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Pediatric Emergency Playbook

Updated 10 days ago

Education
Health
Science & Medicine
Medicine
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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. Please visit our site at http://PEMplaybook.org/ for show notes and to get involved with the show -- see you there!

Read more

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. Please visit our site at http://PEMplaybook.org/ for show notes and to get involved with the show -- see you there!

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119 Ratings
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One of the best

By desertem - Apr 16 2019
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I listen to a lot of podcasts. This is one of my favorites. He is entertaining as well as brilliant. These are mandatory for anyone taking care of sick kids. His delivery and format create maximum retention...

Great podcast

By bbbbbbbbccccccmmmmm - Aug 10 2017
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My best pediatric EM education during residency.

iTunes Ratings

119 Ratings
Average Ratings
110
5
2
2
0

One of the best

By desertem - Apr 16 2019
Read more
I listen to a lot of podcasts. This is one of my favorites. He is entertaining as well as brilliant. These are mandatory for anyone taking care of sick kids. His delivery and format create maximum retention...

Great podcast

By bbbbbbbbccccccmmmmm - Aug 10 2017
Read more
My best pediatric EM education during residency.
Cover image of Pediatric Emergency Playbook

Pediatric Emergency Playbook

Updated 10 days ago

Read more

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. Please visit our site at http://PEMplaybook.org/ for show notes and to get involved with the show -- see you there!

Rank #1: Cyanosis

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Your eyes may fool you...   Keep your differential diagnosis open.

Selected References

Aravindhan N, Chisholm DG. Sulfhemoglobinemia presenting as pulse oximetry desaturations. Anesthesiology. 2000;93:883–884.

  Gharahbaghian L et al. Methemoglobinemia and Sulfhemoglobinemia in Two Pediatric Patients after Ingestion of Hydroxylamine Sulfate. West J Emerg Med. 2009 Aug; 10(3): 197–201

 

 Ginimuge PR et al. Methylene Blue: Revisited. J Anaesthesiol Clin Pharmacol. 2010 Oct-Dec; 26(4): 517–520.

 

 Mack E. Focus on diagnosis: co-oximetry. Pediatr Rev. 2007;28:73–4.

So T-Y et al. Topical Benzocaine-induced Methemoglobinemia in the Pediatric Population. J Pediatr Health Care. 22(6):335–339.

Aug 01 2019
36 mins
Play

Rank #2: The Undifferentiated Sick Infant

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You have all of the skills you need to care for an acutely ill infant.  Learn a few pearls to make this a smoother endeavor.

The Pediatric Assessment Triangle is a rapid, global assessment tool using only visual and auditory clues to make determinations on three key domains: appearance, work of breathing, and circulation to the skin. 

The combination of abnormalities determines the category of pathophysiology: respiratory distress, respiratory failure, CNS or metabolic problem, shock, or cardiopulmonary failure.

Appearance

"TICLS"Tone - the newborn should have a normal flexed tone; the 6 month old baby who sits up and controls her head; the toddler cruises around the room. Interactiveness - Does the 2 month old have a social smile?  Is the toddler interested in what is going on in the room? 

Consolability - A child who cannot be consoled at some point by his mother is experiencing a medical emergency until proven otherwise. 

Look/gaze - Does the child track or fix his gaze on you, or is there the "1000-yard stare"?

Speech/cry - A vigorously crying baby can be a good sign, when consolable - when the cry is high-pitched, blood-curling, or even a soft whimper, something is wrong.  If the child fails any of the TICLS, then his appearance is abnormal.

Work of Breathing

Children are respiratory creatures - they are hypermetabolic - we need to key in on any respiratory embarrassment.

Look for nasal flaring.   Uncover the chest and abdomen and look for retractions.  Listen - even without a stethoscope - for abnormal airway sounds like grunting or stridor.  Grunting is the child's last-ditch effort to produce auto-PEEP.  Stridor is a sign of critical upper airway narrowing.Look for abnormal positioning, like tripodding, or head bobbing

Circulation to the skin

Infants and children are vasospastic - they can change their vascular tone quickly, depending on their volume status or environment.  Without even having to touch the child, you can see signs of pallor, cyanosis, or mottling.  If any of these is present, this is an abnormal circulation to the skin.

Pattern of Abnormal Arms = Category of Pathophysiology

Differential Diagnosis in a Sick Infant: "THE MISFITS"

    Trauma - birth trauma, non-accidental - check for a cephalohematoma which does not cross suture lines and feels like a ballotable balloon, as well as for subgaleal hemorrhage, which is just an amorphous bogginess that represents a dangerous bleed.  Do a total body check.

    Heart disease or Hypovolemia - is there a history of congenital heart disease? Was there any prenatal care or ultrasound done?  Does this child look volume depleted?

    Endocrine Emergencies - Could this be congenital adrenal hyperplasia with low sodium, high potassium, and shock? Look for clitoromegaly in girls, or hyperpigmented scrotum in boys.  Could this be congenital hypothyroidism with poor tone and poor feeding?  Any history of maternal illness or medications? Congenital hyperthyroidism with high output failure?

    Metabolic - What electrolyte abnormality could be causing this presentation? Perhaps diGeorge syndrome with hypocalcemia and seizures? 

    Inborn Errors of Metabolism - there are over 200 inborn errors of metabolism, but only four common metabolic pathways that cause a child to be critically ill.  Searching for an inborn error of metabolism is like looking for A UFO - amino acids, uric acids, fatty acids, organic acids.  If the child's ammonia, glucose, ketones, and lactate are all normal in the ED, then his presentation to the ED should not be explained by a decompensation of an inborn error of metabolism. 

      Seizures - Neonatal seizures can be notoriously subtle - look for little repetitive movements of the arms, called "boxing" or of the legs, called "bicycling"

    Formula problems - Hard times sometimes prompt parents to dilute formula, causing a dangerous hyponatremia, altered mental status, and seizures.  Conversely, concentrated formula can cause hypovolemia

    Intestinal disasters - 10% of necrotizing enterocolitis occurs in full-term babies - look for pneumatosis intestinalis on abdominal XR; also think about aganglionic colon or Hirschprung disease; 80% of cases of volvulus occur within the 1st month of life

    Toxins - was there some maternal medication or ingestion?  Is there some home remedy or medication used on the baby?  Check a glucose ad drug screen

    Sepsis - Saved for last - You'll almost always treat the sick neonate empirically for sepsis - think of congenital and acquired etiologies.

