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Clinical Pearls in Respiratory Diseases

Article  in  The Indian Journal of Pediatrics · December 2010

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Indian J Pediatr (May 2011) 78(5):603–608
DOI 10.1007/s12098-010-0270-3
CLINICAL PEARLS
Clinical Pearls in Respiratory Diseases
Sunit C. Singhi & Joseph L. Mathew & Atul Jindal
Received: 27 September 2010 / Accepted: 5 October 2010 / Published online: 14 December 2010
# Dr. K C Chaudhuri Foundation 2010
Abstract In this section, the authors present some common
and some uncommon respiratory cases that have diagnostic
and/or therapeutic challenges. First case is of an eight- yr-
old child having Acute onset Wheeze and fever, second one
is of a 1.5- yr- old Wheezing child not responding to
inhaled bronchodilators and corticosteroids, third of a 4-yr-
old with Respiratory distress and wheezing with underlying
ventricular septal defect, and fourth of a 5-yr- old with fever
for 1 month, epistaxis from right nostril for 15 days,
polyuria for 10 days, impaired consciousness and discolor-
ation of right orbit. Each one had some unique pointers to
correct diagnosis and management. The authors share
clinical learning points from these cases with a concise
review of the topic.
Keywords Wheezing child . Acute asthma . Foreign body
aspiration . Hyperglycemia . Pneumonia . Diabetic
ketoacidosis . Rhinocerebral zygomycosis
Case 1: Acute Onset Wheeze and Fever
An eight-year-old child was referred with acute onset fever
and progressive worsening of respiratory distress for 1 wk.
He had received intravenous antibiotics and oxygen by face
mask for 3 days at another hospital, and was referred
because he did not improve. At presentation, the child had
tachypnea, chest indrawing, bilateral wheeze and crackles.
S. C. Singhi (*) : J. L. Mathew : A. Jindal
Department of Pediatrics, Advanced Pediatrics Center,
Postgraduate Institute of Medical Education and Research,
Chandigarh, India
e-mail: drsinghi_chd@dataone.in
There was no history of similar episode in the past or
family history of asthma. Management for acute severe
asthma was initiated; however there was no improvement
despite 3 cycles of inhaled bronchodilator, intravenous
corticosteroid, magnesium sulfate, ketamine and terbutaline
infusions as per standard protocol for acute severe asthma.
Question 1
What is your diagnosis
a) Status asthmaticus
b) Foreign body
c) Pneumonia
d) Myocarditis with congestive Cardiac Failure
A chest radiograph was obtained. It showed alveolar
infiltration on both sides and a right sided effusion.
Intercostal drainage revealed pus. The final diagnosis was
pneumonia complicated by empyema.
Question 2
How frequent is wheezing in children with acute respiratory
tract infection?
Are there clinical pointers that differentiate between
severe pneumonia with wheezing and acute severe
asthma?
Discussion
It has been reported that up to 75% of children with
‘pneumonia’ or ‘severe pneumonia’ diagnosed as per WHO
criteria, have associated wheezing; this has been docu-
604 Indian J Pediatr (May 2011) 78(5):603–608

mented in hospital-based [1] and community studies [2].

