When the shock wave and burns two injury-causing factors at the same time or successive effects on the body and caused by the composite injury, called the burn rush compound injury. In the instant of material explosion quickly formed a huge energy release of the chemical reaction process, causing high temperature and high pressure gas rapid expansion, resulting in the destruction of the surrounding media, deformation and displacement, the rapid expansion of the air medium around the source of the explosion to form three compression waves, their overlap on the formation of three shock waves; explosion while the surrounding temperature also increased sharply; variable speed scattered fragments and other injury-causing factors caused by the overlap and compound damage. In times of war, especially nuclear war, impact injuries are quite common. In times of peace and construction, mostly seen in chemical plants, mines or ammunition depots and other explosions. In the clinical injury due to simple shock wave is often less common, the vast majority of composite injury in the form of manifestation.
First, the mechanism of injury caused by the burn shock compound injury
1, shock wave injury: the explosion moment due to the release of tremendous energy, resulting in a large number of explosion products that change the gas, explosion products expansion, in addition to energy transfer to the surrounding air medium, and the formation of the original shock wave around it, with the front end of the explosion products and shock waves to the same speed propagation, common injury, when the explosion products stop anti-shock wave using separate propagation of injury. Therefore, it is said that shock wave injury including primary injury, secondary injury and three mechanisms of injury.
2, heat: the explosion of the original explosion instantly can produce a huge amount of energy, so that the surrounding gas temperature rises sharply, the formation of high-temperature heat, resulting in burns on the body surface; in the nuclear explosion also due to radiation, light radiation caused by radioactive injury, discharge burn compound injury. Therefore, the injury and the end of the burn compound injury mainly depends on the severity of the burns, and severe burn compound injury often shows two injury factors aggravate each other, promote each other, that is, the results of the so-called compound effect.
Second, the pathological characteristics of the burning compound injury
Burning compound injury is often complex and serious injuries. Immediately after the injury died from organ fragmentation, limb severance, body cavity destruction, etc. is mostly the result of a powerful shock wave direct injury. General body surface burns are striking, while the internal shock injury and stress changes are easily concealed, neglecting a series of pathological changes in the internal organs. Under the action of shock waves, the human body contains gas tissue is most vulnerable to injury (such as lung, tympanic membrane), followed by fluid-containing organs and parenchymal organs.
1, the lung: whether the whole body or the chest after local exposure to shock waves, the lung is the main target organ of shock wave action, more opportunities for injury than other organs. The main pathological changes of lung impact injuries are pulmonary hemorrhage and pulmonary edema. According to the lung impact injury injury analysis, the lung injury is divided into three degrees: the lung has more point or sheet hemorrhage, the total bleeding area accounted for more than 50% of the total lung area for severe lung injury; bleeding area accounted for 10% -50% of the total lung area for moderate lung injury; the total bleeding area is less than 10% of the total lung area for mild lung injury. Experimental studies have shown that the most severe lung injury can appear as obvious hemorrhagic solids with pink frothy edema fluid overflowing from the cut surface. Light microscopy showed diffuse hemorrhage in the alveolar cavity, filling with edematous fluid, fusion of the alveolar cavity or emphysema-like changes; reduction of the capillary bed in the alveolar wall, some capillaries were tortuous, prolonged, dilated, and congested, with marked edema in the interstitial lung, and widening of the alveolar septum and perivascular space.
The experimental study showed that the lung injury in the single burn group was mild, with no obvious bleeding, mainly congestion and edema; patchy bleeding and obvious edema were seen in the lung of the single punch group; and the burn and punch group had the most severe injury, with large patchy bleeding and obvious edema, and slow absorption of bleeding. It was also confirmed that the burn-and-punch complex injury caused the most severe damage to the lung endothelium, and severe pulmonary edema and pulmonary hemorrhage was one of the main causes of life-threatening injuries, and pulmonary hemorrhage was mainly caused by the shock wave effect, manifested as increased pulmonary edema and prominent vascular lesions. CEC levels, which reflect endothelial cell injury clinically, are elevated and peak at 8 hours post-injury.
