Ghai Essential Pediatrics8th

of the upper respiratory tract such as adenovirus, influ­ enza, parainfluenza virus, enterovirus and Epstein-Barr virus. It may, however, be a prodrome of measles and rubella or may be caused by S. pyogenes especially group Abeta-hemolyticstreptococci. Mycoplasmapneumoniaeand Candida albicans have also been incriminated.

Clinical features of tonsillopharyngitis include fever, malaise, headache, nausea and sore throat. Younger children maynot complain of sore throat but often refuse to feed normally. It is difficult to distinguish the clinical syndromes due to viral or streptococcal infections. Hoarseness, cough and rhinitis are more common in viral infection. In these, the onset is gradual and there is less toxemia. In streptococcal infections, cervical lymph nodes are enlarged, the illness is acute with high fever and there is absence of nasal discharge or conjunctivitis. Tonsils are swollen and covered with exudates in both types of infections.

A possibility of acute pharyngitis due to group A beta­ hemolyticstreptococcimay be consideredin a patient who has exudates in throat, tender enlarged cervical nodes along with absence of nasal or conjuctival congestion. Throat swab culture for group A beta-hemolytic strepto­ cocci helps in the definitive diagnosis. A rapid antigen detection test (RADT) for identification of group A beta­ hemolytic Streptococcus gives the result within 10 min and has moderate (80-90%) sensitivity and high (>95%) specificity. Enzyme immunoassays are preferred to latex agglutination tests. Testing for antistreptolysin O (ASO) and anti DNAase B antibodies is not useful.

Complications of sore throat include acute glomerulo­ nephritis, rheumatic fever, otitis media, sinusitis and peritonsillar andretropharyngeal abscesses. The infection may spread down the tracheobronchial tree to cause tracheobronchitis and pneumonia.

Differential Diagnosis

Herpangina is an acute febrile illness due to group A

Coxsackie virus. Patients have dysphagia, sore throat and papulovesicular lesionssurroundedby erythema over the tongue, pharynx, anterior tonsillar pillars and soft palate. Pharynx appearscongested.Diphtheria is characterized by moderatefever, severetoxemia, sore throat and membrane formation over the fauces or palate. Patients with pharyngoconjunctival fever have fever, conjunctivitis, pharyngitis and cervical lymphadenitis due to infection with adenovirus type 3. Infectious mononucleosis is characterized by lymphadenopathy, morbilliform rash, hepatosplenomegaly and sometimes, aseptic meningitis.

Treatment

Warm saline gargles are prescribed for older children. Youngerchildrenareencouragedto sip warm tea/liquids. Paracetamol is administered for fever. Soft food such as custardor rice andlentilgruelisgiven because swallowing

Disorders of Respiratory System -

is painful. Oral antihistaminics, e.g. chlorpheniramine or promethazine are useful in symptomatic relief. However, routine use of cough suppressants (e.g. dextromethor­ phan, codeine) and expectorants (ambroxol, guaifensin) should be avoided.

Antibiotics are not required in patients with viral infections. Patients with documented streptococcal infec­ tion (i.e. by throat culture or RADT) should receive anti­ biotic therapy in order to decrease the duration of symp­ toms, reduce morbidity and prevent complications. Options oforaltreatment include (i) penicillin V 250mg q 8-12 hr, (ii) amoxycillin 30-40 mg/kg/day, (iii) erythro­ mycin 40-50 mg/kg/day or (iv) cephalexin 50 mg/kg/ day, given for 10 days; or (v) azithromycin 10-12 mg/ kg/day for 5 days. Where noncompliance is likely, asingle intramuscular injection of benzathine penicillin (0.6-1.2 MU) may be given. Cotrimoxazole, which is commonly used for sinusitis and otitis media, is not an appropriate medication for sore throat.

The therapy for diphtheria is described in Chapter 10.

Recurrent Sore Throat

A detailed history is obtained and physical examination conducted. Para.nasal sinuses and ears should be examinedfor the fociofinfection. Smoky anddusty atmos­ phere should be avoided. Dampness in the environment and overcrowding predispose the child to recurrent upper respiratory tract infections.

Each episode of bacterial pharyngitis should be treated with adequate doses of antibiotics for at least 10 days. Presence of beta-lactamase producing bacteria in the pharynx may inactivatepenicillinandleadtorecurrentsore throat. This should be treated with amoxycillin plus clavulinic acid or clindamycin. In selected cases, penicillin prophylaxis maybeadministeredfor3--6months,especially ifgroup A beta-hemolytic streptococcal infection ispresent.

Tonsillectomy is often recommended for recurrent attacks of sore throat. It does not prevent recurrence of pharyngeal infections. Tonsillectomy should be advised only if there are more than 5-6 episodes of tonsillitis in a year or tonsillar or peritonsillar abscess. It may reduce the incidence of infection with group A beta-hemolytic streptococcus. Tonsillectomy is recommended in diph­ theria carriers, in presence of retention cysts in tonsils or if the tonsilsare a focus of infection for suppurative otitis media. There is no indication for tonsillectomy after rheumatic fever or glomerulonephritis.

Suggested Reading

Casey JR, Pichichero ME. Metaanalysis of short course antibiotic treat­ ment for group A streptococcal tonsillopharyngitis. Pediatr Infect Dis J 2005;24:909-17

Kabra SK, Kaur J. Upper respiratory tract infection. In: Essential Pe­ diatric Pulmonology, 2nd edn. Kabra SK, Lodha R, (eds). New Delhi, Nobel Vision 2010;49-54

ACUTE LOWER RESPIRATORY TRACT INFECTIONS_ _

Acute lower respiratory tract infections are the leading causeof death in childrenbelow 5 yr ofage.Theseinclude croup syndromes, bronchitis, bronchiolitis and pneu­ monia.

