WEBVTT

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Today's topic is a very general topic but a very very burning

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topic for pediatricians. The topic is approach to respiratory distress in

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children. I shall be taking this topic under following heads, introduction about

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the respiratory diseases in children, some basic findings in the clinical signs

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and symptoms and the most important diseases like acute epiglottis,

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group syndrome involving the upper respiratory tract, acute bronchiolitis,

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bronchial asthma, pneumonia in the lower respiratory tract in brief. So let

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us see the respiratory anatomy. We have got the anterior nares, the

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nasal cavity, we have got the nasal pharynx, the oropharynx, the oral

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oral cavity here. So then you have got the hypopharynx. Any disease

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occurring up to this is your upper respiratory tract infection. After

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the glottis, whatever infection occurs, it is your lower respiratory tract infection.

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Once again, you have got the epiglottis here, acute epiglottis which this

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this epiglottis is there to prevent passage of food to the

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windpipe. You can see the cross section of the nasal cavity, oral

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cavity, the larynx, glottis and larynx. So respiratory infections in

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children account for 50% or more of consultations with general practitioner for

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acute illness in young children and one third in older children. Respiratory

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illnesses lead to 30 to 35% of acute pediatric admissions to hospital.

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They are the commonest cause of death in children between 1 and

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14 years in our country. Upper respiratory tract infection is most common

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acute infection followed by bronchial asthma as the chronic infection. Now what

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are the causes? Viruses cause 80 to 90% of childhood respiratory infections.

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The most important are RSV, respiratory syncytial virus, rhinovirus,

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influenza, parainfluenza and adenovirus. An individual virus can cause

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several different patterns of illness. RSV can cause bronchiolitis, croup, pneumonia

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or common cold. The important bacterial respiratory pathogens are Streptococcus pneumoniae

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and other streptococci, H. influenzae, Bordetella pertussis which causes whooping cough,

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Mycoplasma pneumoniae, Mycobacterium tuberculosis remains an important pathogen still. Some

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pathogens cause predictable epidemics such as RSV bronchiolitis every

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winter, whereas others example Pneumococcus show little seasonal variation. So what are

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the host and environmental factors? Poor socioeconomic status that

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is overcrowding, damp housing and poor nutrition, large family size, maternal

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smoking, boys more than girls, prematurity especially infants who have required

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artificial ventilation, congenital abnormalities of lungs and heart, rarely immune

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deficiency, congenital A gamma globulinemia or acquired like

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HIV infections and malignancies. Just have a look on this pie diagram.

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The pneumonias both in children and neonates, they account for

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24% of all the diseases in children and that's a major chunk.

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What is a acute respiratory infection with a distress? A clinical state

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characterized by increased respiratory rate and increased respiratory efforts.

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It refers to any type of subjective difficulty in breathing. The features

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of respiratory distress are tachypnea, dyspnea, nasal flaring, chest

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wall retractions, edited sounds with or without head bobbing. We can

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grade the acute respiratory distress in mild, moderate and severe. In the

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mild, the child will be having only tachypnea and dyspnea or shortness

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of breath. In moderate, there will be tachypnea again, minimal chest retractions

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and flaring of alar nares. In the severe variety, we market tachypnea

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more than 70 breaths per minute, apneic episodes or bradypnea and

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irregular breathing. Lower chest wall retractions, head bobbing, that

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is use of sternocleidomastoid muscles and cyanosis. The

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upper limit of respiratory rate in children is 0 to 2 months,

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60 per minute, 3 to 12 months, 50 per minute, 1 year

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to 5 years, 40 per minute, 5 years to 12 months, 30

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per minute. What are the causes of breathing difficulty in children? Upper

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respiratory tract involvement like croup, acute epiglottis, Ludwig's angina,

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retropharyngeal abscess, foreign body aspiration, diphtheria, laryngospasm

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or acute anaphylaxis. Lower respiratory tract involvement, pneumonias,

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bronchiolitis, asthma, pleural effusion, empyema and hemothorax. Hemothorax,

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atelectasis and hypersensitive pneumonitis. I shall be covering only few of

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them because beyond the scope of this lecture, there are certain non

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pulmonary causes also we can give rise to respiratory distress in children

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like congestive heart failure due to heart disease or severe anemia, metabolic

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acidosis due to renal failure, diabetic ketoacidosis, renal tubular acidosis, shock

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and lactic acidosis, psychogenic hyperventilation, anxiety, panic attacks,

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CNS infections, cerebral edema, tumors, raised ICP and brain stem

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compressions, spinal cord injury and GBS syndrome severe type. What

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are the clinical features? Fever, cough and rapid breathing. It can occur

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in lower respiratory tract infections like pneumonia, bronchiolitis and virus associated wheeze.

