ERCAST
current issues in emergency medicine, reviews, opinion and curbside consults

This is part two of a two part series on chronic pain.

 

Pearls:

  • Set realistic expectations when treating patients with chronic pain.

  • For the vast majority of patients, antidepressants are the first-line pharmacologic choice for the treatment of chronic pain.

  • Patients who present after the acute phase of a painful condition, whether it’s 1 week or 2 years from the injury, are treated the same.  Treatment recommendations are evidence-based and the goal is a return to function.  Methods of treating chronic nerve dysfunction include exercise, physical therapy, tolerance of discomfort, yoga, meditation, and the pharmacology of the  pain agents.  If present, comorbid anxiety, depression, and substance abuse are all addressed.

  • When patients are in the chronic phase of pain, we want to move away as quickly as possible from the opioids, muscle relaxants, and the belief that the pain will ever completely go away.  Patients benefit immensely from starting the rehabilitation of chronic pain early, by employing non-pharmacologic methods and setting realistic expectations.  When they present several years into a painful condition, treatment recommendations are the same, but the process is much harder and slower.

Important links mentioned in this show

  • Specific pharmacologic therapies for chronically painful conditions.

    •  Antidepressants

      • Almost every antidepressant that works on serotonin and norepinephrine has some benefit for neuropathic pain.

      • SNRI's (duloxetine, venlafaxine) are the initial drugs of choice, because they work well for pain and have the added benefit of treating comorbid depression or anxiety.  Duloxetine has a formal indication for the treatment of diabetic neuropathy and is the primary neuropathic pain antidepressant.  These agents tend to treat depression and anxiety lower doses, but much higher doses are needed to get neuropathic pain benefit.

      • Tricyclic antidepressants (amitriptyline, imipramine, nortriptyline) are effective, but can be hard to tolerate.  They’re anticholinergic and have alpha blocking properties which can cause orthostasis and a prolonged QT interval.  Certain tricyclics have a formal indication for the use in migraines, fibromyalgia, and irritable bowel syndrome.  TCA's have immediate pain benefit at lower doses, but in order to get the mood and anxiety benefits, doses usually need to be much higher.  It’s the opposite of the general dosing rule for SNRI's.

      • The anti-pain benefit of antidepressants is independent of the treatment of depression.

      • Dr. Hersevoort starts most patients with neuropathic pain on antidepressants, because the vast majority are also depressed.

    • Anticonvulsants

      • Virtually all have a benefit for neuropathic pain.

      • Like the antidepressants, there are certain agents which are specifically recommended for neuropathic pain conditions.

        • Carbamazepine (Tegretol) is the drug of choice for trigeminal neuralgia.

        • Gabapentin (Neurontin) is the recommended agent for postherpetic neuralgia.

        • Pregabalin (Lyrica) is formally indicated for fibromyalgia.

      • These agents can be combined with antidepressants, as they have a different mechanism of action.

    • Benzodiazepines

      • These are not recommended for long-term, chronic pain treatment.  They may have synergy with improving the analgesic response in the somatic, acute phase of pain.

      • If used, clonazepam is the best choice.  It has the right length of action, is not tremendously dependency forming, and is easily metabolized.

      • The combination of benzodiazepines and opioids (particularly methadone) can be lethal.

    • Muscle relaxants

      • These benefit patients primarily by making them feel more relaxed and mellow; they don’t truly “relax” the muscles.

      • Like opiates, their use is specific and limited to acute management of real muscle spasm or muscle injury.  Data tells us that they have limited efficacy in chronic pain.

    • Analgesic patches

      • Lidoderm patches can be good adjuncts for some patients.  They have a combination of neurologic benefit and placebo effect.

    • Clonidine

      • This centrally-acting alpha agonist appears to work for just about anything:  opiates, alcohol craving, ADHD, tics.

      • There is a new body of research that it helps for complex regional pain syndrome, or reflex sympathetic dystrophy.

