It is one of the causes of morbidity and

mortality following # in patient with multiple

injury+

FES is an important cause of ARDS

Fat embolism syndrome is defined -- Post

Traumatic Respiratory Distress Syndrome

occurring within 72hrs of skeletal trauma

Earliest manifestations are-- Tachycardia-- Elevation of temperature above 38

deg -- falling PaO2

Fat embolism - this indicates presence of

fat globules in lung parenchyma and

peripheral circulation after fractures of

long bones and other major trauma

Fat embolism Syndrome-A serious manifestation of the

phenomenon of emboli resulting in a

variety of symptoms

Historical Review

In 1861, Zenker described fat droplets in the

lung capillaries of a railroad worker who

sustained a fatal thoracoabdominal crush

injury.

In 1865, Wagner described the pathologic features of fat embolism.

However, in 1873,Von Bergmann became the first to establish the clinical diagnosis of fat embolism syndrome.

In a 38-year-old patient who sustained a comminuted fracture of the distal femur.

Postmortem examination revealed a large amount of pulmonary fat

Button – stated that 10% of battle casualities

in World War 1 suffered from FES

World War 2 postmortem study revealed

incidence of FES in 65% of patients.

Causes TraumaticNon-traumatic

Traumatic # long bonesMultiple #ssurgical instrumentation of the medullary

canal

Non traumaticHaemoglobinopahyCollagen vascular diseaseDiabetes mellitusSevere infectionNeoplasmOsteomyelitisBlood transfusionCardiopulmonary bypassRenal infarctionDecompression syndrome owing to altitudeRenal hemotransplantation

Prevalence

Estimated to be 90% after major traumaClinical prevalence is said to range

from .25% to 1.25%Overall mortality is said to be between 10%

and 20%

Physiochemical theory of FES postulate

Pathophysiology

Mechanical theory

1. Presence of torn blood vessels to permit fat to enter the circulation

2. Liberaration of free fat

1. A transient rise in marrow pressure above venous pressure to allow fat droplets to enter the circulation

Biochemical theoryToxic Obstructive

Toxic theory

Recent work by Barie and colleaguesBarie and colleagues

demonstrates that free fatty acids are bound rapidly by albumin

and transported through the bloodstream and lymphatic channels in this benign form.

Obstructive theory

What is the effect of along bone fractureAn abundance of tissue thromboplastin is released with the marrow elements after long-bone fracture

These blood elements, along with leukocytes,

platelets, and fat globules, combine to increase

pulmonary vascular permeability, both by their

direct actions on the endothelial lining and

through the release of numerous vasoactive

substances.

In addition, these same substances activate

platelet aggregation.

Clinical Findings

most common etiologic factor –

-a high-energy Trauma to long bone or pelvis,

including orthopedic

2nd or 3rd decade of life

or in a patient in the 6th-7th decade of life, when

low-energy fractures of the hip are frequent.

Physical: Cardiopulmonary

Early persistent tachycardia

Patients become febrile with high-spiking temperatures

Patients become tachypneic, dyspneic, and hypoxic due to ventilation-perfusion abnormalities 12-72 hours after injury.

Subconjunctival and oral hemorrhages and petechiae also appear.

Dermatologic

• Alert clinicians may

notice reddish-brown

nonpalpable petechiae

developing over the upper

body, particularly in

•only 20-50% of

patients and

resolve quickly• virtually diagnostic

virtually diagnostic

•axillae,

within 24-

36 hours

of insult or

injury.

Neurologic

Central nervous system dysfunction initially manifests as agitated delirium but may progress to stupor, seizures,

or coma and frequently is unresponsive to correction of hypoxia.

Retinal hemorrhages with intra-arterial fat globules are visible upon funduscopic examination.