Hyperoxia TestThe hyperoxia test is the single most important initial test in suspected congenital heart disease - we can test the child's circulation by his reaction to oxygen on an arterial blood gas.  Place the child on a non-rebreather mask, and after several minutes, perform an ABG.  (Ideally you obtain a preductal ABG in the right upper extremity, and compare that with one on the lower extremity, but this may not be practical.)

In a normal circulatory system, the pO2 should be high - in the hundreds - and certainly over 250 torr. This effectively excludes congenital heart disease as a factor.  If the pO2 on supplemental oxygen is less than 100, then this is extremely predictive of hemodynamically significant congenital heart disease.  Between 100 and 250, you have to make a judgement call, and I would side on worst first.

If you are giving this child 100% O2, and he doesn't improve 100% -- that is, his ABG is not at least 100 - then he has congenital heart disease until proven otherwise. 

Give prostaglandin if the patient is less than 4 weeks old (typical presentation is within the first 1-2 weeks of life).  Start at 0.05 mcg/kg/min.  PGE keep the systemic circulation supplied with some mixed venous blood until either surgery or palliation is decided. 

Summary Points* When you see a sick infant, keep THE MISFITS around to keep you out of trouble.* Before you decide on sepsis, ask yourself, could this be a cardiac problem?* When in doubt, perform the hyperoxia test.* All the rest, you have time to look up.

Before You Go: The Availability HeuristicSelected References

Brousseau T, Sharieff GQ. Newborn Emergencies: The First 30 Days of Life. Pediatr Clin N Am. 2006; 53:69-84.

Cloherty JP, Eichenwald EC, Stark AR: Manual of Neonatal Care, 5th edition. Philadelphia, PA, Lipincott Williams & Wilkins, 2004.

Horeczko T, Young K: Congenital Heart Disease, in Pediatric Emergency Medicine-A Comprehensive Study Guide, 4th Ed. ACEP/McGraw-Hill, 2013.

McGowan et al. Part 15: Neonatal Resuscitation: 2010 American Heart Association Guidelines. Circulation. 2010;122:S909-S919.

Okada PJ, Hicks B. Neonatal Surgical Emergencies. Clin Ped Emerg Med. 2002; 3:3-13.

Sep 01 2015
31 mins
Play

Rank #3: Vomiting in the Young Child: Nothing or Nightmare

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In the young child, vomiting is the great imitator:
Gastrointestinal, Neurologic, Metabolic, Respiratory, Renal, Infectious, Endocrine, Toxin-related, even Behavioral.
To help us organize, below is a review of can't-miss diagnoses by age.

The Neonate: Malrotation with Volvulus

In children with malrotation, 50% present within the first month of life, with the majority occurring in the first week after birth. 90% of children with malrotation with volvulus will present by one year of age.   This is a pre-verbal child’s disease – which makes it even more of a challenge to recognize quickly.

The sequence of events usually is fussiness, irritability, and forceful vomiting.  The vomit quickly turns bilious.

Green vomit is a surgical emergency.

Babies may also present unwell, with bloating and abdominal tenderness to palpation.  Be aware that later stages of malrotation may present as shock – they present in hypovolemic shock due to third-spacing from necrotic bowel and/or septic shock from translocation or perforation.   In the undifferentiated sick neonate, always consider a surgical emergency such as malrotation with volvulus.

In the stable patient, get an upper GI contrast study.

Rapid-fire word association for other vomiting emergencies in a neonate:

  • Fever, irritability and vomiting?  Think meningitis, UTI, or sepsis.
  • Premature, unwell, and vomiting?  Think necrotizing enterocolitis.  Remember, 10% of cases of NEC can be full-term. Look for pneumatosis intestinalis.
  • Systemically ill, afebrile, and vomiting for no other reason?  Think inborn error of metabolism.  Screen with a glucose, ammonia, lactate, and urine ketones.
  • Others include congenital intestinal atresia or webs, meconium ileus, or severe GERD
The Infant: Non-Accidental Trauma

All that vomits is not necessarily from the gut.

Abusive head injury is the most common cause of death from child abuse.   Infants especially present with non-specific complaints like fussiness or vomiting.   Up to 30% of infants with abusive head injury may be misdiagnosed on initial presentation.

Louwers et al. in Child Abuse and Neglect developed and validated a six-question screening tool for use the in ED.  The power of this tool was that it was validated for any chief complaint – it is not an injury evaluation checklist – it is a screen for potential abuse in the undifferentiated child:

  1. Is the history consistent?
  2. Was seeking medical help unnecessarily delayed?
  3. Does the onset of injury fit with the developmental level of the child?
  4. Is the behavior of the child and his interaction with his care-givers appropriate?
  5. Do the findings of the head-to-toe examination match the history?
  6. Are there any other red flags or signals that make you doubt the safety of the child or other family members?

On multivariable analysis, if at least one of the questions was positive, there was an OR of 189 for abuse (CI 97 – 300).  In other words, if any of those six questions are problematic, get your child protective team involved.

Other important diagnoses in the infant: intussusception and pyloric stenosis (rapid review in audio).

The Toddler: Diabetic Ketoacidosis (DKA)

The important diagnosis not to miss in the vomiting toddler or early school age child is the initial presentation of diabetic ketoacidosis.  Children under 5 (especially those under 2) and those from lower socioeconomic groups have a higher risk of DKA as their initial presentation of diabetes.

This is true for any child that isn’t quite acting right – check a finger stick blood sugar as a screen.

The International Society for Pediatric and Adolescent Diabetes (ISPAD) criteria for DKA:

  1. Hyperglycemia, with a blood glucose of >200 mg/dL (11 mmol/L) AND
  2. Evidence of metabolic acidosis, with a venous pH of less than 7.3 or a bicarbonate level of < 15 mEq/L AND
  3. Ketosis, found either in the urine or if directly checked in the blood.

If you have access to checking a serum beta-hydroxybutryrate – the unsung ketone – it can help in diagnosis in unclear cases.

