MRI of the Adrenal Glands and Retroperitoneum

▪ Introduction

Extreme sensitivity to the microscopic lipid—present in the form of cholesterol and cholesterol/lipid-based derivatives and adrenal adenomas—and the ability to detect other substances, such as hemorrhage, are the major reasons why MRI is so useful in adrenal imaging. Deviation from either normal Y-shaped morphology or microscopic lipid content generally connotes pathology. Typical indications for MRI in renal and adrenal imaging include indeterminate adrenal lesion evaluation, endocrinologic workup for potential adrenal adenoma or pheochromocytoma and indeterminate adrenal lesion characterization.

Retroperitoneal pathology is a rare independent indication for MRI, but certain scenarios occasionally arise, such as characterizing indeterminate retroperitoneal masses, especially when tissues with characteristic MR features are implicated, such as retroperitoneal fibrosis, amyloidosis, and sarcomas (ie, liposarcoma with intralesional lipid).

▪ Technique

Technical considerations in adrenal and retroperitoneal MRI are essentially the same as for other abdominal indications (see Chapter 1 ), with a few occasional modifications in the case of the adrenal glands.

Although a standard abdominal protocol suffices for most adrenal indications, certain considerations recommend protocol deviations and/or modifications. The ability to detect and quantitate microscopic fat through in- and out-of-phase images is indispensable in adrenal imaging. Adrenal adenomas distinguish themselves from other lesions (such as adrenal metastases) by the presence of intralesional microscopic fat. In adrenal imaging, supplemental three-dimensional (3-D) in- and out-of-phase sequences with thinner slices (and potentially smaller field of view [FOV] and voxel size) better assess small adrenal lesions—often inadequately evaluated with standard two-dimensional (2-D) sequences.

Rigorous dynamic contrast-enhanced imaging is less critical in adrenal and retroperitoneal imaging, compared with liver and pancreatic imaging, because the issue of enhancement more often reduces to a binary question of presence versus absence of enhancement. The temporal nature of lesion enhancement matters less. Nonetheless, the information gleaned by dynamic imaging, including solid lesion enhancement characteristics—supplemental in discriminating adrenal adenomas from other lesions—validates the effort.

▪ Interpretation

Although the adrenal glands are small organs, because they are surrounded by retroperitoneal fat, they are often fairly conspicuous ( Fig. 7.1 ). Pulse sequences without fat suppression provide hyperintense retroperitoneal fat as a backdrop against which T1- and T2-hypointense adrenal glands are clearly visualized. T1-weighting confers sensitivity to protein and hemorrhage, which appear bright in these images. Of course, macroscopic fat appears equally bright in in- and out-of-phase images, and microscopic fat (occasionally present in clear cell type renal cell carcinoma [RCC]) appears dark in out-of-phase images relative to in-phase images. Macroscopic fat (present in adrenal myelolipomas), hyperintense in in- and out-of-phase images, loses signal in the T1-weighted fat suppressed sequence—the paramagnetic sequence (the precontrast phase of the dynamic sequence).

In addition to establishing the presence of macroscopic fat through signal suppression, the paramagnetic sequence (precontrast T1-weighted fat-suppressed) showcases hemorrhage and other paramagnetic substances, such as protein, and other molecules, such as melanin. This sequence is optimized to receive signal solely from (nonfat) substances with very short T1 values—usually hemorrhage in the realm of adrenal and retroperitoneal imaging.

Contrast enhancement adds supplemental diagnostic information in the case of adrenal imaging and helps to differentiate cystic from solid, when necessary or unclear by other imaging modalities, in cases of adrenal and retroperitoneal lesions. Dynamic enhancement information yields some additional information, such as hyperemia in the setting of inflammation, the frequently avid enhancement of a pheochromocytoma, and provides an additional imaging parameter to approaching retroperitoneal masses, which are often relatively nonspecific.

▪ Adrenal Glands

Normal Features

The adrenal glands are Y-shaped structures inhabiting the superior extent of the retroperitoneum. The adrenal body measures approximately 10 to 12 mm in length, and the medial and lateral limb measures 5 to 6 mm. As a general rule of thumb, adrenal limbs measure 5 mm or less in thickness. The right adrenal gland sits 1 to 2 cm above the upper pole of the right kidney, and the left adrenal gland rests ventral to the upper pole of the left kidney (see Fig. 7.1 ). Adrenal gland dimensions vary, precluding the use of specific normal size criteria. Tandem parallel adrenal embryology explains adrenal microanatomy and physiology, imaging appearance, and the spectrum of adrenal lesions. The outer cortex develops from coelomic mesoderm and accounts for most of the bulk of adrenal tissue, responsible for synthesizing cholesterol-derived hormones—glucocorticoids and mineralocorticoids. The cholesterol compounds constituting the building blocks of the adrenal hormones account for the loss of signal in out-of-phase images. The inner adrenal medulla derives from neural crest cells and produces catecholamines—mostly epinephrine.

