Pediatric EM Morsels Pediatric Emergency Medicine Education Fri, 24 Oct 2014 11:00:38 +0000 en-US hourly 1 Anaphylaxis Fri, 24 Oct 2014 11:00:38 +0000   Sitting next to my son, who is rather red-cheeked with his current fever, consuming a herculean amount of cartoons, I was reminded of one of my favorite shows when...

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Epi Early and Often


Sitting next to my son, who is rather red-cheeked with his current fever, consuming a herculean amount of cartoons, I was reminded of one of my favorite shows when I was young: GI JOE.  “Knowing is half the battle,” was imprinted within my being at an early age.  The Morsels have addressed many topics that hopefully augmented everyone’s “knowing.”  One topic that deserves some attention is Anaphylaxis.

{Yes, we just went from my febrile son, to GI JOE, to Anaphylaxis.  That is the transitive property of Morsel writing.}

Anaphylaxis: More Common than you Think

  • The incidence has increased with the implementation of the broader definition.
  • The incidence ranges from 100,000 to 500,000 per year in the USA.
  • Two-thirds of the annual cases are new cases.
  • Almost 1% of cases are fatal.
  • The incidence in food-related allergies has been increasing, so it is expected that anaphylaxis will also increase.
  • Estimated that a food-induced anaphylaxis presents to the ED every 6 minutes in the USA.


Anaphylaxis: The Criteria

  • The National Institute of Allergy and Infectious Diseases define anaphylaxis as a “serious allergic reaction that is rapid in onset and may cause death” and typically involves two or more organ systems.
  • Anaphylaxis is highly likely when ANY of the following criteria are met:
    • Acute Onset with involvement of skin, mucosal surfaces, or both AND
      1. Respiratory Compromise and/or
      2. Reduced BP or symptoms of end-organ dysfunction
    • Two or more of the following that occur rapidly after exposure to a likely allergen:
      1. Skin/Mucosal tissue involvement
      2. Respiratory Compromise
      3. Reduced BP or symptoms of end-organ dysfunction
      4. Persistent GastroIntestinal symptoms (ex, crampy pain, vomiting)
    • Rapid reduction in BP after exposure to known allergen.


Anaphylaxis: Important Points

  • The severity of an anaphylactic reaction cannot be predicted based on past reactions or risk factors.
  • Young children are tricky!
    • As with most conditions, the very young can be more difficult to diagnose.
    • The preverbal may not be able to express their symptoms clearly.
  • GastroIntestinal Symptoms are important to consider!
    • They are often under appreciated.
    • They have been found in over 50% of cases.
  • BiPhasic Reactions:
    • Occur in about 6% – 11% of children.
    • Usually manifest within the first 8 hours after exposure, but may be delayed up to 72 hours.
  • Treatment:
    • Epinephrine is the preferred 1st line therapy.
    • Antihistamines (H1 and H2 blockers) are useful for urticaria, nasal, and ocular symptoms, but not other symptoms.
    • Steroids have too slow of an onset to matter in the acute phase.


Anaphylaxis: “Epi Early and Often!”

  • Epi Early!
    • Epinephrine is the 1st line therapy for acute anaphylaxis.
    • Delayed administration of epinephrine has been associated with increased morbidity and mortality.
      • Unfortunately, several studies indicate that Epinephrine is either given in a delayed fashion or not at all during the acute phase.
      • This is true for patients/parents, EMS providers, as well as physicians.
    • Dose:
      • 0.01 mg/kg of the 1:1,000 solution; Max of 0.3 mg in children (0.5 mg in adults).
      • Autoinjectors: 0.15 mg dose for pts < 25kg; 0.3 mg for pts < 25 kg.
      • Exact dose is preferred for small infants and children.
    • Route Matters!
      • Intramuscular (IM) administration into the mid-anterolateral thigh is preferred.
      • IM provides faster rise in plasma and tissue concentrations than does the subcutaneous route.
  • Epi Often!
    • Epinephrine has a short half-life.
    • May need to repeat dose after 5 minutes.
    • Up to 20% of patients require more than one dose!
    • It is important to ensure patients have at least 2 doses of self-administered Epinephrine available to them in different environments (So prescribe 2 for home, 2 for school, etc).
  • There are no absolute contraindications to Epinephrine in this clinical setting.
    • Often concerns over adverse effects of epinephrine can delay it being given.
    • Appropriate doses of epinephrine rarely cause severe adverse reactions.


Moral of the Morsel: Epi Early and Often

  • Keep the broader criteria of Anaphylaxis on your radar screen.
  • Ask specifically about GI symptoms.
  • If the patient meets criteria, give Epi without Delay and consider additional dose in 5 minutes if not improving.
  • Get access and give IVF.
  • Other meds like antihistamines should not be given instead of Epinephrine.  They can be used as adjuncts, but do not let them distract the team from getting the Epinephrine in!
  • Patients then will require either prolonged observation (no standard, but often recommended to be 4-6 hrs) or hospitalization.



