Verlauf und therapie einer akzidentellen Maggi®-vergiftung mit tödlichem ausgang

Incidence of life-threatening hypernatremia due to intoxication in adults is rare. Depending on the rate of its onset severe hypernatremia causes cellular dehydration resulting in extracellular fluid shift. CNS symptoms such as convulsions, lethargy and coma are most common. Typical complications are intracranial bleeding in the early course while cerebral edema can occur secondary to seizures or intracranial bleeding as well as a result of brisk lowering therapy of hypernatremia. To prevent those eventually life-limiting complications, intensivists should be familiar with the management of acute hypernatremia. We report on a case of fatal hypernatremia due to accidental ingestion of a sapidity agent. Case report: A 26-year old patient with mental retardation accidentally ingested about 875 ml of a flavor intensifier called "Maggi®" containing a total amount of 227.5 g sodium chloride and 2.62 g sodium glutamate, respectively. Serum-sodium peaked at 176 mmol/l, 4 hours after ingestion. Besides immediate diluting-therapy, infusion of glucose 5% as well as therapy with furosemide was started. Another 10 hours after ingestion, hypertensive crisis, generalized convulsions and respiratory depression occurred. Intubation and mechanical ventilation were started. At that time, CCT and CT angiography showed subarachnoidal bleeding, generalized cerebral edema with imminent cerebral herniation and lack of cerebral venous blood flow. Criteria of brain death were fulfilled and the patient succumbed 10 days after admission. Conclusion: Threatening hypernatremia despite normal renal function is rare, but instantaneous management of this complication can become a vital aspect. Sodium restriction, administration of glucose 5% and diuretics are recommended as a first-line therapy. In case of renal dysfunction or life threatening hypernatremia, extracorporeal elimination procedures like hemodialysis or hemodiafiltration could possibly be necessary within the first 1-2 hours. In chronic cases of hypernatremia, when there was enough time to permit the production of "idiogenic osmoles", more gradual correction of serum sodium is needed to limit rapid intracellular shifts of water and electrolytes. The ideal rate for serum sodium decrease is between 10-15 mmol per day. The role of sodium glutamate in the development of cerebral edema in our case remains unclear. Existing data in the literature suggests that glutamate could enhance the formation of cerebral edema. However, a total amount of 2.62 g glutamate does not seem enough to effectuate cerebral edema alone.