Fat embolism syndrome

Introduction to Fat Embolism Syndrome Fatem embolism syndrome (FES) is a complication of severe injuries such as trauma and fracture. Since 1880, Zenker first discovered fat droplets from the pulmonary vascular bed of severe traumatic deaths and the first clinical diagnosis of fat embolism in Bergan in 1887, although A century, many people have studied from different angles, but because of their great clinical manifestations, some cases are fierce, rapid onset, and even die soon before the typical symptoms appear, and some may not be obvious. Clinical symptoms are only found after autopsy after death. Therefore, it was not until nearly 20 years that he had a further understanding of his pathophysiology. Bagg (1979) and others considered that the syndrome was a post-traumatic respiratory distress syndrome that occurred within 72 hours after fracture trauma. Early signs of tachycardia, elevated body temperature over 38 ° C, decreased arterial oxygen partial pressure (PaO2) and the appearance of "blizzard" shadows in the lungs can be diagnosed. Broder believes that except for injuries, burns, metabolic disorders, decompression sickness, connective tissue disease, serious infections, new organisms, osteomyelitis, etc. can also induce FES. basic knowledge The proportion of illness: 0.002% Susceptible people: no specific population Mode of infection: non-infectious Complications: disturbance of consciousness

Causes of fat embolism syndrome

(1) Causes of the disease

Fat embolism syndrome is caused by fat emboli entering the bloodstream to block small blood vessels, especially blocking the capillaries in the lungs, causing a series of pathological changes and clinical manifestations. The clinical manifestations vary depending on the fat emboli.

Source, formation and fate of fat emboli:

1. Mechanical theory (extravascular source) was proposed by Gauss in 1924, he believes that fat from the bone marrow through the fracture to tear the vein into the bloodstream, and then mechanically block the small blood vessels and capillary beds in the lungs, but the embolism must be Three conditions:

(1) The fat cell membrane ruptures to produce free lipids.

(2) Injured and open veins.

(3) The formation of hematoma in the local or fracture site, the local pressure rises, and the fat enters the ruptured vein.

2. Chemistry (intravascular endogenous) Because of the clinical presence of bone damage, there are fat embolism syndrome, this kind of situation can not be explained by the above theory, so in 1927, Lelman and Moore put forward the chemistry, they It is believed that this is because some factors hinder the natural emulsification of blood lipids, causing the chylomicrons to agglomerate each other to form larger lipid droplets, thereby blocking small blood vessels; or in the state of traumatic stress, the sympathetic nervous system is excited, under the action of neuro-endocrine effects Increased secretion of catecholamines activates adenine cyclase, which increases the amount of 3,5-cyclic adenosine monophosphate, which in turn activates lipase in adipose tissue to cause body fat mobilization.

3. Where the fat embolus goes

(1) When the diameter of the lipid plug is small, and because of its plasticity in the blood vessel, it can enter the systemic circulation directly through the pulmonary vascular bed, deposit a whole body fat plug in the tissue or organ, or discharge through the urine through the glomerulus.

(2) Fat emboli can be engulfed by alveolar epithelial cells and shed in the alveoli with the sputum.

(3) Sevitt believes that the fat plug can enter the systemic circulation through the right atrium through the patent foramen ovale or through the pulmonary-bronchial capillaries.

(4) Peltiers believes that a larger diameter fat plug will inevitably stay in the pulmonary vascular bed and undergo hydrolysis under the action of local lipase to produce glycerol and free fatty acids.

(two) pathogenesis

Fat first forms a mechanical blockage in the blood vessels of the lungs, and then activates adenine cyclase to catalyze inactive lipase changes in the serum due to lipase release from vascular endothelial cells or catecholamines released by the wounded due to traumatic stress. Active lipase, through the action of lipase, the neutral fat is hydrolyzed into free fatty acids, the blocked pulmonary blood vessels are stimulated by free fatty acids, and toxic or chemical vasculitis occurs; vascular endothelial cells blister Deformation, and separation from the basement membrane, destroys the integrity of vascular endothelial cells; increases its permeability, resulting in diffuse interstitial pneumonia of the lungs, acute pulmonary edema, at which time chest tightness, cough, and cough can occur clinically. If the lung lesions continue to increase, the lung X-ray film can show a "blizzard"-like shadow, and there is a more obvious respiratory dysfunction in the clinic. Because the alveolar ventilation function is blocked, the arterial oxygen tension is lowered. Then, there is an arterial blood hypoxemia that threatens the lives of the wounded, resulting in damage to the central nervous system and neurological symptoms.

