Monday, May 25, 2015

Hippocratic Medicine No. 4: Victims of Our Own Success?

Clinical Scenario:
Working a emergency department shift on a typical busy day, you see the next patient slotted is a 36-year-old female coming in with shortness of breath and fatigue. She also has a history of anemia, anxiety, and panic disorder.

About one month prior, she presented to another emergency department (ED) complaining of chest pain for the last several weeks along with other vague complaints. Her heart rate of 101 prevented application of the PERC rule and made her moderate risk by Well’s criteria. A d-dimer was sent and was elevated, so she underwent a computed tomography pulmonary angiography (CTPA) scan looking for pulmonary embolism (PE). This demonstrated non-occlusive pulmonary emboli present in branches of the left upper lobe, right middle lobe, and left lower lobe pulmonary arteries. She was admitted to the hospital and started on rivaroxaban.

About 2 weeks prior to today’s visit, she had presented with continued chest pain and shortness of breath. She underwent another CTPA demonstrating no pulmonary emboli. Her hemoglobin was checked on this visit and found to be 11 g/dl. She was discharged and continued taking her rivaroxaban.

During to today’s visit, in addition to her shortness of breath and fatigue, she is also complaining of vaginal bleeding. It is around the normal time for menses, however it has been going on longer and heavier than usual. Her hemoglobin is checked and is found to be 5.6 g/dl. She is given two units of packed red blood cells and admitted to the hospital.

You can’t help but wonder, was there truly a PE in the first place? Did it require treatment? Did we cause this patient harm by putting her on anticoagulation?

Literature review:

The diagnosis of PE has evolved significantly over the past few decades from a disease only suspected and confirmed on autopsy to small subsegmental pulmonary embolisms (SSPE) found on multi-detector CTPA. Despite the increased diagnosis of PE due to CTPA, there has not been a significant change in associated mortality nor an increase in diagnosis of larger, central pulmonary emboli [2]. What has changed is the increased diagnosis of smaller sub-segmental pulmonary embolism (SSPE) due likely to both the sensitivity of the technology and increased physician vigilance for finding the disease [1].

Not long ago, pulmonary embolism was felt to be under-diagnosed, only found after the patient had died from the condition. With the widespread availability and ease of CTPA, there is increasingly concern for overuse of CTPA, perhaps with associated over-diagnosis and over-treatment. Wiener et al studied the incidence, mortality, and treatment complications of PE in the 5 years preceding the introduction of CTPA and the years that followed [2]. With the introduction of CTPA, he found that the diagnosis of PE almost doubled (62.1 to 112.3 per 100,000) and complications from anticoagulation increased (3.1 to 5.3 per 100,000), while the mortality from PE stayed about the same (12.3 to 11.9). While the increase in diagnosis is probably due to increased awareness of PE as well as availability of testing, some of the increase may also be due to the detection of smaller SSPE on multi-detector CTPA that may not be clinically relevant [3].

As a large proportion of the additional PEs detected (above the prior baseline) are SSPEs [3], and in light of the increase in bleeding complications from anticoagulation, this raises the question as to whether the risks of treatment outweigh the risks of going untreated. A study in CHEST demonstrated that hemodynamically stable patients with segmental or sub-segmental PE had low risk of adverse outcome, although in this study population treatment was at the discretion of the treating physician [6]. In a review paper by Ikesaka and Carrier, they found that patients with suspected PE with a non-diagnostic ventilation-perfusion scan and negative compression ultrasonography of the lower extremities could be safely managed without the use of anticoagulation with a recurrent risk of embolism similar to those without PE on CTPA [1]. In addition, 17% of patients with a low probability ventilation/perfusion (V/Q) scan had an isolated SSPE on CTPA.

Despite many physicians treating it otherwise, CTPA is not a gold standard for PE diagnosis. Up to 11% of CTPA studies read initially positive for SSPE are read as negative when reviewed by experienced thoracic radiologist. These 'false positives' may be caused by indeterminate intra-luminal filling defects that may be caused by patient motion artifact or other imaging artifact [4,7].

In addition to the potential harm in placing someone unnecessarily on anticoagulation, testing for PE can also cause harm. The radiation from the scan can cause promote cancer later in the patient’s life while the contrast can induce nephropathy. In a conservative estimate by Newman and Schriger, they found that in testing for PE, physicians can prevent 6 deaths from PE and 24 major, nonfatal PE events per 10,000 individuals [8]. At the same time, testing also can cause 36 deaths and 37 nonfatal major medical harms per 10,000 from bleeding complications, development of cancer, and contrast-induced nephropathy. This estimates seems to imply that physicians can cause more harm than benefit in testing for PE if the diagnostic test is not applied judiciously to patients.

