bubble_chart Overview

Burn shock is mostly secondary shock, usually occurring within the first few hours or more than ten hours after the burn. It is a type of hypovolemic shock caused by a large amount of plasma leaking from capillaries into the wound and interstitial spaces, leading to a reduction in effective circulating blood volume.

bubble_chart Pathological Changes

Burns are an extremely complex traumatic disease, especially severe large-area burns. Although the disease-causing factors act for a short period, the disease progresses according to its own laws. Burn shock is one of the most important pathological processes. The critical point for the occurrence of burn shock is when the burn area exceeds 15% in adults and 10% in children, with second-degree and deep second-degree burns accounting for more than 50% of the total area. This critical point roughly reflects the human body's compensatory capacity for burns. Beyond this point, relying solely on compensatory capacity is insufficient to prevent the occurrence and progression of shock, and effective anti-shock measures must be taken as soon as possible.

I. Basic changes in microcirculation during burn shock

(1) Changes in microcirculation hemodynamics.

1. Ischemic hypoxia phase: The intense stimulation of burns is transmitted to the central nervous system via the spinal ascending nerve tracts, other afferent nerve tracts, and the ascending reticular activating system. Through the integration within the nervous system, the functions of the hypothalamus and pituitary gland are enhanced, which has both defensive compensatory significance and potential for causing damage. The sympathetic nervous system becomes strongly excited under the enhanced regulation of neuroendocrine functions. The blood concentration of adrenaline can increase to 100-150 times the normal value, norepinephrine to 50-100 times, and Black Catechu phenols to 30-300 times. These substances act on the microcirculatory vessels, causing those with dominant α-receptors to contract strongly.

Burns not only cause local damage but can also increase vascular permeability in distant areas, leading to the exudation and loss of a large amount of plasma fluid from the local wound, especially in large-area burns, directly resulting in a decrease in blood volume and circulating blood volume. Under these conditions, if the vascular bed does not contract, blood pressure will inevitably drop significantly. At this time, the carotid sinus and aortic arch reflexes produce a pressor response. The contraction of smooth muscles in microcirculatory vessels via the sympathetic nervous system helps maintain blood pressure and increase venous return.

During burns, the changes in microcirculation caused by the aforementioned main reasons significantly reduce the nutritional blood flow in the microcirculation, especially in areas with dominant α-receptors, such as the skin, mucous membranes, kidneys, stomach, spleen, and mesenteric regions. The increased blood flow through arteriovenous shunts leads to tissue and cellular ischemia and hypoxia, first causing metabolic changes and then organic changes. If anti-shock measures (such as pain relief, blood volume restoration, and relief of vasospastic contraction) are not timely and effective, the disease will continue to progress.

The changes in this phase, while causing harmful effects such as ischemia and hypoxia, also have adaptive compensatory aspects. For example, increasing peripheral resistance helps maintain mean arterial pressure; reducing the capacity of the microcirculatory vascular bed in large areas of the body ensures blood supply to vital organs for a certain period; and the contraction of blood storage organs increases circulating blood volume. Currently, it is believed that changes in microcirculatory blood flow to tissues and cells are more important than changes in arterial pressure. Clinical attention should be paid to both the reference value of arterial pressure and the changes in microcirculation and their prevention and treatment. Emphasizing the improvement of microcirculation in treatment can significantly enhance outcomes.

In addition to the aforementioned changes, other vasoconstrictive substances begin to take effect during this period. For example, intense constriction of the renal microcirculation leads to renal ischemia, and the renin-angiotensin system starts to function. When systemic blood pressure drops and renal vascular perfusion decreases, the juxtaglomerular apparatus is stimulated to release renin, which remains active within the range of plasma pH changes. Angiotensin II can cause contraction of smooth muscles in small stirred pulses, an effect that helps maintain blood pressure but exacerbates the decline in tissue blood perfusion. Furthermore, angiotensin has other effects, such as promoting the secretion of aldosterone from the zona glomerulosa of the adrenal cortex; stimulating the adrenal medulla to secrete adrenaline; enhancing sympathetic effects in certain parts of the body; stimulating the pituitary to release antidiuretic hormone; and, at low concentrations, reducing sodium excretion by the kidneys, while at high concentrations, increasing sodium excretion.

2. Stagnant Hypoxia Phase The prolonged contraction of capillaries during the ischemic hypoxia phase inevitably leads to metabolic changes in tissues and cells. These changes are primarily caused by hypoxia. Secondly, due to the lack of blood perfusion, metabolic products accumulate and their local concentration increases, such as lactic acid, [H⁺], PW₂, histamine, etc., all gradually increase. During local hypoxia, the production and release of histamine are stimulated and increase, which is related to the increased activity of histidine decarboxylase at this time. After the concentration of H⁺

and histamine increases in the interstitial fluid of tissues and cells lacking blood perfusion, under their combined action, they first cause the relaxation of small stirred pulses, micro stirred pulses, and precapillary sphincters, making these smooth muscles lose sensitivity to Black Catechu phenols. On the other hand, due to the action of histamine, while histamine dilates the stirred pulse side, it can cause a contraction reaction on the venous side. Some believe that the effect of 5-HT on the circulation is also similar. While histamine relaxes microvessels and precapillary sphincters, it also has the effect of contracting larger veins. Due to the above changes, the stirred pulse side of the microcirculation begins to relax and dilate, while the venous side remains contracted. The microcirculation has more blood entering than exiting, that is, perfusion is greater than flow, causing blood stasis in the microcirculation vessels. Once this change reaches a certain degree, it can cause a large amount of blood to stagnate within the microcirculation, and the effective blood volume drops sharply. The stagnant ischemia phase can already affect neural regulatory functions. Because the blood supply and oxygen supply to the brain cannot be guaranteed for long by the body's compensatory adaptation. At this time, a decline in regulatory function may already occur. The above-mentioned stagnant state of the microcirculation causes an increase in intravascular static pressure and an increase in fluid exudation, the amount of which is also considerable. When measuring hematocrit, an increase in hematocrit can be found, reflecting a decrease in plasma volume due to increased exudation, leading to blood concentration.

