Fat embolism syndrome is a rare clinical syndrome caused by the presence of fat globules in the pulmonary circulation following trauma or other insults that release fat into the bloodstream. It is characterized by a clinical triad of hypoxemia, neurological abnormalities, and petechial rash that typically develops 24-72 hours after the initial injury. Diagnosis is clinical based on criteria sets, and treatment is supportive to address respiratory failure, shock, or other complications until it resolves spontaneously in days. Prevention focuses on early immobilization of fractures to reduce fat release and potential prophylactic corticosteroids, though their benefit is controversial.

1. Fat embolism syndrome
Dr. Muhammed Alif

2. INTRODUCTION
● FES – rare syndrome, when severe  associated with resp. failure, neurocognitive deficit
and death
● Remains diagnostic challenge – prompt recognition is important – supportive Rx can be
instituted early
DEFINITION
● Fat embolism – ‘’presence of fat globules in pulmonary circulation’’
● FES – ‘’clinical syndrome that follows an identifiable insult which releases fat into the
circulation resulting in pulmonary and systemic symptoms’’

3. Conditions associated with fat embolism
Trauma related Non-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
• Liposuction
• Bone marrow harvesting and transplant
• Pancreatitis
• Diabetes mellitus
• Osteomyelitis and panniculitis
• Bone tumour lyses
• Steroid therapy
• Sickle cell haemoglobinopathies
• Alcoholic (fatty) liver disease
• Lipid fusion
• Cyclosporine A solvent

4. ● Most commonly associated with fractures of long bones and the pelvis.
● More frequent in closed, rather than open fractures.
● Incidence increases with the number of fractures involved.
● Patients with a single long bone fracture 1–3%.
● Reported up to 33% of patients with bilateral femoral fractures.
● more common in men than in women.
● Incidence is highest in those between 10 and 40 years
○ reflecting the incidence of trauma in this age group
● An overall mortality - 5–15%

5. Pathogenesis
● Mechanism – not clearly understood
● Proposed mechanism - mechanical and
biochemical causes
Fat emboli by direct
entry of fat globules
Via disrupted adipose
tissue or bone marrow
into the bloodstream in
areas of trauma
(mechanical)
via production
of toxic
intermediaries
of fat present
in the plasma
(biochemical).

6. ‘Mechanical’ fat embolism (mechanical theory)
● Fat from disrupted bone marrow or adipose tissue  forced into torn venules in
areas of trauma.
● Fractures of marrow-containing bone  highest incidence of fat embolism
syndrome and cause the largest volume fat emboli.
● Disrupted venules in the marrow remain open by osseous attachments.
● The marrow contents may enter the venous circulation with little difficulty.
● Supported by the description of ‘echogenic material’ passing into the right heart
during orthopedic surgery.
● Produce an increase in pulmonary artery and right heart pressures.

7. ● Material can pass through a patent foramen ovale into the systemic circulation
paradoxical embolism.
● Some studies  demonstrated the appearance of embolic material in the systemic
circulation in the absence of a patent foramen ovale.
● Depend on the embolized fat being sufficiently deformable  forced through the
pulmonary capillaries by the raised right ventricular pressure  microembolism
This theory does not sufficiently explain the 24–72 h delay in development after the
acute injury.

8. Production of toxic intermediaries (biochemical theory)
● A number of biochemical mechanisms involved
● Widely held – embolized fat is degraded in plasma to free fatty acids.
● Neutral fat, found in bone marrow, does not cause an acute lung injury.
● Hydrolyzed over the course of hours to several products, including free fatty acids
 shown to cause ARDS in animal models.
● Free fatty acids  associated with cardiac contractile dysfunction can be a
feature of fat embolism syndrome.
● The plasma lipase concentration is increased in some patients.

9. ● Serum from acutely ill patients - shown to have the capacity to agglutinate chylomicrons,
low-density lipoproteins, and liposomes of nutritional fat emulsions.
● C-reactive protein - elevated in these patients
○ responsible for lipid agglutination
○ may also participate in the mechanism of nontraumatic fat embolism syndrome.
● The delay in development of symptoms  timescale required to produce these toxic
metabolites.
● The onset of symptoms may coincide with the agglutination and degradation of fat
emboli.