Cerebral Edema Criteria:

  • Minor criteria: headache, vomiting, irritability or lethargy; hypertension in the face of hypovolemia.
  • Major criteria: change in mental status, including agitation or delirium; incontinence (especially if inappropriate for the child’s age); sluggish pupils and cranial nerve palsies; relative bradycardia (Cushing’s triad).

Cerebral Edema Action Items:

  • Immediately give mannitol, 1 g/kg over 15-20 minutes.  May repeat it in 2 hours if needed.  Hypertonic saline (3% NaCl) is second-line therapy.
  • Put the head of the bed up 30 degrees.
  • Alert your colleagues and counsel your parents.  Make sure everyone knows what to watch out for.

As you can see, vomiting in the young child can be really anything!  Keep your differential broad, and think by age and by system.

Differential Diagnosis of Vomiting in Children

The general approach to the child with chiefly vomiting starts with the decision: sick or not sick.  If ill appearing, establish rapid IV access, or if needed IO.  Rapid blood sugar and if available a point of care pH and electrolytes.  Be the detective in your history and doggedly go after any red flags as you go methodically by organ system.

  • Do a careful physical exam. The general assessment is always helpful – is the child irritable, listless, agitated?
  • What is his work of breathing?  Effortless tachypnea may be a sign of acidosis or sepsis.
  • Is the abdomen soft or is it tender or distended.  Always look in the diaper area – is there a hernia, is there a high-riding, tender, discolored scrotum without cremasteric reflex?  Ovarian torsion has been reported in infants as young as 7 months.
  • Any skin signs?  Look for petechiae, urticaria, purpura.

In other words, use your best judgement, have the dangerous differentials in the back of your mind, and pull the trigger when red flags mount up.  Otherwise, a good history and a good exam will get you where you need to be.

Take home points for the young child with vomiting:
  1. Neonates are allowed to regurgitate (effortless reflux of stomach contents -- the happy spitter-upper).  They are not allowed to vomit (forceful, unpleasant contraction of abdominal muscles).  Consider surgical causes of forceful vomiting, especially if the child does not look anything other than well.
  2. Bilious is bad – green vomit is always a surgical emergency – do not pass go – get the surgeons involved early
  3. Not all vomiting is GI related – if it is not obviously benign, think methodically by organ system and adjust your targeted history and physical to pick up any leads.
  4. Match the tempo of your treatment to the tempo of the disease.
References

Applegate KE, Anderson JM, Klatte EC. Intestinal malrotation in children: a problem-solving approach to the upper gastrointestinal series. Radiographics. 2006; 26(5):1485-500.

Glaser NS, Wootton-Gorges SL, Buonocore MH et al. Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosis. Pediatr Diabetes. 2006 Apr;7(2):75-80.

Louwers ECFM, Korfage IJ, Affourtit MJ et al. Accuracy of a screening instrument to identify potential child abuse in emergency departments. Child Abuse & Neglect. 2014; (38): 1275–1281.

Lee HC, Pickard SS, Sridhar S et al. Intestinal Malrotation and Catastrophic Volvulus in Infancy. J Emerg Med. 2012; 43(1): e49–e51.

Marcin JP, Glaser N, Barnett P et al. Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema. J Pediatr. 2002; 141(6):793-7.

Parashette KR, Croffie J. Intestinal Malrotation in Children: A Problem-solving Approach to the Upper Gastrointestinal. Pediatrics in Review. 2013; (34)7: 307-321.

Wolfsdorf JI, Allgrove J, Craig ME et al. ISPAD Clinical Practice Consensus Guidelines 2014. Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Diabetes. 2014 Sep;15 Suppl 20:154-79.

This post and podcast are dedicated to Damian Roland, BMedSci (Hons), MB BS, MRCPCH, for his fervor in the care of children and his dedication to quality medical education.

Nausea and Vomiting | Non-Accidental Trauma | DKA

Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

Jan 01 2016
47 mins
Play

Rank #4: Strep Throat

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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

Aug 01 2018
41 mins
Play

Rank #5: Bronchiolitis

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"By the pricking of my thumbs, Something wheezing this way comes."

-- Witches in Macbeth, with apologies to William Shakespeare

 

"Bronchiolitis is like a pneumonia you can’t treat. We support, while the patient heals."

-- Coach, still apologetic to the Bard

 

The Who

The U.S. definition is for children less than two years of age, while the European committee includes infants less than one year of age.

This is important: toddlerhood brings with it other conditions that mimic bronchiolitis – the first-time wheeze in a toddler may be his reactive airway response to a viral illness and not necessarily bronchiolitis.

The What

The classic clinical presentation of bronchiolitis starts just like any other upper respiratory tract infection: with nasal discharge and cough, for the first 1-2 days. Only about 1/3 of infants will have a low-grade fever, usually less than 39°C. We may see the child in the ED at this point and not appreciate any respiratory distress – this is why precautionary advice is so important in general.

Then, lower respiratory symptoms come: increased work of breathing, persistent cough, tachypnea, retractions, belly breathing, grunting, and nasal flaring. Once lower respiratory symptoms are present, like increased work of breathing, they typically peak at day 3. This may help to make decisions or counsel parents depending on when the child presents and how symptomatic he is.

You’ll hear fine crackles and wheeze. A typical finding in bronchiolitis is a minute-to-minute variation in clinical findings – one moment the child could look like he’s drowning in his secretions, and the next minute almost recovered. This has to do with the dynamic nature of the secretion, plugging, obstruction, coughing, dislodgement, and re-plugging.

The Why

Respiratory syncytial virus is the culprit in up to 90% of cases of bronchiolitis. The reason RSV is so nasty is the immune response to the virus: it binds to epithelial cells, replicates, and the submucosa becomes edematous and hypersecretes mucus. RSV causes the host epithelia and lymphocytes to go into a frenzy – viral fusion proteins turn the membranes into a sticky goop – cells fuse into other cells, and you have a pile-on of multinucleated dysfunction. This mucosal chaos causes epithelial necrosis, destruction of cilia, mucus plugs, bronchiolar obstruction, air trapping, and lobar collapse.

High-Risk Groups

Watch out especially for young infants, so those less than 3 months of age. Apnea may be the presenting symptom of RSV. Premature infants, especially those less than 32 weeks’ gestation are at high risk for deterioration.  The critical time is 48 weeks post-conceptional age.

