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Neonatal Resuscitation

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Stridor, Stertor, and Noisy Breathing

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Brief, Huddle, and Debrief in the PED

Fontanelle Facts

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Wound Care at Home

The Abdominal Exam in Children

Hemolytic Uremic Syndrome

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Push-Dose Epi

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Environmental Injuries in Children

PEM Myths

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!

Thank you for providing us listeners with a podcase that is so a well put together. For non-peds healthcare providers, this is such valuable information.

Excellent peds medicine podcast!

My best pediatric EM education during residency.

Great podcast

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 <a href="http://PEMplaybook.org/" rel="nofollow" target="_blank">http://PEMplaybook.org/</a> for show notes and to get involved with the show -- see you there!

Pediatric Emergency Playbook

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.

A Social Visit or Your Most Dangerous Presentation Tonight? 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href="http://pemplaybook.org/wp-content/uploads/2017/12/Slide91.jpg" rel="nofollow" target="_blank"></a> <a href="http://pemplaybook.org/wp-content/uploads/2017/12/Slide92.jpg" rel="nofollow" target="_blank"></a> <a href="http://pemplaybook.org/wp-content/uploads/2017/12/Slide93.jpg" rel="nofollow" target="_blank"></a> <a href="http://pemplaybook.org/wp-content/uploads/2017/12/Slide94.jpg" rel="nofollow" target="_blank"></a> <a href="http://pemplaybook.org/wp-content/uploads/2017/12/Slide95.jpg" rel="nofollow" target="_blank"></a> <a href="http://pemplaybook.org/wp-content/uploads/2017/12/Slide96.jpg" rel="nofollow" target="_blank"></a> <a href="http://pemplaybook.org/wp-content/uploads/2017/12/Slide97.jpg" rel="nofollow" target="_blank"></a> <a href="http://pemplaybook.org/wp-content/uploads/2017/12/Slide98.jpg" rel="nofollow" target="_blank"></a> <a href="http://pemplaybook.org/wp-content/uploads/2017/12/Slide99.jpg" rel="nofollow" target="_blank"></a> <a href="http://pemplaybook.org/wp-content/uploads/2017/12/Slide100.jpg" rel="nofollow" target="_blank"></a> This post and podcast are dedicated to <a href="https://twitter.com/henrygoldstein" rel="noopener nofollow" target="_blank">Henry Goldstein, B.Pharm, MBBS</a> for his tireless dedication to all things #FOAMed, #FOAMped, and #MedEd.  You are awesome.  Make sure to visit <a href="https://dontforgetthebubbles.com/" rel="noopener nofollow" target="_blank">Don't Forget the Bubbles!</a> 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.

The Fussy Infant

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 VolvulusIn 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 GERDThe Infant: Non-Accidental TraumaAll 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:  Is the history consistent? Was seeking medical help unnecessarily delayed? Does the onset of injury fit with the developmental level of the child? Is the behavior of the child and his interaction with his care-givers appropriate? Do the findings of the head-to-toe examination match the history? 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:  Hyperglycemia, with a blood glucose of &gt;200 mg/dL (11 mmol/L) AND Evidence of metabolic acidosis, with a venous pH of less than 7.3 or a bicarbonate level of &lt; 15 mEq/L AND 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: 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. Bilious is bad – green vomit is always a surgical emergency – do not pass go – get the surgeons involved early 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. Match the tempo of your treatment to the tempo of the disease.ReferencesApplegate 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 &amp; 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

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: <ul> <li>Fever, irritability and vomiting?  Think meningitis, UTI, or sepsis.</li> <li>Premature, unwell, and vomiting?  Think necrotizing enterocolitis.  Remember, 10% of cases of NEC can be full-term. Look for pneumatosis intestinalis.</li> <li>Systemically ill, afebrile, and vomiting for no other reason?  Think inborn error of metabolism.  Screen with a glucose, ammonia, lactate, and urine ketones.</li> <li>Others include congenital intestinal atresia or webs, meconium ileus, or severe GERD</li></ul>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. <a href="http://www.ncbi.nlm.nih.gov/pubmed/24325939" rel="nofollow" target="_blank">Louwers et al.</a> 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: <ol> <li>Is the history consistent?</li> <li>Was seeking medical help unnecessarily delayed?</li> <li>Does the onset of injury fit with the developmental level of the child?</li> <li>Is the behavior of the child and his interaction with his care-givers appropriate?</li> <li>Do the findings of the head-to-toe examination match the history?</li> <li>Are there any other red flags or signals that make you doubt the safety of the child or other family members?</li> </ol> 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. <a href="http://www.ncbi.nlm.nih.gov/pubmed/25041509" rel="nofollow" target="_blank">The International Society for Pediatric and Adolescent Diabetes (ISPAD) criteria for DKA</a>: <ol> <li>Hyperglycemia, with a blood glucose of &gt;200 mg/dL (11 mmol/L) AND</li> <li>Evidence of metabolic acidosis, with a venous pH of less than 7.3 or a bicarbonate level of &lt; 15 mEq/L AND</li> <li>Ketosis, found either in the urine or if directly checked in the blood.</li> </ol> If you have access to checking a serum beta-hydroxybutryrate – the unsung ketone – it can help in diagnosis in unclear cases. Cerebral Edema Criteria: <ul> <li>Minor criteria: headache, vomiting, irritability or lethargy; hypertension in the face of hypovolemia.</li> <li>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).</li> </ul> Cerebral Edema Action Items: <ul> <li>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.</li> <li>Put the head of the bed up 30 degrees.</li> <li>Alert your colleagues and counsel your parents.  Make sure everyone knows what to watch out for.</li> </ul> As you can see, vomiting in the young child can be really anything!  Keep your differential broad, and think by age and by system. <a href="http://pemplaybook.org/wp-content/uploads/2016/01/Differential-Diagnosis-of-Vomiting-in-Children.pdf" rel="nofollow" target="_blank">Differential Diagnosis of Vomiting in Children</a> 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. <ul> <li>Do a careful physical exam. The general assessment is always helpful – is the child irritable, listless, agitated?</li> <li>What is his work of breathing?  Effortless tachypnea may be a sign of acidosis or sepsis.</li> <li>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.</li> <li>Any skin signs?  Look for petechiae, urticaria, purpura.</li> </ul> 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: <ol> <li>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.</li> <li>Bilious is bad – green vomit is always a surgical emergency – do not pass go – get the surgeons involved early</li> <li>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.</li> <li>Match the tempo of your treatment to the tempo of the disease.</li></ol>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 &amp; 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 <a href="https://twitter.com/Damian_Roland" rel="nofollow" target="_blank">Damian Roland, BMedSci (Hons), MB BS, MRCPCH</a>, for his fervor in the care of children and his dedication to <a href="http://rolobotrambles.com/" rel="nofollow" target="_blank">quality medical education</a>. <a href="http://www.wikem.org/wiki/Main_Page" rel="nofollow" target="_blank"></a> <a href="http://www.wikem.org/wiki/Nausea_and_vomiting_%28peds%29" rel="nofollow" target="_blank">Nausea and Vomiting</a> | <a href="http://www.wikem.org/wiki/Non-accidental_trauma" rel="nofollow" target="_blank">Non-Accidental Trauma</a> | <a href="http://www.wikem.org/wiki/DKA" rel="nofollow" target="_blank">DKA</a> Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

Vomiting in the Young Child: Nothing or Nightmare

"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 (&lt; 92%), grunting, focal crackles, or high fever (&gt; 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

"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 (&lt; 92%), grunting, focal crackles, or high fever (&gt; 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 <a href="http://www.ncbi.nlm.nih.gov/pubmed/17015575" rel="nofollow" target="_blank">2006 AAP Guidelines</a> and the <a href="http://pediatrics.aappublications.org/content/early/2014/10/21/peds.2014-2742" rel="nofollow" target="_blank">2014 AAP Guidelines</a> 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 <a href="http://www.nejm.org/doi/pdf/10.1056/NEJMoa1301839" rel="nofollow" target="_blank">study</a> 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 <a href="http://www.ncbi.nlm.nih.gov/pubmed/27189681" rel="nofollow" target="_blank">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]</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/17015575" rel="nofollow" target="_blank">American Academy of Pediatrics Subcommittee on Diagnosis and Management of Bronchiolitis. Diagnosis and management of bronchiolitis. Pediatrics. 2006 Oct;118(4):1774-93.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/24442856" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/26658529" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/26382998" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/24753521" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/27549684" rel="nofollow" target="_blank">Florin TA, Plint AC, Zorc JJ. Viral bronchiolitis. Lancet. 2016 Aug 20. [Epub ahead of print]</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/22331343" rel="nofollow" target="_blank">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.</a> <a href="http://pediatrics.aappublications.org/content/pediatrics/131/Supplement_1/S103.full.pdf" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/22929141" rel="nofollow" target="_blank">Lashkeri T, Howell JM, Place R. Capnometry as a predictor of admission in bronchiolitis. Pediatr Emerg Care. 2012 Sep;28(9):895-7.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/26866481" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/26384333" rel="nofollow" target="_blank">Liet JM, Ducruet T, Gupta V, Cambonie G. Heliox inhalation therapy for bronchiolitis in infants. Cochrane Database Syst Rev. 2015 Sep 18;(9):CD006915.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/27446241" rel="nofollow" target="_blank">Mammas IN, Spandidos DA. Paediatric Virology in the Hippocratic Corpus. Exp Ther Med. 2016 Aug;12(2):541-549.</a> <a href="http://www.jpeds.com/article/S0022-3476(16)00043-3/abstract" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/26735994" rel="nofollow" target="_blank">Meissner HC. Viral Bronchiolitis in Children. N Engl J Med. 2016 Jan 7;374(1):62-72.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/24901443" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/24429091" rel="nofollow" target="_blank">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.</a> <a href="http://www.jpeds.com/article/S0022-3476(16)30547-9/abstract" rel="nofollow" target="_blank">Oakley E et al. Nasogastric Hydration in Infants with Bronchiolitis Less Than 2 Months of Age. J Pediatr. 2016. [Article in Press]</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/26928704" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/25349312" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/26833493" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/23758233" rel="nofollow" target="_blank">Skjerven HO et al. Racemic adrenaline and inhalation strategies in acute bronchiolitis. N Engl J Med. 2013 Jun 13;368(24):2286-93.</a> This post and podcast are dedicated to <a href="https://twitter.com/DrLindaMD" rel="nofollow" target="_blank">Linda Girgis MD, FAAFP</a>, for her authenticity, innovation, and clear and honest voice on the the frontlines.  Thank you, <a href="http://drlinda-md.com/" rel="nofollow" target="_blank">Dr Linda</a>. <a href="http://www.wikem.org/wiki/Main_Page" rel="nofollow" target="_blank"></a> <a href="http://www.wikem.org/wiki/Bronchiolitis_(peds)" rel="nofollow" target="_blank">Bronchiolitis</a> Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

Bronchiolitis

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.

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.<a href="http://pemplaybook.org/wp-content/uploads/2017/05/Jaundice_Bilitool_Pediatric-Podcast_Horeczko.jpg" rel="nofollow" target="_blank"></a> 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 <a href="http://bilitool.org/" rel="noopener noreferrer nofollow" target="_blank">Bilitool</a> or Bhutani Nomogram (below). Can I go Home Now? <a href="http://pemplaybook.org/wp-content/uploads/2017/04/F2.large_.jpg" rel="nofollow" target="_blank"></a> 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? <a href="http://pemplaybook.org/wp-content/uploads/2017/04/F3.large_.jpg" rel="nofollow" target="_blank"></a> <a href="http://pemplaybook.org/wp-content/uploads/2017/05/Bililights_Pediatric-Podcast_Horeczko.jpg" rel="nofollow" target="_blank"> </a> Exchange Transfusion Now? <a href="http://pemplaybook.org/wp-content/uploads/2017/04/F4.large_.jpg" rel="nofollow" target="_blank"></a> 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 <a href="http://www.llli.org/" rel="noopener noreferrer nofollow" target="_blank">La Leche League</a> – 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<a href="http://pemplaybook.org/wp-content/uploads/2017/05/Exchange-Transfusion_Pediatric-Podcast_Horeczko.png" rel="nofollow" target="_blank"></a> 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 <a href="http://pediatrics.aappublications.org/content/early/2015/04/21/peds.2015-0699" rel="nofollow" target="_blank"> Benitz WE. Hospital Stay for Healthy Term Newborn Infants. Pediatrics. 2015; 135(5):948-53.</a> <a href="http://pediatrics.aappublications.org/content/114/1/297" rel="nofollow" target="_blank"> Bhutani V et al. Management of Hyperbilirubinemia in the Newborn Infant 35 or More Weeks of Gestation. Pediatrics. 2004; 114(1).</a> <a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3775137/" rel="nofollow" target="_blank"> Bhutani VK, Wong RJ. Bilirubin Neurotoxicity in Preterm Infants: Risk and Prevention. J Clin Neonatol. 2013 Apr-Jun; 2(2): 61–69.</a> <a href="http://pediatrics.aappublications.org/content/pediatrics/129/4/689.full.pdf" rel="nofollow" target="_blank"> Bosschaart N et al. Limitations and Opportunities of Transcutaneous Bilirubin Measurements. Pediatrics. 2012; 129(4).</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/17950138" rel="nofollow" target="_blank"> 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.</a> <a href="http://pediatrics.aappublications.org/content/early/2011/09/08/peds.2011-0206" rel="nofollow" target="_blank"> Gamaleldin R et al. Risk Factors for Neurotoxicity in Newborns With Severe Neonatal Hyperbilirubinemia. Pediatrics. 2011; 128(4):825-31.</a> <a href="http://pedsinreview.aappublications.org/content/32/8/341.short" rel="nofollow" target="_blank"> Lauer BJ, Spector ND. Hyperbilirubinemia in the Newborn. Pediatrics in Review. 2011; 32(8):341-9.</a> <a href="http://pediatrics.aappublications.org/content/124/4/1193" rel="nofollow" target="_blank"> Maisels J et al. Hyperbilirubinemia in the Newborn Infant ≥35 Weeks’ Gestation: An Update With Clarifications. Pediatrics. 2009; 124(4):1193-6.</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/16603425" rel="nofollow" target="_blank"> 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.</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/22802603" rel="nofollow" target="_blank"> Vandborg PK, Hansen BM, Greisen G, Ebbesen F. Dose-response relationship of phototherapy for hyperbilirubinemia. Pediatrics. 2012 Aug;130(2):e352-7.</a> This post and podcast are dedicated to <a href="https://twitter.com/GitaPensaMD" rel="noopener noreferrer nofollow" target="_blank">Gita Pensa, MD</a>, for her commitment to #FOAMed and passion for asynchronous learning and education innovation.

