Ann. Medit. Burns Club - vol. VIII - n. 2 - June 1995

EXPERIENCE WITH THE TREATMENT OF POST-BURN DILUTION. AL HYPONATRAEMIA ASSOCIATED WITH CEREBRAL OEDEMA IN THE SHOCK STAGE IN SCALDED CHILDREN - REPORT ON FOUR CASES

Xin Z*, Shen-hai A.**, Xu-sheng L.**, Tian-de Y.**, Fu-qiang L.**

* Burn Ward, The General Hospital of Liao-Ning Province Armed Police, Shenyang, People's Republic of China
** Burn Institute, Southwestern Hospital, Chongqing

SUMMARY. This paper reports on the treatment of four scalded children seen in a one-year period suffering from dilutional hyponatraemia and cerebral oedema in the post-burn shock stage. The authors present their experience in this field and their method of dealing with complications, as well as matters related to early diagnosis and causes.

Post-burn disturbance of systemic fluid balance often occurs as a result of inadequate early antishock treatment. One of the commonest complications is dilutional hyponatraemia, which can easily lead to cerebral oedema. These two conditions have been recognized as major causes of burn death in children.' Between May 1993 and May 1994 four scalded children were admitted to our burn ward with a diagnosis of early dilutional hyponatraemia complicated by cerebral oedema. All the children were cured by prompt and adequate treatment.

The four children were all male and aged under two years. Total body surface area (TBSA) burned ranged from 15 to 30%. The most serious burns were deep second degree. All the children suffered shock in the early postburn stage (Table 1).

They also all presented symptoms of cerebral oedema, such as dysphoria, somnolence, convulsions, coma and vomiting. As a typical example, we will describe in detail the course of treatment of one of the children, Tan Liang, male, aged 21 months.

Tan Liang was scalded by boiling water in the prothotax and both legs (TBSA 20%, deep second degree). He was allowed to drink about 700 nil of water to satisfy his crying. thirst. He was treated in a local hospital with the intravenous injection of 500 tril of 5% glucose solution. During transfer of the child to our hospital, he vomited once, without production of blood. He was finally admit~ led to our burn ward eight hours post-burn, presenting coma, cool extremities and bipalpebral oedema. Physical examination of the patient showed: body temperature 39.3 'C; pulse 152 bpm; respiratory rate 28 bpm. The patient was immediately given low-flow rate nasal oxygen inhalation, intravenous drip of 5 ing dexamethasone, and direct intravenous injection of 50 tril of 20% mannitol. The immediate blood biochemistry examination showed: serum natrium ion (Na+) 121 mmol/1, and plasma osmotic pressure 250 mOsm/1. Thirty mI 3% NaCI were promptly infused and an ice cap was placed on the child's head. Six hours lata his conditon partially improved, and accordingly 3% Na Cl and colloid were infused successively. Mannitol was also given in relation to the ratio of infused fluid to diuresis, in order to reduce cerebral oedema, and, with the aid of furosemide to remove excessive water from the body, serum Na+ recovered to 127 mmol/1 24 hours post-burn, when the child regained consciousness. Tan Liang was cured by subcrustal healing 26 days post-burn and returned home without any sequelae.

Hypervolia is a common post-burn fluid disorder in children. The main cause is the increase of antidiuretic hormone (ADH) secretion induced by hypovolaemia' and the relatively low ability of free-water clearance by the kidneys. The oral intake of a large volume of salt-free fluid may easily induce dilutional hyponatraemia, which may then lead to cerebral oedema.
It is important to make the clinical diagnosis of dilutional hyponatraemia with cerebral oedema as soon as possible.

1. The diagnosis of dilutional hyponatraemia with cerebral oedema is not difficult if there is a history of intravenous or oral intake of a large volume of salt-free fluid.

2. Symptoms such as fever, convulsions, somnolence, apathy and eyelid oedema should be watched out for in cases of suspected cerebral oedema. The diagnosis should not be delayed until the appearance of tie and coma.

3. It is essential to examine blood biochemistry indices, especially serum natrium and plasma osmotic pressure. Both these indices usually decrease considerably.

On the basis of the above three points it is possible to make the diagnosis of dilutional hyponatraemia.
The principle of the treatment of dilutional hyponatraemia with cerebral oedema is therefore: limitation of water intake, accompanied by dehydration, which gradual~ ly correct the hypotonic state.

1. The first step is to suspend 5% glucose solution treatment and to replace it with colloid solution and hypertonic solution (3% NaCI) in order to raise the serum sodium ion level beyond 125 mmol/1 and the plasma osmotic pressure. It must however be remembered that it is not advisable to attempt complete correction too rapidly, as this may lead to severe circulatory overload. The amount of infusion of 3% sodium solution should depend on the serum natrium ion level and its deficit.

2. Diuresis: 20% mannitol is injected intravenously with the conditional application of furosemide, in order to provoke diuresis. Five to ten mg dexamethasone are administered two or three times daily to stabilize the cerebral cellular membrane and promote water discharge, in order to relieve cellular swelling.

3. Continuous low-flow oxygen for 2-3 days and use of the ice cap are recommended to reduce oxygen consumption and the cerebral cell metabolic rate, alleviate cerebral cellular injury and prevent cerebral sequelae. Sedative drugs such as phenobarbital or diazepam can be administered if patients show signs of twitching.

The most important consideration is the prevention of the development of dilutional hyponatraemia and cerebral oedema. The most effective method is the dissemination of health information. The key point is the avoidance of massive intake of pure water and of the infusion of glucose solution in the early shock stage post-burn.

RESUME. Les auteurs, après avoir décrit le traitement de quatre enfants atteints d'ébouillantement observés au cours d'une période d'une année qui présentaient hyponatrémie par dilution et oedème cérébrale dans la phase de choc post-brûlure, présentent leur expérience dans ce champ et leur méthode pour affronter les complications, comme aussi les questions qui concernent le diagnostic précoce et les causes.

BIBLIOGRAPHY

1. Kerrigan GA.: Water and electrolyte metabolism in pediatrics. In: Bland J.H. (Ed.): "Clinical metabolism of body water and electrolytes", 270-8 1. W.A. Saunders Co., Philadelphia & London, 1963.
2. Dempsten W.J.: Syndrome of inappropriate secretion of antidiuretic hormone. Lancet, 1: 970, 197 1.
3. Graef JW., Cone T.E. (Eds): Fluid and electrolytes. In: "Manual of pediatric therapeutics", 177-204. Little, Brown & Co., Boston, 2nd ed., 1980.