GOAL

The goals of this case are for students to explore the pathogenesis of infective endocarditis by recognizing how the virulence of different microbial pathogens, combined with the acute host response to infection, leads to inflammation and injury at the cardiac and systemic levels, and how the underlying valve and dental disease predispose to risk for infective endocarditis.

PAUSE AND REFLECT ON THE GOAL

CASE VIGNETTE

Paul Griner is a 50-year-old man who presents with a fever with chills and 1-2 months of worsening fatigue.

HPI:      Mr. Griner is brought to the emergency department by his wife, Linette Griner, who states that he has been having fevers, night sweats, and fatigue for at least one month.  Mr. Griner was in his usual state of good health until 2 months ago when he began tiring more and more easily at his job, had to go to bed earlier, and often awoke drenched in sweat.  His oral temperature has been as high as 101.5°F.  She says she had wanted to have him seen earlier for his symptoms.  She is concerned about the fevers and wants to know their cause.  She also mentions he’s had a toothache for a month.

No one has been sick at home and he has never traveled outside of Pennsylvania.  He avoids dentists because his gums bleed so much, and he rarely sees a physician as he feels he is always well.  He has been rubbing an over-the-counter remedy on his sore tooth.

Amy Glick, a scribe working in the ED, who is applying to medical school, catches up with you as you are about to enter the exam room with Mr. Griner. She asks if you would mind if she shadows you on this case. You agree and after the two of you briefly discuss a list of potential differential diagnoses, you go in to meet Mr. Griner.

PMH:   Mr. Griner has never been hospitalized or had major surgery.  He takes no prescription medicine.  He was diagnosed with a heart murmur and mitral valve prolapse (degenerative mitral valve disease) years ago, but only has mild mitral regurgitation and has had no symptoms from it otherwise.

FH:       No known history of valvular disease in immediate family members.

SH:       He graduated from high school and has worked in a factory full-time ever since then.  He does not smoke, and drinks about a six-pack of beer a week.  He reports no use of illegal drugs. He has been in a long-term monogamous relationship with his wife.

ROS:    He has had no cough, sputum production, dysuria, back or flank pain, headache, or stiff neck.  He does not hunt, go hiking, or do any yard work.  He has no rashes and does not report any pain.  He has no orthopnea, paroxysmal nocturnal dyspnea, dyspnea on exertion, edema, palpitations, or syncope.

You and Amy compare notes from the history and brainstorm about how this information changes the list of differentials.

SNAPPS

Amy is interested in your interpretation of the physical exam findings, and how these findings influence your list of differentials. Amy asks “Are these exam findings unrelated or are they manifestations of the same disease process? Why do they happen? How could his valve disease put him at risk for his current febrile illness?”

The EKG shows normal sinus rhythm and is otherwise unremarkable.  The chest X-ray shows clear lung fields and no cardiomegaly.  CBC shows a WBC of 14,500/µL (normal 5,000-10,000) and hemoglobin of 12.1 g/dL (normal 13-17).  ESR (erythrocyte sedimentation rate) is 79 (normal<20); CRP (C-reactive protein) is 5.6 (normal <1.0).   Electrolytes and liver function tests are normal.  Creatinine is 1.3 (normal 0.8-1.3) with a BUN of 24 (normal 9-20).  Urinalysis shows 5 RBCs/hpf.  Three sets of blood cultures are drawn from 3 different sites over several hours.

A transthoracic echocardiogram is ordered and you explain to Mr. Griner how important it is to perform this kind of imaging of his heart.   The echo shows mild LV dilation with an ejection fraction of 70%.  The left atrium is moderately dilated.  There is posterior leaflet mitral valve prolapse with moderate to severe mitral regurgitation, increased from mild on his prior echocardiogram. Estimated pulmonary pressure is normal.  The mitral leaflets appear thickened, although no definitive vegetation is seen. You ask Amy to investigate what signs on echocardiogram, combined with clinical presentation, suggest chronic (rather than acute) and compensated (rather than decompensated) mitral regurgitation.

A CT scan of the head reveals a small right frontal lobe infarct and two other smaller infarcts in the left frontal lobe.  The bilateral infarcts are interpreted as consistent with embolic events.  Cardiology and Infectious Disease consultations are called; they agree that endocarditis is likely, but that better visualization of the mitral valve is needed to confirm the diagnosis. A transesophageal echocardiogram (TEE) is recommended to confirm the diagnosis of infective endocarditis and to evaluate for valvular and perivalvular complications.

Amy asks if the transesophageal echo would have been needed if his cardiac physical exam had been more normal.

You review the modified Duke Criteria with the Infectious Disease team, to understand the cardiac and systemic manifestations of endocarditis.

The next time you see Amy, she tells you that she read that Staphyloccocus aureus and Enteroccocus can also cause infective endocarditis. She has a few questions for you: “Would Mr. Griner’s clinical course have been different with those bacterial infections? Do the same antibiotics and treatment work for those as with Streptoccocus viridans? What if he had a prosthetic heart valve, does that make a difference?”

Mr. Griner’s ESR falls to 22, and the anemia and hematuria resolve.  He is afebrile, the pulse pressure narrows, and the LV apex is no longer hyperdynamic.  He completes the antibiotic course, and follow-up blood cultures are negative.  With rehab, his hand recovers reasonably well.  He feels well, and returns to work.