Fat embolism syndrome: diagnosis, ventilation, and management in trauma

Also known as Fat embolism syndrome · FES · Fat embolism · Orthopaedic embolism · Gurd criteria

Fat embolism syndrome (FES) is a clinical syndrome (triad: respiratory distress, neurological dysfunction, petechial rash) developing after an asymptomatic period of 24-72 hours after TRAUMA (especially long bone/pelvic fractures) or orthopaedic procedures; neurological manifestations may appear 12-72 h after the insult. Fat embolization occurs in the majority of patients with long-bone fractures, but clinical signs occur in only 1-10%. PATHOPHYSIOLOGY: (1) MECHANICAL — mechanical obstruction of capillaries by fat emboli (marrow fat embolises to the pulmonary circulation; fat emboli can deform and pass through the lungs to systemic organs, most commonly brain and kidneys; a patent foramen ovale, found in 27.3% of autopsy hearts, permits paradoxical embolism). (2) BIOCHEMICAL — hydrolysis of fat to free fatty acids injures capillary endothelium - ARDS-like lung injury. CLASSIC TRIAD: (1) RESPIRATORY DISTRESS (hypoxaemia — the subclinical presentation may be hypoxaemia alone). (2) NEUROLOGICAL (altered consciousness, confusion, seizures, coma; rarely infarction). (3) PETECHIAL RASH (characteristic; may be absent — cerebral FES can occur without respiratory or dermatological signs). DIAGNOSIS: clinical (Gurd criteria — major + minor features, at least 1 major and 4 minor; the most commonly used criteria but not clinically validated). MANAGEMENT: SUPPORTIVE (oxygen, lung-protective ventilation — Vt 6 mL/kg predicted body weight, plateau 30 cmH2O or less); early fracture stabilisation within 24 hours is the most effective preventive strategy; corticosteroids reduce FES incidence in meta-analysis (risk reduced 78%, no mortality or infection difference) but remain controversial. OUTCOME: usually good with supportive care; severe cases cause respiratory failure, neurological damage and mortality.

medium30 referencesUpdated 19 Aug 202632 min readVerification in progress

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8 MCQs

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Fat embolism syndrome (FES) = clinical triad (respiratory distress + neurological dysfunction + petechial rash) appearing after an asymptomatic period of 24-72 h after long bone/pelvic fracture (neurological manifestations typically 12-72 h after the insult). Diagnosis: clinical — Gurd criteria (major: respiratory insufficiency, cerebral involvement, petechial rash; minor: fever, tachycardia, jaundice, retinal and renal changes, anaemia, thrombocytopenia, high ESR, fat macroglobulinaemia; at least 1 major + 4 minor); the most commonly used criteria, but not clinically validated. Management: SUPPORTIVE — oxygen, lung-protective ventilation (if ARDS-pattern failure), early fracture FIXATION (stabilisation within 24 h is the most effective preventive strategy), corticosteroids controversial (reduce FES incidence in meta-analysis, no mortality benefit). Outcome: usually good with supportive care. Prevention: early operative fixation (vs delayed/traction).

^[20] ^[26]

FES differential — acute deterioration after trauma

Condition	Timing	Key features	Diagnosis
Fat embolism (FES)	24-72h post-fracture	Triad (resp + neuro + rash), hypoxaemia	Clinical (Gurd); exclude others
Pulmonary embolism	Any time (esp. immobilised)	Unilateral leg swelling, sudden dyspnoea, pleuritic pain	CTPA, D-dimer, echocardiography
Tension pneumothorax	Immediate (or delayed)	Unilateral hyperresonance, tracheal deviation	Clinical; CXR/POCUS
Aspiration pneumonitis	During/after intubation	Post-intubation hypoxaemia, infiltrate	Clinical; CXR
ARDS (non-fat)	Days	Lung injury from sepsis/trauma/pneumonia	Berlin definition
Sepsis	Any time	Fever, source, rising lactate	Cultures, source identification
Intracranial injury	Immediate/delayed	Focal deficit, deteriorating GCS	CT brain

^[26] ^[27]

