- •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
M. D. Peck
typify the burns that are commonly treated either at home or in primary care settings. Community surveys and examination of data from emergency rooms or clinics are preferable methods for establishing the magnitude of the burden of burn injuries throughout a district or region.
Other limitations arise in the interpretation of data from the US. Although the variable race is often studied, the limitations of racial and ethnic designations commonly used are subject to misinterpretation [163]. There are also pitfalls associated with use of length-of-stay as an outcome variable [169]. In one retrospective study of length of stay in burn patients, the variance unexplained by the studied variables was very high, with a coefficient of variance of nearly 100 % [162]. Patients admitted on Fridays may have longer lengths of stay for the same severity of injury as those admitted early in the week because of limited resources for discharge planning over the weekend. Excision and grafting of even small burns will lead to longer length of stay for pain control, immobilization, rehabilitation therapy, and assistance with activities of daily living than treatment of burns with topical antimicrobials only. Administration of intravenous medications, especially antibiotics and narcotics, will increase length of stay. Smoke inhalation injury and high-voltage electrical injury will also increase length of stay beyond the range noted for any given burn size. Lack of social support systems lead to longer hospital stays in the absence of medical factors necessitating continued in-patient care.
Risk factors
Socioeconomic factors
Household income and home value are correlated with fire deaths and burn injuries. In metropolitan Oklahoma City in 1987–90 the fire-related hospitalization and death rate was 3.6/100,000 [29]. However, when the examination of data from Oklahoma City was focused on an area characterized by lower median household income, lower property values, and poorer quality of housing, the fire injury rate was much higher, 15.3/100,000 [122]. Additionally, census tracts with low median incomes in Dallas had the
highest rates of injury related to house fires, over 8 times that in tracts with high incomes [104]. Although there are a multitude of risk behaviors in low-income neighborhoods, such as alcohol and drug abuse that put those communities at risk for residential fires, clearly one important factor is the frequent absence of functioning smoke detectors. From 1991 through 1997 in Dallas, TX, the prevalence of operational smoke detectors was lowest in houses in the census tracts with the lowest median incomes [104].
Fire injuries also show the steepest social class gradient among all childhood injuries in England and Wales, with a 16-fold increase in death from fire and flames in the lowest socioeconomic class compared to the highest [181]. Non-fatal smoke inhalation injuries in an impoverished, multiethnic area of inner-city London in 1996–97 occurred at an incidence of 25/100,000 persons per year, over 30 times higher than the mortality from smoke inhalation in this series [60]. In this same quarter of London, the hospitalization rate for unintentional fire and flame injuries (8.2 per 100,000) was 1.75 times that in the southeastern United Kingdom, which includes urban, suburban and rural neighborhoods (DiGiuseppi 2000a).
Longitudinal observations of patients admitted to a single burn center in New Delhi suggest that overall socioeconomic improvements lead to a reduction in the frequency of injuries severe enough to require admission to a burn center. In 1993, the percapita income in Delhi was US$450/year and 1276 patients were admitted that year; by 2005 the percapita income in Delhi had risen to US$1542 and the number of admissions declined to 695 [7]. Although unproven, compelling is the hypothesis that the gradual decline in fire and burn deaths across the world is following improvements in living conditions and income.
Race and ethnicity
In the US there are striking differences in susceptibility to burn injury by race. From 1991 through 1997, African-Americans in Dallas were 2.8 times more likely to be injured in house fires than whites [104]. In 2008 in the US the rate of non-fatal burns was 161 per 100,000 African-Americans, much high-
26
Epidemiology and prevention of burns
er than the observed rate of 109 per 100,000 in white non-Hispanics. In fact, in black Americans aged 35 to 39 years, the rate was 221 per 100,000 blacks, remarkably higher than the rate in whites in the same age group, which was 135 per 100,000 whites [47]. The emergency department visit rate for burn injuries from 1993 to 2004 in the US was 62 % greater among black than white subjects (340 vs. 210 per 100,000, respectively) [73].
The age-adjusted death rate from burns of all causes in the US in 2006 was highest in blacks (2.43 per 100,000) and lowest in Asians (0.44 per 100,000). Intermediate rates were noted among Native Americans (1.45), white non-Hispanics (1.11), and Hispanics (0.77 per 100,000). [47] Amongst children, there is a striking disparity in fire death rates between black and white children under the age of 15 years, with Af- rican-American children dying in residential fires at a rate nearly three times that of white children. However, by the teenage years of 15–19 years, this difference between the races is no longer present [47]. However, older African-Americans had 4.6 times the death rates of white seniors [87]. In Alabama from 1992 to 1997 the fire fatality rate was highest among older African-Americans [133]. Intriguingly, as household income increases, differences in fire death rates between blacks and whites diminish[137].
