SUMMARY. A 52-year-old patient suffered burns in 69% T13SA. The cause of the accident was a flare-up of his clothing, which was soaked in diluent fluid. Prior to the trauma the patient had been suffering from a duodenal ulcer. Prophylaxis of stress bleeding was performed by H2 blockers. In spite of this treatment, there was massive bleeding from the stomach, and by day 16 post-burn surgical treatment became indispensable. The bleeding continued and the patient had to be treated with terlipresin and subsequently with somatostatin. The side-effect of this treatment was a hypertensive reaction and the onset of severe, haemodynamically significant arrhythmia. The patient was treated with intravenous nitroglycerin and a variety of antiarrhythmics for 46 days. The burned areas were treated by necrectomies and transplants. A further complication was osteomyelitis of the right hip bone. The cause of the thromboeytosis remains unclear. Rehabilitation of the patient still continues.

Burn trauma is always a cause of tremendous stress for the afflicted person. Proof of this is the eleven-fold elevation of the catecholamine level. Bleeding from the gastrointestinal tract and other multiple stress complications can develop several hours or days following the trauma, caused by shock hypoxia, inhalation trauma, endotoxinaemia, and even iatrogenic factors. The psychological causes of stress include intense pain, the need to cope with an unexpected life situation, apprehension of repeated surgery, and fear of further life stigmatized by burn sequelae.

A 52-year-old man suffered burns in 69% T13SA on 24 October 1994. The cause of the accident was the flare-up of his clothing soaked in diluent fluid. Prior to the trauma the patient had been suffering from ulcer disease. First aid was performed in a local hospital where the patient was also treated with dexamethasone (total dose 12 mg). The patient was transported to the Burn Centre in Prague the same day, 8 h after the accident. Releasing incisions were performed and the burn areas were covered with dressing; an intravenous line, nasogastric tube, and urine catheter had already been inserted. The patient was treated in the usual way: fluid resuscitation, including crystalloids, and subsequently plasma, analgesics, intravenous heparin (10,000 u/day) for the prophylaxis of thromboembolic disease, together with H2 receptor inhibitors (cimetidine 1200 mg/day) and enteral feeding to prevent stress bleeding.
In spite of all these preventive measures, massive bleeding from the stomach with haematemesis and melaena occurred on November 7. Treatment with terlipresin was commenced (3 mg/24 h). Because of the failure of conservative therapy, surgical treatment was found the next day to be indispensable. A bleeding ulcer penetrating to the hepatoduodenal ligament was found in the lesser ventricular curvature. Suturing was performed. Bleeding continued and the patient had to be treated with with terlipresin for the following seven days. In view of the continued bleeding, terlipresin was replaced by somatostatin (6 mg/24 h) for 3 days, 4 mg/24 h for 1 day, and 1 mg/24 h for 1 day). During the haemorrhage period the patient was given 28 blood transfusions. The therapy with somatostatin was successful in the treatment of the gastric bleeding, but severe cardiac complications occurred during the terlipresin treatment (Fig. 1).

Hypertensive reactions and severe, haemodynamically significant tachyarrhythmias appeared. Hypertension was treated with nifedipine and nitroglycerin intravenously for 46 days. As the supraventricular tachyarrhythmias produced hypotension and consequently circulatory failure, various antiarrhythmic drugs were repeatedly applied in high doses (digoxin, verapamil, ajmaline, amiodaron and pindolol). There were temporary but significant diffuse ischaernic changes in the patient's ECG (horizontal depressions of ST segment and negativization of T waves). Localized myocardial lesions were not found. The conjunction of terlipresin application and of the rise of hypertension with haernodynamically significant arrhythmias was obvious.
The burned areas were treated by avulsion, necrectomy, xenotransplantation and, finally, autotransplantation.
During the course of hospitalization the patient was treated with several antimicrobial drugs because of infections in the burn wound and the respiratory and urinary tract; the iliofemoral joint and bone were also affected (Fig. 2). Different types of microbe were cultivated (Staphylococcus epidermidis, Staphylococcus aureus, Klebsiella pneumoniae, Pseudomonas aeruginosa, Enterococcus faecium, Enterobacter cloacae, Acinetobacter calcoaceticus, Serratia liquefaciens, Xantomonas maltophilia, Proteus mirabilis, Escherichia coli, and Aspergillus).

