There is none. The presentation varies so much, we need a rule to live by:
Unilateral pelvic pain in a girl is ovarian torsion until proven otherwise. This includes the cases in which you are concerned about appendicitis. They both can be fake-outs.
Often the pain is severe and abrupt, but trying to tease this out is often not fruitful.
Here are the often-reported signs and symptoms associated with ovarian torsion:
Stabbing pain, 70%
Nausea and vomiting, 70%
Sudden, sharp pain in the lower abdomen, 59%
Pain radiating to the back, flank, or groin, 51%
Peritoneal signs, 3%
Fever, less than 2%
And of course…no pain on presentation…30%...intermittent torsion.
As far as Doppler flow goes, you may see one of several scenarios:
Other things you may see on ultrasound include focal tenderness with the probe, or the whirlpool sign – this is a twisted vascular pedicle.
In children, is there an ovarian size (volume) that rules out torsion?”
In the Journal of Pediatric Radiology, Servaes et al catalogued the ultrasound findings in children with surgically confirmed torsion over a 12 year period. In this case series of 41 patients, the median age was 11. The age range was one month old to 21 years of age. They found that in torsed ovaries, the ovarian volume was 12 x that compared to the normal, non-torsed contralateral ovary.
That is to say, in this case series all torsed ovaries were larger than the normal contralateral ovary.
Sudden unilateral lower abdominal or pelvic pain in a female? Think torsion.
Have a low threshold for investigation.
Know the performance characteristics of ultrasound findings and involve a gynecologist early.
This post and podcast are dedicated to Stephanie Doniger, MD for her enthusiasm, spirit, and expertise in #MedEd #FOAMed #FOAMped #POCUS
Abe M, Sarihan H. Oophoropexy in children with ovarian torsion. Eur. J. Pediatr. Surg. 2004;14:168.
Aziz D, Davis V, Allen L, Langer J. Ovarian torsion in children: Is oophorectomy necessary? J. Pediatr. Surg. 2004;39:750-3.
Bristow RE, Nugent AC, Zahurak ML, et al. Impact of surgeon specialty on ovarian-conserving surgery in young females with an adnexal mass. J. Adolesc. Health 2006;39:411.
Chang YJ, Yan DC, Kong MS, et al. Adnexal torsion in children. Pediatr. Emerg. Care. 2008;24:534-7.
Conforti A, Giorlandino C, Bagolan P. Fetal ovarian cysts management and ovarian prognosis: a report of 82 cases. J. Pediatr. Surg. 2009;44:868; author reply 868-9.
Guthrie BD, Adler MD, Powell EC. Incidence and trends of pediatric ovarian torsion hospitalizations in the United States, 2000-2006. Pediatrics 2010;125:532-8. Epub 2010 Feb 1.
Houry D, Abbott JT. Ovarian torsion: a fifteen-year review. Ann. Emerg. Med. 2001;38:156-9.
Huang TY, Lau BH, Lin LW, Wang TL, Chong CF, Chen CC. Ovarian cyst torsion in a toddler. Am. J. Emerg. Med. 2009;27:632, e1-3.
Hurh PJ, Meyer JS, Shaaban A. Ultrasound of a torsed ovary: characteristic gray-scale appearance despite normal arterial and venous flow on Doppler. Pediatr. Radiol. 2002;32:586-8. Epub 2002 May 25.
Kokoska E, Keller M, Weber T. Acute ovarian torsion in children. Am. J. Surg. 2000;180:462-5.
Oltmann SC, Fischer A, Barber R, Huang R, Hicks B, Garcia N. Cannot exclude torsion – a 15-year review. J. Pediatr. Surg. 2009;44:1212-6; discussion 1217.
Chmitt ER et al. Twist and Shout! Pediatric Ovarian Torsion Clinical Update and Case Discussion. Pediatr Emerg Care. 2013; 29(4):518-523.
Servaes S, Zurakowski D, Laufer MR, Feins N, Chow JS. Sonographic findings of ovarian torsion in children. Pediatr. Radiol. 2007;37:446-51. Epub 2007 Mar 15.
Valsky DV. Added value of the gray-scale whirlpool sign in the diagnosis of adnexal torsion. Ultrasound Obstet. Gynecol. 2010;36:630-4.
Normally metabolized into codeine-6-glucuronide (50-70%) and norcodeine (10-15%). Codeine, codeine-6-glucuronide, and norcodeine have low affinity for the μ (mu) receptor.
However, the most active metabolite of codeine is morphine with 200x the affinity for the mu receptor as the codeine derivates. The problem is, people vary in its metabolism from 0-15% of codeine is metabolized to morphine.
Ok, codeine is lame at best, unpredictable at worst.
True. Unless you are hiding a genetic time bomb.
You're an ultra-rapid metabolizer.
Some people have multiple extra copies of the DNA sequence for the CYP2D6 enzyme. Ultra rapid metabolizers funnel a huge proportion of their codeine into morphine metabolism, resulting in a bolus of morphine, ending in apnea.
This combination is no better than placebo -- all of the risks, with no proven benefit. This combination is notoriously abused -- as purple drank or sizzurp. The rapper Pimp C died of this.
Speaking of cough syrups...
The AAP recommends no cough and cold preparations in children under age 6. They have not been adequately studied in young children, and are not recommended for treating the common cold.
What then? You gotta give me something, doctor!
In a study in the Archives of Pediatric and Adolescent Medicine, Dr Paul and colleagues published: Effect of honey, dextromethorphan, and no treatment on nocturnal cough and sleep quality for coughing children and their parents. They compared a buckwheat honey, honey-flavored dextromethorphan (DM) and no treatment 30 min before bed for children with upper respiratory tract infections.
Of the three, honey, dextromethorphan, and no treatment – honey scored the best for symptom improvement and cough frequency.
Over age 1? Cough and cold? Honey. There is no concern about accidental overdose, parents are doing something with a proven effect, and compliance is pretty much 100% -- and Grandma approves.
No proven benefit over placebo. Also widely abused, in pill form ("Skittles") and/or liquid form mixed in alcoholic beverage ("robotripping").
Allow the child to speak for himself whenever possible. After acknowledging the parent’s input, perhaps try “I want to make sure I understand how the pain is for you. Tell me more.”
Engage parents and communicate the plan to them. Elicit their expectations, and give them of preview of what to expect in the ED.
Opioids are meant for pain caused by acute tissue injury, for the briefest period of time feasible. Older school-aged children and adolescents are increasingly at risk for opioid dependence and addiction.
Give detailed advice on how to manage pain at home. Set expectations. Let them know you understand and will help them through your good advice that will carry them through this difficult time. Patients and families often just need a plan. Map it out clearly.
Just say no to: codeine, promethazine with codeine, and dextramethorphan.
This post and podcast are dedicated to Bryan Hayes, PharmD for his practical approach to pharmacologic conundrums and to David Juurlink, MD, PhD for his steadfast dedication to patient safety and clinician education. Check out Bryan's helpful blog and clinical resource, PharmERToxGuy. Check out David anywhere one utters the word Tra-ma-dol.
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.
For intractable epilepsy; sends retrograde signal up corona radiata
Also may be used in: depression, bulimia, Alzheimer, narcolepsy, addiction, and others
Used to infuse basal rate of drug, usually baclofen for spasticity, but pump may contain morphine, bupivicaine, clonidine. Also used for severe MS, stroke, TBI, chronic pain. Verify the medication and identify the toxidrome if symptomatic.
May be left ventricular assist, right ventricular assist, or biventricular assist device.
Elliott RE, Rodgers SD, Bassani L et al. Vagus nerve stimulation for children with treatment-resistant epilepsy: a consecutive series of 141 cases. J Neurosurg Pediatrics. 2011; 7:491-500.
Groves DA, Brown VJ. Vagal nerve stimulation: a review of its applications and potential mechanisms that mediate its clinical effects. Neuroscience and Biobehavioral Reviews. 2005; 29: 493–500.
Panebianco M, Rigby A,Weston J,Marson AG. Vagus nerve stimulation for partial seizures. Cochrane Database of Systematic Reviews. 2015; 4, Art. No.: CD002896.
Ruffoli R, Giorgi FS, Pizzanelli C et al. The chemical neuroanatomy of vagus nerve stimulation. Journal of Chemical Neuroanatomy; 2011; 42: 288–296.
Borowski A, Littleton AG, Borkhuu B et al. Complications of Intrathecal Baclofen Pump Therapy in Pediatric Patients. J Pediatr Orthop. 2010; 30:76–81.
Ghosh D, Mainali G, Khera J, Luciano M. Complications of Intrathecal Baclofen Pumps in Children: Experience from a Tertiary Care Center. Pediatr Neurosurg. 2013; 49:138–144.
Yang TF, Wang JC, Chiu JW et al. Ultrasound-guided refilling of an intrathecal baclofen pump—a case report. Childs Nerv Syst. 2013; 29:347–349.
Yeh RN, Nypaver MM, Deegan TJ, Ayyangar R. Baclofen Toxicity in an 8-year-old with an Intrathecal Baclofen Pump. J Emerg Med. 2004; 26(4): 163–167.
Blume ED, Naftel DC, Bastardi HJ et al. for the Pediatric Heart Transplant Study Investigators. Outcomes of Children Bridged to Heart Transplantation With Ventricular Assist Devices: A Multi-Institutional Study. Circulation. 2006; 113: 2313-2319.
Colón JE, Laborde ME, Nossaman BD. Case Report: Left Ventricular Assist Device in a 12 Year Old Child as a Bridge to Heart Transplantation. Section of Congenital Cardiac Anesthesia, Ochsner Medical Center, New Orleans, Louisiana. 2012.
Fan Y, Weng YG, Huebler M et al. Predictors of In-Hospital Mortality in Children After Long-Term Ventricular Assist Device Insertion. J Amer Coll Cardiol. 2011; 58(11):1183–90
Fraser CD, Jaquiss RDB, Rosenthal DN et al. Prospective Trial of a Pediatric Ventricular Assist Device. N Engl J Med. 2012;367:532-41.
Gazit AZ, Gandhi SK, Canter CC. Mechanical Circulatory Support of the Critically Ill Child Awaiting Heart Transplantation. Current Cardiology Reviews. 2010; 6: 46-53.
VanderPluym CJ, Fynn-Thompson F, Blume ED. Ventricular Assist Devices in Children Progress With an Orphan Device Application. Circulation. 2014;129:1530-1537.
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.
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
Myocardial infarction (MI) in children is uncommon, but underdiagnosed. This is due to two main factors: the etiologies are varied; and the presenting symptoms are “atypical”.
Two main presentations of MI due to congenital lesions: novel and known. The novel presentation is at risk for underdiagnosis, due to its uncommonness and vague, atypical symptoms. There are usually some red flags with a careful H&P. The known presentation is a child with a history of congenital heart disease, addressed by corrective or palliative surgery. This child is at risk for expected complications, as well as overdiagnosis and iatrogenia. Risk stratify, collaborate with specialists.
Anomalous Left Coronary Artery from the Pulmonary Artery (ALCAPA) is an example of what can go wrong during fetal development: any abnormality in the number, origin, course, or morphology of the coronary arteries can present as a neonate with sweating during feeds (steal syndrome), an infant in CHF, or an older child with failure to thrive or poor exercise tolerance.
Normal coronary arteries run along the epicardial surface of the heart, with projections into the myocardium. If part of the artery’s course runs within the myocardium (i.e. the artery weaves into and/or out of the myocardium), then there is a myocardial bridge of the coronary artery. With every systolic contraction, the artery is occluded.
Although a myocardial bridge may not cause symptoms (especially at distal portions), the area it supplies is at risk.
With any minor trauma or exertion, demand may outpace supply, resulting in ischemia.
Diagnosis is made on coronary angiography.
The child with single ventricle physiology may have a Norwood procedure at birth (creation of a neoaorta, atrial septectomy, and Blalock-Taussig shunt), a Bidirectional Glenn procedure at 3-6 months (shunt removed, superior vena cava connected to pulmonary arteries), and a Fontan procedure at about 2-3 years of age (inferior vena cava blood flow is shunted into the pulmonary arteries).
These children depend on their preload to run blood passively into the pulmonary circuit; afterload reduction is also important to compensate for a poor left ejection fraction, as well as to avoid the development of pulmonary hypertension. They are typically on an anticoagulant (often aspirin), a diuretic (e.g. furosemide), and an afterload reduction agent (e.g. enalapril).
Any disturbance in volume status (hyper- or hypovolemia), anticoagulation, or afterload may cause myocardial strain or infarction. Take the child s/p Fontan seriously and involve his specialists early with any concerns.
The body’s inflammatory-mediated reaction to a real or perceived insult can cause short- and long-term cardiac sequelae. Find out how well the underlying disease is controlled, and what complications the child has had in the past.
The red, hot, crispy, flaky child: acute Kawasaki disease
Kawasaki disease (KD) is an acute systemic vasculitis, diagnosed by the presence of fever for five or more days accompanied by four or more criteria: bilateral conjunctival injection, mucositis, cervical lymphadenopathy, polymorphous rash, and palmar or sole desquamation. The criteria may occur (and disappear) at any time during the illness.
Infants are under double jeopardy with Kawasaki Disease. They are more likely to have incomplete KD (i.e. not fulfill strict criteria) and if they have KD, they are more likely to suffer the dangerous consequences of aneurysm formation (chiefly coronary arteries, but also brain, kidney). Have a low threshold for investigation.
Treatment includes 2 g/kg/day IVIG and high-dose aspirin (30-50 mg/kg/day) acutely, then low-dose aspirin (5 mg/kg/day) for weeks to months. Regular and long-term follow-up with Cardiology is required.
The family and child with a history of KD may have psychological trauma and continuous anxiety about the child’s risk of MI. Approximately 4.7% of children who were promptly diagnosed and correctly treated will go on to have cardiac sequelae.
Children who have no detected cardiac sequelae by 8 weeks, typically continue to be asymptomatic up to 20 years later.
Smaller aneurysms tend to regress over time, especially those < 6 mm.
Thrombi may calcify, or the lumen may become stenotic due to myofibroblast proliferation. Children with any coronary artery dilatation from KD should be followed indefinitely.
Giant aneurysms (≥8 mm) connote the highest risk for MI.
Parents often are concerned about recurrence, and any subsequent fever can be distressing. There is a low rate of recurrence for KD: approximately 2%. Infants who have coronary aneurysms are at the highest risk for recurrence.
Up to 15% of cases of SLE begin in childhood. Adult criteria are used, with the caveat that the diagnosis of SLE in children can be challenging; many children only manifest a few of the criteria initially before going on to develop further systemic involvement.
The Systemic Lupus International Collaborating Clinics (SLICC) revised the criteria in 2012. The patient should have ≥4/17 clinical and/or immunologic criteria. The clinical criteria are: acute cutaneous (malar); chronic cutaneous (discoid); oral; alopecia; synovitis; serositis; renal; neurologic; hemolytic anemia; leukopenia; or thrombocytopenia. The immunologic criteria are: ANA; anti-dsDNA; anti-Sm; antiphospholipid; low complement; and/or Direct Coombs (in absence of hemolytic anemia). At least one criterion should be clinical, and at least one should be immunologic.
Children with antiphospholipid syndrome (APS) may occur with or without SLE. Patients are at risk for venous and arterial thrombi formation. APS may also cause structural damage, such as valvular thickening and valvular nodes (Libman-Sacks endocarditis). Mitral and aortic valves are at the highest risk.
Although most children with chest pain will not have MI, those with comorbidities should be investigated carefully.
Direct, blunt trauma to the chest can cause myocardial stunning, dysrhythmias, or an asymptomatic rise in Troponin I. However, some children are at risk for disproportionate harm due to a previously unknown risk factor. Clinically significant cardiac injury occurs in up to 20% of patients with non-penetrating thoracic trauma.
