Category Archives: practice updates

Mentoring and Emergency Medicine – Part 1

Authors: Brit Long, MD (@long_brit, EM Staff Physician at SAUSHEC) and Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) // Edited by: Gus M. Garmel, MD, FACEP, FAAEM (Clinical Professor (Affiliate) of EM, Former Co-Program Director, Stanford/Kaiser EM Residency, Stanford University) and Michael S. Runyon, MD, MPH (Professor of Emergency Medicine, Chief of Academic Affairs and Faculty Development, Department of Emergency Medicine, Carolinas HealthCare System)

Let’s start with two individuals: one is a new intern in her first month of Emergency Medicine residency. She’s been nervous about starting this new career, though this has been her dream. Her residency has a mentoring program, and she has already met with her mentor, established several long-term and short-term goals, and discussed aspects of the intern year, the hospital, the nurses, and patient population. She feels prepared, especially with the support from her mentor.

The second individual is a new graduate, fresh out of residency. He is starting a junior faculty position at an academic department. He and his wife just moved across the country, and he knows very few people at the new hospital. He had a brief meeting with the department head, credentials office, and EHR representative. His department head gave him a list of senior faculty members, but there is no formal faculty development plan. He had a great mentor during residency, but he just retired. Frankly, he feels alone in this new job and hospital.

This is the first in a two-part series on mentoring in emergency medicine. Part 1 will focus on what is mentoring, responsibilities of mentors and mentees, and pearls and pitfalls. Part 2 will focus on the process of mentoring. As we will see, mentoring is an important aspect of medical education and development.

What is mentoring?

Mentoring is a vital component of education, personal growth, and career development in every profession.  In emergency medicine, mentoring is beneficial, fostering career development, job satisfaction, and goal achievement.1-10  Mentoring is defined by a trusted and experienced advisor (the mentor) who has a direct interest in the development and education of another individual (the mentee).1-3 Importantly, mentoring is defined by intentional interaction, with the primary goal of mentee development.1,3 The mentee seeks to receive guidance and wisdom, commonly in a confidential, protective, and supportive environment, from the mentor who actively sets aside time and energy and remains flexible.

This relationship can be short or long, structured or loose. It does not need to be continuous, and contact may be reestablished after breaks. It can occur with a variety of levels. Importantly, both the mentor and mentee gain from this relationship, though at first the mentee seems to benefit the most.1-3

Who is involved?

As described, mentoring includes the mentee and mentor.  Classically, the mentor is the individual with greater experience and knowledge, as well as a more senior position. This can occur at any level including medical student and resident or staff, resident and resident, resident and staff, junior faculty and senior faculty.1,2 Mentors may be from a separate career field or medical specialty, which provides the mentee with different perspectives and opportunities. The mentee is the learner, usually with less experience and less seniority. The mentor provides several major resources to the mentee including guidance, support, counseling, motivation, and education. The goal of this relationship is to improve the mentee’s development in several arenas (discussed further).  It is appropriate for mentees to seek and have multiple mentors, as this can assist them in gaining alternative views, opportunities, and guidance. Mentors may also have several mentees, though mentors must ensure they have adequate time and ability to provide a successful mentoring relationship for each mentee.

What are the goals of mentoring?

One major goal of the mentoring relationship is to help the mentee obtain skills and knowledge required for career and professional satisfaction.  The mentor’s main goal is to assist the mentee along the road for future success in life, obtaining his/her goals. However, success can be defined differently, depending on the individual, and the mentor and mentee may differ in their definitions of success. This should be one of the first items discussed, with the mentee’s goals and definition of success clearly defined, which will avoid confusion during the relationship.1,3 Ideally, the mentee should progress not only as a physician, but as a person.

Why is mentoring important?

Mentoring has multiple benefits, including improved productivity, and most importantly, career satisfaction and development.1-10 Physicians with mentors are more confident in their abilities; one study suggests physicians with a mentor receive a higher salary.5 Professional societies have established the importance of mentoring, many creating formal programs for mentoring with resources. Conferences and faculty workshops and committees have provided many new opportunities for networking and developing vital relationships.

Who benefits?

The relationship primarily benefits the mentee. As discussed, mentees demonstrate greater satisfaction, faster promotion, and more academic productivity in the literature.1-3 Other benefits include professional safety, confidence, project opportunities, networking, greater understanding of medical roles, feedback, funding, and more relationships. Mentors also benefit, though these benefits may not occur as quickly. Mentors can assist in the development of a colleague, are less likely to experience burnout, are exposed to new ideas and excitement, and have an opportunity to share their own values. They demonstrate increased passion and excitement, greater satisfaction, academic advancement, productivity, and creativity.1-3,10

Mentoring Models

Classically, mentoring consists of the mentee and mentor. This may be an assigned or spontaneous relationship. Group mentoring includes one mentor who meets simultaneously with several mentees.2 This group often consists of mentees at different training levels, and junior learners can benefit from other mentees who may be more senior. Another form is telementoring, which is completed by email, video conference, phone, etc. This allows the members to stay connected over a distance.1,2,10

Potential Topics for mentoring…

Mentoring encompasses a wide range of topics. Topics can be separated into three fields: training, personal and professional, and future career, which overlap. Training issues such as mentee progress in his/her residency or career, rotation selection, clinical efficiency, mentee preparation for lectures or presentations, medical knowledge, discussion of cases (interesting, successful, difficult, or challenging), and tests are the major components of this field.1-3,5,10

Personal and professional issues include clinical and ethical conundrums, integrating work and personal life, time management skills, conflict resolution, professionalism, and financial matters. One major component of professional issues includes conflict resolution. Not everyone will “play nice in the sandbox”, as we’ve all had our problem with consultants or other healthcare employees. The mentor can provide valuable advice and support in this arena due to his/her experience and networks. Hospital politics, the residency program, new physicians and senior physicians, and administrators can create conflict.  In cases of difficulty with personal and professional issues, the mentor can act as an advocate, confidant, or safety net for the mentee.  EM is not an easy profession, and mentors can monitor the mentee for signs of professional or personal distress and intervene if needed.1,2

Future issues such as career guidance for residents often focuses on networking, the decision to enter community vs. academic medicine, areas of future study, and niche development. As the resident starts to move towards graduation, fellowship and job opportunities can be discussed. However, this just scrapes the surface of what the relationship offers. This is also important for a junior faculty member (mentee) and senior faculty member (mentor). In this relationship, the senior faculty member can assist with similar topics including networking, projects, committees, and administrative or academic opportunities. Ultimately, these issues require goal setting, both short and long-term.1,2

With these aspects, we now have a background on the participants in the relationship, the benefits, and topics that can be covered. However, what responsibilities do the mentor and mentee have to promote a successful relationship?

