Post-traumatic Fat Embolism Research Articles

Post-traumatic Fat Embolism in Intensive Care

Fat embolism syndrome (FES) is a group of clinical, biological and radiological symptoms resulting from obstruction of the microcirculatory network by microdroplets of insoluble fat. It is a complication most often observed in the aftermath of a polytrauma involving several long bone fractures, but it can also occur outside the traumatic context. The aim of this study was to examine the epidemiological, pathogenic, clinical, paraclinical, therapeutic and evolutionary aspects of fat embolism syndrome. This was a retrospective study including all cases of post-traumatic fat embolism collected in the surgical intensive care unit of the Chu Ibn Rochd in Casablanca over a period of 5 years. 24 cases of post-traumatic fat embolism were collected. Male sex, age less than 40 years and the presence of a femur fracture were the dominant characteristics of the epidemiological profile of the trauma patient presenting with this syndrome occurring mainly within 72 hours of the trauma. The clinico-biological presentation was dominated by respiratory distress, consciousness disorders, anaemia, thrombocytopenia and hypocholesterolaemia. The management of FES was symptomatic, combining early immobilisation of fracture sites, optimal analgesia and maintenance of an effective blood volume. 41.66% of patients required mechanical ventilation and 75% underwent osteosynthesis of their fracture sites. 25% developed ARDS and the mortality rate was 26.08%.

Post traumatic fat embolism: The experience of Ibn Tofail hospital, Marrakech

The post traumatic fat embolism (FE) is a group of pulmonary and systemic manifestations secondary to the obstruction of small vessels by fatty particles in a traumatic context following bone fractures. Our work is a retrospective descriptive study conducted in the intensive care unit of Ibn Tofail Hospital in Marrakech during a period from February 2019 to January 2020. The aim of our study was to describe the epidemiological, clinical, paraclinical, therapeutic and evolutionary profiles related to post-traumatic fat embolism. The diagnosis was based on the Gurd criteria. we collected 9 cases which are characterized by the predominance of young male, a femur fracture and a delay between the trauma and the onset of symptoms greater than 72 hours. The clinical and biological profile was dominated by hypoxemia, ARDS, confusion, anaemia and thrombocytopenia. The management remains symptomatic after the surgical fixation and may require a mechanical ventilation. The outcome of our patients was favorable when FE was isolated. Our study confirms that the post traumatic fat embolism is a serious complication with pulmonary and neurological damage that can worsen patient’s prognosis especially with associated trauma injuries, hence the importance of prevention.

Post-traumatic fat embolism syndrome: a case report

El sindrome de embolismo graso (SEG) post traumatico es una complicacion potencialmente letal y poco sospechada. Se presenta un caso de SEG diagnosticado clinicamente y confirmado por los criterios diagnosticos vigentes; cuyas caracteristicas epidemiologicas, factores de riesgo, cuadro clinico y evolucion favorable despues del tratamiento recibido, fueron de acuerdo a lo publicado. Se realiza una revision de la literatura y se proponen medidas para disminuir el riesgo de su presentacion y mejorar el diagnostico oportuno.

English

English

Is There Any Role of Inhalational Corticosteroids in the Prophylaxis of Post-Traumatic Fat Embolism Syndrome?

Fat embolism syndrome (FES) is primarily a lung parenchymal disorder resulting from interstitial and alveolar inflammation triggered by the lipid metabolites in blood circulation. The 'low-dose' corticosteroid is supposed to have a prophylactic effect on the incidence of the FES and arterial hypoxemia by reducing this inflammatory response. It is expected that inhaled corticosteroids (ciclesonide aerosol) may prevent the development of hypoxemia or fat embolism syndrome in high-risk patients by reducing this inflammatory response. Metered-dose inhaler (MDI) steroid preparations can reach the lung parenchyma with minimal systemic effect. Sixty cases of polytrauma patients presenting within eight hours of injury were randomly allocated into one of the two groups. In Group 1 (n1=30) ciclesonide, 640 mcg, was given with a metered dose inhaler and repeated once again after 24 hours, whereas Group 2 (n2=30) was taken as control and observed for 72 hours for any episode of hypoxia. The outcome was assessed using Schonfeld’s criteria for the eventual outcome of subclinical or clinical FES. Out of 30 patients in each group, six patients developed subclinical FES, whereas three from ciclesonide prophylaxis group and eight from controls developed clinical FES. There is no statistical significance found between the eventual outcomes of subclinical or clinical FES between the ciclesonide prophylaxis and control group. Although there was a trend seen in the possible preventive efficacy of inhalational steroid in the present study, it did not reach the statistically significant level. The prophylactic role of inhalational steroid in post-traumatic subclinical and clinical FES is statistically insignificant in the present study.

