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Pediatric Emergency Playbook

You make tough calls when caring for acutely ill and injured children. Join us for strategy and support, through clinical cases, research and reviews, and best-practice guidance in our ever-changing acute-care landscape. This is your Pediatric Emergency Playbook.
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Apr 1, 2019

PEMplaybook.org

Oct 1, 2018

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Sep 1, 2018

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Aug 1, 2018

Does Your Patient Have Streptococcal Pharyngitis?

No Problem -- I'll just Swab.

Not So Fast...

 

Fagan Nomogram for Likelihood Ratios

1. Decide on your pre-test probability of the disease (choose an approximate probability based on our assessment)
2. Use the likelihood ratio that correlates to your exam.
3. Draw a straight line frm your pre-test probability starting point, to the LR of the feauture/test, take it through to find your post-test probability
4. Use this new post-test probability to help in your decision


Your patient has palatal petechiae, which confers a positive likelihood ratio (LR+) of 2.7
See below how to use this statistic based on your clinical assessment"

Low Probability

Moderate Probability

High Probability

 

List of Likelihood Ratios for Streptococcal Pharyngitis

Symptoms and signs

Positive LR (95% CI)

Negative LR (95% CI)

Sensitivity (95% CI)

Specificity (95% CI)

Scarlatiniform rash

3.91 (2.00-7.62)

0.94 (0.90-0.97)

0.08 (0.05-0.14)

0.98 (0.95-0.99)

Palatal petechiae

2.69 (1.92-3.77)

0.90 (0.86-0.94)

0.15 (0.10-0.21)

0.95 (0.91-0.97)

Chills

2.16 (0.94-4.96)

0.88 (0.79-0.98)

0.21 (0.18-0.24)

0.90 (0.83-0.97)

Anorexia

1.98 (0.83-4.75)

0.53 (0.26-1.10)

0.62 (0.12-1.11)

0.62 (0.12-1.12)

Pharyngeal exudate

1.85 (1.58-2.16)

0.78 (0.74-0.82)

0.38 (0.32-0.44)

0.79 (0.73-0.84)

Vomiting

1.79 (1.56-2.06)

0.85 (0.81-0.90)

0.28 (0.21-0.36)

0.84 (0.79-0.89)

Tender cervical nodes

1.72 (1.54-1.93)

0.78 (0.75-0.81)

0.40 (0.35-0.46)

0.77 (0.71-0.82)

Sibling with sore throat

1.71 (0.82-3.53)

0.92 (0.82-1.03)

0.18 (0.14-0.23)

0.89 (0.83-0.94)

Halitosis

1.54 (0.79-2.99)

0.95 (0.81-1.12)

0.12 (0.05-0.29)

0.92 (0.86-0.99)

Tonsillar and/or pharyngeal exudate

1.40 (1.10-1.77)

0.86 (0.75-0.98)

0.37 (0.28-0.46)

0.74 (0.68-0.78)

Large cervical nodes

1.39 (1.16-1.67)

0.67 (0.53-0.84)

0.64 (0.50-0.76)

0.54 (0.41-0.67)

Lack of cough

1.36 (1.18-1.56)

0.59 (0.48-0.73)

0.73 (0.66-0.78)

0.46 (0.38-0.55)

Tonsillar exudates

1.35 (0.98-1.87)

0.81 (0.63-1.06)

0.46 (0.27-0.67)

0.66 (0.48-0.80)

Tonsillar swelling

1.27 (1.04-1.54)

0.67 (0.52-0.85)

0.70 (0.64-0.76)

0.44 (0.32-0.57)

Dysphagia

1.22 (1.00-1.48)

0.68 (0.51-0.91)

0.72 (0.55-0.85)

0.41 (0.23-0.62)

Headache

1.22 (0.95-1.57)

0.90 (0.77-1.04)

0.39 (0.28-0.51)

0.68 (0.58-0.76)

Lack of coryza

1.21 (1.08-1.35)

0.69 (0.55-0.88)

0.72 (0.64-0.79)

0.40 (0.34-0.48)

Abdominal pain

1.18 (0.92-1.51)

0.95 (0.89-1.03)

0.24 (0.19-0.30)

0.79 (0.75-0.83)

Red tonsils and/or pharynx

1.13 (0.96-1.33)

0.41 (0.16-1.02)

0.93 (0.85-0.96)

0.18 (0.09-0.35)

Reported fever

1.07 (0.96-1.19)

0.86 (0.67-1.11)

0.71 (0.58-0.82)

0.33 (0.23-0.49)

Red tonsils

1.07 (0.86-1.34)

0.82 (0.40-1.69)

0.80 (0.60-1.00)

0.25 (0.00-0.51)

Red pharynx

1.06 (0.95-1.18)

0.56 (0.27-1.17)

0.93 (0.81-0.98)

0.12 (0.03-0.34)

Documented temperature >38° or >38.5°C

1.02 (0.87-1.21)

0.98 (0.83-1.15)

0.50 (0.36-0.63)

0.51 (0.38-0.65)

Summer

0.86 (0.61-1.20)

1.02 (1.00-1.05)

0.13 (0.00-0.33)

0.85 (0.65-1.04)

Arthralgia

0.74 (0.18-3.08)

1.02 (0.97-1.06)

0.09 (0.00-0.25)

0.90 (0.77-1.04)

Conjunctivitis

0.73 (0.46-1.16)

1.02 (0.98-1.05)

0.05 (0.02-0.11)

0.94 (0.85-0.98)

Acute otitis media

0.65 (0.14-2.91)

1.04 (0.93-1.16)

0.03 (0.01-0.05)

0.94 (0.84-1.04)

History of tonsillectomy

0.64 (0.49-0.84)

1.07 (1.03-1.11)

0.11 (0.08-0.13)

0.84 (0.81-0.86)

Hoarseness

0.62 (0.46-0.83)

1.04 (1.03-1.06)

0.06 (0.03-0.12)

0.90 (0.85-0.93)

Diarrhea

0.51 (0.33-0.79)

1.04 (0.99-1.11)

0.03 (0.00-0.06)

0.93 (0.86

Modified from: Shaikh et al. 2012

This post and podcast are dedicated to Sarah Werner for her constant encouragement of the story in all of us.  Check out Write Now with Sarah Werner.

Selected References

Cheung L et al. Throat swab have no influence on the management of patients with sore throats. J Laryngol. 217; 131:977-981.
Ebell MH et al. Rational Clinical Examination: Does This Patient Have Streptococcal Pharyngitis? JAMA. 2000;284(22):2912-2918
Homme JH et al. Duration of Group A Streptococcus PCR positivity following antibiotic treatment of pharyngitis. Diagn Microbiol Infect Dis. 2018 Feb;90(2):105-108.
Nakhoul GN et al. Management of Adults with Acute Streptococcal Pharyngitis: Minimal Value for Backup Strep Testing and Overuse of Antibiotics. J Gen Intern Med. 2013 Jun; 28(6): 830–834.
Oliver J et al. Group A Streptococcus pharyngitis and pharyngeal carriage: A meta-analysis. PLoS Negl Trop Dis. 2018 Mar 19;12(3):e0006335.
Shaikh N, Leonard E, Martin JM. Prevalence of streptococcal pharyngitis and streptococcal carriage in children: a meta-analysis. Pediatrics. 2010 Sep;126(3):e557-64.
Shaikh et al. Accuracy and Precision of the Signs and Symptoms of Streptococcal Pharyngitis in Children: A Systematic Review. J Pediatrics. 2012; 3:487-493.e3

Jul 1, 2018

How do we make the diagnosis?

What now?

 

Concussion in Sport Group Guidelines

Concussion Recognition Tool (for coaches, trainers on field)

Child Sports Concussion Assessment Tool, 5th Ed. (Child SCAT); Ages 5-12

Sports Concussion Assessment Tool, 5th Ed. (SCAT5); Ages 13 and Up

This post and podcast are dedicated to the great K Kay Moody, DO, MPH for her stalwart effort to care for both patient and doctor. Thank you for all that you do to help us to be our best and for promoting #FOAMed #FOAMped and #MedEd.

References

Churchill NW et al. The first week after concussion: Blood flow, brain function and white matter microstructure. Neuroimage Clin. 2017; 14: 480–489.
Ellis MJ et al. Psychiatric outcomes after pediatric sports-related concussion. J Neurosurg Pediatr. 2015; 16:709-718.
Graham R et al. and the Committee on Sports-Related Concussions in Youth; Board on Children, Youth, and Families; Institute of Medicine; National Research Council. Sports-Related Concussions in Youth: Improving the Science, Changing the Culture. Washington (DC): National Academies Press (US); 2014 Feb 4.
Harmon KG et al. American Medical Society for Sports Medicine position statement: concussion in sport. Br J Sports Med. 2013; 47:15-26.
McCrory P et al. Consensus statement on concussion in sport—the 5th international conference on concussion in sport held in Berlin, October 2016. Br J Sports Med. 2016
Purcell LK et al. What factors must be considered in “return to school” following concussion and what strategies or accommodations should be followed? Br J Sports Med. 2018; 0:1-15.
Wang KK et al. An update on diagnostic and prognostic biomarkers for traumatic brain injury. Exp Rev Molec Gen. 2018; 18(2):165-180.
Wang Y et al. Cerebral Blood Flow Alterations in Acute Sport-Related Concussion. J Neurotrauma. 2016 Jul 1; 33(13): 1227–1236.

Jun 1, 2018

PEMplaybook.org

May 1, 2018

PEMplaybook.org

Apr 1, 2018

 

References

Baracco R et al. Pediatric Hypertensive Emergencies. Curr Hypertens Rep. 2014; 16:456.

Belsha CW. Pediatric Hypertension in the Emergency Department. Ann Emerg Med. 2008; 51(3):21-24.

Chandar J et al. Hypertensive crisis in children. Pediatr Nephrol. 2012; 27:741-751.

