1.2Fluid Resuscitation and Early Management

1.2.1Fluid Resuscitation

As mentioned previously, patients with <10 % TBSA burn do not require fluid resuscitation. However, burn encompassing >15 % TBSA will require fluid resuscitation. Several formulas have been proposed for the resuscitation of the burn patient, all requiring crystalloid infusion with or without the addition of colloids. However, the mainstay of fluid resuscitation remains the Parkland formula:

4 ml× %TBSA× weight (kg ) = 24 h fluid requirement, with half given over the

first 8 h and the remainder over the following 16h

While the Parkland formula provides with the total amount for 24 h and starting level for initiation of resuscitation, it is not an absolute. The fluid resuscitation should be guided by physiological parameters and laboratory findings to prevent under/over-resuscitation. The goals of resuscitation should be restoration of intravascular volume, maintenance of organ perfusion and function, while preventing burn wound conversion.

In resuscitating a thermally injured patient, one must be cognizant of the three components of burn shock: cardiogenic shock, distributive shock, and hypovolemic shock. Each has a fundamental role in the pathophysiology of the burn patient and cannot be treated in a similar fashion. The myocardial depressant effects of inflammatory mediators post-burn injury has been well documented [4–8]. This typically last up to 36 h following which the patients’ cardiac function typically becomes hyper-dynamic.

Therefore, during the initial phase of burn resuscitation, the physician not only has to restore the patients’ intravascular volume but also might need to consider inotropic agents to aid the myocardial dysfunction.

1.2.2Endpoint of Burn Resuscitation

Traditionally the endpoints of resuscitation of a thermally injured patient have been determined via physiological parameters; however, the use of global end-organ functions such as urinary output, heart rate, and blood pressure is inadequate in determining the adequacy of resuscitation [9]. The addition of measurements of base deficit and lactate has become commonplace as markers of adequate resuscitation; however, it is difficult to ascertain their importance as markers of burn resuscitation as there are multiple episodes of ischemia and reperfusion injury with fluctuation in serum lactate and base deficit level [10]. In some studies, it appears that elevated lactate and base deficit levels on admission do correlate with overall organ dysfunction and mortality; however, there is no absolute number or threshold, which determines non-survivability [11–14]. Moreover, further studies have concluded that elevated lactate level is an independent risk factor for mortality [15–17].

Since at this juncture, there is no ideal method for determining the endpoints of resuscitation, some researchers have begun to adopt new techniques. Light et al.