(II) Changes in Blood in the Microcirculation

The changes in blood in the microcirculation are the most severe stage of microcirculatory changes in burn shock, with the focus on the stagnant blood in the microcirculation. During shock, there is a decrease in leukocyte deformability and capillary plugging, leukocyte adhesion to the walls of venules, aggregation of red blood cells and platelets, and microthrombus formation. These cause an increase in microcirculatory resistance, which is of great significance in the pathogenesis of shock and has become a new topic in microcirculatory research in shock.

1. Separation of Blood Components Due to stasis, blood flow velocity significantly decreases. Some blood cells move slowly back and forth in the dilated microcirculation vessels, while others are in a stagnant state. Combined with fluid exudation, this leads to a decrease in blood suspension stability, causing the separation of various components, with plasma mostly located before and after capillary branches, and some capillary segments containing only plasma without red blood cells, which are located in the direct pathway of capillary units. Leukocytes and platelets are mostly located in the marginal branches of capillary units. This distribution may be related to the distribution state of formed components in normal blood flow. The axial and marginal flow phenomena are that formed components are in the axial flow, with the largest and most important red blood cells being the axis within the axis. Leukocytes and platelets are lighter and located at the edge of the axial flow, with the marginal flow being plasma. During burn shock, the above-mentioned hemodynamic changes occur, blood flow slows, blood contracts, and blood cells congest in front of narrow venules and small veins. These changes promote the development of various microcirculatory blood changes described below.

2. Increase in Blood Viscosity in the Microcirculation Blood viscosity is inversely proportional to flow velocity. When pressure is constant, an increase in viscosity leads to a decrease in microcirculatory blood flow velocity. The increase in viscosity is mainly due to blood contraction, an increase in the proportion of formed components, and red blood cell aggregation.

⑴The hematocrit is significantly elevated, a phenomenon resulting from microcirculatory congestion and the extravasation of blood components. This phenomenon is also observed in other types of shock, but the hemoconcentration in burn shock is more pronounced. The increase in hematocrit is particularly evident when blood is drawn from the microcirculation. This is due to the congestion and retention of a large number of blood cells in the microcirculation. If blood is drawn from a large vein for testing, the hematocrit may appear normal or below normal due to factors such as hemolysis or fluid infusion.

(2) The occurrence of red blood cell aggregation is mainly due to changes in hemodynamics. Under conditions of blood stasis and slowed flow, red blood cells congest in certain segments of the microcirculation-diffused vessels and aggregate into clumps. At this time, the surface of red blood cells is coated with fibrinogen, which facilitates aggregation. Additionally, the blood in the microcirculation is in a hypercoagulable state, forming fibrin filaments that adhere to the walls, making red blood cells more likely to stick to them. The decrease in the negative charge on the surface of red blood cells is also related to their aggregation. Once aggregated into clumps or stacks, the viscosity of the blood increases, making it less fluid. Red blood cell aggregation is common in burn shock and traumatic hemorrhagic shock. It not only occurs directly due to high temperatures in the injured area but also occurs throughout the microcirculation vessels in the body due to shock, such as in the lungs, liver, intestinal mucosa, kidneys, pancreas, adrenal glands, and heart. This aggregation is not coagulation and can be disaggregated under conditions of improved circulation and increased blood flow.

3. Changes in the shape of red blood cells When red blood cells are directly exposed to temperatures above 50°C, they undergo changes and destruction. In burn shock, red blood cells in the microcirculation, due to changes in hemodynamics, are in an environment of hypoxia, lack of nutrients, acidosis, and metabolic product accumulation, leading to shape changes and becoming spherical, making it difficult for them to pass through capillaries. After red blood cells swell into a spherical shape, for every 6% increase in total red blood cell volume, the resistance to external wind and rain can increase by 90%. Therefore, peripheral resistance is not only due to the action of resistance vessels and resistance devices but also related to changes in blood viscosity and even the shape of blood components. Red blood cells swollen into a spherical shape beyond a certain limit can rupture their membrane and cause hemolysis. Additionally, fibrin filaments floating in the blood easily adhere to red blood cells, and under the force of traction, red blood cells deform and eventually rupture, leading to hemolysis. If factors that increase the fragility of red blood cells are present in the blood of burn patients, hemolysis can also occur. Therefore, hemolysis is generally severe and prolonged in patients with large-area burn shock. Anemia in the late stage of burns is mainly due to blood loss from wounds and internal bleeding, as well as malnutrition and hematopoietic suppression. However, it is currently believed that the obstruction caused by such casts is not severe and can be easily cleared once urine flow returns to normal. Hemoglobin casts in the renal tubules, under conditions of sepsis, can be decomposed by bacteria and their toxins, producing acidic and toxic substances, leading to degeneration and necrosis of renal tubular epithelial cells. This may become one of the causes of acute renal insufficiency and renal failure after burns. The deformation of red blood cells is also reversible. Just as aggregation can be disaggregated, when microcirculation improves, the nutrition and metabolism of red blood cells gradually recover, and their shape can return to normal. Only those changes that exceed a certain limit, due to increased fragility, will progressively destroy and cause hemolysis.

4. Platelet aggregation In burn shock, venous blood tests show a decrease in platelet and white blood cell counts. This is also common in other types of shock. In burn shock, platelet aggregation in the microcirculation is a frequent occurrence. The reasons for platelet aggregation are: ① When blood flow velocity decreases, light components such as platelets and white blood cells move to the side and come closer together; ② Adenosine, hemolytic products, histamine, 5-HT, catecholamines, and internal toxins released during shock tissue hypoxia all promote platelet aggregation. Platelet aggregation does not last long and can be disaggregated with improved circulation, thus recovering in a short time. If aggregation lasts for a long time, metabolic disorders due to hypoxia will cause platelets to decompose and rupture. The released platelet factors 1, 2, 3, and 4 all promote blood coagulation, which is the main danger.

