Vagal Maneuvers in SVT: Give 'em a Leg Up!

You walk into the start of your shift when the nurse urgently calls you into a room where a new patient has been placed with a heart rate of 240.  The patient is alert, oriented, and normotensive but complaining of chest pain that started acutely upon waking up 1 hour ago with palpitations. She then drove herself to the ED.  She reports this happening once before about 1 year ago that required "a special IV medicine."  This is her EKG:

 

Clinical question: How should supraventricular tachycardia (SVT) be evaluated in the ED, and how effective are vagal maneuvers in converting SVT to normal sinus rhythm?

Pathophysiology and Clinical Manifestations

SVT can be broken down both by site of origin and regularity. Regular rhythm tachycardias originating from the atria include sinus tachycardia, atrial tachycardia, atrial flutter, and sinus node reentrant tachycardia. Regular rhythm tachycardias originating from the atrioventricular region include atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and automatic junctional tachycardia. All the irregular rhythm tachycardias originate from the atria and include atrial fibrillation, atrial flutter with variable block, and multifocal atrial tachycardia. In patients with otherwise healthy hearts, the most common type of paroxysmal (sudden onset) SVT is AVNRT (60%), 30% of SVT have AVRT, and 10% have either atrial tachycardia or sinoatrial nodal tachycardia.

Commonly associated clinical symptoms include lightheadedness, chest pain, syncope/presyncope, polyuria (as atria can become enlarged by not fully ejecting blood, thus releasing atrial natriuretic peptide), shortness of breath, and anxiety.  People with pre-existing heart disease, such as CHF or CAD, have increased chance of SVT as both ischemia and stretching of the myocardium increase the risk of arrhythmias. Seventy-five percent of patients with SVT are female.  

Management of SVT

When patients present with new palpitations and tachycardia, the first step is to determine stability.  If the patient is hypotensive, they need to be treated with synchronized cardioversion immediately. If the patient remains normotensive, with or without the above mentioned symptoms, he or she can be initially treated with vagal maneuvers, as they are less invasive and cause less discomfort than chemical or electrical cardioversion.  Vagal maneuvers include carotid sinus massage, facial ice water immersion, and Valsalva maneuver. 

Carotid sinus massage involves massaging the base of the internal carotid artery (which is a major baroreceptor in the body) to stimulate the vagus nerve and theoretically decrease heart rate. A 2015 review article shows this procedure is not without risk and reports a 1% neurologic complication rate associated with the maneuver (think knocking off an atherosclerotic plaque into the brain), ranging from mild dysarthria and visual field defects to dense hemiplegia, and as the procedure has shown only modest efficacy at best, the risks may outweigh the benefits [Collins]. 

A second vagal maneuver is ice water immersion of the face, which stimulates the human diving reflex and acts via the vagal nerve as well to slow heart rate. This method seems to be more effective in younger patients, with some studies showing conversion in as many as 89% of patients under 1 year of age. Its efficacy negatively correlates with increasing age. They keys to effective use of ice water immersion in reversion of PSVT include: complete facial immersion in iced water, or covering the face with an ice pack or cold stimulus of 10*C, for at least 30 s.

Ok now bear down...

Ok now bear down...

There are multiple variations on the Valsalva maneuver, all of which attempt to increase intrathoracic pressure and causing vagal stimulation. This can be as simple as telling a patient to "bear down" as if they are having a bowel movement, having them blow into a straw or syringe, or forcefully cough. A 2015 Cochrane Review showed a range of effectiveness of the Valsalva maneuver. Three studies involving a total of 316 participants were included in this review. Analysis of the results showed that reversion success lies somewhere between 19.4% and 54.3%. Few studies show adverse effects of this maneuver, but it can potentially cause hypotension and syncope.

The 2015 REVERT trial represents biggest recent update in the world of Valsalva literature. The modified Valsalva maneuver is performed by semi-recumbent position patients who produce 40mmHg pressure for 15 seconds and are then repositioned in a supine position with a passive leg raise immediately after the Valsalva strain. The REVERT trial convincingly shows that this modified Valsalva maneuver drastically increases the rate of conversion from SVT to normal sinus rhythm (NSR) within one minute compared to normal Valsalva maneuver without costing any money or adverse affects. To confirm the required intrathoracic pressure, the patients in the study blew into a modified manometer until they achieved 40mmHg for 30 seconds. As this setup is not readily available in all settings, the study also suggested that blowing into a 10mL syringe for 30 seconds achieved comparable intrathoracic pressure. To compare, the normal Valsalva method was successful in converting patients to NSR 17% of the time and the modified Valsalva maneuver converted them 43% of the time, resulting in an absolute difference of 26% and a number needed to treat of 3.8. The modified Valsalva group in the study also required adenosine 19% less often compared to the control group.

Demonstrating modified Valsalva. 

Demonstrating modified Valsalva. 

If the patient fails to respond to the above mentioned vagal maneuvers, and remains stable in SVT, the next line treatment should involve chemical therapy (e.g. adenosine) before moving to synchronized cardioversion.

 

Submitted by Trevor Slezak, MD, PGY-2

Edited by Adam Rieves, MD, PGY-3

Faculty reviewed by Phil Chan, MD (@PhilChanEM)

 

References

Appelboam A, et al. Postural Modification to the Standard Valsalva Manoeuvre for Emergency Treatment of Supraventricular Tachycardias (REVERT): A Randomised Controlled Trial. Lancet 2015. [epub ahead of print] PMID: 26314489

Burns EJ. Supraventricular Tachycardia (SVT). Life in the Fast Lane. 18 March 2017.

Campbell M, Buitrago SR. BET 2: ICE WATER IMMERSION, OTHER VAGAL MANOEUVRES OR ADENOSINE FOR SVT IN CHILDREN. Emerg Med J 2017 34: 58-60

Collins NA, Higgins GL. Reconsidering the effectiveness and safety of carotid sinus massage as a therapeutic intervention in patients with supra ventricular tachycardia. The American Journal of Emergency Medicine. Volume 33, issue 6, pp 807-809. June 2015.

Ganz LI, et al. Clinical manifestations, diagnosis, and evaluation of narrow QRS complex tachycardias. UpToDate. 28 Sep 2016.

Smith GD, et al. The effectiveness of the Valsalva Manouevre for stopping an abnormal heart rhythm. Cochrane Review. 18 February 2015.http://www.cochrane.org/CD009502/VASC_the-effectiveness-of-the-valsalva-manoeuvre-for-stopping-an-abnormal-heart-rhythm

Smith G, Morgans A, Taylor DM, et al. Use of the human dive reflex for the management of supraventricular tachycardia: a review of the literature. Emerg Med J 2012 29: 611-616. March 3, 2012

Evicted: EM Book Club

“Evicted” by Matthew Desomod.

By: Kristen Mueller, MD

Thank you to all who attended our inaugural EM Social Justice book club on August 2, 2017.  For those of you who didn’t have time to read the book, or read it and could not attend, here are some of the highlights from our discussion.

As an overview (from the back cover), “In Evicted, Harvard sociologist and MacArthur “Genius” Matthew Desmond follows eight families in Milwaukee as they each struggle to keep a roof over their heads….Evicted transforms our understanding of poverty and economic exploitation while providing fresh ideas for solving one of the twenty-first-century America’s most devastating problems.  Its unforgettable scenes of hope and loss remind us of the centrality of home, without which nothing else is possible”.  

To write this book, sociologist Matthew Desomond lived in a trailer park in South Milwaukee, WI for several months in 2008, and then in an apartment in north Milwaukee in 2009.  In the trailer park, most of the residents were poor and white.  In the north side, most of the residents were poor and black.  In our discussion, it was striking how even among neighborhoods with extreme poverty, racial segregation continued and encouraged by both landlords and the tenants themselves.

This book struck a particular chord with me, as I lived in Milwaukee, WI from 2006-2010.  During that time I rented a 1 bedroom apartment in the predominantly white suburb of Wauwatosa near the medical campus (MCW) and paid $595/mo in rent.  Despite the fact that I had no job and no regular income beyond student loans, I had middle-class parents to co-sign my application and was enrolled in medical school.  I had no difficulty securing this apartment and maintaining my lease for 4 years.  I also looked like everyone else who lived in the neighborhood.

In the book, several of the families were struggling to find housing--studios, 1 bedrooms, anything--for the same amount of money.  Because of criminal history, previous evictions and lack of family co-signers, many were unable to secure housing in buildings that were up to code or have stable leasing agreements.  Related to this imbalance of power between the landlords and the tenants, and the surprisingly for-profit industry of renting to the lowest socioeconomic class in the region, tenants frequently had no recourse for things like holes in the walls or windows, no running water, no appliances in the apartment, or stopped up toilets, etc. Additionally, I was shocked by the number of reasonable things a person or family could do that could lead to evictions such as calling 911 of an emergency, reporting domestic violence, or having children (just at all--having children disproportionately made it difficult to find and maintain housing).  I was also surprised by how often people would take in strangers to come live in their 1 bedroom apartments to help cover the rent.  

This book also highlighted how difficult it is to break out of the cycle of poverty.  Many of the families highlighted spent 70-90% of their monthly income on rent.  This frequently left less than $30 month for all other expenses such as food for the entire family, clothes, transportation, school supplies, etc.  

To given additional perspective, during my reading I considered The Sphere Project as a reference; this is an international humanitarian nonprofit organization that outlines guidelines for quality and accountability in any humanitarian response, with the guiding principle that people have a right to life with dignity (http://www.spherehandbook.org).  Basic core standards required for any humanitarian response include minimum standards for safety from violence, water, sanitation and hygiene, food security and nutrition, shelter, and health action. While reading Evicted, I was struck by how often the protagonists of this book living in America, touted by some to be the best country in the world, frequently did not have the basic human resources that would be expected in refugee camps in war torn regions or areas recovering from natural disasters.

The protagonists of this book are representative of our BJH ED patient population living in urban St. Louis and beyond.  This book can give additional insight into our patients’ barriers to care, medication compliance and regular follow up.  There is much more that I could say about this book, but I encourage you to read it for yourself and to continue the discussion.  

Thank you for your interest and participation. Our next book club will be “White Like Me: Reflections on Race from a Privileged Son" by Tim Wise on Monday, November 13, 2017.  

Happy reading!

Kristen

 

 

Blast Crisis and Hyperleukocytosis

By: Nicole Messenger, MD

Faculty Reviewer: Chris Holthaus, MD

Let’s do a rapid review of blast crisis and its etiology, since some of this material hasn’t been reviewed since our days in medical school.  Let’s begin with the disease process that most commonly leads to blast crisis-- Chronic Myeloid Leukemia, CML for short.  CML is a myeloproliferative disorder associated with the Philadelphia chromosome [t(9;22)(q34;q11) and/or the BCR-ABL fusion gene, to be specific]. This genetic abnormality results in the formation of a unique gene product (BCR-ABL), which results in a constitutively active tyrosine kinase.


CML has three phases—chronic (stable) phase, accelerated phase, and blast crisis.  Given new tyrosine kinase inhibitory therapy, only 6% of patients embark on the accelerated phase of the disease that leads to blast crisis despite starting therapy during the chronic phase.  However, 10-15% of patients with CML alone will develop blast crisis. In roughly 30% of patients with CML, the lymphoid portion of the disease is the culprit for developing blast crisis. 
Per the World Health Organization, blast crisis is defined when one of the following occurs:

o    Greater than or equal to 20% of the peripheral blood or bone marrow is composed of blast cells (What is commonly identified in the Emergency Department)
o    Large clusters of blasts are observed in bone marrow biopsy
o    And evidence of extramedullary blastic infiltrates


Patients with CML have a 1% per year risk of progression toward blast crisis, therefore a diagnosis of CML is usually known prior to presentation in the emergency department for blast crisis.
Symptoms of disease progression to blast crisis include: night sweats, weight loss, bone pain, fevers, and symptomatic anemia; so do not forget these questions in review of systems regarding your CML patients.

 

Characteristic peripheral blood smear of chronic myeloid leukemia shows basophilia and granulocytosis with neutrophils and immature granulocytes. Reproduced with permission from: McClatchey, KD, MD, DDS. Clinical Laboratory Medicine, 2nd Edition. Philadelphia: Lippincott Williams & Wilkins, 2002. Copyright ©2002 Lippincott Williams & Wilkins

Characteristic peripheral blood smear of chronic myeloid leukemia shows basophilia and granulocytosis with neutrophils and immature granulocytes.

Reproduced with permission from: McClatchey, KD, MD, DDS. Clinical Laboratory Medicine, 2nd Edition. Philadelphia: Lippincott Williams & Wilkins, 2002. Copyright ©2002 Lippincott Williams & Wilkins

 


Lab studies to collect in the Emergency Department for patients with the working diagnosis of blast crisis include CBC with Differential, glucose, and CMP for hepatic and renal functions
It is pertinent to recall that patients presenting in blast crisis can have serious complications such as fever, renal failure, and tumor lysis.  If you are concerned for tumor lysis, get IV fluids on board to help avoid renal failure secondary to deposits of uric acid, as well as to avoid hyperkalemia and hyperphosphatemia.  Tumor cells can hold 4-fold the amount of phosphorus, which when lysed may lead to hypocalcemia that will result in seizures. And remember, hyperkalemia can lead to arrhythmias and cardiac arrest!

Now let’s discuss a more serious complication—hyperleukocytosis and leukostasis.  Hyperleukocytosis is diagnosed empirically when a patient with leukemia has a white blood cell (WBC) count over 100 x 109/L (100,000/microL).  Leukostasis is the symptomatic diagnosis due to tissue hypoxia, most commonly respiratory or neurological distress, secondary to leukocytosis. One study found there is “not a good correlation between the threshold of WBC and/or blast count and the development of signs and symptoms of leukostasis”1.  Leukostasis is believed to stem from the increased production of WBC that increases viscosity in the microcirculation, leading to decreased perfusion of major organs.  To muddy the waters of diagnosis even more, 80% of these patients with hyperleukocytosis will be febrile from inflammatory processes and/or infection. This is why hyperleukocytosis and leukostasis should remain at the top of a physician’s differential. If left untreated, patients presenting in hyperleukocytosis have a mortality of 40% in one week.

Let’s imagine we have a patient with an active hematologic malignancy who presents febrile and in acute respiratory failure, now on 4L of nasal cannula. How should we initially approach this patient?


 First, obtain vitals-- stick a pulse oximeter on the patient-- especially if they are dyspneic.  Obtain a complete history and physical, do not forget to inquire about recent blood transfusions, as this increases the WBC count. Hyperleukocytosis/leukostasis should be a primary concern for this imaginary patient, so a CBC with differential is warranted, as well as CMP, PT/INR, PTT, and fibrinogen. Given the acute respiratory failure, one might consider obtaining and Arterial Blood Gas; here is the problem one will run into—the arterial pO2 will be falsely decreased by the large sum of WBCs’ metabolism.  PT/PTT and fibrinogen levels should also be noted as disseminated intravascular coagulation (DIC) is a common complication.  And to piggyback on the blast crisis work-up, you want to observe any renal failure and/or electrolyte abnormalities.  A chest X-ray should also be ordered if there are respiratory symptoms.  And for altered patients, a head CT should be performed.


Treatment focuses on supportive therapy and getting your Hematologist/Oncologists on board early for cytoreduction!  Optimize oxygenation and start IV fluids, but be cognizant to not overuse fluids in patients already in respiratory distress as this will exacerbate any pulmonary edema.  One study has shown hydroxyurea prior to chemotherapy to be beneficial.  The study titled Management of hyperleukocytosis, found, “standard care for acute hyperleukocytosis must include cytoreduction, proper supportive care, and prevention of tumor lysis. Hydration, alkalization, allopurinol, or urate oxidase should be started immediately. In patients with low platelet count of less than 20,000/mm(3), platelet transfusions should be given to prevent cerebral hemorrhage, as platelets do not add substantially to blood viscosity”.  Avoid blood transfusions as this will increase viscosity; if hemodynamically stable with hemoglobin of less than 7, it is recommended to transfuse to a hemoglobin value no greater than 10. Leukapheresis is an adjunct to the initial resuscitation of the patient with the above mentioned standard of care, but it only transiently decreases peripheral WBC load. Once the patient is stabilized, chemotherapy must be initiated, as it is the first-line treatment for hyperkeulocytosis2. 
For the asymptomatic patient with hyperleukocytosis, hydroxyurea is the first line agent. Not to be given to pregnant patients or patients breastfeeding, but for all others, hydroxyurea was found to decrease white blood cell counts 50 to 80% within the first 48 hours with doses of 50 to 100mg/kg daily.

G-band ideograms (left) and partial karyotype (right) of the CML-associated chromosome translocation t(9;22)(q34;q11.2). Breakpoints are indicated with arrows on the normal chromosome homologs. Translocated segments are framed on the der(9) and Ph ideograms. The translocation results in a slightly longer chromosome 9 [der(9)] and a shorter chromosome 22 [der(22)], which is termed the Philadelphia (Ph) chromosome. Courtesy of Athena Cherry, PhD.

G-band ideograms (left) and partial karyotype (right) of the CML-associated chromosome translocation t(9;22)(q34;q11.2). Breakpoints are indicated with arrows on the normal chromosome homologs. Translocated segments are framed on the der(9) and Ph ideograms. The translocation results in a slightly longer chromosome 9 [der(9)] and a shorter chromosome 22 [der(22)], which is termed the Philadelphia (Ph) chromosome.

Courtesy of Athena Cherry, PhD.


As previously mentioned, monitor platelets because reperfusion injury occurs commonly after WBC reduction and increases occurrence of intracranial hemorrhage; platelets should be greater than 20,000, and if not, platelet transfusion is warranted. And always be concerned for DIC and coagulation abnormalities in this patient population.  Once the patient is stabilized, use leukapheresis as the “bridging therapy” to the definitive therapy of chemoreduction agents like hydroxurea and chemotherapy(3).  Continue fluids as tumor lysis will be a complication with chemotherapy.

