The patient was admitted to our hospital due to sudden headache, unclear speech, and weakness of the left limb for 1 day.

Immediately after the facial fat filling surgery, the patient experienced headaches, nausea, vomiting, and difficulty breathing. These symptoms were followed by slurred speech, weakness in the left limbs, and drooling from the left corner of the mouth. These symptoms were not promptly recognized nor treated. The patient’s symptoms worsened over time. The next day a head computed tomography (CT) scan performed outside the hospital revealed a low-density shadow in the right cerebral hemisphere. Subsequently, the patient presented to our hospital for further diagnosis and treatment.

The patient had no significant medical history such as hypertension, diabetes, coronary heart disease, or hyperlipidemia.

The patient denied any history of head trauma, miscarriage, smoking, alcohol consumption, drug use, or food allergies. There was no abnormality in her family history.

The patient’s blood pressure was 14 kPa/9.5 kPa, her heart rate was 65 beats per minute, and her oxygen saturation was 98%. The patient appeared lethargic, with elastic bandages applied to the forehead, bilateral temples, and bilateral nasolabial groove areas. Bruises were observed on the left thigh (8 cm × 6 cm) and right thigh (8 cm × 4 cm). Clear lung sounds were heard without rales. Cardiac auscultation revealed normal heart sounds without murmurs. The abdomen was soft without tenderness. No edema was present in the lower limbs. The patient exhibited slurred speech, decreased orientation to time and place, and memory impairment. Pupils were round, approximately 3 mm in diameter, with sensitive light reflexes. Eye closure was normal, but the mouth corner deviated to the right when opened, and the tongue deviated to the left when protruded. Muscle strength was graded as 4/5 in the left limbs and 5/5 in the right limbs, with normal muscle tone and reflexes. No pathological signs were elicited. Sensation was intact.

The white blood cell count was 10.32 × 10⁹/L (normal range: 3.5 × 10⁹/L-9.5 × 10⁹/L), and the neutrophil percentage was 84% (normal range: 40%-75%). The D-dimer level was 2.2 μg/mL (normal range: 0.00-0.50 μg/mL). Findings from blood gas analysis, blood biochemistry, myocardial enzyme spectrum, myocardial infarction markers, C-reactive protein, infection markers, blood lipids, and blood glucose were all normal.

The head and neck CT angiography (CTA) revealed a fat embolism in the right common carotid artery bifurcation, proximal right internal carotid artery, and proximal right external carotid artery. It was accompanied by multiple infarcts in the right cerebral hemisphere. Scattered multiple fat-density nodules in the right temporal parietal occipital region were suggestive of emboli (Figure 1A). Pulmonary artery CTA showed no definite embolism. Carotid artery ultrasound revealed thrombosis from the bifurcation of the right common carotid artery to the origin of the internal and external carotid arteries on the right side. Cranial diffusion-weighted imaging (DWI) revealed acute extensive cerebral infarction in the right frontal temporal parietal occipital lobe and basal ganglia area as well as acute lacunar infarction in the left frontal temporal lobe (Figure 1B). The electrocardiogram was normal. Right cardiac echocardiography showed no obvious abnormalities.

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Figure 1 Imaging examinations. A: Computed tomography angiography showed fat embolism in the proximal right internal carotid artery and proximal right external carotid artery; B: Diffusion-weighted imaging showed high signal intensity in the left cerebral hemisphere.

The patient was a young female patient who had no known risk factors for thrombosis nor a history of spontaneous abortion. She experienced headaches, nausea, vomiting, and difficulty breathing, which was followed by slurred speech, weakness in the left limbs, and drooling from the left corner of the mouth after autologous fat facial injection. The cranial DWI revealed acute extensive cerebral infarction in the right frontal temporal parietal occipital lobe and basal ganglia area as well as acute lacunar infarction in the left frontal temporal lobe. Therefore, we agreed with this diagnosis.

In recent years, there has been an increasing number of reports of CFE as a complication of autologous fat grafting to the face. Among the complications caused by the facial fat grafting, CFE is the most severe, accounting for 86% of all cases of fat embolism[8,9]. We conducted a literature review by searching the PubMed and China National Knowledge Infrastructure (CNKI) databases for articles describing CFE following facial autologous fat grafting. For PubMed, we used the following search strategy: “(((fat injection (Title/Abstract)) OR (fat graft (Title/Abstract))) AND ((Surgery, Plastic (Mesh)) OR ((((Esthetic Surgery (Title/Abstract)) OR (Reconstructive Surgery (Title/Abstract))) OR (Cosmetic Surgery (Title/Abstract)))) AND ((Embolism, Fat (Mesh))”. No time limit was set during the search process. Using this search strategy, we identified 52 articles (29 from PubMed and 23 from CNKI). After excluding 22 review articles and 9 case reports unrelated to CFE following facial autologous fat grafting, as well as 3 duplicate articles, a total of 18 articles were included (Figure 2). All retrieved articles were independently reviewed by two authors, and articles meeting the criteria were selected based on consensus.

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Figure 2 Literature search process.

