Fat Embolism: Definition, Symptoms, Causes, Diagnosis, Treatment and Complications

The syndrome most often manifests itself in closed fractures of the pelvis or long bones.

A fat embolism (which through major trauma can progress to Fat Embolism Syndrome) is a type of embolism which consists of fatty material.

They are often caused by physical trauma, such as fractures, soft tissue trauma, or burns.

Fat embolism syndrome is distinct from the presence of fatty emboli, symptoms generally appear 1–3 days after a traumatic injury and are predominantly:

  • Pulmonary (shortness of breath, hypoxemia), neurological (agitation, delirium or coma), dermatological (petechial rash) and hematological (anemia, low platelets).

Manifestations and symptoms

The clinical manifestation of fat embolism syndrome (FES) can begin 12 hours to 3 days after the diagnosis of the underlying clinical disease.

The three most characteristic features are: respiratory distress, neurological features, and petechiae on the skin.

Respiratory distress (present in 75% of cases) can range from mild distress requiring supplemental oxygen to severe distress requiring mechanical ventilation.

For neurological features, those who have fat embolism syndrome may become lethargic, restless, with a drop on the Glasgow Coma Scale (GCS) due to cerebral edema rather than cerebral ischemia .

Therefore, the neurological signs are not lateralized to one side of the body. In the severe form of brain edema, a person may stop responding.

Petechiae rash usually occurs in 50% of patients.

This manifestation of the skin is temporary and can disappear in a day. Fat embolism syndrome can be divided into three types:

Sublinic Fat Embolism Syndrome : manifests as a reduced partial pressure of oxygen (PaO2) in arterial blood gases (ASG) with disordered blood parameters (reduced hemoglobin or thrombocytopenia) associated with fever, pain, malaise, tachypnea, tachycardia.

However, there is no respiratory distress, it is often confused with postoperative symptoms of fever, pain, and malaise.

Subacute fat embolism syndrome (non-fulminant fat embolism syndrome) : All three characteristic features of fat embolism are present: respiratory distress, neurological signs, and petechiae on the skin.

Petechiae are seen on the chest, armpit, shoulder, and mouth. The appearance of dermal capillaries from the fat emboli resulted in a petechial eruption. Petechiae rash occurs in 50 to 60% of cases.

Neurological signs such as confusion, stupor, and coma may be present. These are generally temporary and do not occur on one side of the body. Respiratory distress may be mild and tend to improve on the third day.

Changes in the retina similar to Purtscher retinopathy can also occur. Retinal changes occur in 50% of patients with fat embolism syndrome.

These are cotton swabs and small hemorrhages along the vessels of the retina and the macula.

Ruminant Fat Embolism Syndrome : This type of fat embolism syndrome is much rarer than the previous two types. It usually occurs within the first few hours of the injury.

All three characteristics of fat embolism syndrome existed in the most severe form. The cause of death is usually due to acute right heart failure.


It is not known exactly how fat embolism and posterior fat embolism syndrome occur, but one of the main assumptions is the “mechanical obstruction theory.”

Orthopedic injuries, especially long bone fractures, are the most common cause of fat embolism syndrome (FES).

Fat embolism rates in long bone fractures range from 1% to 30%. The death rate for fat embolism syndrome is approximately 10-20%.

However, fat globules have been detected in 67% of people with orthopedic trauma and can reach up to 95% if a blood sample is taken near the fracture site.

As early surgical fixation of long bone fractures has become common practice, the incidence of fat embolism syndrome has dropped from 0.9% to 11%.

While in theory this can happen with smaller bones, larger bones have more adipose tissue, making fat embolism syndrome more likely.

Although rare, fat embolism syndrome can also be caused by other bodily trauma, such as joint replacement surgery and liposuction.

Fat embolism syndrome can occur even when soft tissue is damaged due to burns. Other rare causes of fat embolism syndrome are:

  • Severe burns
  • Hepatic injury.
  • Closed-chest cardiac massage (during cardiopulmonary resuscitation).
  • Bone marrow transplantation.
  • Liposuction.
  • Parental lipid infusion.
  • Decompression sickness.
  • Extracorporeal circulation.
  • Acute hemorrhagic pancreatitis.
  • Alcoholic liver disease.
  • Long-term corticosteroid therapy.
  • Sickle cell disease
  • Carbon tetrachloride poisoning.
  • Osteomielitis.

Another possible cause of fat embolism syndrome is what is called “chemical theory.”

Regardless of its cause, researchers know that certain people are at higher risk for fat embolism syndrome than others.

Risk factors include:

  • Being a man.
  • Be between 20 and 30 years old.
  • Having a closed fracture (the broken bone does not penetrate the skin).
  • Having multiple fractures, especially in the lower extremities and pelvis.


Once the fat particles enter the bloodstream, they can lodge in various places in the body, most commonly the lungs (up to 75% of cases).

However, it can also enter the brain, skin, eyes, kidneys, liver, and heart circulation, causing capillary damage and subsequently organ damage in these areas. There are two theories that describe the formation of a fat embolism:

Mechanical theory : after trauma, fat is released directly from the bone marrow into the circulation.

