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Smoke Inhalation

Author: Keith A Lafferty, MD; Chief Editor: Rick Kulkarni, MD

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.

Methemoglobinemia occurs in fire due to heat denaturation of hemoglobin, oxides produced


in fire, and methemoglobin-forming materials such as nitrites. Occurrence of
methemoglobinemia is a less common phenomenon than CN and CO toxicity. The
pathophysiologic consequences of methemoglobin formation are a decrease in the oxygen-
carrying capacity of the blood and a shift of the oxyhemoglobin dissociation curve to the left,
similar to carboxyhemoglobin (HbCO).

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

Mortality is related to associated cutaneous burns.

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

The male-to-female ratio is about 3:2.

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

Fires in closed spaces significantly increase the risk of smoke inhalation.

Particular materials in fires may contain dangerous asphyxiants.

Polyurethane, wool, and silk increase the patient's risk of CN toxicity.

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.

A history of respiratory illnesses, such as asthma or chronic obstructive pulmonary disease


(COPD), predisposes patients to respiratory insufficiency.

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 patency of the airway.

o Maintain cervical immobilization in any patient who is obtunded, has distracting


injuries, has been involved in a significant mechanism of injury, has bony tenderness,
or complains of neck symptoms.

o Assess breathing by respiratory rate, chest wall motion, and auscultation of air
movement.

o Assess circulation by level of consciousness, pulse rate, blood pressure, capillary


refill, and by symmetry and strength of pulses.

o Perform a brief neurological evaluation including a determination of the Glasgow


Coma Scale, pupil size and reactivity, and any focal findings.

o Remove all clothing to expose traumatic injuries/burns and to prevent ongoing


thermal injury from smoldering clothes. Evaluate patient's back and perform a log
roll if appropriate.

Respiratory

o Identification of impending respiratory failure is paramount.

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 Hoarseness, change in voice, complaints of throat pain, and/or odynophagia indicate


an upper airway injury that may be severe.

o Carbonaceous sputum should be regarded as a marker of exposure. Transportation


to a burn center with such findings should lower ones threshold for early
endotracheal security.

o Tachypnea may be present.

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.

The secondary survey continues in a complete head-to-toe examination as in any other


trauma evaluation.

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

Acute Respiratory Distress Syndrome

Anaphylaxis

Angioedema

Anxiety

Asthma

Bacterial Pneumonia

Chronic Obstructive Pulmonary Disease and Emphysema

Congestive Heart Failure and Pulmonary Edema

Pneumonia, Aspiration

Pneumonia, Viral

Pneumothorax, Iatrogenic, Spontaneous and Pneumomediastinum

Pneumothorax, Tension and Traumatic

Pulmonary Embolism

Laboratory Studies

Electrolyte testing can identify an anion gap acidosis.

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.

Thermal degradation products of various compounds, including phosphorous-based fire


retardants, are capable of impairing cholinesterase activity. A prospective study measured
serum erythrocyte cholinesterase activity at the scene of residential fires for 49 victims. A
significant lower level of cholinesterase activity was noted in these patients as compared to
controls. Obviously, further investigation into the clinical significance of this lower enzymatic
activity is needed before it can be used clinically.
The pulse oximeter can be misleading in the setting of CO exposure or methemoglobinemia
because it uses only 2 wavelengths of light (the red and the infrared spectrum), which detect
oxygenated and deoxygenated hemoglobin (Hb) only and not any other form of Hb.
Cooximeters transmit 4 wavelengths of light through a blood sample and are capable of
detecting methemoglobin and Hb-CO (in addition to Hb and oxyhemoglobin [HbO 2]).

o Be aware that, on routine blood gas analysis, the percent saturation of Hb is


calculated from the alveolar-arterial difference in partial pressure of oxygen (PaO 2),
which can give a falsely elevated saturation. The difference between saturations
obtained by cooximetry and calculated figures is known as the saturation gap and is
an indicator that a dyshemoglobinemia is present.

o Finally, light reflection in methemoglobinemia is similar to that in reduced Hb, and a


depressed saturation may be shown on pulse oximetry, but the decrease does not
accurately reflect the level of methemoglobinemia. In fact, as levels reach 30% or
higher, the pulse oximeter does not go below 85%.

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

High-resolution CT is readily available in most tertiary care centers.

CT scan may show ground-glass opacities in a peribronchial distribution and/or patchy


peribronchial consolidations.

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

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 atelectasis, consolidation, and ARDS, vital capacity, pulmonary compliance, and


functional residual capacity are reduced.

o In patients with bronchospasm, forced expiratory volume in 1 second (FEV 1), peak
flow, and midexpiratory flow rates are reduced.

o Diagnostic accuracy is 91%.


Procedures

Bronchoscopy can be diagnostic as well as therapeutic, particularly when lobar atelectasis is


present.

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 Erythema, charring, deposition of soot, edema, and/or mucosal ulceration may be


present.

o Impending airway obstruction may be inferred, and intubation may be facilitated by


this technique.

o Diagnostic accuracy is reported to be 86%.

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.

o Patients with inhalation injury complicated by pneumonia who undergo


bronchoscopy have decreased duration of mechanical ventilation, shorter intensive
care unit stays, and trend toward lower mortality. [20]

Prehospital Care

Deliver high-flow oxygen by mask.

If respiratory failure is present, the patient should have assisted ventilation and/or
endotracheal intubation.

Perform cricothyrotomy if airway obstruction is present or impending and an airway cannot


be secured orally.

Secure IV access, but do not delay transport of patient to the hospital in any way.

Obtain CO level at the scene if possible.

In a consecutive case series of 18 patients, cardiac arrest complicating CO toxicity was


uniformly fatal, despite administration of hyperbaric oxygen (HBO) therapy after the initial
resuscitation. The prognosis of this condition should be considered when making triage
decisions for these patients.[17]
Emergency Department Care

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.

Assume elevated levels of HbCO in all fire victims.


o The half-life of CO is 320 minutes on room air, 90 minutes on 100% oxygen, and 23
minutes in a hyperbaric chamber at 3 atmospheres absolute (ATA). Elimination of CO
depends primarily on the law of mass action, so alveolar PO 2, rather than alveolar
ventilation, is the critical factor in its removal.

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 Literature suggests that hypoxic encephalopathy secondary to CO poisoning results


from a reperfusion injury in which the products of lipid peroxidation and free radical
formation contribute to morbidity and mortality. In addition, improvement in
mitochondrial oxidative metabolism, impairment of adherence of neutrophils to
cerebral vasculature (decreases inflammation), and preservation of adenosine
triphosphate activity was shown with HBO therapy. This partially explains why HbCO
levels are poor indicators of the severity of intoxication and why patients with
significant toxicity may have low levels. In fact, at the time of the initial HBO
treatment, patients enrolled in most studies have normal or near-normal COHb
levels.

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 In a well-cited study, perhaps the most methodologically rigorous, Weaver et al have


shown in a prospective, double blind manner that in patients with symptomatic
acute CO poisoning, 3 HBO treatments, in comparison to NBO therapy, decreased
the incidence of cognitive sequelae by 46% at 6 weeks. [24] Furthermore, a benefit
continued to be seen at 12-month follow-up. Essentially, for every 6 patients treated
with HBO, one case of delayed neurologic sequelae could be avoided. The study had
to be stopped before its completion because of the evidence.

