III_D.  PULMONARY EDEMA (High Pressure)

Pathophysiology:

There is an increased risk of high pressure pulmonary edema during this period of rapid fluid flux, especially in the elderly burn patient or a massive burn.^72-73   A significant portion of the edema is reabsorbed back into the intravascular space during this period.  In addition, heart work increases with the increasing demands and heart failure can occur, especially in the patient with limited reserve. 

Low pressure pulmonary edema due to inflammation or sepsis typically occurs later in the hypermetabolic phase.

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. It is also likely that earlier microvascular injury will make the lung more prone to overload edema with hypervolemia.   An increase in pulmonary capillary hydrostatic pressure can occur 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 infusion of salt-containing fluid at a rate faster than needed.  This process is most prevalent in the elderly as pre-existing heart disease.  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. 

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.⁷⁴  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.

Diagnosis:

The usual clinical findings seen with pulmonary edema are a reliable diagnostic clue. If an inhalation injury has occurred, increased secretions, rhonchi, and wheezing are already present, making the determination of an added cardiogenic pulmonary edema difficult. Additional information utilizing a pulmonary artery catheter for determination of wedge pressure may be necessary.  Since an increased body weight after initial resuscitation is already present, changes in body weight and early post burn are often not a very helpful indication of hypervolemia.

Figure 3:  High Pressure Pulmonary Edema

Note the characteristics of perivascular fluid cuffs of cardiogenic pulmonary edema.

Treatment:

There are two main objectives of treatment:

1. Maintain adequate oxygenation to systemic tissues
2. Correct the process that is 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. Low-dose dopamine can assist in the diuresis by increasing blood flow and by its anti-aldosterone effects. If hypervolemia persists, diuretics 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. The edema process is usually readily reversible by decreasing pulmonary wedge pressure.  Mortality is dependent on the status of the underlying disease process.

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