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Cyanide poisoning by fire smoke inhalation a.2 (1)

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2 Review article
Cyanide poisoning by fire smoke inhalation: a European
expert consensus
Kurt Anseeuwa,*, Nicolas Delvaub,*, Guillermo Burillo-Putzed, Fabio De Iacoe,
Götz Geldnerf, Peter Holmströmg, Yves Lamberth and Marc Sabbec
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Smoke inhalation is a common cause of cyanide poisoning
during fires, resulting in injury and even death. In many
cases of smoke inhalation, cyanide has increasingly been
recognized as a significant toxicant. The diagnosis of
cyanide poisoning remains very difficult, and failure to
recognize it may result in inadequate or inappropriate
treatment. Findings suggesting cyanide toxicity include the
following: (a) a history of enclosed-space fire; (b) any
alteration in the level of consciousness; (c) any
cardiovascular changes (particularly inexplicable
hypotension); and (d) elevated plasma lactate. The
feasibility and safety of empiric treatment with
hydroxocobalamin for fire smoke victims have been
reported in the literature. On the basis of a literature review
and a panel discussion, a group of European experts has
proposed emergency management protocols for cyanide
toxicity in fire smoke victims. European Journal of
Emergency Medicine 20:2–9 c 2013 Wolters Kluwer Health
| Lippincott Williams & Wilkins.
European Journal of Emergency Medicine 2013, 20:2–9
Keywords: algorithm, cyanide inhalation, cyanide poisoning, guidelines,
hydrogen cyanide, hydroxocobalamin, nitrites, smoke inhalation,
smoke inhalation injury, thiosulphate
a
Department of Emergency Medicine, ZNA Stuivenberg, Antwerp, bDepartment
of Emergency Medicine, Cliniques Universitaires Saint-Luc, Brussels,
c
Department of Emergency Medicine, University Hospital Gasthuisberg,
Leuven, Belgium, dDepartment of Emergency Medicine, Hospital Universitario
de Canarias, Tenerife, Spain, eDepartment of Emergency Medicine, A.S.L. 1
‘Imperiese’, Imperia, Italy, fKlinikum Ludwigsburg, Ruprecht Karls University,
Heidelberg, Germany, gHelsinki EMS, Helsinki University Hospital, Helsinki,
Finland and hDepartment of Emergency Medicine, Versailles Hospital,
Le Chesnay, France
Correspondence to Kurt Anseeuw, MD, Department of Emergency Medicine,
ZNA Stuivenberg, Lange Beeldekensstraat 267, B-2060 Antwerp, Belgium
Tel: + 32 3 217 78 37; fax: + 32 3 217 75 37; e-mail: kurtanseeuw@yahoo.com
*Kurt Anseeuw and Nicolas Delvau contributed equally to the writing of this
article.
Received 16 February 2012 Accepted 18 June 2012
Introduction
Methodology
During a fire, a complex toxic environment involving flames,
heat, oxygen depletion, smoke and toxic gases is created.
The inhalation of fire smoke, which contains a complex
mixture of gases, seems to be the major cause of morbidity
and mortality in fire victims. Although carboxyhaemoglobin
levels have been shown to be an effective predictor of
mortality, morbidity and duration of hospital stay in smoke
inhalation, hydrogen cyanide (HCN) also seems to be a
major source of concern. Cyanide also represents a major
hazard to firefighters entering fires [1–5].
An international group of experts was independently formed
to discuss the management of victims of cyanide inhalation
by fire smoke in Europe and to define practical guidelines for
prehospital and hospital care providers. The European
Society for Emergency Medicine (EuSEM) endorsed this
initiative and proposed several delegates knowledgeable on
the subject (Council Meeting, March 2011). The aims were
to describe and clarify diagnostic and therapeutic issues in
the complex management of cyanide poisoning in smoke
inhalation victims using a literature review following
evidence-based techniques, and a two-round modified
Delphi method to set up practical guidelines.