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.

o Neurologic abnormalities and a history of loss of consciousness are the primary


clinical features used to define severe CO toxicity. HBO use is indicated in any of
these patients as well as those with a base excess lower than -2 mmol/L, a CO level
greater than 25% (or >15% in pregnancy as fetal hemoglobin binds CO more tightly),
signs of cerebellar dysfunction, cardiovascular dysfunction, pulmonary edema, and in
the extremes of age. Note that the incidence of delayed neurologic sequelae (DNS)
increases with a more symptomatic initial clinical picture, in older patients, and in
those with a prolonged exposure.[23]

o The American College of Emergency Physicians Clinical Policies Subcommittee


recommended in 2008 continued use of HBO in CO poisoning, especially in children
and pregnant women, due to the conflicting results of previous studies. [25]

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 Although not used universally, hydroxocobalamin (vitamin B-12), a hemelike


molecule with a complexed cobalt atom, has become the preferred treatment of CN
toxicity. It has been used in France for more than 30 years and was approved by the
FDA in 2006 for use in the US. CN reacts with high affinity with metals such as ferric
ion and cobalt and binds to numerous critical enzymes in the body. The mechanism
of action is direct binding to CN to form cyanocobalamin that is excreted renally.

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.

o Induction of methemoglobinemia is theoretically dangerous in the setting of HbCO,


due to an even greater reduction in oxygen carrying capacity, and the clinician should
consider withholding the nitrite portion of the kit. Another drawback of this
treatment is the delayed onset of thiosulfate. Finally, this treatment may be more
preventative rather than curative.

o Methemoglobinemia in smoke inhalation is relatively rare and rarely requires


treatment with methylene blue. This antidote is reduced by the nicotinamide
adenine dinucleotide phosphate (NADPH) methemoglobin reductase enzyme and in
return reduces methemoglobin to normal hemoglobin. Indications for treatment are
a change in mental status, acidosis, ECG changes, and ischemic chest pain. Levels
lower than 30% may not require treatment, depending on the patient's
cardiorespiratory reserve.

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.

Studies on experimental induction of smoke inhalation confirm the presence of an acute


surfactant deficiency. Instillation of artificial surfactant shortly after injury was beneficial.
Larger studies are needed before instituting such therapy.

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.

View full drug information

Albuterol (Proventil, Ventolin)

Beta-agonist that is useful in treatment of bronchospasm refractory to epinephrine. Relaxes


bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle
contractility. Airway resistance is decreased, and ventilation is improved.

Vitamin, Water Soluble


Class Summary

This agent binds to CN to form cyanocobalamin, which is renally excreted.


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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

These agents convert a portion of circulating hemoglobin to methemoglobin.

View full drug information

Amyl nitrite (Isoamyl nitrite)

In the presence of nitrites, hemoglobin is converted to methemoglobin, which has a higher


binding affinity for CN than does the cytochrome oxidase complex. Administration produces
a methemoglobin level of 5% and subsequent formation of cyanomethemoglobin, allowing
electron transport and cellular respiration to continue. This medication is given until an IV
line is established and sodium nitrite can be administered.

Sodium nitrite

In the presence of nitrites, hemoglobin is converted to methemoglobin that has a higher


binding affinity for CN than does the cytochrome oxidase complex. Administration produces
a methemoglobin level of 20-30% and subsequent formation of cyanomethemoglobin,
allowing electron transport and cellular respiration to continue.

Sulfur compounds
Class Summary

These agents provide a sulfur moiety to rhodanese, allowing the production of thiocyanate,
which subsequently is excreted by the kidneys.

View full drug information

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

These agents are used in order to convert methemoglobin to oxyhemoglobin.

View full drug information

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.

Further Inpatient Care

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:

History of closed-space exposure for longer than 10 minutes

Carbonaceous sputum production

Arterial PO2 less than 60 mm Hg

Metabolic acidosis

HbCO levels above 15%

Arteriovenous oxygen difference (on 100% oxygen) greater than 100 mm Hg

Bronchospasm

Odynophagia

Central facial burns


Further Outpatient Care

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:

Normal vital signs

Normal physical examination

Short smoke exposure

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 Pulmonary edema (4-9%)

o Pneumonia (3-23%)

o Atelectasis (1-5%)

After the 1987 California forest fire disaster, local EDs saw a dramatic rise in asthmatic
patients.

Another study of firefighters showed certain subgroups to have an exaggerated decline in


postexposure FEV1 that was not predicted by age, smoking history, intensity of exposure, or
the use of self-contained breathing apparatus. Some of these patients, who had no family
history of reactive airway disease, went on to need long-term beta-agonist therapy. The
many case series in the literature clarify that reactive airway disease, in a small sample of
patients with smoke inhalation, is a real potential sequela.

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.

References

1. Bizovi KE, Leikin JD. Smoke inhalation among firefighters. Occup Med. Oct-Dec
1995;10(4):721-33. [Medline].

2. Hall AH, Dart R, Bogdan G. Sodium thiosulfate or hydroxocobalamin for the empiric
treatment of cyanide poisoning?. Ann Emerg Med. Jun 2007;49(6):806-13. [Medline].

3. Demling RH. Smoke inhalation lung injury: an update. Eplasty. May 16 2008;8:e27.
[Medline]. [Full Text].

4. Kao LW, Nanagas KA. Toxicity associated with carbon monoxide. Clin Lab Med. Mar
2006;26(1):99-125. [Medline].

5. Stewart RJ, Yamaguchi KT, Knost PM, Mason SW, Roshdieh BB, Samadani S.
Effects of ibuprofen on pulmonary oedema in an animal smoke inhalation model.
Burns. Dec 1990;16(6):409-13. [Medline].

6. Kimura R, Traber L, Herndon D, Niehaus G, Flynn J, Traber DL. Ibuprofen reduces


the lung lymph flow changes associated with inhalation injury. Circ Shock. Mar
1988;24(3):183-91. [Medline].
7. Hill IR. Particulate matter of smoke inhalation. Ann Acad Med Singapore. Jan
1993;22(1):119-23. [Medline].

8. Buyantseva LV, Tulchinsky M, Kapalka GM, et al. Evolution of lower respiratory


symptoms in New York police officers after 9/11: a prospective longitudinal study. J
Occup Environ Med. Mar 2007;49(3):310-7. [Medline].

9. Weiden MD, Ferrier N, Nolan A, Rom WN, Comfort A, Gustave J. Obstructive


airways disease with air trapping among firefighters exposed to World Trade Center
dust. Chest. Mar 2010;137(3):566-74. [Medline].

10. Barillo DJ, Goode R. Fire fatality study: demographics of fire victims. Burns. Mar
1996;22(2):85-8. [Medline].

11. Reducing the number of deaths and injuries from residential fires. Pediatrics. Jun
2000;105(6):1355-7. [Medline].

12. Marshall SW, Runyan CW, Bangdiwala SI, Linzer MA, Sacks JJ, Butts JD. Fatal
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].

18. Koljonen V, Maisniemi K, Virtanen K, Koivikko M. Multi-detector computed


tomography demonstrates smoke inhalation injury at early stage. Emerg Radiol. Jun
2007;14(2):113-6. [Medline].

19. Cancio LC. Airway management and smoke inhalation injury in the burn patient. Clin
Plast Surg. Oct 2009;36(4):555-67. [Medline].

20. Carr JA, Phillips BD, Bowling WM. The utility of bronchoscopy after inhalation
injury complicated by pneumonia in burn patients: results from the National Burn
Repository. J Burn Care Res. Nov-Dec 2009;30(6):967-74. [Medline].
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].

23. Kao LW, Nanagas KA. Toxicity associated with carbon monoxide. Clin Lab Med. Mar
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].

