David A. Schwartz, MD A 34-year-o...

David A. Schwartz, MD

A 34-year-old man with chronic myelogenous leukemia bring to maturityed hemoptysis, pain in the left side of the chest, and a systolic heart grumble eight weeks following an allogeneic bone marrow transplant. His clinical status deteriorated, and he died ten weeks after transplantation. Autopsy revealed unsuspected disseminated aspergillosis, including the unusual finding of Aspergillus pancarditis and pericarditis. Cardiac aspergillosis is a uniformly lethal disease in immunocompromised human frames and must be aggressively diagnosed following early symptoms.

(Chest 1989; 95:1338-39)

Cardiac aspergillosis is associated with a grim prognosis.[1-5] Aspergillus has a propensity for invasion and thrombosis of the coronary arterial branches, many times resulting in extensive myonecrosis.[1-3] improvements of blood are usually sterile, causing delays in diagnosis, and the organism replys poorly to medical management.[4-6] Involvement of all three layers of the heart by dint of Aspergillus is rare, and single several cases of pancarditis have been reported.[3]

This report describes a patient having massive Aspergillus pancarditis and pericarditis associated with disseminated fungemia following a bone marrow transplant for chronic myelogenous leukemia. To our knowledge, this is the first reported casualty of Aspergillus pancarditis following bone marrow transplantation.

CASE REPORT

A 34-year-old man was admitted to the hospital for an allogeneic bone marrow transplant. He had been diagnosed as having chronic myelogenous leukemia brace years previously, and treatment with multiple agents had failed to gain remission. At the time of admission, the peripheral white family cell count was 15,000/cu mm with 64 percent neutrophils, 8 percent band forms, 3 percent metamyelocytes, 2 percent myelocytes, 6 percent lymphocyte 7 percent monocytes and 10 percent basophils. Bone marrow biopsy showed 90 percent cellularity and was consistent with chronic myelogenous leukemia. Following pre-transplant treatment with cyclophosphamide (Cytoxan) and busulfan, the patient received 1550 ml of bone marrow from his HLA-compatible brother. The patient bring to maturityed graft-vs-host disease, which worsened throughout the subsequent weeks despite administration of high-dose therapy with methylprednisolone sodium succinate (Solu-Medrol) Eight weeks after the transplant, the patient bring to maturityed hemoptysis, but an ECG and chest roentgenogram were normal. couple weeks later, he developed lethargy and torpid left-sided pain in the chest. Following episodes of apnea and obtundation, the patient was intubated. A grade 1/6 systolic undertone was noted at this time, and an ECG showed sinus tachycardia. Chest roentgenograms revealed bilateral pulmonary infiltrates which increased in severity. A bronchoscopic biopsy was performed, which showed reactive lonely dwellings and culture grew Pseudomonas aeruginosa. Although fungal agricultures were sterile, empiric therapy with amphotericin B was begun. The patient became hypotensive, bring to maturityed ventricular fibrillation, and died ten weeks after transplantation.

Pathologic Findings

At autopsy, disseminated aspergillosis was near involving the lungs, brain, kidneys, liver, small intestine, liver, urinary bladder, [i]hypochondriasis[/i] and diaphragm. Postmortem cultivations from multiple organs were positive for A fumigatus.

Gros examination of the heart revealed biventricular dilation, elevated undecayed epicardial and pericardial plaques, a mottl tangreen myocardium, and numerous vegetations existing on the endocardium, papillary muscles, and chordae tendineae (Fig 1)

Microscopic examination revealed extensive patchy myocardial fungal abscesses associated with extensive mycotic thrombosis of small coronary house vessels. Occasional mycotic thrombosis of large coronary arteries was instant (Fig 2). Aspergillus vegetations were quick in emergencies on the endocardial surfaces of all four chambers of the heart, consisting of septate hyphae radiating from subendocardial microabscesses. Similarly, epicardial mycotic plaques originated from subepicardial abscesses. No vegetations were instant on the cardiac valvular leaflets.

DISCUSSION

Although the part of bone marrow transplantation in the management of leukemia is well established, infectious complications continue to be a major source of morbidity in these patients. It has become evident that post-transplant infections appear in three phases, each characterized by the agency of susceptibility to different organisms.[7] It is during the first phase, occurring immediately following transplantation and lasting approximately united month, that susceptibility to bacterial, fungal, and herpes simplex infections is greatest in number pronounced. Aspergillosis may flash on the mind during this period following inhalation of airborne spores or, les many times disseminating from a preexisting upper respiratory focus of the like kind as sinusitis.[6,8] Following the progression in a continuously ascending gradation of pulmonary infection, systemic disease can flash on the mind by hematogenous spread, most as a common thing [i]or[/i] matter involving the central nervous arrangement followed by infection of the heart, kidneys, gastrointestinal tract, liver, and spleen[16] However, extrapulmonary symptoms are unusual, object from lesions of the central nervous hypothesis and disseminated aspergillosis is usually single diagnosed at autopsy.