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Exercise induced dyspnea can occur in asthma, congestive heart failure, severe

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anemia, nocturnal cough, orthopnea and dyspnea, congestive heart failure, fever,

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sore throat, stridor, acute epiglottis, severe chest pain with rapid

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shallow breathing, decreased air entry, pneumonia, pneumothorax, pulmonary embolism, acute

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respiratory distress after sudden choking, hyperinflated chest can occur in foreign body

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inhalations. Fever with altered sensorium, convulsions, fast breathing can occur in encephalitis

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involving brain stem, chest wall retractions, paraplegia in acute flaccid paralysis as

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occurs in Guillain-Barre syndrome, acute respiratory distress with vomiting, altered sensorium,

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hydrocarbon poisoning and fast breathing, altered sensorium, polyuria, and dehydration

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in diabetic ketoacidosis. There are certain abnormal breath sounds. Let's take one

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by one. Stridor, upper airway obstruction. It can occur because of foreign

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body or swelling of the upper airways, grunting, upper airway obstruction, swollen

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airway again, pneumonia. It occurs to recruit more alveoli, wheeze,

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lower airway obstruction as in asthma and crackles that flowed in lungs

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which occurs in pneumonia or it is resolving. So snoring occurs from

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oropharyngeal obstruction. It can be inspiratory, low pitched or irregular. Grunting occurs

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in partial closure of glottis. It is expiratory, occurs in hyaline membrane

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disease. Rattling sound is produced by secretions in the trachea or bronchi.

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Inspiratory course can be felt by placing hand over the chest. Stridor

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occurs in obstruction of larynx or trachea. Inspiratory may be associated with

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an expiratory component, wheeze, lower airway obstruction, continuous musical

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sound. This can be monophonic or polyphonic, predominantly expiratory in nature,

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but it can be inspiratory also that increases the severity of the

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disease. So types of stridor can be inspiratory, collapse of tissue above

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the vocal cord, expiratory down the trachea, wheezing, biphasic narrowing of subglottis

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below the vocal cord. So location of pathology, stridor, upper airway obstruction,

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wheezing, lower airway obstruction. Example is in the stridor narrowing of epiglottis,

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subglottis, larynx and trachea, wheezing, narrowing of bronchi, bronchioles, alveoli, damage,

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secretion, phase, inspiration, expiration or both. Wheezing normally inspiration, expiration

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or both. Quality, high pitched, both high pitched. The disease is stridor,

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angioedema, inhalation injury, congenital anomalies, acute esophagitis, retropharyngeal

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abscess, croup syndrome, laryngomalacia, vocal cord paralysis, subglottic stenosis, papillomatosis,

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foreign body aspiration, trauma to larynx and wheezing in asthma, foreign body,

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pneumonia, heart failure, COPD or lung cancer. What are the warning signs

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of dyspnea? Symptoms, impending respiratory failure that is cyanosis, silent

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chest, poor respiratory efforts, fatigue, exhaustion, agitation, reduced

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level of consciousness. The pre-terminal signs are bradypnea that is the pulse

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rate start becoming slow, desaturation, oxygen concentration start falling,

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altered sensorium. The red flag signs are the red flag signs are

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respiratory rate more than 70 per minute, severe chest indrawing, head nodding

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or grunting, central cyanosis, stridor in a calm child, inability to feed.

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The initial general assessment is the goal is to rapidly assess for

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airway patency, adequacy of gas exchange, circulatory status. So we have

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the ABC approach, appearance, interaction, muscle tone, consolability, speech

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and cry, wheeze or work of breathing, use of accessory muscles and

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bradypnea, change abnormal skin color, pallor and cyanosis. Take a proper history.

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Is it acute, recurrent or chronic? What is the nature of progression?

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Is it associated with cough, fever, rash or chest pain? Preceding events,

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choking, foreign body inhalation, trauma, accident and exposure to chemical or environmental

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irritants, family history, exposure to infection, tuberculosis or allergy. Do the basic

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investigations like CBC with peripheral blood smear, ESR, CRP, blood

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culture and sensitivity, ABG, X-ray chest, echo, pulse oximetry

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and a pulmonary function test. Management includes management of airways, breathing, circulation

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and treatment of etiology, foreign body if if the cause is removal,

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croup, humidified oxygen, IV antibiotics, intubation or tracheostomy may be required.

