Lessons of the month 3: Intravenous poppers abuse: case report, management and possible complications

Discussion

Severe poppers intoxications usually occur because of exaggerated inhalation or ingestion of the fluid. Oral intake compared to inhalation is associated with increased systemic toxicity, including life-threatening methaemoglobinaemia.⁴ Additionally, local acid burns in the mouth and oesophagus with the risk of perforation can occur. In the intravenous abuse in our patient, haemodynamic instability was expected, but our patient was normotensive without any relevant arrhythmias. He had fractionally administered the substance and a bolus application might have far greater effects on the circulatory system. Usually, nitrites induce a decrease of blood pressure, but the short duration of action makes prolonged hypotensive periods unlikely.^4,6 Phosphodiesterase-5-inhibitors have been reported to be commonly abused in combination with poppers. Concurrent use may result in life-threatening hypotension.^7,8 Initially, pulmonary fat embolism was considered, but it is unlikely that the small amount would cause any relevant pulmonary artery obstruction as, in comparison, fat boluses of 1.5 mL/kg rarely cause embolism in lipid rescue therapy used for other intoxications.⁹ Brownish colour of the blood is a typical finding in methaemoglobinaemia.¹⁰ Physiologically, Met-Hb concentrations are about 1–2%. Responsible for the maintenance of these concentrations are erythrocyte cytochrome-b5 Met-Hb-reductase and nicotinamide-adenine-dinucleotide-phosphate (NADPH) Met-Hb-reductase. High Met-Hb concentrations result in generalised tissue hypoxia with consecutive hyperlactataemia. Severity of symptoms usually correlates with the Met-Hb concentration (Table 1).¹¹ In this case, despite Met-Hb concentration of <50%, metabolic acidosis with elevated lactate levels and severe respiratory symptoms were present. Therapeutically, toluidine or methylene blue are used as antidotes. Thereby the Met-Hb reduction through the NADPH-Met-Hb-reductase pathway can be increased four to six-fold. Methylene blue should be given intravenously at a dose of 1–2 mg/kg over 3–5 minutes, and, if ineffective, repeated at 1 mg/kg within 30 minutes.¹² If available, toluidine blue may be used instead of methylene blue as the effect onset and duration are similar, but a slightly better efficacy with fewer side effects has been reported.^5,11,13 Hyperbaric oxygenation may be used as a treatment modality, particularly in patients who do not respond to therapeutic doses of methylene blue.^12,14,15 Veno-arterial extracorporeal membrane oxygenation can be used in patients presenting with refractory cardio-circulatory shock, but it remains unclear whether it is possible to sufficiently load the erythrocytes with oxygen in the presence of methaemoglobinaemia.

Regarding the findings from the content analysis, acetone is a common solvent used to decrease viscosity and increase vapor pressure. It is necessary in many pharmaceutical production processes but can also, when inhaled, cause central nervous effects. The fast-evaporating isopropanol is the hydrolysis product of isopropyl nitrite and often used in various disinfectants. The exact toxic doses are unknown but, when ingested, lethal doses of >100 mL and 3.4 mL/kg have been reported. Nevertheless, these doses are not well validated, and the cut-off regarding toxic intravenous doses is unknown.^16–18 Clinically, isopropanol poisoning manifests with vomiting, diarrhoea, confusion, seizures and cardio-circulatory shock.^16,19 Haemodialysis can be used to remove isopropanol. Ethanol or fomepizole are contraindicated as the degradation product (acetone) is less toxic then isopropanol itself.^16,20 The amount injected by our patient is, in comparison, rather small and clinical presentation made a relevant isopropanol poisoning unlikely.