By

Dr. Jitendra Wadhwani

PG ORTHOPAEDICS

PGIMS, ROHTAK

FAT EMBOLISM SYNDROME

Zenker, a pathologist,1st identified fat embolism syndrome at autopsy 1862.

First diagnosed in 1873 by Dr Von Bergmann

1879 Fenger and Salisbury published description of FES

HISTORY

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 occasionally causes multi system dysfunction, the lungs are always involved and next is brain

DEFINITIONS

FAT EMBOLISM SYNDROME:

Clinical diagnosis, No specific laboratory test is diagnostic

Mostly associated with long bone and pelvic #, and more frequent in closed # then open #

Single long bone fracture 1-5% chance of developing FES, and increases with number of #

Onset is 24-72 hours from initial insult

Mortality: 5-15%

CAUSES

CAUSES CONTD..

Blunt Trauma (90%)

CAUSES CONTD..

Non Trauma: agglutination of chylomicrons and VLDL by high levels of plasma CRP.

– disease-related• Diabetes, acute pancreatitis, burns, SLE, sickle cell crisis

– drug-related• parenteral lipid infusion

– procedure-related• Orthopedic surgery, liposuction

Pathophysiology Exact mechanism unknown, but two main

hypothesis

• Mechanical vs. Biochemical

• MECHANICAL – Fat globules from disrupted bone marrow or adipose tissue are forced into torn venules in areas of trauma.

• BIOCHEMICAL – Hormonal changes caused by trauma and/or sepsis induce systemic release of free fatty acids (FFA) as chylomicrons which cause the systemic FES.

MECHANICAL HYPOTHESIS-

– Fractures of marrow-containing bone (Femur,

Pelvis) have the highest incidence of FES and

cause the largest volume of fat emboli, because

the disrupted venules in the marrow remain

tethered open by their osseous attachments.

– The marrow contents enter the venous

circulation with little difficulty.

CONT..

This theory is supported by research on

Orthopaedic long bone (IM reaming) and

spinal surgeries which cause fat globules to

enter the blood circulation when vigorous

reaming/fixation is done.

Increased Pressure + Volume Extravasation

Measuring fat globules pre and post reaming

shows significant difference in concentration

CONT..

Fat droplets are deposited in the pulmonary

capillary beds and travel through arteriovenous

shunts to the brain. Systems affected include

LUNG, BRAIN and CIRCULATION.

Microvascular lodging of droplets produces local

ischemia and inflammation, with concomitant

release

of inflammatory mediators, platelet aggregation,

and vasoactive amines

BIOCHEMICAL :

FES is dependent upon degradation of the embolized fat

into free fatty acids.

Neutral fat does not cause an acute lung injury, it is

hydrolyzed over the course of hours to several products,

including FFA, which cause ARDS in animal models.

CRP (acute phase reactant), which is elevated in

trauma patients, appears to be responsible in lipid

agglutination (FES) for both traumatic and non-

traumatic FES.

CONT..

The process of Neutral fat cells -> FFA ->

Agglutination with CRP may explain the time

sequence of clinical findings in FES.

Onset of symptoms may coincide with

Agglutination.

This theory is animal model based and

circumstantial at best.

Diagnosis is made CLINICALLY NOT

CHEMICALLY. It does not matter how

much fat globules are in your circulation, it

just matters if you have their side effects.

FES typically manifests 24 to 72 hours after

the initial insult. Rarely <12 hrs or >72 hrs.

CLINICAL PRESENTATION-

TRIAD OF FES

Hypoxemia

Neurological abnormalities

Petechial rash

EARLY SIGNS

Dyspnea

Tachypnea

hypoxemia

PULMONARY:

Hypoxia, rales, pleural friction rub

Breath sounds: Loud harsh, Crepts & wheeze

ARDS may develop(fat emboli obstructs lung vessel

(20microns) platelets and fibrin adhere.)

½ of pts with FES require mechanical ventilation (Bulger,

Archives of Surgery 1997; 132: 435-9)

CXR usually normal early on, later may show

‘snowstorm’ pattern- diffuse bilateral infiltrates

CT chest: ground glass opacification with

interlobular septal thickening

NEUROLOGICAL FINDINGS:

Usually occur after respiratory symptoms.

Incidence 80% patients with FES

Minor global dysfunction most common, but ranges

from mild delirium to coma.

Seizures/focal deficits not common but can occur

Transient and reversible in most cases

CT Head: general edema, usually nonspecific

MRI brain: Low density on T1, and high intensity T2

signal, correlates to degree of impairment

RASH:

Petechial

Usually on conjuntiva , neck, axillae

Results from occlusion of dermal capillaries

by fat globules and then extravasations of

RBC

Fleeting & last short.Resolves in 5-7 days

PATHOGNOMONIC, but only present in 20-

50% of patients

OTHER FINDINGS

Retinopathy (exudates, cotton wool spots, hemorrhage)

Lipiduria

Fever (to 39-40ºC)

DIC

Myocardial depression (prominent S, T depression,

RBBB, arrythmia)

Thrombocytopenia/Anemia

Hypocalcemia

DIAGNOSIS

FES is CLINICAL diagnosis, not biochemical. A high degree of suspicion is needed to make diagnosis . -Common misconception that the presence of fat

globules, either in sputum, urine, or a wedged PA catheter, is necessary to confirm the diagnosis of FES

In 50% of fracture patients, fat globules was demonstrated in the serum, without symptoms of FES.

