Thu, 14 November 2013
What do lung nodules have to do with emergency medicine? Weʼd like to see ourselves as full time resuscitationists and while thatʼs one of our master skills, much of our job involves taking care of non-critical patients and, even more so, having conversations with patients and their families. But arenʼt pulmonary nodules someone elseʼs problem, like the pulmonologist? Yes, and no. The pulmonologist is going to manage things in the long term, but the overwhelming majority of nodules are going to be incidental findings that land in your lap.
You get a phone call from the radiologist on a CT chest, “Thereʼs no PE or sign of dissection, but thereʼs a 5mm non-calcified pulmonary nodule in the right upper lobe” What does that mean? Do you need to pay attention to it? Can you ignore it? What do you tell the patient?
The conversation often goes something like this, “Good news Mr. Jones, we donʼt see a blood clot and, oh by the way, the radiologist saw a small nodule.” For you, someone who is used to getting reports of an incidental pulmonary nodule, itʼs no big deal. For the patient, what they heard is, “You have cancer.” That may sound like hyperbole, but itʼs most patientsʼ first reaction.
Mr. Jones may or may not have cancer and Mr. Jones may or may not ask you questions. We donʼt want to do is to induce fear in the patient by our ignorance but we also donʼt want to dismiss the findings and ignore a possible malignancy.
Is this a bad nodule?
Who needs follow-up and when should they get it?
This comes down to risk and benefit. Risk that this nodule is malignant, the benefit of follow up imaging versus the risk of extra radiation, unnecessary biopsies, surgeries, anxiety, and medical bills. While it’s not well known in emergency medicine, The Fleischner Society is a group in radiology that develops an evidence based consensus guideline on how to follow up pulmonary nodules.
Nodule size and patient risk factors are the principle elements that determine timing and type of follow-up study needed. There are two main pieces of the Fleischner Criteria that are germane to emergency providers:
These guidelines suggest that the likelihood of a small (≤4mm) nodule being cancer in low risk patient is so low that no further follow up is needed. Will some of these nodules turn out to be cancer? Yes, but striving for a zero miss rate in this group is not risk-benefit favorable. The likelihood of the patient having negative sequelae (radiation, unnecessary biopsy, surgery, financial hardship) is greater than the chance of the nodule being cancerous. Itʼs analogous to striving for a 0% MI miss rate. Cost far outweighs benefit.
The Other Side of the Fleischner Coin
Not everyone follows the Fleischner guidelines. Some radiologists recommend follow-up imaging, or at least discussion, for every patient with a newly diagnosed nodule. Pulmonary nodules are a complex topic with multiple factors and variables that dictate the best course of action (or no action). These patients need follow up, preferably with a pulmonologist, to discuss risk level and decide what to do next. When weʼre talking about a one millimeter difference dictating a follow up scan versus doing nothing, one of my colleagues who is a chest radiologist, has this to say, “Depending on how much coffee Iʼve had to drink, I can measure the same nodule 20 times and have it be different every time, so trying to make separate recommendations for nodules that are ≤4mm or 4-6mm is silly to me. “
Tips for communicating with patients
What are you going to say to the patient?
Here are some example scripts for delivering the news of a newly diagnosed nodule...
“Mr Jones, good news, there's no blood clot. The radiologist did mention that he saw a small spot on your lung. The medical term for it is a nodule. It's 5mm, which is about half the width of your little finger or the size of a pea. We see these all the time and 95% turn out to be completely harmless so I don't want you to lose any sleep over this. You will, however need to make sure someone takes a look at this again with a CAT scan to make sure it's not growing. Iʼm going to refer your to our pulmonologist, a lung specialist, who is an expert in lung nodules and will help guide you the rest of the way.”
Maybe Mr. Jones is low risk.... “The chance of this nodule being anything serious is extremely low. The nodule is small, you donʼt smoke and youʼre young. The risk isnʼt zero, but itʼs pretty close. I still think you should follow up to discuss all of the options, but in all likelihood, this will not cause you any problems.”
