Monday, July 27, 2015

Consultant Teachings No. 3: Evaluation of Tendinous Hand Injuries for the Emergency Provider

Clinical Case:  You are working in a community emergency department one evening when a woman presents with a laceration across the fingerpad of her right thumb that she sustained after falling onto a piece of glass.  The laceration itself is pretty small - about a centimeter across - and has minimal bleeding.   The X-ray ordered by the triage nurse is negative for retained foreign body.  Before you just sew this up and send the patient on her way, you appropriately decide to do a thorough hand exam, including for tendonous injury.  The patient keeps saying that its hard to bend her finger because it hurts...
Consultant Teaching: Tendon Injuries to the hand are often complex entities that are subject to ongoing research regarding optimal procedures for management and rehabilitation. The flexor and extensor tendon anatomy is quite complex. Both are divided into numerous “zones” created to help clarify the optimal treatment, which can vary markedly depending on injury location. Missed tendon injuries increase morbidity by complicating later management and are therefore a leading cause of malpractice claims in the world of Emergency Medicine. The most important and fundamental aspect of evaluation in these patients is a detailed hand exam. Outlined below is a guide for the evaluation and management of any patient presenting to the ED with a suspected hand injury.

Flexor Tendon Injuries
The first step is to obtain a detailed history of the mechanism of injury. Was the injury caused by a rusty farm knife or a sharp chard of glass? What was the position of the patient’s hand when the injury occurred? This is a frequently missed point to mention. You can imagine that, if the patient was lacerated with flexed fingers while gripping a knife, the location of the tendon injury itself may be in a very different location than the skin laceration when evaluating the hand in a more extended posture. Just because you can no longer see the damaged tendon in the wound doesn’t mean it’s not there.

Step 1: Observation 
Evaluate the location and depth of the laceration. Look at the resting posture of the hand and the
patient’s digital cascade. When in doubt, you can usually find clues by looking at the resting finger position of the uninjured hand. Your clinical suspicion should be raised if a particular finger rests in a more extended position relative to the others.

Step 2: Passive Range of motion
These hand injuries can be really painful. A good place to start is assessment of passive motion with a maneuver that elicits the tenodesis effect. Try it on yourself - With a relaxed hand, when you passive flex your wrist, your MCP/PIP/DIP joints will extend. Similarly, wrist extension will cause passive flexion of those digits. If you passively extend the patient’s wrist and there is persistent extension of the DIP or PIP joints, you may have a flexor tendon injury in that digit. 

Step 3: A detailed (ie purposeful) neurovascular exam 
Flexor tendon injuries are frequently associated with neurovascular injury because of the palmar
location of these structures. The best way to assess nerve function is with a two-point discrimination exam. This can easily be performed with a paper clip. Remember that each finger has proper digital nerves on its palmar aspect on both the radial and ulnar sides: test them both. *Tip 1* If you get abnormal results that don’t make sense given the injury, test the other hand! Your patient who forgot to mention his terrible neuropathy will appreciate this. *Tip 2* Under NO circumstances should a digital block be performed if you are planning to consult the hand service on call. If analgesia is an issue, let the hand service know and proceed with necessary oral/IV medications until your consulting service is able to evaluate the patient’s neurovascular status. This is not only important for our documentation, but is critical for possible surgical planning.

Sensory territories of the hand (Source: wikipedia)
There are multiple ways to assess the vascular status. Assessment of cap refill, a digital Allen’s test (same concept as the wrist, but with compression of the radial and ulnar palmar arteries of each finger) and pulse oximetry can all help establish whether or not a concomitant vascular injury is present.

Step 4: Flexor Tendon Exam
A quick anatomy review is necessary here because, in the hand, form truly follows function. The flexor digitorum profundus (FDP) and superficialis (FDS) tendons are both extrinsic hand muscles that power finger flexion. The FDP lies deep to FDS and then attaches distally to the distal phalanx of the 2nd-5th digits. The FDS attaches at the base of the intermediate phalanx of these digits. Why is that important to know for your physical exam? Since these muscles share a common belly and are intimately associated with one another, you must carefully isolate the desired tendon on each digit. Asking a patient to “wiggle their fingers” is an easy way to improperly assess hand function and miss isolated tendon injuries. To test the FDS: all adjacent digits must be held with all joints in extension while the patient flexes the finger at the PIP joint. To test the FDP: hold the middle phalanx in extension while asking the patient to flex just their distal phalanx. Another reason not to digital block these patients is that pain with these movements may clue the examiner into a possible partial tear or laceration.

