- •Preface
- •List of contributers
- •History, epidemiology, prevention and education
- •A history of burn care
- •“Black sheep in surgical wards”
- •Toxaemia, plasmarrhea, or infection?
- •The Guinea Pig Club
- •Burns and sulfa drugs at Pearl Harbor
- •Burn center concept
- •Shock and resuscitation
- •Wound care and infection
- •Burn surgery
- •Inhalation injury and pulmonary care
- •Nutrition and the “Universal Trauma Model”
- •Rehabilitation
- •Conclusions
- •References
- •Epidemiology and prevention of burns throughout the world
- •Introduction
- •Epidemiology
- •The inequitable distribution of burns
- •Cost by age
- •Cost by mechanism
- •Limitations of data
- •Risk factors
- •Socioeconomic factors
- •Race and ethnicity
- •Age-related factors: children
- •Age-related factors: the elderly
- •Regional factors
- •Gender-related factors
- •Intent
- •Comorbidity
- •Agents
- •Non-electric domestic appliances
- •War, mass casualties, and terrorism
- •Interventions
- •Smoke detectors
- •Residential sprinklers
- •Hot water temperature regulation
- •Lamps and stoves
- •Fireworks legislation
- •Fire-safe cigarettes
- •Children’s sleepwear
- •Acid assaults
- •Burn care systems
- •Role of the World Health Organization
- •Conclusions and recommendations
- •Surveillance
- •Smoke alarms
- •Gender inequality
- •Community surveys
- •Acknowledgements
- •References
- •Prevention of burn injuries
- •Introduction
- •Burns prevalence and relevance
- •Burn injury risk factors
- •WHERE?
- •Burn prevention types
- •Burn prevention: The basics to design a plan
- •Flame burns
- •Prevention of scald burns
- •Conclusions
- •References
- •Burns associated with wars and disasters
- •Introduction
- •Wartime burns
- •Epidemiology of burns sustained during combat operations
- •Fluid resuscitation and initial burn care in theater
- •Evacuation of thermally-injured combat casualties
- •Care of host-nation burn patients
- •Disaster-related burns
- •Epidemiology
- •Treatment of disaster-related burns
- •The American Burn Association (ABA) disaster management plan
- •Summary
- •References
- •Education in burns
- •Introduction
- •Surgical education
- •Background
- •Simulation
- •Education in the internet era
- •Rotations as courses
- •Mentorship
- •Peer mentorship
- •Hierarchical mentorship
- •What is a mentor
- •Implementation
- •Interprofessional education
- •What is interprofessional education
- •Approaches to interprofessional education
- •References
- •European practice guidelines for burn care: Minimum level of burn care provision in Europe
- •Foreword
- •Background
- •Introduction
- •Burn injury and burn care in general
- •Conclusion
- •References
- •Pre-hospital and initial management of burns
- •Introduction
- •Modern care
- •Early management
- •At the accident
- •At a local hospital – stabilization prior to transport to the Burn Center
- •Transportation
- •References
- •Medical documentation of burn injuries
- •Introduction
- •Medical documentation of burn injuries
- •Contents of an up-to-date burns registry
- •Shortcomings in existing documentation systems designs
- •Burn depth
- •Burn depth as a dynamic process
- •Non-clinical methods to classify burn depth
- •Burn extent
- •Basic principles of determining the burn extent
- •Methods to determine burn extent
- •Computer aided three-dimensional documentation systems
- •Methods used by BurnCase 3D
- •Creating a comparable international database
- •Results
- •Conclusion
- •Financing and accomplishment
- •References
- •Pathophysiology of burn injury
- •Introduction
- •Local changes
- •Burn depth
- •Burn size
- •Systemic changes
- •Hypovolemia and rapid edema formation
- •Altered cellular membranes and cellular edema
- •Mediators of burn injury
- •Hemodynamic consequences of acute burns
- •Hypermetabolic response to burn injury
- •Glucose metabolism
- •Myocardial dysfunction
- •Effects on the renal system
- •Effects on the gastrointestinal system
- •Effects on the immune system
- •Summary and conclusion
- •References