5. Blood coagulation in microcirculation vessels is different from adhesion. Its genetic change is the transformation of fibrinogen into fibrin, which can form fibrin blackend swallowwort root emboli and also entangle blood cells to form thrombi, drifting with the blood flow to other parts causing infarction. These microemboli cannot be dispersed by blood flow but can be dissolved under the action of thrombolytic drugs. Once blood coagulation occurs, the changes in microcirculation are not easily reversible. At this point, the microcirculation vessels are blocked. Although tissue ischemia and hypoxia caused by prolonged blood stasis can lead to a significant accumulation of acidic substances, lowering the pH to below 6.9, and the smooth muscles of microveins and small veins have begun to relax, leading to vasodilation, the blood flow in microcirculation is already difficult to improve. By this advanced stage of shock, the tissues and cells of ischemic and hypoxic organs have undergone changes or even necrosis, and the overall metabolism and function have significantly declined. Any type of shock is caused by changes in the neuroendocrine system and some humoral factors affecting the circulatory system, body fluids, lymph, interstitial fluids, etc., acting on the polynucleotide chains within cells, causing changes in various enzymes within the cells, thereby altering cell metabolism until cell degeneration, necrosis, and disintegration. That is, the extracellular phase develops to the point where various enzymes within the blood vessels change to the extent of causing blood coagulation within the vessels. In addition to the aforementioned reasons, the coagulation of blood in microcirculation should also be noted that tissue injury during hypoxia releases tissue thromboplastin, activating the extrinsic pathway of coagulation; the collagen exposed after vascular endothelial injury activates the intrinsic pathway of coagulation; coupled with the high local concentration of these procoagulant factors, all are promoting factors of DIC. The coagulation of blood in microcirculation consumes various coagulation factors, significantly reducing the concentration of various coagulation factors in the blood of large and larger vessels throughout the body. Therefore, it is common to find uncoagulated blood in autopsies of casualties who died from shock. This is referred to as consumptive coagulopathy. The bleeding tendency in advanced stage shock patients, in addition to consumptive coagulopathy being a significant cause, also involves excessive fibrinolysis.

II. Basic Metabolic Changes During Burn Shock

During burn shock, changes in microcirculation hemodynamics and the formation of DIC occur, characterized by ischemia, hypoxia, and metabolic acidosis. The overall metabolic state during shock is a low metabolic rate. The hypermetabolism of burns has a different pathogenesis and is distinct from the metabolism of burn shock.

During burn shock, cellular ischemia and hypoxia primarily disrupt the aerobic metabolic processes of cells. Due to insufficient oxygen supply, NADH₂ accumulates in the tricarboxylic acid cycle, hindering the oxidation process. Energy deficiency also impedes the phosphorylation process. ATP synthesis decreases, while lactate formation increases. As lactate concentration rises, and when microcirculatory changes in burn shock reach a certain severity, severe hypoxia and incomplete oxidative metabolism lead to a significant increase in the proportion of glycolysis in glucose metabolism, while oxidative phosphorylation is severely impaired. This can be seen as a regression from a higher biological form of metabolism to a lower form during shock. The metabolism of human cells is not uniform across all cell types but varies. In terms of hypoxia tolerance, Type A metabolism is strong in glycolysis and the pentose phosphate pathway. These cells are hypoxia-tolerant, such as less differentiated phagocytes, hormone-producing cells, connective tissue, and epidermis. Type B metabolism is strong in the tricarboxylic acid cycle and oxidative phosphorylation, with abundant mitochondria, and is not hypoxia-tolerant, such as highly differentiated neurons, myocardial cells, hepatocytes, and renal tubular epithelial cells. Type C metabolism is balanced between glycolysis and oxidative phosphorylation. Lactate produced by Type A metabolism can be further oxidized and utilized by Type B metabolism, such as between glial cells and neurons, atrial cells and myocardial cells, Kupffer cells and hepatocytes. In severe shock and hypoxia, both Type B and Type C metabolisms are forced to switch to Type A, leading to the accumulation of lactate in intracellular and extracellular fluids, increasing concentrations, and rising H⁺ concentrations, worsening metabolic acidosis. This ultimately leads to a comprehensive inhibition of cellular metabolism. The relationship between blood lactate levels and the severity of shock shows that higher blood lactate levels correlate with higher mortality rates. Therefore, preventing and treating acidosis is a crucial aspect of shock management. Hypoxia during burn shock is not solely due to microcirculatory changes; metabolic acidosis is also not solely due to lactate. For example, combined respiratory tract injuries can narrow due to inflammation, congestion, and edema, leading to insufficient ventilation. Destruction of alveolar surfactant causes scattered pulmonary atelectasis. Microembolism syndrome leads to pulmonary interstitial and alveolar edema. Decreased 2,3-DPG in red cells impairs oxidative metabolism within the cells, affecting oxygen release in tissues. Additionally, pulmonary microembolism impedes pulmonary blood flow and gas exchange. Other factors such as swelling of collagen fibers and mitochondrial edema reduce urine production, leading to the retention of acidic metabolic products. The increase in H⁺ concentration inside and outside cells is extremely harmful, potentially destroying mitochondrial and lysosomal membranes, leading to complete cellular destruction. When these changes reach a certain extent, they can be fatal. Improving oxygen supply and tissue blood perfusion can provide cells with more oxygen and remove more H⁺, improving the situation. This is essential for rescuing burn shock and is currently achievable.

In cases of extensive burns, lysosomal enzymes released by damaged cells in the injured area, once absorbed into the bloodstream, pose significant systemic risks. After shock occurs, with severely insufficient tissue blood perfusion, ischemic organs and cells are further damaged, releasing more lysosomal enzymes, exacerbating tissue and cellular injury. In summary, during shock, prolonged ischemia, hypoxia, and the action of toxic substances lead to changes within shock cells.