Therefore, Murray's classification of fat embolism syndrome should be determined according to the presence or absence of neurological symptoms, while those with central nervous system symptoms are severe, and those without neurological symptoms are light.

There are two different perspectives on where the main lesions of FES are in the lungs or in the brain:

1. According to the viewpoint of Sevitt, the pathogenic effect of lipid plugs is mechanical obstruction of small blood vessels, and the main lesion is in the brain.

Sevitt pointed out that the occurrence of tissue lesions depends on the size and number of lipid plugs, the extent of small blood vessel collaterals, the time of ischemic hypoxia and the sensitivity of organ tissues to hypoxia, and emphasizes the body and brain lipid plugs. It is the basis of clinical manifestation of FES, and it is the main cause of death. Although pathologically confirmed that fat embolism mainly appears in pulmonary blood vessels, it does not cause obvious lesions. Because of the presence of collateral branches in the pulmonary-bronchial vascular system, it is not easy to cause lung lesions; In some cases, the nervous system symptoms are prominent or preceded by pulmonary symptoms.

2. Peltiers believes that the main lesion of FES is in the lungs.

Weisz pointed out that in judging the brain lesions of lipid plugs, it is necessary to distinguish between hypoxic hypoxia and ischemic hypoxia. It is believed that the brain lesions of FES are mainly caused by hypoxia and hypoxia.

Bivins reported 37 cases of death in FES, the pathological findings: 100% of pulmonary lipid stagnation, 37% of renal sputum, and 0 of brain sputum, but brain edema changed by 75%.

Therefore, Weisz and Bivins agree with Peltier that the primary lesion of FES is in the lung, and the clinical course is mainly the process of pulmonary lipid thrombosis gradually developing into respiratory insufficiency, while brain lesions and their symptoms are secondary.

3. The main manifestations of pathological changes in the lungs

(1) Bone marrow fat enters the blood circulation and forms a fat embolism after reaching the capillary of the lung. In the early stage, it is only a simple mechanical obstruction, the blood flow is interrupted, and the distal tissue of the embolism is ischemia, but the alveolar itself still has respiratory activity.

(2) Due to the toxic effect of free fatty acids on the blood vessels in the lungs, hemorrhagic interstitial pneumonia, acute pulmonary edema, severely interfere with the ventilation function of the alveolar membrane, and respiratory dysfunction occur clinically.

(3) Free fatty acids can reduce alveolar surfactants, thereby increasing pulmonary edema, hemorrhage, and even alveolar collapse.

(4) Due to pulmonary dysfunction, the ratio of ventilation to perfusion is imbalanced, which in turn leads to a sharp drop in arterial oxygen tension.

4. Pathological changes in the brain

(1) Fat embolism brain lesions: The fat plug is mechanically blocked by small blood vessels in the brain. It can be seen by the naked eye that there are extensive punctiform hemorrhage in the white matter and cerebellar hemisphere. There are three types of lobes, namely spherical hemorrhage and annular hemorrhage. Hemorrhagic brain lesions and perivascular hemorrhage; microscopic ischemic demyelination areas can be seen under the microscope, and fat emboli are seen, often accompanied by hemorrhagic microinfarction.

(2) cerebral hypoxia changes, mainly cerebral edema, meningeal and cortical blood vessels congested, and occasionally see a bloody spot on the surface of the brain.

5. Cardiac pathological changes have not yet been reported as a case of death due to cardiac fat embolism, but when fat embolism syndrome occurs, due to the large resistance of the pulmonary vascular bed, the right heart load increases and the right heart enlarges. Impaired by hypoxia, manifested as epicardial hemorrhage, small hemorrhage spots, degeneration or necrosis area under the microscope, sometimes found in the myocardial fibers between the fat embolus.

6. fundus changes fat embolism syndrome can occur retinopathy, such as white flash or cilia-like exudate scattered in different sizes, especially in the center of the nipple or macular depression, diffuse or thin striped bleeding of the retina, Macular edema, vascular congestion, tube diameter or segmented.

