burn shock
Introduction
Introduction to burn shock The majority of burn shock is secondary shock, usually occurring in the first few hours or more than 10 hours after burn. It belongs to hypovolemic shock because of the large amount of plasma in the wound from the capillaries to the wound and tissue. The gap causes a reduction in effective circulating blood volume. basic knowledge Sickness ratio: 0.0001% Susceptible people: no special people Mode of infection: non-infectious Complications: metabolic acidosis, respiratory failure, acute renal failure
Cause
Causes of burn shock
Cause:
The disease is caused by a large area of burns leading to changes in microcirculation, decreased white blood cell deformability and capillary embolism, adhesion of white blood cells to the venules, aggregation of red blood cells and platelets, and microthrombus formation, which cause an increase in microcirculation resistance. In turn, a large amount of localized plasma is exuded from the capillaries to the same space between the wound and the tissue, resulting in a decrease in effective circulating blood volume, thereby causing shock.
Prevention
Burn shock prevention
Patients with delayed resuscitation of burn shock not only suffer from internal shock due to shock, but also fail to get timely treatment of wound treatment, which is prone to infection; in addition, shock and reperfusion injury can impair intestinal barrier function and occur intestine The bacterial translocation causes intestinal infection, so delayed recovery of burn shock can be regarded as an indication for the application of prophylactic antibiotics to prevent systemic infection in the stage of edema back absorption. Silver sulfadiazine can be used for external use of sulfadiazine. Such as effective antibacterial agents, patients with delayed recovery of burn shock due to secondary shock to reperfusion injury, easy to develop into excessive systemic inflammatory response and multiple organ dysfunction syndrome, therefore, due to comprehensive measures to passivate (blunt) excessive The inflammatory response, in addition to the above measures, also includes early surgery to remove wound necrotic tissue to block the source of inflammatory mediators, and severe cases of continuous hemofiltration to remove inflammatory mediators in the blood.
Complication
Burn shock complications Complications metabolic acidosis respiratory failure acute renal failure
There are several main situations in which concomitant damage occurs during shock:
(a) the brain and central nervous system
It has the ability to automatically regulate blood flow. It may not be damaged during mild shock. In severe and persistent shock, it may be damaged. Not only the spontaneous bioelectric activity of the cortex but also the potential changes caused by the afferent nerve can be weakened or even disappeared. The metabolism can also be changed. The nerve cells have high oxygen consumption and are very sensitive to hypoxia. The blood supply to the brain is abundant. If the blood supply is reduced to 30ml/100g/min, syncope occurs. If the blood supply is completely cut off for 5 seconds, it will affect consciousness. When the whole body blood pressure drops below 70mmHg, the blood supply to the brain decreases with the decrease of arterial pressure. The microcirculatory blood vessels in the brain expand when the concentration of H+ and CO2 increases. When the concentration of these substances returns to normal, the blood flow also returns to normal. Among them, the effect of CO2 is more obvious when shock enters a serious stage. Because of low blood pressure, insufficient blood supply to the brain, hypoxia, and significant acidosis, it can cause perivascular glial swelling and capillary endothelium. The cells are swollen, the lumen is narrowed, narrow as a line, and the red blood cells pass through difficulties. This change can form a vicious circle. There is also DIC in the brain microcirculation, which further increases the hypoxia of the brain and increases the permeability of the blood vessels. Therefore, there is brain edema and elevated intracranial pressure. Microcirculation of the brain microcirculation during burns And lipid drop embolization, can damage microvessels to form a small point-like hemorrhage, called cerebral purpura, the injured patients show neurological symptoms, such as agitation, convulsions and coma, brain function changes during shock have its material basis, an important brain metabolism The characteristic is that only the lipoprotein membrane which is easy to pass the blood-brain barrier, such as intravenous NaHCO3 to correct the metabolic acidosis of shock, it is difficult to correct the acidosis of the brain because it is not easy to pass the blood-brain barrier.
(B) heart and myocardial inhibitory factor
Severe burn patients may have cardiac dysfunction. When burn is shocked, blood volume is reduced due to fluid loss, and a large amount of blood stagnates in the microcirculation. Therefore, the effective circulating blood volume is obviously insufficient. As the cardiac output decreases, the arterial pressure also decreases. This reduces coronary blood flow, lowers blood pressure, reversely causes tachycardia to shorten its diastolic phase, and also reduces coronary blood flow. When the average aorta is below 60 mmHg, coronary blood flow decreases, myocardial deficiency Blood hypoxia, if burn patients have respiratory damage and lung lesions hinder gas exchange, myocardial ischemia and hypoxia are more serious. Although the energy of the myocardium is normal, although there are many energy sources available, there are fatty acids and glucose in the order of consumption. Lactic acid, amino acids, ketone bodies, pyruvic acid, etc., myocardial metabolism mainly depends on its mitochondrial tricarboxylate cycle and oxidative phosphorylation, the tricarboxylate cycle is blocked during shock, ATP synthesis is reduced, H+ concentration is increased, and myocardial contractility is decreased.
Acidosis and hyperkalemia in burn shock have an inhibitory effect on the heart. In addition, DIC has also been involved in the microcirculation of the heart in recent years. In the case of burn shock, myocardial inhibitors are currently considered to be myocardial inhibitory factor (MDF), mainly From the pancreas of ischemia and hypoxia during shock, MDF inhibits myocardial contractility and becomes another important cause of cardiac dysfunction during burn shock. The use of aprotinin and glucocorticoids to protect cell integrity and inhibit MDF production is Effective.
