Septic shock

Introduction to septic shock Septic shock, also known as septic shock, refers to sepsis syndrome caused by products such as microorganisms and their toxins, shock, invasion of microorganisms and their toxins, cell wall products, etc. Blood circulation, activates various cellular and humoral systems of the host; produces cytokines and endogenous mediators, acts on various organs and systems of the body, affects its perfusion, leading to ischemia, hypoxia, metabolic disorders, dysfunction, and even more Organ failure. This critical syndrome is septic shock. Therefore, septic shock is the result of the interaction between microbial factors and the body's defense mechanism. The amount of virulence of the microorganisms and the internal environment and response of the organism are important factors in determining the development of septic shock. Severe infections, especially Gram-negative bacterial infections, often cause septic shock. basic knowledge The proportion of illness: 0.15% Susceptible people: no specific population Mode of infection: non-infectious Complications: acute respiratory distress syndrome, brain edema, diffuse intravascular coagulation

Causes of septic shock

Pathogens (30%):

Common pathogens of septic shock are Gram-negative bacteria, such as Enterobacteriaceae (Escherichia coli, Klebsiella, Enterobacter, etc.); non-fermented bacilli (Pseudomonas, Acinetobacter, etc.); Meningococcal; bacilli, etc., Gram-positive bacteria, such as grape ball, streptococcus, Streptococcus pneumoniae, Clostridium, etc. can also cause shock, certain viral diseases, such as epidemic hemorrhagic fever, Susceptible to shock, some infections, such as Gram-negative bacterial sepsis, fulminant meningitis, pneumonia, suppurative cholangitis, abdominal infection, bacillary dysentery (children) are easy to have shock.

Host factor (20%):

Original chronic basic diseases such as cirrhosis, diabetes, malignant tumors, leukemia, burns, organ transplantation and long-term acceptance of immunosuppressive drugs such as adrenal cortex hormones, antimetabolites, bacterial toxic drugs and radiation therapy, or application of indwelling catheters Or venous catheter can induce septic shock, so this disease is more common in hospital infected patients, the elderly, infants, childbirth women, poor physical recovery after major surgery is particularly likely to occur.

Bacterial toxins (30%):

Special types of septic shock toxic shock syndrome (TSS) TSS is a serious syndrome caused by bacterial toxins. The initial reported TSS is caused by Staphylococcus aureus. In recent years, similar signs have been found to be caused by streptococcus. cause.

1. Staphylococcus aureus TSS is caused by exotoxin produced by non-invasive Staphylococcus aureus. The first case was reported in 1978. In the early years, it was more common in menstruating women who used vaginal plugs. There were obvious regional distributions, mainly in the United States, followed by Canada. In some countries in Australia and Europe, with the improvement of vaginal plugs, the incidence of Staphylococcus aureus TSS has decreased significantly after the use of hyperabsorbent vaginal plugs has been stopped; non-menstrual TSS has increased, the skin is affected by skin and subcutaneous tissue, wounds Most of the infections, followed by upper respiratory tract infections, no gender, ethnicity and regional characteristics, almost all cases in China are non-menstrual TSS, from the patient's vagina, cervical local lesions can be isolated from Staphylococcus aureus, but blood culture Negative, pyrogenogenic exotoxin C (PEC) and enterotoxin F (SEF) isolated from this non-invasive S. aureus, collectively referred to as toxic shock syndrome toxin 1 (TSST-1), is considered to be associated with TSS Related to the disease, injection of purified TSST-1 into animals can cause symptoms similar to human TSS. The main clinical manifestations of TSS are acute high fever, headache, confusion, scarlet fever rash, skin desquamation after 1 to 2 weeks (foot) Especially), very low Blood pressure or erect syncope, often multiple system involvement, including: gastrointestinal (vomiting, diarrhea, diffuse abdominal pain); muscle (myalgia, increased blood CPK); mucosa (conjunctiva, pharynx, vagina) congestion; central nervous system System (headache, dizziness, disorientation, change of mind, etc.); liver (jaundice, increased ALT and AST values, etc.); kidney (oliguric or anuria, proteinuria, blood urea nitrogen and creatinine, etc.); heart (can Heart failure, myocarditis, pericarditis and atrioventricular block, etc.; blood (platelet reduction, etc.), menstrual TSS patients often have vaginal discharge, cervical congestion, erosion, attachment may have tenderness, about 3% recurrence.

