Pediatric emergency medicine trisk 481

of pulmonary edema secondary to drowning. (Courtesy of Soroosh Mahboubi, MD, The
Children’s Hospital of Philadelphia.)

FIGURE 90.2 Algorithm for pulmonary assessment for drowning.

Other initial laboratory evaluation should include complete blood cell count
(CBC), electrolytes, and urinalysis. Patients with abnormalities of gas exchange
with normal chest radiographs can usually be managed with supplemental oxygen
and pulmonary physiotherapy. Noninvasive ventilatory support, such as high-flow
humidified nasal cannula oxygen or CPAP, may be beneficial. Any change in
mental status or increase in respiratory distress may reflect arterial hypoxemia
and should also prompt a repeat ABG determination. Continuous SaO2 or serial
PaO2 measurements will guide the physician to continue conservative treatment
or to intensify ventilatory support.
Patients with obvious respiratory distress, hypoxemia (SaO2 less than 90% or
PaO2 less than 60 on 60% inspired oxygen), and extensive pulmonary edema or
infiltration generally require more vigorous treatment. All should be monitored
for heart rate, cardiac rhythm, respiratory rate, and BP. Most will require frequent
blood gas analysis and may be more easily monitored through arterial
cannulation. Intubation, supplemental oxygen, and mechanical ventilation with
positive end-expiratory pressure (PEEP; 5 to 15 cm H2 O) may be needed.
Once BP is stabilized, fluid restriction (to approximately one-half the
maintenance rate) and diuretic therapy (e.g., furosemide 0.5 to 1 mg/kg
intravenously, usual maximum 20 mg/dose) may improve gas exchange. In the


setting of extensive pulmonary damage, pulmonary and cardiovascular
components of the disease are intimately entwined. Optimum management
requires monitoring of blood gases and systemic arterial pressure.
Patients who have experienced significant hypoxemia are often not able to be
aroused. Again, reversal of hypoxemia and acidosis is critical, as well as fluid

resuscitation and avoidance of hyperglycemia. Avoiding hypercapnia and
resultant cerebral hyperemia is generally accepted, but hyperventilation,
barbiturate coma, and other measures initially believed to provide cerebral
protection and prevent or treat elevated intracranial pressure have not been
helpful in these patients.
Hypothermia does appear to have some protective effect. Extreme hypothermia
should be corrected to at least 32°C (89.6°F) to achieve hemodynamic stability
and to minimize the risk of infection. The child should then be allowed to rewarm
passively. Although data in humans are limited, animal studies suggest that
maintenance of mild brain hypothermia may minimize reperfusion injury.
Hyperthermia, a common result of active rewarming, should be avoided. Recent
studies suggest that early initiation of extracorporeal membrane oxygenation
(ECMO) in hypothermic patients with cardiorespiratory insufficiency may
prevent cardiopulmonary failure and improve survival in post-drowning cardiac
arrest.
There is no benefit to prophylactic antibiotics, which should be reserved for
strongly suspected or proven bacterial infection. Exceptions are when grossly
contaminated water is aspirated or when maximal ventilatory support is required
to provide any margin for survival. Bronchoalveolar lavage and steroids have no
demonstrated benefit. However, there is anecdotal evidence supporting the use of
surfactant therapy, which is consistent with the pathophysiology of the disease
process.
Renal function, normal electrolytes, and an adequate hemoglobin level (more
than 10 g/100 mL) should be maintained. If significant hemoglobinuria exists,
diuresis is recommended.

Indications for Discharge or Admission
The patient’s clinical condition in the ED dictates further management and may
provide prognostic clues. It is advisable that patients should be observed for 6 to
12 hours after presentation. Most studies have demonstrated no delayed

symptoms in patients with normal initial oxygen saturations on room air at 6
hours after submersion. Patients who develop symptoms usually do so by 4.5
hours after submersion. Even if initially symptomatic, in most cases symptoms
resolve by 8 hours after submersion.