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Pneumonia, humidified oxygen, antipyretics, antibiotics and IV fluids, bronchiolitis,

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symptomatic moist oxygen inhalation is the main stay of treatment. Antibiotics have

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no role. In the bronchial asthma, humidified oxygen, bronchodilators, steroids, magnesium

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sulfate in severe asthma. So let's see the croup syndrome. It's an

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acute infectious disease. There may be barking or brassy cough, hoarseness and

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inspiratory stridor. This includes the spectrum of disorders like laryngotracheobronchitis,

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acute infectious laryngitis is the other name for laryngotracheobronchitis,

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acute bacterial tracheitis and spasmotic bronchitis. So the host

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of causes viral infections like parainfluenza virus type 1, respiratory syncytial

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virus, parainfluenza type 2 and 3, influenza virus, adenovirus, rhinovirus,

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human bocavirus. Onset of the illness is more gradual, mild cough for

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a few days, brassy barking cough, mild inspiratory stridor. As the obstruction

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increases, stridor becomes prominent and then there will be suprasternal and sternal

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recession. Age is 6 months to 3 years. Mild self limiting disease

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can lead to acute respiratory distress and upper airway obstruction. Inflammation causes

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narrowing just below the vocal cords that is subglottic airway, increasing restlessness

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and anxiousness with tachypnea due to increasing hypoxemia, cyanosis. As the

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obstruction worsens, breath sounds may become inaudible and stridor may apparently decrease.

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This may unfortunately be misinterpreted as clinical improvement and we may lose

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the child if if you are not prompt. You must assess the

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severity of the illness on basis of general appearance, stridor, oxygen saturation

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and respiratory distress. In mild cases, give a ambulatory treatment. In moderately

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severe cases, illnesses may need hospitalization and treatment with nebulized epinephrine

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one in 1,000 in doses of 0.1 to 0.5 ml per kg

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to a maximum dose of 0.5 ml administered through nebulizer for immediate

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relief of symptoms. Epinephrine acts rapidly to decrease vascular permeability, airway edema

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and improve air flow. The action is temporary and repeat administration may

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be necessary. A single dose of dexamethasone 0.3 to 0.6 mg per

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kg reduces the disease severity. Before 24 hours, decrease need for intubation

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and nebulization. Inhalation of budesonide induces of 1 mg twice a

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day for 2 days is useful. If the child does not respond,

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he has to be intubated and mechanically ventilated. Severe croup, hospitalization, ICU,

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oxygen inhalation, steroids, short term ventilation, NIV or invasive or non-invasive.

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So all these these children you examine. Throat examination is rarely required.

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If the child is having a barking cough, inspiratory stridor, coarse wheeze,

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they have may have widespread associated wheeze, increased work of breathing, may

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have fever but no signs of toxicity. The risk factors are narrowing

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of the upper airways, previous admissions with severe croup, uncommon before less

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than 6 months of age and less than 3 months of age.

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Consider alternative diagnosis and causes of upper airway obstruction. You can see

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the steeple sign here. This is the narrowing of the airways.

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You can see the steeple here. Here you can hardly see the

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windpipe. You can see the trachea down below but such a severe

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narrowing. Again, you can see the steeple here. Antibiotics have no role

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in uncomplicated croup as it has a viral etiology. Antitussives such as

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codeine have no proven effect. Humidified air has not been proven to

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change the severity. Heliox has not been shown to better than nebulized

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adrenaline in severe croup. Acute epiglottis, you can see the thumb sign.

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This is a thumb sign of the inflamed swollen epiglottis. This is

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the windpipe here. You can see it is covering the entire windpipe.

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This is the epiglottis. Again here, this is the epiglottis swollen. This

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is the swollen epiglottis. This is the windpipe. Again, another visual, windpipe,

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swollen epiglottis. This is acute inflammation of epiglottis 2 to 7 years

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of age children, bacterial infection because of H. influenzae B and due

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to release of HIV in droxins. Untypable HIV can also cause sometimes

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staph is strepto and in older children group A Streptococcus and HIV.

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Early fever, sore throat, dysphagia, drooling, odynophagia, respiratory distress,

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there's no cough. Clinical triad of respiratory distress, dysphagia and drooling is

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found in epiglottis. Looks ill and toxic, restlessness, drooling,

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sits in a tripod position. There can be high grade fever, increased

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respiratory rate, increased heart rate, inspiratory stridor, had intercostal retractions.

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There may be respiratory fatigue and a muffled voice called dysphonia. Same

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thing again, you can just say acute swelling of the epiglottis tissue

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blocking almost the airway. Acute respiratory obstruction, there may be asphyxiation.

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Diagnosis is clinical and recognition has to be prompt and acted immediately.

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Do not perform a clinical examination. Why? Because waste of time in

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emergency you may close the airway due to swelling of epiglottis. X-ray

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is a thumbprint sign due to swollen epiglottis which are shown in

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the X-rays. Treatment is maintain airway, intubation, tracheostomy, perform clinical examination

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after securing the airway. Antibiotics like ceftriaxone may be used, steroids,

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dexamethasone, humidified air, oxygen and IV fluids can be given. Another

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cause of croup is bacterial tracheitis in younger children, viral upper respiratory

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tract infection. Appears toxic with brassy cough and stridor, classic irregular tracheal

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wall on X-ray, bronchoscopy diagnostic and therapeutic. Purulent secretions can be visualized,

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cultured and mechanically debrided. Bacterial tracheitis is a relative medical emergency as

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like setting obstruction may develop from these tracheal secretions. The responsible pathogen

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is usually staph aureus. Spasmotic croup under cause of

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croup syndrome, children between the age of 1 and 3 years. Preceding

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coryza may or may not be there. Wake child wakes up suddenly

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in the early hours of the morning with brassy cough and noisy

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breathing. Symptoms improve within few hours. The illness may occur on recur

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on subsequent days. The course is generally benign and patients recover completely.

