Pulmonary fat embolism in non-survivors after cardiopulmonary resuscitation.

BACKGROUND: Blunt trauma acting against the human body presents the fundamental cause of pulmonary fat embolism (PFE) and fat embolism syndrome. The aim of the present study was to investigate PFE in non-survivors after cardiopulmonary resuscitation (CPR). METHODS: This was a prospective cohort study conducted in University Hospital Ostrava, Czech Republic. Within a 4-year study period, all non-survivors after CPR because of out-of-hospital cardiac arrest were assessed for the study eligibility. The presence/seriousness of PFE was determined by microscopic examination of cryo-sections of lung tissue (staining with Oil Red O). RESULTS: In total, 106 persons after unsuccessful CPR were enrolled in the study. The most frequent cause of death in the study population (63.2% of cases) was cardiac disease (ischemic heart disease); PFE was not determined as the cause of death in any of our study cases. Sternal fractures were identified 66.9%, rib fractures (usually multiple) in 80.2% of study cases; the median number of rib fractures was 10.2 fractures per person. Serious intra-thoracic injuries were found in 34.9% of cases. Microscopic examination of lung cryo-sections revealed PFE in 40 (37.7%) study cases; PFE was most frequently evaluated as grade I or II. Occurrence of sternal and rib fractures was significantly higher in persons with PFE than between persons without PFE (p = 0.033 and p = <0.001). Number of rib fractures was also significantly higher in persons with PFE. The occurrence of serious intra-thoracic injuries was comparable in both our study groups (p = 0.089). CONCLUSIONS: PFE presents a common resuscitation injury which can be found in more than 30% of persons after CPR. Persons with resuscitation skeletal chest fractures have significantly higher risk of PFE development. During autopsy of persons after unsuccessful CPR, it is necessary to distinguish CPR-associated injuries including PFE from injuries that arise from other mechanisms.

Cerebral fat emboli in a patient with paraplegia caused by bilateral femur fractures.

Cerebral fat embolism is a rare cause of stroke and therefore an overlooked diagnosis. Often it is seen as a consequence of major bone fractures or after arthroplasty, and can lead to respiratory or circulatory collapse. We present a case of a patient with a history of paraplegia after a thoracic spinal cord injury that developed cerebral fat embolism following a bilateral femur fracture. Since the patient was paraplegic and with an altered mental state upon admission, femoral bone fractures were not initially suspected. The case shows the difficulties in diagnosing this condition.

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.

Mortality Rates and autopsy findings in fat embolism syndrome complicating sickle cell disease.

Fat embolism syndrome is a rare but underdiagnosed complication of sickle cell disease associated with high morbidity and mortality. It affects predominantly patients with a previously mild course of their illness and those of non-SS genotypes while there is possibly an association with infection with human parvovirus B19 (HPV B19). Here, we present the mortality rates and autopsy findings of all reported cases to date. A systematic review has revealed 99 published cases in the world literature with a mortality rate of 46%. Mortality varied greatly according to the time of reported cases with no survivors in the 1940s, 1950s or 1960s and no deaths since 2020. 35% of cases had previously undiagnosed sickle cell disease and the latter was only identified at autopsy after developing fat embolism with a fatal outcome. 20% of cases reported after 1986 tested positive for HPV B19 with an associated mortality of 63% whereas in cases that have not documented HPV B19 infection the mortality was 32%. The organs most often staining positive for fat were the kidneys, lungs, brain and heart whereas ectopic haematopoietic tissue was found in 45% of the examined lung specimens.

Devastating neurologic injury associated with fat embolism syndrome.

ABSTRACT: The diagnosis of fat embolism syndrome (FES) may present with a constellation of symptoms and continues to be a diagnosis of exclusion. Fat embolism syndrome is a poorly understood syndrome, which is typically associated with orthopedic trauma, most commonly with long bone fractures. Understanding the presentation of FES is essential to provide timely and appropriate interventions and to ensure optimal patient outcomes. The following is a case report of FES in a 39-year-old man following a motor vehicle collision in which he sustained a comminuted fracture of the right femur. The patient was subsequently diagnosed with FES using Gurd criteria in conjunction with frequent assessment of the patient's clinical picture, as well as exclusion of other differential diagnoses. Nurse practitioners and other providers should understand the constellation of symptoms that may be associated with FES to improve prevention and ensure timely intervention.

