Fat embolism symptoms. Treatment of fat embolism. Why and how pathology develops

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 in which blood vessels become clogged with fat droplets, which leads to impaired blood flow.

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Fat embolism is considered as a systemic inflammatory reaction that develops under the influence of mechanical and biochemical processes: from the site of damage to the bone marrow or subcutaneous tissue, fat particles enter the bloodstream and cause the development of a local inflammatory reaction at the site of deposition. In addition, the release of fat globules into the bloodstream entails a slowdown in blood flow, changes in the rheological properties of blood, and disruption of microcirculation.

Possible consequences of fat embolism include the development of pneumonia, respiratory failure, acute pulmonary failure, renal failure, and ischemic stroke.

Large fat particles are able to pass through the capillaries of the lungs and remain in them. Small fat drops penetrate into the systemic circulation to target organs (brain, heart, skin and retina, less often - kidneys, spleen, liver, adrenal glands), causing the clinical picture of fat embolism.

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Causes and risk factors

Most often, fat embolism occurs as a complication of skeletal injuries (fractures of the pelvis, tibia, femur, damage to fatty tissue) or surgical interventions (extensive surgical interventions on tubular bones, joint replacement, hip osteosynthesis, reposition of fragments, maxillofacial operations, liposuction) .

The occurrence of fat embolism is also possible with the following pathologies:

• tumors;
• severe burns;
• acute pancreatitis, severe pancreatic necrosis;
• toxic and fatty liver degeneration;
• long-term corticosteroid therapy;
• post-resuscitation conditions;
• sickle cell anemia;
• bone marrow biopsy;
• erroneous administration of liposoluble drugs intravenously;
• states of shock.

Risk factors: large volume of blood loss and long period of hypotension, incorrect immobilization and transportation of the patient.

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Forms of pathology

Depending on the speed of development of manifestations and the duration of the latent period, the following forms of fat embolism are distinguished:

• acute– develops within several hours after the injury, one of the severe variants is fulminant, in which massive damage to the musculoskeletal system leads to the rapid entry of a large number of fat globules into the vascular bed and lungs (fat embolism in fractures); this form is fatal in a few minutes;
• subacute– the clinical picture develops within 12–72 hours; may develop 2 weeks or more after injury.

3–13% of all cases of fat embolism are fatal.

Based on the location of the lesion, fat embolism is divided into pulmonary, cerebral and mixed (fat embolism of the lungs, brain, liver, and less often of other organs).

Depending on the causes, fat embolism is classified as occurring during or after surgery, as a result of amputation, trauma, or exposure to certain drugs.

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Symptoms

The clinical picture of fat embolism does not have clearly defined symptoms and is manifested by a variety of symptoms that only allow one to suspect it. Symptoms include nonspecific manifestations: pulmonary, neurological and skin.

On the first day, the pathology may be asymptomatic. The clinical picture is often superimposed on the picture of traumatic shock or traumatic brain injury. The first symptoms of fat embolism in fractures and injuries are usually pulmonary and respiratory disorders:

• a feeling of tightness in the chest, lack of air, pain behind the sternum;
• pleural pain;
• dyspnea;
• signs of acute respiratory distress syndrome (hyperthermia, tachycardia, tachyarrhythmia, fever, cyanosis, etc.);
• dyspnea;
• cough, wheezing, hemoptysis.

In the early stages, general cerebral symptoms appear. As a result of cerebral embolism and hypoxic damage, the following neurological symptoms develop:

• motor restlessness;
• irritability or lethargy;
• convulsive syndrome (both local and generalized convulsions);
• disturbances of consciousness: disorientation, delirium, stupor, coma;
• focal neurological symptoms (impaired ability to speak or understand speech, paralysis, impaired complex movements, anisocoria, visual impairment).

Most often, fat embolism occurs as a complication of skeletal injuries or surgical interventions.

Most patients have petechial rashes on the skin. The appearance of petechiae is caused by blockage of capillaries by fat emboli and damage to them by released fatty acids. Petechiae are localized in the upper half of the body, in the axillary region. They usually disappear within a day.

When examining the fundus, signs of retinal damage are revealed:

• exudate;
• hemorrhages (subconjunctival petechiae);
• plaques, spots;
• intravascular fat globules.

Diagnostics

When making a diagnosis, a set of diagnostic criteria for fat embolism is used, the presence of axillary or subconjunctival petechial rashes, and dysfunction of the central nervous system are identified. The state of consciousness is assessed using the Glasgow Coma Scale. Identify signs of pulmonary edema and hypoxemia (decreased oxygen levels in the blood).

