5.1 Adrenal imaging

Evaluating the adrenal gland with imaging can be challenging. The adrenal glands may be morphologically within normal limits even in the presence of clear hyperfunction. Hyperplasia and small nodules may coexist. Nonfunctioning nodules are frequent and need to be differentiated from culpable hyperfunctioning adenomas or carcinomas. However, the increasingly sophisticated anatomical imaging provided by CT and MRI, together with the functional characterization afforded by radionuclide imaging, allows good correlation with clinical and endocrine parameters.

Embryologically, the adrenal cortex derives from coelomic mesoderm and the medulla from neural crest cells. Development is independent of the kidney and adrenal glands will normally be present in the absence of a kidney. In the newborn the adrenal glands are large structures, being one-third of the size of the kidneys. They involute rapidly, however, and in the adult are small structures. They are situated immediately above and anteromedial to the upper pole of the kidneys, although the left is less suprarenal. The right lies immediately behind the cava, alongside the right diaphragmatic crus. The left lies behind the splenic vein, lateral to the left crus.

The normal adrenal has a characteristic inverted Y- or V-shape with the two limbs fusing anteromedially. The most cranial section has a triangular appearance. Cross-sectional appearance varies according to the exact level. Each limb measures 2.5–4 cm in length and 3–6 mm in thickness. Greater than 1 cm thickness is definitely abnormal. Accessory adrenal tissue (rests) may be found in the kidney, testis, or ovary, and elsewhere in the retroperitoneum.

Arterial supply is from three sources: superior–multiple arteries from the inferior phrenic; middle from the aorta; and inferior from the renal artery. A single vein drains each adrenal. The left is a tributary of the left renal vein, the right leads directly to the cava, although rarely may join a hepatic vein first. The right adrenal vein is shorter and narrower.

The diagnosis of hyperfunction is made clinically and endocrinologically, not radiologically. Imaging is reserved for localization and characterization of adrenal lesions (1, 2).

The adrenals may be calcified as a result of previous haemorrhage infarction or granulomatous infection, e.g. due to tuberculosis. Adrenal cysts may be large and show calcification of the wall. Of adrenal tumours, 10–14% are calcified on CT, but this is rarely demonstrable on plain films. Large adrenal masses may be inferred from displacement or distortion of bowel gas or adjacent organs such as the kidney. Rarely, malignant adrenal lesions will invade the kidney and masquerade as a renal tumour on intravenous urography.

Ultrasonography is widely available and accessible, and does not involve exposure to radiation. It is, however, very poor at visualizing the normal adrenal or small masses, and a normal examination would therefore not exclude an adenoma, adrenal hyperplasia, or small malignant tumours. It could be expected to demonstrate tumours of 2 cm or more in size if the examination is technically complete (Fig. 5.1.1). It is more helpful in children where body fat is less of a problem, and when it is particularly desirable to avoid the radiation exposure of a CT examination.

CT is the mainstay of modern adrenal imaging. The normal adrenal gland can almost always be visualized. The right may be more difficult to identify, being in close apposition to the back wall of the cava and being affected by partial volume effect from the overlying liver. If hyperplasia or a small tumour is suspected, definitive assessment of the adrenals requires thin (1–3 mm) contiguous sections. Modern multidetector CT scanners are currently capable of resolving tumours as small as 5 mm. The use of contrast media is not necessary for detection of adrenal masses, the anatomical demonstration being more important. In some instances however, the pattern of enhancement may help characterize the lesion.

Staging of malignant adrenal tumours requires scanning of the chest and abdomen for local organ invasion, lymphadenopathy, and metastases. Intravenous contrast medium is necessary for maximum sensitivity for hepatic metastases. Hypervascular metastases (e.g. phaeochromocytoma) may be more conspicuous with scans obtained in the arterial phase rather than the portal venous phase of enhancement.

As with CT, MRI allows visualization of the normal and abnormal adrenal gland in the majority of cases. It does not involve exposure to ionizing radiation and hence is preferred in children, the young adult, and the pregnant patient. It has a valuable role particularly in characterization of the indeterminate adrenal lesion using chemical shift imaging (in- and opposed-phase sequences). The ability to image in multiple planes allows improved recognition of adjacent organ involvement, and possibly determination of an adrenal origin of an upper-quadrant mass (Fig. 5.1.2). However, when staging malignancy, it is usually difficult to evaluate the whole body as the examination time would be prolonged, and it is as yet poorly sensitive to small metastases in the lung.