Other populations at high-risk for deterioration: congenital heart disease, pulmonary disease, neuromuscular disorders, metabolic disorders.

Guiding Principles

In the full term child, greater than one month, and otherwise healthy (no cardiac, pulmonary, neuromuscular, or metabolic disease), we can look to three simple criteria for home discharge.

If the otherwise healthy child one month and older is:

Euvolemic

Not hypoxic

Well appearing

He can likely go home.

The How

Below is a list of modalities, treatments, and the evidence and/or recommendations for or against:

Chest Radiograph

Usually not necessary, unless the diagnosis is uncertain, or if the child is critically ill.

Factors that are predictive of a definite infiltrate are: significant hypoxia (< 92%), grunting, focal crackles, or high fever (> 39°C).

Ultrasound

Not ready for prime time.  Two small studies, one by Caiulo et al in the European J or Pediatrics and one by Basile et al. in the BMC Pediatrics that show some preliminary data, but not enough to change practice yet.

Viral Testing

Qualitative PCR gives you a yes or no question – one that you’ve already answered. It is not recommended for routine use. PCR may be positive post-infection for several weeks later (details in audio).

Quantitative PCR measures viral load; an increased quantitative viral load is associated with increased length of stay, use of respiratory support, need for intensive care, and recurrent wheezing. However, also not recommended for routine use.

There is one instance in which viral testing in bronchiolitis can be helpful – in babies less than a month of life, the presence of RSV virus is associated with apnea.

Blood or Urine Testing

Routine testing of blood or urine is not recommended for children with bronchiolitis.  Levine et al in Pediatrics found an extremely low risk of serious bacterial illness in young febrile infants with RSV.

The main thing is not to give in to anchoring bias here. If an infant of 3 months of age or older has a clear source for his low-grade fever – and that is his bronchiolitis – then you have a source, and very rarely do you need to go looking any further. He’s showing you the viral waterfall from his nose, and his increased work of breathing. It’s not going to be in his urine.

Bronchodilators!

Should we use bronchodilators in bronchiolitis?  It seems lately that this is a loaded question – with strong feelings on either side amongst colleagues. The short answer is that the American Academy of Pediatrics, the UK’s National Institute for Health and Care Excellence, as well as the Canadian Pediatric Society currently recommend against them. However, in continental Europe and Australia, the language is softened to “not routinely recommended”.

Pros and Cons in Audio; the 2006 AAP Guidelines and the 2014 AAP Guidelines use same data to come to divergent recommendations.

Steroids

There is no role for steroids in the treatment of bronchiolitis, even in those with a family or personal history of atopy.

Nebulized Hypertonic Saline

May show some benefit in admitted patients, after repeated treatments; no data to support its use in ED patients (no immediate effect).

Nebulized Epinephrine

One randomized controlled double blinded study in eight centers in Norway published in the NEJM showed no benefit to nebulized epinephrine over nebulized saline. Again, probably asking too much of one single intervention.

The Cochrane review found 19 studies that included a total of 2256 children with acute bronchiolitis treated with nebulized epinephrine. There were no differences in length of hospital stay between the placebo and treatment groups, and so they concluded that for inpatients, nebulized epinephrine is not worth the hassle. However – and this may just be an artifact of meta-analysis – there may be some benefit to outpatients. One study of combined high-dose steroid and epinephrine therapy was not statistically significant when other factors were controlled, but Cochrane concluded that nebulized epinephrine itself may be helpful for outpatients. It won’t affect the overall disease time course, but it may make them feel better enough to go home from the ED and continue observation there.

High-Flow Nasal Cannula Oxygen

High-flow oxygen via nasal cannula requires specialized equipment and delivers humidified oxygen at 1-2 L/g/min.  In addition to oxygenation, high flow nasal cannula also likely offers some low-grade positive end-expiratory pressure, which may help with alveolar recruitment. The evidence for its use is based on observational studies, which have found improved respiratory parameters and reduced rates of intubation.  Nasal CPAP also has some promising properties in the right clinical setting.

Antibiotics

Not recommended. When bronchiolitis is from a clear viral source, the risk of accompanying bacteremia is less than 1%. A meta-analysis of randomized clinical trials found that antibiotics in bronchiolitis did not improve duration of symptoms, length of hospital stay, need for oxygen therapy, or hospital admission.

Summary: The Good, the Bad, and the Ugly The Good

Nasal suction and hydration are your best allies. You may elect to give a bronchodilator as a trial once and reexamine, if you’re a bronchodilating believer.

The Bad

Steroids, antibiotics, and a blind obeying of the guidelines. Weigh the risks and benefits of every intervention, including hospitalization – it’s not always a benign thing.

The Ugly

Take a moment to assess the child and make a clinical diagnosis of bronchiolitis, after you’ve excluded cardiac disease, anatomic anomalies, and foreign body aspiration. Wheezing without upper respiratory symptoms is not viral, and it is not bronchiolitis.

When all else fails, remember: in the otherwise healthy, term infant greater than a month of age, if he is well appearing, euvolemic, and not hypoxic, he will often do well with good precautionary advice and supportive care at home. Every thing else: be skeptical, be thorough, and above all, be careful.

References Alansari K, Toaimah FH, Khalafalla H, El Tatawy LA, Davidson BL, Ahmed W. Caffeine for the Treatment of Apnea in Bronchiolitis: A Randomized Trial. J Pediatr. 2016 May 14. pii: S0022-3476(16)30170-6. [Epub ahead of print]

American Academy of Pediatrics Subcommittee on Diagnosis and Management of Bronchiolitis. Diagnosis and management of bronchiolitis. Pediatrics. 2006 Oct;118(4):1774-93.

Beggs S, Wong ZH, Kaul S, Ogden KJ, Walters JA. High-flow nasal cannula therapy for infants with bronchiolitis. Cochrane Database Syst Rev. 2014 Jan 20;(1):CD009609.

Bergroth E, Aakula M, Korppi M, Remes S, Kivistö JE, Piedra PA, Camargo CA Jr, Jartti T. Post-bronchiolitis Use of Asthma Medication: A Prospective 1-year Follow-up Study. Pediatr Infect Dis J. 2016 Apr;35(4):363-8.