References:

1.    Uz, B. “A Medical Emergency: Leukostasis,” Global Journal of Hematology and Blood Transfusion. 2015.
2.    Ruggiero, Rizzo, Amato, and Riccardi, “Management of Hyperleukocytosis,” Curr Treat Options Oncol. February, 2016.
3.    Pham, HP and Schwart, J. “How We Approach a Patient with Symptoms of Leukostasis  Requiring Emergency Leukocytaphereis,” Transfusion. October, 2015.
4.    Uptodate: Blast Crisis and Hyperleukocytosis/Leukostasis.
5.    Tintinalli’s Emergency Medicine: A Comprehensive Study Guide 8th Edition. Tintinalli, et al. 2016.

REBOA: Resuscitative Endovascular Balloon Occlusion of the Aorta

By: Al Lulla, MD (EM PGY-2), Stephanie Charshafian, MD (EM PGY-4)

Faculty Reviewers: Chris Holthaus, MD (EM), Gerald Fortuna, MD (Trauma and Vascular Surgeon)

Case

     You are working your regular Friday night shift when EMS rolls in lights and sirens. From the EMS report, you gather: 28 year old male, single RUQ gunshot wound, found down by a bystander, has been hypotensive en route with systolic BPs in the 70s, coming in and out of consciousness. The patient is now moaning and diaphoretic. As your team rapidly establishes IV access, your first manual BP cuff reading is 64/40. You administer a 1L normal saline bolus and call for uncrossed blood. In the meantime, you quickly perform a FAST scan and note a positive study with fluid in Morrison’s pouch. After your second unit of blood is infusing, you check the patient’s pressure, which is only 72/44. While you are waiting for the trauma team to come down, you ask yourself, would this patient benefit from REBOA? 

Clinical Question:

What is REBOA? What are the indications, contraindications and steps for placing a REBOA catheter? 

Background:

     Hemorrhagic shock from non-compressible torso hemorrhage (NCTH) represents a very significant cause of mortality in trauma patients. NCTH is defined as hemorrhage from trauma to torso vessels, pulmonary parenchyma, solid abdominal organs and/or disruption to the bony pelvis. It is estimated that NCTH accounts for 85% of preventable deaths on the battlefield, 80% of which include acute hemorrhage within the abdomen/torso [1]. For many decades, the gold standard to achieve hemostatic control has included operative management or interventional radiological techniques. Both require patient stability and transport time.  However, when faced with cardiac arrest, sudden cardiovascular collapse, or precarious transport times do patients and providers have any other additional stabilizing options?

     Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) is an emerging technique that may serve as a bridge to definitive management of hemorrhagic shock. REBOA has recently evolved as an important aspect of damage control resuscitation for refractory shock and traumatic arrest that may be utilized by emergency physicians and trauma surgeons in the ED setting [2]. REBOA utilizes a balloon occlusion catheter placed via the common femoral artery (CFA) to temporarily slow bleeding from below the diaphragm. Currently two catheters exist to accomplish this purpose.  The Coda® balloon catheter (ranging from 9-10 French catheters, 100-140 cm length, requiring 12-14 French sheaths) and a newer, smaller, and shorter ER-REBOATM catheter (6 French catheter, 72 cm length, 7 French sheath) FDA approved in 2015.  

     Emergency resuscitative thoracotomy (RT) has long been the mainstay and still remains an option in the management of patients with NCTH and subsequent hemodynamic collapse (For more details on the indications and steps of performing resuscitative thoracotomy, check out: http://www.everydayebm.org/case-based-learning/edthoracotomy). However, REBOA may offer an alternative to thoracotomy as a less invasive and less morbid approach that may provide a higher degree of safety to both the provider and the patient in certain scenarios. In animal models there is evidence to suggest that REBOA may be superior to resuscitative thoracotomy and aortic cross clamping in terms of physiological markers of resuscitation including lactic acid and pH, while having comparable improvement in cerebral and cardiac perfusion after hemorrhage from an iliac artery sheath [3]. 

     In a 2015 human study, overall survival was shown to be greater with REBOA vs. RT (37.5% vs. 9.7%; P=0.03) when comparing REBOA (n=24) vs. RT (n=72) at two level 1 civilian trauma centers with refractory hemorrhagic shock from penetrating or blunt abdominal trauma (patients with suspected or confirmed intrathoracic injury were excluded) [4]. Additionally, there were more deaths in the ED amongst patients undergoing RT vs. REBOA (62.5% vs. 16.7%; P< 0.001). Of note, there were no differences in injury severity scores or mechanism of injury between the two groups.

     Prospective data (Nov 2013-Feb 2015) from the Aortic Occlusion for Resuscitation in Trauma and Acute Care Surgery (AORTA) registry (eight ACS Level 1 centers) examined 114 patients of which 46 underwent REBOA and 68 open aortic occlusion (AO) [5].  Overall survival was 21.1% (REBOA 28.2% vs. open AO 16.1%; P=0.12) with few complications associated with REBOA (embolism 4.3%, pseudo aneurysm 2.1%, limb ischemia 0%). Hemodynamic stability (systolic blood pressure >90 mm Hg for > 5minues) if achieved occurred more often with REBOA than open AO (47.8% vs. 27.9%; P=0.01).  Time to successful aortic occlusion was similar for REBOA and open AO (6.6 +/- 5.6 min vs. 7.2 +/- 15.1; P=0.84).

     A recent 2016 study from a group in Japan offers a different perspective on REBOA associated outcomes [6]. From a retrospective analysis (2004-2011) of the Japan Trauma Data Bank (196 centers), blunt trauma patients who underwent REBOA and able to be analyzed (n=351) were compared to controls who did not undergo REBOA (n=1456) using a propensity matched analysis. The study found significantly lower survival to discharge in the REBOA group compared to the propensity group (26.2% vs. 51.3%; P=<0.0001). The poor outcomes reported in this study have been a highly contested point of debate. Nevertheless, several types of delays have been noted: Japanese trauma surgeons are not typically present in the hospital 24/7, REBOA treated nonsurvivors mean time to transfusion was 124 +/- 94 minutes while their mean to definitive care/OR was 172 +/- 134 minutes. The authors noted that the higher REBOA mortality may be indicative of “’last ditch efforts’ for severity not otherwise identified in the trauma registry.”   

     In regards to balloon occlusion times, some time is needed to allow hemostasis, clot formation, and stabilization but is weighed against longer being worse for organ perfusion.  All patients will experience ischemic/reperfusion physiology following occlusion with more severe derangement seen with Zone 1 occlusion times greater than 60 minutes. Research is ongoing to evaluate partial occlusion times. Outcomes and tolerability of various balloon occlusion times may be further influenced by individual patient characteristics, co-morbid conditions, and pre-inflation hypoperfusion or low/no flow states.

Indications:

     Generally speaking, REBOA can be considered in patients who are in hemorrhagic shock due to confirmed or suspected hemorrhage below the diaphragm. It’s important to note that indications vary depending on the injury patterns and the environment (i.e. combat casualty care vs. civilian trauma center) as well as the resources available at each institution (rural hospital versus tertiary care level 1 trauma center) [7]. Based on the current literature, our institution has formulated the following algorithm for REBOA deployment, which is based on the University of Maryland Shock Trauma Algorithm [4]: 

 

Contraindications:

     The only significant contraindication to placement of REBOA is suspicion or presence of intrathoracic injury, for which a resuscitative thoracotomy would likely be the preferred approach.  Per the manufacturer, REBOA is also contraindicated in pregnant patients (aortic occlusion would deprive the pelvic vasculature and thus fetus of blood flow) as well as pediatric (insertion of REBOA is landmark based and has not been studied or approved for pediatrics) patient populations.

The ER-REBOA (7 Fr) Catheter (Prytime Medical)

Source: Prytime medical http://prytimemedical.com/wp-content/uploads/2017/05/er-reboa-cath-900.png

Source: Prytime medical http://prytimemedical.com/wp-content/uploads/2017/05/er-reboa-cath-900.png

 

Get in the Zone [7]:

Source: Napolitano LM. Resuscitative Endovascular Balloon Occlusion of the Aorta: Indications, Outcomes, and Training. Crit Care Clin. 2017;33(1):55-70.

Source: Napolitano LM. Resuscitative Endovascular Balloon Occlusion of the Aorta: Indications, Outcomes, and Training. Crit Care Clin. 2017;33(1):55-70.

     Prior to placing the REBOA catheter, it’s important to think about where you want your balloon to be inflated. There are three delineated zones that the balloon can occlude, zone 1, zone 2 and zone 3. For REBOA deployment, only zone 1 and zone 3 regions should be considered. Zone 1 is demarcated from the take-off of the left subclavian artery to the celiac trunk, and is ideal when abdominal hemorrhage is suspected. Zone 2 is from the celiac trunk to the lowest renal artery, and should not be considered for REBOA. Zone 3 is from the lowest renal artery to the level of the aortic bifurcation, and is optimal for controlling pelvic hemorrhage [7].   

The Procedure [4,8,9]:

  1.  Garner your personal protective equipment, including a face shield, mask, and sterile gloves. 
  2. Establish arterial access: Via ultrasound, landmark, or cut-down access the common femoral artery (2 cm below the inguinal ligament). This can be done first pass with an arterial micropuncture kit or alternatively by using a pre-placed common femoral arterial line (ideally 18ga to allow 7 French sheath guidewire compatibility). Once in the artery, use a guidewire and Seldinger technique to advance your 7 Fr introducer sheath over the guidewire to cannulate the vessel. Note, a 7 French sheath guidewire is only compatible with an 18-gauge arterial line catheter or larger. For example, if you use a 20-gauge arterial catheter, you may not be able to thread the 7 French sheath guidewire through the catheter because the guidewire is too thick. 
  3. Prep the catheter: Draw up normal saline in a 30 ml syringe and attach to the balloon port. Make sure to test the balloon by fully inflating and then deflating it. The balloon only holds a maximum of 24 ml of saline, and no more should EVER be inflated (please note that you will likely never need this much inflation to occlude the aorta, and insertion of more than 24 ml of saline can rupture your balloon). Attach the arterial pressure transducer to your arterial line lumen and flush your arterial line. 
  4. Measurement: You should measure how far you will need to advance the catheter prior to inserting it. To do this, use tip of the catheter as a starting point. To occlude zone 1, place the tip of the catheter over the sternal notch and measure down to your femoral sheath. To occlude zone 3, place the tip of the catheter over the xiphoid process and again measure down to the femoral sheath. Make sure to mentally mark this on the catheter or write these numbers down in case your case evolves and you need to change from zone 1 to zone 3 (see algorithm above).
  5. Insert the catheter: Prior to inserting the catheter, advance the peel-away orange sheath over the p-tip to straighten it out. Insert the tip of the catheter with the orange sheath into your 7 French introducer and puncture the seal/valve. Advance the catheter approximately 10-20 cm, then slide back (or peel) the orange sheath covering the catheter to allow better visualization of the catheter depth marks as they enter the sheath. Continue to advance the catheter and stop at the sheath entrance whenyour pre-measured catheter mark/distance is reached.
  6. Inflate the balloon: Prior to inflation, make note of how much saline you have in your syringe and that the arterial line is reading (or ready to read). Once you open the stopcock, inflate the balloon slowly until you acquire an arterial line tracing and achieve the minimal adequate blood pressure for your patient scenario.  While the balloon can theoretically accommodate up to 24 mls of saline, you should almost never need this much saline to occlude the aorta. The alleged magic balloon volume is approximately 8 mls (remember: “eight is great”). Make sure to call out and record the amount of saline instilled as well as the time when the balloon is up so an accurate assessment of ischemic time can be recorded.
  7. Secure your catheter, obtain an x-ray if time permits (or ultrasound perhaps TBD), otherwise keep getting on your way to definitive management (OR, IR, etc.). The clock is ticking!

Take Home Points:

  • NCTH is the leading cause of death in trauma patients. REBOA offers a reasonable alternative to resuscitative thoracotomy and aortic cross clamping in patients who don’t respond to volume resuscitation, are in hemorrhagic shock, and don’t need a thoracotomy. 
  • Think about the possibility of REBOA early and get ahead of the curve by placing a common femoral arterial line if they are shocky (easier to do with a pulse).
  • REBOA deployment in zone 1 is optimal for abdominal or any infra-diaphragmatic hemorrhage, while zone 3 deployment is better suited when pelvic or lower extremity non-compressible injury is suspected.  If in doubt, consider doing zone 1 until things have stabilized and you’re definitively sure of the hemorrhagic source.
  • Use the tip of the catheter and distance to your femoral access externally as a guide to measure how far you need to advance your catheter (zone 1=tip at sternal notch; zone 3= tip at xiphoid).
  • Once you inflate the balloon (“8 is great”), remember more time = more ischemia. Make sure your patient is headed towards definitive management as quickly as possible.
  • At this time, REBOA has generally been contraindicated in patients who have an identifiable or suspected chest/aortic injury, or in pregnant or pediatric patients.

References: 

  1. Stein, Deborah. REBOA: Who, What and Why. https://www.youtube.com/watch?v=W8yGPeGkuJg. Accessed May 28th, 2017
  2. Qasim Z, Brenner M, Menaker J, Scalea T. Resuscitative endovascular balloon occlusion of the aorta. Resuscitation. 2015;96:275-9.
  3. White JM, Cannon JW, Stannard A, Markov NP, Spencer JR, Rasmussen TE. Endovascular balloon occlusion of the aorta is superior to resuscitative thoracotomy with aortic clamping in a porcine model of hemorrhagic shock. Surgery. 2011;150(3):400-9.
  4. Moore LJ, Brenner M, Kozar RA, et al. Implementation of resuscitative endovascular balloon occlusion of the aorta as an alternative to resuscitative thoracotomy for noncompressible truncal hemorrhage. J Trauma Acute Care Surg. 2015;79(4):523-30.
  5. Dubose JJ, Scalea TM, Brenner M, et al. The AAST prospective Aortic Occlusion for Resuscitation in Trauma and Acute Care Surgery (AORTA) registry: Data on contemporary utilization and outcomes of aortic occlusion and resuscitative balloon occlusion of the aorta (REBOA). J Trauma Acute Care Surg. 2016;81(3):409-19.
  6. Inoue J, Shiraishi A, Yoshiyuki A, Haruta K, Matsui H, Otomo Y. Resuscitative endovascular balloon occlusion of the aorta might be dangerous in patients with severe torso trauma: A propensity score analysis. J Trauma Acute Care Surg. 2016;80(4):559-66.
  7. Napolitano LM. Resuscitative Endovascular Balloon Occlusion of the Aorta: Indications, Outcomes, and Training. Crit Care Clin. 2017;33(1):55-70.
  8. Weingart S. REBOA. Emcrit. 2015. Available at: https://emcrit.org/podcasts/reboa/. Accessed May 28, 2017. 
  9. http://prytimemedical.com/wp-content/uploads/2017/05/ER-REBOA™-Catheter-Quick-Reference-Guide.pdf

Vitamin C in Sepsis: Splashes in the popular press

Hydrocortisone-Vitamin C-Thiamine in Sepsis

When articles pertaining to emergency medicine and critical care make a splash in the popular press, we’ll do our best to provide a timely appraisal of the evidence.

When articles pertaining to emergency medicine and critical care make a splash in the popular press, we’ll do our best to provide a timely appraisal of the evidence.

 

Marik PE, Khangoora V, Rivera R, Hooper MH, Catravas J, Hydrocortisone, Vitamin C and Thiamine for the Treatment of Severe Sepsis and Septic Shock: A Retrospective Before- After Study, CHEST (2017), doi: 10.1016/j.chest.2016.11.036. 

Bottom Line Up Front

In a single center, before-after ICU study comparing 47 patients with severe sepsis or septic shock and a procalcitonin ≥ 2ng/ml, a regimen of Hydrocortisone, Vitamin C, and Thiamine was shown to have a dramatic absolute risk reduction of 31.9% (NNT= 3.1) in mortality (40.4% vs. 8.5%, p<0.001) when compared to retrospective controls not receiving the 3 drug combination. The inclusion criteria included procalcitonin measurement, which limits its generalizability. However, if these results are replicated in large-scale RCTs it would be practice changing in the management of severe sepsis and septic shock. Only a relatively small benefit would need to be demonstrated to support wide-spread adoption because this regimen is very low-cost and has a reassuring safety profile. However, implementing this intervention should not distract us from doing the things we do know work in sepsis, such as early recognition, resuscitation, appropriate antibiotics and lung-protective strategies for patients at risk for ARDS

 

Does it live up to the hype?

It’s too early to tell. There have been dozens of promising therapies in sepsis that have failed to show benefit in large randomized controlled trials.  Until more research is done, it is prudent to maintain focus and improve compliance on interventions that have been more robustly shown to work.  

A Case

You are working in the trauma and critical care area of your emergency department when a 60-year-old woman comes in with a three-day history of productive cough, fever, and today developing lethargy. She has diabetes and hypertension. On arrival, her vital signs are significant for fever to 39.2, tachycardia to the 130s, blood pressure of 93/50 and tachypnea to 28. She has coarse crackles on the right lower lung fields & she appears lethargic. You begin fluid resuscitation with a 30 mL/kg bolus and attempt to gather collateral information from her family. Her chest x-ray shows a dense right lower lobe pneumonia, and small bilateral effusions. Her CBC shows a white count of 18 and her lactate is 12. After the fluid bolus, her blood pressure improves to 110/60 but her tachypnea worsens & she looks like she is tiring out. She is intubated for respiratory failure & her blood pressure remains soft. Central access is obtained & she is started on norepinephrine with a MAP goal of > 65. Broad spectrum antibiotics are initiated after blood cultures are obtained, and she is admitted to the ICU. There, her lactate has only cleared to 10.

Vasopressor requirements increase despite the addition of vasopressin and she is started on stress dose steroids with minimal improvement in her vasopressor requirement. You ask the attending about the utility of vitamin C and thiamine in septic shock, remembering an article that has been circulating on your Newsfeed the last few days about a group in Virginia that is described as having “cured sepsis” with this intervention. 

Vitamin C: Source: https://en.wikipedia.org/wiki/Vitamin_C#/media/File:L-Ascorbic_acid.svg

Vitamin C: Source: https://en.wikipedia.org/wiki/Vitamin_C#/media/File:L-Ascorbic_acid.svg

Critical Analysis

Study Location: Medical service of the General ICU of a tertiary referral center. 