Neonatal Jaundice

EtCO2 Masterclass

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 ShockAll 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: ActUse 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 ShockMostly 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: ActPulmonary embolism (PE) with overt shock: thrombolyse; otherwise controversial.  PE with symptoms: heparin. Tamponade: if any sign of shock, pericardiocentesis, preferentially ultrasound-guided.  Hypovolemic ShockThe 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: ActTip: 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 ShockThe 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: ActWarm 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.  SummaryThe four take-home points in the approach to shock in children  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. 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. 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. 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

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 <a href="https://www.youtube.com/watch?v=wPKIg3UVL88" rel="nofollow" target="_blank">point-of-care cardiac ultrasound</a>: 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. <a href="https://www.youtube.com/watch?v=a-CkSL4nW-Q" rel="nofollow" target="_blank">Pulmonary embolism</a> 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. <a href="https://www.youtube.com/watch?v=dQPwT20TzVA" rel="nofollow" target="_blank">Tamponade</a> -- 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 <a href="https://www.youtube.com/watch?v=T6Z9DvPPmXg" rel="nofollow" target="_blank">ultrasound-guided</a>.  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 <ol> <li>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.</li> <li>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.</li> <li>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.</li> <li>Rapid-fire word association:</li> </ol> <ul> <li>Epinephrine for cardiogenic shock</li> <li>Intervention for obstructive shock</li> <li>Fluids for hypovolemic shock</li> <li>Norepinephrine for distributive shock</li> </ul> References <a href="http://www.ncbi.nlm.nih.gov/pubmed/23999960" rel="nofollow" target="_blank">Agha BS, Sturm JJ, Simon HK, Hirsh DA. Pulmonary embolism in the pediatric emergency department. Pediatrics. 2013 Oct;132(4):663-7.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/23353941" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/21422387" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/21037469" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/24138869" rel="nofollow" target="_blank">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.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/17080001" rel="nofollow" target="_blank">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.</a> <a href="Crit%20Care%20Med.%202015%20Nov;43(11):2292-302." rel="nofollow" target="_blank">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.</a> This post and podcast are dedicated to <a href="https://twitter.com/_NMay" rel="nofollow" target="_blank">Natalie May, MBChB, MPHe, MCEM, FCEM</a> for her collaborative spirit, expertise, and her super-charged support of #FOAMed.  You make a difference.  Thank you. <a href="http://www.wikem.org/wiki/Main_Page" rel="nofollow" target="_blank"></a> <a href="https://www.wikem.org/wiki/Shock" rel="nofollow" target="_blank">Undifferentiated Shock</a> Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

Approach to Shock

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 &gt;38° or &gt;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

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 <a href="http://pemplaybook.org/wp-content/uploads/2018/06/Slide1.jpg" rel="nofollow" target="_blank"></a> 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 <a href="http://pemplaybook.org/wp-content/uploads/2018/06/Slide2.jpg" rel="nofollow" target="_blank"></a> Moderate Probability <a href="http://pemplaybook.org/wp-content/uploads/2018/06/Slide3.jpg" rel="nofollow" target="_blank"></a> High Probability <a href="http://pemplaybook.org/wp-content/uploads/2018/06/Slide4.jpg" rel="nofollow" target="_blank"></a>   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 &gt;38° or &gt;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 <a href="https://twitter.com/WriteNowPodcast?lang=en" rel="noopener nofollow" target="_blank">Sarah Werner</a> for her constant encouragement of the story in all of us.  Check out <a href="https://www.sarahwerner.com/podcasts/" rel="noopener nofollow" target="_blank">Write Now with Sarah Werner</a>. 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

Strep Throat

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 &gt; 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!

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 <a href="http://pemplaybook.org/wp-content/uploads/2017/08/13_Timeline_Pediatric-Podcast.png" rel="nofollow" target="_blank"> </a> General Advice <a href="http://pemplaybook.org/wp-content/uploads/2017/08/General-advice_horeczko_pediatric-podcast.png" rel="nofollow" target="_blank"> </a> Neonate (birth to one month) Necrotizing Enterocolitis <a href="http://pemplaybook.org/wp-content/uploads/2017/08/1_Pneumatosis-Intestinalis_Horeczko_Pediatric-Podcast.png" rel="nofollow" target="_blank"> </a> Pneumatosis Intestinalis. Essentials: <ul> <li>Typically presents in 1st week of life (case reports to 6 months in chronically ill children)</li> <li>Extend suspicion longer in NICU graduates</li> <li>Up to 10% of all cases of necrotizing enterocolitis are in full-term children</li> <li>Pathophysiology is unknown, but likely a translocation of bacteria</li> </ul> Diagnosis: <ul> <li>Feeding intolerance, abdominal distention</li> <li>Abdominal XR: pneumatosis intestinalis</li> </ul> Management: <ul> <li>IV access, NG tube, broad-spectrum antibiotics, surgery consult, ICU admission</li> </ul> Intestinal Malrotation with Volvulus Essentials: <a href="http://pemplaybook.org/wp-content/uploads/2017/08/2_Corkscrew-Malrotation_Horeczko_Pediatric-Podcast.png" rel="nofollow" target="_blank"> </a> Corkscrew Sign in Malrotation with Volvulus <ul> <li>Bilious vomiting (80-100%) in the 1st month; especially in the 1st week</li> <li>May look well initially, then rapidly present in shock</li> <li>Ladd’s bands: abnormally high tethering of cecum to abdominal wall; peristalsis, volvulus, ischemia</li> </ul> Diagnosis: <ul> <li>History of bilious emesis is sufficient to involve surgeons</li> <li>Upper GI series: corkscrew appearance</li> <li>US (if ordered) may show abnormal orientation of and/or flow to superior mesenteric artery and vein</li> </ul> Management: <ul> <li>Stat surgical consult</li> <li>IV access, resuscitation, NG tube to decompress (bowel wall perfusion at risk, distention worsens)</li> </ul> Hirschprung Disease Essentials: <ul> <li>Problem in migration of neural crest cells</li> <li>Aganglionic colon (80% rectosigmoid; 15-20% proximal to sigmoid; 5% total colonic aganglionosis) colon (known as short-segment disease)</li> <li>Poor to no peristalsis: constipation, perforation, and/or sepsis</li> </ul> Diagnosis: <ul> <li>May be diagnosed early as “failure to pass meconium in 1st 48 hours”</li> <li>In ED, presents as either bowel obstruction or enterocolitis</li> <li>Contrast enema</li> <li>Beware of the toxic megacolon (vomiting, distention, sepsis)</li> </ul> <a href="http://pemplaybook.org/wp-content/uploads/2017/08/Presentation1.png" rel="nofollow" target="_blank"> </a> Management: <ul> <li>Resuscitation, antibiotics, NG tube decompression, surgical consultation; stable patients may need rectal biopsy for confirmation</li> <li>Staged surgery (abdominoperineal pull-through with diverting colostomy, subsequent anastomosis) versus one-stage repair.</li> </ul> Infant and Toddler (1 month to 2 years) Pyloric Stenosis Essentials: <ul> <li>Hypertrophy of pyloric sphincter; genetic, environmental, exposure factorsString Sign in Pyloric Stenosis.</li> </ul> Diagnosis: <ul> <li>Hungry, hungry, not-so-hippos; they want to eat all of the time, but cannot keep things down</li> <li>Poor weight gain (less than 20-30 g/day)</li> <li>US: “π–loric stenosis” (3.14); pylorus dimensions &gt; 3 mm x 14 mm</li> <li>UGI: “string sign”</li> </ul> <a href="http://pemplaybook.org/wp-content/uploads/2017/08/Picture2.png" rel="nofollow" target="_blank"></a> Management: <ul> <li>Trial of medical treatment with oral atropine via NGT (muscarinic effects decrease pyloric tone)</li> <li>Ramstedt pyloromyotomy (definitive)</li> </ul> Intussusception Essentials: <ul> <li>Majority (90%) ileocolic; no pathological lead point</li> <li>Small minority (4%) ileoileocolic due to lead point: Meckel’s diverticulum, polyp, Peyer’s patches, Henoch-Schönlein purpura (intestinal hematoma)</li> </ul> Diagnosis: <a href="http://pemplaybook.org/wp-content/uploads/2017/08/7_Target-Sign_Intussusception_Horeczko_Pediatric-Podcast.png" rel="nofollow" target="_blank"> </a> Target Sign (Donut Sign). <ul> <li>Ultrasound sensitivity and specificity near 100% in experienced hands</li> <li>Abdominal XR may show non-specific signs; used mainly to screen for perforation before reduction</li> </ul> Management: <ul> <li>Hydrostatic enema: contrast (barium or water-soluble contrast with fluoroscopy) or saline (with ultrasound)</li> <li>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</li> <li>Consider involving surgical service early (precaution before reduction)</li> <li>Traditional disposition is admission; controversial: home discharge from ED</li> </ul> Young Child and Older (2 years and up) Appendicitis Essentials: <ul> <li>Appendicitis occurs in all ages, but rarer in infants. Infants do not have fecalith; rather they have some other anatomic or congenital condition. </li> <li>More common in school-aged children (5-12 years) and adolescents</li> <li>Younger children present atypically, more likely to have perforated when diagnosed.</li> </ul> Diagnosis: <ul> <li>Non-specific signs and symptoms</li> <li>Often have abdominal pain first; vomiting comes later</li> <li>Location/orientation of appendix varies</li> <li>Appendicitis scores vary in their performance</li> <li>Respect fever and abdominal pain</li> </ul> <a href="http://pemplaybook.org/wp-content/uploads/2017/08/Appendix.png" rel="nofollow" target="_blank"></a> Management: <ul> <li>Traditional: surgical</li> <li>On the horizon: identification of low-risk children who may benefit from trial of antibiotics</li> <li>If perforated, interval appendectomy (IV antibiotics via PICC for 4-6 weeks, then surgery)</li> </ul> Obstruction <a href="http://pemplaybook.org/wp-content/uploads/2017/08/12_SBO-Incarcerated-Inguinal-Hernia_Horeczko_Pediatric-Podcast.png" rel="nofollow" target="_blank"> </a> SBO. Incarcerated Inguinal Hernia. Essentials: <ul> <li>Same pathophysiology and epidemiology as adults: “ABC” – adhesions, “bulges” (hernias), and cancer.</li> </ul> Diagnosis: <ul> <li>Obstruction is a sign of another condition. Look for cause of obstruction: surgical versus medical</li> <li>Abdominal XR in low pre-test probability</li> <li>CT abdomen/pelvis for moderate-to-high risk; confirmation and/or surgical planning</li> </ul> Management: <ul> <li>Treat underlying cause</li> <li>NG tube to low intermittent wall suction</li> <li>Admission, fluid management, serial examinations</li> </ul>   Take these pearls home: <ul> <li>Consider surgical pathology early in encounter</li> <li>Resuscitate while you investigate</li> <li>Have a low threshold for imaging and/or consultation, especially in preverbal children</li> </ul> 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 <a href="https://twitter.com/ffolliet?lang=en" rel="noopener noreferrer nofollow" target="_blank">Mr Ross Fisher</a> for his passion and spirit of collaboration in <a href="http://ffolliet.com/" rel="noopener noreferrer nofollow" target="_blank">all things #FOAMed</a>.  Thank you, sir!

