Adult Respiratory Distress Syndrome

Adult Respiratory Distress Syndrome

Adult respiratory distress syndrome (adult respiratory distress syndrome, ARDS) in patients with the heart and lung function is normal, because of the lung or pulmonary diseases in the course of the permeability of secondary acute pulmonary edema and hypoxia of respiratory failure. Although its causes vary, but the lung tissue injury in pathology and function more or less the same, are clinical manifestations of acute respiratory distress, refractory hypoxemia because of a similar levy infant respiratory distress, and their etiology and pathogenesis Different, it then called "adult" to show differences.

As the severe trauma, shock, infection and other diseases rescue raising the level of technology, many patients do not die of disease directly, thereby increasing the incidence of ARDS, ARDS onset Jizhou, rapid development, if not early diagnosis and treatment, died Rate of more than 50 percent (25% -90%), and often died of multiple organ failure.

[Etiology and pathogenesis]

ARDS the cause of many, such as severe shock, severe trauma, fractures, fat embolism, severe infection (particularly gram-negative bacillus sepsis were caused by septic shock), inhalation of irritating gases and stomach contents, oxygen poisoning, drowning, Massive blood transfusion, acute pancreatitis, drugs or narcotics, such as poisoning, which can cause pulmonary - capillary acute injury, however this injury mechanism has not yet been fully clarified, and a variety of factors, and the intricate existence and mutually affected.

At present the majority of scholars believe that many neurotransmitters involved in alveolar - vascular endothelial injury, with neutrophil (PMN) is the activation of endothelial cells capillary permeability increase was mainly due. Interstitial lung health of people, only a small number of PMN, in trauma, acute pancreatitis, physical and chemical stimulation or pump circumstances, as in a variety of chemotactic factor PMN role, to PMN in the pulmonary capillary gathered in a large number, and through the Adhesion of factors, such as the complement system activated the C5a, lipopolysaccharide (LPS), will be PMN adhesion to endothelial cells, PMN activation of endothelial cells to release a series of damaging lung tissue and harmful substances, mainly oxygen free Based, multi-and arachidonic acid metabolite.

If all kinds of protein-dissolving enzyme, elastase, serine protease, collagenase, cathepsin, elastase and collagenase can digest the basement membrane, and pulmonary artery walls elastic organizational structure.

Arachidonic acid metabolite by PMN, macrophages complement activation of phospholipase, from the plasma membrane phospholipids in the release of arachidonic acid, through its lipoxygenase and cyclooxygenase grass two metabolic process, the formation of A series of high-activity products (medium). The blood vessels and bronchial contraction caused pulmonary hypertension and airway resistance increased, to unite platelets, blood clots, and the release of fibrin degradation products, proteolytic enzymes, increased capillary Tong Xing. Because pulmonary capillary membrane damage, permeability increase in permeability of pulmonary edema.

[Pathology]

ARDS was Anhong of the lung or liver-Anzi red changed, visible swelling, bleeding, weight increased significantly. 24h microscopy see in the pulmonary microvascular congestion, hemorrhage, micro-thrombosis, pulmonary alveolar and quality of water within a protein glue and infiltration of inflammatory cells. Nearly 72 h, from plasma protein coagulation, cell Cui films, fibers and residue of the Surfactant a transparent membrane, or large focal alveolar wilt depression. At exudative acute lung cells damaged Ⅰ necrosis, the restoration of lung epithelial cell type Ⅱ. Early fibroblast proliferation and collagen deposition, a week after the alveolar separated, transparent film can be fibrosis, with pulmonary secondary infection.

[Pathophysiology]

Because pulmonary vascular endothelial cells and alveolar type Ⅱ cell damage caused interstitial lung and pulmonary edema, congestion, pulmonary surfactant reduced, leading to closure of small airway depression, depression not alveolar Zhang Wei, lung compliance decreased functional residual Gas reduction. So that ventilation / flow ratio imbalance, pulmonary arteriovenous shunt-like increase and diffusion barriers, causing serious damage to the ventilation function hypoxemia and stimulate the carotid sinus aorta of chemical receptors can stimulate the respiratory center reflection cause excessive ventilation, there Respiratory alkalosis. Late in ARDS, as in critical condition, respiratory muscle fatigue failure, a lack of ventilation, lack O2 more severe, with CO2 retention, a mixed acid poisoning.

In addition to the disease such as trauma, infection, poisoning, and other relevant signs and symptoms, mainly for emergencies, respiratory distress, shortness of breath, cyanosis, often accompanied with irritability, anxiety expressions, sweating, and so on. The characteristics of their respiratory distress usually can not be used so as to improve the therapy, or use other primary cardiovascular diseases (such as pneumothorax, pulmonary emphysema, atelectasis, pneumonia, heart failure) explained. Early signs may be no abnormalities, or only heard Shuangfei stem-La, Asthma Ming Yin, the late and blisters can hear the sound, or breathing tube sound. Early X-ray can be no anomaly, or a slight change in the quality of performance for the fuzzy edge of the Fei Wenli increased, followed by a spot Flake, as well as integration of National Cheng Kung University Flake infiltration shadow visible in the large shadow of bronchial inflatable levy .