    • Antiarrhythmics

      • Like antidepressants and anticonvulsants, antiarrhythmics block sodium and calcium channels and in addition to blocking firing of myocardial cells, they also seem to block the firing of damaged nerves.

      • Intravenous lidocaine has shown benefit in some neuropathic pain conditions.

  • How should patients who are currently taking massive doses of prescribed opiates for chronic pain be managed when they present reporting acute pain?  These patients need to be treated by a pain management specialist who can get the patient on a treatment program that incorporates non-pharmacologic therapy as well as the slow but consistent tapering of opiate drug therapy.

Important links mentioned in this show

Direct download: Chronic_Pain_Part_2.mp3
Category:general -- posted at: 3:15 PM

Part one of a two part series on caring for patients with chronic pain

Pearls:

  • With few exceptions, opiate therapy should be reserved for the short-term treatment of acute somatic pain due to tissue injury.

  • Patients with acute pain should be informed early on that once tissue healing starts, opiates will be discontinued and the goal of therapy will be to improve function.  The goal is not a painless life.

  • Opiates are an unfavorable option for those with chronic pain.  

  • Patients who cannot tolerate chronic pain may choose maladaptive substances, such as alcohol or tobacco, as a means of “chemical coping”.

Important links mentioned in this show

 

Case:  A 45 year old man presents with chronic back pain.  Prior imaging reveals mild disc herniation.  He has tried epidural steroid injections and, over the years, has become a consumer of increasing doses of narcotics.

  • What advice can be given about the initial treatment of a patient with the acute onset of pain which is likely to become a chronic condition?  Patients with acute, somatic pain (such as a fractured ankle or vertebral disc herniation) may benefit from opioid therapy, in addition to anti-inflammatories and perhaps muscle relaxers, to treat the acute condition.  The tricky question is knowing when the acute phase ends.  Once the acute mechanical signs begin to resolve, which is usually in a few days, we need to start thinking about neuromuscular function and begin long-term planning.  This may include physical therapy with an endpoint of return to function, not a return to a painless life.

  • Total elimination of pain is often not possible with a significant injury.  If you try to completely eliminate the pain, the patient will be led down a dangerous road to overtreatment, loss of function and, eventually, drug dependency.

  • Chronic pain is when the nervous system goes haywire.  It is pain the lasts and persists longer than expected; it’s pain that is there when it “should not be”.  Somatic pain can be thought of as end-organ pain and neuropathic pain is more central.  With a somatic tissue injury, the peripheral and central pain receptors inform us using the sensation of pain.  Once the pain is relieved, the signal turns off.  In the situation of chronic pain, the organ for reporting and localizing pain is damaged and continues to fire, even after the somatic injury has resolved.

  • Is there a way to differentiate true pain from somatization, factitious disorder, or malingering?  There’s always a psychological component to pain, and in neuropathic or chronic pain, the emotional aspect can be greater than the somatic component.  A good history, physical exam, and proper imaging can usually determine the level of true tissue injury.  If there’s no physical evidence of trauma and no injury that can be found, the assumption can be made that the pain the patient is reporting is, at least in large part, psychological or neurological.  Somatizers who are not faking are the victims of their nervous systems exaggerating symptoms.  If you’re confident that the symptoms are manufactured or exaggerated, simply limit the acute intoxicating treatments and move quickly to the non-intoxicating pathways where the goal is to increase function.  In most cases, more narcotics correlate with less function.

  • What is the role of opioids in the treatment of chronic pain that is not related to cancer?  Opioids are an important tool and, like any treatment, can be used well or poorly.  An evidence-based approach to the treatment of pain can vastly minimize the over and under diagnosing that happens with most treatments.  Narcotics are necessary in acute pain and have a role in cancerous pain or ongoing tissue injury (such as severe arthritis).  In chronic pain, the longer the pain persists without clear somatic signs, opioids become less effective and more harmful.  Opiates are not benign substances, and their use is associated with loss of function due to side effects.  Chronic narcotic therapy contributes to sedation, lethargy, lack of engagement in physical therapy, and limited exercise.  It leads to poor socialization, isolation, and assumption of the sick role as pain patients.

