Een patiënte gered door alcohol

A patient saved by alcohol The medical history of a 43-year-old female patient with auto-intoxication of ethylene glycol is reported. Ethylene glycol is a toxic alcohol leading to severe complications if not treated early. Ethylene glycol itself is relatively nontoxic, however life-threatening toxicity appears after metabolization in the liver. These toxic metabolites lead to metabolic acidosis, renal failure, multiple organ failure and death. A quick diagnosis and therapeutic management are important to avoid formation of the metabolites. Serum drug levels give certainty regarding diagnosis, but are rarely available in time to guide management. There is often a strong suspicion or clear history of auto-intoxication. Shortly after large ingestions, patients may present with sedation or inebriation and have a large osmolar gap, but minimal acidosis. After several hours a profound metabolic acidosis with high anion gap will be present. Management involves supportive care, administration of sodium bicarbonate to correct systemic acidosis, inhibition of the enzyme alcohol dehydrogenase with either fomepizole or ethanol, haemodialysis and treatment with cofactors to optimize nontoxic metabolic pathways. Methanol poisoning is also discussed in this article, as methanol is another toxic alcohol with a similar therapeutic management.

Comparison of measuring serum osmolality and equations estimating osmolality in peritoneal dialysis patients

The osmolar gap increases with kidney failure. A number of equations have been proposed to calculate serum osmolality, allowing determination of the osmolar gap by comparison with measured osmolality. As glucose and icodextrin absorption can potentially interfere with the laboratory measurement of serum sodium, a key component in equations calculating osmolality, we reviewed the performance of 14 equations used to calculate serum osmolality compared to the measurement of serum osmolality in 144 patients with peritoneal dialysis (PD); 81 (56.3%) males, 76 (52.5%) diabetics, mean age of 64.4 ± 16.3 years, 115 (79.9%) prescribed icodextrin and 38 (26.4%) 22.7 g/L glucose dialysates. Measured serum osmolality was 311 (304–320) mosmo/kg (mmol/kg), whereas calculated osmolality for the 14 equations ranged from a median of 274 (269–284) mosmo/kg to 307 (300–316) mosmo/kg. Bland–Altman mean bias showed that measured serum osmolality was greater than the calculated osmolality ranging from 4.0 mosmo/kg to 36.2 mosmo/kg between the 14 equations, with wide 95% limits of agreement (LoA) ranging from −27.1 mosmo/kg to 19.4 mosmo/kg and from −58.5 mosmo/kg to −13.8 mosmo/kg. Only 2 of the 14 equations gave a mean osmolar gap of <10 mosmo/kg and showed no systematic bias, median serum osmolality of 307 (300–316) and 303 (298–312) mosmo/kg, Spearman ρ of 0.57, 0.62, both p < 0.001, respectively. Our study would suggest that only 2 of the 14 equations we compared with measured serum osmolality showed no systematic bias, but still had too great a bias to be useful in clinical practice. As such we propose a new equation to calculate serum osmolality in patients with PD.

Minding The Gap: Severe Anion Gap Metabolic Acidosis Associated With 5-Oxoproline Secondary To Chronic Acetaminophen Use

An 89-year-old man with multiple comorbidities presented to the emergency department with diffuse abdominal pain and dyspnea. He was found to have a severe anion-gap metabolic acidosis with the normal osmolar gap. An initial panel of investigations for common causes of anion-gap metabolic acidosis was unremarkable. Further history revealed long-term daily acetaminophen use. A presumptive diagnosis of 5-oxoprolinemia secondary to chronic acetaminophen use was made. Despite supportive care, the patient did not survive. There is emerging literature on elevated anion gap metabolic acidosis induced by the accumulation of 5-oxoproline, an intermediate organic acid in the gamma-glutamyl cycle. A quantitative profile of urinary organic acids to measure 5-oxoproline is valuable in confirming the diagnosis. Treatment is largely supportive, consisting of cessation of acetaminophen, alkali therapy, and N-acetylcysteine. Clinicians should consider 5-oxoprolemia in patients who present with an otherwise unexplained anion gap metabolic acidosis and a history of chronic acetaminophen use. RESUMEUn homme de 89 ans souffrant de comorbidités multiples s’est présenté à l’urgence avec douleur abdominale diffuse et dyspnée. On a découvert qu’il souffrait d’une acidose métabolique grave à anions nuls avec un écart osmolaire normal. Un premier groupe d’études sur les causes courantes d’acidose métabolique à intervalle anionique n’a pas été remarquable. D’autres antécédents ont révélé une utilisation quotidienne à long terme de l’acétaminophène. Un diagnostic présumé de 5-oxoprolinémie secondaire à l’utilisation chronique d’acétaminophène a été posé. Malgré des soins de soutien, le patient n’a pas survécu. Il existe une littérature émergente sur l’acidose métabolique à intervalle anionique élevé induite par l’accumulation de 5-oxoproline, un acide organique intermédiaire dans le cycle gamma-glutamyle. Un profil quantitatif d’acides organiques urinaires pour mesurer la 5-oxoproline est utile pour confirmer le diagnostic. Le traitement est largement favorable, consistant en l’arrêt de l’acétaminophène, un traitement alcalin et de la N-acétylcystéine. Les cliniciens devraient envisager l’administration de 5-oxoprolemia chez les patients qui présentent une acidose métabolique par gap anionique autrement inexpliquée et des antécédents d’utilisation chronique d’acétaminophène.

Continuous-Infusion Etomidate in a Patient Receiving Extracorporeal Membrane Oxygenation

We describe a 16-year-old, 65-kg male deployed on extracorporeal membrane oxygenation (ECMO) for refractory respiratory failure secondary to ingestion of multiple substances. During his ECMO course, standard sedative and analgesic strategies failed and alternative medications were used. The patient received various dosages of fentanyl, morphine, hydromorphone, clonidine patches, dexmedetomidine, lorazepam, methadone, pentobarbital, olanzapine, and propofol. Despite administration of multiple agents, on day 29 of ECMO the patient experienced elevated blood pressures due to agitation, and continuous infusion etomidate was started. At the time of etomidate initiation, the osmolar gap was 8 mOsm/kg. During etomidate therapy, the blood pressure remained normal, sedative agents were slowly weaned, and the patient required few PRN medications. On day 6 of etomidate, the osmolar gap increased to 127 mOsm/kg and etomidate was discontinued. Continuous-infusion ketamine was started, but the blood pressure was not controlled. Metabolic acidosis is a known side effect of etomidate due to inclusion of propylene glycol as a pharmaceutical solvent in the formulation. Despite high-dose etomidate (20 mcg/kg/min) for approximately 6 days, our patient did not experience metabolic acidosis. Absence of this adverse effect caused us to question the role of the ECMO circuit. To our knowledge, this is the first report of the use of continuous-infusion etomidate during ECMO. Etomidate infusion could be considered in difficult-to-manage patients after other alternatives have failed.