1/ #medtweetorial on bacteremia real or not real?
A 70yM comes in with SBO and tachycardia and leukocytosis. Blood cultures are sent on admission. 1 out of 2 comes back with Clostridium spp (not perfrigens/ septicum). To treat or not to treat?
2/While true bacteremia needs to be aggressively treated, there is also a high rate of contamination. Figuring out which blood cultures represent true infection can be tricky.
3/ What is the contamination rate of blood cultures?
What is the chance a positive blood culture represents bacteremia?
There is a .6-12.5% contamination rate of blood cultures.
4/ However, when it comes to + blood cultures, 20-50% of + blood cultures are contaminants. There number vary widely from institution to institution based on how the cultures are obtained. ncbi.nlm.nih.gov/pmc/articles/P…
5/ This is why it is important to consider the pre-test probability of bacteremia before obtaining cultures (see thread
6/ When thinking about contaminants, most are gram + organisms on the skin. Most gram – bacteremia are true infections. However, even an unlikely pathogen like S. epi, is likely true bacteremia if it grows in 2/2 cultures drawn correctly at 2 different venipuncture sites
7/ less than 1/1000 prob that this would occur by chance). Also, consider if the patient has a source for infection such as a medical device. psnet.ahrq.gov/web-mm/contami…
8/ When the cultures come back with 1 out of 2 + for a gram + organism, it is trickier. S. aureus should always be treated as true bacteremia (87%/93% true infection).
9/ Other GP should be treated as true infection (w % true infection) include Enterococcus (63%/70%), S. pneumoniae (100%100%), B hemolytic strep (97%/67%), Clostridium spp. (not perfringens) (63%/80%). pubmed.ncbi.nlm.nih.gov/20800151/ and academic.oup.com/cid/article/24…
10/½ blood cultures + for these bacteremia is usually due to contamination: CoNS, Bacillus, Corynebacterium, Propionibacterium, Microccous, Aerococcus spp, and viridans group streptococcus.
11/ However, the clinical context should be determined, especially with CONS which can cause endocarditis/joint/device infections.
13/ In conclusion 1. Treat gram - as bacteremia 2. 2/2 bacteria on blood cultures drawn from different sites usually bacteremia 3. S. aureus, Enterococcus, most Strep usually true bacteremia, even in 1/2 cultures. 4. CoNS, Bacillus, Corynebacterium ect. usually contaminants
14/ In the first case, I would treat b/c 60-80 Clostridium spp true bacteremia and has a source, but it is never wrong to ask ID.
1/ Understanding #ANA#tweetorial a collab w/ @MithuRheum
You are seeing a 30yo patient in the clinic who is ? an elevated ANA titer. A few months ago she had 2 weeks of joint pains & a rash. As part of the evaluation, an ANA was+ with a titer of 1:80. What do you do next?
2/ The goal of this tweetorial is to understand the significance of ANA
What is ANA?
What are the rheumatological and non-rheumatologic causes of ANA elevation?
What is the significance of the ANA titer?
What is the significance of the pattern of ANA elevation?
3/ ANA stands for antinuclear antibodies. What is in the nucleus? @sargsyanz reminds us that there are a lot of things in the nucleus, so a positive ANA could indicate antibodies targeting any of these structures.
#medtwitter Can you have a completely normal CSF profile in autoimmune encephalitis? (answer forthcoming)
This table is from a 2019 review. Interestingly in LG11, IgLON5, and GlyR the majority have a completely normal CSF profile including oligoclonal bands. (ncbi.nlm.nih.gov/pmc/articles/P…)
What about MRI? In what percentage of autoimmune encephalitis is the MRI of the head normal?
2/ Pts with cirrhosis are at higher risk of bleeding d/t ⬇️ factors, right? Not necessarily. In cirrhosis, there are ⬇️ in both anticoagulant and procoagulant factors in the liver. Additionally, factor VIII and VWF are usually increased.
3/ INR is only measuring a small part of the coagulation cascade, the extrinsic pathway (Factor VII). Additionally, variceal bleed is driven by ⬆️ portal pressure primarily.
Do you give vitamin K to pts with cirrhosis presenting with elevated INR? I would love to hear your thoughts about the topic.
Here are a few questions about Vit K in cirrhosis I wanted to answer. Please post additional articles on the topics that you know of. Question 1: Is there proof that patients with cirrhosis are Vit K deficient?
3/ It is proposed that patients w/ cirrhosis are at ⬆️ risk for Vit K def. I could find very few studies about this. This study of pediatric pts w/ cholestatic liver disease had high prevalence, but very different pop from most adults w/ cirrhosis. pubmed.ncbi.nlm.nih.gov/19502999/
A pt w/ a hip fracture on POD1 has fever of 100.8. HR 90, BP 110/75, SpO2 96% ambient air. No localizing symptoms. Do you obtain blood cultures?
2/My reflex when I hear fever is to order blood cultures. It’s not wrong to make sure, right? As a resident, I remember grumbling at the ED for not ordering cultures on that CAP patient. First, what are the harms of ordering unnecessary blood cultures?
3/ Aside from the cost, there is a high rate of contamination on blood cultures from 0.6% to over 6%. In conditions with a low pretest probability of bacteremia, this represents a large prob that a + culture is contamination. ncbi.nlm.nih.gov/pmc/articles/P…
1/ #tweetorial Next on the skeptical diagnosis series, I wanted to address cellulitis. I always feel a little angst when I am called to admit a patient w/ cellulitis. Does the patient really have cellulitis? In what % of pts diagnosed with cellulitis is the diagnosis incorrect?
2/ Here, I will focus and diagnosis and mimics. I plan to discuss mng of cellulitis later. Studies show that in 30-33% in patients diagnosed with cellulitis, the diagnosis is incorrect.
3/ Of those with an incorrect diagnosis, around 85% percent do not need hospitalization and 92% did not need antibiotics. Misdiagnosis is associated with millions in increased healthcare costs and up to 9000 nosocomial infections. pubmed.ncbi.nlm.nih.gov/27806170/ pubmed.ncbi.nlm.nih.gov/29453874/