  • Patients often get blamed for their opioid use.  But aren’t doctors in part responsible for opiate addiction, by writing the first prescription?  Patients need to be informed with the first prescription of narcotics that the longer they are on the medication, the harder it will be to get off of them.  As physicians, we are responsible for using the least dangerous, damaging, addicting medication for the shortest possible amount of time.  Patients must be educated about this at the beginning of treatment, and we need to let them know the medication will be tapered later.  It should not come as a surprise when we are no longer willing to be the prescriber of opiate therapy.  Patients should recognize from the outset that our goal is not the total elimination of pain and that, in order to recover long-term, they’re going to have to tolerate some pain so that they can continue to function.  In some ways, more discomfort equals more recovery.

  • Some patients are able to endure living with a degree of pain.  Others feel that any iota of pain is completely intolerable.  Patients who decide that they cannot live a life of pain will often get to a point where they’ve had enough.  They believe that they can’t tolerate anymore suffering and may become what’s termed a “chemical coper”.  They may find a substance or chemical that numbs their experience of life.  The substance is used to avoid and escape.  At this point, the condition is no longer medical; it is psychiatric.

  • Alcohol, tobacco, and marijuana are all substances that patients with chronic pain may use, hoping it will alleviate their discomfort.

    • Alcohol does not treat pain, but it is certainly used to escape reality.  It is dangerous when used in combination with opiates.  Heavy alcohol use leads to worsened symptoms the following day:  anxiety, depression, frustration, and increased pain.

    • Tobacco is used by many for chemical coping.  Like alcohol, it has no analgesic properties.  Nicotine is problematic in chronic pain for at least two reasons.  First, it damages the vascular system and interferes directly with healing.  Thus, tissue injury is not improving, nor will the pain.  Second, tobacco is a hepatic inducer, which increases the metabolism and breakdown of medications, including those prescribed to treat pain.  Therefore, this lowers the effective dose of painkillers.

Marijuana is complicated.  It can increase appetite and curb nausea.  There is some evidence that it can provide chronic pain relief.  The downsides to marijuana are that it impairs lung function, can increase anxiety and depression, and induce psychosis.  It also is constipating and is associated with deleterious cognitive effects.

To Be Continued in "Chronic Pain Part II"

Important links mentioned in this show

Direct download: Chronic_Pain_Part_1.mp3
Category:podcasts -- posted at: 3:02 PM

When we want to clinically clear the adult cervical spine, what do we do? We whip out a handy dandy decision instrument. Canadian C-spine? Yes! NEXUS? Boom, you betcha! But when it comes to kids, there's just nothing out there that even resembles a prospectively validated clearance tool. We're left with are gestalt, experience, and hoping for the best. A recent article (retrospective review) from the Journal of Trauma and Acute Care Surgery found that "...missing a cervical spine injury in asymptomatic preelementary patients is extremely low." The authors suggests that high risk findings for pediatric C-spine injury include:

  • Abnormal neurological exam
  • Decreased mental status
  • Neck Pain
  • Torticollis

But. There's a big but. The authors go on to say, "...however if the child is asymptomatic defined by a normal neurologic examination result, appropriate mental status, with absence of neck pain or torticollis, our first step is to remove the cervical collar. We examine the patient for cervical tenderness if they are able to communicate and observe the child for normal range of motion of the neck. In preverbal patients, we simply observe neck range of motion with the collar removed. If the child seems to move his or her neck without discomfort and full range of motion, then we do not pursue any further radiologic evaluation."

Andy Sloas from the PEM ED podcast joins the show to give his take on this article and the nebulous, contentious, and controversial topic of the pediatric cervical spine...

