Oral Nerve Blocks

Written by: Vytas Karalius, MD, MPH (PGY-2) Edited by: Andrew Cunningham, MD (NUEM ‘19) Expert commentary by: Jeffery Hill, MD, MEd

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Nerve Blocks of the Head & Neck Part III:

Oral Nerve Blocks

“I can’t feel my face when I’m with you…. but I love it.” – The Weeknd

About this series…

This article is part of a series of articles on the nerve blocks of the head and neck.  For more information on other types of useful nerve blocks, please refer to the links below:

Nerve Blocks of the Head & Neck Part I: Facial Nerve Blocks

Nerve Blocks of the Head & Neck Part II: The Occipital Nerve Block

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Oral Nerve Blocks

What are the advantages to oral nerve blocks?

Regional nerve blocks can be used in the ED for their ease, efficacy and efficiency in providing anesthesia for common procedures and complaints.  

Facial nerve blocks are particularly useful and have several advantages:

• Better anesthesia: Provides comparable, sometimes even better, anesthesia

• Less needle pokes: Provides complete anesthesia without multiple needle pokes, making them great for the difficult patient, and results in a happier patient and safer procedure

• Less pain medications: Decreases opiate and other oral analgesic use

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The Set-Up

In addition to the materials you might need for the rest of the procedure, you will need the following items for the nerve block:  

• Anesthetic (see below)

• 5mL or 10mL syringe

• Blunt fill or 18 gauge needle

• 25-27 gauge needle

• Gauze

• Long cotton tipped applicators and/or cotton pledgets

• Personal protective equipment – gloves and eye protection are a must

• Bite block if necessary

• Appropriate, dedicated lighting such as an overhead lamp

Choices of Anesthetic

For oral nerve blocks, use bupivacaine with epinephrine when available. Oral/dental pain can be immensely painful and compromise a patient’s quality of life.  The longer you can provide pain relief until they receive definitive care, the better off they will be. 

Table 1: Commonly used local anesthetics. Courtesy of our NUEM Clinical Pharmacologist, Dr. Kelsea Caruso, PharmD.

Table adapted from Pharmacology and Physiology for Anesthesia, Chapter 17, 291-308.

General Considerations to Reduce Pain Include:

• Using buffered anesthetic 

• Avoiding cold/refrigerated anesthetic – allow time to warm up to room temperature

• Decreasing the rate with which you infiltrate (you’re not pushing adenosine)

Special Considerations for pediatrics:

• Depending on your resources, distraction with iPads, child-life specialists, etc. can help improve your success as well.

• Hide the needle from view while preparing for the procedure.

• Do not forget that the parent can also help with positioning and de-escalating the patient’s anxiety.

Special Considerations for Oral Blocks:

• Topical lidocaine should be used prior to nerve block – this will greatly increase the patients’ comfort, their ability to remain still, and ultimately, your success.

• Method 1: Ask them to swish viscous lidocaine around in their mouth for about 30 seconds, or as long as they can tolerate it.

• Method 2: Soak and generously coat 1-2 cotton tipped applicators (Q-tips) or cotton pledgets with viscous or regular lidocaine and place them in the buccal mucosa at your intended target for 1-5 minutes.

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The Anatomy

Figure 1: The area of distribution of areas innervated by different nerves of the maxilla and mandible.

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Superior Alveolar Nerve Blocks

Step 1: Apply topical anesthetic as discussed earlier to make entry with the needle more comfortable. 

Step 2: Retract the lip.  Insert your needle through the mucobuccal fold at the at the area locations depicted in Figure 2, Figure 3 and Figure 4.

Step 3:  With the bevel facing the maxilla, inject 1-3mL of anesthetic.

Figure 2: For the posterior superior alveolar nerve, enter just posterior to the root of the second molar. [1]

Figure 3: For the middle superior alveolar nerve, enter between the first molar and second premolar. [1]

Figure 4: For the anterior superior alveolar nerve, enter just above the canine tooth. [1]

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Inferior Alveolar Nerve Block

Step 1: Apply topical anesthetic as discussed earlier to make entry with the needle more comfortable.

Step 2: Retract the lip/cheek and with the same hand, palpate the coronoid notch with your thumb.

Step 3: With your syringe, enter at an angle in which you are approaching from the contralateral incisor.

Step 4: Insert the needle about 1-2cm posterior to your thumb.

Step 5: Inject 1-3mL of local anesthetic.

Figure 5: The approach and anatomy of the alveolar nerve block. [1]

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Mental Nerve Block & Infraorbital Nerve Block

• Mental nerve and infraorbital nerve blocks can also be used to supply anesthesia to the mouth and oral cavity.  

  • These can be found in Part I of our series of Nerve Blocks of the Head and Neck: [insert link].

• The infraorbital block can be very useful in conjunction with a superior alveolar block for patients with extensive facial pain stemming from their dental complaints.

• Please note: the mental nerve block does not supply anesthesia to the teeth – only the lips, skin and buccal tissue.  For anesthesia to the bottom teeth, an inferior alveolar nerve block is recommended (Figure 1).  

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Expert Commentary

Thank you for this concise review of a necessary and practical skill for any Emergency Medicine provider.  As you point out performing oral blocks not only can facilitate laceration repair/abscess drainage but they can also immediately relieve a patient’s pain from acute or chronic pulpitis or a developing peri-apical abscess.  

Here are a couple of additional tips/points of reinforcement:

Patient positioning and lighting is key to identifying landmarks - When you are the recipient of these blocks in a dentist office you will note that they have you lying nearly completely and that they have exceptionally bright overhead lights. Trying to perform these blocks with the patient sitting upright is a literal pain in the back and not having a bright light sources means you are going mostly be feel.  So, for all these patients, I recommend lying them back in the bed with the HOB at approximately 20 degrees. And, I recommend either a headlamp, swinging over an overhead light (if available), or bringing in a portable light source.

Superior Alveolar Nerve Blocks can be tough - I often find that those that are first learning dental blocks shy away from the superior alveolar nerve blocks.  I, personally find them to be a bit more difficult than the inferior alveolar nerve blocks and, consequently, also find that my success rate is not as good as with inferior alveolar nerve blocks.  However, when they do work, they are every bit as effective in helping your patient feel better in a dramatic way. And since you will always be better at the procedure you have done 50 times than the procedure you have done once or twice, I heartily encourage offering this to patient’s with upper dental pain.  Over time I have found greater success with the procedure by ensuring that I am placing my needle and instilling my anesthetic about 1 mm above the junction of the buccal and gingival mucosa. If you try to instill into the gingival mucosa, it tends to be quite a painful injection and somewhat less effective as a block.

Talk it up, but Don’t Sell it as a Cure All - I offer dental blocks to nearly all of my patients that present with dental pain.  I think it is a highly effective way to immediately take care of the patient’s pain. When you are talking to your patient’s about the procedure, let them now that they could have up to 8 hours of pain relief but that every patient is different in the way they metabolize the anesthetic and the blocks themselves will have variable effectiveness (how close did you get to the nerve, how much did you still, etc).  I also let them know that there is a chance you might miss your mark and the block won’t be effective which would either necessitate a second attempt or an alternative approach to controlling their pain.

Jeffery Hill, MD, MEd

Assistant Professor of Emergency Medicine

Assistant Residency Program Director

University of Cincinnati Health

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References

Ailes D, Waseem M. Regional Anesthesia (Nerve Blocks). In: Ganti L. (eds) Atlas of Emergency Medicine Procedures. Springer, New York, NY. 2016.

Cepeda MS, Tzortzopoulou A, Thackrey M, Hudcova J, Arora Gandhi P, Schumann R. Adjusting the pH of lidocaine for reducing pain on injection. Cochrane Database Syst Rev. 2010 Dec 8;(12).

Hollander JE, Camacho, M. Assessment and management of facial lacerations. Stack AM, Wolfson AB, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed on March 20, 2019.)

Hsu DC. Clinical use of topical anesthetics in children. Stack AM, Wiley JF, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed on March 20, 2019.)

Jeng CL, Rosenblatt MA. Overview of peripheral nerve blocks. Maniker R, Crowley M, ed. UpToDate. Waltham, MA: UpToDate Inc. https://www.uptodate.com (Accessed on March 20, 2019.)

Spangler RM, Abraham MK. Regional Anesthesia of the Head and Neck. In: Roberts and Hedges’ Clinical Procedures in Emergency Medicine and Acute Care. Elsevier Inc, Philedelphia, PA. 2019: Chapter 30, 545-559.

Suzuki S, Koköfer A, Gerner G.  Local Anesthetics. In Hemmings HC & Egan TD, eds. Pharmacology and physiology for anesthesia: foundations and clinical application, 1st ed. Saunders, Philedelphia, PA. 2013: 291-308.

All images were obtained from: 

[1] Spangler RM, Abraham MK. Regional Anesthesia of the Head and Neck. In: Roberts and Hedges’ Clinical Procedures in Emergency Medicine and Acute Care. Elsevier Inc, Philedelphia, PA. 2019: Chapter 30, 545-559.

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How to Cite This Post

[Peer-Reviewed, Web Publication] Karalius V, Cunningham, A. (2020, Jan 20). Oral Nerve Blocks. [NUEM Blog. Expert Commentary by Friedman, B]. Retrieved from http://www.nuemblog.com/blog/oralnerveblock

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Occipital Nerve Block

Written by: Andrew Rogers, MD (PGY-2) Edited by: Aaron Quarles, MD (NUEM ‘19) Expert commentary by: Ben Friedman, MD

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Nerve Blocks of the Head & Neck Part II:

The Occipital Nerve Block

About this series…

This article is part of a series of articles on the nerve blocks of the head and neck.  For more information on other types of useful nerve blocks, please refer to the links below:

Nerve Blocks of the Head & Neck Part I: Facial Nerve Blocks

Nerve Blocks of the Head & Neck Part III: Oral Nerve Blocks

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Introduction/Overview

An occipital nerve block is a peripheral nerve block performed on the greater and lesser occipital nerves to help treat headache.  Occipital nerve block (ONB) has been used in the treatment of cervicogenic headache, cluster headache, and occipital neuralgia, with demonstrated efficacy in improving pain and reducing headache frequency (1-3).  By definition, occipital neuralgia will respond to ONB, and failure of symptoms to resolve should raise into question of the original diagnosis (2, 3).  

Occipital nerve block may also be efficacious in the treatment of migraine.  In a retrospective cohort study of 562 patients who received at least one greater occipital nerve block (GONB) for the treatment of migraine, 82% had >30% reduction in numeric pain scale from baseline with 58% having a >50% improvement (4).  Recently, a small, randomized, sham-controlled trial of GONB performed in the Emergency Department for migraine refractory to metoclopramide therapy demonstrated greater short-term headache relief (5). GONB may be particularly useful in migraine patients with evidence of occipital nerve irritation or tenderness. 

Indications

• Occipital neuralgia

• Cluster headache

• Cervicogenic headache

• Migraine, particularly with occipital nerve irritation or tenderness

Contraindications

• Medication allergy

• Infection overlying site of injection

• Skull defect

Anatomy

Key anatomy points of review:

• The occipital nerve originates from C2-C3 nerve roots

• The GON perforates the fascia just underneath the superior nuchal ridge

• The GON lies just medial to the occipital artery

Figure 1: Greater Occipital Nerve Anatomy (6)

What to Inject

Typically, a local anesthetic such as lidocaine (1-2%) or bupivacaine (0.5%) (or a combination of the two) is injected..  Lidocaine has a quicker onset, while bupivacaine has a longer lasting effect. Total volume injected is 2-4cc per nerve block. 

A steroid such as such as betamethasone (2-4mg) or triamcinolone (10-20mg) may be added to the local anesthetic (3).  For the Emergency Physician, one should consider how the addition of a steroid may complicate or impact a patient’s follow up with their primary neurologist or primary care physician.  Additionally, one study failed to show a significant difference in headache relief for transformed migraines treated with or without triamcinolone in addition to local anesthetic (7).  

The Procedure:

1. Identify the location of the GONB via one of 3 methods:

   1. Palpate the occipital artery pulse about 2cm lateral to the occipital protuberance.  The greater occipital nerve is just medial to the occipital artery

Alternatively

1. Palpate the occipital protuberance and the mastoid process (on side of interest). Measure 1/3 the distance between the two points starting from the occipital protuberance. Stay just superior to the superior nuchal line to remain over the cranium. (Figure 2) 

Alternatively

1. Identify the point of maximal tenderness in the general region as defined above that may elicit paresthesia in the occipital nerve distribution when palpated

1. Clean the site of injection with an alcohol swab or similar cleaning solution.

2. Using a 23-25G needle, insert the needle at a 90-degree angle toward the occiput until a bony endpoint is obtained.  Aspirate to avoid intravascular injection and to prevent injection into CSF. Inject 1cc at the GON, 1cc medial to the nerve, and 1cc lateral to the nerve.  

3. The procedure can be performed bilaterally. 

Figure 2: Representative schematic to aid in locating the greater occipital nerve, using method 1(b) as described above.

Key Points:

• The greater occipital nerve block can used in the treatment of refractory migraine, cluster headache, occipital neuralgia, or cervicogenic headache

• If palpation of the GON reproduces headache pain or irritation, it may be a good target for GONB

• A GONB can be performed bilaterally if needed

• Use local anesthetics such as lidocaine and/or bupivacaine

• Aspirate while inserting the needle to avoid intravascular injection and to avoid being in CSF

• Inject in a fanning technique just medial to the occipital artery pulse, one third of the distance from the occipital protuberance to the mastoid process, or at the site of maximal tenderness in the region

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Expert Commentary

This well-written and informative review of the greater occipital nerve block (GONB) will help clinicians choose appropriate patients for this procedure and perform it with a high likelihood of success. In my experience, the GONB is easy to learn and easy to utilize clinically because it is a “forgiving” nerve block—patients often seen to respond even if the local anesthetic is not delivered precisely. As Dr. Rogers notes, using a “fan” technique maximizes the chances of success. While corticosteroids are efficacious for migraine, the most common type of headache seen in the ED, I prefer to deliver the corticosteroids separately from the GONB as either an intravenous or intramuscular injection. That way, I am not limited by volume and can administer more local anesthetic. And while a 23 or 25 gauge needle can certainly get the job done, my patients seem to appreciate it more when I use a 27 gauge needle. Finally, while not evidence-based, I think about using the GONB for any type of headache that is refractory to first or second line treatment—I’ve had success using it in a wide variety of atypical headaches (just don’t forget to rule out badness!)

Benjamin W. Friedman, M.D.

Professor

Department of Emergency Medicine

Montefiore Medical Center

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How to Cite this Post

[Peer-Reviewed, Web Publication] Rogers A, Quarles A. (2020, Jan 13). Occipital Nerve Block. [NUEM Blog. Expert Commentary by Friedman, B]. Retrieved from http://www.nuemblog.com/blog/occipitalnerveblocl

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References:

Sources

1. “Occipital Nerve Blocks: When and What to Inject?” Tobin, Joshua; Flitman, Stephen. Headache. 2009. Nov-Dec, 49 (10):1521-33

2. “Occipital Neuralgia.” Garza, Ivan. UpToDate. 25 August, 2017. Accessed 28 January 2019. 

3. “Greater Occipital Nerve Block.” Ward, John.  Seminars in Neurology. 2003; 23(1): 059-062.  Accessed 28 January 2019.

4. “Greater Occipital Nerve Block for Acute Treatment of Migraine Headache: A Large Retrospective Cohort Study.” Allen et al. Journal of the American Board of Family Medicine.  Vol 31, Issue 2. March/April 2018. P 211-218.  

5. “A Randomized, Sham‐Controlled Trial of Bilateral Greater Occipital Nerve Blocks With Bupivacaine for Acute Migraine Patients Refractory to Standard Emergency Department Treatment With Metoclopramide.” Friedman, Benjamin, et. Al. Headache. October 2018.  Vol58, Issue 9. Pp1427-1434. 

6. “Greater Occipital Nerve.” Volker, Joseph.  Earthslab.com. 8 August, 2018. 

7. “Greater Occipital Nerve Block Using Local Anaesthetics Alone or with Triamcinolone for Transformed migraine: a radomised comparative study.” Ashkenazi A, et al. Journal of Neurology, Neurosurgery, and Psychiatry. 2008 April; 79(4):415-7

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Emergency Guide to Stroke Neuroimaging

Written by: Justin Seltzer, MD (PGY-3) Edited by: Luke Neill, MD (PGY-4) Expert commentary by: Babak Jahromi, MD, PhD

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According to the CDC, an ischemic stroke occurs approximately every 40 seconds in the US, with nearly 800,000 documented cases annually.[1] This, combined with an effective national stroke symptom public education program, has resulted in a large number of patients presenting to emergency departments for evaluation of stroke or stroke-like symptoms. Essential to this initial evaluation is neuroimaging, which in the emergency department is mainly CT based. 

However, despite frequent use, many emergency physicians are not familiar enough with stroke imaging to interpret images on their own. A prior post addressed the basics of reading a complete head CT, which you can find here. The goal of this article is to discuss the indications and limitations as well as to provide a basic guide to interpretation of noncontrast CT imaging of the brain (NCCT), CT angiography (CTA) of the head and neck, and CT perfusion (CTP) imaging in acute stroke evaluation.

Acute stroke imaging is obtained in the emergency department for two purposes. 

1. To evaluate rapidly for thrombolysis contraindications like hemorrhage and certain pathology such as vascular malformations and aneurysms. Thrombolysis has a high therapeutic benefit in stroke patients, with a number needed to treat of 10 within 3 hours of symptom onset and less than 20 if administered within 4.5 hours.[2,3] In addition, door to needle time of less than one hour is an established benchmark and quality measure.[3]

2. To identify a causative vascular lesion, which may or may not be amenable or contraindicatory to thrombolysis

Non-Contrast Head CT

NCCT is usually the first imaging modality obtained in the acute evaluation for stroke. Within the thrombolysis window (<4.5 hours), however, this scan is far more likely to detect hemorrhage than infarction. Chalela, et al., reviewed 356 patients evaluated for stroke symptoms at a single center over 18 months. They showed a sensitivity of 89% for detection of acute intracranial hemorrhage; conversely, the sensitivity for ischemic strokes less than 3 hours old was 12%, 16% for those older than 12 hours, and an overall sensitivity of 16%.[4] These findings are consistent with other studies and highlights the limitations of NCCT in acute stroke imaging. 

Despite the poor sensitivity for acute infarction, there are a few ways to improve detection. Windowing adjustments can enhance grey-white matter differentiation, as loss of this in an area anatomically associated with the presenting deficit is suggestive of acute infarction. A window width and center of approximately 50 each achieves adequate grey-white differentiation (Figure 1). Additionally, asymmetric, hyperdense section of cerebral vasculature, known as the “dense vessel” sign, is also highly suggestive of middle cerebral artery (MCA) occlusion.[5] As a side note, IV contrast should not be used outside of angiography to “enhance” the image as it may extravasate into the ischemic parenchyma mimicking hemorrhage.[6] 

Figure 1. NCCT of the brain in an acute right M1 occlusion with a last known well time was approximately 13 hours before. Windowing set at C50/W50 for improved grey-white differentiation. Official read: “A diffuse asymmetric hypodensity and subtle loss of gray-white matter differentiation in the right frontal and parietal region is highly concerning for an acute right MCA stroke.”

CT Angiography of the Head and Neck

The role of CTA in acute stroke evaluation is to identify the culprit vascular lesion and is an excellent addition to the emergent evaluation of acute ischemic stroke. A 2014 pooled analysis of 21 studies from 1993 to 2013 showed CTA has a sensitivity of 83.2% and specificity of 95% with a 97.1% negative predictive value for greater than 50% cerebral vascular stenosis;[7] a 2017 pooled analysis of 7 studies from 2003 to 2012 broadly reported a sensitivity of 93% and specificity of 100% for acute ischemic stroke.[8] CTA of the neck is also obtained to evaluate the contributing cervical vasculature. Since interpretation of angiography is dependent on knowledge of the relevant anatomy, the key structures are reviewed below. If a more detailed review is desired or necessary, several neuroanatomy texts may be found in the references. 

The major cerebral vasculature is supplied by the bilateral internal carotid arteries (ICA; “anterior circulation”) and the paired vertebral arteries (VA) that merge to form the basilar artery (BA; “posterior circulation”). The anterior circulation dominates perfusion of the cerebral hemispheres apart from the occipital lobe. The posterior circulation feeds the remaining structures, mainly the occipital lobe, cerebellum, and brain stem. 

Figure 2. CTA of the neck showing bilateral patent CCAs and VAs.

Anterior circulation

The anterior circulation starts with the ICA, which branches from the common carotid artery (CCA) in the upper neck at around the level of the fourth cervical vertebra. (Figures 2, 3). The ICA has four parts with seven defined segments; in general, segments assist with lesion localization and are provided in parenthesis. The cervical part (cervical segment, C1) is first and enters the skull at the carotid foramen (Figure 5). It is distinguished from its companion external carotid artery by a lack of extracranial branching. Once in the skull, the petrous part (petrous segment, C2) traverses the carotid canal within the petrous portion of the temporal bone (Figure 5). Moving out of the temporal bone, the ICA then crosses into the cavernous sinus, where it is known as the cavernous part (lacerum segment, C3, cavernous segment, C4, clinoid segment, C5). Navigating the bony turns in this area results in a characteristic curvature known as the “carotid siphon” (Figure 6). From here, the vessel passes through the dura, where it becomes the cerebral or supraclinoid part (ophthalmic segment, C6, communicating segment, C7) and gives off the ophthalmic, posterior communicating, and anterior choroidal arteries; these posterior communicating arteries (PCommA) run to the ipsilateral posterior cerebral arteries (PCA), thus connecting the anterior and posterior circulations and forming part of the circle of Willis (Figure 7). At the terminus, the internal carotid arteries bifurcate into the bilateral anterior cerebral arteries (ACA) and MCAs. Acute ICA lesions can cause dramatic symptoms due to restricted blood flow to the ipsilateral ACA and MCA and are large vessel occlusions.[9-12]

Figure 3. CTA of the neck showing the bilateral carotid bifurcations. Artifact from metal in the patient’s teeth.

Figure 4. CTA of the neck showing patent bilateral ICAs as well the the bilateral VAs entering the foramen magnum

The ACAs run between the frontal hemispheres in the longitudinal fissure and supply a large portion of the medial cerebral structures such as the medial frontal and parietal lobes as well as the basal ganglia and parts of the internal capsule. They are smaller than the MCAs and their course is recurrent frontal-occipital and inferior-superior, which can make visualization in the axial plane difficult to appreciate. The paired arteries are connected by the anterior communicating artery (ACommA) early in their course which is the final connection completing the circle of Willis (Figure 7). Lesions within the A1 segment, which runs from the carotid terminus to the ACommA are considered large vessel occlusions though may be better tolerated due to collateral flow through the anterior communicating artery.[9,10,12] 

Figure 5. CTA of the head showing the ICAs as they enter the skull and traverse the petrous portion of the temporal bone.

Figure 6. CTA of the head showing the ICA as it traverses the cavernous sinus; the carotid siphon is well visualized on the left.

The MCAs provide circulation to the remaining frontal and parietal lobes, basal ganglia, and internal capsules, as well as portions of the temporal lobes. They are larger and therefore more easily visualized than the ACAs (Figure 7). A lesion of the M1 segment, which runs from the carotid terminus to the bifurcation into the M2 segments, is considered a large vessel occlusion (Figures 8, 9).[9,10,12] 

Figure 7. CTA of the head showing an intact circle of Willis

Figure 8. CTA of the head showing an acute right M1 occlusion in the axial plane

Figure 9. Coronal MIPS of the same vascular occlusion noted in Figure 8 with clear deficit on the right compared with the left.

Posterior circulation

The posterior circulation starts with the VAs, which are subclavian branches that traverse the cervical spine via transverse foramina (Figures 2, 3). Prior to joining, each vertebral artery gives off an ipsilateral posterior inferior cerebellar arteries (PICA) as well as the contributing vessels that form the anterior and posterior spinal arteries. Upon entering the skull via the foramen magnum, the bilateral vertebral arteries join to form the basilar artery at about the level of the medullo-pontine junction (Figures 4, 5, 6). As the basilar artery moves superiorly it gives off the bilateral anterior inferior cerebellar arteries (AICA), multiple bilateral small perforating pontine arteries, the bilateral superior cerebellar arteries, and then finally terminates with a bifurcation into the bilateral posterior cerebral arteries (PCA). As noted prior, these PCAs connect with the ipsilateral posterior communicating arteries from the anterior circulation (Figure 7). Vertebral, basilar, and early posterior cerebral artery occlusions are considered large vessel occlusions but there is, as of now, limited data on mechanical thrombectomy in these territories.[9,10,12,13]

Application

Reading the scan itself is fairly straightforward based on the vascular anatomy. We recommend starting caudally (usually the aortic arch) in the axial plane and tracing all four cervical vessels cranially until they form the circle of Willis and from there extend out into the major branches. The coronal plane is particularly useful for evaluation of the anterior cervical vessels and the MCAs. Significant asymmetry or loss of contrast opacification in vascular beds anatomically consistent with the presenting symptoms should be considered strokes until proven otherwise. Make note of vascular abnormalities such as significant carotid stenosis, aneurysms, and malformations. 

Additional 2-D and 3-D post-processing images may also be provided. The most common is maximum intensity projection (MIP), which highlights high density structures over low density; this allows for improved visualization of the contrast enhanced vasculature at the expense of the surrounding brain tissue. However, MIP images can be falsely negative and should not be used alone for primary vascular evaluation.[14]

CT Perfusion

Though less common than CTA, CTP may also be acquired in the emergency setting to evaluate for territorial changes in cerebral blood flow suggestive of stroke. It is particularly valuable for identifying core infarct and salvageable ischemic penumbra and is becoming an important part of interventional decision making. It has a similar sensitivity and specificity for acute ischemic stroke as CTA, its use has been validated in multiple interventional stroke studies, and it has been shown to predict core infarct size accurately compared to the gold standard MRI.[7,8,15]

Basic concepts

While the specifics of CTP are complex and beyond the scope of this article, there are a few important concepts. CTP operates under the “central volume principle,” which is represented by the equation CBF = CBV/MTT and defines the relationship between cerebral blood volume (CBV; volume of flowing blood in a set volume of brain tissue), blood flow (CBF; per time unit rate of flowing blood in a set volume of brain tissue), and mean transit time (MTT;  average time for blood to transit a set volume of brain tissue). To illustrate this concept, imagine an acute arterial occlusion. The obstruction causes an immediate increase in MTT due to slowed arterial flow through the affected tissue. To maintain CBF a local compensatory vasodilation occurs, increasing CBV. However, this vasodilation may not be able to compensate for rising MTT, causing a progressively inadequate CBF that may result in infarction.[5,16]

Algorithms translate detected changes in MTT, CBV, and CBF into images that can be used in clinical decision-making. MTT is obtained by measuring the movement of contrast through the affected tissue; this also gives a value known as Tmax, which is the time to achieve peak contrast density. CBV and CBF are calculated relative values (rCBF, rCBV) and based off of the surrounding normal tissue. Composite metrics, such as mismatch ratio, the ratio of penumbra to the core infarct volumes, and mismatch volume, the penumbra volume minus the core infarct volume, are also generated.[11] Though there is no set rule, there is evidence that thrombolysis benefit is maximized and hemorrhage risk minimized with a mismatch ratio of 1.8 or greater, a mismatch volume of 15ml or greater, and a core infarct volume less than 70ml.[17]

Figure 10. Illustrative CTP report for the same acute right M1 occlusion from Figures 8 and 9 showing the core infarct (purple) and associated penumbra (green). Note the large mismatch volume and ratio, indicating a relatively small core infarct relative to the threatened penumbra.

Application

These values are then made into “parametric maps” superimposed onto axial CT slices, allowing for visual identification (Figures 10, 11). Different software may present the values and parametric maps differently; note that our institution uses RAPID (iSchemaView, Menlo Park, CA) and our example figures were generated by this software. Using Figure 10 as an example, we see purple and green areas as well as different volumes and ratios. The purple area corresponds to the volume of tissue with a rCBF less than 30% of the unaffected, healthy tissue and is considered the core infarct area. The green area corresponds to the volume of tissue with a Tmax longer than six seconds and is considered the ischemic penumbra. Though these threshold values were used and validated by the SWIFT PRIME and EXTEND-IA trials, they are not definitive or universal.[15,18] Familiarization with an institution’s software and threshold values is vital to interpreting CTP properly.

Importantly, CTP can be abnormal in other situations such as with chronic infarcts, vasospasm from subarachnoid hemorrhage, microvascular ischemia, and cerebral changes associated with seizure and feeding vessel stenosis.[16] Always interpret CTP in the context of the other imaging findings and anatomic consistency. 

