MI in Children

Myocardial infarction (MI) in children is uncommon, but underdiagnosed.

This is due to two main factors: the etiologies are varied; and the presenting symptoms are “atypical”.

We need a mental metal detector! 

Case examples

Congenital

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

The fussy, sweaty feeder: ALCAPA

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

The stable child with chest pain: myocardial bridge

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

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

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

Diagnosis is made on coronary angiography.

The unwell child post-cardiac surgery: Fontan problems

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

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

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

Autoimmune

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

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

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

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

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

The aftermath: sequelae of Kawasaki disease

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

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

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

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

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

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

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

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

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

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

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

Trauma

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

The motor vehicle collision: blunt myocardial injury

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

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

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

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

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

The high-velocity object: coronary artery dissection or thrombus

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

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

The minor trauma with disproportionate complaint: myocardial bridge

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

Hematologic

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

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

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

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

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

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

The puffy faced child with chest pain: nephrotic syndrome hypercoagulability

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

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

The previously well child now decompensated: undiagnosed thrombophilia

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

The chronically worried, now with a reason: hypercholesterolemia

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

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

Infectious

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

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

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

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

The infant in shock after a ‘cold’: myocarditis

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

The child with tachycardia out of proportion to complaint: myocarditis

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

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

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

Toxins

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

The hyperactive boy with a hyperactive precordium: methylphenidate

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

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

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

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

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

The spice trader: synthetic cannabinoids

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

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

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

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

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

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

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

Riding that train: high on cocaine

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

Cranky: methamphetamine

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

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

Summary

Acute MI is a challenging presentation in children:

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

References

Congenital

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Autoimmune

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

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

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

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

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

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

Trauma

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

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

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

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

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

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

Hematologic

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

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

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

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

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

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

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

Infectious

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

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

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

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

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

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

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

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

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

Toxins

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

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

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

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

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

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

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

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

 

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

Neonatal Jaundice

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

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

Pathologic Jaundice

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

Physiologic Jaundice

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

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

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

Increased production

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

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

Impaired conjugation

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

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

Decreased excretion

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

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

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

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

How Does this All Go Down?

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

More Specifically:

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

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

Critical Action #1:

Assess risk for developing severe hyperbilirubinemia.

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

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

Critical Action #2

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

This will tell you: home or admission.

Use the Bilitool or Bhutani Nomogram (below).

 

Can I go Home Now?

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

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

Critical Action #3:

Assess risk for developing subsequent neurotoxicity.

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

 

Phototherapy Now?

 

Exchange Transfusion Now?

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

Home care

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

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

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

Nursery Care

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

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

Critical Care

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

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

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

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

The dehydration and neurologic dysfunction from hyperbilirubinemia may even cause feverCheck 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 a partial volume exchange.  It is a very delicate procedure that requires multiple hours and often multiple staff.

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

Summary

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

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

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

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

References

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

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

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

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

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

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

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

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

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

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

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

Foreign Bodies in the Head and Neck

Children the world over are fascinated with what can possibly “fit” in their orifices.  Diagnosis is often delayed.  Anxiety abounds before and during evaluation and management.

Most common objects:1,2

Food Coins Toys
Insects Balls, marbles Balloons
Magnets Crayon Hair accessories, bows
Beads Pebbles Erasers
Pen/marker caps Button batteries Plastic bags, packaging

Non-pharmacologic techniques

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.

Procedural Sedation

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.

L’OREILLE – DAS OHR – вухо – THE EAR – LA OREJA – 耳 – L’ORECCHIO

Essential anatomy:

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. 

Pearls:

  • Ask yourself: is it graspable or non-graspable?5
    • Graspable: 64% success rate, 14% complication rate
    • Non-graspable: 45% success rate, 70% complication rate5
  • If there is an insect in the external auditory canal, kill it first. They will fight for their lives if you try to dismember or take them out.  “In the heat of battle, the patient can become terrorized by the noise and pain and the instrument that you are using is likely to damage the ear canal.”5,6  Use lidocaine jelly (preferred), viscous lidocaine (2%), lidocaine solution (2 or 4%), isopropyl alcohol, or mineral oil.
  • Vegetable matter? Don’t irrigate it – the organic material will swell against the fixed structure, and cause more pain, make it much harder to extract, and may increase the risk of infection.