III. Major Functional Changes During Burn Shock

(1) The brain and central nervous system

have the ability to automatically regulate blood flow. They may not be damaged during grade I shock, but can be impaired in severe and prolonged shock. Not only can the spontaneous bioelectrical activity of the cortex and the potential changes caused by afferent nerves weaken or even disappear, but the metabolism of nerve cells can also change. Nerve cells have a high oxygen consumption and are very sensitive to hypoxia. The brain has a relatively rich blood supply; if it decreases to 30ml/100g/minute, syncope occurs; if the blood supply is completely cut off for 5 seconds, consciousness is affected. When systemic blood pressure drops below 70mmHg, the brain's blood supply decreases significantly with the drop in stirred pulse pressure. The microcirculatory vessels in the brain dilate when the concentrations of H⁺ and CO₂ increase, and blood flow returns to normal when these concentrations normalize. Among these, the effect of CO₂ is more pronounced. When shock enters a severe stage, due to excessively low blood pressure and insufficient brain blood supply, hypoxia occurs, along with significant acidosis, which can cause swelling of perivascular neuroglial cells and capillary endothelial cells, narrowing the lumen to a thread-like size, making it difficult for red blood cells to pass through. This change can form a vicious cycle. During shock, DIC also occurs in the brain's microcirculation, further exacerbating brain hypoxia. The permeability of the blood vessels also increases. Therefore, brain edema can occur, increasing intracranial pressure. In burns, the brain's microcirculation is affected by microthrombi and lipid droplet embolisms, which can injure microvessels and form small punctate hemorrhagic foci, known as cerebral purpura. The injured exhibit neurological symptoms such as agitation, spasm, and unconsciousness. The changes in brain function during shock have a material basis. An important characteristic of brain metabolism is that only glucose easily passes through the blood-brain barrier's lipid white membrane. For example, when NaHCO₃ is intravenously injected to correct the metabolic acidosis of shock, it is not easy to correct the brain's acidosis because it does not easily pass through the blood-brain barrier.

O₂ and CO₂ easily pass through the blood-brain barrier. Therefore, brain metabolism produces ATP to maintain nerve cell activity, mainly from glucose and O₂. If glucose consumption is not replenished and hypoglycemia occurs, the material basis for brain metabolism becomes insufficient. When brain neuroglial cell swelling, microcirculatory endothelial cell swelling, brain edema, DIC, etc., cause ischemia, then O₂, glucose, and other nutrients will be severely insufficient. The ischemia and hypoxia of the brain during shock greatly harm its energy metabolism. The brain weighs about 2% of the body weight, and in a resting state, its glucose consumption accounts for about 65% of the whole body. The gray matter nerve cells of the brain account for about 1/5 of the total brain cells, but their oxygen and glucose consumption accounts for about 80% of the total. During ischemia and hypoxia, cortical nerve cells are the first to be affected. The newer parts in evolution are harmed more and faster. In severe cases, nerve cells will consume their own substances, leading to structural damage. When nerve cells turn to consume their own proteins and lipids, the increased protein breakdown produces NH₃, which can form glutamine. This can alleviate the significant harm of NH₃ to nerve cell function. However, forming glutamine also consumes α-ketoglutarate in the tricarboxylic acid cycle, further aggravating the cycle's dysfunction. Thus, the formation of brain glutamine during shock is beneficial for reducing the harm of NH₃, but it is very unfavorable for the tricarboxylic acid cycle. The increase in γ-aminobutyric acid reflects severe dysfunction in nerve cell metabolism.

(2) The heart and myocardial depressant factor

Severely burned patients may experience cardiac insufficiency. During burn shock, the loss of fluids leads to a reduction in blood volume, with a large amount of blood stagnating in the microcirculation, resulting in a significant decrease in effective circulating blood volume. As cardiac output continues to decline, the stirred pulse pressure also decreases, which reduces coronary stirred pulse blood flow. The drop in blood pressure reflexively causes tachycardia, shortening the diastolic period and further reducing coronary stirred pulse blood flow. When the mean main stirred pulse pressure falls below 60mmHg, coronary blood flow decreases, leading to myocardial ischemia and hypoxia. If burn patients have respiratory injuries and pulmonary lesions that impair gas exchange, myocardial ischemia and hypoxia become even more severe. Although the myocardium has many available energy sources under normal conditions, such as fatty acids, glucose, lactate, amino acids, ketone bodies, and pyruvate, in order of consumption, myocardial metabolism primarily relies on the tricarboxylic acid cycle and oxidative phosphorylation in mitochondria. During shock, the tricarboxylic acid cycle is obstructed, ATP synthesis is reduced, and the concentration of H⁺ increases, leading to a decrease in myocardial contractility.

Acidosis and hyperkalemia during burn shock both have inhibitory effects on the heart. Additionally, recent studies have found that DIC also affects the microcirculation of the heart. During burn shock, the myocardial depressant currently believed to be responsible is the myocardial depressant factor (MDF), which primarily originates from the ischemic and hypoxic pancreas during shock. MDF inhibits myocardial contractility, becoming another significant cause of cardiac dysfunction during burn shock. The use of aprotinin and glucocorticoids is effective in protecting cellular integrity and inhibiting the production of MDF.

(3) Pathogenesis of the lung and shock lung

The changes in the lung during burn shock are more complex than in other types of shock. In addition to the respiratory system changes during shock, the respiratory tract can be directly injured by the inhalation of high-temperature gases, leading to an increased incidence of respiratory complications in burn patients. Recent domestic and international statistical data indicate that the majority of burn cases die from respiratory insufficiency. Burn shock patients without respiratory tract injury can develop shock lung and acute respiratory failure, which is also one of the adult respiratory distress syndromes. Recent clinical observations have found that one-third of severe shock patients develop shock lung. X-ray observations show patchy or more diffuse increases in density, with both lungs being roughly similar. Therefore, it is easily mistaken for bilateral lobar pneumonia. Pathological changes include congestion, small hemorrhages, small areas of lung collapse, interstitial edema, alveolar edema, and the formation of alveolar hyaline membranes. Functionally, there is mainly a reduction in alveolar surfactant, decreased lung compliance, increased lung respiratory function, and a decrease in PaO₂. Patients exhibit symptoms of dyspnea.

