[Post-traumatic stroke due to fat embolism]. / Accident vasculaire cérébral post-traumatique sur embolie graisseuse.

Fat embolism syndrome mainly occurs following trauma to the long bones or pelvis. Non-traumatic causes are rarer. Its incidence varies greatly and depends on the number of fractures involved. Two physiopathological theories, one mechanical and the other biochemical, attempt to explain this still poorly understood phenomenon. The complete form of the syndrome results in a combination of pulmonary involvement, neurological disorders and a petechial rash. Given the polymorphism of signs and symptoms, Fat embolism syndrome remains a diagnosis of exclusion. Regarding treatment, the therapeutic strategy combines treatment of the causative process with conservative measures.

Le syndrome d'embolie graisseuse se manifeste majoritairement dans les suites d'un traumatisme des os longs ou du bassin. Les causes non traumatiques sont plus rares. Son incidence varie fortement et dépend du nombre de fractures impliquées. Deux théories physiopathologiques, l'une mécanique et l'autre biochimique, tentent d'expliquer ce phénomène encore mal compris. La forme complète du syndrome se traduit par la combinaison d'une atteinte pulmonaire, de troubles neurologiques et d'une éruption pétéchiale. Étant donné le polymorphisme des signes et des symptômes, le syndrome d'embolie graisseuse reste un diagnostic d'exclusion. Concernant le traitement, la stratégie thérapeutique associe la prise en charge du processus causal combinée à des mesures conservatrices.

Successful therapeutic plasma exchange for a patient with sickle cell disease and fat embolism syndrome after a failure of a response to red cell exchange transfusion.

BACKGROUND: Fat embolism syndrome (FES) is a rare complication, which was reported mostly with milder forms of heterozygous sickle cell disease (SCD). It may present in a catastrophic way with multi-organ failure, particularly involving the pulmonary and neurological systems. Diagnosis is often missed or delayed; and the standard recommended treatment is red cell exchange (RCE) transfusion, which has sub-optimal results, such as debilitating long-term neurological complications. Recently, few reports suggested that the addition of Therapeutic Plasma Exchange (TPE) might further improve the outcome. CASE DESCRIPTION: A 23-year-old woman with homozygote SCD was admitted with bony pains and vaso-occlusive crises. However, her course evolved to respiratory failure requiring mechanical ventilation, decreased level of consciousness, skin rash, severe anemia and thrombocytopenia and a picture consistent with thrombotic microangiopathy. MRI of the brain showed scattered multi-focal ischemic foci and cytotoxic edema. The patient received RCE on the third day after admission without improvement. On the seventh day, TPE was instituted (2 L/day of fresh frozen plasma for 5 days), following which she regained her consciousness and showed an improvement in her laboratory abnormalities. On follow up, she had gradual full neurological recovery and resolution of the MRI findings within a few months. CONCLUSION: FES remains a diagnostic and therapeutic challenge, with significant morbidity and mortality. Success in the management of this reported case with the addition of TPE to RCE supports the notion that TPE may be a potentially helpful modality that deserves further research.

Multisystemic involvement of post-traumatic fat embolism at a Pediatric Trauma Center: a clinical series and literature review.