- •Anesthesia for patients with acute burn injuries
- •Introduction
- •Preoperative evaluation
- •Monitors
- •Pharmacology
- •Postoperative care
- •References
- •Diagnosis and management of inhalation injury
- •Introduction
- •Effects of inhaled gases
- •Carbon monoxide
- •Cyanide toxicity
- •Upper airway injury
- •Lower airway injury
- •Diagnosis
- •Resuscitation after inhalation injury
- •Other treatment issues
- •Prognosis
- •Conclusions
- •References
- •Respiratory management
- •Airway management
- •(a) Endotracheal intubation
- •(b) Elective tracheostomy
- •Chest escharotomy
- •Conventional mechanical ventilation
- •Introduction
- •Pathophysiological principles
- •Low tidal volume and limited plateau pressure approaches
- •Permissive hypercapnia
- •The open-lung approach
- •PEEP
- •Lung recruitment maneuvers
- •Unconventional mechanical ventilation strategies
- •High-frequency percussive ventilation (HFPV)
- •High-frequency oscillatory ventilation
- •Airway pressure release ventilation (APRV)
- •Ventilator associated pneumonia (VAP)
- •(a) Prevention
- •(b) Treatment
- •References
- •Organ responses and organ support
- •Introduction
- •Burn shock and resuscitation
- •Post-burn hypermetabolism
- •Individual organ systems
- •Central nervous system
- •Peripheral nervous system
- •Pulmonary
- •Cardiovascular
- •Renal
- •Gastrointestinal tract
- •Conclusion
- •References
- •Critical care of thermally injured patient
- •Introduction
- •Oxidative stress control strategies
- •Fluid and cardiovascular management beyond 24 hours
- •Other organ function/dysfunction and support
- •The nervous system
- •Respiratory system and inhalation injury
- •Renal failure and renal replacement therapy
- •Gastro-intestinal system
- •Glucose control
- •Endocrine changes
- •Stress response (Fig. 2)
- •Low T3 syndrome
- •Gonadal depression
- •Thermal regulation
- •Metabolic modulation
- •Propranolol
- •Oxandrolone
- •Recombinant human growth hormone
- •Insulin
- •Electrolyte disorders
- •Sodium
- •Chloride
- •Calcium, phosphate and magnesium
- •Calcium
- •Bone demineralization and osteoporosis
- •Micronutrients and antioxidants
- •Thrombosis prophylaxis
- •Conclusion
- •References
- •Treatment of infection in burns
- •Introduction
- •Clinical management strategies
- •Pathophysiology of the burn wound
- •Burn wound infection
- •Cellulitis
- •Impetigo
- •Catheter related infections
- •Urinary tract infection
- •Tracheobronchitis
- •Pneumonia
- •Sepsis in the burn patient
- •The microbiology of burn wound infection
- •Sources of organisms
- •Gram-positive organisms
- •Gram-negative organisms
- •Infection control
- •Pharmacological considerations in the treatment of burn infections
- •Topical antimicrobial treatment
- •Systemic antimicrobial treatment (Table 3)
- •Gram-positive bacterial infections
- •Enterococcal bacterial infections
- •Gram-negative bacterial infections
- •Treatment of yeast and fungal infections
- •The Polyenes (Amphotericin B)
- •Azole antifungals
- •Echinocandin antifungals
- •Nucleoside analog antifungal (Flucytosine)
- •Conclusion
- •References
- •Acute treatment of severely burned pediatric patients
- •Introduction
- •Initial management of the burned child
- •Fluid resuscitation
- •Sepsis
- •Inhalation injury
- •Burn wound excision
- •Burn wound coverage
- •Metabolic response and nutritional support
- •Modulation of the hormonal and endocrine response
- •Recombinant human growth hormone
- •Insulin-like growth factor
- •Oxandrolone
- •Propranolol
- •Glucose control
- •Insulin
- •Metformin
- •Novel therapeutic options
- •Long-term responses
- •Conclusion
- •References
- •Adult burn management
- •Introduction
- •Epidemiology and aetiology
- •Pathophysiology
- •Assessment of the burn wound
- •Depth of burn
- •Size of the burn
- •Initial management of the burn wound
- •First aid
- •Burn blisters
- •Escharotomy
- •General care of the adult burn patient
- •Biological/Semi biological dressings
- •Topical antimicrobials
- •Biological dressings
- •Other dressings
- •Exposure
- •Deep partial thickness wound
