Cerebral fat embolism following autologous fat injection in facial reconstruction: A case report

Abstract

BACKGROUND

Autologous fat injection in facial reconstruction is a common cosmetic surgery. Although cerebral fat embolism (CFE) as a complication is rare, it carries serious health risks.

CASE SUMMARY

We present a case of a 29-year-old female patient who developed acute CFE following facial fat filling surgery. After the surgery, the patient experienced symptoms including headache, nausea, vomiting, and difficulty breathing, which was followed by neurological symptoms such as slurred speech and left-sided weakness. Comprehensive physical examination and auxiliary investigations, including blood tests, head and neck computed tomography angiography, and cranial magnetic resonance diffusion-weighted imaging, were performed upon admission. The clinical diagnosis was acute cerebral embolism following facial fat filling surgery. Treatment included measures to improve cerebral circulation, dehydration for intracranial pressure reduction, nutritional support, and rehabilitation therapy for left limb function. The patient showed a significant improvement in symptoms after 2 weeks of treatment. She recovered left limb muscle strength to grade 5, had clear speech, and experienced complete relief of headache.

CONCLUSION

Our case highlights the potential occurrence of severe complications in patients undergoing fat injection in facial reconstruction. To prevent these complications, plastic surgeons should enhance their professional knowledge and skills.

Key Words: Cerebral fat embolism; Mechanical thrombectomy; Thrombolysis; Steroid therapy; Symptomatic treatment; Case report

Core Tip: Our case highlighted the potential occurrence of severe and potentially life-threatening complications in patients undergoing autologous fat injection in facial reconstruction. To prevent and manage such serious complications, plastic surgeons need to enhance their professional knowledge and skills. It is advisable to use blunt needles and inject slowly under low pressure during autologous fat injection, ensuring continuous aspiration to confirm the absence of blood during injection.

INTRODUCTION

Autologous fat grafting in facial reconstruction is becoming increasingly popular as a cosmetic technique in the field of medical aesthetics due to its simplicity, feasibility, effectiveness, and relatively high safety profile[1]. This technique utilizes the patient’s own adipose tissue for filling and shaping to improve facial contours, fill wrinkles, and restore a youthful appearance. The procedure typically involves extracting adipose tissue from sites with body fat (such as the abdomen or buttocks) under local or general anesthesia. The adipose tissue is then processed and injected into the desired areas of the face for enhancement[2].

Compared to traditional fillers, autologous fat injection offers several advantages. First, there is no risk of rejection as it uses the patient’s own tissue, which avoids potential allergic or immune reactions caused by foreign materials[3]. Second, autologous fat injection can achieve more natural and long-lasting results because adipose tissue itself is biologically active. It is capable of integrating with surrounding tissues and maintaining volume over a long-term period. Additionally, the procedure for autologous fat injection is relatively simple and minimally invasive and has a short recovery time allowing patients to quickly return to normal life and work[4].

With the increasing awareness of beauty and the pursuit of a youthful appearance, autologous fat injection in facial reconstruction has become increasingly favored by patients in recent years. However, its potential risks and rare complications warrant attention despite the widespread acceptance of this technique in the field of aesthetics[5-7]. Cerebral fat embolism (CFE) as a rare but serious complication has raised concerns in the medical community. Here, we highlight a case of acute cerebral infarction following autologous fat injection in the face and delve into the mechanisms, clinical manifestations, treatment methods, and prevention strategies for CFE.

CASE PRESENTATION

The patient was a 29-year-old female who underwent facial fat filling surgery under general anesthesia at a plastic surgery hospital. Fat was extracted from both her thighs and injected into the forehead, bilateral temples, and bilateral nasolabial groove.

Chief complaints

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

History of present illness

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.

History of past illness

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

Personal and family history

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.

Physical examination upon admission

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.

Laboratory examinations

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.

Imaging examinations

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.

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.

MULTIDISCIPLINARY EXPERT CONSULTATION

After admission, the case was discussed with a radiologist and plastic surgeon. The radiologist determined that the head and neck CTA revealed fat embolism in the right carotid artery and scattered multiple fat-density nodules in the right temporal parietal occipital region, which is suggestive of emboli. 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. In addition, the patient had a history of autologous fat facial injection. Therefore, they considered a diagnosis of CFE. The plastic surgeon considered that the patient underwent autologous fat facial injection in the hospital, that there were many injection sites, and the injection process was not clearly defined. Immediately after the facial fat filling surgery, the patient experienced headaches, nausea, vomiting, difficulty breathing, slurred speech, weakness in the left limbs, and drooling from the left corner of the mouth. Combined with the cranial DWI and head and neck CTA imaging, the plastic surgeon agreed with the diagnosis of CFE.

Summary of our department

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.

FINAL DIAGNOSIS

Acute cerebral infarction post-facial fat filling surgery.

