On behalf of the Fellows from the Division of Emergency Medicine at Cincinnati Children’s I am delighted to bring you a new series that will highlight what we are learning during our ongoing didactic conferences. The main goal of the Pediatric Emergency Digest series will be to provide concise teaching points to reinforce in-person learning and to further the conversation. As always, feedback is welcome.

This edition reflects content from October 22nd through the 26th, 2018 and is courtesy of Ashish Shah.

Medical Video Review

Case discussion

  • A young adult female s/p kidney transplant, on hemodialysis (last received few days prior) for failed transplant, presents with shortness of breath that started acutely overnight.  The patient also with a history of hypertension and prior episode of pericardial effusion.
  • She initially presented to the resuscitation bay hypoxic and in severe respiratory distress. Duonebs were initially trialed due to wheezing heard on the exam, without significant improvement.  The patient was refusing to place anything oxygen delivery device on her face.  Bedside ultrasound showed pericardial effusion.  After some reassurance and discussion, she was amenable to starting Bipap. However, soon after Bipap was started, her mental status worsened and she eventually was intubated.  In the PICU, she was placed on the oscillator and then transitioned to the conventional ventilator.  CRRT was started and she was subsequently transitioned to hemodialysis. She was discharged in four days with the working diagnosis of flash pulmonary edema secondary to pericardial effusion.

Key Learning Points

  • How do you maintain control when faced with a critically ill patient who is refusing to do the plan?
  • Take a deep breath. It’s okay to take a step back and then re-engage the patient
  • Remain calm and communicate directly with the patient, including an emphasis on using the patient’s name
  • Have a systematic approach starting with your own rapid cardiopulmonary exam
  • Go back to the basics (ABC’s)
  • How do you communicate with your team when dealing with a very sick patient
    • Maintain control of your team and clearly communicate your concerns that the patient is sick with a comprehensive mental model
    • It is okay to express and acknowledge your anxiety and/or the difficulty of the case before you
    • Request feedback from the team
    • Think ahead and prepare the team for unexpected or expected deterioration
  • Why did this patient deteriorate when BiPAP was initiated?
    • In this patient (not a chronic CO2 retainer), an intervention like BiPAP should NOT cause a decreased mental status
    • Suspect this was secondary to a shift in hemodynamics with the initiation of positive pressure– this patient was likely very preload dependent (teetering on the edge of a sharp cliff). When BiPAP was initiated, this augmented her preload just enough to decrease her cardiac output, causing decreased cerebral perfusion and therefore AMS. At this time, cautiously proceeding with intubation is appropriate, but do your best to optimize this patient

Lessons Learned from the Storz Video Laryngoscope

  • Case 1: an example of a difficult post-arrest edematous, pale airway. Things that may have been helpful = cheek pull to increase the amount of room available, potentially a bougie if <= grade 2b view.
  • While there is not a lot of evidence for pre-laryngoscopy positioning, maximizing positioning (i.e. ear to sternal notch) is helpful.
  • Tongue Control: sweeping to the left versus entering the mouth midline. Little evidence supporting one over another. Either approach works, as long as it is stepwise.
    • Green-Hopkins looked at this exact question in 2015 – sweep vs midline (on video laryngoscopy). Investigators found that midline and sweep had no difference in first pass success, and that sweep leads to increased mucosal injury and aspiration (aOR = 4.1, 95% CI = 1.2 to 14.5; aOR = 7.7, 95% CI = 1.5 to 39.5, respectively) as well as increased time to intubation 42 seconds vs. 31.5 seconds; p < 0.05.