Management of suspected fat embolism syndrome

RECOGNISE THE CLINICAL PICTURE — after an asymptomatic period of 24-72 HOURS after long bone/pelvic fracture (or orthopaedic surgery); neurological manifestations typically 12-72 h after the insult: sudden RESPIRATORY DISTRESS (dyspnoea, hypoxaemia — SpO2 drop), NEUROLOGICAL (confusion, agitation, decreased consciousness, seizures, rarely infarction), PETECHIAL RASH (characteristic but may be absent — cerebral FES can occur without any respiratory or dermatological signs). ALSO: fever, tachycardia, jaundice. Apply Gurd criteria (at least 1 major + 4 minor). EXCLUDE other causes (PE, pneumothorax, sepsis, intracranial injury)^[26]^[27]^[21]
SUPPORTIVE RESPIRATORY CARE (MAINSTAY) — (a) OXYGEN (high-flow — target SpO2 >92%). (b) HFNC or NIV if moderate hypoxaemia. (c) INTUBATE + MECHANICAL VENTILATION if severe or refractory hypoxaemia — LUNG-PROTECTIVE (Vt 6 mL/kg predicted body weight, plateau pressure 30 cmH2O or less, PEEP titrated), the settings validated in acute lung injury/ARDS. (d) FES causes ARDS-like lung injury (hydrolysis of fat to free fatty acids) -> manage as ARDS (prone positioning for severe ARDS, permissive hypercapnia). (e) AVOID fluid overload (worsens pulmonary oedema)^[22]^[23]^[13]
NEUROLOGICAL SUPPORT — (a) Cerebral FES: confusion, seizures, coma — from embolic fat (through PFO or via pulmonary shunts) + cerebral oedema. (b) CT brain (exclude traumatic brain injury, haemorrhage). (c) Seizures: benzodiazepines. (d) Raised ICP (if severe): head elevation, osmotic agents (mannitol, hypertonic saline) — if evidence of oedema. (e) FES is a self-limiting disease — most neurological changes are TRANSIENT. (f) Sedation: minimise (to assess neurology)^[27]^[17]
FRACTURE MANAGEMENT (PREVENT ONGOING EMBOLISATION) — (a) EARLY OPERATIVE FIXATION (intramedullary nailing, plating) — in multiply-injured patients, delayed stabilisation carried a higher incidence of pulmonary complications (ARDS, fat embolism, pneumonia) in randomised comparison; early stabilisation within 24 h is the most effective preventive strategy. (b) AVOID delayed fixation or prolonged traction (higher FES risk). (c) TIMING: as early as practicable once stable (within 24 h). (d) CAVEAT: whether intramedullary nailing/reaming causes FES is debated — in borderline polytrauma patients, primary intramedullary nailing carried a higher incidence of acute lung injury than external fixation (odds 6.69x) — discuss damage-control external fixation in the borderline/unstable patient. (e) Support fracture (splint) before definitive fixation^[5]^[19]^[13]^[12]
ADJUNCTS (CONTROVERSIAL) — (a) CORTICOSTEROIDS: (i) PROPHYLACTIC — a meta-analysis of 7 randomised trials (389 patients) found corticosteroids reduced the risk of FES by 78% (95% CI 43-92%), with no difference in mortality or infection; the trials were small and poor quality, and use remains controversial (inconsistent efficacy, potential adverse effects). (ii) THERAPEUTIC (once FES established) — no established benefit. (iii) NOT routine. (b) HEPARIN and other medical therapies: benefit remains unclear. (c) ASPIRIN, DEXTRAN, ALBUMIN: no established role — many drugs have been tried with inconclusive results. (d) NO SPECIFIC ANTIDOTE — supportive care is mainstay^[4]^[19]^[2]^[17]
MONITORING + SUPPORTIVE CARE + RECOVERY — (a) Continuous SpO2, cardiac monitor, urine output. (b) Serial ABG (hypoxaemia, acidosis). (c) Serial GCS (neurological trend). (d) FBC (anaemia, thrombocytopenia), coagulation (DIC), LFTs (jaundice), renal function. (e) SUPPORTIVE: nutrition, DVT prophylaxis, stress ulcer prophylaxis, infection surveillance. (f) EXPECTED COURSE: most cases resolve spontaneously; neurology resolves over days-weeks. (g) OUTCOME: usually good with supportive care — severe instances cause significant respiratory failure, neurological damage and mortality. (h) REHABILITATION: orthopaedic (fracture healing), neuro/cognitive (if deficits persist)^[8]^[15]

