Algorithm for managing injury from smoke inhalation

R M Langford, R F Armstrong

Thermal injury accounts for 14 000 casualties a vear inthe United Kingdom. With improvements in managingcutaneous burns mortality has steadily reduced sothat inhalational injury from smoke and hot, toxicgases is increasingly important in outcome.' Whenoverlooked, smoke inhalation can lead to early or latedeterioration in the patient's condition due to damageto the airways or lungs. In addition, poisoning mayoccur by inhalation of gases such as hydrogen cyanideor carbon monoxide. These problems were experiencedin the fire at King's Cross in 1987, in which a fifth of thevictims were found at postmortem examination tohave high concentrations of carboxyhaemoglobin.Furthermore, despite controversy over the forensicmethod used there was evidence that cyanide poisoningmay have had a contributory role in some of the deaths.In this unusual fire, however, the heat blast led rapidlyto asphyxiation, thus reducing the duration ofexposure to toxic inhalation.

This disaster, supported by previous experiencewith inhalational burns in this unit, suggested theneed for a protocol to guide clinicians in the earlymanagement of these patients. We have proposed animmediate care plan in the form of an algorithm. Thisaims to promote early recognition and treatment of theairway problems and the poisoning that result from

hot, toxic fumes. The flow chart (figure) was designedto give direction to the admitting clinicians andparamedical staff. Points needing explanation arelabelled on the chart (I to V) and elaborated in the text.

Oxygen administration and measurement (I)In the initial assessment of a burnt patient evidence

of underlying hypoxaemia and poisoning may behidden by smoke stains or burns. Confused oraggressive behaviour may be due to cerebral anoxia andshould not be attributed only to pain. To avoid theimmediate and long term cerebral damage caused byhypoxia, upper airway obstruction, and carbonmonoxide poisoning' early administration of highconcentrations of inspired oxygen is essential. Mostof the commercially available plastic masks (MC,Hudson, etc) achieve variable and unpredictableoxygen concentrations that depend on the patient'srespiratory rate, tidal volume, and rate of inspiratoryairflow. The best choice is one of the high airflowmasks with oxygen enrichment, such as the Venti-mask,4 which can achieve 60% inspired concentration.When 100% oxygen is necessary a tight fitting oronasalmask connected to a breathing system with anexpiratory valve and reservoir bag should be used.

Alternatively, the patient can be intubated andventilated with 100% oxygen. A non-rebreathingsystem should be used in cases of suspected carbonmonoxide or cyanide poisoning to avoid reabsorption.Measuring and interpreting the blood concentration ofoxygen in these patients is difficult. A conventionalblood gas analyser with electrodes measures thetension of oxygen dissolved in the plasma. In healthypatients the oxygen tension determines the percentageof haemoglobin that binds oxygen to form oxyhaemo-globin. Such analysers calculate this functionaloxygen saturation on the assumption that only normalhaemoglobin (capable of binding oxygen) is present.Blood from a fire victim, however, may well containhigh carboxyhaemoglobin concentrations with adangerously low concentration of oxyhaemoglobin(despite high measured oxygen tension and highderived calculated saturation). In these circumstancesonly a blood oximeter that uses spectrophotometryactually measures the concentrations of oxyhaemo-globin, reduced haemoglobin, carboxyhaemoglobin,and methaemoglobin in the sample.The oxyhaemoglobin can then be used to calculate

the oxygen content of the blood, which may beconsiderably lower than the calculated oxygensaturation would suggest. In this way the bloodoximeter will confirm a presumptive diagnosis ofcarbon monoxide poisoning and show any deficiency inoxygen delivery to the tissues. Given their currentpopularity, it should be noted that pulse oximeters areunreliable in the presence of carboxyhaemoglobin andmethaemoglobin' as they too cannot measure each tvpeof haemoglobin independently.

Observe Continue 100% oxygen Intubation (IV) and Observe and giveI..............I...... and give cyanide antidotes intermittent positive pressure routine cutaneous

Consider hyperbaric oxygen ventilation as top priority (V) burn treatment

Algorithm of earlv management of inhalational injury in fire victim. (Roman tnumerals indicate relevant

accompanying text)

Carbon monoxide poisoning (II)Carbon monoxide combines strongly with haemo-

globin, causing impairment of oxygen transport. Inaddition, there is evidence of direct tissue toxicity

BMJ VOLUME 299 7 OCTOBER 1989

Intensive Care Unit,University CollegeHospital, LondonWC1E 6AUR M Langford, FCANAES,senior registrar in anaesthesiaR F Armstrong, FCANAES,consultant anaesthetist

Correspondence to:Dr Armstrong.