2. Streptococcus TSS (STSS), also known as Streptococcal TSS-like Syndrome (TSLS). Since 1983, North American and European groups have reported Group A streptococci-induced toxic shock syndrome (STSS), mainly causing disease. The substance is pyrogenic exotoxin A (SPEA), SPEA as a superantigen (SAg) stimulates monocytes to produce tumor necrosis factor (TNF-) interleukin (IL-1), and directly inhibits the myocardium, causing capillaries Leakage caused shock, in the autumn of 1990 to the spring of 1991, some areas of the Yangtze River Delta (Haian, Wuxi, etc.) found scarlet fever-like disease outbreaks, rare in recent decades, rapid onset, chills, fever, headache Sore throat (40%), pharyngeal congestion, vomiting (60%), diarrhea (30%), fever, scarlet fever-like rash on the second day, recovery period desquamation, peeling, severe symptoms of systemic poisoning, nearly half of them have different degrees Low blood pressure, even coma, a small number of multiple organ dysfunction, from most patients throat swab culture to isolate the more virulent streptococcus mitis (streptococcus mitis), in some cases, the same pathogenic bacteria were detected in the blood, but B-type hemolytic streptococcus Injecting the corresponding antibody from the serum of the recovery period, and injecting the isolated strain into the skin of rabbit or guinea pig can cause local swelling and suppurative damage, accompanied by elevated body temperature, and timely antibacterial (using penicillin, erythromycin or clindamycin) Acupuncture) and antibody shock treatment, most patients recover.

Pathogenesis

The pathogenesis of septic shock is extremely complicated. The microcirculatory disorder theory proposed in the 1960s laid the foundation for the pathogenesis of shock. The current research has reached the cellular and molecular levels, microbes and their toxins and cell wall components (such as lipids). Polysaccharides, LPS, etc.) activate various responsive cells (including mononuclear-macrophages, neutrophils, endothelial cells, etc.) and body fluid systems (such as complement, kinin, coagulation and fibrinolysis) Endogenous mediators, cytokines, etc. play an important role in the pathogenesis. Infectious shock is a combined result of multiple factors interacting with each other and causing each other.

(1) The occurrence and development of microcirculatory dysfunction: During the development of shock, the changes of microvessel volume can undergo various stages of sputum, dilation and paralysis, that is, changes in microcirculation include ischemic oxygen phase, vascular vascular phase and Three stages of diffuse intravascular coagulation (DIC):

1. Ischemia and hypoxia: The characteristics of microcirculation changes in this period are: except for the heart, extracerebral vascular, skin and viscera (especially abdominal viscera) microvascular contraction, microcirculation perfusion is reduced, capillary network ischemic and hypoxic, among which The hydrostatic pressure is reduced, the interstitial fluid enters the microcirculation through the capillaries, and the capillary network is partially filled (self infusion). The mechanism involved in this microcirculation change is mainly the catecholamine, renin released by the sympathetic-adrenal medulla system. - angiotensin system, vasoactive lipids (bioactive substances produced by phospholipase A2, such as platelet activating factor, PAF; and arachidonic acid metabolites such as carotenoid A2, AxA2 and white three) Alkene, Leucotreine, LT), etc.

2. Congestion and hypoxia: This is characterized by an increase in anaerobic metabolites (lactic acid), increased formation of histamine and bradykinin by mast cells, diastolic vasodilation of the arterioles and capillaries, and continuous contraction of venules. Adhesion, impaction, blood stasis in the microcirculation, increased hydrostatic pressure in the capillaries, increased capillary permeability, extravasation of blood plasma, concentration of blood, reduction of effective circulating blood volume, further reduction of blood flow to the heart, and significant decrease in blood pressure Hypoxia and acidosis are more obvious, and the generation of oxygen free radicals increases, causing extensive cell damage.

3, microcirculation failure period: blood concentration, blood cell aggregation, blood viscosity increased, and due to vascular endothelial damage and other causes of clotting system activation caused by DIC, microvascular bed blockage, perfusion more reduced, and bleeding, etc., resulting in more Organ failure causes shock to be difficult to reverse.

