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Breathlessness
Breathlessness
Breathlessness
C1 and C2
Table of contents
01 Case 01 07 Evaluate the clinical findings and formulate
the differential diagnoses
02 Case 02
Justify choice of investigations and be
08 able to interpret the results
03 Case 03
Plan management strategies appropriate for
Identify the aspects of anatomy and
09 children presenting with breathlessness.
04 pathophysiology of the respiratory system
relevant to breathlessness.
Physical examination:
● Lethargy → poor feeding + breathlessness
● Air entry decreased bilaterally
● Febrile 39°C
● Occasional rhonchi
● Tachypneic (60 breaths/min)
● Crepitations
● Tachycardic (170 bpm)
● Soft ejection murmur over the left
● Hypoxic (oxygen saturation is 88%)
sternal edge → innocent murmur
● Hyperinflated chest
● Liver palpable 3 cm below the costal
● Subcostal and intercostal recession
margin → Hyperinflation -> liver
pushed down
Differential Diagnosis
1. Cough + fever + breathlessness + tachypnoea
● LRTI → respiratory infection
Clinical signs & ● Common in infants 1-6 ● High fever and chills ● Age > 5 years
symptoms months old (< 2 yr old) ● Severe malaise ● Wheeze
● RSV (common cause) ● Cough with purulent sputum ● Chest tightness
● Mild coryza ● Breathlessness (nasal flaring) ● Tachycardia
● Low grade fever ● Tachypnoea ● Tachypnoea
● Cough ● Breathlessness
Progresses to: ● Cough
● Tachypnoea
● Respiratory distress
● Wheeze
Pharmacotherapy :
● 3% saline solution via nebulizer has been shown to increase mucus clearance and significantly reduce hospital stay
among non-severe acute bronchiolitis
● Inhaled β₂-agonists.
● Antibiotics are recommended for all infants with
○ Recurrent apnoea and circulatory impairment.
○ Possibility of septicaemia.
○ Acute clinical deterioration.
○ High white cell count.
○ Progressive infiltrative changes on chest radiograph.
Case 02
A six week old infant presented with a 2 day history of breathlessness and poor
feeding. The baby was born at term with a birth weight of 3.2 kg. Since two weeks
after birth, the mother had noticed that the baby always required longer time to
finish her milk feeds. For the past 2 days, the baby had been extremely fretful and the
mother had difficulty in feeding her any milk at all.
On examination, the baby weighed 3.8 kg and appeared tachypneic, with a respiratory
rate of 60 per minute. However, the baby still appeared alert and active.
The pulse rate was 180 per minute, but not bounding. The apex beat was situated
over the 5th intercostal space, 1 cm lateral to the midclavicular line. There was a
gallop rhythm with a grade 3/6 pansystolic murmur heard throughout the
precordium.
There were fine crepitations over the bases of both lung fields. Liver was palpable 3
cm below the right subcostal margin.
A chest X-ray done showed a cardio-thoracic ratio of 0.65. An ECG was done which
showed left axis deviation.
Key Points:
Investigations:
● Six weeks infant (1 month and half)
● At birth 3.2 kg → 3.8 kg at 6 weeks (Failure to thrive) ● CXR → Cardio-thoracic ratio of 0.65.
(Cardiomegaly)
● 2 day history of breathlessness and poor feeding.
● ECG → Left axis deviation. (LVH)- structural
● Required longer time to finish her milk feeds. defect/ heart disease
Extremely fretful for past 2 days
●
? Failure
Provisional Diagnosis: Congestive Heart
● Difficulty in feeding her any milk at all.
Physical Examination:
Clinical presentation
Symptoms of heart failure in infancy:
● Feeding difficulty: poor suck, prolonged time to feed, sweating during feed.
● Recurrent chest infections.
● Failure to thrive
Investigations
● CXR → cardiothoracic ratio >0.50 is a well-known indicator of cardiomegaly
on chest radiographs.
● ECG → sinus tachycardia, LV hypertrophy, ST-T changes, and conduction blocks patterns.
axis deviation
● Echocardiogram → LV systolic dysfunction - ejection fraction (EF) <55%.
VSD
Coarctation of the Aorta
● Small defects: loud Pansystolic murmur grade ● Systolic murmur at interscapular region
2-5 at LLSB ● Normal S1 and S2
● Medium to large defects: increased right-to
-left ventriculular impulses
Pulmonary stenosis
○ Thrill at LLSB
○ Split or loud single S2
● Systolic murmur grade 2-5 at USLB
○ Holosystolic murmur at LLSB without radiating to infrascapular regions,
radiation grade 2-5 axillae and back
● normal / loud S1 , Variable S2
ASD ● Systolic ejection flick may be heard at
left sternal border
● Systolic ejection murmur (grade 2 or 3) @USLB
● Wide split S2
● Grade 1 or 2 diastolic flow rumble at LLSB Provisional Diagnosis: CHF 2° to
PDA Ventricular Septal Defect
● Continuous murmur (grade 1-5) in ULSB
(crescendo in systole and descrescendo into
diastole)
● Normal S1,S2 can be buried by the murmur
Aortic stenosis
General measures
● Supplemental O2: give if acute hypoxia (caution in left- to- right shunt, pulmonary
vasodilation may increase shunting).