The functional information afforded by imaging with radioisotopes is unique and is complementary to the anatomical demonstrations of CT and MRI. Isotope imaging of the adrenal medulla uses the noradrenaline analogue meta-iodobenzylguanidine (MIBG) (3). The tracer is actively taken up in postsynaptic nerve terminals where it is resistant to degradation and can hence be used to demonstrate accumulations of such tissue as in phaeochromocytomas, paragangliomas, and neuroblastomas. Carcinoid tumours and medullary carcinomas of the thyroid also take up the radiopharmaceutical.

The pharmaceutical is labelled with ¹²³I- or ¹³¹I-iodine; ¹²³I-iodine gives a lower radiation dose and better quality images but is less readily available and more expensive. A number of drugs inhibit MIBG uptake: opioids, tricyclic antidepressants, sym-pathomimetics, antipsychotics, cocaine, and importantly antihypertensive agents including labetalol and calcium channel blockers, and such drugs need to be withdrawn if possible before this examination (3, 4).

Scans are usually performed at 24 and 48 h. Uptake is normal in liver, spleen, myocardium, and salivary glands. Urinary excretion may obscure primary or metastatic disease in the pelvis or bladder. Occasionally, bowel uptake is seen which may hinder interpretation. Normal adrenal glands are usually not well visualized although there may be faint uptake.

An alternative radiopharmaceutical is the somatostatin analogue octreotide acetate labelled with ¹²³I or ¹¹¹In (indium), which localizes to somatostatin receptor-bearing tumours including phaeochromocytomas and neuroblastomas (5).

Isotope imaging of the adrenal cortex uses labelled cholesterol analogues: 6-β-iodomethyl-19-norcholesterol labelled with ¹³¹I (NP-59). Adrenocortical scintigraphy is not widely available or used. This may be due to the number of patient visits required, the lag time to final result, a relatively high radiation dose, limited availability, but perhaps most importantly the use of endocrine assessments in conjunction with high resolution anatomical imaging with CT.

Positron emission tomography (PET) has an increasingly recognized role in the assessment of adrenal masses (6, 7). The most commonly used radiopharmaceutical is [¹⁸F]2-fluoro-2-deoxy-D-glucose (FDG), a glucose analogue that is actively taken up and trapped in hypermetabolic cells, usually reflecting malignancy. PET can thus be used to detect metastases to the adrenals, and to indicate that the likelihood that a mass is malignant. Although not yet widely available, other pharmaceuticals such as ¹⁸F-fluorodopamine, ¹⁸F-fluroDOPA and have been used for evaluation of adrenal and other neuroendocrine tumours (4).

The vascular supply and drainage have been described above. Arteriography is rarely indicated for diagnostic purposes. Occasionally it may help indicate an adrenal origin of an uncertain abdominal mass, or be used as a prelude to embolization of vascular tumours.

Sampling of the adrenal effluent is used to determine whether hormone production originates from one or both adrenals, and to determine if nodules detected on CT are functional or not. The left adrenal vein is relatively easy to cannulate via the renal vein but the anatomy of the right is less favourable (direct drainage to the inferior vena cava) and high failure rates have been reported. Nevertheless, some investigators approach 100% success rates (8). Extravasation and venous infarction may complicate injection of the adrenal veins. However, adrenal venography is not necessary for diagnostic purposes, although it may help confirm correct catheter placement.

The indeterminate lesion that is discovered when imaging for other purposes may need histological evaluation. However, endocrine assessment and the newer CT and MR characterization techniques have significantly reduced the requirement for biopsy (9). Biopsy accuracy rates range between 80 and 100% (10, 11). Biopsy cannot differentiate between an adenoma and a carcinoma and thus should be avoided if an adrenocortical carcinoma is suspected; violation of the tumour capsule of an adrenocortical carcinoma significantly worsens the prognosis and metastases in the biopsy needle canal have been described. However, biopsy can be helpful to differentiate between a tumour of adrenal origin and an adrenal metastasis of a solid organ tumour distinct from the adrenal. An adrenal biopsy should only be carried out if the outcome would have a therapeutic consequence. Haemorrhage and pneumothorax are the most common complications of adrenal biopsy.

CT guidance is usual except where the tumour is relatively large when ultrasonography is a good alternative. A posterior approach with the patient prone is the least hazardous but the posterior costophrenic angles may be deep, and transgression of the lungs may be unavoidable with consequent risk of pneumothorax. A transhepatic approach is an alternative on the right, or on rare occasions a safe anterior approach may be identified (9).

Most operators remain reluctant to biopsy adrenal masses that may be phaeochromocytomas due to the risk of precipitating a hypertensive crisis (9). Prior blood or urine biochemistry for exclusion of catecholamine excess is therefore mandatory before any adrenal biopsy.

Cushing’s syndrome is the result of overproduction of cortisol by the adrenal cortex. The distinction between pituitary or ectopic ACTH-driven cortisol production and primary adrenal disorders is made on a clinical and biochemical basis and imaging directed appropriately.

MRI is the best imaging modality for pituitary tumours, which account for about 80% of cases of Cushing’s (Fig. 5.1.3a). The multiplanar presentation is ideal, and intravenous contrast medium administration mandatory, for the detection of small tumours. CT is a reasonable alternative. Thin-section coronal examinations with intravenous contrast are most sensitive for small tumours. There is no justification for imaging the adrenals in pituitary-driven or ectopic Cushing’s, although bilateral adrenal hyperplasia can be expected (Fig. 5.1.3b). Adrenal hyperplasia is manifest as thickening and elongation of the limbs of the adrenal gland. The hyperplasia may be smooth or multinodular, but the glands may look normal.

Adrenal tumours are the cause of Cushing’s syndrome in 15–25% of cases and are well shown with CT and MRI (12, 13). Adenomas are usually between 2 and 4 cm in size. They are uniform in attenuation, rounded, and well demarcated (Fig. 5.1.3c), identical to nonfunctioning tumours. They may be large enough to be seen on ultrasonography although increased body fat may hinder the examination. An active adrenal adenoma will be accompanied by atrophy of the rest of the gland and the contralateral adrenal. Carcinomas are usually larger (more than 4 cm) and may show necrosis, haemorrhage, or calcification (12, 13). Histology cannot indicate malignancy but large tumours are predictive of subsequent malignant behaviour, that is, metastasis or recurrence. Multiplanar imaging as with ultrasonography, MRI, and multidetector CT studies may clarify the organ of origin of large tumours more readily than axial CT. Growth over time (Fig. 5.1.4a) or local invasion of adjacent organs are features of malignancy (Fig. 5.1.4b). As with renal cell carcinoma, there may be invasion of the adrenal vein and extension into the cava (Fig. 5.1.4c).

Rarely Cushing’s syndrome is the result of primary pigmented nodular hyperplasia when multiple small nodules are shown arising from an otherwise atrophic gland; or ACTH independent macronodular hyperplasia when the glands are markedly enlarged and nodular but maintain their shape (12).

There are other radiological features of Cushing’s syndrome. Increased body fat may be radiologically evident, especially on CT and MRI. Chronic steroid overproduction results in skeletal osteoporosis. Diagnosis of osteoporosis is best done with bone mineral densitometry.

Conn’s syndrome results from overproduction of aldosterone either from an adrenal adenoma or bilateral hyperplasia (14). The distinction is crucial as it directly affects surgical management. A unilateral adrenalectomy is often curative for an aldosterone-secreting adenoma but has no role to play in bilateral hyperplasia. The pitfall is to remove a nonfunctional nodule or to fail to appreciate subtle hyperplasia in addition to a nodule. Conn’s is very rarely (less than 1%) the result of an adrenocortical carcinoma.

Aldosterone-producing adenomas are often small (less than 2 cm), compared to cortisol-producing adenomas requiring thin-section (3 mm) CT for detection (Fig. 5.1.5a). The average diameter is between 12 and 18 mm and 20% are less than 10 mm (15). CT can detect 82–88% (16, 17). Tumours less than 1 cm can be difficult to identify. Conn’s tumours usually have the lowest attenuation values of all hyperfunctioning adenomas (Fig. 5.1.5b) (18).

Hyperplastic glands may appear normal or show obvious symmetric enlargement. MRI has no real advantage over CT although high signal returned from the lesion on T2-weighted imaging may aid detection.

The definitive test is adrenal venous sampling with an accuracy rate of close to 100% (8, 14, 19). The ratio between aldosterone and cortisol in the venous blood from each adrenal is compared with peripheral samples. Baseline samples and samples following ACTH stimulation may be taken. A high ratio is present on the side with an adenoma, and a low ratio on the opposite side.

Androgen excess may be of ovarian or adrenal origin. Tumorous adrenal causes are mostly malignant. Imaging choices are similar to the investigation of Conn’s syndrome, that is, CT or MRI with venous sampling (with the addition of ovarian venous aspirates) or dexamethasone-suppressed adrenal scans in diagnostically difficult cases (10).

Feminization, for example gynaecomastia, due to adrenal oestrogen excess is rare. As with androgen excess of adrenal origin, the cause is most often an adrenocortical carcinoma of such a size that CT and ultrasonography are invariably helpful (Fig. 5.1.4c).

This may be responsible for any of the above syndromes or be relatively nonfunctional. They are readily seen on ultrasonography, CT, or MRI, as tumours are usually large at presentation although hyperfunctioning tumours are usually smaller at presentation, as a result of the endocrine effects (Fig. 5.1.4a–d) (20). Heterogeneity of some degree is usual. Calcification occurs in 30%. An adrenal origin may be difficult to determine on standard axial CT imagng if the tumours are large and invasive but CT reconstructions or MRI is more informative, using multiple planes and different sequences. Vascular and adjacent organ invasion is diagnostic of malignancy. They rarely contain significant amounts of intracellular lipid, which can be exploited diagnostically as malignant tumours therefore rarely lose signal on opposed MRI and generally feature low attenuation density values (<10 Hounsfield units (HU)) on CT.

This term refers to adrenal insufficiency. Autoimmune mechanisms are the commonest cause now that the incidence of tuberculosis has been reduced. CT may show atrophy or calcification. Tuberculous infection in the subacute stage produces enlarged adrenals, which may show peripheral enhancement around central necrosis. In the long term the glands calcify (Fig. 5.1.6a,b). Histoplasmosis produces similar appearances and half of patients with disseminated disease develop Addison’s disease (10, 15).

Bilateral adrenal metastases, even when large, rarely result in adrenal insufficiency (less than 20%), but symptoms of Addison’s disease may be confused for those of the malignancy (Fig. 5.1.7) (21).

Acute adrenal insufficiency as the result of bilateral adrenal haemorrhage or hypotension may complicate shock, sepsis, or bleeding disorders. High-attenuation swelling of the adrenals is the finding on CT performed acutely.

Rare causes of hypoadrenalism include haemochromatosis, when CT may demonstrate increased attenuation of liver and pancreas as a result of iron deposition and Wolman’s disease (lipid storage abnormality due to a deficiency of liposomal acid lipase) when the adrenals are enlarged and show diffuse punctate calcification.

Secondary hypoadrenalism is usually due to prolonged steroid therapy, but more rarely is a result of pituitary infarction or haemorrhage.

These tumours arise from the chromaffin cells of the sympathetic nervous system. Thus they most commonly arise in the adrenal medulla but can also be found in the neck, the mediastinum (including intrapericardiac), in a para-aortic position, in an accumulation of sympathetic ganglia at the base of the inferior mesenteric artery known as the organ of Zuckerkandl, and in the pelvis and bladder (Fig. 5.1.2 and 5.1.8) (22).

About 25% of apparently sporadic tumours are associated with familial conditions such as neurofibromatosis, and von Hippel–Lindau and multiple endocrine neoplasia (MEN) syndromes. These patients are more likely to have bilateral or multiple lesions (Fig. 5.1.9) (23).

Phaeochromocytomas are usually but not always benign. As with other adrenal tumours, benign and malignant phaeochromocytomas are distinguished by behaviour (i.e. metastasis or local invasion) rather than histology. However, the results of genetic analysis are usually predictive of malignancy risk and determine screening and follow-up strategies.

Adrenomedullary tumours are usually sizeable (greater than 5 cm) except when associated with the MEN syndromes. Therefore they can often be shown with ultrasonography and appear either homogeneous or heterogeneous with cystic or necrotic elements. CT is preferred, however, and will demonstrate the majority of adrenal phaeochromocytomas (77–98%) (23). About 10% may show calcification. These lesions usually enhance strongly on CT and heterogeneity corresponding to haemorrhage or necrosis is better appreciated after contrast medium enhancement, or on T2-weighted MR images. They are characteristically of high signal on T2-weighted MR sequences (20).The older intravenous iodinated ionic contrast agents can precipitate hypertensive crisis in the absence of pharmacological alpha and beta blockade (24,^). The almost ubiquitous nonionic contrast media used now do not carry the same risk and blockade is not now regarded as necessary (25).