(C) the pathogenesis of lung and shock lung
The change of burn shock lung is more complicated than other shocks. In addition to the respiratory changes during shock, the respiratory tract can be directly damaged by the inhalation of high temperature gas, resulting in an increase in the incidence of respiratory comorbidities of burn patients. Recent statistics at home and abroad. It shows that those who died of respiratory dysfunction in burn cases are the most, and those with respiratory tract injury without respiratory tract injury can have shock lung and acute respiratory failure. It is also one of the adult respiratory distress syndromes. In recent years, 1/3 of severe shocks have been observed in clinical observations. The patient developed shock lungs and observed under the X-ray. The plaque or diffuse density increased. The two lungs were similar. Therefore, it is easy to mistake two lobular pneumonia. The pathological changes are congestion, small bleeding points, and small lungs. Collapse, pulmonary interstitial edema and alveolar edema, formation of alveolar transparent membrane, etc., functional aspects, mainly alveolar surfactant reduction, lung compliance decreased, lung respiratory function increased, PaO2 decreased, the patient has difficulty breathing.
Effect of shock lung on respiratory function
(1) Dispersion disorder: Due to pulmonary interstitial edema, alveolar edema, formation of transparent membrane, etc., the gas dispersion distance is increased, causing a decrease in PaO2, and inhalation of high concentration oxygen can be improved.
(2) Ventilation-blood flow ratio imbalance: the area of the pulmonary microcirculation that is blocked by blood cells or micro-plugs, which are ventilated without blood flow, have vasoconstriction, have ventilation and reduce blood flow, and vice versa, blood flow is normal. The area may have alveoli occupied by exudate, or the bronchioles are blocked by secretions, so that there is blood flow without ventilation, which is also the cause of the decline of PaO2, and the inhalation of high concentration of oxygen can also be improved.
(3) Increased venous blood flow: The main reasons are: 1 normal shunt vasodilation, increased blood flow, 2 pulmonary microembolism, short circuit opening; 3 increased blood flow through non-ventilated area, increased venous blood flow during burn shock The phenomenon of venous blood infiltration into arterial blood occurs, causing PaO2 to decrease, and the improvement of inhalation of high concentration of oxygen is not great, and it is necessary to quickly correct the circulatory disorder of shock to improve. The effect of inhaling 100% oxygen and oxygen for 30 minutes is used as a reference. Helping to judge the severity, due to the above-mentioned important effects of shock lung on respiratory function, can lead to a serious decline in PaO2, and then PCO2 rises, causing respiratory failure and life-threatening.
(4) Kidney
There is often a decrease in urine output during shock. Severe shock can cause oliguria or even no urine. The urine volume often reflects the blood circulation of the kidney. The amount of urine in the early stage of shock is reduced. It may be caused by catecholamines in the circulation causing strong contraction of renal blood vessels and increased secretion of ADH. As a result, it is not categorically determined to be a renal tubular change, or acute renal failure, such as treatment by infusion and vasospasm, which improves the condition and increases the amount of urine. The change is still functional. Two aspects: First, renal vasoconstriction reduces renal blood flow, and renal cortical vasoconstriction is more significant. The glomerular input artery is more conspicuous than the output artery, which makes the blood flow through the glomerulus. A large reduction, so the filtration is reduced; the second is the effective filtration pressure drop, which is caused by the decrease in systemic mean arterial pressure during shock. When the mean arterial pressure drops to 60 mmHg, the glomerular capillary pressure drops to the original urine. The extent of almost complete cessation, when burn shock, should restore the urine volume to the level of 30 ~ 50ml / h as soon as possible, in order to reflect the renal vascular flow can be dimensioned Not to suffer kidney damage, if acute renal failure, severe burn victim is very dangerous.
Symptom
Symptoms of burn shock Common symptoms Burn wounds are sweet and suffocating... Corneal burns burn wounds light coffee... Post-burn nausea and vomiting, post-burn, pulse rate increase, post-burn, urine output, palm scar, deformity, coma, dyspnea
First, clinical manifestations
Burn shock is basically hypovolemic shock, so its clinical signs are similar to trauma or hemorrhagic shock. Its characteristics are as follows:
1, pulse growth rate:
Increased secretion of vasoactive substances in burns, increased myocardial contractility and heart rate, and compensated for increased cardiac output. The heart rate increased in the early stage of burns, and severe burns increased to 130 beats/min or more. If heart rate is too fast, Then, each time the cardiac output is reduced, the peripheral vascular resistance is increased, and the pulse is expressed as a weak number. When the shock is severe, the pulse is more delicate.
2, urine output reduction:
It is an early manifestation of burn shock, which generally reflects the blood perfusion of the tissue, and also reflects the severity of burn shock more sensitively. The amount of urine in the early stage of burn is reduced, mainly due to insufficient blood volume and decreased renal blood flow, but also With vasopressin, the increase in aldosterone secretion limits the amount of water excreted by the kidneys.
3, thirst:
It is an early manifestation of burn shock, which may be related to changes in intracellular and extraosseous pressure and insufficient blood volume, and is also controlled by the hypothalamus-pituitary-adrenal system.