Toxicology Conference

with Preston Dean, MD

Tricyclic Antidepressants

TCA’s block serotonin and norepinephrine reuptake and also have anticholinergic properties

Signs and symptoms

  • Anticholinergic symptoms: urinary retention, decreased GI motility, delirium, hallucinations, dry mouth
  • Cardiac Toxicity: Hypertension,QRS Prolongation, Sinus Tachycardia → Wide Complex Tachycardia
  • Neurologic Toxicity: CNS depression, Seizures


  • Obtain initial EKG and repeat to monitor for change (UpToDate suggests hourly)
  • Frequent renal panels looking for acidosis
  • When to use Sodium Bicarbonate?
    • Hypotension or arrhythmias
    • 1-2mEq/kg Sodium Bicarbonate bolus, may be repeated and followed by continuous infusion after narrowing of QRS seen
    • The alkalinized environment inhibits TCA’s from binding to the rapid sodium channels in the His-Purkinje System and myocardium, thus increasing the TCA- inhibited conduction
  • Treat Seizures with Benzodiazepine

Serotonin Syndrome

Caused by selective serotonin reuptake inhibitors (SSRI’s), selective norepinephrine reuptake inhibitors (SNRI’s), monoamine oxidase inhibitors (MOAI’s), TCA’s, amphetamines, tramadol, dextromethorphan, buspirone, MDMA (ecstasy). Serotonin syndrome is more common when two or more serotonergic medications are ingested

Signs and symptoms

  • Neurologic Symptoms: Confusion, Agitation, Seizures
  • Cardiac Symptoms: QTc Prolongation
  • Autonomic Symptoms: Clonus, Sweating, Dilated Pupils, Hyperthermia


  • Treat seizures with benzodiazepines
  • Otherwise, treatment is supportive

Digoxin Toxicity

Digoxin is a Na/K transporter blocker which leads to increased intracellular calcium and inotropy. Symptoms are more common with chronic toxicity than acute toxicity.

Signs and Symptoms

  • Nausea/Vomiting
  • Hypoglycemia
  • Altered mental status
  • Cardiac arrhythmias: sinus bradycardia, irregular heartbeats, ventricular tachycardia/fibrillation, AV and/or SA block


  • Obtain EKG: Premature ventricular beats (earliest and most common finding),
  • Check electrolytes: Hyperkalemia
  • Treat with Digoxin immune Fab antibodies if symptomatic bradycardia or other arrhythmias

Beta Blockers

Very commonly prescribed to manage a range of disorders. Block the beta receptors in heart, smooth muscle through competitive antagonism of beta receptors, thus decreasing the cellular levels of cAMP

Signs and Symptoms

  • Bronchoconstriction
  • Hypotension
  • Bradycardia
  • HYPOglycemia
  • Altered mental status


  • Antidote: Glucagon (0.1 mg/kg IV which leads to increased cAMP) for symptomatic patients
  • Atropine for bradycardia, but will no completely reverse the cardiotoxic effects of overdose
  • Dextrose for hypoglycemia
  • Vasopressors for resistant hypotension
  • Supportive therapy

Calcium Channel Blockers

Block calcium channels responsive for myocardial contractility, vascular smooth muscle contractility, and pacemaker cells
Remember: This is on your list of One Pill Can Kill

Signs and symptoms

  • Hypotension
  • Bradycardia
  • AV-node block
  • HYPERglycemia


  • Serial EKG and electrolyte monitoring
  • Calcium Chloride to overcome the cardiovascular effects of CCBs
  • Atropine for bradycardia
  • Vasopressors for resistant hypotension
  • Insulin and dextrose leads to inotropy


Alpha-2 receptor agonist – It actively slams the breaks on all central alpha-2 output form the CNS.

Signs and symptoms

  • Altered mental status
  • Can present with initial hypertension (due to effects of alpha-1 agonism): DON’T BE FOOLED. Will progress to hypotension
  • Respiratory depression


  • Isotonic fluids
  • Vasopressors
  • Atropine for bradycardia
  • High dose naloxone with some evidence- trial if marked CNS depression and apnea


Increases insulin release from the beta cells of the pancreas
Remember: This is on your list of One Pill Can Kill

Signs and symptoms

  • Gradual and prolonged hypoglycemia
  • Hypoglycemic seizure
  • Decreased mental status
  • Confusion


  • Do NOT start prophylactic dextrose alone! Will cause transient hyperglycemia which triggers insulin release, leading to worsening hypoglycemia.  Therefore use dextrose AND Octreotide, which antagonizes the insulin release
  • Check glucose q1h while asleep and q2h while awake

Call Drug and Poison Information Center for all ingestions
In Cincinnati the number is: 1-800-222-1222
Check your local numbers and have them close at hand in the ED


Fleisher, G. R. 1., Ludwig, S., & Henretig, F. M. (2000). Textbook of pediatric emergency medicine (4th ed.). Philadelphia: Lippincott Williams & Wilkins.

