southerndoc

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25 year old female presents by way of her PMD. Only complaint was multiple joint pains. Her PMD reports she was febrile to 102, tachycardic to 140, tachypneic at 30, and hypoxic on room air. A chest x-ray obtained there demonstrated "wedge deformity concerning for pulmonary embolism."

She denies chest pain and shortness of breath.

She arrives on a non-rebreather with an O2 saturation of 100%. I take her off the non-rebreather to assess this reported hypoxia (which the PMD never documented a number) and decide to place her back on the mask when her SpO2 rapidly dropped to 62% with a good pleth.

Upon further questioning, I find that she has a history of sickle cell disease. She has no recent travel, no immobility, has no history of adenocarcinomatous cancer, and no familial history of DVT's or PE's. She does report that she is currently taking birth control pills. Her social history is unremarkable for tobacco, alcohol, and drug abuse.

So, what would be your initial impression with her presentation? She was sent in for a rule out PE! When I saw the transfer sheet from the PMD, I nearly fell in the floor. Had he never heard of acute chest syndrome? Perhaps she is having a pulmonary infarction secondary to that.

I explain to the patient our suspicions. The nurses get an IV and we administer a liter of normal saline followed by 1/2 normal saline. She is given 1 gram of ceftriaxone and 100 mg of doxycycline IV. The respiratory therapists start giving her albuterol treatments.

My attending, the hematology fellow, and I decide to send her for the PE protocol CT to see if she has an infarction. Also, radiology had official read her chest x-ray full of infiltrates as "pulmonary edema with bilateral small pleural effusions." Obviously they did not read my comment in the order about the patient being febrile and a sickler.

Her lab data comes back with a WBC count of 18 with 80% segs and 10% bands. Her hemoglobin is 5, with a baseline of 9-10. Labs drawn in her PMD's office -- just 5 hours prior (don't ask why he kept her so long) demonstrated a hemoglobin of 8. Her reticulocyte count is 15. Her troponin (sent because of the tachycardia and some rate related ST depression in the lateral leads) was slightly positive at 0.5 (normal <0.04 at my institution).

Obviously with her level of distress she's MICU bound. I call the MICU resident and the hematology fellow. The hematology fellow agrees that it sounds like acute chest and begins to arrange for an exchange transfusion. I get a Quinten from upstairs and go to place it, but the patient refuses. She doesn't want a transfusion or an exchange transfusion, despite me, the MICU resident, my attending, and the hematology fellow advising her of the mortality risk without it.

What happens when I call the PMD? He insists that it's a PE and that she be heparinized! I started to ask if he had ever heard of acute chest syndrome, but bit my tongue. Her CT was eventually done, and it demonstrated bilateral consolidation pneumoniae with small pleural effusions... no evidence of pulmonary embolism. While the patient was in the scanner, I thought of something and mentioned to the attending that doing the CT probably wasn't the best thing. The hyperosmolarity of the contrast could worsen sickling in her.

I guess I'm posting this for all the newbs out there. If you see a sickler with any evidence of chest pain, shortness of breath, fever, cough, hypoxia, or tachypnea, the first thought through your mind should be acute chest syndrome and not PE. ACS has a high mortality rate, and early antibiotics, aggressive oxygen and pulmonary toilet are necessary to prevent rapid progression. This is the only patient I've had with acute chest who was severe enough to need an exchange transfusion, and for the life of me I cannot reason why she wouldn't allow it.
 

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Here's my "I am up too late, I'm only EMT-trained, and I maybe shouldn't ask this" kind of question:

Who gives two tugs on Aunt Matilda's tea-cozy what the PMD thinks, once the patient sets foot in the ED for the purpose of seeking care from trained and experienced emergency peeps? This ain't no PE. You gave the patient a view of your thought process. Could you maybe help illuminate the reasons for biting your tongue, and letting the PMD beat the PE drum? It would be educational, I think, for those of us a few years behind the working providers out there.

Maybe you simply sensed there was no point in having that conversation?
 
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Febrifuge said:
Who gives two tugs on Aunt Matilda's tea-cozy what the PMD thinks, once the patient sets foot in the ED for the purpose of seeking care from trained and experienced emergency peeps? This ain't no PE. You gave the patient a view of your thought process. Could you maybe help illuminate the reasons for biting your tongue, and letting the PMD beat the PE drum? It would be educational, I think, for those of us a few years behind the working providers out there.
The point was the patient was kept in the PMD's office (an infirmary actually) for more than 7 hours before being transferred to the ED. Appropriate antibiotics weren't given during this time.
 
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southerndoc said:
25 year old female presents by way of her PMD. Only complaint was multiple joint pains. Her PMD reports she was febrile to 102, tachycardic to 140, tachypneic at 30, and hypoxic on room air. A chest x-ray obtained there demonstrated "wedge deformity concerning for pulmonary embolism."

She denies chest pain and shortness of breath.

She arrives on a non-rebreather with an O2 saturation of 100%. I take her off the non-rebreather to assess this reported hypoxia (which the PMD never documented a number) and decide to place her back on the mask when her SpO2 rapidly dropped to 62% with a good pleth.

Upon further questioning, I find that she has a history of sickle cell disease. She has no recent travel, no immobility, has no history of adenocarcinomatous cancer, and no familial history of DVT's or PE's. She does report that she is currently taking birth control pills. Her social history is unremarkable for tobacco, alcohol, and drug abuse.

So, what would be your initial impression with her presentation? She was sent in for a rule out PE! When I saw the transfer sheet from the PMD, I nearly fell in the floor. Had he never heard of acute chest syndrome? Perhaps she is having a pulmonary infarction secondary to that.

I explain to the patient our suspicions. The nurses get an IV and we administer a liter of normal saline followed by 1/2 normal saline. She is given 1 gram of ceftriaxone and 100 mg of doxycycline IV. The respiratory therapists start giving her albuterol treatments.

My attending, the hematology fellow, and I decide to send her for the PE protocol CT to see if she has an infarction. Also, radiology had official read her chest x-ray full of infiltrates as "pulmonary edema with bilateral small pleural effusions." Obviously they did not read my comment in the order about the patient being febrile and a sickler.

Her lab data comes back with a WBC count of 18 with 80% segs and 10% bands. Her hemoglobin is 5, with a baseline of 9-10. Labs drawn in her PMD's office -- just 5 hours prior (don't ask why he kept her so long) demonstrated a hemoglobin of 8. Her reticulocyte count is 15. Her troponin (sent because of the tachycardia and some rate related ST depression in the lateral leads) was slightly positive at 0.5 (normal <0.04 at my institution).

Obviously with her level of distress she's MICU bound. I call the MICU resident and the hematology fellow. The hematology fellow agrees that it sounds like acute chest and begins to arrange for an exchange transfusion. I get a Quinten from upstairs and go to place it, but the patient refuses. She doesn't want a transfusion or an exchange transfusion, despite me, the MICU resident, my attending, and the hematology fellow advising her of the mortality risk without it.

What happens when I call the PMD? He insists that it's a PE and that she be heparinized! I started to ask if he had ever heard of acute chest syndrome, but bit my tongue. Her CT was eventually done, and it demonstrated bilateral consolidation pneumoniae with small pleural effusions... no evidence of pulmonary embolism. While the patient was in the scanner, I thought of something and mentioned to the attending that doing the CT probably wasn't the best thing. The hyperosmolarity of the contrast could worsen sickling in her.

I guess I'm posting this for all the newbs out there. If you see a sickler with any evidence of chest pain, shortness of breath, fever, cough, hypoxia, or tachypnea, the first thought through your mind should be acute chest syndrome and not PE. ACS has a high mortality rate, and early antibiotics, aggressive oxygen and pulmonary toilet are necessary to prevent rapid progression. This is the only patient I've had with acute chest who was severe enough to need an exchange transfusion, and for the life of me I cannot reason why she wouldn't allow it.
Southern,

I'm going to criticize you a little here and I hope you won't take offense. My reason is to suggest ways to for everyone on the board to handle it when a 'foreign attending" wants residents to do something that really isn't wise. In this case I would have:
1. Called the attending and say. "You're very smart to recognize that the patient has a pulmonary infarct. But in this case i think the cause of the infarct is not a PE but rather a sickle vasoocclusive crisis called a "acute chest syndrome." The reason I'm calling you is that my textbook *fill in the title * says that imaging dye is contraindicated in this case since it may worsen the vasoocclusion. Why don't we treat for pneumonia and acute chest sysdrome."
2. Wouldn't give dye. If necessary kick it up to your ED attending, that's his job.

p.s. Probably any FP or IM attending has heard of the diagnosis, but it may have been years since they thought about it. It's not only OK, but your duty to bring up weird stuff.