With the introduction of CTPA, there has been a substantial increase in the diagnosis of PE, especially SSPE, without much apparent clinical benefit with treatment. Are we over-diagnosing more patients and putting them on treatments with potential harm? Do we need to scan or even treat these patients? In this presented case, did this patient truly have a PE given that a repeat scan 2 weeks later was read as completely negative? Did this patient bleed down to a hemoglobin of 5.6 g/dl because of the treatment she was on? 

Take home points:
- Pulmonary embolism may be over-diagnosed and over-treated
- Be aware of the false positive rate with CTPA and consider this when deciding whom to test
- There’s evidence to suggest not all PE’s are the same, but there is insufficient ED-based data to determine who should receive anticoagulation
-Realize that you can cause harm putting a patient on anticoagulation when it is not necessarily needed

Submitted by Steven Hung, PGY-2 (@docHungER)
Edited by Alicia Oberle, PGY-3
Faculty Reviewed by Ryan Schneider, Richard Griffey, and Chris Carpenter (@SAEMEBM)
Image by Maia Dorsett (@maiadorsett)

Want to read more? Click here to read the WashU Journal Club on reducing PE protocol CT ordering rates in the ED.

1. Ikesaka F, Carrier M. Clinical significance and management of sub-segmental pulmonary embolism. J Thromb Thrombolysis. 2015 Apr;39(3):311-4.
2. Wiener RS, Schwartz LM, Woloshin S. Time trends in pulmonary embolism in the United States: evidence of overdiagnosis. Arch Intern Med. 2011;171(9):831-837
3. Carrier M, Righini M, Wells PS, Perrier A, Anderson DR, Rodger MA, Pleasance S, Le Gal G. Subsegmental pulmonary embolism diagnosed by computed tomography: incidence and clinical implications. A systematic review and meta-analysis of the management outcome studies. J Thromb Haemost. 2010 Aug;8(8):1716-22.
4. Jones SE, Wittram C. The indeterminate CT pulmonary angiogram: imaging characteristics and patient clinical outcome. Radiology. 2005 Oct;237(1):329-37.
5. Prasad V, Rho J, Cifu A. The diagnosis and treatment of pulmonary embolism: a metaphor for medicine in the evidence-based medicine era. Arch Intern Med. 2012 Jun 25;172(12):955-8.
6. Vedovati MC, Becattini C, Agnelli G, Kamphuisen PW, Masotti L, Pruszczyk P, Casazza F, Salvi A, Grifoni S, Carugati A, Konstantinides S, Schreuder M, Golebiowski M, Duranti M. Multidetector CT scan for acute pulmonary embolism: embolic burden and clinical outcome. Chest. 2012 Dec; 142(6):1417-24.
7. Wittram C, Maher MM, Yoo AJ, Kalra MK, Shepard JA, McLoud TC. CT angiography of pulmonary embolism: diagnostic criteria and causes of misdiagnosis. Radiographics. 2004 Sep-Oct;24(5):1219-38.
8.Newman DH, Schriger DL. Rethinking testing for pulmonary embolism: less is more. Ann Emerg Med. 2011 Jun;57(6):622-627.e3.

The Hippocratic Medicine series is modeled after the Do No Harm project pioneered at the University of Colorado. The aim of this series is to raise awareness about the avoidance of avoidable care i.e. for how medical overuse has the potential to do patient harm. Because every test or intervention we do has the potential for not just benefit but also harm, we should seek that our patients do better because of the care we provide instead of despite it. The WUSM Hippocratic Medicine Series is supported by a grant provided by the Foundation for Barnes Jewish Hospital.

Tuesday, May 19, 2015

@WUSTL_EM #EMConf: #FOAMed Supplement No. 3

This week we had a combined conference with our neighboring residency at St. Louis University to discuss the important topic of wellness in emergency medicine.  The line-up included talks on sleep,  physician burnout, the impaired physician, second-victim syndrome, and a board panel of attendings to discuss their own "tricks of the trade".  Unlike sexier topics such as critical care, I was able to find a lot less on these topics in the FOAMed world.  While "wellness" may be more nebulous, it remains extremely important not only to our quality of life as physicians, but also to the quality of care we provide to our patients.

1. The Importance of Sleep.
The TED series has a number of talks on sleep.   Russell Foster, a neuroscientist, gave this talk on Why do we sleep?

