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

Jeff Kline is one of the world's leading researchers in thromboembolism. He's also a dad, bodybuilder, former wrestler, and philosopher. 

Direct download: Jeff_Kline_and_the_Art_of_Wrestling.output.mp3
Category:podcasts -- posted at: 12:42pm MST

What I do in the in the first 90 seconds of a code…

We want to avoid simultaneous action paralysis: the feeling that multiple things need to happen at once and then nothing gets done. In a code, it seems like everything has to HAPPEN RIGHT THIS SECOND. While it can feel that way, it’s not the case.

My sequence of events in an emergency department cardiac arrest

When the medics roll in, I am listening for five pieces of information. 

  • What happened, preferably in one sentence
  • What was the initial rhythm
  • What have they done (actions, meds, etc)
  • What was the last rhythm
  • How long has the patient been down, unconscious, and presumably in cardiac arrest.

While that report is coming, I keep my eye on the patient's chest to make sure CPR is not stopping. Continuous quality CPR in the first 90 seconds is important because there is so much potential to pause it: transfer to the stretcher, putting on leads, or “Can you stop it for a second for this or that.” Ideally, I’ll have the LUCAS set up so I can take the cognitive load of thinking about CPR out of the picture. 
We’re  about 30 seconds in, and I’ve got general a look at the patient: what's the airway situation, what’s the vascular access. Now is the first decision point. Do I check the rhythm, secure an ET tube, get vascular access? Well, what makes a difference? Electricity is the first thing that comes to mind. So I have the CPR continue while the patient is settled on our stretcher, keeping the EMS chest pads on, keeping the patient attached to their monitor. At this stage, changing over to our monitor (if they’re already on a perfectly good one) makes no sense. Once we’re ready, stop CPR and check the rhythm while simultaneously using the ultrasound for subxiphoid view of the heart. 

Now I’ve got the rhythm and direct visualization of any cardiac activity.  Whatever the rhythm, I know what I'm going to do. 

We're 90 seconds in and I’m moving to intubate/get ETCO2. I that’s already done, I just keep a finger on the femoral pulse while the CPR is happening. Why do I do this? I want to have my hands on the patient but not do be a primary operator of CPR, bag valve mask squeezing, vascular access - just watching and thinking. The room is quiet, there are no raised voices - tone and volume are conversational and calm.

Register for Blood and Sand Dec 6-10, 2015 in the Bahamas!!

Subscribe to EM:RAP

Direct download: How_to_not_freak_out.output.mp3
Category:podcasts -- posted at: 11:13am MST

Torsades de pointes is very bad.  It easily degenerates into Ventricular Fibrillation (VF) and that’s sudden cardiac death.  How many cases of torsades have you seen in your career? Are your ready for it when you see it? Let’s see, there’s magnesium...uh, and then I seem to recall that drug isoproterenol (that I’ve never used) and then..oh yeah...I’m supposed to do ‘OVERDRIVE pacing’.  Got it. Ummm, how do you do overdrive pacing? How does it work? DOES it work?  

First. Let's set the record straight: emergency doctors don’t do overdrive pacing.  How do I know that? Because there is only one indication for “overdrive pacing” in the ED: torsades de pointes.  But the rate of torsades is 150-250 BPM.  And the most commonly used pacemaker in US ED’s is the Medtronic single-chamber Pacer, which has a maximum RATE of 180 BPM. So how were you planning to OVERDRIVE Torsades, which is running at 250 BPM, when your max pacer rate is 180?  See? You can’t even DO overdrive pacing.  What are you really supposed to do?

Ventricular Tachycardia: 2 flavors

  1. Monomorphic VT
  2. Polymorphic VT
    1. Normal QT
    2. Long QT ----- BEWARE! This is Torsades de pointes

Torsades de Pointes = Polymorphic VT with long QT

  • Torsades occurs when a PVC occurs during the T Wave  (R on T)
  • THIS explains WHY ‘overdrive pacing’ works - see Treatment below

The QT conundrum:

The QT is heart rate-dependent.  When the heart rate is slower, the QT is longer, and vice versa.  In order to determine whether your patient truly has a long QT, the QTc was developed as a calculation that that attempts to normalize the QT interval to a rate of 60 BPM.  