The mentee must:1-3

Demonstrate honesty and integrity in the relationship

Be mindful of mentor time and limitations

Establish long-term and short-term goals

Initiate asking questions, finding projects, and developing skills and ideas

Express interest in the relationship

Take responsibility in his/her development

Work to actively apply mentor feedback and suggestions

Provide the mentor with feedback

Seek other mentors and remind each mentor of other mentors

Inform the mentor of deadlines, successes, and difficulties

Responsibilities of mentors include:1-3

Provide oversight in the development of the mentee

Demonstrate sensitivity to cultural, gender, age, religious, and ethnic differences

Promote mentee interests

Promote mentee education and instruction

Ensure the mentee has clear goals established for development and career

Provide time and energy on a regular, consistent basis

Hold the mentee to high, but reasonable, standards

Push and encourage the mentee to reach his/her full potential

Answer questions and requests in a timely manner

Protect the mentee from possible threats

Pay close attention for new opportunities for the mentee

Advocate and champion for the mentee

Provide a confidential area for the mentee to express concerns and difficulties

Treat the mentee with respect, dignity, and courtesy

Demonstrate honesty in the relationship

Express interest in the relationship with the mentee

Impart knowledge for clinical skills and career development

Assist the mentee in networking and contacting others for help (research, statisticians, IRB)

Assist with applications for positions

Provide feedback, while also accepting feedback from the mentee

Identify areas of success and areas requiring development/limitations

Monitor the mentee for behavioral or physical signs of distress

Pearls in Mentoring

Mentoring requires a mentee willing to learn and develop, as well as a mentor who is capable and passionate. The mentor must be able to listen and commit to the needs of the mentee. Mentoring is an active process that takes time. The relationship is constantly evolving and is not static. The mentor must consider the mentee’s needs and balance that with the desire to succeed.  Both must respect the other. The mentee must consider the time commitment demanded of the mentor, while the mentor must be available and listen in a nonjudgmental, confidential manner. Meeting agendas can assist both in planning and staying focused, protecting the time for both mentor and mentee.

Pitfalls in Mentoring

Several major pitfalls may occur in the relationship. These include inappropriate expectations, taking credit for work that is not one’s own, lack of time and commitment, inappropriate/insensitive interactions, doing work for the mentee inappropriately, not behaving in the mentee’s best interest, breaching confidentiality, failing to anticipate challenges or obstacles, giving up too soon on the relationship. Lack of respect for relationship boundaries and not knowing limitations (the mentor and mentee must acknowledge their own weaknesses and limits) are pitfalls that can destroy the relationship. The mentor must not depend on only his or her own skills, but allow the mentee to develop. One major pitfall is failure to set goals and expectations at the beginning of the relationship when possible, and each meeting should be scheduled in advance, with an agenda on what will be discussed.1-3

Members of minority groups and women can find it difficult to identify possible mentors. This occurs for several reasons.1-3,11,12 Fewer effective mentors for women and under-represented minority groups are present in academic medicine.2,11,12 Differences in communication styles, interaction, and thought processes can be present between genders and minority groups. Fortunately, the numbers of female and minority faculty members are steadily rising. Also, mentors and mentees do not need to be of the same minority group or gender, though it remains imperative that future and current physicians receive mentoring that accommodates differences in culture, gender, and professional goals.1

Back to our physicians…

The intern is doing well with her current mentoring relationship. She can discuss aspects of her development and personal life in a confidential, protected environment. Her goals have been established, and her mentor has already tried to involve her in several projects. Their next meeting will discuss these projects and research.

The new staff physician requested a list of senior faculty from his department head, followed by asking who would be willing to mentor new, junior faculty. He also called his prior mentor and asked if he could run things by him on a regular basis by email or phone, to which his prior mentor agreed. Things are starting to look up, but he still has his work cut out for him.

If you have any other thoughts, please comment below.  Part 2 will cover the process of mentoring including stages and roles, and we will continue following our two mentees. Stay tuned for more!


References/Further Reading:

  1. Garmel GM. Chapter 4: Mentoring in emergency medicine in Practical Teaching in Emergency Medicine. Second Edition. Edited by Rogers RL, Mattu A, Winters ME, Martinez JP, Mulligan Terrence M. John Wiley & Sons, Ltd. Published 2013.
  2. Yeung M, Nuth J, Stiell IG. Mentoring in emergency medicine: the art and the evidence. Cal J Emerg Med 2010;12(2):143-149.
  3. Garmel GM. Mentoring medical students in academic emergency medicine. Acad Emerg Med 2004;11:1351-57.
  4. Detsky AS. Baerlocher MO. Academic mentoring – how to give it and how to get it. J Am Med Assoc 2007;297(19):2134-36.
  5. Jackson VA, Palepu A, Szalacha L, Caswell C, Carr PL, Inui T. Having the right chemistry: a Qualitative study of mentoring in academic medicine. Acad Med. 2003; 78:328–34.
  6. Advisor, Teacher, Role Model, Friend: On Being a Mentor to Students in Science and Engineering. National Academy of Sciences, National Academy of Engineering, Institute of Medicine. Washington, DC: National Academy Press, 1997.
  7. Clutterbuck D. Everyone Needs a Mentor: Fostering Talent at Work, ed 3. London: CIPD House, 2001.
  8. Paice E, Heard S, Moss F. How important are role models in making good doctors? BMJ. 2002; 325:707–10.
  9. Wright DW, Hedges JR. Mentoring faculty members to the next level. SAEM/AACEM Faculty Development Handbook, ed 1. Available at: handbook/4-2_mentoring_faculty_members_next_level1.htm. Accessed February 2017.
  10. Ramanan RA, Phillips RS, Davis RB, Silen W, Reede JY. Mentoring in medicine: keys to satisfaction. Am J Med. 2002; 112:336–41.
  11. Lewis RJ. Some thoughts regarding gender issues in the mentoring of future academicians. Acad Emerg Med. 2003;10:59-61.
  12. Hamilton GC. SAEM under-represented minority research/mentorship task force: attitudes and opinions of under-represented minority medical students regarding emergency medicine as a potential future career choice. Acad Emerg Med. 2004;11:483-84.

