Postoperative mid-sternal lipogranuloma with milky discharge following surgery for gynecomastia: a case report

Article information

Arch Aesthetic Plast Surg. 2026;32(2):41-44

Publication date (electronic) : 2026 April 30

doi : https://doi.org/10.14730/aaps.2025.01522

Jun Mo Kim, Ji Seon Cheon, Woo Young Choi, Jeong Yeol Yang

Department of Plastic and Reconstructive Surgery, Chosun University College of Medicine, Gwangju, Korea

Correspondence: Ji Seon Cheon Department of Plastic and Reconstructive Surgery, Chosun University College of Medicine, 309 Pilmun-daero, Dong-gu, Gwangju 61452, Korea E-mail: jscheon@chosun.ac.kr

Received 2025 October 30; Revised 2026 March 11; Accepted 2026 April 13.

Abstract

INTRODUCTION

Lipogranuloma is a chronic inflammatory process that results from an immune response to lipid material within tissues. It may occur secondary to fat necrosis, trauma, or exogenous lipid injection [1-5]. Histologically, it is characterized by lipid-laden macrophages, multinucleated giant cells, and surrounding fibrosis [1].

Although lipogranulomas have been reported in multiple locations, including subcutaneous tissue, lymph nodes, and internal organs, their presentation in the breast or chest wall may mimic malignancy and cause diagnostic confusion [4,6-8]. In men, lipogranuloma has been described primarily in the scrotum or penis, usually after mineral oil injection [5].

Importantly, in the postoperative setting, lipogranuloma may clinically resemble infection, fat necrosis, or seroma formation by presenting as a firm mass with or without discharge, thereby complicating diagnostic assessment [4,9,10]. Because systemic inflammatory signs may be minimal and imaging findings are often nonspecific, granulomatous lesions of the male breast and chest wall may mimic malignancy or abscess [8-11]. Accurate clinicopathologic correlation is therefore essential to avoid misdiagnosis and unnecessary intervention.

To our knowledge, no case of lipogranuloma in the mid-sternal region following surgery for gynecomastia has been reported. This case is unique not only because it occurred in a male patient in the postoperative setting, but also because of its atypical midline location, away from the nipple-areolar complex, suggesting an uncommon inflammatory pathway or migration of lipid material.

CASE REPORT

A 35-year-old man presented with a firm, nonmobile mid-sternal mass that had appeared 2 months earlier. He had undergone bilateral gynecomastectomy for Simon grade IIa gynecomastia at an outside institution 6 months earlier through a periareolar incision with adjunctive power-assisted liposuction. Approximately 120 mL of lipoaspirate had been removed from each side. Liposuction was performed with a 3-mm cannula in a fan-shaped pattern extending toward the parasternal region, although direct suction over the sternal midline was not intentionally performed. Subcutaneous undermining or mechanical trauma in this area may theoretically have contributed to fat necrosis or lipid migration.

There was no pain, redness, or tenderness, but the patient reported persistent firmness in the central chest area. He had a history of hyperlipidemia but no endocrine abnormalities and no history of hormonal medication use, including finasteride or spironolactone. Two firm nodules measuring 1×1 cm and 1×2 cm were palpable over the sternal midline (Fig. 1). Laboratory findings, including complete blood count, erythrocyte sedimentation rate, and C-reactive protein, were within normal limits. Because the lesion was superficial and well localized on clinical examination, surgical exploration was planned.

Fig. 1.

Mid-sternal nodules following surgery for gynecomastia. Clinical appearance showing two firm, well-defined nodules at the mid-sternal region without erythema or tenderness.

A direct incision over the mass revealed milky white discharge, and bacterial culture showed no growth (Fig. 2). The two cavities were connected beneath the dermis. Surgical debridement and irrigation were performed, and antibiotics were prescribed prophylactically. Histopathologic examination demonstrated lipogranulomatous inflammation with lipid-laden macrophages, multinucleated giant cells, and fibrosis, consistent with a foreign-body reaction (Fig. 3). No epithelial lining, ductal structures, or glandular elements were identified. The absence of epithelial remnants argues against displaced ductal epithelium as the primary pathogenic mechanism and instead supports fat necrosis-associated lipogranulomatous inflammation. No evidence of malignancy or infection was found. At the 2-year follow-up, no recurrence or new lesion was detected (Fig. 4).

Fig. 2.

Intraoperative finding of milky discharge. Milky white fluid expressed through the incision, consistent with lipid material.

Fig. 3.

Histopathologic findings of lipogranulomatous inflammation. Section (hematoxylin and eosin, ×200) demonstrating lipid-laden macrophages and multinucleated giant cells.

Fig. 4.

Two-year postoperative follow-up. Complete healing was achieved without recurrence or new lesion formation.

DISCUSSION

This case demonstrates a rare postoperative complication—lipogranuloma with milky discharge—occurring in the mid-sternal region, distant from the periareolar incision used for surgery for gynecomastia. Two plausible mechanisms may explain the underlying pathogenesis.

