42 nd Annual Post Graduate Radiology Course

Hotel Del Coronado • Coronado, Thursday PM, October 19, 2017 TABLE OF CONTENTS

Thursday PM, October 19, 2017

Liver Logic: LI-RADS Why and How (Cynthia S. Santillan, M.D., FSAR)...... 591

What Lurks Below: Retroperitoneal Tumors & Diseases (Noushin Vahdat, M.D.)...... 601

Variant Vessels: Vascular Liver Abnormalities (Cynthia S. Santillan, M.D., FSAR)...... 617

Don’t Be Fooled: Mimickers of Disease in the Chest, Abdomen and Pelvis (Hamad Aryafar, M.D.)...... 623

Romneycare: Are We Learning from Healthcare Reform? (Alexander Norbash, M.D., M.S.)...... 643

Cold Foot? Peripheral Vascular Imaging for Diagnostic Radiologists (Hamed Aryafar, M.D.)...... 657

SAVE THE DATE - 2018 Fall Symposia 591 592 THIDs, THADs, THEDs Overview Vascular Liver Abnormalities Objectives To review the normal vascular supply and drainage of the liver

To discuss how abnormalities in blood flow can affect the enhancement pattern of the liver on CT and MRI

To review disease processes that affect the vessels of the liver, including thrombosis, tumor invasion, inflammation, and masses, Cynthia Santillan, MD and how to distinguish them from each University of California other

Vascular Supply & Drainage Normal

HV Liver receives 25% of cardiac output

Vascular Supply & Drainage Portal vein = PV 75% inflow

HA Hepatic artery = 25% inflow

Vascular Supply & Drainage Vascular Supply & Drainage Normal Normal

Hepatic Arterial Phase Portal Venous Phase HV HV HA enhanced Maximum parenchymal PV enhanced enhancement PV HV not enhanced PV HA & PV enhanced HA Parenchyma starting HA HV with antegrade to enhance enhancement

593 Vascular Supply & Drainage Vascular Supply & Drainage Normal Abnormal Hepatic Arterial Buffer Response

Delayed Venous Phase PV cannot self-regulate flow HV Progressive decreased HABR increases or decreases enhancement of all arterial inflow in response PV structures to portal flow alterations

HA Decreased Can compensate for 25-60% Portal Flow of decreased portal flow Normal

Hepatic Arterial Phase

Eipel et al, Regulation of hepatic blood flow: the hepatic arterial buffer response revisited. World J Gastroenterol 2010; 16:6046-57

Vascular Supply & Drainage Vascular Supply & Drainage Abnormal Abnormal Hepatic Arterial Buffer Response Hepatic Arterial Buffer Response

Triggers hepatorenal reflex Can worsen functional dearterialization Allows continued clearance of metabolites/chemicals Seen following large

Synthetic function closely resection or living related Decreased Increased donor/recipient tied to portal flow Portal Flow Portal Flow Oxygenation does not drive Associated with Normal response Normal Ischemic cholangitis Hepatic Arterial Phase Hepatic Arterial Phase Infarcts

Eipel et al, Regulation of hepatic blood flow: the hepatic arterial buffer response revisited. World J Gastroenterol 2010; 16:6046-57 Eipel et al, Regulation of hepatic blood flow: the hepatic arterial buffer response revisited. World J Gastroenterol 2010; 16:6046-57

Vascular Supply & Drainage Vascular Supply & Drainage Abnormal THID, THED, THAD Impaired Outflow Transient Hepatic Enhancement Difference

Congestion causes absent or Enhancement abnormality reversed peripheral portal flow that does not correspond to

Central liver & caudate an underlying mass/lesion & resolves on later imaging less affected due to Abnormal accessory venous Seen more frequently now drainage due to multiphase, fast imaging Normal Hepatic Arterial Phase Portal Venous Phase

594 Pre-hepatic Portal Vein Non-Cirrhotics Prothrombotic disorders

Cirrhotics Pre-Hepatic Thrombus occurs in up to 30% Low flow state Extent & chronicity must be reported in transplant candidates

Francoz et al, Portal vein thrombosis, cirrhosis, and liver transplantation. J Hepatology 2012; 57:203-12

Pre-hepatic Pre-hepatic Portal Vein Portal Vein

Non-enhancing portal Laminar Flow vein or branches Splenic return may Assess SMV & preferentially go to left lobe splenic vein Splenic vein enhances prior to Increased enhancement SMV of affected parenchyma in Inconsistent

arterial phase Can mimic thrombus Calcification implies Always confirm on venous chronic thrombus or delayed phases

Desser TS, Understanding transient hepatic attenuation differences. Semin Ultrasound CT MRI 2009; 30:408-17

Pre-hepatic Pre-hepatic Portal Vein Portal Vein Vascular Invasion Cavernous Transformation Increased Can occur as quickly as frequency 6 days after occlusion with tumors

Paracholedochal veins >5cm

& recanalized Indicative of channels in thrombus Tumor Stage 4b HCC

De Gaetano et al, Cavernous transformation of the portal vein: patterns of intrahepatic and splanchnic collateral circulation detected wit Doppler sonography, AJR 1995; 165:1151-55

595 Pre-hepatic Pre-hepatic Portal Vein Portal Vein Vascular Invasion Vascular Invasion Increased T2 signal within Thread and streak sign the vessel Visible during arterial Enhancement phase Blood vessels in & Expansile

around tumor Increased extending into portal signal on vein DWI

Bjorn-Werner R, The thread and streak sign, Radiology 2005; 236:284-85

Pre-hepatic Pre-hepatic Portal Vein Portal Vein Vascular Invasion Vascular Invasion

Previously thought Cholangiocarcinoma more often encases or that less than 5% displaces vessels rather than invading of fibrolamellar HCCs invade the portal vein

