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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Other Posts You May Enjoy

SCUBA Diving Injuries and Treatments

Written by: Aaron Wibberly, MD (NUEM PGY-2) Edited by: Sarah Dhake MD (NUEM Alum ‘19 ) Expert commentary by: Justin Hensley, MD

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Expert Commentary

Thanks for writing about one of the topics that isn’t frequently covered in emergency medicine. SCUBA isn’t terribly dangerous, but early recognition of the problems encountered in these patients can save lives.

First, barotrauma exists because of Boyle’s Law (P1V1=P2V2). There is no way to go around this law of nature, only ways to prevent negative outcomes.

Barotrauma mainly affects the ears but can also affect the sinuses or mask.

Mask squeeze is failure to maintain pressure in facemask as pressure increases. Signs include subconjunctival hemorrhages, lid edema, skin ecchymosis, hyphema, and orbital hemorrhage (1)

Both tympanic membrane ruptures and inner ear problems (round and oval window) can be very disorienting underwater, placing the patient in danger of ascending too quickly or not being able to find their way out.

In an unresponsive diver, the arterial gas embolism is assumed until proven otherwise. Alveolar barotrauma is a life threat that needs emergent treatment.

Decompression sickness is known as “the bends” because of caisson workers. It mainly affected the hips and knees, causing them to maintain a bent over stance. For reasons nobody has yet identified, SCUBA divers are affected in the shoulders and elbows.

The “chokes” are bubbles in the pulmonary and cardiac vasculature, and can cause a “mill wheel” murmur (splash, splash, splash).

Skin bends, known as cutis marmorata, may be related to bubbles in the vasculature, but there is some evidence that it may be centrally mediated and symptomatic of more severe DCS. It frequently causes itching. (2,3)

Neurologic DCS most commonly affects the spinal cord and causes 50-60% of sport diver casualties.

Knowing where your closest hyperbaric chamber exists is of utmost importance. Diver’s Alert Network (DAN) does not publish a database but maintains a referral network that you can speak to after emergency evaluation by calling their 24-hour DAN Emergency Hotline at +1-919-684-9111.

References:

1. Barron, E. (2018). The “Squeeze,” an Interesting Case of Mask Barotrauma. Air Medical Journal, 37(1), 74-75. doi: 10.1016/j.amj.2017.10.003

2. Germonpre, P., Balestra, C., Obeid, G. and Caers, D. (2015). Cutis Marmorata skin decompression sickness is a manifestation of brainstem bubble embolization, not of local skin bubbles. Medical Hypotheses, 85(6), pp.863-869.

3. Kemper TC, Rienks R, van Ooij PJ, and van Hulst RA. (2015). Cutis marmorata in decompression illness may be cerebrally mediated: a novel hypothesis on the aetiology of cutis marmorata. Diving Hyperb Med., 45(2), pp. 84-8.

Justin Hensley, MD

Founder and Editor of EBM Gone Wild

Quality Improvement/Assurance Director,

CHRISTUS Health-Texas A&M-Spohn Emergency Medicine Residency

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How to Cite this Post

[Peer-Reviewed, Web Publication] Wibberly A, Dhake S. (2019, Aug 27). SCUBA Diving Injuries and Treatments. [NUEM Blog. Expert Commentary by Hensley J]. Retrieved from http://www.nuemblog.com/blog/scuba.

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Other Posts You Might Enjoy

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Can't Miss Hand and Wrist Fractures in the ED

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Written by: Justine Ko, MD (NUEM PGY-3) Edited by: Spenser Lang MD (NUEM Alum ‘18 ) Expert commentary by: Matt Levine, MD

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“Can’t Miss” Hand and Wrist Injuries in the ED

In the emergency department, orthopedic complaints make up a large percentage of presentations, up to 50% in the pediatric population and close to 33% in the adolescent and young adult population. Many of these injuries are uncomplicated, but an astute clinician can diagnose subtle and uncommon injury patterns. Three less common injuries are reviewed here. If found, these injuries can alter the management and disposition of the patient. Each of these injuries should be carefully assessed for on physical exam and imaging. 

DISTAL RADIOULNAR JOINT (DRUJ) INJURIES

What exactly is the distal radioulnar joint and why is it important?

The distal radioulnar joint (DRUJ) consists of both the bony radioulnar articulation as well as the soft tissue components, including ligaments. It has significant contributions to the axial load-bearing capabilities of the forearm. The injury can be an isolated injury or associated with forearm fractures and should be tested for with every forearm injury as its presence can alter the disposition and even functionality of the patient. 

When does it occur?

A DRUJ injury may occur, although rarely, in isolation. This is usually related to a fall on outstretched hand (FOOSH). A DRUJ injury is more often associated with a fracture. Common associations include: 

• Distal radial fracture (DRF)

  • DRF + DRUJ = Galeazzi fracture (pictured to the right)

• Ulnar styloid fracture 

How should I assess for a possible DRUJ injury?

• Routine AP and lateral views are poor for determining a DRUJ injury. This is largely a CLINICAL DIAGNOSIS.

• Piano Key Sign: with the patient’s hand in pronation, push on the dorsal aspect of the ulnar head. Depression and rebound of the ulnar head suggest DRUJ instability

• Table Top Test: have patient place hands on a table and apply force. A DRUJ injury will show dorsal depression of the ulna

• Grind Test: hyperextend the wrist and axial load the forearm. A positive sign elicits pain over the joint 

How does this alter management?

When associated with a fracture, operative management is often indicated and consultation with our orthopedist is warranted. When missed, a DRUJ injury will result in instability of the joint and arthrosis. 

PERILUNATE AND LUNATE DISLOCATIONS

It has been reported that these injuries are missed in up to 25% of ED presentations.

How do these injuries occur?

In perilunate and lunate dislocations, the mechanism is usually hyperextension in the setting of trauma. Patients presents with hand and wrist pain/swelling.

How do I distinguish perilunate from lunate dislocations?

Lunate and perilunate dislocations can be easily confused or mistaken for each other. The key to distinguishing these injuries on imaging is the alignment between the metacarpal, carpal, and the radius/ulna bones.

In a normal lateral x-ray, these bones should all align (Figure 1, far left). In a lunate dislocation, the lunate itself is physically removed or out of line with the rest of these bones (Figure 1, far right), resulting in the classic “spilled teacup” appearance on x-ray. In a perilunate dislocation, the lunate sits in line with the radius/ulna, however the capitate/metatarsal bones are dislocated dorsally. 

On an AP film, a break in Gilula’s arc/lines may be used to assess for a perilunate or lunate dislocation (Figure 2).

How Are These Injuries Treated?

In the ED, closed reduction can be attempted. If successful, definitive treatment can occur up to 7 days later. If unsuccessful, operative management is indicated. Definitive treatment involves open reduction and internal fixation. 

How Would I Reduce These Injuries in the ED?

Usually, the assistance of our orthopaedic colleagues is warranted. Finger traps can be used for traction. The wrist should be extended while placing palmar pressure on the lunate. Then, with continued traction, the wrist should be gradually flexed so that the capitate falls back into place within the concavity of the lunate. Once the lunocapitate joint is reduced, the wrist can be extended in traction again for full reduction.

SCAPHOLUNATE DISSOCIATION

What is a scapholunate dissociation?

Scapholunate dissociation is caused by injury to the scapholunate ligament. Injury to this ligament can occur with acute FOOSH injury or be caused by degenerative rupture of the ligament. 

How do I diagnosis it?

These patients present with radial wrist pain. On imaging, the following signs can aid in diagnosis. 

• Terry Thomas sign: This is seen on an AP wrist film and is indicated by a gap >3mm between the scaphoid and lunate bones 

• Cortical Ring sign: occurs when the scaphoid is in a flexed position, making the scaphoid tubercle more prominent. A measure distance less than 7mm between the end of the cortical ring and the proximal end of the scaphoid suggests scapholunate dissociation and instability.  

How do I manage it?

In the ED, patients should be placed in a thumb spica cast for stabilization and referred to orthopaedics for follow up. Operative indication includes injury within 3 weeks and associated imaging and physical exam findings. During this time frame, the SL ligament is still viable for repair. 

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Expert Commentary

Great choice by Dr. Ko to highlight these injuries that are often subtle, yet important because of the comorbidities associated with missing the diagnosis. 

The Galeazzi fracture is a classic EM boards question, because it is important!  It was termed by Campbell as the “fracture of necessity” (modern day translation = “this needs surgery!”) in 1942 because nonoperative management was observed to be associated with recurrent ulna styloid dislocations.  Hughston confirmed this is 1957, reporting that 35/38 cases treated nonoperatively had unsatisfactory outcomes.

