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Asthma exacerbations occur across a wide spectrum of chronic severity; they contribute to millions of emergency department (ED) visits in both children and adults every year. Management of asthma exacerbations is an important part of the continuum of asthma care. The best strategy for ED management of an asthma exacerbation is early recognition and intervention, continuous monitoring, appropriate disposition, and, once improved, multifaceted transitional care that optimizes subacute and chronic asthma management after ED discharge. This article concisely reviews ED evaluation, treatment.
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((Wheezy chest in pediatric age group)) Prepared by: Daniel Rawand Pols Sajad Abdulridha Ali Ghazwan Ardalab Slewa Supervised by: Dr. Siamand Yahya
High pitched, continuous, musical (whistling) sound, occurs when air flows through a narrowed airway. -Can originate from airway of any size -Heard mostly on expiration -Manifestation of lower respiratory tract What is wheezing?
Approach to a wheezing child • Clinical History: • Patient age at onset of wheeze • Course: acute vs gradual • Pattern of wheezing? • Episodic: asthma • Persistent: congenital • Response to bronchodilators? • Is Wheezing associated with multiple systemic illnesses? • Cystic fibrosis and Immunodeficiency diseases
Wheeze associated with feeding? • Wheeze associated with cough? • Change in position? Worsening or improvement • Family hx of asthma?
Physical Examination • General • Vital signs including SpO2 % • Chest examination • Inspection: • Respiratory distress • Chest wall deformity (increased AP diameter) • allergic shiners/nasal polyps • Skin: eczema • Palpation: chest wall asymmetry with expansion, tracheal deviation • Percussion: difference in vocal resonance • Auscultation: • Location of wheeze • Character of wheeze • Other breath sounds associated with wheeze • Cardiac: presence of murmur
Investigations • CXR: AP and lateral views • Children with new onset wheezing of undetermined etiology • Chronic persistent wheezing not responding to treatment • Suspected FB aspiration • CXR findings: • Hyperinflation: • Generalized: suggests diffuse air trapping • Asthma/ Cystic fibrosis/ Primary ciliarydyskinesia • Localized hyperinflation: • Structural abnormalities/ FB aspiration • Other findings: atelectasis, bronchiectasis, mediastinal masses, enlarged LN’s, cardiomegaly, enlarged pulmonary vessels or pulmonary edema.
Chest CT scan: • Mediastinal masses or LN’s • Vascular anomalies • Bronchiectasis • Barium Swallow: • GERD • TEF • Vascular rings • Swallowing dysfunction • Pulmonary Function Tests (PFT’s) • Airway obstruction assessment • Response to bronchodilator
Other investigations: • Sweat Chloride Test: Cystic fibrosis screening in children with chronic lung problems, failure to thrive and diarrhea • Immunoglobulin levels: Screen for immunodeficiency. • Rapid antigen testing, viral cultures, sputum gram stain and culture.
Bronchiolitis It is inflammatory obstruction of small airways. Age: first 2 years. 2- 12 months peak 6 months. more sever at 1-3 months. Seasonal disease, peak during winter & early spring.
Etiology & Epidemiology Predominantly viral: RSV Human metapeumovirus Influenza Adeno Para influenza Mumps, Entero, Rhino Mycoplasma pneumonia Chlamydia pneumonia, Chlamydia Trachomatis.
Etiology & Epidemiology Bronchiolitis common in • Male. • Not being breast fed. • Crowded condition.
Clinical manifestation - Mild URTI, diminished appetite, fever(38.5-39) - Respiratory distress with paroxysmal wheezy cough, dyspnea& irritability. - Infant is tachypnic which interfere with feeding - No other systemic complain. - Apnea(in 20% of hospitalized infants) Infant at risk for apnea: *premature infant *very young infant(1-4 months) * Chronic lung disease.
On examination Sign of respiratory distress (nasal flaring, retraction)+ wheezing. Auscultation : Fine crackle or overt ronchi+ prolongation of expiratory phase. Barely audible breath sound suggest a very sever disease with nearly complete bronchiolar obstruction. Hyperinflation of the lung may permit palpation of liver &spleen.
Investigation CXR: • Hyperinflated lung. • Bilateral interstitial abnormalities with peribronchial thickening. • Up to 20% having lobar, segmental, or sub segmental consolidation.
Investigation WBC & differential count are usually normal. Viral testing: • Rapid immunofluorescene. • Polymerase chain reaction • Viral culture Blood gas analysis: hypoxemia, hypercarbia
Treatment Supportive : mainstay of treatment. - Respiratory distress( hospitalization, positioning, cool&humidified oxygen). • Feeding :risk of aspiration( NG feeding) and parenteral fluids. Bronchodilater. Nebulized epinephrine. Corticosteroid : (oral, inhaler, parentral). Ribavirin . Antibiotic. RSV immunoglobulin. Intubation &mechanical ventilation.
Complication 1-increasingly labored breathing 2-cyanosis 3-dehydration 4-fatigue 5-severe respiratory failure
Chronic inflammatory condition of the lung airways resulting in episodic airflow obstruction airway hyper responsiveness airway remodling.
Bronchial inflammation - Oedema - Excessive mucus production - Infiltration with cells (eosinophils, mast cells, neutrophils, lymphocytes) Genetic predisposition Atopy Bronchial hyperresponsiveness Environmental triggers - Upper respiratory tract infections - Allergens (e.g. house dust mite, grass pollens, pets) - environmental tobacco smoke - Cold air - Exercise -Emotional upset or anxiety -Chemical irritants (e.g. paint, aerosols) Airway narrowing Symptoms: Wheeze Cough Breathlessness Chest tightness
Onset of presentation • Transient wheezer • Onset ≤3 years of age then resolving • Initial risk factor is primarily diminished lung size • Normal lung function by 6 Years of age • Not associated with increased risk of developing clinical asthma • Persistent wheezer • Onset ≤3 years then persisting • Initial risk factors include passive smoke exposure, maternal asthma history and elevated IgE level in the first year of life • Irreversible reduction in lung function at 6 years of age • An increase risk of developing clinical asthma • Late onset wheezer • Onset of wheeze between 3 to 6 years
EARLY CHILDHOOD RISK FACTORS FOR PERSISTENT ASTHMA 1) Parental asthma 2) Allergy 3) Severe lower respiratory tract infection: 4) wheezing apart from cold 5) Male gender 6) Low birth weight 7) Environmental tobacco smoke exposure
Clinical features • -Intermittent dry coughing • -expiratory wheezing • Older children report associated • shortness of breath and • chest tightness • -Asthma should be suspected in any child • with wheezing on more than one occasion.
-Other key features: • •worse at night and in the early morning • •triggers • •Personal or family history of an atopic disease • •Positive response to asthma therapy. • Once suspected, the pattern or phenotype should be • further explored by asking: • •frequency • •triggers • general activities • •sleep disturbance • •How much school has been missed due to • asthma?
Examination • -Examination of the chest is usually normal between • attacks. • -In longstanding asthma • hyperinflation • Harrison sulci • generalized expiratory wheeze • and prolonged expiratory phase. • - Evidence of eczema • - the nasal mucosa for allergic • rhinitis. • Growth
Investigations • CBC :Eosinophilia in a range of 15-20% • Eosinophilia in bronchial mucosa strongly suggest Asthma • Allergy testing • Pulse oximetry • Arterial blood gas analysis • Pulmonary function test : Applicable for children > 6 years • CXR
Asthma pharmacotherapy B2 agonist corticosteroids Anticholinergic agent Leukotreine modifier NSAID theophylline
A stepwise approach to the treatment of chronic asthma • Step 1 ( mild intermittent asthma) • No daily medication needed • Sever exacerbation may need systemic steroids • Step 2 (mild persistent) • Low dose inhaled corticosteroids daily
Step 3 (moderate persistent) -low to medium dose inhaled corticosteroids + long acting inhaled B2 agonist Step 4 ( sever persistent) - High dose inhaled corticosteroids + long acting inhaled B2 agonist + oral corticosteroids (if needed)
Management: • Acute asthma: • Semi sitting position • O2 to keep saturation > 92%. • Fluid if dehydrated. • Beta-2 agonist: Salbutamol each 20 min by mask until improved later on mask hourly if required. • Ipratropium bromide. • Steroids: Prednisolone. • If sever give steroids directly since • the onset of action is slow (4 hrs)
Criteria for admission to hospital Persisting breathlessness, tachypnoea Exhausted Still have a marked reduction in their predicted (or usual) peak flow rate 4) Oxygen saturation (<92% in air). 5) Family in able to cope with the condition
(pMDI) Nebuliser Dry powder inhaler
It is extremely common in infancy. • - caused by • 1) inappropriate relaxation of the lower oesophageal sphincter as a result of functional immaturity. • A predominantly fluid diet, • A mainly horizontal posture • A shortintraabdominal length of oesophagus. • -resolves spontaneously by 12 months of age.
Severe reflux is more common in: 1)children with cerebral palsy or other neurodevelopmental disorders. 2) preterm infants 3) following surgery for oesophagealatresia or diaphragmatic hernia.
Complications of gastrooesophageal reflux • Failure to thrive from severe vomiting • Oesophagitis– haematemesis, discomfort on feeding or heartburn, iron deficiency anaemia • Recurrent pulmonary aspiration – recurrent pneumonia, cough or wheeze, apnoea in preterm infants •Dystonic neck posturing (Sandifer syndrome) • Apparent lifethreatening events (ALTE)
Investigation • May be indicated if • the history is atypical • complications are present • failure to respond to treatment. • Investigations include: • • 24hour oesophageal pH monitoring • • 24hour impedance monitoring. • • Endoscopy with oesophageal biopsies • Contrast studies of the upper • gastrointestinal tract
Management • Uncomplicated gastrooesophageal reflux can be managed by • Parental reassurance • adding inert thickening agents to feeds • (e.g. Nestargel, Carobel) • 3) positioning in a 30° headup prone position after feeds. • 4) acid suppression with either : H2 receptor antagonists • (e.g. ranitidine) • or: proton pump inhibitors • (e.g. omeprazole) • 5) If the child fails to respond to these • measures,other diagnoses such as cow’s milk protein • allergy should be considered • 6) Surgical management: A Nissenfundoplication,