Pediatric emergency medicine trisk 483

Initial management
Remove from contaminated environment
Cardiopulmonary resuscitation as needed
Provide 100% supplemental oxygen
Consider hydroxocobalamin injection (Cyanokit) if concern for cyanide toxicity
Ensure patent airway
Laboratory determinations
Arterial blood gas analysis
Carboxyhemoglobin level, cyanohemoglobin level, troponin
Chest radiograph
Monitor
Heart rate, electrocardiogram, respiratory rate, blood pressure, Sao2
Consider central venous pressure
Consider pulmonary artery catheterization
Fluids
5% dextrose in normal saline at maintenance rates or less to maintain urine
output at 0.5–1.0 mL/kg/hr
Volume expansion in presence of cutaneous burns; normal saline, lactated
Ringer solution, or 5% albumin
Respiratory management
Intubation for:
1. Upper airway obstruction
2. Pao2 <60 mm Hg on 60% oxygen
3. Central nervous system depression with loss of cough and gag reflexes.
Continuous positive airway pressure 5–15 cm H2 O for Pao2 <60 mm Hg on
60% oxygen
Intermittent mandatory ventilation for:
1. Hypoxia unresponsive to continuous positive airway pressure or
2. Paco2 >50 mm Hg
Humidification of inspired gases
Meticulous pulmonary toilette

Consider inhaled bronchodilators


Management and Diagnostic Studies
The details of burn therapy are elaborated in Chapter 104 Burns but, in general,
the goals are stabilization of cardiovascular function without fluid overload and
compromise of gas exchange. Pulse rate and BP should guide administration of
fluid volume. Maintenance of urine output of at least 0.5 mL/kg/hr should provide
adequate tissue perfusion. Careful monitoring of renal and cardiovascular systems
may prevent or minimize acute pulmonary edema and delayed pulmonary
dysfunction secondary to late fluid mobilization and infection.
Oxygen saturation and serial blood gas determinations should be obtained to
guide oxygen supplementation and to assess adequacy of ventilation. Clinicians
should be cautious when utilizing oxygen saturation and PaO2 as diagnostic tools
early in the course of injury as they are usually not initially affected, even in the
case of carbon monoxide poisoning. A reduced PaO2 /FiO2 ratio is associated
with injury to the lung parenchyma and the presence of pulmonary edema,
increased airway pressure, and decreased lung compliance. If there is concern for
carbon monoxide or cyanide inhalation, carboxyhemoglobin and
cyanohemoglobin levels should be obtained through blood gas analysis. Cyanide
poisoning is an often overlooked diagnosis in smoke inhalation victims.
Intubation is indicated if adequate oxygenation (SaO2 greater than 90% or
PaO2 greater than 60 mm Hg) cannot be maintained with an inspired oxygen
concentration of 40% to 60%, if PaCO 2 rises above 50 mm Hg, or if the work of
breathing appears unsustainable. Spontaneous ventilation with continuous
positive airway pressure causes less cardiovascular interference; this patient
should receive humidified gas mixtures and be encouraged to take deep breaths
and cough frequently. If there is severe CNS depression or severe pulmonary
parenchymal damage, mechanical ventilation with PEEP will likely be necessary.
Maximally humidified oxygen should be delivered by mask or artificial airway to

prevent inspissation of debris and occlusion of the airway. If intubation is
necessary, meticulous pulmonary toilette is essential, with frequent suctioning to
remove edema fluid, mucus, and sloughed epithelium that may otherwise occlude
the endotracheal tube.
High-frequency percussive ventilation (hi-fi) is superior to conventional
mechanical ventilation in reducing work of breathing. There is also evidence that
extracorporeal membrane oxygenation (ECMO) may be useful in severely burned
children.
After the first few hours, diuretic therapy (furosemide 0.5 to 1 mg/kg
intravenously), within the limits of cardiovascular stability, may also improve