Cunningham S, Rodriguez A, Adams T, Boyd KA, Butcher I, Enderby B, MacLean M, McCormick J, Paton JY, Wee F, Thomas H, Riding K, Turner SW, Williams C, McIntosh E, Lewis SC; Bronchiolitis of Infancy Discharge Study (BIDS) group. Oxygen saturation targets in infants with bronchiolitis (BIDS): a double-blind, randomised, equivalence trial. Lancet. 2015 Sep 12;386(9998):1041-8.

Flett KB, Breslin K, Braun PA, Hambidge SJ. Outpatient course and complications associated with home oxygen therapy for mild bronchiolitis. Pediatrics. 2014 May;133(5):769-75.

Florin TA, Plint AC, Zorc JJ. Viral bronchiolitis. Lancet. 2016 Aug 20. [Epub ahead of print]

Halstead S, Roosevelt G, Deakyne S, Bajaj L. Discharged on supplemental oxygen from an emergency department in patients with bronchiolitis. Pediatrics. 2012 Mar;129(3):e605-10.

Johnson LW, Robles J, Hudgins A, Osburn S, Martin D, Thompson A. Management of bronchiolitis in the emergency department: impact of evidence-based guidelines? Pediatrics. 2013 Mar;131 Suppl 1:S103-9.

Lashkeri T, Howell JM, Place R. Capnometry as a predictor of admission in bronchiolitis. Pediatr Emerg Care. 2012 Sep;28(9):895-7.

Lehners N, Tabatabai J, Prifert C, Wedde M, Puthenparambil J, Weissbrich B, Biere B, Schweiger B, Egerer G, Schnitzler P. Long-Term Shedding of Influenza Virus, Parainfluenza Virus, Respiratory Syncytial Virus and Nosocomial Epidemiology in Patients with Hematological Disorders. PLoS One. 2016 Feb 11;11(2):e0148258.

Liet JM, Ducruet T, Gupta V, Cambonie G. Heliox inhalation therapy for bronchiolitis in infants. Cochrane Database Syst Rev. 2015 Sep 18;(9):CD006915.

Mammas IN, Spandidos DA. Paediatric Virology in the Hippocratic Corpus. Exp Ther Med. 2016 Aug;12(2):541-549.

Mansbach JM, Clark S, Teach SJ, Gern JE, Piedra PA, Sullivan AF, Espinola JA, Camargo CA Jr. Children Hospitalized with Rhinovirus Bronchiolitis Have Asthma-Like Characteristics. J Pediatr. 2016 May;172:202-204.e1.

Meissner HC. Viral Bronchiolitis in Children. N Engl J Med. 2016 Jan 7;374(1):62-72.

Munywoki PK, Koech DC, Agoti CN, Kibirige N, Kipkoech J, Cane PA, Medley GF, Nokes DJ. Influence of age, severity of infection, and co-infection on the duration of respiratory syncytial virus (RSV) shedding. Epidemiol Infect. 2015 Mar;143(4):804-12.

Oakley E, Borland M, Neutze J, Acworth J, Krieser D, Dalziel S, Davidson A, Donath S, Jachno K, South M, Theophilos T, Babl FE; Paediatric Research in Emergency Departments International Collaborative (PREDICT). Nasogastric hydration versus intravenous hydration for infants with bronchiolitis: a randomised trial. Lancet Respir Med. 2013 Apr;1(2):113-20. Epub 2012 Dec 21.

Oakley E et al. Nasogastric Hydration in Infants with Bronchiolitis Less Than 2 Months of Age. J Pediatr. 2016. [Article in Press]

Principi T, Coates AL, Parkin PC, Stephens D, DaSilva Z, Schuh S. Effect of Oxygen Desaturations on Subsequent Medical Visits in Infants Discharged From the Emergency Department With Bronchiolitis. JAMA Pediatr. 2016 Jun 1;170(6):602-8.

Ralston SL, Lieberthal AS, Meissner HC, Alverson BK, Baley JE, Gadomski AM, Johnson DW, Light MJ, Maraqa NF, Mendonca EA, Phelan KJ, Zorc JJ, Stanko-Lopp D, Brown MA, Nathanson I, Rosenblum E, Sayles S 3rd, Hernandez-Cancio S; American Academy of Pediatrics. Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics. 2014 Nov;134(5):e1474-502.

Roqué i Figuls M, Giné-Garriga M, Granados Rugeles C, Perrotta C, Vilaró J. Chest physiotherapy for acute bronchiolitis in paediatric patients between 0 and 24 months old. Cochrane Database Syst Rev. 2016 Feb 1;2:CD004873.

Skjerven HO et al. Racemic adrenaline and inhalation strategies in acute bronchiolitis. N Engl J Med. 2013 Jun 13;368(24):2286-93.

This post and podcast are dedicated to Linda Girgis MD, FAAFP, for her authenticity, innovation, and clear and honest voice on the the frontlines.  Thank you, Dr Linda.

Bronchiolitis

Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

Dec 01 2016
37 mins
Play

Rank #6: Failure to Thrive

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Failure to Thrive (FTT) is not just for the clinics. We need to be on the lookout, because if we find it, there is already a big problem.

Definitions of Failure to Thrive may quibble on the details, but for us in the ED:

  1. Consistently under 2nd percentile in weight over time
  2. "Falling off" the growth curve over 2 or more points

We can get around the longitudinal requirement by looking at weight as a "spot check" -- if grossly below weight without any other chronic condition, be alarmed.

Failure to thrive results from inadequate calories. This may be due to:

  1. Not enough offered
  2. Not enough taken
  3. Not enough absorbed

Any concern should trigger a more complete H&P (in audio).

Classic instructional video on the mother-infant dyad (scan through for various types).

After a focused H&P, you may need to admit the child for further workup, or to show that he can/cannot gain weight with routine care.

Remember, if you are the first one to bring this up, there is a real problem. By definition, an outpatient plan has failed. We will not be able to distinguish among the various possibilities of organic and non-organic causes (or mix thereof); our job is to be ready to catch it and act on it. The child's development, future intelligence, and welfare are at risk.