Patient Selection: Electronic chart query for patients with the diagnosis of severe sepsis or septic shock (1992 American College of Chest Physicians/Society of Critical Care Medicine Consensus Conference definition).  The “before” group included patients from June – December 2015 and the “after” group included patients from January - July 2016. Forty-seven patients were included in each of the intervention and control group. 

Inclusion Criteria: The intervention was implemented in all consecutive patients with a primary diagnosis of severe sepsis or septic shock, and a procalcitonin level greater than or equal to 2 ng/mL. The included control patients were consecutive patients from the preceding six months using the same inclusion criteria.

Exclusion Criteria: Age less than or equal to 18, pregnant patients, and patients who were not full code on presentation to the ICU were excluded from analysis. 

The Intervention: The intervention group received IV vitamin C 1500 mg Q 6 hours for 4 days, IV thiamine 200 mg Q 12 hours (both for either 4 days or until transfer from the ICU), and IV hydrocortisone 50 mg Q6 hours. Hydrocortisone was also given to the control group with 59.6% receiving it “per current guidelines and at the discretion of the attending physician.”

Outcomes: The primary end-point of the study was survival to hospital discharge. Secondary end points were ICU length of stay, need for renal replacement therapy, duration of vasopressor use, delta in SOFA score, and procalcitonin clearance. 

Results: 47% of patients in each group required vasopressors meeting the definition for septic shock while the remainder were severe sepsis.  Hospital mortality in the control group was 40.4% (expected mortality 39.7%) and 8.5% (expected 41.6%) in the intervention group yielding a number needed to treat of 3.1 to avoid 1 death. 

NNT for death was 3.1 in this study, rounded up to 4 treated patients to avoid one death

NNT for death was 3.1 in this study, rounded up to 4 treated patients to avoid one death

The odds ratio for mortality in patients on the protocol was 0.13 (0.04-0.48 95% CI).  The intervention group had a significantly shorter duration of vasopressors (18.3 vs. 54.9 hours, p<0.001); less need for RRT (10% vs. 33%, p=0.02); greater improvement in SOFA scores (Delta SOFA 72hr 4.8 +/- 2.4 vs. 0.9 +/- 2.7, p<0.001); and greater procalcitonin clearance (86.4% vs. 33.9%, p<0.001). There was no significant difference in ICU LOS (4 days for both groups). 

Limitations: The main limitations of this study are relatively small sample size as well as the retrospective nature of the study.  Due to their inherent limitations, retrospective studies can only be hypothesis generating and limited to associations.  These results are impressive but there have been many interventions in sepsis that have shown initial promise but have failed to be validated on large-scale randomized controlled studies.

The other major limitation regarding the generalizability of this study to broader practice is the use of procalcitonin to identify patients that would benefit from the intervention. This is not a routinely ordered lab at our institution & the utility of procalcitonin as a biomarker in sepsis is still a matter of debate. 

Discussion  

These results need to be replicated at other centers and in a randomized fashion before this intervention should be widely adopted.  The harms associated with vitamin C are almost nil (except with renal dysfunction where oxalate accumulation can occur with mega-dose VitC) and the costs are low making it a potentially safe and cost-effective intervention. 

This intervention was so practice changing at their institution that they feel they no longer have clinical equipoise and will not be able to complete an RCT themselves.  Therefore, an RCT would have to be completed in an institution that does not have this as their standard of care in order to allow randomization to the control arm.

Reversals in medical evidence are common.  An analysis of 363 articles testing standard of care in medicine were reversed 40% of the time over a 10-year period.  There is a figurative graveyard of proposed therapies in sepsis management that were initially promising including statins, hemofiltration, immune globulin, drotrecogin alfa, deltibant, nitric oxide inhibitors, growth hormone, calcitriol, etc.  Sepsis is not a single disease that will have a silver-bullet solution; rather, there are subsets of patients who are likely to benefit from some of the above interventions but we simply do not have the mechanism to identify them yet.  Analogous to the admonishment in finance that “past returns do not guarantee future results,” past failures in sepsis research do not necessarily predict current or future failures and this study demonstrates the need for further investigation.  

Applying the evidence: In this hypothetical case, the potential benefits of the intervention outweigh the known risk for harm and I would have a low threshold to trial the addition of vitamin C and thiamine to her treatment if her care had otherwise been optimized and she continued to worsen. 

 

Written by: Adam Rieves, MD MS

Faculty reviewers: Chris Holthaus, MD, Brian Fuller, MD, MSCI, Chris Carpenter, MD, MSc, FACEP, FAAEM

References:

A Decade of Reversal: An Analysis of 146 Contradicted Medical Practices. Prasad, Vinay et al. Mayo Clinic Proceedings , Volume 88 , Issue 8 , 790 - 798

Marik PE, Khangoora V, Rivera R, Hooper MH, Catravas J, Hydrocortisone, Vitamin C and Thiamine for the Treatment of Severe Sepsis and Septic Shock: A Retrospective Before- After Study, CHEST (2017), doi: 10.1016/j.chest.2016.11.036. 

https://www.uptodate.com/contents/investigational-and-ineffective-therapies-for-sepsis#H2552815

Rhodes A, et al. Surviving Sepsis Campaign: International Guidelines for Management of Sepsis and Septic Shock: 2016Crit Care Med. 2017 Jan 17. doi: 10.1097/CCM.0000000000002255. [Epub ahead of print] PMID: 28098591 OR Intensive Care Med. 2017 Jan 18. doi: 10.1007/s00134-017-4683-6. [Epub ahead of print]

 

 

Emergency Resuscitative Thoracotomy

Case

You are working in an ED with a trauma surgeon when you get the call: “28 year old male single stab wound to the chest, BP 98/57, HR 107, 99% O2, ETA 5 minutes.”  You quickly gown up, and with the help of your nurses and techs, you set up the room for the incoming patient.  You hear sirens as the medics pull into the ambulance bay and, much to your surprise, they are doing CPR. “Doc, he was totally with it, and then arrested a few moments ago!  He was PEA on the monitor.”  As the medics are transferring the patient to the gurney, you ask yourself, “Does this patient need a thoracotomy?” 

Clinical Question

What are the indications, contraindications, and the steps to perform an emergency resuscitative thoracotomy (RT)? 

Background & Guidelines

The emergency resuscitative thoracotomy, sometimes referred to as an ED thoracotomy, is often described as a last-ditch “damage control measure" when resuscitating a patient in traumatic arrest or impending traumatic arrest.  Studies suggest that outcomes after resuscitative thoracotomy are generally poor.  Survival rates have been reported between 9-12% for penetrating thoracic trauma.  Outcomes after blunt trauma are even worse, with survival rates estimated between 1-2% [1]. 

Unfortunately, the Advanced Cardiovascular Life Support (ACLS) algorithm is not designed for patients with traumatic arrest.  ACLS is intended for the patient with cardiac arrest from medical causes, as well as life-threatening primary cardiac conditions.  In the medical arrest, chest compressions continue to circulate blood to the coronary arteries and brain temporarily while the underlying cause of arrest is diagnosed and treated.  If the pump (the heart) is broke, we can take over for the pump via chest compressions as a temporizing measure. 

Alternatively, traumatic arrest is almost never a primary pump (cardiac) failure.  The leading cause for cardiac arrest in the trauma patient is hypovolemic shock in the form of hemorrhage.  If the tank is empty and there is no volume to push through the pump, then pushing on an empty pump via chest compressions will yield very limited benefit.  Other causes of traumatic cardiac arrest include obstructive shock (tension hemo/pneumothorax, pericardial tamponade), cardiac injury, and neurogenic shock (traumatic brain or cervical/high thoracic cord injury).  Isolated chest compressions for obstructive shock have negligible effects unless the tension or tamponade is relieved and/or the cardiac injury is repaired or temporized. 

Advanced Trauma Life Support (ATLS) has been developed as a separate set of basic standards for managing traumatic injury.  Part of the ATLS algorithm refers to the emergency resuscitative thoracotomy (RT).  The majority of patients with thoracic trauma can be managed without operative intervention; however, a subset of patients (roughly 10%) may benefit from thoracotomy [1].  RT is often a controversial procedure that utilizes significant institutional resources and poses risk to both patients and providers in the form of iatrogenic injuries from needle sticks, open rib fractures, and infections.  Given the nature of practicing emergency medicine within the community setting, consideration should also be given to the timely availability of a trauma or thoracic surgeon. Not having a surgeon immediately available for subsequent definitive care in your practice environment would be a contraindication to performing a RT. 

The ATLS indications to perform RT include [2]: 

  • Relieve cardiac tamponade
  • Repair cardiac injury
  • Direct control of exsanguinating intrathoracic injury
  • Cross clamp the aorta 
  • Open cardiac massage
  • Remove air embolism

There have been multiple studies that have been conducted to identify which patients will benefit from RT.  Current practice guidelines have been published by several organizations, including the Eastern Association for the Surgery of Trauma (EAST) and the Western Trauma Association (WTA).

The EAST guidelines published in 2015 focus on identifying candidates for RT based on mechanism of injury (i.e. blunt vs. penetrating) and the presence or absence of signs of life (SOL).  SOL is defined as palpable pulses, measurable blood pressure, electrical cardiac activity, pupillary response, spontaneous breathing or purposeful movement of an extremity.  The authors of the EAST guidelines sought to evaluate whether RT improved outcomes versus resuscitation without performing a thoracotomy.  They performed a systematic review of the literature and identified 72 studies and 10,238 patients.  They developed the above recommendations regarding performing RT [3]

In contrast to the EAST guidelines which are based on the presence or absence of SOL, the guidelines put forth by the WTA (AKA the “WEST” guidelines) stratifies patients based on injury and transport time [4].  

Additionally, a trauma and vascular surgeon in the UK named Dr. Karim Brohi, who also worked with the London Helicopter EMS (HEMS) system set up a website called Trauma.org to make trauma education resources publicly available worldwide.  Trauma.org has also published recommendations on which patients are appropriate to receive RT.

Indications:

  • Penetrating thoracic injury with unresponsive hypotension (BP <70) or arrest with previously witnessed cardiac activity.
  • Blunt thoracic injury with unresponsive hypotension or rapid exsanguination from chest tube (>1500mL).

Relative Indications:

  • Penetrating thoracic injury and arrest without previously witnessed cardiac activity.
  • Penetrating non-thoracic injury or blunt thoracic injury and arrest with previously witnessed cardiac activity. 

Who is most likely to benefit?

  • Penetrating > Blunt trauma
    • Thoracic > Extrathoracic
      • Cardiac
    • Stab wounds > GSW
  • Single injury > Multiple injury
  • Less time since loss of pulses
  • Previously witnessed cardiac activity
  • Signs of life in the ED

Contraindications:
Just as there are multiple different recommended indications for RT, there are multiple different recommended contraindications: 

  • ATLS contraindications include no signs of life (SOL) on arrival, severe traumatic brain injury, or most likely extrathoracic cause of circulatory collapse. 
  • EAST guidelines recommend against RT in pulseless patients without SOL after blunt injury.
  • Trauma.org uses blunt thoracic injury with no witnessed cardiac activity, multiple blunt trauma, or severe head injury. 

Decision to perform emergency resuscitative thoracotomy


This decision can be difficult and is not taken lightly given the extremis of the patient, varying recommended indications and contraindications, extenuating circumstances, or preceding health/co-morbidities that may influence ischemic or reperfusion injury and recovery, resources in your area, and the risk to both patient and provider.  Ultimately, this should be an individualized decision based on the patient in front of you, their likelihood of benefit, and your competence in performing the procedure.

Preparation


Prior to ever attempting this procedure on a patient, you should not only be familiar with the necessary steps and indications, but also with the tools available at your institution.  Does your institution have a “thoracotomy kit” or individual tools that need to be gathered prior to patient arrival?  Do you know where this is and how long it takes to get?  Do you know how to set up the rib spreader appropriately?  With a patient in front of you where seconds and minutes are critical, this should not be your first time touching the tools and you should not have to waste time looking up the procedure. Preparation is key.


Breathe. This is a high stress, high adrenaline procedure, with a risk of iatrogenic injury to the patient and provider.  Make sure to put on a face shield and double glove.  Ask for help if you need it. 

Hold chest compressions: As discussed above, chest compressions do not accomplish much in traumatic arrests, interfere with rapid performance of RT, and increase the risk of iatrogenic injury to yourself as well as the provider performing chest compressions.

Procedure [5, 6]

  1. Quickly use betadine to prep the area.
  2. With the patient supine, raise their left arm superiorly exposing the axilla. You can consider taping their arm if needed.
  3. The patient is likely intubated, at which point you can stop positive pressure ventilation, or advance the ETT into the right main-stem to decompress the left lung making access to the heart easier. 
  4. On the patient’s left, use a number 10 blade to cut inferior to the pectoralis major muscle above the rib in the 5th intercostal space (inframammary fold in a female patient), extending your incision to the anterior axillary line and curve superiorly in the direction of the ribs towards the axilla. 
  5. Using a pair of scissors (i.e. curved mayos) dissect through the intercostal muscles to gain access to the thoracic cavity
  6. Insert the rib spreaders, positioning the crossbars towards the bed.  This is important in the event you want to extend your thoracotomy to the right side (i.e. clamshell thoracotomy).  If the rib spreaders are facing towards the sternum, you will have difficulty doing this.
  7. Spread the ribs wide, approximately 8 to 10 inches.  The wider the better, as exposure is key.
    • At any point, consider extending the incision to a clamshell thoracotomy if you need further exposure or if right sided injuries are expected.  Duplicate the left sided incision on the right, likely using a second provider while you continue the next steps.  Once right sided access is obtained, rib spreader can be moved to the center of the chest if needed.
  8. Once in the chest, grab a pair of small scissors and pick-ups.  Push the lung out of the way.  Locate the heart below the sternum.
  9. Make an incision in the pericardium.  Be cognizant not to cut the phrenic nerve.  To avoid this, make a vertical incision parallel to the phrenic nerve to access the pericardial sac, and bluntly spread the incision with your fingers.  This will allow you to relieve tamponade and deliver the heart to assess cardiac activity and any penetrating cardiac injury.
    • Some algorithms suggest stopping further resuscitation measures if no cardiac activity is seen at this point.
  10. If there is evident cardiac injury, apply direct pressure with your finger. Alternatively, a foley catheter can be placed in the wound and inflated with gentle traction applied.
  11. You can consider repair of the cardiac injury using 3-0 prolene with buttressed sutures.  Make sure to avoid tying off a coronary vessel.
  12. Other obvious intrathoracic injuries with hemorrhage can be temporized with direct pressure, clamping, or 3-0 prolene sutures.
  13. Internal cardiac massage can be started immediately after relief of cardiac tamponade and/or repair of penetrating cardiac injury if the patient does not have a palpable pulse after this point.  Make sure to use two hands with fingers together and extended to GENTLY squeeze the heart from apex to atria and avoid perforation of the thin walled right ventricle with your fingers. 
    • Defibrillate the heart using two small internal paddles, 15-30J, (if available) and if the patient has a shockable rhythm.
  14. Aortic cross clamping can be considered for exsanguinating injuries below the diaphragm.  Avoid cross clamping the esophagus if possible.
  15. If you are able to revive the patient, get them to the OR as quickly as possible for definitive treatment.

Case Conclusion 

In our young, healthy patient with single stab wound to the chest causing cardiac arrest of less than 5 minutes and signs of life at the scene, our patient is an optimal candidate for emergency resuscitative thoracotomy without any contraindications.  While the rate of overall survival is low, our patient has the highest rate of survival based on his injury and his down-time.  And while we cannot guarantee survival in this (or any) patient, his outcome cannot get any worse as he is currently pulseless.  Since our institution has the necessary resources available and immediate access to trauma surgery, we decide to perform an emergency resuscitative thoracotomy in this patient. 

Take home points

  1. Consider thoracotomy in your trauma patients with recent or impending loss of pulses.
    • Thoracic trauma with refractory shock
    • Pulseless with SOL (or previously witnessed cardiac activity) after any trauma
    • Penetrating trauma without SOL and arrest <15 minutes
    • Rapid exsanguination from chest tube
  2. Remember where your thoracotomy trays or tools are and know how to use the rib spreaders.
  3. Get the exposure that you need: Left anterolateral vs. Clamshell.
  4. Deliver the heart, control the bleed, and get the patient to the OR!

Written by Al Lulla, MD and Stephanie Charshafian, MD
Faculty reviewers: Chris Holthaus, M.D. (EM); Doug Schuerer, M.D. (Trauma Surgery)

References

  1. Hunt PA, Greaves I, Owens WA. Emergency thoracotomy in thoracic trauma-a review. Injury. 2006;37(1):1-19.
  2. Rhee PM, Acosta J, Bridgeman A, Wang D, Jordan M, Rich N. Survival after emergency department thoracotomy: review of published data from the past 25 years. J Am Coll Surg. 2000;190(3):288-98.
  3. Seamon MJ, Haut ER, Van Arendonk K, et al. An evidence-based approach to patient selection for emergency department thoracotomy: A practice management guideline from the Eastern Association for the Surgery of Trauma. J Trauma Acute Care Surg. 2015;79(1):159-73.
  4. Burlew CC, Moore EE, Moore FA, et al. Western Trauma Association critical decisions in trauma: resuscitative thoracotomy. J Trauma Acute Care Surg. 2012;73(6):1359-63.
  5. Weingart S. The Procedure of ED Thoracotomy. Emcrit. 2012. Available at: http://emcrit.org/podcasts/procedure-of-thoracotomy/. Accessed December 18, 2016. 
  6. Inaba K, Spangler M. Trauma Surgeons Gone Wild: How to Crack the Chest. EM:RAP Podcast. 2016. Available at: https://www.emrap.org/episode/crackthe/traumasurgeons1. Accessed December 18, 2016. 
  7. Trauma.org
  8. The ATLS Subcommittee, American College of Surgeons' Committee on Trauma, The International ATLS Working group. Advanced trauma life support (ATLS®): the ninth edition. J Trauma Acute Care Surg, 2013; 74(5): 1363–1366
  9. Tan BK, Pothiawala S, Ong ME. Emergency thoracotomy: a review of its role in severe chest trauma. Minerva Chir. 2013;68(3):241-50.
  10. Kalina M, Teeple E, Fulda G. Are there still selected applications for resuscitative thoracotomy in the emergency department after blunt trauma? Del Med J. 2009; 81(5):195-8.
  11. Lorenz HP, Steinmetz B, Lieberman J, Schecoter WP, Macho JR. Emergency thoracotomy: survival correlates with physiologic status. J Trauma. 1992; 32(6):780-5
  12. Tyburski JG, Astra L, Wilson RF, et al. Factors affecting prognosis with penetrating wounds of the heart. J Trauma. 2000; 48:587-590.
  13. Boyd M, Vanek VW, Bourguet CC. Emergency room resuscitative thoracotomy: when is it indicated? J Trauma. 1992; 33: 714–721.   
  14. Millham FH, Grindlinger GA. Survival determinants in patients undergoing emergency room thoracotomy for penetrating chest injury. J Trauma. 1993; 34: 332–336
  15. Morrison J, Poon H, Rasmussen T, Khan M, Midwinter M, Blackbourne L, Garner J. Resuscitative thoracotomy following wartime injury. Journal of Trauma and Acute Care Surgery. 2013; 74(3):825-29.
  16. Danne PD, Finelli F, Champion HR. Emergency bay thoracotomy. J Trauma. 1984; 24: 796–802. 