Chipps BE. Update in pediatric anaphylaxis: a systematic review. Clin Pediatr (Phila). 2013 May;52(5):451-61. PMID: 23393309. [PubMed] [Read by QxMD]

Tiyyagura GK1, Arnold L, Cone DC, Langhan M. Pediatric anaphylaxis management in the prehospital setting. Prehosp Emerg Care. 2014 Jan-Mar;18(1):46-51. PMID: 24028748. [PubMed] [Read by QxMD]

Benkelfat R1, Gouin S, Larose G, Bailey B. Medication errors in the management of anaphylaxis in a pediatric emergency department. J Emerg Med. 2013 Sep;45(3):419-25. PMID: 23478178. [PubMed] [Read by QxMD]

Grossman SL1, Baumann BM, Garcia Peña BM, Linares MY, Greenberg B, Hernandez-Trujillo VP. Anaphylaxis knowledge and practice preferences of pediatric emergency medicine physicians: a national survey. J Pediatr. 2013 Sep;163(3):841-6. PMID: 23566384. [PubMed] [Read by QxMD]

Lieberman P1, Nicklas RA, Oppenheimer J, Kemp SF, Lang DM, Bernstein DI, Bernstein JA, Burks AW, Feldweg AM, Fink JN, Greenberger PA, Golden DB, James JM, Kemp SF, Ledford DK, Lieberman P, Sheffer AL, Bernstein DI, Blessing-Moore J, Cox L, Khan DA, Lang D, Nicklas RA, Oppenheimer J, Portnoy JM, Randolph C, Schuller DE, Spector SL, Tilles S, Wallace D. The diagnosis and management of anaphylaxis practice parameter: 2010 update. J Allergy Clin Immunol. 2010 Sep;126(3):477-80. PMID: 20692689. [PubMed] [Read by QxMD]

Sampson HA1, Muñoz-Furlong A, Campbell RL, Adkinson NF Jr, Bock SA, Branum A, Brown SG, Camargo CA Jr, Cydulka R, Galli SJ, Gidudu J, Gruchalla RS, Harlor AD Jr, Hepner DL, Lewis LM, Lieberman PL, Metcalfe DD, O’Connor R, Muraro A, Rudman A, Schmitt C, Scherrer D, Simons FE, Thomas S, Wood JP, Decker WW. Second symposium on the definition and management of anaphylaxis: summary report–second National Institute of Allergy and Infectious Disease/Food Allergy and Anaphylaxis Network symposium. Ann Emerg Med. 2006 Apr;47(4):373-80. PMID: 16546624. [PubMed] [Read by QxMD]

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Appendicitis Clinical Decision Rules Fri, 17 Oct 2014 11:00:31 +0000   Often the Ped EM Morsels discuss diagnoses that emphasize astute clinical skills and vigilance while minimizing the importance of laboratory testing.  Appendicitis is a great example of this! Many...

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Often the Ped EM Morsels discuss diagnoses that emphasize astute clinical skills and vigilance while minimizing the importance of laboratory testing.  Appendicitis is a great example of this!

Many of you already know my disdain for the ubiquitous WBC count (otherwise known as the “Last Bastion of the Intellectually Destitute” – Amal Mattu) and are also aware of the many Myths that are associated with Appendicitis.  This month’s Annals of Emergency Medicine (2014, Oct; 64(4)) addresses another often encountered issue with Appendicitis: the Clinical Decision Rules.


Clinical Decision Rules

  • The practice of medicine is becoming more complicated everyday.
  • Ideally, we would like to ensure that all patients get superior care regardless of where they receive their care.
  • Clinical Decision Rules are aimed at helping providers deliver consistent and high quality care.
  • Clinical Decision Rules integrate various features (history, exam, simple labs, etc) in an effort to predict the likelihood of a specific disease/condition.
  • Useful Clinical Decision Rules would stratify patients into Low, Moderate, and High Risk Groups.
    • Low Risk – Condition ruled-out. No testing.
    • Moderate Risk – “Test Threshold” – Requires further testing.
    • High Risk – “Treatment Threshold” – Condition ruled-in. No Testing… just treat!


Appendicitis and Clinical Decision Rules

  • There are two widely used Clinical Decision Rules for Appendicitis.
    • Alvarado Score
    • Pediatric Appendicitis Score
  • The Alvarado Score has been found to have better test characteristics than the Pediatric Appendicitis Score (although they vary only slightly).
  • The Alvarado Score is a 10-point Score:
    • 1 point for -
      • Migration of Pain
      • Anorexia
      • Nausea or vomiting
      • Rebound Pain
      • Elevated Temperature (greater than or equal to 99.2 F)
      • Left Shift (greater than or equal to 75% PMNs)
    • 2 points for – 
      • Right Lower Quadrant Tenderness
      • Leukocytosis (greater than or equal to 10,000/microL).
  • The Pediatric Appendicitis Score gives only 1 point for leukocytosis and gives no points for rebound pain while adding 2 points for RLQ pain with coughing, jumping, percussion.
  • Unfortunately, often theses clinical findings are not reliably reproduced (we all know if the ask a patient a question 3 times you’ll get at least 2 different replies – “Did you vomit?” “No.” “Did you vomit?” “No.” “Did you vomit?” “Oh, you mean throw up? Yes I did.”).


