Đang chuẩn bị liên kết để tải về tài liệu:
Chapter 046. Sodium and Water (Part 8)

The rate of correction of hyponatremia depends on the absence or presence of neurologic dysfunction. This, in turn, is related to the rapidity of onset and magnitude of the fall in plasma Na+ concentration. In asymptomatic patients, the plasma Na+ concentration should be raised by no more than 0.5–1.0 mmol/L per h and by less than 10–12 mmol/L over the first 24 h. | Chapter 046. Sodium and Water Part 8 The rate of correction of hyponatremia depends on the absence or presence of neurologic dysfunction. This in turn is related to the rapidity of onset and magnitude of the fall in plasma Na concentration. In asymptomatic patients the plasma Na concentration should be raised by no more than 0.5-1.0 mmol L per h and by less than 10-12 mmol L over the first 24 h. Acute or severe hyponatremia plasma Na concentration 110-115 mmol L tends to present with altered mental status and or seizures and requires more rapid correction. Severe symptomatic hyponatremia should be treated with hypertonic saline and the plasma Na concentration should be raised by 1-2 mmol L per hour for the first 34 h or until the seizures subside. Once again the plasma Na concentration should probably be raised by no more than 12 mmol L during the first 24 h. The quantity of Na required to increase the plasma Na concentration by a given amount can be estimated by multiplying the deficit in plasma Na concentration by the total body water. Under normal conditions total body water is 50 or 60 of lean body weight in women or men respectively. Therefore to raise the plasma Na concentration from 105 to 115 mmol L in a 70-kg man requires 420 mmol 115 -105 x 70 x 0.6 of Na . The risk of correcting hyponatremia too rapidly is the development of the osmotic demyelination syndrome ODS . This is a neurologic disorder characterized by flaccid paralysis dysarthria and dysphagia. The diagnosis is usually suspected clinically and can be confirmed by appropriate neuroimaging studies. There is no specific treatment for the disorder which is associated with significant morbidity and mortality. Patients with chronic hyponatremia are most susceptible to the development of ODS since their brain cell volume has returned to near normal as a result of the osmotic adaptive mechanisms described above. Therefore administration of hypertonic saline to these individuals can cause sudden osmotic