Dr.Sruthi, Dr.Sathyajith G Nair, Dr.C. Jayakumar
AIMS, Kochi
Two -year-old male
spastic cerebral palsy, global developmental delay, status post left sided congenital diaphragmatic hernia correction, with h/o Grade 3 IVH with post haemorrhagic hydrocephalus presented with high grade fever and fast breathing,poor feeding of 7 days duration
He is the first child of non-consanguineous parentage born at 27 weeks birth weight of 1.25kg following premature rupture of membranes via vaginal delivery . He had perinatal depression and on ventilator and there is h/o Ba was referred to AIMS with the suspicion of CDHon day 3 of life soon he underwent CDH repair.
MRI brain showed Periventricular leukomalacia suggesting sequelae of hypoxic ischemic injury and associated hydrocephalus.
At admission he was febrile, tachypnoeic and had nasal flaring.
Vitals: Temp- 101.9’F, PR-120/min, RR-40/min, spO2-98% on room air, CRT<2sec.
PICCLE normal
Strabismus+, cortical thumb present.
No neurocutaneous markers or facial dysmorphism.
Weight-9.8kgs (below 3rd centile) Grade 1 PEM, Height-84cms (50th centile) grade 1 stunting, HC-48cms (b/w 15th -50th centile), MUAC-14cms
Chest examination revealed bilaterally equal air entry, bilateral wheeze and crepitations+
CNS: HMF: Alert, conscious. Cranial Nerves: Intermittent convergent Bilateral squint.
Motor: Hypertonia of all limbs, best observed power is grade 3, Reflexes: Exaggerated reflexes(+++) in all 4 limbs, B/L extensor Plantar response. No signs of meningeal irritation. CVS- S1 and S2+, no murmur. GIT- Soft, Non tender, BS(+), No organomegaly
Figure 1: At admission: showing right middle lobe consolidation.
USG chest done showed consolidatorychanges in right middle and lower lobes. A thin rim of echogenic fluid was seen, more in the right posterolateral aspect, inferiorly with maximum thickness of 12 mm. Chest physiotherapy was started. Serial monitoring of blood counts showed improving trend.
Figure 2: Chest X-Ray showing right sided well defined opacity
As he was having 2-3 high grade fever spikes each day oral Azithromycin and IV clindamycin was added to ceftriqxone
Repeat USG chest done showed loculated pleural effusion/collection involving the right middle and lower lobes with internal echoes and collapsed lung with consolidatory changes measuring 6.4 x 5 x 7.1 cm (volume 122 ml).
CT chest with contrast was done which showed presence of a large thick walled cavity with air fluid level involving superior and lateral basal segments of right lower lobe and partly lateral segment of right middle lobe suggestive of a lung abscess, right mild pleural effusion and enlarged right upper paratracheal and subcarinal nodes.
Figure 3: CT chest with contrast showing right sided thick walled cavity
Thus he underwent CT guided pigtail insertion under anaesthesia
Antibiotics were hiked to IV Vancomycin and IV Piperacillin-Tazobactam with which fever subsided.
Cytopathology evaluation showed neutrophil rich inflammation, consistent with abscess. AFB stain was negative. Gram stain showed moderate inflammatory cells. Owing to the thick consistency of the sample, LDH, ADA, glucose and protein couldn’t be done,culture was sterile. MTB PCR was negative. pH was found to be 6.5. Thereafter, daily drain monitoring was done and antibiotics were continued for a total of 21 days. Vancomycin drug level and RFT were serially monitored and were found to be within normal limits. In view of decreasing trend of the drain output, USG chest was done which showed no sonologically detectable collection/effusion. Drain was kept until nil output was obtained. Repeat chest X-ray showed absence of fluid. Thus pigtail was removed and IV antibiotics changed to oral Linezolid.
Figure 4: Chest X-ray showing resolution of right sided opacity post treatment.
A lung abscess in pediatric patient is an encapsulated collection of purulent material within the pulmonary parenchyma, often secondary to infection. It is generally classified as a complication of either aspiration pneumonia or hematogenous spread of infection.
Etiology includes bacterial Pathogens such as Staphylococcus aureus, Streptococcus pneumoniae, Klebsiella pneumoniae, and Pseudomonas aeruginosa. Anaerobic bacteria such as Bacteroides and Peptostreptococcus are also implicated, especially in cases of aspiration. Fungal Infections in immunocompromised children, fungi like Candida or Aspergillus can cause abscesses. Mycobacterium tuberculosis can lead to lung abscess formation, especially in regions with high tuberculosis prevalence. Accidental inhalation of oropharyngeal secretions or foreign bodies can lead to aspiration pneumonia, which may progress to abscess formation.
Symptoms often include persistent cough, fever, pleuriticchest pain, hemoptysis, and, occasionally, respiratory distress. Physical examination may reveal decreased breath sounds or localized wheezing over the affected area.
Diagnosis includes Chest X-ray typically showing a cavitarylesion with an air-fluid level. A high-resolution chest CT scan provides more detailed information regarding the size, location, and characteristics of the abscess, and can help distinguish it from other pulmonary pathologies.2. Sputum culture, blood cultures, and, in some cases, bronchial lavage or percutaneous aspiration can identify the causative organism. Serologic tests and PCR may be required for specific pathogens like fungi or mycobacteria.
Management includes antibiotic therapy. Empirical antibiotic therapy is guided local resistance patterns and adjusted based on culture results. Typically, treatment includes broad-spectrum antibiotics initially, with subsequent de-escalation as more specific pathogens are identified. If the abscess does not respond to medical management or if there is evidence of significant mass effect or complications, percutaneous drainage or surgical intervention may be warranted. Supportive measures include pain management, hydration, and respiratory support as needed.
With timely and appropriate treatment, most pediatric patients with lung abscesses recover fully. Delayed diagnosis or inadequate treatment can lead to complications such as bronchopleural fistula, empyema, or chronic pulmonary damage.