FAT EMBOLISM SYNDROME By Dr Biplav Sapkota MS Resident ,NAMS
FAT EMBOLISM SYNDROME
By Dr Biplav SapkotaMS Resident ,NAMS
Introduction The term ‘fat embolism’ indicates the presence of
fat globules in the peripheral circulation and lung parenchyma after fracture of long bones, pelvis or other major trauma
‘Fat embolism syndrome’ is a serious manifestation of fat embolism phenomenon characterized clinically by triad of dyspnoea, petechiae and mental confusion.
In 1873, E Von Bergmann was first to establish the clinical diagnosis of fat embolism syndrome.
Although fat and marrow embolism occurs in some 90% of individuals with severe skeletal injuries, less than 10% show any clinical findings..
Incidence Fat Embolism Syndrome (FES) most commonly is
associated with long bone and pelvic fractures, and is more frequent in closed.
Patients with a single long bone fracture have a 1 to 3% chance of developing the syndrome
FES has been noted in up to 33 percent of patients with bilateral femoral fractures.
Incidence is also higher in young men rarely in children, as in children, the bone
marrow contain more of hematopoietic tissue and less of fat.
Causes FES is most common after skeletal injury and it is
most likely to occur in patients with multiple long bone and pelvic fractures.
Trauma related Long bone fractures Pelvic fractures Fractures of other marrow-containing bones Orthopaedic procedures Soft tissue injuries (e.g. chest compression
with or without rib fractures) Burns Bone marrow transplant
Non trauma related• Pancreatitis• Diabetes mellitus• Osteomyelitis• Steroid therapy• Sickle cell haemoglobinopathies• Alcoholic (fatty) liver diseases
Pathophysiology There is considerable controversy over both the
source of fat emboli and their mode of action. Three major theories have been proposed.
1. The mechanical theory2. The biochemical theory3. Coagulation theory
The Mechanical Theory proposed by Gauss in 1924
trauma to long bones
releases fat droplets
Disrupting fat cell in the fractured bone or in
adipose tissue
enter the torn veins near long bone
when the intramedullary press >
the venous press
transported topulmonary vascular bed
large fat globules resultin mechanical
obstruction and are trapped as emboli
in the lung capillaries.
Small fat droplets of 7 – 10 ¼msize may pass via lung & reaches
systemiccirculation causing embolisation to
brain, skin, kidney and retina
However, this theory does not sufficiently explain the 24-72 hr delay in development after the acute injury.
The Biomechanical Theory given by Lehmann and Moore in 1927
embolized fat is degraded in plasma to free fatty acids
it is hydrolysed over the course of hours to several products,including free fatty acids
cardiac contractile dysfunction
affect the pneumocytes, producing abnormalities in gas exchange
Coagulation theory long bone fractures
thromboplastin is released with marrow
elements
activates the complement system and extrinsiccoagulation cascade
Factor VII
Products of Intravascular coagulation
fibrin and fibrin degradation products
increase pulmonary vascular permeability
leukocytes, platelets and fat globules
Clinical Features presents 12-72 hrs after the initial injury.
Patients present with a classic triad of : respiratory manifestations (95%) cerebral effects (60%) and petechiae (33%).
Bulger EM, Smith DG, Maier RV, et al. Fat embolism. A 10-yearreview. Arch Surg 1997;132:435-39. P Glover, L.I.G Worthley. Fat embolism. Critical care andResuscitation 1999;1:275-84
Pulmonary manifestations Respiratory changes are often the first clinical
feature to present. They include• Dyspnoea,• tachypnoea and• hypoxaemia
May progress to respiratory failure and ARDS.Half of the patient of FES requires mechanical ventilation.
CNS manifestations Occur after the development of respiratory
distress Acute confusional state is the most common
symptom Focal neurological sign include hemiplegia,
aphasia,, visual field disturbances and anisocoria may be present.
Fortunately, almost all neurological deficits are transient and fully reversible.
Petechial rash It is the only pathognomic feature of fat
embolism syndrome and usually appears within the first 36 hrs
Due to embolization of small dermal capillaries leading to extravasation of erythrocytes
Selflimiting,disappearing completely within 7 days.
Ocular manifestation: In fundoscopy
cotton wool exudates, macular oedema and macular haemorrhage.
CVS involvement Early persistent tachycardia
Systemic fever: Low grade fever
Diagnosis Diagnosis is usually made on the basis of clinical
findings The most commonly used set of major and minor
diagnostic criteria are those published by Gurd
Gurd & Wilson criteria
Major criteria1. Axillary or subconjunctival
petechiae
2. Hypoxaemia PaO2 <60 mm Hg, FIO2 = 0.4
3. Central nervous system depression disproportionate to hypoxaemia
4. Pulmonary oedema
Minor criteria1. Tachycardia >110 bpm2. Pyrexia >38.5°C3. Emboli present in the
retina on fundoscopy4. Fat globules present in
urine5. A sudden inexplicable drop
in haematocrit or platelet values
6. Increasing ESR7. Fat globules present in the
sputumrequires at least 1 major and 4 minor criteria
Lindeque’s Criteria
Sustained Pao2 <8 kPa Sustained PCO2 of >7.3 kPa or a pH <7.3 Sustained respiratory rate >35 breaths min,
despite sedation Increased work of breathing: dyspnoea, accessory
muscle use,tachycardia, and anxiety
based on respiratory features
More recently, a fat embolism index has been proposed
Schonfeld’s criteria Petechiae 5 Chest X-ray changes (diffuse alveolar infiltrates) 4 Hypoxaemia (Pao2 < 9.3 kPa) 3 Fever (>38°C) 1 Tachycardia (>120 beats min–1) 1 Tachypnoea (>30 bpm) 1
Cumulative score >5 required for diagnosis
Investigations no laboratory test is sufficiently sensitive or
specific
Hematology & Biochemistry anemia (70% of patients) and thrombocytopenia ( up to 50% of patients) Hycocalcemia Elevated serum lipase Hypofibrinogenemia, raised ESR and increased
Prothrombin time may be seen.
circulating fat concentrationsdo not correlate with the severity of the syndrome
Arterial blood gases Decreased PaO2 Decreased PaCO2 Respiratory Alkalosis
Chest x-ray
Normal initailly Classical multi flocculent shadows(snow storm
appearance) Diffuse or patchy consolidation-prominent in
periphery and base Radiological sign remain for up to 3 wks
CT Scan chest ground glass opacification Interlobular septal thickening ill-defined centrilobular and subpleural nodules
MRI
Source:http://www.ispub.com/journal/the_internet_journal_of_anesthesiology/volume_19_number_2/article/acute_fatal_fat_embolism_syndrome_in_bilateral_total_knee_arthroplasty_a_review_of_the_fat_embolism_syndrome.html
showing foci of ischemia(starfield appearance) suggestive of fat embolism syndrome
post op day 2 showing multiple hyperintense areas consistent with multiple emboli post operative day 14 and shows
evolving cortical infarctions
Treatment
Prophylaxis Immobilization and early internal fixation of fracture High doses of corticosteroids Albumin
Medical Medical care includes
adequate oxygenation and ventilation, stable hemodynamics,blood products hydration, prophylaxis of deep venous thrombosis and stress related gastrointestinal bleeding and nutrition.
Various drugs have been tried but with inconclusive results
Corticosteroids as an anti-inflammatory agent, reducing the perivascular haemorrhage and oedema.
Aspirin resulted in significant normalization of blood gases, coagulation proteins, and platelet numbers when compared with controls
Heparin : clear lipaemic serum by stimulating lipase activity
Prognosis
Severe trauma mortality from FES is usually between 5-15%, other are due to other injury or secondary infection.
Most deaths attributed to pulmonary dysfunction
At Last…… Fat embolism syndrome is a rare complication
occurring in 0.5 to 2% of patients following a long bone fracture.
It is believed to be caused by the toxic effects of free fatty acids.
Diagnosis is clinical, based on respiratory, cerebral and dermal manifestations.
Treatment is only supportive, directed mainly at maintaining respiratory functions.
References
Campbell’s Orthopaedics 12th ed Apleys orthopaedics 9th ed Bailley & Love’s short practice of surgery 24th ed Robbins basic pathology,9th edition Orthopaedic pathology,5th edition
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