The bottom line: the QTc is number you should look at.  There are several calculations available- even MDCalc has one.  But just look at the top of the EKG. It turns out the EKG computer does a fine job of calculating the QTc. Use the QTc.

What is a long QTc

The dirty definition:   Long QT = QT > 500 ms 

Beware the patient with syncope or near-syncope with a QTc longer than 500.  You might be staring straight at a patient who just had polymorphic VT with long QTc.  You might be staring at torsades.  Torsades likes to degenerate into VF, and VF is a less than desirable rhythm.

Treatment of Torsades

  1. Stabilize the cardiac myocyte and treat hypomagnesemia: Magnesium 2gm IV q15m
  2. Increase the resting heart rate. Increasing the HR narrows the QT. Narrowing the QT narrows the T wave (ventricular repolarization). A narrow T wave means your ventricle is spending less time repolarizing.  If your T wave is narrow, the chances of throwing a PVC on top of a T (R on T) is much less likely.  So....just increase the heart rate. Oh wait...increase the heart rate AFTER you’ve cardioverted them from polymorphic VT.

Drugs to use after sinus rhythm achieved and you want to speed the heart rate


  • nonselective beta agonist
  • Inotropic, chronotropic, dromotropic
  • dose: 10-20 mcg IVP or drip


Dopamine drip

**Transvenous Pacing: RATE = 110 BPM

Bonus: Hollywood Weingart

Show notes by Joe Bellezzo from the ED ECMO podcast

Direct download: Torsades_De_PointesTorsades.mp3
Category:podcasts -- posted at: 6:05pm MST

Mel Herbert is arguably the most influential medical educator of our time. He sat down with ERCast to discuss...

Direct download: Mel_Herbert_This_Wont_Hurt_A_Bit_ERCast.output.mp3
Category:general -- posted at: 3:45pm MST

What does suicidal ideation really mean? It comes down to mindset and intent. For example: wrist cutting. Is it a suicide attempt, a stress relief, a way to get attention? It could be any of those. The behavior, often called the WHAT, needs to be connected to the WHY.  There can be a bad injury, the 'what', but it's the 'why', the mindset and intent, that determine disposition when all the suturing is done.  The idea of connecting the WHAT and the WHY will recur throughout this discussion, not always in those words, but at least in concept. (credit to Kelly Posner for that 'what' and 'why' phrasing. I heard that in a lecture of hers and thought, "....couldn’t have said it better myself."

How do you assess suicide risk. You can use gestalt, decision tools, or whatever relevant questions come to mind. There’s no one best way, no one ring to rule them all. For those who have listened to the show for a while, you know that I use my own algorithm to organize the information in evaluating a mental health or potentially suicidal patient. It's more of a general overview, but getting to the specific question of

"Is my patient suicidal?" the Columbia Suicide Severity Rating Scale   gives a nice framework for asking questions. This isn’t a deep dive into this scale with its algorithm, decision trees,  etc. We're going to use it today as an example of what questions to ask and how to ask them, how to structure the interview - facilitate the assessment.


The Columbia Suicide Severity Rating Scale is a cascade of 6 questions

Step 1: Is there ideation, a wish to die


  • Have you wished you were dead or wished you could go to sleep and not wake up?
  • Have you actually had any thoughts of killing yourself?
  • Have you wished you were dead and have you had thoughts of killing yourself?

These are very general, the screening of the screening- spreading a wide net with maximal sensitivity but minimal specificity.

If the answer to both of these is no- no wish to be dead, no thoughts of killing themselves, then there’s no expressed suicidal ideation. If there’s no ideation, then there’s a final question, kind of a fail safe: Have you ever done anything, started to do anything, or prepared to do anything to end your life? If the answer to that is yes, then when did it happen? If it’s recent, within the past month or so, then the patient just went from potentially low risk, no stated thoughts of suicide, to high risk.

Step 2: If there is ideation, define it

We've established the patient has had thoughts of wanting to die or not wake up or kill themselves. Is there Suicidal Intent, not a specific plan, just intent?


  • Have you had these thoughts and had some intention of acting on them? 

Is there Suicide Intent with Specific Plan:


  • Have you started to work out or worked out the details of how to kill yourself? Do you intend to carry out this plan? 

And the final question: 

  • Have you ever done anything, started to do anything, or prepared to do anything to end your life? More insight and an idea of history because previous attempts are a risk factor for future attempts.

