The seizurogenecity of naloxone in tramadol overdose

05 May 2012
Volume 4 · Issue 5

Abstract

Tramadol is the most widely prescribed opiate analgesic (National Treatment Agency for Substance Misuse, 2011) and, as a result, is present in a large number of overdoses that present in the pre-hospital arena. Naloxone is indicated for use by ambulance personnel where the GCS is reduced due to a known, or possible, overdose of an opiate containing substance (JRCALC (Joint Royal Colleges Service Liaison Committee), 2006).

A case study of a tramadol overdose shows a close temporal relationship between naloxone administration and a seizure. While seizure is a symptom of tramadol intoxication (Saidi et al, 2008), the speed with which it occurred after naloxone administration seemed too fast to be merely coincidence. A study of the literature shows evidence that naloxone can instigate seizure in the case of a tramadol overdose (Rehni et al, 2008; Raffa and Stone, 2008).

This information is particularly pertinent to the ambulance clinician as the consequence of a seizure can be important, both practically and clinically. The findings do not suggest that naloxone should be withheld, but that the potential for seizure should be noted and any forthcoming seizure dealt with. More research is needed to further define the factors that affect the seizurogenicity of naloxone in tramadol overdose.

Tramadol hydrochloride is an increasingly popular prescription drug, licensed in the UK as an effective analgesic for the management of moderate to severe pain (Joint Formulary Committee, 2011). It is by far the most commonly prescribed opiate analgesic, with over 6 million prescriptions in the UK in 2009, representing a 500 % increase over the previous decade (National Treatment Agency for Substance Misuse, 2011). It is generally prescribed as 50 mg tablets, though is available as 37.5 mg quantities combined with paracetamol, and in larger amounts in a sustained release presentation. Its mode of action is primarily due to the inhibition of the reuptake of monoamines such as serotonin and noradrenalin, but also down to its weak affinity for µ-opioid receptors, the same mechanism by which opiates such as morphine function (Raffa and Friderichs, 1996) (Figure 1).

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