Effects_of_Smoke_Inhalation

COVENTRY UNIVERSETY School of health andg Social Sciences Module 226PM 

Applied anatomy, path physiology & Pharmacology for paramedics Effects of Smoke Inhalation SID 3417067 words 2413 total 2578 Abstract The effects of smoke inhalation and poisons such as cyanide and carbon monoxide provide many difficulties for pre-hospital care providers. This article will review the effects of these poisons on the body and the current treatments available for these conditions including drugs such as Cyanokit (hydrocxocobalamin) which is currently licensed for use in the USA and France and critically review the studies undertaken for Cyanokit. Key words : Cyanokit, cyanide poisoning, smoke inhalation, Carbon monoxide, The first part of this article will focus on the number of fire related deaths around the UK with data from the department for local governments who record all the fire related figures for the UK and at how UK fire services have reduced the number of fires and fire related deaths over the last 50 years. There will then be a focus on how the data relates to the causes of death such as burns or smoke inhalation, followed by the physiological effects of the smoke inhalation and the current treatments in practice. Finally, the article will analyse the state of the art treatments such as hyperbaric oxygen for carbon monoxide poisoning; or Cyanokit "vitamin B12" for cyanide poisoning, with a look at the practicality of whether these treatments could be implemented for pre-hospital services in the UK. Fire safety awareness campaigns on TV, property safety checks and fire alarm fittings have become part of the day to day work for fire fighters and a proactive approach by fire services across the UK. This means that the amount of deaths around the UK has dropped over the last 20 years. However when you look at the data from 2007 it shows that there were 443 fire-related deaths in the UK, just 10 per cent less than the 2006 figure of 491. This included six fire fighter fatalities in 2007 and two in 2006. The total number of deaths in the UK in 2007 is the lowest total recorded since 1950. (Department for Local Governments 2009) These figures represent all fire related deaths in the UK including dwellings, cars and business property fires and data from the MOD. However, this data does not represent the actual cause of death, nor distinguish between burns or flame related fatalities or whether the cause of death was due to smoke inhalation or other causes. The cause of death figures show the most commonly identified cause of death from a fire incident is being overcome by gas or smoke. In 2007, fire and rescue services reported that 193 people died this way, accounting for 44 per cent of all deaths. A further 88 (20%) deaths were attributed jointly to both burns and being overcome by gas or smoke, whilst 115 (26%) were due to burns alone. (Department for Local Governments 2009). So when considering this large percentage of fatalities we can see that the main cause of death is due to being overcome with gas or smoke. So what exactly is suspended in smoke' It depends on the materials and the temperature at which they are burning. Smoke contains a variety of irritants such as soot and dust particles along with asphyxiants such as cyanide and carbon monoxide. Below is a table showing a list of common house hold materials and the asphyxiants they contain: ( D H Napier,1977 ) The main chemical often talked about when we hear of smoke inhalation and house fire is carbon monoxide, so we will look at the effects of carbon monoxide on the human body. The pathophysiology of carbon monoxide poisoning. Upon exposure, CO binds to haemoglobin with an affinity 210 times that of oxygen and also increases the affinity of the remaining sites for oxygen. Thus it decreases both the oxygen-carrying and oxygen- delivery capacity of blood. In addition to generating carboxyhaemoglobin, carbon monoxide has been shown to lead to harm by several other mechanisms including direct disruption of cellular oxidative processes by binding to myoglobin and cytochromes, and during recovery there is marked oxidative stress and inflammatory responses (Weaver 2009). Both the direct hypoxic effects and the subsequent oxidative stress and inflammatory processes lead to varying degrees of end-organ damage, and occasionally death. The severity of poisoning is a function of the duration of exposure and the ambient concentration of CO, and the underlying health status of the exposed individual. Although useful for diagnosis when detected, the initial carboxyhaemoglobin level correlates poorly with outcome (Hampson 2008; Weaver (2007). The pre-hospital treatment for carbon monoxide poisoning is high flow oxygen, although it is difficult to diagnose the extent of the CO poisoning. This is because the way carbon monoxide binds with haemoglobin means that SPo2 levels will appear to be in normal range, due to most of the SPo2 meters in use in the pre-hospital environment use infra red light and the infra red cannot distinguish between CO and O2. This goes against the 2006 JRCAL guidelines by giving