Fat embolism of the renal capillaries. Fat embolism. How is fat embolism treated?

- 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 type 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.

Bulletin of surgery named after. I.I.Grekova. T.159, No. 5. 2000 S.100
V.A. Cherkasov, S.G. Litvinenko, A.G. Rudakov, A.M. Nadymov

Fat embolism occurs most often with fractures of large bones and extensive tissue damage, but there are still poorly understood causes of fat embolism of non-traumatic origin. The range of diseases and conditions in which fat embolism can occur, according to the literature, is expanding every year. We have two observations of fat embolism in pancreatic necrosis and sepsis of unknown etiology.
1. Patient L., 44 years old, was hospitalized in the clinic after abusing alcohol with complaints of girdling abdominal pain, nausea and vomiting. The general condition is serious, signs of intoxication, the abdomen is tense, painful, positive Shchetkin-Blumberg sign, dry tongue, peristalsis cannot be heard, retention of stool and gases. Indicators of “red” blood and urine are within normal limits. There is leukocytosis up to 22.5x109/l, hyperglycemia 11.7 mmol/l. With a preliminary diagnosis of acute pancreatitis, peritonitis, the patient was operated on.
A midline laparotomy was performed. The subcutaneous fat layer had gray-green areas of necrosis. In the abdominal cavity - hemorrhagic effusion, plaques of steatonecrosis, mesocolon infiltrated, gray in color. The pancreas is swollen and black. The pancreas and areas of necrosis of the retroperitoneal tissue were removed, and the abdominal cavity was sanitation and drainage.
With mechanical ventilation, the patient was transferred to the intensive care unit. The next day after surgery, contrast microscopy of venous blood serum with a saturated alcohol solution of Sudan IV revealed 75 fat globules with a diameter of 14 to 735 μm. A diagnosis was made: venous form of fat embolism. Hemosorption was performed, after which no fat globules were found in the blood.
The next day, the patient's condition sharply worsened, microcirculation disorders in the extremities, unstable hemodynamics, pulmonary and cerebral edema, and disseminated intravascular coagulation syndrome appeared. Death occurred due to cardiopulmonary failure, pulmonary and cerebral edema.
At autopsy - acute pancreatic necrosis, retroperitoneal phlegmon, diffuse fibrinous-purulent peritonitis, “shock kidneys and lungs,” cerebral edema, massive fat embolism. The cause of death was multiple organ failure.

2. Patient B., 42 years old, was hospitalized with complaints of abdominal pain, chills, hyperthermia, “flickering spots before the eyes.” Upon admission, the condition was severe, encephalopathy, blood pressure 80/40 mm Hg. Art., pulse - 130 beats/min, respiratory failure. The abdomen is soft, painful in the lower parts, weakly positive Pasternatsky's sign. Moderate anemia, leukocytosis up to 26.7 x 109/l, azotemia, hypocoagulation, protein in the urine and 80-100 leukocytes in the visual field were detected. Pseudomonas aeruginosa was cultured from the blood.
A preliminary diagnosis was made: sepsis, hepatic-renal failure, septic shock, disseminated intravascular coagulation syndrome: hemorrhagic fever with renal syndrome?, poisoning by an unknown poison? Due to increasing respiratory failure, the patient was intubated and transferred to mechanical ventilation, intensive therapy and hemodialysis were performed.
Ultrasound and laparoscopy of the abdominal organs and retroperitoneal space did not reveal any pathological abnormalities. X-ray of the lungs revealed drainage infiltration of the “snow blizzard” type. There was a decrease in pO2 in the blood to 21.6 mm Hg. Art. The echocardiogram shows signs of pulmonary hypertension and dilatation of the right ventricle. When examining the fundus, hemorrhages of the retina of the left eye were determined. On the 4th day from the moment of admission, contrast microscopy of blood serum with Sudan IV was performed. No fat globules were found in the blood from the subclavian vein; 115 fat globules ranging from 14 to 73 µm were detected in the blood from the femoral artery. A diagnosis was made: arterial form of fat embolism.
The patient's condition did not improve after 5 sessions of hemodialysis, 4 blood transfusions and intensive antibacterial therapy. Due to cardiopulmonary failure and multiple organ disorders, death occurred on the 18th day. At autopsy - moderate hypostatic pneumonia, chronic pyelonephritis, necrosis of the bladder wall, pulmonary and cerebral edema, fat embolism. Death occurred from multiple organ failure.
Received by the editor on January 11, 2000.

