Professional Documents
Culture Documents
Smoke inhalation (SI) was described as early as the first century AD, when Pliny
reported the execution of prisoners by exposure to the smoke of greenwood fires.
Many victims of fire accidents have both smoke inhalation and thermal injury.
Inhalation injury from smoke and the noxious products of combustion in fires may
account for as many as 60-80% of fire-related deaths in the United States, many of
which are preventable.[1, 2] Excellent care rendered at today's burn centers has greatly
reduced the mortality from surface burns, while the mortality from pulmonary injury
has been increasing. In fact, respiratory failure is now the most common cause of
death at burn centers.[3] Diagnosis of inhalation injury is not always straightforward,
sensitive screening tests are lacking, and symptoms may be delayed until 24-36 hours
after injury.
Pathophysiology
The 3 primary mechanisms that lead to injury in smoke inhalation are thermal damage,
asphyxiation, and pulmonary irritation.
Thermal damage
Thermal damage is usually limited to the oropharyngeal area, due to the poor conductivity of
air and the high amount of dissipation that occurs in the upper airways. Animal experiments
have shown that 142C inhaled air cools to 38C by the time it reaches the carina. Steam,
volatile gases, explosive gases, and the aspiration of hot liquids provide some exceptions, as
moist air has a much greater heat-carrying capacity than dry air.
Asphyxiation
Tissue hypoxia can occur secondary to several mechanisms. Combustion utilizes oxygen,
which in a closed space may be consumed, significantly decreasing the ambient concentration
of oxygen to as low as 10-13%. The decrease in fraction of inspired oxygen (FIO2) leads to
hypoxia, despite adequate circulation and oxygen-carrying capacity.
Carbon monoxide (CO) causes tissue hypoxia by decreasing the oxygen-carrying capacity of
the blood. Hemoglobin binds CO with an affinity more than 200 times greater than the
affinity for oxygen. Even though this tissue hypoxia is the primary insult, other mechanisms
contribute to its pathophysiology.[4]
CO also causes a left shift in the oxyhemoglobin saturation dissociation curve. CO has been
shown to bind to the cytochrome oxidase chain in vitro. Finally, since CO binds to virtually
all heme molecules, myocardial myoglobin is affected and consequently myocardial
contractility is decreased.
Combustion of plastics, polyurethane, wool, silk, nylon, nitriles, rubber, and paper products
can lead to the production of cyanide (CN) gas. CN also takes the form of solid crystals
bound to sodium and potassium salts. It is also found abound in foods such as cassava and in
apple, pear, apricot, and peach seeds. Hydrogen CN is a colorless gas with a bitter almond
odor to the 40% of the population who are able to detect it. It is 20 times more toxic than CO
and can cause immediate respiratory arrest.
Consider CN toxicity in all patients with smoke inhalation who have CNS or cardiovascular
findings. CN is a chemical asphyxiant that interferes with cellular metabolism by binding to
the ferric ion on cytochrome a3, subsequently halting cellular respiration. As a consequence of
the cessation of the electron transport system, anaerobic metabolism ensues, with
corresponding high lactate acidosis and decreased oxygen consumption.
Pulmonary irritation
Irritants can cause direct tissue injury, acute bronchospasm, and activation of the body's
inflammatory response system. Activated leukocytes and/or humoral mediators, such as
prostanoids and leukotrienes, produce oxygen radicals and proteolytic enzymes. Supporting
the importance of the inflammatory response to the mechanism of tissue destruction, some
studies have shown that the administration of the cyclooxygenase inhibitor, ibuprofen, was
found to reduce the lung lymph flow in animals with smoke inhalation.[5, 6] The direct injury is
a consequence of the size of the particle, its solubility in water, and its acid-base status.
Ammonia produces alkaline injury, while sulfur dioxide and chlorine gas lead to acid injuries.
Other chemicals act via different mechanisms; for instance, acrolein causes free radical
formation and protein denaturation.[7]
The location of injury depends on the solubility of the substance in water. High-solubility
substances such as acrolein, sulfur dioxide, ammonia, and hydrogen chloride cause injury to
the upper airway. Substances with intermediate solubility, such as chlorine and isocyanates,
cause both upper and lower respiratory tract injury. Phosgene and oxides of nitrogen have
low water solubility and cause diffuse parenchymal injury.
In a study evaluating survivors of the 9/11 World Trade Center's collapse, 44% had persistent
lower respiratory symptoms after 19 months of follow up[8] ; hence, the term "World Trade
Center cough." A more recent study shows that 13% (1,720) of participants in the FDNY-
WTC Monitoring Program referred for pulmonary evaluation, received either pulmonary
function testing, methacholine challenge test, high-resolution chest CT scans, or a
combination of these tests. Fifty-nine percent were found to have obstructive airway disease
while few had evidence of interstitial disease.[9]
Epidemiology
Frequency
United States
Burns and fires are the third leading cause of accidental death in all age groups. They
comprise the second leading cause of death in the home for all ages and the leading cause of
death in the home for children and young adults.[10] In 1998, approximately 381,500
residential fires occurred in the US, resulting in 3,250 nonfirefighter deaths, 17,175 injuries,
and nearly $4.4 billion in property loss.[11] These figures do not include the estimated 90% of
fires not reported to fire departments. More than half of all fatal residential fires started
between the hours of 11 pm and 7 am.[10]
Incidence of smoke inhalation increases from less than 10% in patients with a mean total
body surface area (TBSA) burn size of 5% to more than 80% in patients with a mean TBSA
burn size of 85% or more. Smoke inhalation is present in one third of patients treated at burn
centers. The magnitude of smoke inhalation is devastating, as the presence of an inhalation
injury has a greater effect on mortality than either patient age or surface area burned.
International
The US has one of the highest fire fatality rates in the developed world, accounting for 2.3
deaths per 100,000 population.[12] In fact, fire death rates in the US and Canada are twice as
high as in Western Europe and Japan.[10]
Mortality/Morbidity
In patients with a burn and no associated SI or respiratory failure, the mortality rate is less
than 2%. In patients with smoke inhalation alone and no burn or respiratory failure, the
mortality rate is 7%.
For patients with a burn and smoke inhalation, the mortality rate increases to 29%,
suggesting that the burn wounds themselves put an additional stress on the compromised
lung.[13]
Studies have shown that children with CO poisoning alone compared to those with combined
smoke inhalation and CO toxicity had an increase in mortality rate from 0% to 22.6%. [14]
In rat and sheep models, cutaneous burns result in systemic complement activation with
pulmonary sequestration of activated neutrophils, which, in turn, release toxic metabolites,
further injuring the lung.