Newer data with large lesions suggests much higher rates of invasion

Pre-hepatic Superior Vena Cava Cavoportal Collateral Pathway

SVC epigastric/ mammary veins Intrahepatic recanalized paraumbilical vein portal vein

Hot Quadrate

Kapur et al, Where there is blood, there is a way: unusual collateral vessels in superior and sign inferior vena cava obstruction, Radiographics 2010; 30:67-78

596 Intrahepatic Intrahepatic Biliary Biliary Obstruction of the peribiliary Peribiliary plexus = plexus due to biliary dilation or mesh surrounding the inflammation bile ducts impairment of portal inflow

arterial compensation Accounts for some portal inflow to the Tends to be in a peribiliary parenchyma distribution when due to obstruction

Polymorphous pattern when inflammatory

Pradella et al, Transient hepatic attenuation difference (THAD) in biliary duct disease. Abdom Imaging 2009, 34: 626-33 Pradella et al, Transient hepatic attenuation difference (THAD) in biliary duct disease. Abdom Imaging 2009, 34: 626-33

Intrahepatic Intrahepatic Inflammation Inflammation Abscess Adjacent Structures Cholecystits Double target sign

Pancreatitis Increased capillary

Inflammation permeability Increased arterial induced hyperemia inflow Decreased portal Regional arterial inflow due to hyperperfusion edema Sump effect

Colagrande S et al, Transient hepatic intensity differences: part 2, those not associated with focal lesions. AJR 2007; 188:160-66 Colagrande S et al, Transient hepatic intensity differences: part 2, those not associated with focal lesions. AJR 2007; 188:160-66

Intrahepatic Intrahepatic Vascular Vascular AP shunts Signal Abnormalities

Cirrhosis Inc T2 signal due to inc Narrowed sinusoids portal free water hypertension enlarged Impaired hepatocellular peribiliary plexus & enlarged function arterial connections to Decreased sinusoids & portal veins

THED hepatocyte Interventions agent Direct connections uptake between arterial & Ahn et al, Nontumorous arterioportal shunts in the liver: CT and MRI Altered fat findings considering mechanisms and fate, Eur Radiol 2010; 20:385-94 portal systems Colagrande S et al, Transient hepatic intensity differences: part 2, those not associated with focal lesions. content AJR 2007; 188:160-66

597 Intrahepatic Intrahepatic Hereditary Hemorrhagic Hemangioma Telangiectasia

Arteriovenous & portovenous shunting Follow portal vein anatomy Enlarged hepatic arteries Wedge shaped Early venous filling

Torabi et al, CT of nonneoplastic hepatic vascular and perfusion Case courtesy of Christine Menias, MD disorders, Radiographics 2008; 28:1967-62

Intrahepatic Intrahepatic Hemangioma HCC A-P shunts are present in 60% of large HCCs Siphoning/sump effect HCCs often cause perfusion In lesions less than 3 cm, abnormalities due to more frequently due portal compression/ to benign lesions than invasion malignancy

Colagrande S et al, Transient hepatic attenuation differences and focal liver lesions: sump effect due to primary arterial hyperperfusion, J Comput Assist Tomogr 2009; 33:259-65

Intrahepatic HCC Perfusion abnormalities in patients with chronic liver disease require careful inspection of the apex to Post-hepatic: assess for HCC Hepatic Vein

598 Post-hepatic Post-hepatic Congestion Budd-Chiari Fan-shaped enhancement Patchy, heterogeneous enhancement Highly characteristic of acute disease Nutmeg liver Delayed peripheral enhancement Perivascular edema Reversed portal venous flow Enlarged hepatic veins, Edema IVC Central Hepatomegaly enhancement Chronic congestion preserved cirrhosis Gore et al, Passive hepatic congestion: cross sectional imaging features, AJR 1994;162:71-75 Torabi et al, CT of nonneoplastic hepatic vascular and perfusion disorders, Radiographics 2008; 28:1967-62

Post-hepatic Post-hepatic Budd-Chiari Budd-Chiari Flip-flop

Pattern may reverse in delayed Chronic

phase Hepatic veins Contrast cleared by central liver narrowed Stagnant contrast in periphery Peripheral Non-enhancement of hepatic veins atrophy Often markedly narrowed Comma-shaped

Hepatomegaly collateral vessels

Post-hepatic Budd-Chiari

Regenerative nodules

Begin to form within days of occlusion

Typically 1-4cm

Hyperenhancing

Resemble focal nodular hyperplasia when large

Do not “wash-out”

599 600 601 602 Overview WHAT LURKS BELOW: RETROPERITONEAL TUMORS  Retroperitoneal Anatomy

AND DISEASES  Cystic and Solid Non-Neoplastic Processes Noushin Vahdat, MD  Tumors Associate Professor of Radiology

UCSD-VA Medical Center, San Diego

DIVIDED BY FASCIAL PLANES INTO:

Anatomy RETROPERITONEUM And  Anterior Pararenal Space Spaces  Posterior Pararenal Space

 Perirenal or Perinephric(PRS) Space

PAIRED PERIRENAL SPACES ANATOMY AND SPACES

Two inverted cones, containing kidneys and adrenals, outlined by: Gerota fascia Renal forms by apposition of two layers of fascia: Zuckerkandl fascia Fascia and

Creating a potential space extending from anterior pararenal space Perirenal spaces communicate at the level of lower lumbar vertebra

603 ANTERIOR PARARENAL SPACE ANTERIOR PARARENAL SPACE

Confined by: Inferiorly below the kidneys, continuous with:  Perirenal and Posterior Pararenal  Pelvic Retroperitoneum

Contains:  Ascending and Descending colon Robert E. Bechtold, RadioGraphics 1996; 16:811-85 (Pericolonic Component)  Duodenum and Pancreas (Pancreaticoduodenal Component) PRS is open to diaphragm and the Retroperitoneal hematoma bare area of the liver Superiorly Continuous across the midline extending to pelvis