Figure 11. Illustrative CTP report for the same acute right M1 occlusion from Figured 8, 9, and 10 showing territorially increased MTT with subtle reduction in CBF and a small area of asymmetrically elevated CBV in the area corresponding to infarction in Figure 10. This figure visually highlights the relationships between rCBV, cCBF, MTT, and Tmax.

Take Away Points

CT is the primary source of neuroimaging in the emergency department evaluation of stroke patients. NCCT is poor at detecting early acute infarcts directly, however it is excellent for hemorrhage detection. Use of CTA can demonstrate causative vascular lesions and addition of CTP can further delineate ischemia and determine how amenable it might be to intervention. Not all lesions identified by CTA and CTP will be amenable to thrombolysis or thrombectomy, but these are usually the only time effective ways available to emergency physicians to identify those that might be. Educating emergency physicians about these imaging modalities can both improve patient care through more rapid diagnosis in suspected stroke cases as well as help to streamline communication and treatment planning with consulting neurologists and neurointerventionalists. 

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Expert Commentary

This is a well-written synopsis of modern neuroimaging used today’s ED for workup and emergent treatment of acute stroke. The reader should keep in mind that the primary thrust of this blog segment is on acute ischemic stroke - while advanced CT imaging (i.e. CTA) also has a crucial role in hemorrhagic stroke, this is more thoroughly addressed elsewhere.

Practically speaking, today’s CT/CTP/CTA is to suspected stroke what an EKG is to chest pain in the ED. While confirmatory tests (MRI for stroke, troponin for MI) take more time, all actionable data depends on the initial CT/CTP/CTA in acute stroke. I would also categorize the purpose of acute stroke imaging in the ED into two categories, but with perhaps broader brush-strokes:

1. Determine if stroke is ischemic or hemorrhagic (“blood or no blood on CT”), and

2. Determine the next course of action:

   1. If ischemic, do temporal and anatomic criteria mandate IV tPA, endovascular thrombectomy, both, or neither, 

   2. If hemorrhagic, is there mass effect and/or an underlying vascular lesion (arterial or venous) that mandates urgent intervention beyond best medical care.

While NCCT is sufficient to determine whether to proceed with IV tPA in the 0-4.5 hour time-window (with an NNT of 10-20), CTP/CTA are key to determining whether the patient requires emergent endovascular thrombectomy in the 0-24 hour time-window (with an NNT of 2.6-4). As these two time-windows overlap, the most practical approach is increasingly to obtain multi-modality imaging up-front / as rapidly as possible in the ED. It is important to remember that as of 2015, both IV tPA and endovascular thrombectomy are considered standard-of-care, and any patient presenting with acute ischemic stroke must undergo full workup and consideration of both treatments based upon national society / consensus guidelines.

An added note on NCCT versus CTP: while NCCT is the oldest modality in the ED, it continues to have tremendous value in acute stroke imaging. Presence or absence of early stroke changes on NCCT (quantified by the ASPECT score) can at times trump CTP in the 0-6 hr time-window, and CTP within any time-window must be interpreted in context of NCCT findings. For example, CTP may show no abnormality (or even luxury perfusion) in an area of established stroke on NCCT in cases of spontaneous recanalization. On the other hand, CTP can be very helpful in detecting small areas of ischemia not well seen on CT/CTA (even when reading NCCT using optimized 35/35 or 40/40 “stroke windows”), and CTP has higher sensitivity for small/distal branch occlusions than either CT/CTA.

The approach to cerebrovascular arterial anatomy is nicely reviewed. A few additional comments:

1. ICA: acute ICA occlusions are most dramatic when reaching the terminus (thereby blocking the MCA/ACA), but those not reaching the supraclinoid ICA may at times be well-tolerated due to collaterals across the Circle of Willis,

2. VA: the course/anatomy of the VA is rather variable, with one VA (typically the right) being less dominant as we age; similarly, PICA can have a variable origin and territory of supply, and

3. BA: while randomized trials of endovascular thrombectomy for basilar occlusion have not been published, the natural history of BA occlusion is typically devastating/fatal, and a large body of non-randomized data (case series/cohorts) shows marked improvement over this natural history following endovascular thrombectomy for BA stroke in selected patients.

Vice Chair of Regional Neurosurgery

Professor of Neurological Surgery

Department of Neurological Surgery

Feinberg School of Medicine

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How to Cite this Post

[Peer-Reviewed, Web Publication] Seltzer J, Neill L. (2020, Jan 6). Emergency Guide to Stroke Neuroimaging. [NUEM Blog. Expert Commentary by Jahromi B]. Retrieved from http://www.nuemblog.com/blog/2018/4/20/stroke-neuroimaging

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References

1. National Center for Chronic Disease Prevention and Health Promotion , Division for Heart Disease and Stroke Prevention. “Stroke Fact Sheet.” Last Update: September 1, 2017. Accessed from https://www.cdc.gov/dhdsp/data_statistics/fact_sheets/fs_stroke.htm

2. Emberson J, Lees KR, Lyden P, et al., for the Stroke Thrombolysis Trialists’ Collaborative Group. Effect of treatment delay, age, and stroke severity on the effects of intravenous thrombolysis with alteplase for acute ischaemic stroke: a meta-analysis of individual patient data from randomised trials. Lancet. 2014 Nov 29;384(9958):1929-35.

3. Filho JO, Samuels OB. Approach to reperfusion therapy for acute ischemic stroke. UpToDate. Last Update: September 14, 2018. Accessed from https://www.uptodate.com/contents/approach-to-reperfusion-therapy-for-acute-ischemic-stroke

4. Chaela JA, Kidwell CS, Nentwich LM, et al.. Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison. Lancet. 2007 Jan 27; 369(9558): 293–298.

5. Nadgir R, Yousef DM. “Vascular Diseases of the Brain.” In Neuroradiology: The requisites. 4th Ed. (2017). Philadelphia, PA: Mosby/Elsevier

6. Yoon W, Seo JJ, Kim JK, Cho KH, Park JG, Kang HK. Contrast enhancement and contrast extravasation on computed tomography after intra-arterial thrombolysis in patients with acute ischemic stroke. Stroke. 2004 Apr;35(4):876-81.

7. Sabarudin A, Subramaniam C, Sun Z. Cerebral CT angiography and CT perfusion in acute stroke detection: a systematic review of diagnostic value. Quant Imaging Med Surg. 2014 Aug;4(4):282-90.

8. Shen J, Li X, Li Y, Wu B. Comparative accuracy of CT perfusion in diagnosing acute ischemic stroke: A systematic review of 27 trials. PLoS One. 2017 May 17;12(5):e0176622. 

9. Mancall EL. “Vascular Supply of the Brain and Spinal Cord” In Gray's clinical neuroanatomy: The anatomic basis for clinical neuroscience. 1st Ed. (2011). Philadelphia, PA: Elsevier/Saunders.

10. Mtui E, Gruener G, Dockery P. “Blood Supply of the Brain.” In Fitzgerald’s Clinical Neuroanatomy and Neuroscience. 7th Ed. (2016). Edinburgh: Elsevier Saunders.

11. Bouthillier A, van Loveren HR, Keller JT. Segments of the internal carotid artery: a new classification. Neurosurgery. 1996 Mar;38(3):425-32.

12. The Joint Commission. Specifications Manual for Joint Commission National Quality Measures (v2018B). Last Updated: 2018. Accessed from https://manual.jointcommission.org/releases/TJC2018B/DataElem0771.html

13. Filho JO, Samuels OB. Mechanical thrombectomy for acute ischemic stroke. UpToDate. Last Update: March 22 2019. Accessed from https://www.uptodate.com/contents/mechanical-thrombectomy-for-acute-ischemic-stroke

14. Prokop M1, Shin HO, Schanz A, Schaefer-Prokop CM. Use of maximum intensity projections in CT angiography: a basic review. Radiographics. 1997 Mar-Apr;17(2):433-51. 

15. Mokin M, Levy EI, Saver JL, Siddiqui AH, Goyal M, Bonafé A, Cognard C, Jahan R, Albers GW; SWIFT PRIME Investigators. Predictive Value of RAPID Assessed Perfusion Thresholds on Final Infarct Volume in SWIFT PRIME (Solitaire With the Intention for Thrombectomy as Primary Endovascular Treatment). Stroke. 2017 Apr;48(4):932-938.

16. Lui YW, Tang ER, Allmendinger AM, Spektor V. Evaluation of CT perfusion in the setting of cerebral ischemia: patterns and pitfalls. AJNR Am J Neuroradiol. 2010 Oct;31(9):1552-63.

17. Bivard A, Levi C, Krishnamurthy V, McElduff P, Miteff F, Spratt NJ, Bateman G, et al.. Perfusion computed tomography to assist decision making for stroke thrombolysis. Brain. 2015 Jul;138(Pt 7):1919-31. 

18. Campbell BC, Mitchell PJ, Kleinig TJ, Dewey HM, Churilov L, Yassi N, Yan B,et al.; EXTEND-IA Investigators. Endovascular therapy for ischemic stroke with perfusion-imaging selection. N Engl J Med. 2015 Mar 12;372(11):1009-18.

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The Top NUEM Blog Posts of 2019

Edited by: Maury Hajjar, MD (NUEM PGY-2), Niki Patel, MD (NUEM PGY-2), Vytas Karalius, MD, (NUEM PGY-2), Justine Ko (NUEM PGY-3)  Expert commentary by:  Seth Trueger, MD

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Happy New Year, Everyone!

Let’s take a look back at the 2019 NUEM Blog!

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The Top Ten NUEM Blog Posts of 2019

10. REBOA

Recent grads Andew Cunningham, Bill Burns, and Trauma/EM doc Zaffer Qasim walk us through the ever-popular and sublimely named REBOA.

9. The Seriousness of Deliriousness

Thorough discussion of the important but easy to overlook issue of delirium in the ED by Nery Porras, recent grad and current neuro critical care fellow Katie Colton and geriatrician Lee Lindquist.

8. Pelvic Fractures

Justine Ko, Terese Whipple, and Matt Levine walk is through pelvic fractures and the important associated injuries.

7. Verbal Deescalation in the ED

Vidya Eswaran, Zach Schmitz, Abiye Ibiebele, NUEM-blog-founder Michael Macias, recent grad Arthur Moore, and John Bailitz review the complex but important topic of verbal deescalation in the ED.

6. Visual Guide to Splinting

Recent grad and current Stanford med ed fellow, recentish grad John Sarwarkand remote grad Matthew Pirotte provide a surprising amount of information in a small amount of words & images.

5. Post-Intubation Management

It’s easy to fall into the trap getting the tube & high-fiving and walking away; Andra Farcas, recent grad and current Air Force doc Paul Trinquero and recentish grad Andrew Pirotte walk is through the steps to post-intubation management.

4. Flexor Tenosynovitis

Thorough and concise review of flexor tenosynovitis by Kevin Dyer and recent grad Adnan Hussain, featuring expert commentary hand surgeon Avi Giladi (who also had the #4 post in 2018).

3. Tetracaine

Nice review by Jonathan Hung and recent grad and current med ed fellow Matt Klein of an Annals study showing a safe approach to tetracaine for corneal abrasions. Won’t solve the controversy but does include an expert commentary by @DGlaucomflecken

2. Intubation Positioning: Beyond the Sniffing Position

Unfortunately, optimal positioning is not always optimally executed in the ED; this post reviews both “standard” sniffing position and ramping, which, if nothing else, will help push us to better position our patients. Very nice work by recent grad and current neuro critical care fellow Katie Colton, and recent grad Charles Caffrey, and recentish grad Andrew Pirotte!

1. Unstable C-Spine Fractures

The top spot goes to a very nice succinct review by recent grads Sarah Sanders and Alison Marshall featuring beautiful images and a commentary by NLFH faculty Steve Hodges.

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 How to cite this post

[Peer-Reviewed, Web Publication]  Hajjar M, Patel N, Karalius V, Ko J, (2019, December 30 ). The Top NUEM Blog Posts of 2019.  [NUEM Blog. Expert Commentary by Trueger S ]. Retrieved from http://www.nuemblog.com/blog/top-ten-2019.

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Other posts you might enjoy…

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The ED Guide to Neuroimaging: Part 2

Written by: Justin Seltzer, MD (NUEM PGY-3) Edited by: Priyanka Sista, MD, (NUEM PGY-4) Expert commentary by:  Peter Pruitt, MD, MS

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Make sure to check out The ED Guide to Neuroimaging: Part 1

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Part two of this series examines the literature regarding the appropriate use of the head CT in blunt head trauma, a common clinical grey zone in emergency medicine.

The Canadian Head CT Rule (Canadian), New Orleans Criteria (New Orleans), NEXUS II Head CT Rule (NEXUS), and PECARN Pediatric Head Injury Algorithm (PECARN) are four major decision rules designed to assist clinicians with this often difficult decision. This article is dedicated to comparing these rules and providing a reasonable guide for maximizing their individual utility. The provided infographics detail the specifics of each rule for quick reference. 

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To start, there are many shared characteristics between the rules. All apply to blunt head trauma only and, except for NEXUS, specifically to those presenting within 24 hours of injury. They utilize criteria to characterize high risk populations for which emergent head CT is appropriate as well as those low risk enough to forego it. Each boasts near perfect sensitivity and negative predictive values for clinically significant acute intracranial processes. Finally, all were prospective cohort studies and, aside from New Orleans, multi-center. 

However, there are differences between each rule that can impact their applicability to certain situations and populations. 

• Study population: The single center New Orleans Criteria had the smallest study population, with 1429 total patients, while the largest, PECARN, had over 42,000 patients. All aside from NEXUS had some age restrictions. Canadian included adults and pediatric patients older than 16 years and New Orleans included adults and pediatric patients older than 3 years. PECARN was exclusively pediatric and excluded anyone over 18 years old. 

• Inclusion and exclusion criteria: There was significant heterogeneity between the studies on what qualified for inclusion. New Orleans only included patients with known loss of consciousness or post-injury amnesia with a normal neurologic exam. Similarly, Canadian involved patients with GCS ≥13 and witnessed alteration or loss of consciousness. PECARN, on the other hand, was most concerned with mechanism and excluded patients with trivial mechanisms or injuries, such as ground level falls, walking into objects, and isolated scalp involvement. These are further contrasted with NEXUS, which included “all patients with blunt trauma with minor head injury (Glasgow Coma Scale [GCS] score of 15) who present to participating study center.”[1] 

• Decision rule criteria: Certain criteria, such as evidence of skull fracture, persistent vomiting, older age (>60-65 years), were nearly universally present. However, beyond these there is little consensus. NEXUS, likely because it applies to all ages, includes criteria such as alertness, behavior changes, and scalp hematoma similar to PECARN. Only New Orleans included clinical intoxication, while NEXUS was the only rule to include coagulopathy. Mechanism-based criteria were only considered by Canadian and PECARN. 

• Primary outcome: There is significant similarity in terms of primary outcome. NEXUS criteria sought “clinically important intracranial injury,” New Orleans any acute abnormality on CT, and PECARN “clinically important traumatic brain injury.” The definitions varied somewhat but were generally similar. Only Canadian stratified differently, with a set of criteria geared towards identifying the need for neurosurgical intervention specifically and another set for the more familiar “clinically important brain injury.” 

• Methods of Application: NEXUS, Canadian, and New Orleans are all or nothing; meeting even one element results in a head CT and not meeting any means a head CT is likely unnecessary. PECARN is unique in that if the major criteria are not met, minor criteria defer to observation or head CT based in part on non-standardized elements such as physician experience and parental preference. Only in the absence of major and minor criteria can a child be cleared immediately. 

Finally, it is important to understand the level of external validation and comparison to which each of these studies has been subjected. Boudia and colleagues performed an external validation study of both Canadian and New Orleans involving 1582 patients 10 years and older over a 3-year period. They noted some key differences between reported performance and performance between the two metrics. Canadian had 100% sensitivity for need for neurosurgical intervention, while New Orleans was 82% sensitive. Canadian was 95% sensitive for clinically significant head CT findings, compared with 86% sensitivity for New Orleans. Negative predictive values were 100% and 99% for Canadian and New Orleans, respectively.[5] Mower, Gupta, Rodriguez, and Hendey recently published a nearly 10 year validation of NEXUS involving 11,770 patients from four centers, which showed improved sensitivity (99% versus 98.3%), specificity (25.6% versus 13.7%), and negative predictive value (99.7% versus 99.1%) compared with the original study for clinically significant intracranial injury. This study also compared NEXUS and Canadian performance within the same study population for those who met Canadian criteria. NEXUS was found to have superior sensitivity (100% versus 97.3%) but worse specificity (32.6% versus 58.8%) for neurosurgical intervention while having worse sensitivity and specificity (97.7%/12.3% versus 98.4%/33.3%) compared with Canadian medium risk criteria for identification of significant brain injury.[6] Schachar and colleagues compared New Orleans, Canadian, and NEXUS in 2,101 pediatric patients over nearly seven years at a non-trauma center; all showed negative predictive values over 97% however Canadian and NEXUS both showed dramatically lower (65.2% and 78.3%, respectively) sensitivities in this population.[7] Smits and colleagues concluded from a Dutch cohort of 3,181 adult patients that Canadian had a lower sensitivity than New Orleans for traumatic intracranial findings but still identified all neurosurgical cases and had a much higher specificity, resulting in a greater number of avoided unnecessary scans.[8] In contrast, PECARN has been externally validated multiple times, all with near perfect sensitivity and negative predictive value;[9-13] of note, in one study two physically abused children with clinically important traumatic brain injury were misclassified as low risk, highlighting a gap in its criteria.[11]

In summary, the four major head CT decision rules all boast impressive sensitivity and negative predictive value for significant traumatic intracranial injury, though external validation and comparison studies have shown that some rules perform better than others under less controlled conditions. When properly applied to the intended patient populations, we can conclude that these are all useful clinical decision making tools, in particular to identify low risk patients and avoid unnecessary radiation exposure, costs, and resource utilization.

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Expert Commentary

I applaud Dr. Seltzer for his interesting and informative summary of decision instruments for patients with blunt head trauma. It is important to have a clear strategy for managing patients with this complaint, since traumatic brain injury is one of the most common ED complaints, accounting for an estimated 2.8 million annual visits in 2013, and the number of visits are steadily increasing.[1] Using a well validated decision instrument, such as the Canadian CT Head Rule in adults or the PECARN rule in children, reduces the frequency of unnecessary imaging and decreases length of stay while increasing the diagnostic yield (frequency of positive tests) amongst those patients that are imaged.[2,3] With this in mind, integration of these rules into clinical practice is a key component of appropriate resource utilization, and is recommended by multiple clinical practice guidelines.[4–6] However, the use of decision instruments cannot completely replace clinical gestalt, defined as the impression of the patient derived from the clinical evaluation. Unfortunately, studies comparing decision instruments to gestalt are extremely limited.[7] One study compared the PECARN decision instrument to clinician gestalt and found gestalt to be much more specific with similar sensitivity, although clinicians were asked about the criteria used in the decision instruments prior to making their “gestalt” decision.[8] There are no studies comparing the decision instruments used in adults to gestalt, so their relative performance is still open to assessment. Clinical instinct is still a valuable tool, and decision instruments only function to support this core skill. It is also important to consider what constitutes a positive outcome in these studies. Most notably, the Canadian CT Head Rule in its simplest form does not attempt to identify individuals who will have no hemorrhage at all.[9] Instead, the authors pre-defined defines a “clinically important injury”, which allowed patients to have small subdural hematomas or trace subarachnoid hemorrhage while still being considered low risk by the rule. Because these lesions rarely require intervention, the clinical significance of identifying them is minimal.

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Peter Pruitt, MD, MS

Assistant Professor

Department of Emergency Medicine

Northwestern University

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 How to cite this post

[Peer-Reviewed, Web Publication]  Seltzer J,   Sista P, (2019, December 15 ). The ED Guide to Neuroimaging: Part 2.  [NUEM Blog. Expert Commentary by Pruitt P ]. Retrieved from http://www.nuemblog.com/blog/emergency-neuroimaging-pt2.

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Other posts you might enjoy…

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References

1. Mower WR, Hoffman JR, Herbert M, Wolfson AB, Pollack CV Jr, Zucker MI; NEXUS II Investigators. Developing a decision instrument to guide computed tomographic imaging of blunt head injury patients. J Trauma. 2005 Oct;59(4):954-9.

2. Kuppermann N, Holmes JF, Dayan PS, Hoyle JD Jr, Atabaki SM, Holubkov R, Nadel FM, Monroe D, Stanley RM, Borgialli DA, Badawy MK, Schunk JE, Quayle KS, Mahajan P, Lichenstein R, Lillis KA, Tunik MG, Jacobs ES, Callahan JM, Gorelick MH, Glass TF, Lee LK, Bachman MC, Cooper A, Powell EC, Gerardi MJ, Melville KA, Muizelaar JP, Wisner DH, Zuspan SJ, Dean JM, Wootton-Gorges SL; Pediatric Emergency Care Applied Research Network (PECARN). Identification of children at very low risk of clinically-important brain injuries after head trauma: a prospective cohort study. Lancet. 2009 Oct 3;374(9696):1160-70.

3. Haydel MJ, Preston CA, Mills TJ, Luber S, Blaudeau E, DeBlieux PM. Indications for computed tomography in patients with minor head injury. N Engl J Med. 2000 Jul 13;343(2):100-5.

4. Stiell IG, Wells GA, Vandemheen K, Clement C, Lesiuk H, Laupacis A, McKnight RD, Verbeek R, Brison R, Cass D, Eisenhauer ME, Greenberg G, Worthington J. The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001 May 5;357(9266):1391-6.

5. Bouida W, Marghli S, Souissi S, Ksibi H, Methammem M, Haguiga H, Khedher S, Boubaker H, Beltaief K, Grissa MH, Trimech MN, Kerkeni W, Chebili N, Halila I, Rejeb I, Boukef R, Rekik N, Bouhaja B, Letaief M, Nouira S. Prediction value of the Canadian CT head rule and New Orleans for positive head CT scan and acute neurosurgical procedures in minor head trauma: a multicenter external validation study. Ann Emerg Med. 2013 May;61(5):521-7.

6. Mower WR, Gupta M, Rodriguez R, Hendey GW. Validation of the sensitivity of the National Emergency X-Radiography Utilization Study (NEXUS) Head computed tomographic (CT) decision instrument for selective imaging of blunt head injury patients: An observational study. PLoS Med. 2017 Jul 11;14(7):e1002313.

7. Schachar JL, Zampolin RL, Miller TS, Farinhas JM, Freeman K, Taragin BH. External validation of New Orleans (NOC), the Canadian CT Head Rule (CCHR) and the National Emergency X-Radiography Utilization Study II (NEXUS II) for CT scanning in pediatric patients with minor head injury in a non-trauma center. Pediatr Radiol. 2011 Aug;41(8):971-9.

8. Smits M, Dippel DW, de Haan GG, Dekker HM, Vos PE, Kool DR, Nederkoorn PJ, Hofman PA, Twijnstra A, Tanghe HL, Hunink MG. External validation of the Canadian CT Head Rule and New Orleans for CT scanning in patients with minor head injury. JAMA. 2005 Sep 28;294(12):1519-25.

9. Schonfeld D, Bressan S, Da Dalt L, Henien MN, Winnett JA, Nigrovic LE. Pediatric Emergency Care Applied Research Network head injury clinical prediction rules are reliable in practice. Arch Dis Child. 2014 May;99(5):427-31.

10. Lorton F, Poullaouec C, Legallais E, Simon-Pimmel J, Chêne MA, Leroy H, Roy M, Launay E, Gras-Le Guen C. Validation of the PECARN clinical decision rule for children with minor head trauma: a French multicenter prospective study. Scand J Trauma Resusc Emerg Med. 2016 Aug 4;24:98.

11. Ide K, Uematsu S, Tetsuhara K, Yoshimura S, Kato T, Kobayashi T. External Validation of the PECARN Head Trauma Prediction Rules in Japan. Acad Emerg Med. 2017 Mar;24(3):308-314.

12. Babl FE, Borland ML, Phillips N, Kochar A, Dalton S, McCaskill M, Cheek JA, Gilhotra Y, Furyk J, Neutze J, Lyttle MD, Bressan S, Donath S, Molesworth C, Jachno K, Ward B, Williams A, Baylis A, Crowe L, Oakley E, Dalziel SR; Paediatric Research in Emergency Departments International Collaborative (PREDICT). Accuracy of PECARN, CATCH, and CHALICE head injury decision rules in children: a prospective cohort study. Lancet. 2017 Jun 17;389(10087):2393-2402.

13. Nakhjavan-Shahraki B, Yousefifard M, Hajighanbari MJ, Oraii A, Safari S, Hosseini M. Pediatric Emergency Care Applied Research Network (PECARN) prediction rules in identifying high risk children with mild traumatic brain injury. Eur J Trauma Emerg Surg. 2017 Dec;43(6):755-762.

References (Expert Commentary)

1. Taylor CA, Bell JM, Breiding MJ, Xu L. Traumatic Brain Injury–Related Emergency Department Visits, Hospitalizations, and Deaths — United States, 2007 and 2013. MMWR Surveill Summ. 2017;66(9):1-16.

2. Sharp AL, Huang BZ, Tang T, et al. Implementation of the Canadian CT Head Rule and Its Association With Use of Computed Tomography Among Patients With Head Injury. Ann Emerg Med. 2017;33(0):1505-1514.

3. Stiell IG, Clement CM, Rowe BH, et al. Comparison of the Canadian CT Head Rule and the New Orleans Criteria in patients with minor head injury. JAMA. 2005;294(12):1511-1518.

4. Rosenberg A, Agiro A, Gottlieb M, et al. Early Trends Among Seven Recommendations From the Choosing Wisely Campaign. JAMA Intern Med. October 2015:1.

5. Schuur JD, Carney DP, Lyn ET, et al. A top-five list for emergency medicine a pilot project to improve the value of emergency care. JAMA Intern Med. 2014;174(4):509-515.

6. Mills AM, Raja AS, Marin JR. Optimizing Diagnostic Imaging in the Emergency Department. Acad Emerg Med. 2015:n/a-n/a.

7. Schriger DL, Elder JW, Cooper RJ. Structured Clinical Decision Aids Are Seldom Compared With Subjective Physician Judgment, and are Seldom Superior. Ann Emerg Med. 2016.

8. Babl FE, Oakley E, Dalziel SR, et al. Accuracy of Clinician Practice Compared With Three Head Injury Decision Rules in Children: A Prospective Cohort Study. Ann Emerg Med. 2018;71(6):703-710.

9. Stiell IG, Lesiuk H, Wells GA, et al. The Canadian CT head rule study for patients with minor head injury: Rationale, objectives, and methodology for phase I (derivation). Ann Emerg Med. 2001;38(2):160-169.

A Closer Look at the HEART Score

Written by: Abiye Ibiebele, MD (PGY-3) Edited by: Kumar Gandhi, MD (PGY-4) Expert commentary by: D. Mark Courtney, MD, MCSI

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Chest pain accounts for nearly six million annual visits to the Emergency Departments across the United States and accounts for over ten billion in healthcare dollars, and thus the appropriate management of chest pain is part of the daily reality of Emergency Physicians. From one’s first EM rotation in medical school, one learns to always rule out the dangerous causes of chest pain first, of which acute coronary syndrome (ACS) is often first and foremost. A STEMI is called from the field or quickly on arrival to the emergency department and the patient is quickly evaluated by cardiology either in the emergency department or on the way to the cardiac catheterization lab. However, the diagnostic and management challenge remains for those patients that may have ACS without initial EKG changes or an elevation in troponin. To help us, clinical decision rules have been developed to help us identify which patients who present with chest pain we can safely rule out life-threatening ACS in and help risk stratify patients into different risk categories [1]. What follows is a breakdown of the components of the HEART score, a review of how to appropriately assign points and a brief review of the original study and subsequent research since then.

HEART Score

Backus et al. Chest pain in the emergency room: a multicenter validation of the HEART Score. Crit Pathw Cardiol. 2010;9(3):164-169.

History

This is the most subjective area of scoring in the HEART score and one of possible contention between different health care providers. 

The original study broke down historical elements as specific for ACS and nonspecific for ACS as judged by the clinical experience of practiced providers.1 A 0 score, was given for a completely nonspecific history and a 2 score was given for a primarily specific history. For a mixture of nonspecific and specific elements, a 1 score was given. 