Dionne JM et al. Hypertension Canada’s 2017 Guidelines for the Diagnosis, Assessment, Prevention, and Treatment of Pediatric Hypertension. Canadian J Cardiol. 2017; 33:577-585

*Flynn JT, Kaelber DC, Baker-Smith CM, et al; SUBCOMMITTEE ON SCREENING AND MANAGEMENT OF HIGH BLOOD PRESSURE IN CHILDREN. Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents. Pediatrics. 2017; 140(3):e20171904

Gilhotra Y et al. Blood pressure measurements on children in the emergency department. Emergency Medicine Australasia. 2006; 18:148-154.

Lurbe E et al. 2016 European Society of Hypertension guidelines for the management of high blood pressure in children and adolescents. J Hypertens. 2016; 34:1-35.

Patel NH et al. Evaluation and management of pediatric hypertensive crises: hypertensive urgency and hypertensive emergencies. Open Access Emergency Medicine. 2012; 4:85-92.

Yang WC et al. Clinical Analysis of Hypertension in Children Admitted to the Emergency Department. Pediatr Neonatol. 2010; 1:44-51.

 

Addendum: Causes of Malignant Hypertension by Age

Infant to Toddler Preschool to School Age Adolescent to Adult
Renal disease Renal disease Primary hypertension
Coarctation of the aorta Coarctation of the aorta Medication non-adherence
Bronchopulmonary dysplasia Drug induced/toxicologic Renal disease
Increased intracranial pressure Increased intracranial pressure Increased intracranial pressure
Volume overload Pheochromocytoma Pheochromocytoma
Congenital adrenal hyperplasia Primary hypertension Drug induced/toxicologic

Adapted from: Constantine E. Hypertension. In: Textbook of Pediatric Emergency Medicine, 6th Ed. Fleischer GR, Ludwig S, Henretig FM (Eds). Lippincott, Williams & Wilkins, Philadelphia. 2010; p315.

 

This post and podcast are dedicated to Manpreet 'Manny' Singh for his collegiality, collaboration, and overall awesomeness. 

Mar 1, 2018

A Social Visit or Your Most Dangerous Presentation Tonight?

[Details in Audio]

This post and podcast are dedicated to Henry Goldstein, B.Pharm, MBBS for his tireless dedication to all things #FOAMed, #FOAMped, and #MedEd.  You are awesome.  Make sure to visit Don't Forget the Bubbles!

References

Cohen GM, Albertini LW. Colic. Pediatr Rev. 2012; 33(7):332-3.

Friedman SB et al. The crying infant: diagnostic testing and frequency of serious underlying disease. Pediatrics. 2009; 123(3):841-8

Herman M, Le A. The crying infant. Emerg Med Clin North Am. 2007 Nov;25(4):1137-59.

Poole SR. The infant with acute, unexplained, excessive crying. Pediatrics. 1991; 88 (3): 450-5.

Prentiss KA, Dorfman DH. Pediatric Opthalmology in the Emergency Department. Emerg. Med. Clin. N. Am. 2008; 26: 181-198.

Shope TR, Rieg TS, Kathiria NN. Corneal abrasions in young infants. Pediatrics. 2010 Mar;125(3):e565-9. Epub 2010 Feb 8.

Feb 1, 2018

You know how to intubate safely.  You can recite all of the Ps backwards and forwards.

Until you can't.

Real-time trouble-shooting.

[Details in Audio]


This post and podcast are dedicated to Mads Astvad for sharing his enthusiasm, clinical excellence, and #FOAMed warrior spirit.

Tak, min ven!  #SMACConia #Vikingeblod

Jan 1, 2018

Ovarian torsion is like the MI of the pelvis.  Sometimes all it takes is a good story to investigate.

When to worry, when to walk it off, and when to work it up:

 

 

What is the typical presentation of ovarian torsion?

There is none.  The presentation varies so much, we need a rule to live by:

Unilateral pelvic pain in a girl is ovarian torsion until proven otherwise.  This includes the cases in which you are concerned about appendicitis.  They both can be fake-outs.

Often the pain is severe and abrupt, but trying to tease this out is often not fruitful.

Here are the often-reported signs and symptoms associated with ovarian torsion:

Stabbing pain, 70%

Nausea and vomiting, 70%

Sudden, sharp pain in the lower abdomen, 59%

Pain radiating to the back, flank, or groin, 51%

Peritoneal signs, 3%

Fever, less than 2%

And of course…no pain on presentation…30%...intermittent torsion.

What is the mechanism of ovarian torsion?

  1. Structurally abnormal ovary (including cysts) that causes the ovary to flop over and twist on its vascular axis
  2. Hypermobile ovary with vigorous movement twists on its vascular pedicle and cuts off blood supply

The Dual Blood Supply to the Ovaries: Why Doppler Flow can Fool You

What ultrasound findings suggest ovarian torsion?

  1. The enlarged hyper or hypoechoic ovary from generalized edema
  2. Peripherally displaced follicles with hyperechoic central stroma – this is called the string of pearls sign, because the stroma is edematous, leaving the follicles to stand out
  3. A midline ovary – if the ovary magically makes it to midline, something is up
  4. Free fluid in the pelvis – this is seen in the vast majority of cases

As far as Doppler flow goes, you may see one of several scenarios:

  1. Little or no venous flow – this is very common, as we talked about, because the low pressure venous system is the first to take a hit in torsion
  2. Totally absent arterial flow – this is not as common, but totally diagnostic
  3. There may be no flow in diastole, or the flow may even be reversed. Rememver the red and blue of dopple does not correspond to arterial and venous.  Doppler is a vector.  Red is fluid coming towards the probe, blue is programmed to present flow away from the probe.  If you have just one or the other, then by definition there is a problem with the vascular circuit.

Other things you may see on ultrasound include focal tenderness with the probe, or the whirlpool sign – this is a twisted vascular pedicle.  

In children, is there an ovarian size (volume) that rules out torsion?”

In the Journal of Pediatric Radiology, Servaes et al catalogued the ultrasound findings in children with surgically confirmed torsion over a 12 year period.  In this case series of 41 patients, the median age was 11.  The age range was one month old to 21 years of age.  They found that in torsed ovaries, the ovarian volume was 12 x that compared to the normal, non-torsed contralateral ovary.

That is to say, in this case series all torsed ovaries were larger than the normal contralateral ovary.

 

Summary

Sudden unilateral lower abdominal or pelvic pain in a female? Think torsion.

Have a low threshold for investigation.

Know the performance characteristics of ultrasound findings and involve a gynecologist early.

 

This post and podcast are dedicated to Stephanie Doniger, MD for her enthusiasm, spirit, and expertise in #MedEd #FOAMed #FOAMped #POCUS 

 
References

Abe M, Sarihan H. Oophoropexy in children with ovarian torsion. Eur. J. Pediatr. Surg. 2004;14:168.

Aziz D, Davis V, Allen L, Langer J. Ovarian torsion in children: Is oophorectomy necessary? J. Pediatr. Surg. 2004;39:750-3.

Bristow RE, Nugent AC, Zahurak ML, et al. Impact of surgeon specialty on ovarian-conserving surgery in young females with an adnexal mass. J. Adolesc. Health 2006;39:411.

Chang YJ, Yan DC, Kong MS, et al. Adnexal torsion in children. Pediatr. Emerg. Care. 2008;24:534-7.

Conforti A, Giorlandino C, Bagolan P. Fetal ovarian cysts management and ovarian prognosis: a report of 82 cases. J. Pediatr. Surg. 2009;44:868; author reply 868-9.

Guthrie BD, Adler MD, Powell EC. Incidence and trends of pediatric ovarian torsion hospitalizations in the United States, 2000-2006. Pediatrics 2010;125:532-8. Epub 2010 Feb 1.

Houry D, Abbott JT. Ovarian torsion: a fifteen-year review. Ann. Emerg. Med. 2001;38:156-9.

Huang TY, Lau BH, Lin LW, Wang TL, Chong CF, Chen CC. Ovarian cyst torsion in a toddler. Am. J. Emerg. Med. 2009;27:632, e1-3.

Hurh PJ, Meyer JS, Shaaban A. Ultrasound of a torsed ovary: characteristic gray-scale appearance despite normal arterial and venous flow on Doppler. Pediatr. Radiol. 2002;32:586-8. Epub 2002 May 25.

Kokoska E, Keller M, Weber T. Acute ovarian torsion in children. Am. J. Surg. 2000;180:462-5.

Oltmann SC, Fischer A, Barber R, Huang R, Hicks B, Garcia N. Cannot exclude torsion – a 15-year review. J. Pediatr. Surg. 2009;44:1212-6; discussion 1217.

Chmitt ER et al. Twist and Shout! Pediatric Ovarian Torsion Clinical Update and Case Discussion. Pediatr Emerg Care. 2013; 29(4):518-523.

Servaes S, Zurakowski D, Laufer MR, Feins N, Chow JS. Sonographic findings of ovarian torsion in children. Pediatr. Radiol. 2007;37:446-51. Epub 2007 Mar 15.

Valsky DV. Added value of the gray-scale whirlpool sign in the diagnosis of adnexal torsion. Ultrasound Obstet. Gynecol. 2010;36:630-4.

Dec 1, 2017

Dogma often dictates routine care.

There are times when we have to attend to paradigm shifts.

An easy way to save lives?  Just say no to (these) drugs:


Codeine

Normally metabolized into codeine-6-glucuronide (50-70%) and norcodeine (10-15%).  Codeine, codeine-6-glucuronide, and norcodeine have low affinity for the μ (mu) receptor.

However, the most active metabolite of codeine is morphine with 200x the affinity for the mu receptor as the codeine derivates.  The problem is, people vary in its metabolism from 0-15% of codeine is metabolized to morphine.

Ok, codeine is lame at best, unpredictable at worst.

True.  Unless you are hiding a genetic time bomb.

You're an ultra-rapid metabolizer.

Some people have multiple extra copies of the DNA sequence for the CYP2D6 enzyme.  Ultra rapid metabolizers funnel a huge proportion of their codeine into morphine metabolism, resulting in a bolus of morphine, ending in apnea.

