Pediatric Multiple Organ Dysfunction Syndrome

Introduction to pediatric multiple organ dysfunction syndrome Multiple organ dysfunction syndrome (MODS) was named in 1992 on the basis of multiple organ failure (MOF), and multiple organ failure was named in 1980 by Eiseman and Fry. In 1973, it was called sequential system failure (sequential system failure). The concept of multiple organ failure means that more than 2 hours of onset, there are 2 or more organs or systems in a chain sequential or cumulative form, successive and/or simultaneous functional failure, so that the internal environment is not stable. Clinical syndrome. basic knowledge The proportion of illness: 0.0521% Susceptible people: infants and young children Mode of infection: non-infectious Complications: acute renal failure, diffuse intravascular coagulation

Causes of pediatric multiple organ dysfunction syndrome

(1) Causes of the disease

1. Severe infection, sepsis, systemic inflammatory response syndrome This is the most common cause. The toxins and inflammatory necrotic tissue produced by bacteria during severe infection can release lysozyme, fatty acids and vasoactive amines, and can be recycled to the lungs with blood. Causes the reduction and loss of activity of pulmonary surfactant, collapse of alveolar wall, atelectasis, bacterial toxin damage of pulmonary capillary membrane, increased permeability, increased albumin in the interstitial lung, leading to alveolar ventilatory dysfunction, can produce acute lung Incomplete function.

The endotoxin of Gram-negative bacteria can directly damage the myocardial sarcoplasmic reticulum, produce toxic myocarditis, affect myocardial systolic and diastolic function, severe heart failure and even cardiogenic shock, bacterial toxin can not only directly damage liver cells, when infection combined with shock At the same time, it can also cause a sustained decrease in blood supply to the liver and cause liver dysfunction.

2. Severe trauma, shock, ischemia-reperfusion injury, surgical stress, these factors can lead to the destruction of intestinal mucosal barrier function, so that bacteria and endotoxin accumulated in the intestinal tract invade the body to form enterogenous endotoxemia, and then through it Direct or indirect effects can induce damage to the body's organs. A series of histiocytic damage effects of endotoxin during septic shock are mainly due to the toxin-stimulated mononuclear macrophage system releasing excessive inflammatory mediators, forming a chain-amplification reaction. There is a certain intrinsic link between the translocation of endogenous bacteria and endotoxin and excessive inflammatory response and organ dysfunction after severe trauma.

3. Quickly input a large amount of blood, liquid and inappropriate drug application. Adult blood transfusion volume is 1800ml/6h, supplemental crystal solution 6000ml/6h or 14000ml/24h can produce circulatory system overload syndrome.

(two) pathogenesis

1. Out-of-control systemic inflammatory response More than 20 years of clinical research has revealed that the pathogenesis and clinical features of MODS are different from other organ failures. At present, a consensus has been reached on "uncontrolled systemic inflammatory response". The inflammatory response is originally a body against foreign diseases. The protective response of factor invasion, but if it is too strong, the body's inflammatory response is out of control, it will cause instability of the internal environment, apoptosis, immunosuppression, septic shock, organ dysfunction, that is, the body is suffering from bacteria or endotoxin. Under attack, the mononuclear macrophage system is activated to over-express, produce and release a large amount of inflammatory mediators, and influx into the systemic circulation, thereby producing a continuous systemic inflammation cascade effect, which can continuously strengthen itself and become lost. control.

2. Multiple inflammatory mediators In addition, the body's compensatory anti-inflammatory response is accompanied by the initiation of inflammatory response. If it is in dynamic equilibrium, the condition is stable; if the imbalance of the homeostasis will lead to internal environment disorder, the inflammatory response is dominant. That is, SIRS, on the other hand, if the anti-inflammatory response predominates, immune dysfunction, increase the susceptibility of the body infection, produce compensatory anti-inflammatory response syndrome (CARS), regardless of SIRS, or CARS Finally, it leads to MODS. If it is not treated early, it will cause death due to MSOF. MODS is mainly caused by the loss of control of the body's inflammatory reaction. Various inflammatory mediators are the key to the disease. Therefore, MODS should be regarded as a medium in essence. Disease, a variety of mediators involved in the inflammatory response, including a variety of inflammatory cytokines (TNF1, ILs, PAT, LTs, EDRF, VPF, etc.), a variety of inflammatory mediators (PGs, C3, C5, etc.) and oxygen free radicals (1O2 , O2-, H202, OH) and nitric oxide (NO), etc., their release and interaction can form overlapping pathophysiological processes, including endothelial cell inflammation Hypercoagulability and micro thrombosis, abnormal state of blood circulation, myocardial depression, and high metabolic reactions, thereby forming the inflammation and pathology of MODS.