10. Clinical presentation
● Typically manifests 24 to 72 hours after
the initial insult
● Rarely occur as early as 12 hours or as
late as two weeks after the inciting
event
Hypoxemia
Neurological
abnormalities
Petechial rash

11. Signs and symptoms
Respiratory abnormalities
● Pulmonary manifestations are the most
common presenting features of FES.
● Hypoxemia, dyspnea, and tachypnea –
most frequent early findings.
● Hypoxemia  present in 96 percent of
cases.
● ~50% of patients with FES due to long
bone fractures develop severe
hypoxemia and require mechanical
ventilation.
Neurologic abnormalities
● Common
● Typically manifest after respiratory
abnormalities,
● Rare case reports suggest neurological
symptoms can occur in isolation.
● Neurologic manifestations
○ Ranges from the development of an acute
confusional state
○ Altered level of consciousness
○ Seizures
○ Focal deficits

12. Petechial rash
● The characteristic red-brown petechial
● Last component of the triad to develop
● Occurs in only 20 to 50 percent (on average
one third) of cases (picture 1)
● found on the nondependent regions of the
body.
○ Head
○ Neck
○ Anterior thorax
○ Axillae
○ Sub-conjunctiva

13. Other clinical and laboratory findings —
Less common and nonspecific manifestations:
● Anemia and thrombocytopenia (one-third to two-thirds)
● Retinal scotomata (Purtscher's retinopathy)
● Lipiduria
● Fever
● Coagulation abnormalities, rarely disseminated intravascular coagulation (DIC)
● Myocardial depression
● Right ventricle dysfunction
● Hypotension
● Obstructive shock

14. Imaging and laboratory findings
● Chest and brain imaging – frequently performed
● Findings – generally nonspecific
● Chest radiograph – normal in majority patients
Minority – reveal air space disease due to edema or
alveolar hge, prominent in periphery and base
● CT chest – may be normal
b/l demarcated ground glass opacity
Ill defined centrilobular nodules

15. ● V/Q scan – not routinely performed
if performed to investigate for VTE – mottled pattern of sub-
segmental perfusion defect with normal ventilatory pattern
● a/c neurological abnormality – MRI
‘’Starfield pattern’’
diffuse punctate, hyperintense lesion on
DWI, correlates with degree of neurological
impairment
Late or severe findings – edema/petechial hge.

16. Laboratory findings – not specific
● May reveal anemia, coagulation abnormality including DIC
● Lipiduria – rare
● CRP – generally elevated
● Lipase – not constantly elevated
● No specific biomarker – validated for FES

17. DIAGNOSTIC EVALUATION
● Main goals: Exclude alternate diagnoses
Assess severity of disease
Determine the need for supportive care.
Initial assessment
● Suspected in those pts who are at risk – with signs of respiratory failure.
● Should be further increased when neurological or petechiae appears within 24 to 72 hrs
● When suspected, chest imaging, typically chest radiography and/or computed tomography (CT), should be performed.
● CT or MRI brain – those with neurologic symptoms.
● Routine laboratory studies – complete blood count and coagulation studies.
● Measuring free fatty acid
c-reactive protein levels not routinely performed since their diagnostic utility is unclear.
urine or sputum for the presence of fat

18. ● CT pulmonary angiography - not routinely performed for diagnosis.
may help exclude pulmonary
thromboembolism as an etiology for
hypoxemia
● Microbiology studies and echocardiography – help to rule out competing diagnoses
such as pneumonia and heart failure.
● most experts consider FES a clinical diagnosis - further testing is not usually
performed
● In most cases, this noninvasive approach is considered appropriate - the only
therapy that is available for FES is supportive.

19. Invasive testing
● Not routinely performed in most patients with
● Only performed when a competing diagnosis is suspected, for which available therapies could
alter the prognosis.
Pulmonary artery catheter:
● Not routinely placed for fat analysis – neither sensitive nor specific.
● Rarely done when PAC is inserted for alternate reason – eg shock, PHTN
● Absence of fat does not preclude the diagnosis.
Bronchoscopy
● Not routinely performed
● Some evidences – BAL can detect fat droplets within alveolar macrophages as am means of fat embolism
● Absence does not preclude the diagnosis.
● Fat globules present in alveolar macrophages – nonspecific – can be seen in sepsis and multiorgan dysfunction.