^[1]

SAQ — Fat embolism syndrome after femoral nailing

10 minutes · 10 marks

A 24-year-old man was admitted 36 h ago after a motorcycle crash with an isolated closed left femoral shaft fracture; he underwent intramedullary nailing within 6 h. He now has acute onset of dyspnoea (RR 36, SpO₂ 86% on 15 L O₂), confusion and agitation, and a petechial rash over the upper chest and conjunctivae. HR 128, BP 100/70, temp 38.6°C. ABG shows pH 7.30, PaO₂ 52, PaCO₂ 32. Platelets 95 ×10⁹/L.

^[21] ^[24] ^[26] ^[27] ^[4] ^[22] ^[23]

SAQ — Cerebral fat embolism in the multiply-injured patient

10 minutes · 10 marks

A 30-year-old man with bilateral femoral shaft fractures from a motor vehicle crash (no head injury on initial CT) develops acute confusion, agitation and decreased level of consciousness 30 h after admission, with respiratory failure requiring intubation. MRI brain shows a 'starfield pattern' of diffuse punctate T2/FLAIR hyperintense lesions in the deep white matter. Petechiae over the axillae are noted.

^[27] ^[28] ^[29] ^[24] ^[18]

Clinical pearls

High-yield fat embolism syndrome points for CICM/FFICM exam

Triad timing — 24-72 hours after fracture (classic). (1) The triad of lung, brain and skin involvement develops after an ASYMPTOMATIC PERIOD of 24-72 HOURS after the triggering event (long bone/pelvic fracture, major orthopaedic surgery); neurological manifestations typically occur 12-72 h after the initial insult. (2) WHY: fat globules from marrow enter venous circulation -> embolise to lungs/brain -> mechanical obstruction + biochemical injury (hydrolysis of fat to free fatty acids toxic to endothelium) -> takes hours for inflammation + capillary leak to develop -> clinical symptoms. (3) DISTINCT from immediate complications (tension pneumothorax, haemothorax — at time of injury). (4) CLINICAL: any patient who deteriorates 24-72h after long bone fracture -> consider FES (especially if respiratory + neurological + rash).^[26]^[27]
Two mechanisms — mechanical + biochemical. (1) MECHANICAL: (a) Fat globules from marrow (especially long bones — femur, tibia) enter venous sinuses of bone -> venous circulation -> right heart -> PULMONARY capillaries (first capillary bed — fat too large to pass) -> mechanical obstruction of capillaries -> respiratory distress. (b) Fat emboli can deform and pass through the lungs, resulting in systemic embolisation (most commonly brain and kidneys); passage via PULMONARY SHUNTS or PFO (patent foramen ovale — overall incidence 27.3% in an autopsy series of 965 normal hearts) also occurs -> brain (cerebral FES), skin (petechiae), kidneys, retina. (2) BIOCHEMICAL: (a) Hydrolysis of fat to FREE FATTY ACIDS. (b) Free fatty acids injure the capillary endothelium -> inflammatory cascade -> capillary leak -> ARDS-like lung injury, cerebral oedema, multi-organ dysfunction. (c) This explains the DELAYED onset (24-72h — time for biochemical injury to develop). (3) BOTH mechanisms contribute — mechanical (immediate embolisation) + biochemical (delayed inflammatory injury).^[26]^[24]^[18]
Petechial rash — characteristic but may be absent. (1) PETECHIAE (pinpoint red spots — from capillary obstruction by fat microemboli) appear over the upper chest, neck, axillae and conjunctivae. (2) A characteristic petechial rash is part of the classic triad. (3) BUT the rash may be ABSENT — cerebral fat embolism can occur without any respiratory or dermatological signs, and diffuse petechiae are only one of the common clinical findings. (4) CLINICAL: don't REQUIRE the rash to diagnose FES (its absence doesn't exclude). (5) Look carefully (conjunctivae, axillae — easy to miss). (6) Other skin signs: pallor, cyanosis (from hypoxaemia).^[27]^[25]^[13]
Gurd criteria — diagnostic framework. (1) MAJOR features (at least 1): (a) Respiratory distress (hypoxaemia, ARDS). (b) Neurological dysfunction (confusion, coma, seizures). (c) Petechial rash. (2) MINOR features (at least 4): (a) Fever. (b) Tachycardia. (c) Jaundice. (d) Renal dysfunction. (e) Retinal changes (fat emboli/petechiae on fundoscopy). (f) Fat macroglobulinaemia (fat in blood — on special stain). (g) Thrombocytopenia, anaemia, elevated ESR. (3) DIAGNOSIS: at least 1 MAJOR and 4 MINOR criteria — the rule applied in published FES series. (4) LIMITATION: Gurd's criteria are the most commonly used diagnostic tool, but with no gold standard they cannot be clinically validated; diagnosis is clinical with exclusion of other causes (PE, sepsis, TBI). (5) USE: framework for diagnosis — but clinical judgement (classic triad after fracture = FES even if criteria not fully met).^[21]^[20]^[3]