There’s a saying in orthopedics that “the most commonly missed injury is the second injury”.  The radial shaft fracture is usually obvious and can distract the clinician from the less dramatic DRUJ injury.  DRUJ injury is radiographically diagnosed by:

• Fracture at the BASE of the ulna styloid process (not the tip)

• A widened DRUJ (a comparison x ray may be necessary), or

• >5mm of shortening of the radius relative to the distal ulna.

A subtle clinical finding often associated with the Galeazzi fracture is anterior interosseus nerve injury.  It is a branch of the median nerve and is purely motor, so there will be no sensory deficit or paresthesia!  It manifests as loss of pinch strength between the thumb and index finger.  So have the patient make the OK sign and resist as you try to open it!

Mayfield, Johnson and Kilcoyne described a pattern of carpal injury caused by wrist hyperextension, ulnar deviation and intercarpal supination in 1980. In their original research on cadavers, progressive hyperextension force was applied and resulted in a consistent, sequential, progressively more unstable intercarpal injury pattern known as the four stages of carpal instability:

1. Scapholunate dissociation

2. Perilunate dislocation

3. Perilunate and triquetral dislocation

4. Lunate dislocation

Acute scapholunate dissociation is the most common pattern of carpal instability. It occurs secondary to a tear of the scapholunate interosseus ligament.  Scapholunate dissociation can also be chronic secondary to arthritic changes when there is no history of recent trauma.

X rays in lunate and perilunate dislocations are often not as clear and obvious as the diagrams used to teach these injuries.  The key to realizing that there is a carpal bone dislocation is recognizing that the carpal arcs are disrupted on the AP view. The distal and proximal carpal rows should never overlap on this view.  If you recognize this, you will heighten your suspicion and won’t miss these injuries, even if you cannot immediately tell the exact diagnosis.  

The name perilunate dislocation has always been a pet peeve of mine. There is no perilunate bone, so this nomenclature just introduces confusion.  It should simply be called a capitate dislocation, because that it what it really is.

All of these injuries, and more, are further detailed in our Ortho Teaching Files!

Matthew R. Levine, MD

Assistant Professor

Department of Emergency Medicine

Northwestern University

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How to Cite this Post

[Peer-Reviewed, Web Publication] Ko J, Lang S. (2019, Aug 19). Can't Miss Hand and Wrist Fractures in the ED. [NUEM Blog. Expert Commentary by Levine M]. Retrieved from http://www.nuemblog.com/blog/cant-miss-hand-and-wrist-fractures-in-the-ed/.

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Other Posts You Might Enjoy

To learn more about the diagnosis and management of orthopedic injuries from head to toe, check out our Ortho Teaching Files!

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References

1. Bowen WT, Slaven EM. 2014. “Evidence-based management of acute hand injuries in the emergency department.” Emergency Medicine Practice 16 (12):1-28. 

2. “Distal Radial Ulnar Joint (DRUJ) Injuries - Trauma - Orthobullets.” n.d. Accessed March 7, 2018. https://www.orthobullets.com/trauma/1028/distal-radial-ulnar-joint-druj-injuries.

3. Kardashian G, CHristoforou DC, Lee SK. 2011. “Perilunate dislocations.” Bulletin of the NYU Hospital for Joint Diseases 69 (1):87-96.

4. “Lunate Dislocation (Perilunate Dissociation) - Hand - Orthobullets.” n.d. Accessed March 2, 2018. https://www.orthobullets.com/hand/6045/lunate-dislocation-perilunate-dissociation.

5. Pappou, Ioannis P., Jennifer Basel, and D. Nicole Deal. 2013. “Scapholunate Ligament Injuries: A Review of Current Concepts.” Hand (New York, N.Y.) 8 (2): 146–56. https://doi.org/10.1007/s11552-013-9499-4.

6. Reisler T, Therattil PJ, Lee ES. 2015 “Perilunate Dislocation.” Eplasty. 

7. Rodner CM, Weiss APC. “Acute scapholunate and lunotriquetral dissociation.” American Society for Surgery of the Hand. 155-171.

8. Scalcione LR, Gimber LH, Ho AM, Johnston SS, Sheppard JE, Taijanovic MS. 2014. “Spectrum of carpal dislocations and fracture-dislocations: imaging and management.” AJR 203: 541-550.

9. Thomas, Binu P, and Raveendran Sreekanth. 2012. “Distal Radioulnar Joint Injuries.” Indian Journal of Orthopaedics 46 (5): 493–504. https://doi.org/10.4103/0019-5413.101031.

Don't Forget aVL!

Written by: Laurie Aluce, MD (NUEM PGY-3) Edited by: Kimberly Iwaki MD (NUEM Alum ‘18 ) Expert commentary by: Daniel Schimmel, MD

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The Case: 

Patient: 57 year old male

Chief Complaint: Chest Pain 

PMH: Hypertension

Pain: Mid-sternal, non-radiating, 6/10, constant pressure

Onset:  45 minutes ago while watching TV

Associated symptoms: No diaphoresis, light-headedness, nausea, vomiting, or back pain 

Vitals: T 98.8, HR 70, BP 110/68, RR 14, Sat 100% on room air

Physical Exam:

General: Alert, no apparent distress, sitting comfortably in cart 

Cardiac: Regular rate and rhythm, no murmurs/rubs/gallops

Pulmonary: Clear to auscultation bilaterally, no crackles/wheezes

Extremities: Warm and well perfused, 2+ distal pulses, cap refill < 2s 

Labs: In process 

Triage EKG: 

Image from Stephen Smith, MD. http://hqmeded-ecg.blogspot.com/2011/02/inferior-hyperacute-t-waves-clue-is-t.html

What abnormalities do you see in this EKG? 

• Prolonged PR interval

• Slightly widened QRS

• Hyperacute T waves in II, III, aVF

• T wave inversion (TWI) in aVL

• < 1mm ST depression in I, avL

What are you concerned about? What elements of this EKG raise your concern?   

• Inferior myocardial infarction (MI) due to hyperacute T waves in II, III, aVF

• Inferior MI or significant mid left anterior descending (LAD) lesion due to TWI in aVL [3] 

How will you differentiate an inferior MI from a chronic mid LAD lesion? 

Clinical picture and a repeat EKG. If the TWI is due to a chronic mid LAD lesion, it should not change on serial EKGs. If the TWI is due to an inferior MI, you may see it evolve to ST depression in aVL and/or ST elevation in II, III, aVF. [3]

You obtain a repeat EKG with one right-sided lead, V4R:

Image from Edward Burns, MD. https://lifeinthefastlane.com/ecg-library/basics/inferior-stemi/

What abnormalities do you see in the repeat EKG?

• Hyperacute T waves and ST elevation in II, III, aVF

• ST depression and TWI in aVL

• ST depression in V2

• <1mm ST depression in I

• <1mm ST elevation in V4R

What are you concerned about? What elements of this EKG raise your concern?

• Concern for inferior MI

  • ST elevation in II, III, aVF

  • ST depression and T wave inversion in aVL

    • EKG sensitivity for inferior MI increases from 60% to 77% when criteria includes ≥ 1mm reciprocal ST depression in aVL in addition to ≥ 1mm ST elevation in II, III, aVF [1]

• Concern for right ventricle (RV) involvement

  • 25% – 53% of inferior MIs have RV involvement [5]

  • ST elevation in III > II

  • Isoelectric ST segment in V1 with ST depression in V2

  • ST depression and T wave inversion in aVL

    • >1mm ST depression in aVL has sensitivity of 87% and positive predictive value of 90% for RV involvement with acute inferior MI [5]

• Other findings suggestive of RV involvement not pictured in this EKG

  • ST elevation in V2 > 50% the magnitude of ST depression in aVF [4]

  • Right bundle branch block, 2nd and 3rd degree AV block

  • ST elevation in V1

How can your further evaluate for RV involvement?  

You ask for a right-sided EKG to check for ST elevation in V3R-V6R, but your EKG tech doesn’t remember where to place the leads. The tech looks to you for help. Where do you put the leads? 

                 Full Right-Sided EKG                                                         Standard EKG with V4R

Images from Tom Bouthillet. http://www.ems12lead.com/2008/10/17/12-lead-ecg-lead-placement-diagrams/

If you don't have the time to perform a full right-sided EKG, you can perform a standard EKG but switch V4 to V4R as shown with the prior EKG. V4R is considered the best single lead for diagnosing a right ventricular MI.[2] ST elevation ≥ 1 mm in V4R has a sensitivity of 88% and a specificity of 78% for RV infarction. [6]

EKG with V4R-V6R:

Image from Ary Goldberger, MD. UpToDate: Electrocardiogram in the diagnosis of myocardial ischemia and infarction

What abnormality do you see in the right-sided leads?

