Correlation Between Macroscopic Features of Ischemic Skin Injury and Subdermal Plexus Damage in Lipoabdominoplasty

Abstract

Background:

Skin necrosis after lipoabdominoplasty occurs in 1%–2.7% of cases. Before tissue necrosis develops, there is a transition period characterized by distinct ischemic injuries triggered by different mechanisms that can be identified macroscopically in the skin. Until now, these ischemic lesions have not been classified from a pathological macroscopic perspective, nor have their distinct patterns of presentation and evolution been described. This lack of classification has made understanding and appropriate management more challenging. This study aimed to classify the patterns of skin ischemic injury analyzing damage to the subdermal plexus, as revealed through macroscopic pathological examination of the skin lesions.

Methods:

This multicentric, retrospective study included 71 patients who underwent lipoabdominoplasty and developed ischemic lesions postoperatively. The study involved 46 surgeons and 2 hyperbaric oxygen therapy centers, both of which participated by completing a questionnaire that collected information about the associated treatments and lesion features. Skin lesions were classified into 3 groups based on macroscopic pathological criteria: (1) dotted pattern, (2) geometric pattern, and (3) geographic pattern. These classifications were correlated with the treatments performed and lesion locations.

Results:

The most frequent ischemic lesions were observed in the distal part of the abdominal flap (n = 49, 69%), presenting a dotted pattern and a worse prognosis. Lesions in atypical locations (n = 23, 32%) demonstrated an association with the concomitant use of energy devices, exhibiting a geographic macroscopic pattern.

Conclusions:

Ischemic lesions exhibit well-defined and distinct macroscopic patterns, which are closely related to their triggering mechanisms.

Takeaways

Question: Is it possible to classify the patterns of skin ischemic injury based on damage to the subdermal plexus?

Findings: There are distinct macroscopic patterns among ischemic lesions in abdominoplasty, each potentially linked to specific triggering mechanisms. These insights are crucial for improving the understanding, prevention, and treatment of necrosis.

Meaning: There are different patterns of ischemic lesions in abdominoplasty.

INTRODUCTION

Flap ischemia is a multifactorial condition. In traditional abdominoplasty dissection, the abdominal flap is undermined up to the costal margin, cutting the periumbilical perforators and smaller vessels originating from the rectus abdominis muscles. Consequently, the flap relies solely on the intercostal perforators at the costal margins and the vessels extending from the lumbar flank (defined by Huger¹ as zone III). This blood supply must traverse 2 vascular zones to reach the flap tip. The lower midline, being the farthest from the blood supply, is most prone to ischemia.^1,2

Skin necrosis, a rare postoperative complication, can lead to abdominoplasty flap dehiscence, often presenting with decreased temperature in the affected area and slow capillary refill. This complication arises due to insufficient perfusion, with reported rates ranging from 1% to 2.7% in the literature.^3–5

However, a transition period precedes tissue necrosis, during which ischemic areas with varying characteristics and causes are evident. These ischemic injuries may present as irregular or uniform changes in skin color, each with different evolution patterns. The decisive factor for the vascular viability of the abdominal flap is the presence of a reliable blood supply (remaining perforating vessels) and an intact distribution network (subdermal plexus) during liposuction and flap manipulation.^1,3

The subdermal plexus plays a pivotal role in distributing blood flow to the distal portion of the abdominal flap. Collateral blood supply from adjacent vascular zones further supports the subdermal distribution network.⁶ Consequently, all ischemic lesions that may progress to necrosis arise due to disruptions in the functioning of the subdermal plexus. These disruptions can be classified into 2 groups:

1. Ischemic injury with preservation of the subdermal plexus.

2. Ischemic injury with direct damage to the subdermal plexus.

In both scenarios, if there is a definitive interruption of blood flow, regardless of the cause, necrosis will inevitably occur. This study aimed to classify the patterns of skin ischemic injury by analyzing damage to the subdermal plexus, as revealed through macroscopic pathological examination of the skin lesions.