The Pediatric Surgical Abdomen

Pediatric Sports Injuries

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

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

Cyanosis

When should you commit to getting urine? When can you wait? When should you forgo testing altogether?   When do I get urine? Symptoms – either typical dysuria, urgency, frequency in a verbal child, or non-descript abdominal pain or vomiting in a well appearing child. Fever – but first look for an obvious alternative source, especially viral signs or symptoms. No obvious source? Risk stratify before “just getting a urine”. In a low risk child, with obviously very vigilant parents, who is well appearing, you may choose not to test now, and ensure close follow up.   Bag or cath? The short answer is: always cath, never bag.   (Pros and cons in audio) What is the definition of a UTI? According to the current clinical practice guideline by the AAP, the standard definition of a urinary tract infection is the presence of BOTH pyuria AND at least 50 000 colonies per mL of a single uropathogen. Making the diagnosis in the ED: The presence of WBCs with a threshold of 5 or greater WBCs per HPF is required. What else goes into the urinalysis that may be helpful?   Pearl: nitrites are poorly sensitive in children.  It takes 4 hours for nitrites to form, and most children this age do no hold their urine. Pearl: the enhanced urinalysis is the addition of a gram stain.  A positive gram stain has a LR+ of 87 in infants less than 60 days, according to a study by Dayan et al. in Pediatric Emergency Care. When can I just call it pyelonephritis? In an adult, we look for UTI plus evidence of focal upper tract involvement, like CVA tenderness to percussion or systemic signs like nausea, vomiting, or fever.  It is usually straightforward. It’s for this reason that the literature uses the term “febrile UTI” for children.  Fever is very sensitive, but not specific in children. The ill-appearing child has pyelonephritis.   The well-appearing child likely has a “febrile UTI”, without upper involvement.  However, undetected upper tract involvement may be made in retrospect via imaging, if done. How should I treat UTIs? For simple lower tract disease, treat for at least 7 days.  There is no evidence to support 7 versus 10 versus 14 days.  My advice: use 7-10 days as your range for simple febrile UTI in children. Pyelonephritis should be treated for a longer duration.  Treat pyelonephritis for 10-14 days. What should we give them? Sulfamethoxazole and trimethoprim (Bactrim) is falling out of favor, mostly because isolates in many communities are resistant.  There is an association of Stevens-Johnson Syndrome (SJS) with Bactrim use.  This may be confounded by its prior popularity; any antibiotic can cause SJS, but there are more case reports with Bactrim. Cephalexin (Keflex): 25 mg/kg dose, either BID or TID.  It is easy on the stomach, rarely interacts with other meds, has high efficacy against E. coli, and most importantly, cephalexin has good parenchymal penetration. Nitrofurantoin is often used in pregnant women, because the drug tends to concentrate locally in the urine.  However, blood and tissue concentrations are weak.  It may be ineffective if there is some sub-clinical upper tract involvement. Cefdinir is a 3rd generation cephalosporin available by mouth, given at 14 mg/kg in either one dose daily or divided BID, up to max of 600 mg.  This may be an option for an older child who has pyelonephritis, but is well enough to go home. Whom should we admit? The first thing to consider is age.  Any infant younger than 2 months should be admitted for a febrile UTI.  Their immune systems and physiologic reserve are just not sufficient to localize and fight off infections reliably. The truth is, for serious bacterial illness like pneumonia, UTI, or severe soft tissue infections, be careful with any infant less than 4-6 months of age. Of course, the unwell child – whatever his age – he should be admitted.  Think about poor feeding, irritability, dehydration – in that case, just go with your gut and call it pyelonephritis, and admit. What is the age cut-off for a urine culture? In adults, we think of urine culture only for high-risk populations, such as pregnant women, the immunocompromised, those with renal abnormalities, the neurologically impaired, or the critically ill, to name a few. In children, it’s a little simpler.  Do it for everyone. Who is everyone? Think of the urine rule of 10s: 10% of young febrile children will have a UTI 10% of UAs will show no evidence of pyuria Routine urine culture in all children with suspected or confirmed UTI up to about age 10 What do I do then with urine culture results? From a quality improvement and safety perspective, consider making this a regular assignment to a qualified clinician. Check once in 24-48 hours to find possible growth of a single uropathogen with at least 50 000 CFU/mL.  Look at the record to see that the child is one some antibiotic, or the reason why he may not.  Call the family if needed. A second check at 48-72 hours may be needed to verify speciation and sensitivities. The culture check, although tedious, is important to catch those small children who did not present with pyuria and who may need antibiotics, or to verify that the right agent is given. Ok, so your UA is negative…now what? The culture is cooking, but you are not convinced.  Below is the differential diagnosis for common causes of pyuria in children:What kind of follow-up should the child get? The younger the child, the more we worry about missing a decompensation.  Encourage the parents to call the child's primary care clinician for a re-check in a few days, and to discuss whether or not further work-up such as imaging is indicated.  As always, strict return to ED precautions are helpful. Who needs imaging? A more accurate question is: what is an important anomaly to detect? Vesiculo-ureteral reflux – a loose ureteropelvic junction causes upstream reflux when the bladder constricts. Uretero-pelvic junction obstruction – in older children or young adults with hematuria, UTI, abdominal mass, or pain.  Infants born with UPJ obstruction have congenital hydronephrosis. Ureterocoele – a cystic mass in the bladder.  It is not malignant, but can cause ureteral dilation, and hydronephrosis.  Treatment is surgical. Ectopic ureter – either a duplication of the draining system, or an abnormal connection, such as the epidydimis or cervix. Posterior urethral valves – occur only in boys, and they are a bit of a misnomer.  The most common type of congenital bladder outlet obstruction, posterior urethral valves are just extra folds of membrane in the lumen of the prostatic urethra.  Usually ablation by cystoscopy does the trick. Urachal remnant – a leftover from fetal development, and an abnormal connection between the bladder and the umbilicus.  Look for an “always wet” belly button in an infant, or an umbilical mass with pain and fever in an older child. Imaging of choice as an outpatient? Renal and bladder ultrasound (RBUS) after the first UTI is recommended (although incompletely followed in practice). If the RBUS is positive, or with the second UTI, DMSA scan to evaluate possible renal scarring. So, with all of this testing – are we over doing it? Like anything, it’s a balance.  A few tips to avoid iatrogenia by way of a summary. If a child over 3 months of age is well, has no comorbidities, has a low grade fever "in the 38s" (38-38.9 °C) without a source, especially if less than 24 hours, you are very safe to do watchful waiting at home. More to the point, an otherwise well child with an obvious upper respiratory tract infection has a source of his fever. If your little patient has risk factors for UTI, or you are otherwise concerned, send the UA and send the culture.  You can opt out of the culture by middle school in the otherwise healthy child. And finally, deputize parents to carry the ball from here – the child needs ongoing primary care and his pediatrician may elect to do some screening.  Don’t promise or prime them for it – rather, encourage the conversation.  BONUS: Suprapubic aspiration (details in podcast audio; video below)  BONUS BONUS: Infant Clean Catch Technique   Step One: feed the baby, wait twenty minutes.     Step Two: clean the genitals with soap and warm water and dry with gauze.  Have your sterile urine container open and at the ready.     Step Three: one person holds the baby under his armpits with his legs dangling.  The other person gently taps the bladder (100 taps/min), then massages the lower back for 30 seconds.     Step Four: Clean Catch! (can also repeat process)   References Bonsu BK, Shuler L, Sawicki L, Dorst P, Cohen DM. Susceptibility of recent bacterial isolates to cefdinir and selected antibiotics among children with urinary tract infections. Acad Emerg Med. 2006 Jan;13(1):76-81. Coulthard MG, Lambert HJ, Vernon SJ, Hunter EW, Keir MJ, Matthews JN. Does prompt treatment of urinary tract infection in preschool children prevent renal scarring: mixed retrospective and prospective audits. Arch Dis Child. 2014 Apr;99(4):342-7. Dayan PS et al.  Test characteristics of the urine Gram stain in infants

When should you commit to getting urine? When can you wait? When should you forgo testing altogether? When do I get urine? Symptoms – either typical dysuria, urgency, frequency in a verbal child, or non-descript abdominal pain or vomiting in a well appearing child. Fever – but first look for an obvious alternative source, especially viral signs or symptoms. No obvious source? Risk stratify before “just getting a urine”. In a low risk child, with obviously very vigilant parents, who is well appearing, you may choose not to test now, and ensure close follow up. <a href="http://pemplaybook.org/wp-content/uploads/2017/02/UTI-Risk-Factors_Horeczko_Pediatric-Podcast-Emergency.png" rel="nofollow" target="_blank"> </a><a href="http://pemplaybook.org/wp-content/uploads/2017/02/Probability-UTI_Horeczko-Pediatric-Podcast-Emergency.png" rel="nofollow" target="_blank"></a> Bag or cath? The short answer is: always cath, never bag. <a href="http://pemplaybook.org/wp-content/uploads/2017/02/Urine-Trouble_Pediatric-Podcast-Emergency.jpg" rel="nofollow" target="_blank"> </a> (Pros and cons in audio) What is the definition of a UTI? According to the current clinical practice guideline by the AAP, the standard definition of a urinary tract infection is the presence of BOTH pyuria AND at least 50 000 colonies per mL of a single uropathogen. Making the diagnosis in the ED: The presence of WBCs with a threshold of 5 or greater WBCs per HPF is required. What else goes into the urinalysis that may be helpful? <a href="http://pemplaybook.org/wp-content/uploads/2017/02/UA-sensitivity_Horeczko-Pediatric-Podcast-Emergency-Medicine.png" rel="nofollow" target="_blank"> </a> Pearl: nitrites are poorly sensitive in children.  It takes 4 hours for nitrites to form, and most children this age do no hold their urine. Pearl: the enhanced urinalysis is the addition of a gram stain.  A positive gram stain has a LR+ of 87 in infants less than 60 days, according to a study by Dayan et al. in Pediatric Emergency Care. When can I just call it pyelonephritis? In an adult, we look for UTI plus evidence of focal upper tract involvement, like CVA tenderness to percussion or systemic signs like nausea, vomiting, or fever.  It is usually straightforward. It’s for this reason that the literature uses the term “febrile UTI” for children.  Fever is very sensitive, but not specific in children. The ill-appearing child has pyelonephritis.   The well-appearing child likely has a “febrile UTI”, without upper involvement.  However, undetected upper tract involvement may be made in retrospect via imaging, if done. How should I treat UTIs? For simple lower tract disease, treat for at least 7 days.  There is no evidence to support 7 versus 10 versus 14 days.  My advice: use 7-10 days as your range for simple febrile UTI in children. Pyelonephritis should be treated for a longer duration.  Treat pyelonephritis for 10-14 days. What should we give them? Sulfamethoxazole and trimethoprim (Bactrim) is falling out of favor, mostly because isolates in many communities are resistant.  There is an association of Stevens-Johnson Syndrome (SJS) with Bactrim use.  This may be confounded by its prior popularity; any antibiotic can cause SJS, but there are more case reports with Bactrim. Cephalexin (Keflex): 25 mg/kg dose, either BID or TID.  It is easy on the stomach, rarely interacts with other meds, has high efficacy against E. coli, and most importantly, cephalexin has good parenchymal penetration. Nitrofurantoin is often used in pregnant women, because the drug tends to concentrate locally in the urine.  However, blood and tissue concentrations are weak.  It may be ineffective if there is some sub-clinical upper tract involvement. Cefdinir is a 3rd generation cephalosporin available by mouth, given at 14 mg/kg in either one dose daily or divided BID, up to max of 600 mg.  This may be an option for an older child who has pyelonephritis, but is well enough to go home. Whom should we admit? The first thing to consider is age.  Any infant younger than 2 months should be admitted for a febrile UTI.  Their immune systems and physiologic reserve are just not sufficient to localize and fight off infections reliably. The truth is, for serious bacterial illness like pneumonia, UTI, or severe soft tissue infections, be careful with any infant less than 4-6 months of age. Of course, the unwell child – whatever his age – he should be admitted.  Think about poor feeding, irritability, dehydration – in that case, just go with your gut and call it pyelonephritis, and admit. What is the age cut-off for a urine culture? In adults, we think of urine culture only for high-risk populations, such as pregnant women, the immunocompromised, those with renal abnormalities, the neurologically impaired, or the critically ill, to name a few. In children, it’s a little simpler.  Do it for everyone. Who is everyone? Think of the urine rule of 10s: 10% of young febrile children will have a UTI 10% of UAs will show no evidence of pyuria Routine urine culture in all children with suspected or confirmed UTI up to about age 10 What do I do then with urine culture results? From a quality improvement and safety perspective, consider making this a regular assignment to a qualified clinician. Check once in 24-48 hours to find possible growth of a single uropathogen with at least 50 000 CFU/mL.  Look at the record to see that the child is one some antibiotic, or the reason why he may not.  Call the family if needed. A second check at 48-72 hours may be needed to verify speciation and sensitivities. The culture check, although tedious, is important to catch those small children who did not present with pyuria and who may need antibiotics, or to verify that the right agent is given. Ok, so your UA is negative…now what? The culture is cooking, but you are not convinced.  Below is the differential diagnosis for common causes of pyuria in children:<a href="http://pemplaybook.org/wp-content/uploads/2017/02/Dysuria_Horeczko-Emergency-Medicine-Podcast.png" rel="nofollow" target="_blank"></a>What kind of follow-up should the child get? The younger the child, the more we worry about missing a decompensation.  Encourage the parents to call the child's primary care clinician for a re-check in a few days, and to discuss whether or not further work-up such as imaging is indicated.  As always, strict return to ED precautions are helpful. Who needs imaging? A more accurate question is: what is an important anomaly to detect? Vesiculo-ureteral reflux – a loose ureteropelvic junction causes upstream reflux when the bladder constricts. Uretero-pelvic junction obstruction – in older children or young adults with hematuria, UTI, abdominal mass, or pain.  Infants born with UPJ obstruction have congenital hydronephrosis. Ureterocoele – a cystic mass in the bladder.  It is not malignant, but can cause ureteral dilation, and hydronephrosis.  Treatment is surgical. Ectopic ureter – either a duplication of the draining system, or an abnormal connection, such as the epidydimis or cervix. Posterior urethral valves – occur only in boys, and they are a bit of a misnomer.  The most common type of congenital bladder outlet obstruction, posterior urethral valves are just extra folds of membrane in the lumen of the prostatic urethra.  Usually ablation by cystoscopy does the trick. Urachal remnant – a leftover from fetal development, and an abnormal connection between the bladder and the umbilicus.  Look for an “always wet” belly button in an infant, or an umbilical mass with pain and fever in an older child. Imaging of choice as an outpatient? Renal and bladder ultrasound (RBUS) after the first UTI is recommended (although incompletely followed in practice). If the RBUS is positive, or with the second UTI, DMSA scan to evaluate possible renal scarring. So, with all of this testing – are we over doing it? Like anything, it’s a balance.  A few tips to avoid iatrogenia by way of a summary. If a child over 3 months of age is well, has no comorbidities, has a low grade fever "in the 38s" (38-38.9 °C) without a source, especially if less than 24 hours, you are very safe to do watchful waiting at home. More to the point, an otherwise well child with an obvious upper respiratory tract infection has a source of his fever. If your little patient has risk factors for UTI, or you are otherwise concerned, send the UA and send the culture.  You can opt out of the culture by middle school in the otherwise healthy child. And finally, deputize parents to carry the ball from here – the child needs ongoing primary care and his pediatrician may elect to do some screening.  Don’t promise or prime them for it – rather, encourage the conversation. BONUS: Suprapubic aspiration (details in podcast audio; video below) BONUS BONUS: Infant Clean Catch Technique <a href="http://pemplaybook.org/wp-content/uploads/2017/02/Herrero-Technique.png" rel="nofollow" target="_blank"> </a> Step One: feed the baby, wait twenty minutes. Step Two: clean the genitals with soap and warm water and dry with gauze.  Have your sterile urine container open and at the ready. Step Three: one person holds the baby under his armpits with his legs dangling.  The other person gently taps the bladder (100 taps/min), then massages the lower back for 30 seconds. Step Four: Clean Catch! (can also repeat process)   References <a href="https://www.ncbi.nlm.nih.gov/pubmed/16365328" rel="nofollow" target="_blank">Bonsu BK, Shuler L, Sawicki L, Dorst P, Cohen DM. Susceptibility of recent bacterial isolates to cefdinir and selected antibiotics among children with urinary tract infections. Acad Emerg Med. 2006 Jan;13(1):76-81.</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/24351607" rel="nofollow" target="_blank">Coulthard MG, Lambert HJ, Vernon SJ, Hunter EW, Keir MJ, Matthews JN. Does prompt treatment of urinary tract infection in preschool children prevent renal scarring: mixed retrospective and prospective audits. Arch Dis Child. 2014 Apr;99(4):342-7.</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/11862130" rel="nofollow" target="_blank">Dayan PS et al.  Test characteristics of the urine Gram stain in infants</a>

