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PEDIATRICS Vol. 109 No. 5 May 2002, pp. 959-961


EXPERIENCE AND REASON

Chronic Lung Disease After Activated Charcoal Aspiration


    ABSTRACT
 TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 REFERENCES
 
The ingestion of toxic substances is a common pediatric emergency. Activated charcoal is part of the standard treatment for most toxic ingestions and is considered a benign therapy. We report a case of inadvertent administration of activated charcoal into the trachea that resulted in the development of chronic lung disease.

Key Words: activated charcoal • aspiration • pneumonitis

Abbreviations: CT, computed tomography • BAL, bronchoalveolar lavage


    INTRODUCTION
 TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 REFERENCES
 
It has been estimated that >4 million toxic ingestions occur annually in the United States.1 The vast majority of these ingestions never receive proper medical attention; however, about 85 000 children younger than 6 years of age receive medical treatment for these episodes on an annual basis.1 Treatment of these toxic ingestions depends on the ingested agent. However, activated charcoal is frequently a key component of therapy, often used to decrease the absorption and enhance the elimination of the ingested toxins. Activated charcoal has generally been considered a benign therapy, with emesis being the most common reported complication.2 There are rare case reports38 and experimental models9,10 of charcoal aspiration causing significant pulmonary morbidity and/or mortality. We report the development of chronic lung disease after aspiration of activated charcoal.


    CASE REPORT
 TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 REFERENCES
 
A 4-year, 11-month-old girl was referred for evaluation of uncontrolled asthma. She started having respiratory symptoms after an incident in which she received emergency department care for the ingestion of an unknown pill at 2 years of age. Before this episode, she had no history of any respiratory disease or respiratory symptoms. By report, a nasogastric tube was introduced for activated charcoal administration, but it was inadvertently placed in the trachea with lavage of charcoal into the airway. She subsequently required intubation and was mechanically ventilated for 5 days. During the time she was intubated and ventilated, and lung lavage was performed twice in attempts to remove the charcoal. Thereafter, she was diagnosed with asthma and started on inhaled steroid and bronchodilator therapy, which did not result in significant improvement in her symptoms. In addition, she received several courses of oral corticosteroids, which resulted in some minimal improvement, but never complete resolution of her symptoms.

At the time of our initial evaluation (2 years after the charcoal aspiration event), her mother reported a daily dry cough that was worse in the morning. The cough was exacerbated by cold air, exercise, and crying. She did not have a history of wheezing, but did become more dyspneic with activity than other children her age. She was taking the following medications: fluticasone propionate, 110 µg (1 puff twice a day); salmeterol xinafoate, 50 µg (1 puff twice a day); loratadine, (5 mg by mouth every day); and albuterol sulfate, (2 puffs as needed). All the inhaled medications were given with a valved holding chamber. Her past medical history revealed 1 episode of pneumonia and multiple emergency department visits for respiratory distress and coughing, all occurring after the charcoal aspiration episode. The family history revealed no history of asthma or any chronic lung disease. She lived with her mother, father, and 8-year-old brother. There was no environmental tobacco smoke exposure, and there was an outside cat.

On physical examination, her height was 110.2 cm (70th percentile) and weight was 18.9 kg (69th percentile). The only appreciable abnormality was a high-pitched right-sided expiratory wheeze that resolved after spirometry. The prebronchodilator spirometry was normal and revealed the following: forced vital capacity = 0.87 L (88% of predicted), forced expired volume in 1 second = 0.83 L (88%), and forced expiratory flow between 25%–75% of the forced vital capacity = 1.32 L/sec (82%). A computed tomography (CT) scan of the chest that was performed at the age of 5 years, 3 months (3 years, 3 months postcharcoal aspiration) revealed a tree-in-bud pattern that was worse in both lower lobes (Fig 1). Over the ensuing 6 months additional evaluations were performed to determine the cause of the chronic lung disease as well as possible sequela and to determine the optimal treatment. A repeat chest CT scan continued to demonstrate the "tree-in-bud" pattern, with no evidence of bronchiectasis, pleural, or other abnormalities. Evaluation for exercise and sleep-related gas exchange abnormalities included a normal 6-minute walk test and a nocturnal cardiorespiratory study with no desaturations or hypoventilation. A sweat chloride was normal. An immune work-up including tests of lymphocyte numbers and function, immunoglobulin A, G (with subclasses), and M levels, complete blood count, complement levels were normal. In addition, an erythrocyte sedimentation rate, C-reactive protein, and rheumatologic work-up revealed no abnormalities. Flexible fiber-optic bronchoscopy revealed no gross anatomic abnormalities. Bronchoalveolar lavage (BAL) fluid, however, contained black particulate material, which was confirmed to be carbon by the pathologist. The cell count from the BAL demonstrated 62% macrophages, 3% neutrophils, and 35% lymphocytes. Ten percent to 15% of the macrophages contained stainable iron and 15% to 20% of the macrophages contained dark particulate material consistent with carbon. All tests for infectious causes (including viral, bacterial, mycobacterium, fungal, etc) were negative. A lipid-laden macrophage index for aspiration was negative at 52. In addition, a pH probe evaluation for gastroesophageal reflux was normal. The patient underwent thoracoscopic open-lung biopsy as no diagnosis had yet been established with the previously described evaluations. It was elected to perform the biopsy on the left side as it simplified the surgical procedure, and although the initial aspiration was right-sided, the CT scans demonstrated similar disease bilaterally. Two biopsies were performed, one from the left lower lobe (which appeared to be severely affected on the CT scan), and one from the lingula (which appeared to be minimally affected). The left lower segment appeared grossly abnormal with carbonaceous-appearing material evident. The pathology demonstrated deposition of particulate dark material within the bronchioles, interstitium, and peribronchial tissue, with minimal deposition in the alveolar space from the left lower lobe segment (Fig 2). Macrophages containing charcoal were present. In addition, there was intraluminal giant cell reaction with some airways demonstrating obliteration. There were no interstitial or alveolar inflammatory reactions. The lingula segment also demonstrated some mild bronchiolar deposition of granular dark material, and a few macrophages containing charcoal, but minimal inflammatory response.



