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Abstract

  1. Top of page
  2. Abstract
  3. Case Report
  4. Discussion
  5. Declaration of Interests
  6. References

Extensive venous thrombosis is usually seen postmortem in amebic liver abscess because of its dismal prognosis. Herein, we describe amebic liver abscess, whose late diagnosis led to multiple deep thromboses, pulmonary embolism, and right atrial thrombosis, in this patient with patent foramen ovale.


Case Report

  1. Top of page
  2. Abstract
  3. Case Report
  4. Discussion
  5. Declaration of Interests
  6. References

A 23-year-old man, originally from Sri Lanka and living in France for 2 years, consulted in our emergency department for a 1-month history of fever and night sweats, non-productive cough, dyspnea, and involuntary weight loss of 10 kg. He had no remarkable medical history but one of his roommates had recently been treated for tuberculosis. He was febrile (temperature 39°C), with normal blood pressure (120/80 mm Hg) and heart rate (120 beats/min). Physical examination was normal. He had no abdominal pain. Chest radiograph findings were unremarkable. Laboratory investigations showed mild hyponatremia, a leukocyte count of 18,300 cells/mm3 with 84% neutrophils. The C-reactive protein level was 274 mg/L but hepatic test results were abnormal, with liver enzyme (alkaline phosphatase and γ-glutamyltransferase) levels twofold higher than normal values. Two sets of blood cultures were negative.

He was initially isolated for suspected tuberculosis and also given empirical amoxicillin and erythromycin. Sputum smears were negative. Because of sustained dyspnea and fever, contrast-medium chest computed tomography scans were obtained for suspected pulmonary embolism. Images showed a large thick-walled liver abscess (diameter 6.5 cm) located in the hepatic dome, a mild pleural effusion on the right, and inferior vena cava thrombosis (Figure 1A), and a large pulmonary embolism (Figure 1B) and right atrial thrombosis.

image

Figure 1. Contrast-medium enhanced thoracic and abdominal computed tomography scans showing (A) a large liver abscess (black arrow) and an inferior vena cava thrombosis (white arrow), (B) the pulmonary embolism (white arrow), and (C) transthoracic echocardiography showing the right atrial thrombosis (white arrow).

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Hepatic ultrasonography confirmed the presence of an abscess of heterogeneous, compartmentalized appearance, suggestive of a hydatid cyst. Transthoracic echocardiography confirmed the atrial thrombosis (Figure 1C) in the interatrial septum, associated with abnormal color Doppler flow, corresponding to a patent foramen ovale; systolic pulmonary artery pressure was evaluated at 38 mm Hg. The patient refused transesophageal echocardiography. Cerebral magnetic resonance imaging ordered because of recent-onset headaches was normal. Doppler ultrasonography of the lower extremities was normal and he had no underlying comorbidity predisposing to venous thrombosis.

Hemagglutination assay showed a high serum titer of antiamebic antibodies (1/2,560). Ultrasound-guided aspiration of the liver abscess was performed because of the severity of the clinical case and yielded chocolate-colored pus. Autoimmune investigations, congenital and acquired thrombophilia tests, including antiphospholipid antibodies, factor V Leiden, or protein C deficiency, were negative. Other prothrombotic entities, such as Behçet's disease, nocturnal paroxysmal hemoglobinuria, and myeloproliferative syndromes, were excluded in our patient: he did not have any story of aphthosis and hemolysis, his blood numeration was controlled and normal and JAK2 mutation was negative.

Initially, unfractionated heparin was administered and warfarin was subsequently prescribed to maintain an international normalized ratio of 2 to 3. The patient was confined to bed until the atrial thrombus resolved. He received metronidazole, 500 mg three times a day for 14 days and tilbroquinol–tiliquinol for intestinal decontamination. His temperature normalized 2 days later and the atrial thrombus disappeared within 1 week. He was discharged in good health 2 weeks later on oral anticoagulation but was lost to follow-up.

Discussion

  1. Top of page
  2. Abstract
  3. Case Report
  4. Discussion
  5. Declaration of Interests
  6. References

Amebiasis, with the protozoan Entamoeba histolytica, is the leading parasitic cause of death worldwide after malaria and schistosomiasis. E histolytica is an enteric parasite thought to infect about 10% of the world's population.1 Its cysts are usually found and transmitted in contaminated food and water. Amebiasis should be considered among the spectrum of febrile diseases in returning travelers, with other infections such as bacterial or viral infections, tuberculosis, and malaria.2

Amebic liver abscess, often characterized by a painful and enlarged liver associated with fever, is the most common extraintestinal manifestation of amebiasis. Its first differential diagnosis is pyogenic abscess. Left untreated, this abscess can be fatal, primarily because of rupture into the pleura or pericardium, but it can also be complicated by thrombosis of hepatic veins and the inferior vena cava. Most of these cases have been described in autopsy series. Aikat et al.3 observed that 27.5% of portal veins, 29.5% of hepatic veins, and 4% of inferior vena cavae were thrombosed in infected patients, and very seldom in living patients.4 The association of hepatic amebiasis, pulmonary embolism, and right atrial thrombosis has been seen even more rarely.5,6 Thrombotic events can be explained by the contiguity of the abscess, containing trophozoites surrounding dead hepatocytes and liquefied cellular debris,1 with venous structures. Moreover, prolonged endothelial cell activation by amebic molecules and cytokines would induce severe local inflammation leading to necrosis.

The widespread thromboses seen in our patient can primarily be explained by the late diagnosis, favored by the patient's underprivileged socioeconomic status, and the absence of symptoms strongly suggestive of hepatic abscess, like abdominal pain thought to be a classical manifestation.1

Computed tomography is considered as the best method for diagnosing hepatic abscess, with sensitivity as high as 97%7 but ultrasonography, tough observer dependent, is widely accepted as a first time technique for imaging focal hepatic lesions including liver abscesses8 and serological diagnosis is the main diagnostic tool after imaging in the differential diagnosis from pyogenic abscess.

However, because of that absence of pain and the inconclusive images, our radiologist was reluctant to drain a potential echinococcal hydatid cyst. Finally, serological detection of amebiasis made the diagnosis and led to abscess aspiration.

The use of ultrasound aspiration to treat amoebic liver abscess is controversial.9 But a reasonable policy might be to reserve aspiration for individuals whose diagnoses are uncertain and severely ill patients whose abscess rupture seems imminent. In those cases, aspiration can be lifesaving.

Pathophysiologically, the thromboses could be explained by abscess proximity to venous structures. It is likely that the inflammatory process spread directly to the adjacent wall of the right hepatic vein, inducing luminal thrombosis. Our patient had a cardiac thrombosis. Although one case of thrombolysis of a thrombus in the right atrium was reported,10 our patient received only anticoagulant therapy, which achieved thrombus disappearance in less than 1 week.

Our patient's thrombophilia tests were negative. Only one case of intestinal amebiasis, deep vein thrombosis, pulmonary emboli, and antiphospholipid antibodies was published,11 with no subsequent description of that association, but it is known that non-pathogenic anticardiolipin antibodies frequently occur in a wide variety of infections.

The prognosis of amebic hepatic abscess is more severe when its diagnosis and the treatment are delayed, because the inflammatory reaction to it can induce local thrombosis. In that context, amebic abscess should be systematically among the spectrum of febrile diseases in returning travelers and the association of the hepatic vein, vena cava inferior, and/or right atrium thromboses and/or pulmonary embolism should be systematically sought.

Declaration of Interests

  1. Top of page
  2. Abstract
  3. Case Report
  4. Discussion
  5. Declaration of Interests
  6. References

The authors state that they have no conflicts of interest.

References

  1. Top of page
  2. Abstract
  3. Case Report
  4. Discussion
  5. Declaration of Interests
  6. References