A rare case of pulmonary fat embolism with acute respiratory distress syndrome after thigh fat circumferential extraction and hip fat autologous transplantation

Abstract

Pulmonary fat embolism is the most severe form of fat embolism syndrome and typically occurs after fractures. However, it is not commonly reported in patients who have undergone liposuction and fat transplantation. A female patient in her early 40s was admitted to the hospital with chest tightness and shortness of breath that had lasted 2 h. Liposuction and fat transplantation (thigh fat circumference, buttock fat transplantation, and filling) were performed under general anesthesia before disease onset; subsequently, she experienced chest tightness and shortness of breath and exhibited decreased oxygen saturation in the peripheral blood. Chest computed tomography combined with red oil O staining of bronchoalveolar lavage fluid samples enabled early and rapid diagnosis of pulmonary fat embolism. The patient was treated with noninvasive mechanical ventilation and short-term glucocorticoid therapy, following which she showed rapid recovery. Considering that the clinical diagnosis of pulmonary fat embolism is very challenging and this condition is commonly misdiagnosed or missed, early diagnosis and appropriate treatment are critical. We aimed to enhance clinicians’ knowledge and understanding of pulmonary fat embolism to facilitate early diagnosis and treatment.

Introduction

Fat embolism syndrome (FES) refers to a series of symptoms and signs caused by the entry of fat particles or their inflammatory factors as well as vasoactive ammonia into the circulatory system after trauma, followed by the embolization of tissues or organs such as the lungs, brain, and skin. ¹ It often manifests as dyspnea, central nervous system dysfunction, and skin ecchymosis, representing a “triad” of clinical syndromes. Pulmonary fat embolism (PFE) is a serious complication that usually occurs after traumatic fractures; however, it is rarely reported after liposuction and fat transplantation. Due to its rapid onset, rapid progression, and complex clinical manifestations, PFE is frequently misdiagnosed or overlooked in the early stages. Herein, we present a case of PFE associated with acute respiratory distress syndrome following autologous fat transplantation. The clinical diagnosis of PFE poses significant challenges, often leading to misdiagnosis or missed diagnosis. This study aimed to provide clinicians with valuable insights, enhance their understanding of PFE, and underscore the importance of early diagnosis and treatment to avoid misdiagnosis and missed diagnosis.

Case presentation

A female patient in her early 40s was admitted to the emergency department of Affiliated Hospital of Guangdong Medical University in March 2024 for chest tightness and shortness of breath that had lasted for 2 h. Her medical history was unremarkable; she denied having hepatitis, tuberculosis, hypertension, diabetes, or heart disease. Her body mass index was 20.58 kg/m², and she reported no history of smoking. Ten hours prior to her presentation, she had undergone liposuction and a fat grafting procedure (involving thigh fat ring and buttock fat graft filling), which lasted for 2 h under general anesthesia. Approximately 8 h postoperatively, the patient experienced a sudden onset of shortness of breath accompanied with chest tightness and a decrease in peripheral blood oxygen saturation to at least 80%. She was promptly administered noninvasive mechanical ventilation and was transferred to the intensive care unit (ICU). Upon transfer, her vital signs were as follows: body temperature, 37.0°C; blood pressure, 106/61 mmHg; no use of vasoactive drugs such as norepinephrine; respiratory rate, 40 bpm; SPO₂ level, 95%; noninvasive mechanical ventilation mode: P-A/C, FiO₂ = 100%; inspiratory pressure, 19 bpm; respiratory rate, 15 bpm; and PEEP = 8.0 cmH₂O. The respiratory sounds in both lungs were diminished, with moderate moist rales present; dry rales were absent. Both lower extremities were wrapped with elastic bandages and exhibited slight tenderness. Muscle strength and tension in the limbs were normal, and no edema was observed in the lower limbs.