References:

Emergency Medicine Literature of Note review of the article Hale, Diane F., et al. "Absence of clinical findings reliably excludes unstable cervical spine injuries in children 5 years or younger." Journal of trauma and acute care surgery 78.5 (2015): 943-948.

PEM ED review of pediatric C-spine clearance

Direct download: Pediatric_C-spine_clearance.output.mp3
Category:podcasts -- posted at: 9:40 PM

Scott Weingart is a thought leader in critical care and medicine in general. His EMCrit podcast has changed the game in medical education and improved care of crucially ill patients across the planet.

 

Direct download: Weingart_on_the_state_of_things.output.mp3
Category:podcasts -- posted at: 4:56 PM

Six hours means so much when it comes to subarachnoid hemorrhage. That is the inflection point when blood may no longer look like fresh blood on a CT. Several studies have shown that a negative ct done within 6 hours of headache onset effectively excludes clinically significant bleeding (extrapolated to mean aneurysmal subarachnoid hemorrhage). Of course there are other things that can cause severe acute headache in an otherwise healthy person: vascular dissection, dural sinus thrombosis to name a few. So it’s not all CT-LP, but focusing on the question of "LP yes or no" after a negative third generation (or higher) CT,  the evidence suggests that LP may not be mandatory. Can there still be bleeding? Yes, there can. But bleeding from a source that’s going to kill is unlikely. This is a time for shared decision making with your patient.

CT may miss a small number of bleeds that LP will find, but there is also the issue of a false positive tap being more likely than a bleed and the downstream effects of testing and aneurysm treatment.

Dr. Ran Ran joins the show to examine the literature on The Subarachnoid Enigma

 

Upcoming 2015 conferences

June: SMACC Chicago

October: Essentials of Emergency Medicine in Las Vegas

December: Atlantis CME Retreat

References for this Podcast

Blok, Katelijn M., et al. "CT within 6 hours of headache onset to rule out subarachnoid hemorrhage in nonacademic hospitals." Neurology (2015): 10-1212.

Perry, Jeffrey J., et al. "Differentiation between traumatic tap and aneurysmal subarachnoid hemorrhage: prospective cohort study." bmj 350 (2015): h568.

Perry, Jeffrey J., et al. "Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study." Bmj 343 (2011): d4277. 

Claveau, David, and Jerrald Dankoff. "Is lumbar puncture still needed in suspected subarachnoid hemorrhage after a negative head computed tomographic scan?." CJEM 16.3 (2014): 226-228.

Direct download: The_Subarachnoid_Enigma.output.mp3
Category:podcasts -- posted at: 3:38 AM

Can a fever get so high that it causes brain damage? That question was posed to us by a listen with a recent patient whose temperature reached 106.9 Fahrenheit. Andy Sloas from the PEM ED podcast returns to ERCast to gives his take on cooling, workup, and the difference between heat exposure and infectious fever.

Upcoming 2015 conferences

June: SMACC Chicago

October: Essentials of Emergency Medicine in Las Vegas

December: Atlantis CME Retreat

Direct download: Can_fever_melt_the_brain_.output.mp3
Category:general -- posted at: 2:56 PM

In October 2013, Scotty Weingart was on the show and suggested that closed chest CPR has no role in traumatic cardiac arrest. It made sense because, after all, the things that cause a traumatic arrest won't be helped by closed chest compressions. Tension pneumothorax, pericardial tamponade, hypovolemia from exsanguination - pushing on the chest isn't going to reverse any of those. But where is the evidence to support that claim? Don't we always compress the chest when the heart has stopped?

There is, unfortunately, a dearth of data on this topic. Swami and I scoured the known literature and here's what we found...

Lockey DJ et al. Development of a simple algorithm to guide the effective management of traumatic cardiac arrest. Resuscitation 2013; 84: 738-42.