For completeness, it is also important to document motor testing for all muscles with separate nerve innervations, regardless of its proximity to the wound in question.

Extensor Tendon Injuries 
Like the flexor tendons, these also can be diagnostic challenges due to the complex anatomy of the extensor mechanism. This region is comprised of extrinsic muscles that power digit extension, like the extensor digitorum communis (EDC) and an extensor aponeurosis with multiple connecting bands and ligaments. Again, a detailed history will provide valuable insight and context for your exam. Is it a result of a fight-bite injury? A crushing mechanism?

The general principles of the physical exam addressed above regarding observation, passive range of motion and a detailed neurovascular exam still apply. As diagrammed in the image above, for the dorsal hand, it is especially important to assess both the radial and ulnar nerves.

With regard to hand posture, take note if there is a resting flexed position of the digit, a mallet finger, or boutonniere deformity. This should heighten your suspicion for a tendon injury.

Assessment of the Extensor Tendon 
A few important considerations are noteworthy here. First, do not be fooled by the action of the lumbricals! Remember, these muscles provide extension of the PIP and DIP joints via the lateral bands. Have the patient lay their hand flat on a table (extends the MCP joint and helps remove the influence of lumbricals) and extend at the MCP joint against resistance. Extension along an affected digit may still be possible even after complete laceration, due to the multiple contributions to the extensor mechanism. Look closely for a lack of hyperextension or differential extension in the affected finger that may be a sign an extensor tendon injury has occurred. The junctura tendinae are intertendinous fascial connections located around the MCP joint that attach tendons of the EDC and help coordinate their movements. This anatomic structure is important to keep in mind because the junctura may allow for some extension of an injured digit if the tendon injury is proximal to them.

Lastly, if you are concerned about an injury to the “central slip” (eg. a lac or crush injury to the middle phalanx), then an Elson test can be performed. To do this test, flex the PIP 90 degrees over a table and have them extend against resistance. If the central slip is intact, the DIP joint will be supple. If it is ruptured, there will be weak extension of the PIP and a rigid DIP due to the action of the lateral bands.

So, I did my hand exam… What next? Management of these injuries is often multifactorial and depends on the location of the injury, the structures involved, patient and other factors that are beyond the scope of this post. Doing a correct and detailed physical exam is the first, and most important, step in making sure a patient doesn’t walk out of the ED with an undiagnosed tendon or neurovascular injury.  When practicing in the community, if you suspect that there is an associated tendonous injury based on your clinical exam, clean and repair the laceration as you otherwise would but subsequently place the patent in a dorsal blocking splint, with 15-20 wrist flexion with the hand in intrinsic plus position (MCPs at 70-90 degrees and DIP/PIP straight) and make sure they have follow-up with a hand surgeon.  
At the end of the day, it’s important to keep a high level of suspicion - a referral to a hand surgeon for a suspected tendon injury is just as valid as a referral for a definite tendon injury. 

Check out these videos:
Tenodesis effect: 
Elson test:
Generic hand exam:

Submitted by Chris Cosgrove, MD. Ortho PGY2
Reviewed by: Daniel Osei, MD. Hand Attending

EverydayEBM Editor: Maia Dorsett (@maiadorsett)

Thursday, July 23, 2015

@WUSTL_EM #EMConf: #FOAMed Supplement No. 9

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 post additional resources as comments below or tweet to @WUSTL_EM.

