TOW #45: Lymphadenopathy

This week’s topic is a review of lymphadenopathy and how to characterize those lumps and bumps that parents worry about (and us too!). Interesting fact of the day: there are about 600 lymph nodes in the body! One of the fascinating zebras on the differential for lymphadenopathy is Kikuchi disease, a necrotizing lymphadenitis, recently reviewed in an excellent morning report by R3 Josiah Peterson MD PhD.

The teaching materials for the week:

Take-home points on lymphadenopathy:

  1. What’s the definition of lymphadenopathy? Abnormality in size, number, or consistency of lymph nodes (whereas lymphadenitis is an inflammatory or infectious enlargement of lymph nodes). Lymph nodes are normally up to 1cm in the axillary and cervical regions and up to 1.5cm in the inguinal region. “Shotty lymphadenopathy” refers to multiple small, mobile lymph nodes resembling birdshot (~2mm) or buckshot (~8mm) under the skin. This is a common, self-limited finding in children under five typically during viral illnesses. Any node >2cm should be considered abnormal. Generalized lymphadenopathy refers to two or more noncontiguous sites of lymph node enlargement.
  2. Why lymph?: An “ultrafiltrate” of blood, lymph carries immune cells in lymph capillaries through the entire body except the brain and heart. The bone marrow and thymus are the primary lymphoid organs because they generate B and T lymphocytes. Secondary lymphoid organs are lymph nodes, spleen, and mucosa-associated lymphoid tissue (MALT), including the tonsils, appendix, and Peyer patches of the ileum. Because young children’s immune systems are actively developing, we commonly feel enlarged lymph nodes.
  3. What’s on the differential diagnosis? The broad categories are infectious, immune disorders, and malignancy. Under age 5, we know cervical lymph nodes are almost always infectious-don’t forget scalp and dental sources. Supraclavicular nodes are always abnormal, most commonly caused by lymphoma, mycobacterial infection, or sarcoidosis. Generalized lymph node swelling is more likely to be systemic infection (viruses, including EBV, CMV, HIV, syphilis or toxoplasmosis), but also may be a sign of malignancy or autoimmune disorders.
  4. What are key parts of history and physical exam? Ask about systemic symptoms, including fever, weight loss, night sweats, poor appetite, and fatigue. Ask about the time course, and change in the size or number of lymph nodes. Review exposure to insects, animal contacts, travel, and immunizations. Determine locations of lymph nodes, whether unilateral versus bilateral, soft versus hard, mobile versus fixed, and tender versus non-tender. Focus the rest of the exam on chief complaint/symptoms. More worrisome signs for malignancy include hard/ rubbery, immobile, persistent and non-tender lymph nodes (though malignant ones can also be tender).
  5. When should we do a work-up and what should it include? If nothing suggests malignancy, observe for 2-4 weeks, then follow-up. If not resolved, work-up would include viral serologies and CBC, ESR and CRP. Additional testing is done based on history (e.g., Bartonella henselae PCR when concerns for cat scratch, or TB testing for patients at risk). When there is concern for malignancy, including prolonged duration, location, large or increasing size, abnormal texture, and/or the presence of constitutional symptoms, we should refer for biopsy and obtain CXR to look for mediastinal lymphadenopathy.

TOW #43: Seasonal allergies

May is designated National Asthma and Allergy Awareness Month. The pollen currently covering my car is definitely one indication it’s spring and allergy season! Indeed, many among us are suffering from the season’s blooms.

Materials for this week:

Here are take-home points about evaluating stuffy nose/allergic rhinitis:

  1. How many people are affected by allergic rhinitis? Allergic rhinitis (AR) is considered among the most common chronic diseases in children, with a prevalence of up to 40%. As with other atopic disease, prevalence of AR has increased rapidly in the past 30 years. Children who have one form of atopy (allergic rhinitis, asthma, eczema) have a 3x greater risk of developing a second. The mean age of onset in one study was 10 years; by 6 years, 42% had been diagnosed with AR.
  2. What is the clinical definition or AR? Rhinitis is defined as “Inflammation of the membrane lining the nose, characterized by nasal congestion, rhinorrhea, sneezing, itching of the nose and/or postnasal drainage.” AR is a hypersensitivity reaction to allergens due to IgE. Intermittent allergic rhinitis involves symptoms <4 days per week or for <4 weeks. Persistent symptoms occur >4 days per week for >4 weeks. It’s often tricky to evaluate relative to viral-induced symptoms, given there is so much frequency of both, but with AR, itching of nose and eyes is more prominent, rhinorrhea is clear.
  3. What do we see on physical exam? Nasal turbinates may appear edematous, with a pale to bluish hue. Cobblestoning from lymphoid hyperplasia may be seen on the posterior oropharynx. “Allergic shiners” are dark discolorations underneath the eyes due to venous engorgement and suborbital edema. Dennie-Morgan lines are folds under the eyes due to edema. The “allergic salute” is a transverse nasal crease in children who chronically push their palms upward under their noses (to wipe mucus)-(and they really happen – last year my daughter developed one of these!)
  4. What’s the appropriate work-up? You may decide to do skin testing to evaluate specific allergens and aid in environmental control strategies, such as for dust mites. Skin testing is preferred to blood testing, but is not 100% specific and requires clinical correlation with symptoms/triggers.
  5. How do we manage AR? Treatment options are allergen avoidance, pharmacotherapy, and immunotherapy (reserved for severe cases). Best medication class is intranasal steroids, which is approved for kids >2. Next best are non-sedating antihistamines (not as good at decreasing nasal congestion, specifically) or leukotriene receptor antagonists. Sometimes people develop tolerance to one group, so switching drugs can help. Decongestants are not recommended for young children due to side effects and rebound symptoms, and are only occasionally used in older children.

TOW #42: Sleep disorders

This week we broaden the topic for sleep problems beyond the newborn period. There are plenty of sleep-challenged toddlers through teens out there!


Take-home points for pediatric sleep problems:

  1. Epidemiology: In community surveys, 25% to 50% of preschoolers and up to 40% of adolescents experience sleep-related problems. These are common problems so it pays to know them well!
  2. Sleep duration varies by age and by person: There is individual variation in need for sleep, but generally, newborns sleep 16-20 hours and most can sleep longer stretches (4-6+ hour stretches) by 3-6 months. Infants sleep 13 to 15 hours, 2 to 5 year olds sleep 11 to 12 hours, school-age kids sleep 10 to 11 hours, and adolescents ideally 9 hours. Most children drop their naps before age 4 (give or take). Remember, sleep duration includes both daytime and nighttime sleep added together. After babies are about 6 months old, the natural rhythm of sleep follows a 70-100 minute cycle through deep sleep/REM/arousal.
  3. What are common sleep problems at different ages? One of the most common for toddlers is nighttime waking. For many young children, transitioning between sleep stages leads to a fully awake state. Combined with the developmental phase of separation anxiety and fear of the dark, this can increase nighttime demand for the parent. Gradual removal of the parent role in returning to sleep will lead to improved sleep habits. For teenagers, their circadian rhythm shifts and can shift their natural bedtime, often about 2 hours later –  a common problem is disrupting sleep drive with light stimulus from phones and devices. Sometimes teens compensate with long afternoon naps that diminish their sleep drive at night. Strategies include removing devices an hour before bed, not taking naps, avoiding caffeine in afternoon/evening, and trying to stick to a regular bedtime and wake-up within an hour of usual time.
  4. Sleep routines and sleep environment help with regular sleep: A consistent schedule is one of the most important parts of sleep routine. Dr. Canapari recommends keeping it simple enough that one parent can do alone. Use the 3 or 4 “Bs for bedtime”: (Bath), Brush, Book, Bed. (In our house, we added “Ballads” and include nighttime songs.) Environment: quiet, low nightlight, cool, and definitely no TV or other devices. Consider a fan or white noise machine, which can help with sounds in the house or outside (especially in our urban environment!).
  5. What are important issues we screen for? Ask about Bedtime “BEARS”: Bedtime problems, Excessive sleepiness, Awakenings at night, Regularity and duration, and Snoring. If you can only do one, ask about snoring to screen for obstructive sleep apnea (OSA). The articles above review diagnostic criteria of specific disorders. When concern for OSA, or other sleep disorder that is interfering with function, consult with a sleep specialist. Our own SCH sleep clinic experts provide handouts and info here.