Urine Trouble

Pediatric airway management is a skill that integrates the three types of knowledge as described by the ancient Greeks: episteme, or theoretical knowledge, techne, or technical knowledge, and phronesis, or practical wisdom, also called prudence.Here we’ll invoke each type of knowledge and understanding as we go beyond the anatomical issues in pediatric airway management – to the advanced decision-making aspect of RSI and the what-to-do-when the rubber-hits-the road.Case 1: SepsisLaura is a 2-month-old baby girl born at 32 weeks gestational age who today has been “breathing fast” per mother.  On arrival she is in severe respiratory distress with nasal flaring and intercostal retractions.   Her heart rate is 160, RR 50, oxygen saturation is 88% on RA.  She has fine tissue-paper like rales throughout her lung fields.  Despite a trial of a bronchodilator, supplemental oxygen, even nasal CPAP and fluids, she becomes less responsive and her heart rate begins to drop relatively in the 80s to 90s – this is not a sign of improvement, but of impending cardiovascular collapse. She is in respiratory failure from bronchiolitis and likely viral sepsis.  She needs her airway taken over. Is this child stable enough for intubation? We have a few minutes to optimize, to resuscitate before we intubate. Here’s an easy tip: use the sterile flushes in your IV cart and push in 20, 40, or 60 mL/kg NS.  Just keep track of the number of syringes you use – it is the fastest way to get a meaningful bolus in a small child. Alternatively, if you put a 3-way stop-cock in the IV line and attach a 30 mL syringe, you can turn the stop cock, draw up stream from the IV bag into the syringe, turn te stop cock, and push the fluid in the IV.Induction Agent in SepsisThe consensus recommendation for the induction agent of choice for sepsis in children is ketamine. Etomidate is perfectly acceptable, but ketamine is actually a superior drug to etomidate in the rapid sequence intubation of children in septic shock.  It rapidly provides sedation and analgesia, and supports hemodynamic stability by blocking the reuptake of catecholamines.Paralytic Agent in SepsisThe succinylcholine versus rocuronium debate… Succinylcholine and its PROS  82% of RSI in the ED used succinylcholine (According to the National Emergency Airway Registry, in 2005).  We know it, we are comfortable with it. Succinylcholine produces superior intubating conditions when comparing 1 mg/kg succinylcholine versus 0.6 mg/kg rocuronium, succinylcholine is that at 45 seconds.  Succinylcholine and its CONs  Raises serum potassium in everyone, typically 0.5 to 1 mEq/L.  That is not usually a problem, but for those with preexisting or inducible hyperkalemia, it can precipitate an arrest, as in renal failure, underlying neurologic or myopathic conditions like multiple sclerosis, muscular dystrophy, ALS, or those who had a stroke or a burn more than 72 hours prior. We often have limited information in critical situations. Succinylcholine gives us a false sense of security.  In children, there really is no “safe apnea” period. Succinylcholine’s effect on the nicotinic receptors results in mydriasis, tachycardia, weakness, twitching and hypertension, and fasciculations (Think nicotine overdose: M/T/W/Th/F). Succinylcholine’s effect on muscarinic receptors manifest (as in organophosphate overdose): SLUDGE – salivation, lacrimation, urination, defecation, GI upset or more apropos here: DUMBBELLS – diarrhea, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation. Second dose of succinylcholine – beware of the muscarinic effects and bradycardia. Co-administer atropine, 0.01 mg/kg, up to 0.5 mg IV.  Coda: succinylcholine is not that bad – we would not have had such great success with it during the early years of our specialty if it were such a terrible drug.  The side effects are rare, but they can be deadly.  So, what’s the alternative? Rocuronium and its PROs  It has none of the side-effects of succinylcholine  Rocuronium and its CONs  Argument 1: the duration is too long if there is a difficult airway, since rocuronium can last over an hour. Still need to intubate, and now your patient is potentially worse. Argument 2: succinylcholine produces better intubating conditions at 45 seconds compared to rocuronium. At 0.6 mg/kg, rocuronium is inferior to succinylcholine at all time intervals. At 1.0 mg/kg, rocuronium is still inferior at 45 seconds.  At 1.2 mg/kg rocuronium – the dose now commonly recommended – there was no difference in intubating conditions, per a study by Heier et al. in Anethesia and Analgesia in 2000.Case 2: MultitraumaJoseph is a 3-year-old boy who is excited that there are so many guests at his house for a family party and when it’s starting to wind down and the guests begin to leave, he is unaccounted for. An unsuspecting driver of a mini-van backs over him. He is brought in by paramedics, who are now bagging him.Induction Agent in Trauma Need something that is hemodynamically stable – agents such as midazolam or propofol would cause too many problems. Etomidate is a short-acting imidazole derivative that acts on GABA-A receptors to induce loss of consciousness in 5-15 seconds. It can cause apnea, pain on injection, and myoclonus. Etomidate reduces cerebral blood flow, reduces intracranial pressure, and reduces cerebral oxygen consumption, all while maintaining arterial blood pressure and cerebral perfusion pressure. Ketamine is reasonable as well: there is no contraindication to ketamine except for known hydrocephalus. It is safe in head trauma. It is a good choice for the hypotensive trauma patient.  TBI is not a contraindication. In the case of the critically injured child who is normotensive, ketamine will raise his blood pressure and perhaps foster further bleeding.  The goal is a good general perfusion and a balanced resuscitation, ensuring enough cerebral perfusion without disrupting nascent clots.  On the other side of the spectrum, permissive hypotension is not described in children, as hypotension is a late and dangerous sign of shock.Paralytic Agent in TraumaAre your surgeons in an uproar about a long-acting agent and the pupillary response?  Relax, it’s a myth. Caro et al in Annals in 2011 reported that the majority of patients undergoing RSI preserved their pupillary response.  Succinylcholine actually performed worse than rocuronium. In the rocuronium group, all patients preserved their pupillary response.In the critically ill, we rethink your dosing of both the sedative and the paralytic.In a critically ill child or adult, perfusion suffers and it affects how we administer medications.  The patient’s arm-brain time or vein-to-brain time is less efficient; additionally, as the patient’s hemodynamic status softens, he becomes very sensitive to the effects of sedatives. We need to adjust our dosing for a critically ill patient:  Decrease the sedative to avoid falling over the hemodynamic compensation cliff. Increase the paralytic to account for prolonged arm-brain time.Case 3: Cardiac/myocarditis/congenital heart diseaseJacob is a 6-year-old-boy with tricuspid atresia s/p Fontan procedure who’s had one week of runny nose, cough, and now 2 days of high fever, vomiting, and difficulty breathing. The Fontan procedure is the last in a series of three palliative procedures in a child with complex cyanotic congenital heart disease with a single-ventricle physiology. The procedure reroutes venous blood to flow passively into the pulmonary arteries, because the right ventricle has been surgically repurposed to be the systemic pump.  The other most common defect with an indication for a Fontan is hypoplastic left heart syndrome. Typical “normal” saturations are 75 and 85% on RA.  Ask the parents or caregiver. Complications of the Fontan procedure include heart failure, superior vena cava syndrome, and hypercoagulable state, and others. A patient with a Fontan can present in cardiogenic shock from heart failure, distributive shock from an increased risk of infection, hypovolemic shock from over-diuresis or insensible fluid loss – or just a functional hypovolemia from the fact that his venous return is all passive – and finally obstructive shock due to a pulmonary thromboembolism. Types of shock mnemonic: this is how people COHDe – Cardiogenic, Obstructive, Hypovolemic, Distributive.Do we give fluids?Children after palliative surgery for cyanotic heart disease are volume-dependent.  Even if there is a component of cardiogenic shock, they need volume to drive their circuit.  Give a test dose of 10 mL/kg NS.Pressors in Pediatric Shock Children compensate their shock state early by increasing their SVR. Epinephrine (adrenaline) is great at increasing the cardiac output (with minimal increase in systemic vascular resistance; tachycardia)  In children the cardiac deleterious effects are not pronounced as in adults.  Later when the child is stabilized, other medication such as milrinone (ionotrope and venodilator) can be used. Epinephrine is also fantastic for cold shock when the patient is clamped down with cold extremities – the most common presentation in pediatric septic shock. Norepinephrine (noradrenaline) is best used when you need to augment systemic vascular resistance, such as in warm shock, where the patient has loss of peripheral vascular tone.Induction Agent in Cardiogenic ShockA blue baby – with a R –&gt; L shunt – needs some pinking up with ketamine A pink baby – with a L –&gt; R shunt – is already doing ok – don’t rock the boat – give a neutral agent like etomidate. Myocarditis or other acquired causes of cardiogenic shock – etomidate.Case 4: Status EpilepticusJessica is a 10-year-old girl with Lennox-Gastaut syndrome who arrives to your ED in status epilepticus. She had been reasonably controlled on valproic acid, clonazepam, and a ketogenic diet, but yesterday she went to a birthday party, got into some cake, and has had stomach aches – she’s been refusing to take her medications today. On arrival, she is hypoventilating, with HR 130s, BP 140/70, SPO2 92% on face mask. She now becomes apneic.Induction Agent in Status EpilepticusMany choices, but we can use the properties of a given agent to our advantage. She is normo-to-hypertensive and tachycardic. She has been vomiting. A nice choice here would be propofol.  Propofol as both a sedative and anti-epileptic agent works primarily on GABA-A and endocannabinoid receptors to provide a brief, but deep hypnotic sedation.  Side effects can include hypotension, which is often transient and resolves without treatment.  Apnea is the most common side-effect. Ketamine would be another good choice here, for its anti-epileptic activity.Paralytic Agent in Status EpilepticusRocuronium (in general), as there are concerns of a neurologic comorbidity.Housekeeping in RSIWhat size catheter doe I use?  If you know your ETT size, then it is just a matter of multiplication by 2, 3, 4, or 5. Remember this: 2, 3, 4 – Tube, Tape, Tap  The NG/OG/Foley is 2 x the ETT – tube The ETT should be taped at a depth of 3 x the ETT size – tape A chest tube size 4 x the ETT – tapIn summary, in these cases of sepsis, multitrauma, cardiogenic shock, and status epilepticus: Resuscitate before you intubate Use the agent’s specific properties and talents to your benefit Adjust the dose in critically ill patients: decrease the sedative, increase the paralytic Have post-intubation care ready: sedation, verification, NG/OG/foley