28. Sterner JB, Zanders TB, Morris MJ, Cancio LC. Inflammatory mediators in smoke
inhalation injury. Inflamm Allergy Drug Targets. Mar 2009;8(1):63-9. [Medline].

29. Desai MH, Mlcak R, Richardson J, Nichols R, Herndon DN. Reduction in mortality in
pediatric patients with inhalation injury with aerosolized heparin/N-acetylcystine
[correction of acetylcystine] therapy. J Burn Care Rehabil. May-Jun 1998;19(3):210-
2. [Medline].

30. Huang PS, Tang GJ, Chen CH, Kou YR. Whole-body moderate hypothermia confers
protection from wood smoke-induced acute lung injury in rats: the therapeutic
window. Crit Care Med. Apr 2006;34(4):1160-7. [Medline].

31. Hall AH, Saiers J, Baud F. Which cyanide antidote?. Crit Rev Toxicol.
2009;39(7):541-52. [Medline].

32. Shepherd G, Velez LI. Role of hydroxocobalamin in acute cyanide poisoning. Ann
Pharmacother. May 2008;42(5):661-9. [Medline].

33. DiGuiseppi C, Roberts I, Wade A, Sculpher M, Edwards P, Godward C, et al.


Incidence of fires and related injuries after giving out free smoke alarms: cluster
randomised controlled trial. BMJ. Nov 2 2002;325(7371):995. [Medline]. [Full Text].
34. Hampson NB, Zmaeff JL. Outcome of patients experiencing cardiac arrest with
carbon monoxide poisoning treated with hyperbaric oxygen. Ann Emerg Med. Jul
2001;38(1):36-41. [Medline].

References

1. Bizovi KE, Leikin JD. Smoke inhalation among firefighters. Occup Med. Oct-Dec
1995;10(4):721-33. [Medline].

2. Hall AH, Dart R, Bogdan G. Sodium thiosulfate or hydroxocobalamin for the empiric
treatment of cyanide poisoning?. Ann Emerg Med. Jun 2007;49(6):806-13. [Medline].

3. Demling RH. Smoke inhalation lung injury: an update. Eplasty. May 16 2008;8:e27.
[Medline]. [Full Text].

4. Kao LW, Nanagas KA. Toxicity associated with carbon monoxide. Clin Lab Med. Mar
2006;26(1):99-125. [Medline].

5. Stewart RJ, Yamaguchi KT, Knost PM, Mason SW, Roshdieh BB, Samadani S.
Effects of ibuprofen on pulmonary oedema in an animal smoke inhalation model.
Burns. Dec 1990;16(6):409-13. [Medline].

6. Kimura R, Traber L, Herndon D, Niehaus G, Flynn J, Traber DL. Ibuprofen reduces


the lung lymph flow changes associated with inhalation injury. Circ Shock. Mar
1988;24(3):183-91. [Medline].

7. Hill IR. Particulate matter of smoke inhalation. Ann Acad Med Singapore. Jan
1993;22(1):119-23. [Medline].

8. Buyantseva LV, Tulchinsky M, Kapalka GM, et al. Evolution of lower respiratory


symptoms in New York police officers after 9/11: a prospective longitudinal study. J
Occup Environ Med. Mar 2007;49(3):310-7. [Medline].

9. Weiden MD, Ferrier N, Nolan A, Rom WN, Comfort A, Gustave J. Obstructive


airways disease with air trapping among firefighters exposed to World Trade Center
dust. Chest. Mar 2010;137(3):566-74. [Medline].

10. Barillo DJ, Goode R. Fire fatality study: demographics of fire victims. Burns. Mar
1996;22(2):85-8. [Medline].

11. Reducing the number of deaths and injuries from residential fires. Pediatrics. Jun
2000;105(6):1355-7. [Medline].

12. Marshall SW, Runyan CW, Bangdiwala SI, Linzer MA, Sacks JJ, Butts JD. Fatal
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].

18. Koljonen V, Maisniemi K, Virtanen K, Koivikko M. Multi-detector computed


tomography demonstrates smoke inhalation injury at early stage. Emerg Radiol. Jun
2007;14(2):113-6. [Medline].

19. Cancio LC. Airway management and smoke inhalation injury in the burn patient. Clin
Plast Surg. Oct 2009;36(4):555-67. [Medline].

20. Carr JA, Phillips BD, Bowling WM. The utility of bronchoscopy after inhalation
injury complicated by pneumonia in burn patients: results from the National Burn
Repository. J Burn Care Res. Nov-Dec 2009;30(6):967-74. [Medline].

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].

23. Kao LW, Nanagas KA. Toxicity associated with carbon monoxide. Clin Lab Med. Mar
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].
28. Sterner JB, Zanders TB, Morris MJ, Cancio LC. Inflammatory mediators in smoke
inhalation injury. Inflamm Allergy Drug Targets. Mar 2009;8(1):63-9. [Medline].

29. Desai MH, Mlcak R, Richardson J, Nichols R, Herndon DN. Reduction in mortality in
pediatric patients with inhalation injury with aerosolized heparin/N-acetylcystine
[correction of acetylcystine] therapy. J Burn Care Rehabil. May-Jun 1998;19(3):210-
2. [Medline].

30. Huang PS, Tang GJ, Chen CH, Kou YR. Whole-body moderate hypothermia confers
protection from wood smoke-induced acute lung injury in rats: the therapeutic
window. Crit Care Med. Apr 2006;34(4):1160-7. [Medline].

31. Hall AH, Saiers J, Baud F. Which cyanide antidote?. Crit Rev Toxicol.
2009;39(7):541-52. [Medline].

32. Shepherd G, Velez LI. Role of hydroxocobalamin in acute cyanide poisoning. Ann
Pharmacother. May 2008;42(5):661-9. [Medline].

33. DiGuiseppi C, Roberts I, Wade A, Sculpher M, Edwards P, Godward C, et al.


Incidence of fires and related injuries after giving out free smoke alarms: cluster
randomised controlled trial. BMJ. Nov 2 2002;325(7371):995. [Medline]. [Full Text].

34. Hampson NB, Zmaeff JL. Outcome of patients experiencing cardiac arrest with
carbon monoxide poisoning treated with hyperbaric oxygen. Ann Emerg Med. Jul
2001;38(1):36-41. [Medline].

http://emedicine.medscape.com/article/771194-followup#a2651

TRAUMA INHALASI PADA LUKA BAKAR PENDAHULUAN


Luka bakar adalah kerusakan atau kehilangan jaringan yang disebabkan oleh energi panas
atau bahan kimia atau benda-benda fisik yang menghasilkan efek memanaskan
ataumendinginkan. Luka bakar adalah suatu trauma yang disebabkan oleh panas, arus
listrik, bahan kimia dan petir yang mengenai kulit, mukosa dan jaringan yang lebih dalam.
1
Luka bakar merupakan luka yang unik diantara bentuk-bentuk luka lainnya karenaluka
tersebut meliputi sejumlah besar jaringan mati (eskar) yang tetap berada pada
tempatnyauntuk jangka waktu yang lama. (Smeltzer, 2001 : 1911). Luka adalah rusaknya
struktur danfungsi anatomis normal akibat proses patologis yang berasal dari internal maupun
eksternaldan mengenai organ tertentu. (Lazarus, 1994 dalam Potter & Perry, 2006;1853).
Traumainhalasi merupakan faktor yang secara nyata memiliki kolerasi dengan angka
kematian. Padakebakaran dalam ruangan tertutup atau bilamana luka bakar mengenai daerah
muka / wajahdapat menimbulkan kerusakan mukosa jalan napas akibat gas, asap atau uap
panas yangterhisap. Cedera inhalasi disebabkan oleh jenis bahan kimia terbakar
(tracheobronchitis) darisaluran pernapasan. Bila cedera ini terjadi pada pasien dengan luka bakar kulit
yang parahkematian sangat tinggi antara 48% sampai 86%. Edema yang terjadi dapat
menyebabkangangguan berupa hambatan jalan napas.
1,2
Keracunan asap yang disebabkan oleh termodegradasi material alamiah dan materiyang
diproduksi. Termodegradasi menyebabkan terbentuknya gas toksik seperti hidrogensianida,
nitrogen oksida, hidrogen klorida, akreolin dan partikel partikel tersuspensi. Efek akut dari
bahan kimia ini menimbulkan iritasi dan bronkokonstriksi pada saluran napas.Obstruksi jalan napas akan
menjadi lebih hebat akibat adanya tracheal bronchitis danedema.
1,2,3

