Paging the Cardiology Registrar: Acute Coronary Syndrome in the ED


About the Author
Dr. Yousif Ahmad (@narrowcomplex) is a Cardiology Specialty Registrar in London, predominantly working at the Hammersmith Hospital which is one of London’s eight 'Heart Attack Centres', offering a 24/7 primary angioplasty service and a 'Primary Arrhythmia' service. Yousif is currently involved in coronary physiology research, and is passionate about medical education. He is teaming up with Pondering EM for the 'Paging the Cardiology Registrar' series, which will equip the junior ED doctor with the nitty gritty for key cardiac presentations, and importantly, explain what our cardiology colleagues are really interested in when they receive a phone call from the ED.

Pondering Cardiology in the ED
The first thing I would like to speak about is the relationship between Cardiology and the Emergency Department, and the unavoidable changes encountered over the last few years.

A large proportion of patients with acute cardiac disorders first present to the ED. This is often the most important point in the patient’s illness. Prompt recognition and treatment is essential for acutely unwell cardiac patients. We are always taught that ‘time is myocardium’, and it’s true: a delay in treating a patient with an acute myocardial infarction means heart muscle will die. It is consistent across other cardiac disease states: ventricular tachycardia is an inherently unstable situation, and patients will not tolerate it for long if untreated. We have all seen the distress a patient encounters in acute pulmonary oedema, and how rapidly it can become fatal if not managed appropriately and promptly.

But the clinicians who ought to be best suited to treating these patients are being taken further and further away from frontline assessment and emergency treatment. Cardiac services have changed radically over the last ten years, with the increasing adoption of primary angioplasty services and sequential subspecialisation. Importantly, this is a good thing: patient outcomes have been improved by these new systems and processes. But it leaves an important gap that must be filled.

And it must be filled by Emergency Medicine, as this is the domain where these patients are often first assessed and treated. The interface between the ED and Cardiology is now more important than ever, and it is crucial that junior ED staff feel empowered to confidently manage these patients.

There is no place for protecting your patch. Doctors from the ED and acute medical teams often tell me they think Cardiology is shrouded in mystery these days. On our rounds we make decisions on patients and it is not always clear why one patient with a raised troponin is managed conservatively, and another with normal cardiac enzymes is rushed to the cath lab. We should be vocalising our decision-making processes and imparting as much as we can in terms of knowledge and skills to the emergency clinicians tasked with managing these patients in those vital first hours after presentation. I am sure this is not a situation that is unique to Cardiology, but I feel it is crucial for us to provide information and education upstream, so that frontline doctors feel better equipped to manage these acutely unwell patients.

I will touch on acute coronary syndromes in this post.  This is the most frequent cardiac problem encountered in the ED, and I hope that the post will help junior emergency doctors feel confident managing these patients and, crucially, help in your liaisons with the Cardiologists in your hospital.

So you’ve got a patient with chest pain…
When I say patient with chest pain… I really mean a patient with suspected acute coronary syndrome, as I am sure I don’t need to discuss the differential diagnosis of chest pain – or that I’m the best placed to do so regardless.


There is a lot to think about when assessing and managing patients with a suspected ACS. The spectrum of presentation is huge. Just because many patients with ACS appear 'well' from the end of the bed, it does not mean we can become complacent in treating them. Patients suffering acute myocardial infarctions can deteriorate rapidly, and early recognition, risk stratification and management is essential.

The Initial Assessment
Talking through the overall assessment and management of ACS patients is difficult. There is no easy algorithm to follow – you can’t always start with a detailed history, because sometimes you don’t have time to.

The key components in your initial, point of contact assessment are:
  • Is the patient still in pain?
  • What is the haemodynamic status of the patient?
  • What does the 12-lead ECG show?
  • Is there any clinical evidence of heart failure?
  • Have there been any associated arrythmias so far?