The original researchers used clinical gestalt and took into account historical elements such as pattern of pain, onset, duration, relation to exercise, localization, concomitant symptoms and reaction to sublingual nitrates. While this was based on clinical judgment, the historical elements were somewhat based on a prior clinical review which listed specific elements as follows: [3]

Concerning history (read: specific for ACS)

• Chest pain radiating to one or both arms

• Pressure like pain with associated nausea, vomiting, or diaphoresis

• Exertional chest pain

• Response of chest pain to nitroglycerin

• Chest pain similar to prior MI

Non-concerning history for ACS (read: nonspecific for ACS)

• Pleuritic or positional chest pain

• Chest pain reproducible with palpation

• Stabbing quality of pain

• Pain localized to an area on chest smaller than a coin

It is important to note is that for assigning a history score, developers did not take into account risk factors or EKG findings. These are accounted for elsewhere in the HEART score.

EKG

Two points are assigned for ST elevations or depressions, in the absence of a bundle branch block, LVH or use of digoxin [1].

One point is assigned for repolarization abnormalities (new or old) without ST depression. A person can also receive a score of 1 for a bundle branch block or left ventricular hypertrophy [1].

Zero points is assigned for a normal EKG [1].

Age

This component of the HEART score is the most straightforward with scoring as defined in the chart above.

Risk Factors

As in the above chart, having no risk factors results in a score of zero points. Having 1-2 risk factors yields a score of 1. Important thing to note is about having at least 3 risk factors OR a “history of atherosclerotic disease” results in a score of 2 points. [1] 

What does “history of atherosclerotic disease” mean? [1]

• History of revascularization (PCI or CABG)

• History of myocardial infarction

• History of ischemic stroke

• History of peripheral arterial disease

Thus, a patient with a history of any of the above disease should automatically get a 2 for this section of the HEART score.

What were included as risk factors for study purposes? [1,2]

• Hyperlipidemia

• Hypertension

• Diabetes Mellitus

• Cigarette smoking (has to have last smoked within 90 days)

• Family history of coronary artery disease (doesn’t matter if family member was over/under 50 years of age)

• Obesity (defined as BMI over 30)

Troponin 

Also, a straightforward component of the HEART score with scoring as above.

Some notes regarding scoring:

• Original study and validation studies did not use high sensitivity troponin when calculating the HEART score [1,4]

• Follow up studies have used high sensitivity troponins in what is referred to as a “modified HEART score”. Scoring is similar to conventional troponin testing as in above chart. [5,6]

As those of you who have use the HEART score know, you calculate all the points and if a patient has a score between 0-3, they are considered low risk can be discharged home safely. A score between 4-6 is considered moderate risk and should be admitted for further observation and workup. A score of 7-10 is considered high risk and is recommended to have an early invasive intervention. 

Now that we have covered the components of the HEART score, as previously mentioned, below is a brief review of the original study. However, before that, two caveats to using the HEART score:

• For original study and following validation studies, patients who presented with only dyspnea or palpitations without associated chest pain were excluded [1,4]

• HEART score has been shown to be helpful in distinguishing risk even when looking within special populations (diabetics, elderly, and females) [1,2,4,5]

Original Study

Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: value of the HEART score. Neth Heart J. 2008;16(6):191-196.

Study design

Retrospective, single center study at a 265 bed community hospital in the Netherlands

Inclusion Criteria

Patients included were any patient admtted to the ER due to chest pain irrespective of age, prehospital assumptoms and previous medical treatments

• Patients with STEMI were excluded

Methods

Patient’s charts were reviewed and HEART score was calculated as above. Endpoints as described below were identified and differences between groups were statistically analyzed.

Endpoints

Acute MI, revascularization, death and composite endpoint of all three.

Demographics

Total of 122 patients, mean age 61 years old, 60% male, race not specifically measured but overall hospital population >95% White/ Caucassion.

Results

All patients:

24% of all patients reached one or more of above endpoints

Average HEART score for all patients that did not reach an endpoint: 3.71 +/- 1.83

Average HEART score for all patients that did meet an endpoint: 6.51 +/- 1.84

Significant difference p < 0.0001

Heart Score Groups:

For patients with HEART score 0-3, 2.5% reached an endpoint

For patients with HEART score 4-6, 20.3% reached an endpoint

For patients with HEART score 7-10, 73% reached an endpoint

What to do with low risk patients?

• Based on the heart score original study, for low risk patients (HEART score 0-3) the risk of a major adverse cardiac event (MACE) was 2.5%. The original suggestion from the authors of this study is that these patients can be immediately discharged.

• Further validation studies have shown the risk of MACE within 45 days to be 1.9% and of all-cause mortality to be 0.05%. 

• There has also been development of the HEART score pathway, which adds a 3-hour serial troponin to low risk patients. In the initial study, 40 patients were discharged from the ED after two negative troponins and none of those patients had a MACE within 30 days.7

• A 2017 systematic review of 9 studies and 11,217 patients revealed that 1.6% of the low risk patients would have a MACE at 6 weeks8. This study derived the sensitivity of the HEART score to be 96.7%. Another systematic review is ongoing to validate these findings and to further delineate the prognostication value of the HEART score9

• Ultimately, having a discussion with these patients about what low risk means and coming to a shared decision can be a useful tool but in a patient with good outpatient follow-up, it is reasonable to discharge the patient without further cardiac testing,

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Expert Commentary

What clinicians (and patients) care about is post test probability. This is a function of two things, what the pretest probability is and how good your testing tools are. The HEART score, the modified HEART score and the HEART Score Pathway as described above are all ways to try to formalize the process of pretest probability estimation. It is important to realize that the standard ED evaluation is suited to identify STEMI and NSTEMI. However part of the definition of MACE is angina and that is the entire point of stress testing….to discover treatable intermittent cardiac ischemia that may not show up on initial or subsequent ECGs or troponin testing. The HEART score approach has rapidly become the most widely used approach in the US to try to determine who needs a stress test during the index admission vs. who may be able to safely be discharged for follow-up and potential stress testing as an outpatient.

Despite popularity, there are challenges with any HEART score approach. These are as follows. 1) Clinicians like to talk about the HEART score but often don’t document it or do so in a template dot-phrase manner. All decision support pretest probability scores are only as good as the degree of accuracy of the data applied and documented. At times documentation is simply “HEART SCORE low” without the granular details to support this in the record. 2) There is potential for inter-observer disagreement. In work presented in abstract at the 2018 SAEM annual meeting Dr. Steven Ignell reported that residents were less likely to classify patients as low risk than attendings, and that formal application of the HEART score did not result in a larger proportion of low risk classification than by simple gestalt alone (do you think this patient is at 2% risk of 6 week MACE?). However in this work the agreement was better using the HEART score with a weighted Kappa of 0.62 vs 0.29 for gestalt along. So it seems that the HEART score likely identifies a roughly similar cohort of patients but does so with more standardization. The biggest future questions are to what degree in the US a HEART score approach will be optimally integrated with hsTroponin testing, who needs serial hsTroponin testing and who does not, and does timing of pain onset matter? Ongoing and future trials may bring insights into these important process questions.

D. Mark Courtney, MD, MSCI

Associate Professor

Department of Emergency Medicine

Northwestern University

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How to Cite this Post

[Peer-Reviewed, Web Publication] Ibiebele A, Gandhi K. (2019, Dec 9). A Closer Look at the HEART Score. [NUEM Blog. Expert Commentary by Courtney DM]. Retrieved from http://www.nuemblog.com/blog/HEART-score.

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References

1. Six AJ, Backus BE, Kelder JC. Chest pain in the emergency room: value of the HEART score. Neth Heart J. 2008;16(6):191-196.

2. Backus BE, Six AJ, Kelder JC, et al. Chest pain in the emergency room: a multicenter validation of the HEART Score. Crit Pathw Cardiol. 2010;9(3):164-169.

3. Swap CJ, Nagurney JT. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005;294(20):2623-2629.

4. Backus BE, Six AJ, Kelder JC, et al. A prospective validation of the HEART score for chest pain patients at the emergency department. Int J Cardiol. 2013;168(3):2153-2158.

5. Ma CP, Wang X, Wang QS, Liu XL, He XN, Nie SP. A modified HEART risk score in chest pain patients with suspected non-ST-segment elevation acute coronary syndrome. Journal of geriatric cardiology : JGC. 2016;13(1):64-69.

6. Santi L, Farina G, Gramenzi A, et al. The HEART score with high-sensitive troponin T at presentation: ruling out patients with chest pain in the emergency room. Intern Emerg Med. 2017;12(3):357-364.

7. Mahler SA, Riley RF, Hiestand BC, et al. The HEART Pathway randomized trial: identifying emergency department patients with acute chest pain for early discharge. Circ Cardiovasc Qual Outcomes. 2015;8(2):195-203.

8. Van Den Berg P, Body R. The HEART score for early rule out of acute coronary syndromes in the emergency department: a systematic review and meta-analysis. European heart journal Acute cardiovascular care. 2018;7(2):111-119.

9. Byrne C, Toarta C, Backus B, Holt T. The HEART score in predicting major adverse cardiac events in patients presenting to the emergency department with possible acute coronary syndrome: protocol for a systematic review and meta-analysis. Systematic reviews. 2018;7(1):148.

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Penile Injuries

Written by: Jacob Stelter, MD (NUEM ‘19) Edited by: Kimberly Iwaki, MD (NUEM ‘18) Expert commentary by: D. Mark Courtney, MD, MCSI

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Case

A 54 year old male with no significant past medical history presents to the ED around 11pm with the chief complaint of “swollen penis.” He appears notably distressed on initial assessment and complains of penile swelling and pain. Per the history, the patient states that he was having sexual intercourse with his wife, with her on top of him, when he felt a sudden “popping” sensation in his penis followed by swelling, detumescence and pain. Vitals are stable and exam is notable for an enlarged, swollen, ecchymotic, mildly angulated and deformed penis. Diagnosis?

Penile fracture. Yes, penises (or penes) can fracture. The penis can sustain multiple different forms of injury, including fracture, direct trauma, burns and strangulation. It is both dramatic and problematic and requires emergent evaluation. Three of these injuries will be discussed here – penile fracture, zipper injury and penile strangulation.

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Penile Fractures

Anatomy and Pathophysiology

The penis consists of two corpora cavernosa on the dorsal aspect of the penis and one corpus spongiosum on the ventral portion of the penis, all wrapped in a tough fascial layer call the tunica albuginea (1). Penile fractures typically involve an injury to the tunica albuginea that becomes significantly thinner and more stretched during an erection (2). Usually, this involves the tunica albuginea of one of the corpus cavernosum, which can also become injured or lacerated (2, 3). The most common mechanism for penile fracture in the United States is during vigorous vaginal sexual intercourse when the erect penis is misdirected into the female pubic bone (2). This most often occurs with the female-on-top or “cowgirl” positions (2). In the Middle East, the most common practice that leads to penile fracture is “taghaandan” or “to click or snap when forcibly pushing the erect penis down to achieve detumescence” (4). In fact, one study conducted in Iran determined that 69% of penile fractures were related to this mechanism (4).

Figure 1: Normal Penile Anatomy (1)

Presentation

The clinical presentation of a penile fracture is typically a “popping” sensation or sound, followed by significant pain, swelling and detumescence of the penis, often with notable ecchymosis, swelling and deformity on exam (3). Clinically, this is referred to as the “eggplant deformity” (5). The “rolling sign” refers to the physical exam maneuver that identifies where the corporal fracture is located by rolling the penis and palpating a firm, immobile swelling that represents the hematoma overlying the fracture (5).  Most often, this is a clinical diagnosis with little utility for imaging studies. However, if the diagnosis is unclear, ultrasound or MRI can be used to diagnose injuries to the underlying fascia or corpora cavernosa (6).

Figure 2: Penile fracture

Treatment

From an emergency department (ED) management perspective, if a penile fracture is suspected, an emergent urology consultation is indicated. Up to 38% of penile fractures can involve urethral injuries and, while they may present with hematuria and difficulty urinating, these signs are not reliable in ruling out a urethral tear (2).  As a result, a retrograde urethrogram (RUG) or cystoscopy should be performed prior to Foley catheter placement (2). This is important, as acute urinary retention in the setting of a penile fracture is an emergency indication for Foley placement and an urologist may not be readily available to assist with this. Symptom control in the ED should include ice packs to reduce swelling, pain control and Foley placement as indicated (5).  Current urological treatment guidelines recommend immediate surgical repair which includes hematoma evacuation, examination of the urethra, and repair of the corporal fracture and any tears in the surrounding fascia (5,2). If promptly repaired, within 36 hours, most patients have minimal residual effects after sustaining a penile fracture (3).

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Zipper Injury

Zipper injuries involving the penis are another injury that can be encountered by the emergency physician.  Most often, this occurs in children and is more common in uncircumcised males (1). Using a lubricant to attempt to separate the entrapped penis can be successful and is noninvasive (1). In fact, a recent study showed that the use of mineral oil to free a simulated entrapped penis was nearly 100% successful (7).  If unsuccessful, using a wire cutter can help to cut the middle portion of the zipper that connects the two halves to help separate the zipper from the entrapped foreskin (1). Additionally, the zipper can be grasped above and below the entrapment to separate the teeth to free the penis (1). This can be painful, so using local or regional anesthesia is recommended (1).

Figure 3: Zipper median bar bisection (1)

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Penile Strangulation

Penile strangulation injuries are seen occasionally in the ED.  Most often, this results from self-application of rings to the base of the penis and often including the scrotum in an attempt to prolong erections or enhance sexual pleasure.  Multiple case reports have been published, detailing various objects used as cock rings and methods to remove them. Being unable to remove the constricting ring is a medical emergency as it can cause a prolonged erection and can lead to ischemia and eventual necrosis of the penis (8).  There are five published grades of injury resulting from penile strangulation (9):

• Grade I: Penile edema with no urethral or skin injury

• Grade II: Skin injury with constriction of the corpus spongiosum with penile edema and decreased sensation

• Grade III: Injury to both the skin and urethra without urethral fistula

• Grade IV: Urethral fistula formation due to division of the corpus spongiosum

• Grade V: Penile necrosis or amputation of the distal segment

Multiple different tools can be used to remove these rings, including ring cutters found in most emergency departments, dental drills or pliers (8).  Care must be taken to protect the skin of the penis underneath the ring and this can be done by using a tongue depressor or other protective guard. If it is difficult to get anything underneath the constricting band, blood can be drained from the corpora cavernosa in a manner similar to draining a priapism (8).  If this is unsuccessful, an emergent urology consult is indicated to avoid permanent penile damage (8).

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Take Home Points

1. Penile fractures are one of the most common injuries of the penis and are often sustained by vigorous sexual intercourse. ED management of penile fractures includes pain control, swelling reduction with ice, Foley placement once a urethral injury is ruled out and emergent urology consult for operative intervention.

2. Zipper injuries occur most frequently in young, uncircumcised males. Mineral oil is the best way to try to free a zipper-trapped penis. If unsuccessful, try bisection of the median bar of the zipper.

3. Penile strangulation occurs by the self-placement of constricting rings and can end up causing penile necrosis or amputation if the constricting object is not promptly removed.

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Expert Commentary

One of the more difficult aspects of management of these injuries is reassurance and anxiolysis to the patient and perhaps their partner or parent in the case of a child with a zipper injury.   There is often a morbid curiosity on the part of members of the treatment team including other physicians and nurses. For the sake of maintaining a calm patient who trusts in you as you approach the penis with a tool that looks like and may have come from the hospital mechanical maintenance room, try to avoid spectacle and treat the patient with dignity and respect and perhaps a bit of a benzodiazepine.  This will make them feel more comfortable and make your job easier.  

Additionally, don’t trust the history.  There are many reasons patients may not be forthright about the events leading up to and causing a penile fracture.  In my experience half of the patients I have taken care of have denied onset while having intercourse despite later revealing the truth.  Point is….if it looks like a penile fracture, it almost certainly is, regardless of the history that may be unclear or inconsistent with your suspicion.   

Finally, the seriousness of implications of untreated penile injuries at times needs to be impressed upon patients, family members, and treating physicians.  Sometimes these patients arrive intoxicated and wanting to leave. This presents the usual difficulties in determining medical decision making capacity and preventing harm.  Though the above Blog post notes most have a good outcome with repair, un-repaired penile fractures have a high incidence of subsequent deformity and erectile dysfunction.

D. Mark Courtney, MD, MSCI

Associate Professor

Department of Emergency Medicine

Northwestern University

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How to Cite this Post

[Peer-Reviewed, Web Publication] Stelter J, Iwaki K. (2019, Dec 2). Penile Injuries. [NUEM Blog. Expert Commentary by Courtney DM]. Retrieved from http://www.nuemblog.com/blog/penile-injuries

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References

1. Dubin J, Davis JE. Penile emergencies. Emerg Med Clin N Am 2011;29:485-499.

2. Chang AJ, Brandes SB. Advances in diagnosis and management of genital injuries. Urol Clin N Am 2013;40:427-438.

3. Cooper BL, Beres KP. Penile Fracture. J Emerg Med 2017;52(2):238-239.

4. Zargooshi, J. Penile fracture in Kermanshah, Iran: Report of 172 cases. J Urol 2000;164:364-366.

5. Jack  GS, et al. Current treatment options for penile fractures. Rev in Urol 2004;6(3):114-120.

6. Bertolotto M, et al. Penile trauma. Chapter 125 in Abdominal Imaging. 2013. Pp. 1937-1946.

7. Oquist M, et al. Comparative analysis of five methods of emergency zipper release by experienced versus novice clinicians 2016;68(45):S116.

8. Chapman JD. A case of penile strangulation secondary to deliberate placement of a wedding band. J Clin Urol 2016;9(2):131-132.

9. Agarwal AA, et al. Penile strangulation due to plastic bottle neck: A surgical emergency. BMJ Case Rep 2014:1-2.

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Bougie Journal Club

Written by: Amanda Randolph, MD (NUEM PGY-3) Edited by: Katie Colton, MD (NUEM ‘19) Expert commentary by: Howard Kim, MD

Introduction:

Endotracheal intubation is one of the most common and life-saving procedures performed in the Emergency Department (ED), though it is not without risk – approximately 12% of ED intubations result in an adverse event. First-pass success has been linked to improved outcomes, but in the case of a difficult airway, this goal can be challenging. The bougie is typically reserved as a rescue device in these situations. However, a study recently published in JAMA questions this approach, and instead asks whether the routine use of a bougie during all difficult airway attempts would improve first-pass success.   

The Study: 

Effect of Use of a Bougie vs Endotracheal Tube and Stylet on First-Attempt Intubation Success Among Patients With Difficult Airways Undergoing Emergency Intubation: A Randomized Clinical Trial

Driver BE, Prekker ME, Klein LR, et al. Effect of Use of a Bougie vs Endotracheal Tube and Stylet on First-Attempt Intubation Success Among Patients With Difficult Airways Undergoing Emergency Intubation: A Randomized Clinical Trial. JAMA. 2018;319(21):2179–2189. doi:10.1001/jama.2018.6496

Study Design:

This study was a randomized clinical trial performed at Hennepin County Medical Center, an urban academic Emergency Department. 

Population:

Investigators enrolled consecutive patients 18 years and older whom the attending emergency physician planned to intubate using a Macintosh laryngoscope blade (direct or video).

Exclusion criteria included known anatomic distortion of the upper airway (ie angioedema, epiglottitis, laryngeal mass, or malignancy), as the bougie has already been proven more effective in these patients in previous studies. Prisoners and pregnant patients were also excluded.

After intubation, the physician recorded whether any difficult airway features were present: body fluids obscuring the laryngeal view, airway obstruction or edema, obesity, short neck, small mandible, large tongue, facial trauma, or cervical spine immobilization. Patients were then subcategorized based on the presence of 1 or more difficult airway characteristics.

Intervention Protocol:

To optimize a balanced study population, eligible patients were first sorted into 2 strata – those with obesity or cervical immobilization, and those without these features. From that point, patients from each stratum was randomized 1:1 to either bougie or endotracheal tube (ET tube) + stylet for the first attempt. 

The intubating physician was free to direct the procedure as they saw fit, including patient positioning, pre-oxygenation, the use of RSI, and cricoid pressure. The physician could choose between direct laryngoscopy using a Macintosh blade, or video laryngoscopy using a C-MAC or GlideScope.  If video laryngoscopy was chosen, the physician could elect whether to view the video screen. 

• In the bougie group, the physician inserted the bougie into the trachea, an assistant loaded the ET tube, and the operator guided the tube through the vocal cords. If resistance was met, the physician retracted the tube 2cm, rotated 90 degrees and re-advanced. 

• In the ET tube + stylet group, a straight to cuff shape was used. If resistance was encountered, the physician could reshape the tube/stylet as needed. 

If intubation was unsuccessful on the first attempt, the physician was free to change any equipment or devices. Correct tube placement was determined by waveform capnography. 

Outcome Measures:

Primary outcome: first-pass intubation success

• Successful intubation on the first laryngoscopy attempt with device as previously randomized (bougie or ET tube)

Secondary outcomes:

• Hypoxemia (sat < 90%, or > 10% desat during intubation if already hypoxemic)

• First attempt time elapsed (laryngoscope insertion to removal)

• Esophageal intubation

Results:

• In patients randomized to the bougie arm, there was a 14% absolute increase in the rate of first-pass success in patients with at least one difficult airway feature (96% vs 82% bougie vs ET tube +stylet).

  • The bougie approach was superior in subsets of patients with predictors of airway difficulty including C-spine immobilization, obesity, and Cormak-Lehane grades 2-4.

• Even in patients not predicted to have a difficult airway, there was a 7% absolute increase in first-pass success with the bougie approach (99% vs 92% with ET tube + stylet).

• There was a small but significant increase in the time elapsed on first-pass success with the bougie (38 seconds) vs ET tube + stylet (34 seconds).

A more extensive summary of the results is depicted in Table 3:

Interpretation:

This study concludes that the bougie improves first-pass success rate both in difficult airways and standard airways.  The small increase in time to first-pass success when using a bougie is outweighed by the need to fall back on rescue techniques more frequently when starting with an ET tube and stylet.  Therefore, authors propose the use of a bougie as a routine primary intubation device for all patients. This argument is compelling and potentially practice-changing. Most EDs including NMH have adopted the practice of using a bougie right away when there is an obviously difficult airway (laryngeal mass, neck hematoma etc), but otherwise the bougie is often reserved for backup after one or more failed attempts.  This relies on a perhaps now invalid model of an algorithmic approach to the difficult airway in which operators progress through a series of rescue devices and maneuvers. In light of this study, it may be time for a culture shift in EM toward routine bougie use. 

Strengths:

This is a well-designed randomized controlled trial, with a total of 752 patients studied, generating enough power to provide meaningful results. The methodology of using the bougie and the ET tube + stylet was highly standardized. At the same time, the physicians were free to direct the remainder of the intubation strategy, including preoxygenation, medications, patient positioning, operator training, laryngoscope type, and video assistance. This is a realistic approach that would be generalizable to the typical ED experience. The power of this study was sufficient to then create subgroup analyses for each of these factors, and prove they were not confounders. 

Weaknesses:

This study is primarily limited by its single center design and thus may not be generalizable to all Emergency Departments. This particular hospital had been using the bougie routinely prior to this study, which is uncommon. This may have led to overestimation of the bougie’s benefit. Further studies involving multi-centered trials are needed to affirm generalizability. Finally, this study by design could not be blinded, which could have led to biased results.  

Take Home Points:

• This was a single center randomized controlled trial of bougie vs ET tube + stylet for first-pass intubation

• The bougie was significantly more effective in all patients, with or without difficult airway features

• This study is potentially practice-changing and suggests the bougie should be used as a routine primary intubation device for all patients in the ED

• Further studies including a multi-centered trial would be helpful to affirm generalizability

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Expert Commentary

Thank you for the excellent review of this randomized trial of a bougie-first intubation strategy. I agree that this study is potentially practice-changing, with the important caveat that your initial mileage may vary due to the study setting of a single ED with an existing culture of utilizing the bougie. Still, the demonstrated 11% absolute difference in first-pass success among all-comers (including patients with and without difficult airway characteristics) is compelling.    

Intuitively, routine use of the bougie should be a familiar concept to ED physicians. We regularly utilize Seldinger technique in the placement of various vascular access devices, and the bougie can be thought of as the Seldinger technique of the airway. Anecdotally, I feel that the primary benefits of the bougie are improved visualization of the glottic inlet and tactile feedback from tracheal clicks and holdup. Many of us will encounter airways that we do not initially perceive to be difficult based on anatomic features (e.g., non-obese, reassuring Mallampati) only to be perplexed by the visual appearance of the glottic inlet after blade placement (see Kovacs et al., 2017) or complete obscuring of the glottic inlet by rapidly re-accumulating blood or vomitus. In these scenarios, tactile feedback can be reassuring of proper tube placement.  

Importantly, use of the bougie requires the operator to understand three key points: first, many novice users instinctively remove the intubating blade after the bougie is placed but prior to railroading the endotracheal (ET) tube over the bougie; this makes ET tube placement difficult but can be addressed by re-inserting the intubating blade (and confirming that the bougie remains in the correct position). Second, as the study authors point out, the bevel tip of the endotracheal tube can get caught on the arytenoids. This can be addressed by rotating the ET tube and re-attempting insertion. Finally, bougie placement can be difficult with hyper-angulated devices, such as the traditional GlideScope blade or the “D-Blade” for the C-MAC – hence the reason for excluding these devices in the trial. These hyper-angulated devices require the ET tube (and bougie) to navigate a hyper-acute angle for delivery, which is why they come with a special hyper-angulated metal stylet.  

Finally, while I am an advocate of a bougie-first intubation strategy, I would emphasize that it is important not to become too infatuated with or dependent on a single airway technique. For example, a bougie cannot solve the dilemma of a small, restricted mouth that will not accommodate blade placement (e.g., advanced scleroderma), nor will it allow you to navigate an edematous tongue that occludes the entire oropharynx (e.g., severe angioedema). The best airway technicians are facile in a number of airway techniques, are always cognizant of the potential for their primary approach to be unsuccessful, and have a clear algorithm for how to respond to potential obstacles. This requires learning as many airway techniques as possible during your training (e.g. video, direct, LMA, bougie, fiber-optic).

References:

Kovacs G, Duggan LV, Brindley PG. Glottic Impersonation. Can J Anaesth. 2017 Mar;64(3):320. PMID 28028675.

Howard S. Kim, MD MS

Assistant Professor

Department of Emergency Medicine

Northwestern University Feinberg School of Medicine

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How To Cite This Post

[Peer-Reviewed, Web Publication]  Randolph A, Colton K. (2019, Nov 25). Bougie Journal Club. [NUEM Blog. Expert Commentary by Kim H]. Retrieved from http://www.nuemblog.com/blog/bougie.

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Approach to Double Vision in the ED

Written by: Andy Rogers, MD (NUEM PGY-2) Edited by: Dana Loke, MD (NUEM PGY-4) Expert commentary by: Quentin Reuter, MD

Seeing double: toil and trouble?

Introduction

Double vision, or diplopia, is a relatively infrequent presenting symptom in the emergency setting, representing 0.1% of Emergency Department (ED) complaints (1).  Diplopia can result from benign processes, such as dry eyes or idiopathic cranial nerve palsy, to emergent conditions with high morbidity, such as stroke, aneurysm, or inflammatory processes.   Given a wide range of possible outcomes for a less common presenting complaint, it is worth reviewing the neuroanatomy and etiologies of diplopia, as well as a generalized approach to the patient presenting to the ED with double vision.  

Neuroanatomy

The neuroanatomy underlying control of the extraocular muscles and their ability to provide gaze alignment is complex and worth a brief review.  Eye movements are governed by six extraocular muscles, which are controlled by four cranial nerves, summarized in Table 1 and Figure 1 below. The nuclei for the cranial nerves are located in the brainstem.  The nerves course from the brainstem, through the subarachnoid space, the cavernous sinus (Figure 2), the orbital apex, and finally to their respective extraocular muscles. Given the close proximity of nearby structures, lesions can often be localized based on associated symptoms, in addition to gaze palsies, to help guide workup and diagnosis.  For instance, an important additional function of CN III includes the parasympathetic fibers that travel along the oculomotor nerve that contribute to pupillary constriction.

Table 1: Summary of functions of the extraocular muscles, grouped by cranial nerve. (2)

Figure 1: Diagnostic positions of gaze with associated extraocular muscles contributing to movement. (3)

Figure 2: Cavernous sinus and its contents. Note that the cavernous sinus is symmetric about the pituitary fossa (only one side is shown above) (4)

Initial approach to diplopia

Dr. Margolin and Dr. Lam published an excellent review of the approach to diplopia in the ED, summarized in Figure 3 (5).  Critical to the diagnosis is a good history and neurologic exam. Their approach involves the follow steps:

1. Determine if symptoms are monocular or binocular

2. Determine if there are associated neurologic signs or symptoms

3. If isolated diplopia, determine if the palsy localizes to a third or sixth nerve palsy, or if it is a complex motility disorder

4. Screen for giant cell arteritis (also known as temporal arteritis) in all patients over the age of 60

Figure 3: Approach to patient with diplopia, from Margolin and Lam (5)

Monocular or Binocular

The first step in the approach to diplopia in the ED is to determine if the diplopia is monocular or binocular.  Some patients may not know or not have checked prior to presentation. Ask the patient “does the double vision resolve when you close one eye?” 