Pretest Probability Matters

  • The Ebell and Shinholser paper nicely demonstrates the fact that the performance of the Clinical Decision Rule for appendicitis is dependent upon the pretest probability.
    • At a pretest probability of 33%, even an Alvarado Score of 9 or 10 does not cross the Treatment Threshold.
    • At a pretest probability of 66%, even an Alvarado Score of <4 does not define a useful Low Risk group.
  • What determines the clinician’s Pretest Probability??
    • While clinical experience and illness scripts certainly play a role in the estimation of the Pretest Probability,…
    • I would also suggest that the Clinical Variables scored in the Clinical Decision score play a significant role in the determination of a Pretest Probability.
    • So if a patient has migratory pain, nausea/vomiting, fevers, RLQ tenderness and rebound, both the Pretest Probability and the Alvarado Score will be high.
    • Experienced clinicians will often perform as well as Clinical Decision Rules.
  • Stratification is not precise.
    • Determining a Pretest Probability is dependent upon many variables.
    • Deciphering it all into a nice number like “33%” or “50%” or “66%” is difficult.
    • Often we default to a general gestalt.
    • This underscores that fact that our job is as much art as it is science.


Moral of the Morsel

  • The diagnosis of appendicitis is a difficult one.
  • The WBC count still is the Last Bastion of the Intellectually Destitute!
  • Clinical Decision Rules can help when incorporated into a Clinical Pathway that help to standardize care across a regional population.
  • Nothing is better than your clinical experience and acumen.



Ebell MH1, Shinholser J2. What Are the Most Clinically Useful Cutoffs for the Alvarado and Pediatric Appendicitis Scores? A Systematic Review. Ann Emerg Med. 2014 Oct;64(4):365-372. PMID: 24731432. [PubMed] [Read by QxMD]

Kharbanda AB. Appendicitis: do clinical scores matter? Ann Emerg Med. 2014 Oct;64(4):373-5. PMID: 24882663. [PubMed] [Read by QxMD]

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Mollaret’s Meningitis Fri, 10 Oct 2014 11:00:23 +0000   The best part of working in the Emergency Department at Carolinas Medical Center is being surrounded by so many brilliant colleagues.  I learn something new every shift (and, in truth,...

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Mollaret's Meningitis


The best part of working in the Emergency Department at Carolinas Medical Center is being surrounded by so many brilliant colleagues.  I learn something new every shift (and, in truth, is where the majority of these Morsels are baked).  Today’s Morsel is a reflection of that fact.

We evaluate headache often.  With the mantra of “worst first” echoing in our ears we naturally consider meningitis, but, fortunately, we are often able to exclude it based on our exam.  In previous Morsels, we have discussed concerning characteristics of headaches as well as some interesting causes of headaches (AVM, meningococcemia, pseudotumor).  What if, however, the patient has had viral meningitis previously?  What is Mollaret’s Meningitis anyway?


Recurrent Meningitis

Can be separated into two main categories:

  • Recurrent Bacterial Meningitis

    • Bacterial meningitis untreated is almost always fatal.
    • Recurrence implies that it was treated, but there is an underlying cause for the bacteria to gain access to the CSF again. Examples:
      • Congenital middle ear abnormalities
      • Persistent dermal sinus along the spinal column
      • Basilar skull fractures
      • Sinusitis, Mastoiditis, Deep Space Abscess
      • Immunodeficiencies


  • Recurrent Non-purulent Meningitis

    • Recurrent non-purulent meningitis can be due to a wide variety of entities including infectious as well as non-infectious causes.
    • Infectious
      • Bacteria, spirochetes, fungi, protozoa, viruses.
    • Non-Infectious
      • Tumors (ex, epidermoid cysts and craniopharyngioma)
      • Inflammatory Conditions (ex, Sacroid, Systemic Lupus Erythematosus)
      • Drugs (drugs can always cause badness)


Mollaret’s Meningitis

  • In 1944, Pierre Mollaret first described Recurrent Benign Lymphocytic Meningits due to HSV-2.
  • Recurrent (at least 3 episodes), benign and brief (usually 2-5 days) episodes of aseptic lymphocytic meningitis.
  • Lymphocytes have characteristic appearances:
    • Large activated monocytes with several deep clefts in the nuceli called:
      • “Cloverleaf nucleus,” “Footprint-shaped nucleus,” “bean-shaped nucleus.”
      • Also referred to as “Mollaret’s cells.”
    • These cells are most likely present in the first 24 hours of the illness.
  • Onset of disease has been observed from 5 years to 83 years of age. Mean is 35 years of age.


Mollaret’s Meningitis Causes

  • Most cases are due to Herpes Simplex Virus type 2 (HSV-2).
  • HSV-1 and Human herpesvirus 6 (HHV-6) have also been associated.
  • It is a good idea to ask about recent herpes lesion outbreaks in your patients with headaches.


Mollaret’s Meningitis Treatment

  • This is a benign and self-limited disease, so does not officially require therapy.
  • Intravenous acyclovir is often used initially, while diagnosis is being clarified.
    • 10 mg/kg three times a day for 7-10 days.
  • Intermittent or continuous prophylaxis has also been used with the goal of preventing the recurrence.



