Patients with thromboembolism are placed in the intensive care unit. In an emergency, the patient undergoes resuscitation in full. Further treatment of pulmonary embolism is aimed at normalizing pulmonary circulation and the prevention of chronic pulmonary hypertension.
In order to prevent relapse of pulmonary embolism, strict bed rest is required. To maintain oxygenation, continuous oxygen inhalation is performed. Massive infusion therapy is performed to reduce blood viscosity and maintain blood pressure.
In the early period, the appointment of thrombolytic therapy is indicated with the aim of dissolving the thrombus as quickly as possible and restoring blood flow in the pulmonary artery. In the future, to prevent relapse of pulmonary embolism, heparin therapy is performed. With the phenomena of heart attack pneumonia, antibiotic therapy is prescribed.
In cases of the development of massive pulmonary embolism and the inefficiency of thrombolysis by vascular surgeons, surgical thromboembolectomy (removal of a thrombus) is performed. As an alternative to embolectomy, catheter fragmentation of thromboembolism is used. With recurrent pulmonary embolism, a special filter is practiced in the branch of the pulmonary artery, the inferior vena cava.
If there is a suspicion of pulmonary embolism, air or gas embolism, specific symptoms are concerned, it is necessary to consult a doctor in a medical institution. He will listen to complaints, examine the patient and prescribe a set of diagnostic procedures: magnetic resonance imaging and computed tomography of a diseased part of the body, radiography and pulse oximetry.
For the diagnosis of pulmonary embolism, air or fat, perfusion scanning and angiography, echocardiography can be performed. It is very important not only to establish the accuracy of the diagnosis, but also to find out the nature of the emboli, the cause of the appearance, in order to avoid relapse.
Upon completion of the examination, the doctor, based on the symptoms and severity of the disease, prescribes a course of treatment, developing it individually for each patient. In case of fat embolism, medications stimulating the dissolution of fat emboli, as well as glucocorticoids, cardiac glycosides and anticoagulants should be taken.
Air embolism is treated taking into account which site was damaged. If it is a limb, it must be fixed on a hill. When air has entered a vein, it should be aspirated with a syringe. Air embolism is treated in a pressure chamber. Also apply the installation of oxygen, infusion therapy. If the condition worsens, the patient needs to be moved to intensive care.
In the case of gas embolism, the patient needs to enter special drugs to restore vital signs of organs and lung function. In more severe cases, surgical intervention is required.
If the patient has pulmonary embolism, he needs to be hospitalized urgently, connected to a ventilator, and resuscitation is needed. Oxygen therapy and the use of drugs that break down emboli are also necessary for pulmonary embolism. But in most cases, pulmonary embolism requires surgery.
In the event of amniotic fluid embolism, hormones that restore the body’s functions must be taken. In severe cases, intensive care with transfusion of blood components and mechanical ventilation is needed. Since amniotic fluid embolism is a serious pathology during pregnancy, emergency therapy should be performed to eliminate this complication and save the life of the mother and child.
The first information on fat embolism appeared back in 1669. Scientists have described that the introduction of milk or fat into the vascular bed of animals leads to their death. In the 19th century, it was established that the main reason for its development is not trauma, but a source of fat entering the blood, bone marrow.
In the literature you can find a synonym – oil embolism. Causes of oil embolism:
- massive mechanical injuries with fractures of the long tubular bones of the limbs and pelvis;
- fractures of the sternum and ribs, including during artificial heart massage;
- acute pancreatitis;
- bone marrow transplantation;
- the introduction of fat-based drugs, intravenous nutrition with special lipid mixtures.
With the development of this condition, patients experience a feeling of tightness behind the sternum, severe anxiety, shortness of breath, discoloration of the skin, the appearance of small hemorrhages on the skin. If the embolus has entered a large circle of blood circulation, neurological symptoms progressively increase: confusion, cramps, eye symptoms, lethargy, up to a coma.
What is an air embolism? This is the ingress of air particles into the bloodstream. Most often, this type occurs in the vessels of the brain, which means that neurological symptoms come to the fore in the clinic. Causes of air embolism:
- open heart surgery;
- damage to large vessels of the neck and chest;
- getting into the vessel of air during intravenous manipulations.
The characters are neurological disorders by the type of paresis (usually unilateral), focal brain symptoms.
Its occurrence requires immediate medical attention, since there is a high risk of death.
Embolism of the vessels of the head of the brain Sudden occlusion of the cerebral vessel with an embolus, one of the pathogenetic variants of the development of ischemic stroke. Along with blockage of the vessel with an embolus, innervation disorders develop (vasospasm followed by vasoparesis), accompanied by cerebral edema, desolation of the capillary network in the pool.
When the reflex spasm disappears, the embolus can advance into the distal parts of the vessel, and then only the small cortical branches of the arteries turn off. The most common cardiogenic embolism in valvular heart defects, recurrent rheumatic endocarditis, subacute or bacterial endocarditis, myocardial infarction, during operations for heart defects, with cardiosclerosis, which occurs with atrial fibrillation and the formation of parietal thrombi, etc.
The nature of the emboli is different. These can be particles of altered heart valves, parietal thrombi and blood clots from the left atrium, pieces of decaying atherosclerotic plaques in case of atherosclerosis of the aorta or major vessels of the head, sometimes thrombi when the oval foramen of the interatrial septum is not closed, from the veins of the large circle of blood circulation (thrombosis veins of the abdominal cavity, pelvis).
In some cases, cerebral embolism occurs with malignant tumors, purulent processes in the lungs. Bacterial embolism can occur with endocarditis. Less common are fatty (in case of fracture of long tubular bones, in operations with large trauma to the subcutaneous tissue) and gas embolism (in lung operations, application of pneumothorax, and caisson work).
The clinical picture is characterized by the sudden onset of neurological symptoms. Often embolism develops in young people, usually in the afternoon; provoked by physical overstrain, stress. Short-term loss of consciousness is characteristic, epileptic seizures and transient sheath symptoms are often noted.
Sometimes at the same time embolism of the central retinal artery occurs with sudden blindness or the appearance of cattle. If the cause of a stroke is disseminated fat embolism, neurological symptoms are preceded by pulmonary symptoms (shortness of breath, cough, hemoptysis), which are caused by the appearance of fatty particles in the vessels of the lungs.
The nature of focal neurological symptoms is determined by the localization of cerebral infarction, which corresponds to the blood supply to the affected vessel. Embolism in the system of the internal carotid artery (compared with the vertebrobasilar system) is somewhat more common. Bibliogr .: Gusev E.I., Grechko V.E. and Burd G.S. Nervous diseases, M., 1988.
Fatty embolism of cerebral vessels in brain injury (ZhESM) is a mechanical blockage caused by the introduction of demulsified droplets of free fat with a diameter of more than 6 microns into the vessels of the brain. It is practically not observed in isolated TBI, but often occurs when it is combined with damage to other parts of the body, more often with fractures of long tubular bones.
The pathogenesis of fatty embolism of cerebral vessels has not been fully elucidated. The defeat of the capillaries of the brain with ischemia of the blood supply areas of the brain tissue occurs due to that part of the demulsified drops of fat that penetrates through the pulmonary filter into the large circle of blood circulation. Therefore, the clinic JESM manifests itself, as a rule, against the background of simultaneous damage to the lungs and often other organs and parts of the body, which determines the variability of the forms of JESM.
