RESPIRATORY SYSTEM COMMON COLD1. Introduction:1. The common cold is a viral illness 2. The symptoms of rhinorrhea and nasal obstruction are prominent; 3. Systemic symptoms and signs such as myalgia and fever are absent or mild.4. It is often termed rhinitis but includes self-limited involvement of the sinus mucosa and is more correctly termed rhinosinusitis 2. Etiology : 1. Mor Common:1. Rhinoviruses2. Less common:1. Coronaviruses2. Respiratory syncytial viruses3. Human metapneumovirus3. Occasional: 1. Influenza viruses 2. Parainfluenza viruses 3. Adenoviruses 4. Enteroviruses3. EPIDEMIOLOGY 1. Rhinovirus infection : August October & AprilMay4. Age a. Young children have an average of 68 colds per year but 1015% of children have at least 12 infections per year. b. Minimum 3/year as per ARI (WHO) program5. Attack rate is 100% 6. PATHOGENESIS 1. Infection of the nasal epithelium is associated with an acute inflammatory response characterized by release of a variety of inflammatory cytokines and infiltration of the mucosa by inflammatory cells. 2. Inflammation can obstruct the sinus ostium or eustachian tube and predispose to bacterial sinusitis or otitis media7. CLINICAL MANIFESTATIONS1. The onset of common cold symptoms typically occurs 13 days after viral infection. 2. The 1st symptom noted is frequently:a. Sore or scratchy throat, b. Nasal obstruction c. Rhinorrhea. 3. The sore throat usually resolves quickly and, by the 2nd and 3rd day of illness, nasal symptoms predominate. 4. The usual cold persists for about 1 wk, although 10% last for 2 wk 8. The physical findings 1. Increased nasal secretion is frequently obvious to the examiner.2. A change in the color or consistency of the secretions is common 3. Examination of the nasal cavity may reveal swollen, erythematous nasal turbinates, 9. Diagnosis and DD CONDITIONDIFFERENTIATING FEATURES

Allergic rhinitisProminent itching and sneezing; Nasal eosinophils

Foreign bodyUnilateral, foul-smelling secretions; Bloody nasal secretions

SinusitisPresence of fever, headache or facial pain, or periorbital edema or persistence of rhinorrhea or cough for >14 days

StreptococcosisNasal discharge that excoriates the nares

Pertussis persistent or severe cough with woop

8. LABORATORY FINDINGS1) Routine laboratory studies are not necessary for the diagnosis 2) A nasal smear for eosinophils for allergic rhinitis 3) Polymorphonuclear leukocytes in the nasal do not indicate bacterial superinfection.4) The viral pathogens associated with the common cold can be detected by culture, antigen detection, polymerase chain reaction (PCR), or serologic methods. 5) Bacterial cultures or antigen detection are useful only when:a. group A streptococcus,b. Bordetella pertussis c. Nasal diphtheria is suspected. 6) The isolation of other bacterial pathogens is not an indication of bacterial nasal infection and is not a specific predictor of the etiologic agent in sinusitis9. TREATMENT 1. The management of the common cold consists primarily of symptomatic treatment.2. Antiviral Treatment. a. Specific antiviral therapy is not available for rhinovirus b. Ribavirin is approved for treatment of RSV infections c. The neuraminidase inhibitors oseltamivir and zanamivir have a modest effect on influenza viral infections d. pleconaril for treatment of rhinovirus infections is under evaluation 3. Antibacterial therapy is of no benefit in the treatment of the common cold. 10. Symptomatic Treatment 1. Fever is infrequently associated with an uncomplicated common cold and antipyretic treatment is generally not indicated.2. NASAL OBSTRUCTION. 1. xylometazoline, oxymetazoline, or phenylephrine are available as either intranasal drops or nasal sprays 2. They are not approved for use in children 60 infantsii. > 50 2-12 monthsiii. > 40 1-5 yearsIII. Severe Pneumonia:a. Chest retractionb. Grunting c. StridorIV. Severe disease:a. Cyanosisb. Unconsciousnessc. convulsions Treatment of no pneumonia: Home care: by Mothera. Treats fever with paracetamolb. Gives more fluidc. Gives more food than usuald. Continues breastfeedinge. Whicks the nostrils for nasal obstructionf. Gives home remedies for cough: Honey, Tulsi, ginger extractsg. Watches for fast breathing and report to health facilityTreatment mild pneumonia: by health workera. Continue mother care as aboveb. Give co trimoxazloe for 2 days and reviewc. If child improves continue co tri for next 3 daysd. If the child remains in the same state give co trimoxazloe for 2 days and reviewe. If the child has developed severe pneumonia refer to hospital

(Severe)PENEUMONIA IN CHILDRENDefinition:Pneumonia: Inflammation of parenchyma of lungs; often focal involving some lobesBronchopneumonia:Acute inflammation of the walls of the bronchioles with peribronchial inflammation of lung parenchyma; bilateral and symmetrical involvementEpidemiology: 19% of under 5 deaths are due to pneumoniaEtiology of Pneumonias: 1. Infection: viral, bacterial, fungal, parasitic2. Aspiration: food; gastric juice3. Foreign body bronchus4. Hydrocarbons: kerosene ingestion5. Lipoid substance: oil baths and nasal instillation of oil6. Hypersensitivity : airy and grain products, animal dander and protein7. Drugs: anticancer drugs like methotrexate8. Radiation: x ray treatment for cancers Leading Etiologic Agents of Pneumonia Infants and Children: Common pathogens:

AgeBacterial pathogensViral PathogensOther

NeonateGroup B StreptocaccusGram-negative bacilli ( E.coli, K.pneumoniae, Proteus sp, others)S.aureusRSVHerpes simplex virusCMVAdenovirus

1-3 mo.S.pneumoniaeH.Infuenzae type bRSVC.trachomatis

4 mo.-5 yrsS.pneumoniaeH.Influenzae type bParainflenza virus1 and 3,AdenovirusInfluenza viruses A and B

5 yrs and olderS.pneumoniae M.pneumoniae C.pneumoniae

1. Pathogensis:Viral invasion Surface defense knocked down altered secretions bacterial invasion Inflammation consolidation2. Pathology Specific to pathogensStreptococcus peumoniae: Focal often lobar pneumoniaG.A. Streptococcus: Diffuse often involves pleuraStaphylococcus: Unilateral; extensive; hemorrhagic necrosis; cavitation; Pneumatoceles; empyema Mycoplasma: Patchy; edema; airway obstruction; coin shadow 3. Clinical features: 1. Starts as upper respiratory catarrh2. Fever3. Chills4. Tachypnoea 5. Grunt6. Cyanosis7. Chest retraction8. Working of accessory muscles of respiration9. Crackles and wheeze10. Restlessness11. Delirium12. Pleuritic pain4. Additional symptos in Infants :1. Diarrhea2. Vomiting3. Abdominal distension4. Incessant cry 5. Diagnosis: Lab:TC normal in viral increased in bacterialLymphocytosis in viralCRP increasedESR increased CXR:1. Sun ray appearance2. Airbronchogram3. Lobar consolidation4. Perbronchial cuffing5. Silhouette sign 6. Treatment Amoxicillin: high doses of amoxicillin (8090 mg/kg/24 hr) Cloxacillin: 50 to 100 mg/kg/day orally divided every 6 hours. Cefuroxim axitil: Parenteral cefuroxime (150 mg/kg/24 hr), Azithrocyn Levofloxacin Gatrifloxacin Aminoglycosides 7. Causes of Poor response: Antibiotic resistance Viral Aspiration Immunodeficiency Cystic fibrosis 8. Complications Septicemia Meningitis Osteomyelitis Metastasis Empyema Death due to sepsis; resp.failure and other complications

STAPHYLOCOCCAL PNEUMONIA:

Viurlance of S.aureus:1. Staphylococcus aureus is coagulase positive and has many virulence factors that mediate various serious diseases. Eg:a. Coagulase causes plasma to clot by interacting with fibrinogen; produce abscess formationb. Panton-Valentine leukocidin (PVL) is an exotoxin causes leukocyte destruction and tissue necrosisc. Protein A, preventing opsonins and thus inhibiting phagocytosis. d. loose polysaccharide capsule interferes with opsonophagocytosis. e. Catalase: inactivates hydrogen peroxide, promoting intracellular survival of pathogens.f. toxin and -hemolysin that cause local tissue destruction. g. B-lactamase which inactivates most penicillinsh. Methycillin resistant staphylococcus aureus (MRSA) are becoming more prevalent 2. S. aureus is an important pathogen of pneumonia in patients with cystic fibrosis Features of Staph Pneumonia: 1. Staph pneumonia can occur both as community acquired and hospital acquired infections and also ventilator associated pneumonia 2. Clinical features:1. Infants:a. Abdominal distention, high fever, respiratory distress, and toxemia. b. produce Pneumatoceles, pyopneumothorax, and empyema c. Rapid progression of disease and death 2. Older children:a. More common are high fever, abdominal pain, tachypnea, dyspnea, and localized or diffuse bronchopneumonia or lobar disease. b. S. aureus often causes a necrotizing pneumonitis; c. Empyema, pneumatoceles, pyopneumothorax, and bronchopleural fistulas develop frequently.3. Symptoms:1. Starts as upper respiratory catarrh2. Fever3. Chills4. Restlessness5. Delirium6. Pleuritic pain4. Signs:1. Tachypnoea 2. Grunt3. Cyanosis4. Chest retraction5. Working of accessory muscles of respiration6. Crackles and wheeze;7. bronchial breathingComplications: 1. Pneumatocoel formation2. Pyopneumothorax3. Bronchopulmonary fistulas 4. Lung abscess5. Septicemia6. Meningitis7. Osteomyelitis 8. Metastasis9. Empyema10. pyopericardium11. Death due to sepsis; &12. Resp.failure Diagnosis:Staphylococcal pneumonia can be suspected on the basis of chest roentgenograms that may reveal pneumatoceles, pyopneumothorax, or lung abscess.Treatment:1. Antibiotic choice is decided by culture -sensitivity patterns2. Drugs: Empiric therapyi. Community acquired staph pneumonia:1. Co Trimoxazole: 8-12 (TMP) mg/kg/day2. Clindamycin: 20-30 mg/kg/dayii. Methicillin sensitive Staph aureus:1. Penicillinase resistant antibiotics such as:a. Oxacillin } 100-150 mg /kg/day/IV in 4 divided dosesb. Nafcillin }c. Methicillin: 200-300 mg /kg/day/IV in 4 divided doses2. Cephalosporins:a. Cefazolin: 100-150 mg /kg/day/IV in 4 divided dosesb. Cephalexin: 50-100 mg /kg/day/orally in 4 divided dosesiii. For methicillin resistant staph. aureus:a. Vancomycin: 40 mg mg /kg/day/IV in 4 divided dosesb. Linozolid is a recent drugc. Rifampin may be added to vancomycin tharpy3. Othyer measures:i. Inter costal drainage of empyemaii. Fresh blood transfusion

CROUP (ACUTE LARYNGOTRACHEOBRONCHITIS).

1. Croup syndrome is another name for acute laryngotracheo bronchitis, inflammation mainly glottis and subglottic region and it produces brassy cough and hoarse voice; laryngitis may cause life threatening airway obstruction.2. Etiology:a. Viruses:i. The parainfluenza viruses (types 1, 2, and 3) account for approximately 75% of cases; ii. Other viruses associated with this disease include influenza A and B, adenovirus, respiratory syncytial virus (RSV), and measles.b. Spasmodic croup occurs most often in children 1-3 yr of age and is clinically similar to acute laryngotracheobronchitis, except that the history of a viral prodrome and fever in the patient and family are frequently absent. The cause is viral in some cases, but allergic and psychological factors may be important in othersc. Epidemiology:i. Most patients with croup are between the ages of 3 mo and 5 yr, with the peak in the second year of life.ii. Higher in males, iii. Most common during winter iv. Approximately 15% of patients have a strong family history of croup3. 4. a. b. c. Clinical features:i. An upper respiratory tract infection with some combination of rhinorrhea, pharyngitis, mild cough, and low-grade fever for 1 to 3 days before the signs and symptoms of upper airway obstruction become apparent.ii. The child then develops the characteristic "barking" cough, hoarseness, and inspiratory stridor. iii. The low-grade fever may persist, although temperatures may reach 39-40C (102.2-104F); some children are afebrile. iv. Symptoms are characteristically worse at night and often recur with decreasing intensity for several days and resolve completely within a week. v. Agitation and crying greatly aggravate the symptoms and signs. vi. The child may prefer to sit up in bed or be held upright. vii. Older children usually are not seriously ill. d. Physical examination:i. hoarse voice, coryza, slightly increased respiratory rate. ii. On progression: increasing respiratory rate; nasal flaring; suprasternal, infrasternal, and intercostal retractions; and continuous stridor. iii. The child may hypoxic, cyanotic, pale, or obtunded e. Investigations:i. Croup is a clinical diagnosis and does not require a radiograph of the neck. ii. Radiographs of the neck may show the typical subglottic narrowing or "steeple sign" of croup on the posteroanterior view f. Differential Diagnosis: i. Diphtheritic croupii. Aspiration of a foreign bodyiii. Retropharyngeal or peritonsillar abscessiv. Angioedema of the subglottic areasv. Hypocalcemic tetany,g. Complications: i. Pneumonia, cervical lymphadenitis, otitis media, or, rarely, meningitis or septic arthritis may occur during the course of epiglottitis. h. Treatment:i. The mainstay of treatment is airway management.ii. provide cool mist through a tube held in front of the patient by the parent: It moistens airway secretions to facilitate clearance, iii. nebulized epinephrine: A dose of 0.25 to 0.75 mL of 2.25% racemic epinephrine in 3 mL of normal saline can be nebulized as often as every 20 min. iv. Corticosteroids:1. Decrease the edema in the laryngeal mucosa through their anti-inflammatory action. 2. Dexamethasone used a single dose of 0.6 mg/kgIM v. Antibiotics: are not indicated in croup. vi. helium-oxygen mixture (Heliox) have shown clinical vii. should be hospitalized progressive stridor

ACUTE EPIGLOTITIS1. Epiglottitis is an infection of the epiglottis and supraglottic structures2. Etilogy:a. In the past, Haemophilus influenzae type b was the most commonly identified etiology of acute epiglottitis. b. After HiB vaccine invasive disease due to H. influenzae type b in pediatric patients has been reduced c. Therefore, other agents, such as Streptococcus pyogenes, S. pneumoniae, and Staphylococcus aureus, now represent a larger proportion of pediatric cases of epiglottitis. 3. Age:a. 2-4 yr of age, 4. Clinical features:a. This is a dramatic, potentially lethal conditionb. High fever, sore throat, dyspnea, and rapidly progressing respiratory obstruction. c. Drooling is present and the neck is hyperextended in an attempt to maintain the airway. d. The child may assume the tripod position e. Restlessness may be followed by rapidly increasing cyanosis and coma. f. Stridor is a late finding and suggests near-complete airway obstruction. g. The barking cough typical of croup is rare. 5. The diagnosis:1. Visualization of a large, "cherry-red" swollen epiglottis by laryngoscopy. 2. Classic radiographs of a child who has epiglottitis show the "thumb sign" 3. Management:a. Establishing an airway by nasotracheal intubation or, less often, by tracheostomy is indicated urgently. b. The duration of intubation depends on the clinical course probably 2-3 daysc. Pneumonia, cervical adenopathy, or otitis media, Meningitis, arthritis are rarely found in conjunction with epiglottitis.4. Drugs:a. Racemic epinephrine and corticosteroids are ineffective. b. Cultures of blood, epiglottic surface, and, in selected cases, cerebrospinal fluid, should be collected at the time of airway stabilization. c. Ceftriaxone, cefotaxime, or a combination of ampicillin and sulbactam should be given parenterally pending culture d. Epiglottitis resolves after a few days of antibiotics, and the patient may be extubated; antibiotics should be continued for 7-10 days. e. Rifampin prophylaxis (20 mg/kg orally once a day for 4 days;) should be given to all household members 5. Prevention:a. HiB vaccine is routinely given with DPT at 6,12,16 weeks and a booster at 18 months6. Prognosis:a. Untreated epiglottitis has a mortality rate of 6% in some series,

Common causes of acute respiratoly distress in a 2 years old child:1. Respiratory system:a. epiglottitis, b. retropharyngeal abscess, c. peritonsillar abscess, d. croup,e. tracheitis,f. bronchiolitis, g. pneumoniah. Asthmai. Anaphylaxisj. Foreign Body2. CVS:a. Heart failure, b. Pericarditis, c. Myocarditis, d. Cardiac tamponade3. Nervous systema. Depressed ventilation (ingestion, injury, infection), b. Hypotonia, c. Loss of protective reflexes4. GIT:a. GER, b. Aspiration, c. Abdominal distention5. Metabolic/Endocrine:a. Diabetic Keto Acidosis, b. Sepsis6. Hematology:a. Severe anemia, b. Methemoglobinemia7. Trauma to chest wall8. Inhalation injury: toxic gases

PLEURISY

Pleura 1. Thepleurais a two layered sac that holds thelungsand separates them from the chestwall,diaphragm, andheart. 2. The pleura that lines the inside of the chest is called theparietalpleura. 3. The pleura that covers the lungs is called thevisceralpleura. 4. The pleura is separated by a thin layer of fluid. This lets the lungs expand and contract easily duringbreathing. 5. Pleural cavity has negative pressure that helps in inspirationPleurisy 1. Inflammation of pleura2. Inflammatory process is divided into 3 types:1. Dry or plastic2. Serofibrinous or serosanguinous 3. Purulent Dry or Plastic pleurisyEtiology 1. Bacterial 2. Viral3. Tuberculous4. Connective tissue: Rheumatic feverPathology 1. Pathology is usually limited to visceral pleura2. Small amounts of yellow serous fluid collection3. Adhesions between pleural surfacces 4. Deposition of fibrin in the space 5. Fibrothorax Clinical manifestations 1. Stabbing Pain exaggerated by deep breathing, coughing and straining2. It is a dull aching pain in some3. Localized over the chest and also referred to shoulder or back4. Grunting and guarding of respiration5. Child lies on affected side to reduce respiratory movement6. Audible friction rub may be present7. Dull percussion note8. There may be no symptoms in some cases; seen only CXR as haziness DD 1. Epidemic pleurodynia: Bornholm disease; Coxsackie B 2. Trauma to the rib cage3. Lesions of dorsal root ganglia4. Tumors of spinal cord5. Herpes zoster6. Gall bladder disease7. Trichinosis : Infection with the roundworm Trichinella spiralis. Fever; Muscle pain with breathing, chewing, or using large muscles8. TuberculosisTreatment 1. Treat primary cause2. Immobilize the chest with adhesive plaster3. Suppress cough4. Analgesia with NSAID

SEROFIBRINOUS PLEURISY (EFFUSION)

Etiology:1. Lung infections2. Inflammatory bowel disease3. SLE4. Periarteritis 5. Rheumatic fever6. NeoplasmClinical manifestations 1. As fluid accumulate pain may disappear2. Large fluid collection leads to cough, dyspnea, retraction, tachypnea, orthopnea and cyanosis3. Signs:1. Dull percussion note2. Decrease of breath sounds3. Diminished tactile fremitus4. Mdiastinal push to opposite side5. Intercostal fullness6. Rales and ronchi due to lung infection7. Bronchial breathing8. Friction rubs9. Shifting dulness Work up 1. CXR: 1. Homogeneous density2. Absent lung markings3. Absent air bronchogram 4. Obliteration of costo and cardio phrenic angles5. Widening of interlobar septa2. Ultrasonography 3. Diagnostic pleural tap:1. Increase in protein; minimal leukocytosis; increase in LDH2. AFB and gram stain DD 1. Hydrothorax2. Chylothorax 3. Hemorrahge 4. Pyothorax 5. Pleural thickening Complications 1. Fluid may resolve with treatment of pneumonia 2. May turn purulent if untreated3. Adhesions may develop between pleural layers4. Pleural thickening may develop5. Usual to resolve completely over timeTreatment 1. Treat underlying disease2. Drain large collection; rapid draining may produce re expansion pulmonary edema3. Chest tube for re accumulation4. Indication for thoracostomy: pleural fluid has:1. pH < 7.22. Glucose < 50 mg/dL 3. Purulent fluid

PURULENT PLEURISY OR EMPYEMA

Definition: accumulation of pus in pleural spaceEtiology:1. Pneumonia: Strepto, staphylo, Pneumo 2. Rupture of lung abscess3. Thoracic surgery4. Extension of mediastinitis 5. Extension of intra abdominal abscessEpidemiology:5-10% bacterial pneumonia may develop empyema Pathology 3 stages:1. Exudative: fibrinous exudate forms on the pleural surface2. Fibrinopurulent: fibrinous septae forms loculations of fluid and thickening of parietal pleura3. Organizational stage: fibroblast proliferation and thickening of pleura; lung collapse4. Clinical manifestations 1. Presents as bacterial pneumonia2. High fever and chills3. Respiratory distress4. Toxemia 5. Frontal sweatingWork up 1. CXR2. CT scan3. Ultrasound4. Thoracentesis : 1. gram stain and culture2. pH < 7.23. >10 000 wbcs 5. High ESR6. Leukocytosis Complications 1. Bronchopleural fistula pyopneumothorax 2. Pyopericardium 3. Lung abscess4. Peritonitis5. Rib osteomyelitis6. Rupture into subcutis7. Meningitis8. Orthritis 9. Osteomyelitis10. Septicemia 11. Pleural thickening persistent fever Treatment 1. Thoracenetsis 2. Chest tube drainage- fibrinolytics (strptokinase)3. Antibiotics- 3-4 weeks4. Decortication through video assisted thoracoscopy

PNEUMOTHORAX

1. Definition: accumulation of extrapulmonary air within the chest2. Most often it is due to leakage of air from lung3. Not so common in childhood4. Types :1. Primary spontaneous2. Secondary spontaneous3. Traumatic4. Iatrogenic 5. Catamenial Primary Eetiology 1. Pneumonia : high in staph pneumonia2. Bronchiolitis 3. Tuberculosis 4. Cystic fibrosis5. Lung abscess6. Pulmonary infarct7. Rupture of cyst8. Rupture of emphysematous bleb (asthma)9. Foreign body in lung10. Lymphoma Secondary Etiology 1. Traumatic:1. Penetrating injury2. Blunt trauma3. Loud music2. Iatrogenic:1. Thoracotomy 2. Tracheostomy 3. Needle punctutre 4. Mechanical ventilation5. Resuscitation 3. Catamenial: during menstruation Pathophysiology 1. Air in pleural space abolishes negative pressure2. Lung collapses upto 30%3. In tension pneumothorax:1. mediastinal shift 2. Decreased venous return3. Decreased cardiac output4. HypoxemiaClinical manifestations 1. Abrupt onset of symptoms2. Dyspnea, chest pain, cyanosis3. Chest retraction 4. Signs:1. Decreased breath sounds2. Tympanitic percussion note3. Tracheal shiftDD 1. Diaphragmatic hernia2. Emphysema 3. Large cyst or cavity4. Compensatory expansion5. Distended stomach Treatment 1. Tension pneumothorax: emergency needle thoracostomy2. Small and medium pneumothorax may resolve spontaneously3. 100% O2 helps resolution4. For collapse lung: chest tube drainage5. Chemical pleurodesis (doxycyclin in pleural space)6. Thoracoscopic blebectomy Intercostal drainage with under water seal:1. 4th or 5th intercostal space; between the mid- to anterior axillary line 2. 2nd intercostal space at mid-clavicular line

FOREIGN BODY ASPIRATION

1. Children younger than 3 yr of age account for 73% of cases.2. One third of aspirated objects are nuts, particularly peanuts. 3. CLINICAL MANIFESTATIONS: 1. Initial event: Stage I1. Violent paroxysms of coughing, choking, gagging, and airway obstruction occur immediately when the foreign body is aspirated.2. Asymptomatic interval: stage II1. The foreign body becomes lodged and the immediate irritating symptoms subside. 2. This stage accounts for a delayed diagnoses and overlooked foreign bodies. 3. Complications: Satge III1. Obstruction or infection develops 2. Complications include fever, cough, hemoptysis, pneumonia, and atelectasis.4. Symptoms:a. Acute:1. Respiratory distress-with stridor; leaning chin forward and drooling. 2. Inability to speak or cough.3. Partial obstruction: Violent paroxysms of coughing, and wheezing.5. Laryngial FB:b. Complete obstruction asphyxiates the child unless promptly relieved with the Heimlich maneuver. 6. Tracheal foreign bodies:1. Produce stridor and wheezing. 7. Bronchial foreign body:1. During expiration the bronchial foreign body obstructs the exit of air from the obstructed lung, producing obstructive emphysema 8. Acute Management:1. The current guidelines for pediatric basic life support recommend that when airway obstruction from a foreign body is mild, no intervention is required. The patient should be allowed to clear his or her airway by coughing while the clinician watches for signs of impending severe airway obstruction.2. Blind finger sweeps should not be performed in infants or children because the finger may actually push the foreign body further into the airway3. Step I: Jaw Thrust1. The airway may be opened by jaw thrust, and if the foreign body can be directly visualized, it should be removed; 2. If the patient resumes adequate spontaneous ventilation, the patient's body is turned on its side to the recovery position with the head to the side (if in the field). 4. Step II: Back flow and chest thrust1. In the infant younger than 1 yr, a combination of five back blows and five chest thrusts are administered. The foreign body is removed if it is seen.5. Step III:1. A conscious child older than 1 yr is administered a series of five abdominal thrusts (the Heimlich maneuver) with the child standing or sitting. 2. If unconscious, this is done with the child lying down. 3. After the abdominal thrusts, the airway is examined for a foreign body, which should be removed if visualized.6. Step IV:1. When the airway is obstructed and foreign body could not be removed needle cricothyrotomy is indicated2. For foreign body bronchus, child should be treated by bronchoscopic removal of foreign body under anaesthesia.

WHEEZE IN CHILDREN1. Definition:a. Wheezing is a high-pitched whistling sound made while breathing, usually during expiration; b. Factors producing wheeze: Bronchospam, mucosal edema and secretions 2. Causes of wheeze a. Wheeze from birth: i. Congenital Tracheo bronchomalacia ii. Congenital Bronchial stenosisiii. Vascular rings iv. CHD with Lt to Rt shuntb. Isolated episode: Bronchiolitis c. Persistent wheeze from 1 year: i. Cystic fibrosis d. Recurrent wheeze:i. Asthmae. Sudden onset of severe wheeze in a healthy child: i. Foreign body 3. Congenital Bronchial stenosis: a. Rare b. Focal bronchomalaciac. Persistant wheeze from early chilhoodd. persistent dyspnoea and cyanosis after birth e. Stenting or surgery 4. Tracheo broncheomalacia: 1. Male : female = 2 : 12. Insufficient cartilage3. Dynamic collapse; >50 reduction of tracheal diameter during expiration4. Low pitched monophonic wheeze5. Good prognosis6. Associated anomalies: TEF7. Improves over 3 yrs of age5.Vascular rings 1. Double aortic arc2. Right aortic arch with liganetum arteriosum3. Aberrant innominate artery4. Anomalous left pulmonary artery5. Compression of trachea and esophagus6. Wheeze from childhood;7. Aggravated by crying, feeding and neck flexion8. Diagnosis by barium swallow9. Surgical correction 6.CVS causes compressing or narrowing bronchus: 1. Cardiomegaly 2. Left atrial enlargement, 3. Dilated pulmonary artery4. Pulmonary edema 7.Foreign body LRT 1. Sudden onset2. h/o chocking3. Chronic cough4. Persistent wheezing localized to one side5. Recurrent pneumonia6. CXR: pendulum sign in fluroscopy 7. Treatment: Bronchoscopy

8. BRONCHIOLITISIntroduction:1. Bronchiolitis is the most common serious acute respiratory illness in infants and young children. 2. The diagnosis of bronchiolitis is based upon clinical findings including an upper respiratory infection that has progressed to cough, tachypnea, respiratory distress.Etiology:i. Respiratory syncytial virus (RSV) is responsible for >50% of cases. ii. Other agents include parainfluenza, adenovirus, Mycoplasma; Human metapneumovirus can occur as a co-infection with RSV. iii. There is no evidence of a bacterial cause for bronchiolitis. Epidemiology:1. Common among children 2 times/month> 1 time/weekFrequent

1. Treatment: step up step down approach: Step 4: severe persistent:1. Acute severe Asthma: O 2 to maintain 90-95% saturation Nebulization of salbutamol 3 doses at 20 mt interval Nebulization of Ipratropium 0.5 to 1 ml every 20 mts 3 doses IV methylprednisolone 1-2 mg/kg or hydrocotisone 1-2 mg/kg IVF: 20 ml/kg Na Cl to treat shock PMS 2/3 of requirement2. Refractory asthma: Aminophilline 5 mg/kg as infusion Adrenalin .01 mg/kg/dose SC x 3 doses IV Magnesium sulfate 25 mvereg/kg x 2 dose Heliox ( Helium+ Oxygen) Mechanical ventilation3. Severe persistent asthmaa. High dose inhaled corticosteroid, 1000g/dayb. B2 agonist inhalationc. + or - Oral prednisolone 2mg/kgStep 3: moderate persistent d. Medium dose inhaled corticosteroid, 500g/daye. B2 agonist inhalationStep 2: mild persistent:f. Low dose inhaled corticosteroid, 300 g/dayg. Bronchodilators - sos Step 1: mild intermittent:B2 agonist inhalation or oral preparationsRefractory case: Aminophilline 5 mg/kg as infusion Adrenalin .01 mg/kg/dose SC x 3 doses IV Magnesium sulfate 25 mg/kg x 2 dose Heliox ( Helium+ Oxygen) Mechanical ventilationPrevention: Family education Avoid exposure to allergens Avoid smoke Exposure to microbes Prolonged breast feeding Nutrition

BRONCHIECTASIS:Introduction: Ren Laennec, inventor of the stethoscope, first described bronchiectasis in 1819 while observing patients with tuberculosis and the sequelae of pneumonia in the pre antibiotic era Definition: Irreversible abnormal dilatation of the bronchial tree; It represents the end result of non specific and unrelated eventsTypes: Bronchiectasis can be focal or diffuse.Lung defense Lower respiratory tract is sterile one Immune defense is by: leukocytes and Ig.A Mucous coat Ciliary clearance Cough Alterations in any above defences can lead to chronic suppurative lung diseaseEpidemiology Decreasing incidence due to antibiotics and immunization Vit. A prophylaxis Male female ratio is 2:1 In developing countries, bronchiectasis is frequently encountered as one of the sequelae of acute infection.Causes: A. Congenital causes:1. Cystic fibrosis 2. Ciliary dyskinesia including Kartagener's syndrome3. Immune deficiency syndromes Immunoglobulin deficiency syndromes White blood cell dysfunction Complement deficiencies6.Williams - Campbell syndrome: Absence of annular bronchial cartilage7.Marnier - Kuhn syndrome: Congenital tracheo bronchomegaly due to connective tissue disorder; autosomal 8.Alpha 1 - antitrypsin deficiency: 9. Disorders of cilia- Ciliopathy Eg. a) Primary ciliary dyskinesia: b) Kartagener syndrome:B. Acquired causes:1. Infections: Pertusis; Measles; Tuberculosis; Pneumonia ; HIV2. Foreignbody bronchus3.Right middle lobe syndrome: Brock syndrome: Rt middle lobe compression by hilar lymph nodes4.Yellow nail syndrome: Pleural effusion, lymphedema and nail discoloration5.Rheumatoid arthritis 6.Inflammatory bowel disease 7.Youngs syndrome (secondary ciliary dyskinesia) Pathogenesis: Typically, bronchiectasis causes widening of medium-sized airways by 3 mechanisms1. Obstruction: }2. Infection}vicious cycle3. Inflammation}The above mechanisms lead to:1. Alteration in the pulmonary defense mechanisms, 2. Bacterial colonization 3. Endogenous nitric oxide production: reacts with superoxide anion, to form a highly cytotoxic compound thjat affects the bronchial epitheliumPathology: Stages of Bronchiectasis: Prebronchiectasis: Endobronchial infection and inflammation Reversible bronchiectasis: seen only in HRCT: reversible stage Established bronchiectasis: No resolution Three important pathological types are:1. Cylindrical bronchiectasis: is characterized by uniform dilatation of bronchi 2. Varicose bronchiectasis: is characterized by irregular and beaded outline of bronchi, with alternating areas of constriction and dilatation. 3. Cystic or saccular bronchiectasis: is the most severe form of the disease. The bronchi dilate, forming large cysts, which are usually filled with air and fluid. Microbiology of Bronchiectasis: The most commonly found microorganisms are: a) Hemophilus influenza (55%), followed by b) Pseudomonas sp (26%) and c) Streptococcus pneumonia (12%). d) 30% of isolates are resistant to antibioticse) Patients infected with P. aeruginosa have greater extent of bronchiectasis and worse lung function.Clinical features: 1. Persistent or intermittent, sputum production; sputum could be mucoid, mucopurulent or viscous2. Cough more in the morning 3. Foul smelling breath 4. Hemoptysis may range from minor, to life threatening conditions5. Fever, loss of appetite and shortness of breath6. Some patients have pleuritic chest pain7. Poor weight gain8. Late stage: Cor pulmonale 9. Signs: a) variable degrees of crackles or coarse rhonchib) Leathery rales c) Clubbing of digits: Clubbing develops in five steps: 1. Fluctuation and softening of the nail bed (increased ballotability)2. Loss of the normal 60 mm/L are abnormalb) Ciliary beat frequency, using high-speed digital video photography. This requires a biopsy taken from nasal epitheliumc) Measurement of nasal nitric oxide which is low primary ciliary dyskinesia d) Bronchoscopy to exclude foreign body and any endobronchial lesionTreatment: a) Bronchopulmonary hygiene: Physical therapy:1. Postural drainage, 2. Chest percussion, 3. Forced exhalation with pursed lips; 4. Blowing a whistle Drugs:1. Mucolytics, 2. Inhaled broncho-dilators 3. Corticosteroids. 4. Antibiotics- 14 days (oral and nebulized)5. Pneumococcal and influenza vaccinesb) Surgery a) Indications: Failure of medical treatment Obstructing tumor or foreign body Uncontrolled hemorrhage Multi-drug resistant tuberculosis b) Lobar resectionc) Lung transplantation Prevention: a) Childhood immunizationb) Vit.A prophylaxisc) Foreign body removald) Management of pneumonia e) Neonatal screening for Cystic Fibrosis.Alpha 1 - antitrypsin deficiency: i. Emphysema bronchiectasis ii. Autosomal dominant iii. Defective release hepatocytes. iv. Serum levels of alpha1-antitrypsin are decreased, v. Low alveolar concentrations, where the alpha1-antitrypsin molecule normally would serve as protection against antiproteases.vi. Protease excess in alveoli destroys alveolar walls and causes emphysema.vii. Emphysema brochiectasisviii. Cirrhosis liver 9. Disorders of cilia- Ciliopathy Eg. a) Primary ciliary dyskinesia: 1. Autosomal recessive; defect in dynein 2. Disorder beatings of cilia and flagella of sperms 3. Abnormal ciliary motion and impaired mucociliary clearance4. Cilia also are involved in nitric oxide production. Nasal nitric oxide (NO) concentration is dramatically reduced PCD5. The term immotile cilia syndrome (ICS) is no longer used6. It is an important cause for male infertility 7. Female subfertility and tendency to ectopic pregnancy has also been suggested.8. Infections of the middle ear are commonb) Kartagener syndrome:1. Heterotaxia with ciliary dyskinesia (50% 0f PCD)2. Triad of situs inversus, chronic sinusitis, andbronchiectasis;3. Mechanisn of heterotaxia:1. Clockwise movement of cilia in vertebrate embryos generates robustleftward movement of the extraembryonic fluid 2. It triggers normalD-looping of the primitive heart tube and normal asymmetricalcardiac morphogenesis. 3. Motile cilia are required for normaldevelopment of left-right asymmetryc) Youngs syndrome (secondary ciliary dyskinesia) a. Recurrent sinopulmonary infection ; lungs is usually normal but the mucus is abnormally viscousb. Obstructive azoospermia; epididymides were frequently enlarged or cystic c. Considerable symptomatic improvement after adolescence. d. Sweat chloride is normale. No ciliary defectf. Not inherited g. Several studies suggest that contact with mercury might cause the syndrome STRIDOR IN A CHILD1. Stridor is an abnormal, high-pitched sound produced by turbulent airflow through a partially obstructed airway at the level of the supraglottis, glottis, subglottis, and/or trachea2. Causes:Acute stridor a) Laryngotracheobronchitis:b) Aspiration of foreign body :c) Bacterial tracheitis:d) Retropharyngeal abscess:e) Peritonsillar abscess:f) Spasmodic croup:g) Allergic reaction (ie, anaphylaxis):h) Epiglottitis:Chronic stridor i. Laryngomalacia:1. It is the most common cause of inspiratory stridor in the neonatal period and early infancy and accounts for up to 75% of all cases of stridor. 2. Stridor may be exacerbated by crying or feeding. 3. Placing the patient in a prone position with the head up improves the stridor; supine position worsens the stridor. 4. Laryngomalacia is usually benign and self-limiting and improves as the child reaches age 1 year. 5. If significant obstruction or lack of weight gain is present, surgical correction or supraglottoplasty may be considered if tight mucosal bands are present holding the epiglottis close to the true vocal cords or redundant mucosa is observed overlying the arytenoids. ii. Subglottic stenosis:iii. Vocal cord paralysis: iv. Laryngeal webs v. Laryngeal cysts vi. Laryngeal hemangiomas vii. Laryngeal papillomas viii. Tracheomalacia ix. Tracheal stenosis x. Choanal atresia

Evaluation:1. Physical examination for recurrent or persistent stridor is usually normal. 2. Anteroposterior and lateral roentgenograms, contrast esophagography, fluoroscopy, CT, and MRI are potentially useful diagnostic tools. 3. In most cases, direct observation by laryngoscopy is necessary for diagnosis.