Y.T., M.S. and K.O. designed the study; Y.T., M.T. and
M.S. performed experiments; Y.T., M.S. and K.O. collected
data; Y.T., M.S. analyzed data; Y.T., M.S. wrote the
manuscript; K.O. and A.Y. gave technical support and
conceptual advice. All authors read and approved the ﬁnal
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Ethylene glycol intoxication presenting with high anion gap metabolic
acidosis, acute kidney injury and elevated lactate
Thomas Giner, Violeta Ojinaga, Nikolaus Neu, Miriam Koessler and Gerard Cortina
Department of Pediatrics, Medical University of Innsbruck, Innsbruck, Austria
Key words acute kidney injury, ethylene glycol intoxication, high anion gap metabolic acidosis, osmolar gap.
A 15-year-old girl presented to the pediatric emergency
department after being euphoric and increasingly confused at
home. Her past medical history was unremarkable. On admis-
sion she was afebrile and drowsy and Glasgow coma scale
score was ﬂuctuating, but she remained verbal. Cardiovascular
examination was unremarkable and she looked well perfused.
Respiratory rate was 35 breaths/min and oxygen saturation
was 99% in ambient air. Laboratory data were as follows:
serum sodium, 145 mmol/L; serum potassium, 5.2 mmol/L;
serum chloride, 111 mmol/L; serum osmolality, 306 mOsm/
kg; and serum creatinine, 97 lmol/L (up from 70 lmol/L
1 month prior). Arterial blood gas analysis indicated metabolic
acidosis (pH, 7.20; partial pressure of carbon dioxide [pCO
8 mm Hg; bicarbonate, 3.4 mmol/L; base excess, À23.4) with
an elevated anion gap (calculated at 30.6 mmol/L) and
elevated lactate at 28.4 mmol/L (Table 1). The calculated
osmolality was 303.9 mOsm/kg, thus no osmolar gap was
present. Brain and chest imaging were normal, as was electro-
cardiography. Routine toxicology screen for benzodiazepines,
opioids, amphetamines, tetrahydrocannabinol, tricyclic antide-
pressants and ethanol was negative. Urine microscopy, how-
ever, indicated massive crystalluria. Volume expansion with
saline and bicarbonate was carried out. The presence of high
anion-gap metabolic acidosis, altered mental status and acute
kidney injury was highly suggestive of toxic alcohol ingestion.
Given the negative ethanol screen and the presence of calcium
oxalate crystals, ethylene glycol intoxication was probable.
Measurement of serum ethylene glycol, however, is not avail-
able at the present hospital. Nevertheless, we empirically
Table 1 Laboratory data
Variable Admission 12 h later Normal value
pH 7.20 7.38 7.35–7.45
paCO2 (mm Hg) 8 23 35–45
paO2 (mm Hg) 122 104 75–100
Bicarbonate (mmol/L) 3.4 13.4 20–À24
Base excess (mmol/L) À23.4 À9.8 À2.0–3.0
SaO2 (%) 98.5 98.3 -
Lactate (mmol/L) 28.4 9.2 0.5–2.2
Osmolarity (mmOsm/kg) 306 306 280–295
Glucose (mmol/L) 6.5 6.7 4–5.5
BUN (mmol/L) 7.42 9.67 4–14
Creatinine (mmol/L) 97 133 45–84
Sodium (mmol/L) 145 146 134–143
Potassium (mmol/L) 5.2 4.1 3.4–4.5
Chloride (mmol/L) 111 114 96–109
Calcium (mmol/L) 2.38 2.13 2.10–2.55
BUN, blood urea nitrogen; pCO
, partial pressure of carbon
, partial pressure of oxygen; SaO
, arterial oxygen
Correspondence: Gerard Cortina, MD, Department of Pediatrics,
Medical University of Innsbruck, Anichstrasse 35, A-6020 Inns-
bruck, Austria. Email: firstname.lastname@example.org
Received 13 August 2017; revised 9 October 2017; accepted 20
194 T Giner et al.
© 2018 Japan Pediatric Society