1. Pathogenesis of shock lung

⑴ Contraction of pulmonary veins and microveins, small veins The pulmonary venous system is richly innervated and has a smooth muscle layer, responding to sympathetic, vagal stimulation, bradykinin, Black Catechu phenols, 5-HT, histamine, etc., with contraction. During shock, these factors are present, and pulmonary vascular resistance increases, with increased intravascular pressure in the microcirculation, facilitating fluid exudation.

⑵ Pulmonary microembolism syndrome DIC occurring during shock can lead to a large number of microemboli reaching the lungs, causing microcirculatory embolism, increasing resistance, with fibrin degradation products containing permeability-increasing factors, which can increase the permeability of microcirculatory vessels, leading to fluid exudation. Additionally, 5-HT and histamine released from platelet breakdown are substances that cause contraction of the pulmonary venous system vessels.

⑶ Other aspects Such as central heart failure during shock, excessive fluid infusion, oxygen toxicity injury to pulmonary capillaries, etc., can all lead to pulmonary edema. If there is respiratory tract injury, the situation is even more severe. When pulmonary congestion and edema are severe, capillary injury and rupture can form hemorrhages, even patchy hemorrhages.

The pathogenesis of lung collapse is mainly due to the reduced synthesis and decreased activity of alveolar surfactant due to hypoxia. Its main component is dipalmitoyl phosphatidylcholine, synthesized and secreted by type II alveolar epithelial cells. The exudate during pulmonary edema may also accelerate its destruction. Its role is to reduce the surface tension on the inner surface of the alveoli, making alveolar expansion difficult. In addition, obstruction of the small bronchi by secretions can also cause the absorption of the middle qi body of the alveoli they belong to, leading to collapse. Recently, it has been found that during DIC, lung tissue releases PGE₂, which can cause spasm and obstruction of the small bronchi, leading to alveolar collapse.

2. Impact of shock lung on respiratory function

⑴ Diffusion impairment: Due to the effects of interstitial edema, alveolar edema, and the formation of hyaline membranes, the diffusion distance of gases increases, causing a decrease in PaO₂. Inhalation of high-concentration oxygen can improve this condition.

⑵ Ventilation-perfusion ratio imbalance: In the pulmonary microcirculation, areas blocked by aggregated blood cells or microemboli have ventilation but no blood flow. In areas with vasoconstriction, there is ventilation but reduced blood flow. Conversely, in areas with normal blood flow, alveoli may be occupied by exudate, or small bronchi may be obstructed by secretions, resulting in blood flow without ventilation, which is also a cause of decreased PaO₂. Inhalation of high-concentration oxygen can also provide some improvement.

⑶ Venous blood flow increase: The main reasons are: ① Normal shunt vessels dilate, increasing blood flow. ② Pulmonary microembolism, with a large number of shunts opening; ③ Increased blood flow through non-ventilated areas. During burn shock, venous blood flow increases, leading to the phenomenon of venous blood infiltrating into stirred pulse blood, causing PaO₂ to drop, with little improvement when inhaling high concentrations of oxygen. Only by quickly correcting the circulatory disorder of shock can improvement be achieved. The effect of inhaling 100% oxygen for 30 minutes can be used as a reference to help judge the severity. Due to the significant impact of shock lung on respiratory function, it can ultimately lead to a severe drop in PaO₂, and subsequently an increase in PCO₂, leading to respiratory failure and threatening life.

(4) Kidneys

Shock often results in reduced urine output. Severe shock can lead to oliguria, or even anuria. Urine output often reflects the state of renal circulation. The reduction in urine output in the early stages of shock may be due to the strong contraction of renal vessels caused by Black Catechu phenolic substances in the circulation and the increased secretion of ADH. It cannot be conclusively determined as a tubular organic change or acute renal failure. If the situation improves with treatments such as fluid infusion and relief of vascular spasms, and urine output increases, the changes are still functional. The mechanism of the above changes mainly has two aspects: one is the contraction of renal vessels reducing renal blood flow, with the contraction of renal cortical vessels being more significant. Compared to the input stirred pulse and output stirred pulse of the glomerulus, the former contracts more significantly. This greatly reduces the blood flow through the glomerulus, thus reducing filtration; the second is the decrease in effective filtration pressure, caused by the drop in the average stirred pulse pressure throughout the body during shock. When the average stirred pulse pressure drops to 60mmHg, the glomerular capillary pressure drops to a level where the formation of primary urine almost completely stops. During burn shock, urine output should be restored to 30～50ml/h as quickly as possible, reflecting that renal vascular flow can maintain the kidneys without suffering damage. If acute renal failure occurs, it is very dangerous for severely burned patients.

The measurement of central venous pressure helps in judging the condition of the kidneys. During burn shock with blood volume loss, except for the increase in pulmonary stirred pulse pressure due to pulmonary microembolism, which affects the right heart, its CVP value is often lower than normal, possibly 0, or even negative. After sufficient fluid infusion, the central venous pressure can return to normal. If vascular spasms have been relieved at this time, urine output increases to 35ml/h. This indicates no major injury to the kidneys. If oliguria or anuria persists, there may be tubular injury, and the possibility of acute renal failure should be considered highly likely.

bubble_chart Clinical Manifestations

Burn shock is essentially hypovolemic shock, so its clinical manifestations are similar to those of traumatic or hemorrhagic shock, with the following characteristics:

1. Increased pulse rate

In burns, the secretion of vasoactive substances increases, enhancing myocardial contractility and heart rate to compensate and increase cardiac output. Therefore, an increased heart rate is common in the early stages of burns. Severe burns can increase the heart rate to over 130 beats per minute. If the heart rate is excessively fast, the cardiac output per beat decreases, and with increased peripheral vascular resistance, the pulse becomes thin and weak. In severe shock, the pulse becomes even weaker.

2. Decreased urine output

This is an early manifestation of burn shock. It generally reflects the perfusion of tissue blood flow and is also a sensitive indicator of the severity of burn shock. The early decrease in urine output in burns is mainly due to insufficient effective blood volume and reduced renal blood flow, but it is also related to increased secretion of antidiuretic hormone and aldosterone, which limit the kidney's ability to excrete water and sodium.