1. Trauma in Pregnancy by @rbavs
- Excellent run-down of the pearls & pitfalls of trauma resus in pregnancy by emDocs, including the precarious ventilatory status of pregnant patients at baseline and the general safety of trauma CT imaging as needed, as covered by Dr. Bavolek.
- Question-and-Answer based review of the challenges posed by physiologic changes of pregnancy when evaluating the pregnant trauma patient by @precordialthump at LifeInTheFastLane.
- And the follow up, monitoring & management of this patient – LifeInTheFastLane
- Review the EAST guidelines your trauma surgery colleagues will likely be following, from @cliffreid on
- Pro-tips for utilizing FAST exam in the pregnant trauma patient from the EDE Blog. Remember sensitivity is decreased in pregnancy, particularly in later term, and only a tiny amount of fluid posterior to the lower part of the uterus can be considered “physiologic.”

2. Pediatric Sexual Abuse by Dr. Jamie Kondis
- Excellent podcast from the PEM ED Podcast covering the cornerstone exam findings and red flags in pediatric abuse cases.
- High-yield discussion from January 2014 EM:RAP about the approach to the potential pediatric abuse patient.
- Pediatric EM Morsels with a brief piece on exam findings in pediatric abuse – remember there’s really no such thing as a “pathognomonic” bruise or fracture.

3. Morel Lavallée by Dr. Lucy Hormberg
- Learn more about the diagnosis and management of this uncommon but not unheard-of closed degloving injury from the sage minds at St. Emlyn’s.
- Review the ultrasound and MRI features of these lesions on Radiopaedia. 

4. The EKG in Acute ACS by Dr. Lucy Hormberg
- In an interview with @emcrit, @smithECGblog covers several difficult-to-diagnose ACS cases.
- Don’t miss a posterior MI. Review the EKG signs with this UMEM Educational Pearl. 
- Likewise, don’t miss an inferior MI. Review with LifeInTheFastLane. 
- Pericarditis can be difficult to distinguish from ACS. Let the guru of ED EKG himself, @amalmattu, talk you through it during this ECG Case of the Week.
- Another lecture from the great @amalmattu about the significance of changes in the Forgotten Lead, aVR. 

5. Door to Donut: ED Management of PE-likely Patients, by Drs. Gabe Gomez and Kevin Baumgartner
- Simple algorithm to review the workup of potential PE by @emcrit. Includes a link to a 2015 review article by the master of ED PE, @klinelab.
- Notes from an excellent lecture from the All NYC EM Conference covering the assessment of risk of PE in ED patients, posted at emDocs. 
- Applications and limitations of the PERC rule, also from emDocs. 
- Excellent summary of EKG changes seen in RV dysfunction due to PE from ALiEM – important to know as these patients have significantly higher mortality. 

6. Altered Mental Status in the Critically-Ill Patient, by Dr. Brian Wessman.
- Remember, what you start in the ED carries over to the ICU.
- The key to adequate sedation post-intubation is analgesia, as covered by @emcrit.  
- Use a scale to measure effect and titrate your sedation infusions. Again, analgesia first, with spot dosing of another agent (such as benzodiazepine) as needed. Check out this summary from emDocs. 

Never stop learning,
Sam (@CSamSmithMD) and Louis (@Lgaard)

EKG Challenge No. 14 Case Conclusion: The EKG Sign Formerly Known as Prince?

On a Sunday afternoon, an elderly gentleman is brought into the emergency department by his wife complaining of chest pain that began one hour ago.  He is diaphoretic and appears very uncomfortable.  An EKG is obtained.  The patient has no prior EKGs available.

When you first look at the EKG, you note that there appears to be an abundance of PVCs... ventricular trigeminy actually.  Given the patient's clinical appearance, you suspect an acute MI.... now to just sort out the EKG to support your clinical gestalt.

Given the prevalence of ventricular ectopy,  you begin your analysis by identifying sinus beats [although you can use PVCs as well - see these posts (1) and (2)  on Dr. Smith's ECG blog]:
Sinus beats outlined in blue.  Other beats are premature ventricular contractions (PVCs)
 If you take one sinus tracing for each lead:

Secondly, you observe that the tracing follows left bundle branch block (LBBB) morphology.  New LBBB may be considered the criteria "formerly known as" an indication for cath lab activation.