Pifalls:

  • Failure to inspect after removal – is there something else in there?
  • Failure to assess for abrasions, trauma, infection – if any break in skin, give prophylactic antibiotic ear drops
  • Law of diminishing returns: probability of successful removal of ear foreign bodies declines dramatically after the first attempt

 

LE NEZ – DIE NASE – ніс – THE NOSE – LA NARIZ – 鼻 – IL NASO

Essential anatomy:

Nasopharyngeal and tracheal anatomy. Highlighted areas indicate points at which nasal foreign bodies may become lodged.4

Pearls:

  • Consider using topical analgesics and vasoconstrictors to reduce pain and swelling – and improve tolerance of/cooperation with the procedure. Use 0.5% oxymetolazone (Afrin) spray and a few drops of 2 or 4%   Pros: as above.  Cons: possible posterior displacement of the foreign body.7
  • Be ready for the precipitous development of an airway foreign body

Pitfalls:

  • Beware of unilateral nasal discharge in a child – strongly consider retained foreign body.8
  • Do not push a foreign body down the back of a patient’s throat, where it may be aspirated into the trachea.
  • Be sure to inspect the palate for “vacuum effect”: small or flexible objects may be found on the roof of the mouth, just waiting to be aspirated.

 

LA GORGE – DER HALS – горло – THE THROAT – LA GARGANTA – 喉 – LA GOLA

Before we go further –

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.

 Essential anatomy:

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

Beware the “double-ring” sign: this is a button battery13

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.

Not a button battery, not a sharp object, not a long object?

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.

What conditions prompt urgent removal?

Size

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

Character

Sharp objects have a high rate of perforation (35%)1

Pearls:

  • History is essential. Believe the parents and assume there is an aspirated/ingested foreign body until proven otherwise.
  • History of choking, has persistent symptoms and/or abnormal xray? Broncoscopy! Cohen et al.16 found that of 142 patients evaluated at a single site university hospital, 61 had a foreign body. Of the 61 patients, 42 had abnormal physical exams and radiographs and 17 had either abnormal physical exams or radiographs, and 2 had normal physical exams and radiographs, but both had a history of persistent cough.  Bottom line: history of choking PLUS abnormal exam, abnormal films, or persistent symptoms, evaluate with bronchoscopy.
  • For patients with some residual suspicion of an aspirated foreign body (mild initial or improving symptoms; possibly abnormal chest x-ray; low but finite risk), consider chest CT with virtual bronchoscopy as a rule-out strategy.17,18
  • Outpatients who have passed a small and non-concerning object into the stomach or beyond: serial exams and observing stools – polyethylene glycol 3350 (MiraLAX) may be given for delayed passage19

Pifalls:

  • A single household magnet will likely pass through the GI tract, with the aforementioned dimensional caveats. Two or more magnets, however, run the risk of attraction and trans-bowel wall pressure necrosis.
  • Not all magnets are created equal. Neodymium magnet toys (“buckyballs”) were recalled in 2014 (but are still out there!) due to their highly attractive nature.  These magnets must be removed to avoid bowel wall ischemia. 19–21
  • Patients should avoid wearing belt buckles or metallic buttons in case of single magnet ingestion while waiting for the single magnet to pass

DES OUTILS DU MÉTIER – DIE HANDWERKSZEUG – Знаряддя праці

TOOLS OF THE TRADE

LAS HERRAMIENTAS DEL OFICIO – GLI ATTREZZI DEL MESTIERE –  仕事のツール

It’s best to keep your armamentarium as large as you can.

Curette

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.

Right-angle Hook

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

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.

Cyanoacrylate (Dermabond®, SurgiSeal®)

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

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

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.

Docusate Sodium (Colace®)

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.

Magnets

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.

Snare Technique

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.

Balloon Catheters (Katz extractor®, Fogarty embolectomy catheter)

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.”

