((Wheezy chest in pediatric age group))

Prepared by:Daniel Rawand PolsSajad Abdulridha AliGhazwan Ardalab Slewa

Supervised by:Dr. Siamand Yahya

What is wheezing?

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

Causes of Wheezing in Childhood

ACUTE

Reactive airway disease : Asthma

Bronchial edema : •Infection•Inhalation•Increased PVP

Bronchial hypersecretion :

• Infection• Inhalation• Cholinergic drugs

Aspiration : Foreign body Aspiration of gastric contents

CHRONIC OR RECURRENTReactive airway disease…..

Airway compression by mass or blood vessel: • Vascular ring/sling• Bronchial or pulmonary cysts•Lymph node

Dynamic airway collapse: Bronchomalacia/tracheomalacia

Aspiration : Foreign body GORD

Bronchial hypersecretion : Bronchitis, Bonchiectasis, Cystic fibrosis, Primary ciliary dyskinesia

Intrinsic airway lesions: Endobronchial tumors (carcinoid)

Approach to a wheezing child Clinical History:

oPatient age at onset of wheeze

oCourse: acute vs gradual

oPattern of wheezing? Episodic: asthma Persistent: congenitalo Response to bronchodilators?

oIs Wheezing associated with multiple systemic illnesses? Cystic fibrosis and Immunodeficiency diseases

oWheeze associated with feeding?

oWheeze associated with cough?

oChange in position? Worsening or improvement oFamily 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 trappingAsthma/ Cystic fibrosis/ Primary ciliary dyskinesia

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

Bronchiolitis 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 Etiology & Epidemiology Predominantly viral: RSV Human metapeumovirus Influenza Adeno Para influenza Mumps, Entero, RhinoMycoplasma pneumoniaChlamydia pneumonia, Chlamydia Trachomatis.

Etiology & Epidemiology Etiology & Epidemiology

Bronchiolitis common in•Male.•Not being breast fed.•Crowded condition.

Clinical manifestation 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 examinationOn 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 Investigation CXR:•Hyperinflated lung.•Bilateral interstitial abnormalities with peribronchial thickening.•Up to 20% having lobar, segmental, or sub segmental consolidation.

Investigation Investigation WBC & differential count are usually normal.

Viral testing:•Rapid immunofluorescene.•Polymerase chain reaction•Viral culture

Blood gas analysis: hypoxemia, hypercarbia

Treatment 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 Complication 1-increasingly labored breathing2-cyanosis3-dehydration 4-fatigue5-severe respiratory failure

Childhood Asthma

Genetic predisposition

Atopy

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)

Bronchial inflammation - Oedema - Excessive mucus production - Infiltration with cells (eosinophils, mast cells, neutrophils, lymphocytes)

Bronchial hyperresponsiveness

Airway narrowing

Symptoms:WheezeCoughBreathlessnessChest tightness

Onset of presentation

Transient wheezerOnset ≤3 years of age then resolvingInitial risk factor is primarily diminished lung sizeNormal lung function by 6 Years of ageNot associated with increased risk of developing clinical asthma

Persistent wheezerOnset ≤3 years then persistingInitial risk factors include passive smoke exposure, maternal asthma history and elevated IgE level in the first year of lifeIrreversible reduction in lung function at 6 years of ageAn increase risk of developing clinical asthma

Late onset wheezerOnset 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 long standing 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

Days with symptoms

Night with symptoms

Mild intermittent <= 2/week < 2/month

Mild persistent > 2/week< 1/day

>2/month

Moderate persistent

Daily > 1 week

Sever persistent Continual Frequent

Classification of chronic Asthma

•B2 agonist

•corticosteroids•Anticholinergic agent •Leukotreine modifier •NSAID•theophylline

Asthma pharmacotherapy

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)

Classification of severity of acute asthma exacerbations

Mild Moderate Sever Respiratory arrest

symptoms

breathlessness walking Talking, feeding difficulty

Rest, stop feeding

Can lie down Prefers setting Sits upright

Talk in Sentences Phrases words

Alterness May be agitated Usually agitated Usually agitated Drowsy, confusion

signs

RR Increased Increased >30

Use of accessory Muscles

No Commonly Usually Paradoxical respiration

Wheeze Moderate on expiration

Loud, through out exhalation

Loud, inspiration & expiration

Absence of wheeze

Pulse/Min <100 100-120 >120 bradycardia

Pulsus paradoxus Absent <100mmhg 10-25 mmhg >25mmhg absent

Management:

Acute asthma:oSemi sitting position oO2 to keep saturation > 92%.oFluid if dehydrated.oBeta-2 agonist: Salbutamol each 20 min by mask until improved later on mask hourly if required.oIpratropium bromide.oSteroids: Prednisolone.If sever give steroids directly since the onset of action is slow (4 hrs)

Criteria for admission to hospital

 

1)Persisting breathlessness, tachypnoea

2)Exhausted

3)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) 

  Dry powder inhaler

 Nebuliser

Gastro-oesophageal reflux

-It is extremely common in infancy. 

- caused by 1) inappropriate relaxation of the lower oesophageal sphincter as a  result of functional  immaturity. 2)A predominantly  fluid  diet,  3)A mainly horizontal posture 4)A short intra abdominal 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 oesophageal atresia or diaphragmatic hernia.

Complications of gastro oesophageal 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 life threatening events (ALTE)

InvestigationMay be indicated if1)the  history  is  atypical2)complications are present 3)failure to respond to treatment.

Investigations include:•  24 hour oesophageal pH monitoring •  24 hour impedance monitoring. •  Endoscopy with oesophageal biopsies • Contrast  studies  of  the  upper  gastrointestinal  tract   

ManagementUncomplicated  gastro oesophageal  reflux can be managed by1)Parental reassurance 2)adding  inert  thickening  agents  to  feeds  (e.g.  Nestargel,  Carobel)    3) positioning  in  a  30° head up 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  considered6) Surgical  management: A Nissen fundoplication, 

Cystic fibrosis

Cystic fibrosisCystic fibrosisCystic fibrosis (CF) is an inherited (AR) multisystem disorder of children and adult, characterized chiefly by obstruction and infection of airways and by mal digestion and its consequenceCF is the major cause of severe chronic lung disease in children and is responsible for most exocrine pancreatic insufficiency in early life.

• Cystic Fibrosis is an inherited disease.

• For a child to inherit CF, both parents must be carriers of a defective gene on chromosome 7.

- They then have a 50% chance of becoming a carrier.

- A 25% chance of getting CF

- A 25% chance of not being a carrier and not having CF

• A chromosome carries genetic information

• Chromosome 7 carries the cystic fibrosis transmembrane conductance regulator (CFTR)

• CFTR controls salt and water movements in and out of cells

• When CFTR is defective, cystic fibrosis occurs because the CFTR doesn’t work or is completely missing.

• When salt and water don’t move in and out of cells properly, sweat becomes 5 times saltier and a thick, sticky

mucus is produced outside the cell.

It affects the…Lungs Pancreas

• Mucus builds up and obstructs airways

• Build up also makes a suitable environment for bacterial growth

Bacterial growth increases risk of infections

Repeated infections cause lung damage

• Pancreas produces enzymes that help with digestion

• Build up of mucus blocks ducts in pancreas, stopping enzymes form reaching

intestines

Without enzymes, intestines can’t digest food properly

Leads to loss of vitamins and nutrients

Respiratory:- A persistent cough that produces thick mucus- Wheezing or lack of breath- A lowered ability to do exercise- Repetitive lung infections -A persistent stuffy nose and inflamed nasal passages

Digestive:- Foul smelling and greasy stools

- Unusually small amount of weight gain or growth- Intestinal blocking, especially in newborns-Severe constipation

Other: - Infertility is common in both males and females, though more frequently in males

- Salty tasting skin and sweat.

