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

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: 5:40 PM

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: 1:06 AM

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: 1:53 AM

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: 3:15 PM

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: 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...


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