Medical Malpractice Insights: It may be more than “just a sore throat”

Here’s another case from from Medical Malpractice Insights – Learning from Lawsuits, a free monthly opt-in email newsletter. The goal of MMI-LFL is to improve patient safety, educate physicians, and reduce the cost and stress of medical malpractice lawsuits.

Author: Chuck Pilcher MD, FACEP; Editor, Med Mal Insights

It may be more than “just a sore throat”

Retropharyngeal abscesses may be subtle

Facts: A 34 yo female presents to the ED with severe sore
throat and dysphagia of 2 days duration. She is anxious and
crying. Examination shows no tonsillar exudates, no Screen Shot 2017-03-15 at 3.08.43 PMlymphadenopathy, and no fever. Rapid strep test is negative. She is given Decadron, viscous lidocaine, and a prescription for Lortab elixir. She returns the next day appearing ill, and the exam is unchanged. Supportive therapy is continued. Two days later she is seen by her PCP at an Urgent Care center, still afebrile, but with trismus and muffled speech. Her neck is “too tender to touch.” A CT is done and reported the next morning as a likely retro- and para-pharyngeal abscess. She is started on serial IV antibiotics as an outpatient, after a telephone consult with an ENT at a tertiary hospital. She improves slightly, but a f/u CT a week later shows spread of the infection. She is sent to the tertiary hospital for surgery. She develops chronic post-operative pain over the next year and consults an attorney.

Plaintiff: You should have made the diagnosis earlier. If I had re- ceived antibiotics earlier, I would not have needed surgery, and I would not be in pain now.
Defense: A retropharyngeal abscess is rarely obvious early. You didn’t even have a fever. Antibiotics are appropriate initially; surgi- cal drainage should be delayed until there is frank pus. Earlier an- tibiotics might not have made any difference.

Result: After expert review of the medical record, plaintiff attorney elected not to file a lawsuit.


  1. Symptoms of retro- or parapharyngeal abscess include fever, dysphagia (difficulty swallowing), odynophagia (pain with swallowing), neck tenderness, and sometimes dyspnea.
  2. Neck stiffness and swelling are more common in infants and children.
  3. Because this is uncommon, one must remember to think of it in any case of severe sore throat, especially when the “throat” itself looks normal.


    Retropharyngeal Abscess. Kahn JH. Medscape eMedicine, up- dated Jan 27, 2017.

    Deep neck space infections. Chow AW. UpToDate Online, up- dated Jul 16, 2015.

    “Good judgment comes from experience. Experience comes from bad judgment.”

TOXCARD: Hyperthermia in the toxicological setting

Author: Jenna Otter, MD (EM Resident Physician, Temple University Hospital) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit) 


Case Presentation:

A 32 year-old man presents to the emergency department with altered mental status. The patient is agitated but sleepy-appearing. He appears to be uncomfortable, shifting on the stretcher and unable to lie still. An empty bottle of cough syrup is found in his pocket. His vitals are HR 141, rectal temperature 103.6F, BP 214/110, RR 22, SpO2 98% in room air.


What is the differential diagnosis for hyperpyrexia with altered mental status? How is hyperthermia secondary to drug ingestion and toxic syndromes treated?


Drug-related hyperthermia is difficult to distinguish but may be differentiated based on components of history and physical exam. Hyperthermia secondary to toxic syndromes and drug ingestion will not respond to antipyretics like ibuprofen or acetaminophen and external cooling measures are key.

  • Fever is defined as a physiologic elevation in the hypothalamic set-point for body temperature induced by inflammatory cytokines in response to a stressor.
  • Hyperthermia in the toxicological setting differs from fever in that it results from an unregulated increase in body temperature either from increased heat production or decreased heat dissipation, usually resulting from increased skeletal muscle metabolism or activity.
  • Toxicological causes of increased heat production include serotonin syndrome, neuroleptic malignant syndrome, malignant hyperthermia, alcohol withdrawal, sedative-hypnotic withdrawal, and ingestions of sympathomimetics, anticholinergics, and ecstasy. Decreased heat dissipation through poor sweat production also occurs in anticholinergic ingestions.
  • Initially, fever and hyperthermia are difficult to distinguish but may be differentiated based on components of history and physical exam.

Hyperthermia Differential Diagnosis2

Toxic Syndrome CNS Other
Serotonin Syndrome Meningitis Sepsis
Neuroleptic Malignant Syndrome ICH Heat Stroke
Malignant Hyperthermia Hypothalamic stroke Pheochromocytoma
Alcohol/Sedative-Hypnotic Withdrawal Encephalitis Thyrotoxicosis
Sympathomimetic Syndrome (e.g. cocaine, amphetamines, PCP, MDMA, cathinones, etc.)


Status epilepticus Infection (Tetanus, malaria, etc)
Alcohol/Benzodiazepine Withdrawal
Anticholinergic Syndrome
Salicylate Toxicity


Some toxicological causes of hyperthermia and their differentiations:


Table Source: Boyer E and Shannon M. The Serotonin Syndrome. N Engl J Med. 2005; 352:1112-1120. DOI: 10.1056/NEJMra041867.

  • Antipyretics have no role in the management of hyperthermia in the toxicological setting since the fever usually results from muscular hyperactivity, not an alteration in hypothalamic homeostasis.
  • Hyperthermia should be addressed promptly by using external cooling blankets, ice water submersion, evaporative cooling techniques, or cool IV fluids. Benzodiazepines should also be used to reduce excess heat production from muscle hyperactivity.
  • To prevent end-organ damage, the goal should be to reduce rectal temperature to below 40°C within 30 minutes of beginning cooling therapy.
  • In severe cases, internal cooling catheters can be used for more regulated cooling, using thermal regulation devices such as CoolLineR or CoolGardR. If necessary, cold fluids can be given through a NG or OG tube in intubated patients. Also the bladder can be irrigated with cool fluids using a foley catheter.