• ST elevation in V4R-V6R  

What is your diagnosis?

• Inferior MI with RV infarction  

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Take Home Points:

1. Don’t forget aVL. T wave inversion and ST depression in aVL can be a marker of serious cardiac pathology:

   1. Significant mid-LAD lesion

   2. Evolving inferior MI and possible RV involvement

2. If you are concerned for inferior ischemia, obtain a right-sided EKG to evaluate for right ventricular involvement

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Expert Commentary

This is an excellent review of aVL, an important lead for diagnosis and prognosis.  Because it can be a modifier, or is used in conjunction with other criteria for diagnosis, it often gets overlooked.

In the acute setting, aVL can be used to help identify ST elevation myocardial infarction (STEMI) in various locations.  In addition to the aforementioned use in identifying RV involvement in inferior STEMI and mid LAD lesions, aVL is considered a high lateral lead which is fed by diagonal vessels.  As such, acute blockages that affect the proximal LAD with anterior STEMI in V3, V4, anteroseptal involvement in V1, V2 and may also have high lateral involvement in aVL. While I am always watching for shock and unstable arrhythmias taking patients to the cardiac catheterization lab, if I see this distribution with an anterior STEMI, I am even more concerned due to the amount of myocardium subtended by the lesion.  I often preemptively get access for cardiac mechanical support in case cardiogenic shock develops. In this way, the prognostic information from aVL may change practice in the cardiac catheterization lab.

Not to be overlooked, leads I and aVL may be the only leads with ST elevation in an isolated high lateral STEMI in a diagonal vessel.  Diagonal 1 or diagonal 2 may be large vessels and be the only vessel with acute thrombosis. aVL is the reciprocal lead to the inferior leads in inferior STEMI.  Similarly, lead III may move reciprocally, showing ST segment depression in the high lateral STEMI with elevation in aVL.

As nice as it can be to have aVL to prognosticate inferior STEMI, prognosticate anterior STEMI and identify isolated high lateral STEMI, aVL ST segments and T waves can be abnormal for non-acute reasons leading to a lack of specificity.  The most common reason for an abnormal repolarization in aVL is strain in the setting of LVH. So how do we differentiate acute reciprocal changes from strain pattern? 

A frequently overlooked bit of information on the EKG is the QRS-T angle.  Luckily this is reported for us on the EKG at the top. In the setting of T wave inversion, if the angle is greater than 100 degrees, this is more consistent with strain.  Furthermore, if the ST segment leading to the T wave is downwardly concave (think downward parabolic curve) with asymmetry of the T wave, this also is more consistent with strain.  If we look at the presented case’s EKGs, we can dissect them a bit further. In the triage EKG, there isn’t ST segment depression at all. In fact there is elevation with a T wave inversion.  This is concerning. The ST segment may be isoelectric with an inverted T wave, but there should not be ST elevation with a T wave inverted in the opposite direction. This morphology is often used in Sgarbossa criteria to identify STEMI in left bundle branch block.  So in addition to the hyperacute T waves of this triage EKG, aVL is very concerning. In the follow-up EKG, we can see dynamic changes that have occurred in the inferior leads solidifying the diagnosis. But aVL also suggests RV involvement. The ST segment is downsloping, depressed without concavity (more linearly pointing down to the right).  To clinch the diagnosis of RV involvement, we also see the right sided leads with elevation.

It is definitely possible to have a patient with LVH/strain findings and also have an acute inferior STEMI.  As demonstrated successfully in this case, the statement about serial EKGs is a critical one. Even in the setting of a normal EKG, a good story for myocardial infarction should prompt a serial EKG and often a posterior EKG to identify a supposedly electrocardiographically silent STEMI.  Remember STEMI is an EKG diagnosis that is supposed to correlate with the physiologic condition of an acute 100% occlusion of a vessel. In the early period, there can be stuttering pain with opening and closing of the vessel and the EKG may not capture it in that moment or may miss the posterior STEMI if the posterior EKG is not obtained.

To sum up the importance of aVL:

1. Inferior STEMI: Improved diagnosis when aVL has a depressed ST segment with an inverted T wave

2. Inferior STEMI: Considered worse prognosis when aVL has a depressed ST segment with an inverted T wave as it suggests a more proximal RCA occlusion with RV involvement.  ST elevation in V1 or right sided V4 may also be helpful in identifying proximal RCA occlusion with RV branch involvement.

3. Anterior STEMI: aVL STEMI confers a worse prognosis, suggesting more proximal LAD involvement.

4. Isolated high lateral STEMI: ST elevation in leads I and aVL may identify an acute 100% blockage in a diagonal vessel.  Lead III may have reciprocal ST segment depression.

To differentiate strain from ischemic changes in aVL:

1. QRS-T angle:  If greater than 100, may be consistent with strain.

2. ST segment slope:  If concave, consider strain.  If downsloping but the ST segment is more straight as it aims downward, consider an acute event.

3. T Wave inversion:  If there is asymmetry to the inverted T wave, it may be more consistent with strain.

In summary, the EKG has so much data in it.  Pattern recognition can be a wonderful tool for quick diagnosis of clear problems.   But a methodical evaluation of the EKG can still be done quickly and identify what others may miss.

Dr. Daniel R. Schimmel

Assistant Professor of Medicine

Bluhm Cardiovascular Institute

Northwestern University

References:

1. Birnbaum Y, et al. ST segment depression in aVL: a sensitive marker for acute inferior myocardial infarction. Eur Heart J 1993;14(1):4-7.

2. Carley SD. Beyond the 12 lead: Review of the use of additional leads for the early electrocardiographic diagnosis of acute myocardial infarction. Emergency Medicine 2003;15: 143-54.

3. Hassen GW, et al. Lead aVL on electrocardiogram: emerging as important lead in early diagnosis of myocardial infarction. Am J Emerg Med 2014;32(7)785-88.

4. Somers MP, et al. Additional electrocardiographic leads in the ED chest pain patient: right ventricular and posterior leads. Am J Emerg Med 2003;21(7):563-73.

5. Turhan H, et al. Diagnostic value of aVL derivation for right ventricular involvement in patients with acute inferior myocardial infarction. Ann Noninvasive Electrocardiol 2003;8:185-88.

6. Zehender M, et al. Right ventricular infarction as an independent predictor of prognosis after acute inferior myocardial infarction. N Engl J Med 1993; 328:981-88.

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How to Cite this Post

[Peer-Reviewed, Web Publication] Aluce L, Iwaki K. (2019, Aug 12). Don’t Forget aVL. [NUEM Blog. Expert Commentary by Schimmel D]. Retrieved from http://www.nuemblog.com/blog/dont-forget-aVL/.

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Fluid Responsiveness

Written by: Brett Cohen, MD (NUEM PGY-3) Edited by: Duncan Wilson, MD (NUEM Alum ‘18) Expert commentary by: Luisa Morales-Nebreda, MD

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Expert Commentary

I’ll start by saying that the assessment of a patient’s intravascular volume status and fluid responsiveness is one of the most difficult tasks in clinical medicine, yet it remains a crucial one to adequately manage acute circulatory failure.

After decades of dedicated research to the critically ill, we’ve learned that rigid protocols lead to large amounts of fluid administration, and that fluid overload is associated with increased morbidity and mortality in septic shock and ARDS patients. As you mentioned, only half of hemodynamically unstable patients are fluid responsive, prompting clinicians to describe novel tools/methods to better evaluate fluid responsiveness.

How do we define fluid responsiveness? What are the determinants of fluid responsiveness?

Fluid responsiveness has been defined as a 10-15% increase in cardiac output after a 500 cc bolus fluid challenge. I find this arbitrary definition unhelpful, but I do think that understanding what determines a fluid bolus leading to a preload-responsive state is important. 

Figure 1: Frank Starling curve

When giving a fluid bolus, the expectation is that it will increase cardiac preload (by increasing both the stressed volume and mean circulatory filling pressure). Once this condition has been met, the next assumption is that the increase in venous return will lead to a change in stroke volume/cardiac output (venous return = cardiac output). This is the ideal situation! Both ventricles working on the ascending limb of the Frank-Starling curve without any major changes in other determinants of cardiac output (contractility, afterload, diastolic function) Figure 1. Unfortunately, our critically ill patients are not that simple and most times display significant changes in cardiac contractility (e.g., due to acidosis) and afterload (e.g., due to vasoactive agents) that could place them on the flat portion of this curve.