The overwhelming majority of pulmonary nodules are benign. The bigger they are, the higher the chance of malignancy. There is debate as to whether a very small lung nodule in a low risk patient needs follow up at all. Should an emergency provider make the call that no follow up is needed? I think there is too much uncertainty in sorting out all of the variables that go into risk factor assessment. I refer all patients with newly diagnosed nodules for follow up, risk stratification, and further discussion with their PCP or a pulmonologist.
Patients almost always have questions about the significance of their newly diagnosed pulmonary nodule. What they really want to know is if they have cancer. You canʼt know that looking by at a nodule one time. For a small nodule, itʼs about how it grows (or doesnʼt) on repeat studies. The things that make cancer more likely and follow up more urgent include size >4mm, age over 35, history of smoking, and nodules that are not completely calcified.
In the end, it may be cancer, but chances are, your patient is going to be just fine.
Bonus Section... Even more information about pulmonary nodules!
Historically, all patients with non-calcified nodules were recommended to get follow-up chest CTs for 2 years. This was based on the pre helical CT era when most pulmonary nodules were found on chest x-ray. By the time a nodule is seen on CXR, itʼs often big. The old ACCP recommendation for indeterminate solitary nodules was follow up CT at 3-, 6-, 12-, and 24 months. Thatʼs five chest CTs (including the original study), no matter what. When you consider that upwards of 51% of smokers over age 50 have pulmonary nodules, that is a lot of negative CT scans, radiation, unnecessary biopsies, surgeries, anxiety, and money spent. With our ability to diagnose smaller nodules, we needed to change our thinking about what to do with them. Thatʼs what the Fleischner recommendations addressed. Itʼs not one size fits all.
Does it make a difference if the nodule is measured on CT or Chest X-Ray?
These measurements apply only to CT scans. CXR is too inaccurate. The work-up for nodules found on CXR varies depending on the scenario. The first step is to try to get old films to see how long it's been there. If no old films are available, depending on nodule features and clinical story, the patient needs either a CT scan or a short-term follow up CXR (4-6 weeks) to see if it persists. Sometimes it's tough to tell if a nodule is calcified on CXR. If it is obviously calcified, it doesn't need any follow-up.
What does calcification in a nodule suggest? Calcification in a small nodule suggests benign etiology. Mostly. A partially calcified nodule or one with eccentric calcification needs followup. Malignancies, like scar carcinomas (from old granulomas), and mucinous adenocarcinomas can have small calcifications.
How should you think about terms like ground glass, semi-solid, and solid? Does appearance make a difference when it comes to determining nodule behavior?
Thu, 31 October 2013
When a trauma arrest rolls though the door, chaos often ensues. But it doesn't have to be that way. Scott Weingart returns to ERcast to share his thoughts on how to run a rational blunt trauma arrest resuscitation when you are working by yourself or with limited personnel.
Scott W's recipe for blunt trauma arrest
Check for a pulse when the patient arrives. If they’re pulseless, they’re in arrest....
The fundamental philosophy: Do only those actions that will make a difference in your patient's survival
Step 1. Airway
Control the airway. If your patient is already intubated, you're done. If not, intubate or place a supraglottic device.
Step 2. Breathing
Perform bilateral finger thoracostomies. There are very few things in a blunt trauma arrest that you can reverse and save a life. One of those is a tension pneumothorax. If there is no rush of air or improvement of condition, proceed to step 3.
Step 3. Circulation
Perform a bedside cardiac echo.
If there is no cardiac activity, the resuscitation is over and the patient is dead.
If there is cardiac tamponade, remove the blood. In trauma, this usually means cracking the chest (ED throacotomy) and delivering the heart from the pericardium. You can try a pericardiocentesis, but that is less likely to be successful.
If there is cardiac activity, your patient is in hemorrhagic shock. Give blood with massive transfusion protocol.