Fat embolism syndrome prevention

The actual external fixation of the fracture, the operation pays attention to the gentle method, which is very important to prevent the occurrence of fat embolism. If the fracture site is not fixed properly, it is easy to move the patient to induce the disease, and it must be paid attention. Some people think that the fracture should be carried out immediately. Fixation, the incidence of lipid thrombosis is lower than that of conservative therapy, which may be related to the reduction of local abnormal activity of the fracture. In addition, the elevation of the affected limb also has a preventive effect. The numbness of the manipulation and the excessive force of the intramedullary nail can increase the blood emboli. When the symptoms of fat plugs occur, moving the patient at will can aggravate the symptoms.

Prevention of infection and prevention and treatment of shock are important to prevent the occurrence of fat embolism. Patients with shock after trauma, especially those with long-term shock and severe degree, have severe symptoms when developing lipid embolus. In this case, attention should be paid to correcting hypovolemia and blood transfusion. Should be based on fresh blood.

In addition, maintain normal blood pH, correct acidosis, oxygen, and use protease inhibitors, aprotinin is a proteolytic enzyme blocker that inhibits the activity of the kinin system and affects fat metabolism. Stabilize blood pressure, have a preventive effect on lipid plugs, severely ill patients can use 400,000 KIE (aprotinin unit) per day for 6 to 10 hours.

Complications of fat embolism syndrome Complications

No relevant information.

Fat embolism syndrome symptoms common symptoms fatigue tidal breathing high fever dyspnea breathing irregular hypoxemia convulsion

The clinical manifestations of fat embolism syndrome vary widely. Sevitt classifies them into three types, namely, fulminant, complete (typical symptom group) and incomplete (partial symptom group, subclinical), incomplete type according to the lesion. It can also be divided into pure lung type, pure brain type, and both lung type and brain type symptoms, of which the pure brain type is the least common.

The general case may have an incubation period of 4h to 15 days (average about 46h). The clinical symptom time can start from a few hours after the injury to about 1 week, and 80% of the cases occur within 48 hours after the injury.

1. Short-term waking after violent hair loss, and soon coma, sputum, sometimes convulsions, hand and foot swaying and other brain symptoms, can die within 1 to 3 days, due to bleeding points and lung X-ray lesions and other typical symptoms are not complete Clinical diagnosis is difficult, and many cases can be diagnosed at autopsy.

2. Complete type (typical symptom group) After 12~24h waking period, the fever starts, the body temperature rises suddenly, the pulse appears fast, respiratory symptoms (breathing fast, voice, cough) and brain symptoms (consciousness) Obstacle, lethargy, paralysis or coma), as well as weakness in the whole body, symptoms are rapidly aggravated, convulsions or spasms may occur, and when the respiratory center is involved, there may be irregular breathing, tidal breathing, severe respiratory arrest, and bleeding spots on the skin.

3. Incomplete type (partial symptom group) Lack of typical symptoms or asymptomatic, easy to be ignored when not paying attention, such patients, if not handled properly, can suddenly become violent or become a typical symptom group, especially when moving patients or injuries It can be induced during limb movement.

Most fat embolisms are incomplete (partial symptom group), only some symptoms, mild condition, can be divided into the following four types:

(1) Those with no respiratory symptoms: The brain symptoms are mild, and the patient has only fever, tachycardia and skin bleeding points, and there may be a decrease in arterial oxygen partial pressure.

(2) Those without brain and nervous system symptoms: mainly dyspnea, hypoxemia, fever, tachycardia and skin bleeding.

(3) Those who have no obvious brain and respiratory symptoms: mainly manifested as skin bleeding points, fever, tachycardia, which may be the point of attention.

(4) Those who have no skin bleeding points: the most difficult to diagnose.

Gurd summarizes the clinical diagnosis of fat embolism and is divided into primary, secondary and reference criteria.

1 main criteria: subcutaneous hemorrhage; respiratory symptoms and lung X-ray lesions; no neurological symptoms of craniocerebral trauma.

2 secondary criteria: arterial partial pressure of oxygen is lower than 8.0 kPa (60 mmHg); hemoglobin decreased (below 10 g).

3 reference standards: tachycardia, pulse fast; high fever; sudden drop in platelets; urinary fat drops and oliguria; free fat droplets in the blood.

Examination of fat embolism syndrome

Blood gas analysis was performed every day for 3 to 5 days after trauma, and blood routine examination was performed.

The chest X-ray shows a typical "blizzard"-like shadow.

