Most causes of severe pulmonary failure in the surgical patient can be ascribed to one or more of nine causes: the acute respiratory distress syndrome, inability to effectively expand the lungs because of mechanical abnormalities, atelectasis, aspiration, pulmonary contusion, pneumonia, pulmonary embolus, cardiogenic pulmonary edema, and, rarely, neurogenic pulmonary edema.
The acute respiratory distress syndrome or ARDS typically follows shock, trauma or sepsis. Activated coagulation in the injured tissues release coagulative, inflammatory mediators into the circulation. The lungs bear at least some of the brunt of the activated mediators because they receive all the venous blood that returns to the heart. If the injured or infected tissues are in the nonsplanchnic portions of the body, lungs are even further at risk because they contain the first microvasculature that the mediators will encounter. (In the case of injury or infection in the splanchnic viscera, the liver bears the initial brunt of the insult.) The mediators disrupt the microvascular endothelium, and plasma extravasates into the interstitium and, in the case of the lungs, into the alveoli. The resultant pulmonary edema impairs both ventilation and oxygenation; the embolization to the lungs impairs perfusion. Arterial oxygen saturation decreases and carbon dioxide content increases—assuming that no compensatory mechanisms come into play.
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 as a consequence of the interaction between the aggregates and the 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. Infection, disease, injury, and ischemia in nonpulmonary tissues thus lead to damage and dysfunction in previously healthy pulmonary tissues.
The diagnosis of pulmonary failure is made by the development of hypoxemia approximately 24 hours after resuscitation from shock, trauma, sepsis in the absence of other causes of hypoxemia under these conditions — mechanical failure, atelectasis, aspiration, and pulmonary contusion. The chest x-ray usually shows a diffuse infiltrate. The lungs develop a nonspecific inflammatory reaction. Monocytes and neutrophils invade the interstitium. Edema appears within a few hours, alveolar flooding is florid within 1 day, and scar tissue begins to form within a week. If the process is unchecked, the lungs become sodden and resemble liver tissue on gross inspection; scar tissue appears within a week and function-limiting fibrosis begins to develop within 2 weeks. If early treatment is effective, the lungs return to normal, both grossly and microscopically. The process of diagnosis, the pathologic features of ARDS are identical to those of the so-called fat embolism syndrome, which is, for practical purposes, merely a special case of ARDS in which the release of marrow fat into the blood contributes to the development of pulmonary microvascular damage. Nothing is gained by making a distinction between the two entities.
Mechanical failure can arise from chest wall trauma, pain and weakness after surgery and anesthesia, debility caused by the catabolic metabolism of long-term illness, or bronchopleural fistula. Massive trauma to the chest with multiple fractures of multiple ribs or bilateral disruption of the costochondral junctions can result in a free-floating segment of chest wall known as a flail chest: Expansion and relaxation of the rest of the chest wall with spontaneous breathing results in paradoxic motion of the free segment in response to changes in intrathoracic pressure; ventilation becomes compromised; and the arterial PCO2 increases. Lesser degrees of chest wall injury can lead to hypoventilation because of pain associated with breathing. Prolonged mechanical ventilation with loss of muscle mass and power in the diaphragm, accessory muscles of respiration can require ventilatory support until muscle function returns to normal. A bronchopleural fistula — a communication from the airway to the pleural cavity to the atmosphere, either through a chest tube or through a hole in the chest wall — can develop after pulmonary surgery, trauma, or infection. Large air leaks can compromise ventilation to the uninvolved lung as well as to the diseased side because insufflated air preferentially goes to the side with the fistula.
Atelectasis — localized collapse of alveoli—can develop with prolonged immobilization, as during anesthesia or in association with bed rest. The problem is usually full-blown within a few hours after the initiating event. Only mechanical failure (to which it is related), aspiration, cardiogenic pulmonary edema, and pulmonary embolism can produce equivalent levels of hypoxemia so soon. The diagnosis is supported by auscultation of bronchial breath sounds at dependent portions of the lung, occasionally, if severe enough, by x-ray confirmation of plate-like collapse of pulmonary parenchyma. The most reliable confirmation of the diagnosis, however, comes with response to therapy, which can include encouragement of deep breathing and coughing, ambulation, bronchoscopy, and intubation, mechanical ventilation. Atelectasis should respond within a few hours. No other form of pulmonary insufficiency responds as quickly.
