Annals of the MBC - vol. 4 - n' I - March 1991


Borgognone A., Gherardini G., Marinelli F.

Divisione di Chirurgia Plastica e Ricostruttiva e Centro Ustioni, Ospedale S. Eugenio, Roma, Italia

SUMMARY. The multiple aspects which constitute the bum syndrome indicate a possible single mechanism activated by disseminated intravascular coagulation. This coagulation dysfunction could give rise to a process that causes frequent organ failure in burned patients. It was determined that multiple unrelated syndromes could be ascribed to massive clogging of the principal organs which work as strainers. It was observed that typical dysfunctions present in burned patients were caused by fibrinogen degradation products, clogs of platelets, and fibrin debris, which impair lung, kidney and liver filtration. If this mechanism of action is confirmed by further studies, a useful application in the field of therapy will be available for the care of burned patients.


We formerly considered bums in a singular and complicated pathological context; in severe bums, the damage often involved systemic impairment and failure of different organs., This multiple process could however be caused by a unique disorder which bears the semblance of unrelated clinical symptoms. Disseminated intravascular coagulation (DIC) may be interpreted as the real underlying cause of these numerous clinical pathologies (12, 13).

Materials and method

98 patients were admitted to our Bum Unit from January 1988 to August 1989; they were selected for their sex (50 males and 48 females), age (two groups: 1-15 years, 38 patients; over 15 years, 60 patients) and extent of lesions (under 50% of burned body surface: 61 patients; over 50% 37 patients); all burned skin areas were deep second- or third-degree.
Patients were tested every three days in order to monitor plasma prothrombin time (PTT), activated partial thromboplastin time (APTT) and fibrinogen degradation products (FDP), creatinine, nitrogen, glutamate oxalacetate transaminase (GOT), and glutamate pyruvate transaminase (GPT) plasma levels. Arterial blood was also valued for gases, electrolyte concentrations and acid base status, the values ranging respectively between: PTT 10.7-13 sec; APTT 18-27 sec. FDP over 10 nanog/ml was considered normal.
Data obtained from samples were elaborated to investigate anomalies of the coagulation fall and the involvement of renal, respiratory, and hepatic functions.


23 patients (23.4%) displayed grossly modified PTT and APTT (over 16 see; APTT over 31 see); of these, 19 (82.6%) had clinical evidence of coagulopathy and 18 (78.2%) died. Alterations of PTT and APTT depended on the severity of lesions: these patients in fact always had an extent of bum area greater than 50%.
21 patients had elevated FDP levels and 18 (85.7%) of these had raised PTT and APTT.
11 (22.2%) presented mildly to severely impaired hepatic function, with GOT and GPT plasma levels respectively up to 200 U/I and 260 U/1; 6 (54.5%) of these died.
Renal involvement was demonstrated in 19 (19.3%) patients, showing a blood urea nitrogen (BUN) plasma level ranging from 60 to 100 mg/dl, and creatinine over 2.5 mg/dl; their clinical complaints were oliguria and anuria, and finally acute renal failure: 18 (94.7%) of them died.
Only 5 (5.1%) patients developed respiratory complications. Blood gases were: P02 under 60 mmHg; PC02 over 45 mmHg. 4 (80%) of these patients manifested lung failure very similar to the adult respiratory distress syndrome (ARDS); their chest X-rays, repeated every 24 hours, were always characterized by bilateral pulmonary densities; all of them died because of respiratory failure, in spite of positive end expiratory pressure (PEEP) therapy.
A total of 4 (4. 1 %) patients had renal, hepatic and respiratory involvement along with PTT and APTT alterations suggesting DIC. All of them died.
PTT and APTT anomalies associated to renal failure alone were found in 15 (15.3%) patients, while the same anomalies along with respiratory or hepatic failure were found respectively in 4 (4.1%) and 10 (10.2%) patients.


Thermal injury produces a tissue damage which depends especially on the extent and depth of the involved area; however, cellular necrosis secondary to burn trauma starts through the delivery of many tissue by-products. This process causes the extrinsic coagulation fall (3, 7).
The activation of this pathway can overcome the normal inhibiting system which is either used up by trying to counteract the activated coagulation process (5) or lost through the increased permeability of inflamed vessel walls (1, 3, 10, 14, 17, 18).
The evolution of this course may be responsible for the impaired coagulation system which leads to DIC.
It is worth distinguishing two possible outcomes when the extrinsic coagulation pathway has been triggered in accordance with the availability of a sufficient amount of antiproteasis which controls the coagulation fall (2, 4, 6, 8, 9, 2 1).
In the first case this level is sufficient, and the process yields only a small amount of FDP; these, along with platelets, constitute reversible aggregates (21), which are not however, sufficient to give any clinical manifestation (15).
In the other case the antiproteasis level is low, and the process is not adequately counteracted, with a consequent increase in the FDP level.
When microclots reach organs or systems that are considered anatomical strainers, they clog their microcirculation (6, 11, 19).
The clinical result is the multiple systems failure which appears to be the unique sign of the working process.


DIC may be considered the actual cause of seemingly unrelated clinical deficiencies such as hepatic, renal and respiratory failure, the latter sometimes simulating ARDS.
These considerations may be hypothesized by the following:

  1. laboratory data nearly always indicate the presence of DIC when burn patients are routinely screened for haemostasis parameters;
  2. the usual administration of plasma products has been worthwhile in sQlyng many clinical aspects typical of burn patients;
  3. these may be further improved by use of heparin, which should be considered an important support in the bum syndrome.

With regard to coagulation anomalies, we believe that these could be considered an important mechanism through which the bum syndrome develops. A further possible therapeutic field in burn ma~agement has thus been disclosed.

RESUME Les aspects multiples qui constituent le syndrome de la brdlure indiquent un possible mécanisme unique activé par la coagulation intravasculaire disséminée. Cc dysfonctionnement de la coagulation pourrait causer un processus qui provoque fréquemment l'insuffisance organique chez les patients brfilés. Les Auteurs ont déterminé que des syndromes multiples non corrélés pourraient Etre dus au bouchage des principales organes qui forictionnent comme des filtres. Ils ont observé que les dysfonctionnements typiques présents chez les patients bi-é1és étaient causés par les produits de dégradation du fibrinogéne, les agrégats plaquettaires et les fragments de fibrine, qui altérent la filtration polmonaire, rénale et hépatique. Si cc mécanisme d'action est confirmé par des recherches ultérieures, on pourra disposer d'une application utile dans le champ de la thérapie des patients bri]51és.


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