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Introduction to Adrenals
Mitchell Tublin, MD; Ghaneh Fananapazir, MD, FSAR, FSRU, FSABI; Michael P. Federle, MD, FACR
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Anatomy, Embryology, and Physiology

  • The adrenal (suprarenal) glands lie in the perirenal space, usually cephalic to the kidneys. The right adrenal gland lies above the kidney, lateral to the crus of the diaphragm, medial to the liver, and touches the posterior aspect of the inferior vena cava. The left adrenal gland usually lies anterior to the upper pole of the left kidney, posterior to the splenic vein and pancreas. The splenic vein is a useful landmark in identifying the source of left upper quadrant masses that may be of uncertain origin. Adrenal masses generally displace the splenic vein forward, while pancreatic or gastric masses displace it posteriorly.
  • The adrenal cortex and medulla are essentially different organs that lie within the same structure. The cortex is an endocrine gland, secreting primarily cortisol, aldosterone, and androgenic steroids, all of which are derived from cholesterol esters. This contributes to the high lipid content that is characteristic of most adrenal cortical adenomas.
  • The medulla is derived from the neural crest and secretes epinephrine and norepinephrine.
  • Adrenal physiology is controlled by an elaborate interaction between the hypothalamus, pituitary, and adrenals. Stress results in the release of epinephrine and cytokines, which cause the pituitary to secrete adrenocorticotrophic hormone (ACTH), which in turn stimulates the adrenals to secrete cortisol. Cortisol and epinephrine are often regarded as "stress hormones." Elevated serum cortisol has a suppressing effect on the hypothalamus and pituitary, reducing further release of ACTH.
  • Cushing syndrome, due to excess cortisol, is characterized by truncal obesity, hirsutism, amenorrhea, hypertension, weakness, and abdominal striae. It is usually caused by adrenal hyperplasia (75-80% of cases) but may also result from an adrenal adenoma (20-25%), adrenal carcinoma (< 5%), or exogenous corticosteroid medication.
  • Conn syndrome is the eponym sometimes used for excess aldosterone and is characterized by hypertension, hypokalemia, alkalosis, muscle weakness, and cardiac dysfunction. Unlike Cushing syndrome, Conn syndrome is usually caused by an adrenal adenoma (65-70%). Adrenal hyperplasia accounts for most of the remaining cases (25-30%), while adrenal carcinoma is a rare cause.
  • Because patients with Cushing syndrome are symptomatic, the diagnosis of either pituitary or adrenal-induced cortisol excess is typically made biochemically, prior to imaging. Imaging (either MR or CT) performed after diagnosis usually easily localizes the pituitary or adrenal adenoma responsible for Cushing syndrome, thus obviating catheter angiography or other invasive tests. Conn adenomas, however, may be quite small, and traditional imaging may be problematic in the setting of elevated aldosterone.
  • Addison syndrome or disease refers to adrenal insufficiency and is characterized by hypotension, weight loss, and altered pigmentation. Among the causes of slow-onset adrenal insufficiency are autoimmune disease, which is the most common cause in developed countries. Tuberculosis and other infections remain common causes of Addison syndrome in the developing world, whereas metastatic disease and AIDS are encountered in all populations.
  • The most common cause of abrupt-onset adrenal insufficiency is adrenal hemorrhage, which may result from sepsis, shock, anticoagulation, or vasculitis. Abrupt withdrawal of corticosteroid medication and postpartum pituitary necrosis, known as Sheehan syndrome, also result in acute adrenal insufficiency. Prompt recognition and treatment of these conditions is critical.