Step 4. Look for sources of bleeding
Did your patient exsanguinate from a scalp laceration?
Is there bleeding into chest? You would have discovered this with finger throacostomy
Is there bleeding inside the peritoneal cavity? Perform a FAST ultrasound
Is there bleeding in the retroperitoneum? Squeeze the pelvis and bind if there is mobility
Is there bleeding from or into the extremities?
Is CPR beneficial in a trauma arrest?
This is such deeply entrenched dogma that I was shocked when Scott suggested that there is no functional reason that closed chest compressions will help in a traumatic arrest. But when you break down the reversible causes of blunt trauma arrest, it makes sense...
Exsanguination: you cant pump an empty circulatory system
Tension pneumothorax: you can’t pump with a zero venous return system
Pericardial tamponade: you can’t pump a heart that can’t accept any more blood
That being said, I still do CPR in a trauma arrest, but don't let it interfere with critical procedures. What do you think?
Fri, 25 October 2013
In this minicast, The Weingart Strikes Back!
Scott Weingart has some issues with our last episode on managing blood pressure in acute ischemic stroke. But the Swami doesn't take it lying down and has a few things of his own to say.
Join Scott, Swami and Rob at the Essentials of Emergency Medicine Pub Crawl on November 4, 2013 at 7pm
Blu Restaurant 747 Market St, San Francisco, CA
Mon, 14 October 2013
How do you manage blood pressure in acute ischemic stroke?
Should you give thrombolytics up to 4.5 hours after symptom onset?
When do you decide that a CVA is actually a TIA?
What is the age cutoff for using thrombolytics in acute ischemic CVA?
And... What's up with the new American College of Emergency Physicians clinical policy on TPA in stroke?
Sun, 1 September 2013
Video laryngoscopy has changed the game in in airway management, but has it made direct laryngoscopy obsolete? Anand "The Swami" Swaminathan joins Ercast to discuss the controversy and share some of his research.
Links Discussed in this episode
Sun, 28 July 2013
Should we treat asymptomatic hyperglycemia in the emergency department?
Endocrinologist Dr. Liz Stephens sets the record straight when it comes to about asymptomatic hyperglycemia.
How many times have you been in this situation... you’re caring for a diabetic patient with abdominal pain and their blood sugar comes back at 350 mg/dL or maybe they were asymptomatic and came in to see you because their blood sugar was 500 mg/dL. Should you worry? Should you treat? What does your patient get out of you treating their asymptomatic hyperglycemia? Does taking them from 500 to 200 really make a difference? How do you know they’re not teetering on ketoacidosis? The answers to those questions and more on this episode of ERCast.
A 40 year old male with abdominal pain. Blood sugar is 300 mg/dL. They have no history of diabetes. Are they a diabetic?
How high can BG get in a stress response?
Should you give them a dose of IV insulin in the ED?
Is there evidence that giving IV hydration to asymptomatic hyperglycemic patients in the ED improves outcome?
If you want to start your patient on metformin...
What’s the expectation for blood sugar drop with proper metformin dosing?
Insulin Pumps in the ED
Insulin pumps deliver continuous subcutaneous insulin. The subQ catheter is not permanent -the site is changed every 3 days. If needed, you can pull out the site.
If your diabetic patient with an insulin pump comes in with ketoacidosis, turn off the pump, take off the site and manage them with IV insulin. Trying to manage acid base, fluid balance and blood glucose gets too confusing with an insulin pump in the picture.
Kitabchi, Abbas E., et al. "Thirty years of personal experience in hyperglycemic crises: diabetic ketoacidosis and hyperglycemic hyperosmolar state." Journal of Clinical Endocrinology & Metabolism 93.5 (2008): 1541-1552.
Sun, 30 June 2013
Do you ever feel stressed and overwhelmed at work? I sure do. Life in the emergency department is chaotic and packed with pressure from all angles. Sometimes it feels like the world is against us, but it doesn't have to be that way. Start off your next shift on the right foot with pearls of wisdom from Dr Thom Mayer. Dr. Mayer gives tips and advice on calming the mind, focusing attention and moving efficiently through an emergency department shift.