The motor vehicle collision: blunt myocardial injury
Direct trauma (steering wheel, airbag, seatbelt), especially in fast acceleration-deceleration injury, may cause compression of the heart between the sternum and the thoracic spine.
Electrocardiography (ECG) should be performed on any patient with significant blunt chest injury. A negative ECG is highly consistent with no significant blunt myocardial injury.
Any patient with a new abnormality on ECG (dysrhythmia, heart block, or signs of ischemia) should be admitted for continuous ECG monitoring.
Elevation in troponin is common, but not predicted. A solitary elevated troponin without ECG abnormality is of unclear significance. Author’s advice: obtain troponin testing if there is an abnormal ECG, more than fleeting suspicion of BCI, and/or the child will be admitted for monitoring.
Direct trauma (e.g. MVC, baseball, high-velocity soccer ball) may cause damage to the left anterior descending artery or left circumflex artery, at the highest risk due to their proximity to the chest wall. Thrombosis and/or dissection may result, often presenting in a focal pattern of ischemia on the ECG.
Echocardiography may reveal valvular damage related to the injury, as well as effusion and ejection fraction. Since there is often a need to investigate the coronary anatomy, percutaneous coronary intervention (PCI) is recommended.
As mentioned in the congenital section (above), a known variation of a coronary artery’s course involves weaving in and out of the myocardium, creating a baseline risk for ischemia. Even minor trauma in a child with a myocardial bridge may cause acute thrombus, or slow stenosis from resulting edema. Unfortunately, the presence of myocardial bridging is often unknown at the time of injury. Approximately 25% of the population may have myocardial bridging, based on autopsy studies. Take the child seriously who has disproportionate symptoms to what should be a minor injury.
Coagulopathic and thrombophilic states may predispose children to focal cardiac ischemia. The best documented cormorbidity is sickle cell disease, although other pro-thrombotic conditions also put the child at risk.
The child with sickle cell disease and chest pain: when it’s not acute chest syndrome
Sickle cell disease (SCD) can affect any organ system, although the heart is traditionally considered a lower-risk target organ for direct sickling and ischemia. The major cardiac morbidity in sickle cell is from strain, high-output failure and multiple, serial increases in myocardial demand, causing left ventricular hypertrophy and congestive heart failure.
However, there is mounting evidence that acute myocardial ischemia in sickle cell disease may be underappreciated and/or attributed to other causes of chest pain.
Other cardiac sequelae from SCD include pulmonary hypertension, left ventricular dysfunction, right ventricular dysfunction, and chronic iron overload.
Evidence of myocardial ischemia/infarction in children with SCD has been demonstrated on single-photon emission computed tomography (SPECT) scan.
Children who suffer from nephrotic syndrome lose proteins that contribute to the coagulation cascade. In addition, lipoprotein profiles are altered: there is a rise in the very low-density lipoproteins (LDL), contributing to accelerated atherosclerosis. Typically nephrotic patients have normal levels of high-density lipoproteins (HDL), unless there is profuse proteinuria.
Children with difficult-to-control nephrotic syndrome (typically steroid-resistant) may form accelerated plaques that rupture, causing focal MI, as early as school age.
Asymptomatic patent foramen ovale (PFO) is the cause of some cases of cryptogenic vascular disease, such as stroke and MI. However, the presence of PFO alone does not connote higher risk. When paired with an inherited or acquired thrombogenic condition, the venous thrombus may travel from the right-sided circulation to the left, causing distal ischemia. Many of these cases are unknown until a complication arises.
A family history of adult-onset hypercholesterolemia is not necessarily a risk factor for early complications in children, provided the child does not have the same acquired risk factors as adults (e.g. obesity, sedentary lifestyle, smoking, etc). Parents may seek help in the ED for children with chest pain and no risk factors, but adult parents who have poor cholesterol profiles.
The exception is the child with familial hypercholesterolemia, who is at risk for accelerated atherosclerosis and MI.
Myocarditis has varied etiologies, including infectious, medications (chemotherapy agents), immunologic (rheumatologic, transplant rejection), toxins (arsenic, carbon monoxide, heavy metals such as iron or copper), or physical stress (electrical injury, heat illness, radiation).
In children, the most common cause of myocarditis is infectious (viruses, protozoa, bacteria, fungal, parasites). Of these, viral causes are the most common (adenovirus, enterovirus, echovirus, rubella, HHV6).
The verbal child may complain of typical chest complaints, or may come in with flu-like illness and tachycardia or ill appearance out of proportion to presumed viral illness.
The most common presenting features in children with myocarditis are: shortness of breath, vomiting, poor feeding, hepatomegaly, respiratory distress, and fever.
Beware of the poor feeding, tachycardic, ill appearing infant who “has a cold” because everyone else around him has a ‘cold’. That may very well be true, but any virus can be invasive with myocardial involvement. Infants are only able to increase their cardiac output through increasing their heart rate; they cannot respond to increased demands through ionotropy. Look for signs of acute heart failure, such as hepatomegaly, respiratory distress, and sacral edema.
The child with tachycardia out of proportion to complaint: myocarditis
The previously healthy child with “a bad flu” may simply be very symptomatic from influenza-like illness, or he may be developing myocarditis. Look for chest pain and tachycardia out of proportion to presumed illness, and constant chest pain, not just associated with cough.
Acute heart failure may mimic viral pneumonia. Look for disproportionate signs and symptoms.
Younger children may get into others’ medications, be given dangerous home remedies, take drugs recreationally, have environmental exposures (heavy metals), suffer from a consequence of a comorbidity (iron or copper overload) or have adverse events from generally safe medications.
Attention deficit hyperactivity disorder (ADHD) is growing in rate of diagnosis and use of medications. As the only medical diagnosis based on self-reported criteria, many children are given stimulants regardless of actual neurologic disorder; with a higher proportion of children exposed to stimulants, adverse effects are seen more commonly.
Methylphenidate is related to amphetamine, and they both are dopaminergic drugs. Their mechanisms of action are different, however. Methylphenidate increases neuronal firing rate. Methamphetamine reduces neuronal firing rate; cardiovascular sequelae such as MI and CHF are more common in chronic methamphetamine use.
Although methylphenidate is typically well tolerated, risks include dysrhythmias such as ventricular tachycardia.
Some anti-epileptic agents, such as carbamazepine, promote a poor lipid profile, leading to atherosclerosis and early MI. Case reports include school-aged children on carbamazepine who have foamy cells in the coronary arteries, aorta, and vasa vasorum on autopsy. It is unclear whether this is a strong association.
The spice trader: synthetic cannabinoids
Synthetic cannabinoids are notoriously difficult to regulate and study, as the manufacturers label them as “not for human consumption”. Once reports surface of abuse of a certain compound, the formula is altered slightly and repackaged, often in a colorful or mysterious way that is attractive to teenagers.
The misperceptions are: are a) synthetics are related to marijuana and therefore safe and b) marijuana is inherently “safe”. Both tend to steer unwitting teens to take these unknown entities. Some suffer MI as a result.
Exposure to tetrahydrocannabinol (THC) in high-potency marijuana has been linked to myocardial ischemia, ventricular tachycardia, and ventricular fibrillation. Marijuana can increase the heart rate from 20-100%, depending on the amount ingested.
K2 (“kush 2.0”) or Spice (Zohai, Genie, K3, Bliss, Nice, Black Mamba, fake weed, etc) is a mixture of plant leaves doused in synthetic chemicals, including cannabinoids and fertilizer (JWH-108), none of which are tested or safe for human consumption.
Synthetic cannabinoids have a higher affinity to cannabinoid receptors, conferring higher potency, and therefore worse adverse effects. They are thought to be 100 to 800 times more potent as marijuana.
Bath salts (Purple Wave, Zoom, Cloud Nine, etc) can be ingested, snorted, or injected. They typically include some form of cathinone, such as mephedrone, similar to the substance found in the naturally occurring khat plant. Hallucinations, palpitations, tachycardia, MI, and dysrhythmias have been reported from their use as a recreational drug.
Chest pain with marijuana, synthetic cannabinoid, or bath salt ingestion should be investigated and/or monitored.
Riding that train: high on cocaine
Cocaine is a well-known cause of acute MI in young people. In addition to the direct stimulant causes acutely, such as hypertension, tachycardia, and impaired judgement (coingestions, risky behavior), chronic cocaine use has long-term sequelae. Cocaine causes accelerated atherosclerosis. That, in conjunction with arterial vasospasm and platelet activation, is a recipe for acute MI in the young.
Methamphetamine is a highly addictive stimulant that is relatively inexpensive and widely available. Repeated use causes multiple psychiatric, personality, and neurologic changes. Risky behavior, violence, and motor vehicle accidents are all linked to this drug.
Like cocaine, methamphetamine may cause fatal dysrhythmias, acute MI from demand ischemia, and long-term sequelae such as congestive heart failure.
Acute MI is a challenging presentation in children:
AboulHosn JA et al. Fontan Operation and the Single Ventricle. Congenit Heart Dis. 2007; 2:2-11.
Aliku TO et al. A case of anomalous origin of the left coronary artery presenting with acute myocardial infarction and cardiovascular collapse. African Health Sci. 2014; 14(1): 23-227.
Andrews RE et al. Acute myocardial infarction as a cause of death in palliated hypoplastic left heart syndrome. Heart. 2004; 90:e17.
Canale LS et al. Surgical treatment of anomalous coronary artery arising from the pulmonary artery. Interactive Cardiovascaulr and Thoracic Surgery. 2009; 8:67-69.
Güvenç O et al. Correctable Cause of Dilated Cardiomyopathy in an Infant with Heart Failure: ALCAPA Syndrome. J Curr Pediatr. 2017; 15:47-50.
Hastings RS et al. Embolic Myocardial Infarction in a Patient with a Fontan Circulation. World Journal for Pediatric Congenital Heart Surgery. 2014; 5(4)L631-634.
Hoffman JIE et al. Electrocardiogram of Anomalous Left Coronary Artery From the Pulmonary Artery in Infants. Pediatr Cardiol. 2013; 34(3):489-491.
Kei et al. Rare Case of Myocardial Infarction in a 19-Year-Old Caused by a Paradoxical Coronary Artery Embolism. Perm J.2015; 19(2):e107-e109.
Liu Y, Miller BW. ALCAPA Presents in an Adult with Exercise Inlerance but Preserved Cardiac Function. Case Reports Cardiol. 2012; AID 471759.
Möhlenkamp S et al. Update on Myocardial Bridging.Circulation. 2002;106:2616-2622.
Murgan SJ et al. Acute myocardial infraction n the neonatal period. Cardiol Young. 2002; 12:411-413.
Sieweke JT et al. Myocardial infarction in grown up patients with congenital heart disease: an emergening high-risk combination. International Journal of Cardiology. 2016; 203:138-140.
Schwerzmann M et al. Anomalous Origin of the Left Coronary Artery From the Main Pulmonary Artery in Adults. Circulation. 2004; 110:e511-e513.
Tomkewicz-Pajak L et al. Arterial stiffness in adult patients after Fontan procedure. Cardiovasculr Ultrasound. 2014; 12:15.
Varghese MJ et al. The caveats in the diagnosis of anomalous origin of left coronary artery from pulmonary artery (ALCAPA). Images Paediatr Cardiol. 2010; 12(3): 3–8.
Ayala et al. Acute Myocardial Infarction in a Child with Systemic Lupus Erythematosus and Antiphospholipid Syndrome. Turk J Rheumatol. 2009; 24:156-8.
Nakano H et al. Clinical characteristics of myocardial infarction following Kawasaki disease: Report of 11 cases. J Pediatr. 1986; 108(2):198-203.
Pongratz G et al. Myocardial infarction in an adult resulting from coronary aneurysms previously documented in childhood after an acute episode of Kawasaki’s disease. European Heart J. 1994. 15:1002-1004.
Newburger JW et al. Diagnosis, Treatment, and Long-Term Management of Kawasaki Disease. A Statement for Health Professionals From the Committee on Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on Cardiovascular Disease in the Young, American Heart Association. Circulation. 2004;110:2747-2771.
Son MB et al. Kawaski Disease. Pediatr Rev. 2013; 34(4).
Yuan S. Cardiac surgical procedures for the coronary sequelae of Kawasaki disease. Libyan J Med. 2012; 7:19796.
Abdolrahim SA et al. Acute Myocardial Infarction Following Blunt Chest Trauma and Coronary Artery Dissection. J Clin Diagnost Res. 2016; 10(6):14-15.
Galiuto L et al. Post-traumatic myocardial infarction with hemorrhage and microvascular damage in a child with myocardial bridge: is coronary anatomy actor or bystander. Signa Vitae. 2013; 8(2):61-63.
Janella BL et al. Acute Myocardial Infarction related to Blunt Thoracic Trauma. Arq Bras Cardiol. 2006; 87:e168-e171.
Liu X et al. Acute myocardial infarction in a child with myocardial bridge World J Emerg Med. 2011; 2(1):70-72.
Long WA et al. Childhood Traumatic Infarction Causing Left Ventricular Aneurysm: Diagnosis by Two-Dimensional Echocardiography. JACC. 1985; 5(6):1478-83.
Smith S. Right Bundle Branch Block after Blunt Trauma: A Tragic Case. [Blog Post] July 22, 2012. Retrievable at: http://hqmeded-ecg.blogspot.com/2012/07/right-bundle-branch-block-after-blunt.html.
Carano N et al. Acute Myocardial Infarction in a Child: Possible Pathogenic Role of Patent Foramen Ovale Associated with Heritable Thrombophilia. Pediatr. 2004; 114(2):255-258.
Chacko P et al. Myocardial Infarction in Sickle Cell Disease. J Cardiovascl Transl Res. 2013; 6(5):752-761.
De Montalembert M et al. Myocardial ischaemia in children with sickle cell disease. Arch Dis Child. 2004; 89:359-362.
Gladwin MT et al. Cardiovascular Abnormalities in Sickle Cell Disease. JACC. 2012; 59(13):1123-1133.
Osula S et al. Acute myocardial infarction in young adults: causes and management. Postgrad Med J. 2002; 78:27-30.
Silva JMP et al. Premature acute myocardial infarction in a child with nephrotic syndrome. Pediatr Nephrol. 2002; 17:169-172.
Suryawanshi SP. Myocardial infarction in children: Two interesting cases. Ann Pediatr Cardiol. 2011 Jan-Jun; 4(1): 81–83.
Cunningham R et al. Viral myocarditis Presenting with Seizure and Electrocardiographic Findings of Acute Myocardial Infarction in a 14-Month-Old Child. Ann Emerg Med. 2000; 35(6):618-622.
De Vettten L et al. Neonatal Myocardial Infarction or Myocarditis? Pediatr Cardiol. 2011; 32:492-497.
Durani Y et al. Pediatric myocarditis: presenting clinical characteristics. Am J Emerg Med. 2009; 27:942-947.
Erden I et al. Acute myocarditis mimicking acute myocardial infarction associated with pandemic 2009 (H1N1) influenza virus. Cardiol J. 2011; 552-555.
Hover MH et al. Acute Myocarditis Simulating Myocardial Infarction in a Child. Pediatr. 1191; 87(2):250-252.
Lachant D et al. Meningococcemia Presenting as a Myocardial Infarction. Case Reports in Critical Care. 2015; AID 953826.
Laissy JP et al. Differentating Myocardial Infarction from Myocarditis. Radiology. 2005; 237(1):75-82.
Miranda CH et al. Evaluation of Cardiac Involvement During Dengue Viral Infection. CID. 2013; 57:812-819.