In this process, the systemic inflammation cascade reaction, bacterial endotoxin and/or lipopolysaccharide (LPS) are the most important stimuli or predisposing factors, and are the trigger of this chain reaction, when LPS and LPS in the blood circulation Binding protein (LBP) binds to form LPS-LBP complex, binds to receptor CD14 molecule on the surface of mononuclear macrophages, initiates intracellular signaling system and promotes expression, synthesis or release of various inflammatory mediators. Autocrine, paracrine and endocrine pathways act on neutrophils, endothelial cells and various organ tissue cells, promoting the production of acutely related proteins, the release of oxygen free radicals, the initiation of coagulation pathways, and organ dysfunction.

3. Oxygen supply (DO2) and oxygen consumption (VO2) DO2 indicates the compensatory capacity of blood circulation when metabolism is increased or insufficiently perfused. VO2 indicates the amount of oxygen consumed by tissues, which is the highest metabolic rate of patients. Reliable indicators, under physiological conditions, oxygen kinetics is oxygen-independent VO2, that is, when blood passes through the tissue, it relies on increasing oxygen uptake to compensate, but under pathological conditions, such as severe shock, infection, ARDS, etc. Occurrence of hypoxia due to tissue oxygenation disorder due to loss of compensation, the mechanism is:

(1) Loss of regulation ability: The microvascular autoregulation ability is lost, and DO2 and VO2 do not match.

(2) Microthrombus: Microthrombus reduces the number of capillaries.

(3) tissue edema: due to tissue edema, the distance between oxygen into the cell is increased, and the time is prolonged.

Due to microcirculation and mitochondrial dysfunction in patients with MODS, DO2 and VO2 are bound to be impaired. Under normal circumstances, DO2 and VO2 are a closely related organic whole in the blood circulation. One of the main functions is oxygen transport and DO2 maintenance. Stable, when MODS occurs in the body with high metabolic state, VO2 increases with the increase of DO2, DO2 can not meet the needs, leading to insufficient tissue perfusion, oxygen transport and oxygen uptake barrier. At this time, even if DO2 is normal or increased, oxygen supply still occurs. Dependent VO2.

4. Multiple hypotheses In recent years, the study of the pathogenesis of MODS, in addition to the above-mentioned consensus mechanism, has established a variety of hypotheses, such as infection hypothesis, cytokine (macrophage) hypothesis, microcirculatory disorders (oxygen free radicals) Hypothesis, intestinal hypothesis, etc. These hypotheses are obviously not isolated. Many contents are related to each other, overlapping, infection, necrotic tissue (inflammatory reaction) or shock (oxygen deficiency) can directly destroy the stability of the body's normal internal environment. Then, the intestinal barrier function is impaired, endotoxemia is produced, the mononuclear macrophage system is activated, various humoral mediators and inflammatory cytokines are produced and released, and the organ supply is insufficient. The latter two in turn damage the intestinal mucosal barrier. And directly or indirectly cause the insufficiency or failure of the damaged organs, wherein the effects of cytokines and various humoral mediators are very important, and can be said to be the result of the sum of various cytokines and inflammatory mediators.