oxygenation and pulmonary compliance, leading to more effective ventilation.
Chemical and particulate irritation of upper airway receptors may cause reflex
bronchoconstriction and contribute to lower airway obstruction. Bronchodilators
such as nebulized albuterol may help reverse bronchospasm, but relief depends
mostly on removal of secretions and debris from the respiratory tree.
Studies have not demonstrated a role for steroids or prophylactic antibiotics.
When steroids are used, there is evidence that sodium and fluid retention increase,
healing is delayed, and bacterial clearance from the lung is decreased.
Prophylactic antibiotics may contribute to the development of antibiotic-resistant
bacteria.
Recent research has demonstrated some benefit to aerosolized heparin, Nacetylcysteine, and the muscarinic receptor antagonist tiotropium in decreasing
the incidence of atelectasis, reintubation, and overall mortality. Whole-body
hypothermia is effective in controlling bronchoalveolar damage in animal models,
but there are insufficient human data.

Indications for Discharge or Admission
Determination of disposition from the ED will depend on the history and clinical
status. Patients with significant respiratory distress or depressed neurologic status

should be admitted to an intensive care unit (ICU). Patients who appear well on
presentation to the ED but have a significant history of exposure or physical
evidence of significant smoke inhalation should be monitored closely for at least
6 hours for signs of worsening respiratory distress or significant cough.

CARBON MONOXIDE POISONING
Goals of Treatment
The goals of treatment are immediate removal from the source of contamination
and provision of 100% oxygen to foster elimination and to treat/prevent tissue
hypoxia, metabolic acidosis, and resultant cerebral edema.
CLINICAL PEARL AND PITFALLS


Carbon monoxide poisoning may occur in spaces with improper
ventilation, even with doors and windows open.
The classically described cherry red skin color is not sensitive for
diagnosis.
Pao2 and pulse oximetry arterial saturation (Sao2 ) are likely to be
normal in carbon monoxide intoxication.

Current Evidence
In the United States about 50,000 ED visits annually are attributed to carbon
monoxide poisoning. The rate of deaths has declined in recent years to
approximately 1,300 deaths per year, with most cases related to house fires.
Patients exposed to house fire are at a higher risk of associated burns, severe
metabolic acidosis, hemodynamic disorders, cyanide toxicity, and inhalation
pneumonitis. Exposure may occur in a variety of other settings unrelated to
accidental fires, including incomplete combustion of any carbon-containing fuel.
Examples include propane-powered forklifts, gas stoves improperly used to heat
residences, gas-powered generators used in a garage, faulty gas-powered hot

water heaters or central heating units, improperly vented wood- or coal-burning
stoves, and automobile exhaust in garages. Poisoning may occur even with doors
and windows open. Passengers may be poisoned in vehicles or boats with open
backs, or with faulty or blocked exhaust systems.
In the normal person, carboxyhemoglobin levels are less than 1% but may be
2% to 3% in urban dwellers. In smokers, levels of 5% to 10% are common.
Inhaled carbon monoxide has two important effects that cause tissue hypoxia: (i)
It binds to hemoglobin with an affinity 200 to 300 times greater than that of
oxygen, and (ii) it shifts the oxyhemoglobin dissociation curve to the left and
changes the shape from sigmoidal to hyperbolic ( Fig. 90.4 ). The first effect
decreases oxygen content of the blood, whereas the second only allows oxygen
release at lower-than-normal tissue oxygen levels. Other endogenous (e.g.,
anemia) and exogenous (e.g., displacement of ambient oxygen during fires)
factors contribute further to hypoxia. Although oxygen content of the blood is
low, the PaO2 remains normal. Because carotid body receptors respond to PaO2 ,
respiration may not be stimulated until late, when metabolic acidosis activates
other centers. Tissue hypoxia increases cerebral blood flow, cerebrospinal fluid
pressure, and cerebral capillary permeability, which predispose the patient to
cerebral edema.