TOW#36: Short stature

This week we review another very relevant growth topic, short stature, that may cause disproportionate parental concern. Let’s review definitions and most common causes/ concerning findings related to evaluation of short stature.

Materials for this week:

Take-home points for short stature in childhood:

  1. Epidemiology: Most short stature represents familial short stature or constitutional growth delay. Incidence of growth hormone deficiency is pretty rare at 1 in 4,000 to 10,000 short children.
  2. What’s the clinical definition of short stature?: Short stature refers to a child who is 2 standard deviations below the mean height for age and sex (<3rd percentile).
  3. What are patterns of growth with familial short stature and constitutional growth delay? Familial short stature typically follows a pattern of proportional wt/ht growth along a curve below normal that starts before age 3, but with a normal bone age and, ultimately, shorter adult height. Children with constitutional growth delay (“late bloomers”) also slow down before age 3, but follow a normal rate of growth around 5th percentile and catch up later. They often have delayed puberty and below-normal bone age, but ultimately adult height in the normal range. Use mid-parental height to determine what is expected height growth (most children are within 10cm of mid-parental height).
  4. When to do a work-up? Work-up is recommended when the child’s height deficit is severe (<1st percentile for age), the child falls off the curve, especially after age 3 (more concerning for acquired growth hormone deficiency), the growth rate is abnormally slow (<10th percentile for bone age), predicted height differs substantially from mid-parental height, or body proportions are abnormal. Work-up includes bone age x-rays, may include labs (if suspicious for another diagnosis: CBC, ESR, renal function, calcium, phosphorus, TFTs, TTG antibody, sweat test, karyotype, IGF-1, IGFBP-3), referral to endocrinologist.
  5. How do we treat? Most children with short stature can be observed and offered reassurance. Evidence is lacking that short stature causes psychological harm or that there is a long-term psychosocial benefit with growth-enhancing therapy. In a few children who are very short, hormone treatment may be helpful. Human growth hormone treatment increases the growth rate, modestly increases adult height, and is mostly considered safe, but it is expensive (~$50K per inch of height!) and the long-term risk:benefit ratio for essentially healthy children remains unclear. Low-dose oral oxandrolone is a relatively inexpensive option to accelerate growth, but has not been shown to increase adult height. It’s important to support children who may be smaller than classmates; some may need extra help coping with differences based on size.

TOW #35: Urinary incontinence / enuresis

Next week we cover another bread and butter topic in gen peds – urinary incontinence, especially during sleep, which is termed “enuresis.” Below I try to digest some of the notably esoteric-sounding definitions from the International Children’s Continence Society (ICCS), which is the main organization that deals with related diagnoses in children. Understanding differences in degree and type of enuresis helps with determining appropriate treatment. Big take-aways are the importance of treating underlying constipation, being aware of other lower urinary tract symptoms, and associated behavioral diagnoses like ADHD.

Materials for this week:

Take-home points on enuresis:

