Home | | Anesthesiology | Increased Permeability Pulmonary Edema (Noncardiogenic Pulmonary Edema): Acute Lung Injury & ARDS

Chapter: Clinical Anesthesiology: Perioperative & Critical Care Medicine: Critical Care

| Study Material, Lecturing Notes, Assignment, Reference, Wiki description explanation, brief detail |

Increased Permeability Pulmonary Edema (Noncardiogenic Pulmonary Edema): Acute Lung Injury & ARDS

Increased Permeability Pulmonary Edema (Noncardiogenic Pulmonary Edema): Acute Lung Injury & ARDS

Increased Permeability Pulmonary Edema (Noncardiogenic Pulmonary Edema): Acute Lung Injury & ARDS

 

Extravascular lung water increases in patients with increased permeability pulmonary edema due to enhanced permeability or disruption of the capillary–alveolar membrane. The protective effect of plasma oncotic pressure is lost as increased amounts of albumin “leak” into the pulmonary inter-stitium; normal—or even low—capillary hydrostatic pressures are unopposed and result in transudation of fluid into the lungs. Permeability edema is seen with acute lung injury (P:F ratio 300 [P = PaO2 and F = FIO2]) and is often associated with sepsis, trauma, and pulmonary aspiration; when severe (P:F ratio < 200), it is referred to as the acute respiratory distress syndrome (ARDS).

Pathophysiology

 

Acute lung injury and ARDS represent the pul-monary manifestation of the systemic inflamma-tory response syndrome (SIRS). Central to the pathophysiology of acute lung injury and ARDS is severe injury of the capillary–alveolar membrane. Regardless of the type of injury, the lung responds to the ensuing inflammatory response in a similar fashion. The released secondary mediators increase pulmonary capillary permeability, induce pulmo-nary vasoconstriction, and alter vascular reactivity such that hypoxic pulmonary vasoconstriction is abolished. Destruction of alveolar epithelial cells is prominent. Alveolar flooding, with decreased surfactant production (due to loss of type II pneu-mocytes), result in collapse. The exudative phase of ARDS may persist for a varying period; it is often followed by a fibrotic phase (fibrosing alveolitis), which in some cases leads to permanent scarring.

Clinical Manifestations

 

The diagnosis of acute lung injury or ARDS requires the exclusion of significant underlying left ventric-ular dysfunction combined with a P:F ratio of less than 300 (acute lung injury) or less than 200 (ARDS), and the presence of diffuse infiltrates on chest radio-graph. The lung is often affected in a nonhomoge-neous pattern, although dependent areas tend to be most affected.

 

Acute lung injury and ARDS are commonly seen in the settings of sepsis or trauma. Patients present with severe dyspnea and labored respira-tions. Hypoxemia due to intrapulmonary shunting is a universal finding. Although dead space venti-lation is increased, arterial CO2 tension is typically decreased because of a marked increase in minute ventilation. Ventilatory failure may be seen initially in severe cases or may eventually develop due to respiratory muscle fatigue or marked destruction of the capillary–alveolar membrane. Pulmonary hypertension and low or normal left ventricular filling pressures are characteristic hemodynamic findings.

Treatment

 

In addition to intensive respiratory care, treatment should be directed at reversible processes such as sepsis or hypotension. Hypoxemia is treated with oxygen therapy. Milder cases may be treated with a CPAP mask, but most patients require intubation and at least some degree of mechanical ventilatory support. Increased Pplt pressures (>30 cm H 2O) and high VT (>6 mL/kg), however, should also be avoided because overdistention of alveoli can induce iatrogenic lung injury, as can high FIO2(>0.5). While injury from high FIO2hasnot been conclusively demonstrated inhumans, as was previously noted, VT of 12 mL/kg was associated with greater mortality than VT of6 mL/kg and Pplt of less than 30 cm H2O in patients with ARDS. Thus, reduced tidal volumes are associated with the greatest improvement in outcome after ARDS of any intervention subjected to a random-ized clinical trial.

 

If possible, the FIO2 should be maintained at 0.5 or less, primarily by increasing PEEP above the inflection point (see Figure 57–6). Other maneuvers to improve oxygenation include the use of inhaled nitric oxide, inhaled prostacyclin or prostaglan-din E1 (PGE1), and ventilation in the prone posi-tion. These three techniques improve oxygenation in many patients with acute lung injury, but they are not risk free and they have not been associated with an improvement in survival. A recent meta-analysis has concluded that moderate doses of cor-ticosteroids likely improve morbidity and mortality outcomes in ARDS, but the underlying data remain controversial.


 

Morbidity and mortality from ARDS usually arise from the precipitating cause or from complica-tions rather than from the respiratory failure itself. Among the most common serious complications are sepsis, renal failure, and gastrointestinal hem-orrhage. Nosocomial pneumonia is particularly common in patients with a protracted course and is often difficult to diagnose; antibiotics are generally indicated when there is a high index of suspicion (fever, purulent secretions, leukocytosis, and change in chest radiograph). Protected specimen brushings and bronchoalveolar lavage sampling via a flexible bronchoscope may be useful. Breach of mucocuta-neous barriers by various catheters, malnutrition, and altered host immunity contribute to a frequent incidence of infection. Kidney failure may result from various combinations of volume depletion, sepsis, or nephrotoxins. Kidney failure substantially increases the mortality rate for ARDS (to >60%).

Prophylaxis for gastrointestinal hemorrhage with sucralfate, antacids, H2 blockers, or proton pump inhibitors is recommended.

Study Material, Lecturing Notes, Assignment, Reference, Wiki description explanation, brief detail


Copyright © 2018-2020 BrainKart.com; All Rights Reserved. Developed by Therithal info, Chennai.