Even among children with (non-severe) pneumonia, wheez-
ing is reported in 13 to 22% [3]. Of course, wheezing is
much more common in infants than those over one year.
In most children with acute severe asthma, respiratory
rate, chest indrawing, wheezing and oxygenation improve
after 2 to 3 cycles of inhaled bronchodilator and/or i.v or
oral corticosteroids. But in pneumonia, bronchodilator
therapy does not yield similar response.
Clinical predictors of pneumonia in children presenting
with wheeze include history of fever at home, history of
abdominal pain, triage temperature ≥38°C, and triage
oxygen saturation of <92% [4]. Early radiograph of the
chest in wheezing children not responding to inhaled
bronchodilator and intravenous/oral corticosteroid, may
avoid unnecessary use of multiple bronchodilators and help Fig. 1 Baseline Chest Radiograph showing bilateral Hyperinflation
in early diagnosis and management of pneumonia and/or its
complications such as pleural effusion. inhalation technique was done, but the symptoms and signs
Most effusions associated with pneumonia (syn-pneu- persisted.
monic) resolve within a week, with appropriate antibiotic
therapy. Sometimes complicated and/or large effusions Question
present by the end of the first week of illness, requiring
intercostal drainage. What could be the reasons for non-response to inhaled
bronchodilator and corticosteroid therapy in index patient?
(i) Resistance to corticosteroid
Clinical Pearls
(ii) Wrong drug dosage
(iii) Wrong diagnosis
Wheezing is not uncommon in acute pneumonia. In a child
with acute onset wheezing, with history of preceding fever The history was reviewed again. Parents offered addi-
and abdominal pain, and presence of temperature >38°C tional information that the child was found playing with a
and SpO2 <92% at presentation, pneumonia is a more likely string of beads in the mouth on one occasion and had tried
diagnosis. Chest radiography can help in early diagnosis to swallow a peanut on another occasion. A flexible
and management. fibreoptic bronchoscopy was undertaken, which revealed
half a peanut, oriented length-wise and partially obstructing
the right main bronchus. The bronchoscope could not be
Case 2: Wheezing Child Not Responding passed beyond the peanut. Left side airway examination
to Inhaled Bronchodilators and Corticosteroids was normal. The final diagnosis was right main bronchus
obstruction by foreign body (peanut).
A 1.5-yr-old infant presented with three months history of
wheezing. There was no preceding/concomitant history of
upper respiratory infection or pneumonia. Wheezing inten- Discussion
sity increased during sleep, on cold exposure and while
crying. There was no history of sensitivity to dust or other In children with bronchial asthma, once the diagnosis, drug
environmental factors. Family history was unremarkable. and dose (3Ds) are confirmed; non-response to appropriate
Examination revealed a thriving, alert infant, without dose of inhaled corticosteroids could be related to inade-
tachypnea; central trachea, symmetrical chest, bilateral quate compliance, incorrect inhalation technique and
expiratory wheeze and no crackles. Baseline chest radio- canister getting empty without parents realizing it. After
graph showed only bilateral hyperinflation (Fig. 1). Based this, adverse environment/living conditions (exposure to
on a provisional diagnosis of moderate persistent asthma, specific allergens) and co-morbid problems (including
inhaled corticosteroid therapy (using MDI with spacer and upper airway allergy, tonsillo-adenoiditis and para-nasal
baby-mask) was initiated. However, there was no response sinusitis) should also be considered and managed. If the
after three weeks of therapy. In view of failure of expected child is still unresponsive, alternate diagnoses that mimic
therapeutic response, a review of compliance to therapy and asthma in young children; particularly heart disease with
Indian J Pediatr (May 2011) 78(5):603–608 605

cardiac failure, foreign body inhalation, gastro-esophageal
reflux disease could be the cause of apparent treatment
failure.
Foreign body aspiration need not always present with the
classic history of acute onset of coughing, choking,
wheezing, or respiratory distress. This is seen in only
three-fourth of cases [5]; the remainder present later with a
chronic course including repeated chest infections and/or
atelectasis. Airway foreign body can present even with
normal physical examination and radiographic findings [6].
One study reported that nearly one-fifth children had no
radiological signs suggesting localized airway obstruction.
Meticulous history and high index of suspicion, with
relatively low threshold for bronchoscopic examination
may be the only way out in such cases.
A large series of foreign body aspiration in over 1400
patients (87% peanuts, 6% beans and 6% others) reported
the location as right bronchial tree in nearly 55%, left
bronchial tree in about 40%. Around 5% were located in
the trachea and less than 0.5% in both bronchial trees [7].
These latter locations can result in bilateral signs. In
addition, partial obstruction of a relatively large airway
can also present with non-lateralization of clinical and
radiographic findings.
Clinical Pearl
All infants/children with bilateral wheezing do not have
bronchial asthma, and foreign body aspiration can present with
non-lateralization of findings; it should be suspected in non-
responders to inhaled bronchodilators and corticosteroids.
Case 3: Respiratory Distress and Wheezing
in a Child with Ventricular Septal Defect
child was managed initially with restricted fluids, intrave-
nous furosemide and morphine, but the respiratory status of
the child worsened. A chest radiograph was obtained
(Fig. 2).
Question
What do you think is the cause of respiratory distress in this
child?
1. Congestive heart failure
2. Pneumonia with wheeze
3. Acute severe asthma
After chest radiograph showed bilateral hyperinflated
lung fields with normal cardiac silhouette, the diagnosis
was reviewed as asthma. He was managed with inhaled
salbutamol, budesonide and ipratropium along with intra-
venous hydrocortisone and magnesium sulphate infusion
and showed significant response over the next 6 hours. The
therapy was deescalated subsequently.
Discussion
Congenital heart diseases (CHD) often present with
recurrent or chronic breathing difficulties, as do chronic
airway diseases such as asthma. Both are relatively
common, and may sometimes coexist. Clinicians are
sometimes faced with patients in whom both Congenital
Heart Disease (CHD) and airway disease co-exist[8–11]. In
fact, congenital cardiovascular anomalies are believed to be
significantly associated with congenital and acquired
airway disorders [9]. Although the prevalence of asthma
and/or airway hyper-responsiveness (AHR) in children with

A 4- yr old boy, presented with fever and cough since

2 days, and difficulty in breathing since 1 day. During
infancy, he was diagnosed to have a small (5 mm) subaortic
ventricular septal defect with left to right shunt without
pulmonary arterial hypertension. On examination, he had
tachycardia, tachypnea, decreased air entry, prolonged
expiration and wheeze on both sides of chest. SpO2 was
92% on 40% FiO2. Liver was 2 cm. below right costal
margin. A harsh pansystolic murmur was present in left
parasternal area. Initial laboratory investigations revealed
Hemoglobin 14 g/dL, leukocyte count- total 8260/μL,
differential- P 47,L 49, M 3, E 1, serum sodium
141 mEq/L, potassium-3.4 mEq/L, urea- 20 mg/dL,
creatinine- 0.3 mg/dL. Arterial blood gas analysis showed
pH- 7.22, PaO2-65.7 torr, PaCO2- 50 torr, bicarbonate- Fig. 2 Chest radiograph showing bilateral hyperinflated lung fields,
20.1 mEq/L, SaO2- 86.9%. Blood culture was sterile. The flattened domes of diaphragm with normal cardiac silhouette
606 Indian J Pediatr (May 2011) 78(5):603–608

CHD is not known, some authors have suggested that

asthma or AHR is more common in children with CHD
than in the general population [12–15]. Tsubata and co-
workers [12] reported that 6 out of 10 of their patients with
congestive heart failure (CHF) secondary to CHD had AHR
elicited by histamine challenge, while Ackerman et al. [8]
identified an extremely strong association between pulmo-
nary atresia with VSD and persistent AHR. Matsuoka et al.
have suggested that pulmonary congestion in infancy may
increase the risk of atopic asthma in genetically predisposed
children [13, 15]. For clinicians practicing in a developing
country, the clinical significance of the co-existence of
these two conditions may lie mainly in the fact that both
could present in a similar manner, since many CHD as well
as asthma, present chiefly with respiratory distress. It
appears that the loud VSD murmur may have earlier, in
the course of management, diverted attention away from the
possibility of a coexisting asthma. It is possible that many
more similar cases have been so missed, and that even
when rhonchi are auscultated, they could be ignored or
attributed to pulmonary congestion or ‘cardiac asthma’ and
cyanosis to severe bronchopneumonia nd/or CCF. This is
coupled with the fact that the family history in children
with CHD is often focused on family history of heart Fig. 3 Note the peri-orbital bruising discoloration, and nasal bleed
disease, parental age and possible predisposing maternal
illnesses in pregnancy, but not particularly on family or
maternal history of atopy or chronic respiratory illnesses sugar 577 mg/dl, pH-6.9, bicarbonate – 3.6, BE- -28. Non-
such as asthma [14]. contrast computerised tomography of head showed exten-
sive infarct in right cerebral hemisphere with non-
opacification of right middle cerebral and internal carotid
Clinical Pearl arteries (Fig. 4).

All that wheezes is not asthma but the most common Questions
diagnosis in wheezing children is asthma. Asthma and
congenital heart disease can coexist. 1. What in your opinion is the cause of hyperglycemia?
1. Stress induced hyperglycemia
Case 4 2. Diabetic ketoacidosis (DKA)
3. Hyperglycaemic hyperosmolar state
A five- yr- old girl presented with intermittent high grade 4. Raised Intracranial pressure
fever for 1 month that became continuous over last 5 days, 2. What do you think is the cause of raised intracranial
epistaxis from right nostril for 15 days, polyuria for 10 days, pressure?
and impaired consciousness for 1 day prior to admission.
1. Cerebral edema caused by hyperglycaemic state.
There was no history of seizures, headache, vomiting,
2. Intracranial bleed
bleeding from any other mucosal site, or trauma. On
3. Rhinocerebral mucormycosis
examination, the modified Glasgow coma scale (GCS)
score was 3, there was bilateral bluish discoloration of lids
and eyes (Fig. 3), papilledema and unequal pupils, both
reacting to light. Investigations revealed: Hemoglobin Discussion
5.8 g/dL, platelet count 82000/μL, leukocyte count total
4800/μL; differential P-60, L–35, M-3, E-2, normal The likelihood of DKA is strong in a child presenting with
prothrombin time, serum sodium 140 mEq/L, potassium hyperglycemia, severe metabolic acidosis and impaired
1.6 mEq/L, urea 21 mg/dL, creatinine 0.9 mg/dL, blood consciousness in the background of polyuria. Urine showed
Indian J Pediatr (May 2011) 78(5):603–608 607

Fig. 4 CECT showing infarct in right cerebral hemisphere with non-opacification of right middle cerebral and internal carotid arteries

sugar 4+ and ketone 2+, In our experience about two thirds of

children with DKA have fresh onset diabetes[16]. The classic
diagnostic criteria for DKA include hyperglycemia (blood
sugar >250 mg/dl), acidosis (pH <7.3, bicarbonate <18 mEq/
L on blood gas) and ketosis (urine or blood positive for
ketones) whereas hyperglycemic hyperosmolar coma is
defined by glucose of >600 mg/dL, HCO3 ≥15 mEq/L,
serum osmolarity of >320 mOsm/L, and pH ≥7.3 without
significant ketosis. In stress induced hyperglycemia, meta-
bolic acidosis is not so severe.
In any child with DKA or severe acidosis with epistaxis
or proptosis or discoloration of cutaneous tissue at or
around rhino-orbital area, rhino-orbital zygomycosis
(mucormycosis) should be suspected. In the index patient,
CECT showed preseptal cellulitis and thickening of
subcutaneous tissues over both maxillary regions, and
multiple air foci within subcutaneous tissues suggestive of
angio-invasive fungal infection (Fig. 5). Scrapings from
nasal lesion revealed aseptate hyphae on smear examination
and culture grew Rhizopus arrhizus. Patients with phago-
cytic dysfunctions due to neutropenia or ketoacidosis, or
patients with high iron serum concentrations, are at higher
risk of developing zygomycosis. These underlying con-
ditions can influence the clinical presentation and outcome.
The rhino-cerebral form of zygomycosis is the most
frequently reported in the diabetic population.
Fig. 5 CECT showing preseptal cellulitis and thickening of subcuta-
In a series of 929 cases of zygomycosis [17] diabetic neous tissues over both maxillary regions. Multiple air foci are seen
patients represented 36% of the total, with type 1 diabetes within subcutaneous tissues suggestive of angio-invasive fungal
accounting for 20%. Ketoacidosis was found in 48% of infection
608
patients with type 1 diabetes and 34% of those with type 2
diabetes. Among those with diabetes in the series, 66%
presented with sinusitis, most often cerebral (43%) or
orbital (15%) extension. Interestingly, no localized cerebral
infection was observed, suggesting that there was a nasal
portal of entry in these patients. Lung and cutaneous
involvement were reported in 16% and 10% of cases,
respectively. In another study among 179 patients with
sinus zygomycosis, 70% presented with ketoacidosis [18];
and 83% of 41 patients with rhinocerebral zygomycosis
were diabetics.
Clinical Pearl
Children with fresh onset diabetes may present for the first
time with ketoacidosis. Any child with diabetic ketoacido-
sis having rhino-orbital discoloration or epistaxis should be
worked up for rhino-orbito-cerebral mucormycosis.
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