Multiple organ dysfunction syndrome

Introduction to multiple organ dysfunction syndrome Multiple organ dysfunction syndrome (MODS), also known as multiple system organ failure (MSOF) or multiple organ failure (MOF), refers to a concurrent or sequential concurrent acute illness, severe trauma, or major surgery. Acute dysfunction or failure of the above system or (and) organs, usually first affected by the lungs, followed by kidney, liver, cardiovascular, central nervous system, gastrointestinal, immune system and clotting system dysfunction. The onset of multiple organ dysfunction syndrome is characterized by secondary, sequential, and progressive. Clinical type 1, one-stage rapid-onset one-stage rapid onset refers to two or more systemic organ dysfunctions after 24 hours of primary acute etiology. This type of emergency is often severe in primary emergency. For those who die of organ failure within 24 hours of onset, they are generally only due to recovery failure, not as a MODS. 2, the second phase of delayed type II delayed type of hair refers to the first appearance of a systemic organ dysfunction (mostly cardiovascular or renal or pulmonary dysfunction), after which there seems to be a stable phase, after a period of time there are other or more systemic organs disfunction. basic knowledge The proportion of illness: 0.003% Susceptible people: no special people Mode of infection: non-infectious complication:

Cause of multiple organ dysfunction syndrome

Cause

1. Sepsis caused by various surgical infections;

2, severe trauma, burns or major surgery resulting in blood loss, lack of water;

3, shock for various reasons, heartbeat, respiratory arrest after recovery;

4, various causes of limbs, large areas of tissue or organ ischemia-reperfusion injury;

5, combined with acute necrosis or infection of acute abdomen;

6, blood transfusion, infusion, drugs or mechanical ventilation;

7. Patients with certain diseases are more likely to develop MODS, such as chronic diseases of heart, liver and kidney, diabetes, and immune function underground.

Pathogenesis

Under normal circumstances, local infections are necessary for bacterial clearance and tissue repair during infection and tissue damage, and have a protective effect. When the inflammatory response is abnormally amplified or out of control, the effect of the inflammatory response on the body changes from protective to damaging, leading to cell death and organ failure. Whether it is an infectious disease (such as severe infection, severe pneumonia, severe acute pancreatitis), or non-infectious diseases (such as trauma, burns, shock, early acute pancreatitis) can cause MODS. It can be seen that any disease that can cause the body's immune inflammatory response disorder can cause MODS. In essence, MODS is the result of uncontrolled body inflammation.

Infection and trauma are the triggering factors of the body's inflammatory response, and the loss of control of the body's inflammatory response ultimately leads to the destruction of the body itself, which is the root cause of MODS. Inflammatory cell activation and abnormal release of inflammatory mediators, tissue hypoxia and free radicals, destruction of intestinal barrier function, and bacterial and/or toxin translocation are all manifestations of uncontrolled inflammatory response in the body, constituting the pathogenesis of inflammatory MODS in MODS. Three overlapping mechanisms of pathogenesis that are out of control - the theory of inflammatory response, the theory of free radicals, and the theory of intestinal motility.

Prevention of multiple organ dysfunction syndrome

Multiple organ dysfunction syndrome is difficult to control once it occurs, and the mortality rate is quite high. When there are three system or organ dysfunctions, the mortality rate can be as high as 80%, so prevention is even more important. The preventive measures mainly focus on the following points:

1. In the treatment of various emergencies, there should be a holistic concept, and comprehensive diagnosis and treatment should be done as soon as possible.

(1) Analysis based on pathogenic factors such as severe trauma, infection, and major surgery.

(2) clinical manifestations of some organ dysfunction clinical manifestations, such as heart, lung, kidney, brain dysfunction. Some clinical manifestations are not obvious, such as liver, gastrointestinal and coagulation systems.

(3) Auxiliary examination The use of relevant tests or monitoring is very important for the discovery of multiple organ dysfunction, especially where the clinical symptoms are not obvious at an early stage. For example, urine specific gravity, serum creatinine can show renal function, platelet count, prothrombin time can show coagulation function.

2, special central circulation and respiratory changes, early detection and treatment of low blood volume, tissue low perfusion and hypoxia, pay attention to time, from the first aid on the spot, and throughout the entire treatment process.

3. Prevention and treatment of infection is an important measure to prevent multiple organ dysfunction syndrome. Including the treatment of the primary disease, that is, severe infection, including the rational use of antibiotics and the necessary surgical drainage: it also includes the prevention and treatment of certain serious wounds and major surgery.

4, as much as possible to improve the general condition such as nutritional status, water and electrolyte balance.

5, early detection and treatment of organ failure first, blocking the pathological chain reaction, to prevent damage to multiple system organs.

