The most common cause of pulmonary edema during this period is that from fluid shift-induced volume overload, especially in the presence of a smoke inhalation injury. An increase in pulmonary capillary hydrostatic pressure occurs leading to excess fluid crossing from plasma to interstitium. Volume overload is frequently due to a combination of systemic resorption of tissue edema at a rate faster than that which can be cleared by the kidney and a continued excess infusion of salt-containing fluid at a rate faster than needed. The stress response and/or positive pressure ventilation will impair renal clearance of the excess fluid by increasing antidiuretic hormone and aldosterone release and suppressing atrial naturietic factor.

Wedge pressure usually exceeds 20 mmHg in the early stages. Severe plasma hypoproteinemia (value less than 50%) will exaggerate the process, whereas a lesser degree of plasma hypoproteinemia is compensated for by a comparable decrease in interstitial protein content. The excess fluid crossing the plasma membrane will first migrate to the hilar area and accumulate in the loose interstitium around the larger airways and vessels. Dyspnea, diffuse rhonchi, and wheezing are the result of the interstitial edema process, whatever the cause. Only mild hypoxia is usually evident at this stage. The impaired oxygen exchange is in large part correctable by increasing the fractional inspired oxygen in air. The interstitial edema will also increase the lung stiffness (decreased static compliance) leading to a decrease in functional residual capacity.

If the edema process continues after the interstitium has filled with fluid, alveolar edema will occur. Edema in dependent lung occurs first. The alveolar flooding causes shunt fraction to increase, leading to significant hypoxemia as well as a decrease in lung volume and functional residual capacity. Compliance decreases and atelectasis increases, further increasing the shunt. Alveolar edema produces moist rales. However, these findings may be difficult to differentiate clinically from the bronchorrhea induced by an inhalation injury.

There are two main objectives of treatment:

1. Maintain adequate oxygenation to systemic tissues
1. Correct the process producing lung edema

The optimum management for the pulmonary edema alone is "drying the patient out". However, this process may impair tissue oxygenation during this very vulnerable period for the wound and lead to problems greater than the lung edema. A relative hypovolemia will also increase operative risks. It is usually best to make appropriate adjustments in fluid infusion rate and protein replacement to minimize the progression of the process while utilizing positive pressure, if intubated (Table 5-8). Low-dose dopamine will assist in the diuresis by increasing blood flow and by its antialdosterone effects. The continued losses from the burn wound can result in a gradual decrease in blood volume. Therefore vigorous diuresis is normally not needed to correct the hypervolemia and actually is more likely to produce a hypovolemic state. If hypervolemia persists, furosemide can be used. If heart failure is present, as evident from a high filling pressure and low cardiac output, beta agonists can be added.

Those patients meeting the criteria for acute respiratory failure require endotracheal intubation and positive pressure ventilation. Positive pressure plus the addition of PEEP will redistribute the alveolar fluid so that some gas exchange can occur, leading to a decrease in shunt fraction.

The increased pressure will also impair preload and, in turn, decrease capillary pressure. Afterload reduction may be necessary to improve cardiac output. The edema process is usually readily reversible with control of capillary pressure or left-sided filling pressures. Mortality is dependent on the status of the underlying disease process.

Two processes, one due to wound manipulation and the second due to the anesthesia, can produce lung dysfunction with wound excision and grafting procedures:

The manipulation of burn tissue during excision can produce at least a transient decrease in lung compliance from released tissue mediators such as thromboxane. A transient endotoxemia or bacteremia can also occur with its alteration in lung function. However, wound inflammation and infection are much less during this period than later, which is the reason why excisional therapy is safer during the 2 to 5 day period. Repeated excision and grafting procedures, especially on large body burns, usually results in a situation in which the patient is either recovering from an inhalation anesthetic or is preoperative. These patients often remain intubated between excision procedures if there is a concomitant inhalation injury and the burn is large. Most general anesthetics will cause a deterioration in an already marginal respiratory status, putting the patient at high risk for pneumonia and further lung failure during the subsequent phase of injury. Muscle relaxants will further compound this problem. Ketamine anesthesia will help by decreasing some of the anesthesia-induced respiratory depression. Early recognition of the increased risks of a relative hypoventilation in the early postanesthesia period is essential. Ventilatory support systems should be added early to avoid the problem rather then attempting to treat the complications.

PULMONARY EFFECTS OF ANESTHESIA, EXCISION

Resolution of facial edema does not always correspond with resolution of airways edema. In addition, there are many pulmonary problems in the burn patient necessitating an artificial airway. Look at the whole picture!

Once the initial airways edema is resolving, a quiet period (calm before the storm) is often present that predates the bacterial tracheobronchitis and resulting bronchopneumonia. An appreciate of impending problems will result in more aggressive preventive measures.