Magnitude of problem

Journal of Neonatology

0971-2179

National Neonatology Forum

jn-21-3-002

REVIEW ARTICLE

Neonatal Pneumonia

Dutta

Sourabh

Postgraduate Institute of Medical Education and Research, Chandigarh, India. E-mail: sourabhdutta@yahoo.co.in, sourabhdutta67@rediffmail.com

7–92007

213158159

Magnitude of problem

Pneumonia is part of the syndrome of neonatal septicemia. It is difficult to quantify the burden of neonatal pneumonia or discuss its diagnosis and treatment, independent of generalized septicemia. In referral hospitals in India 3% of all inborn babies develop sepsis, of which a third are diagnosed to have pneumonia¹. Intrauterine and early onset pneumonia is found in 10–38% of stillborn babies at autopsy and in 20–63% of liveborn babies who subsequently die². The highest risk of death from pneumonia is in the neonatal period. In a community based field trial in the Gadchiroli district of Maharashtra, Bang et al found that more than 50% of child deaths from pneumonia occurred among neonates³. Case fatality rates are higher for intrauterine or early onset pneumonia than late onset neonatal pneumonia⁴.

Pathogenesis

Depending on the mode of acquisition, neonatal pneumonia is acquired transplacentally (either in utero or during birth), from the birth canal or after birth. Those acquired in utero may cause stillbirth or very early neonatal death and are associated with chorioamnionitis. Intrauterine infection can also occur in the setting of systemic infections in the mother, such as rubella, cytomegalovirus, syphilis, listeriosis, tuberculosis and HIV. Pneumonia acquired during the process of birth is often associated with perinatal asphyxia. Asphyxia is both a cause and effect of perinatally acquired pneumonia. Asphyxia may cause gasping and inhalation of infected amniotic fluid and, on the other hand, infection may cause fetal depression and asphyxia.

Diagnosis

Respiratory distress is characteristic of pneumonia. In case of intra-uterine transmission, the distress starts at birth. Other signs include tachypnea, apneic episodes, hypoxemia and other signs of generalized sepsis. Signs of pleural effusion and empyema may be present in suppurative pneumonias associated with staphylococcal infections. Singhi and Singhi reported the sensitivities of common clinical signs of radiographically diagnosed pneumonia: chest recessions (84%), tachypnea (89%), cough (84%), fever (56%), inability to feed (49%) and cyanosis (12%)⁵. They suggested that chest wall retraction with cough or tachypnea could be used to define neonatal pneumonia in primary health care situations. Mathur et al reported that the positive predictive value of chest retractions for diagnosis of pneumonia among neonates presenting to a referral hospital was 68.7%⁶. They defined neonatal pneumonia for purposes of a tertiary care setting: respiratory distress with either positive blood culture or any two out of (a) maternal risk factors, (b) clinical signs of sepsis, (c) radiographic changes that do not resolve within 48 hrs and (d) positive sepsis screen.

It may be difficult to distinguish respiratory distress syndrome from early onset pneumonia. Both can occur in preterm and term infants and can present clinically and radiologically in similar ways. Respiratory distress syndrome, though commoner in newborn infants delivered at less than 34 weeks of gestation, may present in term asphyxiated babies or infants of diabetic mothers.

In developing countries, a large number of neonates with pneumonia present with hypoxia. This figure is estimated to be 10% in primary care facilities and over 30% in hospitals. The risk factors for death from neonatal pneumonia are early onset disease, hypoxemia, low birth weight and absence of tachypnea^5–7.

Chest radiographs of neonatal pneumonia generally show non-homogenous patchy infiltrates. This may be indistinguishable from aspiration syndromes, pulmonary hemorrhage, pulmonary edema and non-bacterial pneumonias, e.g. fungal and viral. Severe pneumonias may present withdiffuse granularity or complete “white-out” akin to respiratory distress syndrome.

Tracheal aspirate cultures (in ventilated babies) or naso-pharyngeal aspirate cultures give an idea of the organisms that the infant is colonized with but this may not necessarily corroborate with the actual etiologic organism. Blood cultures are positive in a minority of cases.

Etiology

The only definitive way to identify the causative organism is to culture the fluid aspirated by lung puncture, which is an invasive procedure. Among seriously ill infants with lung lesions amenable to needle puncture, one-third of the samples yielded positive cultures. This rate of positive results is unlikely to be obtained in an unselected group of neonates with pneumonia². Two lung aspirate studies have been reported from India^7,8. Both studies yielded positive isolates in about 60% cases. Surprisingly, the commonest organism reported was S pneumoniae in both studies. S aureus, Klebsiella spp and S epidermidis were the other common organisms. Considering that, signs of generalized sepsis usually accompany pneumonia and infective processes are seldom compartmentalized in septic neonates, bacterial isolates from the blood or cerebro-spinal fluid can be considered equivalent to the etiology for pneumonia. As per the WHO Young Infant Study the commonest organisms causing neonatal sepsis (in order of decreasing frequency) are E coli, S aureus, Enterobacter spp and S pyogenes in infants less than 7 days old; and S aureus, S pyogenes, E coli, S pneumoniae and Salmonella spp in those more than 7 days old⁹.

Neonatal pneumonia due to Chlamydia trachomatis has not been well studied in India. In Papua and New Guinea positive C trachomatis nasopharyngeal isolates were found in 33% of infants with severe pneumonia and 18% of those with non-severe pneumonia¹⁰.

Risk factors

The risk factors of early onset pneumonia (< 72 hours) are similar to those of early onset sepsis-preterm, premature rupture of membranes; prolonged rupture of membranes; preterm labour; maternal pyrexia, leucocytosis, foul smelling liquor or uterine tenderness; frequent or unclean vaginal examinations. The risk factors for late onset pneumonia are prematurity and low birth weight, and ventilator-associated pneumonia in ICU settings.

Treatment

Treatment comprises of parenteral antibiotics, oxygen and supportive care. For community acquired neonatal pneumonia, the WHO protocol of Ampicillin and once-daily Gentamycin should be followed¹¹. Whenever there is suspicion of staphylococcal infection, cloxacillin or flucloxacillin should be added in place of Ampicillin. In rural community-based studies, oral Cotrimoxazole and intramuscular Gentamycin have been successfully used by village health workers to lower the mortality due to neonatal sepsis¹². The prevailing flora and their sensitivity patterns should guide antibiotic policy in hospitals. The NNPD paints a frightening picture of multi-drug resistance in Indian neonatal units, with widespread resistance to common antibiotics like Ampicillin, Penicillin, Gentamycin and Cefotaxime¹.

There is a paucity of randomized trials to determine the optimum duration of antibiotic therapy. A study from PGIMER, Chandigarh showed that in the case of S aureus septicemia, a 7-day antibiotic course had significantly higher failure rates than a 14-day course¹³. In non-S aureus sepsis, no evidence of a difference in failure rates between the two regimes could be found.

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