Hematoma POSTERIOR PARARENAL SPACE Urinoma

Bounded by: CYSTIC Lymphocele anteriorly posteriorly NONNEOPLASTIC Seroma

PROCESSES Abscess  Medially limited by psoas muscle Pancreatic  Laterally open toward the flank Pseudocyst,  Inferionly open to pelvis Pancreatic or Peripancreatic Contains fat Necrosis

IMAGING HEMATOMA

 CT - Primary modality Variable appearance IV contrast, 3-mm slice thickness, portal venous phase size, shape, presence and thickness of wall, septa, fat, calcification  Acute- Heterogeneous,  MR - Problem-solving tool High-attenuation on CT, T1 and fat-suppressed T1- Assess high-signal fat or hemorrhage Hyperintense on T1 and T2 T2 and fat-suppressed T2- lymphadenopathy, muscle invasion, cystic change or necrosis, fluid collections, bone marrow edema  Chronic- Low-attenuation on CT Contrast-enhanced T1- Differentiate solid from cystic or necrotic Low signal on MR, hemosiderin lesions, extent, presence and nature of vascular thrombosis

604  Urinoma, Urine leak - CT- Water attenuation, 8 days post right nephrectomy progressively increased attenuation by contrast enhanced urine entering the collection on delayed excretory images Subacute Hemorrhage Commonly with proximal hydroureteronephrosis

Retroperitoneal  Lymphocele - Collection of lymph without epithelial Fibrosis and lining, often seen post lymphadenectomy IgG4-Related Sclerosing CT- Homogenously low attenuation, Disease low attenuation fat can be seen SOLID Pseudotumoral NONNEOPLASTIC Lipomatosis

Histiocytosis PROCESSES Extramedullary Hematopoesis

Amyloidosis

RETROPERITONEAL FIBROSIS (RPF) RPF

Secondary:  Idiopathic in more than 70% of cases.  Drug-induced- Most common known cause of RPF is use of Methysergide (an ergot derivative) in treatment of migraine  As many as 15% of patients have additional fibrotic process  Inflammatory Aortic Aneurysm outside the retroperitoneum.  Traumatic - Hematoma, Urinoma, Radiation, Surgery  Infectious  Granulomatous disorders  Coexistence with autoimmune disorders such as IgG4 related  Histiocytosis (Erdheim-Chester) sclerosing disorders, and response to steroids suggests  Occupational –Asbestos autoimmune origin.  Neoplastic - Desmoplastic to retroperitoneal tumor or paraneoplastic  Endometriosis  Amyloidosis

605 RPF-IMAGING RPF-IMAGING

 Homogeneous soft-tissue below  Medial deviation and tapering of middle third of the ureters at aortic bifurcation L4-5 level, proximal hydronephrosis

 Encasing the aorta, IVC, eventually  CT- Plaque typically has the same ureters, with hydroureteronephrosis attenuation as muscle  Avid enhancement in the active,  Does not displace the aorta and IVC  Little or no enhancement anteriorly, as lymphoma or metastatic in chronic phase nodes often do

RPF- MR RPF-IMAGING- CT

 Medial deviation  Tapering of middle third of the ureters at L4-5 level           Proximal Hydronephrosis  RPF T2-Signal Enhancement Pathophysiology

Active Hyperintense Present Inflammatory edema >  Plaque typically has the same cellularity Mature, or Isointense to low Less attenuation as muscle after steroid Decreased Edema therapy Malignant RPF Heterogeneously hyper Present Hypercellularity > edema

Goenka A H. Radiol Clin N Am 50 (2012) 333-355

RPF RPF

Mature or Post Treatment

Patient with RPF Increased left Axial T2 and para-aortic STIR Axial T1-WI signal with increased Low and intermediate signal intensity enhancement soft tissue encasing the retroperitoneal vessels and kidneys, Axial T1 pre and post Axial STIR 1 year later, post steroid Rx, decreased enhancement

606 18F-FDG-PET, and Gallium 67          Scintigraphy  Isotope uptake parallels RPF activity  Retroperitoneal Fibrosis  Share the common  Sclerosing Mesenteritis histopathologic findings of  Autoimmune Pancreatitis, lymphoplasmocytic High uptake in the Active Stage  Sclerosing Cholangitis inflammation with:

Little or no uptake in the Chronic Fibrotic Stage  Inflammatory Pseudotumor  CD4 or CD8-positive T- lymphocytes and IgG4-positive  Detect Multi-focal fibro-inflammatory disease Fall under the umbrella of IgG4- plasma cells with interstitial related sclerosing diseases fibrosis.

 Assess Therapeutic responce Radiographics 2013; 33:1053-1080  Elevated serum IgG4

                 

Retroperitoneal Fibrosis Sclerosing Mesenteritis

Axial T1 post contrast- Pancreas, “sausage” shaped with multiple cortical lesions in R- kidney peripheral smooth hypoenhancing L- hydro, periaortic soft tissue rim, described in autoimmune encasing the left ureter pancreatitis,

MALIGNANT-RPF EXTRA MEDULLARY HEMATOPOIESIS

 Malignancy- 8% of cases of RPF  Hematopoietic deposits outside the bone marrow  More common in liver, spleen and lymph nodes  Retroperitoneum an uncommon site  Desmoplastic response,  In Hemoglobinopathies, Myelofibrosis, Paraneoplastic fibrosis Leukemia and Lymphoma

 CT- lobular paravertebral mass  Lymphoma is the most common with or without fat underlying malignancy, also sarcoma and carcinomas  MR, variable, • T1 and T2 low signal due to hemosiderin • T1 and T2 high signal due to fat  Imaging often suboptimal and • Enhancement, Variable often mild biopsy required Mesurolle B. AJR; 167, November 1996:1139-1140

