Annals of Burns and Fire Disasters - vol. XIII - n. 4 - December 2000


Ramos C.G.

Department of Anaesthesiology. Hospital de Santo Antonio dos Capuchos. Lisbon. Portugal

SUMMARY. A brief description is given of the pathophysiology of the burn patient. indicating the three periods of its evolution: the resuscitation phase. lasting for the first 36 h: the early post-resuscitation phase. betsseen days 2 and 6; and the inflammation/infection phase. from day 7 until wound closure. Each phase is characterized by specific electrolyte imbalances. the management of ssrhich requires a thorough understanding of the changes that occur over time. For each electrolyte abnormality, an indication is given of the major mechanisms responsible and the main signs and symptoms, as well as their management.


Thermal injuries are responsible for many complications and deaths, and although a progressive improvement in outcome and sure ival after major burns has been recorded the management of such patients remains a challenge for all those involved in their care. The improvements in surviv al have been attributed, among other things, to a better understanding of the pathophysiological nature of thermal injuries.
The burn patient has a number of complex injuries that must be taken care of: in addition. the patient's condition changes substantially during the burn disease's evolution.
The initial post-burn period is characterized by cardiopulmonary instability (caused by- significant fluid shifts between compartments) and in many cases by direct injuries to the airways. With the onset of wound inflammation. immunosuppression, and infection the physiological and metabolic parameters change from those seen initially.
Therapeutics must therefore be based on know ledge of these changes in time. It is important to realize that many of the problems are predictable and can and should be prevented before they happen.
One of the many aspects of the care of the burn patient that must be monitored is the electrolyte balance. The correct approach will be considered with regard to three periods of time in relation to the main changes in each period:

  • the initial resuscitation period (between 0 and 36 h). characterized by hyponatraernia and hyperkalaemia;
  • the early post-resuscitation period (between days and 6). in which we consider hypernatraemia. hypokalaemia, hypocalcaemia, hypomagnesaemia. and hypophosphataetnia:
  • the inflammation-infection period (also known as the hypermetabolic period). which is most evident after the first week. when several imbalances may coexist, depending whether correction was performed. and. if so, how.

First period
In major burns. intravascular volume is lost in burned and unburned tissues: this process is due to an increase in vascular permeability, increased interstitial osmotic pressure in burn tissue. and cellular oedema. with the most significant shifts occurring in the first hours.
Hyponatraemia is frequent, and the restoration of sodium losses in the burn tissue is therefore essential hyperkalaemia is also characteristic of this period because of the massive tissue necrosis.
Hyponatraemia (Na) (< 135 mEq/L) is due to extracellular sodium depletion following changes in cellular permeability.
The extent of this process depends on the sev eritc of shock and can be minimized by early restoration of perfusion- in the injured tissues. Failure to achieve this can cause widespread orffan dysfunction  (Table I).


â BP. C0. CVP. GFR
á HR


Altered consciousness
Cerebral oedema




â = decreased, á = increaased, BP = blood pressure, CO = cardiac output,
CVP = central venous pressure, GFR = glomerular filtration rate, HR = heart rate

Table I - Clinical manifestations of hyponatraema

deficit is based on the following formula: (140-Na+) x 0.6 x weight (kg).
It is fundamental that sodium replacement should be performed xvith resuscitation fluids (lactated Ringer's. normal saline); sometimes two ampoules of sodium lactate are added to each 1000 ml of normal saline in order to increase osmolaritv;' volume replacement with blood and the reduction ofJ additional sodium losses are other important factors.
If a hypertonic solution is used to restore serum sodium. it should not be allowed to increase above 160 mEq/1 and the rate of increase should not exceed 1.5 mEq/h.
Hyperkalaemia (K+) (> 5.5 mEq/1) is mainly caused by- cell lvsis and tissue necrosis.
Manifestations of hyperkalaemia are more pronounced in acute hyperkalaemia, and in particular affect the cardiovascular system (cardiac changes depend on the rate of increase of K+ (Table II)

Cardiovascular ECG chames: T waves
Decreased P waves
QRS s~idenine
PR prolongation
  Heart block
Atria] asvstole
Ventricular tachvcardiaí'fibrillation
Asystole,,,diastolic cardiac arrest
Neuromuscular Confusion
Muscle weakness
ECG = electrocardiooratn

Table II - Clinical manifestations of hyponatraemia

Therapeutics should be performed in several steps:

1. Reverse potassium effects in cellular membrane with calcium chloride 10% (10 ml intravenously over 10 min):

2. Transfer extracellular potassium into cells with

  • glucose (250-500 m1 of Dl017cW)+insulin (5-10 U)

  • sodium bicarbonate (50-100 mEq over 5-10 min)

  • hyperventilation (consider. however. the possible complications ):

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.


ECG chances: C vaaves-
  T "aves flattenin_
  PR prolongation
  ST depression
  Ivivocardial dysfunction
  Labile arterial BP
  ]autonomic dysfunction
  Onhostatic hypotension
  Potentiation of digoxin toxicity


  ~ Ileus
  Respiratory failure


i Polyuria
  ]impaired concentrating abiliy)
  T ammonia production
  T bicarbonate reabsorption

sodium retention


1 insulin. GH
  and aldosterona secretion


Glucose intolerance
  Potentiation of: hppercalcaemia
GH = growth hormone

Table III - Clinical manifestations of hypokalaemia

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




Carpopedal spasm (Trousseau's sign)
  Masseter spasm (Chvostek's sign)
  Tetany / muscle spasms


ECG changes
  responsiveness to: digitalis
  (3-adrenergic agonists
  (- cardiac contractility
  Heart failure


Laryngeal stridor (laryngospasm)


Biliary colic

Table IV - Clinical manifestations of hypocalcaemia

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).






ECG changes
  Potentiation of digoxin toxicity



Table V - Clinical manifestations of hypomagnesaemia

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.


Impaired contractility


  impaired leukocyte / platelet function


Myalgia / arthralgia
  Skeletal myopathy


Metabolic acidosis
  Impaired oxygen delivery


  Renal tubular acidosis


  Hepatic dysfunction


  Reduced vital capacity
  Respiratory failure




Skeletal demineralization

Table VI - Clinical manifestations of hypophosphatacmia.

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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This paper was received on 11 June 2000.

Address correspondence to:
Dr C.G. Ramos. Department of Anaesthesiology
Hospital de Santo António dog Capuchos.
Lísbon, Portugal.


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