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.
This podcast was inspired by and partly based on a post by one of my favorite FOAMed bloggers...
Thu, 21 March 2013
Bath salts (not the kind you put in the tub) and synthetic marijuana - agitated delirium, kidney failure, and death. The new drugs of abuse come with a high cost.
Toxicologist Leon Gussow from The Poison Review blog joins ERcast to give the low down on Bath Salts and Synthetic Marijuana.
Fri, 8 March 2013
The gloves are off and the vitriol is bubbling hot. This is the episode where you get the mic and tell the world what really gets your goat.
Rant off 2013 players
Gerry O'Malley is no fan of patient satisfaction surveys
Ken Grauer say we shouldn't throw away the atropine for some cases of asystole
Graham Walker is hot under the collar about medical workups for psych patients
Matt Dawson and Mike Mallin think we should hold the narcotics and and place femoral nerve block patients with hip fractures
Michelle Lin gives a pearl on keeping central line guidewires going in the right direction
Rob Bryant tells us how to throw the guidewire away
Graeme Pickford gives advice to would-be locums physicians traveling to Australia
Seth Trueger Emergency physician and Health Policy fellow in Washington, DC
Gabe Rose is not a fan of pelvic exams
Andy Sloas rants about, well, I'm not really sure, but he seems quite upset
Jim Miller from Montana thinks we make much ado about nothing when it comes to fecal disimpaction
Rob Bryant's Brass Knuckles Technique for Guidewire Disposal
Thu, 28 February 2013
How did emergency medicine evolve into its current incarnation? It wasn't always a smooth ride. Greg Henry and Don Stader take us through the early days of modern emergency care.
Mon, 11 February 2013
If the rectum were a simple tube, it would be like a fecal sluice gate every time stool arrived. But itʼs not just a tube. It has an elegant sphincter system that can automatically tell solid -from gas- from liquid. What other muscle in the human body has that sort of intelligence? Understanding anal abscesses means understanding anal sphincters because they determine where the pus will spread.
The INTERNAL ANAL SPHINCTER wraps directly around the rectum like a hand holding a stick (the rectum being the stick). The ANAL GLANDS, which lubricate the anorectum, sit just inside the internal sphincter like peas in a pod. Anal abscesses are thought to begin as suppuration of the anal glands.
The EXTERNAL ANAL SPHINCTER wraps around the internal sphincter. The external sphincterʼs job is voluntary control and volitional release of feces. Next to the external sphincter is FAT and then the ISCHIUM.
When anal glands get infected, pus can spread in any direction. Most of the time it goes straight down, causing a PERIANAL ABSCESS. The perianal space is relatively small and usually, the abscess you see next to the anus is all the abscess there is. Sometimes, the infection can involve the intersphincteric (perirectal) space or may be the head of a deeper abscess that has made a serpiginous path to the perianal area. Thatʼs why, even if the perianal abscess is small and innocuous looking, a rectal exam is so important.
The ischiorectal space is an expanse of fat sitting between the external anal sphincter and the ischium. An ISCHIORECTAL ABSCESS starts deep. By the time it reaches the skin, where it can be seen on external exam, the patient is usually sick. While a perianal abscess is right up against the anus, the ischiorectal abscess generally comes to a head several centimeters away from the anal orifice. An ischiorectal abscesses are the most common of the deep infections, but it’s not the only player. There are also intersphincteric and supralevator abscesses (which may not be visible on external exam.
The Dividing Line
The essential dividing line for these abscesses is superficial (perianal) versus deep (perirectal). A superficial/perianal abscess is in our field of play. A deep/perirectal abscess is not – that is for the surgeon. How can you tell deep from superficial? Sometimes you canʼt. The abscess may be too deep for you to feel on digital rectal exam. If there’s a fever, think deep. Pain out of proportion to what you see, think deep. This is one case where your rectal exam is important. If the rectal exam is extremely painful for the patient or you feel induration, fluctuance, or fullness, consult a surgeon. The patient needs an exam under anesthesia and/or imaging study.
Who to drain in the ED
Simple perianal abscess can be incised and drained in the ED. One word of caution on the perianal abscess: they can be associated with a deep/perirectal infection.
