Background

Spontaneous intracardiac echo contrast is often described in the left atrium. It has a characteristic, smoke like look, caused by increased ultrasound scatter due to stasis of cellular components.1 2Patients usually suffer of a cardiac abnormality such as atrial fibrillation (AF), prosthetic mitral valves, enlarged left atrium and right atrial enlargement with elevated ventricular pressure and tricuspid regurgitation.3 4

Microcavitations, however, are a different and distinct echocardiographic phenomenon. Since they consist of microbubbles, they mainly occur in patients with extracorporeal, transcutaneous lines and devices (eg, cardiopulmonary bypass or dialysis machines) in place which serve as port of entry. They have also been described in patients with a mechanical heart valve where they result from the rapid pressure drop during valve closure.5

In this present case, however, the search for the source of the microbubbles was less straight forward.

Case presentation

A man in mid-70s was admitted to our emergency department because of an acute weakness in both legs which had led to a fall. He also reported chest pain, combined with a feeling of tachycardia after his fall. He had not noted any dyspnoea. He felt well in the last few days except for chronic pain of the left leg. His medical history is remarkable for mitral regurgitation and hypertensive heart disease (HFpEF), chronic renal failure KDIGO II, normochromic normocytic anaemia and AF. Cardiovascular risk factors were arterial hypertension, dyslipidaemia and a former nicotine abuse. Current medication was phenprocoumon, bezafibrate, candesartan, bisoprolol and chondroitin sulfate.

At presentation, the patient had a temperature of (39.8°C) with normal blood pressure, heartrate and oxygen saturation. The clinical examination was unremarkable except for a systolic murmur. There was no more weakness in the legs. The ECG showed AF with T-negativities in III. Laboratory tests showed a haemoglobin of 88 g/L, leucocytes of 15.9 x10⁹/L,CRP of 60 mg/L (ref.:<10 mg/L), creatinine of 198 µmol/l (ref.:<104 µmol/l). Blood cultures were negative. The X-Ray of the thorax only showed signs of venous congestion.

We admitted the patient to the normal ward with a telemetric monitoring. The next day, there was no fever, the laboratory values were unchanged. The clinical examination still gave no hints of an acute infection. The diagnosis of an infection of unknown origin was maintained and the search for the source was started with an echocardiography due to the pre-existing mitral regurgitation. Surprisingly, the examination revealed continuous spontaneous microcavitations in the right atrium, right ventricle, right ventricular outflow tract and truncus pulmonalis (figure 1). No right-to-left shunt could be detected. A CT scan of the chest confirmed the findings (figure 2). A second surprising finding were several hypodense hepatic lesions, which lead to the suspicion of a metastatic disease. A colonoscopy was additionally performed, where an ulcerated colonic carcinoma at the ileocecal valve was detected (figure 3). Unfortunately, the patient refused any further examinations or treatment and left the hospital before the workup could be completed. He died 4 months thereafter.

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Figure 1

Echocardiographic view (4-chamber axis) with microcavitation in the right ventricle.

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Figure 2

CT scan of the thorax, with air in the right ventricle (arrows) and also the suspicious lesions in the liver.

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Figure 3

Colonoscopy of the ileocaecum with the suspected carcinogens of the colon.

Outcome and follow-up

Unfortunately, the patient refused any further examinations or treatment, and left the hospital before the workup could be completed. He died 4 months thereafter.

Discussion

The port entry, therefore, must be detected. In our case, it seemed to be the colonic adenoma. Scarce literature underlines the plausibility for our theory and is sequentially presented here to explain the bubbles’ journey from the port of entry to the cardiac cavities.

The first stage is the way to the portal venous system, the venous drainage of the colonic cancer described. Hepatic portal venous gas, is a rare finding, but is described in a variety of intestinal pathologies such as infections, ulcers or ileus.6 Li et al describe hepatic portal gas in a patient with colonic cancer,7 suggesting that neoplastic pathologies can also serve as a port of entry.

The transition of the bubbles from the portal venous system to the cardiac cavities must have been facilitated by the metastases: air usually can be cleared from all organs within minutes to hours, as shown in a study after cardiac surgery.8 The liver also seems to effectively clear hepatic portal gas.9

However, portosystemic and hepatopulmonary shunting is known to occur during radioembolisation of hepatic metastases with particles of 20–60 μm diameters. The shunt fraction of the microparticles varies between 1% and 10%, depending on the angiogenetic characteristics within the neoplasia.8 10 11 These particles are about the same size as the microbubbles described.12

Neoplastic angiogenesis can lead to malformations, making portosystemic shunting possible. In an assessment of angiogenesis in colonic cancer, the vessels were irregular, widely branched and of highly variable calibre,13 assuming that the angiogenesis of the metastases are the same, portacaval and therefore porto-cardiac shunting is highly possible.

For our patient, we could not find any other source of the microbubbles but the colonic neoplasia.

Unfortunately, visualisation of air in the colonic wall as pneumatosis intestinalis or in the portal system as a proof for our hypothesis is lacking, also due to the patient’s unwillingness to undergo further investigations. Nonetheless, we believe that the combination of the pathophysiological mechanisms described above is a valid explanation for our findings.

Microcavitations should always lead to an extended search for a plausible port of entry. Although the translocation of microbubbles through the portal system into the cardiopulmonary circulation is rare, an intestinal neoplasia can still be a plausible source. Elimination of the port of entry offers also the cure for this potentially deleterious disease.