Cyanide exists in several forms, including HCN gas,
potassium and sodium cyanide salts, mercury, copper,
gold and silver cyanide salts. HCN from fire smoke is
probably the most common cause of acute cyanide
poisoning in developed countries [1,6–8].
To our knowledge, only local and national guidelines on
the management of cyanide poisoning by smoke inhalation exist [9]. Therefore, European experts met to
formulate an algorithm to improve the recognition and
management of cyanide poisoning and to enhance survival
rates.
Two algorithms were developed to improve the recognition
and management of cyanide poisoning: a prehospital and a
hospital-based algorithm. More information about the composition of the expert group and methodology can be found
in the Supplemental digital content (see text, Supplemental digital content 1, http://links.lww.com/EJEM/A30,
methodology; see text, Supplemental digital content 2,
http://links.lww.com/EJEM/A31, bibliography).
Literature Overview
Supplemental digital content is available for this article. Direct URL citations
appear in the printed text and are provided in the HTML and PDF versions of this
article on the journal’s website (www.euro-emergencymed.com).
0969-9546 c 2013 Wolters Kluwer Health | Lippincott Williams & Wilkins
Is hydrogen cyanide formed during a fire?
Several investigations have reported that carbon monoxide (CO) and HCN are major combustion products of
DOI: 10.1097/MEJ.0b013e328357170b
Cyanide inhalation Anseeuw et al.
materials commonly found in domestic structures and
high quantities of HCN are released, especially under
pyrolyzing conditions at high temperatures and low
oxygen content. In addition, the recycling of combustion
products within a confined space increases the formation
of HCN, and lower fire ventilation rates increase the
formation of HCN by 6–10 times [10].
The presence and amount of specific smoke constituents
vary within and between fires depending on the nature of
the fire substrate, the rate of burning, the temperature of
the fire and the ambient oxygen level [1,6].
CO is released in fires as a result of incomplete
combustion of carbonaceous materials. During combustion of nitrogen-containing and carbon-containing substances, HCN may be generated by burning synthetics
such as foam (polyurethane), acrylics, paints, nylon and
plastics (polyacrylonitriles, polyacrylamides), as well as
natural materials such as wool, silk, cotton, paper and
wood. In general, the more nitrogen compounds, the
greater the potential release of HCN during combustion.
The increasingly widespread use of polymers makes it
more likely that HCN will be encountered more
frequently in smoke [1,6–8,10–12].
Epidemiology
We must be aware that epidemiological data on cyanide
levels are prone to biases. Because cyanide has a very
short half-life and blood samples are rarely obtained
within a short time, the cyanide concentrations measured
are often erroneously low. The storage of sampled blood
(storage temperature, time between sampling and assay)
and the influence of various incident-specific and victimspecific factors (e.g. carboxyhaemoglobin saturation,
methaemoglobin content) can also contribute towards
the error [6,13].
Several case studies have reported different results. A
documented hotel fire claimed 97 lives and injured more
than 140 individuals. From fire dynamics modelling of this
case, the principal cause of death was attributed to heat
shock and oxygen depletion, explaining why burned
victims had low and nonlethal carboxyhaemoglobin and
blood cyanide levels. Interestingly, the burned victims
had lower carboxyhaemoglobin values, indicating that
smoke inhalation more likely contributed towards the
deaths of nonburned victims [1,14].
3
The Happy Land Social Club fire fatalities provided a
unique opportunity to examine the effects on a homogeneous healthy population that was exposed to an
identical smoke-filled environment. Of the decedents,
92% had carboxyhaemoglobin concentrations over 60%
and 81% of the victims had toxic cyanide levels. However,
no correlation was detected between carboxyhaemoglobin
and blood cyanide levels [1,17].
In another study of 178 deaths because of burns, fire
or smoke inhalation, positive results were found for
carboxyhaemoglobin in 111 cases (72%) and cyanide in 88
cases (62%). Lethal levels (> 50%) were found for
carboxyhaemoglobin in 44 cases (29%) and cyanide levels
(> 1 mg/l) in 48 cases (35%). Significantly higher
carboxyhaemoglobin and cyanide levels were observed
in the intoxicated, very young, very old and death-at-thescene victims, and cyanide levels showed a significant
correlation with carboxyhaemoglobin [18].
