stridor and wheeze-1-1.pptx

sarath267362 279 views 65 slides Dec 06, 2022
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About This Presentation

pediatrics stridor wheeze


Slide Content

WHEEZING AND STRIDOR IN CHILDREN SHIFANA MD MUHAMMED SUHAIL

STRIDOR Audible respiratory noises produced by turbulent airflow through an obstructed upper airway. Etiologies: Infections Acute laryngotracheobronchitis(croup) Acute epiglottitis Bacterial tracheitis Retropharyngeal abscess

2. Congenital causes Laryngomalacia Vocal cord pa ralysis 3.Iatrogenic causes Acquired sub glottic stenosis 4.FB aspiration

ACUTE LARYNGOTRACHEOBRONCHITIS (CROUP) Viral URTI: parainfluenzae type 1,2,3 RSV ( respiratory syncytial virus ), adenovirus, influenza,rhinovirus 6months to 3years Clinical features Low grade fever, common cold Biphasic stridor Barking cough Restless tachypnea and Cyanosis

ASSESSMENT OF SEVERITY OF CROUP

Xray Neck:narrowing of the subglottic region “steeple sign”

Management Conservative : reassurance,cool mist and oral hydration Nebulized epinephrine ( 1:1000 dilution 0 .1- 0.5 ml/kg, to a maximum of 5 mL) provide symptomatic relief single dose of dexamethasone (0.3-0.6 mg/kg, intramuscular) reduces severity, if given within the first 24 hours. Inhaled budesonide (1 mg twice a day for two days) an tibiotics against Staphylococcus and H. influenzae are indicated, if the child fails to improve .

Acute epiglottitis Serious illness Age group:- 3 to 6 years Etiology:H.influenzae type b Clinical features: sudden onset high grade fever, sore throat, muffled voice, inspiratory stridor, dysphagia . Releiving factor:Child Sits in a leaning forward position “ tripod position ” with his neck extended and saliva dribbling.

DIAGN OSIS: Airway management - Intubatio n or Rigid broncoscopy , followed by tracheostomy Humidified oxygen by hood, fluids to maintain hydration, Ceftriaxone or cefotaxime 100mg/kg/day for 7 days Atypical presentation: Flexible endoscopy – edema, erythema of supraglottic structures

Xray soft tissue neck lateral view : Thumbprint sign

Retropharyngeal abscess Eti ology:complication of bacterial pharyngitis or dental infection, with abscess formation in lymph nodes between the pharynx and prevertebral fascia Clinical features:high fever, stridor, drooling and reduced neck mobility. Complication:Spread to the mediastinum is fatal. Diagnosis: lateral neck radiograph and contrast CT.

Management: parenteral antibiotics surgical drainage of abscess by transoral or transcervical approach. Tracheostomy may be necessary to secure the airway .

Bacterial tracheitis Etiology: S . aureus, affects younger children and follows a viral upper respiratory tract infection. The child appears toxic ,brassy cough with biphasic or expiratory stridor. X-ray neck shows an irregular tracheal wall. Diagnosis:Bronchoscopy ; culture and removal of purulent tracheal secretions.

Laryngomalacia Most common congenital anomaly Chief cause of chronic stridor in infancy Clinical features: inspiratory stridor; increase in supine or crying position Flexible endoscopy: Omega shaped epiglottis Short aryepiglottic folds Partial collapse of a flaccid supraglottic airway with inspiration

Management Benign and self limiting Resolve by 18 months Surgical intervention include : Temporary Tracheostomy or supraglottoplasty is done in case of severe respiratory distress . Concomitant gastroesophageal reflux should be managed medically.

Vocal cord paralysis Second most c ommon c ongenital laryngeal anomaly Cause s : excessive stretching of the neck during vaginal delivery Injury to Left recurrent laryngeal Nerve in surgery of PDA Idiopathic Associated with hypoxia ,hydrocephalus and Arnold Chiari malformation

Clinical features : Bilateral cord palsy: high pitched inspiratory stridor and cyanosis Unilateral cord palsy:mild stridor ,weak cry Chance of aspiration in case of vagus nerve paralysis

Diagnosis Fibreoptic laryngos co py Management Treatment required in Bilateral cord palsy: tracheostomy to secure airway Unilateral cord palsy without aspiration, do not need active management as hoarseness improves with time

Acquired subglottic stenosis Most common cause of acquired stridor, follows long term endotracheal intubatio n Mucosal Trauma and inflammation of subglottis leads to scarring Clinical feature : progressive biphasic stridor afte r extubation

Management Minor stenosis requires careful observation severe stenosis requires release of stenosis with CO₂ laser and dilatation, widening with cartilage grafts or excision of stenotic segment, with tracheotomy Special T-shaped silicone tracheostomy tubes are used for temporary stenting until complete healing.

In prolonged intubation , early tracheotomy prevents the complication of post-intubation subglottic stenosis. cuffed tracheostomy tubes should be avoided in children; if a cuffed tube is essential, intermittent deflation is advised .

Foreign body aspiration Con sidered in a cut e o ns et str idor and airway obstruction in children If not expelled by coughing it migrates to lower airway, Lodging in the subglottic region In case of small FB, they lodge in secondary bronchioles and later - presents with pneumonia Management is by rigid bronchoscopy for FB removal, lavage to clear up secretions and antibiotics.

WHEEZING High pitched whistling sound audi bl e without auscultation. Partial obstruction of bronchi and bronchioles lea d ing to narrowing produces wheezing . Due to causes within lumen or in walls of bronchi

Causes Bronchial asthma Wheeze associated with lower respiratory tract infection; Bronchiolitis Tropical eosinophilia Loeffler syndrome Hypersensitivity pneumonitis. Inhaled foreign bodies cause sudden onset unilateral localized wheeze. cystic fibrosis

Bronchial Asthma Chronic inflammatory disease of airways characterized by increased responsiveness of the airways to various stimuli and reversible diffuse airway obstruction . Pathophysiology Edema and inflammation of mucous membrane lining Excessive secretions of mucus, inflammatory cells and cellular debris Spasm of smooth muscle of bronchi.

Classification Atopic – IgE mediated, allergens
Non atopic – non IgE mediated, infections
Mixed
Exercise induced

Triggers of asthma Infections ( viral ) Exercise Weather Emotions : stress Food Endocrine

Clinical features Cold or bouts of non productive cough Wheezing and dyspnea ,with prolonged expiration Cyanosi s, Pulsus paradoxus and cardiac arrythmias indicate severe illness. Child sweats profusely and is apprehensive and restless.

Child shows air hunger and fatigue. Hyperresonant chest severe obstruction : feeble breath sounds ,wheezing disappears. Chronic intermittent cases:barrel shaped chest

Diagnosis Clinical Family h/o asthma or atopic dermatitis or allergic rhinitis Recurrent episodes that resolved Relatively afebrile episode Presence of trigger factors :nocturnal or seasonal exacerbations,exercise induced Clear and mucoid sputum sometimes yellow .

Investigations Absolute Eosinophil count Chest Xray : b/l and symmetric air trapping , Patches of atelectasis , Prominent main pulmonary artery due to pulmonary hypertension. Pulmonary function test – PEFR{peak expiratory flow rate},FEV1{forced expiratory volume},FVC{forced vital capacity} and FEV25-75 - decreased Allergy tests

Peak expiratory flow rate (PEFR) Measured with flow meter Reduced in acute attacks and 15%reduced after exercise challenge Abnormalities Diurnal variation of >20% , <80% of predicted Improvement of >20% after bronchodilator therapy

Spirometry Useful only in children above 6 years FEV1 (the amount of air that can be expelled in the first second of forced expiration) is reduced. FEV1/FVC <80% indicates airflow obstruction and improvement of FEV1 by >12% or 200 ml after bronchodilators indicates reversibility of the airflow obstruction.

The flow volume loop shows concavity in the expiratory flow volume loop (obstruction to expiratory flow).

Allergy test Skin test to identify sensitivity to different antigens. RAST (r adioallergosorbent allergen specific Ig E ) Te st Not diagnostic, limited use . Blood IgE levels may be raised in children with atopic asthma, but is not diagnostic.

Bronchial asthma cannot be cured but can be controlled . Goals of therapy are: (1) maintain near normal pulmonary function; (ii) maintain near normal physical activity; (iii) prevent nighttime cough or wheezing with minimal chronic symptoms; (iv) prevent recurrences; (v) avoid adverse effects of therapy Management

Effective long-term management of asthma involves three major areas: i. Identification and elimination of exacerbating factors ii. Pharmacological therapy iii. Education of patient and parents about nature of disease and steps to avoid acute exacerbation

Identify and Eliminate Exacerbating factors Following measures may help in reducing risk of recurrences: i. The bedroom- clean and free from dust. Wet mopping of the floor is encouraged. ii. Since heavy tapestry attracts dust, light plain cloth sheet to be used as curtains in the child's bedroom. iii. Periodic cleaning of carpets, stuffed furniture, loose clothing and hangings, calendars and books.

iv. The child's bed should be made of light material and aired regularly. v.Caressing of animal pets is discouraged, as the child may be sensitive to their fur. vi. It is usually not necessary to restrict the diet, since food allergy is not the cause in most cases.

vii. Adolescent patients should refrain from smoking. viii. Exposure to strong odors such as wet paint, disinfectants and smoke should be minimized. ix. The child should avoid attics or basements, especially if unoccupied and closed.

Pharmacotherapy SABA{Short acting beta agonists} - salbutamol or terbutaline LABA{Long acting beta agonists}- salmeterol or formoterol ICS{Inhaled corticosteroids} - betamethasone budesonide fluticasone LTRA{Leukotriene receptor antagonists} - monteleukast Mast cell stabilizers - Nedocromil sodium, sodium cromoglyate Theophylline

Pharmacological management Key steps are : Assessment of symptom control Assessment of risk of exacerbation Selection of medication Selection of appropriate inhalational device Monitoring

Selection of appropriate inhalation device • Children <4-year-old: MDI with spacer with face mask • Children >4-year-old: MDI with spacer preferred • Children>12-year-old: MDI used directly. Use of spacer improves drug deposition .

Monitoring and Modification of Treatment After initiating treatment, patients should be seen every 4 -12 weeks. history regarding frequency of symptoms, sleep disturbance, physical activity, school absenteeism, visit to a doctor and need for bronchodilators, and PEFR is recorded. The inhalation technique and compliance is checked.

Patient is assessed as controlled, partially controlled or uncontrolled. If partially controlled or uncontrolled, cause mostly would be poor compliance, wrong technique, Associated infections, inappropriate doses etc, If no cause detected then step up Step down - control is Sustained for 3-6 Months.

Description of asthma in plain language should be made. The spectrum of severity of the illness, likely course and satisfactory outcome is explained. Avoiding environmental triggers Avoidance of all kinds of smoke at home, including tobacco smoke, wood burning and kerosene stove is emphasized. Education of parents

Parents should be advised regarding minimizing the use of carpets, curtains and other dust attracting articles. Parents should maintain daily symptoms They sh ould be educated about how the medications work, proper administration Identification of acute exacerbations Use of peak flow monitoring

Acute Exacerbation of Asthma

Mild Acute Asthma cough, rapid respiration and some wheezing, but no chest indrawing . speak s and drink well. PEFR >80% of predicted ; oxygen saturation >95 % in room air. Give ß₂ agonists by nebulizer or MDI + spacer with or without face mask. If MDI is used, one puff of the agonist is given every minute for up to 10 puffs.

If case of significant improvement,sent home on inhalation or oral B₂ agonists every 6-8 hours Review After 1-2 weeks for reassessment and long term treatment. In case of unsatisfactory response, the patient should be treated as moderate exacerbation.

Acute, Moderate and Severe rapid respiration, chest indrawing, wheezing, pulsus paradoxus, difficulty in speech and feeding; PEFR and oxygen saturation is decreased and sensorium is normal. Patients should receive inhalation B2, agonist as described for treatment of mild asthma. Oxygen inhalation is started and oral prednisolone 1-2 mg/kg administered. The patient is assessed for improvement at the end of 1 hour.

Improvement, continued on inhaled B₂ agonists every 30 minutes, and the interval gradually increased to 4-6 hourly. Oxygen inhalation is stopped, if patient is able to maintain oxygen saturation >95%. Prednisolone is continued once daily for 5-7 days, and then stopped without tapering.

The patient is discharged from hospital when the need for bronchodilators is every 4-6 hours, able to feed and speak well, maintains oxygen saturation >95% in room air and PEFR >75% of predicted. These patients should be educated about the disease, need for regular follow-up and avoidance of triggers. They should be assessed for long-term treatment .

No improvement at the end of 1 hour, inhalation of salbutamol is continued and inhaled ipratropium 250 mg given every 20 minutes. An injection of hydrocortisone 10 mg/kg is given and reassessed at end of 2 hours. If satisfactory response is obtained, the patient is treated like early responders. If case of no response, IV theophylline bolus is followed by continuous infusion.

Such patients respond well to magnesium infusion at a dose of 50 mg/kg (with dextrose over 30 minutes). If no improvement :possible mechanical ventilation. transfer to an intensive care unit include worsening hypoxia or hypercapnia, exhaustion, feeble respiration, confusion, drowsiness, coma or respiratory arrest.

BRONCHIOLITIS Occurs with in first 2 years, highest incidence in first 6 months. Usually in winter Or spring Repeated attack indicate viral infection (RSV) associated with wheezing, or asthma. Chest xray shows hyperinflation with scattered areas of infiltration. Infants with bronchiolitis and atopic dermatitis, high IgE levels Or family history of allergy need follow up for later development of asthma

CONGENITAL MALFORMATIONS : Cause obstruction by; vascular rings due to aberrant right subclavian artery or double aortic arch bronchogenic cysts tracheomalacia

ASPIRATION OF FOREIGN BODY Cause localized area of wheezing, hyperresonance and reduced air entry. History of aspiration may be forgotten. Frequent infection in lung may occur. CYSTIC FIBROSIS Recurrent wheezing, clubbing and malabsorption. X ray chest shows hyperinflation, peribronchial cuffing and pneumonia.

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