(1) Intestinal barrier function: In recent years, the intestinal barrier function has caused clinical concern. The intestinal tract is the largest bacterial and endotoxin reservoir in the body. Under normal circumstances, the physiologically functional intestinal mucosa affects the bacteria and endotoxin in the intestine. It acts as a barrier to prevent it from entering the body. In the case of trauma or infection stress, the barrier function of the intestine is weakened or damaged, thereby causing a large number of bacteria and endotoxins to invade the system through the portal vein and mesenteric lymphatic system, resulting in intestinal endotoxin. Endotoxemia and bacterial translocation and under certain conditions stimulate the chain reaction of cytokines and other inflammatory mediators, causing damage to various organs of the body. Therefore, Mashall et al called the intestinal tract as "post-traumatic multi-organ function." The origin of failure, Wilmore called "central organ", according to a series of in vitro and in vivo studies, suggesting intestinal barrier function, Kupffer cell function, ultra-high metabolic response and far There is an important clinical relationship between organ damage, and intestinal endotoxin can regulate Kupffer cell activity and release it. An endogenous mediator that regulates hepatocyte function, and the reticuloendothelial system of the liver plays an important role in the clearance of bacteria or endotoxins from the portal vein. Its damage causes intestinal-derived bacteria or endotoxins to reach the systemic circulation, thereby increasing the barrier. The systemic effects of impaired, therefore, during the development and progression of MODS, the barrier function of the intestine and the functional status of the gut-liver-lung axis deserve further study.

(2) Apoptosis and necrosis: two basic ways of cell death. Apoptosis is the process of active cell death, requiring gene transcription and protein expression; necrosis is the passive death of cells, and the process of apoptosis does not cause the body. Inflammatory reaction, apoptotic cells form apoptotic bodies, which are recognized by phagocytic cells to phagocytose. After phagocytosis, phagocytic cells are not activated, and cells rupture after necrosis, releasing contents and causing inflammation of the body. Studies have shown that apoptosis is not only in physiological In the state of cell selection, differentiation and clearance of aging cells play an important role, and participate in the pathogenesis of a variety of diseases, the traditional view that in the acute infection, severe trauma, trauma and shock, the body tissue due to ischemia, hypoxia And secondary damage often occurs necrosis, in recent years, people have begun to notice the role of apoptosis in the occurrence of MODS, due to increased apoptosis of vascular endothelial cells, resulting in increased microvascular permeability, inflammatory cell aggregation, inflammation Increase, may also be one of the causes of secondary bleeding, necrosis and DIC: intestinal, liver, heart, kidney and other physical organs The occurrence of a large number of apoptosis may directly lead to organ dysfunction, incompleteness, and even failure; thymocytes, lymphocytes, etc., due to increased number of apoptosis, resulting in decreased immunity, increased susceptibility to bacterial endotoxin, etc. (CARS production) further leads to In the occurrence of MODS, inflammatory effector cells such as mononuclear macrophages and Kupffer cells in the MODS process proliferate in a large amount, and when activated, a large number of cytokines can be produced, and PMN infiltrated into tissues is found to release free radicals through respiratory bursts. The toxic medium reaches the effect of damaging the tissue and expanding the inflammation. After the latter two inflammatory cells hyperproliferate, the body clears it by apoptosis, but if the apoptosis is delayed or the apoptotic cells are not phagocytized in time, delayed necrosis occurs. It will lead to the expansion of inflammation, resulting in uncontrolled systemic inflammation and MODS. Therefore, apoptosis not only participates in MODS, but also plays an important role in the development of MODS. The importance of apoptosis will make MODS A deeper understanding of the understanding, it will be possible to discover new ways of MODS.

5. The iatrogenic factor is an important reason for the occurrence of MODS. Due to the delay or inappropriateness of the rescue management of respiratory management, the shock state and hypoxemia can continue, and the primary damage is further enlarged, thus increasing the MODS. Opportunities to form, various intensive treatments, can also be the cause of MODS formation and deterioration, such as tracheal intubation, improper use of ventilators, intravenous, central and catheter indwelling, high-dose antibiotics, renal corticosteroid use, sedatives, Excessive respiratory stimulants, calories and undernutrition are the main causes of uncontrollable infection and opportunistic infections. The iatrogenic factors or iatrogenic diseases are closely related to the production of MODS. It should be noted that Concentrated treatment is necessary, but any treatment of concentrated treatment has its own shortcomings. As the concentration of treatment increases and time prolongs, the damage to the body will inevitably increase, and the possibility of dysfunction of various organs increases. It also reduces the body's immune defense function and produces CARS, which makes SIRS/CARS unbalanced and creates conditions for MODS.

