What is a fat embolism? Fat embolism syndrome. Pathogenesis of fat embolism

Whatever the injury: a cut, a fracture or an ordinary scratch, the human body perceives it as colossal stress. After all, he needs to do everything so that blood does not leak out, no infection gets into the wound, and also protect the body from all sorts of dangers in the environment.

But the most unpleasant situation can be when the injury was minor, but its consequences turned out to be truly terrifying. One of these consequences is fat embolism, in which the body harms itself by creating blood clots.

What is it?

In medicine, fat embolism is any pathological process in which fat cells may appear in the blood. The slightest amount of fat in a vessel can lead to disastrous consequences.

Like a blood clot that leads to heart attack and stroke, fat, moving through a person’s venous or arterial system, clogs vital ducts. It also creates a life-threatening situation.

Typically, with similar clinical pictures, the following factors for the onset of the disease can be detected in patients:

• large blood loss;
• dizziness;
• overweight;
• nausea.

In the international classification, this disease can be classified as T79.1. If surgery is delayed, fat embolism may recur several times.

In what forms does it appear?

This disease has several main forms, the most common in modern medical practice:

• fulminant embolism - this type is one of the most dangerous forms, because it is almost impossible to save the patient due to the fact that the development of fat embolism occurs in a matter of minutes, and it takes much more time to determine it;
• acute embolism - development begins to occur within 2–3 hours after the patient receives injury, and continues for 1–2 days. It occurs more often than other forms;
• subacute embolism – development occurs from a day to 3 days after a person is injured. One of the most favorable forms of disease development.

How is it classified?

According to the conventional classification, depending on the manifestations, fat embolism can be pulmonary, cerebral or mixed. And it can also be divided, depending on the foci, into cerebral embolism, pulmonary embolism, and development in the liver.

Among other things, it is also classified according to the reasons due to which it could arise. This can occur during surgery or after amputation of limbs, during open fractures, surgical interventions, and even due to improper drug treatment.

Today, doctors have at their disposal only a couple of theories and many speculations about how fat embolism appears and what are the reasons for the development. All this is further complicated by the fact that there are two main types - mechanical and biochemical embolism, with a corresponding, characteristic onset of the disease.

According to the first theory, increased bone marrow pressure during trauma and surgery may be the main cause of fat embolism. It is because of this that fat cells penetrate into the patient’s blood vessels, where, by contacting platelets or ordinary blood cells, they can form a microthrombus, which will travel further through the bloodstream.

In the worst case scenarios, such blood clots reach the brain or heart, clogging, for example, the valves in the latter. Under more favorable circumstances, they gradually fall apart on their own, but this does not happen very often.

Biochemical theory

According to the biochemical theory, cell injuries leading to fat embolism occur due to changes in the endocrine system and, accordingly, the patient’s hormonal background. If the hormonal imbalance occurs at the same time as sepsis, then the penetration of lipoprotein bodies into the blood becomes extremely likely.

Those, in turn, begin to cling to the vessels of the lungs, because of this the bronchi and the blood ducts themselves are damaged, blood circulation is disrupted accordingly and the chance of a fat embolism increases several times.

Fat embolism is caused by trauma. But this pathology also occurs with various errors during surgical intervention in the area of ​​​​tubular bones.

Among other things, pathology can also manifest itself against the background of such actions as: prosthetics, various closed fractures with internal bleeding and open fractures, respectively, as well as any intervention in the fatty layers, be it liposuction or plastic surgery on the dermis and lower epithelial layers.

Also, the cause of fat embolism can be not only trauma and improperly performed surgery, but also various intravenously administered drugs.

Such as corticosteroids or various fat emulsions. That is why it is worth making sure that when using steroids, it is a professional who injects the patient.

What are the symptoms?

One of the most dangerous aspects of this disease is that there may be no symptoms at all for several days. But the patient’s deteriorated condition is usually perceived by both the patient and the doctors themselves as the body’s reaction to the operation. Developing pathologies manifest themselves as follows:

• increased heart rate;
• increased breathing or lack of air;
• various small hematomas and small red spots in the place where subcutaneous bleeding may have occurred;
• a vague state of awareness, disorientation in space;
• elevated temperature and severe thirst, turning into febrile attacks.

Patients usually complain of increased fatigue, and often experience migraines and pain in the heart area, and with high blood pressure, severe dizziness may occur. Typically, other symptoms are easily confused with a micro-stroke or micro-infarction, which are already consequences of this disease.

It is precisely the fact that it is extremely difficult to diagnose that makes fat embolism a very dangerous disease, especially when it comes to fatty accumulations in the lungs, when the patient complains of rapid breathing.

How is it diagnosed?

All that is present in the initial diagnosis is an analysis of the history of general symptoms of the disease. The whole picture is very similar to strokes and heart attacks in a milder form, so this could be either a problem with the central nervous system or other symptoms.

One of the most serious and rare manifestations is the patient entering a coma, and there may be no prerequisites for this at all. Before an exacerbation, a person will look completely healthy, and his condition may even improve if surgery has been performed.

