28 Adrenal Glands


28 Adrenal Glands

Burgener\, Francis A.

The adrenal glands are small retroperitoneal structures readily identified by computed tomography (CT). They are located lateral to the spine at the level of the eleventh and twelfth rib and embedded in the perinephric fat that separates the kidney from the anterior (Gerota) and posterior (Zuckerkandl) renal fascia. On CT, normal adrenals extend 2 to 4 cm in a caudocranial direction and display a variety of shapes. The limbs of the adrenal glands have a uniform thickness of 5 to 8 mm with straight or concave margins. A limb thickness exceeding 10 mm is highly suggestive of adrenal disease with the exception of sites where two limbs converge.

On axial images, the right adrenal gland usually has an oblique linear configuration, paralleling the crus of the diaphragm, and rarely an inverted V, an inverted Y, an X, H, or triangular shape (Fig. 28.1). The right adrenal usually lies 1 to 2 cm superior to the upper pole of the right kidney and immediately posterior to the inferior vena cava. The right adrenal gland is also sandwiched between the right crus of the diaphragm medially and the right lobe of the liver laterally.

The left adrenal most often has an inverted V or an inverted Y shape and occasionally assumes a triangular shape on axial images (see Fig. 28.1). The left adrenal lies lateral to the crus of the left diaphragm and posterior and slightly medial to the tail of the pancreas and the stomach. The lower portion of the left adrenal may be in contact with the anteromedial aspect of the upper pole of the left kidney. The left adrenal is generally slightly caudal to the right adrenal.

Fig. 28.1 Normal anatomy. The right adrenal (short arrow) has an oblique linear configuration paralleling the crus of the diaphragm. The left adrenal (long arrow) has a triangular shape.

Differentiating between a benign adrenal adenoma, an incidental finding in 2% of the general population and an adrenal metastasis, the overall fourth most common metastatic site in the body, is a great challenge in the staging of a tumor patient. Adrenocortical adenomas typically measure less than 4 cm in diameter (average size about 2 cm), enhance only mildly but uniformly after contrast material administration, and depict a relatively rapid contrast washout on delayed scans (Fig. 28.2). Adrenal metastases frequently measure often more than 3 cm in diameter, may be inhomogeneous, particularly when larger, tend to enhance more and less uniformly than adenomas, and demonstrate a relatively slow contrast washout. A contrast washout of 50% at 10 minutes after injection is suggestive of a benign adenoma. However, because of the substantial variability in the vascularity of metastases ranging from hypovascular to hypervascular, benign and malignant lesions cannot reliably be differentiated based on their difference in contrast enhancement and washout rates. Adrenal adenomas contain intracytoplasmic lipids (steroids) to a varying degree. Depending on the amount of these lipids, the density of these lesions is accordingly decreased when compared with soft tissue masses not containing any fat. Therefore, on a nonenhanced scan, a uniform CT density of less than 20 HU in a solid lesion strongly suggests a benign adenoma. Fat suppression techniques in magnetic resonance imaging (MRI) appear even more useful for the differentiation between benign adrenal adenomas and metastases. The approach that appears most promising is the combined use of an in-phase/out-of-phase gradient echo technique. This chemical shift-imaging method allows assessment of the intracellular fat content. Benign adenomas containing intracytoplasmic lipids lose signal intensity on out-of-phase images, whereas metastases do not. However, adenomas that do not contain lipids in sufficient quantities and other benign masses cannot be differentiated from metastases with this technique. More recently, positron emission tomography (PET) scan has been shown to more accurately identify adrenal metastases when the primary tumor takes up F 18 fluorodeoxyglucose.

Adrenal calcifications are associated with tumors, hemorrhage, and infections. Tumor calcifications (Fig. 28.3) are very common in neuroblastomas (80%); not unusual in myelolipomas, pheochromocytomas, and adrenal carcinomas (about 20% each); and rare in cortical adenomas. Calcifications in adrenal hemorrhage (Fig. 28.4) and infections are late sequelae of the disease occurring usually 1 y or later after the insult. Adrenal hemorrhage may be traumatic or nontraumatic (e.g., neonatal stress, surgery, burns, hypotension with shock, pregnancy, hemorrhagic diathesis, coagulopathy, and anticoagulation therapy). Calcification in a hemorrhagic pseudocyst characteristically is curvilinear (“eggshell” calcification). Infections commonly associated with adrenal calcifications include tuberculosis, histoplasmosis, and Waterhouse–Friderichsen syndrome (fulminant meningococcemia). Bilateral adrenal hemorrhage and infections with destruction of more than 90% of the adrenal cortex result in adrenal insufficiency (Addison disease).

The differential diagnoses of focal or diffuse adrenal enlargement are discussed in Table 28.1.