Neurological FES — cerebral embolism. (1) Cerebral FES: fat emboli reach brain (through PFO or pulmonary shunts) -> cerebral microinfarcts + oedema. (2) PRESENTATION: (a) CONFUSION, agitation (early). (b) Decreased consciousness (coma). (c) Seizures. (d) Rarely cerebral infarction, spinal cord ischaemia, haemorrhagic stroke. (e) 'Starfield pattern' on diffusion-weighted MRI (multiple small patchy high-signal lesions — characteristic). (3) DIFFERENTIAL: traumatic brain injury (TBI — but TBI is at time of injury, not 12-72h later), anoxia, metabolic. (4) CT brain: may be normal early (or diffuse oedema); MRI more sensitive (starfield pattern). (5) MANAGEMENT: supportive (seizures — benzos; raised ICP — osmotic). (6) PROGNOSIS: FES is self-limiting — neurology usually TRANSIENT (resolves over days-weeks) — but some have persistent cognitive deficits.^[27]^[29]^[17]
Respiratory management — ARDS-like. (1) FES causes ARDS-like lung injury (capillary leak from free fatty acids + mechanical obstruction by fat emboli). (2) SPECTRUM: mild (hypoxaemia on supplemental O2) -> moderate (NIV/HFNC) -> severe (ARDS — needs intubation). (3) VENTILATION (if intubated): LUNG-PROTECTIVE — Vt 6 mL/kg predicted body weight, plateau pressure 30 cmH2O or less, PEEP titrated, permissive hypercapnia (the lower-tidal-volume strategy that reduced mortality — 31.0% vs 39.8% — in the ARDS Network randomized trial). (4) PRONING (severe ARDS — PaO2/FiO2 under 150 mmHg): prone-positioning sessions of at least 16 hours reduced 28-day and 90-day mortality in the PROSEVA randomized trial. (5) FLUID MANAGEMENT: CONSERVATIVE (avoid overload — worsens pulmonary oedema; capillary leak already present). (6) EXPECTED: respiratory distress peaks in the first 24-72h, then improves. (7) MOST recover without long-term lung damage.^[22]^[23]^[13]
Early fracture fixation reduces FES risk. (1) EVIDENCE: a prospective randomised study (Bone 1989, 178 patients) found that when stabilisation was DELAYED in multiply-injured patients, the incidence of pulmonary complications (adult respiratory-distress syndrome, fat embolism, pneumonia) was higher, with longer hospital and ICU stay; early fracture stabilisation within 24 hours remains the most effective preventive strategy. (2) RATIONALE: (a) Stabilises fracture -> reduces ongoing fat/marrow embolisation (movement of fracture fragments -> more fat released). (b) Reduces pain, inflammation, systemic stress. (c) Allows early mobilisation (reduces DVT, pneumonia). (3) CAVEAT: whether intramedullary nailing itself causes FES is debated; in BORDERLINE polytrauma, primary intramedullary nailing carried a higher incidence of acute lung injury than external fixation with later conversion (odds 6.69x) — damage control external fixation is preferred in the borderline/unstable patient. (4) PRACTICE: early definitive fixation if haemodynamically stable; if unstable -> damage control (external fixation) -> definitive when stabilised.^[5]^[19]^[12]^[13]
Corticosteroids for FES — controversial. (1) PROPHYLACTIC (given before FES develops): (a) A meta-analysis of 7 randomised trials (Bederman 2009, 389 patients) found corticosteroids reduced the risk of FES by 78% (95% CI 43-92%), with only 8 patients needed to treat to prevent 1 case, and no difference in mortality or infection rates. (b) BUT the trials were of poor quality and a large confirmatory randomised trial was recommended; use remains controversial owing to inconsistent efficacy and potential adverse effects. (c) NOT routine. (2) THERAPEUTIC (once FES established): (a) NO proven benefit — many drugs have been used to treat FES with inconclusive results. (3) CURRENT: not routine. May consider in very high-risk (multiple long bones) — discuss with orthopaedics. (4) NOT a substitute for early fixation + supportive care.^[4]^[19]^[17]