607 PRIMARY RP NEOPLASMS MESODERMAL NEUROGENIC Primary RP  Leiomyosarcoma  Schwannoma, Neurofibroma, TUMORS Tumors  Liposarcomas Malignant NS tumor  Desmoid  Ganglioneuroma,  Pleomorphic Sarcoma (MFH) Ganglioneuroblastoma, Originating  Lympangioma Neuroblastoma from RP  Perivascular epithelioid cell tumor  Paraganglioma, Pheochromocytoma Organs GERM CELL / SEX CORD LYMPHOID  Germ cell tumor  Lymphoma Metastasis  Primary sex cord stromal tumor  PTLD  Plasmacytoma  Castleman’s disease 70-80% of solid RP masses are malignant

MESODERMAL RP TUMORS: MESODERMAL RP TUMORS LIPOSARCOMA

Subtype Imaging features  Sarcomas Well Differentiated • Macroscopic fat  Desmoid • Streaky fibrous enhancement  Lymphangioma Myxoid • Water attenuation myxoid components  Perivascular epithelioid cell tumor (PEComa): • Gradual, reticular enhancement AML, clear cell sugar tumor, LAM Dedifferentiated • Contain fatty and solid components • Calcifications Pleomorphic/ • Little to no fat Round cell • Indistinguishable from other RP tumors

MESODERMAL RP TUMORS: WELL DIFFERENTIATED LIPOSARCOMA DDX:  Macroscopic fat  Large (>10cm) Well differentiated liposarcoma  Well encapsulated  Streaky, enhancing septae >2mm

 Renal parenchymal defect (Beak sign)  Feeding artery from kidney

Renal AML

608 WELL DIFFERENTIATED LIPOSARCOMA MESODERMAL RP TUMORS: DDX: MYXOID LIPOSARCOMA

• “Pseudocystic” myxoid component is fluid attenuation / signal but shows gradual enhancement

Adrenal Myelolipoma

MESODERMAL RP TUMORS: MESODERMAL RP MASS: DEDIFFERENTIATED LIPOSARCOMA LEIOMYOSARCOMA

Little to no fat  Most common primary IVC  May contain Calcifications tumor  Indistinguishable from other RP tumors  Large size >10 cm  Necrosis common, hemorrhage  2/3 women

MESODERMAL RP MASS: GARDNER’S SYNDROME

 FAP + extracolonic manifestations  Skull osteomas  Desmoid tumors (in 20%)  Papillary thyroid cancer  Skin lesions

24 year-old male with history of total colectomy

609 MESODERMAL RP MASS: WHAT IS FALSE FOR DESMOID TUMOR? LYMPHANGIOMA

• Simple or multiloculated A. Malignant tumor composed of fibrous tissue cystic mass B. Increased incidence in Gardner’s syndrome but • May have negative majority are sporadic attenuation on CT due to chyle C. A/W abdominal surgery, trauma & estrogen tx • May have calcifications D. Tendency to recur after surgery • Insinuates between normal structures

NEUROGENIC RP MASS:

 Nerve Sheath Tumors:  Schwannoma  Neurofibroma  Malignant NST: growth, pain, irregular / infiltrative, younger patients with NF-1: 50%  Ganglion Cells: Ganglioneuroma, Ganglioneuroblastoma, Neuroblastoma  Paraganglion Cells: Paraganglioma, Pheochromocytoma (adrenal medulla)

NEUROGENIC RP MASS: SCHWANNOMA NEUROGENIC RP MASS: SCHWANNOMA

 F>M, 20-50yrs • Encapsulated, extend along nerve (paravertebral or presacral) • Large: Heterogeneous (cystic changes, Ca+, hemorrhage or myxoid stroma)

Small schwannomas are round and homogeneous

610 NEUROGENIC RP MASS: NEUROFIBROMA NEUROFIBROMA

 M>F 20-40 yrs  Target sign  Isolated (90%)  dense central area of  Multiple: 100% NF-1 collagenous stroma  Dumbbell shaped / Fusiform along course of nerve  Low HU on CT (lipid)  Atrophy of muscle supplied  Widening of neural foramina and scalloping of vertebra

NEUROGENIC RP MASS: NEUROGENIC RP MASS: GANGLIONEUROMA PARAGANGLIOMA  Benign  Para-aortic (Zuckerkandl)  20-40 year  40% malignant  57% functional (catecholamines  40% functional or androgenic hormones)  Fluid fluid level caused by  Paravertebral, insinuate hemorrhage between normal structures  Avid enhancement  Speckled calcs in 20%  Rarely lightbulb bright on T2!  ‘Whirled’ appearance at MRI

NEUROGENIC RP MASS: PARAGANGLIOMA VON-HIPPEL LINDAU

 RCC  Renal cysts  Pheochromocytoma  Pancreas: serous cystadenomas and islet cell tumors (NOS subtype)  Hemangioblastomas  Retinal angiomas  Endolymphatic sac tumors

611 GERM CELL / SEX CORD RP TUMORS GERM CELL / SEX CORD RP MASS: GERM CELL TUMOR

Germ cell tumor  1-2% of GCTs are  Seminoma extragonadal  NSGCT (Embryonal carcinoma, Yolk sac tumor,  Most RP GCT are Choriocarcinoma, Teratoma) metastases from gonadal origin Primary sex cord stromal tumor  Rare Testicular US in patient with RP mass suspicious  Women for GC origin  Non-specific imaging

GERM CELL / SEX CORD RP MASS: TERATOMA BURNED OUT GERM CELL TUMOR

 Solid or cystic  +/- Fat, Ca+  Fat-fluid level

LYMPHOID RP NEOPLASM: LYMPHOID RP TUMORS LYMPHOMA

 Lymphoma • Most common RP  PTLD malignancy  Extramedullary Plasmacytoma • 20% of NHL may be heterogenous  Castleman’s Disease • Surrounds structure w/o compressing (floating aorta)

