Canthotomy

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Written by: Alex Ireland, MD (NUEM PGY-3) Edited by: Gabrielle Ahlzadeh, MD (NUEM PGY-4) Expert commentary by: Gary Lissner, MD

Expert Commentary

The author has written an excellent illustrated review of the technique of lateral canthotomy and cantholysis for traumatic orbital compartment syndrome due to a significant retrobulbar hemorrhage. As with any procedure it is crucial to understand the indications and contraindications of the procedure. In these cases, the indication is the saving or restoring of vision lost due to excessive intraorbital pressure, and the contraindication is generally an opened globe. This is a difficult situation because there is usually limited information and there is a limited amount of time to relieve the orbital compartment syndrome. The timing of the onset of the retrobulbar hemorrhage that created the critical pressure to cause loss of vision is often unknown. The decision to decompress is usually based solely on a clinical examination without having time to obtain orbital radiologic studies and before an ophthalmologist can arrive to evaluate the patient. However, the clinical exam could be limited if the patient is not cooperative or is not conscious.

Initially a determination has to be made if the globe is lacerated or ruptured which could preclude the performance of the canthotomy and cantholysis . Either a ruptured globe or an orbital compartment syndrome can cause loss of vision. A ruptured globe can occur along with a retrobulbar hemorrhage. If the eyeball is opened, no additional external pressure should be placed on the lids or globe in order to prevent additional damage to the eye. An opened globe could be determined by seeing a laceration of the globe, seeing protruding intraocular contents, finding a very soft eye, and/or finding a distorted eye. If the eyeball is opened, a sturdy shield should be placed resting on the surrounding orbital bone to protect the eye from external pressure, and the aide of an ophthalmologist should be sought.

If it is determined that the globe is intact, a decision has to be made on clinical examination findings if a significant retrobulbar hemorrhage exists that would create enough pressure in the orbit to cause loss of vision. There is usually not enough time to wait for imaging studies to be done. The trauma could create a large enough orbital fracture that could decompress the orbital pressure and the orbital compartment syndrome. On the other hand, an orbital fracture can create orbital emphysema. Blowing of the nose by the patient can increase the emphysema and further increase the intraorbital pressure, creating a sight-threatening orbital compartment syndrome.

Acute vision loss is the key clue to a significant orbital compartment syndrome, but many trauma patients may not be able to cooperate for visual testing. The reaction of the pupil to light can be used as a sign of visual loss even in the uncooperative patient. With an orbital compartment syndrome, the pupil of the involved eye will not react well to a bright light and will have an afferent defect. However, if the patient was given narcotics the pupils can become miotic and pupil testing becomes difficult. Visual loss is not diagnostic of an orbital compartment syndrome because the trauma can create other damage that can cause visual loss including intraocular bleeding, retinal disorders, traumatic optic neuropathy, or a lacerated or ruptured globe. Trauma can cause edema and ecchymosis of the lids, but tense proptosis with very firm retropulsion of the involved eye is a key diagnostic finding of a significant retrobulbar hemorrhage. As the orbital bleeding continues, the eye is pushed forward against the tight eye lids and the intraocular pressure increases. A significant intraocular pressure increase can be used as another sign of an orbital compartmental syndrome. Checking the intraocular pressure can be difficult in the presence of massive eyelid swelling. Pulling the lids opened especially if the patient is squeezing can transmit the external pulling pressure to the eye, creating a false reading of a raised intraocular pressure. Using curved instruments, or the blunt end of bent paper clips as shown by the Blog’s author, can help open the lids. Using a topical anesthetic to reduce eye discomfort, or using injectable local anesthetic to relax the orbicularis muscle action can also help to more easily open the eyelids to obtain a more accurate intraocular pressure. Orbital compartment syndrome will limit extraocular motility on the involved side, but the unconscious patient’s motility cannot be easily tested. A significant increase of the orbital pressure and the intraocular pressure can cause pulsation of the retina arteries and full retina veins which can help with the diagnosis of an orbital compartment syndrome if the fundus is viewed.

The Blog gives a precise pictorial and written description of the lateral canthotomy and cantholyisis technique. However, unlike the author’s demonstration photos, most cases with significant traumatic orbital compartment syndrome have massive lid ecchymosis and subconjunctival hemorrhage and a proptotic eye that is pushed forward tightly against the lids. Therefore, there is frequently little room to insert the instruments at the lateral canthal angle. Extreme care must be taken to avoid unwanted damage. The author’s “tip” to insert a Morgan lens (a sclera shell if available can also be used) onto the patient’s eye is a good idea to help protect the eye, but the tight space in some cases can prevent the insertion of the lens. It is important that when working in the tight space to always work with the instruments pointing away from the eye and orbit to prevent injury to the globe, lateral rectus, lacrimal gland, or deeper orbital tissues. Always aim anteriorly toward the anterior orbital boney rim during the canthotomy. As the author suggests, the lids should be pulled or lifted away from the eyeball. Pulling the eyelid nasally and anteriorly helps tighten the crus of the lateral canthal tendon, thus making it easier to feel or strum the crus and cut it during the cantholysis. Always keep the tip of the scissors pointed away from the globe.

An orbital compartment syndrome can also occur with retrobulbar hemorrhage after surgery in the region. In such cases it can be advisable to first open the surgical wounds to determine if release of blood and clots from the depths of the wounds relieves the problem and thus eliminating the need for the canthotomy and cantholysis. In cases of retrobulbar hemorrhage after sinus or nasal surgery, the removal of nasal or sinus packing could release the blood and relieve the orbital compartment syndrome.

The Blog’s author presents a good list of potential complications from the canthotomy and cantholysis procedure. Many of the patients with significant retrobulbar hemorrhage are elderly patients who fall on their face. This group of patients can be on anticoagulants that could have potentiated the initial orbital hemorrhage and could create a problem of continued bleeding. The patients have to be observed after the canthotomy and cantholysis for continued or recurrent orbital bleeding and also for the possibility of a newly created surgical site eyelid bleeding that may not stop spontaneously. Additional surgery could be needed to stop the bleeding. Also to be considered as a complication is the fact that the release of the lateral canthal tendon lid support could cause lower lid ectropion, lid retraction, or lateral canthal deformity. Such deformities sometimes have to be surgically repaired.

In conclusion, the author has written a Blog which gives an excellent guide to perform a canthotomy and cantholysis. It can be difficult to make the decision if the procedure is needed to be done to prevent permanent loss of vision of an eye. The decision has to be based on clinical examination findings and the procedure if needed should not be delayed. After the procedure the patient needs to be observed and to have an evaluation by an ophthalmologist.

Gary S. Lissner, MD

Associate Professor, Chief Ophthalmic Plastics Service, Department of Ophthalmology, Northwestern University Feinberg School of Medicine

References

Yung CW, Moorthy RS, Lindley D, Ringle M, Nunery WR. Efficacy of lateral canthotomy and cantholysis in orbital hemorrhage. Ophthalmic Plast Reconstr Surg. 1994 June; 10(2):137-41.
Lima V, Burt B, Leibovitch I, Prabhakaran V, Goldberg RA, Selva D. Orbital compartment syndrome: the ophthalmic surgical emergency. Surv Ophthalmol. 2009 Jul-Aug; 54(4): 441-9.
Kent TL, Morris CL, Scott IU, Fekrat S. Evaluation and management of orbital hemorrhage. Eye Net magazine. 2018 July.
Jaksha AF, Justin GA, Davies BW, Ryan DS, Weichel ED, Colyer MH. Lateral canthotomy and cantholysis in operations Iraqi Freedom and Enduring Freedom: 2001-2011. Ophthalmic Plast Reconstr Surg. 2018 Jul 3. [Epub ahead of print].

How To Cite This Post

[Peer-Reviewed, Web Publication] Ireland A, Ahlzadeh G. (2019, April 15). Canthotomy [NUEM Blog. Expert Commentary by Lissner G]. Retrieved from http://www.nuemblog.com/blog/canthotomy

Pediatric ECMO: Beyond the Basics of Pediatric Resuscitation

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Written by: Steve Chukwulebe, MD (NUEM PGY-4) Edited by: Spenser Lang, MD (NUEM ‘17) Expert commentary by: Leah Harris, MD and Kiona Allen, MD

Case

A 38-year-old G8P6 female at 39-weeks gestation presents to your emergency department in active labor. The patient has gotten all her prenatal care at your institution, but has not made it to her due date. She reports her water breaking about 2 hours ago. She describes that the ruptured fluid was not clear but dark yellow/green, and she is now experiencing contractions every 2 minutes.

Your bedside doppler reveals reassuring fetal heart tones at a rate of 152. On your initial exam, the cervix is fully dilated and effaced…and you see the baby’s head. As your obstetric colleagues are several minutes away, you check your pulse, dust off the radiant warmer, and prepare your resources for an ED delivery.

The mother delivers within the next few minutes with your OB colleagues still en-route. While she has minimal complications, the newborn is now not doing as well.

Neonatal Exam

Constitutional: Full term boy, covered in meconium

Skin: Appears blue gray, cool to touch

Respirations: For the most part apneic and at times grunting

CV: Heart rate 100

Tone: Flaccid

You take over the resuscitation of the neonate immediately as he is delivered given the above exam. Attempts at stimulation, drying, oral suctioning, and warming still yields a 1-minute APGAR of 3.

NRP/PALS

As per the algorithm below, with continued apnea and SpO2 in the 50’s you begin positive pressure ventilation and continued stimulation [1]. At 15 minutes, despite your attempts with continued PPV, suctioning, and stimulations, the SpO2 continues to be in the 60’s and the heart rate begins trending towards from 100 to the 60’s as well. You decide to intubate the patient, and the tube is passed successfully. Tube placement is confirmed and the x-ray shows fluffy infiltrates bilaterally in both lung fields but no evidence of barotrauma. Attempts at bagging yields minimal resistance, however the highest SpO2 the patient reaches is in the low 80’s at 40 minutes, with improved heart rate to the 120’s. At this point, your pediatric colleagues have found their way to the ED and are ready to take the neonate to the NICU. Two hours later into your shift, you read that the neonate was placed on veno-venous extracorporeal membrane oxygenation (ECMO) and is doing better. After your shift is over, you find your way over to the NICU and you see a pink sedated baby under a radiant warmer and connected to a large ECMO circuit.

Diagnosis: meconium aspiration syndrome complicated by pulmonary vascular hemorrhage and ARDS.

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Had this neonate been in your ED, and your resuscitative measures have been exhausted, at what point do you consider ECMO in the neonatal or pediatric patient? I will review briefly the emergence of ECMO in the neonatal and pediatric literature, as well as its indications and the limited data on its utility in the emergency department setting.

From theory to practice

The first cardiac bypass circuit was created by John Gibbon in 1936 in the operating suite. ECMO is defined as a mechanical circuit outside the body where blood oxygenation and carbon dioxide removal can occur for patients with reversible cardiac or respiratory failure [2]. Through the 1950-1970s, many researchers studied various materials and techniques to further improve membrane oxygenation and attempted to increase the length of time a patient could remain on bypass. However, it was not until 1976 in which Bartlett et al. reported on the first neonate suffering from meconium aspiration syndrome to be successfully treated ECMO [3]. Since then, ECMO has grown and been used in various forms as treatment of respiratory failure in the neonatal and pediatric ICU settings. ECMO is to be considered for any reversible pathologic process that is impeding adequate tissue oxygenation and ventilation.

Indications for ECMO in children

Neonates:

Primary pulmonary hypertension of the newborn
Meconium aspiration syndrome
Persistent fetal circulation
Congenital diaphragmatic hernia

Pediatrics:

Respiratory failure
1. Bronchiolitis
2. RSV
3. Pneumonia
4. ARDS
5. Aspiration
6. Status asthmaticus
Sepsis
Cardiac arrest
1. with reversible conditions or amenable to heart transplantation
2. with favorable neurologic outcomes, some studies show better outcomes with CPR initiated in up to 95 minutes [5], key being excellent CPR with ETCO2 > 10 and early recognition and initiation of eCPR (extracorporeal cardiopulmonary resuscitation)
Hypothermia (cold water drowning)

In general, pediatric ECMO has been found useful in the above settings, however Gehrmann et al. reviewed the indications across various institutions when patients have been refractory to medical therapies. These indications are shown in the table below.

Types

ECMO comes in two types: venoarterial (VA) and venovenous (VV). While the early VA ECMO circuits utilized the roller pump to provide non-pulsatile flow of oxygenated blood, its limitations for infants included the necessity to cannulate the artery via either an open sternotomy or open cannulation of the carotids with the risk of losing a unilateral carotid artery due to ligation [4]. VV ECMO is the newer of the two modalities and rather than accessing a major vein and a major artery, the circuit requires access to either 2 major veins or a single major vein using a double-lumen catheter. However, each modality has its associated risks and benefits as described in the chart below [2].

Outcome Data

Neonates:

Neonates generally have better survival and outcomes on ECMO than older children and adults. One single center retrospective study in the journal of pediatric critical care published that of the 264 neonates placed on ECMO, 211 (80%) survived to discharge and 10-year survival was 71% [5]. The study had 2 cohorts and followed both neonatal and pediatric patients, collecting both demographic and survival data from patients placed on ECMO from 1987 to December 2013. Of those neonates that were alive at 90 days, at a 10-year follow up (ie.10-year conditional survival) 93% were alive. Of the common indications for neonatal ECMO, the 90-day survival and 10-year conditional survival are as follows respectively:

meconium aspiration syndrome (99% and 100%)
congenital heart anomalies (58% and 86%)
congenital diaphragmatic hernia (68% and 74%)
neonatal infection (72% and 100%)

Furthermore, patients who underwent VV ECMO had better 90-day survival and 10-year conditional survival rates than VA ECMO, 92% vs. 69%, and 98% vs. 87% respectively.

Pediatrics:

The same study followed 136 pediatric patients as well showing that the 90-day survival rate was 66% (90 patients) and that the 10-year conditional survival rate was 89%. The study divides the 90-day survival rates for ECMO by splitting it between pneumonia (bacterial, viral, and aspiration, 66, 76, and 83% respectively), other causes of sepsis (33%), trauma (100%), and other respiratory etiology (63%). Again, patients who underwent VV ECMO had better 90-day survival rates than VA ECMO, 78% vs. 50% respectively.

Other retrospective studies report similar survival rates to discharge when ECMO is used for severe respiratory failure, with rates from 39% to 83% depending on the pulmonary diagnosis, with status asthmaticus having survival rates of 83-100% on ECMO [2,6].

Data in ED

While data on emergency department utilization of pediatric ECMO is limited, one study mentions the outcomes from its two cases [7]. The first case was a 3-year-old previously healthy girl who presented with nausea and developed cardiogenic shock in the department from viral myocarditis. This patient was placed on ECMO in the ED and transferred to the cardiac intensive care unit. She was taken off the circuit after 4 days with improved contractility, and eventually discharged home 10 days later neurologically intact. The second case was similar in etiology: a 17-year-old male who presented in respiratory distress and suffered a PEA arrest. This patient achieved ROSC, was placed on ECMO in the ED and was eventually discharged home 31 days later with a favorable neurological outcome.

Conclusions

While some centers continue to grow their extracorporeal membrane oxygenation programs to expand their resuscitative efforts, still few places have the equipment to start the circuit or even at times an on-call staff to prime the machine. In general, few studies report the usage of ECMO in the emergency departments as a means for cardiopulmonary resuscitation of a reversible etiology, and only case reports exist in the pediatric literature. However, even if the ability to start neonatal/pediatric ECMO may not be ever be present in one’s emergency department, prompt recognition and early disposition to tertiary care centers that offer these services could potentially be lifesaving in many appropriate cases.

Expert Commentary

While ECMO (extracorporeal membrane oxygenation) may seem a foreign concept for ED management, it is important to recognize that as recently as the 2009 H1N1 epidemic, utilizing this intervention as a rescue therapy to treat acute severe hypoxic respiratory failure associated with influenza resulted in cases of ECMO initiation in emergency rooms across the world. Your review introduces meconium aspiration – a frequent clinical indication – as a platform to review this technology. Critical to the understanding of ECMO is first to be able to determine the appropriate candidates for this support, then to pick the correct mode (veno-arterial versus veno-veno) and to learn your own institution’s interpretations of inclusion and exclusion criteria. For the purposes of this commentary, we will break down the review into five sections sections: types of ECMO, who goes on ECMO, how to measure and trend hypoxemia, what can you do in the ED to maximize success on ECMO and new advances in ECMO.

ECMO modes:

ECMO is temporary cardiopulmonary bypass used to support a patient with either heart or lung failure. Originally developed from modifications of cardiopulmonary bypass and subsequently adapted for prolonged support, an ECMO circuit has both an oxygenator and a pump and a rate by which the blood passes across the oxygenator filter and has carbon dioxide removed. Children with heart or lung failure who do not respond to conventional medical therapies may be candidates for ECMO support. The ECMO circuit drains blood from the body, exchanges oxygen and carbon dioxide on the red blood cell, warms the blood and pumps it back into the body. Placing a child on ECMO allows time for the heart and/or lungs to improve or to serve as a bridge to other long-term extracorporeal support or transplant.

In this very simple model, the oxygenator functions as the lungs, the pump takes over the work of a beating heart and the flow of the blood across the oxygenator mimics a respiratory rate and removes the carbon dioxide. If a patient’s heart is still adequately functioning as a pump and the indications for ECMO are due to oxygenation and/or ventilation defects, then utilizing ECMO as an isolated pulmonary bypass is preferred and veno-venous cannulation is warranted. Blood is therefore removed from a vein, red blood cells are oxygenated and carbon dioxide removed, and then blood is returned to a vein for the heart to pump. This approach allows for an adequate mixed venous saturation and tissue oxygenation. More importantly it allows for the heart to perfuse the coronary arteries with antegrade flow, does not require that an artery be sacrificed for access, permits a pulsatile waveform to be sensed by organs and can often be performed with a single dual-lumen catheter. Most frequent sites are internal jugular vein or femoral vein. Cannulation can be accomplished by either using 2 separate cannulae or by utilizing a dual lumen internal jugular cannula that spans from superior vena cava (SVC) to inferior vena cava (IVC) in order to remove blood via end and side ports in the cavae and return blood via a side port of the second lumen that is positioned in the right atrium and directed towards the tricuspid valve.

If the patient has had any indications of cardiac injury including but not limited to cardiac arrest, arrhythmias, severe pulmonary hypertension, or evidence of significant cardiac dysfunction, then venoarterial cannulation is indicated as the patient’s heart can no longer be relied upon to pump blood.

ECMO Candidates:

The review elegantly lists criteria for candidacy but there are few others to be considered including mediastinal masses with airway compression and complex airway disease. Usually ECMO is on stand-by for these cases in the operating room.

Measurement of hypoxemia:

While many are using P/F ratio (as Steve commented on in his review), the gold standard remains calculating and trending oxygenation index as a surrogate marker for severity of hypoxemia. Patients with an OI > 25 x 6 hours are demonstrating refractory severe lung failure and should be considered for ECMO.

Pre-ECMO Studies:

If you have a patient scenario develop in the Emergency Department with a high likelihood of progression to ECMO, there are handful of tests/treatments to be ordered prior to initiating ECMO that will make the decision to proceed with ECMO easier for the inpatient team:

1. Is there any evidence of a CNS abnormality or bleed? Order a head ultrasound on the infant or a head CT on the child if able – you want to rule out any CNS bleed that would be worsened by anti-coagulation.

2. Does the child have an underlying congenital heart lesion? Order an ECG and ECHO on every patient – you want to rule out any congenital cardiac lesions and to quantify pulmonary hypertension.

3. Is there any evidence of pulmonary hypertension – regardless of whether this is acquired or idiopathic? If “yes” – then start iNO – you can presume that all mechanisms of respiratory failure are coupled with worsening pulmonary hypertension in the child.

4. Order a type and screen and a CBC. While not ideal, a baby with a hemoglobin of 14 g/dL can be placed on a saline-primed ECMO circuit emergently with the recognition that this will dilute and drop their Hg and interfere with oxygen carrying capacity. For smaller children where the total volume of the ECMO circuit can exceed their own intravascular volume, best to be able to prime the ECMO circuit with blood before placing the patient on the ECMO pump.

New Advances in ECMO:

The ECMO world is pushing the envelope and recognizing that preventing deconditioning and minimizing de-recruitment of both lung tissue and muscle mass is key to recovery or to eventual organ transplantation. Centers across the US and Europe now have their patients walking on ECMO. Who knows, one may walk into an ER near you some day!!