CT is generally used to evaluate the adrenals and to search for ectopic sources (4). MR does not usually have any additional benefit.

Surgical planning for large or locally invasive tumours is helped by the multiplanar capabilities of multidetector CT or MR (Fig. 5.1.2). The mediastinal tumours, and especially the intrapericardiac lesions, are well shown with electrocardiographically gated MRI. The tumour can be expected to be markedly hyperintense on T2-weighted imaging. These lesions are often heterogeneous and vascular. Haemorrhage may occur leading to fluid–fluid levels and areas of high signal on T1-weighted images. Extension into the inferior vena cava is shown with flow-sensitive sequences, or with intravenous contrast enhancement (22, 28).

MIBG scanning is of great value in the imaging of phaeochromocytomas (Fig. 5.1.8). It is especially useful for the detection of extra-abdominal tumours and for the staging of malignant lesions, as the metastases are active (Fig. 5.1.10). It is 87% sensitive, and 97% specific (2, 4, 10). Whole-body imaging is straightforward and may be used for the initial imaging test, or to search for an ectopic tumour following a negative adrenal CT. CT, MRI, and MIBG scanning are equally accurate for detection of primary adrenal tumours.

MIBG is not specific for phaeochromocytoma; other tumours of neural crest origin such as neuroblastoma, carcinoid tumours, medullary carcinoma of the thyroid, Merkel-cell skin tumours, and nonfunctioning paragangliomas also show uptake, but this is not usually a clinical problem.

Other radionuclide methods used to demonstrate phaeochromocytomas include ¹¹¹In-octreotide scanning (2) and positron emission tomography with FDG (Fig. 5.1.11) or other radiopharmaceuticals such as ¹⁸F-fluoroDOPA, ¹⁸F-fluorodopamine, or¹¹C-hydroxyephedrine (4, 6, 22). ¹¹¹In octreotide is more useful for demonstration of metastatic disease than benign tumours (1). FDG and¹⁸F-fluorodopamine appear to be better than MIBG for metastatic disease and FDOPA is superior for extra-adrenal tumours and paragangliomas (23).

This tumour of infancy and childhood can arise in the adrenals (50%), in the abdominal sympathetic chain, or in the mediastinum. MIBG uptake is a feature, and can therefore be used for assessment of metastatic disease, although CT or MRI is more appropriate for the assessment of the local disease. Tumours are often nonhomogeneous on CT and MRI, and calcification is characteristic (which helps differentiate it from Wilm’s tumour of the kidney). Local invasion into the spine, and skeletal metastatic disease, can occur. The multiplanar capability of MRI allows demonstration of vascular and liver involvement, intraspinal spread, and marrow disease (29).

With the exponential increase in the use of modern imaging techniques adrenal masses are often recognized as incidental findings (4–6%). These are almost invariably benign in patients with no history of malignancy. They may be functional in terms of hormone synthesis and this is determined endocrinologically. The vast majority are, however, endocrinologically irrelevant, and are likely, statistically, to be benign if small. They are much more likely to be malignant if there is known primary malignancy, although less than 50% are metastatic. The differentiation of metastasis or malignancy from an incidental adenoma is therefore very important (30).

Comparison with old scans or follow-up examination is important—a lesion that changes in size over 6 months is highly likely to be malignant. A positive biopsy result might be regarded as the most definitive test short of surgery. However, these lesions may be small and difficult to sample without morbidity. A negative result is less reassuring because of concerns about sampling error. However, noninvasive techniques now often allow distinction of an adrenal adenoma from a metastasis.

The CT appearance may give some indication of the nature of an incidentally discovered adrenal mass. It may be evidently a cyst (i.e. thin-walled, well-defined, and of fluid density). If solid, benign lesions are usually homogeneous, although there may rarely be calcification. Frank areas of fat may indicate a myelolipoma. Malignant lesions may be irregular in outline, heterogeneous, perhaps with necrotic areas. The morphological appearance following contrast may be of value. Adjacent organ invasion or demonstration of metastasis is diagnostic.

The presence of a high proportion of intracellular fat in 70% of adenomas allows the use of CT density measurements and chemical shift MR imaging.