Fig. 28.2a–c Contrast material washout of a benign adrenal cortical adenoma. (a) Precontrast. An enlarged, uniformly hypodense right adrenal (arrow) is seen bordered by the inferior vena cava anteriorly, the liver laterally, and the right crus of the diaphragm medially. (b) Postcontrast (30 s after intravenous (IV) contrast material injection). Mild homogeneous enhancement of the enlarged right adrenal is seen. (c) Postcontrast (10 min after IV contrast material injection). Contrast material washout from the enlarged right adrenal is virtually complete.
Fig. 28.3a–d Adrenal tumor calcifications. Neuroblastoma (a). A large mass with irregular speckled central calcification is seen. Pheochromocytoma (b). A huge nonenhancing, low-density lesion with curvilinear calcifications is seen in the left abdomen. Myolipoma (c). A soft tissue mass (arrow) with foci of fat and tiny calcifications is seen. Adrenal cortical adenoma (d). A small soft tissue lesion (arrow) with a tiny calcification is seen.
Fig. 28.4 Calcified adrenal hematoma. Extensive rim calcification in an enlarged left adrenal is evident.

Table 28.1 Focal or diffuse adrenal enlargement


CT Findings


Adrenal pseudotumors

Both normal anatomical and pathologic structures can simulate an adrenal mass, especially on the left side. Such structures include medial lobulation of the spleen, accessory spleen, outpouchings of adjacent stomach or small bowel, colonic interposition between the kidneys and liver, tortuous renal vessels, tortuous splenic artery, portosystemic venous collaterals in portal hypertension (e.g., spontaneous splenorenal shunt), and masses arising from the kidneys, liver, pancreas, or retroperitoneum.

Most of these pseudotumors can be differentiated from a true adrenal lesion with proper administration of intravenous (IV) and oral contrast material. Furthermore, a normal adrenal gland is present in these conditions.

Adrenal cyst and pseudocyst

Small to very large, usually unilateral, round, low-density mass with a smooth, well-defined contour. Rim calcification is rare except in echinococcal cysts and hemorrhagic pseudocysts.

Rare. True cysts are endothelial (e.g., lymphangiomatous or angiomatous), epithelial, or parasitic in origin. Pseudocysts are more common and result from hemorrhage and necrosis.

Adrenal cortical hyperplasia

Fig. 28.5

Diffuse bilateral adrenal enlargement with preservation of the normal glandular shape. Hyperplastic glands usually have smooth outlines. Less commonly, the enlarged adrenals may have a nodular or lumpy appearance, with nodules measuring up to 2 cm in diameter (macronodular hyperplasia).

Cushing syndrome (hypercortisolism) is caused in 80% of cases by bilateral adrenal cortical hyperplasia, but in one third of the patients, the adrenals are normal by CT criteria. The syndrome is 4 times more common in women, with the highest incidence between 20 and 40 y of age.

Conn syndrome (primary aldosteronism) presents in 20% of cases with bilateral nodular adrenal hyperplasia and is characterized by mild hypertension, hypokalemia, sodium retention, and reduced plasma renin levels.

Congenital adrenal cortical hyperplasia (inborn block of adrenal cortical steroid production) causes in utero virilization of female offsprings and precocious puberty in male offsprings.

Adrenal cortical adenoma

Fig. 28.3a–d , p. 807

Fig. 28.6

Fig. 28.7

Unilateral, well-defined, homogeneous mass measuring 2 to 4 cm in diameter. Depending on the lipid content, density ranges from soft tissue to near water. In the latter case, ultrasound may confirm the solid nature. Calcification is rare. IV contrast enhancement typically is mild, and the contrast washout is rapid. Differentiation from metastases is discussed in greater detail in the introductory text to this chapter.

Most common adrenal mass and most frequently nonhyperfunctioning and incidentally diagnosed. Increased occurrence in elderly, obese, or hypertensive patients or with carcinomas of the bladder, kidney, or endometrium.

Hyperfunctioning adrenal adenomas are responsible for 15% of cases with Cushing syndrome.

Aldosteronomas are responsible for 80% of Conn syndrome. The tumor averages less than 2 cm in diameter (range 0.5–3.5 cm) and is located twice as frequently on the left than the right side. On MRI, its signal intensity is typically increased on T2-weighted imaging when compared with nonhyperfunctioning adenomas.


Fig. 28.8

Fig. 28.9

Fig. 28.10

Usually unilateral, large soft tissue mass measuring 3 to 12 cm in diameter. Smaller tumors may be entirely solid. Hemorrhage and necrosis are commonly present in larger tumors, producing central regions of low density to an almost completely cystic appearance that may be difficult to differentiate from a true cyst or pseudocyst. Calcifications are present in up to 20% of cases. After IV contrast administration, a marked enhancement with slow washout is present in nonnecrotic areas.