If a patient has an ischiorectal abscess, thereʼs no reason you canʼt give it a stab to release pressure, but most will need definitive deep exam and management in the OR. The longer an anal or perirectal abscess is left to fester, the higher the chance of sphincter damage and incontinence. You may be reluctant to do an I&D out of fear of damaging the sphincters, but itʼs the delay in treatment thatʼs the real risk for sphincter damage. If you can see the point on the skin, and itʼs going to be a while before getting the patient to the OR, make a small incision to start the drainage.
Many drainage techniques have been described in the literature: small incision and drainage, incision and cut out an ellipse of skin, cruciate incision, loop drainage, pack, no pack. No single method has proven superior. Just like any other abscess, you want to get the pus out and keep the pus draining. As long as what you do maintains an open wound, thatʼs enough. The cruciate incision is loved in surgical textbooks, but it is a huge cut to have in a sensitive area and I donʼt think it has a place in ED management. Since there are so many important sphincters in the perianal area, I avoid aggressive exploration and only probe gently.
Sitz bath and stool softeners.
Every patient with a perianal abscess should be referred to a surgeon. First time infections, and even more so repeat infections, can be associated with anal fistulas.
Direct download: 2011_Essentials_Conference_-_65_-_Juicy_Butt_Pus_And_How_To_Drain_It_-_1280.mp4
Category:Vidcast -- posted at: 6:24 PM
Sat, 26 January 2013
Humerus fractures, shoulder dislocations, broken clavicles, shoulder separations and then some. We cover all the bases of acute shoulder injuries with sports medicine orthopedist Dr. Brett Andres. It's also ERcast's third anniversary, so raise a toast and thanks for listening.
Links mentioned in the podcast introduction
Which proximal humerus fractures need surgical repair?
There is no definite answer to this. New fixation technology gives results that were not possible a few years ago, so more and more of these are getting surgically managed. The main questions are whether or not the humeral head is still on top of the humerus and if the head articulates with the glenoid. I think of this in terms of an ice cream cone, with the humeral shaft the cone and the humeral head the ice cream. If the ice cream is still on the cone, it will probably heal OK. If the ice cream has fallen off the cone, that may benefit from surgical repair.
A split humeral head will have a poor outcome with chronic arthitis- may benefit from surgery
Displaced greater and lesser tuberosity fractures may look benign, but those are the attachment sites of the rotator cuff. May benefit from surgery.
Shoulder dislocations: How long to splint after reduction
Young patients, under 20, have a high re-dislocation rate (as high as 70%). Three weeks immobilization.
Age 20-45 will probably not dislocate again, but stiffness is a problem. Sling after reduction, but begin ROM when pain improves.
Older patients, 60 or greater, are unlikely to re-dislocate but have a higher incidence of rotator cuff repair. They probably don't need prolonged immobilization, but do need follow-up to evaluate for rotator cuff injury.
Clavicle fractures: Which need surgery?
There is a high non-union rate for displaced fractures (no cortical contact).
Brett considers surgery if there is : no cortical contact, overriding 2cm, butterfly type fracture.
How should we immobilize clavicle fractures?
A sling should be sufficient. Some patients like the figure of eight, but it can rest on the fracture fragment and be irritating. A sling for a clavicle fracture is not like a cast- it doesn't help with healing. Begin early ROM when the patient can tolerate.
Although a chronic problem, can cause acute intense pain. Calcium breaks loose and gets into the subacromial space, causing irritation. A patient can have so much pain that examination is difficult. A subacromial bursa injection may help to relieve symptoms.
Subacromial bursa injection (courtesy of Larry Mellick, MD)
Tue, 4 December 2012
Kenji Inaba is one of the most published trauma surgeons on the planet. When it comes to trauma, he has more pearls than an oyster bed. We caught up with him at the Essentials of Emergency Medicine conference in Las Vegas.
Kenji’s Trauma Pearls
If a hemodynamically stable trauma patient has pericardial fluid on ultrasound, does treatment differ if the trauma was blunt or penetrating?
Penetrating: presence of fluid equals blood around the heart and your patient needs to go to the OR immediately.