A complete blood examination upon admission to the hospital revealed the following results: total C-reactive protein level, 23.30 mg/L; white blood cell count, 10.28 × 10⁹/L; neutrophil ratio, 91.7%; absolute neutrophil count, 9.43 × 10⁹/L; and hemoglobin level, 102 g/L. The serum procalcitonin level was 8.540 ng/mL, total cholesterol level was 2.73 mmol/L, triglyceride level was 0.39 mmol/L, high-density lipoprotein cholesterol level was 1.26 mmol/L, and low-density lipoprotein cholesterol level was 1.29 mmol/L. The D-dimer level was 0.93 mg/L, while the B-type natriuretic peptide precursor level was 786 pg/mL. Liver function, kidney function, and myocardial enzyme levels were found to be normal. Arterial blood gas analysis (positive end-expiratory pressure = 8.0 cmH₂O, FiO₂ = 100%) at admission indicated a pH of 7.402, PaCO₂ of 34.3 mmHg, PaO₂ of 113.6 mmHg, HCO₃- of 20.9 mmol/L, and lactic acid level of 1.64 mmol/L, resulting in a PaO₂/FiO₂ ratio of 113.6. Chest computed tomography (CT) revealed scattered patchy fuzzy shadows in the upper lobe of both lungs and the middle lobes of the right lung, accompanied with local grid-like changes (Figure 1(a) to (d)). CT pulmonary angiography (CTPA) revealed no clear signs of embolism (Figure 1(e) to (g)). Bronchoscopy showed bronchial inflammation, with large numbers of macrophages and neutrophils in bronchoalveolar lavage fluid (BALF) samples (Figure 2(a) to (d)). Additionally, red oil O staining demonstrated orange fat droplet cells, with more fat droplets observed outside the cells (Figure 2(e)). Based on these findings and the patient’s history of liposuction and fat transplantation, she was diagnosed with PFE accompanied with acute respiratory distress syndrome (ARDS). The treatment regimen initiated included noninvasive assisted ventilation, methylprednisolone sodium succinate at a dosage of 60 mg/day, and imipenem–cilastatin sodium at 1.0 g every 6 h, along with nutritional support and intravenous infusion of human albumin at 10 g twice daily for 5 days. A subsequent CTPA revealed a filling defect in the lower basal artery of the right lung, which further confirmed the diagnosis of PFE (Figure 3). The patient's condition with respect to respiratory failure showed improvement, with peripheral blood oxygen saturation maintained at 95%–100% in ambient air. Consequently, noninvasive assisted ventilation was discontinued, and oxygen was administered via nasal catheter at a flow rate of 4–5 L/min. Additionally, piperacillin sodium and sulbactam sodium were prescribed at 4.5 g every 8 h for infection prophylaxis. The dose of methylprednisolone sodium succinate was reduced to 30 mg/day for 2 days. The patient was subsequently discharged from the ICU on day 6, continuing treatment with prednisone acetate tablets at 30 mg/day, followed by a tapering dose of 15 mg/day for 5 days. The patient’s condition continued to improve, with her heart rate and peripheral blood SpO₂ fluctuating from 70–100 bpm and 98%–100%, respectively. Prednisone acetate was gradually tapered to 5 mg/day for 3 days before discontinuation. Follow-up chest CT and CTPA demonstrated no pulmonary inflammatory infiltration, pleural effusion, or embolism (Figure 4(a) to (f)). The patient ultimately showed complete recovery and was discharged from the hospital.

Figure 1.

Chest CT and CT pulmonary angiography on hospital admission. (a–d) Patchy fuzzy shadows scattered across the upper lobes of both lungs and the middle lobe of the right lung, with local grid changes present (red arrow). Both lungs were scattered in a large flake of solid shadow, with bilateral pleura thickened and adhesions present and (e–g) the main pulmonary trunk, left and right pulmonary trunks, and their internal pulmonary branches showed no clear signs of embolism, and the local development of the distal branches of both pulmonary arteries was poor. CT: computed tomography.

Figure 2.

Bronchial lavage fluid examination. (a–c) Bedside bronchoscopy showed bronchial inflammation; (d) Wright–Giemsa staining of BALF samples revealed a red cytoplasm, blue nucleus, and orange-red eosinophilic particles. Cell difference counts in BALF samples showed macrophages (59.5%), neutrophils (40.5%), and lymphocytes (0%); (e) red oil O staining of BALF specimen. Cells containing orange fat droplets with positive positivity rate of 65% were easily visible (black arrow). More fat droplets were visible outside the cells (blue arrow). BALF: bronchoalveolar lavage fluid.

Figure 3.

The second test of CTPA showing filling defect in the lower basal artery of the right lungs (red arrow).

Figure 4.

Chest CT after hospital discharge. (a–d) There was virtually no pulmonary infiltration or pleural effusion and (e, f) CTPA showed no clear signs of embolism in the main pulmonary trunk, left and right pulmonary trunks, and their internal pulmonary branches. CT: computed tomography; CTPA: computed tomography pulmonary angiography.

