FAT EMBOLISM SYNDROME

BY MUSTAFA LAITH AND NOOR MOHAMMED

RESOURCES
Apley's and Solomans Consise System of
Orthopedics and Trauma 4th Edition 2014

First aid for surgery clerkship 2ND Ed

2009

Netter Orthopedics 1st edition

DEFINITION
An acute respiratory distress syndrome caused by release of fat
droplets from the marrow as may occur following a long bone
fracture.

It occurs in ~2.5% (range 0.5-4%) of those with fat embolism (a phenomenon that sub clinically
occurs in a vast majority of patients (> 90%) with bone fractures and during orthopaedic prosthetic
procedures).

PATHOPHYSIOLOGY
Fat emboli may occlude pulmonary arterioles, leading to
breathlessness and sudden death. Such emboli result
from fractures of bones containing fatty marrow, or from
massive injury to subcutaneous fat. Globules of lipid
enter the torn veins and thereby lead to embolism. Marrow
tissue may also be seen within pulmonary vessels following
trauma and is frequently seen in autopsy histology in cases
of failed cardiopulmonary resuscitation

 Microdroplets of fat are released into the circulation

at the site of fracture, occluding pulmonary
circulation causing ischemic and hemorrhagic
changes.
Another theory: Release of free fatty acids from the
marrow have toxic effects in all tissues, especially the
lung.

CLINICAL FEATURES
Early warning signs of fat embolism (usually within 72 hours of injury) are a
slight rise of temperature and pulse rate. In more pronounced cases there is
breathlessness and mild mental confusion or restlessness. Pathognomonic
signs are petechiae on the trunk, axillae and in the conjunctival folds and
retinae. In more severe cases there may be respiratory distress and coma, due to
both brain emboli and hypoxia from involvement of the lungs. The features at this
stage are essentially those of ARDS.
There is no infallible test for fat embolism; however, urinalysis may show fat
globules in the urine and the blood PaO2 should always be monitored; values
below 8 kPa (60 mmHg or less) within the first 72 hours of any major injury must
be regarded as suspicious. A chest x-ray may show classical changes in the lungs.

SIGNS AND SYMPTOMS

Symptoms may occur immediately or 23 days after trauma.

Shortness of breath with respiratory rate above 30.
Confusion, restlessness, disorientation, stupor, or coma.
Fleeting petechial rash on chest, axilla, neck, and conjunctiva.
Fever, tachycardia.

CLASSICAL TRIAD

CONFUSION

DYSPNEA

PETECHIAE ON
CHEST

Adult respiratory distress

syndrome

X-ray showing diffuse

pulmonary infiltrates in
both lungs.

Nota Bene
Circulating fat globules larger than 10 m in diameter occur in most adults after closed fractures
of long bones, and histological traces of fat can be found in the lungs and other internal organs.

A small percentage of these patients develop clinical features similar

to those of ARDS; this was recognized as the fat embolism syndrome
long before ARDS entered the medical literature.
Whether the fat embolism syndrome is an expression of the same
condition or whether it is an entirely separate entity is still uncertain.
The source of the fat emboli is probably the bone marrow, and the condition is more common
in patients with multiple fractures.

Source: Apley's and Solomans Consise System of Orthopedics and Trauma 4th Edition 2014

TYPICAL SCENARIO
A 25-year-old male complains of difficulty
breathing.
His family notes he is acting a little confused,
and that he has a spotty purplish rash.
Two days ago, he sustained a femur fracture
after a high-speed motor vehicle collison

COMMON CAUSES
1.
2.
3.
4.
5.
6.
7.
8.

Long bone fracture.

Burns.
Severe infection.
Inhalation anesthesia.
Metabolic disorders.
Cardiopulmonary bypass.
Decompression sickness.
Others: Hemoglobinopathy, collagen disease, diabetes, renal
homotransplantations.

DIAGNOSIS
Hallmark finding:
Arterial hypoxemia. Arterial PO2 < 60 mmHg is suggestive.
Chest x-ray: Progressive snowstorm-like infiltration.
Cryostatfrozen section of clotted blood reveals presence of fat.
Absence of fat globules in urine makes diagnosis unlikely; however,
their presence is not specific for fat embolism.

MANAGEMENT IN SHORT
Management of severe fat embolism is SUPPORTIVE

1.Oxygen: Keep PO2 over 90 mmhg

2. Prompt stabilization of fracture
3. Nursing of patient in sitting position

MANAGEMENT
Management of severe fat embolism is SUPPORTIVE
Symptoms can be reduced with the use of supplemental high inspired oxygen concentrations immediately after injury.

Administer oxygen to decrease hypoxemia and monitor PO2 to maintain it over 90 mmHg

In severe hypoxemia: Mechanical ventilatory support

Prompt stabilization of long-bone fractures also appears to reduce the likelihood of fat
embolism occurring; this also allows the patient to be nursed in the sitting position, which optimizes the
ventilationperfusion match in the lungs

Intramedullary nailing is not thought to increase the risk of developing the syndrome
Use of ethanol, heparin, hypertonic glucose, or steroids has been suggested but their
effectiveness is questionable

PROGNOSIS
Mortality from fat embolism
thought to be as high as 50%
following multiple fractures.