In contrast, in the New Jersey State database of fire
deaths, only a weak correlation was observed between
carboxyhaemoglobin and cyanide levels. However, elevated carboxyhaemoglobin levels were observed in 87%
of patients and elevated cyanide levels in 75% of
patients [2].
In an aircraft fire that killed 23 individuals out of 46,
toxicological reports indicated carboxyhaemoglobin levels
averaging 40% and cyanide levels averaging 2.33 mg/l in
the 23 victims. In contrast, the average carboxyhaemoglobin level was 2.7% and the average cyanide level was
0.04 mg/l in the survivors [19].
In another aircraft fire, 54 individuals died of smoke
inhalation and very low carboxyhaemoglobin levels were
detected, but cyanide was detected in every victim,
pointing out the primary role of HCN versus CO in these
victims [1].
During an insurrection in a prison, 35 inmates died of
smoke inhalation. Most (34%) showed cyanide levels of
2–4 mg/l and carboxyhaemoglobin levels of 5–10%,
indicating that HCN (pyrolysis of polyurethane mattresses) was the main cause of death [20].
Low carboxyhaemoglobin levels were found in another
hotel fire. Cyanide was also measured, but the results
were too sketchy [1,15].
One-hundred and nine fire victims were studied by Baud
and colleagues in the Paris area. The mean blood cyanide
levels in the survivors (0.5 mg/l) and the deceased victims
(3 mg/l) were significantly higher than those in the
control group (0.1 mg/l). There was a marginal positive
correlation between carboxyhaemoglobin and cyanide
levels [1,13].
In a prospective study including 144 patients with either
smoke inhalation or smoke exposure and 43 fire victims,
elevated cyanide blood levels were found in both
survivors (90%) and the deceased (100%). A statistically
significant correlation was observed between cyanide and
carboxyhaemoglobin levels [16].
In conclusion, CO and HCN play an important role in fire
smoke toxicity, and HCN sometimes appears to be the
primary cause of death. A limited correlation between CO
and cyanide levels makes the prediction of cyanide
concentration on the basis of the carboxyhaemoglobin
level almost impossible.
4 European Journal of Emergency Medicine 2013, Vol 20 No 1
Pathophysiology
Fire victims may be exposed to three potential injuries:
burns, trauma and smoke inhalation. However, 60–80%
of deaths at the fire scene are attributable to smoke
inhalation. Smoke is a heterogeneous compound unique to
each fire in both its chemical composition and its toxic
features. The components of smoke that cause damage are:
Smoke inhalation victims of a closed-space fire may
therefore suffer from concurrent poisoning with HCN,
CO and other asphyxiants. CO compromises arterial oxygen
transport, whereas cyanide blocks oxygen utilization at the
cellular level. The synergistic effect of combined CO and
HCN poisoning has been reported [1,6,11].
(1) Heat, with a risk of glottis oedema.
(2) Particulates, which are deposited in the airways
according to their size.
(3) Systemic toxins (up to 150 toxic molecules have been
identified).
(4) Respiratory irritants, causing intense and prolonged
inflammatory reactions.
Diagnosis
In addition, smoke inhalation can also produce oxygen
deprivation because of oxygen consumption by the fire and
asphyxiant gases. Houeto and colleagues studied erythrocyte cholinesterase activity in 49 fire victims and found that
it correlates with neither HCN nor CO. They believe that
oxygen deprivation or as yet undetermined toxic gases may
be responsible for this impairment [1,5,21,22].