Rettig JS et al. Myocarditis in Children Requiring Critical Care Transport. In: "Diagnosis and Treatment of Myocarditis", Milei J, Ambrosio G (Eds). DOI: 10.5772/56177.
De Chadarévian JP et al. Epilepsy, Atherosclerosis, Myocardial Infarction, and Carbamazepine. J Child Neurol. 2003; 18(2):150-151.
McIlroy G et al. Acute myocardial infarction, associated with the use of a synthetic adamantly-canabinoid: a case report. BMC Pharmacology and Toxicology. 2016; 17:2.
Mir A et al. Myocardial Infarction Associated with Use of the Synthetic Cannabinoid K2. Pediatr. 2011; 128(6):1-6
Munk K et al. Cardiac Arrest following a Myocardial Infarction in a Child Treated with Methylphenidate. Case Reports Pediatr. 2015; AID 905097.
Rezkalla SH et al. Cocaine-Induced Acte Mycardial Infarction. Clin Med Res. 2007; 5(3):172-176.
Schelleman H et al. Methylphenidate and risk of serious cardiovascular events in adults. Am J Psychiatry. 2012 Feb;169(2):178-85.
Sheridan J et al. Injury associated with methamphetamine use: a review of the literature. Harm Reduction Journal, 2006; 3(14):1-18.
Stiefel G et al. Cardiovascular effects of methylphenidate, amphetamines and atomoxetine in the treatment of attention-deficit hyperactivity disorder. Drug Saf. 2010 Oct 1;33(10):821-42.
This post and podcast are dedicated to Edwin Leap, MD for his sanity and humanity in the practice of Emergency Medicine. Thank you, Dr Leap for all that you do.
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, 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.
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.
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.
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”.
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.
|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.
Assess risk for developing severe hyperbilirubinemia.
|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|
Check bilirubin and match this with how old the child is -- in hours of life -- at the time of bilirubin measurement.
Use the Bilitool or Bhutani Nomogram (below).
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).
Assess risk for developing subsequent neurotoxicity.
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.
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.
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.
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.
This post and podcast are dedicated to Gita Pensa, MD, for her commitment to #FOAMed and passion for asynchronous learning and education innovation.
|Magnets||Crayon||Hair accessories, bows|
|Pen/marker caps||Button batteries||Plastic bags, packaging|
Set the scene and control the environment. Limit the number of people in the room, the noise level, and minimize “cross-talk”. The focus should be on engaging, calming, and distracting the child.
Quiet room; calm parent; “burrito wrap”; guided imagery; have a willing parent restrain the child in his or her lap – an assistant can further restrain the head.
Most foreign bodies in the ear, nose, and throat in children can be managed with non-pharmacologic techniques, topical aids, gentle patient protective restraint, and a quick hand. Consider sedation in children with special health care needs who may not be able to cooperate and technically delicate extractions. Ketamine is an excellent agent, as airway reflexes are maintained.3 Remember to plan, think ahead: where could the foreign body may be displaced if something goes wrong? You may have taken away his protective gag reflex with sedation. Position the child accordingly to prevent precipitous foreign body aspiration or occlusion.
The external auditory canal. Foreign bodies may become lodged in the narrowing at the bony cartilaginous junction.4 The lateral 1/3 of the canal is flexible, while the medial 2/3 is fixed in the temporal bone – here is where many foreign bodies are lodged and/or where the clinician may find evidence of trauma.
Nasopharyngeal and tracheal anatomy. Highlighted areas indicate points at which nasal foreign bodies may become lodged.4
Remember that a foreign body in the mouth or throat can precipitously become a foreign body in the airway. Foreign body inhalation is the most common cause of accidental death in children less than one year of age.9,10
Go to BLS maneuvers if the child decompensates.
Infants under 1 year of age – back blows: head-down, 5 back-blows (between scapulae), 5 chest-thrusts (sternum). Reassess, repeat as needed.
Children 1 year and up, conscious – Heimlich maneuver: stand behind patient with arms positioned under the patient’s axilla and encircling the chest. The thumb side of one fist should be placed on the abdomen below the xiphoid process. The other hand should be placed over the fist, and 5 upward-inward thrusts should be performed. This maneuver should be repeated if the airway remains obstructed. Alternatively, if patient is supine, open the airway, and if the object is readily visible, remove it. Abdominal thrusts: place the heel of one hand below the xiphoid, interlace fingers, and use sharp, forceful thrusts to dislodge. Be ready to perform CPR.
Children 1 year and up, unconscious – CPR: start CPR with chest compressions (do not perform a pulse check). After 30 chest compressions, open the airway. If you see a foreign body, remove it but do not perform blind finger sweeps because they may push obstructing objects further into the pharynx and may damage the oropharynx. Attempt to give 2 breaths and continue with cycles of chest compressions and ventilations until the object is expelled.
Chest films are limited: 80% of airway foreign bodies are radiolucent.11 Look for unilateral hyperinflation on expiratory films: air trapping.
Most esophageal foreign bodies in children occur at the level of the thoracic inlet / cricopharyngeus muscle (upper esophageal sphincter). Other anatomically narrow sites include the level of the aortic arch and the lower esophageal sphincter.
Coin en face – in the esophagus – lodged at the thoracic inlet.12 The pliable esophagus accommodates the flat coin against the flat aspect of the vertebra.11
This is an emergency: the electrolyte-rich mucosa conducts a focal current from the narrow negative terminal of the battery, rapidly causing burn, necrosis, and possibly perforation. Emergent removal is required.
Button batteries that have passed into the stomach do not require emergent intervention – they can be followed closely.
If there is no obstruction, consider revaluation the next day – may wait up to 24 hours for passage.14 Sharieff et al.15 found that coins found in the mid to distal esophagus within 24 hours all passed successfully.
Infants: objects smaller than 2 cm wide and 3 cm long will likely pass the pylorus and ileocecal valve10
Children and adults: objects smaller than 2 cm wide and 5 cm long will likely pass the pylorus and ileocecal valve9
Sharp objects have a high rate of perforation (35%)1
A small foreign body in the lateral 1/3 of the auditory canal may be amenable to a simple curettage. Hair beads (if the central hole is accessible) may be manipulated out with the angled tip of a rigid curette. Steady the operating hand by placing your hypothenar eminence on the child’s zygoma or temporal scalp, to avoid jutting the instrument into the ear canal with sudden movement. There is a large selection of disposable simple and lighted curettes on the market.
Various eponymous hooks are available for this purpose; one in popular use is the Day hook, which may be passed behind the foreign body.22 An inexpensive and convenient alternative to the commercially available right-hooks is a home-made version: make your own by straightening out a paperclip and bending it to a right angle23 at 2-3 mm from the end (be sure not to use the type that have a friable shiny metallic finish, as the residue may be left behind in the ear canal). If it is completely lodged, use of a right-angle hook will likely only cause trauma to the canal.
Alligator forceps are best for grasping soft objects like cotton or paper. Smooth, round or oval objects are not amenable to extraction with alligator forceps. When using them, be sure to get a firm, central grip on the object, to avoid tearing it into smaller, less manageable pieces.
Pro tip: Look before you grip! Be careful to visualize the area you are gripping, to avoid pulling on (and subsequently avulsing) soft tissue in the ear canal.
Apply cyanoacrylate to either side of a long wooden cotton swab (the lecturer prefers the cotton tip side, for improved grip/molding around object). Immediately apply the treated side to the object in the ear canal in a restrained patient. Steady the hypothenar eminence on the child’s face to avoid dislodgement of the cotton swab with sudden movement. Apply the treated swab to the foreign body for 30-60 seconds, to allow bonding. Slowly pull out the foreign body. Re-visualize the ear canal for other retained foreign bodies and abrasion or ear canal trauma.
Did the cyanoacrylate drip? Did the swab stick to the ear canal?
No problem – use 3% hydrogen peroxide or acetone.24 Pour in a sufficient amount, allow to work for 10 minutes. Both agents help to dissolve ear wax, the compound, or both. Repeat if needed to debond the cyanoacrylate from the ear canal.24,25
Irrigation is the default for non-organic foreign bodies that are not amenable to other extraction techniques. Sometimes the object is encased in cerumen, and the only “instrument” that will fit behind the foreign body is the slowly growing trickle of water that builds enough pressure to expulse it. Do not use if there is any organic material involved: the object will swell, causing much more pain, difficulty in extraction, and possibly setting up conditions for infection.
Position the child either prone or supine, gently restrain (as above). Let gravity work for you: don’t irrigate in decubitus position with the affected ear up. It may be more accessible to you, but you may never get the foreign body out.
To use a butterfly needle: use a small gage (22 or 24 g) butterfly set up, cut off the needle, connect the tubing to a 30 mL syringe filled with warm or room-temperature water. Insert the free end of the tubing gently, and “secure” the tubing with your pinched fingers while irrigating (think of holding an ETT in place just after intubation and before taping/securing the tube). Gently and slowly increase the pressure you exert as you irrigate.
To use an IV or angiocatheter: use a moderate size (18 or 20 g) IV, remove the needle and attach the plastic catheter to a 20 mL syringe, and irrigate as above.
Acetone has been used successfully to remove chewing gum, Styrofoam, and superglue from the ear canal24,26,27 Use in cases where there is no suspicion of perforation of the tympanic membrane.
Cerumen is composed of sebaceous ad ceruminous secretions and desquamated skin. Genetic, environmental, and anatomical factors combine to trap a foreign body in the external canal. Use of a ceruminolytic such as docusate sodium may help to loosen and liberate the foreign body.28 Caveat medicus: Adding docusate sodium will make the object more slippery – this may or may not be an issue given the nature of the foreign body.
In the case where loosening the ear wax may aid extraction (and will not cause a slippery mess), consider filling the ear canal will docusate sodium (Colace), having the child lie with the affected side up, waiting 15 minutes, and proceeding. This is especially helpful when planning for irrigation.
Rare earth magnets (a misnomer, as their components are actually abundant) such as neodymium can be useful in retrieving metallic foreign bodies (e.g. button batteries in the nose or ears).29,30 Magnetic “pick-up tools” – used by mechanics, engineers, and do-it-yourselfers – are inexpensive and readily available in various sizes, shapes, and styles such as a telescoping extender. Look for a small tip diameter (to fit in the ear canal as well as the nose) and a strong “hold” (at least a 3-lb hold).
Alternatively, you may purchase a strong neodymium bar magnet (30- to 50-lb hold) to attach to an instrument such as an alligator forceps, pick-up forceps, or small hemostat (a pacemaker magnet may also work). The magnetic bar, placed in your palm at the base of the instrument, will conduct the charge (depending on the instrument) and allow you to retrieve many metallic objects.31 Although stainless steel is often said to be “non-magnetic”, it depends on the alloy used, and some may actually respond to the strong rare earth magnet. Most stainless steel has a minimum of 10.5% chromium, which gives the steel its 'stainless' properties (essentially corrosion resistance). A basic stainless steel has a “ferritic” structure and is magnetic. Higher-end stainless steel such as in kitchen cutlery have an “austenitic” structure, with more chromium added, and so less magnetic quality. (Ironically, the more “economical” instruments in the typical ED suture kit have less chromium, and so are more magnetic – use these with your neodymium bar magnet to conduct the magnetic charge and extract the metallic foreign body.)
Bottom line: if it’s metal, it’s worth a try to use a magnet. Even if the metal is very weakly magnetic, the strong neodymium magnet may still be able to exert a pull on it and aid in extraction.
A relatively new method, described by Fundakowski et al.32 consists of using a small length of 24-gauge (or similar) wire (available inexpensively online, and kept in your personal “toolkit”; see Appendix B below) to make a loop that is secured by a hemostat (the 24-gauge wire is easily cut into strips with standard trauma scissors). After treatment with oxymetolazone (0.05%) and lidocaine (1 or 2%) topically, the loop is passed behind the foreign body (in the case report, a button battery). Pull the loop toward you until you feel that it is sitting up against the button battery. Now, turn the hemostat 90° to improve your purchase on the foreign body. Pull gently out. This technique is especially useful when the foreign body has created marked edema, either creating a vacuum effect or making it difficult for other instruments to pass.
Small-caliber devices (5, 6, or 8 F) originally designed for use with intravascular or bladder catheterization may be used to extract foreign bodies from the ear or nose.7,33 A catheter designed specifically for foreign body use is the Katz extractor. Inspect the ear or nose for potential trauma and to anticipate bleeding after manipulation (especially the nose). Deflate the catheter and apply surgical lubricant or 2% lidocaine jelly. Insert the deflated catheter and gently pass the device past the foreign body. Inflate the balloon and slowly pull the balloon and foreign body out. Re-inspect after extraction.
NB, from the manufacturer of the Katz extractor, InHealth: “the Katz Extractor oto-rhino foreign body remover is intended principally for extraction of impacted foreign bodies in the nasal passages. This device may also be used in the external ear canal, based upon clinical judgment.”
The mother’s kiss was first described in 1965 by Vladimir Ctibor, a general practitioner from New Jersey.34 “The mother, or other trusted adult, places her mouth over the child’s open mouth, forming a firm seal as if about to perform mouth-to-mouth resuscitation. While occluding the unaffected nostril with a finger, the adult then blows until feeling resistance caused by closure of the child’s glottis, at which point the adult gives a sharp exhalation to deliver a short puff of air into the child’s mouth. This puff of air passes through the nasopharynx, out through the non-occluded nostril and, if successful, results in the expulsion of the foreign body. The procedure is fully explained to the adult before starting, and the child is told that the parent will give him or her a “big kiss” so that minimal distress is caused to the child. The procedure can be repeated a number of times if not initially successful.”34
This technique is an approximation of the above mother’s kiss technique – useful for unwilling parents or unsuccessful tries.10,25 The author prefers to position the child sitting up. A self-inflating bag-mask device is fitted with a very small mask: use an abnormally small mask (otherwise inappropriately small for usual resuscitative bag-mask ventilation) to fit over the mouth only. Choose an infant mask that will cover the child’s mouth only. Occlude the opposite nostril with your finger while you form a tight seal with the mask around the mouth. Deliver short, abrupt bursts of ventilation through the mouth – be sure to maintain good seals with the mask and with your finger to the child’s nostril – until the foreign body is expulsed through the affected nostril.
For the very uncooperative child with a nasal foreign body amenable to positive pressure ventilation who fails the mother’s kiss and bag-mask technique, a continuous positive pressure method may be used. Connect one end of suction tubing to the male adaptor (“Christmas tree”) of an air or oxygen source. Connect the other end of the suction tubing to a male-to-male adaptor (commonly used for chest tube connections or connecting / extending suction tubes). Insert the end of the device into the child’s unaffected nostril. The air flow will deliver positive pressure ventilation continuously.
To minimize this risk, some authors recommend limiting to a maximum of four attempts using any positive pressure method.10
Optimize your visualization with a nasal speculum. The nostrils, luckily, will accommodate a fair amount of distention without damage.
Hold the speculum vertically to avoid pressure on and damage to the vessel-and-nerve-rich nasal septum. Hold the handle of the speculum in the palm of your hand comfortably and while placing your index finger on the patient’s ala. This will help to control the speculum and your angle of sight. Your other hand is then free to use a hook or other tool for extraction.
Lighting is especially important when using the nasal speculum: a focused procedure light or head lamp is very helpful. The author keeps a common camping LED headlamp in his bag for easy access.
Various commercial and non-commercial suction devices are on the market for removal of foreign bodies. All connect to wall suction, and vary by style, caliber of suction, and tip end interface. A commonly available suction catheter is the Frazier suction tip (right), a single-use device used in the operating room.
