Tag Archives: toxicology

How You Train is How You Fight

Simulation makes us more effective. I think it’s good to consider how one would deal with emergency situations in every day life, and practice the response. There are ALWAYS learning points.

My four year old son Kal brought along his rubber red bellied black snake on a New Year’s Day bush walk with my family. Too good an opportunity to miss, so we practiced managing a snakebite scenario. What we did and what we learned are summarised in this three minute video:

This was a worthwhile exercise. Learning points were:

1. Carry a knife to help cut up the teeshirt (if you don’t carry bandages)

2. Call for help early – it takes several minutes to apply the pressure immobilisation bandage, so ideally these things are done in parallel rather than series.

3. Know how to get your coordinates from your smart phone. Several free apps are available.
On an Apple iPhone, they are displayed on the ‘Compass’ app but ONLY if you have enabled location services (Settings->Privacy->Location Services->Compass)

location services compass-10










Learn more about pressure immobilisation technique and its indications from the Australian Resuscitation Council

Flumazenil for BZD overdose: getting away with it

Standard teaching in benzodiazepine (BZD) overdose is that the reversal agent flumazenil is best avoided because of the risk of seizures, particular in those patients who are BZD dependent and those who may have co-ingested proconvulsant substances such as tricyclic antidepressants.

Data from the UK’s National Poisons Information Service indicate that these principles are often flouted in the UK, and they usually get away with it, even in patients who had had seizures prior to flumazenil therapy. This will not change my practice though.

Objective Benzodiazepine (BZD) overdose (OD) continues to cause significant morbidity and mortality in the UK. Flumazenil is an effective antidote but there is a risk of seizures, particularly in those who have co-ingested tricyclic antidepressants. A study was undertaken to examine the frequency of use, safety and efficacy of flumazenil in the management of BZD OD in the UK.

Methods A 2-year retrospective cohort study was performed of all enquiries to the UK National Poisons Information Service involving BZD OD.

Results Flumazenil was administered to 80 patients in 4504 BZD-related enquiries, 68 of whom did not have ventilatory failure or had recognised contraindications to flumazenil. Factors associated with flumazenil use were increased age, severe poisoning and ventilatory failure. Co-ingestion of tricyclic antidepressants and chronic obstructive pulmonary disease did not influence flumazenil administration. Seizure frequency in patients not treated with flumazenil was 0.3%. The frequency of prior seizure in flumazenil-treated patients was 30 times higher (8.8%). Seven patients who had seizures prior to flumazenil therapy had no recurrence of their seizures. Ventilation or consciousness improved in 70% of flumazenil-treated patients. Flumazenil administration was followed by one instance each of agitation and brief seizure.

Conclusions Flumazenil is used infrequently in the management of BZD OD in the UK. It was effective and associated with a low incidence of seizure. These results compare favourably with the results of published randomised controlled trials and cohort studies, although previous studies have not reported the use of flumazenil in such a high-risk population. This study should inform the continuing review of national guidance on flumazenil therapy.

Flumazenil use in benzodiazepine overdose in the UK: a retrospective survey of NPIS data
Emerg Med J. 2012 Jul;29(7):565-9

Nebulised naloxone

This appears to be a useful option when iv access is difficult and the patient is relatively stable.

The protocol specified nebulisation of 2 mg of naloxone with 3 mL of normal saline as empiric treatment for suspected opioid overdose or undifferentiated depressed respirations as long as the patient had some spontaneous respiratory effort, no apnoea, and no severe cardiorespiratory compromise.

BACKGROUND: Emergency medical services (EMS) traditionally administer naloxone using a needle. Needleless naloxone may be easier when intravenous (IV) access is difficult and may decrease occupational blood-borne exposure in this high-risk population. Several studies have examined intranasal naloxone, but nebulized naloxone as an alternative needleless route has not been examined in the prehospital setting.

OBJECTIVE: We sought to determine whether nebulized naloxone can be used safely and effectively by prehospital providers for patients with suspected opioid overdose.

