On initial examination, the patient reported that he had fallen and could not get up. He also reported symptoms of fatigue with generalized weakness that started 4 months previously and had progressively worsened until admission. He denied having chest pain and worsening of shortness of breath. He appeared awake and alert and had a mild left facial droop. He was afebrile, his blood pressure was 102 mm Hg systolic and 60 mm Hg diastolic; pulse rate, 44 beats/min; respiratory rate, 24/min; and oxygen saturation, 91% in room air. There was no jugular venous distention or bruit on neck examination. Decreased air entry at the right lung base was found, with no wheeze, rales, or rhonchi. Results of abdominal examination were unremarkable. A neurologic examination revealed normal muscle strength and tone. An osteopathic structural examination revealed a normal spinal curve for the patient's age. Examination of the lower extremity showed venous stripping. No edema was present, and pulses were palpable bilaterally. The patient's skin appeared dry.
A complete blood cell count showed a white blood cell count of 8.32 (reference range, 4.6–10.2). Hematocrit was 42% (reference range, 43.5%–53.7%); hemoglobin, 13 g/dL (reference range, 14.1–18.1 g/dL); and platelet count, 248 ×103/μL (reference range, 142–424 ×103/μL). Chemical analysis revealed the following: sodium, 140 mEq/L (reference range, 136–146 mEq/L); potassium, 3.9 mEq/L (reference range, 3.5–5.1 mEq/L); chloride, 101 mEq/L (reference range, 98–106 mEq/L); CO2, 32.2 mEq/L (reference range, 23–29 mEq/L); glucose, 143 mg/dL (reference range, 83–100 mg/dL); blood urea nitrogen, 36 mg/dL (reference range, 8.0–25.0 mg/dL); and creatinine, 1.2 mg/dL (reference range, 0.7–1.3 mg/dL). Cardiac studies found B-type natriuretic peptide, 757 pg/mL (reference range, 0–100 pg/mL); first creatine kinase, 1444 U/L (reference range, 32–250 U/L); second creatine kinase, 713 U/L; first creatine kinase-MB fraction, 21.6 ng/mL (reference range, 0–10.4 ng/mL); second creatine kinase-MB fraction, 5.2 ng/mL; first troponin I, 0.33 mg/mL (reference range, 0–0.4 mg/mL); second troponin I, 0.16 mg/mL; and digoxin, 3.2 ng/mL (reference range, 0.8–2.1 ng/mL).
Results of a 12-lead resting electrocardiogram done prior to examination showed atrial fibrillation with a ventricular response rate of 63 beats/min and diffuse ST-T abnormalities.
An enhanced multidetector CT scan of the brain revealed an old left temporal occipital infarct. No abnormal enhancement was seen. A chest radiograph revealed changes consistent with cardiomegaly and an intact pacemaker defibrillator system (
Figure 1) and showed a retrocardiac nodular density in the lateral view (
Figure 2). This was a new finding compared with that obtained by chest radiographic examination done 4 months earlier and 1 year earlier.
Multidetector CT scan of the chest was done before and after intravenous contrast was injected. Findings were consistent with those seen on the chest radiograph in the anteroposterior (
Figure 3) and lateral (
Figure 4) views. The aorta showed some atheromatous change, and the aortic root measured 4 cm. No hilar or mediastinal lymphadenopathy was seen. There were what appeared to be aneurysms of the CABGs on the right and left sides. The right-sided graft revealed a proximal aneurysm with maximum dimension of 4 cm, with an intraluminal clot and a true lumen of 16 mm (
Figure 5). Distally, there was a second aneurysm measuring almost 4.4 cm, with a clot and a true lumen of about 9 mm (
Figure 6). The left CABG revealed a proximal aneurysm measuring 2.6 cm, with a true lumen of about 2 cm (
Figure 7). A second aneurysm was found distal to the first, measuring 2.4 cm, with a small true lumen (
Figure 8).
It was determined that the patient had a transient ischemic attack. Blood clots found in the patient's bladder, most likely caused by long-term use of indwelling urinary catheters for chronic urinary retention and benign prostatic hypertrophy, were flushed out by a large catheter. His insulin therapy was reduced, owing to the controlled hospital diet, and he was also converted to oral furosemide from intravenous administration. The patient did very well after diuresis. His digoxin level decreased to within the therapeutic range. His strength improved with minimal intervention. His facial droop resolved. Serial cardiac markers and an electrocardiogram ruled out acute myocardial injury.
The patient and his family refused any evaluation for repair of the four aneurysms, and the patient obtained a do-not-resuscitate order. With stable cardiopulmonary status, the patient was discharged to an extended care facility for rehabilitation.