You Can't PATCH Up An ICH

Clinical Scenario: A 65-year-old male with a history of coronary artery disease, hypertension, and diabetes presents to the ED complaining of a severe headache, nausea, and vomiting. He is protecting his airway and has no focal neuro deficits. A head CT shows a large left-sided intraparenchymal hemorrhage. As you’re about to page Neurosurgery, you scroll through his medication list and notice that he takes aspirin and clopidogrel daily. You know that the neurosurgeons frequently ask for platelet transfusions in these patients- should you just go ahead and order a couple of packs now?

Clinical Question: Does platelet transfusion improve short- or long-term outcomes for patients with spontaneous intracerebral hemorrhage (ICH) who are taking antiplatelet agents?

Literature Review: The first high-quality RCT on this topic, the PATCH trial, was recently published in the Lancet. Baharoglu and colleagues performed a multi-national, multi-center, randomized, open-label, masked-endpoint trial to assess the efficacy of platelet transfusion for patients taking antiplatelet agents who develop a non-traumatic ICH. Patients were eligible for enrollment if they met the following criteria:

  • 18+ years old
  • Non-traumatic ICH and a GCS of 8-15
  • Able to receive platelets within 6 hours of last known normal and within 90 minutes of brain imaging
  • Known to have been taking aspirin, carbasalate (an aspirin derivative that is frequently used in the UK), clopidogrel, or dipyridamole for at least 7 days
  • Pre-event modified Rankin score of 0 or 1.

Patients were excluded if they met any of the following criteria:

  • Presence of comorbid neurosurgical conditions (epidural hematoma, subdural hematoma
  • CT findings suspicious for underlying AVM or aneurysm
  • Significant intraventricular hemorrhage,
  • Expected surgical intervention for clot evacuation within 24 hours
  • Previous history of severe reaction to platelet transfusion
  • Use of vitamin K antagonists (unless INR <1.3 on presentation)
  • Known coagulopathy or thrombocytopenia with platelet count <100k,
  • Inability to provide consent prior to ICH due to mental disability, or imminent death.

Patients were randomized in a 1:1 ratio to receive “standard care” (not strictly defined, but presumed by the authors to correspond to current European neurosurgical guidelines) or “standard care” plus platelet transfusion. Randomization was blinded by means of a secure computerized system. Patients and treating physicians were aware of allocations, but outcome assessors and study investigators not involved in direct patient care were blinded. The primary outcome was shift towards death or dependence rated on the modified Rankin scale (mRS) at 3 months.

Overall, 190 patients were enrolled and randomized, 97 to transfusion and 93 to standard care. Baseline characteristics including severity of hemorrhage, GCS score on presentation, and comorbidities (other than PVD, more common in the platelet group) were similar between the groups. In the intention-to-treat analysis, the odds of a shift towards death or dependence on the mRS were actually higher in the transfusion group (adjusted common OR 2.05, 95% CI 1.18-3.56, p = 0.014). Secondary analysis showed that patients in the transfusion group were more likely to have a mRS of 4-6 (moderately severe disability, severe disability, or death) at 3 months (OR 2.04, 95% CI 1.12-3.74, p=0.0195). 42% (n=40)of participants receiving platelets had a “serious adverse event” during their index hospitalization, as compared to 29% (n=28) of participants receiving standard care.  The most serious adverse events were ICH enlargement or urinary or pulmonary infections.

The study did have some weaknesses. It was relatively small compared to other stroke trials, leading some chance imbalances between the groups; however, standard size calculations were performed and enrollment targets were achieved. It had very rigorous exclusion criteria (19% met at least one exclusion criteria), which render the trial inapplicable to a large number of patients presenting with ICH (especially the requirement that no surgery be planned within 24 hours). Study investigators did not keep screening logs, so it is not possible to evaluate the trial for inclusion bias. Finally, the investigators relied on patient/relative report and/or chart review rather than objective lab platelet function testing (which is expensive and not widely available) to identify patients taking antiplatelet agents, raising the possibility that some patients included were not actually taking these medications

Overall, however, the PATCH trial strongly suggests that the routine practice of treating patients with non-traumatic ICH who are taking antiplatelet agents with platelet transfusion is not helpful, and possibly harmful. It may be time to start discussing the risks and benefits of this treatment more thoroughly with our patients and consultants.

References:

  1. Baharoglu et al. “Platelet transfusion versus standard care after acute stroke due to spontaneous cerebral haemorrhage associated with antiplatelet therapy (PATCH): a randomised, open-label, phase 3 trial.” Lancet 2016; 387: 2605–13

Kevin Baumgartner PGY2

Faculty Reviewed by Peter Panagos, MD, FACEP, FAHA

It's Okay to Delay Your Sequence... a Little.

Case: A 68 year old man with a history of CVA, CAD, HTN, and COPD presents from his nursing home with several days cough and fever.  He is brought in by EMS on nonrebreather mask and appears to be in severe respiratory distress with oxygen saturations in the 80's.  After he is placed on BiPap, chest x-ray demonstrates infiltrates consistent with pneumonia.  The decision to intubate the patient is made after he fails BiPap due to intolerance of the mask (he repeatedly attempted removing the mask) and continued poor oxygen saturation.  Endotracheal intubation was successfully performed with RSI, though the patient briefly desaturated to 75% during the process. 

Clinical question: Would delayed sequence intubation have benefited this patient and avoided desaturation?

Rapid sequence intubation, or RSI, is the preferred means of emergency airway management, allowing for a definitive airway in a short period of time and avoiding prolonged bag-valve-mask ventilation with the goal of minimizing the risk of aspiration [1].  In RSI, both an induction agent and a neuromuscular blocking agent are administered in quick succession.  Etomidate and succinylcholine are two commonly used medications for induction and paralysis, respectively.  The major disadvantage of RSI is the potential for a "cannot intubate, cannot ventilate" situation [2].  In a patient similar to the one above, this could lead to a precipitous drop in oxygen saturation and increases the risk of cardiac arrest from hypoxemia. 

One alternative that could ameliorate pre-existing hypoxemia is delayed sequence intubation, or DSI.  During DSI, the induction agent is first given to facilitate preoxygenation either by nonrebreather mask or non-invasive positive pressure ventilation (NIPPV).  After a period of preoxygenation, the patient is then given a paralytic and intubated.  DSI can be especially useful in situations where the patient has altered mental status or agitation that precludes adequate preoxygenation with a nonrebreather or NPPV mask.  Successful preoxygenation by this method would theoretically provide the patient with a better oxygen reserve and buffer against desaturation during intubation attempts [2].  

A prospective, observational study done by Weingart, et al. published in the Annals of Emergency Medicine investigated the degree of improvement in preoxygenation after a brief period of sedation with ketamine prior to intubation.  Patient selection consisted of a convenience sample of 64 patients who were uncooperative with preoxygenation (e.g. not tolerating or removing the mask, inability to remain on the stretcher).  Patients were administered 1 mg/kg of ketamine IV and preoxygenated for 3 minutes with high-flow nonrebreather or NIPPV if the nonrebreather did not raise SpO2 to >95%.  The study found that saturations after increased from a mean of 89.9% to 98.8% immediately before intubation, a difference of 8.9% (95% confidence interval 6.4% to 10.9%).  Two patients, both asthmatics, did not require intubation after DSI and were able to tolerate and be admitted on NIPPV [3].  Although the major shortcoming in the study is the lack of randomization with a control arm, the study does demonstrate that DSI with ketamine can create a more favorable peri-intubation oxygen saturation, potentially providing a buffer against hypoxemic peri-intubation cardiac arrest.  

 

Submitted by Phil Chan (@PhilChanEM), PGY-4

Faculty reviewed by Brian Fuller, MD, MSCI

 

References

[1] Salhi BA, Ander DS. Chapter 122. Intubation and Airway Support. Principles and Practice of Hospital Medicine. New York, NY: McGraw-Hill; 2012.

[2] Vissers RJ, Danzl DF. Chapter 29. Intubation and Mechanical Ventilation. Tintinalli’s Emergency Medicine, 8e. New York, NY: McGraw-Hill; 2016.

[3] Ann Emerg Med. 2015;65:349-355.

An NSAID for Your Broken Bone?

Case:  A 24 year old male with no past medical history presents with a closed distal radius and ulna fracture after a cycling accident.  After closed reduction and splinting, his pain is much improved.  You tell him that he will be discharged with oxycodone for pain as needed, but he asks if he can just take ibuprofen because oxycodone and other opioids make him sleepy, and he needs to return to work tomorrow.  

Clinical Question: Should patients with acute fractures avoid NSAIDs?

Extremity fractures are relatively common presentations in the ED. Recent literature from the orthopedic world has suggested that usage of NSAIDs (non-steroidal anti-inflammatory drugs) in the setting of acute fractures hinders the healing process and leads to worse outcomes.  Given that we often try to provide non-narcotic methods to control pain in the ED, removing a whole class of drugs like NSAIDs should not be done without strong evidence that they result in poorer outcomes for patients. 

A paper published in the Journal of Bone and Mineral Research in 2002 treated rats with a COX-2 (cyclo-oxygenase 2) selective NSAID, then studied signs of healing based on radiologic, histologic, and mechanical measures.  The authors showed that endochondral ossification was markedly deficient in both rats treated with a COX-2 inhibitor, suggesting that pro-inflammatory prostaglandins (suppressed by COX-2 inhibitors) are necessary for normal fracture healing.  Similarly, fracture healing is impaired in mice that have a mutation in the COX-2 gene [1].  A recent systematic review of the existing data published in the Journal of Bone and Joint Surgery in 2012 found similar results.  This review included 316 relevant papers, and concluded that the preponderance of evidence showed that inhibiting COX-2 disrupted early fracture healing in multiple animal models, although in vivo studies in humans have not yet substantiated this finding.  A limitation of the review was that the majority of the studies were small and of variable quality with numerous potentially confounding variables. Nevertheless, the authors concede that a short term course of NSAIDs in the setting of acute fracture is likely safe and may not impede healing to a significant degree [2]. Larger and more robust human studies are needed to better delineate the effects of NSAIDs on fracture healing and patient-oriented outcomes, but a single dose of NSAIDs may be acceptable in patients who should avoid opioid analgesics. 

Submitted by Jarrod Dornfeld, PGY-2

Edited by Phil Chan (@PhilChanEM), PGY-4

Faculty Reviewed by Albert Kim, MD, MACM

 

References

[1] Simon AM, Manigrasso MB, O'Connor JP. Cyclo-Oxygenase 2 Function Is Essential for Bone Fracture Healing. J Bone Mineral Research. 2002;17(6):963-976.

[2] Kurmis AP, Kurmis TP, O’Brien JX, Dalén T. The Effect of Nonsteroidal Anti-inflammatory Drug Administration on Acute-Phase Fracture Healing: A Review. J Bone Joint Surg. 2012;94(9): 815-823

 

You're Putting that Needle Where?!

Case: 34 year old with history of extensive IV drug abuse and insulin-dependent diabetes presents to the ED in hypovolemic shock from DKA.  Multiple attempts at IV access in the field failed. Once transitioned from the EMS stretcher to the bed, the ED team immediately starts an assessment.  While the MD progresses through the A-B-Cs, the nurses start to look for IV access and the techs disrobe him.  Nursing is unable to identify an veins on exam that would be amenable to IV placement.  One of the tech’s jokingly points out that the patient has multiple penile veins that could be used for large bore placement.

Clinical Question: Is it safe and effective to place intrapenile or intracavernosal catheter to achieve access?

Anatomy

The venous vessels of the male penis form two primary systems - the superficial system involving the skin which ultimately drains into the superficial dorsal vein and the sinusoids of the corpora cavernosa draining into the deep dorsal vein. There are many communications between the superficial and deep systems facilitating rapid drainage.

https://en.wikipedia.org/wiki/Corpus_cavernosum_penis#/media/File:Gray588.png

Animal Studies

Nicol D, Watt A, Wood G, Wall D, Miller B. Corpus cavernosum as an alternative means of intravenous access in the emergency setting. Aust N Z J Surg. 2000 Jul;70(7):511-4.

The canine penis is anatomically and physiologically similar to the human penis, and these authors conducted a small prospective comparative study (3 male dogs) to assess the clinical utility of intracavernosal (IC) access for fluid resuscitation and drug administration. A standard intravenous catheter was placed (gauge and location not named) to serve as the control for the 19-gauge butterfly needle placed in the penile corpora cavernosa. Placement of the intracavernosal catheter was confirmed by the aspiration of blood. The infusion pressure of all fluids was controlled by a pneumatic infusion device.

Three primary tests were conducted:

  1. A normal saline infusion by IV and IC catheters were started at various pressures and flow rates were compared (see Table 1).
  2. Each dog was exposed to epinephrine (0.5 mg IC) and monitored for 5 minutes, then atropine (600 mg IC) and monitored again with HR, MAP, CVP recorded.
  3. The dogs were bled down to a MAP of 60 and then each resuscitated with a different fluid (normal saline, Haemaccel [colloid], autologous whole blood) while MAP and CVP were recorded.

The IC catheters infused normal saline slower than the control IV catheters but were relatively comparable. See Table 1 for details. Both epinephrine and atropine given via the IC route increased the MAP and HR, respectively, with the peak effect occurring within 1 minute (no control to compare). Lastly, all dogs were successfully resuscitated as indicated by a CVP that that was equal or greater than pre-bleeding levels and a MAP that was the same or within 10% of the pre-bleeding pressures.

Conclusions: Intracavernosal access in the canine model can facilitate moderate volume infusion rates and administration of vasoactive medications with systemic effects. Although more research is warranted, it can be considered as an alternative means of vascular access when more traditional methods fail.

 

Abolyosr A, Sayed MA, Elanany F, Smeika MA, Shaker SE. Blood transfusion and resuscitation using penile corpora: an experimental study. Urology. 2005 Oct;66(4):888-91.

This small experimental study was conducted to evaluate the utility of transfusing blood and/or resuscitation via the intracavernosal route. The authors elected to use 2 different animal models to analyze transfusion rate: the donkey and dog.

A total of 3 donkeys underwent 3 separate sessions of IV blood withdrawal (2 units each session) and IC auto-transfusion (in the same session) with each session separated by 1 week. The transfusion was performed via 18-gauge IV cannula with the site changed for each unit transfused. Times blood transfusion and establishment of corporeal access times were recorded. The rate of transfusion for each unit was calculated. Manual compression was applied to the site of the needle puncture for a maximum of 5 minutes after completion of the blood transfusion.  The penile shaft was observed throughout the procedure and 1 hour afterward. A total of 3 dogs had blood withdrawn until a MAP of 60 mmHg was achieved.  The same blood was transfused back into the dogs using a 19-gauge butterfuly needle inserted into the corpora cavernosa using a pressure bag to maintain infusing pressure at 150mmHg.

In the donkey cohort, the average time to establish IC access was 22 seconds with a range of 14 to 48 seconds.  The average time to transfuse a unit of blood was 14.2 minutes with a range of 13.2 to 16.1 minutes.  The average rate of transfusion was 31.7 mL/min.  In all donkeys, the penis returned to its pre-transfusion state by the end of the transfusion.  Complications including extravasation, hematoma formation, or color changes were not seen.

In the dog cohort, the average rate of transfusion was 35.2 ml/min with a range between 33.1 and 37 mL/min.  All dogs had been successfully resuscitated with a return of their MAP close to baseline. 

Conclusions: “Every point along the corpora cavernosa of that precious organ—the penis—may offer potential vascular access to rescue a man’s life and replenish his blood in some critical situations.”

 

Human Studies

Godec CJ, Cass AS. The penis-a possible alternative emergency venous access for males? Ann Emerg Med. 1982 May;11(5):266-8.

This study started as a retrospective review of 33 cases of males being evaluated for impotence.  During evaluation, a tourniquet was placed at the base of the penile shaft preventing venous outflow from the penis.  A recorded volume of normal saline was injected into the corpus cavernosum through a 19-gauge scalp vein needle. The changes in penile circumference and pressures inside the corpus were recorded simultaneously. Then the tourniquet was released, and the time between the release of tourniquet and return of pressure and tumescence to the preinjection level was recorded. This time represented drainage time of the fluid injected from the corpora cavernosa into the penile venous system.

The drainage time from corpora cavernosa was recorded in 10 patients, and the volume drained in the first two to four seconds ranged from 27% to 85%, with an average of 56%.  The average peak drainage per second was 13.4 cc per second, with a range Of 4 cc to 22 cc per second.  One patient was noted to have subcutaneous hematoma which resolved the next day. Patients did not report any pain.

Conclusions: An intracavernosal catheter has several advantages.  It is always available in male patients, obviates the need for venous cutdown, and can facilitate high capacity resuscitation.  In male patients with hypovolemic shock with no other IV access, the IC route may be a useful alternative.

 

Shafik A, El Sibai O, Shafik IA, Shafik AA. Corpora cavernosa as an alternative route for transfusion. Front Biosci. 2006 Sep 1;11:2535-7.