One study reported that a more specific type of intra-alveolar crystallization was found in the alveoli after burn shock compound injury, with a smooth surface and uniform texture being a plate-like structure arranged in multiple parallel layers, mainly seen 12-72 hours after injury, with lighter crystalline staining 3 days after injury and less common after 7 days. It was further demonstrated that the early crystals in the alveoli were found in areas where hemolysis of red blood cells occurred, and crystals were not seen in the hemorrhagic areas where red blood cells were intact. They were surrounded by more type II alveolar epithelial cell hyperplasia and mononuclear cell infiltration, with an increase in interstitial fibroblasts, even forming solid alveolar lesions. As a large number of crystals form, they block the alveolar cavity and thus may aggravate pulmonary hemorrhage and cause pulmonary respiratory dysfunction.
2. Heart: The instantaneous overpressure and negative pressure of the shock wave can lead to pathological changes in the heart, such as myocardial fracture, endocardial punctate hemorrhage, early degenerative necrosis, etc. The lesions increase significantly in 6 hours, with focal myocardial necrosis and punctate hemorrhage in the interstitium. Electron microscopy reveals discrete myogenic fibers, swollen mitochondria, vacuolization, etc. The heart may show extensive hemorrhage, masses and small scattered hemorrhages of varying degrees in all layers of the ventricular wall. The plasma CK-MB, cTnI and myocardial MDA were significantly elevated within 24 hours after injury, indicating that the myocardial damage caused by the two causative factors of the burn-punch composite injury was significantly aggravated and tended to worsen, and was positively correlated with the severity of myocardial degeneration and necrosis. Compared with the single burn injury group, the recovery is slow and the risk period is longer.
3, brain: burn punch compound injury whether the whole body or chest exposed to the effect of shock waves, autopsy found that in addition to the occurrence of hemorrhage, edema, bruising in the lungs, no other organs were seen in the bulk of the obvious damage. However, ultrastructural changes in hippocampal and brainstem tissues were found not only under electron microscopy, but also in parallel with the lung injury. The structural damage was observed 3 hours after the injury and was significantly aggravated with the prolonged observation time, mainly manifested as: shrinkage and defect of axon pulp in brainstem tissues, swelling in the sheath, and decrease of electron density; disappearance of axon cytoplasm, formation of myelin-like structures, swelling of basement membrane, and increase of swallowing and drinking vesicles in hippocampus, etc. The mechanism of injury may be related to ischemia and hypoxia in brain tissue. There are lamellar hemorrhages of different sizes in brain tissue, parenchymal structure sparing, edema, focal lysis degeneration, swelling and cavitation of mitochondrial endoplasmic reticulum in neurons, widening of perivascular gaps, swelling of endothelial cells, etc.
4. Gastrointestinal tract: Mild to moderate subplasma hemorrhage in the gastrointestinal tract can be found, with colonic injuries being more common.
Third, the clinical characteristics of the composite injury of moderate burn punch
1.Severe shock and fatal damage with severe damage to multiple organs and parts, with a high morbidity and mortality rate. In the instant of shock wave action can produce significant biological effects, especially close blast injuries, the shock wave running at high speed generated by the dynamic pressure (98.07-254.97kPa that is 737.4-1917mmHg, can cause lethal injury) of the throw, impact, direct extrusion, the injured fall, displacement and organ rupture bleeding and fractures; debris injuries; and the explosion center of the flame and scorching gas caused by skin burns and inhalation injuries. It is reported that the incidence of shock in 36 cases of burn and punch compound injury patients reached 94.1%.
2, the scope of trauma is large, the development of injuries is fast, the blood volume loss is more, the degree of shock is heavy and long.
3, the incidence of lung impact injury is high, the lung is the main target organ of shock wave action, and is also the easy injury site of burn-impact compound injury. The lung microvascular endothelial cell damage is significantly worse than simple burns or shock wave damage. The main manifestations are pulmonary hemorrhage, alveolar and interstitial edema, alveolar rupture, ventilatory and ventilatory dysfunction, or hypoxemia that is difficult to reverse.