Secretion of high amounts of catecholamines results in paroxysmal attacks characterized by hypertension, diaphoresis, tachycardia, and anxiety. Elevated urinary metanephrine and vanillylmandelic acid levels are characteristic. Approximately 10% are bilateral, 10% malignant, 10% extra-adrenal (organ of Zuckerkandl at origin of inferior mesenteric artery, para-aortic sympathetic chain, gonads, urinary bladder, and mediastinum), 10% familial (associated with Sipple or multiple endocrine neoplasia [MEN II] syndrome, mucosal neuroma or MEN III syndrome, von Hippel–Lindau syndrome, or neurofibromatosis).


Fig. 28.11

Fig. 28.12

Fig. 28.13

Unilateral, usually small, well-defined mass, but occasionally measuring up to 12 cm in diameter. The lesion consists primarily of fatty tissue that may contain foci of calcifications in 20%. Less commonly, the tumor is of soft tissue density with small regions of fatty tissue.

Rare benign asymptomatic tumor consisting of myeloid (megakaryocytes) and erythroid elements and mature fat cells. Flank or abdominal pain may develop secondary to hemorrhage or necrosis.

Mesenchymal adrenal tumors

CT features are not characteristic except in cavernous hemangiomas that present as low-density masses with central and/or peripheral calcifications (phleboliths) and a distinctive enhancement pattern (peripheral discontinuous ring of nodules) seen immediately after IV contrast material administration.

Extremely rare. Besides hemangiomas, other lesions such as lymphangiomas, fibromas, neurofibromas, myomas, and hamartomas, as well as their malignant counterparts, occur.


Fig. 28.14

Fig. 28.15

Fig. 28.16

Fig. 28.17

Irregular, usually unilateral soft tissue mass frequently containing low-density areas due to hemorrhage and necrosis and punctate to coarse calcifications. Considerable inhomogeneous enhancement is typically evident after IV contrast material administration. Invasion of the kidney and retroperitoneal lymph nodes with extension across the midline and encasement of the inferior vena cava, aorta, and its major vessels is characteristic in the advanced stage.

Approximately 80% occur in children younger than 3 y. Vanillylmandelic acid and homovanillic acid in urine are characteristic. Metastases (bone 60%, lymph nodes 40%, liver 15%, intracranial 14%, and lungs 10%) are already present in the majority of children at the time of diagnosis. Histologic spectrum ranges from the highly malignant sympathicogonioma to the relatively benign ganglioneuroma Adult neuroblastomas are rare and extra-adrenal sites are more frequent (e.g., mediastinum, retroperitoneum, and pelvis), and calcifications are uncommon.

Adrenal cortical carcinoma

Fig. 28.18

Fig. 28.19

Unilateral, inhomogeneous soft tissue mass usually measuring more than 4 cm at the time of diagnosis. Tumor diameters in excess of 10 cm are not unusual. They commonly contain low-density areas due to necrosis. Contrast enhancement is inhomogeneous, and the washout is delayed. Dystrophic calcifications are more common than in adenomas. Frequent complications, especially in larger lesions, include tumoral hemorrhage and central necrosis.

Occurs at any age and presents commonly with abdominal pain and palpable mass. Fifty percent of adrenal cortical carcinomas are hormonally active (twice as common in women), and patients may develop Cushing syndrome.

Adrenal metastases

Fig. 28.20

Fig. 28.21

Fig. 28.22

Unilateral or bilateral. Usually relatively small lesions, but may attain any size. The density of the metastases is similar to the primary tumor or other metastatic deposits, provided they are comparable in size. Small metastases tend to be homogeneous, but with increase in size, intratumoral hemorrhage and necrosis occur more frequently. Marked contrast enhancement with delayed washout is typical after IV contrast material administration. Direct extension occurs from renal and pancreatic carcinomas. Differentiation of small adrenal metastases from adrenal adenomas is discussed in greater detail in the introductory text of this chapter.

Hematogenous adrenal metastases originate in order of decreasing frequency from carcinomas of the lung, breast, gastrointestinal tract, or thyroid, and melanomas. A small adrenal mass in a patient with a known tumor is, however, more likely a cortical adenoma than a metastatic deposit.

Primary adrenal lymphoma is exceedingly rare and of the non-Hodgkin variety. In secondary lymphoma, retroperitoneal lymphadenopathy is usually present.

Adrenal granuloma

Fig. 28.23

Fig. 28.24

Unilateral or, more commonly, bilateral adrenal enlargement, often with hypodense regions representing necrosis. Calcification may subsequently develop which can become quite dense. Such calcifications in the absence of a soft- tissue mass strongly suggest chronic granulomatous disease rather than tumor. Contrast enhancement is usually modest.

Tuberculosis, histoplasmosis, and blastomycosis are the most frequent infectious sources.

