Adult Respiratory Distress Syndrome

Transcription

1 Critical Care Medicine Adult Respiratory Distress Syndrome Leonard J. Sonne, MD, FACP, FCCP* *Chief, Division of Pulmonary Physiology and Medicine, Department of Medicine, King Faisal Specialist Hospital and Research Centre LJ Sonne, Adult Respiratory Distress Syndrome. 1983; 3(3): KEYWORDS: Respiratory distress syndrome, adult Introduction The adult respiratory distress syndrome (ARDS), a common cause of acute respiratory failure, is characterized by a protein- and cell-rich pulmonary edema resulting from increased permeability of the pulmonary vasculature. The diffuse capillary injury usually occurs in the setting of systemic infection, endotoxemia, shock, aspiration, trauma, pancreatitis, cardiopulmonary bypass, overdose, or pulmonary infection. Following a latent period of up to 48 hours, the patient presents with tachypnea, dyspnea, cyanosis, stiff lungs, severe hypoxemia (PO 2 <55) refractory to high concentrations of inspired O 2 (FIO 2 >0.6), and diffuse alveolar infiltrates on chest x-ray (Figure 1). The mortality is approximately 50 percent. Pathogenesis The prevailing theory of the pathogenesis of ARDS is summarized in Figure 2. 1 ARDS occurs in the setting of massive complement activation such as pancreatitis, endotoxemia, or shock, liberating C5a. 2 In turn, C5a, via the leukotriene pathway (nonprostaglandin lipo-oxygenase products of unsaturated fatty acids) induces intravascular leukocyte agglutination with microembolization or microvascular occlusion in situ. 3 Consistent with this mechanism is the observation that circulating C5a and leukocyte aggregates characterize the early phases of ARDS. Pulmonary microvasculature is then injured by superoxide radicals and proteases released from the activated leukocytes. The leukocyte aggregates may form locally in the pulmonary vasculature or embolize from a systemic source. Injury to endothelial and Type I alveolar (gas exchanging) cells allows the leakage of a cell- and protein-rich fluid into the alveoli and results in the formation of hyaline membranes. Surfactant activity is also reduced. 4 The superoxide radicals inactivate pulmonary antiproteases and are important in the pathogenesis of pulmonary fibrosis. Bronchoalveolar lavage fluid from patients with ARDS has large numbers of neutrophils, proteolytic activity derived from them, and decreased antiproteolytic activity. 5,6 The inflammation is further amplified by reaction with fibrinogen and platelets. Thrombocytopenia, disseminated intravascular coagulation and vascular thrombosis are found in a high percentage of patients with ARDS. 7-9 The Type I alveolar cells are replaced by the cuboidal, surfactant-secreting Type II cells. This represents a general reaction to lung injury. Recovery occurs if Type II cells differentiate into Type I cells; otherwise, fibrosis and obliteration of the capillary bed result.

2 Figure 1. X-ray picture in ARDS.

3 Figure 2. Mechanisms of pathogenesis and points of therapeutic intervention in ARDS. Circles indicate ameliorating or therapeutic steps. indicates inhibitory influence on pathophysiologic mechanism. Pulmonary hypertension is a poor prognostic sign. Superinfection with bacteria or fungi is common. It is difficult to ascertain whether factors such as protease release and reduced surfactant activity are important in the pathogenesis of ARDS or are merely markers of injury. Little is known about the key events of intercellular organization which lead to fibrosis. The diagnosis is made in patients with predisposing conditions with previously normal lungs who develop progressive dyspnea, tachypnea and typical progressive pulmonary infiltrates (Figure 1). Arterial hypoxemia results that is refractory to high concentrations of inspired oxygen.