Race
One study in New Jersey reports on the demographics of fire fatalities and notes that victims
who perished did not parallel the ethnic census of the time.[2, 10]
Whites accounted for 53% of fatalities and comprised 49% on the census.
African Americans accounted for 38% of fatalities and 13% of the census.
Sex
Age
The New Jersey study also showed that children and the elderly represented a
disproportionate percentage of people injured by fire.[10] People younger than 11 years or
older than 70 years constituted 22% of the population but accounted for 40% of all fire
fatalities. These statistics closely match national figures.
A comprehensive study in Dallas looked at all house fires from 1991-1997.[15] Many of the
findings parallel those of the New Jersey study.
Relative risk of injury was 1.8 for men, 1.4 for boys, 2.8 for blacks, and 2.6 for elderly
persons.
In addition, among the injured, the proportion of injuries that were fatal was higher in
persons older than 65 years (53%) and in those younger than 10 years (67%) compared with
those aged 10-64 years (30%).
The lowest income tracts had the highest rate of injury. The rate of injury in households with
a median income below $20,000 per year was 8 times that of tracts with a median income
greater than $80,000 per year. In fact, tracts with extremely low incomes, less than $10,000
per year, had rates of injury 20 times that of the above.
Houses built in the 1950s and 1960s were somewhat more likely to burn than houses built
before this time. This may be a case of "selection of the fittest" houses, with those houses
most prone to burn having already done so leaving the most structurally sound ones still
standing.
Fires caused by arson occurred predominately in census tracts with lower median incomes.
Eighty percent of fires occurred in homes with median incomes of less than $40,000 per year.
Causes of the house fires were arson (25.5%), electrical wiring/equipment (16.6%), heating
equipment (15.8%), cooking (11.4%), smoking (5.5%), children playing with fire (4.5%), and
unknown/other (20.6%).
The rate of fire-related injury in houses in Dallas without a functioning smoke detector was
8.7 times that of homes with functioning smoke detectors. Houses that are most likely to
have fires were least likely to have functioning smoke detectors.
As a result of this study, a program in Dallas now provides and installs smoke detectors in
census tracts with the highest rates of injuries and deaths related to house fires.
History
Conditions at the scene may yield critical information, such as loss of consciousness or
deaths in the same environment.
CO measurement at the scene correlates much better with toxicity than does the
measurement in the ED.
Physical
Inhalation injury can range from an immediate threat to a patient's airway and respiratory
status to only minor mucosal irritation. Follow a trauma management protocol.
Primary survey
o Assess breathing by respiratory rate, chest wall motion, and auscultation of air
movement.
Respiratory
o Smoke inhalation and burns to the upper airway trigger the inflammatory cascade
with associated vasodilation and capillary leak. Treat any signs or symptoms of
airway compromise early and aggressively before rapid progression to upper airway
obstruction ensues.
o Wheezing, rales and rhonchi, and use of accessory respiratory muscles may be
noted.
Patients with facial burns should be carefully evaluated for smoke inhalation.
o One study has shown a 59% incidence of respiratory injury with burns involving the
nose, lips, brows, and neck area compared with a 22% incidence in patients with
either peripheral or no facial burns.
o Again, early airway security is paramount before edema and airway compromise
develop.
o Patients with facial burns showed an increased mortality and more of a need for
ventilatory support.
Large cutaneous burns indicate an inability to escape flame and a risk for smoke inhalation
injury.
Causes
Based on a study looking at the characteristics of survivors and casualties of fire fatalities,
specific risk factors seem to elevate the rate of mortality.[12]
Age is an important predictor, with elderly persons (>64 y) and young persons (< 10 y) being
the most likely to die as a result of a fire.
Persons having a physical or cognitive disability have a higher mortality rate than matched
controls, as do persons under the influence of alcohol or other drugs. For these vulnerable
populations, if a nonvulnerable potential rescuer was present, the fatality rate dropped from
49% to 39%.
The absence of a functioning smoke detector increases the risk of death in a fire by about
60%.
Differentials
Anaphylaxis
Angioedema
Anxiety
Asthma
Bacterial Pneumonia
Pneumonia, Aspiration
Pneumonia, Viral
Pulmonary Embolism
Laboratory Studies
Elevated lactate levels may result from metabolic acidosis secondary to hypoxia, CO, CN,
methemoglobinemia, inadequate resuscitation, or unrecognized trauma. Lactate levels
higher than 10 mmol/L are a sensitive indicator of CN levels higher than 1 mg/mg; therefore,
they should be treated as such.[16] Note that in most institutions, CN levels can take hours to
days for results; therefore, one must rely on clinical and indirect laboratory data.
BUN and creatinine levels should be obtained for baseline renal function in patients in shock
or rhabdomyolysis. Patients with large cutaneous burns, crush injuries, or prolonged
immobilization should have their serum creatine kinase (CK) checked and, if appropriate,
urine myoglobin.
Lead-containing paint is common in structures built before 1977, and this element can
become aerosolized and absorbed directly into the bloodstream from the lungs. While it is
true that severe smoke inhalation has been shown to increase serum lead levels more than
2-fold, no evidence suggests that these elevations are clinically relevant. [17]
Imaging Studies
Chest radiography
Obtain chest x-ray films (CXRs) in patients with a history of significant exposure or pulmonary
symptoms.
Most x-ray film findings are normal after smoke inhalation; initial CXR is only 8% sensitive for
smoke inhalation.
Findings may include atelectasis, pulmonary edema, and acute respiratory distress syndrome
(ARDS).
Insensitivity of the CXR and lack of reliability of clinical signs of inhalation injury may
necessitate use of other diagnostic techniques.
CT of the chest
Findings may be present on CT scan as early as a few hours after inhalation injury. [18]
CT of the brain
CT of the brain may show signs of cerebral infarction due to hypoxia, ischemia, and
hypotension.
An interesting and well-reported finding for severe CO toxicity is bilateral globus pallidus low-
density lesions. These lesions may be delayed for up to several days.
This finding is highly specific for CO insult unlike focal cortical hypoperfusion, which is
nonspecific.
Xenon ventilation-perfusion scan is less commonly utilized than chest radiography, chest CT,
and bronchoscopy.
