Sepsis

Introduction to sepsis Sepsis refers to the systemic inflammatory response syndrome (SIRS) caused by infection, which is clinically confirmed to have bacteria or highly suspicious infections. Although sepsis is caused by infection, once it develops, it follows its own pathological processes and laws, so sepsis is essentially the body's response to infectious factors. basic knowledge The proportion of illness: 0.002% Susceptible people: no special people Mode of infection: non-infectious Complications: shock stress ulcer metabolic acidosis diffuse intravascular coagulation

Cause of sepsis

Bacterial endotoxin (20%):

Bacterial endotoxin can induce sepsis. Uncontrolled inflammatory reactions, immune dysfunction, high metabolic status and multiple organ dysfunction in the pathophysiology of sepsis can be triggered directly or indirectly by endotoxin.

Inflammatory mediator (10%):

Infectious factors in sepsis activate the mononuclear macrophage system and other inflammatory cells, and produce and release a large number of inflammatory mediators. In sepsis, endogenous inflammatory mediators, including vasoactive substances, cytokines, chemokines, oxygen free radicals, acute phase reactive substances, bioactive lipids, plasma enzyme system products, and fibrinolysis pathways The effect forms a network effect and causes extensive damage to various systems and organs throughout the body. At the same time, certain cytokines, such as tumor necrosis factor (TNF)-, may play an important role in the occurrence and development of sepsis.

Immune dysfunction (10%):

The main features of sepsis immune disorder are loss of delayed allergic reaction, inability to remove pathogens, and susceptibility to iatrogenic infections. The mechanism of sepsis immune dysfunction, on the one hand, is an important regulation of the immune system, cell T cell dysfunction, inflammatory mediators drift to anti-inflammatory response, inflammatory factors are reduced, anti-inflammatory factors increase; on the other hand, immune paralysis That is, apoptosis and immune non-reactivity, T cells do not respond to specific antigen stimulation or secrete cytokines.

Intestinal bacterial/endotoxin translocation (8%):

Since the 1980s, people have noticed that the body's largest bacterial and endotoxin reservoir--intestinal dysfunction caused by stress, and the infection caused by intestinal bacterial/endotoxin translocation and subsequent pus Toxicosis and multiple organ dysfunction are closely related. Studies have shown that the stress response after severe injury can cause intestinal mucosal barrier destruction, intestinal flora imbalance and decreased immune function, resulting in intestinal bacterial/endotoxin translocation, triggering excessive inflammatory response and organ dysfunction.

Coagulation disorders (5%):

The coagulation system plays an important role in the pathogenesis of sepsis. It promotes the inflammatory reaction and forms a key factor in the occurrence and development of sepsis. Endotoxin and TNF can activate the exogenous coagulation pathway by inducing the release of tissue factor from macrophages and endothelial cells, and endotoxin-activated factor XII can further activate the endogenous coagulation pathway, eventually leading to disseminated intravascular coagulation ( DIC).

Genetic polymorphism (5%):

The clinical manifestations and prognosis of different individuals infected with the same pathogen are clinically different, suggesting that genetic factors such as gene polymorphism also affect the human's susceptibility and tolerance to stress, clinical manifestations, and differences in drug treatment response. An important factor.

Sepsis prevention

The most effective way to treat and prevent sepsis is to treat and prevent it based on the pathogenesis of sepsis, but unfortunately the pathogenesis of sepsis is still not fully elucidated. In this case, for the cause of the disease Prevention should be done in all aspects of clinical practice, and efforts to reduce the risk factors for infection may play an important role in the treatment and prevention of sepsis. With the advancement of medical research, large-sample, multi-center clinical randomized controlled trials will bring more evidence-based medical evidence to the treatment of sepsis. The clarification of the mechanism of sepsis in the future will definitely be the treatment of sepsis. Prevention brings new hope.

Sepsis complications Complications, shock stress ulcer, metabolic acidosis, disseminated intravascular coagulation

The complications of sepsis are clinical manifestations in the pathophysiology of sepsis. Common complications include shock, acute lung injury/acute respiratory distress syndrome, deep vein thrombosis, stress ulcer, and metabolic Acidosis, disseminated intravascular coagulation (DIC) until multiple organ dysfunction. Mastering its pathogenesis will help to better prevent its complications.

Symptoms of sepsis Common symptoms Increased heart rate, toxic granules, shortness of breath, leukocytosis, leukopenia, hypothermia, hypothermia

symptom

Sepsis is a manifestation of systemic inflammation:

1. chills, high fever, or low fever, the onset of rapid development.

2. Indifferent or irritated, coma.

3. Heart rate is fast, pulse is fine, shortness of breath or difficulty.

4. Liver and spleen.

5. Shock, G + bacteria sepsis occurred in shock late, the limbs are warmer. G-bacteria septic shock early, long duration, cold limbs.