When diagnosing fat embolism, laboratory data are taken into account:

• decrease in hemoglobin;
• increased ESR;
• decreased platelet count;
• decreased fibrinogen levels;
• decreased hematocrit (volume of red blood cells in the blood);
• the presence of drops of neutral fat in the urine measuring 6 microns, fat globules in the blood plasma, sputum, and cerebrospinal fluid;
• presence of fat on skin biopsy in the area of ​​petechiae.

Instrumental studies are more informative. A chest x-ray can evaluate changes resulting from pulmonary fat embolism. The X-ray shows the appearance of small focal shadows and an increase in the pulmonary pattern: manifestations of diffuse infiltration of the lungs, characteristic of the development of ARDS.

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An ECG can detect unmotivated persistent tachycardia, cardiac arrhythmias, which indicate overload of the right half of the heart or myocardial ischemia.

The unfavorable prognosis lies in the fact that fat embolism occurs against the background of severe conditions; early diagnosis and adequate treatment of fat embolism improves the prognosis.

Computed tomography of the brain determines cerebral edema, the presence of petechial hemorrhages, foci of necrosis, and perivascular infarctions. Magnetic resonance imaging visualizes diffuse hyperechoic areas, revealing the etiology of cerebral embolism. Fundoscopy can detect the presence of fatty angiopathy in the fundus retina. Monitoring using pulse oximetry and control of intracranial pressure are also used.

Treatment

Treatment of fat embolism consists of relieving the main clinical manifestations of the injury or disease that caused it. Main directions of therapy:

• ensuring oxygen delivery to tissues, oxygen therapy and respiratory support;
• carrying out infusion therapy for systemic microcirculation disorders, eliminating spasm of peripheral vessels, replenishing the volume of circulating blood, rheological, transfusion therapy by administering biological fluids, correction of water-electrolyte balance using colloid and crystalloid solutions. The administration of albumin is indicated, which is capable of restoring circulating blood volume, binding free fatty acids and reducing the degree of damage to pulmonary functions;
• with – dehydration therapy using osmotic diuretics;
• therapy of brain hypoxia with the use of antihypoxants, barbiturates and opiates;
• metabolic therapy – course administration of nootropic drugs;
• sedative therapy;
• correction of the coagulation and fibrinolysis system using anticoagulants, in particular heparin, which, along with anticoagulant properties, has the ability to activate lipoproteins and accelerate the enzymatic reactions of triglyceride hydrolysis, helping to cleanse the lungs of fat globules;
• intensive hormonal therapy, the use of corticosteroids - provide protection against free oxygen radicals and enzymes;
• the use of drugs whose action is aimed at reducing the concentration of fat globules in the blood, restoring the physiological dissolution of disemulsified fat and to prevent disemulsification (Lipostabil, Essentiale);
• detoxification and detoxification therapy - forced diuresis, exchange plasmapheresis. Plasmapheresis operations normalize the rheological properties of blood, its electrolyte, morphological, biochemical composition and hemodynamic parameters;
• surgical treatment, timely surgical stabilization of fractures (transosseous pin osteosynthesis with pin-rod devices, intramedullary osteosynthesis with a pin);
• correction of immune status under the control of immunological research data.

The clinical picture of fat embolism does not have clearly defined symptoms and is manifested by a variety of symptoms that only allow one to suspect it.

Possible complications and consequences

Possible consequences of fat embolism include the development of pneumonia, respiratory failure, acute pulmonary failure, renal failure, and ischemic stroke.

Forecast

3–13% of all cases of fat embolism are fatal. However, the unfavorable prognosis lies in the fact that fat embolism occurs against the background of severe conditions; early diagnosis and adequate treatment of fat embolism improves the prognosis.

Prevention

Prevention of fat embolism includes: prevention of injury in high-risk patients, timely and correct immobilization of the limb in case of injury, early surgical stabilization of pelvic and tubular bone fractures, stabilization of bone fragments, adherence to infusion therapy techniques.

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Fat embolism refers to the blockage of blood vessels by droplets of fat. As a rule, this is the fat of one’s own body, as an exception - foreign fat, introduced into certain organs of the body for diagnostic or therapeutic purposes as a solvent for medicinal or contrast agents, for example, during radiography (bladder, renal pelvis, etc.).

The overwhelming majority of fat embolisms occur due to trauma accompanied by damage to long tubular bones. In fact, every injury of this kind produces a fat embolism, although most often “silent”, i.e. "non-clinical", and therefore non-lethal form.

According to various authors, cases of fatal fat embolism due to gunshot injury are 1-2%. In routine surgical practice, severe forms of fat embolism account for about 1.5% of all operations; Among all fat embolisms, deaths do not exceed 1.3%.

From the above data it follows that the “non-clinical” form of fat embolism is an almost constant background of any injuries, surgical and military-traumatic, while fatal and severe ones, i.e. clinical cases are rare. At the same time, with gunshot trauma, severe forms are observed 2-3 times more often than with surgical or orthopedic trauma.