As even bronchoscopic examination may fail to detect injury caused by inhalation of fine
particulate aerosol material that may reach terminal bronchioles, consider xenon ventilation-
perfusion scans in any patient suspected of having an inhalation injury even if bronchoscopic
examination has been negative. This is because bronchoscopy does not evaluate the lower
airways and, although 90% of particles measuring 5-10 microns in diameter impact in the
upper airways, those measuring 0.5-3 microns reach the terminal bronchioles. In fact,
particles this size may escape some filtration devices worn by firefighters.
Unequal lung field radiation density and/or retention of the radiolabeled gas in the lung field
for longer than 90 seconds constitutes a positive scan.
Although the accuracy is reported as 86%, xenon ventilation-perfusion scan lacks specificity
in patients with preexisting pulmonary disease. [19]
This test may be more appropriate for use in a burn unit or intensive care unit rather than
the ED.
Other Tests
Perform electrocardiogram (ECG) in any patient presenting with smoke inhalation. Potential
for decreased oxygen delivery from asphyxiation, dyshemoglobinemia, and cessation of
electron transport system can result in myocardial ischemia.
Pulmonary function test results are abnormal soon after inhalation injuries.
o In patients with bronchospasm, forced expiratory volume in 1 second (FEV 1), peak
flow, and midexpiratory flow rates are reduced.
o Bronchoscopy is the criterion standard for diagnosis of smoke inhalation injury. [18]
This procedure examines the airways from the oropharynx to the lobar bronchi.
Although it may be performed in the ED, the intensive care unit or burn unit may be
a more appropriate setting, especially in patients who are intubated.
o Studies have shown up to a 96% correlation between bronchoscopic findings and the
triad of closed-space smoke exposure, HbCO levels of 10% or greater, and
carbonaceous sputum.
o Another study reports that serial bronchoscopy was twice as sensitive for diagnosing
inhalation injury as clinical findings alone.
Prehospital Care
If respiratory failure is present, the patient should have assisted ventilation and/or
endotracheal intubation.
Secure IV access, but do not delay transport of patient to the hospital in any way.
Presently, no specific treatment exists to ameliorate the tissue damage and reduce the
vulnerability to infection induced by smoke inhalation. Once the CO toxicity, CN toxicity,
and methemoglobinemia have been corrected, subsequent treatment is predominantly
supportive.
High-flow humidified oxygen is critical to reverse or prevent hypoxia and assist displacement
of CO from Hb.
The most urgent concern in patients is the patency of the upper airway and adequacy of
ventilation.
o About 50% of patients with an inhalation injury require endotracheal intubation. The
proportion of patients requiring this procedure is higher for those who also have a
burn injury: 62% with a burn versus 12% without a thermal injury.
o It is of vital importance that the magnitude of the swelling in the areas of the face
and mandible be closely scrutinized when making decisions about the need for an
artificial airway. The threshold for intubation should be lower than in other patients
due to the potential of rapid development of airway edema. This is especially true of
the pediatric patient. Delays create the possibility that critical airway compromise
may be unrecognized or develop quickly, making endotracheal intubation technically
impossible.
If systemic paralysis is necessary, succinylcholine can be used safely in the immediate post-
burn phase and up to several days out. Inflate tube cuff to minimal levels, even allowing a
small leak, in order to prevent iatrogenic tracheal damage in patients with an already
compromised tracheal mucosa.
Studies have shown that positive pressure ventilation with low tidal volumes (3-5 mL per kg)
and positive end-expiratory pressure (PEEP) initiated immediately after the inhalation injury
significantly increases short-term survival and is associated with decreased tracheobronchial
cast formation. The mechanism by which PEEP works may be from "splinting" the alveoli and
preventing bronchial cast formation and protein-rich fluid from entrapping the airway. [19]
Other studies have shown that high-frequency percussive ventilation (HFPV) also decreases
mortality, pneumonia, and barotrauma. This modality generates pulsatile flow at up to 600
cycles per minute, which entrains the humidified gas by effect on molecular diffusion.
Clearance of airway secretions may improve, and continued patency of the lower airways
may be allowed. In patients with inhalation injury and less than 40% TBSA burns HFPV
decreases both morbidity and mortality. While not as commonly used in the ED, many burn
centers consider this standard therapy.[19, 21, 22]
Administer IV fluids to maintain a euvolemic state and to ensure adequate tissue perfusion.
Use formulas (eg, Parkland) to calculate fluid resuscitation if severe burns are present.
o CO is not only responsible for most prehospital deaths due to smoke inhalation, it is
also the leading cause of injury/death from all poisons worldwide. [23]
The main reason for use of HBO therapy is to prevent delayed neurological sequelae.
o A classic study demonstrated that dogs breathing 13% CO died within 1 hour after
achieving CO-Hgb levels from 54% to 90%. However, exchange transfusion with
blood containing 80% CO-Hgb to otherwise healthy dogs resulted in no toxic effects,
despite resultant CO-Hgb levels of 57-64%. This further supports the notion that CO
toxicity is not dependent on CO-Hgb formation or, in other words, solely upon a
relative anemia.
o At this time, 6 prospective, randomized controlled trials have compared HBO with
normobaric oxygen (NBO) therapy for CO poisoning. Four of these studies show a
benefit for CO poisoning; two do not. The data and conclusions drawn from these
studies are conflicting and highlight the controversy surrounding the utility of HBO.
o Though there has been much debate regarding the accuracy of neuropsychometric
testing, including the fact that patients who are depressed and who have attempted
suicide with non-CO means perform as poorly as CO-exposed patients, they remain
an objective means to evaluate cognitive function.
Management of CN toxicity has historically involved the creation of an alternate binding site
for CN to compete with cytochrome oxidase and also to provide substrate necessary to
convert CN to a nontoxic metabolite.
o In vitro studies indicate that hydroxocobalamin penetrates cells and can act
intracellularly. Side effects are chromaturia and reddening of the skin. Empiric
administration to patients subsequently confirmed to have CN poisoning has been
shown to be associated with 67% survival. It has a rapid onset of action, is easy to
administer, does not interfere with cellular oxygen use, is well tolerated, and is safe
for smoke inhalation patients. Additionally, it is not associated with hypotension or
the formation of a dyshemoglobinemia found in previous antidote kits. [2, 26, 27]
o The traditional CN antidote kit contains amyl and sodium nitrite to create a
methemoglobin level of 3% and 20-30%, respectively, which, in turn, has a higher
affinity for CN than for cytochrome a3. Also included is sodium thiosulfate, which
provides substrate for the enzyme rhodanese, which combines thiosulfate and CN to
form a nontoxic compound, thiocyanate, which is excreted renally.
A small subset of patients manifests bronchospasm and may benefit from the use of
bronchodilators, although this is not well documented. This is especially true of patients with
underlying COPD or asthma.
