Pediatric emergency medicine trisk 480

Occasionally massive hemolysis may occur. Electrolyte abnormalities that occur
after massive aspiration in laboratory animals rarely achieve clinical significance
in human victims. However, infants and toddlers may ingest large amounts of
water during submersion events, and if fresh water, may lead to symptomatic
dilutional hyponatremia.
Even small (1 to 3 mL/kg) quantities of fresh water cause disruption of
surfactant, a rise in surface tension in the lungs, and alveolar instability. Capillary
and alveolar membrane damage allows fluid to leak into the alveoli, with
subsequent pulmonary edema. Aspiration of salt water (osmolality greater than
normal saline) does not denature surfactant but creates an osmotic gradient for
fluid to accumulate in the lungs, which dilutes surfactant. Both fresh- and saltwater aspiration decrease pulmonary compliance, increase airway resistance and
pulmonary artery pressure, and diminish pulmonary flow. As nonventilated
alveoli are perfused, an intrapulmonary shunt develops, leading to a fall in partial
pressure of arterial oxygen (PaO2 ). Tissue hypoxia then leads to metabolic
acidosis. The victim is usually able to correct a rise in partial pressure of arterial
carbon dioxide (PaCO 2 ). Aspiration of bacteria, gastric contents, and foreign
materials may cause additional trauma to the lungs.
Hypoxemia results in loss of consciousness. If anoxia ensues, irreversible
central nervous system (CNS) damage begins after 4 to 6 minutes. Fear or cold
may trigger the diving reflex (commonly encountered in infancy), which shunts
blood to the brain and heart primarily and affords several minutes of additional
perfusion. Cold water is relatively protective of the CNS, but probably only if
immersion hypothermia develops very rapidly or before compromise of
oxygenation. Hypothermia is more rapid in the victim who is younger (because of
greater surface area:volume ratio) or is struggling in or swallowing icy water. If
laryngospasm or aspiration occurs before a fall in core body temperature and
cerebral metabolic rate, protection is probably minimal.
Cardiovascular effects are primarily those expected with myocardial ischemia,
severe systemic acidosis, hypothermia, and intravascular volume changes. After
aspiration of fresh water, the transient rise in intravascular volume later
contributes to problems of cerebral and pulmonary edema.

Clinical Recognition
In the first moments after rescue, the appearance of the child who has drowned
may range from nearly normal to apparently dead. Body temperature may be low,
even in warm water. Respiratory efforts may be absent, irregular, or labored, with
pallor or cyanosis, retractions, grunting, and cough productive of pink, frothy


material. The lungs may be clear, or there may be rales, rhonchi, and wheezing.
Infection may develop as a consequence of aspirated mouth flora or organisms in
stagnant water, but this is not usually important in the first 24 hours.
Respiratory function may improve spontaneously or deteriorate rapidly as
pulmonary edema and small airway dysfunction worsen. Deterioration may also
occur slowly over 12 to 24 hours. Intense peripheral vasoconstriction and
myocardial depression may produce apparent or actual pulselessness.
The child may be alert and normal or have any level of CNS compromise.
Superficial evidence of head trauma may be noted if the submersion episode was
a secondary event. Head CT most typically shows diffuse loss of gray–white
differentiation and/or bilateral basal ganglia edema/infarction.

Triage Considerations
Outcome depends on the duration of submersion, the degree of pulmonary
damage by aspiration, the effectiveness of initial resuscitative measures, and the
degree of hypothermia. Many children with submersion injuries are salvageable,
and all should receive the benefit of excellent cardiopulmonary resuscitation
(CPR), without delay, at the scene. They should be given oxygen as needed if
hypoxemia is present with an oxygen saturation of <92% on room air. Physical
examination is insensitive to hypoxemia; a seriously hypoxemic child may be
alert and talking. Since cardiac arrest from drowning is primarily caused by the
inadequate oxygenation, CPR should follow the traditional airway–breathing–

circulation (ABC) sequence, rather than the circulation–airway–breathing (CAB)
sequence, starting with five initial rescue breaths and followed by chest
compressions. Once the child has arrived at an emergency facility (and
cardiovascular stability is achieved), pulmonary and neurologic assessment
should guide further treatment.

Initial Assessment
Initial assessment should focus on signs of neurologic, respiratory, and
hemodynamic compromise. One prospective study devised a prediction rule for
children submerged in non-icy water who presented to the emergency department
(ED) in a comatose state: lack of pupillary light reflex, male gender, and
hyperglycemia were variables used to predict unfavorable outcome (vegetative
state or death). A retrospective study of children presenting to the ED after warmwater submersion suggested that hemodynamic, rather than neurologic, status was
more highly predictive of poor neurologic outcome.
More recent studies indicate that patients with asystole on arrival in the ED
have uniformly poor neurologic outcomes, unless the child is deeply hypothermic


from ice-water drowning. The emergency physician may reasonably discontinue
resuscitative efforts after consideration on a case-by-case basis. Pulse oximetry
has been shown to be a better indicator of a patient’s cardiorespiratory status than
heart rate or blood pressure (BP), which might be increased due to anxiety or
catecholamine release.

Management and Diagnostic Testing
Effective therapy of drowning depends on the reversal of hypoxemia, metabolic
acidosis, and hypothermia. The pulmonary status is assessed initially with a chest
radiograph ( Fig. 90.1 ) and with measurement of arterial oxygen saturation
(SaO2 ) and arterial blood gas (ABG), as in Figure 90.2 . If oxygenation is
normal on breathing room air, the child can be assumed to have suffered

drowning without aspiration. Observation for 6 to 12 hours with repeat SaO2 or
ABG determination should be sufficient to assess the possibility of late
deterioration in gas exchange.


FIGURE 90.1 Drowning in a 4-month-old girl. A: There is bilateral disseminated alveolar
pattern, more on the left than on the right, consistent with the pulmonary edema of drowning.
This change may be the result of neurogenic pulmonary edema rather than aspirated water. B:
Two days later, the patient has been extubated and there is marked improvement in appearance