4, irritability and non-amine:
It is a manifestation of brain cells and thus poor blood perfusion. It appears earlier in symptoms and can reflect the severity of burn shock. It is also a sensitive indicator of treatment response. When brain cerebral hypoxia is severe, it may be paralyzed, manic, and conscious. Even coma, but need to be differentiated from cerebral edema and early infection.
5, nausea and vomiting:
It is one of the early symptoms of burn shock. The common cause is cerebral hypoxia. The vomit is generally the contents of the stomach. In severe shock, there may be brown or bloody vomit, suggesting that the digestive tract mucosa is severely congested, edematous or erosive. Acute gastric dilatation or paralytic ileus should be considered.
6, poor peripheral circulation:
In the early stage of burns, the skin is white, the limbs are cold, and sometimes the hair is slightly blemishes. The superficial veins are poorly filled. After pressing the nail bed and skin capillaries to make it white, the time to restore normal blood color is prolonged.
7, blood pressure and pulse pressure changes:
In the early stage of vascular contraction, the surrounding resistance increases, and the blood pressure tends to increase, especially the diastolic blood pressure. Therefore, the pulse pressure difference becomes smaller, the subsequent generation is incomplete, the capillary bed is enlarged, the blood stagnates, and the effective circulating blood volume decreases, and the blood pressure begins to decrease. Shock has been more serious. In the blood pressure changes, the pulse pressure becomes smaller and appears earlier.
Second, the basic changes of microcirculation during burn shock
(a) Changes in microcirculatory hemodynamics.
1. Ischemic hypoxia: a strong stimulation of burns, through the spinal nerves and other afferent nerve bundles, the upward reticular activation system into the central, through the integration of the nervous system, promote the hypothalamus and pituitary The function is strengthened, which not only has the meaning of defense compensation, but also causes damage. The sympathetic nerve is strongly excited under the regulation of neuroendocrine function. The concentration of adrenaline can be increased to 100-150 times of the normal value. Norepinephrine can be used. Increasing to 50-100 times, catecholamines can be increased to 30-300 times, they act on microcirculatory blood vessels, so that those are strongly contracted by the dominant blood vessels.
Burns can cause vascular permeability increase not only locally, but also in distant sites. It can exude and lose a large amount of plasma fluid from local wounds, especially large-area burns, which directly leads to a decrease in blood volume and a decrease in circulating blood volume. Under this circumstance, if the vascular bed does not undergo a contraction reaction, the blood pressure will inevitably decrease significantly. At this time, the carotid sinus, the aortic arch reflex is a pressor response, and the microcirculatory vascular smooth muscle is contracted by the sympathetic nerve. Conducive to maintaining blood pressure and increasing blood flow back.
In the case of burns, the microcirculation changes caused by the above-mentioned main causes greatly reduce the nutrient blood perfusion of the microcirculation, especially the sites where the receptors predominate, such as the skin, mucous membrane, kidney, stomach, spleen and intestine. In the upper arterial supply area, etc., the blood flow of the venous short circuit increases, causing tissue, cell ischemia and hypoxia, first metabolic changes, followed by qualitative changes in the generator, in this period, if anti-shock measures (such as pain Elimination, shock of blood volume, release of vasospasm, etc.) failed to be timely and effective, and the disease will continue to develop.
In addition to causing ischemia and hypoxia, which is extremely harmful to the body, this change also affects the other side of compensation, such as increasing peripheral resistance, which is conducive to the maintenance of mean arterial pressure in the aorta; The capacity of the circulatory vascular bed is such that the blood supply to vital organs is guaranteed for a certain period of time; when the blood storage organ receives contraction, the blood storage and circulation have an effect of increasing the circulating blood volume. It is currently considered that the microcirculation is for tissues and cells. The change of blood perfusion is more important than the change of arterial pressure. It should pay attention to the clinical reference value of arterial pressure, but also pay more attention to the changes of microcirculation and its prevention and treatment, such as the improvement of microcirculation in treatment, the effect There will be a significant increase.
In addition to the above changes, there are other vasoconstrictors that begin to function in this period, such as strong contraction of the renal microcirculation, causing renal ischemia, renin-angiotensin system begins to function, when systemic blood pressure drops, renal vascular perfusion When reduced, the near-ball device is excited to release renin, which is active in the range of changes in plasma pH. Angiotensin II can cause arteriolar smooth muscle contraction, and its effect is beneficial to maintain blood pressure, but strengthens tissue blood perfusion. The decline, in addition, angiotensin has other effects, such as promoting the secretion of aldosterone in the adrenal spheroidal band; promoting the adrenal medulla to secrete adrenaline; in some parts of the body can improve the sympathetic effect; stimulate the pituitary release of vasopressin; blood concentration is not When high, the kidneys are reduced in sodium, and when the concentration is high, the kidneys are increased in sodium.