Sometimes it's pretty clear what's going on, there has been an event and they've said that they were trying to kill themselves. They don't have to have actually hurt themselves. It’s the intent to die. 

Things that are not on the Columbia Scale that I ask in patient encounters

  • If a patient comes in after an attempt or has been thinking about it, “What did you think would happen when you did X?” 
  • A follow up question to that is, “How do you feel now that you’re not dead, that you’re here talking to me?”


When we explore the ideation a little more deeply, there a few aspects that color the picture. 

  • Is this incessant or fleeting ideation? 
  • Have you attempted suicide before?
  • In a patient with ideation but hasn't attempted, one of the most important question is:  Why haven’t you killed yourself? What’s stopping you from doing it? 
  • This gives insight into protective factors and makes a huge difference. Protective factors decrease the chance of completing suicide. Things like family, like religious beliefs. If someone says they haven't jumped off a bridge yet because they just haven't gotten up the nerve. Is that a protective factor? Not much of one. If they haven't attempted because they don’t want to leave their family and it’s against their religious beliefs, are those protective? Yes, not like a force field, or being superman, but more than nothing. 

Something I heard recently that isn’t something we’d normally ask, this was from  Kelly Posner, the developer of the Columbia tool. Ask...

  • Did you want to kill yourself? No? Did any part of you want to kill yourself? 

As long as you’re organized, systematic, you learn the Why behind the What, the mindset and intent, if there even is intent, you’ll be off to a good start. But despite our best assessment, a great evaluation, an estimate that the patient is low risk, the reality is that is suicide is often an impulsive act, things change, the mind changes, an event can tip someone over the edge in a moment. For many, suicidal ideation is short lived, less than an hour, and the time between deciding on suicide and attempting is often less than 10 minutes.

While we want to assess the factors that are associated with suicide, hopelessness, previous attempts, feeling trapped like there’s no exit, the extent of suicidal ideation, we can't always outsmart the tides of the human psyche.  But there are other things that we can do to decrease someone's risk of killing themselves and one of those is completely unrelated to mental health.It is the means by which suicide happens. It is impossible to restrict all the means of suicide. People hang themselves,  are you going to take all the rope out of their house, or take away their car so they can't crash it or die from carbon monoxide, take away their shoes so they can’t run into traffic?

What is the likelihood of death from different means of suicide attempt?

  • Overdose and sharp instruments 1-2%
  • Gas 45%
  • Hanging 61%
  • Firearms 82%

No matter where you stand politically on firearms, there’s no denying that use of a firearm gives one of, if not the best, chances of dying from a suicide attempt.

If you remove the lethal means, the chance of dying is lower. Not zero, but lower. History gives us many examples of this. Prior to the 1960’s, in the UK, the most common method of death from suicide was gas asphyxiation, after a less toxic gas source was used, that rate dropped precipitously.  Other methods were used, but the overall rate of suicide death dropped. In Sri Lanka, suicide by pesticide was the most common method. When less toxic pesticides were introduced, the number of attempts didn’t drop but the number of suicide deaths plummeted. IN the Israeli army, a compulsory military force made up mostly of adolescents, 18 and 19 year olds, many soldiers were dying, not from missile attacks, but from suicide by firearm. The army instituted a policy that firearms couldn't be taken home on weekends (a time when an impulsive act of suicide attempt ma occur). The suicide rate dropped by 40%.

When the immediately lethal means are removed, does it make a difference? Yes. The evidence is there, the chance of dying is lower. But  we don’t always ask our depressed and suicidal patients about whether or not they own or have access to firearms, or plan on buying a firearm. Say you have a suicidal patient, even one who's low risk, and there is access to firearms. One way you can phrase it is this: "There’s no way to predict what’s going to happen when you go home. You feel better now, safe leaving the hospital, but that can change. When there’s access to a firearm, and someone feels suicidal  the chance of dying just went up, dramatically. I don’t want you to die, your family doesn’t want you to die, and you don’t want to die."  I have never had a situation where a discharged  patient and their family weren’t in agreement to get the guns out of the house or in some way made no access during the period of crisis.


  • When your suicidal patient comes in, or someone potentially suicidal, get the story, the what and the why. How are those connected. What was the link between what they did and and why they did it. Their mindset and intent.
  • And then, a risk assessment. Is there ideation? If there is ideation, explore it. You can use the my method, Columbia Scale, combinations of the two (which is what I do). There are other tools out there as well. No matter what the tool, think of it as a way to organize questions and collect information, to can inform your risk assessment. It does not trump your clinical judgment and gestalt, it facilitates. 



Suicide Risk Assessment in the ED podcast 

  • Large, Matthew, et al. "Risk factors for suicide within a year of discharge from psychiatric hospital: a systematic meta-analysis." Australian and New Zealand Journal of Psychiatry 45.8 (2011): 619-628.
  • Shah, Seema, et al. "Adolescent suicide and household access to firearms in Colorado: results of a case-control study." Journal of Adolescent Health 26.3 (2000): 157-163.
  • Simon, Robert I. "Gun safety management with patients at risk for suicide."Suicide and Life-Threatening Behavior 37.5 (2007): 518-526.
  • Levin, Aaron. "Several Signs Should Alert Clinicians to Suicide Risk." (2014).
  • Pinholt, Ellen M., et al. "“Is There a Gun in the Home?” Assessing the Risks of Gun Ownership in Older Adults." Journal of the American Geriatrics Society 62.6 (2014): 1142-1146.
  • Wintemute, Garen J., et al. "Mortality among recent purchasers of handguns."New England Journal of Medicine 341.21 (1999): 1583-1589.
  • Fisher, Lauren B., James C. Overholser, and Lesa Dieter. "Methods of committing suicide among 2,347 people in Ohio." Death studies ahead-of-print (2014): 1-5.
  • Barber, Catherine W., and Matthew J. Miller. "Reducing a suicidal person’s access to lethal means of suicide: a research agenda." American journal of preventive medicine 47.3 (2014): S264-S272.
  • Spicer, Rebecca S., and Ted R. Miller. "Suicide acts in 8 states: incidence and case fatality rates by demographics and method." American Journal of Public Health 90.12 (2000): 1885.
Direct download: Suicide_Podcast.output.mp3
Category:general -- posted at: 10:29am MST

Deep venous thrombosis of the calf causes an undue amount of consternation. What's the best way to manage these?Anticoagulate, serial ultrasound, do nothing? We break down the evidence to help you decide.

What are we worried about with calf DVT?

  1. Will it become a PE?
  2. Will the clot propagate proximally?
  3. Does treatment make a difference for recurrence?
  4. Does treatment make a difference for post phlebitic syndrome?

The numbers

Propagation to proximal veins

  • Without anticoagulation: around 15%. Wide variation in numbers
  • Propagation with anticoagulation: around 2%
  • Propagation is probably higher with risk factors such as malignancy and an unprovoked clot
  • Caveat: isolated gastrocnemius and soleal vein clots progress at about 3% untreated. Felt to be lower risk than the other deep veins of the calf. Lower risk of extension. No clear evidence on what to do.

Pulmonary Embolism

  • Without anticoagulation up to 6%
  • With anticoagulation 0-6%, biggest study 3%, but PEs mostly asymptomatic 
  • 1 reported fatal PE, but unknown if this patient was anticoagulated


  • Short term recurrence without treatment: up to 30%
  • Short term treatment with treatment 0-3%,
  • Recurrence is higher if two calf veins involved, increased clot burden

Compression stockings and post thrombotic syndrome 

Post thrombotic syndrome (PTS) is a horrible consequence of DVT.  Reflux from valve injury and venous hypertension lead to chronic edema, pain, and leg ulcerations. If there’s something that can mitigate that in our patients, we’d want them to have it. The incidence of PTS  in proximal DVTs is around 50%, depending on the source you read. In calf DVTs, it’s lower: somewhere around 10 to 24%.

There is good evidence that compression stockings can decrease the incidence of PTS.

  • Lancet 1997: about 200 patients with acute DVT compression stockings versus none. Compression stockings reduced the rate of PTS by about 50%.
  • Annals of internal medicine 2004: Below the knee compression stockings to prevent the post thrombotic syndrome. Half of the patients with no compression stockings developed PTS versus a quarter who wore stockings. How long did they wear the stockings? 2 years. Why two years? It’s because that’s the time window when the majority of PTS develops. When you break down the numbers of the study, there was an NNT of 4. Treat four patients with compression stockings to prevent one post thrombotic syndrome. That is a huge return on investment. A frequent question: Do patients need to wear the stockings 24/7. The study protocols were said just during the day, so,... just during the day.