References

Birth to 24 months: Boys Weight-for-length percentiles and Head circumference-for-age percentiles

Birth to 24 months: Boys Length-for-age percentiles and Weight-for-age percentiles

Birth to 24 months: Girls Weight-for-length percentiles and Head circumference-for-age percentiles

Birth to 24 months: Girls Length-for-age percentiles and Weight-for-age percentiles

Jaffe AC. Failure to Thrive. Pediatrics in Review. 2011; 32(3)

Prutsky GJ et al. When Developmental Delay and Failure to Thrive Are Not Psychosocial. Hospital Pediatrics. 2016; (1):6

Jul 01 2019
36 mins
Play

Rank #7: EKG Killers: Part One

May 01 2018
37 mins
Play

Rank #8: The Fussy Infant

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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.

Mar 01 2018
46 mins
Play

Rank #9: Neonatal Jaundice

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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 measurement.  Identify 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.

May 01 2017
39 mins
Play

Rank #10: Approach to Shock

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Do we recognize shock early enough?
How do we prioritize our interventions?
How can we tell whether we’re making our patient better or worse?

World wide, shock is a leading cause of morbidity and mortality in children, mostly for failure to recognize or to treat adequately.

So, what is shock?

Simply put, shock is the inadequate delivery of oxygen to your tissues.  That’s it.  Our main focus is on improving our patient’s perfusion.

Oxygen delivery to the tissues depends on cardiac output, hemoglobin concentration, the oxygen saturation of the hemoglobin you have, and the environmental partial pressure of oxygen.

At the bedside, we can measure some of these things, directly or indirectly.  But did you notice that blood pressure is not part of the equation?  The reason for that is that blood pressure is really an indirect proxy for perfusion – it’s not necessary the ultimate goal.

The equation here is a formality:

DO2 = (cardiac output) x [(hemoglobin concentration) x SaO2 x 1.39] + (PaO2  x 0.003)

 

 
Shock CAN be associated with a low blood pressure, but shock is not DEFINED by a low blood pressure.

 

 
Compensated Shock: tachycardia with poor perfusion.  A child compensates for low cardiac output with tachycardia and a increase in systemic vascular resistance.

 

 
Decompensated Shock: frank hypotension, an ominous, pre-arrest phenomenon.

Shock is multifactorial, but we need to identify a primary cause to prioritize interventions.

 

 
How they "COHDe": Cardiogenic, Obstructive, Hypovolemic, and Distributive.

 

Cardiogenic Shock

All will present with tachycardia out of proportion to exam, and sometimes with unexplained belly pain, usually due to hepatic congestion.  The typical scenario in myocarditis is a precipitous decline after what seemed like a run-of-the-mill URI.

Cardiogenic shock in children can be from congenital heart disease or from acquired etiologies, such as myocarditis.  Children, like adults, present in cardiogenic shock in any four of the following combinations: warm, cold, wet, or dry.

"Warm and Dry"

A child with heart failure is “warm and dry” when he has heart failure signs (weight gain, mild hepatomegaly), but has enough forward flow that he has not developed pulmonary venous congestion.  A warm and dry presentation is typically early in the course, and presents with tachycardia only.

"Warm and Wet"

If he worsens, he becomes “warm and wet” with pulmonary congestion – you’ll hear crackles and see some respiratory distress.  Infants with a “warm and wet” cardiac presentation sometimes show sacral edema – it is their dependent region, equivalent to peripheral edema as we see in adults with right-sided failure.

“Warm” patients – both warm and dry and warm and wet -- typically have had a slower onset of their symptoms, and time to compensate partially. Cool patients are much sicker.

"Cold and Dry”

A patient with poor cardiac output; he is doing everything he can to compensate with increased peripheral vascular resistance, which will only worsen forward flow.  Children who have a “cold and dry” cardiac presentation may have oliguria, and are often very ill appearing, with altered mental status.

"Cold and Wet"

The sickest of the group, this patient is so clamped down peripherally that it is now hindering forward flow, causing acute congestion, and pulmonary venous back-up.  You will see cool, mottled extremities.

Cardiogenic Shock: Act

Use point-of-care cardiac ultrasound:

Good Squeeze? M-mode to measure fractional shortening of the myocardium or anterior mitral leaflet excursion.

Pericardial Effusion? Get ready to aspirate.

Ventricle Size? Collapsed, Dilated,

Careful with fluids -- patients in cardiogenic shock may need small aliquots, but go quickly to a pressor to support perfusion

Pressor of choice: epinephrine, continuous IV infusion: 0.1 to 1 mcg/kg/minute.  Usual adult starting range will end up being 1 to 10 mcg/min.

Avoid norepinephrine, as it increases systemic vascular resistance, may affect afterload

Just say no to dopamine: increased mortality when compared to epinephrine

 

Obstructive Shock

Mostly one of two entities: pulmonary embolism or cardiac tamponade.

Pulmonary embolism in children is uncommon – when children have PE, there is almost always a reason for it – it just does not happen in normal, healthy children without risk factors.

Children with PE will either have a major thrombophilic comorbidity, or they are generously sized teenage girls on estrogen therapy.

Tamponade -- can be infectious, rheumotologic, oncologic, or traumatic.  It’s seen easily enough on point of care ultrasound.  If there is non-traumatic tamponade physiology, get that spinal needle and get to aspirating.

Obstructive Shock: Act

Pulmonary embolism (PE) with overt shock: thrombolyse; otherwise controversial.  PE with symptoms: heparin.

Tamponade: if any sign of shock, pericardiocentesis, preferentially ultrasound-guided.

 

Hypovolemic Shock

The most common presentation of pediatric shock; look for decreased activity, decreased urine output, absence of tears, dry mucous membranes, sunken fontanelle.  May be due to obvious GI losses or simply poor intake.

Rapid reversal of hypovolemic shock: may need multiple sequential boluses of isotonic solutions. Use 10 mL/kg in neonates and young infants, and 20 mL/kg thereafter.

Hypovolemic Shock: Act

Tip: in infants, use pre-filled sterile flushes to push fluids quickly.  In older children, use a 3-way stop cock in line with your fluids and a 30 mL syringe to "pull" fluids, turn the stop cock, and "push them into the patient.

Titrate to signs of perfusion, such as an improvement in mental status, heart rate, capillary refill, and urine output.

When concerned about balancing between osmolality, acid-base status, and volume status, volume always wins.  Our kidneys are smarter than we are, but they need to be perfused first.