Signs Raise in temprature (39-40deg C)Tachypnea 30min or higherTachycardia-- > 140min or higher, BP is

usually WNLLong tract signs extensor posturing and

deceribrate rigidityUrinary incontinencehealthy patient with

long bone # showing urinary incontinence needs to be ruled out for FES

Sub clinical

Nonfulminant subacute

Fulminant types

Sub clinicalOnset after injury 12-72 hrsMortality rate 0 %Clinical presentation -

nonspecific or absent symptoms moderate hypoxemia(Pao2 <80mm Hg in room air)

moderate hypocapnia (Paco2<=30 mm Hg during spontaneous breathing) moderate decrease of platelet count (<200,000 micro L)

Nonfulminant subacuteOnset after injury 12-96 hrsMortality rate 0 -5%Clinical presentation

dyspnea, tachypnea ,fever, tachycardia ,petechiaecerebral signshypoxemia (Pao2 <60mm Hg in room

air) anemiathrombocytopenia and coagulation

abnormalities lung opacities on chest radiograph

Fulminant typesOnset after injury few hrsMortality rate >50%Clinical presentation

frank pulmonary edemamoderate to severe

hypotension cerebral signssevere hypoxemia

and acidosis

Management of Fat Embolism

Lab.Findings & Radiographic evaluation.

Treatment

Lab. Findings1. 1.ABGa)Hypoxemia(pO2<60mm Hg).2. b) Acidosis(pH<7.3).3. 2.HAEMATOLOGY-4. a)Hb-low. b)Platelets- low 5. C)6. d)PT/PTTK-high7. e)ESR-elevated.

Biochemistry1.Fat macroglobinemia2.Urine & Sputum fat globules.3.Serum FFA’s-Increased.4.Hypocalcemia(relative).5.Levels of Cortisol,Glucagon &

Catecholamines increase in proportion to the stress response to injury.

ECGRight axis deviation.

S-waves in lead –II.

Q-waves in lead –III.

ST-segment changes.

Radiographic EvaluationCHEST X-RAY-initially

appears normal.Dysnea -within 72 hours

diffuse B/L infilterates(SNOWSTORM appearance)

s/o—ARDS.

SNOWSTORM

CT-HEAD-Cerebral edema & Haemorrhagic infarcts in white matter may be seen.

Diagnosing FES

Gurd‘criteria

one sign from major and at least

four signs from the minor criteria category

Gurd major‘criteria

petechiae in a “vest” distribution

hypoxia, with a PaO 2 less than 60 mm Hg

pulmonary edema

cerebral manifestations.

Gurd‘minor criteriatachycardia, with a

heart rate greater than 110 beats/minute

pyrexia, with a temperature higher than 103° F (39.4° C)

retinal changes

fat in urine or sputum

an unexplained drop in hematocrit or platelet count

an increasing erythrocyte sedimentation rate

jaundice

renal changes.

TREATMENT 3 CORNERSTONES OF TREATMENT

RESPIRATORY SUPPORTRanges from O2 admn to full resp. support

with mechanical ventilation.On pulse oximetry— a)If PaO2<90mm=ABG analysis.

b)If PaO2 b/w 60-90mm=O2 by mask,serial ABGs,wait &watch for any deterioration. c)If PaO2<60mm=INTUBATE & VENTILATE. PEEP if required.

TREATMENT OF SHOCK

SEVERITY OF FAT EMBOL. IS DIRECTLY PROPORTIONAL TO DEGREE OF SHOCK.

ADDITIONAL THERAPIES1)STEROIDS--they also decrease inflam.reaction in

lungs caused by FFAs. Decrease capillary leakage by stabilizing

lysosomal & capillary membranes.

Prophyllactic dose of Methyl Pred.in high risk patients=10mg/kg body wt./q8h i.v(in 100ml saline).

2)ALCOHOL-Decreases ser. Lipase activity,limits lipolysis of fat & decr.FFAs

3)APROTININ-Protease inhibitor.Decr. Plat. Aggreg.& serotonin release.Decr. Incidence of fat emb. From 15% to 5%.

4)HYPERTONIC GLUCOSE-Metabol. Decreases production of FFAs.

.

TIMING OF # STABILIZATIONRIGID EARLY IMMOBILIZATION.

Seibel et al-10 days of skeletal traction of fracture femur with respect to early definitive # treatment-

a) x2 duration of ventilatory failure. b) x4 no. of fracture complications. c) x10 no. of positive blood cultures.

TYPE OF STABILIZATIONReamed v/s Unreamed Femoral nailing.

Pape et al-In patients with thoracic injury reaming has high rates of ARDS(33% v/s 8% for unreamed).

Many studies disproove/attempt to disproove it.

So it is INCONCLUSIVE/DEBATABLE.