ChapterPDF Available
CHAPTER
44
747
Functional Respiratory Disorders
Miles Weinberger, MD, FAAP
Manju S. Hurvitz, MD, FAAP
Mutasim Abu-Hasan, MD
Introduction
Functional respiratory disorders (FRDs) are characterized by symptoms
without medical explanation. Those likely to be encountered in children
include chronic cough, dyspnea, and dysfunctional breathing; other clinical
symptoms of FRDs include sighing, chest or throat tightness, and pain. Func-
tional respiratory disorders should not be considered diagnoses of exclusion.
They have recognizable characteristics that permit identication. Routine
investigation for all other causes of the same symptoms is usually not jus-
tied and only causes unnecessary testing and treatment. For each of the
FRDs discussed in this chapter, the unique presentation is described,
diagnostic criteria presented, and the treatment approach provided.
Habit Cough Syndrome
There are multiple causes of a chronic cough (Table 44-1). Habit cough is
an involuntary chronic cough without medical explanation. Terminology that
has been used for this disorder includes cough tic, psychogenic cough, and
somatic cough disorder. In considering these alternative terms, it is important
to understand that the symptom patients experience is obvious to an observer
as a cough, not a tic. While some patients might have a psychogenic basis,
there is little evidence to support that for most. Somatic cough disorder is
a general description, not a specic diagnosis. The term habit cough had
its origin in a 1966 publication by Boston allergist Bernard Berman, who
identied 6 children in his practice over a 5-year period who were cured
with “the art of suggestion.”15 A further advantage of the term is its
benignity in explaining the disorder to children and their parents.
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Table 44-1. Etiologies of Chronic Cough Among Diagnoses of 346 Childrena
Cause Percent of 346 children
Protracted bacterial bronchitis141.0
Asthma215.9
Spontaneous resolutions without diagnosis 14.0
Bronchiectasis39.0
Tracheomalacia46.1
Habitual54.3
Pertussis63.5
Aspiration72.3
Mycoplasma 1.4
Pneumonia80.9
Cystic brosis90.3
Primary ciliary dyskinesia10 0
Uvula impinging on epiglottis11 0
Tonsils impinging on epiglottis12 0
Achalasis13 0
Diuse panbronchiolitis14 0
Tuberculosis 0
aChang AB, Rober tson CF, van Asperen PP, et al. A multicenter stud y on chronic cough in children: burden
and etiologi es based on a standardized m anagement pathway. Chest. 2012;142(4):943–950.
The presentation is a repetitive cough, often occurring several times per
minute though with interpatient variability, classically harsh and barking,
and continuing for many hours that can include all waking hours. Habit cough
commonly follows a viral respiratory infection, a common cold. Caregivers
often describe an initial typical cough of a cold that changes after 1 to 2 weeks.
That description is present in a 1694 publication (Figure 44-1).16 It becomes
the repetitive barking cough characteristic of this disorder. The cough may
interfere with going to sleep, but a sine qua non of this disorder is the cough’s
total absence once the patient is asleep.15,17–19 Habit cough has continued to be
described in this manner since the Berman publication in 1966,15 sometimes
with different terminology but with the same presenting characteristics.15,17–22
Variations seen in one series found about 10% with a softer cough manifested
by a repetitive throat-clearing sound.18
Chang,
Robert son, et
al. is not in
Refs.
AUTHOR:
Why are
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table? The table
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correct?
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AUTHOR: You
already
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2 queries; I just
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Chapter 44 —Functional Respirator y Disorders
The median age of children with habit cough at several centers has been about
10 years with a range from 4 to 18 years.18,19 The prevalence of habit cough
at major referral centers has been an average of 7 per year at the University
of Iowa18 and 9 per year at the Brompton Hospital in London, England.19 An
example of the classic barking cough presentation can be seen and heard at
https://www.milesweinberger.com/copy-of-chronic-cough-1.
The diagnosis of habit cough is based on the unique presentation of the daily
repetitive cough that is absent once asleep. None of the other causes of chronic
cough in Table 44-1 have that characteristic presentation. Other proposed
causes of chronic cough are sinusitis,23 postnasal drip (aka upper airway cough
syndrome),24,25 and gastroesophageal reux,26,27 all of which diminish as legiti-
mate causes of chronic cough when critically examined. Although asthma
sometimes presents with cough, it rarely mimics the repetitive cough of
habit cough that is absent during sleep. Moreover, a short course of an oral
corticosteroid can readily distinguish the steroid-responsive cough of
asthma from the habit cough.28 (See also Chapter 12, Asthma.)
Various forms of suggestion therapy have been used to treat habit cough.15,18,22,29
Suggestion therapy was used most extensively over a 40-year period at the
University of Iowa Pediatric Allergy & Pulmonary Clinic.19 A guide to the
15-minute session commonly used is in Box 44-1. A demonstration of the
method is available at www.habitcough.com. The prognosis for habit cough
with suggestion therapy is good, with long-term remission in most cases.
Absence of a specic treatment plan can result in prolonged symptoms. In a
report from Mayo Clinic (Rochester, MN), 44 of 60 patients diagnosed with
habit cough required an average of 6 months beyond the diagnosis for sponta-
neous resolution, and 16 continued to be symptomatic for a mean duration of
5.9 years.30 A report from the Brompton Hospital looked at the outcome from
reassurance alone. Cough subsequently resolved in 59% of patients within
4 weeks but persisted, on average, signicantly longer when the parents were
skeptical or did not accept the diagnosis.19 In contrast, the cough can be abated
after about 15 minutes of suggestion therapy, with residual symptoms fading
over the next few days or weeks.
Figure 44-1. Description of habit cough
in a 1694 medical book.
AUTHOR:
Why are
different
references cited
on each line
throughout the
table? The table
is repor ting the
results of one
specic st udy,
correct?
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D.J. is a 12-year-old boy who is brought to your oce by his mother with a
complaint of cough for 3 months without systemic symptoms. A trial of inhaled
corticosteroid and a short-acting bronchodilator have not produced improve-
ment. The cough is present throughout the waking hours. It is not present once
he is asleep. It is disruptive of activities, including school; he had been sent home
multiple times. Your examination ndings are normal except for a dry, harsh,
“honking” cough. The referring physician had performed chest radiography,
sinus radiography, and spirometry. Are all normal.
Comment: The presentation is diagnostic of the habit cough syndrome. While
the chest radiograph and spirometry were reasonable, though not essential,
to ensure there is no other explanation for the cough, the sinus radiograph is
not indicated since it will provide neither positive nor negative information.23,31
The indicated treatment is suggestion therapy, which was associated with a
95% success rate among 85 children seen at the University of Iowa Pediatric
Allergy & Pulmonary Clinic by 6 clinicians.18
CASE REPORT 44-1
Guide for Suggestion Therapy Treatment of Habit Cough
Box 44-1
ū Express condence, communicated verbally and behaviorally, that the therapist
will be able to show the patient how to stop the cough.
ū Explain the cough as a vicious cycle of an initial irritant, now gone, that had set
up a pattern of coughing that caused irritation and further symptoms.
ū Encourage suppression of the cough to break the cycle. The therapist closely
observes for the initiation of the muscular movement preceding coughing and
immediately exhorts the patient to hold the cough back, emphasizing that each
second the cough is delayed makes further inhibition of cough easier.
ū An alternative behavior to coughing is oered in the form of inhaling a generat-
ed mist or sipping body-temperature water with encouragement to inhale the
mist or sip the water every time the patient begins to feel the urge to cough.
ū Repeat expressions of condence that the patient is developing the ability to
resist the urge to cough.
ū When some ability to suppress cough is observed (usually after about
10 minutes), ask in a rhetorical manner if the patient is beginning to feel
that they can resist the urge to cough (eg, “You’re beginning to feel that
you can resist the urge to cough, aren’t you?”).
ū Discontinue the session when the patient can repeatedly answer positively
to the question, “Do you feel that you can now resist the urge to cough on
your own?” This question is only asked after the patient has gone 5 minutes
without coughing.
ū Tell the patient that what we just did can be done by the patient on their own
at home.
From Lokshin B, Li ndgren S, Weinberger M, et al. Ou tcome of habit cough in children treate d with a brief
session of suggestion therapy. Ann Allergy. 1991;6 7(6):5 79- 582.
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Chapter 44 —Functional Respirator y Disorders
Habit Throat Clearing
Habit throat clearing appears to be related to the habit cough syndrome. Of
140 children diagnosed with the habit cough syndrome over a 20-year period at
the University of Iowa, a repetitive, softer throat-clearing sound rather than the
more typical barking cough was the presenting symptom in 10% of the patients;
11% exhibited both the barking cough and the softer throat-clearing patterns of
coughing.18 Habit throat clearing has been attributed by some to gastroesopha-
geal reex (GER). However, an association of GER and habit throat clearing
was not found in 186 patients referred for possible GER disease who underwent
consecutive ambulatory impedance studies.32 Response to suggestion therapy
was as effective in these patients as in those with the harsh barking cough.
Habit Sneezing
Habit sneezing is a much less common disorder than the habit cough syn-
drome, but there have been a substantial number of case reports. In the oldest
reported case, a 40-year-old woman had repetitive sneezing that was even-
tually stopped by suggestion.33 Two case reports in children were published
(8- and 10-year-old girls).34 Both children experienced severe repetitive
sneezing multiple times per minute that was absent once asleep. Habit
sneezing generally appears more as a cough through the nose than a true
sneeze. There is no mucus excretion; it is essentially a dry sneeze. As with
habit cough, a precipitating factor is likely to have been present (an irritant
in the case of the 40-year-old woman). In a 9-year-old girl observed by one of
this chapter’s authors, the initiating factor was a bug up her nose. Suggestion
therapy similar to that used for habit cough was rapidly effective.
Functional Causes of Dyspnea
Dyspnea is the subjective experience of uncomfortable breathing that can
vary in quality and intensity. Dyspnea can occur for many reasons (Box 44-2).
Pulmonary, cardiac, and neuromuscular disorders can cause dyspnea when they
decrease appropriate ventilation and gas exchange. Functional disorders asso-
ciated with dyspnea are those that have no physiologic basis.35 Dyspnea is also
perceived during hyperventilation attacks that involve a medically unexplained
Causes of Dyspnea
Box 44-2
Physiologic Dyspnea
Bronchospasm from asthma
Obstructive pulmonary disease
Restrictive pulmonary disease
Cardiac abnormalities
Anemia
Functional Dyspnea
Vocal cord dysfunction
Hyperventilation
Exertional dyspnea
Dyspnea perception
without physical correlate
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increase in a normal function (breathing). Functional dyspnea can also occur
without any physiologic dysfunction.
Vocal cord dysfunction (VCD) has an anatomic component, but the cause of
that anatomic component is functional in that there is no organic reason for
the dysfunction. Normal functions of the vocal cords include protection of the
airway by adduction to prevent aspiration, permitting unrestricted ow of air
into the lungs by abduction, and speech. The movement of the vocal cords is
controlled by the intrinsic laryngeal muscles. All intrinsic laryngeal muscles
except the cricothyroid muscle are innervated by the recurrent laryngeal
nerves, which are branches of the vagal nerves.36 Although much of the
function of the vocal cords is reexive and automatic, they must interact with
volitional control at higher levels of the central nervous system. The precise
interactions between cortical and subcortical control systems and reexive
pattern generators are essential for normal laryngeal function.
Dyspnea occurs with VCD when the dysfunction results in airway obstruc-
tion at the level of the larynx. That occurs because there is failure of the
vocal cords to open and allow air to enter the lungs during inspiration.
Essentially, the complex interaction of the vagal and central nervous system
goes awry. There are 2 physiologic abnormalities of VCD: adduction of
the vocal cords during inspiration and persistent adduction during both
inspiration and expiration. Videos of both are available for viewing at
https://www.milesweinberger.com/copy-of-exercise-induced-dyspnea.
The most common abnormality is adduction of the vocal cords during inspira-
tion. The vocal cords should abduct to permit free ow of air during inspira-
tion. Adduction during inspiration is essentially a paradoxical movement of
the vocal cords, causing stridor on inspiration and dyspnea because of
Figure 44-2. Spirometry before and af ter exercise
of a 15-year-old girl showing a marked decrease in the
inspiratory por tion of the ow-volume loop in asso-
ciation with dyspnea and an inspiratory wheeze-like
sound (technically a high-pitched stridor; see video
with audio at https://www.milesweinberger.com/
copy-of-exercise-induced-dyspnea).
From Weinberger M, A bu-Hasan M. Pseudo -asthma: when
cough, wheezi ng, and dyspnea are not asthma. Pediatrics.
2007;120(4):855–864.
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Chapter 44 —Functional Respirator y Disorders
increased resistance to airow on inspiration. Spirometry shows marked
attening of the inspiratory portion of the ow-volume loop as a result of
marked obstruction to airow only during inspiration (Figure 44-2).37
Persistent adduction during both inspiration and expiration results in inter-
ference of airow to and from the lungs during both phases of respiration,
causing stridorous sounds on both phases (Figure 44 -3).37 Because of the
persistent decrease in airow throughout the whole respiratory cycle, dyspnea
is much more severe and alarming when there is persistent adduction.
A report in adults indicated a third pattern where adduction occurs only on ex-
piration.38 That has not been reported in children. An American Thoracic Society
podcast discussing how dyspnea from vocal cord dysfunction can be distiguished
from other causes of dyspnea can be heard at https://www.thoracic.org/about/
ats-podcasts/evaluation-and-management-of-vocal-cord-dysfunction.php.
There are 2 distinct phenotypes of vocal cord dysfunction. Some patients have
VCD limited to being exercise-induced (EIVCD). Others have spontaneously
occurring vocal cord dysfunction (SVCD) that may or may not occur also with
exercise.39 The latter (SVCD) is more distressing to the patient since there is
not a predictable trigger for the disorder. Speech therapy by skilled speech
pathologists is reported to have been effective in enabling those with SVCD
to control the problem.40
The use of speech therapy has also been reported for EIVCD, but the prac-
ticality of that during competitive activity raises questions of its actual value.
Based on the vagal innervation of the vocal cords,39 a trial of an anticholinergic
aerosol, ipratropium metered-dose inhaler, has been used prior to planned
exercise with success in preventing EIVCD.37 Evidence that vagal stimulation
can cause abnormal function of the vocal cords provides further rationale for
Figure 44-3. Spirometry before and after the
spontaneous onset of dyspnea in a 14-year-old girl
showing marked decrease in both the inspiratory
and expiratory portion of the ow-volume loop in
association with an inspirator y wheeze-like sound
(technically a high-pitched stridor on inspiration)
and a monophonic wheeze on expiration (see video
with audio at https://www.milesweinberger.com/
copy-of-exercise-induced-dyspnea).
From Weinberger M, Abu-Hasan M. Pseudo -asthma:
when cough, whe ezing, and dyspnea are not ast hma.
Pediatrics. 2007;120(4):855–864.
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this approach.41,42 While not subjected to a controlled clinical trial, multiple
patients with well-documented EIVCD have experienced effective blocking
of their paradoxical vocal cord movement.37,40
Extended follow-up in 28 patients with VCD found 26 patients asymptomatic
when contacted a median of 5 months (range of 1 week to 5 years) after the
evaluation and diagnosis.39 Two of 17 patients with EIVCD were still using
ipratropium metered dose inhaler prior to exercise for prevention. All 11
patients with SVCD were no longer having VCD symptoms when contacted.
An imitator of EIVCD is exercise-induced laryngomalacia (EIL).43 In some
cases, this may be a residuum of infantile laryngomalacia.44 Inspiratory stridor
occurs in patients with EIL only when vigorous exercise results in sufcient
air movement to invaginate the arytenoids or pull down the epiglottis over the
airway, depending on the specic anatomy.45 When exercise testing identies
upper airway obstruction, visualization is necessary to distinguish EIVCD
from the much less common EIL.46 The treatment of EIL, if needed, is
supraglottoplasty (Figure 44-4).47,48
In summary, VCD can occur with paradoxical vocal cord adduction during
inspiration instead of the normal abduction. Some will have persistent adduc-
tion during inspiration and expiration. VCD can be limited to occurring only
Figure 44-4. A. Laryngomalacia with
obstruction by invaginated arytenoid
induced by high airow during aerobic
exercise. B. Laryngoplasty repair.
Reproduced w ith permission from Arora R , Gal TJ,
Hagan LL. An unusual case of laryngomalacia
presenting as asthma refractory to therapy.
Ann Allergy Asthma Immunol. 2005;95(6):607-611.
A
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Chapter 44 —Functional Respirator y Disorders
with exercise or can occur spontaneously. While these are often distinct
phenotypes, some patients will manifest both SVCD and EIVCD. Speech
therapy can provide the patient with SVCD with the ability to stop VCD
when it occurs. Pre-exercise treatment with an anticholinergic appears to be
an effective prevention for EIVCD. A high rate of natural resolution occurs
for both forms of VCD.
Exertional Dyspnea Other Than EIVCD
Physicians may be predisposed to attribute exertional dyspnea to asthma
because it is a common cause. However, in the absence of other symptoms
of asthma, present or past, it is unlikely to be the cause of exercise-induced
dyspnea (EID). Even in the presence of a modest degree of measurable
exercise-induced bronchospasm (EIB), EID does not necessarily warrant
a diagnosis of asthma. EIB is a pathophysiological response that can be
measured using lung function testing. Exercise-induced asthma (EIA), on
the other hand, is a clinical diagnosis based on demonstration of EIB as the
cause of EID. This issue was demonstrated by Burnett et al49 who reported
an EIB prevalence of 43% in college athletes, most having no dyspnea or any
respiratory symptoms. This raised the question of the clinical relevance of
a modest degree of EIB in the absence of dyspnea on exertion or other
symptoms of asthma.50
Evaluation of exercise-induced dyspnea rst warrants a trial of pre-exercise
use of a bronchodilator, such as albuterol. The complete and reliable pre-
vention of exercise-induced dyspnea supports the diagnosis of asthma. The
absence of complete and reliable prevention does not justify any other attempts
at asthma pharmacotherapy. Instead, if there is minimal or no improvement in
dyspnea from a trial of albuterol, alternative diagnoses should be considered,
and cardiopulmonary exercise testing is needed to identify other causes
of EID.46
Of 117 children and adolescents referred to the pulmonary clinic at the
University of Iowa Children’s Hospital because of EID, 100 had been pre-
viously diagnosed with asthma. They were referred because they had not
responded to usual treatment for EIA. Symptoms were reproduced during
exercise testing and the etiology identied. Although most of the patients
previously had been diagnosed with asthma, only 11 could be demonstrated
to have EIA. Other diagnoses associated with reproduced EID included vocal
cord dysfunction in 13 patients, laryngomalacia in 2 patients (1 of whom had
unilateral vocal cord paralysis), exercise-induced hyperventilation in 1 patient,
and supraventricular tachycardia in 1 patient. Restrictive abnormalities sug-
gestive of a minor degree of chest wall stiffness were seen in 15 patients.
Seventy-four of those 117 patients demonstrated only normal physiologic
exercise limitation; 48 of these 74 had normal to high cardiovascular
conditioning, and 26 had poor conditioning (Figure 44-5).51
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EIB
11
13
15
2
1
1
74
VCD
EIL
EIH
EISVtach
Physiologic
Restrictive
Figure 44-5. The diagnoses among 117 sequential children and adolescents evaluated
for exercise-induced dyspnea. Diagnoses determined by treadmill exercise testing with
physiologic monitoring.
Abbreviations: EIB, exercise-induced bronchospasm; EIH, exercise-induced hyperventilation; EIL, exercise-
induced laryngomalacia; EISVtach, exercise-induced supraventricular tachycardia; Physiologic, normal
physiologic limitation without other abnormality; Restrictive, apparent restriction of chest wall movement;
VCD, vocal cord dysfu nction.
From Weinberger M , Abu-Hasan M. Pse udo-asthma: when cou gh, wheezing, and dys pnea are not asthma.
Pediatrics. 2007;120(4):862; with permissio n. Original data from Ab u-Hasan M, Tannous B, Weinbe rger M.
Exercise -induced dyspnea in ch ildren and adolescent s: if not asthma then what? Ann Allergy Asthma Immunol.
2005;94(3):366-371.
Normal physiologic exercise limitation occurs when lactic acidosis increases
during anaerobic metabolism, resulting in an attempt to compensate for this
metabolic acidosis by increasing ventilation to create respiratory alkaloses.
However, this increased respiratory drive occurs when maximal ventilation
already has been reached. That is associated with a low pH that cannot be
compensated by a respiratory alkalosis from further increasing ventilation.
That causes progressive dyspnea, which is interpreted by even some well-
conditioned children and adolescents as pathologic rather than normal
physiologic limitation. Successful athletes in aerobic sports learn to adjust
their activity when necessary to maintain a maximal tolerated level that
may be increased with further conditioning. The treatment is counseling to
explain the physiology of exercise so that the patient understands the etiology
of their dyspnea and the necessity of pacing in addition to conditioning.
Dyspnea Without Physiologic Correlates
Although not associated with physiologic abnormality, a patient’s perception
of dyspnea may still be troublesome. The sensation of dyspnea is stronger in
patients with anxiety and has been reported in patients with anxiety disorders
NOTE: This
gure is being
re-rendered at a
higher
resolution.
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Image at left is the
re-rendered version.
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Chapter 44 —Functional Respirator y Disorders
in the absence of cardiopulmonary disease.52 These observations demonstrate
the importance of cerebral cognition in this complex symptom. Patients
with this disorder have been misdiagnosed as having asthma and treated
as such. Once recognized by a physician, treatment of the anxiety is the
appropriate measure.
Dysfunctional Breathing
Hyperventilation
Hyperventilation refers to an increase in alveolar ventilation in excess of
metabolic needs. That can result in respiratory alkalosis with a reduction in
arterial partial pressure of carbon dioxide below the normal range for age
(Pa
co
2 < 4.66 kPa [< 35 mm Hg]) and a consequent rise in pH above 7.4. The
resulting respiratory alkalosis with its effect on calcium ionization causes
feelings of light-headedness, numbness, or tingling periorally and on the
ngers or toes. It can progress to carpopedal spasm.
While some drug overdoses, such as aspirin, can create increased ventilation,
which can also occur from metabolic disorders (eg, Kussmaul breathing during
diabetic ketoacidosis), the details of those are beyond the scope of this publica-
tion. Hyperventilation in children typically presents as a spontaneous event
related to anxiety, panic, nervousness, or stress. The term “acute hyperventi-
lation” is used to describe these brief episodes, which can occur in children
and adults. Chronic hyperventilation is a documented entity in adults but not
described in the pediatric population.53 Hyperventilation can be associated just
with anxiety or can be a part of a panic attack. There is characteristically an
abrupt onset of intense fear or discomfort that reaches a peak within minutes.
Symptoms can include palpitations, sweating, and trembling along with the
sensation of dyspnea that provokes the hyperventilation.54 Somatic complaints
can also occur.55
On examination, children and adolescents appear anxious or distressed with
usually rapid deep breathing that can involve the use of accessory muscles
of respiration. The apparent increased work of breathing and description by
the patient that they are experiencing air hunger can cause a misdiagnosis of
asthma. Lower airway sounds are unusually clear with absence of the poly-
phonic wheezes that characterize asthma. The presence of a normal pulse
oximetry, 95% or greater, is reassuring to the examiner encountering this
patient. A blood gas (capillary or venous is adequate) can conrm hyperventi-
lation if the pH is high and the Pco2 i s low.
Immediate treatment of acute hyperventilation can include rebreathing into
a bag. That increases the Pco2, decreases the pH, and thereby eliminates
symptoms caused by the alkalosis. Reassuring and calming the patient can
further decrease the anxiety and fear associated with an anxiety-induced panic
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attack. For a patient prone to have such episodes, counseling and explaining
what is being felt are essential so that future episodes are not mistaken for
acute asthma or some other illness.
Repetitive Sighing
Sighing is a normal activity, sometimes as an expression of relief. It involves
taking a deep inspiration followed by exhalation and a subsequent normal
breathing pattern. Repetitive involuntary sighing is known as the sighing
syndrome.56 As with other habit disorders, the sighing is absent once asleep.
Anxiety and stress are speculated to be associated. Although one young child
is reported to have sighing associated with asthma,57 another report that
included both adults and children suggested the potential for mistakenly
diagnosing repetitive sighing as asthma.58 When asked why they are sighing,
the common answer is just that they felt more air was needed. While the
syndrome is called sighing dyspnea in some publications, the child with
recurrent sighing generally does not express a feeling of dyspnea. The
sighing occurs most commonly when the patient is quiet, does not interfere
with activity, and does not seem to disturb the child as much as the parent.
This generally appears to be a benign condition that nonetheless disturbs the
parents who bring the child to a physician for evaluation. The child, however,
is often unconcerned and experiencing no distress. No treatment is needed
other than explaining the benignity of this minor functional deviation from
usual respiration. Since it is harmless and generally self-limited, repetitive
sighing generally warrants only benign neglect.
Dysfunctional Breathing Complicating Asthma
Dysfunctional breathing can occur in children with asthma and complicate
the clinical assessment of severity and control of the disease.59 61 However,
dysfunctional breathing seems to occur much less frequently in children
with asthma than in adults with asthma.62 A study of 203 children with
asthma, aged 5 to 18 years, used a Nijmegen Questionnaire63 and related that
to the results of an Asthma Control Questionnaire.64 Although the Nijmegen
Questionnaire is primarily used to assess hyperventilation in adults, the
results demonstrated 5% of children at a specialized asthma clinic had a high
Nijmegen score that correlated with poor asthma control. That suggests that
poor asthma control warrants investigation for dysfunctional breathing.
Breathing retraining has been used for adults with asthma and dysfunctional
breathing with benet.65 While that has also been suggested as of value for
children with asthma,66 controlled trials have not been performed. Nonethe-
less, poor asthma control justies observation to determine if the patient’s
symptoms or breathing pattern were disproportionate to the degree of
measured airway obstruction or gas exchange.
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key points
}Functional respiratory disorders are symptoms without medical explanation.
}Functional respiratory disorders are not diagnoses of exclusion; they are based
on specic characteristics.
}Misdiagnosis results in overtreatment of the symptoms.
}The treatment of functional disorders is behavioral, not pharmacologic.
Some FNs do
not have PMID
and /or doi:
FN #5, 15, 16,
17, 21, 28, 30,
32, 56, 58.
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Disregard.
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Article
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Objective To assess the impact of breathing retraining on asthma symptoms and dysfunctional breathing (DB) in children. Breathing retraining can improve DB but there is a lack of evidence in pediatrics. Methods Participants attended outpatient physiotherapy appointments and received individually tailored interventions, particularly Buteyko breathing techniques. The primary outcome was the change in the Asthma Control Test (ACT) score or change in childhood ACT (CACT) score from first to final appointment. The ACT and CACT are validated in children more than or equal to 12 years and children aged 4 to 11, respectively. The secondary outcome measure was the change in Nijmegen Questionnaire (NQ) score from first to the final appointment (score range, 0‐64) with a score of more than or equal to 23 indicating DB symptoms. Results One hundred and sixty‐nine children with asthma attended and completed a mean of six physiotherapy sessions, over a mean of 15 weeks. Patients were aged 2 to 18, mean 10 years. Fifty‐five patients were more than or equal to 12 years old and 114 were less than or equal to 11 years. One hundred and seven patients were receiving BTS/SIGN asthma guideline step 1 to 3 therapy and 62 were on step 4 to 5 therapy. The mean ACT score improved by 4.4 (P < 0.0001), the mean CACT score improved by 4.9 (P < 0.0001), and the mean NQ score change improved by −9.3 points (P < 0.0001). Conclusion In addition to standard medical therapy, individually tailored physiotherapy interventions improved asthma control and DB in children on all levels of asthma treatment. A randomized controlled study is required to determine whether these improvements are due to the intervention.
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Exercise-induced dyspnea in children and adolescents can occur for many reasons. Although asthma is the common cause, failure to prevent exercise-induced asthma by pretreatment with a bronchodilator, such as albuterol, indicates that other etiologies should be considered. Other causes of exercise-induced dyspnea include exercise-induced vocal cord dysfunction, exercise-induced laryngomalacia, exercise-induced hyperventilation, chest wall restrictive abnormalities, cardiac causes, and normal physiologic limitation. When exercise-induced dyspnea is not from asthma, cardiopulmonary exercise testing with reproduction of the patient's dyspnea is the means to identify the other causes. Cardiopulmonary exercise testing monitors oxygen use, carbon-dioxide production, end-tidal pCO2 (partial pressure of carbon dioxide), and electrocardiogram. Additional components to testing are measurement of blood pH and pCO2 when symptoms are reproduced, and selective flexible laryngoscopy when upper airway obstruction is observed to specifically identify vocal cord dysfunction or laryngomalacia. This approach is a highly effective means to identify exercise-induced dyspnea that is not caused by asthma. [Pediatr Ann. 2019;48(3):e121-e127.].
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Goals: To identify the association of throat clearing (TC) with gastroesophageal reflux disease (GERD) during objective reflux monitoring in a large number of patients studied in our esophageal testing laboratory. Background: TC is frequently reported and considered to be an atypical symptom of GERD. Atypical GERD symptoms have been widely investigated and empirically treated with proton pump inhibitors. Study: We reviewed ambulatory impedance-pH studies of 186 patients referred for evaluation of possible GERD from January 2011 to December 2015 to evaluate the symptom association (SA) of TC with both an abnormal number of reflux episodes and also abnormal esophageal acid exposure (EAE). Patients were divided into 2 groups; group 1: TC is the only reported symptom, group 2: TC is one of the symptoms. All patients were studied off proton pump inhibitors therapy. Results: Group 1 where TC was the only symptom in 27/186 (14.5%) patients. There was no significant difference in positive SA between this group (6/27; 22%) and group 2 (43/159; 27%) (Z score P=0.59). There was also no significant association between SA and abnormal EAE whether TC was the only presenting symptom (χ, P=0.7) or one of the reported symptoms (χ, P=0.10). None of the 6/27 had abnormal EAE. Conclusion: Although TC is often considered a possible GERD-related symptom, we found a low probability of objective association. TC is not likely to be the only presenting symptom, and if it happens, it is unlikely to be associated with GERD. Perhaps, TC should not be considered as a GERD symptom, even as an atypical one.
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Rationale: In primary ciliary dyskinesia (PCD), factors leading to disease heterogeneity are poorly understood. Objectives: To describe early lung disease progression in PCD and identify associations between ultrastructural defects and genotypes with clinical phenotype. Methods: Prospective, longitudinal (5 years), multicenter, observational study. Inclusion criteria: < 19 years at enrollment; > 2 annual study visits. Linear mixed effects models including random slope and random intercept were used to evaluate longitudinal associations between ciliary defect group (or genotype group) and clinical features (percent predicted FEV1, weight and height z-scores). Measurements and main results: 137 participants completed 732 visits. The group with absent inner dynein arm, central apparatus defects and microtubular disorganization (IDA/CA/MTD; n=41) were significantly younger at diagnosis and in mixed effects models had significantly lower percent predicted FEV1, weight and height z scores than the isolated outer dynein arm (ODA) defect (n=55) group. Participants with CCDC39 or CCDC40 mutations (n=34) had lower percent predicted FEV1, weight and height z-scores than those with DNAH5 mutations (n=36). For the entire cohort, percent predicted FEV1 decline was heterogeneous with a mean (standard error, SE) decline of 0.57 (0.25) percent predicted/year. Rate of decline was different from zero only in the IDA/MTD/CA group (mean (SE) -1.11 (0.48) pp/yr; p=0.02). Conclusions: Participants with IDA/MTD/CA defects, which included individuals with CCDC39 or CCDC40 mutations, had worse lung function and growth indices compared to those with ODA defects and DNAH5 mutations, respectively. The only group with a significant lung function decline over time were participants with IDA/MTD/CA defects.
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Respiratory distress during exercise can be caused by exercise-induced laryngeal obstruction (EILO). The obstruction may appear at the level of the laryngeal inlet (supraglottic), similar to supraglottic collapse observed in infants with congenital laryngomalacia (CLM). This observation has encouraged surgeons to treat supraglottic EILO with procedures proven efficient for severe CLM. This article summarizes key features of the published experience related to surgical treatment of EILO. Supraglottoplasty is an irreversible procedure with potential complications. Surgery should be restricted to cases where the supraglottic laryngeal obstruction significantly affects the quality of life in patients for whom conservative treatment modalities have failed.
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Objectives: Our therapeutic approach to a habit/tic cough is simple reassurance in a single consultation. To quality assure our practice, we followed up children to determine outcomes at least 3 months after diagnosis. Design: Consecutive children diagnosed over 6 years were studied. Medical records were analyzed retrospectively and parents answered a scripted verbal survey. Results: Fifty-five patients were diagnosed (median age 9.9 years), with a median cough duration of 3 months (IQR 2-7.5 months, range up to 3 years). In 51/55 (93%) cases, cough was absent during sleep. 51/55 (93%) received prior medications with median 3 therapeutic trials, none of which resolved the cough. Follow-up was possible in 39/55 (71%) children after a median duration of 1.9 years. In 32/39 (82%), the cough had resolved completely (59% within 4 weeks, including 12% on the day), and it improved in 6/39 (15%). In the 26/39 (67%) parents who said they believed the diagnosis, there was 96% resolution of the cough, versus the 13/39 (33%) who were sceptical or disbelieving, when there was only 54% resolution. 7/39 (18%) children were later diagnosed with a tic disorder, functional symptoms, or a behavioural/psychiatric disorder. Conclusions: Habit cough can be diagnosed from the characteristic history; the crucial question is whether the cough disappears during sleep. We have shown successful long term outcomes following a single consultation with simple reassurance, but it is important that the child and parents believe the explanation. It is not uncommon for subsequent tic disorders or behavioral issues to emerge.