If you can’t get your patient to the OR right away and they start to become unstable, a pericardiocentesis with pericardial catheter placement may be an option. The catheter can allow for intermittent drainage until the patient can get definitive care in the operative theater. If that's not an option or your patient is crashing, crack the chest.
Does the amount of pericardial effusion matter?
No. In penetrating thoracic trauma, even a small amount of fluid can rapidly increase leading to rapid decompensation.
Blunt: Cardiac injury resulting in hemopericardium is much less common than with penetrating trauma. If the patient is stable, the likelihood of the fluid representing blunt cardiac rupture is less likely than the fluid having been there before the trauma. It can be hard to tell acute bleeding from a chronic effusion, just ask the ultrasound podcast guys -even they can't tell. The first thing you want to know is whether or not there is tamponade physiology. What's that look like? Like there's a little man bouncing on the RV as if it were a trampoline. See video below.
Is there utility getting dedicated thoracic and lumbar spinal images on a patient who is going to get a CT scan of the chest, abdomen and pelvis?
No. You can get sufficient information about significant thoraco-lumbar spinal fractures from the bone windows and reconstructed images from a CT of the chest, abdomen and pelvis. Dedicated imaging of the spine adds a significant amount of radiation without giving additional actionable information.
What is blood volume cutoff for draining hemothorax?
300cc is a rough estimate, but there is no absolute cutoff. Compared with CXR, CT is much better at estimating amount of blood in the chest, but measuring exact volume is easier said than done. In the end, it often comes down gestalt.
Looks like a little bit of blood: watch and wait
Looks like more than a little bit of blood: chest tube
What are the risks of retained hemothorax?
Empyema and adhesions/fibrothorax. These are rare complications.
Kenji Bonus Pearl
When draining a hemothorax, give a single dose of antibiotics before placing the chest tube. What is the ideal antibiotic? Unknown, but currently under study.
Sat, 27 October 2012
Is it safe to cardiovert a hemodynamically stable patient with recent onset atrial fibrillation? The evidence says yes, but not everyone is a believer...
I've talked quite a bit about atrial fibrillation on ERCast, and the topic that generates the most emails, by a wide margin, is cardioverting the hemodynamically stable patient with recent onset atrial fibrillation or flutter (RAFF). Recent onset is defined by dysrhythmia onset within 48 hours of presentation. Forty eight hours is considered the time window for safe (minimal thromboembolic risk) RAFF cardioversion.
But why would we even consider cardioverting a RAFF patient in the ED?
The palpitations, shortness of breath, dizziness, and weakness caused by RAFF were the reason they came to see you. Having done hundreds of ED RAFF cardioversions, I can tell you, that when patients get out of RAFF, they feel much better. Leaving a RAFF patient in a fib presents an extra level of complexity. What is your plan for discharge if you are going to leave the RAFF patient in atrial fibrillation? Most of the time, it involves anticoagulating and referring them to cardiology for cardioversion at a later date. Is that really a better option? If it were a matter of patient safety, i.e. performing delayed cardioversion with full anticoagulation is safer than ED RAFF cardioversion, then there would be no discussion-we would err on the side of patient safety. But there is no evidence that delayed cardioversion with full anticoagulation and echocardiogram to rule out clot in the atrium is any safer than cardioverting RAFF patients in the ED.
Do you have to go straight to cardioversion?
There are several options for the hemodynamically stable RAFF patient in the ED.
Option one: Have the patient come back tomorrow so they can be rechecked within 48 hours of symptom onset, since that is the known window of safety for cardioversion without anticoagulation. Fifty percent of RAFF patients will convert spontaneously within 24 hours and there is no rule that says cardioversion has to happen this minute. I instruct patients to not eat after midnight (so they can have an empty stomach for procedural sedation-not that there's evidence to support this, but I'd rather have a patient with an empty stomach than one with a belly full of Egg Mcmuffins and Vegemite), come back in the morning and, if they’re still in a fib, proceed with cardioversion. If there is rapid ventricular response associated with the RAFF, I will IV rate control in the ED and give an oral rate control agent (usually diltiazem) prior to discharge.