Wed, 29 May 2013
Rivaroxaban for acute deep venous thrombosis
When we have a standard therapy for a disease, in this case vitamin K antagonists (VKA) for deep venous thrombosis (DVT), and a new therapy comes out, what do we want to know about the new drug? Is it at least as effective as the old therapy? Because if it’s not, that ends the conversation. If it’s at least as effective, that opens the door to further discussion. We also want know if the new therapy is safe, or at least no more dangerous that what we’re already using. Then we want to know the cost, because new therapies aren’t cheap. Bringing a drug to market costs a lot of money and who gets to cover that cost? The people buying the medication: patients, insurance companies, the government.
Let's take a look at rivaroxaban for treatment of DVT and see if it's something we should add to our treatment quiver or a case of 'the enemy of good is better'.
Part one. The evidence
Who was studied?
The main study looking at rivaroxaban treatment for DVT study was by the EINSTEIN group published in NEJM 2010. There was a follow-up study using the same drug for PE but for now, we’ll stick to DVT. About 3500 patients with acute symptomatic DVT were split into two groups. Group one got standard therapy with LMWH and an oral vitamin K antagonist. Group two got rivaroxaban 15 mg/kg bid for three weeks and then 20 mg per day for the duration of therapy- 3, 6 or 12 months. One thing I don’t like about this study is that it was funded Bayer (the company that makes the drug) but that’s the reality with almost all large drug trials. An upside of the trial is that there was a good representation of the different causes of DVT- unprovoked, surgery, trauma, immobilization, estrogen, cancer, previous VTE.
Efficacy and safety
The primary efficacy outcome was recurrent venous thromboembolism. Both groups were statistically the same: 2.1% for rivaroxaban and 3% for standard therapy. The primary safety outcome, major bleeding or what was dubbed ‘clinically relevant non-major bleeding’, was the same for both groups : 8.1%.
Major bleed rates were around 1% for both groups, and that held up in the follow-up study looking at rivaroxaban for PE. But what is a major bleed? It may mean something different to you than your colleagues. In these trials, a major bleed was defined as: clinically overt with at least a 2g/dL hemoglobin drop, bleeding that led to at least a 2 units blood transfusion, intracranial or retroperitoneal or critical site bleed, or bleeding that contributed to death.
A meta-analysis in BMJ 2012 looked at the available data on new anticoagulants (for multiple indications, not just DVT) and found similar results as the NEJM study, but came to the conclusion that rivaroxaban was associated with a reduced risk of bleeding. Click here for an in-depth analysis by Professor Simon Carley.
The BMJ meta-analysis showed that rivaroxaban had non-inferior efficacy and decreased bleeding rates compared to VKAs. I don't agree with the argument that this drug has superiority because of fewer bleeding compications. The rate of serious bleeding was 1% for both rivaroxaban and VKAs. If you put lipstick on a pig, it’s still a pig. Bleeding happens and the new stuff is just as bleedy or just as not bleedy, which ever way you want to slice it.
A footnote to all of this data is that in the two main NEJM rivaroxaban studies on VTE and PE, INR was therapeutic about 50-60% of the time. If INR was therapeutic 100% of the time, would rivaroxaban have looked so good? We’ll probably never know because that’s the problem with warfarin and one of the selling points of this new drug: VKA metabolism is erratic. A 2011 Swedish study found INR in therapeutic range 76% in 18,000 patients on VKAs. How would rivaroxaban have fared against this cohort?
Should warfarin be voted out of office?
If the new therapy is no better and no worse than the old therapy as far as recurrent VTE and bleeding, why would we vote the incumbent out of office? If this were politics, how would you campaign against each candidate? Warfarin has a long track record and we can bring out a lot of its dirty laundry.