Croup

The term croup is used for a variety of conditions inwhich a peculiar brassy cough is the main presenting feature. Inspiratorystridor, hoarseness orrespiratorydistress may not always be associated with croup. The diseases include acute epiglottitis, laryngitis, laryngotracheobronchitisand spasmodic laryngitis.

Epiglottitis

Supraglottitisincludes both epiglottitis and inflammatory edema of the hypopharynx. Haemophilus influenzae type B

is the most frequent cause. Other microbes like pneu­ mococcus, beta-hemolytic Streptococcus and Staphylococcus

are not common etiologies. The illness usually starts with a minor upper respiratory tract illness which progresses rapidly within the course of a few hours. The child suffers from high fever and has difficulty in swallowing. The breathing becomes noisy but is generally softer than in case of laryngotracheobronchitis. The child is not able to phonate and often sits up leaning forwards with his neck extendedand saliva dribbling fromhis chinwhichappears to be thrust forwards. The accessory muscles of respiration are active and there is marked suprasternal and subcostal retraction of the chest. As the child becomes fatigued, the stridor diminishes. The diagnosis of epiglottitis is made by a cautious direct laryngoscopy, wherein the epiglottis appears angry red and swollen. Injudicious attempt to examine the throat may, rarely, cause death by sudden reflex spasm of the larynx. It is therefore prudent not to force a child, panting for breath, to lie down for throat examination or to send him to the radiology department for an urgent X-ray film if the clinical diagnosis is other­ wise obvious. In case these procedures are considered essential, the equipment and personnel for respiratory resuscitation should always be readily available.

Laryngitis and Laryngotracheobronchitis (Infectious croup)

These conditions are nearly always caused by viral infections, usually with parainfluenza type l. Other viruses incriminated include respiratory syncytial and parainfluenza types 2 and 3, influenza virus, adenovirus and rhinovirus. Bacterial etiology or bacterial super­ infection are unusual. In infectious croup, theonset of the illness is more gradual. Usually, there is a mild cold for a few days before the child develops a brassy cough and mild inspiratory stridor. As the obstructionincreases, the stridor becomes more marked and the suprasternal and sternal recession with respiration become manifest. The

child becomesrestlessand anxious withfast breathing due to increasing hypoxemia. Eventually cyanosis appears. As the obstruction worsens, breath sounds may become inaudible and stridor may apparently decrease. This may unfortunately be misinterpreted as clinical improvement by an unwary physician.

Spasmodic Croup

It occurs in children between the age of 1 and 3 yr. There is sometimes no preceding coryza. The child wakes up suddenly in the early hours of the morning with brassy coughandnoisybreathing. Thesymptomsimprovewithin a few hours. The illness may recur on subsequent days. The course is generally benign and patients recover completely. The cause is unknown. Humidification of the room in which the child is nursed is all that is necessary.

Differential Diagnosis

The syndromes of croup should be distinguished from each other and also from the croup associated with diphtheria in which a membrane is seen on laryngoscopy or occasionally with measles. Rarely the croup may result from angioneurotic edema. A retropharyngeal abscess maycause respiratory obstruction. Aspirationof aforeign bodyis an important cause of obstruction. It maybe rarely confused with wheezing in asthma.

Management

Achild with epiglottitisneedshospitalization. Humidified oxygen should be administered by hood. Face masks are not well tolerated by these children. As oxygen therapy maskscyanosis, acarefulwatchshouldbekept for impend­ ing respiratory failure. Sedatives should not be given. Unnecessary manipulation of the patient may induce laryngeal spasm. Fluids should be administered for adequate hydration of the patient by intravenous route. Antibiotics such as cefotaxime or ceftriaxone 100 mg/kg/ day is recommended in patients with epiglottitis, but not in laryngotracheobronchitis or laryngitis. Endotracheal intubationor tracheostomymaybe indicatedifthe response to antibiotics is not adequate and obstruction is worsening.

A child with acute laryngotracheobronchitis should be assessed for severity of illness on basis of general appearance, stridor (audible withorwithout stethoscope), oxygen saturation and respiratory distress (Table 14.3). Mild cases can be managed on ambulatory basis with symptomatic treatment for fever and encouraging the child totake liquids orally. Parentsmay beexplainedabout the progression of diseases and to bring the child back to hospital in case of worsening of symptoms.

A patient with moderately severe illness may need hospitalizationand treatment with nebulised epinephrine (1:1000 in doses of 0.1-0.5 ml/kg to a maximum dose of 5 ml administered through nebulizer for immediate relief of symptoms. While epinephrine acts rapidly to decrease vascular permeability, airway edema and improves

airflow, the action is temporary and repeat administration may be necessary at 2--4 hr. Recent studies have shown that a single intramuscular dose of dexamethasone (0.3- 0.6 mg/kg) reduces disease severity in the first 24 hr with decreased need of intubation and adrenaline nebulization and shortened duration of hospital stay. Inhalation of budesonide in doses of 1 mg twice a day for two days is useful.

Severe croup may need hospitalization, preferably in intensive care, with oxygen inhalation and need for steroids (similar to moderate severity). Worsening distress may need short term ventilation.