This is a small prospective case series of 15 men with difficult venous access due to burns (7), scarred veins from repeated injections (6), or extensive trauma (2).  After multiple failed attempts to obtain IV access, the providers placed an intracavernosal catheter for access.  An 18-gauge intravenous cannula was inserted into the shaft of the penis. Blood was aspirated to verify that the needle was in a sinusoid.  The thick and fibrous tunica albuginea encasing the corpus facilitated anchoring of the cannula during blood or fluid infusions. During infusion of blood or normal saline, the penile shaft elongated which disappeared after termination of infusion.  To prevent hematoma, following termination of the blood transfusion and withdrawal of the needle, the penile shaft at the site of needle insertion was compressed between fingers for 1-2 minutes.

In shock states, it took only few seconds to insert the cannula into the corpus (compared to femoral access or saphenous cut down which requires a mean of 3.18 to 5.63 minutes).  Not once did a failure to successfully cannulate the corpus occur. No difficulties were encountered by varying rates of intracavernosal infusion from slow to rapid or repeating the infusion during the same or subsequent days.  Subcutaneous penile hematoma occurred in 2 patients but disappeared spontaneously.

The ability to obtain an erection was followed in 5 men for mean period of 6.3±1.4 SD months (range 4-8) after discharge. All patients reported normal sexual activity after the catheters were discontinued.  No changes in the flaccid or erect penis, swellings or curvatures of the shaft, or pain/discomfort during erection or coitus were reported.  Additionally, fibrosis of corpus cavernosum or priapism which might occur after repeated injection did not occur.

Conclusion: “In conclusion, the CC can serve as a simple, easy, rapid, and safe method for vascular access in conditions for administration of fluid or blood when other conventional routes are inaccessible.”

 

BOTTOM LINE: While it may not be first, second, or even third line,  intracavernosal cannulation is a potential means to facilitate rapid access in a male patient with limited options; and although intraosseous access is typically the mainstay for emergent vascular access in resuscitation, intracorporal access can be an option when an intraosseous needle is not available, such as in a resource limited or mass casualty situation.  Although the risk of hematoma formation or other penile injury was low in these studies, their small sample size makes it difficult to draw strong conclusions regarding potential complications.  

 

Submitted by Dr. Danny Kolinsky, PGY-4

Edited by Dr. Phil Chan (@PhilChanEM), PGY-4

Faculty reviewed by Dr. Rose Naunheim

No Guarantees: MRI in the diagnosis of acute posterior stroke

Clinical scenario: An elderly male is brought in by EMS one evening after he developed sudden onset of vertigo 1 hr prior to arrival.  He was watching a show when he suddenly felt that the world was spinning.  On initial presentation, he had intermittent, unilateral nystagmus and was unable to walk on his own for unsteadiness and fear that he would fall.  He had no other focal neurologic deficits or extremity ataxia.  His NIHSS was 0.   The physicians felt unsure about the diagnosis of acute posterior circulation stroke, so after discussion with the patient, a hyperacute MRI was performed and was negative.  However, after returning fromMRI, the patient developed worsening nystagmus and agreed to received tPA despite negative imaging.

Clinical question:  What is the sensitivity of DWI (Diffusion Weight Imaging) MRI for acute posterior circulation stroke and should this be used to help make decisions regarding tPA administration?

Literature Review:  Posterior circulation strokes are notoriously difficult to diagnose.  This is because their presentation is dominated by non-specific symptoms such as nausea/vomiting and dizziness as opposed to the more obvious neurologic presentations of weakness, numbness and slurred speech found with anterior circulation strokes.  The NIHSS itself is strongly geared towards detecting deficits due to anterior circulation pathology.  Probably because they are difficult to diagnose, posterior circulation strokes are also missed more often.  In one recently published retrospective study of 465 patients seen at both academic and community centers, 37% of posterior circulation strokes were initially misdiagnosed compared to 16% of anterior strokes (p < 0.001) [1].   

Failing to consider the diagnosis of posterior stroke is one etiology of missed diagnosis.  In the above mentioned study, only 8% of missed strokes were triaged as stroke codes [1].   A fair number of missed strokes also were missing neurologic exams (18% at an academic hospital and 65% at a community hospital).  Even when neurologic exams are charted, documentation (and by assumption) examination of neurologic findings associated with posterior circulation stroke (eye movements, coordination and gait) is often omitted [2].  But even when a full neurologic exam is performed, the diagnosis of posterior circulation stroke is not always crystal clear.  As posterior circulation strokes can present more of a diagnostic dilemma, it would be nice if emergency physicians could rely on imaging to be more confident in the diagnosis of stroke (or lack thereof).  This is especially true prior to discharging a patient home with an alternative diagnosis or administering tPA to a patient presenting within the treatment window.  Unfortunately, such confidence may not be possible.  Several studies have examined the false negative rate of DWI imaging in ischemic stroke and their results are far from comforting:

An initial study from the late 1990's retrospectively estimated the false negative rate of DWI imaging in ischemic stroke [3].  They evaluated the imaging of 139 patients who were admitted to a stroke center between 1998 to 1999 with signs and symptoms suggestive of arterial ischemic stroke and in whom symptoms persisted for at least 24 hours.  All patients had initial MRI within the first 48 hours of presentation (93/139 within the first 24 hrs).   All patients who had a negative initial MRI had a follow-up MRI prior to hospital discharge.  The study identified 8 patients who initially had negative DWI imaging but had a positive MRI 8 to 70 hrs later. Significantly, 6 of 8 false negative MRIs were located in the posterior circulation, giving an overall false negative rate for posterior circulation CVA of 31%.

Another prospective study enrolled 401 patients with stroke symptoms between March 2002 and March 2005 [4].  All the patients had an MRI within 24 hrs of symptom onset and a follow-up MRI at 30 days.  103/401 patients (25.6%) had negative initial imaging.  Of these 103 patients, 26 were eventually diagnosed with stroke at 30 days based on a combination of imaging and clinical data.  The false negative rate for DWI in patients with a brain stem stroke location was 30%.  DWI imaging also missed a large number of lacunar infarcts that were found on follow-up imaging. 

These first two studies may be considered limited due to their age, as they are 16-17 years and 11-14 years old respectively. However, a more recently performed retrospective study found similar results.  This study was performed at an institution where hyperacute MRI  is incorporated into the tPA protocol [5].  The authors reviewed the records of 569 patients who received tPA from 2004 to 2010.  518 of these had a DWI lesion.  Four turned out to be stroke mimics, including one which had a false-positive DWI lesion.  The overall sensitivity of DWI for a stroke anywhere in the brain was 92%.  Factors associated with having DWI-negative initial imaging included having a less severe stroke (NIHSS 4 vs. 7), a better outcome (% modified Rankin scale 0-1: 80.9% vs. 61.8%), a longer time to imaging  (120 minutes vs. 109 minutes) and having a posterior circulation stroke.  Indeed, DWI imaging was found to be negative in 34.9% patients with posterior circulation strokes.

So, is there anything better to than DWI imaging to help with this difficult diagnosis? Indeed there is, and it’s cheaper than an MRI.  Studies of the HINTS exam (Head impulse test-nystagmus-test of skew) suggest that it outperforms MRI with a sensitivity of 100% and specificity of 86% for stroke in patients presenting with acute vestibular syndrome [6]. However, in this study, the test was performed by a neuro-ophthalmologist. The sensitivity and specificity of this bedside test when performed by emergency physicians is still to be determined [7].

Take home:  DWI imaging will be negative in about a third of patients with acute posterior circulation stroke.  Consideration for administration of tPA should be done of the basis of physical exam (HINTS), clinical gestalt and discussion of the risks and benefits with the patient.

Submitted by Maia Dorsett (@maiadorsett), PGY-4

Faculty Reviewed by Peter Panagos (@panagos_peter)

 

References:

1. Arch, A. E., Weisman, D. C., Coca, S., Nystrom, K. V., Wira, C. R., & Schindler, J. L. (2016). Missed Ischemic Stroke Diagnosis in the Emergency Department by Emergency Medicine and Neurology Services. Stroke, 47(3), 668-673.

2. Savitz, S. I., Caplan, L. R., & Edlow, J. A. (2007). Pitfalls in the diagnosis of cerebellar infarction. Academic emergency medicine, 14(1), 63-68.

3. Oppenheim, C., Stanescu, R., Dormont, D., Crozier, S., Marro, B., Samson, Y., ... & Marsault, C. (2000). False-negative diffusion-weighted MR findings in acute ischemic stroke. American Journal of Neuroradiology, 21(8), 1434-1440.

4. Sylaja, P. N., Coutts, S. B., Krol, A., Hill, M. D., Demchuk, A. M., & VISION Study Group. (2008). When to expect negative diffusion-weighted images in stroke and transient ischemic attack. Stroke, 39(6), 1898-1900.

5. Simonsen, C. Z., Madsen, M. H., Schmitz, M. L., Mikkelsen, I. K., Fisher, M., & Andersen, G. (2015). Sensitivity of diffusion-and perfusion-weighted imaging for diagnosing acute ischemic stroke is 97.5%. Stroke, 46(1), 98-101.

6. Kattah, J. C., Talkad, A. V., Wang, D. Z., Hsieh, Y. H., & Newman-Toker, D. E. (2009). HINTS to diagnose stroke in the acute vestibular syndrome three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging.

I've Got the Antidote! Pradaxa reversal in the bleeding patient

Clinical Scenario: In the middle of a busy night in the critical care area, an elderly woman comes in from an outside hospital with a known intracranial hemorrhage after a mechanical fall. While reviewing her medication list, you notice that she has A-fib and is taking Pradaxa for stroke prevention. You vaguely recall an email about a new reversal agent for this blood thinner. Can you do anything to prevent this woman’s bleed from worsening? Should she get Prothrombin Complex (PCC), or something else?

As you desperately try to find the Pradaxa email in your ever-more-crowded inbox, another patient rolls in. He’s a middle-aged man with multiple prior abdominal surgeries and a day of nausea and vomiting. His abdomen is distended and a CT of the abdomen and pelvis shows a closed-loop small bowel obstruction with signs of ischemia. You notice that this patient, too, is on Pradaxa. Given his need for emergent surgery, what should you do to minimize his risk of serious intraoperative and postoperative bleeding?

Literature ReviewThe development of the novel oral anticoagulants, or NOACs, was hailed by many physicians as a bold step forward in the fight against thrombo-embolic disease. Unlike their much-maligned predecessor, warfarin, these agents (which include direct thrombin inhibitors such as dabigatran (Pradaxa) and factor Xa inhibitors such as rivaroxaban (Xarelto) and apixaban (Eliquis)) do not require bridging with other agents upon initiation and do not suffer from warfarin’s innumerable interactions with medications and food products. Furthermore, labs are not routinely drawn for monitoring in patients on the NOACs, while patients on warfarin require frequent INR checks for titration. Preliminary research has indicated that they are just as efficacious as warfarin in preventing stroke and other thrombo-embolic complications, but with less risk of serious or life-threatening bleeding, especially intracranial hemorrhage [1]. Finally - anticoagulants for busy patients who hate blood draws and love grapefruit!

The introduction of the NOACs did, however, cause some consternation in the emergency medicine community. Warfarin, although it was (and is) a messy drug with an unfortunate side effect profile, is easily reversed with vitamin K and FFP or PCC. Patients on warfarin who present to the ED with an acute hemorrhage (subarachnoid, gastrointestinal, traumatic, or otherwise) or who require emergent surgery can be reversed quickly, and the efficacy of their reversal can be tracked with a simple, widely available laboratory test, the prothrombin time / international normalized ratio (PT / INR). The NOACs had no such reversal agent, and no easily available lab test to track reversal in the case that it was required or attempted. Some suggested using PCC, with some support in the literature, but many emergency physicians were concerned that widespread use of the NOACs would lead to a plague of irreversible anticoagulation, to the detriment of some of their sickest patients.

Keenly aware of these concerns, the pharmaceutical giants behind the NOACs raced to develop specific reversal agents for their products. The first to gain FDA approval was idarucizumab (Praxbind), an anti-Pradaxa drug developed by Boehringer Ingelheim Pharmaceuticals (who are now proudly advertising that only Pradaxa has a specific FDA-approved reversal agent, although Portola is actively developing a reversal agent for the factor Xa inhibitors). Praxbind is now available at BJH and other BJC hospitals. But is this antidote the real deal? Has it been shown to improve patient-centered outcomes? How and when should we use it?

Idarucizumab is a humanized monoclonal antibody developed to bind dabigatran. It was initially developed, humanized, and tested in a rat model by Schiele and colleagues in 2013. They demonstrated that idarucizumab bound dabigatran with about 350 times greater affinity than dabigatran bound thrombin, and that infusion of idarucizumab into rats previously given dabigatran rapidly normalized laboratory tests of clotting function.1 A later study of idarucizumab in a porcine model again confirmed that addition of idarucizumab to blood taken from dabigatran-treated animals normalized coagulation parameters. This study also showed that idarucizumab, unlike PCC, did not cause over-correction of thrombin generation [2]. Further animal testing, also in a porcine model, demonstrated that administration of idarucizumab to dabigatran-treated animals significantly reduced bleeding after blunt liver trauma [3].

Glund and colleagues performed the first study of idarucizumab in human volunteers in late 2014. They showed that idarucizumab had no effect on coagulation parameters in the absence of dabigatran, that peak exposure was achieved essentially instantaneously, and that the compound’s half life was very short, roughly 45 minutes [4]. The same investigators also demonstrated that idarucizumab normalized coagulation parameters in healthy volunteers treated with dabigatran in a dose-dependent fashion. These effects were immediate, and were sustained over a 72 hour period in volunteers given at least 2 grams of idarucizumab [5].

On the strength of these results, a multicenter prospective cohort study called RE-VERSE AD was designed and approved to determine the real-world safety and efficacy of idarucizumab for the reversal of dabigatran in patients with serious bleeding, or who required emergent surgical or procedural intervention. In June 2015, the RE-VERSE AD investigators published their preliminary results, derived from the first 90 patients enrolled in the trial[6]. The dose tested in this trial (5 g IV, administered as two infusions of 2.5 g no more than 15 minutes apart) was calculated to fully bind the 99th percentile of total body dabigatran load observed in the RE-LY trial that demonstrated the efficacy of dabigatran in stroke[7].  Patients were eligible for inclusion if they were at least 18 years old and taking dabigatran. Patients were assigned to two groups: those with “over, uncontrollable, or life-threatening bleeding that was judged by the treating clinician to require a reversal agent” to group A, and those who required urgent surgery or other procedures that required normal hemostasis to group B. The primary outcome was the maximum percentage reversal of anticoagulation at 4 hours after administration of idarucizumab; this was determined by dilute thrombin time or ecarin clotting time (both tests correlate well with the presence of unbound dabigatran). Secondary outcomes included restoration of hemostasis.

51 patients were enrolled in group A, and 39 were enrolled in group B. Of the patients in group A, 18 had ICH, 20 had GI bleeding, 9 had bleeding “from trauma,” and 11 had “other” causes of bleeding. Of note, 22 patients (11 in group A, 11 in group B) were found to have normal dilute thrombin time at baseline, and 9 of these patients (4 in group A, 5 in group B) also had normal ecarin clotting time at baseline; these patients were excluded from the primary efficacy analysis. All patients analyzed had 100% reversal of anticoagulation at 4 hours.

Analysis of the secondary clinical outcomes was less helpful. Of the 51 patients in group A, 3 had no assessment of bleeding severity at baseline, and the time to cessation of bleeding could not be ascertained in 13 patients. In the remaining patients, the median investigator-reported time to cessation of bleeding was 114 hours, but there was no control group for comparison. In group B, one patient received idarucizumab to reverse a massive overdose of dabigatran, two patients were deemed too unstable for surgery, and 36 patients underwent surgery or procedure as planned. Of these, 33 (92%) had “normal intraoperative hemostasis” as reported by the surgeon or proceduralist. Obviously, these secondary outcomes were somewhat soft and subjective, and given the absence of a control group, it is not possible to draw firm conclusions about the effect of idarucizumab on patient-centered clinical outcomes.

RE-VERSE AD is ongoing, and publication of the final results should be enlightening. Its major limitation, of course, is the absence of a control group an overall small number of patients. The investigators commented that they felt that it would be unethical to randomize patients to a placebo agent or to another unproven reversal therapy, given the very strong laboratory data supporting the efficacy of idarucizumab and the absence of clear evidence demonstrating the efficacy of any alternative reversal agent. Animal and volunteer studies of dabigatran reversal with PCC, the most reasonable alternative agent, have produced mixed results [8].

While the ethical concerns raised by the authors are understandable, the absence of a control group does severely limit our ability to draw patient-centered conclusions from the RE-VERSE AD trial. However, given the absence of a plausible and proven alternative reversal agent, and the overwhelming laboratory evidence of anticoagulation reversal demonstrated in this and other trials, one could reasonably argue that idarucizumab is the best available treatment and should become standard of care. In fact, the Neurocritical Care Society and Society of Critical Care Medicine have formally recommended that idarucizumab be used as the first-line reversal agent in patients taking dabigatran who present with intracranial hemorrhage [8].

Take home Points: Idarucizumab rapidly and completely reverses the anticoagulant effects of dabigatran, as demonstrated by laboratory assessment of clotting parameters. While high-quality patient-centered outcome data are still lacking, it is reasonable to give idarucizumab to patients on dabigatran who are experiencing serious bleeding or who will require an emergent surgery or invasive procedure.

Submitted by Kevin Baumgartner, PGY-1

Faculty Reviewed: Evan Schwarz

Everyday EBM Editor: Maia Dorsett

References

  1. Schiele et al. “A specific antidote for dabigatran: functional and structural characterization.” Blood 2013 May 2;121(18):3554-62

  2. Honickel et al. “Reversal of dabigatran anticoagulation ex vivo: Porcine study comparing prothrombin complex concentrates and idarucizumab.” Thromb Haemostasis 2015; 113:728-740

  3. Grottke et al. “Idarucizumab, a specific dabigatran reversal agent, reduces blood loss in a porcine model of trauma with dabigatran anticoagulation.” JACC 2015 Sept; 66(13):1516-23

  4. Gund et al. “A randomised study in healthy volunteers to investigate the safety, tolerability and pharmacokinetics of idarucizumab, a specific antidote to dabigatran.” Thromb Haemostasis 2015; 113:943-951

  5. Glund et al. “Safety, tolerability, and efficacy of idarucizumab for the reversal of the anticoagulant effect of dabigatran in healthy male volunteers: a randomised, placebo-controlled, double-blind phase 1 trial.” Lancet 2015; 386:680-90

  6. Pollack et al. “Idarucizumab for dabigatran reversal.” N Engl J Med 2015; 373:511-20

  7. Connolly et al. “Dabigatran versus warfarin in patients with atrial fibrillation.” N Engl J Med 2009; 361:1139-51.

  8. Frontera et al. “Guidelines for reversal of antithrombotics in intracranial hemorrhage.” Neurocrit Care 2016; 24:6-46

A Comfortable Miss Rate? Who Needs an LP after CT?

