By now, I have had some direct experience working with patients that were afflicted with the swine flu and who required hospitalization. Early on, NYC doctors heard that most of the people who test positive for influenza A are actually infected with the swine flu. Therefore we employed a rapid flu screen since it detects both influenza A and B. Surprisingly, this rapid flu test in its capacity to screen for the swine flu turned out to be a dud; with this particular virus it is only 19% sensitive.
PCR will detect the H1N1 flu
virions more reliably and this test appears sensitive, but it takes days to receive the result. Thus, the problem with
PCR is that if you want to decide on using anti-
virals within the time frame that these drugs will be effective, you cannot wait for this more sensitive and specific test. Therefore, in
choosing whom to prescribe
Tamilfu to, you must use your clinical skills. There is no reliable rapid laboratory analysis that will answer this question for you. The
PCR test is useful for statistical analysis and in some cases post-mortem, but it is useless in the clinic.
That brings up the next topic I want to address. I know of a patient who died from this virus and his
pre-existing medical conditions were relatively unremarkable. After admission to hospital with URI symptoms, he became progressively more
hypoxic. Chest CT showed diffuse infiltrates. He received
Tamiflu, steroids, and antibiotics, but he still required a lot of supplemental oxygen. Without the non-
rebreather mask his oxygen saturation was in the 80's, but on supplemental oxygen it improved to mid-90's.
Tamiflu did not save him, even though he was on it for a whole week and it was started shortly after he developed symptoms -within 48 hours to be precise.
PCR eventually confirmed the H1N1 infection. It may be that while
Tamiflu will help with typical flu symptoms and shorten the course of the illness, it may not help those who develop life threatening viral pneumonia. If you have the genetic composition to react in this way to this virus and develop diffuse pulmonary infiltrates, don't place a whole lot of hope on
Tamiflu. For this particular patient, there may also have been an inflammatory reaction around the
myocardium, since he suddenly went into cardiac arrest. The hypoxia was under control. He didn't have any significant
pre-existing cardiac disease. Cardiac arrhythmia seems to be the most plausible explanation here, and it is known to arise when the
myocardium is inflamed.
Such severe reaction to this virus appears rare since we are not seeing widespread admissions to the ICU, while most people with this virus recover and go home within just a few days. However, there are some who develop life threatening complications and the H1N1 deaths seem to occur among the young and middle aged individuals. Whenever their
pre-existing medical conditions are mentioned, these afflictions sound relatively minor. The fatal mechanism might involve precisely this form of severe viral-inspired pulmonary inflammation. Considering the above
patient's course, I am not sure that
Tamiflu is going to be all that important in reducing swine flu associated mortality.
The NYC government
website lists 32 deaths thus far and provides some superficial information about New Yorkers who were hospitalized, as well as those who died from this virus. What's missing is an in depth evaluation of how these folks died. Until that information is analyzed and released, you are left only with my conjectures.