One possible explanation is displacement of residual ductal epithelium with secondary ductal ectasia [9,11]. In patients with gynecomastia, ductal remnants may persist beneath the nipple-areolar complex. These epithelial elements could theoretically be displaced along subcutaneous tissue planes during surgical manipulation or liposuction and subsequently produce lipid-rich secretions, thereby triggering a localized granulomatous reaction. However, no epithelial lining or ductal structures were identified on histopathologic examination in the present case. Therefore, displacement of ductal epithelium is unlikely to be the principal pathogenic mechanism.

Alternatively, the lesion may have resulted from postoperative fat necrosis with secondary lipogranulomatous inflammation [1,3,5]. Mechanical trauma from liposuction or subcutaneous dissection extending toward the parasternal region may have caused adipocyte disruption, lipid release, and a foreign-body-type giant cell reaction. Given the lesion’s distance from the nipple-areolar complex and the absence of epithelial elements on histological examination, postoperative fat necrosis appears to be the more plausible explanation in this case.

In addition to these two proposed mechanisms, previous reports of implant-related lipogranuloma support the broader concept that displaced lipid or foreign material can provoke granulomatous inflammation remote from the original operative site. Granulomatous complications after gynecomastia and other breast procedures have been reported. Weniger et al. [10] described palisading granulomas at liposuction incision sites in patients undergoing surgery for gynecomastia, possibly associated with retained lubricant or suture material. Similarly, axillary and chest wall lipogranulomas have been reported after rupture of silicone or hydrogel breast implants, in which migrated silicone tracked along tissue planes and triggered delayed inflammatory responses [4,9]. These observations reinforce the concept that mechanical disruption and material migration along subcutaneous planes may result in granulomatous reactions at anatomically distant sites. The present case further expands this spectrum by demonstrating a midline sternal lipogranulomatous lesion following surgery for gynecomastia.

Although fat necrosis may theoretically occur at any site of mechanical trauma, certain anatomical and biomechanical characteristics may have contributed to mid-sternal localization in this patient. The relatively thin subcutaneous fat layer, increased dermal tension, and limited tissue compliance along the sternal midline may impair the dispersion of disrupted adipose material, thereby favoring focal lipid accumulation and a sustained inflammatory response. Furthermore, negative pressure and repeated cannula sweeps during liposuction could have facilitated tracking of liquefied adipose debris along subcutaneous tunnels toward the parasternal region.

Clinically, granulomatous lesions of the male breast and chest wall may mimic infection, seroma, or malignancy [5,12]. The principal differential diagnoses include fat necrosis, chronic abscess, and epidermal inclusion cyst. Fat necrosis typically presents with oil cyst formation and calcification, whereas chronic abscess is associated with positive bacterial culture results and neutrophilic infiltration. Epidermal inclusion cysts demonstrate a keratinizing squamous epithelial lining, which was absent in this case.

In the present case, preoperative imaging was not performed. Radiologic evaluation may be useful in selected patients, particularly when lesions are atypical or enlarging, or when the diagnosis remains uncertain. Imaging findings in granulomatous or postoperative breast lesions are often nonspecific, with substantial overlap among inflammatory, postoperative, and malignant conditions. On ultrasonography, these lesions may appear as hypoechoic or heterogeneous masses with indistinct margins, findings that may be seen in granulomatous mastitis, fat necrosis, or carcinoma [8,11-13]. Magnetic resonance imaging may demonstrate irregular margins and heterogeneous or early enhancement patterns that closely resemble invasive malignancy. In male patients, benign inflammatory or reactive conditions, including granulomatous mastitis and postsurgical changes, are well documented to mimic carcinoma on imaging [11-13]. Furthermore, previous procedures such as liposuction may result in subcutaneous fibrosis, fat necrosis, or fluid collections that further complicate radiologic interpretation [14].

Histopathologic examination demonstrated lipid-laden macrophages and multinucleated giant cells without epithelial components or microbial growth, confirming the diagnosis of lipogranuloma [1,3]. Although small postoperative lipogranulomatous or fat-necrotic lesions may occasionally resolve spontaneously, conservative observation was considered less appropriate in this case because of progressive enlargement of the mass and the patient’s substantial concern about possible neoplasia. Given the diagnostic uncertainty and the patient’s preference for definitive management, early surgical exploration was performed rather than continued observation.

From a preventive standpoint, meticulous surgical technique is essential. Minimizing subcutaneous undermining along the sternal border, ensuring complete glandular removal, achieving adequate hemostasis, and reducing dead space through meticulous closure and appropriate compression may reduce postoperative lipid accumulation. Postoperatively, adequate compression and prompt management of seroma or hematoma may further decrease the risk of secondary inflammatory reactions at distant sites.

This report is limited by the absence of preoperative imaging and the relatively short duration of follow-up. In addition, although postoperative fat necrosis appears to be the most plausible mechanism, definitive confirmation of lipid tracking along subcutaneous planes cannot be established on the basis of histopathologic findings alone. Larger case series or imaging-pathologic correlation studies are needed to further clarify the underlying pathophysiology.

This case highlights that lipogranulomatous inflammation may present at sites distant from the primary operative field following surgery for gynecomastia. Awareness of this entity is important when evaluating postoperative chest wall masses to avoid diagnostic confusion and unnecessary intervention.

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