A 2014 Lancet study,  suggested that there was no benefit to compression stockings. The above two trials used stockings or no stockings, this one used the 30-40 mm Hg graduated compression stockings or placebo, which was a 5 mmHg stocking. Results: no benefit of compression stockings over placebo socks. Does this study show that stockings don't make a difference? Or was the placebo not actually a placebo since there was still some degree of compression, albeit light.  I think you could interpret all of this data in several ways.

  • First  - more recent data suggests compression stockings  don't work (although I disagree with that interpretation)
  • Second - there are several studies showing benefit with a low NNT... NNT of 4 for a horrible sequelae.
  • Third - a light grade of compression, such that was used in the recent Lancet stud,y gives the same result as high pressure compression.

ACCP recommends compression stockings for proximal DVTs (ankle pressure of 30-40 mm Hg). Start as soon as possible and continue for 2 years. That is a grade 1A recommendation. How this will change based on more recent evidence remains to be seen. Distal DVTs, even more unclear.

Duration of treatment

  • For proximal DVTs, 3 months of treatment but for calf DVTs, no benefit found if treatment extended beyond 6 weeks. 
  • The ACCP, American College of Chest Physicians, kind of recommends 6 weeks. Mostly of a discussion in the evidence review that there’s no benefit in treatment beyond 6 weeks.
  • Post surgical patients with 2 or more veins involved, 12 weeks (3 months of treatment)

Type of treatment

No superior agent. Unfractionated heparin, LMWH, vitamin K antagonists-nothing superior. Many providers are using oral Xa inhibitors, but these are unstudied (yet still heavily used). You can extrapolate that LMWH is aba inhibitor, albeit by a different mechanism, so an oral Xa inhibitor should be effective too, but we don’t have direct evidence to answer that question.

Different treatment recommendations and guidelines

2012 ACCP: serial ultrasound for low risk clots and treat high risk clots (cancer, close to the popliteal vein, history of prior DVT)

National Clinical Guideline Centre: did not mention the treatment of isolated distal DVT because the guideline “... focused on proximal DVT rather than isolated calf vein DVT as the latter is less likely to cause post thrombotic syndrome than proximal DVT and also less likely to embolize to the lungs."

International Consensus Statement on Prevention and Treatment of Venous Thromboembolism: 3 months of oral anticoagulants for all calf clots

Up to date: Treat for 3 months (based on poor evidence) versus 2 weeks of serial US

Hematologist Tom Deloughery

  • Muscular Calf Vein (soleus or gastrocnemius) Thrombosis: 10 days of therapeutic LMWH or rivaroxaban.  
  • Calf Vein Thrombosis: 6 weeks of rivaroxaban

Jeff Kline 3 weeks of rivaroxaban. Permanent anticoagulation for active cancer, unprovoked clot

Rob O: 6 weeks anticoagulant and 2 years compression stockings

References for this podcast

Links mentioned in this show

Direct download: Calf_Clots_ercast.output.mp3
Category:podcasts -- posted at: 11:40am MST

A trauma patient with persistent, yet unexplained hypotension may be suffering from neurogenic shock. What's that? Anand Swaminathan joins the show to help break down the diagnosis and treatment. 

Register for Essentials of Emergency Medicine and get access to Essentials LA on August 27, 2015

 **Correction: the original title of this post was "spinal shock" which, of course, is a different entity than neurogenic shock. The term spinal shock is also used interchangibly with neurogenic shock during the conversation. The entity we are referring to in this show is indeed neurogenic, and not spinal shock.

A primer on Neurogenic Shock courtesy of EM Lyceum

Neurogenic shock is a form of distributive shock unique to patients with spinal cord injuries. Fewer than 20% of patients with a cervical cord injury have the classic diagnosis of neurogenic shock upon arrival to the emergency department, and it is a relatively uncommon form of shock overall (Guly, 2008). Patients with injuries at T4 or higher are most likely to be affected by neurogenic shock (Wing, 2008). It is caused by the loss of sympathetic tone to the nervous system, ultimately leading to an unopposed vagal tone (Stein, 2012). Many times the terms “spinal shock” and “neurogenic shock” are used interchangeably, although they are two separate entities. Spinal shock consists of the loss of sensation and motor function immediately following a spinal cord injury (Nacimiento, 1999). During this period of spinal shock, reflexes are depressed or absent distal to the site of the injury. Spinal shock may last for several hours to several weeks post injury (Nacimiento, 1999).

