Seizure metabolic acidosis with

Management of methanol and ethylene glycol poisoning is similar. Symptomatic support of respiration and circulation is augmented by correction of metabolic acidosis with intravenous bicarbonate infusion, and control of seizures with diazepam. Ethanol inhibits the metabolism of methanol and ethylene glycol to the toxic metabolites, and can give time for further treatment. The goal is to maintain blood ethanol concentrations between 100 and 150 mg per decilitre, sufficient to saturate alcohol... 

The major concern of the emergency department physicians was the lethargy, hypotonia, and seizure activity. Initial laboratory studies revealed that the child had a normal complete blood count and smear. Other blood tests revealed metabolic acidosis with a bicarbonate concentration of 11 mEq/L (normal is 20-25 mEq/L) and an anion gap of 22 mEq/L (normal is < 15 mEq/L). His serum glucose, calcium, and magnesium concentrations were normal. To exclude the diagnosis of meningitis, a spinal tap was performed. The cell counts and chemistries of the cerebrospinal fluid were normal. The physicians considered that the child might have sepsis and administered antibiotics and intravenous fluids. Prior to administration of antibiotics, blood, urine, and cerebrospinal fluid were sent for bacterial culture. 

The normal concentration of methemoglobin is <1.5% of total hemoglobin. In otherwise healthy individuals, methe-mogiobin levels up to 20% cause only cyanosis. Concentrations between 20% and 50% may cause dyspnea, exercise intolerance, fatigue, weakness, and syncope. More severe symptoms of dysrhythmias, seizures, metabolic acidosis, and coma are associated with methemoglobin concentrations of 50% to 70%, and levels >70% may be lethal. All of these symptoms are a consequence of hypoxia associated with the diminished O2 content of the blood and with a decreased O2 dissociation from hemoglobin species in which some, but not ah, subunits contain heme iron in the ferric state (i.e., shift of dissociation curve to the left). The PO2 is normal in... 

C. This may be followed by an abrupt relapse with coma, shock, seizures, metabolic acidosis, coagulopathy, hepatic failure, and death. Yersinia enterocolit-ica sepsis may occur. 

Chronic or large ingestions of propylene glycol have been associated with the development of hyperosmolar anion-gap metabolic acidosis, renal dysfunction, hemolysis, cardiac arrhythmias, and seizures. 

Most patients with pyruvate-carboxylase deficiency present with failure to thrive, developmental delay, recurrent seizures and metabolic acidosis. Lactate, pyruvate, alanine, [3-hydroxybutyrate and acetoacetate concentrations are elevated in blood and urine. Hypoglycemia is not a consistent finding despite the fact that pyruvate carboxylase is the first rate-limiting step in gluconeogenesis. 

Cardiovascular Effects. In a recent report on the clinical treatment of phenol poisoning, Langford et al. (1998) provide a summary of a case report in which a woman accidentally consumed an ounce of 89% phenol which had been mistakenly been given to her in preparation for an in-office procedure. Her immediate reaction upon consuming the phenol was to clutch her throat and collapse, and within 30 minutes she was comatose and had gone into respiratory arrest. Treatment was initiated with an endotracheal intubation. Ventilation with a bag and mask led to the detection of a lamp oil odor. Within an hour she developed ventricular tachycardia which responded to cardioversion however, she subsequently developed (in the first 24 hours) supraventricular and ventricular dysrhythmias, metabolic acidosis, and experienced a grand mal seizure. After a 15-day hospital stay, she was completely recovered with no evidence of impaired motility or compromised gastrointestinal or cardiovascular systems. 

Metabolic acidosis follows, and an increased anion gap results from accumulation of lactate as well as excretion of bicarbonate by the kidney to compensate for respiratory alkalosis. Arterial blood gas testing often reveals this mixed respiratory alkalosis and metabolic acidosis. Body temperature may be elevated owing to uncoupling of oxidative phosphorylation. Severe hyperthermia may occur in serious cases. Vomiting and hyperpnea as well as hyperthermia contribute to fluid loss and dehydration. With very severe poisoning, profound metabolic acidosis, seizures, coma. 