The authors' algorithm states that in all traumatic arrests, you should look for a penetrating injury to the chest or epigastrium. If you find one, crack the chest ASAP.

If you don’t see a penetrating injury, consider a medical cause for the arrest.

There are a few key procedures in trauma arrest and the study recommends using the HOT mnemonic.

  • H – Hypovolemia (control external hemorrhage, pelvic binding, long bone splinting and give blood)
  • O – Oxygenation (Airway management)
  • T – Tension PTX (Bilateral decompression and chest tubes)
  • Swami and I add in a second T for tamponade, making it the HOTT mnemonic.

If these three things are addressed and there’s no ROSC, you should consider stopping resuscitation. This simple list emphasizes a systematic approach so that you open the chest when it’s indicated without thinking about it too much.

Leis CC et al. Traumatic Cardiac Arrest: Should Advanced Life Support Be Initiated? Acute Care Surgery 2013; 74: 634-8.

Advanced life support in this article means advanced procedures, not ACLS and CPR. The authors argue that we should resuscitate patients in traumatic arrest stating that 49.1% attain ROSC and 6.6% have a good neurologic outcome, including 23.1% of children.

ALS here included IV fluids, intubation, chest tube insertion, pericardiocentesis and FAST in the field. There was no mention of chest compressions.

Bottom Line: The question as to whether or not closed chest CPR in traumatic cardiac arrest has not been well studied. In the literature we found,  chest compressions were rarely mentioned (if at all). Logistically, compressions can get in the way of life saving procedures and haven't been shown to help (nor have they been shown not to help). Considering the pathophysiology of traumatic arrest, compressions don’t make a lot of sense in the emergency department, since pumping on a closed chest in a patient with no volume (hemorrhagic shock), a hole (pericardial effusion), or obstructed outflow (tension PTX) isn’t going to help.

Links mentioned at the end of the show

Find out more and register for ATLANTIS CME

Essentials of Emergency Medicine

SMACC 2015

Direct download: No_CPR_in_trauma_arrest_.output.mp3
Category:general -- posted at: 2:28 PM

Something very cool is happening in emergency medicine, specifically low risk chest pain. What I mean by that is figuring out who is low risk and what to do about it. This is one of the biggest areas of CYA, for the uninitiated, cover your ass, medicine. And for good reason, it’s a big cause of lawsuits and if we get it wrong, people can die. We just had two episodes on cardiac CT addressing this very topic and one thing that came up in the last show with Rory Spiegel, was that the Cardiac CT did not perform any better than just using risk assessment and cardiac enzymes. But what does that mean? What is risk assessment in the ED? Is it, “Holy moly, that sounds like cardiac chest pain for sure, bang, you’re admitted.” Or is it, “C’mon, that’s not cardiac chest pain.” Well, that’s indeed a small part of it, but there has been improvement on assessing risk using enzymes and risk scores. The TIMI score has been out there for a while but it’s not as nuanced an instrument as we’d like. The HEART score may be a better and more usable tool in the ED.

Links for this episode

Amal Mattu's full explanation of Chest Pain ADP, Low risk chest pain, medico-legal aspects of chest pain, chest pain guidelines

University of Maryland Low Risk Chest Pain ADP

Shared Decision Making Graphic

Heart Score Calculator 

Stay up-to-date by subscribing to EM:RAP Today!

We are hungry for a sensible, safe and consistent pathway for evaluating chest pain. A new chest pain ADP has emerged from from the primordial soup, and it comes from none other Dr. Amal Mattu. Here is a link to Amal’s full explanation of the ADP and chest pain risk assessment and I recommend you to listen to it to get the full flavor of what he’s talking about. But for now, a  recap….