The clinical manifestations of JESM are based on the primary vegetative-stem symptom complex, which includes characteristic disorders of autonomic functions and a peculiar neurological symptomatology. This is due to the relatively selective defeat of higher vegetative centers due to the known features of vascularization of the hypothalamic region, compared with other areas of the brain.
The aggravation of the manifestations of brain pathology in patients with traumatic brain injury combined with extracranial injuries, taking into account the similarity of a number of neurological symptoms, needs to be differentiated between traumatic compression of the brain and ZhESM. Most of all, their clinic is brought together by the occurrence of consciousness disorders after the “bright interval”.
With traumatic compression of the brain, as a rule, it is possible to trace the gradual aggravation of consciousness disorders, increasing headaches in intensity, progressive, locally caused focal hemispheric symptoms and only the subsequent occurrence of stem symptoms, which are irreversibly increasing in severity.
The fatty embolism of the cerebral vessels is characterized by the suddenness of the occurrence of disorders of consciousness, ranging from mild forms of its disturbance (agitation or stunning with disorientation, delirium) to coma. Waviness and instability are possible, both in the manifestation of the depth of the change in consciousness, and in the entire symptom complex of multi-focal neurological disorders that were absent during the “bright interval” or joined the previously existing symptoms caused by brain injury.
With compression of the brain, there is a tendency to bradycardia, arterial hypertension, respiratory rhythm disturbances, subfebrile condition, with JESM – tachycardia, blood pressure drops, severe shortness of breath without respiratory rhythm disturbance, hyperthermia. For JESM, a displacement of the midbrain structures is uncharacteristic, with unilateral intracranial hematomas, as a rule, a shift of 4 mm or more is noted.
petechiae on the skin, mucous membranes of the oral cavity and eyes, traumatic retinopathy, detection of fat in the urine, sputum, enlarged drops of fat in the blood serum, helps to recognize JESM, but these phenomena usually appear after a day or more. The greatest difficulties in the diagnosis of fatty embolism of cerebral vessels arise in patients with combined TBI with a diencephalic form of a brain contusion or intraventricular hemorrhage, pleuropulmonary shock, massive blood loss, in which nonspecific embolism symptoms manifest themselves the killing of existing violations of vital functions can be explained by the severity of the established damage, and specific signs (petechial rash, fat in the urine, etc.
) are absent or do not have time to manifest. Prevention of fatty embolism of cerebral vessels in patients with combined TBI provides reliable immobilization of fractures of the extremities, avoiding relocation and nosocomial transport, the implementation of anti-shock measures. Treatment of fatty embolism of cerebral vessels should include measures to combat traumatic injuries with cerebral edema, hypoxia, impaired cardiovascular activity, ACS, mineral metabolism.
The use of drugs aimed at improving blood microcirculation, normalizing the dispersion of fatty particles (contrycal, heparin, lipostabil, decholine, etc.), antihistamines is shown. The prognosis in patients with combined TBI complicated by JESM is determined by the severity of the injuries, the form of the course of fat embolism, timeliness and completeness of therapeutic measures. With fulminant and acute forms of this complication, most victims die in the first 12 hours. after an injury.
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The clinical picture varies depending on the type and size of the affected vessel. If there is a violation of the outflow of blood along large peripheral veins, typical signs of thrombosis occur. The affected area swells, increases in size. When squeezing, severe pain is determined. The skin in the area of pathology is cyanotic, local hyperthermia occurs. A systemic reaction is moderate tachycardia, caused by the deposition of a certain volume of fluid and a decrease in bcc.
An air embolism of small branches of the pulmonary artery causes coughing, hemoptysis, episodes of syncope, shortness of breath over 20 breaths, tachycardia within 100-120 beats per minute. Hemodynamic disorders are absent. When blocking large trunks, a picture of an acute pulmonary heart develops. The patient has severe hypotension, swelling of the cervical veins, an increase in the size of the liver, an increase in CVP, psychomotor agitation, and an increase in cardiac impulse. The skin is pale, cold, covered with sticky sweat.
Damage to the coronary arteries leads to acute myocardial infarction. Typical pain behind the sternum of a compressive nature is noted. The use of nitrates does not give the expected effect. Blood pressure decreases up to shock figures. Possible pulmonary edema of cardiac origin. A typical picture of AMI is not always observed. In 40% of cases, the disease proceeds in an atypical version, manifested by pains in the abdomen, throat, left arm, etc.
Embolization of the blood supply structures of the brain causes a stroke. In the brain tissue, a focus of necrosis is formed, on the localization of which the clinical symptomatology depends. The most common signs of ischemic stroke include paresis and paralysis, a local decrease in muscle tone, paresthesia, speech disorders, blurred vision, dizziness, headache, impaired stability, drop attacks, weakening of skin sensitivity.
The elimination of the effects of air entering the vessels is performed using medical and hardware methods of treatment. The amount of help needed depends on the condition of the patient, the severity of the violation of vital functions, the availability of necessary equipment in the clinic. Typically, a remediation plan includes the following methods of exposure:
- Nonspecific medication. The treatment is aimed at minimizing the clinical signs of the disease and preventing complications. The patient is prescribed steroid hormones, cardiotonics, loop diuretics, vasodilators, antioxidants. At the recovery stage, multivitamin complexes and nootropic drugs are used. With severe respiratory failure, the patient is transferred to mechanical ventilation in the forced ventilation mode.
- Hardware Air embolism is treated with hyperbaric oxygenation and controlled hypothermia. HBO is carried out under a pressure of 2-3 atmospheres, the number of sessions varies from 5 to 12. The duration of each of them is 45 minutes. When using hypothermia, the patient’s body is cooled to 34 ° C. Both barotherapy and cold contribute to an increase in the solubility of gases in the blood, which makes it possible to destroy a blood clot inaccessible for removal by surgery.
- Operational. An optimal method for extracting an embolus during intracardiac EB is its aspiration through the subclavian catheter. In this case, several hundred milliliters of blood are removed, which may require massive infusion therapy or blood transfusion. With an accurate determination of the location of the embolus, an opening of the vessel or venous sinus is possible.
Air embolism (VE) is an acute pathological condition that occurs when air enters the blood vessel from outside. The amount of simultaneously injected gas should be at least 10-20 ml, otherwise it will dissolve in the blood without harm. Pathology is considered quite rare, it accounts for no more than 2% of all possible types of vascular occlusion.
Pulmonary thromboembolism (pulmonary embolism) – sudden blockage of the branches or trunk of the pulmonary artery with a thrombus (embolus) formed in the right ventricle or atrium of the heart, the venous channel of the pulmonary circulation and brought with blood flow. As a result, pulmonary embolism stops the blood supply to the lung tissue. The development of pulmonary embolism often occurs rapidly and can lead to the death of the patient.