The increase in deaths from fat embolism in military trauma is associated with modern military technology; Of particular importance are numerous injuries to the limbs and the compressive effect of explosions that shake certain fat depots of the body, not to mention the nature of the wounds and the conditions of transportation of the wounded.

The main danger with regard to the development of fat embolisms is bone damage, especially in people after 25-30 years of age, when the bone marrow of the tubular bones mainly becomes fatty. With age, the danger of these embolisms increases even more, as fat becomes more fusible (a relative increase in liquid oleic acid in the composition of fat) and its total mass in the bones increases due to atrophy of the cancellous beams.

The danger of developing fat embolisms during gunshot fractures, especially in the diaphysis of long tubular bones, has also increased in recent wars because the living force of projectiles has sharply increased. Therefore, the semi-liquid bone marrow of the diaphyses is destroyed by hydrodynamic explosive action over a much larger area than the bone itself.

Indeed, with shrapnel wounds, fat embolism occurs 3-4 times more often than with bullet wounds (Yu. V. Gulkevich). This can be associated with the greater living force of the fragments, with their intense concussion and compression effect on such delicate tissue as adipose tissue.

However, the appearance of drops of free fat in the fatty tissue is observed not only when injured or crushed. There are observations that severe shock to the skeleton or fat depots without visible histological changes in them can also cause fat embolism. This is proven by the occurrence of fat embolism in a fall from a height that does not result in fractures, as well as in a fall on the stump without bone damage. Fat embolism can also develop with very minor injuries to the bone marrow, for example during punctures for diagnostic purposes.

For the occurrence of fat embolism, the location of the damage is important. The largest number of fatal fat embolisms is observed with injuries to the tibia and pelvic bones.

The nature of the damage also matters. The largest number of embolisms are caused by closed injuries. This is explained by the fact that with such injuries, free fat ends up in confined spaces and under pressure, which facilitates its entry into the veins.

Clinically and anatomically, the vast majority of fat emboli are of mild or moderate intensity and are therefore neither a cause of death nor significant functional impairment. This is evidenced by mass materials relating to peacetime injuries and wounds.

Thus, it is known that fat embolism can be observed after childbirth (compression of the pelvic tissue), after surgical operations (outside the bones), after bone resection, some orthopedic procedures, after burns, severe body cramps, i.e. without any external trauma. Most often, such cases are clinically even elusive.

As for fat embolism in burns, it does not seem to be a rare phenomenon.

The comparative rarity of fatal fat embolism in gunshot wounds is partly explained by the fact that fat embolism does not have time to develop into a leading complication and is “overtaken” in importance by other causes of death - such as shock, bleeding, etc.; in addition, fatal forms of fat embolism most often occur as a delayed complication (see below).

K l a s i f i k a c i a . Depending on the moment of injury, fat embolism can be immediate (ultra-early), early and late, i.e. slow or delayed.

By immediate, or very early (apoplectiform), fat embolism we mean cases when the moment of embolism almost coincides with the moment of injury; they are separated, for example, by a few seconds or minutes. If several hours pass between the onset of embolism and injury, then such embolism can be called early. If this period extends to several days or weeks, then such cases are classified as late (slow or delayed). Very early and early forms are typical for injuries of the subcutaneous tissue, late forms are mainly associated with bone fractures.

Very early and early forms of fat embolism are usually embolisms of the small circle only. Such emboli, being massive, can be fatal. However, in the vast majority of cases, pulmonary emboli are either a transient symptom or they are asymptomatic (“non-clinical forms” of fat embolism).

It is therefore clear that very early and early embolisms always turn out to be embolisms of the small circle, regardless of whether the embolism was the cause of death or a concomitant, random phenomenon.

Delayed forms of fat embolism mostly cover not only the small, but also the systemic circulation.

K l i n i h e s k a p t i n a fat embolism is varied, which depends on the amount of fat simultaneously entering the vessels from the traumatic focus, on the total duration of the embolism, i.e. from repeated embolisms, often following one after another at various intervals. The first or small amounts of fat may be completely imperceptible, especially in healthy and strong people with normal heart and lung activity.

Classic cases of pulmonary embolism are characterized by a picture of acute pulmonary failure and asphyxia. These phenomena are usually observed when 2/3 to 3/4 of the vessels of the small circle are blocked. Sometimes the clinical picture is close to that of shock.

In longer-lasting cases of fat embolism, symptoms of pulmonary edema and pneumonia are observed.

E m b o l i n g a l o g o c p u g a (Fig. 83) is the first and, for the most part, the only result of fat resorption from the lesion. In non-mortal cases, fat is partly eliminated through the airways, and partly undergoes breakdown during the process of lipodyeresis, an inherent function of the lungs.