Min Z1, Baddley JW2. Mollaret’s meningitis. Lancet Infect Dis. 2014 Oct;14(10):1022. PMID: 25253408. [PubMed] [Read by QxMD]
Poulikakos PJ1, Sergi EE, Margaritis AS, Kioumourtzis AG, Kanellopoulos GD, Mallios PK, Dimitrakis DJ, Poulikakos DJ, Aspiotis AA, Deliousis AD, Flevaris CP, Zacharof AK. A case of recurrent benign lymphocytic (Mollaret’s) meningitis and review of the literature. J Infect Public Health. 2010 Dec;3(4):192-5. PMID: 21126724. [PubMed] [Read by QxMD]

Abu Khattab M1, Al Soub H, Al Maslamani M, Al Khuwaiter J, El Deeb Y. Herpes simplex virus type 2 (Mollaret’s) meningitis: a case report. Int J Infect Dis. 2009 Nov;13(6):e476-9. PMID: 19329344. [PubMed] [Read by QxMD]

Davis LE. Acute and recurrent viral meningitis. Curr Treat Options Neurol. 2008 May;10(3):168-77. PMID: 18579020. [PubMed] [Read by QxMD]

Capouya JD1, Berman DM, Dumois JA. Mollaret’s meningitis due to human herpesvirus 6 in an adolescent. Clin Pediatr (Phila). 2006 Nov;45(9):861-3. PMID: 17041177. [PubMed] [Read by QxMD]

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Facial Nerve Palsy Fri, 03 Oct 2014 11:00:06 +0000 There are many conditions that exist in both Pediatric and Adult patients who present to the ED.  Some of them require special consideration when you are evaluating the special population...

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Bell's Palsy

There are many conditions that exist in both Pediatric and Adult patients who present to the ED.  Some of them require special consideration when you are evaluating the special population of pediatric patients (please don’t say “kids aren’t little adults”… that drives me crazy).  For instance, DKA management often requires different considerations in children.  Another entity that requires some additional considerations is Facial Nerve Palsy.


Facial Nerve Palsy in Kids – Basics:

  • Facial Nerve Palsy is commonly encountered throughout one’s lifetime, but is relatively rare in kids.
    • Less common in younger children and infants than it is in teenagers and adults.
    • So don’t be cavalier when diagnosing a young child with “Bell’s Palsy.”
  • Outcomes are related to underlying cause as well as severity upon presentation.


Facial Nerve Palsy Severity Grading

  • The House-Brackmann Facial Nerve Grading System is used to grade the severity of the palsy.
    • Grade 1Normal function
    • Grade 2 – Mild dysfunction: normal symmetry at rest, able to completely close the eye with minimal effort.
    • Grade 3 – Moderate dysfunction: noticeable but not severe synkinesis, with effort can close eye, asymmetric mouth movement with maximal effort.
    • Grade 4 – Moderately severe dysfunction: obvious weakness, incomplete eye closure, asymmetric mouth movement.
    • Grade 5 – Severe dysfunction: only barely perceptible motion, asymmetric at rest.
    • Grade 6No movement.


 Facial Nerve Palsy Causes to Consider in Kids

Abridged list– but the big ones to consider are:

  • Idiopathic (Bell’s Palsy) 
    • Often reported to be the most common cause of Facial Nerve Palsy in kids (40-70% of cases).
    • More recent literature demonstrate lower percentages, likely from being able to detect other potential infectious cause.
  • Infection
    • Otitis media, mastoiditis, parotitis, meningitis
    • EBV, Mycoplasma pneumoniae, HSV, VZV, tuberculosis, HIV, poliomyelitis, mumps
    • Lyme Disease (the most prevalent causes in endemic areas!)
    • Ramsay-Hunt Syndrome (Herpes Zoster cephalicus) – look for vesicles on TM or in mouth
  • Inflammatory Conditions
  • Trauma
    • Fracture of the temporal bone
    • Skull base fractures
    • Perinatal trauma (compression from forceps)
    • Trauma to parotid / cheek region
    • Barotrauma
  • Neoplasm
    • Leukemias
    • Parotid tumors
    • Brainstem masses
    • Cholesteatoma
  • Others


Facial Nerve Palsy Evaluation

  • The evaluation is predicated upon a thorough history and physical exam, mindfully considering the above potential causes.
  • Key Points to Contemplate:
    • Condition is progressively worsening over 3 weeks or lacks improvement after 3 months – concerning for CNS or neoplastic process.
    • Recurrent Facial Nerve Palsy – is rare, therefore warrants specialty evaluation.
    • Bilateral Facial Nerve Palsy – likely due to a Lyme Disease or EBV infection or neurological cause (Guillan-Barre Syndrome).
    • Aural Symptoms – Bell’s Palsy can have this, but so too can Ramsay-Hunt Syndrome, Otitis Media, Cholesteatoma, or tumors! Be thorough with your physical exam.
    • Recent Immunizations - Facial Nerve Palsy has been related to rabies, polio, tetanus, and influenza vaccinations. Causation is a different story.
    • Failure to Thrive, Persistent Fever – Consider occult neoplasms.
    • Other Cranial Nerves Involved or Abnormalities on Neuro Exam – No longer a simple Facial Nerve Palsy… investigate for badness.
  • Imaging?
    • Neuro-imaging would be recommended for:
      • Any signs of Central Nervous System involvement,
      • Suspect malignancy,
      • Suspect trauma,
      • Evidence of Middle Ear Cholesteatoma,
      • Peripheral Facial Nerve Palsy progressing beyond 3 weeks,
      • Peripheral Facial Nerve Palsy without improvement after 6 months,
      • Recurrent Facial Nerve Palsy
    • Be cautious with a patient who is younger than 2 years of age… Bell’s Palsy is less likely.


