Annals of Burns and Fire Disasters - vol. XIII - n. 2 - June 2000

ACUTE RENAL FAILURE IN SEVERE BURNS. CONCLUSIONS AFTER ANALYSES OF DEATHS DURING 1998

Belba M, Belba G.

Clinic of Burns and Plastic Surgery, University Centre Hospital, Tirana, Albania

SUMMARY. This article focuses on the presence of acute renal failure (ARF) in deceased patients during 1998. We describe the clinical situations in which ARF occurs. These include burn shock, massive necrotic tissue (especially in electrical and chemical), burns, endotoxic shock from gram-negative bacteria, and hypercatabolic states with multiple organ failure. We believe that there are two essential aspects that medical staff must keep in mind in the treatment of severe burns - prevention and the treatment of ARF.

Burns are one of the most serious of all pathologies, also with regard to the surgical and intensive care aspect of treatment. Although this is a surgical pathology, the burn patient experiences certain clinical situations in which intensive care becomes very important.
Thus, unlike other surgical pathologies, burns as an illness require initial intensive care for two or three days. This period coincides with the treatment of burn shock. During debridement or surgical interventions the patient is in a septic condition that lasts two to three weeks, depending on the elimination of nerotic tissue. In this period the patient needs intensive care and repeated anaesthetic procedures. The wound closure phase finds the patient in a catabolic condition with a negative nitrogen balance, requiring nutritional support in order to gain weight.
In prolonged courses of pathology there may be a disequilibrium of all physiopathological. indices (hydroelectrolytic and acid-base balance, haernatological condition, and nutrition). Failure to correct these in due time may subsequently aggravate the general prognosis and open up the way to complications. Among the possible complications that may occur in the treatment of severe burns is acute renal failure (ARF).
When we analysed deaths that occurred in our centre in 1998, we found that the frequency of ARF was low, but presented high mortality. In this article we will concentrate on this type of ARF, its time of appearance, treatment, and the clinical course. Parallel to these data we will provide other general data about the causes of death during 1998

Clinical material

During 1998 we hospitalized and treated 224 patients in the Intensive Care Unit in our Clinic of Burns and Plastic Surgery in Tirana. Of these, 170 were children and 54 were adult and elderly patients and, of these, 23 died (17 children and 6 adults). The overall mortality rate was 10.3%. The mortality in children was 10.0% and in adults 11.1%. The mean burn surface in the deceased patients was considerable (38% third degree). The most frequent aetiological causes of burns were scalds and flame. One-third of the patients presented immediately to our clinic; twothirds delayed from Six to twelve hours, having been sent on from district hospitals. Some 20% of the patients also suffered from other illnesses, such as dystrophy, miodystrophy, depression, and other conditions. Nearly all the patients presented to the clinic with burn shock. Death usually occurred in the first week post-burn and less frequently in other weeks. We have arranged the cases in groups on the basis of the cause of death (Table 1)

Table II presents the relationship between death and ARF as a directly fatal complication or as a consequence.

The analysis of mortalities indicates the most critical clinical situations and also gives details about particular cases.