Kiona Allen, MD

Assistant Professor of Pediatrics, Cardiology

Leah Harris, MD

Professor of Pediatrics, Pediatric Clinical Care

How To Cite This Post

[Peer-Reviewed, Web Publication] Chukwulebe S, Lang S. (2019, April 8). Pediatric ECMO: Beyond the basics of pediatric resuscitation [NUEM Blog. Expert Commentary by Harris L & Allen K]. Retrieved from http://www.nuemblog.com/blog/pediatric-ecmo

Resources

Pediatrics AA, Association AH. Textbook of neonatal resuscitation. 2006.
Gehrmann LP, Hafner JW, Montgomery DL, Buckley KW, Fortuna RS. Pediatric Extracorporeal Membrane Oxygenation: An Introduction for Emergency Medicine Physicians. J Emerg Med. 2015;49(4):552-60.
Bartlett RH, Gazzaniga AB, Jefferies MR, Huxtable RF, Haiduc NJ, Fong SW. Extracorporeal membrane oxygenation (ECMO) cardiopulmonary support in infancy. Trans Am Soc Artif Intern Organs 1976;22:80—93.
Mok YH, Lee JH, Cheifetz IM. Neonatal Extracorporeal Membrane Oxygenation: Update on Management Strategies and Long-Term Outcomes. Adv Neonatal Care. 2016;16(1):26-36.
Alsoufi B, Osman A, Nazer R, et al. Survival outcomes after rescue extracorporeal cardiopulmonary resuscitation in pediatric patients with refractory cardiac arrest. J Thorac Cardiovasc Surg 2007; 134:952–9.
Swaniker F, Kolla S, Moler F, et al. Extracorporeal life support outcome for 128 pediatric patients with respiratory failure. J Pediatr Surg. 2000;35(2):197-202.
Nevet A, Polak T, Dagan O, Waisman Y. Extracorporeal Membrane Oxygenation as a Resuscitation Measure in the Pediatric Emergency Department. Isr Med Assoc J. 2015;17(10):639-41.

Posted on April 8, 2019 by NUEM Blog and filed under Pediatrics and tagged ECMO VV ECMO VA ECMO.

Visual Guide to Splinting

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Written by: Danielle Miller, MD (NUEM PGY-4) Edited by: John Sarwark, MD (NUEM ‘16) Expert commentary by: Matthew Pirotte, MD

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Expert Commentary

Great work by the authors to create such a handy guide to splinting. Like so many procedures in the emergency department, splinting is like snowboarding – easy to learn difficult to master! My love for emergency ortho has led me to really work on my own splinting techniques and to have a healthy respect for this skill.

The only quibbles that I would have for the otherwise excellent chart (and they are minor) are the following:

1. Mid-shaft humerus: Rare will the patient be who can manage this with just a sling. There is tons of painful fracture movement to deal with here. The appropriate splint (a coaptation splint) is extremely challenging to place but worth it for the patient with such a painful fracture

2. Distal radius fractures: After reduction I really like a double sugar-tong splint as opposed to a single. I worry about elbow extension (even involuntary at night) degrading the integrity of my splint and therefore my reduction.

My biggest teaching point with respect to splinting in the ED is the under-appreciated art of molding splints. Getting the plaster or fiberglass correctly placed, padded, and wrapped is really the easy part. The emergency provider must grasp the critical orthopedic concept that “crooked splints make straight bones.” Your splint needs to be working for you not just sitting there observing! If you have made a reduction your splint generally needs to be keeping in in place. This sounds more complicated than it is, follow my 3-step plan to learn how to make and mold splints:

Step 1: understand the concept of a 3-point mold.

The concept of the 3-point mold creates a fulcrum proximal to the fracture site and bends the splint to keep the reduction from falling away. The 3-point mold looks like this.

Sharp-eyed readers might have noted that this is a pediatric fracture but have no fear, the splinting and molding is very similar to that of an adult. As you can see above the splint needs to be pushed and molded while it dries to keep that distal fragment from falling back. Start going into rooms with ortho residents and you’ll grasp this concept very quickly.

Step 2: start doing your own distal radius fracture reductions and splinting

Quentin Reuter MD (NUEM ’18) splinting a DRF

Unless there is nerve entrapment or some other complicating factor there is rarely a need to consult on DRF fractures in the emergency department. I basically taught myself to splint by really learning how to manage distal radius fractures. There are any number of high-quality videos out there. This is a good one that demonstrates my favorite molding technique as well. The nice thing about a DRF is that with a good hematoma block you can take the time to get it right. A pair of finger traps thrown in your shift bag is a good trick, they are a high-theft item so watch out for prowling residents. The nice thing about reducing DRFs is that you end up needing to place and mold a relatively complex splint. I like a double sugar tong followed by a good mold incorporating 3-points along with some mild flexion and ulnar deviation at the wrist. You also need to pay attention to what is going on at the elbow. Putting in all together for your mold you must manage the position of the elbow, wrist flexion, and wrist ulnar deviation all while putting good pressure on your mold points., It takes a bit of time to get right but your patients (and consultants) will thank you!

Step 3: build on what you’ve learned and apply it to other common fractures

Once you understand the principles of reduction, splinting, and molding you are ready to tackle a host of other fractures. Bimalleolar/trimalleolar ankle fractures, both bone midshaft forearm fractures in school aged kids, and boxer’s fractures are all great places to start. This is a fun and rewarding part of our practice that any emergency provider can do with a bit of practice.

Always remember to check and document your nerve function after splint placement!

Matthew Pirotte, MD

Assistant Program Director, Northwestern Emergency Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication] Miller D, Sarwark J. (2019, April 1). Visual Guide to Splinting [NUEM Blog. Expert Commentary by Pirotte M]. Retrieved from http://www.nuemblog.com/blog/splinting

The Seriousness of Deliriousness: Delirium in the ED

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Written by: Nery Porras, MD (NUEM PGY-2) Edited by: Katie Colton, MD (NUEM PGY-4) Expert commentary by: Lee Lindquist, MD

Introduction:

Imagine: you arrive to your shift, surrounded by the beeping and buzzing of monitors, an intoxicated patient already on the bed in front of your computer. You gamely walk in to the room of your first patient, a 74 year-old man for whom the tracking board reads “something is not right.” You see a quiet, subdued elderly man who looks at first glance generally well. The family member in the room starts talking immediately, concerned that something is just not right with this man – he seems depressed, and has been forgetting names. As she talks you hear a commotion from the next room and poke your head around the divider to see if you can help. There you see an older woman fighting with EMS and her EKG leads, surrounded by nurses trying to keep her from jumping off the stretcher. These widely disparate presentations potentially represent ends of the spectrum of the important but often missed diagnosis of acute delirium.

Emergency physicians are trained in the diagnosis and initial management of life and limb-threatening medical conditions. Delirium is an under-recognized but highly morbid condition that we are under-prepared to diagnose and treat in a busy ED. Trained in pattern recognition, we currently lack an easy and reliable method to diagnose acute delirium. The DSM-V identifies 5 key features that characterize this diagnosis:

Disturbance in attention and awareness
Develops over a short period of time, represents a change from baseline, and tends to fluctuate during the course of the day
An additional disturbance in cognition
The disturbances are not better explained by another preexisting, evolving or established neurocognitive disorder
There is evidence that the disturbance is caused by a medical condition, substance intoxication or withdrawal, or medication side effect

What’s the big deal with a somewhat confused elderly patients?

As the US population ages, elderly Americans are becoming the predominant users of healthcare with over 20 million older American visits to the ED each year (Han, et al 2013); these older patients are preferentially affected by delirium. One study notes delirium to be present in 8-17% of all elderly ED patients and in 40% of nursing home patients (Inouye 2014). Acute delirium can be the presentation of potentially life-threatening conditions including metabolic derangements, sepsis, and hypoxia. Interestingly one study showed that patients in their eighties with myocardial infarction are more likely to present with delirium than chest pain (Inouye 2014).

The diagnosis of delirium itself confers morbidity beyond the underlying condition that it can reflect. When comparing groups of elderly patients in the ED, those with delirium were found to be markedly more likely to die within 6 months than those without delirium – 36% versus 10%, respectively (Han 2013). Another study found that elderly patients diagnosed with delirium had 12-month mortality of 10-26%, rates comparable to sepsis or acute MI (Gower 2012). Despite the remarkable danger of this condition, emergency physicians are bad at making this diagnosis – per one report missing 57-83% of cases of delirium (Han 2013).

What does a patient with delirium look like?

The fluctuating presentation of delirium makes it difficult to recognize but we should be attentive to certain hallmarks, including alterations in attention and awareness and acute changes in cognition. These can be associated with hallucinations or other perceptual disturbances. Collateral information and family input can be critical in detecting changes from baseline function and cognition. The more acute temporal course of delirium is important to distinguish from underlying dementia, which is itself one of the most important risk factors for delirium. The most common presentation, the hypoactive form, is a quiet, subdued, withdrawn state. This is distinguished from the hyperactive form notable for hypervigilance, irritability and restlessness. Hypoactive and mixed-type deliriums are the most common presentations in the ED, representing up to 96% of acute cases in the ED (Han 2013). Unfortunately, the hypoactive form is both more commonly missed and associated with a worse prognosis (Inouye 2014).

So, how do I diagnose delirium? Can this be done in the ED?

As the personal, medical, and financial risks of delirium are increasingly recognized, research has focused on creating better tools for recognition and diagnosis. Traditionally this diagnosis has required an extended interview and evaluation, usually performed by a psychiatrist or geriatrician; these methods are rarely available in the ED or inpatient setting. Inouye and her colleagues built upon the DSM definition of delirium to create the Confusion Assessment Method (CAM) tool to quickly and easily screen for delirium.

The CAM algorithm for diagnosis of delirium, using standardized psychiatric evaluation for delirium for validation, showed a sensitivity of 94%-100% and a specificity of 90%-95% for the diagnosis of delirium (Inouye 1990). The CAM was later adapted and validated for use in the ED (Lewis 1995) and most recently that CAM has been modified to be even more ED friendly. In 2013 the Geriatric Emergency Department Guidelines were put together by ACEP, SAEM, AGS (American Geriatric Society) and ENA (Emergency Nurses Association in which they delineate a real-world adaptation of the CAM, the bCAM. In conjunction with the Delirium Triage Screen, these two tools are quick, easy and practical method of assessing for delirium in the ED.

What should be in your differential diagnosis when you suspect delirium?

You have made the step of recognizing that your elderly patient is off their baseline; what should you consider as part of your work-up? Consider the acronym “I WATCH DEATH” (below), a helpful reminder of the broad (and overlapping) differential of diagnoses that exist for acute delirium. For a more nimble tool particularly useful in the ED evaluation of the delirious elderly patient, the “ABCDEF” acronym (below) was developed by Rosen et al (Rosen 2016) to identify overlooked precipitating causes.

What can I do to acutely de-escalate a delirious patient?

As always, consider non-invasive measures first – recruiting family for this can be critical. Alleviating pain and discomfort and frequent re-orientation can help calm an acutely agitated patient.

Pharmacological interventions should be reserved for the agitated patient with overt psychotic manifestations. The use of restraints should be avoided if possible as the use of restraints themselves can worsen delirium. If medications are required, low doses of haloperidol of 0.5-1 mg can be used, although caution must be exercised with regard to QTc prolongation in patients with polypharmacy (Gower 2012). Atypical antipsychotics can be considered as well; the chart below details one potential protocol for pharmacologic management of acute delirium.

Take Home Points:

Delirium is under-recognized and under-diagnosed but carries marked increases in morbidity and mortality in the elderly population.
This diagnosis can and should be made in the ED; consider diagnostics aids like the CAM.
Delirium is often the presenting symptom of an underlying pathology and a broad differential should be consider.
Pharmacological interventions are a last resort; if needed low does of haloperidol or other atypical antipsychotics can be considered.

Expert Commentary

I love that delirium in the emergency department is being discussed! As a geriatrician, so many of my older adult patients are brought into the ED with these symptoms and it is vital that delirium is recognized and treated effectively. Delirium is a serious problem among older adults – and their families and supporters. It carries a high risk of extended hospitalizations, morbidity, and mortality. Katie and Nery did an excellent job describing the full spectrum of Delirium – ranging from hypo to hyperactive delirium. The hypoactive delirium symptoms are frequently missed because older adults affected by this are very quiet and often appear distracted. With “the squeaky wheel getting the grease”, we are more likely to recognize and respond to the older adult with hyperactive delirium instead.

I fully concur that collateral information is important. I would emphasize that we need to encourage patient families and supporters to stay with the patient – even after the patient is being admitted and moved to the inpatient setting. What can be most frustrating is that families will sometimes leave once the patient is called from the waiting room or after they have been seen by one staff member. We need to reaffirm with families that they need to remain at bedside and continue to remain at bedside when the patient is admitted. Having a loved one nearby will help both physicians in obtaining more information as well as the patient is reorienting and soothing them. I have seen too often that family members will leave from the ED, since the patient is being admitted, and subsequently, the patient’s agitation worsens. Important lesson: Please tell families to follow the patients to the inpatient floors/rooms and continue to stay with them.

Besides the family, collateral information should be obtained from the patient’s prior residence. So many older adult patients are transferred from skilled nursing facilities (SNF), or senior residences/communities (e.g. assisted living, memory care) for worsening confusion and delirium. I would suggest that ED teams contact the SNF nurses to determine collateral information. It would also be helpful to become familiar with the places that house seniors in their area (e.g. set up a tour, ask for clinical/nurse station phone numbers) so that communication can flow more easily.

From a clinical practice, the most common causes of delirium that I see are medication-related (withdrawal, polypharmacy) and dehydration. Doing a medication/brown bag review is always my first step. What I see is that older adults will sometimes start an OTC medication (e.g. diphenhydramine, sleep aid, or a pain medicine/sleep aid combo like a “acetaminophen PM”) and that will cause the acute confusion. Dehydration is also a common cause for delirium among older adults since we lose our thirst mechanism as we age and do not feel the need to drink. With summer weather, it is easy for a senior to become dehydrated with the first symptoms being delirium.

I would like to point out that UTIs are frequently misdiagnosed as a cause for delirium. What does that mean? We have been taught that UTIs can be the culprit for delirium - but it is usually not. Actually, checking a UA for confusion alone is no longer recommended by the CDC. The CDC recommends that urinary symptoms (e.g. frequency, dysuria) are present for UA testing. Why? Many older adults have asymptomatic bacteriuria – so much so that UTIs are frequently over-diagnosed in the ED as the culprit for delirium. When the culture comes back days later, there is a lack of evidence for the UTI. Even on the graphic presented by Katie and Nery on infections causing delirium – UTI is not listed. What I will do is ask for collateral information about any prior urinary symptoms from the families, fevers/chills, leukocystosis, and check for suprapubic tenderness on exam to assess urinary issues as a culprit for delirium.

Lastly, avoid benzodiazepines to treat delirium in older adults. I realize that it is listed on the infographic but this class of medicines are likely to exacerbate the delirium. Benzos can be used for alcohol withdrawal symptoms/delirium tremens but that is it. The ABIM Choosing Wisely Campaign has noted this “Don’t use benzodiazepines or other sedative-hypnotics in older adults as first choice for insomnia, agitation or delirium.” Non-pharmacologic methods are by far the best to treat delirium.

Delirium is not fun for our older adults or their families. The quicker we can recognize the symptoms of delirium and ameliorate the cause in the ED, the better everyone’s lives are. I congratulate Nery and Katie for a great discussion of delirium and I hope that it will impact how we treat our seniors with delirium!

Resources:

ABIM Choosing Wisely – Geriatrics. Available at: http://www.choosingwisely.org/societies/american-geriatrics-society/
Mody L, Juthani-Mehta M: Urinary tract infections in older women: a clinical review. Jama 2014, 311(8):844-854.
McKenzie R, Stewart MT, Bellantoni MF, Finucane TE: Bacteriuria in individuals who become delirious. Am J Med 2014, 127(4):255-257.
Nicolle L.E., Bradley S., Colgan R., Rice J.C., Schaeffer A., Hooton T.M. Infectious Diseases Society of America Guideline for the diagnosis and treatment of asymptomatic bacteriuria in adults. Clin. Infect. Dis. 2005;40:643–654.

Lee Lindquist, MD, MPH

Associate Professor of Medicine

General Internal Medicine and Geriatrics

How To Cite This Post

[Peer-Reviewed, Web Publication] Porras N, Lindquist L. (2019, March 25). The seriousness of deliriousness: delirium in the ED [NUEM Blog. Expert Commentary by Lindquist L]. Retrieved from http://www.nuemblog.com/blog/delirium

Resources

Gower, Lynn, et al. “Emergency Department Management of Delirium in the Elderly.” Western Journal of Emergency Medicine, vol. 13, no. 2 Jan. 2013, pp. 194-201.
Grossmann, Florian F. et al. “Screening, detection and management of delirium in the emergency department – a pilot study on the feasibility of a new algorithm for use in older emergency department patients: the modified Confusion Assessment Method for the Emergency Department (MCAM-ED).” Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine, vol. 22, no. 1, 2014, p. 19.
Geriatric Emergency Department Guidelines. (2014). Annals of Emergency Medicine, 63(5). doi:10.1016/j.annemergmed.2014.02.008
Han, Jin H., et al. “Delirium in the Older Emergency Department Patient: A Quiet Epidemic.” Emergency Medicine Clinics of North America, vol. 28, no. 3, 2010, pp. 611-631.
Inouye, Sharon K, et al. “Delirium in elderly people” The Lancet, vol. 383, no. 9934, 2014, pp. 911-922.
Inouye, Sharon K. “Clarifying confusion: The Confusion Assessment Method.” Annals of Internal Medicine, vol. 113, no. 12, 1990, pp. 941-948.
Inouye SK. The Confusion Assessment Method (CAM):Training Manual and Coding Guide. 2003; New Haven: Yale University School of Medicine.
Lewis LM et al. “Unrecognized delirium in ED geriatric patients.” American Journal of Emergency Medicine. vol. 13, 1995, pp. 142-45.
Monette, Johanne, et al. “Evaluation of the confusion assessment method (CAM) as a screening tool for delirium in the emergency room.” General Hospital Psychiatry, vol. 23, no. 1 , 2001, pp. 20-25.
Rosen, Toney, et al. “Assessment and Management of Delirium in Older Adults in the Emergency Department.” Advance Emergency Nursing Journal, vol. 37, no. 3, 2015

Posted on March 25, 2019 by NUEM Blog and filed under Neurology and tagged delirium elderly hyperactive hypoactive.

Lovenox in NSTEMI

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Written by: Terese Whipple, MD (NUEM PGY-3) Edited by: Andrew Ketterer, MD (NUEM Alum ‘17) Expert commentary by: Michael Macias (NUEM Alum ‘17)

The Case

A 64 year old female with history of diabetes and hypertension is brought to your emergency department (ED) by EMS for “acid reflux.” She has new T wave inversions in leads II, III, and aVF with a troponin of 0.12. The patient is given aspirin, nitroglycerine, and ticagrelor, but before signing your heparin drip order, you ask yourself:

Would enoxaparin (LMWH) be a better option?

The Recommendation:

The AHA and ACC guidelines state, “In patients with NSTE-ACS, anticoagulation, in addition to antiplatelet therapy, is recommended for all patients irrespective of initial treatment strategy. Treatment options include:

Enoxaparin: 1 mg/kg subcutaneous every 12 hours, continued for the duration of hospitalization or until PCI is performed. An initial IV loading dose is 30 mg (Level of evidence A)
Unfractionated heparin (UFH) IV: initial loading dose 60 IU/kg (max 4000 IU) plus 12 IU/kg/h (max 1000 IU/h) adjusted per activated PTT in according to specific hospital protocol (Level of evidence B)”[2]
Bivalirudin/Fondaparinux- These are other options outside the scope of this post

The Evidence:

So why is the evidence for enoxaparin Level A and UFH level B? Multiple randomized controlled trials have examined this issue:

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The ESSENCE (Efficacy and Safety of Subcutaneous Enoxaparin in Non-Q-Wave Coronary Events) trial was the first major RCT to demonstrate the efficacy of enoxaparin over UFH. Although it was conducted in the late 90s, before GIIb/IIIa inhibitors or early invasive intervention were commonplace, it demonstrated a statistically significant decrease in the risk of death, MI, or recurrent angina in those randomized to treatment with enoxaparin (16.6%) v. UFH (19.8%) (p=.019). Incidence of major bleeding was similar in both groups.
TIMI-II: Enoxaparin was found to be superior with no increase in hemorrhage. Outcomes measured were death, MI, and urgent revascularization at 8 and 43 days, respectively, for enoxaparin (12.4%, 17.3%) and UFH (14.5%, 19.7%) (P=.048).
SYNERGY: In patients undergoing early PCI, enoxaparin was not inferior to UFH in the treatment of NSTEMI. However, enoxaparin was associated with more major bleeding (3.7% v 2.5%, p=.028). Both bleeding and efficacy were potentially confounded by crossover from LMWH before randomization to UFH upon randomization and vice versa … more below.
A to Z: Studied the efficacy and safety of enoxaparin and tirofiban compared w/ UFH and tirofiban. Incidence of death, MI, refractory ischemia with enoxaparin (8.4%) v. UFH (9.4%) were similar with similar bleeding incidences. Enoxaparin was found to be not inferior to UFH.
A systematic review conducted in 2004 of approximately 22,000 patients extending across the evolution of ACS treatment from conservative management to early PCI, demonstrated that enoxaparin is more effective than UFH in preventing MI and death.