In the sputum you can sometimes see blood, as well as drops of fat. Typically, fat appears in sputum no earlier than 25-30 hours from the moment of injury.

Some of the fat that enters the lungs is absorbed by the lymphatic system and penetrates the lymph nodes of the mediastinum.

E m b o l i y b o r sh o g o k p u g a, as a rule, is the second stage, i.e. further development of fat embolism.

The bulk of fat that falls into the large circle should therefore be considered as fat that has passed through the small circle. Such passage is ensured, on the one hand, by the physical properties of fat as a liquid, as well as by the distensibility and abundance of capillaries in the small circle, and on the other hand, by respiratory movements, during which, as is known, the lumens of the arterioles of the lungs undergo significant rhythmic expansion. The arteriovenous connections of the small circle, which open compensatoryly during sequentially layered embolisms, may also have some significance. The significant diameter of these connections (about 30 μ) ensures the passage of relatively large drops of fat and air bubbles (in case of air embolism) through the lung.

Rice. 83. Fat embolism of the lung. Death 3 days after injury.

Fat brought into a small circle can itself cause spastic contraction of the blood vessels of the lungs. At the same time, this fat cannot be artificially pushed into a large circle with the help of amyl nitrite [Far (Th. Fahr)], nor can it be emulsified, for example, by introducing bile salts, decholine, gardinol and other fat emulsifying agents.

The intensity of the embolic process in the organs of the large circle is associated with the intensity of their arterial blood supply (massive embolisms of the brain, kidneys, heart, on the one hand, and individual drops of fat in the liver, on the other), as well as the caliber and abundance of capillary systems (brain, skin) . Of great importance are the reflex influences from the embolized vessels of the small circle on the vessels of the organs of the large circle. Thus, with experimental fat embolism of the small circle in rabbits, it is often possible to obtain an embolism of the coronary arteries of the heart in the order of the pulmonary-coronary reflex with the development of microinfarctions.

It is hardly fair to say that fat, unlike air, does not cause spasms and that this is why drops of fat often float freely in the blood mass, while air bubbles are tightly enveloped by the wall of the vessel. Microscopic examination of embolisms in humans does not allow us to establish such a pattern.

The presence of an open oval window can contribute to the spread of fat into the greater circle. However, this factor is of limited importance.

With large fat embolisms, symptoms of brain failure and cardiac weakness occur due to the corresponding localization of the embolism. Fat embolisms of the central nervous system are especially dangerous. Signs of renal failure are usually not observed. Lipuria, i.e. The presence of fat in the urine is rare with fat embolism. Fat in the urine may disappear and reappear. Detecting it presents some difficulties, since fat droplets in the bladder are located on the surface and cannot be detected until all the urine has been released from the bladder. It is recommended to keep the resulting urine in the cold. Then collect its surface layer and stain it for fat.

No matter how the symptoms develop from the organs of the large circle (brain, heart, kidneys), one or another disorder of the lungs often serves as an important background for it.

Other symptoms of fat embolism include increased temperature (apparently of central origin, sometimes in connection with pneumonia), petechial rashes on the skin and mucous membranes. Petechiae of the shoulder girdle and upper torso are especially characteristic.

The occurrence of fat embolism and the severity of its course are somewhat influenced by age, the development of the skeletal system and bone marrow, as well as general health, in particular heart and lung disease.

In case of heart disease, blockage of a significant number of capillaries of the small circle does not allow the weakened heart to overcome this obstacle with sufficient speed, and then expansion and paralysis of the heart occurs before the fat moves into the system of the large circle by the force of heart contractions. Therefore, fat embolism of the large circle is observed mainly in strong and healthy young people.

At the same time, it is known that even large amounts of fat in the blood (in diabetes, for example, up to 20% instead of the normal 0.6-0.7%) never cause fat embolism, since the drops of fat in such lipemia are very small (in 1000 times smaller than an erythrocyte), having the character of “chylomicrons”, unable to merge into large drops. But if such a fusion occurred to some extent, it would not increase the danger of embolism, since fat globules up to 10-12 μ in diameter can still freely pass through a small circle. For the same reason, the experiment fails to induce fat embolism using milk. In other words, for the development of fat embolism, it is important not just an increase in fat in the blood, but its presence in the form of droplets of a certain size, i.e. the emulsion state and the total mass of fat.

The emulsion state of fat in the blood can change significantly both due to the fragmentation of droplets and as a result of the merging of small droplets into larger ones. This has a direct bearing on fat emulsions that are not stabilized by protein films (as seen in milk fat globules) to prevent droplets from coalescing.