- •Total wound excision
- •Serial wound excision and conservative management
- •Full thickness burns
- •Excision and autografting
- •Topical antimicrobials
- •Large full thickness burns
- •Serial excision
- •Mixed depth burn
- •Donor sites
- •Techniques of wound excision
- •Blood loss
- •Antibiotics
- •Anatomical considerations
- •Skin replacement
- •Autograft
- •Allograft
- •Other skin replacements
- •Cultured skin substitutes
- •Skin graft take
- •Rehabilitation and outcome
- •Future care
- •References
- •Burns in older adults
- •Introduction
- •Burn injury epidemiology
- •Pathophysiologic changes and implications for burn therapy
- •Aging
- •Comorbidities
- •Acute management challenges
- •Fluid resuscitation
- •Burn excision
- •Pain and sedation
- •End of life decisions
- •Summary of key points and recommendations
- •References
- •Acute management of facial burns
- •Introduction
- •Anatomy and pathophysiology
- •Management
- •General approach
- •Airway management
- •Facial burn wound management
- •Initial wound care
- •Topical agents
- •Biological dressings
- •Surgical burn wound excision of the face
- •Wound closure
- •Special areas and adjacent of the face
- •Eyelids
- •Nose and ears
- •Lips
- •Scalp
- •The neck
- •Catastrophic injury
- •Post healing rehabilitation and scar management
- •Outcome and reconstruction
- •Summary
- •References
- •Hand burns
- •Introduction
- •Initial evaluation and history
- •Initial wound management
- •Escharotomy and fasciotomy
- •Surgical management: Early excision and grafting
- •Skin substitutes
- •Amputation
- •Hand therapy
- •Secondary reconstruction
- •References
- •Treatment of burns – established and novel technology
- •Introduction
- •Partial thickness burns
- •Biological membranes – amnion and others
- •Xenograft
- •Full thickness burns
- •Dermal analogs
- •Keratinocyte coverage
- •Facial transplantation
- •Tissue engineering and stem cells
- •Gene therapy and growth factors
- •Conclusion
- •References
- •Wound healing
- •History of wound care
- •Types of wounds
- •Mechanisms of wound healing
- •Hemostasis
- •Proliferation
- •Epithelialization
- •Remodeling
- •Fetal wound healing
- •Stem cells
- •Abnormal wound healing
- •Impaired wound healing
- •Hypertrophic scars and keloids
- •Chronic non-healing wounds
- •Conclusions
- •References
- •Pain management after burn trauma
- •Introduction
- •Pathophysiology of pain after burn injuries
- •Nociceptive pain
- •Neuropathic pain
- •Sympathetically Maintained Pain (SMP)
- •Pain rating and documentation
- •Pain management and analgesics
- •Pharmacokinetics in severe burns
- •Form of administration [21]
- •Non-opioids (Table 1)
- •Paracetamol
- •Metamizole
- •Non-steroidal antirheumatics (NSAID)
- •Selective cyclooxygenasis-2-inhibitors
- •Opioids (Table 2)
- •Weak opioids
- •Strong opioids
- •Other analgesics
- •Ketamine (see also intensive care unit and analgosedation)
- •Anticonvulsants (Gabapentin and Pregabalin)
- •Antidepressants with analgesic effects
- •Regional anesthesia
- •Pain management without analgesics
- •Adequate communication
- •Psychological techniques [65]
- •Transcutaneous electrical nerve stimulation (TENS)
- •Particularities of burn pain
- •Wound pain
- •Breakthrough pain
- •Intervention-induced pain
- •Necrosectomy and skin grafting
- •Dressing change of large burn wounds and removal of clamps in skin grafts
- •Dressing change in smaller burn wounds, baths and physical therapy
- •Postoperative pain
- •Mental aspects
- •Intensive care unit
- •Opioid-induced hyperalgesia and opioid tolerance
- •Hypermetabolism
- •Psychic stress factors
- •Risk of infection
- •Monitoring [92]
- •Sedation monitoring
- •Analgesia monitoring (see Fig. 2)
- •Analgosedation (Table 3)
- •Sedation
- •Analgesia
- •References
- •Nutrition support for the burn patient
- •Background
- •Case presentation
- •Patient selection: Timing and route of nutritional support
- •Determining nutritional demands
- •What is an appropriate initial nutrition plan for this patient?
