LETTER TO THE EDITOR

An (un)usual cause of haemoptysis

DOI:10.1111/j.1752-699X.2008.00062.x

A 40-year-old man presented to the emergencydepartment in December 2004 with a 1-week historyof increasing haemoptysis; he had neither fever norother symptoms. He was a smoker and anamnesisrevealed heroine addiction from the age of 16 to27 years, hepatitis C virus infection, but no chestdisease, tuberculosis in particular. Hepatomegaly wasfound during physical examination, routine labora-tory tests resulted in an increase in serum ami-notransferases and a chest radiograph showed nosignificant findings. Endonasal fibroscopic examina-tion revealed nasal crusts, hyperhaemic vocal cordsand blood deposition in Morgagni’s ventriculus.Bronchial endoscopy showed haemorrhage from theapical–dorsal bronchus of the upper left lobe, withoutendoluminal lesions or signs of inflammation. Thepatient rejected hospitalization and was dischargedwith prescription of antibiotic therapy. Several epi-sodes of haemoptysis recurred in the following days,so the patient returned to the hospital and was admit-ted to our division. Mild hypoxemia was found onarterial gas analysis. Microscopy and culture ofsputum and bronchoalveolar lavage fluid for bacteriaand mycobacteria isolated no organisms. Also, sero-logical and immunological examinations provednegative. Computed tomography of the chest con-firmed the presence of blood deposition in the upperdorsal region of the left hemithorax, in the absence ofother parenchymal or pleural findings (Fig. 1). Selec-tive bronchial angiography was then performed butno pathological findings were identified. Medicaltherapy with tranexamic acid was established andhaemoptysis gradually reduced with complete resolu-tion in a few days. Once all the common causes forhaemoptysis were excluded, given the personalhistory of drug addiction and the nasal crusts foundat fibroscopic examination, toxicological screeningwas performed, which resulted positive for cocaine(in traces). The patient subsequently admittedcocaine abuse, via intranasal route, in the days pre-ceding the onset of haemoptysis. No relapses werereported at 2 months follow-up.

Bleeding of airways in habitual cocaine smokers orintravenous users has been described previously. Evenif a direct causal correlation could not be proved, to

date, this is the only report of haemoptysis begunafter cocaine use via intranasal route. Despite recentstudies focusing on smoking of alkaloid (‘crack’)cocaine, more than two-thirds of approximately3 million current cocaine addicts in Europe do notuse ‘crack’ (1). Moreover, intranasal administration ofpowdered cocaine is the gateway for addiction; it iscommon among young and neophyte users and isoften the first way that substance-dependent indi-viduals use cocaine (2).

Although extensive literature has been devoted tocardiovascular problems related to cocaine abuse, con-siderably less information about its pulmonary com-plications is available. Haemoptysis in habitual cocainesmokers and intravenous users has been reported pre-viously in a proportion of patients widely ranging from5·7% (3) to 26% (4), pathogenetic hypothesis includ-ing (i) ischemic endothelial or epithelial damage sec-ondary to vasoconstriction; and (ii) direct toxicdamage to endothelium (5). Both these mechanismscould be effective for intranasal route of administra-tion. Moreover, autoptic examinations of individualswith positive toxicological tests for cocaine have shownalveolar haemorrhage in 71% of cases, pointing outthat this pulmonary complication is much more fre-quent than is clinically evident (5). Despite this,cocaine abuse is generally not considered among thecauses of haemoptysis and therefore not properlyinvestigated in these patients.

We believe that cocaine abuse should be routinelytaken into account in the differential diagnosis amongthe causes of haemoptysis, even in the absence of spe-cific history or needle tracks, before labelling it as‘cryptogenetic’. Higher index of suspicion is requiredin the otherwise healthy young adult patient or in thepresence of comorbidities frequently associated withaddiction, such as chronic viral infections. Thisshould help in lowering the rate of ‘cryptogenetic’haemoptysis, which is currently up to 30% in medicalliterature.

Filippo Fassio, Fabio Almerigogna and Ilaria CecioniUniversity of Florence, Immunology and Cell Therapies

Unit,Viale Morgagni,85 Florence 50134, Italy

The Clinical Respiratory Journal

187The Clinical Respiratory Journal (2008) • ISSN 1752-6981© 2008 The Authors. Journal compilation © 2008 Blackwell Publishing Ltd

References

1. European Monitoring Centre for Drugs andDrug-Addiction. Annual Report 2005: The State of theDrugs Problem in Europe (ISSN 1609–6150). Lisbon, TheOffice for Official Publications of the EuropeanCommunities, 2005.

2. Foltin RW, Haney M. Intranasal cocaine in humans: acutetolerance, cardiovascular and subjective effects. PharmacolBiochem Behav. 2004;78: 93–101.

3. Tashkin DP, Khalsa ME, Gorelick D, Chang P, SimmonsMS, Coulson AH, Gong H Jr. Pulmonary status of habitualcocaine smokers. Am Rev Respir Dis. 1992;145: 92–100.

4. Suhl J, Gorelick DA. Pulmonary function in male freebasecocaine smokers. Am Rev Respir Dis. 1988;137(Suppl):A488.

5. Bailey ME, Fraire AE, Greenberg SD, Barnard J, Cagle PT.Pulmonary histopathology in cocaine abusers. Hum Pathol.

1994;25: 203–7.

Figure 1. CT scan of the chest showing the presence of blooddeposition in the upper dorsal region of the left hemithorax.

LETTER TO THE EDITOR

188 The Clinical Respiratory Journal (2008) • ISSN 1752-6981© 2008 The Authors. Journal compilation © 2008 Blackwell Publishing Ltd