604 D'Arsigny, Ford, O'Donnell

Localised upper airway obstruction in a patientwith acquired immunodeficiency syndrome

Christine L D'Arsigny, Sally Ford, Denis E O'Donnell

Division ofRespiratory & CriticalCare Medicine,Department ofMedicine, Queen'sUniversity, RichardsonHouse, 102 StuartStreet, KingstonGeneral Hospital,Kingston, Ontario,Canada K7L 2V7C L D'ArsignyS FordD E O'Donnell

Correspondence toDr Denis E O'Donnell

Accepted 23 April 1998

SummaryWe describe a case of rapidly progressiveupper airway obstruction due to trachealPseudomonas abscesses in a patient withacquired immunodeficiency syndrome.The case highlights the aggressive natureof Pseudomonas infections and the diffi-culty of eradicating this organism inpatients infected with the human immu-nodeficiency virus.

Keywords: airway obstruction; Pseudomonas infection;tracheal abscess; acquired immunodeficiency syndrome

A 40-year-old homosexual man, with a 1 0-yearhistory of human immunodeficiency virus(HIV) infection, was admitted to hospital with2 weeks of worsening shortness of breath, feverand cough. Three months previously, he hadbeen admitted with Pseudomonas aeruginosabacteraemia. One month later, he was re-admitted with sinusitis and a new left upperlobe infiltrate. Blood and sputum cultures werenegative and he improved on empiric anti-pseudomonas antibiotics. He was admitted on1 January 1996 with a febrile neutropenia (leu-cocytes = 0.4 x 1i0/l, normal range 4.0-11.0)with a neutrophil nadir of 0.06 (normal range2.0-7.5 x 109/l) and cough. This was on abackground of chronic mild neutropenia overthe previous year and was presumed to beaggravated by therapy with azido-thymidine(AZT) and rifabutin. However, discontinua-tion of these drugs resulted in only partial

recovery of leucocytes to 0.9 x 1O9/i. Blood cul-tures again were negative and chest radio-graphs remained unchanged from the previousadmission (figure 1). He showed clinicalimprovement after 2 weeks of antibiotics andempiric antifungal therapy (fluconazole, 800mg once daily). He was admitted again onemonth later with fever and cough. Bloodcultures were again negative and the chestradiograph remained unchanged from the pre-vious admission. He showed clinical improve-ment after 2 weeks of antibiotics and wasdischarged. In the 2 weeks prior to his mostrecent admission, he developed progressivedyspnoea, productive cough, fever, and chills.The patient had no history of respiratory tractinfections with Pneumocystis carinii or tubercu-losis.

Physical examination revealed a thin,lethargic-looking man in moderate respiratorydistress. His respiratory rate was 28 breaths/min, blood pressure 180/70 mmHg, heart rate107 beats/min, and his temperature was 39°C.There were findings suggestive of oral candi-diasis. Pulmonary auscultation revealed dimin-ished breath sounds, but no wheezing orstridor. Laboratory values revealed a whitecount of 6.6 x 109/l with neutrophils of 3.1 x109/l; his CD4 count was 4. His haemoglobinwas 10.8 g/dl, platelets were 321 x 109/l, andelectrolytes and renal function were normal.The lactate dehydrogenase (LDH) was el-evated at 1208 IU/l (LDH/PaO2 = 16.7), withan alkaline phosphatase of 652 IUll. Transami-

Figure 1 Chest radiograph from 1 January 1996 on the left and from 30 January on the right. The second filmshows narrowing of the tracheal air column and no progression of the left upper lobe lesion

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Upper airway obstruction in a patient with AIDS

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Figure 2 CT scan of the upper airway. Obstructionof the mid-trachea is evident with > 50% reduction inits internal diameter. A right extrinsic tracheal mass isseen protruding into the tracheal lumen

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Figure 3 Maximal flow-volume loop in the patient(solid line) compared with age-matched predictedloop. Note severe reduction in maximal expiratory andinspiratory flows: expiratory flow rates are

disproportionately reduced

nases and bilirubin were normal. Arterial bloodgases on room air yielded a pH of 7.42, PaO2 of9.6 kPa, PaCO2 of 4.9 kPa, and bicarbonate of24 mmol/l. A chest radiograph identified an

unexpected, new narrowing of the tracheal aircolumn compared to a film one month earlier(figure 1, right). The ill-defined left upper lobeinfiltrate, which was first noted six weeksearlier, was still present, but moderatelyimproved.

Helical computed tomography (CT) of thetrachea confirmed the obstruction in the mid-trachea with > 50% reduction in the internallumen (figure 2). There was also a large, softtissue density within the tracheal wall withextension into the tracheal lumen. A CT scan

Figure 4 Pathologic specimen of the trachea andsurrounding tissues. Multiple ulcerated lesions are seenwith thickening of the tracheal wall. The internaldiameter is reduced by >75%

of the chest identified a poorly demarcatedinfiltrate with a cystic component in the leftupper lobe, and moderate bilateral air spacedisease which was not appreciated on the chestradiograph the previous day.A maximal flow-volume loop was performed

to evaluate the functional significance ofanatomical airway narrowing (figure 3). Thisshowed markedly diminished maximal expira-tory flows: peak expiratory flow rate = 1.2 1/s(14% predicted); maximal mid-expiratory flowrate = 0.35 1/s (9.4% predicted); maximal flowat 75% of vital capacity (VC) was 0.52 1/s(6.8% predicted) and at 25% of the VC was

0.26 l/s (9.9% predicted); peak inspiratory flowrate = 1.7 1/s (28% predicted). The dispropor-tionate reduction in expiratory flows relative to

inspiratory flows over the mid-volume rangesuggest a component of variable intrathoracicupper airway obstruction, as well as fixed upperairway obstruction pattern (figure 3).Bronchoscopy revealed severe narrowing of

the mid-trachea, spanning 3-5 cm in lengthwith a large ulcerated lesion along the anteriortracheal wall. There were copious amounts ofmuco-purulent secretions. Gram staining re-vealed large quantities of Gram-negative or-

ganisms, and staining for acid-fast bacilli andPneumocystis carinii were negative. While await-ing final bronchial culture results, the patientwas started on broad-spectrum, anti-pseudomonal antibiotics.The patient declined intubation or resuscita-

tion in the event of further clinical deteriora-tion. He was, therefore, treated with chestphysiotherapy, suctioning and close assessmentof his respiratory status, along with the broad-spectrum antibiotics. The patient died acutely

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606 D'Arsigny, Ford,Ford, O'Donnell

during sleep from a respiratory arrest, 56 hoursafter admission.An autopsy was obtained and showed 75%

stenosis of the tracheal lumen (figure 4). Therewere multiple tracheal ulcerations within thelumen with areas of ulceration as well asabscesses within the tracheal wall with diffusedestruction of cartilage, suggesting the poten-tial for dynamic instability of the trachea.There was also peritracheal fibrosis suggestingrelative chronicity of the lesion. The patient'slung parenchyma had diffuse haemorrhage andmicro-abscesses, along with a cavity in the leftupper lobe. Tracheal brushings and sputumcultures showed heavy growths of Pseudomonasaeruginosa, sensitive to the antibiotics that hewas receiving. Fungal cultures from trachealbrushings and lung secretions were negative,and no other pathogens were isolated.

Discussion

The presence of localised upper airway ob-struction in HIV is rare and sparsely describedin the literature. Different aetiologic possibili-ties include bacterial infections' and infectionswith cytomegalovirus,2 herpes simplex virus,and fungal organisms.3 Tracheal malignancy,including primary and metastatic carcinoma,lymphoma and Kaposi's sarcoma4 have alsobeen reported. Although an inflammatoryprocess was suspected in our patient due to therapid progression of the airway narrowing, thepossibility of localised Pseudomonas abscesseswas not specifically entertained and, to ourknowledge, has not previously been describedin HIV patients. There is one report of mixedbacterial tracheitis from Staphylococcus aureusand Pseudomonas aeruginosa by Valor et al,1 buttheir patient did not have a discrete abscess.The mechanism offormation for the tracheal

abscesses in our patient was not ascertained.However, given this patient's history of previ-ous Pseudomonas bacteraemia, we suspect thathis chronic sinusitis and lung infections werealso caused by the same organism. The autopsyfindings were suggestive of a chronic inflamma-tory process in the trachea (ie, peritrachealfibrosis and cartilage erosion), with lack of ademonstrable communication from the lung

abscesses to the trachea. Tracheal infectionmay, therefore, have been related to chronicpseudomonal sinusitis. Although multiplepathogens may co-exist in the lungs inend-stage HIV infection, only Pseudomonas wascultured from the trachea and lung secretionsin this patient. Other potential pathogens,including fungi, were not identified.

Patients with HIV have abnormal hostdefence mechanisms which may predisposethem to Pseudomonas infections.5 Chronic neu-tropenia, aggravated by antiviral agents, mayhave additionally predisposed this patient topersistent Pseudomonas infection. Despite ap-propriate antibiotic therapy, a third of HIVpatients have recurrent infections.6 Any site ofrecurrence is possible and mortality then esca-lates to 80%.6Although the cause of this patient's death

was multifactorial, critical airway narrowingprobably contributed to his demise. We specu-late that the tracheal occlusion was due to bothdynamic instability of the trachea from carti-lage erosion and structural narrowing fromextraluminal compression and tracheal ab-scesses. That the airway narrowing was criti-cally reduced is verified by the severe obstruc-tive pattern on the maximal flow-volume loop.This patient also had fulminant bilateral Pseu-domonas pneumonia and an inability to clearhis secretions which, in combination with thecritical airway narrowing, probably culminatedin his demise.

Learning points* critical airway narrowing can occur in the

absence of physical signs (ie, stridor)* fulminant bilateral pseudomonal pneumonia can

occur in the HIV-infected host in the presence ofonly minor radiographic abnormality

* consider pseudomonal abscess formation inpatients with HIV presenting with localisedupper airway obstruction

* chronic pseudomonal infection in patients withHIV are difficult to eradicate and carry a highmortality

1 Valor RR, Polnitsky CA, Tanis DJ, Sherter CB. Bacterialtracheitis with upper airway obstruction in a patient with theacquired immunodeficiency syndrome. Am Rev Resp Dis1992;146:1598-9.

2 Imoto EM, Stein RM, Shellito JE, Curtis JL. Central airwayobstruction due to cytomegalovirus-induced necrotizingtracheitis in a patient with AIDS. Am Rev Resp Dis1990;142:884-6.

3 Patete ML, Mellon D. Extrinsic tracheal compression-anewly described complication of acquired immune deficiencysyndrome (AIDS). Ear Nose ThroatJ 1995;74:189-92.

4 Beitler AJ, Ptaszynski K, Karpel JP. Upper airway obstruc-tion in a woman with AIDS-related laryngeal Kaposi'ssarcoma. Chest 1996;109:836-7.

5 Kielhofner M, Atmar RL, Hamill RJ, Musher DM.Life-threatening Pseudomonas aeruginosa infections inpatients with human immunodeficiency virus infection. ClinInfect Dis 1992;14:403-11.

6 Mendelson MH, Gurtman A, Szabo S, et al. Pseudomonasaeruginosa bacteremia in patients with AIDS. Clin Infect Dis1994;18:886-95.

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