METHODS

This retrospective, multicentric study was conducted across 9 months (January to September 2024) in accordance with the Declaration of Helsinki, with signed written informed consent obtained from all participants. The study included 71 female patients who underwent circumferential liposuction and abdominoplasty and subsequently developed ischemic lesions during the postoperative period. These patients were treated at different centers and received various associated treatments, including conventional liposuction (suction-assisted liposuction [SAL]); power-assisted liposuction (PAL); and energy-based devices such as ultrasound, radiofrequency, and/or plasma. Treatments were administered either individually or in combination and were classified accordingly.

The study involved 46 surgeons and 2 hyperbaric oxygen therapy centers, both of which participated by completing a questionnaire. Data were collected through a simple questionnaire completed by the surgeons or specialized hyperbaric medicine treatment centers. The questionnaire recorded details about (1) the type of surgery performed, (2) the associated treatments administered, (3) the progress of the injuries, and (4) the location of the lesions. Additionally, 1 or more digital photographs of each patient’s lesion(s) were taken at the time of diagnosis and attached to the responses. The inclusion criteria were patients who had undergone lipoabdominoplasty and presented with skin ischemic lesions in any area addressed during surgery. The associated treatments (SAL, PAL, or energy-based devices) combined with lipoabdominoplasty were analyzed in correlation with the macroscopic pattern and location of the lesions.

Macroscopic Pathology Classification

The ischemic skin injuries were classified according to macroscopic pathology criteria^7,8 by the authors and then classified into 3 main groups:

1. Dotted pattern: noncontinuous, progressive, and coalescent lesion; small, circular areas of skin discoloration; and red, purple, or darkened dots (Fig. 1).

2. Geometric pattern: well-defined discoloration, edges, and angles. (See figure, Supplemental Digital Content 1, which displays a geometric pattern in the lower abdomen [A]. Note the square-shaped lesion area not continuously interposed by a segment of normal tissue, corresponding to the fold of the garment fabric. B, Geometric pattern in the lower abdomen, standing out from other areas of vascular damage, https://links.lww.com/PRSGO/E270.)

3. Geographic pattern: irregular edges, uniform red or purple discoloration, and nonprogressive, resembling maps or large patches (Fig. 2).

Fig. 1.

Macroscopic skin ischemic patterns. A, Dotted pattern lesion in the lower abdomen. Note the characteristic triangular shape. B, Dotted pattern lesion magnified to highlight the coalescent characteristic.

Fig. 2.

A, Geographic pattern in the upper abdomen. B, Geographic pattern in the upper abdomen. Note the regular borders and homogeneous texture.

Lesion Location

The lesions were divided into 2 groups based on their location:

1. Typical: infraumbilical triangle area.

2. Atypical: any location other than group 1, such as the flank, back, or upper abdomen.

Statistics

The statistical procedure adopted considered the analysis of the association between surgical approaches and different locations and patterns of lesions, and the results were presented in terms of absolute and relative frequencies, in addition to the statistical significance of the hypothesis tests performed. The Fisher exact test was used in the bivariate association analysis to verify the existence of significant differences in the distribution of the categories of variables. The χ² test of homogeneity compared the frequencies of the lesion patterns and locations for each treatment. A significance level of α equal to 0.05 was adopted for all statistical tests performed; therefore, for a P value of 5% or more, the null hypothesis should not be rejected. All statistical analyses were performed with R software version 4.4.2.

RESULTS

Among the 71 patients, 58 (41%) underwent lipoabdominoplasty combined with 1 or more types of energy-based devices. The remaining 13 patients received only associated liposuction, with 9 (6%) undergoing PAL and 4 (2.8%) undergoing conventional liposuction (SAL).

Ischemic Lesions

The surgical approach (SAL, PAL, or energy devices) combined with lipoabdominoplasty was correlated with the macroscopic pattern of the lesions (Table 1). Statistical analysis showed significance, associating the combination of treatments (energy-based devices) with the geographic pattern of skin lesions (all but renuvion + PAL). The use of PAL alone showed an association between surgical treatment and the lesion pattern. SAL applied alone did not demonstrate any association with location, although all cases that performed SAL presented the dotted pattern. This fact is attributed to the small number of patients who underwent this type of treatment in the sample.

Table 1.

