Yesterday afternoon I was on a Society of Critical Care Medicine's webcast on the ICU and H1N1 preparedness. Despite my very busy day, I had paid my $50 bucks for the privilege, and, damn it, I was going to get my money's worth. So, I made it, albeit a few minutes late.
Breathless at my monitor, I was promptly reminded by Randy Wax that in the Mexican experience over 70% of the patients with respiratory failure received antibiotics prior to hospitalization. And these are just the ones that required breathing support, representing only 18% of all the hospitalized H1N1 cases. In the recent Spanish study of H1N1 victims requiring ICU care, on the other hand, all patients received initial empiric antibiotic therapy, with 63% being treated with a fluoroquinolone.
These numbers are concerning for several reasons. Granted, these were the sickest of the sick H1N1 patients, where the ICU ethos is rightly to throw the kitchen sink and ask questions later. And it is important to note that a number of patients in the Spanish group did have a superinfection with a bacterial pathogen. But what happens if in an onslaught of cases in our hospitals later in the fall and winter engenders prodigious overuse of antibiotics in these patients?
Before there was an H1N1 pandemic, there had already existed and established pandemic of antibiotic resistance in our communities and healthcare institutions. One of these superbugs is Clostridium difficile, affectionately called C diff, which causes florid diarrhea and potentially life-threatening inflammation of the colon. This bug gets very happy when its neighbors in the gut succumb to death from antibiotics. Unopposed by its foes, it proliferates out of control and elaborates a toxin which squeezes the large intestine of all its contents, causing cramping, distention of the colon and frequent watery bowel movements. What used to be thought of as a nuisance infection primarily in chronically ill hospitalized patients, in recent years, has mutated into a much more virulent form and is now galloping in an epidemic fashion through nearly every state in the US. More ominous is the fact that, much like its brother-in-arms MRSA, C diff is now causing diarrhea in the community setting, among people without any chronic illnesses. Furthermore, this superbug is more likely to recur despite adequate treatment and to cause much more severe disease in its victims than the bug we used to know and love (well, not really love) a decade ago.
So, how is all this relevant to the H1N1 story? One word: antibiotics! And more specifically, fluoroquinolones. This new and improved C diff seems to love fluoroquinolones. The reason for this oversized affection is that is has developed resistance to them. Practically speaking, it now has a further survival advantage over its neighbors when fluoroquinolones hit the gut.
What does all of this amount to? Well, I go back to my previous assertion that an ounce of flu prevention is going to be worth far more than a pound of cure; we need to take prevention efforts at both the personal and public levels extremely seriously. Short of that, we, both healthcare professionals and its consumers, need to say an emphatic "no" to antibiotics unless we are sure that they will help -- after all this is no longer a "might help won't hurt scenario". Finally, physicians and hospitals need to put systems into place where a critically ill patient can still get the kitchen sink before any questions are asked. But this magnitude of therapeutic interventions, including antibiotics, must be assiduously de-escalated in the absence of evidence of a bacterial superinfection. These systems need to be in place before the predicted onslaught of flu season cases. Otherwise, we may be in a situation of "our treatment was successful, but the patient died". This kind of Pyrrhic victory we can all do without!