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caused by unbound carbon monoxide dissolved inthe plasma.' Several workers consider that it is thistissue toxicity that produces the svmptoms and thecerebral damage and suggest that carboxvhaemoglobinconcentrations correlate poorly with clinical conditionand prognosis.- Others point out a good associationbetween carboxyhaemoglobin concentrations andclinical state and describe concentrations of >400'Scausing coma and >60% collapse. Carboxvhaemo-globin may also be measured as a diagnostic test:concentrations over 15% on admission suggest smokeinhalation. Back calculation with a nomogram has beenrecommended as a means of estimating concentrationsat the time of exposure.'Carbon monoxide poisoning presents with symptoms

and signs ranging from nausea and headache to comaand convulsions. In a burnt patient anv alteration inthe neuropsychiatric state or consciousness should beviewed with suspicion. Laboratory bench tests orblood oximeters measure carboxyhaemoglobin byspectrophotometry. Carbon monoxide meters (such asthe Bedfont Micro Smokerlyzer) are available tomeasure exhaled carbon monoxide. Metabolic acidosismay be distinct.The immediate treatment of carbon monoxide

poisoning is with high concentrations of oxygen.Several workers recommend giving hyperbaricoxygen," '( which increases the amount of oxvgendissolved in plasma, thereby improving oxygendeliverv to the tissues. This also combats the directlytoxic effects of carbopi monoxide in tissues. Hyperbaricoxygen is especially recommended in (a) patients whoare or have been unconscious; (b) patients withneurological symptoms; (c) patients with cardiaccomplications; (d) patients with carboxyhaemoglobinconcentrations >40%S); and (e) pregnant women.Comatose patients should be transferred early,but late referral for hyperbaric oxygen may beworth while. For the nearest hyperbaric chambertelephone the Royal Navy, Portsmouth (0705) 822351ext 24875/41769/22008.

Cyanide poisoning (III)Fumes from smouldering plastics such as poly-

urethane, nylon, and Acrilan contain hydrogencyanide gas."' Inhaling these fumes results in rapidsystemic absorption and cyanide poisoning. Cyanideparalyses mitochondrial respiration by bindingreversibly with enzymes containing ferric ions.In particular, cytochrome oxidase is affected andoxidative phosphorylation stops.

Clinical signs of cyanide poisoning are produced bycellular hypoxia and therefore affect several systems.Commonly, abnormalities of the central nervoussystem occur with headaches, dizziness, and fits. In theearly stages the hypoxia causes stimulation of therespiratory centre with tachypnoea and dyspnoea laterfollowed by bradypnoea and apnoea. Cardiovascularsigns include hypertension and tachycardia leadingeventually to hypotension and cardiovascular collapse.

Diagnosis-Unlike with industrial exposure orattempted suicide bv ingestion the evidence forcyanide poisoning in a fire is circumstantial. Measuringblood cyanide concentrations is difficult as cyanidedisappears rapidlv from stored blood specimens.Furthermore, the actual process of measurement takesseveral hours and is usually not available locally.Nevertheless, a sample of heparinised whole bloodshould be sent immediately to the regional poisons unitlabelled with the time of sampling and the time sincethe poisoning occurred. Concentrations of 13 timol/lare commonly seen in smokers. Concentrations of>50 ytmol/l are associated with altered consciousness,and concentrations of > 100 limol/l are lethal.'l Because

of the difficulty in measuring cyanide, thiocyanateconcentrations are considered useful bv some' but notall workers.'4 Burns units may find a simple hydrogencyanide gas detector (such as the Drager tube) useful asan early diagnostic aid. Findings supporting cyanidepoisoning are a normal arterial oxygen tension, adecrease in measured (as opposed to calculated) arterialoxygen saturation due to cvanhaemoglobin, anincreased mixed venous oxygen saturation (>75%),and a decrease in the arteriovenous difference inoxygen content (normally 5 ml/100 ml). Additionally, asevere metabolic acidosis, high lactate concentration,and increased anion gap (> 12 [imol) may suggestcellular hypoxia. The usefulness of high carboxv-haemoglobin concentration as a marker of cyanideinhalation is controversial.''

Treatment of cyanide poisoning (III)Unlike cyanide poisoning by ingestion systemic

absorption of further cyanide stops on removal of thefire victim from the scene. At this stage the cyanide isalready present in the blood and tissues. Emergencytreatment starts with transfer to hospital and givingoxygen. The urgent objectives are to reduce bloodcyanide concentrations and promote detachment ofcyanide from cytochrome oxidase in the tissues. Thereare three principal methods.