Many chest pain pathways have relied on the TIMI score, but that is a somewhat cumbersome tool for our needs. The HEART score shows promise as a decision instrument with more utility in the emergency department. The HEART score uses 5 criteria: history, EKG, age, risk factors, and troponin to determine risk of a 6 week major adverse cardiac event. Each one of these pieces has three parts. For example, risk factors: no risk factors, zero points; 1-2 risk factors, 1 point; 3 or more risk factors, 2 points. If a patient has everything, everything positive in the heart score, that’s 10 points -high risk. Low risk is 3 points or less. A low risk score gives a 1.7% 30 day risk of major adverse event. Add in a second negative (delta) troponin, and the risk goes down to under 1%.

Direct download: Amal_Mattu_Low_risk_chest_pain.output.mp3
Category:general -- posted at: 11:51 PM

Guest post by Rory Spiegel, A.K.A Captain Basil, A.K.A EM NERD

In today’s age of Modern Medicine, we consistently favor the objective findings provided by medical technology over the more subjective judgments of the experienced clinician. Yet the precision of these tools has rarely demonstrated superiority when compared to the experience and wisdom of the practicing physician.  Nowhere is this more evident than with the recent introduction of CT coronary angiogram (CTCA) for the work-up of chest pain in the Emergency Department. The lure of CTCA is rooted in our fear of uncertainty and the promise that this test may provide a safe non-invasive measure to quell these doubts.  Despite the overwhelming lack of evidence demonstrating CTCA’s efficacy over the more traditional risk stratification methods of history, physical, EKG and biomarkers, CTCA continues to make a push into the hearts and minds of Emergency Physicians.

The claims of CTCA’s successes are based off the negative predictive ability demonstrated in a number of cohorts of low-risk chest pain patients. In four large prospective trials, authors found that following a negative CTCA a diminutively low number of patients had an MI within the next 30 days (1,2,3,4). What proponents of this test fail to mention is that none of the patients in these cohorts, independent of the type of downstream testing they received, had a bad outcome during the 30-day follow up period. In the ACRIN-PA trial, the largest of these cohorts, only 2 of the 1357 patients who did not rule in for MI during their initial presentation experienced an MI within the next 30 days, independent of what was found on their CTCA (4). Seemingly just by meeting entry criteria to be enrolled in these trials, patients identified themselves as being at such a low-risk that they were destined for a good outcome independent of the testing strategy they received.

We now have four trials randomizing low-risk chest pain patients to either a standard work up or CTCA following a negative Emergency Department work up. Each study demonstrated that CTCA adds no additional prognostic value to our standard risk stratification strategies and likely leads to increased invasive procedures. In a meta-analysis of these four trials published in JACC in 2013, Hulten et al found a significant increase in the number of invasive angiographies, PCIs and revascularizations performed in the patients randomized to the CTCA arm (5). The only arguable benefit these trials were able to identify, in patients randomized to receive CTCA, was a moderate reduction in the length of stay. Even these temporal benefits are an illusion though, as many patients in the traditional care arm experienced a prolonged length of stay because they were subjected to unnecessary provocative testing that required admission to observation units (4).

The concept that CTCA adds diagnostic utility to the traditional ED chest pain work-up has been consistently disproven. Proponents continue to argue for the utilization of CTCA in the Emergency Department, suggesting that CTCA will provide additional risk stratification of patients with CAD, and allow us to determine which patients will benefit from more aggressive medical therapy. Until the FACTOR-64 Trial, published in in JAMA in 2014, this concept had not been validated in a prospective fashion (6).  Muhlestein et al enrolled 1000 high-risk patients and randomized them into traditional management of CAD or the use of CTCA to guide medical management. The authors found no difference in the primary endpoint: rate of death, MI or unstable angina (UA) between the groups (7.6% vs 6.2%). Additionally the patients randomized to the CTCA group received far more diagnostic caths (5.1% vs 13.3%), PCIs (1.8% vs 6.0%), and CABGs ( 1.3% vs 2.9%) than patients in the traditional management group. Even the concept that CTCA will allow for a reduction in patients receiving aggressive medical management is flawed. In the FACTOR-64 cohort, patients randomized to the CTCA group were upgraded to more aggressive management far more frequently than patients in the control group(6). Clearly in patients at high risk for CAD, CTCA adds little to the downstream management and likely will lead to overdiagnosis and overtreatment.