BTW without chest pain probably wouldn't have made chest syndrome diagnosis since pulmonary infarcts hurt. Would have gone with pneumonia and Bone VOCS.
 
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BKN said:
Southern,

I'm going to criticize you a little here and I hope you won't take offense. My reason is to suggest ways to for everyone on the board to handle it when a 'foreign attending" wants residents to do something that really isn't wise. In this case I would have:
1. Called the attending and say. "You're very smart to recognize that the patient has a pulmonary infarct. But in this case i think the cause of the infarct is not a PE but rather a sickle vasoocclusive crisis called a "acute chest syndrome." The reason I'm calling you is that my textbook *fill in the title * says that imaging dye is contraindicated in this case since it may worsen the vasoocclusion. Why don't we treat for pneumonia and acute chest sysdrome."
2. Wouldn't give dye. If necessary kick it up to your ED attending, that's his job.

p.s. Probably any FP or IM attending has heard of the diagnosis, but it may have been years since they thought about it. It's not only OK, but your duty to bring up weird stuff.

BTW without chest pain probably wouldn't have made chest syndrome diagnosis since pulmonary infarcts hurt. Would have gone with pneumonia and Bone VOCS.
I probably should have said something to the PMD. My attending and hematology were ok in doing the CT to see if there was a pulmonary infarct, plus there was a discrepancy on the official read of the chest x-ray. In retrospect, and I fault myself for not thinking of this sooner, a hyperosmolar contrast dye probably wasn't the wisest thing to administer to a patient with active sickling.

By the way, that wasn't criticizing me.
 

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What about when they do have a PE? Had a chronic sickler who was complaining of a new chest pain and was noted to be mildly hypoxic. Spund her chest and she did have a moderately sized PE. Suppose I could have VQ scanned her . . .
 

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southerndoc said:
The point was the patient was kept in the PMD's office (an infirmary actually) for more than 7 hours before being transferred to the ED. Appropriate antibiotics weren't given during this time.
Aha, so that was my "I'm up too late, and I totally missed the point" question. Sigh. That'll happen sometimes, I reckon. :laugh: Sorry 'bout that.
 

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Seaglass said:
What about when they do have a PE? Had a chronic sickler who was complaining of a new chest pain and was noted to be mildly hypoxic. Spund her chest and she did have a moderately sized PE. Suppose I could have VQ scanned her . . .
In my experience given the clinical situation posted I think that acute chest and PE are both on the differential in your sickle cell patient with fever, chest pain, hypoxia, and an abnormal CXR (which will make your VQ scan more difficult to interpret). Obviously the CBC favors VOC/acute chest/ pulmonary infarction over the PE. (Sickle cell itself and the OCP use I guess are your PE risk factors). I think you can pursue the VQ (with the caveat above plus uf you truly have infarction you will have VQ deficits there). It may actually also be helpful to consider a high resolution CT without contrast as this may better characterize your lung findings.

We had a similar case when I was a resident although the hemoglobin was actually around baseline and acute chest was favored as the working diagnosis by the EM resident and attending. The patient decompensated more and got intubated by me pretty quickly after that while still in the department. EKG actually showed characteristic changes (which you so rarely see). Hemodynamics actually improved after intubation and some volume. Antibiotics had already been started by the EP. We opted to anticoagulate with a heparin drip (because of the EKG changes and something feeling more like PE--very unspecific) and got nuclear to come in and do the VQ which had a clear ventilation-perfusion mismatch consistent with PE. There was a lot of discussion (IR had come in thinking we perhaps needed intralesional lytics) but she was ultimately much better and eventually extubated. Interestingly she ended up also having a Protein C and Protein S deficiency as well. [And apparently had a family history of that which no one (including her) knew]
 
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V/Q was not an option in this patient due to the massive consolidations that were present in her lungs. That would automatically make it a high probability scan.