Imaging and histological findings of fat embolism in the vena cava

We describe an unusual case of a post-traumatic fat embolism in the vena cava and left femoral vein identified on CT before the onset of fat embolism syndrome. The patient was successfully treated by insertion of a vena cava filter and venous thrombectomy. This is the first occurrence of early identification of a large fat embolus allowing its extraction before occurrence of severe respiratory failure.

Uso de corticoide na profilaxia para síndrome de embolia gordurosa em pacientes com fratura de osso longo

The "Evidence-based Telemedicine - Trauma & Acute Care Surgery" (EBT-TACS) Journal Club conducted a critical review of the literature and selected three recent studies on the use of corticosteroids for the prophylaxis of fat embolism syndrome. The review focused on the potential role of corticosteroids administration to patients admitted to the intensive care unit (ICU) at risk of developing post-traumatic fat embolism. The first study was prospective and aimed at identifying reliable predictors, which occurred early and were associated with the onset of fat embolism syndrome in trauma patients. The second manuscript was a literature review of the role of corticosteroids as a prophylactic measure for fat embolism syndrome (FES). The last manuscript was a meta-analysis on the potential for corticosteroids to prophylactically reduce the risk of fat embolism syndrome in patients with long bone fractures. The main conclusions and recommendations reached were that traumatized patients should be monitored with non-invasive pulse oximetry and lactate levels since these factors may predict the development of FES, and that there is not enough evidence to recommend the use of steroids for the prophylaxis of this syndrome.

A40 Reversible Cytotoxic Cerebral Oedema in Post-Traumatic Cerebral Fat Embolism prior to Operative Repair of Femoral Fracture. The Efficacy of Hypothermia Induction

A40 Reversible Cytotoxic Cerebral Oedema in Post-Traumatic Cerebral Fat Embolism prior to Operative Repair of Femoral Fracture. The Efficacy of Hypothermia Induction

Correlation between outliving period and trauma severity in persons died from posttraumatic fat embolism

Posttraumatic fat embolism follows the injury. The fat emboli in circulation could cause death in three ways: isolated lung fat embolism, systemic fat embolism and fat embolism syndrome (FES). In forensic pathology, only two trauma scores, based on disintegration of anatomic structures, could be used for objectivization, comparison and establishment of severity of injuries. One of them is Injury Severity Score--ISS, based on Abbreviated Injury Scale--AIS. The second one is Hannover Polytrauma Score--HPTS, based on the total sum of all injuries and age of the injured person. The objectives of this paper were to establish the correlation between outliving period and trauma severity (based on ISS and HPTS values), in persons died from posttraumatic fat embolism and/or its complications, and to establish which of these score systems could be better for prediction of development of the posttraumatic fat embolism. The retrospective autopsy study was performed and it included the material of the Institute of Forensic Medicine in Belgrade for period 1988-2001. The autopsy reports and clinical medical data were analyzed, for persons died from posttraumatic fat embolism and/or its complications. In all cases, the fat embolism was the single cause of death, verified by autopsy. In each case, ISS and HPTS values were obtained. The sample was statistically prepared (chi2 test, correlation coefficient, regression line). The sample included 50 persons: 41 males and 9 females. The proportion of men was statistically significant (chi2 = 20.480; p < 0.001). Average age of male was 55.26 years (SD = 21.39) and of female was 55.78 (SD = 17.45). There was no statistically significant disproportion among the age distribution of the sample (chi2 = 6.4; p > 0.05). The outliving period varied from 1-14 days: the average was 5.92 (SD = 3.39; Med. 5.50; Mod. 2). The average value of 1SS was 19 (SD = 7.70; Med. 19; Mod. 14), and for HPTS average value was 28.16 (SD = 12.87; Med. 26.50; Mod. 12). In literature, there have been data about critical ISS value: 12-20. HPTS value of 20 to 35 was lethal in 25%. Each injured of our sample had, at least, one long bone or pelvic fracture. There was negligible negative correlation between outliving period and 1SS and HPTS values in our sample: coefficient of linear correlation r = -0.117, t = 0.83 and r = -0.088, t = 0.59. Our sample was representative (t = 8.37). These data pointed out that the outliving period of the observed patients, died from post-traumatic fat embolism, was not in relation to general severity of injuries but to fat embolism per se and its consequences. There was low positive correlation between ISS and HPTS values: r = 0.296, t = 2.147, coefficient of determination r2 = 0.0876 and linear regression HPTS = 18.7588+0.4948 ISS. These data indicated that direct correlation between scores was only about 9% and the rest of correlation i.e. 91% depended on other factors. There was negative negligible correlation between outliving period and severity of injury based on ISS and HPTS, in patients died from posttraumatic fat embolism. So, these score systems are useless for prediction of duration of the outliving period in the injured died from fat embolism as well as for prediction of posttraumatic fat embolism as cause of death.