Under pathological conditions, the emulsion state of blood fat can be significantly disrupted due to a slowdown in blood flow when the physicochemical constants of fat emulsifiers change, for example, during ether or chloroform anesthesia, when dead tissue histamine enters the blood, which easily destroys fine fat emulsions. In conditions of severe trauma, all of the above factors, such as circulatory disorders, absorption of histamine-like compounds from the lesion, operations under anesthesia, are present more or less constantly. A number of authors see the leading factor in the pathogenesis of fat embolism in the inactivation of blood fat emulsifiers, and not in fat from fat depots (see below).

Pathological diagnosis of fat embolism is macroscopically difficult. The issue should be resolved after microscopic examination, mainly of the lungs, brain, kidneys and heart.

When examining the blood of the pulmonary artery, flecks of fat are sometimes found in it; When pieces of lung are treated with potassium alkali (2% solution), droplets of fat appear on the surface of the liquid. You can perform a blood test in a dark field.

Acute swelling, sometimes edema, as well as the presence of acute pneumonic foci in the lungs, sometimes with suppuration, may be of some importance in recognizing fat embolism.

In the brain there is some smoothing of the convolutions, indicating an increase in intracranial pressure. There are scattered small hemorrhages here and there. Gray and white matter are affected equally frequently.

Rice. 84. Fatty decomposition of the myocardium at the site of fat embolism.

In the clinic, the diagnosis of fat embolism is very often not established when its presence is undeniable. Often, clinicians’ assumptions are directed in a completely different direction - they talk about shock, air embolism, apoplexy, etc. A true idea of ​​the frequency of fat embolism, its varieties and organopathological relationships can only be gleaned from a systematic histological examination of the organs of those who died from trauma .

The histological picture of fat embolism consists of two closely related points: blockage of arterioles and capillaries with fat and degenerative-necrobiotic changes in the surrounding tissues (Fig. 84).

In the lungs, the bulk of the fat completely fills the lumens of large sections of arterioles and capillaries; There is especially a lot of fat in the areas of branching vessels. The droplet state of fat freely floating in the blood is relatively rare. This indicates a dense blockage of the vessels (see Fig. 83), as well as increased resistance for the right heart, since the transformation of spherical drops of fat into elongated cylinders suggests a closer fit of the embolus to the vessel wall due to the continued action of surface forces tending to remove the embolus from states of deformation, i.e. give it the shape of a ball again.

The force of throwing fat causes not only the deformation of the drops, their pressing into the vessels, but also the fragmentation of large drops. The same force is probably of great importance for the passage of fat droplets through the capillary network. At the same time, the close contact of fat drops with the wall of the vessel gives rise to a reflex spasm: it is known that arteries and arterioles respond to any attempts to cause their acute expansion mechanically with a spastic contraction. Apparently, this contraction of arterioles at the site of their blockage is one of the reasons for the tight compression of fat droplets in the lumen of the vessel. It can also serve as an additional obstacle to their advancement into the capillaries until the spasm is resolved.

Changes in the brain and spinal cord such as purpura are usually observed no earlier than two days after the injury. This also applies to the so-called annular hemorrhages, which are peculiarly constructed microinfarctions of the brain: in the center of the hemorrhage lies a vessel, closed either by droplets of fat or by a hyaline thrombus; further to the periphery there is a zone of necrosis, behind which there is the hemorrhage itself.

B kidney X The main site of damage is the glomeruli and afferent arterioles. The unevenness of damage to the glomeruli is associated with the intermittent nature of blood circulation in individual nephrons, with their different functional state at the time of embolism (working and reserve glomeruli). The last thing you have to think about is freeing the glomeruli from fat, since it is not possible to detect fat in the tubules or in the lumens of the glomerular bursae. This is consistent with the fact that lipuria occurs rarely, although in the literature there are persistent indications that fat is secreted by the kidneys.

B m i o k a p d e fat in the arterioles and capillaries is distributed unevenly. In places of greatest blockage, foci of fatty decomposition of varying sizes are found (see Fig. 84) and typical micromyomalacia, sometimes with a marginal zone of leukocytes. This focality of fatty degeneration corresponds to the picture of a “tiger” heart at autopsy. Fragmentation of the myocardium, hemorrhages along the conduction systems of the heart, and retrograde embolism of the venous system of the heart coming from the coronary sinus are also observed. With pulmonary embolisms, such emboli transport through the veins of the heart becomes possible not only because the pressure in the right heart increases sharply, but also due to the fact that the pressure in the left heart, in particular in the coronary arteries, decreases. The role of conductors of fat in these conditions is apparently played by the Vabesian vessels, which open into the right heart.