If during the initial diagnosis they suspect the appearance of pulmonary embolism or some other type, then doctors refer the patient for additional examination:

• general analysis of urine and blood, with which you can cover the largest number of possible diseases, including fat embolism;
• biochemical blood test, which is carried out for specific suspicions and in cases where the disease is not associated with injuries;
• X-ray of the skull, due to which blockage of cerebral vessels and subsequent hemorrhages can be excluded;
• other studies that would allow us to exclude diseases with similar symptoms (of which there are actually quite a lot);
• MRI, which will identify the source of inflammation and determine the causes of its occurrence.

But what to do when the doctor has made a diagnosis? How to treat embolism and prevent life-threatening complications?

How is an MRI performed?

How does the treatment proceed?

Under no circumstances should embolism be treated with folk remedies; this provokes its development. This disease is too dangerous and complex for such measures; ordinary blood thinning solutions cannot help the patient.

Initially, the patient undergoes conventional therapy, which must necessarily include oxygen therapy using nasal catheters. If it is not possible to identify the pathology in time, this method of treatment is ineffective and a waste of the patient’s precious time.

If conventional therapy does not produce any results, respiratory therapy is started, in which they try to keep the oxygen pressure in the vessels at a high level. This only allows you to save a person’s life for a little longer and keep the patient in a stable condition. But after all these undertakings, drug therapy is mandatory to eliminate the blood clot.

Here there may already be several treatment methods, depending on whether doctors are dealing with pulmonary embolism or another form of the disease. And also depending on the general rules of the clinic and approved drugs in certain countries.

Fat embolism is an extremely dangerous and difficult disease to identify; fortunately, according to statistics, symptoms of the disease are quite rare. But it is worth remembering that the most common is fat embolism during a fracture, so appropriate tests should be carried out to identify this disease.

How long it takes for treatment can only be determined by doctors; it all depends on what signs the patient has. Treatment of fat embolism in fractures occurs in stages. If detected in a timely manner, it is quite harmless, however, if neglected, it can cause a lot of trouble and lead to disastrous consequences.

Video: Fat Embolism Syndrome

With fat embolism (FE), embolization of the microvasculature occurs with fat droplets. First of all, the capillaries of the lungs and brain are involved in the pathological process. Which is manifested by the development of acute respiratory failure, hypoxemia, ARDS of varying severity, diffuse brain damage. Clinical manifestations usually develop 24 to 72 hours after injury or other exposure.

In typical cases, the clinical manifestations of PVCs develop gradually, reaching their maximum approximately two days after the first clinical manifestations. The fulminant form is rare, but death can occur within a few hours of the onset of the disease. PVCs are more common in young patients, but mortality is higher in older patients.

It is believed that if the patient was deeply intoxicated at the time of the injury, PVCs rarely develop. There are several theories on the mechanism of occurrence of fat embolism (mechanical, colloidal, biochemical), but, most likely, in each specific case different mechanisms leading to PVCs are implemented. Mortality, based on the number of diagnosed cases, is 10-20%.

Common causes of PVCs

Skeletal trauma (about 90%) of all cases. The most common cause is a fracture of large tubular bones, and primarily a fracture of the femur in the upper or middle third. With multiple bone fractures, the risk of PVCs increases.

Rare causes of PVCs

• Hip replacement;
• Intramedullary osteosynthesis of the femur with massive pins;
• Closed reduction of bone fractures;
• Extensive surgical interventions on tubular bones;
• Extensive soft tissue injury;
• Severe burns;
• Bone marrow biopsy;
• Fatty liver degeneration;
• Long-term therapy with corticosteroids;
• Acute pancreatitis;
• Introduction of fat emulsions.

Diagnosis of PVCs

Symptoms of fat embolism:

• Patients may complain of vague chest pain, lack of air, and headache.
• There is an increase in temperature, often above 38.3º C. Fever in most cases is accompanied by a disproportionately high tachycardia.
• Most patients with PVCs are drowsy and have oliguria.

If patients, 1-3 days after a skeletal injury, have increased body temperature, drowsiness and oliguria, then the presence of PVCs should first be assumed.

Main manifestations of fat embolism

• Arterial hypoxemia (PaO2<60-70 мм рт. ст., SрO2 < 90-92%);
• Signs of ARDS (usually with severe PVCs);
• Dysfunction of the central nervous system (motor restlessness, convulsions, delirium, coma). It is characteristic that after normalization of oxygenation, there is no noticeable regression of neurological symptoms;
• Petechial rashes develop 24-36 hours after injury in 30-60% of patients with PVCs. They are localized in the upper half of the body, more often in the axillary region. Hemorrhages on the oral mucosa, eye membranes and conjunctiva are also characteristic. The rash usually disappears within 24 hours;
• Sudden decrease in hemoglobin on days 2-3;
• Thrombocytopenia, or rapid decrease in platelet count, decrease in fibrinogen levels;
• Detection of neutral fat in blood, urine, cerebrospinal fluid, sputum (fat is detected in alveolar macrophages);
• Detection of fat during skin biopsy in the area of ​​petechiae;
• Detection of retinal fatty angiopathy.

