La enfermedad por quemaduras como modelo de respuesta inflamatoria sistémica

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Abstract

La quemadura corporal es una violenta agresión que modifica todos los mecanismos de la homeostasis orgánica y por su connotación clínica y social es un problema que enfrentan los servicios médicos en la sociedad contemporánea. Desde el punto de vista fisiopatológico, en el paciente quemado se desarrolla un Síndrome de Respuesta Inflamatoria Sistémica (SRIS) caracterizado por la hiperactivación de todos los mecanismos de defensa. La disregulación de estos mecanismos conduce al daño de los tejidos propios cuyas consecuencias se expresan en alteraciones morfofuncionales de todos los sistemas. Con independencia de la etiología, evolución inicial, manejo terapéutico y respuesta individual, la sepsis generalmente complica la evolución del gran quemado. En este trabajo, se presentan elementos clínicos e histopatológicos de la enfermedad por quemadura y se comentan los mecanismos moleculares de la respuesta inflamatoria sistémica destacando el papel de los mediadores de la comunicación intercelular.

Translated abstract

A body burn is a violent agression that modifies all the mechanisms of organic homeostasis and is also a problem facing the medical services in the contemporary society because of its clinical and social connotation. From the physiopathological viewpoint, a burned patient develops a systemic inflammatory response characterizaed by hyperactivation of all its defense mechanisms. The de-regulation of such mechanisms leads to damage of tissues which is expressed as morpho-functional modifications of all systems. Regardless of the ethiology, initial evolution, therapeutic management and individual response, sepsis generally complicates the evolution of burn injuries. This paper sets forth the clinical and histopathological elements of burn-related diseases and comments on the molecular mechanisms of systemic inflammatory response, underlining the role of the intercellular signalling mediators.

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Most cited references 58

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Septic Shock in Humans

Joseph E Parrillo (1990)

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Selected treatment strategies for septic shock based on proposed mechanisms of pathogenesis.

Charles Natanson (1994)

To review selected new therapies for septic shock designed to inhibit bacterial toxins or endogenous mediators of inflammation. Scientific journals, scientific meeting proceedings, and Food and Drug Administration advisory committee proceedings. Preclinical and clinical data from trials using core-directed antiendotoxin antibodies and anticytokine therapies for sepsis and studies in animal models of sepsis from our laboratory. Ten clinical trials using core-directed antiendotoxin antibodies produced inconsistent results and did not conclusively establish the safety or benefit of this approach. Both anti-interleukin-1 and anti-tumor necrosis factor (TNF) therapies have been beneficial in some animal models of sepsis but did not clearly improve survival in initial human trials, and one anti-TNF therapy actually produced harm. Neutrophils, another target for therapeutic intervention, protect the host from infection but may also contribute to the development of tissue injury during sepsis. In a canine model of septic shock, granulocyte colony-stimulating factor increased the number of circulating neutrophils and improved survival, but an anti-integrin (CD11/18) antibody that inhibits neutrophil function worsened outcome. Nitric oxide, a vasodilator produced by the host, causes hypotension during septic shock but may also protect the endothelium and maintain organ blood flow. In dogs challenged with endotoxin, the inhibition of nitric oxide production decreased cardiac index and did not improve survival. No new therapy for sepsis has shown clinical efficacy. Perhaps more accurate clinical and laboratory predictors are needed to identify patients who may benefit from a given treatment strategy. On the other hand, the therapeutic premises may be flawed. Targeting a single microbial toxin such as endotoxin may not represent a viable strategy for treating a complex inflammatory response to diverse gram-negative bacteria. Similarly, the strategy of inhibiting the host inflammatory response may not be beneficial because immune cells and cytokines play both pathogenic and protective roles. Finally, our scientific knowledge of the complex timing of mediator release and balance during sepsis may be insufficient to develop successful therapeutic interventions for this syndrome.

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Leukotoxin, a linoleate epoxide: its implication in the late death of patients with extensive burns.

K Kosaka, K. M. Suzuki, M Hayakawa … (1994)

Burn death based on circulatory shock is often encountered after recovery from primary shock in patients with deep and extensive burns, i.e., late death. Several toxic substances have been proposed, however, the responsible substance remains obscure. Since we have found leukotoxin, a highly cytotoxic linoleate epoxide biosynthesized by neutrophils, in the burned skin, in the present study we determined plasma leukotoxin concentrations in various degree of 30 burn patients. C-reactive protein and circulatory white blood cells were also measured. A significantly high mortality rate of patients with extensive burns (burn surface area over 70%) was observed compared with that in patients with burn surface area under 70%, and significantly high leukotoxin concentrations were observed within a week, and 3 weeks after the thermal injury in patients with extensive burns compared with those in patients with burn surface area under 70%. There were two peaks of plasma leukotoxin concentrations, i.e., the early phase (within 1 week) and the late phase (over 1 week) in patients with extensive burns. Plasma leukotoxin concentrations significantly correlated with burn surface area in the early phase, and similar correlations were observed in the late phase. A significantly high mortality rate (61%) of patients with peak leukotoxin concentrations over 30 nmol/ml was observed compared with 8% for those below 30 nmol/ml. Plasma leukotoxin concentration correlated significantly to C-reactive protein concentration, log (leukotoxin nmol/ml) = 0.042 x C-reactive protein (mg/dl) + 0.74, (r = 0.83, P < 0.01) in the late phase. From these results, it is concluded that leukotoxin is produced in patients with burns particularly in the late phase of extensive burns, and leukotoxin might play an important role in the tissue destructive procedure associated with severe burns.

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Author and article information

Journal

Journal ID (publisher-id): ibi

Title: Revista Cubana de Investigaciones Biomédicas

Abbreviated Title: Rev Cubana Invest Bioméd

Publisher: ECIMED (Ciudad de la Habana, , Cuba )

ISSN (Print): 0864-0300

ISSN (Electronic): 1561-3011

Publication date (Print and electronic): August 1999

Volume: 18

Issue: 2

Pages: 77-85

Affiliations

[01] Ciudad de La Habana, orgnameInstituto de Ciencias Básicas y Preclínicas Victoria de Girón. Cuba

Article

Publisher ID: S0864-03001999000200002 Publisher ID: S0864-0300(99)01800202

SO-VID: 036c2af0-2604-46ff-aefa-cfaba61b5607

License:

This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

History

Date received : 29 September 1998

Date accepted : 19 July 1999

Page count

Figures: 0, Tables: 0, Equations: 0, References: 48, Pages: 9

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SciELO Cuba

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