● Diet: sufficient caloric intake to enable growth. (feed via NG tube) refer to dietician
● Diuretics: reduce volume load.
● ACE inhibitors: reduce afterload.
● Respiratory support: reduces preload and volume load, and MV assists left ventricular
function.
● Inotropic support: if acute cardiac decompensation is detected.
Specific treatment
VSD
- Small defect: No treatment; high rate of spontaneous closure.
● SBE prophylaxis + Yearly follow up for aortic valve prolapse, regurgitation.
● Surgical closure indicated if prolapsed aortic valve.
- Large defects:: Early primary surgical closure.
● Pulmonary artery banding followed by VSD closure in multiple VSDs.
Case 03
A 10 year old boy presented with acute onset of breathlessness for one day. He had
been having fever for the past 5 days, associated with vomiting and abdominal pain.
At the same time, he also had frequent micturition. On the day of admission, he
had made a turn for the worse and was not able to walk about.
ABG results
pH : 7.05 (reduced)
• Insulin therapy in DKA should begin with a rate of 0.05 - 0.1 unit/kg/h
Goals of therapy
about 1 - 2 hours after starting fluid replacement therapy (to reduce the
- Correct dehydration
- Correct acidosis and reverse ketosis risk of cerebral oedema and exacerbation of hypokalemia)
- Restore blood glucose to near normal
-BG level typically decreases at a rate of 2-5 mmol/L/hr, depending
- Avoid complications of therapy
on the timing and amount of glucose administration, hence
- Identify and treat any precipitating event
duration & dose of insulin has to be carefully monitored to avoid
hypokalemia
Fluid replacement
- Minimally dehydrated & can tolerate orally →
give oral fluids
- Moderately dehydrated → 0.9% NS over 48hr
- Severely volume depleted but not in shock →
10-20 ml/kg 0.9% NS over 1-2hr
- Shock → 0.9% NS 10-20 ml/kg ASAP, then
reassess after each bolus. Continue infusion over
48 hr ECG changes:
• Hypokalaemia: prolonged PR interval, T-wave flattening and
inversion,ST depression, prominent U waves and apparent long QT
interval.
• Hyperkalaemia: tall, peaked and symmetrical T waves, and
shortening of the QT interval.
Potassium replacement
Acidosis
• Bicarbonate therapy may cause paradoxical CNS acidosis, hypokalaemia and increasing
osmolality.
Decision-making involving the health care of older children and MREC guideline stated that assent for minors aged less
adolescents should include, to the greatest extent feasible, the than 7 years is not required as they are deemed
assent of the patient as well as the participation of the parents and incapable of comprehending the research process.
the physician. If physicians recognize the importance of assent, they Assent for minors aged 7 to less than 18 years is
empower children to the extent of their capacity. required and investigators must first obtained the
permission of the parents or guardians for the
Assent should include at least the following elements:
participation of the minor in the research and to solicit
1. Helping the patient achieve a developmentally appropriate assent from the minor. However, emancipated minors
awareness of the nature of his or her condition. can consent to participation in research without the
2. Telling the patient what he or she can expect with tests and permission or consent of the parent or guardian.
treatment(s).
3. Making a clinical assessment of the patients understanding
of the situation and the factors influencing how he or she is
responding (including whether there is inappropriate pressure
to accept testing or therapy).
4. Soliciting an expression of the patient's willingness to accept
the proposed care.
Identify the aspects of anatomy and
pathophysiology of the respiratory
system relevant to breathlessness.
Ventilation Drive
Primary motor cortex → respiratory
muscle
ungs (Mechanoreceptors)
- airways, trachea, lung, and pulmonary vessels provide sensory information
to the respiratory center in the brain with regards to lung volume, airway
stretch, and vascular congestion.Two primary types of thoracic sensors: slow
adapting stretch spindles (vloume) and rapid adapting irritant receptors
(chemicals).
- Transmits → Cranial nerve X (the vagus nerve) to increase the breathing
rate, the volume of breathing, or to stimulate cough.
- A notable example is the Pulmonary stretch reflex, also called the
Herring-Breuer reflex, which prevents the lungs from over-inflating by
sending inhibitory impulses to the inspiration center.
Describe the common paediatric
conditions causing breathlessness
I. Pneumonia
- Infection/ Inflammation of interstitial tissue of the lungs.
Causes:
- Can be classified by age-specific versus pathogen-specific organisms.
Neonates →risk for bacterial pathogens present in the birth canal, and this includes organisms
- Group B streptococci, Klebsiella, Escherichia coli, and Listeria monocytogenes.
