Adrenal Cysts and Myelolipomas

Classification of cystic lesions

In diagnostic imaging, five main types of cysts are distinguished, differing in origin and structure:

1. Endothelial (vascular). Most common (45%). Predominantly diagnosed in women (about 2/3 of cases); bilateral in 8% of observations. An important histological feature is that functional adrenal cortex tissue may persist in the wall.
2. Hemorrhagic (pseudocysts). Account for 39% of cases. Formed as a result of hemorrhage into a vascular or lymphangioendothelial cavity. Blood causes fibrosis and hemosiderin deposition. The mass enlarges due to a continuous influx of fluid and new hemorrhages. They occur in middle-aged women and are sometimes associated with Beckwith-Wiedemann syndrome (Beckwith-Wiedemann syndrome).
3. Parasitic. Most commonly caused by *Echinococcus*. They consist of two layers: the inner (germinal) layer synthesizes fluid, scolices, and the laminated membrane, while the outer layer provides nutrition for the parasite.
4. True (epithelial). Rare lesions of mesothelial origin. They can be embryonic, retention cysts, or develop within adenomas.
5. Lymphangiomas (Lymphangioma). An extremely rare pathology (0.06%), representing a thin-walled cavity lined with flattened endothelial cells.

MRI and ultrasound semiotics of cysts

A simple cyst is a typical incidentaloma that often remains unchanged in size for years. On MRI, it shows a homogeneous hypointense signal on T1-weighted images (T1WI) and a hyperintense signal on T2-weighted images (T2WI). Internal architecture is absent, and the wall is not thickened. Upon gadolinium administration, neither the capsule nor the contents enhance.

Parasitic lesions have a specific ultrasound appearance divided into five types:

• Type 1: Simple cavity without septa.
• Type 2: Specific 'water lily' sign — ultrasound shows detachment of the inner membrane.
• Type 3: Multiple complex septa and floating debris.
• Types 4 and 5: Scarring processes, wall thickening, and calcification.

Adrenal myelolipomas

Myelolipoma is a neoplasm composed of adipose tissue. It is usually asymptomatic, but large nodules can cause abdominal pain or hemorrhage. Interestingly, in 10% of cases, they are accompanied by adrenocortical dysfunction leading to Cushing's disease, hyperandrogenism, or hypertension due to excess catecholamines and aldosterone.

On MRI, the lesion appears large, with multiple foci of bright (hyperintense) signal on T1WI. The presence of fat is proven by signal drop on fat-suppressed sequences (fat saturation) and out-of-phase chemical-shift sequences (out-of-phase chemical-shift). The CT appearance is also specific: X-ray attenuation ranges from -30 to -50 HU, which fully corresponds to retroperitoneal adipose tissue. Treatment for small nodules is conservative, and for large ones, surgical.

Incidentaloma evaluation algorithm

The main task of the radiologist when discovering an incidental nodule is to prove its benignity (benignity). The algorithm consists of the following steps:

• Unenhanced CT. If the lesion is homogeneous with an attenuation of $\le$ 10 HU, the diagnosis of a benign adenoma is confirmed.
• Attenuation > 10 HU. CT with contrast washout calculation is required. Adenoma is confirmed if absolute washout is $\ge$ 60% and relative washout is $\ge$ 40%. When using chemical shift MRI, the signal must quantitatively decrease by more than 30%.
• Heterogeneous lesions. Imaging does not provide 100% accuracy. A multidisciplinary team (MDT) review is required.
• PET/CT. Not used as a first-line method. However, if the study was performed for another reason, radiopharmaceutical uptake at or below the liver level favors an adenoma.

Endocrine disorders and the role of diagnostic imaging

Clinically proven dysfunction requires imaging to locate the source of the problem. The goal is to find the lesion, assess its extent (unilateral or bilateral), and plan treatment.

Disorders are divided into three groups:

1. Cortical hyperfunction: Cushing's syndrome, Conn's syndrome, adrenogenital syndrome.
2. Medullary hyperfunction: pheochromocytomas, diffuse hyperplasia.
3. Cortical hypofunction (Addison's disease): caused by autoimmune aggression, granulomatoses (tuberculosis, sarcoidosis, histoplasmosis), amyloidosis, metastatic involvement, or hemorrhagic necrosis. Secondary deficiency due to ACTH deficiency also occurs.

Class and exam questions

What else to study on this topic

• Pathogenesis and imaging features of Beckwith-Wiedemann syndrome.
• MRI semiotics of malignant lesions and adrenal liposarcomas.
• Formulas for calculating absolute and relative CT contrast washout.
• Features of radiopharmaceutical uptake in PET/CT in metastases.
• Radiological manifestations of granulomatous lesions in Addison's disease.

Other topics in the section "Diagnostic Radiology of the Abdominal Organs"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.