According to the change of blood flow, the septic shock can be divided into high dynamic type (high row and low resistance type) and low dynamic type (low row high resistance type). If the former is not corrected in time, it will eventually develop into low power type and high. The occurrence of kinetic shock may be related to the release of histamine and bradykinin; the short circuit of arteriovenous vein is open, which constitutes a non-nutritive blood flow channel of microcirculation, and the blood passes through the short circuit to return the heart, and the output of the heart can be normal or even increased. The visceral microcirculation vegetative blood perfusion is reduced; endotoxin activates histidine dehydrogenase, accelerates the formation of histamine, and increases the release of histamine from mast cells; plus the direct damage of endotoxin to vascular smooth muscle cell membrane leads to membrane The ability to function normally to reduce calcium ions is associated with decreased vascular tone, and the occurrence of low-power shock is associated with alpha receptor excitation.

(B) the cellular mechanism of shock: microcirculatory disorders are important in the occurrence of shock, but cell damage can occur before hemodynamic changes, that is, the metabolic disorder of the cells can be primary, possibly directly by endotoxin Caused by the earliest occurrence of membrane dysfunction, membrane damage caused by the failure of Na+-K+-ATPase on the membrane, resulting in increased intracellular Na+, decreased K+, edema in the cells, mitochondria is the first organelle to change when shocked, when After it is damaged, it can cause the following changes: 1 its respiratory chain function is disordered, causing metabolic disorder; 2 its oxidative phosphorylation function is reduced, the tricarboxylic acid cycle is not working properly, ATP production is reduced, lactic acid is accumulated; The ion pump has obstacles, the intracellular and extracellular Na+, K+, Ca++, Mg++ plasma concentration difference transfer, K+ and Ca++ are lost from mitochondria, the intracytoplasmic Ca++ is increased, and the phospholipase A2 on the membrane is activated to decompose the membrane phospholipid, resulting in membrane Injury, its permeability increases, Na+ and water enter the mitochondria, causing it to swell, structural damage, lysosome contains a variety of enzymes, is the main digestive system in the cell, lysosomal membrane during shock Permeability increased, plasmin release, resulting in cell death autolysis.

In addition to activating the body fluid system, endotoxin can also directly act on various reactive cells to produce cytokines and metabolites:

1. Endothelial cells: cause cytotoxic reactions (NO) and the like.

2, neutrophils: make it chemotactic aggregation, conditioning and phagocytosis; synthesis of PAF, TxA2, prostaglandin (PGE), LTB4, etc.; release oxygen free radicals, lysosomal enzymes, elastase and so on.

3. Platelets: aggregation, synthesis of TxA2, etc.

4. Mononuclear macrophages: release of tumor necrosis factor (TNF), interleukin-1 (IL-1), lysosomal enzyme, plasminogen activin and the like.

5, basophils and mast cells: release of histamine, PAF, LT and so on.

6, pituitary and hypothalamus: release ACTH, -endorphin and thyroid stimulating hormone releasing hormone (TRH).

The importance of TNF in shock has been widely recognized. TNF can bind to specific receptors of various cells in the body and produce various physiological effects: TNF and IL-1, IL-6, IFN-, PAF and other cytokines. There is synergy, which is important in vascular endothelial cell injury, while transforming growth factor (TGF-1) can alleviate the effects of TNF and other factors. TNF can activate neutrophils and lymphocytes, and make the membrane sticky. The expression of the attached protein is increased, the adhesion between leukocytes and endothelial cells is enhanced, and the expression of adhesion proteins on the inner leukocyte membrane is also enhanced, resulting in endothelial cell damage and permeability enhancement, promoting blood coagulation, etc., animal experiments prove that the infusion large dose After TNF, it can produce hemodynamics, blood biochemical and pathological changes that are similar to septic shock, causing the animal to die rapidly.

