Clinical Pearl: A Parent’s Kiss for Nasal Foreign Body Removal

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Author: Ashley Grigsby, DO PGY-1
Indiana University Emergency Medicine/Pediatrics
Originally published: Modern Resident April/May 2015

Every little boy knows the best place for anything is up your nose. That is, until they show up in your emergency department (ED).

The Case:
Three-year-old previously healthy male presents after he put his older sister’s jewelry bead up his right nostril two hours ago. Vitals are normal. As you walk in the room, he is breathing comfortably and appears well, but his big brown eyes see you coming and immediately start welling up with tears. He’s sitting in his mom’s lap; he’s anxious and wants no part of you coming near him.

Clinical Pearl: "Light Bulb Sign" in Posterior Shoulder Dislocation

Author: Nathan Haas, MD

University of Michigan
Originally Published: Modern Resident, June/July 2014

Posterior shoulder dislocations are relatively uncommon, comprising only 2-4% of all shoulder dislocations. Thus, posterior dislocations often go undiagnosed, and can lead to severe consequences for both the patient and emergency physician (EP). A high index of suspicion and a firm grasp of associated radiologic findings are key to making the diagnosis.

Posterior shoulder dislocations are classically associated with seizures, electrocution and severe trauma. As a group, the internal rotators of the humerus (teres major, pectoralis major and latissimus dorsi) are more powerful than the external rotators (infraspinatus, posterior deltoid and teres minor), leading to internal rotation during global muscle contraction from electrical activity (seizure, electrocution, electroconvulsive therapy, etc.). This internal rotation is what allows the humeral head to dislocate posteriorly from the glenoid fossa, and also produces the characteristic "light bulb sign" of the humeral head seen in posterior shoulder dislocations.

The AP view of the normal shoulder demonstrates the normal asymmetry of the humeral head in anatomic position. The larger portion is on the medial side, seated in the glenoid fossa. With internal rotation in the setting of a posterior dislocation, this larger portion rotates out of view producing the more round and symmetric "light bulb sign" of the humeral head in the second image. It is important to note that this pertains only to the AP view, and not the axillary or lateral view of the shoulder.



*Image 1: Normal AP view of shoulder
Source: Dr. M Daya; ebmedicine.net

Reprinted with permission from EB Medicine, publisher of Emergency Medicine Practice, from: Daya M, Nakamura Y. Shoulder girdle fractures and dislocations. Emergency Medicine Practice. 2007; 9(10):4, www.ebmedicine.net

*Image 2: Posterior dislocation, "light bulb sign"
Source: Dr. Alexandra Stanislavsky; radiopaedia.org

While the axillary or scapular Y views often help demonstrate posterior shoulder dislocations, the "light bulb sign" of the humeral head is often present on the AP view. Other signs include the rim sign (>6mm gap between the medial humeral head and anterior glenoid rim), the trough sign/reverse Hill-Sachs lesion (compression fracture of anteromedial humeral head), or fracture of the lesser tuberosity.

References:

1. Shoulder Girdle Fractures And Dislocations. EB Medicine. Web. 20 May 2014. http://www.ebmedicine.net/topics.php?paction=showTopicSeg&topic_id=120&seg_id=2471
2. Stanislavsky A. Posterior Shoulder Dislocation. Radiopaedia. Web. 20 May 2014. http://radiopaedia.org/cases/posterior-shoulder-dislocation
3. Tosif, S. Posterior Shoulder Dislocation. Life in the Fast Lane. Web. 20 May 2014. http://lifeinthefastlane.com/posterior-shoulder-dislocation/

Why is My Arm Swollen?

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Author: Pollianne Ward, MD
Temple University Hospital
Originally Published: Modern Resident February/March '13

A 16-year-old female presented to a children's hospital emergency department with two weeks of intermittent left shoulder pain. Over the last few days, her left arm had become diffusely swollen and painful with mottling of the skin, coolness of her left hand and paresthesias on the lateral forearm. Exam revealed strong radial and brachial pulses with her arm dependent, and decreased pulses when she raised her arm. She was a competitive swimmer and practiced up to four hours per day and symptoms were worse after exercise.