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Clinical Scenario: A middle-aged man with a history of hypertension, diabetes mellitus, obesity, and peripheral vascular disease presents to the ED after an episode of syncope about 30 minutes ago. He is now completely alert and oriented and complains of a severe headache. Your initial workup, including basic labs, EKG, troponin, and non-contrast head CT, is unremarkable, and you prepare to admit him for observation and an inpatient syncope workup. The hospitalist service calls back to request a lumbar puncture to rule out subarachnoid hemorrhage before the patient comes up to the floor. Should you get the LP?

Clinical Question: In patients with a non-diagnostic non-contrast head CT, is a lumbar puncture necessary to completely rule out subarachnoid hemorrhage?

Literature Review:  In medical school, we all learn that head CT alone is not sufficient to rule out a subarachnoid hemorrhage (SAH) in a patient with a sufficiently suspicious history- you also need a lumbar puncture (LP), to evaluate for blood in the CSF or xanthochromia. On standardized tests, no patient with risk factors and a sudden-onset headache gets to escape the LP needle… but is this the right way to go about things in clinical practice?

Most experts and clinical guidelines continue to recommend LP after negative head CT in patients at high risk of SAH. In the 2012 guidelines for the diagnosis and treatment of SAH, the American Heart Association and American Stroke Association recommend that “head CT, if nondiagnostic, should be followed by lumbar puncture (Class I, Level of Evidence: B).”[1] This recommendation is based mainly on older studies demonstrating decline in the sensitivity of head CT over the course of days.

However, newer studies using modern multi-detector CT scanners may have identified a subclass of patients in whom an LP is not required to rule out SAH.  Perry and colleagues performed a multi-center prospective cohort study to assess the sensitivity of modern third-generation CT in ED patients being evaluated for SAH [2]. Patients presenting to 11 Canadian tertiary care referral centers between November 2000 and December 2009 with suspected SAH were prospectively enrolled. Alert (GCS=15) patients over 15 years of age presenting with non-traumatic acute headache or syncope associated with headache were included in the study. Exclusion criteria included the presence of focal neurologic deficits or papilledema, known history of CNS abnormality (such as neoplasm, aneurysm, or shunt), recurrent headaches, and transfer from another center with an established diagnosis of SAH. The gold standard for diagnosis of SAH was subarachnoid blood on non-contrast head CT, any visually identified xanthochromia on CSF analysis, or RBCs in the final tube of CSF collected AND aneurysm identified on CT angiography. A major weakness of the study was that not all patients enrolled had both a head CT and a lumbar puncture. In an attempt to correct for this weakness, all patients who did not have a definitive diagnosis based on neuroimaging OR a negative LP were followed for six months to ascertain their outcomes. By the conclusion of the study, 3,132 patients had been enrolled; of these, 240 had confirmed SAH. For all comers, the sensitivity of head CT was 92.9% (95% CI 89.0%-95.5%) and the negative predictive value was 99.4% (99.1%-99.6%). However, for patients who were scanned within six hours of headache onset, the sensitivity of head CT was 100% (97.0%-100%), and the negative predictive value was 100% (99.5%-100%). Likelihood ratios were not reported; however, using data available in the paper, they were calculated as a negative likelihood ratio of 0.07 (0.05-0.11) for all comers, and an impressive 0.00 (0.00-0.03) for patients scanned within six hours of headache onset. 

 

The results of this study were later replicated by Backes and colleagues [4]. In this retrospective single-center cohort study, patients presenting to the ED with a history suspicious for SAH between 2005 and 2012 were enrolled. Patients with clinical suspicion of a non-traumatic SAH and a normal level of consciousness (GCS=15) were included. Exclusion criteria included unknown time of symptom onset, focal neurologic deficits on presentation, referral from another hospital with a confirmed diagnosis of SAH, and LP in the month before presentation. At the study site, all patients with suspicion of SAH undergo non-contrast head CT, and all patients with a nondiagnostic head CT undergo LP with CSF analysis at least 12 hours after symptom onset; patient databases were reviewed to generate a study population of 250 patients who met criteria.  In all comers, head CT had a sensitivity of 95.4% (89.5%-98.5%), negative predictive value of 96.6% (92.2%-98.9%), and negative likelihood ratio of 0.05 (0.02-1.11). In patients scanned within 6 hours of symptom onset, sensitivity was 98.5% (92.1%-100%), negative predictive value 98.6% (92.3%-100%), and negative likelihood ratio 0.02 (0.00-0.10). In fact, only one patient with a non-diagnostic head CT had any findings on LP; this was a patient with atypical symptoms who was subsequently found to have a bleeding cervical AVM. The authors conclude that in patients with typical symptoms who present and are scanned within six hours of headache onset, there is no need for an LP after non-diagnostic head CT to rule out SAH. Weaknesses of this study included its small sample size and retrospective design.

 

There are, of course, many patients who still warrant an LP after non-diagnostic head CT. Patients with an altered level of consciousness or focal neurologic deficits were excluded from the above studies and require more intensive diagnostics. These findings are not generalizable to patients with an unknown time of symptom onset, significant anemia, pediatric patients, or patients who present to community centers that lack 24/7 coverage by experienced neuroradiologists—note that both studies were performed at academic tertiary referral centers. Some experts also raise the possibility that stopping the ED workup after a non-diagnostic head CT might miss minor “sentinel” bleeds [5], citing a 1987 study showing that head CT missed “sentinel” bleeds in 55% of patients, while LP, when performed, was positive in all patients later diagnosed with SAH[6]. However, this study was performed in 1987, prior to the introduction of modern third-generation CT scanners, and any attempt at replication would likely show improved testing characteristics for CT alone.

Clinical Takehome : In alert adult patients with a suspected non-traumatic SAH and no focal neurologic deficits who are scanned within 6 hours of symptom onset, a non-diagnostic head CT is sufficient to exclude SAH in patients with a low to moderate pre-test probability of SAH.

Submitted by Kevin Baumgartner, PGY-1

Faculty Reviewed by Brian Cohn

 

Additional related #FOAMed resources:

LP for subarachnoid hemorrhage: The 700 Club

SGEM #134: on what British docs say about LP    

 

References

1. Connolly et al. “Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guide for healthcare professionals from the American Heart Association/American Stroke Association.” Stroke 2012 Jun; 43(6): 1711-1737 

2. Perry et al. “Sensitivity of computed tomography performed within six hours of onset of headache for diagnosis of subarachnoid haemorrhage: prospective cohort study.” BMJ 2011; 343 

3. Alan Schwartz. “Diagnostic Test Calculator.” Department of Medical Education, University of Illinois at Chicago. [http://araw.mede.uic.edu/cgi-bin/testcalc.pl] 

4. Backes et al. “Time-dependent characteristics of head computed tomography in patients suspected of nontraumatic subarachnoid hemorrhage.” Stroke 2012 Aug; 43(8):2115-9 

5. Singer RJ, Ogilvy CS, Rodorf G. “Clinical manifestations and diagnosis of aneurysmal subarachnoid hemorrhage.” UpToDate. Literature review complete through September 2015; article last updated September 2013. 

6. Leblanc R. “The minor leak preceding subarachnoid hemorrhage.” J Neurosurg 1987; 66(1):35

For the Sake of the Trach: Tracheostomy Basics & Complications in the ED

Clinical scenario: You’re working in the ED when you receive a pre-arrival page: 62 y M with trach in respiratory distress, unable to obtain sats, ETA 5 min.  As you are setting up suction in the resuscitation bay, EMS arrives with a pale, elderly male gasping for air.  What's your next move?

Review: Although (hopefully) not something we see in the emergency department every day, this is absolutely something we need to be comfortable stabilizing, if not definitively managing, on our own. In order to have a better understanding of tracheostomy complications, it’s important to understand some terminology and anatomy first.  

Differentiating tracheostomies from laryngectomies 
A critical piece of information to obtain in patients with a tracheostomy is to determine whether or not they have had a laryngectomy as well. A tracheostomy is simply an opening in the trachea created with an incision through the anterior neck. Some reasons for needing a tracheostomy include chronic mechanical ventilation, maxillofacial trauma, or upper airway obstruction such as from a mass. A laryngectomy—usually performed on patients with laryngeal cancer—is a complete removal of the larynx with separation of the airway from the mouth, nose, and esophagus. Since there is no connection between the mouth and the patient’s airway, laryngectomy patients can NEVER be orally
intubated. Outwardly, a laryngectomy patient looks like any other patient who has had a tracheostomy, so it is impossible to tell if a patient has had a laryngectomy simply by looking at his or her neck. While occluding the stoma of a patient who has only had a tracheostomy may not cause complete loss of the ability to ventilate (assuming that have at least a somewhat patent upper airway), occlusion of the stoma in a larygectomy patient will absolutely in all cases make it impossible for the patient to breathe, since the stoma is the only possible connection to the lungs in a laryngectomy patient. Despite being a “never” event, attempts at oral ventilation on a laryngectomy patient have been reported in the past [1].   If a patient with a total laryngectomy requires bagging and the trach tube is displaced, the stoma is the only way to ventilate them.  As an initial measure, an laryngeal-mask airway or neonatal mask can be applied to the stoma and used for bagging.


Tracheostomy basics 
To better understand tracheostomies in general, some basics are worth reviewing. Tracheostomies can be performed percutaneously at the bedside in the intensive care unit or surgically in the operating room. Various methods for a tracheostomy exist, but the neck incision is usually made midway between the cricoid cartilage and the sternal notch, well below where a cricothroidotomy is usually performed, and the trachea itself may be opened with a vertical or horizontal incision. A few safety features are sometimes integrated into the tracheostomy: stay sutures and Bjork flaps. Stay sutures are temporary sutures placed through 2-3 tracheal rings that allow for the trachea to be pulled back up to the skin should decannulation occur. This allows for visualization and easier reinsertion of the tracheostomy tube, thereby decreasing the risk of creating a false passage if the tracheostomy tube needs to be reinserted before the tract fully matures in about 7 days. Stay sutures are usually removed after 7 days, so patients presenting to the ED are not likely to have these. A Bjork flap is an upside-down U-shaped section of trachea that not only creates the tracheostomy, but the free edge of the flap is sutured to the skin of the neck, essentially creating a path for tracheostomy tube reinsertion and reduces the risk of creating a false passage when reinserting a tracheostomy tube prior to tract maturation [2]. 

Tracheostomy Tube Features 
Tracheostomy tube designs vary widely but most tracheostomy tubes have a number of parts in common. A few important details to know about every tube include the size of the tube, the brand or type, and whether or not the tube has a cuff. For example, when speaking with a consultant, one might say, “this patient has a size 6 cuffed Shiley.” The cuff is an important feature of many
tracheostomies as it allows for the airway to be sealed off, allowing for positive pressure ventilation and reducing the risk of aspiration. Deflating the cuff will allow the patient to breath through his or her mouth to some degree (assuming a patent upper airway), which serves as a backup for ventilation should the tube become occluded. Having the cuff down also allows for the patient to phonate when they occlude their tracheostomy tube, since air will be able to pass around the deflated cuff and tube through the vocal cords. Some tracheostomy tubes will have both an outer cannula and inner cannula, which allows for the inner cannula to be removed and cleaned or replaced without changing the entire tracheostomy tube. The downside to having an inner cannula, however, is that the effective inner diameter of the tube is decreased, so the patient may experience increased resistance to airflow.


Tracheostomy tube complications 
Setting up for the patient
Patients with tracheostomy tubes will on occasion present to our emergency department, and as the initial responders to these emergencies, it is important to be aware of the common or potentially life threatening complications associated with tracheostomy tubes. In the patient who is not rapidly decompensating, eliciting a brief history focused on the tracheostomy tube should be performed. Necessary details such as when the tracheostomy was placed, what size tube the patient uses, and why the tracheostomy was needed may be management altering pieces of information. When the patient arrives to the ED, supplies and equipment should be assembled in anticipation of potential worsening of the patient's complication. Personal protective equipment (face shield, gloves, fluid-resistant gown), suction catheters, Yankauer suction, replacement tracheostomy tubes (of the same and also one size smaller), tracheostomy tube ties, and a supplemental oxygen source should all be at the bedside ready for immediate use. Endotracheal tubes with intubating equipment (if the patient has a patent upper airway) should be readily available as well, if not at the bedside. 


Tracheostomy tube obstruction
Secretion buildup will often result in a narrowing of the effective tube diameter, commonly leading to increased resistance to flow and manifesting as respiratory distress in the patient. Inadequate suctioning, poor hydration, and decreased mobility are all risk factors for obstruction from secretions. The initial step in patients with a possible tube obstruction is to attempt passing a suction catheter through the tracheostomy tube. Instilling a few milliliters of sterile saline may help loosen secretions. If the suction catheter cannot be passed easily beyond a few centimeters or the length of the tube, the tube may either be obstructed or dislodged. In tubes with an inner cannula, the inner cannula should be removed and inspected or replaced, but if there is still resistance to passing a suction catheter, the tracheostomy tube is likely dislodged with the distal tip in the soft tissues of the neck and will need to be removed immediately and replaced [2]. 


Accidental decannulation
Although most patients will have a mature tracheostomy tract when they present to the ED, it is prudent to ask when the tracheostomy was placed. Tracheostomies that are less than 7 days old presenting with a decannulation of the tube should never be replaced blindly because of the risk of creating a false passage upon reinsertion. In a patient with a mature tract, he or she should be optimally positioned for reinsertion, preferably laying supine with a shoulder roll to extend the neck, which will help align the tissue planes and mimic the position by which the tracheostomy was originally created (likely supine on a operating table). Preoxygenating the patient oronasally or via the stoma will reduce the risk of oxygen desaturation should any difficulties arise during the procedure. Always use an obturator or introducer if available to avoid injuring the soft tissues with the end of the tracheostomy tube. Water-soluble lubricant or a lidocaine containing jelly should be applied to the tube. Holding the tube and obturator as one unit, the tube should be inserted with the tip initially pointed perpendicular to the stoma and then gently curved downward into the trachea following the bend of the tube. If the tube has been out of the stoma for more than several hours, the stoma may have begun to stenose and require dilation by an otolaryngologist prior to reinserting a tube. A chest x-ray should be performed to confirm placement. Alternatively, if available, a nasopharyngoscope or bronchoscope can be used to directly visualize the carina via the tracheostomy tube, which would guarantee proper tracheal placement.  For a video demonstration, see this you tube video.


Bleeding from the tracheostomy
Tracheostomy bleeds can be from a number of possible sources. Superficially, the skin underlying the flange of the tracheostomy tube should be checked, as malpositioning of the tube or patient may result in pressure ulceration. The tracheostomy tube may need to be removed to fully inspect the stoma and surrounding skin, and local bleeding can be controlled with pressure or topical silver nitrate. Often, granulation tissue, which are new growths of connective tissue and small blood vessels, can arise from the stoma site, or even within the trachea itself. Minor bleeding from around the stoma can similarly be treated with pressure or silver nitrate. Granulation tissue within the trachea is diagnosed by direct visualization with a nasopharyngoscope or bronchoscope, and needs to be definitively treated by ENT, usually by cauterization. Other potential sources of tracheostomy bleeding may come from the tube eroding into the thyroid vessels, thyroid gland, or tracheal wall. A tracheoinnominate fistula is perhaps the most feared complication of a tracheostomy tube and occurs when the tip of the cannula erodes through the anterior tracheal wall and into the innominate artery. This rare condition occurs in less than 1% of all patients with a tracheostomy tube but carries a mortality rate approaching 100% given the catastrophic bleeding into the airway. Approximately 75% of patients with a tracheoinnominate fistula will present within 3 to 4 weeks of tracheostomy tube placement, and some of these patients will have an initial "sentinel bleed" that may be relatively minor before developing massive hemorrhage [2,4]. Hemorrhage in these cases can be temporized by hyperinflating the cuff of the tracheostomy tube or endotracheal tube placed through the stoma as an attempt to tamponade the bleeding. These patients will need emergent thoracic and ENT consultation. Endovascular embolization of the innominate artery may be another option in these patients and has been demonstrated to be successful in a few case reports [5]. 


Cardiac arrest
Suppose a patient with a tracheostomy is brought into the emergency department with CPR in progress. Provided that the patient's stoma remains patent, a small cuffed endotracheal tube (e.g. a 6.0 tube) can be inserted through the stoma to ventilate a tracheostomy patient in this code scenario. Intubation of the stoma is not only is much faster than attempting oral intubation, but also avoids the potential attempt at oral intubation on a laryngectomy patient (which, again, should never occur) if his or her medical history is unknown. A laryngeal mask airway (LMA) can be placed over the stoma to ventilate if an endotracheal tube is not readily available, but the patient's mouth and nose should be covered if upper airway patency is unknown. Alternatively, should the stoma be stenosed (for example, if the tracheostomy tube has been out for hours) and the patient is known to have a patent upper airway, the stoma can be occluded and the patient can be ventilated with bag-valve-mask via the mouth and nose. 


Take Home Points 
Tracheostomy complications can quickly become life-threatening, and knowing some basic concepts about tracheostomies can allow us to better respond to and take care of patients with these complications. As with any patient, getting an adequate history should be the first step, and in particular, knowing if the patient has had a laryngectomy can prevent the “never event” of an orotracheal intubation attempt. Before performing any interventions on a patient where there is time to set up (i.e. on a relatively stable patient), one should gather appropriate equipment such as personal protective gear, extra tubes, and suction. Finally, consider the potential for a tracheo-innominate fistula in a bleeding tracheostomy patient given the extremely high associated mortality. 

Submitted by Phil Chan, PGY-3
Faculty Reviewed by jason wagner  (@TheTechDoc)
Everyday EBM Editor: Maia Dorsett (PGY-4, @maiadorsett) 

References

[1] El-Sayed IH, et al. Identifying and Improving Knowledge Deficits of Emergency Airway Management of Tracheotomy and Laryngectomy Patients: A Pilot Patient Safety Initiative. Int J Otolaryngology. 2010;2010:1-7.
[2] Morris LL, et al. Tracheostomy Care and Complications in the Intensive Care Unit. Crit Care Nursing. 2013;33(5):18-30.
[3] D. Doyle J, Scales DC. Tracheostomy. In: Hall JB, Schmidt GA, Kress JP. eds. Principles of Critical Care, 4e. New York, NY: McGraw-Hill; 2015. http://accessmedicine.mhmedical.com/content.aspx?bookid=1340&Sectionid=80032214. Accessed September 24, 2015.
[4] Epstein SK. Late Complications of Tracheostomy. Respir Care 2005;50(4):542-549.
[5] Hamaguchi S, Nakajima Y. J Vasc Surg. 2012;55:545-547

Gettin' jiggy wit it ... Stick a Catheter in it? Consider the Peripheral IJ.

Clinical scenario: You are taking care of a patient with a history of IV drug use who presents to the emergency department with a large abscess in her arm requiring drainage under conscious sedation. Nursing is unable to obtain IV access after multiple attempts. You look for an EJ or an ultrasound-guided peripheral IV and find no suitable sites. The patient is likely to be discharged so a central line seems unnecessary. You scope out the patient's neck under ultrasound and see the plump internal jugular (IJ) vein and wonder, why don't I just put an IV in that? 

Clinical Question: Is there any literature to support or refute the use of the peripheral IV in a central vein? 

Literature Review: In patients who are critically ill with difficult IV access, the decision to move forward with intraosseous or central venous access is relatively clear. However, stable patients requiring intravenous access that have no sites amenable to ultrasound guided peripheral IVs or external jugular access and are likely to be discharged present more of a conundrum.
One proposed alternative to placement of central venous access for these patients is the "peripheral IJ", an angiocatheter placed into the internal jugular vein. Anatomically speaking, a "peripheral IJ" is not a central line. Like the external jugular vein, which also drains into the subclavian, the catheter tip is far superior to the cavo-atrial junction and thus does not constitute central access. 

In 2009, a Letter to the Editor published in the Journal of Emergency Medicine described a technique in which the internal jugular was cannulated under ultrasound guidance with a 48 mm -peripheral angio catheter. The technique described involved the following steps: 

1. Place the patient in trendelenberg
2. Prep the neck with chlorhexadine as you would for a central line
3. Use a linear ultrasound probe covered in a sterile probe cover and sterile gel to identify the internal jugular vein
4. Cannulate the vein and advance catheter over needle
5. Flush & Dress with bio-occlusive dressing
No sterile drapes were used. 

In the report, the technique (anecdotally) had been safely performed many times, but presented no supporting data. 

Following this initial letter, two subsequent case series have been published supporting the peripheral-IJ as a reasonable alternative for temporary venous access. The first case series of 9 patients placed them in patients with unobtainable IV access [2]. 64 mm angiocatheters were used to cannulate the IJ under ultrasound guidance using the above-described technique. All catheters were labeled for removal within 72 hrs. All patients were followed up via chart review one year later. Two of 9 catheters failed due to kinking within the first 48 hrs. There were no apparent adverse outcomes in any patient including deep vein thrombosis, bacteremia, endocarditis or pneumothorax. A second group conducted a prospective case series in which 9 patients underwent placement of a ‘‘peripheral IJ” (PIJ), when other access could not be obtained and the patient did not initially require a central line [3]. The authors attempted follow-up with all patients within a week. On follow-up, the seven patients who were successfully contacted denied any fevers, chills, swelling or pain at the site of catheter entry. One likely reason for the decrease in complication rate is that the placement of a "peripheral IJ" does not require dilation of the vessel.

Take Home: In the patient with a need for short-term intravenous access and in whom ultrasound peripheral IVs or external jugular access cannot be obtained, consider placement of a peripheral-IJ. This procedure should be completed under sterile precautions above that used for standard ultrasound guided IV. Larger studies are needed to verify the safety of this technique on a broader scale. If you’re patient is morbidly obese (a common theme for difficult IV access) keep in mind that an even longer IV catheter may be required to keep it safely intravenous after placement.


Submitted by Daniel Kolinsky, PGY-3

Edited by Maia Dorsett (@maiadorsett), PGY-4
Faculty Reviewed by Evan Schwarz 

References
1. Moayedi S. Ultrasound-guided venous access with a single lumen catheter into the internal jugular vein. J Emerg Med 2009;37:419.

2. Zwank, M. D. (2012). Ultrasound-guided catheter-over-needle internal jugular vein catheterization. The American journal of emergency medicine, 30(2), 372-373.
3. Teismann, N. A., Knight, R. S., Rehrer, M., Shah, S., Nagdev, A., & Stone, M. (2013). The ultrasound-guided “peripheral IJ”: internal jugular vein catheterization using a standard intravenous catheter. The Journal of emergency medicine, 44(1), 150-154.

The Times They Are A Changin': the "No Zone" Approach to Management of Penetrating Neck Trauma

Clinical Case: You're working a busy evening shift when a middle aged woman is brought in by EMS from the scene of a car accident.  She has a deep laceration to her anterior neck near the level of the cricoid cartilage from a glass shard.  She is neurologically intact, talking with a normal voice and is in no respiratory distress.  However, there is a continuous and brisk oozing of blood from the wound.

Clinical Question: What imaging is indicated in hemodynamically stable, neurologically intact patients with penetrating neck injuries?  What should the typical disposition be?

Literature Review:
Any neck wound that extends deep to the platysma is considered a penetrating neck wound, and it is estimated that they represent 5-10% of all trauma patients who arrive to the emergency department. Two common ways of anatomically dividing the neck include using the sternocleidomastoid to divide the neck into anterior and posterior triangles, or dividing the neck into three zones [1]:


    In the event of penetrating injury to the neck, airway compromise should be immediately assessed, with early intubation for airway protection if there is any concern for expanding neck hematoma or concerns for airway injury.  An attempt can be made to orotracheally intubate (bougies have been suggested as excellent initial adjuncts [2]), but plans should be made to move to early cricothyroidotomy if the airway is unable to be secured from above. After securing the airway and establishing hemodynamic stability, the neck wound should be carefully inspected.  Injuries that breach the platysma may have caused significant underlying injury, and it is best to avoid probing these wounds at the bedside, as this could disrupt hemostasis.  Aside from risk of vascular disruption, patients with penetrating neck injuries warrant consideration of tracheal and esophageal compromise.  Signs of tracheal injury include air bubbling at the wound, hemoptysis, subcutaneous emphysema, and stridor.  Esophageal injuries can be initially be asymptomatic, and a missed injury can lead to neck space infection and mediastinitis [3].   Emergent surgical consultation is warranted, as patients with hemodynamic instability and/or "hard signs" of vascular or aerodigestive tract injury should go for emergent neck exploration [3].

    Classically, management of hemodynamically stable patients with penetrating neck injuries was based on an anatomic "zone-based" approach mentioned above, with zone II injuries often going directly to surgical exploration and zone I and III injuries undergoing angiography, bronchoscopy, and esophagoscopy.  This approach was developed in the 1970’s, but it had several problems [4].  First, there may be poor correlation between the location of the neck wound and internal organ involvement, as there may be traversing of zones internally. Secondarily, the adoption of a mandatory-exploration policy lead to a high negative exploration rate (53% - 56%)[4,5].

    With the rapid improvement and dissemination of the use of  CT over the past few decades, a “No Zone” management approach based on careful physical exam with CT angiography has been shown in surgical literature to decrease resource utilization and unnecessary surgical exploration, making the rigid zone approach less relevant [3].   Several studies have examined the sensitivity and specificity of CT angiography in stable patients with penetrating neck injury.  A study by Inaba et. al. prospectively evaluated an algorithm in which patients with "soft signs" of injury (venous oozing, non-expanding hematoma, minor hemoptysis, dysphonia, dysphagia, or small amount of subcutaneous emphysema) underwent an initial evaluation with CT-angiography and asymptomatic patients were observed [6].  Over a 31-month period, 453 patients with penetrating neck trauma were prospectively evaluated in their study.  186 of these patients had "soft signs" of clinical injury, and underwent CT angiography as their initial method of evaluation.  38.2% of these patients had an injury to zone II of the neck.  Using an aggregate gold standard of the final diagnosis at discharge which included operative exploration, catheter-based angiography, bronchoscopy, esophagogram and esophagoscopy results and clinical follow-up (duration not specified),  the sensitivity and specificity of CT Angiography for vascular or aerodigestive injury was 100% and 97.5 % respectively.  There were two patients who had false-positive findings of vascular injury (irregularities in the ICA) that were not present on follow-up with surgical exploration and/or angiography, and three patients had air tracking suspicious for aerodigestive tract injury that was not confirmed on follow-up imaging and endoscopic studies. 

    As mentioned above, the "No Zone" approach combining clinical exam with imaging evaluation has the potential to decrease unnecessary neck exploration. A study by Osborn et. al. examined the rate of negative neck explorations in patients who were taken to the OR who did not have hard signs of injury.  They compared the rate of negative neck explorations amongst those patients who had a CT-A as part of their initial evaluation and those who did not, and found that CT angiography significantly reduced the negative neck exploration rate [7]:

    Source: Osborn et al. (2008)
     In their review of penetrating neck trauma management, Shiroff at al. shared the algorithm below, comparing the traditional vs. "no zone" approach:

    Image Source:  Reference 3



    Take Home Points: Patients with penetrating neck trauma who are hemodynamically unstable or  display hard signs of vascular or aerodigestive should receive immediate surgical consultation with consideration for operative or invasive management.  As the traditional, anatomic approach to management of penetrating neck trauma is associated with a high rate of negative neck exploration, patients with soft signs of injury should be initially evaluated with CT angiography which has a high sensitivity for clinically-significant injury.

    Submitted by Philip Chan, PGY-3
    Edited by Maia Dorsett (@maiadorsett), PGY-4
    Faculty reviewed by jason wagner (@TheTechDoc)

    References
    [1] Tintinalli’s Emergency Medicine, 7e.  Ch 257. 
    [2] Daniel, Y., de Regloix, S., & Kaiser, E. (2014). Use of a Gum Elastic Bougie in a Penetrating Neck Trauma. Prehospital and disaster medicine, 29(02), 212-213.
    [3] Shiroff, A. M., Gale, S. C., Martin, N. D., Marchalik, D., Petrov, D., Ahmed, H. M., ... & Gracias, V. H. (2013). Penetrating neck trauma: a review of management strategies and discussion of the ‘No Zone’approach. The American Surgeon, 79(1), 23-29.
    [4] Prichayudh, S., Choadrachata-anun, J., Sriussadaporn, S., Pak-art, R., Sriussadaporn, S., Kritayakirana, K., & Samorn, P. (2015). Selective management of penetrating neck injuries using “no zone” approach. Injury.
    [5] Varghese, A. (2013). Penetrating neck injury: a case report and review of management. Indian Journal of Surgery, 75(1), 43-46.
    [6] Inaba, K., Branco, B. C., Menaker, J., Scalea, T. M., Crane, S., DuBose, J. J., ... & Demetriades, D. (2012). Evaluation of multidetector computed tomography for penetrating neck injury: a prospective multicenter study. Journal of Trauma and Acute Care Surgery, 72(3), 576-584.
    [7] Osborn, T. M., Bell, R. B., Qaisi, W., & Long, W. B. (2008). Computed tomographic angiography as an aid to clinical decision making in the selective management of penetrating injuries to the neck: a reduction in the need for operative exploration. Journal of Trauma and Acute Care Surgery, 64(6), 1466-1471.

    On Broken Teeth: Emergency Management of Dental Fractures

    Clinical Scenario: One evening in the ED, a teenage boy is brought in by his mother for dental trauma after an altercation at school.  The boy reports that he was pushed to the ground in the scuffle, hitting face first into the concrete. On exam, pinkish-red material was visible at base of what remains of his frontal incisorsIt's been awhile since you took care of dental trauma and you decide to read more about it. 

    Clinical Question: What are the different layers of teeth and how do they impact severity of dental injury? What are the risk factors for dental injury? How are dental fractures graded and what steps should the ED physician take to protect remaining tooth fragments? 

    Source: wikipedia.org
    Review: Traumatic dental injuries (TDI) are a common occurrence in both children and adults. Approximately 1 in 3 adults sustain dental trauma during their lifetime, the majority which occur in childhood. A wide variety of risk factors have been described in the literature. These include patient specific factors like ADHD, epilepsy, cerebral palsy, propensity for risk-taking behavior, and anatomic factors like over-jet (the horizontal distance between posterior surface of the maxillary incisors and the anterior surface of the mandibular incisors) and inadequate lip coverage. In a review of rates of TDI in epileptic patients, over half had suffered TDI, many with multiple injuries. Environmental factors include poor socioeconomic status, living in an overcrowded environment and poor road safety [1]. Etiologies of TDI are broad with the most common mechanism of injury being falls. Adolescents and adults are more likely to sustain TDI through organized sporting activities, traffic accidents and violent means including fighting and assault.  In children, dental fractures can be a presentation of non-accidental trauma, and therefore a complete a full physical exam, including skin exam, should be performed

    With regard to anatomy, primary dentition consists of 20 teeth – 8 incisors, 4 canines and 8 molars, classically lettered A – T. The permanent dentition includes 28 to 32 teeth – 8 incisors, 4 canines, 8 premolars and 8 - 12 molars. The 32 permanent teeth are numbered from right to left on top and left to right on the bottom [2].

    With regard to anatomy of the individual teeth, from the inside out a tooth is composed of pulp, dentin and enamel [2]. The visible portion of the tooth is referred to as the crown and consists all three layers. As the tooth extends underneath the gum line, the enamel portion thins and the dentin and pulp extend in to the alveolar bone covered by a thin layer of cementum. The apex of the tooth is the entry point of the neurovascular bundle supplying each tooth. Finally,  the periodontal ligament is a collagenous strructure that extends from the alveolar bone to the cementum surrounding the root of the tooth.


    Image source: Tintinalli, JE et al: Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th Ed via Accessmedicine.com
    The primary traumatic dental injury classifications are concussion, subluxation, extrusion, luxation, intrusion, avulsion and fracture [3].  Examination of a TDI should include visual inspection, percussion testing, manual evaluation of tooth mobility and consideration for radiographic imaging to evaluate for associated alveolar bone injury and widening of the periodontal ligament space. Sensitivity testing (cold testing) is often less useful at the time of injury due to transient lack of pulpal response.   

    Dental fractures aka "broken teeth" require different management based on the extent of the injuryThe Ellis classification, which subdivides dental fractures into three classes of injury is useful for ED providers because it determines emergent care of the dental fracture [4]: 
                  -    Ellis I fractures involve only the enamel.  They typically require no emergency treatment. If sharp edges are present, those can be smoothed for patient comfort. Dentist follow up can be at the patient’s convenience.
                  -    Ellis II fractures involve the dentin but not the pulp  and  can be identified on exam by the creamy yellow color of dentin compared to the whiter, harder enamel.  These fractures require more urgent care.  Because dentin is a microtubular structure, Ellis II fractures threaten the integrity of the pulp and can lead to contamination of the pulp by oral flora . After recognizing an Ellis II fracture, the ED provider should anesthetize, clean and dry the tooth (Peridex can be used to sterilize the tooth) and seal the exposed dentin, which can be done with dental cement . Urgent dental follow up in the next 24 hours is recommended. Patients will require frequent visits and radiographs.
                  -   Ellis III fractures are full thickness and expose the pulp.  They can be identified by visualization of the pink-red pulp as well as bleeding from the pulp on cleaning of the tooth. Like Ellis II injuries, the pulp is at risk with these injuries but at a greater extent given the direct exposure of pulp to the oral environment. Ellis class III injuries require a two step sealing procedure. After anesthetizing, cleaning and drying the tooth, bleeding should be controlled with careful direct pressure. The first sealant layer is a calcium hydroxide base. On top of this base, the same dental cement coverage is applied. Like Ellis II injuries, Ellis III injuries require urgent dental follow up preferably within 24 hours.   

    For children with injuries to primary teeth, pulp exposure is more often encountered given the relatively larger size of the pulp. The same approach to different fracture types are recommended for children. Children will often require a pulpotomy to better protect the pulp from infection, but this requires more specialized tools and can be performed by the dentist in rapid follow up.

    Because dental fractures can have associated injuries, it is important to examine for associated intraoral lacerations, tooth subluxation or avulsion. Subluxations and avulsions may require repositioning of the tooth and splinting to adjacent teeth with zinc oxide based dressings like Coe-Pak  [little trick of the trade: since the applications of dental splints requires teeth to be dry, cut off the end of oxygen tubing and attach to the air or oxygen on the wall to blow air onto the teeth and dry them prior to application of an adhesive dental splint]. 

    With all of these injuries, patients should be discharged with oral analgesics, a soft diet and urgent dental follow-up. Generally, topical anesthetics should be avoided. Routine use of systemic antibiotics has not demonstrated benefit, but patient specific factors, associated injuries and co-morbidities should be considered [5].    
      
    Take-Home Points:  Dental fracture management depends on the Ellis classification. Anything more than an Ellis I fracture requires some degree of a protective coating applied in the ED and referral to urgent dental follow up.  Always examine patients thoroughly for other associated injuries and watch for NAT. 

    Submitted by Sara Manning (@EM_SaraM), PGY-4
    Faculty Reviewed by Rob Poirier

    Everyday EBM Editor: Maia Dorsett (@maiadorsett)  

    In case you were thinking that "Broken Teeth" would be a good name for a band, it's already taken.  Thank you google.  