Additional manifestations of PVCs

However, the independent significance of additional manifestations is small. All of them can occur with any severe skeletal injury.

Instrumental studies

• MRI in many cases makes it possible to establish the etiology of cerebral embolism;
• CT scan of the skull allows us to exclude other intracranial pathology;
• X-ray of the lungs confirms the presence of ARDS and allows to exclude pneumothorax.

Monitoring

Pulse oximetry should be used even for mild manifestations of PVCs, as the situation can change quickly. In case of severe lesions of the central nervous system, control of intracranial pressure is required.

Treatment

Many therapies that have been proposed for the treatment of PVC have been ineffective: glucose administration to reduce the mobilization of free fatty acids, ethanol administration to reduce lipolysis. Severe injuries are often accompanied by the development of coagulopathy. In the first few days (usually within three days), administration (including low molecular weight heparins) increases the risk of bleeding, increases the concentration of fatty acids in plasma, and, in most cases, is not indicated.

There is no evidence that commonly prescribed drugs for the treatment of PVCs, such as Essentiale, lipostabil, nicotinic acid, hepasol, contrical, sodium hypochlorite, can improve treatment outcomes. So treatment is mainly symptomatic.

Maintaining PaO2 > 70-80 mm Hg. Art., SpO2 ≥ 90 ≤ 98% - the goal of respiratory therapy. In mild cases, oxygen therapy through nasal catheters is sufficient. The development of ARDS in patients requires special approaches and mechanical ventilation regimens.

Reasonable limitation of the volume of infusion therapy and the use of diuretics can reduce the accumulation of fluid in the lungs and help reduce ICP. Until the patient's condition stabilizes, saline solutions (Ringer's solution) and albumin solutions are used. Albumin not only effectively restores intravascular volume and slightly reduces ICP, but also by binding fatty acids may be able to reduce the progression of ARDS.

For severe cerebral manifestations of PVCs, sedative therapy and artificial ventilation are used. There is a certain correlation between the depth of the coma and the degree of increase in ICP. The management of these patients is in many ways similar to the management of patients with traumatic brain injury of another origin. It is necessary to prevent body temperature from rising above 37.5°C, for which non-steroidal analgesics are used, and, if necessary, physical cooling methods.

Broad-spectrum antibiotics are prescribed, usually 3rd generation cephalosporins, as initial therapy. If clinically significant coagulopathy develops, the use of fresh frozen plasma is indicated.

The effectiveness of corticosteroids in the treatment of PVCs has not been proven. But they are often prescribed in the hope that they will be able to prevent further progression of the process. For PVCs, corticosteroids are recommended in high doses. 10-30 mg/kg bolus over 20-30 minutes. Then 5 mg/kg/hour by dispenser for 2 days. If methylprednisolone is not available, other corticosteroids (dexamethasone, prednisolone) are used in equivalent dosages.

Prevention of fat embolism

Prevention of PVCs is indicated for patients with fractures of two or more long tubular bones of the lower extremities and fractures of the pelvic bones. Preventive measures include:

• Effective and early elimination of hypovolemia and blood loss;
• Adequate pain relief;
• Early, in the first 24 hours, surgical stabilization of fractures of the pelvis and large tubular bones is the most effective preventive measure.

The frequency of complications in the form of PVCs and ARDS increased significantly (4-5 times) if surgical intervention was postponed to a later time. Note that chest trauma and traumatic brain injury are not a contraindication to early intramedullary osteosynthesis of long bones. The effectiveness of corticosteroids for the prevention of PVCs and post-traumatic hypoxemia has been proven, although the optimal regimens and doses of drugs have not been established. Methylprednisolone is used more often - 15-30 mg/kg/day. within 1-3 days. But there is data confirming the effectiveness of lower doses: methylprednisolone at a dose of 1 mg/kg every 8 hours for 2 days. Corticosteroids are especially indicated if early fracture stabilization has not been achieved.

- This is multiple occlusion of blood vessels by lipid globules. Manifests itself in the form of respiratory failure, damage to the central nervous system, and retina. The main symptoms include headache, encephalopathy, floating eyeballs, paralysis, paresis, chest pain, shortness of breath, tachycardia. The diagnosis is made based on the clinical picture, the presence of predisposing factors in the anamnesis and the identification of large lipid particles in the blood. Specific treatment includes mechanical ventilation, fat disemulsifiers, anticoagulants, glucocorticosteroids, sodium hypochlorite. In addition, nonspecific therapeutic measures are carried out.

ICD-10

T79.1 O88.8

General information

Fat embolism (FE) is a severe complication that develops mainly with damage to long tubular bones as a result of blockage of vascular beds by lipid complexes entering the bloodstream. The frequency of occurrence ranges from 0.5-30% of the total number of trauma patients. Usually diagnosed in patients aged 20-60 years. The minimum number of embolisms is recorded among people injured while intoxicated. Mortality is 30-67%; this indicator directly depends on the severity and type of injuries, the speed of medical care.