Main point:

Hyperthermia secondary to drug ingestion differs from infection-related fevers in that it results from an unregulated increase in body temperature, usually from increased skeletal muscle activity. Drug-related hyperthermia is difficult to distinguish but may be differentiated based on components of history and physical exam. Hyperthermia secondary to toxic syndromes and drug ingestion will not respond to antipyretics like ibuprofen or acetaminophen and external cooling measures are key.


  1. Simon H. Hyperthermia. N Engl J Med. 1993; 329:483-487. DOI: 10.1056/NEJM199308123290708.
  2. LoVecchio F. Chapter 210: Heat Emergencies. In: Tintinalli J, ed. Tintinalli’s Emergency Medicine. 8th ed. McGraw Hill; 2016: 1365-1370.
  3. Boyer E and Shannon M. The Serotonin Syndrome. N Engl J Med. 2005; 352:1112-1120. DOI: 10.1056/NEJMra041867.

The Hand: An Expedited Examination and Key Points Regarding ED Diagnoses

Authors: Alin Gragossian, DO (EM Resident Physician, Drexel University), Matthew A. Varacallo, MD (Orthopedics Resident Physician, Drexel University), and Richard J. Hamilton, MD (EM Professor and Chair, Drexel University) // Edited by: Erica Simon, DO (@E_M_Simon) & Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital)

A 31-year-old male, the victim in a low-speed MVC versus pedestrian, arrives to the trauma bay via EMS. As the stretcher rolls by you see an alert patient, yelling in pain. A c-collar is in place, and a splint supports what appears to be a mangled right hand and an open right forearm fracture. As your trauma team hurriedly connects monitors, you note initial VS: HR 110, BP 132/96, RR 14, SpO2 98% RA.

You’re reassured by your primary survey: ABCs are intact; the radial and ulnar pulses of both upper extremities are palpable. Your secondary survey is significant for what appears to be a serious injury to the dorsal aspect of the distal right upper extremity: a large skin avulsion revealing extensor tendons of the hand and an open distal radius fracture.

CT imaging and radiographs demonstrate that the patient is without additional injuries, save those identified on your exam. After administering analgesia, cefazolin, and updating a tetanus, the patient wheels off to the OR for washout, re-approximation, and repair. As you complete the trauma paperwork, you replay the hand examination in your mind.  Was there anything that your team overlooked?

If it’s been a while since you’ve treated a patient with a hand complaint, let’s review some high-yield material.


Hand complaints represent nearly 12% of injury-related visits to ED setting.1,2 Trauma involving the hands imparts a significant burden on healthcare systems given the frequent requirement for referral, and potential necessity for surgical intervention. According to a 2009 study of 134 patients presenting for the evaluation of hand lacerations secondary to electric saws, mean treatment costs per injury (including hospitalization) were $30,704, with an average loss of 64 productive work days.3 As limitations in dexterity can significantly impact activities of daily living and quality of life, the early identification and treatment of neurovascular, tendon, and bone injuries of the hand are paramount.4

History & Physical

When obtaining a history, question patients regarding the type of injury (burn, laceration, injection injury, etc.), the mechanism, time elapsed between injury and evaluation, and the possibility of occupational exposures. Hand dominance, prior hand injury, and prior hand surgeries should be documented.5

Physical Exam
Table 1 offers a quick reference guide for use when performing muscle and tendon function evaluation of the hand and wrist.6,7

Table 1. Muscle and Tendon Function of the Hand and Wrist
Table 1. Muscle and Tendon Function of the Hand and Wrist

Examination of the hand should include an assessment of nerve function:

Median Nerve

  • Motor: thumb abduction and opposition => test by asking the patient to place his hands in anatomic position.  Apply resistance to the thumbs while prompting the patient to move them towards the ceiling.
  • Sensory: innervates the central aspect of the palm and terminates distally in the radial 3.5 digits of the hand => test sensation by assessing two-point discrimination. Normal two-point discrimination is 5mm at the volar fingertips. Sensory testing should be repeated 2-4 times on each side of each digit.5,6

Radial Nerve

  • Motor: thumb extension => test the patient’s thumb extension against resistance.
  • Sensory: the superficial branch of the radial nerve and its terminal branches provide sensation to the central and radial aspects of the dorsum of the hand, and the dorsal-radial aspect of the thumb => test sensation by performing two-point discrimination on the dorsum of the thumb.5,6

Ulnar Nerve

  • Motor: innervates the adductor pollicis muscles and controls thumb adduction => test by asking the patient to cross her fingers, or abduct her fingers against resistance.
  • Sensory: provides sensation to the dorsal-ulnar aspect of the hand and into the fingertips of the fourth and fifth digits => test ulnar nerve sensation by assessing two-point discrimination of the fourth and fifth digits.5,6
Figure 1. Cutaneous Nerve Supply of the Hand O’Rahilly R. Basic Human Anatomy: Chapter 10: The Hand. 2008. Available from:
Figure 1. Cutaneous Nerve Supply of the Hand
O’Rahilly R. Basic Human Anatomy: Chapter 10: The Hand. 2008. Available from:


The radial and ulnar arteries perfuse the hand. The radial artery forms the deep palmar arch, and the ulnar artery forms the superficial palmar arch.5,7 Vascularity may be evaluated through palpation (temperature and pulses), Doppler (if required), and capillary refill. While some advocate the use of the Allen’s test during the vascular examination, it is important to note that this test lacks sensitivity and specificity as findings vary according to the time employed (e.g. – injury transecting the radial artery may initially present with a normal Allen’s test, however subsequent radial artery vasospasm and thrombosis may result in an later abnormal Allen’s test), and operator experience.8


When it comes to hand injuries, malrotation resulting from fracture is an indication for ED reduction. When the fingers are flexed, a cascade directed towards the scaphoid tubercle should be observed (Figure 2). If abnormalities in alignment are identified, radiographs and consultation are advised.