Pediatric airway management is a skill that integrates the three types of knowledge as described by the ancient Greeks: episteme, or theoretical knowledge, techne, or technical knowledge, and phronesis, or practical wisdom, also called prudence. Here we’ll invoke each type of knowledge and understanding as we go beyond the anatomical issues in pediatric airway management – to the advanced decision-making aspect of RSI and the what-to-do-when the rubber-hits-the road. Case 1: Sepsis Laura is a 2-month-old baby girl born at 32 weeks gestational age who today has been “breathing fast” per mother.  On arrival she is in severe respiratory distress with nasal flaring and intercostal retractions.   Her heart rate is 160, RR 50, oxygen saturation is 88% on RA.  She has fine tissue-paper like rales throughout her lung fields.  Despite a trial of a bronchodilator, supplemental oxygen, even nasal CPAP and fluids, she becomes less responsive and her heart rate begins to drop relatively in the 80s to 90s – this is not a sign of improvement, but of impending cardiovascular collapse. She is in respiratory failure from bronchiolitis and likely viral sepsis.  She needs her airway taken over. Is this child stable enough for intubation? We have a few minutes to optimize, to resuscitate before we intubate. Here’s an easy tip: use the sterile flushes in your IV cart and push in 20, 40, or 60 mL/kg NS.  Just keep track of the number of syringes you use – it is the fastest way to get a meaningful bolus in a small child. Alternatively, if you put a 3-way stop-cock in the IV line and attach a 30 mL syringe, you can turn the stop cock, draw up stream from the IV bag into the syringe, turn te stop cock, and push the fluid in the IV.Induction Agent in Sepsis The consensus recommendation for the induction agent of choice for sepsis in children is ketamine. Etomidate is perfectly acceptable, but ketamine is actually a superior drug to etomidate in the rapid sequence intubation of children in septic shock.  It rapidly provides sedation and analgesia, and supports hemodynamic stability by blocking the reuptake of catecholamines.Paralytic Agent in Sepsis The succinylcholine versus rocuronium debate… Succinylcholine and its PROS <ul> <li>82% of RSI in the ED used succinylcholine (According to the National Emergency Airway Registry, in 2005).  We know it, we are comfortable with it.</li> <li>Succinylcholine produces superior intubating conditions when comparing 1 mg/kg succinylcholine versus 0.6 mg/kg rocuronium, succinylcholine is that at 45 seconds.</li> </ul> Succinylcholine and its CONs <ul> <li>Raises serum potassium in everyone, typically 0.5 to 1 mEq/L.  That is not usually a problem, but for those with preexisting or inducible hyperkalemia, it can precipitate an arrest, as in renal failure, underlying neurologic or myopathic conditions like multiple sclerosis, muscular dystrophy, ALS, or those who had a stroke or a burn more than 72 hours prior. We often have limited information in critical situations.</li> <li>Succinylcholine gives us a false sense of security.  In children, there really is no “safe apnea” period.</li> <li>Succinylcholine’s effect on the nicotinic receptors results in mydriasis, tachycardia, weakness, twitching and hypertension, and fasciculations (Think nicotine overdose: M/T/W/Th/F).</li> <li>Succinylcholine’s effect on muscarinic receptors manifest (as in organophosphate overdose): SLUDGE – salivation, lacrimation, urination, defecation, GI upset or more apropos here: DUMBBELLS – diarrhea, urination, miosis, bradycardia, emesis, lacrimation, lethargy, salivation.</li> <li>Second dose of succinylcholine – beware of the muscarinic effects and bradycardia. Co-administer atropine, 0.01 mg/kg, up to 0.5 mg IV.</li> </ul> Coda: succinylcholine is not that bad – we would not have had such great success with it during the early years of our specialty if it were such a terrible drug.  The side effects are rare, but they can be deadly.  So, what’s the alternative? Rocuronium and its PROs <ul> <li>It has none of the side-effects of succinylcholine</li> </ul> Rocuronium and its CONs <ul> <li>Argument 1: the duration is too long if there is a difficult airway, since rocuronium can last over an hour. Still need to intubate, and now your patient is potentially worse.</li> <li>Argument 2: succinylcholine produces better intubating conditions at 45 seconds compared to rocuronium. At 0.6 mg/kg, rocuronium is inferior to succinylcholine at all time intervals. At 1.0 mg/kg, rocuronium is still inferior at 45 seconds.  At 1.2 mg/kg rocuronium – the dose now commonly recommended – there was no difference in intubating conditions, per a study by Heier et al. in Anethesia and Analgesia in 2000.</li></ul>Case 2: Multitrauma Joseph is a 3-year-old boy who is excited that there are so many guests at his house for a family party and when it’s starting to wind down and the guests begin to leave, he is unaccounted for. An unsuspecting driver of a mini-van backs over him. He is brought in by paramedics, who are now bagging him.Induction Agent in Trauma <ul> <li>Need something that is hemodynamically stable – agents such as midazolam or propofol would cause too many problems.</li> <li>Etomidate is a short-acting imidazole derivative that acts on GABA-A receptors to induce loss of consciousness in 5-15 seconds. It can cause apnea, pain on injection, and myoclonus.</li> <li>Etomidate reduces cerebral blood flow, reduces intracranial pressure, and reduces cerebral oxygen consumption, all while maintaining arterial blood pressure and cerebral perfusion pressure.</li> <li>Ketamine is reasonable as well: there is no contraindication to ketamine except for known hydrocephalus. It is safe in head trauma. It is a good choice for the hypotensive trauma patient.  TBI is not a contraindication.</li> <li>In the case of the critically injured child who is normotensive, ketamine will raise his blood pressure and perhaps foster further bleeding.  The goal is a good general perfusion and a balanced resuscitation, ensuring enough cerebral perfusion without disrupting nascent clots.  On the other side of the spectrum, permissive hypotension is not described in children, as hypotension is a late and dangerous sign of shock.</li></ul>Paralytic Agent in Trauma Are your surgeons in an uproar about a long-acting agent and the pupillary response?  Relax, it’s a myth. Caro et al in Annals in 2011 reported that the majority of patients undergoing RSI preserved their pupillary response.  Succinylcholine actually performed worse than rocuronium. In the rocuronium group, all patients preserved their pupillary response.In the critically ill, we rethink your dosing of both the sedative and the paralytic. In a critically ill child or adult, perfusion suffers and it affects how we administer medications.  The patient’s arm-brain time or vein-to-brain time is less efficient; additionally, as the patient’s hemodynamic status softens, he becomes very sensitive to the effects of sedatives. We need to adjust our dosing for a critically ill patient: <ul> <li>Decrease the sedative to avoid falling over the hemodynamic compensation cliff.</li> <li>Increase the paralytic to account for prolonged arm-brain time.</li></ul>Case 3: Cardiac/myocarditis/congenital heart disease Jacob is a 6-year-old-boy with tricuspid atresia s/p Fontan procedure who’s had one week of runny nose, cough, and now 2 days of high fever, vomiting, and difficulty breathing. The Fontan procedure is the last in a series of three palliative procedures in a child with complex cyanotic congenital heart disease with a single-ventricle physiology. The procedure reroutes venous blood to flow passively into the pulmonary arteries, because the right ventricle has been surgically repurposed to be the systemic pump.  The other most common defect with an indication for a Fontan is hypoplastic left heart syndrome. Typical “normal” saturations are 75 and 85% on RA.  Ask the parents or caregiver. Complications of the Fontan procedure include heart failure, superior vena cava syndrome, and hypercoagulable state, and others. A patient with a Fontan can present in cardiogenic shock from heart failure, distributive shock from an increased risk of infection, hypovolemic shock from over-diuresis or insensible fluid loss – or just a functional hypovolemia from the fact that his venous return is all passive – and finally obstructive shock due to a pulmonary thromboembolism. Types of shock mnemonic: this is how people COHDe – Cardiogenic, Obstructive, Hypovolemic, Distributive.Do we give fluids? Children after palliative surgery for cyanotic heart disease are volume-dependent.  Even if there is a component of cardiogenic shock, they need volume to drive their circuit.  Give a test dose of 10 mL/kg NS.Pressors in Pediatric Shock <ul> <li>Children compensate their shock state early by increasing their SVR.</li> <li>Epinephrine (adrenaline) is great at increasing the cardiac output (with minimal increase in systemic vascular resistance; tachycardia)  In children the cardiac deleterious effects are not pronounced as in adults.  Later when the child is stabilized, other medication such as milrinone (ionotrope and venodilator) can be used.</li> <li>Epinephrine is also fantastic for cold shock when the patient is clamped down with cold extremities – the most common presentation in pediatric septic shock.</li> <li>Norepinephrine (noradrenaline) is best used when you need to augment systemic vascular resistance, such as in warm shock, where the patient has loss of peripheral vascular tone.</li></ul>Induction Agent in Cardiogenic Shock A blue baby – with a R –&gt; L shunt – needs some pinking up with ketamine A pink baby – with a L –&gt; R shunt – is already doing ok – don’t rock the boat – give a neutral agent like etomidate. Myocarditis or other acquired causes of cardiogenic shock – etomidate.Case 4: Status Epilepticus Jessica is a 10-year-old girl with Lennox-Gastaut syndrome who arrives to your ED in status epilepticus. She had been reasonably controlled on valproic acid, clonazepam, and a ketogenic diet, but yesterday she went to a birthday party, got into some cake, and has had stomach aches – she’s been refusing to take her medications today. On arrival, she is hypoventilating, with HR 130s, BP 140/70, SPO2 92% on face mask. She now becomes apneic.Induction Agent in Status Epilepticus Many choices, but we can use the properties of a given agent to our advantage. She is normo-to-hypertensive and tachycardic. She has been vomiting. A nice choice here would be propofol. <ul> <li>Propofol as both a sedative and anti-epileptic agent works primarily on GABA-A and endocannabinoid receptors to provide a brief, but deep hypnotic sedation.  Side effects can include hypotension, which is often transient and resolves without treatment.  Apnea is the most common side-effect.</li> <li>Ketamine would be another good choice here, for its anti-epileptic activity.</li></ul>Paralytic Agent in Status Epilepticus Rocuronium (in general), as there are concerns of a neurologic comorbidity.Housekeeping in RSI What size catheter doe I use?  If you know your ETT size, then it is just a matter of multiplication by 2, 3, 4, or 5. Remember this: 2, 3, 4 – Tube, Tape, Tap <ul> <li>The NG/OG/Foley is 2 x the ETT – tube</li> <li>The ETT should be taped at a depth of 3 x the ETT size – tape</li> <li>A chest tube size 4 x the ETT – tap</li></ul>In summary, in these cases of sepsis, multitrauma, cardiogenic shock, and status epilepticus: <ul> <li>Resuscitate before you intubate</li> <li>Use the agent’s specific properties and talents to your benefit</li> <li>Adjust the dose in critically ill patients: decrease the sedative, increase the paralytic</li> <li>Have post-intubation care ready: sedation, verification, NG/OG/foley</li></ul>

Adventures in RSI

EKG Killers: Part One

How do you approach the child who may be altered?  Altered mental status in children can be subtle.  Look for age-specific behaviors that range from irritability to anger to sleepiness to decreased interaction. In the altered child, anchoring bias is your biggest enemy.  Keep your mind open to the possibilities, and be ready to change it, when new information becomes available. For altered adults, use AEIOU TIPS (Alcohol-Epilepsy-Insulin-Overdose-Uremia-Trauma-Infection-Psychosis-Stroke). Try this for altered children: remember that they need their VITAMINS! V – Vascular (e.g. arteriovenous malformation, systemic vasculitis) I – Infection (e.g. meningoencephalitis, overwhelming alternate source of sepsis) T – Toxins (e.g. environmental, medications, contaminated breast milk) A – Accident/abuse (e.g. non-accidental trauma, sequelae of previous trauma) M – Metabolic (e.g. hypoglycemia, DKA, thyroid disorders) I – Intussusception (e.g. the somnolent variant of intussusception, with lethargy) N – Neoplasm (e.g. sludge phenomenon, secondary sepsis, hypoglycemia from supply-demand mismatch) S – Seizure (e.g. seizure and its variable presentation, especially subclinical status epilepticus)  Case One: Sleepy Toddler16-month-old who chewed on his grandmother's clonidine patch Clonidine is an alpha-2 agonist with many therapeutic indications including hypertension, alcohol withdrawal, smoking cessation, perimenopausal symptoms.  In children specifically, clonidine is prescribed for attention deficit hyperactivity disorder, spasticity due to cerebral palsy and other neurologic disorders, and Tourette’s syndrome. The classic clonidine toxidrome is altered mental status, miosis, hypotension, bradycardia, and bradypnea.  Clonidine is on the infamous list of “one pill can kill”. Treatment is primarily supportive, with careful serial examinations of the airway, and strict hemodynamic monitoring. Naloxone can partially counteract the endogenous opioids that are released with clonidine's pharmacodynamics. Start with the usual naloxone dose of 0.01 mg/kg, up to the typical adult starting dose is 0.4 mg. In clonidine overdose, however, you may need to increase the naloxone dose (incomplete and variable activity) up to 0.1 mg/kg.  Titrate to hemodynamic stability and spontaneous respirations, not full reversal of all CNS effects.  Case Two: In Bed All DayA 7-year-old with fever, vomiting, body aches, sick contacts.  Altered on exam. Should you get a CT before LP? If you were going to perform CT regardless, then do it. Adult guidelines: age over 60, immunocompromised state, history of central nervous system disease, seizure within one week before presentation, abnormal level of consciousness, an inability to answer two consecutive questions correctly or to follow two consecutive commands, gaze palsy, abnormal visual fields, facial palsy, arm drift, leg drift, and abnormal language. Children: if altered, and your differential diagnosis is broad (especially if you may suspect tumor, bleed, obvious abscess). Influenza is often overlooked as a potential cause of altered mental status.  Many authors report a broad array of neurological manifestations associated with influenza, such as altered mental status, seizures, cranial nerve abnormalities, hallucinations, abnormal behavior, and persistent irritability.  All of this is due to a hypercytokinemic state, not a primary CNS infection.  Case Three: Terrible Teenager14-year-old brought in for "not listening" and "acting crazy"; non-complaint on medications for systemic lupus erythematosus (SLE). SLE is rare in children under 5. When school-age children present with SLE, they typically have more systemic signs and symptoms.  Teenagers present like adults.  All young people have a larger disease burden with lupus, since they have many more years to develop complications. Lupus cerebritis: high-dose corticosteroids, and possibly IV immunoglobulin.  Many will need therapeutic plasma exchange (TPE), a type of plasmapheresis.  Summary In altered mental status, keep your differential diagnosis open Pursue multiple possibilities until you are able to discard them Be ready to change your mind completely with new information Make sure your altered child gets his VITAMINS (Vascular, Infectious, Toxins, Accident/Abuse, Metabolic, Intussusception, Neoplasm, Stroke)    References Beckman HB, Frankel RM. The effect of physician behavior on the collection of data. Ann Intern Med 1984; 101:692. Fujita K, Nagase H, Nakagawa T et al. Non-convulsive seizures in children with infection-related altered mental status. Pediatrics International. 2015; 57(4):659–664. Gallagher J, Luck RP, Del Vecchio M. Altered mental status – a state of confusion. Paediatr Child Health. 2010 May-Jun; 15(5): 263–265.  Hasbun R, Abrahams J, Jekel J, Quagliarello VJ. Computed tomography of the head before lumbar puncture in adults with suspected meningitis. N Engl J Med. 2001; 345(24):1727-33. Oliver WJ, Shope TC, Kuhns LR. Fatal Lumbar Puncture: Fact Versus Fiction—An Approach to a Clinical Dilemma. Pediatrics. 2003; 112(3) Schwartz J et al. Guidelines on the Use of Therapeutic Apheresis in Clinical Practice—Evidence-Based Approach from the Writing Committee of the American Society for Apheresis: The Sixth Special Issue. Journal of Clinical Apheresis. 2013; 28:145–284. Zorc JJ. A lethargic infant: Ingestion or deception? Pediatr Ann 2000; 29: 104–107   This post and podcast are dedicated to Teresa Chan, HBSc, BEd, MD, MS, FRCPC for her boundless passion for and support of #FOAMed, for her innovation in education, and for her dedication to making you and me better clinicians and educators.  Thank you, T-Chan.  Altered Mental Status Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

