Some opioids such as tramadol, pethidine, dextromethorphan and tapentadol increase serotonergic activity. Fentanyl and methadone also do this but to a lesser extent.These opioids may increase the risk of serotonin toxicity when combined with antidepressants. Some selective serotonin reuptake inhibitors block the metabolism of opioids. This may reduce the concentrations and analgesic effect of some opioids such as codeine and tramadol, and increase the concentrations and risk of adverse effects of other opioids such as methadone.Fluoxetine and irreversible monoamine oxidase inhibitors -tranylcypromine and phenelzinehave prolonged actions and may interact for weeks after they have been discontinued.• autonomic hyperactivity -fevers, tachycardia, diaphoresis, tachypnoea• altered mental state.Serotonin toxicity generally only occurs when serotonergic opioids are given with another serotonergic drug such as an antidepressant, even at therapeutic doses (see Box). 3 The highest risk opioid drugs are tramadol, pethidine and dextromethorphan. 7 The highest risk serotonergic drugs are the irreversible monoamine oxidase inhibitor (MAOI) antidepressants, tranylcypromine and phenelzine. 8 The risk and precautions with different combinations are summarised in the Table. 3,6,7,9 The highest risk for serotonin toxicity by far is with irreversible MAOIs and pethidine, tramadol or dextromethorphan.There have been occasional case reports of serotonin toxicity with low-risk opioid and antidepressant combinations, such as oxycodone and buprenorphine/naloxone (Suboxone) with other serotonergic medicines. [10][11][12][13] Many of these reports have very obvious alternative medical explanations for all the signs of the alleged severe serotonin toxicity. 14 However, it also seems likely that moderate serotonin toxicity may occasionally be precipitated by any opioid in susceptible individuals taking an antidepressant, perhaps due to indirect effects of opioids on serotonin release. A high index of suspicion is therefore needed. 8 Similarly, antidepressants such as agomelatine, mianserin and reboxetine have a very low risk of serotonin syndrome but caution still might be warranted in combination with very high-risk serotonergic drugs. 3,5,7

ObjectiveWe report the only two adult cases of NH4OH ingestion described in literature at the Peradeniya Teaching Hospital in Sri Lanka. Both cases showed clinical evidence of gastrointestinal toxicity and using intestinal fatty acid binding protein (IFABP), a novel biomarker, we attempted to quantify the extent of enterocyte damage. Procalcitonin was also measured as a maker of bacterial sepsis to ascertain whether there was a link between enterocyte damage and infection secondary to bacterial translocation.CasesA 45-year-old, previously well man was brought in by family with a reduced level of consciousness after ingestion of an unknown quantity of industrial NH4OH (29% solution) with suicidal intent. Peak IFABP and procalcitonin levels were 1274 pg/mL and 2.0 ng/mL, respectively, 7.7 hours following presumed ingestion. A 23-year-old, previously well woman presented 24 hours after consuming 100 mL of NH4OH (5.4% solution) used as a cleaning product. She presented with ongoing vomiting and oropharyngeal pain. Her peak IFABP and procalcitonin levels were 865 pg/mL and 5.8 ng/mL, respectively, 27.2 hours following ingestion.ConclusionWe report the only two adult cases of NH4OH ingestion and describe severe gastrointestinal damage both clinically and biochemically. IFABP, currently only a marker used in research settings, was elevated in both cases but only marginally below that of levels seen in mesenteric ischaemia (levels greater than 1300 pg/mL). The use of a marker for enterocyte damage especially in ingestion of caustic solutions can allow clinicians to monitor progress, predict complications and evaluate the need for further invasive procedures.

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