Post-traumatic fat embolism syndrome (FES) is a severe complication consequent to bone fractures. The authors describe its clinical features and management in a population of teenagers by detailing demographics, organ involvement, laboratory, and imaging findings, as well as outcome. Moreover, a systematic review of pediatric published case reports of post-traumatic FES is provided. First, a series of eight episodes of post-traumatic FES that occurred in seven patients (median age 16.0 years, IQR 16.0-17.5) admitted to a pediatric intensive care unit (PICU) in an 8-year period was analyzed through a retrospective chart review. Secondly, a systematic research was performed on PUBMED database. Trauma patients ≤ 18 years without comorbidities in a 20-year period (2002-2022) were included in the review. Neurological impairment was present in five out of seven patients, and a patent foramen ovale was found in four cases. Hemodynamic instability requiring vasoactive drugs was recorded in four patients. A severe form of acute respiratory distress syndrome (ARDS) occurred in five cases, with the evidence of hemorrhagic alveolitis in three of them. In the literature review, eighteen cases were examined. Most cases refer to adolescents (median age 17.0 years). More than half of patients experienced two or more long bone fractures (median: 2 fractures). Both respiratory and neurological impairment were common (77.8% and 83.3%, respectively). 88.9% of patients underwent invasive mechanical ventilation and 33.3% of them required vasoactive drugs support. Neurological sequelae were reported in 22.2% of patients. CONCLUSION: Post-traumatic FES is an uncommon multi-faceted condition even in pediatric trauma patients, requiring a high level of suspicion. Prognosis of patients who receive prompt support in an intensive care setting is generally favorable. WHAT IS KNOWN: •Post-traumatic fat embolism syndrome is a severe condition complicating long bone or pelvic fractures. •Little is known about clinical features and management in pediatric age. WHAT IS NEW: •Post-traumatic fat embolism syndrome can cause multiple organ failure, often requiring an intensive care management. •Prompt supportive care contributes to a favorable prognosis.

Rare Presentation of a Patient with Cardiac Arrest Due to Cerebral Fat Embolization Following Polytrauma.

Cerebral fat embolism (CFE) syndrome is a known complication that can occur following polytrauma, particularly in cases involving fractures of long bones, but cardiac arrest is a rare presentation following cerebral fat embolization.1 Our patient met with a road traffic accident (RTA), sustaining multiple long bones injuries with hypovolemic shock. After 10 hours of admission and achieving hemodynamic stability, the patient developed cerebral fat embolization. He developed sudden cardiac arrest and was resuscitated. We instituted ventilator support, inotropic infusion, antibiotics, and intravenous (IV) fluids. Our patient regained consciousness without neurological deficit over a period of 10 days and underwent surgery for all three major fractures with due precautions. The patient was discharged after 3 weeks of treatment from the hospital. How to cite this article: Rathod N, Rathod V, Parikh B, et al. Rare Presentation of a Patient with Cardiac Arrest Due to Cerebral Fat Embolization Following Polytrauma. J Assoc Physicians India 2023;71(11):89-93.

Identifying and Treating Severe Bone Marrow Necrosis and Fat Embolism Syndrome in Pediatric Patients With Sickle Cell Disease: A Case Report.

Fat embolism syndrome after bone marrow necrosis is an extremely rare complication in sickle cell disease associated with significant morbidity and mortality. A high index of suspicion is required for diagnosis. This case report will assist pediatric clinicians and hematologists to recognize this severe complication in patients with sickle cell disease and to promptly initiate treatment. Red flags include severe bone pain, respiratory distress, neurological impairment, decreasing platelet count, peripheral leukocyte left shift, elevated nucleated red blood cells, and significant elevation in plasma ferritin and lactate dehydrogenase. We report a pediatric patient who was diagnosed early, received urgent red cell exchange transfusion and plasma exchange, and ultimately survived this devastating complication.

Cerebral fat embolism syndrome at a single trauma center.