HCN is a potent and rapidly acting poison. Signs and
symptoms appear within seconds to minutes after exposure
to moderate to high concentrations. The effect of a gas
always depends on two parameters: the concentration and
the duration of exposure. The cyanide ion, having a high
affinity for metalloproteins, inhibits about 40 enzyme
systems. It has an affinity in decreasing order for cobalt,
ferric iron (Fe3+) in methaemoglobin, cytochrome oxidase
and ferrous iron (Fe2+) in haemoglobin. It is thus principally
fixed on the cytochrome aa3 oxidase, present in high
concentrations in the mitochondria, inhibiting oxidative
phosphorylation and resulting in a shift from aerobic to
anaerobic metabolism. This anaerobic metabolism leads to
cellular ATP depletion and lactic acidosis. Organs rich in
cytochrome oxidase (brain, heart, liver) will be most affected.
Our bodies can detoxify cyanide using several mechanisms including conversion into nontoxic thiocyanate by
the enzyme rhodanese and conversion into cyanocobalamin by binding to hydroxocobalamin. These mechanisms
are overwhelmed by exposure to all but very small
concentrations of cyanide because of the depletion of
sulphur donors [6–8,11,21,23–25].
The effects of CO are produced through different
mechanisms:
(1) Combining with haemoglobin to carboxyhaemoglobin
and reducing the oxygen capacity;
(2) Left shifting the oxygen–haemoglobin dissociation
curve and thus impairing tissue oxygen availability;
(3) Combining with myoglobin and thus impairing
cardiac and skeletal oxygen availability; and
(4) Inhibition of cytochrome enzymes [1,5,21].
Poisoning can be diagnosed on the basis of different
criteria: clinical, biological or analytical.
Early manifestations of cyanide toxicity reflect neurologic
and respiratory stimulation, in an attempt to compensate
for tissue hypoxia, and include giddiness, confusion,
headache, vertigo and dizziness; nausea and vomiting;
palpitations; and hyperventilation or shortness of breath.
Later symptoms of acute cyanide poisoning reflect
neurological, respiratory and cardiovascular depression
arising from the inability to compensate for tissue hypoxia.
Eventually, seizures, bradycardia, hypotension, coma, respiratory and cardiac arrest will ensue. Cardiovascular
effects have been found in a canine model with two
distinct phases: the first phase includes features of a
hyperdynamic state, whereas the second phase follows a
pattern consistent with cardiovascular failure. The importance of bradycardiac heart failure, with preservation of
contractility, is introduced in this study. Cyanide also causes
permanent neurological disability, ranging from various
extrapyramidal syndromes to postanoxic vegetative
states [4,11,12,23–31].
Besides clinical signs and symptoms, biological or
analytical criteria can be used to predict cyanide
poisoning. Different studies have found a significant
correlation between plasma lactate and blood cyanide
levels, both in fire victims and in victims of pure cyanide
poisoning. A plasma lactate concentration of at least 90 mg/
dl is a sensitive and specific indicator of cyanide poisoning.
In general, high lactate values are strongly suggestive of
cyanide poisoning following smoke inhalation and may thus
be used as a severity marker of cyanide toxicity.
Unfortunately, lactic acidosis is nonspecific and is also
found in a huge number of critical illnesses, even in CO
poisoning. Serial lactate measurements can be useful in
assessing the severity of cyanide poisoning. Theoretically,
venous blood arteriolization should be present, but this
finding has been poorly documented [11,13,26,32–34].
In contrast to CO, there is no rapid detection method for
HCN in blood and it takes time to obtain analytical
confirmation. Lab analysis will confirm the diagnosis, but
treatment should start without waiting for the lab results.
Because of its short half-life, a blood sample should be
taken as soon as possible, if possible at the scene of the
fire. The relationships between cyanide concentrations
and the severity of symptoms are described as follows:
concentrations in the range of 0.5–1 mg/l are considered
Cyanide inhalation Anseeuw et al.
as mild, between 1 and 2 mg/l as moderate, between 2
and 3 mg/l as severe and greater than 3 mg/l as lethal.
Studies were performed to evaluate the cyanide breath
concentration as an indicator of systemic cyanide poisoning [8,12,27,35,36].
Clinical smoke inhalation severity scores (composed of
history, clinical examination and vital signs) seem to be
the single strongest predictor of CO and HCN poisoning [4,5,21,28,29,31].