Promethazine with codeine

This combination is no better than placebo -- all of the risks, with no proven benefit.  This combination is notoriously abused -- as purple drank or sizzurp.  The rapper Pimp C died of this.

Speaking of cough syrups...

The AAP recommends no cough and cold preparations in children under age 6.  They have not been adequately studied in young children, and are not recommended for treating the common cold.

What then?  You gotta give me something, doctor!

Ok, Honey!

In a study in the Archives of Pediatric and Adolescent Medicine, Dr Paul and colleagues published: Effect of honey, dextromethorphan, and no treatment on nocturnal cough and sleep quality for coughing children and their parents.  They compared a buckwheat honey, honey-flavored dextromethorphan (DM) and no treatment 30 min before bed for children with upper respiratory tract infections.

Of the three, honey, dextromethorphan, and no treatment – honey scored the best for symptom improvement and cough frequency.

Over age 1?  Cough and cold?  Honey.  There is no concern about accidental overdose, parents are doing something with a proven effect, and compliance is pretty much 100% -- and Grandma approves.

Dextromethorphan

No proven benefit over placebo.  Also widely abused, in pill form ("Skittles") and/or liquid form mixed in alcoholic beverage ("robotripping").

Alternatives to Codeine

Details in Audio:

Morphine liquid

Acetaminophen and Hydrocodone

 

PEARLS AND PITFALLS IN PEDIATRIC PAIN

Allow the child to speak for himself whenever possible. After acknowledging the parent’s input, perhaps try “I want to make sure I understand how the pain is for you. Tell me more.”

Engage parents and communicate the plan to them. Elicit their expectations, and give them of preview of what to expect in the ED.

Opioids are meant for pain caused by acute tissue injury, for the briefest period of time feasible. Older school-aged children and adolescents are increasingly at risk for opioid dependence and addiction.

Give detailed advice on how to manage pain at home. Set expectations. Let them know you understand and will help them through your good advice that will carry them through this difficult time. Patients and families often just need a plan. Map it out clearly.

And...

Just say no to: codeine, promethazine with codeine, and dextramethorphan.

Selected References

Dhaliwal G, Hsu D. Tramadol Ultra Rapid Metabolizers at Risk for Respiratory Depression. Pain Physician. 2016; 19(2):E361.

European Medicines Agency. Restriction on the use of codeine for pain relief in children—CMDh endorses PRAC recommendation [press release]. June 28, 2013.

FDA. Most Young Children With a Cough or Cold Don't Need Medicine.

Hartling L et al. How Safe Are Common Analgesics for the Treatment of Acute Pain for Children? A Systematic Review. Pain Res Manag. 2016; 2016: 5346819.

Grond S, Sablotzki A. Clinical pharmacology of tramadol. Clin Pharmacokinet. 2004;43(13):879-923.

Jin J. Risks of Codeine and Tramadol in Children. JAMA. 2017 Oct 17;318(15):1514. doi: 10.1001/jama.2017.13534.

Kelly LE et al. More Codeine Fatalities After Tonsillectomy in North American Children. Pediatrics. 2012; 129(5).

Kirchheiner J, Schmidt H, Tzvetkov M, et al. Pharmacokinetics of codeine and its metabolite morphine in ultra-rapid metabolizers due to CYP2D6 duplication. Pharmacogenomics J. 2007;7(4):257–265

Orliaguet G et al. A Case of Respiratory Depression in a Child With Ultrarapid CYP2D6 Metabolism After Tramadol. Pediatrics. 2015; 135(3).

Poonai N. Analgesia for children in acute pain in the post-codeine era. Curr Pediatr Rev. 2017 Aug 28. doi: 10.2174/157339631366617082911563.1.

 

This post and podcast are dedicated to Bryan Hayes, PharmD for his practical approach to pharmacologic conundrums and to David Juurlink, MD, PhD for his steadfast dedication to patient safety and clinician education.  Check out Bryan's helpful blog and clinical resource, PharmERToxGuy.  Check out David anywhere one utters the word Tra-ma-dol.

Nov 1, 2017

Not all head trauma is minor.

Not all minor head trauma is clinically significant.

 

How can we sort out the overtly ok from the sneakily serious?

 

 

Mnemonics for bedside risk stratification of minor pediatric blunt head trauma, based on PECARN studies:

[Details in Audio]

 

Blunt Head Trauma in Children < 2 years of Age

 

 

Blunt Head Trauma in Children ≥ 2 years of Age

 

 

Image Gently Campaign

 

Medical Imaging Record (maintain like an immunization card)

 

Brochure for Parents: Just in Time Education

 

Selected References

Dayan PS et al. Association of Traumatic Brain Injuries with Vomiting in Children with Blunt Head Trauma. Ann Emerg Med. 2014; 63(6):657-665.

Dayan PS et al. Headache in Traumatic Brain Injuries from Blunt Head Trauma. Pediatrics. 2015; 135(3):504-512.

Horeczko T, Kuppermann N. To scan or not to scan: pediatric minor head trauma in your office, clinic or emergency department. Contemporary Pediatrics. 2012;29(8):40-47.

Kupperman et al. Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009;374(9696):1160-70.

Lee LK et al. Isolated Loss of Consciousness in Children with Minor Blunt Head Trauma. JAMA Pediatr. 2014; 168(9):837-843.

Magana JN, Kuppermann N. The PECARN TBI Rules Do Not Apply To Abusive Head Trauma. Acad Emerg Med. 2017; 24(3)382-384.

Rogers AJ et al. Children with Arachnoid Cysts who Sustain Blunt Head Trauma: Injury Mechanisms and Outcomes. Acad Emerg Med. 2016; 23:358-361.

 

This post and podcast are dedicated to Kevin Klauer, DO, EJD, FACEP for his dedication to education, and for his unique balance of safety and keeping it real.  Thank you.

Oct 1, 2017

Comfortable with G-tubes, tracheostomies, and VP shunts?

Good. 

Get ready for the next level: Vagus Nerve Stimulators, Intrathecal Pumps, and Ventricular Assist Devices.

 

Details in Audio:

Vagus Nerve Stimulators

For intractable epilepsy; sends retrograde signal up corona radiata

Also may be used in: depression, bulimia, Alzheimer, narcolepsy, addiction, and others

VNS magnets

Are VNS safe in MRI?

Are VNS safe in everyday life?

Intrathecal Pumps

Used to infuse basal rate of drug, usually baclofen for spasticity, but pump may contain morphine, bupivicaine, clonidine.  Also used for severe MS, stroke, TBI, chronic pain.  Verify the medication and identify the toxidrome if symptomatic.

Ventricular Assist Devices

May be left ventricular assist, right ventricular assist, or biventricular assist device.

 

References

Vagus Nerve Stimulators (VNS)

Elliott RE, Rodgers SD, Bassani L et al. Vagus nerve stimulation for children with treatment-resistant epilepsy: a consecutive series of 141 cases. J Neurosurg Pediatrics. 2011; 7:491-500.

Groves DA, Brown VJ. Vagal nerve stimulation: a review of its applications and potential mechanisms that mediate its clinical effects. Neuroscience and Biobehavioral Reviews. 2005; 29: 493–500.

Panebianco M, Rigby A,Weston J,Marson AG. Vagus nerve stimulation for partial seizures. Cochrane Database of Systematic Reviews. 2015; 4, Art. No.: CD002896.

Ruffoli R,  Giorgi FS, Pizzanelli C et al. The chemical neuroanatomy of vagus nerve stimulation. Journal of Chemical Neuroanatomy; 2011; 42: 288–296.

Intrathecal Pumps

Borowski A, Littleton AG, Borkhuu B et al. Complications of Intrathecal Baclofen Pump Therapy in Pediatric Patients. J Pediatr Orthop. 2010; 30:76–81.

Ghosh D, Mainali G, Khera J, Luciano M.  Complications of Intrathecal Baclofen Pumps in Children: Experience from a Tertiary Care Center. Pediatr Neurosurg. 2013; 49:138–144.

Yang TF, Wang JC, Chiu JW et al. Ultrasound-guided refilling of an intrathecal baclofen pump—a case report. Childs Nerv Syst. 2013; 29:347–349.

Yeh RN, Nypaver MM, Deegan TJ, Ayyangar R. Baclofen Toxicity in an 8-year-old with an Intrathecal Baclofen Pump. J Emerg Med. 2004; 26(4): 163–167.

Ventricular Assist Devices

Blume ED, Naftel DC, Bastardi HJ et al. for the Pediatric Heart Transplant Study Investigators. Outcomes of Children Bridged to Heart Transplantation With Ventricular Assist Devices: A Multi-Institutional Study. Circulation. 2006; 113: 2313-2319.

Colón JE, Laborde ME, Nossaman BD. Case Report: Left Ventricular Assist Device in a 12 Year Old Child as a Bridge to Heart Transplantation. Section of Congenital Cardiac Anesthesia, Ochsner Medical Center, New Orleans, Louisiana. 2012.

Fan Y, Weng YG, Huebler M et al. Predictors of In-Hospital Mortality in Children After Long-Term Ventricular Assist Device Insertion. J Amer Coll Cardiol. 2011; 58(11):1183–90

Fraser CD,  Jaquiss RDB, Rosenthal DN et al. Prospective Trial of a Pediatric Ventricular Assist Device. N Engl J Med. 2012;367:532-41.

Gazit AZ, Gandhi SK, Canter CC. Mechanical Circulatory Support of the Critically Ill Child Awaiting Heart Transplantation. Current Cardiology Reviews. 2010; 6: 46-53.

VanderPluym CJ, Fynn-Thompson F, Blume ED.  Ventricular Assist Devices in Children Progress With an Orphan Device Application. Circulation. 2014;129:1530-1537.

This post and podcast are dedicated to Joe Bellezzo, MD, FACEP and Zack Shinar, MD, FACEP for bringing us all up to speed.  Listen to their fantastic ED ECMO podcast here.

Aug 1, 2017

Abdominal pain is common; so are strongly held myths and legends about what is concerning, and what is not.

 

One of our largest responsibilities in the Emergency Department is sorting out benign from surgical or medical causes of abdominal pain.  Morbidity and mortality varies by age and condition.  