Discussion

FES occurs when fat particles or inflammatory factors enter the circulatory system after trauma, embolizing tissues such as the lungs and brain. When fat globules form in the lung, termed as PFE, a small proportion of patients with FES develop this uncommon and deadly condition. ¹ It commonly occurs when fat particles reach the pulmonary capillary bed through torn veins after fat cells rupture from fractured bones; however, it is rare after liposuction or fat transplantation.^2,3 Lung lipases hydrolyze fat particles into toxic glycerol and free fatty acids, damaging alveolar and endothelial cells.^4,5 Additionally, long bone fractures activate complement and coagulation, causing intravascular coagulation, increased pulmonary permeability, and lung injury.^5,6 The diagnosis in most cases exhibiting microscopic fat embolism relies on clinical symptoms and laboratory results, while macroscopic fat embolism can be detected using CT/MRI, which shows fat droplets in the vasculature, or biopsy/autopsy, which confirms fat globules causing vascular occlusion.^7,8 Early diagnosis and treatment are crucial to patient health.

The patient in the current case had no high-risk factors for thrombosis or history of spontaneous abortion. Given her history of fat grafting, fat embolism was considered the primary cause of her pulmonary clots. Unfortunately, specific details such as the harvested fat volume, injected fat volume, and instrument specifications (e.g. needle and cannula type or gauge) were unavailable due to lack of access to surgical records from the other medical institution. The CTPA test at admission did not reveal any sign of embolism, while BALF cytopathological examination showed several orange fat droplet cells and more fat droplets outside the cells, which was essential for the early diagnosis of fat embolism. Fat particles embolized pulmonary capillaries or small blood vessels after entering the body’s circulatory system, and the imaging manifestations were scattered or large non-infectious infiltrating lesions, showing widespread and diffuse distribution; in severe cases, there were blizzard-like changes or complicated signs of right heart congestion.^9,10 In a study on 40 patients from 19 countries, chest CT was 100% accurate in diagnosing PFE. ¹¹ Therefore, imaging is not only valuable for the diagnosis and treatment of PFE but also a reliable method for post-treatment follow-ups. Lipids in lung tissue can be detected via lung biopsy; however, owing to its invasive nature, it is not considered feasible. Wright–Giemsa and red oil O staining of BALF from this case revealed lipid-rich macrophages and fat droplets. Although it aids early diagnosis of PFE, it may also indicate lipid accumulation, sepsis, or hyperlipidemia, making its role in diagnosing PFE controversial.^12,13 The patient did not exhibit any such condition; therefore, the diagnosis of macroscopic PFE was finally confirmed using clinical manifestations, imaging data, and predisposing factors.

FES is generally self-limiting, with a fatality rate of 10%–15%, and prognosis is related to the degree of respiratory dysfunction. Respiratory support is the most basic treatment. This patient was given noninvasive mechanical ventilation in time to maintain oxygen supply and achieve good therapeutic effects, effectively preventing the need for invasive mechanical ventilation. Special treatment of glucocorticoids can reduce fat droplet size and number, alleviating the toxic effects of free fatty acids. ¹⁴ Most patients show favorable prognosis with fluid rehydration, oxygen inhalation, and hormone therapy, while few patients progress to ARDS, requiring mechanical ventilation and extracorporeal membrane oxygenation treatment. Albumin, aprotinin, dextran, aspirin, and hyperbaric oxygen also have a certain adjuvant therapeutic effect. ¹⁵ The patient received methylprednisolone sodium succinate at a daily dose of 60 mg, which was gradually reduced with improvement in the patient’s condition. Early corticosteroid use in PFE with ARDS is effective in inhibiting inflammation, stabilizing pulmonary surfactants, and reducing the toxic effects of free fatty acids, thereby relieving capillary leakage, lung damage, and lung edema.^14,16 In addition, systemic anticoagulant therapy with heparin and other anticoagulant drugs is used to treat PFE.^6,10 However, notably, the use of heparin in the treatment of PFE may cause serious potential complications, such as intracranial hemorrhage; thus, the selection and adjustment of heparin dosage require further study.^17,18

Conclusion

FES, a possibly fatal complication, can also arise from fat suction and fat injection procedures. Early-stage dyspnea and hypoxemia in these patients should be considered regarding PFE possibilities. For the early and rapid diagnosis of PFE, chest CT combined with red oil O staining of BALF samples has great diagnostic value. Prompt diagnosis and appropriate treatment are critical to the patient’s prognosis in cases of PFE.