Possible ARDS Following Cosmetic Lipolysis: A Case Report Urging Caution in Aesthetic Medicine

Introduction

Fat-dissolving agents, such as phosphatidylcholine, deoxycholate, or hyaluronic acid derivatives, are injected into subcutaneous fat to break down adipose tissue. Although these procedures are considered minimally invasive, they are not without risk. Reports of pulmonary complications, particularly acute respiratory distress syndrome (ARDS), highlight the potential severity of adverse outcomes associated with unregulated or improperly performed injections. Several case reports and series have documented serious pulmonary complications – such as pulmonary fat embolism, silicone embolism syndrome, and ARDS – following cosmetic fat-altering procedures. In this context, the study by Chaghamirzayi et al further delineated the clinical characteristics, diagnostic modalities, and outcomes of macroscopic fat embolism (MAFE) and microscopic intravascular fat embolism (MIFE) after liposuction. While MIFE refers to microscopic entry of fat into the circulation, leading to fat embolism syndrome, MAFE is characterized by macroscopic entry of fat with direct vascular obstruction [1]. A recent systematic review analyzing 137 reported cases of fat grafting–related complications demonstrated that 32.0% of patients presented with cardiopulmonary involvement. Diagnostic modalities were heterogeneous, including imaging studies and histopathological examinations. Supportive care was the primary therapeutic approach, yet the overall mortality reached 34.3%, and 88.6% of survivors were left with permanent sequelae [2]. Gai et al reported the case of a 19 year old woman who developed acute respiratory failure with bilateral pulmonary opacities visible on computed tomography (CT) shortly after undergoing liposuction and fat grafting; bronchoalveolar lavage revealed lipid-laden macrophages, confirming pulmonary fat embolism, and the patient recovered with noninvasive ventilation and steroidal treatment [3]. Another case in Brazil involved ARDS attributed to fat embolism in the postoperative period after liposuction and fat grafting; the patient responded well to alveolar recruitment maneuvers and lung-protective mechanical ventilation [4]. Kao et al conducted a systematic review of 40 patients (from 19 countries) with pulmonary fat embolism following liposuction and fat grafting. Chest CT confirmed pulmonary fat embolism in 100% of cases. Among all patients, 76% required mechanical ventilation, and 33% died. Notably, 69% of cases presented within 24 hours, and among those early-onset cases, 75% required mechanical ventilation and 33% resulted in death [5]. In the realm of silicone injections, a 28 year old woman developed seizures, respiratory failure, and ARDS following unlicensed gluteal silicone injections, which proved fatal despite intensive care unit (ICU) care [6]. Similarly, illegal silicone injections have been linked to diffuse alveolar damage, pneumonitis, hemorrhage, and ARDS – even requiring extracorporeal membrane oxygenation in some instances [7]. Collectively, these reports underscore that procedures marketed as minimally invasive, such as lipolysis injections or illicit silicone use, can precipitate life-threatening pulmonary complications. Early detection through imaging and bronchoalveolar lavage, combined with prompt respiratory support and corticosteroid therapy, is essential to improving outcomes [8].

Vietnam is one of the countries in the Asia-Pacific region witnessing a rapid rise in the demand for cosmetic procedures, particularly among women. In recent years, the number of individuals seeking aesthetic treatments has increased significantly, contributing to the proliferation of unlicensed cosmetic clinics. This trend raises serious public health concerns, as many complications are often underreported or deliberately concealed. Our clinical case of severe ARDS following the injection of fat-dissolving agents serves as a critical warning in the context of the widespread operation of unauthorized aesthetic practices.