- •Formulations for nutritional support
- •Monitoring nutrition support
- •Optimal monitoring of nutritional status
- •Problems and complications of nutritional support
- •Conclusion
- •References
- •HBO and burns
- •Historical development
- •Contraindications for the use of HBO
- •Conclusion
- •References
- •Nursing management of the burn-injured person
- •Introduction
- •Incidence
- •Prevention
- •Pathophysiology
- •Severity factors
- •Local damage
- •Fluid and electrolyte shifts
- •Cardiovascular, gastrointestinal and renal system manifestations
- •Types of burn injuries
- •Thermal
- •Chemical
- •Electrical
- •Smoke and inhalation injury
- •Clinical manifestations
- •Subjective symptoms
- •Possible complications
- •Clinical management
- •Non-surgical care
- •Surgical care
- •Coordination of care: Burn nursing’s unique role
- •Nursing interventions: Emergent phase
- •Nursing interventions: Acute phase
- •Nursing interventions: Rehabilitative phase
- •Ongoing care
- •Infection prevention and control
- •Rehabilitation medicine
- •Nutrition
- •Pharmacology
- •Conclusion
- •References
- •Outpatient burn care
- •Introduction
- •Epidemiology
- •Accident causes
- •Care structures
- •Indications for inpatient treatment
- •Patient age
- •Total burned body surface area (TBSA)
- •Depth of the burn
- •Pre-existing conditions
- •Accompanying injuries
- •Special injuries
- •Treatment
- •Initial treatment
- •Pain therapy
- •Local treatment
- •Course of treatment
- •Complications
- •Infections
- •Follow-up care
- •References
- •Non-thermal burns
- •Electrical injury
- •Introduction
- •Pathophysiology
- •Initial assessment and acute care
- •Wound care
- •Diagnosis
- •Low voltage injuries
- •Lightning injuries
- •Complications
- •References
- •Symptoms, diagnosis and treatment of chemical burns
- •Chemical burns
- •Decontamination
- •Affection of different organ systems
- •Respiratory tract
- •Gastrointestinal tract
- •Hematological signs
- •Nephrologic symptoms
- •Skin
- •Nitric acid
- •Sulfuric acid
- •Caustic soda
- •Phenol
- •Summary
- •References
- •Necrotizing and exfoliative diseases of the skin
- •Introduction
- •Necrotizing diseases of the skin
- •Cellulitis
- •Staphylococcal scalded skin syndrome
- •Autoimmune blistering diseases
- •Epidermolysis bullosa acquisita
- •Necrotizing fasciitis
- •Purpura fulminans
- •Exfoliative diseases of the skin
- •Stevens-Johnson syndrome
- •Toxic epidermal necrolysis
- •Conclusion
- •References
- •Frostbite
- •Mechanism
- •Risk factors
- •Causes
- •Diagnosis
- •Treatment
- •Rewarming
- •Surgery
- •Sympathectomy
- •Vasodilators
- •Escharotomy and fasciotomy
- •Prognosis
- •Research
- •References
- •Subject index
Epidemiology and prevention of burns
sylvania, 2 % of burn admissions were for self-inflict- ed injuries, and another 2 % for assault-by-burning; 95 % were unintentional [78]. Only 2.4 % of admissions to burn centers in Taiwan, ROC, from 1997 to 2003 were for self-inflicted injuries [217].
India has the highest number of cases of intentional self-harm by burning in the world. The majority of victims are young women, as opposed to Europe, where they are more often men in their fourth or fifth decade of life [88, 116].
Comorbidity
Because epilepsy is often untreated in LMIC, it is a frequent initiating factor in many severe burns [139]. During a seizure the epileptic may fall into an open fire or onto a stove. The severity of injury is sometimes and unfortunately exacerbated by traditional beliefs that epilepsy is contagious; victims in Ethiopia are often left to burn because of fear by potential rescuers of contacting the disease by touching the victim [211]. Burns precipitated by epileptic seizures occurred in 44 % of adult burn injuries in a community survey in rural Ethiopia, and 29 % of adult burns admitted to the hospital were precipitated by epileptic seizures [54]. Epilepsy was the most common personal risk factor, other than age, in remote subsistence village of the highlands of Papua New Guinea during 1971 to 1986, where the mortality rates from fire and flames were nearly 15 per 100,000, many times higher than reported rates from other countries [33]. In rural Bangladesh, 0.7 % of all deaths to women (15–44 years of age) were caused by falls into fires during seizure activity; this is an annual rate of approximately 2 per 100,000 [75].
Many Muslim epileptics insist on fasting during the holy month of Ramadan and hence miss their anti-epileptic medications. Therefore, burns in epileptics are commonly seen during Ramadan in Islamic populations. These burns are typically sustained during seizures while in the kitchen or falling on the hot ground (which can reach temperatures over 115 °F). In a prospective study of burns in epileptics in Saudi Arabia, 40 % of injured patients sustained the burn while fasting because they did not take their anti-epileptic medications [11, 12].
Peripheral neuropathy is a disorder commonly caused by leprosy and diabetes mellitus, and results
in sensory loss of the extremities. People with sensory peripheral neuropathy are vulnerable to burn injuries, especially hot water scalds [110]. Handling hot cooking utensils or warming neuropathic feet too close to a fire can also cause deep burns.
One of the reasons that the elderly are at higher risk of sustaining injuries is because of coexisting medical conditions. Seventy-seven percent of burn center patients aged 59 years or older in a singlecenter study had one or more preexisting medical conditions at the time of injury, and in 57 % of patient’s judgment, mobility or both were impaired [132]. In another study, 50 % of octogenarians admitted for burn treatment sustained injury because of a cerebrovascular accident [45]. Physical or cognitive disabilities are distinct risk factors for burns, especially for scald burns or for death from residential fires. Thirty-seven patients with disabilities were admitted to a burn center in Toronto between 1984 and 1992; the majority of them (84 %) were admitted for scald burns in the home. Although some were elderly as well (median age was 58 years), the extent of disability was significant in all cases, including spinal cord disorders or injuries, epilepsy or other neurological disorders. Given the relatively small size of burn (mean was 10 % TBSA), the mortality rate was 22 %, which is high compared to 4 % in the general burn population. The average length of stay for disabled burn patients was 2.8 days per percent body surface area burned, in comparison to the general population of burn patients in whom length of stay is approximately one day per percent burn [16, 22]. Although the relative risk of burns in the elderly with dementia has not yet been established, expert opinion among burn centers is that dementia is a significant risk factor for burns. Indeed, elderly patients with dementia tend to have poorer outcomes from burns injuries, and rehabilitation is very limited [9].
Agents
Flame burns and scalds occur at approximately the same frequency in children under the age of 18 years in some LMIC, including China and Iran [117, 234] . In general, however, and particularly in younger children, scald burns are more common than flame burns
33
M. D. Peck
in children. For example, three pediatric hospitals in Mexico noted that the majority of emergency room visits for burns in children under 10 years of age was because of exposure to boiling liquids, most commonly overly hot bath water [99]. Over 75 % of children under the age of 18 hospitalized for treatment of burns in Taiwan, Republic of China, were injured by scalding liquids [221]. In burn centers in the US, scald burns account for nearly half the admissions of children under five years of age. For very young children under two years, flame burns cause only 5 % of admissions; contact burns are more common in this age group, involving over 20 % of admissions (Table 3).
Even when older children up to the age of 18 years are included in analysis, scald burns still outnumber fire and flame injuries by a ratio of 1.6:1 in US burn centers and 5:1 in all US hospitals [201, 16]. Nonetheless, older children and young teenagers between five and 16 years of age experience fewer scald burns than their younger siblings: only 23 % of admissions are for scalds, compared to 38 % for flame burns (Table 3).
Scald burns are very common in adults as well. A study of discharges from all hospitals in Pennsylvania in 1994 (including hospitals without burn centers as well as the six hospitals with burn centers) showed that 56 % of admissions were for treatment of scald burns [78].
Nonetheless, flame burns overall cause more admissions to US burn centers than any other single cause of thermal injury. Through the adult decades, flame burns continue to be the cause for 35 % to 42 % of admissions, and scalds for 15 % to 18 % (Table 3).
Fortunately, the majority of burns of any etiology are small to moderate in size: 86 % of burns admitted to US burn centers 1999–2008 involved less than 20 % of the body surface area [16].
Clothing ignition is a common cause of severe flame burns. Although conflagrations caused 78 % of the deaths in the elderly in the US in 1984, 11 % of fatalities were from clothing ignitions [87]. Women of the Indian subcontinent wearing loose flammable saris (made of cotton or synthetic textiles) are vulnerable to fire deaths when their clothing is ignited while cooking near open flames, particularly if the cooking source is an open fire pit or a small kerosene stove on the ground [66]. Ninety-three percent of burn injuries in rural Ethiopia occurred inside the
home where open fires were used in the common room and often ignite clothing [58]. Likewise, ignition of grass skirts in warm coastal areas of Papua New Guinea account for nearly half of hospitalizations for burns [32].
Flammable fuels are often the agents of fire acceleration or heat production in incidents that result in flame burns. The unsafe use of gasoline was implicated in 87 % of patients in whom the cause of the burn could be identified at single-site retrospective study of burns admitted from 1978 to 1996 in the US [28]. Liquefied petroleum gas (LPG) has replaced kerosene in many households in LMIC as per-capita income has risen and availability of smaller and more affordable LPG cylinders has improved. In Delhi, LPG-related burns were responsible for over 10 % of admissions from 2001 to 2007 [7].
Electrical and chemical burns are rarely reasons for admission in children, occurring less than 2 % of the time, but account for 4 % to 5 % of admissions of adults from 20 to 60 years of age (Table 3). The frequency of admissions for contact burns declines precipitously with age: although one-fifth of admissions of children under two years are for contact burns, only about 5 % of adult admissions are for contact burns (Table 3).
Residential fires
The products of combustion consist of fire gases, heat, visible smoke, and toxicants. The hazards created by these products of combustion include effects of heat on the upper airway, toxicant damage to the sub-glottic respiratory system, impaired vision due to smoke density or eye irritation, and narcosis from inhalation of asphyxiants. These effects lead contribute to restricted vision, loss of motor coordination, impaired judgment, disorientation, physical incapacitation and panic. The resultant delay or prevention of escape from the burning structure leads to injury and death from inhalation of toxic gases and from thermal burns. Extricated survivors may go on to die later in the hospital from complications such as respiratory failure, septic shock, and multiple organ system failure, all of which are rooted in the initial exposure to products of combustion [94].