Whole body or chest exposure to shock waves in the circulation of blood instantly pressed heart, lung small intravascular pressure has nearly a hundred-fold increase, thus causing the lung injury.
Pulmonary fractional flow can be increased within a few hours after the pulmonary shock injury, and in 8 hours after the injury pulmonary fractional flow increased dramatically from 4.7% before the injury to 21%.
Early X-ray chest radiographs after burn injury show increased lung texture, thickening, blurring, decreased translucency, uneven density and shallow lumpy or lamellar cloudy shadow, which decreases or disappears 4-8 days after injury, pulmonary alveoli and fluid pneumothorax, mediastinal emphysema and rib fracture. The detection rate of focal pulmonary alveolar emphysema, pleural effusion and mediastinal emphysema was higher than that of X-ray chest plain film within 6 hours after the injury, especially a small amount of pericardial effusion was not easily detected on X-ray plain film; the cloudy flocculent shadow with increased density suggested alveolar and interstitial hemorrhage and edema.
4, infection occurs early. Systemic infection is the main complication of burn and punch compound injury, but also the main cause of death. According to the statistics of 46 cases of burn and punch compound injury patients, the incidence of systemic infection is 19.57%, of which the morbidity and mortality rate reaches 88.89%, which is significantly higher than that of patients with simple burns. It is also reported that 13 burn washout compound injury dog early death of blood bacterial culture 100% positive.
5, more complications, the chance of MODS increased. Burning compound injury patients often combined with serious internal environmental stability disorders occur, hypoxemia, and coagulation mechanism disorders. Burning compound injury as the first blow, resulting in hypovolemic shock, hypoperfusion, ischemia-reperfusion injury, although the patient through the shock, but the heart, lungs, liver, intestines and other organs are still in “hidden shock”, ischemia and hypoxia, lack of oxygen metabolism to produce lactic acid, a large number of oxygen radical release. All types of immune cells in the body are in an “activated” state. If serious infection and sepsis occur, it can lead to MODS.
Diagnosis
Pulmonary heart type as the main performance.
1, history of blast burns, post-injury impaired consciousness, respiratory distress symptoms.
2, skin swelling in the anterior chest area with extensive subcutaneous hemorrhagic spots.
3, dry and moist rales were heard in the lungs.
4, persistence of hypoxemia.
5, blood gas analysis of blood hypoxemia, metabolic acidosis with respiratory alkalosis.
6, blood picture, changes in erythrocyte pressure volume.
7, myocardial enzyme profile including CK-MB, cTnI determination.
8.X-ray chest film and CT examination show patchy cloudy flocculent shadow, pleural effusion, hemopneumothorax, etc.
V. Treatment
Treatment principles: light to moderate burn compound injury according to the principles of burn treatment, treatment is relatively smooth, very few visceral complications. The treatment of severe and extra-severe burn washout compound injuries should be combined with the clinical situation in the early stage, focusing on the resuscitation measures of pulmonary impact injury and correction of shock.
Measures.
1, the prevention and treatment of shock
Resuscitation rehydration fluid can basically be supplemented by the expected amount of simple burns, but with appropriate supplementation of crystalloid and a certain amount of whole blood. However, extra heavy patients require rapid rehydration, striving to input 2000-2500ml of fluid in the first 2 hours. Firstly, sodium lactate Ringer’s solution should be used to reduce the degree and duration of shock, followed by whole blood and plasma to increase the colloid osmotic pressure and reduce plasma extravasation. It has been reported that the rehydration amount of the first 24 hours is 2.0-2.5ml/Kg.1% TBSA crystal, colloid fluid; the rehydration amount of the second 24 hours is 2/3 of the amount of the first 24 hours. According to the results of experimental studies suggest that the burn washout compound injury and red blood cell membrane stiffness increased, deformability decreased, blood rheological properties deteriorated, the administration of HSD (sedation 7.5% sodium chloride solution for 15 min), can significantly reduce the whole blood viscosity and whole blood reduction viscosity, can significantly expand the volume, peripheral vascular resistance decreased, improve the hemodynamic status. During resuscitation, urine volume (1-2ml/Kg.h), hematocrit, electrolytes, oxygen saturation (SpO2) and hemodynamic parameters were closely monitored.