Although the pathophysiology of smoke inhalation involves irritants setting off the
inflammatory response, no benefit has been shown with corticosteroid therapy. In fact, many
studies report an increased rate of pulmonary infection. [28]
Inhalation injuries clearly predispose the airways to infection after several days because of
cellular injury, reduction of mucociliary clearance, and poor macrophage function. Despite
this, prophylaxis with parenteral antibiotics has not shown any benefit. Acute bacterial
colonization and invasion peaks at 2-3 days after smoke inhalation injury. Consider cultures
and possible treatment at this time.
Oxidant injury eventually leads to cast formation of cellular debris in the airways, thus
contributing to pulmonary failure. A pediatric study has shown that aerosolized heparin/N-
acetylcystine decreases the incidence of atelectasis, reintubation rates, and overall mortality.
[29]
In the animal model, whole-body hypothermia has recently been shown to suppress oxidant
bronchoalveolar damage and pulmonary inflammation. [30] Mechanistically, this appears to
halt the progression of bronchoalveolar-capillary permeability.
Medication Summary
Oxygen is the primary medication used in the treatment of smoke inhalation. Bronchodilators
may be of benefit in patients displaying signs of bronchospasm. After this, specific antidotes
of methylene blue for methemoglobinemia and thiosulfate/sodium nitrite for CN poisoning
are indicated. Certain patients with CO toxicity may require hyperbaric therapy.
Bronchodilators
Class Summary
These agents act to decrease the muscle tone in the small and large pulmonary airways.
Hydroxocobalamin (Cyanokit)
B-12 precursor that minds cyanide to its cobalt ion forming cyanocobalamin. The cobalt ion
has greater affinity for cyanide than does cytochrome oxidase. Cyanocobalamin is excreted
renally. Has few adverse effects and has several advantages over other cyanide treatments
including ease of administration, rapid onset of action, good safety profile, no effect on the
oxygen carrying capacity of blood, and is safe in victims of smoke inhalation.[31, 32] Low-dose
hydroxocobalamin in combination with sodium thiosulfate used successfully to prevent
cyanide toxicity due to prolonged sodium nitroprusside infusions.
Antidotes
Class Summary
Sodium nitrite
Sulfur compounds
Class Summary
These agents provide a sulfur moiety to rhodanese, allowing the production of thiocyanate,
which subsequently is excreted by the kidneys.
Sodium thiosulfate
After formation of methemoglobin and production of cyanomethemoglobin, thiosulfate acts
as a sulfur donor to the endogenous enzyme rhodanese. This enzyme removes CN from the
cyanomethemoglobin complex and forms thiocyanate, which is excreted renally. CN also is
removed directly from cytochrome oxidase and is converted to thiocyanate in the presence of
thiosulfate via the enzyme rhodanese.
Reducing agents
Class Summary
Methylene blue
Tetramethyl thionine chloride moiety that is reduced (it is an electron acceptor) in the
presence of NADPH and methemoglobin reductase to leukomethylene blue. Leukomethylene
blue then becomes available to reduce methemoglobin to oxyhemoglobin.
May be ineffective in treating patients with G-6-PD deficiency because, in the hexose
monophosphate shunt, G-6-PD is essential for the generation of NADPH. Without NADPH,
methylene blue cannot act as a reducing agent in the transformation of methemoglobin to
oxyhemoglobin.
Patients with smoke inhalation should be monitored for 4-6 hours in the ED. While there is
no definite criteria for admission, the following patients should be strongly considered for
hospitalization:
Metabolic acidosis
Bronchospasm
Odynophagia
Although the literature is lacking regarding definite discharge criteria, patients whom
otherwise do not meet admission criteria may be sent home after an observation period of 6
hours providing the following criteria are met:
Transfer
Treat patients with isolated smoke inhalation appropriately in any modern intensive care
unit. However, transport patients with significant cutaneous burns (who otherwise meet
criteria for transfer to a burn center) when stable.
Modern burn care has decreased the mortality rate in patients with thermal burns. A large
retrospective chart review from 1972-1996 has shown that increasing burn size, older age,
inhalation injury, and female sex increase the risk of death, while operative intervention and
upper limb burns decrease the risk of death. [8]
Deterrence/Prevention
A study shows that smoke detectors reduce the risk of death by about 60% in all subgroups of
people.
This is in contrast to past data that suggest that these early warning devices may not be
effective in populations that have difficulty responding to an alarm in a timely manner, such
as children, older adults, persons with disabilities, or those impaired by alcohol or other
drugs.
These new data clearly exemplify the point that all homes should have a working smoke
detector in every room.
Although smoke detectors have been widely adopted by the public, and 93% of US
households have one in place, it is estimated that 30-45% of these are not operational,
usually due to nonreplacement or removal of batteries.
DiGuiseppi et al have shown that just merely giving out free smoke alarms in a deprived,
multiethnic, urban community did not reduce injuries related to fire. [33] This was because few
alarms had been installed or properly maintained.
Complications
While the mortality rate for isolated smoke inhalation injury is lower than 10%, the addition
of a cutaneous burn could almost quadruple this mortality rate.
Complications may include the following:
o Subglottic stenosis
o Bronchiectasis
o Pneumonia (3-23%)
o Atelectasis (1-5%)
After the 1987 California forest fire disaster, local EDs saw a dramatic rise in asthmatic
patients.
Patient Education
For excellent patient education resources, visit eMedicine's Lung and Airway Center,
Procedures Center, and Poisoning Center. Also, see eMedicine's patient education articles
Smoke Inhalation, Bronchoscopy, and Carbon Monoxide Poisoning.
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2006;26(1):99-125. [Medline].
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11. Reducing the number of deaths and injuries from residential fires. Pediatrics. Jun
2000;105(6):1355-7. [Medline].
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residential fires: who dies and who survives?. JAMA. May 27 1998;279(20):1633-7.
[Medline].
13. Muller MJ, Pegg SP, Rule MR. Determinants of death following burn injury. Br J
Surg. Apr 2001;88(4):583-7. [Medline].
14. Chou KJ, Fisher JL, Silver EJ. Characteristics and outcome of children with carbon
monoxide poisoning with and without smoke exposure referred for hyperbaric oxygen
therapy. Pediatr Emerg Care. Jun 2000;16(3):151-5. [Medline].
15. Istre GR, McCoy MA, Osborn L, Barnard JJ, Bolton A. Deaths and injuries from
house fires. N Engl J Med. Jun 21 2001;344(25):1911-6. [Medline].