It may seem that as treatment of NSTEMI has evolved to include antiplatelet therapy and early invasive intervention, the superiority of enoxaparin has been negated. However, both the SYNERGY and A to Z trials were potentially confounded by the fact that a majority of patients received pre-randomization therapy. A subgroup analysis performed on those patients who received only enoxaparin in the SYNERGY trial and no pre-treatment anticoagulation demonstrated the superiority once again of enoxaparin over UFH in regards to the combined outcome of death and MI (13.3% vs. 15.9% , p= 0.004). The bleeding risk also seemed to be increased by pre-randomization therapy. The subgroup analysis showed no significant difference in major bleeding between UFH and enoxaparin when the patients received enoxaparin only (OR 1.04, CI 0.83-1.3).

If changing anticoagulation potentially increases bleeding risk, what about those destined for PCI?

The practices and procedures involved in PCI are beyond the scope of emergency medical practice, however the medications that we choose in the ED have downstream effects on patient care. Therefore, if we chose to use enoxaparin in the ED, we need to make sure that it won’t interfere with the ability of the patient to undergo PCI, and that it won’t increase their risk of adverse outcomes. Fortunately, this has been evaluated in controlled trials:

STEEPLE (Safety and Efficacy of Enoxaparin in PCI patients, an international randomized evaluation). This trial examined the safety and efficacy of IV bolus (0.5 mg/kg or 0.75 mg/kg) of LMWH at time of PCI.[7]
- Bleeding: Incidence of non-CABG-related bleeding complications in first 48 hours - 5.9% with 0.5 mg/kg enoxaparin (p=0.01 vs. UFH), 6.5% with 0.75 mg/kg enoxaparin (p= 0.051 vs. UFH), and 8.5% with UFH.
- Conclusion: IV bolus 0.5 mg/kg enoxaparin associated with reduced rates of bleeding, 0.75 mg/kg associated with similar bleeding risk to UFH. For the combined end point of bleeding and ischemic events, both doses of LMWH were non-inferior to UFH.
- 1-year mortality rates were comparable between patients receiving enoxaparin and UFH (2.3% for 0.5 mg/kg, 2.2% for 0.75 mg/kg, 1.9% for UFH)
CRUSADE (Can rapid risk stratification of unstable angina patients suppress adverse outcomes with early implementation of ACC/AHA guidelines). This trial studied the efficacy and safety of LMWH compared with UFH in high risk NSTEMI patients also receiving early GPIIb/IIIa inhibitor therapy.
- In patients who underwent PCI within 48 hours the ORs for risk of death and reinfarction were similar for LMWH compared to UFH (OR 0.93, CI 0.67-1.31).
- In patients who underwent PCI >48 hours into hospitalization, LMWH therapy was associated with reduced rates of death or reinfarction (OR 0.57, 95% CI = 0.44-0.73) and transfusion (OR 0.66, 95% CI = 0.52-0.84).
- Conclusion: Early invasive management with LMWH and GP IIb/IIIa inhibitor in NSTEMI is safe and doesn’t result in increased bleeding complications. In fact, it actually improves outcomes for those who don’t undergo PCI within 48 hours. 9

Take Home Points:

Enoxaparin has been proven to be at least non-inferior and likely even superior to UFH when it comes to reducing the risk of death and MI in the setting of NSTEMI.
Bleeding risk with enoxaparin compared to UFH appears to be equal (with the exception of the Synergy trial).
Enoxaparin is safe and efficacious for use during PCI.
Dialogue should occur between ED providers and interventional cardiologists to ensure their comfort with enoxaparin use and to prevent bleeding complications. If everyone is on board with using enoxaparin, it will likely get your patient anticoagulated more expediently than they otherwise would while waiting for pharmacy to mix up your heparin drip.

Expert Commentary

Dr. Whipple, thank you for an excellent review of the literature supporting the use of lower molecular weight heparin (LMWH) for Non-ST-Elevation Myocardial Infarction (NSTEMI). There are two important points to discuss here before we even talk about LMWH, specifically: (1) What is the evidence behind good ole unfractionated heparin (UFH) in patients with NSTEMI? (2) Based on the evidence for UFH, is there a subgroup of patients who are likely to benefit more than others?

What is the evidence behind good ole unfractionated heparin (UFH) in patients with NSTEMI?

If you look at the AHA/ACC guidelines, UFH is listed as a Class I recommendation. Like any recommendations in guidelines, it is always important to look back at the data behind it. Specifically with respect to UFH, this data is weak but unfortunately is the best we have. Many of studies supporting the use of UFH in NSTEMI involved patients with “unstable angina” in the era before modern laboratory diagnostics (most studies used creatinine kinase), dual anti-platelet therapy (DAPT), GpII/IIIa inhibitors, early invasive strategies, and revascularization [10]. This is a very different population than NSTEMI patients today. In general, these studies did find a strong trend in reduction of composite endpoints (mainly recurrent angina, death or MI) however this was only during hospitalization (short term endpoints) and this is the main crux of the AHA/ACC guideline recommendations. Further in the guidelines favor, the Cochrane review also concluded that UFH in NSTEMI reduces the rate of MI with a relative risk of 0.4 (0.25-0.63) [11]. However what both the guidelines and Cochrane review failed to consider is the benefits of UFH to our patients at a later time point. Deeper analysis of the Cochrane review reveals that the majority of their data points came from the FRISC study, which used only a six-day end point for their outcomes. A meta-analysis performed by Oler in 1996, took into account a time period beyond the UFH treatment duration (2-12 weeks) and found no significant difference in outcomes:

“Because the anticoagulant effects of heparin are brief, any benefit of therapy is unlikely to last beyond the duration of treatment. Consistent with this theory, we found no reduction in the risk of MI or death between 2 and 12 weeks following randomization in patients with unstable angina who received heparin and aspirin compared to those who received aspirin alone. This result underscores that heparin is a short-acting, temporizing therapy, and not an intervention that alters underlying atherosclerotic disease. - Oler et al. 1996”

Not only do the studies that the guidelines base their data off fail to consider more later end points, they also include a different patient population, in a different era of acute coronary syndrome management. Since heparin has now become the standard of care for management of NSTEMI, no further placebo- controlled trials of heparin will ever exist.

Based on the evidence for UFH, is there a subgroup of patients who are likely to benefit more than others?

Based on the discussion above, there isn’t strong evidence to support UFH use in all comers with NSTEMI however based on its mechanism of action, it is likely to benefit those with high risk NSTEMI (TIMI Risk Score), or those who will undergo coronary intervention or revascularization. Intuitively this makes sense and jives with the evidence in the AHA/ACC guidelines. Patients who are placed on UFH and bridged to PCI/revascularization will benefit from the theoretical plaque stabilization. Those who are observed without any intervention will not, as once heparin is discontinued, their ongoing plaque burden and coronary anatomy will be unchanged, placing them at risk for a “rebound” event.

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In the emergency department we are burdened with making decisions with minimal initial information and only a few hours of observation. That being said, making a confident decision about which NSTEMI patients will need PCI/revascularization (and therefore will benefit from UFH) may prove very difficult. Therefore it may be more prudent to consider when certain situations make intervention less likely. These situations may include:

Patients without ACS symptoms but with elevated troponin:
- Renal disease
- hypotension
- Sepsis
- Toxic ingestion
- Significant metabolic derangement
- Anemia
- Heart failure (without suspicion for ischemic etiology)
- Supraventricular tachycardia (SVT)
- Other presentations where troponin elevation is suspected to be related to a supply/demand issue
Patients with atypical history and high bleeding risk

The best course of action in these situations is to discuss the utility of UFH with the consulting cardiologist or admitting hospitalist about what is right for your patient based on the risk and benefits of anticoagulation, as well as your clinical suspicion for true acute coronary syndrome.

UFH or LMWH?

Now that we have a better understanding of the utility of UFH in NSTEMI, the use of LMWH becomes more clear. The same considerations just discussed should be similarly applied to the use of LMWH. As your literature review demonstrates, LMWH appears to be as good (if not better) than UFH with a similar bleeding risk profile. It is also easier to administer, requires less monitoring and has a lower risk of accidental supra-therapeutic anticoagulation. While it seems that it may be an obvious decision to switch to LMWH, remember that there is always a significant time lag between evidence and its incorporation into clinical practice. Therefore as you mentioned in your take home points, clear communication with other services is key. Before you go rogue giving LMWH to all your NSTEMI patients, I recommend having a evidence based discussion with your cardiologists and hospitalists to ensure everyone is on the same page.

Michael Macias, MD

NUEM Alumus 2017

University of California, San Diego

How To Cite This Post

[Peer-Reviewed, Web Publication] Whipple T, Ketterer A. (2019, March 18). Lovenox in NSTEMI [NUEM Blog. Expert Commentary by Macias M]. Retrieved from http://www.nuemblog.com/blog/lovenox-NSTEMI

Optic Neuritis

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Written by: Steve Chukwulebe, MD (NUEM PGY-4) Edited by: Victor Gappmaier, MD (NUEM Alum ‘18) Expert commentary by: Shira Simon, MD, MBA

Case:

31-year-old female, with no significant past medical history, presents to the emergency department with a mild headache and blurry, decreased vision in the right eye for the past 2 days. Other historical elements include that the patient has been experiencing pain with eye movement. However, she denies difference in color perception. She also denies any trauma to the eye, recent fevers, chills, malaise, exposures, or travel. The left eye is unaffected.

Exam:

Normal vitals and a well appearing female of stated age

Ocular exam reveals normal appearing eyes without chemosis, proptosis, conjunctival injection, scleritis, icterus, or foreign bodies

Non-dilated funduscopic exam is unremarkable

Visual acuities are OD: 20/40 and OS: 20/20

Tonometry reveals right and left eye pressures are < 20 mmHg

Slit lamp exam is without cells or flare

Fluorescein stain is without any corneal uptake

CN 3-12 are intact, and no focal neurologic deficits on exam

Differential Diagnosis [1,2]:

Painless Vision Loss

Central retinal artery occlusion
Central retinal vein occlusion
Retinal detachment
Vitreous detachment/vitreous hemorrhage
Tumor/Mass
Stroke

Painful Vision Loss

Acute angle closure glaucoma
Scleritis
Anterior uveitis (iritis)
Optic neuritis
Keratitis
Corneal abrasion/trauma
Temporal arteritis

The challenge in diagnosing optic neuritis is to exclude other causes of acute monocular vision loss. Therefore, a normal appearing eye, slit lamp exam, fluorescence stain, and intraocular pressures eliminates scleritis, uveitis, keratitis/abrasion, and glaucoma respectively [5]. Additionally, the history is less suggestive of other urgent and emergent ocular pathologies such as retinal detachment and central retinal artery occlusion.

Some physical exam findings more specific to optic neuritis include:

Afferent pupillary defect
Optic disk swelling and papilledema, which can be seen by ultrasound [6]
Decreased perception in the saturation of deep red colors
Decreased visual acuities ranging from 20/25 to 20/190, and even no light perception[4]
Eye pain, especially with eye motion, is seen in 92 percent of patients
Loss of color vision out of proportion to the decrease in visual acuity
Retro-orbital headache

Further diagnostics may include an MRI of the brain and orbits, but is not necessary for the diagnosis of optic neuritis [5]. MRI can help characterize the disease burden and assess the risk for the development of multiple sclerosis [7].

Given the patient’s age and constellation of symptoms, both neurology and ophthalmology consultation were performed with the leading concerning diagnosis being optic neuritis. The patient was admitted for further evaluation with a dilated ocular exam, MRs of the brain, and treatment.

Pathophysiology and Clinical Disease:

Optic neuritis is an inflammatory and demyelinating process that usually presents with monocular vision loss [3-4]. While there are many causes for optic neuritis, the demyelinating lesions seen in optic neuritis are similar to those that have been associated with multiple sclerosis. Patients are typically women between the ages of 20-40. Patients often develop progressive symptoms over a period of a few hours to several days.

Treatment and Timing:

Typical treatment is high dose intravenous steroids for three days. Another treatment regimen that has been described is intravenous methylprednisolone (250 mg four times per day) for three days, followed by oral prednisone (1 mg/kg per day) for 11 days, and then a four-day taper [8, 9].

If the diagnosis is uncertain, then is it acceptable to delay treatment for an MRI or specialist consultation the following morning?

The Optic Neuritis Treatment Trial described treatment of optic neuritis with high dose intravenous methylprednisolone. The initial multicenter trial enrolled 457 patients from July 1, 1988, through June 30, 1991. They ultimately randomized 389 patients with acute optic neuritis (and without known multiple sclerosis) to receive intravenous methylprednisolone (250 mg every six hours) for 3 days followed by oral prednisone (1 mg per kilogram of body weight) for 11 days, oral prednisone (1 mg per kilogram) alone for 14 days, or placebo for 14 days. They then assessed the neurologic status of the subjects for a period of two to four years and published their results in 1993. Also by following the subjects longitudinally, the authors were able to reanalyze the data and publish again in 2003. From the initial study, it was learned that high the steroids hastened the recovery of visual function, but did not affect long term visual outcomes when compared to both placebo and oral prednisone [10, 11, 12] after six months, and ten-year follow-up. It was found that a 3-day course of methylprednisolone reduced the rate of development of multiple sclerosis over a 2-year period [12]. Multiple sclerosis developed within the first two years in 7.5 percent of the IV methylprednisolone group vs. 14.7 percent of the oral prednisone group vs. 16.7 percent of the placebo group. The adjusted rate ratio for the development of definite multiple sclerosis within two years in the intravenous methylprednisolone group was 0.34 as compared with the placebo group and 0.38 as compared with the oral-prednisone group. However, after a 5-year period the treatment effect was no longer significant for the same group of patients.

Therefore, in a scenario when a provider may delay high dose steroids for a neurology and ophthalmology consultation, or for an MRI, it can be inferred that this delay will not affect long term outcomes for the patient. However, given that early treatment hastens symptom recovery and delays progression to multiple sclerosis, it may be beneficial to start high dose IV steroids in the emergency department in patients if optic neuritis is the suspected diagnosis.

Expert Commentary

This is a very good review of optic neuritis. There are just a few, additional nuanced points I’d like to mention, as well as some tips on counseling the patient.

Visual field changes: A central visual field deficit is commonly seen with this entity. It is most easily detected on formal visual field testing in the ophthalmology clinic (Humphrey or Goldmann visual fields), though some patients may report this on their own in the acute care setting.
Optic nerve swelling: In the ONTT, only 35% of patients had disc swelling (65% had normal appearing optic nerve heads on fundoscopy), so evaluating with ultrasound would not be revealing in most cases.
MRI for diagnosis: MRI is actually very important for the diagnosis of optic neuritis, as inflammation of a different part of the optic nerve (other than the nerve head) can only be visualized radiographically. MRI of the orbits and brain should be obtained with thin slices through the orbits, with fat suppression, and gadolinium (in addition to FLAIR sequences to look for demyelination).
Differential diagnosis: While this article talks about optic neuritis from demyelination related to possible MS, it’s important to bear in mind that there are other causes of optic neuritis: autoimmune disease (e.g., lupus), infections (e.g., syphilis or Lyme), other inflammatory conditions (e.g., sarcoidosis), other demyelinating processes (like neuromyelitis optica), or it can be idiopathic.

When counseling the patient about prognosis, it may be helpful to remember the “10-20-40-60” rule. I had been taught this, and it helps quickly summarize the ONTT prognostic statistics (that are outlined very nicely in this article). The “10-20-40-60 rule” mnemonic reminds us that at 10 years: there is a 20% chance of developing MS after an episode of idiopathic optic neuritis if there were no white matter lesions found on MRI; a 40% chance regardless of MRI findings; and, a 60% chance if 1+ white matter lesions are found on MRI.

It is also helpful to let the patient know that visual recovery is often excellent. Most patients return fairly close to their baseline vision within 3-5 weeks, although they may note some lingering difficulties with contrast sensitivity and color vision. An afferent pupillary defect may also persist.

Shira Simon, MD, MBA

Assistant Professor of Ophthalmology and Neurology

Northwestern Medicine

How to Cite This Post

[Peer-Reviewed, Web Publication] Chukwulebe S, Gappmaier V. (2019, March 11). Optic Neuritis. [NUEM Blog. Expert Commentary by Simon S]. Retrieved from http://www.nuemblog.com/blog/optic-neuritis

Resources

Dargin JM, Lowenstein RA. The painful eye. Emerg Med Clin North Am. 2008;26(1):199-216, viii.
Vortmann M, Schneider JI. Acute monocular visual loss. Emerg Med Clin North Am. 2008;26(1):73-96, vi.
The clinical profile of optic neuritis. Experience of the Optic Neuritis Treatment Trial. Optic Neuritis Study Group. Arch Ophthalmol. 1991;109(12):1673-8.
UpToDate
Germann CA, Baumann MR, Hamzavi S. Ophthalmic diagnoses in the ED: optic neuritis. Am J Emerg Med. 2007;25(7):834-7.
Teismann N, Lenaghan P, Nolan R, Stein J, Green A. Point-of-care ocular ultrasound to detect optic disc swelling. Acad Emerg Med. 2013;20(9):920-5.
Beck RW, Arrington J, Murtagh FR, Cleary PA, Kaufman DI. Brain magnetic resonance imaging in acute optic neuritis. Experience of the Optic Neuritis Study Group. Arch Neurol. 1993;50(8):841-6.
Beck RW, Cleary PA, Anderson MM, et al. A randomized, controlled trial of corticosteroids in the treatment of acute optic neuritis. The Optic Neuritis Study Group. N Engl J Med. 1992;326(9):581-8.
Sellebjerg F, Nielsen HS, Frederiksen JL, Olesen J. A randomized, controlled trial of oral high-dose methylprednisolone in acute optic neuritis. Neurology. 1999;52(7):1479-84.
Beck RW, Gal RL, Bhatti MT, et al. Visual function more than 10 years after optic neuritis: experience of the optic neuritis treatment trial. Am J Ophthalmol. 2004;137(1):77-83.
Beck RW, Trobe JD, Moke PS, et al. High- and low-risk profiles for the development of multiple sclerosis within 10 years after optic neuritis: experience of the optic neuritis treatment trial. Arch Ophthalmol. 2003;121(7):944-9.
Beck RW, Cleary PA, Trobe JD, et al. The effect of corticosteroids for acute optic neuritis on the subsequent development of multiple sclerosis. The Optic Neuritis Study Group. N Engl J Med. 1993;329(24):1764-9.

Posted on March 11, 2019 by NUEM Blog and filed under Ophthalmology and tagged optic neuritis demyelination optic nerve MS.

Verbal De-escalation in the ED

Written by: Vidya Eswaran, MD (NUEM PGY-3), Zach Schmitz, MD (NUEM PGY-2), Abiye Ibiebele, MD (NUEM PGY-2) Edited by: Michael Macias, MD and Arthur Moore, MD (NUEM Alum ‘17) Expert commentary by: John Bailitz, MD

Introduction

I’ve been suffering in that waiting room for hours!
That worthless tech stabbed me with a needle ten times!!
If you don’t give what I want right now, I am going to hurt someone!!!

Every emergency physician can recall a time when they hear these words or similar phrases echoing throughout the Emergency Department (ED). As a patient becomes increasingly agitated, nearby staff and visitors become distracted, and ultimately concerned about everyone’s safety. Emergency Physicians can help restore the calm amidst the chaos by recognizing subtle clues and intervening early.

According to the Bureau of Labor Statistics, those who work in the healthcare sector had three times the rate of illness and injury from violence compared to all private industries [1]. In a survey of emergency medicine residents, 65.6% reported an experience of physical violence by a patient, 96.6% reported verbal harassment from a patient, and 52.1% reported sexual harassment by a patient. Often these patients were under the influence of drugs or alcohol, had a psychiatric disease, or an organic cause of their agitation, such as dementia [2]. In Australian emergency departments, 3 of every 1000 ED visits are associated with an episode of violence or acute behavioral disturbance [3].

When violence by a patient is imminent or has already occurred, the patient requires immediate restraint by either chemical or physical means [4]. ACEP guidelines for patient restraints supports the careful and appropriate use of restraints or seclusion if “careful assessment establishes that the patient is a danger to self or others by virtue of a medical or psychiatric condition and when verbal de-escalation is not successful [5].” Verbal “de-escalation techniques aim to stop the ascension of aggression to violence, and the use of physically restrictive practices, via a range of psychosocial techniques [6],” and should be tried before one simply grabs “5 and 2.”

Clinical Approach to Agitation

How do you determine which patients would benefit from verbal de-escalation?

Look for the agitated patient, the one who has an angry demeanor, using loud and aggressive speech, seems tense and is grasping their bed rails or clenching their fists, the one who is pacing or fidgeting [4]. These patients are in the pre-violent stage, and may have the potential to be successfully talked down. If a patient has already engaged in violent acts, it is too late to intervene with verbal de-escalation methods.

What principles should be used to assist with verbal de-escalation of the agitated patient?

In 2012 the American Association for Emergency Psychiatry offered a consensus statement on verbal de-escalation and created ten key domains to guide care of agitated patients. These domains offer a great framework for how to approach the agitated patient before the situation escalates [7].