A modification to suction can be made with the Schuknecht foreign body remover (left; not to be confused with the suction catheter of the same name): a plastic cone-shaped tip placed on the end of the suction catheter to increase vacuum surface area and seal.
If a child aspirates and occludes his airway, return to BLS maneuvers (as above). If the child becomes obtunded, use direct laryngoscopy to visualize the foreign body and remove with the Magill forceps. Hold the laryngoscope in your left hand as per usual. Hold the Magill forceps in your right hand – palm side down – to grasp and remove the foreign body.
Beware the “vacuum palate”: a flat (especially clear plastic) foreign body hiding on the palate
Take seriously the complaint of foreign body without obvious evidence on initial inspection – believe that something is in there until proven otherwise
Control the environment, address analgesia and anxiolysis, have a back-up plan
MERCI – DANKE – Дякую – THANK YOU – GRACIAS – ありがとう— GRAZIE
Appendix A: Prevention
At the end of the visit, after some rapport has been established, counsel the caregivers about age-appropriate foods and “child-proofing” the home. This is a teachable moment – and only you can have this golden opportunity!
0-6 months: breastmilk or formula
6-9 months: introduce solid puree-consistency foods
9-12 months: small minced solids that require no chewing (well cooked, soft, chopped foods)
Although molars (required for chewing) erupt around 18 months, toddlers need to develop coordination, awareness to eat hard foods that require considerable chewing.
Not until 4 years of age (anything that requires chewing to swallow):
Nuts and seeds
Chunks of meat or cheese
Hard or sticky candy
Chunks of peanut butter
Chunks of raw vegetables
Child-proofing the home
Refer parents to the helpful multi-lingual site from the American Academy of Pediatrics:
An abbreviated list: use age-appropriate toys and “test” them out before giving them to your child to verify that there are no small, missing, or loose parts. Secure medications, lock up cabinets (especially with chemicals), do not store chemicals in food containers, secure the toilet bowl, and unplug appliances.
Parents should understand that “watching” their child alone cannot prevent foreign body aspiration: a recent review found that in 84.2% of cases, incidents resulting in an airway foreign body occurred in the presence of an adult.35
Best overall tip: get down on all fours and inspect your living area from the child’s perspective. It is amazing what you will find when you are least expecting it.
Appendix B: The Playbook's ENT Foreign Body Toolkit
Although your institution should supply you with what you need to deal with routine problems, we all struggle with having just what we need when we need it. High-volume disposable items such as cyanoacrylate (Dermabond), curettes, supplies for irrigation, alligator forceps, and the like certainly should be supplied by the institution. However, some things come in very handy as our back-up tools.
NB: we should be cognizant of the fact that tools that must be sterilized or autoclaved are not good candidates for our personal re-usable toolkits.
These items can all be found inexpensively – shop around online, or in home improvement stores:
This post and podcast are dedicated to Linda Dykes, MBBS(Hons) for her can-do attitude and collaborative spirit. Thank you for sharing your knowledge, experience, and heart with the world.
– John Mason
Place a towel roll under the scapulae to align oral, pharyngeal, and tracheal axes:
Use airway adjuncts such as the oropharyngeal airway or a nasal trumpet.
Use the two-hand ventilation technique whenever possible:
(See Adventures in RSI for more)
(details in audio)
Pros: Best studied; sizes for all ages
Cons: Cannot intubate through aperture
Pros: Better ergonomics with updated design; bite bloc; port for decompression
Cons: Cannot pass appropriate-sized ETT through tube
Pros: Little training needed; high success rate; single inflation port
Cons: Flexion of tube can impede ventilation or cause leaks; only sized down to 12 kg (not for infants and most toddlers)
Pros: Easy to place; can intubate through aperture
Cons: Not for neonates less than 4 kg
Pros: Molds more accurately to supraglottis; no need to inflate; good seal pressures
Cons: Cannot intubate through (without fiberoscopy)
• If you can bag the patient, you're winning.
• If you have difficulty bagging, or anticipate or encounter a difficult airway, then don't forget your friend the supraglottic airway (SGA).
• Ego is the enemy of safety: SGAs are simple, fast, and reliable.
• Just do it.
Black AE, Flynn PE, Smith HL, Thomas ML, Wilkinson KA; Association of Pediatric Anaesthetists of Great Britain and Ireland. Development of a guideline for the management of the unanticipated difficult airway in pediatric practice. Paediatr Anaesth. 2015 Apr;25(4):346-62.
Schmölzer GM, Agarwal M, Kamlin CO, Davis PG. Supraglottic airway devices during neonatal resuscitation: an historical perspective, systematic review and meta-analysis of available clinical trials. Resuscitation. 2013 Jun;84(6):722-30.
Supraglottic Airway on WikEM
This post and podcast are dedicated to Tim Leeuwenburg, MBBS FRACGP FACRRM DRANZCOG DipANAES and Rich Levitan, MD, FACEP for keeping our minds and our patients' airways -- open. You make us better doctors. Thank you.
Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP
Pediatric; Emergency Medicine; Pediatric Emergency Medicine; Podcast; Pediatric Podcast; Emergency Medicine Podcast; Horeczko; Harbor-UCLA; Presentation Skills; #FOAMed #FOAMped #MedEd
Symptoms – either typical dysuria, urgency, frequency in a verbal child, or non-descript abdominal pain or vomiting in a well appearing child.
Fever – but first look for an obvious alternative source, especially viral signs or symptoms.
No obvious source?
Risk stratify before “just getting a urine”.
In a low risk child, with obviously very vigilant parents, who is well appearing, you may choose not to test now, and ensure close follow up.
The short answer is: always cath, never bag.
(Pros and cons in audio)
According to the current clinical practice guideline by the AAP, the standard definition of a urinary tract infection is the presence of BOTH pyuria AND at least 50 000 colonies per mL of a single uropathogen.
Making the diagnosis in the ED:
The presence of WBCs with a threshold of 5 or greater WBCs per HPF is required.
What else goes into the urinalysis that may be helpful?
Pearl: nitrites are poorly sensitive in children. It takes 4 hours for nitrites to form, and most children this age do no hold their urine.
Pearl: the enhanced urinalysis is the addition of a gram stain. A positive gram stain has a LR+ of 87 in infants less than 60 days, according to a study by Dayan et al. in Pediatric Emergency Care.
In an adult, we look for UTI plus evidence of focal upper tract involvement, like CVA tenderness to percussion or systemic signs like nausea, vomiting, or fever. It is usually straightforward.
It’s for this reason that the literature uses the term “febrile UTI” for children. Fever is very sensitive, but not specific in children.
The ill-appearing child has pyelonephritis. The well-appearing child likely has a “febrile UTI”, without upper involvement. However, undetected upper tract involvement may be made in retrospect via imaging, if done.
For simple lower tract disease, treat for at least 7 days. There is no evidence to support 7 versus 10 versus 14 days. My advice: use 7-10 days as your range for simple febrile UTI in children.
Pyelonephritis should be treated for a longer duration. Treat pyelonephritis for 10-14 days.
Sulfamethoxazole and trimethoprim (Bactrim) is falling out of favor, mostly because isolates in many communities are resistant. There is an association of Stevens-Johnson Syndrome (SJS) with Bactrim use. This may be confounded by its prior popularity; any antibiotic can cause SJS, but there are more case reports with Bactrim.
Cephalexin (Keflex): 25 mg/kg dose, either BID or TID. It is easy on the stomach, rarely interacts with other meds, has high efficacy against E. coli, and most importantly, cephalexin has good parenchymal penetration.
Nitrofurantoin is often used in pregnant women, because the drug tends to concentrate locally in the urine. However, blood and tissue concentrations are weak. It may be ineffective if there is some sub-clinical upper tract involvement.
Cefdinir is a 3rd generation cephalosporin available by mouth, given at 14 mg/kg in either one dose daily or divided BID, up to max of 600 mg. This may be an option for an older child who has pyelonephritis, but is well enough to go home.
The first thing to consider is age. Any infant younger than 2 months should be admitted for a febrile UTI. Their immune systems and physiologic reserve are just not sufficient to localize and fight off infections reliably.
The truth is, for serious bacterial illness like pneumonia, UTI, or severe soft tissue infections, be careful with any infant less than 4-6 months of age.
Of course, the unwell child – whatever his age – he should be admitted. Think about poor feeding, irritability, dehydration – in that case, just go with your gut and call it pyelonephritis, and admit.
In adults, we think of urine culture only for high-risk populations, such as pregnant women, the immunocompromised, those with renal abnormalities, the neurologically impaired, or the critically ill, to name a few.
In children, it’s a little simpler. Do it for everyone.
Who is everyone? Think of the urine rule of 10s:
10% of young febrile children will have a UTI
10% of UAs will show no evidence of pyuria
Routine urine culture in all children with suspected or confirmed UTI up to about age 10
From a quality improvement and safety perspective, consider making this a regular assignment to a qualified clinician.
Check once in 24-48 hours to find possible growth of a single uropathogen with at least 50 000 CFU/mL. Look at the record to see that the child is one some antibiotic, or the reason why he may not. Call the family if needed.
A second check at 48-72 hours may be needed to verify speciation and sensitivities.
The culture check, although tedious, is important to catch those small children who did not present with pyuria and who may need antibiotics, or to verify that the right agent is given.
The younger the child, the more we worry about missing a decompensation. Encourage the parents to call the child's primary care clinician for a re-check in a few days, and to discuss whether or not further work-up such as imaging is indicated. As always, strict return to ED precautions are helpful.
A more accurate question is: what is an important anomaly to detect?
Vesiculo-ureteral reflux – a loose ureteropelvic junction causes upstream reflux when the bladder constricts.
Uretero-pelvic junction obstruction – in older children or young adults with hematuria, UTI, abdominal mass, or pain. Infants born with UPJ obstruction have congenital hydronephrosis.
Ureterocoele – a cystic mass in the bladder. It is not malignant, but can cause ureteral dilation, and hydronephrosis. Treatment is surgical.
Ectopic ureter – either a duplication of the draining system, or an abnormal connection, such as the epidydimis or cervix.
Posterior urethral valves – occur only in boys, and they are a bit of a misnomer. The most common type of congenital bladder outlet obstruction, posterior urethral valves are just extra folds of membrane in the lumen of the prostatic urethra. Usually ablation by cystoscopy does the trick.
Urachal remnant – a leftover from fetal development, and an abnormal connection between the bladder and the umbilicus. Look for an “always wet” belly button in an infant, or an umbilical mass with pain and fever in an older child.
Renal and bladder ultrasound (RBUS) after the first UTI is recommended (although incompletely followed in practice).
If the RBUS is positive, or with the second UTI, DMSA scan to evaluate possible renal scarring.
Like anything, it’s a balance. A few tips to avoid iatrogenia by way of a summary.
If a child over 3 months of age is well, has no comorbidities, has a low grade fever "in the 38s" (38-38.9 °C) without a source, especially if less than 24 hours, you are very safe to do watchful waiting at home.
More to the point, an otherwise well child with an obvious upper respiratory tract infection has a source of his fever.
If your little patient has risk factors for UTI, or you are otherwise concerned, send the UA and send the culture. You can opt out of the culture by middle school in the otherwise healthy child.
And finally, deputize parents to carry the ball from here – the child needs ongoing primary care and his pediatrician may elect to do some screening. Don’t promise or prime them for it – rather, encourage the conversation.
Suprapubic aspiration (details in podcast audio; video below)
Infant Clean Catch Technique
Step One: feed the baby, wait twenty minutes.
Step Two: clean the genitals with soap and warm water and dry with gauze. Have your sterile urine container open and at the ready.
Step Three: one person holds the baby under his armpits with his legs dangling. The other person gently taps the bladder (100 taps/min), then massages the lower back for 30 seconds.
Step Four: Clean Catch! (can also repeat process)
Bonsu BK, Shuler L, Sawicki L, Dorst P, Cohen DM. Susceptibility of recent bacterial isolates to cefdinir and selected antibiotics among children with urinary tract infections. Acad Emerg Med. 2006 Jan;13(1):76-81.
Coulthard MG, Lambert HJ, Vernon SJ, Hunter EW, Keir MJ, Matthews JN. Does prompt treatment of urinary tract infection in preschool children prevent renal scarring: mixed retrospective and prospective audits. Arch Dis Child. 2014 Apr;99(4):342-7.
Finnell SM, Carroll AE, Downs SM; Subcommittee on Urinary Tract Infection. Technical report—Diagnosis and management of an initial UTI in febrile infants and young children. Pediatrics. 2011 Sep;128(3):e749-70.
Michael M, Hodson EM, Craig JC, Martin S, Moyer VA. Short versus standard duration oral antibiotic therapy for acute urinary tract infection in children. Cochrane Database Syst Rev. 2003;(1):CD003966.
Shaikh N et al. Identification of children and adolescents at risk for renal scarring after a first urinary tract infection: a meta-analysis with individual patient data. JAMA Pediatr. 2014 Oct;168(10):893-900.
Shah AP, Cobb BT, Lower DR, Shaikh N, Rasmussen J, Hoberman A, Wald ER, Rosendorff A, Hickey RW. Enhanced versus automated urinalysis for screening of urinary tract infections in children in the emergency department. Pediatr Infect Dis J. 2014 Mar;33(3):272-5.
Subcommittee on Urinary Tract Infection, Steering Committee on Quality Improvement and Management, Roberts KB. Urinary tract infection: clinical practice guideline for the diagnosis and management of the initial UTI in febrile infants and children 2 to 24 months. Pediatrics. 2011 Sep;128(3):595-610.
This post and podcast are dedicated to Brad Sobolewski, MD, MEd for his innovation and tenacity in all things #FOAMed, #FOAMped, and #MedEd. Thanks, Brad, for your enthusiasm, energy, and for your fantastic PEM Currents and PEM Blog.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
N.B.: This month's show notes are a departure from the usual summary. Below is a reprint (with permission) of a soon-to-be released chapter, Horeczko T. "Acute Pain in Children". In Management of Pain and Procedural Sedation in Acute Care. Strayer R, Motov S, Nelson L (eds). 2017. Rather than the customary blog post summary, the full chapter (with links) is provided as a virtual reference.
Pain is multifactorial: it is comprised of physical, psychological, emotional, cultural, and contextual features. In children often the predominant feature may not be initially apparent. Although clinicians may focus on the physical component of pain, much time, energy, and suffering can be saved through a holistic approach. What is the age and developmental stage of the child? How is the child reacting to his condition? What are the circumstances? What is the family or caregiver dynamic?
We rely much on how patients and families interact with us to gauge pain. Assessing and managing children’s pain can be challenging, because they may not exhibit typically recognized signs and symptoms (Srouji 2010). Further, children participate in and absorb their family’s culture and specific personality from a very young age (Finley 2009). Knowing the context of the episode may help. For example, a very anxious caregiver can easily transmit his or her anxiety to the child, which may either inhibit or amplify presentation of symptoms (Bearden 2012).
The guiding principles in pediatric pain assessment and management are: know the child; know the family; and know the physiology. Children have long suffered from an under-treatment of their pain, due both to our incomplete acknowledgement of their pain and our fear of treatment (Howard 2003). As the pendulum on pain management swings one way or the other, do not let your pediatric patient get knocked by the wayside. Take a thoughtful approach: know the signs and symptoms, and aggressively treat and reassess.
Each stage of development offers a unique framework to the child’s signs and symptoms of pain. In pre-verbal children, use your observational skills in addition to the parent’s report of behavior. Verbal children can self-report; younger children require pictorial descriptions, while older children and adolescents may use standard adult scales. In all ages, ask open-ended questions and allow the child to report and speak for himself whenever possible.
