FAT EMBOLISM
F
|
at embolism syndrome was first diagnosed by Dr. Von
Bregman in 1873. In 1879, Fenger and Salisbury published the description of fat
embolism.
Individual fat cells are called as adipocytes, which
are found throughout the connective tissues and thus it is named as adipose
tissue.
Fig 1.0 Show fat (yellow colour) and muscle.
This tissue is present all over the body and acts as a
protective barrier. Sometimes this is used in medication purpose, where certain
medications are used to deliver into the body; these medications are applied as
patch and thus their release is absorbed into the fat underneath the skin and
is released into the circulation slowly for longer duration of drug action.
They store energy in form of triglycerides inside
them.
They also have paracrine function and endocrine
functions.
White adipose tissue may
represent the largest endocrine tissue of humans. Its pleiotropic nature is
based on the ability of fat cells to secrete numerous hormones, growth factors,
enzymes, cytokines, complement factors and matrix proteins. Adipose tissue also
expresses receptors for most of these factors that are implicated in the
regulation of many processes including food intake, energy expenditure,
metabolism homeostasis, immunity and blood pressure homeostasis.
Adipose tissue is
dynamically involved in cell function regulation through a complex network of
endocrine (signals travel through the circulatory system to reach all parts of
the body), paracrine (signals sent only to cells in the vicinity of the cell
station), and autocrine (only affecting cells that are the same type) signals
that influence the response of many tissues, including hypothalamus, pancreas,
liver, skeletal muscle, kidneys, endothelium, and the immune system, among
others. This secretory nature has prompted the view of white adipose tissue as
an extremely active endocrine tissue
[for more details, please read the paper on adipose tissue as endocrine organ on this link https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648822/]
[for more details, please read the paper on adipose tissue as endocrine organ on this link https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3648822/]
There are two different types of adipose tissues –
1.
White adipose tissue
2.
Brown adipose tissue
1. Greater
omentum
2. Mesentery
3. Retroperitoneal
spaces
4. Around
kidneys
5. Bone
marrow
6. In
spaces of hands and soles of feet
7. Beneath
visceral pericardium
8. In
orbits around the eyeballs
9. Around
the mammary glands in females.
The amount of fat varies according to the gender.
Histologically they appear round, polygonal with a single nucleus around the
periphery, this is called as signet ring appearance.
Brown adipose tissue is present predominantly in
babies, located in regions around their back (interscapular region), aorta,
neck, mediastinum.
Brown adipose tissue is thermogenic in nature, it
prevents excessive heat loss from the baby’s body and prevents hypothermia.
Histologically this tissue is filled with capillaries
and thus takes up more stain and appears crowded. It also contains numerous
mitochondria; Golgi apparatus, rER and sER in small quantities [rER = rough
Endoplasmic Reticulum, sER = smooth Endoplasmic Reticulum].
Fat emboli – Fat particles or droplets that travel
through the body via circulation.
Fat embolization – the process by which fat particles
get deposited into the blood vessel.
Fat embolization syndrome – Serious manifestation of
the fat embolism, occasionally causes multi-system dysfunction.
Morality rate is 10 – 20%
Onset is 24 – 72 hours from initial result.
Causes –
1. Trauma
related – Long bone fractures, soft tissue injuries, burns, liposuction, Bone
marrow harvesting and transplant.
2. Non
trauma related – pancreatitis, diabetes milletus, osteomyelitis, panniculitis,
steroid therapy, bone tumor lysis, alcohol fatty liver disease, fat infusion.
3. Drug
related – heavy infusion of lipids at rates faster than usual, agglutination of
endogenous or infused fat as intra-lipid.
Closed fractures have a higher tendency to cause FES
as compared to the open fractures; 90% is caused by fractures of long bones. In
non-traumatic causes, it may be because of the fat or marrow necrosis, or due
to increase in the concentration of lipids in the blood stream.
May occur in sickle cell crisis or when hypoxia occurs
to bone marrow.
Risk Factors for FES –
1. Males
2. Age
10-39 years
3. Post-traumatic
hypovolemic state
4. Reduced
cardio-pulmonary reserve.
5. Multiple
fractures
6. Femoral
shaft fractures
7. Concomitant
pulmonary reserve
8. Joint
replacement with high volume prosthesis, etc.
Pathophysiology –
1. Mechanical
hypothesis
2. Biochemical
hypothesis
Mechanical hypothesis may indicate there is
obstruction to the capillaries or blood vessels. Smaller fat emboli travel
through the capillaries and may reach the brain or kidney creating renal and
nervous dysfunction.
Biochemical hypothesis suggests that circulating free
fatty acids may hamper the gaseous exchanges in the alveoli and pneumocytes,
co-existing shock, hypovolemia and sepsis may impair liver function and may
further aggravate the condition. Hormonal changes after trauma induce systemic
release of fatty acids as chylomicrons. Acute phase proteins may coalesce the
chylomicrons, this explains why the non-traumatic FES takes 12 hours.
If the Fat emboli obstruct alveoli and platelets and
fibrin accumulate (<20 microns), it causes inflammation and then endothelial
damage leading to ARDS (Acute Respiratory Distress Syndrome).
Clinical Features –
1. Asymptomatic
in the initial 12-48 hours.
2. Pulmonary
dysfunction.
3. Neurologic
dysfunction.
4. Dermatological
signs.
Pulmonary -
1. ARDS.
2. Pleural
rub,
3. Hypoxia
4. CXR
– Snow storm appearance is seen (bilateral diffuse infiltrates).
5. CT
chest – ground glass opacification, with interlobular septal thickening.
Neurologic –
1. Usually
occur after the respiratory involvement.
2. Minor
global dysfunction may range from delirium to coma.
3. Seizers/focal
deficits.
4. CT
– General oedema
Dermatological –
1. Petechiae
2. Usually
on the neck, conjunctiva, neck, axilla, upper limbs.
3. Results
from occlusion of capillaries of upper limb and then extravasation of RBC’s
4. Usually
fast resolving (5-7 days)
5. Pathognomic
feature but usually present in 20% of the people.
Early signs – Dyspnoea, tachypnoea, hypoxemia.
Triad of FES – Hypoxia, neurological dysfunction and
petechiae.
Other findings –
1. Retinopathy
(exudates, cotton wool spots)
2. Lipiduria
3. Fever
4. DIC
5. Myocardial
depression (right heart strain)
6. Hypocalcaemia
.
Diagnostic criteria –
Gurd’s criteria is used majority
Other indices used are – Schoenfeld index and Lindeque
index.
Lab investigations –
1. Arterial
blood gas estimation
2. Haematological
tests
3. Biochemical
tests
4. Urine
and sputum examination.
Treatment –
1. High
dose of corticosteroids.
2. Immobilization
and early fixation of the hip.
3. Fixation
within 24 hours helps in reduction of ARDS by 5 folds.
4. Maintain
oxygen and ventilation.
5. Maintain
haemodynamic stability
6. Make
sure the patient is hydrated
7. Prophylaxis
in DVT (deep vein thrombosis)
8. Nutritional
care
Heparin has also been
used in treatment of FES.
Prognosis –
1. Most
deaths contributed to pulmonary dysfunction.
2. Fulminant
form represents as acute cor-pulmonale, respiratory failure or embolic
phenomenon.
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