1. Burn shock. Two patients, one a child and the other elderly, died of burn shock, with burns respectively in 80% and 50% TBSA. The causative agent was flame. The respiratory tract was also damaged. In these two cases we observed irreversible shock. Intensive reanimation with solutions and colloids was unsuccessful. The immediate cause of death was cardiorespiratory failure in the presence of ARF.
2. Toxic situation. All five patients were children aged about 2 yr, with a mean burn surface of 35% (thirdor second-degree). Although presenting late, the children overcame the burn shock phase and presented normal diuresis for three or four days. Later, as a result of absorption and the release of toxic burn products, the patients reacted negatively to therapy. They did not have the strength to survive later developments. Laboratory examinations revealed leukopaenia, early anaemia (after the second day), severe hypoproteinaemia, and "obstinate" hyperglycaemia. In spite of treatment the children died on day 3 or 4, before the onset of the typical symptomatology of septicaemia.
3. Cardiac arrest. There was only one case, a child with second-degree burns caused by clean water in 50% TBSA. We considered this case to be specific because from the second day the condition was evident and treatment was initiated for myocarditis. Clinically, we observed low cardiac output with consequences in the peripheral microcirculation. In spite of general intensive care with cardiotonics the patient died on day 3 post-burn.
4. Septic shock. Six children with this diagnosis died (mean BSA approximately 30%.) The children had not been treated in proper manner - two of them were very poorly. i On hospitalization all the patients presented a grain-negative infection, confirmed later by bacteriological analysis. The patients suffered septic shock at the end of the first week and died with a picture of paralytic ileus accompanied by irreversible ARF.
5. Septicaemia and staphylococcal scalded skin syndrome. We had only two cases, in which the septic course was accompanied by generalized eruptions of the skin similar to exfoliative dermatitis (in unburned skin). At the same time the wounds deteriorated with manifestations of renecrotization also in parts where there was a tendency for epithelialization. The diagnosis was also confirmed bacteriologically. In both cases ARF was fatal. The patients died on day 20 of treatment.
6. Non-ketotic hyperglycaemic-hyperosmolar coma. We made this diagnosis in one elderly patient with burns in 30% BSA. The nature of the accident was such that he received no immediate medical assistance - he presented to the clinic after 12 h. The patient had ARF symptoms which adequate rehydration prevented from aggravating. The patient did not present oliguria. In the next few days biochemical examination of the blood showed high levels of uraernia, creatinaemia, hyperglycaemia, acidosis, and polyuria. The patient did not regain equilibrium despite insulin treatment. He went into a non-ketotic coma from which died on day 13. According to the literature, this type of coma has a high mortality (over 50%). It occurs after hyperglycaemia and osmotic diuresis, but requires some predisposing factor, which in this case was local infection.¹In addition to the other factors the patient was old and had been very severely burned.
7. ARF. There were only three cases of manifest ARF These regarded one child and two adults with burns in about 40% BSA. Following ascertainment of ARF, diuresis was maintained with the help of diuretics. After some days the renal indices fell progressively, with high levels of uraernia and creatinaemia. The patients died respectively on the third, eleventh, and fourteenth day of treatment. A fundamental pathognomonic sign was the presence of myoglobinuria, especially in the two patients with electrical and chemical burns. Our opinion is that the aetiological factor of development of ARF was the great mass of tissue damaged by the thermal agent.
8. Multiple organ failure. In three children treatment of the burns was unsuccessful, and a tendency for non-healing of the wounds was observed. The children presented dystrophy and reduced immune forces, and they did not respond to therapy. The massive wounds became chronic and eventually led to multiple organ failure. In the final days the children lost strength and the immediate cause of death was the spread of infection from the wound. Two children died respectively on days 30 and 40 of treatment.

ARF is one of the possible complications of severe burns. In this study we do not present the incidence of this complication in burns - we describe the incidence of cases leading to the patient's death during 1998. We thus analysed 23 deaths, in 17 of which ARF was present. Of these patients only three died from primary ARF. Of the other patients, 14 died of indirect causes owing to various burns complications. ARF refers to clinical situations with the abrupt interruption of essential kidney functions. These situations are accompanied by a rapid and progressive increase in uricaemia and creatinaemia, with or without oliguria (< 500 ml/day). 
If we analyse the general causes of ARF we can theoretically group them into three types:

• pre-renal or functional ARF (inadequate perfusion)
• renal ARF (tubular, glomerular, or tubulo-interstitial damage)
• post-renal ARF (obstruction)

In everyday burns treatment practice we meet only the first two types of ARF. The third type is seen only very rarely, when coincidentally the burn also patient suffers from kidney calculosis. In most cases ARF is pre-renal and is caused by retardation and rehydration deficits. Immediately after the burn, the patient suffers from extracellular dehydration, which presents clinically as severe hypotension (shock state). As we treated burn shock contemporaneously, we were able to reduce the incidence of ARF and we consequently recorded a statistically very low mortality in this phase of the burn. In general, the clinical conditions in which ARF may occur after severe burns are as follows:

1. Hypovolaemia during burn shock, which proceeds proportionally to the severity of the pathology. This hypovolaemia is responsible in nearly all cases for pre-renal ARF tending towards renal ARF as result of inadequate treatment.
2. Massive presence of necrotic tissues after third- and fourth-degree electrical and chemical burns. From the first moment this can cause renal ARF or acute tubular necrosis. In such patients there is evidence of myoglobinuria and haemoglobinuria in the first urinary portions. This condition is more serious if the patient is aged or presents concomitant diseases. Analogously, the same clinical situation appears in patients with deep necrotic avulsion or in burns combined with the crush syndrome.
3. Septic period of the burn illness with or without bacteraernia. The presence of bacteraemia indicates that the clinical situation is aggravated as a result of systemic infection. If the condition develops unfavourably, the patient will suffer from endotoxaemia of septic shock, which may cause pre-renal or renal ARF. This last condition is subdivided into acute tubular necrosis and tubulo-interstitial nephropathy. The clinical picture is dominated by persistent hypotension due to the release of circulating toxins.
4. Hypercatabolic state after prolonged and unsuccessful treatment. This condition is manifested by dystrophy in all organs. The kidneys are mainly affected by renal ARF. We would emphasise that renal function is damaged gradually but increasingly until complete non-function.

In the above clinical situations, the treatment of severe burns has a poor prognosis if we consider patients suffering from ARF accompanied by other pathologies. This is because the burn itself is a very severe pathology with high mortality.
The object of laboratory examinations in cases of ARF is to assess progressive uraemia, acidosis, hyperkalaemia, and hyponatraemia. It is also possible to observe a progressive increase of creatinaemia, together with oligoanuria. Cases have to be monitored dynamically and continuously, in order to detect any alterations as early as possible.
It is also important to analyse the indices of renal failure as these reflect different aetiologies.With regard to ARF, it is essential to treat the cause. In severe burns, immediate preventive treatment is important - the only cases to be considered "unfortunate" should be those where the kidney is damaged directly. It is therefore imperative to initiate immediate appropriate treatment of hypovolaemic shock to prevent renal hypoperfusion. There must also be rigorous attention during the period of septicaemia in order to maintain non-vulnerability of the general equilibrium. It is necessary to monitor laboratory and clinical parameters closely for any sign of septic shock. Antibiotics should be used only at the proper time and in the proper quantity in order to protect the kidney from infection and from their toxicity.' Consultation with a nephrologist, with a view to possible dialysis, may also be in the patients' interest, if compatible with their clinical condition. Surgical intervention is useful because it eliminates necrotic tissue and reduces the frequency of ARF.

Conclusions

1. A comparison of data relative to the year 1998 with those of previous years indicates that the generalmortality of severely burned patients treated in our 3
   Intensive Care Unit fell considerably. This wasdue to the application of an intensive care protocol and its use adapted to each single case.
2. Our study indicated that ARF was a concomitant pathology in 73.9% of deaths, while primary ARF was evident in only 13%. A comparison of these data with those of previous studies shows that the incidence of primary ARF was lower than the incidence of pulmonary complications, but higher than the incidence of gastrointestinal complications.
3. Apart from its low frequency, primary ARF has a high mortality and is very difficult to treat. The essential moments in the treatment of the severely burned patient with a predisposition for ARF are, first, prevention by rehydration and, second, treatment with diuretics.¹⁰ We would emphasize that dialysis treatment is not so beneficial as in other pathologies.¹¹
4. Considering the high incidence of ARF as a concomitant disease, it is the medical staffs duty to increase vigilance and therapeutic capacity, especially during the septic phase of the burn illness.

RESUME. Ce travail considre la présence de 1'insuffisance rénale aigud (IRA) dans nos patients décédés en 1998. Les Auteurs fficrivent les situations cliniques oii FIRA se manifeste, qui incluent le choc de brûlure, le tissu nécrotique massif, particuli~rernent dans les brûlures électriques et chimiques, le choc endotoxique cause par les bactéries A Gram négatif, et les conditions hypercataboliques avec insuffisance organique multiple. Selon les Auteurs les deux aspects les plus importants dans le traitement des brûlures graves sont la prévention et le traitement de l'IRA.