Interesting enough, this patient had a CT PE protocol last winter when she presented with chest pain and shortness of breath. Looking through the records, that presentation was not consistent with acute chest syndrome since she was not febrile, hypoxic, etc.

I guess my main beef out of all this situation is the delay in antibiotics.

By the way, if this patient did have a PE, what would be the standard treatment? Is heparin indicated? It doesn't seem to be from a traditional clot in a sickler, but would instead be from a mass of sickled cells. This is considering the patient had no risk factors for DVT (prolonged immobilization, lower extremity trauma, airline flights, etc.).
 

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I agree with your comments BKN about taking the time to explain to the PMD your findings on your evaluation. Its all in the wording of how you present it. Saying you are wrong, the patient has this....isnt going to go far. Saying something like given x,y,z (adding the new info the PMD didnt have like cxr, labs) the patient has this and going over the plan in a confident manner will go much further. And will keep the PMD referring to your ED without losing face.

I also think some of the PMD referrals can trap you, like when the triage sheet or PMD referral says "sent from PMD to r/o PE". Even if you are sure it isnt, if she did have a PE and you didnt scan her, it would be difficult to defend yourself. You'd have to document really well explaining why you disagree with that diagnosis. Most of the PMD that refer to us will just write chest pain, please eval/treat. But those that I see with a r/o ______ (insert badness here), drive me crazy....especially when they are WAY off!
 

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southerndoc said:
I guess my main beef out of all this situation is the delay in antibiotics.
You are right. The delay in antiobiotics was not appropriate. Just an observation, when I was doing my ICU time, often we would not get called about the patient until the patient had been in the department for 6 hours or more, septic, and no antibiotics given. Education and system changes are key to fixing this problem, and giving our patients the best care possible.

Would a echocardiogram help to rule out a PE? With her symptoms, if it were a PE, it would likely to have been a fairly big one, and should show some effects on the r ventricle?
 
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Annette said:
Would a echocardiogram help to rule out a PE? With her symptoms, if it were a PE, it would likely to have been a fairly big one, and should show some effects on the r ventricle?
I did one at the bedside. No effusions, good LV function (EF~70%), a some RV dilation, but it wasn't larger than the LV. RV pressure was 46 mmHg. No visible clots in the RV (I normally don't mention this, but I have seen them before!).

Lower extremity duplexes (bedside again) were negative.

One of the advantages of my program is that we ultrasound everybody.
 

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southerndoc said:
25 year old female presents by way of her PMD. Only complaint was multiple joint pains. Her PMD reports she was febrile to 102, tachycardic to 140, tachypneic at 30, and hypoxic on room air. A chest x-ray obtained there demonstrated "wedge deformity concerning for pulmonary embolism."

She denies chest pain and shortness of breath.

She arrives on a non-rebreather with an O2 saturation of 100%. I take her off the non-rebreather to assess this reported hypoxia (which the PMD never documented a number) and decide to place her back on the mask when her SpO2 rapidly dropped to 62% with a good pleth.

Upon further questioning, I find that she has a history of sickle cell disease. She has no recent travel, no immobility, has no history of adenocarcinomatous cancer, and no familial history of DVT's or PE's. She does report that she is currently taking birth control pills. Her social history is unremarkable for tobacco, alcohol, and drug abuse.

So, what would be your initial impression with her presentation? She was sent in for a rule out PE! When I saw the transfer sheet from the PMD, I nearly fell in the floor. Had he never heard of acute chest syndrome? Perhaps she is having a pulmonary infarction secondary to that.

I explain to the patient our suspicions. The nurses get an IV and we administer a liter of normal saline followed by 1/2 normal saline. She is given 1 gram of ceftriaxone and 100 mg of doxycycline IV. The respiratory therapists start giving her albuterol treatments.

My attending, the hematology fellow, and I decide to send her for the PE protocol CT to see if she has an infarction. Also, radiology had official read her chest x-ray full of infiltrates as "pulmonary edema with bilateral small pleural effusions." Obviously they did not read my comment in the order about the patient being febrile and a sickler.

