traumatic shock
Introduction
Introduction to traumatic shock Severe trauma, especially with a certain amount of bleeding, often causes shock, called traumatic shock. Injury shock is more common in some patients suffering from severe injuries, such as fractures, crush injuries, major surgery. Loss of plasma or whole blood to the body, plus bleeding at the injury site, edema and fluid exuded into the interstitial space can not participate in the circulation, which can reduce the circulating blood volume, and the injured tissue gradually necrosis or decomposition, resulting in vascular inhibition. Proteolysis products, such as histamine, protease, etc., cause microvascular dilatation and increased wall permeability, and also reduce the effective circulating blood volume, and the tissue is more ischemic. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: disseminated intravascular coagulation
Cause
Causes of damaging shock
Reason for shock
Trauma can trigger a series of pathophysiological changes, the basic changes are the existence of uneven distribution of body fluids, peripheral blood vessels can be expanded, cardiac discharge function can be normal, and even compensatory increase, and tissue perfusion pressure is insufficient.
Traumatic shock can be associated with low-volume shock caused by blood loss and loss of fluid, including chemical mediators, injury factors, oxygen free radicals, the effects of toxic substances, and changes in neuroendocrine, which enhances the permeability of microvessels. Exudation is a low-volume shock caused by vascular injury, so it should belong to vasogenic shock. Although it is low-volume shock, it is different from low-volume shock caused by blood loss. Traumatic shock is associated with A large amount of body fluid is lost, and a large amount of body fluid is isolated in the extravascular space, which activates the inflammatory mediator more and develops into acute inflammatory response syndrome (SIRS).
Microcirculatory disorders (ischemia, congestion, disseminated intravascular coagulation) cause microcirculation arterial blood perfusion insufficient, important vital organs due to hypoxia and functional and metabolic disorders, is a common law of various types of shock, microcirculation during shock The changes can be roughly divided into three phases, namely microcirculation ischemic phase, microcirculation hepatic phase and microcirculation coagulation phase (see Hemorrhagic Shock for details).
The development from the hemorrhagic phase of the microcirculation to the microcirculation coagulation phase is a manifestation of the deterioration of shock. It is characterized by the presence of fibers in the microcirculation (especially the capillary veins, venules, venules) on the basis of microcirculation congestion. Protein thrombosis, and often focal or diffuse hemorrhage; tissue cells degeneration and necrosis due to severe hypoxia.
DIC mechanism
Stress response
Stress response causes elevated blood coagulability, causes of shock (such as trauma, burns, bleeding, etc.) and shock itself is a strong stimulus that can cause stress, sympathetic excitation and pituitary-adrenal activity Strengthened, increased blood platelets and coagulation factors, enhanced platelet adhesion and aggregation, providing the necessary material basis for blood coagulation.
clotting factor
The release and activation of clotting factors, and some causes of shock (such as trauma, burns, etc.) can release and activate clotting factors themselves. For example, damaged tissue can release a large amount of tissue thromboplastin and initiate exogenous coagulation. The process; large area burns destroy a large number of red blood cells, and the phospholipids and red blood cells in the red blood cell membrane destroy the released ADP, which promotes the blood coagulation process.
Microcirculatory disorder
Microcirculatory disorders, tissue hypoxia, local histamine, kinins, lactic acid, etc., on the one hand cause capillary dilation and congestion, increased permeability, slow blood flow, increased blood concentrating red blood cell viscosity, favoring thrombosis Formation; on the other hand damage capillary endothelial cells, expose the gelatin, activate Factor XII and allow platelet adhesion and aggregation.
Hypoxia
Hypoxia reduced the function of the mononuclear phagocytic system, and it was unable to clear thrombin enzymes, thrombin and fibrin in time. As a result, disseminated intravascular coagulation occurred under the above factors.
It should be noted that in different types of shock, the formation of disseminated intravascular coagulation may be different in the morning and evening, for example, in the case of burns and traumatic shock, due to a large amount of tissue destruction, due to endotoxin to blood vessels due to toxic shock Direct damage to the endothelium can result in disseminated intravascular coagulation earlier, whereas in hemorrhagic shock, disseminated intravascular coagulation occurs later.
