Rosie’s Sept E-shift

1. What is the clinical utility of troponins in ESRD?

I know this seems like a boring question, because sometimes we brush a side an elevated trop with a dialysis patient so I was surprised when I read in Tintanelli (bolded no less) that levels of CK, Trop I, Trop T, aren’t significantly elevated in ESRD undergoing regular dialysis and are specific markers of ischemia. Therefore how are we ever able to use troponin in these patients?

Despite (maybe popular) belief, elevated troponin levels are unlikely caused from decreased clearance from failing kidneys. The exact mechanism of increased troponin is unknown.  Troponin T can be elevated ( > 0.10) in asymptomatic patients 30-85% of the time.  TnT actually can increase after dialysis, and TnI can decrease after dialysis.  (I have stuck to speaking only of TnT as this is what we use at St. John)  However, an elevated troponin is not normal and infers greater risk to the patient. It’s been shown that TnT is an independent predictor of multivessel disease.  An elevated TnT is associated with all cause mortality, poor short term prognosis, and increased cardiovascular events in ESRD patients.  There has been evidence to suggest that a chronically elevated troponin comes from microvascular ischemic changes, subclinical myocardial necrosis, and a hypertrophic left ventricle.  None of these are good and goes to infer greater risk to the patient and to predict a higher likelihood of CAD.

My question is more specific to a symptomatic patient complaining of ischemic symptoms, with no EKG changes, and an elevated troponin.  What do we do with that? Level B evidence states that a patient presenting with possible ACS AND an > 20% increase in baseline troponin defines an ACS.  A chronic, unchanging baseline troponin can aid in identifying mortality and cardiovascular risk in ESRD patient too but may not be necessary to further investigate ACS at that time.  http://jasn.asnjournals.org/content/19/9/1643.full

2. The AHA/ACC guidelines for NSTEMIs just came out and I thought I would review the treatment options that were updated in the new guidelines. I stayed focus on medical therapy as to not make this a novel.  

Oxygen is recommended in all NSTEMI patients who have an oxygen saturation less than 90%, respiratory distress, or other high risk features of hypoxemia.

Nitro is recommended in NSTEMI patient who have continued signs of ischemia: sublingual nitro 0.3-0.4 q 5 min x 3.  Then a decision should be made about a drip.  A Nitro drip should be considered in patient with HF, HTN, and persistent ischemia.

Analgesics.  It is reasonable to give morphine, given there is no contraindications, to a NSTEMI patient with persistent pain despite anti-ischemic agents.   NSAIDs (other than aspirin) are contraindicated.

Beta-blockers. A beta-blocker should be initiated within 24 hours if there are no contraindications (HF, cardiogenic shock, asthma, certain heart blocks)

Anti-platelets. All patients with NSTEMIs should be given a full dose aspirin.  If a patient can’t take an aspirin, then load with Plavix (300 mg or 600 mg).

If an early invasive or ischemic-guided strategy* is planned: patient needs dual anti-platelet medication. In addition to aspirin, you may give a loading dose with Plavix, or Brilinta 180 mg. This is the area that I’ve seen rarely do in the ED and I can’t figure out why.  I will speak with a cardiologist and they will plan the patient for a cath in the morning…and they still only tell me to give aspirin.  Anybody have thoughts on this?

Plavix and Brilinta or both P2Y12 inhibitor and are equally recommended in the management of NSTEMI.  (Dual antiplatelet therapy with these plus aspiring is a Class 1, Level of Evidence B)

GPIIb/IIIa.  These antiplatelets are reasonable to give in NSTEMI patient with intermediate/high risk features of ACS (eg positive troponin) who are planned for cath.   An example is Integrilin. (Class IIb, LOE B)

Anticoagulation: Anticoagulation therapy is recommended in all patients with NSTEMIs regardless of their initial treatment strategy.  I thought it was interested that Lovenox had a Class 1, LOE A compared to UFH which was Class 1, LOE B.

Fibrinolytic therapy.  Don’t use in NSTEMIs.