Distinguish from pulmonary embolism (PE). (1) TIMING: FES 24-72h; PE any time (esp. after immobilisation — days-weeks). (2) SOURCE: FES from marrow (fracture); PE from DVT (leg veins). (3) FEATURES: (a) FES: triad (resp + neuro + rash), ARDS-like, PETECHIAL RASH. (b) PE: pleuritic pain, haemoptysis, unilateral leg swelling, ECG changes (S1Q3T3, RV strain), echo (RV dilation). (4) INVESTIGATIONS: (a) FES: clinical (Gurd), MRI brain (starfield), bronchoalveolar lavage (fat in macrophages — supportive, not definitive). (b) PE: CTPA (filling defect), D-dimer, echocardiography. (5) MANAGEMENT: (a) FES: supportive (no anticoagulation). (b) PE: anticoagulation (or thrombolysis if massive). (6) DON'T confuse — different treatments. (But trauma patient may have BOTH — assess).^[26]^[2]
Cardiac FES — rare but recognised. (1) The cardiovascular system is among the organs most seriously affected by FES; fat emboli can reach the coronary circulation (through PFO or pulmonary shunts). (2) PRESENTATION: (a) Chest pain (ischaemic). (b) ECG changes (ST, T-wave). (c) Troponin rise. (d) Arrhythmia. (3) DIFFERENTIAL: traumatic cardiac contusion (blunt chest injury — but contusion is at time of injury), MI (atherosclerotic — but patient usually young trauma). (4) MANAGEMENT: supportive, treat arrhythmia. (5) Usually resolves (microinfarcts — not large territory). (6) Rare — but consider in a trauma patient with cardiac signs after the FES latency window.^[17]^[27]
Retinal FES — diagnostic clue. (1) Fat emboli can lodge in the RETINAL circulation (through systemic embolisation) — retinal ischaemia is a recognised feature of FES. (2) FUNDOSCOPY: (a) Fat globules (yellow-white, glistening — in retinal arterioles). (b) Petechial haemorrhages. (c) Cotton-wool spots (microinfarcts). (3) CLINICAL: in a trauma patient with FES suspicion -> examine fundi (may reveal fat emboli — supportive evidence). (4) LIMITATION: requires ophthalmology/dilated fundus (not always feasible in ICU); small emboli may be missed. (5) SUPPORTIVE for diagnosis (not definitive).^[27]
Bronchoalveolar lavage (BAL) fat-laden macrophages — supportive test. (1) In FES, fat from embolised globules is engulfed by alveolar macrophages. (2) BAL (bronchoscopy + lavage): sample alveolar fluid -> stain for fat (Oil Red O or Sudan) -> fat-laden macrophages. (3) SUPPORTIVE for FES (if positive). (4) LIMITATIONS: (a) Not specific (fat-laden macrophages also seen in other conditions — aspiration, ARDS). (b) Not sensitive (may be negative early). (c) Requires bronchoscopy (invasive — not always feasible). (5) NOT required for diagnosis (FES is clinical). (6) USE: if diagnosis uncertain + BAL available -> supportive evidence.^[2]
Differential diagnosis — acute deterioration in trauma patient. (1) FES (24-72h post-fracture — triad; neurological features may appear 12-72 h after the insult). (2) PULMONARY EMBOLISM (DVT — any time, immobilisation). (3) TENSION PNEUMOTHORAX (immediate or delayed). (4) ASPIRATION PNEUMONITIS (during/after intubation). (5) ARDS (from sepsis, pneumonia, trauma, transfusion — TRALI). (6) SEPSIS (source — pneumonia, line, wound). (7) TRAUMATIC BRAIN INJURY (deteriorating — extradural, subdural — need CT). (8) HYPOXAEMIA from other cause (fatigue, opioids). (9) EVALUATE: clinical (timing, features), CXR (pneumothorax, infiltrates), CT brain (intracranial), CTPA (PE if suspected), cultures (sepsis), echocardiography (cardiac). DON'T assume FES without excluding others.^[26]^[27]^[2]
Prognosis and recovery. (1) OUTCOME: the condition is usually associated with a good outcome with supportive care; severe instances can lead to significant respiratory failure, neurological damage and even mortality — mostly in the ARDS/multi-organ failure phenotype. (2) RESPIRATORY: most cases resolve spontaneously; most recover without long-term lung damage. (3) NEUROLOGICAL: usually transient (days-weeks) — but some have persistent cognitive deficits (especially if severe/prolonged coma). (4) SKIN: petechiae resolve (days — no scarring). (5) FRACTURE: depends on orthopaedic injury (fixation, healing). (6) PREDICTORS of poor outcome: severe respiratory failure, prolonged coma, multi-organ failure. (7) REHABILITATION: orthopaedic (fracture healing + mobility), neuro/cognitive (if deficits), pulmonary (if residual impairment). (8) RECURRENCE: rare (no predisposition — usually a one-time event after fracture).^[8]^[15]^[13]