CTCA in the low risk patient who has already been ruled out for ACS using history, physical exam, EKG and biomarkers, fails to add further diagnostic utility. Additionally its use to help guide medical management of CAD seems to lead to increased testing and treatment without decreasing the rate of MI or death. The next question becomes, “How does CTCA perform in the high-risk patient in whom we suspect ACS?” Though the data on this question is certainly not as robust as that for the low-risk patient, there are a number of trials to guide us.

The first of these trials is a secondary analysis of the ROMCAT II cohort published in JACC in August 2014. In this analysis, Puchner et al examined how effective CTCA was in identifying ACS independent of other diagnostic tools (EKG, biomarkers) (7). The authors found that when using the traditional threshold for positive study (> 50% stenosis), CTCA was only 78.4% sensitive for ruling out ACS. In order for CTCA to reach a clinically acceptable sensitivity, the test threshold had to be lowered to the point where no obstructive CAD was visualized on CTCA (7). What these findings suggest, though the authors do not state, was in a number of patients who were diagnosed with ACS during their initial Emergency Department visit detected by EKG or biomarkers, were actually missed by the CTCA. Thus in the high-risk patient with either EKG changes or elevated troponin values, a negative CTCA is not sufficient to exclude ACS.

The next trial examining the diagnostic accuracy of CTCA in high-risk patients is the NXT Trial, which was published in JACC in late 2014 (8). In this trial, CTCA was used as a straw man comparator to another non-invasive tool for the diagnosis of CAD, CT fractional flow reserve (FFR). This trial compared both CTCA and CT-FFR to the gold standard of angiographic calculated FFR in patients with at least a 30% stenosis. At the typical threshold of 50% stenosis, CTCA was only 94% sensitive for identifying hemodynamically important stenosis (FFR< 0.80). Additionally when this threshold of 50% stenosis is employed, the specificity is equally clinically unacceptable at 34% (8).

Essentially the diagnostic characteristics are not unlike those of a D-Dimer assay. In the high-risk patients, the ones we are truly concerned with in the diagnosis of ACS, its sensitivity is not acceptable to safely rule out the disease process in question. In the low risk patients its poor specificity will lead to overtesting, overdiagnosis and overtreatment.

Finally, a brief comment regarding the patient’s expectations and desires. Champions of this test have noted that when given the option, patients choose CTCA over other testing strategies, said to desire the definitive answers it provides. This general endorsement speaks less to the efficacy of the test itself and more to our misinterpretation of the data when communicating the benefits of CTCA to our patients. We have clear evidence demonstrating that CTCA does not add any further risk stratification to the traditional Emergency Department workup. Patients only think it provides an additional level of security because of how it is presented to them. The evidence suggests that in the low-risk patient, CTCA adds no diagnostic value and will only lead to needless downstream interventions.

Certainly a more honest shared decision making moment would be similar to the one proposed by Dr. Jeremiah Schuur and Dr. Joshua Kosowsky in their letter to the editor (9) in response to Lit et al’s paper examining the use of CTCA in an Emergency Department population 4). In this letter they suggest the use of a more evidence-based consent when discussing the risks and benefits of CTCA. It goes as follows:

Sir, although you only have a 1 in 100 chance of having a heart attack in the next month, I do not feel safe sending you home. So, I ordered an expensive test that will not reduce your risk of a heart attack, but it could cause kidney damage or cancer.

Goldstein JA, Gallagher MJ, O’Neill WW, Ross MA, O’Neil BJ, Raff GL. A randomized controlled trial of multi-slice coronary computed tomography for evaluation of acute chest pain. J Am Coll Cardiol 2007;49:863–71.