Imaging Techniques and Protocols

  • Adrenal Protocol: CT

    • CT is the modality of choice for evaluating adrenal masses. It consists of a low-dose NECT. If the adrenal mass is ≤ 10 HU, this is diagnostic of an adrenal adenoma, and no further imaging is required. If the adrenal mass is > 10 HU, CECT is performed at 70 seconds and 15 minutes, and relative and absolute washout are calculated. Masses > 10 HU with an absolute washout of ≥ 60% or a relative washout of ≥ 40% are lipid-poor adenomas. Masses with significant macroscopic fat can be diagnosed as myelolipomas, and those with attenuation differences ≤ 10 HU are indicative of cysts or hemorrhage.
    • Adrenal Protocol: MR

      • Intracellular lipid content of adrenal adenomas can also be detected using chemical shift MR. Signal loss on opposed-phase images compared to in-phase images is considered to be diagnostic for adrenal adenoma. Given that a subgroup analysis shows chemical shift analysis inferior to CT in assessing nodules > 20 HU, CT is favored over MR in assessing adrenal nodules.
      • FGD PET/CT
      • FDG PET/CT is the modality of choice for evaluating large (> 4 cm) or enlarging masses where metastatic disease is the presumed diagnosis.

      Approach to Adrenal Mass

      • Adrenal nodules are commonly encountered on radiologic examination with a prevalence of 4% on CT. Most adrenal lesions are nonfunctioning adrenal adenomas. However, some may have a functional component to them, or may represent other adrenal masses, such as myelolipoma, pheochromocytoma, adrenocorticocarcinoma, lymphoma, or metastatic disease. Knowledge of when and how to work-up the incidentally discovered adrenal nodule is important to not overutilize resources but also not underdiagnose clinically significant adrenal masses.
      • Is it an adenoma?
      • If it's not an adenoma, what is it?
      • What else should I suggest regarding adrenal nodules?
      • Are all fat-containing adrenal masses adenomas?
      • How should we image for suspected pheochromocytoma?
      • How should we image for suspected adrenal metastases?

      Selected References

      1. Glazer DI et al: Management of incidental adrenal masses: an update. Abdom Radiol (NY). 45(4):892-900, 2020
      2. Mayo-Smith WW et al: Management of incidental adrenal masses: a white paper of the ACR incidental findings committee. J Am Coll Radiol. 14(8):1038-44, 2017
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      Anatomy, Embryology, and Physiology

      • The adrenal (suprarenal) glands lie in the perirenal space, usually cephalic to the kidneys. The right adrenal gland lies above the kidney, lateral to the crus of the diaphragm, medial to the liver, and touches the posterior aspect of the inferior vena cava. The left adrenal gland usually lies anterior to the upper pole of the left kidney, posterior to the splenic vein and pancreas. The splenic vein is a useful landmark in identifying the source of left upper quadrant masses that may be of uncertain origin. Adrenal masses generally displace the splenic vein forward, while pancreatic or gastric masses displace it posteriorly.
      • The adrenal cortex and medulla are essentially different organs that lie within the same structure. The cortex is an endocrine gland, secreting primarily cortisol, aldosterone, and androgenic steroids, all of which are derived from cholesterol esters. This contributes to the high lipid content that is characteristic of most adrenal cortical adenomas.
      • The medulla is derived from the neural crest and secretes epinephrine and norepinephrine.
      • Adrenal physiology is controlled by an elaborate interaction between the hypothalamus, pituitary, and adrenals. Stress results in the release of epinephrine and cytokines, which cause the pituitary to secrete adrenocorticotrophic hormone (ACTH), which in turn stimulates the adrenals to secrete cortisol. Cortisol and epinephrine are often regarded as "stress hormones." Elevated serum cortisol has a suppressing effect on the hypothalamus and pituitary, reducing further release of ACTH.
      • Cushing syndrome, due to excess cortisol, is characterized by truncal obesity, hirsutism, amenorrhea, hypertension, weakness, and abdominal striae. It is usually caused by adrenal hyperplasia (75-80% of cases) but may also result from an adrenal adenoma (20-25%), adrenal carcinoma (< 5%), or exogenous corticosteroid medication.
      • Conn syndrome is the eponym sometimes used for excess aldosterone and is characterized by hypertension, hypokalemia, alkalosis, muscle weakness, and cardiac dysfunction. Unlike Cushing syndrome, Conn syndrome is usually caused by an adrenal adenoma (65-70%). Adrenal hyperplasia accounts for most of the remaining cases (25-30%), while adrenal carcinoma is a rare cause.
      • Because patients with Cushing syndrome are symptomatic, the diagnosis of either pituitary or adrenal-induced cortisol excess is typically made biochemically, prior to imaging. Imaging (either MR or CT) performed after diagnosis usually easily localizes the pituitary or adrenal adenoma responsible for Cushing syndrome, thus obviating catheter angiography or other invasive tests. Conn adenomas, however, may be quite small, and traditional imaging may be problematic in the setting of elevated aldosterone.
      • Addison syndrome or disease refers to adrenal insufficiency and is characterized by hypotension, weight loss, and altered pigmentation. Among the causes of slow-onset adrenal insufficiency are autoimmune disease, which is the most common cause in developed countries. Tuberculosis and other infections remain common causes of Addison syndrome in the developing world, whereas metastatic disease and AIDS are encountered in all populations.
      • The most common cause of abrupt-onset adrenal insufficiency is adrenal hemorrhage, which may result from sepsis, shock, anticoagulation, or vasculitis. Abrupt withdrawal of corticosteroid medication and postpartum pituitary necrosis, known as Sheehan syndrome, also result in acute adrenal insufficiency. Prompt recognition and treatment of these conditions is critical.