Monocular Diplopia

Monocular diplopia persists with one eye closed.  This localizes the lesions to the affected eye and reflects that the issue is not with misalignment of gaze.  It is almost always benign and most often due to dry eyes and refractive error (5, 6). Referral to an ophthalmologist is appropriate and no further imaging is indicated unless warranted by other features of the patient’s presentation.

Binocular diplopia

Binocular diplopia resolves with one eye closed.  This indicates ocular misalignment that can be due to an issue with the muscle, nerve, or CNS.  

Binocular diplopia with associated neurologic signs

Diplopia with other associated neurologic signs is concerning.  Acute onset of symptoms may be due to intracranial hemorrhage, cerebrovascular disease, or rapidly progressive neurologic disorder.  Initiation of stroke protocol is valuable for several reasons. It allows for rapid diagnosis of hemorrhagic or ischemic stroke, evaluates for cerebral aneurysm, and involves Neurology quickly in the patient’s care.  Some neurologic signs and symptoms, or clusters of signs and symptoms can help identify the etiology (5-7). See Table 2 below.

Binocular diplopia without associated neurologic signs (Isolated diplopia)

In all patients presenting with diplopia, careful examination of the extraocular movements and pupils are important to localizing the lesion.  Note that diplopia can be due to weakness in one direction or entrapment of the muscle limiting range of motion. Both etiologies must be kept in mind.  Figure 1 is a good reference to identify what muscles and nerves may be affected based on directional limitations in extraocular movements. Some important questions to ask include (6):

• Are the two images side by side, on top of each other, or on a diagonal? – helps to tease out the plane of action of the affected muscles and their respective nerves

• What field of gaze makes the double vision worse? – this represents the field of vision of a paretic muscle or opposite the field of action of a restricted muscle

• Can you move your head to correct the vision? – Oblique diplopia due to CN IV paresis often can be distinguished with tilting of the head. Vertical diplopia can be improved with neck extension or flexion. 

• Is there pain with eye movement? – suggests myopathy or orbital process

Isolated 4th nerve palsies:

The trochlear nerve innervates the superior oblique muscle.  Patients often complain of vertical or diagonal diplopia that may correct with head tilt.  CN IV palsies are most commonly due to trauma or are idiopathic in nature (6). In idiopathic CN IV palsies, the patient should be referred to ophthalmology. The palsy often resolves within two weeks.  Important neurologic signs to look for with a CN IV palsy are cerebellar signs. The trochlear nerve exits on the dorsum of the brainstem and may be compressed by a posterior fossa tumor.  

Isolated 6th nerve palsies:

The abducens nerve, or 6th cranial nerve, innervates the lateral rectus muscle. In a 6th nerve plasy, patients will complain of a horizontal diplopia.  There is often inward deviation of the affected eye (esotropia) and symptoms are made worse with lateral gaze to the affected side (6).  This nerve palsy is often idiopathic in etiology, with diabetes mellitus as a risk factor. Be careful to assess for bilateral 6th nerve palsy.  The abducens nerve has a long, isolated course intracranially; tumors can affect the bilateral abducens nerve before other areas of the brain are affected. 

Isolated 3rd nerve palsy:

The oculomotor nerve innervates four muscles and carries parasympathetic fibers that control pupil constriction.  Its course is closely related to the posterior cerebral artery and posterior communicating artery. A palsy of the 3rd nerve (especially with pupillary involvement) may be due to cerebral aneurysm and must emergently be evaluated with CTA, MRA, or intravascular angiography.   An acute isolated 3rd nerve palsy may be due to expanding aneurysm that is at risk of imminent rupture (7).  Pupil sparing 3rd nerve is rarely due to an aneurysm and more often ischemic injury (6,7).  

Internuclear ophthalmoplegia (INO) 

In the setting of horizonal diplopia, also look for internuclear ophthalmoplegia (INO).  An INO is impaired horizontal movement with weak adduction of the affected eye and abduction nystagmus of contralateral eye (8).  This localizes the lesion to the medial longitudinal fasciculous (MLF) in the dorsomedial brainstem tegmentum. The MLF connects the 6th nerve nucleus and medial rectus subnucleus of the 3rd nerve nucleus to coordinate lateral conjugate gaze movement.  In patients <45 years old, it is most commonly caused by multiple sclerosis and is often bilateral (73%) (9).  In older patients, especially those with vascular risk factors, it is caused by cerebrovascular disease and is usually unilateral.   Up to a third have other causes, including infection, tumor, trauma, myasthenia gravis, and Guillain-Barre. Look for historical clues and other neurologic exam findings.  Presence of an INO requires MRI workup. 

Complex motility abnormality

If the diplopia doesn’t isolate to a specific cranial nerve, consider what nerves may be involved and where they are close together to consider anatomic abnormalities. This includes the cavernous sinus, orbital apex, and brainstem.  Brainstem lesions will often have other neurologic deficits identified on exam.  

Cavernous sinus

Cavernous sinus lesions will affect multiple cranial nerves but should not affect visual acuity as the optic nerve does not pass through in relation to the other structures (5,7).  The pituitary gland also resides between the cavernous sinuses. Pituitary mass or apoplexy can compress laterally causing ophthalmoplegia. Another key concern is septic cavernous sinus thrombosis.  These patients will often be septic and febrile. Conversely, consider asking your septic patients if they have double vision! Consider CT and CT venogram of brain and orbits. 

Orbital apex

The orbital apex involves all extraocular muscles, sympathetic fibers, and cranial nerves 2/3/4/6/V1/V2.  Here, the optic nerve is in close anatomic relation to the nerves and muscles of ocular motility. Any ophthalmoplegia with decreased vision or numbness in V1 or V2 distribution should raise concern for orbital apex pathology (5,7).  Consider CT with contrast of the orbits.  

Giant Cell Arteritis

Giant cell arteritis (also known as temporal arteritis) is an important diagnosis to always consider in an elderly patient presenting with diplopia. Missing this diagnosis can lead to permanent vision loss. Diplopia is actually an uncommon finding in GCA, occurring in roughly 5% of cases. However, diplopia has the second highest positive likelihood ratio (LR 3.4) for GCA (the highest being jaw claudication – LR 4.2) (10).  In an elderly patient presenting with diplopia, be on the lookout for other signs and symptoms suggestive of GCA, such as jaw claudication, fevers, vision loss, temporal headaches, PMR, or elevated inflammatory markers.  

Key Points

• Diplopia is a relatively rare presenting complaint in the Emergency Department, and it can portend a wide range of disease, from the benign to the emergent

• A good history and physical exam are key to diagnosis

• Use your physical exam and the presence of other neurologic signs and symptoms to try to localize the lesion and guide imaging choice

• Screen for temporal arteritis in the >60 population

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Expert Commentary

Diplopia is a rare but potentially dangerous chief complaint, making up approximately 0.1% of all ED visits. [1]  In one study of 260 ED patients with non-traumatic, binocular diplopia, 64% had primary diplopia (i.e. no identifiable cause found, likely from microvascular ischemic disease) and 36% had secondary diplopia (i.e. caused by some discernible pathology).  Of patients with secondary diplopia, stroke accounted for nearly 50%, with multiple sclerosis (MS), tumor, aneurysm, myasthenia gravis (MG), and carotid cavernous fistula (CCF) accounting for the other diagnoses. [1]  Given the dangerous etiologies at play, clinicians must approach these patients in a systematic and cautious manner.  (Figure 1)

In patients presenting with diplopia, the first concern must be the possibility of stroke and the need to consider time-sensitive treatment with thrombolytics.  Cranial nerves (CN) 3, 4, and 6 are supplied by the vertebrobasilar arterial system and strokes affecting these nerves most often present with cerebellar dysfunction and/or “crossed signs” or contralateral hemiparesis from involvement of the corticospinal tracts. [2]  Thrombolytic treatment must be considered if the patient is presenting within the appropriate time window and stroke is suspected.  If the patient is outside of the tPA window but suspicion remains for an ischemic process, these patients may benefit from neurologic consultation and MR imaging.  

After considering stroke, look for other associated signs or symptoms that may lead to the correct diagnosis.  If a patient has fevers, facial infections, or meningismus one must consider orbital cellulitis, cavernous venous sinus thrombosis (CVST), meningitis, or encephalitis.  If a patient had a traumatic injury, consider orbital wall fractures, retrobulbar hematoma, increased intracranial pressure (ICP), and intracranial hemorrhage. If a patient has proptosis, chemosis, headaches, and/or facial sensory changes, consider cavernous sinus pathology such as CCF, aneurysm, CVST, mass, or Tolosa-Hunt syndrome (idiopathic inflammatory changes within the cavernous sinus).  If a patient has a severe headache, CN 6 palsy, and/or AMS, consider subarachnoid hemorrhage or other causes of increased ICP. Notably, up to 5% of ruptured PCOM aneurysms present with a CN 6 palsy. [3]  Lastly, if patients have concomitant vision changes/loss, consider pathology of the orbital apex such as mass, infection, and thyroid eye disease.  

If no associated signs or symptoms exists, evaluate the patient for an isolated CN palsy. (Figure 2)  The Margolin paper discusses the importance of obtaining a CTA brain in patients with isolated CN 3 palsy to rule out an intracranial aneurysm.  I would also highlight the importance of obtaining a CTA when patients have an isolated CN 6 palsy as 16% of patients with cavernous sinus carotid aneurysm presented with isolated CN 6 palsy in one study. [4]  In patients with internuclear ophthalmoplegia (INO), admission for MR and neurology consultation is appropriate to rule out stroke and MS, the most common causative pathologies.  Finally, clinicians must consider systemic disease entities such as giant cell arteritis (GCA), MS, and MG. GCA is a vision-threatening disease and must be considered in patients over the age of 60 with transient or persistent diplopia as it is a presenting complaint in 6-27% GCA patients. [5]

Finally, a word of caution when approaching patients with diplopia.  The Margolin article suggests that some patients with isolated diplopia can have non-emergent outpatient follow-up once an aneurysm has been excluded.  Others have also recommended that a CT brain is not useful in the setting of isolated diplopia citing one study showing CT had a sensitivity of 0% in 11 patients with isolated secondary diplopia as the rationale. [6]  I believe these recommendations are unrealistic for many reasons.  First, diplopia is encountered only infrequently in the ED, making the gains of avoiding a CT brain and inpatient neurologic workup minimal.  Furthermore, the neuro-ophthalmologic exam is challenging, and some patients can present with partial palsies or deficits involving multiple cranial nerves, making diagnosis of a specific CN challenging.  Clinicians must also be 100% confident that no other signs or symptoms exist such as jaw claudication in GCA or subtle vision changes and papilledema for pseudotumor cerebri prior to discharge, a difficult task in a busy ED.  Ensuring reliable and urgent neurologic follow-up and outpatient MR imaging can also be difficult or impossible in many health systems. Patients will also likely appreciate obtaining a definitive diagnosis for a concerning neurologic symptom like diplopia in a timely manner.   Moreover, of the 11 patients with isolated secondary diplopia for which CT was not useful in the Nazerian article, two had strokes, another patient had a mass, and another had a CFF that the CT missed. [1]  Diagnoses such as stroke, aneurysm, MS, GCA, and neoplasm can all have morbid ramifications if not expediently diagnosed.  

As such, in patients with isolated diplopia, it may be appropriate for ED clinicians to rule out aneurysm with vascular imaging and admit for neurology consultation and MR to evaluate for more sinister pathology.  ED clinicians should at the very least discuss the case with a consulting neurologist to ensure appropriate management. While the majority of patients with isolated diplopia will go on to be diagnosed with microangiopathic ischemia, given the above concerns, it would seem reasonable for ED clinicians to err on the side of caution and get help from their local neurology colleagues for these challenging patients. 

Citations:

1. Nazerian P, Vanni S, Tarocchi C, et al. Causes of diplopia in the emergency department: diagnostic accuracy of clinical assessment and of head computed tomography. Eur J Emerg Med 2014;21:118-24.

2. Rowe F, UK VISg. Prevalence of ocular motor cranial nerve palsy and associations following stroke. Eye (Lond) 2011;25:881-7.

3. Burkhardt JK, Winkler EA, Lasker GF, Yue JK, Lawton MT. Isolated abducens nerve palsy associated with subarachnoid hemorrhage: a localizing sign of ruptured posterior inferior cerebellar artery aneurysms. J Neurosurg 2018;128:1830-8.

4. Stiebel-Kalish H, Kalish Y, Bar-On RH, et al. Presentation, natural history, and management of carotid cavernous aneurysms. Neurosurgery 2005;57:850-7; discussion -7.

5. Haering M, Holbro A, Todorova MG, et al. Incidence and prognostic implications of diplopia in patients with giant cell arteritis. J Rheumatol 2014;41:1562-4.

6.Kisilevsky E, Kaplan A, Micieli J, McGowan M, Mackinnon D, Margolin E. Computed tomography only useful for selected patients presenting with primary eye complaints in the emergency department. Am J Emerg Med 2018;36:162-4.

Figure 1: Approach to the patient with diplopia

Figure 2: Clinical exam for CN 3 palsy, CN 6 palsy, and INO

Figure 2A: Complete CN 3 palsy

Figure 2B: Complete CN 6 palsy

Figure 2C: Internuclear Ophthalmoplegia

Quentin Reuter, MD

Assistant Professor of Emergency Medicine

Northeast Ohio Medical University

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Citations

Sources:

1. “Causes of Diplopia in the Emergency Department: Diagnostic Accuracy of Clinical Assessment and of Head Computed Tomography.” Nazerian et al. European Journal of Emergency Medicine. 21 April 2014 (2):118-24. Doi 10.097/MEJ.0b01323283636120

2. “Actions of Extraocular Muscles.” UpToDate.com. Accessed 11/22/18. 

3. Image adapted from: “Diagnostic Positions of Gaze.” UpToDate.com Accessed 11/22/18. 

4. Image from: “ZSFG Neuro Report: Multiple Cranial Neuropathies – Spotlight on the Cavernous Sinus.”  Stern, Rachel. UCSF Internal Medicine Chief Resident Hub. Published 28 Oct 2016. Accessed 20 November 2018. https://ucsfmed.wordpress.com/2016/10/28/zsfg-neuro-report-multiple-cranial-neuropathies-spotlight-on-the-cavernous-sinus/

5. “Approach to a Patient with Diplopia in the Emergency Department.” Margolin, Edward and Lam, Cindy.  Journal of Emergency Medicine. Volume 54, Issue 6. June 2018. pp799-806. Accessed 16 November 2018. 

6. “Overview of Diplopia.” Bienfang, Don. UpToDate. Last updated 20 June 2017. Accessed 17 November 2018. 

7. “Third Cranial Nerve (Oculomotor Nerve) Palsy in Adults.” Lee, Andrew. UpToDate. Last updated 19 June 2017. Accessed 17 November 2018. 

8. “Internuclear Ophthalmoparesis.” Frohman, Teresa; Frohman, Elliot.  UpToDate. Last updated 4 December 2017. Accessed 18 November 2018. 

9. “Internuclear Ophthalmoplegia Unusual Causes in 114 of 410 Patients.” Keane, James.  Arch Neurol. 2005;62(5):714–717. doi:10.1001/archneur.62.5.714

10. “Does This Patient Have Temporal Arteritis?” Smetana, Gerald; Shmerling, Robert. JAMA. 2002;287(1):92–101. doi:10.1001/jama.287.1.92

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How To Cite This Post

[Peer-Reviewed, Web Publication]  Rogers A, Loke D. (2019, Nov 18). Approach to Double Vision in the ED. [NUEM Blog. Expert Commentary by Reuter Q]. Retrieved from http://www.nuemblog.com/blog/double-vision.

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Other Posts You May Enjoy

Procedural Sedation

Written by: Mike Conrardy, MD (NUEM PGY-3) Edited by: Will LaPlant, MD (NUEM PGY-4) Expert commentary by: Seth Trueger, MD, MPH

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I Want to be Sedated… 

Mastering Procedural Sedation in the Emergency Department

Procedural sedation, which is not called conscious sedation given the goal is to ensure the patient is not fully conscious, comes in a variety of flavors. Propofol, ketamine, or “ketofol” (the two used together) are typically preferred by emergency physicians, yet there are other options that may be more appropriate depending on the circumstances. In this article, we will provide a brief overview of the basics of procedural sedation, then dive deeper to provide more information about the specific agents that can be used for procedural sedation, including the pros and cons of each.

How many people are necessary to perform procedural sedation?

Generally it is recommended to have three personnel for procedural sedation (typically at least one doctor to perform the procedure and two other providers to provide sedation and monitor the patient), although using two providers (one doctor and one nurse) has been shown to have a similar complication rate.

What type of monitoring is necessary during the procedure?

Monitor vitals, telemetry, SpO2, EtCO2, and the patient’s level of sedation by physical exam. I prefer having EtCO2 if it is available, although remember EtCO2 can lead to false positives (e.g. suspected apnea when apnea is not present), but also provides earlier recognition of hypoventilation.

What other supplies should I have ready?

Oxygen by face mask has been shown to reduce likelihood of hypoxemic episodes. In addition to the above monitoring equipment, at the bedside you should have a bag-valve-mask, oral airway, nasal airway, suction, and intubation supplies ready in case they are needed. A good acronym for remembering all the supplies is SOAP ME: Suction, Oxygen, Airway equipment, Preoxygenation, Monitoring, Medications, ETCO2. As with most procedures, preparation is the most important step.

What are the most common complications of procedural sedation?

Aspiration (<2%), intubation (<2%), laryngospasm (<5%), nausea/vomiting (<5%), respiratory depression (10-20%), hypotension (10-20%), and emergence reactions if using ketamine (up to 20%).

What if my patient is pregnant?

Unfortunately, we have limited data on the safety of procedural sedation in pregnant patients. We do know that pregnant patients are more prone to hypoxemia, can be more difficult to intubate due to physiologic changes to the airway, and have a higher risk of aspiration when sedated after 16 weeks of pregnancy. Clinicians must weigh the risks and benefits of performing sedation in a pregnant patient, but if a procedure is emergent, delay is not a reasonable option. To reduce the risk of aspiration, utilize left lateral decubitus positioning and consider using pre-procedural metoclopramide and antacids. 

Etomidate, propofol, and ketamine may all have an impact on brain development in pregnancy, but evidence in pregnancy is limited for all these medications and they have not been shown to be teratogenic. Propofol may be preferred given it is short acting and is used commonly for general anesthesia in pregnancy. Given that some benzodiazepines have been shown to be teratogenic, midazolam should not be used. 

Prior to giving a sedating agent, is pretreatment necessary?

It is not necessary, but using ondansetron or another antiemetic prior to sedation may reduce vomiting and aspiration (and is at least generally safe and uncomplicated). Midazolam may also useful in conjunction with ketamine to reduce some of the post-sedation side effects, i.e. agitation and emergence reactions, although increases the risk of respiratory depression. More specifics are described below.

After sedation, when can a patient be discharged?

Once a patient is back to their neuromuscular and cognitive baseline, typically 30 minutes after the procedure, they can go home. Our practice is to PO trial a patient prior to discharge and ideally have them go home with a friend or family member who can monitor them at home for a few hours.

Agents:

Propofol:

• Onset/Duration: Onset of ~40 seconds, duration of ~5 min.

• Dose: 0.5 – 1 mg/kg loading dose followed by 0.5 mg/kg doses every 3-5 min or 20mg pushes every 1-2 mins PRN.

• Pros: Short-acting sedative/amnestic, easy to redose, near immediate effect, decreased muscle tone for orthopedic procedures.

• Cons: No analgesia, has pain on injection, can cause hypotension and respiratory depression. 

• Special notes: 

  • Use a larger vein, such as in the antecubital fossa. 

  • Recommended to pretreat with opioid (fentanyl, typically 50-100mcg) or ketamine for procedural pain. The downside of opioid pretreatment is greater risk of respiratory depression.

  • Injection pain can be reduced with intravenous 1% lidocaine mixed with propofol or prior to injecting propofol while occluding the vein. The dose is of lidocaine is 0.5mg/kg or approximately 3-4cc of 1% lidocaine. 

  • Reduce the mg/kg dose in elderly and use lean body weight (calculator) in obese patients. No change is required in patients with impaired liver or kidney function.

Ketamine:

• Onset/Duration: Onset of 30 seconds to 1 minute when given IV, duration of 10-20 min.

• Dose: When used alone, dose is 1-2mg/kg given over 1-2 min followed by 0.5 mg/kg doses every 5-10 min PRN.

• Pros: Dissociative sedative/analgesic with minimal respiratory depression, no impairment of protective airway reflexes, and no hypotension.

• Cons: Ketamine can cause emergence reactions or post-sedation agitation (up to 20%), laryngospasm, nausea/vomiting, hypersalivation, tachycardia, and may increase ICP/IOP. 

• Special Notes:

  • Midazolam 0.05 mg/kg (2-4mg typically) immediately prior to ketamine can reduce rates of emergence reactions although increases rates of respiratory depression.

  • Avoid in patients with psychotic disorders.

  • Recommended for patients who may have a potentially difficult airway because there is less risk for respiratory depression.

  • This is the first-line medication for children above 3 months of its impeccable airway safety and provides both sedation and analgesia as a single agent (no need for opioids).

 Combined Ketamine and Propofol, AKA “Ketofol”:

• Onset/Duration: Same as above for each medication.

• Dose: 0.5 mg/kg of each medication followed by propofol 0.5 mg/kg doses every 3-5 min or 20 mg pushes every 1-2 mins prn. Of note, individual provider choice of dose for each medication varies widely.

• Pros: Potential benefit is ability to use lower doses of both ketamine and propofol with potentially lower risk of adverse events such as hypotension, respiratory depression, emesis, emergence reactions. 

• Cons: May reduce side effects of each medication individually, yet now dealing with the side effects of two medications rather than one alone.

• Special notes: 

  • Research on ketofol is mixed. Systematic reviews have shown that it causes fewer events of respiratory depression and hypotension/bradycardia, yet these events were mostly transient and clinically insignificant. Overall, ketofol has not been shown to reduce clinically significant adverse events or to prolong procedural duration.

Etomidate:

• Onset/Duration: Near immediate onset when given IV, duration of 5-15 min.

• Dose: 0.1-0.15 mg/kg given over 30-60 seconds, redose every 3-5 min.

• Pros: Easy to dose, minimal hemodynamic effect.

• Cons: No analgesia, myoclonus (up to 80%), respiratory depression (10%), nausea/vomiting, pain with injection, and potential for adrenal insufficiency.

• Special Notes:

  • Recommended to pretreat with opioid (fentanyl, typically 50-100mcg) for procedural pain. The downside of opioid pretreatment is greater risk of respiratory depression.

  • In rare cases of severe myoclonus, treat with 1-2 mg IV midazolam every minute until resolved. Some providers pretreat with 0.015 mg/kg etomidate to prevent myoclonus.

  • Dose must be reduced for patients who are elderly or have renal/hepatic dysfunction.

  • Not recommended for orthopedic procedures given the frequency of myoclonus.

Midazolam (requires opioid co-administration):

• Onset/Duration: Onset of 2-5 min, duration of 30-60 min.

• Dose: 0.02-0.03 mg/kg or 0.5-1 mg doses IV every 2-5 min prn, typically not exceeding 5 mg total.

• Pros: Provides anxiolysis and amnesia.

• Cons: Not as effective for true procedural sedation as shorter acting medications, no analgesia, higher risk of respiratory depression when combined with fentanyl compared to other medications.

• Special Notes:

  • When combining with fentanyl for pain/sedation, give midazolam doses as above first until the desired anxiolysis is achieved, typically 1-2 doses, then give 0.5 mcg/kg doses of fentanyl every 2 min PRN, carefully titrated to effect, with maximum dose of 5 mcg/kg or approximately 250 mcg.

  • Prolonged sedation is high risk in patients who are elderly, obese, or have hepatic/renal dysfunction.

  • Use for anxiolysis rather than for true procedural sedation.

Barbiturates (Methohexital):

• Onset/Duration: Immediate onset, duration of < 10 min.

• Dose: 0.75-1 mg/kg followed by 0.5 mg/kg doses IV every 2 min prn.

• Pros: Fast onset, short duration sedation.

• Cons: No analgesia, causes hypotension/tachycardia, can precipitate seizures.

• Special Notes: 

  • You are probably never going to use this drug unless you are in a very resource limited setting, but you might as well know it is an option.

Dexmedetomidine:

• Onset/Duration: Onset of 5-10 min, duration of 60-120 min.

• Dose: Not well studied for procedural sedation, options are intranasal 2-3 mcg/kg or bolus of 0.5-1.0 mcg/kg over 10 min followed by infusion of 0.2-0.7 mcg/kg/hr.

• Pros: Preserved muscle tone and respiration, much like natural sleep, provides some analgesia.

• Cons: Potentially unpredictable effect, not well studied, risk of hypotension/bradycardia, longer acting.

• Special Notes:

  • Delayed time to onset may limit application in the ED

  • Dexmedetomidine is just not ready for primetime yet, but worth further investigation.

Nitrous oxide:

• Onset/Duration: Immediate onset, off within seconds.

• Dose: 30-50% mixture with 30% oxygen.

• Pros: Provides analgesia, anxiolysis, and sedation all in one.

• Cons: Not typically available in emergency departments, needs scavenging system.

• Special Notes:

  • Have been trying for years to get this constantly vented into all our patient rooms, but still no luck with our administration.

Summary Points:

• Propofol, ketamine, ketofol, and etomidate are our typical first-line medications in the emergency department for procedural sedation.

• Ketamine is preferred for kids.

• In adults, propofol or ketofol is best for hemodynamically stable adults requiring procedural sedation, particularly for joint reductions because it does not cause myoclonus and is easy to titrate.

• Etomidate provides greater hemodynamic stability and is best for cardioversion or procedures in patients with hemodynamic compromise, but the downside is myoclonus which may reduce procedural success.

• Ketamine alone is best in patients with a difficult airway or at high risk for respiratory compromise because it does not cause respiratory depression.

• Use what you are most comfortable with, and remember that adequate preparation is key.

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Expert Commentary

Thank you for the excellent and concise review. It’s been interesting to see procedural sedation practices change over the course of my training and career, as newer safe and easy options (propofol and ketamine) gained rapid popularity but have been challenged by drug shortages and well-publicized celebrity tragedies. Here is my typical practice, which is certainly not the only correct way but my strong preference:

A few factors on when to think about procedural sedation:

-Any painful procedure, particularly for potential for longer duration. This includes incision and drainage (especially Bartholin’s) and disimpaction. I’ve gotten some odd looks for suggesting it but it works out better for everyone involved. 

-Consultant’s procedures, particularly big traumatic injuries which look nasty and like they need to be fixed. It’s easy to forget how terrible it is for the patient.

When I think about avoiding:

-medically complex patients

-difficult airways

-procedures that can wait

-procedures with low likelihood of success even under the best circumstances. If they need to go to the OR no matter what, that might be the best place to start.

My one exception are situations that are currently painful and need to be fixed now and can be fixed quickly, e.g. dislocated ankles. The likelihood of success with 100mcg of fentanyl within seconds to resolve a huge amount of pain now is exceedingly favorable.

The worst situation is trying to avoid procedural sedation with “just some morphine and maybe a little lorazepam” which quickly devolves into “a little more morphine” and “hmm maybe another dose of lorazepam.” Now it’s a procedural sedation that is both ineffective and unsafe.

My general process:

First I print out a checklist I made with the following preparation steps (details below):

RSI box (succinylcholine)

VL

airway cart (LMA, PEEP valve, DL gear)

nasal ETCO2 (plus ETT adapter)

4mg ondansetron now

bottle ketamine

bottle propofol

room ready (including suction, bag, anything required for the procedure)

Department ready?

Am I ready?

Procedure plan

Post-procedure planning (sling, splint)

The general principle is to set up at least as much as if I were performing RSI. A lot of this may seem like over-preparation, but the more I prepare, the luckier I get. Here is some more detail on each item:

RSI box (succinylcholine)

2 main purposes for the RSI box. First, if things go south, I will be intubating the patient, and need the medications to do so (i.e. NMBA). Second, if I am using ketamine, there is a small but nontrivial chance of laryngospasm, and of jaw thrust and bagging do not fix it, the patient needs NMBA. This is not a time to debate roc vs sux, so I always have sux in the room (even if roc isn’t slower when dosed appropriately at ≥1.2mg/kg, I don’t want to have to argue about it at the RCA). The easiest way for me to get these medications in the room is grabbing our RSI box, but this will depend on your department; simply grabbing a vial of sux with 1.5mg/kg is sufficient.