Multiple organ dysfunction syndrome complications Complication

This disease is a serious infection, severe trauma and other complications, is a critical manifestation of the disease, can occur heart, liver, kidney and other important organs of the functional failure, can occur gastrointestinal, central nervous system function damage, DIC occurs Wait. During the development of SIRS to MODS, ALI, acute renal failure, disseminated intravascular coagulation (DIC), acute gastrointestinal bleeding, and excessive inflammatory reactions can occur throughout the process.

Symptoms of multiple organ dysfunction syndrome common symptoms brain dysfunction renal failure irritability biliary stagnation liver function abnormality coagulopathy dysfunction hypovolemic shock

1. Clinical features of MODS In addition to the common point of organ failure, MODS has many clinical features that are significantly different from other organ failure.

(1) Closely related to infection, severe hypoxia, shock and trauma: In this type of patient, despite the clinical manifestations of infection such as fever and increased white blood cells, about half of them lack bacteriological evidence, and about 1/3 of them did not find infections even after autopsy. It is difficult to distinguish between sepsis or SIRS in clinical practice.

(2) high metabolism and high oxygen consumption: the patient's basal metabolism can reach 2 to 3 times normal. Despite the support of nutrient metabolism, the patient still exhibits a rapid depletion state, which is called auto-cannibalism.

(3) Physique is often accompanied by simultaneous or sequential organ damage: primary (also known as immediate) MODS often occurs during cardiopulmonary resuscitation or refractory shock, associated with organ perfusion and reperfusion injury . Secondary (also known as delayed type) MODS is the first attack on infection, shock, trauma, etc. to activate the body's inflammatory cells; the intestinal barrier function is impaired; the anti-inflammatory mechanism in the body is weakened; the inflammatory tissue secretions remain, etc., so that the body is in the pre- In the stimulating state, the body again encounters a runaway inflammatory reaction that occurs when the second stroke occurs.

(4) Lack of specific pathological changes: MODS lacks specificity in pathology, mainly for a wide range of acute inflammatory reactions, such as inflammatory cell infiltration, tissue cell edema, and the like. Shock is mainly caused by ischemic injury. Chronic organ failure is mainly caused by tissue necrosis and hyperplasia, organ atrophy and fibrosis.

(5) The possibility of reversal: Although the condition is dangerous, once cured, the clinical course may not leave a chronic disease. MODS has its own unique syndrome, but it also has the characteristics of the primary disease. Often reflected in the order and severity of the occurrence of various organ failure.

(6) Number of organ damage: There is no unified understanding of the number of organs involved in the diagnosis of MODS. The systemic failure is usually diagnosed according to the lungs, heart, kidney, brain, gastrointestinal, blood and liver. However, the organ failure caused by the primary disease should be excluded. Such as pneumonia leading to respiratory failure, heart failure, shock leading to renal failure, generally should not be considered as MODS. In 1991, ACCP/SCCM in the United States divided MODS into primary and secondary categories, also known as instant and delayed. Cardiac arrest and refractory shock can often lead to immediate onset MODS. After shock, hypoxia, and trauma correction, there may be a period of clinical remission, often due to re-infection, the so-called second phase blow, which triggers the body's immune inflammation to go out of control and develops delayed-type MODS. According to the clinical course, some people have classified MODS into acute phase, infection phase and low nutrition period. The mortality rate of MODS is positively correlated with the number of debilitating organs.

2.MODS affected system organs

(1) Lung: In the development of MODS, the order of systemic or organ dysfunction often shows relative regularity. The lungs are often the most commonly observed organ with the highest incidence of failure, which may be related to the anatomical features of the lung itself, the vulnerability to various pathogenic factors, and the ease of observation and monitoring. Lung endothelial cells are abundant, and cell damage rapidly leads to vasoconstriction and increased capillary permeability, resulting in pulmonary edema. MODS often manifests itself as acute pulmonary failure, a syndrome characterized by progressive hypoxemia and respiratory distress, or ARDS. Its pathological basis is mainly the destruction of alveolar membrane integrity, the reduction of pulmonary surfactant, the decrease of lung compliance, and atelectasis. Refractory hypoxemia attenuates oxygen transport and provides soil for lung infection. It is known that the lungs are not only gas-exchanged organs, but also places where hormones and media are produced and inactivated. Therefore, pulmonary dysfunction not only leads to reduced oxygen transport in the whole body, tissue oxygen metabolism disorders, but also may cause changes in the contents of certain media such as kinins, serotonin and angiotensin.

(2) Gastrointestinal tract: The role of the gastrointestinal tract in the formation of MODS is receiving increasing attention. Intestinal mucosal barrier function is impaired or depleted early in the pathogenesis of MODS, which is particularly prominent in severe trauma with shock and reperfusion injury. Various basic diseases of MODS such as sepsis and septic shock are severe stress reactions, and children may have varying degrees of gastrointestinal mucosal erosion, ulceration and bleeding. Because the gastrointestinal tract is the largest bacterial and endotoxin reservoir in the human body, damage to the intestinal barrier can cause intestinal bacterial translocation and endotoxemia in the portal vein, thereby activating liver mononuclear macrophages and initiating systemic inflammatory response; using systemic antibiotics Treatment causes some resistant strains to grow too fast, and children are prone to severe sepsis and systemic infections. Therefore, it is currently believed that the gastrointestinal tract of children with MODS can be an important source of pathogens causing serious infections.