Cardiac Output = Heart Rate x Stroke Volume

Stroke Volume is determined by: contractility, preload, afterload

How do we measure fluid responsiveness?

Despite a great amount of evidence showing that “static” measurements, such as central venous pressure (CVP) are poor predictors of fluid responsiveness, they continue to be widely used. I don’t mean to say that measuring CVPs is useless. After all, perfusion is determined by the pressure gradient between MAP (mean arterial pressure) and CVP, and CVP is a good marker of preload (just NOT of preload responsiveness). 

To circumvent this limitation, we can use “dynamic” measurements of heart-lung interactions during mechanical ventilation. Specifically, if changes in intrathoracic pressure under positive pressure ventilation lead to cyclic changes in stroke volume (stroke volume variation or SVV), pulse pressure (pulse pressure variation PVV), or vena cava diameter it indicates that both ventricles are preload-dependent and the patient is fluid responsive. Limitations to these 3 methods include: a) patients need to be mechanically ventilated and without spontaneous breaths (during which changes in intrathoracic pressure become unreliable) b) tidal volume of at least 8 cc/Kg and normal respiratory system compliance (in order to generate significant swings in intrathoracic pressure, tidal volume needs to be on the high end and your lungs/chest wall can’t be stiff). 

So you can think about how limited these maneuvers are in the ICU setting. Most intubated patients take spontaneous breaths (unless paralyzed or deeply sedated). If paralyzed for ARDS, they need to be on low-tidal volume ventilation and their lungs are generally pretty stiff.

As you mentioned a maneuver that is unaffected by these limitations is the passive leg raise test (PLR). Importantly, PLR raises preload by shifting venous blood not only from your lower extremities, but mainly from your splanchnic compartment (where ~70% of unstressed volume reservoir lies). This is why in order to adequately perform the maneuver, patients are placed in a semi-recumbent position (rather than horizontal) and the bed is adjusted to 45֯, followed by assessment of cardiac output changes within 60 seconds (NOT blood pressure changes).

PLR is one of the most validated maneuvers for assessment of fluid responsiveness, and as you described, many downstream methods to measure cardiac output have been used, including: a) velocity time integral of the left ventricular outflow tract b) peak velocity of the carotid artery c) changes in end-tidal CO2. 

Given the widespread use of critical care echocardiography and their inherent practicality, I think echocardiographic indices are the most useful dynamic parameters to predict fluid responsiveness.

What to expect and my two cents on fluid responsiveness

Given the pace of technology, innovation in hemodynamic monitoring methods will likely improve in the not too distant future. Pocket echo probes and non-invasive wearable sensors measuring cardiac output will make assessment of fluid responsiveness much easier and reliable. Check out:

Michard et al. Intensive Care Medicine (2017) 43:440-442 https://link.springer.com/article/10.1007%2Fs00134-016-4674-z

Vincent et al. Intensive Care Medicine (2018) 44:922-924 https://link.springer.com/article/10.1007%2Fs00134-018-5205-x

For now, I go to the bedside and after a physical exam perform a basic point-of-care ultrasound to assess heart function, look for interstitial lung edema (B lines) and IVC collapsibility before and after a PLR maneuver (if tolerated). Combining information from these maneuvers not only allows you to better assess a patient’s current volume status and likelihood to be fluid responsive (hyperdynamic LV, absent B lines, collapsible IVC), but can also help you identify what type of shock your patient has and if giving fluid could make things worse (RV failure). 

When a patient is likely fluid responsive, I give a small/moderate fluid bolus (250-500 cc) then come back to the bedside to repeat my assessment with the tools I feel most comfortable. Then I ask myself: are things getting better? (Improved mental status/blood pressure, increased in urine output and decreased vasoactive agent requirement). And then do it all over again!

Luisa Morales-Nebreda, MD

Fellow, Pulmonary & Critical Care Medicine

Department of Medicine

Northwestern University

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How to Cite this Post

[Peer-Reviewed, Web Publication] Cohen B, Wilson D. (2019, Aug 5). Fluid Responsiveness. [NUEM Blog. Expert Commentary by Morales-Nebreda L]. Retrieved from http://www.nuemblog.com/blog/fluid-responsiveness.

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Spontaneous Bacterial Peritonitis

Written by: Kevin Dyer, MD (NUEM PGY-4) Edited by: Paul Trinquero, MD (NUEM Alum ‘19) Expert commentary by: Steven K. Herrine, MD

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Background

Spontaneous bacterial peritonitis (SBP) is an infection of ascitic fluid without an evident intra-abdominal or surgically-treatable source [1]. The pathophysiology is poorly understood, but likely relates to bacterial translocation across an edematous bowel wall (due to portal hypertension) into the immunologically impaired ascitic fluid. SBP is common in patients with severe hepatic dysfunction (present in 20% of hospitalized patients with ascites) and carries a mortality rate of 10% [2,3]. The high incidence, grave mortality, and potential benefit of early treatment make SBP a can’t-miss diagnosis for the emergency physician.

Clinical Features

The classic triad of SBP is fever, abdominal pain, and increasing ascites [4]. However, like most other “classic triads” in medicine, patients rarely present with all three and instead are much more likely to have only 1 or 2 of these features. The most common signs and symptoms are fever (69%), abdominal pain (59%), altered mental status (54%), and abdominal tenderness (49%). Other less common signs and symptoms include diarrhea (32%), paralytic ileus (30%), hypotension (21%), and hypothermia (17%) [5]. In one study, 13% of patients with SBP were asymptomatic [6].

Importance of Paracentesis

As mentioned above, the clinical signs and symptoms of SBP are variable  and sometimes subtle, making it a difficult clinical diagnosis. Instead, diagnosis hinges on the results of an ascitic fluid sample obtained via a diagnostic paracentesis. Ascitic fluid findings indicative of SBP include an elevated absolute polymorphonuclear leukocyte (PMN) count ≥250 cells/mm3, a positive ascitic fluid bacterial culture, and exclusion of secondary causes of bacterial peritonitis (e.g. perforated viscous, intra-abdominal abscess). For the ED physician, a PMN level ≥250 cells/mm3 necessitates initiation of antibiotics as soon as possible, if they were not already started empirically [7].

Not only do patients at risk for SBP need a diagnostic paracentesis, but because treatment is time sensitive, it should be performed as quickly as is feasible. A study by Kim et al showed a 3.3 percent increase in in-hospital mortality for each hour paracentesis was delayed and revealed that delayed paracentesis for patients ultimately diagnosed with SBP led to a 2.7-fold increased risk of death [8-9].

Treatment

Empiric therapy should be initiated in patients with ascites who have a temperature >100°F, abdominal pain and/or tenderness, altered mental status, or ascitic PMNs ≥250 cells/mm3. First line treatment is a third-generation cephalosporin such as Ceftriaxone 2g per day or Cefotaxime 2g q8hrs [10]. For those with a severe penicillin allergy, fluoroquinolones are a viable alternative provided the patient has not been on a prophylactic fluoroquinolone. Common choices are levofloxacin 750mg daily or ofloxacin 400mg BID [10-11].

An additional therapeutic consideration is albumin infusion. Current guidelines from the American Association for the Study of Liver Diseases (AASLD) recommend the administration of albumin at a dose of 1.5g/kg for patients with either a BUN >30mg/dL, a serum creatinine >1.30mg/dL, or a total bilirubin >4mg/dL. A meta-analysis of 4 studies demonstrated a significant reduction in renal impairment (8% vs 31%) and a decrease in mortality (16% vs 35%) in patients who received 1.5g/kg of albumin within 6 hours of diagnosis of SBP [12-13].

Take Home Points

• Spontaneous bacterial peritonitis is an infection of ascitic fluid without an evident intra-abdominal or surgically-treatable source. 

• Diagnosis is nearly impossible to make clinically due to variable, and sometimes subtle, presenting symptoms and therefore hinges on obtaining a fluid sample via a diagnostic paracentesis.

• Early diagnostic paracentesis in the ED may improve mortality for hospitalized patients with ascites.

• Polymorphonuclear leukocyte (PMN) count ≥250 cells/mm3 raises suspicion for SBP and should prompt initiation of empiric antibiotics - first line is 2g of Ceftriaxone and second line is a fluoroquinolone. 

• In addition, AASLD guidelines recommend 1.5g/kg of albumin for patients with SBP who have BUN >30mg/dL, creatinine >1.3mg/dL, or bilirubin >4mg/dL as this may decrease mortality and reduce the incidence of renal impairment.