VL

If things go south, this is not the time for the intern to practice their DL. I always have the hyperangulated VL ready to go at the head of the bed, with a combo Mac VL/DL blade and a traditional Mac DL as backup, with stylets loaded with tubes ready to go. 

Airway cart 

We have nicely built airway carts with everything I need for bagging, difficult bagging, and difficult intubation. Primarily, what I want is gear for bagging, i.e. LMA and PEEP valve. All the usual backup is here as well (oral/nasal airways, bougie, cric gear).

Nasal ETCO2 (and ETT adapter)

The literature on end tidal in procedural sedation is interesting but I think generally answers a different question than the one I care about. I don’t look for qualitative changes in waveforms or quantitative changes in ETCO2 to predict hypoventilation; rather, it is the quickest and easiest way to see if the patient is breathing. No staring at their chest hoping to see chest rise. Simply look at the monitor: either there is a waveform and they are breathing, or there is not and they are not. It’s like a sedative for me, similar to supervising an intern using VL instead of DL: it makes the procedure much less stressful for me.

Additionally, by using ETCO2, it is now safe to provide supplemental oxygen via nasal cannula or reservoir facemask so if things go south, there is a much wider safety margin (i.e. the patient is preoxygenated for intubation).

4mg ondansetron now

As discussed above, it might help, it may not, and it’s safe and easy.

bottle Ketamine

bottle Propofol

I’ll discuss my medication strategies below, but the bottom line is I like to have multiple 100s of mg of each medication ready for each patient, because when I need to redose, it can be needed in a very short time.

Room ready

Other equipment I make sure is ready: suction, bag for mask ventilation. Other items like do I need vaseline gauze for splinting over an abrasion?

Is the Department ready?

Was an 80 year old with abdominal pain just roomed? Should I lay eyes on them and make a quick decision about an obvious CT? Is there a hospitalist hanging around who I can tell about another patient to send upstairs before I get stuck in a sedation for 45 minutes? Should I discharge anyone?

Am I ready?

Do I need to go to the bathroom? Has it been hours before I’ve had any calories?

Procedure plan

I always make sure to have a clear plan for the procedure—not just the sedation—well before we start. Who is doing what? What technique are we using? What are backup plans? Of course these questions apply to the sedation as well.

If a non-EM physicians is performing the procedure (e.g. ortho, or gen surg pulling a tunneled line) I try to make sure that they understand my definition of “ready” is not the same as in the OR, and I make sure they are ready to start the actual procedure as soon as the meds are working. This is not a judgment in any way; rather, the ER simply isn’t the OR.

Post-procedure planning

Few things are more frustrating than getting a difficult shoulder reduced only to have it slip out while someone is hunting down the sling I forget to get beforehand, that I knew I would need (see also: ordering post-intubation meds with RSI meds in an intubation). Obviously if something needs to be splinted we need the gear and whoever is doing the splint. And, if there are abrasions going under the splint, petroleum gauze, etc.

Medication choices

I typically choose between ketamine and propofol on a spectrum. 

Factors on the propofol side: young, healthy, BP/respiratory reserve, shorter procedure, ortho procedure (propofol is much better at loosening up patients, plus these often end quickly).

Factors on the ketamine side: older, more comorbidities, less respiratory reserve, longer procedures, non-reduction procedures, more protractedly-painful procedures (e.g. I&D).

Obviously these are not absolutes and I tend to plan on using ketofol quite a bit. I usually have enough cognitive space and hands available to dose them separately (generally 0.5mg/kg ketamine first, then 0.5mg/kg propofol as needed) but in more constricted settings I will mix 1:1 if I don’t have the bandwidth. 

I will say I have been tending to more and more ketamine-only sedations. Usually I start with the intention of using ketamine-first ketofol, particularly if the patient needs to be loosened up for a reduction, but I am continually surprised by how little I end up needing the propofol.

As noted above, for solo propofol, I pretreat with fentanyl as propofol is not inherently analgesic. 

I appreciate the debate about midazolam for pretreatment for ketamine, but the rates of substantial post-sedation agitation are low enough that I simply treat that when it happens, as not all but most ketamine respiratory depression only happens with co-administered sedatives. 

Other than lack of availability of other options, there is no reason to use fentanyl/midaz anymore.

Lastly, I’ve stopped using etomidate. The rate of myoclonus is simply too high. Myoclonus easily defeats the reduction, and even for cardioversion, it makes checking the rhythm, getting an ECG, monitoring the sat, etc. very difficult. Ultimately, it’s just a headache we don’t need, particularly as we have so many other safe and effective agents.

As I said above, these are more my style preferences than the only absolutely correct choices, and I am always happy to at least discuss adapt to the circumstances including others’ preferences (or trying something different so the residents can gain experience with different techniques).

Seth Trueger, MD, MPH, FACEP

Assistant Professor

Northwestern Emergency Medicine

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Citations

1. Brown TB, Lovato LM, Parker D. Procedural sedation in the acute care setting. Am Fam Physician 2005; 71:85.

2. Swanson ER, Seaberg DC, Mathias S. The use of propofol for sedation in the emergency department. Acad Emerg Med 1996; 3:234.

3. Miner JR, Burton JH. Clinical practice advisory: Emergency department procedural sedation with propofol. Ann Emerg Med 2007; 50:182.

4. Euasobhon  P, Dej‐arkom  S, Siriussawakul  A, Muangman S, Sriraj  W, Pattanittum P, Lumbiganon  P. Lidocaine for reducing propofol‐induced pain on induction of anaesthesia in adults. Cochrane Database of Systematic Reviews 2016, Issue 2. Art. No.: CD007874. DOI: 10.1002/14651858.CD007874.pub2.

5. Messenger DW, Murray HE, Dungey PE, et al. Subdissociative-dose ketamine versus fentanyl for analgesia during propofol procedural sedation: a randomized clinical trial. Acad Emerg Med 2008; 15:877.

6. Strayer RJ, Nelson LS. Adverse events associated with ketamine for procedural sedation in adults. Am J Emerg Med 2008; 26:985.

7. Adnolfatto G et al. Ketamine-Propofol Combination (Ketofol) versus propofol alone for Emergency Department Procedural Sedation and Analgesia: A Randomized Double-Blind Trial. Annals of Emergency Medicine. 2012;59(6):504-512.e2

8. Miner JR et al. Randomized, Double-Blinded, Clinical Trial of Propofol, 1:1 Propofol/Ketamine, and 4:1 Propofol/Ketamine for Deep Procedural Sedation in the Emergency Department. Annals of Emergency Medicine. 2015;65(5):479-488.e2

9. Yan JW, McLeod SL, Iansavitchene A. Ketamine-Propofol Versus Propofol Alone for Procedural Sedation in the Emergency Department: A Systematic Review and Meta-analysis. Acad Emerg Med 2015; 22:1003.

10. Miner JR, Danahy M, Moch A, Biros M. Randomized clinical trial of etomidate versus propofol for procedural sedation in the emergency department. Ann Emerg Med 2007; 49:15.

11. Falk J, Zed PJ. Etomidate for procedural sedation in the emergency department. Ann Pharmacother 2004; 38:1272.

12. Sacchetti A, Senula G, Strickland J, Dubin R. Procedural sedation in the community emergency department: initial results of the ProSCED registry. Acad Emerg Med 2007; 14:41.

13. Keim SM, Erstad BL, Sakles JC, Davis V. Etomidate for procedural sedation in the emergency department. Pharmacotherapy 2002; 22:586.

14. Hüter L, Schreiber T, Gugel M, Schwarzkopf K. Low-dose intravenous midazolam reduces etomidate-induced myoclonus: a prospective, randomized study in patients undergoing elective cardioversion. Anesth Analg 2007; 105:1298.

15. Horn E, Nesbit SA. Pharmacology and pharmacokinetics of sedatives and analgesics. Gastrointest Endosc Clin N Am 2004; 14:247.

16. Bahn EL, Holt KR. Procedural sedation and analgesia: a review and new concepts. Emerg Med Clin North Am 2005; 23:503.

17. Frank RL. Procedural sedation in adults outside the operating room. Wolfson AB, and Grayzel J (Ed.) UpToDate (2018).

18. Hsu DC and Cravero JP Pharmacologic agents for pediatric procedural sedation outside of the operating room. Stack AM and Randolph AG (Ed.) UpToDate (2018).

19. G. Haeseler, M. Störmer, J. Bufler, R. Dengler, H. Hecker, S. Piepenbrock, et al. Propofol blocks human skeletal muscle sodium channels in a voltage-dependent manner. Anesth Analg, 92 (2001), pp. 1192-1198

20. J. Ingrande, H. J. M. Lemmens; Dose adjustment of anaesthetics in the morbidly obese, BJA: British Journal of Anaesthesia, Volume 105, Issue suppl_1, 1 December 2010, Pages i16–i23.

21. Neuman G and Koren G. Safety of Procedural Sedation in Pregnancy. J Obstet Gynaecol Can. February 2013, pages 168-173.

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How To Cite This Post

[Peer-Reviewed, Web Publication]  Conrardy M, LaPlant W. (2019, Nov 11). Procedural Sedation. [NUEM Blog. Expert Commentary by Trueger S]. Retrieved from http://www.nuemblog.com/blog/procedural-sedation.

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Ultrasound Confirmation of Endotracheal Tube Placement

Written by: Maurice Hajjar, MD (NUEM PGY-2) Edited by: Alex Ireland, MD (NUEM PGY-4) Expert commentary by: John Bailitz, MD

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Introduction

Although the cuff is inflated and the laryngoscope is removed, no emergent intubation is complete without first confirming the correct placement of the endotracheal tube (ETT). A variety of indicators exist that can confirm ETT placement into the trachea rather than the esophagus—chest rise, condensation in the tube, auscultation of breath sounds, lack of abdominal breath sounds, visualization with a video or fiberoptic laryngoscope, and both quantitative waveform capnography and qualitative (or colorimetric) capnometry. 

However, situations exist in which these techniques may be unavailable, impractical, or can even fail or mislead providers. A hectic cardiac arrest scenario may present the perfect storm. Chest compressions preclude providers from visualizing chest rise. Gastric contents or blood can mask tube condensation or preclude visualization of the cords with a video laryngoscope. Colorimetric capnometry can have low sensitivity in patients without a palpable pulse and can also be falsely positive if exposed to blood or gastric contents [1]. The sensitivity of quantitative waveform capnography decreases significantly in cardiac arrest as it requires adequate pulmonary circulation which may be absent in this or other low flow states [2,3]. Furthermore, despite increasing use, it may be unavailable at the institution altogether [4]. 

Taken together, there is a relatively high risk of esophageal intubation in this scenario which bears disastrous consequences. Any single method of confirming ETT placement is imperfect; as such, there is room for unique modalities in emergent intubations. 

Using Point of Care Ultrasound to Confirm Endotracheal Tube Placement

Why it works

Point of care ultrasound (POCUS) is readily available in emergency departments (EDs) and intensive care units in most settings and both intensivists and emergency providers have at least some training in its use at the bedside. Conceptually, the use of transtracheal US to confirm ETT placement relies on the differing anatomy of the trachea and esophagus. Recall that the trachea remains open due to cartilaginous rings while the esophagus will collapse unless filled (e.g., by an ETT). Thus, an esophagus with an ETT will be more readily visualized adjacent to the trachea than one without. 

The sonographic appearance of the trachea is characterized by a bright, hyperechoic curvilinear structure with posterior shadowing and reverberation artifact (Figure 1). If the trachea was intubated, then a single bullet sign [5] (Figure 2) will be visualized, which is an increase in both the echogenicity and the posterior artifact indicating the presence of an air-filled ETT. 

Figure 1: Sonographic view of trachea showing air-mucosa interface with posterior reverberation and shadowing artifact. [Photo courtesy of John Bailitz, MD]

Figure 2: Clip demonstrating the bullet sign: a single air-mucosa interface with increased posterior shadowing and artifact indicates the trachea has been intubated. [Photo courtesy of John Bailitz, MD]

Conversely, if the esophagus is intubated, then a double tract sign [6] (Figure 3) will be visualized, which is the appearance of a “second” trachea, or a similar hyperechoic line with posterior shadowing and reverberation artifact lateral to that of the trachea. This second air-mucosa interface indicates that the esophagus is stented open by an air-filled ETT.

Figure 3: Clip demonstrating the double tract sign: the appearance of a second air-mucosa interface with posterior artifact adjacent to the trachea indicates the esophagus has been intubated. [Photo courtesy of John Bailitz, MD]

How it is used

As alluded to above, the primary use of US in confirming ETT placement is determining that the trachea, rather than the esophagus, has been intubated. This can be confirmed either statically or dynamically. In static confirmation, the US probe is used post-intubation to visualize either the bullet sign or the double tract sign. Additionally, if the operator is uncertain, she or he could lightly move the ETT up and down to ascertain if there is movement in the region of the trachea or esophagus7. In dynamic confirmation, the US probe is used during intubation to visualize the increase in artifact as the tube passes into the trachea or the appearance of artifact as the tube passes into the esophagus.

Of note, transtracheal US cannot be used to determine the distance of the ETT from the carina or to determine if the right mainstem bronchus has been intubated. Thoracic ultrasound, however, can be used to observe bilateral pleural sliding but requires multiple ventilations. Additionally, anatomical variance may cause the esophagus to be positioned directly posterior to the trachea, leading to false positive tracheal intubations [8]. 

Technique [6–8]

1. Use a high frequency linear probe with sonographic gel applied liberally. 

2. Place the probe superior to the suprasternal notch in a transverse orientation, being careful to minimize downward pressure.

3. Adjust sonographic depth (depending on body habitus) to visualize the trachea and, if visible, the esophagus which will typically lie posterolateral to the trachea. 

4. Interpret:

   1. If performing static confirmation post-intubation, look for the bullet sign or the double tract sign.

   2. If performing dynamic confirmation during intubation, look for an increase in motion artifact posterior to the trachea or the appearance of a “second” trachea (double tract sign). 

Brief Review of Evidence

A meta-analysis pooled data from 11 studies and 969 intubations and showed an aggregate sensitivity of 98% and specificity of 94% in emergency intubations, with capnography as the gold standard [5]. More recently, a meta-analysis of 17 studies and 1,596 patients showed a sensitivity of 98.7% and specificity of 97.1%, with a positive likelihood ratio of 34.4 and a negative likelihood ratio of 0.019. This compares favorably to pooled data from studies examining capnography, which in one meta-analysis showed slightly lower sensitivity but similar specificity (93% and 97%, respectively)2,10. Furthermore, POCUS has several distinct advantages over capnography as mentioned above. 

POCUS is a skill familiar to many ED providers. A pilot study in a non-emergent, controlled operating room setting of patients intubated by anesthesiologists demonstrated that ED providers with no formal airway US training could identify tracheal intubations with a sensitivity and specificity approaching 100% [8]. In a cadaver study, the performance of residents compared favorably to that of ultrasound fellowship-trained emergency physicians, ranging from 91-100% sensitivity and 48-96% specificity depending on cadaver body habitus [11].

In the emergent setting, ultrasound assessment not only has high sensitivity and specificity for tracheal intubation but can be performed rapidly. A study of patients being intubated for impending respiratory failure, cardiac arrest, or trauma found that ED residents trained in airway US could identify tracheal intubation using ultrasound with 98.9% sensitivity, 94.1% specificity, and a 93% concordance with criterion standard quantitative capnography. Furthermore, confirmation of ETT tube with ultrasonography could be performed within an average of nine seconds [6].  During CPR, real-time tracheal ultrasonography was 100% sensitive and 85.7% specific for detecting tracheal versus esophageal intubation compared to the combined criterion standard of waveform capnography and auscultation. Furthermore, this study examined ultrasonography performed during chest compressions, suggesting that ultrasonography can be a highly reliable method of ETT confirmation without interrupting compressions [12]. 

Summary

• Established methods of confirming ETT placement in an emergent intubation are imperfect. 

• Quantitative waveform capnography has reduced sensitivity in the setting of a cardiac arrest or other low-flow states and requires multiple ventilations prior to confirmation. 

• Ultrasound can rapidly be used to confirm ETT placement with comparable sensitivity and specificity to criterion standards without requiring ventilation or an interruption of chest compressions.

• Providers with some familiarity with US can use it to distinguish between tracheal and esophageal intubations reliably.

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Expert Commentary

Thank you for his outstanding review of an exciting and relatively new application in Emergency Ultrasound. Although the literature on this topic has exploded in the last few years, tracheal ultrasound was already included in the 2015 ACLS Guidelines as a reliable method to confirm endotracheal intubation. 

As a longtime ultrasonographer and resuscitationist, I find this application particularly useful in two common ED situations. The first is out of hospital cardiopulmonary arrest in which the patient was already intubated by paramedics in the field. As the patient arrives in the resuscitation bay, there are a number of competing priorities. Rapid confirmation of correct endotracheal tube placement during chest compressions allows the team to quickly move on to other priorities. The second is the difficult intubation of the crashing ED patient. Particularly, in patients who are obese or otherwise have distorted airway anatomy, the ultrasound machine provides real time visualization of the endotracheal tube placement, or a rapid confirmation immediately after. In either situation, the ultrasound machine will certainly be helpful not only for confirmation of ETT location, but further for ruling out pneumothorax and main stem intubation, before moving onto other causes of cardiac arrest such as cardiac tamponade, massive PE, and blood loss. 

Regarding technique, dynamic visualization during intubation may be difficult particularly if external laryngeal manipulation while is being preformed. So static visualization immediately after placement is often more feasible. Forceful, or up and down movement of the tube may dislodge an endotracheal tube, damage the airway, or stimulate a cough or vomiting in the non-paralyzed patient. Instead, simply gently rotating the tube from side to side creates an easily visible change in the tracheal air column if correctly located, or “esophageal sliding” of the mucosa over the endotracheal tube if incorrectly placed in the esophagus.

Final shout outs to the authors of this well written blog. But also to Dr. Michael Gottlieb, full disclosure my former fellow, for his considerable research in this area. Dr. Gottlieb first identified the need for better confirmatory methods as an EM intern. Although I was initially skeptical as a resuscitationist, Dr. Gottlieb quickly convinced me with a well-done literature review during which he identified a gap in the existing literature. Dr. Gottlieb then took the initiative and turned one research question into an exciting are of scholarship for his career and the many fellows that followed that benefitted from Dr. Gottlieb’s mentoring. This is such a wonderful example of turning a simple clinical question into a rich and rewarding area of leadership through scholarship!

John Bailitz, MD

Vice Chair for Academics

Department of Emergency Medicine

Northwestern Feinberg School of Medicine

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Citations

1. MacLeod BA, Heller MB, Gerard J, Yealy DM, Menegazzi JJ. Verification of endotracheal tube placement with colorimetric end-tidal CO2 detection. Ann Emerg Med [Internet] 1991 [cited 2019 Jan 8];20(3):267–70. Available from: http://www.ncbi.nlm.nih.gov/pubmed/1899985

2. Li J. Capnography alone is imperfect for endotracheal tube placement confirmation during emergency intubation. J Emerg Med [Internet] 2001 [cited 2019 Jan 8];20(3):223–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/11267809

3. Takeda T, Tanigawa K, Tanaka H, Hayashi Y, Goto E, Tanaka K. The assessment of three methods to verify tracheal tube placement in the emergency setting. Resuscitation [Internet] 2003 [cited 2019 Jan 8];56(2):153–7. Available from: https://www.sciencedirect.com/science/article/pii/S0300957202003453

4. DeIorio NM. Continuous end-tidal carbon dioxide monitoring for confirmation of endotracheal tube placement is neither widely available nor consistently applied by emergency physicians. Emerg Med J [Internet] 2005 [cited 2019 Jan 13];22(7):490–3. Available from: http://www.ncbi.nlm.nih.gov/pubmed/15983084

5. Das SK, Choupoo NS, Haldar R, Lahkar A. Transtracheal ultrasound for verification of endotracheal tube placement: a systematic review and meta-analysis. Can J Anesth Can d’anesthésie [Internet] 2015 [cited 2019 Jan 11];62(4):413–23. Available from: http://www.ncbi.nlm.nih.gov/pubmed/25537734

6. Chou H-C, Tseng W-P, Wang C-H, et al. Tracheal rapid ultrasound exam (T.R.U.E.) for confirming endotracheal tube placement during emergency intubation. Resuscitation [Internet] 2011 [cited 2019 Jan 9];82(10):1279–84. Available from: http://www.ncbi.nlm.nih.gov/pubmed/21684668

7. Chao A, Gharahbaghian L. Tips and Tricks: Airway Ultrasound [Internet]. Am. Coll. Emerg. Physicians Emerg. Ultrasound Sect. 2015 [cited 2019 Jan 13];Available from: https://www.acep.org/how-we-serve/sections/emergency-ultrasound/news/june-2015/tips-and-tricks-airway-ultrasound/#sm.00000hnz0e2u2ofnizwz7io2f5wg6

8. Werner SL, Smith CE, Goldstein JR, Jones RA, Cydulka RK. Pilot study to evaluate the accuracy of ultrasonography in confirming endotracheal tube placement. Ann Emerg Med [Internet] 2007 [cited 2019 Jan 9];49(1):75–80. Available from: http://www.ncbi.nlm.nih.gov/pubmed/17014927

9. Gottlieb M, Holladay D, Peksa GD. Ultrasonography for the Confirmation of Endotracheal Tube Intubation: A Systematic Review and Meta-Analysis. Ann Emerg Med [Internet] 2018 [cited 2019 Jan 16];72(6):627–36. Available from: http://www.ncbi.nlm.nih.gov/pubmed/30119943

10. Gottlieb M, Bailitz J. Can Transtracheal Ultrasonography Be Used to Verify Endotracheal Tube Placement? Ann Emerg Med [Internet] 2015 [cited 2019 Jan 11];66(4):394–5. Available from: http://www.ncbi.nlm.nih.gov/pubmed/25805115

11. Gottlieb M, Bailitz JM, Christian E, et al. Accuracy of a novel ultrasound technique for confirmation of endotracheal intubation by expert and novice emergency physicians. West J Emerg Med [Internet] 2014 [cited 2019 Jan 13];15(7):834–9. Available from: http://www.ncbi.nlm.nih.gov/pubmed/25493129

12. Chou H-C, Chong K-M, Sim S-S, et al. Real-time tracheal ultrasonography for confirmation of endotracheal tube placement during cardiopulmonary resuscitation. Resuscitation [Internet] 2013 [cited 2019 Jan 10];84(12):1708–12. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23851048

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How To Cite This Post

[Peer-Reviewed, Web Publication] Hajjar M, Ireland A. (2019, Nov 4). Ultrasound Confirmation of ETT Placement. [NUEM Blog. Expert Commentary by Bailitz J]. Retrieved from http://www.nuemblog.com/blog/us-ett.

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Leaving Against Medical Advice

Written by: Brett Cohen, MD (NUEM PGY-3) Edited by: Will Ford, MD, MBA (NUEM ‘19) Expert commentary by: Larry Weiss, MD

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Background

Leaving the ED prior to a completed workup is relatively common and can place both providers and patients at risk.

• AMA discharges make up about 2% of all discharges in the USA [1]

• Patients that are discharged AMA are associated with a higher mortality than planned discharges [2] (ORadj 2.05; 95% [CI 1.48-2.86])

• Patients that are discharged AMA are more likely to initiate lawsuits against their providers [3], some studies suggest that they may be up to 10 times more likely to sue the Emergency Physician compared to other ED patients [5]

Despite these risks, patients have a fundamental right to refuse medical care, even when doing so may not be in their own best interests.[4]

Risk Factors for an AMA Discharge [1, 5]

Left Without Being Seen

In this scenario, the patient has not yet interacted with a physician. There is not much to do here as long as the provider never met the patient, if so, they would be in a different category. There are no known cases where the ED, or ED Providers, have been sued and found to be at fault or responsible for an outcome. People have the right to walk in and walk out as they choose. 

The Eloped Patient

If the provider has met the patient and they leave the department before completion of their work-up or before having had the AMA discharge conversation, they are considered to have eloped. Most departments have their own policy for this situation, it is recommended to follow your own departmental policy. If not, here are a few things to do:

• Look for the patient a few times (once every 20 minutes for an hour)

• If witnessed by RN, have them document the time the patient left as well as the status of their IV. If an IV is still in place, first try to contact the patient and then their emergency contact. If no success, contact the police non-emergently to aid in locating the patient. 

• Review sent labs, if there are any critical values contact the patient or their emergency contact and advise to return to this or the closest ED. If there are any life-threatening findings and the patient is unable to be contacted, contact the police non-emergently. 

• Document the time you were made aware the patient left as well as your attempts to contact them. If prior to desertion the patient was awake and alert and appeared to have capacity, document this. If the patient is at risk and you are truly uncertain of capacity, notify the police and document as such.

How to Navigate an AMA Discharge in the Emergency Department

The capacity of a patient to make the decision to leave the hospital against medical advice is the most important feature of the AMA discharge process. There are four basic elements to capacity: [1]

1. The ability to communicate with the provider

2. The understanding of treatment options including the option of refusal

3. The ability to reason and explain ‘why’ he or she is making the choice

4. The understanding of consequences of choices

A conversation with a patient that desires to be discharged AMA is one of the most important parts of this process. Through the IDEA method, the physician will be able to assess the capacity of the patient, reinforce the need to continue care if clinically indicated, as well as lay a foundation for follow-up care:

Investigate

• Investigate barriers to communication (and resolve them if able)

• Investigate patient’s rational for wanting to leave AMA

• Investigate if anyone else can help convince the patient (family, friend, PCP)

Discuss

• Discuss working or actual diagnosis and findings

• Discuss recommended course of treatment including alternatives and comfort measures you can provide

• Discuss risks of refusing treatment, including disability/death

Evaluate Understanding

• Have the patient explain their diagnosis/findings in their own words. “I understand” is not enough

• Have the patient explain the consequences of them leaving AMA

Allow the AMA

• Go over discharge instructions including reasons to return

• Ensure the patient understands that they can return at any time

• Have the patient sign the AMA form. For a witness, use a family member if possible, or an RN

Patients that Lack Capacity

Patients have a fundamental right to refuse care, however those that lack decision-making capacity or are at risk for harm to self or others cannot refuse treatment, and therefore cannot leave AMA. The ED provider has an obligation to try and restore decision-making capacity as soon as possible. Some steps to do this include:

• Locating a surrogate decision maker

  • If there is no designated healthcare POA, in most states the hierarchy is: Adult Spouse > Adult Children > Parents of Patient

• Locating an Advance Directive

• Reassessments of Capacity over time (sober reassessments)

A common dilemma arises when the right to refuse care is taken away from a patient, and there are two laws which protect the ED physician in these cases:

• Emergency Consent: Physicians are authorized to provide treatment to a patient without capacity when interventions are needed to prevent serious physical harm or death, and the need is certified by at least two physicians writing in the medical record [7]

• Federal law allows for restraint or seclusion only when needed to ensure the immediate physical safety of the patient, a staff member, or others and must be discontinued at the earliest possible time based on an individualized patient assessment and reevaluation [8]

Documentation

A well written addendum for an AMA discharge will include the following:

• Discussion of the treatment(s) offered

• Discussion of the risks/benefits of further treatment and for no treatment

• Reasons for refusal

• Efforts taken at negotiating with the patient including possible alternative treatments, risks/benefits of alternative courses as well as comfort measures offered

• Steps taken to secure a written informed refusal

• An assessment that the patient has capacity to make the decision, and if there are concerns or gray areas involving capacity note what they were and why it was resolved in the manner chosen

Example Addendum

The patient expresses the desire to leave against medical advice (AMA). Their reasoning for leaving AMA is due to ***. They presented with a chief complaint of *** and I have explained my concern that based on their complaint in addition to my history, physical exam, and studies returned to date that this may represent ***. In addition, I explained that their work-up is currently incomplete and I would recommend *** to complete it. I also explained my concern that leaving at this time places them at risk for their condition worsening, critical illness, and death or permanent disability including ***. I have also offered an alternative treatments options including ***.

The patient explained in their own words all of my concerns including the consequences of refusing further treatment including death or permanent disability. I have also discussed my concerns with *** who was also unable to convince the patient to stay. The patient is clinically sober and has no injury that would affect their cognition. In addition, they appear to have intact insight, judgement and reason and in my opinion has the capacity to make their own healthcare decisions. 