METHODS: We performed a retrospective analysis of all consecutive cases administered nebulized naloxone from January 1 to June 30, 2010, by the Chicago Fire Department. All clinical data were entered in real time into a structured EMS database and data abstraction was performed in a systematic manner. Included were cases of suspected opioid overdose, altered mental status, and respiratory depression; excluded were cases where nebulized naloxone was given for opioid-triggered asthma and cases with incomplete outcome data. The primary outcome was patient response to nebulized naloxone. Secondary outcomes included need for rescue naloxone (IV or intramuscular), need for assisted ventilation, and adverse antidote events. Kappa interrater reliability was calculated and study data were analyzed using descriptive statistics.

RESULTS: Out of 129 cases, 105 met the inclusion criteria. Of these, 23 (22%) had complete response, 62 (59%) had partial response, and 20 (19%) had no response. Eleven cases (10%) received rescue naloxone, no case required assisted ventilation, and no adverse events occurred. The kappa score was 0.993.

CONCLUSION: Nebulized naloxone is a safe and effective needleless alternative for prehospital treatment of suspected opioid overdose in patients with spontaneous respirations.

Can nebulized naloxone be used safely and effectively by emergency medical services for suspected opioid overdose?
Prehosp Emerg Care, 2012 vol. 16 (2):289-292

Salicylate poisoning and pseudohyperchloraemia

Severe salicylate poisoning can cause metabolic acidosis from an accumulation of salicylic acid, lactic acid, and ketone bodies. A high anion gap acidosis is therefore the typical metabolic abnormality seen. A case series illustrates salicylate poisoning presenting with a normal gap (hyperchloraemic) acidosis – one patient had a chloride of 111 mmol/l and the other 123 mmol/l. This can occur when some analysers falsely read an elevated chloride in the presence of high concentrations of salicylate.

Severe salicylate poisoning is classically associated with an anion gap metabolic acidosis. However, high serum salicylate levels can cause false increase of laboratory chloride results on some analyzers. We present 2 cases of life-threatening salicylate poisoning with an apparently normal anion gap caused by an important laboratory interference. These cases highlight that the diagnosis of severe salicylism must be considered in all patients presenting with metabolic acidosis, even in the absence of an increased anion gap.

Falsely Normal Anion Gap in Severe Salicylate Poisoning Caused by Laboratory Interference
Ann Emerg Med. 2011 Sep;58(3):280-1

Intravenous lipid emulsion as antidote

Emergency physician intensivist Grant Cave and colleagues review the literature on intravenous lipid emulsion (ILE) therapy for human poisoning in this month’s Emergency Medicine Australasia

Intravenous lipid emulsion (ILE) has been demonstrated to be effective in amelioration of cardiovascular and central nervous system sequelae of local-anaesthetic and non-local-anaesthetic drug toxicity in animal models. Sequestration of lipophilic toxins to an expanded plasma lipid phase is credited as the predominant beneficial mechanism of action of ILE. Systematic review of published human experience is however lacking. We determined to report a comprehensive literature search of all human reports of ILE application in drug poisoning. Forty-two cases of ILE use (19 local-anaesthetic, 23 non-local-anaesthetic) were identified, with anecdotal reports of successful resuscitation from cardiovascular collapse and central nervous system depression associated with ILE administration in lipophilic toxin overdose. Although significant heterogeneity was observed in both agents of intoxication, and reported outcomes; case report data suggest a possible benefit of ILE in potentially life-threatening cardio-toxicity from bupivacaine, mepivacaine, ropivacaine, haloperidol, tricyclic antidepressants, lipophilic beta blockers and calcium channel blockers. Further controlled study and systematic evaluation of human cases is required to define the clinical role of ILE in acute poisonings.

Review article: Intravenous lipid emulsion as antidote: A summary of published human experience.
Emerg Med Australas. 2011 Apr;23(2):123-41

An editorial by Guy Weinberg, the researcher who first demonstrated the effect of ILE on bupivacaine toxicity, has some interesting observations and recommendations:

  • Each of the first six case reports of lipid resuscitation from local anaesthetic systemic toxicity (LAST) were noted to have one or more of either underlying ischaemia, conduction defect or low cardiac output. For patients in these susceptible groups, reduce the dose of local anaesthetics used in nerve blocks
  • There is laboratory evidence that epinephrine (adrenaline) can impair lipid resuscitation. Weinberg believes that epinephrine should be used only in small doses, if at all, in treating LAST
  • In bupivacaine toxicity, use it early rather than later, as outcomes are likely to be better when intervention occurs before tissue perfusion has been compromised and too much pressor therapy has been used

Weinberg informs us that more examples of lipid resuscitation can be found at the educational website: http://www.lipidrescue.org/ and the registry site: http://www.lipidregistry.org/.

