A 50-year-old male patient with a history of arterial hypertension, type 2 DM, and heart failure, diagnosed 8 months before hospitalization. He consulted in another institution for 1 week of functional class deterioration, progressive edema in the lower limbs, orthopnea, hematemesis, and melaena. He underwent an upper gastrointestinal (GI) endoscopy which revealed a prepyloric ulcer with active bleeding at the edges, requiring sclerotherapy. He was then referred to our institution; at admission, he was without dyspnea at rest or nasal flutter, arterial tension (AT) 159/66 mmHg, heart rate 90 beats per minute, respiratory rate 20 breaths per minute, and SaO2 89% without supplemental oxygen. There was no evidence of ulcers in the nasal or oral cavity, no jugular engorgement, heart sounds were rhythmic without murmurs, no gallop or pericardial rub, decreased breath sounds at the base of the right lung, but no rales or wheezing. A painful and enlarged liver was found, but no ascites or collateral circulation reported, associated with grade III edema in the lower limbs. Neurological examination revealed no lateralization but time and space disorientation. The laboratory results can be seen in Table 1. Transthoracic echocardiogram reported a left ventricular ejection fraction (LVEF) of 40%, without any further alterations, diagnosing a decompensated chronic heart failure (profile B) with concomitant hypertension.
The patient was then transferred to the ICU. Management with vasodilators, diuretics, and non-invasive mechanical ventilation was initiated. A chest x-ray showed pulmonary congestion and a rounded, thick-walled image at the right pulmonary base (Figure 1). A chest computerized tomography (CT) scan showed a cavitated image in the lateral segment of the middle lobe with a nodule inside, in addition to varicose bronchiectasis and centrilobular nodules in the lower lobe (Figures 2 and 3). The patient was followed with bronchoscopy and bronchoalveolar lavage (BAL), in which transbronchial biopsies were taken, with results reporting generalized purulent endobronchitis. Bacilloscopic and polymerase chain reaction (GeneXpert) for tuberculosis were negative, as well as tests for syphilis, HIV, C, and B hepatitis. Direct studies for fungi detected hyaline septate hyphae, the galactomannan test for Aspergillosis was positive at 4.73 (negative value < 0.5), and cultures were positive for A. fumigatus. Cytology was negative for malignancy, but the biopsy showed chronic inflammation and necrosis associated with fungal structures suggestive of Aspergillus (Figures 4-6). A diagnosis of IPA was made and management with liposomal amphotericin B was initiated.
Abdomen ultrasonography reported normal-sized kidneys, with no ascites but a filling defect in the right hepatic vein that extended to the right atrium. A transesophageal echocardiogram was performed, describing a LVEF 39% and lesions suggesting vegetations of 9 mm x 11 mm in the aortic valve, 24 mm x 19 mm in the right atrium and 19 mm x 16 mm with a 26 mm filiform element in the crista terminalis. Due to the neurological manifestations at admission, a brain CT scan was performed, reporting a left frontal periventricular hypodensity. One week later, the patient presented with a left inferior monoparesis and nominal aphasia, so he was followed with a nuclear magnetic resonance of the brain finding multiple lesions along the corpus callosum, right cerebellar hemisphere, diffuse leptomeningeal enhancement and changes due to volume loss of the parenchyma (Figure 7). A lumbar puncture was unremarkable. Due to the characteristics of the lesions, an angio-invasive fungal parenchymal compromise was considered, despite having a normal spinal tap.
Having pulmonary, cardiac, and CNS involvement, IA was diagnosed and posaconazole was added to amphotericin B. The possibility of aortic valve replacement and right lower lobe lobectomy was deferred, pending on the evolution of the patient once the antifungal management was initiated. The patient received 8 weeks of in-hospital management and despite the poor prognosis, clinical stability and regression of pulmonary, cardiac, and CNS lesions were achieved (Figures 8 and 9). The patient was then discharged with posaconazole to complete treatment for 1 year. At follow-up, he presented in good clinical condition. Control studies showed an echocardiogram with a notable regression in the size of the lesions, the largest being 11 mm in the right atrium, a chest CT scan with a decrease in centrilobular nodules and no further progression of lesions and a brain MRI with an improvement of lesions due to less enhancement and a decrease in size of edema.