Neonates are a unique group in pain assessment. The neonate (birth to one month of age) has not yet acquired social expression of pain, and his nascent nervous system is only now learning to process it. Do not expect typical pain behaviors in neonates. Facial grimacing is a weak indicator of pain in neonates (Liebelt 2000). When this behavior is present, look for a furrowed brow, eyes squeezed shut, and a vertically open mouth. Tachycardia, tachypnea, and a change in behavior can be indicators not only to the presence of pain, but possibly to its etiology as well.
Neonatal observational scales have been validated in the intensive care and post-operative settings; ED-specific quantitative scales are lacking. CRIES is a 10-point scale, using a physiologic basis similar to APGAR: Crying; Requires increased oxygen administration (distress and breath-holding); Increased vital signs; Expression; and Sleeplessness (Krechel 1995). CRIES (Table 1) was validated for post-operative patients; to adapt its use for the ED, the most conservative approach is to substitute “preoperative baseline” with normal range for age. Although the numerical values of CRIES have not been validated to date in the ED, the clinician may find the domains included in CRIES to be a useful cognitive construct in assessing neonatal pain.
Neonatal pain pathways are particularly plastic; prompt assessment of and increased alertness to neonatal pain may help to mitigate long-lived pain sensitivity and hyperalgesia (Taddio 2002). In other words, treat the neonate’s pain seriously, as you may save him long-term pain sequelae in the future.
This group will begin to exhibit more reproducible, reliable signs and symptoms of pain.
For infants of less than one year of age, the Neonatal Infant Pain Scale (NIPS) uses observational and physiologic parameters to detect pain (Table 2). A score of 0-2 indicates no pain present. A score of 3-4 indicates mild to moderate pain; non-pharmacologic techniques may be tried first. A score of 5 or greater indicates severe pain; some pharmacologic intervention is indicated (Lawrence 1993).
For children greater than one year who are preverbal, a well performing scale is the FLACC score: Face, Legs, Activity, Cry, Consolability (Table 3).
Contextual and caregiver features predominate in this group. Frequent reassessments are helpful, as the initial trepidation and fright in triage may not accurately reflect the child’s overall pain status.
Increasing language development offers the hope of more information to the clinician, but be careful not to ask leading questions. Do not jump directly to “does this hurt?”. Preschoolers will say ‘yes’ to anything, in an attempt to please you. School-age children may passively affirm your “statement”, if only to validate their human need for care or attention. Start with some ice-breaking banter, lay down the foundations for rapport, and then ask open-ended questions. Be careful not to allow the caregiver to “instruct” the child to tell you where it hurts, how much, how often, etc. Rather, engage the parents by asking them what behavior they have noticed. Eliciting history from both the child and the parent will go a long way in constructing a richer picture of the etiology and severity of the pain, and will help to build rapport and trust.
Adolescents vary in their development, maturity, and coping mechanisms. You may see a mixture of childhood and adult behaviors in the same patient; e.g. he may be initially stoic or evades questioning, then later exhibits pseudo-inconsolability. Do what you can to see the visit from the adolescent’s perspective, and actively transmit your concern and intention to help – many will respond to a warm, open, non-judgemental, and helpful attitude. The overly “tough” adolescent is likely secretly fearful, and the “dramatic” adolescent may simply be very anxious. Take a moment to gauge the background behind the presentation.
You may use the typical adult scale of 0 (no pain) to 10 (worst pain), or the Faces Pain Scale–Revised (FPS-R). The FPS-R uses more neutral and realistic faces and, unlike the Wong Baker scale, does not use smiling or crying faces to anchor the extremes of pain (Tsze 2013).
Pain includes two major components: generation and perception. Generation of pain involves the actual propagation of painful stimuli, either through nociceptive pain or neuropathic pain. Nociceptive pain arises from free nerve endings responding to tissue damage or inflammation.
Nociceptive pain follows a specific sequence: transduction (an action potential triggered by chemical mediators in the tissue, such as prostaglandins, histamine, bradykinin, and substance P); transmission (the movement of the action potential signal along the nerve fibers to the spinal cord); perception (the impulse travels up the spinothalamic tract to the thalamus and midbrain, where input is splayed out to the limbic system, somatosensory cortex, and parietal and frontal lobes); and modulation (the midbrain enlists endorphins, enkephalins, dynorphin, and serotonin to mitigate pain) (Pasero 2011). As clinicians we can target specific “stations” along the pain route to target the signal more effectively.
Simple actions such as ice, elevation, local anesthetics, or splinting help in pain transduction. Various standard oral, intranasal, or IV analgesics may help with pain’s transmission. Non-pharmacologic techniques such as distraction, re-framing, and others can help with pain perception. The sum of these efforts encourage pain modulation.
A phenomenon separate from nociceptive pain is neuropathic pain, the abnormal processing of pain stimuli. It is a dysregulated, chaotic process that is difficult to manage in any setting. Separating nociceptive from neuropathic symptoms may help to select specific pain treatments and to clarify treatment goals and expectations.
Neonates are exquisitely sensitive to many analgesics. Hepatic enzymes are immature and exhibit decreased clearance and prolonged circulating levels of the drug administered. Once the pain is controlled, less frequent administration of medications, with frequent reassessments, are indicated.
The neonate’s vital organs (brain, heart, viscera) make up a larger proportion of his body mass than do muscle and fat. That is to say, the volume of distribution is unique in a neonate. Water-soluble drugs (e.g. morphine) reach these highly perfused vital organs quickly; relatively small overdosing will have rapid and exaggerated central nervous system and cardiac effects. The neonate’s small fat stores and muscle mass limit the volume of distribution of lipophilic medications (e.g. fentanyl, meperidine), also making them more available to the central nervous system, and therefore more potent. Other factors that predispose neonates to accidental analgesic overdose are their decreased concentrations of albumin and other plasma proteins, causing a higher proportion of unbound drug. Renal clearance is also decreased in the first few months of life.
Clinical note: in the ED, neonates often require analgesia for procedures more than for injury. Non-pharmacologic techniques predominate (see below). Make liberal use of local anesthetics such as eutectic mixture of local anesthetics (EMLA; for intact skin, e.g. IV access, lumbar puncture) and lidocaine-epinephrine-tetracaine gel (LET; for superficial open skin and soft tissue application). Oral sucrose (30%) solutions (administered either with a small-volume syringe or pacifier frequently dipped in solution) are effective for minor procedures (Harrison 2010, Stevens 2013) via the release of dopamine and through distraction by mechanical means. Neonates with severe pain may be managed with parenteral analgesics, on a monitor, and with caution.
With increasing body mass comprised of fat stores in conjunction with an increase in metabolism, this group will require a different approach than the neonate. For many medications, these children will have a greater weight-normalized clearance than adults (Berde 2002). They will often require more frequent dosing. Infants and toddlers have a larger functioning liver mass per kilogram of body weight, with implications for medications cleared by cytochrome p-450.
Clinical note: some drugs, such as benzodiazepines, will have both a per-kilogram dosing as well as an age-specific modification. When giving analgesics or anxiolytics to young children, always consult a reference for proper dosing and frequency.
This group retains some hyper-metabolic features of younger children, but the dose-effect relationship is more linear and transparent. Physiologic clearance is improved, and from a physical standpoint, these are typically lower-risk children. From a psychological standpoint, this group may need more non-pharmacologic consideration and support to modulate pain optimally.
The first line of treatment in all pain management is non-pharmacopeia (Horeczko 2016). Not only is this the safest of all techniques, but often the most effective. Some are simple comfort measures such as splinting (fracture or sprain), applying cold (acute soft tissue injury) or heat (non-traumatic, non-specific pain), or other targeted non-pharmacology.
Many a pain control regimen is sabotaged without consideration of non-pharmacologic techniques, which may augment, or at times replace, analgesics. Think of non-pharmacopoeia as your “base coat” or “primer” before applying additional coats of analgesic treatment. With the right base coat foundation, you have a better chance of painting a patient’s symptoms a more tolerable and long-lasting new color.
A tailored approach based on age will allow the practitioner to employ a child’s developmental strengths and avoid the frustration that results in asking the child to do what he is not capable of doing. A brief review of Piaget’s stages of development will help to meet the child at his developmental stage for best effect (Piaget 1928, Sheppard 1977) during acute painful presentations and minor procedures.
Sensorimotor stage (from birth to age 2): Children use the five senses and movement to explore the world. They are egocentric: they cannot see the world from another’s viewpoint. At 6 to 9 months, object permanence is established: understanding that objects (or people) exist even without seeing them.
Preoperational stage (from ages 2 to 7): Children learn to use language. Magical thinking predominates. They do not understand rational or logical thinking.
Concrete operational stage (from age 7 to early adolescence): Children can use logic, but in a very straightforward, concrete manner (they do well with simple examples). By this stage, they move from egocentrism to understanding another point of view. N.B. Some children (and adults) never completely clear this stage.
Formal operational stage (early adolescence to adult): children are capable of abstract thinking, rationalizing, and logical thinking.
It is important to assess the child’s general level of development when preparing and guiding him through the minor procedure or distracting him until his pain is controlled. It is not uncommon for acutely ill or injured to regress temporarily in their behavior (not their development) as a coping mechanism.
Neonate and Infant (0-12 months)
Involve the parent, and have the parent visible to the child at all times if possible. Make advances slowly, in a non-threatening manner; limit the number of staff in the room. Use soothing sensory measures: speak softly, offer a pacifier, and stroke the skin softly. Swaddle the infant and encourage the parent to comfort him during and after the procedure. Engage their developing sensorimotor skills to distract them.
Toddler to Preschooler (1-5 years)
Use the same techniques as for the infant, and add descriptions of what he will see, hear, and feel; you can use a doll or toy to demonstrate the procedure. Use simple, direct language, and give calm, firm directions, one at a time. Explain what you are doing just before doing it (do not allow too much time for fear or anxiety to take root). Offer choices when appropriate; ignore temper tantrums. Distraction techniques include storytelling, bright and flashy toys, blowing bubbles, pinwheels, or having another staff member play peek-a-boo across the room. The ubiquitous smart phone with videos or games can be mesmerizing at this age.
School age (6-12 years)
Explain procedures using simple language and (briefly) the reason (understanding of bodily functions is vague in this age group). Allow the child to ask questions, and involve him when possible or appropriate. Distraction techniques may include electronic games, videos, guided imagery, and participation in the minor procedure as appropriate.
Adolescent (13 and up)
Use the same techniques for the school age child, but can add detail. Encourage questioning. Impose as few restrictions as possible – be flexible. Expect more regression to childish coping mechanisms in this age group. Distraction techniques include electronic games, video, guided imagery, muscle relaxation-meditation, and music (especially the adolescent’s own music, if available).
No amount of knowledge of the above physiology, pharmacology, or developmental theory will help your little patient in pain without a well constructed and enacted plan. Aggressively search out and treat your pediatric patient’s presence and source of pain. Frequent reassessments are important to ensure that breakthrough pain treatment is achieved, when re-administration is indicated, or when a change of plan is necessary. This is the time to involve the parents or caregivers to let them know what the next steps are, and what to expect.
Start with the least invasive modality and progress as needed. After non-pharmacologic treatments such as splinting, ice, elevation, distraction, and guided imagery, have an escalation of care in mind (Figure 2).
From a pharmacologic perspective, various options are available. Your pain management plan will differ depending on whether a painful procedure is performed in the ED (Table 4). Once pain is addressed, create a plan to keep it managed. Consider the trajectory of illness and the expected time frame of the painful episode. Include practicalities such as how well the pain may be controlled as an outpatient. Poorly controlled pediatric pain is more often managed as an inpatient than the same condition in an adult. Speak frankly with the parents about what drug is indicated for what type of pain and that treatment goals typically do not include absence of all pain, but function in face of the pain, in anticipation for clinical improvement.
A special note on codeine: Tylenol with codeine (“T3”) has never been a very effective pain medication, as up to 10% of patients lack enzymatic activity to metabolize it into morphine, its active form (Crews 2014). New evidence is emerging on the erratic and unpredictable individual metabolism of codeine. Some children are ultra-rapid-metabolizers of codeine to morphine, causing a rapid “bolus” of the available drug, with respiratory depression and death in some cases (Ciszkowski 2009, Racoosin 2013). Author’s advice: take codeine off your formulary.
Most common non-traumatic head and neck complaints can be managed non-pharmacologically (e.g. headache: improved hydration, sleep, stress, nutrition) or with PO medications, such as NSAIDs. The anti-inflammatory nature of ibuprofen (10 mg/kg PO q 4-6 h prn, up to adult dose) for example, will treat the cause as well as the symptoms of ear pain, sore throat, and muscular pain. Ibuprofen may be more effective than acetaminophen (paracetamol) for odontogenic pain (Bailey 2013). For most applications, acetaminophen may be as effective; however, the combination of both NSAIDs is not likely to be more effective than either agent individually (Merry 2013).
True migraine headache may be treated with all of the above, and rescue therapy may include prochlorperamide (0.15 mg/kg IV, up to 10 mg ) (Brousseau 2004), often given with diphenhydramine (1 mg/kg PO or IV, up to 50 mg) and IV fluids. Ketoralac (0.5 mg/kg IV, up to 10 mg) may be substituted for ibuprofen (Paniyot 2016). Other specific therapies may be considered, although evidence for them varies.
After ruling out important pulmonary (e.g. the under-recognized spontaneous pneumothorax) and cardiac (e.g. pericarditis, myocarditis) etiologies, many chest complaints are amenable to NSAIDs. There is often a large component of anxiety in the child and/or parents in chest pain; no amount of medication will assuage them without addressing their concerns as well.
Abdominal pain in children is challenging, as it is common, often benign, but may be disastrous if the etiology is missed. For mild pain, consider acetaminophen as indicated (15 mg/kg/dose q 4-6 h prn, up to 650 mg). The oral route is preferred, but intravenous acetaminophen is an option for patients unable to tolerate PO, or for those in whom the per rectum (PR) route is contraindicated (e.g. neutropenia) (Babl 2011, Dokko 2014). For children with moderate to severe abdominal pain in whom a nil per os (NPO) status is ideal, consider rehydration/volume repletion, and small, frequent aliquots of a narcotic agent. Surgical pain is not “erased” by opioids (Thomas 2003, Poonai 2014); treating pain improves specificity to certain surgical emergencies with retained diagnostic accuracy (Manterola 2007). If there is inter-departmental concern about prolonged effects, sedation, limitation in the physical exam, or there is a need to “see if the pain will come back”, you may opt to use fentanyl initially for its shorter half-life. More frequent re-assessments may help the surgical team in its deliberations. Transition quickly to a longer-acting opioid as soon as possible.
Fracture pain should be addressed immediately with splinting and analgesia. Oral, intranasal, and intravenous routes are all acceptable, depending on the severity of the injury and symptoms.
Intranasal (IN) medications offer the advantage of a fast onset for moderate-to-severe pain (Graudins 2015), either as monotherapy or as a bridge to parenteral treatment (Table 4). The ideal volume of IN medication is 0.25 mL/naris, with a maximum of 1 mL/naris. Common concentrations of fentanyl limit its mg/kg use to the school-aged child; intranasal ketamine may be used for pain (i.e. sub-dissociative dose) up to adult weight.
Long-bone injuries are a good opportunity to employ a speedy modality that requires little technical skill in administration: nebulized fentanyl. Clinically significant improvement in pain scales are achieved with 3 mcg/kg/dose of fentanyl administered via standard nebulizer in children 3 years of age or older (Miner 2007, Furyk 2009). Nebulized fentanyl is a rapid, non-invasive alternative to the IN route for older children, adolescents, or adults, in whom the volume of IN medication would exceed the recommended per naris volume (Deaton 2015).
