Keywords
pediatric - supraventricular tachycardia - burns - inhalational injury - cocaine -
unintentional drug exposure
Introduction
Twenty to thirty percent of all severe burns suffered in a fire are associated with
inhalational injury, the presence of which increases the risk of mortality threefold.[1]
[2] Inhalational injury, however, is not always immediately obvious in the pediatric
patient who may be awake and alert, but too young to effectively communicate. Therefore,
certain criteria should increase suspicion for injury. Any patient who has been trapped
in a fire in an enclosed structure is at risk. Patients may present with facial buns,
singed nasal hairs, and soot on the nose and face. There may also be signs of respiratory
distress such as stridor, drooling, hoarseness, or wheezing. In pediatric patients,
the agitation and confusion often associated with toxic inhalation may be mistaken
for expected behavior in a toddler who is afraid and/or injured.[3] Perhaps the most challenging aspect is the unknown nature of what substance may
have been inhaled. Any number of toxins are released in the combustion process initiated
by a structure fire. This potential for an unknown toxin allows for a wide variety
of neurologic and cardiovascular derangements to potentially be part of the presentation
of pediatric inhalational injury. The following case report describes a toddler whose
final diagnoses included cocaine intoxication. It is possible that the cocaine was
inhaled while trapped in a high heat, fast burning garage fire.
Case Report
A 3-year-old girl was brought to the trauma bay after being extracted from a home
garage fire. According to the paramedic report, the patient was initially hypoxic
with percent oxygen saturations in the 70s, which improved with supplemental oxygen.
On arrival, the patient's oxygen saturation was greater than 92% with a simple face
mask at 6 L per minute. The remainder of the child's vital signs included a blood
pressure of 107/82 mm Hg, a heart rate of 160 beats per minute, and a temperature
of 38.4°F.
Additional examination was notable for an extremely agitated, well-nourished, well-developed
child with 2% total body surface area partial thickness burn to the forehead. The
patient was crying and restless, but the exam was otherwise normal. In the trauma
bay, the patient was given 2 mg of intravenous midazolam with only mild improvement
in her agitation. Of note, this was the only medication administered to the child
during transport and while in the emergency department. Additional past medical history
was not immediately available as no caregivers were present at the bedside in the
trauma bay.
Initial laboratories were notable for a carboxyhemoglobin of 21% (poisoning is considered
to have occurred at carboxyhemoglobin levels of over 10%, and severe poisoning is
associated with levels over 20–25%). The patient was admitted to the burn-intensive
care unit for further monitoring secondary to concern for possible inhalational injury.
Shortly after arrival to the intensive care unit, the patient developed sudden onset
of supraventricular tachycardia (SVT) with a heart rate of 250 beats per minute ([Fig. 1]).
Fig. 1 Electrocardiogram (EKG) obtained during patient's episode of tachycardia. The EKG
demonstrates regular, narrow complex tachycardia with absent P waves typical of atrioventricular
node reentrant tachycardia.
During the episode, blood pressure by noninvasive cuff was 80/40 mm Hg; the patient
was alert, but continued to be inconsolable. Adenosine 0.05 mg/kg was administered
via rapid intravenous bolus without response. A second dose of adenosine 0.1 mg/kg
of was given with immediate resolution of the SVT. Her heart rate returned to 150
beats per minute and blood pressure increased to 100/62 mm Hg. After this intervention,
the patient was noted to have a markedly increased work of breathing in addition to
a continued level of agitation that was out of proportion to the size and location
of the burn. The decision was made to intubate the patient out of concern for evolving
inhalational injury. Following intubation, it was challenging to adequately sedate
the child despite concurrent drips of fentanyl, versed and dexmedetomidine. A low-dose
infusion of cis-atracurium was necessary to safely reduce the remaining excessive
movements the patient continued to exhibit. The patient had a 5-year-old sister that
was rescued from the same fire and admitted for treatment of her burns as well. The
sibling was also tachycardic and agitated to a degree inconsistent with presenting
visible injuries, although not quite as severely. Per hospital policy, child protective
services were contacted due to the unclear circumstances surrounding the fire and
because the siblings appeared to be unattended in the structure. A urine toxicology
screen was requested for both children, both of which came back positive for cocaine.
Following 4 hours of oxygen therapy, the patient's carboxyhemoglobin decreased to
4%. Bronchoscopy revealed only mild inhalational injury and the patient was successfully
extubated on hospital day 2. There were no further episodes of SVT, and the patient
received no additional cardiac workup. She was discharged after a thorough investigation
by social work and child protection services.
Discussion
This case highlights the importance of a comprehensive differential when treating
small children in the acute trauma setting. Although inhalational injury can cause
broad and severe physiologic changes, the presence of SVT in the child was an unexpected
finding that called for additional workup. Suspicion for another etiology was also
heightened by the patient's extreme agitation and a sibling that shared several elements
of this peculiar presentation. In addition to physical exam, a detailed history can
also be key to expanding the differential. In our patient's case, we did not have
the past medical history of the child at initial presentation and even after interviewing
the patient's caregiver the circumstances surrounding the fire remained unclear.
Our patient's presenting symptoms of hypoxia, elevated carboxyhemoglobin level, and
agitation, as well as facial burns (although minor) appeared consistent with inhalational
injury. Both cyanide toxicity and CO poisoning can be associated with agitation and
confusion and cyanide toxicity may be associated with cardiac arrhythmias (including
SVT). In adults with cyanide poisoning who experience cardiac complications, approximately
30% may be diagnosed with SVT.[3]
Since the laboratory tests revealed that cyanide was not to blame for this patient's
range of symptoms, the cocaine-positive urine screen provides a likely explanation
for the patient's SVT. Cocaine has a biological half-life of 45 to 90 minutes and
is rapidly metabolized by plasma and liver esterases. The cocaine urine toxicology
test evaluates for the presence of benzoylecgonine, an inactive metabolite that can
be detected for up to a week after cocaine exposure.[4] The tachyarrhythmia, agitation, and elevated temperature on presentation are symptoms
consistent with cocaine intoxication. These effects are the result of sympathomimetic
stimulation by dopamine and norepinephrine and central dopamine and serotonin reuptake
inhibition. There is little data on frequency and type of arrhythmia associated with
cocaine toxicity, but in research animals, virtually every type of rhythm disturbance
can be induced.[5] These disturbances can be due to the ion-channel effects of cocaine, the increase
in sympathetic nervous system stimulation, and/or myocardial ischemia.[6] In pediatric patients who are unintentionally exposed to cocaine, tachycardia, seizures,
and agitation are the most common presenting symptoms.[7] Case reports from the late 1980s and early 1990s also suggest that small children
and infants can have detectable cocaine levels secondary to passive inhalation.[8]
[9] Eventually we were able to obtain further history from the caregiver suggesting
that an acquaintance with a history of drug abuse had been spending time in the garage.
Although the timeline of events leading up to the patient presenting to the trauma
bay remains unclear, it is possible that the positive urine screen for cocaine was
secondary to unintentional inhalation of or exposure to the drug. The exposure could
have been secondary to proximity to the drug user while they were inhaling cocaine,
or the presence of some amount of drug stored in the garage that burned in the fire.
