Rank #1: Vomiting in the Young Child: Nothing or Nightmare
Gastrointestinal, Neurologic, Metabolic, Respiratory, Renal, Infectious, Endocrine, Toxin-related, even Behavioral.
To help us organize, below is a review of can't-miss diagnoses by age.
The Neonate: Malrotation with Volvulus
In children with malrotation, 50% present within the first month of life, with the majority occurring in the first week after birth. 90% of children with malrotation with volvulus will present by one year of age. This is a pre-verbal child’s disease – which makes it even more of a challenge to recognize quickly.
The sequence of events usually is fussiness, irritability, and forceful vomiting. The vomit quickly turns bilious.
Green vomit is a surgical emergency.
Babies may also present unwell, with bloating and abdominal tenderness to palpation. Be aware that later stages of malrotation may present as shock – they present in hypovolemic shock due to third-spacing from necrotic bowel and/or septic shock from translocation or perforation. In the undifferentiated sick neonate, always consider a surgical emergency such as malrotation with volvulus.
In the stable patient, get an upper GI contrast study.
Rapid-fire word association for other vomiting emergencies in a neonate:
- Fever, irritability and vomiting? Think meningitis, UTI, or sepsis.
- Premature, unwell, and vomiting? Think necrotizing enterocolitis. Remember, 10% of cases of NEC can be full-term. Look for pneumatosis intestinalis.
- Systemically ill, afebrile, and vomiting for no other reason? Think inborn error of metabolism. Screen with a glucose, ammonia, lactate, and urine ketones.
- Others include congenital intestinal atresia or webs, meconium ileus, or severe GERD
All that vomits is not necessarily from the gut.
Abusive head injury is the most common cause of death from child abuse. Infants especially present with non-specific complaints like fussiness or vomiting. Up to 30% of infants with abusive head injury may be misdiagnosed on initial presentation.
Louwers et al. in Child Abuse and Neglect developed and validated a six-question screening tool for use the in ED. The power of this tool was that it was validated for any chief complaint – it is not an injury evaluation checklist – it is a screen for potential abuse in the undifferentiated child:
- 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.
- Hyperglycemia, with a blood glucose of >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 < 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.
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.
Applegate KE, Anderson JM, Klatte EC. Intestinal malrotation in children: a problem-solving approach to the upper gastrointestinal series. Radiographics. 2006; 26(5):1485-500.
Glaser NS, Wootton-Gorges SL, Buonocore MH et al. Frequency of sub-clinical cerebral edema in children with diabetic ketoacidosis. Pediatr Diabetes. 2006 Apr;7(2):75-80.
Louwers ECFM, Korfage IJ, Affourtit MJ et al. Accuracy of a screening instrument to identify potential child abuse in emergency departments. Child Abuse & Neglect. 2014; (38): 1275–1281.
Lee HC, Pickard SS, Sridhar S et al. Intestinal Malrotation and Catastrophic Volvulus in Infancy. J Emerg Med. 2012; 43(1): e49–e51.
Marcin JP, Glaser N, Barnett P et al. Factors associated with adverse outcomes in children with diabetic ketoacidosis-related cerebral edema. J Pediatr. 2002; 141(6):793-7.
Parashette KR, Croffie J. Intestinal Malrotation in Children: A Problem-solving Approach to the Upper Gastrointestinal. Pediatrics in Review. 2013; (34)7: 307-321.
Wolfsdorf JI, Allgrove J, Craig ME et al. ISPAD Clinical Practice Consensus Guidelines 2014. Diabetic ketoacidosis and hyperglycemic hyperosmolar state. Pediatr Diabetes. 2014 Sep;15 Suppl 20:154-79.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
Rank #2: The Fussy Infant
[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!
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.
Rank #4: Bronchiolitis
-- 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 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:
He can likely go home.The How
Below is a list of modalities, treatments, and the evidence and/or recommendations for or against:Chest Radiograph
Usually not necessary, unless the diagnosis is uncertain, or if the child is critically ill.
Factors that are predictive of a definite infiltrate are: significant hypoxia (< 92%), grunting, focal crackles, or high fever (> 39°C).Ultrasound
Not ready for prime time. Two small studies, one by Caiulo et al in the European J or Pediatrics and one by Basile et al. in the BMC Pediatrics that show some preliminary data, but not enough to change practice yet.Viral Testing
Qualitative PCR gives you a yes or no question – one that you’ve already answered. It is not recommended for routine use. PCR may be positive post-infection for several weeks later (details in audio).
