title: Early anion gap metabolic acidosis in acetaminophen overdose.
abstract: OBJECTIVE
  The study aimed to determine the incidence and clinical significance of early high (>15 mEq/L) anion gap metabolic acidosis in acetaminophen (APAP) overdose.
  
  
  METHODS
  A retrospective review of a cohort of 74 patients presenting within 24 hours of APAP overdose was conducted.
  
  
  RESULTS
  Early high anion gap metabolic acidosis was present in 41% of patients on admission and persisted for 1.5 ± 0.1 days. The anion gap was associated with an elevated lactate level (4.5 ± 1 mmol/L) (r(2) = 0.66, P < .05), which persisted for 1 day. The lactate level increased in proportion to the APAP concentration (r(2) = 0.75, P < .05). Patients with increased anion gap had a higher incidence of confusion (48% vs 3%; P < .001) and lethargy (39% vs 6%; P = .003). Early high anion gap metabolic acidosis was found in the absence of shock or liver failure. All patients were treated with N-acetylcysteine and, despite the early high anion gap metabolic acidosis, none developed hepatic failure or hypoglycemia.
  
  
  CONCLUSIONS
  Early high anion gap metabolic acidosis in patients with APAP overdose is self-limited and does not predict clinical or laboratory outcomes. Persistent or late metabolic acidosis in the absence of liver failure is not likely due to APAP and should prompt a search for other causes of metabolic acidosis. Finally, APAP overdose should be considered in patients presenting to the emergency department with altered mental status, as this is a treatable condition when detected early.
authors.affiliation: Division of Pulmonary and Critical Care, Department of Internal Medicine, Kings County Hospital Center, Brooklyn, NY 11203, USA.
authors.forename: Joe G
authors.initials: JG
authors.lastname: Zein
authors.forename: David J
authors.initials: DJ
authors.lastname: Wallace
authors.forename: Gary
authors.initials: G
authors.lastname: Kinasewitz
authors.forename: Nagib
authors.initials: N
authors.lastname: Toubia
authors.forename: Christine
authors.initials: C
authors.lastname: Kakoulas
mesh_terms: D000082:Acetaminophen / Q000506:poisoning*; D000136:Acid-Base Equilibrium; D000140:Acidosis, Lactic / Q000139:chemically induced* / Q000175:diagnosis / Q000453:epidemiology* / Q000378:metabolism / Q000628:therapy; D000328:Adult; D018712:Analgesics, Non-Narcotic / Q000506:poisoning*; D000704:Analysis of Variance; D015984:Causality; D016009:Chi-Square Distribution; D003221:Confusion / Q000139:chemically induced; D062787:Drug Overdose / Q000150:complications; D004636:Emergency Service, Hospital / Q000706:statistics & numerical data; D005260:Female; D006801:Humans; D015994:Incidence; D019344:Lactic Acid / Q000097:blood; D053609:Lethargy / Q000139:chemically induced; D008297:Male; D009518:New York / Q000453:epidemiology; D009825:Oklahoma / Q000453:epidemiology; D011379:Prognosis; D012189:Retrospective Studies; D012720:Severity of Illness Index; D018709:Statistics, Nonparametric; D013997:Time Factors
chemical_list: D018712:Analgesics, Non-Narcotic; D019344:Lactic Acid; D000082:Acetaminophen