The cardiac arrhythmias are life-threatening, so the patient must be closely monitored, with facilities available for possible resuscitation. Drugs such as quinidine and procainamide are contraindicated, but lidocaine, propranolol, or phenytoin has been used safely and effectively. The arterial blood gas levels, pH, and electrolyte concentrations should be monitored so that metabolic acidosis or hypokalemia can be identified that would further aggravate the arrhythmias. Electrical pacing may be required if the antiarrhythmic drugs fail. Hyperpyrexia is treated by cooling. Seizures may be managed by intravenous doses of diazepam. 

Phosphate An intracellular shift of phosphate occurs along with potassium as fluid rehydration commences.The phosphate deficit can also be worsened with correction of the metabolic acidosis. Controlled, randomized studies have shown that routine phosphate repletion is not necessary, but some practitioners think it prudent to provide supplemental phosphate if serum phosphate levels are less than 1 mEq/L, potentially reducing the risk of seizure or tissue ischemia. During intravenous phosphate administration, serum calcium concentrations should be monitored carefully to avoid hypocalcemia and tetany (Fisher and Kitabchi, 1983). 

A gasping syndrome in small premature infants who had been exposed to intravenous formulations containing benzyl alcohol 0.9% as a preservative has been described (SEDA-10, 421) (SEDA-11, 475) (6-8). The affected infants presented with a metabolic acidosis, seizures, neurological deterioration, hepatic and renal dysfunction, and cardiovascular collapse. Death was reported in 16 children who received a minimum of 99 mg/kg/day of benzyl alcohol. This metabolic acidosis is caused by accumulation of the metabolite benzoic acid and is mainly related to an excessive body burden relative to body weight, so that the load of the metabolite may exceed the capacity of the immature liver and kidney for detoxification. The FDA has recommended that neither intramuscular flushing solutions containing benzyl alcohol nor dilutions with this preservative should be used in newborn infants. 

Acute poisoning with isoniazid in children (48) and adults (13,26,35) causes recurrent seizures, profound metabolic acidosis, coma, and even death. In adults, toxicity can occur with the acute ingestion of as little as 1.5 g of isoniazid. Doses larger than 30 mg/kg often produce seizures and 80-150 mg/kg or more can be rapidly fatal. The first signs and symptoms of isoniazid toxicity usually appear 0.5-2.0 hours after ingestion, by which time peak absorption occurs (49), and include nausea, vomiting, slurred speech, dizziness, tachycardia, and urinary... 

Acute intoxication with phenylbutazone is dominated by metabolic acidosis, which can progress to coma, seizures, hypotension, shock, and oliguria. Kidney and liver reactions, acute bone marrow depression, and acute perforation of peptic ulcer have all been described (5,11,35). 

After a valproate overdose a 27-year-old man developed seizures, hypernatremia, respiratory failure, metabolic acidosis, liver failure, and bone marrow depression (125). His plasma valproic acid concentration was 1414 pg/ml. Treatment with hemodialysis was effective in enhancing valproic acid clearance, while hemoperfu-sion was relatively less effective, because of saturation of the column. Overall, the half-Ufe of the drug was reduced from over 20 hours before treatment to less than 3 hours during hemodialysis/hemoperfusion drug removal was probably favored by saturation of drug binding to plasma proteins, which resulted in a low unbound fraction (32% at the start of treatment). He was comatose for 5 days but recovered fully thereafter. 

Animals may manifest toxicity to salicylates with signs and symptoms similar to those seen in humans. These may include fever, hyperpnea, seizures, respiratory alkalosis, metabolic acidosis, gastric hemorrhage, and kidney damage. Methemoglobinemia has also been seen in animals following salicylate toxicity. Activated charcoal has been used in animals. Methylene blue or ascorbic acid may be utilized for the treatment of methemoglobinemia. 

There is no specific antidote. Supportive care should be instituted for all patients with history of serious boric acid exposure. Substantial recent ingestions may benefit from administration of activated charcoal. Fluid and electrolyte balance, correction of acid/base disturbance, and control of seizures are essential to therapy. Hemodialysis has been successfully used to treat acute boric acid poisoning. Sodium bicarbonate may be used for any metabolic acidosis. 

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