Oxygen to a patent, with SPo2 meter reading of above 94%. But you have to look at the clinical picture and if a patent has come out of a fire, the pre-hospital provider can not relay on the SPo2 meter as a accrete way of measuring SPo2 levels. In hospital, treatment for carbon monoxide is the same as the pre-hospital treatment. That is, the use of high oxygen ie 100% . However, there are a lot of promising ongoing testing and studies for the use of Hyperbaric oxygen for carbon monoxide poisoning which is seen as the gold standard for dealing with this form of poisoning. Delivery of oxygen under higher than atmospheric pressure, hyperbaric oxygenation therapy, greatly increases the amount of oxygen that can be dissolved in plasma, thereby improving tissue oxygenation. At 3 atmospheres absolute, dissolved oxygen can supply the body’s basal oxygen requirements with normal cardiac output in the absence of functional haemoglobin. (Boerema, I et al ,(2006). The more quickly tissue can regain oxygen after an episode of smoke inhalation, the less damage will be caused as a result of hypoxia, thereby improving cognitive function. However one of the big problems with hyperbaric oxygen chambers is that if the patient is presenting with other injuries such as complex burns following a house fire or crush injuries following a building collapsing with fire damage means that the hyperbaric chamber is often not set up for dealing with these other types of injuries. But if they were able to manage more complex injuries such as large burns, patients may have a better outcome through the use of hyperbaric oxygen treatment as bacteria cannot survive at 3 atmospheres which could help with infection as a result of burns,(Gibbns M (1993). However, smoke inhalation is a complex condition and it is not just the carbon monoxide which is the cause of fatalities. There is a lot of research suggesting that cyanide could be one of the main causes of death, and “smoke inhalation is the most common cause of cyanide poisoning in western countries.” (Boron SW 2006) Cyanide poisoning is difficult to diagnose in the pre-hospital setting. According to the SOBI Swedish Orphan Biovitrum signs and symptoms of cyanide poisoning include nausea and vomiting, headache, altered mental status ( e.g confusion, disorientation), chest tightness, dyspnoea or hyperpnoea, seizures or coma, mydriasis with exposure to fire in an enclosed area, and soot present around the mouth, nose and/or pharynx. All of the above signs and symptoms could also be signs and symptoms present with carbon monoxide poisoning. They could, however, be present without either cyanide or carbon monoxide poisoning and could just be down to an irritant after exposure to smoke. Furthermore, the anxiety of being in a house fire and having concerns about family members and also the possibility of losing a home due to fire can result in many of the above symptoms. Cyanide poisoning affects the body’s oxygen delivery system and if we look at the path physiology of the condition “cyanide is highly lethal because it deffuses into tissues and binds to target sights within seconds (shepherd R ,2007) The toxicity of cyanide is largely attributed to the cessation of aerobic cell metabolism. Cyanide courses intercellular hypoxia by reversibly binding to the cytochrome oxidase within the mitochondria. Cytocrome oxidase is necessary for the reduction of oxygen to water in the forth complex of oxidation phosphorylation. (Hall AH et al, 2009) Oxidative phosphorylation is essential to the synthesis of adenosine triphosphate and the continuation of cellular respiration. As supplies of adenosine triphosphate become depleted, mitochondria cannot extract or use the oxygen they are exposed too (Borron SW (2007). So even if you have the patient intubated and ventilated at a adequate rate and volume, with 100% oxygen going into the respiratory system, if the body cannot utilise the oxygen being delivered then all the good work of intubation and ventilation is done in vain. Cyanide poisoning needs to be treated aggressively and early, preferably on scene. Until recent years the antidote for cyanide poisoning was a three substance concoction of amyl nitrite pearls (inhaled), sodium nitrite and sodium thiosulfate (infusion). However, this was only recommended to be administered in hospital after blood results were obtained and these results are dependant on the hospital and could take hours or even days in a worst case scenario. Furthermore, this antidote when mixed has very serious side effects and patients need to be monitored in an intensive care unit. For the last 10 years the French pre-hospital services have been using a drug called hydroxycobalamin and in 2006 the federal drug administration approved the use of this drug sold under the brand name Cyanokit for known cyanide poisoning or for high suspicion of cyanide poisoning due to smoke inhalation in enclosed space fires. Cyanokit comes in vials of 2.5g of hydroxocobalamin. After reconstruction with 100ml of dilutents, then each ml of the reconstituted solution contains 25mg of hydroxocobalamin. Cyanokit has no