Consider an aggressive, multi-modal approach to control symptom up front. For example, for a simple forearm fracture, you may opt to give an oral opioid, perform a hematoma block, and offer inhaled nitrous oxide for reduction, rather than a formal intravenous procedural sedation (Luhmann 2006).
Skin and soft tissue injuries or abscesses often require solid non-pharmacopoeia in addition to local anesthetics. For IV cannulation, consider EMLA if the patient is stable and a minor delay is acceptable.
Topical ethyl chloride vapo-coolant offers transient pain relief due to rapid cooling and may be used just prior to an IV start (Farion 2008). Try this: engage your young child’s imagination to distract him and say, “have you ever held a snow ball? You are in luck – it’s just like that – here, do you feel it?”.
Vibratory adjuncts such as the “BUZZY” bee can be placed near the IV cannulation site to provide mechanical and cognitive distraction (Moadad 2016).
Needleless lidocaine injectors may facilitate IV placement without obscuring the target vein (Spanos 2008, Lunoe 2015). The medication is propelled into the dermis by a CO2 cartridge that makes a loud popping sound; try this to alleviate anxiety, just before using it: “your skin looks thirsty – it needs a drink – there you are!”.
As with any minor procedure, when you tell the child what you are doing, be sure to do it right away. Do not delay or build suspense.
Lidocaine-epinephrine-tetracaine gel (LET) is used for open or mucosal wounds. Apply as soon as possible in the visit. The goal of LET is to pretreat the wound to allow for a painless administration of injectable anesthetic. A common practice to apply LET two or three times at 15-minute intervals for deeper anesthesia, in an attempt to avoid injection altogether. Researchers are currently working to offer an evidence base to this anecdotal practice.
Pediatric burns should be assessed carefully and treated aggressively. Submersion of the affected extremity in room-temperature water (if possible) or applying room-temperature saline-soaked gauze will both thwart ongoing thermal damage, soothe the wound, and provide foundational first-aid. Minor burns can be treated topically and with oral medications. Major burns require IN, IM, or IV analgesics with morphine. Treatment may escalate to ketamine (Gandhi 2010), in analgesic or dissociative dosing, depending on the context. Post-traumatic disorders are common in burns; effective pain management is ever-more important in these cases.
Children with acute exacerbations of their chronic pain or episodic painful crises require special attention. Some examples of children with recurring pain are those suffering from sickle cell disease, juvenile idiopathic arthritis, complex regional pain syndrome, and cancer. Find out whether these symptoms and circumstances are typical for them, and what regimen has helped in the past. Previous unpleasant experiences may prime these children with amplified anxiety and perception of pain (Cornelissen 2014). Target the disease process and do your best to show the patient and his family you understand his condition and needs.
An equally challenging scenario is the child with chronic pain. Treat the entire patient with a multimodal approach. Limit opioids as possible. As an opioid-sparing strategy or as rescue therapy, consider sub-dissociative ketamine, especially for conditions such as sickle cell crisis, complex regional pain syndrome, autoimmune disorders, or chronic pain due to sub-acute trauma (Sheehy 2015). Intranasal ketamine may be used for sub-dissociative pain control at 0.5 – 1 mg/kg (Andolfatto 2013, Yeaman 2013). Intravenous infusions of ketamine at 0.1 – 0.3 mg/kg/h may be initiated in the ED and continued 4 – 8 h/d, up to a maximum of 16 h total in 3 consecutive days (Sheehy 2015). In vaso-occlusive episodes, dexmedetomidine has been shown to be an effective adjunct for severe pain poorly responsive to opioids and/or ketamine (Sheehy 2015b).
Children with cognitive impairment such as those with various genetic or metabolic syndromes, or primary neurologic conditions such as some with cerebral palsy are a challenge to assess and treat properly. These children not only cannot explain their symptoms, but they also have atypical expressions of pain. Pain responses in severely intellectually disabled children include a full-blown smile (which may or may not accompany inappropriate laughter), stiffening, and non-cooperation (Hadden 2002). Other observed behaviors include the freezing phenomenon, in which the child acutely feels the pain, and he abruptly pauses without moving his face for several seconds. Look also for episodes of unexplained pallor, diaphoresis, breath-holding, and shrill vocalizations. The FLACC has been revised (r-FLACC) for children with cognitive impairment and appears to be reliable for acute care (Malviya 2006).
The most distressing and perplexing presentation is the parent who brings his or her child with cognitive impairment for “fussiness”, “irritability”, or “I think he’s in pain”. Often, this is after significant investigations have been performed, sometimes repeatedly. Poorly controlled spasticity is an often under-appreciated cause of unexplained pain; treat not with opioids, but with GABA-receptor agonists, such as baclofen or benzodiazepines.
Take special precautions in the administration of opioids or benzodiazepines in children with metabolic disorders (e.g. mitochondrial disease) or various syndromes (e.g. Trisomy 21). They may have a disproportionate reaction to the medication. Start with a low dose in these children and reassess frequently, titrating in small aliquots as needed.
After careful, meticulous investigation in the ED to rule out occult infection, trauma, electrolyte imbalance, or surgical causes, the child with cognitive impairment who continues to be symptomatic despite ED treatment may be admitted for observation. However, in some cases, the addition of gabapentin to the typical regimen has been shown to manage unexplained irritability in these children (Hauer 2007) by treating visceral hyperalgesia.
The child with multi-trauma is in need of meticulous critical care. Frequent assessments of pain analgesic response (typically via the intravenous route) are necessary to gauge the child’s trajectory. Unexplained tachycardia may be the early signs of shock. Without controlling the child’s pain, it is difficult to distinguish the extreme tachycardia from pain or from blood loss. If intubated, control the pain first with a fentanyl drip, then use a sedative in addition as needed to keep him comfortable.
Children undergoing palliative care require a multidisciplinary approach. This includes engaging the patient’s car team as well as “treating” members of the patient’s family. Examples include the natural course of devastating chromosomal, neurologic, and other congenital conditions; terminal cancer; and trauma, among others (Michelson 2007). Family dynamics and family members’ needs are often overlooked; the family as a whole must be considered. Focus on the productive and beneficial treatments that can be offered. Treat pain promptly, but speak with the parents about end-of-life goals as early as possible, as any analgesic or sedative may have an untoward effect. You do not want to be caught in the position of potentially precipitously providing cardiopulmonary resuscitation in a child undergoing palliative care, because of a lack of understanding of how increasingly large doses of pain medications can affect breathing and circulation (AAP 2000).
Children with ongoing opioid requirements may present not so much with an exacerbation of their chronic pain, but a complication of its treatment. Identify, assess and aggressively treat constipation, nausea and vomiting, pruritus, and urinary retention (Friedrichsdorf 2007); treating side-effects of pain management may be just as important for quality of life as treating the pain itself.
Allow the child to speak for himself whenever possible. After acknowledging the parent’s input, perhaps try “I want to make sure I understand how the pain is for you. Tell me more.”
Engage parents and communicate the plan to them. Elicit their expectations, and give them of preview of what to expect in the ED.
Opioids are meant for pain caused by acute tissue injury, for the briefest period of time feasible. Older school-aged children and adolescents are increasingly at risk for opioid dependence and addiction.
Premature infants present a challenge in pain control. Their pain is under-recognized, as they often display atypical responses to painful stimuli. Treatment is equally difficult, as they are particularly sensitive to analgesia-sedation. This is important, as this group is even more likely to undergo painful procedures due to their higher-risk status.
Give detailed advice on how to manage pain at home. Set expectations. Let them know you understand and will help them through your good advice that will carry them through this difficult time. Patients and families often just need a plan. Map it out clearly.
Andolfatto G, Willman E, Joo D, Miller P, Wong WB, Koehn M, Dobson R, Angus E, Moadebi S. Intranasal ketamine for analgesia in the emergency department: a prospective observational series. Acad Emerg Med. 2013 Oct;20(10):1050-4.
Bailey E, Worthington HV, van Wijk A, Yates JM, Coulthard P, Afzal Z. Ibuprofen and/or paracetamol (acetaminophen) for pain relief after surgical removal of lower wisdom teeth.Cochrane Database Syst Rev. 2013 Dec 12;(12):CD004624.
Brousseau DC, Duffy SJ, Anderson AC, Linakis JG. Treatment of pediatric migraine headaches: a randomized, double-blind trial of prochlorperazine versus ketorolac. Ann Emerg Med. 2004 Feb;43(2):256-62.
Cornelissen L, Donado C, Kim J, Chiel L, Zurakowski D, Logan DE, Meier P, Sethna NF, Blankenburg M, Zernikow B, Sundel RP, Berde CB. Pain hypersensitivity in juvenile idiopathic arthritis: a quantitative sensory testing study. Pediatr Rheumatol Online J. 2014 Sep 6;12:39.
Crews KR, Gaedigk A, Dunnenberger HM, Leeder JS, Klein TE, Caudle KE, Haidar CE, Shen DD, Callaghan JT, Sadhasivam S, Prows CA, Kharasch ED, Skaar TC; Clinical Pharmacogenetics Implementation Consortium. Clinical Pharmacogenetics Implementation Consortium guidelines for cytochrome P450 2D6 genotype and codeine therapy: 2014 update. Clin Pharmacol Ther. 2014 Apr;95(4):376-82.
Deaton T, Auten JD, Darracq MA. Nebulized fentanyl vs intravenous morphine for ED patients with acute abdominal pain: a randomized double-blinded, placebo-controlled clinical trial. Am J Emerg Med. 2015 Jun;33(6):791-5.
Farion KJ, Splinter KL, Newhook K, Gaboury I, Splinter WM. The effect of vapocoolant spray on pain due to intravenous cannulation in children: a randomized controlled trial. CMAJ. 2008 Jul 1;179(1):31-6.
Furyk JS, Grabowski WJ, Black LH. Nebulized fentanyl versus intravenous morphine in children with suspected limb fractures in the emergency department: a randomized controlled trial. Emerg Med Australas. 2009 Jun;21(3):203-9.
Graudins A, Meek R, Egerton-Warburton D, Oakley E, Seith R. The PICHFORK (Pain in Children Fentanyl or Ketamine) trial: a randomized controlled trial comparing intranasal ketamine and fentanyl for the relief of moderate to severe pain in children with limb injuries. Ann Emerg Med. 2015 Mar;65(3):248-254.e1.
Luhmann JD, Schootman M, Luhmann SJ, Kennedy RM. A randomized comparison of nitrous oxide plus hematoma block versus ketamine plus midazolam for emergency department forearm fracture reduction in children. Pediatrics. 2006 Oct;118(4):e1078-86.
Lunoe MM, Drendel AL, Levas MN, Weisman SJ, Dasgupta M, Hoffmann RG, Brousseau DC. A Randomized Clinical Trial of Jet-Injected Lidocaine to Reduce Venipuncture Pain for Young Children. Ann Emerg Med. 2015 Nov;66(5):466-74.
Malviya S, Voepel-Lewis T, Burke C, Merkel S, Tait AR. The revised FLACC observational pain tool: improved reliability and validity for pain assessment in children with cognitive impairment. Paediatr Anaesth. 2006 Mar;16(3):258-65.
Merry AF, Edwards KE, Ahmad Z, Barber C, Mahadevan M, Frampton C. Randomized comparison between the combination of acetaminophen and ibuprofen and each constituent alone for analgesia following tonsillectomy in children. Can J Anaesth. 2013 Dec;60(12):1180-9.
Miner JR, Kletti C, Herold M, Hubbard D, Biros MH. Randomized clinical trial of nebulized fentanyl citrate versus i.v. fentanyl citrate in children presenting to the emergency department with acute pain. Acad Emerg Med. 2007 Oct;14(10):895-8.
Poonai N, Paskar D, Konrad SL, Rieder M, Joubert G, Lim R, Golozar A, Uledi S, Worster A, Ali S. Opioid analgesia for acute abdominal pain in children: A systematic review and meta-analysis. Acad Emerg Med. 2014 Nov;21(11):1183-92.
Sheehy KA, Muller EA, Lippold C, Nouraie M, Finkel JC, Quezado ZM. Subanesthetic ketamine infusions for the treatment of children and adolescents with chronic pain: a longitudinal study. BMC Pediatr. 2015 Dec 1;15:198.
Sheehy KA, Finkel JC, Darbari DS, Guerrera MF, Quezado ZM. Dexmedetomidine as an Adjuvant to Analgesic Strategy During Vaso-Occlusive Episodes in Adolescents with Sickle-Cell Disease. Pain Pract. 2015 Nov;15(8):E90-7.
Spanos S, Booth R, Koenig H, Sikes K, Gracely E, Kim IK. Jet Injection of 1% buffered lidocaine versus topical ELA-Max for anesthesia before peripheral intravenous catheterization in children: a randomized controlled trial. Pediatr Emerg Care. 2008 Aug;24(8):511-5.
Voepel-Lewis T, Merkel S, Tait AR, Trzcinka A, Malviya S. The reliability and validity of the Face, Legs, Activity, Cry, Consolability observational tool as a measure of pain in children with cognitive impairment. Anesth Analg. 2002 Nov;95(5):1224-9.
Yeaman F, Oakley E, Meek R, Graudins A. Sub-dissociative dose intranasal ketamine for limb injury pain in children in the emergency department: a pilot study. Emerg Med Australas. 2013 Apr;25(2):161-7
This post and podcast are dedicated to Sergey M. Motov, MD, FAAEM, for his integrity, hard-won expertise, humility, and innovation. Thank you for making us better doctors, Sergey, and for getting us ever closer to a pain-free ED.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
-- Witches in Macbeth, with apologies to William Shakespeare
-- 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 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.
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.
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.
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.
Below is a list of modalities, treatments, and the evidence and/or recommendations for or against:
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).
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.
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.
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.
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.
May show some benefit in admitted patients, after repeated treatments; no data to support its use in ED patients (no immediate effect).
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 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.
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.
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.
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.
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.
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
Images courtesy of Radioglypics (Open Access Radiology Education). Used with permission.
Now that we have our adult anatomy reviewed, let's go through the development of the elbow in a child.
We are all born with primary ossification centers -- the basic shapes of our long bones. Secondary ossification centers then develop around the ends of our long bones, and make interpretation of films in the context of suspected injury difficult.
More pragmatic and utilitarian than a prosaic mnemonic, CRITOE helps us to remember the order of ossification of the pediatric elbow.
Although children develop at different rates, the order of ossification is programmed into us. Images courtesy of Radiopaedia.
By age one, the capitellum ossifies. On the AP view, imagine a little white oval balloon floating in the darkness between the radius and the humerus.
By age three, the capitellum gets another little balloon to join the party. The radial head is a bony little balloon that floats just above the floor. If you see both little balloons floating on either ends of the space between the humerus and the radius – you know this child is about three years old.
By the age of five, the capitellum and radial head are no longer little floating balloons, but now taking on shapes that resemble what they will look like as an adult. By age five, you’ve grown out of balloons, and have moved on to Frisbees. The internal epicondyle (meaning the medial epicondyle) starts to ossify by age five – a little bony Frisbee.
By age seven, another little Frisbee flies around. On the AP view, the trochlea is superimposed on the humerus – if you look at the distal medial humerus, you’ll see the trochlea like a little oval Frisbee taking shape (see combined film below).
By age nine, the olecranon of the ulna is ossifying. In a nine year old, you’ll see a capitellum, radial head, internal epicondyle, trochlea, and olecranon.
By age 11, you start to ossify your external epicondyle (lateral epicondyle).
These three things can save us: fat pads, the anterior humeral line, and the radiocapitellar line. Non-annotated images courtesy of Heidi Nunn.
Normal anterior fat pad
Baumann’s angle (carrying angle): Normal is 70 to 75 degrees. A difference between extremities of just 5 degrees or more is abnormal.
