A 65-year-old man with alcohol-induced cirrhosis presented with two days of fatigue and total body pain. He claims every part of him hurts: his limbs, his back, his head.
He has no fever, and has normal vital signs and appears comfortable. He is icteric with dry mucous membranes, poor dentition, and no cervical nodes. His liver edge is not palpable, and the abdomen is soft and flat. Extremities are warm with 1+ pitting edema to the ankles. He claims to be in pain, but he is unimpressive on inspection and has no tenderness to palpation of the torso or any limb. I percuss down his spine, and he does not react. He has an old scar over his left inguinal area.
I ask about it, and he claims it was from a “valve placement,” but he has no median sternotomy or transverse thoracotomy scar. I wonder if he is confused and actually only received a coronary stent. He has a 2/6 crescendo-decrescendo ejection murmur in the aortic area and along the left lower sternal border. It radiates to both carotids. No diastolic component. There is an associated early ejection sound just after S1. Aortic stenosis of a native or replaced valve? I progress across his precordium toward the apex and hear a separate 2/6 holosystolic decrescendo murmur radiating into the anterior axillary line. Mitral regurgitation as well?
The chest x-ray reveals a normal heart size and no pulmonary vascular congestion. A metal caged stent is sitting in his aortic outflow area. This is the housing of a transcatheter prosthetic aortic valve. The leaflets themselves are not radiopaque, and only the stent framework is visible. The valve was placed via a femoral cutdown and the cage expanded to push the native diseased cusps up against the aortic annulus without obstructing the ostia of either coronary artery within each sinus. I discover this was placed in 2012 for critical aortic stenosis because of high operative risk associated with end-stage liver disease.
WBC returns at 27, and he has thrombocytopenia to 80. Chronic, low-grade platelet consumption could be the result of artificial valve leaflets shearing cellular components as they are forcefully ejected by the left ventricle day after day. But platelet consumption can also be the sequelae of damaged endothelium secondary to hematogenous bacterial transit. The aortic murmur and aortic ejection sound could represent bacterial contamination of the prosthesis leaflets. I also could not attribute his apical holosystolic murmur radiating into the axilla to his aortic prosthesis, and I had to wonder if he had mitral regurgitation from endocarditis.
Aortic and mitral valve endocarditis can occur together as their annuli are fused at the fibrous trigone. Bacteria can simply creep along from one valve to the other or drop from an aortic cusp onto the anterior leaflet of the mitral valve. I now have enough concern that even his well appearance and absence of fever cannot exclude bacterial advancement.
I add blood cultures. Bedside ultrasound shows no secondary pericardial effusion as an outward extension of aortic annular infection. IVC collapses on inspiration. We start a saline bolus.
He is immunocompromised to my eye from impaired hepatic synthetic abilities evidenced in daily icterus, but his bilirubin and INR may be no different from baseline. I keep in mind that the first sign of any systemic illness in this particular man will be an acute decline in liver function. It is his most fragile system and in that sense will be most sensitive to catabolic stimuli, whether intravascular bacteria or otherwise. Rising bilirubin should first point us toward valve leaflets, not biliary canaliculi.
He is admitted, and a second CBC shows platelets have dropped to 47. Blood cultures return with Streptococcus viridans in all bottles. IV antibiotics are begun, and a transthoracic echocardiogram is negative. The high suspicion for endocarditis prompts a transesophageal echocardiogram, but it only shows thickening of one native aortic valve leaflet as it sits just lateral to the cage stent, apposed to the annulus. He is managed nonoperatively given hemodynamic stability with sufficient leaflet coaptation at the aortic prosthesis and mitral valve, normal gradients, the absence of annular abscess with dehiscence, purulent pericardial effusion, septic response, or embolic manifestations. The inpatient team places a PICC line to complete a two-week course of vancomycin. Dental consult notes advanced periodontal disease and extracts a fractured, subluxed tooth. He never has an elevation in temperature. He is discharged looking well and no longer complaining of total body pain.
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