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Cause is unknown. Humidification of the room in which the child is

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nursed is all that is necessary. Retropharyngeal abscess, potential suppurative

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complications of bacterial pharyngitis may present with stridor, high fever, reduced mobility

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of the neck and appear toxic. Complications include spread of infection into

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mediastinum. Mediastinitis is potentially fatal. Lateral neck radiograph reveals the bulge

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in the posterior pharyngeal wall. Treatment is by surgical drainage and broad

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spectrum parenteral antibiotics. There are certain congenital causes, commonest being congenital

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laryngeal anomaly, 60% of all causes and the most common cause of

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infant stridor that is in the early neonatal period and infancy

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with laryngomalacia. Inspiratory stridor sometimes aggravated when the child is supine or

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crying because the trachea falls and it is because the supportive tissue

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in the trachea of the larynx is not there which which normally

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develops as the child grows. Flexible endoscopy reveals partial collapse or flashes

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of supraglottic airway with inspiration. Gastroesophageal reflux should be managed. Laryngomalacia

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benign and self limited most cases resolved by 18 months of the

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age. Surgical intervention is advised for either respiratory distress or failure to

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thrive. Vocal cord paralysis, second most common congenital laryngeal anomaly, bilateral

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vocal cord paralysis will present with a high pitched inspiratory stridor and

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cyanosis. Iatrogenic by excessive stretch of the neck during vaginal delivery producing

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an outpalsy of the recurrent nerve but can also be idiopathic. Other

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causes may include Arnold-Chiari malformation, hydrocephalus or hypoxia. Unilateral

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vocal cord paralysis presents with a mild stridor or with signs of

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aspiration. Congenital subglottic stenosis is third most common cause of stridor.

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Then there can be vascular rings, subglottic hemangioma, congenital sacculocis,

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laryngeal web and laryngeal atresia. So they're very very rare causes. There

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are certain iatrogenic causes we we cause acquired subglottic stenosis. The most

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common cause of acquired is stridor. It most often results from long

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term endotracheal intubation and subsequent scar formation. Laryngeal granuloma may

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also result from prolonged intubation. Endoscopy reveals a vocal cord granuloma. Recurrent

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respiratory papilloma can also give rise to stridor. Acute bronchiolitis is the

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common serious acute lower respiratory tract infection in infants. Age group 1

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to 6 months and it can occur rarely up to 2 to

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3 years and but very severe in babies less than 1 year.

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Occurs in winter and spring. Respiratory syncytial virus is the parainfluenza virus,

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adenovirus, influenza virus and rarely Mycobacterium pneumoniae. Protection against

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RSV is maintained by antibody IgG 3 subclass. These antibodies have shorter

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half life and do not cross the placenta in substantial amount so

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as to offer protection to the infant. That means the transmission from

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mother to the baby is hardly any. High quantities of secretory IgG

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antibodies to RSV present in the colostrum and breastfeeding reduces the likelihood

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of an infant being hospitalized with acute bronchiolitis. So if the baby

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is breastfed, he is less likely to suffer from bronchiolitis or if

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he suffers, it will be very very minimal. Pathogenesis includes inflammation of

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the bronchial mucosa leading to thickening, formation of mucus plugs and cellular

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debris. Bronchial spasm in some cases, bronchial lumen is already narrow in

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infants is further reduced as airway resistance in irreversibly related to the

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fourth power of the radius. Even slight narrowing of the bronchial lumen

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causes marked increase in airway resistance both during inspiration and expiration. During

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expiration, the bronchioles are partially collapsed and egress of air from the

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lungs is severely restricted resulting in air trapping inside the alveoli causing

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emphysematous changes. When obstruction becomes complete, the trapped air in the lungs

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may be absorbed causing atelectasis. Due to diminished ventilation and diffusion, hypoxemia

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00:20:23.800 --> 00:20:27.200
it produce in almost all of these infants. Retention of carbon dioxide

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leads to respiratory acidosis. The presence of eosinophils in the blood and

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respiratory secretions suggests that the viral infection initiates the wheezing attack in

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a child who is already sensitized. Clinical features, a few days following

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an upper respiratory tract infection, breathing becomes fast and respiratory distress develops.

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Majority of infants have mild symptoms and recover in 3 to 7

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days. Those with severe disease may develop retraction of lower intercostal spaces

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and suprasternal and sternal recession. Age is 6 months

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to 3 years. In severe infection, the infant is dyspneic and may

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appear cyanosed. Fever is moderately high. Accessory muscles of respiration are working.