Domain 1: Respect the patient’s and your personal space. First and foremost in any patient encounter, especially one with an agitated patient, is your safety. Aim to keep at least 2 arms lengths distance between you and the patient. This offers you room for your own personal safety, and is seen as non-confrontational and non-threatening in the eyes of the patient. Ensure that both you and the patient have an unobstructed pathway to the exits and that you do not stand in the way of the patient’s path to leaving the room.

Domain 2: Do not be provocative. The majority of our interpersonal interactions is communicated not by the words we say, but how we say them. Our body language is crucial and we must be mindful of it when attempting to calm a patient. Keep your hands visible and at ease, bend your knees slightly, avoid excessive direct eye contact and approach your patient from an angle instead of head-on. These positions convey a non-threatening demeanor.

Domain 3: Establish verbal contact. The first person to interact with the patient should be the one who leads the verbal de-escalation. Introduce yourself and tell the patient your role and orient them to their surroundings. Then, ask the patient what they would like to be called. This gives the patient the impression that you believe he or she is important and has some control over the situation.

Domain 4: Be concise and caring. Use short sentences and simple vocabulary to get your point across. Give your patients time to process what you have said and to respond before continuing. You should be prepared to repeat your message multiple times until your patient understands.

Domain 5: Identify wants and feelings. In order to provide empathetic care, you must understand your patient’s perspective. Listen carefully to what your patient says to pick up clues and respond to their desires. One tactic is to say “I really need to know what you expected when you came to the ED today. Even if I can’t provide it, I would like to know so that we can work on it together.”

Domain 6: Listen closely to what the patient is saying. This is closely related to Domain 5. Practice closed loop communication, repeat what the patient has told you to ensure you have understood them correctly.

Domain 7: Agree, or agree to disagree. Look for something that you can agree with in what the patient is saying. “I agree, waiting can be frustrating” or “Yes, I understand that the nurse has stuck you three times.” However, if you can’t find something to agree with the patient about, do not lie - agree to disagree.

Domain 8: Lay down the law and set clear limits. Draw a line which the patient must not cross. Let him or her know that harming himself or others is unacceptable and will result in specific consequences (seclusion, arrest, prosecution). This should not be portrayed as a threat, but rather be conveyed in a respectful manner. You can preface it with “Your behavior is making our staff uncomfortable and that makes it difficult for us to help you.”

Domain 9: Coach the patient on how to stay in control. Give the patient tactics they can use to help de-escalate the situation. “If you sit down we can discuss why you are here.”

Domain 10: Be optimistic and provide hope that the patient will be able to get to a favorable outcome. “I don’t want you to stay here longer than you need to. Let’s work together to help you get out of here feeling better.” Be sure to debrief with the patient and staff after the de-escalation, so that there is a strategy in place if this were to happen again.

Other strategies include recruiting the patient’s friends and family to help and to employ the three Fs technique - feel, felt, found [8]. “I understand that you feel X. Others in the same situation have felt that way to. Most have found that doing Y can help [4].”

Think of verbal de-escalation as a procedure just like intubations or central lines - with practice, comes mastery. Rehearse what you plan to say, and do mental run-throughs of de-escalations. Watch and learn from others who do this well. The English Modified De-Escalating Aggressive Behaviour Scale (EMDABS) is a validated tool you can use to assess your performance during de-escalations [9].

Summary

Unfortunately, physical and chemical restraint of the severely agitated patient is sometimes needed to protect ED staff, visitors, and the patient themselves. [10,11]. But by recognizing subtle signs of agitation early, we can often utilize effective verbal-de-escalation techniques to create safety for everyone!

Check out our infographic for an easy to use mnemonic which summaries key points.

Expert Commentary

Thank you for this outstanding review of an incredibly important topic topic with tragically little supporting evidence to guide best practice. Colleagues and patients in multiple different practice settings throughout Chicago have repeatedly taught me several key pearls and pitfalls when dealing with the agitated patient.

For the mildly agitated patient, always open with an apology that empathically validates the patient or visitor emotions. “I am very sorry that you have been suffering in the waiting room for so long. That must have been very frustrating. My sincere apologies.” Never reply with a sharp justification or any explanation. Just acknowledge their frustration, own it, and the patient will quickly move past the emotion. Often times, this first connection forms the foundation of a healthy patient physician relationship and even a thank you letter to your ED Director.

For the patient whose agitation is escalating despite appropriate efforts by trained ED staff, call security or hit the duress button for back up before stepping into any potentially risky situation. If you are single covered at 3 AM, you cannot become another patient. When help arrives, ask security to simply stand in the hallway as you begin your DEFUSE techniques. Politely but purposefully excuse inexperienced staff members who have themselves become agitated and entered into a shouting match with patients or visitors. Always keep your own emotions in check and debrief with everyone involved after each learning opportunity.

Finally, when the sedation is needed for patient and staff safety, assemble your team, and proceed with the utmost professionalism. As a physician, you have no role in the physical restraint process unless absolutely necessary. Your security staff has been trained in proper physical restraints while chemical sedation catches up with the dangerous patient. If the patient is acutely agitated without concerns for respiratory depression, utilize 5 mg of Haldol + 5 mg of versed instead of the traditional 2 mg of Ativan. Everyone in the ED will become safer more quickly and the patient will wake up more rapidly for reassessment.

Just remember, “Patients First” always starts with everyone’s safety first!

John Bailitz, MD

Program Director, Northwestern Emergency Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication] Eswaran V, Schmitz Z, Ibiebele A, Macias M, Moore A. (2019, March 4). Verbal De-escalation in the ED. [NUEM Blog. Expert Commentary by Bailitz J]. Retrieved from http://www.nuemblog.com/blog/verbal-deescalation

References

Nonfatal Occupational Injuries and Illnesses Requiring Days Away From Work, 2014.Bureau of Labor and Statistics News Release. 2015. http://www.bls.gov/news.release/archives/osh2_11192015.pdf
Schnapp et al. Workplace Violence and Harassment Against Emergency Medicine Residents, WJEM 2016: 17(5) 567-573. https://www-ncbi-nlm-nih-gov.ezproxy.galter.northwestern.edu/pmc/articles/PMC5017841/pdf/wjem-17-567.pdf
Downes et al. Structured team approach to the agitated patient in the emergency department. Emergency Medicine Australasia (2009) 21, 196-202 http://onlinelibrary.wiley.com.ezproxy.galter.northwestern.edu/doi/10.1111/j.1742-6723.2009.01182.x/epdf
Moore, G and Pfaff, J. Assessment and emergency management of the acutely agitated or violent adult.Up to Date. https://www-uptodate-com.ezproxy.galter.northwestern.edu/contents/assessment-and-emergency-management-of-the-acutely-agitated-or-violent-adult?source=search_result&search=Assessment%20and%20emergency%20management%20of%20the%20acutely%20agitated%20or%20violent%20adult&selectedTitle=1~150#H17
ACEP Policy on Patient Restraints https://www.acep.org/Clinical---Practice-Management/Use-of-Patient-Restraints/
Price et al. Learning and performance outcomes of mental health staff training in de-escalation techniques for the management of violence and aggression. The British Journal of Psychiatry (2015) 206, 447-455 http://bjp.rcpsych.org.ezproxy.galter.northwestern.edu/content/bjprcpsych/206/6/447.full.pdf
JS Richmond et al. Verbal De-escalation of the Agitated Patient: Consensus Statement of the American Association for Emergency Psychiatry Project BETA De-escalation Workgroup. Western Journal of Emergency Medicine: Integrating Emergency Care with Population Health 2012: 13(1) 17-25. http://escholarship.org/uc/item/55g994m6
Nickson, C. De-Escalation. Life in the Fast Lane. 2014. http://lifeinthefastlane.com/ccc/de-escalation/
Mavandadi et al. Effective ingredients of verbal de-escalation: validating an English modified version of the ‘De-Escalating Aggressive Behaviour Scale’. Journal of Psychiatric and Mental Health Nursing, 2016, 23, 357-368. http://onlinelibrary.wiley.com.ezproxy.galter.northwestern.edu/doi/10.1111/jpm.12310/epdf
Weingart, S. Podcast 060 – On Human Bondage and the Art of the Chemical Takedown. EMCrit. 2011. http://emcrit.org/podcasts/human-bondage-chemical-takedown/
Nickson, C. Chemical Restraint. Life in the Fast Lane. 2014. http://lifeinthefastlane.com/ccc/chemical-restraint/

Posted on March 4, 2019 by NUEM Blog and filed under Psychiatry and tagged verbal de-escalation psychiatry violence patient safety.

Intraosseous Lines

Written by: Dana Loke, MD (NUEM PGY-3) Edited by: Victor Gappmaier, MD (NUEM Alum ‘18) Expert commentary by: John Sarwark, MD

Since its development in the 1940s, intraosseous (IO) access has been a mainstay of resuscitation in both pediatric and adult patients[1]. IO access has been used in medical emergencies requiring immediate access when peripheral IV access is either not possible or time-prohibiting, such as cardiac arrest, status epilepticus, shock, trauma, and burns[2]. There is mounting evidence supporting the continued use of IO lines both in-hospital and pre-hospital. Studies have demonstrated similar outcomes between IO and IV access with return of spontaneous circulation, further supporting their use during cardiac arrest3. In fact, the International Liaison Committee on Resuscitation (ILCOR) stated in 2010 that “Delivery of drugs via an endotracheal tube is no longer recommended – if IV access cannot be achieved, drugs should be given by the IO route”[4]. Currently, IO access is achievable in two ways: manually or with commercially-available drill-inserted devices (such as the EZ-IO).

Why use an IO instead of a central line during a resuscitation?

Besides the obvious advantage that IO insertion is quicker, it is also cheaper than central line insertion. On average IO lines cost about $100 compared to $300 for central lines[4]. Additionally, there are far fewer complications associated with IO lines compared to central lines. All medications that can be given via central line can also be given via IO line. Blood can be drawn and sent for lab analysis just as with IV access. Although an IO line only has one lumen, there are multiple possible insertion sites, and multiple IO lines can be placed in the same patient simultaneously. Furthermore, IO lines are easy to remove when more definitive vascular access has been obtained.

But perhaps one of the biggest advantages of an IO is that it requires less training and experience to insert than a central line. Their ease of use allows trained RNs, techs, and novice providers to obtain vascular access without interrupting assessment by senior providers. In fact, a recent study showed that IO access can effectively be taught as a four-step approach to medical students[5].

Contraindications

There are a few important contraindications to IO access for the EM physician to be aware of. The first is any fracture at or proximal to the insertion site, as this can cause extravasation of fluids or medication and increases the risk of compartment syndrome[2]. The second is cellulitis or evidence of other infection such as abscess at the insertion site, similar to other procedures like central lines and PIV access[2]. Sites of prior attempts should not be used for a second attempt. Lastly, patients at risk for fracture (for instance, osteogenesis imperfecta or osteopetrosis) should not be given an IO line[4].

Technique

Although manual insertion of an IO line is possible using a Cook or Jamshidi needle, commercial devices such as the EZ-IO are widely available and should always be used for IO insertion if available. The EZ-IO kit includes the IO needle set (with 45 mm, 25 mm, and 15 mm needles), power driver, IO tubing, and adhesive dressing as shown in the image below[6]. The 25 mm needle is the standard needled used for adults. If the humerus is used or there is excessive tissue (i.e. muscular or obese patients), then the 45 mm needle should be used. The 15 mm is generally used in children or any adults <40 kg.

There are multiple sites in which IO access can be obtained as shown in the image below [4,5]:

Proximal humerus – insert about 1 cm above the surgical neck (which can be found by sliding a finger up the anterior humeral shaft until the greater tubercle is felt)
- Of note, this is the preferred insertion site during resuscitation, especially those involving abdominal trauma, as medications and fluids enter the circulation faster as they reach the central circulation via the SVC and bypass the pelvic and abdominal vessels.
Proximal tibia – insert 2 finger breadths below the patella and 1-2 cm medial to the tibial tuberosity in adults
Distal tibia – insert 3 cm proximal to the most prominent aspect of the medial malleolus
Femur, iliac crest, sternum – not routinely used and may require a special device

After choosing the correct needle and site, clean the site with alcohol swabs or chlorhexidine, and connect the needle set to the power driver (i.e. the drill). Remove the needle cap and insert the needle by drilling with a consistent downward pressure perpendicular to the bone surface. It is customary to feel a sudden loss of resistance, as the needle “gives” when entering the medullary space. Remove the power driver from the needle and secure the site with the adhesive dressing. At this point, you can aspirate blood for lab analysis and then connect primed IO tubing to flush the IO line. Now the line is ready for use to primed IV tubing. Make sure to document the time of insertion as IO lines should not be left in for more than 24 hours.

Medications

Any medication that can be given intravenously can also be given intraosseously[2]. This includes contrast media and blood transfusions[7]. Some amount of hemolysis of transfused blood has been documented when given intraosseously, although this is of unclear clinical significance[4]. According to multiple studies, the IO route is pharmacokinetically equivalent to the IV route and therefore there is no need to change medication doses when administering via IO8.

Labs

While any lab can be sent from an IO blood sample, it is important to be cognizant of the correlation between certain labs when obtained via IO vs IV. Labs that have good correlation include hemoglobin/hematocrit, chloride, glucose, urea, creatinine, and albumin[4]. However, other labs including WBC, platelets, serum CO2, sodium, potassium, calcium do not correlate well or in any predictable way with venous samples4.

Removal

All IO lines should be removed within 24 hours of the insertion time or earlier if there is any sign of extravasation (i.e. progressive pain or swelling at the insertion site). After disconnecting all infusions, the EZ-IO needle and hub can be removed by attaching a 10 cc luer-locked syringe to the hub and rotating clockwise while pulling back[4]. As with all potential sharps, the device should be disposed of in a biohazard sharps container.

Complications

Although rare, there are several complications of IO access to be aware of. These include osteomyelitis, fracture, extravasation, compartment syndrome, and necrosis of the epiphyseal plate[4]. However, perhaps the most common complication is injury to self or others while obtaining access. To avoid injury, warn conscious patients about the procedure and in unconscious patients make sure to stabilize the site.

Key Points

IO lines are a mainstay of resuscitation and used when peripheral IV access is either not possible or time-intensive.
Compared to central access in resuscitations, IO access is cheaper, quicker, safer, and easier to obtain.
Contraindications to IO insertion include fracture at or proximal to the insertion site, cellulitis or other infection overlying the insertion site, prior attempt at the insertion site, or bone disease such as osteogenesis imperfecta or osteopetrosis.
Make sure to choose the appropriate needle and insertion site prior to obtaining IO access.
All medications that can be given intravenously can be given intraosseously at the same doses.
Remember that not all lab values from an IO sample correlate with IV samples. Accurate IO labs include: hemoglobin/hematocrit, chloride, glucose, urea, creatinine, and albumin.
IO lines should be removed within 24 hours of insertion.
Complications are rare but include osteomyelitis, fracture, extravasation, compartment syndrome, and necrosis of the epiphyseal plate.

Expert Commentary

Intraosseous lines in the emergency department have always made perfect sense to me so I appreciate the scrappy enthusiasm for them in this article. In my opinion, they are an incredibly logical alternative to “crash” central lines. I mean, seriously, in a scenario where a patient is coding or about to code, why in god’s name should we be farting around with a femoral line? People get stuck with needles. Arteries are inadvertently punctured. There’s a huge mess and it’s often not sterile. An IO goes in clean and easy within seconds and boom, you’ve got yourself access, and essentially central access at that. You can put pretty much anything in it, although I did hear in my time around the ICU circuit in residency that the exception to this is TPN. That’s largely a piece of meaningless chin stroking trivia but, hey, maybe it will make you sound smarter on MICU rounds tomorrow AM.

The needle sizes can be a bit confusing in a tense situation. To avoid any issues, just remember this to keep it simple: USE THE BLUE NEEDLE. I have yet to have a patient who was so obese they needed the yellow needle in their tibia, and the pink one is exclusively just for kids. The best route is indeed via the humerus as the flow rate is reportedly as good as a subclavian line. Folks tend to jump for the tibia as their go-to site, and that’s perfectly fine but if you’re doing this out of uncertainty with the landmarks of the humerus it’s easier than you think. One way I was taught was to place your hands in an inverted “V” over the proximal humerus, and where your thumbs meet over the bone there is your target for your drill.

Not to be a Robert Downer Junior but I should remind everyone that there was an article in Annals this year entitled “Intraosseous Vascular Access Is Associated With Lower Survival and Neurologic Recovery Among Patients With Out-of-Hospital Arrest.” The title really states it all, showing a lower rate of “favorable” modified Rankin score in the patients that got IO over IV. Another study from Resuscitation last year titled “Intraosseous compared to intravenous drug resuscitation in out-of-hospital cardiac arrest” also showed decreased rates of ROSC and survival to hospitalization (but not to discharge) in the IO group. Bear in mind the IO’s in these articles are placed in the field and not in the hospital, although I can’t think there’s too much difference in technique between us and our friends out in the rigs.

I’m not going to get into the nitty gritty of each of these papers and I certainly don’t think we are actively making moves to remove them from our practice in our specialty but keep your eyes open for more discussion and research on this in the coming months to years. I still like the IO and it’s still a part of my practice and I encourage you to use it as well. Drill, baby, drill!

John P Sarwark, MD

NUEM Alumnus 2016

How to Cite This Post

[Peer-Reviewed, Web Publication] Loke D, Gappmaier V (2019, February 25). Intraosseous Lines [NUEM Blog. Expert Commentary by Sarwark J]. Retrieved from http://www.nuemblog.com/blog/io

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References

Foëx, B.A. (2000). Discovery of the intraosseous route for fluid administration. J Accid Emerg Med, 17(2) 136-137.
Faga, M., & Wolfe, B. (2016). Vascular access in hospitalized patients. Hospital Medicine Clinics, 5(1), 1-16.
Clemency, B., Tanaka, K., May, P., Innes, J., Zagroba, S., Blaszak, J., Hostler, D., Cooney, D., McGee, K., & Lindstrom, H. (2017). Intravenous vs. intraosseous access and return of spontaneous circulation during out of hospital cardiac arrest. Am J Emerg Med , 35(2), 222-226.
Nickson, C. (2015, June 10). Intraosseous access. Retrieved February 26, 2018, from https://lifeinthefastlane.com/ccc/intraosseous-needle-insertion/
Afzali, M., Kvisselgaard, A.D., Lyngeraa, T.S., & Viggers, S. (2017). Intraosseous access can be taught to medical students using the four-step approach. BMC Med Educ, 17(1), 50.
Teleflex. (2018). Intraosseous access. Retrieved February 26, 2018, from https://www.teleflex.com/usa/product-areas/vascular-access/emergency-trauma-products/intraosseous-access/
Winkler, M., Talley, C., Woodward, C., Kingsbury, A., Appiah, F., Elbelasi, H., Landwher, K., Li, X., & Fleischmann, D. (2017). The use of intraosseous needles for injection of contrast media for computed tomographic angiography of the thoracic aorta. J Cardiovasc Comput Tomogr, 11(3), 203-207.
Von Hoff, D.D., Kuhn, J.G., Burris, H.A. 3rd, & Miller, L.J. (2008). Does intraosseous equal intravenous? A pharmacokinetic study. Am J Emerg Med, 26, 31–38

Posted on February 25, 2019 by NUEM Blog and filed under Procedures and tagged IO intraosseous IV access IV.

Diagnose on Sight: Rhabdomyolysis

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Written by: David Kaltman, MD (NUEM PGY-3) Edited by: Charles Caffrey, MD (NUEM Alum ‘18) Expert commentary by: Josh Waitzman, MD

Case: A 25 year-old man with no significant past medical history presents to the ED with discolored urine. He states that he does not exercise regularly, but two days ago he went to a spinning class with several co-workers. He endorses increasingly severe bilateral lower extremity soreness over the past 24 hours that has not improved with ibuprofen. Overnight, he began to note discoloration of his urine, prompting his presentation. Vital signs are unremarkable. Physical exam is notable for diffuse and equivalent tenderness to palpation of his thighs; his lower extremities are neurovascularly intact distally.

Clinical Questions: What should be the disposition of this patient: home vs. medical floor vs. ICU? Is the initial CK useful in this risk stratification?

This patient has a classic case of exercise-induced rhabdomyolysis. Rhabdomyolysis is a clinical syndrome and is variously defined; most criteria use CK > 5x upper limit of normal as a cutoff. The most common etiologies in adults are:

Trauma, often crush injury or prolonged downtime
Prolonged exertion, particularly in hot weather and in those who are not well conditioned
Toxicologic, including alcohol, sympathomimetics, PCP, carbon monoxide, statins, envenomations
Viral infection

Patients often present with myalgias, weakness, and dark urine. In severe cases, nausea and mental status changes (secondary to uremia or other metabolic catastrophe) may be present. Muscle necrosis leads to the release of intracellular contents into the systemic circulation, making hyperkalemia and hypocalcemia the most immediately life-threatening problems.