Prevention
Traumatic shock prevention
1. Actively prevent infection.
2. Do a good job of on-site treatment of trauma, such as timely hemostasis, analgesia, and heat preservation.
3. For patients who have lost blood or lost fluid (such as vomiting, diarrhea, hemoptysis, gastrointestinal bleeding, excessive sweating, etc.), they should promptly replenish or transfuse blood.
Complication
Traumatic shock complications Complications disseminated intravascular coagulation
Shock can often cause disseminated intravascular coagulation. Once disseminated intravascular coagulation occurs, the microcirculatory disorder will be more serious, and the shock condition will worsen. This is because: 1 extensive microvascular obstruction further aggravates microcirculatory disorders and makes it back. The blood volume is further reduced; 2 the consumption of coagulation substances, the activation of fibrinolysis and other factors cause bleeding, thereby reducing blood volume; 3 soluble fibrin polymer and its lysate can block the mononuclear phagocytic system, thus enabling Endotoxin from the intestine cannot be adequately eliminated.
Due to the occurrence of disseminated intravascular coagulation and the increasing aggravation of microcirculation, the systemic hypoxia and acidosis will become more and more serious due to the severe deficiency of systemic microcirculation perfusion caused by blood pressure reduction; severe acidosis It can rupture the lysosomal membrane in the cell, release lysosomal enzymes (such as proteolytic enzymes, etc.) and certain shock drivers (such as endotoxin), which can cause serious or irreversible damage to the cells, thus The functional metabolic disorders of various vital organs, including the heart and brain, are also more serious, which causes great difficulties in treatment. Therefore, this period is also called the refractory period of shock.
Symptom
Symptoms of septic shock Common symptoms Pulse fine-speed gravity shock pulse compression small irritability pulse pressure small skin pale ambition indifferent dizziness cold sweat response slow
The diagnosis of hypovolemic shock is generally not difficult. It is important to make an early diagnosis. It is necessary to diagnose shock after the blood pressure drops. Sometimes it may be too late. Whenever there is a lot of blood loss, water loss or serious trauma, it should be When thinking about the possibility of shock, during the observation process, if the patient is found to have mental excitement, irritability, cold sweat, accelerated heart rate, small pulse compression, decreased urine output, etc., it should be considered that there is shock, such as the sick population is thirsty, the mind Indifferent, unresponsive, pale skin, cold sweat, cold limbs, shallow and fast breathing, rapid pulse, systolic blood pressure below 12kPa (90mmHg) and less urine, should be considered to have entered the shock inhibition period, as for infectivity The diagnosis of shock may be based on the presence of a serious infection in the patient, some clinical manifestations of the shock compensatory period, or sudden hyperventilation. High-resistance septic shock has some acquired shock performance, diagnosis It is not difficult, but the low-resistance septic shock patients lack the shock performance of these observations, the diagnosis is difficult, and some special examinations are needed to confirm the diagnosis. .
The monitoring of shock can further confirm the diagnosis through the monitoring of shock patients, and can better judge the condition and guide the treatment.
According to the evolution of shock, shock can be divided into two stages, namely shock compensation period and shock inhibition period, or pre-shock or shock period.
Shock compensation period
Trauma with bleeding, when the loss of blood volume has not exceeded 20%, due to the body's compensatory effect, the patient's central nervous system excitability increased, sympathetic nerve activity increased. The performance industry is nervous or irritated, pale, cold hands and feet, accelerated heart rate, excessive ventilation. Normal or slightly higher blood pressure, which reflects the increase in diastolic blood pressure in the contraction of small arteries, so the pulse compression is small. Normal or reduced urine output. At this time, shock can be corrected quickly if handled properly. If not handled properly, the condition develops and enters the inhibition period.
2. Shock inhibition period
The patient is indifferent and unresponsive, and may even have unconsciousness or coma, cyanosis, cold sweat, rapid pulse rate, decreased blood pressure, and reduced pulse pressure difference. In severe cases, the skin and mucous membranes of the whole body are obviously purpura, the limbs are cold, the pulse is unclear, blood pressure is not detected, and there is no urine. There may also be metabolic acidosis. The appearance of ecchymosis or gastrointestinal bleeding in the skin and mucous membranes indicates that the condition has progressed to the stage of generalized intravascular coagulation. Progressive dyspnea, pulse rate, irritability, purpura or pinkish sputum, arterial oxygen partial pressure drops below 8kPa (60mmHg), although a large amount of oxygen can not improve symptoms and increase oxygen partial pressure, often prompt breathing The existence of a difficult syndrome.