Causes

The essence of the pathological process is the obstruction of blood vessels with drops of fat. This leads to disruption of blood flow in important structures of the body - the brain and spinal cord, lungs, heart. Conditions that can cause PVCs include:

1. Injuries. The main cause of lipid embolism is fractures of the diaphysis of the femur, tibia, and pelvis. The risk of developing pathology increases with volumetric and multiple injuries accompanied by crushing of bone tissue. It is believed that the pathology occurs in 90% of people with injuries to the musculoskeletal system. However, its clinical manifestations develop only in a relatively small number of cases. In addition, dyslipidemia, which can provoke vascular obstruction, occurs in patients with burns and damage to a large volume of subcutaneous fat.
2. Shocks and post-resuscitation illness. The formation of emboli occurs during shocks of any origin in 2.6% of cases. The reason is an increase in catabolic processes, a metabolic storm. Symptoms often develop towards the end of 2-3 days after the patient recovers from a critical condition.
3. Intravenous administration of oil solutions. Cases of iatrogenic origin of the disease are isolated. Fat occlusion occurs due to exogenous fats that enter the bloodstream due to erroneous actions of a medical professional. In addition, fat embolism is sometimes diagnosed in athletes who use synthol to increase muscle mass.
4. Hypovolemia. With severe hypovolemia, hematocrit increases, the level of tissue perfusion decreases, and congestion occurs. All this causes the formation of large fat droplets in the circulatory system. Dehydration develops with prolonged vomiting, diarrhea, insufficient drinking water in hot climates, and excessive use of diuretics.

Pathogenesis

According to the classical theory, fat embolism is the result of direct entry of bone marrow particles into the bloodstream at the time of injury. The globules then spread throughout the body through the bloodstream. Particle sizes >7 µm cause pulmonary artery occlusion. Small drops of fat bypass the lungs and penetrate the bloodstream of the brain. Cerebral symptoms occur. There are other assumptions regarding the mechanisms of development of the process.

According to supporters of the biochemical theory , Immediately upon injury and after it, plasma lipase is activated. This becomes a stimulus for the release of fats from storage sites, hyperlipidemia develops, and the formation of coarse fat droplets occurs. The colloid-chemical version is that the de-emulsification of fine emulsions begins due to a slowdown in blood flow in the affected area.

From the hypercoagulation theory it follows that the cause of the formation of fat droplets is a disorder of microcirculation, hypovolemia, and oxygen starvation. Lipid globules with a diameter of 6-8 microns are formed, which create the basis for disseminated intravascular coagulation. The continuation of the process is systemic capillaropathy, which leads to fluid retention in the lungs and endointoxication with lipid metabolism products.

Classification

Fat embolism can occur in the pulmonary, cerebral or mixed form. The respiratory form develops with predominant occlusion of the branches of the pulmonary artery and manifests itself in the form of respiratory failure. The cerebral variety is the result of blockage of the arteries and arterioles that supply blood to the brain. The mixed form is the most common and includes signs of both pulmonary and cerebral damage. The period before the first symptoms appear varies widely. Based on the latent period, the following forms of the disease are distinguished:

• Lightning fast. Manifests immediately after injury and has a critically rapid course. The patient's death occurs within a few minutes. The mortality rate for this type of embolism is close to 100%, since providing specialized care in such a short time is impossible. Occurs only with multiple or massive injuries. The frequency of occurrence is no more than 1% of cases of PVCs.
• Acute. Occurs less than 12 hours after injury in 3% of patients. It is a life-threatening condition, but the mortality rate does not exceed 40-50%. Death occurs from pulmonary edema, acute respiratory failure, or extensive ischemic stroke.
• Subacute. Appears within 12-24 hours in 10% of patients; after 24-48 hours – in 45%; after 48-70 hours – in 33% of victims. There are cases where signs of embolism developed after 10-13 days. The course of subacute forms is relatively mild, the number of deaths does not exceed 20%. The chances of survival increase if signs of the disease develop while the patient is in the hospital.

Symptoms of fat embolism

The pathology is manifested by a number of nonspecific symptoms that can also occur in other conditions. Occlusion of the pulmonary vessels leads to a feeling of tightness in the chest, chest pain, and anxiety. Objectively, the patient exhibits shortness of breath, cough accompanied by hemoptysis, foam at the mouth, pallor, sticky cold sweat, anxiety, fear of death, acrocyanosis. Persistent tachycardia, extrasystole, and compressive pain in the heart occur. Atrial fibrillation may develop. Changes in the respiratory system occur in 75% of patients and are the first symptoms of pathology.

The consequence of cerebral embolism is neurological symptoms: convulsions, impaired consciousness up to stupor or coma, disorientation, severe headaches. Aphasia, apraxia, and anisocoria may be present. The picture resembles that of a traumatic brain injury, which makes diagnosis much more difficult. Paralysis and paresis may develop, local loss of sensitivity, paresthesia, and decreased muscle tone may occur.

