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Indian Pediatr 2015;52:
63-64 |
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Lipoid Pneumonia - An Unusual Cause of Acute
Respiratory Distress Syndrome
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Anil Sachdev, Preeti Anand and Dhiren Gupta
From Division of Pediatric Critical care and
Pulmonology, Department of Pediatrics, Institute of Child Health, Sir
Ganga Ram Hospital, New Delhi, India.
Correspondence to: Dr Anil Sachdev, Director
Pediatric Emergency, Critical Care and Pulmonology, Department of
Pediatrics, Institute of Child Health, Sir Ganga Ram Hospital, Rajinder
Nagar, New Delhi 110060, India.
Email: [email protected]
Received: July 02, 2014;
Initial review: August 21, 2014;
Accepted: October 06, 2014.
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Background: Lipoid
pneumonia is a rare form of pneumonia caused by aspiration of fatty
substances. Case characteristics: Acute respiratory distress
syndrome in an infant due to accidental aspiration of baby oil massage.
Intervention: Large volume bronchoalveolar lavage. Outcome:
Gradual recovery over a period of 5 months. Message: Aspiration
of lipids cause prolonged and refractory hypoxemia.
Keywords: Bronchoalveolar lavage, Fiberoptic
bronchoscopy, Lipoid pneumonia.
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E xogenous lipoid pneumonia is an uncommon
condition resulting from the aspiration or inhalation of fatty
substances like mineral oils or petroleum jelly [1,2]. We report a child
developing acute respiratory distress syndrome (ARDS) after accidental
ingestion of baby massage oil. She was successfully treated with
multiple bilateral large volume bronchoalveolar lavages (BAL) carried
out with fiberoptic flexible bronchoscope.
Case Report
A 10-month-old girl presented to us fifteen days
after accidental ingestion of baby massage oil. Post-ingestion, she had
vomited once, and developed progressive cough and dyspnea in the next
three days. Her clinical condition worsened despite oral antibiotics and
she was admitted elsewhere. In view of poor response to treatment,
patient was referred to our hospital for further management.
At admission, she had severe respiratory distress and
hypoxemia. Initial chest radiograph showed bilateral diffuse ground
glass appearance suggestive of alveolar-interstitial pattern of
opacities. She was electively intubated and ventilated with pressure
regulated volume controlled mode. In view of persistent respiratory
acidosis (pH 7.21), high plateau pressure (32 cmH 2O)
and refractory hypoxemia (PaO2/FiO2
<150), she was shifted to high frequency oscillatory ventilation (HFO-V,
Sensormedics 3100A). She required high mean airway pressure (27cm H2O),
FiO2 0.7, amplitude 45,
frequency 10Hz and inspiratory time 33%. In view of the hemodynamic
instability, boluses of normal saline and dopamine infusion (10
mcg/kg/min) were used for 48 hours. Hypoxemia and respiratory acidosis
improved gradually over next 72 hours, and she was shifted to
conventional ventilation on day 4. The weaning trial failed on day 7 of
admission and chest X-ray continued to show ground glass haziness
of both lung fields. The sepsis screen sent at admission was negative.
Endotracheal aspirate sent on admission was positive for
lipid-laden macrophages; gram stain and culture were non-contributory.
On seventh day of admission, we performed fiberoptic
flexible bronchoscopy through endotracheal tube. The tracheobronchial
tree was smeared with pale yellow oily secretions. Large volume (50mL
saline for each lung) Bronchoalveolar lavage (BAL) was done; it was
positive for lipid-laden macrophages and the cultures were sterile. She
was started on intravenous methylprednisolone (2 mg/kg/day)followed by
its oral preparation for next 8 weeks. During her stay, contrast
enhanced computed tomography of chest also showed bilateral ground glass
haziness of both lungs, lower lobes more involved than upper lobes (Fig.
1). Single lung large volume BAL was performed twice a week, while
she was on invasive ventilation, followed by weekly BAL; the child was
successfully extubated on day 11 of admission. She was electively weaned
and extubated to non-invasive ventilation (BIPAP) with supplement
oxygen. Over the next 4 months she was shifted from BIPAP to continuous
positive airway pressure mode. She could be weaned from oxygen after 5
months of hospital stay. Patient developed clubbing of all fingers by
end of 3 weeks of stay in the hospital.
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Fig. 1 Contrast enhanced CT of chest
(axial section in lung window) showing ground glass appearance,
air trapping and consolidation.
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She received oral prednisolone and azathioprine (2
mg/kg/day) for 9 months. Initially, prednisolone was started with 2
mg/kg/day and dose was gradually tapered. Six months after discharge,
she had normal growth and development with reversal of clubbing and
normal chest X-ray.
Discussion
Acute exogenous lipoid pneumonia is due to acute
ingestion of mineral, vegetable or animal fats [3]. Chronic exogenous
lipid pneumonia usually results from repeated episodes of aspiration or
inhalation of oils over an extended period. It is usually seen in
children with anatomic (cleft palate) or functional defects
[2]. The aspirated fat is phagocytosed by macrophages leading
to destruction of alveoli. Most of the oil coalesces, forming large fat
drops surrounded by fibrous tissue and giant cells, creating paraffinoma.
The inflammatory response can destroy the alveolar walls and the
interstitium, and the resultant fibrosis can occasionally progress to
end-stage lung disease [2,3].
Acutely, patient typically presents with cough,
dyspnea and low-grade fever. Crackles or rhonchi may be heard on
auscultation of chest. Laboratory investigations reveal hypoxemia,
leukocytosis and raised erythrocyte sedimentation rate [1,2]. Diagnosis
is established on the basis of history of exposure with presence of
lipid laden macrophages in respiratory samples such as BAL fluid or
sputum [4]. Hadda, et al. [3] reported a case of a 20-year-old
male who presented with acute respiratory distress syndrome following
accidental mineral oil aspiration.
The key to treatment is identifying and discontinuing
exposure to the offending agent, providing adequate supportive therapy
and treating complications [1,2,5,6]. Use of azathioprine with steroids
has been reported in pulmonary fibrosis patients to prevent progression
of fibrosis [6,7]. Fibrosis is reported as an end result in lipoid
pneumonia but azathioprine use for the treatment has not been earlier
reported [1,2]. Steroids either alone or in combination with intravenous
immunoglobulin and large volume bronchial lavage have been used with
reasonable success [5,8-10].
Contributors: AS: Case management and
critical review of the manuscript; PA: Data collection and
manuscript preparation; DG: Drafting the manuscript.
Funding: None; Competing interests: None
stated.
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