Thoracic outlet syndrome (TOS) is an uncommon condition with varying presentations and a constellation of signs and symptoms that make diagnosis very tricky. It is characterized by compression of the neurovascular bundle exiting the thoracic outlet, involving the subclavian artery, vein and Brachial plexus. Historically, it was categorized by the anatomic abnormality causing the compression, such as cervical or first rib, scalene muscle hypertrophy, costoclavicular and hyperabduction syndrome.

Six Clinical Pearls from Intern Year

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Author: Casey Grover, MD
Stanford/Kaiser Emergency Medicine
Originally Published: Modern Resident October/November 2011

Looking back after finishing a year as an emergency medicine intern, the lessons that I remember the most come from the mistakes that I have made. I had one particularly rough month late in my internship that was filled with bounce backs and mismanaged cases. I learned six important lessons that will hopefully help to avoid another such month in the future.

1. Review every study that you order. While you may have ordered a chemistry panel just to check the creatinine, it's embarrassing to miss a sodium of 121.
   
2. Document your discharge decision process. If a patient has a problem or bounces back, it is extremely helpful to have documented everything (i.e., normal vitals, well appearance, consultant recommendations) that you considered when sending that patient home.
   
3. Review discharge vital signs. Vital signs are actually important – they reflect the patient's underlying physiology. Document normal vital signs when sending patients home; and when discharging someone with abnormal vitals, document your rationale and plan.
   
4. Document your discussions with consultants. Record at what time and to whom you spoke, as well as what they recommended. This allows others to see the basis of your decisions, which is essential if an adverse outcome occurs.
   
5. Be suspicious of patients signed out to you. Review the labs and vital signs of the patient you will be taking care of, and address all of their medical issues. Approach the case with fresh eyes and be willing to consider other diagnoses than those billed to you in sign out.
   
6. Approach procedures carefully. While it's fun to do procedures, be aware that complications may arise – particularly in a patient who is high risk for bleeding. Review labs and history, particularly for things like coagulopathy, that may make procedures difficult.

Tips for Tackling the Pediatric Trauma

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Author: Shyam Sivasankar, MD
Emergency Medicine Resident
Stanford-Kaiser Emergency Medicine
AAEM/RSA Publications Committee Member

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I am very fortunate to train at a facility with a child life specialist present in the emergency department. Their presence has helped me learn a lot about running pediatric trauma surveys and resuscitations, and I have picked up a few pearls along the way. The following are some of their tips, tricks, and suggestions.


1. Calming Distractions 

A trauma resuscitation can be quite overwhelming for an adult, let alone for a child. Use age appropriate interventions for each child including, but not limited to:

• Infants and Toddlers:
• Stuffed animals (for comfort) 

• Bubbles (to encourage deep breathing and relaxation) 

• Elmo Calls (Facetime™ with Elmo, a fun game for distraction) 

• School Age/ Teens: 
• iPads (or smart phones for distraction and teaching moments with patients) 

• Simply Sayin’ (a smart phone application, created in part by Phoenix Children’s Hospital. This application provides illustrations, a free-draw option, and video clips to help both patients and their parents understand what is happening while simultaneously lowering the anxiety level in the room.) 

• Stress ball for relaxation and stress management 

• Deep breathing techniques to support relaxation  

Electrical Storm: Don’t Just “Push Another Milligram of Epi”

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Author: Khalid M Miri, OMSIV
Western University of Health Sciences, College of Osteopathic Medicine of the Pacific

"Are you ready to call it?" "Not yet, let’s push one more of epi." Sound familiar? Despite doing proper CPR, defibrillating, and pushing all the ACLS meds, you know deep down that after the first few rounds of chest compressions, your cardiac arrest patient has a tiny chance of surviving to discharge in good neurological condition. You have seen too many codes that go on too long and all you know to do is keep pushing epinephrine and hope that your patient is that one rare case that will achieve sustained ROSC. Have you ever wished you had another option, something that might work when epinephrine and amiodarone do not? Well, an additional option may exist. During a specific condition — refractory ventricular fibrillation — research shows that using a beta blocker can have a better chance of bringing that patient out of their dysrhythmia than when using epinephrine and antidysrhythmics alone.

