Wheezy chest in pediatrics

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  • For cystic fibrosis to occur, a child’s parents must both be carriers of a defective gene on chromosome 7. If both parents are carriers, a child then has a 50% chance of also becoming a carrier, a 25% chance of contracting cystic fibrosis and a 25% chance of not being a carrier and not contracting cystic fibrosis.
  • This gene on chromosome 7 contains information for a protein called the cystic fibrosis transmembrane conductance regulator (CFTR). The protein CFTR controls the movement of salt and water in and out of the cell. When the gene is defective, like in CF, the CFTR doesn’t work properly or may be completely missing. This causes sweat to be up to five times saltier than normal. It also causes thick, sticky mucus to be produced on the outside of the cell (Genetic Science Learning Center, 2009).
  • The two organs that are mainly affected by this mucus are the lungs and the pancreas. The mucus builds up and obstructs the airways in the lungs. This build up of mucus can lead to bacterial growth, increasing risk of infections and the probability of lung damage. The pancreas produces enzymes that assist with digestion but the build up of mucus can also block the ducts in the pancreas, stopping the enzymes from reaching the intestines. Without these enzymes the intestines are unable to digest food properly, leading to a loss of vitamins and nutrients.
  • Wheezy chest in pediatrics

    1. 1. ((Wheezy chest in pediatric age group)) Prepared by: Daniel Rawand Pols Sajad Abdulridha Ali Ghazwan Ardalab Slewa Supervised by: Dr. Siamand Yahya
    2. 2. 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
    3. 3. Causes of Wheezing in Childhood ACUTE CHRONIC OR RECURRENT Reactive airway disease….. Reactive airway disease : Asthma Bronchial edema : •Infection •Inhalation •Increased PVP Bronchial hypersecretion : • Infection • Inhalation • Cholinergic drugs Aspiration : Foreign body Aspiration of gastric contents 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)
    4. 4. Approach to a wheezing child Clinical History: oPatient age at onset of wheeze oCourse: acute vs gradual oPattern of wheezing? Episodic: asthma Persistent: congenital o Response to bronchodilators? oIs Wheezing associated with multiple systemic illnesses? Cystic fibrosis and Immunodeficiency diseases
    5. 5. oWheeze associated with feeding? oWheeze associated with cough? oChange in position? Worsening or improvement oFamily hx of asthma?
    6. 6. 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
    7. 7. 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 ciliary dyskinesia Localized hyperinflation: Structural abnormalities/ FB aspiration Other findings: atelectasis, bronchiectasis, mediastinal masses, enlarged LN’s, cardiomegaly, enlarged pulmonary vessels or pulmonary edema.
    8. 8. •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
    9. 9. 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.
    10. 10. Bronchiolitis
    11. 11. 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.
    12. 12. Etiology & Epidemiology Predominantly viral: RSV Human metapeumovirus Influenza Adeno Para influenza Mumps, Entero, Rhino Mycoplasma pneumonia Chlamydia pneumonia, Chlamydia Trachomatis.
    13. 13. Etiology & Epidemiology Bronchiolitis common in •Male. •Not being breast fed. •Crowded condition.
    14. 14. 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.
    15. 15. 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.
    16. 16. Investigation CXR: •Hyperinflated lung. •Bilateral interstitial abnormalities with peribronchial thickening. •Up to 20% having lobar, segmental, or sub segmental consolidation.
    17. 17. Investigation WBC & differential count are usually normal. Viral testing: •Rapid immunofluorescene. •Polymerase chain reaction •Viral culture Blood gas analysis: hypoxemia, hypercarbia
    18. 18. 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.
    19. 19. Complication 1-increasingly labored breathing 2-cyanosis 3-dehydration 4-fatigue 5-severe respiratory failure
    20. 20. Childhood Asthma
    21. 21. Genetic predisposition Atopy Bronchial inflammation - Oedema - Excessive mucus production - Infiltration with cells (eosinophils, mast cells, neutrophils, lymphocytes) 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
    22. 22. 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
    23. 23. 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
    24. 24. 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.
    25. 25. -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?
    26. 26. 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   
    27. 27. 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  CXR years
    28. 28. Classification of chronic Asthma 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
    29. 29. Asthma pharmacotherapy •B2 agonist •corticosteroids •Anticholinergic agent •Leukotreine modifier •NSAID •theophylline
    30. 30. 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
    31. 31. 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)
    32. 32. Classification of severity of acute asthma exacerbations Mild Moderate Sever Respiratory arrest 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 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 symptoms breathlessness Drowsy, confusion signs
    33. 33. 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)
    34. 34. 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
    35. 35.   (pMDI)   Nebuliser   Dry powder  inhaler
    36. 36. Gastro-oesophageal reflux
    37. 37. -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.   
    38. 38. 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.
    39. 39. 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)
    40. 40. Investigation May be indicated if 1)the  history  is  atypical 2)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   
    41. 41. Management Uncomplicated  gastro-oesophageal  reflux can be managed by 1)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  considered 6) Surgical  management: A Nissen fundoplication, 
    42. 42. Cystic fibrosis
    43. 43. Cystic fibrosis Cystic 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 consequence CF is the major cause of severe chronic lung disease in children and is responsible for most exocrine pancreatic insufficiency in early life.
    44. 44. • 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
    45. 45. • 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.
    46. 46. It affects the… Lungs Pancreas • Mucus builds up and obstructs airways • Pancreas produces enzymes that help with digestion • Build up also makes a suitable environment for bacterial growth • Build up of mucus blocks ducts in pancreas, stopping enzymes form reaching intestines Bacterial growth increases risk of infections Repeated infections cause lung damage Without enzymes, intestines can’t digest food properly Leads to loss of vitamins and nutrients
    47. 47. 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.
    48. 48. 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
    49. 49. Diagnosis -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.
    50. 50. 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.
    51. 51. Diagnosis DNA testing Pancreatic function test: Microbiological studies: Sputum culture: Radiology: Pulmonary function test:
    52. 52. Treatments for CF • 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
    53. 53. Treatments for CF (continued) • 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
    54. 54. Gene Therapy • 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
    55. 55. Foreign bodies of the airways
    56. 56. Foreign bodies of the airways Epidemiology 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.
    57. 57. Clinical 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.
    58. 58. Complication •Obstruction, erosion or infection develops. •Atelectasis, recurrent or persistent pneumania. •Persistent wheezing unresponsive to bronchodilator& diminished local breath sounds •Persistent cough.
    59. 59. 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.
    60. 60. FB aspiration  FB occludes middle lobe bronchus  Atelectasis of Rt middle lobe  Hyperinflation of upper and lower lobes
    61. 61. Treatment ABC Conscious : Heimlich maneuver FB removal Back blow or chest thrusts (PALS) Unconscious: 100% oxygen through the mask, rigid bronchoscopy and object removal
    62. 62. Reference: -Nelson Essentials of Pediatrics, 6th Edition -nelson textbook of pediatrics 19th edition -illustrated textbook of paediatrics 4th http://www.medicinenet.com/anatomy_of_an_a sthma_attack_pictures_slideshow/article.htm

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