PANCREAS / SPLEEN / ADRENAL GLANDS
PANCREAS
ANATOMY / VARIANTS
PANCREATITIS
CANCER
SOLID EPITHELIAL NEOPLASM
CYSTIC EPITHELIAL NEOPLASM
INCIDENTAL PANC CYST GUIDELINES
SPLEEN
ADRENAL GLANDS
ANATOMY
Adrenal cortex: derived from mesoderm and consists of the following layers:
Zona glomerulosa (mineralocorticoids)
Zona fasciculata (glucocorticoids)
Zona reticularis (androgens)
Adrenal medulla: chromaffin cells derived from neural crest cells from SNS that secrete catecholamines into bloodstream
Avg thickness ~3 mm for medial/lateral limbs; >10 mm can be used as hyperplasia threshold
Arteries:
Superior adrenal: 6-8; from inferior phrenic arteries
Middle adrenal: 1; from abdominal aorta
Inferior adrenal: 1; from renal arteries
Veins:
Right adrenal drains into IVC
L adrenal drains into L renal vein
Presynaptic SNS fibers from paravertebral ganglia end directly on secretory cells of medulla.
APPROACH TO ADRENAL LESIONS
ADRENAL ADENOMA & INDETERMINATE MASSES
MALIGNANT (POTENTIALLY MALIGNANT) ADRENAL GLANDS
ADRENOCORTICAL CARCINOMA
Very rare w prevalence approx 1/1,000,000. Highly aggressive w/ poor prognosis
~66% are functional producing a disordered array of hormones that may manifest as Cushing syndrome, hyperaldosteronism, and virilization.
Imaging:
Large >4 cm and unilateral; irregular tumor margins
Central necrosis/hemorrhage w/ heterogeneous enhancement.
Calcification is common. Fat is rare.
Early local vascular invasion of renal vein or IVC
20% have distant mets at presentation lungs, liver nodes, bone.
IMAGING FEATURES
CANNOT be distinguished from other tumors by imaging alone. Need clinical hx and lab values (urinary and plasma fractionated metanephrines)
Highly vascular and prone to hemorrhage
US: hypoechoic suprarenal lesion +/- cystic change
NECT: >10 HU
CECT:
Delayed washout kinetics typically similar to adrenal CA and mets, but rapid washout like adenoma is possible.
Heterogeneous enhancement 2/2 necrosis, cystic degeneration, hemorrhage.
MR: Variable T1/T2 signal 2/2 hemorrhage, cystic degeneration, necrosis; T2 light bulb hyperintensity
Ga-68 DOTATATE: ectopic, recurrent and metastatic tumors. (see below)
PHEOCHROMOCYTOMA
Intra-adrenal paraganglioma; neuroendocrine tumor that typicaly originates from the adrenal medulla.
Composed of chromaffin cells that secrete catecholamines and cause uncontrolled secondary HTN and episodic headaches/diaphoresis.
Hereditary type: small bilateral adrenal lesions in young patient.
Syndromes:
MEN2A/B: b/l intraadrenal pheos
NF1
vHL
Carney's triad (gastric leiomyosarcoma, pulmonary chondroma, paraganglioma)
Hereditary paraganglioma-pheochromocytoma syndrome: SDHD gene mutation.
Sporadic type: large > 3 cm, unilateral mass in older pt
90% arise in adrenal, 90% unilateral, ~90% are benign
Called paraganglioma when tumor arises in other chromaffin cells of sympathetic ganglia. Typically subdiaphragmatic but can be anywhere along sympathetic chain from neck to bladder.
Organ of Zuckerkandl (along Ao bifurcation to level of bladder) and urinary bladder are relatively common sites.
ADRENAL METS
4th MC site of hematogenous mets after lungs, liver and bone.
Adrenal mets are present >25% of patients w known primary malignancy.
Melanoma (50%), lung/breast (30-40%), renal/GIT (10-20%)
Rich adrenal blood supply for endocrine function. As a result, adrenal glands are common site for hematologic mets (lung, breast, melanoma)
Unilateral or bilateral; central necrosis +/- hemorrhage
Usually <5 cm, larger if melanoma.
Must differentiate b/n isolated benign adrenal lesion (typically adenoma) and mets during initial staging:
Most mets show prolonged washout pattern unlike adenoma. Rapid washout if hypervascular mets.
DIFFUSE ADRENAL DISORDERS
ADRENAL HEMORRHAGE
Can be spontaneous but in adults is usually due to anticoagulation or an underlying malignancy.
Hemorrhage can appear mass-like and is often heterogeneous on CT but does not enhancement of postcontrast images.
When prior imaging is available, it should be suspected in the event of rapid onset of an adrenal mass.
In this context F/U imaging can be helpful to confrim resolution and/or interval decrease in size.
ADRENAL HYPERPLASIA
Enlargment of adrenal glands
Adrenal body > 10 mm, limbs >5 mm
Typically bilateral and smooth w/ maintained shape
Majority are nonfunctional. minority demonstrate subclinical or clinical adrenal dysfunction.
ADRENAL CALCIFICATION
Adrenal calcifications are not infrequent bu rarely cause adrenal hypofunction.
Can be 2/2 hemorrhage, granulomatosis w polyangiitis, TB, and histoplasmosis.