Compared to the other drugs your patients are taking, warfarin is a great drug and a horrible drug. It’s great because it thins the blood and it’s horrible because it makes patients bleed, has variable and erratic metabolism, needs frequent monitoring and patients have dietary restrictions. In the 2010 EINSTEIN NEJM study, INR was therapeutic (2.0-3.0) just over half the time and low about a quarter of the time (and this was in a clinical trial where you would expect tight control). Let’s face it, warfarin is a fussy drug and your patient will need to give themselves LMWH shots until goal INR is reached. Self administration of LMWH can be a barrier to treatment. It’s expensive and, if treatment becomes prolonged, REALLY expensive.
The new stuff, rivaroxaban, is no worse than the old stuff as far as efficacy and bleeding. So how is it better? It’s orally dosed so no shots are needed. It has more reliable metabolism, less drug interaction, no dietary restrictions, no monitoring. But like any new drug, you know it’s not going to be cheap and then there’s the problem of reversibility - the Achilles heel of the new anticoagulants. Let’s take a look at these two issues. First, cost.
Part two. Cost
My local pharmacy prices for LMWH, warfarin and rivaroxaban...
LMWH + warfarin for 3 months
LMWH: 70 dollars a dose. Five days at two doses a day: $700.
Warfarin for 95 days: about 10 dollars
INR testing: $44 dollars per test. There are a few INR checks in the first week and the total number of tests is going to vary but let’s say 8 total tests that’s one every other week once therapeutic and some extra in the beginning before therapeutic. Say $350 for all the INR testing in a three-month period.
Total cash payout $1060
That’s only the money, not the other pains challenges that come with the warfarin package: diet, requirement of frequent testing, variable metabolism. It’s no secret that warfarin is metabolized differently by different people (and even in the same person depending on the circumstances)
Rivaroxaban for 3 months
First 3 weeks, or 21 days at 15 mg bid is $450
69 days of 20 mg per day, at 11 bucks a pill: $759.
Total cash payout $1209
Part 3. Reversal
The the elephant in the room, and not such a quiet elephant, is bleeding. No matter how great the drug, if it causes a life threatening complication we can’t reverse, like severe bleeding, is it really worth it? In many cases no. That’s still the problem with dabigatran and why most ED docs, especially those who have cared for patients with dabigatran bleeds, are not fans.
What do we know about rivaroxaban reversal?
There are a few studies that give some idea on reversal, but there’s not a mountain of evidence where we can say, “Yup, we’ve got this covered.”
Rivaroxaban pharmacology basics
Half life 5-9 hours.
Can it be dialyzed? No, it’s 95% protein bound.
Is there a product that can reverse rivaroxaban’s anticoagulant effect? What about PCC? Yes. Kind of. Probably. Maybe.
The study that’s most quoted about reversing rivaroxaban was published in Circulation 2011. Twelve healthy males were given rivaroxaban for three days. Rivaroxaban prolonged the PT and another test called endogenous thrombin potential. OK, blood is thinner. So we’re following these two lab tests then given Cofact - a four factor PCC. This has factors II, VII, IX and X, protein C and S, and antithrombin. As an aside, four factor PCC was just FDA approved in the United states. Back to the study. So here are our healthy male subjects, a wad of cash in their pockets, and the’ve been taking rivaroxaban for three days. Blood is thin, clotting tests are abnormal and in goes the PCC. What happened?
PCC immediately normalized the prothrombin time. The control reversal agent was saline which, not surprisingly, did nor correct the PT. We know that when PCC works for warfarin, it works right away. In healthy subjects taking rivaroxaban, it did just that. The PT was normal right away. The endogenous thrombin potential was also normalized by PCC, but not by saline. Lab tests corrected. Good so far. But what about actual bleeding? No human studies on this, but there is some animal data.
Reversal of rivaroxaban associated bleeding
2012 Anesthesiology- Rabbits given rivaroxaban and then PCC had improved lab tests but their ears bled just as long. Possibly under-dosing of PCC in this trial, but, no difference between the two groups.