2. Congestive hypoxia: The long-term contraction of capillaries during ischemic hypoxia is bound to cause changes in tissue and cell metabolism. These changes are mainly caused by hypoxia, followed by lack of blood perfusion and accumulation of metabolites. The increase of local concentration, such as lactic acid, [H+], PW2, histamine, etc., gradually increased. The formation and release of histamine increased during local hypoxia, which was caused by the activity of histidine decarboxylase. Highly related, H+ concentration and histamine concentration in the tissue lacking blood perfusion, after the intercellular fluid is elevated, under their joint action, the small arteries, arterioles, and anterior capillary sphincters are first relaxed, so that these smooth muscle pairs The catecholamine loses its sensitivity. On the other hand, due to the action of histamine, histamine can cause the venous side to contract during the expansion of the arterial side. It is believed that the 5-HT countermeasure cycle is similar to the introduction of histamine. While relaxing the micro-animals, the anterior capillary sphincter, there is also the effect of contracting the larger veins. Due to the above changes, the arterial side of the microcirculation begins to relax. Zhang, while the vein side is still contracting, the blood of the microcirculation is more and less, that is, the irrigation is greater than the flow, which causes the blood stasis in the microcirculation blood vessels. As long as this change reaches a certain level, the blood can be stagnated in a small amount. Within the cycle, the effective blood volume drops sharply, and the congestive ischemic period can affect the neuromodulation function, because the supply of blood to the brain and the supply of oxygen cannot be guaranteed by the compensation of the body for a long time, and adjustment may occur at this time. The decline of function, the hemostatic state of the above microcirculation, the intravascular static pressure rises, the liquid exudation increases, and the amount thereof is also considerable. When measuring the hematocrit, the hematocrit can be found to increase, reflecting the plasma volume due to exudation. Increase and decrease, prepare blood for concentration.
(B), changes in blood in the microcirculation
The change of blood in the microcirculation is the most serious stage of the microcirculation of burn shock. The focus of the change is the stagnant blood in the microcirculation. The white blood cell deformability and capillary embolism appear in shock, and the white blood cell adhesion in the venule , red blood cells and platelet aggregation, as well as microthrombus formation, etc., which cause increased microcirculation resistance, which is of great significance in the pathogenesis of shock, and has become a new topic in the study of shock microcirculation.
1. Separation of blood components Due to congestion, the blood flow rate drops significantly. Some blood cells move slowly back and forth in the expanding microcirculatory blood vessels, and some are in a stagnant state, and the leakage of liquid leads to a decrease in blood suspension stability. Separation of the ingredients in the preparation of the ploughing, the plasma is mostly located before and after the capillary branching, in the few capillaries, there is only plasma and no red blood cells, the red blood cells are located in the direct pathway of the capillary unit, and the white blood cells and platelets are mostly located in the capillary unit. In the marginal branches, this distribution may be related to the distribution of the formation in the normal blood flow. The axial flow and the lateral flow phenomenon are that the formation is in the axial flow, and the important and largest red blood cells are the axes in the axis, the white blood cells and The platelets are light, at the edge of the axial flow, and the lateral flow is plasma. When the burn is shocked, the hemodynamic changes occur, the blood becomes slow, the blood contracts, and the blood cells stagnate in front of the narrow venules and venules. It promotes the development of blood changes in various microcirculations described below.
2. Increased blood viscosity in the microcirculation. The viscosity of the blood is inversely proportional to the flow rate. When the pressure is constant, the viscosity of the microcirculation decreases as the viscosity increases. The increase in viscosity is mainly due to blood contraction and formation. The proportion is increased and red blood cells are cohesive.
(1) The hematocrit is obviously increased. This phenomenon is caused by microcirculation congestion and extravasation of blood components. This phenomenon is also observed in other types of shock, but the blood concentration of burn shock is more significant. Blood collection is checked by microcirculation. The increase in product is particularly obvious, because a large number of blood cell stagnation is retained in the microcirculation. If a large venous blood test is taken, sometimes the hematocrit may be normal or lower than normal due to factors such as hemolysis or infusion.
(2) Red blood cell cohesion occurs, which is mainly caused by hemodynamic changes. In the condition of blood stasis and slow flow rate, the red blood cell clogging procedure sticks to agglomerates in some segments of the microcirculation-diffusing blood vessels. When the surface of the red blood cells is covered with fibrinogen, it is conducive to cohesion. In addition, at this time, the blood in the microcirculation is hypercoagulable, forming fibrin filaments attached to the wall, and red blood cells are also easy to adhere thereto, and the negative charge on the surface of the red blood cells is also lowered. It is related to cohesion. When it is agglomerated into agglomerates or agglomerates, the viscosity of the blood increases and it is less likely to flow. In the case of burn shock and traumatic hemorrhagic shock, red blood cell adhesion is common, not only because of high temperature. Direct action occurs in the injured area, and red blood cell adhesion is common in shock and traumatic hemorrhagic shock. It occurs not only in the direct action of high temperature but also in the injured area, and also occurs in the microcirculation vessels throughout the body due to shock. For example, in the microcirculation of the lungs, liver, intestinal mucosa, kidney, pancreas, adrenal gland, and heart, this cohesion is not coagulated, and the blood flow is accelerated after the circulation is improved. Still depolymerization member.