Pain out of proportion to exam, paresthesias, pallor, poikilothermia, pulselessness, and paralysis
The 6 Ps of compartment syndrome are not sensitive in children.
The only thing that may alert you to increasing compartment pressures in children is an increasing need for analgesics.
Untreated compartment syndrome results in thrombosis, edema, ischemia, and disabling contracture.
Lateral Condyle Fracture
Medial Epicondyle Fracture
Radial head and radial neck fractures
Radial head subluxation (nursemaid’s elbow)
Medial epicondylar apophysitis (Little leager’s elbow)
The most important pediatric elbow injury is the supracondylar fracture. Grade I is minimally displaced and needs a cast; Grade II is displaced, but with the posterior cortex intact; after closed reduction, the child may still need surgery; Grade III fractures all need closed reduction, internal fixation, and close monitoring for compartment syndrome.
CRITOE gives us the order of ossification for the pediatric elbow – capitellum, radial head, internal epicondyle, trochlea, external epicondyle, and olecranon -- typically occurring at year 1, 3, 5, 7, 9, and 11 – remember the order is the most important thing – all ossification centers should be accounted for. Make sure one is not missing – or where one has been “created” traumatically.
If you don't see the obvious fracture, you can be "saved" by the sail sign and/or a posterior fat pad. Also, make sure to look for the anterior humeral line – on the lateral view, a line drawn down the anterior humerus – if it intersects with the middle third of the capitellum, that is normal – it not, suspect a supracondylar fracture.
The radiocapetellar line runs along the radial neck through the radial head and should line up nicely with the capitellum. If not, assume a fracture-dislocation.
Close communication and coordination with the orthopedist will help us to get the right care at the right time – there is some variability with orthopedic practice, so be open to that – we can make out biggest impact by making the right diagnosis, and aggressively treating pain and effectively providing procedural sedation when needed.
This post and podcast are dedicated to Andy Neill, MBBS. Thank you for your humanism and your dogged dedication to connect with the learner and simplify complex concepts. Welcome back, Andy!
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
The differential diagnosis of GI bleeding in children is broad.
GI bleeding in the neonate (less than one month of age) is serious until proven otherwise.
If this in obvious anal fissure, then no further work-up is necessary. Counsel on proper feeding and follow-up.
Evaluate for potential swallowed maternal blood by examining mother with a chaperone, then perform the Apt test.
Consider allergic proctocolitis if the child is well. Counsel the breastfeeding mother on diet modification. If formula fed, the child should feed through thus until the primary care physician decides whether to start the sticky process of changing up formulas.
If unclear, consider a complete blood count and/or further work-up and admission if unwell.
The three most dangerous diagnoses in the neonate are necrotizing enterocolitis, malrotation with volvulus, and inherited coagulopathy. It is important to note that 15% of necrotizing enterocolitis occurs in full-term babies; malrotation can present simply in shock, without initial overt bleed. Inherited conditions may not be known to the family early on, as they have not yet heard back from the neonatal screening done at birth.
Genitourinary bleeding; hematuria; or uric acid crystals: the classic fake out here is the orange or pink stained diaper – that is actually residue from deposits of uric acid crystals in the urine, an almost always benign phenomenon in which the concentrated crystals oxidize and stain the diaper, frightening the parents.
Think -- pink stain, without clot:
Through the first year to age 5, things like infectious colitis and gastritis are common.
Think about intussusception, cryptic liver disease, or esophageal bleeding. Check the skin – is that a dark purple palpable rash on the buttocks? Think Henoch-Schoenlein purpura.
Meckel’s diverticulum is the most common congenital malformation of the GI tract, and the most common cause of GI bleeding in the toddler. It is a remnant of the omphalomesenteric tract – it came from a long tube that once connected the yolk sac to the lumen of the midgut. A stranded island of gastric tissue secretes acid in the intestine, where it doesn’t belong. Sometimes these islands never cause much trouble.
When it does present itself, a Meckel’s diverticulum usually follows the rule of twos:
Presents by age 2
Affects 2% of the population
Often 2 inches in length
May include 2 types of mucosa
Found within 2 feet of the ileocecal valve.
Not actively bleeding: technetium-99 pertechnate scintigram (Meckel’s scan).
Actively bleeding: radio-labeled red blood-cell scan (resuscitate and call your surgeons!)
Epistaxis; food-related misadventures
Mallory-Weiss tears after forceful vomiting; trivial hemoptysis after viral symptoms; pill esophagitis in the child is just learning to swallow medications. Always consider foreign body ingestion.
Varices from cryptic liver disease; hemorrhagic gastritis; vascular malformation, such as a Dieulafoy lesion, where a tortuous small artery ends just superficial to the gastric mucosa, and can erode through and erupt.
Approximately a quarter of patients with inflammatory bowel disease (IBD) -- both Ulcerative Colitis and Crohn disease – will present by age 20. Children and adolescents may present with the classic symptoms of IBD: abdominal pain, weight loss, bloody diarrhea, but many present atypically with isolated signs like poor growth, anemia, or delayed puberty.
You may also suspect IBD in the child with other extra-intestinal symptoms like oral ulcers, clubbing, erythema nodosum, jaundice, or hepatomegaly.
On history and physical examination, you may get one of three cardinal presentations
Fatigue, history of anemia, in a stable child who comes to the ED with bloody diarrhea
Chronic diarrhea, chronic abdominal pain, and poor weight gain or weight loss
A fulminant presentation, with severe abdominal pain, frankly bloody stools, tenesmus, fever, leukocytosis, and hypoalbuminemia.
On exam, look for general appearance, glossitis from B2 deficiency, hair loss and brittle nails form protein loss, purpura (from vitamin C and vitamin K deficiencies). Look for evidence of episcleritis or uveitis. Listen for rubs as in pericarditis. Do a good abdominal exam, especially looking for hepatomegaly. Perirectal skin tags are not uncommon. Children with IBD may form urinary calculi form oxalate crystal deposition. Do a thorough skin and neurologic exam.
Treatment for both ulcerative colitis and Crohn’s disease is similar.
Induction therapy: children with mild disease get aminosalicylates; those with moderate disease get steroids; and those with severe disease get cyclosporine.
Maintenance regimens to prevent relapse include aminosalicylates, mercaptopurine, and azathioprine.
Surgical treatments for refractory colitis include an ileal pouch and anal anastomosis – also called a J pouch, a type of neorectum created surgically by folding loops of ileum back on themselves and stitching them together to create a larger rectal reservoir where the rectum once was. A neorectum allows the child to have voluntary control of his stools again.
Life-threatening GI bleeding in children is, thankfully, rare, but we have to be prepared.
Give blood for compensated shock, prepare for massive transfusion if giving more than 40 mL/kg total blood products.
The reasons for upper GI bleed in adults are vastly different from those of children. In adults, mostly the life-threats are due to liver disease, varices, or hemorrhagic gastritis.
In children, critical upper GI bleed is often secondary to critical illness (hemorrhagic gastritis or stress ulcer), or vascular malformation. Critical lower gastrointestinal bleeding may be from Meckel's diverticulum or other congenital angiodysplasia.
Get your patient urgent endoscopy as soon as possible after arrival if there is active bleeding. Otherwise, according to the Belgian guidelines, stable children may have endoscopy within the first 24 hours of hospitalization. The reported efficacy of endoscopy for controlling upper GI bleeding in children is approximately 90%.
Nasogastric tube? No routine role (unreliable to rule out or stratify upper GI bleed).
Proton pump inhibitor? No good data, but no major common contraindications.
Octreotide, vasopressin, broad-spectrum antibiotics? May use adult data to extrapolate in the proper etiologic context.
This is a rare, but potentially life threatening situation, so anticipate how the child can decline, and get your team assembled: your pediatric intensivist, gastroenterologist, and surgeon – especially if we can’t ge the upper GI bleed to abate with endoscopy. The sooner you activate the team, the better.
The broad differential diagnosis may be paralyzing, and frustrating, since much of it we cannot discern in the ED.
Consider actionable, high-yield etiologies based on age and appearance.
Well appearing? Think rectal fissure, maternal blood, or allergic proctocolitis
Ill appearing? Think necrotizing enterocolitis, malrotation, or an inherited coagulaopathy.
Infants, and Young Children
Well appearing? Think infectious colitis and gastritis.
Ill appearing? Think intussusception and Meckel’s diverticulum.
Older Children and Adolescents
Well appearing? Think Mallory Weiss tear from vomiting, or gastritis
Ill appearing? Think metabolic, cryptic liver disease, or inflammatory bowel disease.
For everyone – a careful history and a good physical exam will point you tto the etiology, or risk-stratify for further outpatient evaluation and management.
Chaïbou M, Tucci M, Dugas MA, Farrell CA, Proulx F, Lacroix J. Clinically significant upper gastrointestinal bleeding acquired in a pediatric intensive care unit: a prospective study. Pediatrics. 1998 Oct;102(4 Pt 1):933-8.
Colle I, Wilmer A, Le Moine O, Debruyne R, Delwaide J, Dhondt E, Macken E, Penaloza A, Piessevaux H, Stéphenne X, Van Biervliet S, Laterre PF. Upper gastrointestinal tract bleeding management: Belgian guidelines for adults and children. Acta Gastroenterol Belg. 2011 Mar;74(1):45-66.
Thomson MA, Leton N, Belsha D. Acute upper gastrointestinal bleeding in childhood: development of the Sheffield scoring system to predict need for endoscopic therapy. J Pediatr Gastroenterol Nutr. 2015 May;60(5):632-6.
This post and podcast are dedicated to Carlo D'Apuzzo, MD for his creativity, innovation, and dedication to the highest standards of emergency care. Le tue pillole sono buona medicina. Grazie, Carlo per tutto quello che fai per il mondo #FOAMed.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
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?
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.
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 dysfunction
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.
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.
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.
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.
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.
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
Clysis comes from the same Greek word that “a flood” – hypodermoclysis refers to flooding the subcutaneous space with fluid, so that it can be absorbed systemically.
Well, it turns out, what is old is new again.
In 1913, Dr Day first described this technique for a child with severe diarrhea who could not tolerate fluids by mouth. Hypodermoclysis then began to gain popularity with a peak of use in the 1940s, until an innovative breakthrough in 1950. Dr David Massa, a resident anesthesiologist at the Mayo clinic, invented the first catheter-over-needle apparatus.
With increasing safety and ready access of IV catheters, IV quickly overshadowed SC.
The subcutaneous route of hydration has also been used effectively in geriatric and palliative care for decades, and it is only now beginning to gain popularity again in its original population: children.
In a nutshell, you place a butterfly needle or angiocatheter in the subcutaneous space and you run fluids into it. The tissues quickly absorb the fluids, making them available systemically. That’s it. Everything else is just finesse.
The ideal candidate for hypodermoclysis is the stable patient, with mild to moderate dehydration who fails a trial of fluids by mouth, or who needs a bridge to gaining IV access later, after a slow subcutaneous fluid bolus is given.
Place a topical anesthetic cream, such as EMLA, cover with occlusive dressing (IV dressing), wait 15-20 min
"Pinch an inch" of skin anywhere, but the most practical site in young children is between the scapulae
Insert a 25-gauge butterfly needle or 24-gauge angiocatheter (preferred by the author), secure
Inject 150 U hyaluronidase SC, if available
Infuse 20 mL/kg isotonic solution over one hour, repeat as needed or use "bolus" as bridge to IV access
You can set the line to gravity, and if it is dripping in, you may leave it be. If you see a very slow drip by gravity, or worse, nothing is dripping, you can set the line on a pump, to deliver up to 20 mL/kg over an hour. Infusion at this rate optimizes the balance we want in minimal discomfort while maximizing the flow rate.
This is not a “bolus” in the true sense – but then, when you compare it to the alternative – like IV therapy – and we see a time and cost savings. Dr Mace and colleagues in the American Journal of Emergency Medicine report substantially decreased cost and ED length of stay when comparing the material and human resources needed to place an IV in a squirmy young child, compared with a simple subcutaneous stick.
There will be swelling – that is the goal. It is really painless, and your patient may lie down on his back with the pump going – it is actually pretty comfortable for most children and adults to do.
Here’s a tip – since there will be swelling, we want to be careful about how we secure the line, so how you tape it down to the skin is important – we want to avoid a pulling sensation, which can be the beginning of the end of the tolerance for the procedure. Cover that with an occlusive dressing, as you would an IV site. The footprint of the occlusive dressing is relatively small, so it will travel up on top of the subcutaneous mound you’re creating. As the line exits the occlusive patch, place a thin layer of gauze between the skin and the IV tubing, so that the tubing doesn’t press into the skin. Then—as far away from the puncture site as possible—tape it down securely. The idea is not to tape on the growing mound itself, because the mound may pull at the anchored skin and set a nuclear chain reaction of annoyance and restlessness – and potentially a failed procedure.
The swelling will look indurated, a pinkish red. It’s not an allergic reaction: even with the old preparations of hyaluronidase, allergic reactions were rare, and now they are very rare with the recombinant preparation. It is supposed to swell and look ugly. The subcutaneous tissues will swell to a point where you have a steady state fluid administration rate, and as soon as you stop the infusion, the remaining fluid will start to subside as it is absorbed.
Kuensting et al. in the Journal of Emergency Nursing in 2013 compared subcutaneous fluid infusion with intravenous fluid infusion in children with difficult IV access. They found the mean time from order entry to subcutaneous fluid infusion to be 20 min, compared to the failed IV access group with an average infusion start time of 1.5 hours. The latter group eventually received subcutaneous fluids. The investigators also found a shorter ED length of stay in the subcutaneous group.
In the same study, a subgroup received subcutaneous fluids initially, and later an IV. They found a trend in ease of IV access after subcutaneous fluid therapy. In other words, if your little patient with difficult IV access is hemodynamically stable and amenable to a bolus over an hour, you may choose to start with hypodermoclysis and reevaluate.
Much has been studied and written about the predictors of difficult IV access in children. The most often cited are: age < 3 years, weight less than 5 kg, prematurity, obesity, and darker skin tones, where the contrast of vein to skin may not be so apparent.
The three main predictors of the score validated by Riker et al. in Annals of Emergency Medicine include the most practical and universal of features: vein palpability, vein visibility, and patient age.
If you’re anticipating difficult IV access in the child who can stand to wait an hour for a slow bolus, you may start with the subcutaneous route to get those veins plumper and more visible, to improve your chances of IV access in the very near future.
Certain medications have been used safely via subcutaneous infusion; always check dose, rate, and compatibility.
You don’t need to use larger needles or angiocathters for older children, adolescents or adults. A 25-gauge butterfly or 24-gauge angiocatheter works well from an infant to an elder. In one study of adults, a half a liter of saline was infused by gravity via a 24-gauge catheter. With IVs, the shorter and larger the bore, the faster the infusion.
In subcutaneous infusion, it is not the size of the catheter, but the osmotic gradient that determines the rate of absorption.
It’s actually increasingly readily found – and available in generic form. If you have it, please use it – it will make a believer out of you and others.
Hypodermoclysis will work without hyaluronidase – the process of subcutaneous rehydration just takes a lot longer to work. In a double-blind cross-over trial Thomas et al. in 2007 compared subcutaneous administration of lactated ringer’s solution by gravity with and without hyalurondase. The hyaluronidase group received their fluids 5 times faster. The average rate of the hyaluronidase group was 382 mL/h versus the fluid only group, who did not receive hyalurinodase; they were substantially slower, at 82 mL/h. It’s worth using if you have it, but still potentially useful if you don’t.