Ischemic Skin Lesions Correlated to the Treatment Performed

Pattern	Treatment						Fisher, P
	US + PAL	P + PAL	RF + PAL	US + P + PAL	PAL	SAL
Dotted pattern (n = 49)	11	13	1	12	8	4	0.0426
Geometric pattern (n = 6)	1	2	0	1	1	1
Geographic pattern (n = 23)	4	6	2	10	1	0
χ2, P	0.007	0.012	0.368	0.011	0.007	0.074

P, plasma; RF, radiofrequency; US, ultrasound.

The Fisher exact test was applied to analyze the association between the type of treatment (combination or individual) and the patterns of skin lesions, which indicated a statistically significant association (P = 0.0426). A tendency toward a higher frequency of lesions associated with combined treatments was observed.

Type of Injury and Location

The lesions were classified based on their location and macroscopic appearance, as shown in Figure 3.

Fig. 3.

Skin lesion distribution by location and macroscopic appearance. A, Typical (geometric, n = 6, in yellow and dotted, n = 49, in blue). B, Atypical (geographic, n = 23, in red).

Surgical Approach and Location

The most frequent ischemic lesions occurred in the distal part of the abdominal flap (n = 49, 69%), presenting a dotted, coalescent, and progressive pattern (Table 2). PAL and SAL demonstrated a statistically significant association between the location and pattern of injury. Additionally, in this distal area of the flap, lesions with a geometric pattern featuring well-defined angles were identified (n = 6). All patients exhibiting this pattern of distal injury developed partial or full-thickness necrosis. Five patients had both geometric and dotted patterns of injury concurrently.

Table 2.

Surgical Approach Added to the Lipoabdominoplasty Correlated to Skin Lesion Location

Location	Treatment						Fisher, P
	US + PAL	P + PAL	RF + PAL	US + P + PAL	PAL	SAL
Typical location (n = 48)	6	12	3	16	7	4	0.046
Atypical location (n = 23)	4	7	2	9	1	0
χ2, P	0.527	0.251	0.655	0.002	0.003	0.046

P, plasma; RF, radiofrequency; US, ultrasound.

Lesions in atypical locations were more frequent with the concomitant use of energy devices (n = 23, 32%), exhibiting a well-defined, nonprogressive geographic macroscopic pattern. The Fisher test was applied to analyze the association between the type of treatment (combination or individual) and the location, which indicated a statistically significant association (P = 0.046). Flanks and upper abdomen were the most frequent locations (87%). Ten patients exhibiting this pattern showed total or partial remission of the lesion after combined treatments using hyperbaric chambers and vasodilators. Only 1 patient had a geographic pattern lesion in an atypical region (back) without the use of energy devices (only PAL).

Three patients presented with concomitant lesions in both the distal region of the flap and atypical locations. Twenty patients had lesions exclusively in atypical locations.

DISCUSSION

Flap ischemia is multifactorial. In traditional abdominoplasty dissection, the flap is undermined all the way to the costal margin, cutting the periumbilical perforators and the smaller vessels arising from the flat muscles. The flap then relies solely on the intercostal perforators at the costal margins and the vessels extending from the lumbar flank (territory defined by Huger¹ as zone III). This blood supply must cross 2 vascular zones to reach the flap tip. The lower midline, being the farthest from the blood supply, is the most prone to ischemia. Tension in skin closure further exacerbates ischemia.²

Despite being a rare complication, skin necrosis can lead to abdominoplasty flap dehiscence, often presenting with decreased temperature and slow capillary refill. The occurrence rate ranges from 1% to 3% in the literature. The sequelae are often caused by insufficient perfusion secondary to blood flow interruption (due to microthrombi, direct trauma, or vasoconstriction), excess traction, tight garments, or underlying pathology associated with poor wound healing, such as diabetes, lupus, and sickle cell disease.^3,9

Regarding the prevention of ischemic lesions, certain medications can aid in maintaining blood flow when the subdermal plexus remains intact. Pedretti et al¹⁰ demonstrated that pentoxifylline, when administered subcutaneously, effectively enhances skin flap survival by promoting tissue repair mechanisms, stimulating angiogenesis and reepithelization, and reducing fibrogenesis. Pentoxifylline can be safely used orally at a dose of 400 mg, 4 times a day to improve the vascular performance of the flap and aid in the treatment of ischemic skin lesions.

