How to manage wheeze in preschool children (ages 1 to 5 years)

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at NSU

Asthma is the most common chronic respiratory disease, affecting up to 10% of adults and 30% of children (90% of patients with asthma have allergic rhinitis, 30% of patients with allergic rhinitis have asthma).

Key points

Preschool wheeze should be divided into:

- “episodic viral” wheeze (EVW) - triggered by URIs
- “multiple trigger” wheeze (MTW) - triggered by URIs but also exercise, smoke and allergen exposure

These 2 phenotypes can change within an individual over time.

Wheeze Phenotypes in Preschool Children (click to enlarge the image):



Lower respiratory tract illnesses with wheeze are common, occurring in 30% of all preschool children (defined as aged between 1 and 5 years).

No treatment prevents progression of preschool wheeze to school age asthma, so treatment is driven solely by current symptoms

In all but the most severe cases, episodic symptoms should be treated with episodic treatment.
If trials of prophylactic treatment are contemplated, they should be discontinued at the end of a strictly defined time period because many respiratory symptoms remit spontaneously in preschool children.

Oral steroids (prednisolone) are not indicated in preschool children with attacks of wheeze who are well enough to remain at home and in many children, especially those with episodic viral wheeze, who are admitted to hospital.

What is wheeze?

The term wheeze is often used imprecisely. Some languages do not even have a word for wheeze. Wheeze is a high pitched whistling sounds associated with increased work of breathing. Studies have shown that physicians auscultating the chest accurately identify wheeze; parents and nurses were much less reliable.

Here is what wheezing sounds like (click to play the embedded video):



How common is wheeze in preschool children?

Preschool wheeze is very common: 26% of infants have at least one episode of wheeze by the age of 18 months.

Early aeroallergen sensitization is predictive of ongoing symptoms and loss of lung function at school age.

Is this wheeze asthma?

This question is commonly asked by parents. What most parents actually want to know is whether their child will go on with symptoms and the need for treatment into school age and beyond. Severe preschool wheeze which is multiple trigger wheeze is associated with more airflow obstruction and airway pathology (eosinophilic inflammation and remodeling) similar to childhood and adult asthma.

Does preschool wheeze lead to asthma?

Several clinical predictive indices for future risk of asthma have been developed based on:

- atopic manifestations
- indirect evidence of airway inflammation, such as peripheral blood eosinophil count
- severity of preschool wheeze

All predictive indices have a high negative predictive value and a poor positive predictive value (typically positive predictive values 44-54, negative 81-88).

Children who have only episodic viral wheeze (EVW) have no increased risk of atopy or respiratory symptoms in the long term once they reach the age of 14.


Modified Asthma Predictive Index (mAPI) (click to enlarge the image). A positive mAPI greatly increased future asthma probability (eg, 30% pretest probability to 90% posttest probability) http://buff.ly/ZJfMgQ

Can we prevent preschool wheeze progressing to school age asthma?

No. Early use of inhaled corticosteroids does not affect progression of disease. There are no disease modifying drug treatments. Treatment should solely be focused on current symptoms.

What are the treatment strategies for children with preschool wheeze?

- ensure that the home environment is optimal - not exposure to tobacco smoke; parental smoking “not in front of the children” does not protect them from harm

- no drug strategies reduce future risk of asthma

- if inhaled drugs are prescribed, repeated education of the parents in the correct use of spacers is essential. If inhaled drugs in particular do not seem to be working, check that they are being properly administered rather than escalate treatment

How to treat episodic viral wheeze?

Intermittent symptoms should be treated with intermittent therapy (and in practice this is likely to be what parents do anyway).

As needed use: A trial of montelukast in preschool children with troublesome viral induced wheeze is worth attempting (evidence is mixed). Start treatment at the first sign of a viral cold and discontinuing it when the child is clearly better, rather than for a fixed period of days.

How to prevent wheezing?

Regular nebulized budesonide does not prevent viral exacerbations of wheeze. No evidence to support the use of inhaled corticosteroids in children with episodic viral wheeze.

I would be unwise to go above a fluticasone dose of 150 µg twice a day, given the number and duration of viral colds in normal preschool children and the risk of side effects including growth suppression and adrenal failure with higher doses.

No evidence to support the use of regular inhaled corticosteroids in preschool children who do not wheeze between viral colds.