5 to 13 years old
- S. pneumoniae is still the most commonly identified organism.
- Mycoplasma pneumonia
*When children develop pneumonia, their lungs become stiff. One of the body’s responses to stiff lungs and hypoxia (too little
oxygen) is fast breathing. When the pneumonia becomes more severe, the lungs become even stiffer. Chest indrawing may
develop. Chest indrawing is a sign of severe pneumonia.
- Symptoms of atypical pneumonia (Mycoplasma pneumoniae, Legionella pneumophila and Chlamydophila pneumoniae)
· Low grade fever (often)
· Nonproductive cough
· Dyspnea
· Normal auscultation/labs
· Interstitial bilateral infiltrates on CXr.
· Erythema multiforme: Multiple skin lesions with blue livid center, pale intermediate zone, and dark red peripheral
rim.
· Common extrapulmonary features include fatigue, headaches, sore throat, myalgias, and malaise.
*Legionella features: High fever >39°C, contaminated water, diarrhea, confusion (hyponatremia) and CXr: patchy, unilateral,
lobar infiltrates (consolidation).
• Cough: recurrent/persistent non-productive cough that worsens at night or accompanied by wheeze or breathlessness. Cough in the
absence of respiratory infections, usually with laughing, crying or exposure to tobacco smoke.
• Wheezing: Recurrent wheezing during sleep or with triggers such as activity, laughing, crying or exposure to tobacco smoke or air
pollution
• Difficult or heavy breathing or shortness of breath occurring with crying, laughing or playing.
• Reduced activity: not running, playing, or laughing at the same intensity as other children.
• Therapeutic trial with moderate dose inhaled steroids: Clinical improvement in 2-4 wks of controller treatment and worsening when
treatment is stopped.
IV. Croup
• A result of viral inflammation of the larynx, trachea and bronchi, hence the term laryngotracheobronchitis.
● 3 months to 3 years old child
• The most common pathogen is parainfluenza virus (74%), (types 1, 2 and 3).
Others:
- Respiratory Syncytial Virus, Influenza virus types A and B, Adenovirus, Enterovirus, Measles, Mumps and Rhinoviruses and rarely
Mycoplasma pneumoniae and Corynebacterium Diptheriae.
Clinical Features
• Low grade fever, cough and coryza for 12-72 hours, followed by:
• Increasingly bark-like cough and hoarseness.
• Stridor that may occur when excited, at rest or both.
• Respiratory distress of varying degree.
Elicit history and physical signs
in children with breathlessness
History
1. History of presenting illness
a. Onset + Duration (eg, 12-72hrs of fever and coryza followed by cough, suggestive
of croup)
b. Associated symptoms: Cough (nature of cough - barking cough indicating
croup) , fever, tachypnea (LRTI), noisy breathing, trouble sleeping, poor feeding
c. Any previous admissions due to similar symptoms
2. Sick contact + Travel history
3. Birth complications in neonates
a. Preterm babies
4. Social history
a. Living conditions, overcrowding, allergies, pets
5. Family history of asthma / eczema
Physical signs
1. General inspection
a. Pink, BMI (weight + height)
b. Level of consciousness
c. Signs of respiratory distress
2. Inspection of the chest
a. Throat: Any foreign bodies (if indicated in hx) (obstruction → breathlessness)
b. Chest deformities
c. Check for any chest indrawing / intercostal recession or hyperinflation (indicate
bronchiolitis)
3. Auscultation
a. Listen for any wheeze or stridor (croup)
b. Auscultate for rales / rhonchi / crepitations and air entry
Evaluate the clinical findings and
formulate the differential diagnoses
Condition Clinical findings
Pneumonia Reduced breath sounds, dull on percussion, crepitations, bronchial breath sounds
CCF Bilateral basilar rales, dull on percussion, coolness of peripheries, jugular venous
distention, kussmaul sign
Epiglottitis Odynophagia, pain over larynx on palpation, respiratory distress, hypoxia, toxic
appearance, dysphagia, stridor, drooling, muffled voice, absence of hoarseness, cough
Bacterial bronchopneumonia
● Elevated WBC (> 20 000 cu.mm) mainly neutrophils - tachypnea , high fever
Bronchial Asthma
Viral bronchopneumonia
Bronchiolitis
Chest Radiography
● Increased lung radiolucency , normal lung fields or areas
of increased density
● Hyperinflation with horizontal ribs , flattened diaphragm
● Patchy atelectasis often in right upper lobe
● Peribronchial thickening
Asthma:
Bronchiolitis:
- Supportive treatment
- Give humidified 02 (conc. determined by pulse oximetry reading)
- Assisted ventilation in the form of nasal or facemask CPAP or full ventila tion is
required in a small percentage of infants
- RSV (highly contagious) so take appropriate measurements to prevent spread in
the hospital setting
Croup:
- When the upper airway obstruction is mild, the stridor and chest recession
disappear when the child is at rest. The child can usually be managed at
home.
Pneumonia :