Given that the patient was unwilling to stay I *** to increase the probability of a good outcome. I ensured there were no communication barriers with the patient by ***. A written informed refusal document was *** signed by the patient after our conversation. Outpatient follow-up was offered with ***. The patient was encouraged to seek care immediately if they would like to complete the work-up or if they have any new concerns.

This conversation was witnessed by ***

AMA paperwork was*** completed and signed.

References

1. Ethics Seminars: A best practice-approach to navigating the against-medical-advice discharge. Acad Emerg Med. 2014 Sep;21(9):1050-7. doi: 10.1111/acem.12461

2. Increased Risk of Mortality and Readmission among Patients Discharged Against Medical Advice. Southern, William N. et al. The American Journal of Medicine , Volume 125 , Issue 6 , 594 – 602

3. Monico EP, Schwartz I. Leaving against medical advice: facing the issue in the emergency depart- ment. J Healthcare Risk Manage 2009;29:6–15.

4. Cruzan v. Missouri Department of Health, 497 U.S. 261 (1990); Schloendorff v. Society of New York Hospital, 105 N.E. 92 (N.Y. 1914).

5. Bitterman RA. Against medical advice: When should you take “no” for an answer? Lecture presented at ACEP Scientific Assembly. Chicago, Oct. 30, 2008.

6. The importance of a proper against-medical-advice (AMA) discharge: how signing out AMA may create significant liability protection for providers. Frederick Levy, Darren P. Mareiniss, Corianne Iacovelli. J Emerg Med. 2012 Sep; 43(3): 516–520.  Published online 2011 Jun 28. doi: 10.1016/j.jemermed.2011.05.030

7. Georgia Department of Human Resources. O.C.G.A. §§ 37-3-163(e), 37-7-163(e). Jun 29, 2014. 

8. U.S. Government. Federal Register 42 C.F.R. § §482.13(e). Available at: http://www.gpo.gov/fdsys/pkg/CFR-2010-title42-vol5/pdf/CFR-2010-title42-vol5-sec482-13.pdf. Accessed Jun 29, 2014. 

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Expert Commentary

Brett and William provided a truly outstanding summary of the AMA process and its risks. I’ll just emphasize a few things. When allowing a patient to refuse recommended care and leave the ED, the single most important thing to document is the capacity to understand. The U.S. Supreme Court stated that patients have a liberty interest (i.e.: the right to be left alone) in refusing medical care.[1] Many legal authorities argue that liberty is our most important fundamental right. Therefore, we must be very careful when forcing unwanted medical care on any patient. As Brett and William stated, the two exceptions to the informed consent doctrine are suicidal patients and those who lack the capacity to understand. These patients lose the right to refuse necessary emergency care.

As Brett and William stated, patients who sign out AMA are more likely to sue physicians. An honest plaintiff attorney will tell them they do not have a viable case because they refused medical care, unless they argue the patient was too confused to refuse care. The burden will be on you to document such confusion. In one third of cases, emergency physicians fail to document anything about capacity to understand. [2]

One may document capacity in a number of ways. The ACE Test is a quick way to provide such documentation.[3] Other options include the Folstein Mini-Mental Status Examination, several different “mini mini” batteries, or writing a simple conclusory statement. During the course of my career, I often only had enough time to use the latter option. A conclusory statement is a statement with only a conclusion and no evidence. For example, “The patient clearly has the capacity to understand.” This is far better than writing nothing about the mental status. Such a statement reflects the art of medicine, which often carries a lot of weight in most courtrooms.

Finally, some very prominent academicians in EM now recommend not using the AMA form because it is too confrontational and it does not provide complete protection from litigation. The AMA process should never be confrontational. Remember, patients usually refuse medical care for non-medical reasons unrelated to your plan of care. [4] We practice in the world’s most dangerous legal environment. It would be reckless not to use the AMA form because courts expect us to use these forms. [5-7] A number of state Supreme Courts rendered decisions against physicians in AMA cases because they did not use the proper forms.,, Regarding protection from litigation, nothing provides complete protection. After all, up to 83% of all lawsuits against physicians are groundless, having no basis in fact. [8] Using an AMA form may not prevent a groundless lawsuit, but it may prevent you from losing the lawsuit.

References:

1. Cruzan v Director, Mo. Dep’t of Health, 497 U.S.261 (1990).

2. Dubow et al.  Emergency department discharges against medical advice.  J Emerg Med  1992; 10:513-516.

3. www.jointcentreforbioethics.ca/tools/ace.shtml.  

4. Jerrard DA, Chasm RM.  Patients leaving against medical advice (AMA) from the emergency department: Disease prevalence and willingness to return.  J Emerg Med  2011; 41:412-417.

5. Sawyer v Comerci, 563 S.E.2d 748 (Va. 2002).

6. Drummond v Buckley, 627 So.2d 264 (Miss. 1993).

7. Thomas v Sessions, 818 S.W.2d 940 (Ark. 1991).

8. Localio AR et al.Relation between malpractice claims and adverse events due to negligence.Results of the Harvard Medical Practice Study III.New Engl J Med1991; 325:245-251.

Larry D Weiss, MD, JD, FAAEM, MAAEM

Professor of Emergency Medicine

University of Maryland School of Medicine

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How to Cite This Post

[Peer-Reviewed, Web Publication] Cohen B, Ford W. (2019, Oct 28). Leaving Against Medical Advice. [NUEM Blog. Expert Commentary by Weiss L]. Retrieved from http://www.nuemblog.com/blog/ama.

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Pediatric Ankle Injuries

Written by: Nikita Patel, MD (NUEM PGY-2) Edited by: Paul Trinquero, MD (NUEM ‘19) Expert commentary by: Kristen Loftus, MD, MEd

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Expert Commentary

This is a succinct, high-yield review of pediatric ankle injury management. I appreciate the focus on radiograph-negative injuries, as only a minority will have a fracture identified on radiographs (~12%).

 You highlight a key point about the use of the Ottawa Ankle Rules (OAR). A few things I would emphasize/add:

• You most definitely do not need an x-ray on every pediatric patient with an ankle injury (though x-rays are obtained ~85-95% of the time).

• The OAR have indeed been well-validated in children. In clinical practice, the problem you run into with the pediatric population is that: 1) kids commonly refuse to bear weight even with mild ankle injuries and 2) in pediatric patients (as opposed to adults), isolated distal fibular tenderness typically suggests a low risk ankle injury where x-rays won’t change your management.

• The Low Risk Ankle Rule (LRAR) addresses these 2 key issues of using the OAR in kids, and it may be worth considering adopting the use of this clinical decision rule for pediatric ankle injuries. It was initially validated in children and is associated with a larger decrease in unnecessary radiographs compared to the OAR. [Boutis K, Komar L, Jaramillo D, et al. Sensitivity of a clinical examination to predict need for radiography in children with ankle injuries: a prospective study. Lancet. 2001;358:2118-21.]

No discussion on pediatric orthopedic injuries would be complete without a review of the Salter-Harris classification. There is a lot of practice pattern variation in the management of patients with negative radiographs but growth plate tenderness on exam (i.e. the potential Salter-Harris I fracture). The Boutis et al. group has done some great work in this area, and you highlight several key studies in your excellent review of the literature. I personally feel well-supported by this emerging evidence, and my practice pattern is to place patients in a removable ankle lacer (if able to bear weight) or a pneumatic walking boot (if unable to bear weight), with crutches as needed, and outpatient follow-up with their pediatrician versus Sports Medicine, rather than Orthopedics.

Kirsten V. Loftus, MD MEd

Division of Pediatric Emergency Medicine

Ann and Robert H. Lurie Children’s Hospital of Chicago

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How to Cite This Post

[Peer-Reviewed, Web Publication] Patel N, Trinquero P. (2019, Oct 21). Pediatric Ankle Injuries. [NUEM Blog. Expert Commentary by Loftus K]. Retrieved from http://www.nuemblog.com/blog/peds-ankle.

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Needlestick Injuries

Written by: Logan Wedel, MD (NUEM PGY-2) Edited by: Hashim Zaidi, MD (NUEM ‘19) Expert commentary by: Tim Loftus, MD, MBA

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So You Just Sustained A Needlestick Injury… Now What?

A Brief Guide For Healthcare Professionals

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Needlestick injuries continue to be a common source of work related injury among health care professionals.

Since the Needle-Stick Safety and Prevent act of 2000, non-surgical needle sticks have decreased by 31.6% (2001-2006). Over this same time period, incidents within the surgical setting have increased 6.5%.

However the most recent data from the CDC still estimates 385,000 injuries a year, which equates to more than 1,000 needle stick injuries per day amongst health care professionals. Unfortunately, this is believed to be a gross under-estimation secondary to the vast amount of incidents that go un-reported.

So I Got Stuck… What Is My Actual Risk?

High Risk

• Inoculation from deep or open wound

• Stick with a hallow bore needle / Needle used for blood draw

Low Risk

• Suturing needle

• Discarded needle

No Risk

• Unused needle

• No break in the skin

Good News! The risk of occupational transmission is low!

Transmission Rates by Disease - From a Source Positive Patient

Hepatitis B: 1% - 62% (Depending on exposure type and infectivity of source patient)

• Risk of developing clinical evidence of infection ranges from 1% - 31%

• Risk of developing serologic evidence of infection ranges from 23% - 62%

• Fortunately, this disease is the most easily prevented. Staying up to date on vaccines is the #1 way to prevent HBV infection!

Hepatitis C: 1.8%

• Has ranged from 0% - 7% in some studies

• Extremely low transmission rates from mucous membrane exposure

Human Immunodeficiency Virus (HIV): 0.3%

• Rates drop to 0.09% with mucous membrane exposure

Immediately After Exposure

Safely cease the procedure. Have another operator take over if available.

• The best way to prevent transmission after contact is to wash the site thoroughly with soap and water

• Take your time to perform this well

• Flush the nose and mouth if they were exposed

• Copious irrigation of the eyes if there was ocular exposure

Reporting

This is the last thing you want to be doing, but....

• It is critical to report the incident. Each institution has its own protocol that health care professionals are required to follow. The first step usually deals with informing the charge nurse or unit manager if you are in a healthcare facility. Follow your local institutional protocols to document and report the exposure.

• Every healthcare facility has protocols for occupational exposure. Remember-this is not a unique event and these exposures happen. If there is uncertainty on how to proceed, see if the institution has infection control personnel, occupational health agents, or other administrators or staff who would be familiar with the process.

• This happens. Follow the institutional process and remember this is not uncommon. By not reporting or following protocol you risk transmission of blood borne infectious agents without timely diagnosis and treatment.

Management + Blood Draws

1. Collect the Source Patient's Blood -- Disclose the Incident

• If unable to acquire (patient no longer present, refuses, or unknown source), post-exposure prophylaxis will need to be considered carefully

• Council the source patient on the standard practice to test for blood born infectious agents given the exposure

• Determine the source patient's baseline disease characteristics and any treatment history

2. Your Blood Work

• Determine your baseline disease characteristics

• Hepatitis B status

  1. Vaccinated with or without response

  2. Un-vaccinated without infection

  3. Evidence of current infectivity

  4. Hepatitis B immune globulin (HBIG) may be utilized post exposure particularly for those who are not vaccinated

• Hepatitis C status

• HIV status

3. Follow Up Blood Work - Short and Long Term Monitoring

• Hepatitis B: repeat test at 6 months post exposure

• Hepatitis C: repeat testing at 2, 4, 8 weeks post exposure

• HIV : repeat testing at 6 weeks, 3 months, 6 months, 1 year post exposure

Post Exposure Prophylaxis

Hepatitis B

• Hepatitis B Immune Globulin Alongside Vaccination Series

• Roughly 75% effective and preventing infection

• Administer ASAP - effectiveness after 7 days is unclear

Hepatitis C

• No available post exposure prophylaxis

• Follow your blood work to monitor disease status

Human Immunodeficiency Virus (HIV):

• Three Drug Cocktail: Truvada QD (Tenofovir 300mg + Emtricitabine 200mg) + Raltegravir 400mg BID is the preferred regimen

• Dual Nucleoside Reverse Transcriptase Inhibitor +

  • Integrase Inhibitor

  • Protease Inhibitor

  • Non Nucleoside Reverse Transcriptase Inhibitor

• Multiple Regimens Exist: Can target specific resistance patterns. Expert consultation can be made with local experts or by calling the National Clinicians’ Post-Exposure Prophylaxis Hotline (PEPline) at 888-448-4911.

• Initiate ASAP - effectiveness unknown after 72 hours

• 28 Day Regimen

• Close physician/laboratory follow up to monitor toxicity

Prevention

Always take the the time to apply proper personal protective equipment (PPE)

• It will save you time and save you stress

Gowns, Gloves, Goggles

• Common mistake to forget eye protection

• Double glove in higher risk circumstances

Safe practices: Never reuse needle / Never re-cap needle

• Safe needle disposal

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Expert Commentary

Thank you to Dr. Wedel on an excellent review and summation of what is a frequent and yet frustrating topic for EM physicians.  The evaluation and management of potential blood or body fluid exposures is an area riddled with logistical nuances that frequently change and can be state and institution-specific.  As such, it can be very helpful to mentally break the topic down as has been done so nicely here, into considerations of risk, reporting, testing, and management (including PEP). There are a few important points and nuances that deserve further discussion:

Safety 

Safety is of utmost priority - safety for yourself, your colleagues, and your patients and their family members.  These events are vastly underreported for a variety of reasons, but often this is the first step in tracking these events, mitigating downstream morbidity, addressing issues upfront, and preventing transmission.  A safety culture is built on a daily basis by each and every one of us. 

Nature of Exposure

This post focuses on occupational exposures to healthcare workers, which are relevant to us, but are by far not the only possible or definite exposure we will see.  The more detailed and thorough history we can elicit in these situations may make the difference between initiation or not of post-exposure prophylaxis, as an example.  It is incumbent upon us in emergency medicine to remain up to date on state and local laws and regulations as well as institutional policies and procedures, which help guide us to correctly managing these situations.  As an example, the evaluation and management plan of an exposed healthcare worker may differ compared to that of a patient’s family member, pregnant female, or law enforcement officer or other government official. The more details we can gather regarding the nature of exposure and possible risk of blood-borne pathogen transmission will help us in these nuanced situations. 

Post-Exposure Prophylaxis

This is nicely outlined by Dr. Wedel - to highlight a few points:

1. HBV - immunization is key.  Please ensure your own HBV immunization status is up to date and obtain history of HBV immunization in all patients who are able to provide this. 

2. Tetanus - depending on the nature of the exposure, be mindful that tetanus immunization may be necessary.  

3. HIV - post-exposure prophylaxis has been shown to be very effective in this situation, decreasing likelihood of HIV transmission by as much as 81%.  The effectiveness is best the sooner it gets started after the exposure and is recommended within 72 hours. While there are widely used and preferred regimens, the specific details of each situation may alter the choice of PEP regimen, including kidney function, source patient’s HIV status and resistance patterns, pregnancy, cost, dosing frequency, and side effect profile.  The decision to initiate PEP should be involve a detailed and informed conversation with the patient, as 50% of HCW’s have reported side effects to PEP and as many as 33% have prematurely stopping taking the medicines. 

Consent

Make sure to consider one’s local practice environment, policies, and procedures with respect to potential body fluid exposure testing and treatment. Certain states, such as Illinois, require consent, pre-test information, and other considerations when performing HIV testing in the ED setting.  However, as is the case in Illinois with the AIDS Confidentiality Act and in as many as 35 other states, informed consent and pre-test information may not be required when HIV testing is either medically indicated or in cases of blood or body fluid exposure with certain individuals, including health care workers, law enforcement officers, and paramedics. Be mindful that exception from informed consent does not compel the source patient to submit to testing if a blood specimen is not already available, as this usually requires a court order.  Further, exception from informed consent does not waive us of the responsibility to thoroughly discuss with these patients the rationale behind testing, reporting, and details of unconsented HIV testing.

Overall, blood and body fluid exposure in the health care setting is extremely common and relatively easy to manage, but often gets relegated to standard institutional protocols that may or may not be applied appropriately given the unique circumstances of each patient encounter.  Thank you again to Dr. Wedel for an excellent review, as a thoughtful approach to these situations can help guide us in having a detailed, informed conversation with our patients surrounding transmission risk, testing procedures, post exposure prophylaxis, and rationale behind follow-up timing and testing procedures.  

There are many resources out there to help us, including each institution’s corporate/occupational health, risk management, state and local laws and regulations, and the PEPline. 

• AIDS Confidentiality Act (410 ILCS 305): http://www.ilga.gov/legislation/ilcs/ilcs3.asp?ActID=1550&ChapterID=35

• Cowan E & Macklin R. Unconsented HIV Testing in Cases of Occupational Exposure - Ethics, Law, and Policy. Acad Emerg Med. 2012. 19(10):1181-1187. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3473147/pdf/nihms-402780.pdf  doi:10.1111/j.1553-2712.2012.01453.x.

• ACEP Policy Statement: https://www.acep.org/patient-care/policy-statements/bloodborne-pathogens-in-emergency-medicine/

Timothy Loftus, MD, MBA

Assistant Professor

Department of Emergency Medicine

Northwestern University

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How to Cite this Post

[Peer-Reviewed, Web Publication] Wedel L, Zaidi H. (2019, Oct 14). Needlestick Injuries. [NUEM Blog. Expert Commentary by Loftus T]. Retrieved from http://www.nuemblog.com/blog/needlestick.

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Other Posts You Might Enjoy…

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References

1. "CDC Guidance for Evaluating Health-Care Personnel for Hepatitis B Virus Protection and for Administering Postexposure Prophylaxis Management." Centers for Disease Control and Prevention, U.S. Department of Health & Human Services, https://www.cdc.gov/mmwr/PDF/rr/rr6210.pdf.

2. "Exposure to Blood: What Healthcare Personnel Need to Know." Centers for Disease Control and Prevention, U.S. Department of Health & Human Services, https://www.cdc.gov/HAI/pdfs/bbp/Exp_to_Blood.pdf.

3. "HIV/AIDS PEP." Centers for Disease Control and Prevention, U.S. Department of Health & Human Services, https://www.cdc.gov/hiv/basics/pep.html.

4. "HIV/AIDS Post Exposure Prophylaxis (PEP)." Centers for Disease Control and Prevention, U.S. Department of Health & Human Services, https://www.cdc.gov/hiv/risk/pep/index.html

5. "Oral Health: Occupational Exposure to Blood." Centers for Disease Control and Prevention, U.S. Department of Health & Human Services, https://www.cdc.gov/oralhealth/infectioncontrol/questions/occupational-exposure.html.

6. "The National Surveillance System for Healthcare Workers." Centers for Disease Control and Prevention, U.S. Department of Health & Human Services, https://www.cdc.gov/nhsn/PDFs/NaSH/NaSH-Report-6-2011.pdf

7. "Updated U.S. Public Health Service Guidelines for the Management of Occupational Exposures to HBV, HCV, and HIV and Recommendations for Postexposure Prophylaxis." Centers for Disease Control and Prevention, U.S. Department of Health & Human Services, https://www.cdc.gov/mmwr/preview/mmwrhtml/rr5011a1.htm.

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Non-Accidental Trauma - A Can’t Miss Diagnosis

Written by: Dana Loke, MD (NUEM PGY-4) Edited by: Ashley Amick, MD (NUEM ‘18) Expert commentary by: Lauren Riney, DO

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Introduction

Non-accidental trauma (NAT) is a leading cause of pediatric traumatic injury and death. In 2014 alone, there were 1546 reported deaths from NAT and 3.6 million child abuse referrals submitted to Child Protective Services (CPS). [1] NAT is most commonly encountered in young children, but can occur at any age. The classic signs and symptoms of NAT will be reviewed here, but it is important to realize that occult injury is common. Compared with accidental pediatric trauma, patients with NAT have been shown to have higher injury severity scores, rates of intensive care unit admission, and mortality. Furthermore, the diagnosis of NAT is delayed in 20% of cases, increasing the risk of poor outcomes.[2] Therefore, the Emergency Physician (EP) must maintain a high index of suspicion for NAT to prevent the grave consequences of missed diagnosis for the patient and any other children in the home.

Red Flags and Risk Factors

NAT is a frequently missed diagnosis, but there are some red flags and risk factors that should make the EP take pause and consider this diagnosis. Children at greatest risk are generally toddler and younger, and often come from dysfunctional family units. A recent study found that 97% of NAT cases have antecedent familial dysfunction, such as substance abuse (alcohol or drugs), psychiatric disorder, history of violence or incarceration, or child withdrawal. [3] Additionally, over 70% of reported NAT deaths in 2014 were in children under 3 years old. [1]

Red Flags

• Injuries inconsistent with the caregiver’s history

• Reported mechanism of injury is unexpected for the child’s developmental status (for instance, a 2 week old infant rolling off of a bed)

• Delayed presentation

Risk Factors

• Age under 5 account for 81.5% of cases; children under 1 are most vulnerable [3]

• Prematurity

• Multiple medical conditions

• Young parent

• Female parent (although males are more likely to inflict fatal NAT)

• Poor social support

• Unplanned or unwanted pregnancy

• Poor prenatal care

• Shorter birth intervals between children

• Increased number of separations from the child in the first year

Abuser Characteristics

• Poor self-esteem

• Depression and suicide attempts

• Life stressors

• Personal history of being abused as a child

• Exposure to foster care or abandonment as a child

• Engagement in criminal activity or corporal punishment as a child

Many other suspected risk factors have been studied. There is no consensus regarding whether a particular race is at greatest risk for NAT however black children have a greater risk of mortality from NAT. [4] Similarly, there is no consensus regarding socioeconomic status as it relates to NAT risk, but studies have shown that incidence of non-accidental head trauma and its severity rise during times of economic recession. [4]

Presentation

Figure 1: Bruising patterns that suggest child abuse. [6]

Bruising

Bruising is the most common manifestation of NAT but has low specificity. In any child presenting with bruising, it is imperative to note the location, shape and pattern of the lesion and ensure this is clearly documented. Bruising located over soft tissue areas such as the cheeks, neck, genitals, buttocks, torso, and back, are more likely to represent NAT than bruises over bony prominences. [4] The shape of the bruise should be considered as well, since the bruise often reflects the shape of the causative object. Common objects used to inflict injury include belts, cords, shoes, kitchen utensils, hangers, and teeth. [4] Additionally, patterned bruises should raise suspicion for NAT since they generally do not occur with accidental trauma. Lastly, any bruising in non-mobile infants is suspicious for NAT as well. [5]

Figure 2: Forced immersion burn of buttocks with bilateral, symmetric leg involvement in a “stocking” pattern. [7]

Burns

Burns occur in 8-12% of NAT cases. [2] The most common types of burns from NAT are scald burns and thermal contact burns. Scald burns are the most common and typically occur from forced immersion in hot liquids, usually of the buttock, or in a stocking-and-glove distribution. Scald burns generally have sharp demarcation, uniform depth, and lack splash or drip marks that would be seen in an accidental immersion. Thermal burns occur from contact with hot objects, of which branding with metal implements or cigarettes is a common presentation. Concerning features of burns include:

• Location on the hands (especially the dorsum), legs, feet, or buttocks

• Patterned contact burns in the shape of an object (such as a fork, clothing iron, curling iron, or cigarette lighter)

• Sharp stocking-and-glove pattern with sparing of the flexed protected areas (the classic forced immersion burn pattern)

Figure 3: Classic metaphyseal lesion. White arrows denote femoral metaphyseal separation and black arrow denotes a proximal tibial lesion or “bucket handle.” [1]

Fractures

There are various non-accidental fracture patterns, several with high specificity as described below: 

• Classic metaphyseal lesion (CML) – Also known as “bucket handle fractures” or “corner fractures,” these fractures are highly specific in children less than one year old. They result from a shearing force applied to a long bone, which causes avulsion of the metaphysis. These fractures are not associated with falls.

• Multiple posterior and/or lateral rib fractures – These fractures also have a high correlation with NAT in children less than one year old. They arise from a specific mechanism – grasping the child around the torso and exerting a squeezing/compressive force. These fractures are more likely to affect the rib head and neck given the closer proximity to the transverse processes of the spine. NAT should especially be considered when healing fractures are found in a child without recent CPR.

Figure 4: Posterior and lateral rib fractures of differing ages indicative of NAT [4]

• Clavicular fractures and spiral fractures of long bones in nonambulatory children

• Multiple fractures, especially if in different stages of healing

• Scapular fractures

• Sternal fractures

• Spinous process fractures

Of note, spiral fractures of long bones generally result from twisting injuries (indicating NAT), but can occur accidentally from falls in ambulatory children. Therefore, these fractures (especially if coupled with clavicular fractures) are more specific for NAT in younger patients, and the specificity decreases with advancing age. Other described non-accidental patterns to consider include epiphyseal separations, vertebral body fractures and separations, digital fractures, linear and complex skull fractures, and subperiosteal bone formation. These patterns have low to moderate specificity for NAT. [1] 

Abusive Head Trauma

Abusive head trauma (AHT) is the most fatal form of non-accidental injury in children. In fact, about 80% of deaths from NAT are caused by AHT and only 15% of patients with AHT survive without any sequelae. [4] AHT is a spectrum of injuries including collisions with stationary objects, direct blows to the head, and a repetitive acceleration- deceleration injury, also known as “Shaken Baby Syndrome.” Infants are particularly vulnerable to traumatic brain injury from shaking due to the relative weight of the head compared to the body, coupled with weak neck musculature. [1] If AHT is suspected, a non-contrast head CT should be obtained even with a nonfocal neurologic examination, because occult intracranial injury is common. Make sure to use age-appropriate dose reduction to minimize radiation exposure and if the CT scan is normal, consider further work-up with an MRI.

Figure 5: Fundus of child with AHT with too-numerous-to-count retinal hemorrhages indicated by the black arrows. [8] The white arrow indicates small pre-retinal hemorrhages. The white arrowhead denotes hemorrhage extending into the peripheral retina. The black arrowhead denotes a healthy optic disc.

Ocular Manifestations

Although there are many ocular manifestations associated with non-accidental head injuries, retinal hemorrhages occur most often (about 60-85% of non-accidental head injuries). [4] Suspicion for NAT should be especially heightened when retinal hemorrhages are found in combination with signs of head trauma. Other ocular manifestations of NAT include periorbital hematoma, eyelid laceration, subconjunctival hemorrhage, subluxed or dislocated lens, cataracts, glaucoma, anterior chamber angle regression, iridiodialysis, retinal dialysis or detachment, intraocular hemorrhage, optic atrophy, or papilledema. [4] 

Management and Disposition

All patients with suspected NAT should be admitted for protection and coordination of care even if they are clinically stable. Child Protective Services (CPS) must be notified, and engagement with the institutional social worker and child abuse team is recommended. It is important to note patients with NAT often have worse outcomes than other assault patients despite similar mechanisms of injury with intent to harm. [9] These patients often require close monitoring with Intensive Care Unit (ICU) resources. Patients with NAT should undergo a full skeletal survey as indicated in Figure 6 with additional imaging (CT, MRI) tailored to each patient. For instance, CT abdomen and pelvis should be obtained per general trauma guidelines, particularly if there is suspicion for solid organ or visceral injury. 

Figure 6: Elements of the Skeletal Survey. Although a full skeletal survey is currently the standard of care for patients with NAT, there are ongoing research efforts to tailor X-ray imaging more specifically to each patient. [1]

Other diagnoses to consider in these patients include metabolic bone disease (such as rickets, Caffey disease, and osteogenesis imperfecta), blood dyscrasias, benign enlarged subarachnoid spaces (BESS), glutaric aciduria type 1 (which causes brain atrophy and subdural fluid collections). [1] However NAT is far more common than these diagnoses and carries significant morbidity and mortality when overlooked so should be considered and worked-up prior to these diagnoses.

Key Points

• Pediatric NAT causes significant morbidity and mortality, and therefore EPs must maintain a high degree of suspicion for this diagnosis.

• Red flags during evaluation include a changing or inconsistent history, injuries inconsistent with the history, an unexpected mechanism of injury based on the child’s developmental status, and delayed presentation despite significant injury.

• Risk factors for NAT include children younger than school age (with children younger than 1 being most vulnerable), family dysfunction, prematurity, multiple medical conditions, young/female parent, poor social support, unplanned or unwanted pregnancy, poor prenatal care, numerous separations from the child in the first year of life, and history of psychiatric issues, stressors, criminal activity, or childhood abuse or abandonment in the abuser.

• Although physical exam findings can be non-existent or non-specific, highly specific findings include bruising over soft tissue areas; bruises/burns that are patterned take the form of an object; any bruising in a non-mobile child; scald burns on the hands, legs, feet, or buttocks; and stocking-and-glove patterned burns.

• Highly concerning fracture patterns include classic metaphyseal lesions (“bucket handle fractures” or “corner fractures”), multiple posterior and/or lateral rib fractures, clavicular or spiral long bone fractures in any nonambulatory child, multiple fractures, fractures in different stages of healing, scapular fractures, sternal fractures, and spinous process fractures.