Conversion of haemoglobin to methaemoglobin by theantidote promotes the binding of cyanide to the threeferric haem groups in each methaemoglobin molecule.The percentage of methaemoglobin achieved plusthe percentage of carboxyhaemoglobin should bemeasured and not allowed to exceed 40%/0, thusavoiding excessive reduction of oxygen carryingcapacity. Therefore, in the case of fire victims cautionshould be exercised until the concentration ofcarboxyhaemoglobin is known. Antidotes used toproduce methaemoglobin are amyl nitrite, sodiumnitrite, and 4-dimethylaminophenol. It shouldbe noted that sodium nitrite can induce distinctvasodilatation and hypotension.

Augmentation of the endogenous cyanide detoxificationsystem-Normally cyanide is converted slowly to theessentially non-toxic thiocyanate in the bloodstreamand by enzymes such as rhodanase in the mitochondria.Giving sodium thiosulphate and thus providing anextra source of sulphur will accelerate this process.

Chelation of the cyanide- Dicobalt edetate combineswith cyanide to form an inert complex, cobalticyanide.A potentially serious consequence of its use, however,is cobalt toxicity. This is more likely in the absence ofcyanide. Although dicobalt edetate has been the agentof choice in the United Kingdom, it should be usedonly in cases of severe poisoning, whether suspected orproved. When the patient is still conscious someworkers propose that the less toxic antidotes should beused.'6The protocol for the treatment of cyanide poisoning

has recently been the subject of a joint study in Geneva,under the auspices of the World Health Organisation,by the International Programme on Chemical Safetyand the Commission of the European Communities.TVThe following section summarises the recommenda-tions of their document IPCSICEC Evaluation ofAntidotes in Poisoning by Cyanide.

FIRST AID MEASURES

These measures are to be undertaken only in cases ofunequivocally severe poisonings.

Trained staff (wearing protective clothing andbreathing apparatus if hydrogen cyanide or liquidcyanide preparations are involved should

* stop further exposure

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* start artificial ventilation with 100% oxygen by anon-rebreathing system* give 0 2-0-4 ml amyl nitrite through an Ambu bag.

If a doctor is present immediately on the scene he orshe should

* start artificial ventilation with 100% oxygen by anon-rebreathing svstem* give 0 2-0 4 ml amyl nitrite through an Ambu bag.

HOSPITAL TREATMENT

Hospital doctors must establish whether specificantidotal treatment was given at the time of theincident before further doses are given, especially inthe case of agents that form methaemoglobin.

In cases of severe poisoning when the patient isin deep coma with dilated, non-reactive pupils anddeteriorating cardiorespiratory function (bloodcyanide concentrations 1 15-154 pmol/l (3-4 mg/l))

* start artificial ventilation with 100% oxygen* start cardiorespiratory support

Then give

* either 10 ml of 30o sodium nitrite solution (300 mg)intravenously over 5-20 minutesor 5 ml 5o/0 dimethylaminophenol solution (250 mg or3-4 mg/kg) intravenously over one minuteor 20 ml 1 5% dicobalt edetate solution (300 mg)intravenously over one minuteor 10 ml 40%, hydroxocobalamin solution (4 g)intravenously over 20 minutes* and 50 ml 25% sodium thiosulphate solution(12 5 g) intravenously over 10 minutes.

In cases of moderately severe poisoning whenthe patients have suffered a short period of uncon-sciousness, convulsions, vomiting, or cyanosis (bloodcyanide concentrations 77-115 [tmol/l (2-3 mg/l))

* give 100% oxygen but for no longer than 12-24 hours* observe in intensive care* give 50 ml 25% sodium thiosulphate solution(12 5 g) intravenously over 10 minutes.

In cases of mild poisoning when patients havenausea, dizziness, and drowsiness (blood cyanideconcentrations <77 [tmol/l (<2 mg/I))* give oxygen* reassurance* prescribe bed rest.

The above scheme was developed to deal with allmodes of cyanide poisoning. In smoke inhalation,however, there may be doubt initially about thepresence of cyanide poisoning. In these circumstances,therefore, we recommend using the fairly safeantidotes amyl nitrite and sodium thiosulphate.Thereafter, only when concentrations of carboxy-haemoglobin and methaemoglobin are known and thepatient's clinical progress has been reviewed should theother agents be used.