Quantitative PCR measures viral load; an increased quantitative viral load is associated with increased length of stay, use of respiratory support, need for intensive care, and recurrent wheezing. However, also not recommended for routine use.
There is one instance in which viral testing in bronchiolitis can be helpful – in babies less than a month of life, the presence of RSV virus is associated with apnea.Blood or Urine Testing
Routine testing of blood or urine is not recommended for children with bronchiolitis. Levine et al in Pediatrics found an extremely low risk of serious bacterial illness in young febrile infants with RSV.
The main thing is not to give in to anchoring bias here. If an infant of 3 months of age or older has a clear source for his low-grade fever – and that is his bronchiolitis – then you have a source, and very rarely do you need to go looking any further. He’s showing you the viral waterfall from his nose, and his increased work of breathing. It’s not going to be in his urine.Bronchodilators!
Should we use bronchodilators in bronchiolitis? It seems lately that this is a loaded question – with strong feelings on either side amongst colleagues. The short answer is that the American Academy of Pediatrics, the UK’s National Institute for Health and Care Excellence, as well as the Canadian Pediatric Society currently recommend against them. However, in continental Europe and Australia, the language is softened to “not routinely recommended”.
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]
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.
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.
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.
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.
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.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
Rank #5: Neonatal 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
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
This post and podcast are dedicated to Gita Pensa, MD, for her commitment to #FOAMed and passion for asynchronous learning and education innovation.
Rank #6: Strep Throat
Fagan Nomogram for Likelihood Ratios
1. Decide on your pre-test probability of the disease (choose an approximate probability based on our assessment) 2. Use the likelihood ratio that correlates to your exam. 3. Draw a straight line frm your pre-test probability starting point, to the LR of the feauture/test, take it through to find your post-test probability 4. Use this new post-test probability to help in your decision
Your patient has palatal petechiae, which confers a positive likelihood ratio (LR+) of 2.7 See below how to use this statistic based on your clinical assessment"Low Probability Moderate Probability High Probability List of Likelihood Ratios for Streptococcal Pharyngitis Symptoms and signs Positive LR (95% CI) Negative LR (95% CI) Sensitivity (95% CI) Specificity (95% CI) Scarlatiniform rash 3.91 (2.00-7.62) 0.94 (0.90-0.97) 0.08 (0.05-0.14) 0.98 (0.95-0.99) Palatal petechiae 2.69 (1.92-3.77) 0.90 (0.86-0.94) 0.15 (0.10-0.21) 0.95 (0.91-0.97) Chills 2.16 (0.94-4.96) 0.88 (0.79-0.98) 0.21 (0.18-0.24) 0.90 (0.83-0.97) Anorexia 1.98 (0.83-4.75) 0.53 (0.26-1.10) 0.62 (0.12-1.11) 0.62 (0.12-1.12) Pharyngeal exudate 1.85 (1.58-2.16) 0.78 (0.74-0.82) 0.38 (0.32-0.44) 0.79 (0.73-0.84) Vomiting 1.79 (1.56-2.06) 0.85 (0.81-0.90) 0.28 (0.21-0.36) 0.84 (0.79-0.89) Tender cervical nodes 1.72 (1.54-1.93) 0.78 (0.75-0.81) 0.40 (0.35-0.46) 0.77 (0.71-0.82) Sibling with sore throat 1.71 (0.82-3.53) 0.92 (0.82-1.03) 0.18 (0.14-0.23) 0.89 (0.83-0.94) Halitosis 1.54 (0.79-2.99) 0.95 (0.81-1.12) 0.12 (0.05-0.29) 0.92 (0.86-0.99) Tonsillar and/or pharyngeal exudate 1.40 (1.10-1.77) 0.86 (0.75-0.98) 0.37 (0.28-0.46) 0.74 (0.68-0.78) Large cervical nodes 1.39 (1.16-1.67) 0.67 (0.53-0.84) 0.64 (0.50-0.76) 0.54 (0.41-0.67) Lack of cough 1.36 (1.18-1.56) 0.59 (0.48-0.73) 0.73 (0.66-0.78) 0.46 (0.38-0.55) Tonsillar exudates 1.35 (0.98-1.87) 0.81 (0.63-1.06) 0.46 (0.27-0.67) 0.66 (0.48-0.80) Tonsillar swelling 1.27 (1.04-1.54) 0.67 (0.52-0.85) 0.70 (0.64-0.76) 0.44 (0.32-0.57) Dysphagia 1.22 (1.00-1.48) 0.68 (0.51-0.91) 0.72 (0.55-0.85) 