References30Show

[1]Gurd AR, Wilson RI The fat embolism syndrome. Journal of bone and joint surgery (British volume), 1974.PMID 4547466
[2]Newbigin K, Souza CA, Torres C, et al. Fat embolism syndrome: State-of-the-art review focused on pulmonary imaging findings. Respiratory medicine, 2016.PMID 26895808
[3]Timon C, Keady C, Murphy CG Fat Embolism Syndrome — A Qualitative Review of its Incidence, Presentation, Pathogenesis and Management. Malaysian orthopaedic journal, 2021.PMID 33880141
[4]Bederman SS, Bhandari M, McKee MD, et al. Do corticosteroids reduce the risk of fat embolism syndrome in patients with long-bone fractures? A meta-analysis. Canadian journal of surgery, 2009.PMID 19865573
[5]Bone LB, Johnson KD, Weigelt J, et al. Early versus delayed stabilization of femoral fractures. A prospective randomized study. Journal of bone and joint surgery (American volume), 1989.PMID 2925704
[6]Rothberg DL, Makarewich CA Fat Embolism and Fat Embolism Syndrome. Journal of the American Academy of Orthopaedic Surgeons, 2019.PMID 30958807
[7]Luff D, Hewson DW Fat embolism syndrome. BJA education, 2021.PMID 34457354
[8]Mellor A, Soni N Fat embolism. Anaesthesia, 2001.PMID 11167474
[9]Schonfeld SA, Ploysongsang Y, DiLisio R, et al. Fat embolism prophylaxis with corticosteroids. A prospective study in high-risk patients. Annals of internal medicine, 1983.PMID 6354030
[10]Kallenbach J, Lewis M, Zaltzman M, et al. 'Low-dose' corticosteroid prophylaxis against fat embolism. Journal of trauma, 1987.PMID 3312625
[11]Lindeque BG, Schoeman HS, Dommisse GF, et al. Fat embolism and the fat embolism syndrome. A double-blind therapeutic study. Journal of bone and joint surgery (British volume), 1987.PMID 3818718
[12]Pape HC, Rixen D, Morley J, et al. Impact of the method of initial stabilization for femoral shaft fractures in patients with multiple injuries at risk for complications (borderline patients). Annals of surgery, 2007.PMID 17717453
[13]Parisi DM, Koval K, Egol K Fat embolism syndrome. American journal of orthopedics (Belle Mead, N.J.), 2002.PMID 12650535
[14]Cantu CA, Pavlisko EN Liposuction-Induced Fat Embolism Syndrome: A Brief Review and Postmortem Diagnostic Approach. Archives of pathology and laboratory medicine, 2018.PMID 29939780
[15]Kwon J, Coimbra R Fat embolism syndrome after trauma: What you need to know. Journal of trauma and acute care surgery, 2024.PMID 39213184
[16]Lempert M, Halvachizadeh S, Ellanti P, et al. Incidence of Fat Embolism Syndrome in Femur Fractures and Its Associated Risk Factors over Time — A Systematic Review. Journal of clinical medicine, 2021.PMID 34205701
