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.
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
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.
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.
Maintenance of hemodynamic stability from 36 hours to 6 days after the burn injury.
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.