Aspiration of gastric contents or blood can occur in any patient who cannot protect the airway, eg, one who has just been injured or anesthetized or who is debilitated or obtunded for any reason. Gastric acid or particulate matter in the airways leads to disruption of the alveolar and microvascular membranes, causing interstitial and alveolar edema. The resultant hypoxemia is usually evident within a few hours, is associated with a localized infiltrate on x-ray. Recovery of gastric contents by suctioning from the endotracheal tree confirms the diagnosis.
Pulmonary contusion arises from direct trauma to the chest wall, the underlying lung parenchyma. Hypoxemia associated with a localized infiltrate on x-ray develops over 24 hours as the injured lung becomes edematous.
Pneumonia can arise primarily or can be superimposed on aspiration, pulmonary contusion, or ARDS. Generally, the diagnosis of that form of pulmonary failure is made by recovery of bacteria and purulent material from the endotracheal tree, hypoxemia, signs of systemic sepsis, and a localized infiltrate on x-ray. Recently, there has been interest in a Clinical Pulmonary Infection Score (CPIS) derived from these parameters. The CPIS provides a quantitative value that aids in accurate diagnosis of pneumonia. Diagnosis of the CPIS bronchoscopy, with bronchoalveolar lavage and culture, may be a useful adjunct to distinguish pneumonia from ARDS.
Pulmonary embolism typically presents with sudden deterioration of pulmonary function 3 days or more after an event — such as an operation, injury, or the beginning of immobilization—that can stimulate deposition of clot in a large systemic vein. Patients with cancer are at particularly high risk, and in any patient the greater the magnitude of operation or injury, the greater the chance of venous thrombosis and embolization. The chest film is usually nonspecific. A fairly definite diagnosis can often be made by high-definition computed tomograms of the chest. The study requires transfer to the radiology suite and the use of large amounts of radiographic contrast material. Pulmonary arteriography carries the same risks — transfer to the radiology suite and use of contrast — and requires right-heart catheterization, but it does have advantages. It gives a definitive diagnosis with one test. At the end of the diagnostic study, an indwelling catheter can be placed proximal to the clot and used for infusion of lytic agents.
Clot emboli must be organized to be clinically significant; embolism to the lung of fresh soft clot rarely causes any difficulty. The pulmonary endothelium contains potent fibrinolysins that can break up any poorly organized embolus. Sudden deterioration in pulmonary function sooner than 3 days after an event that stimulates clot formation is only rarely caused by an embolus; the deterioration is more likely to be caused by mechanical failure, atelectasis, aspiration, or pneumonia.
Cardiogenic pulmonary edema arises from high left atrial and pulmonary microvascular hydrostatic pressures. Patients who have suffered an acute myocardial infarction can present this way, as can patients with underlying myocardial or coronary artery disease when faced with fluid shifts and surgical stress. Occasionally, the rapid administration of intravenous fluid — especially in elderly patients with poor myocardial performance—will outstrip the heart’s ability to pump, pulmonary edema will result. Acute valvular disease, though quite rare after injury or cardiac surgery, is another possible cause of inability of the left heart to pump effectively. The diagnosis oh that form of pulmonary failure is made on the basis of hypoxemia, rales, a third heart sound, perihilar infiltrates, Kerley’s lines, and cephalization of blood flow on x-ray along with elevated pulmonary arterial wedge pressures on Swan-Ganz catheterization. A wedge (or left atrial) pressure of 24 mm Hg can produce cardiogenic pulmonary edema even in the presence of an intact endothelium; wedge pressures less than 24 mm Hg will not produce pulmonary edema in and of themselves, but pressures exceeding 16 mm Hg can worsen the edema associated with increased permeability. The goal for the wedge pressure in a patient with uncomplicated cardiogenic pulmonary edema in the absence of an inflammatory process in the lungs should be 20 mm Hg or less; the goal in a patient with an inflammatory process should be 16 or, better, 12 mm Hg.
Neurogenic pulmonary edema is associated both experimentally and clinically with head injury and increased intracranial pressure. The exact mechanism by which this occurs is unknown, but it is probably related to sympathetic discharge with postmicrovascular vasoconstriction in the lungs and a resultant increase in pulmonary microvascular hydrostatic pressure. This form and oxygenation defect is rare, and other causes should be considered also in patients with head injury.