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Author: 2nd Lt. James D. Covelli, Uniformed
Services University of the Health Sciences F. Edward Hébert
School of Medicine, Class of 2013
Introduction: Pulmonary arterial hypertension
(PH) is a devastating condition that results in small vessel
fibrosis and destruction. There are numerous potential etiologies,
and treatment of PH is based on the World Health Organization (WHO)
Classification System. Group 5 of the WHO Classification System
includes PH with unclear multifactorial etiologies such as
hematologic disorders, metabolic disease and sarcoidosis.
Case Presentation: We report a case of a
61-year-old Caucasian male with a history of Aspergillus empyema in
1997 requiring thoracotomy with decortications, and long-term
therapy with itraconazole. Evaluation for immunosuppressive
disorders was negative, and he had otherwise been healthy prior to
the infection. He presented approximately 12 years later with new
onset slowly progressive dyspnea, cough and orthopnea. He had
evidence of left heart failure at that time and was treated
aggressively with diuretics and afterload reduction. Tricuspid
regurgitation was seen on echocardiogram (ECHO) with no evidence of
valvular pathology or systolic or diastolic dysfunction. At initial
cardiac catheterization, severe pulmonary hypertension with a mean
pulmonary artery pressure of 63 mmHg (normal 15-25 mmHg) without
evidence of obstructive coronary artery disease was present. He
demonstrated vasodilator responsiveness with inhaled nitric oxide.
Following aggressive diuresis, ECHO demonstrated markedly abnormal
right heart function, with preserved left ventricular function.
Computed tomography imaging revealed marked pulmonary artery
enlargement, mediastinal lymphadenopathy and multiple dense
calcifications predominantly in the left hilar and subcarinal
regions, associated with marked decreased size of the left chest
cavity. Pulmonary function testing demonstrated severe restriction.
Laboratory testing revealed an increased ESR of 34 mm/hr and
C-reactive protein elevated at 2.99 mg/dL, but otherwise, there was
no evidence of an autoimmune disorder. With the addition of
Sildenafil and inhaled prostacyclin to his diuretic regimen, his
functional capacity has improved along with improvement in
Discussion: Pulmonary hypertension following
fungal empyema has not been previously reported, but it has been
described secondary to fibrosing mediastinitis as a complication of
sarcoidosis. We postulate our patient developed a similar process
secondary to aspergillus empyema. Clinicians should be aware that
patients with fungal empyema may be at increased long-term risk for
pulmonary hypertension secondary to a process similar to fibrosing
mediastinitis, and this may be successfully treated with
conventional pulmonary hypertension therapies.
July 2012 Issue of IMpact