Is it Really the Salt that Matters?

Intensivists have repeatedly been warning on the potential effect side effects when infusing bigger quantities of normal saline like acidosis and potentially worse outcomes. It is well recognized that infusion of normal saline can lead to metabolic acidosis, but the link between the acidity of saline solution and the acidaemia it can produce might be not straightforward!

This article from the beginning of this year shows a surprising insight on the various components involved when using normal saline infusions and comes to the conclusion that the acidaemia complicating saline infusions is actually unrelated to the acidity of the normal saline solution itself. It turns out that in vitro the acidity of a normal saline solution is mainly due to dissolved CO2 and PVC degradation of the bag containing the solution. The metabolic acidosis by saline infusions in vivo though mainly results from from buffer base dilution and is not directly related to the pH of the infusion at all. Got interested?

Reddi B, et al. Int J Med Sci. 2013 Apr;10(6):747-50


I Know That I Know Nothing, Socrates

Therapeutic hypothermia – Here we go again. Another quite invasive therapy we offered to patients in the last couple of years might actually not help as we thought it would. This seems to become another deja-vu and might just show the saying which is so true for intensive care: ‘Less is more’.

Just last month the New England Journal of Medicine published this international multi-center trial where 950 patient initially were enrolled to receive hypothermic treatment at 33°C or 36°C. 939 patients finally where followed up for neurologic function (CPC scale and Rankin scale) and death. And guess what… There is no difference what so ever!

The evidence of this study implicates that therapeutic hypothermia might not be of any benefit. So what do we do now? Is this the end of the hypothermic era?

Nielsen N, et al. New Engl J Med. 2013 Dec;369(23):2197-206

Don’t Keep Cool

Hypothermia is back in the focus of discussions and was not only used for treatment after cardiac arrest. If hypothermia would protect after cerebral ischemia after an arrest it might be also useful after other impacts like stroke or meningitis.

To answer this question a french multi-center study was started involving 49 intensive care units. Patients with communitiy acquired bacterial meningitis and a GCS of less than 8 for less than 12 hours were enroled. The hypothermia group was cooled to 32-34°C for 48 hours and then passively rewarmed. Primary outcome was GCS at three months. After including 98 patients the study had to be stopped on the request of the data ans safety monitoring board due to concerns over excess mortality in the hypothermia group. Analysis showed no improve of outcome but might actually be harmful to patients.

Hypothermia doesn’t seem to be the magic bullet here either.

Mourvillier B, et al. JAMA. 2013 Nov;310(20):2174-83