Diagnosis Diagnosis - Screening: most newborn with CF can be identified by determination of immunoreactive trypsinogene and limited DNA testing on blood spots, coupled with confirmatory sweat analysis. This screening test is about 95% sensitive. -History: child having : Cough and wheeze, SOB, sputum production, hemoptysis, stool type( e.g fatty, oily, pale) and frequency , weight loss or poor weight gain

DiagnosisDiagnosis-Most children with CF present with:malabsorption,Failure to thrive,Recurrent chest infection.

-Examination:Full assessment of: *Respiratory system.*Liver and GIT system.*Growth and development.

Diagnosis Diagnosis Investigation:Sweat test: most definite test. By chloridometer is recommended for analysis of chloride in these samples+ve when CL is equal or more than 60 meq/L which is dx for CF in conjunction with one of the followings:•Typical chronic obstructive pulmonary dis.•Exocrine pancreatic insuffisiency•Positive family hx.

DiagnosisDiagnosisDNA testingPancreatic function test:Microbiological studies:Sputum culture:Radiology:Pulmonary function test:

• Medications– Medications are used to treat lung disease– Many are inhaled using a nebulizer– Medications used are:

• Mucolytics, which loosen lung mucus• Bronchodilators, which expand the airways• Steroids, which decrease inflammation• Antibiotics, fight infections

• Chest physical therapy– Considered standard therapy– Used to clear mucus from the lungs– Person is clapped on the back

Treatments for CF

• Nutrition– Good nutrition– High-calorie diet– Vitamins

• Pancreatic enzymes– Pancreatic enzyme supplements, taken with everything consumed, help

absorb nutrients

• Transplantation – Transplants are used for end-stage disease. – The transplants used are:

• Double-lung transplant• Heart-lung • Liver

Treatments for CF (continued)

• Gene therapy is an experimental technique that uses genes to treat diseases.

• Gene therapy can replace a mutated gene or inactivating a mutated gene.

• It is promising but risky. It needs more research to see if it is safe.• Gene therapy has been used for cystic fibrosis, in which the healthy

CFTR gene is inserted into the lung cells

Gene Therapy

Foreign bodies of the airwaysForeign bodies of the airways

Foreign bodies of the airwaysForeign bodies of the airwaysEpidemiology and etiolagy:•Most patient are younger than 4 years.•73% are older infants and toddlers•1/3 of aspirated objects are nuts•Raw carrot, apple, dried beans, pop corn& sun flower or water melon seeds•Mainly in right side.

Clinical manifestationClinical manifestation- Sudden onset of cough, chocking & wheezing.Stages of symptoms:•Initial events; there is violent paroxysms of coughing, chocking, gagging& possibly airway obstruction.•Asymptomatic interval; foreign body become lodged.

Complication Complication •Obstruction, erosion or infection develops.•Atelectasis, recurrent or persistent pneumania.•Persistent wheezing unresponsive to bronchodilator& diminished local breath sounds•Persistent cough.

Diagnosis Diagnosis Postero anterior & lateral chest radiogragh(expiratory film) obstructive emphysema (air trapping) with shifting of mediastinum toward the opposite site.Lateral decubitus chest film or fluoroscopy.Flexible bronchoscoy.

FB aspirationFB aspirationFB occludes middle lobe

bronchusAtelectasis of Rt middle

lobeHyperinflation of upper and

lower lobes

Treatment Treatment ABCConscious : Heimlich maneuverFB removal Back blow or chest thrusts (PALS)Unconscious: 100% oxygen through the mask, rigid bronchoscopy and object removal

Reference:-Nelson Essentials of Pediatrics, 6th Edition

-nelson textbook of pediatrics 19th edition

-illustrated textbook of paediatrics 4th

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