Idiopathic Facial Nerve (Bell’s) Palsy Treatment

  • Eye Care!
    • The most important therapy consideration!
    • Artificial Tears during daytime.
    • Moisturizing eye ointment (ex, Lacrilube) during sleep.
  • Steroids?
    • There is adult literature that supports the use of steroids; however the literature does not contain many pediatric patients.
    • In addition, the vast majority of children with Bell’s Palsy improve without therapy, so studies are often underpowered to determine a difference between those who received steroids and those who did not.
    • If you elect to use steroids:
      • Prednisolone 1 mg/kg (max 60mg) per day x 7 days and then taper off.
      • Best to initiate within first week of onset.
      • Consider other comorbidities (diabetes, hypertension, occult leukemia) before prescribing.
        • Some would advocate for a screening CBC because of this.
  • Acyclovir
    • Has not been shown to be helpful on its own with adults or children.
    • In adults, there is some evidence that it is beneficial when used with steroids.




Ozkale Y1, Erol I, Saygı S, Yılmaz I. Overview of Pediatric Peripheral Facial Nerve Paralysis: Analysis of 40 Patients. J Child Neurol. 2014 May 8. PMID: 24810082. [PubMed] [Read by QxMD]

Malik V1, Joshi V, Green KM, Bruce IA. 15 minute consultation: a structured approach to the management of facial paralysis in a child. Arch Dis Child Educ Pract Ed. 2012 Jun;97(3):82-5. PMID: 22315344. [PubMed] [Read by QxMD]

Pavlou E1, Gkampeta A, Arampatzi M. Facial nerve palsy in childhood. Brain Dev. 2011 Sep;33(8):644-50. PMID: 21144684. [PubMed] [Read by QxMD]

Wang CH1, Chang YC, Shih HM, Chen CY, Chen JC. Facial palsy in children: emergency department management and outcome. Pediatr Emerg Care. 2010 Feb;26(2):121-5. PMID: 20093994. [PubMed] [Read by QxMD]

Shih WH1, Tseng FY, Yeh TH, Hsu CJ, Chen YS. Outcomes of facial palsy in children. Acta Otolaryngol. 2009 Aug;129(8):915-20. PMID: 18923943. [PubMed] [Read by QxMD]

Bilavsky E1, Scheuerman O, Marcus N, Hoffer V, Garty BZ. Facial paralysis as a presenting symptom of leukemia. Pediatr Neurol. 2006 Jun;34(6):502-4. PMID: 16765834. [PubMed] [Read by QxMD]

Singhi P1, Jain V. Bell’s palsy in children. Semin Pediatr Neurol. 2003 Dec;10(4):289-97. PMID: 14992461. [PubMed] [Read by QxMD]

Salman MS1, MacGregor DL. Should children with Bell’s palsy be treated with corticosteroids? A systematic review. J Child Neurol. 2001 Aug;16(8):565-8. PMID: 11510926. [PubMed] [Read by QxMD]

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Neonatal Leukemia Fri, 26 Sep 2014 11:00:15 +0000 We have discussed numerous common neonatal issues (ex, Analgesia, Umbilical Granuloma, Neonatal Tooth, Hyperbilirubinemia).  Many of us have learned that neonates are challenging and demand respect.  Even the most proficient practitioner...

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Neonatal Leukemia

We have discussed numerous common neonatal issues (ex, Analgesia, Umbilical Granuloma, Neonatal Tooth, Hyperbilirubinemia).  Many of us have learned that neonates are challenging and demand respect.  Even the most proficient practitioner will be apprehensive of the sick neonate, given that there are so many conditions to consider with so few clinical clues to help sort through them (ex, ALTE, Omphalitis, PGE1, Neonatal Resuscitation, Hypothermia).

While severe infections, congenital anomalies, and unusual metabolic conditions need to be pondered, it seems completely unfair that you should also have to consider cancer in neonates!!

Neonatal Leukemia - because life is not fair.


Neonatal Leukemia – Basics

  • Neonatal Leukemia is, fortunately, rare!
    •  Estimates of 1-5 per MILLION live births.
      • While rare, it does occur (our group just diagnosed a neonate with a WBC >900,000).
    • <1% of all childhood leukemia is diagnosed during the neonatal period.
  • Neonatal leukemia is not the same as childhood leukemia.
    • Neonatal leukemia is more likely to present with poor prognostic factors.
    • Neonatal ALL has a disease-free survival rate of ~10% compared to >70% in older children.
    • Neonatal leukemia is the leading cause of death in neonate due to neoplastic disease.
  • Trisomy 21 (Down Syndrome) and 11q23 translocation are the most common chromosomal aberrations associated with neonatal leukemia.
  • Timing of Presentation:
    • Some show signs at birth.
    • Some within a few days of birth.
    • Others present between the 3rd and 6th week of life.
      • This group may present in a more vague manner with failure to thrive, pallor, fever, and lethargy.


