DOI 10.1378/chest.96.3.672 1989;96;672-674Chest

 C G Elliott, T V Colby, T M Kelly and H G Hicks aspiration of activated charcoal.Charcoal lung. Bronchiolitis obliterans after

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672 Charcoaf Lung (Elliott et a!)

Charcoal Lung*

selected reports

Bronchiolitis Obliterans AfterAspiration of Activated Charcoal

Charles G. Elliott, M.D. ,FC.C.P;t

Thomas V Colby, M.D. ,FCC.P;t Thomas M. Kelly, M.D.;t and

Harry G. Hicks, M.D4

Activated charcoal usually provides effective and safe

treatment for drug overdose. We describe a patient whodeveloped bronchiolitis obliterans and respiratory failure

following aspiration of activated charcoal. This patient hada markedly reduced vital capacity with roentgenographic

evidence of airtrapping. Chest roentgenograms did not

demonstrate the large amount of charcoal identified atpostmortem examination. (Che8t 1989; 96:672-74)

I #{176}‘the United States, more than 400,000 suicide attempts

occur annually; and at least 28,000 are successful.’

Standard management of sedative and tricyclic drug poison-

ing includes removal of drug from the stomach by lavage or

induced emesis and the instillation of activated charcoal.23

Aspiration of gastric contents represents a well-recognized

hazard following drug overdose, but pulmonary injury

following the aspiration of activated charcoal has not beenreported. We report a 16-year-old patient who developed

obliterative bronchiolitis after aspirating activated charcoal.

CASE REPORT

A previously healthy 16-year-old white woman took approximately

60 nortriptyline (Pamelor). Upon arrival in the emergency room,

she was combative. A 16 French nasogastric tube was placed, and

the stomach was lavaged until clear of pill fragments. Activated

charcoal (75 g, Actidose with sorbitol) was given through the

nasogastric tube. Ten minutes later, a grand mal seizure accompa-

nied cardiac arrest. Cardiopulmonary resuscitation and DC coun-

tershock restored a stable cardiac rhythm and blood pressure after

90 minutes. Drug screen detected only amitriptyline (673 p.g/dL).

She was transferred to the LDS Hospital. Upon arrival, she was

comatose and was supported with positive pressure ventilation

(p eak pressure 52 cm H20, plateau pressure = 37 cm H20, tidal

volume = 700 ml, rate = 18 breaths per minute). Chest auscultation

revealed scattered end-expiratory wheezes over all lung fields. A

chest roentgenogram disclosed alveolar infiltrate within both lungs

and a right subpulmonic pneumothorax. Arterial blood gas values

were pH of7.40, PaCO2 of5l.5 mm Hg, and Pa02 of54 mm Hg at

F1o2 = 0.8 without positive end expiratory pressure. The WBC was

14.4 x 10� with ten band cells, 86 PMNs, two lymphs, one mono,

and one eosinophil. The ECG showed a wide QRS tachycardia. A

chest tube drained the right pneumothorax, but subcutaneous

*From the Departments ofMedicine, LDS Hospital and University

of Utah, Salt Lake City; and the Departments of Pathology, LDSHospital and the Mayo Clinic, Rochester, MN.

tAssociate Professor.

lPathologist.Reprint requests: Dr Elliott. Pulmonary Division, LDS Hospital,Salt Lake City 84143

emphysema worsened. Fiberoptic bronchoscopy was performed to

look for a tracheal laceration. A tracheal laceration was not found,

but the endoscopist noted extensive charcoal staining of both

mainstem bronchi. During the next 24 hours, 33 ml of thin grey

sputum was suctioned. Arterial blood gas values improved to a pH

of 7.46, PaCO2 of 42.6 mm Hg, Pa02 of 62 mm Hg at F1o2 = 0.45

with 5 cm H20 PEEP The coma resolved, she remained afebrile,

and her ventilatory function improved. She was extubated 15 days

after admission and was discharged four days later with a pH of

7.41, PaCO2 of 46, and Pa02 of 64 while breathing 02 at 4 LPM

(altitude 4,600 ft).

Six days later, she returned complaining offever, cough, dyspnea,

and headaches. Her rectal temperature was 40.3#{176}C;BP, 102/60; VR,

44; and HR, 120. Chest examination revealed paradoxic sternal

motion and late inspiratory rales over both lower lobes. The WBC

was 9,700 with 69 PMNs, 20 band cells, nine lymphocytes, one

basophil, and one eosinophil. The chest roentgenogram demon-

strated small pneumatocoeles, but no new parenchymal infiltrate

was apparent. Arterial blood gas values while breathing ambient

air were Pa02, 42 mm Hg; PaCO2, 35.6 mm Hg; pH, 7.47; and

P(A-a)02, 34 mm Hg. Sputum Gram stain showed Gram-positive

cocci and Gram-negative bacilli. Ceftizoxime, 1 g, and erythromy-

cm, 1 g, were given intravenously every six hours. Sputum culture

yielded alpha-streptococci. Complement fixation antibodies were

negative for Mycoplasma and Legionella species. A DNA probe for

mycoplasma and DFA stain for Legionella were also negative. Blood

cultures were without growth. Her fever abated, and she was

discharged on 02 4 LPM and erythromycin 500 mg po every sixhours.

She returned two days later complaining of dyspnea. She was

afebrile, but the heart rate was 130 beats per minute and the

breathing rate was 40 per minute. Coarse rales were heard over

both lower lobes. The sternum moved paradoxically, and the

respiratory muscles contracted forcefully. Result of cardiac exam

was normal. The arterial Pco2 had increased to 51.4 mm Hg, and

the pH was 7.38. Spirometric measurements were FVC of 0.86 L

and FEy,, 0.64 L. Severe respiratory acidosis ensued requiring

tracheal intubation and positive pressure ventilation. Spontaneous

ventilatory measurements included a rate of3&’minute, tidal volume

of 400 ml, and maximal inspiratory pressure greater than 60 cmH20. Static thoracic compliance remained between 20 and 30 ml!

cm H20. Tracheotomy was performed. Dead space to tidal volume

(VDNT) ratio while breathing spontaneously was 0.67. Within two

weeks, she was weaned from the ventilator. Her arterial blood gas

values were: pH of 7.36; PaCO2, 54.4; and Pa02, 92 mm Hg while

breathing, F1o2, 0.3. During the next five weeks, PaCO2 progres-

sively increased to 76 mm Hg, tidal volume increased to 565 ml,

and ventilatory rate remained 24 per minute. Dead space to tidal

volume ratio was 0.72. Chest roentgenogram and computerized

tomography examination disclosed pneumatocoeles predominantly

in the left upper lobe. Mechanical ventilation was reinstituted. Two

weeks later, VD/VT was 0.90. A perfusion lung scan revealed normal

perfusion except in the cystic left upper lobe. Charcoal was not

seen in the segmental bronchi during fiberoptic bronchoscopy.

Respiratory failure progressed, and she died ten weeks after

admission and 14 weeks after her suicide attempt.

Postmortem Examination

The autopsy revealed extensive charcoal deposition along the

airways in all regions of the lung (Fig 1, top). Histologically, this

was accompanied by bronchiolitis obliterans with fibrous oblitera-

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CHEST I 96 I 3 I SEPTEMBER, 1989 673

FIGURE 1 . Top, Gross photograph of the lung at autopsy showing

extensive charcoal deposition in a centrilobular distribution (arrows)

along medium-sized and small airways. Histologically, the charcoal

deposition is centered on small airways and associated with scarring

and fibrous obliteration of the bronchioles (bronchiolitis obliterans)

and a prominent giant cell reaction (hematoxylin-eosin x 30 (center)

and 400 (bottom).

tion and stenosis of most of the small airways (Fig 1, center). In

some foci, bronchiolectasis was an accompanying feature. Embed-

ded within the bronchiolar scar tissue were massive amounts of

black material associated with a foreign body giant cell reaction

(Fig 1, bottom). No material consistent with food was noted, and

there was no pneumonia at the time of death.

DIScUSSIoN

Activated charcoal is a valuable agent for the treatment

of most toxic ingestions. It is commonly believed to be

innocuous, and large doses are given to avoid administering

too little of an effective nontoxic substance . � Aspiration of a

thick suspension of activated charcoal and gastric contents

has been associated with obstruction of the trachea and

endotracheal tube in an eight-month-old girl,� but our case

is the first report of extensive bronchiolitis obliterans and

progressive respiratory failure associated with massive as-

piration of activated charcoal.

Several physiologic and roentgenographic features of this

case deserve emphasis. First, wheezing and obstruction of

the larger airways were not prominent, although the occur-

rence of pneumothorax and the subsequent demonstration

of air trapping suggest that charcoal obstructed smaller

airways. Arterial hypoxemia, reduced total thoracic compli-

ance, and bilateral diffuse infiltrates on chest roentgenogram

characterized the initial presentation. These features de-

scribe the adult respiratory distress syndrome, a disorder

which commonly follows the aspiration of gastric contents.6

The difference between this presentation and the obstruc-

tion of large airways reported by Pollack et al� may reflect

the larger diameter of adult air�vays and the use of a more

liquid charcoal suspension in the present case.

Although the initial physiologic and roentgenographic

features resembled ARDS, the subsequent course diverged

substantially from the natural history of ARDS and sup-

ported a pathogenetic role for charcoal in the production of

bronchiolitis obliterans. Arterial hvpoxemia improved during

the first three weeks, but hypercapneic acidosis caused by

progressive increases of VD/VT ensued over the next two

months. The vital capacity was severely decreased although

roentgenographic lung volumes remained normal suggesting

air trapping. The standard chest roentgenograms and com-

puted tomography of the chest demonstrated pneumato-

coeles, but neither technique detected the charcoal which

remained in the lungs. These physiologic and roentgeno-

graphic observations suggested diagnoses of bronchiolecta-

sis7 and adult bronchopulmonary dysplasia� rather than

bronchiolitis obliterans due to aspiration of charcoal.

The exact pathogenetic role of activated charcoal in our

case remains uncertain. The charcoal particles and/or ma-

terial adsorbed to its surface, eg, drug particles, clearly

induced a fibrosing granulomatous reaction. Conceivably,

the charcoal alone, other gastric contents alone, or both in

concert were responsible for the bronchiolitis obliterans.

Bronchiolitis obliterans accompanied by hypoxemia and

hypercapnea has been associated with aspiration of gastric

contents containing food particles�’#{176} but not with aspiration

of gastric contents and activated charcoal. The fact that

thorough gastric lavage preceded administration of activated

charcoal and that the charcoal was present in massive

amounts and was the only material associated with bronchi-

olar scarring favors a pathogenetic role for the charcoal.

The treatment of this disorder begins with prevention.

When cardiopulmonary arrest accompanies reflux of gastric

contents, postural drainage of secretions is not possible.

Under these circumstances, rapid intubation of the trachea

with simultaneous cricoid pressure should decrease aspira-

tion. If massive charcoal aspiration occurs, bronchoscopy

with suctioning and lavage may decrease the extent of the

subsequent reaction.

ADDENDUM

After this report was submitted, we identified a report of

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674 Per&sting Hypereo�nopMia and Myocard�1 ActMty(Frustac!eta!)

respiratory failure complicating aspiration ofactivated char-

coal (Menzies DC, Busuttil A, Prescott LF. Br Med J 1988;

297:459-60).

ACKNOWLEDGMENT: The authors thank Mr. Bruce Paddock ofPaddock Laboratories, Inc. for financial support of the colorphotographs.

REFERENCES

1 Fleming TC. Suicide, the hush-hush killer. Postgrad Med 1981;

70:13-16

2 Plum F, Posner JB. Disturbances of consciousness and arousal.

In: Wyngaarden JB, Smith LH, eds. Cecil’s textbook of medi-

cine. Philadelphia: WB Saunders Company, 1988; 2070

3 Klaasen CD. Principles oftoxicology. In: Goodman LS, Gilman

AG, eds. The pharmacological basis of therapeutics, 7th ed.

New York: Macmillan Publishing Company, 1985; 1599-601

4 June CH. lkisoning. In: Chernow B, Lake CR, eds. The

pharmacologic approach to the critically ill patient. Baltimore:

Williams and Willdns, 1983; 667-685 Ebllack MM, Dunbar BS, Holbrook PR, Fields Al. Aspiration

of activated charcoal and gastric contents. Ann Emerg Med

1981; 10:528-296 Fowler AA, Hamman 1W, Good JT, Benson KN, Baird M,

Eberle DJ, et al. Adult respiratory distress syndrome: risk with

common predispositions. Ann Intern Med 1983; 98:593-977 Slavin C, Nunn JF, Crow J, Dore CJ. Bronchiolectasis-a

complication ofartificial ventilation. Br Med J 1982; 285:931-34

8 Churg A, Golden J, Fligiel S. Hogg JC. Bronchopulmonary

dysplasia in the adult. Am Rev Respir Dis 1983; 127:117-20

9 Schwartz DJ, Wynne JW, Gibbs CP, Hood CI, Kuck EJ. The

pulmonary consequences of aspiration of gastric contents at pH

greater than 2.5. Am Rev Respir Dis 1980; 121:119-26

10 Wynne JW, Modell JH. Respiratory aspiration of stomach

contents. Ann Intern Med 1977; 87:466-74

Persisting Hypereosinophilia andMyocardlal Activity in the FibroticStage of Endomyocardial Disease*Andrea Frustaci, M.D.; Abdel KaJAr Abdulla, M.D.;

Gianfederico Fbssati, M.D.; and Ugo Manzoli, M.D.

An unusual case of endomyocardial fibrosis is reportedcomplicating an idiopathic hypereosinophilic syndrome.

Persisting hypereosinophilia, degranulated eosinophils inthe blood, and myocardial activity have been found accom-

panying the fibrotic phase of endomyocardial disease. Thisoccurrence supports the unitarian theory on tropical and

temperate endomyocardial disease and suggests in such acondition the use of steroids or cytotoxic drugs in additionto surgery. (Cheat 1989; 96:674-75)

I � has been recently recognized’ that Loffler’s endocarditis2

and Davies’ endomyocardial fibrosis� are different phases

ofthe same pathologic process.�7 Separation ofthese entitieshas been accomplished for many years on the basis of the

disappearance of degranulated eosinophils in the blood, as

in the heart ofpatients in the fibrotic phase of endomyocar-

*Fmm the Departments ofCardiology (Drs. Frustaci and Manzoli)

and Cardiac Surgery (Dr. Possati), Catholic University Rome,Italy; and the Department of Pathology (Dr. Abdulla), NationalHeart Hospital, London, England.

Reprint requests: Ds� Frustaci, Cardiology Department, PoliclinicoGemelli, Largo Gemelli 8, 00168, Rome, Italy

dial disease.We report an unusual case of endomyocardial fibrosis

where persisting hypereosinophilia and myocardial activitywere found.

CASE REPORT

A 49-year.old woman was admitted because of nocturnal and

exertional dyspnea associated with chest discomfort. Twelve years

earlier, she had developed recurrent anginal pain with an unaltered

ECG coronary arteriography had been performed, which had

revealed a normal coronary network; nevertheless, anginal symp-toms had persisted, showing scant responsiveness to therapy withnitrates and calcium antagonists At that time, moderate idiopathic

hypereosinophilia (78Wcu mm) was found.

Nine years later, a dyspneicsyndrome supervened, which becameprogressive and insensitive to therapy with digitalis and diuretics.

At a new clinical examination, rales were audible at the basalpulmonary fields; at cardiac auscultation a grade 4/6 holosystolic

murmur, best heard over the mitral area and conducted to the

axilla, was found. Relevant laboratory data included an increased

sedimentation rate (37 mm) and white blood cell count

(10,250/cu mm), with evident hypereosinophilia (18 percent) and

degranulated eosinophils in the blood (20 percent).

Following extensive investigations, including markers for tumor

and leukemias and tests for parasitic infection and allergic reaction,

the abnormal and chronic increase of eosinophils was attributed to

an idiopathic hypereosinophilic syndrome. Among noninvasive

cardiac examinations, the ECG showed sinus tachycardia (110 beatsper minute), left atrial hypertrophy, low QRS voltages in the

peripheral leads, and diffuse T-wave abnormalities. A chest x-ray

film revealed pulmonary congestion and cardiomegaly, mostly due

to enlargement ofthe left atrial chamber.At cardiac catheterization a moderate pulmonary hypertension

(maximal pulmonary arterial pressure, 50 mm Hg) was recorded,with increased left ventricular end-diastolic pressure (22 mm Hg)showingatypical “square-root” aspect. Left ventricular angiography

presented an “ace-of-hearts” configuration with amputation of the

apex. In addition, it showed a preserved left ventricular systolic

function and a moderately severe (3/4) mitral regurgitation. At the

end ofcatheterization, a left ventricular endomyocardial biopsy was

undertaken, with extraction of five fragments consisting histologi-

cally ofthickened, dense collagen tissue.

Following hemodynamic, angiographic, and histologic findings, a

diagnosis of endomyocardial fibrosis was entertained, and the

patient was submitted to surgery, which included mitral replace-

ment by a prosthetic valve (Bjork-Shiley 27) and left ventricularendocardial decortication following the approach of Dubost et al8

and of Metras et al.� The patient tolerated the procedure well. She

made a good postoperative recovery and had good symptomatic

improvement; however, some chest discomfort was still present;

this was thought to be possibly correlated to a persistence of

hematologic imbalance (hypereosinophilia), and a careful morpho-

logic analysis of surgical samples was undertaken.

At microscopic examination a typical three zonal layering of

endocardium consisting of collagen tissue, fibroelastic tissue, andgranulation tissue was observed, together with fibrous septae linking

the endocardium with the myocardium (Fig 1). These are the

characteristic histologic features of endomyocardial fibrosis.In the myocardium, in addition to the increase of interstitial

fibrous tissue and some areas of fibrous replacement, several foci of

inflammatory infiltrates, consisting predominantly of degranulated

eosinophils, were found. The degranulated eosinophils and other

mononuclear cells were close to the adjacent myocytes which

occasionally showed areas of fraying (Fig 2). Due to the persistence

of hypereosinophilia with degranulated eosinophils in the blood

and the presence of myocardial activity steroid treatment (predni-

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DOI 10.1378/chest.96.3.672 1989;96; 672-674Chest

C G Elliott, T V Colby, T M Kelly and H G HicksCharcoal lung. Bronchiolitis obliterans after aspiration of activated charcoal.

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