Chapter 99. Burns: Postresuscitation Phase (Days 2 to 6)

• 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.

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.

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.

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.

Infection surveillance is crucial during this early period in order to detect bacterial bronchitis before pneumonia develops. Unlike typical bronchopneumonia, presenting with a localized infiltrate, the entire tracheobroncheal tree becomes colonized with pathogens, and the resulting infection is often a diffuse bronchopneumonia. Sputum smears and monitoring of the character of the sputum are useful as early guides. Systemic antibiotics are not given prophylactically but are initiated when a bacterial tracheobronchitis becomes evident. This approach is summarized in Fig. 99-3.

Repeated excision and grafting procedures, especially on large body burns, usually result in a situation in which the patient either is recovering from an inhalational anesthetic or is awaiting surgery. Most general anesthetics cause deterioration in an already marginal respiratory status and put the patient at further increased risk for pneumonia and respiratory failure during the subsequent phase of injury. Muscle relaxants compound this problem.

Pathophysiologic Changes

Fluid Losses

Evaporation from the surface of the burn becomes a major source of water loss that persists until the wound is closed. This loss is related to the water vapor pressure at the surface.4 A reasonable estimate of loss can be obtained from the following formula, where TBS is the total body surface area:

Red blood cell mass can decrease markedly during this period because of breakdown and decreased production of red blood cells.5,6 Lipid peroxidation of the red blood cell membrane after burn injury is well described. The hematocrit characteristically falls to between 30% and 35% or lower several days after the burn injury. Besides increased red blood cell breakdown, there is decreased red blood cell production by the bone marrow—an effect characteristic of any chronic injury state. Red blood cell production does not return to normal until after the wound is closed.

Fluid Gains

Intravascular fluid is gained during the postresuscitation period as a result of absorption of edema. Edema resorption is much more rapid in the case of superficial burns where lymphatics are intact and begins at about day 2 or 3. Edema resorption is much slower after full-thickness injury because of the lack of local lymphatics and venules. However, the magnitude of tissue edema is not a valid reflection of the circulating volume and never should be used to judge the correct rate of fluid replacement.

Systemic Metabolic Changes and Circulatory Responses

The ebb, or hypometabolic, phase characteristic of the initial burn shock period begins to change into the flow, or hypermetabolic, phase over the next 3 to 5 days.7,8 Tachycardia, ranging from modest to significant (100 to 120 beats per minute), is seen frequently and results partly from persistent elevation of catecholamine levels. Systemic vascular resistance begins to decrease. The vasodilatation results in an increase in the capacity of the vascular space and, therefore, an increased need for colloid and red blood cells.

Oxygen consumption usually peaks 5 to 7 days after the burn.7 The transition to the flow state also initiates an increase in body temperature, which increases further with the release of pyrogens from the burn wound. The characteristic increase in body temperature by 1 to 2°F makes it more difficult to diagnose infection. Patients with subclinical glucose intolerance (typically obese or elderly patients) may develop hyperglycemia, especially with a large burn. Increased catabolism leads to increased urea production, especially if inadequate glucose calories are being provided. The rate of body protein loss is massive as a result of the increased levels of catecholamines and cortisol, as well as inflammatory cytokines, which markedly stimulate gluconeogenesis using protein as a substrate.9,10 Decreased levels of human growth hormone and testosterone amplify the catabolism.11 A total of 20% to 30% of calories come from proteins, as opposed to the protein sparing, which occurs in starvation, where fat is the main fuel. Loss of the amino acid glutamine is particularly pronounced because it is used heavily as a fuel source by the gut as well as a precursor for the antioxidant glutathione.12 Muscle losses of a kilogram a day are common with large burns. Over a 10-day period, 10% to 15% of body protein stores can be lost, resulting not only in muscular weakness, including weakness of the intercostal muscle and diaphragm, but also in decreased wound healing and immune function. Because of the large increase in oxidant release due to inflammation, the levels of endogenous antioxidants fall rapidly, increasing the risk of further oxidant injury and generalized organ dysfunction.13

Hemodynamic Management

Understanding the physiologic and metabolic changes during this period is the key to successful management. The major decisions relate to fluid therapy and the ongoing assessment of the adequacy of perfusion.

Selection of Fluid

A common error is continued infusion of isotonic crystalloid during a period when major losses of sodium do not occur. A 5% glucose-containing solution with a low sodium content and an increased potassium content is the primary replacement fluid for evaporative and urinary losses during this period. Initiation of nutrition is also essential, preferably by the enteral route. To restore blood volume and maintain the protein binding required for predictable pharmacokinetics, protein losses should be replaced. A serum albumin level of 2.5 g/dL is a reasonable goal. It is also frequently necessary to replace red blood cells. The hematocrit should be kept at least at a level of 30% to optimize delivery of oxygen to tissues. Hemodynamic management is summarized in Fig. 99-4.