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Expert Commentary

The blog authors make many excellent points about the recognition and management of SBP in the emergency department. From the standpoint of a hepatologists, several concepts and developments regarding this dangerous diagnosis are worth emphasizing. 

• Clinical context is vital in making management decisions: a patient with advanced chronic liver disease, manifested by high MELD score, is more likely to have SBP than an individual with acute or less advanced disease. 

• Prompt paracentesis is the key to proper management. It is considered safe to perform diagnostic paracentesis in all patients but those with evident hyperfibrinolysis or those in DIC. Some have advocated for midline paracentesis to avoid vascular structures, but LLQ has been demonstrated to be safer. (Sakai 2005)

• Only a small amounts of fluid is required to make the diagnosis of PMN > 250 cells/mL. Even a drop in a hemocytometer can be sufficient

• Patients on prophylactic antibiotics due to previous SBP or low-protein ascites should raise concern for resistant organisms. It is important to sample the ascites in these individuals before commencing antibiotic therapy. 

• The use of dipstick (leukocyte esterase) diagnosis is supported by some literature but use has been limited mostly to developing nations (Mendler 2010)

• There is a growing body of literature that supports initial intravenous therapy followed by transition to oral antibiotics in clinical scenarios meeting certain conditions. (Angeli 2006)

References:

1. Sakai H, Sheer TA, Mendler MH, Runyon BA. Choosing the location for non-image guided abdominal paracentesis. Liver International 2005;25:984-986. 

2. Mendler MH, Agarwal A, Trimzi M, Magridal E, Tsushima M, Joo E, Santiago M, et al. A new highly sensitive point of care screen for spontaneous bacterial peritonitis using a leukocyte esterase method. J Hepatol 2010;53:477-483

3. Angeli P, Guarda S, Fasolato S, Miola E, Craighhero R, Del Piccolo F, Antona C, et al. Switch therapy with ciprofloxacin vs intravenous ceftazidime in the treatment of spontaneous bacterial peritonitis in patients with cirrhosis: similar efficacy at lower cost. Aliment Pharmacol Ther 2006;23:75-84

Steven K. Herrine, MD

Professor of Medicine, Division of Gastroenterology and Hepatology

Vice Dean for Academic Affairs

Sidney Kimmel Medical College at Thomas Jefferson University

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How to Cite this Post

[Peer-Reviewed, Web Publication] Dyer K, Trinquero P. (2019, July 29). Spontaneous Bacterial Peritonitis. [NUEM Blog. Expert Commentary by Herrine S]. Retrieved from http://www.nuemblog.com/blog/sbp.

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References:

1. Such J, Runyon BA. Spontaneous bacterial peritonitis. Clin Infect Dis 1998; 27:669.

2. Nickson, Chris. “Spontaneous Bacterial Peritonitis.” Life in the Fast Lane Medical Blog, 17 Dec. 2012, https://www.lifeinthefastlane.com/ccc/spontaneous-bacterial-peritonitis

3. Guiney, Allan. “Should All Admitted Patients with Ascites Get a Paracentesis?” Core EM, 7 Dec. 2017, coreem.net/journal-reviews/paracentesis-for-all

4. “Episode 123.0 – Paracentesis Journal Update.” Core EM, 27 Nov. 2017, coreem.net/podcast/episode-123-0

5. McHutchison JG, Runyon BA. Spontaneous bacterial peritonitis. In Surawicz CM, Owen RL (Eds.), Gastrointestinal and Hepatic Infections, WB Saunders Company, Philadelphia 1995. P.455.

6. Runyon BA. Monomicrobial nonneutrocytic bacterascites: a variant of spontaneous bacterial peritonitis. Hepatology 1990; 12:710Runyon BA. Monomicrobial nonneutrocytic bacterascites: a variant of spontaneous bacterial peritonitis. Hepatology 1990; 12:710.

7. Runyon, B. (2018) Spontaneous bacterial peritonitis in adults: Clinical manifestations. In K.D. Lindor (Ed.), UpToDate. Retrieved April 2, 2018, from https://www.uptodate.com/contents/spontaneous-bacterial-peritonitis-in-adults-clinical-manifestations

8. Kim JJ, Tsukamoto MM, Mathur AK, et al. Delayed paracentesis is associated with increased in-hospital mortality in patients with spontaneous bacterial peritonitis. Am J Gastroenterol 2014; 109:1436.

9. Kumar A, Roberts D, Wood KE, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med 2006; 34:1589.

10. Runyon, B. (2018) Spontaneous bacterial peritonitis in adults: Treatment and prophylaxis. In K.D. Lindor (Ed.), UpToDate. Retrieved April 2, 2018, from https://www.uptodate.com/contents/spontaneous-bacterial-peritonitis-in-adults-treatment-and-prophylaxis

11. Navasa M, Follo A, Llovet JM, et al. Randomized, comparative study of oral ofloxacin versus intravenous cefotaxime in spontaneous bacterial peritonitis. Gastroenterology 1996; 111:1011.

12. Salerno F, Navickis RJ, Wilkes MM. Albumin infusion improves outcomes of patients with spontaneous bacterial peritonitis: a meta-analysis of randomized trials. Clin Gastroenterol Hepatol 2013; 11:123.

13. Pescatore, Rick. “Should You Give Albumin in Spontaneous Bacterial Peritonitis (SBP)?” R.E.B.E.L. EM - Emergency Medicine Blog, 6 July 2017, rebelem.com/should-you-give-albumin-in-spontaneous-bacterial-peritonitis-sbp

Pelvic Fractures

Written by: Justine Ko, MD (NUEM PGY-3) Edited by: Terese Whipple, MD (NUEM PGY-4) Expert commentary by: Matt Levine, MD

Pelvic Ring Fractures

Overview

Pelvic ring fractures make up about 3% of skeletal fractures [1]. In the emergency department, they are often seen with high-impact blunt trauma, such as MVCs, crush injuries, or falls.

The pelvis consists of the sacrum and the two innominate bones, which are made up of the ilium, ischium, and pubis [2]. The sacrum and the innominate bones together form a posterior arch and an anterior arch that join to make a ring, also known as the pelvic inlet. The stability of the pelvis is enforced by ligaments: the sacroiliac ligaments, the sacrospinous ligaments, and sacrotuberous ligaments [2]. The ligaments and bones together give the pelvis vertical and rotational stability. 

Pelvic ring fractures carry a significant mortality, ranging from 15-25% in closed fractures, and as much as 50% in open fractures [3]. They are often associated with other high-mortality injuries as well, such as chest injuries, spinal injuries.

What are the mechanisms associated with these injuries?

The Young-Burgess classification system categorizes injury patterns based on the mechanism of injury and the forces applied: anteroposterior compression (APC), lateral compression (LC), and vertical shear (VS) [1]. The most common mechanism is lateral compression, which occurs when lateral forces are applied to the pelvis (as the name would suggest). APC injuries result in the classic “open book” pelvic fractures (Figure 1). 

Figure 1

Figure 2

• Anteroposterior compression: causes disruption of the pubic symphysis. A normal pubic symphysis should not exceed 5mm. Injuries where the symphysis widening is <2.5cm, with no significant posterior column injury or other fractures, are usually considered stable. APC injuries are often associated with significant blood loss, as the pelvic volume increases and can store more blood [4].

• Lateral Compression: considered rotationally unstable. This mechanism causes the pelvic volume to decrease, and therefore, is associated with less blood loss [4].

• Vertical shear: the most unstable, often associated with axial loading of the hemipelvis, such as with a fall or a jump from a height. 

What exam findings should I look for?

During a trauma workup, visual inspection for leg-length discrepancy or rotation of the pelvis may provide clues to a hip or pelvic injury. You may assess for stability of the pelvis by applying downward and medial pressure to the bilateral iliac crests. Apply pressure gently and slowly to avoid disruption of any possible clots that may have formed.

A digital rectal exam should also be performed to assess for spinal cord injury and frank blood. In males, the meatus should be assessed for possible bladder or urethral injury.

X-ray reading tips

• Check the 3 circles! (Figure 3)

  • Pubic inlet

  • Two obturator foramina

  • Check for irregularities along the circles

  • In general, a vertical fracture pattern will be associated with APC or VS mechanisms. Horizontal fracture patterns will be associated with LC. [7]

Figure 3

• Check the lines! 

  • ilioischial line (orange line in Figure 4)- disruption suggest posterior column fracture [5]. The posterior column involves the posterior half of the acetabulum and extends to the ischial tuberosity [4]. 

  • iliopectineal line (red line in Figure 4)- disruption suggests anterior column fracture [5]. The anterior column involves the anterior half of the acetabulum and extends to the lateral half of the superior pubic ramus [4].

  • It’s a circle! If it breaks in one location, it likely broke in another place. Be wary of isolated rami fractures in the setting of high-impact trauma!

Figure 4

Management

• As always, still stick to your ABCs!

  • Initiate blood transfusion early for patients in shock 

  • Hemodynamic instability occurs in about 10% of these injuries [1]

• Try to obtain IV access above the pelvis if a pelvic fracture is suspected.

• Stabilize the pelvis with a TPOD or a sheet for patients with open book pelvic fractures

  • Apply over the GREATER TROCHANTERS

  • Do not apply a compressive device for isolated lateral compression pelvic fractures as the device can cause further compression and worsen the displacement [4].

• If the hemorrhage or hypotension is suspected to be from pelvic hemorrhage, activate IR early.

• If stable, obtain a CTA of the pelvis to assess for vascular injury

What other injuries should I look for?

• Urologic Injury: incidence in pelvic fractures is ~5%. Patient with blood at the meatus will need a retrograde urethrogram and then a cystogram [4].

• Neurologic Injury:  pelvic fractures can be associated with plexus injuries and even cauda equina syndrome. Check for rectal tone and saddle anesthesia [4].

• Gynecologic injury:  blood a the introitus can represent urethral injury or an open pelvic fracture [4].

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Expert Commentary

Dr Ko has provided a high yield concise guide of the key cognitive and clinical features of pelvic fractures.  A few points worthy of further emphasis:

When examining for pelvic instability, do not rock on the pelvis to further open it.  Instead, compress medially to feel instability while closing, rather than opening, the pelvis.

For most studies we order, we have the luxury of waiting for a formal report. Pelvis x rays are one of the few radiographic studies that the Emergency Physician must be able to rapidly interpret independently at the bedside for patient management!  Do not just eyeball the film.  It is impossible to find multiple pelvic fractures that way. Go over every arc, curve, and ring visually.  If something appears possibly abnormal, compare to the other side for (a)symmetry.  And if you find one break in the pelvic ring, scrutinize for more, there almost always are.  Many of these are in the posterior ring, the part of the pelvis for which plain films are least sensitive. CT will help evaluate the posterior elements if feasible.

Understanding the classic LC, APC, VS mechanism classifications lend insight into when a binder will help.  Realize, however, that in vehicular trauma, often the forces are multidirectional, so there will be mixed injury patterns.  Ask yourself what you are trying to achieve by placing the binder.  If it is closing the open book to tamponade hemorrhage, then go for it!  If it is to provide some stability to a VS injury so you can move the patient without their pelvis flopping around than OK but it won't be therapeutic.  If it is an LC injury where the femoral head has crushed through the acetabulum, avoid using a binder, you will only further intrude bony fragments into the pelvis!  

Call IR the instant you realize there is a bleeding pelvic fracture.  It takes time to prepare the suite, especially overnight!

Matt Levine, MD

Assistant Professor of Emergency Medicine

Northwestern Feinberg School of Medicine

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How To Cite This Post

[Peer-Reviewed, Web Publication] Ko J, Whipple T. (2019, July 22). Pelvic Fractures. [NUEM Blog. Expert Commentary by Levine M]. Retrieved from http://www.nuemblog.com/blog/pelvic-fracture.

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References

Halawi MJ. Pelvic ring injuries: Emergency assessment and management. Journal of Clinical Orthopaedics and Trauma. 2015;6(4):252-258. 

1. Khurana B, Sheehan SE, Sodickson AD, Weaver MJ. Pelvic ring fractures: What the orthopedic surgeon wants to know. RadioGraphics. 2014;34:1317-1333

2. Weatherford B. Pelvic ring fractures. Orthobullets website. https://www.orthobullets.com/trauma/1030/pelvic-ring-fractures. Accessed October 14, 2018.

3. Walls RM, Hockberger RS, Gauche-Hill M. (2018). Rosen's emergency medicine: Concepts and clinical practice (9th ed.). Philadelphia, PA: Elsevier/Saunders.

4. Murphy A, Jones J. Pelvic radiograph (an approach). Radiopaedia website. https://radiopaedia.org/articles/pelvic-radiograph-an-approach. Updated August 2018. Accessed October 14, 2018. 

5. Tile M. Pelvic ring fractures: should they be fixed? J Bone Joint Surg Br Vol. 1988;70(1):1–12.

6. Singh, AP. Pelvic fractures: Presentation and treatment. https://boneandspine.com/pelvic-fractures-presentation-and-treatment/

Images: 

Case courtesy of Dr Jeremy Jones, https://radiopaedia.org Radiopaedia.org. From the case https://radiopaedia.org/cases/28928" rID: 28928

Clostridium Difficile

Written by: Luke Neill, MD (NUEM PGY-4) Edited by: Keith Hemmert, MD (NUEM ‘18) Expert commentary by: Michael Angarone, DO

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Expert Commentary

Dr. Neill has provided an excellent overview of the important points from the latest iteration of the IDSA/SHEA guidelines for the diagnosis and management of Clostridioides difficile (formerly Clostridium difficile) infection (CDI). There are a few important changes to this current update to the guidelines. For the diagnosis of C. difficile infection the guidelines recommend hospitals to not test persons on laxatives, that have formed stools or another diagnosis for the patient’s diarrhea. This is an important change in the way that most practitioners think of testing for C difficile and will result in less tests being performed.  Hospitals that do not adopt pretesting criteria for testing stool for C diffiicile should develop a multi-step testing algorithm, such as glutamate dehydrogenase test followed by toxin test, arbitrated by C difficile PCR. The guidelines do not recommend probiotics for primary prevention of CDI stating that there is insufficient data to recommend the use of these agents. This is contrary to a recent Cochrane review from 2017 that analyzed 31 studies and found that in individuals at high risk for CDI may benefit from probiotics, with a number needed to benefit of 12.  The biggest change in this version of the guidelines is that metronidazole is no longer recommended for therapy. Patients should be treated with either oral vancomycin or fidaxomicin. For multiple recurrent CDI (>2 episodes), patients should be considered for fecal microbiota transplantation. This is the first time that FMT has been recommended as a treatment option in the IDSA/SHEA guidelines. The changes in this guideline should not change the way that most practitioners approach CDI, with the exception of the above important changes.

Reference:

1.       McDonald LC, Gerding DN, Johnson S, et al. Clinical practice guidelines for Clostridium difficile infection in adults and children: 2017 update by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA) [published online February 15, 2018]. Clin Infect Dis.doi: 10.1093/cid/cix1085

2.       Cochrane Database Syst Rev. 2017 Dec 19;12:CD006095.  Probiotics for the prevention of Clostridium difficile-associated diarrhea in adults and children. PMID 29257353

Michael P. Angarone, DO

Assistant Professor

Department of Medicine (Division of Infectious Diseases) and Medical Education

Northwestern University, Feinberg School of Medicine

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How To Cite This Post

[Peer-Reviewed, Web Publication] Neill L,  Hemmert K. (2019, July 15). Clostridium Difficile. [NUEM Blog. Expert Commentary by Angarone M]. Retrieved from http://www.nuemblog.com/blog/clostridium-difficile

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Tetracaine

Written by: Jonathan Hung, MD, (NUEM PGY-3) Edited by: Matt Klein, MD (NUEM ‘18) Expert commentary by: Dr. Glaucomflecken

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Introduction

Corneal abrasions are a commonly encountered eye-related presentation in the emergency department (ED) [1]. Patients will often have a significant amount of pain from even minor abrasions. Topical anesthetics such as tetracaine have been found to be effective in treating the pain and are now routinely used in the ED [2]. However, the use of topical anesthetics for corneal abrasions in the outpatient setting is controversial due to concerns over safety and delayed healing. These traditional concerns over the prolonged use of topical anesthetics are based on early animal studies and case reports in humans [3]. The current literature suggests that topical anesthetics are, in fact, safe and effective if given as a short course with appropriate follow up, but further studies with larger patient populations are needed to support these findings [4]. A recent study published in Annals of Emergency Medicine is one of the largest studies to date that examines the safety of discharging patients home from the ED with a short supply of tetracaine for corneal abrasions.

Study

Waldman N, Winrow B, Densie I, et al. An Observational Study to Determine Whether Routinely Sending Patients Home With a 24-Hour Supply of Topical Tetracaine From the Emergency Department for Simple Corneal Abrasion Pain Is Potentially Safe. Ann Emerg Med. 2017. 

Study Design

The study design was a single-center, retrospective cohort study with ethics approval given by the Human Ethics Committee at the University of Otago. 

