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Familiar
as they
may be,
beta-
blockers
are potent
medications
with real
side effects.
The leading candidate for infection was endocar-
ditis, a bacterial invasion of the heart valves. I hadn’t
heard a telltale heart murmur during my exam, but
that ruled out nothing. Valve-encrusting bacteria,
debris and immune complexes (antibodies bound
to their targets in a molecular death grip) can seed
the bloodstream to inflame or block distant blood
vessels. Endocarditis is a bear to treat, requiring four
to six weeks of intravenous antibiotics.
LOTS OF TESTS
“What could be the cause, doctor?” a second daugh-
ter asked.
“It could be many things,” I answered. “From a
blood disorder, to infection, to the immune system
attacking the body’s own blood vessels. Is he tak-
ing anything besides the heart and blood pressure
medications?”
As his daughter had pointed out, Mr. Mendez
had suffered a heart attack a month ago, but had
recovered nicely and was on a standard post-attack
and stent regimen: Lipitor, a statin to lower choles-
terol; Plavix, an anti-platelet drug; atenolol, a beta-
blocker; and Lisinopril, a blood pressure reducer.
“No supplements?” I continued. “He hasn’t trav-
eled anywhere? No fevers? No joint pains? Never
smoked?”
The answer, from first to last, was no.
Casting a wide net, I ordered ultrasounds of the
arteries and veins of the legs, and cultures of blood
and urine to pick up possible invading bacteria,
inflammatory markers indicating infection, tests
of kidney and liver function, serum electrolytes,
blood cell counts, and a urinalysis to look for the
rod-shaped debris that kidney tubules shed when
infected or inflamed.
Depending on the workup results, that could lead
to an echocardiogram to look at the heart valves or
a CT scan with intravenous contrast to trace the
arterial system.
“These special tests will take a while,” I explained
to Mr. Mendez and his family.
As I turned, it struck me that Mr. Mendez looked
pretty hale. I stepped back and asked him in Spanish,
“At this moment it is mostly the toes that bother
you, no?”
He bobbed his head, “Mas o menos, doctor.” More
or less.
It was weird because, usually, blue is pretty bad.
It’s the sickly hue of oxygenless blood. Hands and
feet and babies are never supposed to be blue. How
could he be so healthy otherwise, despite such a
serious symptom?
A while later, the first results came in: white and
red cells, platelets, all normal; coagulation profile, on
target; kidney and liver function, electrolytes, all good.
Infection seemed unlikely, given the normal white
count, no fever and normal vital signs. The sedimen-
tation rate, a crude measure of overall inflammation
that’s particularly sensitive to endocarditis, also
checked out as normal.
That left mostly autoimmune diseases or break-
away atherosclerosis. Precise diagnosis of the former
relies on specific patterns of protein markers and
maybe some biopsies, the latter on angiograms and
other vascular studies.
I considered admitting him despite how stable he
looked. It’s hard to tell a patient and family, “Hey,
those blue toes could be a harbinger of something
terrible. So just go home and have your family doc-
tor run some tests. You’ll know soon.”
VITAL SIGNS