Procedural Simulation

with Matt Mittiga and Michelle Eckerle

This month at the fellow’s procedural simulation, Dr. Mittiga and Dr. Eckerle facilitated a case of a 7-month old with supraventricular tachycardia (SVT).

Identification of SVT

  • Absent P-waves on the EKG
    • Increase the speed of the EKG paper from 25mm/s (normal) to 50mm/s to stretch the EKG
  • Minimal to no heart rate (HR) variability (rare cases of transient changes in HR with volume resuscitation but it will return to SVT range)
  • Rates:
    • 220-240: Infant
    • 180-200: Childhood
  • Stable vs Unstable SVT
    • Unstable with any sign of poor perfusion (hypotension for age, altered mental status, signs of shock)


  • Ventricular Arrhythmias
    • Rare
    • Risk with A-V reentrant tachycardia (WPW)
    • Important to place defibrillator pads
  • Asystole
    • Uncommon but can occur with adenosine administration
    • Start CPR and epinephrine

Treatment of SVT


  • Extremely short half-life (<10 seconds)
  • Make sure to obtain proximal PIV or Humeral IO
  • Starting dose is 0.1mg/kg (max starting 6mg, 2nd dose 12mg), if not successful in conversion with starting dose, double the dose and attempt again if stable
  • Methods of administration: 3-way stopcock (1 connection with adenosine, 1 connection with a 5-10ml flush, 1 connection to the patient). Step 1 push adenosine, Step 2 push 5-10ml normal saline flush.
    • The best way is 2 person technique with 1 pushing the medication and 1 controlling stopcock

Ice to the face

  • Diving reflex from an increase in parasympathetic response and should respond in 30-40 seconds
  • Do not obstruct the airway

Valsalva maneuver

  • Revert Trial: Modified Valsalva maneuver vs standard semi-recumbent maneuver
    • Modified Valsalva maneuver: semi-recumbent position patients produce 40mmHg pressure for 15 seconds and then repositioned in a supine position with a passive leg raise immediately after the Valsalva strain
    • Standard semi-recumbent
    • Multi-center RCT: patients with SVT allocated to modified vs standard maneuver
    • Primary Outcome: the return of sinus rhythm at 1 min
    • Results
      • 428 pts with SVT in the primary analysis
      • Standard Valsalva Arm: 37/214 (17%)
      • Modified Valsalva Arm: 93/214 (43%)
      • Absolute Difference = 26.2%
      • NNT = 3

Synchronized Cardioversion

  • If unstable tachycardia
  • Start with 0.5 J/Kg to 1 J/kg, can increase to 2 J/kg if needed
  • Be sure to print EKG tracing when giving adenosine OR synchronized cardioversion

Take Home Point

The REVERT Trial showed a statistically significant increase in return of sinus rhythm with modified Valsalva maneuver.


You can substitute a 10cc syringe for the maneuver for 15 seconds as it provides similar pressure as in the trial.


Appelboam A, Reuben A, Mann C, Gagg J, Ewings P, Barton A, Lobban T, Dayer M, Vickery J, Benger J; REVERT trial collaborators.  Postural modification to the standard Valsalva manoeuvre for emergency treatment of supraventricular tachycardias (REVERT): a randomised controlled trial. Lancet. 2015 Oct 31;386(10005):1747-53. doi: 10.1016/S0140-6736(15)61485-4. Epub 2015 Aug 24.