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Fig 1. CT scan demonstrating diffuse parenchymal infiltration of lower lobes (left > right), with characteristic "tree-in-bud" pattern.

 


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Fig 2. Biopsy specimen from the left lower lobe demonstrating intraparenchymal irregular dark particles consistent with charcoal, and associated multinucleated giant cell reaction.

 

    DISCUSSION
 TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 REFERENCES
 
Pulmonary aspiration of charcoal is a rare complication of the treatment for toxic ingestions. The majority of the pulmonary complications from charcoal ingestion have been considered to result from the ingestion of gastric contents along with the charcoal and not directly from the charcoal itself.11 Fatal cases have been reported. In some, aspiration of gastric contents was reported,5 while in others no documentation was provided, making it difficult to make conclusions.6 However, our patient had isolated pulmonary aspiration of charcoal and has developed a chronic long-term inflammatory response. There are case reports of inadvertent activated charcoal aspiration into the lung that resulted in the development of acute respiratory distress syndrome3 with apparent resolution, although long-term follow-up was not provided. In our case, there was need for acute ventilation after the instillation, however, long-term follow-up has demonstrated significant morbidity with daily symptoms that can not be attributed to any other pulmonary pathology, other than the aspirated charcoal. To our knowledge, this is the first case report demonstrating long-term chest CT abnormalities and lung inflammation (based on BAL cytology and biopsy histopathology) after charcoal aspiration.

Until recently, activated charcoal has been considered an inert substance void of serious complications. However, 2 recent experimental studies have demonstrated that instillation of charcoal into the lung can have adverse pathophysiologic consequences. Arnold et al10 instilled charcoal directly into the lung of rats and demonstrated acute changes in pulmonary microvascular permeability and the development of lung edema. Lee et al9 used a similar model and demonstrated that obliterative bronchiolitis lesions developed after intratracheal instillation of charcoal. These 2 studies give a potential framework for the development of long-term pulmonary sequela from charcoal aspiration observed in this patient. Additional animal model evaluation of the long-term effects of intratracheal charcoal administration would be useful and interesting.

There is a single report of a postmortem case in which a biopsy demonstrated bronchiolitis obliterans after aspiration of activated charcoal.4 The similarities in this case are striking in that chronic lung disease developed after the aspiration event, and the biopsy demonstrated black material (presumably charcoal) within the airways with obliteration of the bronchioles, and a giant cell reaction.4 However, they also demonstrated fibrous obliterans associated with airway stenosis and bronchiolectasis on biopsy, none of which were present on our biopsy specimen. Additionally, chronic respiratory insufficiency developed in that case report, which ultimately was the cause of death, that did not occur in our patient.4 The reasons for the more severe course are not evident in their case report, although, one can conjecture that aspiration of gastric contents with the charcoal and the prolonged ventilation after the initial event were at least contributory.

Our finding on the CT scans of a tree-in-bud pattern has not been previously been reported in charcoal aspiration events. The "tree-in-bud" pattern is a nonspecific finding commonly seen in diseases affecting bronchioles. Collins et al12 provide an excellent review discussing the structural pathology that causes this CT scan appearance, as well as a differential diagnosis. The "tree-in-bud" CT pattern is seen in conditions that cause severe bronchiolar impaction with obliteration of the distal bronchioles and contiguous branches.12 This pathology was demonstrated on the biopsy specimens in our case. Other conditions associated with the "tree-in-bud" CT finding are infectious diseases involving bronchioles (such as tuberculosis, atypical mycobacterium, viral, parasitic, fungal), allergic bronchopulmonary aspergillosis, cystic fibrosis, papillomatosis, aspiration pneumonia, etc.

Treatment of acute ingestions is a common problem encountered in pediatric emergency rooms. Activated charcoal is frequently administered and is generally considered to be a safe therapy for the majority of these ingestions. To decrease the complications from this therapy, it is imperative that one determine the patients’ mental status and ability to protect their airway. Protecting the patient’s airway (even if this requires intubation with a cuffed endotracheal tube) should be considered if the patient’s mental status and/or ability to prevent aspiration is impaired. In addition, adhering to established techniques for the placement of nasogastric tubes is critical, and verifying placement is necessary to prevent similar cases from occurring. It is likely that aspiration of activated charcoal with gastric contents will result in a more severe acute course. However, when charcoal inhalation does take place, we recommend that long-term follow-up be considered, as charcoal-related pulmonary complications may persist.

Gavin R. Graff, MD, James Stark, MD, John W. Berkenbosch, MD, George W. Holcomb, III, MD and Robert E. Garola, MD

University of Missouri Hospital and Clinics
Columbia, MO 65212
Children’s Mercy Hospital
Kansas City, MO 64108

-->
    FOOTNOTES
 
Received for publication Sep 10, 2001; Accepted Nov 29, 2001.

Address correspondence to Gavin R. Graff, MD, Department of Child Health, University of Missouri, One Hospital Drive, Columbia, MO 65212. E-mail: graffg{at}health.missouri.edu


    REFERENCES
 TOP
 ABSTRACT
 INTRODUCTION
 CASE REPORT
 DISCUSSION
 REFERENCES
 

  1. Shannon M. Ingestion of toxic substances by children. N Engl J Med.2000; 342 :186 –191[Free Full Text]
  2. American Academy of Clinical Toxicology, European Association of Poisons Centres and Clinical Toxicologists. Position statement: single-dose activated charcoal. J Toxicol Clin Toxicol.1997; 35 :721 –741[Medline]
  3. Harris C, Filandrinos D. Accidental administration of activated charcoal into the lung: aspiration by proxy. Ann Emerg Med.1993; 22 :1470 –1473[CrossRef][Medline]
  4. Elliott CG, Colby TV, Kelly TM, Hicks HG. Charcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal. Chest.1989; 96 :672 –674[Abstract/Free Full Text]
  5. Menzies DG, Busuttil A, Prescott LF. Fatal pulmonary aspiration of oral activated charcoal. BMJ.1988; 297 :459 –460
  6. Litovitz TL, Smilkstein M, Felberg L, Klein-Schwartz W, Berlin R, Morgan JL. 1996 annual report of the American Association of Poison Control Centers Toxic Exposure Surveillance System. Am J Emerg Med.1997; 15 :447 –500[CrossRef][Medline]
  7. Justiniani FR, Hippalgaonkar R, Martinez LO. Charcoal-containing empyema complicating treatment for overdose. Chest.1985; 87 :404 –405[Abstract/Free Full Text]
  8. Sabga E, Dick A, Lertzman M, Tenenbein M. Direct administration of charcoal into the lung and pleural cavity. Ann Emerg Med.1997; 30 :695 –697[CrossRef][Medline]
  9. Lee AG, Wagner FM, Chen MF, Serrick C, Giaid A, Shennib H. A novel charcoal-induced model of obliterative bronchiolitis-like lesions: implications of chronic nonspecific airway inflammation in the development of posttransplantation obliterative bronchiolitis. J Thorac Cardiovasc Surg.1998; 115 :822 –827[Abstract/Free Full Text]
  10. Arnold TC, Willis BH, Xiao F, Conrad SA, Carden DL. Aspiration of activated charcoal elicits an increase in lung microvascular permeability. J Toxicol Clin Toxicol.1999; 37 :9 –16[CrossRef][Medline]
  11. Tomaszewski C. Activated charcoal—treatment or toxin? J Toxicol Clin Toxicol.1999; 37 :17 –18[CrossRef][Medline]
  12. Collins J, Blankenbaker D, Stern EJ. CT patterns of bronchiolar disease: What is "tree-in-bud"? AJR Am J Roentgenol.1998; 171 :365 –370[Free Full Text]

PEDIATRICS (ISSN 1098-4275). ©2002 by the American Academy of Pediatrics

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