    References:
    1. Glendor, U, “Aetiology and risk factors related to traumatic dental injuries a review of the literature.” 2009. Dental Traumatology. Vol 25: 19 – 31. 
    2. Tintinalli, JE et al, : Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th Ed via Accessmedicine.com 
    3. Dentaltraumaguide.org
    4.DiAngelis et al, “International Association of Dental Traumatology guidelines for the management of traumatic dental injuries: 1. Fractures and luxations of permanent teeth.” 2012 Dental Traumatology. Vol 28: 2 – 12. 
    5. ANDREASEN, J. O., STORGÅRD JENSEN, S. I. M. O. N., & SAE‐LIM, V. A. R. A. W. A. N. (2006). The role of antibiotics in preventing healing complications after traumatic dental injuries: a literature review. Endodontic Topics, 14(1), 80-92.

    Theme Image Source: http://www.windsorstar.com

    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  


    References
    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.

    An Imperfect Science: Diagnosis of CSF Shunt Malfunction

    Clinical scenario: Your patient is a 20 yo male with a history of VP shunt placement as a child for obstructive hydrocephalus. He was brought to the emergency department by his family because of decreased responsiveness over the past day. On arrival to the emergency department, he has aniscoria (L greater than R), no verbal response, and withdraws his extremities symmetrically. An emergent non-contrast head CT shows no change in ventricular size from prior CT scan one year prior and a VP shunt series demonstrates no evidence of fracture of the shunt line. Clearly, something is critically wrong with the patient, but is it his VP shunt to blame?

    Clinical question: What is the spectrum of shunt complications? What is the sensitivity of clinical exam and various imaging modalities in detecting shunt malfunction?

    Literature Review: There are multiple forms of CSF shunts, the most common of which is the Ventriculo-Peritoneal shunt (as opposed to ventriculo-atrial & ventriculo-pleural) which shunts CSF into the peritoneal cavity. A CSF shunt is composed of a proximal catheter, reservoir, valve and distal catheter [1]. The proximal catheter starts in the frontal horn of the lateral ventricle and exits through a burr hole to connect to the reservoir which is located in the subcutaneous tissue (this is what is accessed when neurosurgery taps a shunt). Flow from the reservoir to the distal catheter is regulated by a one way valve. Programmable shunts allow for the setting of a specific pressure above which fluid drains through a valve. This is sometimes adjusted in one direction or another for VP shunt patients who experience headaches, lightheadedness or other symptoms related to the pressure when their evaluation is negative for obstruction, infection etc. For VP shunts, the distal catheter is then tunneled into the peritoneum


    Image Source: Cancer Research UK / Wikimedia Commons


    As an emergency physician, one must be familiar with the presentation and diagnosis of shunt complications because they are relatively common; incidence of VP shunt failure is close to 40% at one year and 50% at two years from initial shunt placement, at least in the pediatric population where it has been most actively studied[2]. There are multiple types of shunt malfunctions leading to increased intracranial pressure, including but not limited to:

    1. Mechanical Obstruction - Most proximally, the catheter can be obstructed by blood, debris or in-growth of the choroid plexus. The catheter position within the lateral ventricle can also migrate. Kinking or fracture along the catheter track at any point will also lead to shunt failure, as will distal obstruction which can occur when the catheter adheres to the omentum or erodes into intra-abdominal organs.

    2. Infection - This often presents with shunt failure, and occurs most commonly within 6 months of placement due to intraoperative contamination with skin flora. The overall incidence of shunt infection is common (8-10%).

    3. Ventricular Loculations - Loculations within the ventricle can create non-communicating pockets of CSF that are not drained by the VP shunt. If these grow, they can cause symptoms of hydrocephalus.

    At least in very young children, depressed level of consciousness, nausea/vomiting, headache, irritability, and fluid tracking along the shunt site are highly predictive of shunt malfunction (see positive LR below). However, none of these clinical signs and symptoms are adequately sensitive to rule out shunt malfunction in their absence [2,3]. Some signs like abdominal pain/peritonitis are less commonly seen, but more highly predictive of shunt infection.

    LR, Sensitivity, & Specificity for clinical signs and symptoms associated with shunt failure in two large pediatric studies


    In addition to overall clinical exam and picture, radiographic imaging plays a central role in the emergency department evaluation of VP shunt malfunction.

    CT scans are the most commonly used imaging modality to evaluate for shunt malfunction. While enlarged ventricles (when compared with prior imaging studies) are the canonical feature of shunt obstruction, other CT findings correlated with increased intracranial pressure include effacement of the cortical sulci, loss of the basal cisterns and periventricular edema due to transependymal CSF absorption [4]. Based on multiple retrospective pediatric studies using surgical shunt revision as a "gold standard", CT has a sensitivity for shunt malfunction of anywhere between 53% to 92% [4,5; see Table below]. In one small retrospective study of 174 adults evaluated for shunt malfunction with both shunt series and head CT, head CT had a sensitivity of only 52%, a specificity of 78% and negative predictive value of 88% for shunt malfunction [6]. This study only included patients who had had shunt series performed, so it may have underestimated the sensitivity of CT by excluding patients who were evaluated with CT alone. While this is a wide range of estimations for sensitivity, the important point is that a negative head CT does not completely rule out a shunt malfunction.

    Shunt series radiographs are used to identify mechanical shunt defects such as shunt discontinuity or kinking. Studies in both children [4,7] and adults [6] support the conclusion that although the yield and sensitivity of radiographic shunt series is very low (see Table below), it is not zero. Shunt series rarely (~ 1-2%) detect abnormalities not identified on initial CT that prompt surgical revision. Therefore, shunt series are still indicated in the evaluation of potential shunt malfunction.


    Table 2 from Boyle and Nigrovic, 2015. Reference 4.


    In some cases, more commonly in pediatric institutions, MRI protocols have been instituted to reduce cranial radiation in children [4,8,9]. This has been made possible in part due to advances in MRI technology that have allowed for development of "ultra-fast" or Rapid MRI protocols that can acquire images in a span of ~ 1-4 minutes. Rapid Cranial MRI has been studied in comparison to CT for detection of ventricular shunt malfunction in the pediatric population, and appears to be comparable at least with respect to specificity and accuracy [8]. When considering using MRI in place of CT, the provider should be aware that some VP shunts have a programmable shunt valves that can be affected by the magnetic force of the MRI machine and may need to be readjusted after the exam. For this reason, it is common practice to obtain coned-down radiographs of a small indicator usually located near the proximal portion of the distal catheter to identify the setting prior to MR and then again after MR. If the programmed setting has changed, the neurosurgeon can use a magnet to reprogram the setting. The radiologist uses an indicator that looks like a clockface to determine the settings. 


    Image source: http://www.ajnr.org
    Take home Points: Malfunction and infection are common complications of CSF shunts. No single clinical exam finding or image study is sufficient to rule out shunt malfunction, and clinical management should take into account patient history, overall clinical picture, diagnostic data and neurological assessment.
     

    Submitted by Maia Dorsett @maiadorsett
    Faculty Reviewed by Peter Panagos and Richard Griffey
     

    References
    1. Wallace, A. N., McConathy, J., Menias, C. O., Bhalla, S., & Wippold, F. J. (2014). Imaging Evaluation of CSF Shunts. American Journal of Roentgenology, 202(1), 38-53.2.Garton, H. J., Kestle, J. R., & Drake, J. M. (2001). Predicting shunt failure on the basis of clinical symptoms and signs in children. Journal of neurosurgery, 94(2), 202-210.3. Piatt Jr, J. H., & Garton, H. J. (2008). Clinical diagnosis of ventriculoperitoneal shunt failure among children with hydrocephalus. Pediatric emergency care, 24(4), 201-210.4. Boyle, T. P., & Nigrovic, L. E. (2015). Radiographic Evaluation of Pediatric Cerebrospinal Fluid Shunt Malfunction in the Emergency Setting. Pediatric emergency care, 31(6), 435-440.
    5.Lehnert, B. E., Rahbar, H., Relyea-Chew, A., Lewis, D. H., Richardson, M. L., & Fink, J. R. (2011). Detection of ventricular shunt malfunction in the ED: relative utility of radiography, CT, and nuclear imaging. Emergency radiology, 18(4), 299-305.
    6. Griffey, R. T., Ledbetter, S., & Khorasani, R. (2007). Yield and utility of radiographic “shunt series” in the evaluation of ventriculo-peritoneal shunt malfunction in adult emergency patients. Emergency radiology, 13(6), 307-311.
    7. Desai, K. R., Babb, J. S., & Amodio, J. B. (2007). The utility of the plain radiograph “shunt series” in the evaluation of suspected ventriculoperitoneal shunt failure in pediatric patients. Pediatric radiology, 37(5), 452-456.
    8.Boyle, T. P., Paldino, M. J., Kimia, A. A., Fitz, B. M., Madsen, J. R., Monuteaux, M. C., & Nigrovic, L. E. (2014). Comparison of rapid cranial MRI to CT for ventricular shunt malfunction. Pediatrics, 134(1), e47-e54.
    9. Koral, K., Blackburn, T., Bailey, A. A., Koral, K. M., & Anderson, J. (2012). Strengthening the argument for rapid brain MR imaging: estimation of reduction in lifetime attributable risk of developing fatal cancer in children with shunted hydrocephalus by instituting a rapid brain MR imaging protocol in lieu of head CT. American Journal of Neuroradiology, 33(10), 1851-1854.10.

    A Balancing Act

    It’s another busy day in the ED when an elderly female comes in from triage with fever, cough, and new oxygen requirement. Even before the patient comes back you are concerned for pneumonia with sepsis. The patient is tachycardic and hypotensive with a shock index greater than one. You institute early antibiotics and fluids and systematically begin to aggressively resuscitate her. The patient requires nearly four liters of normal saline before her blood pressure stabilizes. Your attending suggests that your liberal use of normal saline will induce a hyperchloremic metabolic acidosis, and perhaps you should have used lower chloride containing fluid, like lactated ringers. You perform a brief literature review on the topic of balanced resuscitation using lower chloride containing fluids.

    Literature Review:
    Strong Ion Difference (Kishen et al)
    The main difference between normal saline and balanced fluids, such as lactated ringers, is the strong ions difference (SID), that is, the difference between cations (e.g. Na+) and anions (e.g. Cl-).  Normal saline has a SID of zero (equal parts Na+ and Cl-) where as Lactated ringers has a SID of 28, which is due to the additional cations such as Ca+, K+, and lower anion (Cl-) content.  Importantly, normal plasma SID content ranges from 38-44mmol/L, therefore balanced fluids more closely approximates physiologic SID.  As the SID becomes narrower, as is the case with significant normal saline administration, a non-gap metabolic acidosis develops. [1]

    The use of normal saline in large volumes has been shown to produce a reliable drop in serum pH as demonstrated by Scheinraber et al, in a study among patients undergoing elective surgery. [2] However, the development of a hyperchloremic acidosis is of unclear clinical significance. Early animal models in dog kidneys demonstrated that compared to non-chloride fluids, chloride containing solution led to renal vasoconstriction and decline in glomerular filtration rate. Similarly a randomized, double blind crossover study in healthy humans demonstrated a significant reduction in renal blood flow and renal tissue perfusion, after the administration of two liters of normal saline compared to low chloride (98 mEq/L) Plasma-Lyte solution. [3] However, the effect of isotonic saline in acutely ill patients is still not as clear. A prospective cohort study among 175 ICU patients demonstrated that higher chloride levels (109.4 vs 115.1mEq) was an independent factor for increased mortality, although a limitation of this study was they could not distinguish the cause of hyperchloremia (iatrogenic, renal dysfunction, or endogenous hyperchloremia) [4]
    Traditional and 'balanced' fluid content (crashingpatient.com)
    A large retrospective cohort study of critically ill adults with vasopressor dependent sepsis showed lower in-hospital mortality in patients who received balanced (lower chloride) fluids versus isotonic saline, 19.6% versus 22.8% (RR 0.86; 95% CI,0.78-0.94). A limitation of this study was that patients receiving balanced solutions were younger, less likely to have chronic heart and renal failure, and more likely to receive steroids, colloids and invasive monitoring. [5] A 2014 retrospective study in 109,836 patients that met SIRS criteria and received crystalloid fluid resuscitation, showed that low-chloride loads were associated with lower in-hospital mortality. This mortality difference remained even after adjustment for severity of illness and total fluid volume administered. [6]

    Similarly, a before and after study by Yunos et al involving 1644 ICU patients, reported the use of chloride-restricted fluids was associated with lower serum creatinine and decreased rates of renal replacement therapy (6 vs 10%) compared to controls. Like the study by Shaw et al, the difference was independent of severity of illness or total fluid volume administered. However, as mentioned by the authors, determining which component of lower-chloride fluid may have led to the observed effect is difficult, as there was simultaneous administration of lower sodium content, as well as increase in the administration of acetate, lactate, and gluconate. Importantly, this study showed no difference in mortality. [7][8]

    Take home points: Administration of large volume of isotonic saline is associated with a metabolic acidosis. Animal models have demonstrated decreased renal perfusion with chloride containing fluids. Several retrospective studies indicate that chloride is an independent risk factor for mortality in acutely ill patients. More and more literature in humans seems to indicate that a ‘balanced resuscitation’ may decrease morbidity, and possibly mortality, in patients receiving large volumes of crystalloids as part of their resuscitation.  A single nonrandomized study demonstrated a correlation between low chloride fluids and decreased use of renal replacement therapy. Blinded, randomized, prospective studies are needed to further elucidate this observed effect.

    Expert Commentary:

    Dr. Schwarz, an Assistant Professor here at Wash U, and both an Emergency Physician and Toxicologist has provided some of his own thoughts on the topic. 

    First, I’d like to thank Louis for picking a great topic and generating discussion about a very important subject.  I initially became interested in this topic a few years ago.  Originally, I was much more interested in the mechanism by which normal saline (NS) caused a non-anion gap metabolic acidosis, and that’s when I learned about the strong ion difference and a ‘balanced resuscitation.’  As a full disclosure while I found the pathophysiology really interesting, I initially didn’t think it had much clinical relevance.  However as more investigators have studied this, I’ve come to believe that my initial impressions were incorrect and changed my practice.

     The last time I reviewed the literature, I didn’t see a randomized, controlled trial comparing resuscitation with NS and lactated ringers in the ED.  However I do believe that there are studies out there that are applicable to the ED.  A retrospective study compared patients undergoing elective or emergent general surgery that received either NS or a ‘balanced fluid.’1  Unadjusted mortality and the number of patients developing major complications were higher in the group that received NS; after adjusting with propensity scoring, the mortality was no longer significantly different between the 2 groups.  However, patients that received NS were 4.8 times more likely to require dialysis. In a meta-analysis of patients with sepsis, patients that received a ‘balanced resuscitation’ had a lower mortality than patients receiving NS.2  The trend, however, was not significant.

    In a promise to keep this short, I won’t review all the other literature that has been published on this topic and kept the discussion on the 2 articles that I did include short.  I’ll also concede that the literature is not perfect, and as I mentioned earlier, I’m also still waiting for that perfect ED-based study to be completed.  However the cost of NS or a ‘balanced solution’ such as lactated ringers is nearly equivalent.  I’m also not aware of significant complications from administering lactated ringers in most patients. So when the risks, costs, and benefits of implementing a ‘balanced resuscitation’ verses a standard resuscitation with NS are viewed together, I think there is enough evidence to consider changing your resuscitation strategy.

    Now like many EDs, lactated ringers is not kept in our department.  It is on shortage but so is NS.  Neither of those are reasons not to use it.  So what do I do? Since I haven’t been able to convince pharmacy to keep lactated ringers in the ED yet, I do my best to guess early on which patients are going to need large-volume resuscitations.  If I think they are going to likely need more than 2-3 liters of fluid, I order additional lactated ringers from the pharmacy when I place their initial orders. In an hour after the patient has received the first few liters of NS, the lactated ringers should be there from the pharmacy.  If they need further resuscitation I can use it or return if they no longer need it.  For those that are interested to read more about this topic, I’d direct you to the upcoming May 2015 edition of Emergency Physicians Monthly. From my understanding, it’s brilliantly written! (Sorry for my shameless plug)


    Jamtgaard References:
     [1] Kishen R, Honoré PM, Jacobs R, et al. Facing acid–base disorders in the third millennium – the Stewart approach revisited. International Journal of Nephrology and Renovascular Disease. 2014;7:209-217. doi:10.2147/IJNRD.S62126.
    [2] Scheingraber et al. Rapid Saline infusions produces hyperchloremic acidosis in patients undergoing gynecologic surgery. Anesthesiology 1999;90;1265
    [3] Chowdhury A et al. .  A randomized, controlled, double-blind crossover study on the effects of 2-L infusions of 0.9% saline and plasma-lyte® 148 on renal blood flow velocity and renal cortical tissue perfusion in healthy volunteers.  Ann Surg. 2012;256(1):18-24
     [4] Boniatti MM et al.  Is hyperchloremia associated with mortality in critically ill patients? A prospective cohort study. J Crit Care. 2011;26:175–179. doi: 10.1016/j.jcrc.2010.04.013
    [5] Raghunathan K, Shaw A, Nathanson B et al. Association between the choice of IV crystalloid and in-hospital mortality among critically ill adults with sepsis*. Crit Care Med 2014; 42: 1585–91
    [6] Shaw A et al.  Association between intravenous chloride load during resuscitation and in-hospital mortality among patients with SIRS. Intensive Care Medicine. 2014;40(12):1897-1905. doi:10.1007/s00134-014-3505-3.
    [7] Waikar SS, Saving the Kidneys by Sparing Intravenous Chloride?.JAMA. 2012;308(15):1583-1585. doi:10.1001/jama.2012.14076.
    [8] Yunos N et al. Association between a chloride-liberal vs chloride restrictive intravenous fluid administration strategy and kidney injury in critically ill adults. JAMA 2012; 308: 1566– 72.

    Schwarz References
    1. Shaw et al.  Major Complications, Mortality, and Resource Utilization after Open Abdominal Surgery: 0.9% saline compared to Plasma-Lyte. Ann Surg 2012;255:821-829.
    2. Rochwerg et al. Fluid Resuscitation in Sepsis. A Systematic Review and Network Meta Analysis. Ann Intern Med 2014;161:347-355.


    Submitted by Louis Jamtgaard +Louis Jamtgaard , PGY-3
    Faculty Reviewed by Evan Schwarz @TheSchwarziee