[17]Taviloglu K, Yanar H Fat embolism syndrome. Surgery today, 2007.PMID 17186337
[18]Richards RR Fat embolism syndrome. Canadian journal of surgery, 1997.PMID 9336522
[19]Miyake T, Okada H, Kanda N Advances and uncertainties in fat embolism syndrome: a review. Trauma surgery and acute care open, 2026.PMID 42375760
[20]Talbot M, Schemitsch EH Fat embolism syndrome: history, definition, epidemiology. Injury, 2006.PMID 16990059
[21]Gallardo X, Castañer E, Mata JM, et al. Nodular pattern at lung computed tomography in fat embolism syndrome: a helpful finding. Journal of computer assisted tomography, 2006.PMID 16628042
[22]Brower RG, Matthay MA, Morris A, et al. Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The New England journal of medicine, 2000.PMID 10793162
[23]Guérin C, Reignier J, Richard JC, et al. Prone positioning in severe acute respiratory distress syndrome. The New England journal of medicine, 2013.PMID 23688302
[24]Hagen PT, Scholz DG, Edwards WD Incidence and size of patent foramen ovale during the first 10 decades of life: an autopsy study of 965 normal hearts. Mayo Clinic proceedings, 1984.PMID 6694427
[25]Al-Khuwaitir TS, Al-Moghairi AM, Sherbeeni SM, et al. Traumatic fat embolism syndrome. Saudi medical journal, 2002.PMID 12518208
[26]Shaikh N, Parchani A, Bhat V, et al. Fat embolism syndrome: clinical and imaging considerations: case report and review of literature. Indian journal of critical care medicine, 2008.PMID 19826589
[27]Algahtani HA, Shirah BH, Abdelghaffar N, et al. Cerebral fat embolism syndrome: diagnostic challenges and catastrophic outcomes: a case series. Journal of Yeungnam medical science, 2023.PMID 36069083
[28]Buskens CJ, Gratama JW, Hogervorst M, et al. Encephalopathy and MRI abnormalities in fat embolism syndrome: a case report. Medical science monitor, 2008.PMID 18971877
[29]Kontani S, Nakamura A, Tokumi H, et al. [A case of cerebral fat embolism after artificial bone replacement operation for femoral head fracture]. Rinsho shinkeigaku (Clinical neurology), 2014.PMID 25142536
[30]Akoh CC, Schick C, Otero J, et al. Fat embolism syndrome after femur fracture fixation: a case report. The Iowa orthopaedic journal, 2014.PMID 25328460

Fat embolism syndrome: diagnosis, ventilation, and management in trauma

Also known as Fat embolism syndrome · FES · Fat embolism · Orthopaedic embolism · Gurd criteria

medium30 referencesUpdated 19 Aug 202632 min readVerification in progress

Practise this topic

8 MCQs

Condition

Timing

Key features

Diagnosis

Fat embolism (FES)

