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INITIAL TREATMENT OF ACUTE PULMONARY FAILURE

DIAGNOSIS OF PULMONARY FAILURE IN SURGICAL PATIENTS

Most causes of pulmonary failure in the surgical patient can be ascribed to one or more of nine causes: the pulmonary failure of shock, trauma, and sepsis; mechanical failure caused by deranged respiratory system mechanics; atelectasis; aspiration; pulmonary contusion; pneumonia; pulmonary embolism; cardiogenic pulmonary edema; and, rarely, neurogenic pulmonary edema.

The pulmonary failure of shock, trauma, and sepsis arises from extrapulmonary trauma, infection, or ischemia–reperfusion in the setting of shock. Products of coagulation and inflammation are carried intravascularly from the damaged tissues and carried to the lungs (or to the liver, in the case of the splanchnic circulation, and from there to the lungs), where they set up an acute inflammatory reaction. The extrapulmonary causes are many and range from necrotizing infections to noninfective inflammatory responses (such as pancreatitis) to reperfusion of ischemic limbs to soft-tissue injury.

The concept of pulmonary failure secondary to extrapulmonary ischemia–reperfusion, coagulation, and inflammation, which is common in surgical patients, can be subsumed into a broader category of pulmonary failure known as the acute respiratory distress syndrome (ARDS). ARDS is defined by the Berlin criteria as the acute onset of hypoxemia with bilateral infiltrates on chest x-ray or CT scan as well as a PaO2:FIO2 ratio less than 300, not fully explained by cardiac failure or fluid overload.

The causes of ARDS include those that are responsible for the pulmonary failure of shock, trauma, and sepsis, and also include severe pneumonia and aspiration. The end result in all of these conditions is activation of macrophages and other inflammatory cells in the lungs. The mediators disrupt the microvascular endothelium, increasing its permeability. Plasma extravasates into the interstitium and, in the case of the lungs, into the alveoli. The resultant pulmonary edema impairs both ventilation and oxygenation; microembolization to the lungs impairs perfusion. Arterial oxygen saturation decreases and carbon dioxide content increases, assuming that no compensatory mechanisms come into play. Lastly, to make things worse, the inflammatory process in the lungs releases mediators into the systemic circulation that can lead to inflammation and dysfunction in the liver, gut, and kidneys.

A number of different mediators of coagulation and inflammation have been implicated as causes of the increased permeability. Proteases, kinins, complement, oxygen radicals, prostaglandins, thromboxanes, leukotrienes, lysosomal enzymes, and other mediators are released from aggregates of platelets and white cells or from the endothelium or plasma because of the interaction between the aggregates and vessel wall. Some of these substances are chemoattractants of more platelets and white blood cells, and a vicious cycle of inflammation develops that worsens the disruption of the vascular endothelium.

Pathologically, ARDS (and the pulmonary failure of shock, trauma, and sepsis) is characterized by diffuse alveolar damage and a nonspecific inflammatory reaction, with the loss of alveolar epithelium and ...

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