Magnesium and Electrolytes in Head Injury Cases

Factors associated with hypophosphatemia include nasogastric suction, liver disease, sepsis, alcoholism, and acidosis associated with diabetic ketoacidosis. Various drugs such as P-binding antacids, catecholamines, beta-adrenergic agonists, Na bicarbonate, acetazolamide, and (when administered via a gastro-tube) sucralfate can contribute significantly to the development of hypophosphatemia [16] . Also, refeeding hypophosphatemia after starvation for a period as short as 48 hrs occurs commonly in critically ill patients in the ICU [17] . Poor nutritional status predisposes to this syndrome. Thus, as with hypomagnesemia, a combination of many factors may put ICU patients at risk for hypophosphatemia. Polyuresis induced by cerebral injury increases this risk even further, as demonstrated by the results of our study. Hypophosphatemia is associated with weakness of respiratory muscles [11] [12] [13] , respiratory infections [12] , and ventricular tachycardia [14] . Thus, clinical outcome in ICU patients may be adversely affected by hypophosphatemia.

The mechanism through which patients with severe head injury could be put at risk for the development of electrolyte disorders is unclear. A shift of electrolytes from the extracellular to the intracellular compartment may have taken place; electrolyte loss through induction of polyuresis by cerebral injury may also have played a role. Residual urine volume was higher in group 1 than in group 2; however, the time period in which urine volumes were produced in group 1 is unknown, because we were unable to determine the last time that the patients had urinated before the occurrence of head injury. In addition, spontaneous urine loss could have occurred in group 1 patients at the scene of their accident; this would lead to an underestimation of residual urine levels.

Almost all patients in group 1 had diuresis in excess of 300 mL/hr in the period immediately preceding ICU admission and in the first 3 hrs of ICU stay, and urine production was significantly higher in group 1 than in group 2. Although this does not prove that polyuresis was the cause of electrolyte deficiencies in group 1, it seems likely that high urine production and renal excretion of electrolytes contributed to the occurrence of electrolyte disorders. Nine patients in group 1 had received a single dose of mannitol before electrolyte measurement; however, the average time interval between mannitol administration and electrolyte assessment was <60 mins. Moreover, there was no significant difference in electrolyte levels between group 1 patients who had received mannitol and those who had not. Thus, it seems highly unlikely that mannitol administration alone caused the differences between groups 1 and 2, although it may have been a contributing factor in some patients.

It is difficult to determine to what extent outcome in our patients was affected by the presence of electrolyte disorders. Survival was significantly lower in group 1; to some extent, this was to be expected in view of the difference in morbidity as indicated by higher APACHE II scores and the severity of disease in group 1. On the other hand, some of the factors leading to higher APACHE II scores in group 1 could be associated with electrolyte disorders present in group 1. For example, tachycardia and tachycardic arrhythmias leading to higher APACHE II scores in group 1 may have been, in part, induced by electrolyte depletion; episodes of low blood pressure were, in some cases, induced by tachycardia; and high Na levels and low K levels found in group 1 led directly to attribution of APACHE II score points. The use of antiarrhythmic medication in the course of ICU stay was higher in group 1, but it is unclear to what extent electrolyte disorders played a role in this difference. Moreover, measures to correct electrolyte disorders were initiated promptly when low levels of electrolytes were found in our patients. Thus, it remains unclear as to what extent these disorders contributed to the occurrence of arrhythmias in our patients.

In most ICUs, Na and K are measured routinely at admission in all patients, including those with cerebral injury. However, Mg and P are not measured on a routine basis; therefore, deficiencies in levels of these electrolytes are likely to remain undetected for a longer period of time. We feel that intensivists and others treating patients with severe head injuries should be aware of this potential problem and that levels of Mg and P should be measured on a routine basis in all patients with severe head injury.

We conclude that patients with brain injury are at a high risk for the development of hypomagnesemia and hypophosphatemia, as well as hypokalemia and (to a lesser degree) hypocalcemia. Increased urinary loss appears to be one of the factors contributing to electrolyte depletion; other, as yet unknown factors, induced by neurologic trauma may also play a role. Levels of Mg and P, as well as K, Na and Ca, should be determined frequently in these patients, and if necessary, adequate supplementation should be initiated promptly.

Critical Care Medicine
Volume 28 Number 6 June 2000

Kees H. Polderman MD, PhD
Frank W. Bloemers MD
Saskia M. Peerdeman MD
Armand R. J. Girbes MD, PhD

From the Surgical Intensive Care Unit (Drs. Polderman and Girbes) and the Departments of Surgery (Dr. Bloemers) and Neurosurgery (Dr. Peerdeman), University Hospital Vrije Universiteit, Amsterdam, The Netherlands.

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