Fat embolism syndrome without respiratory failure

We present a case of post-traumatic fat embolism syndrome according to Gurd's criteria. At no time did the patient have respiratory failure. Neurological symptoms were coma and focal signs, these evolved favourably until complete recovery.

Management of post-traumatic fat embolism in the emergency department

Fat embolism following trauma is not commonly seen in the emergency department, since the signs and symptoms of post-traumatic fat embolism usually occur several hours or even days later. However, fat embolism is one of the major causes of death secondary to skeletal injuries. Everyday, there are a significant number of orthopaedic injuries or trauma presentations to every Emergency Department, which have potential to develop post-traumatic fat embolism. This article is intended to give an overview of pathophysiology, clinical manifestation and management of post-traumatic fat embolism. Through understanding the pathophysiology of post-traumatic fat embolism, emergency staff can actually play an important role in the preventive management of fat embolism following traumatic injury. Hulman described fat embolism as the mechanical blockage of the lumina of blood vessels by circulating fat particles. The first case of post-traumatic fat embolism was published by Zenker in 1862. From Zenker's studies, he stated that the embolised fat originated from the contents of a lacerated stomach although his patient also had fractured ribs. In 1990, the studies of Levy and Liu et al, suggested that more than 90% of traumatic injuries were found to have fat embolism in organs and tissues. Considering the complications of orthopaedic trauma, fat embolism is an important cause of secondary death. Fat embolism can occur 12 to 48 hours or even up to 10 days post traumatic injury. Schwartz et al, states that, the progress of the fat embolism is affected by the degree of mobility of injured tissue and the condition of circulation. The mobilisation of fat emboli is also affected by the presence of hypovolaemia.

Fulminating Fat Embolism Syndrome Caused by Paradoxical Embolism through a Patent Foramen Ovale

The post-traumatic fat embolism syndrome is a multisystem disorder characterized by pulmonary and neurologic dysfunction, pyrexia, and a petechial rash1–4. More than a century after the first descriptions of the fat embolism syndrome, the cause of fat emboli and the pathogenesis of the systemic manifestations of this disorder remain incompletely understood. We describe a patient undergoing treatment of a femoral fracture in whom massive fat embolism was demonstrated by transesophageal echocardiography. Acute cor pulmonale developed, precipitating paradoxical fat embolism across a patent foramen ovale, with the subsequent development of the fat embolism syndrome. Embolism of fat across a . . .

Prostanoid production and pulmonary hypertension after fat embolism are not modified by methylprednisolone

Bilateral cemented arthroplasty (BCA) in anaesthetized mongrel dogs produces particulate fat and marrow embolism of the lung. Methylprednisolone sodium succinate (MPSS) has been advocated for post-traumatic fat embolism to prevent acute lung injury. We used the BCA procedure to produce acute fat and marrow embolism, and tested the efficacy of MPSS (30 mg.kg-1) in preventing physiological and pathological markers of acute lung injury. Dogs (n = 6) pre-treated with MPSS demonstrated similar acute increases in pulmonary artery pressure (PAP) within one minute of BCA (17.8 +/- 7.3 mmHg) as the untreated (control n = 7) dogs (18.6 +/- 12.6). Pulmonary vascular resistance (PVR) increased to the same degree in both groups (455 +/- 323 and 319 +/- 137 dyne.sec.cm-5) and PaO2 decreased by 18.3 +/- 6.4 mmHg in the control group as opposed to 12.4 +/- 7.7 mmHg in the MPSS group within five minutes of BCA. Circulating arterial and mixed venous plasma concentrations of thromboxane B2 (TxB2) increased within one minute of BCA in both groups with no increase in the transpulmonary gradient. Arterial plasma 6-keto prostaglandin F1 alpha (6-keto PGF1 alpha) increased (0.91 +/- 0.29 ng.ml-1 and 0.87 +/- 0.43 ng.ml-1) in both groups one minute after BCA. Mixed venous 6-keto PGF1 alpha plasma concentration also increased, but a significant transpulmonary 6-keto PGF1 alpha gradient was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Post-traumatic Fat Embolism—Its Clinical and Subclinical Presentations

