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The term "nosocomial pneumonia" refers to the pneumonia that develops in the hospital with no evidence of lung infection present on admission, i.e., it is hospital-acquired. Although another form of nosocomial infection, namely, wound infection, is more common, the mortality rate for pneumonia is much higher. Burn patients with a combination of inhalation injury and a major body burn have the greatest risk of pneumonia, with a rate exceeding 50%.^78-81 The high incidence is due to the presence of virulent organisms in the hospital environment and the immunosuppressed state of the burn patient. Lung bacterial clearance is significantly impaired in the presence of a burn and inhalation injury.^81-82 The major events occurring in the majority of nosocomial lung infections are described.

Nearly 100% of major burn patients with a respiratory problem have colonized their oropharynx with pathogens. There are a number of routes and events by which colonization occurs.

Aspiration of infected secretions is the next step following colonization. Aspiration is potentiated by sedation or any process that impairs normal clearance of oral secretions., e.g. a nasogastric tube. Pooled contaminated secretions present above the cuff of an endotracheal tube can readily be aspirated into the tracheobronchial tree. Suctioning of the oropharynx before cuff deflation or extubation is, of course, mandatory. The endotracheal tube (or tracheostomy) itself increases the potential for aspiration of secretions because the glottis and vocal cords cannot be effectively closed and secretions can track down both the inside and outside of tube. The causes of tracheobronchial aspirations are as follows:^83-87

· Pharmacologic impairment to clerarance of secretions, e.g., sedation, anesthesia, paralysis

· Anatomic impairment to clearance of secretions, e.g., oropharyngeal edema, trauma, nasogastric tube, endotracheal tube, oral airway, etc.

· Direct contamination of lower airways by catheters, lavage fluid, or deflation of the cuff on endotracheal tube.

Altered lung host defenses can dramatically increase the potential for lung infection as a result of the aspiration of bacteria. The altered defenses that are most prominent in the process of lung infection will be described.^83-87

Impaired Cough - Impairment of this reflex is a common occurrence in the burn patient. A decrease in the state of consciousness markedly suppresses both the initiation of the reflex and the quality of the cough. This will be the case with the need for narcotics for pain control and during recovery from anesthesia. The ability to take a large inspiration, necessary for an adequate cough, will be impaired by a chest burn and also by muscle weakness from catabolism. The presence of an endotracheal tube although maintaining an adequate airway, can decrease the ability to generate a sufficient propulsive force to clear sections effectively. Any aspirated, infected oral secretions will then have the opportunity to proliferate.

Impairment of Mucociliary Action - The airways are lined with ciliated mucous-coated epithelia that beat toward the pharynx, thereby assisting in the continued clearance of particles and microorganisms. This is particularly useful in the smaller airways, which are less effectively cleared by coughing. The ciliary action is directly injured by heat and chemicals in inhaled smoke.^8,32

Airway Plugging - The combination of tenacious secretions, mucosal slugh and impaired clearance lead to frequent plugging of small and medium sized airway, atelectasis and increased risk of infection.^8,32

Impairment of Alveolar Macrophage Function - Bacteria or particles deposited in the alveoli are rapidly phagocytized by the alveolar macrophage, which destroys them by direct killing via oxygen radical release. Chemoattractants are released from the macrophage, which attract neutrophils to assist in the containment process. The microorganism-laden macrophages are cleared via the mucociliary system or may also migrate through the interstitial space to be cleared by the lymphatics, thus entering the regional lymph nodes and systemic circulation. A number of factors in the burn patient will impair macrophage function. Inhalation anesthetics, inhalation injury, malnutrition, anemia, and hypoxia will impair macrophage function, thereby increasing the risk of lung infection.^89.90

Impairment of Containment - The postburn immunodeficiency state involving both the cellular and humoral component of resistance will impair the ability of the lung defenses to contain infection. Another major factor that impairs the containment process is increased lung water. The movement of edema fluid allows a rapid spread of bacteria to uninvolved areas both as a vehicle for carrying bacteria and as an impairment of the sequestration and containment process.⁹¹

Excess Use of Antibiotics - The burn patient develops a sepsis syndrome as a result of the inflammatory response to injury. This process makes it difficult to diagnose a superimposed infection often leading to an excessive use of antibiotics and the development of resistant organisms.