0,1% of the world’s population dies from TELA annually. About 90% of patients who died from pulmonary embolism did not have a correct diagnosis at the time and the necessary treatment was not carried out. Among the causes of death of the population from cardiovascular diseases, pulmonary embolism is in third place after IHD and stroke. Pulmonary embolism can lead to death in non-cardiological pathology, occurring after operations, injuries, childbirth. With timely optimal treatment of pulmonary embolism, a high rate of mortality reduction to 2 – 8% is observed.
Prevention of cerebral thromboembolism
The most common causes of pulmonary embolism are:
- deep vein thrombosis (DVT) of the lower leg (in 70 – 90% of cases), often accompanied by thrombophlebitis. Thrombosis of simultaneously deep and superficial veins of the lower leg may occur.
- thrombosis of the inferior vena cava and its tributaries
- cardiovascular diseases predisposing to the appearance of blood clots and emboli in the pulmonary artery (IHD, the active phase of rheumatism with mitral stenosis and atrial fibrillation, hypertension, infectious endocarditis, cardiomyopathies and non-rheumatic myocarditis)
- septic generalized process
- oncological diseases (usually cancer of the pancreas, stomach, lungs)
- thrombophilia (increased intravascular thrombosis in violation of the hemostatic regulation system)
- antiphospholipid syndrome – the formation of antibodies to platelet phospholipids, endothelial cells and nervous tissue (autoimmune reactions); manifested by an increased tendency to thrombosis of various localizations.
Risk factors for venous thrombosis and pulmonary embolism are:
- prolonged immobility (bed rest, frequent and prolonged air travel, trips, paresis of limbs), chronic cardiovascular and respiratory failure, are accompanied by a slowdown in blood flow and venous congestion.
- taking a large number of diuretics (massive loss of water leads to dehydration, increased hematocrit and blood viscosity);
- malignant neoplasms – some types of hemoblastoses, true polycythemia (a high content of red blood cells and platelets in the blood leads to their hyperaggregation and the formation of blood clots);
- prolonged use of certain medications (oral contraceptives, hormone replacement therapy) increases blood coagulation;
- varicose disease (with varicose veins of the lower extremities, conditions are created for stagnation of venous blood and the formation of blood clots);
- metabolic disorders, hemostasis (hyperlip >
Embolism is a pathological condition, which is based on occlusion of the lumen of the vessel by a pathological particle (embolus).
Under normal conditions, blood is a liquid medium in which there is a specific set of cells and nutrients of a certain size that ensure the vital activity of the body.
When a foreign substance appears, organ trophism and local blood supply are disturbed.
There are several types of pathology, depending on the origin of the particles that caused it:
- Amniotic fluid embolism.
- Solid Embolism.
- Embolism with blood clots.
The severity of the consequences of the disease is due to the location of the particles. The most dangerous are occlusions of the pulmonary, coronary and cerebral arteries. They most often cause death.
The causes of embolism are various. Blood clots along the walls of the left ventricle occur when the heart muscle is damaged. This is characteristic of aneurysm of the heart, an extensive myocardial infarction. In a large circle of blood circulation, embolism of arteries occurs when a blood clot moves from the heart to the periphery, causes thrombosis in the extremities, in the mesentery of the intestine, splenic, renal and cerebral vessels.
For this, the following matters:
- the ability of the heart to eject blood under high pressure to open the auxiliary vessels and increase blood flow;
- properties of the vessels themselves to eliminate spasm.
With heart diseases with chronic or acute heart failure, severe atherosclerosis, such results can not be expected.
Manifestations of the disease depend on the diameter of the vessel and the organ or part of the body that is fed from it. A sign of embolism of an limb artery is acute pain. The mechanism of pain is considered to be overstretching of the artery wall at the site of thrombus insertion and irritation of nerve fibers. Spasm of the vessel occurs reflexively. At night the pain intensifies.
On palpation, you can feel the absence of a pulse below the site of thrombosis. The skin of the limb turns white, it becomes cold to the touch. Cyanotic spots appear at your fingertips. There is a decrease in skin sensitivity.
Gangrene of the foot after embolism of the shin vessel
After 6 – 8 hours from the moment of embolism, provided that the blood supply is completely stopped, symptoms of tissue necrosis (gangrene) appear. In this case, the pain becomes very intense. Dry gangrene usually develops.
With fat embolism
Clinical manifestations occur 1 to 2 days after an injury, surgery or other critical condition. There are two types of embolism:
- pulmonary – occurs in 60% of all cases, the patient suddenly has suffocation, blue face, cough with hemoptysis, pulmonary edema is possible;
- cerebral – sudden loss of consciousness or loss of orientation, agitation, delirium, convulsions.
- At the same time, signs of acute heart failure appear: a drop in blood pressure, tachycardia, and rhythm disturbance.
You can read more about fat embolism in this article.
The scheme of damage to the cerebral arteries
Pulmonary embolism is a complication of not only heart disease, but also surgical interventions. After surgery, it develops unexpectedly during the patient’s recovery period against the background of a general improvement, even before discharge from the hospital. Statistics determine up to 6% of this postoperative complication. The frequency directly depends on the duration of the operation.
With heart diseases (acute myocardial infarction, aneurysm, malformations, atrial fibrillation), an embolism in the pulmonary artery is possible. The largest vessel is not always clogged. Most often, the embolus enters the narrower artery of the lower lobe of the right lung. With the defeat of the main vessel, a lethal outcome occurs. Clinical symptoms do not have time to develop, but when examining the deceased, they pay attention to the sharp redness of the upper parts of the body.
If the embolus is localized in small branches, it causes pulmonary infarction. The patient complains of a sharp sudden pain in the side, shortness of breath, cough, sometimes with hemoptysis. Following a heart attack, pneumonia develops, pleurisy.
Three groups of symptoms can be distinguished:
- neurovascular – anxiety, fear, pain in the heart, palpitations, decreased blood pressure;
- pulmonary – pains in the side, hemoptysis, cough, shortness of breath;
- general – fever, yellowness of the skin and sclera, leukocytosis in a blood test.
Embolism of the abdominal aorta is more common with rheumatic heart disease. The embolus is located on the branching of the aorta and leads to subsequent secondary thrombosis. The main symptoms are sudden pain in the legs, their blanching and cooling, the disappearance of pulsation in the arteries of the foot. Pain is given to the perineum, lower abdomen, sacrum.
The effects of embolism can be paralysis and numbness of the legs. The patient is in a state of shock. Gangrene develops rapidly. If smaller arteries are affected, patients complain of weakness in the legs, lameness and pain when walking. In men, an erectile dysfunction occurs.
Renal artery embolism leads to kidney infarction. Patients note sharp lower back pain in the absence of dysuric phenomena (pain during urination, frequent urges). Two days later, blood appears in the urine. Possible increase in blood pressure. In severe cases, pain throughout the abdomen, bloating, vomiting, stool and urine retention.
Each type of embolism has its own causes.
Atrial fibrillation and other heart rhythm disturbances;
Aneurysm of the left ventricle;
Diseases of the venous system of the pelvis and limbs (thrombophlebitis, varicose veins, post-thrombophlebitis syndrome);
Large operations on the pelvic organs, abdomen and limbs;
With air embolism:
Traumatic damage to large veins;
Gross violations of the technique of intravenous manipulation;
Surgical interventions in gynecology with a violation of the technique of their implementation, abortion and difficult birth.
