Objectives At the end of this session, Understand pathophysiology of common respiratory tract infections. Approach respiratory tract infections.
Introduction Acute respiratory Infection (ARI) Is acute infection of air way ranging from nose to parenchyma of the lung Leading cause of morbidity and mortality in < 5 children Nearly 20% of ARI cases are acute lower respiratory tract infections, mainly pneumonia .
Major Risk factors Pollution Lack of breast feeding Congenital abnormalities of heart /lung Immunodeficiency Malnutrition Young infants Smoking exposure Over-crowededness Poor socio-economic status
Classification of ARI Acute upper respiratory tract infection Acute lower respiratory tract infection
Peculiarities of airway in children the cricoids ring is the narrowest part of the airway in the child; the vocal cords are in the adult large tongue large omega shaped epiglottis anterior larynx which is at a higher level large head short trachea, greater angle of carina; left main bronchus more horizontal the nasal passage which is approximately the same size as the cricoid ring in children obligate nose breathers
Cont’d… INFANT ADULT Narrowest point = cricoid cartilage
Acute upper respiratory tract infection 1.Common Cold A cute Viral upper resiratory infection characterized by rhinorrhea and nasal obstruction systemic symptoms and signs such as headache, myalgia , and fever are absent or mild. Rhinosinusitis-involvement of the sinus and nasal mucosa Etiologies Rhinoviruses (Frequent) , Coronaviruses ,RSV, Parainfluenza viruses ,Adenoviruses
Young children = 6-8 colds per yr, 10–15% of children have at least 12 infections per yr. Transmitted Via : direct contact, aerosol inhalation Clinical Manifestation typically occurs 1-3 days after viral infection. sore or scratchy throat, followed by nasal obstruction and rhinorrhea. Cough is associated with ∼30% of colds Influenza viruses, RSV, and adenoviruses are more likely associated with fever and other constitutional symptoms The usual cold persists for about 1 wk, although 10% last for 2 wk
Physical findings Increased nasal secretion is usually obvious swollen, erythematous nasal turbinate, although this finding is nonspecific and of limited diagnostic value. Diagnosis - clinical diagnosis: exclude other conditions that are potentially more serious or treatable
Rx Symptomatic treatment- hydration, antipyretics No need of antibiotics Complication Otitis media Sinusitis Exacerbation of asthma Pneumonia
2.SINUSITIS Inflammation of the sinuses. can be viral, bacterial or fungal Sinus Age of pneumatization (aeration) Ethmoidal At birth Maxillary 4yrs Sphenoidal 5 yrs Frontal 7-8yrs
Etiology Predisposing factors: viral URTI, allergic rhinitis, tobacco exposure, immuno-deficiency, CF, GERD, Cleft palate. The bacterial pathogens include Streptococcus pneumoniae ,nontypable Haemophilus influenzae, Moraxella catarrhalis M. catarrhalis, S. pneumoniae , and coagulase -negative staphylococci are commonly recovered from children with chronic sinus disease.
Clinical Manifestation Can be Acute, Subacute, Chronic, and Recurrent Nasal congestion, purulent nasal discharge (unilateral or bilateral), fever, and cough. Less-common symptoms include bad breath ( halitosis) , a decreased sense of smell ( hyposmia ), and periorbital edema Physical examination might reveal Erythema and swelling of the nasal mucosa with purulent nasal discharge Sinus tenderness may be detectable in adolescents and adults.
Diagnosis Clinically: Severe respiratory symptoms, including temperature of at least (39 o C) and purulent nasal discharge for 3-4 consecutive days, day time cough > 10 days , suggest a complicating acute bacterial sinusitis.