The reason these are the essential starting points – above the full history – is they govern the next steps in management, at a point when time cannot be lost. If there are no immediately concerning features when you work through this list (i.e. pain-free, good blood pressure, no significant ST segment deviation, no heart failure, sinus rhythm) then you have time to take a proper history and make a more comprehensive assessment. If any of the above features are obviously in play, then you need to think about immediately involving Cardiology with a view to deciding if the patient needs to go straight to the cath lab.

The History
So let’s assume you have some time to get a proper history. As we all know, the history is not always helpful. Sometimes patients can’t volunteer the salient points we want to extract. But get what you can. 

Key points to try and elicit:
The characteristic of the pain: this isn’t something to live or die on, but it can be useful. We all know the typical description of pain this is supposed to represent myocardial ischaemia (crushing central chest pain, radiating to the jaw or left arm, associated with breathlessness and nausea or vomiting). But many patients with severe coronary disease have atypical symptoms. So you can’t rely on this entirely, and don’t be fooled by thinking you can.

The timing of the pain. How long has the patient been in pain for? Is this the first ever episode of pain, or has it happened before? What was the patient doing? Was it on exertion or at rest? Exertional pain suggests a more stable situation than pain at rest.

Established history of coronary disease. Has the patient had an infarct before? Have they had a bypass or previous PCI? Is the presentation now similar to previous presentations with proven ACS?

Risk factors for coronary disease: smoking, diabetes, hypertension, lipid disease.

Other things we might be interested in: renal failure (if we need to take the patient to the lab and accordingly give contrast): anaemia or bleeding (as we may be thinking of giving potent antithrombotic drugs); intercurrent medical problems such as life-limiting malignancy; the general functional status of the patient; peripheral vascular disease(in terms of planning access routes for angiography)

The ECG
This is obviously crucial. But don’t make the mistake of divorcing the clinical assessment of the patient from the ECG. Looking at the patient can often tell you if they’re having an infarct. Subtle ST changes in a young patient with only a few seconds atypical pain and no risk factors is unlikely to represent a STEMI.

I interpret ECGs in a very, very simple way. I describe them in a similar way. Telling someone over the phone the ECG shows 'an inferior NSTEMI' is not very helpful; neither is stating that it shows a 'junctional bradycardia'. Far more useful is actually describing the ECG so the person on the other side of the phone knows, as far as possible, exactly what you are looking at (so better to say something like 'sinus rhythm with deep T wave inversion in V1-V4'; or 'bradycardic at 35 bpm, regular, no visible p waves, narrow QRS').

So for ACS and all other ECGs I generally take this approach:
  1. Fast, slow or pretty much normal?
  2. Regular or irregular?
  3. Are p waves clearly and consistently visible and what is their relation to the QRS complexes?
  4. What is the PR interval? (you can just read this from the printout)
  5. What is the QRS duration/morphology? (can also read from the printout, narrow/broad?) 
  6. What do the ST segments and T waves show? Is there ST elevation, ST depression, or T wave inversion? Do these changes respect a coronary artery territory?

Never forget to check serial ECGs. A changing ECG is the hallmark of ischaemia.

By building up the ECG like this, you will be able to accurately delineate the abnormalities and – crucially – describe them to somebody clearly over the phone. If it’s barndoor, massive ST elevation then you probably don’t need to worry about going through every point, but it’s a good habit to get into.

Example 1


So there are obvious abnormalities here. Taking the approach above:

  1. Slow
  2. Looks regular (always map the ECG out if you’re dealing with an arrhythmia)
  3. P waves are visible but there appears to be no relationship to the QRS complexes
  4. PR interval is not-applicable, due to the above.
  5. The QRS is broad at 118ms
  6. There is significant ST elevation in II, III and aVF with ST depression in I and aVL. There is also some more subtle ST elevation in V5 and V6.