 

Distributive Shock

The most common cause of distributive shock is sepsis, followed by anaphylactic, toxicologic, adrenal, and neurogenic causes.  Septic shock is multifactorial, with hypovolemic, cardiogenic, and distributive components.

Children with sepsis come in two varieties: warm shock and cold shock.

Distributive Shock: Act

Warm shock is due to peripheral vascular dilation, and is best treated with norepinephrine.

Cold shock is due to a child’s extreme vasoconstriction in an attempt to compensate.  Cold shock is the most common presentation in pediatric septic shock, and is treated with epinephrine.

Early antibiotics are crucial, and culture everything that seems appropriate.

 

Shock: A Practical Approach

 

"How FAST you FILL the PUMP and SQUEEZE"

Sometimes things are not so cut-and-dried.  We'll use a practical approach to diagnose and intervene simultaneously.

Look at 4 key players in shock: heart rate, volume status, contractility, and systemic vascular resistance.

How FAST you FILL the PUMP and SQUEEZE

First, we look at heart rate -- how FAST?

Look at the heart rate – is it sinus?  Could this be a supraventricular tachycardia that does not allow for enough diastolic filling, leading to poor cardiac output?  If so, use 1 J/kg to synchronize cardiovert.  Conversely, is the heart rate too slow – even if the stroke volume is sufficient, if there is severe bradycardia, then cardiac output  -- which is in liters/min – is decreased.  Chemically pace with atropine, 0.01 mg/kg up to 0.5 mg, or use transcutaneous pacing.

If the heart rate is what is causing the shock, address that first.

Next, we look at volume status.

How FAST you FILL the PUMP and SQUEEZE

Look to FILL the tank if necessary.  Does the patient appear volume depleted?  Try a standard bolus – if this improves his status, you are on the right track.

Now, we look at contractility.

How FAST you FILL the PUMP and SQUEEZE

Is there a problem with the PUMP?  That is, with contractility?  Is this in an infarction, an infection, a poisoning?  Look for signs of cardiac congestion on physical exam.  Put the probe on the patient’s chest, and look for effusion.  Look to see if there is mild, moderate, or severe decrease in cardiac contractility.  If this is cardiogenic shock – a problem with the pump itself -- begin pressors.

And finally, we look to the peripheral vascular resistance.

How FAST you FILL the PUMP and SQUEEZE

Is there a problem with systemic vascular resistance – the SQUEEZE?

Look for signs of changes in temperature – is the patient flushed?  Is this an infectious etiology?  Are there neurogenic or anaphylactic concerns?  After assessing the heart rate, optimizing volume status, evaluating contractility, is the cause of the shock peripheral vasodilation?  If so, treat the cause – perhaps this is a distributive problem due to anaphylaxis.  Treat with epinephrine. The diagnosis of exclusion in trauma is neurogenic shock.  Perhaps this is warm shock, both are supported with norepinephrine.  All of these affect systemic vascular resistance – and the shock won’t be reversed until you optimize the peripheral squeeze.

 

Summary

The four take-home points in the approach to shock in children

  1. To prioritize your innterventions, remember how patients COHDe: Cardiogenic, Obstructive, Hypovolemic, and Distributive. Your patient's shock may be multifactorial, but mentally prioritize what you think is the MAIN case of the shock, and deal with that first.
  2. To treat shock, remember: How FAST You FILL The PUMP and SQUEEZE: Look at the heart rate – how FAST.  Look at the volume status – the FILL.  Assess cardiac contractility – the PUMP, and evaluate the peripheral vascular tone – the SQUEEZE.
  3. In pediatric sepsis, the most common type is cold shock – use epinephrine (adrenaline) to get that heart to increase the cardiac output. In adolescents and adults, they more often present in warm shock, use norepinephrine (noradrenaline) for its peripheral squeeze to counteract this distributive type of shock.
  4. Rapid-fire word association:
  • Epinephrine for cardiogenic shock
  • Intervention for obstructive shock
  • Fluids for hypovolemic shock
  • Norepinephrine for distributive shock

References

Agha BS, Sturm JJ, Simon HK, Hirsh DA. Pulmonary embolism in the pediatric emergency department. Pediatrics. 2013 Oct;132(4):663-7.

Dellinger RP, Levy MM, Rhodes A, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med. 2013; 41:580-637.

Jaff MR et al. for the American Heart Association Council on Cardiopulmonary, Critical Care, Perioperative and Resuscitation; American Heart Association Council on Peripheral Vascular Disease; American Heart Association Council on Arteriosclerosis, Thrombosis and Vascular Biology. Management of massive and submassive pulmonary embolism, iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement from the American Heart Association. Circulation. 2011; Apr 26;123(16):1788-830.

Levy B et al. Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables in cardiogenic shock. A prospective, randomized pilot study. Crit Care Med. 2011; 39:450.

Micek ST, McEvoy C, McKenzie M, Hampton N, Doherty JA, Kollef MH. Fluid balance and cardiac function in septic shock as predictors of hospital mortality. Crit Care. 2013; 17:R246.

Osman D, Ridel C, Ray P, et al. Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge. Crit Care Med. 2007; 35:64-8.

Ventura AM, Shieh HH, Bousso A, Góes PF, de Cássia F O Fernandes I, de Souza DC, Paulo RL, Chagas F, Gilio AE. Double-Blind Prospective Randomized Controlled Trial of Dopamine Versus Epinephrine as First-Line Vasoactive Drugs in Pediatric Septic Shock. Crit Care Med. 2015;43(11):2292-302.

This post and podcast are dedicated to Natalie May, MBChB, MPHe, MCEM, FCEM for her collaborative spirit, expertise, and her super-charged support of #FOAMed.  You make a difference.  Thank you.

Undifferentiated Shock

Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

Jun 01 2016
38 mins
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Rank #11: Vaccine Preventable Illness Part One

Jul 01 2017
39 mins
Play

Rank #12: The Pediatric Surgical Abdomen

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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!

Aug 01 2017
30 mins
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Rank #13: Concussion

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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.

Jul 01 2018
34 mins
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Rank #14: Altered Mental Status in Children (REBROADCAST)

May 01 2019
36 mins
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Rank #15: Pediatric Status Epilepticus

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Do you have a plan for your little patient when he just won’t stop seizing?  What do you do when your typical treatment is not enough? Get up-to-date in the understanding and management of pediatric status epilepticus.