Workup should include:

Serial physical exams for compartment syndrome
ECG, given the likelihood of electrolyte derangements
Labs: Chemistry panel (including Mg and Phos), CBC, urinalysis, total creatine kinase (CK) *note: urine myoglobin is specific but not sensitive; its half-life is only 1-3 hours
If very ill-appearing, consider adding DIC panel, LDH, and hepatic chemistries

Does the total initial CK level in the ED correlate with risk of acute renal failure? Not really. The risk of renal failure depends more on concurrent conditions such as sepsis, acidosis, hypovolemia, and comorbidities. However, multiple reviews have shown that the risk is higher when the total level approaches 15,000. One 2013 retrospective review of 2,000 patients did not find any significant correlation until CK levels exceeded 40,000. On the other end, one prospective study showed that no patients with CK levels <5,000 went on to develop renal failure.

Management

Initial management should include identifying and treating the underlying cause (detoxification, removing offending agent, cooling, etc.), and then treating to prevent renal failure and other long term complications. Prompt IV fluid resuscitation can generally begin with a bolus of 1-2L. Much like DKA, do not give more than this until the patient is able to urinate. Once urination is proven, titrate fluid resuscitation to achieve about 250mL/hr of UOP (3mL/kg/hr). Urinary alkalinization with a bicarbonate drip is a controversial treatment that may have a renal protective effect; no randomized controlled trials to date have demonstrated benefit. This may be a reasonable option in severe cases if the urine is very acidic (pH<6.5) and if your hospital has an ICU experienced with a urinary alkalinization protocol. Signs of renal failure should merit nephrology consultation and consideration of dialysis.

Disposition

Consider:

Discharge with close follow up for patients who are generally healthy, have normal creatinine, downtrending CK, and can reliably consume lots of fluids at home
Medical admission for patients with AKI, co-morbidities (pre-existing or trauma, heat injury)
ICU admission for impending renal failure (unable to void, highly elevated creatinine, severe metabolic acidosis), arrhythmia, DIC, concern for early compartment syndrome

Case Conclusion

The patient is able to urinate after receiving 2L of NS. His initial CK is 45,000 but serum creatinine and potassium are within normal limits. He is admitted to the general medicine service where he receives aggressive IV fluid resuscitation. Fortunately, he does not develop acute kidney injury and is later discharged in his usual state of health with only a newfound aversion to bicycles.

Expert Commentary

The above is a really nice presentation of a mild-to-moderately severe case of rhabdomyolysis. A few additional points of emphasis:

Although we like to think about rhabdo as a disease of excess Cross Fit, the history often includes a broad variety of causes.

I think the most common rhabdomyolysis history in a patient on whom nephrology is consulted is “found down after a fall.” Patients can spend hours or days with prolonged muscle compression and resulting muscle breakdown. Individuals who have this presentation tend to be older and more frail, and often have more medical comorbidities like CKD, DM and HTN that predispose them to acute kidney injury.

In addition to the nice list of causes that Dr. Kaltman provides, I’d add a few other rarer, but can’t miss conditions, including

- seizure and electrocution injuries (which break down muscle from prolonged activation)

- compartment syndrome (from burns or vascular occlusion, including ECMO cannulation)

- eating quail (called “coturnism”). I’ve never actually seen this, but please call nephrology if you do! It makes for great cocktail party chatter.

I agree with the statements re: CK levels for diagnosis of rhabdomyolysis. There is no CK level that perfectly excludes rhabdomyolysis, but it is hard to attribute an AKI to rhabdomyolysis without a CK in the tens of thousands. CK can be added onto a mint green tube in our laboratory, which makes it an easy test to add on after you see hyperkalemia or AKI.

A very useful and rapid screening test for rhabdomyolysis is the urinalysis, which will often show large blood but few or no RBCs on microscopy. Both myoglobin and hemoglobin contain heme, which is recognized by the urine dipstick as “blood”; however free myoglobin (from rhabdomyolysis) or free hemoglobin (from hemolysis) do not appear in the urine as RBCs. The test can be done in under 30 minutes and allow for rapid diagnosis and initiation of therapy. Urine myoglobin can also be checked, but has a longer turnaround time.

Prompt treatment of the patient with aggressive (1-2L per hour to start) IV crystalloid resuscitation is critical to the management of rhabdomyolysis. I can’t overstate enough how important volume is. If a patient is failing medical management, it is often from under-resuscitation. I don’t necessarily buy into the “proving they can make urine” before giving more volume—keep giving volume and trial high dose diuresis or dialysis if the patient is showing clinical signs of volume overload.

In terms of which fluid to use, classically the recommendation has been for saline because balanced crystalloids contain potassium. However, the amount of potassium in LR is quite low, and LR has never been shown to cause hyperkalemia in patients.

If patients are acidemic and have a normal/high calcium, isotonic bicarbonate is probably the crystalloid of choice. However, if the patient is hypocalcemic prior to receiving bicarbonate, treating their acidosis with bicarbonate can in further calcium binding to albumin, lower serum ionized calcium and symptomatic hypocalcemia.

TL;DR

Don’t forget about rhabdomyolysis in older people who are found down.
In true rhabdomyolysis CK should be 10,000+ to explain a severe kidney injury.
The UA is a fast test that can suggest rhabdomyolysis with large blood and few RBCs.
Be aggressive with early isotonic fluid resuscitation. We can always take fluid off later with dialysis if we need to.
LR or NS are reasonable fluid choices. Isotonic bicarbonate is great as long as the patient is both acidemic and does not have a low calcium.
Call nephrology if you are worried about your patient or if they say that they ate quail.

Josh Waitzman, MD

Nephrology Fellow

Northwestern Medicine

How to Cite This Post

[Peer-Reviewed, Web Publication] Kaltman D, Caffrey C (2019, February 18). Diagnose on Sight: Rhabdomyolysis [NUEM Blog. Expert Commentary by Waitzman J]. Retrieved from http://www.nuemblog.com/blog/rhabdomyolysis

References

Bosch, X., et al. (2009). "Rhabdomyolysis and acute kidney injury." N Engl J Med 361(1): 62-72.
Brown, C. V., et al. (2004). "Preventing renal failure in patients with rhabdomyolysis: do bicarbonate and mannitol make a difference?" J Trauma 56(6): 1191-1196.
Chatzizisis, Y. S., et al. (2008). "The syndrome of rhabdomyolysis: complications and treatment." Eur J Intern Med 19(8): 568-574.
Chavez, L. O., et al. (2016). "Beyond muscle destruction: a systematic review of rhabdomyolysis for clinical practice." Crit Care 20(1): 135.
McMahon, G. M., et al. (2013). "A risk prediction score for kidney failure or mortality in rhabdomyolysis." JAMA Intern Med 173(19): 1821-1828.
Parekh, R. (2014). Chapter 127: Rhabdomyolysis. Rosen's Emergency Medicine. R. H. John Marx, Ron Walls, Saunders: 1667-1675.

Posted on February 18, 2019 by NUEM Blog and filed under Renal and tagged rhabdomyolysis myoglobin CK.

Post-Intubation Checklist

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Written by: Andra Farcas, MD (NUEM PGY-2) Edited by: Paul Trinquero, MD (NUEM PGY-4) Expert commentary by: Andrew Pirotte, MD

Developing a Post-Intubation Checklist

Multiple studies have shown checklists in medicine can be beneficial. They have been used to reduce rates of catheter-related blood stream infections and ventilator associated pneumonias and to improve team performance in various settings.

In the ED setting, a peri-intubation checklist for trauma patients resulted in more use of rapid sequence intubation and a trend towards improvement in post-intubation sedation rates.[1] This checklist included meds for pre-intubation (pre-treatment, induction, paralytics) and information about which intubation device was used but had only one line for post-intubation medications and did not include other post-intubation safety measures.

One of the few studies that we could find specifically focused on a post-intubation checklist was a MICU study by McConnell, et al. They looked at the proportion of patients who had an ABG drawn within 60 minutes of mechanical ventilation initiation, as well as rates of respiratory acidosis and acidemia. They found that after initiating a post-intubation checklist and timeout, the rates of ABGs increased, which led to earlier recognition of inappropriate ventilation settings.

There are a lot of pre-intubation checklists available for public use. For example, a great podcast/blogpost by Scott Weingart on the topic was developed into a checklist by Jeffrey Siegler and Christ Huntley. Their versions can be found at https://emcrit.org/emcrit/post-intubation-package/.

Our goal was to design a checklist specifically for the post-intubation setting that could potentially be implemented in our emergency department. We took ideas from aforementioned studies and existing checklists, as well as personal experience. In addition to covering a broad array of post-intubation tasks, we wanted to focus especially on post-intubation sedation and initial vent settings. In regards to these important tasks, what we do in the ED matters. Not only are the first few hours a critical period in the course of illness, but there is significant downstream momentum associated with choices made in the Emergency Department.

The SPICE trial showed a link between deep early sedation and prolonged ventilation and increased mortality.[6] Conversely, an analgesia only, no-sedation approach has been shown to reduce time on the ventilator.[7] Consequently, we advocate for an analgesia-first approach. Fentanyl is a commonly used opioid for this purpose because of its rapid onset and short half-life. An easy starting point is a 0.5 - 1mcg/kg fentanyl push, followed by a drip starting at 25mcg/hr and uptitrated by 25mcg every 15-30 minutes (concurrent with another bolus as needed to control pain).

If pain is under control and additional sedation is needed, there are many options. Propofol is commonly used and is easily titratable. Start with a bolus of 5 mcg/kg/min (for 5 min) and start the drip at 5 to 10 mcg/kg/min, increasing by 5-10mcg/kg/min intervals every 5 min as needed (usual range 5-50mcg/kg/min). In the case of hypotension precluding the use of propofol, consider ketamine. Try to avoid benzodiazepines as these have been shown to increase risk of delirium.

Similarly, the initial vent settings that we chose in the ED matter and they can affect duration of ventilation, ICU length of stay, hospital length of stay, and other patient-oriented outcomes.[2] Not all illnesses requiring intubation and mechanical ventilation are the same and consequently vent-settings are not a one size fits all selection. Try to tailor settings to the individual patient and illness and choose one of the following broad strategies[9]:

Lung Protective Strategy (ARDS, lung injury, default for most patients): goal is to minimize additional injury via volutrauma or barotrauma. Set the tidal volume at 6-8cc per kg (of ideal body weight). Soon after intubation, drop Fio2 to 30% and PEEP to 5cm then titrate according to ARDSNet strategy for goal oxygen saturation 88-95%.
Obstructive Strategy (asthma or COPD): goal is to minimize air trapping by maximizing expiration time. Hence, set a low rate (perhaps 10) which will minimize I:E ratio (perhaps 1:4). Tidal volume can be standard 8cc/kg. This strategy may require permissive hypercapnea.
Severe acidosis (DKA, severe sepsis, etc.): Goal is to mimic the pre-intubation minute ventilation. Set the respiratory rate to match pre-intubation rate (usually at least 25-30).

Below is our designed post-intubation checklist:

Expert Commentary

This column highlights the need for optimized post-intubation management. This process requires attention to detail and patient needs. Effective management not only involves delivery of adequate analgesia and sedation, but also efficient titration of the ventilator. Each of these aspects of post-intubation management can be multi-faceted and challenging. To assist with these processes and to simplify tasks, a checklist can be of great value.

Checklists can help create a stepwise clinical approach and trigger timely delivery of individual tasks. Checklists can also help prevent omission of vital steps. A task as simple as a chest X-ray to confirm endotracheal tube placement and positioning can be overlooked in an emergent situation. The checklist provided in the review provides a simple, direct pathway to assist with post-intubation management, and avoid task omission. In addition, this checklist can help emphasize strategies in the post-intubation period. For example, the use of an “analgesic first” pathway for patient comfort following intubation.

As stated in the blog post, evidence now suggests “analgesic first” pathways improve patient outcomes. The clinician should strive to enhance analgesia prior to escalating sedation. Sedation has its role in post-intubation management, but should be employed only if escalated analgesic efforts fail. “Analgesic first” pathways decrease ICU length of stay, decrease complications, and improve outcomes. In addition to managing patient comfort, the clinician must also focus on optimizing ventilation and oxygenation.

Successful ventilator management requires attention to detail and the clinical scenario. Every patient has different ventilation and oxygenation needs. In addition to frequently reevaluating the patient clinically, a common and effective strategy for optimizing a ventilated patient is use of frequent blood gas measurement. Titration of ventilation and oxygenation can be aided greatly with serial blood gas monitoring. The use of blood gas data can also guide the provider utilizing a specific ventilation strategy (eg Lung-protective strategy). Common problems in early post-intubation management include excessive oxygen delivery and hypoventilation. Both of these can be identified by blood gas sampling. Once optimal ventilation and oxygenation is achieved, the clinician can proceed with further diagnostic and stabilization pathways.

Within the airway community, much focus is placed on optimized laryngoscopy and endotracheal tube delivery, no desaturation during intubation, interesting new equipment, etc. However, managing an airway does not conclude with delivery of the endotracheal tube. All clinicians managing airways would benefit greatly from accompanying this enthusiasm for intubation with focused and detailed care (often supplemented by checklists) in the post-intubation period.

Special thanks to Dr. Jordan Kaylor and Dr. Matthew Pirotte

Andrew Pirotte, MD

Department of Emergency Medicine, University of Kansas Hospital

Clinical Assistant Professor, University of Kansas Medical Center

How To Cite This Post

[Peer-Reviewed, Web Publication] Farcas A, Trinquero P (2019, February 11). Post-Intubation Checklist [NUEM Blog. Expert Commentary by Pirotte A]. Retrieved from http://www.nuemblog.com/blog/post-intubation

References

Conroy, M.J., Weingart, G.S., Carlson, J.N. Impact of checklists on peri-intubation care in ED trauma patients. American Journal of Emergency Medicine, 2014; 32:541-544.
Fuller, B.M., Ferguson, I.T., Mohr, N.M., Drewery, A.M., Palmer, C., Wessman, B.T. et al. Lung-Protective Ventilation Initiated in the Emergency Department (LOV-ED): A Quasi-Experimental, Before-After Trial. Annals of Emergency Medicine, 2017; 70(3):406-418.
Guthrie, K., Rippey, J. Emergency Department Post-Intubation Checklist. Agency for Clinical Innovation, 2013. https://www.aci.health.nsw.gov.au/__data/assets/pdf_file/0003/273792/emergency-department-post-intubation-checklist-charles-gairdner.pdf. Accessed May 26, 2018.
McConnell, R.A., Kerlin, M.P., Schweickert, W.D., Ahmad, F., Patel, M.S., Fuchs, B.D. Using a Post-Intubation Checklist and Time Out to Expedite Mechanical Ventilation Monitoring: Observational study of a Quality Improvement Intervention. Respiratory Care, 2016; 61(7):902-912.
Nickson, C. Post-intubation care. Life In The Fast Lane, Jan 5 2013. https://lifeinthefastlane.com/ccc/post-intubation-care/. Accessed May 26, 2018.
Shehabi, Y., Bellomo, R., Reade, M., Bailey, M., Bass, F., Howe, B. et al. Early Intensive Care Sedation Predicts Long-Term Mortality in Ventilated Critically Ill Patients. American Journal of Respiratory and Critical Care Medicine, 2012; 186(8):724-731.
Strøm, T., Martinussen, T., Toft, P. A protocol of no sedation for critically ill patients receiving mechanical ventilation: a randomised trial. The Lancet, 2010; 375:475-480
Weingart, S. Podcast 84 – The Post-Intubation Package. EMCrit RACC, Oct 16 2012. https://emcrit.org/emcrit/post-intubation-package/. Accessed May 26, 2018.
Weingart, S. Managing Initial Mechanical Ventilation in the Emergency Department. Annals Of Emergency Medicine, 2016; 68(5):614-61

Posted on February 11, 2019 by NUEM Blog and filed under Pulmonary and tagged intubation post-intubation sedation analgesia checklist.

Intubation Positioning: Beyond Sniffing

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Written by: Katie Colton, MD (NUEM PGY-4) Edited by: Charles Caffrey, MD (NUEM Alum ‘18) Expert commentary by: Andrew Pirotte, MD

The patient

On a recent Thursday night in a single-attending ED, we received a call that a patient was several minutes out with respiratory distress. He had been enjoying his routine post-dinner cocaine insufflation and became dyspneic, per bystanders. We could hear yelling in the back of the ambulance and EMS reported that they were only able to get an oxygen saturation, which was about 70%.

The scene

Two minutes later, EMS rushed in with a patient who looked to be in his mid-50s who was clearly struggling to breathe; it required 6 people to transfer him to our cart. He was altered, hypoxic, approximately 500 pounds, and needing an airway in the near future. While there are many considerations for the difficult airway, what are particular positioning options that may increase the chances of success in this patient?

“Positioning is 90% of the battle”

Beyond the technical difficulties posed by the morbidly obese patient, there are physiologic differences that complicate their oxygenation and ventilation. Due to the weight of the chest and larger abdomen they will have a decreased functional residual capacity and total lung capacity. Supine position can complicate pre-oxygenation, endotracheal intubation (ETI), and cause hypotension in these patients.

Many providers are still trained almost entirely in ETI with a supine patient, but there is growing evidence that a head-up position can improve pre-oxygenation and facilitate ETI.

Some authors advocate for an aggressive ramped position, using either a pre-formed foam ramp or a stack of pillows or blankets, like in the pictures below. I would argue that unless you have a stack of pillows at the ready and a number of spare hands this technique may be difficult in the less-controlled setting.

So then what?

Newer studies – and anecdotal experience - are showing good results with upright intubation through simple manipulation of the head of the bed. One example of this is the back-up head-elevated position as seen below[2]. First, by brief placement of the patient into Trendelenburg, the patient is brought all the way to the top of the bed (1 in image), and then the back of the bed is ramped up to at least 30 degrees above the horizontal (2 in image), with the head placed into the “sniffing” position with a towel roll (3 in image).[2] In their retrospective analysis, Khandelwal et al. found a lower rate of intubation-related complications as compared to a supine cohort, 9.3% vs 22.6%.[2]

(Khandewal 2016)How to place the patient in the advised back-up, head-elevated position. — (Khandewal 2016)
How to place the patient in the advised back-up, head-elevated position.

A team from IU showed improved intubation success with head of bed elevation in both a simulated [4] and ED setting [3]. This approach allows the patient to be positioned during preoxygenation. Redundant tissue falls away from the face and chest, improving the patients ability to breathe for themselves and the ease of BVM, if needed. Khandelwal et al found lower risk of aspiration and esophageal tube placement. For every 5 degree increase in head of bed angulation above the horizontal, Turner et al found increased likelihood of first pass success with ETI.

In short, consider using the bed to your advantage in these difficult patients. It takes time to overcome habits but there is good evidence for changing up your positioning plan.

Case Conclusion

The patient’s head of the bed was ramped up to 45 degrees. Utilizing rapid sequence intubation, the resident took one look with a size 4 Macintosh acquiring a Grade II view, and was able to place an 8-0 tube. A follow-up chest x-ray showed appropriate placement and frank pulmonary edema. The patient was treated for pulmonary edema and admitted to the ICU.

Expert Commentary

As with all clinical excellence, the devil is in the details. Skillful airway management requires attention to detail, notably patient positioning. This case and review serve as a reminder that close attention to setup and positioning can help enhance successful airway management.

Positioning is critical to airway success. Particularly in the setting of higher body-mass index patients, optimized positioning is a critical step to safe and successful airway management. As suggested by the review, simply placing the patient in supine positioning is not optimal and should be avoided if possible. Improved positioning can be achieved in several ways, but often the most straight-forward is by raising the head of the bed, or stacking towels and pillows. This position is often referred to as the “sniffing” position.

The sniffing position refers to bringing the sternal notch and the ear into the same plain (see blog post image). This positioning not only improves ergonomics for the clinician, but provides enhanced laryngoscopy and endotracheal tube delivery success. In addition, sniffing positioning compliments and enhances other airway optimization strategies.

One significant benefit of the sniffing position is preventing collapse of soft tissue and occlusion of the airway. The relief of redundant tissue with the sniffing position likely improves high-quality mask ventilation, as the tissue collapse into the posterior oropharynx is less prominent. Physiological benefits of sniffing position also include decreased lung atelectasis and improved delivery of oxygen during airway preparation. Considering these points, utilization of the sniffing position (rather than supine positioning), vitally strengthens the airway management pathway.

Positioning remains crucial to optimized airway delivery. The sniffing position does not require expensive equipment or great skill; it is a straight-forward, useful, and impactful strategy to enhance airway management. As emergency airway management continues to evolve, much focus has been on enhancing laryngoscopy. In addition, there have been great strides in technology and monitoring equipment. But even with the best equipment and technology, simple strategies such as optimizing positioning can lead to high-yield results.

Special thanks to Dr. Jordan Kaylor and Dr. Matthew Pirotte

Andrew Pirotte, MD

Department of Emergency Medicine, University of Kansas Hospital

Clinical Assistant Professor, University of Kansas Medical Center

How to Cite This Post

[Peer-Reviewed, Web Publication] Colton K, Caffrey C (2019, February 4). Intubation Positioning: Beyond Sniffing [NUEM Blog. Expert Commentary by Pirotte A]. Retrieved from http://www.nuemblog.com/blog/intubation-positioning.