Racial differences in burn admissions occur by age group in data collected by the American Burn Association for the National Burn Registry.3 Whereas for children under five years of age, 22 % of admissions to burn centers were black children and 44 % were white children, only 15 % of seniors aged 60 years or older were black and nearly 75 % were white (Table 3). In parallel with the decline of prevalence of blacks in the hospitalized burn population as age increases, Hispanic representation at burn centers was only 4 % of the elderly, compared to nearly 20 % of children under five
3The 2009 report of the National Burn Repository reviews the combined data set of acute burn admissions for the period 1999 – 2008. Seventy-nine hospitals (including 51 verified by the ABA as centers of excellence) from 33 states plus the District of Columbia contributed to this report, totaling 127,016 records. Sixty-two hospitals contributed more than 500 cases. Data were not dominated by any single center and appeared to represent a reasonable cross section of US hospitals.
(Table 3). Hospital discharge rates for treatment of burns in Pennsylvania in 1994 showed that blacks were hospitalized for burns more than twice as frequently as whites (46.6 vs. 20.6 per 100,000, respectively) [78].
Age-related factors: children
Despite their remarkable resilience, children across the world are commonly seriously injured, with pain and suffering, disability and occasionally death as the outcome. The highest fire-related death rates in children across the world occur in infants and children under four years of age. After age 15, death rates begin to climb again, presumably because of greater exposure to hazards, experimentation and risk-tak- ing, as well as employment [232]. In the US, fires and burns were the third leading cause of unintentional injury death in the US in 2006 for children one to nine years of age [47].
Non-fatal burns in children are extremely common as well. In 2008 in the US, the crude rate of nonfatal burns was 156 per 100,000 in children under the age of 18 [47]. Strikingly, the rate for children up to three years of age was a staggering 358 per 100,000, and the fifth leading cause of unintentional non-fatal injury in US infants is burns [47]. The fact that 93 % of these young children were treated and released from emergency rooms suggests that the burns were probably minor scald and contact burns. In fact in the US, 67 % of the children hospitalized for burn injuries sustained burns of less than 10 % TBSA [201].
Compared to HIC, children under five years of age in LMIC have a disproportionately higher rate of burns [170]. For example, in Brazil, Côte d’Ivoire and India, nearly half of all childhood burns occur in infants [89, 189, 225]. Even in HIC, children who live in poor districts are at high risk of residential fire related injuries [105].
Various issues impact the likelihood that a child will be burned. These include literacy among mothers, knowledge of the risk of burns and of the means to secure health care, ownership of the house, kitchens separated from other living areas, use of fire-retardant chemicals in fabrics and upholstery, installation of smoke alarms and residential water sprinklers, appropriate first-aid and emergency response systems, and the existence of good quality health care services
27
M. D. Peck
Table 3. Summary of data from the National Burn Repository of the American Burn Association 1999–2008
Age in years |
White |
Hispanic |
Black |
Scald |
Flame |
Contact |
Electrical |
Chemical |
Burns |
Mortality |
|
|
|
|
|
|
|
|
|
> 10 % |
|
|
|
|
|
|
|
|
|
|
TBSA |
|
0–0.9 |
42 % |
17 % |
24 % |
55 % |
6 % |
22 % |
> 1 % |
> 1 % |
67 % |
> 1 % |
N=3675 |
|
|
|
|
|
|
|
|
|
|
1–1.9 |
42 % |
21 % |
22 % |
57 % |
4 % |
20 % |
> 1 % |
> 1 % |
67 % |
> 1 % |
N=9387 |
|
|
|
|
|
|
|
|
|
|
2–4.9 |
47 % |
20 % |
20 % |
46 % |
16 % |
13 % |
2 % |
> 1 % |
60 % |
1 % |
N=7987 |
|
|
|
|
|
|
|
|
|
|
5–15.9 |
57 % |
14 % |
18 % |
23 % |
38 % |
6 % |
2 % |
> 1 % |
54 % |
> 1 % |
N=13,457 |
|
|
|
|
|
|
|
|
|
|
16–19.9 |
66 % |
12 % |
13 % |
17 % |
40 % |
4 % |
2 % |
2 % |
50 % |
2 % |
N=7230 |
|
|
|
|
|
|
|
|
|
|
20–29.9 |
60 % |
13 % |
16 % |
18 % |
35 % |
4 % |
4 % |
3 % |
47 % |
2 % |
N=19,033 |
|
|
|
|
|
|
|
|
|
|
30–39.9 |
61 % |
13 % |
15 % |
18 % |
36 % |
4 % |
5 % |
4 % |
45 % |
3 % |
N=17,657 |
|
|
|
|
|
|
|
|
|
|
40–49.9 |
64 % |
9 % |
17 % |
17 % |
38 % |
4 % |
5 % |
4 % |
46 % |
4 % |
N=18,421 |
|
|
|
|
|
|
|
|
|
|
50–59.9 |
66 % |
8 % |
17 % |
16 % |
39 % |
5 % |
4 % |
3 % |
44 % |
6 % |
N=12,523 |
|
|
|
|
|
|
|
|
|
|
60–69.9 |
69 % |
6 % |
16 % |
16 % |
40 % |
4 % |
2 % |
2 % |
43 % |
9 % |
N=6987 |
|
|
|
|
|
|
|
|
|
|
70–79.9 |
72 % |
4 % |
14 % |
15 % |
42 % |
4 % |
> 1 % |
> 1 % |
40 % |
16 % |
N=4825 |
|
|
|
|
|
|
|
|
|
|
80+ |
77 % |
3 % |
13 % |
16 % |
38 % |
6 % |
> 1 % |
> 1 % |
36 % |
25 % |
N=3594 |
|
|
|
|
|
|
|
|
|
|
(Census |
(70 %) |
(6 %) |
(12 %) |
|
|
|
|
|
|
|
2000) |
|
|
|
|
|
|
|
|
|
|
[170]. Compared with children in the state of Tennessee (1980–1995) whose mothers had a college education, children whose mothers had less than a high school education had nearly 20 times greater risk of dying in a fire. Similarly, children whose mothers had three or more other children had over six times greater risk of dying in a fire when matched with children whose mothers had no other children. Likewise, when contrasted with children whose mothers were 30 years or older, children whose mothers were younger than 20 years of age had almost four times increased risk of dying in a fire. Fortunately, children characterized thusly comprise only 1.5 % of the population. Nonetheless, the fatal fire rate for this high-risk group was 28.6 per 100,000, far exceeding the national norms for fire fatalities [197].
Children are more susceptible to burns than adults. The curiosity and desire to experiment of children is matched neither by their capacity to understand the potential of danger nor by their ability to respond to it [180]. Beginning at six months of age, children start reaching for objects and crawling, and are fully mobile by 18 months. This escalation in motor skills and activity increases the chance that children will encounter hot liquids and solids, electrical cords, candles, fireplaces, microwaves, treadmills, hair curlers and curling irons, ovens and stoves, chemicals, and other harmful agents. For instance, the majority of scald burns in children between the ages of six and 36 months are from hot foods and liquids spilled in the kitchen or dining room [149].
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Epidemiology and prevention of burns
Hot liquid and vapor injuries were the leading specific causes for children 12 to 17 months in a review of injuries in Californian children under the age of four years (Fig. 2). This age coincides with developmental achievements such as independent mobility, exploratory behavior, and hand-to-mouth activity. Although the child is able to gain access to hazards, he or she has not yet developed cognitive hazard awareness and avoidance skills [5]. Just as poisoning is linked to grasping and drinking behavior of children one to three years of age, scald burns are more common in children between one and five years of age than in any other age group [16].
Once risks are encountered, the child may lack the ability to escape danger. And because their cognitive development is not as advanced as motor development, they are not aware of the potentially damaging consequences of their behavior. For example, fires resulting from children’s play are the leading cause of residential fire deaths in children under 10 years [149]. Therefore developmental stage becomes a risk factor for burn injuries [201].
Although the home is full of hazards, the young child views his or her dwelling as the centerpiece of their physical existence, in which they must eat, sleep, play, and resolve conflicts. Most home environments were not configured by architects to minimize the risk of injury to children. The space set aside for preparing and consuming food is such an example. Most women (mothers, grandmothers, aunts, nieces and older female children) find themselves involved in multiple tasks while preparing
Fig. 2. Rates of injury hospitalization and death per 100,000 for children under four years of age in California 1996–1998 [5]. Rates are illustrated by three month intervals for the major categories of injury. The rate of burn and fire injuries peak between 12 and 18 months, similar to the pattern seen with foreign bodies in the airway and gastrointestinal tract. Rates of poisoning are begin to rise at the same period of childhood as burns, but do not decrease until after
27 months of age, nearly ¾ year later than the onset of the decrease in burns
meals, including caring for the younger children. It is not surprising that low-income families are functioning in overcrowded conditions with only basic utilities and utensils, throughout which they are stressed by hunger, fatigue, frustration and fear. The prevention of scald or flame burns may be the last item on the agenda of the teenage sister charged with making dinner and caring for her younger siblings while her parents are away at work. In this regard, there is little difference between impoverished families in LMIC and HIC, thus explaining why scald burns in young children are universally common.
However, the presence of adults does not eliminate risk to children. In Greece the incidence of burns from contact with hot exhaust pipes while riding motorcycles 17 per 100,000 per year; many of these burns occur in children, who are passengers on the rear of the motorcycle. The responsibility of assuring safety to the child passenger rests with the motorcycle operator; the presence of contact burns from the exhaust pipe suggests negligence of this responsibility [130]. Similarly, review of childhood injuries treated at a large urban hospital in the US from 1972 through 1993 showed that adults were present 54 % of the time that children were injured by fireworks; for whatever reason, the presence of adults did not protect the children from harm [206]. Nonetheless, parents are aware of the importance of their responsibility of protecting children from the risk of burns, and consider lack of supervision around the home to be negligence, as noted in a
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