TREATMENT

The patient received venoclysis with butylphthalide and sodium chloride injection (25 mg twice daily) and Shuxuetong injection (6 mL once daily) to improve the brain circulation. She also received intramuscular injection of galamatamine hydrobromide injection (5 mg once daily) to repair the nerves. These drugs were used for 14 days. At the same time, intravenous infusion of mannitol (25 g every 8 hours) was given to reduce cerebral edema for 7 days. In addition, rehabilitation of the left limb was given including intradermal injection treatment, simulated acupuncture treatment, partition moxibustion treatment, electronic biofeedback treatment (electromyography), large joint loosening training, instrument training, and endurance training once daily for 14 days.

OUTCOME AND FOLLOW-UP

The patient had no adverse effects during the course of treatment. The slurred speech and weakness in the left limbs gradually improved, and the patient’s headache gradually subsided. After 2 weeks of treatment in the hospital, the patient was discharged. At discharge the patient’s muscle strength in the left limbs recovered to grade 5, her speech was mostly clear, and the headache was completely resolved.

DISCUSSION

Epidemiology

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.

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].

Table 1 Cases of cerebral fat embolism following facial injections.

Ref.	Year	Country	Age(years)	Anesthesia	Dose (mL)	Injection site	Infarction artery/site	Treatment	Outcomes
Cheng et al[10]	2023	China	31	General	0.6	Temples and tear troughs	Left internal carotid artery, anterior cerebral artery, and middle cerebral artery	Decompressive craniectomy and provided symptomatic and supportive treatments	Death
Qian et al[11]	2021	China	28	General	77	Temple, forehead, and cheeks	Frontal, temporal, and parietal lobes and the basal ganglia	Dehydration, infection prophylaxis, gastric protection, and seizure prophylaxis	Mild improvement
Lee et al[12]	2011	Korea	44	Intravenous	NR	Periocular	MCA	Ocular massage, carbon dioxide, and oxygen therapy	Vision loss
Liu et al[13]	2021	China	18	Local	NR	Temporal region	ECA and ICA	Decompressive craniectomy	Death
Kang et al[14]	2016	Korea	32	Local	NR	Glabella	ACA and MCA	Thrombolytic agents	Vision loss and neurological deficits mildly improved
Wang et al[15]	2014	China	22	General	49	Temporal and frontal	ECA and ICA	Mannitol and decompressive craniectomy	Vision loss and neurological deficits mildly improved
Zhou et al[16]	2019	China	22	Local	50	Temporal region	ICA and MCA	Embolectomy	Incomplete cure
Miao et al[17]	2021	China	22	General	10	Temporal region	Posterior cerebral artery and MCA	Decompressive craniectomy, mannitol, vasoactive drugs, ceftriaxone, and methylprednisolone	Incomplete cure
Hong et al[18]	2014	Korea	31	General	NR	Glabella	MCA	Ocular massage, anterior chamber paracentesis, and volume expansion	Vision loss
Liu et al[19]	2018	China	47	NR	NR	Jaw	ECA and MCA	Thrombolytic agents, antiplatelet aggregation, and reduce intracranial pressure	Incomplete cure
Wang et al[20]	2018	China	22	Local	NR	Temporal region	MCA and superficial temporal artery	Decompressive craniectomy	Incomplete cure
	2018	China	30	Local	NR	Temporal region	Right hemisphere, superficial temporal artery	Decompressive craniectomy	Left limbs paralysis
Lee et al[21]	1996	Korea	42	Local	0.5	Nasolabial groove	NR	NR	NR
Renard et al[22]	2019	France	50	Local	NR	Right eye	MCA and ACA	NR	NR
Lee et al[23]	2012	Korea	26	Local	NR	Face	Right parietal lobe	Steroids	NR
Thaunat et al[24]	2004	France	39	Local	17	Temporal, eyelids, and glabella	ACA	NR	Mutism and paraplegia
Lu et al[25]	2021	China	35	NR	NR	Temporal region	Left frontal and parietal cortices	Intravenous thrombolysis	Mild improvement
Yoon et al[26]	2003	Korea	39	Local	5	Glabella	ICA	Mechanical ventilation and steroids	Death
Ji et al[27]	2018	China	30	NR	NR	Bilateral temporal regions	ICA and ECA	Embolectomy	Death
Ji et al[27]	2018	China	23	NR	NR	Bilateral temporal regions	Left frontal and parietal lobes	Antiplatelet drugs and oxygen therapy	Vision loss

ACA: Anterior cerebral artery; ECA: External carotid artery; ICA: Internal carotid artery; MCA: Middle cerebral artery; NR: Not reported.

Pathogenesis

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.

Pathogenesis and clinical presentation

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 presentation and diagnosis

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].

Treatment and prevention

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.

CONCLUSION

Our case underscored the potential for severe and life-threatening complications following autologous fat grafting to the face. To mitigate the risk of such complications, plastic surgeons must enhance their expertise and skills during facial fat grafting procedures.