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Prolong expiration, fine crepitations and rhonchi, breath sounds may be faint or

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inaudible in severe cases. Respiratory distress is out of proportion to the

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physical signs. Hyperinflation results in the liver and spleen being pushed down

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00:21:11.600 --> 00:21:15.300
and they are palpable. When the chest becomes over inflated, the anteroposterior

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diameter of the chest is increased. Increasing resonance is noted if you

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do a percussion. X-ray shows hyperinflation of infiltrated diaphragm is pushed down.

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The lungs fields appear abnormally translucent. Leukocyte count is normal or slightly

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00:21:28.300 --> 00:21:33.100
elevated. A rapid test using monoclonal antibodies on nasopharyngeal aspirate can identify

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the respiratory syncytial virus. Bronchiolitis is a self limiting illness. Symptoms subside

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in 3 to 7 days. Death may occur in 1% of the

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severely ill patient due to respiratory failure. Normally in babies less than

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1 year of age. The relationship of acute bronchiolitis to bronchial asthma

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in later life is observed in about 25% cases of acute bronchiolitis.

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Bronchial asthma is more likely in children with personal or family history

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of an allergic illness. You can it can mimic bronchial asthma,

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congestive heart failure, foreign body in trachea and bacterial pneumonia. Treatment is

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symptomatic in mild cases and can be cared at home with humidified

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00:22:12.400 --> 00:22:17.600
atmosphere. If the respiratory distress increases or there's feeding problem,

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child should be hospitalized in hospital and he is nursed in a

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humid atmosphere preferably in sitting position at angle of 30 to 14

289
00:22:25.800 --> 00:22:30.500
degrees with head and neck elevated. Moist oxygen is given continuously even

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00:22:30.500 --> 00:22:34.200
in the absence of cyanosis. Very sick infant may need a concentration

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00:22:34.200 --> 00:22:38.900
of 60% oxygen given through hood. Pulse oximetry should be performed regularly

292
00:22:38.900 --> 00:22:43.100
to keep oxygen saturation of more than 92% fluids and electrolyte balance

293
00:22:43.100 --> 00:22:47.600
should be maintained in all babies. Antibiotics have got no role. Ribavirin

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00:22:48.000 --> 00:22:52.500
is controversial that it has been tried. Beta 2 adrenergic drugs and

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ipratropium are not recommended for infants less than 6 months of age.

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00:22:56.300 --> 00:23:00.200
A recent review on use of bronchodilators in bronchiolitis suggests the beneficial

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00:23:00.200 --> 00:23:05.300
effect of inhale salbutamol with ipratropium and epinephrine. So depending on

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the situation, the child has got bronchospasm, you may use this. If

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the patient shows improvement, the bronchodilator may be given for 4 to

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00:23:12.200 --> 00:23:17.000
6 hourly. Continuous positive airway pressure or assisted ventilation may be required

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00:23:17.000 --> 00:23:21.200
to control respiratory failure if it is there. ECMO can be given

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00:23:21.300 --> 00:23:26.000
if the other measures fail. The next is acute bronchial asthma in

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00:23:26.000 --> 00:23:29.600
children. I'll be covering very in very brief. Bronchial asthma is a

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00:23:29.600 --> 00:23:34.300
disease characterized by increased responsiveness of the airways to various stimuli. Widespread

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00:23:34.300 --> 00:23:39.300
narrowing of the airways causes paroxysmal dyspnea, wheezing or cough. Edema and

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00:23:39.300 --> 00:23:43.900
inflammation of mucus membrane lining the airways. There is excessive secretion of

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00:23:43.900 --> 00:23:49.000
mucus, inflammatory cells and cellular debris and spasm of the smooth muscles

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00:23:49.000 --> 00:23:52.700
of the bronchi. So there are three factors which lead to airway

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00:23:52.700 --> 00:23:56.600
obstruction in the asthma. Edema and inflammation of the mucus membrane lining

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00:23:56.600 --> 00:24:00.900
the airways, excessive secretion of mucus, inflammatory cells and cellular debris and

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00:24:00.900 --> 00:24:05.000
spasm of the smooth muscle of bronchi. So the clinical features are

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00:24:05.000 --> 00:24:09.600
steeple recurrent cough to severe wheezing, dyspnea with prolonged expiration and wheezing,

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00:24:09.600 --> 00:24:15.300
active accessory muscles of respiration, sweating profusely, cyanosis, apprehensive

314
00:24:15.300 --> 00:24:19.500
child, restless and fatigued. There may be air hunger. If you examine,

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00:24:19.500 --> 00:24:24.300
there may be hyper resonant chest, persistence of hyperinflation of the chest

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00:24:24.300 --> 00:24:29.000
even after subsidence of asthmatic attack signify that the apparent relief from

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00:24:29.000 --> 00:24:32.800
bronchospasm will be short lived. Now breath sounds may become feeble or