Cont’d Sinus aspirate culture- Gold standard Radiographic studies – can’t differentiate viral, bacterial, or allergic causes (sinus plain films, CT scans) - not diagnostic Opacification, mucosal thickening, Presence of an air-fluid level
Treatment Amoxicillin-1 st line treatment alternatives -cefpodoxime, clarithromycin, cefixime Azithromycin and trimethoprim- sulfamethoxazole are no longer indicated because of a high prevalence of antibiotic resistance. The duration of therapy 7 days after resolution of symptoms. Frontal sinusitis : ceftriaxone until substantial clinical improvement is achieved Complications Periorbital cellulitis and orbital cellulitis Intracranial complications: epidural abscess, meningitis cavernous sinus thrombosis, subdural empyema , and brain abscess
3.Acute Tonsilopharyngitis Approximately 30% of URTI illnesses feature a sore throat as the primary symptom The most important agents causing pharyngitis are viruses : adenoviruses, enteroviruses,rhinoviruses,RSV,EBV Bacterial : group A β- hemolytic streptococcus Other organisms Mycoplasma pneumoniae Neisseria gonorrhoeae , Fusobacterium necrophorum Corynebacterium diphtheriae
Epidemiology Streptococcal pharyngitis is relatively uncommon before 2-3 yr of age has a peak incidence in the early school years, and declines in late adolescence and adulthood. Illness occurs most often in winter and spring and spreads among siblings and classmates
Pathogenesis Colonization of the pharynx by GABHS either asymptomatic carriage or acute infection M protein is the major virulence factor that facilitates resistance to phagocytosis by polymorphonuclear neutrophils Scarlet fever is caused by GABHS that produces 1 of 3 streptococcal erythrogenic exotoxins (A, B, and C) that can induce a fine papular rash Type-specific immunity develops during infection and provides protective immunity to subsequent infection with that particular M serotype, and, therefore, scarlet fever can occur up to 3 times.
Clinical features Rapid onset of fever, vomiting, sore throat, absence of cough. Enlarged and tender anterior cervical lymph-nodes. Hyperemic pharynx. Edematous Tonsils with w hile non adherent exudates .
Adenovirus pharyngitis - can feature concurrent conjunctivitis and fever ( pharyngoconjunctival fever ). EBV pharyngitis - there may be prominent tonsillar enlargement with exudate , cervical lymphadenitis, hepatosplenomegaly , rash, and generalized fatigue as part of the infectious mononucleosis syndrome. Lemierre syndrome is a serious complication of F. necrophorum pharyngitis and is characterized by septic thrombophlebitis of the internal jugular veins with septic pulmonary emboli, producing hypoxia and pulmonary infiltrates.
Cont’d…
Scarlet fever Scarlet fever manifested by: red finely papular rash strawberry tongue(white then red) erythematous pharyngitis with exudates easly blanchable
Diagnosis Clinical Throat culture - gold standard Rapid antigen detection tests High specificity Less sensitive than culture Serologic tests DDx for Exudative pharyngitis - EBV - Adenoviruses - Diphteria
Treatment Antibiotics Penicillines/Erythromycine-10 days Antipyretics Fluid Tonsillectomy when indicated The primary benefit of treatment is the prevention of acute rheumatic fever , which is almost completely successful if antibiotic treatment is instituted within 9 days of illness . Tonsillectomy lowers the incidence of pharyngitis for 1-2 yr among children with recurrent, culture-positive GABHS pharyngitis that has been severe and frequent (>7 episodes in the previous year, or >5 in each of the preceding 2 yr).
Acute Inflammatory Upper Airway Obstruction/Airway Emergencies Obstruction of the portion of the airways located above the thoracic inlet Inflammation involving the vocal cords and structures inferior to the cords is called laryngitis, laryngotracheitis , or laryngotracheobronchitis . Stridor is a harsh, high-pitched respiratory sound, which is usually inspiratory but can be biphasic and is produced by turbulent airflow
Cont’d… Upper airway obstruction is accounting for approximately 15% of all critically ill patients. Infectious etiologies account for 90% of these, with viral croup accounting for 80%. Epiglottis accounts for 5% of severe cases Other significant causes include other infectious etiologies (bacterial tracheitis, tonsillar pathology, mononucleosis, and diphtheria)
Common causes of upper airway obstruction Causes of acute upper airway obstruction that are potentially life-threatening