Figure 2. Assessment of Malrotation Steinman S. Seattle Children’s Hospital Finger Fractures: Don’t Forget the Malrotation. 2017. Available from:
Figure 2. Assessment of Malrotation
Steinman S. Seattle Children’s Hospital Finger Fractures: Don’t Forget the Malrotation. 2017. Available from:

Special Examinations

Carpal Tunnel

Tinel’s and Phalen’s tests may be utilized to assess for the presence of carpal tunnel syndrome. A positive Tinel’s sign is elicited when the examiner taps the median nerve as it passes through the carpal tunnel, eliciting a report of paresthesias in median nerve distribution. A positive Phalen’s test occurs when paresthesias are experienced in median nerve distribution after > 60 seconds of maximum wrist flexion.8

Ulnar Motor Weakness

Froment’s test identifies ulnar nerve motor dysfunction (specifically, a weakness of the adductor pollicis). The patient is instructed to grasp a thin object between the thumb and radial aspect of the index finger.   If the examiner is able to remove the thin object, or the patient flexes the IP joint (flexing the flexor pollicis longus, innervated by the anterior interosseous nerve) to increase the grasping force, the test is said to be positive. If the patient simultaneously hyperextends the first metacarpophalangeal joint, this is said to be a positive Jeanne’s test, again indicating ulnar motor weakness.9

Figure 3. Froment's Test Ujash S. Physical Exam of the Hand. 2017. Available from:
Figure 3. Froment’s Test
Ujash S. Physical Exam of the Hand. 2017. Available from:
Figure 4. Positive Jeanne's Test Ujesh, S. Physical Exam of the Hand. 2017. Available from:
Figure 4. Positive Jeanne’s Test
Ujesh, S. Physical Exam of the Hand. 2017. Available from:


In the ABCs of Emergency Radiology, Chan and Touquet offer a number of excellent recommendations on the basics of ED radiographs:

The Rules of Two:1

  • Two views: one view is one too few
  • Two joints: image the joint above and below a long bone
  • Two sides: compare the other side if unsure of pathology
  • Two abnormalities: look for a second abnormality
  • Two occasions: compare current films and old films (if available)
  • Two visits: repeat films before and after procedures
  • Two specialists: if possible, obtain a formal radiology report
  • Two examination modalities: US, CT, or MRI should be considered as appropriate to the clinical scenario

Speaking of imaging, ultrasound is quickly becoming a popular mechanism for identifying foreign bodies. Prior to the employment of US, epidemiological studies estimate that nearly 38% of non-radiopaque foreign bodies went unidentified during initial ED encounters (1982 publication).11 A recent study by Saboo and colleagues demonstrated sensitivities of 94–98% for ultrasound detection of both radiolucent and radiopaque foreign bodies (n =123 patients, 7.5 MHz transducer).12 As US may be difficult to perform on the small surfaces of the hands, a water bath may be utilized with a high frequency linear transducer to generate high resolution images.

Figure 5. Water Bath for Hand US Lin, Michelle. Tricks of the Trade: Underwater Ultrasonography. 2011. Available from:
Figure 5. Water Bath for Hand US
Lin, Michelle. Tricks of the Trade: Underwater Ultrasonography. 2011. Available from:

Urgent or Emergent  Surgical Intervention

The following offers a review of hand conditions requiring urgent or emergent ED attention.

 Acute Compartment Syndrome

Compartment syndrome of the hand is relatively uncommon, but may occur secondary to trauma, insect bites, snake bites (2-8%13), high-pressure injection, contrast infusion, and crush injuries.12 The hand is anatomically separated into ten compartments; those most commonly at risk for the development of elevated intra-compartmental pressures include: the interossei (dorsal and palmar), the thenar and hypothenar, the adductor, and the finger compartments.14 Symptoms associated with acute compartment syndrome are classically characterized as the “six Ps” – pain, pallor, paresthesias, poikilothermia, pulselessness, and paralysis. The most reliable indicator is pain out of proportion to physical examination findings.12 It is paramount that fasciotomy be performed within 8 hours of the onset of symptoms as axonal and myocyte damage may be irreversible outside of this time frame.15-17


Replantation, the surgical reattachment of a finger, hand, or arm that has been severed, is a topic best discussed with the orthopedic/hand specialist –  patient outcomes depend upon the skill of the surgical team, patient co-morbidities, and the extent of the injury.18 Primary indications for replantation after trauma include amputations to the thumb at any level, involvement of multiple digits, amputations through the palm, amputations at or proximal to the wrist, and almost all amputated parts in the pediatric patient.18 Consideration for replantation should be given for individual digit amputations distal to the insertion of flexor digitorum superficialis, ring avulsion injuries, and amputations through or above the elbow.18

Primary contraindications to replantation include patients with severe vascular disorders, crush injuries, or injuries with mangling of the severed limb.18

Flexor tenosynovitis

 Flexor tenosynovitis is an infection of the flexor tendon sheath that is characterized by Kanavel’s Signs: finger held in flexion, pain with passive extension, pain with palpation of the flexor tendon sheath, and fusiform swelling.19 Flexor tenosynovitis may result from minor trauma as the distance from the volar dermis to the flexor sheath is 1-2 millimeters.19 If suspected, initiate broad-spectrum antibiotic therapy, and consult for surgical intervention.19

High-Pressure Injection Injuries

Patients utilizing high-pressure injection equipment often present to the ED for the evaluation of an injury to the non-dominant hand (equipment most commonly held in the dominant hand).20,21 Injury severity is dependent upon the force of injection, volume of material injected, and the composition of the material injected.20 While injuries may initially appear relatively benign, specialty consultation is a must as tracking of the injected material may ultimately result in gross contamination of subcutaneous tissue and deep muscle. Upon ED arrival, imaging should be performed to assess for the presence of foreign bodies, and parenteral antibiotic therapy initiated.20,21 In terms of morbiditiy, as compared to all other finger injuries, those due to high-pressure injection are three times as likely to require amputation.19


  • A rapid hand exam can be performed in the following manner:
    • As the patient make an “OKAY” sign with thumb and first finger (median nerve). Spread the fingers apart maximally (ulnar nerve). Dorsiflex the wrist fully (radial nerve). These can be combined into an OKAY sign with remaining fingers spread apart and the wrist dorsiflexed to get an all-in-one motor exam.
    • Check sensation of the median and ulnar nerve by testing two-point discrimination at the index and small finger pads respectively. Radial nerve sensation can be tested over the dorsum of the thumb.
  • For carpal tunnel syndrome, perform Tinel’s and Phalen’s tests. Remember, a positive test occurs when the patient reports paresthesias in median nerve distribution.
  • Acute compartment syndrome must go to the OR within 8 hours of onset.
  • Kanavel’s Signs are key physical exam findings for flexor tenosynovitis: finger held in flexion, pain with passive extension, pain with palpation of the flexor tendon sheath, and fusiform swelling.
  • Beware of high-pressure injection injuries. They look more benign than they truly are, and warrant a careful physical examination of the hand and consultation.