16. Baud FJ, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of
smoke inhalation. N Engl J Med. Dec 19 1991;325(25):1761-6. [Medline].
17. Lahn M, Sing W, Nazario S, Fosberg D, Bijur P, Gallagher EJ. Increased blood lead
levels in severe smoke inhalation. Am J Emerg Med. Oct 2003;21(6):458-60.
[Medline].
19. Cancio LC. Airway management and smoke inhalation injury in the burn patient. Clin
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21. Nieman GF, Cigada M, Paskanik AM, et al. Comparison of high-frequency jet to
conventional mechanical ventilation in the treatment of severe smoke inhalation
injury. Burns. Apr 1994;20(2):157-62. [Medline].
22. Hall JJ, Hunt JL, Arnoldo BD, Purdue GF. Use of high-frequency percussive
ventilation in inhalation injuries. J Burn Care Res. May-Jun 2007;28(3):396-400.
[Medline].
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2006;26(1):99-125. [Medline].
24. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon
monoxide poisoning. N Engl J Med. Oct 3 2002;347(14):1057-67. [Medline].
25. Wolf SJ, Lavonas EJ, Sloan EP, Jagoda AS. Clinical policy: Critical issues in the
management of adult patients presenting to the emergency department with acute
carbon monoxide poisoning. Ann Emerg Med. Feb 2008;51(2):138-52. [Medline].
26. Kung SW, Chan YC, Lau FL. Hydroxocobalamin for acute cyanide poisoning in
smoke inhalation. Ann Emerg Med. Jan 2008;51(1):108; author reply 108-9.
[Medline].
27. Borron SW, Baud FJ, Barriot P, Imbert M, Bismuth C. Prospective study of
hydroxocobalamin for acute cyanide poisoning in smoke inhalation. Ann Emerg Med.
Jun 2007;49(6):794-801, 801.e1-2. [Medline].
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29. Desai MH, Mlcak R, Richardson J, Nichols R, Herndon DN. Reduction in mortality in
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2. [Medline].
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2001;38(1):36-41. [Medline].
http://emedicine.medscape.com/article/771194-followup#a2651
INSIDEN
Kurang lebih 2,5 juta orang mengalami luka bakar di Amerika Serikat setiaptahunnya. Dari
kelompok ini, 200.000 pasien memerlukan penanganan rawat jalan dan100.000 pasien
dirawat di rumah sakit. Sekitar 12.000 meninggal setiap tahunnya. Anak kecildan orang tua
merupakan populasi yang beresiko tinggi untuk mengalami luka bakar. Kaumremaja laki-laki dan pria
dalam usia kerja juga lebih sering menderita luka bakar (Smeltzer,2001 : 1911). Di rumah sakit
anak di Inggris, selama satu tahun terdapat sekitar 50.000 pasienluka bakar dimana 6400 diantaranya masuk
ke perawatan khusus luka bakar
2
. Antara tahun 1997-2002 terdapat 17.237 anak di bawah usia 5 tahun mendapat perawatan di
gawat daruratdi 100 rumah sakit di Amerika. Rumah Sakit Cipto Mangun Kusumo Jakarta pada tahun
1998di laporkan 107 kasus luka bakar yang dirawat, dengan angka kematian 37,38%
sedangkan diRumah Sakit Dr. Sutomo Surabaya pada tahun 2000 dirawat 106 kasus luka
bakar, kematian26, 41 %. Studi North-West England menemukan angka rata-rata yang datang ke rumah
sakitdengan trauma inhalasi akibat luka bakar adalah 0,29 per 1000 populasi tiap
tahun.Perbandingan antara laki-laki dan perempuan yaitu 2:1. Referensi lain menyebutkan
bahwakurang lebih sepertiga (20-35%) pasien luka bakar yang dating ke Pusat Luka Bakar
G
as iritan : bekerja dengan melapisi mukosa saluran nafas dan menyebabkan reaksiinflamasi. Amonia,
klorin, kloramin lebih larut air sehingga dapat menyebabkan luka bakar pada saluran nafas atas
dan menyebabkan iritasi pada mata, hidung, dan mulut.
G
as iritan lain yaitu sulfur dioksida, nitrogen dioksida, yang kurang larut air
sehinggamenyebabkan trauma paru dan distress pernafasan.2.
G
as asfiksian : karbon dioksida, gas dari bahan bakar (metana, etena, propane,asetilana), gas-gas
ini mengikat udara dan oksigen sehingga menyebabkan asfiksia.3.
G
as yang bersifat toksik sistemik : CO yang merupakan komponen terbesar dari asap,hidrogen sianida
merupakan komponen asap yang berasal dari api, hidrogen sulfide.
G
as-gas ini berhubungan dengan pengangkutan oksigen untuk produksi energi bagisel.
Sedangkan toksin sistemik seperti hidrokarbon halogen dan aromatik menyebabkan kerusakan
lanjut dari hepar, ginjal, otak, paru-paru, dan organ lain.4.
G
as yang menyebabkan alergi, dimana jika asap terhirup, partikel dan aerosolmenyebabkan
bronkospasme dan edema yang menyerupai asma.
Hidung : Bulu-bulu hidung berguna untuk menyaring udara yang masuk, debu dengandiameter > 5
mikron akan tertangkap, selaput lendir hidung berguna untuk menangkapdebu dengan
diameter lebih besar, kemudian melekat pada dinding rongga hidung.Anyaman vena (Plexus
venosus) berguna untuk menyamakan kondisi udara yang akanmasuk paru dengan kondisi
udara yang ada di dalam paru. Konka (tonjolan dari tulangrawan hidung) untuk memperluas
permukaan, agar proses penyaringan, pelembaban berjalan dalam suatu bidang yang luas, sehingga
proses diatas menjadi lebih efisien.2.
Pharing, terdapat persimpangan antara saluran napas dan saluran pencernaan. Bilamenelan
makanan, glotis dan epiglotis menutup saluran napas untuk mencegahterjadinya aspirasi. Pada
pemasangan endotrakeal tube glotis tidak dapat menutupsempurna, sehingga mudah terjadi
aspirasi laring. Terdapat pita suara / plika vokalis, bisamenutup dan membuka saluran napas, serta
melebar dan menyempit.
G
unanya adalahmembantu dalam proses mengejan, membuka dan menutup saluran napas
secaraintermitten pada waktu batuk. Pada waktu mau batuk plika vokalis menutup, saat
batuk membuka, sehingga benda asing keluar. Secara reflektoris menutup saluran napas
padasaat menghirup udara yang tidak dikehendaki dan untuk proses bicara.3.