Retropharyngeal Abscess/Lateral pharyngeal abscess Most commonly occurs in children <3-4 year of age Up to 67% have or a recent history of ear, nose, or throat infection. The lymph nodes in the deep neck spaces communicate with each other, allowing bacteria from either cellulitis or node abscess to spread to other nodes. Infection of the retropharyngeal nodes can result from: Usually from extension of a localized oropharyngeal infection Dental infection Vertebral osteomyelitis Penetrating trauma to the oropharynx
Etiology : Polymicrobial ( GABHS,Oropharyngeal anaerobic bacteria, S aureus) Clinical Features Common in children below 3-4yrs Fever Irritability Reduced oral intake , Drooling of saliva Neck stiffness Torticoli s Limitation of neck movement Sore throat & neck pain Muffled voice Stridor Respiratory distress Bulging of posterior pharynx Cervical LAP
Diagnosis Lateral neck X-ray: increased width or air-fluid level in the retropharyngeal space Incision and drainage of pus provides definite diagnosis Contrast CT scan DDx acute epiglottitis foreign body aspiration meningitis lymphoma hematoma vertebral osteomyeliti s
Treatment IV antibiotics with/without surgical drainage A 3rd-generation cephalosporin combined with ampicillin-sulbactam or clindamycin to provide anaerobic coverage is effective. Vancomycin and clindmycin Parenteral treatment is maintained until the patient is afebrile and clinically improved. Oral therapy should be continued to complete a 14-day course . Surgical drainage
Complications Upper air way obstruction Rupture → aspiration pneumonia → mediastinitis Thrombophlebitis of internal jugular vein Erosion of carotid artery sheath and septic emboli
Peritonsillar abscess C aused by bacterial invasion through the capsule of the tonsil, leading to cellulites and/or abscess formation in the surrounding tissues. The typical patient with a peritonsillar abscess is an adolescent with a recent history of acute pharyngotonsillitis . Clinical Features Sore throat,fever,trismus,dysphagia Asymmetric tonsillar bulge with displacement of the uvula
Etiology Most commonly group A streptococci and mixed oropharyngeal anaerobes with more than 4 bacterial isolates per abscess Treatment Surgical drainage/Tonsillectomy and antibiotic therapy effective against group A streptococci and anaerobes
Submandibular space infections (Ludwig's angina) It is a bilateral infection of the submandibular space This infection most commonly arises from an infected second or third mandibular molar tooth It is an aggressive, rapidly spreading cellulitis without lymphadenopathy with potential for airway obstruction The infection begins in the floor of the mouth It is characteristically an aggressive, rapidly spreading " woody " or brawny cellulitis involving the Submandibular space. The infection is a rapidly spreading cellulitis without lymphatic involvement and generally without abscess formation (initially)
Etiologies Streptococcus viridans . Oral anaerobes, including Peptostreptococcus species, Fusobacterium nucleatum gram-negative aerobes and Staphylococcus aureus in immunocompromised patients
Clinical manifestation fever, chills, and malaise, as well as mouth pain, stiff neck, drooling, and dysphagia lean forward to maximize the airway diameter They may have a muffled voice or be unable to speak at all. Stridor and cyanosis are considered ominous signs On physical examination tender, symmetric, and "woody" induration The floor of the oropharynx is usually elevated and erythematous , and is tender to palpation
DIAGNOSIS Based on the presence of suggestive clinical findings When needle aspiration or incision and drainage is indicated, samples should be obtained for Gram stain and culture Treatment Airway management most cases can be managed initially by close observation and intravenous antibiotics Tracheostomy under emergency conditions may be required in more severe cases. Penicillin G plus metronidazole or Clindamycin
Acute Epiglottitis (Supraglottitis) Life threatening infection Age groups affected 2-4 yrs, but as late as 7 yr. Etiology most common cause H. influenzae type b(pre vaccination era) Now Streptococcus pyogenes S.pneumoniae S. aureus Non-typable H.Influenza
Clinical manifestation Sudden onset Rapidly progressing respiratory obstruction Fever Toxicity sore throat Voice/cry - muffled Soft stridor Drooling of saliva Hyper extended neck (to maximize the diameter of the obstructed airway) Children with epiglottitis generally lack hoarseness, cough, and stridor until late in the disease process .
This child's "tripod" positioning (trunk leaning forward, neck hyperextended , chin thrust forward) is indicative of epiglottitis.