612 PRIMARY RP NEOPLASMS: PATTERN OF SPREAD DIAGNOSTIC CLUES

 Pattern of spread  Lesions that extend between normal structures:  Tumor characteristics (fat, solid/cystic, fluid-fluid levels, vascularity, Ca)  Lymphangioma  Younger age  Ganglioneuroma  Neurogenic tumors, Germ cell tumors, Lymphangioma,  Lymphoma Desmoid  Labs  Neurofibroma  Ganglioneuroma: 57% functional (catecholamines or androgens)  Paraganglioma: 40% elevated catecholamines  Germ cell tumor: elevated hCG and AFP

PRESENCE OF FAT PRESENCE OF MYXOID STROMA

 Myxoid Sarcomas  Lipoma  Neurogenic tumors  Liposarcoma  Schwannoma  Teratoma (may have fat-fluid level)  Neurofibroma  PEComa  Ganglioneuroma (younger patients)  EMH  Gangioneuroblastoma  Malignant nerve sheath tumor

TUMOR NECROSIS HYPERVASCULARITY

 Sarcoma (esp. Leiomyosarcoma)  Paragangliomas  Paragangliomas  Hemangiopericytomas  May have fluid-fluid levels from hemorrhagic necrosis  Sarcomas  Castleman’s disease

613 CYSTIC COMPONENTS

 Entirely cystic  Lymphangioma  Mucinous cystadenoma THANK YOU

 Mixed solid and cystic  Neurogenic tumors [email protected]

REFERENCES

 Goenka AH MD, Shah S MD, Remer E MD. Imaging of the retroperitoneum. Radiology Clinics of America 50 (2012) 333-355.  Rajiah P MBBS MD FRCR, Sinha R MD FRCR, Cuevas C MD, Dubinsky T MD, Bush WH Jr MD, Kolokythas O MD. Imaging of uncommon retroperitoneal masses. Radiographics 2011; 31:949-976.  Murphey MD, Carroll JF, Flemming DJ, Pope TL, Gannon FH, Kransdorf MJ. From the archives of the AFIP: Benign musculoskeletal lipomatous lesions. Radiographics 2004; 24:1433-1466.  Nishino, M MD, Hayakawa K MD, Minami M, MD, Yamamoto A MD, Ueda H MD, Takasu K MD. Primary retroperitoneal neoplasms: CT and MR imaging findings with anatomic and pathologic diagnosic clues. Radiographics 2003; 23:45-57.

614 615 616 617 618 619 620 621 622 623 624 Disclosures Pitfalls of imaging as related to IR • None procedures Acknowledge UCSD Partners: Hamed Aryafar MD Thomas Kinney, MS, MD Associate Clinical Professor of Anne Roberts, MD Vascular and Interventional Steven Rose, MD Isabel Newton, MD, PhD Radiology

Introduction Objective

• Interventional Radiology is often asked to review • Review some examples of potential pitfalls of imaging for possible intervention. pre-procedural imaging. – Frequently before any formal diagnosis is present. • Methods to alleviate potential problems that may • Outside referrals may often lead to incorrect arise. assumptions or diagnoses. • Mainly case based review

30 M with history of prior talc pleurodesis for Case 1 spontaneous left pneumothorax > 1 yr ago

T10

625 Current study CT imaging

Prior comparison Diagnostic Interpretation: 2 cm enhancing pleural based mass lesion T9 level Diagnostic consideration pseudoaneurysm related to prior chest tube placement in past. Recommend Neuro IR Consult

T9 T10 T11 T12 Formal Spinal Angiogram: Flush Thoracic Aortogram

Selective angiogram in search of tumor/ aneurysm

Celiac SMA

Pre and post Diagnosis: Talcoma Contrast CT scans • Talc pleurodesis is commonly used for the treatment of pleural effusions and recurrent spontaneous pneumothoraces • Following this procedure, pleural abnormalities are common and include pleural thickening, loculated effusions, nodules, and masses • Masses related to talc sclerosis are most commonly found in the posterior caudal aspects of the thorax: para- mediastinal or para-vertebral. • Characteristic high attenuation • FDG uptake has been noted in talc-related pleural disease (SUV may be >15 U)-which may mimic cancer (granulomatous reaction to talc)

* Avila NO, et al, AJR 2006; 186:1007-1012/ Murray JG, et al AJR 1997; 169:89-91

626 Case 2

• 46 M status post Stab Wound to the chest 1 week ago • Presents to ED with SOB • CT abdomen pelvis

More delayed

Treatment? Angiographic findings

• Embolize with coils? – Dense opacification of lesion • Embolize with gelfoam? – "Cotton wool" • Follow up CT in 1 month? appearance • Do nothing? • Pooling of contrast medium

627 Angiographic findings Case 3

– Normal-sized feeders • 69 F with RUQ pain – No neovascularity – No arteriovenous shunting – Typically retain contrast beyond venous phase

Dx: Hemagioma of the liver Venous malformation of the liver

Diagnosis: Acute Returns 2 months post laparascopic cholecystitis cholecystectomy with RUQ pain Treatment: Laparascopic cholecystectomy Dx: Post surgical abscess

After 2 weeks of antibiotics IR guided drainage recommended

• Persistent abscess

628 CT guided procedure

Diagnosis: Retained Gallstone post Case 4 surgery • Patient went back to surgery for removal of • 67 M with abdominal pain, concerning CT, stone. transferred from outside institution for care.

Emergent open surgical repair

• Retroperitoneal approach • Aortic reconstruction with graft. • Did not go through with complete Aorto-bi-iliac repair due to acute nature.

629 3 months later

• Patient returns to the emergency room with abdominal pain.

Diagnosis and treatment?

• Aortic endograft repair? • Repeat open surgical repair? • Put a needle into it?