B p e h e n and the fat content is the lowest, which is affected by the anatomical features of the blood supply to the organ. Drops of fat in the vessels of the liver are usually small and free; therefore, they are not so much in the nature of emboli, but rather in the nature of chylomicrons, freely transported through the bloodstream and reflecting either the fact of fragmentation, i.e. emulsification of fat from primary emboli of the small circle, or the fact of colloidal instability of plasma lipoids, their mobilization. A significant portion of fat is absorbed by Kupffer and liver cells.

Fat can also be found in the vessels of the spleen, skin, mucous membranes, and endocrine glands, such as the pituitary gland. These findings are accompanied by petechiae.

In the histological picture of fat embolism, attention is drawn to the absence of any significant reactive processes. On the one hand, this indicates the recent occurrence of embolism, on the other hand, the non-toxicity of emboli, which represent a purely physical and mechanical factor, and, moreover, not foreign in biochemical terms.

The significant freshness of the changes in the organs also suggests that fat embolism of the small, and even more so of the large circle, if it is massive enough, leads to very significant disruptions in the vital functions of the organs.

The presence of inflammatory foci in the lungs during fat embolism can be explained by the fact that the lungs are primarily exposed to the most massive embolism. The ischemic, or infarct-like, foci that arise after some period of time can undergo decay and suppuration, and, moreover, early, for example, 1-2 days after the injury.

With fat embolism, two phases of the process are observed: first, small circle embolism occurs, and then large circle embolism. There is a description of only isolated cases of selective fat embolism of the large circle with an open foramen ovale.

The presence of the second phase also implies damage to the lungs. Histological examination of fat embolism confirms that practically without a small circle embolism a large circle embolism cannot occur (Yu. V. Gulkevich and V. N. Zamaraev). On the contrary, a small circle embolism may not be combined with a large circle embolism.

Preferential damage to the lungs may also be due to the fact that the average blood pressure in the pulmonary circulation is less than, for example, in the brain or kidneys; That is why the introduction of labeled fat even into the carotid arteries, into the portal vein still gives preferential pulmonary embolism. A fundamentally new point of view has also been put forward, pointing to a reduction in the activity of heparin (normally produced mainly by the lungs), which can clarify lipemic plasma, i.e. change the emulsion state of fat.

M e X a n i z m f i p o v o y e m b o l i has its own characteristics. Let us consider separately: the formation of free fat in the area of ​​injury, the moment of fat resorption, small circle embolism and large circle embolism.

The formation of free fat in the area of ​​injury is directly related to the disruption of the integrity of adipose tissue. The resulting droplets of fat partially merge with each other, float in the mass of spilled blood, without mixing with it and without forming an emulsion. High temperature also acts similarly to injury, at which both melting of fatty tissue and rupture of capillaries can be observed.

Free fat can remain in the lesion for a significant period of time without being affected by tissue lipase. This action eventually comes; Then, in the process of fat hydrolysis, fatty acids and soaps appear, which irritate the tissue and which, if resorbed, turn out to be quite toxic.

Free fat has the properties of a liquid that can take on different shapes in vessels (spherical, cylindrical), and also penetrate into the thinnest capillary vessels, closing them. It was indicated that fat can pass through a small circle. Massive droplets, for example over 10-15 μ, are unlikely to reach a large circle, unless one takes into account the presence of an open foramen ovale and the arteriovenous connections in the lung, which have a diameter of about 30 μ. The droplets in the resorption focus itself and in the small circle range in size from several microns to 1 cm.

Particles of crushed tissue, such as cells and even small pieces of bone marrow in case of bone fractures, are easily mixed into the mass of fat. In other words, fatty embolism of the lungs in conditions of trauma has every chance of being simultaneously a parenchymal cell embolism, not to mention the accidental entry of foreign bodies into the vein.

Absorption of free fat occurs through lymphatic vessels, but mainly through veins. With fractures and especially crushed bones, the lymphatic pathways are usually blocked and the venous pathways open wide.

It has long been noted that the classic patterns of fat embolism do not develop immediately after injury, which is so typical, for example, for air embolism, but after some time (“light interval”). This period can cover both hours and days.

An explanation for this circumstance should be sought, on the one hand, in local factors relating to the area of ​​injury, and on the other hand, in general factors regulating blood, in particular venous, pressure, colloidal stability of plasma lipids, sufficiency of heparin, etc.

Local factors promoting fat resorption are as follows. In case of a fresh injury, masses of liquid and coagulated blood, together with scraps of tissue and leaked fat, fill the resulting spaces, in particular the entire wound canal and all its slit-like branches. These masses

being in a confined space, together with the applied bandage, they exert significant pressure on soft tissues, including bleeding vessels. As is known, stopping bleeding occurs mainly due to such pressure. Due to the equalization of pressure inside and outside the vessels, bleeding stops, primarily from the veins, even if, due to their anatomical structure, they are incapable of collapse (for example, bone marrow veins).

This entire “balanced” system can be easily disrupted, for example, by changing the dressing, changing the ratio of soft and dense tissues, muscle tone during transportation, during traction, etc. As a result of this, significant movements of liquid and dense contents are possible, and in some places they open again the lumens of damaged veins, even if they were covered with blood clots. It is obvious that accidental contact of such veins with a fatty bloody mass can lead to absorption of the latter and embolism, especially since the newly applied bandage, as well as newly emerging hemorrhages at the site of injury, will increase the pressure and thereby promote the movement of liquid fatty masses along the line of least resistance , i.e. into gaping veins. Due to the fact that the specific gravity of fat is less than one, the accumulated masses of fat will always be located in the superficial (peripheral) parts of the injury area along the line of contact of the liquid contents of the Canal with its wall. Obviously, the masses of fat will be absorbed first of all. This will also be facilitated by boundary tension forces and the relatively low viscosity of fat.

There are observations that the coagulated mass of blood in a fresh bone wound in the first hours does not contain any significant amount of liquid blood and fat. Only with repeated punctures is fat found in the form of free masses. This circumstance also, to a certain extent, explains the comparative frequency of delayed fat embolisms.

Among the general factors contributing to the development of fat embolism, it should be taken into account that as the patient recovers from a serious condition associated with bleeding, shock, cooling, etc., the activity of the heart improves, blood pressure increases, local spastic phenomena at the site of injury decrease , and the veins, slightly collapsed, to some extent only compressed and communicating (through damaged walls) with masses of fat and blood, fill up and begin to conduct blood again. However, filling the venous system in the area of ​​injury may be insufficient due to damage to the arteries and capillary systems. Then the venous pressure easily becomes negative, and a deficiency in the filling of the veins occurs, which, in the presence of gaping holes in their walls, contributes to the flow of fluid accumulated in the wound cavity into the veins.

Consequently, the mechanism of resorption of bloody masses from the lesion has much in common with what is observed in air embolism: both here and there there is a suction effect of veins that are not sufficiently filled naturally.

There are other possible interpretations of the late occurrence of fat embolisms, especially when large bones are crushed. The restoration of general blood circulation in a wounded person, which occurs, for example, after providing first aid, is accompanied by an increase in arterial and venous pressure in the area of ​​injury. At the same time, a fresh wound channel can be conditionally considered as communicating with the arterial and venous systems. Experiencing pressure from the bandage and surrounding tissue, this channel is relatively stable in volume, as is the hematoma filled with free fat that fills it. An increase in blood pressure, accompanied by additional hemorrhage, leads to an increase in pressure in the canal cavity, i.e. to the appearance near the mouth of veins opening or for some reason opening into the wound with a pumping force (vis a tegro). Under these conditions, fluid from the canal cavity will move in the direction of weakly positive, and at times negative, pressure in the draining veins. Such negative pressure can be associated, for example, with the act of breathing, heart contractions, or displacement of the wounded limb to the upper level. p.Fat embolism is almost inevitable under these conditions.

It is obvious that an increase in pressure in the wound canal can be caused by such manipulations as changing dressings, traction, transport trauma, and sometimes associated with additional hemorrhages into the canal, contraction of the muscles surrounding the canal, etc.

Of greatest importance are rapid and massive fat resorptions that occur over a short period of time, as well as repeated resorptions, even if they are separated by a short interval. Massive, but very prolonged fat emboli are also included in the group of “concomitant”, i.e. not related to causes of death.

According to experimental observations, animals can tolerate injections of huge doses of fat if they first and repeatedly receive small portions intravenously. Perhaps this is due to the fact that preliminary microembolism removes or softens the severity of the above-mentioned reflex reactions in the form of widespread vasospasm characteristic of embolism.

The amount of fat that causes a fatal fat embolism in humans is not known. According to literature data, it ranges from 12 to 120 cm 3. Casuistic observations indicate the possibility of fatal fat embolism in humans with the resorption of several cubic centimeters of fat.

Experiments on dogs have shown that the amount of fat that causes death is twice (and according to some authors, four times!) the total amount of fat contained in the femur.

For a rabbit, the minimum lethal dose of fat is 0.9 cm 3 per 1 kg of weight (this amount is assumed to be administered at a time). A mouse can tolerate intravenous administration of olive oil in a volume of 3 cm 3 per 1 kg of weight.

The given variety of figures says little about observational errors. There is no doubt that different animals and humans have unequal endurance in relation to mechanical blockage of small vessels (fat, air, etc.), and this endurance is associated not only with the structure of the vascular system of the lungs, but also with the activity of the heart. It is obvious, for example, that for a seriously wounded person who has experienced blood loss, and perhaps shock, and is therefore in conditions of low blood pressure, the question of the dose of fat acquires only relative importance. Under these conditions, even very small doses of fat can have serious consequences, being, as it were, the last link in the general chain of functional disorders that accompany a serious injury.

It is also a mistake to transfer experimental data obtained with vegetable oil to embolism with natural fat in the bone marrow or fiber of the same individual.

The inconsistency of data regarding the pathogenesis of fat embolism is apparently associated with the underestimation of some additional physiological factors and the overestimation of purely mechanical concepts, reducing the issue to the physical release of tissue fat, to its transport from the site of injury and to mechanical blockage of blood vessels.

Similar experiments were carried out with lycopodium spores [Fahreus 1960].

As early as 1927, Lehman and Myp questioned the origin of fat in embolism from fat depots, given the observation that even the entire mass of fat contained in the femur was not sufficient to cause a fatal embolism. In their opinion, the main role belongs to special products of tissue breakdown in the area of ​​injury. These products change the solubility of plasma fats, i.e. e. colloidal state of lipoids, which become the source of large fat aggregates that clog blood vessels. LeQuere and Shapiro et al. (1959) showed that embolic fat contains at least 10% cholesterol; that is why this fat gives birefringence and a positive Schultze reaction. Fat depots contain only about 1% cholesterol. This suggests that embolic fat does not only come from the site of injury. The same authors indicate that fat embolism can occur without trauma, for example, during inhalation anesthesia, decompression, decompression sickness, administration of hemolytic agents, and bleeding. In rabbits subjected to decompression, there is a noticeable increase in serum lipoids B IN CONNECTION with a decrease in the activity of heparin, which has the property of moderating the amount of lipoids, i.e. clear lipemic plasma. At the same time, the mobilization of lipoids in the plasma increases, and their metabolism becomes insufficient. According to these authors, fat embolism, therefore, consists in the inactivation of fat emulsifiers, in the occurrence of colloidal instability of lipoids, and perhaps in insufficient production of endogenous heparin by the lungs themselves.

The provisions put forward deserve attention. At the same time, they do not refute either the significance of the injury or the entry of free fat into the bloodstream, i.e. moment of mechanical blockage, which is often leading in pathogenesis.

P I H I N O Y C m e p t and with fat embolism is either pulmonary failure or failure of vital organs of the large circle (brain, heart).

It is incorrect to reduce the degree of danger of fat embolism and the cause of death with it only to the mass of fat trapped in the small circle, i.e. to the number of clogged vessels. Reflex-spastic phenomena associated with irritation of the hemo- and vasoreceptors of the lung, with the possible irradiation of these irritations to nearby (mainly the heart) and distant organs, are of enormous and at the same time individual importance.

The experiments of A. B. Fokht and V. K. Lindeman (with the introduction of lycopodium), later experiments of L. Kozhin and N. A. Struev (embolism with killed anthrax bacilli) showed the leading importance of reflex effects on the heart, blood pressure, respiration, on the own vessels of the lungs. In N. A. Struev’s experiments with embolism of pulmonary vessels under conditions of removal of irritation from the vagus nerves (when they were cut), animals tolerated the embolism much easier.

In practice, pulmonary failure is soon combined with heart failure, because the presence of fat in the blood of the pulmonary circle leads to an increase in its viscosity, which, in addition to the very fact of massive blockage and spastic contractions of blood vessels, creates insurmountable resistance to the driving force of the right heart. The flip side of the same phenomena will be insufficient blood supply to the left heart, myocardial hypoxemia. In other words, heart failure during fat embolism is always of great, and in some cases, for example, with coronary artery embolism, of leading importance.

Fat embolism can occur not only in direct connection with injury. Fat in quantities that cause death can be absorbed from hollow organs, such as the bladder, or from body cavities when administered for therapeutic or diagnostic purposes.

Spontaneous fat embolism is observed with severe fatty liver, for example, with fatty cirrhosis of pellagriks, alcoholics, with choline deficiency, etc. Droplets of fat, merging, form fatty “cysts”, and when liver cells are destroyed, they enter the blood and are carried into the lungs, without causing any special clinical consequences. It is possible that the release of such microemboli into a large circle, in particular into the vessels of the brain, underlies some mental disorders in this category of patients.

Topic of the lesson. CIRCULATION DISORDERS. THROMBOSIS. EMBOLISM. INFARCTION. DISSEMINATED INTRAVASCULAR BLOOD COLOGTING (DIC SYNDROME)

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.

Every person is prone to skeletal bone injuries. Each of them requires immediate treatment, otherwise the development of complications cannot be ruled out. One of these pathologies is fat embolism, which has its own specific characteristics, types and methods of therapy.

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 the disorder 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.

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