HOWEVER Growing literature on the use of bronchoscopy with

bronchoalveolar lavage to detect fat droplets in alveolar macrophages as a means to diagnose fat embolism. Sensitivity and specificity are unknown, being studied in Trauma patients

FES = 1 major + 4 minor + fat microglobulinemia

Still widely used today

Gurd’s Criteria

FES = femur fracture ± tibia fracture + 1 feature

Based on respiratory parameters

Lindeque’s Criteria

3 TYPES- In 1962

SUBCLINICAL FES

NON FULMINANT FES

FULMINANT FES

SEVITT’S CLASSIFICATION-

SUBCLINICAL FES:

Around 3 days post trauma

Probably occurs in almost all long bone

fractures of the lower extremity and

fractures of the pelvis

Characterised by decreased PaO2, decreased

Hb% and decreased platelets. No clinical

signs and symptoms of respiratory

insufficiency.

NONFULMINANT FES:

- Any time ,upto 6 days post trauma

-Clinical signs and symptoms are clearly evident.

Petechiae, tachycardia, respiratory failure, and signs

of CNS embolism.

Thrombocytopaenia, anaemia, and coagulation

abnormalities can be found, as can pulmonary

alveolar and interstitial opacities on chest x ray

There is no definitive test for this version of

the syndrome, as most of the changes

described can occur as a result of trauma as

well as a result of fat

embolism, the diagnosis remains a clinical

one, and the significance is uncertain

FULMINANT FES:

Occurs very suddenly and rapidly after injury,

and progresses very quickly, often resulting in

death within a few hours of the initial trauma.

Clinical features are acute respiratory failure, acute

cor pulmonale and embolic neurological changes.

These occur shortly after injury and often result in

the death of the patient.

Pats. with multiple fractures are particularly

susceptible to this form of the syndrome,

which, although it is relatively rare, is of

immense clinical significance because of its

high mortality.

MANAGEMENT

TREATMENT IS LARGELY SUPPORTIVE

Constant Positive Airway pressure(CPAP)

Mechanical Ventilation

Antibiotics

Nutritional support

Corticosteroids

Heparins

Have all been used

INITIAL TREATMENT

Adequate airway

Start IV line – correct fluid deficit

Basic investigation – including baseline chest X-ray

and ABG assay (v. imp).

Nasogastric tube – should be inserted in patient

with severe trauma and gastric contents suctioned

to prevent aspiration and ARDS

MONITORING

TPR, BP

I/O chart – maintain output 50-100cc/hr

CVP – to correct fluid deficit

If overload pulmn. Edema (4-8cm H2O)

Pulmonary haemodynamics– PCWP for accurate mean

of deficit correction (5-12mm of Hg)

Arterial blood gas monitoring

SPECIFIC DRUG THERAPY:

Many drugs have tried, most without demonstrable

benefit in established ARDS except Corticosteroids

but with some prophylactic benefit.

Drugs which may be tried in Fat embolism associated

ARDS are:

1.Ethanol : Lipase inhibitor, low incidence when level

>20mg.

2.Heparin : PL aggregation useful in DIC assoc ARDS

also.Controversial in trials.10000-15000 iu stat & 10000

iu 4-6hly with PTT at 1.5-2.5 INR.

3.Hypertonic glucose: block post traumatic

mobilization of FFA – may improve oxygenation.

4.Corticosteroids – stabilize cell member, PMN

adhesion, prevent surfactant reduction, protect

capillary endothelium, compliment activation and

minimize transudation.

CORTICOSTEROIDS –

ØValue in ARDS of Fat embolism, aspiration, sepsis,

shock and cerebral edema.

ØHelpful in late stage in recovering patients in

reducing fibrotic change.

ØImprove and preserve arterial oxygenation and

stimulate proliferation and maturation of Type II

pneumocyte.

CORTICOSTEROIDS -

Prophylactic dose 10mg/Kg Q8H

Or

80mg/kg bolus

Or

1-2gm IV over 24 hrs. & maintain for 48-96 hrs by

gradual reduction

ATLS Protocol :

1. Early immobilization of fracture and early

definitive reduction (open or closed).

2. Maintain intravascular volume to maintain

cardiovascular stability (hypovolemic shock

resuscitation), may use colloids (albumin) as it

can expand fluid and bind FFA.

3. Mechanical ventilation with PEEP

4. IV Ethanol has been used in Russia, Europe and some American centres to decrease rate of FES.

J Bone Joint Surg Am. 1977 Oct;59(7):878-80

“A raised level of alcohol in the blood was associated with a lower incidence of fat embolism” all other variables controlled.

- Other studies

- Can J Surg. 1970 Jan;13(1):41-9

- Br Med J. 1978 May 13;1(6122):1232-4

ROLE OF FRACTURE STABILIZATION

Highly debated issue

- Accumulated evidence over past decade support

early fixation within 24 hours of injury.

Early IF – decompress # hematoma as ongoing

source of fat emboli and retained necrotic debris,

eliminate pain and physiologic stress with continued

# motion, optimize pulmn function, contributes to

reduced ventilatory dependence and improve

survival.

But transient increasing pulmn Ar pressure and

worsening pulmn gas exchange observed during

reaming of medullary canal. So undreamed nailing

is suggested for femoral fixation in multiple #

patients.

PROGNOSIS

Mild -undetected

Mod -low mortality

Severe -fatal unless if treatement

instituted early. Survivors have pulmonary sequele.