In half of the patients, a petechial rash is detected in the armpits, on the shoulders, chest, and back. This usually occurs 12-20 hours after the onset of signs of respiratory failure and indicates overstretching of the capillary network by emboli. When examining the patient's fundus, damage to the retina is detected. Hyperthermia develops, in which the body temperature reaches 38-40°C. This is due to irritation of the thermoregulatory centers of the brain by fatty acids. Traditional antipyretic drugs are ineffective.

Complications

Help for patients with PVCs should be provided in the first minutes after the development of signs of vascular occlusion. Otherwise, fat embolism leads to the development of complications. Respiratory failure ends in alveolar edema, in which the pulmonary vesicles fill with fluid leaking from the bloodstream. In this case, gas exchange is disrupted, the level of blood oxygenation decreases, and metabolic products accumulate, which are normally removed with exhaled air.

Obstruction of the pulmonary artery by fat globules leads to the development of right ventricular failure. The pressure in the pulmonary vessels increases, the right parts of the heart become overloaded. In such patients, arrhythmia, atrial flutter and atrial fibrillation are detected. Acute right ventricular failure, as well as pulmonary edema, are life-threatening conditions and in many cases lead to the death of the patient. Such developments can only be prevented by providing assistance as quickly as possible.

Diagnostics

An anesthesiologist-resuscitator, as well as consultant doctors: cardiologist, pulmonologist, traumatologist, ophthalmologist, radiologist, take part in the diagnosis of embolisms of lipid origin. Laboratory data play a significant role in making the correct diagnosis. PVC has no pathognomic signs, so its intravital detection occurs only in 2.2% of cases. The following methods are used to determine pathology:

1. Objective examination. A clinical picture corresponding to the disease is revealed, the heart rate is more than 90-100 beats per minute, the respiratory rate is more than 30 times per minute. Breathing is shallow, weakened. Moist coarse bubbling rales are heard in the lungs. The SpO2 indicator does not exceed 80-92%. Hyperthermia within febrile levels.
2. Electrocardiography. The ECG shows a deviation of the electrical axis of the heart to the right and nonspecific changes in the ST segment. The amplitudes of the P and R waves increase, in some cases a negative T wave occurs. Signs of right bundle branch block may be detected: expansion of the S wave, change in the shape of the QRS complex.
3. X-ray. X-rays of the lungs show diffuse infiltrates of the lung tissue on both sides, predominant in the periphery. The transparency of the pulmonary background decreases as the edema increases. A fluid level may appear indicating the presence of pleural effusion.
4. Laboratory diagnostics. The detection of lipid globules measuring 7-6 microns in plasma has a certain diagnostic value. It is preferable to take biomaterial from the main artery and central vein. The media from both basins are studied separately. Identification of globules increases the risk of developing occlusion, but does not guarantee its occurrence.

Differential diagnosis is carried out with other types of embolism: air embolism, thromboembolism, vascular obstruction by a tumor or foreign body. A distinctive feature of PVCs is the presence of microdroplets of fat in the blood in combination with the corresponding radiological and clinical picture. With other types of vascular occlusion, lipid globules are absent in the blood.

Treatment of fat embolism

Therapy is carried out using conservative medicinal and non-medicinal methods. To provide medical care, the patient is placed in the intensive care unit. All therapeutic measures are divided into specific and nonspecific:

• Specific. Aimed at disemulsification of fats, correction of the coagulation system, and ensuring adequate gas exchange. For the purpose of oxygenation, the patient is intubated and transferred to artificial ventilation. To synchronize with the device, it is allowed to administer sedatives in combination with peripherally acting muscle relaxants. Restoring the normal consistency of lipid fractions is achieved through the use of essential phospholipids. Heparin is administered to prevent hypercoagulation.
• Nonspecific. Non-specific techniques include detoxification using infusion therapy. Prevention of bacterial and fungal infections is carried out by prescribing antibiotics, nystatin. Sodium hypochlorite is used as an antimicrobial and metabolic agent. From the 2nd day the patient is prescribed parenteral nutrition with subsequent transfer to enteral tube nutrition.

An experimental method of treatment is the use of blood substitutes based on PPO compounds. The drugs improve hemodynamics, restore normal rheological properties of blood, and help reduce the size of lipid particles.

Prognosis and prevention

In subacute cases, fat embolism has a favorable prognosis. Timely assistance can stop pathological phenomena, ensure the necessary perfusion in vital organs, and gradually dissolve emboli. In the acute form of the disease, the prognosis worsens to unfavorable. The fulminant course leads to the death of the patient in almost 100% of cases.

Prevention during operations involves the use of low-traumatic techniques, in particular percutaneous pin osteosynthesis, performed in a delayed manner. It is recommended to avoid using skeletal traction, since this method does not ensure a stable position of the fragments and can lead to the development of late embolization. Before hospitalization, the fastest possible stop of bleeding, if any, is required, adequate analgesia, and maintenance of blood pressure at a normal physiological level. A specific method is the introduction of ethyl alcohol in a 5% glucose solution.