Adenomas are often readily apparent as hypoattenuating compared to kidney or liver on unenhanced CT (Fig. 5.1.3c and 5.1.5b). Mean attenuation values of adenomas are 2 HU,and of nonadenomas 30 HU (31). On thin-section unenhanced scans a density of 10 HU or less is indicative of a high proportion of intracellular fat, which suggests an adenoma with high specificity (98%) though poorer sensitivity (71%) (32–33).An upper threshold of 2 HU will be 100% specific for benign adrenal lesions at the cost of sensitivity. Quantitative enhancement and wash-out characteristics have been used effectively by many authors and relates to the fact that benign lesions lose enhancement more rapidly than malignant. The most commonly used threshold is 40% relative wash-out on a 15 min delayed scan (30, 34). This technique is proven even for lipid-poor adenomas.

Early users of MRI suggested that high signal intensity on T2-weighted images indicated a malignant lesion, benign lesions generally having signal intensity similar to normal adrenal; however, it became apparent that there was too much overlap (20–30%) for this to be a useful feature. Gadolinium contrast medium enhancement was likewise unreliable, even with the use of dynamic acquisitions (34). The most robust technique appears to be the use of chemical-shift imaging (30, 35). This utilizes the fact that the presence of fat within benign adenomatous cells alters the local magnetic environment, and hence the resonant frequency of the precessing protons. This results in a reduction of signal intensity of benign lesions (whose cells contain both lipid and water) on out-of-phase imaging. This feature can be seen in 95% of adrenal adenomas (Fig. 5.1.12). Normal adrenals also display this phenomenon but nonadenomatous lesions do not.

There is recent work indicating that MR spectroscopy can characterize adrenal masses as adenomas, carcinomas, phaeochromocytomas, or metastases but at present this can only be used for masses larger than 2 cm (36).

FDG-PET relies on the altered metabolism of cancer cells trapping this radiopharmaceutical which enters the glycolytic pathway in the place of glucose. It has been shown to accurately differentiate benign and malignant adrenal masses in the cancer patient with specificities of 90–96%, and sensitivities of 93–100% (6, 7). It is the most accurate test therefore to confirm that an adrenal mass is metastatic in the cancer patient. It is expensive but availability has rapidly increased in recent years.

A reasonable approach to the incidentally discovered adrenal lesion, whether in the setting of a known malignancy or not, is to perform density measurement on thin-section unenhanced CT, or delayed wash-out if indeterminate. On unenhanced CT if the density is less than 0 HU, malignancy is excluded. If less than 10 HU, malignancy is almost certainly excluded. In the range 10–20 HU in- and out-of-phase MRI is helpful. If greater than 20 HU it is less likely to resolve the issue due to the lack of intracellular lipid, and FDG-PET may be helpful.

Myelolipomas are benign and contain elements of fat and bone marrow (30). The fat is diagnostic and can be demonstrated on ultrasonography (hyperechoic), CT (low attenuation), or MRI (high signal on T1-weighting, focal loss of signal on fat-suppressed images, but not on opposed-phase sequences) (Fig. 5.1.13). However, fat is not always a dominant feature and the appearance of the lesion is then nonspecific. Haemorrhage may complicate the imaging features.

Adrenal cysts are endothelial (lymphangiomas and haemangiomas), epithelial (retention cysts, embryonal, or cystic adenomas), pseudocysts (resulting from previous haemorrhage), or echinococcal (hydatid). Of adrenal cysts, 15% show mural calcification, particularly in hydatid disease (37, 38).

The CT appearance of acute adrenal haemorrhage is of high-attenuation material expanding the adrenal gland or periadrenal haemorrhage leading to stranding, and an indistinct adrenal contour (Fig. 5.1.14). The high density may not be appreciated if only contrast-enhanced scans are available. Subacute haematomas are isodense with normal adrenal and indistinguishable from adenomas. Old adrenal haematomas may lead to calcification. Because of the paramagnetic effects of blood such as haemosiderin and methaemoglobin, MRI can be diagnostic of adrenal haematoma, although there will be a complex variation depending on the age of the lesion.

Adrenal tissue can be found in ectopic sites such as the coeliac plexus region, the broad ligaments, the testes, and the ovaries. These rests may then enlarge in pathological conditions such as congenital adrenal hyperplasia (Fig. 5.1.15) (39), or following ACTH stimulation such as occurs in Addison’s or Cushing’s diseases. This phenomenon may lead to the misdiagnosis of testicular or other tumours (40).