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e1654 MENOCH et al
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CASE REPORT
Any injured patient who is cool and examination results were negative. So- rhythmprintoutrevealed absentp waves,
tachycardic is considered to be in shock nographic views of the heart revealed with narrow complex QRS at a rate of
until proven otherwise.1 We describe no effusion. Two normal saline boluses 237 (Fig 1). A 12-lead ECG was obtained,
the diagnostic challenge when evalu- (2 L) and fentanyl 1.5 mcg/kg were in- which revealed no beat to beat variabil-
ating persistent tachycardia in the fused intravenously. Her secondary ity. Cardiology provided a bedside con-
setting of multiple system trauma with survey consisted of an actively bleeding sult to assist in confirming the diagnosis
hemorrhagic shock. This is a unique 12 cm forehead laceration with partial of SVT.
case given the secondary condition of scalp de-gloving and nasal laceration Thirty minutes after arrival (shortly
cardiogenic shock due to supraven- with separation of her right nare. The after cardiology arrival and SVT di-
tricular tachycardia (SVT) complicat- remainder of the survey was negative, agnosis), her heart rate continued to be
ing ongoing hemorrhagic shock. with normal chest and pelvis radio- sustained at 220 beats per minute, and
graphs. her BP fell to 88/52 mm Hg, then 65/34
CASE PRESENTATION Her heart rate remained between 210 mm Hg. At this time, she quickly be-
and 220 beats per minute with BP of 114 came pale and diaphoretic, while still
A 17-year-old female patient presented
to the pediatric emergency department to 116/51 to 68 mm Hg with good per- mentating well. Adenosine was rapidly
(ED) with a complicated facial lacera- fusion and mentation during this time pushed at an intravenous (IV) dose of
tion after a multiple system trauma. She of initial assessment. Acute blood loss 0.1 mg/kg. On the ECG, the SVT was
was driving restrained in a vehicle was considered to be the most likely terminated with a pause, followed by
without an airbag when she lost control cause of the continued tachycardia, and ventricular escape beats, then by re-
and hit a fence. She lost consciousness rapid transfusion protocol was initiat- sumption of a normal sinus rhythm at
for an unknown duration. Upon emer- ed after the 2 normal saline boluses. a rate of 120 beats per minute (Fig 2).
gency medical services arrival, she was Before this, initial arrival bedside She immediately felt better, with mar-
noted to have a complicated laceration hemoglobin/hematocrit was 11.9/35. ked improvement of her skin color and
to her nose and partial de-gloving of her In the mean time, further assessment of perfusion, and her BP improved to 120/
forehead with significant ongoing hem- her facial wound with an attempt at 60 mm Hg, which was maintained
orrhage, but she had no other obvious controlling the hemorrhage was per- throughout the rest of her ED course. A
injuries and a Glasgow Coma Scale of formed by the surgery service. Ongoing repeat hemoglobin/hematocrit revealed
15. Her vitals remained stable en route evaluation of her sustained tachycardia a drop to 6.5/19 after a total of 2 L of
to the ED with a heart rate of 98 to 110 continued. Her medical history included normal saline and 3 U of packed red
beats per minute and a blood pressure a history of glycogen storage disease blood cells.
(BP) of 117 to 120/74 to 78 mm Hg. type I status post liver transplant 4 There was no ventricular preexcitation
Upon arrival she was placed on a mon- years ago with a normal echocardio- on her resting ECG, providing evidence
itor, and her initial vital signs in the ED gram (ECHO) and electrocardiogram against Wolff Parkinson White (WPW)
were as follows: heart rate, 219 beats per (ECG) at pretransplant evaluation that syndrome. Hepatology was consulted
minute; respiratory rate, 30; BP, 114/51 same year. She was taking tacrolimus 4 after her heart rate stabilized during
mm Hg; and oxygen saturation, 100% mg twice a day. Hemorrhagic shock the ED course, confirming the presence
on room air. She was alert and com- remained the most likely etiology of the of normal liver function and the history
plaining of pain at her forehead lacera- tachycardia; however, other than the of a normal pretransplant cardiac
tion. Her primary survey consisted of facial laceration, there were no signs of evaluation. They also informed that the
a patent and stable airway with c-spine any internal bleeding, and bedside he- tacrolimus should not play a causative
precautions, equal chest rise with clear moglobin was only mildly decreased. role in the SVT, nor should her liver
breath sounds bilaterally, no chest wall The heart rate of 220 beats per minute function be a concern regarding
tenderness or crepitus, clear heart was out of proportion to her hemor- metabolism of cardiac medications in
sounds without murmur, regular rhythm, rhage, and there was no improvement general. After repair of her wound and
tachycardic with 1+ distal pulses and after aggressive volume resuscitation inpatient telemetry observation, cardi-
2+ central pulses, active bleeding from or pain control after 20 minutes. It was ology did not recommend any further