The use of externally based energy technologies (plasma and radiofrequency) can promote variable and, sometimes, unpredictable degrees of subcutaneous tissue retraction, regardless of the mechanism of action, and some degree of thermal energy is generated, acting on the fibroseptal network or interstitial connective tissue. Thermal energy promotes coagulation, dehydration, and protein denaturation of these structures, causing scar shortening, and consequently increasing the tension and traction of adjacent tissues.¹¹

Transitional Ischemic Injury

Before tissue necrosis sets in, there is a transition period during which ischemic injuries can be identified macroscopically in the skin. Ischemic areas of varying characteristics and causes precede the definitive lesion. These injuries may present with changes in skin color and texture, which can be irregular or uniform and may evolve differently over time.⁷

It is essential to understand that different causative mechanisms will lead to different transitional ischemic lesions, but all have the potential to progress to tissue necrosis. Until the present study, ischemic damage had not been classified from a pathological macroscopic perspective, nor stratified into distinct profiles of presentation and evolution. Previously, all transitional ischemic lesions were considered similar, which made understanding and managing them appropriately difficult.

The decisive factor for the vascular viability of the abdominal flap is the presence of a reliable source of blood supply (remaining perforating vessels) and an intact distribution network (subdermal plexus) during liposuction and flap manipulation.^11,12 The subdermal vessels have a degree of axiality that plays an important role in flap vascularization. Since Imanishi¹³ proposed the concept of the thin flap in 1988, several thin flaps in the abdominal region have been reported. Knowledge of the characteristics of the subdermal plexus, particularly the direction of blood flow, may be critical for designing thin flaps, as this plexus is the remaining and primary source of vascular nutrition for the flap.^13,14

In this series, we were able to identify ischemic injuries that occurred with either a preserved or damaged subdermal plexus, based on macroscopic findings and corresponding pathophysiological mechanisms. Both conditions can lead to partial or total obstruction of blood flow, either temporarily or permanently.

Ischemic Injury With Preservation of the Subdermal Plexus

Experimental studies have suggested that ischemic areas may be associated with the presence of microthrombi, even when the subdermal plexus remains intact.^13–15 These studies indicate that the underlying mechanisms are related to a reduction in vessel lumen, which subsequently leads to the formation of microthrombi and focal perivascular hemorrhage. The thrombus is replaced by immature granulation tissue, rich in newly formed capillaries, fibroblasts, collagen, and with a reduced inflammatory infiltrate. According to the literature, these findings are specific to cellular and microscopic changes, resulting in a characteristic macroscopic appearance (dotted pattern) that visually represents these microscopic alterations and signifies a partial or total obstruction of blood flow as a chain reaction.^7,8,16

In this group, macroscopic pathology analysis revealed coalescent dotted skin lesion patterns that evolved during several days and responded minimally to treatments such as vasodilators and hyperbaric therapy, eventually leading to definitive necrosis. These lesions were consistently found in the distal region of the abdominal flap, typically with a triangular shape (a characteristic area). A poor response to treatment indicates that, similar to the intact plexus, there is a mechanical obstruction caused by microthrombi.

This finding supports the idea that when a traction force is applied to an elastic structure, such as a flap, the greatest deformation occurs nearest to the point of traction. This deformation in the distal flap leads to the narrowing of local vessels, increasing the risk of stasis, turbulent blood flow, and subsequent microthrombus vascular occlusion. Once microthrombi form, the condition becomes nearly irreversible. Importantly, this mechanism operates independently of direct damage to the subdermal plexus; instead, the mechanical deformation of the tissue disrupts the local vascular architecture, triggering a cascade of events that can result in ischemia.

This process also explains why this portion of the flap is more sensitive to external compression (such as from garments) as a promoter of vascular obstruction. However, in this study, we identified a distinct macroscopic pattern of lesions that was likely triggered primarily by external compression. In these cases, we observed a lesion with a well-defined geometric pattern, corresponding to the area of greatest external pressure (folds in the compression fabric), which caused obstruction with a very specific macroscopic appearance (well-defined angles). These areas with sharp angles stood out from the other regions of vascular distress and, in some cases, showed areas with preserved vascularization. Therefore, this type of lesion can be considered a subgroup of obstructive lesions with a preserved subdermal plexus, located in typical areas.