Secondly, in order to improve myocardial contractility and heart beat output, dilate renal and mesenteric vessels, and increase renal blood flow and glomerular filtration rate in the early stage of burned and washed compound injury, micro dopamine (2-5ug/Kg.min) or dobutamine can be administered intravenously. The combination of scopolamine (654-2) and dexamethasone can also be used. 20mg of 654-2 infusion once every 6 hours can improve microcirculation, increase oxygen supply to tissue cells and reduce the release of inflammatory mediators. Dexamethasone 10-20mg once in 8 hours and discontinued after 3 days can improve the stress and tolerance to hypoxia in traumatic shock. Experimentally, the combination of the two can improve the degree of hemodynamic index disorder, reduce the lung body index and reduce the degree of pulmonary edema.
2.Adequate oxygen supply
Patients with burn-impact complex injuries should establish a good airway early. Anyone with pulmonary impact injury and/or inhalation injury should undergo tracheotomy as early as possible (i.e. before 6 hours after injury or if airway obstruction occurs) to ensure the patency of the airway. According to the parameters required for oxygen supply, namely DO2=1.34×Hb×CO×SaO2, efforts should be made to increase Hb, CO and SaO2. ensure that Hb is 100-120g/L; Hct33-35%, SaO2 is positively correlated with PaO2 in a wide range, and increase PaO2 to ensure airway patency, and appropriately increase the concentration of inhaled oxygen (FiO2) so that the oxygenation index ( PaO2/ FiO2) is greater than 300 mmHg or more, so as to ensure good oxygen supply to important organ tissues. To increase CO (cardiac output), it lies in increasing preload (rehydration and expansion), appropriately decreasing afterload as well as applying positive inotropic drugs to increase the volume per beat. For this purpose, regular monitoring of blood gas analysis is performed. If the respiratory rate exceeds 35 breaths/min, PaO2 has a tendency to decrease, and PaO2 is lower than 80-70 mmHg, mechanical ventilation should be used promptly, and PEEP 5-8 cmH2O should be added if necessary. to ensure airway patency, in addition to regular airway humidification and removal of airway secretions, fiberoptic bronchoscopy should be performed once daily to observe airway and lung lesions, and alveolar high-dose lavage plus exogenous pulmonary surface active substance (PS). And closely observe the dynamic changes of ARDS.
3.The management of trauma
According to the evolution of the pathophysiological changes of impact injury, the lung injury starts to reduce or improve in 3 days after the injury, so 1-2 large area scab cutting and microdermal implantation are performed on the wound surface of Ⅲ degree burns around 3 days after the injury to remove the inflammatory media and endotoxicity of scab and subscab edema fluid, block or reduce the uncontrolled inflammatory reaction, reduce the incidence of systemic sepsis and visceral complications, and improve the healing rate.
The treatment of injured organs requires shortening the time to be operated, thorough removal of necrotic tissues without blood flow, excision of organs that cannot be repaired such as spleen and intestinal canal, partial excision or repair of liver, pancreas and one kidney depending on the injury, and cautious one-stage anastomosis of the injured colon in severe shock. Those with hemopneumothorax causing respiratory distress should immediately perform closed drainage of the chest cavity.
4.Apply early intestinal nutrition
Early intestinal nutrition can improve intestinal blood perfusion after burn injury, maintain the structure and function of intestinal mucosa, reduce intestinal injury and endotoxin displacement. Reduce intestinal-derived hypermetabolism. At the same time, oral glutamine and arginine.
5.Prevent and control infection
The lung injury is the most serious in burn and punch complex injury, with pulmonary hemorrhage and alveolar and interstitial edema, loss of airway mucosal barrier defense function, resident bacteria and nosocomial pathogens (including fungi) leading to respiratory tract infection is not uncommon. Therefore, targeted antibiotics are used to regulate the immune function of the body and prevent or control the infection as soon as possible.