24-72h post-fracture

Triad (resp + neuro + rash), hypoxaemia

Clinical (Gurd); exclude others

Pulmonary embolism

Any time (esp. immobilised)

Unilateral leg swelling, sudden dyspnoea, pleuritic pain

CTPA, D-dimer, echocardiography

Tension pneumothorax

Immediate (or delayed)

Unilateral hyperresonance, tracheal deviation

Clinical; CXR/POCUS

Aspiration pneumonitis

During/after intubation

Post-intubation hypoxaemia, infiltrate

Clinical; CXR

ARDS (non-fat)

Days

Lung injury from sepsis/trauma/pneumonia

Berlin definition

Sepsis

Any time

Fever, source, rising lactate

Cultures, source identification

Intracranial injury

Immediate/delayed

Focal deficit, deteriorating GCS

CT brain

Clinical pearls

References30Show

[1]Gurd AR, Wilson RI The fat embolism syndrome. Journal of bone and joint surgery (British volume), 1974.PMID 4547466
[2]Newbigin K, Souza CA, Torres C, et al. Fat embolism syndrome: State-of-the-art review focused on pulmonary imaging findings. Respiratory medicine, 2016.PMID 26895808
[3]Timon C, Keady C, Murphy CG Fat Embolism Syndrome — A Qualitative Review of its Incidence, Presentation, Pathogenesis and Management. Malaysian orthopaedic journal, 2021.PMID 33880141
[4]Bederman SS, Bhandari M, McKee MD, et al. Do corticosteroids reduce the risk of fat embolism syndrome in patients with long-bone fractures? A meta-analysis. Canadian journal of surgery, 2009.PMID 19865573
[5]Bone LB, Johnson KD, Weigelt J, et al. Early versus delayed stabilization of femoral fractures. A prospective randomized study. Journal of bone and joint surgery (American volume), 1989.PMID 2925704
[6]Rothberg DL, Makarewich CA Fat Embolism and Fat Embolism Syndrome. Journal of the American Academy of Orthopaedic Surgeons, 2019.PMID 30958807
[7]Luff D, Hewson DW Fat embolism syndrome. BJA education, 2021.PMID 34457354
[8]Mellor A, Soni N Fat embolism. Anaesthesia, 2001.PMID 11167474
[9]Schonfeld SA, Ploysongsang Y, DiLisio R, et al. Fat embolism prophylaxis with corticosteroids. A prospective study in high-risk patients. Annals of internal medicine, 1983.PMID 6354030
[10]Kallenbach J, Lewis M, Zaltzman M, et al. 'Low-dose' corticosteroid prophylaxis against fat embolism. Journal of trauma, 1987.PMID 3312625
[11]Lindeque BG, Schoeman HS, Dommisse GF, et al. Fat embolism and the fat embolism syndrome. A double-blind therapeutic study. Journal of bone and joint surgery (British volume), 1987.PMID 3818718
[12]Pape HC, Rixen D, Morley J, et al. Impact of the method of initial stabilization for femoral shaft fractures in patients with multiple injuries at risk for complications (borderline patients). Annals of surgery, 2007.PMID 17717453
[13]Parisi DM, Koval K, Egol K Fat embolism syndrome. American journal of orthopedics (Belle Mead, N.J.), 2002.PMID 12650535
[14]Cantu CA, Pavlisko EN Liposuction-Induced Fat Embolism Syndrome: A Brief Review and Postmortem Diagnostic Approach. Archives of pathology and laboratory medicine, 2018.PMID 29939780
[15]Kwon J, Coimbra R Fat embolism syndrome after trauma: What you need to know. Journal of trauma and acute care surgery, 2024.PMID 39213184
[16]Lempert M, Halvachizadeh S, Ellanti P, et al. Incidence of Fat Embolism Syndrome in Femur Fractures and Its Associated Risk Factors over Time — A Systematic Review. Journal of clinical medicine, 2021.PMID 34205701
[17]Taviloglu K, Yanar H Fat embolism syndrome. Surgery today, 2007.PMID 17186337
[18]Richards RR Fat embolism syndrome. Canadian journal of surgery, 1997.PMID 9336522
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