Adrenal abscesses are rare in adults but occur more frequently in neonates secondary to meningococcal infections (Waterhouse–Friderichsen syndrome).

Addison disease (adrenal insufficiency) may be a late sequela of granulomatous disease, especially histoplasmosis. Autoimmune disease (idiopathic) and pituitary insufficiency are more common causes.

Adrenal hemorrhage

Fig. 28.25

Fig. 28.26

Unilateral or bilateral homogeneous adrenal masses measuring up to 3 cm. Lesions are either hyperdense or of soft tissue density. Progressive decrease in size and density of the adrenal masses on follow-up examinations. Calcifications may develop as late sequelae. Development of a hemorrhagic pseudo-cyst, often with curvilinear (eggshell) calcification, is another late presentation.

Anticoagulation therapy is the most common cause. Bleeding diathesis, sepsis, shock, trauma, major surgery, and pregnancy are other predisposing factors. Bilateral involvement may result in acute adrenal insufficiency that is potentially fatal. If not fatal,

Addison disease may be a late sequela. Posttraumatic adrenal hemorrhage is limited in 85% to the right side. Right adrenal hemorrhage is also a complication of liver transplantation.

In the neonate, adrenal hemorrhage may be associated with birth trauma, hypoxia (prematurity), septicemia, and bleeding disorders.

Fig. 28.5 Cortical hyperplasia. Diffuse bilateral adrenal enlargement with nodular appearance (arrows) is seen.
Fig. 28.6 Adrenal cortical adenoma. A well-defined, homogeneous, low-density mass (arrow) is seen.
Fig. 28.7 Adrenal cortical adenoma. An enlarged left adrenal (arrow) with little contrast enhancement is seen.
Fig. 28.8 Pheochromocytoma. A round, well-defined, homogeneous soft tissue mass (arrow) originating in the right adrenal is seen. Note also the milk of calcium bile (lime bile syndrome).
Fig. 28.9 Pheochromocytoma. A large mass (arrow) is seen with central regions of low density due to necrosis. Increased density of the perirenal fat is caused by hemorrhage from the pheochromocytoma.
Fig. 28.10 Pheochromocytoma. A large cystlike lesion without enhancement is seen in the left abdomen. The finding is the sequela of extensive necrosis and hemorrhage within the original tumor.
Fig. 28.11 Myelolipoma. An ovoid predominantly fatty lesion (arrow) is seen originating in the right adrenal.
Fig. 28.12 Myelolipoma. A well-defined soft tissue mass (arrow) is seen containing a small focus of fatty tissue.
Fig. 28.13 Myelolipoma. A soft tissue lesion (arrow) containing several foci of fatty tissue and tiny calcifications is seen.
Fig. 28.14 Neuroblastoma. A large inhomogeneous soft tissue mass with calcifications (arrow) is seen in the right subhepatic region with extension into the retroperitoneum. Note also the peripheral low-density lesion in the liver representing metastases.
Fig. 28.15 Neuroblastoma. A large mass with extensive speckled calcifications is seen.
Fig. 28.16 Ganglioneuroma. A homogeneous round lesion (arrows) with similar to slightly less density than the surrounding muscle is seen.
Fig. 28.17 Ganglioneuroma. An ovoid mass (arrow) with patchy enhancement is seen originating from the left adrenal.
Fig. 28.18 Adrenal cortical carcinoma. A huge soft tissue mass with multiple hypodense areas caused by tumor necrosis is evident in the left abdomen.
Fig. 28.19 Adrenal cortical carcinoma. A large mass (arrow) with slightly hypodense central regions is seen.
Fig. 28.20 Adrenal metastasis. A right adrenal metastasis (arrow) originating from a bronchogenic carcinoma is seen.
Fig. 28.21 Adrenal metastases. An enlarged and deformed left adrenal (arrow) with multiple hypodense nodules is seen. A small hypodense metastasis (arrowhead) is also seen in the nonenlarged right adrenal. The primary tumor was a bronchogenic carcinoma.
Fig. 28.22 Bilateral adrenal metastases. Large bilateral adrenal metastases (arrows) are seen originating from a liposarcoma.
Fig. 28.23 Adrenal histoplasmoma. An enlarged, triangular, left adrenal (arrow) is seen with slightly reduced attenuation centrally when compared to its periphery.
Fig. 28.24 Adrenal tuberculoma. An enlarged right adrenal with scattered irregular dense calcifications and small hypodense foci is seen.
Fig. 28.25 Adrenal hematoma (subacute). An enlarged left adrenal (arrow) without enhancement is seen.
Fig. 28.26 Calcified adrenal hematoma. An enlarged right adrenal gland (arrow) with irregular central calcifications is seen.

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Jul 6, 2020 | Posted by in GENERAL RADIOLOGY | Comments Off on 28 Adrenal Glands

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