The prognosis of elderly acute respiratory distress syndrome is extremely poor, with a mortality rate of up to 50% to 60%, and there is still no specific therapy. Only targeted or supportive treatment can be performed, actively treating the primary disease, improving ventilation and tissue hypoxia, preventing further lung injury and pulmonary edema, which are the main principles of treatment. Specifically, as follows:
I. Treatment of the primary disease
In the treatment of the primary disease, special attention should be paid to the control of infection, as infection is not only a common cause of ARDS but also can seriously affect the prognosis once ARDS is complicated by infection. Blood culture should be performed, and sensitive antibiotics should be selected for intravenous, adequate dosing.
II. Improve ventilation and tissue hypoxia
During ARDS, due to widespread atelectasis and pulmonary edema, lung compliance decreases, and the function of pulmonary ventilation and gas exchange is severely impaired, leading to severe tissue hypoxia, and routine oxygen inhalation cannot effectively correct it. Therefore, mechanical ventilation treatment is required. Indications for mechanical ventilation: if the inhaled oxygen concentration is greater than 50%, the arterial blood oxygen saturation (SaO2)
1. High-frequency ventilation (HFV) and high-frequency jet ventilation (HFJV): HFV can reduce peak airway pressure and minimize the lung injury and barotrauma caused by it. However, oxygenation decreases with the decrease in mean airway pressure, which is particularly true for ARDS patients. HFJV can significantly increase oxygenation but also increase mean airway pressure, reduce venous return and cardiac output. Therefore, HFV and HFJV are no longer used for the treatment of ARDS.
2. PEEP: It can expand collapsed alveoli and reinflate atelectatic alveoli, thus correcting the ventilation/perfusion (V/Q) ratio disorder, increasing functional residual capacity and lung compliance. It is conducive to the diffusion of oxygen through the alveolar membrane. Therefore, PEEP can effectively increase PaO2. However, experiments show that PEEP cannot prevent lung injury. In summary, PEEP itself cannot prevent or cure ARDS, but it can accelerate the repair process by improving oxygenation, avoid further lung tissue damage from high FiO2, and provide an opportunity for comprehensive treatment as a supportive therapy.
3. New mechanical ventilation methods:
① Assistive controlled ventilation or intermittent mandatory ventilation is currently recommended, where patients rely on spontaneous breathing while occasionally receiving positive pressure breathing from the ventilator. However, it is not suitable for patients with extremely fatigued respiratory muscles.
② Other types of mechanical ventilation, including volume-controlled inverse ventilation; low tidal volume ventilation with appropriate PEEP; extracorporeal membrane oxygenation therapy, etc., have different efficacy, with their own advantages and disadvantages.
Third, multi-link reduction of lung and systemic injury
1. Glucocorticoids: Adrenal cortical hormones can alleviate allergic, inflammatory, and toxic reactions; relieve bronchospasm; inhibit PMN and platelet aggregation, prevent microthrombosis, and stabilize lysosomal membranes. Reduce the release of lysosomal enzymes and related mediators; increase the synthesis of pulmonary surfactant substances, and alleviate microatelectasis, etc., which are used in the early stage of ARDS, but there is much controversy, mainly about the dose and timing of medication. Delaying medication for too long is not appropriate, and there are also reports that the mortality rate of high-dose methylprednisolone is still higher than that of the control group.
2. Vasodilators: Including atropine and PGE1 have a relieving effect on ARDS and experimental RDS, but there is no evidence at present.
3. Other: Such as methylxanthines, pentoxifylline can affect intercellular signal transduction, reduce PMN and AM activation, and antagonize TNF, inhibit the production of PIA2 enzyme and IL-1 and their cytokine responses, inhibit OR release, and alleviate lung injury. In addition, there are drugs like Pulmadine, which are currently in the experimental stage.