Thursday, September 5, 2013
Worrier In Chief
The vascular surgeon was equivocal, amputation versus watchful waiting. Toes can autonecrose (self amputate), but when the black tide of dead tissue spread towards the ankle our options became limited. As the white count began to rise, I had the wound care nurse unwrap the limb. Fluffs of inflammatory transudate soaked the dressing but no signs of active infection.
The leukocytosis (high infection count) was bothersome. Although the course of vancomycin had been long finished, the specter of clostridium difficile remained. And of course there was the polycythemia to deal with. A bone marrow disorder, the white count could shoot up for almost any reason, especially since he had been taken of the hydrea (treatment for polycythemia) as a precaution while treating the bowel infection.
So there were multiple possibilities: inflammatory reaction to necrotic tissue, C Diff, polycythemia, other infection? When the diarrhea began it was almost a relief. Cultures were resent, vancomycin and flagyl started, and daily INR's to track the interaction between coumadin (started to allay the risk of clotting with untreated polycythemia-hydrea on hold because of C Diff) and antibiotics.
Saul, though, had no fever, no abdominal pain, and the diarrhea slowed within days of starting antibiotics. But the white count (infection) was now heading towards thirty and the platelets were over a million. I tracked down the infectious disease specialist while in the hospital and briefly discussed oral antibiotics vs intravenous Tygacil. I paged the hematologist and we debated restarting hydrea in case this was just a noninfectious leukamoid reaction.
When cases are starting to get out of control, I like to sit and talk to the patient. Saul, bless his heart, was probably too demented to understand the complexities. His daughter, however, was involved and interested. We discussed the upcoming surgery. We talked of my clinical impasse between infection and inflammation. She was more concerned with her dad's comfort than prolonging his life.
And Saul was as happy as a lark. His functional abilities were declining, but his biggest complaint was being stuck in the room due to isolation from his infection.
Ultimately I decided to give the antibiotics a little more time. I held off on hydrea, and gambled that the high white count was more a reaction to the foot necrosis and less so infection. I watched tentatively at his bedside, visiting the nursing home daily.
Saul's dilemma bubbled up in my mind, even at home. Occasionally waking in the middle of the night with a startle, I wondered if I was missing something.
With time the white and platelet count started to abate. The diarrhea disappeared. A surgical date was set and another flurry of calls was made to figure out the anticoagulation. Coumadin needed to be stopped, lovenox was risky given the HITT syndrome, and no one wanted to put him in the hospital for agatroban. The hematologist thought that Arixtra would do, and be a nice middle ground.
Saul is by no means out of the woods, but there are signs of improvement.
When people ask what an Internist does, I sometimes have to pause. Unlike common perception, our job is much more complex then treating colds. We are not just followers of our specialists directions. What always surprises medical students is that when the lab results come back, or the phone rings in the middle of the night, the specialists are long gone. Often I have to take all the information I have gleaned over time, and make the call.
Hydrea or no hydrea.
Infection or inflammation.
Aggressive treatment or palliative care.
I guess I would say that my job is to think deeply, build consensus, and help families plan. I do this for a few in the hospital, seventy in the nursing home, and two thousand outpatients.
Call me an Internist, a primary care doctor, or a flea. The sign on my office door will tell you how I feel about it.
Worrier In Chief
Posted by Jordan Grumet at 11:57 AM