With fat embolism:
Massive limb injuries;
Intravenous administration of banned fat-containing drugs;
Spontaneous air entry into the circulatory system of a healthy person is practically excluded. The pressure in most vessels is excessive in relation to the atmosphere, therefore, gas suction in case of damage to the vascular wall is not observed. The exception is the internal jugular vein, the pressure in which when inhaling is lower than atmospheric. The situation with dehydrated patients looks different. Due to the decrease in bcc, the pressure in the central vessels becomes negative, a violation of the integrity of the vessel wall can lead to the ingress of gases from the environment. Common causes of aerial occlusion include:
- Injury Atmospheric gases penetrate the blood during lung barotrauma (sharp ascent from depth, improperly selected ventilation mode), chest injuries, accompanied by rupture of blood vessels. VE is also detected against the background of injuries of other anatomical zones in the absence of timely stopping of profuse bleeding.
- Childbirth. The penetration of gases becomes possible with rupture of the placental venous sinuses. Air into the damaged vessels is pumped under pressure during uterine contractions. The disease develops regardless of the magnitude of the central venous pressure. Symptoms can occur not only directly in childbirth, but also after 1-2 days.
- Medical procedures. Manipulations with a high risk of the formation of VE include operations on the vessels, organs of the chest, brain, if during the intervention an autopsy of the venous sinus is performed. In addition, air can enter the blood supply system when the infusion system is loosely connected to a central venous catheter or during infusion therapy. This happens with a negative CVP.
- mechanical – clogging with solid foreign substances and particles;
- clogging with body fat and elements of the body’s own tissues;
- fluid and gas embolism;
- blockage caused by the accumulation of bacteria;
- thrombotic embolism (with the development of thromboembolic disease);
- embolism with medications when they enter the vascular lumen.
- by surgery.
- Frontal opercular syndrome, manifested by a distortion of the face, gross aphasia and dysarthria;
- Shoulder or hand paralysis syndrome, in which the entire arm, forearm and hand are not movable, or only the hand in the presence or absence of cortical sensitivity disorders, depending on whether the sensory cerebral cortex is involved in the affected area along with the motor cortex;
- Syndrome of an isolated aphasia of Brock or Wernicke with a lesion of the dominant hemisphere in a patient
- The syndrome of denial of the left halves of the visual fields in case of damage to the occipital lobe of the non-dominant hemisphere in a patient.
- prolonged use of drugs, in the list of side effects of which there is an increase in blood viscosity;
- prolonged stay in one position, followed by a sharp rise – this can happen, for example, in the postoperative period;
- sustained high blood pressure;
- progressive heart failure;
- history of strokes;
- diagnosed and progressive varicose veins;
- malignant neoplasms;
- increased drowsiness;
- some stun;
- disorientation in space.
Large air bubbles in the bloodstream can lead to occlusion of any vessels. Most often, the pulmonary veins, blood vessels of the heart, arterial trunks that feed the brain are blocked. When the pulmonary artery is affected, regional intravascular hypertension, pancreatic overload and acute right ventricular failure are noted. Further, the left ventricle is involved in the process, cardiac output is reduced, peripheral blood circulation is disturbed, shock develops. Aerial embolism of LA is accompanied by the occurrence of bronchospasm, ventilation-perfusion imbalance, pulmonary infarction and respiratory failure.
In case of impaired blood flow in the cerebral vessels, the formation of pathology occurs as an ischemic stroke. In a certain part of the brain, the blood supply is disturbed, the neurotissue experiences oxygen starvation and dies. A site of necrosis is formed, multiple small hemorrhages in the brain tissue occur. The further course of the disease depends on the location of the affected area. Paresis, paralysis, impaired cognitive function, malfunctions in the activity of internal organs can be detected.
Brief description of thromboembolic disease
Pathological embolization of cerebral vessels and the development of methods to combat it are the subjects of many studies of domestic and foreign experts. Effective and long-term removal of blood clots from the blood will allow them to prevent the development of such phenomena as ischemia (decreased blood supply) and heart attack (cessation of blood flow).
Thromboembolic disease (or thromboembolism) is a pathology in which clogging of blood vessels by thrombi circulating in the composition of the blood mass sharply develops. The disease often ends in an ischemic heart attack, also called a brain stroke. Pathology is extremely dangerous for health and life. It is preceded by thrombosis, the causes of which may be:
- endocardial damage: consequences of endocarditis and an attack of myocardial infarction;
- vascular endothelial damage: consequences of aortic aneurysm, thrombophlebitis, vasculitis, atherosclerosis;
- hyperactivity of blood coagulation functions;
- pathological slowdown of blood flow.
For the most part, blood clots form in the internal lumen of the veins of a large circle of blood circulation and often affect the vessels of lung tissue. However, blood clots can also be observed in the arteries of a large circle of blood circulation, then they form in the aorta, left chambers of the heart and other main arteries. Over time, blood clots come off the wall of the artery (veins) and are transported together with the blood to the part of the vessel that cannot pass, and therefore clog it, reducing or completely blocking blood circulation.
Brain embolism leads to a heart attack of the central nervous system, the absence of its blood supply and the necrosis of cellular material. Only timely and adequate medical care can limit cellular necrosis, but in all cases it ends with dysfunctions of the central nervous system. Deviations from the norm can occur to one degree or another, paralysis of the extremities and violation of facial expressions are often observed.
It is impossible to predict the consequences of cerebral infarction. One of the consequences of thromboembolic disease can also be the development of insufficient supply of the central nervous system with nerve cells – innervation disorders, such as vasospasm and subsequent vasoparesis, which are accompanied by cerebral edema and the desolation of the pool of the affected capillary network.
In addition, cerebral embolism is the main cause of hemorrhage – hemorrhage from rupture of a blood clot by a blood clot and subsequent premature death. The disease in most cases manifests itself in the elderly and develops gradually. Pathology is associated with deterioration of the blood lines, age-related changes in the organization and provision of metabolic processes, as well as the accumulation of fat and other deposits in the inner lumen of the vessels.
Depending on the localization of the thromboembolic process, the following variants of pulmonary embolism are distinguished:
- massive (thrombus is localized in the main trunk or main branches of the pulmonary artery)
- embolism of segmental or lobar branches of the pulmonary artery
- embolism of small branches of the pulmonary artery (usually bilateral)
Depending on the volume of the disabled arterial blood flow during pulmonary embolism, the following forms are distinguished:
- small (less than 25% of the pulmonary vessels are affected) – accompanied by shortness of breath, the right ventricle is functioning normally
- submassive (submaximal – the volume of the affected pulmonary vessels from 30 to 50%), in which the patient has shortness of breath, normal blood pressure, right ventricular failure is not very pronounced
- massive (volume of switched off pulmonary blood flow more than 50%) – loss of consciousness, hypotension, tachycardia, cardiogenic shock, pulmonary hypertension, acute right ventricular failure
- fatal (the volume of the disconnected blood flow in the lungs is more than 75%).
Tela can occur in a severe, moderate or mild form.