20. ● Study – trauma and acute chest syndrome in sickle cell disease
BAL may be useful – diagnostic criteria vary and lack standardization,
Sn, Sp – unknown
● Another study – trauma patients – FES  asso. With high % of alveolar macrophage contain
lipid inclusion bodies (>30%)
some pts with non trauma related ARDS  had same %
● Trans bronchial bx, video assisted biopsy – no role

21. DIFFERENTIAL DIAGNOSIS
● Pulmonary embolism
● Amniotic fluid embolism syndrome
● Tumour embolism
● Foreign body embolism
● Air embolism
● Alveolar filling disorders
● Vasculitic disorders

22. DIAGNOSIS
● Clinical diagnosis – can be made when the classic triad occurs in an appropriate clinical
setting.
● Non specifc manifestations – diagnosis  clinical exclusion
● Diagnostic criteria  Gurd’s, Schonfeld's, and Lindeque.
None has been validated or compared
Not widely used in practice
● Tissue obtained for other reasons or at autopsy  fat globules can be histologically
appreciated
● Areas of optical clearing and after staining with Oil Red O.
● When present may confirm the clinical suspicion for FES.

23. Gurd’s criteria
Major criteria
• Axillary or subconjunctival petechiae
• Hypoxaemia PaO2 <60 mm Hg; FIO2 = 0.4)
• Central nervous system depression
disproportionate to hypoxaemia
• Pulmonary oedema
Minor criteria
• Tachycardia <110 bpm
• Pyrexia <38.5oC
• Emboli present in the retina on fundoscopy
• Fat present in urine
• A sudden inexplicable drop in hematocrit or
platelet values
• Increasing ESR
• Fat globules present in the sputum
1 major and 4 minor criteria
Schonfeld’s criteria
Petechiae 5
Chest X-ray changes (diffuse alveolar infiltrates) 4
Hypoxaemia (Pao2, <9.3 kPa) 3
Fever (>38oC) 1
Tachycardia (>120 beats/min) 1
Tachypnoea (>30 bpm) 1
Cumulative score >5 required for diagnosis
Score > 5
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: dyspnea, accessory muscle use,
tachycardia, and anxiety

24. Treatment
● No definitive treatments for fat embolism syndrome
● Largely supportive – resolves spontaneously.
Treatment of the cause:
● Early correction of fractures may prevent FES
● Unknown whether or not this strategy works as a treatment for those with established FES,
● Most clinicians advocate for early treatment of the underlying cause as a rational approach to treating FES.
Supportive care:
● Supportive care – mainstay of therapy for clinically symptomatic FES.
● Involves fluid resuscitation, oxygenation, and when indicated, noninvasive or invasive mechanical ventilation.
● Rarely, patients require:
- intracranial pressure monitoring for massive cerebral involvement
- vasopressors, mechanical cardiac support devices, or extracorporeal membrane oxygenation for refractory
shock.
● Supportive therapy is continued until FES resolves or death occurs.

25. Systemic corticosteroids – controversial.
● The rationale for the administration - based upon their anti-inflammatory effects & evidence that supports their role in
preventing FES.
● For patients with life-threatening cases of FES, a limited trial (eg, 1 to 5 days) of systemic corticosteroids (eg,
hydrocortisone 100 mg three time daily intravenously or methylprednisolone 1 to 1.5 mg/kg/day) is appropriate.
● Administration should be weighed against the increased risk of steroid-associated infections.
Heparin: Routine administration - not advised.
● Proposed as an agent that may increase the clearance of intravascular lipids.
● Risk of hemorrhage
● Lack of trials demonstrating benefit and Theoretical harm from an increase in free fatty acid production – Prevents its
administration in the absence of a true indication for anticoagulation (eg, venous thromboembolism).

26. PROGNOSIS
● Fully recover spontaneously.
● In most cases  findings are transient and fully reversible, within a few days,
● features may persist beyond one week in severe cases.
● Individual studies – mortality rates ranges from 5 to 15 %.
● True mortality – probably lower (suggested by a meta-analysis – 2 deaths among the 166
patients with FES who received supportive care alone (1.2 %).
● The etiology of death is typically related to severe respiratory failure, refractory shock, or
brain death.

27. Prevention
Early immobilization of fractures:
● reduces the incidence of FES.
● risk - further reduced by operative correction, rather than conservative management.
Intraosseous pressure limitation — reduces the intravasation of intramedullary fat and other debris.
● venting hole – between the greater and the lesser trochanter.
● Cementless fixation of hip prostheses
● Unreamed intramedullary femoral shaft stabilization
Prophylactic corticosteroids — controversial
● Should only be considered on a case-by-case basis.
● Always weigh the potential benefits of preventing FES against the risk associated with their administration.
● many surgeons do not use - associated adverse effects, most patients recover with supportive care alone.
● meta-analysis - reduced incidence of FES and hypoxemia -mortality was not decreased.

28. Thank you…