The 2004 ACC/AHA STEMI guidelines included new LBBB as a indication for Cath lab activation in patients presenting with symptoms suspicious for acute MI.  This was changed in the 2013, largely due to data suggesting that this was responsible for a large number of "false positive" cath lab activations [1].  Two separate studies involving patients with LBBB evaluated for suspected STEMI found an overall low prevalence of coronary lesions amenable to PCI [2,3].

In "normal" LBBB, repolarization is characterized by ST segment and T wave deviation away from the major direction of the terminal QRS waveform - also known as "appropriate discordance" [1]. Hence, in leads where the QRS is positive, the ST segment (and often the T wave) are deflected in the opposite direction and vice versa:

Appropriate discordance makes it more difficult, but not impossible, to assess for acute myocardial infarction with underlying LBBB.  In 1996, Sgarbossa and colleagues retrospectively derived and independently validated a clinical prediction rule for EKG diagnosis of acute myocardial infarction in the context of LBBB using positive biomarkers as a gold standard [4].   These three criteria are illustrated in the figure below:

Image source: ecg12lead; Table source: Sgarbossa et. al. (1996)

There are few important things to note about the Sgarbossa criteria.  First, Sgarbossa criteria only need to be met in a single lead.  Second, the three criteria are not equal in their sensitivity or specificity with respect to predict myocardial infarction and thus are awarded different points within the model.   In the initial study, concordant ST elevation was found to have a sensitivity of 73% (95% CI 64-80) and specificity of 95% (95% CI 86-96), while concordant ST segment depression had a sensitivity of only 25% (95% CI 18-34) and specficity of 96% (95% CI 91-99).   The third criteria, discordant ST segment elevation > 5 mm, has a sensitivity of 31% (95% CI 23-39) and specificity of 92% (95% CI 85-96).  Thus, the Sgarbossa criteria were specific, but not necessarily sensitive, for acute myocardial infarction as diagnosed by positive biomarkers.

Source: Sgarbossa et. al. (1996)

A meta-analysis of subsequent studies evaluating the Sgarbossa criteria was published in 2008 [5].   Based on calculated sensitivities and specificities (see below), this study recommended at the Sgarbossa score of > 3 (i.e. only concordant ST elevation anywhere  or concordant ST depression in V1, V2 or V3) physicians should treat for acute myocardial infarction.  A Sgarbossa score of 2 (i.e. meeting the discordant criteria alone) was deemed "inadequate to diagnose myocardial infarction."

Source: Reference 5

Smith et. al. (2012)  addressed the low sensitivity of the initial Sgarbossa criteria by postulating that changing the third component (excessive discordance) to a proportional rule instead of a 5 mm absolute cutoff would increase both the sensitivity and specificity of the criteria.  They defined "Abnormal, excessive discordance" as a ST/S ratio of < -0.25. 
Image Source: Smith et. al. (2012)
The authors proposed a "modified" unweighted Sgarbossa criteria:

            1. Concordant ST elevation > 1 mm in any lead
            2. ST segment depression > 1 mm in V1, V2 or V3
            3. ST/S ratio < -0.25 in any lead with > 1 mm of ST segment elevation or depression

The EKG was considered positive for ischemia if any of the above criteria were met.

Based on a data set using angiographic occlusion or troponin value > 10 ng/mL as their cutoff for "true MI", they calculated a sensitivity of 91% (95% CI 76-98) and specificity 90% (83-95) for the Modified Sgarbossa criteria.

If we apply the Sgarbossa and Modified Sgarbossa criteria to our patient's EKG, the patient meets criteria for acute myocardial infarction.

The patient did go to the cardiac catheterization laboratory and was found to have a 100% occlusion of the mid-LAD:
Cath lab diagram demonstrating 100% occlusion of mid-LAD
So what would happen if this patient did not meet Sgarbossa criteria?  Remember Sgarbossa criteria are far from sensitive.  The modified Sgarbossa criteria significantly improve on this, but has not yet been validated in a distinct set of EKGs.  What would you do?

When this patient presented, the cardiologist was at first reticent to take him to the cath lab.  Rather than arguing technicalities on a Sunday afternoon, the attending physician, Heather Webb (@webbmd) used what I would say are some of the most important criteria in a patient who looks sick and has severe chest pain, diaphoresis and a presumed new left bundle branch block to demand that the patient go: Clinical Gestalt.