Intravenous lipid emulsion: Why wait to save a life?
Emerg Med Australas. 2011 Apr;23(2):113-5

In his editorial Weinberg refers to the review article by Jamaty et al, whose suggested regimen included 20% ILE 1.5mL/kg bolus then 0.25–0.5 mL/kg/min for 30–60 min.

OBJECTIVE: To assess the evidence regarding the efficacy and safety of intravenous fat emulsion (IFE) in the management of poisoned patients.
METHODS: We performed a systematic review of the literature with no time or language restriction. The electronic databases were searched from their inception until June 1, 2009 (Medline, EMBASE, ISI web of science, Biological abstract, LILACS, ChemIndex, Toxnet, and Proquest). We also examined the references of identified articles and the gray literature. The target interventions eligible for inclusion were administration of any IFE before, during, or after poisoning in human or animals. All types of studies were reviewed. Eligibility for inclusion and study quality scores, based on criteria by Jadad and the STROBE statement, were evaluated by independent investigators. The primary outcome was mortality. Secondary outcomes included neurologic, hemodynamic, and electrocardiographic variables, as well as adverse effects.
RESULTS: Of the 938 publications identified by the search strategies, 74 met the inclusion criteria. We identified 23 animal trials, 50 human, and 1 animal case reports. Overall, the quality of evidence was weak and significant heterogeneity prevented data pooling. Available data suggest some benefits of IFE in bupivacaine, verapamil, chlorpromazine, and some tricyclic antidepressants and beta-blockers toxicity. No trial assessed the safety of IFE in the treatment of acute poisoning.
CONCLUSION: The evidence for the efficacy of IFE in reducing mortality and improving hemodynamic, electrocardiographic, and neurological parameters in the poisoned patients is solely based on animal studies and human case reports. The safety of IFE has not been established.

Lipid emulsions in the treatment of acute poisoning: a systematic review of human and animal studies.
Clin Toxicol (Phila). 2010 Jan;48(1):1-27

The Guidelines from the Association of Anaesthetists of Great Britain and Ireland, also endorsed by the Australian and New Zealand College of Anaesthetists, outline the dose and indications for ILE in LAST. The full guideline can be accessed by clicking the image below:

Hyperbaric O2 for the sick and the well with CO poisoning

A French study, large by hyperbaric oxygen trial standards, did not confirm that hyperbaric oxygen therapy improves recovery from pure CO poisoning. In addition, in comatose patients, repeating hyperbaric oxygen therapy resulted in worse outcomes compared to one session.

I don't care if it doesn't work - something looking like a retro-sci-fi time machine is COOL.

INTRODUCTION: Although hyperbaric oxygen therapy (HBO) is broadly used for carbon monoxide (CO) poisoning, its efficacy and practical modalities remain controversial.

OBJECTIVES: To assess HBO in patients poisoned with CO.

DESIGN: Two prospective randomized trial on two parallel groups.

SETTING: Critical Care Unit, Raymond Poincaré Hospital, Garches, France.

SUBJECTS: Three hundred eighty-five patients with acute domestic CO poisoning.

INTERVENTION: Patients with transient loss of consciousness (trial A, n = 179) were randomized to either 6 h of normobaric oxygen therapy (NBO; arm A0, n = 86) or 4 h of NBO plus one HBO session (arm A1, n = 93). Patients with initial coma (trial B, n = 206) were randomized to either 4 h of NBO plus one HBO session (arm B1, n = 101) or 4 h of NBO plus two 2 HBO sessions (arm B2, n = 105). PRIMARY ENDPOINT: Proportion of patients with complete recovery at 1 month.