Neonatal Leukemia – Signs and Symptoms

  • Hyperleukocytosis

    • Present in the majority of ALL cases (85%), but only 49% of AML cases.
    • WBC > 50 x 10^9/L
    • Complications due to Hyperleukocytosis:
      • Leukostasis Syndrome
        • White Cells plug up the micro-circulation.
        • Heart Failure
        • Respiratory Failure (hypoxia, pulmonary infiltrates, tachypnea)
        • Neurologic insults (somnolence, coma, retinal hemorrhage)
  • Hepatosplenomegaly

    • Seen in about 80% of the cases.
    • Liver is more often enlarged than the spleen.
    • Other Lymphadenopathy is seen in only ~25% of cases.
  • Leukemia Cutis

    • Seen in about 60% of cases.
    • Caused by cutaneous leukemic infiltrates.
    • A firm blue, red, or purple nodular eruption.
    • Blueberry muffin baby.” – similar to what is seen with congenital infections.
    • Reported to be the INITIAL presenting sign in about 50% of cases!
      • Keep this on your list of items to look for in the neonate!
      • May precede the other signs by as much as 4 months!
  • Additional Findings

    • Bone Marrow Suppression (due to infiltrative disease)
      • Anemia
      • Thrombocytopenia
      • Neutropenia
    • CNS Infiltration
      • Seizures
      • Cranial Nerve Palsies
      • Bulging Fontanelle
      • Intracranial Hemorrhage
      • Infarction
    • Respiratory
      • Pulmonary Hemorrhage
      • Pneumonia
    • Sepsis


Neonatal Leukemia – on the Differential

  • Leukemoid Reaction
    • Causes elevated WBC counts and Hepatomegaly.
    • May also have BlueBerry Muffin Baby appearance.
    • Seen with Congenital Infections.
      • TOxoplasmosis, Rubella, CMV, HErpes, Syphilis, Listeria.
      • Also with Sepsis.
      • Typically have Intrauterine growth retardation and/or microcephaly.
  • Other Congenital Neoplasms (Neuroblastoma)
  • Hemolytic Disease of the Newborn
  • Congenital HIV Infection


Neonatal Leukemia – Initial Work-up

  • The definitive diagnosis will not be made in the ED, but your suspicion for it should lead you to obtain:
    • CBC with Differential
    • Peripheral Smear
    • Work up for Congenital Infections!
  • During the admission, the child will have Bone Marrow Aspirate performed to help make definitive diagnosis.



Orbach D1, Sarnacki S, Brisse HJ, Gauthier-Villars M, Jarreau PH, Tsatsaris V, Baruchel A, Zerah M, Seigneur E, Peuchmaur M, Doz F. Neonatal cancer. Lancet Oncol. 2013 Dec;14(13):e609-20. PMID: 24275134. [PubMed] [Read by QxMD]

van der Linden MH1, Creemers S, Pieters R. Diagnosis and management of neonatal leukaemia. Semin Fetal Neonatal Med. 2012 Aug;17(4):192-5. PMID: 22510298. [PubMed] [Read by QxMD]

Isaacs H Jr. Fetal and neonatal leukemia. J Pediatr Hematol Oncol. 2003 May;25(5):348-61. PMID: 12759620. [PubMed] [Read by QxMD]

Sande JE1, Arceci RJ, Lampkin BC. Congenital and neonatal leukemia. Semin Perinatol. 1999 Aug;23(4):274-85. PMID: 10475541. [PubMed] [Read by QxMD]

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Optimize Chest Compressions Fri, 19 Sep 2014 12:00:49 +0000   On occasion, I get the honor of being to “asked” to help with my daughter’s homework. It isn’t common, fortunately, as I don’t recall middle school algebra that well, but...

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Chest Compressions Basics


On occasion, I get the honor of being to “asked” to help with my daughter’s homework. It isn’t common, fortunately, as I don’t recall middle school algebra that well, but recently I was emphasizing the fact that you cannot expect excellent results from complicated systems (equations) if you fail to do the basics correctly.

Often we get distracted with “advanced” strategies and techniques. While advanced procedures can be effective, suboptimal performance of the basics will undermine the entire project.  This concept, I think, is easily reflected when we are involved in resuscitations.  Focusing on the choice between lidocaine, procainamide, and amiodarone is fruitless if the team is not performing the basics optimally.  Without question, The Basics are the Best!

We all know that the American Heart Association has emphasized the focus on the basics, and we recently discussed the need to de-emphasize pulse checks, but let us now look at how to optimize our chest compressions!


What are Quality Chest Compressions

  • For pediatrics patients quality chest compressions require:
    • Rate of 100 compressions per min
    • Compression Depth of 1/3 AP diameter
    • Compressions that allow for complete recoil of the chest!
      • This is just as vital as the depth and the rate, but often under appreciated!
      • It is during recoil phase that the heart chambers fill with blood and the coronary arteries have blood flow.


Quality Chest Compressions Matter

  • Goal of delivering CPR is Return of Spontaneous Circulation (ROSC) and Maintaining Cerebral Perfusion.
    • Obvious ROSC is important, but survival with good neurologic outcome is the real goal.
  • Quality chest compressions can generate good MAP.
    • This is integral to having a chance to provide cerebral perfusion!
    • Sutton et al. showed that quality chest compressions can generate systolic BP >80 and diastolic BP >30!
  • Quality chest compressions can lead to improved survival.
    • When compared to suboptimal chest compressions, quality chest compressions have been associated with improved survival in the first 24 hours.
    • Obviously, this does mean overall survival, but you have to start somewhere.