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

adalahdengan trauma inhalasi


4,6
ETIOLOGI
Kebanyakan trauma inhalasi terjadi akibat kerusakan langsung pada permukaan epitelyang
dapat menyebabkan konjungtivitis, rhinitis, faringitis, laryngitis, trakeitis, bronchitis
danalveolitis. Absorbsi sistemik dari toksin juga terjadi. Susah untuk membedakan
apakahinsufisiensi pernafasan disebabkan oleh trauma langsung pada paru atau akibat
pengaruhmetabolik, hemodinamik dan komplikasi lanjut dari suatu infeksi permukaan luka bakar.
2
Trauma inhalasi disebabkan oleh berbagai inhalan. Inhalan dibedakan atas 4 macamyaitu:
2,7
1.

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.

ANATOMI DAN FISIOLOGI


Menurut Price SA, Wilson LM, 1946, anatomi pernafasan agar udara bisa mencapai paru-
paru adalah hidung, laring, trakhea, bronkhus dan bronkhiolus. Fungsi masing-masing bagian
ini sebagai berikut:1.

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 dorsalis, yang merupakan area inspirasi.


Letak neuronnya sangat dekat dan berhubungan rapat dengan traktus solitarius yangmerupakan
ujung sensorik nervus vagus dan glosofaringeus. Sebaliknya masing-masing saraf ini menghantarkan isyarat-
isyarat sensorik dari kemoreseptor perifer,dengan cara ini membantu ventilasi paru.2.

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 :-

Luka bakar pada wajah-

Alis mata dan bulu hidung hangus-

Adanya timbunan karbon dan tanda-tanda inflamasi akut di dalam orofaring-

Sputum yang mengandung arang atau karbon-

Wheezing, sesak dan suara serak -

Adanya riwayat terkurung dalam kepungan api-

Ledakan yang menyebabkan trauma bakar pada kepala dan badan-

Tanda-tanda keracunan CO (karboksihemoglobin lebih dari 10% setelah berada


dalamlingkungan api) seperti kulit berwarna pink sampai merah, takikardi, takipnea,
sakitkepala, mual, pusing, pandangan kabur, halusinasi, ataksia, kolaps sampai koma.
PEMERIKSAAN PENUNJANG
1,2,3
1.

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

ElektrolitUntuk memonitor abnormalitas elektrolit sebagai hasil dari resusitasi cairandalam


jumlah besar
y

Darah lengkapHemokonsentrasi akibat kehilangan cairan biasanya terjadi sesaat


setelahtrauma. Hematokrit yang menurun secara progresif akibat pemulihan
volumeintravaskular. Anemia berat biasanya terjadi akibat hipoksia atauketidakseimbangan
hemodinamik. Peningkatan sel darah putih untuk melihatadanya infeksi.2.

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.

BreathingJika didapatkan tanda-tanda insufisiensi pernapasan, susah bernapas, stridor,


batuk,retraksi suara nafas bilateral atau tanda-tanda keracunan CO maka dibutuhkan
oksigen100% atau oksigen tekanan tinggi yang akan menurunkan waktu paruh dari CO
dalamdarah.
1,2,3
3.

CirculationPengukuran tekanan darah dan nadi untuk mengetahui stabilitas hemodinamik.


Untuk mencegah syok hipovolemik diperlukan resusitasi cairan intravena. Pada pasiendengan
trauma inhalasi biasanya dalam 24 jam pertama digunakan cairan kristaloid40-75% lebih
banyak dibandingkan pasien yang hanya luka bakar saja.
1,3
4.

Neurologik Pasien yang berespon/sadar membantu untuk mengetahui kemampuan mereka


untuk melindungi jalan nafas dan merupakan indikator yang baik untuk mengukur kesuksesan resusitasi.
Pasien dengan kelainan neurologik seringkali memerlukananalgetik poten.
2
5.

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

Kortikosteroid : digunakan untuk menekan inflamasi dan menurunkan edema


y

Antibiotik : Mengobati infeksi sekunder yang biasanya disebabkan olehStaphylococcus


Aureus dan Pseudomonas Aeruginosa pada pasien-pasiendengan kerusakan paru
y

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

Bronkodilator untuk pasien-pasien dengan bronkokonstriksi. Pada kasus-kasus berat


bronkodilator digunakan secara intavena.

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.

Rajpura A., Inhalation Injury, available atwww.burncenter.com, Januari 20112.

Emily B Nazarian., Inhalation Injury, available atwww.emedicine.com, Januari 20113.

Herold, L Cerny, Inhalation Injury, available


atwww.ynovaburnandreconstructivesurgery.com, Januari 20114.

Michael D Peck., Smoke Inhalation Injury, available atwww.ameriburn.org, 20055.

Robert A Benner, Inhalation Injury, available atwww.burnresource.com, 2001-20026.

Argenta, L.C., Inhalation Injury, Basic Science for Surgeon : A Review, Saunders, North
Carolina, 20047.

Craig Feied, Inhalation Injury, available atwww.NCEMI.com, 20068.

G
uyton, AC., Pernafasan, Buku Ajar Fisiologi Kedokteran, Edisi 9, E
G
C, 20009.

Luhulima, J. W., Thorax, Anatomi Program Pendidikan Dokter, Jilid 4, BagianAnatomi


FKUH, Makassar, 200110.

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.

Robert H. Demling., Pulmonary Problems in The Burn Patient, available atwww.burnsurgery.org,


200016.

Awori N., Luka Bakar, Bedah Primer Trauma, E


G
C, Jakarta, 200017.