2009 Journal of Thrombosis and Hemostasis looked at mesenteric bleeding in rats given rivaroxaban followed by PCC. PCC at a dose of 50 units per kilogram almost completely normalized bleeding time, whereas 25 units per kilogram did not. Going back to the healthy human volunteer study, 50 units/kg of PCC was the effective dose used. At 25 units/kg, PCC had no effect.
So there is some animal data that says that PCC has little effect on bleeding, and other evidence that says PCC reverses bleeding. But a rat’s gut is not a human’s brain. Can we infer that the correction of bleeding in this surrogate model applies to the catastrophic brain bleed you are seeing in resuscitation bay one? Maybe, but it’s still unknown. The evidence is better for rivaroxaban than for dabigitran. In the previously mentioned study on healthy subjects given rivaroxaban, subjects were also given dabigatran at another time and PCC had no effect on the clotting tests. There is, however, some animal evidence that PCC may help with dabigitran associated bleeding.
What about our old friend FEIBA, factor eight inhibitor bypassing activity? Not everyone has PCC, but a lot of shops have FEIBA. There is some lab and animal data in baboons and rats given rivaroxaban that FEIBA reduces prothrombin time and bleeding time.
On the horizon: recombinant and plasma derived factor Xa antidote, monoclonal antibodies Still in testing, we’ll let you know more when and if they’re ready for prime time.
Rivaroxaban starts with a loading dose: 15 mg twice daily for three weeks followed by 20mg once daily. Starting with twice daily dosing gives better thrombus regression than staring once daily.
We have another 10a antagonist that we’ve been using for a long time: low molecular weight heparin. LMWH is dosed by weight yet rivaroxaban is not. Rivaroxaban is mostly protein bound, giving it a low volume of distribution. This means that most of the drug going to moving about in the vascular bed, not body tissue. In a pharmacokinetics study of forty eight patients with a mix of males and females, light (<50kg), average (70-80 kg), and heavy (120kg) subjects were given rivaroxaban. Anticoagulant effect was similar between genders. In the different body weights, there was a little more anticoagulant effect in the light group and a little less in the heavy group, but not enough of a difference for dose adjustment.
Should you use this drug?
So what to do? We have two therapeutic pathways for DVT. I think you can be honest with your patients and, if they are candidates for both, give them the option.
Efficacy, about the same.
Complication rate, about the same. This is always an interesting part of the conversation. “You have a condition that can potentially kill you, a blood clot. The treatment for this is to make your blood thinner. Good thing there, because that’s going to help you in the long run. The down side to this treatment is that thin blood means you’ll bleed easier. Eight percent is a fair number to give, or you can say 1% serious bleeding. There you have a number needed to harm. How does that compare to number needed to treat? It’s going to be the same with rivaroxaban and warfarin, because the efficacy for recurrent VTE is the same.
Wed, 24 April 2013
What is the fetal radiation exposure from CT pulmonary angiogram and ventilation perfusion scan (V/Q)?
What do you tell pregnant patients about how much fetal radiation there is from a radiographic study? Do you use rads, grays, seiverts, micrograys? Here's any easy way to think about it... The threshold we want to avoid is 0.1 gray. 0.1 gray at any time during gestation is regarded as the practical threshold beyond which induction of congenital abnormalities is possible. Do you know how much 0.1 gray is in relation to rest of the universe? Don't worry, nobody else does either. To help with perspective, think of 0.1 gray as $100 or 100 points, we'll use dollars here.
Estimated fetal radiation exposure from diagnostic imaging studies
0.1 gray = $100
A chest x-Ray is one tenth of a penny.
Ct pulmonary angiogram is 25 to 50 cents.
A V/Q scan is 50 to 75 cents, less with a partial dose V/Q, which is often used in pregnancy. So for CT and V/Q , we'll say 50 cents each.
Background radiation during 9 months gestation: $5.
