Complicated infective endocarditis: a case series

A 57-year-old Chinese woman presented to our hospital with generalized weakness. Her medical history included hypertension and early liver cirrhosis caused by chronic viral hepatitis C (platelet count 104,000/μl). She had undergone mitral valve replacement (MVR) with a Hancock II 27-mm prosthesis (Medtronic, Minneapolis, MN, USA) for mitral valve prolapse 1 month earlier. Her blood pressure was 100/60 mmHg, her breathing rate was 12 breaths/minute, her heart rate was 121 beats/minute, and her body temperature was 36.5 °C. She appeared acutely ill and was dehydrated. The result of an initial chest x-ray was normal, and the patient’s electrocardiogram showed sinus tachycardia. Transthoracic echocardiography (TTE) showed normal prosthetic valve motion without evidence of vegetation or paravalvular leakage, but the patient’s mean diastolic pressure gradient was elevated at 10.3 mmHg (Fig. 1a) [2]. She had been discharged on warfarin and other medications after successful MVR without complications. Transesophageal echocardiography (TEE) (Fig. 1b and Additional file 1: Video 1) showed hyperdynamic echogenic material attached to the prosthetic MV. During preparation for redo surgery with administration of appropriate antibiotics, the patient suddenly had a generalized seizure with decreased mentation. Brain computed tomography (CT) and magnetic resonance imaging (Fig. 2a, b) revealed acute hemorrhage with perilesional edema in the bilateral cerebellum causing obstructive hydrocephalus, suggestive of MA rupture. She was transferred to the intensive care unit with an indwelling external ventricular drain (EVD) for monitoring. We performed a redo MVR with a Hancock II 27-mm prosthesis after resolution of her hemorrhage.

A 70-year-old Korean woman presented with generalized weakness and headache. Her medical history included diabetes mellitus and hypertension. Her physical examination revealed her blood pressure was 163/81 mmHg and her pulse rate was 91 beats/minute. Brain CT revealed a chronic left subdural frontotemporal hemorrhage. After burr hole trephination was performed, generalized edema developed because of acute kidney injury (creatinine level 0.86 → 1.89 mg/dl). A peripherally inserted central catheter (PICC) was placed. The patient developed a fever (38.1 °C) after 3 weeks, without a definite source of infection. TEE revealed a globular, mobile, echogenic mass (1.91 × 1.0 cm) (Fig. 3a, b) attached to the tricuspid valve. Blood cultures revealed Staphylococcus aureus sensitive to vancomycin. The patient’s fever subsided after treatment with antibiotics, but a vegetation and persistent septicemia were noted after 2 weeks. We performed coronary angiography prior to possible valve surgery and observed no significant coronary obstruction, but a large saccular aneurysm was detected in the infrarenal abdominal aorta (Fig. 4a and Additional file 2: Video 2). CT indicated this was a newly developed abdominal aortic aneurysm (maximum diameter 5.2 cm) (Fig. 4b, c) that had not been present 2 years previously (Fig. 4d). The appearance was suggestive of an MA associated with IE. We recommended valve surgery and endovascular stenting or surgical removal of the MA in sequence, but the patient’s guardians refused. The patient was discharged to a private convalescent hospital and was lost to follow-up. We suspect IE developed in association with PICC placement and that persistent septicemia, despite use of proper antibiotics, led to an MA.

A 76-year-old Korean woman with acute onset of flank pain caused by splenic infarction and abscess was transferred to our hospital with percutaneous drainage (Fig. 5). She had been diagnosed with a stroke in our hospital 3 months earlier. Other than fever (38.1 °C), she had stable vital signs. Although splenic infarction or embolism is common, splenic abscess is rare. In every patient diagnosed with splenic infarction, a search for the possible source of emboli should be performed, and IE is the most common cause [3]. There was no evidence of IE in this patient, but slightly increased mitral regurgitation (grade 1–2) (Additional file 3: Video 3 and Additional file 4: Video 4) was noted by TTE. TEE revealed a thickened, nonhomogeneous area with an echo-dense appearance around the aortic root (Fig. 6a) and discontinuous endocardial tissue (Fig. 6b) with flow communication detected by color and pulsed wave Doppler ultrasound (Fig. 6c, d). This patient needed surgery for locally uncontrolled infection [4]. A weblike structure with interruption of endocardial tissue continuity was noted (Fig. 7a), and thrombi were observed within the pocket (Fig. 7b). The patient recovered fully and was discharged.