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

to the neck may be helpful in reducing the tight eschar and


therefore decrease the pressure exerted on the trachea.
Whenever UAO is suspected the most experienced clinician
in airway management should perform endotracheal intubation.
Securing the endotracheal tube can be difficult due to
the burn wound and the rapid swelling that occurs within the
first 72 h. Mlcak and his co-workers reported on a technique
of airway security that has been used effectively on burn
children [21].
4.1.1. Bronchial hygeine therapy
Airway clearance techniques are an essential component of
respiratory management of patients with smoke inhalation.
Bronchial hygiene therapy is a termused to describe several of
the modalities intended to accomplish this goal. Therapeutic
coughing, chest physiotherapy, early ambulation, airway
suctioning, therapeutic bronchoscopy and pharmacologic
agentshavebeeneffectiveinthe removalof retainedsecretions.
Therapeutic coughing functions to promote airway clearance
of excess mucus and fibrin cast in the tracheal bronchial
tree. The impairment of the cough mechanism will result in
retained secretions, bronchial obstruction, atelectasis, and/or
pneumonia. A cough may be either a reflex or a voluntary
action. During a voluntary cough, alveolar, pleural, and
subglottic pressures may rise as much as 200 cm H2O. A
failure of the cough mechanism may be due to pain, drugs or
artificial airways. When this occurs, it is often necessary to
perform the following techniques which may be used to
improve the voluntary cough and aid in airway clearance. The
patient is asked to start a small breath and small cough, then a
bigger breath and harder cough, and finally a really deep
breath and hard cough. This technique is especially effective
for postoperative patients who tend to splint from pain.
Another technique involves the therapist placing the index
and middle finger flat in the sternal notch and gently
massaging inward in a circular fashion over the trachea. This
is most effective in obtunded patients or in patients coming
out of anesthesia. Patients with artificial airways cannot cough
normally since a tube is either between the vocal cords
(endotracheal) or below the cords (tracheostomy). Adequate
pressure cannot be built up without approximation of the
cords. These patients may have a cough stimulated by
inflating the cuff on the tube, giving a large, rapid inspiration
by a manual resuscitation bag, holding the breath for 12 s,
and rapidly allowing the bag to release and exhalation to
ensue. This technique is normally performed by two therapists
and is made more effective by one therapist performing
vibration and chest compressions from the time of the
inspiratory hold, all during exhalation. Coughing and deep
breathing is encouraged every 12 h to aid in removing
retained secretions [22].
4.2. Chest physiotherapy
Chest physiotherapy has come to mean gravity-assisted
bronchial drainage with chest percussion and vibrations.
Studies have shown that a combination of techniques are
effective in secretion removal [2326].
Bronchial drainage/positioning is a therapeutic modality
which uses gravity-assisted positioning designed to improve
pulmonary hygiene in patients with inhalation injury or
retained secretions. There are 12 basic positions in which
patients can be placed for postural drainage. Due to skin grafts,
donor sites, and the use of air fluid beds, clinical judgment
dictates that most of these positions are not practical. In fact,
positioning in the Trendelenburg and various other positions
may acutely worsen hypoxemia. Evidence has shown that a
patients arterial oxygenation may fall during positioning[27].
To accomplish the same goal it is common practice, in
intensive care units, to turn patients side to side every 2 h so as
to aid in mobilizing secretions.
Percussion aids in the removal of secretions from the
tracheal bronchial tree. Percussion is done by cupping the
hand so as to allow a cushion of air to come between the
percussors hand and the patients chest. If this is done
properly, a popping sound will be heard when the patient is
percussed. There should be a towel between the patient and
the percussors hand in order to prevent irritation of the skin.
Percussion is applied over the surface landmarks of the
bronchial segments which are being drained. The hands
rhythmically and alternately strike the chest wall. Incisions,
skin grafts, and bony prominences should be avoided during
percussion [22].
Vibration/shaking is a shaking movement used to move
loosened secretions to larger airways so that they can be
coughed up or removed by suctioning. Vibration involves rapid
shaking of the chest wall during exhalation. The percussor
vibrates the thoracic cage by placing both hands over the
percussed areas and vibrating into the patient, isometrically
contracting or tensing the muscles of their arms and
shoulders. Mechanical vibrations have been reported to
produce good clinical results. Gentle mechanical vibration
may be indicated for patients who cannot tolerate manual
percussion. Chest physiotherapy techniques should be used
every 24 h for patients with retained secretions. Therapy
should continue until breath sounds improve [22].
4.3. Early ambulation
Early ambulation is another effective means of preventing
respiratory complications. With appropriate use of analgesics,
even patients on continuous ventilatory support can be taken
out of bed and placed into a chair. The sitting position has
several beneficial effects which include:
_ the patient can breathe with regions of the lungs which are
normally hyperventilated;
_ muscular strength and tone are preserved;
_ contractions are prevented and exercise tolerance is
maintained.
4.4. Airway suctioning
Airway suctioning is another method of clearing an airway.
Normal bronchial hygiene is usually accomplished by the
mucociliary escalator process. When these methods are not
effective in maintaining a clear airway, tracheobronchial
suctioning is indicated [2831]. Nasotracheal suctioning is
intended to remove from the trachea accumulated secretions,
and other foreign material which cannot be removed by the

patients spontaneous cough or less invasive procedures.


Nasotracheal suctioning has been used to avoid intubation
which was solely intended for the removal of secretions.
Nasotracheal suctioning refers to the insertion of a suction
catheter through the nasal passages and pharynx into the
trachea in order to aspirate secretions or foreign material. The
first step in this process is to hyperoxygenate the patient with
100% oxygen. The patient should be positioned in an inclined
position in which the head of the bed is raised at a 458 angle
and the catheter slowly advanced through the nares to a point
just above the larynx. The therapist or nurse then listens for
air sounds at the proximal end of the catheter.When airflow is
felt to be strongest and respiratory sounds are loudest, the tip of
the catheter is immediately above the epiglottis.Oninspiration,
the catheter is advanced into the trachea. After the vocal cords
have been passed, a few deep breaths are allowed and the
patient is reoxygenated. Suction is begun while the catheter is
slowly withdrawn from the trachea. The patient should not be
suctioned for more than 15 s without being reoxygenated.
Suctioning is notwithout potential hazards [32]. Complications
include irritation of the nasotracheal mucosa with bleeding,
abrupt drops in PO2, vagal stimulation, and bradycardia.
Preoxygenating and limiting suction time have been shown
to decrease or eliminate the fall in the PO2.
4.5. Therapeutic bronchoscopy
When all other techniques fail to remove secretions, the use of
the fiberoptic bronchoscope has proven to be of benefit. In
addition to its diagnostic functions, bronchoscopy retains
important therapeutic applications. Copious secretions
encountered in patients with inhalation injury may require
repeated bronchoscopic procedures when more conservative
methods are unsuccessful. The modern fiberoptic bronchoscope
is small in diameter, flexible, and has a steerable tip
which can be maneuvered into the fourth or fifth generation
bronchi for examination or specimen removal [22].
4.6. Pharmacological adjuncts
Bronchodilators can be helpful in some cases. Inhalation
injury to the lower airways results in a chemical tracheobronchitis
which can produce wheezing and bronchospasms.
This is especially true for patients with pre-existing reactive
airway diseases. Most drugs which are used in the management
of bronchospasms are believed to act on the biochemical
mechanism which controls bronchial muscle tone. Aerosolized
sympathomimetics are effective in two ways: they result
in bronchial muscle relaxation and they stimulate mucociliary
clearance. The newer bronchodilators are more effective and
have fewer side effects than the older generation drugs [22].
Racemic epinephrine is used as an aerosolized topical
vasoconstrictor, bronchodilator, and secretion bond breaker.
The vasoconstrictive action of racemic epinephrine is useful in
reducing mucosal and submucosal edema within the walls of
the pulmonary airways. A secondary bronchodilator action
serves to reduce potential spasm of the smooth muscles of
the terminal bronchioles. Water, employed as a diluent for
racemic epinephrine, serves to lower both adhesive and
cohesive forces of the retained endobronchial secretions, thus
serving as a bond-breaking vehicle. Racemic epinephrine has
also been used for the treatment of post-extubation stridor. Its
mode of action is thought to be related to the vasoconstrictive
activity, with the resultant decrease in mucosal edema.
Aerosolized treatments may be given every 24 h as long as
the heart rate is not excessively increased [22].
Aerosolized N-acetylcysteine is a powerful mucolytic agent
in use in respiratory care. N-Acetylcysteine contains a thiol
group; the free sulfhydryl radical of this group is a strong
reducing agent which ruptures the disulfide bonds which
serve to give stability to the mucoprotein network of
molecules in mucus. Agents which break down these disulfide
bonds produce the most effective mucolysis [33]. N-Acetylcysteine
is an irritant to the respiratory tract. It can cause
mucosal changes, and it may induce bronchospasm. For this
reason, patients are evaluated for signs of bronchospasm and
a bronchodilator may be added if necessary. N-Acetylcysteine
has proven to be effective in combination with aerosolized
heparin for the treatment of inhalation injury in animal
studies [34].
Heparin/N-acetylcysteine combinations have been used as
scavengers for the oxygen free radicals produced when
alveolar macrophages are activated either directly by chemicals
in smoke or by one or more of the compounds in the
arachidonic cascade. Animal studies have shown an increased
P/F ratio, decreased peak inspiratory pressures, and a
decreased amount of fibrin cast formation with heparin/
acetylcystine combinations. In a retrospective review Desai
et al. showed that the use of Heparin/N-acetylcysteine to be
effective in pediatric patients with inhalation injury [35].
Results indicate a significant decrease in the reintubation
rates, incidence of atelectasis and improved mortality for
patients treated with Heparin/N-acetylcysteine therapy.
Therefore, a standard treatment for patients with inhalation
injury might include 500010,000 units of heparin and 3 ml
normal saline nebulized every 4 h, alternating with 35 ml of
20% N-acetylcysteine for 7 days. This insures that the patient
receives an aerosolized treatment every 2 h. Baseline and daily
clotting studies are recommended for the entire length of the
aerosolized Heparin/N-acetylcysteine treatments [22].
Table 1 shows the Inhalation Injury treatment protocol
used at the Shriners Hospital for Children, Galveston Burn
Table 1 Inhalation injury treatment protocol
Titrate humidified oxygen to maintain SaO2s > 90%
Cough, deep breath exercises every 2 h
Turn patient side to side every 2 h
Chest physiotherapy every 4 h
Aerosolize 3 ccs of 20% N-acetylcysteine every 4 h with a
bronchodilator
Alternate aerosolizing 5000 units of Heparin with 3 ccs of
normal saline every 4 h
Nasotracheal suctioning as needed
Early ambulation on post-operative day 5
Sputum cultures for intubated patients every Monday,
Wednesday, Friday
Pulmonary function studies prior to discharge and at out-patient
visits
Patient/family education regarding inhalation injury
The protocol is continued for 7 days.

Hospital. This protocol has been in place and used clinically


since 1990 with over 560 patients treated.
4.6.1. Mechanical ventilation
Over the past 30 years, and especially over the past decade,
there has been an increase in new ventilatory techniques
which present alternatives for the treatment of patients with
smoke inhalation. Unfortunately, although the number of
options available to the clinician has appeared to increase
exponentially, well controlled clinical trials defining the
specific role for each of the modes of ventilation and
comparing them to other modes of ventilation has not been
forthcoming. Based upon current available data, the recommendations
from the American College of Chest Physicians
consensus conference on mechanical ventilation generally
serve as guidelines[36]. The general consensus concludes:
_ The clinician should choose a ventilatormode that has been
shown to be capable of supporting oxygenation and
ventilation and that the clinician has experience in using.
_ An acceptable oxygen saturation should be targeted.
_ Based primarily on animal data, a plateau pressure of
greater than 35 cm H2O is cause for concern. With clinical
conditions that are associated with a decreased chest wall
compliance, plateau pressures greater than 35 cm H2Omay
be acceptable.
_ To accomplish the goal of limiting plateau pressures, PCO2
should be permitted to rise (permissive hypercapnia) unless
other contraindications exist that demand a more normal
PCO2 or pH.
_ Positive end-expiratory pressure (PEEP) is useful in supporting
oxygenation. An appropriate level of PEEP may be helpful
in preventing lung damage. The level of PEEP required
should be established by empirical trials and reevaluated on
a regular basis.
_ Large tidal volumes (810 ml/kg) with PEEP may be needed to
improve oxygenation if the use of protective ventilatory
strategies become ineffective. Peak flow rates should be
adjusted as needed to satisfy patient inspiratory needs.
A new multicenter study by the Acute Respiratory Distress
Syndrome Network of the National Heart, Lung, and Blood
Institute (NHLBI) is the first large randomized study comparing
high versus low tidal volumes for patients with ARDS [37]. The
trial compared traditional ventilation treatment, which
involved an initial tidal volume of 12ml/kg of predicted body
weight and an airway pressure measured of 50 cmH2O or less,
to ventilation with a lower tidal volume, which involved an
initial tidal volume of 6 ml/kg of predicted body weight and a
plateau pressure of 30 cm H2O or less. The volume-assistcontrol
mode was used for the ventilation study. The trial was
stopped after the enrollment of 861 patients because mortality
was lower in the group treated with lower tidal volumes than
in the group treated with traditional tidal volumes and the
number of days without ventilator use during the first 28 days
after randomization was greater in this group [37].
This study was the first large randomized investigation that
documented a decrease inmortality with the use of lower tidal
volumes for the treatment of patients with ARDS. In light of
this new evidence, the tidal volumes used when initiating
mechanical ventilation should be 68 ml/kg of predicted body
weight. If the patient becomes obstructed with fibrin cast and
presents with an acute increase in PCO2 and decrease in PaO2,
the clinician should first provide aggressive pulmonary toilet,
then consider changing over to volume ventilation with higher
tidal volumes. If ventilation continues to worsen, tidal
volumes of 810 ml/kg may be needed to provide adequate
mechanical ventilation.
4.7. Modes of ventilation
4.7.1. Control mode
In the control mode of ventilation, the ventilator cycles
automatically at a rate selected by the operator. The
adjustment is usually made by a knob calibrated in breaths/
min. The ventilator will cycle regardless of the patient need or
desire for a breath, but guarantees a minimum level of minute
ventilation in the apneic, sedated or paralysed patient. The
control mode of ventilation is often utilized in patients with
the adult respiratory distress syndrome due to the high peak
pressures needed to achieve adequate chest expansion. The
major disadvantage with this mode is that the patient cannot
cycle the ventilator and thus the minute ventilation must be
set appropriately.
4.7.2. Assist-control mode
In the assist-control mode of ventilation in which every breath
is supported by the ventilator, a back-up control rate is set;
however, the patient may choose any rate above the set rate.
Using this mode of ventilation, the tidal volume, inspiratory
flow rate, flow waveform, sensitivity and control rate are set
[3840].
Advantages are that assist-control ventilation combines
the security of controlled ventilation with the possibility of
synchronizing the breathing pattern of the patient and
ventilator, and it ensures ventilatory support during each
breath.
Disadvantages are as follows:
_ Excessive patient work occurs in case of inadequate peak
flow or sensitivity settings, especially if the ventilator drive
of the patient is increased.
_ It is sometimes poorly tolerated in awake, nonsedated
subjects and can require sedation to insure synchrony of
patient and machine.
_ It can cause respiratory alkalosis.
_ It may worsen air trapping with patients with chronic
obstructed lung disease [36].
4.7.3. Synchronized intermittent mandatory ventilation
(SIMV)
This mode of ventilation combines a preset number of
ventilator-delivered mandatory breaths of preset tidal volume
with the facility for intermittent patient-generated spontaneous
breaths [41,42].
Advantages are as follows:
_ The patient is able to perform a variable amount of
respiratory work and yet there is the security of a preset
mandatory level of ventilation.