Take Home Points: Left bundle branch block makes the diagnosis of acute myocardial infarction more difficult.  The original Sgarbossa criteria developed in 1996 aimed at identifying myocardial infarction in the context of LBBB were specific but poorly sensitive.  These were improved with development of the Modified Sgarbossa criteria, which incorporated the concept for proportionality in the evaluation of ST/S discordance.  Remember that these rules do not fully account for  your pretest probability or clinical gestalt of when a patient is having an MI.  If the patient looks like they are having an MI and has a new left bundle branch block, they should probably go to the cath lab regardless.  Now for Prince's Song of the Heart...

Submitted by Maia Dorsett, PGY-4 (@maiadorsett)
Faculty Reviewed by Doug Char and Joan Noelker

Interested in reading additional resources (Thanks to @tbouthillet for sharing):
 -  ECG Medical Training  on the Modified Sgarbossa criteria
- Dr. Smith's ECG blog on Modified Sgarbossa criteria with links to additional cases
- ALiEM discussion of Modifed Sgarbossa criteria with management algorithm for new LBBB

1. Cai, Q., Mehta, N., Sgarbossa, E. B., Pinski, S. L., Wagner, G. S., Califf, R. M., & Barbagelata, A. (2013). The left bundle-branch block puzzle in the 2013 ST-elevation myocardial infarction guideline: from falsely declaring emergency to denying reperfusion in a high-risk population. Are the Sgarbossa Criteria ready for prime time?. American heart journal, 166(3), 409-413.
2. Larson, D. M., Menssen, K. M., Sharkey, S. W., Duval, S., Schwartz, R. S., Harris, J., ... & Henry, T. D. (2007). “False-positive” cardiac catheterization laboratory activation among patients with suspected ST-segment elevation myocardial infarction. Jama, 298(23), 2754-2760.
3.Jain, S., Ting, H. T., Bell, M., Bjerke, C. M., Lennon, R. J., Gersh, B. J., ... & Prasad, A. (2011). Utility of left bundle branch block as a diagnostic criterion for acute myocardial infarction. The American journal of cardiology, 107(8), 1111-1116.
4. Sgarbossa, E. B., Pinski, S. L., Barbagelata, A., Underwood, D. A., Gates, K. B., Topol, E. J., ... & Wagner, G. S. (1996). Electrocardiographic diagnosis of evolving acute myocardial infarction in the presence of left bundle-branch block. New England Journal of Medicine, 334(8), 481-487.
5. Tabas, J. A., Rodriguez, R. M., Seligman, H. K., & Goldschlager, N. F. (2008). Electrocardiographic criteria for detecting acute myocardial infarction in patients with left bundle branch block: a meta-analysis. Annals of emergency medicine, 52(4), 329-336.
6. Smith, S. W., Dodd, K. W., Henry, T. D., Dvorak, D. M., & Pearce, L. A. (2012). Diagnosis of ST-elevation myocardial infarction in the presence of left bundle branch block with the ST-elevation to S-wave ratio in a modified Sgarbossa rule. Annals of emergency medicine, 60(6), 766-776.

Wednesday, July 22, 2015

If There's a Delay, Consider TXA: On Anti-fibrinolytic Therapy for Management of Aneurysmal Subarachnoid Hemorrhage

Clinical Scenario: While working in a community emergency department you see a middle aged otherwise healthy female who developed a thunderclap headache two hours ago while lifting weights.  She is very nauseated, has intermittent vomiting, but is able to respond to your questions. An emergent Head CT shows subarachnoid hemorrhage involving the suprasellar, interpeduncular, and ambient cisterns with associated ventriculomegaly.  You call the neurosurgeon at the closest tertiary care hospital and he asks whether you considered giving tranexamic acid (TXA) prior to transport.
Clinical question: Does TXA improve outcomes for patients with spontaneous subarachnoid hemorrhage? Does it increase the risk for thrombotic event/stroke? 