RESULTS: In trial A, there was no evidence for a difference in 1-month complete recovery rates with and without HBO [58% compared to 61%; unadjusted odds ratio, 0.90 (95% CI, 0.47-1.71)]. In trial B, complete recovery rates were significantly lower with two than with one HBO session [47% compared to 68%; unadjusted odds ratio, 0.42 (CI, 0.23-0.79)].

CONCLUSION: In patients with transient loss of consciousness, there was no evidence of superiority of HBO over NBO. In comatose patients, two HBO sessions were associated with worse outcomes than one HBO session.

Hyperbaric oxygen therapy for acute domestic carbon monoxide poisoning: two randomized controlled trials
Intensive Care Med. 2011 Mar;37(3):486-92

Algorithm for Body Packers

‘Mules’ or body packers are people who transport illegal drugs by packet ingestion into the gastrointestinal tract. A large study of body packers apprehended by United State Customs officials at JFK International Airport, New York describes experience with body packers and an algorithm for conservative and surgical management.

Of 56 patients requiring admission out of a total of 1250 subjects confirmed to be body packers, 25 patients (45%) required surgical intervention, whereas 31 patients (55%) were successfully managed conservatively.


  • Plain abdominal x-ray was diagnostic in 49 patients (88% of all hospitalised patients).
  • Non-contrast CT of the abdomen and pelvis is required if AXR is negative
  • Forty-eight per cent of body packers had positive urine toxicology for illicit substances.


  • Indications for intervention included:
  • bowel obstruction
  • packet rupture/toxicity
  • delayed progression of packet transit on conservative management.
  • Patients with packets found predominantly in the proximal gastrointestinal tract failed conservative management more frequently than those with packets found in the distal gastrointestinal tract.

Multiple intraoperative manoeuvres were used to remove the foreign bodies:

  • gastrotomy
  • enterotomy
  • colotomy.

Wound infection was the most common complication and is associated with distal enterotomy and colotomy.

The authors recommend a confirmatory radiological study to demonstrate complete clearance of packets

Establishment of a definitive protocol for the diagnosis and management of body packers (drug mules).
Emerg Med J 2011;28:98-10

Body position in poisoning

You come across a patient in the community who has taken an overdose of pills. The ambulance is on its way and you have no medical equipment. Is there any first aid that might help? How should you position the patient if they are unconscious?

Authors of a BestBet in the EMJ searched the literature to answer the three-part question:
In [orally poisoned patients] does [a specific body position] result in [a better outcome for the patient]?

The limited evidence they found from just two papers suggests that drug absorption is lowest in patients lying on their left side, so you might want to consider placing an unconscious overdose patient in the left-sided recovery position prior to definitively managing them in hospital. The theoretical increased risk of pulmonary aspiration on the left side should be considered however. The table shows just how limited this evidence base is – but the idea is an interesting one.

Optimal body position in oral poisoning cases
Emerg Med J 2010;27:952-953 Full text from the BestBets site

Specialised chemical burns

Certain chemical burns require a little extra thought than just irrigation and good wound care – which may even be contraindicated. An article in The Journal of Emergency Medicine addresses these, and some of the points are summarised below, with some additional information from Toxbase:

Hot tar (bitumen)

  • Immerse contaminated area in cool water until the bitumen has hardened and cooled.
  • Adherent material may be left in place to avoid causing further injury by removal attempts, and will spontaneously detach after a few days.
  • If a finger or limb is completely surrounded, split the bitumen to prevent a tourniquet effect.
  • To remove bitumen, apply a lipid or polysorbate based agent and a clean non-adherent dressing. Suitable products include melted butter, sunflower oil, liquid paraffin, and petroleum or polysorbate based antibiotic ointments. Solvents such as alcohol, acetone, kerosene, ether or gasoline are not suitable.
  • Change the dressing frequently, and reapply the product as necessary, until the bitumen is completely removed. This may take up to 72 hours.
  • Treat as a thermal burn.