_ SIMV allows for a variation in level of partial ventilatory


support from near total ventilatory support to spontaneous
breathing.
_ It can be used as a weaning tool.
Disadvantages are:
_ Hyperventilation with respiratory alkalosis.
_ Excessive work of breathing due to the presence of a poorly
responsive demand valve, suboptimal ventilatory circuits or
inappropriate flow delivery could occur.
_ In each case, extra work is imposed on the patient during
spontaneous breaths.
4.7.4. Pressure control mode
In pressure-controlled ventilation all breaths are time or
patient triggered, pressure-limited, and time-cycled. The
ventilator provides a constant pressure of air to the patient
during inspiration. The length of inspiration, the pressure
level, and the back-up rate of are set by the operator. Tidal
volume is based upon the compliance and resistance of the
patients lungs, the ventilator system as well as on the preset
pressure. Pressure control ventilation has become a frequently
used mode of ventilation for the treatment of ARDS.
4.7.5. Pressure support ventilation (PSV)
Pressure support ventilation (PSV) is a pressure-targeted, flowcycled,
mode of ventilation in which each breath must be
patient triggered. It is used both as a mode of ventilation
during stable ventilatory support periods and as a weaning
method [4346]. It is primarily designed to assist spontaneous
breathing and therefore the patient must have an intact
respiratory drive.
Advantages are:
_ It is generally regarded as a comfortable mode of ventilation
for most patients.
_ Pressure support reduces the work of breathing.
_ It can be used to overcome the airway resistance caused by
the endotracheal tube.
_ Pressure support may be useful in patients who are difficult
to wean.
Disadvantages are:
_ The tidal volume is not controlled and is dependent on
respiratory mechanics, cycling frequency, and synchrony
between the patient and ventilator.
_ Pressure support may be poorly tolerated in some patients
with high airway resistances because of the preset high
initial flow rates [22].
4.7.6. Alternate modes of ventilation
During the last decade, a new concept has emerged regarding
acute lung injury. In severe cases of adult respiratory distress
syndrome (ARDS), only a small part of the lung parenchyma
remains accessible to gas delivered by mechanical ventilation
[46,47]. As a consequence, tidal volumes of 10 ml/kg or more
may overexpand and injure the remaining normally aerated
lung parenchyma and could worsen the prognosis of severe
acute respiratory failure by extending nonspecific alveolar
damage. High airway pressures may result in overdistension
and local hyperventilation of more compliant parts of the
diseased lung. Overdistension of lungs in animals has
produced diffuse alveolar damage [4850]. This is the reason
why alternative modes of ventilation, all based on a reduction
of end-inspiratory airway pressures and/or tidal volumes
delivered to the patient, have been developed and are used by
many clinicians caring for patients with severe forms of acute
or chronic respiratory failure. Three alternative modes of
ventilation, high-frequency percussive ventilation (HFPV),
inverse ratio ventilation (IRV), and airway pressure release
ventilation (APRV) will be briefly discussed.
4.7.7. High-frequency percussive ventilation (HFPV)
High-frequency percussive ventilation (HFPV) is a term used to
describe a high-frequency time-cycled pressure ventilator
commonly known as the VDR ventilator. The use of HFPV
facilitates a lung protective strategy by providing ventilation at
lower mean airway pressures. With this mode of ventilation,
subtidal volumes are delivered in a progressive stepwise
fashion until a preset oscillatory equilibrium is reached and
exhalation is passive.
High-frequency percussive ventilation is a new technique
that has shown some promise in the ventilation of patients
with inhalation injury [5153] Clinical studies indicate that this
mode of ventilation may aid in reducing pulmonary barotrauma
[52,53]. In a retrospective study, Cortiella et al. has
shown a decrease incidence of pneumonia, peak inspiratory
pressure and a improved P/F ratio in children ventilated with
the use of HFPV as compare to controls [54].
In the first prospective randomized study on HFPV, Mlcak
have shown a significant decrease in the peak inspiratory
pressures needed to ventilate pediatric patients with inhalation
injury [55]. No significant differences were found for
incidence of pneumonia, P/F ratios or mortality.
Based upon clinical experience the following guidelines are
given for initial set up of the HFPV in children. The pulsatile
flow (PIP) rate should set at 20 cm H2O. The pulse frequency
(high rate) should be set between 500 and 600. The low
respiratory rate should be set at about 1520. Oscillatory PEEP
levels should be initially set at about 5 cm H2O and demand
peep set on 3 cm H2O. The I:E ratio should be set at 2:1.
Ventilator settings are adjusted based upon the patients
clinical condition and blood gas values. To improve oxygenation
the ventilator can be set up in a more diffusive mode
(increased pulse frequency) and to eliminate carbon dioxide
the ventilator can be set up in a more convective mode
(decreased pulse frequency) [22].
Clinicians must be familiar with the technique used and its
possible limitations. There must be adequate humidification
of the respiratory gases or severe necrotizing tracheobronchitis
can occur. Special delivery devices for providing
adequate humidification during HFPV are required.
4.7.8. Inverse ratio ventilation (IRV)
Inverse ratio ventilation (IRV) is the use of an inspiratory/
expiratory (I:E) ratio greater than 1:1. The rationale behind this
is to maintain a high mean airway pressure and to hold peak
alveolar pressure within a safe range. The second theoretical

concept underlying inverse ratio ventilation is the prolongation


of inspiration to allow for recruitment of lung units with a
long time constant. Deep sedation and/or paralysis is nearly
always required with this mode of ventilation. At this time
there is no conclusive evidence based data comparing inverse
ratio ventilation to conventional mechanical ventilation in
patients with inhalation injury.
4.7.9. Airway pressure release ventilation (APRV)
Airway pressure release ventilation (APRV) is a pressureregulated
mode of ventilatory support that allows for timecycled
decreases in pressure to facilitate CO2 elimination. This
mode may permit spontaneous breathing while limiting
airway pressures and may therefore limit the amount of
sedative, analgesic, and neuromuscular blocking agents
infused. Several studies suggested improved oxygenation
compared with pressure-controlled ventilation [56]. Evidencebased
recommendations to use this mode of ventilation in
inhalation injury await outcome studies.
4.8. Typical ventilator settings required for conventional
mechanical ventilation
A large multicentered study by the NHLBI evaluated the use of
Volume Ventilation with low versus high tidal volume on
ARDS. This study documented a decreased incidence of
mortality in patients with ARDS who were ventilated with
small tidal volumes [37]. Based upon this study, it has become
clinically accepted practice to use small tidal volumes when
initially setting up mechanical ventilation.
Table 2 describes the authors typical guidelines for initial
ventilator settings in children [22]. The guidelines for adults
are given in the text below.
4.8.1. Tidal volumes
In volume-cycled ventilation, a machine-delivered tidal
volume is set to be consistent with adequate gas exchange
and patient comfort. The tidal volume selected for burned
patients normally varies between 6 and 8 ml/kg of predicted
body weight. Numerous factors, such as lung/thorax compliance,
system resistance, compressible volume loss, oxygenation,
ventilationandbarotrauma, are consideredwhenvolumes
are selected [57]. Of critical importance is the avoidance of
overdistension. This can generally be accomplished by insuring
that peak airway and alveolar pressures do not exceed a
maximum target. Many would agree that a peak alveolar
pressure greater than 35 cm H2O in adults raises concern
regarding the development of barotrauma and ventilatorinduced
lung injury increases [58,59]. The clinicianmust always
look at the patient to insure adequate chest expansionwith the
setting of the tidal volume. Expired tidal volumes should be
measured for accuracy at the connection between the patients
ventilator circuit and the artificial airway. This insures that the
volume selected reaches the patient and is not lost in the
compressible volume of the ventilator tubing.
The range of tidal volumes will vary depending on the
disease process, with some diseases requiring maximum tidal
volumes and others needing less. Severe interstitial diseases
such as pneumonia and ARDS may require a tidal volume of 8
10 ml/kg to adequately inflate the lungs and improve gas
exchange if protective ventilatory strategies become inadequate.
However, the acceptable range of 68 ml/kg allows the
clinician to make more precise adjustments in volume, as
needed by the patient.
4.8.2. Respiratory rate
Setting of the mandatory ventilator respiratory rate is
dependent on the mode of ventilation selected, the delivered
tidal volume, dead space to tidal volume ratio, metabolic rate,
targeted PCO2 levels, and level of spontaneous ventilation.
With adults, set mandatory rate normally varies between 4
and 20 breaths/min, with most clinically stable patients
requiring mandatory rates in the 812 range [57]. In patients
with inhalation injury, mandatory rates exceeding 20 per min
may be necessary, depending on the desired expired volume
and targeted PCO2 . It is important to have targeted arterial
blood gas values set to aid the clinical team in proper
management (Table 3) [22]. Along with the PCO2 , pH, and
patient comfort, the primary variable controlling the selection
of the respiratory rate is the development of air trapping and
auto PEEP [60]. Auto PEEP is gas trapped in alveoli at end
expiration, due to inadequate time for exhalation, bronchoconstriction
or mucus pulgging. It results in an increase in the
work of breathing.
The respiratory rates of children and infants all need to be
set substantially higher than those of adults. For pediatrics,
the respiratory rate can be set at from 12 to 45 depending on
the disease state and the level of targeted PCO2 one wishes to
achieve. Slower respiratory rates are useful in the patient with
obstructed airways because slower rates allow more time for
exhalation and emptying of hyperinflated areas [22].
Arterial blood gases should be assessed after the patient
has been on the ventilator for approximately 20 min and the
respiratory rate adjusted accordingly.
4.8.3. Flow rates
The selection of peak inspiratory flow rate during volume
ventilation is primarily determined by the level of spontaneous
inspiratory effort. In patients triggering volume breaths,
patient effort, work of breathing, and patient ventilator
synchrony depend on the selection of peak inspiratory flow.
Table 2 Mechanical ventilation guidelines in children
Variable Settings
Tidal volumes 68 ml/kg
Respiratory rates 1245 breaths/min
Plateau pressures <30 cm H2O
I:E ratios 1:11:3
Flow rates 40100 l/min
PEEP 8 cm H2O

