NON-INFECTIVE PNEUMONIA

Non-infective pneumonias denote alveolar inflammation due to chemical (aspiration), allergic (hypersensitivity) or physical injury (smoke). However, most of them are rapidly complicated by superadded infections.

Aspiration pneumonia: Clinical presentation of aspi­ration pneumonias depend on the type of aspirate, e.g.

(a) gastric contents/oral feeds, e.g. milk, (b) volatile hydrocarbons, e.g. kerosene and (c) thick viscous lipoid substances, e.g. oils, discussed as follows:

Milk-aspiration syndrome: Aspiration of milk/gastric content is common in infants or debilitated children with following risk factors—(a) oropharyngeal defects, e.g. cleft palate, (b) esophageal problems, e.g. strictures or gastroesophageal reflux, (c) neuromuscular incordi­nation in preterms, comatose or floppy child, and (e) severe respiratory distress.

Clinically, these cases present with a biphasic course- (a) immediate bouts of cough or apnea (choking) due to mechanical obstruction or reflex laryngospasm, followed by; (b) a silent phase of 1-2 hours; and then (c) progressive respiratory distress due to chemical pneumonitis and secondary infection.

Signs of pneumonia appear only after 1-2 hours of aspiration with development of crepitations/rhonchi, etc. Presence of high fever indicates secondary infection.

Diagnosis rest on-(a) history of vomiting/choking during feeds, (b) presence of vomitus/milk on immediate airway suction, and (c) bilateral perihilar or diffuse reticular infiltrates on chest X-ray after 2 hours of aspiration (Fig. 16.11E). Immediate X-ray may be normal. Management includes—(a) immediate endotracheal suction, (b) oxygen or ventilatory support, (c) fluid and electrolyte therapy, (d) antibiotics-Penicillin/ clindamycin with an aminoglycoside to cover anaerobic oral flora or gram-negative hospital flora. Role of prophylactic antibiotics is controversial.

Prognosis depends on severity of underlying disease and quantum of aspiration, with immediate mortality of ~25%. In survivors, clinical and radiological signs resolve in next 10-14 days.

Hydrocarbon pneumonia: Accidental ingestion of hydrocarbons, e.g. kerosene, petrol, turpentine, etc. is a common cause of poisoning in rural Indian children, specially toddlers (1-3 year).

Pathogenesis: While actual quantity of ingestion is usually very small due to unpleasant taste, these low viscosity volatile fluids easily trickle down the airways to—(a) destroy pulmonary surfactant (atelectasis), (b) initiate inflammatory reaction (pulmonary edema), followed by (c) secondary infection (pneumonia).

Clinical manifestations may not correlate with quantum of aspirate and include—(a) immediate bouts of cough/ vomiting, followed by (b) a silent phase for ~6-12 hours and then, (c) progressive development of pulmonary edema. Development of high fever suggests secondary pneumonia.

Lung signs are often disproportionately less than X-ray abnormalities. Signs of systemic toxicity, e.g. seizures and coma are rare and usually indicate hypoxic injury rather than direct substance toxicity.

Diagnosis depends on history and chest skiagram, which should be delayed for minimum 6 hours after ingestion to allow development of radiological signs, e.g. pulmonary edema (early) or extensive infiltrates, patchy atelectasis and consolidation (late). Air-leaks, e.g. pneumothorax or subcutaneous emphysema are common.

Management includes:

• No immediate intervention is needed in most cases and nasogastric lavage or induction of emesis is contraindicated due to fear of aspiration, except in cases with ingestion of hydrocarbon solvents with toxic substances, e.g. organophosphorus compounds and presenting within 2 hours. In such cases, gastric lavage may be necessary to minimize absorption, but should be done only after insertion of a cuffed endotracheal tube to prevent aspiration.

• Close observation for next 6 hours, followed by chest X-ray to exclude developing pneumonia. (No patient must be sent home before 6-12 hours of observation).

• Hospitalization of symptomatic cases with supportive therapy, e.g. O₂ or ventilatory support and chest physiotherapy. Development of ARDS necessitates positive-pressure ventilation, though many workers suggest early intubation to prevent progressive

CNS depression. Bronchodilators, e.g. salbutamol nebulizations may be used in select cases.

• Prophylactic antibiotics are not routinely indicated, except in symptomatic cases with possible secondary infection. Steroids are contraindicated.

Prognosis depends on—(a) volume of ingestion, (b) age of patient, (c) severity of lung signs and (d) efficacy of treatment, with overall mortality of lt;5-10%. Most cases recover after stormy course within a week.

Lipoid pneumonia is a chronic, interstitial pneumonia due to aspiration of high-density oils, e.g. oily nasal drops, drugs (cod liver oil), feeds (ghee) or petroleum jelly. Indian custom of instilling massage oil in nostrils and ears during early infancy is an important risk factor for lipoid pneumonia.

Pathologically, development of lipoid pneumonia evolves through three stages: (a) initial interstitial proliferative and exudative inflammation, followed by

(b) diffuse fibrosis or secondary infection, and lastly, (c) formation of multiple nodules, i.e. paraffinomas.

Clinically, most cases are initially asymptomatic and present after many months with persistent cough, progressive dyspnea and recurrent chest infections.