2. Physican Burnout & The Impaired Physician.
There has been a fair amount of attention to the risk of suicide amongst physician in the public media. The article, Why Do Doctors Commit Suicide?  published in the NY Times draws attention to importance of peer support in physician coping.

For EM-specific resources, emdocs produces the EM Mindset series, which is written by EM physicians and describes our specific practice of medicine.  It has a lot to offer the young EM physician. Some posts in this series touch directly on mechanisms for resilience, including:
            James Adams:  Frameworks & Habits of an EP
            Rob Orman :  The Successful EM Mindset
            Steve Carroll: Masters of the Undifferentiated Patient
Finally, you can also read this article that was discussed during today's lecture on factors contributing to "burnout" during EM residency.

3. The Second Victim: The TED series has a number of talks that focus on humanizing the physician and discussing medical errors.  Brian Goldman's talk, entitled Doctors Make Mistakes, Can we Talk about that? is particularly well done.

4. Advice from Others:  Check out the How I Work Smarter series from ALiEM.
My particular favorite?  Rob Rogers' post,  because of this great advice which I have taken to heart:

                    ' Someday when you are sitting on your front porch in a rocking chair
                      thinking about the “good ole days” you aren’t going to have thoughts
                      of “I wish I had written one more paper or traveled for one more lecture."'

Enjoy ... or maybe take a nap instead. #ChooseWellness


Tuesday, May 12, 2015

@WUSTL_EM #EMConf: #FOAMed Supplement No. 2

Welcome to @WUSTL_EM #EMConf, the #FOAMed Edition. The purpose of this weekly column is to identify #FOAMed resources that reinforce and expand on the concepts/facts discussed during weekly conference.  Please e-mail to share additional resources (or just post them as comments below).
This week in @WUSTL_EM #EMConf ....

1. Neurology Core Content with Education Resident Sean Cavanaugh:
- see this post from EM Lyceum on tPA in ischemic stroke (including blood pressure management, age cutoffs etc.) as well as this one on  management of intracranial hemorrhage.
 - In patients with vertigo and concern for posterior circulation stroke, learn to perform the HINTS exam.  Our own EM Journal Club reviewed the HINTS exam in this podcast, with supplemental videos provided on the website.
- Get certified to perform the NIH Stroke Scale correctly by working through the online module provided by the National Stroke Association here.
- Good resources for "on the shift" reminders of the NIH stroke scale and contraindications to tPA are ALiEM's PV cards on the subject.

- I highly recommend this post from EM Lyceum covering pharmacologic management of seizures, imaging in first time seizure, and diagnosis of pseudoseizures.
-ALiEM has some good resources regarding phenytoin loads: this "Trick of the Trade" post on single dose oral load for phenytoin in the ED and this one on understanding phenytoin equivalents.
- EM basic has this podcast on general seizure management and this post on febrile seizures.

2. Sepsis: Shock & Awe with Dr. Wes Watkins
 - Rebel EM did this post summarizing the results of the ProMISe, ARISE, and ProCESS trials.  If you prefer the podcast version, you can listen to the RebelCast here.
- SGEM evaluated the ProMISe trial in  Podcast #113
- Our own blog advocated a balanced approach to fluid choice for resuscitation in sepsis in this post.
- Approach to assessment of volume status with ultrasound via the Ultrasound Podcast.

3. Physostigmine for Anticholingeric Toxicity with Dr. Wes Watkins:
 - Life in the Fast Lane gives a "how to administer" for physostigmine.
 - A further review of use of physostigmine for anticholingeric toxicity from the EM Pharm D blog.

4. Difficult Diagnosis with Maureen Gross - we discussed the "gray area" of diagnosis of septic arthritis.  For further reading regarding this difficult-to-make diagnosis see Chris Carpenter's 2013 review in EP Monthly. Also check out this emdocs post on septic arthritis as well.

5. Sleep Cycle with Maureen Gross: Could not find much FOAMy material on the subject, but you can check out this review article on sleep cycle and pharmacologic sleep aids for the emergency physician.

6. Ortho Radiology with Dr. Ruoff: Northwestern has this great Ortho teaching website that allows one to work through a series of cases.


