Relevant Pericardial Effusion Caused by Cytomegalovirus Infection in An Immunocompetent Patient

A Case Report

Tabea Hutter; Dirk Springe; Lukas Ebnöther; Marcos Delgado


J Med Case Reports. 2018;12(14) 

In This Article

Case Presentation


A 72-year-old Caucasian woman presented at her general practitioner complaining that she had been suffering from progressive shoulder pain for 2 weeks and dyspnea on exertion for 1 week. Our patient's past medical history included a case of arterial hypertension, treated with cilazapril and atenolol/chlorthalidone, as well as dyslipidemia, treated with atorvastatin. Our patient has been smoking about 5 cigarettes each day for the last 30 years but she does not consume alcohol on a daily basis. Our patient is retired and lives with her husband. They have two children and three grandchildren. In the initial examination carried out by her general practitioner, a blood sample was taken and a chest X-ray was carried out, showing elevated inflammation parameters and a large unilateral pleural effusion. As our patient's general condition deteriorated she was admitted to the hospital.


Upon admission to the hospital our patient was afebrile (with a temperature of 37.3 °C). Our patient's blood pressure was 91/59 mmHg and she had a heart rate of 82 beats/min (given that she was undergoing treatment with atenolol). A 2/6 systolic heart murmur was evident from her clinical examination. There was no visible engorgement of the neck veins, nor signs of lower leg edema. Her breath sounds were attenuated on the left side and her neurologic examination was normal.

Her blood results showed elevated C-reactive protein (CRP, upon admission 256.7 mg/L; reference < 7.5 mg/L) and leukocytosis (leukocytes upon admission 21.5 10^9/L, reference 3.5–10.0 10^9/l) with slight monocytosis present in the leukogram. Additionally, she showed elevated levels of aspartate amino transferase (ASAT) and alanine amino transferase (ALAT) as well as alkaline phosphatase and gamma-glutamyltransferase (GGT), whilst her bilirubin levels were within the normal range. She presented with slightly impaired renal function upon admission but this was normalized after hydration. The aspiration of the pleural effusion revealed exudate without signs of a bacterial infection (cell number 4 10^9/L, out of which 85.5% were polynuclear cells and 13.5% were mononuclear cells; pH 7.57, glucose 7.5 mmol/L, protein 39 g/L, lactate dehydrogenase [LDH] 213 U/L; no growth of microorganisms). A transthoracic echocardiography revealed pericardial effusion with consecutive hemodynamic changes but no pericardial tamponade. The left ventricle was normal in shape with normal systolic function (left ventricular ejection fraction 60%), but there was evidence of dysfunctional relaxation. The heart valves were normal. The right ventricle was normal in shape and function (Figure 1 and Figure 2).

Figure 1.

Transthoracic echocardiogram with subcostal view. Pericardial effusion with compression of the RA right atrium, RV right ventricle, LV left ventricle

Figure 2.

Apical four chamber transthoracic echocardiogram view. Displacement of the RA right atrium, RV right ventricle, LV left ventricle

A computed tomography (CT) scan showed dilatation of the inferior vena cava and of the liver veins, as well as a hepatomegaly, resulting either from venous congestion or from an inflammatory process.

Several additional blood tests were done in order to rule out a rheumatologic etiology: rheumatoid factor, anti-citrullinated protein antibody, anti-nuclear antibody, anti-neutrophil cytoplasmic antibody, double-stranded deoxyribonucleic acid (dsDNA), anti-Sm antibody, anti-mitochondrial antibody, and complements C3 and C4. The results of all of these tests were normal. To determine a possible infectious cause, serologic testing was performed for hepatitis B and C, human immunodeficiency virus (HIV), Borrelia burgdorferi, Epstein-Barr virus (EBV), CMV, chlamydia, enterovirus, and mycoplasma. The results showed an acute CMV reinfection.


As a result of the hemodynamic changes caused by the pericardial effusion, our patient was admitted to the intensive care unit (ICU) where she was stabilized with intravenous fluids and vasoactive medications. Our patient's respiratory status remained stable with oxygen administered through a nasal cannula and she did not show any symptoms of any neurological disorders. Given that an ultrasound-guided pericardiocentesis carried a high risk of liver injury due to hepatomegaly, the surgical team performed a pericardial window. Pericardial and liver biopsies were obtained during the procedure. The histologic results showed mild hepatic steatosis and signs of chronic fibrinous pericarditis. The cytopathology report of the pericardial effusion showed reactive mesothelial changes and signs of a lymphohistiocytic reaction. Our patient's post-interventional clinical outcome was uncomplicated, and she was transferred from the ICU to the ward. The results of the previously ordered rheumatologic tests were all negative. The serology results were positive for an acute CMV infection. The IgM seroconversion occurred during her hospital stay (negative result upon admission) while the immunoglobulin G (IgG) levels were elevated in all blood samples. The IgG avidity was high (CMV IgG avidity 0.462; reference < 0.25), confirming the coexistence of a past CMV infection with a new CMV reinfection due to IgM seroconversion.

As our patient was not known to suffer from immunodeficiency, no antiviral therapy was indicated. Our patient left the hospital, against medical advice, before a CMV polymerase chain reaction (PCR) or additional tests could be ordered.

After she left the hospital, her infection parameters and hepatic transaminase levels normalized completely, and there was no recurrence of the pleural or pericardial effusions. In a blood sample taken 19 months after hospitalization, her transaminase levels and infection parameters remained within the normal range, but a new CMV serology was not performed by the doctor in charge.