Case Report

TIMELINE OF EVENTS:

The timeline of events was as follows. On day -45, the patient underwent session 1, which consisted of breast filler injection. No acute complications reported. On day -21, the patient underwent session 2, which consisted of a second breast filler injection. No acute complications reported. On day -2, the patient underwent session 3, which consisted of breast filler and fat-dissolving injections to the abdominal wall, shoulders, and thighs. The agents administered were Lignospan (lidocaine hydrochloride with epinephrine), Vline Body (water and lecithin), and Botox (botulinum toxin). At 30 minutes after the injection, she experienced the onset of bilateral chest pain, predominantly over the right anterior chest wall near the injection site; it was described as tightness and firmness without erythema, warmth, or swelling. Mild dyspnea also occurred. A transient episode of diarrhea developed and resolved within 24 hours. At 48 hours after injection, the patient experienced progressive worsening of chest pain and dyspnea. She remained afebrile, with no cough, sputum production, or other systemic symptoms. On day 0 (hospital admission), the patient presented to a primary health care facility with worsening respiratory symptoms, and was subsequently transferred to the respiratory center of a central hospital.

CLINICAL FINDINGS:

On admission, the patient was alert and oriented. Her vital signs were stable, with a heart rate of 80 beats per minute, blood pressure of 100/60 mmHg, body temperature of 37°C, and peripheral oxygen saturation (SpO₂) of 91% while receiving supplemental oxygen at 6 L/min via face mask. Chest auscultation revealed bilateral coarse crackles. Cardiac examination showed normal first and second heart sounds without murmurs. No erythema, swelling, or warmth was observed on the skin, although mild tenderness was noted over the right anterior chest wall at the site of a prior injection.

INVESTIGATIONS:

Initial laboratory evaluation showed a white blood cell count of 12.4 G/L with neutrophilic predominance (83.5%), hemoglobin level of 104 g/L, and a low procalcitonin concentration (0.07 μg/mL). The C-reactive protein level was moderately elevated (53.2 mg/L). Erythrocyte sedimentation rate (ESR) was markedly elevated, measuring 97 mm/h at the first hour and 120 mm/h at the second hour. Additional findings included serum albumin level of 34.1 g/L, D-dimer level of 0.47 μg/mL, brain natriuretic peptide level of 151 pg/mL, and interleukin 6 level of 39.47 pg/mL. Overall, leukocytosis and neutrophilia were only mild, and procalcitonin remained low. Liver function tests, renal function, cardiac biomarkers, creatine kinase, and serum electrolytes were within normal limits. On the third day after admission, the patient’s hemoglobin level dropped to 84 g/L (Table 1).

A multiplex polymerase chain reaction panel for respiratory pathogens yielded negative results. Chest multidetector computed tomography at presentation (Figure 1) excluded pulmonary embolism and macroscopic fat embolism but demonstrated diffuse bilateral pulmonary infiltrates. Transthoracic echocardiography revealed a pulmonary artery systolic pressure of 25 mmHg, preserved left ventricular ejection fraction (66%), and normal right ventricular size and function.

Follow-up multidetector computed tomography at the referral hospital (Figure 2) demonstrated bilateral diffuse ground-glass opacities and inflammatory consolidations, with a normal pulmonary arterial tree and no evidence of thromboembolism. Mild bilateral bronchial dilatation was also observed. Echocardiography confirmed normal left ventricular dimensions and preserved systolic function (ejection fraction of 79%), with mild pulmonary hypertension but no wall motion abnormalities, valvular disease, or intracardiac vegetations.

Peripheral blood and bone marrow examinations demonstrated hypercellular marrow on both aspirate and biopsy specimens, without evidence of parasitic infestation or hematologic malignancy.

TREATMENT:

The patient was diagnosed with ARDS in the setting of cosmetic surgery, with fat microembolism (MIFE) strongly suspected as the underlying cause. Initial empirical therapy consisted of intravenous ceftaroline, levofloxacin, and methylprednisolone 40 mg/day. At the referral hospital, supportive management included transfusion of packed red blood cells to maintain hemoglobin levels above 90 g/L, together with intravenous methylprednisolone 80 mg/day, meropenem 3 g/day and linezolid 1200 mg/day. Following this adjustment, the patient’s respiratory status gradually improved.