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00:24:32.800 --> 00:24:36.700
inaudible or absent. This is an ominous sign. Absence of wheezing in

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00:24:36.700 --> 00:24:42.000
presence of cyanosis on respiratory sign. Again ominous sign. Pulsus paradoxus indicates

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00:24:42.000 --> 00:24:47.200
severe illness. Again a very ominous sign. Severe hypoxemia may result cyanosis

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00:24:47.200 --> 00:24:51.700
and cardiac arrhythmias against a very ominous sign all like threatening. As

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the child improves, the air flow increases and wheezing may reappear. With

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00:24:55.700 --> 00:25:02.830
remission, the wheeze disappears. Severe hypoxemia may result Perhaps

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00:25:02.830 --> 00:25:06.430
some small segments of the lung may occur. The various triggers are

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viral infection of the respiratory tract, dust mites, pollens, environmental tobacco smoke,

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00:25:11.730 --> 00:25:16.430
particulate matter, wood or coal burning smoke, cold dry air, exercise, rhinitis

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00:25:16.430 --> 00:25:21.730
and sinusitis. The goals of therapy are maintain near normal pulmonary function,

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00:25:21.830 --> 00:25:26.930
maintain near normal physical activity, prevent nighttime cough or wheezing with minimal

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00:25:26.930 --> 00:25:32.130
chronic symptoms, prevent recurrences, avoid adverse effects of therapy. So

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00:25:32.130 --> 00:25:37.430
the treatment includes bronchodilators, that is salmeterol, salmeterol,

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00:25:37.530 --> 00:25:41.030
formoterol. Then we have got the xanthines, we have got the mast

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00:25:41.030 --> 00:25:46.030
cell stabilizers like sodium cromoglycate and ketotifen. Then is the inhaled

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00:25:46.030 --> 00:25:50.330
corticosteroids. We have got the beclomethasone, budesonide. Then we have got the

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00:25:50.330 --> 00:25:55.330
leukotriene antagonists that is montelukast. The pharmacological management includes

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00:25:55.330 --> 00:26:00.430
assessment of symptom, assessment of risk,

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00:26:01.330 --> 00:26:06.530
exacerbation, selection of medications, selection of appropriate inhalation device

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00:26:06.530 --> 00:26:11.630
and monitoring. Selection of appropriate inhalation device includes meter dose MDI, MDI

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00:26:11.630 --> 00:26:15.430
with spacer, MDI with spacer with face mask, dry powder inhalation and

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00:26:15.430 --> 00:26:19.530
nebulizer. For children below four years of age, we give MDI with

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00:26:19.530 --> 00:26:23.730
spacer with face mask can be used. For children four years of

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00:26:23.730 --> 00:26:28.230
age and more, MDI with spacer is preferred. For children 12 years

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00:26:28.230 --> 00:26:32.130
of age, MDI may be used directly. So pharmacotherapy, what it does?

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00:26:32.230 --> 00:26:37.830
Relaxes smooth muscle, dilates the airways, decreases inflammation and prevents exacerbation.

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00:26:38.030 --> 00:26:43.430
The various modalities are I have already enumerated. Just to repeat bronchodilators

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00:26:43.530 --> 00:26:48.730
like salmeterol, formoterol, steroids, dexamethasone, mast cell stabilizers,

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00:26:48.730 --> 00:26:54.130
leukotriene modifiers, theophylline. Bronchodilators give immediate symptomatic relief

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00:26:54.230 --> 00:26:59.530
which is short-acting and long-acting adrenaline, terbutaline and salmeterol.

348
00:26:59.630 --> 00:27:04.130
Terbutaline and salmeterol are specific beta-2 agonists. So these are the various

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00:27:04.130 --> 00:27:07.830
doses schedule. I'm not going to in detail. We have got the

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00:27:07.830 --> 00:27:13.230
beclomethasone. All these are available as MDIs. Beclomethasone, budesonide,

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00:27:13.330 --> 00:27:18.730
fluticasone or more is the ciclesonide. Now there are certain add-on

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00:27:18.730 --> 00:27:24.230
drugs on controller drugs. They are the tiotropium, anti-IgE

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00:27:24.230 --> 00:27:29.530
that is omalizumab, interleukin-5 and anti-interleukin-5R,

354
00:27:29.630 --> 00:27:35.130
anti-interleukin-4 that is dupilumab and systemic corticosteroids, tablet

355
00:27:35.130 --> 00:27:40.130
suspension, IM, IV, prednisolone, prednisolone, methylprednisolone, hydrocortisone. These are given

356
00:27:40.130 --> 00:27:43.530
short-term five to seven days and the effects seen after four to

357
00:27:43.530 --> 00:27:48.030
six hours. So to begin with, we always start with a The

358
00:27:48.030 --> 00:27:53.330
rescue drugs are your bronchodilators. For us it is the aclidinium,

