Diagnosis Of Fat Embolism Research Articles

Fat Embolism Syndrome: A Rare Case Report

Background: Fat embolism syndrome (FES) is a life-threatening complication in patients with orthopedic trauma, especially long bone fractures. The diagnosis of fat embolism is made by clinical features alone with no specific laboratory findings. FES has no specific treatment and requires supportive care, although it can be prevented by early fixation of bone fractures. Here, we report a case of FES in a patient with a right closed femoral fractrure severe comminutive, which was diagnosed initially by Gurd’s criteria and subsequently confirmed by typical appearances on Magnetic Resonance Imaging (MRI) of the brain. The most important for fat embolism syndrome management is divided two-fold: preventative and supportive. Patient: A 43-year-old male fell from a high-rise building approximately 3 days before admission. A deformity was observed on the right thigh and the patient felt intense pain. After a few hours, the patient became weak and experienced a loss of consciousness. He was diagnosed with Fat Embolism Syndrome (FES) by using Gurd’s criteria. The diagnosis was confirmed after excluding other diagnoses with similar clinical presentation.

Fat Embolism and Severe Natural Disease: Challenges for Certification

Detectable intravascular fat has been reported in up to 90% of patients with long bone fractures. However, the more clinically significant fat embolism syndrome (FES) is less common. Despite its common occurrence, determining the significance of fat embolism as a cause of death remains controversial; however, helpful objective criteria through a tiered approach have recently been proposed. Patients with coexisting natural disease and fat embolism present an additional challenge for interpretation. We present an illustrative 59-year-old woman with severe comorbidities who died 11 days following a femoral neck fracture and discuss how the use of special techniques to demonstrate embolic fat and published guidelines for diagnosis were helpful in death certification. The case also provides a beautiful morphologic illustration of the accumulation of lipid laden alveolar macrophages as intravascular fat is absorbed into the tissues over time. Such macrophages can also be clinically detected by bronchoalveolar lavage, which can provide some objective support for a clinically suspected diagnosis of fat embolism.

The study of diagnostic test of using the ten-point scale for the early fat embolism syndrome

Objective To explore the clinical value of the ten-point scale in the early diagnosis of fat embolism syndrome.Methods The data of 129 patients with fat embolism syndrome diagnosed by Gurd criteria admitted from January 1993 to February 2012 were analyzed retrospectively.At the same time,another 97 patients with single or multiple long bone fracture and/or pelvic fracture without fat embolism admitted from July 2005 to February 2012 were enrolled as control group.Patients were excluded if they had any of the following diseases:simple brain trauma,thoracic injury,spine fracture,hemorrhagic shock and the complications of cardiopulmonary cerebral resuscitation (CPCR).The patients of two groups were comparable in respect of clinical setting.The clinical data were analyzed and scored by the ten-point scale.The x2 test were applied to statistical works.Results Among all the clinical characteristics,the incidence of increased D-dimer was the highest (74.1％) in early fat embolism syndrome,followed by the progressive decrease in hemoglobin (63.6％) and hypoxemia (57.4％),and the occurrence of dyspnea was the lowest (17.8％).The percentage of total scores over ten points in patients with fat embolism syndrome group was higher than that in those without fat embolism syndrome (x2 =202.6,P ＜ 0.01).The sensitivity of tenpoint scale was 96.12％ and the specificity was 99.8％.Conclusions Ten-point scale could be used to make early diagnosis of fat embolism syndrome,thereby reducing the occurrence of misdiagnosis and misseddiagnosis. Key words: Ten-point scale; Fat embolism syndrome; Early diagnosis; Differential diagnosis

Fat embolism syndrome: Clinical and imaging considerations: Case report and review of literature

Fat embolism syndrome (FES) is a serious clinical disorder occurring after trauma, orthopedic procedures and rarely in non-traumatic patients. Fat emboli develop in nearly all patients with bone fractures, but they are usually asymptomatic. Small number of patients develop signs and symptoms of various organ system dysfunction due to either mechanical obstruction of capillaries by fat emboli or due to hydrolysis of fat to fatty acids. A triad of lung, brain and skin involvement develop after an asymptomatic period of 24 to 72 hours. This symptom complex is called FES. The incidence reported is up to 30%, but many mild cases may recover unnoticed. Diagnosis of fat embolism is clinical with nonspecific, insensitive diagnostic test results. Treatment of fat embolism syndrome remains supportive and in most cases can be prevented by early fixation of large bone factures. Here we report two cases of traumatic fat embolism, which were diagnosed initially by Gurd's criteria and subsequently confirmed by typical appearance on magnetic resonance imaging (MRI) of the brain in these patients. These patients were successfully treated with supportive management. In conclusion, diagnosis of FES needs high index of suspicion, exclusion of other conditions and use of clinical criteria in combination with imaging. Magnetic resonance imaging of the brain is of great importance in diagnosis and management of these patients.

Cerebral fat embolism diagnosed by magnetic resonance imaging at one, eight, and 50 days after hip arthroplasty: a case report

To describe cardiovascular collapse during a cemented hip hemiarthroplasty in a patient who, despite a successful cardiopulmonary resuscitation, remained in a persistent vegetative state due to cerebral fat embolism diagnosed by magnetic resonance imaging (MRI). A 75-yr-old woman with no medical history underwent cemented hip hemiarthroplasty under spinal anesthesia for a right femoral neck fracture. Shortly after insertion of the prosthesis, a sudden oxygen desaturation, hypotension, bradycardia, and cardiac arrest occurred. The patient was successfully resuscitated, but did not regain consciousness. The patient developed high-grade fever, thrombocytopenia, anemia, and oliguria. MRI scans of the brain revealed multiple high intensity signals throughout the white matter, the basal ganglia, the cerebellum, and the brain stem. The diagnosis of fat embolism was made on the basis of clinical findings and MRI images. Although her cardiorespiratory status improved over the next week, the patient remained in a persistent vegetative state. When fat embolism is suspected, serial MRI scans of the brain should be performed to diagnose the etiology of cerebral embolism as well as to evaluate the severity of brain damage.

Anatomical-pathological considerations in the etiology and diagnosis of fat embolism

Anatomical-pathological considerations in the etiology and diagnosis of fat embolism

EVALUATION OF THE GURD TEST FOR FAT EMBOLISM

1. Blood from forty-one healthy volunteers, seventy-one patients with fractures but without symptoms of fat embolism and seven patients with clinical evidence of fat embolism was examined microscopically for fat droplets and chemically for triglycerides. 2. Fat droplets, after Millipore filtration of the blood, were seen evenly distributed in all three groups. 3. There was no significant difference in triglyceride concentration between serum and filtrate in the three groups. 4. The results do not support the thesis that the Gurd test is a reliable aid in the diagnosis of fat embolism.

Fat particles in plasma: The macroglobule: Its relevance to the concept of fat embolism

The present study indicates that large fat globules, 5 microns or more in diameter, are often found in the blood of normal individuals. This demonstration contests the value of the finding in the diagnosis of fat embolism. These fat macroglobules possess a composition analogous to that of chylomicrons. The question is raised whether they are artifactually produced in vitro by an unstable emulsion or whether they exist in vivo. Until the nature of the phenomenon is clarified, the noncommittal term “fat macroglobulemia” is suggested. A relation probably exists between fat macroglobulemia and the not uncommon presence of fat in the lungs at autopsy.

Diagnosis of Fat Embolism

To the Editor:— Physicians and patients could benefit from ophthalmoscopy in cases of possible fat embolism. Evarts' discussion of the management of this condition (194: 899, 1965) omitted the diagnostically useful retinopathy of Purtscher, or traumatic retinal angiopathy. Whitish gray opaque patches in the retina are seen near blood vessels, sometimes accompanied by hemorrhages. These are observed two to four days after bone injuries, or postoperatively in cases in which there has been much handling of fat tissues. This retinopathy was described by Jacobi in 1868, later studied by the Austrian ophthalmologist Purtscher in 1910. Size of lesions and degrees of visual impairment vary; transient small field defects may occur, but optic-nerve atrophy is not rare. The Viennese Urbanek (1934) correlated the clinical picture with histologically demonstrated fat emboli in retinal vessels, confirmed by Walsh in 1947.

FAT EMBOLISM

The history of experimental fat embolism dates as far back as 1669, when Lower1did some work on lipemia and its effect on the circulation in animals. Since that time a tremendous amount of work has been done,2both clinically and experimentally, on the accurate detection of fat embolism. As far as we know, roentgen examination has never been used for this purpose. Therefore we are presenting for the first time the results of experimental work which show the value of the roentgenograms of the chest in the diagnosis of fat embolism. EXPERIMENTAL PROCEDURE AND RESULTS We used eleven dogs in our experiments, selecting whenever possible an animal weighing close to 12.5 Kg. Sterile oleic acid was given intravenously to six animals and sterile olive oil to five. Doses of varying amounts were used in each experiment. Owing to the researches of Landois,3who found that olein

The clinical diagnosis of fat embolism

F AT embohsm can be defined as the introduction of Iiquid fat into the circmation and its transportation by the bIood stream to occIude the finer bIood vesseIs in various parts of the body. This condition is a frequent resuIt of fractures of the long bones or any other trauma which is associated with damage to adipose tissue. In the majority of cases only an insignificant grade of fat emboIism is produced by the types of injury mentioned. In a few instances, however, especiaIIy when the Iong bones of the Iower extremity are fractured, a Iarge quantity of fat may gain access to the bIood vesseIs and so interfere with the bIood suppIy of the vita1 organs that death resuIts. In most fractures of the Iong bones three factors are present which promote the deveIopment of fat emboIism. They are: (I) The destruction of fat ceIIs in the bone marrow and in the surrounding intermuscuIar tissues so that a Iarge amount of Iiquid oi1 is produced. (2) The tearing of the venuIes in the Haversian canaIs of the bones which cannot coIIapse readiIy because of the rigid waIIs in which they are encased. (3) A mechanism such as muscular spasm or manipuIation of the broken bones which increases interna pressure in the region of the fracture and so favors entrance of the fat into the veins. In the majority of fractures of the Iower extremities (80 per cent) the processes of repair are effective and prevent the entrance of any considerabIe quantity of fat into the bIood stream. For this reason, serious cases of fat emboIism are not common and when they occur it is probable that mechanica interference with the broken bones has interfered with the processes of repair.’ The way in which fat emboIism deveIops in the human subject is not known in a11 its detaiIs. Many have the conception that the fat enters the bIood as a coherent coIumn of oi1 which bIocks the puImonary artery and causes immediate asphyxia. This eventuaIity may occur in rare instances, but in the vast majority of cases it is more probabIe that the fat is forced into the veins at intervaIs as insuIts of various sorts are offered to the injured extremity. Symptoms are produced when sufficient emboIi accumuIate in the Iungs to impede the pulmonary circuIation. CIinicaIIy the serious and fatal cases of fat emboIism are separated into two types: I. Pulmonary Fat Embolism. In this type the fat is transported through the veins, the right heart, the puImonary artery, and finaIIy Iodges in the arterioIes and capiIIaries of the lungs. The flow of the puImonary circuIation is impeded and the patient shows signs of asphyxia. 2. Systemic or Cerebral Fat Embolism. In this type the fat emboIi in the puImonary capilIaries are forced by pressure in the right side of the heart into the puImonary veins, the Ieft side of the heart, and the aorta, whence they are distributed a11 over the body. Most of these emboIi reach the brain and cause definitedamage of the brain substance. Because of this the patient deveIops a coma which becomes deeper and deeper unti1 his death.