√ EMLA or any topical anesthetic used for intact skin, placed as soon as the decision is made
√ A 25-gauge butterfly needle or 24-gauge angiocatheter
√ IV tubing, gauze to pad, tape to anchor
√ 150 U hyaluronidase, the same dose, regardless of age or size
√ Isotonic fluids – you can start with 20 ml/kg
√ And finally a well informed team made up by the patient, the parents, and your staff, so that everyone knows what to expect for a successful subcutaneous fluid administration.
Allen CH, Etzwiler LS, Miller MK, Maher G, Mace S, Hostetler MA, Smith SR, Reinhardt N, Hahn B, Harb G; INcreased Flow Utilizing Subcutaneously-Enabled Pediatric Rehydration Study Collaborative Research Group. Recombinant human hyaluronidase-enabled subcutaneous pediatric rehydration. Pediatrics. 2009 Nov;124(5):e858-67.
Cabañero-Martínez MJ, Velasco-Álvarez ML, Ramos-Pichardo JD, Ruiz Miralles ML, Priego Valladares M4, Cabrero-García J. Perceptions of health professionals on subcutaneous hydration in palliative care: A qualitative study. Palliat Med. 2016 Jun;30(6):549-57.
Mace SE, Harb G, Friend K, Turpin R, Armstrong EP, Lebel F. Cost-effectiveness of recombinant human hyaluronidase-facilitated subcutaneous versus intravenous rehydration in children with mild to moderate dehydration. Am J Emerg Med. 2013 Jun;31(6):928-34.
Riker MW, Kennedy C, Winfrey BS, Yen K, Dowd MD. Validation and refinement of the difficult intravenous access score: a clinical prediction rule for identifying children with difficult intravenous access. Acad Emerg Med. 2011 Nov;18(11):1129-34.
Thomas JR, Yocum RC, Haller MF, von Gunten CF. Assessing the role of human recombinant hyaluronidase in gravity-driven subcutaneous hydration: the INFUSE-LR study. J Palliat Med. 2007 Dec;10(6):1312-20.
Zaloga GP, Pontes-Arruda A, Dardaine-Giraud V, Constans T; Clinimix Subcutaneous Study Group. Safety and Efficacy of Subcutaneous Parenteral Nutrition in Older Patients: A Prospective Randomized Multicenter Clinical Trial. J Parenter Enteral Nutr. 2016 Feb 17. pii: 0148607116629790. [Epub ahead of print]
This post and podcast are dedicated to Christina L. Shenvi, MD, PhD, for her dedication to excellence in patient care and enthusiasm in #FOAMed, Emergency Medicine, and Geriatric Emergency Medicine. There are many shared lessons learned in the care of children, elders, and families. Thank you.
Catch Dr Shenvi on the innovative GEMcast.
Powered by #FOAMed -- Tim Horeczko, MD, MSCR, FACEP, FAAP
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.
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.
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.
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 – <0.2 %
1 Predictor – 3%
2 Predictors – 40%
3 Predictors – 93.1%
4 Predictors – 99.6%
Now, remember, this is to be used in children in whom you already have some suspicion of a septic joint. So, 0 predictors, generally you’re alright. 1 predictor, you may start to worry. Once you have 2 predictors, your chances jump for 3% to 40%. You really have to go looking.
The Kocher caveat is that there is no single test or single decision rule that will stop you from investigating if you are concerned enough. Don’t have too much faith in this imperfect decision tool – we use it because we need somewhere to start. Treat and push for the aspiration of the hip if you are left in doubt. Septic arthritis can be devastating if not identified early.
Kocher MS et al. Differentiating between septic arthritis and transient synovitis of the hip in children: an evidence-based clinical prediction algorithm. J Bone Joint Surg Am. 1999 Dec;81(12):1662-70.
Kocher MS et al. Validation of a clinical prediction rule for the differentiation between septic arthritis and transient synovitis of the hip in children. J Bone Joint Surg Am. 2004 Aug;86-A(8):1629-35.
This post and podcast are dedicated to the estimable yet graciously humble Andrew Tagg BSC(Hons), MBBS, MRCSEd, ACEM for his dedication to #FOAMed, Emergency Medicine, Pediatric Emergency Medicine, and all things caffeinated. Thank you for your dedication, generosity, and your example.
World wide, shock is a leading cause of morbidity and mortality in children, mostly for failure to recognize or to treat adequately.
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 is multifactorial, but we need to identify a primary cause to prioritize interventions.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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
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
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)
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.
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.
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.
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
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?
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.
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.
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.
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.
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.
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:
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.
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.
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.
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:
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.
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
On arrival, he was in compensated shock, with tachycardia.
He decompensates and needs blood.
40 mL/kg of blood products given at any time within the first 24 hours.
6-8 units of packed red blood cells (PRBCs)
The typical initial transfusion of PRBCs in children is 10 mL/kg.
Massive transfusion in children is defined as 40 mL/kg of any blood product.
Once you start to give a child with major trauma the second 10 mL/kg dose of PRBCs – start thinking about other blood components, and ask yourself whether you should initiate your massive transfusion protocol.
The goal is to have the products ready to use in the case of the dynamic trauma patient.
Direct measures the four components of clot formation. When there is endolethial damage and bleeding, the sequence that your body takes to address it is as follows:
Red wine glass: a normal tracing with a normal reaction time and a normal amplitude. That patient just needs support and monitoring.
Champagne glass: a coagulopathic TEG tracing – thinned out, with less amplitude. This patient needs specific blood products.
Puffer fish or blob: a hyperfibrinolytic tracing. That patient will needs clot-stablizer.
TEG – like the FAST – can be repeated as the clinical picture changes.
Lethal triad of hypothermia, acidosis, and coagulopathy.
Keep the patient perfused and warm.
Each unit of PRBCs contains 3 g citrate, which binds ionized calcium, causing hypotension. In massive transfusion, give 20 mg/kg of calcium chloride, up to 2 g, over 15 minutes. Calcium chloride is preferred, as it is ionically readily available – just use a larger-bore IV and watch for infiltration. Calcium gluconate could be used, but it requires metabolism into a bioavailable source of calcium.
Prothrombin complex concentrate (PCC) is derived from pooled human plasma and contains 25-30 times the concentration of clotting factors as FFP. Four-factor PCCs contain factors II, VII, IX and X, while 3-factor PCCs contain little or no factor VII.
The typical dose of PCC is 20-50 units/kg
In the severely hemorrhaging patient – you don’t have time to wait for the other blood products to thaw – PCC is a powder that is reconstituted instantly at the bedside.
Tranexamic acid (TXA), is an anti-fibrinolytic agent that functions by stopping the activation of plasminogen to plasmin, and the degradation of fibrin. The Clinical Randomisation of an Antifibrinolytic in Significant Hemorrhage (CRASH-2) investigators revealed a significant decrease in death secondary to bleeding when TXA was administered early following trauma.
Based on the adult literature, one guideline is to give 15 mg/kg loading dose of TXA with a max 1 g over 10 minutes followed by 2 mg/kg/h for at least 8 h or until bleeding stops.
Our goal here is damage control. Apply pressure whenever possible. Otherwise, resuscitate, identify the bleeding source, and slow or stop the bleeding with blood products or surgery.
In adults, we speak of “permissive hypotension” (also called “balanced resuscitation” or “damage control resuscitation”). The idea is that if we bring the adult patient’s blood pressure up to normal, we may be promoting clot rupture. To avoid this, we target a MAP of 65 and look for clinical signs of sufficient perfusion. Adults tolerate hypotension relatively well, and is sufficient until we send them to the OR or interventional radiology suite.
In children, this is simply not the case. Hypotension in children is a sign of pre-arrest. Remember, they compensate with an increased systemic vascular resistance and tachycardia to maintain blood pressure.
We should not allow children to become hypotensive – severe tachycardia alone should prompt us to resuscitate.
In other words, permissive hypotension is not permissible for children.
Fox et al in Academic Emergency Medicine found a sensitivity of 52%; with a 95% confidence interval [CI] = 31% to 73%.
Often children even with high-grade splenic and liver lacerations can be managed non-operatively. If they are supported adequately, they are observed in the ICU and can avoid surgery in many cases. Unfortunately, a negative FAST cannot help with detecting or grading the laceration for non-operative management. In other words, feel free to use ultrasound – especially for things that we in the ED will react to and intervene on – but CT may help to manage the traumatized child non-operatively.
CT Head and Neck, non-contrast: in concerning mechanisms of injury, patients that are difficult to assess (especially those under 3 months), those with a GCS of 13 or lower.
CT Chest, IV contrast: for suspicion of vascular injury that needs exploration, especially in penetrating trauma. Otherwise, chest xray will tell you everything you need to know in children – especially in blunt trauma. Hemo or pneumothoraces are readily picked up by US or CXR. Rib fractures on CXR predict pulmonary contusions. If you are concerned about great vessel injury, then CT Chest may be helpful; otherwise consider omitting it.
CT Abdomen and Pelvis, IV contrast: helpful in grading splenic and liver lacerations with goal to manage non-operatively. Abdominal tenderness to palpation, significant bruising, or a seat belt sign are concerning and would generally warrant a CT. Also, consider in liver function test abnormalities, or hematuria.
Extremity injuries: in general can be evaluated with physical exam and plain films. However, some injuries in high-risk anatomically complex areas such as the hand and wrist, tibial plateau, and midfoot may be missed by plain films, and CT may be helpful here.
Fox JC, Boysen M, Gharahbaghian L, Cusick S, Ahmed SS, Anderson CL, Lekawa M, Langdorf MI. Test characteristics of focused assessment of sonography for trauma for clinically significant abdominal free fluid in pediatric blunt abdominal trauma. Acad Emerg Med. 2011 May;18(5):477-82.
Holscher CM, Faulk LW, Moore EE, Cothren Burlew C, Moore HB, Stewart CL, Pieracci FM, Barnett CC, Bensard DD. Chest computed tomography imaging for blunt pediatric trauma: not worth the radiation risk. J Surg Res. 2013 Sep;184(1):352-7.
Nosanov L, Inaba K, Okoye O, Resnick S, Upperman J, Shulman I, Rhee P, Demetriades D. The impact of blood product ratios in massively transfused pediatric trauma patients. Am J Surg. 2013 Nov;206(5):655-60.
Scaife ER, Rollins MD, Barnhart DC, Downey EC, Black RE, Meyers RL, Stevens MH, Gordon S, Prince JS, Battaglia D, Fenton SJ, Plumb J, Metzger RR. The role of focused abdominal sonography for trauma (FAST) in pediatric trauma evaluation. J Pediatr Surg. 2013 Jun;48(6):1377-83.
This post and podcast are dedicated to Larry Mellick, MS, MD, FAAP, FACEP. Thank you for your dedication to medical education, and sharing your warm bedside manner, extensive knowledge and talents, and your patient interactions with the world.
Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP
When you think of trauma in children, think of Charlie Brown. Large head, no neck, his chest and abdomen form an underdeveloped, amorphous shape.
Alternatively, think of children as apples – they are rounder than they are tall, with a large increased surface area. Apples don’t have a hard shell or thick rind to protect them. If you drop them, you may not see any evidence of damage to the outside, but there can be considerable bruising just under the surface.
A 5-year-old boy who was playing with his older brother in front of their home when the ball rolled into the street. He ran after it, and was struck by a sedan going approximately 30 mph.
This is the so-called Wadell’s triad that occurs in a collision of auto versus pedestrian or auto versus bicycle. The initial impact is the greatest, and will vary depending on the child’s height and what part of his body reaches up to the bumper of the car. Depending on the height of the child and the height of the car, the initial impact will cause a femur fracture, a pelvic fracture, or direct abdominal trauma. The second impact happens as the child is flung onto the grill or the hood of the car, causing usually thoracic trauma. The third impact can be the coup de grace – to add insult to major injury, the child is then propelled forward, worsening the two previous impacts’ injuries and adding a third – severe blunt head trauma.
If your patient has any subtle change in mental status, intubate early. In pediatric trauma, we need to be proactive. Hypoxia is our enemy.
Thankfully cervical spine injuries in children are uncommon, and when they do occur, they typically occur at the child’s fulcrum, which is at C2. Compare this with an adult’s injury pattern with our fulcrum at C7. Be careful and minimize manipulation of the cervical spine, but do what you must to visualize the chords and place the tube. Keep the neck midline, and realize that the child’s usual decrease respiratory reserve is even more affected by trauma. Preoxygenate and pass that tube quickly.
Chest tube sizing in pediatrics is straightforward if we remember that the traditional chest tube size is 4 x the ETT size.
Try using a pigtail catheter.
It’s roughly where you would put on a generous dose of deodorant. Insertion here minimizes the risk of damage to nerves, vessels and organs.
In a 40-year review of ED thoracotomy, Moore et al. analyzed 1,691 patients who received ED thoracotomy. Overall all-cause adult survival was 6.1%. In children ? 15 years of age, overall all-cause survival was considerably less, at 3.4%.
In a large case series and review of the literature for pediatric ED thoracotomy, Allen et al. found a survival rate in penetrating trauma of 10.2%, with a much lower survival rate in blunt pediatric arrest, at 1.6%. Adolescents had more penetrating injuries, and younger children had more blunt trauma.
To synthesize, the rarity of ED thoracotomy in children is due to the fact that:
If you have access to resuscitative endovascular balloon occlusion of the aorta or REBOA, this may be an option to temporize the child to get him to the relative control of the operating room. REBOA involves accessing the common femoral artery, passing a vascular sheath, floating a balloon catheter to the appropriate section of the aorta, and inflating the balloon to occlude blood flow.
Brenner et al. described a case series of 6 patients from two Level I trauma centers. They used REBOA for refractory hemorrhagic shock due to either blunt or penetrating injury. After balloon occlusion, blood pressure improved sufficiently to take the patient either to interventional radiology or to the OR. Four patients lived, two died. The AORTA trial is underway to investigate its use in trauma.
Allen CJ, Valle EJ, Thorson CM, Hogan AR, Perez EA, Namias N, Zakrison TL, Neville HL, Sola JE. Pediatric emergency department thoracotomy: a large case series and systematic review. J Pediatr Surg. 2015 Jan;50(1):177-81.
American College of Surgeons Committee on Trauma; American College of Emergency Physicians Pediatric Emergency Medicine Committee; National Association of Ems Physicians; American Academy of Pediatrics Committee on Pediatric Emergency Medicine, Fallat ME. Withholding or termination of resuscitation in pediatric out-of-hospital traumatic cardiopulmonary arrest. Pediatrics. 2014 Apr;133(4):e1104-16.
Holscher CM, Faulk LW, Moore EE, Cothren Burlew C, Moore HB, Stewart CL, Pieracci FM, Barnett CC, Bensard DD. Chest computed tomography imaging for blunt pediatric trauma: not worth the radiation risk. J Surg Res. 2013 Sep;184(1):352-7.
Scaife ER, Rollins MD, Barnhart DC, Downey EC, Black RE, Meyers RL, Stevens MH, Gordon S, Prince JS, Battaglia D, Fenton SJ, Plumb J, Metzger RR. The role of focused abdominal sonography for trauma (FAST) in pediatric trauma evaluation. J Pediatr Surg. 2013 Jun;48(6):1377-83.
Pediatric Trauma on WikEM
This post and podcast are dedicated to Dr Al Sacchetti, MD, FACEP. Thank you for promoting the emergency care of children and for spreading the message that you don’t need subspecialty training to take good care of acutely ill and injured children.
Powered by #FOAMed — Tim Horeczko, MD, MSCR, FACEP, FAAP
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:
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:
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 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.
If you have access to checking a serum beta-hydroxybutryrate – the unsung ketone – it can help in diagnosis in unclear cases.
Cerebral Edema Criteria:
Cerebral Edema Action Items:
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.
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.
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