Friday, May 8, 2015

EKG Challenge No. 13 Case Conclusion: Sometimes The Pain Ain't From Cocaine

You are working one evening in the emergency department when you walk in to see your 4th chest pain patient of the night.  Your current patient is a 50-something year old male who's years of homelessness and cocaine abuse have made him appear older than his stated age.  He tells you that  he has been having left sided chest pain on and off for the last 3 hrs.  He received ASA and nitro x 2 in the ambulance and now feels much better.  You examine his EKG from today:

EKG #1 (day of presentation)

You then compare it to his EKG from two days ago when he came in for chronic diarrhea (and had mentioned some intermittent chest pain):

EKG #2 (EKG from two days prior to presentation)

... and compare it again with his EKG from 1 year before during an admission for chest pain in which he had a negative cardiac stress test:
EKG #3 (EKG from one year prior to presentation)

Initially, you compare his first and second EKG.  You think, "those T waves in V2 and V3 look weird, but they are unchanged from previous".  However, you note that this prior EKG was only a couple days before and you compare them with the EKG from a year before... when those strange, biphasic T waves were not present.

Whenever you see T wave abnormalities in a patient with possible unstable angina, you need consider an electrocardiographic syndrome of critical LAD stenosis that was first described by Hein Wellens and colleagues in 1982 and thus is referred to as Wellen's Syndrome

Wellens' Syndrome is a clinical-electrocardiographic syndrome with the following criteria [1,2]:
 - Prior history of chest pain - i.e. the patient is now chest pain free
- Little or no cardiac enzyme elevation
- No pathologic precordial Q waves
- Little or no ST-segment elevation
-  Symmetric or deeply inverted T waves in leads V2 and V3 (and occasionally the other precordial leads as well) OR  biphasic T wave in leads V2 and V3

As noted above, Wellens' syndrome has variable electrocardiographic presentations.  It comes in one of two forms:  symmetric, deep T wave inversions (75% of cases) or biphasic T waves (25% of cases) [2,3].  These T wave inversions are notable for their steep angle of descent and depth.  While changes in V2, V3 are typical, T-wave abnormalities may also be present in the other precordial leads (V1, V4, V5, V6) as well.  Wellens' syndrome is dynamic, which is one of the features that distinguishes it from more benign causes of precordial T wave inversion such as LVH with strain.  Dr. Steve Smith's ECG blog has this post on distinguishing benign T wave inversion from Wellens' syndrome.
Figure 1 from the original paper describing Wellens' syndrome (Ref 3).  Note the two patterns of precordial T wave abnormalities.

Wellens' syndrome was first identified by a retrospective study of patients presenting with unstable angina [3].  This study found a strong correlation between one of two distinct patterns of T wave abnormalities in V2 and V3 and high risk for progression to large anterior wall myocardial infarction.  This association was re-confirmed with a follow-up prospective study of 204 patients admitted to their hospital between 1980-1985 with unstable angina and findings of Wellens' syndrome on the EKG.  180 of these patients underwent cardiac catheterization.  All had evidence of LAD lesions,  29% of which were proximal to the first septal perforator.  In general, patients who had medical management vs. angioplasty were more likely to die of sudden cardiac death  (8/30 for medical management vs. 3/115) [4].

Given the high risk of progression to left anterior wall myocardial infarction and death, patients with Wellens' syndrome should NOT undergo a cardiac stress test. [2]  They should go cardiac catheterization sooner rather than later (probably from the ED in ideal circumstances) as they are extremely high risk for progression to anterior STEMI:
Figure 2 from the original paper demonstrating progression from Wellens' to STEMI (and death).

After intervention and with time, ninety percent of patients with Wellens' syndrome will regain a normal ST-T segment [4].  While an exact time period for resolution of EKG changes was not specified in Wellens' paper,  ST-T wave abnormalities were more likely to persist in patients who continued to have chest pain, undergo medical therapy, or had extensive collateral circulation on cardiac catheterization suggesting longer term and more permanent cardiac injury.

So what happened with our patient?  After his second presentation with unstable angina and biphasic T waves, the emergency physician diagnosed him with Wellens' syndrome and admitted him to the Cardiology service where he was taken for cardiac catheterization and underwent stenting of a 90% lesion in his proximal LAD.  While his hospital discharge summary announced that "it was felt that his chest pain was still most likely to costochondritis or cocaine use",  the change in T wave morphology on his post-cath EKG suggests otherwise:

Clinical Take Home: Proper risk stratification and correct disposition of patients presenting with possible acute coronary syndrome is a common and difficult problem faced by pre-hospital personnel and emergency physicians. While anterior T wave abnormalities can have a wide differential diagnosis with both benign and concerning causes  [including but not limited to persistent juvenile T wave inversion, pulmonary embolism, ongoing cardiac ischemia and neurocardiogenic injury], in a now pain free patient with symptoms of unstable angina a critical LAD stenosis with high risk for progression to large anterior wall MI must be considered.  These patients should undergo cardiac catheterization sooner rather than later as they are at very high risk for progression to massive acute anterior wall myocardial infarction.  Do not under any circumstances send them for a stress test, as this may trigger massive MI and cardiac arrest.  Finally, be a patient advocate.  Although coronary vasospasm from cocaine use can cause a pseudo-Wellens' syndrome, this is a diagnosis of exclusion. Just because a patient uses drugs does not mean that he/she does not have underlying coronary artery disease. 

