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 _______________________________________________ Sepsisgroups mailing list [email protected] http://lists.sepsisgroups.org/listinfo.cgi/sepsisgroups-sepsisgroups.org _______________________________________________ Sepsisgroups mailing list [email protected] http://lists.sepsisgroups.org/listinfo.cgi/sepsisgroups-sepsisgroups.org
