Fat embolism syndrome
Fat embolism syndrome | |
---|---|
Other names | Fat embolism |
Supportive care[4] | |
Prognosis | 10% risk of death[2] |
Frequency | Rare[4] |
Fat embolism syndrome occurs when
Fat embolism most commonly occurs as a result of
Treatment is mostly
Signs and symptoms
Symptoms of fat embolism syndrome (FES) can start from 12 hours to 3 days after diagnosis of the underlying clinical disease. The three most characteristic features are: respiratory distress, neurological features, and skin
- Subclinical FES - It manifests as reduced tachypnoea, tachycardia. However, there is no respiratory distress. However, it is often confused with post-operative symptoms of fever, pain, and discomfort.[5]
- Subacute FES (non-petechiae. Petechiae are seen on the chest, axilla, shoulder, and mouth.[5] Occulsion of dermal capillaries by the fat emboli result in petechial rash. Petechiae rash occurs in 50 to 60% of the cases.[7] Neurologic signs such as confusion, stupor, and coma may be present. These are usually temporary and do not happen on one side of the body. Respiratory distress can be mild and tends to improve on the third day. Retinal changes similar to Purtscher's retinopathy may also be present.[5] Retinal changes happens in 50% of the patients with FES. These are the cotton wool exudates and small haemorrhages along the retinal vessels and macula.[7]
- Fulminant FES - This type of FES is much rarer than the above two types. It usually happens within the first few hours of the injury. The three characteristics of FES existed in the most severe form. Cause of death is usually due to acute right heart failure.[5]
Causes
Orthopaedic injuries, especially fractures of the long bones, are the most common cause of fat embolism syndrome (FES). The rates of fat embolism in long bone fractures vary from 1% to 30%. The mortality rate of fat-embolism syndrome is approximately 10–20%.[7] However, fat globules have been detected in 67% of those with orthopaedic trauma and can reach as high as 95% if the blood is sampled near the fracture site. As the early operative fixation of long bone fractures became a common practice, the incidence of FES has been reduced to between 0.9% and 11%.[6]
Other rare causes of fat embolism syndrome are:[7][6]
- Severe burns
- Liver injury
- Closed chest cardiac massage (during cardiopulmonary resuscitation)
- Bone marrow transplantation
- Liposuction
- Parenteral lipid infusion
- Decompression sickness
- Extracorporeal circulation
- Acute haemorrhagic pancreatitis
- Alcoholic liver disease
- Prolonged corticosteriod therapy
- Sickle cell disease
- Carbon tetrachloride poisoning
- Osteomyelitis
Pathophysiology
Once fat emboli enter the blood circulation, they can lodge at various sites of the body, most commonly in 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 cause organ damage in these areas. There are two theories that describe the formation of a fat embolus:[6]
- Mechanical theory - Following trauma, fat is released directly from the bone marrow into the circulation. This is because after trauma, an elevated pressure in the cor pulmonale, leading to acute right heart failure.[5]
- Biochemical theory - Following trauma, an inflammation causes bone marrow to liberate fatty acids into the venous circulation.[6] This is achieved through the increased activity of lipoprotein lipase which break down triglycerides into free fatty acids.[7] Both the release of fatty acids and the inflammation causes damage to the capillary beds[6] of the lungs and other organs, causing interstitial lung disease, chemical pneumonitis,[7] and acute respiratory distress syndrome (ARDS).[6] This theory can help to explain non-traumatic causes of fat embolism.[7]
Diagnosis
Fat embolism is presence of fat particles in the micro-circulation of the body. Meanwhile, fat embolism syndrome is the clinical manifestation as the result of fat particles lodging in the body micro-circulation.[6] There are three major diagnostic criteria proposed for fat embolism syndrome, however, none of them are validated and accepted universally.[6] However, Gurd and Wilson's criteria for fat embolism become more commonly used when compared to the other two diagnostic criteria.[9]
Gurd and Wilson's criteria
- Axillary or subconjunctival petechiae
- Hypoxaemia PaO2 <60 mm Hg, FIO2 = 0.4
- Central nervous system depression disproportionate to hypoxaemia
- Pulmonary oedema
- Tachycardia more than 110 beats per minute
- Pyrexia more than 38.5 °C
- Fat globules present in urine
- Changes in renal function (reduced urine output)
- Drop in haemoglobinvalues (more than 20% of the value upon admission)
- Drop in haematocritvalues
- Drop in platelet values (more than 50% of the value upon admission)
- Increasing erythrocyte sedimentation rate (ESR) (greater than 71 mm per hour)
- Fat globules present in the sputum
- Emboli present in the retina on fundoscopy
A least two positive major criteria plus one minor criteria or four positive minor criteria are suggestive of fat embolism syndrome.[6] Fat embolism syndrome is a clinical diagnosis. There are no laboratory tests sensitive or specific enough to diagnose FES. Such laboratory tests are only used to support the clinical diagnosis only.[7] Chest X-ray may show diffuse interstitial infiltrates while chest CT scan will show diffuse vascular congestion and pulmonary oedema. Bronchoalveolar lavage has been proposed to look for fat droplets in alveolar macrophages however it is time-consuming and is not specific to fat embolism syndrome. Looking for fat globules in sputum and urine is also not specific enough to diagnose FES.[6]
Prevention