Diagnosis and differentiation of fat embolism syndrome

Diagnostic criteria

Where there are more than 2 main criteria for clinical symptoms, or only 1 for the main criteria, and 4 or more for the secondary or reference criteria, the diagnosis can be confirmed. If there are no major criteria, there are 1 minor criteria and 4 or more reference standards. Can be diagnosed as a recessive fat embolism.

Main standard

(1) Subcutaneous hemorrhage: 2 to 3 days after injury, the front of the shoulder, the upper part of the clavicle, the front chest, the abdomen and other skin loose parts appear, can also be seen in the conjunctiva or fundus, 1 to 2 days after the injury can appear in batches , quickly disappeared, can occur repeatedly, therefore, the fracture patients should pay attention to check within a few days of admission.

(2) Respiratory symptoms: The main symptoms are dyspnea, cough, and cough (often bloody), but the wet voice is not a symptom. The typical lung X-ray shows a "blizzard" shadow on the whole lung, and often has a right An image with increased cardiac load, but this shadow may not be found, and if there is no secondary infection, it can disappear quickly. Therefore, for suspicious cases, it can be repeatedly checked by a portable X-ray machine.

(3) Brain symptoms: mainly manifested as headache, restlessness, insomnia, excitement, paralysis, confusion, lethargy, coma, paralysis, urinary incontinence and other symptoms, although there are few focal symptoms, but occasionally there may be strabismus, pupils ranging Large and diabetes insipidus, etc., therefore, when some fracture cases have unexplained brain symptoms, fat embolism should be suspected.

2. Secondary criteria

(1) Arterial oxygen partial pressure: It is valuable for early diagnosis and guidance treatment. If it is below 8.0 kPa (60 mmHg), it means hypoxemia, which is diagnostic. In severe cases, it can only be 6.67 kPa (50 mmHg) or lower. The time of hypoxemia appears inconsistent, sometimes within a few hours after injury, sometimes later; some early normal or only subclinical hypoxemia, therefore, severe trauma should be monitored daily and repeated It is generally believed that hypoxemia is late and the symptoms are mild.

The cause of hypoxemia is mainly the abnormal ventilation and blood flow ratio in the early stage, and the oxygen diffusion disorder in the alveolar; the acute shunt is caused by the acute shunt in the late stage, and the low blood oxygen is used in the early stage due to excessive breathing. The concentration decreased, respiratory alkalosis occurred; in the late stage, the concentration of carbon dioxide increased significantly, and metabolic acidosis occurred.

(2) Decreased hemoglobin (100g/L or less): Kontschorer (1936) first proposed a decrease in peripheral hemoglobin when lipid is applied (40 to 50g/L in 12h). He believes that it is a hemolysis caused by a certain toxin, but some people think that It is the result of pulmonary hemorrhage, and some people think that it is caused by increased red blood cell aggregation. Pipkin believes that this phenomenon occurs before the appearance of lesions on the X-ray of the lungs. It is a powerful diagnostic clue, so it should be checked once a day within a few days after admission.

3. Reference standard

(1) tachycardia: Gurd believes that the pulse is above 120 beats/min.

(2) High fever: more than the general fracture symptoms, the body temperature of 38 ° C or more has diagnostic significance.

(3) oliguria and fat droplets in the urine: generally floating in the upper layer of urine, so the patient must be found when the urine is completely empty, or by catheterization.

(4) thrombocytopenia: platelets can be drastically reduced, some people think that it is caused by low blood volume, or the influence of DIC, and some people think that it is related to adipose droplet agglutination.

(5) ESR: The erythrocyte sedimentation rate is increased, which can be divided into two types, one is ascending immediately after injury; the other is sharply rising on the third day after fracture. Therefore, it can be measured once in the afternoon and 5 days after injury. Gurd believes that 70mm/h or more has diagnostic significance.

(6) Increase in serum lipase: 32.7% of patients with traumatic Peltiers have serum lipase rise, starting from 3 to 4 days after injury and reaching a peak in 7 to 8 days, so this test is very meaningful within 3 to 7 days. It is believed that 18.4% of serum lipases in trauma patients increase (some drugs have an effect on lipase activity, such as ethanol can reduce its activity, heparin can increase its activity, should pay attention when checking), when lung fat plug occurs, the lung parenchyma of the disease area can be Lipase is secreted to break down the neutral fat embolus. This lipase can occur in the systemic circulation, causing an increase in serum lipase, which is diagnostic.

(7) Free fat in blood: The incidence of free fat droplets in the blood of trauma patients is increased by fluorescence microscopy. Among the 20 cases of acute trauma, 6 cases have fat droplets. Some people think that the diameter of blood fat droplets is 10-20 m. Diagnostic significance, Gurd reported that serum was filtered through a microporous filter, and the content of triglyceride and fat globules were determined by Sudan IV staining, which can be used to diagnose fat embolism, but some people think that its diagnostic value is not reliable.

4. Diagnostic classification Because the clinical symptoms and signs of fat embolism syndrome are very atypical, the diagnosis is difficult. It should be comprehensively analyzed in combination with the medical history and various related indicators. Gurd divides the diagnosis into three levels according to the above indicators:

(1) Suspicious diagnosis: severely fractured traumatic patients, after initial treatment, sudden brain symptoms and high fever, pulse rate, difficulty in breathing, cough, snoring, and even pulmonary edema in a short period of time, and light or moderate Hypoxemia, at the same time can exclude shock, infection, DIC and existing patients with cardiopulmonary disease, should be highly suspected of fat embolism, and should be further examined immediately.

(2) Early diagnosis: severe fractures have obvious hypoxemia, and can not be explained by other reasons. Although there are no major diagnostic indicators mentioned above, there are still obvious secondary indicators, such as anemia (hemoglobin is less than 100g/L). , thrombocytopenia, etc., can be initially diagnosed, but should be closely observed and should start treatment (including respiratory support therapy).

(3) Clinical diagnosis: The criteria are as described above.

At present, the diagnosis of lipid thrombosis syndrome is still under investigation. Some people think that once brain symptoms appear, continuous observation of blood and urine free fat droplets should be carried out. For example, there are multiple lipid droplets with a diameter >10-50 m in the low power field. Positive, Sevitt et al have used a renal biopsy, which is considered to be diagnosed as long as the fat globule is found, but the operation is dangerous and not widely used. Kelly tries to use ultrasonic to detect the fat plug. The method is simple, but it is still in the exploration stage. Pollak proposed the injury. Continuous observation of blood oxygen analysis within 4 days, blood routine and blood, urine fat droplets, help early diagnosis, Lihiri reported venipuncture blood 10ml, after coagulation, remove serum, blood clots quickly frozen section staining, such as fat The ball was positive. There were 7 cases of typical lipid thrombosis syndrome, 16 cases of fractures, and 10 cases were positive. Among them, 7 cases were treated with hormone therapy in the early stage, no lipid thrombosis occurred, 3 cases were untreated, 2 cases occurred. Typical lipid thrombosis syndrome; 6 cases of negative no symptoms, indicating that this method has guiding value for predicting the incidence of lipid thrombosis and early treatment.

Differential diagnosis

Attention should be paid to the identification of brain trauma, shock, sepsis, poisoning, pulmonary contusion and pneumonia.

1. Shock: Fat embolism generally does not decrease blood pressure, there is no peripheral circulatory failure, blood is not concentrated without shock, but diluted, and hemoglobin decreases, thrombocytopenia, decreased hematocrit, etc., but both have DIC phenomenon in the late stage. Therefore, some people think that lipid plug is the result of disseminated intravascular coagulation. Wersy et al reported in 21 cases of 21 cases of children, one third of which had shock, that shock can increase the fat absorption of the injured part, and the pulse of 2 to 3 days after injury. Sudden increase, in addition to shock, clinical attention should be paid to fat embolism, sepsis (infection or coexisting septic shock, can cause fat embolism).

2. Craniocerebral injury: If there is no brain injury, if you have neurological symptoms, you should pay attention to the possibility of fat embolism.

3. respiratory distress syndrome (respiratory distress syndrome): fat embolism is one of the causes of respiratory distress, and trauma, shock, sepsis, inhalation pneumonia, oxygen poisoning, excessive blood transfusion, extracorporeal circulation, etc. The distress syndrome is the same. The different points are local embolism caused by fat plug. Hemorrhage and exudation occur in the embolization area, forming interstitial edema, pulmonary fibrosis, black, abscess and necrotic area, and gradually causing fibrosis. The capsule changes, so gas exchange is difficult, and the oxygen partial pressure drops. This is the theoretical basis for applying artificial respiration in recent years.

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