Adrenal lesion differential diagnosis depends on cystic (or nonsolid because hemorrhage is included in this category) versus solid tissue composition ( Fig. 7.2 ). Presence or absence of enhancement classifies adrenal lesions into the respective categories. With the exception of hemorrhage, nonsolid etiologies exhibit nonspecific free water imaging features. Solid lesion tissue composition often demonstrates specific imaging features suggesting the underlying diagnosis. Microscopic fat connotes adenoma, and macroscopic fat equals myelolipoma. High fluid content and hypervascularity explain the T2 hyperintensity and avid enhancement of pheochromocytoma, respectively. Other solid lesions, such as lipid-poor adenoma, metastasis, and adrenal cortical carcinoma are less specific.

Cystic (Nonsolid) Lesions

Adrenal cystic lesions are rare, with an incidence of less than 1%. Adrenal cystic lesions divide into two main categories: 1) true endothelial (lymphatic—lymphangiomatous and vascular—hemangiomatous) and epithelial cysts (40%–45%) and 2) pseudocysts (40%)—usually represents the sequela of previous hemorrhage, but also includes infectious (parasitic) cysts and other rare cystic lesions. Hemorrhage constitutes a third nonsolid category (although metastases are included in the differential diagnosis of adrenal hemorrhage, technically belying the term nonsolid ) ( Table 7.1 ).

TABLE 7.1

Differential Diagnosis of Adrenal Hemorrhage

Unilateral	Bilateral
Blunt trauma	Stress
Liver transplant (right-sided)	Hemorrhagic diatheses
Primary or metastatic tumors	Thromboembolic disease
Uncomplicated pregnancy	Complicated pregnancy
Spontaneous/idiopathic	Meningococcal septicemia

Adrenal Cysts

Adrenal cystic lesions are almost always asymptomatic and virtually always detected incidentally during imaging studies. Symptoms manifest only with large size through mass effect on adjacent organs. Nonspecific imaging features usually fail to discriminate among the different cystic types. Most lesions share features of typical cysts: internal free water signal, absent central enhancement, and a thin or imperceptible wall ( Fig. 7.3 ). Internal contents of pseudocysts from previous hemorrhage exhibit a greater degree of heterogeneity (see Fig. 7.3 ).

Mimickers of adrenal cysts and pseudocysts, which are not incidental, include parasitic (echinococcal) cysts, pheochromocytoma, and cystic neoplasms. Adrenal echinococcal cysts share imaging features with echinococcal cysts infesting other body parts, such as the liver (see Chapter 2 ). At the early stages of development, the hydatid cyst simulates adrenal pseudocysts and true cysts. With continued development, characteristic features corroborate the diagnosis (eg, daughter cysts, floating membrane). The extreme T2 hyperintensity of the pheochromocytoma conjures cystic etiology in T2-weighted images, but avid enhancement confirms solid tissue, excluding fluid contents. Solid tumors—such as metastases and adrenal cortical carcinoma—with cystic degeneration and necrosis harbor solid neoplastic, occasionally subtle, components. Subtracted images improve solid tissue conspicuity.

Adrenal Hemorrhage

Although not exactly cystic, adrenal hemorrhage—except when induced by underlying adrenal metastases—is nonsolid. Lack of enhancement best establishes the absence of solid tissue, which benefits from the incorporation of subtracted images, given the precontrast T1 hyperintensity of hemorrhage. Rich adrenal arterial supply—hormonally enhanced under certain conditions—with limited venous drainage through a single adrenal vein (prone to spasm induced by catecholamines) predisposes to hemorrhage.

Distortion of the adreniform shape depends on the degree of hemorrhage. Methemoglobin T1 hyperintensity in acute/subacute hemorrhage signals the diagnosis ( Fig. 7.4 ). Follow-up imaging shows involution and confirms the diagnosis, although potentially identifying or excluding underlying lesions.

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