Value of emergency toxicological investigations in differential diagnosis of coma.

Helliwell, M; Hampel, G; Sinclair, E.A.; Huggett, Anthony C.; Flanagan, Robert J.

doi:10.1136/bmj.2.6194.819

Cited by 52 publications

(11 citation statements)

References 14 publications

(4 reference statements)

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“…It is claimed that an inaccurate diagnosis is not affecting mortality (8,12), nor being the cause of complications (13). However, knowing the correct diagnosis could enable optimal treatment of acute poisoning by reducing the need for supervision and costly treatments, and facilitating the identification of cases that require prompt drug-specific treatment (10,12,13,17). Thus, both morbidity and costs may be reduced.…”

Section: Introductionmentioning

confidence: 95%

Clinical vs. Laboratory Identification of Drugs of Abuse in Patients Admitted for Acute Poisoning

Bjornaas

Hovda

Mikalsen

et al. 2006

Clinical Toxicology

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Section: Introductionmentioning

confidence: 95%

Clinical vs. Laboratory Identification of Drugs of Abuse in Patients Admitted for Acute Poisoning

Bjornaas

Hovda

Mikalsen

et al. 2006

Clinical Toxicology

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“…Complete reversal of coma occurred within ten minutes of administration in 49 patients. Full toxicological screening (Helliwell et al, 1979) in 45 identified ethanol at a mean plasma concentration of 3.54g/l (range 2.40-5.90 g/1) as the sole cause of unconsciousness in 38 cases; phenobarbitone (21 mg/1) was the only drug present in addition to ethanol (3.1 g/1) in a further patient. Dextropropoxyphene was the agent responsible for coma in the other 6 patients in addition to alcohol.…”

Section: Methods and Resultsmentioning

confidence: 98%

“…In the second part of this study we assessed the role for naloxone in cases in which the NPIS were requested to carry out toxicological screening (Helliwell et al, 1979). Sixty-four requests were made when opiates were suspected of contributing to the coma, either from circumstantial evidence, e.g.…”

Section: Methods and Resultsmentioning

confidence: 99%

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An Investigation of the Role of the Specific Opioid Antagonist Naloxone in Clinical Toxicology

Jefferys

Volans

1983

Human Toxicology

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1 An assessment of the current role of naloxone in clinical toxicology has been made in a series of three separate epidemiological studies. 2 Through the National Poisons Information Service we found that the role of naloxone in opioid poisoning is often not appreciated by the enquirer and that toxicological screening is often requested before the diagnostic use of naloxone. 3 The recommended dose of naloxone (0.4-1.2 mg i.v.) is not always adequate. In 51 cases where naloxone was effective, doses of up to 3.2 mg were necessary (mean 1.8 ± 0.3 mg SEM i.v.). 4 In 31 cases of non-opioid poisoning, naloxone in doses of 0.4-1.2 mg i.v. caused no deterioration, whilst six patients in whom no opioids were detected showed clinical improvement. 5 In 300 cases of suspected ethanol-induced coma, 49 showed reversal of coma with naloxone, and in 38 cases ethanol was the sole cause of coma (mean plasma concentration 3.54 ± 0.62 g/l SEM). 6 These results suggest that the role of naloxone in clinical toxicology is not fully appreciated. There is a need for further education as to its indications in opioid poisoning, together with additional studies to define more accurately the dose/response relationship. In addition, the role of naloxone in coma induced by ethanol and certain other non-opioids needs to be evaluated further.

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“…Specimens of blood (10 ml) and urine (20 ml) were requested in the latter stages of the survey in order to provide objective confirmation of the diagnosis. The specimens were analysed for a wide range of drugs by a combination of colour tests, thin-layer and gas chro matography [Helliwell et al, 1979].…”

Section: Methodsmentioning

confidence: 99%

Acute Trazodone Poisoning: Clinical Signs and Plasma Concentrations

et al. 1984

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A total of 70 patients presenting with suspected acute trazodone poisoning were notified to the Poisons Unit (National Poisons Information Service for England) from August 1980 until March 1983. Detailed follow-up information was obtained on 41 patients, 22 of whom were thought to have ingested trazodone alone. In these latter patients drowsiness (11), ataxia (5), nausea/vomiting (4) and dry mouth (2) were the manifestations of toxicity reported most frequently, only 2 patients became unconscious (grade 2 or 3 coma), and all recovered uneventfully with no more than minimal supportive therapy. The presence of trazodone was confirmed in 8 out of 9 patients from whom specimens (blood and urine) were received. The highest plasma trazodone concentrations (15 and 19 mg/l, respectively) were both associated with only drowsiness and ataxia. However, in 2 further patients moderate plasma trazodone concentrations (4.2 and 8.2 mg/l, respectively) were associated with deep (grade 3–4) coma, although 1 of these latter patients had also ingested ethanol (plasma concentration 3.0 g/l). Although acute trazodone poisoning does not appear to be associated with cardiac arrhythmias or convulsions, these results emphasise that drowsiness and ataxia are commonly encountered, while coma may occur in severe cases. The possible contribution of metabolites of trazodone to toxicity and the potentiating effect of co-ingested drugs or alcohol must be remembered.

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Value of emergency toxicological investigations in differential diagnosis of coma.

Cited by 52 publications

References 14 publications

Clinical vs. Laboratory Identification of Drugs of Abuse in Patients Admitted for Acute Poisoning

Clinical vs. Laboratory Identification of Drugs of Abuse in Patients Admitted for Acute Poisoning

An Investigation of the Role of the Specific Opioid Antagonist Naloxone in Clinical Toxicology

Acute Trazodone Poisoning: Clinical Signs and Plasma Concentrations

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