Pediatric Acute Respiratory Distress Syndrome

　　1. Etiology

　　The primary diseases or underlying diseases that cause ARDS are many, and their occurrence is often related to one or more increased risk factors. Such as infectious or hemorrhagic shock, head trauma, and other neurological pulmonary edema, burns, drug poisoning, pancreatitis, and massive blood transfusion, and other indirect causes; it can also be caused by direct causes such as smoking or inhalation of chemical substances, aspiration pneumonia, pulmonary infection, pulmonary embolism, pulmonary contusion, and radiation pneumonia.

　　2. Pathogenesis

　　The ultimate result of the above reasons is the diffuse increase in permeability of the pulmonary capillary epithelium, which ultimately leads to pulmonary edema; the alveoli and small airways are filled with edema fluid, mucus, blood, and other exudates, resulting in the formation of hyaline membrane, causing significant right-to-left pulmonary shunting, making the lungs rigid; at the same time, due to the large consumption and destruction of pulmonary surfactant substances, the proliferation of type II alveolar epithelial cells, and finally the thickening of alveolar septa accompanied by inflammation and fibrous hyperplasia.

　　Respiratory and circulatory failure. Circulatory failure, the patient initially experiences palpitations, sweating, pale complexion, rapid and weak pulse; then it develops into cold limbs, cyanosis, and a rapid drop in blood pressure, disappearance of pulse, and even inability to measure blood pressure, ultimately leading to cardiac arrest. A few patients with pre-existing coronary atherosclerosis may develop myocardial infarction. Lactate dehydrogenase (LDH, LD) is a glycolytic enzyme. Lactate dehydrogenase exists in the cytoplasm of all tissue cells in the body, with a higher content in the kidneys. Dynamic electrocardiogram (Holter monitoring): It is a method that can continuously record and analyze the changes of the electrocardiogram of the heart under activity and rest for a long time. Also known as Holter monitoring. The electrocardiogram is the objective indicator of the occurrence, conduction, and recovery process of cardiac excitation. The electrocardiogram is the earliest, most commonly used, and most basic diagnostic method in the diagnosis of coronary heart disease.

　　1. Acute injury period

　　If ARDS is induced by trauma, the time of the acute injury period is relatively clear. If it is caused by oxygen toxicity, it is difficult to determine the time of injury. During this period, there are no characteristic signs of lung or ARDS, although some children may have hyperventilation, hypocapnia, and respiratory alkalosis. However, the arterial oxygen partial pressure (PaO2) is still normal, and chest auscultation and X-ray examination are normal, except for primary injury in the lungs.

　　2. Latent period

　　Also known as the surface stability period, lasting from 6 to 48 hours after the previous stage. During this period, the child's heart and lung functions are stable, but hyperventilation continues to exist. Chest X-rays show fine reticular infiltrates and interstitial lung edema. Continuous observation has found that children who eventually develop ARDS in this stage have significantly different hemoglobin concentration, arterial oxygen partial pressure, pulmonary vascular resistance, and pH from those who do not develop ARDS. Therefore, although the children appear stable on the surface during this period, they may still develop ARDS and should be vigilant.

　　3. Acute respiratory failure stage

　　Sudden shortness of breath, difficulty breathing, irritating cough, coughing up white frothy sputum or blood-stained sputum, increased heart rate, a sense of fear accompanied by cyanosis, flaring of the nostrils, three凹陷 signs, the lungs may sometimes be heard to wheeze, and the condition of hypoxia does not improve after oxygen inhalation and increased ventilation.

　　4. Severe physiological disorder stage

　　The boundary between the acute respiratory failure stage and this stage is not clear. If the child develops a rare hypercapnia with ARDS, it indicates a worsening condition, but it is not necessarily irreversible. Chronic pulmonary lesions in severe ARDS may require months of respiratory support to disappear. However, some children with hypoxemia and hypercapnia may have no response to ventilation treatment and eventually die from refractory respiratory failure and metabolic disorders, so this period is also known as the terminal stage.

　　How should children be prevented from developing acute respiratory distress syndrome?

　　Early blood gas analysis may show progressive hypoxemia and metabolic acidosis. As the condition gradually progresses, carbon dioxide retention may occur. Early PaO2 may be less than 8.0kPa (60mmHg) and arterial oxygen saturation (SaO2) may decrease. PaCO2 may be less than 4.7kPa (35mmHg). In the late stage, PaO2 continues to decrease, and PaCO2 may be higher than normal. The alveolar-arterial oxygen pressure difference (A-aDO2) can increase abruptly, mainly reflecting an increase in right-to-left shunting in the lungs. Due to significant pulmonary edema and a lack of surfactant, the lungs become rigid. Pulmonary function tests show a decrease in tidal volume and a significant decrease in vital capacity. X-ray findings may be normal or show mild interstitial changes in the early and middle stages, manifesting as increased pulmonary markings, blurred edges, and subsequently appearing patchy shadows; in the middle and late stages, patchy shadows increase, appear glassy, or scattered small patchy alveolar consolidation shadows; in the late stage, both lungs show generalized increased density, and there are widespread fusions of consolidation to varying degrees, exacerbation of interstitial edema, and more significant alveolar edema than before, with a marked bronchial gas phase.