  1. Goldstein JA, Chinnaiyan KM, Abidov A, et al. The CT-STAT (Coronary Computed Tomographic Angiography for Systematic Tri- age of Acute Chest Pain Patients to Treatment) trial. J Am Coll Cardiol 2011;58:1414–22.
  2. Hoffmann U, Truong QA, Schoenfeld DA, et al. Coronary CT angiography versus standard evaluation in acute chest pain. N Engl J Med 2012;367:299–308.
  3. Litt HI, Gatsonis C, Snyder B, et al. CT Angiography for safe discharge of patients with possible acute coronary syndromes. N Engl J Med 2012;366:1393–403.
  4. Hulten E, Pickett C, Bittencourt MS, et al. Outcomes after coronary computed tomography angiography in the emergency department: a systematic review and meta-analysis of randomized, controlled trials. J Am Coll Cardiol. 2013;61:(8)880-92.
  5. Muhlestein JB, Lappé DL, Lima JA, et al. Effect of screening for coronary artery disease using CT angiography on mortality and cardiac events in high-risk patients with diabetes: the FACTOR-64 randomized clinical trial. JAMA. 2014;312:(21)2234-43.
  6. Puchner SB, Liu T, Mayrhofer T, et al. High-risk plaque detected on coronary CT angiography predicts acute coronary syndromes independent of significant stenosis in acute chest pain: results from the ROMICAT-II trial. J Am Coll Cardiol. 2014;64:(7)684-92
  7. Nørgaard BL, Leipsic J, Gaur S, et al. Diagnostic performance of noninvasive fractional flow reserve derived from coronary computed tomography angiography in suspected coronary artery disease: the NXT trial (Analysis of Coronary Blood Flow Using CT Angiography: Next Steps). J Am Coll Cardiol. 2014;63:(12)1145-55.
  8. Schuur et al. CT Angiography for Possible Acute Coronary Syndrome. N Engl J Med 2012; 367:83-86 July 5, 2012
Direct download: Revenge_of_the_nerd.output.mp3
Category:general -- posted at: 6:46 AM

Use of CT scans for the evaluation of renal colic increased 10 fold between 1996 to 2007. Is this good for patients? Have they benefitted from the detailed information that CT scanning? The answer is no. Several studies have revealed that we are not only irradiatiting patients at an increasingly alarming rate, their outcomes are not improving because of it. In this episode, recorded at the Cabo CME retreat, ERCast meets up with Matt Dawson and Mike Mallin from The Ultrasound Podcast to discuss the article Ultrasonography versus computed tomography for suspected nephrolithiasis.

Study Breakdown

  • About 3ooo patients with suspected renal colic divided into 3 groups defined by initial diagnostic study
    • CT scan
    • Radiology Ultrasound
    • Point of Care Ultrasound
    • Results: Using CT as the initial study increased radiation exposure but did not reduce adverse outcomes.
    • ERCast editorial: Another way to look at: Starting with ultrasound as the initial imaging modality decreased radiation exposure and did not increase adverse outcomes. Whether you see the cup as half full or half empty, starting with US in an uncomplicated case of suspected renal colic seems like the right call. If you start with CT on everybody, then everybody gets irradiated.

For a more detailed discussion on this topic, check out the Broomedocs Podcast.

References

Smith-Bindman, Rebecca, et al. "Ultrasonography versus computed tomography for suspected nephrolithiasis." New England Journal of Medicine371.12 (2014): 1100-1110.

Westphalen, Antonio C., et al. "Radiological imaging of patients with suspected urinary tract stones: national trends, diagnoses, and predictors." Academic Emergency Medicine 18.7 (2011): 699-707.

Moore, Christopher L., and Leslie Scoutt. "Sonography first for acute flank pain?." Journal of Ultrasound in Medicine 31.11 (2012): 1703-1711.

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