Six months after injury the patient started physiotherapy out of bed. A gastroscopic investigation was performed and scarring was found in the healed ulcer. An echocardiographic investigation was carried out on the same day. The kinetics of all the myocardial walls was quite normal and no impairment of myocardial function was found.
Fourteen days later the patient started to complain of pain in the right hip. Coxitis was diagnosed and Staphylococcus attreus was cultivated from the joint. Antimicrobial treatment was recommenced and correct external fixation was carried out because of dislocation of the right lower extremity towards the pelvis.
Another unusual phenomenon was a change in the thrombocyte count. The decreased number of thrombocytes was due to burn shock and massive bleeding. But the increase in the number of thrombocytes to more than one million is hard to explain. The patient was treated with dipyridamole and low-molecular heparin for this abnormality (Fig. 3).

Fig. 3 - Thrombocytes.

Discussion

Four questions arise with regard to this patient:

1. Was the gastric bleeding preventable?
2. Were the haernodynamically significant arrythmias the consequence of previous medical therapy?
3. What was the aetiology of the right hip bone inflammation ?
4. What was the cause of the thrombocytosis?

For the prophylaxis of gastrointestinal tract ulceration one can use as soon as possible food administration, antacids, H2 receptor inhibitors, and sucralphate .4 This patient was treated from the time of admission to the Burn Centre with H2 receptor inhibitors - cimetidine intravenously in continual doses and enteral feeding through a nasogastric tube. Gastric bleeding in this patient, who was suffering from ulcer disease, occurred in spite of all the preventive measures. At present we use mostly ranitidin and sucralphate in patients with a history of ulcer disease.
The prevalence of ischaernic heart disease among males in their fifties is high. It can be manifested by heart failure or arrhythmias. Severe vasoconstrictive hypertension and haemodynamically significant supraventricular tachyarrhythmias appeared in our patient during and after terlipresin therapy. Terlipresin is a synthetic polypeptide - an analogue of natural hormone from the posterior lobe of the hypophysis. It has extreme vasoconstrictive effects. Somatostatin is a 14-amino acid oligopeptide that inhibits gastrointestinal endocrine and exocrine secretion and motility as well as resorption within the digestive tract.
The ECG ischaemic changes in this patient were only temporary, since the echocardiographic investigation carried out in a later period showed a normal picture. For this reason the cardiac complications were considered a probable consequence of the previous medical therapy.
The right hip joint inflammation could have been caused by haematogenic transport of microbes or per continuitatem with the joint. It is difficult to establish what type of microbial translocation was more probable in this patient because of the multiple surgical procedures performed in the right lower limb.
The explanation of the remarkable thrombocytosis is unclear. The aggregability of thrombocytes was normal and the finding in bone marrow was also normal. The patient will be followed up in the haematology department for the possibility of the development of myeloproliferative disease without any relation to the burn trauma.

RESUME. Un patient âgé de 52 ans a été atteint de brûlures en 69% de la surface corporelle. La cause de l'accident était la flambée de ses vêtements imbibés de diluant. Précédemment le patient souffrait d'ulcères duodénales. Les Auteurs ont effectué la prophylaxie de l'hémorragie par stress moyennant les bloquants de l'H2, mais malgré ce traitement une hémorragie massive gastrique s'est produite et 16 jours après la brûlure le traitement chirurgical s'est révélé indispensable. Lhémorragie a continué et il fallait traiter le patient avec le terlipresin et ensuite par la somatostatine. Ueffet collatéral de ce traitement a été une réaction hypertensive et des arythmies hémodynamiquernent significatives. Le patient a été traité pendant 46 jours avec la nitroglycérine intraveineuse et divers médicaments antiarythmiques. Les zones brûlées ont été traitées avec des nécrectomies et des transplantations. Une autre complication successive a été l'ostéomyélite du col du fémur droit. La cause de la thrombocytose n'est past claire. La réhabilitation du patient continue.

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