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/]

There are two different types of adipose tissues –
1.    White adipose tissue
2.    Brown adipose tissue

White adipose tissue is found in –
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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