Amount of radiation to increase the risk of cancer before age 20 by one one-hundredth of a percent, or one in ten thousand, $10.
On the scale of $100, CT and VQ give less than $1 of fetal radiation exposure. Considering the risk of a bad outcome from PE, especially in a pregnant patient, where it is one of the leading causes of maternal mortality, err on the side of the workup.
So what study to do? My approach is to perform a V/Q scan in a pregnant patient with a normal chest x-ray. The caveat to this is early in the first trimester, where the decision may be more emotion than data based (on my part). At this stage of gestation, the fetus is about the size of a cashew nut and, with a V/Q. retained urine in the bladder seems like a lot of focused radiation to the entire fetus. In this patient group, I start with CTPA.
Jeff Kline's approach to using the D-dimer in pregnancy
In normal pregnancy, 60% of patients will have a d-dimer above standard threshhold. In the first trimester: negative PERC rule, with the caveat of an increased heart rate of 105 (HR rises in pregnancy) plus a negative d-dimer makes PE unlikely. The d-dimer cutoffs are 50% higher for each trimester. If your regular cutoff is 500 ng/mL, pregnancy corrected cutoffs:
Tom Deloughery's Protocol for Rivaroxaban for Venous Thromboembolic Disease
Paraspinous block for headache
Wed, 3 April 2013
There are times when the safety of IV contrast can be a confusing quagmire. We know that iodinated contrast for CT scans can hurt the kidneys. But is it harmful for someone who already has renal failure and is on dialysis? What about the breastfeeding mother? Will IV contrast harm her infant? How should we pretreat patients who have had a previous reaction to IV contrast? These questions and more answered on this episode of ERCast.
If you want to be uber-educated, check out The American College of Radiology’s (ACR) Manual on Contrast Media. As this type of document goes, it’s actually pretty concise, and something you may want to keep as a reference.
Q: Is it safe to give iodinated contrast to a breastfeeding mother?
Less than 1% of contrast is excreted in the breast milk and less than 1% of that is absorbed by the child’s gut. If the patient is concerned about even this level of exposure, she can always discard the next 24 hours of breast milk (the so-called ‘pump and dump’), but the ACR feels it’s safe for breastfeeding to continue without interruption after administration of iodinated contrast.
Q: If we give iodinated contrast to a dialysis patient, do they need to be dialyzed immediately, or can they wait until their next regularly scheduled dialysis?
A: Most patients can wait until their next regularly scheduled dialysis. If a patient has severe underlying cardiac disease and the small osmotic load of contrast will potentially send them into pulmonary edema, then urgent dialysis may be indicated. Does a potential risk warrant a default of immediate - post contrast dialysis? Probably not. I think a more reasoned approach is to assess the patient after they have received contrast. If there are signs of volume overload, then dialyze. If not, then dialysis can wait.
There is also a theoretical risk of making an oliguric patient anuric, but limited evidence to give a clear answer. Bottom line from the American College of Radiology:
“Unless an unusually large volume of contrast medium is administered or there is substantial underlying cardiac dysfunction, there is no need for urgent dialysis after intravascular iodinated contrast medium administration.” For a specialty that defines itself by beating around that bush, that is a pretty clear statement. No clinical correlation recommended, nothing in the differential diagnosis includes that this patient who you just sent home is going to die from this incidentaloma.
The Renal Fellow Network has an excellent synopsis on dialysis post CT contrast. Worth a read
Q: What is the best way to pretreat patients who have had a previous reaction to iodinated contrast?
A: Many EDs give a two pronged pretreatment: steroids and antihistamines with a one hour delay between treatment and injection of contrast.
The steroid studies have shown that pretreatment several hours before contrast decreases the incidence of reactions. The limited data on a single steroid dose two hours before contrast injection shows no benefit. This goes along with our current thinking about steroids - they take several hours to work.
H1 blockers: Probably useful when given one hour before contrast injection.
H2 blockers: Unclear if they have beneficial effect. There is little downside to giving an H2 blocker along with an H1 blocker, but it should not be used as a substitute.