References / Further Reading:

  1. Niska R, Bhuiya F, Xu J. National Hospital Ambulatory Medical Care Survey: 2007 emergency department summary. Natl Health Stat Report. 2010;(26):1-31.
  2. Maroukis BS, Chung KC, MacEachern M, Mahmoudi E. Hand trauma care in the United States: a literature review. Plastic and Recon Surg. 2016 Jan; 137(1): 100e-111e.
  3. Hoxie SC, Capo JA, Dennison DG, Shin AY. The economic impact of electric saw injuries to the hand. J. Hand Surg. 2009 Jun; 34A: 886-889.
  4. Soucacos P. Indications and selection for digital amputation and replantation. J Hand Surg Br. 2001;26(6):572–581.
  5. Tintinalli J, Stapczynski J, Cline D, Ma OJ et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8th edition. McGraw-Hill Education / Medical; 2015.
  6. Chung KC. Hand and Wrist Surgery. Elsevier Health Sciences; 2012.
  7. Morton DA, Foreman K, Albertine KH. eds. The Big Picture: Gross Anatomy New York, NY: McGraw-Hill; 2011.
  8. Jarvis MA, Jarvis CL, Jones PR, Spyt TJ. Reliability of Allen’s test in selection of patients for radial artery harvest. Ann Thorac Surg. 2000;70(4):1362-5.
  9. Ujash S. Physical Exam of the Hand. 2017. Accessed 15 March 2017. Available from:
  10. Chan O and Touquet R. General Principles: How to Interpret Radiographs. In ABC of Emergency Radiology. 3rd 2013. West Sussex, UK. Wiley-Blackwell Publishing.
  11. Lewis D, Jivraj A, Atkinson P, Jarman R. My patient is injured: identifying foreign bodies with ultrasound. Ultrasound. 2015;23(3):174-80.
  12. Saboo S, Saboo SH, Soni SS, et al. High-resolution sonography is effective in detection of soft tissue foreign bodies. J Ultrasound Med 2009; 28: 1245–9.
  13. Anz A, Schweppe M, Halvorson J, Bushnell B, Sternberg M, Andrew Koman L. Management of venomous snakebite injury to the extremities. J Am Acad Orthop Surg. 2010 Dec; 18(12): 749-59.
  14. Chandraprakasam T and Kumar R. Acute compartment syndrome of forearm and hand. Indian J Plast Surg. 2011; 44(2):212-218.
  15. Oak NR, Abrams RA. Compartment Syndrome of the Hand. Orthop Clin North Am. 2016;47(3):609-16.
  16. Whitesides TE, Heckman MM. Acute compartment syndrome: update on diagnosis and treatment. J Am Acad Orthop Surg 1996;4(4):209–18. 21.
  17. Von keudell AG, Weaver MJ, Appleton PT, et al. Diagnosis and treatment of acute extremity compartment syndrome. Lancet. 2015;386(10000):1299-310.
  18. Sabapathy SR, Venkatramani H, Bharathi RR, Bhardwaj P. Replantation surgery. J Hand Surg Am. 2011;36(6):1104-10.
  19. Ong YS, Levin LS. Hand infections. Plast Reconstr Surg. 2009;124(4):225e-233e.
  20. Eroglu O, Sari E, Vural S, Coskun F. Warning: This may be as dangerous as firearm injuries; “grease-gun injury”: A case report. The Pan African Medical Journal. 2015;20:40. doi:10.11604/pamj.2015.20.40.5892.
  21. Hogan CJ, Ruland RT. High-pressure injection injuries to the upper extremity: a review of the literature. J Orthop Trauma. 2006;20(7):503-11.

EM@3AM – Acute Coronary Syndrome

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 69 year-old male with a history of hypertension, hyperlipidemia, and smoking presents with pre-cordial chest pain radiating to his right upper extremity, associated with shortness of breath. The patient reports the onset of his symptoms one hour prior to arrival, while mowing his lawn. He characterizes his chest pain as an 8/10 “tightness” and notes nausea that “comes in waves.” ROS is negative for recent illness, travel, and hospitalization within the previous 90 days. The patient denies personal or familial history of DVT/PE.

 Triage VS: BP 157/98, HR 102, RR 22, T99.8°F Oral, SpO2 98% on room air

What diagnosis do you suspect? What’s the next step in your evaluation and treatment?

Answer: Acute Coronary Syndrome (ACS)1-4

  • ACS: Consists of unstable angina, NSTEMI, and STEMI
  • Risk Factors: Hypertension, diabetes, dyslipidemia, tobacco use, family history of CAD (i.e. – CAD in a male primary relative younger than 55 years of age, or CAD in a female primary relative younger than 65 years of age), HIV/AIDS, SLE, cocaine use.1 
  • Presentation: Chest pain or pressure radiating to the neck, jaw, or upper extremities; mid-epigastric pain, diaphoresis, nausea with or without emesis.2
    • Increased likelihood of acute MI:3
      • Chest pain with radiation to right arm or shoulder: positive likelihood ratio (+LR) 4.7; 95% CI 1.9-12
      • Chest pain with radiation to both arms or shoulders: +LR 4.1; 95% CI 2.5-6.5
      • Chest pain associated with exertion: +LR 2.4; 95% CI 1.5-3.8
  •  Evaluation:
    • Focused H&P, serial EKGs, cardiac biomarkers, chest radiograph
      • Troponin I most sensitive marker of cardiac myocyte damage (positive in NSTEMI and STEMI).1
  •  Treatment:1
    • Administer non-enteric coated, chewable ASA.
    • Antithrombotic therapy and/or anti-platelet therapy as appropriate per the diagnosis.
    • Nitrates to relieve chest discomfort (caution in the setting of inferior STEMI => perform R-sided EKG to rule out RV infarct,  a pre-load dependent condition).
    • Supplemental oxygen therapy for patients with shortness of breath, signs of acute heart failure, or cardiogenic shock.
  •  Pearls:
    • Females, diabetics, and the elderly often present atypically.
    • Keep in mind there are numerous ACS mimics: aortic dissection, PE, pneumonia, pericarditis, myocarditis, pleurisy, PUD, etc.
    • Previous non-invasive cardiac stress testing does not rule out coronary artery disease.4 