Abdominal Surgical Emergencies in Children: A Relative Timeline

General Advice

Neonate (birth to one month)

Necrotizing Enterocolitis

Pneumatosis Intestinalis.

Essentials:

  • Typically presents in 1st week of life (case reports to 6 months in chronically ill children)
  • Extend suspicion longer in NICU graduates
  • Up to 10% of all cases of necrotizing enterocolitis are in full-term children
  • Pathophysiology is unknown, but likely a translocation of bacteria

Diagnosis:

  • Feeding intolerance, abdominal distention
  • Abdominal XR: pneumatosis intestinalis

Management:

  • IV access, NG tube, broad-spectrum antibiotics, surgery consult, ICU admission

Intestinal Malrotation with Volvulus

Essentials:

Corkscrew Sign in Malrotation with Volvulus
  • Bilious vomiting (80-100%) in the 1st month; especially in the 1st week
  • May look well initially, then rapidly present in shock
  • Ladd’s bands: abnormally high tethering of cecum to abdominal wall; peristalsis, volvulus, ischemia

Diagnosis:

  • History of bilious emesis is sufficient to involve surgeons
  • Upper GI series: corkscrew appearance
  • US (if ordered) may show abnormal orientation of and/or flow to superior mesenteric artery and vein

Management:

  • Stat surgical consult
  • IV access, resuscitation, NG tube to decompress (bowel wall perfusion at risk, distention worsens)

Hirschprung Disease

Essentials:

  • Problem in migration of neural crest cells
  • Aganglionic colon (80% rectosigmoid; 15-20% proximal to sigmoid; 5% total colonic aganglionosis) colon (known as short-segment disease)
  • Poor to no peristalsis: constipation, perforation, and/or sepsis

Diagnosis:

  • May be diagnosed early as “failure to pass meconium in 1st 48 hours”
  • In ED, presents as either bowel obstruction or enterocolitis
  • Contrast enema
  • Beware of the toxic megacolon (vomiting, distention, sepsis)

Management:

  • Resuscitation, antibiotics, NG tube decompression, surgical consultation; stable patients may need rectal biopsy for confirmation
  • Staged surgery (abdominoperineal pull-through with diverting colostomy, subsequent anastomosis) versus one-stage repair.

Infant and Toddler (1 month to 2 years)

Pyloric Stenosis

Essentials:

  • Hypertrophy of pyloric sphincter; genetic, environmental, exposure factorsString Sign in Pyloric Stenosis.

Diagnosis:

  • Hungry, hungry, not-so-hippos; they want to eat all of the time, but cannot keep things down
  • Poor weight gain (less than 20-30 g/day)
  • US: “π–loric stenosis” (3.14); pylorus dimensions > 3 mm x 14 mm
  • UGI: “string sign”

Management:

  • Trial of medical treatment with oral atropine via NGT (muscarinic effects decrease pyloric tone)
  • Ramstedt pyloromyotomy (definitive)

Intussusception

Essentials:

  • Majority (90%) ileocolic; no pathological lead point
  • Small minority (4%) ileoileocolic due to lead point: Meckel’s diverticulum, polyp, Peyer’s patches, Henoch-Schönlein purpura (intestinal hematoma)

Diagnosis:

Target Sign (Donut Sign).
  • Ultrasound sensitivity and specificity near 100% in experienced hands
  • Abdominal XR may show non-specific signs; used mainly to screen for perforation before reduction

Management:

  • Hydrostatic enema: contrast (barium or water-soluble contrast with fluoroscopy) or saline (with ultrasound)
  • Air-contrast enema: air or carbon dioxide (with either fluoroscopy or ultrasound); higher risk for perforation than hydrostatic (1% risk), but generally safer than perforation from contrast
  • Consider involving surgical service early (precaution before reduction)
  • Traditional disposition is admission; controversial: home discharge from ED

Young Child and Older (2 years and up)

Appendicitis

Essentials:

  • Appendicitis occurs in all ages, but rarer in infants. Infants do not have fecalith; rather they have some other anatomic or congenital condition. 
  • More common in school-aged children (5-12 years) and adolescents
  • Younger children present atypically, more likely to have perforated when diagnosed.

Diagnosis:

  • Non-specific signs and symptoms
  • Often have abdominal pain first; vomiting comes later
  • Location/orientation of appendix varies
  • Appendicitis scores vary in their performance
  • Respect fever and abdominal pain

 

Management:

  • Traditional: surgical
  • On the horizon: identification of low-risk children who may benefit from trial of antibiotics
  • If perforated, interval appendectomy (IV antibiotics via PICC for 4-6 weeks, then surgery)

Obstruction

SBO. Incarcerated Inguinal Hernia.

Essentials:

  • Same pathophysiology and epidemiology as adults: “ABC” – adhesions, “bulges” (hernias), and cancer.

Diagnosis:

  • Obstruction is a sign of another condition. Look for cause of obstruction: surgical versus medical
  • Abdominal XR in low pre-test probability
  • CT abdomen/pelvis for moderate-to-high risk; confirmation and/or surgical planning

Management:

  • Treat underlying cause
  • NG tube to low intermittent wall suction
  • Admission, fluid management, serial examinations

 

Take these pearls home:

  • Consider surgical pathology early in encounter
  • Resuscitate while you investigate
  • Have a low threshold for imaging and/or consultation, especially in preverbal children

 

Selected References

Necrotizing Enterocolitis

Neu J, Walker A. Necrotizing Enterocolitis. N Eng J Med. 2011; 364(3):255-264.

Niño DF et al. Necrotizing enterocolitis: new insights into pathogenesis and mechanisms. Nature. 2016; 13:590-600.

Walsh MC et al. Necrotizing Enterocolitis: A Practitioner’s Perspective. Pediatr Rev. 1988; 9(7):219-226.

Malrotation with Midgut Volvulus

Applegate KE. Intestinal Malrotation in Children: A Problem-Solving Approach to the Upper Gastrointestinal Series. Radiographics. 2006; 26:1485-1500.

Kapfer SA, Rappold JF. Intestinal Malrotation – Not Just the Pediatric Surgeon’s Problem. J Am Coll Surg. 2004; 199(4):628-635.

Lee HC et al. Intestinal Malrotation and Catastrophic Volvulus in Infancy. J Emerg Med. 2012; 43(1):49-51.

Martin V, Shaw-Smith C. Review of genetic factors in intestinal malrotation. Pediatr Surg Int. 2010; 26:769-781.

Nehra D, Goldstein AM. Intestinal malrotation: Varied clinical presentation from infancy through adulthood. Surgery. 2010; 149(3):386-391.

Hirschprung Disease

Amiel J, Sproat-Emison E, Garcia-Barcelo M, et al. Hirschsprung disease, associated syndromes and genetics: a review. J Med Genet 2008; 45:1.

Arshad A, Powell C, Tighe MP. Hirschsprung's disease. BMJ 2012; 345:e5521.

Aworanti OM, McDowell DT, Martin IM, Quinn F. Does Functional Outcome Improve with Time Postsurgery for Hirschsprung Disease? Eur J Pediatr Surg 2016; 26:192.

Clark DA. Times of first void and first stool in 500 newborns. Pediatrics 1977; 60:457.

Dasgupta R, Langer JC. Evaluation and management of persistent problems after surgery for Hirschsprung disease in a child. J Pediatr Gastroenterol Nutr 2008; 46:13.

De Lorijn F, Reitsma JB, Voskuijl WP, et al. Diagnosis of Hirschsprung's disease: a prospective, comparative accuracy study of common tests. J Pediatr 2005; 146:787.

Doig CM. Hirschsprung's disease and mimicking conditions. Dig Dis 1994; 12:106.

Khan AR, Vujanic GM, Huddart S. The constipated child: how likely is Hirschsprung's disease? Pediatr Surg Int 2003; 19:439.

Singh SJ, Croaker GD, Manglick P, et al. Hirschsprung's disease: the Australian Paediatric Surveillance Unit's experience. Pediatr Surg Int 2003; 19:247.

Suita S, Taguchi T, Ieiri S, Nakatsuji T. Hirschsprung's disease in Japan: analysis of 3852 patients based on a nationwide survey in 30 years. J Pediatr Surg 2005; 40:197.

Sulkowski JP, Cooper JN, Congeni A, et al. Single-stage versus multi-stage pull-through for Hirschsprung's disease: practice trends and outcomes in infants. J Pediatr Surg 2014; 49:1619.

Pyloric Stenosis

Aspelund G, Langer JC. Current management of hypertrophic pyloric stenosis. Semin Pedaitr Surg. 2007; 16:27-33.

Dias SC et al. Hypertrophic pyloric stenosis: tips and tricks for ultrasound diagnosis. Insights Imaging. 2012; 3:247-250.

Kawahara H et al. Medical treatment of infantile hypertrophic pyloric stenosis: should we always slice the olive? J Pediatr Surg. 2005; 40:1848-1851.

Mack HC. Adult Hypertrophic Pyloric Stenosis. Arch Inter Med. 1959; 104:78-83.

Meissner PE et al. Conservative treatment of infantile hypertrophic pyloric stenosis with intravenous atropine sulfate does not replace pyloromyotomy. Pediatr Surg Int. 2006; 22:1021-1024.

Mercer AE, Phillips R. Can a conservative approach to the treatment of hypertrophic pyloric stenosis with atropine be considered a real alternative to pyloromyotomy? Arch Dis Child. 2013; 95(6): 474-477.

Pandya S, Heiss K, Pyloric Stenosis in Pediatric Surgery.Surg Clin N Am. 2012; 92:527-39.

Peters B et al. Advances in infantile hypertrophic pyloric stenosis. Expert Rev Gastroenterol Hepatol. 2014; 8(5):533-541.

Intussusception

Apelt N et al. Laparoscopic treatment of intussusception in children: A systematic review. J Pediatr Surg. 2013; 48:1789-1793.

Applegate KE. Intussusception in Children: Imaging Choices. Semin Roentgenol. 2008; 15-21.

Bartocci M et al. Intussusception in childhood: role of sonography on diagnosis and treatment. J Ultrasound. 2015; 18 Gilmore AW et al. Management of childhood intussusception after reductiion by enema. Am J Emerg Med. 2011; 29:1136-1140.:205-211.

Chien M et al. Management of the child after enema-reduced intussusception: hospital or home? J Emerg Med. 2013; 44(1):53-57.

Cochran AA et al. Intussusception in traditional pediatric, nontraditional pediatric, and adult patients. Am J Emerg Med. 2011; 523-527.

Loukas M et al. Intussusception: An Anatomical Perspective With Review of the Literature. Clin Anatomy. 2011; 24: 552-561.

Mendez D et al. The diagnostic accuracy of an abdominal radiograph with signs and symptoms of intussusception. Am J Emerg Med. 2012; 30:426-431.

Whitehouse et al. Is it safe to discharge intussusception patients after successful hydrostatic reduction? J Pediatr Surg. 2010; 45:1182-1186.

Appendicitis

Amin P, Chang D. Management of Complicated Appendicitis in the Pediatrc Population: When Surgery Doesn’t Cut it. Semin Intervent Radiol. 2012; 29:231-236

Blakely ML et al. Early vs Interval Appendectomy for Children With Perforated Appendicitis. Arch Surg. 2011; 146(6):660-665.

Bundy DG et al. Does This Child Have Appendicitis? JAMA. 2007; 298(4):438-451.

Cohen B et al. The non-diagnostic ultrasound in appendicitis: is a non-visualized appendix the same as a negative study? J Pediatr Surg. 2015 Jun;50(6):923-7

Herliczek TW et al. Utility of MRI After Inconclusive Ultrasound in Pediatric Patients with Suspected Appendicitis. AJT. 2013; 200:969-973.

Janitz et al. Ultrasound Evaluation for Appendicitis. J Am Osteopath Coll Radiol. 2016; 5(1):5-12.

Kanona H et al. Stump Appendicitis: A Review. Int J Surg. 2012; 10:4255-428.

Kao LS et al. Antibiotics vs Appendectomy for Uncomplicated Acute Appendicitis. Evid Based Rev Surg. 2013;216(3):501-505.

Petroianu A. Diagnosis of acute appendicitis. Int J Surg. 2012; 10:115-119.

Mazeh H et al. Tip appendicitis: clinical implications and management. Amer J Surg. 2009; 197:211-215.

Puig S et al. Imaging of Appendicitis in Children and Adolescents. Semin Roentgenol. 2008; 22-28.

Schizas AMP, Williams AB. Management of complex appendicitis. Surgery. 2010; 28(11):544-548.

Shogilev DJ et al. Diagnosing Appendicitis: Evidence-Based Review. West J Emerg Med. 2014; 15(4):859-871.

Wray CJ et al. Acute Appendicitis: Controversies in Diagnosis and Management. Current Problems in Surgery. 2013; 50:54-86

Intestinal Obstruction

Babl FE et al. Does nebulized lidocaine reduce the pain and distress of nasogastric tube insertion in young children? A randomized, double-blind, placebo-controlled trial. Pediatrics. 2009 Jun;123(6):1548-55

Chinn WM, Zavala DC, Ambre J. Plasma levels of lidocaine following nebulized aerosol administration. Chest 1977;71(3):346-8.

Cullen L et al. Nebulized lidocaine decreases the discomfort of nasogastric tube insertion: a randomized, double-blind trial. Ann Emerg Med. 2004 Aug;44(2):131-7.

Gangopadhyay AN, Wardhan H. Intestinal obstruction in children in India. Pediatr Surg Int. 1989; 4:84-87.

Hajivassiliou CA. Intestinal Obstruction in Neonatal/Pediatric Surgery. Semin Pediatr Surg. 2003; 12(4):241-253.

Hazra NK et al. Acute Intestinal Obstruction in children: Experience in a Tertiary Care Hospital. Am J Pub Health Res. 2015; 3(5):53-56.

Kuo YW et al. Reducing the pain of nasogastric tube intubation with nebulized and atomized lidocaine: a systematic review and meta-analysis. J Pain Symptom Manage. 2010 Oct;40(4):613-20.  .

Pediatric Surgery

Irish MS et al. The Approach to Common Abdominal Diagnoses in Infants and Children. Pedaitr Clin N Am. 1998; 45(4):729-770.

Louie JP. Essential Diagnosis of Abdominal Emergencies in the First Year of Life. Emerg Med Clin N Am. 2007; 25:1009-1040.

McCullough M, Sharieff GQ. Abdominal surgical emergencies in infants and young children. Emerg Med Clin N Am. 2003; 21:909-935.

Pepper VK et al. Diagnosis and Management of Pediatric Appendicitis, Intussusception, and Meckel Diverticulum. Surg Clin N Am. 2012

 

This post and podcast are dedicated to Mr Ross Fisher for his passion and spirit of collaboration in all things #FOAMed.  Thank you, sir!

Jun 1, 2017

Myocardial infarction (MI) in children is uncommon, but underdiagnosed.  This is due to two main factors: the etiologies are varied; and the presenting symptoms are “atypical”.

We need a mental metal detector! 

Case examples

Congenital

Two main presentations of MI due to congenital lesions: novel and known.  The novel presentation is at risk for underdiagnosis, due to its uncommonness and vague, atypical symptoms.  There are usually some red flags with a careful H&P.  The known presentation is a child with a history of congenital heart disease, addressed by corrective or palliative surgery.  This child is at risk for expected complications, as well as overdiagnosis and iatrogenia.  Risk stratify, collaborate with specialists.

The fussy, sweaty feeder: ALCAPA

Anomalous Left Coronary Artery from the Pulmonary Artery (ALCAPA) is an example of what can go wrong during fetal development: any abnormality in the number, origin, course, or morphology of the coronary arteries can present as a neonate with sweating during feeds (steal syndrome), an infant in CHF, or an older child with failure to thrive or poor exercise tolerance.

The stable child with chest pain: myocardial bridge

Normal coronary arteries run along the epicardial surface of the heart, with projections into the myocardium.  If part of the artery’s course runs within the myocardium (i.e. the artery weaves into and/or out of the myocardium), then there is a myocardial bridge of the coronary artery.  With every systolic contraction, the artery is occluded. 

Although a myocardial bridge may not cause symptoms (especially at distal portions), the area it supplies is at risk.

With any minor trauma or exertion, demand may outpace supply, resulting in ischemia. 

Diagnosis is made on coronary angiography.

The unwell child post-cardiac surgery: Fontan problems

The child with single ventricle physiology may have a Norwood procedure at birth (creation of a neoaorta, atrial septectomy, and Blalock-Taussig shunt), a Bidirectional Glenn procedure at 3-6 months (shunt removed, superior vena cava connected to pulmonary arteries), and a Fontan procedure at about 2-3 years of age (inferior vena cava blood flow is shunted into the pulmonary arteries).

These children depend on their preload to run blood passively into the pulmonary circuit; afterload reduction is also important to compensate for a poor left ejection fraction, as well as to avoid the development of pulmonary hypertension.  They are typically on an anticoagulant (often aspirin), a diuretic (e.g. furosemide), and an afterload reduction agent (e.g. enalapril). 

Any disturbance in volume status (hyper- or hypovolemia), anticoagulation, or afterload may cause myocardial strain or infarction.  Take the child s/p Fontan seriously and involve his specialists early with any concerns.

Autoimmune

The body’s inflammatory-mediated reaction to a real or perceived insult can cause short- and long-term cardiac sequelae.  Find out how well the underlying disease is controlled, and what complications the child has had in the past.

The red, hot, crispy, flaky child: acute Kawasaki disease

Kawasaki disease (KD) is an acute systemic vasculitis, diagnosed by the presence of fever for five or more days accompanied by four or more criteria:  bilateral conjunctival injection, mucositis, cervical lymphadenopathy, polymorphous rash, and palmar or sole desquamation.  The criteria may occur (and disappear) at any time during the illness.

Infants are under double jeopardy with Kawasaki Disease.  They are more likely to have incomplete KD (i.e. not fulfill strict criteria) and if they have KD, they are more likely to suffer the dangerous consequences of aneurysm formation (chiefly coronary arteries, but also brain, kidney).  Have a low threshold for investigation.

Treatment includes 2 g/kg/day IVIG and high-dose aspirin (30-50 mg/kg/day) acutely, then low-dose aspirin (5 mg/kg/day) for weeks to months.  Regular and long-term follow-up with Cardiology is required.

The aftermath: sequelae of Kawasaki disease

The family and child with a history of KD may have psychological trauma and continuous anxiety about the child’s risk of MI.  Approximately 4.7% of children who were promptly diagnosed and correctly treated will go on to have cardiac sequelae.

Children who have no detected cardiac sequelae by 8 weeks, typically continue to be asymptomatic up to 20 years later. 

Smaller aneurysms tend to regress over time, especially those < 6 mm.

Thrombi may calcify, or the lumen may become stenotic due to myofibroblast proliferation.  Children with any coronary artery dilatation from KD should be followed indefinitely.

Giant aneurysms (≥8 mm) connote the highest risk for MI. 

Parents often are concerned about recurrence, and any subsequent fever can be distressing.  There is a low rate of recurrence for KD: approximately 2%.  Infants who have coronary aneurysms are at the highest risk for recurrence.

The older child with vague chest complaints and hypercoagulability: Systemic Lupus Erythematosus and Anti-Phospholipid Syndrome

Up to 15% of cases of SLE begin in childhood.  Adult criteria are used, with the caveat that the diagnosis of SLE in children can be challenging; many children only manifest a few of the criteria initially before going on to develop further systemic involvement.

The Systemic Lupus International Collaborating Clinics (SLICC) revised the criteria in 2012.  The patient should have ≥4/17 clinical and/or immunologic criteria.  The clinical criteria are: acute cutaneous (malar); chronic cutaneous (discoid); oral; alopecia; synovitis; serositis; renal; neurologic; hemolytic anemia; leukopenia; or thrombocytopenia.  The immunologic criteria are: ANA; anti-dsDNA; anti-Sm; antiphospholipid; low complement; and/or Direct Coombs (in absence of hemolytic anemia).  At least one criterion should be clinical, and at least one should be immunologic

Children with antiphospholipid syndrome (APS) may occur with or without SLE.  Patients are at risk for venous and arterial thrombi formation.  APS may also cause structural damage, such as valvular thickening and valvular nodes (Libman-Sacks endocarditis).  Mitral and aortic valves are at the highest risk.

Although most children with chest pain will not have MI, those with comorbidities should be investigated carefully.

Trauma

Direct, blunt trauma to the chest can cause myocardial stunning, dysrhythmias, or an asymptomatic rise in Troponin I.  However, some children are at risk for disproportionate harm due to a previously unknown risk factor.  Clinically significant cardiac injury occurs in up to 20% of patients with non-penetrating thoracic trauma.

The motor vehicle collision: blunt myocardial injury

Direct trauma (steering wheel, airbag, seatbelt), especially in fast acceleration-deceleration injury, may cause compression of the heart between the sternum and the thoracic spine.

Electrocardiography (ECG) should be performed on any patient with significant blunt chest injury.  A negative ECG is highly consistent with no significant blunt myocardial injury.

Any patient with a new abnormality on ECG (dysrhythmia, heart block, or signs of ischemia) should be admitted for continuous ECG monitoring.

Elevation in troponin is common, but not predicted.  A solitary elevated troponin without ECG abnormality is of unclear significance.  Author’s advice: obtain troponin testing if there is an abnormal ECG, more than fleeting suspicion of BCI, and/or the child will be admitted for monitoring.

Hemodynamically labile children should be resuscitated and a stat transesophageal echocardiogram obtained.

The high-velocity object: coronary artery dissection or thrombus

Direct trauma (e.g. MVC, baseball, high-velocity soccer ball) may cause damage to the left anterior descending artery or left circumflex artery, at the highest risk due to their proximity to the chest wall.  Thrombosis and/or dissection may result, often presenting in a focal pattern of ischemia on the ECG.

Echocardiography may reveal valvular damage related to the injury, as well as effusion and ejection fraction.  Since there is often a need to investigate the coronary anatomy, percutaneous coronary intervention (PCI) is recommended.

The minor trauma with disproportionate complaint: myocardial bridge

As mentioned in the congenital section (above), a known variation of a coronary artery’s course involves weaving in and out of the myocardium, creating a baseline risk for ischemia.  Even minor trauma in a child with a myocardial bridge may cause acute thrombus, or slow stenosis from resulting edema.  Unfortunately, the presence of myocardial bridging is often unknown at the time of injury.  Approximately 25% of the population may have myocardial bridging, based on autopsy studies. Take the child seriously who has disproportionate symptoms to what should be a minor injury.

Hematologic

Coagulopathic and thrombophilic states may predispose children to focal cardiac ischemia.  The best documented cormorbidity is sickle cell disease, although other pro-thrombotic conditions also put the child at risk.

The child with sickle cell disease and chest pain: when it’s not acute chest syndrome

Sickle cell disease (SCD) can affect any organ system, although the heart is traditionally considered a lower-risk target organ for direct sickling and ischemia.  The major cardiac morbidity in sickle cell is from strain, high-output failure and multiple, serial increases in myocardial demand, causing left ventricular hypertrophy and congestive heart failure.

However, there is mounting evidence that acute myocardial ischemia in sickle cell disease may be underappreciated and/or attributed to other causes of chest pain.

Other cardiac sequelae from SCD include pulmonary hypertension, left ventricular dysfunction, right ventricular dysfunction, and chronic iron overload.

Evidence of myocardial ischemia/infarction in children with SCD has been demonstrated on single-photon emission computed tomography (SPECT) scan.

The puffy faced child with chest pain: nephrotic syndrome hypercoagulability

Children who suffer from nephrotic syndrome lose proteins that contribute to the coagulation cascade.  In addition, lipoprotein profiles are altered: there is a rise in the very low-density lipoproteins (LDL), contributing to accelerated atherosclerosis.  Typically nephrotic patients have normal levels of high-density lipoproteins (HDL), unless there is profuse proteinuria.

Children with difficult-to-control nephrotic syndrome (typically steroid-resistant) may form accelerated plaques that rupture, causing focal MI, as early as school age.

The previously well child now decompensated: undiagnosed thrombophilia

Asymptomatic patent foramen ovale (PFO) is the cause of some cases of cryptogenic vascular disease, such as stroke and MI.  However, the presence of PFO alone does not connote higher risk.  When paired with an inherited or acquired thrombogenic condition, the venous thrombus may travel from the right-sided circulation to the left, causing distal ischemia.  Many of these cases are unknown until a complication arises.

The chronically worried, now with a reason: hypercholesterolemia

A family history of adult-onset hypercholesterolemia is not necessarily a risk factor for early complications in children, provided the child does not have the same acquired risk factors as adults (e.g. obesity, sedentary lifestyle, smoking, etc).  Parents may seek help in the ED for children with chest pain and no risk factors, but adult parents who have poor cholesterol profiles.

The exception is the child with familial hypercholesterolemia, who is at risk for accelerated atherosclerosis and MI.

Infectious

Myocarditis has varied etiologies, including infectious, medications (chemotherapy agents), immunologic (rheumatologic, transplant rejection), toxins (arsenic, carbon monoxide, heavy metals such as iron or copper), or physical stress (electrical injury, heat illness, radiation).

In children, the most common cause of myocarditis is infectious (viruses, protozoa, bacteria, fungal, parasites).  Of these, viral causes are the most common (adenovirus, enterovirus, echovirus, rubella, HHV6).

The verbal child may complain of typical chest complaints, or may come in with flu-like illness and tachycardia or ill appearance out of proportion to presumed viral illness.

The most common presenting features in children with myocarditis are: shortness of breath, vomiting, poor feeding, hepatomegaly, respiratory distress, and fever.

The infant in shock after a ‘cold’: myocarditis

Beware of the poor feeding, tachycardic, ill appearing infant who “has a cold” because everyone else around him has a ‘cold’.  That may very well be true, but any virus can be invasive with myocardial involvement.  Infants are only able to increase their cardiac output through increasing their heart rate; they cannot respond to increased demands through ionotropy.  Look for signs of acute heart failure, such as hepatomegaly, respiratory distress, and sacral edema.

The child with tachycardia out of proportion to complaint: myocarditis

The previously healthy child with “a bad flu” may simply be very symptomatic from influenza-like illness, or he may be developing myocarditis.  Look for chest pain and tachycardia out of proportion to presumed illness, and constant chest pain, not just associated with cough.

The “pneumonia” with suspicious chest x-ray: myocarditis

Acute heart failure may mimic viral pneumonia.  Look for disproportionate signs and symptoms.

Toxins

Younger children may get into others’ medications, be given dangerous home remedies, take drugs recreationally, have environmental exposures (heavy metals), suffer from a consequence of a comorbidity (iron or copper overload) or have adverse events from generally safe medications.

The hyperactive boy with a hyperactive precordium: methylphenidate

Attention deficit hyperactivity disorder (ADHD) is growing in rate of diagnosis and use of medications.  As the only medical diagnosis based on self-reported criteria, many children are given stimulants regardless of actual neurologic disorder; with a higher proportion of children exposed to stimulants, adverse effects are seen more commonly.

Methylphenidate is related to amphetamine, and they both are dopaminergic drugs.  Their mechanisms of action are different, however.  Methylphenidate increases neuronal firing rate.  Methamphetamine reduces neuronal firing rate; cardiovascular sequelae such as MI and CHF are more common in chronic methamphetamine use.

Although methylphenidate is typically well tolerated, risks include dysrhythmias such as ventricular tachycardia.

The child with seizure disorder and chest pain: anti-epileptics

Some anti-epileptic agents, such as carbamazepine, promote a poor lipid profile, leading to atherosclerosis and early MI.  Case reports include school-aged children on carbamazepine who have foamy cells in the coronary arteries, aorta, and vasa vasorum on autopsy.  It is unclear whether this is a strong association.

The spice trader: synthetic cannabinoids

Synthetic cannabinoids are notoriously difficult to regulate and study, as the manufacturers label them as “not for human consumption”.  Once reports surface of abuse of a certain compound, the formula is altered slightly and repackaged, often in a colorful or mysterious way that is attractive to teenagers.

The misperceptions are: are a) synthetics are related to marijuana and therefore safe and b) marijuana is inherently “safe”. Both tend to steer unwitting teens to take these unknown entities.  Some suffer MI as a result.

Exposure to tetrahydrocannabinol (THC) in high-potency marijuana has been linked to myocardial ischemia, ventricular tachycardia, and ventricular fibrillation.  Marijuana can increase the heart rate from 20-100%, depending on the amount ingested.

K2 (“kush 2.0”) or Spice (Zohai, Genie, K3, Bliss, Nice, Black Mamba, fake weed, etc) is a mixture of plant leaves doused in synthetic chemicals, including cannabinoids and fertilizer (JWH-108), none of which are tested or safe for human consumption. 

Synthetic cannabinoids have a higher affinity to cannabinoid receptors, conferring higher potency, and therefore worse adverse effects.  They are thought to be 100 to 800 times more potent as marijuana.

Bath salts (Purple Wave, Zoom, Cloud Nine, etc) can be ingested, snorted, or injected.  They typically include some form of cathinone, such as mephedrone, similar to the substance found in the naturally occurring khat plant. Hallucinations, palpitations, tachycardia, MI, and dysrhythmias have been reported from their use as a recreational drug.

Chest pain with marijuana, synthetic cannabinoid, or bath salt ingestion should be investigated and/or monitored.

Riding that train: high on cocaine

Cocaine is a well-known cause of acute MI in young people.  In addition to the direct stimulant causes acutely, such as hypertension, tachycardia, and impaired judgement (coingestions, risky behavior), chronic cocaine use has long-term sequelae.  Cocaine causes accelerated atherosclerosis.  That, in conjunction with arterial vasospasm and platelet activation, is a recipe for acute MI in the young.

Cranky: methamphetamine

Methamphetamine is a highly addictive stimulant that is relatively inexpensive and widely available.  Repeated use causes multiple psychiatric, personality, and neurologic changes.  Risky behavior, violence, and motor vehicle accidents are all linked to this drug. 

Like cocaine, methamphetamine may cause fatal dysrhythmias, acute MI from demand ischemia, and long-term sequelae such as congestive heart failure.

Summary

Acute MI is a challenging presentation in children:

  • Easily missed: uncommon and atypical
  • Varied etiology
  • Respect vague symptoms with a non-reassuring H&P
  • Try to detect it: CATH IT!

References

Congenital

AboulHosn JA et al. Fontan Operation and the Single Ventricle. Congenit Heart Dis. 2007; 2:2-11.

Aliku TO et al. A case of anomalous origin of the left coronary artery presenting with acute myocardial infarction and cardiovascular collapse. African Health Sci. 2014; 14(1): 23-227.

Andrews RE et al. Acute myocardial infarction as a cause of death in palliated hypoplastic left heart syndrome. Heart. 2004; 90:e17.

Canale LS et al. Surgical treatment of anomalous coronary artery arising from the pulmonary artery. Interactive Cardiovascaulr and Thoracic Surgery. 2009; 8:67-69.

Güvenç O et al. Correctable Cause of Dilated Cardiomyopathy in an Infant with Heart Failure: ALCAPA Syndrome. J Curr Pediatr. 2017; 15:47-50.

Hastings RS et al. Embolic Myocardial Infarction in a Patient with a Fontan Circulation. World Journal for Pediatric Congenital Heart Surgery. 2014; 5(4)L631-634.

Hoffman JIE et al. Electrocardiogram of Anomalous Left Coronary Artery From the Pulmonary Artery in Infants. Pediatr Cardiol. 2013; 34(3):489-491.

Kei et al. Rare Case of Myocardial Infarction in a 19-Year-Old Caused by a Paradoxical Coronary Artery Embolism. Perm J.2015; 19(2):e107-e109.

Liu Y, Miller BW. ALCAPA Presents in an Adult with Exercise Inlerance but Preserved Cardiac Function. Case Reports Cardiol. 2012; AID 471759.

Möhlenkamp S et al. Update on Myocardial Bridging.Circulation. 2002;106:2616-2622.

Murgan SJ et al. Acute myocardial infraction n the neonatal period. Cardiol Young. 2002; 12:411-413.

Sieweke JT et al. Myocardial infarction in grown up patients with congenital heart disease: an emergening high-risk combination. International Journal of Cardiology. 2016; 203:138-140.

Schwerzmann M et al. Anomalous Origin of the Left Coronary Artery From the Main Pulmonary Artery in Adults. Circulation. 2004; 110:e511-e513.

Tomkewicz-Pajak L et al. Arterial stiffness in adult patients after Fontan procedure. Cardiovasculr Ultrasound. 2014; 12:15.

Varghese MJ et al. The caveats in the diagnosis of anomalous origin of left coronary artery from pulmonary artery (ALCAPA). Images Paediatr Cardiol. 2010; 12(3): 3–8.

Autoimmune

Ayala et al. Acute Myocardial Infarction in a Child with Systemic Lupus Erythematosus and Antiphospholipid Syndrome. Turk J Rheumatol. 2009; 24:156-8.

Nakano H et al. Clinical characteristics of myocardial infarction following Kawasaki disease: Report of 11 cases. J Pediatr. 1986; 108(2):198-203.

Pongratz G et al. Myocardial infarction in an adult resulting from coronary aneurysms previously documented in childhood after an acute episode of Kawasaki’s disease. European Heart J. 1994. 15:1002-1004.

Newburger JW et al.  Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease. A Statement for Health Professionals From the Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Circulation. 2004;110:2747-2771.

Son MB et al. Kawaski Disease. Pediatr Rev. 2013; 34(4).

Yuan S. Cardiac surgical procedures for the coronary sequelae of Kawasaki disease. Libyan J Med. 2012; 7:19796.

Trauma

Abdolrahim SA et al. Acute Myocardial Infarction Following Blunt Chest Trauma and Coronary Artery Dissection. J Clin Diagnost Res. 2016; 10(6):14-15.

Galiuto L et al. Post-traumatic myocardial infarction with hemorrhage and microvascular damage in a child with myocardial bridge: is coronary anatomy actor or bystander. Signa Vitae. 2013; 8(2):61-63.

Janella BL et al. Acute Myocardial Infarction related to Blunt Thoracic Trauma. Arq Bras Cardiol. 2006; 87:e168-e171.

Liu X et al. Acute myocardial infarction in a child with myocardial bridge World J Emerg Med. 2011; 2(1):70-72.

Long WA et al. Childhood Traumatic Infarction Causing Left Ventricular Aneurysm: Diagnosis by Two-Dimensional Echocardiography. JACC. 1985; 5(6):1478-83.

Smith S. Right Bundle Branch Block after Blunt Trauma: A Tragic Case. [Blog Post] July 22, 2012. Retrievable at: http://hqmeded-ecg.blogspot.com/2012/07/right-bundle-branch-block-after-blunt.html.

Hematologic

Carano N et al. Acute Myocardial Infarction in a Child: Possible Pathogenic Role of Patent Foramen Ovale Associated with Heritable Thrombophilia. Pediatr. 2004; 114(2):255-258.     

Chacko P et al. Myocardial Infarction in Sickle Cell Disease. J Cardiovascl Transl Res. 2013; 6(5):752-761.

De Montalembert M et al. Myocardial ischaemia in children with sickle cell disease. Arch Dis Child. 2004; 89:359-362.

Gladwin MT et al. Cardiovascular Abnormalities in Sickle Cell Disease. JACC. 2012; 59(13):1123-1133.

Osula S et al. Acute myocardial infarction in young adults: causes and management. Postgrad Med J. 2002; 78:27-30.

Silva JMP et al. Premature acute myocardial infarction in a child with nephrotic syndrome. Pediatr Nephrol. 2002; 17:169-172.

Suryawanshi SP. Myocardial infarction in children: Two interesting cases. Ann Pediatr Cardiol. 2011 Jan-Jun; 4(1): 81–83.

Infectious

Cunningham R et al. Viral myocarditis Presenting with Seizure and Electrocardiographic Findings of Acute Myocardial Infarction in a 14-Month-Old Child. Ann Emerg Med. 2000; 35(6):618-622.

De Vettten L et al. Neonatal Myocardial Infarction or Myocarditis? Pediatr Cardiol. 2011; 32:492-497.

Durani Y et al. Pediatric myocarditis: presenting clinical characteristics. Am J Emerg Med. 2009; 27:942-947.

Erden I et al. Acute myocarditis mimicking acute myocardial infarction associated with pandemic 2009 (H1N1) influenza virus. Cardiol J. 2011; 552-555.

Hover MH et al. Acute Myocarditis Simulating Myocardial Infarction in a Child. Pediatr. 1191; 87(2):250-252.

Lachant D et al. Meningococcemia Presenting as a Myocardial Infarction. Case Reports in Critical Care. 2015; AID 953826.

Laissy JP et al. Differentating Myocardial Infarction from Myocarditis. Radiology. 2005; 237(1):75-82.

Miranda CH et al. Evaluation of Cardiac Involvement During Dengue Viral Infection. CID. 2013; 57:812-819.

Rettig JS et al. Myocarditis in Children Requiring Critical Care Transport. In:  "Diagnosis and Treatment of Myocarditis", Milei J, Ambrosio G (Eds). DOI: 10.5772/56177.

Toxins

De Chadarévian JP et al. Epilepsy, Atherosclerosis, Myocardial Infarction, and Carbamazepine. J Child Neurol. 2003; 18(2):150-151.

McIlroy G et al. Acute myocardial infarction, associated with the use of a synthetic adamantly-canabinoid: a case report. BMC Pharmacology and Toxicology. 2016; 17:2.

Mir A et al. Myocardial Infarction Associated with Use of the Synthetic Cannabinoid K2. Pediatr. 2011; 128(6):1-6

Munk K et al. Cardiac Arrest following a Myocardial Infarction in a Child Treated with Methylphenidate. Case Reports Pediatr. 2015; AID 905097.

Rezkalla SH et al. Cocaine-Induced Acte Mycardial Infarction. Clin Med Res. 2007; 5(3):172-176.

Schelleman H et al. Methylphenidate and risk of serious cardiovascular events in adults. Am J Psychiatry. 2012 Feb;169(2):178-85.

Sheridan J et al. Injury associated with methamphetamine use: a review of the literature. Harm Reduction Journal, 2006; 3(14):1-18.

Stiefel G et al. Cardiovascular effects of methylphenidate, amphetamines and atomoxetine in the treatment of attention-deficit hyperactivity disorder. Drug Saf. 2010 Oct 1;33(10):821-42.

 

This post and podcast are dedicated to Edwin Leap, MD for his sanity and humanity in the practice of Emergency Medicine.  Thank you, Dr Leap for all that you do.

May 1, 2017

Most newborns will have some jaundice.  Most jaundice is benign.

So, how can we sort through the various presentations and keep our newborns safe?

Pathologic Jaundice

When a baby is born with jaundice, it’s always bad.  This is pathologic jaundice, and it’s almost always caught before the baby goes home.  Think about ABO-incompatbility, G6PD deficiency, Crigler-Najjar, metabolic disturbances, and infections to name a few.  Newborns are typically screened and managed.

Physiologic Jaundice

Physiologic jaundice, on the other hand, is usually fine, until it’s not.

All babies have some inclination to develop jaundice.  Their livers are immature.  They may get a little dehydrated, especially if mother’s milk is late to come in.  In today’s practice, we are challenged to catch those at risk for developing complications from rising bilirubin levels.

Hyperbilirubinemia is the result of at least one of three processes: you make too much, you don’t process it enough, or you don’t get rid of it fast enough.

Increased production

Bilirubin mostly comes from the recycling of red blood cells. Heme is broken down in in the liver and spleen to biliverdin then bilirubin.

Normal, full term babies without jaundice run a little high -- bilirubin production is two to three times higher than in adults, because they are born with a higher hematocrit.  Also, fetal hemoglobin is great at holding on to oxygen, but has a shorter life span, and high turn-over rate, producing more bilirubin.

Impaired conjugation

Think of bilirubin as your email.  Unconjugated bilirubin is your unread email.  To process it or get rid of it – you have to open it.  Of course, the more unread messages that accumulate, the more unwell you feel.

Conjugated bilirubin is your opened and processed email.  So much easier to sort out, deal with, and get rid of.

Decreased excretion

Both unread email and unconjugated bilirubin continue to float around in your inbox.  Unconjugated bilirubin keeps getting reabsorbed in the intestinal mucosa through enterohepatic circulation.

Processed email and conjugated bilirubin are easier to sort out.  Conjugated bilirubin is water soluble, so it goes right into the read folder in your gallbladder, and is excreted off your inbox.  Later on down the line in the intestine, conjugated bilirubin can’t be reabsorbed through the intestinal mucosa.  Like when you open an email and forget about it – it passes on through, out of your system.

Newborns are terrible at answering emails.  There is a lot of unread unconjugated bilirubin is floating around.  The liver and spleen are just not able to keep up.

Also, newborns have a double-whammy administrative load.  Normally, bacteria in the gut can further break down conjugated bilirubin to urobilin and get excreted in the urine.  The infant’s gut is relatively sterile, so no admin assistance there.  Just to add to the workload a poor little newborn has to do – he is being sabotaged by extra beta-glucuronidase which will take his hard-earned conjugated bilirubin and unconjugate it again, then recycle it, just like email you “mark as unread”.

How Does this All Go Down?

The recommended followup is 48 hours after discharge from the nursery for a routine bilirubin check, often in clinic, and often via the transcutaneous route.

More Specifically:

Infant Discharged Should Be Seen by Age
Before age 24 h 72 h
Between 24 and 48 h 96 h
Between 48 and 72 h 120 h

The neonate will end up in your ED off hours, if there is concern, if his status deteriorates, or simply by chance.  We need to know how to manage this presentation, because time is of the essence to avoid complications if hyperbilirubinemia is present.

Critical Action #1:

Assess risk for developing severe hyperbilirubinemia.

This will tell you: check now in ED or defer to clinic (default is to check).

Risk Factors for Developing Hyperbilirubinemia
Total serum bilirubin/Transcutaneous bilirubin in high-risk zone
Jaundice in first 24 hours
ABO incompatibility with positive direct Coombs, known hemolytic disease, or elevated ETCO
Gestational age 35-36 weeks
Prior sibling had phototherapy
Cephalohematoma or bruising
Exclusive breastfeeding, especially with poor feeding or weight loss
East Asian Race

Critical Action #2

Check bilirubin and match this with how old the child is -- in hours of life -- at the time of bilirubin measurement.

This will tell you: home or admission.

Use the Bilitool or Bhutani Nomogram (below).

 

Can I go Home Now?

Risk Stratification for Developing Severe Hyperbilirubinemia. Bhutani et al. Pediatrics. 1999.

In general, babies at low-risk and low-intermediate risk can go home (see below).  Babies at high-intermediate or high risk are admitted (see below).

Critical Action #3:

Assess risk for developing subsequent neurotoxicity.

This will tell you: a) phototherapy or b) exchange transfusion

 

 

Phototherapy Now?

 

 

Exchange Transfusion Now?

Threshold for Initiating Exchange Transfusion by Risk Stratum. Bhutani et al. Pediatrics. 1999.

Home care

The neonate who is safe to go home is well appearing, and not dehydrated.  His total bilirubin is in the low to low-intermediate risk for developing severe hyperbilirubinemia, and he is not at high risk for neurotoxicity based on risk factors.

Babies need to stay hydrated.  Breast feeding mothers need encouragement and need to offer feeds 8-12 times/day – an exhausting regimen.  The main message is: stick with it.  Make sure to enlist the family's help and support to keep Mom hydrated, eating well, and resting whenever she can.  Supplementing with formula or expressed breast milk is not routinely needed.  Be explicit that the neonate should not receive water or sugar water – it can cause dangerous hyponatremia.  A moment of solid precautionary advice could avert a disaster in the making.

The child’s pediatrician will help more with this, and you can remind nursing mothers of the excellent La Leche League – an international group for breastfeeding support.  They have local groups everywhere, including a hotline to call.

Nursery Care

If the baby is at high intermediate or high risk for hyperbilirubinemia, then he should be admitted for hydration, often IV.  Most babies with hyperbilirubinemia are dehydrated, which just exacerbates the problem.

Bililights or biliblankets, provide the baby with the right blue spectrum of light to isomerize bilirubin to the more soluble form.  Traditionally, we have thought them to be more effective or safer than filtered sunlight.  A recent randomized control trial by Slusher et al. in the New England Journal of Medicine compared filtered sunlight versus conventional phototherapy for safety and efficacy in a resource-poor environment.  These were all term babies with clinically significant jaundice in Nigeria.  To standardize the intervention, they used commercial phototherapy canopies that remove most UV rays. None of them became dehydrated or became sunburned.  The filtered sunlight resulted in a 93% successful treatment versus 90% for conventional phototherapy.  My take away: we now have some evidence basis for using filtered sunlight as an adjunct for babies well enough to go home.

Critical Care

Although rare, the critically ill neonate with hyperbilirubinemia requires immediate intervention.

He will be dehydrated – possibly in shock.  He will be irritable.

Or, he may just have a dangerously high bilirubin level – at any minute he could develop bilirubin induced neurologic dysfunction, or BIND, especially when bilirubin concentrations reach or surpass 25 mg/dL (428 micromol/L).  The bilirubin is so concentrated that it leeches past the blood brain barrier and causes neuronal apoptosis.  BIND is a spectrum from acute bilirubin encephalopathy to kernicterus, all involving some disorder in vision, hearing, and later gait, speech, and cognition.

Acute bilirubin encephalopathy starts subtly.  The neonate may be sleepy but hypotonic or have a high-pitched cry; he maybe irritable or inconsolable, jittery or lethergic.

The dehydration and neurologic dysfnction from the hyperbilirubinemia may even cause fever.  Check the bilirubin in any neonate you are working up for sepsis.

Acute bilirubin encephalopathy may progress to an abnormal neurologic exam, seizures, apnea, or coma.

Kernicterus is the final, permanent result of bilirubin encephalpathy.  The child may have choreoathetoid cerebral palsy with chorea, tremor, ballismus, and dystonia.  He may have sensorineural hearting loss, or cognitive dysfunction.

It is for this reason that any child sick enough to be admitted should be considered for exchange transfusion.  Most babies need just a little gentle rehydration and bililights, but to be sure, the admitting team will look at a separate nomogram to gage the child’s risk and decide whether to pull the trigger on exchange transfusion.  For our purposes, a ballpark estimate is that if the total serum bilirubin is 5 mg/dL above the phototherapy threshold, or if they have any red flag signs or symptoms, then exchange transfusion should be started.

Exchange transfusion involves taking small aliquots of blood from the baby and replacing them with donor blood.  It’s often a manual procedure, done with careful monitoring.  It can be done with any combination of umbilical arteries or veins with peripheral arteries or veins.  In general, arteries are the output, veins are for transfusion. The baby may need a double-volume exchange, which ends up replacing about 85% of circulating blood, a single-voume exchange, replacing about 60% of blood, or any fraction of that with apartial volume exchange.  It is a very delicate procedure that requires multiple hours and often multiple staff.

For our pruposes, just be aware that the jaundiced baby in front of you may need escalation of his care.

Summary

Find out the hour of life of the baby at the time of bilirubin measurementIdentify risk factors for developing severe hyperbilirubinemia and/or neurotoxicity

The child with low to low-intermediate risk may be a good outpatient candidate provided he is well, not dehydrated, and follow-up is assured.

The child with high-intermediate to high-risk for developing severe hyperbilirubinemia should be admitted for hydration, bililights, and/or assessment for exchange transfusion.

The unwell child with or without current neurologic findings should have immediate exchange transfusion.

References

Benitz WE. Hospital Stay for Healthy Term Newborn Infants. Pediatrics. 2015; 135(5):948-53.

Bhutani V et al. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics. 2004; 114(1).

Bhutani VK, Wong RJ. Bilirubin Neurotoxicity in Preterm Infants: Risk and Prevention. J Clin Neonatol. 2013 Apr-Jun; 2(2): 61–69.

Bosschaart N et al. Limitations and Opportunities of Transcutaneous Bilirubin Measurements. Pediatrics. 2012; 129(4).

Colletti JE, Kothari S, Jackson DM, Kilgore KP, Barringer K. An emergency medicine approach to neonatal hyperbilirubinemia. Emerg Med Clin North Am. 2007 Nov;25(4):1117-35, vii.

Gamaleldin R et al. Risk Factors for Neurotoxicity in Newborns With Severe Neonatal Hyperbilirubinemia. Pediatrics. 2011; 128(4):825-31.

Lauer BJ, Spector ND. Hyperbilirubinemia in the Newborn. Pediatrics in Review. 2011; 32(8):341-9.

Maisels J et al. Hyperbilirubinemia in the Newborn Infant ≥35 Weeks’ Gestation: An Update With Clarifications. Pediatrics. 2009; 124(4):1193-6.

Smitherman H, Stark AR, Bhutani VK. Early recognition of neonatal hyperbilirubinemia and its emergent management.  Semin Fetal Neonatal Med. 2006 Jun;11(3):214-24.

Vandborg PK, Hansen BM, Greisen G, Ebbesen F. Dose-response relationship of phototherapy for hyperbilirubinemia. Pediatrics. 2012 Aug;130(2):e352-7.

This post and podcast are dedicated to Gita Pensa, MD, for her commitment to #FOAMed and passion for asynchronous learning and education innovation.

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