After 5 days of treatment, she was transitioned to oxygen via face mask at 8 L/min, maintaining SpO₂ above 95%. Antimicrobial therapy with meropenem and linezolid, as well as methylprednisolone, was continued. By day 7, oxygen support was reduced to nasal cannula at 4 L/min with sustained SpO₂ above 95%. Follow-up chest radiography showed regression of pulmonary infiltrates, and the methylprednisolone dose was tapered to 40 mg/day.

On day 11, the patient maintained SpO2 above 95% on room air. A follow-up chest CT scan revealed substantial improvement of bilateral pulmonary lesions (Figure 3). Oral corticosteroids were then gradually tapered: methylprednisolone 32 mg/day for 4 days, followed by 16 mg/day for 5 days, and 8 mg/day for 1 week after discharge.

OUTCOME AND FOLLOW-UP:

Following hospital discharge, the patient remained clinically stable and reported no recurrence of dyspnea. Oxygen saturation was maintained within the normal range on room air, and her functional status progressively improved. No new respiratory or systemic complications were observed during follow-up.

Discussion

PATHOGENESIS:

ARDS following cosmetic injections can result from multiple pathogenic mechanisms. One potential cause is mechanical fat embolism, whereby fat droplets or injected substances inadvertently enter the vascular system and obstruct the pulmonary capillaries, leading to ventilation–perfusion mismatch and respiratory compromise. A second mechanism involves a systemic inflammatory response, triggered by immunological reactions to foreign substances or their degradation products. This immune-mediated injury can result in diffuse alveolar damage, a hallmark of ARDS. Additionally, infectious complications arising from non-sterile injection techniques or contaminated materials can lead to sepsis, subsequently progressing to ARDS as part of a systemic inflammatory cascade. Understanding these underlying mechanisms is essential for timely diagnosis and targeted management of this potentially life-threatening complication [9,10]. In this patient, multiple cosmetic procedures had been performed in the weeks preceding presentation; however, all earlier interventions were uneventful and did not result in any acute complications. Among these, lipolysis injections warrant particular attention. Although the published literature is limited, some reports suggest that lipolysis injections may induce local tissue necrosis, fat microembolism, or immune-mediated inflammatory responses, which could contribute to the development of ARDS. The lack of microbiological evidence of infection, only modest elevation of inflammatory markers, and the patient’s rapid clinical and radiological improvement following corticosteroid therapy support a non-infectious, immune-mediated mechanism rather than acute infectious pneumonia. Further systematic evaluation of lipolysis-related cases is needed to elucidate the underlying pathophysiological pathways, including the potential roles of MIFE and exaggerated inflammatory responses [2].

DIAGNOSIS AND MANAGEMENT:

In their systematic review, Chaghamirzayi et al reported that patients with isolated MAFE typically developed symptoms such as respiratory distress, chest pain, or cardiac arrest within 12 hours of the procedure, with a mortality rate of 33.3%. In cases in which MAFE and MIFE coexisted, neurological deficits, cardiopulmonary complications, and cardiac arrest were observed, with mortality reaching 80%. The abrupt onset of dyspnea, chest pain, and cardiac arrest within 12 hours highlights the fulminant and life-threatening nature of this condition. By contrast, patients with MIFE alone often presented with respiratory or neurological manifestations, fever, or subcutaneous hemorrhage within or beyond 72 hours after the procedure, with a lower mortality rate of 15.4% [1]. In our case, chest pain occurred as early as 30 minutes after the procedure; however, hospital admission was delayed until 48 hours later, largely due to limited expertise at an unlicensed cosmetic facility.