Flexor Tenosynovitis

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Written by: Kevin Dyer, MD (NUEM PGY-3) Edited by: Adnan Hussain (NUEM Alum ‘17) Expert commentary by: Aviram Giladi, MD

Case Presentation

A 29 year old right-handed male with no significant past medical history presents to the ED with left hand pain for the past 4 days. He reports that the pain started in the MCP joint of his left 2nd digit and was just “achy” at first, a mild 3/10. He noted associated swelling and erythema over the joint as well. Symptoms slowly became worse and he went to an urgent care facility yesterday where he was diagnosed with gout and sent home with NSAIDs and Norco. Overnight the pain became markedly worse, 8/10, and he began having subjective fevers. He denied any trauma to the area, no history of gout, no immune compromising diseases or medications, and no IV drug use. In the ED his vitals were stable and he was afebrile. He appeared uncomfortable. His left 2nd digit had fusiform swelling, pain with passive extension, tenderness to percussion along the flexor sheath, and was held in slight flexion at rest. The MCP was noted to be erythematous with the erythema extending to the palmar surface of the hand.

Background

This patient’s exam was concerning for flexor tenosynovitis (FTS), an infection of the flexor tendon and its synovial sheath that can result in deformity, tendon necrosis and adhesions leading to loss of function, or loss of limb, especially if treatment is delayed [1]. The flexor tendon sheath consists of visceral and parietal layers and functions to provide a gliding surface and nutrition to the extrinsic tendons of the digits. Once bacteria are inoculated into the space between the two layers, the synovial fluid becomes a medium for bacterial growth and the closed nature of the sheath limits the host’s immune response to fight infection [2].

Most patients with FTS will endorse a traumatic injury occurring 2-5 days prior to ED presentation [2]. Pang et al noted that 57 of their 75 patients (76%) with flexor tenosynovitis were caused by a traumatic event [4]. Of these, 81% were caused by a puncture wound. Often times, the inciting injury may have been trivial and patients may not endorse an event. Therefore, it is incredibly important to still consider the diagnosis of FTS even if a traumatic component is missing from the patient’s history.

Patients should be asked about associated symptoms such as fever, chills, anorexia, and malaise. Additionally, questions assessing the patient’s handedness, immune status, proximal extent of the pain, and other sites of pain should also be asked.

Microbiology

The most likely causative bacteria for FTS are skin flora. A review of four studies published within the past 10 years showed that out of 201 cases, 92 (46%) were caused by Staphylococcus with 20 (10%) being methicillin-resistant Staphylococcus aureus(MRSA). Streptococcus species were the cause of 30 cases (15%), gram negative bacteria were the cause of 28 cases (14%), and 18 (9%) were olymicrobial. Interestingly, 49 (24%) cases of confirmed FTS were culture negative, which has been attributed to early use of intravenous antibiotics or an aggressive immune response [4].

Diagnosis

The clinical diagnosis of FTS is based on the work of Dr. Allen B. Kanavel who described the four cardinal signs as:

Fusiform swelling.
Pain with passive extension of the digit.
Tenderness over the flexor sheath.
The digit held in slight flexion at rest.

No published study has validated the sensitivity and specificity of Kanavel’s signs, nor has there been a study validating inter-observer reliability. However, several studies have looked at the presence of the individual signs in patients diagnosed with the condition. Studies published by Pang et al and Nikkah et al had a combined 91 patients [3,6]. The most common sign was fusiform swelling and was present in 89 of 91 patients (98%). The second most common was pain on passive extension (73%), followed by tenderness over the flexor sheath (67%), and finger held in slight flexion (67%). Dailiana et al reported that only 54% of their 41 patients exhibited all four of Kanavel’s signs [5]. However, all of their patients displayed tenderness over the flexor sheath, which has been described by several authors as the most important sign when distinguishing FTS from other infections of the hand [4,5,8,9].

Image from EM in 5, used with permission from Anna Pickens, MD (10).

Work up for patients with suspected FTS should include plain films to rule out a retained foreign body and fractures [2]. Laboratory studies should include white blood count (WBC), C-reactive protein (CRP), and erythrocyte sedimentation rate (ESR). Bishop et al studied 71 patients with clinically diagnosed FTS, 69 of which were confirmed by operative findings or positive intraoperative cultures [7]. All 69 patients had elevation of at least one of the three inflammatory markers, a positive predictive value of 100%. They reported negative predictive values for WBC, ESR and CRP as 4%, 3%, and 13%, respectively. The two patients without FTS were diagnosed with calcific tendinitis, both patients had normal inflammatory markers. These results suggest that a positive inflammatory marker when FTS is suspected makes the likelihood of infection extremely high. However, normal inflammatory markers cannot reliably rule out an infection.

Treatment

The two cornerstones for treating FTS are prompt administration of IV antibiotics and emergent hand surgery consultation. Antibiotic treatment should be guided by local antibiotic susceptibilities as well as the mechanism of infection. As discussed above, Staphylococcus, including MRSA, and Streptococcus species account for 61% of FTS cases whereas an additional 23% of cases are caused by gram negatives or are polymicrobial. Therefore, broad spectrum antibiotics are required. A common approach is to use vancomycin with piperacillin/tazobactam [2]. Consultation with an infectious disease specialist or a clinical pharmacist should be considered for patients with antibiotic allergies, immunocompromise, or chronic infections.

Learning Points

FTS can cause a loss of hand function or a loss of limb if treatment is delayed.
Patients may not endorse a traumatic event and the diagnosis must still be considered despite this.
The clinical diagnosis of FTS is made using Kanavel’s Signs:
- Fusiform swelling.
- Pain with passive extension of the digit.
- Tenderness over the flexor sheath.
- The digit held in slight flexion at rest.
Staphylococcus and Streptococcus species account for 61% of infections.
The two cornerstones of treatment are:
- Broad antibiotics – Vancomycin and Zosyn is sufficient
- Emergent Hand Surgery Consultation

Expert Commentary

Thank you for putting together this nice case report. Hand infections are common, and the challenge for the emergency provider is in deciding which patients are appropriate for a surgical consult (and for the surgery team, deciding which patients need surgery). In the era of strong IV antibiotics, the timing and indications for intervention are shifting. With early intervention using strict extremity elevation (hanging from the ceiling if possible) and IV antibiotics, we are avoiding surgery for some patients. This includes some with early FTS, before all of the Kanaval ’cardinal signs’ are evident. IV antibiotics have made it so that some patients with FTS, a condition traditionally considered to require surgery, are able to avoid surgery altogether. Maintaining a high index of suspicion for these problems is important in seizing these opportunities.

When specifically thinking about FTS, the notable challenge is that most patients (around 50% or more, as highlighted in the Dailiana article review) will present with only one or two ‘cardinal’ findings. Identifying any potential inciting event – whether small puncture, cut, or even working in the garden – helps to increase your index of suspicion. As the case highlights, many patients have a red joint, hand pain, or other presenting complaints that muddy the picture. The obvious FTS patients are relatively easy to identify, but the other 50% or more can be very challenging to diagnose.

Many infection, gout, arthritis flare, “hand that’s swollen and red”, etc. patients have such pain that a good exam is difficult. But, deciding on one of the four types of hand infection surgical emergencies – abscess, septic arthritis, purulent FTS, or necrotizing fasciitis – is critical. If the patient will not tolerate passive extension of the finger, my preferred way to evaluate for FTS without being unnecessary cruel is by manually compressing the tendons in the distal 1/3 of the volar forearm. You can try this on yourself – let your arm relax and then squeeze your forearm at the junction between the middle and distal 1/3 (where flexor tendons start to become distinct from muscles) and you can make your fingers flex; relax on the forearm and they will return to resting posture. If that maneuver creates focal pain in the swollen finger, my concern for FTS goes up.

Overall, high index of suspicion is critical. Rule FTS out, not in – convince yourself the patient doesn’t have a potential surgical problem by doing whatever evaluation and early treatment you think is appropriate and following the course, rather than delaying intervention until the presentation is more obvious. And, whenever in doubt, keep the patient NPO and consult a specialist so that a treatment plan can be put together without unnecessary delay or risk.

Aviram Giladi, MD, MS

The Curtis National Hand Center, MedStar Union Memorial Hospital

How to Cite this Post

[Peer-Reviewed, Web Publication] Dyer K, Hussain A (2019, January 28). Flexor Tenosynovitis [NUEM Blog. Expert Commentary by Giladi A]. Retrieved from http://www.nuemblog.com/blog/flexor-tenosynovitis.

References

Kennedy CD, Huang JI, Hanel DP. In brief: Kanavel’s signs and pyogenic flexor tenosynovitis.ClinOrthopRelat Res 2016;474:280–4.
Hyatt MT, Bagg MR. Flexor Tenosynovitis.OrthopClin N Am 2017;48:217-27
Pang HN, Teoh LC, Yam AK, et al. Factors affecting the prognosis of pyogenic flexor tenosynovitis. J Bone Joint Surg Am 2007; 89:1742.
Draeger RW, Bynum DK Jr. Flexor tendon sheath infections of the hand. J Am AcadOrthopSurg 2012;20:373–82.
Dailiana ZH, Rigopoulos N, Varitimidis S, et al. Purulent flexor tenosynovitis: factors influencing the functional outcome. J Hand SurgEurVol 2008;33:280–5.
Nikkhah D, Rodrigues J, Osman K, Dejager L. Pyogenic flexor tenosynovitis: one year’s experience at a UK hand unit and a review of the current literature. Hand Surg 2012; 17:199.
Bishop GB, Born T, Kakar S, et al. The diagnostic accuracy of inflammatory blood markers for purulent flexor tenosynovitis. J Hand Surg Am 2013;38:2208–11.
Boles SD, Schmidt CC. Pyogenic flexor tenosynovitis.Hand Clin 1998;14:567–78.
Pollen AG. Acute infection of the tendon sheaths. Hand 1974;6:21–5.
Pickens, Anna. "Flexor Tenosynovitis." EM in 5. N.p., 20 Apr. 2014. Web. 10 May 2017.

Posted on January 28, 2019 by NUEM Blog and filed under Orthopedics and tagged flexor tenosynovitis infection hand.

Unstable Cervical Spine Fractures

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Written by: Sarah Sanders, MD (NUEM PGY-4) Edited by: Alison Marshall, MD (NUEM Alum ‘17) Expert commentary by: Steve Hodges, MD

Fractures of the cervical spine are injuries that must be approached with caution. Some are stable, some are unstable, and mismanagement can lead to life-altering sequelae. Remembering which fractures fit into which category is imperative for optimum emergency department care.

A quick review of cervical spine anatomy is a helpful starting point:

All the cervical spine anatomy images are credited to Netter, FH Atlas of Human Anatomy, Sixth Edition.

All the cervical spine anatomy diagrams are credited to Agur, AMR & Dalley, AF of Grant’s Atlas of Anatomy: Twelfth Edition.

The common mnemonic “Jefferson Bit Off A Hangman’s Thumb,” is used to remember the unstable fractures, which will be reviewed in this post.

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Ultimately, understanding the mechanism of injury is crucial in identifying and accurately managing these injuries. The below PV cards are organized by mechanism and tailored down to be an on-shift reference.

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In conclusion, cervical spine injuries required a high index of suspicion and caution by the emergency medicine physician as their variability and potential for neurological impairment is high. Hopefully this review can provide you with additional insight and ease of memory when the next Level 1 trauma rolls through the door.

Expert Commentary

Thanks for this insightful post. You've done a really nice job in laying out the most salient points. It is important to have an understanding of the anatomy and this is a great review. Knowing the factors that put people a high risk for injury is also paramount. Certain chronic disease states and anatomic variances, as you note, do put select patient populations at risk for specific injury. The mechanism of injury is something we always talk about, but when it comes to neck trauma we need to really pay attention to all available history including paramedic reports, or even cell phone video, to get the best possible picture or the mechanism of injury. I can not stress enough the importance of a detailed neurological exam including sensation(s) and reflexes. Any asymmetric finding should raise your level of suspicion for severe injury. Moving to advanced imaging is especially important if there is a complaint of a focal neurological deficit; be that transient, subjective or blatantly obvious.

Athletes or motorcyclist who have suspected cervical spine injury, who have protective shoulder pads and/or helmets pose a unique challenge. Eventually the protective devices are going to need to be removed. There are many opinions on how best to do this and whether an x-ray should be done before attempting the removal of protective gear. From personal experience; it can be difficult to remove protective gear; I recommend getting "all hands on deck" and using an methodical slow organized approach. More recent thought is that cervical spine imaging should incorporate procedures for removal of equipment before initial radiographic evaluation.[1] Once the gear is removed a c-collar should then be applied and you can proceed with imaging.

Recommendations for imaging the cervical spine for trauma has changed quit a lot over the last several years. The National Emergency X-Radiography Utilization Study (NEXUS) and the Canadian C-Spine Rule (CCR) have been validated and have allowed our practice to advance such that we can effectively practice clinical medicine. However, a word of caution on using these criteria with patients who could be impaired. Sometimes the mild dementia, delirium or subtle drug, alcohol intoxication can lead us astray when we rely solely on these criteria. The cross table lateral films and specifically flexion/extension views have fallen out of favor. Most patients without focal neurological complaint or deficit are imaged with plain CT. If your patient has a focal neurological complaint or deficit, a suspected ligamentous or disc injury an MRI should be done. Depending on the exam and risk factors I would consider either a CTA or and MRA to evaluate for vascular injury.

You asked about c-collars specifically. What is available to you will be somewhat hospital - vendor specific. I prefer the Aspen or the Miami collar, they are very similar in function overall and superior to the pre-hospital EMS ones. When a patient has to be transported to another facility; make sure that the patient has full immobilization with back board and head-side blocks with the collar and head secured to the side blocks. An immobilized patient that requires intubation can make an easy air way difficult and a difficult airway terrifying. Make sure you have all your equipment prepared, including a surgical method, before you intubate. The person holding c spine immobilization needs to knows their role.....don't let go and don't move. This is the time when a video assisted intubation should be used. Use either the intubating bronchoscope or a video laryngoscope. This article talks a bit about managing airway in cervical spine injury and is a nice reference.[2]

Closing thoughts: maintain a high level of suspicion for injury in the setting of a focal neurological deficit, immobilize early immobilize often and don't be shy about intubating before transferring.

https://doi.org/10.1067/mem.2001.116333 Annals of Emergency Medicine; Baldwin et. al., "Football protective gear and cervical spine imaging" July 2001 Volume 38, Issue 1, Pages 26–30
10.4103/2229-5151.128013 International Journal of Critical Illness and Injury Science; Austin et. al., "Airway management in cervical spine injury" Jan-Mar; 4(1): 50–56

Steven W. Hodges, MD, FACEP

Assistant Medical Director

Northwestern Lake Forest Hospital

How To Cite This Post

[Peer-Reviewed, Web Publication] Sanders S, Marshall A (2019, January 21). Unstable Cervical Spine Fractures [NUEM Blog. Expert Commentary by Hodges S]. Retrieved from http://www.nuemblog.com/blog/cervical-spine-fractures.

References

Adams, J. Lin, M. Mahadevan, SV. “Spine Trauma and Spinal Cord Injury.” Section VIII, Chapter 75. Emergency Medicine: Clinical Essentials. Second Edition. P652 - 657.
Agur, AMR; Dalley AF. Grant’s Atlas of Anatomy. Twelfth Edition. Chapter 4: Back. 2009.
Bergenheim, AT, Forssell, A. “Vertical Odontoid Fracture. Case Report.” Journal of Neurosurgery. Vol 74 (4) p665-667. 1991.
Netter, F. Atlas of Human Anatomy. Section Head & Neck. Sixth Edition. 2014.
Wheeless, CR. “Cervical Spine.” Wheeless Textbook of Orthopedics by Duke University. April 26 2016. 2 Jan 2017. http://www.wheelessonline.com/ortho/cervical_spine

Posted on January 21, 2019 by NUEM Blog and filed under Trauma and tagged cervical fracture unstable trauma Jefferson.

PJP Pneumonia

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Written by: Julian Richardson, MD, MBA (NUEM PGY-2) Edited by: Sarah Sanders, MD (PGY-4) Expert commentary by: Michael Angarone, DO

Pneumocystis pneumonia (PCP) is one of the most common AIDS-defining opportunistic infections. It is a fungal disease that affects patients with an impaired immunity. Though it is most commonly associated with HIV and AIDS, the advent of HAART has been associated with a decreasing prevalence of PCP within the HIV population.[6] While the prevalence has been decreasing in the HIV population, it has been increasing in patients receiving immunosuppressive therapy.[2]

PCP in the non-HIV patient is becoming an important diagnosis but is less recognized in its early stages. PCP is now mostly diagnosed in the non-HIV population and is associated with higher mortality rates. When comparing PCP in the non-HIV versus HIV population at a single center, over nine years the ratio of non-HIV to HIV PCP patients increased from 1.7 to 5.6 and mortality at day fourteen was 25.9% v 1.4%, respectively.[1] Part of the explanation for the high mortality is that the non-HIV population frequently presents with less symptoms and diagnosis via microscopic examination, which is quicker, more often produces a false-negative compared to real-time polymerase-chain reaction (PCR). By lack of early recognition of PCP in the non-HIV patient and delay in diagnosis, there is a lag in treatment initiation which contributes to the higher mortality rate of the non-HIV patients with PCP.[4]

The clinical features and diagnostic work-up are non-specific and it takes a high-index of clinical suspicion to ensure these patients are treated appropriately. The symptoms of PCP are generally fever, non-productive cough, and progressive dyspnea. With regards to imaging, chest x-ray can be normal in ten percent of these patients or non-specific or inconclusive in thirty percent of these cases. The classic finding on chest x-ray is bilateral reticular infiltrates. Definitive diagnosis is identification of the Pneumocystis organism, which can be done by induced sputum, BAL or lung biopsy. Tests that can identify the organism include PJ DFA or PJ PCR. Induced sputum is just as good as BAL for those with AIDS, which may not be true for other populations. Both the induced sputum culture and BAL are time-consuming and thus PCR is becoming essential to assist with rapid diagnosis.[3,5]

Treatment

Bactrim is the mainstay of treatment for both non-HIV and HIV PCP. In the non-HIV population, Bactrim has been shown to be highly effective and reduces PCP-related mortality by 83%.[7] The prophylactic dose is 80-160mg daily while the treatment dose is 15-20mg/kg/day (both dosed based on the trimethoprim component) divided every six to eight hours for twenty-one days. Adverse reactions are commonly seen in HIV patients and can range from rash, fever, leukopenia, thrombocytopenia, azotemia, hepatitis, and hyperkalemia. Given the efficacy of bactrim compared to alternative regimens, it is suggested that supportive care be initiated prior to initiating alternative regimens which are listed below.[5]

Alternative regimens (for treatment) all twenty-one days [5]

Pentamidine (4mg/kg IV daily)
Primaquine (30mg PO daily) + Clindamycin (900mg IV every six hours or 600mg PO every eight hours)
Atovaquone: 750mg PO twice a day

When should steroids be utilized?

Steroids should be given for moderate to severe disease. Moderate to severe disease is defined as PO2 <70mmHg or A-a gradient >35mmHg on room air. The steroids are dosed on a twenty-one day prednisone taper, starting at 40mg PO twice a day. PO regimens taper from 40 mg BID for 5 days to 40 mg daily for 5 days to 20 mg daily for 11 days. If the patient is unable to tolerate PO, IV methyprednisolone can be given at seventy-five percent of the prednisone dose. When considering steroids, early initiation is important and an ABG should be obtained in the emergency department.[5]

Managing Treatment Failure

Clinical failure is defined as lack of improvement or worsening respiratory function after four to eight days of PCP treatment. In patients with mild to moderate disease, this occurs in about ten percent of cases. It should be noted that in the absence of corticosteroids administration, clinical deterioration is not uncommon. ED providers must also consider co-infection with additional microbes, while the inpatient team may discuss bronchoscopy. Depending on disease severity, options for alternative therapies include atovaquone, clinidamycin, and primaquine, however these decisions should be held in conjunction with the patient’s primary physician and/or infectious disease doctor.[5]

Expert Commentary:

Pneumocystis jerovecii pneumonia (PJP) is a life threatening and severe infection that traditionally affected individuals with AIDS. As described in the blog piece the epidemiology of affected patient populations has changed over the past 20 years with effective HIV therapy. It is currently more common to see PJP in persons that have had an organ transplant, stem cell transplant, those on glucocorticoid therapy and those receiving therapies that deplete their T-lymphocytes. A major risk factor for the development of PJP is the use of glucocorticoid medications. On average the median dose of steroids associated with the development of PJP is 30mg/day.[1] At Northwestern Medicine we recently published on our experience with PJP in the Solid Organ Transplant recipient population. We found 15 cases of PJP over a 15 year period. Among these 15 patients, six required intensive care unit management and three (20%) died from there infection. Low absolute lymphocyte count, especially <500 cells/mm3, had the strongest association with development of PJP.[2] This data demonstrates that the key immune cells that help defend against the development of PJP are the lymphocyte and in particular the CD4+ T-lymphocyte. The presentation of PJP in non-HIV infected individuals is similar to that in HIV-infected with fever, dry cough and progressive dyspnea, but many non-HIV infected individuals may present with fulminant respiratory failure. Fortunately trimethoprim-sulfamethoxazole remains the treatment of choice for this infection, with adjunctive steroids used for those with severe respiratory compromise. For the emergency room provider PJP should be on the list of potential causes of pneumonia or respiratory compromise not just in HIV-infected persons, but in those with compromised immune systems. Like all infections early recognition and early treatment result in better patient outcomes.

