Annals of Burns and Fire Disasters - vol. IX - n. 3 - September 1996


Dauti L, Andrea A., Osman X.H.

Hospital 2, Department of Burns and Plastic Surgery, Tirana, Albania

SUMMARY. This paper considers the nature of burn shock, which is the main cause of mortality unless local and systemic treatment is correctly administered. The primary and secondary manifestations are described. The effects of burn shock are described in relation to 75 burn patients. Sodium plasma concentrations were significantly reduced, while potassium plasma levels rose considerably in 29 patients. An increase in glycaemia was seen in 28 cases; 29 cases presented haemoglobinuria and bilirubinuria due to haernolysis. Serious complications were prevented by fluid replacement and the treatment of hydroelectrolytic and metabolic disturbances. All the patients who died were suffering from critical burns and were admitted to the Burns Department after a considerable delay.


Burn shock is the first consequence of deep and extensive burns and constitutes the main cause of mortality if local and systemic treatments are not correct and timely.
Burn shock - a type of hypovolaemic shock - in the first stages is dominated by disturbances in membrane permeability accompanied by oedema, exudation and evaporation. Secondary manifestations of these processes include plasma loss, haemoconcentration, increased blood viscosity and all the haemodynamic consequences that these imply. Without intensive therapy, circulatory shock will follow.

Materials and method

Bum shock was observed in our patients with intermediate and full-thickness burn involving 15% BSA (and less than 15 % in patients aged over 65 or under IS years).
During the study period, 75 patients were treated in our Burn Center (8% of all patients); the main cause of death was burn shock. Burn shock usually appeared within the first 2-12 hours after the thermal trauma and always before 24-36 hours. In these last cases the patients were admitted to the hospital after some delay.
In critical burns, disturbances in membrane permeability in the burn area may result in secondary disturbances in various organs, as a result of reduced perfusion and consequent hypoxia.
The loss of fluid and protein, particularly alburnins, causes a decrease in oncotic-osmotic pressure.
Determination of sodium and potassium in plasma after severe burn injuries showed a significant drop in sodium concentration; potassium levels rose markedly in 29 cases, while hyponatraemia with normal levels of potassium was observed in 6 cases.
In 28 cases an increase in glycaemia was observed. This was the consequence of the disturbances of glucose metabolism and the increase of glycogen secretion in the pancreas B cells of pancreas. We believe that ketacholamines could be high, but we were unable to determine this.
In 29 cases, haemoglobinuria and bilimbinuria were observed. These were caused by haemolysis.
The correct and rational treatment of burn shock, fluid replacement, and the treatment of hydroelectrolytic and metabolic disturbances improve the function of the visceral organs and prepare the patient for surgery. This treatment prevents the occurrence of serious life-threatening complications. All such procedures have to be carried out as soon as possible.

In our study all the patients who died were patients with critical burns who were not admitted in good time (Table 1).

Delay of hospitalization after trauma (hours)

N' cases %


16 21.4


36 48.0


18 24.0


5 6.6

Table 1 - Number of patients with burn shock in relation to time of hospitalization in our Burn Centre

The treatment of burn patients with burn shock was based on the Baxter/Parkland formula: 4 m] x body weight x % burned BSA (half administered in the first 8 hours and the remaining half in the following 16 hours).
Infusion therapy consisted of lactated Ringer's solution and sodium bicarbonate. Valium was given for pain relief; Phenergan and pethidine were also used. Vitamin C was administered 1-1.5 gr/day as the enzymatic regulator of cellular processes. Oxygen therapy was used in all cases.


The hydroelectrolytic disturbances occurring after injuries are responsible for conditions that favour the development of burn shock.
Disturbances in membrane permeability are accompanied by oedema, plasma loss, haemoconcentration, increased blood viscosity, and hypomobility of circulating plasma. Hypo-oedema and haemoconcentration reduce capillary perfusion, which can lead to organ damage. Hypoxia blocks the Krex cycle, and there is consequently an interruption of glucose metabolism and the onset of metabolic acidosis. These disturbances may lead to cell disturbances in the burn area and the main organs. The most serious complication is acute post-burn pulmonary distress, in which case the prognosis is reserved.


  1. Critical burns are frequently accompanied by hypovolaemic shock.

  2. The time of hospitalization of patients with critical burns is very important in relation to the treatment of burn shock and prognosis.

  3. Early treatment of burn shock decreases mortality.

RESUME. Cet article considère la condition de choc causée par les brûlures, qui est la cause principale de la mort si le traitement local et systémique n'est pas correct. Les Auteurs, après avoir considéré les manifestations primaires et secondaires du choc, présentent les résultats de leurs observations de 75 patients brûlés. Les concentrations plasmatiques de sodium étaient réduites en manière significative, tandis que les niveaux plasmatiques de potassium étaient élevés dans 29 patients. La glycémie était élevée dans 28 cas, et 29 cas présentaient l'hémoglobinurie et la bilirubinurie à cause de l'hémolyse. Les complications graves peuvent être évitées par le remplacement des fluides et le traitement des problèmes hydroelectrolytiques et métaboliques. Les patients décédés, tous atteints de brûlures critiques, ont été hospitalisés dans le Centre de Brûlés avec un fort délai.


  1. Arturson G.: Bum shock. Scand. J. Plast; Reconstr. Surg., 8: 112-8, 1974.
  2. Mayer A.C.: Bums shock and plasma volume regulation. Saint-Luis, 151:355,1978.
  3. Pepi G.: New concepts for the treatment of burn patients during shock period. Metingi Medical, 1979.
  4. Schumer W. et a].: Treatment of shock. Philadelphia, 3: 200, 1974.
  5. Andrea A.: Study of combustional shock. Folc Medical Review, 2:67, 1980.
  6. Astrup P.: The acid base metabolism. A new approach. Lancet:1035, 1969.
  7. Dauti I.: Surgical treatment of early burn. Dissertation: 24-30, 1986.
  8. Monafo W.W: New concepts in burn shock efficacy ofhypertonic lactated saline solution. Rev. Latino-amer. Chir. Plast., 17: 63-74, 1973.
  9. Perna L.: Hydroelectrolytic and nutritive reanimation in burns.Metingi Medical, Tirana, 1986.
  10. Arturson G.: Experimental and clinical studies of capillary permeability in burns. Bahamas Int. Conf. on Burns: 151-82, 1963.
  11. Hall VK: The treatment of burn shock. Bums, 5: 107-12, 1978.
  12. Zhuka E: Treatment of burn shock patients during the first 48 hours.Surgical considerations. 5: 15, 1983.

This paper was received on 1 June 1995.

Address correspondence to: Dr 1. Dauti, Hospital 2, Department of Burns and Plastic Surgery, Tirana, Albania.


Contact Us