3. Remove potassium from the body by means of diuretics, potassium exchange resins. or. in serious cases, haemodialvsis.
It is mandatory to monitor carefully ECG and K+.

Second period
The early post-resuscitation phase is a period of transition from the shock phase to the hypermetabolic phase, and fluid strategies should change radically with a view to restoring losses due to water evaporation.The main changes in this period are:
A. Hypernatraemia (Na+) (> 115 mEq/1). This is caused by several mechanisms: intracellular sodium mobilization. reabsotption of cellular oedema, urinary retention of sodium (because of the increase in renin, angiotensin. and ADH), and the use of iso-/hypertonic fluids in the resuscitation phase.Hypernatraemia presents in various forms, depending on the amount of water retained: peripheral oedema, ascites, pleural effusion, and interstitial/a1-eolar oedema (with possible impaired ventilation) may dominate, or alternatively manifestations of dehydration may be more significant.
Therapeutics is performed with hypotonic~fluids (low sodium content, with or without glucose): NaCl 0.45% or DSc NaCI 0.-15%: in some cases it may be necessary to add diuretics. The amount of water necessary to bring Na+ back to normal is given by the formula: 0.6Jx weight (kg) x (Na+ initial/NaT desired -1).
Correction should be performed in such a way that the decrease in Na` does not exceed 1.5 mEq/h (there is a danger of cerebral oedema if correction is too quick).
B. Hypcoalaemia. This is most prevalent in the period following the first -18 h post-burn and is characterized by K+ < 3.5 mEq/l. It may be due to increased potassium losses (urinary-, gastric. faecal) and the intracellular shift of potassium because of the administration of carbohydrates; this imbalance is also increased by coexistinff hypomagnesaemia.

The symptoms can affect several organs, with greater or lesser severity (Table III) cardiac hypersensitivity to the arrhythmogenic effects of catecholamines, digoxin, and calcium are among the most dangerous complications.K Jo-is
In an attempt to prevent hypokalaemia it is advised to add '20-30 mEq/1 of potassium to the hypotonic fluids in order to compensate for urinary losses and intracellular shift; it is also mandatory to correct precipitating factors such as increased pH, hypomagnesaemia, and several drugs.
Potassium deficit is given by the formula (3.5 - K+) x 0.4 x. weight (kg).
It is fundamental to monitor the ECG and plasma K+ during correction of hypokalaemia to avert complications.
Potassium is usually replaced as chloride salt because any coexisting chloride deficiency may limit the ability of the kidney to conserve potassium; mild hypokalaemia (K+ > 2 mEq/1) is corrected by intravenous KCl infusion, usually at a rate of < 10 mEq/h; if severe hypokalaemia is present (i.e., when K+ is less than 2 mEq/1 or there are ECG changes or paralysis), the intravenous KCl infusion rate may reach 40 mEq/h; and in cases of digitalic toxicity, KCl should be administrated in bolus (0.5 mEq every 3 to 5 min) until ECG normalization.'2'°
C. Hypocalcaemia (Ca2+) (< 4.5 mEq/1 or < 8.5 mg/dl). This is apparent after the first 48 h post-burn and is more prevalent on day 4, lasting until 7 weeks post-burn. Whenever possible, it is advised to monitor the ionized fraction, which represents about 45% of total circulating calcium, as it is independent of pH and albumin and therefore gives more accurate values.'`°-'3
This electrolyte change occurs as a result of the calcium shift between fluid compartments and increased urinary losses.'
Clinical manifestations may affect all the organ systems, especially the cardiovascular and neuromuscular system (Table IV). 3-a