359
00:27:53.430 --> 00:27:58.630
terbutaline. Then the controller drugs are steroids. We always add a

360
00:27:58.830 --> 00:28:04.030
short-term low-dose steroids along with the salmeterol. Whenever the child

361
00:28:04.030 --> 00:28:08.630
gets and the child will be maintained on low-dose steroids via device,

362
00:28:08.630 --> 00:28:14.030
I already explained. And whenever he gets attack, he'll be advised

363
00:28:14.030 --> 00:28:19.030
a inhaled aclidinium inhalations as and when required. So

364
00:28:19.030 --> 00:28:23.530
what is the management of life-threatening asthma? Oxygen inhalation, adrenaline is given

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00:28:23.530 --> 00:28:29.230
subcutaneously, may be given. Inhalation of salmeterol or terbutaline and ipratropium.

366
00:28:29.330 --> 00:28:33.530
Hydrocortisone 5 mg per kg IV and arrangements are made to transfer

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00:28:33.530 --> 00:28:37.430
the patient to ICU. If the patient shows improvement, salmeterol or terbutaline

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00:28:37.430 --> 00:28:41.230
inhalation is continued every 20 to 30 minutes. Hydrocortisone 5 mg per

369
00:28:41.230 --> 00:28:44.530
kg continued for six to eight hours till patient starts accepting orally.

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00:28:44.630 --> 00:28:48.630
If patient does not improve or deteriorates, a slow IV infusion of

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00:28:48.630 --> 00:28:53.030
magnesium sulfate 50 mg per kg is given for 30 minutes. Alternatively,

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00:28:53.030 --> 00:28:56.530
a loading dose of theophylline may be infused. If there's no improvement

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00:28:56.530 --> 00:29:00.930
with this management, patient is prepared for mechanical ventilation. Patient also screened

374
00:29:00.930 --> 00:29:06.330
for acidosis or any complication developing like pneumothorax or electrolyte imbalance.

375
00:29:06.430 --> 00:29:10.230
So these are various modalities by which we treat the children like

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00:29:10.230 --> 00:29:15.330
nebulizer, we have the meter dose inhalers, we have the rotahaler, MDI

377
00:29:15.330 --> 00:29:20.430
with spacer and baby mask, use of meter dose inhalers, MDIs. Education

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00:29:20.430 --> 00:29:24.730
of parents is very important. Education of patients and their parents is

379
00:29:24.730 --> 00:29:29.430
an important aspect of management. A description of the etiopathogenesis of asthma

380
00:29:29.430 --> 00:29:32.830
should be made. Severity of the illness, course of and outcome is

381
00:29:32.830 --> 00:29:37.430
explained. Avoidance of all kinds of smoke at home, active or passive.

382
00:29:37.430 --> 00:29:41.330
Maintaining a record of daily symptoms such as cough, wheeze and breathlessness.

383
00:29:41.430 --> 00:29:44.430
A record of sleep disturbance, absence from school due to illness is

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00:29:44.430 --> 00:29:49.030
advised. So the last one is pneumonia. This I this I think

385
00:29:49.030 --> 00:29:52.330
I have already covered about full lecture on pneumonias. Pneumonia may be

386
00:29:52.330 --> 00:29:57.330
classified anatomically as lobar, lobular pneumonia, bronchopneumonia and

387
00:29:57.430 --> 00:30:02.530
interstitial pneumonia. Pathologically, there's consolidation of alveoli or infiltration of the interstitial

388
00:30:02.530 --> 00:30:07.530
tissue with inflammatory cells or both. Causes are viral, RSV, influenza, parainfluenza,

389
00:30:07.530 --> 00:30:12.430
adenovirus, coronavirus, bacterial now 40 to 60% of cases. Common bacteria cause

390
00:30:12.430 --> 00:30:17.530
pneumonia are gram-negative Klebsiella in first two months, gram-positive pneumococci is staff

391
00:30:17.530 --> 00:30:21.930
between three months and three years. Streptococcal pneumonia actually influenza and staff

392
00:30:22.030 --> 00:30:25.730
after three years it is pneumococci, streptococcal pneumonia and staff. There can

393
00:30:25.730 --> 00:30:31.330
be atypical organisms, Chlamydia and Mycoplasma. Pneumocystis carinii zero causes

394
00:30:31.330 --> 00:30:36.330
pneumonia in immunocompromised children. Fungal histoplasmosis and coccidioidomycosis.

395
00:30:36.430 --> 00:30:41.430
Miscellaneous include ascariasis, Loeffler syndrome, aspiration of food, nose drugs,

396
00:30:41.430 --> 00:30:46.430
cirrhosis and hypersensitivity pneumonitis. Rarely pneumonia may present with symptoms of

397
00:30:46.430 --> 00:30:51.630
acute abdominal emergency. This is attributed to a referred pain from pleura.