A total of 18 case studies were included, covering cases from China, South Korea, and France related to CFE following facial injections. The age range was 18-50 years, with the majority falling between 20-30 years. General anesthesia was predominantly used in most cases. Injection sites primarily involved the temples, temporal regions, forehead, and cheeks. The locations of emboli encompassed the internal carotid artery, anterior cerebral artery, and middle cerebral artery. Emboli were treated with surgical interventions (such as decompressive craniectomy, embolus removal), pharmacotherapy (including thrombolytic agents, antibiotics, steroids), and supportive measures (such as oxygen therapy, mechanical ventilation). Treatment outcomes varied, with some cases showing symptomatic improvement, while others exhibited limited or no improvement. Severe cases resulted in mortality (Table 1)[10-27].

Fat embolism is commonly seen after long bone fractures. However, the rapid development of cosmetic medicine has led to an increase in patients opting for the facial fat grafting technique. This in turn leads to an increase in associated complications. CFE following facial fat grafting surgery mainly occurs in middle-aged and young women, with a predominance among East Asian women.

Facial autologous fat grafting typically involves harvesting fat from areas with abundant adipose tissue such as the abdomen, buttocks, inner thighs, or upper arms. The fat particles are purified through centrifugation and then injected into the desired facial areas. The predisposing factors for CFE are believed to be increased local pressure and the rich vascular network in facial tissues[28]. Excessive injection pressure or rapid injection speed may lead to increased local pressure. Once fat emboli enter the bloodstream, they can cause endothelial injury and inflammatory reactions, resulting in inflammatory responses and thrombus formation in the vessel wall[29]. These inflammation and embolism events may further lead to blood flow obstruction and tissue ischemia.

Our patient underwent facial fat grafting surgery to address facial concavity. Immediately after the surgery, she experienced headaches, speech impairment, and hemiparesis. She had no known risk factors for thrombosis or history of spontaneous abortion, both of which can cause stroke. CTA of the head and neck upon admission revealed fat embolism at the bifurcation of the right carotid artery as well as scattered fat-density nodules in the right cerebral hemisphere. There were no significant abnormalities in the pulmonary artery. Considering the patient’s history of facial fat grafting surgery, the detected cerebral infarction was attributed to fat embolism.

Fat embolism, a rare complication of cosmetic fat grafting, predominantly affects the frontal area, nose, nasolabial folds, brow, temples, periorbital region, and scalp. The retrograde flow of autologous fat during injection into facial arteries or veins, especially when encountering sufficient pressure, is considered a plausible mechanism for CFE[30,31]. Additionally, intercommunication between the extracranial and intracranial arterial systems allows fat emboli to transit from extracranial arteries to intracranial arteries, as evidenced by imaging studies.

Clinical manifestations of CFE vary widely, ranging from mild delirium to vision loss, hemiparesis, and coma. Some cases may present with seizures and focal neurological deficits[32]. Fat emboli can localize to central areas that control catecholamine release thereby increasing catecholamine levels and leading to the paroxysmal sympathetic hyperactivity[33,34]. Paroxysmal sympathetic hyperactivity can present as tachycardia, hypertension, tachypnea, irregular motor tone, and hyperthermia[35]. Severe cases can lead to coma and death[36]. The mortality rate of CFE ranges between 5%-15%, but patients with combined respiratory failure usually have higher mortality rates[37]. These symptoms are similar to stroke, but onset can occur immediately after fat injection or several hours later.

CFE caused by facial fat grafting is confirmed by clinical diagnosis and differentiated by imaging examinations. Differentiating fat embolism from other causes of cerebral infarction on plain head CT scans is challenging, and DWI can reveal scattered high-signal lesions. Magnetic resonance spectroscopy has been proposed as a more effective diagnostic tool than DWI for fat embolism identification[10,38,39].

Currently, there is no specific treatment for CFE, and supportive care remains the gold standard. Some researchers have suggested alcohol infusion as a therapeutic option, although its efficacy is based on limited case reports[40]. Given the inflammatory response triggered by cholesterol crystals from fat emboli in the cerebral circulation, steroid therapy has been proposed as a potential treatment. However, Bederman et al[41] found no significant correlation between corticosteroid use and patient outcomes.

The early use of hyperbaric oxygen has also been shown to be an effective treatment. It can increase blood oxygen pressure and oxygen content, improve the availability of oxygen to brain tissue and microcirculation, and promote the development of collateral circulation. The function of brain cells in the penumbral area is then restored, and the risk of severe neurological symptoms is decreased[41,42].

Anticoagulant drugs have been proposed for CFE treatment. Anticoagulant drugs can stimulate clearance of lipids from the circulation to decrease lipase activity. However, their use is potentially dangerous[43]. Furthermore, fat emboli can be dissolved by saponin (a lipid-soluble drug)[42,44]. However, the effectiveness of this approach is unclear. Mechanical thrombectomy has been attempted in select cases to relieve neurological symptoms associated with fat emboli[36,45].

Preventing CFE primarily involves optimizing injection techniques during facial fat grafting. Plastic surgeons should be well-versed in facial vascular anatomy. Blunt-tipped cannulas, minimal injection pressure, slow injection rates, and aspiration before fat injection can prevent inadvertent vessel puncture.