(3) Metabolic changes during shock, electrolyte and acid-base balance disorders:

Under shock stress, glycogen and fat catabolism are hyperactive, initial blood sugar, fatty acids and triglycerides are increased; glycogen depletion with shock, blood sugar is reduced, insulin secretion is reduced, glucagon is secreted, and early shock Respiratory augmentation due to direct stimulation of bacterial toxins to the respiratory center or reflex stimulation of effective circulating blood volume, excessive ventilation, resulting in respiratory alkalosis; followed by insufficient oxygenation of the organ oxygenation, biooxidation occurs Obstacles, tricarboxylic acid cycle inhibition, ATP production decreased, lactic acid formation increased, leading to metabolic acidosis, deep and rapid breathing; late shock, often due to central nervous system or lung function damage caused by mixed acidosis, may occur Changes in respiratory rhythm or amplitude, insufficient ATP production every time the sodium pump on the membrane fails, resulting in abnormal distribution of ions inside and outside the cell: Na+ influx brings water, causing cell edema, mitochondria swelling, matrix changes; K+ flows out of the cell The concentration of Ca++ inside and outside the cell is thousands of times. The difference in concentration depends on the permeability of the cytoplasmic membrane to Ca++ and the external pumping effect. Calcium ++ influx occurs when the membrane is damaged, and Ca++ overload in the cytoplasm can produce a lot of harmful effects, such as activation of phospholipase A2, hydrolysis of membrane phospholipids to produce arachidonic acid, the latter by cyclooxygenase and The lipid oxidase metabolic pathway produces prostaglandins (PGF, PGE2, PGD2), prostacyclin (PGI2), TxA2 and LT (LTB4, LTC4, LTD4, LTE4) and other inflammatory mediators. These products can affect vascular tone and microvascular permeability. Sexuality, and acts on platelets and neutrophils, causing a series of pathophysiological changes that play an important role in the development of shock.

(4) Changes in the function and structure of important organs during shock:

1. Kidney: Renal vascular smooth muscle AV is short-circuited, renal cortical vasospasm in shock, and near-medullary microcirculation short circuit is open to a large extent, causing cortical blood flow to be greatly reduced and medullary blood flow is relatively guaranteed. If shock persists, renal tubule Necrosis due to ischemia and hypoxia, interstitial edema, easy to complicated with acute renal failure, and DIC, glomerular capillary plexus with extensive thrombosis, resulting in renal cortical necrosis.

2. Lung: The changes of pulmonary circulation during shock are mainly pulmonary microvascular contraction, increased resistance, large number of AV short circuits, insufficient pulmonary capillary perfusion, and pulmonary blood flow into the pulmonary vein without alveolar gas exchange, resulting in imbalance of ventilation and perfusion ratio and oxygen diffusion function. Obstruction, PO2 decline, and systemic hypoxia, this condition is called adult respiratory distress syndrome (ARDS), neutrophils are considered to be an important factor in the pathogenesis of ARDS, complement activation product C5a attracts neutrophil accumulation The lungs circulate and adhere to the surface of the pulmonary capillary endothelium, releasing a variety of injurious mediators such as proteolytic enzymes, elastase, collagenase, arachidonic acid metabolites (prostaglandins, TxA2, LT, etc.), oxygen self groups, etc. Injury of lung parenchymal cells, endothelial cells, fibroblasts, etc., increased alveolar capillary permeability, plasma extravasation and interstitial edema, TNF, IL-1 cytokine release also leads to neutrophil chemotaxis and The lung is stagnant and increases its adhesion to endothelial cells. In the case of ischemia and hypoxia, the secretion of alveolar surfactant is reduced, and lung compliance is reduced. It is easy to cause atelectasis, and can also cause alveolar epithelium and capillary endothelium to swell, aggravating the imbalance between alveolar ventilation and perfusion. In the shock, plasma fibronectin (Fn) is often reduced by synthesis, accelerated degradation and increased consumption. Can cause alveolar capillary membrane structural defects, as well as bacteria, toxins, fibrin degradation products difficult to remove, is also conducive to the production of ARDS.

3, heart: high oxygen consumption of the heart, coronary vascular perfusion has a great influence on myocardial function, arterial pressure is significantly reduced, when the diastolic blood pressure drops below 5.3 kPa (40 mm), the coronary perfusion is greatly reduced, myocardial ischemia and hypoxia Subcellular structure changes significantly, sarcoplasmic reticulum calcium-reducing ability is weakened, Na+-K+-ATPase and adenylate cyclase activity on sarcolemma are decreased, metabolic disorder, acidosis, hyperkalemia, etc. can affect myocardial Function, myocardial inhibitory factor and -endorphin from the pituitary gland have inhibitory effects on the cardiovascular system. Oxygen free radicals produced during myocardial ischemia-reperfusion can also cause myocardial inhibition and injury, although the heart beat during shock It can be normal, but the ventricular function is abnormal, which is reflected in the decrease of cardiac ejection fraction, ventricular dilatation, myocardial fiber degeneration, necrosis and rupture, interstitial edema, and DIC, microthrombus formation in myocardial blood vessels.