Diagnosis Laryngoscopy large, swollen cherry red epiglottis Lateral neck x-ray swollen epiglottis – thumb sign NB- avoid oral examination – risk of reflex laryngeal spasm
Cherry red epiglottis Classic radiographs of a child who has epiglottitis show the “thumb sign”
Treatment Precaution Do not manipulate the throat Do not put patient in supine positions is a medical emergency and warrants immediate treatment with an artificial airway placed under controlled conditions Endotracheal intubation Tracheostomy Racemic epinephrine and corticosteroids are ineffective Ceftriaxone, cefepime,or meropenum since 10-40% of H.influeza type B are resistant for Ampicillin. for 7-10 days. Ceftriaxone and vancomycin in patients with MRSA Prophylaxis : Rifampin 20 mg/kg for all household members include a child within the home who is younger than 4 yr of age and incompletely immunized, younger than 12 mo of age and has not completed the primary vaccination series, or immunocompromised
Croup (Acute laryngotracheobronchitis) The most common cause of UAO Age groups affected 3mo-5 yr Etiology Para influenza (I & II)-75% RSV-9% Adenovirus Influenza virus
Clinical Features Preceding flu-like symptoms (combination of rhinorrhea, pharyngitis , mild cough, and low-grade fever for 1-3 days before the signs and symptoms of upper airway obstruction become apparent) Agitation and crying greatly aggravate the symptoms and signs. Barking /Brassy cough Hoarseness triads of croup Inspiratory Stridor Respiratory distress Physical examination can reveal a hoarse voice, coryza, normal to moderately inflamed pharynx, and a slightly increased respiratory rate
Rarely, the UAO progresses and is accompanied by an i ncreasing respiratory rate; nasal flaring; suprasternal, infrasternal, and intercostal retractions; and continuous stridor . Croup is a disease of the upper airway, and alveolar gas exchange is usually normal. Hypoxia and low oxygen saturation are seen only when complete airway obstruction is imminent. The child who is hypoxic, cyanotic, pale, or obtunded needs immediate airway management. Spasmodic Croup???
Features of Upper Airway Disorders
Croup scoring- the Wesley croup score Signs Grades Stridor None With agitation At rest score 1 2 Cyanosis None With agitation At rest Score 4 5 Retraction None mild Moderate Severe Score 1 2 3 Air entry Normal Decreased Markedly decreased Score 1 2 Mental status Normal Disoriented Score 5
Diagnosis Croup is a clinical diagnosis and does not require a radiograph of the neck Radiographs of the neck can show the typical subglottic narrowing, or steeple sign, of croup on the posteroanterior view However, the steeple sign may be absent in patients with croup, may be present in patients without croup as a normal variant, may rarely be present in patients with epiglottitis Radiography after airway stablization for atypical presentation or clinical course. Doesn’t corellate with the diseases severity.
Management of croup Mild croup – occasional barking cough, without audible stridor at rest Dexamthasone 0.6mg/kg IM single dose educate the parents about disease observe Moderate to severe cases (progressive stridor , restlessness, cyanosis, pallor or depressed sensorium ) Admission Don’t disturb the patient Give parentral fluids Give oxygen Avoid sedatives
Cont’d… Nebulized Racemic epinephrine (0.25-0.75ml 2.25% max 0.5ml)in3ml of NS or L- Epinephrine 0.5 ml/kg max 5 ml q 20 min Caution in patient with tachycardia and heart conditions ( TOF,Ventricular outflow obstruction) B/C of possible S/E Steroids : Dexamthasone 0.6mg/kg IM single dose Antibiotics not indicated Artificial airway for severe cases
Bacterial Tracheitis Bacterial tracheitis is an acute bacterial infection of the upper airway that is potentially life threatening. Staphylococcus aureus is the most commonly isolated pathogen. Moraxella catarrhalis, nontypable H. influenzae , and anaerobic organisms have also been implicated. The mean age is between 5 and 7 yr Bacterial tracheitis often follows a viral respiratory infection (especially laryngotracheitis)
Clinical Manifestations Typically, the child has a brassy cough, apparently as part of a viral laryngotracheobronchitis High fever and “ toxicity” with respiratory distress can occur immediately or after a few days of apparent improvement. The patient can lie flat , does not drool, and does not have the dysphagia associated with epiglottitis The usual treatment for croup ( epinephrine) is ineffective.
Diagnosis Clinical high fever, purulent airway secretions, and an absence of the classic findings of epiglottitis. Intubation purulent material is noted below the cords during endotracheal intubation X-rays are not needed but can show the classic findings Irregularity of the margins of the tracheal mucosa below the subglottis and/or presence of irregular or linear shadows (membranes) in the tracheal lumen are common
Lateral radiograph of the neck of a patient with bacterial tracheitis, showing pseudomembrane detachment in the trachea ( candle droppings sign ) ( )
Management Maintenance of an adequate airway is of primary importance Intubation only 50-60% of patients require intubation for management younger patients are more likely to need intubation. Suctioning these secretions, although occasionally affording temporary relief, usually does not sufficiently obviate the need for an artificial airway Tracheostomy Avoid agitating the child
Cont’d… Antibiotics – coverage against S. aureus Combination of ceftriaxone and cloxacilline is used The prognosis for most patients is excellent Patients usually become afebrile within 2-3 days of the institution of appropriate antimicrobial therapy, but prolonged hospitalization may be necessary
Complications of UAO Inability to relieve the obstruction can cause: Brain damage Breathing failure Pulmonary edema pneumothorax pneumomediastinum
OTITIS MEDIA Commonest childhood infection second only to common cold Over 80% of children will have experienced at least one episode of otitis media (OM) by the age of 3 yr. The peak incidence and prevalence of OM is during the 1st 2 yr of life. OM is the leading reason for physician visits and for use of antibiotics and figures importantly in the differential diagnosis of fever.