contraindications in the emergency setting, but the drug does have some side effects such as hypertension and red discolouration of the skin and mucous membranes that may last up to 15 days. Also, a quite marked dark red colouration of urine during the three days after administration. The urine discolouration may last up to 35 days after administration of Cyanokit (M Saint eMA 2010). There have been some promising results in a controlled study, on cyanide poisoned dogs. The dogs were poisoned via intravenous administration of a lethal dose of potassium cyanide. The dogs then received sodium chloride 9mg/ml, 75mg/kg or 150 mg/kg hydroxocobalamin, administered intravenously over 7.5 minuets. The 75mg/kg and 150mg/kg doses are approximately equivalent to 5g and 10g of hydroxocobalamin. Survival at hour 4 and at day 14 was significantly greater in 75mg/kg and 150mg/kg hydroxocobalamin dose groups compared with dogs receiving sodium chloride 9 mg/ml alone: Survival of cyanide-poisoned dogs Parameter Treatment Sodium chloride Hydroxocobalamin 9 mg/ml 75 mg/kg 150 mg/kg (N = 17) (N = 19) (N = 18) Survival at Hour 4, N (%) 7 (41) 18 (95)* 18 (100)* Survival at Day 14, N (%) 3 (18) 15 (79)* 18 (100)* (M Sante 2010) The active substance in Cyanokit, Hydroxocobalamin (vitamin B12a) reacts with cyanide in the body. This action produces cyanocobalamin, that is a none-poisonous compound that is excreted in patient's urine, and reduces the levels of cyanide in the body and inhibits cyanide from attaching itself to cytochrome oxidase, a cellular enzyme. The enzyme cytochrome oxidase is essential for providing intercellular energy, this drug helps to limit and reduces the effects of cyanide. The negative side to this treatment is that it is relatively new and costly. When Swedish Orphan Biovitrum Ltd lunched Cyanokit in the UK the NHS price for a pack of 2 vials containing 2.5g each of hydraxocobalamin (together with infusion administration equipment) was £772 (excluding VAT). Looking back on this article we can see that the local fire services and their education strategy along with strict UK health and safety legislation is having a strong impact on the amount of fire related deaths in the UK. However, house and cars fires will still happen and even with better education, more fire alarms and greater fire safety awareness, people will still die as a result of fires and smoke inhalation. So the onus really needs to be on the medical care the patients receive when they are rescued from fires. It is this treatment which may have the capability to save whole families. With regards to treatment for carbon monoxide poisoning it could be said that everything is being done that can be with the current evidence based practice. However, hyperbaric oxygenation therapy has its place and we can see the benefits when it comes to the recovery rate of patients. Despite this the number of hyperbaric chambers are limited in the UK at this present time with limited facilities for maintaining patients with multiple injuries. When it comes to other asphyxiants such as cyanide the reality is that the UK needs to catch up with the rest of the world and look at new drugs such as Cyanokit of hydraxocobalamin. It has been proven through the controlled testing on dogs that there is potential to save lives through the use of this form of treatment, regardless of cost and when we look at the cost its not to different to thrombolytics witch we use on a regular bases, after all cyanide is a toxin and potentially a reversible course of cardiac arrest post smoke inhalation. With the introduction of HART teams across the UK responding to house fires and terrorist attacks and CBRN incidents, Cyanokit may be a good drug for HART to carry as standard kit. It could be stated that there is better care for people suffering from smoke inhalation and a greater understanding of the pathophysiology of the condition around the world. On the other hand, pre-hospital providers in the UK need better education and understanding of the condition and to have access to the new treatments available on the market to stay at the forefront of pre-hospital care. Reference list Borron SW Baud Fj, Megarbane B, bis- mouth C Hydroxocabalamin for severe acute cyanide poisoning by ingestion or inhalation. Am j Emerg Med. 2007;25 (5):551-558. Communities and Local Government, Fire statistics and Social Research Branch 2006 ISBN 1-40980-046-0 Gibbons M. Hyperbaric therapy treatment for hit home care. adv Resp Ther 1993:2(5):19-35, 52. Hampson Neil B critical care Medicin 2008; 36(9) ;2523-7 Jwan-luc Fortin, MD Stanislas Woaroux, J.P Giocanti, MD Gillles capellir, MD Michel Ruttimann, MD. The journal of Emergency Medicine, Vol 39, No.3, pp. 320-324, 2010 JRCALL Guidelines 2006 SOBI Swedish Orphan Biovitrum Ltd 2010 cyanokit fact sheet. SOBI Swedish Orphan Biovitrum, 1 Fordham House court, fordham Estate, Newmarket / Weaver L K, Hampson Neil B journal of the Undersea and hyperbaric Society, inc 2006;33(4); 257-63 Hall AH, D Dart R, Bogdan G. Sodium thiosulfate or Hydroxocobalamin for the treatment of cyanide poisoning Ann Emerg Med. 2007: 49(6):806-813