Chapter 1: | Historical Perspective and the Development of Modern Burn Care |
Fluid resuscitation, by contrast, was rarely practiced before WWII. In 1945 the Medical Research Council of the United Kingdom reviewed 1200 admissions from 1937 through 1941 to the Glasgow Royal Infirmary and discovered that one-half of deaths occurred within the first 24 hours and 72 percent within 3 days. Only 4 patients received intravenous plasma or serum.7 Similarly, Artz and Fox found that the “majority” of burn patients in this era died from inadequate or inappropriate fluid replacement.18
Three developments formed the foundation for the method of burn resuscitation used today. First, Underhill, writing in 1930 about his experiences following the Rialto Theatre fire in New Haven, Connecticut, of 1921, argued that the toxemia theory was “an obstruction.” Rather, anhydremia, or loss of water from the blood, magnified “the circulatory deficiency” (ie, shock). “The thick, sticky blood…finds great difficulty in passing through the capillaries…the tissues in general suffer from inadequate oxygenation…the heart pumps only a portion of its normal volume.” Tissue damage and inflammation caused increased capillary permeability and loss of plasma-like fluid. This was manifested by an increase in hemoglobin, which could also be used as an index of resuscitation. Therapy should consist of intravenous, oral, subcutaneous, and/or rectal infusions of saline solutions, at a rate not to exceed 1.5 liters per hour.42
Second, Blalock in 1931 demonstrated that thermal injury in unresuscitated dogs caused loss of over half of the total plasma volume as interstitial edema fluid. He concluded that “fluid loss probably is the initiating factor in the decline of blood pressure”—not toxemia. He also revealed the protein content of edema fluid to be almost as high as that of blood. Interestingly, he did not (at that time) propose that these fluid losses be replaced, but incorrectly speculated that tannic acid and other escharotics might effect a reduction in fluid loss rates.43
The third major contribution was the demonstration that plasma, now available in sufficient quantities for clinical use, could be used to resuscitate burn patients when guided by burn-size-based formulae to estimate plasma dose. Use of plasma for burn resuscitation was described by several authors after 193944-46; consistent with Underhill’s recommendations, complex formulae based on frequent determinations of the hematocrit or hemoglobin were used to adjust the infusion rate. Mass production of plasma was begun by the Blood for Britain program under Dr Charles Drew et al. in August 1940.47 As a consequence, plasma was used in the treatment of the approximately 300 thermally injured casualties admitted to the US Naval Hospital Pearl Harbor following the Japanese attack.10 At the National Research Council meeting of January 7, 1942, chaired by I. S. Ravdin, Harkins proposed for far-forward military use (where laboratory facilities for calculation of the hematocrit were not available) the first formula for resuscitation based on burn size, known as the first aid formula. Fifty ml of plasma were to be given per percent total body surface area burned (TBSA), “in divided doses.”46,48 Later, he defined a more rapid initial rate of infusion—one-third of the estimated volume given in the first 2 hours, one-third in the next 4 hours, and one-third in the next 6 hours.49 It should be noted that this volume is considerably less than would be recommended by later formulae. After the Cocoanut Grove fire, Cope and Rhinelander reported giving plasma to all but 10 of the 39 patients admitted to MGH. In a fortuitous modification of the NRC formula,
In Cope and Moore’s follow-up paper of 1947, a further refinement called the surface area formula is described: 75 ml of plasma and 75 ml of isotonic crystalloid solution per TBSA, with one-half given over the first 8 hours and one-half over the second 16 hours. The urine output was to be used as the primary index of resuscitation.51 Subsequent refinements of this basic concept included the following:
The net effect of this effort was the virtual elimination of postburn renal failure during the early 1950s and a reduction in burn shock as the cause of postburn death by approximately 13%. Currently, the hazards of over-resuscitation (extremity and abdominal compartment syndromes, airway and pulmonary edema, progression of wound depth)56