• There is a wide range of ocular manifestations in NAT but the most common manifestation is retinal hemorrhage(s).

• AHT carries the highest mortality rate of all the injuries associated with NAT. Any suspicion for AHT warrants consideration of a non-contrast head CT.

• Notify Child Protective Services (CPS) and admit these children for further NAT work-up including a full skeletal survey.

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Expert Commentary

Excellent overview of NAT in the Emergency Department with emphasis on risk factors and manifestations. I want to add a few pearls about NAT and then will focus my commentary on NAT management in the ED as well as discussion with families, as this was recently a large quality improvement project in our pediatric tertiary care center.

Neglect is the most common form of child abuse accounting for about two-thirds of all forms of abuse and often accompanies other forms of abuse. (1) Neglect is involved in about 50% of all cases of fatal child abuse. (1) Among children less than 1 year of age, 25% of fractures are a result of abuse. (2) Consider two things: does the explanation the provider stated account for the fracture the child has sustained? Is the child developmentally capable of the action being described? After 2 years of age, the history and physical exam should determine the imaging required. Over 5 years of age, the yield of unsuspected fractures from a skeletal survey is only 9%, making this group more amenable to selective radiographic studies. (3) 

Diagnosis of NAT in children remains a challenge due to provider bias, preconceptions, and failure to recognize the presentation as possible abuse. (4,5) As a result, these injuries may go undetected, leading to further injury prior to diagnosis. An estimated 25% of children ultimately diagnosed with NAT have a sentinel injury prior to their abuse diagnosis. (6,7) Of abused children with a previous sentinel injury, the most common were a bruise (80%), a torn frenulum (11%), or a fracture (7%). (8) A large retrospective chart review estimated 80% of deaths from unrecognized abusive head trauma may have been prevented by earlier detection of NAT. (6) The American Academy of Pediatrics (AAP) states that “ANY injury to a young, pre-ambulatory infant” suggests abuse. (9)

Figure 1: Standardized Physical Abuse Guideline.

At our institution, a team of pediatric emergency medicine physicians and child abuse pediatricians convened to develop and implement a standardized NAT guideline for providers in the ED when evaluating children with suspected NAT (Figure 1 Standardized Physical Abuse Guideline). This work stemmed from a chart review showing there was significant variability in the evaluation and management of children with concern for NAT in our Pediatric Emergency Department. The guideline was based on current peer reviewed literature as well as local expert consensus. It is divided into three separate age groups:  < 6 months, 6-12 months, and >12-36 months. Age groups were determined based on risk of injury at different age levels in described literature, acquisition of milestones as age progresses, and increased ability for young children to show specific signs of injury with increasing age.  

Lastly, the evaluation of NAT is stressful for both families and healthcare providers. The second page of our NAT guideline gives a sample script for EPs when discussing the non-accidental trauma evaluation for children. It states, “Any time a child comes to the hospital with this injury/these injuries, we evaluate for other injuries. Sometimes a child can have internal injuries such as fractures, head injury or abdominal injuries that we cannot see on the outside. Just like you, we want to make sure that your child is okay, so it is important to do this testing. We will also have our social worker come talk to you. This is a standard part of our evaluation. We are happy to answer any questions along the way”. It is important to acknowledge that this process is stressful, time consuming, and not comfortable for the child. Explaining each part of the process is important. Ensure that you use language that is non-accusatory. As EPs, we are not the ones to identify who the perpetrator is/was, but rather ensure the full NAT evaluation is completed and allow social work and/or Child Protective Services to determine further action. 

Non-accidental trauma remains too prevalent in our country. Literature continues to show that unrecognized NAT leads to worse injuries and sometimes fatality. Continuing knowledge and education about injuries suspicious for NAT for EPs remains imperative. Standardized evaluations and real time order sets can increase appropriate management of NAT in the Emergency Department.  

References:

1. Dubowitz H. Epidemiology of Child Neglect. CAN 2011, pp 28-34.

2. Kaczor K, Clyde Pierce M. Abusive Fractures. CAN 2011, pp 275-295.

3. Martich KV. Imaging of Skeletal Trauma in Abused Children. CAN 2011, pp 296-308.

4. Higginbotham N, Lawson KA, Gettig K, et al. Utility of a child abuse screening guideline in an urban pediatric emergency department. J Trauma Acute Care Surg. 2014;76(3):871-877. 

5. Tiyyagura GK, Gawel M, Koziel JR, et al.  Barriers and facilitators to detecting child abuse and neglect in general emergency departments. Annals of Emergency Medicine. 2015;66(5):447-454. 

6. Jenny C, Hymel K, Ritzen A, et al. Analysis of missed cases of abusive cases of head trauma. JAMA. 1999;282:621-6.

7. Rangel EL, Cook BS, Bennett BL, et al. Eliminating disparity in evaluation for abuse in infants with head injury: use of a screening guideline. Journal of Pediatric Surgery. 2009; 44(6):1229-34.

8. Sheets LK, et al. Injuries in Infants Evaluated for Child Physical Abuse. Pediatrics. 2013, pp 701-707.

9. Christian CW, Committee on Child Abuse and Neglect. The evaluation of suspected child physical abuse. Pediatrics. 2015;135:e1337–e1354.

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Lauren C. Riney, DO

Assistant Professor

Division of Emergency Medicine

UC Department of Pediatrics

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How to Cite this Post

[Peer-Reviewed, Web Publication] Loke D, Amick A. (2019, Oct 7). Non-Accidental Trauma. [NUEM Blog. Expert Commentary by Riney C]. Retrieved from http://www.nuemblog.com/blog/nonaccidental-trauma.

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References

1. Pfeifer, C.M., Hammer, M.R., Mangona, K.L., & Booth, T.N. (2017). Non-accidental trauma: the role of radiology. Emerg Radiol, 24, 207-213.

2. Kim, P.T. & Falcone, R.A. (2017). Non-accidental trauma in pediatric surgery. Surgical Clinics of North America, 97.1, 21-33.

3. Child maltreatment 2014. Report, Children’s Bureau. Washington, DC: U.S. Department of Health and Human Services; 2014. Available at: http://www.acf. hhs.gov/sites/default/files/cb/cm2014

4. Paul, A.R. & Adamo, M.A. (2014). Non-accidental trauma in pediatric patients: a review of epidemiology, pathophysiology, diagnosis and treatment. Transl Pediatr, 3, 195-207.

5. Maguire, S., Mann, M.K., Sibert, J. & Kemp, A. (2005). Are there patterns of bruising in childhood which are diagnostic or suggestive of abuse? A systematic review. Arch Dis Child, 90, 182-186.

6. Boos, S.C. (2017). Physical child abuse: Recognition. Retrieved April 21, 2017, from http://www.uptodate.com

7. Hobbs, C.J. (1986). When are burns not accidental? Archives of Disease in Childhood, 61, 357-361.

8. Binenbaum G., Rogers, D.L., Forbes, B.J., Levin, A.V., Clark, S.A., Christian C.W., Liu, G.T., & Avery R. (2013). Patterns of retinal hemorrhage associated with increased intracranial pressure in children. Pediatrics, 132, 430-434.

9. Litz, C.N., Ciesla, D.J., Danielson, P.D. & Chandler, N.M. (2017). A closer look at non-accidental trauma: Caregiver assault compared to non-caregiver assault. Journal of Pediatric Surgery, 52, 625-627.

Assessment of the Suicidal Patient

Written by:  Kaitlin Ray, MD (NUEM PGY-4) Edited by: Matt Klein, MD (NUEM ‘18) Expert commentary by: Julie Cooper, MD (NUEM ‘11)

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Approach to Assessing Suicidal Ideation in the Emergency Department

As the 10th leading cause of death in the United States, suicide has become a pervasive public health issue taking over 44,000 lives annually [1]. Each year, over 12 million emergency department (ED) visits are related to mental health and substance abuse issues, and over 650,000 patients are evaluated for suicide attempts [2]. An estimated 9.3 million American adults reported having suicidal thoughts in 2015, among which 2.7 million thought through a suicide plan. Of those adults who have thought through a plan, half 1.3 million actually attempted suicide [3]. Unfortunately, suicidal ideation is one of the most common psychiatric chief complaints encountered by emergency medicine physicians, and the ED is playing an increasingly critical role in providing acute psychiatric care [3]. 

The unfortunate reality is that many mental health programs and community initiatives have limited resources and are at maximum capacity [2]. As such, the ED is often the only available option for management of acute and subacute psychiatric illness [2]. In fact, the Joint Commission’s National Patient Safety Goal (NPSG) orders that general hospitals “conduct a risk assessment that identifies specific characteristics of the individual served and environmental features that may increase or decrease the risk for suicide”. Further, the National Action Alliance Clinical Care and Intervention Task Force specifies that suicide assessment “should be completed by a professional with appropriate and specific training in assessing for and evaluating suicide risk…and [the professional] must have the skills to engage patients in crisis and to elicit candid disclosures of suicide risk in a non-threatening environment” [4]. 

In an attempt to meet these goals and provide psychiatric care to those in need, EM physicians are faced with the unique expectation to execute an organized, efficient, and effective approach to suicide assessment that ensures patient and public safety. The process of eliciting the aforementioned ‘candid disclosure’ can be a daunting task during an emergent visit without a previously established relationship [2]. This problem is further complicated by the increasing reliance on the ED for acute psychiatric care which can exacerbate overcrowding, leading to decreased quality of care and increased likelihood of medical error. Further, mental health associated visits are 2.5x more likely to result in an admission requiring resource intensive care, which can negatively impact quality of care for other patients [5].

The continued emphasis on screening for suicidal ideation in the ED necessitates EM physicians to understand and perform a suicide risk assessment [6]. Of note, it is critical to differentiate suicide screening and suicide assessment. Screening refers to a standardized instrument or protocol that identifies individuals at risk for suicide; a process often performed in triage independent of chief complaint or presenting symptoms. Assessment refers to a comprehensive evaluation performed by a clinician to not only confirm suspected suicide risk, but also to estimate immediate danger to the patient and implement a treatment plan [4]. The focus of this piece is targeted toward the assessment and evaluation of a patient once already determined to be at risk for suicide per various screening methods (Mental Health Triage Scale, Behavioral Health Screening, Manchester Self-Harm Rule, ReACT Self-Harm Rule, P4 Screener, Beck Depression Scale, Geriatric Depression Scale) [7]. 

Suicide assessment and evaluation in the ED is an imperfect science with a limited evidence base to guide management [4]. Further, neither the American Psychiatric Association nor the American College of Emergency Physicians (ACEP) have issued guidelines addressing acute ED management of suicidal patients, leading to markedly varied practice patterns in hospitals across the United States [2]. While there are efforts to develop a quantitative method through which to identify those at highest risk of suicide, there is no universally accepted scoring system, and currently clinical judgment remains the most essential factor [6].

In the majority of emergency departments across the country, the EM physician is responsible for the assessment and disposition of patients with suicidal ideation. Multiple factors are taken into account when defining the role of an EM physician during this process including the following: 

• Providing a safe environment: Take care to ensure the safety of both the patient and other health care providers. This process often requires taking patient’s clothing in exchange for a hospital gown, searching and withholding personal belongings, 1:1 observation, and physical or chemical restraints if deemed appropriate. Conduct the evaluation in a non-judgmental fashion, preferably in a private or semi-private setting utilizing open-ended questions [2]. 

• Ruling out “reversible” causes of depression/suicidal ideation: Consider toxic ingestions, infectious processes, toxic-metabolic etiology, and trauma as possible causative factors when clinically indicated. ACEP issued a Level B recommendation regarding obtaining routine laboratory testing in alert, cooperative patients with normal vital signs and a non-focal history and physical. Routine urine drug screens (UDS) are a Level C recommendation and should not delay patient evaluation or transfer to more advanced psychiatric care [2]. Of note, one should insist on a clinically sober assessment, not based on BAC, given the disinhibiting effect of alcohol. 

• Assessing the degree of imminent risk to the patient: Arguably the most challenging yet critical component of the process. The Suicide Prevention Resource Center (SPRC) has developed a 5-step process to guide the clinical assessment of patients with suicidal ideation and is one that can be implemented in the ED setting [8]. SAFE-T, the Suicide Assessment Five-Step Evaluation and Triage, is a simple methodical approach that focuses on identifying risk factors for suicide, identifying protective factors, conducting the suicide inquiry, determining the risk level of the patient, and finally documenting the clinical assessment [8]. Each component will be elaborated on separately.

Identifying risk factors for suicide:

• Prior history of suicide attempts: The single strongest predictor of suicide with these patients being 6x more likely to make another attempt [2].

• Current lethal plan: Highly predictive of future suicide attempt [6].

• Older age: While younger patients typically have more attempts at suicide, older patients are more likely to succeed2. The highest rates of suicide are found among middle-aged populations between 45-64 years old [1].

• Coexisting psychiatric disorder: Major Depressive Disorder, schizophrenia, personality disorder, borderline personality disorder, bipolar disorder, PTSD [2]

• Recent psychosocial stressor: Ask about marital status, employment, social support, homelessness, financial stressors

• Caucasian Race: Highest suicide rates among whites, specifically white males who account for 7/10 suicides in the US [1]. The 2nd highest suicide rate is among American Indians/Alaska Natives, where suicide is now the leading cause of death in those aged between 10-34 years of age [3].

• EtOH/Drug Abuse: Chronic use elevates suicide risk long term, while acute intoxication disinhibits and impairs thought process, increasing suicide risk in a more immediate context [6].

• Other factors to consider [6]:

  • Gender: Women attempt suicide 4x more frequently than men; however men are 3x as successful as women in completing suicide [2].

  • Access to firearms: Utilization of firearms accounts for 50% of all suicides in the US, with higher rates among men1. Poisoning is the most common method among females [3].

  • Impulsivity: Look for behaviors and statements from the patient that establish a pattern of impulsive behavior [2].

  • Family history of suicide/mental illness

  • History of childhood trauma

  • Chronic physical illness

Identifying protective factors for suicide

• No past suicidal ideation: Denies feelings of hopelessness and depression [6]

• Supportive family and social network [9]

• Willingness to seek and accept help [9]

• Strong personal relationships [9]

• Female gender [9]

• Ethical, moral, or religious suicide taboos [9]

• Employment and financial stability [9]

• Having dependents [9]

• Positive self-esteem [9]

Conducting suicide inquiry [8]

• Ideation: Frequency? Intensity? Duration? How often in past 48 hours? Past month?

• Plan: Inquire about timing, location, lethality, availability, and any preparatory acts that may be involved

• Behaviors: Past attempts? Aborted attempts? Any rehearsals—tying a noose? Loading a gun?

• Intent: Evaluate the extent to which the patient intends to carry out the plan and believes the act to be lethal versus self-injurious. If possible discuss with patient their reasons to die vs. reasons to live.

Determining risk level and need for interventions

• A patient’s risk level and subsequent treatment disposition is based on clinical judgment! 

• Charted below is a general rule of thumb in guiding a patient’s disposition from the ED [8]:

Documenting the clinical assessment

• Documentation is the fifth and final component of a suicide assessment in the ED. Be clear to document the patient’s estimated risk level as well as the rationale for doing so. Specify the treatment plan that will address the patient’s current risk [8]. 

Perhaps the most challenging portion of assessing a suicidal psychiatric complaint is determining the patient’s disposition. In many facilities, a formal psychiatric assessment would require an inpatient hospitalization. Additionally, it is state (not federal) laws that govern conditions in which you may involuntarily hold a patient for an emergency psychiatric evaluation, with a hold >72 hours typically requiring a court order. Unfortunately there is no clear evidence to support the use of suicide contracts in the ED—i.e. written or verbal agreements between the physician and the patient in which the patient agrees to abstain from self-harm behaviors while in the ED and for a set amount of time thereafter. While psychotropic medications are rarely initiated in the emergency department, it may be reasonable to prescribe a short course of anxiolytics as a bridge to psychiatric follow up in a patient determined safe for discharge home. Patients determined safe for outpatient follow-up should be given strict return precautions in addition to resources that include emergency and crisis phone numbers. Finally, as with all other life threatening conditions that come through the ED, documentation regarding the risk assessment and disposition of the patient is critical [2].

Ultimately, until our mental health and community resources have the means to meet the growing psychiatric demands of our country, the emergency department will continue to be a resource to provide acute psychiatric care. Limited evidence-based recommendations and no official standardized guidelines exist to assist emergency physicians in assessing risk of suicidality; however, adhering to the basic process of identifying high risk features in addition to protective factors, while simultaneously asking direct questions regarding suicidal ideation, plan, behavior, and intent, can guide EM physicians towards making an appropriately and timely disposition for the suicidal patient.

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Expert Commentary

Thanks so much for this excellent review of the approach to the patient with suicidal ideation. What a complex task to perform in our already complex practice, but also what a pleasure to care for someone when the major tool in our toolbox is taking the history!  This review correctly notes that the emergency physician “must have the skills to engage patients in crisis and to elicit candid disclosures of suicide risk in a non-threatening environment”. So, what exactly are those skills? 

First, we know that the typical ED environment is not always conducive to sensitive conversations. I once heard a resident walk up to a patient in the hallway and say “Hi! I heard you were suicidal!”. Whether the patient is mean, intoxicated, or has some kind of perceived secondary gain, observe your cognitive biases and overcome the urge to minimize their perceived risk.  Consider location bias when they are in a hallway, anchoring bias when staff tell you “they were just discharged yesterday”. Those all may be reasons a patient is destabilized and at high risk, so be on alert. Many of these patients wait for hours, have difficult lives and none of us went into medicine to be mean to vulnerable people. Get them the sandwich and a warm blanket, create some privacy and pull up a chair. 

Conversations surrounding mental health and suicidality can trigger intense feelings of shame or embarrassment (in both the patient and clinician), elicit anxiety surrounding the consequences of seeking help or conjure memories of negative experiences with the mental health system. Language really does matter when it comes to building trust and conveying empathy. I always start my history open ended with “how did you end up here today?” and assume no knowledge of the events that brought them in. The details of how a person actually came to be in the ED can shine a light on their risk. Did they come seeking help themselves? Did another person encourage them who may have important collateral information? Was law enforcement involved? If they are not forthcoming I might try “I heard …   is that correct?” 

If a patient doesn’t bring up suicidal thoughts on their own I often start with “It sounds like you have been feeling really badly leading up to today, were you worried about your safety?”. I’ll work up to “were you worried you might harm or kill yourself?” and try to tease out “how close” they might have gotten by asking “did you actually do something to try to harm yourself or was there something you were worried about doing?” For an attempt that doesn’t seem serious to me (a small over the counter ingestion or superficial self-injurious behavior like cutting) I will ask what they thought was going to happen when they did that. Often it might be a serious attempt in their eyes. When considering protective factors I always ask “what kept you from going through with it?”. This might bring up mitigating factors that reduce their suicide risk.  

The assessment of a suicidal patient can be an opportunity to switch gears during a shift and focus on the kind of communication that is fundamental to the practice of medicine.  If you’re looking to build your skills, consider seeking feedback from mental health professionals like psychiatrists, nurses or social workers in your department or observe them on shift to learn language you might integrate. That is how I picked up one of my favorite tools for an emotional patient encounter: expressing gratitude. If a patient acknowledges suicidal feelings, try “thank you so much for sharing that with me, I know it was hard and we are here to help.”

Julie Cooper, MD

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How To Cite This Post

[Peer-Reviewed, Web Publication] Ray K,  Klein M. (2019, Sept 30). Assessment of the Suicidal Patient. [NUEM Blog. Expert Commentary by Cooper J]. Retrieved from http://www.nuemblog.com/blog/assessment-SI.

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Resources:

1. American Foundation for Suicide Prevention. (2015). Suicide Statistics — AFSP. Retrieved from https://afsp.org/about-suicide/suicide-statistics/

2. Bernard, C., Gitlin, D., & Patel, R. (2011). The Depressed Patient and Suicidal Patient in the Emergency Department: Evidence based management and treatment strategies. Emergency Medicine Practice, 13(9). Retrieved from ebmedicine.net

3. Suicide Facts at a Glance 2015. Retrieved from http://www.cdc.gov/violenceprevention

4. Suicide Prevention Resource Center. (2014, September 1). Suicide Screening and Assessment. Retrieved from http://www.sprc.org/sites/default/files/migrate/library/RS_ suicide%20screening_91814%20final.pdf

5. Owens, P., Mutter, R., & Stocks, C. (2010). Mental health and substance abuse-related emergency department visits among adults, 2007 (92). Agency for Healthcare Research and Quality.

6. Ronquillo, L., Minassian, A., Vilke, G. M., & Wilson, M. P. (2012). Literature-based Recommendations for Suicide Assessment in the Emergency Department: A Review. The Journal of Emergency Medicine, 43(5), 836-842. doi:10.1016/j.jemermed.2012.08.015

7. Brim, C., Lindauer, C., Halpern, J., & Storer, A. (2012). Clinical Practice Guideline: Suicide Risk Assessment. Institute for Emergency Nursing Research. Retrieved from https://www.ena.org

8. Jacobs M.D., Douglas. National Suicide Prevention Lifeline. (2017, January 14). SAFE-T: Suicide Assessment Five-step Evaluation and Triage for Mental Health Professionals. Retrieved from http://www.stopsuicide.org

9. Simon, Robert I. "Assessing protective factors against suicide: questioning assumptions." Psychiatric Times, Aug. 2011, p. 35. Academic OneFile, go.galegroup.com.ezproxy.galter.northwestern.edu/ps/i.do?p=AONE&sw=w&u=

northwestern&v=2.1&it=r&id=GALE%7CA264271238&asid=e996d06fc529b9a60a6d5306fb8c8fd4. Accessed 1 Feb. 2017.

Preeclampsia

Written by: Priyanka Sista, MD (NUEM PGY-4) Edited by: Matt Klein, MD (NUEM ‘18) Expert commentary by: Shannon Lovett, MD

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Expert Commentary

Thank you for this succinct guide to the diagnosis and management of preeclampsia in the ED. 

“The eyes do not see what the mind does not know…..”. The biggest pitfall in the management of preeclampsia in the ED, is failing to consider and recognize the diagnosis. Recognition and prompt treatment of preeclampsia in the ED setting can be challenging due to the variety of presenting complaints. It is important to note that preeclampsia may occur anytime from 20 weeks gestation up to 6 weeks postpartum. 

Postpartum preeclampsia tends to be more diagnostically challenging and depending on your facility, these patients are more likely to present to the ED than pregnant patients who often present to their obstetrician or to labor and delivery. Preeclampsia in the postpartum period most frequently occurs in the first 48 hours after delivery, but should be considered up to 6 weeks postpartum. Patients with postpartum preeclampsia often do not have hypertensive disease or preeclampsia during pregnancy. 

The complaints associated with preeclampsia may be broad and vague- including but not limited to: headache, vision changes, swelling or rapid weight gain, nausea and vomiting, shortness of breath, and abdominal pain. Consider preeclampsia or eclampsia in the critical female patient that arrives in the ED with little known history- for example actively seizing, or in respiratory distress with pulmonary edema. 

The treatment of preeclampsia can be broken down into three parts: treating the hypertension, reducing the risk or recurrence of seizures, and delivery of the fetus and the placenta. In the ED- our focus is on the first two, and involving our obstetric colleagues immediately. Blood pressure is most commonly treated with labetolol or hydralazine IV in the ED, and Mag should be given immediately for seizure prophylaxis (or to reduce recurrence of seizures in eclampsia). 

Lastly, our obstetric and gynecology colleagues at ACOG have recognized the frequency that postpartum patients present to the ED, and have created this ED checklist that can be used as a reference for the management of postpartum preeclampsia-  https://www.acog.org/-/media/Districts/District-II/Public/SMI/v2/19sm03a170703PPPreeclamCheckED1.pdf?dmc=1&ts=20190327T1949153065. Preeclampsia is a syndrome with potentially devastating consequences to mother and baby, and our early recognition and treatment can improve outcomes.

Shannon Lovett, MD

Associate Professor

Loyola University Medical Center

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How To Cite This Post

[Peer-Reviewed, Web Publication] Sista P, Klein M. (2019, Sept 23). Preeclampsia. [NUEM Blog. Expert Commentary by Lovett S]. Retrieved from http://www.nuemblog.com/blog/preeclampsia.

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Clearing C-Spine in Intoxicated Blunt Trauma Patients

Written by: Jason Chodakowski, MD (NUEM PGY-4) Edited by: Duncan Wilson, MD (NUEM ‘18) Expert commentary by: Matt Levine, MD

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Saturday night in the ED.  A 28 year old man presents after a low speed motor vehicle accident.  Police report that he was seen swerving in the road before rear ending a parked car at approximately 25 mph.  He presents to the ED without visible signs of trauma. His trauma exam reveals no cervical spine tenderness, but he is heavily intoxicated with a GCS of 13.  Head CT and cervical spine CT are negative and he is currently sleeping in the hallway, periodically waking up to remove his cervical collar. You have very low suspicion that he has a significant cervical spine injury, but you ask yourself, can I clear his cervical spine given his level of intoxication?

Evaluating C-Spine Injuries

The Eastern Association for the Surgery of Trauma (EAST) Practice Management Guidelines Committee recommends the following approach to the care of patients with suspected cervical spine injuries: [1]

• In awake, alert patients with trauma without neurologic deficit or distracting injury who have no neck pain or tenderness with full range of motion of the cervical spine, imaging is not necessary and the cervical collar may be removed.

• All other patients in whom cervical spine injury is suspected should have radiographic evaluation, preferably with cervical spine CT imaging.

  • In patients with negative CT imaging but persistent neck pain, the patient may have a cervical ligamentous injury.  Three treatment options exist:

    • Continue the cervical collar

    • Cervical collar may be removed after negative MRI

    • Cervical collar may be removed after negative and adequate flexion/extension plain films.

The Canadian C-Spine and National Emergency X-Radiography Utilization Study (NEXUS) criteria are two widely used, prospectively validated decision rules that can be used by clinicians to clinically rule out clinically significant cervical spine injury, thereby obviating the need for imaging.

Canadian C-Spine criteria [10]: If the patient has all of the below, then radiography is not necessary:

1. No High Risk Factors: Age >/=65; Dangerous Mechanism, paresthesias in extremities

2. AND has presence of at least one low risk factor: simple rear-end MVC, sitting position in ED, ambulatory at any time, delayed onset of neck pain, and absence of midline c spine tenderness

3. AND able to range neck actively (i.e. rotate neck 45 degrees left and right)

National Emergency X-Radiography Utilization Study (NEXUS) criteria [9]: If the patient meets all of the below criteria, no radiology is required.

1. No posterior midline cervical-spine tenderness

2. No evidence of intoxication

3. A normal level of alertness

4. No focal neurologic deficit

5. No painful distracting injuries

C-Spine Clearance in Intoxicated Patients

Intoxicated patients are an important population to consider in the setting of suspected cervical spine injury: not only do they make up nearly half of all blunt and penetrating trauma patients [2], but intoxication and reduced level of consciousness disqualify the use of the above decision-rules, thereby necessitating CT imaging. CT is insensitive for ligamentous injuries and current practice dictates that after a negative CT c-spine these patients (and obtunded patients generally) are left in a c-collar until they can be reassessed unaltered or have additional imaging performed, usually MRI. 

A wealth of gradually accumulating data challenges the need to keep obtunded patients (and therefore plausibly intoxicated patients) in prolonged immobilization or to obtain MRI after a single negative CT c-spine, notably: 

• Smith et al [3]: meta-analysis, 16785 obtunded trauma patients 

  • 99.9% Sn and 99.9% Sp for CSI; NPV 100%

• Panczykowski et al [4]: meta-analysis, 14327 obtunded or intubated patients

  • 99.9% Sn and 99.9% Sp for unstable cervical spine injury

• Patel et a [5]: systematic review, 1718 obtunded blunt trauma patients

  • NPV 100% for unstable CSI, 91% for any stable CSI

• Raza et al [6]: meta-analysis, 1850 obtunded blunt trauma patients

  • 93.7% Sn and 99%.7% Sp; NPV 99.7%

• Hogan et al [7]: retrospective review, 1400 blunt trauma patients

  • NPV 98.9% for ligamentous injury; 100% for unstable CSI

EAST Practice Management Guidelines reflect these findings, conditionally recommending c-collar removal after a negative high-quality CT c-spine alone. [5]

Most recently, a prospective observational study of intoxicated patients with blunt trauma was published by Bush et al [8] in JAMA Surgery in 2016. The authors followed 1696 adult blunt trauma patients who underwent 2mm-thickness, three-view CT c-spine, finding that among intoxicated patients (alcohol or other drugs) a single negative CT c-spine alone had a NPV of 99.2% for all cervical spine injuries and 99.8% for unstable cervical spine injuries. Of the 632 intoxicated patients, only 1 had an unstable ligamentous injury that was missed on CT and later identified on MRI.  This patient had quadriplegia on initial evaluation. The incidence and types of CSI were similar between intoxicated and sober groups. 

