Canadian Health&Care; Mall

Conclusion Our patient is interesting for many reasons. Even though the LAC-USC Medical Center has many cases of amebiasis, in this patient the diagnosis was delayed for over two weeks. The patient was initially treated for a community-acquired bacterial pneumonia and tuberculosis. When he did not respond to adequate antibiotic therapy, bronchoscopy was performed to exclude lung cancer. The lack of abdominal findings and the history of hemoptysis and cigarette use contributed to the misdiagnosis. Hemoptysis is not uncommon in pleuropulmonary amebiasis,’ and in fact, massive hemoptysis has been reported. This sign also is associated with pulmonary tuberculosis particularly in many patients from areas where tuberculosis is endemic. Elevated alkaline phosphatase levels, a nonspecific marker for amebic liver abscess, are also present in tuberculosis involving the liver. Other clues present in this case might have led an alert mind to the right diagnosis. During bronchoscopy, a cottage cheese-like material was observed. The patient was noted to have one to two cups of sputum for the first two to three days which resolved spontaneously. In retrospect, we can ascribe this to the spontaneous drainage of the abscess through the hepatobiliary fistula. The inability of the CT scan clearly to define the liver abscess was unfortunate but not unusual. In a series of 23 patients with amebic liver abscesses who had CT scans nine had pleural effusions, and in none of these patients could the integrity of the diaphragm be established, which was true in our case. Although a tissue diagnosis of amebiasis was not made, this patients constellation of findings establishes the diagnosis. His travel to an endemic area, documentation of a single liver lesion with extension through the diaphragm, a clinical course compatible with a hepatobronchial fistula, high amebic titers and a response to metronidazole incontrovertibly point to pleuropulmonary amebiasis.