Option two: Cardiovert right now- either chemically with procainamide or straight to electricity. I’d say about 80% of the time, the experienced a-fibbers want to go straight to electricity and not mess around. They also don’t want to have to come back for a recheck. The new onset a fib patients will opt for the 'come back the next day ad recheck' option more often than a patient with previous episodes, but even the majority of first timers go for cardioversion during the current ED visit. I like the Ottawa Aggressive Protocol for managing RAFF and will offer 1g IV procainamide over 1 hour as an initial step, especially if the patient is hesitant to proceed with sedation and electricity.
Option 3: Do no ED cardioversion at all. Anticoagulate (or start on a daily aspirin if a low CHADS score and no plan for future cardioversion) and refer the patient to cardiology. You can also start your patient on LMWH and set them up for an urgent TEE to look for atrial clots. Some hospitals do not have ready access to transesophogeal echocardiogram (TEE) and, in this case, the patient will get a few weeks of anticoagulation before cardioversion.
There is an option 4, which doesn't get the bold highlight, and that is to rate control, give a dose of low molecular weight heparin, and admit all RAFF patients to the telemetry unit. This is still done in many hospitals in the United States, but I'm not sure why.
Let’s address the elephant in the room...
Is it safe to cardiovert RAFF patients?
How do you really KNOW there is no clot in the atrium? How do you know you aren’t going to stun the atrium, make some sort of thrombogenic medium and cause a stroke in a few days? Is there a way to know this without doing a TEE? A study in Heart 2011 suggested that N-terminal pro-brain natriuretic peptide (NTproBNP) level can help to tell if patients have been in afib for a short or long period of time and whether or not there is a clot in the atrium. This was a small study and may ultimately allow us to do cardioversions in patients who aren’t sure of how long they’ve been in afib, but there’s not enough evidence to support it NTroBNP in clinical practice. Use of D-dimer to detect atrial clot has been tried with varying success but the evidence isn’t convincing. But why even worry about biomarkers? If the patient knows exactly when their symptoms started and they present within 48 hours of onset, do we need to go through any extra steps beyond an H and P and having a conversation?
Let’s take a look at a December 2011 Annals of Emergency Medicine article titled: Is discharge to home after emergency department cardioversion safe for the treatment of recent onset atrial fibrillation? This was a “Best Available Evidence” review that looked 5 papers addressing the safety of ED cardioversion.
The authors's synopsis of the 5 reviewed papers was that most of the complications related to cardioversion come from procedural sedation. When I am having a PARQ (Procedures, Alternatives, Risks and Questions) conversation with the patient, one of the main things I focus on is how we are going to do the sedation, the potential risks and what we will do to mitigate those risks.
As far as complications from cardioversion itself, in the five studies reviewed, there were some chest wall burns and 2 episodes of ventricular tachycardia. One v-tach converted spontaneously and 1 was successfully shocked. Sometimes, in the back of our minds, we worry that we are going to cause a more serious arrhythmia if we shock a patient with a-fib. There have been a few reported cases of ventricular tachycardia but it is extremely rare, and the two in this paper were short lived.
Our main worry is that we are going to cause a stroke
Combining the outcome data of the 5 studies in this 'best available evidence' paper, there were zero reported post cardioversion thromboembolic events after ED discharge with follow up periods ranging from 7 to 30 days. Zero is pretty impressive, and when we’re talking about something like stroke, zero risk is about where we want to be. But like most things in medicine and life, there is no 'all or nothing' and the risk cannot really be zero.
The first study that directly looked at the risk of stroke and conversion to sinus rhythm in the setting of RAFF was from Annals of Internal Medicine 1997 titled Risk for Clinical Thromboembolism Associated with Conversion to Sinus Rhythm in Patients with Atrial Fibrillation Lasting Less Than 48 hours. Three hundred fifty seven hospitalized patients converted to sinus rhythm within 48 hours of a fib onset. Some converted spontaneously and some were cardioverted. Out of those 357, there were three thromboembolic events shortly after conversion from fib to sinus. All three of these patients were in their 80s and all three converted spontaneously.
Should we give a dose of LMWH before ED cardioversion?