4 Pathophysiology and Management The exudation of fluid into the alveoli leads to marked hypoxemia. Patients present with an arterial PO 2 <55 while breathing an inspired O 2 concentration of >50 percent. There is loss of surfactant activity which results in decreased compliance and alveolar collapse. The hypoxia is due to an increased right-to-left shunt and perfusion of poorly aerated alveoli. 10 Mechanical ventilation with an inspiratory plateau and positive end-expiratory pressure (PEEP) are used to improve oxygenation. PEEP increases the functional residual capacity and decreases the alveolar collapse, thus reducing shunting. This is illustrated in Figure 3. However, PEEP does not diminish pulmonary edema. 11 The optimal amount of PEEP is determined by the maximum oxygen transport, cardiac output times arterial oxygen content. 12,13 The optimal PEEP can be estimated by calculating the total static compliance (tidal volume divided by the difference between the inspiratory plateau pressure and end-expiratory pressure). 12 The level of PEEP with the highest compliance occurs at the point where alveolar collapse is maximally improved without overdistension of the lung. PEEP decreases cardiac output by decreasing venous return and perhaps by depressing ventricular function. 14,15 The "optimal PEEP" as defined above varies in conjunction with levels of cardiac output, fluid administration, and tidal volume. 13 Figure 3. PEEP increases functional residual capacity and decreases alveolar collapse. Swan-Ganz catheter measurement of the pulmonary artery wedge pressure is the most common clinical method of assessing the left ventricular filling pressure. These catheters are useful to avoid fluid overload. A lateral chest x- ray should be obtained to be sure that the catheter is located below the left atrium; otherwise the wedge pressure may reflect airway pressures. 16,17 Since patients treated with mechanical ventilation tend to retain fluid, the wedge pressure should not exceed 18 mmhg and probably be maintained at the lower limits of normal to avoid fluid overload without dehydrating the patient. The administration of crystalloid versus colloid intravenous fluids is controversial. Crystalloids should probably be used early in ARDS when there is a marked increase in vascular permeability because colloids will increase pulmonary edema. In the later stages of ARDS, administration of colloids may increase the serum oncotic pressure and decrease pulmonary edema. The minimal concentration of inspired O 2 that can maintain an arterial PO 2 of 55 should be used because the amount of oxygen that can be safely administered in ARDS is unknown. The concentration of oxygen that is nontoxic to a normal lung may produce toxicity that may lead to pulmonary fibrosis in ARDS. 18 The use of pharmacologic doses of methylpred-nisolone, 30mg/kg, is controversial. They inhibit complementinduced neutrophil aggregation and may reduce alveolar-capillary permeability in ARDS. 19 However, steroids also reduce lung macrophage function and bacterial clearance and should be discontinued after hours if no clinical response is seen. Ibuprofen has been used in the treatment of ARDS on the grounds that it, unlike aspirin, interferes with leukotriene synthesis and thereby prevents leukocyte agglutination. Its use is experimental at this time.