      Imaging Techniques and Protocols

      • Adrenal Protocol: CT

        • CT is the modality of choice for evaluating adrenal masses. It consists of a low-dose NECT. If the adrenal mass is ≤ 10 HU, this is diagnostic of an adrenal adenoma, and no further imaging is required. If the adrenal mass is > 10 HU, CECT is performed at 70 seconds and 15 minutes, and relative and absolute washout are calculated. Masses > 10 HU with an absolute washout of ≥ 60% or a relative washout of ≥ 40% are lipid-poor adenomas. Masses with significant macroscopic fat can be diagnosed as myelolipomas, and those with attenuation differences ≤ 10 HU are indicative of cysts or hemorrhage.
        • Adrenal Protocol: MR

          • Intracellular lipid content of adrenal adenomas can also be detected using chemical shift MR. Signal loss on opposed-phase images compared to in-phase images is considered to be diagnostic for adrenal adenoma. Given that a subgroup analysis shows chemical shift analysis inferior to CT in assessing nodules > 20 HU, CT is favored over MR in assessing adrenal nodules.
          • FGD PET/CT
          • FDG PET/CT is the modality of choice for evaluating large (> 4 cm) or enlarging masses where metastatic disease is the presumed diagnosis.

          Approach to Adrenal Mass

          • Adrenal nodules are commonly encountered on radiologic examination with a prevalence of 4% on CT. Most adrenal lesions are nonfunctioning adrenal adenomas. However, some may have a functional component to them, or may represent other adrenal masses, such as myelolipoma, pheochromocytoma, adrenocorticocarcinoma, lymphoma, or metastatic disease. Knowledge of when and how to work-up the incidentally discovered adrenal nodule is important to not overutilize resources but also not underdiagnose clinically significant adrenal masses.
          • Is it an adenoma?
          • If it's not an adenoma, what is it?
          • What else should I suggest regarding adrenal nodules?
          • Are all fat-containing adrenal masses adenomas?
          • How should we image for suspected pheochromocytoma?
          • How should we image for suspected adrenal metastases?

          Selected References

          1. Glazer DI et al: Management of incidental adrenal masses: an update. Abdom Radiol (NY). 45(4):892-900, 2020
          2. Mayo-Smith WW et al: Management of incidental adrenal masses: a white paper of the ACR incidental findings committee. J Am Coll Radiol. 14(8):1038-44, 2017