Fat embolism syndrome overview
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A fat embolism is a type of embolism that is often (but not always) caused by physical trauma. Fat emboli can occur whenever there is a pulmonary embolism. The fat embolism syndrome (FES) is characterized by the triad of hypoxemia, mental status changes and petechiae. The syndrome is usually trauma related and seen with closed fractures of the long bones or pelvis.
In 1861, Zenker first discovered fat embolism (FES), after he found pulmonary capillary fat deposition in a patient who suffered from crush injury. In 1873, Bergmann described the first clinical case of FES in a patient who suffered a distal femur fracture. In 1875, Czerny explored cerebralsymptoms associated with FES.
There is no established system for the classification of fat embolism syndrome.
Fat embolism syndrome (FES) is the presence of fat globules in the circulation post traumatic insult which can lodge into the small sized capillaries in the lung, brain and skin leading to devastating clinical manifestations. The two widely accepted theories which explain the pathophysiology of FES are mechanical and biochemical theory. The mechanical theory proposes that there is mechanical obstruction by fat cells from the bone marrow in the end-capillaries after trauma. Biochemical theory attributes the clinical manifestations of FES to the pro inflammatory effect of fat emboli.
The causes of fat embolism syndrome can be divided into trauma and non-trauma related. The most common cause of fat embolism syndrome is long bone fracture especially the femur. Other causes include orthopedic procedures, liposuction, pelvic fractures and soft tissue injury.
Differentiating Fat Embolism Syndrome from other Diseases
Fat embolism syndrome should be differentiated from other diseases presenting with chest pain, shortness of breath, tachypnea and neurological deficits. FES must be differentiated from meningitis, pneumonia, pulmonary embolism, stroke, thrombotic thrombocytopenic purpura.
Epidemiology and Demographics
The exact incidence of FES is unknown and is estimated to be of <1% to >30% of all trauma cases. It commonly affects individuals 10-40 years of age. Fat embolism syndrome more commonly affects men more than women.
The risk factors playing an important role in the development of fat embolism are blunt trauma, acute pancreatitis, diabetes mellitus, long bone fractures and liposuction.
There is insufficient evidence to recommend routine screening for fat embolism syndrome.
Natural History, Complications and Prognosis
Fat embolism syndrome commonly occurs 12-24 hrs after the inciting event. It can occur as early as 12 hrs and as late as 2 weeks. Patients are often dyspneic, tachypneic and hypoxic. Complications of fat embolism syndrome include disseminated intravascular coagulation, right ventricular dysfunction, acute respiratory distress syndrome and shock. Most patients recover with supportive treatment. Mortality occurs in 5-15% of patients.
History and Symptoms
A detailed history and early detection of symptoms is vital for the diagnosis of fat embolism (FES). It is entirely a clinical diagnosis. Patients with fat embolism may have a positive history of long bone fracture, orthopedic procedure, plastic surgical procedure or parenteral lipid transfusion. The symptoms may take 24-48 hours to become apparent and can be categorized as pulmonary, neurological and cutaneous symptoms.
Fat embolism syndrome(FES) is characterized by multisystem dysfunction most commonly presents in 12 to 72 hours after the initial insult. It is a clinical diagnosis and requires high degree of suspicion. The classic triad of clinical manifestations are petechiae, hypoxemia and neurological abnormalities. Pulmonary manifestations are the most common initial signs of FES and include dyspnea, tachypnea, hypoxemia, and respiratory failure of which the hypoxemia is the earliest feature that . Other findings on physical examination are retinal exudates, scotomatas and intravascular fat globules.
There are no electrocardiogram(ECG) findings associated with fat embolism syndrome.
Chest X-ray in fat embolism syndrome is done in fat embolism to rule out the complications such as acute respiratory distress syndrome and any other possible diagnosis, for example, pulmonary embolism or pulmonary edema. It takes 12-24 hours for the abnormalities to appear on chest X-ray which include bilateral air space opacities, snow-storm appearance, increased pulmonary vascular markings and dilated right heart.
High resolution computed tomopraphy (HRCT) of the lung shows thickening of the interlobular septa, bilateral ground-glass opacities and centrilobular nodular opacities. CT scan of the head is also done in patients with neurological deficits.
Magnetic resonance imaging (MRI) is performed in patients in patients with neurological deficits and shows the following reversible abnormalilties such as "starfield" pattern of diffuse, punctate, hyperintense lesions
Echocardiography may be helpful in the diagnosis of fat embolism syndrome. Findings of fat embolism syndrome include demonstartion of echogenic material passing through the right atrium followed by increased pulmonary pressures and right heart pressures and subsequent paradoxical embolization of this material through a patent foramen ovale (PFO).
Other Imaging Findings
Pulmonary ventilation/perfusion scan may be helpful in the diagnosis of fat embolism syndrome. Findings include demonstration of multiple subsegmental perfusion defects.
Other diagnostic studies
There are no other diagnostic studies done to diagnose fat embolism syndrome.
The mainstay of treatment of fat embolism syndrome is supportive care, anticoagulation in some cases and corticosteroid therapy in severe respiratory distress. The main steps followed in conservative management include in ICU supportive care, fluid resuscitation, supplemental oxygen, mechanical ventilation and intracranial monitoring.
Surgical intervention is not recommended for the management of fat embolism syndrome.
Effective measurement for the primary prevention of fat embolism include early fixation of long bone fractures, external fixation with a plate and screw and use of small-diameter nails.
The secondary prevention of fat embolism syndrome is the same as primary prevention.