  1. What are the definitions of incontinence and enuresis? Urinary incontinence is the involuntary leakage of urine, which can be continuous or intermittent and can occur during the day or at night. Generally, urinary incontinence is not considered pathologic until a child reaches age 5 years, according to the DSM-5. Enuresis refers to intermittent incontinence that happens while the child is asleep (mostly at night but can also happen with daytime naps). Lower urinary tract (LUT) symptoms should be assessed (frequency, urgency, hesitancy, dysuria, etc). Primary monosymptomatic nocturnal enuresis (PMNE) is defined as “lifelong continuous enuresis without any other history of lower urinary tract symptoms and without a history of bladder dysfunction.” Children with enuresis and any LUT symptoms have nonmonosymptomatic enuresis (NMSE) (This was formerly called diurnal enuresis). Recent stressors, UTI, and constipation can all lead to secondary enuresis, which is enuresis occuring after a period of regular bladder control.
  2. How many children are affected by bedwetting? What are other associated conditions? 15% of children will have primary monosymptomatic nocturnal enuresis (PMNE) at age 6 years, but only 1% to 2% of adolescents will continue to have wetting by the late teen years. About 1/3 of children who have bedwetting 2 or more nights per week also have daytime urinary symptoms (thus classified as NMSE). Children with enuresis have a ~20% to 30% incidence of comorbid behavioral conditions, such as ADHD, oppositional defiant disorder, and conduct disorder.
  3. What screening questions can distinguish type of enuresis? Ask about whether patients have 1) been previously dry for 6 months, 2) have daytime urine control issues, 3) constipation or fecal soiling, and/or 4) severe recent stress.
  4. How do we treat primary nocturnal enuresis (PMNE)? We are seeking to treat 3 primary physiologic disturbances involving the kidney, brain, and bladder: nocturnal polyuria, diminished sleep arousal, and reduced nocturnal bladder capacity or bladder overactivity. As far as fluid intake, a good guideline is to drink two thirds of daily fluid during school, and then one-third of the fluid in the afternoon/ evening, with no fluid an hour before bed. Children should go to the bathroom before bed and anytime they wake up. The bedwetting alarm is 1 of 2 first-line treatments recommended by the ICCS, and has the best long-term outcomes. It helps by improving arousal from sleep. Effective bed alarms use vibratory or auditory stimuli or both. Some experts believe the auditory alarms may be more effective because they alert parents as well. The alarm should be used consistently, and the child should be motivated to participate. Oral desmopressin (DDAVP) is the other first-line treatment, with caution used because of hyponatremia (intranasal is no longer recommended due to more severe hyponatremia). If used, limit fluid consumption in evening (ICCS suggests 200mL) starting 1 hour before the medication is given and until the child wakes the next morning. Long-term use does not seem to be harmful, but many of the guidelines suggest trial off the medication every 3 months to see if the child still needs it.
  5. How do we treat NMSE? Treatment includes addressing 1) Underlying constipation or fecal incontinence, 2) LUT dysfunction and daytime voiding symptoms, 3) Behavioral conditions. Urotherapy is recommended for LUT symptoms, which involves parent and patient education on normal elimination habits and a structured behavioral program to improve bladder and bowel function. A 48-hour daytime frequency and volume chart over a weekend period is recommended to provide more details to evaluate LUT dysfunction.

TOW #33: Eating disorders

This week’s topic is Eating Disorders, in recognition of National Eating Disorders Awareness week. This is a tough diagnosis for multiple reasons. Thankfully we have our wonderful adolescent medicine colleagues locally to provide expert guidance on this topic, so help is close by.

Materials for this week:

Take home points to review about Eating Disorders:

  1. Epidemiology: Once thought of as primarily a problem for white upper middle class females, unfortunately, the number of males and minority tweens/teens of both genders with disordered eating has increased in recent years, with up to 14% meeting criteria for disordered eating NOS. About 0.5% of female adolescents are diagnosed with anorexia and 1.5% with bulimia. Teens are particularly high risk during times of transition, and also in highly competitive athletics.
  2. Clinical definition: Eating disorders involve dysfunctional eating habits (may include restrictive eating and binge/purging), weight changes, and body image distortion with intense fear of gaining wt. Suspect in patients who fail to maintain weight in adolescence (especially concerning if <85% of ideal body wt, IBW), or who have amenorrhea, cold intolerance, constipation, headaches, fainting or dizziness. Ask about satisfaction with weight, efforts to control weight, exercise, and changes in diet. The female athlete triad is defined by low energy with or without eating disorder, hypothalamic amenorrhea, and osteoporosis. (DSM-5 criteria are in Tables 1 & 6 in the Peds in Review article).
  3. Physical exam: Some patients have normal exams, and patients with bulimia may have normal weight. Vital sign changes are important including bradycardia, hypothermia, and orthostatic changes. Skin findings may include acrocyanosis, lanugo, peripheral edema, and muscle atrophy. “Russell sign” is callus/abrasion over the MCP/PIP joints from tooth scraping while inducing vomiting. Also look for worn tooth enamel and salivary gland enlargement from purging.
  4. Work-up: Review wt trajectories/changes, and compare weight to median BMI (50th percentile BMI for age on growth chart, which is the ideal body wt). The current weight is divided by the IBW. In primary care it is more important to diagnose medical complications of eating disorders and refer for psychological management. Labs to consider initially are BMP (electrolyte, BUN, glucose abnormalities), ESR (to rule out systemic inflammation), and CBC (assess for malignancy/anemia).
  5. Management: Eating disorders represent complex physical and mental health disorders with high mortality rates. Refer to adolescent medicine for multidisciplinary care. If acutely ill/worsening, determine if patient meets criteria for inpatient admission in consultation with adolescent specialists (see AAP guidelines for hospitalization in Table 4 of this review). Provide regular follow-up as PCP for overall health/support and encouragement to engage in treatment. SSRIs may be considered for concurrent depression/anxiety, especially with bulimia.