How do you approach the child who may be altered? Altered mental status in children can be subtle.  Look for age-specific behaviors that range from irritability to anger to sleepiness to decreased interaction. In the altered child, <a href="http://www.sciencedirect.com/science/article/pii/S1053535710001411" rel="nofollow" target="_blank">anchoring bias</a> is your biggest enemy.  Keep your mind open to the possibilities, and be ready to change it, when new information becomes available. For altered adults, use AEIOU TIPS (Alcohol-Epilepsy-Insulin-Overdose-Uremia-Trauma-Infection-Psychosis-Stroke). Try this for altered children: remember that they need their VITAMINS! V – Vascular (e.g. arteriovenous malformation, systemic vasculitis) I – Infection (e.g. meningoencephalitis, overwhelming alternate source of sepsis) T – Toxins (e.g. environmental, medications, contaminated breast milk) A – Accident/abuse (e.g. non-accidental trauma, sequelae of previous trauma) M – Metabolic (e.g. hypoglycemia, DKA, thyroid disorders) I – Intussusception (e.g. the somnolent variant of intussusception, with lethargy) N – Neoplasm (e.g. sludge phenomenon, secondary sepsis, hypoglycemia from supply-demand mismatch) S – Seizure (e.g. seizure and its variable presentation, especially subclinical status epilepticus)  Case One: Sleepy Toddler 16-month-old who chewed on his grandmother's clonidine patch Clonidine is an alpha-2 agonist with many therapeutic indications including hypertension, alcohol withdrawal, smoking cessation, perimenopausal symptoms.  In children specifically, clonidine is prescribed for attention deficit hyperactivity disorder, spasticity due to cerebral palsy and other neurologic disorders, and Tourette’s syndrome. The classic clonidine toxidrome is altered mental status, miosis, hypotension, bradycardia, and bradypnea.  Clonidine is on the infamous list of “one pill can kill”. Treatment is primarily supportive, with careful serial examinations of the airway, and strict hemodynamic monitoring. Naloxone can partially counteract the endogenous opioids that are released with clonidine's pharmacodynamics. Start with the usual naloxone dose of 0.01 mg/kg, up to the typical adult starting dose is 0.4 mg. In clonidine overdose, however, you may need to increase the naloxone dose (incomplete and variable activity) up to 0.1 mg/kg.  Titrate to hemodynamic stability and spontaneous respirations, not full reversal of all CNS effects.  Case Two: In Bed All Day A 7-year-old with fever, vomiting, body aches, sick contacts.  Altered on exam. Should you get a CT before LP? If you were going to perform CT regardless, then do it. Adult guidelines: age over 60, immunocompromised state, history of central nervous system disease, seizure within one week before presentation, abnormal level of consciousness, an inability to answer two consecutive questions correctly or to follow two consecutive commands, gaze palsy, abnormal visual fields, facial palsy, arm drift, leg drift, and abnormal language. Children: if altered, and your differential diagnosis is broad (especially if you may suspect tumor, bleed, obvious abscess). Influenza is often overlooked as a potential cause of altered mental status.  Many authors report a broad array of neurological manifestations associated with influenza, such as altered mental status, seizures, cranial nerve abnormalities, hallucinations, abnormal behavior, and persistent irritability.  All of this is due to a hypercytokinemic state, not a primary CNS infection.  Case Three: Terrible Teenager 14-year-old brought in for "not listening" and "acting crazy"; non-complaint on medications for systemic lupus erythematosus (SLE). SLE is rare in children under 5. When school-age children present with SLE, they typically have more systemic signs and symptoms.  Teenagers present like adults.  All young people have a larger disease burden with lupus, since they have many more years to develop complications. Lupus cerebritis: high-dose corticosteroids, and possibly IV immunoglobulin.  Many will need therapeutic plasma exchange (TPE), a type of plasmapheresis.  Summary <ul> <li>In altered mental status, keep your differential diagnosis open</li> <li>Pursue multiple possibilities until you are able to discard them</li> <li>Be ready to change your mind completely with new information</li> <li>Make sure your altered child gets his VITAMINS (Vascular, Infectious, Toxins, Accident/Abuse, Metabolic, Intussusception, Neoplasm, Stroke)</li> </ul> References <a href="http://www.ncbi.nlm.nih.gov/pubmed/6486600" rel="nofollow" target="_blank">Beckman HB, Frankel RM. The effect of physician behavior on the collection of data. Ann Intern Med 1984; 101:692.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/25523443" rel="nofollow" target="_blank">Fujita K, Nagase H, Nakagawa T et al. Non-convulsive seizures in children with infection-related altered mental status. Pediatrics International. 2015; 57(4):659–664.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/21532787" rel="nofollow" target="_blank">Gallagher J, Luck RP, Del Vecchio M. Altered mental status – a state of confusion. Paediatr Child Health. 2010 May-Jun; 15(5): 263–265. </a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/11742046" rel="nofollow" target="_blank">Hasbun R, Abrahams J, Jekel J, Quagliarello VJ. Computed tomography of the head before lumbar puncture in adults with suspected meningitis. N Engl J Med. 2001; 345(24):1727-33.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/?term=Fatal+Lumbar+Puncture%3A+Fact+Versus+Fiction%E2%80%94An+Approach+to+a+Clinical+Dilemma" rel="nofollow" target="_blank">Oliver WJ, Shope TC, Kuhns LR. Fatal Lumbar Puncture: Fact Versus Fiction—An Approach to a Clinical Dilemma. Pediatrics. 2003; 112(3)</a> <a href="http://italkid.org/Guidelines%20on%20the%20Use%20of%20Therapeutic%20Apheresis%20in.pdf" rel="nofollow" target="_blank">Schwartz J et al. Guidelines on the Use of Therapeutic Apheresis in Clinical Practice—Evidence-Based Approach from the Writing Committee of the American Society for Apheresis: The Sixth Special Issue. Journal of Clinical Apheresis. 2013; 28:145–284.</a> <a href="http://www.ncbi.nlm.nih.gov/pubmed/10693211" rel="nofollow" target="_blank">Zorc JJ. A lethargic infant: Ingestion or deception? Pediatr Ann 2000; 29: 104–107</a> This post and podcast are dedicated to <a href="https://twitter.com/TChanMD" rel="nofollow" target="_blank">Teresa Chan, HBSc, BEd, MD, MS, FRCPC</a> for her boundless passion for and support of #FOAMed, for her innovation in education, and for her dedication to making you and me better clinicians and educators.  Thank you, T-Chan. <a href="http://www.wikem.org/wiki/Main_Page" rel="nofollow" target="_blank"></a> <a href="https://www.wikem.org/wiki/Altered_Mental_Status_%28Peds%29" rel="nofollow" target="_blank">Altered Mental Status</a> Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

Altered Mental Status in Children

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:    Consistently under 2nd percentile in weight over time "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:    Not enough offered Not enough taken Not enough absorbed    Any concern should trigger a more complete H&amp;P (in audio).    Classic instructional video on the mother-infant dyad (scan through for various types).   After a focused H&amp;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 

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: <ol> <li>Consistently under 2nd percentile in weight over time</li> <li>"Falling off" the growth curve over 2 or more points</li> </ol> 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: <ol> <li>Not enough offered</li> <li>Not enough taken</li> <li>Not enough absorbed</li> </ol> Any concern should trigger a more complete H&amp;P (in audio). <a href="https://www.youtube.com/watch?v=9Cq7Jy3Ln5g" rel="noreferrer noopener nofollow" target="_blank"> Classic instructional video on the mother-infant dyad</a> (scan through for various types). After a focused H&amp;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 <a href="https://www.cdc.gov/growthcharts/data/who/GrChrt_Boys_24HdCirc-L4W_rev90910.pdf" rel="noreferrer noopener nofollow" target="_blank"> Birth to 24 months: Boys Weight-for-length percentiles and Head circumference-for-age percentiles</a> <a href="https://www.cdc.gov/growthcharts/data/who/GrChrt_Boys_24LW_100611.pdf" rel="noreferrer noopener nofollow" target="_blank"> Birth to 24 months: Boys Length-for-age percentiles and Weight-for-age percentiles</a> <a href="https://www.cdc.gov/growthcharts/data/who/GrChrt_Girls_24HdCirc-L4W_9210.pdf" rel="noreferrer noopener nofollow" target="_blank"> Birth to 24 months: Girls Weight-for-length percentiles and Head circumference-for-age percentiles</a> <a href="https://www.cdc.gov/growthcharts/data/who/GrChrt_Girls_24LW_9210.pdf" rel="noreferrer noopener nofollow" target="_blank"> Birth to 24 months: Girls Length-for-age percentiles and Weight-for-age percentiles</a> 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

Failure to Thrive

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.

How do we make the diagnosis? What now? <a href="http://bjsm.bmj.com/content/early/2017/04/26/bjsports-2017-097699" rel="noopener nofollow" target="_blank">Concussion in Sport Group Guidelines</a> <a href="http://www.parachutecanada.org/downloads/resources/CRT5.pdf" rel="noopener nofollow" target="_blank">Concussion Recognition Tool (for coaches, trainers on field)</a> <a href="http://www.parachutecanada.org/downloads/resources/child-sport-concussion-assessement-tool-5.pdf" rel="noopener nofollow" target="_blank">Child Sports Concussion Assessment Tool, 5th Ed. (Child SCAT); Ages 5-12</a> <a href="http://bjsm.bmj.com/content/51/11/848.long" rel="noopener nofollow" target="_blank">Sports Concussion Assessment Tool, 5th Ed. (SCAT5); Ages 13 and Up</a> This post and podcast are dedicated to the great <a href="https://twitter.com/KKayMoodyDOMPH" rel="noopener nofollow" target="_blank">K Kay Moody, DO, MPH</a> 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 <a href="https://www.ncbi.nlm.nih.gov/pubmed/28280686" rel="noopener nofollow" target="_blank">Churchill NW et al. The first week after concussion: Blood flow, brain function and white matter microstructure. Neuroimage Clin. 2017; 14: 480–489.</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/26359916" rel="noopener nofollow" target="_blank">Ellis MJ et al. Psychiatric outcomes after pediatric sports-related concussion. J Neurosurg Pediatr. 2015; 16:709-718.</a> <a href="https://www.ncbi.nlm.nih.gov/books/NBK169016/" rel="noopener nofollow" target="_blank">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.</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/23243113" rel="noopener nofollow" target="_blank">Harmon KG et al. American Medical Society for Sports Medicine position statement: concussion in sport. Br J Sports Med. 2013; 47:15-26.</a> <a href="http://bjsm.bmj.com/content/early/2017/04/26/bjsports-2017-097699" rel="noopener nofollow" target="_blank">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</a> <a href="http://bjsm.bmj.com/content/early/2018/03/02/bjsports-2017-097853" rel="noopener nofollow" target="_blank">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.</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/29338452" rel="noopener nofollow" target="_blank">Wang KK et al. An update on diagnostic and prognostic biomarkers for traumatic brain injury. Exp Rev Molec Gen. 2018; 18(2):165-180.</a> <a href="https://www.ncbi.nlm.nih.gov/pubmed/26414315" rel="noopener nofollow" target="_blank">Wang Y et al. Cerebral Blood Flow Alterations in Acute Sport-Related Concussion. J Neurotrauma. 2016 Jul 1; 33(13): 1227–1236.</a>