The clinical manifestations of shock generally change with the evolution of shock.
Examine
Examination of traumatic shock
Central venous pressure
The venous system accommodates 55% to 60% of the whole body's blood volume. The change of central venous pressure is usually changed early by arterial pressure. It is affected by many factors, mainly including:
1 blood volume.
2 venous vascular tone.
3 right ventricular discharge ability.
4 chest or pericardial pressure.
5 venous return blood volume, the normal value of central venous pressure is 0.49 ~ 0.98kPa (5 ~ 10cmH2O), in the case of hypotension, the central venous pressure is less than 0.49kPa (5cmH2O), indicating insufficient blood volume; higher than 1.47kPa ( 15cmH2O), suggesting cardiac insufficiency, excessive venous vascular bed contraction or increased pulmonary circulation resistance; above 1.96 kPa (20cmH2O), it indicates congestive heart failure, continuous measurement of central venous pressure and observation of changes, than single The results obtained by one measurement are reliable.
2. Pulmonary wedge pressure
Central venous pressure does not directly affect the pressure in the pulmonary veins, left atrium, and left ventricle. Therefore, left ventricular pressure may have increased before central venous pressure rise, but not by central venous pressure measurements, using Swan-Gans pulmonary artery. The floating catheter is inserted into the superior vena cava from the surrounding vein, and the balloon is inflated to flow through the right atrium and the right ventricle into the pulmonary artery. The pulmonary artery pressure and pulmonary wedge pressure are measured to understand the pulmonary vein, left atrium and left ventricular end-diastolic phase. The pressure, which reflects the resistance of the pulmonary circulation, the normal value of pulmonary artery pressure is 1.3 ~ 2.9kPa, the normal value of pulmonary wedge pressure is 0.8 ~ 2.0kPa, the increase indicates the increase of pulmonary circulation resistance, pulmonary edema, the pulmonary wedge pressure exceeds 4.0kPa When the pulmonary artery wedge pressure has increased and the central venous pressure is not increased, the infusion should be avoided too much to prevent pulmonary edema, and the pulmonary circulation resistance should be considered. The pulmonary artery can be used for blood sampling and mixed venous blood gas analysis to understand the lungs. The internal arteriovenous shunt, that is, the degree of change in the ratio of ventilation/perfusion of the lung, has certain complications in the application of the catheter. Therefore, it is only used when the severe shock patient is rescued and necessary. The time for the catheter to be placed in the pulmonary artery should not exceed 72 hours.
3. Cardiac output and cardiac index
In shock, the cardiac output is generally reduced, but in septic shock, the cardiac output can be higher than the normal value, so if necessary, need to be measured to guide the treatment, through the pulmonary artery cannula and temperature dilution method, measured The cardiac output and the calculated cardiac index, the normal value of the cardiac index was 3.20 ± 0.20 / L (min · m2).
4. Arterial blood gas analysis
The normal value of arterial partial pressure of oxygen (PaO2) is 10 to 13.3 kPa (75 to 100 mmHg), the normal value of arterial carbon dioxide partial pressure (PaCO2) is 5.33 kPa (40 mmHg), and the normal value of arterial blood is 7.35 to 7.45. In shock, If the patient has no lung disease, PaCO2 is generally lower or within the normal range due to excessive ventilation. If the ventilation is better than 5.9-6.6 kPa (45-50 mmHg), it is often severe pulmonary insufficiency. Symptoms, PaO2 is lower than 8.0kPa (60mmHg), there is no significant increase after inhaling pure oxygen, often the signal of respiratory distress syndrome, through blood gas analysis, can also understand the evolution of metabolic acidosis during shock.
5. Arterial blood lactate determination
The normal value is 1~2mmol/L. Generally speaking, the longer the duration of shock, the more severe the blood perfusion disorder, the higher the arterial blood lactate concentration, and the higher the lactate concentration, indicating that the condition is serious and the prognosis is poor. When the lactate concentration exceeds 8mmol/L, the mortality rate is up to 100%.