3. Changes in the shape of red blood cells When red blood cells are directly exposed to temperatures above 50 °C, changes and destruction occur. In the case of burn shock, red blood cells in the microcirculation are hypoxic, lacking nutrients, acidosis and In the environment of metabolites, the shape changes and becomes spherical. At this time, it is not easy to pass through the capillaries. After the red blood cells are swollen and spherical, the total volume of red blood cells increases by 6%, and the resistance of the external wind and rain can increase by 90%, thus forming the periphery. The resistance is not only the function of the resistance blood vessel and the resistance device, but also related to the blood viscosity and even the change of the shape of the blood. The swelling of the spherical red blood cells exceeds a certain limit, the plasma membrane can be broken and hemolysis occurs. The blood in which the fibrin filament floats is easily attached to the red blood cells. Under the action of the pulling force, the red blood cells are deformed and finally ruptured to cause hemolysis. If there is a factor that increases the fragility of red blood cells in the blood of the burned patient, hemolysis may also occur. Therefore, in general, patients with large-area burn shock have more hemolysis, and last longer, burning Late anemia, mainly invasive and exudative, visceral hemorrhage and other blood loss and malnutrition, hematopoietic inhibition and other original protein tubular obstruction of the lumen, but it is currently considered that this type of tubular obstruction is not serious, after the urine flow returns to normal Easy to remove, the hemoglobin tube type in the renal tubules, under conditions of sepsis, can be decomposed by the action of bacteria and its toxins, producing acidic products and toxic substances, causing degeneration and necrosis of epithelial cells of the renal tubules, which may become urgent after burns. One of the causes of renal insufficiency and renal failure, the deformation of red blood cells is also reversed, just as cohesion can depolymerize, when the microcirculation is improved, the nutrition and metabolism of red blood cells are gradually restored, and the shape can be restored to normal, only those When the change exceeds a certain limit, the brittleness increases, and it will gradually destroy and hemolyze.
4, platelet adhesion burn shock venous blood test platelet and white blood cell count decreased, other types of shock are also the same, burn shock, platelet aggregation in the microcirculation is a frequent phenomenon, platelet adhesion causes: 1 blood flow When the speed drops, platelets, white blood cells, etc. are lightly formed and close to each other; 2 adenosine, hemolysate, histamine, 5-HT, and catecholamines and endotoxin released during hypoxia Platelet adhesion, platelet adhesion time is not long, can still be depolymerized due to improved circulation, therefore, can be recovered in a short period of time, if the adhesion time is long, due to lack of oxygen, metabolic disorders, platelets will break down and break The released platelet factors 1, 2, 3, 4, etc. all promote blood coagulation, which is the main risk.
5, microcirculation blood vessels in blood coagulation is different from adhesion, the genetic change is fibrinogen into fibrin, which can form fibrin micro-plugs, but also can be wrapped around blood cells to form a blood clot, with blood flow drifting to other parts causing infarction, The micro-plug can not be dissipated by blood flow, and can be dissolved under the action of thrombolytic drugs. Once blood coagulation occurs, the microcirculation changes are not easy to recover, and the microcirculatory blood vessels are blocked, although the blood stagnates due to prolonged stagnation of blood. Tissue ischemia, hypoxia can cause a large amount of acidic substances to accumulate, the pH value drops below 6.9, venules and venule smooth muscles have begun to relax, blood vessels dilate, but the blood flow of microcirculation has not been easy to improve, In the late stage of shock, the tissue of the ischemic and hypoxic organs, the cells appear to change or even necrosis, and the metabolism and function of the whole body are significantly decreased. Any type of shock is caused by neuroendocrine and some changes in body fluids. Various factors such as lymphatic and interstitial fluids act on the polynucleotide chain in the cell, causing changes in various enzymes in the cell. Change cell metabolism until cell degeneration, necrosis and disintegration, that is, the development of various enzymes in the extracellular phase to the blood vessels to achieve the degree of blood coagulation in the blood vessels, blood coagulation in the microcirculation, in addition to the reasons for surgery, It should be pointed out that the tissue clotting-activated enzyme released by tissue damage during hypoxia activates the external pathway of coagulation; the intrinsic pathway of collagen-activated coagulation exposed after vascular endothelial injury; and the local concentration of these procoagulant factors is high, both are DIC Promoting factors, microcirculation blood coagulation, consumption of various coagulation factors, so that the concentration of various blood coagulation factors in the blood of large and large blood vessels is significantly reduced, therefore, the blood is often found in the autopsy of the injured person who suffered from shock. Non-coagulation, called loss coagulopathy, bleeding tendency in patients with advanced shock, in addition to loss of coagulopathy is an important reason, there are factors of excessive fibrinolysis.
Third, the basic changes in metabolism during burn shock
Microcirculation hemodynamic changes and DIC formation occur during burn shock. Its metabolism is characterized by ischemia, hypoxia and metabolic acidosis. The total metabolic state during shock is low metabolic rate. The hypermetabolism of burn has its other pathogenesis. The principle is different from the metabolism of burn shock.