0.41 (0.23-0.62) Headache 1.22 (0.95-1.57) 0.90 (0.77-1.04) 0.39 (0.28-0.51) 0.68 (0.58-0.76) Lack of coryza 1.21 (1.08-1.35) 0.69 (0.55-0.88) 0.72 (0.64-0.79) 0.40 (0.34-0.48) Abdominal pain 1.18 (0.92-1.51) 0.95 (0.89-1.03) 0.24 (0.19-0.30) 0.79 (0.75-0.83) Red tonsils and/or pharynx 1.13 (0.96-1.33) 0.41 (0.16-1.02) 0.93 (0.85-0.96) 0.18 (0.09-0.35) Reported fever 1.07 (0.96-1.19) 0.86 (0.67-1.11) 0.71 (0.58-0.82) 0.33 (0.23-0.49) Red tonsils 1.07 (0.86-1.34) 0.82 (0.40-1.69) 0.80 (0.60-1.00) 0.25 (0.00-0.51) Red pharynx 1.06 (0.95-1.18) 0.56 (0.27-1.17) 0.93 (0.81-0.98) 0.12 (0.03-0.34) Documented temperature >38° or >38.5°C 1.02 (0.87-1.21) 0.98 (0.83-1.15) 0.50 (0.36-0.63) 0.51 (0.38-0.65) Summer 0.86 (0.61-1.20) 1.02 (1.00-1.05) 0.13 (0.00-0.33) 0.85 (0.65-1.04) Arthralgia 0.74 (0.18-3.08) 1.02 (0.97-1.06) 0.09 (0.00-0.25) 0.90 (0.77-1.04) Conjunctivitis 0.73 (0.46-1.16) 1.02 (0.98-1.05) 0.05 (0.02-0.11) 0.94 (0.85-0.98) Acute otitis media 0.65 (0.14-2.91) 1.04 (0.93-1.16) 0.03 (0.01-0.05) 0.94 (0.84-1.04) History of tonsillectomy 0.64 (0.49-0.84) 1.07 (1.03-1.11) 0.11 (0.08-0.13) 0.84 (0.81-0.86) Hoarseness 0.62 (0.46-0.83) 1.04 (1.03-1.06) 0.06 (0.03-0.12) 0.90 (0.85-0.93) Diarrhea 0.51 (0.33-0.79) 1.04 (0.99-1.11) 0.03 (0.00-0.06) 0.93 (0.86
Modified from: Shaikh et al. 2012
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
Rank #7: Approach to Shock
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.
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
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
Mostly one of two entities: pulmonary embolism or cardiac tamponade.
Pulmonary embolism in children is uncommon – when children have PE, there is almost always a reason for it – it just does not happen in normal, healthy children without risk factors.
Children with PE will either have a major thrombophilic comorbidity, or they are generously sized teenage girls on estrogen therapy.
Tamponade -- can be infectious, rheumotologic, oncologic, or traumatic. It’s seen easily enough on point of care ultrasound. If there is non-traumatic tamponade physiology, get that spinal needle and get to aspirating.Obstructive Shock: Act
Pulmonary embolism (PE) with overt shock: thrombolyse; otherwise controversial. PE with symptoms: heparin.
Tamponade: if any sign of shock, pericardiocentesis, preferentially ultrasound-guided.
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.
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.
The 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
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.
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.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
Rank #8: Concussion
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.
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.
Rank #11: The Pediatric Surgical Abdomen
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 Pneumatosis Intestinalis.
- 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
- Feeding intolerance, abdominal distention
- Abdominal XR: pneumatosis intestinalis
- IV access, NG tube, broad-spectrum antibiotics, surgery consult, ICU admission
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
- 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
- Stat surgical consult
- IV access, resuscitation, NG tube to decompress (bowel wall perfusion at risk, distention worsens)
- 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
- 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)
- 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.
- Hypertrophy of pyloric sphincter; genetic, environmental, exposure factorsString Sign in Pyloric Stenosis.
- Hungry, hungry, not-so-hippos; they want to eat all of the time, but cannot keep things down
- Poor weight gain (less than 20-30 g/day)
- US: “π–loric stenosis” (3.14); pylorus dimensions > 3 mm x 14 mm
- UGI: “string sign”
- Trial of medical treatment with oral atropine via NGT (muscarinic effects decrease pyloric tone)
- Ramstedt pyloromyotomy (definitive)
- 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
- 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
- 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.
