Fat embolism refers to passage of fat globules in the lung parenchyma and peripheral circulation.
Fat embolism syndrome is a serious consequence of fat emboli producing a distinct pattern of clinical symptoms and signs.
Fat embolism syndrome is a occurs when embolic fat macroglobules pass into the small vessels of the lung and other sites leading to endothelial damage, respiratory distress, cerebral dysfunction and other symptoms.
Ernst Von Bergmann is credited with making the first clinical diagnosis of fat embolism in 1873 though Zenker in 1862 had described it on an autopsy.
Fat embolism occurs in 90% of all trauma patients. Fat embolism syndrome accounts for for only 2-5% of patients who have long-bone fractures.
Thus most of the cases of fat embolism are asymptomatic [That means these cases do not progress to full fledged fat embolism syndrome.
Asymptomatic fat embolism to the pulmonary circulation almost always occurs with major trauma, including elective surgical procedures such as intramedullary nailing of long bones.
Timely intervention in cases with fat embolism syndrome is life saving which otherwise is associated with high mortality rate.
An overall mortality of 5-15% has been described with fat embolism syndrome.
Pathophysiology of Fat Embolism Syndrome
The exact mechanism of fat embolism and resultant fat embolism syndrome is not clearly understood.
Mechanical and biochemical causes have been proposed.
Fat emboli may occur either by direct entry of depot fat globules from disrupted adipose tissue or bone marrow into the bloodstream in areas of trauma (mechanical) or via production of toxic intermediaries of fat present in the plasma (biochemical).
It is thought that release of fat emboli leads to occlusion of the microvasculature, triggering an inflammatory response leading to skin, lung and neural dysfunction.
Pulmonary changes lead to respiratory distress not unlike acute respiratory distress syndrome. It is usually the initial manifestation typically appearing within 24 hours after the injury.
The initial symptoms are probably caused by mechanical occlusion of multiple blood vessels with fat globules that are too large to pass through the capillaries.
The late presentation is thought to be a result of injury to the pulmonary capillary endothelium caused by free fatty acids that were hydrolyzed by lipoprotein lipase and releasing local toxic mediators.
Effects of these mediators are increased vascular permeability, resulting in alveolar damage and respiratory distress.
Cerbral and renal effects are caused by fat emboli that pass to systemic circulation. A patent foramen ovale is seen in 20-30% people and this may how fat emboli pass from pulmonary circulation to systemic.
In brain, patient may have gross encephalopathy, localized cerebral edema, and white-matter changes.
Causes of Fat Embolism Syndrome
- Fractures of long bones, ribs and pelvic bones.
- Orthopedic procedures such as intramedullary nailing of the long bones, hip or knee replacements.
- Massive soft tissue injury.
- Severe burns.
- Bone marrow biopsy.
- Non-traumatic settings occasionally lead to fat embolism. These include conditions associated with
- Fatty liver.
- Prolonged corticosteroid therapy.
- Acute pancreatitis.
- Sickle cell crisis
- Cardiopulmonary bypass
- Decompression sickness
- Parenteral lipid infusion
- Sickle cell crisis
There would be history of trauma or other procedures or other relevant history.
Diagnosis of fat embolism syndrome is clinical. Fat embolism syndrome typically presents 24-72 hours after the initial injury. Patient presents with following
- Respiratory changes;
- Neurological abnormalities;
- Petechial rash.
Respiratory changes are often the first clinical feature to present.
Most early findings include dyspnoea, tachypnoea, and hypoxaemia. The severity of these symptoms varies. In most severe form it may progress to respiratory failure and a syndrome acute respiratory distress syndrome like condition.
About one-half of the patients with fat embolism syndrome caused by long bone fractures develop severe hypoxaemia andrespiratory insufficiency and require mechanical ventilation.
Neurological features resulting from cerebral embolism and often present in the early stages but generally after the development of respiratory distress.
The symptoms range from mild confusion and drowsiness to severe seizures. Common presentation is confusion and focal neurological signs [Hemiplegia, aphasia,apraxia, visual field disturbances etc.]
Petechial rash is last to develop and is seen in about 60%. These occur due to embolization of small dermal capillaries leading to extravasation of erythrocytes. Conjunctiva, oral mucous membrane, and skin folds of the upper body, especially the neck and axilla are common sites.
The rash appears within the first 36 h and is self-limiting,disappearing completely within 7 days.
Other major signs are oliguria [decreased urine output], hematuria [blood in urine] and anuria [failure of the kidneys to produce urine].
- Respiratory insufficiency
- Cerebral involvement
- Petechial rash
- Pyrexia (usually >39°C)
- Sustained pO2 <8 kPa
- Sustained respiratory rate >35/minute, in spite of sedation
- Retinal changes – cotton wool exudates and small haemorrhages, occasionally fat globules seen in retinal vessels
- Renal signs
- High ESR
- Fat macroglobulinemia
- Diffuse alveolar infiltrates ‘snow storm appearance’ on chest x-ray
- Pulmonary Embolism
- Thrombotic Thrombocytopenic Purpura
Following lab studies may guide the diagnosis of fat embolism syndrome
Routine Blood Examination
- Thrombocytopenia [decreased platelet count], anemia, and hypofibrinogenemia are indicative of fat embolism syndrome. However, they are nonspecific.
- Decreased haematocrit occurs within 24-48 hours due to intra-alveolar haemorrhage.
- Elevated lipase levels [not specific and can occur in any bone trauma.
- Decreased calcium
Examination of urine, blood and sputum may detect fat globules that are either free or in macrophages. But this test has low sensitivity and a negative result does not exclude fat embolism.
Cytology of pulmonary capillary blood [ obtained from a wedged pulmonary artery catheter] may reveal fat globules in patients. This may be beneficial in early detection of patients at risk.
Blood Gas Examination
Blood gases will show low oxygen [hypoxia] and higher carbon dioxide levels [hypocapnia].
Unexplained increase in alveolar-to-arterial oxygen tension difference, especially if it occurs within 24-48 hours of a sentinel event is strongly suggestive of the syndrome.
- Serial chest radiographs reveal increasing diffuse bilateral pulmonary infiltrates within 24-48 hours of the onset of clinical findings. The CXR may show evenly distributed, fleck-like pulmonary shadows (snow storm appearance), increased pulmonary markings and dilatation of the right side of the heart.
Parenchymal changes consistent with lung contusion, acute lung injury, or acute respiratory distress syndrome (ARDS) may be evident, depending on the burden of secondary lung injury.
Nodular or ground-glass opacities in the setting of trauma suggest fat embolism.
Transesophageal echocardiography (TEE) may show repeated showers of emboli on TEE have been noted to increase right heart and pulmonary artery pressures but lack correlation with the actual development of fat embolism syndrome.
Nuclear ventilation-perfusion imaging of the lungs may be normal or may demonstrate subsegmental perfusion defects.
Bronchoalveolar lavage specimens have been evaluated in trauma patients and sickle-cell patients with acute chest syndrome, and the results have been mixed. At present its use is controversial.
There is no specific medical therapy for fat embolism and fat embolism syndrome.
The care of the patient aims at supporting physiologic derangements. Following measures are important
- Adequate oxygenation and ventilation
- Maintenance of hemodynamic stability- crsytalloids or colloids
- Blood/blood products transfusion
- Prophylaxis of deep venous thrombosis
At risk patients [as in trauma] should be put on continuous pulse oximetry for early detection of desaturation. This allows prophylactic administration of oxygen and thereby decreasing the chances of hypoxic injury and systemic complications of fat embolism syndrome.
Prompt surgical stabilization of long bone fractures reduces the risk of the syndrome.
Prophylactic placement of inferior vena cava filters may help reduce the volume of fat that reaches the heart in at-risk patients but the risk of the surgery should be weight against benefits..
- The mortality rate from fat embolism syndrome is 5-15%
- Neural deficit and coma may last for days or weeks. Residual deficits like personality changes, memory loss and cognitive dysfunction may remain.
- Pulmonary residual diffusion capacity deficits may exist even after a year, the time by which other lung deficits resolve.
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