  1. Qazi M and Patel P. Acute Coronary Syndrome. In: Ferri’s Clinical Advisor 2017. Philadelphia: Saunders Elsevier, 2017: 25-29.e1.
  2. Kumar A and Cannon C. Acute Coronary Syndromes: Diagnosis and Management, Part I. Mayo Clin Proc. 2009; 84(10): 917-938.
  3. Swap C and Nagurney J. Value and limitations of chest pain history in the evaluation of patients with suspected acute coronary syndromes. JAMA. 2005; 294(20): 2623-2629.
  4. Walker J, Galuska M, Vega D. Coronary disease in emergency department chest pain patients with recent negative stress testing. West J Emerg Med. 2010; 11(4): 384-388.

For Additional Reading:

EKG Findings in ACS:

ST Elevation in aVR:

Risk Stratification:

Management of Low-Risk Chest Pain:

EM@3AM – Anticholinergic Toxicity

Author: Erica Simon, DO, MHA (@E_M_Simon, EM Chief Resident, SAUSHEC, USAF) and Daniel Sessions, MD (EM Associate Program Director, SAUSHEC, USAF / Medical Toxicologist, South Texas Poison Center) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital) and Brit Long, MD (@long_brit, EM Attending Physician, SAUSHEC, USAF)

Welcome to EM@3AM, an emdocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 62 year-old female, escorted by her son, presents to the emergency department for altered mental status. The son reports his mother as being in her usual state of health during a visit the night prior, but per the family maid, was severely confused upon awakening one hour prior to arrival.  A phone call to the patient’s daughter reveals a ROS positive only for a medication change: chlorpromazine prescribed for hiccups.

 Triage VS: BP 172/101, HR 127, RR 28, T103.2°F Oral, SpO2 98% on room air

Accucheck: 137

Upon initial evaluation the patient is oriented only to herself. Her pupils are 5mm bilaterally, she is flushed, her skin is dry, and her capillary refill is > 3 seconds. Her abdominal exam is remarkable for a palpable, distended bladder.

What do you suspect as a diagnosis? What’s the next step in your evaluation and treatment?

Answer: Anticholinergic Toxicity1-5

  • Precipitating Causes: Amantadine, antihistamines, antiparkinsonian medications, antipsychotics, cyclic antidepressants, dicyclomine, atropine, phenothiazines, scopolamine, Jimson weed.1 
  • Presentation: Classically “hot as a hare, dry as a bone, red as a beet, blind as a bat, mad as a hatter, full as a flask, tachy as a pink flamingo.”
  • Evaluation:
    • Focused H&P:1
      • Perform a medication reconciliation
      • VS: obtain rectal temperature, look for tachycardia
      • Neurologic examination: possible altered mental status, mydriasis, visual deficits
      • Additional exam findings: patient commonly flushed with dry skin and a prolonged capillary refill.  Palpate the abdomen in search of a distended bladder.
  • Treatment:1
    • Delirium/Agitation: benzodiazepines
      • Avoid haldoperidol – may worsen symptoms
    • Urinary retention: foley placement
    • Hyperthermia: active cooling with misting/fanning, cooled IV fluids; benzodiazepines for shivering
    • Hypotension: IVF; if intractable, consider norepinephrine
    • EKG demonstrating conduction delays: sodium bicarbonate to overcome impaired sodium conduction
    • Although physostigmine has traditionally been recommended only for patients with life-threatening anticholinergic toxicity (given concern regarding its associated complications, i.e. – severe agitation, seizures, persistent hypertension, and hemodynamic compromise secondary to tachycardia),3 newer data report its relative safety and efficacy in reversing the anticholinergic toxidrome; specifically anticholinergic delirium.4,5 
  •  Pearls:
    • Consider anticholinergic toxicity in the differential diagnosis of an altered patient with residual urine > 200-300 mL.2
    • Exercise caution in the use of physostigmine if there is concern for TCA toxicity, arrhythmias, or QRS/QTc prolongation, as upon administration physostigmine displays a dose dependent AV nodal conduction delay.2
    • In 2013, the American Association of Poison Control Centers reported three deaths secondary to an anticholinergic drug (benztropine).3


  1. Thornton S and Ly B. Over-the Counter Medications. In: Emergency Medicine: Clinical Essentials. Philadelphia, Saunders Elsevier. 2013; 1334-1342.e1.
  2. Stilson M, Kelly K, Suchard J. Physostigmine as an antidote. Cal J Emerg Med. 2001. 2(4): 47-48.
  3. Mowry J, Spyker D, Cantilena L, McMillan N, Ford M. 2013 Annual report of the American Association of Poinson Control Centers’ National Poison Data System (NPDS): 31st annual report. Clin Toxicol. 2014; 52: 1032-1238.
  4. Watkins J, Schwarz E, Arroyo-Plasencia A, Mullins M; Toxicology Investigators Consortium Investigators. The use of physostigmine by toxicologists in anticholinergic toxicity. J Med Toxicol. 2015; 11(2):179-184.
  5. Dawson A and Buckley N. Pharmacological management of anticholinergic delirium – theory, evidence, and practice. Br J Clin Pharmacol. 2016; 81(3): 516-524.

