Abstract
An amoebic liver abscess (ALA) caused by Entamoeba histolytica remains a significant cause of morbidity and mortality in tropical regions. Although hepatic rupture into adjacent thoracic structures is a recognised but rare complication, it can be fatal if undiagnosed or untreated. Hepatic abscesses can rupture and spread the infection to the thoracic cavity, resulting in the formation of a hepato-thoracic fistula, rarely. We report an autopsy case of a middle-aged female who died suddenly following nonspecific systemic symptoms. Postmortem examination revealed a large ALA that had ruptured through the diaphragm, leading to massive pleural empyema. This autopsy case report underscores the importance of early clinical suspicion, imaging, and surgical management to prevent such catastrophic outcomes.
Keywords
Introduction
Ruptured amoebic liver abscess (ALA) can silently extend into thoracic cavity, causing fatal empyema and underscoring the need for early diagnosis. Amoebiasis, caused by Entamoeba histolytica, is a globally prevalent parasitic infection most often seen in tropical and subtropical regions 1 where it contributes notably to the burden of disease and mortality. It typically affects the gastrointestinal tract and remains asymptomatic in most cases. 2 Initially, it is a benign condition; in approximately 90% of individuals, the infection does not produce clinical symptoms. However, in some instances, the parasite can invade tissues beyond the intestine via portal transmission of the pathogen, leading to complications such as dysentery or, more notably, abscess formation in the liver, and mainly affects the males from 18–50 year age group and sometimes in children. 2
In India, the prevalence of this infection varies widely, ranging from 3.6% to 47.4%, depending on the area. 3 Among the extraintestinal manifestations, ALA represents the most frequent and clinically significant form.4,5 Although ALA usually presents with fever, hepatomegaly and pain in the right upper quadrant, right shoulder tip pain and/or pain between the scapulae, haemoptysis is also frequently observed. Clinical signs that may point toward thoracic involvement in amoebiasis include right-sided elevation of the diaphragm, enlarged liver, pleural effusion, opacity at the right lung base, and blunting of the costophrenic and costodiaphragmatic angles.6,7
Prompt diagnosis, with imaging such as ultrasound or contrast-enhanced computed tomography, and serological or antigen testing, followed by treatment with drainage and antibiotic (metronidazole) therapy can be life-saving. In advanced cases, surgical drainage or decortication may be necessary.2,7
Several large case series have documented significant numbers of patients diagnosed with hepatic amoebic abscesses. In one study over 18 years, 501 cases were analysed. 8 An untreated ALA may rupture into neighbouring structures like the pleural spaces in 2–3% of cases, leading to severe tissue injury.5,8,9
In this study, we present an autopsy case of a young adult female who was found to have a massive right-sided pleural empyema secondary to a ruptured ALA. The infection had extended through the diaphragm, forming a hepato-thoracic fistula that was not clinically diagnosed during life. This case emphasises the importance of early recognition of hepatic amoebiasis and the severe consequences of its extension to the thorax, which may only be revealed during a postmortem examination.
Case report
A 22-year-old female was brought to a hospital with a history of weakness, common cold, cough, abdominal pain, and loose stools, followed by sudden loss of consciousness at home. She was brought to the emergency department, where she was declared dead on arrival. The corpse was transferred to the mortuary for a medicolegal autopsy examination. History from the family members revealed that she was 22 weeks pregnant and had episodes of abdominal pain for the last month. Laboratory tests for viral markers were negative.
On autopsy, external examination revealed a malnourished female dead body with abdominal distension and right lower limb oedema. Postmortem changes, such as lividity, were present over the back of the body and were fixed, and rigour mortis had passed off. Greenish discolouration of the right iliac fossa was present. Cyanosis of the lips and nail beds of both hands was present. The oral cavity showed poor oral hygiene. The skull and brain were unremarkable. On opening the thoracic cavity, there was an empyema thoracis with approximately 5 litres of thick, greyish-brown, curdy anchovy-sauce-like pus in the right pleural cavity (Figure 1A). The right lung was collapsed and corrugated with pus, which was adherent to the lung surface and the inner thoracic wall (Figure 1B). Around 500 ml of straw-coloured fluid was present on the left side of the thoracic cavity, and the left lung showed congestion and oedema.

(A) Right thoracic cavity filled curdy anchovy-sauce-like pus. (B) Collapsed right lung shown with yellow arrow, corrugated with amoebic pus. (C) Right lobe of liver densely adherent to diaphragm inferiorly at ALA cyst area. (D) Cavity of ALA eroded the diaphragm and formed a fistula with right thorax. (E) Cavity with size 11 cm × 7 cm × 7 cm deep, filled with greyish-brown anchovy paste-like material with necrotic tissue. (F) Eroded fistulous tract measuring 4 cm × 4 cm in size with surrounding necrotic tissues. ALA: amoebic liver abscess (Color version available online).