This is because after trauma, elevated pressure in the medullary cavity (central cavity of the bone where bone marrow is stored) of the bone causes the release of fat globules into the venous system that feeds the bone.

This explains the obstruction of the fat embolism in the pulmonary capillaries.

However, it does not explain fat embolism in other parts of the body (brain, skin, heart and eyes) because the small diameters of the pulmonary capillaries do not allow the fat emboli to pass through the pulmonary circulation back to the ventricle. left of the heart to be pumped throughout the body.

For those without patent foramen ovale (a hole that connects the right atrium directly to the left atrium of the heart), fat emboli can still be found in other parts of the body besides the lungs.

If fat globules obstruct 80% of the capillary network of the lung, it will cause acute right heart failure leading to death.

Blockage of fat globules in pulmonary capillaries can cause increased pulmonary capillary pressure.

This increased pressure makes the lungs stiffer and increases the workload of the right heart.

Back pressure in the right heart causes dilation of the right heart through the cor pulmonale causing acute right heart failure.

Biochemical theory : After trauma, an inflammation causes the bone marrow to release fatty acids into the venous circulation. This is accomplished through the increased activity of lipoprotein lipase that breaks down triglycerides into free fatty acids.

Both fatty acid release and inflammation cause damage to the capillary beds of the lungs and other organs, causing interstitial lung disease, chemical pneumonitis, and acute respiratory distress syndrome (ARDS).

This theory can help explain the non-traumatic causes of fat embolism.


Fat embolism is the presence of fat particles in the body’s microcirculation. Meanwhile, fat embolism syndrome is the clinical manifestation as a result of fat particles that lodge in the body’s microcirculation.

There are three main diagnostic criteria proposed for fat embolism syndrome, however, none of them are universally validated and accepted.

However, the Gurd and Wilson criteria for fat embolism are more commonly used when compared to the other two diagnostic criteria.

Gurd and Wilson criteria for fat embolism syndrome

Major criterion
  • Axillary or subconjunctival petechiae.
  • Hypoxemia PaO2 <60 mm Hg, FIO2 = 0.4.
  • Central nervous system depression disproportionate to hypoxemia.
  • Pulmonary edema .
Minor criteria
  • Tachycardia more than 110 beats per minute.
  • Pyrexia more than 38.5 ° C.
  • Fatty globules present in the urine.
  • Changes in kidney function (reduced urine output).
  • Decrease in hemoglobin values ​​(more than 20% of the value at admission).
  • Decrease in hematocrit values.
  • Drop in platelet values ​​(more than 50% of the value on admission).
  • Increased erythrocyte sedimentation rate (ESR) (more than 71 mm per hour).
  • Fatty globules present in sputum.
  • Emboli present in the retina on funduscopy.

A minimum of two positive major criteria plus one minor or four positive minor criteria suggest fat embolism syndrome.

Fat embolism syndrome is a clinical diagnosis.

There are no specific or sensitive enough laboratory tests to diagnose fat embolism syndrome.

These laboratory tests are only used to support clinical diagnosis only.

Chest X-ray may show diffuse interstitial infiltrates, whereas CT scan of the chest will show diffuse vascular congestion and pulmonary edema.

Bronchoalveolar lavage has been proposed to look for fat droplets in alveolar macrophages; however, it is time consuming and not specific to fat embolism syndrome.

The search for fat globules in sputum and urine is also not specific enough to diagnose fat embolism syndrome.


Treatment for fat embolism syndrome generally revolves around supportive care. You will be admitted to the hospital, probably in the intensive care unit.

Your oxygen levels will be monitored and you may be given oxygen, if needed. Some people will need help breathing with mechanical ventilation.

You may also receive IV fluids and medications that will increase blood volume. This helps remove harmful free fatty acids from the body.

Your doctor may prescribe steroids and heparin, a blood thinner, but these medications have not been shown to be highly effective. Its use must be carefully monitored.

Fat embolism is a serious condition. About 10 to 20 percent of people with the syndrome will not recover.

However, when treatment is quick and careful, most people with fat embolism will make a full recovery without long-lasting side effects.

Pharmacological interventions

Therapeutic treatments developed specifically for fat embolism syndrome have been largely unsuccessful.

The first experiments attempted to use dextrose to decrease the mobilization of free fatty acids or ethanol to decrease lipolysis; however, none have shown clinical benefits.

Heparin anticoagulation was found to be beneficial in animal models, but is no longer commonly used in clinical practice due to the risk of bleeding and unproven benefits.

Corticosteroid therapy has been proposed as a potential therapy for fat embolism syndrome by limiting free fatty acid levels, stabilizing membranes, and inhibiting complement-mediated leukocyte aggregation.

Meta-analysis of seven randomized trials using prophylactic corticosteroids in patients with long bone fractures found that corticosteroids reduce the risk of fat embolism syndrome by 77% (95% CI 40–91%).

This same trial reported no difference in mortality, infection, or avascular necrosis in corticosteroid-treated patients compared to control patients. This meta-analysis, however, included only one recent trial.

