The American Diabetes Association goals for inpatient management of diabetes can be found here. The goal fingerstick for non-critically ill patients is 140-180 mg/dL. Even though we don’t always do it (read: rarely do it), it is ideal to calculate a patient’s inpatient insulin regimen based on body weight. Sliding scales should not be the sole form of insulin administration as there is actually no evidence to support their use!
Sliding scale insulin is extra coverage and usually consists of short-acting insulin like lispro (Humalog) or insulin aspart (Novolog). These forms of insulin start working in 15-60 minues and peak in 1-3 hours.
Short-acting insulin vs. regular insulin for a sliding scale? Studies have found that there is no significant difference in outcomes, but generally regular insulin should be used for patients who are NPO, on TPN or continuous tube feeds.
To create an insulin sliding scale, calculate your patient’s “insulin sensitivity factor.”
ISF = 1700/total daily dose of insulin
For example: if someone takes 20 U insulin glargine (Lantus) and 2 U insulin lispro (Humalog) with meals, their total daily dose of insulin is 20 + 2*3= 26. 1700/26=65, so 1 U Humalog for sliding scale would be expected to lower their fingerstick glucose by 65.
The University of Pittsburgh put out a patient safety study with a preset protocol for low, moderate, and high-risk patient sliding scales that can be found here.
Important note: bedtime or “QHS” sliding scales should, generally speaking, be more gentle than mealtime sliding scales, as there is a risk for overnight hypoglycemia.
You have a patient who presents with persistent bleeding, and heme/onc recommends a workup for bleeding disorders. One of the tests is a “mixing study.” This literally consists of mixing a patient’s plasma with normal plasma to see if there is a factor deficiency (aPTT corrects) or factor inhibitor (aPTT does not correct).
This is a good overview of a general approach to an abnormal PT or aPTT. (The whole PDF is a good review of workup for hypercoagulable disorders.)
Something like 10% of the US population reports an allergy to penicillin. However, as this CDC info sheet makes clear, <1% are truly allergic. That being said, if someone has ever had a reported reaction to a penicillin, think carefully before prescribing!
Remind me what the penicillins are again? Obviously, anything with “penicillin” in the name (like penicillin G, benzathine penicillin), and derivatives like nafcillin, oxacillin, ampicillin, amoxicillin, and extended-spectrum forms like piperacillin and ticaricillin. The latter are important because they are found in medications like Zosyn and Unasyn which we typically think of as “big gun” antibiotics.
Is it a true drug allergy? The difference between anaphylaxis and drug side effect can be life-saving. Allergy is an IgE-mediated reaction characterized by vasodilation (drop in blood pressure, flushing, tachycardia) and edema (wheezing, abdominal pain/gut edema) and in its most severe form, may cause anaphylactic shock. Hives are characteristic. On the other hand, side effects may be described as a “red rash,” nausea/diarrhea, dizziness, yeast infection. A family history of penicillin allergy doesn’t matter. Not discussed here are delayed allergic reactions, like SJS/TEN, serum sickness, DRESS, or other forms of organ damage. If someone has had a delayed reaction, they should never be given penicillins.
Questions to ask:
How quickly did your reaction happen? (Minutes, hours, days)
Did you have shortness of breath or swelling?
If there was a rash, was there blistering or peeling?
Did your doctors tell you there was organ damage? (liver, kidney dysfunction, changes in the blood counts, etc?)
How long has it been since they took a penicillin? The data shows that over 80% of people who had a penicillin allergy 10 years ago won’t be allergic if they are given a penicillin drug again. Allergies change over the course of a person’s life, and sometimes what you were allergic to as a kid is no longer a problem.
What are the risks of cross-sensitivity with cephalosporins and carbapenems? There is a reported 10% incidence of cross-sensitivity among penicillins, cephalosporins, and carbapenems (beta-lactam antibiotics). I found this review helpful in preparing this post, and one of the key takeaways is: “Persons who make IgE in response to cephalosporins seem to produce it only in response to a particular cephalosporin, whereas persons who make clinically significant IgE in response to penicillin tend to react to core penicillin break-down products.”
What’s the deal with skin testing? Penicillin skin sensitivity testing is a critical tool for determining if someone is still at risk for an allergic reaction. It can be ordered for inpatients or outpatients, and can be done in conjunction with a pharmacist or allergist. If you are skeptical about the allergy (and brave) you can order a “test dose” or graded challenge of the medication, and if the patient tolerates it, put them on regular doses.
I don’t have the time/energy to do skin testing, what can I use instead? People who are allergic to penicillin are more likely to have a reaction to a lower generation cephalosporin than higher generation. Cephalosporins to avoid: cephalexin, ceftriaxone, and cefpodoxime. Cefazolin and cefuroxime, because of their side chains, are less likely to react. This review describes people who can be trialed on alternative beta-lactams and people who should continue to have complete avoidance. Going outside the beta-lactams, the world is your oyster: quinolones, vancomycin (or daptomycin), sulfa drugs (Bactrim), and aminoglycosides (gentamicin).
Let’s say you get a septic patient who has a history of “ESBL.” What does this mean, and what can you empirically treat with?
ESBL, or extended spectrum beta lactamases, refers to a group of bacteria that have developed resistance against beta-lactam antibiotics: penicillins, cephalosporins, and aztreonam. Common suspects include fecal and urinary organisms like E. coli and Klebsiella
If you can’t use penicillins (piperacillin-tazobactam or Zosyn) or cephalosporins (which include heavy hitters like cefepime and ceftazidime), what are you left with? Carbapenems: meropenem is used more frequently, although imipenem and ertapenem are also options. It is sometimes possible to “power through” with high-dose cefepime (2 g q8h) but it’s best to have bacterial sensitivities before plowing down this path.
You also have the option of adding on fosfomycin and/or tigecycline sensitivities if you are stuck treating a difficult UTI.
We’ve all heard horror stories of patients getting digital necrosis from peripheral pressors:
However, the data shows that you CAN run pressors safely through peripheral IVs with close monitoring and proper selection of an IV site. How?
The Journal of Critical Care from 2015 reviewed the available literature of the use of peripheral pressors in adults.This review concluded that there are very rare side effects in the first 6 hours of use, and that best practice is to place IVs in veins >4 mm in diameter (use an ultrasound to confirm!) and monitor at least every 2 hours for extravasation. There was poor quality data reporting adverse outcomes from site of administration of pressors–out of 85 studies included, there was only one randomized study. Furthermore, as this study notes, the rate of adverse effects is low when a good-sized vein in the forearm is used, and pressors can be restarted at another peripheral site when extravasation does occur.
Muddy brown casts are diagnostic for ATN, or acute tubular necrosis, which is an intrinsic form of AKI. But if you don’t see muddy brown casts, can ATN be ruled out? The literature on this is surprisingly light. There is one study of 267 patients with AKI who were classified as low or high pretest probability for ATN and had urine samples analyzed. The study concludes: “In patients with a low pretest probability of ATN (initial diagnosis of prerenal AKI), lack of casts or RTEC on urinary sediment examination had a sensitivity of 0.73 and specificity of 0.75 for a final diagnosis of prerenal AKI. The negative predictive value of lack of casts or RTEC in patients with low pretest probability of disease was 91%.” One important point to take away is that your pretest probability matters a lot for how confident you should be about making a diagnosis.
This review, by the same group, has a nice discussion section about making the diagnosis of ATN through a combination of methods, including microscopy, and use of FeNa and FeUrea.