Ischemic Injury With Subdermal Plexus Damage

A specific macroscopic pathology pattern was observed in this group. The lesions were all located in atypical and varied areas (flank, back, upper abdomen) and presented well-defined (geographic) features, with uniform discoloration and distinct margins. The lesion showed a delimited area at a single point in time, without a progressive coalescent feature.⁷ An important finding is that this type of lesion can be either permanent or transient, responding in some cases to salvage measures.

In this group, 10 out of 23 (43%) patients showed total or partial remission of the lesion after combined treatments using hyperbaric chambers and vasodilators (Fig. 4). This behavior is attributed to the fact that these lesions were linked to direct trauma to the subdermal plexus, either mechanical (trauma caused by the liposuction cannula) or thermal (caused by energy devices). The causative agent can lead to transient disruption in the plexus, such as edema in the endothelial cell layer without structural breakdown, temporarily obstructing its flow. On the other hand, more severe injuries, such as damage to the intima layer of the vessel, complete thermal injury to the plexus, or destruction by mechanical trauma, result in definitive interruption and subsequent total necrosis of the affected area, either due to anatomical discontinuity or microthrombi formation. This is evident in 13 out of 23 (56%) cases, where even after combined treatment, the lesions evolved into necrosis.

Fig. 4.

Area of partial remission of ischemic injury (blue arrows) and area of remaining injury (yellow arrows) after treatment in a hyperbaric oxygen chamber.

Ultimately, all lesions are related to some degree of vascular occlusion. Permanent obstructive lesions (due to microthrombi and definitive trauma to the plexus) have the worst prognosis, whereas partial endothelial lesions may be transient.^6,16 Therefore, accurate and early diagnosis of the type of injury and its triggering mechanism is crucial. In this series, the best success rates occurred when salvage treatment was initiated within the first 12–24 hours. After 48 hours, all cases showed little or no response to treatment.

Causality

It is important to note that this study does not establish a causal relationship between the methods or devices used in conjunction with lipoabdominoplasty and vascular injury. Instead, this series identifies a tendency toward an association between external factors and injury to the plexus. Statistical analysis showed significance, associating the combination of treatments (energy-based devices) with the geographic pattern of skin lesions. However, direct causal factors cannot be pinpointed because many patients received multiple associated treatments (58 patients, 41%), introducing a potential bias into the analysis. To demonstrate a causal correlation, the design of the study should be modified.

Several factors may contribute to the development of ischemic injuries, leading to lesions that exhibit mixed characteristics. Moreover, the same patient may show varying lesion patterns at different locations. Notably, a tendency toward association was observed in patients using energy devices, which resulted in distinctive injuries located in atypical regions, following a geographic pattern. In contrast, distal lesions with dotted patterns seem to be related to factors such as devascularization, tension, or traction on the flap, as seen in abdominoplasty procedures.

A total of 46 different surgeons with different learning curves and experience, using various combined techniques and approaches, and distinct levels of flap thickness and definition, can introduce bias in the causal mechanisms of ischemic injury. Despite the study’s limitations, which include sample heterogeneity resulting from diverse treatments, surgeons, medical centers, and ischemia treatment protocols, patients were treated as their own controls. This methodology facilitated individualization and effectively addressed the heterogeneity of the sample during data collection.

For the first time, this study correlated macroscopic skin pathology lesions with the damage process of the subdermal plexus. Lesions with a geographic pattern in atypical locations may be fully or partially reversible and are associated with the use of energy devices. However, lesions with a dotted pattern in the distal part of the flap have a worse prognosis. Based on these findings, it can be concluded that distinct macroscopic patterns exist among ischemic lesions, each potentially linked to specific triggering mechanisms. These insights are crucial for improving the understanding, prevention, and treatment of necrosis.

DISCLOSURE

The authors have no financial interest to declare in relation to the content of this article.