A prospective study of post-traumatic fat embolism among a group of Chinese patients suffering from fractures demonstrated an incidence of 8.75% in fracture patients with overt clinical features and a mortality rate of 2.5%. In a multiple-fracture group the incidence of fat embolism was 35%. The significant findings of 64% of the patients with a low arterial pO2 and 52% with positive cryostat tests for fat globules suggested a high incidence of subclinical presentation. The presence of large vacuoles in the cryostat sections is demonstrated and its significance discussed. The 'iceberg' phenomenon of fat embolism syndrome should be well recognized, particularly in patients with multiple fractures.

Embolies graisseuses post-traumatiques

Between 1977 and 1982, fifty cases of post-traumatic fat embolism were treated in a general intensive care unit. Average age of patients was 25.5 ± 13 years; there was no male majority. Mean free interval was 39 ± 27 h. 12 cases (24%) had single fractures and 38 (76%) multiple fractures. Forty-four patients had a fractured femur. Thirty-two patients presented the complete clinical syndrome with general, respiratory, neurological and cutaneous signs. Thrombocytopaenia and hypocholesterolaemia were the biological signs most often seen. In forty-four patients, orthopaedic treatment consisted of immediate immobilization, usually with traction. Twenty-six patients were reoperated on : intramedullary nail for twenty patients, plate for the other six. Fat embolism appeared in spite of surgery in six cases; it worsened after surgery in six others. Seven patients had per- or postanaesthetic problems. Fourteen per cent of patients died. The decrease in mortality was mainly due to an improvement in mechanical ventilation techniques. Early surgical fixation remained the rule if there was no serious respiratory distress or haemodynamic instability, although it did not seem to change the mortality rate in this group of patients.

Fat embolism syndrome

Patients with the fat embolism syndrome are reported to have a severe course, with mortality as high as 15 percent. Recent studies have attributed improved prognosis to one or another treatment modality. We reviewed the 54 patients with clinical evidence of the posttraumatic fat embolism syndrome documented at the Foothills Hospital from 1968 to 1977. The criteria for diagnosis were fever (54/54), hypoxemia (52/52), diffuse pulmonary infiltrates

Fat Embolism Syndrome: Changing Prognosis

Patients with the fat embolism syndrome are reported to have a severe course, with mortality as high as 15 percent. Recent studies have attributed improved prognosis to one or another treatment modality. We reviewed the 54 patients with clinical evidence of the posttraumatic fat embolism syndrome documented at the Foothills Hospital from 1968 to 1977. The criteria for diagnosis were fever (54/54), hypoxemia (52/52), diffuse pulmonary infiltrates (49/54), changes in sensorium (41/54), and petechiae (39/54). Therapy included supplemental oxygen (54), assisted ventilation with positive end-expiratory pressure (5), and corticosteroids (7). There were no deaths. Patients who have the fat embolism syndrome without associated life-threatening disease have a relatively good prognosis with modern therapy, in contrast to reports in most of the published literature.

The role of shock in the pathogenesis of fat embolism after trauma

Experimental studies and pathological investigations indicate that intrusion of fat into the circulation is common after trauma. This may not have any effect unless frank hypovolaemia a supervenes upon changes in the blood vessels, manifested by a deficient vasomotility in shock. After fat embolism disseminated intravascular coagulopathy may occur as a consequence of the haematological changes and disturbances of capillaries. The morphological appearance of massive post-traumatic fat embolism evolves from the compensatory effect of accumulated synergistic factors that primarily induced the changes. From this point of view fat embolism should be recognized in the additional important role of an epiphenomenon of post-traumatic shock.

Post-traumatic fat embolism : Bellotti C., Formaggio G., Gatti G. and Regalia F. (1975). Three cases of post-traumatic fat embolism. Minerva Ortopedica26, 331 (Italian)

Post-traumatic fat embolism : Bellotti C., Formaggio G., Gatti G. and Regalia F. (1975). Three cases of post-traumatic fat embolism. Minerva Ortopedica26, 331 (Italian)

Relations between coagulability of the blood and post-traumatic fat embolism

Relations between coagulability of the blood and post-traumatic fat embolism