Thanks! V helpful
On Wed, 11 Jun 2014 13:48:47 +0000
Terry Clemmer <[email protected]> wrote:
Tom
Streptococcus and especially Group A is an interesting
organism. It can be accompanied by an immune-reaction
that affects distant organs. Examples include the more
commonly known Post-streptococcal Glomerulonephritis and
Rheumatic Heart Disease. Less known but well documented
is a pleurisy with pleural effusions that are not
accompanied by pneumonia. Pericarditis has also been
described. This is not a common complication but I have
seen about a half dozen in my 40 year career. Some
geographical areas have higher rates than others. For
example in the Rocky Mountain area we have higher rates
of rheumatic heart disease, when I practiced in Hawaii we
saw a lot of Strep. Induced glomerulonephritis.
I think this is the most likely etiology of your
patients pleural effusions and they do usually resolve in
time but it can be weeks or even months. CHF is common
with sepsis up to 30-40 percent of cases will have
myocardial depression with reduces EFs on ECHO with a few
being very severe and presenting as cardiogenic shock.
They usually recover within a few days to a week and
return to normal. I have not seen prolonged pleural
effusions with this situation.
Terry P. Clemmer, MD
Director: Critical Care Medicine
LDS Hospital
Professor of Medicine
University of Utah School of Medicine
Salt Lake City, Utan 84143
Work Phone: 801-408-3661
Work Fax: 801-408-1668
-----Original Message-----
From: Sepsisgroups
[mailto:[email protected]] On
Behalf Of Tom Morris
Sent: Tuesday, June 10, 2014 11:44 AM
To: [email protected]
Subject: [Sepsis Groups] Pleural effusions and low alb
Dear All
Hope all okay - am just reflecting on a case on our
ward of a previously fit 35 year old guy, discharged from
ICU after severe sepsis from arm cellulitis and Group A
Strep in blood. He's had a good week of Benpen and
Clindamycin, but left with bilateral moderate pleural
effusions and a RR of 24, in the context of albumin 24.
Questions:
i) how common is sepsis induced myocardial dysfunction,
or is that all more likely to be iatrogenic fluid
overload? Thought it was a bit odd that lung fields
clear on examination and no parenchymal changes of
pulmonary oedema on CXR
ii) If he'd had acute lung injury during the acute
process, could that have resolved into pleural effusions?
Am assuming that this wouldn't respond to frusemide
quite as well as the top two would do. He wasn't
ventilated by the way.
Many thanks
Tom Morris
ID/GIM Str
Sent from my iPhone
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