Fat embolism is a pathology that is accompanied by problems with blood flow. Painful processes appear after blockage of blood vessels occurs. Blockage occurs due to the settling of tiny fatty particles. Fat enters the blood system, and irreversible processes begin. In our article we will talk in detail about what a fat embolism is.

To begin with, let us inform you that the disease most often appears as a consequence of injuries. A special risk group consists of people who are prone to severe internal bleeding and people with increased body weight.

An embolism is a blockage of a vessel. This complex condition leads to tissue death. In most cases, the pulmonary arteries are blocked, since particles of foreign bodies along with the blood very quickly enter the lungs through the bloodstream. This can lead to breathing problems and sometimes death. The treatment of this disease is carried out by a resuscitator.

If timely emergency medical assistance is provided, the blockage of the venous lumen will be successfully eliminated.

Embolism comes in different types. Each type differs in what blocks the lumen:

• Thromboembolism - the venous lumen is blocked by a blood clot or a torn piece of it.
• Gas embolism - when trace elements in a gas state enter the vessels. In most cases it is air.
• Drug-induced disease.

This is just a short list of various embolisms. But the essence of the disease always remains the same.
A child suffers from embolism many times less often than an adult.

Causes of the disease

Fat particles have the ability to clog various small vessels in many organs of the human body. Most often, the disease affects the lungs, brain, heart and kidneys.

Fat embolism can begin to develop as a background process in diseases such as:

1. Severe injury that damages and displaces bones. This is the root cause that is encountered most often.
2. State of shock. We are talking about anaphylactic or traumatic shock conditions.
3. State of clinical death.
4. In rare cases, with acute hepatitis in a complex form.

Doctors have developed several options for how the disease supposedly develops. We list the main versions:

• When injured, the integrity of the fatty tissue is disrupted. Fatty drops from the affected area are transferred to the venous vessels, then, in the direction of blood flow, they enter the capillary vessels of other organs or the lungs.
• When injured or in a state of shock, the fatty elements that are found in the blood are transformed from tiny particles into large droplets and block blood vessels.
• Blood thickening, which occurs due to excessive bleeding during injuries or complex diseases, leads to an increase in coarse drops of fat in its composition.

Forms of the disease

Medicine classifies embolism into various groups based on the complexity of the condition and the speed of development of the disease. Let's highlight the main forms:

• Lightning embolism. This type of disease develops instantly, the patient dies within two minutes.
• Acute embolism. The disease appears several hours after injury or shock.
• Subacute embolism. The course occurs in the form of hidden symptoms and lasts about two days. Then the symptoms appear.

Based on where the blockage of the vessel is located, fat embolism can be divided into the following types:

• pulmonary - when the capillaries in the lung are affected;
• cerebral - when the capillaries of the brain are affected;
• mixed - when capillaries throughout the body are affected: it can be the heart, lung, kidneys and even the retina.
  The mixed form of the disease occurs most often.

Symptoms

Let's talk about the signs of the disease. They directly depend on what type of disease is diagnosed. Let's consider each case separately.

Symptoms of pulmonary embolism

When it comes to pulmonary embolism (PE), a painful sensation of a compressive nature appears: a tingling sensation behind the sternum.

Respiratory function is impaired: the patient suffers from shortness of breath. Sometimes breathing may stop altogether. The heartbeat becomes faster and faster. An acute cough appears with sputum in the form of foam or blood.

Brain embolism

When diagnosing a diagnosis such as cerebral embolism, the following signs are noted: the patient’s consciousness is disturbed, acute pain in the head of a paroxysmal nature appears, a state of delirium and hallucinations, the pupils twitch and float.

Sometimes paralysis and muscle cramps occur. The central nervous system is depressed, which can result in a coma. The body temperature rises to forty degrees; this condition cannot be eliminated with the help of medications.

Symptoms of mixed embolism

With mixed embolism, all the symptoms that we wrote about in the two previous paragraphs are observed. In addition, damage to the capillaries on the skin and mucous membrane increases.

A red rash appears in the form of dots, which indicates tiny effusions of blood that can be found on the entire skin, especially the upper part, as well as in the oral cavity and on the eyeballs.

In addition, symptoms of destruction of the capillaries of the kidneys appear, which manifests itself in an instant decrease in urine and a change in its composition.

Diagnosis

The first diagnosis of the disease consists of analyzing the history of symptoms. The patient experiences severe problems with the central nervous system, fever and other symptoms, even coma.

Confirmation of the diagnosis is carried out using additional tests. Among which are the following:

• general blood analysis;
• general urine analysis;
• biochemical blood test, which can identify causes of the disease that are not related to injury;
• CT scan of the cranial area to confirm or rule out changes within the skull;
• X-ray, which will make it possible to exclude pneumothorax.

The most accurate method for studying embolism is MRI. This procedure will make it possible to see the affected organ and understand the main cause of the disease.

Treatment

Before we start talking about the treatment of embolism, let's pay special attention to important information. It lies in the fact that it is impossible to cure embolism of any type using traditional and alternative medicine methods, since this can only result in death. This disease requires immediate treatment in a hospital setting and even intensive care.

Treatment before hospital

When there is a threat of fatty blockage of blood vessels during severe injuries, it is necessary to begin providing emergency rescue even at the stage before entering the hospital in order to reduce the risk of complications to a minimum.

It is necessary to treat fat embolism of a preventive type if the patient experiences the following symptoms:

• traumatic shock;
• long-term arterial hypotension;
• the pelvic bones are crushed;
• hips and legs were crushed;
• long absence of transportation to the hospital;
• improper immobilization.

In the presence of factors that aggravate the disease, it is necessary to properly immobilize the injured limbs.

This is necessary in order to prevent tearing of the tissues that are located around the bone. In addition, it is important to correctly take measures to administer painkillers in order to prevent the development of traumatic shock.

Then, it is necessary to transfer the patient to a special transport, this will allow him to be safely delivered to the hospital department.

If there is such a need, then it is necessary to provide respiratory support, as well as stabilize complications. Sometimes it becomes necessary to administer large doses of corticosteroids and take preventive measures for the occurrence of thrombosis in the deep veins of the legs and arms.

Treatment in the therapeutic department

Fat embolism is treated in a hospital setting. If an urgent need arises, the patient is transferred to the intensive care unit.

All treatment procedures consist of many actions that should be performed in order to improve the quality of oxygen supply to tissues in the body.

• Everyone, without exception, undergoes the procedure of artificial ventilation of the lungs if there is confusion and other mental abnormalities. Ventilation can continue for a long time, until the person regains consciousness and his health improves.
• Demulsifiers are introduced into the body - this substance is capable of dissolving fat that is in the body and turning it into a special emulsion of fine dispersion.
• To stop the spread of DIC syndrome and the appearance of thromboembolism, it is necessary to carry out therapy using heparin.
• Surgical intervention.
• Sometimes they resort to a method called arterial embolization.

Forecast

In general, the prognosis is regarded as unfavorable. About ten percent of patients die from fat embolism.

The essence of the unfavorable course of treatment is that embolism can occur as a background process in incredibly severe health conditions. It is this condition that provokes death, and embolism only aggravates the severity.

Prevention

During damage to the musculoskeletal system, during first aid, as well as on the first day, it is necessary to carefully monitor the patient’s condition. Every procedure performed by doctors must be extremely careful.

The patient can be transported only after special bandages are applied to immobilize the condition. The patient must be brought out of shock.

If surgical intervention cannot be avoided, then it is necessary to do it as quickly as possible while reducing the likelihood of injury. Liquids can only be injected into a vein using the drip method. Before carrying out these manipulations, a sponge must be applied to the vessels.

During a skull injury, it is difficult to diagnose a fat embolism, so it is important to undergo an examination by a neurologist.

Fat embolism is very rare in children.

Complications

Fat embolism in itself is a complication, as it is extremely dangerous. Even with proper and high-quality treatment, it leads to problems with blood supply. This affects the condition of the whole organism. All chronic illnesses become acute. The most serious consequences are the death of the patient.

In our article you learned about what a fat embolism is. What it is? This is a serious condition of the body that requires immediate treatment. We wish you good health!

The term “embolism” refers to the pathological occlusion of blood vessels by substances that normally cannot be present in them. Fat embolism, therefore, is a pathology in which blood vessels become clogged with droplets of fat, causing disruption of blood flow with all the ensuing consequences.

Most often, this pathology develops against the background of traumatic injury to the tubular bones, which causes damage to the bone marrow. In addition, fat embolism can develop in other pathological conditions, such as cardiogenic shock. Due to the fact that the signs of fat embolism are similar to other pathologies, for example, or, the likelihood of an incorrect diagnosis and, as a result, death increases.

The risk group includes young men, who are more likely to develop this complication after skeletal fractures.

Causes

This complication develops when tiny drops of fat enter the blood vessels. This happens for various reasons, for example, after surgery to amputate limbs or in overweight people when fractures occur. Increased bone marrow pressure can also lead to the development of this pathological condition.

Fat embolism occurs especially often in cases where people lose a lot of blood (during operations, with extensive traumatic injuries). In people with low blood pressure, the risk of developing this complication is also quite high.

Of course, not every traumatic injury to the skeleton is accompanied by a fat embolism - a complication is observed in 10% of cases. At the same time, the mortality rate for this pathology is quite high and is about 50%.

There are other reasons that can cause this complication, for example:

• severe burns;
• traumatic extensive damage to soft tissues;
• liver injuries.

It also occasionally happens that a fat embolism develops in a person who has undergone closed cardiac massage.

The mechanism of development of pathology is quite multifaceted. The main role in the pathogenetic mechanism is played by increased bone marrow pressure, which promotes the penetration of fat particles into the veins. Some researchers suggest that when the blood thickens, for example, with large blood loss, lipase is activated in it, which leads to an increase in the number of fat cells.

According to another theory, the development of this formidable complication occurs due to changes in the size of plasma fats.

Varieties

Today in medical practice there is the concept of three types of fat embolism:

• pulmonary;
• mixed;
• cerebral (brain, kidney).

The type of pathology depends on the location of the fat particles - in the lung tissue, in the kidney or brain tissue, as well as in various organs of the body. According to the type of course, embolism can be fulminant, in which death occurs within a few minutes. But acute and subacute forms are more common. In acute cases, the disease manifests itself within a few hours after the traumatic injury, and in subacute cases, in the period from 12 hours to 3 days.

In acute and subacute forms, the likelihood of death is reduced, since doctors have time to dissolve fat cells and resume normal blood circulation.

Clinical manifestations

The first symptoms of the pathological condition appear a day after suffering injuries or critical conditions. They are expressed by the appearance of very small hemorrhages, which are most often localized on the skin of the shoulders, neck, chest and armpits. These hemorrhages are sometimes so small that it can be difficult to see them without a magnifying glass. They can persist on the human body for several hours or several days. Symptoms such as hemorrhages indicate that there is a blockage in the capillaries with traumatic damage.

Sometimes, hemorrhages are found in the fundus and conjunctiva. In addition, examining the fundus of the eye gives the doctor the opportunity to see small fatty blood clots in the lumens of blood vessels. If we talk about the main symptoms, they are represented by four characteristic syndromes.

The first syndrome is associated with disorders of the central nervous system. It is represented by symptoms such as:

• disturbance of consciousness;
• development of paresis and paralysis;
• unbearable headaches;
• nystagmus;
• rave;
• convulsions and even coma.

The second syndrome is hyperthermic. A person’s temperature rises to febrile levels and nothing can bring it down. The reason for such a persistent temperature lies in the fact that it occurs against the background of irritation of the thermoregulatory structures of the brain by fatty acids.

In addition to these, there are other symptoms characteristic of this pathology, namely, disturbances in cardiac and respiratory activity (the third clinical manifestation). A person complains of shortness of breath, even stopping breathing, pain behind the sternum, cough with blood in the sputum,... When listening to the lungs, you can identify the presence of fine rales, and when listening to the heart, it is possible to determine the accent of the second tone.

And the last, fourth clinical manifestation concerns the already described petechial hemorrhages throughout the body.

Separately, it should be said about pulmonary syndrome, which develops in the lungs. This is the most common form of pathology, which occurs in 60% of patients, and is characterized by the following symptoms:

• the appearance of a dry cough;
• secretion of bloody, foamy sputum;
• cyanosis and shortness of breath.

Sometimes the only visible symptom in a pathology such as pulmonary fat embolism is arterial hypoxemia.

In the cerebral form, that is, with damage to the brain, the above-described symptoms associated with disruption of the central nervous system predominate. And the mixed form, in which damage occurs not only to the lungs and brain, but also to the vessels of other organs, in particular the kidneys, manifests itself with mixed symptoms.

Very often, against the background of a fat embolism of the lungs or brain, it develops, requiring the insertion of a breathing tube and the start of mechanical ventilation. Such measures help prevent oxygen starvation of tissues and restore microcirculatory function.

Treatment

In case of extensive injuries, burns and after severe clinical conditions, it is necessary to prevent complications such as fat embolism. In order to prevent the development of symptoms, measures are taken to improve blood circulation through the vessels and restore the functions of the respiratory system. The administration of heparin to thin the blood and the installation of special vena cava filters that can retain fatty clots are also indicated.

Treatment for fat embolism varies depending on the severity of the symptoms. In case of pulmonary and cerebral embolism, it is mandatory to connect a ventilator. Among medications, treatment involves the administration of drugs such as: ethyl alcohol with glucose (intravenous drip), as well as rheopolyglucin and glucose solution.

In addition, treatment is carried out with the drugs decholin, essentiale, lipostabil, that is, drugs that can break down fat clots. Sometimes glucocorticosteroids are prescribed. Nonspecific treatment involves detoxification therapy. Treatment can also be surgical and consists of stabilizing bones during fractures using the installation of rod devices.

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Diseases with similar symptoms:

Pulmonary failure is a condition characterized by the inability of the pulmonary system to maintain normal blood gas composition, or it is stabilized due to severe overstrain of the compensatory mechanisms of the external respiration apparatus. The basis of this pathological process is a violation of gas exchange in the pulmonary system. Because of this, the required volume of oxygen does not enter the human body, and the level of carbon dioxide constantly increases. All this causes oxygen starvation of organs.

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.

• Common causes of PVCs
• Rare causes of PVCs
• Diagnosis of PVCs
• Main manifestations of fat embolism
• Treatment
• Prevention of fat embolism

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;
• Liposuction;
• Bone marrow biopsy;
• Fatty liver degeneration;
• Long-term therapy with corticosteroids;
• Acute pancreatitis;
• Osteomyelitis;
• 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), the administration of heparin (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 (0.9% sodium chloride, 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. Methylprednisolone 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.

Why and how pathology develops

Fat particles clog small vessels - capillaries - of various organs: first of all, the lungs, then the brain, kidneys, and heart.

Fat embolism develops against the background of the following pathologies:

There are several versions of the mechanism of development of fat embolism. Here are the main ones:

Forms of fat embolism

Depending on the severity of the condition and the speed of development of the embolism, doctors distinguish the following forms:

• Lightning fast. The embolism develops very quickly, and the patient's death occurs in just a few minutes.
• Spicy. Develops during the first hours after the occurrence of the cause (trauma, shock).
• Subacute. It occurs in a latent form for 12–72 hours, and only then do symptoms appear.

Depending on the location, fat embolism is divided into pulmonary (lung capillaries are affected), cerebral (brain capillaries), mixed (capillaries of the whole body, including lungs, brain, heart, kidneys, skin, retina, etc.) . Most often it is the mixed form that appears.

The photo shows damage to the pulmonary capillaries after a fracture of the tibia and fibula. One can judge the pulmonary form of fat embolism or, if other organs are also affected, a mixed fat embolism.

Symptoms

Manifestations of different types of fat embolism:

Pulmonary	Compressive, stabbing pain behind the sternum, breathing problems (shortness of breath, suffocation, respiratory arrest), rapid heartbeat, and sometimes cough with the release of foamy or bloody sputum.
Cerebral (brain)	Impaired consciousness, attacks of severe headaches, delirium, hallucinations, twitching of the pupils, “floating” pupils, paralysis, muscle cramps, depression of the central nervous system up to coma, high body temperature (39–40 degrees), which is not reduced by medications.
Mixed	All of the above symptoms. Plus signs of damage to the capillaries of the skin, mucous membranes: pinpoint red rashes (small hemorrhages) on the skin of the entire body (more on the upper half), in the eyeballs, in the mouth. Symptoms of damage to the renal capillaries also appear: a sharp decrease in the amount of urine formed, a change in the composition of urine.

Diagnostics

The famous physician Pashchuk A. Yu. developed the following scale of symptoms, using which doctors can suspect fat embolism in patients with trauma and shock:

If the score is more than 10, even in the absence of symptoms, a latent form of fat embolism can be suspected. With a score of more than 20, doctors are dealing with severe fat embolism.

The following criteria accurately confirm the diagnosis:

Often there is no time for such detailed studies as fundus examination, chest x-ray, so fat embolism is diagnosed using a symptom scale, urine and blood tests.

Why is pathology dangerous?

The main danger posed by fat embolism is the possibility of death.

Death occurs for the following reasons:

• If more than 2/3 of the capillaries of the lungs are affected, acute respiratory failure develops, which leads to hypoxia of all body tissues and death.
• When a large number of cerebral vessels are affected, multiple small hemorrhages in the brain occur, which can also cause irreversible changes and death.

Treatment methods

It is carried out urgently and immediately.

If consciousness and breathing are impaired, even in the absence of a confirmed diagnosis, the patient is connected to a ventilator to prevent further changes in the lungs and death due to respiratory arrest.

After confirmation of the diagnosis, drug therapy is used.

Patients are given drugs that destroy large drops of fat in the blood and turn them into the same small particles that they should be normally. Such medications include Lipostabil, Essentiale, Decholin. Anticoagulants are used to thin the blood: for example, Heparin.

Also, glucocorticosteroids (Prednisolone, Dexamethasone), protease inhibitors (Kontrikal), antioxidants (vitamin C, vitamin E) are used to eliminate the state of shock, strengthen the body's cells and improve metabolism in tissues.

All this allows you to stabilize the composition of the blood, improve blood circulation, and prevent irreversible changes in the body’s cells.

Nonspecific treatment is also used, aimed at improving the general condition of the patient and eliminating the risk of other complications of injuries. To maintain vital functions, a solution of glucose with insulin, electrolytes (potassium, magnesium), and amino acids is infused. To prevent infectious complications in injuries, Timalin, T-activin, and gamma globulin are used. To prevent purulent-septic complications, doctors prescribe Nystatin, Polymyxin, and aminoglycosides.

Forecast

In most cases it is unfavorable. About 10% of patients die from fat embolism itself. However, the unfavorable prognosis lies in the fact that fat embolism occurs against the background of very severe conditions, which in themselves can provoke the death of the patient.

Etymology of the disease

What is a fat embolism? The disease is a pathology associated with the penetration of fats into blood cells. The main cause of the disease is considered to be injury to bone tissue, especially in patients with increased blood loss or excessive body weight.

Medical specialists distinguish several varieties of this disease, and each form occurs depending on the course of the pathology:

• fulminant - characterized by rapid development, and the process itself takes about several minutes, resulting in death;
• acute - spread occurs over several hours after injury;
• subacute - more than one day is spent on development.

There is also a conditional division of the disease into groups, and the patient can be diagnosed with pulmonary, cerebral or mixed fat embolism. In most cases, fats have a negative effect on the brain, lungs and liver areas. The remaining internal organs are affected much less frequently by the disease.

Factors of occurrence

Fat embolism syndrome can develop due to the influence of certain types of factors. Medical experts tend to adhere to two theories as to what the causes may be.

The first theory implies that the formation of the disease is associated with an increase in pressure in the bone marrow after injury or as a result of surgery. After the penetration of fat cells into the blood, the formation of so-called microthrombi occurs, which subsequently moves throughout the entire area of ​​​​the body. The second is biochemical. What it is? She says that a violation at the cellular level is directly related to a negative change in the hormonal levels of the human body.

Simultaneously with this factor, sepsis may occur, causing disruption of proper blood flow.

Additional factors influencing the development of the disease include:

• performing a surgical procedure to remove excess fat;
• closed bone fractures;
• hip joint replacement;
• receiving severe burns to a large area of ​​the skin;
• bone marrow biopsy;
• diagnosing concomitant diseases, for example, osteomyelitis or acute pancreatitis.

