The rationale for the ultrasound assessment of superficial tissues in patients with lymphedema does not lie in identifying intrinsic damage to the lymphatic system itself, as the resolution of standard ultrasound equipment used for this type of examination does not allow direct visualization of lymphatic vessels. Specifically, when affected by disease, the deeper canalicular component containing lymphatic collectors may become visible due to dilation and disruption of the fibrous scaffold; however, the subepidermal lymphatic plexus cannot be directly evaluated.
The objective, therefore, is to identify indirect tissue alterations that reflect lymphatic dysfunction, such as differences in echogenicity and thickness of the various layers of the skin and subcutis. In unilateral lymphedema, the healthy contralateral limb is always used as a point of comparison; in bilateral cases, previous examinations serve as the reference point.
Although the number of studies evaluating the role of ultrasound in lymphedema is still limited, several have laid the groundwork for its systematic use in clinical assessment. Of particular relevance is the study by Tassenoy et al. (2011), an observational study involving seven women with unilateral breast cancer who developed lymphedema. Limb volume increase was measured using water-displacement plethysmography, and ultrasound findings were correlated with MRI to assess tissue-structure changes [20].
Similarly, the retrospective study by Suehiro et al. (2013) examined 35 patients with secondary lower-limb lymphedema by evaluating the skin and subcutis at eight standardized points. In the subcutaneous tissue, three grades of echogenicity were identified. This study highlighted that variations in tissue echogenicity correlate with lymphedema stage according to the International Society of Lymphology, and that such evaluation is feasible using probes operating at 11 MHz [21].
One of the most influential studies demonstrating the feasibility of a standardized ultrasound assessment protocol in lymphedema was conducted by Mander et al. (2019). This study precisely identified distinct ultrasonographic patterns representing progressive histological degeneration in the dermo-epidermal complex (DEC) and subcutis (SUBC) of the upper limb after mastectomy. These findings laid the foundation for a more objective evaluation of lymphatic-system compromise [20,21,22].
Based on Mander’s work, characteristic ultrasound patterns can be identified in both the dermo-epidermal complex and the subcutis, each reflecting progressive stages of histological alteration. Specifically, for the dermo-epidermal complex, the following patterns may be observed:
• Dermal edema
This condition is characterized by increased DEC thickness and reduced echogenicity (hypoechoic dermis). It is caused by the dilation of the subepidermal lymphatic plexus, leading to leakage of fluid into the dermal interstitium and the formation of vessel-like structures between collagen bundles lacking endothelial lining (a phenomenon known as dermal backflow). The papillary dermis is typically affected earlier than the reticular dermis due to differences in vascular and lymphatic distribution and collagen architecture.
Some authors suggest an association between dermal edema and paresthesias, attributed to stretching and irritation of sensory nerve endings.
This acute-stage pattern is sonographically identified as F-DEC (fluid dermo-epidermal complex).
• Dermal sclerosis with infiltrative changes
This pattern shows a marked increase in DEC thickness, increased echogenicity (hyperechoic dermis), and loss of the typical trilaminar DEC structure. These findings are due to cellular infiltration and early collagen-fiber deposition.
This pattern reflects a subacute or evolving stage and is identified as S-DEC (sclerotic dermo-epidermal complex). It is considered partially reversible.
• Dermal sclerosis with fibrotic involution
This condition is characterized by the loss of the dermo-hypodermal interface, resulting in a homogeneous echogenic appearance across tissues, making it difficult or impossible to accurately measure individual layers. These changes are due to chronic collagen deposition, ultimately leading to dermal fibrosis.
This chronic, irreversible stage is identified as M-DEC (mixed or markedly sclerotic dermo-epidermal complex).
The normal pattern of the dermo-epidermal complex is labeled N-DEC.
Regarding the subcutaneous tissue, the following patterns may be observed:
• Dilation of lymphatic ducts
In this condition, the hyperechoic signal of the fibrous connective septa disappears and the subcutis becomes globally thickened. This disappearance is due to the dilation of the lymphatic collectors running within the fibrous strands, which leads to a marked separation of the adipose lobules (a cobblestone appearance). In some cases, dilated lymphatic collectors may cause a rupture of the fibrous septa, resulting in the formation of so-called lymph lakes. Unlike dilated lymphatic collectors, lymph lakes collapse under pressure from the ultrasound probe.
This pattern is identified as F-SUBC (fluid subcutaneous).
• Edema and infiltrative phenomena of adipose lobules
This condition is characterized by increased echogenicity of the subcutaneous tissue, poor visualization of the fibrous framework, and overall thickening of the subcutis. It is caused by an infiltration of fluid and cells into the stromal component of adipose lobules—i.e., at the intercellular level— resulting in a sclerotic-edematous appearance known as “snow-fall”. In addition, mechanical pressure within the lobules may lead to the formation of a network of microscopic fissures in which fluid can accumulate.
• Subcutaneous sclerosis with fibrotic involution
This condition shows increased echogenicity and reduced thickness of the subcutis. It results from the replacement of adipose lobules with fibrotic tissue and collagen fibers, producing a fibro-sclerotic pattern. When the subcutis reaches this stage, and when a dermo-epidermal complex already shows dermal fibrosis, the dermo-hypodermal interface may become indistinguishable.
These latter two patterns are classified as S-SUBC (sclerotic subcutaneous).
The normal pattern of the subcutis is labeled N-SUBC.
In clinical practice, differentiation between patterns is not always clear-cut, and features of different patterns may coexist within the same ultrasound image, producing blended or transitional appearances.