Concussion

The Notorious VBG

Myocarditis

It's a busy shift.  Today no one seems to have a chief complaint.Someone sends a troponin on a child.  Good, bad, or ugly, how are you going to interpret the result?And while we’re at it – what labs do I need to be careful with in children – sometimes the normal ranges of common labs can have our heads spinning!Read on to go from bread-and-butter pediatric blood work to answer the question – what’s up with troponin, lactate, d-dimer, and BNP in kids?  A fundamental tenet of emergency medicine:  We balance our obligation to detect a dangerous condition with our suspicion of the disease in given patient.Someone with a cough and fever may simply have a viral illness, or he may have pneumonia.  Our obligation is to evaluate for the pneumonia.  It’s ok if we “miss” the diagnosis of a cold. It could be bad if we don’t recognize the pneumonia.  How do we decide?  Another fundamental concept:  The threshold.Depending on the disease and the particular patient, we have a threshold for testing, and the threshold for treating.  Every presentation – and every patient for that matter – has a complicated interplay between what we are expected to diagnose, how much we suspect that particular serious diagnosis, and where testing and treating come into play.   What's wrong with "throwing on some labs"?Easy to do right?  They are but a click away… Often a good history and physical exam will help you to calibrate your investigational thresholds.  This is especially true in children – the majority of pediatric ambulatory visits do not require blood work to make a decision about acute care.  If your patient is ill, then by all means; otherwise, consider digging a bit deeper into the history, get collateral information, and make good use of your general observation skills. First, a brief word about basic labs.   The punchline is, use a pediatric reference.If you don’t have a trusted online reference available during your shift, make sure you have something like a Harriett Lane Handbook accessible to you. Don’t rely on your hospital’s lab slip or electronic medical record to save you, unless you are sure that they use age-specific pediatric reference ranges to flag abnormal values. Believe it or not, in this 21st century of ours, some shops still use adult reference ranges when reporting laboratory values on children.  Notable differences in basic chemistriesPotassium: tends to run a bit higher in infants, because for the first year of life, your kidneys are inefficient in excreting potassium. BUN and creatinine: lower in children due to less muscle mass, and therefore less turnover (and usually lack of other chronic disease) Glucose: tends to run lower, as children are hypermetabolic and need regular feeding (!) Alkaline phosphatase: is always high in normal, growing children, due to bone turn over (also fond in liver, placenta, kidneys) Ammonia: high in infancy, due to immature liver, trends down to normal levels by toddlerhood ESR and CRP: low in healthy children, as chronic inflamation from comorbidities is not present; both increase steadily with age Thyroid function tests: all are markedly high in childhood, not as a sign of disease, but a marker of their increased metabolic activity   Big Labs  TroponinReliably elevated in myocarditis, and may help to distinguish this from pericarditis (in addition to echocardiography) Other causes of elevated troponin in children include: strenuous activity, status epilepticus, toxins, sepsis, myocardial infarction (in children with congenital anomalies).  Less common causes of troponemia are: Kawasaki disease, pediatric stroke, or neuromuscular disease. Don't go looking, if you won't do anything with the test. Brain natriuretic peptide (BNP)In adults, we typically think of a BNP &lt; 100 pg/mL as not consistent with symptoms caused by volume overload. Luckily, we have data in children with congenital heart disease as well.  Although each company's assay reports slightly different cut-offs, in general healthy pediatric values match healthy adult values. One exception is in the first week of life, when it is high even in healthy newborns, due to the recent transition from fetal to newborn circulation. Use of BNP in children has been studied in both clinic and ED settings. Cohen et al. in Pediatrics used BNP to differentiate acute heart failure from respiratory disease in infants admitted for respiratory distress. They compared infants with known CHF, lung disease, and matched them with controls. Later, Maher et al. used BNP in the emergency department to differentiate heart failure from respiratory causes in infants and children with heart failure and those with no past medical history. The bottom line is:BNP reliably distinguishes cardiac from respiratory causes of shortness of breath in children with a known diagnosis of heart failure. D-dimerTo cut to the chase: d-dimer for use as a rule-out for pulmonary embolism has not been studied in children. The only data we have in using d-dimer in children is to prognosticate in established cases. It is only helpful to track therapy for children who have chronic clots. This is where our adult approach can get us into trouble. Basically, think of the d-dimer in children like it doesn’t even exist. It’s not helpful in our setting for our indications.   An adult may have an idiopathic PE – in fact, up to a third of adults with PE have no known risk factor, which makes decision tools and risk stratification important in this population.Children with PE almost always have a reason for it. There is at least one identifiable risk factor in up to 98% of children with pulmonary embolism. The majority have at least two risk factors. If you’re suspecting deep venous thrombosis, perform ultrasonography, and skip the d-dimer. If you’re worried about PE, go directly to imaging. In stable patients, you may elect to use MR angiography or VQ scan, but most of us will go right to CT angiography. Radiation is always a concern, but if you need to know, get the test. This is yet another reminder that your threshold is going to be different in children when you think about PE – they should have a reason for it. After you have excluded other causes of their symptoms, if they have risk factors, and you are still concerned, then do the test you feel you need to keep this child safe.You are the test.Risk factors only inform you, and you’ll have to just pull the trigger on testing in the symptomatic child with risk factors. LactateA sick child with sepsis syndrome? The short answer – yes. In the adult literature, we know that a lactate level above 4 mmol/L in patients with severe sepsis was associated with the need for critical care. This has been studied in children as well, and an elevated lactate in children – typically above 4 – was a predictor of prolonged ICU course and mortality in septic patients.The acute recognition and treatment of sepsis is first and foremost, clinical.And it’s all about perfusion and providing oxygen to the tissues. Lactate and other laboratory testing is not a substitute for clinical assessment – it should be used as an extension of your assessment.  There are two main reasons for an elevated lactate: the stress state and the shock state. The stress state is due to hypermetabolism and an increase in glycolysis, as an example, in early sepsis. The shock state is due to tissue hypoxia, seen in septic shock. The confusion and frustration with lactate is that we often test the wrong people for it. We could use it to track treatment, and see if we can clear the lactate; decreased lactate levels are associated with a better outcome in adults. Serial clinical assessments are even more useful to gauge your success with treatment. We should use lactate to detect occult shock. Children compensate so well for shock, that subtle tissue hypoxia may not be detected until later. It may inform your decision for level of care, intensive care versus some other lower level. Have you every been in this situation:"Why, oh why, did we send a lactate?"There are times when a lactate is ordered – maybe by protocol or maybe accidentally – or maybe in retrospect, the patient didn’t need it. Here is a quick mnemonic to remember the reasons for an elevated lactate: LACTATES  L – liver – any liver disease affects how lactate is metabolized by the Cori cycle A – albuterol (or for our international friends, salbutamol), beta-agonists like albuterol, increase lactate production via cyclic amp C – “can’t breathe” – respiratory distress and increased work of breathing shifts the ratio of aerobic and anerobic repiration T – toxins – all kinds of wonder drugs and recreational drugs do it – look up your patient’s list if you’re suspicious A – alcohol, not an infrequent offender T – thiamine deficiency – think of this in your cachectic or malnourished patients E – epinephrine – a by-product of the cori cycle, how lactate is metabolized. Difficult to interpret lactates when a patient is on an epinephrine drip. S – seizure or shock – most commonly septic, but can be any type: cardiogenic, bstructive, hypovolemic, distributive. Bottom line: high serum lactate levels have been associated with morbidity and mortality in children with sepsis and trauma, the two best-studied populations. A summary of how labs can help you – or hurt you – in pediatric emergency medicine: Have a good reference for normal values and always be skeptical of how your lab reports them. Troponin testing is great for the child with suspected cardiogenic shock, myocarditis, or in unwell children with congenital heart disease. BNP in children can be used just like you do in adults – to get a sense of whether the presenting symptoms are consistent with heart failure. D-dimer is mostly a waste of time in the PED. Lactate can be useful in the right patient – use it to risk-stratify the major trauma patient or the patient with sepsis that may be suffering from occult shock. And lastly, make sure that you are mindful of your threshold for testing, and our threshold for treatment. If will vary by disease and by the patient at hand.    References Troponin Gupta SK, Naheed Z. Chest Pain in Two Athletic Male Adolescents Mimicking Myocardial Infarction. Pediatr Emer Care. 2014;30: 493-495. Kelley WE, Januzzi JL, Christenson RH. Increases of Cardiac Troponin in Conditions other than Acute Coronary Syndrome and Heart Failure. Clinical Chemistry. 2009; (55) 12:2098–2112. Kobayashi D, Aggarwal S, Kheiwa A, Shah N. Myopericarditis in Children: Elevated Troponin I Level Does Not Predict Outcome. Pediatr Cardiol. 2012; 33:1040–1045. Koerbin G, Potter JM, Abhayaratna WP et al. The distribution of cardiac troponin I in a population of healthy children: Lessons for adults. Clinica Chimica Acta. 2016; 417: 54–56. Liesemer K, Casper TC, Korgenski K, Menon SC. Use and Misuse of Serum Troponin Assays in Pediatric Practice. Am J Cardiol. 2012;110:284 –289. Newby KL et al. for the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. J Am Coll Cardiol. 2012; 60(23): 2427-2463. Schwartz MC, Wellen S, Rome JJ et al. Chest pain with elevated troponin assay in adolescents. Cardiology in the Young; 2013. 23: 353–360. BNP Auerbach SR, Richmond ME, Lamour JM. BNP Levels Predict Outcome in Pediatric Heart Failure Patients Post Hoc Analysis of the Pediatric Carvedilol Trial. Circ Heart Fail. 2010;3:606-611. Cohen S, Springer C, Avital A et al. Amino-Terminal Pro-Brain-Type Natriuretic Peptide: Heart or Lung Disease in Pediatric Respiratory Distress? Pediatrics. 2005;115:1347–1350. Fried I, Bar-Oz B, Algur N et al. Comparison of N-terminal Pro-B-Type Natriuretic Peptide Levels in Critically Ill Children With Sepsis Versus Acute Left Ventricular Dysfunction. Pediatrics. 2006; 118(4): 1165-1168. Koch A, Singer H. Normal values of B type natriuretic peptide in infants, children, and adolescents. Heart. 2003;89:875–878. Maher KO, Reed H, Cuadrado A et al. , B-Type Natriuretic Peptide in the Emergency Diagnosis of Critical Heart Disease in Children. Pediatrics. 2008;121:e1484–e1488. Mir TS, Marohn S, Laeer S, Eistelt M. Plasma Concentrations of N-Terminal Pro-Brain Natriuretic Peptide in Control Children From the Neonatal to Adolescent Period and in Children With Congestive Heart Failure. Pediatrics. 2002;110(6)1:6. Mir TS, Laux R, Hellwege HH et al. Plasma Concentrations of Aminoterminal Pro Atrial Natriuretic Peptide and Aminoterminal Pro Brain Natriuretic Peptide in Healthy Neonates: Marked and Rapid Increase After Birth. Pediatrics. 2003;112:896–899. D-Dimer Goldenberg NA, Knapp-Clevenger RA, Manco-Johnson MJ. Elevated Plasma Factor VIII and d-Dimer Levels as Predictors of Poor Outcomes of Thrombosis in Children for the Mountain States Regional Thrombophilia Group. Pediatrics. 2003;112:896–899. Manco-Johnson MJ. How I treat venous thrombosis in children. Blood. 2006; 107(1)21-31. Naqvi M, Miller P, Feldman L, Shore BJ. Pediatric orthopaedic lower extremity trauma and venous thromboembolism. J Child Orthop. 015;9:381–384. Parasuraman S, Goldhaber SZ. Venous Thromboembolism in Children. Circulation. 2006;113:e12-e16. Strouse JJ, Tamma P, Kickler TS et al. D-Dimer for the Diagnosis of Venous Thromboembolism in Children. N Engl J Med. 2004;351:1081-8. Lactate Andersen LW, Mackenhauer J, Roberts JC et al. Etiology and therapeutic approach to elevated lactate. Mayo Clin Proc. 2013; 88(10): 1127–1140. Bai et al. Effectiveness of predicting in-hospital mortality in critically ill children by assessing blood lactate levels at admission. BMC Pediatrics. 2014; 14:83. Scott HF, Donoghue AJ, Gaieski DF et al. The Utility of Early Lactate Testing in Undifferentiated Pediatric Systemic Inflammatory Response Syndrome. Acad Emerg Med. 2012; 19:1276–1280. Shah A, Guyette F, Suffoletto B et al. Diagnostic Accuracy of a Single Point-of-Care Prehospital Serum Lactate for Predicting Outcomes in Pediatric Trauma Patients. Pediatr Emer Care. 2013; 29:715-719. Topjian AA, Clark AE, Casper TC et al. for the Pediatric Emergency Care Applied Research Network. Early Lactate Elevations Following Resuscitation From Pediatric Cardiac Arrest Are Associated With Increased Mortality. Pediatr Crit Care Med. 2013; 14(8): e380–e387. This post and podcast are dedicated to Daniel Cabrera, MD for his vision and his leadership in thinking 'outside the box'.  Troponin     |     BNP     |     D-Dimer     |     Lactate Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