If you were confident in interpreting ECGs by glancing at them you could just say that this shows inferolateral ST elevation with complete heart block and an unreliable ventricular escape rhythm.
But if not you can build up a fuller interpretation by being systematic. Inferior ST elevation with some lateral changes. Bradycardia. Regular. Visible p waves but no relationship between p and QRS. Broad QRS.

 Example 2


Again the abnormalities are obvious, and there’s nothing wrong with just saying there is significant anterior ST elevation with reciprocal change. But when you have more subtle or challenging ECGs – or when you are dealing with rhythm disturbance predominantly above ACS – then being systematic is advantageous. Taking the approach above:
  1. Not slow, not fast
  2. Looks regular
  3. P waves aren’t clearly or consistently visible
  4. PR interval not applicable, due to the above
  5. The QRS is narrow at 94ms
  6. There is significant ST elevation in V1-V3 with ST depression in V4-V6, II, III and aVF.

If you were confident in interpreting ECGs by glancing at them you could just say that this shows anterior ST elevation with reciprocal inferolateral ST depression and a junctional rhythm. But again you can build that up by being systematic. Anterior ST elevation. Inferolateral ST depression. Regular, narrow complex, no p waves.

Specific ECG changes to be wary of in ACS, beyond barn-door ST elevation
ST-elevation in aVR with global ST depression elsewhere – this often represents a stenosis in the left main stemand, with an appropriate clinical picture, suggests the patient may need urgent invasive management in the cath lab.

LBBB, particularly when Sgarbossa’s criteria are fulfilled with a score of over 3 points (these criteria help improve accuracy for diagnosing an infarct in the presence of LBBB); they are:
  • ST elevation ≥1 mm in a lead with a positive QRS complex (ie: concordance) - 5 points
  • ST depression ≥1 mm in lead V1, V2, or V3 - 3 points
  • ST elevation ≥5 mm in a lead with a negative (discordant) QRS complex - 2 points
ST-depression in V1-3 – this may represent a posterior STEMI and need to go straight to the lab.

Deep T-wave inversion or biphasic T waves in V1-3 – this may represent a critical LAD stenosis and need to go to the lab urgently.

Dynamic/changing ST segments or T waves.

The Initial Management
The first question you need to answer based on your assessments for far is whether the patient needs to go to the lab urgently. If you think so, do not delay in contacting Cardiology.

The emergency treatment that can and should be given in ED is the following:
  • Continuous cardiac rhythm monitoring: this is important, as these patients are at risk of ventricular arrhythmias or AV block
  • Analgesia (but ensure you let the Cardiologists know what you have given – a patient who is pain-free with no analgesia is a different situation to one who is pain-free after 10mg of IV morphine)
  • Aspirin 300mg
  • Sublingual nitrates
  • If you are sure you are dealing with ACS, and there is no concern over bleeding, then further antithrombotic therapyis needed. The second antiplatelet agent is not a big deal (clopidogrel 600mg, prasugrel or ticagrelor) as the outcomes between those three options are fairly similar. Equally, most people won’t mind too much what form of low-molecular weight heparin you give. What is important is that you don’t administer this treatment lightly for anybody with vague chest pain, because there are substantial bleeding risks.

Point-of-care echocardiography, for a broad assessment of LV function and regional compromise of the LV, is helpful if performed by somebody appropriately skilled and trained. If you have these skills, please do not withhold them as the information can be invaluable to us.

Further treatment beyond this for a true ACS really ought to be undertaken by the Cardiologists, especially if the patient needs to go to the cath lab.

Beware of the fallacy of 'stabilising' a sick STEMI patient. Sometimes we have delays in getting people to the lab because the doctors looking after them want to insert arterial lines, central lines, get a nitrate infusion started, or put the patient on inotropes. It is important to understand that a sick patient with an occluded coronary artery cannot be stabilised outside of the catheter lab. They need the artery opening and there is no other temporising measure. Equally, if your Cardiologists try to tell you that the patient 'needs stabilising' before being transferred to the lab then you must also fight against this. The only thing that will help these patients is getting the occluded vessel open. That’s it.