3. Thirst

This is an early manifestation of burn shock. It may be related to changes in intracellular and extracellular osmotic pressure and insufficient blood volume, and is also controlled by the hypothalamus-pituitary-adrenal cortex system.

4. Dysphoria

This is a manifestation of cerebral hypoxia due to poor blood perfusion. It appears early and can reflect the severity of burn shock, and is also a sensitive indicator of treatment response. Severe cerebral hypoxia can lead to delirium, mania, impaired consciousness, or even unconsciousness. However, it needs to be differentiated from cerebral edema and early infection.

5. Nausea and vomiting

These are early symptoms of burn shock. The common cause is also cerebral hypoxia. Vomitus is usually gastric contents, but in severe shock, it can be coffee-ground or bloody, indicating severe congestion, edema, or erosion of the gastrointestinal mucosa. If vomiting is excessive, acute gastric dilation or paralytic ileus should be considered.

6. Poor peripheral circulation

In the early stages of burns, pale skin and cold limbs are often observed, sometimes with grade I cyanosis at the extremities, poor filling of superficial veins, and prolonged recovery time of normal skin color after pressing the nail bed and skin capillaries.

7. Changes in blood pressure and pulse pressure

In the early stages of burns, vasoconstriction and increased peripheral resistance often lead to elevated blood pressure, especially diastolic pressure, resulting in a smaller pulse pressure. Later, as compensation fails, the capillary bed expands, blood stasis occurs, and effective circulating blood volume decreases, leading to a drop in blood pressure. This indicates that the shock has become more severe. Among blood pressure changes, a decrease in pulse pressure appears earlier.

8. Laboratory tests

Necessary laboratory tests help in the early diagnosis of burn shock and the assessment of disease progression. The laboratory changes in burns mainly reflect the following three aspects: ① The stress response of the pituitary-adrenal axis, manifested by a decrease in eosinophils, lymphocytes, and platelets, and an increase in catecholamines in the blood. ② Hypovolemia, low blood flow, and tissue hypoxia, generally manifested as hemoconcentration, increased red blood cell count, hemoglobin, and hematocrit, decreased central venous pressure, metabolic acidosis, decreased mixed venous oxygen partial pressure, normal or decreased carbon dioxide partial pressure, normal or decreased mixed venous blood pH, decreased venous blood carbon dioxide combining power, and decreased blood buffer base and base excess. In terms of metabolism, it is manifested by increased blood sugar, non-protein nitrogen, and blood potassium, and decreased blood sodium. ③ Reflection of dysfunction of internal organs, which varies depending on the surface manifestations of organ dysfunction.

The early diagnosis of burn shock is mainly based on early clinical manifestations and necessary laboratory tests. The purpose of early diagnosis is to initiate early treatment, which can often prevent its occurrence or reduce its severity.

bubble_chart Treatment Measures

Burn shock is a hypovolemic shock, with severe cases accompanied by shock lung and other organ injuries. Some patients also have inhalation injuries, leading to impairments in both the circulatory and respiratory systems. Therefore, the early resuscitation of burn patients should follow general resuscitation principles, including maintaining airway patency, preserving respiratory function, and supporting cardiovascular function.

Fluid resuscitation is an effective measure to prevent and treat burn shock. It is crucial to establish intravenous access promptly to ensure smooth fluid administration.

1. Resuscitation Fluid Therapy

Various early burn fluid resuscitation formulas have long been established internationally, such as the Evans formula and the Brooke formula. Based on the Evans formula, many domestic institutions have developed their own early burn fluid resuscitation formulas based on their experiences. Most formulas are similar, with only slight differences in total fluid volume and the ratio of colloids to crystalloids. The commonly used formula in many domestic institutions is: for the first 24 hours post-burn, administer 1.5 ml of colloid and electrolyte solution per 1% burn area per kilogram of body weight (2.0 ml for children), plus additional water. Generally, adults require 2000 ml of water, while the amount for children is calculated based on age or weight. The ratio of colloid to electrolyte or balanced salt solution is usually 0.5:1, but for severe deep burns, it can be 0.75:0.75. The infusion rate should be faster initially, with half of the total volume administered within the first 8 hours post-burn, and the remaining half over the next 16 hours. For the second 24 hours, half of the total volume is administered, with water still at 2000 ml.

Another commonly used domestic formula is:

II, III degree burn area (%) × 100 ± 1000 = total fluid volume for the first 24 hours post-burn (ml).

For patients who are overweight or underweight, adjust by adding or subtracting 1000 ml. Of the total volume, 2000 ml is the baseline water requirement. One-third of the remaining volume is colloid solution, and two-thirds is balanced salt solution.

The Parkland formula recommends administering 4 ml of lactated Ringer's solution per 1% burn area per kilogram of body weight within the first 24 hours. The rationale is that after a burn, capillary permeability increases, allowing both crystalloids and proteins to pass through the capillary walls. Therefore, neither colloids nor crystalloids can fully remain within the vessels to maintain blood volume, as a significant portion leaks into the interstitial space. Thus, the infused fluid must expand the entire extracellular fluid compartment, including both intravascular and extravascular spaces, to maintain circulatory volume. This necessitates a significantly larger volume of fluid. Since sodium is the primary electrolyte in extracellular fluid, administering sodium-containing crystalloids is more reasonable than colloids. Some scholars also advocate for the use of hypertonic saline solutions. In recent years, many scholars have recognized that administering large amounts of crystalloids, water, and salts within the first 24 hours post-burn can overload the patient, potentially leading to hypoalbuminemia and significant tissue edema, which may further predispose the patient to infection after shock. Therefore, it is still recommended to administer an appropriate amount of colloids within the first 24 hours, which can reduce the total fluid volume, alleviate excessive fluid load, and better support anti-shock efforts, reabsorption, and post-shock treatment.

The type of intravenous fluid administered depends on the situation. In addition to oral intake, water can be supplemented with a 5% glucose solution. Colloidal fluids are generally preferred, with plasma being the first choice. Alternatively, 5% albumin or whole blood can be used, especially for extensive deep burns where partial whole blood transfusion may be necessary. Plasma expanders such as dextran, 409 solution, and 706 solution can also be selected, but the dosage within 24 hours should generally not exceed 1000-1500 ml. The purpose of using balanced salt solutions is twofold: to avoid hyperchloremia caused by excessive chloride ion content when only saline is supplemented, and to correct or alleviate metabolic acidosis caused by burn shock. If the area of deep burns is extensive and significant metabolic acidosis or hemoglobinuria occurs, part of the balanced salt solution can be replaced with a simple isotonic alkaline solution to correct metabolic acidosis or alkalinize the urine. To rapidly excrete free hemoglobin from the urine and reduce the risk of kidney irritation and dysfunction, in addition to alkalinizing the urine and appropriately increasing fluid intake to enhance urine output, diuretics can be intermittently administered while correcting blood volume. Commonly used diuretics include 20% mannitol or 25% sorbitol at 100-200 ml every 4 hours. If the effect is not significant, ethacrynate sodium or furosemide can be added or substituted. Additionally, for elderly patients, those with inhalation injuries, cardiovascular diseases, or combined brain injuries, diuretics can be intermittently administered to prevent excessive fluid infusion.

It must be emphasized that any formula can only serve as a reference and should not be mechanically followed. It is important to avoid either insufficient or excessive fluid replacement. Insufficient fluid often makes shock difficult to control and can lead to acute renal failure; excessive fluid can cause an overload on the circulatory system and edema in the brain and lungs, and increase local exudation in burns, which is conducive to bacterial proliferation and infection. Therefore, adjustments can be made based on the following fluid infusion indicators: ① Appropriate urine output. When renal function is normal, urine output mostly reflects the circulatory status. Generally, adults should maintain a uniform urine output of 30-40ml per hour. If it is below 20ml, fluid replacement should be accelerated; if it is above 50ml, it should be slowed down. Those with hemoglobinuria require more urine output; those with cardiovascular diseases, combined brain trauma, or elderly patients require less. ② Calmness, clear consciousness, and cooperation are signs of good circulation. If the patient is dysphoric and restless, it is mostly due to insufficient blood volume and cerebral hypoxia, and fluid replacement should be accelerated. If the fluid replacement has reached or exceeded the general level and the patient becomes dysphoric and restless, the possibility of cerebral edema should be alerted. ③ Good peripheral circulation and strong pulse and heartbeat. ④ No obvious thirst. If there is polydipsia, fluid replacement should be accelerated. ⑤ Maintain blood pressure and heart rate at a certain level. Generally, it is required to maintain systolic blood pressure above 90mmHg, pulse pressure above 20mmHg, and heart rate below 120 beats per minute. Changes in pulse pressure are earlier and more reliable. ⑥ No obvious blood concentration. However, in severe large-area burns, early blood concentration is often difficult to completely correct. If blood concentration is not obvious and the circulatory status is good, it should not be forcibly corrected to normal to avoid excessive fluid infusion. ⑦ Stable breathing. If there is an increase in breathing, the cause should be identified, such as hypoxia, metabolic acidosis, pulmonary edema, acute pulmonary insufficiency, etc., and the fluid infusion volume should be adjusted in time. ⑧ Maintain central venous pressure at a normal level. Generally, low blood pressure, low urine output, and low central venous pressure indicate insufficient return of blood to the heart, and fluid replacement should be accelerated; high central venous pressure with low blood pressure and no other explanation mostly indicates poor cardiac output. Fluid replacement should be cautious, and the cause should be investigated. Due to the many factors affecting central venous pressure, especially in cases with a large amount of fluid replacement, measuring pulmonary artery pressure (PAP) and pulmonary artery wedge pressure (PWAP) can be considered to further understand cardiac function and take corresponding measures.

Among the fluid infusion indicators, the overall condition is the primary concern. Severe large-area burns change rapidly in the early stages, and it is necessary to have a dedicated person closely observe the condition and adjust treatment in a timely manner to achieve rapid and accurate results. The intravenous fluid infusion channel must be good, and if necessary, two can be established to adjust the infusion speed at any time, ensuring uniform infusion and preventing interruption.

2. Maintain good respiratory function

During shock, especially in cases with inhalation injury, gas exchange function is often suppressed, and severe cases may be complicated by acute respiratory failure. Therefore, maintaining good respiratory function is an important measure to prevent and treat burn shock. Mainly, it is to keep the respiratory tract unobstructed. For example, frequently suctioning sputum and shed mucous membranes in the respiratory tract to eliminate mechanical obstruction; when head and neck deep burns edema or inhalation injury causes difficulty in breathing, a tracheotomy should be performed in time, and hesitation should be avoided. Because prolonged obstruction, hypoxia can not only aggravate shock, but even lead to respiratory failure or cardiac arrest, and if neck edema significantly increases before performing an emergency tracheotomy, not only is the surgery difficult, but it is also easy to accidentally injure major blood vessels, pleura, and other important tissues; to relieve bronchospasm and reduce respiratory mucous membrane congestion and edema, aminophylline and adrenal corticosteroids can be intravenously dripped. If there is hypoxia, oxygen should be given, and in severe cases, a respirator can be used to assist breathing.

3. Application of sedative and analgesic drugs

Severe pain after burns and patient fear are strong stimuli to the central nervous system, so sedation and analgesia have a certain role in the prevention and treatment of shock. Generally, pethidine or morphine is used. When used repeatedly, barbiturates can be used intermittently; after blood volume is replenished, drugs such as phenergan can also be used. If dysphoria and restlessness occur due to insufficient blood volume, increasing the dose of sedatives cannot calm the patient, and sometimes excessive dosage can inhibit respiration and increase cerebral hypoxia, thereby worsening dysphoria.