Her lab data comes back with a WBC count of 18 with 80% segs and 10% bands. Her hemoglobin is 5, with a baseline of 9-10. Labs drawn in her PMD's office -- just 5 hours prior (don't ask why he kept her so long) demonstrated a hemoglobin of 8. Her reticulocyte count is 15. Her troponin (sent because of the tachycardia and some rate related ST depression in the lateral leads) was slightly positive at 0.5 (normal <0.04 at my institution).

Obviously with her level of distress she's MICU bound. I call the MICU resident and the hematology fellow. The hematology fellow agrees that it sounds like acute chest and begins to arrange for an exchange transfusion. I get a Quinten from upstairs and go to place it, but the patient refuses. She doesn't want a transfusion or an exchange transfusion, despite me, the MICU resident, my attending, and the hematology fellow advising her of the mortality risk without it.

What happens when I call the PMD? He insists that it's a PE and that she be heparinized! I started to ask if he had ever heard of acute chest syndrome, but bit my tongue. Her CT was eventually done, and it demonstrated bilateral consolidation pneumoniae with small pleural effusions... no evidence of pulmonary embolism. While the patient was in the scanner, I thought of something and mentioned to the attending that doing the CT probably wasn't the best thing. The hyperosmolarity of the contrast could worsen sickling in her.

I guess I'm posting this for all the newbs out there. If you see a sickler with any evidence of chest pain, shortness of breath, fever, cough, hypoxia, or tachypnea, the first thought through your mind should be acute chest syndrome and not PE. ACS has a high mortality rate, and early antibiotics, aggressive oxygen and pulmonary toilet are necessary to prevent rapid progression. This is the only patient I've had with acute chest who was severe enough to need an exchange transfusion, and for the life of me I cannot reason why she wouldn't allow it.
Truthfully, I am not entirely sure that the PMD was completely off base with his diagnosis. After all, nobody seems to have a real clear idea what the true etiology behind the acute chest sydrome is (or what the best treatment is for that matter...except that ABx, nebs, and hemotransfusion seem to help... at least most of the time). Most do seem to think that it may involve a occlusion/embolism etiology with a little bit of the bugs (infection), but hey thats just my take on it and we are certainly anything but experts here where I work, except that it seems that there are a lot of sicklers in the south bronx and this does seem to afflict them rather often (most common cause of death?). Anyway, you are right Southerndoc. Regardless of whether you have heard of the sydrome or for that matter understand the pathophysiology behind it (I certainly wouldn't claim to), if you have a patient that is febrile, tachy, hypoxic, and borderline to frank unstable and you don't think that patient needs some sort of bug juice before their trip upstairs you probably need your head checked out or at the very least the ego draining experience of having a resident point out something that you should have already known. (you have a blanket excuse for ignorance or stupidity if you are a resident or student...)
 

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I agree with several of the others here. It is not entirely ridiculous to think of PE in a sickler.

While 102 is a little high for a PE fever, PEs manifest with tachypnea, tachycardia, hypoxia and fever.

I understand your frustration with the PMD though. But remember, we, as EMP's, are trained quite differently than the vast majority of the rest of medicine. We don't generate differentials of most likely to least likely but based on lethality. And we are quite comfortable entertaining multiple diag. and treating them until we get a better idea. It is beat into us to always think and entertain the lethal rare diseases. This is quite different as to how the rest of medicine practices.

It definately would have been a good idea to explain to the PMD why you were thinking what you were thinking. I would have covered her with ABX and gotten some imaging (probably a CT scan at my institution).
Managing a sick patient is frustrating and it sounds like you did a great job. But remember not to pigeon-hole your own differential! :)
 

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Just a note on the contrast agent issue:

The issue with hyperosmolar contrast agent stems from the times when we still used 'ionic' contrast agents (e.g. conray, renografin). They had osmolalities in the 1200 range and indeed made your cells sickle (and the average patient puke due to the rapid plasma osmolality changes).

For the past 15 years or so, we use 'low-osmolar', for the most part 'non-ionic' contrast agents (e.g. Omnipaque). They are more in the 500-600 range and the impact on systemic osmolality is considerably less.

For the past 5 years, we have a contrast agent that is iso-osmolar to regular blood (Visipaque). It should have not influence on the sickling of RBCs whatsoever.