The Referral
This is important. You need to get the salient information across. You also need to know what we aren’t interested in. Don’t just tell us what the ECG shows. We do want a little bit of detail on the patient. Equally, in the middle of the night we don’t want to know exactly which statins the patient has been intolerant to over the last decade. The balance is admittedly difficult.

We want to avoid a scenario like this:


In reality, referring an ACS patient should not take more than a minute or two. Below is a list of the essential information the Cardiologist wants to hear:
  • Does the patient have chest pain? (It is not an infrequent scenario when we are asked to review a possible STEMI who has never had any pain)
  • Has the pain abated?
  • What does the 12-lead ECG show?
  • What is the patient’s heart rate andblood pressure?
  • Is the patient in pulmonary oedema?
  • Does the patient have established history of coronary disease? and if so do you know when they last had their coronaries imaged or intervened on with stents/bypass?
  • What are the risk factors for coronary disease?
  • Is there anything else going on we need to be wary of (anaemia, bleeding etc)
  • What treatment has the patient had in the ED?
  • Has there been a point of care assessment of the LV function yet?
  • Does the patient look like they are having an infarct from the end of the bed?


The last point is key. Emergency clinicians are used to dealing with sick patients. An end of the bed assessment as to how the patient looks generally is key for us when we cannot physically see the patient. Do they look like they’re having a heart attack, or are they lying there comfortably with an abnormal ECG?

And that really is all the information that the Cardiologist could possibly want. It would take ten minutes to assimilate the information, and two minutes to relay it. By using the above reference points systematically, you will always be prepared for any questions you may be asked and you will always be supplying the pertinent information to the person who needs to decide on the next stages of management.

Summing up
While Cardiologists become more subspecialised and move further away from the frontline, Cardiology itself and patients with acute cardiac disorders remain a huge contributor to the workload of the ED. The interface between Cardiology and Emergency Medicine is closer than ever, and more important than ever.


Junior ED doctors need to be equipped to deal with these patients, and promptly recognise a sick Cardiology patient. Cardiologists can be difficult to refer to, but by maintaining first principles and approaching each aspect of the case systematically it is easy to build and portray a clear picture for the Cardiologist you are referring to.

References
  • Steg PG, James SK, Atar D, et al. ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation: The Task Force on the management of ST-segment elevation acute myocardial infarction of the European Society of Cardiology (ESC). Eur Heart J 2012;33:2569–619
  • Emergencies in Cardiology (2 ed.). Edited by Saul G. Myerson, Robin P. Choudhury, and Andrew R. J. Mitchell. Oxford University Press.
  • American College of Emergency Physicians; Society for Cardiovascular Angiography and Interventions, O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2013 Jan 29;61(4):e78-140.
  • Yamaji H, Iwasaki K, Kusachi S, Murakami T, Hirami R, Hamamoto H, et al. Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography. ST segment elevation in lead aVR with less ST segment elevation in lead V(1). J Am Coll Cardiol. 2001 Nov 1;38(5):1348-54
  • Rhinehardt J, Brady WJ, Perron AD, Mattu A. Electrocardiographic manifestations of Wellens’ syndrome. Am J Emerg Med. 2002 Nov;20(7):638-43.

Avoid couchlock! Four things to know about cannabis pharmacology

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With medical marijuana now legal in 23 states and the District of Columbia — and recreational weed available in Colorado and Washington State — knowing the pharmacokinetics of THC has never been more important, both for consumers and the physicians who must counsel and treat them. Recently, the New York Times’ Pulitzer Prize-winning columnist Maureen Dowd got into trouble in Denver when she overdosed on a cannabis candy bar and experienced 8 hours of paranoia and couchlock. My recent Emergency Medicine News column describing 4 things Maureen should have known about weed before venturing to the “mile high city” has been posted online. You can read it here.

Another Example of Defensive Medicine

The ultrasound images above show a circular clot in the superficial femoral vein. The image on the left is without compression and the image on the right is with compression. Normally blood vessels flatten out when compressed. Since the vessel did not flatten with compression it confirmed the presence of a blood clot.

While discussing a case with one of the nurses with whom I work, I saw how once again defensive medicine had affected my medical practice.

I gave a few examples of defensive medicine in a post several years ago and I also mentioned how sometimes doctors have to prove a negative when dealing with patients. Both of those posts are pertinent to this case.

A patient with a history of a clotting disorder has arthroscopic knee surgery. He has had two prior blood clots in his leg and one prior blood clot in his lung, so he’s on lifelong Coumadin. His doctors told him to stop taking the Coumadin for the week prior to his surgery to prevent bleeding during surgery. The surgery went well and he was discharged the same day.

The following day he started taking Coumadin again. However, he also noticed some pain in his calf. The pain was there after his surgery, but it seemed to be a little worse the following day. He took some pain medication and kept ice on it.

Two days out from his operation he was still having some pain in his calf, so he called the orthopedist. The orthopedist told him to go straight to the emergency department for an ultrasound of his leg to make sure that he didn’t have another blood clot. The possibility of a blood clot worried the patient, so he followed the doctor’s recommendations.

When I saw him, based on his clinical exam I could tell – with a reasonable degree of medical certainty – that he didn’t have a blood clot. His leg wasn’t red or swollen. We measured the circumference of both legs at the thigh and at the calf. His normal leg was actually a centimeter larger in diameter than the leg that underwent surgery. The pain was in the belly of the calf muscle – where orthopedists will sometimes apply pressure to get the leg in the correct position during a surgery. There was no thigh pain and there were no palpable cords.
It was a Saturday evening, so doing an ultrasound to look for a blood clot meant that we would have to call in the ultrasound tech from home and the patient would have to sit in the emergency department for at least a couple of more hours.

I told him “Based on my exam, it is pretty unlikely that you have a blood clot in your leg. Keep taking your Coumadin, keep putting ice on the tender area, keep taking your pain medications, and follow up with your doctor on Monday.”
He said “I have a history of blood clots in my leg before, it feels like a blood clot now, and my orthopedist said I need an ultrasound. You need to do the ultrasound.”

Now if there wasn’t any concern about liability or other repercussions, I probably would have told him that the ultrasound wasn’t indicated and that we didn’t need to do it that night.

But there is a concern about liability and other repercussions.

Even if the patient didn’t have a blood clot on this visit, what would happen if the patient developed a blood clot the following day? And what if that blood clot broke off, caused a pulmonary embolism, and the patient died? How could I prove that there was no clot present when I evaluated the patient – especially when purported “expert” witnesses testify under oath that it is “grossly negligent” to miss a diagnosis of pulmonary embolism in a teenager after knee surgery? It is much easier to order a test than it is to defend your reasonable and evidence-based approach for not ordering the test in the event of a bad outcome.
What if the patient had a clot despite the lack of physical findings for a blood clot? We often hear the phrase “nobody’s perfect”, but if you don’t order testing and miss a diagnosis, there is really not much tolerance for less than perfection in cases like this. It is much easier to order a test than it is to defend your reasonable and evidence-based approach for not ordering the test in the event of a bad outcome.
I’ve seen more than a few specialists and primary care docs who send a patient to the emergency department for testing and who then complain to hospital administrators that the dumb emergency physicians don’t do the tests that they wanted.
And let’s not forget that sending a patient home without getting the tests that the patient wanted is a sure way to tank your patient satisfaction scores.

So we ordered the ultrasound and called in the ultrasound tech.

A few hours later we got back the report from the radiologist showing no DVT. The patient got to go home and I’m sure that he slept better.
I’m sure that the orthopedist was able to sleep better, also.
The whole episode didn’t have much of an effect on my sleep pattern. I knew the patient didn’t have a blood clot when I first examined him … but now I had objective proof of my clinical findings and everyone got what they wanted.