398
00:30:51.830 --> 00:30:56.930
Atypical pneumonias may sometimes be associated with meningismus and convulsions. On

399
00:30:56.930 --> 00:31:00.030
examination, there is a flaring of alae nasi, retraction of lower chest

400
00:31:00.030 --> 00:31:05.330
and intercostal spaces. When do you hospitalize cases of pneumonia?

401
00:31:05.830 --> 00:31:10.830
Moderate to severe pneumonia having respiratory distress, tachypnea, retractions, grunting, nasal flaring

402
00:31:10.830 --> 00:31:17.230
or head bobbing and SpO2 less than 90%. Children

403
00:31:17.230 --> 00:31:21.930
less than six months of age with suspected bacterial pneumonia. Dehydration, vomiting

404
00:31:21.930 --> 00:31:26.930
or inability to take oral medication, presence of comorbid conditions. Example

405
00:31:26.930 --> 00:31:32.030
immunological disorders, hematological, cardiac and chronic pulmonary conditions, genetic

406
00:31:32.030 --> 00:31:37.230
syndromes and neurocognitive disorders. Improper compliance to therapy or follow-up.

407
00:31:37.430 --> 00:31:42.530
Just to conclude, acute respiratory infections are an important cause of morbidity

408
00:31:42.530 --> 00:31:46.730
and mortality in children. Early recognition of the life-threatening symptoms and prompt

409
00:31:46.730 --> 00:31:50.630
hospitalization and treatment is the goal of every physician caring for children.

410
00:31:50.730 --> 00:31:55.630
We can have primary prevention by adequate nutrition, increasing immunization coverage rate,

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00:31:55.630 --> 00:32:00.430
reducing indoor pollution, health education, exclusive breastfeeding till six months of age

412
00:32:00.430 --> 00:32:05.930
and initiation of complementary feeding. Vaccines again diphtheria,

413
00:32:05.930 --> 00:32:11.230
pertussis and measles, influenza, RSV measles can decrease the mortality

414
00:32:11.230 --> 00:32:15.530
associated with ARI. Vaccination against pneumococcus and Haemophilus influenza type B may

415
00:32:15.530 --> 00:32:19.030
decrease the incidence and deaths associated with pneumonia in children. We can

416
00:32:19.030 --> 00:32:23.430
have a secondary prevention by early diagnosis and treatment, differentiation or identification

417
00:32:23.430 --> 00:32:28.030
of clinical condition by degree of severity, initiation of appropriate antibiotics, timely

418
00:32:28.030 --> 00:32:33.030
and appropriate measures and monitoring and follow-up. Thank you so much

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00:32:33.030 --> 00:32:35.330
sir for taking your time out with us and giving such a

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00:32:35.330 --> 00:32:39.630
wonderful session today. So I request all the attendees, if you have

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00:32:39.630 --> 00:32:43.030
any doubts or questions, please post in the chat box okay in

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00:32:43.030 --> 00:32:46.430
this session we'll be taking your questions now. So sir we have

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00:32:46.430 --> 00:32:49.330
a few of the questions, we'll take those questions. Yeah yeah no

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00:32:49.330 --> 00:32:53.930
problem. Sir the first question is what role do vaccinations play in

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preventing respiratory infections in children? See vaccinology is a subject

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by itself. All the vaccines are good, they are They have been

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I mean proved beyond doubt that do prevent against the disease against

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which they are meant. So like if you give RSV vaccine, you

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can roll out the RSV pneumonias, you can roll out the bronchiolitis

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or if your very mild. So if you give roll out the

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give the vaccine H influenzae which is a part of the pentavalent

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vaccine. So certain infections are roll out. If you give a pneumococcal

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vaccine, that is roll out. Or the measles vaccine. So I mean

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I think I've given discussed in my lecture also. So all these

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vaccines are good. We are giving the vaccines right right at six

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weeks. That includes your HIV, pneumococcal, diphtheria,

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pertussis that is whooping cough. So these three vaccines are given right

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at started at six months. Then you have got the measles. You

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can give we are given influenza vaccine. I mean they are part

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of the AIP schedule but not part of the NIS schedule. So

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all these vaccines which are available should be given. They are full-proof

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and they protect against these diseases. That's throughout the message I want

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to convey. Any other question? Thank you sir for answering. We have

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one more question sir. How can recurrent respiratory infections in children be

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minimized? I think that I told you in the concluding session. A

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good health education, practice of hand hygiene, controlling the controlling

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the atmosphere where the child is living, very difficult and proper immunization,

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a good food. That's how you can prevent if there is somebody

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is a smoker that has to be to advise to go out

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and do it or abstain from it because passive smoking is as

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bad as active smoking. Thank you so much sir for taking your

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time out with us and giving such a wonderful session today. Thank

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you. Thank you everyone for joining us today. Hope you have enjoyed

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our session and learned something new to upgrade yourself in your daily

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life practices. To know more about the upcoming sessions, please visit Thank

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you sir once again. Okay bye.