Smoke is defined as the airborne solid and liquid particulates and fire gases created during combus-
34
Epidemiology and prevention of burns
tion and when materials undergo decomposition or transformation by heat [20]. Pyrolysis is the decomposition of a material from heat and does not require the normal atmospheric level of oxygen, leading to incomplete combustion. The toxicant gases produced in a fire can be categorized into separate classes: the asphyxiants which induce unconsciousness, and the irritants which inflame the eyes and respiratory tract. The major threat in most fire atmospheres is carbon monoxide, an asphyxiant produced by incomplete combustion.
The vast majority of deaths due to fires in the US each year occur because of exposure to products of combustion in structure conflagrations. From 1992 to 2001, two-thirds of fire deaths in the US occurred in residential fires [76]. (Although residential fires are the primary cause of fire mortalities, they account for only half of structure fire injuries and less than onethird of the dollar loss for fires.) Residential fires accounted for 76 % of the years of life lost in 2006 in the US due to flame burns [47].
Although most victims of fatal fires die from smoke inhalation, a few will die of thermal injury directly. Temperatures higher than 300 °F are reached within five to ten minutes in building fires, and in an aircraft cabin the temperatures near 500 °F in just five to six minutes [69, 98]. Flashover5 can occur in less than 10 minutes in even a slowly progressing residential fire, at which time temperatures soar from 1100 °F to over 2000 °F in seconds, creating an environment in which survival is unprecedented. In the absence of inhalation of products of combustion and pyrolysis, death can be caused by heat-induced laryngospasm or by vagal-reflex mediated cardiac arrest [202].
Although a well-burning fire produces much more carbon dioxide than carbon monoxide (CO), materials in most structure fires smolder because of rapid depletion of oxygen in the interior of the building. Although the pathophysiology of CO poisoning is well-under-
5Flashover is defined as a transitional phase in the development of a compartment fire in which surfaces exposed to thermal radiation reach ignition temperature more or less simultaneously and fire spreads rapidly throughout the space resulting in full room involvement or total involvement of the compartment or enclosed area. (NFPA 921 - 1992, Guide for Fire and Explosion Investigations, National Fire Protection Association, Quincy, MA, (1992).)
stood, there remains no readily apparent explanation for the observation that the range of carboxyhemoglobin (COHb) tolerated is very wide. Although COHb saturation greater than 35 % can cause death in some people, others have survived COHb saturations as high as 64 % [94]. The average COHb level in fire fatalities is 60 %, with a range of 25 to 85 % [202]. About 10–15 % of CO binds to myoglobin and cytochrome A3, blocking production of ATP and causing muscular weakness, thus exacerbating the difficulties the victim encounters during escape maneuvers [229].
Unfortunately, COHb levels rise rapidly in house fires. When the CO level in inspired air reaches 5 %, COHb rises to 10 % in 10 seconds and to 40 % (a fatal level in some people) in only 30 seconds [209]. A study in East Denmark from 1982–1986 demonstrated that the blood alcohol concentration averaged about 190–200 mg/dl in fatalities from residential fires, and the mean COHb was about 60 % [214]. However, it is clear that some people with pre-existing functional impairments are at risk for increased CO toxicity at lower COHb levels, including children and the elderly, the physically disabled, and those impaired by alcohol, drug or medication intoxication [60, 104]. Largely for this reason, children under age five years and the elderly over 65 years account for 45 % of home fire deaths [108]. Patients with coronary artery disease cannot increase coronary blood flow when COHb rises above 10 % [25]. In addition to inhibiting cognitive responses, ethanol also potentiates the effects of CO such that lower levels of COHb are associated with fatality [46].
Although hydrogen cyanide (HCN), which is produced by the combustions of materials that contain nitrogen such as wool, silk, acrylonitrile polymers, nylons, and polyurethanes, is 20 times more toxic than CO, its role as a causative agent in human fire fatalities is less clear than that of CO. For example, in many fire deaths, COHb is in the toxic range, but cyanide levels are not toxic [119]. Nonetheless, low levels of COHb in other fire fatalities suggest that other toxic gases such as HCN may play a role in causing death [8].