Trakea. Dikelilingi tulang rawan berbentuk tapal kuda (otot polos dan bergaris) sehingga bisa
mengembang dan menyempit. Trakea bercabang menjadi 2 bronkus utama.4.
Bronkus. Merupakan percabangan trakea, terdiri dari bronkus kanan dan kiri.
Antara percabangan ini terdapat karina yang memiliki banyak saraf dan dapat
menyebabkan bronkospasme dan batuk yang kuat jika dirangsang. Bronkus kiri dan kanan tak
simetris.Yang kanan lebih pendek, lebih lebar dan arahnya hampir vertikal. Yang kiri
lebih panjang dan lebih sempit dengan sudut lebih tajam. Bronkus ini kemudian
bercabangmenjadi bronkus lobaris, bronkus segmentasi, bronkus terminalis, asinus yang
terdiri dari bronkus respiratorius yang terkadang mengandung alveoli, duktus alveolaris dan
sakusalveolaris terminalis.5.
Paru. Terdiri dari paru kanan dan kiri yang kanan terdiri dari 3 lobus, kiri 2 lobus.Dibungkus oleh selaput
yang disebut pleura visceralis sebelah dalam dan pleura parietalis sebelah luar yang
menempel pada rongga dada. Diantara kedua pleura terdapat
kavum interpleura yang berisi cairan. Di dalam saluran napas selain terdapat lendir, juga bulu-
bulu getar / silia yang berguna untuk menggerakkan lendir dan kotoran ke atas.
8,9,10
Fisiologi pernapasan menurut
G
uyton dkk, respirasi meliputi 2 bidang yakni respirasieksterna dan respirasi interna. Respirasi eksterna
adalah pengangkutan oksigen dari atmosfer sampai ke jaringan tubuh dan pengangkutan
karbon dioksida dari jaringan sampai keatmosfer. Sementara bagaimana oksigen digunakan
oleh jaringan dan bagaimana karbondioksida dibebaskan oleh jaringan disebut respirasi
internal. Proses respirasi merupakan proses yang dapat dibagi menjadi 5 tahap yaitu :1.
V
entilasi. Udara bergerak masuk dan keluar paru-paru karena ada selisih tekanan yangterdapat
antara atmosfer dan alveolus akibat kerja mekanik dari otot-otot. Selamainspirasi, volume toraks
bertambah besar karena diafragma turun dan iga terangkat akibatkontraksi beberapa otot yaitu otot
sternokleidomastoideus mengangkat sternum ke atasdan otot seratus, skalenus dan interkostalis
eksternus mengangkat iga-iga. Toraksmembesar ke tiga arah : anteroposterior, lateral dan
vertikal. Peningkatan volume inimenyebabkan penurunan tekanan intrapleura, dari sekitar -4
mmHg (relatif terhadaptekanan atmosfer) menjadi sekitar -8 mmHg bila paru-paru
mengembang pada waktuinspirasi. Tekanan saluran udara menurun sampai sekitar -2 mmHg
(relatif terhadaptekanan atmosfer) dari 0 mmHg pada waktu mulai inspirasi. Selisih tekanan
antarasaluran udara dan atmosfer menyebabkan udara mengalir ke dalam paru-paru
sampaitekanan saluran udara pada akhir inspirasi sama lagi dengan tekanan atmosfer.
Selama pernapasan tenang, ekspirasi merupakan gerakan pasif akibat elastisitas dinding dada
dan paru-paru atau saat ekspirasi dinding dada turun dan lengkung diafragma naik ke atas
menyebabkan volume toraks berkurang. Pengurangan volume toraks ini
meningkatkantekanan intrapleura maupun tekanan intrapulmonal. Selisih tekanan antara
saluran udaradan atmosfer menjadi terbalik, sehingga udara mengalir keluar dari paru-paru
sampaitekanan saluran udara dan tekanan atmosfer menjadi sama kembali pada akhir ekspirasi.2.
Difusi Tahap kedua dari proses pernapasan mencakup proses difusi gas-gas
melintasimembran alveolus-kapiler yang tipis (tebalnya kurang dari 0,5 m). Kekuatan
pendoronguntuk pemindahan ini adalah selisih tekanan parsial antara darah dan fase gas.
Padawaktu oksigen diinspirasi dan sampai di alveolus maka tekanan parsial ini
akanmengalami penurunan sampai sekitar 103 mmHg.
8,9,10,11
Penurunan tekanan parsial initerjadi berdasarkan fakta bahwa udara inspirasi tercampur
dengan udara dalam ruangsepi anatomik saluran udara dan dengan uap air. Ruang sepi anatomik ini
dalam keadaannormal mempunyai volume sekitar 1 ml udara per pound berat badan. Hanya udara bersih
yang mencapai alveolus yang merupakan ventilasi efektif, tekanan parsial oksigendalam darah
vena campuran (P
V
O2) di kapiler paru kira-kira sebesar 40 mmHg. Karenatekanan parsial oksigen dalam kapiler lebih
rendah daripada tekanan dalam alveolus(PAO2 = 103 mmHg), maka oksigen dapat dengan
mudah berdifusi ke dalam alirandarah. Perbedaan tekanan CO2 antara darah dan alveolus
yang jauh lebih rendah (6 mmHg) menyebabkan karbon dioksida berdifusi ke dalam alveolus. Karbon
dioksida inikemudian dikeluarkan ke atmosfer, dimana konsentrasinya pada hakekatnya
nolkendatipun selisih CO2 antara darah dan alveolus amat kecil.3.
Hubungan antara ventilasi-perfusi. Pemindahan gas secara efektif antara alveolus dankapiler
paru-paru membutuhkan distribusi merata dari udara dalam paru-paru dan perfusi(aliran
darah) dalam kapiler. Dengan perkataan lain, ventilasi dan perfusi dari unit pulmonar harus
sesuai. Nilai rata-rata rasio antara ventilasi terhadap perfusi (
V
/Q) adalah0,8. Angka ini didapatkan dari rasio rata-rata laju ventilasi alveolar normal (4
L/menit).Ketidak-seimbangan antara proses ventilasi-perfusi terjadi pada kebanyakan
penyakit pernapasan.