Literature Review
In people who suffer from aneurysmal subarachnoid hemorrhage, rebleeding is a cause of significant death and disability, peaking in incidence 24 hrs from the initial presenting event [1].   More than a third of rebleeding events occur within 3 hrs and more than half within 6 hrs [2].  It is thought that part of the mechanism of rebleeding is dissolution of the clot at the site of the aneurysm.  While securing the aneurysm via coiling or clipping is the standard of care to prevent rebleeding, in instances where there is an delay of care is unavoidable, it was been postulated that anti-fibrinolytic therapy, which may mitigate this process, may decrease the incidence of rebleeding.

One form of anti-fibrinolytic therapy is TXA, a synthetic analog of the amino acid lysine that works as a hemostatic agent by binding to the lysine binding sites on plasminogen, thereby competitively inhibiting its conversion to plasmin and subsequently fibrin degradation Existing studies suggest that TXA decreases bleeding in menorrhagia and cardiopulmonary bypass, as well as to improves mortality in trauma patients dying of massive hemorrhage [3,4,5,6].  Does this hemostatic benefit apply to spontaneous subarachnoid hemorrhage?

A large number of studies regarding anti-fibrinolytic therapy for aneurysmal subarachnoid hemorrhage have been published.    These were assessed in a 2013 Cochrane meta-analysis aimed at addressing the overall clinical effects of such therapies on rates of rebleeding and overall morbidity/mortality in aneurysmal SAH [7].  This was prompted in part because of concern that even if antifibrinolytics decreased risk of rebleeding, this would be offset by an increased risk of cerebral ischemia, which tends to develop between 4-14 days after initial SAH.  The Cochrane review included only randomized trials that compared antifibrinolytic to placebo vs. control and assessed subsequent outcomes on an intention to treat basis.   Their systematic review included 10 studies [with a pooled patient sample of 1904 who received TXA, 597 placebo, and 348 control].  Nine of these studies used TXA as the antifibrinolytic agent and one used epsilon-amino-caproic acid (39 patients).  These studies were extremely heterogeneous in their anti-fibrinolytic treatment regimens.  One study treated for less than 72 hrs (before onset of potential cerebral ischemia) [8] and others treated up to six weeks (through peak time of cerebral ischemia).  Two of the studies concurrently treated patients with therapy (such as nimodipine) to reduce the risk of cerebral ischemia [8,9].  Their analysis found that that TXA did not affect the overall morbidity (risk of poor outcome was RR 1.02; 95% 0.91-1.15) or mortality (death from all causes RR 1.00; 95% CI 0.85-1.18). Administration of TXA did decrease the risk of rebleeding (RR 0.65, 95% CI 0.44 to 0.97; 78 per 1000 people), but this was offset by the increased the risk of cerebral ischemia (RR 1.41, 95% CI 1.04 to 1.91; 83 per 1000 people). 

There was was considerable heterogeneity between the older studies and the newer studies, which may be attributed to newer studies using specific treatments to prevent the risk of cerebral ischemia. 

While this overall analysis suggests that TXA may not significantly benefit long term outcome in aSAH, the majority of the studies administered the drug for a prolonged period time of > 10 days, at which point definitive aneurysmal treatment via endovascular or surgical intervention should be achieved.  One study examined short term  (mean of 15.3 +/- 16 hrs) use of an anti-fibrinolytic therapy (E-Aminocaproic acid - EACA) on risk of rebleeding, mortality and favorable neurologic outcome at 3 months [10].  They prospectively studied 248 patients with aSAHPatients were not randomized, but the two groups were similar with regard to baseline characteristics predictive of rebleeding risk and neurologic outcome, including anticoagulation and Hunt-Hess grade (with the exception of blood pressure which was not assessed).  The authors compared the outcomes of 73 patients who received EACA with those of 175 patients who did not.  They found that there was a significant decrease in rebleeding in EACA-treated patients (2.7% vs. 11.4%), as well as a general trend towards favorable neurologic outcome in those who received anti-fibrinolytic therapy.  While we will continue to await randomized, placebo-controlled trials to determine if (and which) antifibrinolytic therapy improves outcome for patients with aSAH, the AHA/ASA guidelines have incorporated anti-fibrinolytic therapy into the recommendations for medical measures to prevent rebleeding [2]:

Current AHA/ASA Guidelines for Medical Management to Prevent Rebleed in Aneurysmal SAH (Ref 2)

  Take home: TXA may reduce the risk of rebleeding in aneurysmal subarachnoid hemorrhage, but current evidence does not strongly support a benefit regarding survival or morbidity.   In studies using prolonged anti-fibrinolytic therapy, the benefit conferred by decreased risk of rebleed was offset by increase in cerebral ischemia.  However, more recent trials of short-term antifibrinolytic therapy have had promising, but far from definitive results.  Current AHA/ASA guidelines encourage its use for patients who will have a delay in aneurysm obliteration.

Submitted by Melissa Kroll, PGY-3
Edited by Maia Dorsett, PGY-4
Faculty Reviewed by Peter Panagos  

1.Guo, L. M., Zhou, H. Y., Xu, J. W., Wang, Y., Qiu, Y. M., & Jiang, J. Y. (2011). Risk factors related to aneurysmal rebleeding. World neurosurgery, 76(3), 292-298.
2. Connolly, E. S., Rabinstein, A. A., Carhuapoma, J. R., Derdeyn, C. P., Dion, J., Higashida, R. T., ... & Vespa, P. (2012). Guidelines for the management of aneurysmal subarachnoid hemorrhage a guideline for healthcare professionals from the American heart association/American stroke association. Stroke, 43(6), 1711-1737.
3. Jimenez, J. J., Iribarren, J. L., Lorente, L., Rodriguez, J. M., Hernandez, D., Nassar, I., ... & Mora, M. L. (2007). Tranexamic acid attenuates inflammatory response in cardiopulmonary bypass surgery through blockade of fibrinolysis: a case control study followed by a randomized double-blind controlled trial. Crit Care, 11(6), R117.
4. Lethaby, A., Farquhar, C., & Cooke, I. (2000). Antifibrinolytics for heavy menstrual bleeding (Cochrane Review). The Cochrane Library, (4).
5. Williams-Johnson, J. A., McDonald, A. H., Strachan, G. G., & Williams, E. W. (2010). Effects of tranexamic acid on death, vascular occlusive events, and blood transfusion in trauma patients with significant haemorrhage (CRASH-2) A randomised, placebo-controlled trial. The West Indian medical journal, 59(6), 612-624.
6. Morrison, J. J., Dubose, J. J., Rasmussen, T. E., & Midwinter, M. J. (2012). Military application of tranexamic acid in trauma emergency resuscitation (MATTERs) study. Archives of surgery, 147(2), 113-119.
7.Baharoglu, M. I., Germans, M. R., Rinkel, G. J., Algra, A., Vermeulen, M., van Gijn, J., & Roos, Y. B. (2013). Antifibrinolytic therapy for aneurysmal subarachnoid haemorrhage. The Cochrane Library.
8.Hillman, J., Fridriksson, S., Nilsson, O., Yu, Z., Säveland, H., & Jakobsson, K. E. (2002). Immediate administration of tranexamic acid and reduced incidence of early rebleeding after aneurysmal subarachnoid hemorrhage: a prospective randomized study. Journal of neurosurgery, 97(4), 771-778.
9.Roos, Y. B. W. E. M., & STAR Study Group. (2000). Antifibrinolytic treatment in subarachnoid hemorrhage A randomized placebo-controlled trial. Neurology, 54(1), 77-77.
10. Starke, R. M., Kim, G. H., Fernandez, A., Komotar, R. J., Hickman, Z. L., Otten, M. L., ... & Connolly, E. S. (2008). Impact of a protocol for acute antifibrinolytic therapy on aneurysm rebleeding after subarachnoid hemorrhage. Stroke, 39(9), 2617-2621.

Monday, July 20, 2015

EKG Challenge No. 14: Elderly gentleman BIBW (brought in by wife) ....

On a Sunday afternoon, an elderly gentleman is brought into the emergency department by his wife complaining of chest pain that began one hour ago.  He is diaphoretic and appears uncomfortable.  An EKG is obtained:

You have no prior EKGs available for comparison, but the patient denies any prior history of acute MI or CHF.  Interpret the EKG.   What do you think is going on?   What do you do next?