Optimize Chest Compressions

  • Since chest compressions are so important, one of the most important roles a team leader has is to ensure they are being optimized.
    • Use a BackBoard!
      • Even with adults this is important, but particularly true in children.
      • Often the compression of the gurney’s mattress will significantly diminish the actual AP compression of the patient!
      • The backboard can be easily overlooked and if not present, all of the efforts are being undermined!!
    • Get the timing down! Use a Metronome!
      • Often it is recommended to do compressions to the beat of a song…
        • But even if we all sing the same song, the tempo of that song can easily be misjudged.
      • Take the guess work out of it… is an automatic timing system.
        • Use a metronome to help define what 100/min is.
        • There is “an app for that.”  Some apps will use your smartphone’s flash to signal that rate… which give nice visual cues to the compressor.
        • There are also “fancy” commercial products available that can give cues to the timing and depth of compressions, but they aren’t free.
    • Use End-Tidal CO2 to provide feedback.
      • Studies show that EtCO2 can be a surrogate maker of blood flow produced during compressions in both adult and pediatric patients.
        • CPR is a low flow state, and as such, EtCO2 becomes less dependent upon CO2 production and ventilation and is more related to Cardiac Output.
        • Since pediatric arrests are usually due to respiratory (or infectious) etiology, do not rely on the initial EtCO2 value.
        • The value is more reliable after 1 min of compressions.
      • Goal EtCO2 of between 10-15 during chest compressions.
        • Can be used as a feedback device… as it indicates quality compressions are being done.
        • If EtCO2 <10, ROSC is unlikely. Double check your quality characteristics!
      • If EtCO2 increases substantially during chest compressions, this likely indicates ROSC.
        • Using this method can help decrease interruptions in chest compressions for “pulse checks.”
        • Just seeing an increase would not lead me to stopping compressions… I’d likely complete that 2 min cycle before checking for pulse.
    • Mandate the Rotate!
      • While we work with many true heroes, this is not a time to allow someone’s self-sacrifice to interfere with quality chest compressions.
        • Even the strongest and biggest person will get tired.
        • The power to do quality chest compressions is similar to that of running or swimming.
        • While the compressor may be a physically fit individual, he/she will not sprint at the same rate the entire time.
      • Studies show there is a measurable and significant decrement in quality of chest compressions at 2 minutes for both adult and pediatric patients!
        • Interestingly, the rate and depth often stays the same, but the compressor begins to lean on the chest.
        • This decreases the chest recoil!!  We cannot have that.
      • Do not ask if the compressor is “ok.”
        • Tell him or her that it is time to rotate rapidly and have the next person prepped and ready to take over without interruption!
        • Even if it is Superman, tell him it is time to rotate for the sake of optimizing your chest compressions!


Hamrick JL1, Hamrick JT, Lee JK, Lee BH, Koehler RC, Shaffner DH. Efficacy of chest compressions directed by end-tidal CO2 feedback in a pediatric resuscitation model of basic life support. J Am Heart Assoc. 2014 Apr 14;3(2):e000450. PMID: 24732917. [PubMed] [Read by QxMD]

Sutton RM1, French B2, Niles DE3, Donoghue A3, Topjian AA3, Nishisaki A3, Leffelman J3, Wolfe H3, Berg RA3, Nadkarni VM3, Meaney PA3. 2010 American Heart Association recommended compression depths during pediatric in-hospital resuscitations are associated with survival. Resuscitation. 2014 Sep;85(9):1179-84. PMID: 24842846. [PubMed] [Read by QxMD]

Badaki-Makun O1, Nadel F, Donoghue A, McBride M, Niles D, Seacrist T, Maltese M, Zhang X, Paridon S, Nadkarni VM. Chest compression quality over time in pediatric resuscitations. Pediatrics. 2013 Mar;131(3):e797-804. PMID: 23439892. [PubMed] [Read by QxMD]

Sutton RM1, French B, Nishisaki A, Niles DE, Maltese MR, Boyle L, Stavland M, Eilevstjønn J, Arbogast KB, Berg RA, Nadkarni VM. American Heart Association cardiopulmonary resuscitation quality targets are associated with improved arterial blood pressure during pediatric cardiac arrest. Resuscitation. 2013 Feb;84(2):168-72. PMID: 22960227. [PubMed] [Read by QxMD]

Tress EE1, Kochanek PM, Saladino RA, Manole MD. Cardiac arrest in children. J Emerg Trauma Shock. 2010 Jul;3(3):267-72. PMID: 20930971. [PubMed] [Read by QxMD]

Kleinman ME, de Caen AR, Chameides L, Atkins DL, Berg RA, Berg MD, Bhanji F, Biarent D, Bingham R, Coovadia AH, Hazinski MF, Hickey RW, Nadkarni VM, Reis AG, Rodriguez-Nunez A, Tibballs J, Zaritsky AL, Zideman D; Pediatric Basic and Advanced Life Support Chapter Collaborators. Part 10: Pediatric basic and advanced life support: 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. Circulation. 2010 Oct 19;122(16 Suppl 2):S466-515. PMID: 20956258. [PubMed] [Read by QxMD]

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Intussusception & Altered Mental Status Fri, 12 Sep 2014 20:10:38 +0000 Evaluating the child with altered mental status can be very challenging.  As with adults, there are a myriad of potential etiologies and it can be difficult to prioritize the order...