The clinical course of pulmonary embolism can be:
- acute (fulminant) when there is an instant and complete blockage by a thrombus of the main trunk or both main branches of the pulmonary artery. Acute respiratory failure, respiratory arrest, collapse, ventricular fibrillation develop. A fatal outcome occurs in a few minutes, pulmonary infarction does not have time to develop.
- acute, in which there is a rapidly increasing obstruction of the main branches of the pulmonary artery and part of the lobar or segmental. It begins suddenly, rapidly progresses, the symptoms of respiratory, cardiac and cerebral insufficiency develop. It lasts a maximum of 3 to 5 days, complicated by the development of pulmonary infarction.
- subacute (prolonged) with thrombosis of large and medium branches of the pulmonary artery and the development of multiple pulmonary infarction. It lasts several weeks, slowly progresses, accompanied by an increase in respiratory and right ventricular failure. Repeated thromboembolism may occur with exacerbation of symptoms, in which death often occurs.
- chronic (recurrent), accompanied by recurrent thrombosis of the lobar, segmental branches of the pulmonary artery. It manifests itself as repeated pulmonary infarction or repeated pleurisy (often bilateral), as well as gradually increasing hypertension of the pulmonary circulation and the development of right ventricular failure. Often develops in the postoperative period, against the background of existing oncological diseases, cardiovascular pathologies.
There are several criteria for the systematization of renewable energy. Air embolism is classified by the nature of the course (fulminant, acute and subacute), the path of air into the bloodstream (iatrogenic, traumatic), the direction of movement of the embolus (orthograde, retrograde, paradoxical). In clinical practice, the separation of the forms of the disease according to the type of affected vessel is used, including the following pathology options:
- Arterial. Clogging of large arterial trunks (coronary, pulmonary, cerebral) is observed. It occurs in 30-35% of cases, develops with lightning speed, is severe, with severe clinical symptoms. The patient dies within a few hours, sometimes minutes. For the formation of AVE, more than 40-50 cm 3 of gas, which simultaneously enters the bloodstream, are needed.
- Venous It is found in 65-70% of cases. It leads to a violation of the venous outflow. Symptoms progress relatively slowly, life-threatening conditions are rarely detected. Prone to subacute current. With blockage of small veins and venules, it can be asymptomatic, and blood flow is ensured by the collateral system. An exception is air occlusion of the pulmonary veins, through which oxygen-rich blood flows from the lungs to the heart.
Air embolism treatment
External signs of a manifestation of brain embolism depend on the location of the affected vessel. However, doctors managed to identify some symptoms that indicate clogging of the internal lumens of the vessels that feed the central nervous system. In particular, they include:
- bouts of dizziness;
- loss of consciousness (fainting);
- development of shortness of breath with minor physical exertion;
- a feeling of chronic fatigue;
- cough with sputum production, including the development of hemoptysis;
- pallor of the skin;
- arrhythmic heart rate;
- the appearance of seizures.
In rare cases, embolism can manifest itself after physical exertion or stress tests, psychoemotional stress. For the most part, clogging of the vessels leads to the observation of symptoms at rest, inclusive. When observing signs that may indicate the development of embolism, an appropriate examination should be immediately taken.
The key to success in curing pathology is the timely diagnosis and adequate therapeutic effect. Embolism is differentiated with vascular crises, ruptures of aneurysms, attacks of heart attacks and the development of malignant tumors. Only professionally performed diagnostics can distinguish thromboembolic disease from other pathologies.
Thrombosis of cerebral vessels may occur in different ways depending on the location of the lesion and the size of the affected area. Usually its symptoms appear at rest and develop gradually. The first sign of blockage in the blood vessels of the brain is confusion. A person looks sleepy and does not respond to external stimuli, but consciousness is preserved. The most common signs of pathology are noted:
- muscle weakness or paralysis of half the body or face;
- speech impairment;
- difficulty swallowing;
- loss of coordination of movements;
- sudden loss of vision.
Thrombosis of cerebral veins and sinuses manifests itself as a severe headache. About a third of patients experience seizures and paralysis of half the body. Less common are double vision, impaired speech and consciousness.
To accurately diagnose cerebral vascular thrombosis, computed or magnetic resonance imaging is used. The second type of study is preferable, since it gives an idea of the vascular bed even when the blood flow stops. To detect thrombosis of large arteries, ultrasound examination of blood vessels and transcranial dopplerography are used.
Sudden pain behind the sternum or in one of the half of the chest;
Drop in blood pressure (90/50 and below);
Shortness of breath and shortness of breath (over 20);
Tachycardia (more than 100) and heart rhythm disturbances;
Severe general weakness;
Cough and hemoptysis (join later).
Lack of coordination of movements;
Movement disorders such as paresis and paralysis;
Severe burning pain in the abdomen;
Bloody fluid stool;
Tachycardia and lowering blood pressure;
Lack of rumbling and intestinal motility;
Pain in the projection of the affected kidney;
Red color of urine;
Oliguria (the amount of urine is below normal).
Sudden pain at the site of localization of the embolus, which then spreads to the entire limb;
Pallor of limb skin;
Cooling of the affected segment and its numbness;
The impossibility of active and passive movements;
Signs of gangrene (bubbles with dark fluid, black spots).
Many patients are interested in what is embolism? This is a pathology in which clogging of blood vessels by foreign bodies leads to a halt in the blood supply to the internal organ. Embolas – bodies that narrow the lumen in a vessel – can be air bubbles, an accumulation of fatty tissue or blood clots.
In embolism, species are always associated with severe pathologies in the body. This is an extremely dangerous phenomenon that requires immediate treatment. Vascular embolism always leads to very serious consequences, provokes the development of irreversible processes in the body, and often causes the patient to die. From the moment the embolus enters the blood vessel to the development of severe consequences, from 6 to 12 hours pass. In some cases, the embolism can be sluggish, chronic.
The presence of a blood clot in one of the blood vessels leads to the fact that blood flow begins to bypass the damaged area along the collateral blood vessels. Pathophysiology distinguishes 3 types of embolism, which differ in the causes of blood flow disturbance, types of emboli and localization of the blood channels, in which a blockage formed and closed the lumen.
Embolism arising from a blockage of a vessel by a thrombus (thromboembolism) is characterized by an overlap of the lumen of the pulmonary or carotid artery with a clot of platelets. An air or gas embolism occurs when an air or gas bubble enters a blood vessel. The fatty type of pathology develops due to the ingress of fat cells and other nutrients into the bloodstream.
Emboli clog the subclavian artery, visceral aorta and its branches, iliac arteries, blood vessels of the legs and pelvis. In some, extremely rare cases, embolism can develop simultaneously in large and small blood vessels.
Embolism, the symptoms of which depend on the location of the emboli, has a pronounced clinical picture that manifests itself immediately after a partial clogging of the lumen in the blood vessel. Embolism in the pulmonary arteries can be characterized by such signs:
- sharp pain in the chest area, mainly on one of its sides;
- excessive sweating;
- general weakness of the body;
- a sudden drop in blood pressure to critical levels.
Septic embolism, in which a foreign body enters the venous channel, has the same symptomatic picture as with pulmonary type pathology. The appearance of a blood clot, air bubbles, or fat cells in the carotid artery provokes a severe headache, fainting, speech becomes slurred, and motility of the limbs is impaired. The patient experiences dizziness, loses coordination.
Violation of blood flow in the mesenteric artery provokes severe, unbearable pain in the abdomen, feces become fluid, blood streaks are visible in them. The patient feels a strong bloating, lowers blood pressure, heart palpitations.
If a blood clot, air, or an accumulation of fat cells clogs the lumen of an artery leading to the kidneys, the patient changes the color of urine, it turns red, and pain in the lower back appears. Circulatory disorders in the upper and lower extremities are the most common type of embolism. Symptoms – severe pain in the area of the damaged blood vessel, pallor and cooling of the skin, impaired motor function of the limbs.
The ingress of fat cells into a blood vessel with further clogging of the lumen always leads to an exacerbation of chronic diseases. So, in patients with bronchial asthma, a cough begins to intensify, at the end of which sputum appears with blood clots. During pregnancy, embolism may develop, in which particles of amniotic fluid enter the bloodstream of the mother’s body.
The methods of treatment for embolism depend on the type of pathology. Clogging of blood vessels with blood clots requires immediate hospitalization of the patient with further thromboembolectomy – surgery to remove blood clots. If it is not possible to carry out this operation, the fibrinolysis method is used, which involves the dissolution of blood clots.
With single accumulations of platelets, the therapeutic method of anticoagulation is used, its purpose is to make the blood less dense and prevent the re-formation of a blood clot. Taking medications depends on the symptoms. The patient may be prescribed diuretics, glucocorticosteroids, hormone therapy. It is mandatory to carry out preventive antibiotic therapy to prevent the development of infectious diseases and increase immunity.
When symptoms of air embolism occur, the patient must be laid down and his legs raised above head level. Syringe aspiration is used to remove air from a blood vessel. In some cases, with multiple blockage of blood vessels by air drops, it is necessary to carry out treatment in pressure chambers and transfer the patient to mechanical ventilation.
In the treatment of fat embolism, an installation with an oxygen mixture is prescribed, the use of hormonal drugs and medications that dissolve fat cells. For the relief of symptoms, anticoagulants and glycosides of the heart group are prescribed.
Embolism, regardless of its type, is an extremely serious pathology, which can lead to serious, irreversible consequences and cause death. In order to prevent an ailment, you need to carefully monitor your health, regularly undergo a medical examination and treat any concomitant diseases, especially varicose veins.
The main principle of preventing the development of occlusion is the timely diagnosis of diseases of the cardiovascular system and internal organs. With the development of the first symptoms: the appearance of impaired consciousness, a change in the function of breathing and palpitations, the occurrence of pain and anxiety, you should immediately seek medical help.
Symptoms of pulmonary embolism depend on the number and size of thrombosed pulmonary arteries, the rate of development of thromboembolism, the degree of pulmonary tissue blood supply disturbance, the patient’s initial condition. With pulmonary embolism, a wide range of clinical conditions is observed: from an almost asymptomatic course to sudden death.
The clinical manifestations of pulmonary embolism are nonspecific, they can be observed in other pulmonary and cardiovascular diseases, their main difference is a sharp, sudden onset in the absence of other visible causes of this condition (cardiovascular failure, myocardial infarction, pneumonia, etc.). For the pulmonary embolism in the classic version, a number of syndromes are characteristic:
- acute vascular insufficiency. A drop in blood pressure (collapse, circulatory shock), tachycardia is noted. Heart rate can reach more than 100 beats. per minute.
- acute coronary insufficiency (in 15-25% of patients). It is manifested by sudden severe pain behind the sternum of a different nature, lasting from several minutes to several hours, atrial fibrillation, extrasystole.
- acute pulmonary heart. Due to massive or submassive pulmonary embolism; manifested by tachycardia, swelling (pulsation) of the cervical veins, positive venous pulse. Edema with acute pulmonary heart does not develop.
- acute cerebrovascular insufficiency. There are cerebral or focal disorders, cerebral hypoxia, in severe form – cerebral edema, cerebral hemorrhage. It manifests itself as dizziness, tinnitus, deep fainting with convulsions, vomiting, bradycardia or coma. Psychomotor agitation, hemiparesis, polyneuritis, meningeal symptoms can be observed.
- acute respiratory failure is manifested by shortness of breath (from a feeling of lack of air to very pronounced manifestations). The number of breaths is more than 30-40 per minute, cyanosis is noted, the skin is ash-gray, pale.
- moderate bronchospastic syndrome is accompanied by dry wheezing.
- pulmonary infarction, myocardial pneumonia develops 1 to 3 days after pulmonary embolism. There are complaints of shortness of breath, cough, chest pain from the affected side, aggravated by breathing; hemoptysis, fever. Small bubbling wet rales, the pleural friction noise become audible. In patients with severe heart failure, significant effusions in the pleural cavity are observed.
3. Feverish syndrome – subfebrile, febrile body temperature. It is associated with inflammatory processes in the lungs and pleura. The duration of the fever is from 2 to 12 days.
4. Abdominal syndrome is caused by acute, painful swelling of the liver (in combination with intestinal paresis, peritoneal irritation, hiccups). It manifests itself as acute pain in the right hypochondrium, belching, vomiting.
5. Immunological syndrome (pulmonitis, recurrent pleurisy, urticaroid rash on the skin, eosinophilia, the appearance of circulating immune complexes in the blood) develops at 2-3 weeks of illness.
- getting injuries, fractures of the upper or lower extremities;
- excessive intravenous administration of preparations containing fatty elements;
- severe pancreatic necrosis.
Acute pulmonary embolism can cause cardiac arrest and sudden death. When the compensatory mechanisms are triggered, the patient does not die immediately, but in the absence of treatment, secondary hemodynamic disturbances very quickly progress. The patient’s cardiovascular diseases significantly reduce the compensatory capabilities of the cardiovascular system and worsen the prognosis.
With embolization of peripheral arteries, trophic ulcers are formed, zones of necrosis arise. Violation of the venous outflow in the limbs leads to edema. Changes in the circulatory system of internal organs cause a weakening or complete cessation of their activity. Acute renal or hepatic insufficiency, intestinal paresis, insufficiency of heart and lung function may develop.
Treatment of cerebral thromboembolism
Diagnosis of embolism is difficult because it is limited in time. Pathological changes develop suddenly and very quickly lead to irreversible conditions. It matters the patient’s questioning about past illnesses, examination and checking the pulse on the limbs.
Information about starting thrombosis can give:
- blood coagulation test;
- set of signs on the ECG;
- chest x-ray;
- ultrasound examination of large veins and abdominal organs.
Vascular angiography is performed according to clinical indications in large vascular centers and specialized departments.
Possible catheterization of the cavities of the heart.
In specialized clinics and centers where a specialized study and treatment of the organs of the cardiovascular system is carried out, several diagnostic methods are used to detect brain embolism. The choice of a particular method of examination depends on the characteristics of the patient’s body, its age and other individual characteristics, as well as past illnesses.
