ADRENAL LESIONS 10/09/2012. Adrenal + lesion. Introduction. Common causes. Anatomy. Financial disclosure. Dr. Boraiah Sreeharsha. Nothing to declare
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1 ADRENAL LESIONS Financial disclosure Nothing to declare Dr. Boraiah Sreeharsha MBBS;FRCR;FRCPSC Introduction Adrenal + lesion Adrenal lesions are common 9% of the population Increase in the detection rate Improvement in the imaging modalities With resultant improvement in the diagnostic rate Anatomy Common causes Rare causes Understanding the basics of imaging options Algorithm to come to a diagnosis Anatomy Common causes Ad-renal 5 grams Shapes - Y/V/T Cortex mesodermal origin Medulla neural crest origin Metastasis Hemorrhage Hyperplasia 1
2 Uncommon causes Hyerfunctioning lesion Solid lesions Adrenocortical carcinoma, Hemangioma; angiosarcoma; ganglioneuroma Solid fatty - collision tumor; myelolipoma Cystic Hydatid cyst, endothelial cyst Cortex Cushing (cortisol from zona fasciculata) Conn (aldosterone from zona glomerulosa) Hyperandrogenism (androgen form zona reticularis) Medulla Imaging and., CT CT and MRI PET I-123 MIBG / In-111 Octreotide Blood / Urine analysis (plasma catecholamines, urine VMA and metanephrine) Biopsy Adrenal vein sampling Unenhanced scan Portal venous phase scan Washout protocol Unenhanced + 70 (60-80) sec enhanced scan + 10 (10-15) mins delayed scan Relative WO = Enhanced HU Delayed HU /Enhanced HU Absolute WO = Enhanced HU Delayed HU / Enhanced HU Unenhanced HU MR In brief. Utilization of chemical shift principle - T1 in-phase and T 1 out-of-phase (intralesional fat content drops signal on out of phase images) Gad enhancement is not essential Metastasis Adrenocortical carcinoma Collision tumor Conn syndrome Hemorrhage 2
3 Most common adrenal lesion, and is benign About 70 % are intracytoplasmic lipid rich in the adrenal cortex and 30% are lipid poor Lipid rich adenomas have low HU Lee et al => mean 2.2 HU; at a threshold value of 0HU, unenhanced CT has a sensitivity of 47% and specificity of 100% Rapid enhancement and wash-out <30HU at 10 mins has been shown to be diagnostic Wash-out of >50% is specific At sec HU is usually <110 (not FDG avid) Boland et al (meta-analysis) at a threshold of 10HU, sensitivity of 71% and specificity of 98% Comparison of T1 in-phase with T1 out-of-phase Spleen is usually taken as the reference organ Sensitivity % Specificity % Can be difficult for <1cm lesions due to low resolution Unenhanced CT Low HU T1 in-phase T1 out-of-phase T2 Gad enhancement 3
4 Metastasis DWI ADC Little intracytoplasmic fat Lee et al => mean - 39HU Can have rapid enhancement but washout is usually prolonged Not smooth in contour; heterogeneous enhancement Metastasis Functioning medullary tumor Typically unilateral and benign; well circumscribed 10% extra adrenal paragangliomas Clinically hypertension and palpitations due to catecholamine secretion (however, <1% of hypertension cases are due to pheochromocytoma) Plasma catecholamines, urine VMA and metanephrine => sensitivity % (false negative from exogenous drugs and episodic catecholamine production) T2W Can have hemorrhage, necrosis, calcification Hyper-enhancing; >110HU at sec; >50% wash out Markedly hyperintense on T2; salt and pepper type enhancement Positive on I123-MIBG/In111-Octreotide metastasis; extra adrenal lesions 4
5 Adrenocortical carcinoma T1 FS + Gad T1 FS + Gad Rare Bilateral in about 10% 50-80% - functional => Cushing syndrome/conn/virilization Usually large; necrosis; hemorrhage; calcification(30%); invasion of adjacent structures; venous extension; metastasizing F18-FDG avid AGGRESSIVE LOOKING Adrenocortical carcinoma Collision tumor CT + CT + 2 Histologically different tumors in adrenal gland Rare benign/benign; benign/malignant; malignant/malignant s, metastasis, myelolipoma, carcinoma.. Metastasis in an adenoma is the main entity of concern CT and PET; biopsy Conn syndrome Conn syndrome Primary Hyperaldosteronism (most common cause of secondary hypertension) CT - CT - 80 % due to (aldosterone producing) adenoma (APA ) 20% due to hyperplasia (unlike Cushing where hyperplasia accounts for 80%) Also in adrenocortical carcinoma Clinical symptoms, hypernatremia/hypokalemia/alkalosis + nodule on CT => surgery 5
6 Hemorrhage Hemorrhage Not common Traumatic/unilateral > non traumatic/bilateral Adrenal insufficiency 90% destruction; can be catastrophic Anticoagulation, stress, metastasis, pheochromocytoma Varied appearance CT; MR Other Adrenal lipoma Adrenal lipoma Myelolipoma Myelolipoma Myelolipoma Myelolipoma Hyperplasia Hyperplasia 6
7 Algorithm to assess an adrenal lesion Hydatid cyst BENIGN In summary, BENIGN Imperative to consider background history Previous imaging is extremely helpful MR is not always confirmatory for tiny lesions CT washout is the best modality for adenomas Simple follow up imaging should not be forgotten! BENIGN Biopsy References Lee MJ, Hahn PF, Papanicolaou N, et al. Benign and malignant adrenal masses: CT distinction with attenuation coeficients, size, and observer analysis. Radiology 1991; 179; Boland GW, Lee MJ, gazelle GS, Halpern EF, McNicholas MM, Mueller PR. Characterization of adrenal massess using unenhanced CT: an analysis of the CT literature. AJR Am J Roentgenol 1998: 171: Mayo-Smith WW, Boalnd GW, Noto R, Lee MJ. State of the art Adrenal Imaging. Radiographics 2001; 21: Otal P et al. Imaging features of uncommon adrenal masses with histopathologic correlation. Radiographics 1999; 19: Elaini A et al. Improved detection and characterization of adrenal disease with PET CT. Radioraphics 2007: 27: Caoili EM et al: Adrenal masses: characterization with combined unenhanced and delayed enhanced CT. Radiology. 222(3):629-33, 2002 Blake MA et al: : an imaging chameleon. Radiographics. 24 Suppl 1:S87-99, 2004 Thank you Caoili EM et al: Delayed enhanced CT of lipid-poor adrenal adenomas. AJR Am J Roentgenol. 175(5):1411-5,
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