In the case of burn shock, the ischemia and hypoxia of cells, the core effect is the disorder of the aerobic metabolism process of the cells. At this time, due to insufficient oxygen supply, NADH2 is accumulated in the tricarboxylate cycle, the oxidation process is difficult to carry out, the energy is insufficient, and the phosphorylation process is also Impeded impediment, ATP synthesis decreased, lactic acid formation increased, lactic acid concentration increased, when the microcirculation of burn shock reached a certain degree of severity, severe hypoxia, oxidative metabolism is incomplete, and glucose metabolism is greatly increased by the proportion of glycolysis, while oxidation The process of phosphorylation is severely impeded, which is also seen as a metabolic at shock, from the advanced form of biological purchases back to the generation form, the metabolism of human cells is not a variety of cells, but different For hypoxia tolerance, type A metabolism is strong in glycolysis and pentose pathways, such cells are resistant to hypoxia, such as low-differentiated phagocytic cells, hormone-producing cells, nodular tissue and epidermis B type metabolism is strong in the process of tricarboxylate and oxidative phosphorylation. Their mitochondria are abundant and are not resistant to hypoxia, such as high differentiation of nerve cells, cardiomyocytes, liver. Cells, renal tubular epithelial cells, etc., type C metabolism is a relatively balanced process of glycolysis and oxidative phosphoric acid. The product of type A metabolism can be continuously oxidized by type B metabolism, such as glial cells and nerve cells, strong cells of the atrioventricular With the main muscle cells; Kupffer cells and liver cells, shock and hypoxia, B and C metabolism are forced to change to type A, lactic acid accumulates in the intracellular fluid and external fluid, the concentration is increasing, and the H+ concentration is increased. Metabolic acidosis is getting heavier and heavier, eventually leading to the overall inhibition of cell metabolism, the relationship between arterial blood lactate level and the severity of shock, the higher the blood lactate level, the higher the mortality rate. It can be seen that the prevention and treatment of acidosis is the rescue of shock. One of the important aspects, hypoxia in burn shock is not only due to changes in microcirculation; metabolic acidosis is not only due to lactic acid, for example, combined with respiratory tract damage due to inflammation, congestion, edema and stenosis, inadequate ventilation, alveolar surface Destruction of active substances causes scattered lung atrophy, pulmonary interstitial and alveolar edema caused by microembolism syndrome, 2,3DPG reduction in red blood cells, oxidation in red blood cells Metabolic disorders release oxygen in the tissue. In addition, pulmonary microembolism also interferes with the exchange of blood flow and gas. It can reduce the swelling of collagen fibers and the edema of mitochondria itself, and also keep acidic metabolites in the body. The increase of H+ concentration inside and outside is extremely harmful to the cells, which can destroy the membrane of mitochondria and the membrane of lysosome, thus completely destroying the cells. When the change reaches a certain extent, it can kill and improve oxygen supply and tissue. Blood perfusion can make the cells get more oxygen, take more H+, and the situation will improve. This is necessary to save burn shock, and it can be done now.
In large-area burns, the lysosomal enzymes released by damaged cells in the injured area have a great harm to the whole body after local inhalation of blood. After the shock occurs, the blood perfusion in the tissue is seriously insufficient, and the ischemic organs of the whole body The tissue can release more lysosomal enzymes when the cells are damaged, further aggravating the damage of the tissue cells. In short, the tissue in shock will cause shock cells under the action of long-term ischemia, hypoxia and toxic substances. Changes within.
Fourth, the main function changes in burn shock
(a) the brain and central nervous system
It has the ability to automatically regulate blood flow. It may not be damaged during mild shock. In severe and persistent shock, it may be damaged. Not only the spontaneous bioelectric activity of the cortex but also the potential changes caused by the afferent nerve can be weakened or even disappeared. The metabolism can also be changed. The nerve cells have high oxygen consumption and are very sensitive to hypoxia. The blood supply to the brain is abundant. If the blood supply is reduced to 30ml/100g/min, syncope occurs. If the blood supply is completely cut off for 5 seconds, it will affect consciousness. When the whole body blood pressure drops below 70mmHg, the blood supply to the brain decreases with the decrease of arterial pressure. The microcirculatory blood vessels in the brain expand when the concentration of H+ and CO2 increases. When the concentration of these substances returns to normal, the blood flow also returns to normal. Among them, the effect of CO2 is more obvious when shock enters a serious stage. Because of low blood pressure, insufficient blood supply to the brain, hypoxia, and significant acidosis, it can cause perivascular glial swelling and capillary endothelium. The cells are swollen, the lumen is narrowed, narrow as a line, and the red blood cells pass through difficulties. This change can form a vicious circle. There is also DIC in the cerebral microcirculation, which further increases the hypoxia of the brain and increases the permeability of the blood vessels. Therefore, there is brain edema and elevated intracranial pressure. Thrombosis and lipid droplet embolization can damage microvessels and form small punctate hemorrhage, called cerebral purpura. The wounded exhibit neurological symptoms such as agitation, convulsions and coma. Brain function changes during shock are based on its material metabolism. The important feature is that only the lipoprotein membrane that glucose easily passes through the blood-brain barrier, such as intravenous NaHCO3 to correct the metabolic acidosis of shock, it is difficult to correct the acidosis of the brain because it is not easy to pass the blood-brain barrier.