Definition of status epilepticus:Continuous seizure activity of 5 minutes or greater

– OR –

Recurrent activity without recovery between intervals.  (This definition includes clinically apparent seizures as well as those seen only on EEG.)

During a seizure, GABA receptors in the neuron’s membrane are internalized and destroyed.  Seizure activity itself starts this self-defeating process – this is the first reason we need to act as quickly as possible and take advantage of the GABA receptors that are still recruitable.

Excitatory receptors – the NMDA receptors – are acutely upregulated and mobilize to the neuron’s surface.  This is the second reason to act quickly and avoid this kindling effect.

In other words – time is brain.

Or… is it something else as well?

Pediatric status epilepticus is analogous to the multi-organ dysfunction syndrome in severe sepsis.  Status epilepticus affects almost every organ system. 

Cardiac – dysrhythmias, high output failure, and autonomic dysregulation resulting in hypotension or hypertension. 

Respiratory – apnea and hypoxia, ARDS, and potentially aspiration pneumonia.  Renal – rhabdomyolysis, myoglobinuria, and acute renal failure.

Metabolic – lactic acidosis, hypercapnia, hyperglycemia, sometimes hypoglycemia, hyperkalemia, and leukocytosis.

Autonomic – hyperpyrexia and breakdown of cerebral circulation. 

DeLorenzo et al.: Mortality correlated with time seizing.  Once the seizure has met the 30 min mark, Delorenzo reported a jump from 4.4% mortality to 22%!  If the seizure lasts greater than 2 hours, 45%.  Time spent seizing is a vicious cycle: it’s harder to break the longer it goes on, and the longer it goes on, the higher the mortality.

Think about treatment of pediatric status epilepticus in terms of time: prehospital care, status epilepticus (greater than 5 min), initial refractory status epilepticus (greater than 10 min), later refractory status (at 20 min), and coma induction (at 25 minutes).

Case 1: Hyponatremic Status Epilepticus

Give 3 mL/kg of 3% saline over 30 min.

Stop the infusion as soon as the seizure stops.

Case 2: INH toxicity

Empiric treatment -- you are the test.  If we know the amount of ingestion in adults or children, we give a gram-for-gram replacement, up to 5 grams. 

If a child under 2 years of age arrives to you in stats epilepticus, give 100 mg of IV pyridoxime for potentially undiagnosed congenital deficiency.

Case 3: Headache and Arteriovenous Malformation

Unlike in adults, stroke in children is divided evenly between hemorrhagic and ischemic etiologies. 

The differential is vast: cardiac, hematologic, infectious, vascaulr, syndromic, metabolic, oncologic, traumatic, toxic. 

Treatment: stabilization, embolization by interventional radiology, elective extirpation when more stable.  Other options for stable patients include an endovascular flow-directed microcatheter using cyanoacrylate. Radiosurgery is an options for others.

Non-convulsive Status Epilepticus

Risk factors include age < 18, especially age < 1, no prior history of seizures, and traumatic brain injury.  This would prompt you to ask for continuous EEG monitoring for non-convulsive status epilepticus, especially when there is a change in mental status for no other reason.  Also, a prolonged post-ictal state or prolonged altered mental status.  Other considerations are those who had a seizure and cardiac arrest -  ROSC without RONF, those with traumatic brain injury, and those needing ECMO – all within the context of seizures.

SUMMARY POINTS

The longer the seizure lasts, the harder it is to break – act quickly

Have a plan for normal escalation of care, and Search for an underlying cause

Recognize when the routine treatment is not enough.Before You Go

“Healing is a matter of time, but it is sometimes also a matter of opportunity.”

“Extreme remedies are very appropriate for extreme diseases.”

 – Hippocrates of KosSelected References

Abend NS et al. Nonconvulsive seizures are common in critically ill children. Neurology. 2011; 76(12):1071-7

Baren J. Pediatric Seizures and Strokes: Beyond Benzos and Brain Scans. ACEP Scientific Assembly. October 8th, 2009. Boston, MA.

Brophy et al. Guidelines for the Evaluation and Management of Status Epilepticus. Neurocrit Care. 2012; DOI 10.1007/s12028-012-9695-z

Capovilla G et al. Treatment of convulsive status epilepticus in childhood: Recommendations of the Italian League Against Epilepsy. Epilepsia. 2013; 54 Suppl 7:23-34

Chin RFM et al., for the NLSTEPSS Collaborative Group. Incidence, cause, and short-term outcome of convulsive status epilepticus in childhood: prospective population-based study. Lancet. 2006; 368: 222–29.

Chen JW, Chamberlain CG. Status epilepticus: pathophysiology and management in adults. Lancet Neurol. 2006; 5:246-256.

DeLorenzo RJ. Comparison of status epilepticus with prolonged seizure episodes lasting from 10 to 29 minutes. Epilepsia. 1999 Feb;40(2):164-9.

LaRoche SM, Helmers SL. The New Antiepileptic Drugs: Scientific Review. JAMA. 2004;291:605-614.

Minns AB, Ghafouri N, Clark RF. Isoniazid-induced status epilepticus in a pediatric patient after inadequate pyridoxine therapy. Pediatr Emerg Care. 2010; 26(5):380-1.

Ogilvy CS et al. Recommendations for the Management of Intracranial Arteriovenous Malformations: A Statement for Healthcare Professionals From a Special Writing Group of the Stroke Council, American Stroke Council. Stroke. 2001; 32: 1458-1471

Rosati A et al. Efficacy and safety of ketamine in refractory status epilepticus in children. Neurology. 2012; 79:2355-2358.

Schwartz ID. Hyponatremic seizure in a child using desmopressin for nocturnal enuresis.  Arch Pediatr Adolesc Med. 1998 Oct;152(10):1037-8

Trommer BL, Pasternak JF.  NMDA receptor antagonists inhibit kindling epileptogenesis and seizure expression in developing rats. Brain Res Dev Brain Res. 1990 May 1;53(2):248-52.

Waterhouse EJ et al. Prospective population-based study of intermittent and continuous convulsive status epilepticus in Richmond, Virginia. Epilepsia. 1999 Jun;40(6).

Sep 01 2015
24 mins
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