OBJECTIVES: Based on a 16-year case series, we sought lessons about diagnosis and treatment of cerebral fat embolism syndrome. MATERIALS AND METHODS: Using discharge codes at a Level 1 Trauma Center, we performed a retrospective chart review of clinical characteristics, diagnostic studies, treatments, and outcome in cerebral fat embolism syndrome. RESULTS: Thirty-nine (40%) of 97 patients with fat embolism syndrome were diagnosed with cerebral fat embolism syndrome, with 29 (74%) presenting with coma. All had abnormal brain magnetic resonance imaging, with scattered cytotoxic edema (starfield pattern) in 29 (74%). All but two of the 21 patients with dilated fundoscopy showed retinal embolism. Among 29 patients with transcranial Doppler, the presence of microembolic signals in 15 (52%) was associated with fever (p = 0.039), right-to-left intracardiac shunting (p = 0.046) and a trend towards initial coma. In 11 patients with serial transcranial Dopplers and treatment with high-intensity statin therapy, the frequency of microembolic signals tended to decrease after therapy was initiated. Of the 28 (72%) of the 39 patients discharged, 16 (57%) had mild to moderate disability at last follow up. CONCLUSIONS: The recognition of cerebral fat embolism syndrome may be improved with routine inclusion of brain magnetic resonance imaging, dilated fundoscopy, and transcranial Doppler. We share our empiric management algorithm for cerebral fat embolism syndrome using these studies and with consideration of experimental therapies in select patients to prevent ongoing cerebral injury.

Two Cases Surviving Macro Fat Emboli Complications Following Gluteal Fat Grafting.

Media attention has in recent years created an increased patient demand for gluteal contouring and augmentation. Gluteal augmentation and contouring with autologous fat transfer, colloquially referred to as the "Brazilian butt lift" (BBL), can be performed safely and effectively, with an overall complication rate ranging from 1.5% to 6.8%. However, there have been an alarming number of lethal events from intravenous passage of injected fat and fatal pulmonary embolism due to macro-fat emboli (MAFE). MAFE (fat emboli >1 cm in diameter), distinct from micro-fat emboli, can quickly result in catastrophic cardiopulmonary compromise and death. Accurate mortality estimates are limited by difficulties in determining accurate values for the total number of BBL procedures performed because most of these cases are performed at budget clinics. Accurate morbidity estimates are limited by a lack of published outcomes and a low level of evidence in published studies. The first case of survival of MAFE secondary to BBL was reported in 2019 by Peña et al. Few highly morbid complications secondary to MAFE have been reported because such events are almost universally lethal. We present 2 recent cases of survival after MAFE in the setting of gluteal fat transfer following expedient transfer to a tertiary care setting, allowing for timely and successful intervention. We illustrate examples of how MAFE is a highly lethal complication of gluteal fat grafting. Early recognition and immediate aggressive vital support to stabilize the patient are key for survival.

Fat Embolism After Autologous Facial Fat Grafting.

BACKGROUND: Autologous facial fat grafting has gained popularity in recent years and is considered to be safe. This paper presents the case of a patient who died due to massive cerebral microfat embolism after facial fat grafting. OBJECTIVES: The aim of this study was to raise awareness and provide more evidence on the prevention and treatment of this potentially lethal complication of facial fat grafting. METHODS: A detailed report was made of the case. Two online databases were searched for similar cases of facial fat embolism resulting in neurologic and/or visual symptoms. Thereafter a literature search was conducted to verify the etiology, current treatment options, and preventive measures. RESULTS: Forty-nine cases with similar events were found in the literature. The most common injected area was the glabella (36.1%), and an average of 16.7 mL fat was injected. The main complications were visual impairment, with 88.5% of cases resulting in permanent monocular blindness, and neurologic symptoms, some of which never fully recovered. Including the present patient, 7 cases were fatal. Fat embolism can occur in the veins and arteries of the face. Two possible pathways for fat embolism exist: the macroscopic, mechanical pathway with immediate signs, and the microscopic, biochemical pathway with delayed symptoms. Mechanical embolectomy and corticosteroids are suggested treatment options but evidence for their efficacy is lacking. Several different preventive measures are described. CONCLUSIONS: Although facial fat grafting is considered a safe procedure, one should be aware of the risk of fat embolism. Underreporting of this adverse event is likely. With no effective treatment and often detrimental outcomes, preventive measures are of utmost importance to improve patient safety.

Macro Fat Embolism After Gluteal Augmentation With Fat: First Survival Case Report.

