Adult respiratory distress syndrome . Respiratory failure caused by various acute lung injuries, characterized by non-cardiogenic pulmonary edema, respiratory distress (distress), and hypoxemia.
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- 1 Etiology
- 2 Pathophysiology
- 3 Signs, symptoms and diagnosis
- 4 Complications and prognosis
- 5 Treatment
- 1 Mechanical ventilation
- 6 Sources
Adult respiratory distress syndrome (ARDS), a frequent medical emergency, is precipitated by various acute processes that directly or indirectly injure the lung, such as sepsis, primary viral or bacterial pneumonia, aspiration of gastric contents, direct chest trauma, prolonged or deep shock, burns, fat embolism, drowning by immersion, massive blood transfusion, cardiopulmonary bypass, O2 toxicity, acute hemorrhagic pancreatitis, inhalation of smoke or other toxic gases and the intake of certain drugs. The incidence of ARDS is estimated to be> 30% in sepsis. Although called “adult”, this syndrome can also affect children.
Initial lung injury is poorly understood. Animal studies suggest that activated platelets and leukocytes accumulate in the capillaries, interstitium, and airspace, which can release prostaglandins, toxic O2 radicals, proteolytic enzymes, and other mediators (such as tumor necrosis factor and interleukins), They damage cells, facilitate inflammation and fibrosis, and modify broncomotor tone and vascular reactivity.
When the pulmonary capillaries and alveolar epithelia are injured, blood and plasma leak out into the interstitial and intraalveolar spaces, with consequent alveolar fluid occupation and atelectasis, the latter partly due to lower surfactant activity. The lesion is not homogeneous and predominantly affects the declining areas of the lung. In 2 or 3 days, interstitial and bronchoalveolar inflammation occurs with proliferation of epithelial and interstitial cells. Collagen accumulates rapidly, producing severe interstitial fibrosis within 2 to 3 weeks. These pathological changes cause a reduction in lung compliance, with less functional residual capacity, alterations in the ventilation / perfusion ratio, an increase in physiological dead space, severe hypoxemia and pulmonary hypertension .
Signs, symptoms and diagnosis
ARDS usually develops within 24 to 48 hours after the initial injury or illness. Dyspnea first occurs, often accompanied by rapid, shallow breathing. Intercostal and suprasternal retraction can be observed with inspiration. The skin may appear cyanotic or mottled and does not improve when O2 is administered. Auscultation can detect snoring, wheezing, or rales, but is sometimes normal.
Early diagnosis requires a high index of suspicion in the presence of dyspnea in situations that predispose to ARDS. The presumptive diagnosis can be made with arterial blood gas and chest radiography. This analysis initially demonstrates acute respiratory alkalosis: very low PaO2, with normal or low PaCO2 and high pH. Chest radiography usually shows bilateral diffuse alveolar infiltrates similar to acute pulmonary edema of cardiac origin, but the cardiac silhouette is usually normal. However, radiological abnormalities typically show several hours of lag compared to functional abnormalities, so hypoxemia may appear disproportionately severe compared to radiological edema.
Following immediate treatment for hypoxemia, several diagnostic steps are indicated. When there is doubt that the patient is in heart failure, a Swan-Ganz catheter may be helpful. Pulmonary arterial interlocking pressure is typically low (<18 mm Hg) in ARDS and high (> 20 mm Hg) in heart failure. If pulmonary embolism, which may resemble ARDS, is considered possible, appropriate diagnostic procedures (such as pulmonary angiography) should be performed after stabilizing the patient. the pneumoniaPneumocystis carinii and sometimes other primary lung infections may resemble ARDS and should be considered in immunosuppressed patients; In these cases, a lung biopsy or bronchosalveolar guided bronchoscopy can be useful.
The American-European Consensus Conference defines ARDS as PaO2 / FiO2 <200 (regardless of positive end-expiratory pressure), bilateral infiltration on frontal chest radiography, and PAWP £ 18 mm Hg when measured or not present. evidence of left atrial hypertension.
Complications and prognosis
Secondary bacterial superinfection of the lungs, especially by gram-negative aerobic bacteria (such as Klebsiella, Pseudomonas and Proteus spp.) And by gram-positive Staphylococcus aureus, especially the methicillin-resistant strains; Multiple organ failure, especially kidney failure, and complications due to life support techniques, which are associated with high mortality and morbidity, can occur. Tension pneumothorax may occur suddenly associated with central venous catheter placement or with positive pressure ventilation (PPV) and positive pressure at the end of expiration (PEEP), whose early recognition and treatment are essential to avoid death. Pneumothorax should be suspected in a tachycardia, hypotension and a sudden increase in the peak inspiratory pressure required for mechanical ventilation. Pneumothorax that appears in late stages of ARDS is considered an ominous sign because it is usually associated with severe lung injury and the need for high ventilatory pressures. If adequate intravascular volume replacement is not performed, PPV and PEEP can reduce venous return, decreasing cardiac output and overall O2 transport to tissues, contributing to secondary multiorgan failure.
