Really enjoyed @UnremarkableLab last night where we discussed HTN in the hospital.
You are an intern on night float and get called that a patient's BP is 195/110. You:
For anyone who participated, I found this article a really helpful read. I also would suggest listening to the Annals of Call Podcast(acpjournals.org/doi/10.7326/A1…).
Some key points the article made: 1. 72% of pts in hospital have HTN 2. 1 study the article cites- 94 pts given IV hydral (only 4 needed)>17 had adverse effects from hypotension 3. Study of pts given IV treatment for HTN- 56% had BP ⬇️ >25%, 2 hypotensive, 6 had to hold BP med
4. Study of 2,189 pts give IV hydral or labetolol. Only 3% indicated. Use IV meds HTN associated with ⬆️ LOS. 5. Even giving a oral med like nifedipine was associated with rapid BP.
Ask about symptoms: chest pain, SOB, AMS, severe headache (not mild to moderate), visual changes, or acute end organ damage> if acutely symptomatic, HTN emergency and should be treatment aggressively (but still be careful to avoid overly rapid fall in BP).
Review if any reason why BP should be be more aggressively controlled in the hospital: 1. Stroke given TPA 2. Unstable bleed that HTN could ⬆️bleeding risk 3. Aortic dissection 4. Recent neurosurgical procedure
ect.
If not, you have some time to figure it out.
When I call back, I ask about pain/agitation/anxiety. Is the HTN a manifestation of pain that is not being adequately controlled? Then I look look back at the med list and see if there are HTN meds that are being held/missed. I will usually restart home meds 1st.
There are also oral agents which have a fast onset like nifedipine (probably best to avoid), carvedilol, clonidine and catopril. It is important to remember that a pt is the hospital is under stress and BP in hospital may not reflect their normal BP.
Most of HTN's adverse effects occur over years and most cases in hospital are asymptomatic. In the case of asympmatic BP elevation, we can do significant harm by lowering BP too quickly. Pretty # do not always = better pt outcomes.
I have replaced the term HTN urgency w/ permissive HTN (even in non-stroke pts). Like treating diabetes in the hospital, over aggressive treatment can lead to harm. Sometimes, you need to tolerate a little HTN in the hospital with good PCP f/u outpt.
• • •
Missing some Tweet in this thread? You can try to
force a refresh
1/Why do distal tube diuretics cause hyponatremia more often than loop diuretics? Important roles of the nephron include both the ability to dilute and concentrate the urine. The ability to concentrate the urine is maintained by hypertonic medullary gradient (d/t Na & urea).
2/Loop diuretics impair Na/Cl transport in the loop of Henle> loss of a hypertonic renal medulla. The nephron loses the ability of concentrate the urine causing increased water loss (hypotonic renal losses). However, the ability to dilute urine is maintained.
3/Since losing more dilute fluid, hyponatremia does not usually develop.
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.
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/