4. Cardiac Function Adjunctive Therapy

In cases of severe burn shock where, despite vigorous fluid resuscitation, the heart rate significantly increases to over 140 beats per minute, especially when fluid resuscitation is delayed or insufficient, and hypoxia-induced damage is confirmed by electrocardiogram, pharmacological treatment should be considered to protect cardiac function. Shock that cannot be corrected by fluid resuscitation, increased central venous pressure indicating fluid overload, and cardiac insufficiency are clear indications for medication. Cardiac glycosides such as Rehmannia, Cedilanid, and Strophanthin K often require a loading dose within 24 hours, followed by a maintenance dose. These drugs enhance myocardial contractility, thereby increasing cardiac output. Dopamine strengthens myocardial contractility, reducing the heart's burden and alleviating pulmonary and renal circulatory resistance. Administering a small dose intravenously can be effective. RA642, which increases blood pressure, enhances cardiac output, reduces peripheral and pulmonary circulatory resistance, and increases blood flow to coronary, renal, and mesenteric arteries, is a promising drug for assisting cardiovascular function during shock resuscitation.

5. Reducing Peripheral Vascular Resistance

The use of α^-adrenergic blockers can improve microcirculatory blood flow and enhance tissue perfusion. Before administration, ensure adequate blood volume to prevent vascular bed expansion, which could cause or exacerbate relative hypovolemia, and appropriately correct metabolic acidosis.

6. Renal Function Adjunctive Therapy

In cases of severe extensive burn shock, deep burns, or electrical burns leading to hemoglobinuria or myoglobinuria, fluid overload, pulmonary and cerebral edema due to inhalation injury and combined craniocerebral trauma, and renal injury from chemical poisoning such as inorganic phosphorus, good renal function is essential for diuresis or toxin elimination. If diuresis is insufficient after necessary fluid resuscitation, diuretics such as mannitol or sorbitol are used. Furosemide or ethacrynic acid can be used alone or in combination with mannitol, provided blood volume is adequate. During dehydration therapy with significant diuresis, monitor for sodium and potassium loss.

7. Correcting Acid-Base Imbalance

Shock often leads to metabolic acidosis due to increased lactate production from anaerobic metabolism. Early in burns, respiratory alkalosis may occur due to hyperventilation from stress, pain, shock, and inhalation injury hypoxia. These factors directly or indirectly affect the body's acid-base balance and blood pH stability. Inadequate recognition and management can exacerbate complex functional disturbances, potentially leading to a vicious cycle and complicating treatment. Therefore, timely diagnosis and management of complex conditions and acid-base imbalances are crucial.

8. Hormone Therapy

This is generally reserved for patients with difficult resuscitation or adrenal cortical insufficiency. For difficult resuscitation cases, high doses should be administered early. Some recommend a single intravenous dose of 2000-3000 mg of hydrocortisone sodium succinate, or even higher, while others suggest 1000 mg, with a repeat dose if necessary. It is also advisable in cases of pulmonary or cerebral edema.

9. Application of Oxygen Free Radical Scavengers

In cases of severe burns, the leukocytes in the blood vessels of the burned tissue are activated, and the NAD(P)H oxidase on the cell membrane is activated, enhancing the metabolism of the pentose phosphate pathway, producing oxygen free radicals O₂, OH·O^-₂, H₂O₂, iron ions, etc., causing more severe damage to the cells. The use of oxygen free radical scavengers can alleviate the damage to various internal organs or tissue cells caused by shock, thereby improving the survival rate of burns. Dimethyl sulfoxide (DMSO) and superoxide dismutase (SOD) are used to scavenge oxygen free radicals; catalase is used to scavenge H₂O₂; sodium benzoate (sod. benzoate) is used to scavenge OH·O^-₂; apolactoferin or deferoxamine is used to scavenge iron ions; and vitamin E is used to alleviate pulmonary vascular damage. The combined use of SOD and catalase can scavenge O^-₂ and H₂O₂, which can eliminate lung damage.

10. Plasma Exchange Therapy During Shock Period

Using a continuous blood cell separator or a continuous blood cell adder, the patient's plasma is removed while an equal amount of frozen fresh plasma of the same type is transfused. For children under 5 years old, it is preferable to exchange with whole blood of the same type. Adult respiratory distress syndrome after severe burns, persistent grade III hemoglobinuria and myoglobinuria after severe electrical burns, and some resuscitation fluid therapies may not be effective. After severe burns, many serum factors that enhance vascular permeability and cause cell membrane dysfunction are involved in the pathophysiology of shock circulation. The application of plasma exchange therapy to eliminate these serum factors can help resuscitate shock. However, the use of plasma removal and exchange transfusion therapy may lead to complications such as hepatitis, hypokalemia, transfusion reactions, hemolysis, and air embolism. Therefore, close monitoring is necessary, frequently observing vital signs, recording fluid intake and output, measuring cardiac output, etc. Routine blood tests, platelet counts, coagulation tests, blood gas analysis, and chest X-rays should also be performed.

11. Severe Burn Patients

The reasons for the difficulty in early shock resuscitation are complex and often multifactorial. In addition to improper handling of shock itself, common main reasons include: ① These patients have undergone long journeys and jolts, with insufficient anti-shock measures, leading to difficult resuscitation. Severe burn patients should, in principle, be treated locally. When transfer is necessary, it must be done after the shock has stabilized to avoid grade III shock. ② The emergence of systemic infection is often an important reason for the difficulty in early shock resuscitation in severe large-area burns, even leading to resuscitation failure. Therefore, early anti-infection measures should be taken for severe burn patients, including intravenous infusion of broad-spectrum antibiotics, strict protection of the wound surface, and prevention of re-contamination, which are very important. ③ Inhalation injury, combined injuries, especially those with severe brain trauma, internal organ injury, pelvic or femur fracture, and massive hemorrhage, the reasons for the difficulty in shock resuscitation, in addition to the severity of the injury itself, are mainly due to insufficient understanding of the injury condition and improper handling, mostly due to insufficient fluid infusion; a few cases are due to excessive fluid infusion, as well as misdiagnosis or fistula disease diagnosis. Combined poisoning is also often the case. Therefore, a detailed understanding of the injury situation and careful examination are indeed important.