There are several theories addressing why atrial fibrillation causes clots to form in the atrium. One is that prolonged fibrillation causes stagnation of blood and subsequent clot formation. Another is that conversion from fib to sinus, either spontaneously or via cardioversion, depresses left atrial function which leads to clotting. We worry about both of these when considering cardioversion of ED RAFF patients. Regarding theory two, clot formation as a result of cardioversion, wouldn’t it make sense to give some anticoagulation like LMWH at the time of cardioversion to decrease the risk of clot formation? In the 1997 Annals of Internal Medicine study mentioned above, no difference in thromboembolic stroke risk was seen between patients who did and did not receive acute anticoagulation with either warfarin or heparin. Take that with a grain of salt because this study was not powered to define/detect a small difference in benefit from anticoagulation in RAFF. The 1997 Annals study showed a 0.8% rate of thromboembolism and most others report a 0.0% rate. A clinical trial designed to detect a decrease in thromboembolic risk would need thousands of patients with treatment and non treatment arms to see if there's any benefit giving anticoagulation for RAFF cardioversion. At that point, when you are giving thousands of patients acute anticoagulation to try and prevent a rare event, you’re likely to see more harm from the treatment itself than benefit in preventing strokes. Some, such as the American College of Chest Physicians, recommend considering acute heparin for high risk patients getting cardioversion, but even they recognize that there’s no evidence to support this approach.
When discharging a patient with new onset atrial fibrillation after a successful cardioversion, there are a few key points I put into the conversation.
"Atrial fibrillation is usually not a one time occurrence and will invariably recur. The next time it happens, you don't need to come immediately to the ED if you aren't having chest pain, SOB, feeling dizzy, etc. Give it some time if you can tolerate the symptoms. Most episodes are short lived and, for the longer ones, there is a 48 hour window in which we can cardiovert.”
"You need to establish care with a cardiologist to get an echocardiogram and discuss long term a fib management."
If this is a patient with new onset a fib or one who is not on an anti-platelet agent or anticoagulant, I will also calculate the patient’s CHADS VASC score on MDcalc and give them a printout showing their future stroke risk. Many of these folks are not even taking aspirin - I at least start them on that. Should you start oral anticoagulants in the ED? I personally don’t but have them follow up with cardiology or their primary provider ASAP. The decision of whether or not to start anticoagulation is a huge conversation. One of my partners feels differently. He starts patients on anticoagulation right there in the ED if patients are high risk. But this, my friends, is a talk for another day.
Tue, 2 October 2012
There is no perfect way to rule out pulmonary embolism. But what if we could change the game and move the d-dimer cutoff higher in the low risk patient? From 500 ng/ML to 1000ng/mL. You’d think that the specificity of the test would improve - fewer false positives. But what would we sacrifice in sensitivity? Would we start missing PE’s? On this episode of ERcast, we’ to talk about doing just that - raising the d-dimer threshold in low risk patients. The idea for raising the d-dimer threshold comes from an article by Jeff Kline et al in the April 2012 Journal of Thrombosis and Hemostasis titled D-dimer threshold increase with pretest probability unlikely for pulmonary embolism to decrease unnecessary computerized tomographic pulmonary angiography
By the numbers...what happens when we raise the d-dimer threshold? Sensitivity decreases and specificity increases.
Using a d-dimer cutoff of <500ng/mL
Wells Score ≤4
Revised Geneva Score ≤6
Using a d-dimer cutoff <1000 ng/mL
Revised Geneva Score ≤6
What should we take away from this paper? This was essentially a thought exercise in increasing the cutoff for a diagnostic test. It was not an outcome study. What happens when the d-dimer threshold is increased? Theoretically many fewer CTPAs (fewer patients exposed to radiation and risk of contrast induced nephropathy) and... more missed PEs. The question is one of balance. We know we do too many CTPAs. So, is a 1.5% (absolute) increased risk of missing PEs worth doubling the exclusion rate, or in other words, halving the number of CTPAs? It can be debated either way. What’s the right answer? There is no right answer. It’s complicated to understand ourselves. Some shared decision making with your patient may be in order.
Also discussed in this Podcast
Ketamine for status epilepticus Neuro Critical Care 2012
Emergency Medicine News commentary on ketamine for status epilepticus
IST-3 Lancet 2012
SMART-EM podcast on thrombolytics for actue stroke