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Ranzani, Marcelo Fernando, et al.Pneumonia lipodica associada forma digestiva da doena de Chagas

Digestive Chagas disease with concomitant lipoidpneumonia*

MARCELO FERNANDO RANZANI, NILSON SEBASTIO MIRANDA, ULISSES FREDERIGUE JUNIOR,SRGIO MARRONE RIBEIRO, J USSARA MARCONDES MACHADO

A 50-year-old woman with chagasic esophageal achalasia and megacolon presented withnonproductive cough, chest pain and dyspnea. A chest X-ray showed bilateral opacity suggestive

of lobar pneumonia. Open lung biopsy revealed lipoid pneumonia resulting from aspiration of mineral oil from a mineral oil- based laxative that the patient had been taking regularly for the lastthree years. The authors discuss concomitance of chagasic megacolon and esophageal achalasiawith lipoid pneumonia and make recommendations regarding the use of mineral oil-based productsby these patients.

.Key words: Pneumonia, aspirtion/etiology. Pneumonia, lipid/etiology. Esophageal achalasia/pathology.

Chagas disease/complications.

*Study conducted at the Faculdade de Medicina de Botucatu (Botucatu School of Medicine) UNESP.Correspondence to: Departamento de Doenas Tropicais e Diagnstico por Imagem. Hospital das Clnicas - Faculdade de Medicina de Botucatu- UNESP. Distrito de Rubio J unior S/No - CEP 18618-970Submitted: 17 August 2003. Accepted, after review: 20 November 2003.

INTRODUCTIONA 50-year-old woman presented with

nonproductive cough, chest pain and dyspnea. Thirty years prior, the patient had presented signsof intestinal subocclusion and, after a laparotomy,was diagnosed with megacolon. On that occasion,indirect hemagglutination for Chagas disease waspositive. The patient remained free of symptomsuntil 15 years later, at which time she began toexperience episodes of constipation that spannedincreasingly greater periods of time, often as longas 10 days. She then started using laxatives on adaily basis and giving herself weekly enemas.

CASE REPORT Three years prior to the most recent

treatment, after an even more prolonged episodeof constipation, the patient was hospitalized foran intestinal lavage. During hospitalization, shereceived, per oral, mineral oil, a practice shemaintained after discharge. With the use of 40to 50 mL of this substance daily, the patient wasable to evacuate her bowels every 3 to 4 dayswith resorting to enemas. Four months prior toseeking treatment again, she began to presentdyspnea upon heavy exertion, and mild, sporadicchest pain upon drawing a breath, as well as a


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Figure 3 Alveolar space filled with numerous macrophagescontaining a great quantity of lipid vacuoles in theircytoplasm

dry cough, mainly in the morning. She wasadmitted under suspicion of heart disease. Achest X- ray revealed alveolar opacities withpoorly-defined borders in the posterior segmentof the upper lobe of the right lung and in thelower lobe of the left lung, as well as a smallopacity in the left lung base (Figure 1). On thisoccasion, the patient presented no signs orsymptoms of infection or consumption, whichare common in cases of tuberculosis andpulmonary mycosis. The patient was thereforesubmitted to a computed tomography scan of the chest, which revealed a ground- glass pattern

with poorly-defined borders, involving both lowerlobes but more pronounced in the right lobe.Esophageal achalasia, with an air-fluid level, wasalso observed (Figure 2). The predominance of right-sided lesions, together with the esophagealachalasia, suggested aspiration. Since theground- glass pattern revealed an inflammatoryprocess of light intensity, it was not consideredcompatible with suppurative pneumonia.

An open- lung freeze biopsy wasrecommended and performed, and thehistopathological analysis showed partitioning of

the alveolar walls with lymphatic ectasia andpneumocyte hyperplasia.

Within the alveolar space, great numbers of histiocytes, with microvascularization within thecytoplasm, were observed.

Figure 1 Anteroposterior chest X-ray showing alveolar opacitywith poorly defined borders in the posterior segment of thelower right lobe and a small opacity in the left lung base

Figure 2 Computed tomography of the chest showing aground-glass pattern with poorly defined borders involvingboth lower lobes, more pronounced in the right lobe


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Ranzani, Marcelo Fernando, et al.Pneumonia lipodica associada forma digestiva da doena de Chagas

DISCUSSIONChagas disease is caused by a protozoan

parasite known as Trypanosoma cruzi . The initialinfection may pass unnoticed or may manifest aseither a mild or severe form of the disease, thelatter being more common in endemic regions.Undetected infection is the more common scenario.In such individuals, the disease may evolve slowlyand gradually into one of the chronic forms of thedisease, which typically present cardiac or digestiveabnormalities. The digestive form manifests asdysphagia in the presence of esophageal achalasiaand, in the presence of megacolon, as severe

intestinal constipation.(4-6)

The basic pathogenic phenomenom thatdetermines the digestive form of the disease isdenervation within the walls of the autonomicnervous system myenteric plexuses, especially theparasympathetic plexuses. (7)

In Brazil, chronic chagasic colopathy is acondition that is frequently seen, especially in theelderly, and results in progressively more severeintestinal constipation and alternating periods of diarrhea. In the later stages, after megacolon hasbeen established, patients may remain constipatedfor extended periods, requiring the aid of laxativesand high colonics. (4)

Chagasic esophagopathy is another commonalteration seen in cases of the digestive form of the disease. This condition mainly affectsindividuals older than 30 and manifests asdysphagia, primarily when dry, hard or cold foodsare consumed. Such patients tend to ingest greaterquantities of liquid at mealtimes in order to facilitatedeglutition and relieve the symptoms. (4)

Esophageal dysfunction progresses throughaccumulation of ingested material in the superiorportion of the esophagus, facilitating the aspiration

of this material. This condition is more commonin individuals in whom the cough reflex has beenlost or suppressed due to neuromusculardisturbances, or due to the use of sedatives orother drugs. In such cases, aspiration pneumoniabecomes established. (8-10)

Mineral oil commonly inhibits airway protectiveresponses, such as glottal closure and cough, andis also capable of retarding mucociliary clearance.Mineral oil aspiration may be imperceptible,creating a condition that is easily confused withpneumonia. The substance is relatively inert and

is not metabolized by tissue enzymes. It consistsof a mixture of long-chain saturated hydrocarbonsderived from petroleum. When aspirated, mineraloil emulsifies and appears as drops, or vacuoles,of free lipids in the macrophage cytoplasm.

Therefore, an area of alveolar and interstitialaccumulation of lipid-filled macrophages develops,surrounded by lymphoplasmacytic infiltrate. Overtime, this area evolves into fibrosis, and oil-filledgiant cells encircle the site, forming a structureknown as a paraffinoma. The appearance of thistype of lesion in imaging exams may lead to adiagnosis of pulmonary neoplasm. However,

mineral oil aspiration can present a variety of radiological findings. Those most commonly seenin lipoid pneumonia are ground-glass opacities,interstitial abnormalities and pulmonaryconsolidations, any and all of which may appearin isolation or concomitantly in the samepatient. (2,3,11,12)

In light of the possibility that thesecomplications may occur, it is recommended thatindividuals at risk for bronchoaspiration avoid theuse of mineral oil. In addition, it is stronglysuggested that mineral oil be prescribed for shortperiods (less than one week) only since chronicuse increases the risk of aspiration. The authors of this report propose that, in Brazil, mineral oil notbe prescribed for individuals with chagasicmegacolon since there is a risk that, in suchpatients, its use will become chronic. This warningcarries additional weight in cases of intestinalChagas disease involving esophageal achalasia. (13,14)

REFERENCES1. Bandla HPR, Davis SH, Hopkins NE. Lipoid pneumonia:

a silent complication of mineral oil aspiration.

Pediatrics. 1999;103:19.2. Cox JE, Choplin RH, Chiles C. Case report. Chemical-shift MRI of exogenous lipoid pneumonia. J ComputAssit Tomogr. 1996;20:465-7.

3. Spickard A II I, Hirschmann J V. Exogenous lipoidpneumonia. Arch Intern Med. 1994;154:686-92.

4. Ferreira MS, Lopes ER, Chapadeiro E, Dias J CP,Ostermayer AL. Doena de Chagas. In: Veronesi R,Foccacia R, editores. Tratado de infectologia. SoPaulo: Atheneu; 1996. p.1175-213.

5. Chagas C. Nova enti dade mrbida no homem.Resumo geral de estudos etiolgicos e clnicos. MemInst Oswaldo Cruz. 1911;3:219-75.

6. Rezende J M, Moreira H. Forma digestiva da doenade Chagas. In: Brener Z, Andrade ZA, Barral- Netto M.


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Trypanosoma cruzi e doena de Chagas. 2a ed. Rio

de J aneiro: Guanabara-koogan; 2000. p.297-3437. Lopes ER, Chapadeiro E. Anatomia patolgica dadoena de Chagas humana. In: Dias J CP, Coura JR.Clnica e teraputica da doena de Chagas, umaabordagem prtica para o clnico geral. Rio de J aneiro:Fiocruz; 1997. p.67-84.

8. Gimenez A, Franquet T, Erasmus J J , Martinez S, EstradaP. Thoracic complications of esophageal disorders.Radiographics. 2002;22:247-58.

9. Kobzik L. O pulmo. In: Cotran RS, Kumar V, Collins T.Robins, patologia estrutural e funcional. 6a ed. Rio de

J aneiro: Guanabara Koogan; 2000. p.626-79.

10. Berg BW, Saenger JS. Exogenous lipoid pneumonia. N

Engl J Med. 1998;338:512.11. Lee JS, Im JG, Song KS, Seo J B, Lim TH. Exogenouslipoid pneumonia: high-resolution CT findings. EurRadiol. 1999;9: 287-91.

12. Gimnez A, Franquet T, Prats R, Estrada P, Villalba F,Bagu S. Unsual primary lung tumors: a radiologic pathologic overview. Radiographics. 2002;22:601-19

13. Langdon DE, Bowen DL. A risk of mineral oil. N Engl JMed. 1998;339:1947-8.

14. Bowen DL. A spokesperson for the food and drugadmini stration comments. N Engl J Med.1998;339:1947-8.

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