The diaphragmatic surface of the right lobe of the liver was adherent to the diaphragm, and the liver parenchyma was congested but showed yellowish discolouration around the cyst (Figure 1C). On further exploration, the diaphragm was eroded with a through-and-through perforation in the posteromedial region, with a fistulous tract (4 cm × 4 cm) communicating with the subdiaphragmatic liver surface to the right pleural cavity (Figures 1D and 1F). The right lobe of the liver contained a large solitary cavity (11 cm × 7 cm × 7 cm deep) filled with similar greyish-brown anchovy paste-like material and the wall was surrounded by greyish necrotic tissue (Figure 1E). The uterus was enlarged, measuring 21 cm×14 cm×8 cm, and 1.680 kilograms in weight, and showed a single, intrauterine dead female foetus attached to the placenta with the umbilical cord. Length of umbilical cord was 32 cm, female foetus size was appropriate to the gestation of 22 weeks, eyebrows, eyebrows, eyelashes, and scalp hairs present. The weight of the foetus was 680 grams, nails were distinct and soft, the skin was red, wrinkled and covered with vernix caseosa. Meconium present till transverse colon. Two centres of ossification in the upper part of the sternum, and ossification centre of the calcaneum was present. There was no pathology or any evidence of Entamoeba histolytica infection found in placenta, umbilical cord and the foetus. The cause of death of the foetus is the death of the mother.
On histological examination, the ruptured abscess cavity from the liver, filled with necrotic debris, hepatocytes, and inflammatory infiltrates dominated by neutrophils, without a well-formed capsule (Figure 2A). Periodic acid-Schiff (PAS) stain confirmed the presence of trophozoites of Entamoeba histolytica, characterised by eccentric nuclei and ingested erythrocytes (Figure 2B). The ruptured wall of the diaphragm shows necrotic debris and trophozoites of Entamoeba histolytica. Lung histology showed necrotic debris and congested parenchyma. The thyroid showed a multinodular goitre. Other organs, including the heart, kidneys, and spleen, were congested but without significant pathology. The cause of death given in this case was septicaemia with empyema thoracis secondary to ruptured ALA.

Discussion
Hepato-thoracic fistula formation secondary to ALA is rare. The organism exhibits a two-stage life cycle: the cyst stage, which is responsible for transmission and infection, and the trophozoite stage, which leads to tissue invasion and spread of the disease. 10 The clinical presentation depends on the perforation site and can vary from mild illness to severe, and potentially fatal complications. Thoracic complications, including pleural effusion, empyema, or pulmonary necrosis, may result from direct extension of the abscess through the diaphragm.11,12 We found stage 2 of this infection in our case, where histopathology showed scattered trophozoites on H & E and PAS stain (Figure 2A and 2B). This case exemplifies a rare but lethal complication of ALA – trans diaphragmatic rupture into the pleural cavity leading to pleural empyema and could be misdiagnosed as complicated pneumonia.2,12
The course of this condition may extend from several weeks to months, particularly in individuals residing in endemic regions. In the present case, clinical symptoms evolved within 1 week; however, previous reports have documented much shorter durations, with symptom onset occurring within a few days. 12 Among individuals infected with E. histolytica, fewer than 1% develop ALAs. 13 Poor socioeconomic status, inadequate nutrition, and long-term alcohol use are key factors that increase the risk of developing amoebiasis. Our case belongs to a poor socioeconomic status, but there was no history of inadequate nutrition or alcohol use. Direct transdiaphragmatic extension of the pathogen can lead to right-sided pleural effusion or empyema, as seen in our case. The mechanism involves enzymatic digestion and pressure necrosis of the diaphragm by the abscess contents or via haematogenous or lymphatic routes.7,9,14
The classic description of anchovy-sauce pus, composed of necrotic liver tissue and inflammatory cells, is a hallmark of ALA and helps distinguish it from pyogenic abscesses. 14 Global estimates suggest that nearly 40 million people are affected yearly. However, this figure may be inflated due to the frequent misidentification of the non-pathogenic Entamoeba dispar as E. histolytica during diagnostic testing. 15 Transmission typically occurs via ingestion of food or water contaminated with cysts, with food handlers and mechanical vectors serving as potential contributors to the spread of infection. 16
A case involving a 16-month-old child has been reported, where the ALA ruptured into multiple cavities, including the pleural, pericardial, peritoneal, and gastric spaces. 17 Another extensive series from China reported 503 cases of ALA over a 21 year period, with complications related to abscess rupture occurring in approximately 22% of the patients. 18
An ALA develops in approximately 3% to 9% of individuals with amoebiasis. Among those affected, complications arise in about 20% to 40% of cases, with reported mortality rates ranging from 2% to 18%. 19
Serological testing using ELISA to detect anti-amoebic antibodies is commonly employed for assessing seroprevalence in population studies and diagnosing extraintestinal amoebiasis cases.7,20 During an extensive search of the Google search engine, we could not find any autopsy report on such conditions. However, we only found cases that were reported during their life and recovered after treatment was provided. So, autopsy continues to play a critical role in identifying such occult presentations and guiding public health measures in endemic areas.
Conclusions
ALA remains a silent killer, particularly when complicated by rupture into the thoracic cavity. Early diagnosis, clinical vigilance in high-risk individuals, and prompt management are essential to reduce fatal outcomes. This case reinforces the need for awareness among clinicians regarding the thoracic complications of ALA and their grave prognostic implications.
Footnotes
Authors contributions
MK contributed to conception, design and drafting of the article. SKT, VS, DR, and NA contributed to critical revision and approval of the version to be published.
Funding
The authors received no financial support for the research, authorship, and/or publication of this article.
Declaration of conflicting interests
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