Definitions Acute otitis media -inflammation of the middle ear presenting with rapid onset of symptoms(Lasting <2weeks) Chronic otitis media -persistent discharge from the middle ear for 2 weeks or longe r
Predisposing factors Young age Incidence greater in boys than in girls Low socioeconomic status Immunodeficiency Passive smoking Congenital Anomalies - unrepaired palatal clefts cold weather months Sibling with recurrent otitis media Down syndrome (craniofacial dysmorphism) URTI (viral, bacteria) Breast feeding reduces incidence of otitis media
Etiology Common pathogens: Streptococcus pneumoniae (50%) Haemophilus influenzae (25-45%) Moraxella catarrhalis (10-15%) Less common causes Staph.aureus (acute, chronic) Pseu.aeruginosa (chronic) Anaerobic organisms Group A streptococcus
Pathogenesis Bacteria gain access to the middle ear when the normal patency of Eustachian tube is blocked by: Local infection Pharyngitis Enlarged adenoids Obstruction of secretions from the middle ear to the pharynx, result in middle ear infection The shorter and more horizontal orientation of the tube in infants and young children may increase the likelihood of reflux from the nasopharynx and impair passive gravitational drainage through the eustachian tube.
Clinical Features Neonates & infants may be asymptomatic or may present with non-specific manifestations: Fever Irritability Vomiting Diarrhea Ear pulling Older children present with Fever Irritability Vomiting/Diarrhea URTI Pain (one, both ears) Ear discharge
Cont’d… Chronic otitis media Foul-smelling ear discharge Perforation of tympanic membrane Impaired hearing
Diagnosis Clinical Otoscopy and tympanometry: Important characteristics of the tympanic membrane consist of contour, color, translucence, structural changes if any, and mobility Bulging erythematous membrane with impaired mobility opacification denotes either scarring, or more commonly, underlying effusion Structural changes include scars, perforations, retraction pockets, and a more severe complication of OM, cholesteatoma formation Culture of ear discharge
Treatment Antibiotics Antipain /Antipyretic Ear Wicking First line antibiotics Amoxicillin = high dose for 10 days. Azithromycin (for penicillin allergy)
Complications Chronic suppurative otitis media Acute/Chronic mastoiditis Facial palsy Acquired cholesteatoma Chronic tympanic perforation Hearing loss (conductive, SNHL)
1.Bronchiolitis Inflammatory obstruction of small air ways characterized by bronchiolar obstruction with edema, mucus, and cellular debris Peak age-3-6 months may be followed by bacterial super infection
Etiology RSV Most common cause (>50% of cases) virtually the only etiology during epidemics(80%) Para influenza virus I,II,III (25%) Others: adenovirus,Mycoplasma ,Rhino viruses, Influenza virus Risk factors common in those who have not been breast-fed, and those who live in crowded conditions Older family members are a common source of infection Infants with pre-existent smaller airways and diminished lung function have a more-severe course
Pathopysiology bronchiolar obstruction with edema, mucus, and cellular debris. Resistance in the small air passages is increased during both inspiration and exhalation, but because the radius of an airway is smaller during expiration, the resultant respiratory obstruction leads to expiratory wheezing, air trapping, and lung hyperinflation.
Clinical Manifestations Symptoms of mild URTI Fever (subnormal to markedly elevated) Respiratory distress with paroxysmal wheezy Cough, dyspnea ,Poor feeding Apnea may be more prominent than wheezing early in the course of the disease, particularly with very young infants (<2 mo old) or former premature infants. Retraction, nasal flaring, cyanosis overt wheezes , with prolongation of the expiratory phase of breathing. Complete ostraction →elimnate turbulance that creat wheezing → thus lack owheezing is not reasuring Ventilation-perfusion mismatch-Hypoxemia
Diagnosis Clinical , particularly in a previously healthy infant presenting with a first-time wheezing episode during a community outbreak CXR- can reveal hyperinflated lungs with patchy atelectasis PCR, rapid immunofluorescence, or viral culture) is helpful if the diagnosis is uncertain or for epidemiologic purposes
DDX Bronchial asthma bacterial Pneumonia CHF, Congenital heart disease Foreign body aspiration, Aspiration pneumonia One or more of the following favors the diagnosis of asthma Repeated episodes of wheezing Absence of a viral prodrome(sudden onset with out a preceding infection) Family history of asthma or atopy Eosinophilia An immediate favorable response to a single dose of aerosolized albuterol
Treatment Most cases are self limiting who are experiencing respiratory distress (hypoxia, inability to take oral feedings, extreme tachypnea) should be hospitalized Supportive care Humidified Oxygen Fluid -NPO/ NGT feeds to avoid risk of aspiration Bronchodilators/ Nebulized epinephrine Antibiotics- if bacterial superinfection Ribavirin
Course and Prognosis Most critical phase –First 48-72 hours after the onset of cough and dyspnea Desperately ill, apneic spells, respiratory acidosis Recovery -10-12 days Case Fatality Rate <1%, with death attributable to apnea, respiratory arrest, or severe dehydration. After this critical period, symptoms can persist Poor prognostic factors congenital heart disease bronchopulmonary dysplasia Immunodeficiency age <12 wk, preterm birth
Prevention: hand hygiene- best measure Palivizumab , an intramuscular monoclonal antibody to the RSV F protein. Reduced risk of hospitalization but cant prevent bronchiolities by other virus and decrease mortality. Indicated for Child born < 29 wk, those with co-morbidity( heart disease, CLD of prematurity), as prophylaxis for child with immunocompromized and neuromascualr dis order.
2.Pneumonia Inflammation of the lung parenchyma associated with consolidation of the alveolar spaces Leading cause of under 5 mortality Accounts for ¾ of ARI deaths Incidence and mortality highest in infants Viral pneumonia is the most common cause of morbidity Bacterial pneumonia are common in developing countries (60% in developing, and 10-30% in developed countries)
Epidemiology 158 million episodes of pneumonia per year of which ≈154 million are occurring in developing countries pneumonia is estimated to cause ≈3 million deaths, An estimated 33% of all deaths, among children younger than 5 yr worldwide (World Health Report 2015) Incidence of pneumonia up to 10 times higher in developing countries and 99% of deaths occur in this areas. Main cause of childhood morbidity and mortality( particularly in less than five years)
Cont’d… In Ethiopia it accounts for 28% of under 5 children deaths. It is estimated that 65% of these pneumonia deaths could be prevented if appropriate preventive and treatment interventions were applied at national scale. Treatments such as oral antibiotics, in addition to the effective prevention interventions ( breastfeeding and adequate complementary feeding.)
Etiology Identifying organism a challenge: no reliable diagnostic method S. pneumoniae important bacterial cause regardless of age Mycoplasma pneumoniae and Chlamydia pneumoniae responsible for mild to severe LRIs, particularly for age > 5 yr In younger patients: mostly respiratory viruses
Etiologic agents for pneumonia is age dependent Neonates (<1 month) Group B streptococcus, Escherichia coli, other gram-negative bacilli, Streptococcus pneumoniae , Haemophilus influenzae (type b, * nontypable) 1–3 month Febrile pneumonia Respiratory syncytial virus, other respiratory viruses ( parainfluenza viruses, influenza viruses, adenoviruses), S. pneumoniae , H. influenzae (type b,nontypable ) Afebrile pneumonia Chlamydia trachomatis, Mycoplasma hominis , Ureaplasma urealyticum , cytomegalovirus
3–12 months RSV, other respiratory virus S. pneumoniae , H. influenzae (type b, nontypable), C. trachomatis , Mycoplasma pneumoniae , group A streptococcus 2–5 yr Respiratory viruses, S. pneumoniae , H. influenzae (type b, nontypable) M. pneumoniae , Chlamydophila pneumoniae S. aureus, group A streptococcus
Cont’d… 5–18 yr M. pneumoniae , S. pneumoniae , C. pneumoniae , H. influenzae (type b, nontypable), influenza viruses, adenoviruses, other respiratory viruses ≥18 yr M. pneumoniae , S. pneumoniae , C. pneumoniae , H. influenzae (type b,nontypable ), influenza viruses, adenoviruses, Legionella pneumophila
Routes of infections Inhalation Aspiration Direct inoculation Blood borne
Risk factors Lack of EBF Under nutrition Indoor pollution Low birth weight Crowding Viral respiratory tract infection Lack of immunization
Pathology Lobar pneumonia Causes consolidation of large areas of the lung Congestion Red hepatization Grey hepatization Resolution Bronchopneumonia - Patchy consolidation Interstitial
Pathogenesis Normally the lower respiratory tract is kept sterile by different defense mechanisms include Prevention of aspiration-epiglottal and cough reflex Trapping of pulmonary secretion by mucus and ciliary action Alveoli macrophage Neutralization by specific and non-specific immune processes Complement, opsonins, antibodies
CLINICAL MANIFESTATION Cough: chief symptom Increased respiratory rate: WHO Infants younger than 2 months old 60 and more 2 months up to 12 mons 50 or more 12 months up to 5 years 40 or more Grunting Sign of severe distress and impending respiratory failure Nasal flaring (air hunger) Pulse oximetry
Cont’d… Retractions: intercostal, supraclavicular, subcostal Increased effort to breathe, decreased lung compliance Fever Auscultate: crackles at end of inspiration usually indicate parenchymal disease Decreased breath sounds BBS
Viral pneumonia fever is usually present; temperatures are generally low Gradual onset symptoms Non-productive cough Other sx : headache, fatigue, myalgia , rhinorrhea, sore throat CXR: diffuse infiltrates WBC count can be normal or elevated but is usually not higher than 20,000/mm 3 , with a lymphocyte predominance C-reactive proteins are normal or slight elevations.
Bacterial pneumonia High grade fever Productive cough Chest pain Ill appearance elevated WBC count, in the range of 15,000-40,000/mm 3 , and a predominance of granulocytes. A large pleural effusion, lobar consolidation, Elevated ESR, and C-reactive protein (CRP) level Infants and young children less likely to have “classic”signs of pneumonia. Often: fever, tachypnea and subtle signs such as lethargy, irritability, vomiting, diarrhea and poor feeding.
Classification I .Clinically 1. Community acquired pneumonia Typical/’’Classic’’ Pneumonia -S. pneumonia(90% of bacterial pneumonia), -HIB, S.aureus Atypical pneumonia-40-50% -Afebrile, clear chest,CXR -extensive infiltration -Viruses and mycoplasma
Cont’d… 2. Hospital acquired pneumonia - After 72 hours of admission or - within 7-30 days of hospital discharge 60% aerobic gram negative - mostly enterobactericae ( klebseilla,E.coli and enterobacter ) -Less commonly-Pseudomonas 10-15% -S. aureus
Cont’d… II . Anatomic/Radiologic classification 1.Alveolar/Air space Pneumonia/ lobar -Air brnchogram is characteristic -Lobar type of consolidation -S.pneumonia,Klebseilla,HIB 2.Bronchopneumonia -Patchy and segmental distribution -Staph.aureus,strep. pyogens,HIB 3.Interstitial pneumonia inflammatory process is more or less confined with in the wall that surrounds the alveoli and bronchioles Reticular or reticulonodular infiltrates Patchy or homogenous opacity viral or mycoplasmal
IV. Based on severity 1.Pneumonia fever, cough + fast breathing 2.Sever pneumonia- pneumonia and any of following General danger signs Grunting Nasal flaring sub costal and intercostal retraction 3.Very sever pneumonia central cyanosis severe respiratory distress not able to drink or breast feed or vomiting everything convulsions, lethargy or unconsciousness No more used Included in sever pneumonia
Diagnosis Clinical CBC/ Leukocytosis C- reactive protein CXR Routine CXR is not always necessary Indicated in severe pneumonia Confirmation of the diagnosis when clinical findings are inconclusive when potential complications are suspected Exclusion of alternate explanations for respiratory distress deteriorating or unresponsive to antimicrobial therapy Recurrent pneumonia
Cont’d… CXR Findings Viral pneumonia , afebrile pneumonia of infancy hyperinflation with bilateral interstitial infiltrates peribronchial cuffing Bacterial pnuemonia Consolidation/ "round pneumonia" pneumatocele (S.aureus) Evidence of complication(pleural effusion……) Bacteriology Pleural fluid analysis, cell count, gram stain, culture Blood culture Antigen detection tests Reliable DNA or RNA tests for the rapid detection of virus, ASO titer….
Recurrent pneumonia is defined as 2 or more episodes in a single year or 3 or more episodes ever, with radiographic clearing between occurrences. An underlying disorder should be considered if a child experiences recurrent bacterial pneumonia
2.In patient management Age <6 mo Sickle cell anemia with acute chest syndrome Multiple lobe involvement Immunocompromised state Toxic appearance Moderate to severe respiratory distress Dehydration Vomiting or inability to tolerate oral fluids or medications No response to appropriate oral antibiotic therapy(failed OPD treatment) Social factors (e.g., inability of caregivers to administer medications at home or follow up appropriately)
Supportive treatment Bed rest Nutritional supplementation ( maintainace fluid) oxygen supplementation Antipyretics Physiotherapy and breathing exercise
Cont’d… Neonate and imunocompromised Ampicillin +Gentamycin Children Crystalline penicillin If no improvement in 48hrs Ceftriaxone
3.Treatment of complications Empyema-Antibiotics 4-6wks Chest tube drainage Chest physiotherapy Lung abscess-Broad spectrum antibiotics anaerobic coverage, 4-6wks Surgery chest physiotherapy
Reasons for poor response Complications, such as Empyema Bacterial resistance Nonbacterial etiologies such as viruses and aspiration of foreign bodies or food Bronchial obstruction from endobronchial lesions, foreign body, or mucous plugs Pre-existing diseases Other noninfectious causes NB:A repeat chest x-ray is the 1st step in determining the reason for delay in response to treatment.
Complications Direct spread of bacterial infection within the thoracic cavity parapneumonic effusion Empyema/ pyopneumothorax Pneumatocele Lung abscess pericarditis Myocarditis Hematologic spread Septicemia septic arthritis Osteomylitis Meningitis
Parapneumonic effusion/ Empyema Empyema is an accumulation of pus in the pleural space Primary pulmonary infection(55%) Ruptured lung abscess Thoracic trauma and surgery(20%) Mediastinitis/Esophageal perforation Subdiaphragmatic infections(2%) 70% of empyemas occur in <2 years of age
Epidemiology Empyema is most frequently encountered in infants and preschool children It occurs in 5-10% of children with bacterial pneumonia and in up to 86% of children with necrotizing pneumonia
Etiology Pneumonia is the most common cause 30-40 % develop parapneumonic effusion Staph. Aureus (is most common in developing nations and Asia as well as in post-traumatic empyema ) Strep.pneumoniae and strep pyogens (commonest in non traumatic cases) Hemophillus influenzae Less Common Anaerobes Enterobactericeae tuberculosis, fungi, and malignancy are less common causes
Pathology Empyema has 3 stages the exudative stage , fibrinous exudate forms on the pleural surfaces In the fibrinopurulent stage , fibrinous septa form, causing loculation of the fluid and thickening of the parietal pleura the organizational stage , there is fibroblast proliferation; pockets of loculated pus may develop into thick-walled abscess cavities or the lung may collapse and become surrounded by a thick, inelastic envelope
Clinical Manifestations The initial signs and symptoms are primarily those of bacterial pneumonia. Most patients are febrile, develop increased work of breathing or respiratory distress, and often appear more ill. Physical findings Dullness may be found on percussion. Breath sounds are decreased or absent and there are a diminution in tactile fremitus a shift of the mediastinum away from the affected side crackles and rhonchi if extensive pneumonia is present
Diagnosis Radiographically, all pleural effusions appear similar, but the absence of a shift of the fluid with a change of position indicates a loculated empyema Septa may be confirmed by ultrasonography or CT Pleural tab and analysis Color Cell count with differential Gram stain Culture Chemistry
Treatment Systemic antibiotics 4-6wks Thoracentesis and possibly chest tube drainage with or without a fibrinolytic agent(Streptokinase , urokinase ) Video-assisted thorascopic surgery (VATS), or open decortication Chest physiotherapy
Ask 4 things while clerking a patient with pneumonia for prevention Immunization Nutrition HIV Housing condition THANK YOU!!!
Reference - Nelson Textbook of Pediatrics 21 st Edition - UpTodate