Fat embolism occurs in injuries with fractures of long tubular bones and pelvic bones. In this case, its development ranges from 0.5 to 30%. It also happens with other known diseases and disorders. The pathology is quite dangerous, the probability of death is from 3 to 67%.

At the same time, modern medical science has not fully studied this problem, which complicates the practice of using preventive and therapeutic methods of influence. So how to react and overcome?

Causes

Embolism (from the ancient Greek “invasion”) is a pathological process as a result of which particles enter the blood that should not be there under normal conditions. If these particles (emboli) accumulate in high concentrations, they can lead to blockage of the vessel, which will further affect the blood supply to the organ/tissue.

Fat embolism is determined by the fact that droplets of fat clog the vessels of the microvasculature, involving capillaries in the pathological process. The pathology develops rapidly, and the first manifestations are detected 1-3 days after injury or other exposure.

This pathology has no age or gender restrictions, as well as the influence of the general condition of the body. And yet, there is a certain type of injury and certain types of impact on the human body that can lead to the development of a disease.

Embolization can develop:

• for fractures of tubular bones;
• with a fracture of the pelvic bones;
• in case of multiple injuries with damage to bone tissue;
• after bone marrow surgery;
• after amputation;
• against the background of diabetes mellitus and acute pancreatitis;
• after receiving burn injuries;
• with long-term use of corticosteroid drugs;
• after a liposuction session;
• as a complication of osteomyelitis.

The disease can proceed, taking on the signs of pneumonia, traumatic brain injury, ARDS in adults and a number of other diseases. This significantly complicates the diagnosis of the pathological process, which as a result affects mortality statistics.

Signs

Droplets of fat that enter the blood do not immediately manifest themselves. They move through the bloodstream, mixing with blood elements. Some clog into small vessels, while others continue to move, gradually accumulating. So after a day, a large number of capillaries throughout the body are blocked.

The pathology does not have a specific localization, since the circulatory system passes through the entire body. The first signs of the pathological process are minor hemorrhages. They mainly appear in the neck, shoulders, chest, and armpits, many of them invisible to the naked eye.

After pulmonary capillary embolization, shortness of breath occurs. Reduced oxygen content in the blood leads to cyanosis, a dry cough. Embolism in the heart area leads to the development of tachycardia. Other symptoms include fever and confusion.

Fat emboli can “sit” in place or move, which is much more dangerous. This is precisely the difficulty of diagnostics: it is almost impossible to predict how the particles will behave at a given moment.

However, it is possible to conclude with a high probability what organ pathologies will develop when a fat clot enters:

• heart muscle – acute heart failure;
• kidneys – renal failure (symptom – oliguria);
• lungs – respiratory failure;
• brain - stroke and so on.

This is why it is so difficult to predict the consequences of the disease. And that’s why deaths are recorded so often.

Diagnostics

If the disease is so unpredictable, how can it be detected? A comprehensive diagnosis will be required.

1. Magnetic resonance imaging will help in detecting cerebral fat embolism.
2. Computed tomography can rule out other intracranial lesions.
3. An X-ray examination of the lungs will confirm the symptoms of ARDS, which in turn will rule out pneumothorax.
4. Pulse oximetry and intracranial pressure monitoring.
5. Blood test for hemoglobin, fibrinogen, platelet count levels. Detection of fat in the blood.
6. Analysis of urine, cerebrospinal fluid, sputum.
7. Skin biopsy to detect fat.
8. Examination of the eyeballs for fatty retinal angiopathy.

After surgery, amputation or therapeutic manipulations for injuries, the patient spends several days in the hospital. Thus, it is much easier to monitor the condition, which increases the likelihood of timely detection of pathology.

Therapeutic effect

Due to the special nature of the disease, urgent treatment is required, which is carried out in intensive care.

Early surgical stabilization of the injury helps reduce the risk of fat embolism in injuries with fractures. Immobilization through skeletal traction in this case can be dangerous. Therefore, the optimal solution in the treatment of injuries of large tubular bones is surgical fixation of fragments (pin osteosynthesis).

As for the drug course of treatment, unfortunately, no direct drugs have been developed for this group of pathologies. And yet a number of prescriptions are possible. Therapeutic measures here are aimed at relieving the main symptoms of injury or illness. This means that it is not a fat embolism that is being treated, but a traumatic disease.

Although fat embolism is a quickly affecting and dangerous disease, it can be combated. The main thing is to detect it in time and take appropriate therapeutic measures. One of the main points of early prevention is the provision of high-quality first aid to the victim. Immediate but gentle transport to a medical facility.

Cardiologist

Higher education:

Cardiologist

Kabardino-Balkarian State University named after. HM. Berbekova, Faculty of Medicine (KBSU)

Level of education – Specialist

Additional education:

"Cardiology"

State educational institution "Institute for Advanced Medical Studies" of the Ministry of Health and Social Development of Chuvashia

Trauma is a serious shock to the body. It can undermine health and provoke severe complications. One of them is fat embolism. Typically, such a pathology manifests itself in injured patients with excess body weight with significant blood loss. Experts note: if therapeutic measures are not taken in time, the possibility of recurrence of fat embolism increases several times.

Fat embolism: features of pathology

Fat embolism is a consequence of an injury that provokes the formation of blood clots in the form of fat particles in the vessels of the circulatory system. The pathology is most often caused by damage to the ribs and pelvic bones. The use of various orthopedic fixators only increases the possibility of the formation of fat emboli. The first impetus for the progression of fat embolism is negative changes in the properties of blood that disrupt blood circulation in small vessels.

Pathology manifests itself against the background of oxygen deficiency and a decrease in circulating blood volume. Blood vessels and corresponding organs are filled with fat particles, which over time group into microthrombi. Lipid metabolism products and enzymes have a toxic effect on the body. The membranes of blood vessels and lungs are injured, sometimes causing disseminated intravascular coagulation syndrome (blood clotting disorder due to significant release of thromboplastic substances from tissues).

The course of fat embolism is greatly influenced by disturbances in the structure of red blood cells. In pathology, among normal red blood cells, their altered forms (in the form of sickles, spikes, balls) or red blood cells of unnaturally small sizes are observed. Their number depends on the severity of the injury and its consequences. In accordance with the clinical picture of development, several forms of pathology are distinguished:

• pulmonary;
• cerebral;
• mixed.

In addition, fat emboli are divided according to the time of occurrence. They can be:

• lightning (sudden death);
• acute (occurs in the first hours after injury);
• subacute (death within a three-day period).

Reasons for the development of pathology

There are four versions of the occurrence of fat embolism:

• classical - fat fragments from the injured area enter the passages of the veins and with blood enter the pulmonary vessels, blocking their lumens;
• enzymatic - in case of injury, fat-like substances in the blood under the influence of an enzyme (lipase) are transformed from a dispersed state into droplets, negatively affecting surface tension. Fat fragments from the bone marrow activate the secretion of lipase, which contributes to the further development of the process;
• colloid-chemical - fat-like substances in the blood are transformed from emulsion particles into droplets under the influence of the injury itself;
• hypercoagulability – a complex of post-traumatic disorders leads to the development of blood clotting disorders due to an imbalance of lipid metabolism.

In 90% of cases, the progression of the pathology is provoked by skeletal injuries, more often these are damage to large tubular bones. The likelihood of fat embolism increases with multiple fractures. More rare causes of the development of pathology include:

• connecting fragments of hip bones with large pins;
• replacement of worn-out hip joint tissue with artificial endoprostheses;
• closed reduction of displaced bone fragments;
• massive surgical interventions for lesions of tubular bones;
• significant soft tissue injury;
• severe burns;
• surgical correction of the figure;
• collecting a bone marrow sample;
• excess accumulation of fats in the liver;
• long-term treatment with corticosteroids;
• acute inflammation of the pancreas;
• inflammation of the bone marrow;
• introduction of fat emulsions.

Symptoms of fat embolism

Fat embolism can “mimic” – the onset of formation of fat droplets in the blood is not accompanied by symptoms. Gradually they group and clog vessels of different sizes. Symptoms of a dangerous condition will appear when fat emboli “occupy” a significant part of the blood vessels. This usually happens within one to two days. Fat drops provoke ruptures of blood vessels, which is manifested by hemorrhages - most often in the upper parts of the chest and in the armpits. After this obvious symptom, others arise:

• significant shortness of breath;
• cough;
• increased heart rate;
• “bloodshot” eyes, pain in the eye sockets;
• cyanosis of the skin;
• fever;
• loss of consciousness.

Fat drops are able to move with the blood flow (mobile), or can be fixedly attached to the wall of a certain vessel (immobile). If the embolus is mobile, the pathology develops within a few hours. Its manifestations depend on the organ affected by the embolus. For example, if a drop of fat clogs a coronary vessel, heart failure and cardiac arrest occur. If the embolus penetrates the kidney vessels, fat embolism will cause kidney failure. And if a drop of fat clogs a cerebral artery, a stroke or cerebral infarction develops.

In accordance with the localization of emboli, the pathology is expressed:

1. Central nervous system disorders:

• headache;
• disorders of consciousness and psyche;
• paralysis and paresis;
• delusional states;
• weak manifestations of clinical signs of irritation of the meninges;
• pendulum-like eye movements;
• disorders of pyramidal cells of the cerebral cortex;
• muscle twitching;
• coma state;

1. Respiratory dysfunctions:

• chest pain;
• wet cough with blood clots;
• severe shortness of breath;
• bubble wheezing;
• sustained tachycardia;

1. Permeability and fragility of capillaries (reddish rash in the mouth, conjunctiva, cheeks, neck, shoulders, chest, back);
2. Fever (up to 40°C).

In febrile signs of fat embolism, antipyretic drugs are ineffective because cerebral thermoregulation is impaired by fatty acids.

Features of pathology in heart diseases

The negative impact of fat embolism on the condition of blood vessels is undoubtedly. But it also affects the activity of the heart muscle. In cardiac pathologies, blockage of a large number of small vessels in the pulmonary circulation does not give the weak organ the opportunity to overcome the existing obstacles to blood flow. Ideal conditions are created for the expansion of the heart and its paralysis - this can occur before heart contractions push fat droplets into the vessels of the systemic blood circulation.

When the coronary vessels are damaged, at autopsy, in areas of myocardial blockage, lesions of different sizes, sometimes bordered by leukocytes, are noticeable. This condition is called “tiger” heart. At the same time noticeable:

• disintegration of myocardial muscle fibers into separate fragments;
• hemorrhages in the conduction system of the heart muscle;
• retrograde venous embolism.

Fat emboli move through the cardiac veins not only due to a sharp increase in pressure in the right parts of the heart muscle, but also due to a drop in pressure in the coronary arteries. The Viessen vessels, which communicate with the right side of the heart, also contribute to the movement of fat. Experts believe that when determining the danger of fat embolism, reflex convulsive phenomena caused by irritations of the lung and their transmission to other organs, including the heart, are important.

Pulmonary failure can cause heart failure - fat-like substances in the blood of the pulmonary circulation increase its viscosity and create resistance to the work of the right parts of the heart muscle. The flip side of these phenomena is insufficient filling of the left side of the heart with blood and oxygen starvation of the myocardium. Such facts indicate that heart failure always plays a large role in fat embolism, and the leading role in coronary artery embolism.

Diagnosis of fat embolism

Diagnosis of fat embolism is usually carried out on the basis of clinical data. Laboratory studies are of secondary importance. The diagnosis is confirmed if the patient has several disorders simultaneously:

• round whitish spots near the blood vessels of the eyes, swollen retina;
• tachycardia over 90 beats per minute;
• body temperature above 38°C;
• signs of shock lung syndrome (shortness of breath, anxiety, rapid heartbeat);
• change in consciousness;
• low amount of urine excreted by the kidneys;
• fat droplets with a diameter of about 6 microns; microscopic cylindrical bodies from coagulated protein, blood cells, renal tubular epithelium (urinalysis);
• anemia, signs of increased or decreased blood clotting (blood test);
• diffuse infiltrate in the lungs (x-ray).

There are various scoring diagnostic methods, in which each criterion corresponds to a certain score. Their count allows us to determine the presence of latent and manifest fat embolism.

Fat embolism therapy

Treatment options include:

• saturating the body with oxygen;
• ventilation;
• stabilization of hemodynamics;
• infusion of blood products according to clinical indications;
• prevention of deep vein thrombosis.

Specific therapy for fat embolism consists of providing the body tissues with oxygen. Artificial pulmonary ventilation (ALV) is carried out if the patient’s consciousness is impaired - he is overly excited, behaves inappropriately, and is unable to perceive speech. For such manifestations, mechanical ventilation is indicated even in the absence of manifestations of respiratory failure and acid-base balance disorders. Medicines are also used in the treatment of fat embolism, but their effectiveness is not convincing enough. Drugs used:

• corticosteroids - to relieve inflammation, reduce hemorrhages and swelling;
• Aspirin - to normalize blood gases, coagulation of proteins and platelets;
• Heparin - to stimulate lipase activity. But this can be potentially dangerous if an increase in free fatty acids is part of the pathogenesis. In addition, there is the possibility of an increased risk of bleeding in patients with multiple traumas;
• N-acetylcysteine;
• Lipostabil and Essentiale - to restore the physiological dissolution of disemulsified fat.

• forced diuresis (increased volume of urine produced);
• plasmapheresis (blood collection, purification and return to the bloodstream);
• ultraviolet and laser irradiation of blood.

Intensive therapy aims to support and restore the basic functions of the body and is symptomatic. Surgery is indicated to stabilize bone fractures. If possible, the most gentle method is used - rod devices are used.

Prevention of pathology

Measures to prevent fat embolism in patients who have undergone massive trauma or surgical therapy include:

• carrying out adequate medical measures in case of injury;
• replenishment of blood loss and elimination of bleeding;
• correct fixation of the affected parts of the patient’s body (pneumatic splints);
• competent transportation of the patient to a medical facility;
• implementation of early therapy aimed at slowing down platelet aggregation;
• taking medications that help normalize lipid metabolism;
• monitoring the patient's condition.

Prevention lasts three to four days after injury or surgery.

Fat embolism is initially dangerous, because in itself it is a complication of existing pathologies. Even with qualified therapy, it can disrupt blood flow and affect the condition of the entire body, and with exacerbation of chronic diseases it can provoke death. Modern diagnostic methods have made it possible to significantly reduce the mortality rate of fat embolism, but the prognosis remains unfavorable.