Introduction
Amebic liver abscess (ALA) is a dangerous manifestation of Entamoeba histolytica infection. While most ALAs remain confined to the liver, a subset may rupture into the thoracic cavity, elevating mortality risk. Early recognition and differentiation from reactive pleural effusion are critical for guiding management and improving outcomes. Here we present a case of intrathoracic rupture of ALA with diaphragmatic disruption, along with a concise literature review to illuminate diagnostic and therapeutic approaches.
Case presentation
A 46-year-old man with well-controlled HIV infection presented with right shoulder and upper abdominal pain. Imaging revealed a solitary hepatic abscess with diaphragmatic disruption, right pleural effusion, and portal vein thrombosis. Initial stool microscopy and antigen tests were inconclusive, but polymerase chain reaction (PCR) detected Entamoeba histolytica in stool, liver aspirate, and pleural fluid, establishing a definitive diagnosis of amebiasis.
The patient began oral metronidazole. By day 2, oxygen needs rose and the pleural effusion worsened. Empiric broad-spectrum antibiotics were added due to concern for secondary infection, and metronidazole was intensified. By day 3, drainage catheters were placed in both the hepatic abscess and the pleural space. The liver aspirate appeared anchovy sauce-like, a classic macroscopic feature of ALA. Although histology did not reveal E. histolytica, PCR confirmation across specimen types provided diagnostic certainty.
Clinical course and management
Drains allowed rapid clinical stabilization. Cultures were negative for bacteria, rendering antibiotic therapy unnecessary beyond short courses. After stabilization, anticoagulation for portal vein thrombosis was initiated with edoxaban, given the thrombosis risk and bleeding considerations related to thoracic drainage. To eradicate residual intestinal cysts, paromomycin was prescribed.
Imaging follow-up showed progressive shrinkage of the liver abscess and resolution of diaphragmatic disruption and portal vein thrombosis over several months. Six-month follow-up revealed no recurrence and normalization of D-dimer levels.
Discussion: diagnostic challenges and role of imaging
Imaging played a pivotal role in diagnosing intrathoracic rupture. Contrast-enhanced CT typically shows a solitary, rim-enhancing hepatic lesion with surrounding edema. In cases of rupture, signs include diaphragmatic disruption, pleural thickening, and increasing pleural effusion with thoracic extension of the lesion. Distinguishing intrapleural rupture from reactive pleural effusion is essential because rupture carries a worse prognosis and often requires prompt drainage.
In this case, the diaphragmatic breach and transdiaphragmatic spread to the pleural space on CT, combined with pleural and hepatic aspirates that later yielded E. histolytica DNA by PCR, provided decisive evidence. While microscopic examination of pleural or liver aspirates has low sensitivity for E. histolytica, PCR demonstrated high sensitivity and specificity, even when conventional methods failed. Importantly, a higher cycle threshold (Ct) in pleural fluid compared with stool and liver aspirates suggested lower pathogen burden in the pleural space but still indicated infection.
Therapeutic considerations
First-line therapy for ALA remains metronidazole (typical dosing: 500–750 mg three times daily for 7–10 days). Drainage is indicated when there is poor clinical response, large abscesses (>5 cm), left lobe involvement, or complications such as rupture. In this patient, rapid pleural effusion progression and signs of respiratory compromise justified aggressive drainage of both pleural and hepatic collections.
Portal vein thrombosis occurs in a substantial fraction of ALA cases. Anticoagulation decisions require balancing thrombotic risk against bleeding, particularly around thoracic procedures. After stabilization, edoxaban was chosen in this case, complemented by paromomycin to eradicate residual intestinal cysts. No adverse bleeding events were observed.
Review of the literature shows eight previously reported cases of ALA with confirmed intrathoracic rupture, all treated with drainage and metronidazole. This pattern underscores the importance of early radiographic assessment, timely drainage, and integrated antimicrobial and anticoagulation strategies in managing this life-threatening complication.
Clinical implications and conclusions
This case reinforces several key points for clinicians: (1) maintain a high index of suspicion for intrathoracic rupture in ALA with new chest symptoms or rapidly accumulating pleural effusion; (2) rely on imaging to identify diaphragmatic disruption and pleural extension; (3) employ prompt pleural and hepatic drainage when rupture is suspected; (4) use PCR to confirm Entamoeba histolytica when microscopy and serology are inconclusive; (5) tailor anticoagulation to thrombosis and bleeding risk, particularly with thoracic interventions.
Amebic liver abscess confined to the liver is manageable, but rupture into the thoracic cavity necessitates a multidisciplinary approach. With timely drainage, appropriate antimicrobial therapy, and carefully balanced anticoagulation, patients can achieve durable recovery, as demonstrated by this case and the reviewed literature.
Conclusion
Intrathoracic rupture of amebic liver abscess is rare but deadly without prompt diagnosis and intervention. Imaging-guided drainage, combined with targeted anti-amebic therapy and cautious anticoagulation, offers the best chance for full recovery and prevention of recurrence.
