systemic metabolic defect (idiopathic calcinosis):
• Prior surgical procedure (iatrogenic calcinosis):

References

Nunley JR and Jones LME. Calcinosis Cutis. eMedicine. Jan 27, 2009

Supported vs Unsupported Grafts

Supported endografts have the graft skeleton throughout their course, while unsupported grafts only have it at the attachment sites.

Unsupported grafts have a greater propensity for kinking compared to supported grafts. In addition, the natural history of type IA endoleaks is different between supported and unsupported endografts. While small type IA endoleaks in unsupported grafts can be watched for at least 1 month after placement (spontaneous resolution is possible), type IA endoleaks in supported grafts don't usually resolve spontaneously and may rupture.

Expected Findings after Percutaneous Gastrostomy

Don't panic findings after percutaneous gastrostomy:

• Pneumoperitoneum
• Abdominal wall hematoma
• Gastric hematoma

You should worry if you see subcutaneous emphysema, free peritoneal fluid, pneumatosis intestinalis, or a loculated abdominal fluid collection.

References

Wojtowycz MM, Arata JA Jr, Micklos TJ, Miller FJ Jr. CT findings after uncomplicated percutaneous gastrostomy. AJR Am J Roentgenol. 1988 Aug;151(2):307-9.

Types of Endoleaks

Blood flow into the aneurysm sac following endovascular repair can be classified as:

• Type I (seal failure): Blood flow is due to ineffective seal with the native vessel at the proximal (IA) or distal (IB) end of the graft. Usually occur early. A Type I endoleak is repaired immediately.
• Type II (retrograde flow): Blood is from retrograde from small vessels, such as lumbar arteries or the inferior mesenteric artery. Delayed images are sometimes needed, Most have a benign course, but increasing sac size is of concern. Management depends on the surgeon. Some follow the aneurysm and intervene if it increases, while others choose to intervene.
• Type III (defect): Rare. Blood flow due to ineffective sealing of overlapping grafts (IIIA) or rupture of the graft (IIIB). Usually occurs early due to technical issues. Late cases occur due to device breakdown. Associated with a sudden elevation of intrasac pressure. A Type III endoleak is repaired immediately.
• Type IV (porosity): Rare. Blood flow is due to porosity of the graft. No treatment is usually indicated as these resolve within a month.
• Type V (endotension): The exact cause of these is unknown.

References

• Agarwal PP, Chughtai A, Matzinger FR, Kazerooni EA. Multidetector CT of thoracic aortic aneurysms. Radiographics. 2009 Mar-Apr;29(2):537-52.
• Stavropoulos SW, Charagundla SR. Imaging techniques for detection and management of endoleaks after endovascular aortic aneurysm repair. Radiology. 2007 Jun;243(3):641-55.