Mother’s kiss

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

Positive Pressure Ventilation with Bag Valve Mask

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.

Beamsley Blaster (Continuous Positive Pressure) Technique

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.

With this technique there is a theoretical risk of barotrauma to the lungs or tympanic membranes.  However, there is only one case reported in the literature of periorbital subcutaneous emphysema.

To minimize this risk, some authors recommend limiting to a maximum of four attempts using any positive pressure method.10

Nasal speculum

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.

Suction tips / catheters

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.

 Laryngoscope and Magill Forceps

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.

 Take-home Points

 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

Motto

Like a difficult airway: plan through the steps

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!

Age-appropriate foods

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):

            Hot dogs

            Nuts and seeds

            Chunks of meat or cheese

            Whole grapes

            Hard or sticky candy

            Popcorn

            Chunks of peanut butter

            Chunks of raw vegetables

            Chewing gum

Child-proofing the home

Refer parents to the helpful multi-lingual site from the American Academy of Pediatrics:

http://www.healthychildren.org/English/safety-prevention/at-home/Pages/Childproofing-Your-Home.aspx

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:

  • Head lamp, LED camping style: $5-15
  • Neodymium magnet “pick-up tool”: $5-15
  • Neodymium bar magnet: $6-20
  • Wire, 24-gauge, spool of 25 yards (for snare technique): $6
  • Day hook: $15-20

References

  1. Chapin MM, Rochette LM, Annest JL, Haileyesus T, Conner KA, Smith GA. Nonfatal Choking on Food Among Children 14 Years or Younger in the United States, 2001–2009. Pediatrics. 2013;132(2):275-281. doi:10.1542/peds.2013-0260.
  2. Committee on Injury V. Policy Statement—Prevention of Choking Among Children. Pediatrics. 2010:peds.2009-2862. doi:10.1542/peds.2009-2862.
  3. Brown L, Denmark TK, Wittlake WA, Vargas EJ, Watson T, Crabb JW. Procedural sedation use in the ED: management of pediatric ear and nose foreign bodies. Am J Emerg Med. 2004;22(4):310-314.
  4. Heim SW, Maughan KL. Foreign bodies in the ear, nose, and throat. Am Fam Physician. 2007;76(8):1185-1189.
  5. DiMuzio J, Deschler DG. Emergency department management of foreign bodies of the external ear canal in children. Otol Neurotol Off Publ Am Otol Soc Am Neurotol Soc Eur Acad Otol Neurotol. 2002;23(4):473-475.
  6. Leffler S, Cheney P, Tandberg D. Chemical immobilization and killing of intra-aural roaches: an in vitro comparative study. Ann Emerg Med. 1993;22(12):1795-1798.
  7. Kiger JR, Brenkert TE, Losek JD. Nasal foreign body removal in children. Pediatr Emerg Care. 2008;24(11):785-792; quiz 790-792. doi:10.1097/PEC.0b013e31818c2cb9.
  8. Kadish HA, Corneli HM. Removal of nasal foreign bodies in the pediatric population. Am J Emerg Med. 1997;15(1):54-56.
  9. Tahir N, Ramsden WH, Stringer MD. Tracheobronchial anatomy and the distribution of inhaled foreign bodies in children. Eur J Pediatr. 2009;168(3):289-295. doi:10.1007/s00431-008-0751-9.
  10. Rempe B, Iskyan K, Aloi M. An Evidence-Based Review of Pediatric Retained Foreign Bodies. Pediatr Emerg Med Pract. 6(12).
  11. Digoy GP. Diagnosis and management of upper aerodigestive tract foreign bodies. Otolaryngol Clin North Am. 2008;41(3):485-496, vii – viii. doi:10.1016/j.otc.2008.01.013.
  12. Loren Yamamoto, Inaba A, DiMauro R. Radiologic Cases in Pediatric Emergency Medicine; University of Hawaii. Radiol Cases Emerg Med. http://www.hawaii.edu/medicine/pediatrics/pemxray/zindex.html. Accessed February 20, 2015.
  13. Painter K. Energizer makes button battery packages safer for kids. USA Today.
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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.