Diagnosis:

• Anaplastic neoplasm without clear differentiation. Pathology favors sarcoma.

630 Elderly man Case 5 admitted with chronic SOB

Referred to IR for thoracentesis

Chest tube placement

• Pt’s symptoms never improved • Despite thoracentesis or chest tube • No change of pneumothorax • Despite using higher pleural evacuation pressures!

Companion case Diagnosis: Pneumothorax Ex vacuo

• Benign uncommon form of PTX  Initially defined as condition in which acute bronchial obstruction and lobar collapse occurs and gas in drawn into the pleural space  Now: refers to development of gas in pleural space because lung is unable to expand to fill the thoracic cavity after removal of fluid • Seen with malignant effusions (fibrous peel over visc pleura) • Patients have minimal symptoms • Chest tube may not evacuate PTX/ life expectancy often < 6 months

Acad Radiol 2005; 12:980-986[UCSF]/ AJR( Boland GW) 1998; 170:943-6

631 Case 6 53M with history of IV Drug Use

• Treated for bacteremia • TEE negative for endocarditis • CT abd/pelvis

Abscess vs Hematoma?

• Had vague history of a fall, pt was drunk and did not remember well. • Fluid collection was painful. • VIR consulted for aspiration/drainage.

VIR aspiration Diagnosis: Morel Lavallee

• Fluid was serosanginous, non-purulent, thin.

632 Case 7

• Can recur • Tx: Aspiration +/- compression • May need surgical resection of capsule

Elderly male with left flank pain, ↑ WBC Xanthogranulomatous Pyelonephritis

 5th –7th decade, Female > Male  Diffuse (90%), Segmental  Plasma cells + lipid-laden macrophages (xanthoma cells)  Anemia (70%), elevated LFT’s (25%), diabetes (10%)  Enlarged, malfunctioning kidney with central obstructing calculus  DDx: hydronephrosis, avascular tumor

Potential Pitfall: XGP http://www.webpathology.com/

Pt with history of Ethanol abuse Case 8 admitted with nausea, and abdominal pain. History of pancreatitis

Dx: Large pancreatic pseudocyst Plan: Drainage

633 Post drainage: Pt doing worse, septic Left upper quadrant drain added with peritonitis. Reimaged that night. Diagnosis: Gastric outlet obstruction. -Patient could have been treated with Reformat of original CT: NG Tube alone. -Without gastropexy, he spilled gastric contents into peritoneal space. -Was eventually stabilized by supportive care, NGT, and additional drainage of leaked gastric contents.

Dx: Apparent spill from the pseudocyst Consult: consider adding additional drainage catheter to drain spilled material

Case 9

• 88 M with hematuria, renal failure, hydronephrosis 19201904

IMPRESSION: 4.7 x 3.3 x 5.8 cm right pelvic mass. CT pelvis with contrast is recommended for further evaluation. Consult IR for Biopsy

Further evaluation requested

634 Diagnosis: Bladder diverticulum Case 10

• Secondary to increased intra-vesicular pressure • 56 F with cirrhosis of unclear origin • Result from BPH, urethral stricture, bladder neck • Followed by hepatology for portal hypertension contracture • Request for TIPS procedure for portal • Most often Males, > 55 years of age decompression • Location: typically solitary along lateral wall of bladder • Most are asymptomatic, some associated with GU anomalies ; malignancy can occur in 1-10% of bladder diverticula

8 Months earlier

1 year earlier

• Portal-systemic gradient 22 mmHg

Post 5 different embolization procedures

Dx: Pseudoaneurysm related to prior biopsy

635 Post embolization Case 11

• Symptoms (recurrent ascites) improved, but did not resolve • Hepatopetal flow (instead of hepatofugal) • Patient currently listed for transplant, TIPS contra-indicated.

• 44 y/o M with gradual onset left upper abdominal/left flank pain described as a fullness along his flank over the course of a month. • Pain rated 7-8/10. • Denies f/c/n/v, denies dyuria.

636 Hydroureter: consult for percutaneous nephrostomy for decompression

637 638 Post-procedural Course MRI Lumbar Spine 3 years ago

• Patient with initial improvement immediately following the procedure, followed by recurrent pain and fullness in left upper abdomen/flank. • eGFR stable at 76 ml/min • Urine gram stain and culture negative

Diagnosis: Congenital Megaureter

• Dilated ureter (> 6 mm) tapers to normal caliber just proximal to bladder • Left side more common • Tc-99m-DTPA renography → early stasis pattern, prompt washout after diuresis.

Differential diagnosis: Etiology • Obstructive Hydronephrosis – Both medulla and cortex become atrophic; no polycalyces • Megaureter – Evidence of obstruction, intrinsic (e.g., stones, tumor) or extrinsic (e.g., retroperitoneal fibrosis or tumor) – Adynamic distal ureteral segment, which has normal • Post-obstructive Atrophy: Residual dilatation after caliber chronic obstruction – Excess collagen and fibrosis; deficient or disordered – History helps to differentiate from megacalices/ureter muscle in wall of distal ureter • Postoperative Pyeloplasty • Vesicoureteral Reflux – Grade 3-5 reflux may cause irreversible dilatation of ureters and calyces – Best shown on VCUG – Tortuous dilated ureter; no "adynamic" juxtavesical segment • Renal Papillary Necrosis – Usually 1 to several sloughed papillae – Club-shaped calyces

639 Treatment Case 12 (final)

• Surgery performed in 20-30% of cases: Excision of • 48 M with metastatic colon cancer responding to juxtavesical segment and ureteroneocystostomy chemotherapy. • Evaluate for progression of disease

Biopsy results: benign Consult IR for biopsy inflammatory tissue

Review of the imaging: Diagnosis: Pulmonary infarct

• Occurs in a minority of patients (less than 15%) • Usually associated with small vessel occlusion (< 3 mm) • Wedged shaped pleurally based without air bronchograms • Usually in the lower lobes

640 Conclusion Thank you!

• Beware of diagnoses that can lead to IR procedures • Enlist help of others as needed • Understand the diagnosis first before undertaking therapy (review prior imaging!) • Hopefully review of these cases will help you stay out of trouble • Good luck!!!

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645 ',** History of regulation (1978) and the CAB Adjusted $

Since 1938, the federal Civil Aeronautics Board (CAB) had regulated all domestic interstate air transport routes as a public utility, setting 896 fares, routes, and schedules. that flew only intrastate routes, however, were not regulated by the CAB. Those airlines were regulated by the governments of the states in which they operated. The CAB promoted air travel, for instance by generally attempting to hold fares down in the short-haul market, to be subsidized by higher fares in the long-haul market. The CAB also was obliged to ensure that the airlines had a reasonable rate of return.

2,622

Wikipedia: http://en.wikipedia.org/wiki/Airline_Deregulation_Act

2,775 http://paleofuture.gizmodo.com/air-travel-today-is-a-damn-bargain-951705216

33 Airline Chapter 11 Bankruptcies since 1978 Thursday, October 17, 2013 Reports Most Profitable Quarter in Company History

Airline Airline Woodrow Bellamy III

New York Airways Air Canada American Airlines parent company AMR Corp., on Thursday reported a net profit of $530 Aeroamerica Flash Airlines million for the third quarter of 2013, the most profitable quarter in its company's history. Florida Airlines US Airways Air Bahia Aloha Airlines The net profit was a $420 million year-over-year improvement for AMR Corp., and also came Mountain West Airlines-Idaho Northwest Airlines with revenue of $6.8 billion, the highest quarterly revenue ever reported by the American LANICA Airlines parent. The report comes as American and US Airways Group prepare to defend Air Aloha Airlines their proposed merger against a lawsuit filed by the Department of Justice (DoJ).

Cochise Airlines ATA Airlines Aero Virgin Islands Skybus Airlines "We are pleased to report our highest quarterly net profit in American's history, excluding Altair Airlines reorganization and special items," said Tom Horton, chairman and CEO of AMR Corp. Partnair Eos Airlines "Continued execution on our product, network and alliance strategy, combined with cost Pan American World Airways efficiencies from restructuring and fleet renewal, creates strong momentum towards our America West Airlines Primaris Airlines planned merger with US Airways. And we are especially pleased to set aside $59 million this Trans World Airlines quarter in expectation of making our first profit-sharing payout since 2001 to our people who US Airways Arrow Air have done so much to put American back on top." Mexicana American Airlines American took delivery of ten Airbus A319s, eight Boeing 737-800s and one Boeing 777-300ER during the third quarter.

If American and US Airways as American Airlines Group largest airline by revenue and profit, with earnings of >$40 Billion.

Related: Aviation Today's Checklist

        

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654 655 656 657 658 Disclosure Cold Foot – Peripheral vascular • None disease for the diagnostic radiologist

Hamed Aryafar MD Associate Professor of Radiology/ Interventional Radiology

Topics Topics

• Background • Background • Non invasive testing • Non invasive testing – Segmental pressures/ pulse volume – Segmental pressures/ pulse volume recordings recordings – Ultrasound – Ultrasound – TCPO2 test – TCPO2 test

PAD Risk Factors

• Male sex • Increased risk of • Increasing age developing lower – ≥70 years extremity PAD with – 50-69 years and history of smoking or – Smoking: 2- to 6-fold diabetes – Diabetes: 2- to 4-fold – <50 years, with – High cholesterol: 1- to 2- diabetes and one other fold atherosclerosis risk – Hypertension: 1.5- to 2.5- factor fold • Alcohol use – Hyperhomocystinemia: 2- • BMI ≥25 to 3-fold • Family history – C-reactive protein: 2-fold

Gandhi S, et al. Prog Cardiovasc Dis. 2011;54:2-13. Hirsch AT, et al. ACC/AHA 2005 Practice PAD guidelines. Circulation. 2006; 113:e463-e654.

659 PVD in Clinical Manifestations of PVD

12

10

8 • Asymptomatic 6 • Intermittent claudication Americans 4 • Chronic limb ischemia (millions) 2

0 PVD PVD with PVD w int. claud CAD

As US demographics change to older population PVD may be more prevalent

Intermittent Claudication Claudication or not?

• Aching, pain, tiredness, tightness, cramping in the buttocks, thigh, calf, or foot brought on by exercise and relieved by rest – Reproducible with a consistent level of exercise from day to day – Completely resolves within 10 minutes after exercise stops – Occurs again at the same distance once walking resumes – “Angina of the leg”

PAD Signs, Symptoms, and PAD Signs, Symptoms, and Complications (cont) Complications (cont) • Rest pain • Ischemic ulceration and gangrene – Pain on the dorsum of the foot or deep in the forefoot – Ischemia severe enough to cause tissue loss without exertion due to ischemia at rest – Thought to be the natural endpoint to rest pain – Often occurs at night and awakens patients – High risk for limb loss – Can be relieved by dangling the foot over the edge of – Together with rest pain, considered critical limb the bed (gravity) ischemia (CLI) – “Unstable angina of the foot” – “Acute myocardial infarction (MI) of the foot”

660 High Resistance Arterial Systems Low Resistance Arterial Systems High tone at rest, capacity for increase Organs that need constant blood supply e.g., carotid & renal arteries e.g., Musculoskeletal arteries

Monophasic waveform Dicrotic notch No reversal in diastole ( Pressure ) Pressure Triphasic waveform = velocity Reversal early diastole = volume flow ( Vel & Vol )

Courtesy of Steve Rose Courtesy of Steve Rose

Effect of Stenosis Effect of Stenosis

Continuity Principle: In an unbranching conduit, Energy losses (heat) rise exponentially the volume of blood flow must remain constant with increasing stenosis severity at all points along the course of the conduit.

Critical stenosis: If a reduction in lumen diameter ( stenosis ), Approx 50% diameter then velocity must increase proportionately Approx 75% area to maintain constant volume of flow.

Courtesy of Steve Rose Courtesy of Steve Rose

Topics Vascular Lab Testing for PAD

• Background • Interpretation of ABI – >1.30 = Non-compressible vessels • Non invasive testing – 0.91 - 1.30 = Normal – ≤0.90 = Abnormal – Segmental pressures/ pulse volume • 0.5 - 0.90 = Mild-to-moderate PAD recordings • 0.00 - 0.50 = Severe PAD – Ultrasound • Claudication can occur anywhere from 0.1-1.0 – <0.5 is consistent with CLI – TCPO2 test – “One level of disease” can decrease ABI by 0.3

Rooke W, et al. 2011 ACC/AHA PAD guidelines update. J Am Coll Cardiol. 2011;58(19):2020-2045. Hirsch AT, et al. ACC/AHA 2005 PAD guidelines. Circulation. 2006; 113:e463-e654. TASC Working Group. J Vasc Surg. 2000;31(suppl 1):S66-S67.

661 Vascular Lab Testing for PAD (cont) Doppler Waveforms (Velocity)

Noninvasive Exam ABIs and Doppler Waveforms Upstream occlusive disease - Adjunct to segmental P’s

Normal: Triphasic High resistance

Abnormal: Monophasic Low resistance

Courtesy of Steve Rose

Vascular Lab Testing for PAD (cont) Vascular Lab Testing for PAD (cont)

• Toe pressures • Pulse volume recordings (PVRs) – Systolic BP in the great toe – Waveforms showing the quality of the pulse wave at – Predictive of ability to heal different levels of the leg – Normal is >60 mm Hg (ideally >80 mm Hg in – Suggestive of the location/severity of blockage diabetics) • Exercise ABIs – Important adjunct in patients with diabetes (non- – Analogous to a treadmill test compressible tibial arteries from calcification) – Only necessary for patient with a convincing history • Segmental pressures but normal ABIs at rest – BP measurements at several locations along the leg – Suggestive of location of blockage

Hirsch AT, et al. ACC/AHA 2005 PAD guidelines. Circulation. 2006;113:e463-e654. TASC Working Group. J Vasc Surg. 2000;31(suppl 1):S66-S67. Hirsch AT, et al. ACC/AHA 2005 PAD guidelines. Circulation. 2006;113:e463-e654. TASC Working Group. J Vasc Surg. 2000;31(suppl 1):S66-S67.

Pulse Volume Recording (PVRs) PVR

Pneumatic cuffs thigh, calf, ankle Approx. 65 mmHg Volume changes converted to electrical signal - Plethysmography - Arterial inflow Not affected by calcified arteries - Useful in diabetics with medial calcinosis

662 Exercise Stress Test

• PVR Normal  Abnormal Exercise until pain - Treadmill, toe stands

Measure ABI’s q 30 sec

Positive: > 20% drop ABI or 20 mmHg drop

Below baseline > 2 min

Courtesy of Steve Rose Courtesy of Steve Rose

Topics

• Background • Non invasive testing – Segmental pressures/ pulse volume recordings – Ultrasound – TCPO2 test

663 Ultrasound Spectral Display • Inexpensive • Widely available tool X axis = Time Y axis = Velocity ( or f ) of • No real risks (ionizing radiation, contrast, etc) Δ given RBC’s @ specific • Does require expertise (Vascular technologist) moment in time Limitations: Brightness = Number of RBC’s Poor acoustic penetration moving @ specific velocity @ Bone given moment in time Air Excessive fat Small field of view (+/- 5 cms ) Operator dependent Courtesy of Steve Rose

Angle of Doppler insonation Grey Scale

• Detects US frequency shifts caused by reflection from moving RBC’s • Remember that Doppler is only accurate at or less than 60 degrees

Color flow Normal Spectral tracing

• Triphasic • Reversal of flow during diastole • Peak Velocities not markedly elevated (ratio more important than absolute)

664 AbNormal Spectral tracing AbNormal Spectral tracing

At STENOSIS Immediately After • PSV 2 X or more of stenosis proximal segment • Parvus Tardus (loss • Spectral broadening of upstroke) • Aliasing • Diastolic flow (if collaterals present) • Turbulent flow • Biphasic

AbNormal Spectral tracing Bypass Graft evaluation

Downstream • PSV 2X indicative of stenosis • Monophasic • PSV < 45 cm/s worrisome for • Poor upstroke impending thrombosis • No diastolic flow • Will not always have traditional triphasic waveform (biphasic • Poor velocities normal) • Should evaluate inflow, anastomosis, and outflow

Topics Transcutaneous Oxygen Tension (TcPO2) • Background Known advanced PAD • Non invasive testing – Segmental pressures/ pulse volume Tissue healing: recordings - Amputation level - Healing ulcers – Ultrasound – TCPO2 test Combined with ankle, toe B/Ps

Courtesy of Steve Rose

665 Conclusions: TcPO2 Recording • Be familiar with non invasive testing methods Cathode – anode available Occlusive seal • Become Vascular certified if you do enough Free O2 diffuses through skin volume Electrical current • Understand the clinical aspect of the PAD to Good prognosis: better interpret the studies - Baseline 20 mmHg • Non invasive labs can provide revenue through additional imaging (CTA, MRA) and procedures - Rise after O by 10 mmHg 2 (IR, vascular surgery, cardiology)

Courtesy of Steve Rose

666 667 668 SAVE THE DATE

Hotel Del Coronado • Coronado, California

43 rd Annual Post Graduate Radiology Course October 22 – 26, 2018

20 th Annual Breast Imaging and Interventions Update October 26 - 28, 2018