What to Monitor

Assessment of the adequacy of perfusion, tissue oxygenation, and fluid and electrolyte balance can be difficult during this period of evolving hemodynamics. Oxygen consumption increases gradually with the transition from the ebb state to the flow state. The absolute value of body weight cannot be used to reflect blood volume during this transition. However, if weight is increasing, excess fluid (and salt) is probably being given. One should anticipate a gradual increase of 1 to 2°F in body temperature over normal; this increase is due to hypermetabolism. Further increases are common with wound manipulation.

The wound undergoes dramatic changes during this period as inflammation develops. In addition, wound colonization and the potential for wound infection increase. This process of deepening of the burn (called wound conversion) is seen most commonly in deep second-degree burns and can occur even with optimal management. Processes such as wound desiccation, hypovolemia, increased tissue pressure, and hypothermia all can accentuate the potential for conversion. The most common cause, however, is local infection.

Pathophysiologic Changes in the Burn Wound

Intense inflammation is seen at about 7 to 10 days in deep burns. The rate of onset of inflammation depends on the blood flow to the wound, with inflammation occurring more rapidly in more superficial burns. A marked increase in wound vascularity is also seen. As wound blood flow increases, so do water loss and heat loss. Heat and water losses are further accentuated by the increase in core temperature that develops with the onset of hypermetabolism.14

Management of Burn Wound Infection

Pathogenesis of Burn Wound Infection

With loss of the outer skin barrier, bacteria can populate the burn wound.15 Most of these early colonizing bacteria are endogenous, originating from the heat-injured skin (especially hair follicles, glands, and so on), the nares and oropharynx, and the perineal and stool microflora. In addition, systemic host defenses are significantly impaired after a major burn17 (Table 99-1). Movement of organisms via hand contact, by patient and by personnel, from area to area on the patient—or between patients—is the major factor leading to bacterial contamination of the wound.

Use of Topical Antibiotics

The mainstay of infection control is the use of topically applied antibiotics. Silver sulfadiazine is the most common and least toxic. Mafenide is more potent and is reserved for the treatment of deep infections because of its toxicity (carbonic anhydrase inhibitor).14,15

Diagnosis of Wound Infection

In order to assess the wound for infection, a definition of infection must be well understood. Burn wounds are never sterile, even in the presence of topical agents or systemic antibiotics. The presence of bacteria on the wound surface or in the nonviable tissue is called colonization. Infection of the wound (or local wound sepsis), in contrast, indicates invasion of the underlying viable tissue. As infection progresses, the viable tissue and its blood vessels are invaded, and sepsis develops.14

The clinical diagnosis of wound infection is difficult. Fever, leukocytosis, tachycardia, and intermittent temperature spikes are seen characteristically in the burn patient with or without infection. Wound purulence is a reliable indicator of infection only if the purulence is in the subeschar space.11

The organism most often involved in wound infection, particularly in the first week, is Staphylococcus aureus.14,15 Infection with gram-negative organisms is more evident after the first week. Pseudomonas aeruginosa is present on the wounds of approximately 25% of burn patients. Enterococci and Candida albicans are now seen with increasing frequency, each being found in the wounds of about 50% of burn patients.

A reliable method of diagnosing a burn wound infection is bacterial analysis of a full-thickness wound biopsy.14,16 It has been established that 105 organisms per gram of tissue is the bacterial load that is preinvasive and indicates infection and the need for systemic antibiotics.

Early Wound Excision and Grafting

Early excision and grafting should be considered for all burns that will not heal by primary intention within 3 weeks. Full-thickness burns require grafting unless they are smaller than 3 to 4 cm in diameter. The more rapidly the wound is closed, the better. At least in theory, burns covering less than 30% of the TBS can be closed rapidly because adequate donor sites are available. Larger burns are more difficult, if not impossible, to graft early. Deep partial-thickness burns are also difficult to assess clearly as regards time to healing. Considerable judgment and assessment skills, therefore, are essential (Fig. 99-5).

Pain and Stress Control

Management of pain and anxiety is of extreme importance and should begin soon after the burn injury to avoid accentuation of the stress response to injury, with further catabolism. Since pain and stress are present at all times and are amplified by wound management, a continuous background use of narcotics—often patient-regulated or continuously infused kind—is used. Low doses of benzodiazepines are also used. Burn patients are very prone to the extrapyramidal side effects of phenothiazines.15,19,20 In many cases, the dosages of all drugs must be increased because of rapid drug clearance when the patient is in the hypermetabolic state.23