Diagnosis rests on history and characteristic X-ray appearance, i.e. bilateral perihilar densities, radiating from hilum in a fan-like manner.

Management is non-specific with treatment of inter­current infections and prognosis is guarded due to progressive lung pathology.

Hypersensitivity pneumonia, also termed hypereosino- philic lung syndromes often mimics asthma (wheezy child), due to bronchial/pulmonary reaction to a known/ unknown allergen.

Loeffler syndrome is a pulmonary hypersensitivity reaction to many antigens/allergens, e.g. (a) worm infestations, e.g. ascaris, toxocara, etc., or (b) drugs, e.g. aspirin, sulfonamides, penicillin, etc.

These cases presents as a chronic disease with-(a) paroxysmal attacks of cough, wheezing, dyspnea without fever, (b) transient, generalized pulmonary infiltrates (miliary mottling), and (c) eosinophilia. Treatment includes wormicidal agents and supportive bronchodilator therapy during attacks.

Tropical pulmonary eosinophilia is a hypersensitivity reaction to microfilariae, characterized by—(a) paroxy­smal cough, wheezing and dyspnea, (b) absolute eosinophil count gt;2000/ml, and (c) presence of micro­filariae or anti-microfilarial antibodies in blood. Chest skiagram is normal or reveals miliary mottling.

Treatment may be started empirically in endemic regions with PO Diethylcarbamazine 5 mg/kg/day for 14-21 days, which may be repeated in partially responsive cases. Response is monitored clinically and by serial eosinophil counts. (Ch 10.35)

Allergic bronchopulmonary aspergillosis (ABPA) is the hypersensitivity response to inhaled aspergillus spores, usually in children with chronic lung diseases. These cases present with recurrent cough/wheeze with occasional expectoration of pathognomonic brown plugs in sputum. Chest X-ray may reveal proximal bronchiectasis.

Diagnosis is supported by positive skin allergen test or presence of aspergillus-specific IgE antibodies. Total IgE levels usually exceed gt;1000 ng/ml.

Low-dose steroids (PO prednisolone 0.5 mg/kg/d) for 4-8 weeks is the treatment of choice, along with specific anti-fungal therapy.

Smoke injury: Thermochemical injury to respiratory mucosa is an important cause of morbidity and mortality in burns, due to inhalation of soot (thermal injury) or noxious gases, e.g. carbon monoxide (chemical injury).

Clinical presentation depends on duration and severity of exposure and may be divided into four stages:

a. Immediate respiratory distress during first 8-12 hours due to bronchospasm, laryngeal edema and alveolar exudation, which must be treated with IV steroids and endotracheal intubation/tracheostomy, if necessary.

b. Pulmonary edema after 8-12 hours, treated with diuretics, fluid restriction and ventilatory assistance.

c. Secondary infection after 4-5 days, usually caused by Staph. aureus or Pseudomonas and treated with antibiotics.

d. Cervical eschar formation with constriction of air­ways after 3-5 days, in cases with full thickness burns of respiratory mucosa. It needs to be treated with bronchoscopic vertical division of burn crust, if necessary.

Carbon monoxide poisoning and asphyxia may also lead to CNS changes, i.e. irritability, visual impairment, altered sensorium and occasionally, coma.

Management depends on clinical staging (discussed earlier), though even asymptomatic cases should be observed for 24 hours after exposure to smoke/fire, for signs of smoke injury or Carbon monoxide poisoning.

Acute Respiratory Infections (ARI) Control Program

Considering the fact that—(a) ARI account for ~20% mortality in under-five children, and (b) diagnosis and differentiation of viral and bacterial ARIs is often difficult in resource limited settings, National ARI Control Programme was launched in 1989, to focus on the clinical-approach based management of these cases, as per WHO guidelines.

It is currently a component of comprehensive RMNCH+A strategy (reproductive, maternal, neonatal, child and adolescent health) of National Health Mission, implemented through existing health infrastructure using Integrated management of Neonatal and Child­hood Illness (IMNCI) guidelines (Ch 29).

Under IMNCI guidelines, a child aged 2 months-5 years with respiratory illness is classified as:

• No pneumonia (cough and cold), in absence of fast breathing or other following signs, who can be treated at home with home remedies without antibiotics and follow-up after 5 days.

• Pneumonia with respiratory rate gt;50 in infants or gt;40 in older children, who should be treated with PO Amoxycillin 40-50 mg/kg/d q8-12 hr for 5 days and follow-up after 2 days.

• Severe pneumonia with lower chest indrawing, central cyanosis or any danger sign, i.e. inability to feed, seizure, coma or vomiting, should be immediately referred for hospitalization after a dose of IM antibiotics.

This classification does not apply to children lt; 2 months, who should be immediately referred for hospitalization in presence of any signs of severe disease.

Major component of ARI control program are—(a) to train paramedical staff at the community level for early diagnosis and appropriate treatment/referral of ARI cases, using standard case management guidelines, (b) to encourage rational treatment practices while limiting the irrational use of antibiotics, and (c) to prevent predisposing illnesses for pneumonia, e.g. measles, pertussis and diphtheria by effective immunization.

16.10