The survival rate of patients with severe ARDS who receive correct treatment is 60%; If severe ARDS hypoxemia is not recognized and treated, cardiopulmonary arrest occurs in 90% of patients. Those who respond rapidly to treatment often develop minimal or no residual lung dysfunction. Patients who require prolonged ventilatory support with FiO2> 50% may more often develop pulmonary fibrosis. In the majority of patients who survive acute disease, pulmonary fibrosis usually resolves within months, although the mechanisms are unknown.
The principles of treatment are similar whatever the cause. Oxygenation should be maintained and the cause of the underlying acute lung injury should be corrected. Meticulous attention is required to avoid nutritional depletion, O2 toxicity, superinfection, barotrauma, and renal failure, which may be exacerbated by intravascular volume depletion. While the diagnosis is ruled out, life- threatening hypoxemia should be treated with elevated FiO2 and controlled with serial blood gases or noninvasive oximetries. Endotracheal intubation with mechanical ventilation and PEEP may be necessary to deliver O2, since hypoxemia is usually refractory to inhalation of O2 in a face mask.
Intravascular volume is usually depleted when ARDS begins, because sepsis is one of the associated causes, because treatment with diuretics was administered before this diagnosis was suspected or because the initiation of PPV reduces venous return. Despite the existence of alveolar edema, IV fluids should be administered if necessary to recover peripheral perfusion, urine excretion, and BP. Controlling vascular volume is essential because both hypovolemia and overhydration are dangerous. Physical findings and central venous pressure values can be confusing in critically ill patients undergoing mechanical ventilation, and if severe hypoxemia persists, poor skin perfusion, altered mental status, or reduced excretion. urine (<0.5 ml / kg / h), a reliable index of intravascular volume is immediately required. A Swan-Ganz catheter is often used to determine volume infusion, especially if PEEP is required. However, these catheters carry risks. To make the contribution of liquids it is essential to closely monitor their intake and excretion. In general, patients with ARDS respond better when a “dry” treatment is chosen, that is, fluid restriction with judicious use of diuretics, as long as cardiac output and tissue perfusion are not altered. To make the contribution of liquids it is essential to closely monitor their intake and excretion. In general, patients with ARDS respond better when a “dry” treatment is chosen, that is, fluid restriction with judicious use of diuretics, as long as cardiac output and tissue perfusion are not altered. To make the contribution of liquids it is essential to closely monitor their intake and excretion. In general, patients with ARDS respond better when a “dry” treatment is chosen, that is, fluid restriction with judicious use of diuretics, as long as cardiac output and tissue perfusion are not altered.
If sepsis is or may be the cause of ARDS, empirical antibiotic therapy should be started until the culture results arrive. Cultures and Gram staining of sputum or tracheal aspirates can help detect lung superinfection early and determine antibiotic therapy. Infections should be drained indoors. Feeding begins at 48 to 72 h, the enteral route being preferable because it protects the intestinal mucous lining.
Steroids do not produce any demonstrated beneficial effect in acute ARDS, although isolated reports suggest some benefit in patients with ARDS in the late fibroproliferative phase, which develops 7 to 10 days after mechanical ventilation. The coexistence of pulmonary infections should be excluded in these patients, since they are usually feverish and have leukocytosis with or without infection.
Many therapeutic and prophylactic approaches to ARDS have been unsuccessful or of little use. Treatments that have not improved or prevented ARDS include monoclonal antibodies against endotoxin, monoclonal antibodies against tumor necrosis factor, interleukin 1 receptor antagonist, prophylactic (early) PEEP, membrane oxygenation extracorporeal and extracorporeal CO2 extraction, albumin iv, volume expansion, and cardiotonic drugs to increase systemic O2 distribution, steroids in the early stages of ARDS, parenteral ibuprofen to inhibit cyclooxygenase, prostaglandin E1, and pentoxifylline. Some approaches look promising, but need more study.
The prone posture can significantly improve oxygenation in some patients, possibly because this posture diverts perfusion and gas exchange to more normal areas, which were previously not in decline. However, it is unclear if this posture improves gas exchange in severe ARDS and if it can reduce the duration of mechanical ventilation and improve overall survival. It is difficult to position the patient.
Inhalation of nitric oxide significantly improves pulmonary hypertension and arterial oxygenation in patients with severe ARDS without producing systemic hypotension. It remains to be seen whether nitric oxide improves survival and whether its prolonged use determines further lung damage by degradation products derived from it, such as peroxynitrite anion.