Sickle cell disease and fat embolism: a rare complication of vaso-occlusive crisis.

A 61-year-old woman was admitted to the hospital for management of a painful vaso-occlusive crisis. She had a history of sickle cell beta-thalassaemia and end-stage renal disease managed with intermittent haemodialysis. While hospitalised, she became lethargic and unresponsive and developed acute chest syndrome. Initial MR scan of brain, cerebrospinal fluid examination and continuous electroencephalogram were unremarkable, but subsequent MR scan of brain identified a right transverse venous sinus thrombosis and extensive supratentorial and infratentorial microhaemorrhages consistent with fat emboli. We; therefore, discuss a case of non-traumatic fat embolism syndrome, a rare complication of sickle cell disease.

Fat Embolism Syndrome in Sickle Cell ß-Thalassemia Patient With Osteonecrosis: An Uncommon Presentation in a Young Adult.

Fat embolism syndrome is a relatively infrequent presentation in sickle cell thalassemia patients. It most commonly occurs in long bone fractures in the setting of trauma. However, nonorthopedic trauma and nontraumatic cases have been reported to contribute to fat embolism. The fat embolic syndrome is an underdiagnosed, life-threatening, and debilitating complication of sickle-ß-thalassemia-related hemoglobinopathies. It is primarily seen in milder versions of sickle cell disease, including HbSC and sickle cell ß-thalassemia, with the mild prior clinical course without complications; hence, diagnosis can be easily missed. Pathogenesis of fat embolic syndrome is a combination of mechanical obstruction from fat globules released into systemic circulation at the time of bone marrow necrosis and direct tissue toxicity from fatty acids and inflammatory cytokines released from fat globules. Prompt diagnosis and early initiation of treatment can reduce morbidity and mortality and result in better outcomes and prognosis. Red cell exchange transfusion is the mainstay of therapy with mortality benefits. Overall mortality and neurological sequelae continue to be high despite increased red cell exchange transfusion in the last few years. In this article, we discussed a case of a 34-year-old male patient with a history of sickle cell thalassemia and avascular necrosis of the hip, who presented with fever, hypoxia, encephalopathy, and generalized body aches, found to have thrombocytopenia and punctate lesions on magnetic resonance imaging brain, which led to the diagnosis of the fat embolism syndrome. Only a few sickle cell ß-thalassemia with fat embolic syndrome cases have been reported.

Ursodeoxycholic acid protects against lung injury induced by fat embolism syndrome.

Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) is a life-threatening disease with a high mortality rate, which was a common complication of fat embolism syndrome (FES). Ursodeoxycholic acid (UDCA) has been reported to exert potent anti-inflammatory effects under various conditions. In vivo, perinephric fat was injected via tail vein to establish a rat FES model, the anti-inflammatory effects of UDCA on FES-induced lung injury were investigated through histological examination, ELISA, qRT-PCR, Western blot and immunofluorescence. In vitro, human lung microvascular endothelial cells (HPMECs) were employed to understand the protective effects of UDCA. The extent of ALI/ARDS was evaluated and validated by reduced PaO2 /FiO2 ratios, increased lung wet/dry (W/D) ratios and impaired alveolar-capillary barrier, up-regulation of ALI-related proteins in lung tissues (including myeloperoxidase [MPO], vascular cell adhesion molecule 1 [VCAM-1], intercellular cell adhesion molecule-1 [ICAM-1]), elevated protein concentration and increased proinflammatory cytokines levels (TNF-α and IL-1ß) in bronchoalveolar lavage fluid (BALF). Pre-treatment with UDCA remarkably alleviated these pathologic and biochemical changes of FES-induced ALI/ARDS; our data demonstrated that pre-treatment with UDCA attenuated the pathologic and biochemical changes of FES-induced ARDS, which provided a possible preventive therapy for lung injury caused by FES.

[Purtscher's retinopathy as a complication to a cemented resection tumour prosthesis].

