Can a generalized tonic‑clonic seizure cause a severe high anion‑gap metabolic acidosis (bicarbonate 11 mmol/L, anion gap ≈ 26 mEq/L) in a 13‑year‑old girl?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 21, 2026View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Can a Generalized Tonic-Clonic Seizure Cause Severe High Anion-Gap Metabolic Acidosis?

Yes, a generalized tonic-clonic seizure can absolutely cause severe high anion-gap metabolic acidosis with bicarbonate of 11 mmol/L and anion gap of 26 mEq/L in a 13-year-old girl, and this acidosis typically resolves spontaneously within 60–90 minutes without specific treatment. 1

Mechanism and Expected Severity

Seizure-induced lactic acidosis is a well-established phenomenon that occurs immediately following grand mal seizures due to intense muscular activity and tissue hypoxia. The metabolic derangement can be profound:

  • Immediately post-seizure, mean venous lactate reaches approximately 12.7 mEq/L, with bicarbonate dropping to around 17 mmol/L and arterial pH falling to approximately 7.14 1
  • The anion gap elevation correlates directly with lactate accumulation, as lactate is an unmeasured anion 1
  • In your patient with bicarbonate of 11 mmol/L and anion gap of 26 mEq/L, these values are consistent with—though slightly more severe than—typical post-ictal lactic acidosis 1

Time Course and Spontaneous Resolution

The acidosis resolves spontaneously through lactate metabolism and hydrogen ion removal, typically normalizing within 60 minutes. 1 Specifically:

  • At 60 minutes post-seizure, lactate falls to approximately 6.6 mEq/L, bicarbonate rises to 23.6 mmol/L, and pH normalizes to 7.38 1
  • This spontaneous resolution occurs without any specific intervention beyond supportive care 1
  • The rapid improvement distinguishes seizure-related acidosis from other causes of severe lactic acidosis 1

Critical Distinguishing Feature

Seizure-induced lactic acidosis does NOT cause hyperkalemia, despite severe systemic acidemia. 1 This is a unique characteristic that helps differentiate it from other causes of severe metabolic acidosis:

  • Serum potassium remains stable throughout the acidotic episode and recovery phase 1
  • Other causes of severe metabolic acidosis (e.g., diabetic ketoacidosis, toxic ingestions) typically present with hyperkalemia when pH drops below 7.2 2

Essential Differential Diagnosis

While seizure-induced lactic acidosis is the likely explanation, you must actively exclude other causes of severe high anion-gap metabolic acidosis, particularly in a 13-year-old: 3

Immediate exclusions required:

  • Diabetic ketoacidosis: Check glucose (should be >250 mg/dL in DKA), serum/urine ketones 3, 4
  • Toxic ingestions: Obtain comprehensive toxicology screen including methanol, ethylene glycol, salicylates; calculate osmolar gap using 2 × [Na⁺] + (glucose/18) 3, 4
  • Sepsis/shock: Assess for signs of tissue hypoperfusion (tachycardia, prolonged capillary refill >2 seconds, altered mental status beyond post-ictal period, hypotension) 2

Key laboratory evaluation:

  • Arterial blood gas, complete metabolic panel, serum lactate 3
  • If anion gap >27 mEq/L with suspected toxic alcohol ingestion, emergent hemodialysis is indicated due to mortality exceeding 20% 4

Management Approach

For seizure-induced lactic acidosis, treatment is purely supportive—no bicarbonate therapy is indicated. 3, 1

  • Bicarbonate administration is contraindicated unless arterial pH falls below 6.9–7.0, as it generates CO₂ and may worsen outcomes 3
  • Ensure adequate oxygenation and ventilation to facilitate lactate metabolism 1
  • Monitor serial electrolytes and repeat blood gas at 60 minutes to confirm expected spontaneous improvement 1
  • If acidosis persists or worsens beyond 90 minutes, aggressively pursue alternative diagnoses 3, 1

Clinical Pitfall to Avoid

Do not assume all severe acidosis post-seizure is benign lactic acidosis. 3 The seizure itself may have been triggered by an underlying metabolic derangement (hypoglycemia, toxic ingestion, inborn error of metabolism in younger patients) that requires specific treatment 2, 3. Always obtain glucose immediately, as hypoglycemia <3 mmol/L can both precipitate seizures and cause acidosis 2.

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

High Anion Gap Metabolic Acidosis in Pediatric Patients

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Guideline

Management of Abnormal Anion Gap

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2026

Related Questions

What causes high anion gap metabolic acidosis?
What are the causes and treatment options for a patient with high anion gap metabolic acidosis, considering potential underlying conditions such as lactic acidosis, ketoacidosis, or toxic ingestions, and taking into account the patient's medical history, including diabetes or kidney disease?
What does an anion gap of 15.2 indicate and how should I manage the high‑anion‑gap metabolic acidosis in a patient with lactate 7.3 mmol/L, glucose 456 mg/dL, bicarbonate 15 mmol/L, pH 7.30, hypertension, bilateral crackles, left pleural effusion, and severe pallor?
What are the causes of anion gap metabolic acidosis?
Is a patient with severe metabolic acidosis and hyperkalemia, as indicated by bicarbonate (HCO3) level of 6, anion gap of 21, and potassium (K+) level of 5.5, in breach of Health Canada's safety guidelines for discharge?
According to the latest ESPAC‑4 trial data, what is the 5‑year overall survival percentage for a 62‑year‑old patient with a 3‑cm pancreatic head adenocarcinoma who underwent a standard pancreatoduodenectomy with R0 (margin‑negative) resection and has lymph‑node involvement (N1) and perineural invasion, and what first‑line adjuvant chemotherapy regimen (gemcitabine plus capecitabine: drug names, doses, schedule) is recommended for optimal survival?
How should impulsive behavior that emerges after initiating or increasing an SNRI be evaluated and managed?
What is the appropriate diagnostic work‑up for suspected Biermer (pernicious) anemia?
What is bupropion?
What is the endoscopic appearance of gastric atrophic mucosa?
What is the appropriate evaluation and management for a Baker's cyst?

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.