For a deep dive review of pretreatment, check out this 2006 article from the British Medical Journal
Q: Is there a role for pre-treatment to decrease the chance of contrast induced nephrotoxicity (CIN)?
A: A bigger question is: why does CIN happen in the first place? No one really knows. There are theories ranging from direct renal tubular toxicity to vasoconstriction. Since the cause isn’t clear, treatment is somewhat a patchwork of guesswork.
There is no evidence that gives a clear creatinine cutoff as to when we should or should not give contrast. The ACR feels that a creatinine of less than 2 mg/dL is safe for IV contrast, but that’s a fuzzy line. Is a creatinine of 1.9 mg/dL safer than 2.1? I’ll put it this way: clinical correlation recommended.
How should we pretreat patients we’re worried about CIN? Hydration is a good bet. There is decent evidence that pretreating with IV 0.9% NS decreases the incidence of CIN. How much, how long, how fast to infuse? Unknown.
The bigger mystery lies in pretreatment with sodium bicarbonate and N-acetylcystine (NAC). These have both fallen in and out and then in and then back out of vogue. Where they are now in the sphere of medical thinking is a mystery to me.
Bicarb: there is some evidence to say it decreases CIN and other evidence that it makes no difference.
Does it work? Conflicting evidence.
NAC: here is what the ACR has to say about NAC pretreatment:
The efficacy of N-acetylcysteine to reduce the incidence of CIN is controversial. Multiple studies and a number of meta-analyses have disagreed as to whether this agent reduces the risk of CIN. There is evidence that it reduces serum creatinine in normal volunteers without changing cystatin-C (cystatin-C is reported to be a better marker of GFR than serum creatinine). This raises the possibility that N-acetylcysteine might be simply lowering serum creatinine without actually preventing renal injury. There is insufficient evidence of its efficacy to make a definitive recommendation. N-acetylcysteine should not be considered a substitute for appropriate pre-procedural patient screening and adequate hydration.
Does it work: The jury is still out.
Q: Who should have their creatinine checked before IV contrast?
A: Some of this is evidence based, some is OGSAR based (old guys sitting around a room). Below are the ACR consensus recommendations taken directly from the document.
Patients who are scheduled for a routine intravascular study but do not have one of the above risk factors do not require a baseline serum creatinine determination before intravascular iodinated contrast medium administration.
*Metformin does not confer an increased risk of CIN. However, metformin can very rarely lead to lactic acidosis in patients with renal failure. Therefore, patients who develop CIN while taking metformin are susceptible to the development of lactic acidosis. To assess the risk of lactic acidosis, it is probably prudent to stratify the risk of CIN in patients taking metformin who will be exposed to intravascular iodinated contrast medium .
Nephrogenic Systemic Fibrosis
We’ve been talking about safety of iodinated contrast for CT scans, but what about gadolinium - the contrast used for MRI? It’s much less common for us to order an MRI than CT and even less common to give gadolinium, but it occasionally comes up. Is there a problem with Gadolinium and the kidneys? We used to think, and not that long ago, that gadolinium was safe for the kidneys. About as safe as injecting saline. The risk of direct nephrotoxicity is indeed extremely low - there have been some cases of gadolinium related kidney injury, but for the most part, it’s not directly nephrotoxic. The problem is something called Nephrogenic Systemic Fibrosis or NSF. NSF is a condition of progressive fibrosis throughout the body. It usually starts with skin thickening and pruritis but can involve several organs including the heart, lungs, esophagus, skeletal muscles. It can even be fatal. Not so good. The exact mechanism is unclear, but the primary risk factor for developing NSF is renal insufficiency. The screening for who is a risk for NSF is much like the screening for who is at risk for kidney injury from CT scans. Avoid gadolinium in patients on dialysis, acute kidney injury or chronic renal insufficiency with a depressed GFR. A GFR less than 30 scrubs the mission - do not inject.
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