Acute respiratory distress syndrome in children
Introduction to acute respiratory distress syndrome in children
Acute respiratory distress syndrome (ARDS), also known as shock lung syndrome, is an acute respiratory distress and hypoxemia syndrome characterized by pulmonary microcirculation disturbance during rescue or treatment. It is a non-specific response of the lung to severe injury in different situations and is characterized by severe progressive respiratory failure, although inhalation of high concentrations of oxygen cannot be corrected. In recent years, although the prognosis has been improved due to the early diagnosis of intrinsic and the application of end-expiratory positive pressure breathing apparatus, the mortality rate is still high. In 1967, Ashbaugh et al. proposed an intrinsic neonatal respiratory distress syndrome, but in order to distinguish it from the latter, it is recommended to name it adult respiratory distress syndrome.basic knowledge
The proportion of the disease: 0.01% - 0.02% (the incidence rate of children under 3 years old is about 0.01% - 0.02%, mostly due to severe pneumonia)
Susceptible people: young children
Mode of infection: non-infectious
Complications: respiratory failure, sepsis, pulmonary edema in children, acute pulmonary edema
Causes of acute respiratory distress syndrome in children
The primary cause (35%):
There are many primary or underlying diseases that cause ARDS, which are often associated with one or more risk factors such as infectious or hemorrhagic shock, head trauma and other neuropathic pulmonary edema, scald, drug poisoning, pancreatitis. Caused by indirect causes such as massive blood transfusions.
Environmental factors (25%):
Because children's immunity is lower than that of adults, especially in the case of normal adults, there is no problem in the environment, but children may be caused by smoking or inhaling chemicals.
Disease factors (18%):
Many times, children with other lung diseases cause this symptom, such as children with aspiration pneumonia, lung infection, pulmonary embolism, pulmonary contusion and radiation pneumonitis.
Other factors (12%):
The child's own immunity is low, and the main organs of the respiratory system may not be fully developed, resulting in insufficient force, which makes breathing difficult to respiratory distress.
The end result of the above reasons is the diffuse increase of pulmonary capillary epithelial permeability, which eventually causes pulmonary edema; the alveolar and small airways are filled with edema fluid, mucus, blood and other exudation, resulting in the formation of transparent membrane of the lung, causing obvious right to left The intrapulmonary shunt makes the lungs stiff; at the same time, type II alveolar epithelial cells proliferate due to the massive consumption and destruction of pulmonary surfactant, and eventually the alveolar septal thickening is accompanied by inflammation and fibrosis.
Prevention of acute respiratory distress syndrome in children
Prevent accidents. Prevent drug poisoning or other poisoning. Do a good job of vaccination. Actively prevent and cure children with pneumonia and various infectious diseases. Timely detection and correct treatment of primary diseases, prevention of cross-infection, maintenance of oral cleansing, prevention of food or drug reflux.
The most effective measures for the treatment of ARDS are prevention, timely detection and correct treatment of the primary disease, elevated heart function and stability of the head and chest of the child, can improve lung function and oxygenation; often change position to reduce atelectasis Children with artificial respirators should be given special monitoring; prevent cross-infection, keep the mouth clean, prevent food or drug reflux; supply nutritious and digestible food.
Complications of acute respiratory distress syndrome in children Complications, respiratory failure, sepsis, pulmonary edema, acute pulmonary edema
Breathing, circulatory failure. The disease has a rapid onset and rapid development. If it is not diagnosed early, the mortality rate is as high as 50% or more (25%-90%), and it often dies in multiple organ failure. If the sepsis caused by severe infection is not controlled, the prognosis is extremely poor. Bone marrow transplantation has an ARDS mortality rate of almost 100%. Continued pulmonary vascular resistance increases, indicating a poor prognosis. ARDS caused by fat embolization, after active treatment, mechanical ventilation treatment can achieve 90% survival. Acute pulmonary edema and ARDS caused by irritating gases can also achieve better results in time. Most patients with ARDS can be relieved quickly, and most of them can return to normal. Although survivor lung volume and lung compliance are close to normal, most ARDS patients may still have varying degrees of interstitial lung disease.