In isolated and very rare cases, fat embolism syndrome can be affected by factors that are not associated with injury to individual parts of the body.

Symptomatic manifestations

Thromboembolism is a fairly serious disease, not only because it develops relatively actively and can lead to death in a short period of time, but also because at the initial stages of its development it does not show any visible symptomatic signs. The primary symptom of the disease is the occurrence of pain, but patients attribute this to the consequences of injury or surgical treatment. Once the disease has reached its optimal point, symptoms begin to appear.

The most common ones include:

• cardiopalmus;
• active respiratory process;
• the formation of small redness in places where small vessels bleed;
• disturbance of consciousness;
• the appearance of a feverish state.

The patient may experience a constant feeling of fatigue, accompanied by headaches, dizziness, or chest pain.

If the disease is formed as a result of the influence of the factors considered above, then the symptomatic signs have a slightly different nature of manifestation. In this case, the patient has a dysfunction of the central nervous system, headaches have the nature of attacks relative to their manifestation, the patient loses the ability to adequately respond to the surrounding reality. Often the patient may be tormented by a cough, and when sputum is separated, blood may be observed in it. During all symptomatic manifestations, the respiratory process begins to noticeably weaken, which provokes the formation of so-called fine-bubble wheezing. In almost all cases, the patient’s body temperature actively rises to almost the maximum level, while taking antipyretic medications does not give positive results.

Diagnostic measures and treatment methods

The first priority when diagnosing this disease is to carefully examine the patient’s sting regarding the manifestation of symptomatic signs. After this, the patient is sent to conduct a certain series of studies in order to confirm or refute the suspected diagnosis. These activities include:

• laboratory examination of a general blood and urine test to study the general condition of the patient’s body and the presence of concomitant diseases;
• biochemical blood test to detect the indirect cause of the disease;
• computed tomography of the skull to review and identify possible negative disorders;
• radiography.

Magnetic resonance therapy is considered the most functional and effective, since it can help identify the main cause of the disease.

Once the diagnosis is confirmed, treatment for fat embolism first begins with supplying the required amount of oxygen to the brain area. The following therapeutic measures are divided into:

1. Therapeutic. They include treatment with oxygen, but over time this method has lost its increased effectiveness, since the disease is not always detected on time. After this, the patient requires respiratory therapy.
2. Medication. The standard form of treatment for the disease involves the use of sedatives simultaneously with artificial ventilation (usually used when severe cerebral disorders are detected). This also includes taking analgesic drugs to normalize body temperature and broad-spectrum antibiotics. Some medical experts argue that the use of methylprednisolone or prednisolone is necessary at this time, as they help stop the development of the disease. If necessary, diuretics can be included in the use to reduce the accumulation of fluid in the lung area.

Carrying out therapeutic measures must be timely, since the disease can lead to death in a minimum period of time.

Preventive actions

Preventive measures undoubtedly play an important role, especially for those patients who are prone to developing this type of disease and who are in the so-called risk group. These include patients who have relatively recently undergone surgical treatment or have been severely injured. All existing preventive measures regarding this problem imply that the patient receives appropriate and competent medical care in case of injury, normalizing the process of blood circulation and stopping bleeding if it occurs, correct transportation of the patient to a medical facility after injury, and, if necessary, timely provision and implementation of initial therapeutic measures, the use of appropriate medications and constant monitoring of the general condition of the patient.

The duration of preventive measures, as a rule, is about several days after surgical treatment has been performed or an injury has been sustained.

The patient must be aware of possible subsequent complications. Thromboembolism associated with blockage in itself is a complication process, and it is for this reason that it is considered a rather dangerous pathology. Even if the patient received highly qualified and timely medical care, this does not mean that the blood supply remains normal. All these consequences negatively affect the functionality of the body as a whole, as it provokes the active occurrence and impact on the body of numerous and varied chronic diseases. Of course, death is considered the most serious and most common complication.

Thus, this disease poses a serious threat to the patient’s life. The prognosis for the patient's future life depends on the quality and timeliness of treatment. Modern medicine has become much improved, which is confirmed by a decrease in the number of cases where the disease ends in death. However, this factor is not always confirmed, since some forms of the disease can be difficult to diagnose.