A 42-year-old man is brought to the emergency department immediately after having a seizure. His family describes a medical history of generalized tonic-clonic seizures. The patient has been on valproic acid for the past 10 years but stopped taking the drug 6 months ago as he had no seizures in the last 9 years. He is otherwise healthy and had been doing well until this seizure episode. He does not use tobacco, alcohol, or illicit drugs. The patient is afebrile. Blood pressure is 105/68 mm Hg, pulse is 96/min, and respirations are 18/min. Pulse oximetry shows 99% on room air. The patient appears confused and lethargic. Chest auscultation is unremarkable, and the abdomen is soft and nontender. A limited neurologic examination is nonfocal. Laboratory results are as follows:
| Serum chemistry | |
| Sodium | 140 mEq/L |
| Potassium | 4.0 mEq/L |
| Chloride | 103 mEq/L |
| Bicarbonate | 17 mEq/L |
| Blood urea nitrogen | 20 mg/dL |
| Creatinine | 0.8 mg/dL |
| Glucose | 98 mg/dL |
Arterial blood gas shows pH 7.24. Chest x-ray and urinalysis are within normal limits, and a CT scan of the head is unremarkable. Which of the following is the most appropriate next step in management of this patient's metabolic acidosis?
This patient has anion gap metabolic acidosis that is likely due to postictal lactic acidosis. Seizure activity, especially a tonic-clonic seizure, can significantly raise serum lactic acid levels due to skeletal muscle hypoxia and impaired hepatic lactic acid uptake. The postictal lactic acidosis is typically transient and self-limited and typically resolves within 90 minutes. Therefore, the most appropriate management of this patient is observation and a repeat chemistry panel after approximately 2 hours. If the metabolic acidosis has not resolved, other potential causes of anion gap metabolic acidosis (eg, intoxication, sepsis) should be investigated.
(Choice A) The risks and benefits of treating acute metabolic acidosis with sodium bicarbonate are not entirely clear; however, it is generally recommended in patients with severe acute metabolic acidosis with pH <7.1. Administration of sodium bicarbonate may cause myocardial depression and increased lactic acid production; therefore, in patients with pH >7.1, the relatively small benefits of sodium bicarbonate do not typically outweigh the risks.
(Choice B) An elevation in the serum amylase level is nonspecific as it can occur in a variety of disease processes (eg, acute pancreatitis, HIV, lymphoma, rheumatologic disease). Serum amylase levels do not play a role in the management of metabolic acidosis.
(Choice C) The common causes of metabolic acidosis due to ketosis include diabetes, alcoholism, and starvation. Ketosis due to seizure activity is not typical.
(Choice E) Serum ammonia levels have minimal clinical use and do not play a role in the management of metabolic acidosis.
(Choice F) Norepinephrine acts as a positive inotrope and vasoconstrictor and is often used in patients with lactic acidosis due to hypotension and poor organ perfusion (eg, sepsis) that persists following fluid resuscitation. Although this patient's metabolic acidosis is likely due to lactic acidosis, the inadequate oxygen delivery to skeletal muscle due to seizure activity was transient and is now resolved. This patient's confusion and lethargy are consistent with a typical postictal state rather than cerebral hypoperfusion.
Educational objective:
Postictal lactic acidosis commonly occurs following a tonic-clonic seizure. It is a transient anion gap metabolic acidosis that resolves without treatment within 90 minutes following resolution of seizure activity.