Blood Concentration Changes in Extensive Superficial Burns, and Their Significance for Systemic Treatment

Underhill, Frank P.

doi:10.1001/archinte.1923.00110190034003

Cited by 73 publications

(10 citation statements)

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“…Before the 19th century, it was demonstrated that after a burn, fluid is lost from the blood, so that blood becomes thicker, and in 1897, saline infusions for severe burns were first advocated (40,41). Cope and Moore (42) demonstrated that hypovolemia resulted from fluid and protein translation into burned and nonburned tissues, whereas Underhill et al (43) demonstrated that unresuscitated burn shock results in increased hematocrit values in burned patients. In recent years, many mechanisms have been addressed to cause fluid loss, and many inflammatory mediators have been identified that seem to induce systemic burn shock after thermal injuries (4,44).…”

Section: Discussionmentioning

confidence: 99%

Burn Plasma Transfer Induces Burn Edema in Healthy Rats

Kremer

Abé²,

Weihrauch³

et al. 2008

Shock

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Thermal injuries greater than 20% body surface area (BSA) result in systemic shock with generalized edema in addition to local tissue destruction. Burn shock is induced by a variety of mediators, mainly immunomodulative cytokines. This experimental study evaluates if burn shock can be induced in healthy rats by transfer of burn plasma (BP) with mediators. Thermal injury was induced by hot water (100 degrees C water, 12 s, 30% BSA) in male syngenic Wistar rats. Donor rats were killed 4 h posttrauma, and BP was harvested. Burn plasma was transferred to healthy animals by continuous intravenous infusion in three types of dilution (100%, 10%, and 1%). Positive controls were directly examined 4 h after thermal injury, and negative control rats had a continuous infusion done with sham burn (SB) plasma (37 degrees C water, 12 s, 30% BSA). Afterwards, intravital fluorescence microscopy was performed in postcapillary mesenteric venules at 0, 60, and 120 min. Edema formation was assessed by relative changes over time in fluorescence intensity of fluorescein isothiocyanate-albumin in the intravascular versus the extravascular space. The interactions of leucocytes and endothelium were evaluated by quantification of leukocyte sticking. Additionally, microhemodynamic (volumetric blood flow, erythrocyte velocity, venular wall shear rate, venular diameters) and macrohemodynamic parameters (blood pressure, heart frequency, temperature) were assessed online (arterial catheter). For statistics, an ANOVA was performed with Bonferroni adjustment procedure. Differences were considered significant when P < 0.05. There are no statistically significant differences in microhemodynamics or macrohemodynamics between study groups. Burn plasma infusion and thermal injury lead to significant increases in fluorescein isothiocyanate-albumin extravasation, whereas SB plasma shows no significant changes. Even BP diluted in 0.9% saline (10% and 1%) results in a similar transvascular flux of plasma proteins as direct thermal injury. Differences between positive controls and BP infusion are not significant, whereas all groups are statistically different from the SB group (P<0.05). Leukocyte sticking is significantly increased in all groups except the SB group, and the number of adherent leukocytes is dose dependent. The present study demonstrates that as early as 4 h after thermal injury, there are sufficient factors (e.g., cytokines) in BP to induce systemic burn shock in healthy rats even in diluted plasma (1%). However, the "key" cytokines are not identified at this point. The burned tissue is no longer required for burn shock induction, and the pathophysiologic process seems to be self-perpetuating as early as 4 h posttrauma. Leukocytes are activated by thermal injury and BP infusion. The role of leukocyte-endothelium interactions for edema formation remains uncertain and requires further investigation.

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Section: Discussionmentioning

confidence: 99%

Burn Plasma Transfer Induces Burn Edema in Healthy Rats

Kremer

Abé²,

Weihrauch³

et al. 2008

Shock

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“…Before the nineteenth century, investigators demonstrated that after a burn, fluid is lost from the blood and blood becomes thicker; and in 1897, saline infusions for severe burns were first advocated [14,15]. However, a more complete understanding of burn pathophysiology was not reached until the work of Frank Underhill [16]. He found that unresuscitated burn shock correlates with increased hematocrit values in burned patients, which are secondary to fluid and electrolyte loss after burn injury.…”

Section: The Systemic Responsementioning

confidence: 99%

Pathophysiology of burns

Keck

Herndon

Kamolz

et al. 2009

Wien Med Wochenschr

112

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Burn injury represents a significant problem worldwide. Advances in therapy strategies, based on better understanding of the pathophysiologic responses after burn injury have improved the clinical outcome of patients with burn injuries over the past years. This article describes the present understanding of the pathophysiology of a burn injury including both the local and systemic responses, focusing on the many facets of organ and systemic effects directly resulting from hypovolemia and circulating mediators following burn trauma.

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“…Dupuytren was perhaps the fi rst to describe an approach to fl uid replacement in burns patients that was based on the management of cholera during the 1 830 s [1] . Following the Rialto Theater fi re in Connecticut in 1921, Underhill showed that ' burn shock ' was the result of fl uid shifts and proposed that a salt and protein solution should be used in the management of burn patients [2] . Cope and Moore published the Burn Budget Formula in 1947 based on their experiences with the Coconut Grove fi re victims, using colloid, saline and lactated Ringer ' s solution [3] .…”

Section: Discussionmentioning

confidence: 99%