8
Tiga unit pernapasan abnormal secara teoritis menggambarkan unit ruangsepi yang
mempunyai ventilasi normal, tetapi tanpa perfusi, sehingga ventilasi terbuang percuma (
V
/Q = tidak terhingga). Unit pernapasan abnormal yang kedua merupakan unit pirau, dimana tidak ada
ventilasi tetapi perfusi normal, sehingga perfusi terbuang sia-sia(
V
/Q = 0). Unit yang terakhir merupakan unit diam, dimana tidak ada ventilasi dan perfusi.4.
Transpor oksigen dalam darah Oksigen dapat diangkut dari paru-paru ke jaringan- jaringan melalui dua
jalan: secara fisik larut dalam plasma atau secara kimia berikatan
dengan hemoglobin sebagai oksihemoglobin (HbO2). Ikatan kimia oksigen
denganhemoglobin ini bersifat reversibel. Dalam keadaan normal jumlah O2 yang larut
secarafisik sangat kecil karena daya larut oksigen dalam plasma yang rendah. Hanya sekitar 1%dari jumlah
oksigen total yang diangkut. Cara transpor seperti ini tidak memadai untuk mempertahankan
hidup.
8
Sebagian besar oksigen diangkut oleh hemoglobin yangterdapat dalam sel-sel darah merah.
Dalam keadaan tertentu (misalnya : keracunankarbon monoksida atau hemolisis masif
dimana terjadi insufisiensi hemoglobin) makaoksigen yang cukup untuk mempertahankan hidup
dapat ditranspor dalam bentuk larutanfisik dengan memberikan oksigen dengan tekanan yang lebih
tinggi dari tekananatmosfer (ruang oksigen hiperbarik). Satu gram hemoglobin dapat
mengikat 1,34 mloksigen.
8
Pada tingkat jaringan, oksigen akan berdisosiasi dari hemoglobin dan berdifusike dalam plasma.
Dari plasma, oksigen berdifusi ke sel-sel jaringan tubuh untuk memenuhi kebutuhan jaringan yang
bersangkutan. Meskipun kebutuhan jaringan bervariasi, namun sekitar 75% dari hemoglobin
masih berikatan dengan oksigen padawaktu hemoglobin kembali ke paru-paru dalam bentuk
darah vena campuran. Jadisesungguhnya hanya sekitar 25% oksigen dalam darah arteria yang
digunakan untuk keperluan jaringan.5.
Pengendalian Pernapasan. Yang disebut pusat pernapasan adalah suatu kelompok neuronyang
terletak bilateral di dalam substansia retikularis medula oblongata dan pons. Dibagimenjadi 3
daerah utama yaitu :1.
Kelompok neuron medula oblongata ventralis, yang merupakan area ekspirasi.Merupakan kelompok
neuron respirasi ventralis yang bila terangsang merangsangotot-otot ekspirasi. Area ekspirasi
selama pernapasan tenang dan normal bersifat pasif. Bila dorongan ekspirasi menjadi jauh lebih besar dari
normal maka isyarat-isyarat tertumpah ke area ekspirasi dari mekanisme osilasi dasar area
inspirasi,meningkatkan tenaga kontraktil yang kuat ke proses ventilasi paru.3.
Area di dalam pons yang membantu kecepatan pernapasan yang disebut area pneumotaksis. Pusat
pneumotaksis menghantarkan isyarat penghambat ke areainspirasi, yang mempunyai efek
membatasi isyarat inspirasi. Efek sekundernya
terjadi bila pembatasan inspirasi memperpendek masa pernapasan, maka siklus pernapasan
berikut akan terjadi lebih dini. Jadi isyarat pneumotaksis yang kuat dapatmeningkatkan
kecepatan pernapasan 30-40 x per menit. Sementara yang lemah hanya beberapa kali per menit.
8,11
PATOFISIOLOGI
Trauma inhalasi terjadi melalui kombinasi dari kerusakan epitel jalan nafas oleh panasdan zat kimia, atau
akibat intoksikasi sistemik dari hasil pembakaran itu sendiri. Hasil dari pembakaran tidak
hanya terdiri dari udara saja, tetapi merupakan campuran dari udara, partikel padat yang
terurai di udara (melalui suatu efek iritasi dan sitotoksik). Aerosol daricairan yang bersifat
iritasi dan sitotoksik serta gas toksik dimana gabungan tersebut bekerjasistemik. Partikel
padat yang ukurannya lebih dari 10 mikrometer tertahan di hidung dannasofaring. Partikel
yang berukuran 3-10 mikrometer tertahan pada cabang trakeobronkial,sedangkan partikel
berukuran 1-2 mikrometer dapat mencapai alveoli.
1,2
G
as yang larut air bereaksi secara kimia pada saluran nafas atas, sedangkan gas yangkurang larut
air pada saluran nafas bawah. Adapun gas yang sangat kurang larut air masuk melewati barier kapiler
dari alveolus dan menghasilkan efek toksik yang bersifat sistemik.Kerusakan langsung dari
sel-sel epitel, menyebabkan kegagalan fungsi dari apparatusmukosilier dimana akan
merangsang terjadinya suatu reaksi inflamasi akut yang melepaskanmakrofag serta aktivitas
netrofil pada daerah tersebut. Selanjutnya akan dibebaskan oksigenradikal, protease jaringan,
sitokin, dan konstriktor otot polos (tromboksan A2, C3A, C5A).Kejadian ini menyebabkan
peningkatan iskemia pada saluran nafas yang rusak, selanjutnyaterjadi edema dari dinding saluran
nafas dan kegagalan mikrosirkulasi yang akanmeningkatkan resistensi dinding saluran nafas dan
pembuluh darah paru. Komplians paruakan turun akibat terjadinya edema paru interstitial
sehingga terjadi edema pada saluran nafas bagian bawah akibat sumbatan pada saluran nafas
yang dibentuk oleh sel-sel epitel nekrotik,mukus dan sel-sel darah.
1,2
Trauma inhalasi diklasifikasikan menjadi 3, antara lain :
1,2,3,4
1.
Trauma pada saluran nafas bagian atas ( trauma supraglotis)Trauma saluran nafas atas dapat
menyebabkan ancaman hidup melalui obstruksi jalannafas sesaat setelah trauma. Jika proses
ini ditangani secara benar, edema salurannafas dapat hilang tanpa sekuele beberapa hari.2.
Trauma pada saluran nafas bawah dan parenkim paru (trauma subglotis)
Trauma ini dapat menyebabkan lebih banyak perubahan signifikan dalam fungsi parudan mungkin akan
susah ditangani. Trauma subglotis merupakan trauma kimia yangdisebabkan akibat inhalasi
hasil-hasil pembakaran yang bersifat toksik pada luka bakar. Asap memiliki kapasitas
membawa panas yang rendah, sehingga jarangdidapatkan trauma termal langsung pada jalan nafas
bagian bawah dan parenkim paru,trauma ini terjadi bila seseorang terpapar uap yang sangat
panas.3.
