A 73-year-old woman from the Middle East presented with mild generalized pruritus without associated cutaneous lesions. The symptoms did not improve or worsen with daily activities such as showering or exposure to sunlight. Over the previous 2 months, the patient had noticed weight loss and difficulty swallowing solid foods. She reported no constitutional symptoms, such as fever, night sweats, jaundice, or changes in urine or stool color. She had right upper quadrant (RUQ) abdominal pain and dyspnea.
On physical examination, the patient’s vital signs were within normal limits. No cutaneous lesions, splenomegaly, signs of hepatic disease, or jaundice were observed. Her medical history included hypertension, chronic kidney disease, and peptic ulcer disease. Her family history was unremarkable, and no other family members had pruritus. The patient had no history of smoking, alcohol consumption, or substance abuse.
Diagnostic evaluation included urinalysis, complete blood count, liver function tests, serum creatinine and urea measurements, alkaline phosphatase (AlkP), alanine aminotransferase (ALT), and gamma-glutamyl transferase (GGT). The patient had elevated serum urea, creatinine, ALT, AlkP, and GGT levels and a reduced hematocrit (
Table 1). All other blood test results were within the normal range. All urinalysis findings were within the normal range except for proteinuria.
| Test | Results (Reference) |
|---|
| Urea | 54 mg/dL (17 - 43) |
| Creatinine | 1.42 mg/dL (0.6 - 1.3 in females) |
| ALT | 45 IU/L (up to 31 in females) |
| Alkaline phosphatase (AlkP) | 447 IU/L (64 - 360) |
| Gamma-glutamyl transferase (GGT) | 288 U/L (up to 32 in females) |
| WBC | 7.7 mil/cumm (4 - 10) |
| RBC | 3.9 mil/cumm (3.7 - 5.2 in females) |
| Hemoglobin | 11.7 g/dL (11.5 - 15 in females) |
| Hematocrit | 34% (35 - 47 in females) |
Although elevated blood urea and creatinine levels were considered possible causes of pruritus, the presence of RUQ pain, elevated ALT, and high creatinine levels prompted comprehensive abdominopelvic sonography. Sludge and stones were found in the gallbladder. Because of dysphagia and weight loss, the physician recommended upper endoscopy. Given the increased vulnerability of older patients to complications during certain medical procedures, the physician requested a cardiology evaluation before endoscopy.
The cardiologist performed echocardiography and electrocardiography (ECG). The ECG showed AF rhythm (
Figure 1). Atrial fibrillation was also detected during echocardiography. The estimated ejection fraction was 45%. During diastole, 3 large echogenic atrial masses measuring 36 × 25 mm were observed protruding into the left ventricle and left ventricular outflow tract (Video 1). Additional findings included severe right ventricular enlargement, moderate right ventricular systolic dysfunction, mild mitral regurgitation (MR), and mild-to-moderate mitral annular calcification. Abnormal septal motion was also detected. The tricuspid valve leaflets were thickened and retracted, and severe tricuspid regurgitation (TRVC = 13 mm) was observed. The systolic pulmonary artery pressure (SPAP) was 47 mm Hg.
ECG without P waves because of atrial fibrillation (AF).
After the masses and AF rhythm were detected on echocardiography, coronary angiography was promptly performed to rule out potential vascular disease. Coronary angiography showed no abnormalities in the coronary arteries. Therefore, the cardiologist recommended consultation with a cardiac surgeon. The cardiac surgeon advised surgical intervention to remove the masses and perform valvoplasty. During surgery, 4 masses were discovered, although echocardiography had shown 3 masses. After surgery, the masses were sent to a pathologist for further examination (Video 2) (
Figure 2). The pathologist reported fibrin material admixed with leukocytes and clot formation with ingrowing vascular channels (
Figure 3), suggesting a thrombus.
This figure shows atrial masses. A, this part of the figure shows the largest atrial mass (1) and atrium (2); B, atrial masses after surgery.
A, histopathological morphology of the clot showing fibrin material admixed with some leukocytes, hematoxylin and eosin staining, high-power field (400×). B, histopathological morphology of the clot showing fibrin material admixed with some leukocytes, hematoxylin and eosin staining, low-power field (100×). C, Histopathology of organizing thrombi with ingrowing proliferating vascular channels, hematoxylin and eosin staining, low-power field (100×). The first arrow (1) shows the organizing thrombi, and the second arrow (2) shows the vascular channel.
The patient was transferred to the intensive care unit after cardiac surgery. Regrettably, she did not survive in the intensive care unit because of right-sided heart failure and hepatic failure.