Severely poisoned patients may on occasion fail torespond to the initial dose of a specific antidote.Although repeated doses of hydroxocobalamin orsodium thiosulphate, or both, are unlikely to beassociated with toxicity, expert advice should besought before a repeated dose of any other specificantidote is given. Intensive supportive treatment isof paramount importance in these circumstances.Finally, the above scheme raises the question of

whether amvl nitrite should be made available toambulance crews and paramedical staff at the scene ofthe accident.

Indication for intubation (IV)When airway obstruction is suspected indirect

laryngoscopy or fibreoptic laryngoscopy or broncho-scopy is an invaluable investigation in the handsof experts. Indications for intubation2' are (a) un-consciousness or failure to maintain an airway;(b) evidence of severe carbon monoxide or cyanidepoisoning; (c) stridor; (d) facial burns and depressionof the central nervous system; (e) facial burns andcircumferential burns of the neck; (t) full thicknessburns of the nose or lips; and (g) visible oedema of thepharynx and larynx. Nasotracheal tubes are morecomfortable and require less sedation. This will allowspontaneous respiration with continuous positiveairway pressure (or intermittent positive pressureventilation as appropriate).

Respiratory failure (V)The onset of respiratory failure may be recognised

clinically with increasing respiratory rates anddyspnoea. Criteria for respiratory support are(a) respiration rate >30/min; (b) vital capacity<12-15 ml/kg; (c) arterial oxygen tension <11 0 kPawhen breathing 40% oxygen; (d) arterial oxygentension <6-0 kPa when breathing air; and (e) arterialcarbon dioxide tension high enough to cause fall in pHto 72.When severe hypoxaemia occurs with good

ventilatory response (arterial carbon dioxide <6 0 kPa)continuous positive airway pressure by mask can beeffective." Otherwise intermittent positive pressureventilation through a nasotracheal tube will allowsatisfactory treatment of respiratory failure with easysedation and management of the patient. Early venousaccess for fluids and monitoring of central venouspressure (under scrupulous asepsis) is recommendedbefore dressings, ointments, and oedema renderthe task too difficult. The place of tracheostomy iscontroversial, but modern attitudes are less critical"xand it may lead to less long term laryngeal scarring.'9

We thank Dr G N Volans (poisons unit, New CrossHospital), Dr 'F Meredith (international programme onchemical safety, division of environmental health, WorldHealth Organisation), Dr I West (department of forensicmedicine, Guy's Hospital), Dr P A ToselJnd (Guy'sHospital), Dr D Chambers (coroner, inner north London),and Dr P V Cole and Mr C J Vesey (St Bartholomew'sHospital) for their expert advice and Miss Annmarie Worlevfor typing the manuscript. Finally, we thank Dr M Mercier,international programme on chemical safety, department ofenvironmental health, World Health Organisation, forpermission to use the document on cyanide poisoning.The algorithm is available in poster form from the authors.

I Home Office. Firt statistics, L'nzied Kingdom. London: HNMSO, 1986.2 lVenus B, MiatsLida T, Copiozo JB, Mathru M\. Prophylactic intubation and

continuous positive airwav pressure in the management of inhalation injlurvin burn victims. Crnl Cure Med 1981;9:519-23.

3 Mvers RAM, Snyder SK, Emhoff TA. Sub acute sequelae of carbon monoxidcpoisoning. .Ann EenergMed 1985;14:1163-7.

4 Campbell EIM1. How to use the Venturi ma-sk. Lancet 1982;ii: 1206.5 Tremper KK, Barker SJ. Pulse oximetry. Anaesthesiology 1989;70:98-108.6 Goldbaum LR, Orellano F, Degal E. Mechanisms of the toxic action of carbon

monoxide. Ann Clin Lab Sci 1976;6:372-6.7 Norkool DM, Kirkpatrick JN. rreatment of acute carbon monoxide poisoning

with hyperbaric oxygen: a review of 115 cases. Ann Emerg Aled 1985;14:1168-71.

8 Clark CJ, Campbell D, Reid WH. Blood carboxyhaemoglobin and cyanidelevels in fire survivors. Lancet 1981;i: 1332-5.

9 Broome JR, Pearson RR, Skrine H. Carbon monoxide poisoning, forgottennot gone! BrJ7 Hosp Med 1988;39:298-305.

10 Anonvmous. 'I'reatment of carbon monoxide poisoning. Drug Ttler Bull1988;26(20):77-9.

11 Wald PH, Balmes JR. Respiratory effect of short term high intensity toxic

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inhalations: smoke gases and fumes. Journal of Intensive Care Medicine1987;2:260-78.