Symptoms of neurogenic shock consist of bradycardia and hypotension (Grigorean, 2009). Bradycardia is typically not present in other forms of shock, and may provide a clue to clinicians that a patient has sustained a spinal cord injury. However, emergency physicians should recognize that hemorrhagic shock needs to be first ruled out, even in patients with bradycardia, many patients with hemorrhagic shock are not tachycardic (Stein, 2012). Cardiac dysfunction is another feature of neurogenic shock, and patients may present with dysrhythmias following injury to the spinal cord (Grigorean, 2009).

The American Spinal Injury Association (ASIA) has classified injuries based on motor and sensory findings at the time of injury. ASIA A and B injuries are the worst; with A being a complete motor and sensory loss with no preserved function in the sacral segments S4-S5. ASIA B includes patients who have sacral sparing, meaning that they have function of S4 and S5 (Marino, 2003). Neurogenic shock is rarely encountered in the emergency department, however, it is important to recognize that almost 100% of patients who sustain complete motor cervical ASIA A or ASIA B injuries develop bradycardia. Thirty five percent of these patients ultimately require vasopressors, so management of neurogenic shock is imperative for emergency physicians (McKinley, 2006). There is no conclusive data regarding the optimal time to start vasopressors, however, it is important to maintain appropriate hemodynamic goals in patients with spinal cord injuries.

Hemodynamic goals in patients with spinal cord injuries are unique. A systolic blood pressure <90 mmHg must be corrected immediately (Muzevich, 2009). The American Association of Neurological Surgeons and the Congress of Neurological Surgeons Guidelines for the Acute Management of Spinal Cord Injuries both recommend a MAP at 85 to 90 mm Hg for the first seven days following a spinal cord injury based on observational descriptions of the hemodynamics in spinal cord injured patients (Levi, 1993Licina, 2005).

Patients who are suspected of being in neurogenic shock should receive adequate fluid resuscitation prior to initiating vasopressors (Wing, 2008). However, there are no current recommendations regarding the first line vasopressor for neurogenic shock (Stein, 2012). Depending on a patient’s hemodynamics, this vasopressor will likely be norepinephrine, phenylephrine, or dopamine.

Norepinephrine is an excellent first line vasopressor in neurogenic shock due to its alpha and some beta activity, thus leading to its ability to improve blood pressure and heart rate (Stein, 2012). Phenylephrine is another common choice because it is easy to titrate and can be given through a peripheral line. A disadvantage of phenylephrine is the fact that it can lead to reflex bradycardia due to its lack of beta agonism. This drug may be most appropriate in patients who are not bradycardic (Wing, 2008). Dopamine is another option, however, it may lead to diuresis and ultimately worsened hypovolemia (Stein, 2012). It does have beta agonism, and in bradycardic patients may be favored over phenylephrine (Muzevich, 2009). Dopamine is unlikely to be tolerated in patients who are experiencing dysrhythmias.


Direct download: Neurogenic_Shock_ERCast.mp3
Category:general -- posted at: 7:06pm MST

There's no getting around night shifts in the emergency department. Most of us work nights to some degree or another and find them less than pleasant. Are there ways to mitigate the misery? Haney Mallemat joins ERCast to discuss nightshifts and so much more....

In this episode

Finding your niche and following your passion in medicine and life

Tranexamic acid (TXA) used for oral mucosal bleeding

Listener emails

  • Acute care nurse practitioners in the emergency department
  • Warming patients after hypothermia

Night Shifts

  • Complex decision making
  • What's the deal with caffeine?
  • Optimal shift sequencing
  • Zolpidem (Ambien) and melatonin
  • Casino Shifts

Important links mentioned in this show

Check out Primary Care RAP! Clicking this link will give you a 20% discount that’s automatically applied at checkout.

Register for Essentials of Emergency Medicine, Oct 13-15 Las Vegas

Register for Blood and Sand, Dec 6-10 Bahamas

Direct download: Night_Shifts_ercast.output.mp3
Category:general -- posted at: 7:53pm MST

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



  • 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: 9:15am MST

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


  • 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: 9:02am MST