O2 and CO2 are easy to enter the blood-brain barrier, so brain metabolism produces ATP to maintain the activity of nerve cells, mainly glucose and O2. If glucose consumption is not supplemented and hypoglycemia occurs, the material basis of brain metabolism is insufficient. When brain glial cells are swollen, microcirculatory vascular endothelial cells are swollen, brain edema, DIC, etc. cause ischemia, O2, glucose and other nutrients are severely deficient, and cerebral ischemia and hypoxia during shock are harmful to energy metabolism. Very large, the weight of the brain is about 2% of the weight. In the quiet state, its glucose consumption accounts for about 65% of the whole body. The gray matter cells of the brain account for about 1/5 of the total amount of brain cells, while the oxygen consumption and Glucose accounts for about 80% of the total. In the case of ischemia and hypoxia, cortical nerve cells are the first to be affected. The more evolved, the more harmful the part is, the faster it will be. In severe cases, the nerve cells will consume themselves. Substance destroys the structure. When the nerve cells turn to consume their own proteins and lipids, the NH3 produced by proteolysis can form glutamine, which can lift the NH3 to God. A major hazard to cell function, however, the formation of glutamine requires the consumption of alpha-ketoglutaric acid in the tricarboxylate cycle, which in turn aggravates the barrier of the tricarboxylate cycle. It can be seen that brain glutamine is formed during shock, which is harmful to reduce NH3. The benefits, but hinder the tricarboxylate cycle is very unfavorable, and the increase of -aminobutyric acid is a serious reflection of the metabolic dysfunction of nerve cells.
(B) heart and myocardial inhibitory factor
Severe burn patients may have cardiac dysfunction. When burn is shocked, blood volume is reduced due to fluid loss, and a large amount of blood stagnates in the microcirculation. Therefore, the effective circulating blood volume is obviously insufficient. As the cardiac output decreases, the arterial pressure also decreases. This reduces coronary blood flow, lowers blood pressure, reversely causes tachycardia to shorten its diastolic phase, and also reduces coronary blood flow. When the average aorta is below 60 mmHg, coronary blood flow decreases, myocardial deficiency Blood hypoxia, if burn patients have respiratory damage and lung lesions hinder gas exchange, myocardial ischemia and hypoxia are more serious. Although the energy of the myocardium is normal, although there are many energy sources available, there are fatty acids and glucose in the order of consumption. Lactic acid, amino acids, ketone bodies, pyruvic acid, etc., myocardial metabolism mainly depends on its mitochondrial tricarboxylate cycle and oxidative phosphorylation, the tricarboxylate cycle is blocked during shock, ATP synthesis is reduced, H+ concentration is increased, and myocardial contractility is decreased.
Acidosis and hyperkalemia in burn shock have an inhibitory effect on the heart. In addition, DIC has also been involved in the microcirculation of the heart in recent years. In the case of burn shock, myocardial inhibitors are currently considered to be myocardial inhibitory factor (MDF), mainly From the pancreas of ischemia and hypoxia during shock, MDF inhibits myocardial contractility and becomes another important cause of cardiac dysfunction during burn shock. The use of aprotinin and glucocorticoids to protect cell integrity and inhibit MDF production is Effective.
(C) the pathogenesis of lung and shock lung
The change of burn shock lung is more complicated than other shocks. In addition to the respiratory changes during shock, the respiratory tract can be directly damaged by the inhalation of high temperature gas, resulting in an increase in the incidence of respiratory comorbidities of burn patients. Recent statistics at home and abroad. It shows that those who died of respiratory dysfunction in burn cases are the most, and those with respiratory tract injury without respiratory tract injury can have shock lung and acute respiratory failure. It is also one of the adult respiratory distress syndromes. In recent years, 1/3 of severe shocks have been observed in clinical observations. The patient developed shock lungs and observed under the X-ray. The plaque or diffuse density increased. The two lungs were similar. Therefore, it is easy to mistake two lobular pneumonia. The pathological changes are congestion, small bleeding points, and small lungs. Collapse, pulmonary interstitial edema and alveolar edema, formation of alveolar transparent membrane, etc., functional aspects, mainly alveolar surfactant reduction, lung compliance decreased, lung respiratory function increased, PaO2 decreased, the patient has difficulty breathing.
1, the pathogenesis of shock lung
(1) Pulmonary veins and venules, systolic pulmonary veins of venules are rich in innervation and smooth muscle layer, and have a contractile response to sympathetic, vagal stimulation, bradykinin, catecholamine, 5-HT, histamine, etc. All the factors exist, and the pulmonary vascular resistance increases, and the intravascular pressure in the microcirculation increases, which is favorable for liquid exudation.
(2) DIC in the micro-thrombosis syndrome during shock, there may be a large number of micro-plugs to the lungs causing microcirculation embolization, resulting in increased resistance, and fibrin degradation products have an increase in permeability factor, which may cause an increase in the overall circulation of microcirculatory vessels. Extravasation of the fluid, in addition to 5-HT and histamine released by platelet breakdown, is a substance that causes vasoconstriction of the pulmonary venous system.
(3) Other aspects such as central heart failure during shock, excessive infusion, oxygen poisoning damage to pulmonary capillaries, etc., can cause pulmonary edema, if there is respiratory damage, the situation is more serious, pulmonary congestion, edema, capillary Damage rupture can form bleeding spots and even plaque-like bleeding.
The pathogenesis of lung collapse is mainly due to the decrease in the synthesis of alveolar surfactant due to hypoxia and the decrease in activity. The main component is di-fatty acid lecithin, which is synthesized and secreted by type II alveolar epithelial cells, and the exudate of pulmonary edema. It may also accelerate its destruction. Its role is to reduce the surface tension of the inner surface of the alveoli, so the alveolar expansion is difficult. In addition, the fine branch gas is blocked by secretions in the near, which can also cause the gas in the alveoli to be absorbed and atrophied. Recently, the release of PGE2 in lung tissue when DIC was detected can cause obstruction of bronchioles and cause alveolar atrophy.