For those treated conservatively with immobilisation of long bone fractures, the incidence of FES is 22%. Early operative fixation of long bone fractures can reduce the incidence of FES especially with the usage of internal fixation devices. Patients undergoing urgent fixation of long bone fractures has a rate of 7% of acute respiratory distress syndrome (ARDS) when compared to those undergoing fixation after 24 hours (39% with ARDS). However, movement of the fracture ends of the long bones during the operative fixation can cause transient increase of fat emboli in the blood circulation. Cytokines are persistently elevated if the long bone fractures is treated conservatively using immobilisation. The cytokine levels would return to normal after operative fixation. Although ream nailing increases pressure in the medullary cavity of the long bones, it does not increase the rates of FES. Other methods such as drilling of holes in the bony cortex, lavaging bone marrow prior to fixation, and the use of tourniquets to prevent embolisation have not been shown to reduce the rates of FES.[6]
Corticosteroid therapy such as methylprednisolone (6 to 90 mg/kg) has been proposed for the treatment of FES, however, it is controversial. Corticosteroid can be used to limit free fatty acid levels, stabilising membranes, and inhibit leukocyte aggregation. A meta-analysis conducted in 2009 reported prophylactic corticosteroids can reduce the risk of FES by 77%. However, there is no difference in mortality, infection, and avascular necrosis when compared to the control group. However, a randomised trial conducted in 2004 reported no differences in FES incidence when comparing treatment with the control group.[6] Administration of corticosteroids for 2 to 3 days is not associated with increased rates of infection.[5] However, there is insufficient data to support the use of methyprednisolone once FES is established.[5]
Heparin has been used in the prevention of venous thrombosis in post-operative patients; however its regular use in those with FES has been contraindicated due to increase risk of bleeding in those with polytrauma.[5] Placement of inferior vena cava filters has been proposed to reduce the amount of emboli going into the lung vascular system, however, this method has not been studied in detail.[6]
Treatment
Once FES develops, the person should be admitted into
History
In 1861, Zenker first reported on the autopsy findings of fat droplets found in the lungs of a railway worker who died due to severe thoraco-abdominal crush injury. In 1873, Bergmann diagnosed fat embolism clinically in a patient with fractured femur. In 1970, Gurd defined the characteristics of this phenomenon.[7] Gurd later modified the fat embolism criteria together with Wilson, thus producing Gurd and Wilson's criteria for fat embolism syndrome in 1974.[7] In 1983, Schonfeld suggested a scoring system for the diagnosis of fat embolism syndrome. In 1987, Lindeque proposed another scoring system that diagnose fat embolism syndrome by using respiratory changes alone. However, none of them have become universally accepted in the medical community.[6]
In 1978, Formula One racing driver Ronnie Peterson died from FES, after sustaining multiple fractures in a racing accident.
In 2015, Singaporean couple Pua Hak Chuan and Tan Hui Zhen were charged with the abuse and
References
- ^ PMID 19825491.
- ^ a b c d e f g h i Laurence, Knott (19 February 2014). "Fat embolism syndrome". patient.info. Retrieved 14 March 2018.
- ^ PMID 29763060.
- ^ S2CID 51969468.
- ^ PMID 23661916.
- ^ PMID 23724388.
- ^ S2CID 8190157.
- ISSN 1743-1816.
- ^ PMID 18702388. Retrieved 14 March 2018.
Diagnosis is usually made on the basis of clinical findings but biochemical changes may be of value. The most commonly used set of major and minor diagnostic criteria are those published by Gurd (See Table 2 ).
- ^ "14, 16.5 years' jail for couple who tortured tenant to death". Today. Singapore. 1 December 2017. Retrieved 20 April 2022.
- ^ "AGC replies to questions raised by the public". The Straits Times. Singapore. 19 December 2017. Retrieved 20 April 2022.
Further reading
- Shaikh, Nissar (2009). "Emergency management of fat embolism syndrome". Journal of Emergencies, Trauma, and Shock. 2 (1): 29–33. PMID 19561953.
- Silva, Douglas Fini; Carmona, César Vanderlei; Calderan, Thiago Rodrigues Araújo; Fraga, Gustavo Pereira; Nascimento, Bartolomeu; Rizoli, Sandro (2013). "The use of corticosteroid for the prophylaxis of fat embolism syndrome in patients with long bone fracture". Revista do Colegio Brasileiro de Cirurgioes. 40 (5): 423–426. PMID 24573593.
- Lewis, Sharon L.; Dirksen, Shannon Ruff; Heitkemper, Margaret M.; Bucher, Linda (2013-12-02). Medical-Surgical Nursing: Assessment and Management of Clinical Problems, Single Volume. Elsevier Health Sciences. p. 1523. ISBN 9780323086783.
- Nolan, Jerry; Soar, Jasmeet (2012-06-28). Anaesthesia for Emergency Care. OUP Oxford. p. 86. ISBN 9780199588978.
- Bederman SS, Bhandari M, McKee MD, Schemitsch EH (2009). "Do corticosteroids reduce the risk of fat embolism syndrome in patients with long-bone fractures? A meta-analysis". Can J Surg. 52 (5): 386–93. PMID 19865573..
- Dondelinger, Robert F. (2004). Imaging and Intervention in Abdominal Trauma. Springer Science & Business Media. p. 477. ISBN 9783540652120.
- George, Ronald B. (2005-01-01). Chest Medicine: Essentials of Pulmonary and Critical Care Medicine. Lippincott Williams & Wilkins. p. 222. ISBN 9780781752732.
- Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; Mitchell, Richard (2007-05-24). Robbins Basic Pathology. Elsevier Health Sciences. p. 505. ISBN 1437700667.