Toksisitas sistemik akibat inhalasi gas toksik seperti karbon monoksida (CO)
dansianida.Inhalasi dari gas toksik merupakan penyebab utama kematian cepat akibat api,meskipun
biasanya trauma supraglotis, subglotis dan toksisitas sistemik terjadi bersamaan. Intoksikasi
CO terjadi jika afinitas CO terhadap hemoglobin lebih besar dari afinitas oksigen terhadap
hemoglobin, sehingga ikatan CO dan hemoglobinmembentuk suatu karboksihemoglobin dan
menyebabkan hipoksia.
GAMBARAN KLINIS
1,2,3,4,12,13,14
Oleh karena onset terjadinya tidak segera dan sering tidak ditangani sesegeramungkin, maka
perlu diketahui tanda-tanda yang dapat mengarahkan kita untuk bertindak dan harus mencurigai bahwa
seseorang telah mengalami trauma inhalasi antara lain :-
Laboratorium
y
Pulse oximetry
Digunakan untuk mengukur saturasi hemoglobin yang meningkat palsu akibatikatan CO terhadap
hemoglobin sehingga kadar karboksihemoglobinseringkali diartikan sebagai oksihemaglon
y
Analisa
G
as DarahUntuk mengukur kadar karboksihemoglobin, keseimbangan asam basa dankadar
sianida. Sianida dihasilkan dari kebakaran rumah tangga dan biasanyaterjadi peningkatan kadar
laktat plasma
y
Foto ThoraksBiasanya normal dalam 3-5 hari, gambaran yang dapat muncul sesudahnya
termasuk atelektasis, edema paru, dan ARDS3.
Laringoskopi dan bronkoskopi fiberoptik Keduanya dapat digunakan sebagai alat diagnostik
maupun terapeutik. Pada bronkoskopi biasanya didapatkan gambaran jelaga, eritema, sputum
dengan arang, petekie, daerah pink sampai abu-abu karena nekrosis, ulserasi, sekresi,
mukopurulen.Bronkoskopi serial berguna untuk menghilangkan debris dan sel-sel nekrotik
padakasus-kasus paru atau jika suction dan ventilasi tekanan positif tidak cukup memadai.
PENATALAKSANAAN
Diagnosis yang cepat terhadap trauma inhalasi adalah penting untuk penanganancepat agar
terhindar dari gagal nafas yang berakibat kematian. Pengobatan untuk traumainhalasi adalah
bersifat suportif.1.
AirwayJika dicurigai seseorang dengan trauma inhalasi maka sebelum dikirim ke pusat luka bakar
sebaiknya dilakukan intubasi cepat untuk melindungi jalan nafas sebelum
terjadi pembengkakan wajah dan faring yang biasanya terjadi 24-48 jam setelahkejadian,
dimana jika terjadi edema maka yang diperlukan adalah trakeostomi ataukrikotiroidotomi jika
intubasi oral tidak dapat dilakukan.
2,4,15,16,17
2.
Luka bakar Periksa seluruh tubuh untuk mengetahui adanya trauma lain dan luka bakar.
Cuci NaCl kulit yang tidak terbakar untuk menghindari sisa zat toksik yang bermakna.
2
6.
Medikasi
1,2
Amyl dan Sodium Nitrit untuk mengobati keracunan sianida tetapi harus berhati-hati jika ditemukan
pula tanda-tanda keracunan CO karena obat inidapat menyebabkan methahemoglobinemia.
Oksigen dan Sodium tiosulfat juga dapat sebagai antidotum sianida, antidotum yang lain
adalahhidroksikobalamin dan EDTA.
y
KOMPLIKASI
1,2
1.
Trauma paru berat, edema, dan ketidakmampuan untuk oksigenasi atau ventilasi yangadekuat
dapat menyebabkan kematian2.
Keracunan CO dan inhalasi dari hasil pembakaran yang lain secara bersamaan
dapatmenyebabkan hipoksemia, trauma organ dan morbiditas.
PROGNOSIS
Pada trauma inhalasi ringan biasanya self limited dalam 48-72 jam. Berat ringannyatrauma
langsung pada parenkim paru tergantung pada luas dan lamanya paparan serta jenisinhalan yang
diproduksi secara bersamaan.
DAFTAR PUSTAKA1.
Argenta, L.C., Inhalation Injury, Basic Science for Surgeon : A Review, Saunders, North
Carolina, 20047.
G
uyton, AC., Pernafasan, Buku Ajar Fisiologi Kedokteran, Edisi 9, E
G
C, 20009.
Snell, RS., Cavitas Thoracis, Anatomi Klinik Untuk Mahasiswa Kedokteran, Bagian1, Edisi
3, E
G
C, 199711.
Putz, R., Alat Pernafasan, Atlas Anatomi Manusia Sobotta, Jilid 1, Edisi 21, E
G
C,200612.
Holleran, RS., Burn Trauma, Air and Surface Patient Transport Principles andPractice, Third
edition, Mosby, Ohio, 200313.
Lynge, DC., Traumatic Injury, Surgical Problems and Procedurs in Primary Care,Mc
G
raw Hill, Washington, 200114.
Way, LW., Burn and Other Thermal Injuries, Current Surgical Diagnosis andTreatment, 11
th
Edition, Mc
G
raw Hill, Boston, 200315.
Beasly R.Thorne H.
G
rabb & Smiths Plastic Surgery Six Edition. AssociateProfessor of Plastic Surgery.NYU
Medical Center. New York. 2007. 139-141
Airway
UAO (Acute upper airway obstruction) terjadi hampir seperlima sampai sepertiga korban
kebakaran dengan trauma inhalasi dan mortalitas terbesar disebabkan oleh progresi yang
cepat dari edema faring hingga obstruksi jalan nafas bagian atas dengan asfiksia (19).
The
worsening of upper airway edema is most prominent in
supraglottic structures. Serial nasopharyngoscopic evaluations
demonstrate obliteration of the aryepiglotic folds,
arytenoid eminences, and interaryteniod areas by edematous
tissues that prolapse to occlude the airway [20]. For patients
with large surface burns that require rapid fluid administration,
these changes may be accentuated. Burns of the neck,
especially in children, can cause unyielding eschars that
externally compress and obstruct the airway. Escharotomies
burns 3 3 ( 2 0 0 7 ) 2 1 3