Fat embolism syndrome overview: Difference between revisions
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{{Fat embolism syndrome}} | {{Fat embolism syndrome}} | ||
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==Overview== | ==Overview== | ||
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. | 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. |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Feham Tariq, MD [2]
Overview
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.
Historical Perspective
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 cerebral symptoms associated with FES.
Classification
- There is no established system for the classification of fat embolism syndrome.
Pathophysiology
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.
Causes
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 [disease name] from other Diseases
- [Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as:
- [Differential dx1]
- [Differential dx2]
- [Differential dx3]
Epidemiology and Demographics
- The prevalence of [disease name] is approximately [number or range] per 100,000 individuals worldwide.
- In [year], the incidence of [disease name] was estimated to be [number or range] cases per 100,000 individuals in [location].
Age
- Patients of all age groups may develop [disease name].
- [Disease name] is more commonly observed among patients aged [age range] years old.
- [Disease name] is more commonly observed among [elderly patients/young patients/children].
Gender
- [Disease name] affects men and women equally.
- [Gender 1] are more commonly affected with [disease name] than [gender 2].
- The [gender 1] to [Gender 2] ratio is approximately [number > 1] to 1.
Race
- There is no racial predilection for [disease name].
- [Disease name] usually affects individuals of the [race 1] race.
- [Race 2] individuals are less likely to develop [disease name].
Risk Factors
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.
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.
Diagnosis
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.
Physical Examination
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.
Laboratory Findings
- There are no specific laboratory findings associated with [disease name].
- A [positive/negative] [test name] is diagnostic of [disease name].
- An [elevated/reduced] concentration of [serum/blood/urinary/CSF/other] [lab test] is diagnostic of [disease name].
- Other laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].
Imaging Findings
- There are no [imaging study] findings associated with [disease name].
- [Imaging study 1] is the imaging modality of choice for [disease name].
- On [imaging study 1], [disease name] is characterized by [finding 1], [finding 2], and [finding 3].
- [Imaging study 2] may demonstrate [finding 1], [finding 2], and [finding 3].
Other Diagnostic Studies
- [Disease name] may also be diagnosed using [diagnostic study name].
- Findings on [diagnostic study name] include [finding 1], [finding 2], and [finding 3].
Treatment
Medical Therapy
- There is no treatment for [disease name]; the mainstay of therapy is supportive care.
- The mainstay of therapy for [disease name] is [medical therapy 1] and [medical therapy 2].
- [Medical therapy 1] acts by [mechanism of action 1].
- Response to [medical therapy 1] can be monitored with [test/physical finding/imaging] every [frequency/duration].
Surgery
- Surgery is the mainstay of therapy for [disease name].
- [Surgical procedure] in conjunction with [chemotherapy/radiation] is the most common approach to the treatment of [disease name].
- [Surgical procedure] can only be performed for patients with [disease stage] [disease name].
Prevention
- There are no primary preventive measures available for [disease name].
- Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].
- Once diagnosed and successfully treated, patients with [disease name] are followed-up every [duration]. Follow-up testing includes [test 1], [test 2], and [test 3].