In this case report, a 53-year-old female with a pathological subtrochanteric femur fracture received a cemented resection tumour prosthesis. The patient was post-operatively diagnosed with Purtscher's retinopathy due to fat embolisation. Purtscher's retinopathy has previously been described in trauma patients, however, no previous reports exist with patients treated with prosthesis. No treatment guideline is available. There is a risk of permanent visual impairment, and it is recommended, that patients presenting reduced vision post-operatively are referred to an ophthalmologist without delay for correct diagnosis.

Análisis estructural macular bilateral tras síndrome de embolismo graso / Bilateral macular structural analysis after fat embolism síndrome

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Embolia gaseosa arterial: una rara complicación de la biopsia con aguja gruesa en el diagnóstico del nódulo pulmonar solitario / Arterial Gas Embolism: A Rare Complication of Core Needle Biopsy in the Diagnosis of Solitary Pulmonary Nodule

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VEGF mediates fat embolism-induced acute lung injury via VEGF receptor 2 and the MAPK cascade.

Fat embolism (FE) is a lethal medical emergency often caused by fracture of long bones and amputation of limbs. Vascular endothelial growth factor (VEGF) promotes angiogenesis and increases vascular permeability. We tested the hypothesis that VEGF plays a critical role in FE-induced acute respiratory distress syndrome (ARDS) and acute lung injury (ALI). Fat tissues were collected from male Sprague-Dawley rats, and animal oil was extracted and mixed with water to form fatty micelles. The micelles were then injected into the tail vein to produce FE and ALI in rats. Lung weight gain was measured as the index of pulmonary edema. The expression of pulmonary VEGF was evaluated by real-time PCR and western blot analysis. Inducible nitric oxide synthase (iNOS) and phosphorylation of mitogen-activated protein kinase (MAPK) were determined by western blot analyses. Interleukin-1ß (IL-1ß) was quantified by ELISAs. Hematoxylin and eosin staining was used to evaluate the pathological damage of ALI. In this study, we found that animal oil-induced FE significantly increased pulmonary VEGF expression and MAPK phosphorylation. We also evaluated the inflammatory response after FE and found that iNOS and IL-1ß significantly increased after FE. Systemic administration of SU-1498, an antagonist of VEGF receptor 2 (VEGFR-2), significantly attenuated the FE-induced inflammatory response and histological damage. This study suggested that VEGF is involved in FE-induced ARDS via the VEGFR-2 and MAPK cascades, which induce IL-1ß release and iNOS upregulation. Blockade of could be used to treat FE-induced pulmonary damage.

Woman with acute onset involuntary limb movements.

CLINICAL INTRODUCTION: An 88-year-old woman presented with acute onset of involuntary limb movements for one day. Two days prior she had fallen a suffered a left hip contusion but no head trauma. There was no fever or difficulty breathing. Her heart rate was 72 bpm with blood pressure of 109/68 mm Hg. Physical examination revealed restricted left hip motion due to pain and a sustained twisted posture of the upper extremity without paresis. Glasgow Coma Scale was 15, and there was no evidence of Kernig's or Brudzinski's sign. She underwent a hip X-ray and non-contrast CT scan (figures 1 and 2).emermed;36/7/415/F1F1F1Figure 1Anteroposterior X-radiograph of the hip.emermed;36/7/415/F2F2F2Figure 2A non-contrast brain CT. QUESTION: What is the most likely cause of the clinical presentation?Acute meningitisCerebral fat embolismHaemorrhagic strokeHypertensive encephalopathy For answer see page 2 For question see page 1.

[A case of bone marrow necrosis and fat embolism in a sickle-cell disease patient]. / Un cas de nécrose médullaire compliquée d'embolie graisseuse chez un patient drépanocytaire.

We report here a case of bone marrow necrosis and fat embolism syndrome in a 23-year-old sickle-cell disease (HbSS) patient. A brutal and severe bicytopenia conducted to suspect bone marrow necrosis, confirmed by bone marrow aspiration and analysis. This was the first life-threatening medical event for this patient. In the present case, a complex alloimmunization against blood group antigens complicated the treatment because of the risks associated with the transfusion strategy. These rare complications of sickle-cell disease may be fatal, but an efficient symptomatic treatment generally allows for recovery. Medical biologists should be aware of the danger of bone marrow necrosis in sickle-cell disease, so that they can help clinicians and accurately diagnose this serious complication.