6. Laboratory examination of disseminated intravascular coagulation
For patients suspected of diffuse intravascular coagulation, examination of the extent of platelet and clotting factor consumption, as well as examination of fibrinolytic properties, platelet counts below 80 × 109 / L, fibrinogen less than 1.5 g / L, prothrombin time is more than 3 seconds longer than normal, and the co-coagulation test is positive, can be diagnosed as diffuse intravascular coagulation.
Diagnosis
Diagnostic diagnosis of traumatic shock
diagnosis
The diagnosis of hypovolemic shock is generally not difficult. It is important to make an early diagnosis. It is sometimes too late to diagnose shock after a drop in blood pressure. Whenever there is a lot of blood loss, water loss or serious trauma, you should think about the possibility of shock. During the observation process, if the patient is found to have mental excitement, irritability, cold sweat, accelerated heart rate, small pulse compression, and decreased urine output, it should be considered that there is shock. Such as the sick population thirsty, ambiguous, unresponsive, pale skin, cold sweat, cold limbs, shallow and fast breathing, rapid pulse, systolic blood pressure below 12kPa (90mmHg) and less urine Shock inhibition period. As for the diagnosis of septic shock, it may be considered according to the presence of a serious infection in the patient, some clinical manifestations of the shock compensation period, or sudden hyperventilation. High-resistance septic shock has some manifestations of shock performance, and diagnosis is not difficult. However, patients with low-resistance septic shock lack the shock performance of these observations, and the diagnosis is difficult. Some special examinations are needed to confirm the diagnosis.
The monitoring of shock can further confirm the diagnosis through the monitoring of shock patients, and can better judge the condition and guide the treatment.
(1) General monitoring
It is often possible to determine whether shock exists and its evolution.
Mental state
Can reflect the condition of brain tissue perfusion. The patient was conscious and responded well, indicating that the circulating blood volume was sufficient. Ambition or irritability, dizziness, vertigo, or syncope from sitting to sitting position, often indicates that the circulating blood volume is insufficient, shock still exists.
2. Limb temperature, color
Reflect the situation of body surface perfusion. When the limbs are warm, the skin is dry, and the nails or lips are lightly pressed, the local temporary ischemia is pale, and after the compression, it quickly turns rosy, indicating that the shock is getting better. In shock, the skin of the limbs is often pale, damp and cold; when the nails or lips are lightly pressed, the color becomes pale, and the rosy is slow after the compression.
3. Blood pressure
During shock compensation, severe vasoconstriction keeps blood pressure at or near normal. Therefore, blood pressure should be measured regularly and compared. The blood pressure gradually decreased, the systolic blood pressure was lower than 12 kPa (90 mmHg), and the pulse pressure was less than 2.67 kPa (20 mmHg), which is evidence of the presence of shock. The blood pressure rises and the pulse pressure increases, indicating that the shock has improved.
4. Pulse rate
Pulse speed often occurs before blood pressure drops. Sometimes blood pressure is still low, but the pulse is clear, the hands and feet are warm, often indicating that shock tends to improve. The shock index (pulse rate/systolic blood pressure [calculated in mmHg]) can help determine whether or not there is shock and its extent. The index is 0.5, which generally means no shock; more than 1.0 to 1.5 means that there is shock; above 2.0, it means severe shock.
5. Urine volume
It is an indicator reflecting the renal blood perfusion, which can also reflect the blood perfusion of vital organs. Place the indwelling catheter and observe the urine volume per hour. The urine volume is less than 25ml per hour, and the specific gravity increases, indicating that the renal vasoconstriction still exists or the blood volume is still insufficient; the blood pressure is normal, but the urine volume is still small, and the specific gravity is lowered, and acute renal failure may have occurred. When the urine volume is stable at 30 ml or more per hour, it indicates that the shock is corrected.
(2) Special monitoring
The pathophysiological changes in shock are complex. In severe or long-term hypovolemic shock and septic shock, changes in hemodynamics, etc., are often not fully reflected in the above-mentioned monitoring programs, and further special monitoring projects are needed to better Determine the condition and take the correct treatment (see laboratory check).
