I recently cared for a patient who was an injection drug user who presented with fever, tachycardia, and redness/swelling of the forearm near an injection site. Her initial workup was remarkable for an elevated white blood cell count, hyponatremia to the high 120s, and hyperlactatemia. The patient was not eager to be hospitalized (as I have found is often the case with patients who inject drugs), and during our conversation about the risks:benefits of hospitalization and aggressive treatment with IV antibiotics and supportive care for what I felt was likely a very serious soft tissue infection with sepsis, I mentioned that the patient’s blood level of sodium was low and that I was concerned this was a serious and grave sign that their infection might be quite severe. When I went home after the shift, I wondered what that was founded on other than knowing that sodium was included in the LRINEC score and having had some experience in the past seeing patients with serious / necrotizing skin/soft tissue infections (SSTIs) who presented with hyponatremia.
I did a brief literature search and turned up a few articles, including one publication from one of our program’s recent graduates looking at our county hospital’s population of IVDU-associated STTIs.
Briefly, what I found in these articles was:
a.) Hyponatremia is a commonly-reported finding in patients with skin and soft tissue infections, and it seems to be found more commonly in patients with IVDU-associated infections. It was found in 41% of the patients from the Detroit group, 38% of the San Francisco group (compared to 27% of non-IVDU patients), and in the study looking specifically at necrotizing infections (from UCLA Harbor, with 31% of the 124 patients reporting IVDU) 56% of the patients had hyponatremia.
b.) When present, hyponatremia seems to be related to worse outcomes and is prognostically generally a bad sign. The group from SFGH did not report the association between low sodium and outcomes, but the group from Detroit and UCLA both showed significantly higher mortality in the patients with low serum sodiums at presentation.
Another question I asked myself was why do these patients get hyponatremia? I don’t think anyone knows for sure, but the authors from UCLA Harbor postulated the following in their paper:
Sepsis leads to increased muscle glucose uptake, increased lactate production and decreased utilization, an increase in the calculated ratio of muscle membrane permeabilities to Na+ and K+, and an increased intracellular Na+ concentration. These effects may be mediated by complement activation. In addition, sepsis has been linked to an increase in antidiuretic hormone level as well as adrenocortical insufficiency, both of which may lead to hyponatremia. Finally, severe NSTIs lead to marked third spacing of fluids, which may be replaced by free water, leading to hypovolemic hyponatremia.
More to come when I finish this post. Time to go to shift.