It's a busy shift.  Today no one seems to have a chief complaint. Someone sends a troponin on a child.  Good, bad, or ugly, how are you going to interpret the result? And while we’re at it – what labs do I need to be careful with in children – sometimes the normal ranges of common labs can have our heads spinning! Read on to go from bread-and-butter pediatric blood work to answer the question – what’s up with troponin, lactate, d-dimer, and BNP in kids?  A fundamental tenet of emergency medicine:    We balance our obligation to detect a dangerous condition with our suspicion of the disease in given patient. Someone with a cough and fever may simply have a viral illness, or he may have pneumonia.  Our obligation is to evaluate for the pneumonia.  It’s ok if we “miss” the diagnosis of a cold. It could be bad if we don’t recognize the pneumonia.  How do we decide?  Another fundamental concept:    The threshold. Depending on the disease and the particular patient, we have a threshold for testing, and the threshold for treating.  Every presentation – and every patient for that matter – has a complicated interplay between what we are expected to diagnose, how much we suspect that particular serious diagnosis, and where testing and treating come into play.    What's wrong with "throwing on some labs"? Easy to do right?  They are but a click away… Often a good history and physical exam will help you to calibrate your investigational thresholds.  This is especially true in children – the majority of pediatric ambulatory visits do not require blood work to make a decision about acute care.  If your patient is ill, then by all means; otherwise, consider digging a bit deeper into the history, get collateral information, and make good use of your general observation skills. First, a brief word about basic labs.    The punchline is, use a pediatric reference. If you don’t have a trusted online reference available during your shift, make sure you have something like a Harriett Lane Handbook accessible to you. Don’t rely on your hospital’s lab slip or electronic medical record to save you, unless you are sure that they use age-specific pediatric reference ranges to flag abnormal values. Believe it or not, in this 21st century of ours, some shops still use adult reference ranges when reporting laboratory values on children.  Notable differences in basic chemistries Potassium: tends to run a bit higher in infants, because for the first year of life, your kidneys are inefficient in excreting potassium. BUN and creatinine: lower in children due to less muscle mass, and therefore less turnover (and usually lack of other chronic disease) Glucose: tends to run lower, as children are hypermetabolic and need regular feeding (!) Alkaline phosphatase: is always high in normal, growing children, due to bone turn over (also fond in liver, placenta, kidneys) Ammonia: high in infancy, due to immature liver, trends down to normal levels by toddlerhood ESR and CRP: low in healthy children, as chronic inflamation from comorbidities is not present; both increase steadily with age Thyroid function tests: all are markedly high in childhood, not as a sign of disease, but a marker of their increased metabolic activity    Big Labs    Troponin Reliably elevated in myocarditis, and may help to distinguish this from pericarditis (in addition to echocardiography) Other causes of elevated troponin in children include: strenuous activity, status epilepticus, toxins, sepsis, myocardial infarction (in children with congenital anomalies).  Less common causes of troponemia are: Kawasaki disease, pediatric stroke, or neuromuscular disease.  Don't go looking, if you won't do anything with the test.  Brain natriuretic peptide (BNP) In adults, we typically think of a BNP &lt; 100 pg/mL as not consistent with symptoms caused by volume overload. Luckily, we have data in children with congenital heart disease as well.  Although each company's assay reports slightly different cut-offs, in general healthy pediatric values match healthy adult values. One exception is in the first week of life, when it is high even in healthy newborns, due to the recent transition from fetal to newborn circulation. Use of BNP in children has been studied in both clinic and ED settings. <a href="http://www.ncbi.nlm.nih.gov/pubmed/15867046" rel="nofollow" target="_blank">Cohen et al. </a>in Pediatrics used BNP to differentiate acute heart failure from respiratory disease in infants admitted for respiratory distress. They compared infants with known CHF, lung disease, and matched them with controls. Later, <a href="http://www.ncbi.nlm.nih.gov/pubmed/18519452" rel="nofollow" target="_blank">Maher et al.</a> used BNP in the emergency department to differentiate heart failure from respiratory causes in infants and children with heart failure and those with no past medical history. The bottom line is:BNP reliably distinguishes cardiac from respiratory causes of shortness of breath in children with a known diagnosis of heart failure.  D-dimer To cut to the chase: d-dimer for use as a rule-out for pulmonary embolism has not been studied in children. The only data we have in using d-dimer in children is to prognosticate in established cases. It is only helpful to track therapy for children who have chronic clots. This is where our adult approach can get us into trouble. Basically, think of the d-dimer in children like it doesn’t even exist. It’s not helpful in our setting for our indications.   An adult may have an idiopathic PE – in fact, up to a third of adults with PE have no known risk factor, which makes decision tools and risk stratification important in this population.Children with PE almost always have a reason for it. <a href="http://pemplaybook.org/wp-content/uploads/2016/04/Slide41.jpg" rel="attachment wp-att-496 nofollow" target="_blank"></a> There is at least one identifiable risk factor in up to 98% of children with pulmonary embolism. The majority have at least two risk factors. If you’re suspecting deep venous thrombosis, perform ultrasonography, and skip the d-dimer. If you’re worried about PE, go directly to imaging. In stable patients, you may elect to use MR angiography or VQ scan, but most of us will go right to CT angiography. Radiation is always a concern, but if you need to know, get the test. This is yet another reminder that your threshold is going to be different in children when you think about PE – they should have a reason for it. After you have excluded other causes of their symptoms, if they have risk factors, and you are still concerned, then do the test you feel you need to keep this child safe.You are the test. Risk factors only inform you, and you’ll have to just pull the trigger on testing in the symptomatic child with risk factors.  Lactate A sick child with sepsis syndrome? The short answer – yes. In the adult literature, we know that a lactate level above 4 mmol/L in patients with severe sepsis was associated with the need for critical care. This has been studied in children as well, and an elevated lactate in children – typically above 4 – was a predictor of prolonged ICU course and mortality in septic patients.The acute recognition and treatment of sepsis is first and foremost, clinical. And it’s all about perfusion and providing oxygen to the tissues. Lactate and other laboratory testing is not a substitute for clinical assessment – it should be used as an extension of your assessment.  There are two main reasons for an elevated lactate: the stress state and the shock state. The stress state is due to hypermetabolism and an increase in glycolysis, as an example, in early sepsis. The shock state is due to tissue hypoxia, seen in septic shock. The confusion and frustration with lactate is that we often test the wrong people for it. We could use it to track treatment, and see if we can clear the lactate; decreased lactate levels are associated with a better outcome in adults. Serial clinical assessments are even more useful to gauge your success with treatment. We should use lactate to detect occult shock. Children compensate so well for shock, that subtle tissue hypoxia may not be detected until later. It may inform your decision for level of care, intensive care versus some other lower level. Have you every been in this situation:"Why, oh why, did we send a lactate?" There are times when a lactate is ordered – maybe by protocol or maybe accidentally – or maybe in retrospect, the patient didn’t need it. Here is a quick mnemonic to remember the reasons for an elevated lactate: LACTATES <a href="http://pemplaybook.org/wp-content/uploads/2016/04/Slide52.jpg" rel="attachment wp-att-495 nofollow" target="_blank"></a> L – liver – any liver disease affects how lactate is metabolized by the Cori cycle A – albuterol (or for our international friends, salbutamol), beta-agonists like albuterol, increase lactate production via cyclic amp C – “can’t breathe” – respiratory distress and increased work of breathing shifts the ratio of aerobic and anerobic repiration T – toxins – all kinds of wonder drugs and recreational drugs do it – look up your patient’s list if you’re suspicious A – alcohol, not an infrequent offender T – thiamine deficiency – think of this in your cachectic or malnourished patients E – epinephrine – a by-product of the cori cycle, how lactate is metabolized. Difficult to interpret lactates when a patient is on an epinephrine drip. S – seizure or shock – most commonly septic, but can be any type: cardiogenic, bstructive, hypovolemic, distributive. Bottom line: high serum lactate levels have been associated with morbidity and mortality in children with sepsis and trauma, the two best-studied populations.  A summary of how labs can help you – or hurt you – in pediatric emergency medicine: <ol> <li>Have a good reference for normal values and always be skeptical of how your lab reports them.</li> <li>Troponin testing is great for the child with suspected cardiogenic shock, myocarditis, or in unwell children with congenital heart disease.</li> <li>BNP in children can be used just like you do in adults – to get a sense of whether the presenting symptoms are consistent with heart failure.</li> <li>D-dimer is mostly a waste of time in the PED.</li> <li>Lactate can be useful in the right patient – use it to risk-stratify the major trauma patient or the patient with sepsis that may be suffering from occult shock.</li> <li>And lastly, make sure that you are mindful of your threshold for testing, and our threshold for treatment. If will vary by disease and by the patient at hand.</li> </ol> References Troponin Gupta SK, Naheed Z. Chest Pain in Two Athletic Male Adolescents Mimicking Myocardial Infarction. Pediatr Emer Care. 2014;30: 493-495. Kelley WE, Januzzi JL, Christenson RH. Increases of Cardiac Troponin in Conditions other than Acute Coronary Syndrome and Heart Failure. Clinical Chemistry. 2009; (55) 12:2098–2112. Kobayashi D, Aggarwal S, Kheiwa A, Shah N. Myopericarditis in Children: Elevated Troponin I Level Does Not Predict Outcome. Pediatr Cardiol. 2012; 33:1040–1045. Koerbin G, Potter JM, Abhayaratna WP et al. The distribution of cardiac troponin I in a population of healthy children: Lessons for adults. Clinica Chimica Acta. 2016; 417: 54–56. Liesemer K, Casper TC, Korgenski K, Menon SC. Use and Misuse of Serum Troponin Assays in Pediatric Practice. Am J Cardiol. 2012;110:284 –289. Newby KL et al. for the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents. ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations. J Am Coll Cardiol. 2012; 60(23): 2427-2463. Schwartz MC, Wellen S, Rome JJ et al. Chest pain with elevated troponin assay in adolescents. Cardiology in the Young; 2013. 23: 353–360. BNP Auerbach SR, Richmond ME, Lamour JM. BNP Levels Predict Outcome in Pediatric Heart Failure Patients Post Hoc Analysis of the Pediatric Carvedilol Trial. Circ Heart Fail. 2010;3:606-611. Cohen S, Springer C, Avital A et al. Amino-Terminal Pro-Brain-Type Natriuretic Peptide: Heart or Lung Disease in Pediatric Respiratory Distress? Pediatrics. 2005;115:1347–1350. Fried I, Bar-Oz B, Algur N et al. Comparison of N-terminal Pro-B-Type Natriuretic Peptide Levels in Critically Ill Children With Sepsis Versus Acute Left Ventricular Dysfunction. Pediatrics. 2006; 118(4): 1165-1168. Koch A, Singer H. Normal values of B type natriuretic peptide in infants, children, and adolescents. Heart. 2003;89:875–878. Maher KO, Reed H, Cuadrado A et al. , B-Type Natriuretic Peptide in the Emergency Diagnosis of Critical Heart Disease in Children. Pediatrics. 2008;121:e1484–e1488. Mir TS, Marohn S, Laeer S, Eistelt M. Plasma Concentrations of N-Terminal Pro-Brain Natriuretic Peptide in Control Children From the Neonatal to Adolescent Period and in Children With Congestive Heart Failure. Pediatrics. 2002;110(6)1:6. Mir TS, Laux R, Hellwege HH et al. Plasma Concentrations of Aminoterminal Pro Atrial Natriuretic Peptide and Aminoterminal Pro Brain Natriuretic Peptide in Healthy Neonates: Marked and Rapid Increase After Birth. Pediatrics. 2003;112:896–899. D-Dimer Goldenberg NA, Knapp-Clevenger RA, Manco-Johnson MJ. Elevated Plasma Factor VIII and d-Dimer Levels as Predictors of Poor Outcomes of Thrombosis in Children for the Mountain States Regional Thrombophilia Group. Pediatrics. 2003;112:896–899. Manco-Johnson MJ. How I treat venous thrombosis in children. Blood. 2006; 107(1)21-31. Naqvi M, Miller P, Feldman L, Shore BJ. Pediatric orthopaedic lower extremity trauma and venous thromboembolism. J Child Orthop. 015;9:381–384. Parasuraman S, Goldhaber SZ. Venous Thromboembolism in Children. Circulation. 2006;113:e12-e16. Strouse JJ, Tamma P, Kickler TS et al. D-Dimer for the Diagnosis of Venous Thromboembolism in Children. N Engl J Med. 2004;351:1081-8. Lactate Andersen LW, Mackenhauer J, Roberts JC et al. Etiology and therapeutic approach to elevated lactate. Mayo Clin Proc. 2013; 88(10): 1127–1140. Bai et al. Effectiveness of predicting in-hospital mortality in critically ill children by assessing blood lactate levels at admission. BMC Pediatrics. 2014; 14:83. Scott HF, Donoghue AJ, Gaieski DF et al. The Utility of Early Lactate Testing in Undifferentiated Pediatric Systemic Inflammatory Response Syndrome. Acad Emerg Med. 2012; 19:1276–1280. Shah A, Guyette F, Suffoletto B et al. Diagnostic Accuracy of a Single Point-of-Care Prehospital Serum Lactate for Predicting Outcomes in Pediatric Trauma Patients. Pediatr Emer Care. 2013; 29:715-719. Topjian AA, Clark AE, Casper TC et al. for the Pediatric Emergency Care Applied Research Network. Early Lactate Elevations Following Resuscitation From Pediatric Cardiac Arrest Are Associated With Increased Mortality. Pediatr Crit Care Med. 2013; 14(8): e380–e387. This post and podcast are dedicated to <a href="https://twitter.com/CabreraERDR" rel="nofollow" target="_blank">Daniel Cabrera, MD</a> for his vision and his leadership in thinking 'outside the box'. <a href="http://www.wikem.org/wiki/Main_Page" rel="nofollow" target="_blank"></a> <a href="https://www.wikem.org/wiki/Troponin" rel="nofollow" target="_blank">Troponin</a>     |     <a href="https://www.wikem.org/wiki/BNP" rel="nofollow" target="_blank">BNP</a>     |     <a href="https://www.wikem.org/wiki/D-dimer" rel="nofollow" target="_blank">D-Dimer</a>     |     <a href="https://www.wikem.org/wiki/Lactate" rel="nofollow" target="_blank">Lactate</a> Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP

Big Labs, Little People

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