When a patient with hyponatremic encephalopathy experiences respiratory arrest, therapy is unlikely to result in an outcome without brain damage ( AlVseLM 1992).
Among the 1 per cent of postoperative patients who become hyponatremic, more than 15 per cent develop encephalopathy (Ayys..JDd..,..Ad§ft.1996). Every postoperative patient is at risk of developing hyponatremia, and prophylactic measures are indicated. The most important measure includes the avoidance of intravenous hypotonic fluid to postoperative patients unless the patient is hypernatremic. The use of hypotonic fluid in postoperative patients has no place in modern medical practice as it can potentially lead to permanent brain damage or death; isotonic (154 mmol/l) NaCl is virtually always preferable.
Symptomatic hyponatremia is a medical emergency, with a morbidity in excess of 15 per cent (Ayys...and...ADMf...199.6). In patients with hyponatremic encephalopathy, the morbidity and mortality following correction by water restriction alone are unacceptable. Patients with hyponatremic encephalopathy should be constantly monitored, preferably in an intensive therapy unit. The first step in management of such patients is to ascertain that there is a secure airway, with assisted ventilation if required. Therapy should be initiated with intravenous hypertonic sodium chloride (514 mmol/l), using an infusion pump, with administration of a loop diuretic such as furosemide (frusemide). The infusion is designed to increase plasma sodium at a rate of about 1 mmol/l/h. If the patient has active seizures, the rate of hypertonic fluid administration should be adjusted such that the rise in plasma sodium is about 8 to 10 mmol/l/h over the initial 4 h, or until cessation of seizure activity. Therapy with hypertonic NaCl should be discontinued when either the patient becomes asymptomatic or the plasma sodium reaches a value in the range of 124 to 132 mmol/l. The plasma sodium should not be increased by more than 20 mmol/l during the initial 48 h of therapy and should not be acutely elevated to hyper- or normonatremic levels.
These guidelines require modification if patients are symptomatic at higher levels of plasma sodium (124-131 mmol/l) ( Fras.eLaD.d...,Ari§.ff..,1990; Aiy$...M.M 1992).
During the period that active correction of symptomatic hyponatremia is being carried out, plasma electrolytes should be monitored every 2 h until the patient has become neurologically stable. This regimen may require modification in patients with renal or cardiac disease. An estimate of the patient's total body water should be made at the start of therapy of symptomatic hyponatremia. Correction of the plasma sodium should initially be planned using intravenous 514-mmol/l NaCl, often combined with a loop diuretic (furosemide). The technique is as follows: infuse 514-mmol/l NaCl at a rate calculated to increase plasma sodium at a rate of 1 mmol/l/h for 24 h. For a 54-kg woman (assuming 26 liters of total body water) who is symptomatic and whose plasma sodium is 108 mmol/l, the aim is to raise the plasma sodium to about 128 mmol/l in 24 to 48 h. This is accomplished by infusing (using an infusion pump) 514-mmol/l NaCl at a rate calculated to increase plasma sodium at 1 mmol/l/h, i.e. (26 liters x 20 mmol/l) = 520 mmol NaCl in 48 h. Using 514-mmol/l NaCl, this will be
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