The diagnosis of cyanide poisoning is challenging because
of the lack of pathognomonic symptoms and signs. To start
with, diagnosis should be based on an index of suspicion,
altered mental state and lactic acidosis. The suspicion of
cyanide poisoning is heightened by the findings of
hypotension combined with bradycardia [1,6,8,12,21,37].
Treatment
HCN is fast acting; thus, the speedy and empiric
treatment of fire smoke victims is critical for achieving
successful intervention. Management involves removing
the victim from the source of the cyanide, basic life
support and administration of high-flow 100% oxygen.
Supplemental oxygen is a crucial part of supportive care
in cyanide poisoning, as it treats CO poisoning and may
reactivate cyanide-inhibited mitochondrial enzymes. The
use of hyperbaric oxygen for cyanide toxicity remains
controversial: some studies have reported beneficial
effects, whereas others have failed to report any improved
outcome [11,21,35].
If necessary, additional supportive measures (e.g. blood
pressure support, treatment of seizures, etc.) have to be
adopted. Some report advocate aggressive cardiovascular
support to increase hepatic clearance of cyanide by
rhodanese, which may be successful in treating cyanide
poisoning. Most authors, however, advise the administration of an antidote when suspecting cyanide toxicity. Fire
smoke victims presenting with normal vital signs, a
normal clinical examination and no lactate increase can be
safely discharged home [4–8,11,21,29,38].
Three large families of antidotes exist: methaemoglobinforming agents [nitrites, 4-dimethylaminophenol (4-DMAP)],
sulphur donors (thiosulphate) and cobalt compounds (dicobalt edetate, hydroxocobalamin) [11,12,25].
Nitrites reduce blood cyanide by forming methaemoglobin, which chelates cyanide to form cyanomethaemoglobin. 4-DMAP also neutralizes cyanide by inducing
methaemoglobin. As cyanomethaemoglobin dissociates,
it allows free cyanide to be converted into thiocyanate by
rhodanese. Significant side-effects such as vasodilatation,
hypotension, nephrotoxicity and haemolysis have been
observed during treatment. 4-DMAP can generate
methaemoglobin concentrations above 30%, exceeding
the threshold value above which cardiovascular collapse
and death can occur [6,12,25,37,39–43].
5
Methaemoglobin generators have the potential to impair
the oxygen-carrying capacity of haemoglobin by displacing oxygen from it. In smoke inhalation victims, with
concomitant hypoxaemia of multiple causes and possible
pulmonary injury, there is an obvious added risk
associated with the formation of methaemoglobin. The
additive oxygen-depriving effects of nitrites and CO can
even be lethal, particularly in those with a pre-existing
low cardiopulmonary reserve. This has been shown by the
work of Moore and colleagues [7,21,37,39,42,43].
The enzyme rhodanese forms the less toxic thiocyanate,
which is cleared renally by adding a sulphur atom to the
cyanide. This reaction is accelerated more than three
times by the administration of thiosulphate. Although the
brain is highly susceptible to cyanide toxicity, thiosulphate does not readily penetrate cells and the mitochondria and its effectiveness is limited by its delayed onset of
action, short half-life and small distribution volume. It is
often used in conjunction with other rapid-acting agents
rather than as a single antidote [11,25,39,42,44].
Cobalt compounds are rapid and powerful cyanide
antidotes because of the strong affinity of cyanide to
cobalt. Dicobalt edetate works by chelation of cyanide to
form cobalticyanide. Adverse effects of dicobalt edetate
include deleterious cardiovascular effects, urticaria, seizures and anaphylactic shock. The solution contains free
cobalt ions, resulting in severe cobalt toxicity in the
absence of cyanide. For those reasons, it is now
recommended as a second-line antidote [25,42,44].