4. Liver: The liver is supplied by double blood. The smooth muscle of the portal system is very sensitive to catecholamine. In addition, the gradient of blood flow pressure difference in the portal system is small, and the flow rate is relatively slow. Therefore, the liver is prone to ischemia and ischemia, blood stasis and DIC. The liver is the body's metabolism, detoxification and synthesizing organs such as clotting factors and fibrinolysis. The liver function is impaired after persistent hypoxia, which may cause systemic metabolic disorders and lactate accumulation, weakened barrier function and DIC formation, often making shock difficult. Treatment, hepatocyte degeneration and necrosis in the central area of the hepatic lobules, and microthrombus formation in the central vein.

5, the brain: brain tissue high oxygen demand, its glycogen content is very low, mainly relying on blood flow supply, when the blood pressure drops below 7.9kPa (60mmHg), the brain irrigation flow is insufficient, the brain is hypoxia, the star The shape cells first swell and compress the blood vessels, and the vascular endothelial cells also swell, causing microcirculatory disorders and abnormal blood flow, which aggravate cerebral hypoxia. After the ATP storage is exhausted, the sodium pump disappears and causes brain edema, such as short-term It is impossible to restore the cerebral circulation, and it is difficult to reverse the development of cerebral edema.

6, other: intestinal sympathetic nerve is rich in distribution, blood circulation is reduced in shock, intestinal mucosal ischemia, injury, followed by edema, hemorrhage, bacterial invasion, endotoxin into the blood circulation to increase shock, in addition to histidine decarboxylase activation release Histamine, resulting in abdominal visceral and portal vascular bed congestion, plasma leakage and exacerbation of shock, severe ischemia and hypoxia, pancreatic lysosomes release proteolytic enzymes and cause serious consequences.

Septic shock prevention

1. Actively prevent infections and various diseases that are likely to cause septic shock, such as sepsis, bacterial dysentery, pneumonia, epidemic cerebrospinal meningitis, peritonitis, etc.

2, do a good job of on-site treatment of trauma, such as timely hemostasis, analgesia, heat preservation and so on.

3, patients with blood loss or excessive fluid loss (such as vomiting, diarrhea, hemoptysis, gastrointestinal bleeding, a lot of sweating, etc.) should promptly replenish or transfuse blood.

Complications of septic shock Complications Acute respiratory distress syndrome cerebral edema diffuse intravascular coagulation

Septic shock is a circulatory disorder syndrome with high morbidity and mortality. The complications caused by it pose a great threat to the life of patients.

1. Respiratory distress syndrome (RDS): Acute respiratory distress syndrome refers to a clinical syndrome characterized by alveolar capillary damage after severe intrapulmonary and external attacks such as severe infection, trauma, shock, and acute lung injury is a serious stage. Or type.

2, cerebral edema: cerebral edema refers to the pathological phenomenon of increased brain water, leading to increased brain volume, is the response of brain tissue to various pathogenic factors.

3, diffuse intravascular coagulation (DIC): shock can be seen in the reduction of capillary folds, the diameter of the tube is shortened, the appearance of broken lines, poor filling, blood color purple, slow blood flow loss of uniformity, severe There is coagulation. Fundus examination showed small arteriolar spasm, venous stasis, arteriovenous ratio from normal 2:3 to 1:2 or 1:3, severe retinal edema. Increased intracranial pressure can be seen in papilledema.

Symptoms of septic shock Common symptoms Shortness of breath, fever, chills, urinary alkali, low temperature, coma, low blood pressure, weak pulse, or even no... Achilles cold, irritability, chills, chills, infection, coma

Except for a few cases of high-resistance and low-resistance shock (warm shock), most patients have sympathetic excitability: the patient is clear, but irritated, anxious, nervous, pale complexion, pale lips and nails, and limbs The end is wet and cold. Can have nausea and vomiting. Reduced urine output. The heart rate increases, the breathing is deep and fast, the blood pressure is normal or low, and the pulse pressure is small. Arterial spasm can be seen in the fundus and nail fold microcirculation.