Population

The study was performed at the ED of Southland Hospital, Invercargill, New Zealand. A computer search of the hospital’s ED information system was conducted looking for all eye-related diagnoses and charts were reviewed between February 1, 2014 to October 31, 2015. Patients were initially selected if they were seen in the ED with an injury or illness involving the cornea. 

Intervention protocol

Patients with simple corneal abrasions were discharged home with undiluted 1% tetracaine hydrochloride in addition to the standard treatment of acetaminophen and chloramphenicol eye ointment. Instructions were given to place tetracaine in the eye as often as every 30 minute over the first 24 hours.  

Outcome Measures

• ED rechecks 

• Persistent fluorescein uptake

• Ophthalmology clinic referrals

• Complications

Results

There was a total of 1,576 ED presentations of corneal abrasions of which 532 were simple corneal abrasions (SCA) and 1,044 were defined as nonsimple corneal abrasions (NSCA). Tetracaine was given to 57% (303) of SCA patients and 14% (141) of NSCA patients. Overall, there were no serious complications or uncommon adverse events in either the SCA or NSCA group (0/459). The relative risk of patients with SCA receiving tetracaine and returning to the ED, having fluorescein uptake, or requiring a referral to ophthalmology was low compared to the standard treatment group. 

Interpretation

This study is one of the largest studies to examine the safety of outpatient tetracaine use in simple corneal abrasions. More importantly, it gives a robust conclusion similar to previous smaller studies in that there was no evidence that using topical tetracaine for a short duration caused harm. The strengths of this study include the large patient population and good patient follow-up. Furthermore, the physicians that administered tetracaine did not know that an observational study was planned, thus increasing the internal validity. However, the researchers were not blinded to the hypothesis which could have led to bias when collecting data. This was also a retrospective study and therefore due to the lack of randomization, those who received tetracaine may have differed from those who did not. Another limitation was that it was not known if all the patients administered the tetracaine as instructed after leaving the ED. Also, the diagnosis of simple corneal abrasion was limited to what the physician documented in the chart. The external validity is limited since this was a single-center study and about 71% of the patients were males. Overall, this study further strengthens the role of tetracaine in treating pain secondary to simple corneal abrasions and may gradually change practice patterns in the emergency department despite traditional teaching. 

Take Home Points

• Topical tetracaine is effective in treating pain due to corneal abrasions

• Patients with simple corneal abrasions can benefit from a short course of topical tetracaine to treat pain 

• Topical tetracaine use over a 24-hour period is generally safe 

• Emergency medicine physicians should consider incorporating topical tetracaine in their practice for treating SCAs 

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Expert Commentary

This is an interesting observational study regarding the safety of prescribing a limited supply of topical tetracaine to patients who present to the emergency department with what the authors describe as “simple corneal abrasions.” It is well documented in the literature that long term use of topical anesthetics can lead to a variety of serious ophthalmic complications, including persistent epithelial defects, neurotrophic ulceration, secondary infectious keratitis, corneal scarring and perforation. However, many of these reports describe long term use of anesthetics ranging from 7 days to 6 months which have helped establish the long-held dogma that topical anesthetics are only appropriate for use during surgery or clinic examination. This study, as well as several smaller previous studies, has attempted to challenge that dogma in an effort to better treat the immense pain often associated with corneal abrasion.

The authors did a great job trying to distinguish between simple and non-simple corneal abrasions. This can be very difficult, even for an ophthalmologist. What may look like a simple corneal abrasion can easily turn out to be a different diagnosis altogether. Herpes simplex keratitis can present as a geographic ulcer, lighting up with fluorescein much like a corneal abrasion without the tell-tale sign of dendritic lesions to accompany it. Dry eye disease can result in confluent, punctate epithelial defects which can look like a corneal abrasion without the magnification afforded by a slit lamp. These conditions should not be treated with topical anesthetics and will only delay the patient in receiving appropriate care. Stating that topical anesthetics are safe for simple corneal abrasions assumes that the examiner is able to accurately diagnose a simple abrasion. In this study, several patients were misdiagnosed as simple abrasions and ultimately required follow up with ophthalmology. Patients who need to see ophthalmology for a non-simple abrasion may be less likely to follow up in a timely manner if they are given topical anesthetic that will effectively mask the pain. This can result in more extensive corneal scarring from a variety of diagnoses such as delayed rust ring removal or treatment of infectious keratitis.

The authors make a compelling point that a limited supply of tetracaine in a subset of corneal abrasions intended to last no more than 24 hours is safe with no significant difference in the number of ED rechecks, ophthalmology clinic referrals, persistent fluorescein uptake, or complications. If this is indeed true, is treating with topical anesthetic worth it? At best, you are providing a minimally-painful healing process which will be complete in 48-72 hours regardless of topical anesthetic use. At worst, you are masking pain of a potentially vision-threatening process that may have been misdiagnosed as a simple abrasion. I contend that setting patient expectations regarding pain (very severe for first 24 hours, then rapid improvement) and discussing more conservative comfort measures like icing and patching are sufficient.

Lastly, I want to discuss the treatment for simple and non-simple corneal abrasions. It is unclear whether or not the patients in this study were treated with topical antibiotics. It is possible that patients with simple corneal abrasions were sent home with a 24 hour supply of tetracaine and no topical antibiotics. Without an epithelial barrier, the underlying corneal stromal is prone to infection. Topical antibiotics act as a preventive measure and are particularly important if a patient is using topical anesthetic, which could mask the pain of infectious keratitis. Although not all sources agree, there is general consensus among ophthalmologists that all corneal abrasions require topical antibiotics at the time of diagnosis.

In conclusion, I agree that a 24 hour prescription of topical anesthetic in a simple corneal abrasion is likely safe. However, given the rapid healing time, consideration should be made to counseling patients on pain expectation and comfort measures in place of topical anesthetic. Lastly, prescribing more than a 1 day supply of topical anesthetic is unnecessary given the rapid improvement in pain after the first 24 hours

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Dr. Glaucomflecken, MD

https://www.drgcomedy.com/

https://twitter.com/dglaucomflecken

http://gomerblog.com/author/glaucomflecken/

How To Cite This Post

[Peer-Reviewed, Web Publication] Hung J,  Klein M. (2019, July 8). Tetracaine. [NUEM Blog. Expert Commentary by Dr. Glaucomflecken]. Retrieved from http://www.nuemblog.com/blog/tetracaine.

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Other Posts You May Enjoy

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References

1. Verma A, Khan FH. Corneal abrasion. MedscapeAvailable at: http://emedicine.medscape.com/article/1195402-overview. Accessed November 1, 2017.

2. Waldman N, Densie IK, Herbison P. Topical tetracaine used for 24 hours is safe and rated highly effective by patients for the treatment of pain caused by corneal abrasions: a double-blind, randomized clinical trial. Acad Emerg Med 2014;21:374–82.

3. Chang YS, Tseng SY, Tseng SH, et al. Cytotoxicity of lidocaine or bupivacaine on corneal endothelial cells in a rabbit model. Cornea 2006;25:590–6.

4. Swaminathan A, Otterness K, Milne K, Rezaie S. The Safety of Topical Anesthetics in the Treatment of Corneal Abrasions: A Review. J Emerg Med. 2015;49(5):810-815. 

Sink or Swim: The management of submersion injuries

Written by: Michael Conrardy , MD (NUEM PGY-2) Edited by: Gabby Ahlzadeh, MD (NUEM ‘19) Expert commentary by: Kristina McAteer, MD

Introduction

If you are an emergency physician, you likely will see submersion injuries often throughout your career. In the United States, from 2005-2014, there are approximately ten deaths per day from unintentional drowning, and about 3,536 annually. This number increases to eleven per day if you include boating-related deaths. One in five deaths involve children under the age of fourteen, and drowning is the second leading cause of death for children ages 1-14 [1,2]. Approximately 80% of all victims are male [2], and when considering adolescents and adults, alcohol is involved in up to 70% of cases [3]. Statistics for nonfatal drowning events are difficult to obtain, but studies estimate that they may occur several hundred times more frequently than reported deaths [4,5].

Example Case

While working in the emergency department on Friday night, three college students are brought in by EMS after “drinking alcohol and jumping in Lake Michigan.” Patient #1 received CPR for ten minutes en route, has a temperature of 32 degrees Celsius, signs of head trauma, and a cervical collar in place. Patient #2 experienced a short period of submersion and is in mild respiratory distress. Patient #3 was submerged for only a brief period of time and is completely asymptomatic.

Emergency Department Management of Submersion Injuries
Patient #1 - Severely Symptomatic Patients

Initial Management:

In serious cases of drowning, top concerns are hypoxemia, hypothermia, subsequent cardiac arrest, and other signs of trauma.

1. If in cardiac arrest, start ACLS and consider underlying causes such as hypoxemia or hypothermia

2. Remove wet clothing and use rewarming techniques

3. Chest x-ray, blood gas, labs, end tidal CO2. Initial CXR is often normal but can be helpful in tracking the patient’s condition.

4. Assess for signs of trauma and obtain appropriate imaging. It is important to note that cervical spine injuries are uncommon (<5%) in cases of drowning, and cervical collars should not distract from airway management [6].

Management of airway, ventilation, oxygenation:

Fluid aspiration can lead to loss of surfactant, pulmonary edema, and hypoxemia from V/Q mismatch. Hypoxemia is the primary cause of end-organ damage in submersion injuries (typically cardiac and neurologic) and treating it should be your top priority. Here are some general guidelines:

• Airway: Intubate patients if unable to protect airway, O2Sat < 90% despite supplemental O2, or PaCO2 >50

• Ventilation: Positive pressure opens alveoli and improves ventilation in drowning.

  • Unable to protect airway: Start with bag-valve-mask and then intubate. Use ARDS settings of Vt 6-8 mL/kg, Pplateau < 30mmHg, and increased PEEP.

  • Able to protect airway: Use non-invasive positive pressure ventilation in alert, symptomatic patients for goal O2Sat > 94% [6].

• Oxygenation: Use maximum available supplemental O2 initially and wean as tolerated.

Medications:

No medications need to be routinely used for submersion injuries. Bronchospasm can occur, and if suspected should be treated with inhaled beta-adrenergic agonists. Glucocorticoids have not been shown to be helpful in preventing subsequent lung injury and may interfere with healing, and not enough data exists to support routine administration of exogenous surfactant. Antibiotics should only be used in cases where signs of infection develop or if the patient was submerged in grossly contaminated water [7].

ECMO:

Data on use of ECMO to treat patients with severe pulmonary edema or signs of ARDS are extremely limited, although initial results are encouraging [9]. This is an area of ongoing research, and perhaps we may eventually see early initiation of ECMO as standard practice for severely symptomatic patients.

Patient #2 - Mildly Symptomatic Patients

The main takeaway from patient #2 is that all patients who are symptomatic on arrival to the ED (requiring ventilatory assistance or supplemental O2) should be admitted to the hospital. Airway, ventilation, and oxygenation should be managed as above, and serial chest x-rays can help monitor for development of pulmonary edema in symptomatic patients [6].

Patient #3 - Asymptomatic Patients

Although most research on safe discharge has been in children, it is generally accepted that asymptomatic patients can be safely discharged after 4-6 hours of monitoring. Patients should have normal pulmonary exam, SaO2>95% on room air, and GCS>13 [6,10]. Some clinicians advocate for observing up to eight hours based on a study that observed one pediatric patient who did not develop symptoms until seven hours post-submersion [11], although six hours in the ED with return precautions is probably adequate in most cases. Many clinicians obtain basic labs on all patients and a chest x-ray prior to discharge to confirm that there are no signs of pulmonary edema, although no strong evidence supports these practices.

Key Takeaways:

• Hypoxemia is the main cause of harm, prioritize the airway and use positive pressure

• Initial chest radiographs are often normal, but can be used to track a patient’s clinical status

• Blood gas is the most useful laboratory test in symptomatic patients, additional testing (e.g. ECG, CBC, chem, troponin) is particularly useful in patients with altered mental status

• Asymptomatic patients may be safely discharged after six hours of monitoring

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Expert Commentary

The terminology can be confusing with such terms as drowning, nonfatal drowning, submersion injury, dry drowning, wet nonfatal drowning, and so on.  Most recently (2010) the AHA recommended a more straightforward approach and supported the Utstein definition which hopefully offers some clarification, relieves some of the angst when approaching this population, and standardizes research and reporting.  The Utstein defines a drowning as “a process resulting in a primary impairment from submersion or immersion in a liquid medium.” [1]

The key is to keep it simple.  Is your patient symptomatic from the exposure?  If so, focus on the ABC’s and get to work! 

You will often see pediatric patients as drowning victims.  Drowning is a leading cause of accidental death in children under 5 years of age, particularly in states where swimming pools or beaches are more accessible. The states of California, Arizona and Florida lead the way [2].  The second peak is in older ages (15-25 yo), primarily males, and involves more rivers, lakes and beaches. [3].  The distinction between fresh and salt water drownings is no longer considered important as the volume of aspirated water is so small that the theorized electrolyte shifts do not have any real physiological impact [4]. Both wash out pulmonary surfactant.  

As appropriately pointed out it is often is not the drowning that causes mortality. It is therefore necessary to consider concomitant trauma, toxic ingestions (at the very least alcohol leading to impaired judgment!), and hypothermia.  Hypoxemia and the resultant hypoxia is ultimately the cause for death, often impacting multiple organ systems, and thus it is your job to reverse the hypoxemia as quickly as possible!  Supplemental oxygen, BIPAP (Bilevel positive airway pressure), endotracheal intubation and if necessary, ECMO (extracorporeal membrane oxygenation) are management options.  There is a neuroprotective effect of hypothermia and in some cases patients make a complete recovery despite a prolonged resuscitation.  Age > 14, duration of submersion > 5 minutes, time to basic life support > 10 minutes, resuscitation duration > 25 minutes, GCS (Glascow coma scale) <5, persistent apnea and requirement of CPR in the emergency department and arterial blood pH <7.1 have all been associated with a poor prognosis.  [5]

1. Vanden Hoek TJ, Morrison LJ, Shuster M, et al. Part 12: Cardiac Arrest in special situations 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergent Cardiovascular Care. Circulation 2010; 122: S829.

2. Brenner Ra. Prevention of drowning in infants, children, and adolescents. Pediatrics 2003; 112:440.

3. DeNivola, LK, Falk, JL, Swanson ME, et al. Submersion injuries in children and adults. Crit Care Clin 1997;12:477.

4. Orlowski JP, Szpilman D. Drowning, Resucue, resuscitation and reanimation. Pediatr Clin. North Am 2001. 48:627.

5. Quan L, Mack CD, Schiff MA.  Association of water temperature and submersion duration and drowning outcome. Resuscitation 2014.85:790.

Kristina McAteer, MD

Assistant Professor of Emergency Medicine

Brown University

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How To Cite This Post

[Peer-Reviewed, Web Publication] Conrardy M,  Ahlzadeh G. (2019, July 1). Sink or Swim: The management of submersion injuries. [NUEM Blog. Expert Commentary by McAteer Kristina]. Retrieved from http://www.nuemblog.com/blog/drowning.

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Other Posts You May Enjoy

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References

1. Centers for Disease Control and Prevention, National Center for Injury Prevention and Control. Web-based Injury Statistics Query and Reporting System (WISQARS) [online]. Available from: URL: http://www.cdc.gov/injury/wisqars.

2. CDC. Wide-ranging online data for epidemiologic research (WONDER). Atlanta, GA: CDC, National Center for Health Statistics; 2016 [online]. Available at http://wonder.cdc.gov.

3. Driscoll TR, Harrison JA and Steenkamp M. Review of the role of alcohol in drowning associated with recreational aquatic activity. Inj Prev. 2004; 10: 107-13.

4. Bierens JJ, Knape JT and Gelissen HP. Drowning. Curr Opin Crit Care. 2002; 8: 578-86.

5. Orlowski JP. Drowning, near-drowning, and ice-water drowning. JAMA : the journal of the American Medical Association. 1988; 260: 390-1.

6. Schmidt AC, Sempsrott JR, Hawkins SC, Arastu AS, Cushing TA and Auerbach PS. Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Drowning. Wilderness Environ Med. 2016; 27: 236-51.

7. Layon AJ and Modell JH. Drowning: Update 2009. Anesthesiology. 2009; 110: 1390-401.

8. Chandy D, Weinhouse GL. Drowning (submersion injuries). UpToDate. Danzl DF, Grayzel, J (Ed). 2017.

9. Burke CR, Chan T, Brogan TV, et al. Extracorporeal life support for victims of drowning. Resuscitation. 2016; 104: 19-23.

10. Causey AL, Tilelli JA and Swanson ME. Predicting discharge in uncomplicated near-drowning. The American journal of emergency medicine. 2000; 18: 9-11.

11. Noonan L, Howrey R and Ginsburg CM. Freshwater submersion injuries in children: a retrospective review of seventy-five hospitalized patients. Pediatrics. 1996; 98: 368-71.