Patients may be assigned to one of three groups: alert, blunted, or comatose.
Patients in the first group should be observed in the ED (as above). If they
maintain normal oxygenation and normal work of breathing they can be
discharged to home. Patients in the second group should be admitted for careful
monitoring.
Patients in the third group have experienced severe CNS asphyxia. The
prognosis for this group includes a much greater risk of death or severe
anoxic/ischemic encephalopathy. Risk increases with depth of coma on
presentation. Comatose patients who present flaccid with fixed, dilated pupils
rarely survive intact regardless of treatment, although coexistent hypothermia has
provided some remarkable exceptions.
Upon discharge from the ED all caretakers should be educated on drowning
prevention. The American Academy of Pediatrics recommends the installation of
a 4-sided fence that prevents direct access to a swimming pool. The fence should
be at least 4 ft high, climb-resistant, and the distance between the bottom of the
fence and the ground should be less than 4 in. The gate should be self-latching
and self-closing. Parents and caregivers should be advised that small children
should always be under the direct supervision of an adult while around bathtubs,
pools, or other bodies of water.

SMOKE INHALATION
Goals of Treatment
The goals of emergency care include early intubation (if there are signs of airway
compromise), stabilization of respiratory and cardiovascular status, and

maintenance of fluid and electrolyte balance. One must recognize concomitant
carbon monoxide or cyanide poisoning or other inhalants that contribute to
morbidity.
CLINICAL PEARLS AND PITFALLS
Early intubation should be accomplished if there is any evidence of
airway burns or edema.
Severe smoke inhalation can occur without cutaneous burns.

Current Evidence
Respiratory complications of smoke inhalation rank with carbon monoxide
poisoning as a major cause of early death from fire. Although serious cutaneous


injury may occur in the absence of pulmonary involvement, inhalation injury is
present in up to one-third of all burn injuries and accounts for up to 90% of all
burn-related mortality.
The severity of carbon monoxide inhalation and respiratory problems is related
to the duration of exposure, the occurrence in a closed space (more likely in very
young or elderly victims), the nature of materials involved, and the presence of
products of incomplete combustion. Severe hypovolemic shock, massive tissue
destruction, extensive fluid resuscitation, and infection further complicate direct
inhalational trauma. The mechanism of destruction can be categorized in the
following categories: upper airway injury, lower airway injury, pulmonary
parenchymal injury, and systemic toxicity (carbon monoxide and cyanide).
The relatively low heat capacity of dry air and the excellent heat exchange
properties of the nasopharynx usually limit direct thermal injury to the upper
airway. Dry air above 160°C (320°F) has little effect on the lower airway. The
greater heat capacity of steam increases the risk of lower airway damage. In
addition, continuing combustion of soot particles carried deeply into the lung may
exacerbate thermal injury to the lower airways and pulmonary parenchyma.

Chemical injury may occur at any level of the respiratory tract. Oxides of
sulfur and nitrogen combine with lung water to form corrosive acids. Incomplete
combustion of any carbon-containing material, such as wood, may produce
carbon monoxide. Combustion of cotton or plastic generates aldehydes that cause
protein denaturation and cellular damage. Burning polyurethane may produce
cyanide gas. Fire retardants that contain phosphorus may produce phosgene gas.
The upper airway filters most soot particles, but those carried into the lung may
adsorb various substances and cause reflex bronchospasm to further extend
chemical damage.
Immediate effects of smoke inhalation on the lower airway and alveoli include
loss of ciliary action, mucosal edema, bronchiolitis, alveolar epithelial damage,
and impaired gas exchange, particularly oxygenation. Areas of atelectasis or air
trapping, and loss of surfactant activity, worsen ventilation–perfusion mismatch
and hypoxemia. Hours later, sloughing of tracheobronchial mucosa and
mucopurulent membrane formation increases the degree of obstruction, poor gas
exchange, and likelihood of infection. Beyond the first 24 hours, pulmonary
pathology that results from smoke inhalation is largely indistinguishable from
adult respiratory distress syndrome, which arises from other insults. Patient with
inhalation injury are at increased risk for pneumonia and multisystem organ
failure. Children who die from smoke inhalation may sustain serious respiratory
damage in the absence of cutaneous injury.