TOW #32: Heart murmurs

February is Heart Month. In honor of Valentine’s Day this week, we will do a heart-related topic and review one of the biggies in evaluating pediatric hearts: assessing heart murmurs!

Materials for this week:

Take-home points for heart murmurs:

  1. What do typical innocent murmurs sound like? These are typically vibratory (or musical), of low intensity, and best audible at the left-sternal border (LSB). They are usually midsystolic—never purely diastolic—and nonradiating. Their intensity varies with position-typically loudest lying down and decreased while sitting up. Innocent murmurs (like pathologic ones) are louder with fever, anemia, or any increased cardiac output. The two most common innocent murmurs are Still’s murmur (typically early systole vibratory “twangy” murmur at LLSB most common in ages 2-6) and pulmonary outflow murmurs (mid-systolic crescendo-decrescendo murmur at LUSB).
  2. What murmurs are loudest at LLSB and LUSB? At the left lower sternal border (LLSB), we are usually dealing with Still’s murmur but the most common pathologic murmur to consider is VSD – typically holosystolic and may radiate more than Still’s. Murmurs loudest at the LUSB: usually pulmonary outflow murmurs, but also consider supraclavicular murmur (also innocent) or ASD or pulmonary stenosis.
  3. What are two continuous murmurs? Common continuous murmurs in childhood are venous hum and PDA. Venous hum is an innocent murmur heard on the low anterior part of the neck lateral to the sternocleidomastoid muscle, but can extend below the clavicle (usually on the right). It is usually louder during diastole and while the patient is upright. PDA is the classic “machinery” like murmur heard most often during S2 over the second left intercostal space, or in the left infra- or supraclavicular region.
  4. What clinical features are suggestive of pathologic murmurs? Murmurs with long duration (pansystolic/holosystolic), greater intensity (grade≥3), and harsh quality are more suggestive of cardiac lesion/defect. Be concerned about murmurs in the setting of decreased exercise/activity tolerance, palpitations, chest pain, syncope, or a family history of congenital heart disease, arrhythmias, or sudden cardiac death. A systolic murmur that gets louder with Valsalva is consistent with hypertrophic cardiomyopathy (due to reduction of venous return to the heart and resultant narrowing of the left ventricular outflow).
  5. What further evaluation of murmurs should we consider? To avoid unnecessary costs, most often it is helpful to directly refer a suspected pathologic murmur to a pediatric cardiologist for further workup. If you are going to a study first, an EKG has the lowest cost and may help identify some patients at risk.

TOW #31: Sick child

Many young children present with fever this time of year (indeed, it’s been record census at Children’s throughout recent weeks). We need to decide the degree of illness and appropriate disposition. This week’s topic is an opportunity to delve into this process and literature behind how we decide if a child is “sick or not sick.”