Cardiac electrical storm (ES) is often defined as three or more episodes of sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) within 24 hours. It is a dangerous arrhythmia that leads to refractory VF and will kill most of its victims despite treatment with the current ACLS recommendations of epinephrine, antidysrhythmics, CPR, and defibrillation.[1]

Digoxin Toxicity: Myths, Truths and Management

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Author: Andrew V. Bokarius, MD
Emergency Medicine Resident
University of Chicago
AAEM/RSA Publication Committee Member

The Case:
A 68-year-old male with a history of heart failure presents with weakness, confusion, and visual disturbances including yellow/green halos and scotomas. Digoxin is on the list of current medications. Vitals are notable for bradycardia with a HR of 55. The patient is awake but confused.

The Clinical Decision-Making:
While your differential diagnosis may include calcium channel toxicity, beta blocker toxicity, sick sinus syndrome, clonidine toxicity, organophosphate poisoning, and other potential diagnoses, digoxin toxicity should be at the top of the list.

You quickly recall how digoxin works: it inhibits the Na/K ATPase, causing intracellular sodium levels to rise. Sodium is then exchanged for calcium via a Na/Ca transporter. The intracellular calcium concentration is thus increased, thereby increasing contractility. Furthermore, digoxin also may increase vagal tone and can lead to bradyarrhythmias.

When SCUBA diving goes wrong – Decompression Illness

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Jonathan Morgan, MSIV

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Medical Student

Lake Erie College of Osteopathic Medicine-Bradenton

A 54 year-old male presents to your emergency department complaining of dizziness that started shortly after completing a dive. He is a biologist who was studying the nearby river. He reports that about 10 minutes after surfacing he became profoundly dizzy. He also reports nausea that has since resolved. He thinks his hearing is normal. He can walk, but stumbles sideways.

His companions administered oxygen immediately and called 911. He is currently alert, oriented, complaining of only dizziness. His vitals are: BP 130/70, Pulse 76, RR 14, Temp. 37.0 C, SpO2 98% on room air.

What do you need to know about his dive?

Basic information includes maximum depth of the dive, time at maximal depth, decompression or safety stops used, previous dives within 12 hours, and type of gas and equipment used. [1]

Drowning in your own Blood: Managing Massive Hemoptysis

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Author: Jonathan Morgan, MSIV Lake Erie College of Osteopathic Medicine-Bradenton

Case:
EMS calls; they are 5 minutes out
with a 50-year-old female patient in cardiac arrest with massive airway bleeding. She began coughing up blood and collapsed several minutes prior to EMS arrival. She is currently intubated with a 7.0 ETT, 3 doses of epinephrine have been administered, and CPR is ongoing; she has been alternating between

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PEA and asystole. Family reported a recent diagnosis of lung cancer.

What defines massive hemoptysis?
There is no consensus on the definition of “massive.” Many sources use a definition of 600cc of expectorated blood per hour, but proposed cutoffs run between 200 and 1000 mL/hr. [1] However, estimating blood volumes can be difficult and it may only take 100-400mL of blood in the airway to cause impaired gas exchange.[1,2] Because of this, some proposals call for inclusion of other clinical data including evidence of impaired gas exchange or hemodynamic derangements to define “massive.”[3]

What is the likely etiology of this patient’s cardiovascular collapse? 
Asphyxiation rather than exsanguination is the most likely cause of cardiovascular collapse in massive hemoptysis.[4] 90% of cases of massive hemoptysis are caused by bleeding in the bronchial circulation, which is exposed to systemic pressures; bleeding in the low pressure pulmonary circulation accounts for only 5% of cases.[2]

Ocular Emergency: Chemical Burns, A Non-Ophthalmologist Approach to Initial Treatment and Referral

Image from Maxxl2 - Wikimedia Commons

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Author: 
Fernando Pellerano, MS-V Universidad Iberoamericana (UNIBE) School of Medicine

Chemical burns represent potentially blinding ocular injuries and constitute a true ocular emergency requiring immediate assessment and initiation of treatment. The sequelae of an ocular burn can be severe and particularly challenging to manage. An appropriate initial emergency management may be the most important factor in determining visual outcome.[1]

Chemical eye injuries can occur from any exogenous material contacting the eye. This includes alkalis (e.g., lye, cements, plasters, airbag powder, bleach, and ammonia), acids (e.g., battery acid, pool cleaner, and vinegar), solvents, detergents, and irritants (e.g., mace).[2] Severity of the eye injury depends on the pH, concentration, and the nature of the chemical.