6. The relationship between SIRS and MODS When the body is seriously infected, shock, trauma or major surgery, it can immediately produce complex defense confrontation, causing the immune system's stress response, including the release of various inflammatory mediators. The defensive process in which multiple systems are involved is called Systemic Inflammatory Response Syndrome (SIRS). The body is accompanied by compensatory anti-inflammatory reactions while initiating an inflammatory response. The two are two aspects of the body's opposition. Balance, the condition is stable; if the imbalance of the steady state leads to imbalance of the body, shock occurs when the SIRS is dominant, apoptosis and organ dysfunction; while CARS predominates, immunosuppression occurs, and some patients may also appear The combined antagonistic syndrome response syndrome, the interaction between pro-inflammatory and anti-inflammatory forces, continues to strengthen each other, ultimately resulting in more impaired immune imbalance (immunologic dissonance).

The factors that cause the body to be hit are divided into two categories: infection and non-infection. The SIRS caused by infectious factors is called sepsis, non-infectious factors such as trauma, and the clinical manifestations of acute non-suppurative pancreatitis are sepsis. However, there are no bacteria, viruses and other pathogens. It is said that SIRS is more suitable. The meaning is more extensive and more meaningful than sepsis. In the above two SIRS processes, if it can be actively treated, it can terminate its development, such as failing to control its development. , can be developed into MODS/MSOF.

SIRS is a new concept jointly proposed by the American Association of Chest Physicians and the Critical Care Medicine Association (ACCP/SCCM) in 1991 and has received extensive attention in the medical community. It represents a systemic inflammatory response in critical illness caused by infection or non-infectious factors. In general, when the body is hit by disease factors, the body's inflammatory response system and the anti-inflammatory response system (SIRS/CARS) are out of balance, and excessive inflammatory mediators are released, leading to excessive inflammatory reactions, such as continued development or deterioration, which can lead to Acute lung injury (ALI), acute respiratory distress syndrome (ARDS), MODS, MSOF, etc., have basically reached a consensus: 1 serious infection, multiple trauma, shock, acute pancreatitis, etc. are common causes of SIRS SIRS is characterized by systemic excessive inflammatory response; 2MODS is an important complication of SIRS development; 3SIRS to MODS development can occur simultaneously or sequentially ALI, acute renal failure, disseminated intravascular coagulation (DIC), acute Gastrointestinal hemorrhage, excessive inflammatory response throughout the entire process, Hayden recommended in 1994 clinical application of SIRS, MODS name, and proposed SIRS diagnostic criteria The following 2 or more conditions: 1 body temperature > 38 ° C or < 36 ° C; 2 heart rate is greater than the normal average of each age group plus 2 standard deviation; 3 respiratory rate is greater than the normal average of each age group plus 2 standard deviation; 4 blood leukocytes> 12 × 109 / L or < 4 × 109 / L, or rod-shaped nuclear cells > 10%, in June 1996, the second World Congress of Pediatric Critical Care Medicine proposed pediatric SIRS diagnostic criteria are shown in Table 1.

Prevention of pediatric multiple organ dysfunction syndrome

1. Actively prevent and treat various infectious diseases.

2. Actively prevent and treat all kinds of trauma.

Pediatric multiple organ dysfunction syndrome complications Complications, acute renal failure, diffuse intravascular coagulation

The disease is a serious infection, serious trauma and other complications, is a manifestation of critical illness, can occur heart, liver, kidney and other important organs of the functional failure, can occur in the gastrointestinal tract, central nervous system function damage, DIC occurs Et al, SIRS to MODS development process can occur simultaneously or sequentially ALI, acute renal failure, disseminated intravascular coagulation (DIC), acute gastrointestinal bleeding, excessive inflammatory response throughout the entire process.

Symptoms of pediatric multiple organ dysfunction syndrome common symptoms shock no urinary urinary heart failure pupillary liver function impairment coma lung atelectasis hypoxemia

1. Clinical features of MODS

In addition to the commonality of organ failure, MODS has many clinical features that are significantly different from other organ failures.

(1) It is closely related to infection, severe hypoxia, shock and trauma: in this type of patients, despite the presence of fever, increased clinical manifestations of white blood cells, etc., about half of them lack bacteriological evidence, and about 1/3 of the infections were not found 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 in the infection, shock, trauma, etc. to activate the body's inflammatory cells; 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 In the pre-excited state, the body again encounters a runaway inflammatory reaction that occurs during the second stroke.

(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, etc., while shock is mainly caused by ischemic injury, chronic organ failure Tissue cell necrosis and hyperplasia, organ atrophy, fibrosis.

(5) The possibility of reversal: Although the condition is dangerous, once it is 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 manifested in the occurrence of various organ failures. Order and severity aspects.

(6) Number of organ damage: There is no unified understanding of the number of organs involved in the diagnosis of MODS. Usually, the systemic failures of the lungs, heart, kidney, brain, gastrointestinal, blood and liver are diagnosed, but 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 regarded as MODS. In 1991, US ACCP/SCCM classified MODS into primary and secondary. Two types, also known as immediate and delayed, cardiac arrest and refractory shock can often lead to immediate onset of MODS, shock, hypoxia, and wound correction, there may be a period of clinical remission, often due to re-infection , the so-called second phase blow, triggering the body's immune inflammation out of control, the occurrence of delayed type MODS, according to the clinical course, some people will divide MODS into acute phase, infection period and low nutrition period, MODS mortality and failure organs The number is positively correlated.

2.MODS affected system organs

(1) Lung: In the development of MODS, the order of systemic or organ dysfunction often shows relative regularity. The lung is often the highest observed clinically occurring failure rate, the earliest organ, which may be related to the anatomy of the lung itself. Characteristics, easy to be affected by various pathogenic factors and easy to observe and monitor, lung endothelial cells are abundant, cell damage quickly leads to vasoconstriction and capillary permeability increase, pulmonary edema occurs, MODS often first manifests as acute lung Functional failure, a syndrome characterized by progressive hypoxemia and respiratory distress, ARDS, whose pathological basis is mainly the destruction of alveolar integrity, causing a decrease in pulmonary surfactant, decreased lung compliance, atelectasis, and stubbornness. Hypoxemia attenuates oxygen transport and provides a soil for lung infection. It is known that the lung is not only a gas-exchanged organ, but also a place where some hormones and mediators are produced and inactivated. Therefore, pulmonary dysfunction not only leads to a decrease in oxygen transport in the whole body. Tissue cell dysfunction of oxygen, and may cause certain mediators such as kinins, serotonin and angiotensin in the blood circulation Changing the content.

(2) Gastrointestinal tract: The role of the gastrointestinal tract in the formation of MODS is receiving more and more close attention. The intestinal mucosal barrier function is damaged or depleted earlier in the pathogenesis of MODS, which is combined with shock and recurrence in severe trauma. The perfusion injury is particularly prominent. Various basic diseases of MODS such as sepsis and septic shock are severe stress reactions. Children with different degrees of gastrointestinal mucosal erosion, ulcers and hemorrhage, because the gastrointestinal tract is the largest in the human body. Bacterial and endotoxin reservoirs, intestinal barrier damage can cause intestinal bacterial translocation and portal endotoxemia, thereby activating liver mononuclear macrophages, triggering systemic inflammatory response; using systemic antibiotics to cause certain drug resistance The diseased strain grows too fast, and the child is prone to severe sepsis and systemic infection. Therefore, it is currently believed that the gastrointestinal tract of children with MODS can be an important source of pathogenic bacteria causing serious infection.

(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 during shock is an important cause of acute heart failure, cardiac function The main manifestations of 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, use of immune mediators, antibodies, vasopressors, and acute tubular dysfunction caused by deposition of immune complexes. Performance of oliguria or anuria, retention of metabolites, imbalance of electrolyte balance and weakened chemical detoxification, although renal function is essential, renal failure complicates the treatment of critically ill children, but children do not die mainly from kidney disease, often with renal failure Respond only to the severity of the underlying disease.

(5) Liver: Liver dysfunction is mainly characterized by short-term serum bilirubin, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, metabolic function changes including carbohydrate metabolism, glycogen storage, gluconeogenesis and blood glucose itself Aspect changes, energy deamination of amino acids, barriers to the conversion of carbohydrates and lipids to energy, decreased urea production capacity to eliminate ammonia, low plasma protein synthesis, and excessive oxidation of fatty acids that produce ATP can lead to increased ketone bodies. The detoxification ability is reduced, and the above liver function changes are the result of the combined effects 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 Due to the metabolite of epoxyacetic acid, the child's body temperature is unstable, vascular tone changes, blood pressure and heart rate fluctuate, and there may be 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, become a cause of blood coagulation mechanism activation and platelet destruction, and can promote DIC Formation and the development of acute anemia crisis.

Examination of pediatric 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 metabolites, disordered electrolyte balance, decreased urea production capacity of 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, increased lactate dehydrogenase, total bilirubin >85.5mol/L (5mg/dl) and SGOT or LDH as normal values More than 2 times.

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

3. The pathogen is checked for infectious diseases, and the culture of the bacteria is positive.

4. Urine check for oliguria or no urine, proteinuria, hematuria, etc.

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

Diagnosis and diagnosis of multiple organ dysfunction syndrome in children

diagnosis

1. Diagnostic criteria for pediatric MODS.

2. Diagnostic criteria for organ and organ failure in infants and children <12 months of pediatric and >12 months pediatric system organ failure diagnosis criteria:

(1) Cardiovascular system:

1 blood pressure (systolic blood pressure): <12 months of children: <5.3 kPa (40 mmHg); > 12 months of children: <6.7 kPa (50 mmHg).

Or continuous intravenous drug, such as dopamine [> 5g / (kg · min)], to maintain blood pressure above the above criteria.

2 heart rate: normal body temperature, quiet state, continuous measurement for 1 min.

A. <12 months: <60 times/min or >200 times/min.

B.>12 months: <50 times/min or >180 times/min.

3 cardiac arrest.

4 serum pH < 7.2 (PaCO2 is not higher than normal).

(2) Respiratory system:

1 Respiratory frequency: normal body temperature, quiet state, continuous measurement for 1 min.

A. <12 months: <15 times/min or >90 times/min.

B.>12 months: <10 times/min or >70 times/min.

2PaCO2>8.7 kPa (65 mmHg).

3PaO2 < 5.3 kPa (40 mmHg) (no oxygen, except for cyanotic heart disease).

4 mechanical ventilation is required (not including children within 24 hours after surgery).

5PaO2/FiO2 <26.7 kPa (200 mmHg) (except cyanotic heart disease).

(3) nervous system: 1Glasgow coma score: 7; 2 pupil fixed, scattered (except drug influence).

(4) Blood system: 1 acute anemia crisis: hemoglobin <50g / L (5g / dl); 2 white blood cell count: 2 × 109 / L (2000 / mm3); 3 platelet count: 20 × 109 / L ( 20,000/mm3).

(5) Kidney system:

1 serum BUN: 35.7mmol / L (100mg / dl); 2 serum creatinine: 176.8mol / L (2.0mg / dl) (previously no kidney disease); 3 due to renal dysfunction need dialysis.

(6) Gastrointestinal system: 1 stress ulcer bleeding requires blood transfusion; 2 toxic intestinal paralysis, high abdominal distension.

(7) Liver system: total bilirubin > 85.5 mol / L (5 mg / dl) and SGOT or LDH is more than 2 times normal (no hemolysis), hepatic encephalopathy > II.

Differential diagnosis

1. How to determine the degree of failure and staging is usually divided into dysfunction, late in dysfunction (or early exhaustion), three stages of functional failure, the diagnostic criteria for each organ dysfunction in MODS can not be judged by the previous single organ failure criteria, Some systems such as immunization, the endocrine system currently lacks a standard of judgment.

2. The identification of primary and secondary MODS has different opinions on the mechanism of primary and secondary MODS, and there is no specific standard for classification. However, most scholars speculate on the main mechanisms of the two (including molecular biological mechanisms). Differently, as the disease progresses or the course continues, the primary will be converted to secondary.

3. Local causes and dying state and identification of MODS In clinical practice, care should be taken not to confuse local causes of acute illness in children (such as severe pneumonia with respiratory obstruction) and chronic disease dying state with the concept of MODS. Confusion of these concepts leads to treatment strategies. And the error in prognosis judgment is not conducive to the exchange and comparison of medical literature. It must be emphasized that severe blows and strong therapeutic interventions are necessary conditions for the occurrence of MODS. It is a syndrome in which critical illness occurs during intensive treatment. The current need for workers to improve is mainly the medical level supported by single organ function such as respiratory failure, heart failure, shock, and brain edema.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.