- 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
- 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)
- Same pathophysiology and epidemiology as adults: “ABC” – adhesions, “bulges” (hernias), and cancer.
- 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
- 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
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.
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.
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.
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.
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
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. .
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
Rank #12: Big Labs, Little People
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:
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
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 < 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.
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.
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.
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
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.
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.
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.
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.
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'.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
Rank #14: Adventures in RSI
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
- 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.
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
- 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.
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:
- Decrease the sedative to avoid falling over the hemodynamic compensation cliff.
- Increase the paralytic to account for prolonged arm-brain time.
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
- 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.
A blue baby – with a R –> L shunt – needs some pinking up with ketamine
A pink baby – with a L –> 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.
- 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.
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
- 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 – tap
- 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
Rank #15: Altered Mental Status in Children
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 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.
- 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)
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.
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.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
Rank #16: Blunt Head Trauma
How can we sort out the overtly ok from the sneakily serious?
Mnemonics for bedside risk stratification of minor pediatric blunt head trauma, based on PECARN studies: [Details in Audio]
Blunt Head Trauma in Children < 2 years of Age
Blunt Head Trauma in Children ≥ 2 years of Age
Image Gently Campaign
Medical Imaging Record (maintain like an immunization card)Brochure for Parents: Just in Time Education
This post and podcast are dedicated to Kevin Klauer, DO, EJD, FACEP for his dedication to education, and for his unique balance of safety and keeping it real. Thank you.
Rank #17: Hypertension in Children
Baracco R et al. Pediatric Hypertensive Emergencies. Curr Hypertens Rep. 2014; 16:456.
Belsha CW. Pediatric Hypertension in the Emergency Department. Ann Emerg Med. 2008; 51(3):21-24.
Chandar J et al. Hypertensive crisis in children. Pediatr Nephrol. 2012; 27:741-751.
Dionne JM et al. Hypertension Canada’s 2017 Guidelines for the Diagnosis, Assessment, Prevention, and Treatment of Pediatric Hypertension. Canadian J Cardiol. 2017; 33:577-585
*Flynn JT, Kaelber DC, Baker-Smith CM, et al; SUBCOMMITTEE ON SCREENING AND MANAGEMENT OF HIGH BLOOD PRESSURE IN CHILDREN. Clinical Practice Guideline for Screening and Management of High Blood Pressure in Children and Adolescents. Pediatrics. 2017; 140(3):e20171904
Gilhotra Y et al. Blood pressure measurements on children in the emergency department. Emergency Medicine Australasia. 2006; 18:148-154.
Lurbe E et al. 2016 European Society of Hypertension guidelines for the management of high blood pressure in children and adolescents. J Hypertens. 2016; 34:1-35.
Patel NH et al. Evaluation and management of pediatric hypertensive crises: hypertensive urgency and hypertensive emergencies. Open Access Emergency Medicine. 2012; 4:85-92.
Yang WC et al. Clinical Analysis of Hypertension in Children Admitted to the Emergency Department. Pediatr Neonatol. 2010; 1:44-51.
Addendum: Causes of Malignant Hypertension by Age Infant to Toddler Preschool to School Age Adolescent to Adult Renal disease Renal disease Primary hypertension Coarctation of the aorta Coarctation of the aorta Medication non-adherence Bronchopulmonary dysplasia Drug induced/toxicologic Renal disease Increased intracranial pressure Increased intracranial pressure Increased intracranial pressure Volume overload Pheochromocytoma Pheochromocytoma Congenital adrenal hyperplasia Primary hypertension Drug induced/toxicologic
Adapted from: Constantine E. Hypertension. In: Textbook of Pediatric Emergency Medicine, 6th Ed. Fleischer GR, Ludwig S, Henretig FM (Eds). Lippincott, Williams & Wilkins, Philadelphia. 2010; p315.
This post and podcast are dedicated to Manpreet 'Manny' Singh for his collegiality, collaboration, and overall awesomeness.
Rank #18: Please STOP LIMPING!
S – Septic Arthritis
The most urgent part of our differential diagnosis. The hip is the most common joint affected, followed by the knee. Lab work can be helpful, as well as US of the hip to look for an effusion, but sometimes, regardless of the results, the joint just has to be tapped to know for sure.
T – Toddler’s fracture
This is usually a torque injury when the wobbling toddler pivots quickly or trips and falls. Toddler’s fractures happen in children 1 to 3 years of age, and occur in the distal 1/3 of the tibia. Sometimes a cast is needed, but currently there is a new trend in foregoing casting in mild cases.
O – Osteomyelitis
Bacteremia – from any source – can seed into any bone. It’s not very common, but it happens: approximately 2% of children who present to an ED with limp will have osteomyelitis. Plain films, ESR, and CRP are a fair screen to start. For more than the casual concern, MRI is the best modality to evaluate, followed by radionuclide scintigraphy. Although not the first choice modality, CT can show periosteal changes, such as inflammatory new bone formation or periosteal purulence.
P – Perthes disease
This is the famous Legg-Calvé-Perthes idiopathic avascular necrosis of the hip, usually affecting children from 3 to 12 years. They present with a slow onset pain and with an antalgic gait. Patients will have trouble with internal rotation and abduction of the hip. Radiographs may be initially normal. MRI can show the culprit: decreased perfusion to the femoral head and subsequent necrosis.
L – Limb-Length Discrepancy
Parents may notice that he seems “wobblier” than he should be. It may be that we are just now appreciating a congenital anomaly. Get out the paper tape, and measure from the anterior superior iliac spine to the medial malleolus and compare both sides. Children with limb-length discrepancy only need a non-urgent referral to pediatric orthopedics to look for congenital dysplasia of the hip, or other growth abnormalities. Some are treated with orthotics. Surgical options vary. Epiphysiodesis destroys the growth plate on the unaffected side, which evens out the growth. Other options are limb-lengthening or limb-shortening procedures.
I – Inflammatory
Transient Synovitis. This is what we want them to have right? The typical age is between 3 and 6 years, sometimes just after a URI. To be comfortable with this diagnosis, we should have considered all of the dangerous diagnoses, the child should be well, afebrile, in minimal discomfort, and he should respond almost completely to an NSAID. He’s the one running up and down the department after treatment – or just from sheer boredom after observation.
M – Malignancy
Primary bone tumors such as Ewing’s sarcoma or osteogenic sarcoma typically affect older children. Limping, however, may be a presenting symptom of leukemia. If you have any suspicion of the general wellness of the child, get a screening CBC, and perhaps a peripheral blood smear. Whatever you do, make sure you get close follow up for these kids that are on your malignancy radar -- the blast crisis may not have occurred yet – but it can happen hours to days later.
Plain films are insensitive for leukemic involvement of bone but they may show diffuse osteopenia, or metaphyseal bands – symmetrical high-uptake markings around the joint. They look like stacks of paper within normal bone – you can see them also in anemia, lead poisoning, and other causes. Also look for periosteal new bone formation, sclerosis, or lysis.
P – Pyomyositis
This usually presents with vague irritability, pain, and fever, and sometimes with a subacute minor trauma. These children don’t look to well.
Also think about just run-of-the-mill myositis, usually from a viral cause, such as influenza. Typically the calves are affected and are always tender. Hydration and supportive therapy are indicated for viral causes.
For bacterial focal pyomyositis, give empiric antibiotics, admit them for major inpatient workup, and think about early surgical consultation if you think you need sepsis source control.
I – Iliopsoas Abscess
Children most often will develop a primary abscess from bacteremia from an unresolved infection. Adults more commonly form secondary abscesses from Crohn’s disease, post-op complications, a vertebral infection, or even a bad chronic urinary tract infection. Lest you think this is a dramatic presentation, think again: iliopsoas abscesses present also with vague symptoms of back, flank, abdominal, or hip pain, sometimes with fever. The median time from symptoms to diagnosis in children is a whopping 20+ days, according to one study. If iliopsoas abscess is starting to get your attention, get the CT or MRI.
N – Neurologic
Not to scare you, but children do have strokes; unlike adults, half are hemorrhagic, half are thromboembolic. Typically they’ll have some underlying pathology that will alert you, such as a cardiac lesion, sickle cell disease, or some infectious or metabolic history. The good news is that it won’t just be a limp – you’ll have some other neuro sign or symptom to go after.
Guillain Barré is another thing to consider – early lower extremity weakness may present as a limp or refusal to walk. Maybe it’s not the hip that should be tapped, but the spinal canal.
Think also about muscular dystrophy or peripheral neuropathy and its possible underlying etiology.
G – Gastrointestinal and Genitourinary
What else could be going on? Appendicitis may be faking you out here. Perhaps there is a hernia, or testicular or ovarian torsion, all of which can present as lateralizing pain and not wanting to walk. Think outside the box.Phases of Gait
The gait cycle has three phases: contact, stance, and propulsion. Contact is the time from heel strike to just when the foot is flat. Stance is from the foot being flat to lifting the heel from the ground. The stance phase is when you bear most of your weight. The propulsion phase is when your weight transfers to your toes, and you push off.
Antalgic Gait -- "hobbling" gait; normal contact phase, but stance phase is abbreviated; propulsion is normal. The patient is trying to limit the time spent bearing weight on that side.
Trendelenburg Gait -- the affected side's hip abductor muscles are too weak or painful to stabilize the pelvis; the unaffected side dips to the floor. May be superior gluteal neuropathy, or a biomechanical problem, such as avascular necrosis, congenital dysplasia of the hip, or slipped capital femoral epiphysis.
Circumduction Gait -- the patient swings his foot laterally (due to a foot or ankle pathology), or to avoid tripping in limb-length discepancy.
Stiff-leggged Gait -- the patient walks with knees locked, in an attempt to avoid using the gastrocnemius muscles; concerning for myositis.
Equinus Gait -- toe-walking, as seen in myositis, also to avoid exacerbating pain from the calves.Lag of Internal Rotation of the Hip
Look for symmetry of internal rotation, or lateralizing pain or "guarding" with range of motion.
Keep the pelvis flush to the bed, and simultaneously rotate the lower extremity laterally, which will cause internal rotation of the hip.
Avascular necrosis will not allow full internal rotation, since the joint space is narrowed with this maneuver, causing impingement of the sensitive necrotic head of the femur.
Note any pain, asymmetry, and angle of internal rotation achieved.Kocher Criteria
In their original paper in 1999, Dr Kocher et al. performed a retrospective analysis of children who were being evaluated for a septic joint versus transient synovitis over a 15 year period, in a major referral center. They came up with four independent predictors of a septic joint, and calculated the probability of septic arthritis based on the number of features present. In 2004 the same group validated their prediction tool, with a slightly decreased sensitivity and specificity in the validation population.
In short, the Kocher criteria are not perfect, but it’s the best evidence we have at the moment.
The four predictors are:
Inability to walk
Fever of 38.5 C of greater
ESR > 40 mm/h
WBC > 12,000
Bonus mnemonic: Walk FEW: Inability to Walk | Fever | ESR | WBC
The probability of septic arthritis increases with increasing predictor. In this prediction model, each predictor has the same weight.
Probability of Septic Arthritis (Kocher et al. 1999)
0 Predictor –
Rank #19: Airway Master Moves
This post and podcast are dedicated to Mads Astvad for sharing his enthusiasm, clinical excellence, and #FOAMed warrior spirit.
Tak, min ven! #SMACConia #Vikingeblod
Rank #20: Pediatric Headache: Some Relief for All
We can make headache as easy or as complicated as we like, but let's break it down to what we need to know now, and what the parents need to know when they go home.
Primary headaches: headaches with no sinister secondary cause – like tension or migraine – are of course diagnoses of exclusion (cluster headache is exceedingly rare in children).
Secondary headaches: headaches due to some underlying cause -- are what we need to focus on first.
Ask yourself three main questions:
Is it a tumor?
Is it an infection?
Is it a bleed?Is it a tumor?
Some historical features are high-yield in screening for signs or symptoms consistent with a space occupying lesion.
Progression and worsening of symptoms over time
Pain only in the occiput
Headache that is worse with Valsalva – ask if coughing, urinating, or defecating affects the headache
Does this headache wake the child from sleep?
Is it worse in the morning just after getting up?
Conversely, the absence of some historical features may increase suspicion of a space-occupying lesion
No family history of migraine
No associated aura with the headache.Who needs neuroimaging?
The short answer is, if the child has an abnormal exam finding, then obtain a non-contrast head CT in the ED. If you’re worried enough to get imaging, then you should not feel great about sending him to an expedition to MRI.
The reassuring point is that for a child with a normal neuro exam, we have time to figure this out. For the recurrent headache, outpatient MRI really is the way to go if at all possible – not only do we forgo unnecessary radiation, but MRI is more likely to reveal the cause – or rule out the concern.
Medina et al. in Pediatrics reported on children with headache suspected of having a brain tumor. They stratified patients into low, intermediate, and high risk, based on clinical predictors from the history and physical. All had imaging. They then calculated probability of tumor in each group.
The low risk group had a 0.01% probability of tumor. The intermediate group 0.4%, and the high-risk group had only a 4% probability of tumor. The take-home message is that in the stable patient with a normal neurologic exam and no red flags, time is on our side.
The American Academy of Neurology's most recent guidelines, published first in 1994 and revised in 2004.
1. Neuroimaging on a routine basis is not indicated with recurrent headaches and a normal neurologic exam
2. Neuroimaging should be considered in children with an abnormal exam.
3. Neuroimaging should be considered in children with recent onset of severe headache, change in the type of headache, or associated features that suggest neurologic dysfunctionIs it an infection?
This is nothing new: if you think you need to perform a lumbar puncture, then you’re right. Go after the diagnosis when it meets your threshold for testing.
The difficulty is in the child who just has a headache, plus or minus symptoms that may be viral syndrome.
Dr Curtis et al. in Pediatrics did a systematic review of Clinical Features Suggestive of Meningitis in Children. In the history, only obvious features were helpful in this study: bulging fontanel in the infant or neck stiffness in the older child. Both increased the likelihood of meningitis by 8-fold.
In the physical examination, the only reliable predictors in this study were poor general appearance or a change in behavior.
You will catch those cases, because you would have tuned into meningitis early on -- especially in the unvaccinated.
What about all-comers with fever and headache? The presence of a high fever (so greater than 40 °C) only conferred a positive likelihood ratio of 2.9, only marginally predictive. Reassuring is that for temperatures less than 40 °C, the LR was 1 for meningitis.
In other words, a fever less than 40 °C was just as likely to be present with or without meningitis.Is it a bleed?
Does this child have some underlying disorder? For example, sickle cell disease, hypertension, rheumatologic disease, or some other endocrine or metabolic disease, such as a mitochondrial disorder?
In chronically ill children, consider cerebral sinus venous thrombosis, vasculitis, ischemia, or hemorrhage.
Arteriovenous malformation (AVM) is the hemorrhage we fear the most.
We really don’t know enough about arteriovenous malformations in the brain to say what is the typical presentation. They may be completely asymptomatic, until they rupture. Even the headache presentation is variable.
Think, headache PLUS.
New headache plus…vomiting.
Headache plus…it’s unilateral and new for the patient.
Headache plus…a new seizure.
Headache plus…focal neuro deficits, that may be transient, due to a vascular steal phenomenon.
Two illustrative cases of arteriovenous malformation:
1. An eleven-year-old girl presents to the ED with new headache, nausea, and vomting in the morning, then had a generalized seizure later that day, and presents with a low GCS. She was intubated, CT confirmed the AVM. She had a right frontal intraparenchymal bleed with midline shift. She underwent clot evacuation and extirpation of the intertwined arteries and veins.
2. A nine-year old girl presented to the ED with headache for two days, constant, then one day of nausea and vomiting. On presentation, she was altered, and had slow-reacting pupils. She also underwent evacuation, and only on histopathology did they find a single, arterialized vein.Primary Headache: Presumptive Impression
Tension headaches are the most common in children and adults. As in adults, the tension headache is band-like, pressure, tighetening, and often associated with muscle aches in the neck and shoulders.
Find out how often they occur, and whether there is any pattern of worsening symptoms, or if the symptoms seem to be related to sleep hygiene, video games, too much digital screen time. Also, screen for lack of exercise, poor diet, stress, and all of the other good questions you usually ask.
Treat the cause or counsel about lifestyle modification, and offer PO hydration and an NSAID, like ibuprofen or acetaminophen (paracetamol).
Non-pharmacologic techniques like heat packs, rest, stress relief, and a little TLC always help. Be careful not to encourage overreacting to the headache – sometimes we see a pattern of headache, attention, and more headache that can take root. Also look for overuse of medications, which may be the culprit in up to 50% of chronic headaches. Taking NSAIDs 3 or more times per week is associated with medication-induced headache, or cephalalgia medicamentosa.
We often fail to identify migraine headaches in children in the ED, likely for two reasons: prevalence of migraine increases with age, and children don’t present exactly like adults.
Stewart et al. in Neurology, report a prevalence of migraine in children that increases with age: 3 to 7 years of age was 2%; 7 to 11 years of age, 7%; and 11 to 20 years of age, 20%
Pearl: migraines are most commonly bilateral and temporal in children. They resemble "adult" tension headaches, but are much more severe.
We may not be able to sort this out in the ED. The point here is that migraines in children are more common that we may expect, and they can interfere with school performance, with social development, or even with family dynamics and overall stress burden.Primary Headache Diagnosis: Not (Usually) "Our Thing"
You noticed that we treated before we knew exactly the etiology; such is Emergency Medicine.
We may not be able to make a specific, definitive primary headache diagnosis in the ED, but we should be aware of the criteria to help counsel patients and families.Tension headache is the most common, but it requires multiple, similar episodes: Migraine headache (without aura) requires less episodes, but more specific features:
Primary Headache Management
So how do we treat primary headaches? If you feel this is a mild tension headache, fluids by mouth and a simple NSAID are probably all that is needed, in addition to a heaping dose of reassurance. Ibuprofen (10 mg/kg/dose q 6h, up to 600 mg) for a short course has the most evidence basis. Acetaminophen (paracetamol) (15 mg/kg/dose q6 h) for a short course may also be given.
Abortive treatments with the triptans may have been tried at home, but if they are coming to see us, we are past the point where triptans will be helpful.
For the primary headache that is resistant to NSAIDs, IV therapy may be considered.
If you’re going for IV, a nice evidence-based migraine cocktail is the following:
1. A bolus of 20 ml/kg of normal saline, up to a liter
2. Ketorolac (0.5 mg/kg; max, 30 mg)
3. Diphenhydramine (2 mg/kg; max, 50 mg)
4. Prochlorperazine (0.1 mg/kg; max, 10 mg)
Dr Kaar et al. in Pediatric Emergency Care evaluated the safety and efficacy of their institution’s standardized pediatric migraine practice guideline in the emergency department, which used ths cocktail, based on the best evidence available. In their retrospective chart review, they found the average visual pain scale drop from 7.8 to 2.1
There were no adverse events reported.
So, really you can treat children with migraines very similarly to adults.
For everyone who is going home, take just a moment to talk about the importance of sleeping well, eating well, getting exercise, limiting digital screen time, and trying to improve ways of dealing with stress.
When all else fails, and the parent has “heard it all”: get them started on a headache diary.
Take a piece of paper, fold it in half, and start a template for them to work on in a spiral notebook. Start a sample entry for them, with the date and time the headache started, what it felt like, what was happening just before, what made the headache better, any dose of medications given, how long it lasted, and what the patient did after. There are even free apps that will track the headache pattern.
This is the first thing a neurologist will start them on – and it’s sometimes a selling point to the parent that the time spent waiting for a referral to a neurologist is not waste – they will actually be in better shape and can move things along faster. It also gives them some sens of control of what can be a draining situation.Summary and Mental Road Map
If you were thinking meningitis or acute bleed, especially with fever or meningismus, get a CT first if you see signs of increased intracranial pressure, or if there is an abnormal neuro exam. Otherwise go straight to the lumbar puncture (LP).
In the afebrile child with a normal exam, give symptomatic relief, briefly counsel them, and arrange for follow-up.
In the afebrile child with an abnormal exam, obtain a CT in the ED. If negative, either admit for MRI if you are still concerned, or consider LP for idiopathic intracranial hypertension (pseudotumor cerebri).
Talk with parents early about expectations, and offer them some friendly advice on prevention. Refer patients to the primary care provider or neurologist if the presentation is more involved.
After a good history and physical examination in the ED that results in no red flags, we have time on our side. Help the family through the process by explaining the next steps and what can be done in the meantime. Compassion and a plan: sometimes these are our most powerful allies.
Lewis DW, Ashwal S, Dahl G, Dorbad D, Hirtz D, Prensky A, Jarjour I; Quality Standards Subcommittee of the American Academy of Neurology; Practice Committee of the Child Neurology Society. Practice parameter: evaluation of children and adolescents with recurrent headaches: report of the Quality Standards Subcommittee of the American Academy of Neurology and the Practice Committee of the Child Neurology Society. Neurology. 2002 Aug 27;59(4):490-8.
Lewis D, Ashwal S, Hershey A, Hirtz D, Yonker M, Silberstein S; American Academy of Neurology Quality Standards Subcommittee; Practice Committee of the Child Neurology Society.Practice parameter: pharmacological treatment of migraine headache in children and adolescents: report of the American Academy of Neurology Quality Standards Subcommittee and the Practice Committee of the Child Neurology Society.Neurology. 2004 Dec 28;63(12):2215-24.
Richer L, Billinghurst L, Linsdell MA, Russell K, Vandermeer B, Crumley ET, Durec T, Klassen TP, Hartling L. Drugs for the acute treatment of migraine in children and adolescents. Cochrane Database Syst Rev. 2016 Apr 19;4:CD005220.
This post and podcast are dedicated to Mark Wilson, PhD, BSc, MBBChir, FRCS(SN), MRCA, FIMC, FRGS for his #FOAMed generosity, candor, humility, and dedication to the care of the acutely ill and injured. Thank you.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP