Vol 39 # 2 June 2007 - Kma.org.kw

June 2007KUWAIT MEDICAL JOURNAL 185Fig. 2: HRCT of case 1 showing centrilobular nodular opacities (thinarrows) and branching linear opacities (thick arrow) (tree-in-bud pattern)with itraconazole. Despite treatment she developedworsening respiratory failure and died. Permissionfor autopsy was declined.Fig. 1: Chest X-ray of case 1 showing poorly defined bilateral nodularopacitiesconsistent with A s p e rg i l l u s. The mucosa andsubmucosa were inflamed and there was squamousmetaplasia. Serum immunoglobulin level showed apattern consistent with acute phase reaction but noevidence of immunoglobulin deficiency. A d i a g n o s i sof A s p e rg i l l u spsuedomembranous tracheobro n c h i t i swas made. The disease was differentiated fromallergic bronchopulmonary aspergillosis (ABPA) bythe following: (1) the absence of peripheraleosinophilia, (2) the absence of the appearances ofABPA on endobronchial biopsy (e.g. allergic mucinand eosinophils), (3) the presence of inflammatorypsuedomembranes that are not known to occurwith ABPA, and (4) the progression of the diseasedespite high doses of systemic stero i d s .Amphotericin B was commenced and the patientwas transferred to the intensive care unit fori n c reasing shortness of breath and stridor. Shei m p roved significantly on Amphotericin B butwhen switched to oral itraconazole she deterioratedand Amphotericin B was re-started. Two monthsafter admission, she coughed up a large grayishtracheobronchial cast, histology of which revealedorganized inflammatory psuedomembranes. Thepatient improved gradually and was dischargedfrom hospital after a three-month stay. She hadreceived a total dose of 2705 mg of Amphotericin Band was discharged on no antifungal therapy.One year later the patient was readmitted tohospital with increasing shortness of bre a t h .Sputum cultures grew Aspergillus, and a CT chestshowed areas of bronchiectasis and new nodularopacities. She was presumed to have reactivation ofinvasive aspergillosis and was started on treatmentCase 2A 74-year-old male with COPD presented withshortness of breath and cough. A chest radiographshowed hyperinflation but was otherwise unre m a r k a b l e .Peripheral white blood cell count was normal.S p i rometry revealed an FEV1 of 0.58l (23%predicted). He was admitted to hospital with adiagnosis of COPD exacerbation and was treatedwith bronchodilators, cefuroxime, erythro m y c i nand systemic corticosteroids. Cefuroxime was laterswitched to cefotaxime. Despite five days of tre a t m e n t ,the patient’s condition pro g ressed to acuterespiratory failure necessitating transfer to theintensive care unit and endotracheal intubation. Hedeveloped leukocytosis with a neutro p h i l i cpredominance. Arepeat chest X-ray showed diffusereticulonodular infiltrates. A high resolution CTchest revealed extensive bilateral centrilobularnodular and branching linear opacities andb ronchial wall thickening. Sputum culture waspositive for A s p e rg i l l u sf u m i g a t u s. On bro n c h o s c o p i cexamination, copious thick white secretions wereobserved throughout the entire tracheobronchialtree with adherent plaques in the right main-stembronchus and psuedomembranes more distally inthe right lower lobe. Bronchoscopic biopsiesshowed numerous fungal hyphae ( a s p e rg i l l u s )within material consistent with psuedomembranes.B ronchial washings grew A s p e rg i l l u s f u m i g a t u s.Both the bronchoscopy findings and the CTappearances were consistent with psuedomembranoustracheobronchitis, and the patient wasstarted on treatment with nebulized andintravenous liposomal Amphotericin B. Despitetreatment, the patient developed signs of septicshock and died eight days later of respiratory andrenal failure.