I haven't seen (and searched for) any literature comparing the various generations of contrast agents in the setting of sickle cell anemia, either clinically or on the bench.
If you have to do a CT with contrast on a sickler, ask the CT tech or the radiologist whether they can use Visipaque. It is mainly used for patients with diabetic renal disease, the cost is about 50% over regular low-osmolar agents and it is a bit tricky to handle due to its high viscosity. Given that most sicklers have some degree of nephropathy, you could justify the use on that ground alone.

PS.
I never had the problem of a sickler clotting too much. They rather tend to bleed out because they don't clot all that well.

PS2.
A patient with T 102 and a wedge shaped opacity in the lung has pneumonia. If it is a sickler it is pneumonia with acute chest. Unless someone did his residency in Dickinson, ND they should know how acute chest looks like.
 
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Even in the 500-600 Osm range, it is still quite hyperosmolar when compared to serum (280-300). Even many of the "iso-osmolar" contrast agents are in fact slightly hyperosmolar (350-400).

My institution does not carry Visapaque to my knowledge. Even if it did, with its higher viscosity, one must ask if it will be sufficient for a PE protocol CT. The injection timing must be just right, and if the viscosity makes injection slower than usual contrast, then the scan may be a limited study.

PE is not entirely out of the differential, and I didn't mean to imply that. However, the chances of this being an embolic event from a thrombosis is relatively small. More likely would have been a fat embolus from a bone infarction secondary to the sickling episode. This, however, is not treated with anticoagulants.
 

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This is not meant to be a dig at PMD's, but once the patient is in the ED, you're holding the reins, so to speak. Suggestions are always appreciated, but you're the one responsible for the workup you order, whether it was your idea or not. If you agree that it's a PE in this case, fantastic. If you rightly became concerned about acute chest syndrome, your duty is to work up & treat for that, not to allow the well-intentioned PMD to lead you and the patient down the road to hell.

totalbodypain said:
Truthfully, I am not entirely sure that the PMD was completely off base with his diagnosis.
The PMD is not off base in that yes, there is likely a pulmonary infarction occurring. Where he or she is wrong is in regard to the etiology and treatment. Classical PE (thrombotic) and acute chest in sicklers (vaso-occlusive) have quite different approaches from the therapeutic standpoint. Heparinizing this patient and watching her go down the pipes would not be the best course of action.
 

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Even many of the "iso-osmolar" contrast agents are in fact slightly hyperosmolar (350-400).
Visipaque is at 290 mosmol/kg

Even if it did, with its higher viscosity, one must ask if it will be sufficient for a PE protocol CT.
The power injector won't care. It'll squeeze that stuff in at 4cc/sec no matter what. The viscosity is more of an issue if you have to hand inject during angiography or if the tech creates bubbles while drawing it into the injector. Also, contrast should be stored in a contrast warmer prior to use, that way the viscosity drops to about 1/2.

The injection timing must be just right,
It allways has to be right. Hence such applications as 'smartprep' or test-injections.

then the scan may be a limited study.
In a sickler the scan is likely to be a limited study due to problems with IV access. The vein of choice (R antecubital) was probably blown by some pediatric intern 15 years earlier. Ports don't take power injections and some PICCs are not approved for it either.

As I said, I have never looked into the literature for the specific topic of LOSM or IOSM contrast in sicklers. If I was in a situation where I needed to look for PE or do an angio, I would use Visi, and as little of it as possible.
 

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f_w said:
Visipaque is at 290 mosmol/kg



The power injector won't care. It'll squeeze that stuff in at 4cc/sec no matter what. The viscosity is more of an issue if you have to hand inject during angiography. Also, contrast should be stored in a contrast warmer prior to use, that way the viscosity drops to about 1/2.



It allways has to be right. Hence such applications as 'smartprep' or test-injections.



In a sickler the scan is likely to be a limited study due to problems with IV access. The vein of choice (R antecubital) was probably blown by some pediatric intern 15 years earlier. Ports don't take power injections and some PICCs are not approved for it either.

As I said, I have never looked into the literature for the specific topic of LOSM or IOSM contrast in sicklers. If I was in a situation where I needed to look for PE or do an angio, I would use Visi, and as little of it as possible.
Thanks, I still learn stuff on SDN
 
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