Where Do We Go From Here?

Given the high incidence of intoxication in blunt trauma patients who are collared and require c-spine clearance, it is worth considering whether an otherwise neurologically intact intoxicated patient with a negative high-quality CT c-spine requires prolonged immobilization. This is of particular importance in patients that become combative and demand removal of their cervical collar.  In such cases, ED physicians may be forced to sedate the patient in order to keep the cervical collar on or obtain an MRI, which may place the patient at risk. While the data is admittedly limited, it does demonstrate that the incidence of clinically significant c-spine injury in the setting of a negative CT scan is very low, with some authors stating it approaches zero. Given this, it may be justifiable to remove an intoxicated patient’s cervical collar in the setting of a reassuring clinical exam and negative CT scan in settings when the risk of keeping the patient in a cervical collar until sober is deemed to outweigh the risks of missed cervical spine injury.

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Expert Commentary

Everything we recommend in medicine is a risk-benefit analysis.  If there is extremely little to benefit, then do not recommend. If the risk exceeds the benefit, then do not recommend.  Keep this in mind when considering various cervical collar scenarios, and the concept of being risk-averse vs being risk-neurotic.

Most of us think we are risk averse, but no one thinks they are risk neurotic.  However, many witnessed practices regarding the use of cervical collars are exactly that.  For instance, a patient that had an MVC yesterday presents with neck pain after waking up this morning.  They have been moving all over, showered, dressed, etc. There is some midline tenderness so now they must lie flat and still and wear a collar. They are not allowed to walk, use the toilet, or move themselves onto a CT table even though they got themselves in and out of the car this morning.  This is risk neurosis. This patient has gained nothing from wearing this collar. Furthermore, we have inconvenienced ourselves by having to now logroll this patient for imaging studies, not to mention the bedpan for the negative pregnancy test. Why are we doing this to ourselves and our patients?  Risk neurosis.

Do not confuse this with the MVC patient who had immediate neck pain, was removed from the car by EMS and immediately placed in a collar.  That patient has not moved around yet and declared themselves low enough risk yet. It is reasonable to handle them with care until the doctor can assess, and possibly image before considering collar removal.  Risk averse.

Back to the intoxicated patient demanding collar removal.  My risk-benefit calculator which is continuously churning in my head considers the two options:  

1. Sedate and restrain a neurologically intact patient without signs of spine injury, despite not meeting strict clearance criteria due to intoxication.  This puts him at risk for violent behavior, over sedation, aspiration, prolonged ED length of stay, etc. Even if the patient is hiding a fracture, is the struggle to restrain him protecting his spine or putting it at risk?

2. Do not make him wear the collar but make him stay in the ED until he can be clinically reassessed (when sober).  Even if he has a c spine fracture, how likely is deterioration during this time? 

Which is riskier for the patient’s spine, the restraint to force a collar on or the relatively peaceful collarless period?  My risk-benefit calculator tells me the peaceful collarless period is safest.

So remember to ask yourself when faced with a cervical collar scenario what are the risks and benefits of applying this collar?  Is there any real benefit? And then ask yourself the truly difficult but introspective question: Am I being risk averse or am I being risk-neurotic?

Matt Levine, MD

Assistant Professor of Emergency Medicine

Northwestern Feinberg School of Medicine

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Citations

1. Como, John J., et al. "Practice management guidelines for identification of cervical spine injuries following trauma: update from the eastern association for the surgery of trauma practice management guidelines committee." Journal of Trauma and Acute Care Surgery 67.3 (2009): 651-659.

2. Rivara, Frederick P., et al. "The magnitude of acute and chronic alcohol abuse in trauma patients." Archives of Surgery 128.8 (1993): 907-913.

3. Smith, Jackie S. "A synthesis of research examining timely removal of cervical collars in the obtunded trauma patient with negative computed tomography: an evidence-based review." Journal of Trauma Nursing 21.2 (2014): 63-67.

4. Panczykowski, David M., Nestor D. Tomycz, and David O. Okonkwo. "Comparative effectiveness of using computed tomography alone to exclude cervical spine injuries in obtunded or intubated patients: meta-analysis of 14,327 patients with blunt trauma: A review." Journal of neurosurgery 115.3 (2011): 541-549.

5. Patel, Mayur B., et al. "Cervical spine collar clearance in the obtunded adult blunt trauma patient: a systematic review and practice management guideline from the Eastern Association for the Surgery of Trauma." The journal of trauma and acute care surgery 78.2 (2015): 430.

6. Raza, Mushahid, et al. "Safe cervical spine clearance in adult obtunded blunt trauma patients on the basis of a normal multidetector CT scan—a meta-analysis and cohort study." Injury 44.11 (2013): 1589-1595.

7. Hogan, Gerard J., et al. "Exclusion of Unstable Cervical Spine Injury in Obtunded Patients with Blunt Trauma: Is MR Imaging Needed when Multi–Detector Row CT Findings Are Normal? 1." Radiology 237.1 (2005): 106-113.

8. Bush, Lisa, et al. "Evaluation of cervical spine clearance by computed tomographic scan alone in intoxicated patients with blunt trauma." JAMA surgery 151.9 (2016): 807-813.

9. Hoffman, J.R., et. al. “Validity of a set of clinical criteria to rule out injury to the cervical spine in patients with blunt trauma. National Emergency X-Radiography Utilization Study Group.” NEJM. 2000. 343(2):94-99.

10. Stiell, IG, et. al. “The Canadian C-Spine rule for Radiography in Alert and Stable Patients.” JAMA. 2001. 286(15):1841-8.

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How To Cite This Post

[Peer-Reviewed, Web Publication] Chodakowski J, Wilson D. (2019, Sept 16). Clearing C-Spine in Intoxicated Blunt Trauma Patients. [NUEM Blog. Expert Commentary by Levine M]. Retrieved from http://www.nuemblog.com/blog/cspine-clearance-etoh.

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Rise and Shine: A Review of the WAKE-UP Trial

Written by: Gabrielle Bunney, MD (NUEM PGY-2) Edited by: Alex Ireland, (NUEM PGY-4) Expert commentary by: Chris Richards, MD, MS

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Introduction

Wake up strokes have always been a clinical conundrum. Current practice guidelines from the American Stroke Association on the treatment of acute ischemic strokes specify a maximum of 4.5 hours from time of symptom onset to the delivery of alteplase therapy. [1] However, patients often awaken with these symptoms or are unable to give a clear history of symptom onset and thus are not eligible for alteplase therapy. Initial non-contrast computed tomography can identify whether or not an acute hemorrhage is present, but confirmatory imaging for ischemic stroke involves magnetic resonance imaging (MRI). Studies are now looking at the utility of early MRI in the diagnostic and therapeutic pathways of acute ischemic stroke. These studies are specifically looking at a positive signal on diffusion-weighted imaging (DWI) and a negative signal on FLAIR imaging to identify recent cerebral infarction. Multiple studies have found that there is adequate sensitivity and specificity of DWI-FLAIR mismatch to suggest stroke onset within 4.5 hours. [2-4] Armed with these new data, this paper’s goal was to determine whether patients with an unknown time of symptom onset, but with a mismatch on DWI and FLAIR MRI imaging, would benefit from thrombolysis with intravenous alteplase. 

Study

Thomalla G, Simonsen CZ, et. al “MRI-Guided Thrombolysis for Stroke with Unknown Time of Onset | NEJM.” New England Journal of Medicine, Oxford University Press, www.nejm.org/doi/full/10.1056/NEJMoa1804355. [5]

Study Design

This study was a multi-center, randomized, double blind, and placebo controlled clinical trial. It involved 70 experienced stroke research centers in eight European countries. There was a central image-reading committee that reviewed all images for patient enrollment to evaluate inclusion and exclusion, and to arbitrate disagreements. 

Population

Patients between the ages of 18 and 80 were eligible for the study if they clinically had an acute stroke and were able to perform their activities of daily living prior to this event. The patient had to awaken with these symptoms, be unsure about the time of onset secondary to confusion or aphasia, or have a timeline of symptoms greater than 4.5 hours, without an upper limit. 1,362 patients underwent screening. 859 were excluded, leaving 503 that were randomized. 254 of those were given alteplase and 249 received placebo. 

Intervention Protocol

Selected patients underwent DWI and FLAIR MRI imaging. Those who had a mismatch, defined as an abnormal signal on DWI, but no signal on FLAIR, were then randomized. Excluded were those with intracranial hemorrhage, lesions larger than one third of the middle cerebral artery territory, those who were to undergo thrombectomy, those with severe stroke, defined as greater than 25 on the National Institute of Health Stroke Scale (NIHSS), and those that had any other contraindication to alteplase aside from time from last known normal. Those that were randomized into the alteplase group were given 0.9mg/kg of alteplase with 10% administered as a bolus and the rest given as an infusion over 60 minutes. Assessments were then conducted between 22 and 36 hours after randomization, between 5 and 9 days, and finally at 90 days. 

Outcome Measures

This study had two end point measurements: efficacy and safety. The primary efficacy outcome measurement was favorable clinical outcome defined as a score of 0 to 1 on the modified Rankin scale 90 days after randomization. Secondary efficacy outcome measurements ranged from depression scores to activities of daily living measurements. 

The primary safety outcome was death and a composite outcome of death or dependence (4-6 on the modified Rankin scale) at 90 days. Secondary safety endpoints were symptomatic intracranial hemorrhage and the incidence of parenchymal hematoma type 2 on MRI 22 to 36 hours after randomization. 

Results

The demographics between the alteplase and placebo groups were similar for age, sex, and medical history. However, in the alteplase group there was a higher rate of intracranial occlusion of the internal carotid artery. The average time for treatment of the alteplase and placebo groups was 3.1 and 3.2 hours after symptom recognition, respectively. 

Alteplase was found to be associated with favorable outcome at 90 days, with 53.3% in the alteplase group and only 41.8% in the placebo group having a modified Rankin score between 0 and 1 at 90 days, p=0.02. The secondary efficacy endpoints lacked power due to the fact that the study was terminated early because of a loss of funding. Table 2 from the original article describes the efficacy findings.

The safety groups were sized 251 in the alteplase group due to 5 patients not receiving alteplase and 244 in the placebo group due to 4 patients not receiving placebo. Death or dependency was found in 13.5% of the alteplase group and 18.3% of the placebo group, p=0.17. However, death at 90 days was higher in the alteplase group at 4.1%, while in the placebo group it was 1.2%, p=0.07. There were numerically more parenchymal hemorrhages in the alteplase group than in the placebo group, with 10 in the alteplase group and 1 in the placebo group. Table 3 from the original article describes the safety outcomes.

Interpretation

The primary efficacy outcome of this study, favorable functional outcome at 90 days, was higher in the group that received alteplase than in the group that received placebo and was statistically significant. Additionally, the primary safety outcome of death or disability was higher in the placebo group than in the alteplase group, though this was not found to be statistically significant. Death at 90 days was found to be numerically higher in the alteplase group than the placebo group, although not statistically significant. In extrapolating the data from the paper, the number needed to treat is 9.4 and the number needed to harm is 36.3. The ratio of these numbers suggests that treatment provides a greater benefit than risk. 

There are several limitations to this study. The trial was stopped early due to lack of funding, and so we may be overestimating the benefit or underestimating the risk. The authors estimated that they needed approximately 800 patients to have sufficient power, yet enrolled only 503. Bleeding complications and death at 90 days were numerically higher in the alteplase group, though this was not statistically significant. Trials such as ATLANTIS A and B, and ASK, were all stopped early due to harm because of increased bleeding in the alteplase groups. [6-8] It is unknown whether the addition of 297 patients to meet the pre-specified enrollment target of 800 in the WAKE-UP trial would have resulted in statistical significance. 

The population of this study had a median NIHSS of 6 out of 42, a relatively low stroke severity. The DAWN, DEFUSE, NINDS, and SITS-MOST trials, all significant studies in the progression of stroke research, had NIHSS medians of 17, 16, 14, and 12, respectively. [9-12] It is unclear if MRI-guided alteplase therapy would benefit patients with more severe strokes. Additionally, this paper excluded patients who were selected for thrombectomy. Patients selected for thrombectomy have large clot burdens in the internal carotid artery or middle cerebral artery that often have a modified Rankin score greater than 6. [13] By not including these patients, the WAKE-UP trial does not show the benefit of medical treatment in these sicker patients with a larger clot burden. 

Lastly, the study was only performed in experienced research stroke centers with readily available diagnostic pathways and MRI. Of the 1,362 patients imaged and screened, only 37% met intervention criteria. Many did not have DWI-FLAIR mismatch, and some did not have any DWI lesion, suggesting a transient ischemic attack or a stroke mimic. A smaller hospital is unlikely to have the experience or equipment to be able to screen these more difficult patients for the few that can actually proceed to intervention. 

Future Areas of Research

A replication of this study with additional subjects and sufficient power to confirm the beneficial effect of alteplase in MRI-guided thrombolysis would be the next step. Inclusion of alteplase plus thrombectomy in appropriate patients presenting after 4.5 hours with mismatch on DWI-FLAIR is another possible study. For example, TWIST (ClinicalTrials.gov Identifier: NCT03181360) and TIMELESS (ClinicalTrials.gov Identifier: NCT03785678) are two large clinical trials that will hopefully give more information about expanding the time window for thrombolysis. [14,15]

Review

• MRI DWI-FLAIR mismatch may be able to allow more patients to receive alteplase therapy after an acute ischemic stroke

• Alteplase still shows benefit for treating stroke even with an unknown timeline when used in conjunction with MRI DWI-FLAIR mismatch

• Similar to prior studies, alteplase is associated with numerically higher instances of intracranial hemorrhage 

• Further research needs to be done to increase the power of this study

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Expert Commentary

Really nice summary of the recent WAKE-UP* trial, and you bring up important considerations about both the pros and the cons of this study. WAKE-UP addressed an important clinical question: is it safe and effective for patients who have no other disqualifying reasons aside from their last known normal time to receive thrombolysis, if imaging shows a small area of infarction but a large area of ischemia? As you mention, intervention patients in the study: a) received intravenous tissue plasminogen activator (IV tPA) when otherwise they would not have, b) had increased odds of having a favorable outcome compared to standard of care, c) though with numerically greater instances of hemorrhage. 

WAKE-UP fits into a narrative with two other important recent trials, DAWN* and DEFUSE-3*that studied the outcomes of patients with last known normal (LKN) times greater than conventional LKN time cut-offs (4.5 hours for IV tPA and 6 hours for endovascular therapy) and have found efficacy of reperfusion in these extended windows for select patients. A third trial, EXTEND,* has been presented in abstract form and has demonstrated clinical improvement in select AIS patients receiving IV tPA up to 9 hours from LKN time (https://abstractsonline.com/pp8/#!/4715/presentation/13367). Importantly, these trials that expand the time window for reperfusion used imaging-based criteria for inclusion: WAKE-UP used MR, DAWN used a non-contrast CT scan compared to severity of clinical syndrome, DEFUSE-3 used CT perfusion along with a computer software program to identify the infarcted “core” and the ischemic penumbra, and EXTEND required a penumbral mismatch on CT perfusion or MRI.

From a pathophysiological perspective, this makes sense. If imaging can identify a large area of ischemia and small area of infarction, reperfusion should potentially result in the salvage of at least some of those reversibly damaged cells. It should also result in less pronounced hemorrhagic side effects because the area of known infarction is less – remember, not only neurons die in infarcted brain, so do blood vessel endothelium cells, a contributing factor in post-reperfusion hemorrhage. [16]

Looking into the future of acute stroke care, these clinical trials give promise for individualized acute stroke treatment. Rather than being beholden to a rigid time cut-off (that evidence is showing is not one-size-fits-all), we can look to imaging to inform acute treatment decision. We have learned from subgroup analysis from DEFUSE-3 that some patients slowly progress in their stroke pathophysiology, meaning that even beyond 24 hours, some patients have a favorable core to penumbra ratio. [17] Other patients quickly progress in their stroke pathophysiology and may match their ischemic core to their salvageable penumbra well before traditional time-cut offs. [18]

It is possible that image-based selection criteria could be integral to the screening of all candidates for acute reperfusion therapy in the future. As WAKE-UP, EXTEND, DAWN, and DEFUSE-3 have shown us, there are some patients that can be reasonably considered for treatment beyond traditional time cut-offs. The same imaging criteria that extended the window for patients in these studies may be the same criteria that, in the future, could identify patients within the traditional time window who are likely to not benefit from treatment and who may have an increased risk of hemorrhagic conversion. One can image a patient without evidence of a salvageable penumbra presenting at 3 hours, for example, for whom the risks of IV tPA may, in fact, outweigh the potential benefits. 

Lastly, I would hazard readers from interpreting the results of WAKE-UP, EXTEND, DAWN, and DEFUSE-3 as providing comfort in delaying thrombolysis or endovascular therapy for patients in extended time windows who would otherwise have indications for reperfusion. For IV tPA, longer delay is associated with increased risk of symptomatic intracranial hemorrhage and more timely treatment is associated with better outcomes. In the 2015 endovascular therapy trials, [19-23] even for patients within 6 hours of LKN, more timely treatment was associated with better outcomes. Even if the imaging protocols used in WAKE-UP, EXTEND, DAWN, and DEFUSE-3 can identify “slow progressors” that can be treated outside current treatment windows, these patients’ stroke are still progressing as time goes by. [18] Systems that promote timely evaluation of patients with stroke systems should be expected to help patients in extended time window, as they do patients within traditional time windows. {24,25]

Studies like WAKE-UP that test traditional inclusion and exclusion criteria for reperfusion give promise for safer and more effective stroke treatment. We look forward to future clinical trials, like TIMELESS* and TWIST*, that hopefully will give further clarity on this clinical question.

WAKE-UP [5]: Efficacy and Safety of MRI-based Thrombolysis in Wake-up Stroke Trial

DAWN [10]: Diffusion Weighted Imaging (DWI) or Computerized Tomography Perfusion (CTP) Assessment With Clinical Mismatch in the Triage of Wake Up and Late Presenting Strokes Undergoing Neurointervention Trial

DEFUSE-3 [9]: Endovascular Therapy Following Imaging Evaluation for Ischemic Stroke 3 Trial

EXTEND [26]: EXtending the time for Thrombolysis in Emergency Neurological Deficits Trial

TIMELESS: Tenecteplase in Stroke Patients Between 4 and 24 Hours Trial (https://clinicaltrials.gov/ct2/show/NCT03785678)

TWIST: Tenecteplase in Wake-up Ischaemic Stroke Trial (https://clinicaltrials.gov/ct2/show/NCT03181360)

Chris Richards, MD, MS

Assistant Professor

Department of Emergency Medicine

Northwestern University

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How to Cite this Post

[Peer-Reviewed, Web Publication] Bunney G, Ireland A. (2019, Sept 9). Rise and Shine: A Review of the WAKE-UP Trial. [NUEM Blog. Expert Commentary by Richards C]. Retrieved from http://www.nuemblog.com/blog/wake-up-trial.

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Citations

1. Powers WJ, Rabinstein AA, Ackerson T, et al. 2018 Guidelines for the Early Management of Patients With Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association. Stroke 2018;49:e46-e110.

2. Aoki, Junya, et al. “FLAIR Can Estimate the Onset Time in Acute Ischemic Stroke Patients.” Journal of the Neurological Sciences, vol. 293, no. 1-2, 2010, pp. 39–44., doi:10.1016/j.jns.2010.03.011

3. Petkova, Mina, et al. “MR Imaging Helps Predict Time from Symptom Onset in Patients with Acute Stroke: Implications for Patients with Unknown Onset Time.” Radiology, vol. 257, no. 3, 2010, pp. 782–792., doi:10.1148/radiol.10100461.

4. Thomalla, Götz, et al. “DWI-FLAIR Mismatch for the Identification of Patients with Acute Ischaemic Stroke within 4·5 h of Symptom Onset (PRE-FLAIR): a Multicentre Observational Study.” The Lancet Neurology, vol. 10, no. 11, 2011, pp. 978–986., doi:10.1016/s1474-4422(11)70192-2.

5. Thomalla G, Simonsen CZ, et. al “MRI-Guided Thrombolysis for Stroke with Unknown Time of Onset | NEJM.” New England Journal of Medicine, Oxford University Press, www.nejm.org/doi/full/10.1056/NEJMoa1804355.

6. Albers, Gregory W., et al. “ATLANTIS Trial.” Stroke, vol. 33, no. 2, 2002, pp. 493–496., doi:10.1161/hs0202.102599.

7. Clark, Wayne M., et al. “Recombinant Tissue-Type Plasminogen Activator (Alteplase) for Ischemic Stroke 3 to 5 Hours After Symptom Onset.” Jama, vol. 282, no. 21, Jan. 1999, p. 2019., doi:10.1001/jama.282.21.2019.

8. Donnan, G. A. “Streptokinase for Acute Ischemic Stroke with Relationship to Time of Administration: Australian Streptokinase (ASK) Trial Study Group.” JAMA: The Journal of the American Medical Association, vol. 276, no. 12, 1996, pp. 961–966., doi:10.1001/jama.276.12.961.

9. Albers, Gregory W, et al. “Thrombectomy for Stroke with Selection by Perfusion Imaging.” New England Journal of Medicine, vol. 378, no. 19, 2018, pp. 1849–1850., doi:10.1056/nejmc1803856.

10.  Nogueira, Raul G, et al. “Thrombectomy 6 to 24 Hours after Stroke.” New England Journal of Medicine, vol. 378, no. 12, 2018, pp. 1161–1162., doi:10.1056/nejmc1801530.

11.  “Tissue Plasminogen Activator for Acute Ischemic Stroke.” New England Journal of Medicine, vol. 333, no. 24, 1995, pp. 1581–1588., doi:10.1056/nejm199512143332401.

12. Wahlgren, Nils, et al. “Thrombolysis with Alteplase for Acute Ischaemic Stroke in the Safe Implementation of Thrombolysis in Stroke-Monitoring Study (SITS-MOST): an Observational Study.” The Lancet, vol. 369, no. 9558, 2007, pp. 275–282., doi:10.1016/s0140-6736(07)60149-4.

13. Campbell, Bruce C V, et al. “Endovascular Thrombectomy for Stroke: Current Best Practice and Future Goals.” Bmj, vol. 1, no. 1, 2016, pp. 16–22., doi:10.1136/svn-2015-000004.

14. “Tenecteplase in Wake-up Ischaemic Stroke Trial (TWIST).” ClinicalTrials.gov, clinicaltrials.gov/ct2/show/NCT03181360.

15. “Tenecteplase in Stroke Patients Between 4 and 24 Hours (TIMELESS).” ClinicalTrials.gov, https://clinicaltrials.gov/ct2/show/NCT03785678

16. Yaghi S, Eisenberger A, Willey JZ. Symptomatic intracerebral hemorrhage in acute ischemic stroke after thrombolysis with intravenous recombinant tissue plasminogen activator: a review of natural history and treatment. JAMA neurology 2014;71:1181-5. PMCID: 4592535.

17. Christensen S, Mlynash M, Kemp S, et al. Persistent Target Mismatch Profile >24 Hours After Stroke Onset in DEFUSE 3. Stroke 2019;50:754-7. PMCID.

18. Rocha M, Jovin TG. Fast Versus Slow Progressors of Infarct Growth in Large Vessel Occlusion Stroke: Clinical and Research Implications. Stroke 2017;48:2621-7. PMCID.

19. Berkhemer OA, Fransen PS, Beumer D, et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med 2015;372:11-20. PMCID.

20. Campbell BC, Mitchell PJ, Kleinig TJ, et al. Endovascular therapy for ischemic stroke with perfusion-imaging selection. N Engl J Med 2015;372:1009-18. PMCID.

21. Fransen PS, Berkhemer OA, Lingsma HF, et al. Time to Reperfusion and Treatment Effect for Acute Ischemic Stroke: A Randomized Clinical Trial. JAMA neurology 2015:1-7. PMCID.

22. Goyal M, Demchuk AM, Menon BK, et al. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J Med 2015;372:1019-30. PMCID.

23. Jovin TG, Chamorro A, Cobo E, et al. Thrombectomy within 8 hours after symptom onset in ischemic stroke. N Engl J Med 2015;372:2296-306. PMCID.

24. Prabhakaran S, Ruff I, Bernstein RA. Acute stroke intervention: a systematic review. JAMA 2015;313:1451-62. PMCID.

25. Higashida R, Alberts MJ, Alexander DN, et al. Interactions within stroke systems of care: a policy statement from the American Heart Association/American Stroke Association. Stroke 2013;44:2961-84. PMCID.

26. Churilov L, Ma H, Campbell BC, Davis SM, Donnan GA. Statistical Analysis Plan for EXtending the time for Thrombolysis in Emergency Neurological Deficits (EXTEND) trial. International journal of stroke : official journal of the International Stroke Society 2018:1747493018816101. PMCID.

Chemical Sedation of the Agitated Patient in the ED

Written by: Zach Schmitz, MD (NUEM PGY-3) Edited by: Jason Chodakowski (NUEM PGY-4) Expert commentary by: Spenser Lang, MD (NUEM 2018)

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Expert Commentary

Chemical Sedation of the Agitated Patient

This is a wonderful infographic from Dr. Schmitz discussing the various tools at the disposal of the emergency physician regarding agitated patients. Unfortunately, this type of encounter in the Emergency Department occurs rather frequently. Agitated patients can represent danger to themselves, staff, and even other patients, and thus the shrewd emergency physician should be prepared to act quickly and efficaciously. Importantly, organic illness can manifest with agitation as well, and trainees do well to remember that the cause of the agitation is just as important as the management.

I want to highlight the ethical aspect of chemical sedation. Given that this is a relatively frequent encounter in the ED, physicians and nurses risk becoming desensitized to these patients. The decision to chemically sedate a patient is paramount to taking away a patient’s autonomy, so should never be taken lightly. Also, in an academic environment, it is especially important to model professionalism in this vulnerable population. For this reason, I tend to discourage the use of terms such as “chemical takedown” and “B52.”  Still, the safety of the patient and staff remains the most important factor, and if this is in question, it’s time to proceed rapidly and efficaciously.

I always attempt verbal de-escalation – in the “agitated but cooperative” population this will often work (see http://www.nuemblog.com/blog/verbal-deescalation). More often, an experienced nurse or tech can have a tremendous impact on these patients. However, if I am called back to the bedside for a 2nd time to attempt this process, that is usually another trigger for medications. If I have been called twice, that means this patient is taking up an abundance of nursing and support staff, putting other patients at relative risk. At this point I offer oral medications (olanzapine, benzodiazepines) if the patient is receptive, or proceed with IM medications if necessary.

Once you have made the decision to chemically sedate the patient, it is important to do so safely. Gather the necessary staff – this will include security if available, at least one person per limb, plus someone able to control a patient’s head. Before any needles come near the body, it is of utmost important to ensure the limbs are controlled, to avoid accidental needle sticks for the staff. For the best positioning for patients in restraints, see the image below. I always recommend keeping the head of the bed elevated to around 30 degrees. After the patient is appropriately sedated, feel free to remove the restraints if appropriate and safe, and monitor with both pulse oximetry and end-tidal capnography if there is concern for significant respiratory depression.

Image from: Scott Weingart. Podcast 060 – On Human Bondage and the Art of the Chemical Takedown. EMCrit Blog. Published on November 13, 2011. Accessed on March 8th 2019. Available at [https://emcrit.org/emcrit/human-bondage-chemical-takedown/ ].

I want to point out one of the tables above comparing the time of onset in the most common medications administered for agitation. As you can see, both antipsychotics and benzodiazepines have significant delays to onset when given intramuscularly. With this significant delay in onset, it can be tempting to redose the medications. I find nursing staff, since they typically remain at the bedside of these patients, can become impatient with a slow time of onset. As the table shows, midazolam works much more quickly than lorazepam and can prevent a second dose of medications which may be unnecessary and potentially harmful to the patient. As part of my process of administering these medications, I try to counsel everyone involved (security, nursing staff) about what to expect and what our next step will be if the first attempt truly fails.

Spenser Lang, MD

Assistant Professor

Department of Emergency Medicine

University of Cincinnati Medical Center

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How to Cite This Post

[Peer-Reviewed, Web Publication] Schmitz Z, Chodakowski J. (2019, Sept 2). Chemical Sedation. [NUEM Blog. Expert Commentary by Lang S]. Retrieved from http://www.nuemblog.com/blog/chemical-sedation .

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