Fat Embolism and Perioperative Care

Introduction:

Trauma is most frequently linked to fat embolism. The most prevalent causes are fractures of the long bones and the pelvis, orthopedic surgery, total hip arthroplasty, and other traumatic traumas. In addition, fat embolisms can be brought on by burns and soft tissue injuries, albeit they happen much less commonly than fractures. According to the most widely accepted explanation regarding the cause of fat embolism, fat globules (also known as emboli) are generated when fat cells in broken bones are disrupted and enter the body through tears in the vascular marrow beds. According to a different idea, the emboli form as a result of free fatty acid accumulation brought on by alterations in fatty acid metabolism brought on by trauma or illness. The capillary-alveolar membrane in the lung and the capillary beds in the cerebral circulation are both hazardous when fatty acid levels are elevated, regardless of the source.

90 % of people with serious skeletal injuries experience traumatic fat embolism. However, the clinical symptoms are typically modest and go unnoticed.10 % of these people experience fat embolism syndrome (FES). Fat embolism is considered a block of arterioles and capillaries by lipid globules. If the block in the circulation is from fatty tissue, it is called a fat-tissue embolism.

What is the Eitiolgy behind Fat Embolism?

The causes of fat embolism:

1) Traumatic Etiology:

The most frequent cause of fat embolism is trauma to the bones, such as fractures of long bones that allow fatty marrow to enter the bloodstream, bone concussions, orthopedic surgical operations, etc. Whereas trauma to soft tissue, e.g., laceration of adipose tissue and in puerperium due to injury to pelvic fatty tissue.

2) Non-Traumatic Etiology:

• Extensive burns.
• Diabetes mellitus (increased levels of blood sugar levels).
• Fatty liver.
• Pancreatitis (inflammation of the pancreas).
• Sickle cell anemia (alternation in the red blood cell of the body that causes lower oxygen-carrying capacity).
• Decompression sickness.
• Inflammation of bones and soft tissues.

What is the Pathogenesis behind Fat Embolism?

The pathogenesis of fat embolism:

• Mechanical Theory:

Fluid fat mobilization may occur following bone or soft tissue trauma. The fat globules released from the injured area may cause abrupt venous circulation. Eventually, most of the fat is halted in the lungs' tiny blood veins. However, fat globules may penetrate and enter the bloodstream before settling in other organs.

• Emulsion Instability Theory:

This theory explains the pathogenesis of fat embolism in non-traumatic cases. According to this idea, a disruption in the normal emulsification of fat causes chylomicrons, fatty acids, and plasma lipids to aggregate and form fat emboli.

• Intravascular Coagulation Theory:

In stress, releasing some factors activates disseminated intravascular coagulation ( DIC) and aggregation of fat emboli.

• Toxic Injury Theory:

By this theory, excessive plasma levels of free fatty acid cause chemical damage to the tiny blood capillaries in the lungs, increasing vascular permeability and ultimately causing pulmonary edema.

What are the Complications of Fat Embolism?

Fat globules' size, number, and ability to pass through the lungs and enter the systemic circulation all play a role in fat embolism.

1) Pulmonary Fat Embolism:

Because the tiny fat globules are unlikely to significantly impede the large pulmonary capillary bed, the presence of multiple fat emboli in the lung's capillaries is a typical postmortem finding in patients who die from fractures. However, widespread obstruction of pulmonary circulation due to extensive pulmonary embolism can occur and result in sudden death. Microscopically, the lungs show hyperemia, edema, petechial hemorrhages, and adult respiratory distress syndrome (ARDS) changes. Pulmonary infarction is usually not a feature of fat embolism because of the small size of globules. The fat globules in the pulmonary arteries, capillaries, and alveolar spaces appear as vacuoles in routine stains. Frozen section or confirmation of globules by fat stains such as Sudan dyes (like Sudan black, Sudan III, and IV), oil red O, and osmic acid.

2) Systemic Fat Embolism:

Through the pulmonary circulation, such as the patent foramen ovale, pulmonary arteriovenous shunts, and spinal venous plexuses, certain fat globules may enter the body and become entrapped in the capillaries of many organs, including the brain, kidney, skin, etc.

• Brain:

The pathological findings in the brain are petechial and minute parenchyma hemorrhages (bleeding into brain parenchyma proper). Microscopically, microinfarct of the brain, edema, and hemorrhages are seen. The CNS (central nervous system) manifestations include delirium, convulsions, stupor, coma, and sudden death.

• Kidney:

Renal fat embolism in the glomerular capillaries may cause decreased filtration. Other effects include tubular damage and renal insufficiency.

• Other organs:

In addition to the brain and kidneys, petechiae in the skin, conjunctiva, serosal surfaces, fat globules in the urine, and sputum are other symptoms of systemic fat embolism.

What Is the Investigation for Fat Embolism?

A) Investigations

• Arterial blood gas analysis and an alveolar-to-arterial oxygen tension difference associated with fat embolism syndrome strongly suggest the diagnosis.

• Erythrocyte sedimentation rate (ESR).

• Cytological analysis of urine, blood, and sputum examination.

B) Imaging Studies:

1. Chest Radiography: To rule out any consolidation or diffuse infiltration in the chest area.

2. To reveal any hemorrhage or pathology within the body or organs:

   • CT (Computerized Tomography) and MRI(Magnetic Resonance Imaging).

   • Transcranial doppler sonography.

   • Transesophageal echocardiography (TEE).

Some criteria to rule out fat embolism syndrome:

Lindeque’s Criteria:

1. Sustained (partial pressure of oxygen) PaO2 less than 60 mm Hg.

2. Sustained (partial pressure of carbon dioxide) PaCO2 greater than 55 mm Hg or pH less than 7.3.

3. Sustained respiratory rate greater than 35 per min even after adequate sedation.

4. Increased work of breathing evaluated by dyspnea, use of accessory muscles, tachycardia, and anxiety.

Gurd and Wilson’s Criteria for Fat Embolism Syndrome:

Major Criteria:

• Petechial rash.

• Respiratory insufficiency.

• Cerebral involvement.

Minor Criteria:

• Tachycardia.

• Fever.

• Retinal transformations.

• Jaundice.

• Renal signs.

Laboratory Values:

• Thrombocytopenia.

• Anemia.

• High erythrocyte sedimentation rate.

• Fat macroglobulinemia.

What is the Treatment for Fat Embolism?

Treatment of fat embolism syndrome consists of providing adequate arterial oxygenation. The high oxygen flow rate is delivered to keep the arterial oxygen tension in the standard range. Further, supervision of intravascular volume is crucial because shock can worsen lung injury induced by fat embolism syndrome. Albumin is suggested for volume resuscitation as the balanced electrolyte solution not only restores blood volume but also binds with the fatty acids and may thus decrease lung injury. Medications, including steroids, heparin, alcohol, and dextran, are ineffective.

Conclusion:

Although rare, fat embolism syndrome is a potentially lethal complication that occurs secondarily to trauma, specific orthopedic surgical interventions, liposuction, and particular chronic disease conditions. Diagnosis of fat embolism syndrome (FES) and identifying this syndrome remains challenging and demands a high degree of doubt for even experienced clinicians. Although careful clinical analysis remains the gold standard for diagnosing fat embolism syndrome (FES), immediate distinction and treatment are critical in controlling poor outcomes, thereby declining mortality.