Hyperkalaemia potentiates cardiac abnormalities due to hypocalcaemia; treatment is therefore of particular importance in the post-burn period because non-correction may lead to delayed response to fluid replacement in the shock phase.
We should consider the use of intravenous calcium in the presence of certain symptoms (hypotension, tetany) or if Ca2+ is less than 3.5 mEq/1, with calcium chloride 10% (3-5 ml) or calcium gluconate 10% (10-20 ml) for 10-15 min, followed by elemental calcium (0.3-2.0 mg/kg/h); calcium infusion should be slow, owing to the risk of arrhythmia - it can also be responsible for the development of acidosis or phlebitis. It is essential to monitor ECG, blood gas, and serum Mg2+ (in order to exclude hypomagnesaemia) during calcium replacement. If it is possible to use the oral route, elemental calcium (500-1000 mg), should be given every 6 h; if hypocalcaemia continues to persist, an intermittent intravenous dose is advised, as required by each individual patient.
Correction should be continued until Ca2+ is greater than 4 mEq/1 or the ECG returns to normal.
Intravenous calcium should not be added to phosphate or bicarbonate in order to prevent precipitation.
D. Hypomagnesaemia (Mg2+) (< 1.5 mE/1). This appears also later than the first 48 h, and is most prevalent on day 3 day post-burn; this condition frequently coexists with hypocalcaemia and hypokalaemia and can cause treatmentresistant hypokalaemia.'" The commonest cause is excessive magnesium loss. The symptoms are few, except for severe hypomagnesaemia (Mg2+) (< 1 mEq/1) (Table V).

Magnesium deficiency is usually treated with magnesium sulphate solutions: in mild cases, oral or intramuscular routes can be used (10 mEq every 4-6 h), while symptomatic or severe depletion should be treated with a parenteral magnesium infusion of 48 mEq over 24 h. If serious symptoms are present (seizures, arrhythmias), it may be necessary to perform an intravenous administration of 8-16 mEq for 30-60 min (in some cases for only 5-10 min), followed by 2-4 mEq/h as continuous infusion; subsequent therapy should be guided by the serum magnesium level.
It is mandatory to monitor vital signs, renal function (if there is any impairment of renal function, the magnesium dose should be reduced by 50%), and the patellar deep tendon reflex (if this becomes depressed or disappears, magnesium infusion should be discontinued).
E. Hypophosphataemia. This is indicated by a serum phosphate concentration below 2.5 mg/dl and is considered serious if less than 1 mg/dl. This condition appears on about day 3 post-burn and is most prevalent on day 7.
Measurement of serum phosphate levels should be performed daily during the early post-burn phase, especially if renal function is impaired or if there is massive tissue injury or necrosis. The results should be carefully evaluated because ingestion of carbohydrates decreases serum phosphate.
Phosphate deficiency may result from several mechanisms, including fluid resuscitation, mobilization of interstitial oedema, increased circulating catecholamines, respiratory alkalosis, ingestion of phosphate-binding antacids, sucralfate, and carbohydrates, increased urinary and gastrointestinal losses, and concomitant electrolyte imbalances (hypokalaemia, hypomagnesaemia, hypocalcaemia).
Hypophosphataemia may cause tissue hypoxia because of an increased affinity of haemoglobin from oxygen and a consequent decrease in tissue ATP; this deficiency is asymptomatic in mild cases but can present as multi-organ dysfunction if severe (Table VI).
Hypophosphataernia should be prevented prior to the initiation of carbohydrate administration, gastric acid neutralization (with phosphate-binding antacids or sucralfate), or the administration of diuretics.

Prevention (if serum levels drop below 2 mg/dl) and treatment of asymptomatic hypophosphataemia are achieved by oral supplementation with elemental phosphorus, correction of other electrolyte abnormalities (hypomagnesaemia, hypocalcaemia, hypokalaemia), and maintenance of the acid-base balance; the oral route has the advantage of avoiding hypocalcaemia and metastatic deposition of calcium phosphate salts. If symptomatic, correction requires intravenous replacement with solutions of sodium or potassium phosphate, 2-5 mg/kg, infused over 6 h, with treatment continuing until the serum phosphate concentration exceeds 1 mg/dl."' After day 10 post-burn, the phosphorus delivered in diet and fluids is usually enough to keep serum phosphate levels above 3 mg/dl; occasionally, intravenous supplementation may be necessary if hypophosphataemia persists.

RESUME. L'Auteur décrit brièvement la pathophysiologie du patient br6lé et indique les trois périodes de son evolution: la phase de la reanimation qui persiste pendant les premières 36 h; la phase précoce post-reanimation, entre les jours 2 et 6; et la phase de 1'inflamtmation/infection, depuis le jour 7 jusqu'à la guerison des lesions. Chaque phase est caractéris6e par des d6séquilibres électrolytiques spécifiques, dont la gestion nécessite une compr6hension complète des modifications qui se produisent dans le temps. Pour chaque anomalie 1'Auteur indique les m6canismes principaux responsables et les signer et les symptómes les plus importants, comme aussi le traitement le plus approprié.

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