(3) Cardiovascular system: Cardiac dysfunction or failure in children with MODS is mainly caused by prolonged tissue hypoxia, bacterial toxins and various inflammatory mediators. The production of myocardial inhibitory factor in shock is an important cause of acute heart failure. The main manifestations of heart failure are decreased myocardial contractility, decreased cardiac output, decreased cardiac index, increased pulmonary wedge pressure, and increased myocardial enzymes.

(4) Kidney: In MODS, renal dysfunction or renal failure is often a late manifestation due to hypoperfusion, immune mediators, antibodies, vasopressors, and acute tubular dysfunction caused by deposition of immune complexes. The child showed oliguria or no urine, metabolite retention, electrolyte balance disorder and weakened chemical detoxification. Although renal function is critical and renal failure complicates critical care, children do not die primarily from kidney disease, and kidney failure often only reflects the severity of the underlying disease.

(5) Liver: Liver dysfunction is mainly manifested by increased serum bilirubin, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase in a short period of time. Changes in metabolic function include changes in carbohydrate metabolism, glycogen storage, gluconeogenesis, and blood glucose self-stabilization. The deamination of amino acids that produce energy, the barrier to the conversion of carbohydrates and lipids to energy, the ability to remove ammonia from ammonia, the lowering of plasma protein synthesis, and the rapid oxidation of fatty acids that produce ATP can lead to an increase in ketone bodies and a decrease in detoxification ability. . The above changes in liver function are the result of a combination of ischemia, hypoxia and toxins.

(6) Central nervous system: The effect of MODS on the central nervous system is the reduction of cerebral blood flow and the influence of toxic media on the central nervous system. The damage can be directly caused by ischemia or indirectly due to toxic mediators such as pseudo-neurotransmitters, oxygen free radicals or Caused by an epoxy acetate metabolite. Children with unstable body temperature, changes in vascular tone, fluctuations in blood pressure and heart rate, and varying degrees of cerebral edema, and even cerebral palsy.

(7) Blood system: various serious infectious diseases, shock, diseases with antigen-antibody reaction, vasculitis, etc., can cause endometrial abnormalities, which become the cause of blood coagulation mechanism activation and platelet destruction, and can promote DIC Formation and the development of acute anemia crisis.

Examination of multiple organ dysfunction syndrome

Blood test

(1) Acute anemia crisis: hemoglobin <50g/L (5g/dl).

(2) White blood cell count: White blood cell count and neutrophils were significantly increased at the time of infection, and the white blood cell count was 2 × 109 / L (2000 / mm 3 ).

(3) Platelet count: 20 × 109 / L (20,000 / mm3).

2. Blood test

(1) Progressive hypoxemia: PaCO2 > 8.7 kPa (65 mmHg), PaO2 < 5.3 kPa (40 mmHg), PaO2 / FiO2 < 26.7 kPa (200 mmHg).

(2) impaired renal function: retention of metabolic products, disordered electrolyte balance, and decreased urea production capacity to exclude ammonia. Serum BUN35.7mmol/L (100mg/dl), serum creatinine176.8mol/L (2.0mg/dl).

(3) Impaired liver function: increased serum bilirubin, increased aspartate aminotransferase, increased alanine aminotransferase, and increased lactate dehydrogenase. Total bilirubin>85.5mol/L (5mg/dl) and SGOT or LDH were more than twice the normal value.

(4) Others: increased myocardial enzymes, low plasma protein synthesis, and increased ketone bodies.

3. Detection of pathogens Infectious diseases are cultured positively.

4. Urine examination oliguria or no urine, proteinuria, hematuria and other changes.

According to clinical needs, X-ray chest X-ray, B-ultrasound, electrocardiogram, brain CT and other examinations were selected.

Diagnosis and identification of multiple organ dysfunction syndrome

diagnosis

The degree and stage of failure are usually classified into dysfunction, late insufficiency (or early failure), and stage III of functional failure. The diagnostic criteria for incomplete function of each organ in MODS cannot be judged by the previous single organ failure criteria. Certain systems, such as immune and endocrine systems, currently lack a standard of judgment.

Differential diagnosis

The identification of primary and secondary MODS differs in the mechanism of primary and secondary MODS, and there is no specific standard for typing. However, most scholars speculate that the main mechanisms of the two (including the molecular biological mechanism) are different, and the primary transformation will be secondary to the progression of the disease or the progression of the disease.

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