Status epilepticus acidosis

A 10-year-old child had status epilepticus controlled with a combination of valproate, oxcarbazepine, and 48 hours of propofol infusion in a dose of 5.5 mg/kg/ hour. After weaning from propofol, a classic ketogenic diet was instituted in an attempt to provide long-term control of the seizures. A day later status epilepticus recurred and propofol was restarted at a rate of 6-9 mg/ kg/hour to suppress seizure activity (the diet, valproate, and oxcarbazepine were also continued). Shortly thereafter, he developed the classical constellation of malignant ventricular arrhythmias, hyperlipidemia, rhabdomyolysis, lactic acidosis, and biventricular cardiac failure. He did not survive. 

Two men, aged 7 and 17 years, presented with refractory status epilepticus. Both were treated with high-dose propofol infusions to achieve burst suppression on the electroencephalogram. During the second day of propofol infusion there was progressive severe lactic acidosis, hypoxia, pyrexia, and rhabdomyolysis, followed by hypotension, bradydysrhythmias, and renal dysfunction, leading to death. The total doses of propofol were 1275 mg/ kg over 2.7 days and 482 mg/kg over 2 days. 

Pentazocine in overdose can cause generalized tonic-clonic seizures, hypertension, hypotonia, dysphoria, hallucinations, delusions, and agitation, with a poor response to naloxone (15). Others have reported status epilepticus, coma, respiratory depression, acidosis, severe hypotension, and ventricular dysrhythmias. 

The transfer of intracellular K" into ECF invariably occurs in acidosis as H shifts intraceHularly and shifts outward to maintain electrical neutrality. As a general rule, K concentrations are expected to rise 0.2 to 0.7 mmol/L for every 0.1 unit drop in pH. When the underlying cause of the acidosis is treated, normokalemia will rapidly be restored. Extracellular redistribution of may also occur in (1) dehydration, (2) shock with tissue hypoxia, (3) insulin deficiency (e.g., diabetic ketoacidosis), (4) massive intravascular or extracorporeal hemolysis, (5) severe burns, (6) tumor lysis syndrome, and (7) violent muscular activity, such as that occurring in status epilepticus. Finally, important iatrogenic causes of redistribution hyperkalemia include digoxin toxicity and P adrenergic blockade, especially in patients with diabetes or on dialysis. ... 

B. Specific drugs and antidotes. Pyridoxine (vitamin Bg) is a specific antidote and usually terminates diazepam-resistant seizures and results in improved mental status. Administer at least 5 g IV (see p 499) if the amount of INH ingested is not known If the amount is known, give an equivalent amount in grams of pyridoxine to grams of ingested INH. Concomitant treatment with diazepam may improve outcome. If no pyridoxine is available, high-dose diazepam (0.3-0.4 mg/kg) may be effective for status epilepticus. Pyridoxine treatment may also hasten the resolution of metabolic acidosis. 

A. Severe metabolic acidosis resulting from intoxication by methanol, ethylene glycol, or salicylates or from excessive lactic acid production (eg, resulting from status epilepticus or shock). 

Federman MD, Kelly R, Harrison RE. Refractory metabolic acidosis as a complication of high-dose midazolam infusion for pediatric status epilepticus. Clin Neuropharmacol 2009 32(6) 340-1. 

The authors reported that the clinical manifestations of coma, status epilepticus, cardiogenic shock, metabolic acidosis, and pulmonary edema were compatible with previously reported fatal cases of acute diphenhydramine poisoning. 

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