　　Children with acute respiratory distress syndrome need to be treated in a timely manner, and after treatment, it is necessary to provide the child with enhanced nutrition, a diet high in protein and vitamins. Fast food and other unhealthy diets should be avoided..

　　1. Treatment

　　The treatment principle is to actively treat the primary disease, effectively correct hypoxemia, and as soon as possible eliminate interstitial and alveolar edema.

　　1. Oxygen therapy

　　Oxygen can be administered through a nasopharyngeal tube when PaO2 is between 9.33-10.66kPa (70-80mmHg). However, as the condition progresses, the common oxygenation method cannot correct hypoxemia, and positive pressure ventilation is required. Generally, when PaO2 is below 7.99kPa (60mmHg), and nasal cannula oxygen therapy is ineffective, and respiratory distress is evident, it is necessary to promptly adopt positive pressure ventilation, commonly using Continuous Positive Airway Pressure (CPAP) and Positive End-Expiratory Pressure (PEEP). When treating ARDS, the application of ventilators should pay attention to the following points:

　　(1) It is advisable to use a volume-controlled ventilator to maintain a relatively constant tidal volume. The compliance of the ventilator should be small [for treating small infants with ARDS, it should be less than 0.098kPa/m2 (1cmH2O/m2)].

　　(2) Choose a slightly faster frequency and extend the inspiratory time appropriately to ensure uniform distribution of gas in the alveoli, with a respiratory ratio of 1:(1-1.25).

　　(3) It is advisable to use sedatives or muscle relaxants as early as possible to reduce the incidence of pulmonary pressure injuries.

　　2. Control fluid intake

　　It is very important to strictly control fluid volume. Due to increased pulmonary capillary permeability during ARDS and the need for fluid expansion during shock treatment, there is a large amount of fluid in the body, so it is necessary to strictly control fluid intake, generally 1000-1200ml/m2 per day, and pay attention to administering a certain proportion of colloid solution to increase colloid osmotic pressure, such as plasma, human serum albumin, and fresh blood. It is best to avoid using stored blood as much as possible.

　　3. Improve microcirculation and cardiovascular function

　　Anticholinergic drugs and α-adrenergic receptor blockers, such as atropine, anisodamine, phentolamine, and others, can be used when there is vasoconstriction and poor blood perfusion; heparin and low molecular weight dextran, certain Chinese herbs for promoting blood circulation and removing blood stasis are beneficial to improving microcirculation and preventing thrombosis; diuretics have a significant effect on eliminating pulmonary edema; if the child has heart failure, rapid acting digitalis preparations can be used to improve heart function.

　　4. Adrenal Cortex Hormones

　　The role of hormones in this disease is still controversial, but hormones can improve capillary permeability, reduce pulmonary edema, eliminate inflammatory reactions, and promote the formation of surfactant. Generally, hydrocortisone is used at a dose of 10-30mg/(kg·d), once every 6 hours, the principle is high dose, short duration, generally not exceeding 48 hours, and sometimes good therapeutic effects can be achieved.

　　5. Other treatments

　　Including active treatment of the underlying disease and control of infection, careful nursing, strengthening respiratory management, maintaining nutrition, and closely monitoring complications of mechanical ventilation. In recent years, therapies successfully applied in the rescue of ARDS include:

　　(1) High-frequency ventilation (HFV) and high-frequency/low-frequency mixed ventilation (C-HFV).

　　(2) Extracorporeal Membrane Oxygenation (ECMO).

　　(3) Application of exogenous surfactant, there are successful reports of using bovine or porcine lung surfactant to rescue ARDS and neonatal RDS in Beijing and Shanghai.

　　(4) Hemofiltration, used to remove vasoactive substances and free radicals in the blood.

　　II. Prognosis

　　Due to rapid progression of the disease and poor prognosis, the mortality rate can reach up to 50%; mastering intubation and mechanical ventilation techniques, strengthening respiratory management, and actively treating complications can improve the cure rate. Although the lung volume and lung compliance of survivors can approach normal, most ARDS patients may still have varying degrees of interstitial lung lesions.