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- Pulmonary problems must be controlled during this period to allow for an aggressive surgical excisional approach.
- Fluid management changes dramatically to a strategy of replacing evaporative water losses.
- Postburn anemia will develop and necessitate increased blood transfusions.
- Monitoring must be primarily noninvasive to avoid line sepsis.
- Nutritional support should begin at this point, using enteral alimentation.
- Controlled surgical excisions should begin as soon as the patient is hemodynamically stable, to avoid having extensive burns still in place when the infection-inflammation phase begins.
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The early postresuscitation phase is a period of transition from the ebb, or shock, phase to the flow, or hypermetabolic, phase. Major cardiopulmonary and wound changes occur that alter patient care substantially from that given during resuscitation. In general, cardiopulmonary stability is optimal during this period because wound inflammation and infection have not yet developed. Early wound excision and grafting are initiated during this period because operative risks, especially blood loss and septicemia, are substantially less than after inflammation and infection develop.
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Five major abnormalities impair pulmonary function during this period: (1) continued upper airway obstruction, (2) decreased chest wall compliance, (3) tracheobronchitis, (4) pulmonary edema, and (5) lung dysfunction induced by surgery (and anesthesia). Upper airway and facial edema caused by the heat-induced tissue and mucosal damage begins to resolve between days 2 and 4. The decision to extubate (Fig. 99-1) is a difficult one because there is no good test for determining the adequacy of airway patency.1,2 Laryngoscopy to determine the presence of cord edema is helpful, as is deflation of the cuff to determine if air moves around the tube. The impaired compliance of the chest wall caused by deep burns is improved, but certainly not eliminated, by escharotomy. Early excision of the full-thickness wound can improve chest wall motion by removing both edema and noncompliant tissue.
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The chemical burn to the airways results in a spectrum of clinical manifestations during this period. At the very least, mucosal irritation will persist for several days and cause bronchorrhea, cough, and increased mucus production. The damaged ciliary function of the airways leads to a high risk for infection, manifested first (in the next 3 to 4 days) by a bacterial tracheobronchitis that is often followed by bronchopneumonia. Bacterial colonization is inevitable. If infection can be controlled and secretions cleared, the acute process will resolve over the next 7 to 10 days. However, the risk of infection persists for several weeks, extending well into the inflammation period. The treatment of lung dysfunction during this phase is summarized in Fig. 99-2. The clearance of soot, mucopurulent exudate, and sloughing mucosa is essential to avoid progression of the lung injury.
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