Gluteal augmentation with fat has become one of the most common cosmetic procedures worldwide. Gluteal augmentation is designed to increase the volume and contour of the gluteal region. Intramuscular lipoinjection has been linked to multiple reports of severe complications, including death due to macro fat embolism (MAFE). The authors present the first reported case of survival and successful recovery after MAFE secondary to gluteal augmentation with fat. A 41-year-old woman, ASA II, was scheduled for augmentation mammaplasty, liposuction, and gluteal augmentation with fat. The patient was operated under general anesthesia with a total intravenous anesthesia technique. A total of 3.5 liters of fat was liposuctioned with no complications. The patient was then positioned in a lateral decubitus position for gluteal augmentation with fat. Right after the last injection, the anesthesiologist noticed a sudden change in capnography followed by hypotension, bradycardia, and hypoxemia. The first reaction in the operating room was to consider that the patient was experiencing a severe episode of fat embolism. She was then resuscitated and transferred to a tertiary facility for intensive care management. To our knowledge, this is the first case report of successful resuscitation in a patient experiencing severe MAFE after gluteal augmentation with fat. We believe that this patient survived the event due to early detection, aggressive management, and proper transfer to an intensive care unit. Level of Evidence: 5.

Case 254: Posttraumatic Migrating Fat Embolus Causing Fat Emboli Syndrome.

History An otherwise healthy 18-year-old man was admitted to the emergency department with a closed displaced fracture of the left femoral shaft ( Fig 1 ) after a high-velocity motorbike accident. At admission, other physical examination findings were unremarkable. Initial unenhanced and contrast material-enhanced (120 mL of Iomeron 400; Bracco Imaging, Milan, Italy) computed tomography (CT) was performed in the arterial and venous phases from the head to the knees. No abnormalities were noted in the brain or chest at initial CT. [Figure: see text] Within a few hours, the patient developed sudden mental confusion and severe hypoxemia, with rapidly worsening tachypnea and perturbed arterial blood gas with low partial pressure of oxygen (61 mmHg [8.1 kPa]; normal range, 75-100 mmHg [10.0-13.3 kPa]) and low partial pressure of carbon dioxide (32 mmHg [4.3 kPa]; normal range, 38-42 mmHg [5.1-5.6 kPa]). A second contrast-enhanced chest CT examination and initial brain magnetic resonance (MR) imaging were performed. Femoral fracture was stabilized with external fixation, and the patient was admitted to the intensive care unit, with progressive neurologic recovery at day 3 and respiratory improvement at day 4. Treatment included intubation with mechanical ventilation and intravenous administration of steroids and noradrenaline. Afterward, the femoral fracture was stabilized with an intramedullary nail. The patient made a full neurologic recovery 1 month after the accident.

Suspected coronary fat embolism after liposuction.

A 38-year-old female presented with chest pain and ST elevation on electrocardiogram after an outpatient liposuction procedure. Emergent coronary angiography revealed complete occlusion of multiple coronary arteries, with fat embolism as the suspected etiology. Attempts to restore distal coronary flow with balloon dilatation, aspiration with Pronto catheter, and distal adenosine administration resulted in minimal improvement in flow. The material aspirated was consistent with fat. With supportive therapy, including Impella CP support, the patient's clinical condition improved. To our knowledge, this is the first reported case of multiple coronary occlusion after liposuction.

Cerebral Fat Embolism: Recognition, Complications, and Prognosis.

Fat embolism syndrome (FES) is a rare syndrome caused by embolization of fat particles into multiple organs including the brain. It typically manifests with petechial rash, deteriorating mental status, and progressive respiratory insufficiency, usually occurring within 24-48 h of trauma with long-bone fractures or an orthopedic surgery. The diagnosis of FES is based on clinical and imaging findings, but requires exclusion of alternative diagnoses. Although there is no specific treatment for FES, prompt recognition is important because it can avoid unnecessary interventions and clarify prognosis. Patients with severe FES can become critically ill, but even comatose patients with respiratory failure may recover favorably. Prophylactic measures, such as early stabilization of fractures and certain intraoperative techniques, may help decrease the incidence and severity of FES.