However, in those children with severe episodic wheeze who require repeated admission to hospital or have prolonged disruptive symptoms managed at home, a trial of prophylactic inhaled corticosteroids can be given for 6-8 weeks.

How should we treat multiple trigger wheeze (MTW)?

Step 1: Trial of inhaled corticosteroids or montelukast for a defined period, 4-8 weeks)

Step 2: Stop treatment.

Step 3: Restart treatment if symptoms recur; then reduce treatment to the lowest level that controls symptoms.

Algorithm for the diagnosis and management of early childhood asthma, JACI, 2012:



What about asthma action/treatment plans?

Treatment plans outline self management actions to be taken depending on the severity of symptoms and peak flow measurements and are widely recommended. Many physicians may recommend asthma action plans, but there is no evidence of efficacy in school age children.

Asthma Action Plans

- Asthma Action Plan, adapted by Dr. Dimov (PDF)
- Asthma Action Plan, with added common medications, not branded for a specific physician  (PDF)
- NIH generic Asthma Action Plan (PDF)



What is the role of nebulized therapy?

There is no role for nebulised therapy to deliver bronchodilator apart from in children too sick to use inhalers. For all other purposes, the evidence is clear that metered dose inhalers (MDIs) and spacers are at least as good as nebulizer, or better.

Nebulizers should not be used in preschool wheeze; inhaled drugs delivered by metered dose inhaler (MDI) and spacer are at least as efficacious.

If inhaled drugs in particular do not seem to be working, check that they are being properly administered rather than escalating treatment (videos demonstrating the correct technique are available from AllergyGoAway.com).

How to Use a Metered Dose Inhaler (MDI) (albuterol, Xopenex, Flovent, Symbicort, Dulera, Alvesco, Qvar). The three videos below show three techniques: with a spacer and without spacer. The videos are by the CDC.









Although several predictive indices for future asthma risk have been proposed, negative predictive value is excellent but positive predictive value is poor.

References

Managing wheeze in preschool children. BMJ 2014;348:g15. (Published 4 February 2014)
http://www.bmj.com/content/348/bmj.g15

Published: 02-05-2014
Updated: 02-07-2014

Difficult to control asthma in a child - what to do?

Author: V. Dimov, M.D.
Reviewer: S. Randhawa, M.D.

A 9-year-old African American girl with asthma diagnosed at age 15 months, and with a history of allergic rhinitis and atopic dermatitis is referred for evaluation. The atopic dermatitis has improved with age. She now has symptoms mostly during the winter. Her rhinitis is better controlled with the use of intranasal steroid, however her asthma has proved challenging to control. She has been diagnosed with asthma at age 15 months and she has been treated with inhaled steroids for the last several years, including Advair 115/21 for the last year. She still needs to use albuterol 3-4 times per day, including before exercise. Her symptoms are manifested by chest tightness and cough, not much wheezing, but definitely the chest tightness is one of her predominant symptoms. The triggers of her symptoms include infections, exercise and changes in weather. She has symptoms once to twice per week, including during the night once to twice a week and the last course of oral steroids was 5 months ago. She was never hospitalized with asthma and has no emergency room visits. She had spirometry done 5 months ago which showed FEV1 of 74%, which actually decreased by 10% with bronchodilator use. She had ImmunoCAP specific IgE testing for allergens and it was all negative apart from a positive to one of the trees, oak. She also complains of congestion and itchy eyes which are worse during the spring and fall, and snoring at night. She was evaluated with a sleep study which showed mild sleep apnea. They do not report a history of recurrent skin infections. She was treated with for a respiratory infection earlier this year with antibiotics and chest x-ray done years ago was negative.

Past medical history is positive for asthma, rhinitis and atopic dermatitis. Past surgical history is negative. She has no known drug allergies.

Family history is positive for mother with allergic rhinitis, sister with asthma and allergic rhinitis.

On social history, she is exposed to second-hand smoke from a neighbor in the apartment complex and also her father is a smoker. They have no pets at home. There is no carpet and no visible mold in the house.

On birth history, she was born via C-section. She was born at term and she was breast fed for a short period of time.

Her current outpatient prescriptions include Advair 115/21 one inhalation b.i.d. with Aero-Chamber, albuterol p.r.n., Pataday eye drops, Zyrtec and Nasacort one spray in each nostril daily.