Submitted by Maia Dorsett (@maiadorsett), PGY-3
Faculty Reviewed by Brent Ruoff
Thank you to Julianne Dean and Chris Palmer for the cases (and patient advocacy)

[1]Tandy, T. K., Bottomy, D. P., & Lewis, J. G. (1999). Wellens’ syndrome. Annals of emergency medicine, 33(3), 347-351.
[2]Rhinehardt, J., Brady, W. J., Perron, A. D., & Mattu, A. (2002). Electrocardiographic manifestations of Wellens' syndrome. The American journal of emergency medicine, 20(7), 638-643.
[3] de Zwann, C., Bar F.W., Wellens, H.J. (1982). Characteristic electrocardiographic pattern indicating a critical stenosis high in left anterior descending coronary artery in patients admitted because of impending myocardial infarction." American heart journal, 103(4), 730-736.
[4] de Zwaan, C., Bär, F. W., Janssen, J. H., Cheriex, E. C., Dassen, W. R., Brugada, P., ... & Wellens, H. J. (1989). Angiographic and clinical characteristics of patients with unstable angina showing an ECG pattern indicating critical narrowing of the proximal LAD coronary artery. American heart journal, 117(3), 657-665.

Wednesday, May 6, 2015

@WUSTL_EM #EMConf : #FOAMed Supplement No. 1

Welcome to @WUSTL_EM #EMConf, the #FOAMed Edition. The purpose of this weekly column is to identify #FOAMed resources that reinforce and expand on the concepts/facts discussed during weekly conference.  Please e-mail to share additional resources (or just post them as comments below).

This week, we covered:

1. Core Content - Neuro with Dr. Hilbert. Discussed signs/symptoms/treatment of meningitis.
  - Peruse this Paucis-Verbis card from ALiEM on when you should get a CT prior to LP for meningitis.
- Listen to this 2010 EMcrit podcast on severe CNS infections.

2. Toxicology with Dr. Mullins - Management of Oral Hypoglycemic overdoses.
  - The Crashing Patient did this post on Hypoglycemia, including a review of the different oral hypoglycemics.
- The Poison Review touched on octreotide for sulfonylurea overdose in this blog post reviewing this article.

3. Critical Care with Dr. Palmer - Non-invasive Ventilation and Basics of Ventilator Management
 - Scott Weingart's Dominating the Vent Part 1 and Dominating the Vent Part 2 are great EM-based tutorials on Ventilator Management
-  Our own Dr. Fuller's algorithm posted on this blog for Troubleshooting Hypoxia on the Vent
-  Our own EMJClub covered benefits of low tidal volume ventilation 
- Brian Fuller & Brian Cohn wrote this article for epmonthly on "Protecting the Intubated Patient".

4.  Trauma Conference -Resuscitation of the patient in hemorrhagic shock
 - You can listen to this EMCrit podcast on resuscitation of the trauma patient in hemorrhagic shock.
-  You can read this excellent post on predicting need for Massive Transfusion in trauma from Life in the Fast Lane.
- For a discussion of more recent literature, read Rory Spiegel's EM Nerd post regarding the findings of the PROPPR trial regarding optimum transfusion strategies.


Monday, May 4, 2015

EKG Challenge No. 13: "I feel much better now"

You are working one evening in the emergency department when you walk in to see your 4th chest pain patient of the night.  Your current patient is a 50-something year old male who's years of homelessness and cocaine abuse have made him appear older than his stated age.  He tells you that he he has been having left sided chest pain on and off for the last 3 hrs.  He received ASA and nitro x 2 in the ambulance and now feels much better.  You examine his EKG from today:
EKG #1 (day of presentation)

You then compare it to his EKG from two days ago when he came in for chronic diarrhea and chest pain, but was chest pain free at the time:

EKG #2 (EKG from two days prior to presentation)

... and compare it again with his EKG from 1 year before during an admission for chest pain in which he had a negative cardiac stress test:
EKG #3 (EKG from one year prior to presentation)
What is your differential?  What is your management and dispo plan? 

Read the Case Conclusion here.