Table 3 Targeted arterial blood gas goals


Variable Goal
pH 7.257.45
PaO2 5580 mmHg or SaO2 of 8895%
PaCO2 3555 mmHg (permissive hypercapnia
can be used if pH _ 7.25)

Peak inspiratory flows should ideally match patient peak


inspiratory demands. This normally requires peak flows to be
set at 40100 l/min, depending on expired volume and the
inspiratory demand [36].
4.8.4. Inspiratory/expiratory (I:E) ratio
The time allowed for the inspiratory and expiratory phases of
mechanical ventilation is commonly referred to as the
inspiratory/expiratory (I:E) ratio. The inspiratory part of the
ratio includes the time to deliver the tidal volume before the
exhalation valve opens and exhalation begins. The expiratory
part of the ratio includes the time necessary for the tidal
volume to exit through the exhalation valve before the next
inspiration begins. The inspiratory time should be long
enough to deliver the tidal volume at flow rates that will
not result in turbulence and high peak airway pressures. The
usual I:E ratio is 1:11:3 [61].
In severe lung disease it is acceptable to prolong the
inspiratory time to allow for better distribution of gas and
enhance oxygen diffusion. When a longer inspiratory time is
required, careful attention should be given to sufficient
expiration to avoid stacking of breaths and impeding venous
return. Prolonged inspiratory time creates a more laminar
flow, which helps to keep the peak pressures lower. Rapid
inspiratory times are tolerated in patients with severe airway
obstruction. The rapid inspiratory time allows for a longer
expiratory phase, which may help to decrease the amount of
overinflation [22].
4.8.5. Inspired oxygen concentration
As a starting point and until the level of hypoxemia is
determined, a patient placed on a ventilator should receive an
oxygen concentration of 100%. The concentration should be
systematically lowered as soon as arterial blood gases dictate.
In general, as a result of the concerns regarding the effects of
high oxygen concentration on lung injury, the lowest
acceptable oxygen level should be selected as soon as possible.
In patients who are difficult to oxygenate, oxygen concentrations
can be minimized by optimizing PEEP and mean airway
pressures and selecting a minimally acceptable oxygen
saturation [62].
4.8.6. Positive end-expiratory pressure (PEEP)
PEEP is applied to recruit lung volumes, elevate mean airway
pressure, and improve oxygenation [63]. The level of PEEP used
varies with the disease process. PEEP levels should start at
8 cm H2O and be increased in 2.5 cm increments. Increasing
levels of PEEP in conjunction with a prolonged inspiratory time
aids in oxygenation and allows for the safe level of oxygen to
be used. The use of pressure volume curves to determine the
best PEEP level has been recommended to aid in over
stretching the alveoli. This technique has certain limitations
and is dificult to perform in the clinical setting. The use of PEEP
trials can determine the best PEEP without causing a decrease
in cardiac output.
Optimal PEEP is the level of end-expiratory pressure that
results in the lowering of intrapulmonary shunting, significant
improvement in arterial oxygenation, and only a small change
in cardiac output, arteriovenous oxygen content differences or
mixed venous oxygen tension.
4.8.7. Weaning and discontinuing ventilatory support
As the conditions that warranted placing the patient on
mechanical ventilation stabilizes and begins to resolve,
attention must be placed on removing the ventilator as
quickly as possible. Patients receiving mechanical ventilation
for respiratory failure should undergo a formal assessment of
discontinuation if the following criteria are met: [64]
1. Evidence for some reversal of the underlying cause of
respiratory failure.
2. Adequate oxygenation (PaO2/FiO2 > 200250; requiring
positive end expiratory pressure [PEEP] _ 58 cm H2O;
FiO2 _ 0.40.5) and pH _ 7.25.
3. Hemodynamic stability-requiring no or low dose vasopressor.
4. The capacity to initiate an inspiratory effort.
If the patients meet the above criteria, they should undergo
a spontaneous breathing trial. The spontaneous breathing
trial includes either a t-tube trial for 30 min or pressure
support/CPAP for 1 h. Respiratory mechanics considered
adequate prior to or during a spontaneous breathing trial
are as follows: [64]
1. Respiratory rate <38 in children, <24 in adults.
2. Spontaneous tidal volume _4ml/kg.
3. Expired minute volume <15 l/min.
4. Negative inspiratory force >30 cm H2O.
5. Audible leak around the endotracheal balloon cuff.
In general, use of respiratory mechanics evaluate a
patients ability to sustain spontaneous ventilation. They do
not assess a patients ability to protect the upper airway. For
this reason, traditional indices often fail to reflect the true
clinical picture of a patient with an inhalation injury. For a
complete evaluation prior to extubation, bronchoscopic
examination will aid in determining if the airway edema
has decreased enough to attempt extubation.
Prior to a scheduled extubation it is recommended that
reintubation equipment be set up and that the person doing
the extubation be experienced in emergency intubations.
If the patient demonstrates signs of inspiratory stridor, the
use of racemic epinephrine by aerosol has been effective in
reducing the mucosal edema and may prevent the patient
from being reintubated.

Respiratory management of inhalation injury


Ronald P. Mlcak a,b,*, Oscar E. Suman c,d, David N. Herndon c,d

burns 3 3 ( 2 0 0 7 ) 2 1 3