2. The effect of shock lung on respiratory function
(1) Dispersion disorder: Due to pulmonary interstitial edema, alveolar edema, formation of transparent membrane, etc., the gas dispersion distance is increased, causing a decrease in PaO2, and inhalation of high concentration oxygen can be improved.
(2) Ventilation-blood flow ratio imbalance: the area of the pulmonary microcirculation that is blocked by blood cells or micro-plugs, which are ventilated without blood flow, have vasoconstriction, have ventilation and reduce blood flow, and vice versa, blood flow is normal. The area may have alveoli occupied by exudate, or the bronchioles are blocked by secretions, so that there is blood flow without ventilation, which is also the cause of the decline of PaO2, and the inhalation of high concentration of oxygen can also be improved.
(3) Increased venous blood flow: The main reasons are: 1 normal shunt vasodilation, increased blood flow, 2 pulmonary microembolism, short circuit opening; 3 increased blood flow through non-ventilated area, increased venous blood flow during burn shock The phenomenon of venous blood infiltration into arterial blood occurs, causing PaO2 to decrease, and the improvement of inhalation of high concentration of oxygen is not great, and it is necessary to quickly correct the circulatory disorder of shock to improve. The effect of inhaling 100% oxygen and oxygen for 30 minutes is used as a reference. Helping to judge the severity, due to the above-mentioned important effects of shock lung on respiratory function, can lead to a serious decline in PaO2, and then PCO2 rises, causing respiratory failure and life-threatening.
(4) Kidney
There is often a decrease in urine output during shock. Severe shock can cause oliguria or even no urine. The urine volume often reflects the blood circulation of the kidney. The amount of urine in the early stage of shock is reduced. It may be caused by catecholamines in the circulation causing strong contraction of renal blood vessels and increased secretion of ADH. As a result, it is not categorically determined to be a renal tubular change, or acute renal failure, such as treatment by infusion and vasospasm, which improves the condition and increases the amount of urine. The change is still functional. Two aspects: First, renal vasoconstriction reduces renal blood flow, and renal cortical vasoconstriction is more significant. The glomerular input artery is more conspicuous than the output artery, which makes the blood flow through the glomerulus. A large reduction, so the filtration is reduced; the second is the effective filtration pressure drop, which is caused by the decrease in systemic mean arterial pressure during shock. When the mean arterial pressure drops to 60 mmHg, the glomerular capillary pressure drops to the original urine. The extent of almost complete cessation, when burn shock, should restore the urine volume to 30 ~ 50ml / h as soon as possible, in order to reflect the renal vascular flow can Who will not suffer kidney damage, if acute renal failure occurs, serious burn victim is very dangerous.
The measurement of central venous pressure is helpful to judge the condition of the kidney. When the blood volume of shock is shocked, the pulmonary artery pressure is increased due to pulmonary microembolism, which affects the right heart. The CVP value is often lower than the normal value, which can be 0. Even a negative value, after the infusion is sufficient, the central venous pressure can be restored to normal. If the vasospasm has been relieved, the urine volume is increased to 35 ml/h, which means that the kidney has no major damage, such as still oliguria or no urine. There may be tubular damage, and the possibility of acute renal failure should be considered.
Examine
Burn shock check
Generally, according to the clinical manifestations, the diagnosis of burn shock can be made. If conditions permit, necessary laboratory tests such as plasma osmotic pressure, hematocrit, red blood cell count, hemoglobin count, hemoglobin, etc., can help early diagnosis of burn shock. For therapeutic reference, the purpose of early diagnosis is to treat it early, often to prevent it from happening or to reduce its severity.
(1) Laboratory inspection
The necessary laboratory tests are helpful for the early diagnosis of burn shock and the judgment of the progress of the disease. The test changes of burns are mainly reflected in the following three aspects: 1 pituitary-adrenal response, eosinophils, lymphocytes and thrombocytopenia , the content of catecholamine in blood increased; 2 low blood volume, low blood flow and tissue hypoxia, generally expressed as blood concentration, increased red blood cell count, increased hemoglobin and hematocrit, central venous pressure decreased, metabolic acid Poisoning, arterial oxygen partial pressure is reduced, carbon dioxide partial pressure is normal or decreased, arterial blood pH is normal or decreased, venous blood carbon dioxide binding is reduced, blood buffer alkali and residual alkali are reduced, etc. Metabolism, manifested as blood sugar, blood non-protein Nitrogen, increased blood potassium, low blood sodium, etc. 3 The reflection of visceral dysfunction varies with the surface of visceral dysfunction.
(2) Blood pressure measurement
The measurement of central venous pressure is helpful to judge the condition of the kidney. When the blood volume of shock is shocked, the pulmonary artery pressure is increased due to pulmonary microembolism, which affects the right heart. The CVP value is often lower than the normal value, which can be 0. Even a negative value, after the infusion is sufficient, the central venous pressure can be restored to normal. If the vasospasm has been relieved, the urine volume is increased to 35 ml/h, which means that the kidney has no major damage, such as still oliguria or no urine. There may be tubular damage, and the possibility of acute renal failure should be considered.
Diagnosis
Diagnosis of burn shock
The diagnosis of this disease is not difficult. The shock caused by burns has a history of extensive burns. Therefore, there is very little need for differential diagnosis in clinical practice. In addition to some patients with burns and trauma, it is necessary to check the change of blood volume.
