Fat embolism is a multiple occlusion of blood vessels by lipid globules. It manifests itself in the form of respiratory failure, damage to the central nervous system, the retina of the eye. The main symptoms include headache, encephalopathy, floating eyeballs, paralysis, paresis, chest pain, shortness of breath, tachycardia. The diagnosis is made on the basis of the clinical picture, the presence of predisposing factors in the anamnesis and the detection of large lipid particles in the blood. Specific treatment includes ventilators, fat desemulsifiers, anticoagulants, glucocorticosteroids, sodium hypochlorite. In addition, non-specific therapeutic measures are carried out.
Fat embolism (FE) is a severe complication that develops mainly with damage to long tubular bones as a result of blockage of vascular pools by lipid complexes that have entered the bloodstream. The frequency of occurrence ranges from 0.5-30% of the total number of trauma patients. It is usually diagnosed in patients aged 20-60 years. The minimum number of embolisms is registered among people who have been injured while intoxicated. The mortality rate is 30-67%; this indicator directly depends on the severity and type of damage, the speed of medical care.
Reasons of fat embolism
The essence of the pathological process is the obturation of blood vessels by drops of fat. This leads to a violation of blood flow in important structures of the body – the brain and spinal cord, lungs, heart. Among the conditions that can cause FE are:
- Injury. The main cause of lipid embolism is fractures of the diaphysis of the femurs, tibia, and pelvis. The risk of developing pathology increases with volumetric and multiple injuries accompanied by bone crushing. It is believed that pathology occurs in 90% of people with injuries of 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, damage to a large volume of subcutaneous fat.
- Shocks and post-resuscitation illness. Emboli formation occurs with shocks of any origin in 2.6% of cases. The reason is an increase in catabolic processes, a metabolic storm. Symptoms often develop by the end of 2-3 days after the patient is brought out of critical condition.
- Intravenous administration of oil solutions. Cases of iatrogenic origin of the disease are isolated. Fat occlusion occurs due to exogenous fats that have entered the bloodstream due to erroneous actions of a medical professional. In addition, fat embolism is sometimes diagnosed in athletes using synthol to increase muscle mass.
- Hypovolemia. With severe hypovolemia, an increase in hematocrit occurs, the level of tissue perfusion decreases, stagnation 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, excessive intake of diuretics.
According to the classical theory, a fat embolism is the result of a direct hit of bone marrow particles into the bloodstream at the time of injury. Further, globules with blood flow spread in the body. When the particle size is >7 microns, they cause blockage of the pulmonary arteries. Small drops of fat bypass the lungs and penetrate into the circulatory network of the brain. There is a cerebral symptomatology. There are other assumptions about the mechanisms of development of the process.
According to the proponents of the biochemical theory, plasma lipase is activated immediately upon injury and after it. This becomes an incentive for the release of fats from the deposit sites, hyperlipidemia develops, coarse fat droplets form. The colloidal-chemical version is that the desemulsification of fine emulsions begins due to the slowing of blood flow in the affected area.
It follows from the hypercoagulation theory that the cause of the formation of fat droplets is a microcirculation disorder, hypovolemia, oxygen starvation. Lipid globules with a diameter of 6-8 microns are formed, which form the basis for disseminated intravascular coagulation. The continuation of the process is systemic capillaropathy, which leads to fluid retention in the lungs and endointoxication by lipid metabolism products.
Classification of fat embolism
Fat embolism can occur in a pulmonary, cerebral or mixed form. The respiratory form develops with predominant occlusion of the branches of the pulmonary artery and manifests itself in the form of respiratory failure. The cerebral variety is the result of blockage of the arteries and arterioles that provide blood supply to the brain. The mixed form is the most common and includes signs of both pulmonary and cerebral lesions. The period before the first symptoms appear varies widely. According to the time of the latent interval , the following forms of the disease are distinguished:
- Lightning fast. Manifests itself immediately after the injury, is characterized by a critically rapid course. The patient’s death occurs within a few minutes. Mortality in this type of embolism is close to 100%, because it is impossible to provide specialized care in such a short time. It occurs only with multiple or massive injuries. The frequency of occurrence is no more than 1% of cases of FE.
- Spicy. Occurs in less than 12 hours from the moment of 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, extensive ischemic stroke.
- Subacute. It manifests itself 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 when signs of embolism developed after 10-13 days. The course of subacute forms is relatively easy, the number of deaths does not exceed 20%. The chances of survival increase if the signs of the disease develop while the patient is in the hospital.
Symptoms of fat embolism
Pathology is manifested by a number of nonspecific symptoms that can occur in other conditions. Occlusion of the pulmonary vessels leads to a feeling of tightness in the chest, pain behind the sternum, anxiety. Objectively, the patient has shortness of breath, cough, accompanied by hemoptysis, foaming from the mouth, pallor, sticky cold sweat, anxiety, fear of death, acrocyanosis. There is persistent tachycardia, extrasystole, compressing pains in the heart. Possible development of atrial fibrillation. 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. There may be aphasia, apraxia, anisocoria. The picture resembles that of a traumatic brain injury, which makes diagnosis much more difficult. It is possible to develop paralysis, paresis, there is a local loss of sensitivity, paresthesia, a decrease in muscle tone.
Half of the patients have petechial rash in the armpits, on the shoulders, chest, back. This usually occurs 12-20 hours after the appearance of signs of respiratory failure and indicates overgrowth of the capillary network by emboli. When examining the fundus of the patient, 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 with fatty acids. Traditional antipyretic drugs are ineffective at the same time.
Care for patients with FE should be provided in the first minutes after the development of signs of vascular occlusion. Otherwise, a fat embolism leads to the development of complications. Respiratory failure ends with alveolar edema, in which the pulmonary vesicles are filled with fluid sweating from the bloodstream. At the same time, gas exchange is disrupted, the level of blood oxygenation decreases, metabolic products accumulate, normally moving away with exhaled air.
Obturation 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 are overloaded. In such patients, arrhythmia, fluttering 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. It is possible to prevent such a development of events only with the fastest possible assistance.
An anesthesiologist-resuscitator, as well as consulting doctors: cardiologist, pulmonologist, traumatologist, ophthalmologist, radiologist take part in the diagnosis of embolisms of lipid origin. Laboratory research data play a significant role in making the correct diagnosis. FE has no pathognomic signs, so its lifetime detection occurs only in 2.2% of cases. The following methods are used to determine pathology:
- Objective examination. The 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, large-bubbly wheezes are heard in the lungs. The SP2 index does not exceed 80-92%. Hyperthermia within febrile values.
- Electrocardiography. The ECG shows a deviation of the electrical axis of the heart to the right, non-specific changes in the ST segment. The amplitudes of the P and R teeth increase, in some cases there is a negative T wave. Signs of blockade of the right leg of the Gis beam may be detected: expansion of the S wave, a change in the shape of the QRS complex.
- X-ray. Diffuse infiltrates of the lung tissue on both sides, predominant on the periphery, are visible on the radiographs of the lungs. The transparency of the pulmonary background decreases as the swelling increases. There may be a fluid level indicating the presence of pleural effusion.
- Laboratory diagnostics. The detection of lipid globules in plasma with a size of 7-6 microns has a certain diagnostic value. It is preferable to take biomaterial from the main artery and central vein. The study of media from both basins is carried out separately. Detection of globules increases the risk of occlusion, but does not guarantee its occurrence.
Differential diagnosis is performed with other types of embolisms: air, thromboembolism, vascular obstruction by a tumor or a foreign body. A distinctive feature of FE is the presence of microdrops of fat in the blood in combination with the corresponding radiological and clinical picture. In other types of vascular occlusion, lipid globules are absent in the blood.
Treatment of fat embolism
Therapy is carried out by 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 non-specific:
- Specific. They are aimed at deemulsification of fats, correction of the coagulation system, ensuring adequate gas exchange. For the purpose of oxygenation, the patient is intubated and transferred to artificial ventilation. To synchronize with the device, sedatives may be administered in combination with peripheral muscle relaxants. Restoration of the normal consistency of lipid fractions is achieved by using essential phospholipids. To prevent hypercoagulation, heparin is administered.
- Non-specific. Non-specific techniques include detoxification by 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 probe enteral.
The experimental method of treatment is considered to be the use of blood substitutes based on PFC compounds. The drugs improve hemodynamic parameters, restore normal rheological properties of blood, and help reduce the size of lipid particles.
Prognosis and prevention
In the subacute course, fat embolism has a favorable prognosis. Timely assistance allows to stop pathological phenomena, provide the necessary perfusion in vital organs, gradually dissolve emboli. In the acute variant of the disease, the prognosis worsens to unfavorable. The lightning-fast course leads to the death of the patient in almost 100% of cases.
Prevention during operations consists in the use of low-traumatic techniques, in particular percutaneous spoke osteosynthesis, performed in a delayed manner. It is recommended to abandon the use of skeletal traction, since this method does not provide a stable position of the fragments and can lead to the development of late embolization. Before hospitalization, it is required to stop bleeding as quickly as possible if it is present, adequate analgesia, and maintaining the blood pressure level at a normal physiological level. A specific method is the introduction of ethyl alcohol in a 5% glucose solution.