Hydroxocobalamin detoxifies by chelation of cyanide to
form cyanocobalamin, or vitamin B12, which is excreted
renally. Hydroxocobalamin is well tolerated, with only
minor adverse effects (skin discoloration, chromaturia,
urticaria, allergy) and it does not reduce oxygen-carrying
capacity. Data from both human and animal studies shows
that administration of hydroxocobalamin increases blood
pressure, because of its nitric oxide-scavenging effects,
and may be beneficial in counteracting hypotension in
cyanide-poisoned patients. Pharmacokinetic and pharmacodynamic data suggest a predominantly extracellular
partitioning of the antidote, but also intracellular and
cerebrospinal fluid penetration. Because of its half-life,
single-dose therapy, in sufficient quantity to bind all
cyanide present, is likely to be adequate. When
administered by an infusion, it dissolves almost immediately into the different tissue compartments, resulting in
a rapid onset of action [12,25,40,42,44–52].
Prospective and retrospective human and animal data
have described antidotal properties, with reported
survival rates ranging from 42 to 72% for prehospital
administration of hydroxocobalamin for suspected cyanide poisoning by fire smoke inhalation [25,37,40,48]
Hydroxocobalamin can be used successfully in patients
with cardiorespiratory instability, and also remains useful
6 European Journal of Emergency Medicine 2013, Vol 20 No 1
in patients with a cardiorespiratory arrest because of
cyanide poisoning. Bebarta and colleagues compared
hydroxocobalamin with thiosulphate and sodium nitrite
with thiosulphate for cyanide poisoning treatment.
Showing no difference in mortality, serum acidosis or
serum lactate, the hydroxocobalamin group showed a
faster return to the baseline mean arterial pressure than
the thiosulphate group. This may have important clinical
consequences. The recommended dose of hydroxocobalamin is 70 mg/kg (5 g). A second dose of 5 g should be
given in case of cardiac arrest or persistent cardiovascular
instability. Doses of 2.5 g have been shown to be
insufficient to avoid neurological sequelae. The use of
hydroxocobalamin can be combined with the administration of thiosulphate, but they should never be mixed in
the same vial because of the formation of inefficient
thiosulphatocobalamin [5,11,25,37,40,46–49,52–55].
The safety profile and rapid onset of action of hydroxocobalamin render prehospital or hospital empiric treatment of smoke inhalation-associated cyanide poisoning a
reality [5,6,21,25,37,44].
Many agents have been explored as prophylactic cyanide
antagonists. Cobinamide and sulfanegen seem to be
Fig. 1
Cyanide poisoning by fire smoke inhalation
Prehospital algorithm
Smoke inhalation incident
Evaluate:
Fire in an enclosed space
Duration of exposure
Number of victims
Administer O2 100%
Severe poisoning
GCS≤9
Intermediate
poisoning
GCS 10−13 and/or
abnormal ABC
No neurological
and/or haemodynamic
symptoms
GCS≥14
Collect blood samples, if possible
Hydroxocobalamin
5 g (70 mg/kg) i.v.a
Hydroxocobalamin
5 g (70 mg/kg) i.v.b
Monitoring
Transfer to hospital
Prehospital algorithm. GCS, Glasgow Coma Scale.
a
If cardiac arrest, administer 10 g of hydroxocobalamin. bIf several victims, begin with 2.5 g and top up to 5 g.
Cyanide inhalation Anseeuw et al.
Algorithms
effective as intramuscular cyanide antidotes in mouse
models, but further human testing is necessary [11,56].
On the basis of the above review, two algorithms for the
treatment of smoke inhalation victims were developed.
Although the use of any specific cyanide antidote in
cyanide poisoning is unquestionable, the overall evidence
for any specific antidote remains weak. With respect to
practicality and safety advantages, the use of hydroxocobalamin seems most appropriate, but a large multicentre, randomized study is necessary to confirm this
approach.
Prehospital algorithm
Because of the rapid onset of cyanide toxicity, we
advocate the administration of an antidote as soon as
possible, even prehospital. Although Europe has a culture
of prehospital medical care, the first actors may differ
from system to system. The prehospital algorithm was
Fig. 2
Cyanide poisoning by fire smoke inhalation
Hospital algorithm
Smoke inhalation incident
Other injuries
(burns, trauma, etc.)
