FAT EMBOLISM SYNDROME(FES)

DR AFTAB HUSSAIN

HistoryFirst diagnosed in 1873 by Dr Von Bergmann

In 1879 Fenger and Salisbury published description of Fat embolism syndrome

Fat Emboli: Fat particles or droplets that travel through the circulation

Fat Embolism: A process by which fat emboli passes into the bloodstream and lodges within a blood vessel.

Fat Embolism Syndrome (FES): serious manifestation of fat embolism occasionallycauses multi system dysfunction, the lungs are

always involved and next is brain

FE vs. FESFat embolization is a well-known complication

of skeletal trauma and surgery involving instrumentation of the femoral medullary canal.

Fat embolism syndrome (FES) is a physiological response to fat within the systemic circulation.

Fat embolization and FES are not synonymus.

The embolization of fat can be detected in almost all patients who sustain a pelvic or femoral fracture, but the incidence of FES is less than 1%.

Fat Embolism SyndromeMortality: 10-20%Clinical diagnosis, No specific laboratory test

is diagnostic.Mostly associated with long bone and pelvic

fractures, and more frequent in closed fractures.

Single long bone fracture has 1-3% chance of developing FES, and increases with number of fractures.

Onset is 24-72 hours from initial insult.

Causes of fat embolism TRAUMA RELATED: Blunt trauma: Long bone (Femur, tibia, pelvic)

factures orthopedic proceduresSoft tissue injury(chest compression with or

without rib fracture) BurnLiposuctionBone marrow harvesting and transplant.

NON TRAUMA RELATEDPancreatitis Diabetes mellitusOsteomyelitis and panniculitisBone tumor lysisSteroid therapySickle cell hemoglobinopathyAlcoholic liver diseaseFat infusion

Most common cause of FES is blunt trauma.

90 % occurs after blunt trauma complicated by long-bone fractures

Closed fractures had higher incidence compared to open fractures. The intramedullary bone pressure is lower in case of open fractures, which reduces the bulk of fat emboli propelled into the blood stream.

Non-traumatic fat embolism It occurs due to the process of fat or marrow

necrosis or by the increased concentration of lipids in the blood.

It may be caused by agglutination of chylomicrons and VLDL by high levels of plasma CRP.

As in Acute pancreatitis in patients with types I, IV, and V hyperlipidaemia and avascular necrosis of bone in patients with corticosteroid-induced hyperlipidaemia.

Drug-related causes of FES

Infusion of lipids at rates greater than the normal clearance capacity of lipids.

Agglutination of lipid emulsion particles with fibrin.

Agglutination of endogenous or infused exogenous fat such as Intra lipid.

FES can occur in SC crisis.

Bone marrow necrosis as a result of hypoxia may release fat.

Risk factors

Pathophysiology of FESExact mechanism unknown, but two main

hypothesis

1.Mechanical Hypothesis

2.Biochemical Hypothesis

Mechanical HypothesisObstruction of vessels and capillaries

Increase in inter medullary pressure forces fat and marrow into bloodstream.

Bone marrow contents enter the venous system and lodge in the lungs as emboli.

Smaller fat droplets travel through the pulmonary capillaries into the systemic

circulation: Embolization to cerebral vessels or renal vessels also leads to central nervous system and renal dysfunction

Biochemical HypothesisToxicity of free fatty acids

Circulating free fatty acids directly affect the pneumocytes, producing abnormalities in gas exchange.

Coexisting shock, hypovolemia and sepsis impair liver function and augment toxic effects of free fatty acids.

Hormonal changes caused by trauma or sepsis induce systemic release of free fatty acids as chylomicrons.

Acute-phase reactants( C-reactive proteins) cause chylomicrons to coalesce.

It explains non traumatic forms of fat embolism syndrome and why symptoms take 12 hours to develop.

FE in ARDSFat emboli obstructs

lung vessel (20microns), platelets and fibrin adhere to it

Lipase increases FFA

Inflammatory changes->endothelial damage->ARDS

CLINICAL FEATURESAsymptomatic for the first 12-48 hours

Pulmonary DysfunctionNeurological (nonspecific)Dermatological Signs

Pulmonary

Hypoxia, rales, pleural friction rubARDS may develop.CXR usually normal early on, later may show

‘snowstorm’ pattern- diffuse bilateral infiltrates

CT chest: ground glass opacification with interlobular septal thickening.

Neurological findingsUsually occur after respiratory symptomsIncidence- 80% patients with FESMinor global dysfunction is most common-

ranges from mild delirium to coma. Seizures/focal deficitsTransient and reversible in most cases.CT Head: general edema, usually nonspecificMRI brain: Low density on T1, and high

intensity T2 signal, correlates to degree of impairment.

Dermatological findingsPetechieUsually on conjunctiva, neck, axilla, upper

limbs.Results from occlusion of dermal capillaries

by fat globules and then extravasations of RBC.

Resolves in 5-7 days. Usually fast resolving.Pathognomic, but only present in 20-50% of

patients.