Just think, it only cost the system a few thousand extra dollars.

———————–

This and all posts about patients may be fictional, may be my experiences, may be submitted by readers for publication here, or may be any combination of the above. Factual statements may or may not be accurate. If you would like to have a patient story published on Dr.WhiteCoat.com, please e-mail me.

Boring Question: Steroids for Tinea?

The Case

An otherwise healthy 30-year-old woman presents to the emergency department with a pruritic rash on her upper thigh that she has had for nine days. Thinking it was poison ivy, she had been using topical corticosteroids on the area. When the rash didn’t improve, she decided to seek care. She is otherwise well; she reports no fevers, joint pain, or tick exposure. On exam she has two lesions each about 2 cm in diameter (similar to image below). The lesions are slightly raised and scaly. She has no palpable lymphadenopathy. The emergency physician diagnoses tinea cruris and instructs her to stop the corticosteroid. Instead, he prescribes clotrimazole 1% twice daily.

tinea

She returns to the emergency department two days later because the lesions have grown four times in size. They are intensely pruritic, and she notices that they swell with the summer heat at night. Two physicians are working in the department on this particularly slow day, and both examine her. Both physicians agree with the original diagnosis.

  • Physician A suggests combined clotrimazole/betamethasone cream to treat the tinea and reduce inflammation.
  • Physician B is sceptical of using steroids in a tinea infection. She is concerned that steroids may delay resolution of the fungal infection. She suggests continuing with the antifungal treatment alone.

The clinical question

“Is co-treatment with topical steroids in tinea infections associated increased failure or relapse rates?”

Analysis

Search Strategy

 I entered the search terms “tinea” AND “topical steroids” in the Google Scholar search engine. I reviewed titles then read papers that were related. I reviewed the bibliographies and “cited by” of each to find additional papers. I also searched the Cochrane Review Database for “tinea”.

 The evidence

A Cochrane review (published while writing this blog post!) “Topical antifungal treatments for tinea cruris and tinea corporis” highlights that the quality of evidence on co-treatment with steroids is not strong. The meta-analysis of the corticosteroid subgroup combined data from six studies comparing azoles and azole/steroid combinations. Authors concluded that there was no difference in mycological cure rates (RR=0.99 [0.92-1.07]) between the two groups and that clinical cure rates were significantly better in the combination group (RR=0.67 [0.57-0.84], NNT 6). [1].

An older study by Smith et al (1992) reported failure rates of 45% (combined) vs 7% (antifungal alone) [2]. Similarly Nada et al (1994) found a failure rate of 66% (combined) vs 4% (antifungal alone) [3]. In both of these studies, however, the antifungal medication used was different between the antifungal alone vs combined group, which makes it difficult to interpret these results. A review from a pediatric dermatology group found that all cases of refractory tinea referred to their group were associated with topical steroid use (n= 6 cases) [4]. Three trials show no difference in failure between combined therapy and antifungal therapy groups [5,6,7]. One [5] showed symptomatic benefit of steroids while one [6] did not. A more recent study suggests that some combinations of antifungals and steroids may even be synergistically beneficial [8].

 AN IMPORTANT POINT: If you are not sure of the diagnosis, don’t use steroids (and if you think it is tinea don’t use steroids alone) because it complicates the picture. Topical steroids may cause the rash lose some of its distinguishing characteristic qualities. Tinea Incognito is an group of tinea infections that are misdiagnosed because of changes to the skin and tissues related to topical corticosteroid use. 

The Bottom Line

When used in conjunction with antifungals, corticosteroids may improve symptoms and are unlikely to be associated with an increased risk of treatment failure.

  • Given the weak evidence on the topic, it makes most sense to discuss the potential benefits and drawbacks of co-treatment with patients, and let them decide what they prefer.