Fat Embolism Syndrome Secondary to Bone Marrow Necrosis in Patients with Hemoglobinopathies.

Bone marrow necrosis with subsequent embolization of the fat and necrotic tissues into the systemic circulation causing fat embolism syndrome and multiorgan failure is a rare complication of patients with hemoglobinopathies. The exact etiology of this condition is not known. Because it occurs more often in patients with compound heterozygous conditions than in sickle cell disease, some patients are unaware of their predisposition. The initial symptoms are nonspecific, such as back and/or abdominal pain, fever, and fatigue, which may rapidly progress to respiratory failure and severe neurologic compromise. Common laboratory tests reveal anemia without reticulocytosis, thrombocytopenia, leukoerythroblastic picture with immature white cells and nucleated red blood cells, increased lactate dehydrogenase, high ferritin, and, sometimes increased creatinine. The diagnosis can be delayed because of an apparent lack of awareness about bone marrow necrosis with fat embolism syndrome, its rarity, and its similarities with other conditions such as thrombotic thrombocytopenic purpura. Although a bone marrow biopsy is diagnostic, waiting for it delays definitive treatment, which appears to be essential for the recovery of end-organ damage, such as neurologic and pulmonary damage. In our experience, either multiple units of red blood cell transfusion or, preferably, red cell exchange initiated promptly, is lifesaving.

Pathogenesis, diagnosis and treatment of cerebral fat embolism.

In this study, we analyzed two cases of pure cerebral fat embolism and reviewed related literatures to explore the pathogenesis, clinical manifestations, diagnosis and treatment of cerebral fat embolism, improve the treatment efficiency and reduce the misdiagnosis rate. In our cases, patients fully returned to consciousness at the different times with good prognosis, normal vital signs and without obvious sequelae. For patients with the limb fractures, who developed coma without chest distress, dyspnea or other pulmonary symptoms 12 or 24 h post injury, cerebral fat embolism should be highly suspected, except for those with intracranial lesions, such as delayed traumatic intracerebral hemorrhage, etc. The early diagnosis and comprehensive treatment can improve prognosis.

[Fat embolism syndrome in skeletal trauma: particularities of the diagnosis, economic aspects and the role of non-invasive ventilation in intensive care].

The article deals with a multicenter study that demonstrates the possibility and feasibility of noninvasive ventilation in patients with skeletal trauma complicated wiith fat embolism syndrome. The authors found additional criteria for the severity of the condition of patients with trauma. Important criteria for the choose a type of ventilation (non-invasive and invasive) is the lack of consciousness, desynchronization of a patient with ventilator and the need for a specialized regimes or miorelaxation to synchronize with the respirator.

Fat embolism: the hidden murder for trauma patients!

INTRODUCTION: fat embolism syndrome (FES) is an acute respiratory disorder that occurs when an inflammatory response causes the embolization of fat and marrow particles into the bloodstream. The exact incidence of FES is not well defined due to the difficulty of diagnosis. FES is mostly associated with isolated long bone trauma, and it is usually misdiagnosed in other trauma cases. The scope of this study was to identify and search the current literature for cases of FES in nonorthopedic trauma patients with the aim of defining the etiology, incidence, and main clinical manifestations. METHODS: we perform a literature search via the PubMed journal to find, summarize, and incorporate reports of fat embolisms in patients presenting with non-orthopedic trauma. RESULTS: the final literature search yielded 23 papers of patients presenting with fat embolism/FES due to non-orthopedic trauma. The presentation and etiology of these fat embolisms is varied and complex, differing from patient to patient. In this review, we highlight the importance of maintaining a clinical suspicion of FES within the trauma and critical care community. CONCLUSION: to help trauma surgeons and clinicians identify FES cases in trauma patients who do not present with long bone fracture, we also present the main clinical signs of FES as well as the possible treatment and prevention options.