A 2004 randomized trial found no difference in the incidence of fat embolism syndrome among patients treated with methylprednisolone.

While still controversial, some doctors give corticosteroids to patients with long bone fractures as prophylaxis for fat embolism syndrome. Methylprednisolone is the most widely used steroid and doses range from 6 to 90 mg / kg.

The placement of inferior venal cava filters has been recommended as a method to reduce the shower of emboli to the pulmonary vasculature.

Inferior vena cava filters as prophylactic treatment to prevent fat embolism syndrome have not been sufficiently studied.


For patients treated conservatively with immobilization for long bone fractures, the incidence of fat embolism syndrome is 22%.

Eliminate slip hazards from your home, make sure your shoes fit well, and practice balance-enhancing exercises like yoga.

But if your bones are broken or if you need orthopedic surgery for any reason, keep these points in mind:

If you think you have broken a long bone in your body, limit your movement. The more immobile you are, the more you reduce your chances of developing a fat embolism.

If surgery is needed to repair the broken bone, the sooner it is done, the better. Surgery started within 24 hours of interruption carries a lower risk of fat embolism than delayed bone establishment.

If you have a long, broken bone or if you are having orthopedic surgery, talk to your doctor about using prophylactic steroids. Some research shows that they are effective in preventing a fat embolism.

Early surgical fixation of long bone fractures can reduce the incidence of fat embolism syndrome, especially with the use of internal fixation devices.

Patients who undergo urgent fixation for long bone fractures have a 7% rate of acute respiratory distress syndrome (ARDS) compared to those who undergo fixation after 24 hours (39% with acute respiratory distress syndrome). acute respiratory).

However, movement of the fracture ends of the long bones during surgical fixation can cause a transient increase in fat emboli in the bloodstream.

Cytokines are persistently elevated if long bone fractures are treated conservatively by immobilization.

Cytokine levels would return to normal after surgical fixation. Although nailing the ream increases pressure in the medullary canal of the long bones, it does not increase the rates of fat embolism syndrome.

Other methods, such as drilling holes in the bone cortex, flushing the bone marrow prior to fixation, and using tourniquets to prevent embolization have not been shown to reduce rates of fat embolism syndrome.

Corticosteroid therapy such as methylprednisolone (6 to 90 mg / kg) has been proposed for the treatment of fat embolism syndrome, however it is controversial.

The corticosteroid can be used to limit free fatty acid levels, stabilize membranes, and inhibit leukocyte aggregation.

A meta-analysis conducted in 2009 reported that prophylactic corticosteroids can reduce the risk of fat embolism syndrome by 77%.

However, there is no difference in mortality, infection and avascular necrosis compared to the control group.

However, a randomized trial conducted in 2004 reported no difference in the incidence of fat embolism syndrome when comparing treatment with the control group.

Corticosteroid administration for 2 to 3 days is not associated with increased infection rates.

However, there is insufficient data to support the use of methyprednisolone once fat embolism syndrome is established.

Heparin has been used in the prevention of venous thrombosis in postoperative patients.

However, its regular use in people with fat embolism syndrome has been contraindicated because it increases the risk of bleeding in people with multiple trauma.

The placement of inferior vena cava filters has been proposed to reduce the number of emboli entering the pulmonary vascular system, however, this method has not been studied in detail.

Supportive treatment

Once fat embolism syndrome develops, the person should be admitted to the intensive care unit (ICU), preferably with central venous pressure (PVC) monitoring.

Central venous pressure monitoring would be helpful in guiding volume resuscitation.

Supportive treatment is the only proven treatment method; Supplemental oxygen can be given if a person has mild respiratory distress.

However, if a person has severe respiratory distress, continuous positive pressure ventilation (CPAP) or mechanical positive end-expiratory pressure (PEEP) ventilation may be indicated.

Fluid replacement is necessary to prevent shock. Human albumin resuscitation is recommended because it can restore blood volume in the circulatory system, while also binding to free fatty acids to reduce lung injury.

In severe cases, dobutamine should be used to support right ventricular failure. Frequent recording of the Glasgow Coma Scale is required to access the neurological progression of a person with fat embolism syndrome.

The placement of an intracranial pressure monitor may be helpful in directing the treatment of cerebral odema.

Complications of fat embolism syndrome

Once you have recovered from fat embolism or fat embolism syndrome, there are usually no long-term complications.


In 1861, Zenker first reported autopsy findings of fat droplets found in the lungs of a railroad worker who died of a severe thoracoabdominal crush injury.

In 1873, Bergmann clinically diagnosed a fat embolism in a patient with a fractured femur.

In 1970, Gurd defined the characteristics of this phenomenon. Gurd later modified the criteria for fat embolism together with Wilson, thus producing the Gurd and Wilson criteria for fat embolism syndrome in 1974.

In 1983, Schonfeld suggested a scoring system for the diagnosis of fat embolism syndrome. In 1987, Lindeque proposed another scoring system that diagnoses fat embolism syndrome by using respiratory changes alone.

However, none of them are universally accepted in the medical community.