her complex facial laceration, Glasgow difficult to discern discrete p-waves on inpatient work-up for the SVT but did
Coma Scale of 15, and no other wounds the telemetry monitor during the du- arrange outpatient follow-up since it
or contusions when exposed. Bedside ration of her initial evaluation, which was triggered by a less than routine
focused abdominal sonogram for trauma was concerning for SVT. The telemetry event. Her status postliver transplant
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CASE REPORT
which we will mention in detail) that infants and children. The most com- our trauma patient), the pharmaco-
caused our patient’s SVT rather than mon example of this is WPW syndrome logic agent of choice for the rapid
decreased myocardial perfusion due to with an accessory pathway that con- conversion is adenosine, breaking the
blood loss since her BP remained stable ducts both antegrade and retrograde. reentry circuit by slowing or blocking
for the majority of her presentation and However, AVRT can be supported by an conduction in the AV node and will
recovered after cardioversion. accessory pathway, which only con- terminate the SVT in 72% to 77% of
Arrhythmias are not common in chil- ducts in the retrograde direction, a so cases.11,12
dren,7 regardless of traumatic injury, called “concealed” accessory pathway In the evaluation of sustained tachy-
and presenting to the pediatric ED with due to the absent footprint on a resting cardia occurring with blunt trauma
first time arrhythmia is also not com- ECG. Characteristic ECG findings in management and ongoing hemor-
mon. Suspicion for a tachyarrhythmia WPW include a shortened PR interval rhage, there has to be a high level of
should remain high when the rate is and slurred onset of the QRS complex clinical suspicion for arrhythmia. It is
sustained regardless of interventions known as the d wave (Fig 3). This can be best to use a step-wise approach to
such as IV fluids for hydration, fever found with structurally normal hearts, evaluate sustained tachycardia with
control, pain control, and calming as well as in hypertrophic cardiomy- blood loss being the most common
techniques for anxiety, and evaluation opathy or Ebstein anomaly. In patients likely etiology. This explains the clinical
for any structural injury (such as with WPW, syncope is a potential war- rationale for our incremental approach
pneumothorax or myocardial injury) ning sign of rapid ventricular conduc- as the patient continued to show ade-
with bedside imaging. Patients should tion and atrial fibrillation. Atrioventricular quate perfusion and acceptable BP and
be on telemetry monitoring while node reentry tachycardia is more mentation. In accordance with ad-
treatment ensues. SVT is the most common in older children and vanced trauma life support (ATLS)
common malignant pediatric tachyar- adolescents.9 In this form of SVT, re- guidelines for the trauma patient, re-
rhythmia.8 The category of SVT can be entry is entirely conducted within the suscitation of ongoing hemorrhage
divided into 3 major subcategories: AV node. with rapid IV crystalloid infusion in the
reentrant tachycardias using an ac- An intervention that interrupts the re- first 10 to 15 minutes (our patient re-
cessory pathway, reentrant tachy- entrant circuit in will interrupt the ceiving 2 boluses of normal saline
cardias without an accessory pathway, tachycardia for both AVRT and atrio- during this short time), then the initi-
and ectopic or automatic tachycardias.9 ventricular node reentry tachycardia.8 ation of the rapid transfusion protocol
SVT refers to all tachycardia originat- Treatment choice of SVT depends on to compensate for the ongoing bleed-
ing above the ventricles; however, this the clinical stability of the patient. A ing (moving to colloid administration
discussion will refer to reentrant types confirmatory 12-lead ECG should be when no response is seen with crys-
of tachycardia that are specifically de- obtained before treatment. Vagal talloid per ATLS) was performed. While
pendent on the atrioventricular (AV) stimulation is the first-line treatment. If giving this therapy time to work, eval-
node.10 unsuccessful or not applicable (as with uation for any cardiac tamponade
Classically, SVT has an unvarying heart
rate and therefore a fixed cycle length,
usually with a narrow complex QRS (it
can be wide complex if aberrant con-
duction, possessing a similar configu-
ration as ventricular tachycardia) with
the absence of clearly discernible p
waves. The majority of SVT in children is
caused by either AV nodal or AV reentry.
These reentrant forms of SVT can have
abrupt onset and cessation with the
only complaint being patient aware-
ness of a rapid heart rate.
AVRT, our patient’s ultimate diagnosis,
involves an accessory pathway and is FIGURE 3
the most common mechanism of SVT in ECG revealing WPW.
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e1658 MENOCH et al
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Supraventricular Tachycardia in the Pediatric Trauma Patient: A Case Report
Margaret Menoch, David Hurst, Peter Fischbach and Jesse J. Sturm
Pediatrics 2013;131;e1654; originally published online April 29, 2013;
DOI: 10.1542/peds.2012-1607
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