Because oxygen is consumed during combustion, the oxygen level in the inspired air (O2) can drop from 21 % to levels that affect coordination, mentation and consciousness. When O2 drops to 17 %, coordination is impaired, when it drops to 14 %
35
M. D. Peck
judgment becomes faulty, and below 6 % unconsciousness occurs [94].
Acrolein is formed from the smoldering of all plant materials (including wood and the natural fibers used in decorations and furnishings), and is a potent sensory and pulmonary irritant. It is extremely irritating to the eyes at concentrations as low as a few parts per million [170].
Level of consciousness and thus ability to escape are affected by drugs and alcohol [8]. One-third to one-half of victims of fatal fires have ingested alcohol [81, 133, 207]. Ethanol intoxication significantly impairs the ability to escape from fire and smoke and is a contributory factor in smoke-related mortality. Whereas victims found near escape exits had blood alcohol levels (BALs) averaging 88 mg/dl, the mean BAL was 268 mg/dl in those found dead in bed, presumably having made no attempt to escape [27]. Moreover, if even one person in the house is impaired by alcohol or drug usage, others in the dwelling are at increased risk of death from fire as well [190].
Perhaps the most deadly combination leading to fatal fires is alcohol and cigarettes. Not only in higher socioeconomic neighborhoods is smoking in bed while inebriated one of the most common causes of death by fire, but also in indigenous communities in North America. Seventy-six percent and 90 % of the adult victims of residential fires in Canadian Indians in Manitoba and Alberta, respectively, were under the influence of alcohol at the time of death [79, 106].
Risk factors for fatal and non-fatal house fire injuries include young or old age, male gender, nonwhite race, low income, disability, smoking and alcohol use [227]. Single, detached mobiles homes had the highest rate of fire deaths of all types of residences [227]. In rural areas, risk of death from a residential fire in a mobile (manufactured) home is 1.7 times the risk in a singleor multiple-family home [190]. In addition, the presence of an ablebodied adult who is not impaired by alcohol or drugs will significantly the odds of survival in a house fire [124]. Burn injuries and fire fatalities are more common in older homes and from fires started in the bedroom or living room from heating equipment, smoking or children playing with fire [104].
Non-electric domestic appliances
In many households in LMIC, especially in rural areas lacking electrification, open flames are common, including floors of huts with open hearths which are used for cooking and warmth, candles, and small kerosene and naphtha stoves and lanterns. The fire risk from these sources are contributed by lack of enclosure for open fires, floor-level location of fires and stoves, instability of appliances, nearby storage of volatile and flammable fuels, flammable clothing and housing materials, and lack of exits [34].
A large number of burn injuries and fire deaths in LMIC are related to the nature of non-electric domestic appliances that are used for cooking, heating, lighting or all three. The incidence of injuries is largely associated with the use of stoves and lamps, and from kerosene (termed paraffin in some countries) and petroleum as well as butane, liquid petroleum gas and alcohol. Associated problems include appliance design and construction, fuel combustion and instability, and mechanical inefficiency. Ignorance of safe usage techniques is also contributory. Industry and government regulations and standards are either nonexistent or not adequately enforces [165].
Informal settlements in densely populated urban areas are often scenes for fires that lead to incalculable property damage and horrific loss of life. From 2002 to 2004, approximately 12 % of households in South Africa were “shacks”, living quarters assembled from highly combustible and toxic materials and usually assembled close to one another on uneven ground. Kerosene is used as fuel for small stoves; the more inexpensive the stove, the more likely it is to tip over or malfunction. During a simulated shack fire triggered by a kerosene stove that was knocked over while burning, the temperature in the shack reached an excess of 1670°F in less than four minutes [159]. Shack fire burns are the second most common reason for admission to burn centers in Cape Town, and the most common cause of shack fires in these cases is the use of kerosene stoves [83].
Serious injuries from kerosene stoves have been documented in Egypt, Ethiopia, India, Nigeria, Pakistan and other LMIC [6, 70, 85, 90, 120, 123, 148, 196]. The underlying problem of kerosene stove-related fires often lies with design issues. Poor design allows
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