You can read the case conclusion here.

Wednesday, July 15, 2015

@WUSTL_EM #EMConf: #FOAMed Supplement No. 8

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 post additional resources as comments below or tweet to @WUSTL_EM.
1. Things I Wish I'd Known as an Intern aka Approach to the patient by @CSamSmithMD
- I have shared the emdocs mindset multiple times on this #FOAMed supplement, and I must stress how good this series is.  It reinforces so much of what is wonderful about emergency medicine and is full of great advice about how to be a good (maybe even great?) emergency medicine physician.  Most recently,  I HIGHLY recommend this post by Larissa Velez which addresses a lot of the values discussed in Sam's talk.
- The power of the placebo effect is stressed in this EM Lit of Note post.

2. Trauma Resuscitation [thanks to Louis Jamtgaard (@Lgaard) for sending in most of these these links]
- * Every emergency medicine physician (especially our new third years moving into the role of the trauma senior) should watch Cliff Reid's video:  Making Things Happen
- In his lecture, Dr. Jamtgaard covered the unreliability of  blood pressure estimation based on pulse exam in trauma patients.  Rebel EM covered this data in this post.
- Want to read more about permissive hypotension? See these posts by LITFL and EMDocs on the subject.
- Assessment & management of extremity hemorrhage is covered in this post by LITFL.
- For more on tranfusion in trauma: see massive transfusion as covered by EMDocs and discussion of the PROPPR trial by EMCrit and EMNerd.
- The use of TXA in traumatic hemorrhage was critically appraised by our own journal club.  Read the results of the discussion and listen to the podcast.

3. C-spine Radiology - Taming of the Sru has this post with link to a video on interpretation of C-spine CT.

4. Joint Reductions in the Upper Extremities
- See this video  from Temple University on shoulder reduction using intra-articular injection and Cunningham technique shared with @WUSTL_EM via twitter by @ZackRepEM
- Mike Cadogan wrote this post on elbow dislocations for Life in the Fast Lane.
- Orthobullets has this post on management of MCP dislocations. Remember - flex that wrist!

Maia (@maiadorsett)

Wednesday, July 8, 2015

@WUSTL_EM #EMConf: #FOAMed Supplement No. 7

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).

1.  Starting the year off with Approach to Chest Pain
- See this RebelEM post reviewing the HEART score to risk stratify chest pain patients in the ED.
- EM Literature of Note reviewed the HEART score in this post.
- Review Amal Mattu's approach to low risk chest pain in this excellent podcast by ERCAST
- For some primary literature, you can review Hess et. al. (2012) on employment of a Shared Decision Making Aid to reduce OBS admission for stress testing.
- Don't miss this  recent article by Weinstock et. al. on the low risk for cardiac events for patients admitted to the hospital with two negative troponins and non-concerning EKG changes.

2. Resuscitation Fluids: A Primer
- Didn't follow the Glycocalyx explanation on the first go around?  I don't think most people do.  Don't worry, Life in the Fast Lane has this explanation of the glycocalyx and its role in critical illness which you can access here.
- Our own Evan Schwarz reviews the importance of fluid choice in sepsis here.
- Dr. Wessman recommended several New England Journal of Medicine  articles during his talk, including this one on resuscitation fluids and this one on Albumin vs. Crystalloids.

3. EMS: Systems of Care
The PHARM blog did an excellent job compiling & summarizing the results of the best articles in prehospital medicine in 2014.  You can access this list here. Amongst these articles was this one on how Statewide Regionalization of Care can lead to improved outcome in Cardiac arrest patients.

Finally, please take the time and go here to sign a petition supporting an Air Ambulance for Northern Ireland in memory of the great Dr John Hinds, master of prehospital medicine, teacher of many and tireless advocate for improvement and support of prehospital care.

4. Ultrasound: eFAST
- check out this entertaining "clarification" of the eFAST by Cliff Reid and the Ultrasound podcast team.

5. Patient Satisfaction
- see Emergency Medicine Cases on Effective Patient Communication, Patient Centered Care and Patient Satisfaction.