Ketoconazole can prevent ARDS by suppressing the formation and release of tumor necrosis factor in macrophages. Its beneficial effect in small preliminary studies has to be confirmed in larger well controlled studies. Initial studies with synthetic aerosol surfactant in adult patients with ARDS have been disappointing. The development of better quality aerosol delivery devices and mammalian natural surfactant preparations can improve alveolar stability, reduce atelectasis and intrapulmonary blood shunt, and increase the antibacterial and anti-inflammatory properties of the fluid that lines the alveoli; Currently, studies are underway on these treatments.
Most patients require endotracheal intubation and assisted ventilation with a volume-limited mechanical ventilator. Endotracheal intubation and PPV should be considered when the respiratory rate is> 30 breaths / min or if a FiO2 with a face mask> 60% is required to maintain Po2 at about 70 mm Hg for several hours. As an alternative to intubation, a positive pressure airway mask can effectively deliver PEEP to patients with moderate or mild ARDS. These masks are not recommended for patients with low levels of consciousness, given the risk of aspiration, and should be replaced by a ventilator if the patient progresses to severe ARDS or shows signs of respiratory muscle fatigue with increased respiratory rate. and arterial Pco2.
Conventional values for a volume-limited ventilator in ARDS are a tidal volume of 10 to 15 ml / kg, a PEEP of 5 to 10 cm H2O, a FiO2 of £ 60%, and mixed frequency assisted / controlled control-activated mode. the patient. This technique can be replaced by intermittent mandatory ventilation with an initial respiratory rate of 10 to 12 breaths / min with PEEP.
There is concern about whether high volumes and ventilator pressures may aggravate lung lesions in ARDS, although this effect has not been demonstrated. Too low a PEEP can also injure the lung, as it allows unstable terminal lung units to open and close repeatedly. This problem can be avoided with small tidal volumes (6 to 8 ml / kg) and higher PEEP (between 10 and 18 cm H2O).
The goal of low tidal volumes is to prevent ventilator-generated breaths from exceeding the upper inflection point (deflection) of the patient’s pressure-volume curve and causing pulmonary overdistension (see Fig. 67-1). After this point, the lung becomes quite stiff, and small increases in tidal volume determine large increases in the plateau pressure of the ventilator (the pressure required to maintain insufflation of the lung and chest wall when the inspiratory flow has ended). For technical reasons, the upper inflection point is not usually measured directly, but rather the plateau pressure of the ventilator is determined, which in most patients should not exceed 25 to 30 cm H2O (or 20 to 25 cm H2O according to some researchers). At low tidal volume, the ventilator’s respiratory rate can be increased to maintain adequate arterial pH and PCO2. Despite this, some patients develop hypercapnia and respiratory acidosis, which they usually tolerate well. If the arterial pH falls below 7.2, the slow bicarbonate infusion can be started.
Theoretically, the PEEP selected should be several centimeters of water higher than the lower inflection point of the pressure-volume curve of the patient to facilitate the incorporation and insufflation of many alveoli. If this lower inflection point is not determined directly, a PEEP of 10 to 15 cm H2O is usually sufficient. With satisfactory PEEP, the FiO2 of the ventilator can be safely reduced to <50 to 60%, such that the patient has a PaO2 of 60 mm Hg or an arterial saturation of O2 (SaO2) of 90%. For the transport of O2 to the tissues to be adequate, the cardiac index must be 3 l / min / m2; volume replacement or administration of parenteral cardiotonic drugs is sometimes necessary.
As an alternative, pressure-controlled mechanical ventilation can be used, especially in patients with severe ARDS. Inspiration pressure and duration are selected and the tidal volume is modified with the inspiratory impedance; High inspiratory pressures in the ventilator are thus avoided, but hypercapnia usually occurs. This approach is usually combined with an inverse quotient ventilation, in which the duration of inspiration is selected to be equal to or greater than that of expiration. This technique operates and re-expands more lung units than PEEP alone (in part because it produces an intrinsic PEEP or auto-PEEP), so that a potentially damaging FiO2 value can be further reduced.
Ease of ventilation removal is based on continued evidence of improved lung function (reduced need for O2 and PEEP), radiological improvement, and resolution of tachypnea. Patients can be removed from the ventilator without prior lung disease with ease, and difficulties in doing so indicate recent or untreated infection, excessive hydration, bronchospasm, anemia, electrolyte disturbances, cardiac dysfunction, or poor nutritional status resulting in respiratory muscle weakness. If these diseases are treated, the ventilator can be removed using intermittent mandatory ventilation to reduce mechanical frequency, often with some degree of pressure support ventilation or by attempts to spontaneously breathe for longer and longer periods through a T-piece connected to the endotracheal tube. A low PEEP (5 cm H2O) is usually maintained throughout the fan removal process.