Diagnosis - The usual criteria for diagnosing pneumonia are fever, leukocytosis, purulent sputum, new or increasing infiltrates on radiographs, and pathogens growing from the sputum.

These criteria are of much less value in the burn patient where other sources of infection and burn inflammation an initiate a sepsis syndrome. For example, approximately 75% of critically ill burn patients have a colonized upper airway, usually with gram-negative organisms. The purulent sputum may simply be aspirated oropharyngeal secretions. Pulmonary infiltrates are also a common finding in the postburn patient. Approximately 30% of new infiltrates in these patients turn out not to be pneumonia. Based on these facts, clinical criteria alone are not sufficiently accurate to allow a precise diagnosis of the presence or absence of nosocomial pneumonia.⁸⁷ More invasive testing such as obtaining samples with a fiberoptic bronchoscope using a brush technique, are indicated. Bronchoalveolar lavage sampling is another approach.

Table 1: Criteria for Diagnosing Pneumonia
Clinical Signs	Differential Diagnosis
Fever, leukocytes	Non-pulmonary infection, Burn wound, infllammation
Pulmonary Infiltrate	Inhalation-induced inflammation, postoperative atelectasis, aspiration
Purulent sputum	Oropharyngeal colonization

Since eradication of an established pneumonia in the burn patient is very difficult, prevention is of primary importance.^92-94

Maintaining adequate oxygen delivery to the burn wound and other tissue at risk for infection is necessary by optimizing blood volume, hemoglobin, and cardiac output. Nutritional status, both adequate calories and protein, using the correct mix of nutrients must be maintained. In addition, underlying chronic diseases that are also immunosuppressive, such as diabetes, must be kept in as good a control as possible.

Maintaining an adequate cough mechanism is of utmost importance in the patient at risk for pneumonia, particularly in the absence of positive-pressure support, since there is a greater risk of hypoventilation and atelectasis. Analgesics and sedation must be used carefully. It is necessary to provide adequate pain relief, especially if splinting due to a chest wall burn is present. In addition, adequate sleep is required to maintain muscle activity. Oversedation and analgesia are, of course, counterproductive unless mechanical ventilatory support is being provided.

An endotracheal tube, although adequate for maintenance of a patent and protected airway, impairs the ability to clear thick secretions by coughing. It is very difficult to propel secretions the length of the tube. If continued intubation is expected to be necessary for many weeks, conversion to a tracheostomy performed in the first 7 to 10 days will greatly assist the clearance of secretions. The tracheostomy should not be placed through burned tissue. If the neck is burned, early excision and grafting of the neck area is indicated, and the subsequent tracheostomy can be performed through the skin graft in 24 to 48 hours.

The cough reflex alone will be insufficient to maintain small airway patency. Frequent position changes, hyperinflation, and postural drainage will be necessary to move the small and moderate airway secretions to the proximal airways so that cough clearance can occur. Ambulation is the ideal approach. The intubated, ventilated patient with a lung injury who cannot ambulate is best managed using side-to-side position change. The side-to-side rotating bed is ideal for this purpose because the need for pushing on the painful burn areas to move the patient is eliminated.

Beside improved mucous clearance, maintaining local containment of the infection is needed, by avoiding increased lung water. Lung edema impedes bacterial containment.

Decreasing the potential cross-contamination of bacteria from personnel or equipment to the patients airway will certainly decrease the risk of colonization with a virulent resistant hospital organism. Avoiding unnecessary use of broad-spectrum antibiotics will also decrease risks. Thus, the risk-reduction methods are:

· Minimize personnel or equipment transfer of bacteria with compulsive handwashing and surveillance for bacterial reservoirs.

Once oropharyngeal colonization occurs, the risks of aspirating the infected secretions should be minimized. Positioning with the head elevated will decrease orofacial edema and improve secretion clearance. Transfer of bacteria from the upper to the lower airway by way of endotracheal tubes and suction catheters needs to be controlled by careful aseptic technique.

Initial empiric therapy is indicated after which the antibiotics chosen need to be as specific for the organs involved as possible to avoid development of resistant strains.^91-96

Antibiotic dosing in the burn patient is more complex due to the more rapid elimination and the larger area of distribution (burns and edema).⁹⁶

IV_A. NOSOCOMIAL PNEUMONIA