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Intussusception Altered Mental Status

Evaluating the child with altered mental status can be very challenging.  As with adults, there are a myriad of potential etiologies and it can be difficult to prioritize the order of the evaluation.  Does this patient have an intracranial process or maybe just simple hypogylcemia?  Or maybe we need to consider serious bacterial infections and intoxicants instead?

Many of you will recall the mnemonic “TIPS AEIOU” [Trauma, Infection, Psych, Space Occupying Lesion, Alcohol, Electrolytes, Insulin, Opiates, Uremia] to help consider a number of the potential etiologies of altered mental status.  I use this often, but it is important to remember that along with “infection” and “insulin” the “I’s” also stand for “Intussusception.”


Intussusception Basics

  • Occurs when one segment of bowel telescopes into the adjacent segment.
  • Second most common abdominal emergency (appendicitis is #1).
  • Most often this occurs near the ileocecal valve.
  • Most are idiopathic.
  • ~5% are associated with lead points or disease


Intussusception Presentation

  • “Classic” presentation (Abdominal Pain, Currant Jelly Stools, and vomiting) is only seen in 20%- 33% of cases.
  • 75% without obviously bloody stools will have positive occult blood.  
    • Great reason to check heme occult for the vomiting child without diarrhea.
  • Abdominal Mass is commonly found (when looked for).
  • Fever, anorexia, diarrhea, and dehydration can be seen and can lead to misdiagnosis.
  • Many cases are missed upon initial evaluation — we must always remain vigilant!


Intussusception and Altered Mental Status

  • Along with the classic and common presentations, patients with intussusception may also present with altered mental status.
  • This altered mental status is often thought of as the child being inconsolable.
    • Most practitioners will have intussusception high on the DDx in the child with inconsolability and vomiting.
  • Additionally, significant somnolence and lethargy can be seen with intussusception!
    • Numerous cases have been reported that highlight this fact.
    • Cause of the lethargy is unclear.
    • Presence of lethargy does not, necessarily, portend a worse outcome (but does contribute to delayed diagnosis, which can lead to more morbidity/mortality).
  • Cases of intussusception and altered mental status often also have history of:
    • Vomiting,
    • Heme-positive stool,
    • Abdominal Pain,
    • or Abdominal Mass


POCUS and Altered Mental Status

  • So how can Point of Care Ultrasound (POCUS) help with the evaluation of altered mental status in a child?
  • POCUS can be used to AUGMENT the physical exam.
    • Studies have shown the POCUS can be used by emergency practitioners (in a variety of locales) to rule-in the diagnosis of intussusception.
    • The evaluation should not (yet) be used to rule-out the diagnosis; however, it’s utility can help prioritize the next most appropriate step.
      • For instance, consider the 18 month old presenting with lethargy and episodes of non-bilious emesis.  You perform POCUS:
        • If consistent with intussusception, then call your surgeon and your radiologist.
        • If not consistent with intussusception, it may still be present, but you may want to get that Head CT and give antibiotics before getting abdominal imaging.


Moral of the Morsel

Altered Mental Status?  Augment your exam with POCUS.  It may be intussusception.



Halm BM. Reducing the time in making the diagnosis and improving workflow with point-of-care ultrasound. Pediatr Emerg Care. 2013 Feb;29(2):218-21. PMID: 23546429. [PubMed] [Read by QxMD]

Gingrich AS1, Saul T, Lewiss RE. Point-of-care ultrasound in a resource-limited setting: diagnosing intussusception. J Emerg Med. 2013 Sep;45(3):e67-70. PMID: 23777777. [PubMed] [Read by QxMD]

Stolz LA1, Kizza H, Little K, Kasekende J. Intussusception detected with ultrasound in a resource-limited setting. Lancet. 2013 Jun 8;381(9882):2054. PMID: 23746905. [PubMed] [Read by QxMD]
Raymond-Dufresne É1, Ghanayem H. Towards evidence-based emergency medicine: best BETs from the Manchester Royal Infirmary. BET 2: Can emergency physicians safely rule in or rule out paediatric intussusception in the emergency department using bedside ultrasound? Emerg Med J. 2012 Oct;29(10):854-5. PMID: 23038721. [PubMed] [Read by QxMD]

Birkhahn R1, Fiorini M, Gaeta TJ. Painless intussusception and altered mental status. Am J Emerg Med. 1999 Jul;17(4):345-7. PMID: 10452429. [PubMed] [Read by QxMD]

Hickey RW1, Sodhi SK, Johnson WR. Two children with lethargy and intussusception. Ann Emerg Med. 1990 Apr;19(4):390-2. PMID: 2321825. [PubMed] [Read by QxMD]

Heldrich FJ. Lethargy as a presenting symptom in patients with intussusception. Clin Pediatr (Phila). 1986 Jul;25(7):363-5. PMID: 3709021. [PubMed] [Read by QxMD]

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