Toxic effects
of smoke
Refer to
other protocols
Administer O2 100%
History (type of fire, duration of exposure)
Clinical examination
Technical examination – imaging
Lactates
HbCO
Arterial and venous blood gas
Laboratory as needed
CO poisoning
5. ECG
6. Thorax radiographs (only if necessary)
7. CN analysis (not required for acute treatment)
Treat if
clinical signs or HbCO>10%
Follow local
guidelines
Other poisoning
(acrolyne, phosgene,
benzine, etc.)
HOCo, 5 g
High (70 mg/kg) i.v.
Lactatea
after 2 h
Prehospital
antidote
Lactatea
Normal
Need for
end-organ monitoring
1.
2.
3.
4.
Normal
(1)
(2)
(3)
High
Lactatea
High
HOCo, 5 g
(70 mg/kg) i.v.
High
Normal
High
Normal
If needed, consider transfer to reference centre
Hospital algorithm. CO, carbon monoxide; CN, cyanide; HOCo, hydroxocobalamin.
a
Consider other causes (e.g. hypovolaemia).
Lactatea
after 2 h
Cyanide
poisoning
Lactatea
after 2 h
Consider sodium
thiosulphate
No antidote
7
Normal
Consider
discharge
8 European Journal of Emergency Medicine 2013, Vol 20 No 1
designed in such a way that it could be used by
paramedics, nurses and emergency physicians (Fig. 1).
We propose dividing patients into three groups, depending
on the degree of cyanide poisoning. We grade the degree of
poisoning using the Glasgow Coma Scale (GCS) and vital
signs. Severe poisoning is characterized by a GCS lower
than 9 and/or severe haemodynamic instability (defined as
heart rate below 40 bpm and/or systolic tension below
90 mmHg). Intermediate poisoning is described as a GCS
from 10 to 13 with or without abnormal vital signs, and the
absence of significant cyanide toxicity is characterized by a
GCS at least 14. Using the GCS as the major determinant
may result in overtreatment, but for us, this is the only
reliable clinical parameter prehospitally to characterize
cyanide poisoning.
We advocate the administration of high-flow 100% oxygen
to all smoke inhalation victims and transportation to an
emergency department. Blood sampling for analytical
analysis is proposed, as long as it does not delay patient
treatment.
Early administration of 70 mg/kg (5 g) hydroxocobalamin
is advocated for all intermediate or severely poisoned
patients. If a smoke inhalation victim presents with
cardiorespiratory arrest or haemodynamical instability,
10 g hydroxocobalamin must be administered immediately, even during cardiopulmonary resuscitation. Giving
the utmost importance of rapid treatment, we propose
administering 2.5 g if multiple intermediate smoke
inhalation victims are present at the scene, knowing that
this is an insufficient dose, provided that the antidote is
immediately topped up to 5 g at the hospital.
All patients who received hydroxocobalamin or presented
symptoms of cyanide poisoning should be admitted for
end-organ monitoring. Asymptomatic patients, without
antidotal therapy and negative lactates, can be safely
discharged home after a short observation period.
Conclusion
There is growing evidence of cyanide toxicity in fire smoke
victims presenting to the emergency department. Reducing mortality and morbidity attributed to cyanide inhalation primarily depends on early recognition and the timely
administration of an antidote. Several specific cyanide
antidotes are available, but given the practical and safety
advantages, hydroxocobalamin is the preferred antidote. We
developed two algorithms to improve the recognition and
management of cyanide poisoning. Evaluation of these
guidelines and the effect of implementation are planned.
Acknowledgements
Conflicts of interest
Merck Serono Company supported the logistics of the
Paris meeting. All experts received an honorarium from
Merck Serono Company for taking part in the meeting.
Professor Geldner received a honorarium from Merck
Germany for giving lectures. He also participated at a
National Advisory Board. For the remaining authors there
are no conflicts of interest.
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4
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A lactate concentration at least 90 mg/dl must be
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