The specialist begins the examination with the study and analysis of the patient’s living conditions, his psycho-emotional environment, diet and diet, patient explanations about complaints about the state of health and information about the illnesses. Then, laboratory, instrumental and hardware studies are carried out, in particular:
- instrumental study of blood pressure values;
- ultrasound examination of the vessels of the neck and head;
- instrumental listening to heart murmurs;
- laboratory general analysis of blood and urine;
- laboratory biochemical blood test;
- electrocardiography (ECG);
- phonocardiography – hardware listening and noise analysis;
- Magnetic resonance imaging;
- CT scan;
- X-ray studies using high-contrast substances.
If necessary, other diagnostic measures are prescribed and carried out, which depend on the features of the development of pathology or other pathogenic processes occurring in the patient’s body.
- vitamins C and K;
- the medal.
Other medical preparations may be used, however, the possibility of their use is determined by a specialist. Self-medication for brain embolism is unacceptable. Surgical intervention is an extremely radical method of exerting a therapeutic effect. Its features depend on the stage of the disease, the localization of the affected area and compliance with safety requirements for the patient’s life.
One of the most confusing issues in the problem of cerebral vessels (cerebrovascular diseases) is embolism from “unknown sources”. It is believed that in patients with a violation of the blood coagulation system in the direction of its strengthening, while taking contraceptives, a chronic disease or a metastatic tumor, embolism of the cerebral vessels may develop suddenly.
Sometimes, when listening to the patient’s heart, such causes of auscultatory phenomena as a click of an opening with mitral valve stenosis, or such a form of arrhythmia as transient atrial fibrillation are not recognized. As a result, in many patients, especially those aged 20 to 50 years, with the sudden development of embolic stroke, it is not possible to detect its causes.
The magnitude, location and to some extent the very nature of the embolus determines the size, location and nature of the heart attack caused by it in the parenchyma of the brain tissue. Large enough emboli that can clog the trunk of the middle cerebral artery (2-3 mm). This type of embolism leads to massive brain damage involving the cerebral cortex and underlying white matter, as well as deep gray and white matter, in the pathological process.
Cardiac arrhythmias of any type are combined with symptomatic cerebral and systemic emboli. Particular attention should be paid to the high frequency of embolism in case of sick sinus syndrome and atrial fibrillation, against the background of atrial fibrillation in patients with rheumatic heart valve disease. Therefore, in order to prevent embolism, such patients are shown long-term administration of anticoagulants (warfarin sodium).
It was noted that clinically manifest embolism is especially common in patients with atrial fibrillation, regardless of the cause that caused it. It is estimated that the frequency of embolism in cerebral vessels among patients with atrial fibrillation not associated with valvular lesions reaches 4-7% per year, and in most cases the first stroke leads to deep disability of such a patient.
The formation of a parietal thrombus with subsequent embolism is relatively common in patients with atherosclerotic lesions of the cardiovascular system and myocardial infarction, regardless of whether there is papillary muscle dysfunction, congestive heart failure, or cardiac ventricular aneurysm.
Patients with atrial fibrillation, which are associated with a high risk of stroke, currently have an alternative to the long-term use of warfarin. The device is designed to close the ear of the left atrium and prevent the migration of blood clots formed in the brain, which can cause ischemic stroke.
Cardiac surgery and surgical valve replacement are associated with a particularly high risk of embolism. Less common cause of cerebrovascular embolism is surgery on the chest, after which embolism from the pulmonary veins, as well as the head and neck (arterioarterial embolism from the aorta or carotid arteries) are possible.
Fractures of the cerebral vessels result in fatty or air embolism of the long bones, surgical interventions on the organs of the chest cavity and diagnostic angiography with intravascular administration of the contrast medium through the catheter. Both variants of embolism give multiple sites of point hemorrhages.
The most significant complication of using an artificial heart is embolism from the cavity of the heart to the vessels of the brain. Congenital defects of the heart walls can be the cause of paradoxical embolism in the patient. Thrombotic and tumor material, infectious or fibrous marantic deposits that accumulate on the surface of the endocardium in the heart chambers or on the valves can be transported with a blood stream.
Deposits on the aortic valve and the left atrioventricular valve with rheumatic or marantic endocarditis are observed simultaneously with systemic or cerebral emboli and are diagnosed on the basis of the patient’s medical history, objective and laboratory examinations. Typical flat deposits under the cusps of the left atrioventricular valve and, to a lesser extent, the aortic valve (Liebmaia-Sachs endocarditis) have been described in patients with systemic lupus erythematosus.
They can be a source of embolism in the vessels of the brain, but more often they become foci of the development of bacterial endocarditis. Thrombotic deposits in acute and subacute bacterial endocarditis in patients lead to septic embolism. Such emboli can cause extensive cerebral infarctions that are no different from non-infectious embolic infarcts during occlusion of large cerebral arteries.
They also cause small heart attacks with microscopic abscesses. Meanwhile, large brain abscesses do not combine with embolism in subacute bacterial endocarditis. Mycotic (fungal) aneurysms caused by septic emboli cause subarachnoid and intracranial hemorrhages.
If you suspect a cerebrovascular embolism, it is always necessary to remember the possibility of endocarditis in the patient and exclude it. Atrial myxoma leads to tumor embolism. The substrate of emboli in myxoma is deposits on the surface of the endocardium. In the case of myxoma, the differential diagnosis helps to identify signs of pulmonary hypertension, a high erythrocyte sedimentation rate (ESR), and symptoms of a systemic disease (fever, malaise).
Mitral valve prolapse during the formation of a parietal thrombus is combined with cerebral embolism, but their formation mechanisms have not been studied enough to predict the incidence of repeated embolism in patients. It is supposed to be low. When making a diagnosis of mitral valve leaflet prolapse, the patient should undergo echocardiography.
- assessment of lung function and, if necessary, their artificial ventilation or oxygen therapy;
- maintaining normal temperature with antipyretic drugs;
- intravenous fluid administration to improve blood flow;
- decrease in high blood pressure.
In the diagnosis of pulmonary embolism, the main task is to establish the location of blood clots in the pulmonary vessels, to assess the degree of damage and the severity of hemodynamic disturbances, to identify the source of thromboembolism to prevent relapse.
The complexity of the diagnosis of pulmonary embolism dictates the need for such patients to be in specially equipped vascular departments that have the widest possible capabilities for conducting special studies and treatment. The following examinations are performed for all patients with suspected pulmonary embolism:
- a thorough history, assessment of risk factors for DVT / pulmonary embolism and clinical symptoms
- general and biochemical analyzes of blood, urine, a study of the gas composition of blood, a coagulogram and a study of D-dimer in blood plasma (a method for the diagnosis of venous blood clots)
- ECG in dynamics (to exclude myocardial infarction, pericarditis, heart failure)
- X-ray of the lungs (to exclude pneumothorax, primary pneumonia, tumors, fractures of the ribs, pleurisy)
- echocardiography (to detect increased pressure in the pulmonary artery, overloads of the right heart, blood clots in the cavities of the heart)
- lung scintigraphy (impaired blood perfusion through the lung tissue indicates a decrease or absence of blood flow due to pulmonary embolism)
- angiopulmonography (to accurately determine the location and size of the thrombus)
- Ultrasound of the veins of the lower extremities, contrast phlebography (to >
CT angiography of the pulmonary arteries. An extended parietal thrombus in the lumen of the main trunk of the left pulmonary artery
Diagnosis of VE is carried out by an anesthesiologist-resuscitator in tandem with the patient’s direct physician. Clinical examination data, combined with information obtained using hardware-based diagnostic techniques, usually leave no doubt about the diagnosis. Difficulties arise in determining the type of embolism. It is necessary to differentiate vascular occlusion caused by air, gas bubbles formed endogenously with a sharp change in environmental pressure (decompression sickness, gas embolism), thrombus, tumor, foreign body, conglomerate of bacterial cells. Diagnostic measures include:
- Physical. Conducted in the intensive care unit or at the location of the patient. During the examination, indirect signs of thrombosis are detected and a preliminary diagnosis is made. It should be borne in mind that the disease does not always occur with a full range of symptoms, the frequency of occurrence of some of them does not exceed 50-60%.