Suggested Reading

Bjornson C, Russell KF, Vandermeer B, Duree T, Klassen TP, Johnson DW. Nebulized epinephrine for croup in children. Cochrane Database Syst Rev 2011;2:CD006619

Knutson D, Aring A. Viral croup. Arn Fam Physician 2004;69: 535-40 Russell KF, Liang Y, O'Gorman K, Johnson DW, Klassin TP. Gluco­ corticoids for croup. Cochrane Database Syst Rev 2011; (1): CD001955

Pneumonia

Pneumonia may be classified anatomically as lobar or lobular pneumonia, bronchopneumonia and interstitial pneumonia. Pathologically, there is a consolidation of alveoli or infiltration of the interstitial tissue with inflam­ matory cells or both.

Etiology

Viral pneumonia caused by respiratory syncytial virus, influenza, parainfluenza or adenovirus may be responsi­ ble for about 40% of the cases. In over two-thirds of the cases, common bacteria cause pneumonia. In the first 2 months, the common agents include gram-negative bacteria such as Klebsiella, E. coli and gram-positive organisms like pneumococci and staphylococci. Between 3 months and 3 yr commonpathogensinclude S. pneumoniae, H. infiuenzae and staphylococci. After 3 yr of age, common bacterial pathogens include pneumococci and staphy­ lococci. Gram-negative organisms cause pneumonia in early infancy, severe malnutrition and immunocompro­ rnised children.

Atypical organisms including Chlamydia and Myca­ plasma spp. may cause community acquired pneumonia

in adults and children. Pneurnocystis jiroveci, histo­ plasmosis and coccidioidomycosis may cause pneumonia in immunocomprornised children.

Other causes of pneumonia include ascaris, aspiration of food, oily nose drops, liquid paraffin and kerosene poisoning. The etiology remains unknown in one-third of cases of pneumonia.

Clinical Features

Risk factors for pneumonia include low birth weight, malnutrition, vitamin A deficiency, lack of breastfeeding, passive smoking, large family size, family history of bronchitis, advanced birth order, crowding, young age and air pollution. Indoor air pollution is one of the major risk factor for acute lower respiratory tract infection in children in developing countries. Onset of pneumonia may be insidious starting with upper respiratory tract infection or may be acute with high fever, dyspnea and gruntingrespiration. Respiratory rate is always increased.

Rarely, pneumonia may present with symptoms of acute abdominal emergency. This is attributed to referred pain from the pleura. Apical pneumonia may be associated with meningismus and convulsions. In these patients the cerebrospinal fluid is always clear.

On examination, there is flaring of alae nasi, retraction of the lower chest and intercostal spaces. Signs of consolidation are present in lobar pneumonia.

Pneumococcal Pneumonia

Respiratory infections due to S. pneumoniae are transmitted by droplets and are more common in the winter months. Overcrowding and diminished host resistance predis­ poses the children to infection withpneumococci. Bacteria multiply in the alveoli and an inflammatory exudate is formed. Scattered areas of consolidation occur, which coalesce around the bronchi and later become lobular or lobar in distribution. There is no tissue necrosis. Pathological process passes from the stage of congestion to red and gray hepatization before the final stage of resolution.

Clinicalfeatures. Incubation period is 1 to 3 days. The onset is abrupt with headache, chills, cough and high fever. Cough is initially dry but may be associated with thick

rusty sputum. Child may develop pleuritic chest pain. Respiration is rapid. In severe cases there may be grunting, chest indrawing, difficulty in feeding and cyanosis. Percussion note is impaired, air entry is diminished, crepitations and bronchial breathing may be heard over areas of consolidation. Bronchophony and whispering pectoriloquy may be observed. Meningismus may be present in apical pneumonia.

Diagnosis. The diagnosis is based on history, physical examination, X-ray findings of lobar consolidation (Fig. 14.1) and leukocytosis. Bacteriological confirmation is difficult; sputum is examined by Gram staining and culture. Blood culture may be positive in 5-10% of cases. Demonstration of polysaccharide antigen in urine and blood do not have sufficient specificity for confirming pneumococcal pneumonia as it may be also be positive in children with colonization in throat.

Treatment. Antibiotic therapy may be empiric while awaiting confirmation of etiology. While the treatment of choice for pneumococcal pneumonia is penicillin (penicillin V 250mg q 8-12 hr orally, penicillin G 0.5 MU/ kg/day IV or procaine penicillin 0.6 MU IM daily, for 7 days), amoxycillin (30-40 mg/kg/day for 7 days) with or without clavulanic acid is a useful alternative.

The need for oxygen administration should be guided by signs of respiratory distress (rapid breathing, chest retractions, nasal flare), presence of cyanosis or hypoxernia on pulse oximetry. Patients may be dehydrated, and require IV fluids. Fever should be managed with para­ cetamol.

Staphylococcal Pneumonia

Staphylococcal pneumonia occurs in infancy and child­ hood. The pulmonary lesion may be primary infection of

the parenchyma; or may be secondary to generalized staphylococcal septicemia. It may be a complication of measles or influenza; other risk factors include cystic fibrosis, malnutrition and diabetes.

In infants, the pneumonic process is diffuse initially, but soon the lesions suppurate, resulting in bronchoalveolar destruction. The illness is characterized by the formation of multiple pneumatoceles. The pneumatoceles fluctuate in size and finally resolve and disappear within a period of few weeks to months. Staphylococcal abscesses may erode into the pericardium causing purulent pericarditis. Empyema in a child below two yr of age is nearly always secondary to staphylococcal infections.

Clinical manifestations. The illness usually follows upper respiratory tract infection, pyoderma or a purulent disease. The patient is toxic and sick looking. Cyanosis may be present. Progression of the symptoms and signs is rapid. Pulmonary infection may occasionally be complicated by disseminated disease, with metastatic abscesses in joints, bone, muscles, pericardium, liver, mastoid or brain.