This week’s teaching materials:

Take-home points for identifying the sick child:

  1. What’s the frequency of febrile illnesses in young children?: Young children under 5 typically experience 3-6 febrile illnesses per year, and the likelihood of serious disease for these children is about 1-3%. The epidemiology of these illnesses has evolved over time with our immunization available and new viral testing available, as highlighted in this review in JAMA Peds.
  2. How do we make a diagnosis of serious illness?: Unfortunately, there is no identified set of signs and symptoms that definitively rule in or out a serious illness in all patients. In one review of 30 studies, high fever, cyanosis, rapid breathing, poor peripheral perfusion, and petechial rash were confirmed as warning signs for serious infection in children. The presence of cyanosis or poor peripheral perfusion raised the probability of severe illness from 1% to between 25% and 30%. Fever over 40 degrees C had a post-test probabillity of 5% for a serious illness. Parental concern was also identified as a strong red flag.
  3. How important is our “instinct” in these situations? Clinician instinct (“gut instinct”) is among the best performing assessments among clinicians when trying to determine whether a child has a serious illness. This skill develops over time. We can use active observation from the moment we walk in the room and throughout the visit. Experienced providers have been found to rely heavily on stimulus response information while assessing children with acute illness. Children with serious illness typically do not respond normally to age-appropriate activities or stimuli.
  4. Clinical Prediction Rules: In the study linked above comparing clinical prediction rules (CPRs), the best performing in a primary care setting was the Five Stage Decision Tree (FSDT), which uses the physician’s gut feeling, the patient’s age and temperature, and presence of dyspnea and diarrhea. The UK’s National Institute for Health and Care Excellence (NICE) Guideline on Feverish illness in children also did fairly well in ruling out serious illness.
  5. Finally, don’t forget to “phone a friend” in these situations – without doubt, I have found the insight of colleagues invaluable in assessing children I am concerned about, and helping make a plan.

TOW #30: Headache

Next week’s topic is headaches. Evaluating them in our patients can sometimes feel like they result in our own, so I am hoping a review of this topic can result in fewer for all involved. Our own local expert neurologist, Dr. Heidi Blume, wrote the Pediatrics in Review article, which is really comprehensive.

Materials for this week:

Take-home points for pediatric headaches:

  1. How many children report headaches? Depending on the study definition and time period, 17% to 90% of children report headaches, with an overall prevalence of 58% reporting some form of headache in the past year. By adolescence, girls report headaches more often than boys.
  2. What are the main types of headaches? Classifying the headache into one of 4 basic patterns helps with evaluation and diagnosis of the cause: 1) acute; 2) acute recurrent (or episodic); 3) chronic progressive; and 4) chronic nonprogressive. Most primary headache disorders are of an acute recurrent or chronic non-progressive type. Most concerning for something serious is the chronic progressive pattern.
  3. What are the red-flags for secondary headache from space-occupying lesions? Progressive pattern of severity or frequency; sleep-related headache, absence of family history of migraine, headache <6 months’ duration, change in headache type, confusion, abnormal neurologic findings, lack of visual aura symptoms, and vomiting.
  4. What work-up should be done? Neuroimaging should be considered in children who have abnormal results on neurologic examination, seizures, or red-flags by history. It should not be used routinely when there’s a normal neuro exam and recurrent headaches that are non-progressive. Some recommend using imaging for chronic headaches as a tool to reassure the patient and family, which may be therapeutic in and of itself.
  5. How should we manage headaches? Use SMART  as an acronym for headache management: regular S=sleep, M=meals, A=activity, R=relaxation & stress management, T=trigger avoidance. (See our expert Dr. Blume’s thorough review!) I really like Dr. Julie Bledsoe’s reminder to her patients when there are brain-related diagnoses: “we have to do the basics well” including sleep routine, nutrition, and physical activity. We can avoid triggers, and maybe even medications, through doing the basics well. When we do have to use medications for frequent headaches, it’s recommended to limit to one rescue and one prophylactic medicine, and to try to use rescue only 2-3 times per week to avoid medication rebound headaches. One option to consider for analgesia is Naproxen, which has longer duration and is not typically associated with rebound headaches.

TOW #26: Otitis media

Next week’s topic is otitis media, a quintessential topic year-round in pediatrics, but particularly during viral season. Indeed, we currently have an 8 yr old at home with recent URI and 24 hours of otalgia… at her request, pediatrician mom pulled out the trusty portable otoscope from med school last night (it’s gotten good use through the years!). Sure enough, a bulging, purulent TM with severe erythema… so how do we treat, and how does that vary by age group? Let’s review!

Materials for next week:

A few take-home points:

  1. How common is acute otitis media (AOM) and what are the pathogens? AOM is the most common condition for which medications are prescribed in children. Antibiotic stewardship has become an important goal in appropriately diagnosing and treating AOM. In the current vaccine era, S. pneumonia and non-typeable Haemophilus influenzae (H. flu) are now equally prevalent (~40-45%), followed by Moraxella catarrhalis (10-15%). Much less common are staph and group A strep. Viruses are also common and usually concurrent with the bacteria; in one study, 92% of AOM fluid had a bacteria, 70% had a virus, and 66% had both a virus and bacteria.
  2. What are the criteria to diagnose AOM? This has evolved somewhat through the years. The most recent guidelines have 3 main diagnostic components: 1) AOM is diagnosed in children who present with moderate to severe bulging of the tympanic membrane (TM) or new onset of otorrhea not due to acute otitis externa; 2) AOM may be diagnosed in children with “mild bulging of the TM” AND either “recent (less than 48 hours) onset of ear pain” (including rubbing, tugging, or holding in a nonverbal child) or “intense erythema of the TM;” 3) Diagnosis should NOT be made in children without middle ear effusion based on pneumatic otoscopy or tympanometry (we enhance the accuracy of diagnosis with pneumatic techniques especially for inconclusive visual findings). Studies have found a bulging TM has the highest predictive value for AOM, followed by a cloudy TM and impaired TM mobility. Note, slight redness of the TM does not indicate AOM, though moderate to severe erythema (including hemorrhagic) does correlate with AOM.
  3. How should we treat otalgia of AOM? Pain should be assessed with AOM, and we should provide clear guidance on how to manage it with oral analgesics. My daughter got a dose of ibuprofen last night (preferred at our house given the longer half life and dosing every 6 hours, and better taste of the generic brand compared to acetaminophen, per my kids’ taste buds!). It’s important to counsel that the ear pain may require scheduled pain medication for a day or two. We no longer have prescription topical otic analgesics on the market, as the prior medications were pulled by the FDA due to concerns about lack of safety and efficacy. To my knowledge, OTC otic analgesics (such as homeopathic or herbal remedies) have not been adequately studied to recommend them.
  4. When should we use antibiotics to treat? Antibiotics should be provided for children under 2 when AOM is diagnosed, unless it’s unilateral AOM and non-severe presentation (afebrile, mild otalgia), then we can use observation when jointly decided with parents. For children over 2 yo we can treat, or observe if they are non-severe, based on joint decision making. One recent RCT showed that middle ear effusion did indeed persist longer for children not treated (as above). For my daughter, given her age group and unilaterality, we are currently trying the watchful waiting approach and hoping for resolution (promising sign she slept well and had no complaints of pain this morning!). In her last bout a couple of years ago, after days of otalgia (pediatrician mom was stubbornly holding out), she had great improvement within 24 hours of starting antibiotics; it was a good reminder they really are warranted in some cases.
  5. What antibiotic treatment should we use? As pediatricians, we should probably be able to answer this in our sleep! High-dose amoxicillin (80-90mg/kg divided BID, up to 3g daily) remains the initial antibiotic of choice. Although beta-lactamase production is common among certain AOM pathogens (e.g., H. flu, M. catarrhalis), severe, invasive disease is often associated with Group A strep (susceptible to amox), or S. pneumoniae, whose resistance from penicillin-binding-proteins can be overcome by using high-dose regimens. Treatment duration is 10 days for children with severe disease or under 2 years of age. Shorter duration is appropriate for children >2yo with mild disease: 7 days in 2 to 5 years old, and 5-7 days in children over 5. We use amoxicillin-clavulanate (Augmentin, 90mg/kg/day divided BID) for children who either received amox in the past 30 days, have had recurrent infection unresponsive to amox, or have concurrent purulent conjunctivitis concerning for otitis-conjunctivitis syndrome (more likely non-typeable H. flu). If patients are allergic to penicillin, then we should choose a 2nd or 3rd generation cephalosporin (macrolides are not recommended), orally, or we can do 1-3 days of ceftriaxone IM (most respond to 1 dose, but there’s less treatment failure with 3).