5 Proper management of the underlying illness is important. Repeated cultures of sputum, wounds, urine, blood, and stool should be taken and appropriate narrow spectrum antibiotics used to treat infection and avoid superinfection. Electrolytes and serum osmolality must be monitored because the syndrome of inappropriate antidiuretic hormone is common in acute respiratory failure. 20 Administration of antacids will reduce the incidence of stress ulcers. Vitamin K administration will frequently correct coagulation abnormalities in ICU patients receiving antibiotics. Extracorporeal membrane oxygenation does not improve survival and is no longer used in the treatment of ARDS. 21 The principles of management of ARDS are outlined in Table 1. Essential Table 1, Management of ARDS Management of underlying illness Mechanical ventilation with inspiratory plateau and PEEP Minimal inspired concentration of O 2 to maintain an arterial PO 2 of 55. Avoid FIO 2>0.6 Repeated cultures of sputum, wounds, urine, blood and stool Narrow spectrum antibiotics to treat infection Close monitoring of electrolytes and assessment of volume status Antacids Helpful if available Swan-Ganz catheter monitoring Controversial Steroids methylprednisolone (30 mg/kg) Crystalloid versus colloid fluids Ibuprofen Prognosis The mortality of patients with ARDS is approximately 50 percent. The lung mechanics of patients who recover return to normal within 6 months, although minor abnormalities of gas exchange may persist. 22 REFERENCES 1. Rinaldo JE, Rogers RM: Adult respiratory-distress syndrome: changing concepts of lung injury and repair. TV Engl J Med 306( 15): Hammerschmidt DE, Weaver LJ, Hudson LD, et al: Association of complement activation and elevated plasma- C5a with adult respiratory distress syndrome. Lancet 1(8175): Jacob HS, Craddock PR, Hammerschmidt DE, et al: Complement-induced granulocyte aggregation: an unsuspected mechanism of disease. N Engl J Med 302(14): Alveolar response to injury, editorial. Thorax 36(11): Lee CT, Fein AM, Lippmann M, et al.: Elastolytic activity in pulmonary lavage fluid from patients with adult respiratorydistress syndrome. TV Engl J Med 304(4): McGuire WW, Spragg RG, Cohen AB, et al.: Studies on the pathogenesis of the adult respiratory distress syndrome. J Clin Invest 69(3): Bone RC, Francis PB, Pierce AK: Intravascular coagulation associated with the adult respiratory distress syndrome. Am J Med 61(5): Schneider RC. Zapol WM, Carvalho AC: Platelet consumption and sequestration in severe acute respiratory failure. Am Rev Respir Dis 122(3): Tomashefski JF, Reid L, Zapol WM: The pulmonary vascular lesions of the adult respiratory distress syndrome. Am Rev Respir Dis 125(Abstr): Dantzker DR, Brook CJ, Dehart P, et al.: Ventilation-perfusion distributions in the adult respiratory distress syndrome. Am

6 Rev Respir Dis 120(5): Miller WC, Rice DL, Unger KM, et al.: Effect of PEEP on lung water content in experimental noncardiogenic pulmonary edema. Crit Care Med 9(1): Suter PM, Fairley B, Isenberg MD: Optimum end-expiratory airway pressure in patients with acute pulmonary failure. N Eng J Med 292(6): Suter PM, Fairley HB, Isenberg MD: Effect of tidal volume and positive end-expiratory pressure on compliance during mechanical ventilation. Chest 73(2): Calvin JE, Driedger AA, Sibbald WJ: Positive end-expiratory pressure (PEEP) does not depress left ventricular function in patients with pulmonary edema. Am Rev Respir Dis 124(2): Robotham JL, Lixfeld W, Holland L, et al.: The effects of positive end-expiratory pressure on right and left ventricular performance. Am Rev Respir Dis 121(4): Shasby DM, Dauber IM, Pfister S, et al.: Swan-Gantz catheter location and left atrial pressure determine the accuracy of the wedge pressure when positive end-expiratory pressure is used. Chest 80(6): Tooker J, Huseby J, Butler J: The effect of Swan-Ganz catheter height on the wedge pressure-left atrial pressure relationships in edema during positive-pressure ventilation. Am Rev Respir Dis 117(4): Witschi HR, Haschek WM, Klein-Szanto AJ, et al.: Potentiation of diffuse lung damage by oxygen: determining variables. Am Rev Respir Dis 123(1): Sibbald WJ, Anderson RR, Reid B, et al.: Alveolo-capillary permeability in human septic ARDS. Effect of high-dose corticosteroid therapy. Chest 79(2): Szatalowicz VL, Goldberg JP, Anderson RJ: Plasma antiduretic hormone in acute respiratory failure. Am J Med 72(4): Zapol WM, Snider MT, Hill JD, et al.: Extracorporeal membrane oxygenation in severe acute respiratory failure. A randomized prospective study. JAMA 242(20): Elliot CG, Morris AH, Cengiz M: Pulmonary function and exercise gas exchange in survivors of adult respiratory distress syndrome. Am Rev Respir Dis 123(5):