12 Hall AH, Rumack BH. Clinical toxicology of cyanide. Ann Emerg Med1986;15:1067-74.

13 Stevenson RN, Kingswood C, Cohen SL, Vesey CJ. Cyanide and fire victims.Lancet 1988;ii: 1145.

14 Holland MA, Kozlowski LM. Clinical features and management of cyanidepoisoning. Clin Pharm 1986;5:737-41.

15 Barillo DJ, Goode R, Rush BF, Reng Lang Lin, Freda A, Anderson EJ. Lackof correlation between carboxyhaemoglobin and cyanide in smokeinhalation injurv. Curr Surg 1986;43:421-3.

16 Daunderer M. Fatal smoke inhalation of hydrogen cyanide from smoulderingfires. Fortschr Med 1979;97:1401-5.

17 Smith RA, Kirby RR, Gooding JM, Civetta JM. Continuous positive airwaypressure (CPAP) by face mask. Cnt Care Med 1980;8:483-4.

18 Astrachan DI, Kirchner JC, Goodwin WJ. Prolonged intubation vstracheostomy complications-practical and psychological considerations.Laryngoscope 1988;98:1165-9.

19 Sataloff DM, Sataloff RT. Tracheotomy and inhalation injury. Head NeckSurg 1984;6:1024-31.

20 Bartlett RH, Niccole M, Travis MJ, Allyn PA, Furnas DW. Acutemanagement of the upper airway in facial burns and smoke inhalation.Arch Surg 1976;3:744-9.

(Accepted 7 August 1989)

Lesson of the Week

Communicating with Asian patients

Kathryn A Stevens, R F Fletcher

Patients from the Asiansubcontinent who do notspeak or read Englishneed the help of aqualified interpreter orwritten information orvideos in their ownlanguage

Dudley Road Hospital,Birmingham B18 7QHKathryn A Stevens, BSC,state registered dietitian,department ofnutrition anddieteticsR F Fletcher, FRCP,consultant physician, diabetesand endocrine unit

Correspondence to:Miss Stevens.

BrTMedJ 1989;299:905-6

Patients cannot hope to benefit fully from the advicegiven in a consultation or be expected to comply withtreatment if they cannot understand the informationthat is given to them. Many of our patients are of Asianethnic origin, and some have obvious difficultieswith written and spoken communication. Though aprevious report recommended providing teachingmaterials in Asian languages,' there is doubt aboutthe usefulness of such written material because ofuncertainty about the level of literacy among patients.To help us develop suitable material in the dieteticdepartnment we carried out a survey of our patientsto assess the possible value of different ways ofcommunicating with them.

Patients, methods, and resultsPatients of Asian ethnic origin from the Indian

subcontinent who attended the general outpatientsdepartment at this hospital over seven days in May1988 were invited to answer a short questionnaire.Only one patient refused, and 150 patients wereinterviewed by an Asian interpreter. Relatives were notasked to interpret.The patient's ability to read English and an Asian

language was assessed by asking the patient to readaloud a short, simple sentence in the appropriatelanguage. Each sentence was different to reduce thepossibility of the patient guessing the content.The patients' ages ranged from 13 to 74; 96 were

women. Eighty five could read an Asian language:Punjabi (43), Urdu (22), Hindi (10), Bengali (5), andGujarati (5).A total of 76 of the 150 patients could speak English,

TABLE I-Literacy among 150 patients of Asian origin seen inoutpatient clinics

Literacy No of patients

Read English only 20Read English and an Asian language 33Read an Asian language only 52Read no language 45

TABLE iI-Numbers of men and women of Asian origin who couldspeak English according to age

Men WomenAge

(years) No No speaking English No No speaking English

13-28 1 1 1 1 32 2129-60 3 1 22 56 1861-74 12 2 8 2

zA doctor examines a patient in the casualty department after a roadaccident

and 53 could read it as well (table I). All of the men andtwo thirds of the women aged 13 to 28 could speakEnglish but the proportion fell to under a fifth of themen and one quarter of the women aged 61 to 74 (tableII). Fifteen patients said that they could read, but theywere unable to do so when tested.

DiscussionOur patients fell into three groups of roughly equal

sizes. One third read English, and often an Asianlanguage as well, one third read an Asian languageonly, and one third could not read. Among thosespeaking Asian languages, about half spoke Punjabi,but four other languages were also spoken. Thus theneeds of our patients for help in understandinginformation about their health care are highly variable.One hundred and twenty five of our patients wanted

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