The diagnosis of ARDS in the context of cosmetic procedures relies on a combination of clinical, radiological, and laboratory findings. Clinically, patients may present with progressive dyspnea, hypoxemia, and altered mental status. Chest CT typically reveals bilateral ground-glass opacities, while brain magnetic resonance imaging may be indicated in cases with suspected cerebral involvement. Laboratory investigations should include arterial blood gas analysis, inflammatory markers (eg, C-reactive protein, procalcitonin, interleukin 6), and microbiological cultures if infection is suspected. Although chest CT imaging excluded pulmonary embolism and MAFE, MIFE could not be definitively ruled out, as CT has limited sensitivity for this condition. Given the temporal relationship to the cosmetic injections and the rapid onset of symptoms, MIFE remained a strong diagnostic consideration, and the patient was treated accordingly in line with established guidance. A key limitation in this case is that bronchoscopy with bronchoalveolar lavage to identify lipid-laden macrophages was not performed, due to the patient’s respiratory instability at presentation. Similarly, urinalysis for fat droplets, as suggested in standard diagnostic protocols, was not obtained, representing another shortcoming of the diagnostic workup. When evaluated against the Gurd and Wilson criteria for fat embolism syndrome, our patient fulfilled several supportive features [11]. Major criteria included respiratory insufficiency, which was clearly present, and unexplained anemia, which was also documented. Among the minor criteria, tachycardia and fever were absent; however, hypoxemia, elevated inflammatory biomarkers (C-reactive protein, interleukin 6), and a markedly increased ESR of 97 mm/h at the first hour and 120 mm/h at the second hour) indicated a significant systemic inflammatory response. Although the full set of diagnostic tests was not completed, the constellation of findings – acute respiratory distress, hypoxemia, unexplained anemia, elevated ESR, and the temporal association with cosmetic injections – is consistent with the diagnostic framework for fat embolism syndrome. This further supports the suspicion of microscopic fat embolism as a plausible mechanism underlying the patient’s presentation.

Management is largely supportive and includes oxygen supplementation, with escalation to high-flow nasal cannula or mechanical ventilation in severe cases. Systemic corticosteroids can be beneficial in reducing inflammation and capillary leak, although their use should be individualized. Empirical antibiotic therapy is indicated when there is clinical suspicion of secondary infection. Admission to the ICU is warranted for patients with severe hypoxemia or respiratory failure.

The patient’s prognosis was relatively favorable due to timely intervention with high-flow nasal cannula oxygen therapy, systemic corticosteroids, and intravenous antibiotics. The patient responded well to treatment, with rapid improvement in pulmonary lesions.

RECOMMENDATIONS:

An important limitation of this report is the lack of detailed procedural information. Specific data regarding the total volume of each substance injected, the precise injection technique (eg, needle vs cannula, depth of injection), and the professional accreditation of the practitioner were not available, as the procedures were performed in an unlicensed cosmetic facility. This lack of documentation underscores a critical issue: unregulated aesthetic interventions not only increase the risk of complications but also hinder proper clinical assessment and management when adverse events occur. The absence of standardized procedural records can delay diagnosis, obscure causal relationships, and limit the ability to compare cases across the literature. Our case therefore highlights the urgent need for strict regulation of cosmetic procedures and for such interventions to be carried out only in accredited medical centers with appropriate documentation and emergency preparedness. In our patient, the unavailability of accurate procedural details posed a significant challenge in identifying the exact cause of lung injury and limited the ability to determine the mechanism of ARDS. This further illustrates how unsafe cosmetic practices can compromise patient safety and scientific understanding.

To minimize the risk of ARDS and related complications, fat-dissolving injections should be administered only by licensed and trained healthcare professionals under sterile conditions. Patients must be thoroughly counseled on the potential for life-threatening adverse events. Close post-procedural monitoring is critical for early recognition and intervention. Furthermore, stricter regulatory oversight is necessary to prevent unlicensed or unsupervised cosmetic interventions that may pose significant public health risks.

Conclusions

This case highlights a possible association between lipolysis injections and the development of ARDS. Although evidence from a single case report is inherently limited and does not allow for causal inference, the clinical course suggests a non-infectious, immune-mediated mechanism. The findings underscore that even minor cosmetic procedures, such as fat-dissolving injections, can occasionally result in severe, life-threatening complications. Therefore, all aesthetic interventions should be performed only in licensed medical facilities equipped with adequate emergency response capabilities. Clinicians involved in both cosmetic and respiratory care should remain vigilant for this rare but potentially fatal complication, as early recognition and prompt immunosuppressive therapy may improve outcomes. Further studies are warranted to clarify the potential risks and underlying pathophysiology.