Yale SH, Limper AH. Pneumocystis carinii pneumonia in patients without acquired immunodeficiency syndrome: associated illness and prior corticosteroid therapy. Mayo Clin Proc. 1996;71(1):5.
Werbel WA, Ison MG, Angarone MP, Yang A, Stosor V. Lymphopenia is associated with late onset Pneumocystis jirovecii pneumonia in solid organ transplantation. Transpl Infect Dis. 2018 Mar 7:e12876

Michael Angarone, DO

Assistant Professor of Medicine, Infectious Diseases

Northwestern Medicine

How To Cite This Post

[Peer-Reviewed, Web Publication] Richardson J, Sanders S (2019, January 14). PJP Pneumonia [NUEM Blog. Expert Commentary by Angarone M]. Retrieved from http://www.nuemblog.com/blog/PJP

Resources

Bienvenu, Anne-Lise, et al. “Pneumocystis Pneumonia Suspected Cases in 604 Non-HIV and HIV Patients.” International Journal of Infectious Diseases, vol. 46, 2016, pp. 11–17., doi:10.1016/j.ijid.2016.03.018.
“DPDx - Pneumocystis.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 30 Dec. 2017, www.cdc.gov/dpdx/pneumocystis/index.html.
“Fungal Diseases.” Centers for Disease Control and Prevention, Centers for Disease Control and Prevention, 26 Apr. 2017, www.cdc.gov/fungal/diseases/pneumocystis-pneumonia/index.html.
Liu, Yao, et al. “Risk Factors for Mortality from Pneumocystis Carinii Pneumonia (PCP) in Non-HIV Patients: a Meta-Analysis.” Oncotarget, Vol. 8, No. 35, Apr. 2017, doi:10.18632/oncotarget.19927.
“PCP Adult and Adolescent Opportunistic Infection.” National Institutes of Health, U.S. Department of Health and Human Services, 25 July 2017, aidsinfo.nih.gov/guidelines/html/4/adult-and-adolescent-opportunistic-infection/321/pcp.
Rosen, Peter, et al. “HIV Infection and AIDS.” Rosen's Emergency Medicine: Concepts and Clinical Practice, Elsevier, 2018.
Stern, Anat, et al. “Prophylaxis for Pneumocystis Pneumonia (PCP) in Non-HIV Immunocompromised Patients.” Cochrane Database of Systematic Reviews, Jan. 2014, doi:10.1002/14651858.cd005590.pub3.

Posted on January 14, 2019 by NUEM Blog and filed under Pulmonary and tagged PCP pneumonia HIV.

REBOA

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Written by: Andew Cunningham, MD (NUEM PGY-4) Edited by: Bill Burns, MD (NUEM Alum ‘17) Expert commentary by: Zaffer Qasim, MBBS, FRCEM, FRCPC(EM), EDIC

REBOA: Ready for Prime Time?

For years, the resuscitative thoracotomy has been the sole weapon in the physician’s arsenal against a loss of a perfusing pressure in the crashing trauma patient. With the advent of new endovascular technologies, novel methods to control hemorrhage are being refined, among them Resuscitative Endovascular Balloon Occlusion of the Aorta or REBOA. With this newer method getting a lot of attention in the emergency and trauma communities, it’s time to take a look at what it is, how successful it is, and where we are going with it.

What Is It?

Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a possible alternative to resuscitative thoracotomy in cases of non-compressible torso hemorrhage (NCTH) that present to the Emergency Department in extremis.1
REBOA works via the insertion of a catheter through the femoral artery to allow an endovascular balloon to be deployed within the aorta, allowing for bleeding control and augmentation of afterload in hemorrhagic shock.2
REBOA can be deployed in Zone III of the Aorta, as depicted in the image below, for pelvic hemorrhage, or in Zone I of the Aorta for abdominal hemorrhage.3

The primary indications for REBOA include:
- PEA arrest secondary to abdominal or pelvic hemorrhage within 10 minutes of the onset of arrest
- Severe hypovolemic shock secondary to abdominal or pelvic hemorrhage
- Unstable hemodynamics refractory to volume resuscitation in patients with abdominal or pelvic hemorrhage2
The major contraindications include age older than 70, significant comorbidities, prolonged PEA arrest (lasting longer than 10 minutes), or high suspicion for proximal aortic injury (REBOA may exacerbate bleeding from thoracic sources).2

Does It Work?

A study at U of Arizona showed that 45% of patients who received thoracotomy may have benefited from REBOA based on autopsy results, but only 32% of the patients receiving a thoracotomy did not have a contraindication for it, and of those who did not have a contraindication, only roughly half would have potentially benefited. Compared to prior literature, this may suggest that REBOA is not as useful in patients in extremis.1
Although the literature does suggest that REBOA reduces the amount of overall hemorrhage, there is still no definitive evidence in humans of a decrease in mortality.4
There are still risks of complications in humans, including arterial injury and limb ischemia.3 In animal models, REBOA has also resulted in renal failure, liver failure, intestinal ischemia, and multiple other injuries which result from occlusion of the aorta.5

Given that REBOA still obstructs distal flow, just like cross-clamping the aorta in a resuscitative thoracotomy, it is still reserved as a last resort maneuver. The effects of aortic occlusion can be reviewed below6:

Where Is It Going?

An alternative to REBOA may be Selective Aortic Arch Perfusion (SAAP); in this similar yet separate endovascular approach, a catheter that has two ports is utilized instead of the single-port REBOA catheter. This allows for both occlusion of the aorta and selective administration of blood, pressors, or other medications directly to the heart and brain. Where REBOA may be useful for exclusively shock, SAAP may have advantages in cardiac arrest secondary to trauma.7
A new, smaller REBOA catheter, the 7 French ER-REBOA, may cause fewer injuries and also allows for simultaneous blood pressure monitoring.8
Partial REBOA, or P-REBOA, allows for controlled blood flow to the body distal to the area of occlusion, in efforts to limit ischemia.5

Is It Feasible for ER Docs to Perform?

Yes! Some of the larger studies performed in Japan required placement by either a surgical or emergency medicine-trained attending.9
In England, there are case of REBOA being deployed in the pre-hospital setting to act as a bridging method for resuscitation during transport.7 As the relay between the hospital and Emergency Medical Services, it is an EM physician’s responsibility to be aware of this method and its utility in her area.

Take-Home Points

REBOA is a newer up-and-coming method of controlling hemorrhage secondary to abdominopelvic trauma that may act as an alternative to resuscitative thoracotomy.
Although more data still needs to be collected, REBOA has not yet shown to clearly improve mortality, and does come with certain risks and complications.
There are more novel methods of REBOA undergoing research and development, including SAAP, ER-REBOA, and P-REBOA, which may strengthen the utility of REBOA and reduce some of the complication risks.
REBOA is within an EM physician’s scope of practice, and may play a role in EMS in the future. As such, it is our duty to be aware of it and follow along with its developments.

Expert Commentary

Thanks for a great post on an evolving temporary hemorrhage control concept. Hemorrhage, and torso hemorrhage in particular, remains the largest cause of death in trauma in the first 24 hours. In the right patient, REBOA can be another effective procedure in the emergency physician’s toolbox. Some additional points to consider:

1. Access is key! The rate limiting step is early common femoral artery (CFA) access. It’s important to emphasize accessing the common as placing the sheath in one of the smaller branch vessels could increase the risk of iatrogenic injury. I advocate using ultrasound to define the anatomy and routinely placing a CFA arterial line in your “big sick” patients to maintain skills. As you state, this step is well within the wheelhouse of the Emergency Physician, and the foundation to build on to train in placing REBOA

2. Patient selection is critical! The available data generally has the inclusion/exclusion criteria listed, but definitions on who is “unstable” vary. In my opinion, an arbitrary blood pressure cutoff of <90mmHg in someone with torso hemorrhage should not automatically trigger REBOA. I think these patients should get a CFA line, and then proceed to REBOA only if not responding to initial resuscitative measures or rapidly deteriorating to imminent arrest.

3. Placement before arrest will likely lead to better outcomes. The evolving data shows that the group that benefits most in terms of mortality are the nonresponders who will imminently arrest unless they have a lifesaving procedure. In the arrested patient, as mentioned, determining the time of arrest is crucial. This can certainly be challenging with prehospital arrest.

4. While the data does not show improved mortality compared to thoracotomy, there does seem to be a trend to improved neurologically intact survival – this is our ultimate goal and speaks to the ability to use REBOA proactively, before traumatic arrest happens

5. It is absolutely critical that REBOA is used in a system that can rapidly deliver these patients to definitive care (OR/IR). The consequences of prolonged balloon occlusion as listed are dire. Based on collective clinical experience and translational animal data, I would not recommend occluding beyond 45 minutes to 1 hour in Zone 1.

6. REBOA in the US is currently used only at level 1 and 2 trauma centers. I think (as the British have shown), the biggest benefit is likely at smaller centers and ultimately prehospital. Success here will be based on procedural considerations (like p-REBOA to prolong safe inflation times), appropriate training, and systems issues (expedited transfer to definitive care).

Zaffer A. Qasim, MBBS, FRCEM, FRCPC(EM), EDIC

Assistant Professor of Clinical Emergency Medicine

UPenn Medicine

How to Cite This Post

[Peer-Reviewed, Web Publication] Cunningham A, Burns W (2019, January 7). REBOA [NUEM Blog. Expert Commentary by Qasim Z]. Retrieved from http://www.nuemblog.com/blog/REBOA

References

Joseph B, Ibraheem K, Haider AA, et al. Identifying potential utility of resuscitative endovascular balloon occlusion of the aorta: An autopsy study. J Trauma Acute Care Surg. 2016;81:S128-S132.
Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA). Vol 2016. LIFTL.
Napolitano LM. Resuscitative Endovascular Balloon Occlusion of the Aorta: Indications, Outcomes, and Training. Crit Care Clin. 2017;33:55-70.
Morrison JJ, Galgon RE, Jansen JO, Cannon JW, Rasmussen TE, Eliason JL. A systematic review of the use of resuscitative endovascular balloon occlusion of the aorta in the management of hemorrhagic shock. J Trauma Acute Care Surg. 2016;80:324-334.
Perkins ZB, Lendrum RA, Brohi K. Resuscitative endovascular balloon occlusion of the aorta: promise, practice, and progress? Curr Opin Crit Care. 2016;22:563-571.
Russo RM, Neff LP, Johnson MA, Williams TK. Emerging Endovascular Therapies for Non-Compressible Torso Hemorrhage. Shock. 2016;46:12-19.
Bebarta V. REBOA - Ready for Prime Time? ACEP EM Education.
Weingart S. Podcast 170 - the ER REBOA Catheter with Joe DuBose. Vol 2016. EMCrit Blog.:Available at [http://emcrit.org/podcasts/er-reboa].
Saito N, Matsumoto H, Yagi T, et al. Evaluation of the safety and feasibility of resuscitative endovascular balloon occlusion of the aorta. J Trauma Acute Care Surg. 2015;78:897-903; discussion 904.

Posted on January 7, 2019 by NUEM Blog and filed under Trauma and tagged REBOA trauma thoracotomy.

Herpes Zoster

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Written by: Kevin Dyer, MD (NUEM PGY-3) Edited by: Simiao Li-Sauerwine, MD (NUEM Alum ‘18) Expert commentary by: David Zull, MD

The Patient

A 76-year-old man with a history of metastatic colon cancer (on Bevacizumab), HTN, and DM2 presents with a skin rash on his back wrapping around to his groin. He went on to say that 4 days ago he began having a dull, aching pain in this region and about 18 hours ago this rash appeared. He denied having a rash in any other location, and also denied oral sores, vision changes, confusion, neck pain, fevers, cough, or shortness of breath. His last infusion of bevacizumab was 9 days prior to ED presentation and he did not receive the shingles vaccine.

Upon examination he had a unilateral erythematous vesicular rash in the distribution of his T12 and L1 dermatomes that was classic for Herpes Zoster (HZ) along with erythema at the base that was concerning for an underlying cellulitis. His labs were remarkable for a white count of 2,200 and an absolute neutrophil count of 1,200.

Given his immunocompromised status, he was given Acyclovir 750mg (10mg/kg) IV and Ancef 2g IV in the ED and admitted for continued IV anti-viral therapy.

Discussion

To me, this case was much more interesting than the average case of HZ given the patient’s immunocompromised status and it served as an important reminder that there are several pitfalls and complications surrounding HZ that the ED physician must be aware of and constantly on the lookout for.

Post-Herpetic Neuralgia (PHN)

PHN is defined as pain that persists more than 30 days after the onset of rash. Both the incidence (8-70%) and duration are directly correlated with the patient’s age.[1-3] Symptoms of PHN include pain, numbness, dysesthesias, and allodynia. While PHN is not applicable to the patient with an acute attack of HZ, it is included here because it is the most common complication of HZ and should be included in the counseling given to patients who are discharged from the ED.

Herpes Zoster Ophthalmicus

Herpes Zoster Ophthalmicus (HZO) is an ocular and peri-ocular disease that is the result of virus reactivation in the trigeminal ganglion.

Patients with HZO may present with a vesicular eruption along the trigeminal dermatome, conjunctivitis, episcleritis, and lid droop. Clinicians should also pay particular attention the nose and be on the lookout for vesicular lesions at the base, side, or tip of the nose. Commonly known as Hutchison’s sign, lesions on the nose indicate involvement of the nasociliary branch and are strong predictors of ocular involvement, which occurs in 50-72% of HZO cases.[4,5]

Corneal involvement can lead to significant vision loss and should be evaluated for via fluoroscein staining in all patients with suspected HZO. Keratitis may present as punctate or dendriform lesions that are easily mistaken for Herpes Simplex Keratitis.[5]

Herpes Zoster Oticus

Often referred to as Ramsay Hunt Syndrome (RHS), Herpes Zoster Oticus manifests as a triad of ipsilateral facial paralysis, ear pain, and vesicles in both the auditory canal and auricle. RHS is considered a polyneuropathy affecting cranial nerves V, VII, VIII, IX, and X.7 Involvement of these nerves leads to tinnitus, hearing loss, hyperacusis, dysgeusia, and vertigo. It is worth noting that when compared to those with Bell’s Palsy, patient’s with RHS were found to have more severe palsy and a less favorable recovery.[8]

Panel A displaying a crusted lesion in the ear of a patient with RHS. Panel B highlights the CN VII palsy that can be seen in RHS.[9]

Disseminated Zoster

Disseminated cutaneous HZ is a complication that is often accompanied by visceral organ involvement.[10] Though it is more common in immunocompromised hosts, it can also be seen in immunocompetent patients, as well. As the name implies, patients with disseminated zoster will have midline-crossing vesicular skin lesions in multiple dermatomes. Visceral involvement can be life threatening and may present as fulminant pneumonia, hepatitis, or encephalitis.11

Skin Infection

Patients with HZ lesions are at an increased risk for skin superinfection regardless of immune status. The most likely causative agents are Staphylococcus and Streptococcus species. When encountering a patient with HZ, the clinician should be sure to look for signs of bacterial infection and treat with antibiotics in addition to antivirals.

Treatment

In immunocompetent patients, antiviral therapy should be started within 72 hours of rash occurrence or if new lesions continue to occur as this is a sign of ongoing virus replication.[13] For immunocompromised patients, antiviral therapy should be started regardless of when the lesions appeared.

The three antivirals currently recommended for use are acyclovir, valacyclovir, and famciclovir, with dosing regimens as follows:

Acyclovir – 800mg, 5 times per day for 7 days

Valacyclovir – 1000mg, 3 times per day for 7 days

Famciclovir – 500mg 3 times per day for 7 days

A meta-analysis of placebo-controlled trials have shown that patients who received acyclovir within 72 hours of rash onset are more likely to have resolution of neuritis and PHN.[14] A commonly used alternative option is valacyclovir which, when compared to acyclovir, has equal efficacy in the resolution of cutaneous lesions, and the added benefit of accelerated resolution of neuritis.[15] The TID dosing is also thought by many clinicians to lead to better patient compliance. The caveat to this, however, is valacyclovir is much more expensive than acyclovir and can be cost prohibitive depending on the patient’s insurance status.

Patients should be treated with intravenous acyclovir 10 mg/kg if they are immunocompromised, have disseminated zoster, are found to have sight threatening disease on exam, or if they have symptomatic meningitis, encephalitis, or myelitis.[12]

Disposition

The overwhelming majority of patients with HZ can be treated as outpatients with an oral agent as discussed above. Admission is indicated for patients who meet the criteria for IV acyclovir as outlined in the previous section.

Take Home Points

When caring for a patient with herpes zoster, be on the lookout for herpes zoster ophthalmicus, herpes zoster oticus, signs of disseminated zoster, and underlying cellulitis.

Initiate antivirals if the onset of rash is within 72 hours of presentation or if the patient is immunocompromised.

Oral antivirals are acceptable for the majority of patients with herpes zoster, but those who are immunocompromised, have disseminated zoster, sight threatening involvement, or signs of CNS involvement should be treated with IV acyclovir.

Expert Commentary

It is estimated that up to one third of the population will develop Herpes Zoster virus infection (shingles) sometime during our lifetime, such that it is a very common ED presentation. Emergency physicians should be keenly aware of the complications of HZV and be able to recognize it early. Antiviral treatment within the first 72 hours of the skin eruption can limit progression of lesions, halt development of new lesions, minimize infectious risk to household contacts, decrease the risk of complications of HZV infection, and in particular ameliorate the severity of post herpetic neuralgia.

Ramsay Hunt syndrome is typically limited to a triad of Bell’s palsy (7th Nerve palsy), ear pain and vesicles in the auditory canal and external ear. The skin lesions are often subtle and frequently limited to just a few papules such that the syndrome is often missed. Other cranial nerves (5,8,9,10) can also be involved in Ramsay Hunt syndrome, most notably 8th nerve involvement with tinnitus, hearing loss or hyperacusis, and vertigo.

Herpes Zoster ophthalmicus is usually limited to punctate keratitis and is not vision threatening. Dendritic lesions can occur in HZV but they are referred to as pseudodendrites because they are composed of heaped up epithelial cells with no epithelial defects. These pseudodendrites do not take up fluorescein since the epithelium remains intact but fluorescein often collects at the edges thereby outlining the dendrites. In contrast, the dendrites of HSV are comprised of denuded epithelium which do take up fluorescein. The HSV dendrite can lead to corneal erosion, scarring, and even perforation. HZV can also affect the corneal stroma and not the corneal epithelium leading to white rounded opacities with no overlying fluorescein uptake. Pink eye can result from conjunctivitis or iritis but is often overlooked. The most feared ocular complication of V-1 Zoster is acute retinal necrosis which leads to rapidly progressive vision loss often complicated further by retinal detachment.

Disseminated herpes zoster is defined as the presence of more than 20 lesions outside the involved dermatome. This unusual presentation is more common in immunosuppressed patients. Lesions in an ipsilateral adjacent dermatome are usually not of concern. Disseminated zoster can resemble acute varicella or smallpox, as well as acute vesiculating drug eruptions like erythema multiforme and toxic epidermal necrolysis. Disseminated HZV is distinguished by the onset primarily in one dermatome before dissemination of lesions. Systemic organ involvement can occur with dissemination of HZV including pneumonia, hepatitis, aseptic meningitis, encephalitis, motor neuropathy, myelitis, GBS, and CNS vasculitis with stroke.

Post herpetic neuralgia, a common complication of HZV infection, is best prevented by prompt antiviral therapy in the acute phase. Although steroids may have some benefit in ameliorating the severity of pain in the acute setting, they have not been shown to decrease the development of PHN. Pain management of PHD frequently requires use of TCA’s, gabapentin or pregabalin.

A common complication of HZV dermatomal lesions is secondary bacterial infections with staph aureus, usually with an impetiginous superficial purulent discharge with or without local cellulitis. Staph septicemia and toxic shock syndrome is a rare complication in dermatomal zoster but is well described in primary varicella infections in neonates and immunocompromised children.

The emergency physician should have a low threshold for initiating antiviral therapy acute shingle, typically Valcyclovir 1gm TID or Acyclovir 800mg five times per day, for 7 days in immunocompetent hosts with uncomplicated disease, or 14 days in compromised hosts and those experiencing complications of HZV.