Early SignsDyspnea TachypneaHypoxemia

Triad of FESHypoxemiaNeurological abnormalitiesPetechial rash

Other findingsRetinopathy (exudates, cotton wool spots,

hemorrhage)LipiduriaFeverDICMyocardial depression (Right heart strain)Thrombocytopenia/AnemiaHypocalcemia.

Diagnostic CriteriaGurd criteria most

commonly used.

Other indexes areSchonfeld IndexLindeque Index

Gurd & Wilson Criteria

Schonfeld Fat Embolism Syndrome Index

It ranks signs and symptoms of FES in relation to their incidence of presentation.

Score >5 required for diagnosis of fat embolism syndrome

Schonfeld FES Index sign score

Petechial rash 5

Diffuse alveolar infiltrate 4

Hypoxemia pao2<70 mm Hg, FIO2-100%

3

confusion 1

Fever ( >100.4 F) 1

Heart rate >120 beats/min 1

Respiratory rate >30/min 1

Lindeque's criteriaAcc. to Lindeque FES can be diagnosed on

the basis of respiratory system involvement alone.

Laboratory Studies Arterial Blood Gases (ABGs)

Urine and sputum examination

Haemotological Tests

Biochemical tests

Imaging• Chest x-ray

– shows multiple flocculent shadows (snow storm appearance). picture may be complicated by infection or pulmonary edema.

Imaging contd.

MRI Brain - Image showing minimal hypodense

changes in periventricular region, which are more evident in DWI and T2WI as areas of high signals.

Treatment and managementProphylaxisImmobilization and early internal fixation of

fracture.  Fixation within 24 hours has been shown to

yield a 5 fold reduction in the incidence of ARDS.

Continuous pulse oximeter monitoring in high-risk patients may help in detecting desaturation early, allowing early institution of oxygen and possibly steroid therapy.

High doses of corticosteroids.

Supportive Medical Care

Maintenance of adequate oxygenation and ventilation

Maintenance of hemodynamic stability.Administration of blood products as clinically

indicated.HydrationProphylaxis of deep venous thrombosis .Nutrition.

Treatment and management contd.

Treatment and management contd.

Oxygenation and ventilation

 High flow rate oxygen is given to maintain the arterial oxygen tension in the normal range.

 Mechanical ventilation and PEEP may be required to maintain arterial oxygenation.

Treatment and management contd.

Hemodynamic stabilityMaintenance of intravascular volume is

important, because shock can exacerbate the lung injury caused by FES.

Albumin has been recommended for volume resuscitation in addition to balanced electrolyte solution, because it not only restores blood volume but also binds with the fatty acids and may decrease extent of lung injury

SteroidsSteroid prophylaxis is controversial to

prevent FES.It causes blunting of inflammatory response

and complement activationProspective studies suggests prophylactic

steroids benefit in high risk patients.Preoperative use of methylprednisolone may

prevent the occurrence of FESOnce FES established, steroids have not

shown improved outcomes.

Results of Randomized, Controlled Trials of Corticosteroids for Prevention of Fat Embolism Syndrome

Dose Model Timing Duration of study

Effect on disease incidence

30mg/kg Dog Before event

60min None

10mg/kg q8h for 24 hrs

Human trauma

At admission

No data Declining

7.5mg/kg q6h for 12hrs or placebo

Human Trauma

Within 12hrs

2 days Declining

Heparin

Heparin has also been proposed for treatment as it "clears" lipemic plasma in vivo by causing the release of lipoprotein lipase into the circulation, but no evidence exists for its use in FES.

PrognosisThe fulminant form presents as acute cor

pulmonale, respiratory failure or embolic phenomena, leading to death within a few hours of injury.

Most death contributed to pulmonary dysfunction

Hard to determine exact mortality rate

Estimated less than 10%

The incidence of FES ranges from < 1 to 29% in different studies.

Actual incidence of FES is not known, as mild cases often go unnoticed.

A high index of suspicion is needed to diagnose FES.

A combination of clinical criteria and MRI brain will enable early and accurate diagnosis of FES.

RefrencesAltaf Hussain: “A Fatal Fat Embolism.” The Internet Journal of

Anesthesiology, 2004. Volume 8 Number 2.

Fabian T. “Unraveling the fat embolism syndrome”. N Engl J Med 1993;329:961–63

U. Galway, J. E. Tetzlaff & R. Helfand : “Acute Fatal Fat Embolism Syndrome In Bilateral Total Knee Arthroplasty – A Review Of The Fat Embolism Syndrome”. The Internet Journal of Anesthesiology. 2009 Volume 19 Number 2

Latif, A., Bashir, A., Aurangzeb. "Fat Embolism and Fat Embolism Syndrome; Management Trends." Professional Med J 15.4 (2008): 407-413.

Harrisons principles of Internal medicine 18th edition.

Nissar Shaikh, Emergency management of fat embolism syndrome.” J Emerg Trauma Shock. 2009 Jan-Apr; 2(1): 29–33

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