[Diagnosis]

The main cause RADS basis for the original cause of morbidity and, in the past without Feibujihuan and exclude left heart failure; sudden sexual respiratory distress, more than 35 per minute, breathing, oxygen commonly used method can not be improved; X - Ray to see first interstitial, after the invasion to diffuse the shadow of the alveolar; blood gas analysis revealed that PaO2 <8 kPa (60mmHg), early PaCO2 <4.6kPa (35mmHg), alveolar gas and blood oxygen difference (PA-aDO2) and the lung-flow (QS / QT) increased oxygenation index (PaO2/FIO2) <300 (PaO2 units mmHg).

[Diagnosis]

With cardiogenic pulmonary edema of identification, cardiogenic pulmonary edema, difficulty breathing and posture-related, bubble-like cough Xue Tan, the strong heart, diuretics, such as better treatment, pulmonary edema and more in the La-lung at the bottom, Pulmonary capillary wedge pressure> 1.58kPa (16cmH2O). ARDS respiratory distress little to do with posture, non-bubble-like Xue Tan Xue Shui-thin, oxygen inhalation conventional circumstances, PaO2 still a decrease, La-wide, often high-pitch "-burst", reduced pulmonary capillary wedge pressure Or normal. ARDS sometimes have to identify with and bronchial pneumonia.

ARDS treatment, including oxygen therapy to improve ventilation function and to correct the lack of oxygen, and causes must be promptly removed so that the primary disease under control, ARDS to heal.

First, adrenal glucocorticoid Application

Glucocorticoid vascular endothelial cells to protect against WBC, platelet aggregation and adhesion wall, a micro-thrombosis; lysosomal membrane stability, reduce complement activity and inhibit cell membrane phospholipid metabolism, reduce the synthesis of arachidonic acid to prevent Prostaglandin and thromboxane A2 production, protection of Ⅱ-cell lung surfactant; with anti-inflammatory and the promotion of interstitial lung fluid absorption; easing bronchial spasms; inhibit the latter part of pulmonary fibrosis. According to the irritation that the current gas inhalation, fractures caused by trauma, such as non-fat embolism caused by infection of ARDS, the use of glucocorticoid sooner the better, the incidence four days after use, less effective. The use of the principle as soon as possible, large and short-range treatment. Such as dexamethasone 20-30 mg, on the 1st, 2-3, the linked two days, if effective, continue to use the few days that is parked. But ARDS with a serious infection or sepsis glucocorticoid should Jiyong or anti.

Second, oxygen therapy

O2 is imperative to correct missing the important measures, such as missing O2 are not corrected, will cause irreversible damage to important organs. General must be a high concentration of oxygen absorption (> 50%), but as far as possible inhalation of low oxygen concentration, as long as the SaO2> 90% to prevent oxygen poisoning occurred.

Third, PEEP ventilation (PEEP)

Breathing machine for a certain volume or delivery of gas flow into the lungs, respiratory and pulmonary inspiratory phase in a positive pressure in the breath of breath until the end of the airway open, mouth, airway and alveolar pressure higher than atmospheric pressure of the type of mechanical ventilation . ARDS PEEP can improve the ventilation function, its principles are as follows: to wilt subsidence of the small airway, alveolar expansion of interstitial lung and pulmonary edema dissipated and improve lung compliance, more functional residual capacity, reduce the physical void cavity, increased alveolar Ventilation, improve the ventilation / flow ratio imbalance, reduced pulmonary arteriovenous shunt-like, lower power and breathe oxygen consumption, thereby enhancing PaO2. The use of PEEP circulating blood volume should be effective enough, PEEP to the pressure from low-level 0.29-0.49 kPa (3-5cmH2O), gradually increasing to 0.98 kPa (10cmH2O), the general should not be超过0.98 kPa, will be affected because of blood from top to bottom cavity The flow of blood back. PEEP pressure> 2.5 kPa, spontaneous pneumothorax rate as high as 14 percent, with mediastinal emphysema. When a stable condition, gradually reduce the value of PEEP, but to maintain SaO2> 90% can be.

4, liquid reasonable input

To ensure adequate blood volume, blood pressure and stability, under the premise of access requirements of a mildly negative balance (-500 ml - 1000ml). For the promotion of tissue fluid dissipated, for furosemide 40-60 mg / d. Damage to the endothelial cells in the vascular permeability increases, colloidal liquid can be infiltrated into mesenchymal, increase pulmonary edema, it should not be completed in early ARDS colloid. Apart from excessive bleeding due to trauma, to blood transfusion, Yi Yi and micro-filter with the new blood transfusion, blood inventory to avoid micro-particles with micro-thrombosis caused pulmonary capillary endothelial cells.

5, nutrition supplies and the incidence of treatment

Patients with ARDS often a lack of nutrition, should be given high nasal feeding and intravenous nutrition, in order to maintain sufficient energy supply, to avoid metabolic functions and dielectric disorder.