It was difficult to pool results between studies because of differing definitions of organ dysfunction or nonparametric data. Multiorgan and single-organ dysfunctions were either undefined (46) or used organ dysfunction severity scores such as the Multiorgan Dysfunction Score (MODS) (43, 45, 59) or the Sepsis-Related Organ Failure Assessment (60) score (47). To further increase heterogeneity of outcomes, organ dysfunction scores were reported as scores for one organ (43), daily scores (43, 45), or total score over 10 days (48). The incidence of multiorgan failure was reported in two studies (45, 46) with an overall nonsignificant result between groups (RR, 1.28; 95% confidence interval, 0.48–3.32; P = 0.64). Individual results reported in Table 5 on the whole studies found no difference between the groups or favored hemodynamic fluid guidance. No study revealed results in favor of HUO steered fluid resuscitation.
Results for fluid volumes administered in the first 24 h were conflicting, with some studies (42–46) (Table 5) using significantly higher volumes in the hemodynamic group in the first 24 h, whereas others (47) found a nonsignificant increase in the control group. Of note, the study finding decreased fluid volumes in the hemodynamic group (47) utilized a measure of fluid responsiveness (SVV%) as a titration endpoint compared with the measure of preload (ITBVI) utilized in other studies. When reporting daily fluid requirements expressed as mL/kg per TBSA%, an overall meta-analysis was unable to be calculated because of the nonparametric expression of data (Table 5).
Despite a number of studies showing a large increase in the fluid volume, there were no specific studies reporting pulmonary edema (43, 45), abdominal compartment syndrome (42, 44), and either no escharotomy procedures required (42) or no significance between groups (48). A combined analysis found a nonsignificant RR between groups for the incidence of renal failure (42, 43, 46) (RR, 0.77; 95% confidence interval, 0.39–1.43; P = 0.38) (Fig. 4).
Incidence of sepsis (without a specific definition) was investigated by two studies (45, 46), but a random-effects model (i2 = 56.4) overall found no difference between the two groups (RR, 1.35; 95% confidence interval, 0.54–3.39; P = 0.53).
Overall, this study had equivocal results. Although a mortality advantage was demonstrated in Figure 2 for all comparative trials, the result relied heavily on one cohort study with weak methodology (49). Two studies (43, 45) did report significantly better organ function on days 2 and 3, but a meta-analysis was unable to be performed. There were a number of limitations to this review, including the small number of studies, low subject numbers, and lack of assessor blinding. Pooled effect sizes could not be calculated for some outcome measures because of reporting of medians and IQR or heterogeneity of outcomes. However, the limited evidence indicates that a large multicenter randomized trial is warranted.
The understanding of shock overall has moved from global parameters to one of abnormalities of microcirculation and cellular metabolism, with sophisticated, relatively noninvasive technologies capable of real-time measurement (63, 66). There is some evidence mainly from observational studies that, during burn resuscitation, macroscopic parameters (blood pressure, urine output) can be satisfactory yet tissue perfusion inadequate (18, 20, 53, 57). While decreased UO indicates renal hypoperfusion, normal urine output cannot exclude the presence of malperfusion.
There are a number of reasons alternate endpoints to HUO may theoretically have an advantage in burns resuscitation. In the initial 48 h of burn, shock patients are known to be in the “ebb” stage with a generalized capillary leak, low PAOP, depressed cardiac function, and high systemic vascular resistance. After 48 to 72 h, cardiovascular parameters alter with systemic vasodilatation and high cardiac output. A number of authors utilizing hemodynamic endpoints (43, 52) reported earlier normalization of this stage with almost normal cardiac output at 5 h (52). It is not yet known whether this is a mechanical effect from targeting increased preload or the effect of improving oxygen delivery.
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