Symptoms of acute respiratory distress syndrome in children Common symptoms Lip hair, nose, fan, face, bruising, acute dyspnea, dyspnea, breath sounds, respiratory failure, central apnea
Acute onset, more common in severe trauma, shock, severe infection, sudden increase in breathing, severe respiratory distress can occur 24 to 48 hours, breathing often with nasal or sputum, obvious cyanosis and chest depression, but no cough And bloody sputum, lung signs are rare, sometimes can hear bronchial breath sounds and occasional dry and wet voices, late lungs have physical signs, such as turbidity, decreased breath sounds and obvious tubular breath sounds, typical clinical After the process can be divided into the following four periods:
1. Acute injury period: ARDS is induced by trauma, and the time of acute injury is relatively clear. If it is caused by oxygen poisoning, it is difficult to determine the time of injury. There is no characteristic sign of lung or ARDS in this period, although some children have Hyperventilation, hypocapnia and respiratory alkalosis, but arterial partial pressure of oxygen (Pa02) is still normal, chest auscultation and X-ray examination are normal, with the exception of primary injury in the lungs.
2. Incubation period: also known as surface stability period, lasting 6~48h after the last period. In this period, the heart and lung function of the child are stable, but the hyperventilation persists. The small reticular infiltration and interstitial effusion can be seen in the chest radiograph. Continuous observation showed that the children who eventually developed ARDS had significant differences in hematocrit, arterial oxygen partial pressure, pulmonary vascular resistance and pH from those who did not develop ARDS. Therefore, although the surface of the child was stable during this period, However, it is possible to develop into an ARDS and need to be vigilant.
3. Acute respiratory failure: Sudden shortness of breath, difficulty breathing, irritating cough, coughing up white foam or blood stasis, increased heart rate, fear accompanied by cyanosis, nose flapping, three concave signs, sometimes audible and roaring in the lungs After the sound, oxygen and increased ventilation, the hypoxic state did not improve.
4. Severe physical dysfunction: The transition from acute respiratory failure to the current period is not obvious. If the child has abnormal hypercapnia with ARDS, it indicates that the condition is heavier, but not irreversible. Severe lung disease of severe ARDS. The lesions need to be respiratory support for several months to disappear, but some children with hypoxemia and hypercapnia do not respond to ventilation therapy, and eventually die of refractory respiratory failure with metabolic disorders, therefore, This period is called the end period.
Examination of acute respiratory distress syndrome in children
In the early stage of blood gas analysis, progressive hypoxemia and metabolic acidosis can be seen. When the disease progresses, carbon dioxide retention can occur. The early Pa02 is less than 8.0 kPa (60 mmHg) and the arterial oxygen saturation (S02) is decreased. PaC02 is less than 4.7 kPa. 35mmHg), the late Pa02 continues to decline, PaCO2 can be higher than normal, calculate the alveolar arterial oxygen pressure difference (A-aDO2) can increase rapidly, mainly reflecting the increase of right-to-left shunt in the lung, due to obvious pulmonary edema and surfactant deficiency, The lungs became stiff, pulmonary function tests showed a decrease in lung tidal volume and a significant decrease in lung capacity. X-ray findings showed no abnormalities or mild interstitial changes in the early and middle stages, showing increased lung texture, blurred edges, and subsequent patches. In the middle and late stages, the patchy shadows increase, the ground glass is worn, or the shadows scattered in the small alveolar consolidation; the late two lungs generally increase in density, showing that the two lungs have varying degrees of fusion consolidation, The edema is aggravated, alveolar edema is also obvious, and the bronchial gas phase is obvious.
Diagnosis and diagnosis of acute respiratory distress syndrome in children
1. There are basic lesions such as severe infection or shock.
2. The above-mentioned patients suddenly developed respiratory distress during the onset of 24 to 48 hours, and progressive aggravation (adult breathing > 35 times / min, children up to 50 ~ 80 times / min).
3. Severe cyanosis and chest depression, oxygen is difficult to correct.
4. Lung signs are less, clinical symptoms, lung signs and X-ray performance are not proportional.
5. In addition to severe hypoxemia, blood gas has an increase in progressive A-aDO2. Generally, A-aDO2 > 26.6 kPa (200 mmHg) has a lung partial flow of more than 10%.
6. The lung insertion pressure is normal, indicating that the pulmonary capillary venous pressure is not high. According to the progressive hypoxemia that occurs during the rescue treatment of the primary disease, the usual oxygen therapy cannot be corrected, and the blood gas analysis and X-ray changes can make a diagnosis. .
ARDS needs to be differentiated from acute cardiogenic pulmonary edema, obstructive atelectasis, primary pulmonary infection, aspiration pneumonia and other systemic diseases caused by cyanosis and dyspnea.