Back to the Case…

You discuss the above evidence with the patient. She opts to use the anti fungal and also decides to restart with the steroid cream. She notices symptomatic relief during the first few days of combined treatment. Over the next couple of weeks her infection resolves!

Reviewing with Staff | Dr. Seth Trueger, MD

By Seth Trueger, MD   (Attending Emergency Physician at University of Chicago)

Nice summary, and quite fortuitous that the Cochrane review came out while writing it! Not surprisingly, there isn’t a lot of high quality study in this area, but the few hundred patients that made it into the Cochrane review show a pretty decent clinical improvement with the addition of topical steroids to antifungals, with a statistically insignificant increase in adverse effects. While steroids can lead to tinea incognito, if the diagnosis is clear, it makes sense to use them.

Seth Trueger MD MPH
Emergency Medicine
University of Chicago

References

  1. El-Gohary M, van Zuuren EJ, Fedorowicz Z, Burgess H, Doney L, Stuart B, Moore M, Little P. Topical antifungal treatments for tinea cruris and tinea corporis. Cochrane Database of Systematic Reviews 2014, Issue 8. Art. No.: CD009992. DOI: 10.1002/14651858.CD009992.pub2.
  2. Smith EB, Breneman DI, Griffith RF, et al. (1992). Double-blind comparison of naftine cream and clotrimazole/betamethasone diproprionate cream in the treatment of tinea pedis. J Am Dermatol; 26: 125-27. PMID: 1732321
  3. Nada M, Hanafti S, Al-Omari H et al. (1994). Naftifine versus miconazole/hydrocortisone in inflammatory dermatophyte infections. Int J Dermatol; 33: 570-572. PMID: 7960355
  4. Alston S, Cohen B, Braun M. (2003). Persistent and recurrent tinea corporis in children treated with combination antifungal/corticosteroid agents. Pediatrics; 111(1): 201-203. PMID: 12509578
  5. Wortzel MH. (1982). A double blind study comparing the superiority of a combination anti-fungal (clotrimazole)/steroid (betamethasone diproprionate). Cutis; 30: 258-261. PMID: 6751707
  6. Evans EG, James IGV, Seaman RAJ, Richardson MD. (1993) Does naftifinehave anti-inflammatory properties? A double blind study with 1% clotrimazole/1% hydrocortisone in clinically diagnosed fungal infection of the skin. J Am Acad Dermatol; 129:437 PMID: 8217779
  7. Katz HI, Bard JB, Cole GW, et al. (1984). SCH 370 (clotrimazole-betamethasone diproprionate cream) in patients with tinea curis or tinea corporis. Cutis;34:183 PMID: 6383734
  8. Havlickova B & Friedrich M. (2008). The advantages of topical combination therapy in the treatment of inflammatory dermatomycoses. Mycoses; 51(S4): 16-26. PMID:18783560

Author information

Eve Purdy
Medical Student Editor at BoringEM
Fourth year medical student at Queen's University-happily consuming, sharing, creating and researching #FOAMed

The post Boring Question: Steroids for Tinea? appeared first on BoringEM and was written by Eve Purdy.

Figure 1 Image of the Week #3

A 39 year-old woman presented with this nodular rash and an insidious onset of shortness of breath. A chest X-ray was obtained as shown above. What is abnormal finding on the chest x-ray and what is the syndrome that culminates the imaging finding and rash together?


 

Pondering. 

 

Answer. 


Image of the Week - Löfgren Syndrome

This is Lӧfgren Syndrome, which is the manifestation of Sarcoidosis which includes 
erythema nodosum, hilar adenopathy, and arthritis. With this very specific 
presentation, a diagnosis of Sarcoidosis can be made without a biopsy. 
Fortunately, this form of Sarcoidosis has an excellent prognosis and can be 
managed with NSAIDs.


See more cases like this on Figure 1.


More FOAMed Resources: