Please Clarify
Tweet Doctor, can you please clarify the route of administration?
ICN Nip’n Tuck
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The ICN site has been undergoing some changes over the past couple of months and we hope your use of the site has benefitted as a result. We think it looks better and that it is more streamlined and intuitive to navigate. Now we need your help! We are just a bunch of physicians who thought that the intensive care community needed a resource like this (The ED guys have been into this sort of thing for a bit longer, but we are catching up), but we can't claim to be artistic masters. We want to update the ICN logo, you know .. the orange box up there on the top left corner of your screen; here it is:
As there are over 1500 registered ICN members, we figure there must be at least a handful of you out there that could do a better job than us. So get out your crayons, pastels and Etch-a-Sketches and get all Goya on our logo. The logo will be used for the website, the soon-to-be released newsletter, tweets, Google+ noise and bookmark emblem, so it needs to work in a range of sizes. Also, try to match the site's colour scheme (blue, white, orange) but otherwise go nuts!
Send your masterpieces in to us and the winner will be selected by a completely biased, subjective and open to bribery panel of self-proclaimed experts who will place you upon a shining pedastal for all the online world to see. We might even shower you in glory at the forthcoming Bedside Critical Care Conference in September. So get cracking! |
{jcomments on}
Suprapubic Catheter Foley Balloon Coming out of What?
A few days ago, I picked up a patient who was transferred to our facility for urology consult. Patient had a suprapubic catheter for various reasons and was having gross hematuria. The outside facility had taken out the catheter and replaced it with a new one. Per report, while the patient waiting for lab results for her new hematuria, she was complaining of some groin discomfort.
The nurse did a quick pelvic inspection and saw the foley balloon coming out of the vagina. The physician checked himself and concluded the patient must have a vesicovaginal fistula. The patient was transferred primarily for this abnormality on exam.
Vesiocovaginal what?
 | A vesicovaginal fistula is a connection between the vagina and the bladder. It usually occurs after vaginal surgery, most common after open hysterectomies. The patients present with watery (urine) vaginal discharge a few weeks after the surgery. |
So how do you go about confirming it? And what do you do if you do? Call urology for emergent surgery?
So we placed another suprapubic catheter and flushed 60 cc of our improvised concoction of methylene blue and 250cc of normal saline. Then we did a speculum pelvic exam and looked for blue staining anywhere. And what did we find?
Nothing. No signs of urine or bluish stain. We waited a bit and still nothing.
We came to the conclusion that when the outside hospital nurse initially placed the suprapubic catheter, the end must have came back out of urethra without anyone seeing it. When they filled the balloon, it was already outside the urethra around the entrance of the vagina.
We called the urologist just to confirm our suspicion and they mentioned it’s not uncommon for a suprapubic catheter to accidentally come out of the urethra on initial insertion.They stated it happens all the time in the OR.
Either way, methylene blue was the test of choice to figure out whether or not there was a fistula or not. Rather than a speculum exam, a tampon could be used as well for assessment. Tintinalli mentions if methylene blue can not confirm a fistula, indigo carmine dye should be used as well.
If a fistula is found or highly suspected, the treatment isn’t emergent surgery or even admission. A urethra foley is kept in place to keep the bladder drained with likely fistula repair in the next few weeks in an outpatient setting. The patient can still be discharged (which I always find as a win in my book).
We kept the catheter in and sent the patient back home.
I don’t get it.
A man came in today who claimed that he was allergic to "water", then in parentheses in the allergy section it says: "takes quick showers". Just kill me now. Them showers must have to be damn quick. And take an epi pen in there with you...The human body is 50-65% water. By rights, this man should have died years ago. But unfortunately, he is still with us and chooses to present himself to our ER. He has a legitimate problem, but somehow its hard to get past the whole water thing.
There is actually a scientific name for this: aquagenous urticaria. Only 30 people in the whole wide world have this allergy. There is no cure. Their is a 14 year old girl who is allergic to water. Every time she comes in contact with it she develops a rash or blisters. So she applies a barrier foam that has allowed her to function somewhat. My question is what about her body's water content. How come that doesn't cause a reaction? Hmmmmm...
Another allergy someone had recently is an allergy to "cold". "I have just been diagnosed with it" she said. Woman, you are in the wrong part of the country and I suggest you move south my dear. I know someone who is allergic to the sun. Bummer. Here's a good one: "I'm allergic to holy water at church. Whereever it touches me, I break out in hives". Hmmmm.....maybe God is trying to tell you something....
emergency room nurse
I don’t get it.
A man came in today who claimed that he was allergic to "water", then in parentheses in the allergy section it says: "takes quick showers". Just kill me now. Them showers must have to be damn quick. And take an epi pen in there with you...The human body is 50-65% water. By rights, this man should have died years ago. But unfortunately, he is still with us and chooses to present himself to our ER. He has a legitimate problem, but somehow its hard to get past the whole water thing.
There is actually a scientific name for this: aquagenous urticaria. Only 30 people in the whole wide world have this allergy. There is no cure. Their is a 14 year old girl who is allergic to water. Every time she comes in contact with it she develops a rash or blisters. So she applies a barrier foam that has allowed her to function somewhat. My question is what about her body's water content. How come that doesn't cause a reaction? Hmmmmm...
Another allergy someone had recently is an allergy to "cold". "I have just been diagnosed with it" she said. Woman, you are in the wrong part of the country and I suggest you move south my dear. I know someone who is allergic to the sun. Bummer. Here's a good one: "I'm allergic to holy water at church. Whereever it touches me, I break out in hives". Hmmmm.....maybe God is trying to tell you something....
emergency room nurse
I don’t get it.
A man came in today who claimed that he was allergic to "water", then in parentheses in the allergy section it says: "takes quick showers". Just kill me now. Them showers must have to be damn quick. And take an epi pen in there with you...The human body is 50-65% water. By rights, this man should have died years ago. But unfortunately, he is still with us and chooses to present himself to our ER. He has a legitimate problem, but somehow its hard to get past the whole water thing.
There is actually a scientific name for this: aquagenous urticaria. Only 30 people in the whole wide world have this allergy. There is no cure. Their is a 14 year old girl who is allergic to water. Every time she comes in contact with it she develops a rash or blisters. So she applies a barrier foam that has allowed her to function somewhat. My question is what about her body's water content. How come that doesn't cause a reaction? Hmmmmm...
Another allergy someone had recently is an allergy to "cold". "I have just been diagnosed with it" she said. Woman, you are in the wrong part of the country and I suggest you move south my dear. I know someone who is allergic to the sun. Bummer. Here's a good one: "I'm allergic to holy water at church. Whereever it touches me, I break out in hives". Hmmmm.....maybe God is trying to tell you something....
emergency room nurse
ECG of the Week – 13th August 2012
ECG of the Week – 13th August 2012
ECG of the Week – 13th August 2012
Presidential Assassinations (Part Two): James A. Garfield
The Assassination Attempt At 9:20 AM on July 2, 1881 James A. Garfield, 20th President of the United States, arrived ...
Continue reading
Continue reading
Crushing Chest pain, but the ECG is not obvious; later there is both RBBB and LBBB
A 63 year old male presented with crushing chest pain. Prehospital BP was 70, but higher in the ED.
Here is the initial ECG at 1033 PM:
Although the ECG is subtle and many or most physicians will not recognize it, it is diagnostic of anterior STEMI. Nothing else has this morphology.
It is important to know that 40-50% of anterior STEMI have upward concavity of the ST segments on the initial ECG.(1, 2, 3)
1. Kosuge M. Am Ht J 1999; 137:522-7. 2. Smith SW. J Em Med 2006;31:69-77 3. Smith SW. Annals of EM 2012;60:45-56
The emergency physician knew that the patient was ill, but did not initially diagnose STEMI. He then noticed the STE in aVL, but not the anterior injury. He did not activate the cath lab immediately, but did immediately consult both an interventionalist and a general cardiologist. They did not see the STEMI, but agreed that this sounded serious and the cath lab was activated.
While waiting for the cath lab, this was recorded at 2303:
At cath, there was severe 3 vessel disease, with an ostial LAD occlusion that was opened. The patient underwent a balloon pump for cardiogenic shock.
Here is an EKG shortly after leaving the cath lab:
He went for CABG x 4.
Here is the initial ECG at 1033 PM:
 |
| There is ST segment elevation in V1 - V3. Is it normal ST elevation? There are several reasons why it is NOT normal STE and is due to LAD occlusion. 1) there is ST segment depression in inferior leads, and STE in aVL 2) there is ST depression in V5 and V6. These two features alone make it diagnostic. But one can also use the formula: 3) The QTc is 448, and thus the formula for differentiating normal anterior STE from anterior STEMI has a value of 24.41. (See the side bar of the front page of this blog for the formula). |
Although the ECG is subtle and many or most physicians will not recognize it, it is diagnostic of anterior STEMI. Nothing else has this morphology.
It is important to know that 40-50% of anterior STEMI have upward concavity of the ST segments on the initial ECG.(1, 2, 3)
1. Kosuge M. Am Ht J 1999; 137:522-7. 2. Smith SW. J Em Med 2006;31:69-77 3. Smith SW. Annals of EM 2012;60:45-56
The emergency physician knew that the patient was ill, but did not initially diagnose STEMI. He then noticed the STE in aVL, but not the anterior injury. He did not activate the cath lab immediately, but did immediately consult both an interventionalist and a general cardiologist. They did not see the STEMI, but agreed that this sounded serious and the cath lab was activated.
While waiting for the cath lab, this was recorded at 2303:
 |
| There is now right bundle branch block, still with pathologic STE in V1-V3 and aVL, and STD in V5 and V6 |
At cath, there was severe 3 vessel disease, with an ostial LAD occlusion that was opened. The patient underwent a balloon pump for cardiogenic shock.
Here is an EKG shortly after leaving the cath lab:
 |
| This appears to me to be sinus rhythm with alternating LBBB and RBBB (not multiform PVCs). There is persistent ST elevation, consistent with poor microvascular reperfusion. The ST/S ratio in the LBBB complexes in V1-V3 is proportionally excessive (>0.25). There is concordant ST elevation in lead V4. There is nearly excessive proportionally discordant ST depression (0.28) in V5 and V6. As for the RBBB complexes |
Crushing Chest pain, but the ECG is not obvious; later there is both RBBB and LBBB
A 63 year old male presented with crushing chest pain. Prehospital BP was 70, but higher in the ED.
Here is the initial ECG at 1033 PM:
Although the ECG is subtle and many or most physicians will not recognize it, it is diagnostic of anterior STEMI. Nothing else has this morphology.
It is important to know that 40-50% of anterior STEMI have upward concavity of the ST segments on the initial ECG.(1, 2, 3)
1. Kosuge M. Am Ht J 1999; 137:522-7. 2. Smith SW. J Em Med 2006;31:69-77 3. Smith SW. Annals of EM 2012;60:45-56
The emergency physician knew that the patient was ill, but did not initially diagnose STEMI. He then noticed the STE in aVL, but not the anterior injury. He did not activate the cath lab immediately, but did immediately consult both an interventionalist and a general cardiologist. They did not see the STEMI, but agreed that this sounded serious and the cath lab was activated.
While waiting for the cath lab, this was recorded at 2303:
At cath, there was severe 3 vessel disease, with an ostial LAD occlusion that was opened. The patient underwent a balloon pump for cardiogenic shock.
Here is an EKG shortly after leaving the cath lab:
He went for CABG x 4.
Here is the initial ECG at 1033 PM:
|
| There is ST segment elevation in V1 - V3. Is it normal ST elevation? There are several reasons why it is NOT normal STE and is due to LAD occlusion. 1) there is ST segment depression in inferior leads, and STE in aVL 2) there is ST depression in V5 and V6. These two features alone make it diagnostic. But one can also use the formula: 3) The QTc is 448, and thus the formula for differentiating normal anterior STE from anterior STEMI has a value of 24.41. (See the side bar of the front page of this blog for the formula). |
Although the ECG is subtle and many or most physicians will not recognize it, it is diagnostic of anterior STEMI. Nothing else has this morphology.
It is important to know that 40-50% of anterior STEMI have upward concavity of the ST segments on the initial ECG.(1, 2, 3)
1. Kosuge M. Am Ht J 1999; 137:522-7. 2. Smith SW. J Em Med 2006;31:69-77 3. Smith SW. Annals of EM 2012;60:45-56
The emergency physician knew that the patient was ill, but did not initially diagnose STEMI. He then noticed the STE in aVL, but not the anterior injury. He did not activate the cath lab immediately, but did immediately consult both an interventionalist and a general cardiologist. They did not see the STEMI, but agreed that this sounded serious and the cath lab was activated.
While waiting for the cath lab, this was recorded at 2303:
|
| There is now right bundle branch block, still with pathologic STE in V1-V3 and aVL, and STD in V5 and V6 |
At cath, there was severe 3 vessel disease, with an ostial LAD occlusion that was opened. The patient underwent a balloon pump for cardiogenic shock.
Here is an EKG shortly after leaving the cath lab:
|
| This appears to me to be sinus rhythm with alternating LBBB and RBBB (not multiform PVCs). There is persistent ST elevation, consistent with poor microvascular reperfusion. The ST/S ratio in the LBBB complexes in V1-V3 is proportionally excessive (>0.25). There is concordant ST elevation in lead V4. There is nearly excessive proportionally discordant ST depression (0.28) in V5 and V6. As for the RBBB complexes |
Crushing Chest pain, but the ECG is not obvious; later there is both RBBB and LBBB
A 63 year old male presented with crushing chest pain. Prehospital BP was 70, but higher in the ED.
Here is the initial ECG at 1033 PM:
Although the ECG is subtle and many or most physicians will not recognize it, it is diagnostic of anterior STEMI. Nothing else has this morphology.
It is important to know that 40-50% of anterior STEMI have upward concavity of the ST segments on the initial ECG.(1, 2, 3)
1. Kosuge M. Am Ht J 1999; 137:522-7. 2. Smith SW. J Em Med 2006;31:69-77 3. Smith SW. Annals of EM 2012;60:45-56
The emergency physician knew that the patient was ill, but did not initially diagnose STEMI. He then noticed the STE in aVL, but not the anterior injury. He did not activate the cath lab immediately, but did immediately consult both an interventionalist and a general cardiologist. They did not see the STEMI, but agreed that this sounded serious and the cath lab was activated.
While waiting for the cath lab, this was recorded at 2303:
At cath, there was severe 3 vessel disease, with an ostial LAD occlusion that was opened. The patient underwent a balloon pump for cardiogenic shock.
Here is an EKG shortly after leaving the cath lab:
He went for CABG x 4.
Here is the initial ECG at 1033 PM:
|
| There is ST segment elevation in V1 - V3. Is it normal ST elevation? There are several reasons why it is NOT normal STE and is due to LAD occlusion. 1) there is ST segment depression in inferior leads, and STE in aVL 2) there is ST depression in V5 and V6. These two features alone make it diagnostic. But one can also use the formula: 3) The QTc is 448, and thus the formula for differentiating normal anterior STE from anterior STEMI has a value of 24.41. (See the side bar of the front page of this blog for the formula). |
Although the ECG is subtle and many or most physicians will not recognize it, it is diagnostic of anterior STEMI. Nothing else has this morphology.
It is important to know that 40-50% of anterior STEMI have upward concavity of the ST segments on the initial ECG.(1, 2, 3)
1. Kosuge M. Am Ht J 1999; 137:522-7. 2. Smith SW. J Em Med 2006;31:69-77 3. Smith SW. Annals of EM 2012;60:45-56
The emergency physician knew that the patient was ill, but did not initially diagnose STEMI. He then noticed the STE in aVL, but not the anterior injury. He did not activate the cath lab immediately, but did immediately consult both an interventionalist and a general cardiologist. They did not see the STEMI, but agreed that this sounded serious and the cath lab was activated.
While waiting for the cath lab, this was recorded at 2303:
|
| There is now right bundle branch block, still with pathologic STE in V1-V3 and aVL, and STD in V5 and V6 |
At cath, there was severe 3 vessel disease, with an ostial LAD occlusion that was opened. The patient underwent a balloon pump for cardiogenic shock.
Here is an EKG shortly after leaving the cath lab:
|
| This appears to me to be sinus rhythm with alternating LBBB and RBBB (not multiform PVCs). There is persistent ST elevation, consistent with poor microvascular reperfusion. The ST/S ratio in the LBBB complexes in V1-V3 is proportionally excessive (>0.25). There is concordant ST elevation in lead V4. There is nearly excessive proportionally discordant ST depression (0.28) in V5 and V6. As for the RBBB complexes |
Crushing Chest pain, but the ECG is not obvious; later there is both RBBB and LBBB
A 63 year old male presented with crushing chest pain. Prehospital BP was 70, but higher in the ED.
Here is the initial ECG at 1033 PM:
Although the ECG is subtle and many or most physicians will not recognize it, it is diagnostic of anterior STEMI. Nothing else has this morphology.
It is important to know that 40-50% of anterior STEMI have upward concavity of the ST segments on the initial ECG.(1, 2, 3)
1. Kosuge M. Am Ht J 1999; 137:522-7. 2. Smith SW. J Em Med 2006;31:69-77 3. Smith SW. Annals of EM 2012;60:45-56
The emergency physician knew that the patient was ill, but did not initially diagnose STEMI. He then noticed the STE in aVL, but not the anterior injury. He did not activate the cath lab immediately, but did immediately consult both an interventionalist and a general cardiologist. They did not see the STEMI, but agreed that this sounded serious and the cath lab was activated.
While waiting for the cath lab, this was recorded at 2303:
At cath, there was severe 3 vessel disease, with an ostial LAD occlusion that was opened. The patient underwent a balloon pump for cardiogenic shock.
Here is an EKG shortly after leaving the cath lab:
He went for CABG x 4.
Here is the initial ECG at 1033 PM:
|
| There is ST segment elevation in V1 - V3. Is it normal ST elevation? There are several reasons why it is NOT normal STE and is due to LAD occlusion. 1) there is ST segment depression in inferior leads, and STE in aVL 2) there is ST depression in V5 and V6. These two features alone make it diagnostic. But one can also use the formula: 3) The QTc is 448, and thus the formula for differentiating normal anterior STE from anterior STEMI has a value of 24.41. (See the side bar of the front page of this blog for the formula). |
Although the ECG is subtle and many or most physicians will not recognize it, it is diagnostic of anterior STEMI. Nothing else has this morphology.
It is important to know that 40-50% of anterior STEMI have upward concavity of the ST segments on the initial ECG.(1, 2, 3)
1. Kosuge M. Am Ht J 1999; 137:522-7. 2. Smith SW. J Em Med 2006;31:69-77 3. Smith SW. Annals of EM 2012;60:45-56
The emergency physician knew that the patient was ill, but did not initially diagnose STEMI. He then noticed the STE in aVL, but not the anterior injury. He did not activate the cath lab immediately, but did immediately consult both an interventionalist and a general cardiologist. They did not see the STEMI, but agreed that this sounded serious and the cath lab was activated.
While waiting for the cath lab, this was recorded at 2303:
|
| There is now right bundle branch block, still with pathologic STE in V1-V3 and aVL, and STD in V5 and V6 |
At cath, there was severe 3 vessel disease, with an ostial LAD occlusion that was opened. The patient underwent a balloon pump for cardiogenic shock.
Here is an EKG shortly after leaving the cath lab:
|
| This appears to me to be sinus rhythm with alternating LBBB and RBBB (not multiform PVCs). There is persistent ST elevation, consistent with poor microvascular reperfusion. The ST/S ratio in the LBBB complexes in V1-V3 is proportionally excessive (>0.25). There is concordant ST elevation in lead V4. There is nearly excessive proportionally discordant ST depression (0.28) in V5 and V6. As for the RBBB complexes |
EMRAP 2012 Product Demo:iCare Ocular Tonometer We are trying…
EMRAP 2012 Product Demo:iCare Ocular Tonometer
We are trying out a potential new addition to the EM:RAP family. There are so many products out there for use in the ED we thought we would try and provide a little info on some of them. We receive no revenue from these companies and we are not endorsing any of the products in these videos.
Fluidos iniciales en el trauma: ¿salvan a alguien?
Antes de saber cómo ayudar a un paciente, debemos aprender a no dañarlo. Acá va un primer consejo.
E’ solo un ascesso…
Avere mal di denti è di per sé una grande sofferenza, ma i problemi sicuramente aumentano se succede di notte o nei week end. Il pronto soccorso diventa allora l'ultima-unica spiaggia cui...
[[ This is a content summary only. Visit my website for full links, other content, and more! ]]
[[ This is a content summary only. Visit my website for full links, other content, and more! ]]
E’ solo un ascesso…
Avere mal di denti è di per sé una grande sofferenza, ma i problemi sicuramente aumentano se succede di notte o nei week end. Il pronto soccorso diventa allora l'ultima-unica spiaggia cui...
[[ This is a content summary only. Visit my website for full links, other content, and more! ]]
[[ This is a content summary only. Visit my website for full links, other content, and more! ]]
E’ solo un ascesso…
Avere mal di denti è di per sé una grande sofferenza, ma i problemi sicuramente aumentano se succede di notte o nei week end. Il pronto soccorso diventa allora l'ultima-unica spiaggia cui...
[[ This is a content summary only. Visit my website for full links, other content, and more! ]]
[[ This is a content summary only. Visit my website for full links, other content, and more! ]]
Crowding & Boarding Review in Health Affairs
Rabin, E., K. Kocher, et al. "Solutions To Emergency Department 'Boarding' And Crowding Are Underused And May Need To Be Legislated." Health Affairs. 2012 Aug; 31(8): 1757-1766.doi: 10.1377/hlthaff.2011.0786Health Aff August 2012 vol. 31 no. 8 1757-1766
It's like your paper was boarding, too RT@mdaware after 366 days of peer review, our crowding/boarding article is out: content.healthaffairs.org/content/31/8/1...
-- borborygmi (@nickgenes) August 6, 2012
Crowding & Boarding Review in Health Affairs
Rabin, E., K. Kocher, et al. "Solutions To Emergency Department 'Boarding' And Crowding Are Underused And May Need To Be Legislated." Health Affairs. 2012 Aug; 31(8): 1757-1766.doi: 10.1377/hlthaff.2011.0786Health Aff August 2012 vol. 31 no. 8 1757-1766
It's like your paper was boarding, too RT@mdaware after 366 days of peer review, our crowding/boarding article is out: content.healthaffairs.org/content/31/8/1...
-- borborygmi (@nickgenes) August 6, 2012
Crowding & Boarding Review in Health Affairs
Rabin, E., K. Kocher, et al. "Solutions To Emergency Department 'Boarding' And Crowding Are Underused And May Need To Be Legislated." Health Affairs. 2012 Aug; 31(8): 1757-1766.doi: 10.1377/hlthaff.2011.0786Health Aff August 2012 vol. 31 no. 8 1757-1766
It's like your paper was boarding, too RT@mdaware after 366 days of peer review, our crowding/boarding article is out: content.healthaffairs.org/content/31/8/1...
-- borborygmi (@nickgenes) August 6, 2012
When doctors disagree
A recent study ( http://www.ncbi.nlm.nih.gov/pubmed/22849819) talked about when disagreements between the ER diagnosis and the inpatient diagnosis. It goes on to say how the ER over-diagnosed pneumonia and urinary infections in older patients. All I have to say is, "You bet I over diagnosis." The ER is like a fish bowl. It is a clear glass bowl that every one can look into and criticize what you are doing but they never come in to try it themselves. This criticism usually comes after all the crap has been clean off the fan. I feel (and know because I do it) that a lot of these over-diagnosis come from just trying to get the patient care. If I call a hospitalist with an admission, they ask "what is the diagnosis?" Many times I want to tell them – "I do not have a firm diagnosis but they just do not look good." The hospitalist would laugh and tell me to call them back when I have a real diagnosis. So what do I do to avoid this, I over-diagnosis. In the ER, we call it throwing out a big net. We go and see patient. We come out of the room thinking the patient needs to be admitted but I cannot quite put my finger on why. We then throw out a big net ordering a lot of tests hoping that something comes back positive so we have a "reason" to admit the patient. The easiest are pneumonia and urinary infections. Almost all old people have a dirty urine or something on their chest xray that I can construe to be a pneumonia. Once I have one of these, I have an admission. Is this the best practice?? No. But it is what we have to do in this environment. I have to find something to get the patient admitted. There is no more admitting the patient just to watch them. The hospital and doctors will not get paid without a firm diagnosis. Also, I do not get penalized for over-diagnosing. I get penalized for missing that 1 in a million case. Old people like to hid bad disease with only small complaints. They also like to die quickly if they are missed. We find a diagnosis, give them antibiotics, and admit them. As long as the pay structure is how it is and malpractice is how it is, there will always be ER over-diagnosis. And once the ER has stabilized the train wreck patient, the rest of medicine will always critique a day later why I did not do this or that.
Busting the myth: The 10% cephalosporin-penicillin cross-reactivity risk
To give or not to give a cephalosporin in penicillin-allergic patients?
It turns out that prior to 1980, penicillins and cephaloporins were often produced using the same fungus and the chance for contamination during the manufacturing process was high. The belief was that the beta-lactam ring similarities must be the cause. How wrong we were.
More recent studies have determined that the actual risk of cross-reactivity relates more to a side chain similarity and probably not the beta-lactam ring at all. Therefore it makes sense that if a penicillin and a cephalosporin share that particular (R-1) side-chain similarity, the risk of cross-reactivity is increased. Such is the case with amoxicillin or ampicillin with:
- 1st generation cephalosporins: cefadroxil, cefatrizine, cephalexin, cephradine
- 2nd generation cephalosporins: cefaclor, cefprozil
- Overall cross-reactivity rate between cephalosporins and penicillins in patients reporting a penicillin allergy = 1%.
- Overall cross-reavtivity rate in patients with a confirmed penicillin allergy = 2.5%.
Other key findings to note:
- The true incidence of an allergy to penicillin in patients believed to have such allergy is <10% (it's like we have a built in 10-fold safety factor).
- Cross-reactivity between penicillins and MOST 1st and 2nd generation cephalosporins is negligible.
- Cross-reactivity between penicillins and ALL 3rd and 4th generation cephalosporins is negligible.
- If a patient has an allergy to amoxicillin or ampicillin, avoid cefadroxil, cefaclor, cefatrizine, cefprozil, cephalexin, and cephradine.
Bottom Line:
You can feel comfortable clicking past the flashing allergy alert as you enter that ceftriaxone order in your patient with a documented penicillin allergy. If the patient has an allergic reaction, it's more likely a unique allergy to that cephalosporin than any cross-reactivity with a penicillin.
References:
Campagna JD, Bond MC, Schabelman E, Hayes BD. The use of cephalosporins in penicillin-allergic patients: A literature review. J Emerg Med. 2012;42(5):612-20. Pubmed .
Busting the myth: The 10% cephalosporin-penicillin cross-reactivity risk
To give or not to give a cephalosporin in penicillin-allergic patients?
It turns out that prior to 1980, penicillins and cephaloporins were often produced using the same fungus and the chance for contamination during the manufacturing process was high. The belief was that the beta-lactam ring similarities must be the cause. How wrong we were.
More recent studies have determined that the actual risk of cross-reactivity relates more to a side chain similarity and probably not the beta-lactam ring at all. Therefore it makes sense that if a penicillin and a cephalosporin share that particular (R-1) side-chain similarity, the risk of cross-reactivity is increased. Such is the case with amoxicillin or ampicillin with:
- 1st generation cephalosporins: cefadroxil, cefatrizine, cephalexin, cephradine
- 2nd generation cephalosporins: cefaclor, cefprozil
- Overall cross-reactivity rate between cephalosporins and penicillins in patients reporting a penicillin allergy = 1%.
- Overall cross-reavtivity rate in patients with a confirmed penicillin allergy = 2.5%.
Other key findings to note:
- The true incidence of an allergy to penicillin in patients believed to have such allergy is <10% (it's like we have a built in 10-fold safety factor).
- Cross-reactivity between penicillins and MOST 1st and 2nd generation cephalosporins is negligible.
- Cross-reactivity between penicillins and ALL 3rd and 4th generation cephalosporins is negligible.
- If a patient has an allergy to amoxicillin or ampicillin, avoid cefadroxil, cefaclor, cefatrizine, cefprozil, cephalexin, and cephradine.
Bottom Line:
You can feel comfortable clicking past the flashing allergy alert as you enter that ceftriaxone order in your patient with a documented penicillin allergy. If the patient has an allergic reaction, it's more likely a unique allergy to that cephalosporin than any cross-reactivity with a penicillin.
References:
Campagna JD, Bond MC, Schabelman E, Hayes BD. The use of cephalosporins in penicillin-allergic patients: A literature review. J Emerg Med. 2012;42(5):612-20. Pubmed .
Busting the myth: The 10% cephalosporin-penicillin cross-reactivity risk
To give or not to give a cephalosporin in penicillin-allergic patients?
It turns out that prior to 1980, penicillins and cephaloporins were often produced using the same fungus and the chance for contamination during the manufacturing process was high. The belief was that the beta-lactam ring similarities must be the cause. How wrong we were.
More recent studies have determined that the actual risk of cross-reactivity relates more to a side chain similarity and probably not the beta-lactam ring at all. Therefore it makes sense that if a penicillin and a cephalosporin share that particular (R-1) side-chain similarity, the risk of cross-reactivity is increased. Such is the case with amoxicillin or ampicillin with:
- 1st generation cephalosporins: cefadroxil, cefatrizine, cephalexin, cephradine
- 2nd generation cephalosporins: cefaclor, cefprozil
- Overall cross-reactivity rate between cephalosporins and penicillins in patients reporting a penicillin allergy = 1%.
- Overall cross-reavtivity rate in patients with a confirmed penicillin allergy = 2.5%.
Other key findings to note:
- The true incidence of an allergy to penicillin in patients believed to have such allergy is <10% (it's like we have a built in 10-fold safety factor).
- Cross-reactivity between penicillins and MOST 1st and 2nd generation cephalosporins is negligible.
- Cross-reactivity between penicillins and ALL 3rd and 4th generation cephalosporins is negligible.
- If a patient has an allergy to amoxicillin or ampicillin, avoid cefadroxil, cefaclor, cefatrizine, cefprozil, cephalexin, and cephradine.
Bottom Line:
You can feel comfortable clicking past the flashing allergy alert as you enter that ceftriaxone order in your patient with a documented penicillin allergy. If the patient has an allergic reaction, it's more likely a unique allergy to that cephalosporin than any cross-reactivity with a penicillin.
References:
Campagna JD, Bond MC, Schabelman E, Hayes BD. The use of cephalosporins in penicillin-allergic patients: A literature review. J Emerg Med. 2012;42(5):612-20. Pubmed .
Welcome to the blog team: Bryan Hayes, PharmD
Bryan Hayes, PharmD, DABAT
On a quick web search, I think Bryan may be the first ED clinical pharmacist ever to have a meducation blog!
Here is a little blurb bio about Bryan:
- Clinical Assistant Professor, University of Maryland (UM) Schools of Pharmacy and Medicine
- Clinical Pharmacy Specialist, EM & Toxicology, UM Medical Center
Welcome to the blog team: Bryan Hayes, PharmD
Bryan Hayes, PharmD, DABAT
On a quick web search, I think Bryan may be the first ED clinical pharmacist ever to have a meducation blog!
Here is a little blurb bio about Bryan:
- Clinical Assistant Professor, University of Maryland (UM) Schools of Pharmacy and Medicine
- Clinical Pharmacy Specialist, EM & Toxicology, UM Medical Center
Welcome to the blog team: Bryan Hayes, PharmD
Bryan Hayes, PharmD, DABAT
On a quick web search, I think Bryan may be the first ED clinical pharmacist ever to have a meducation blog!
Here is a little blurb bio about Bryan:
- Clinical Assistant Professor, University of Maryland (UM) Schools of Pharmacy and Medicine
- Clinical Pharmacy Specialist, EM & Toxicology, UM Medical Center
Clinical skills – Does anyone use Ophthalmoscopes anymore?
This may well turn into a bit of rant, but that’s OK….why? Well that would just mean that it’s turning back into what it started as…which was a rant, but in true education style I have paused on my rant and reflected…and now I’m back to ranting.
So, one of your colleagues tells you about a lady in her 30s turns up to the ED with a really high BP. Really high, like >250 systolic. In Virchester the first, second, third and if it’s after 7pm or the weekend the fourth question is ‘what have they taken’, but on this occasion the answer really does seem to be nothing.
Hmmm, so we are really looking for endogenous causes of a really high BP, (but secretly wondering whether to ask the drugs question again later). Key to future decisions about this will be an assessment of the end organ damage associated with a really high BP. So where shall we look? Well the eyes of course as they are the window to the cardiovascular system, the fundus is the one place in the body where we can actually see the vasculature in detail, and it’s an essential component of the exam for hypertension.
So, you send a succession of docs off to have a look at the fundi and the answer comes back that they are normal. Really? Well I must alter my thoughts then! A normal exam in the presence of hypertension at this level would seriously question the diagnosis and we are back to thinking about ultra-acute conditions such as drug ingestion. Except we are not. The patient has gross retinal changes with flame haemorrhages all over the retina, they’ve just been missed. This is important as we now have clear evidence of end organ damage and this now seems very unlikely to be something that’s going to go away on it’s own and we need to intervene now, but why was this important finding missed? Time for a bit of team reflection here and the results were surprising. Many docs just don’t use direct ophthalmoscopy as a skill in the ED much anymore and if they do then the sole question seems to be ‘does this patient have papilloedema?’ The richness of data available in other parts of the retina seems to have been lost in the mists of time and undergraduate OSCEs, and I’m not entirely sure that we are that good at picking up papilloedema to be honest.
[Ed - The OSCE rant is one for another day - students can go through the process but not actually notice what is going on. A bit like doing a driving test and looking in the mirror before you pull out, but not being able to spot the truck hurtling towards you in the reflection.]
So, you go and observe your colleagues examining the eye and it’s really interesting. Wrong hand, wrong eye, wrong position, etc. and you enquire…how often do you do this, and the answer is virtually never. It seems to be a skill that is no longer practiced in hospital based clinical medicine. I can’t speak about primary care but it does seem that a significant number of primary care docs refer patients to Optometrists for an opinion, so my impression is that this is probably not just a hospital issue.
Now, at this point I was into full rant about the quality of medical eduction & clinical practice but you have to ask….is this a skill that all docs need? How often is it a ‘game changer’ of a technique that really alters what you do to a patient in the ED and I must admit that I am struggling to find many situations (apart from accelerated hypertension) where it matters, but I’m looking for more! (Ed – vein occlusion, arterial occlusion maybe???)
So what can we do? Well there are options of course. We can teach and practice (Ed – love it), and we can belittle our colleagues who cannot do it (Ed – not so sure now), or we can perhaps look to make it easier. Mrs C, also a doc, is in her own words hopeless with a direct Ophthalmoscope and wonders how we manage to see anything at all, but that’s because she is an Ophthalmologist and would not dream of using one preferring the use of a x78 lens with a slit lamp or an x20 lens with an indirect. These give you binocular images which makes picking up all the other things we might be interested in (retinal tear/bleed/detachment) SO much easier!
There are potential solutions out there of course. A paper in the EMJ looked at the use of the pan-Ophthalmoscope (see pic) and it showed some benefit in a small study, but I’d love to hear from others who are actually using it.
The other alternative is that we could just abandon the time and effort required to effectively perform this relatively simple technique in favour of learning how to use a something more exciting and thrilling like a new chest drain, cric set or thoracotomy saw, but I’m not so sure. All these things are important and it’s unfair to make a comparison, but I would like to raise a little cheer for the basics of clinical examination. As EPs, like family physicians we rely on our basic clinical skills and acumen. We should do our best to retain and teach them.
And this case – can’t tell you as confidentiality etc, but as a learning moment it was super. One really great case with fantastic findings will (I hope) inspire all involved to keep using that rather expensive Ophthalmoscope hung on the walls in every cubicle. It’s more than a light for checking pupillary responses…
Rant – Reflection – Rant over 
vb
Simon Carley