Diagnosis. The diagnosis of staphylococcal pneumonia is suspected in a newborn or an infant with respiratory infection who has evidence of staphylococcal infection elsewhere in thebody. The characteristic complications of pyopneumothorax and pericarditis are highly suggestive. Pneumatoceles are present in X-ray films (Fig. 14.2), characteristically in pneumonia due to staphylococci or Klebsiella. These pneumatoceles persist as thin walled asymptomatic cysts for several weeks. Staphylococci can be cultured from the blood.

Treatment. The child should be hospitalized and isolated to prevent the spread of resistant staphylococci to the other patients. Fever is controlled with antipyretics; intravenous fluids may be required. Oxygen is administered to relieve dyspnea and cyanosis.

Empyema isaspiratedandthe pusis sent for culture and sensitivity. Prompt antibiotic therapy should be initiated withcoamoxiclav,oracombinationofcloxacillinandathird­ generationcephalosporin,e.g. ceftriaxone.If thepatient does not show improvement in symptoms within 48 hr, therapy withvancomycin,teicoplaninorlinezolidmaybenecessary. Therapy should continue till all evidence of the disease disappearsbothclinicallyandradiologically, whichusually takes2 weeksinuncomplicatedcases. Therapyiscontinued for 4--6 weeks in patients with empyema or pneumothorax. Following initial IV therapy, the remaining course may be completed with oral antibiotics.

Complications. Pneumatoceles do not require specific measures. Empyema and pyopneumothorax are treated by intercostal drainage under water seal or low pressure aspiration. Metastatic abscesses require surgical drainage. Significant pleural thickening that prevents complete expansion of the underlying lung may require decor­ tication. Early thoracoscopic drainage of empyema helps prevent pleural thickening. Installation of streptokinase or urokinase inpleural cavity or loculatedpleural effusion may also be useful.

Haemophilus Pneumonia

Haemophilus influenzaeinfectionsoccurusuallybetween the age of three months and three years and are nearly always associated with bacteremia. Infection usually begins in the nasopharynx and spreads locally or through the blood­

stream. Mostnasopharyngealinfectionsaremildand confer immunity from subsequent serious illness after the early

months of life. As the infants have transplacentally transferred antibodies during the first 3 to 4 months of life, infections are relatively less frequent during this period.

Clinical features. The onset of the illness is gradual with nasopharyngeal infection. Certain viral infections such as

those due to influenza virus act synergistically with H. influenzae. The child has moderate fever, dyspnea, grunt­

ing respiration and retraction of the lower intercostal spaces.

Complications include bacteremia, pericarditis, empyema, meningitis and polyarthritis.

Treatment. Haemophilus infection is treated with ampicillin at a dose of 100 mg/kg/day or coamoxiclav. Cefotaxime (100 mg/kg/day) or ceftriaxone (50-75 mg/kg/day) are recommended in seriously ill patients.

Streptococcal Pneumonia

Infection of the lungs by group A beta hemolytic strep­ tococci is secondary to measles, chickenpox, influenza or whooping cough. Group B streptococcal pneumonia is an important cause of respiratory distress in newborns. Pathologically it causesinterstitialpneumonia, which may be hemorrhagic. Tracheobronchial mucosa may be ulcerated and lymphnodesenlarged. Serosanguineous or thinly purulent pleural effusion is frequently associated.

Disorders of Respiratory System -

Clinical feature. The onset is abrupt with fever, chills, dyspnea, rapidrespiration,bloodstreaked sputum, cough and extreme prostration. Signs of bronchopneumonia are generally less pronounced, as the pathology is usually interstitial. X-ray film shows interstitial pneumonia, seg­ mental involvement, diffuse peribronchial densities or an effusion.

Complications. Thinserosanguineousor purulent empyema is a usual complication. Pulmonary suppuration is less frequent. Ten percent of the patients have bacteremia. When pneumatoceles are present, the condition mimics staphylococcal pneumonia.

Treatment. Therapy for streptococcal pneumonia is carried out as outlined for pneumococcal pneumonia. The response is gradual but recovery is generally complete. Empyema is treated by closed drainage with indwelling intercostal tube.

Primary Atypical Pneumonia

The etiological agent of primary atypical pneumonia is Mycoplasma pneumoniae. Thediseaseistransmittedbydroplet

infection, chiefly in the winter months. The illness is uncommon in children below the age of four yr, although subclinical and mild infections are reported in infants.

Primary atypical pneumonia involves the interstitial tissue with round cell infiltration. The alveolar septae are edematousandmucosaof the broncl1ioles is inflamed and ulcerates. Obstruction of the terminal bronchioles causes emphysema and atelectasis. Pleura may show patchy fibrinous exudates.

Clinicalfeatures. Following an incubation period of 12-14 days, patients have malaise, headache, fever, sore throat, myalgia and cough. Cough is dry at first but later associated with mucoid expectoration, which may be blood streaked. Dyspnea is unusual. There are very few physical signs, except mild pharyngeal congestion, cervical lymphadenopathy andfew crepitations. Hemolytic anemia may be seen.

X-ray findings are more extensive than suggested by the physical findings. Poorly defined hazy or fluffy exudates radiate from the hilar regions. Enlargement of the hilar lymph nodes and pleural effusion are reported. Infiltrates involve one lobe, usually the lower.

Diagnosis. It is difficult to distinguish Mycoplasma pneu­

monia from viral or rickettsial pneumonia. The leucocyte

count is usually normal. Cold agglutinins are elevated in many patients. M. pneumoniae may be cultured from the

pharynx and sputum. The diagnosis is made rapidly by demonstration of IgMantibodybyELISAduringthe acute stage. IgG antibodies are seen on a complement fixation test after one week of illness.

Treatment. Patients are treated with macrolide antibiotics (erythromycin, azithromycin or clarithromycin) or tetra­ cycline (for older children) for 7 to 10 days.

Chlamydia Pneumoniae

It may cause pneumonia in younginfants. Clinicalfeatures include spasmodic cough. A history of purulent conjunc­ tivitis during early neonatal period may be present.

Pneumonia Due to Gram-negative Organisms

The etiological agentsare E. coli, Klebsiella andPseudomonas.

These organisms affect small children (<1 yr of age) or children with malnutrition and deficient immunity. Pseudomonas may colonize airways of patients with cystic fibrosis andcausesrecurrentpulmonaryexacerbations. The clinical features are similar, but patients can be very sick. Signs of consolidation are minimal, particularlyin infants. Constitutional symptoms are more prominent than respiratory distress. X-ray shows unilateral or bilateral consolidation. Infectionwith E. coli or Klebsiella pneumoniae may be associated with pneumatoceles.

Treatment. Intravenous use of third generation cephalo­ sporins (cefotaxime or ceftriaxone, 75-100 mg/kg/day) with or without an aminoglycoside is recommended for 10 to 14 days. Ceftazidime or piperacillin-tazobactam are effective in patients with Pseudomonas infection.

Viral Pneumonias

Respiratory syncytial virus is the most important cause in infants under 6 months of age. At other ages, influenza, parainfluenza and adenoviruses are common. The bronchialtreeoralveoli are involved resultinginextensive interstitial pneumonia. Features of consolidation are usuallynotpresent. Radiological signs consist of perihilar and peribronchial infiltrates.

Ingestion of Aliphatic Hydrocarbons

Keroseneexerts itstoxiceffects on thelungs andthecentral nervous system. It is poorly absorbed from the gastro­ intestinal tract. Milk and alcohol promote its absorption. It haslow viscosity and less surfacetension, andtherefore, diffuses quickly from the pharynx into the lungs. Administration of oil apparently decreases its absorption from the gastrointestinal tract but is not recommended. Clinical features of hydrocarbon pneumonia include cough, dyspnea, high fever, vomiting, drowsiness and coma. Physical signs in lungs are minimal. X-ray film of the chest shows ill defined homogeneous or patchy opacities; occasionally featuresresemble rniliary mottling.

Vomiting is not induced. Gastric lavage is usually avoided to prevent inadvertent aspiration. The patient is kept on oxygen. The routine use of antibiotics and/or corticosteroids is not recommended.

Loeffler Syndrome

Larvae of many nematodes, during their life cycle, enter the portal circulation, liver and then through the hepatic

vein and inferior vena cava into the heart and lungs. In the lungs, the larvae penetrate the capillaries, enter the alveoli, plug the bronchi with mucus and eosinophilic material due toallergicreaction. There are fleeting patchy pulmonary infiltrations. Some cases may be due to drug reaction to aspirin, penicillin, sulfonamide orirnipramine.

Clinical features include cough, low fever, feeling unwell and scattered crepitations. There is eosinophilia and X-ray lungs shows pulmonary infiltrates of varying size, which superficially resemble miliary tuberculosis. Treatment is symptomatic.

Suggested Reading

Bradley JS, Byington CL, Shah SS, et al. Pediatric Infectious Diseases Society and the Infectious Diseases Society of America. The manage­ ment of community-acquired pneumonia in infants and children older than 3 months of age: clinical practice guidelines by the Pediatric Infec­ tious Diseases Society and the Infectious Diseases Society of America. Clin Infect Dis 2011; 53:617-30

Harris M, Clark J, Coote N, et al. British Thoracic Society Standards of Care Committee. British Thoracic Society guidelines for the manage­ ment ofcommunityacquiredpneumoniain children: Update 2011. Tho­ rax 2011;66 SIII-3

Kabra SK, Lodha R, Pandey RM. Antibiotics for community-acquired pneumonia in children. Cochrane Database Syst Rev 2010; 3:CD004874 Sarthi M, Lodha R, Kabra SK. Pneumonia. Indian J Pediatrics 2009;76:

Sll-7

Acute Respiratory Tract Infection (ARTI) Control Program

Acute lower respiratory tract infection (LRTI) is a leading cause of mortality in children below 5 yr of age. The etio­ logical agent is bacterial in 50-60% children. The common bacteria causing LRTI in preschool children include H. infiuenzae, S. pneumoniae and staphylococci. All these agents are sensitive to antibacterials like cotrimoxazole. Hence,judicioususeof cotrimoxazoleinchildrensuffering from LRTI may prevent death due to pneumonia. World Health Organization (WHO) has recommended certain criteria for diagnosis of pneumonia is children at primary health care level for control of LRTI deaths in developing countries where the infant mortality is more than 40/ 1000 live births. Clinical criteria for diagnosis of pneumonia include rapid respiration with or without difficulty in respiration. Rapidrespirationis defined as respiratory rate of more than 60, 50 or 40 per minute in children below 2 months of age, 2 months to 1 yr, and 1 to 5 yr of age, respectively. Difficulty in respiration is defined as lower chest indrawing.

The World Health Organization recommends that, in a primary care setting, if a child between 2 months and 5 yr of age presents with cough he should be examined for rapid respiration, difficulty in breathing, presence of cyanosis or difficulty in feeding (Table 14.4). If the respiration is normal and there is no chest indrawing and difficulty in feeding, the patient is assessed to be having an upper respiratory tract infection and can be managed

at home. If the child has rapid respiration but there is no chest indrawing, he/she is suffering from pneumonia and can be managed at home with oral cotrimoxazole for 5 days.

Patients with chest indrawing are considered to have severe pneumonia and need hospitalization and therapy with parenteral penicillin. The presence of severe chest indrawing or cyanosis indicates very severe pneumonia, requiring hospital admission and therapy with IV penicillin (or ampicillin) with gentamicin and supportive care.

In children below 2 months of age presence of any of the following indicates severe disease: fever (38°C or more), convulsions, abnormally sleepy or difficult to wake, stridor in a calm child, wheezing, not feeding, tachypnea, chest indrawing, altered sensorium, central cyanosis, grunting or apneic spells and distended abdomen. Such children should be referred to hospital for admission and treated with parenteral ampicillin and gentamicin along with supportive care.

Suggested Reading

Basis for WHO recommendations on the management of pneumonia in children at first level health facilities. WHO/ARI/91.20 Geneva: World Health Organization, 1991

Bronchiolitis

This is a common, serious acute lower respiratory infection in infants. Affected infants are between the ages of 1 and 6 months, but the disease can affect children up to their second birthday. Disease usually occurs in winter and spring. Respiratory syncytial virus (RSV) is implicated in most cases. Other causative organisms

include parainfluenza virus, adenovirus, influenza viruses and rarely M. pneumoniae. Protection against RSV

is mediated by antibodies of IgG3 subclass. These antibodies have shorter half life and do not cross the placenta in substantial amount so as to offer protection to the infant. High quantities of secretory IgA antibodies to RSV are present in the colostrum and breast feeding reduces the likelihood of an infant being hospitalized with acute bronchiolitis.

Pathogenesis

The inflammation of the bronchiolar mucosa leads to edema, thickening, formation of mucus plugs and cellular debris. Bronchiolar spasm occurs in some cases. The bronchial lumen, which is already narrow in the infants, is further reduced. As airway resistance is inversely related to the fourth power of the radius, even slight narrowing of the bronchiolar lumen causes marked increase in the airway resistance, both during inspiration and expiration. During expiration, the bronchioles are partially collapsed and egress of air from the lungs is severely restricted resulting in trapping of the air inside the alveoli causing emphysematous changes. When obstruction becomes complete, the trapped air in the lungs may be absorbed causing atelectasis. Due to diminished ventilation and diffusion, hypoxemia is produced in almost all of these infants. Retention of carbon dioxide leads to respiratory acidosis. The presence of eosinophils in the blood and respiratory secretions suggest that the virus infection initiates the wheezing attack in a child who is already sensitized.

Clinical Features

A few days following an upper respiratory tract infection, breathing becomes fast and respiratory distress develops. Majority of infants has mild symptoms and recover in 3-7 days. Those with severe disease may develop retraction of lower intercostal spaces and suprastemalnotchby 3-5 days.

In severe infection the infant is dyspneic and may appear cyanosed. The fever is moderately high. Accessory muscles of respiration are working. Expiration is prolonged; fine crepitations and rhonchi are auscultated. Breath sounds may be faint or inaudible in severe cases. Respiratory distress is out of proportion to the physical signs. Hyperinflation results in the liver and spleen being pushed down. When the chest becomes over inflated, the anteroposterior diameter of the chest is increased and increased resonance is noted on percussion.

X-ray chest shows hyperinflation (Fig. 14.3) and infiltrates. Diaphragm is pushed down. The lung fields appear abnormally translucent. The leukocyte count is normal or slightly elevated. A rapid test, using monoclonal antibodies, on nasopharyngeal aspirate can identify RSV.

Fig. 14.3: Chest X-ray. Bronchiolitis showing hyperinflation

Course and Prognosis

Bronchiolitis is generally a self limiting illness. The symptoms subside in three to seven days. Death may occur in one percent of the severely ill patients due to respiratory failure. The relationship of acute bronchiolitis to bronchial asthma in later life is observed in about 25% cases of acute bronchiolitis. Bronchial asthma is more likely in children with personal or family history of an allergic illness.

Differential Diagnosis

Bronchial asthma. Bronchiolitis is often confused with bronchial asthma. The latter is unusual below the age of one year; a family history of asthma is usually present. Several attacks occur in the same patient with or without a preceding respiratory infection. Response to broncho­ dilators is more consistent in children with asthma as compared to bronchiolitis.

Congestive heart failure. Congestive heart failure is suggested, if there is cardiomegaly on X-ray film of chest, tachycardia, large tender liver, raised JVP, edema and rales on auscultation of the lungs.

Foreign bodies intrachea. These are diagnosed by the history of aspiration of foreign body, localized wheeze and signs of collapse or localized obstructive emphysema.

Bacterial pneumonia. In bacterial pneumonia, the signs of obstruction are less pronounced, fever is high and adventitious sounds in the lungs are prominent.

Treatment

Treatment of bronchiolitis is essentially symptomatic. Infants with mild disease can be cared for at home in a

humidified atmosphere. If respiratory distress increases or feeding problems appear, child should be hospitalized.

In hospital, the child is nursed in a humid atmosphere preferably in sitting position at angle of 30° to 40° with head and neck elevated. Moist oxygen is given conti­ nuously even in the absence of cyanosis. Very sick infants may need a concentration of 60% oxygen given through hood. Pulse oximetry should be performed regularly to keep oxygen saturation of more than 92%. Fluids and electrolyte balance should be maintained.

Antibiotics have no role. Ribavirin, an antiviral agent has no role in the treatment of infants who were previously healthy. The medication, however, shortens the course of illness in infants with underlying congenital heart disease, chronic lung disease and immunodeficiency. Ribavirin is delivered by a nebulizer 16 hr a day for 3-5 days in such cases.

Beta2-adrenergic drugs and ipratropium are not recommended for infants less than 6 months. A recent review on the use of bronchodilators in bronchiolitis suggests a beneficial effect of inhaled salbutamol with ipratropium and epinephrine. If a patient shows improvement, the bronchodilators may be given every 4-6 hourly. Continuous positive airway pressure (CPAP) or assisted ventilation may be required to control respiratory failure. Extracorporeal membrane oxygenation is effective, if respiratory failure is not controlled by mechanical ventilation.

SuggestedReadngi

Blom D, Ermers M, Bont L, et al. Inhaled corticosteroids during acute bronchiolitis in the prevention of post-bronchiolitic wheezing. Cochrane Database Syst Rev 2007;CD004881

Hartling L, Fernandes RM, et al. Steroids and bronchodiJators for acutebronchiolitisinthe first two yr of life: systematic review and meta­ analysis. BMJ 2011;342:1714

Spurling GK, Fonseka K, Doust J, Del Mar C. Antibiotics for bronchi­ olitis in children. Cochrane Database Syst Rev 2007;1:CD005189

Zorc JJ, Hall CB. Bronchiolitis: recent evidence on diagnosis and management. Pediatrics 2010;125:342-9

BRONCHIAL ASTHMA

Bronchial asthma is a disease characterized by an increa­ sed responsiveness of the airways to various stimuli. It manifests by widespread narrowing of the airways caus­ ing paroxysmal dyspnea, wheezing or cough. The diffuse obstruction to the airflow is reversible in a large majority of cases, either spontaneously or in response to treatment. Bronchial reactivity is a necessary component of asthma.

Pathophysilogy

Airway obstruction in asthma is caused by (i) edema and inflammation of mucous membrane lining the airways; (ii) excessive secretion of mucus, inflammatory cells and cellular debris; and (iii) spasm of the smooth muscle of bronchi. Obstruction is diffuse but not uniform.

Asthma has been classified as atopic (lgE mediated, triggered by allergens), nonatopic (nonlgE mediated, triggered by infection), mixed, exercise induced or aspirin induced. Inhalation of an allergen leads to a biphasic response with early and late reactions ultimately causing bronchoconstriction.

Early reaction starts within 10 min of the exposure to allergen. It is characterized by release of histamine, leukotrienes, prostaglandins, platelet activating factor and bradykinin from the mast cells following the interaction of allergen with specific mast cell bound IgE. All these substancescause bronchoconstriction, mucosaledemaand mucus secretion which manifests as airway obstruction. This phase is inhibited by 2-agonist drugs.

Late phase occurs in about two-thirds of patients. It develops 3-4 hr later and peaks at 8-12 hr. The release of mast cell mediators is not prevented by premedication with 2-agonist. However, it is inhibited by premedication with steroids suggesting that airway narrowing is mainly due toan inflammatoryreaction and mucosaledema. This phase presents as clinical asthma.

Airway resistance is increased more during exhalation because airways close prematurely during expiration. Lungs are hyperinflated; elasticity and frequency­ dependent compliance of the lungs is reduced. Breathing involves more work resulting in dyspnea. Perfusion of inadequately ventilated lungs causes hypoxemia.

In early stages of illness the partial pressure of CO2 falls because of hyperventilation. When obstruction becomes more severe, alveolarhypoventilationsupervenes,leading to hypercarbia and respiratory acidemia.

Pathology

Airway inflammation is considered to be the basic pathology in asthma. This is initiated by degranulation of mast cells and release of various mediators of inflam­ mation, which damage the airways leading to epithelial shedding and mucus secretion. Inflammatory mediators also influence reactivity via neural mechanisms.

Triggers of Episodes of Asthma

Viral infections. Viral infections in young children and exercise in older child or adult appear to be more frequent triggers of airway narrowing. Viral infections interfere with the integrity of mucosal surfaces by opening up tight intraepithelial cell junctions and induce shedding of epithelium.

Role of exercise. Exercise induced asthma occurs in genetically susceptible individuals with hyper-reactive airways. The loss of water from the respiratory tract induces mucosal hyperosmolarity, which stimulates mediator release from mast cells.

Weather change. Suddenchange in the weather mightresult in (i) loss of heat and water from lower airways and

Disorders of Respiratory System -

(ii) sudden release of airborne allergens in atmosphere, resulting in exacerbation of asthma.

Emotional factors. Emotional stress operated through the vagusnerve,initiatesbronchialsmoothmusclescontractility.

Role of food. Allergy to food proteins or additives in food might have a minor role in the pathogenesis of asthma. These should be incriminated only on a very strong association with the illness.

Endocrine factors. Some endocrine changes including puberty may increase symptoms of asthma.

Clinical Features

The clinical features of asthma are variable. Symptoms vary from simple recurrent coughtosevere wheezing. The symptoms occur with change in season, aggravated by exercise and more at night. Acute asthma may usually beginwith a cold, orboutsofspasmodiccoughing. Inearly phase of the episode, the cough is nonproductive. The patientbecomesdyspneic, with prolonged expiration and wheezing. Accessory muscles of respiration are exces­ sively used. The child sweats profusely, may develop cyanosis and becomes apprehensive and restless and appear fatigued.

In severe episodes the child may show air hunger. The chest is hyper-resonant because of excessive air trapping. As the obstruction becomes severe, the airflow decreases markedly. As a result the breath sounds become feeble. Wheezing which was earlier audible may disappear. This is an ominous sign. Absence of wheezing in the presence of cyanosis and respiratory distress should not be considered as an evidence ofclinical improvement. As the child improve, the airflow increases and wheezing may reappear. With remission, the wheeze disappears.

Severe hypoxemia in asthma results in cyanosis and cardiac arrhythmias. Pulsus paradoxus indicates severe illness. Mucus plugs occluding the bronchial tree may cause collapse of small segments of the lung. Persistence of hyperinflation of the chest even after subsidence of the asthmatic attack signifies that the apparent relief from bronchospasm will be short lived. In chronic intermittent cases the chest becomesbarrelshaped. Clubbingoffingers, however, is unusual.

Diagnosis

A prolonged whistling sound heard at the mouth during expiration is called a wheeze. Recurrent attacks of wheez­ ing indicate bronchial asthma. Although intermittent attacks of coughing may be due to recurrent viral infec­ tions, the diagnosis of bronchial asthma should be consi­ dered. Cough, which is associated with asthma generally, worsens after exercise. Sputum is generally clear and mucoid but expectoration of yellowishsputum (attributed to large number of eosinophils) does not exclude he diagnosis of asthma. Chronic spasmodic cough may suggest occult asthma.

Investigations

The diagnosis of asthma is clinical in most cases, hence pulmonary function tests may not play significant role. These investigations have an important role in diagnosis of doubtful cases and in monitoring the response to treatment. The important parameters in spirometry include PEFR, FEVl, PVC and FEV25-75. All parameters are decreased in asthma. FEVl is commonly used parameter for documentation of severity of asthma. FEV25-75 is effort independent and is probably more sensitive indicator of airway obstruction. PEFR can be measured easily with peak expiratory flow meter, while for other parameters spirometer is required. PEFR may be used as diagnostic tool in doubtful cases as well as monitoring of treatment. Abnormality in PEFR suggestive of asthma include: a diurnal variation of more than 20%, ::;80% of predicted and improvement of 20% after bronchodilator therapy.

Absolute eosinophil counts. Significance of eosinophilia for distinguishing between allergic, vasomotor or infectious nature of the chronic respiratory obstructive disease is limited. Wheneosinophilia ispresent,bronchial obstruction generally responds well to antispasmodic therapy and the condition is often reversible. The eosinophil count may be low in cases associated with infection. Steroid medication in asthma causes eosinopenia.

Chest X-rayfilm. The X-ray film of the chest shows bilateral and symmetric air trapping in case of asthma. Patches of atelectasis of varying sizes due to mucus plugs are not unusual. Main pulmonary artery is prominent due to pulmonary hypertension. Bronchial cuffing mayoccurdue to the presence of edema fluid in perivascular and peribronchial interstitial space.Extensive areas of collapse or consolidation should suggest an alternative diagnosis. Chest X-ray film may often be normal.

Allergy test. Skin test and radioallergosorbent allergen specific IgE (RAST) havelimited usefulness. Few children need skin tests to identify sensitivity to different antigens since the role of desensitization therapy is not established.

Differential Diagnosis

Bronchiolitis. Bronchiolitis always occurs within the first 2 yr, usually within the first 6 months of life. It is commoner in winter or spring months. Generally there is a single attack. Repeated attacks indicate viral infection associated wheeze or asthma. Hyperinflation of chest with scattered areas of infiltration may be seen on chest X-ray. Asthma may start at any age; more than 3 episodes are usual and wheezing is prominent. Infants diagnosed as bronchiolitis with familyhistory of allergy, having atopic eczema or whose IgE levels are elevated are likely to develop asthma.

Congenital malformation causing obstruction, e.g. vascular rings such as aberrant right subclavian artery or double aortic arch,bronchogeniccysts and tracheomalacia should be excluded in differential diagnosis.

Aspiration of foreign body. Wheeze, if present is generally localized. The history of foreign body aspiration may be forgotten. An area with diminished air entry, with or without hyperresonance on percussion especially in children, may be due to obstructive emphysema because of a check-valve type of obstruction due to the foreign body. Most children develop frequent infections in the lung around the foreign body.

Hypersensitivity pneumonitis. An acute or chronic lung disease may be observed following inhalation of organic dust such as molds, wood or cotton dust, bird droppings, fur dust, grain or following exposure to certain chemicals or drugs such as epoxy resins, PAS and sulfonamides. In the acute form of illness, these children show from fever, chills, dyspnea, malaise, aches and pain, loud inspiratory rales (crackles) atbases of lung andweight loss. X-ray chest shows interstitial pneumonia. Bronchial markings are prominent. The levels of IgE antibodies to the specific antigen are increased. The skin test shows Arthus phenomenonwith local hemorrhage, edema and localpain within 8 hr of the test. Diagnosis is established by lung biopsy.

Cystic fibrosis. Children with cystic fibrosis may present with recurrent wheezing but over a period of time they develop clubbing. There may be clinical evidence of mal­ absorption. X-ray film may show evidence of hyper­ inflation, peribronchial cuffing and pneumonia. Diagnosis is established by estimating sweat chloride levels.

Management

The effective longterm management of asthma involves:

1.Identification and elimination of exacerbating factors

ii.Pharmacological therapy

iii.Education of patient and parents about the nature of disease and the steps required to avoid acute exacer­ bation.

Identification and Elimination of Exacerbating Factors

Factors associated with development and precipitation of asthma include passive smoking, allergic disorders,

inadequate ventilation athomeleading to dampness, cold air, cold food, smoke, dust and pets in the family. Acute respiratory infectiondue tovirusesis thecommonestcause of exacerbation of asthma. The following measures help in reducing the triggers of asthma:

•The bedroom of the child should be kept clean and as

free from dust as possible. Wet mopping of the floor should be done because dry dusting increases exposure of the child to house dust.