Fat embolism

When adipose tissue cells enter the bloodstream in the form of drops or globules of free bone marrow, visceral or subcutaneous fat, a pathological condition or clinical syndrome such as fat embolism develops - with partial or complete obstruction of blood vessels, impaired microcirculation and homeostasis. 

Epidemiology

According to clinical statistics, fatty traumatic embolism occurs from 67% [1]to 95% of  [2]people with severe skeletal injuries, but symptoms appear in 10-11% of cases. Quite often, mild manifestations remain unrecognized, many cases of fat embolism syndrome are not diagnosed or diagnosed incorrectly.

Fat embolism is an almost inevitable consequence of long bone fractures. Approximately 0.9–2.2% of these cases result in multisystem pathology of fat embolism syndrome (FES). [3]The  [4]classic triad of features described in FES is hypoxemia, neurologic abnormalities, and petechial rash, which usually appear 12–36 hours after injury.

The frequency of fat embolism in isolated injuries of tubular bones is estimated at 3-4%, with fractures of long bones in children and adolescents - in 10%.

In 40% of patients, fatty embolism is detected after surgical fixation of bone shaft fractures. [5], [6]

Causes of the fat embolism

Most often, fat embolism is caused by fractures of the long (tubular) bones and the pelvis. So, fat embolism in hip fractures is observed in almost a third of patients, and this condition can occur after any fracture affecting the shaft of the femur. 

Fat embolism may develop with fractures of the bones of the lower leg (peroneal and tibial), shoulder or forearm, as well as fat embolism with amputation of a limb.

Other possible reasons are noted, in particular:

• polytrauma of the skeleton with multiple fractures and soft tissue damage;
• orthopedic surgery, especially total hip arthroplasty and knee replacement;
• bone marrow transplant;
• severe burns;
• diffuse changes in the pancreas  with pancreatitis.

Fatal fatty liver embolism develops with its acute necrosis against the background of dystrophy and severe alcoholic obesity.

One of the many  symptoms of sickle cell anemia  is a fatty embolism of the retinal vessels. [7]

Possible fatty embolism with injections, for example, with the introduction of a radiopaque agent Lipiodol into a lymphatic vessel (during lymphography); glycerin-containing corticosteroid solutions; fillers (fillers) of soft tissues; [8]autologous fat injections (autotransplantation) with lipofilling.

By the way, fat embolism syndrome can be a  complication after liposuction  (lipoplasty) - removal of excess fat. [9], [10]

Risk factors

In addition to the above reasons, risk factors for the development of fatty embolism are:

• insufficient immobilization of patients with fractures;
• significant blood loss;
• crush injuries to the bones of the limb;
• the procedure for surgical reposition of broken bones and displaced fragments in case of comminuted fractures, as well as intraosseous (intramedullary) osteosynthesis in case of diaphysis fractures;
• operations on the maxillofacial bones, including plastic;
• cardiac surgery with sternotomy (dissection of the sternum) and the transition to artificial circulation;
• decompression (decompression) sickness;
• long-term use of corticosteroids.

Fat embolism of the vessels of the lungs and brain can cause  parenteral nutrition of  patients. [11], [12]

Pathogenesis

Explaining the pathogenesis of fat embolism, the researchers put forward many versions, but two are considered the closest to the real mechanism of the development of this syndrome: mechanical and biochemical. [13]

Mechanical is associated with the release of adipocytes (fat cells) into the venous bloodstream due to a post-traumatic increase in pressure in the cavity of tubular bones - the marrow canal filled with bone marrow and adipose tissue - and in individual cells of cancellous bone tissue. Fat cells form emboli (10-100 microns in diameter), which clog the capillary bed. [14]

The adherents of the biochemical theory argue that the particles of endogenous fat in the blood during the process of enzymatic hydrolysis by lipase are converted into glycerol and fatty acids and are transformed into fat emboli. They first enter the vascular system of the lungs, causing impaired blood vessel patency and respiratory symptoms. Smaller fat globules enter the general bloodstream, causing systemic manifestations. [15]

In addition, adipocytes in the bone marrow produce adipocytokines and chemoattractive cytokines, which, entering the bloodstream, can affect the functions of various organs and systems. [16]

Symptoms of the fat embolism

Embolized fat droplets can enter microvessels throughout the body. Thus, FES is a multiple organ disease and can damage any microcirculatory system in the body. Fat has been reported to embolize the lungs, brain, skin, retina, kidneys, liver, and even the heart.[17]

The first signs of fat embolism syndrome usually appear within 12-72 hours after injury. There are clinical symptoms such as:

• shallow rapid breathing (tachypnea) and shortness of breath;
• punctate rash - petechiae - on the chest and shoulders, on the neck and in the armpits, on the mucous membrane of the mouth and the conjunctiva of the lower eyelids (due to the closure of the skin capillaries with fat emboli);
• tachycardia;
• pulmonary edema;
• hyperthermia (as a result of a disorder of cerebral circulation);
• decreased urine output.

The intensity and range of symptoms that occur depend on the degree of fat embolism (mild, moderate, or severe). There are lightning, acute and subacute forms of fatty embolism. In a subacute condition, three characteristic features are present:  respiratory distress syndrome , skin petechiae, and dysfunctions of the central nervous system.

Occlusion of the capillary network of the lungs with fat globules - fatty embolism of the lungs - leads to hypoxemia, that is, a lack of oxygen in the blood.

A fatty cerebral embolism causes numerous petechial hemorrhages in the white matter, edema and lesions of the basal ganglia, cerebellum and interlobar septa, which in more than 80% of patients is accompanied by cerebral hypoxia and CNS depression with headache, disorientation, agitation, convulsions, confusion with delirium.

Among the focal neurological symptoms, there may be unilateral muscle paresis or increased tone of the lower extremities, conjugate deviation of the eyes (strabismus), speech disorder in the form of aphasia. [18]

Complications and consequences

Neurological consequences and complications of fat embolism can include ischemic / hemorrhagic strokes, retinal ischemia, autonomic dysfunction, diffuse brain damage, stupor, and coma. Microvascular damage to the retina leads to hemorrhagic retinal damage seen in 50% of patients. [19]These lesions go away on their own and disappear within a few weeks. [20]Residual visual impairment is rare.

The development of compartment syndrome  and complex regional pain syndrome is noted .

Closing the lumen of 80% of the pulmonary capillaries leads to increased capillary pressure and causes acute right ventricular failure, which can be fatal. Up to 10-15% of cases of fatty embolism are fatal.

Diagnostics of the fat embolism

Currently, the diagnosis of this condition is based on clinical manifestations, and for this there is a scale of major (major) and minor (minor) symptoms. [21]

Blood tests for hematocrit, platelet counts, arterial blood gases and oxygen content, and detection of fat globules in peripheral blood plasma using infrared spectroscopy can be helpful in making a diagnosis. Patients with long bone fractures should monitor blood oxygen levels by continuous pulse oximetry.

Early detection and verification of fat embolism is facilitated by instrumental diagnostics: plain radiography of the lungs and chest; ECG; duplex ultrasound of the veins of the lower extremities; [22]CT / MRI of the brain. [23],  [24],  [25], [26]

Differential diagnosis

Differential diagnostics with thromboembolism and cardiogenic pulmonary edema, pneumonia, meningococcal septicemia, cerebral hemorrhage, anaphylactic reaction of various etiologies is carried out.

Treatment of the fat embolism

In fat embolism syndrome, treatment consists in maintaining respiratory function and adequate oxygenation of the blood by means of artificial ventilation through a mask (with constant positive pressure), and in cases of acute respiratory distress syndrome - endotracheal ventilation. [27],  [28], [29]

Infusion resuscitation is performed - intravenous fluid administration - to avoid the development of shock, maintain the volume of blood circulation and restore the rheological properties of the blood. [30]

Systemic corticosteroids (methylprednisolone) are also used. [31]

In severe cases, when the cause is fatty pulmonary embolism, inotropic support of right ventricular failure with adrenostimulants and adrenomimetics may be required  .

In recent years, resuscitators have begun to use  plasmapheresis and plasma exchange techniques . [32], [33]

Prevention

The adopted strategy for the prevention of fat embolism is aimed at early surgical stabilization of fractures, especially of the tibia and femur.

Forecast

With early fixation of fractures and adequate supportive therapy, the prognosis of fat embolism is favorable. [34],  [35]In other cases, this condition can be fatal.