Physical examination

HEENT examination showed some dry discharge in both nostrils and boggy turbinates which are mildly erythematous. Chest was clear to auscultation bilaterally. Cardiovascular system showed clear S1, S2. Abdomen was soft, nontender and nondistended. Extremities showed no clubbing, cyanosis or edema and skin showed mild lesions of atopic dermatitis on upper extremities.

Procedures: Skin prick test and spirometry. The skin prick test was negative to cat, dog, cockroach, dust mite, trees, grasses, weeds, ragweed and mold and had a good reaction to histamine. The size of the wheel was 6 x 6 mm. She had spirometry which initially showed FVC of 79% and FEV1 of 66%. FEV1 improved significantly with the administration of nebulized albuterol. There was an improvement of 19% in FEV1 from 1.47 L to 1.77 L, so the bronchodilation test was positive.

What is the most likely diagnosis?

This is a child with severe asthma, including night symptoms with inadequate response to Advair at the dose of 115/21. She does not provide a certain history of reflux disease, although she has some night cough, but no heartburn or metallic taste in her mouth. She has not been on Singulair in the past and we discussed the possibility of vitamin D deficiency or insufficiency in patients with severe asthma, and other comorbidities. She is not a likely candidate for the diagnosis of vocal cord dysfunction (VCD) as she does not have symptoms of VCD (voice change, etc.) during her asthma attacks. Her rhinitis is most likely nonallergic with negative skin prick test today and negative specific IgE 7 years ago, apart from the mild sensitization to oak. There is no history of food allergy. She has mild eczema which is easy to control with moisturizers.

What treatment approach would you suggest?

Considering that even with the moderate dose of Advair she did not have full control of her symptoms in the past and she needed to use albuterol 3-4 times a day, I would suggest a trial of a different combination of inhaled steroids and long-term beta agonist, namely Symbicort at a dose of 160/4.5 two puffs twice a day with an AeroChamber. The formoterol in Symbicort has some short-acting and long-acting bronchodilator effects and she may have better control of symptoms with that. Also, I would recommend adding Singulair 5 mg chewable tablet to her regimen and taking a multivitamin for the vitamin D component, 1 tablet p.o. daily. Considering that her skin prick was negative, I would probably discontinue cetirizine at this point. She, however, can continue to use the Nasacort at a dose of 1 spray each nostril twice a day to control her nasal inflammation, which is most likely due to nonallergic rhinitis at this point. I suggested followup in approximately 1-2 months for repeat spirometry to verify that these changes in her treatment have the desirable effect. If there is a suspicion for GERD, we can consider a PPI addition to the therapy at that point.

It is very important for her not be exposed to tobacco smoke. A 2012 study showed that when household members smoked, children had up to 70% higher risk of wheezing through age 4 (http://goo.gl/bTTyy).



Severe asthma - differential diagnosis and management (click to enlarge the image).

Related reading

Worldwide, 40% of children, 33% of male non-smokers, 35% of female non-smokers are exposed to second-hand smoke http://goo.gl/xFGef

Published: 07/12/2010
Updated: 01/12/2012

Severe asthma in children - differential diagnosis and management

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at NSU

Asthma is the most common chronic respiratory disease, affecting up to 10% of adults and 30% of children (JACI, 2011).



Severe asthma - differential diagnosis and management (click to enlarge the image). Related: Common Asthma-related Comorbidities. Medscape, 2011, (figure).

If asthma treatment is not working, check DAT:

- Diagnosis - not asthma at all (VCD, CF, FBA), asthma plus AR, GERD
- Adherence - compliance with medication - 24% of asthma exacerbations are attributable to ICS medication nonadherence (http://goo.gl/1i8ET). Poor adherence to asthma medications (less than 80%) was seen in 75% of children (JACI, 2011).
- Technique - NEB, HFA with spacer, DPI, etc.

3 C's of care - communication, continuity, concordance (finding common ground) are critical for asthma management (http://goo.gl/8gJM6).

Children who are referred to specialist care with asthma that does not respond to treatment (problematic severe asthma) are a heterogeneous group.

In many children with severe asthma, the diagnosis is wrong or adherence to treatment is poor. Therefore, the first step is a detailed diagnostic assessment to exclude an alternative diagnosis (“not asthma at all”), followed by a multidisciplinary approach to exclude comorbidities (“asthma plus”) and to assess whether the child has difficult asthma (improves when the basic management needs, such as adherence and inhaler technique, are corrected) or true, therapy-resistant asthma (still symptomatic even when the basic management needs are resolved). In particular, environmental causes of secondary steroid resistance should be identified.

Licensed therapeutic approaches include:

- high-dose inhaled steroids and LABA
- Symbicort maintenance and reliever (SMART) regimen (with budesonide and formoterol fumarate)- anti-IgE therapy

Unlicensed treatments include methotrexate, azathioprine, ciclosporin, and subcutaneous terbutaline infusions.

Pediatric data are needed on cytokine-specific monoclonal antibody therapies and bronchial thermoplasty.


Asthma Inhalers (click to enlarge the image).

Inhaled corticosteroid (ICS)

Relative binding affinity for glucocorticoid receptor (GR): mometasone > fluticasone > budesonide > triamcinolone.

Relative anti-inflammatory potency: mometasone = fluticasone > budesonide = beclomethasone > triamcinolone.

References

Management of severe asthma in children. Prof Andrew Bush MD, Sejal Saglani MD. The Lancet, Volume 376, Issue 9743, Pages 814 - 825, 4 September 2010.

Evidence-based asthma management in children — what’s new? MJA 2011; 194 (8): 383-384.
One in 20 children has severe asthma that doesn't respond to standard therapies. http://goo.gl/omDI

An approach to recalcitrant, severe asthma - AAAAI Ask the Expert, 2011.

Common Asthma-related Comorbidities. Medscape, 2011, (figure) http://j.mp/qJqwNY and http://j.mp/omHVc6

24% of asthma exacerbations are attributable to ICS medication nonadherence (http://goo.gl/1i8ET)

Single inhaler therapy in asthma (SMART) linked to poor day-to-day control of symptoms and increasing inflammation. Clin Exp Allergy. 2012 Jan 18.

Figures:



Published: 09/03/2010
Updated: 03/08/2013

Treatment of Pediatric Asthma

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at NSU

Asthma is the most common chronic respiratory disease, affecting up to 10% of adults and 30% of children (JACI, 2011).

Asthma pathogenesis

Dust mites play a major role in asthma pathogenesis.

Bronchial provocation with particles: dust mite fecal particles are 30 µm in diameter (same size as pollen grain). They do not stay airborne and do not cause allergic comjunctivitis. Pollen grains are airborne, have spicules and cause 90% of allergic conjunctivitis cases.

10% of inhaled pollen grains and mite fecal particles enter lungs. Dust mite fecal particles and pollen grains are 1000 times larger than penicillin spores. A single mite fecal particle will produce a small focus of inflammation in lung.

Not all wheezing is asthma

Wheezing occurrences in children:

- single episode in 30% to 50% of children before 5 yr of age
- 40% who wheeze before 3 yr of age continue at 6 yr (“persistent wheezers”)
- 50% of infants who wheeze once will wheeze again within several months


Wheezing in Children - Phenotypes (click to enlarge the image).

Childhood asthma phenotypes:

- transient early wheezers - wheeze sometime during first year of life; risk factors include prematurity, history of parental smoking during pregnancy, and passive exposure to tobacco smoke; such patients do not respond to inhaled bronchodilators or inhaled corticosteroids (ICS); wheezing tends to remit as child’s airway gets larger (between ages 2-3 yr)

- nonatopic wheezers - 0 to 6 yr of age; wheeze associated exclusively with viral infection; usually no eczema or family history; wheezing tends to remit by 6 yr of age

- atopic wheezers - past 5 yr of age, allergic - have positive blood and skin testing to inhalant allergens; tend to present within 2 to 3 yr of age, and continue to wheeze; wheezing not related to URTI



Childhood asthma phenotypes (click to enlarge the image).

A 2012 study described 2 "new" phenotypes for young children with wheezing: "boys atopic multiple-trigger" and "girls nonatopic uncontrolled wheeze". JACI, 2012.

Toward a definition of asthma phenotypes in childhood: early viral wheezers, multitrigger wheezers (MTWs), and nonatopic uncontrolled wheezers (NAUWs). Some children have “allergic bronchitis” rather than “asthma”. JACI, 2012.

Modified Asthma Predictive Index (API):

Children under the age of 3 with ALL of the following:

- 4 wheezing exacerbations in past year
- with one physician-confirmed episode
- plus one major criteria OR 2 minor criteria

Major criteria - 1 of the following:

- parental history (mother who had childhood asthma only, father with exercise-induced asthma)
- physician-diagnosed atopic eczema
-allergic sensitization to one aeroallergen

Minor criteria - 2 of the following:

- allergic sensitization to milk, eggs, or peanuts (positive skin or blood test sufficient)
- wheezing unrelated to respiratory illness (ie, cold)
- blood eosinophilia 4% of total white blood cell (WBC) count

Positive API = 10 times more likely to have persistent asthma.


Modified Asthma Predictive Index (mAPI) (click to enlarge the image). A positive mAPI greatly increased future asthma probability (eg, 30% pretest probability to 90% posttest probability) http://buff.ly/ZJfMgQ

mAPI relies heavily on wheezing. However, asthma can occur in children without wheezing.

Cough-variant asthma

Chronic, persistent cough - without wheezing - may be the only manifestation of asthma. More than 60% bronchial obstruction is needed to produce wheezing - asthma can occur without wheezing - spirometry is required for diagnosis.

Cough-variant asthma presents as dry cough at night. It worsens with exercise (EIA) and nonspecific triggers (cold air).

Cough-variant asthma responds to asthma therapy with ICS.

Cough-variant asthma is diagnosed with pulmo­nary function testing (PFTs) with response to bronchodilator.

The most common cause of chronic cough in children is cough-variant asthma.

Guidelines

National Heart, Lung, and Blood Institute (NHLBI) guidelines for diagnosis and management of asthma (2007) are only available online. Key concepts:

- severity dictates therapy
- distinction between intermittent and persistent asthma - "rule of 2s”
- 4 levels of asthma severity - intermittent; 3 sublevels of persistent
- inhaled corticosteroids (ICS) preferred for all levels of persistent asthma
- use of asthma action plans
- spirometry recommended

Rule of 2s - if symptoms are present for more than 2 days per week or for more than 2 nights per month, asthma categorized as persistent. Within this category, disease must be classified as mild, moderate, or severe. However, as severity of asthma not constant, must monitor patients for changes; as severity changes, therapy should change too.

The category of “mild intermittent” asthma was eliminated in the 2007 guidelines - now it is just called “intermittent” asthma.

The concepts of “impairment”, “risk”, and “control” were introduced in the 2007 guidelines:

- impairment - refers to symptoms
- risk - refers to likelihood that the patient will eventually have exacerbation of asthma and present to emergency department (ED) or hospital, or need course of oral corticosteroids
- control - refers to the level of patient’s asthma control

ICS therapy probably does not make difference in prevention of airway remodeling.

Classification of asthma severity:

- impairment domain - daytime and nighttime symptoms (rule of 2's), use of short-acting beta-agonist (SABA), interference with normal activities

- risk domain - number of exacerbations per year (if more than 2, daily controller medication is needed). Increased risk is conferred by parental history of asthma or history of eczema.

Childhood Asthma Control Test (ACT) is validated down to age 4 yr. Adult ACT questionnaire should be used for teenagers (cutoff age is 11 years).

Treatment steps:

- step 1 - SABA as needed
- step 2 - low-dose ICS monotherapy vs. leukotriene receptor antagonist (LTRA)
- step 3 - low-to-medium dose ICS plus long-acting beta-agonist (LABA)
- step 4 - high-dose ICS therapy plus LABA and (if needed) systemic corticosteroids. Omalizumab (Xolair; anti-IgE antibody) is prescribed before placing patient on daily oral corticosteroids.

"Rule of 2s” is used to determine level of control. If any of these are positive, consider a daily controller medication:

- daytime symptoms more than 2 days/wk
- rescue β2 -agonist use more than 2 times per week
- nighttime symptoms more than 2 nights/mo
- more than 2 asthma exacerbations per year
- more than 2 rescue β2-agonist canisters/yr

When to step down therapy?

If patient is well-controlled for 3 months, consider stepping down therapy.

When to step up therapy?

If the patient is not well-controlled, step up therapy and re-evaluate in 2 to 6 weeks. If the patient is very poorly controlled, step up therapy 2 steps, consider short course of steroids, and reassess in 2 weeks.

There was an increase in the use of preventive asthma medication from 18% in 1988–1994 to 35% in 2005–2008 among children with asthma (Pediatrics, 2012).

Which ICS to choose?

- delivery system best for patient’s developmental stage
- optimal lung deposition

Particle size may play a role in lung deposition of ICS - ciclesonide (Alvesco) has smaller particle size that results in good lung deposition.

When to consider long-term ICS treatment:

- positive API and more than 3 wheezing episodes in previous 12 mo lasting more than 1 day and affecting sleep

- consistent requirement for SABA treatment (more than 2 times/wk, on average, over 1-2 mo); 2 exacerbations in 6 mo requiring oral corticosteroids

As severity increases, increase ICS dose:

Children younger than 5

- budesonide inhalation suspension (Pulmicort Respules)
- fluticasone propionate (Flovent)
- mometasone tripattern inhaler (Asmanex Twisthaler)

Children 5 to 11 yr of age

- low-dose ICS (budesonide dry powder inhaler (DPI) or inhalation suspension (Pulmicort Respules)
- beclomethasone hydrofluoroalkane (HFA)
- add long-acting β agonist (LABA) or leukotriene receptor antagonists (LTRA)


ICS treatment options for pediatric asthma (click to enlarge the image).


Asthma Inhalers (click to enlarge the image).

Inhaled corticosteroid (ICS)

Relative binding affinity for glucocorticoid receptor (GR): mometasone > fluticasone > budesonide > triamcinolone.

Relative anti-inflammatory potency: mometasone = fluticasone > budesonide = beclomethasone > triamcinolone.



Severe asthma - differential diagnosis and management (click to enlarge the image).

Algorithm for the diagnosis and management of early childhood asthma, JACI, 2012:



References

New NHLBI guidelines for asthma: is anything really new? Michael J. Welch, MD. Audio-Digest Pediatrics, Volume 56, Issue 01, January 7, 2010.
Advances in pediatric asthma in 2010: Addressing the major issues. Szefler SJ. J Allergy Clin Immunol. 2011 Jan;127(1):102-15.
Immunopathogenesis of Asthma in Childhood. Thomas A.E. Platts-Mills. Audio-Digest Pediatrics, Volume 55, Issue 02, January 21, 2009.
Asthma management update. Hary T. Katz, MD. Audio-Digest Pediatrics, Volume 55, Issue 02, January 21, 2009.
The Asthma Predictive Index: A very useful tool for predicting asthma in young children. Jose A. Castro-Rodriguez. JACI, 2010.
Predicting the long-term prognosis of children with symptoms suggestive of asthma at preschool age. J Allergy Clin Immunol. 2009.
The Asthma Predictive Index: Not a useful tool in clinical practice. J Allergy Clin Immunol. 2010.
A clinical index to define risk of asthma in young children with recurrent wheezing. Castro-Rodriguez JA, Holberg CJ, Wright AL, Martinez FD. Am J Respir Crit Care Med. 2000;162:1403–1406.
Patterns of fetal and infant growth are related to atopy and wheezing disorders at age 3 years - Thorax http://goo.gl/UGB8a
Inhaled steroids can suppress growth of children who are 2 years of age weighing less than 15 kg (high dose per kg). AAAAI, 2011.
Compared with low doses, moderate doses of ICS may not have benefits in asthmatic children. Pediatrics, 2010. Doubtful conclusion.
Asthma Predictive Index not better than simple prediction based only on preschool wheeze? (performance was low for both). JACI, 2011.
Achieving control of asthma in preschoolers. CMAJ, March 9, 2010; 182 (4).
House dust mite sensitization in toddlers predicts wheeze at age 12 years (JACI, 2011).
Timeline of Major Advances in Treatment of Asthma from 1812 through 2012 - NEJM, 2012.

Published: 06/01/2010
Updated: 01/02/2014

Pediatric sinusitis

Author: V. Dimov, M.D., Allergist/Immunologist and Assistant Professor at University of Chicago
Reviewer: S. Randhawa, M.D., Allergist/Immunologist and Assistant Professor at NSU

Nasal physiology

Mucociliary clearance can be tested by placing saccharin on the inferior turbinate and timing the onset of sweet taste in the mouth. The normal range is 7-11 minutes.

There is normal asymmetry of nasal mucosa swelling, with one side of nose swollen as a result of dilatation of veins in the inferior turbinate and the other side "open" - 80% of the population exhibits a nasal cycle, with reciprocal changes in airflow over 1-2 hours.

Anatomy of paranasal sinuses

Sinus is a Latin word for “fold” or “pocket”. Paranasal sinuses have an embryogenic origin from the nasal passage and are an integral component of the airway. Drainage pathways of the sinuses are complex and can be blocked during inflammation. Ostia are the sinus openings in the nasal cavity. They are 2-6 mm wide.

Paranasal sinuses have an embryogenic origin from the nasal passage and are an integral component of the airway. Drainage pathways of the sinuses are complex and can be blocked during inflammation.

The outflow tract of the maxillary sinus is positioned high on medial wall, therefore intact mucociliary apparatus required to move mucus and debris from sinus into nose.

The ethmoid sinus consists of 3 to 15 air cells (on left and right sides), separated by thin bony partitions. Each air cell drains by tiny ostium into middle meatus and the ostia are easily obstructed during URI.

The frontal sinus develops from anterior ethmoid cell and achieves supraorbital position by 6 years of age. It is an uncommon site of infection in pediatrics.

The sinus ostia are the drainage routes for paranasal sinuses - because of their small diameter (1.0-2.5 mm), they are easily occluded by mucosal inflammation. This is is similar to the blockage of Eustachian tube that can lead to otitis media.

How large are the ostia of the sinuses?

The size of ostium of the maxillary sinus is 2.5 mm, the ostia of the other sinuses are smaller - in the range of 1 mm.

Location of the openings of the sinuses

- Inferior meatus - opening of nasolacrimal duct.
- Middle meatus - frontal, maxillary and anterior ethmoids
- Superior turbinate - posterior ethmoids and sphenoid sinuses

Mnemonic

Sinuses listen to the following radio channels: FM AM / PS SS

Frontal sinus, Maxillary sinus, and
Anterior ethmoids drain into Middle meatus
Posterior ethmoids and Sphenoid sinus drain into
Sphenoethmoidal recess above Superior turbinate

Sinusitis

Sinusitis of less than 4 weeks’ duration is considered acute. Chronic sinusitis persists for more than 4 weeks.

Recurrent sinusitis is defined as 4 or more episodes of sinusitis per year. Each episode lasting 7-10 days and no symptoms during intervening periods. Sinusitis is mostly preceded by rhinitis and is rarely found without rhinitis.

The 1997 Rhinosinusitis Task Force thus proposed the term Rhinosinusitis instead of Sinusitis (reiterated in 2007 guidelines).

Diagnosis

The diagnosis is clinical most of the time.

Radiographic findings suggestive of acute sinusitis:

- diffuse opacification - most common finding in children with acute bacterial sinusitis
- mucosal swelling greater than 4 mm
- presence of air-fluid level - may not occur in children

Maxillary sinus aspiration recovered bacteria from 75% of children with abnormal radiographic findings (Wald et al, 1981).

History of persistent upper respiratory symptoms predicted abnormal findings on radiographs in 88% of children younger than 6 yr of age and in 70% of children older than 6 yr of age (Wald et al, 1986).

The frequency of bacterial sinusitis peaks by 6 years of age.

According to the current guidelines, the diagnosis of acute bacterial sinusitis does not require radiographic imaging in children younger than 6 yr of age with persistent upper respiratory symptoms. The diagnosis is based on clinical findings only. There is no consensus about the need for imaging for children older than 6 yr of age with persistent symptoms and for all children with severe or worsening symptoms.

Do you need an X-ray to diagnose sinusitis in children?

Acute sinusitis in children is likely if the symptoms persist for tnan 10 but less than 30 days and they are not improing. This predicts abnormal X-ray in 88% of children yonger than 6 years. They can be treated with an antibiotic withouth an X-ray.

The "story" is different in children older than 6 years - 30% of them had a normal X-ray and this group may not need an antibiotic. Only 75% of children with abnormal X-rays had a positive bacterial sinus aspirate.

Sinus Imaging for Diagnosis of CRS in Children - plain radiography has limited utility - CT and MRI have a major role (http://goo.gl/cNHHK).

Pathogens in pediatric sinusitis

From aspiration of maxillary sinus ((Wald et al, 1981):

- Streptococcus pneumoniae, 30% to 40%
- Haemophilus influenzae, 20%
- Moraxella catarrhalis, 20%
- Streptococcus pyogenes (group A streptococci), 4%
- no bacteria recovered from 25% of samples

The widespread use of pneumococcal vaccine has resulted in changes in prevalence. The recent data is from tympanocentesis studies of children with acute otitis media and showed decreased rate of infection with S pneumoniae and increased rate of infection with H influenzae. The data can be extrapolated to sinusitis - some ENTs consider the middle ear "a paranasal sinus."

Antibiotic resistance

- 35% of isolates of H influenzae and 100% of isolates of M catarrhalis are resistant to b-lactam antibiotics
- 25% to 50% of isolates of S pneumoniae resistant to penicillin (half are highly resistant)

"Plain old" amoxicillin will not help in those cases.

Treatment of Acute Sinusitis

Recommendations form the current guidelines

For children with uncomplicated mild to moderate acute bacterial sinusitis without risk factors (age less than 2 yr; recent use of antibiotics; attendance at daycare), give amoxicillin or amoxicillin-clavulanate, 45 to 90 mg/kg per day (in 2 divided doses).

In acute sinusitis in children, you often have to use high dose amoxicillin (90 mg per kg) - 45 mg per kg is not helful because of resistance.

In penicillin allergy, you can use cefdinir, cefuroxime, or cefpodoxime for children with mild allergy; clarithromycin or azithromycin for children with type-1 hypersensitivity (but these have low activity against Haemophilus).

If there is no effect within 72 hr, consider increasing dose of amoxicillin-clavulanate to 80 to 90 mg/kg per day (2 divided doses).

Amoxicillin-clavulanate to 80 to 90 mg/kg per day should be used in:

- patients who do not improve within 72 hr

- those who have recently received antibiotics

- moderate to severe disease

These higher doses achieve concentration needed to eradicate most highly-resistant S. pneumoniae

How long should you treat with an antibiotic?

The minimum ciurse is 10 days. A simple rule is to treat until the patient becomes symptom free plus 7 more days.

When to change the antibiotic?

If children are treated with an antibiotic, they should start to get better within 48 hours, and should feel substantially better within 72 hours. If they do not feel better within 72 hours (3 days), you either got the wrong diagnosis or the wrong antibiotic. It is reasonable to start with amoxicillin/clavunate, and if there is no effect within 72 hours, switch to cefpodoxime.

What is the role of corticosteroids nose sprays?

Some studies show modest benefit of intranasal corticosteroids. Intranasal decongestants (eg, oxymetazoline form 3 days) or saline irrigation may be useful.

References


Pediatric sinusitis. Ellen R. Wald, MD. Audio-Digest Pediatrics, Volume 55, Issue 14, July 21, 2009.
Acute and Chronic Rhinosinusitis: Practical Clinical Treatment Strategies. Nancy Otto, PharmD. Medscape, 11/2008.

Sinusitis Practice Guideline Aims to Improve Diagnosis, Cut Antibiotic Use. AFP, 2007.
Antibiotic Treatment for Rhinosinusitis - Levofloxacin recommended for children with penicillin allergy? Medscape, 2012.

Related reading


FIT Corner Questions. Chapter 78 of the 6th edition of Middleton’s Allergy Principles and Practice, edited by N. Franklin Adkinson, et al. September 27, 2006. Chapter 78: Nasal Polyps and Sinusitis.

Humming increases airflow between the sinus and nasal cavities, which could protect against sinus infections. NYTimes, 2010.

Frequent otitis media during infancy linked to atopic dermaitis and asthma in later life. Medscape, 2010.

Unlike otitis media, visit rate for acute sinusitis among children did not decrease after pneumococcal conjugate vaccine, Pediatrics, 12/2010. http://goo.gl/gkwYm

Pediatrics and Medicine

The best price for azithromycin is at Costco: 18 tablets for $18.
SNOT-16 Assessment Tool for Acute Sinusitis takes 5 minutes - copyright protected by Washington University. Medscape, 2011.
Intranasal Treatment for Clogged Ears: ears are connected to the back of the nose via a tunnel called Eustachian tube. http://goo.gl/2XwD9
Mnemonics for sinusitis: PODS and C-PODS (end of PDF here)

Published: 05/29/2010
Updated: 03/30/2012