Elemental sodium

  • – utilised in the manufacturing of methamphetamine.
  • will spontaneously ignite above 115°C
  • Contact with water releases sodium hydroxide and hydrogen gas. It is the heat released in the reaction with the water in air that then ignites locally produced hydrogen gas.
  • Burns involving the metallic forms of sodium, potassium, and lithium (alkali metals) produce both thermal and chemical injury to the tissue. The thermal tissue damage is due to the extreme exothermic reaction that metallic sodium undergoes when exposed to water.
  • At times, water, when mixed with either elemental sodium or potassium, undergoes an explosive reaction.
  • Avoid water irrigation; if metal is still present in the tissues, the added water could ignite it.
  • All clothing should first be removed from the victim. If retained metal exists, the affected area should be covered in mineral oil. Removal of embedded sodium should then be undertaken with forceps.
  • Mineral oil is a practical, and potentially safer, alternative to isopropyl alcohol for the storage of elemental sodium.

Chromic acid

  • – a corrosive, oxidizing acid. After skin has been exposed to chromium, burns covering as little as 10% of body surface area (BSA) have proven fatal.
  • Burns involving as little as 1% of total BSA have resulted in acute renal failure.
  • Wash thoroughly with copious amounts of water and treat as a thermal burn.
  • Application of 10% ascorbic acid solution at least three times per day may improve the rate of healing
  • Prompt excision of burned, contaminated areas is recommended to prevent absorption of the chemical.

White phosphorus

  • – will ignite spontaneously in 30°C air temperature; typically stored in water.
  • burns of > 10% can have associated mortality.
  • Three stages of systemic toxicity exist: (1) gastrointestinal symptoms (nausea, vomiting and “smoking stool”). Symptoms of headache, seizures, and coma, as well as the potential for cardiovascular collapse, may occur in the initial phase. Decreasing serum calcium concentrations; (2) symptom-free period; (3) (4 to 8 days post-exposure) neurological toxicity, bleeding diathesis, hepatic failure, renal failure, and shock.
  • Continuous coverage with water will protect both the patient and staff from ignition and fumes that result from white phosphorus’s contact with air.
  • Brushing particulate not incorporated in wounds can accomplish a significant amount of decontamination. This brushing should be followed by continuous irrigation until all particles are removed. Those debriding and decontaminating an exposed patient should have a safe method of disposing of particles: a container of cold water would suffice.
  • A way to identify phosphorous particles for removal is the use of a Wood’s lamp, which will cause the white phosphorous to fluoresce.
  • Excision may be necessary to remove the chemical if deeply entrenched in fascia.


  • – a corrosive aromatic hydrocarbon that can be absorbed at toxic levels through all routes of absorption
  • causes extensive denaturisation of tissue proteins, producing an eschar with shallow ulcers
  • Rescue personnel should use butyl rubber gloves and aprons, and conduct decontamination in a well-ventilated area.
  • wipe exposed areas immediately with low-molecular-weight polytheylene glycol (PEG 300 or 400)
  • however Toxbase states: “The use of solvents (such as glycerol, polyethylene glycol and isopropanol) has been suggested. One (animal) study (Hunter et al, 1992) indicated that isopropanol was more effective than water, but there is no evidence in humans that solvents are more effective than washing with copious amounts of water.”
  • if the burn covers a large skin area, high pressure shower irrigation before PEG application is preferable
  • Any water applied must be applied in high pressure, as small amounts might dilute the phenol present on the skin and thus expand not only the involved area but also the amount of phenol absorbed.

Hydrofluoric acid

  • HF is highly corrosive and causes damage by two mechanisms. It produces a corrosive burn from the high concentration of hydrogen ions. It also penetrates tissues due to the lipophilic nature of fluoride, and causes liquefactive necrosis.
  • Tissue penetration leads to systemic reactions with effects on the cardiac, respiratory, nervous, and gastrointestinal systems. The fluoride ion precipitates calcium, leading to hypocalcemia, and may interfere with enzyme systems by binding magnesium and manganese, as well as important nerve conduction functions that depend on calcium.
  • Copious irrigation of HF-burned skin with water should begin immediately. Most HF burns will respond well to this.
  • Pain that persists after irrigation is a marker that the fluoride ion needs detoxification. This can be accomplished through superficial topical treatment, infiltrative treatment, or intra-arterial treatment.
  • The preferred topical agent is calcium gluconate gel.

Special considerations in hazardous materials burns.
J Emerg Med. 2010 Nov;39(5):544-53