Sign

Sepsis is often accompanied by signs of above or below normal body temperature, increased or decreased leukocytosis, tachycardia, shortness of breath, or abnormally elevated ventilation per minute, such as two or more symptoms in the clinic. It can diagnose sepsis; when it comes to organ failure, it is called severe sepsis. There are 500,000 patients with sepsis every year in the United States, and the survival rate is only 55% to 65%. In recent years, on the basis of a large number of clinical and experimental studies, people have gained a lot of new understanding of sepsis, and the detection methods for sepsis have been improved, and anti-infective treatment and supportive treatment have been greatly improved. Mortality in patients with sepsis has decreased.

Examination of sepsis

1. Monitoring: Accurate understanding of the disease state of patients with sepsis is an indispensable part of the treatment of septic shock. It is especially important to reflect the indicators of hemodynamics and microcirculation perfusion. Therefore, it is a common monitoring indicator for sepsis. The method and clinical significance are important skills of doctors.

(1) Central venous pressure (CVP) and pulmonary artery pressure (PAWP). CVP and PAWP reflect right ventricular end-diastolic pressure and left ventricular end-diastolic pressure, respectively, which are pressure indicators reflecting the preload. The central venous catheter should be placed as early as possible in patients with severe sepsis, and the pulmonary artery floating catheter should be placed according to the condition.

(2) Central venous oxygen saturation (ScvO2) and mixed venous oxygen saturation (SvO2). In the early stage of severe sepsis and septic shock, even if the body's blood pressure, heart rate, urine volume and CVP are in the normal range, the perfusion of the whole body tissue has already occurred, and ScvO2 and SvO2 can be earlier. Reflects the perfusion state of the tissue. Studies have shown that SvO2 <70% in severe sepsis and septic shock suggests a significant increase in mortality.

(3) Blood lactic acid. Blood lactate is a sensitive indicator of whether the tissue is in a low perfusion state and whether it is hypoxic. If the lactate level is higher than 4mmol/L, the mortality rate is significantly increased. Dynamic monitoring of changes in blood lactate or calculation of lactate clearance is more valuable in assessing disease status.

(4) Tissue oxygen metabolism. Hypoperfusion of gastrointestinal blood flow caused by sepsis can lead to ischemia and hypoxia of mucosal cells, increased H+ release and accumulation of CO2. The pH of the digestive tract mucosa (pHi) is an indicator that currently reflects the oxygenation status of gastrointestinal tissue cells.

Diagnosis of sepsis

1. Diagnostic indicators : Because the diagnostic indicators of previous "infection + SIRS performance" are considered too sensitive, the current clinical diagnosis of adult sepsis requires clear infection or suspicious infection plus the following indicators:

(1) general condition: fever (>38.3 °C) or hypothermia (<36 °C); increased heart rate (>90 beats / min) or > standard deviation above normal age 2; respiratory increase (>30 times / Points); consciousness changes; significant edema or fluid positive balance > 20 ml / kg, duration of more than 24h; hyperglycemia (blood sugar > 7.7mmol / L) without diabetes history.

(2) Inflammatory markers: leukocytosis (>12×109/L or leukopenia (<4×109/L) or normal but immature cells>10%; plasma C-reactive protein>normal 2 standard deviation; plasma Procalcitonin > normal value 2 standard deviations.

(3) hemodynamic parameters: hypotension (systolic blood pressure <90 mmHg, mean arterial pressure <70 mmHg or adult systolic blood pressure drop >40 mmHg, or 2 standard deviations below normal age); mixed venous blood Oxygen saturation (SvO2) > 70%; cardiac index (CI) > 3.5 L/min/m2.

(4) Organ dysfunction parameters: oxygenation index (PaO2/FiO2) <300; acute oliguria (urinary volume <0.5 ml/kg/h); creatinine increase 44.2 mol/L; abnormal coagulation function (international normalized ratio > 1.5 or activated partial thromboplastin time > 60s); intestinal paralysis: disappearance of bowel sounds; thrombocytopenia (<100 × 109 / L); hyperbilirubinemia (total bilirubin > 70mmol / L).

(5) Tissue perfusion parameters: hyperlactosis (>3 mmol/L); prolonged capillary refilling time or spotted skin.

It should be noted that the new diagnostic criteria do not emphasize that it is necessary to add the above 5 or more of the above symptoms to the diagnosis of sepsis, and more emphasis on the combination of abnormal indicators combined with clinical specialties. The condition changes to make a clinical diagnosis of sepsis more in line with clinical practice.

2. Severe sepsis : a combination of sepsis with organ dysfunction.

3. Septic shock : Other causes unexplained, acute circulatory failure characterized by hypotension, is a special type of severe sepsis. include:

(1) systolic blood pressure < 90mmHg or systolic blood pressure decreased by > 40mmHg at least 1h, or dependent on infusion and drugs to maintain blood pressure, mean arterial pressure < 60mmHg;

(2) Capillary refill time > 2s;

(3) cold limbs or skin spots on the limbs;

(4) hyperlactosis;

(5) Reduced urine output.

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