As the shock develops, the patient is irritable or unconscious. Breathing shallow speed. The heart sound is low and blunt. The pulse is fine, and the pressure is slightly heavier. Superficial vein collapse. The blood pressure drops, and the systolic blood pressure drops below 10.6 kPa (80 mmHg). In the original hypertension, the blood pressure is reduced by 20% to 30% compared with the basal level, and the pulse pressure is small. The skin is damp and cold, and this sputum is often pronounced. Less urine, or even no urine.

DIC and important organ failure can occur in the late stage of shock.

Examination of septic shock

1, blood: white blood cell counts are mostly increased, between 15 × 109 ~ 30 × 109 / L, neutrophil increased with nuclear left shift phenomenon, hematocrit and hemoglobin increased as a marker of blood concentration, concurrent with DIC platelets Reduced sex.

2, pathogen examination: routine blood (or other body fluids, exudate) and pus culture (including anaerobic culture) before the antibiotic treatment, separation of pathogenic bacteria for drug susceptibility test, sputum lysate test (LLT) facilitates the detection of endotoxin.

3, urine routine and renal function test: in the occurrence of renal failure, urine specific gravity from the initial high to low and fixed (about 1010); blood urea nitrogen and creatinine increased; urine / serum creatinine ratio <20; Urinary osmotic pressure decreased, urine / blood percolation ratio <1.1; urine Na (mmol / L) excretion > 40; renal failure index > 1; Na excretion fraction (%) > 1, above examination with prerenal renal function Not fully identified.

4. Blood biochemical examination of acid-base balance: CO2CP is a clinically measured parameter, but in respiratory failure and mixed acidosis, blood gas analysis must be performed simultaneously to determine blood pH, arterial blood pCO2, standard HCO3- And the actual HCO3-, buffer alkali and alkali remaining, etc., urine pH determination is simple and easy, blood lactic acid content determination has prognostic significance.

5, serum electrolyte determination: shock blood line is mostly low, blood potassium levels vary, depending on renal function status.

6, serum enzyme determination: serum ALT, CPK, LDH isozyme measurement can reflect liver, heart and other organs damage.

7, blood rheology and related DIC examination: blood flow slowed during shock, capillary stasis, blood cells, fibrin, globulin, etc., blood viscosity increased, so the initial blood is hypercoagulable, followed by fiber The lysis of the sputum is converted to hypocoagulability. The examination of DIC includes both consumptive coagulopathy and fibrinolysis: the former has platelet count, prothrombin time, fibrinogen, and kaolin thromboplastin time; the latter includes Thrombin time, fibrin degradation products (FDP), plasma protamine paracoagulation (3P) and ethanol gel test, and euglobulin dissolution test.

8, other: ECG, X-ray examination, etc. can be carried out as needed.

Diagnosis of septic shock

diagnosis

For patients with infectious diseases that are prone to concurrent shock, patients should be closely observed for changes in blood, blood samples, pathogens, urine and renal function tests, blood biochemical tests, serum electrolytes, serum enzymes, and blood rheology. Check and so on to diagnose.

Differential diagnosis

Septic shock should be differentiated from hypovolemic shock, cardiogenic shock, anaphylactic shock, and neuronal shock. Hypovolemic shock is caused by massive hemorrhage (internal or external bleeding), loss of water (such as vomiting, diarrhea). , intestinal obstruction, etc.), loss of plasma (such as large area burns, etc.) caused by a sudden decrease in blood volume, cardiogenic shock caused by low blood pressure, often secondary to acute myocardial infarction, acute pericardial occlusion, serious Arrhythmia, various myocarditis and cardiomyopathy, acute pulmonary heart disease, etc., anaphylactic shock is often caused by allergic reactions to certain drugs (such as penicillin) or biological products, neurogenic shock can be traumatic, drama Pain, cerebrospinal injury, anesthesia accident, etc., due to nerve action, the peripheral blood vessels are dilated, and the effective blood vessel volume is relatively reduced.

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