- Laboratory At the initial stages of the development of renewable energy, laboratory testing is not very informative. Changes in the composition of blood gases, acid-base balance, and electrolyte balance are noted. With damage to internal organs and the development of multiple organ failure, an increase in the activity of liver enzymes occurs, an increase in the concentration of creatinine and urea in the blood. Destructive processes in muscle tissue cause an increase in myoglobin levels.
- Instrumental. When conducting precardial, transesophageal or transcranial dopplerography, it is possible to establish the fact of the presence of air in the vessels. The study is qualitative, it is impossible to determine the volume of gas with its help. The capnogram indicates an increase in the concentration of carbon dioxide at the end of exhalation; when measuring CVP, an inadequate increase in indicators is revealed. On the ECG, ventricular extrasystoles, P wave changes, and ST segment depression are detected.
Prognosis and prevention
The outcome is favorable in cases where air can be removed with the help of less traumatic subclavian access. With intracranial or pulmonary localization of the embolus, the prognosis worsens, since it is almost impossible to extract it by surgical methods. The use of HBO and hypothermia does not allow to quickly normalize blood flow, therefore, the likelihood of irreversible consequences increases. With the defeat of peripheral veins and arteries, there is usually no threat to life, but the restoration of the affected tissues takes a long time, complete regeneration is not always possible.
Air embolization most often occurs during medical manipulations, therefore, measures for its prevention fall entirely on the staff of the medical institution. During interventions on the superior vena cava, the patient should be in the Trandelenburg position, catheterization of the subclavian vein at the moment when the needle remains open (disconnecting the syringe, removing the conductor) is performed on a deep exhalation of the patient. With low CVP, the completed infusion systems should be timely blocked.
Preventive measures are divided into several sections.
taking anticoagulants (aspirin, cardiomagnyl, warfarin);
Monitoring of blood coagulation indicators (APTT, PTI INR), especially in people at risk for thromboembolic complications;
Timely and adequate treatment of heart rhythm disturbances;
Elimination of venous pathology of the lower extremities;
Installation of cava filters in people at risk;
Elastic compression of the legs and prophylactic doses of anticoagulants in people at risk who have surgery;
Dosed physical and mental stress.
Prevention of air embolism:
Compliance with the rules of smooth ascent from high depths by divers;
Correct and fast treatment of wounds with damage to venous vessels;
The correct laying of women on the operating table during gynecological operations, thorough and quick dressing of damaged veins;
Strict adherence to the technique of intravenous injection;
Prevention of fat embolism:
Fast and persistent immobilization of a damaged limb;
Early surgical interventions or other methods of reposition, leading to stabilization of bone fragments;
Compliance with the rules of intravenous administration of drugs.
Article author: Volkov Dmitry Sergeevich | K.M. surgeon, phlebologist
Education: Moscow State University of Medicine and Dentistry (1996). In 2003, he received a diploma from the educational and scientific medical center for managing the affairs of the President of the Russian Federation.
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Embolism of the cerebral arteries is most often observed against the background of risk factors for cardiac pathology: People with hypertension should regularly take antihypertensive drugs, limit salt intake, and increase physical activity. A safe pressure level is 110 -120/70 – 80 mm Hg. Art. In patients with diabetes mellitus, one should strive for a glycosylated hemoglobin index of less than 7%.
With elevated cholesterol, the level of lipids in the blood should be monitored, a diet with restriction of animal fats should be followed, and statins should be taken as prescribed by the doctor. It is recommended to stop smoking and alcohol abuse. Thrombosis of cerebral vessels – blockage of the lumen of an artery or vein, leading to oxygen starvation of the brain and stroke.
The main signs of the disease are impaired speech, vision, motor coordination and paralysis. Damage to the veins can cause prolonged headaches. Vascular thrombosis must be urgently addressed. To do this, substances that dissolve blood clots or surgical intervention are used. Any person can reduce the risk of such a pathology by taking medical examinations in time, monitoring blood sugar and cholesterol levels and blood pressure indicators.
It is necessary to refrain from smoking, overeating and follow a healthy diet. If you notice the first signs of a blood clot, you can prevent a catastrophe. What are the symptoms if a blood clot in the arm, leg, head, heart? What are the signs of a formation that has come off? Thrombosis of the cerebral sinuses or veins of the meninges can occur spontaneously.
Symptoms will help to seek help and treatment in a timely manner. Thrombosis of the sinus of the brain occurs due to untreated infectious diseases. It can be sagittal, transverse, venous. Symptoms will help you start treatment in a timely manner in order to minimize the negative consequences. Often, deep vein thrombosis poses a serious threat to life.
Acute thrombosis requires immediate treatment. Symptoms on the lower extremities, especially the lower leg, may not be immediately diagnosed. Surgery is also not always required. Due to abnormalities in the development of the fetus, hypoplasia of the arteries of the brain may develop. It happens back, right, left or connecting. Signs of violations can go unnoticed with lesions of the small arteries.
In the case of large cerebral arteries, treatment must be started immediately. Due to a number of diseases, even due to stoop, subclavian thrombosis can develop. The reasons for its appearance in the artery, vein are very diverse. Symptoms are manifested by blueness, pain. The acute form requires immediate treatment.
The reasons why cerebellar stroke can occur are quite diverse. Stroke can be ischemic, hemorrhagic, stem. The treatment is long, recovery requires a long rehabilitation. The consequences are problems with speech, movement. A real threat to life is a stroke. It can be hemorrhagic, ischemic.
Symptoms resemble a heart attack, and are also similar to other diseases. Treatment is a long, complete recovery after a stroke of the stem brain is almost impossible. Only timely recognition of subarachnoid hemorrhage will save a life. Symptoms of traumatic and non-traumatic brain hemorrhage are clearly defined. Diagnosis involves CT, and treatment involves surgery. With a stroke, the consequences are exacerbated.
With the early provision of full assistance to patients, the prognosis for life is favorable. With severe cardiovascular and respiratory disorders against the background of extensive pulmonary embolism, mortality exceeds 30%. Half of relapses in pulmonary embolism develop in patients who have not received anticoagulants. Timely, correctly conducted anticoagulant therapy halves the risk of relapse of pulmonary embolism. To prevent thromboembolism, early diagnosis and treatment of thrombophlebitis, the appointment of indirect anticoagulants to patients at risk are necessary.
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