David N. Zull, MD, FACEP, FACP

Professor of Emergency Medicine & Internal Medicine

Northwestern University

How to Cite This Post

[Peer-Reviewed, Web Publication] Dyer K, Li-Sauerwine S (2018, December 17). Herpes Zoster [NUEM Blog. Expert Commentary by Zull D]. Retrieved from http://www.nuemblog.com/blog/herpes-zoster

Resources

Choo PW, Galil K, Donahue JG, Walker AM, Spiegelman D, Platt R. Risk factors for postherpetic neuralgia. Archives of internal medicine 1997;157:1217-24.
Gnann JW, Jr., Whitley RJ. Clinical practice. Herpes zoster. The New England journal of medicine 2002;347:340-6.
Ragozzino MW, Melton LJ, 3rd, Kurland LT, Chu CP, Perry HO. Population-based study of herpes zoster and its sequelae. Medicine 1982;61:310-6.
Zaal MJ, Volker-Dieben HJ, D'Amaro J. Prognostic value of Hutchinson's sign in acute herpes zoster ophthalmicus. Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie 2003;241:187-91.
Pavan-Langston D. Herpes zoster ophthalmicus. Neurology 1995;45:S50-1.
Shaikh S, Ta CN. Evaluation and management of herpes zoster ophthalmicus. American family physician 2002;66:1723-30.
Adour KK. Otological complications of herpes zoster. Annals of neurology 1994;35 Suppl:S62-4.
Robillard RB, Hilsinger RL, Jr., Adour KK. Ramsay Hunt facial paralysis: clinical analyses of 185 patients. Otolaryngology--head and neck surgery : official journal of American Academy of Otolaryngology-Head and Neck Surgery 1986;95:292-7.
Espay AJ, Bull RJ. Petrositis in Ramsay Hunt Syndrome with multiple cranial neuropathies. Arch Neurol 2005;62(11):1774-5.
Locksley RM, Flournoy N, Sullivan KM, Meyers JD. Infection with varicella-zoster virus after marrow transplantation. The Journal of infectious diseases 1985;152:1172-81.
Jantsch J, Schmidt B, Bardutzky J, Bogdan C, Eckardt KU, Raff U. Lethal varicella-zoster virus reactivation without skin lesions following renal transplantation. Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association 2011;26:365-8.
Dworkin RH, Johnson RW, Breuer J, et al. Recommendations for the management of herpes zoster. Clinical infectious diseases : an official publication of the Infectious Diseases Society of America 2007;44 Suppl 1:S1-26.
Cohen JI, Brunell PA, Straus SE, Krause PR. Recent advances in varicella-zoster virus infection. Annals of internal medicine 1999;130:922-32.
Jackson JL, Gibbons R, Meyer G, Inouye L. The effect of treating herpes zoster with oral acyclovir in preventing postherpetic neuralgia. A meta-analysis. Archives of internal medicine 1997;157:909-12.
Beutner KR, Friedman DJ, Forszpaniak C, Andersen PL, Wood MJ. Valaciclovir compared with acyclovir for improved therapy for herpes zoster in immunocompetent adults. Antimicrobial agents and chemotherapy 1995;39:1546-53.

Posted on December 17, 2018 by NUEM Blog and filed under Dermatology and tagged zoster shingles.

Topical Hemostatics

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Written by: Alex Ireland, MD (NUEM PGY-3) Edited by: Andrew Moore, MD (NUEM Alum ‘18) Expert commentary by: Joseph Posluszny, MD

Expert Commentary

The above summary of the mechanism of actions, indications for and limitations of topical hemostatic agents is comprehensive and thorough.

As with most summaries of hemostatic agents, we focus on the mechanism of action or aspect of coagulation by which the agent works. Clinically, it may be easier to take a different approach.

Sometimes, the most difficult aspect of applying a topical hemostatic agent is determining the appropriate agent given the clinical scenario- all work in some fashion, but which will work best?

To help approach this, an initial question to help frame what to do in the trauma bay or ED would be: does this wound require just a hemostatic agent as a covering/dressing to promote hemostasis or are both assisted hemostasis and pressure needed to control the bleeding? For superficial, low volume, but persistently bleeding wounds, topical agents like Dermabond, thrombin (with gelfoam) and Surgicel are ideal. For deep, complex wounds that require hemostatic agents and pressure, QuikClot Gauze, Ativene and Combat Guaze are more effective.

Hospitals and EMS systems purchase a variety of topical hemostatic agents. It is imperative to become familiar with these agents and be prepared for their indications before you are presented with bleeding uncontrolled by conventional dressings or pressure.

Joseph Posluszny, MD

Assistant Professor of Surgery

Trauma and Critical Care, McGaw Medical Center of Northwestern University

How to Cite this Post

[Peer-Reviewed, Web Publication] Ireland A, Moore A (2018, December 10). Topical Hemostatics [NUEM Blog. Expert Commentary by Posluszny J]. Retrieved from http://www.nuemblog.com/blog/topical-hemostatics

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Posted on December 10, 2018 by NUEM Blog and filed under Trauma and tagged topical hemostatics trauma dermabond topical thrombin combat gauze hemcon quikclot.

Implicit Bias

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Written by: Vidya Eswaran, MD (NUEM PGY-3) Edited by: Meghan Quigley, MD (NUEM Alum ‘17) Expert commentary by: Bernard L. Lopez, MD, MS, CPE, FACEP, FAAEM

First, do no harm, it’s an oath we take when we are given the title of physician. On the surface it sounds easy enough - nobody practices medicine intending to harm patients. Yet as we all know, mistakes are easy to make, especially in the emergency department. We work in a fast-paced, high acuity environment with limited information and time to make decisions. We depend on pattern recognition, heuristics and, often, generalizations to aid in our decision-making. Accordingly, we open ourselves to inadvertent errors, especially if our decision aids are based on stereotyping. Implicit biases are defined as unconscious beliefs that affect our understanding, actions and decisions. These biases can be both favorable and unfavorable, and are activated involuntarily - without the individual’s knowledge.[1] Implicit biases are ubiquitous - we all have them. Our biases are learned at a young age and are based on our cultural backgrounds and upbringing.[2] Biases do not make us racist, sexist, ageist, or any other -ist, however it is imperative that we understand that these biases exist and that they can affect our patient care.

Studies show that race contributes to differences in ESI scoring for triaging patients in ED waiting rooms,[3] to analgesic administration, and even to the therapeutic options offered to patients with coronary artery disease.[4] These disparities are presumably multifactorial, but implicit biases likely have a role to play. When using the Implicit Association Test, the current gold standard in implicit bias assessment, physicians routinely express an implicit pro-white/anti-black bias.[2] Just because we have these biases, however, does not mean we have to act upon them. In one study, Johnson et al. found that emergency physicians expressed more pro-white/anti-black bias when their EDs were overcrowded and they were personally caring for over 10 patients.[5] Such stressful environments may cause us to fall back onto our implicit biases. So what can we do to prevent biases from affecting our clinical care? Here are ten easy strategies that physicians and hospitals can implement to create a safer environment for our minority patients:

1. Take an Implicit Association Test online (and take them often!). Our biases are not immutable, and data over time is more valuable than a single result. With the results of your IAT in hand, take a minute at the end of your shift to evaluate your patient interactions. Do you think your biases affected your patient care? What could you do in the future to prevent this from happening? Simple awareness that biases exist can make a significant impact.

2. We utilize our stereotypes when we do not know our patients. Healthcare disparities have been shown to decrease when providers take a minute to learn a personal, not necessarily medically relevant, fact about their patients.[6] Where are they from? Do they have kids? What do they do for work? When we think about patients as individuals we are much less likely to generalize or stereotype.

3. Do you live in the same community as your patients? If not, get to know where your patients come from. Ask a community organizer to arrange for a tour of neighborhoods where your patients live or invite patients to speak at your hospital about their experiences both inside and out of the healthcare system.

4. Recognize situations when you are susceptible to unconscious biases, and take steps to prevent those situations from arising. This may require buy-in from hospital administrators to help ease the cognitive burden or additional tasks (reading triage EKGs, accepting interhospital transfers, etc) during busy shifts. This will likely help boost physician wellness as well!

5. In some cases it is impossible to ease cognitive load from an administrative standpoint. It’s up to us then to develop coping strategies during these times. Being well fed and hydrated are important first steps. Make sure to go to the bathroom. Take two minutes out of your shift for breathing or meditation exercises. These steps can go a long way to improve your physical and mental wellbeing and prevent mistakes.

6. Promote racial diversity at all levels of your hospital/departmental organization. Increased exposure to people of diverse backgrounds has been shown to decrease prejudices and racial anxiety.

7. Encourage administrators to consider surveying patients on their ED experience and how biases may have impacted their patient-physician interaction.

8. Support projects that encourage positive images of persons of color, LGBT and women. Distribute stories and pictures widely that portray stereotype-busting images. Biases can be mitigated just by seeing these positive images on a regular basis.

9. Encourage and participate in research regarding biases and health disparities and test interventions to combat them. Without data, we are nothing.

10. Consider professional training sessions on implicit bias and diversity and inclusion for your physician group. Encourage discussion - you’ll learn that you are not the only one with biases and can learn how your colleagues deal with similar struggles.

Expert Commentary

This is a great post on the topic of unconscious bias and how it affects us as physicians (and as human beings). Unconscious biases are simply part of how we are wired as human beings. We have them and cannot help but have them. They affect almost every human interaction and are especially important in healthcare as poor interpersonal communications may lead to mistreatment and misdiagnosis. However, while we cannot help but have them, we can work with them.

Stereotypes, while often thought of in a negative way, are simply patterns of the mind developed by our conscious and unconscious experiences and are examples of our unconscious biases. These unconscious patterns help us to function in a speedy and efficient manner. Pattern recognition can help but can also have negative consequences. We use and rely on our pattern recognition (stereotypes) to move quickly in times of stress (such as a busy ED). This makes us more "efficient" in completing tasks. However, we may erroneously complete these tasks if we have biases that take us down the wrong pathways.

Awareness that these unconscious cognitive biases exist and can have both positive and negative consequences in our dealings with people is the key take-home from this post. Recognizing that they come into play the busier and more stressful things get might help us to slow down a little to make better decisions. The suggestion in the ten-item list of getting to know the members of the community, encouraging positive images of those with whom you may be unfamiliar, participating in research and promoting racial diversity all help to change our unconscious biases and potentially lessen its negative effects.

If you take the IAT, recognize that it is not a measure of racism, sexism, or any other -ism - it is a measure of association only. If you can reduce the cognitive load (much easier said than done in a busy ED), take whatever steps one can (this typically requires systems changes) to lessen the urgency to make too quick of a decision based on unconscious biases.

Working with your unconscious bias is possible. It is necessary for providing the best care possible to our patients.

Bernard L. Lopez, MD, MS, CPE, FACEP, FAAEM

Associate Provost for Diversity and Inclusion, Thomas Jefferson University

How to Cite This Post

[Peer-Reviewed, Web Publication] Eswaran V, Quigley M (2018, December 3). Implicit Bias [NUEM Blog. Expert Commentary by Lopez B]. Retrieved from http://www.nuemblog.com/blog/implicit-bias

Resources:

https://www.jointcommission.org/assets/1/23/Quick_Safety_Issue_23_Apr_2016.pdf
Chapman E, Kaatz A, and Carnes M. Physicians and Implicit Bias: How Doctors May Unwittingly Perpetuate Health Care Disparities. J Gen Intern Med. 2013 Nov, 28(11): 1504-1510.
Vigil JM, Coulombe P, Alcock J, Kruger E, Stith SS, Parshall M, Chichowski SB. Patient Ethnicity Affects Triage Assessments and Patient Prioritization in U.S. Department of Veterans Affairs Emergency Departments. Medicine (Baltimore). 2016 Apr;95(14):e3191.
Just Medicine
Johnson T, Hickey RW, Switzer GE, Miller E, Winger DG, Nguyen M, and Hausmann LR. The Impact of Cognitive Stressors in the Emergency Department on Physician Implicit Racial Bias. Acad Emerg Med. 2016 Mar; 23(3): 297-305.
Blair IV, Steiner JF, Havranek EP. Unconscious (Implicit) Bias and Health Disparities: Where do we go from here? Perm J. 2011 Spring; 15(2):71-78.

Posted on December 3, 2018 by NUEM Blog and filed under Ethics and tagged implicit bias.

The UTI that isn’t: Why a common condition presents such a diagnostic challenge.

Written by: Ashley Amick, MD (NUEM Alum ‘18) Edited by: Michael Macias, MD (NUEM Alum ‘17) Expert commentary by: Alexander Lo, MD — **Written by:** Ashley Amick, MD (NUEM Alum ‘18) **Edited by:** Michael Macias, MD (NUEM Alum ‘17) **Expert commentary by**: Alexander Lo, MD

This is Part 2 of the blog post on the diagnosis of UTIs. Check out Part 1 here

Urinary tract infection (UTI) is the most common commonly diagnosed infection in the United States. However, a high incidence of diagnoses does not render those diagnoses appropriate. Increasing evidence suggests that this common condition poses a serious diagnostic challenge. Erroneously identified UTIs frequently result in inappropriate treatment, as well as delays in management of the true underlying pathology. In an era where ever more terrifying multi-drug resistant organisms continue to emerge, increasing emphasis is placed on evidence-based practice and antimicrobial stewardship. In the acute care setting, where information is limited and time is scarce, guideline-based management can aid the Emergency Physician (EP) in improving both individual and community-level outcomes.

Despite increased awareness of UTI’s role in antimicrobial stewardship and cost-effective care, leading interest groups have failed to create a consensus definition of UTI. (For an interesting experiment ask your colleagues what they consider diagnostic criteria for UTI, and prepare for wide variability). Generally speaking, UTI is a diagnosis arrived at by two core features: 1) laboratory testing suggestive of infection, of which urine culture is considered gold standard; and 2) clinical symptomatology.

Herein lies a major quandary for the Emergency Physician EP – culture data is not available in a timely fashion, and determining what defines a “symptom” of a UTI is, at best, elusive. In the absence of culture data, the EP must rely upon a urinalysis (UA), with or without microscopy, as a surrogate. Certain elements of the UA are thought to be particularly predictive of a true infection, including leukocyte esterase, nitrite, white blood cells, red blood cells, and bacteria. However, when considered either alone or in combination, there is variable sensitivity and specificity of nearly all elements of a dipstick or UA. Even when both leukocyte esterase and nitrite are present, the sensitivity and specificity is too poor to definitively diagnose or exclude a UTI.

Part of the poor predictive performance of UAs may be attributed to poor collection techniques and the presence of chronic bactiuria. Obtaining a clean-catch sample in the emergency department setting can be a formidable challenge. Studies suggest less than 10% of ED patients use proper midstream clean-catch techniques. Concerningly, 50% of patients with a contaminated urine sample receive inappropriate intervention and antibiotics. Proper education on sampling techniques as well as and in and out catheterization when appropriate, should be routinely employed.

Despite adequate sample collection, UA interpretation is frequently confounded by the presence of asymptomatic bactiuria (ASB). While definitions vary, the Infectious Disease Societies of America (IDSA) define ASB as isolation of a specified quantitative count of bacteria (105 cfu/ml from clean catch specimens) in a patient without symptoms or signs referable to urinary infection, such as frequency, urgency, dysuria, or suprapubic pain. ASB is common in the geriatric population, and prevalence increase with age and in institutionalized patients. ASB, like UTI, will frequently yield a UA positive for bacteria, LE, nitrate, and pyuria, therefore rending the UA of little use in differentiating between these two conditions. Given these considerations, the clinical symptoms become the most important factor in making the correct diagnosis.

When considering the diagnosis of UTI, beginning with an assessment of patient signs and symptoms seems not only rational, but intuitive. However, in the ever-increasing drive for efficiency, UAs are frequently drawn indiscriminately to expedite work-up. In a recent study of patient treated for UTI in an ED population, 2/3 of patients diagnosed with a UTI had a UA collected as part of an order set, often before being evaluated by a clinician. It was also found that antibiotics were administered inappropriately in 59% of those patients, due to lack of clinical signs or symptoms to substantiate a diagnosis of UTI. Going about the diagnostic work-up in a backwards way invites not only anchoring bias when a UA is positive, but places pressure on the clinician to treat a UTI that isn’t. Clinicians require discipline in looking beyond an abnormal UA, and work to objectively determine if the criteria for UTI are met based on symptomatology – or better yet – order UAs only when symptoms warrant further investigation.

Determining what constitutes a symptom – at least a symptom that should prompt a urinalysis – remains controversial. According to the CDC and SHEA guidelines, symptoms consistent with a UTI include fever and lower genitourinary symptoms such as dysuria, urgency, frequency, suprapubic pain, and costovertebral angle discomfort. Noteworthy is the omission of falls, altered mentation, and general malaise in the elderly in the absence of an indwelling catheter. (See the related post: ‘delirium as a symptom of UTI, physiology or pseudoaxiom?’ for further discussion)

According to the most contemporary guidelines, these nonspecific symptoms without localizing symptoms or fever, are no longer sufficient to support the diagnosis of UTI. This represents a shift in not only traditional clinical teaching, but a departure from prior guidelines. This change results from a realization that both asymptomatic bactiuria and altered mentation are prevalent in the geriatric population, and there is a paucity of evidence supporting a causal link between these findings. Despite these new recommendations, altered mentation, confusion, weakness, and falls are among the most frequent reasons for obtaining a UA in the geriatric population. In a population where ASB is prevalent, and procuring a clean urine sample is challenging, geriatric patients are at high risk of morbidity from inappropriate antibiotic therapy and unnecessary testing. Perhaps more concerning is that with a presumptive diagnosis of UTI, little thought may be devoted to other potential diagnoses – at least until the patient fails to improve.

Expert Commentary

Over 50 million U.S. adults > 65 years of age (“older adults”), account for over 20 million Emergency Departments (ED) visits each year [1]. Many of these patients have unmet and complex underlying medical needs that are often understated by their chief complaints. The tempting application of traditional ‘one complaint; one algorithm’ approach taught to many emergency physicians, may often result in long-term, downstream, adverse outcomes. One of those relevant to the accompanying blog, is the traditional “if grandma is delirious, look for and treat the UTI” doctrine. A review of the literature proves that the evidence linking UTI’s to delirium in older adults is lacking [2]. Many older adults are bacteriuric; most do NOT have to be treated [3]. The delirium is not a reason to treat bacteriuria [4]. It is also just as likely that it is the other comorbid conditions causing the delirium, since 75% of older adults have two or more comorbid chronic conditions [5]. many of which have the potential to cause delirium at any time[6]. The patient may likely require admission for the delirium, but a more comprehensive investigation into its etiology is more helpful than treating the easy target of a contaminated urine sample

Alexander S Lo, MD, PhD

Assistant Professor of Emergency Medicine, Northwestern University

How to Cite this Post

[Peer-Reviewed, Web Publication] Amick A, Macias M (2018, November 26). The UTI that isn’t: Why a common condition presents such a diagnostic challenge [NUEM Blog. Expert Commentary by Lo A]. Retrieved from http://www.nuemblog.com/blog/uti-part2

Resources

Little, P., et al. "Dipsticks and diagnostic algorithms in urinary tract infection: development and validation, randomised trial, economic analysis, observational cohort and qualitative study." Health Technol Assess 13.19 (2009): 1-73.
Van Nostrand, Joy D., Alan D. Junkins, and Roberta K. Bartholdi. "Poor predictive ability of urinalysis and microscopic examination to detect urinary tract infection." American journal of clinical pathology 113.5 (2000): 709-713.
Schulz, Lucas, et al. "Top Ten Myths Regarding the Diagnosis and Treatment of Urinary Tract Infections." The Journal of emergency medicine (2016).
Bent, Stephen, and Sanjay Saint. "The optimal use of diagnostic testing in women with acute uncomplicated cystitis." The American journal of medicine 113.1 (2002): 20-28.
Klausing, Benjamin T., et al. "The influence of contaminated urine cultures in inpatient and emergency department settings." American Journal of Infection Control (2016).
Gupta, Kalpana, et al. "International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women: a 2010 update by the Infectious Diseases Society of America and the European Society for Microbiology and Infectious Diseases." Clinical infectious diseases 52.5 (2011): e103-e120.
Nicolle, Lindsay E., et al. "Infectious Diseases Society of America guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults." Clinical Infectious Diseases (2005): 643-654.
Detweiler, Keri, Daniel Mayers, and Sophie G. Fletcher. "Bacteruria and Urinary Tract Infections in the Elderly." Urologic Clinics of North America 42.4 (2015): 561-568.
Kiyatkin, Dmitry, Edward Bessman, and Robin McKenzie. "Impact of antibiotic choices made in the emergency department on appropriateness of antibiotic treatment of urinary tract infections in hospitalized patients." Journal of hospital medicine (2015).
Horan, Teresa C., Mary Andrus, and Margaret A. Dudeck. "CDC/NHSN surveillance definition of health care–associated infection and criteria for specific types of infections in the acute care setting." American journal of infection control 36.5 (2008): 309-332.

Posted on November 26, 2018 by NUEM Blog and filed under Infectious Disease and tagged UTI UA geriatrics.

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