* Early invasive strategy is straight forward – plan for cath. A ischemic-guided calls for a cath if: 1) Patient still experiences ischemic symptoms despite maximal medical therapy, 2) Objective evidence of ischemia (ie EKG changes, positive stress test) or 3) High clinical indicators of a high morbidity risk (ie high TIMI)

Rosie’s E-shift

1. Is succinylcholine safe to use in kidney injury?

Succinylcholine, in the normal individual, can transiently raise serum potassium by 0.5-1.0 mEq/L within 5 minutes of IV administration and lasts less than 10 minutes. Rarely does this cause any complications. This rise is likely from potassium release from cells as a result of depolarization. However, there are certain situations where SCh is contraindicated: (trauma, burns, rhabdo, etc). Hyperkalemia in these cases can lead to fatal cardiac dysrhythmias. This is believed to occur because in these situations there tends to be a proliferation of postsynaptic acetylcholine receptors beyond the NM junction. Therefore when there is a K+ flux, it is not restricted to just the NMJ receptors; potassium can trigger other ACh receptors leading to adverse effects.

Case reports show that there is sufficient evidence to support the current consensus that SCh can be safely administered to patient with renal failure. Of nine studies: 6 studies didn’t find an excessive risk of hyperkalemia or its adverse cardiac effects. Three case reports there wasn’t enough evidence to directly correlate SCh with adverse cardiac effects. In one case report, authors contributed hyperkalemia to uremic neuropathy and a repeated dose of SCh. The other two reports were sketchy on to post-treatment K or any EKG changes of hyperK.

In renal failure, if pretreatment K is high – data is unclear. So then stay away from SCh. Too risky. Not enough data to support a consensus.

I noticed in the case reports, most of the comparisons were drawn from CKD vs normal renal function. I would be more cautious to use SCh in AKI as adaptive measures to protect the body against hyperkalemia haven’t developed in AKI as it has in CKD. And of course if there’s any preexisting hyperkalemia then SCh is contraindicated.

2. In a patient presenting with pelvic pain after receiving treatment with methotrexate for an ectopic, when should we be worried about a ruptured ectopic?

Methotrexate is an acceptable alternative to surgery for the treatment of early, unruptured ectopic pregnancy in hemodynamically stable patients. Methotrexate is contraindicated in patients with alcoholism, PUD, immunodeficiency, or active disease of the lungs, kidney, liver, or hematopoietic system. It is relatively contraindicated in ectopic gestational sacs measuring greater than 3.5 cm or embryonic cardiac activity seen on ultrasound.

Treatment failure with MTX is significant however. Treatment failures, up to 20-36%, have been reported in several cohort studies. Treatment failure is also higher when the beta-hcg is greater than 5000. Therefore, in a patient presenting with abdominal pain who is status post MTX, a rupture ectopic pregnancy must be in your differential.

The clinical picture gets fuzzy when you consider side effects of MTX therapy. Side effects of MTX include lower abdominal pain lasting up to 12 hours around day 3 to 7 post treatment. Pain is typically from tubal abortion or tubal distention. Pain is self-limiting and responds to NSAIDs. Abdominal pain from a ruptured ectopic is therefore difficult to exclude   Some prognostic things to consider to determine if this is a ruptured ectopic is: initial b-hcg level, severe abdominal pain, and larger tubal size. If any of these are present; treatment failure should be high on the differential and an ultrasound is warranted. ACEP clinical policy states for any worrisome features including severe abdominal pain – an ultrasound is warranted. If there are no worrisome features, then simply arranging follow-up on an outpatient basis is ok too.

Dr LaLonde’s E-shift

The great Dan LaLonde’s July E-shift!

1. Does everyone with renal colic need a CT scan?

A non-contrast CT has been described as the best imaging study to confirm the diagnosis of a urinary stone and is widely accepted as the first line imaging study. It’s obviously very easy to order and takes minutes to complete. There are many pitfalls including cost and the use of ionizing radiation. Moreover, most kidney stones will pass spontaneously, and the odds of a non-contrast CT detecting an alternative diagnosis are low. The use of ultrasonography has changed our practice as well. Personally, I try to order ultrasound on many of my patients, especially young people. A recent article in the BMJ aimed to predict the presence of uncomplicated ureteral stones and the lower likelihood of acutely important alternative findings. The researchers called it the STONE score, and it uses the top five factors associated with ureteral stones: male sex, short pain duration, non-black race, nausea or vomiting, and microscopic hematuria.

Sex
	Female	0
	Male	2
Timing
	> 24 hours	0
	6-24 hours	1
	< 6 hours	3
Origin (Race)
	Black	0
	Non-black	3
Nausea
	None	0
	Nausea alone	1
	Vomiting alone	2
Erythrocytes
	Absent	0
	Present	3

 

For patients with low (0–5 points), moderate, (6–9 points), and high (10–13 points) scores, the probability of stones was 9%, 51%, and 89%, respectively. There is more research to be done, however this could become a very useful clinical tool and save some of our patients some radiation.