Diphenhydramine Overdose in the ED

Image Credit: Flickr Andrew Ranta

Author: Kaylinn Dokken, OMSIV
Western University of Health Sciences

You are just at the beginning of your shift when paramedics call in and notify you that they are bringing in a 35 year old female who reports that she took 3,000 mg of diphenhydramine in a suicide attempt. Her BP is 145/80, her pulse is 160 beats per minute (bpm) with sinus tachycardia on the monitor, and her respiratory rate is 24 breaths per minute. Upon presentation, the patient is disoriented, continuously writhing, and having intermittent myoclonic jerks. An initial EKG is obtained and is shown below.

Clonidine Toxicity: A Brief Review

Image Credit: Flickr Pranjal Mahna

Author: Matt Rosen, MSIV
Georgetown School of Medicine

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Background:
Clonidine was once a popular antihypertensive agent, and while its use as a primary blood pressure agent has declined, it continues to have a role in hypertension management for some patients. Clonidine is also being used in other applications such as treatment of migraines, treatment of vasomotor symptoms associated with menopause or withdrawal, and in a number of pediatric applications such as pre-anesthesia, postoperative pain management, and panic/anxiety disorders.[1, 5]

Retinal Detachment: What You Need to Know

Image Credit: Subhadra Jalal - Flickr

Author: Stephanie Cihlar, MSIII
Medical Student
Loyola University Chicago Stritch School of Medicine
AAEM/RSA Publications Committee Member

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Introduction
Retinal detachment is one of the most common ophthalmic emergencies, affecting approximately 1 in 10,000 people per year.[1] Because of the risk of permanent vision loss, it is important that emergency physicians are able to identify a retinal detachment and consult a retinal specialist as soon as possible.

Pathophysiology
Retinal photoreceptors (rod and cones) are metabolically highly active cells. In fact, the choroidal circulation responsible for nourishing these cells has the highest blood flow per cubic centimeter of tissue found in the human body.[2] In a retinal detachment, the neurosensory layer of the retina is peeled away from its underlying supporting tissues, the retinal pigment epithelium and choroid. The photoreceptors undergo ischemic damage, which can lead to vision loss and blindness in a matter of hours.[3]

Maisonneuve Fracture - A can’t miss diagnosis!

Author: Benjamin Lindquist, MD

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Chief Resident
Stanford/Kaiser Emergency Medicine Residency

A 50 year-old male pedestrian presented to the emergency department by ambulance after having his left foot struck by a bicyclist while the foot was firmly planted on the ground. He complained of severe pain to his medial ankle but denied knee or hip pain. He had no other injuries. On examination, he had slight eversion at the ankle with significant tenderness over the medial malleolus. He also had tenderness over his proximal fibula. He had normal strength, sensation and pulses.

X-ray showed widening of the medial tibiotalar joint space (Image A) and a comminuted fracture of the proximal fibula (Image B). These findings are suggestive of a Maisonneuve fracture with syndesmotic ligament disruption. He was placed in a splint and referred to orthopedic surgery. Ten days later, he underwent operative fixation of his syndesmotic ligament injury.

In evaluating patients with ankle injury, it is imperative to assess for concomitant proximal fibular fractures. As in this case, it is common for patients to complain only of ankle pain and not pain around the proximal fibula. However, Maisonneuve fractures are often unstable and require surgical fixation, whereas isolated fibular fractures or deltoid ligament sprains are managed nonsurgically.

Image A: Anteroposterior view L ankle

Image B: Anteroposterior view L tibia-fibula

References:

Taweel NR, Raikin SM, Karanjia HN, Ahmad J. The proximal fibula should be examined in all patients with ankle injury: a case series of missed maisonneuve fractures. J Emerg Med. 2013;44(2):e251-5. PMID: 23079149