Moore CL et al. Derivation and validation of a clinical prediction rule for uncomplicated ureteral stone—the STONE score: Retrospective and prospective observational cohort studies. BMJ 2014 Mar 26; 348:g2191

 

 

2. Morphine in the setting of Acute MI?

This wasn’t exactly a clinical question that I thought of, but I overheard some of the cardiac fellows talking about the effects of morphine in Acute MI (AMI). Morphine is widely used in chest pain patients, especially those having an AMI. It serves several functions including reducing preload, reducing afterload, vasodilatation, and pain control (duh). This can help in decreasing myocardial oxygen consumption. The administration of morphine during an AMI has also been associated with poor outcomes. A recent article in the Journal of the Academic College of Cardiology aimed to evaluate the drug-drug interaction of clopidogrel (Plavix) and morphine. They hypothesized that morphine lowers the plasma levels of clopidogrel active metabolite as well as its effects on platelets. This was a randomized double blinded placebo control study of 24 patients receiving a loading dose of Plavix and morphine IV or placebo. They found that “morphine delays clopidogrel absorption, decreases plasma levels of clopidogrel active metabolite, and retards and diminishes its effects, which can lead to treatment failure in susceptible individuals.” I’m not sure if this would change my management at all, but it’s definitely thought provoking.

Hobl EL et al. Morphine decreases Clopidogrel Concentrations and Effects. J Am Coll Cardiol. 2014 Feb 25;63(7):630-5

3. Pediatrics: Prednisone or Dexamethasone in an acute asthma exacerbation?

Asthma is obviously something we see every day, and we all prescribe glucocorticoids for severe exacerbations. The anti-inflammatory action of glucocorticoids effectively reduces the airway edema and secretions associated with acute asthma exacerbations. Depending on which pediatric attending you are working with, you might send someone home on oral prednisone or Decadron. I feel like I use Decadron a lot more compared to my intern year, but I never really questioned why. Oral prednisone or dexamethasone are a reasonable choice for ED treatment. A recent meta-analysis in the Journal of Pediatrics compared a five day course of oral prednisone with dexamethasone (single IM dose or two PO doses) for asthma exacerbations in the ED revealed no difference in rate of relapse and were both equal in efficacy. However, dexamethasone showed a lower rate of emesis, both in the ED and at home. The same study also commented that it is not necessary to deliver glucocorticoids via the intravenous route, even in the subset of hospitalized patients. The dosages of each medication are reviewed below:

Prednisone or Prednisolone	1-2 mg/kg (maximum 60 mg/day) PO for 1st dose. Subsequent dose of 0.5 – 1 mg/kg PO twice daily x 3-10 days
Methylprednisolone	1-2 mg/kg (maximum 125 mg/day) IV
Dexamethasone	0.6 mg/kg (maximum 16 mg/day) PO, IM, or IV

Keeney GE et al. Dexamethasone for Acute Asthma Exacerbations in Children: A Meta-analysis.Pediatrics Vol. 133 No. 3 March 1, 2014
pp. 493 -499

 

4. A new (at least new to me) way to drain abscesses

Incision and Drainage (I&D) is the first line treatment for cutaneous abscesses. There is much controversy about packing them, leaving them open or placing a drain. Patients claim the packing causes pain, and there is compliance issues with the changing and removal of the packing. However, if you don’t pack an abscess, it may heal with infected material remaining inside the cavity. I came across an interesting article in this month’s Journal of Emergency Medicine. It describes placement of a subcutaneous drain using a part of a sterile glove. Here are the instructions with photos (click on link below to see Figures).

 

1. The cuff is removed from the glove (Figure 1 and 2).
2. The cuff is cut, leaving an improvised drain (Figure 3)
3. Make a 1cm incision over the fluctuant area. Explore and break apart any loculations.
4. Make a second 1cm incision opposite to the fluctuant area.
5. Insert the drain into one incision and pass it out through the other incision (Figure 4).
6. Tie the loop drain
7. Apply absorbent dressing to completed loop drain (Figure 5).

 

The patient is then expected to cut the drain when there is no more pus draining from the site. There are some limitations including increased need for the patient to follow discharge instructions (removing the drain) and performing dressing changes independently. External drains can also be cumbersome and unnerving to the patient.

I + D Figures

Thompson D et al. LOOP DRAINAGE OF CUTANEOUS ABSCESSES USING A MODIFIED STERILE GLOVE: A PROMISING TECHNIQUE. The Journal of Emergency Medicine, Vol. 47, No. 2, pp. 188–191, 2014