 For Additional Reading:

Physostigmine for Anticholinergic Toxicity:

Physostigmine for Management of Anticholinergic Toxidrome

Posterior Circulation Strokes and Dizziness: Pearls and Pitfalls

Authors: Alec Pawlukiewicz, BA (Vanderbilt University School of Medicine) and Drew A. Long, BS (@drewlong2232, Vanderbilt University School of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

Case Presentation

You are working the night shift in the ED, and you see the next patient is a 38-year-old female complaining of dizziness.  Her vital signs include HR 82, BP 115/70, RR 12, O2 saturation 99%, and T 37 C.  She describes her dizziness as a sensation of the room spinning, and her dizziness began yesterday and has worsened today.  It is associated with severe nausea and vomiting. Her past medical history is notable for type I diabetes.  She has never had any previous episodes of dizziness.  Is she having a posterior stroke? How can you evaluate this patient for a life-threatening cause of dizziness?


Worldwide, stroke is a major cause of disability and mortality.1  In the U.S., around 795,000 strokes occur every year.2 Posterior circulation strokes account for approximately 20% of ischemic strokes.3 Unfortunately, many of these posterior strokes are initially misdiagnosed or remain undiagnosed.4 Misdiagnosis of posterior circulation strokes presenting with dizziness is common, occurring in up to 35% of cases.5 The common causes of posterior circulation strokes include embolic causes, atherosclerosis (and subsequent stenosis), small vessel disease, and arterial dissection.6-9 The posterior circulation supplies approximately 20% of the brain.10  See Figure 1 for the anatomy of the posterior circulation and Table 1 for the areas supplied.

Screen Shot 2017-03-10 at 5.13.27 PM

Table 1: Areas Supplied by Posterior Circulation11

Artery Area Supplied
Vertebral Artery Brainstem
PICA Cerebellum
Basilar Artery Thalamus
Posterior cerebral Auditory/vestibular structures
Medial temporal lobe Visual occipital cortex

Clinical Presentation

The clinical presentation of posterior circulation strokes can vary widely and depends on the location of the infarct. Posterior circulation strokes commonly present with symptoms of altered mental status, vision changes, speech changes, nystagmus, vertigo, ataxia, limb weakness, headache, and a variety of other focal neurological deficits.12,13 Of note, these focal neurological deficits may be absent or subtle, leading to difficulty diagnosing posterior strokes.13,14 One particularly challenging presentation of posterior circulation stroke is patients with acute vestibular syndrome (AVS), which often manifests with vertigo or “dizziness.”  This review will focus on dizziness or vertigo and the posterior circulation.

Categorizing Dizziness

A common, classic first step in evaluating a patient with dizziness is to have them characterize what they mean by “dizzy,” as dizziness is an imprecise descriptor.  Dizziness is often used by patients to describe a wide variety of experiences, which can be categorized into one of four categories.  These include vertigo (illusion of motion, often spinning), near syncope (feeling of impending fainting), disequilibrium (loss of balance while walking), and nonspecific dizziness.15  Unfortunately, having the patient describe what they mean by “dizzy” has been shown to be an unreliable indicator of the underlying pathology.16,17  A study by Newman-Toker et al. found that patients frequently changed their descriptors of the type of dizziness if questioned in a different manner after only 10 minutes.18 These studies bring into question the utility of a patient’s description and characterization of “dizziness.”

A newer method of categorizing “dizziness” deals with the timing and triggers of its onset.14 One study has shown that despite the unreliability of the description of the dizziness, patients often reliably relate the context and timing of its onset.19 These categories are displayed in Table 2.

Table 2.  Categories of Timing and Triggered Based Vestibular Syndromes14

Vestibular Syndrome  Duration Asymptomatic Periods Triggers?
Acute Vestibular Syndrome > 24 Hours No No
Triggered Episodic Vestibular Syndrome < 1 minute Yes Yes
Spontaneous Episodic Vestibular Syndrome Minutes to hours Yes No, but may have exacerbating factors

Vestibular Syndromes include Acute Vestibular Syndrome (AVS), Triggered Episodic Vestibular Syndrome, and Spontaneous Episodic Vestibular Syndrome.  Table 2 lists defining characteristics of these syndromes. Table 3 lists common benign and dangerous causes of these categories of dizziness. The dizziness associated with posterior circulation strokes often falls into the category of AVS.  AVS is characterized by a rapid onset of vertigo, in addition to nausea/vomiting and gait unsteadiness.  AVS is often associated with head motion intolerance and nystagmus that can last for days to weeks.20

Table 3. Benign and Dangerous Causes of Dizziness14

Vestibular Syndrome Common Benign Cause Dangerous Cause(s)
Acute Vestibular Syndrome Vestibular neuritis Stroke
Triggered Episode Vestibular Syndrome BPPV Posterior Fossa Tumor
Spontaneous Episodic Vestibular Syndrome Vestibular migraine TIA, Cardiac Dysrhythmia

Peripheral vs. Central Causes of AVS

The differential diagnosis of AVS can be broken into peripheral and central causes. It is imperative the Emergency Physician consider central causes of vertigo. Central causes include those disorders that affect the structures of the central nervous system such as the cerebellum and the brainstem. The most common, dangerous central cause of AVS is a posterior circulation stroke. Peripheral causes are those that affect CN VIII and the vestibular apparatus.  The most common peripheral causes of AVS are vestibular neuritis and labyrinthitis.20 A list of signs and symptoms associated with peripheral and central causes is shown in Table 4. The Emergency Physician (EP) must keep in mind many of the distinguishing features of peripheral lesions may also be present in central lesions. For example, while auditory symptoms are typically associated with peripheral processes, their presence does not exclude a central process.21

The evaluation for stroke in AVS is particularly important in those patients who are older, have hypertension or cardiovascular disease, are on anticoagulation, or have other classic stroke risk factors.22 However, the EP must keep in mind younger age is not sufficient reason to exclude the potential diagnosis of stroke. It is estimated one in five strokes causing AVS affects a patient less than 50 years of age and one in ten patients less than 40 years of age.20 One study found 50% of patients misdiagnosed after suffering a posterior circulation stroke were under the age of 50.23 The overall mortality described by this study was 40%, with a 50% prevalence of significant neurological disability among the survivors.23 These findings convey the significance of thorough assessment for central pathologies in patients with AVS.

Table 4: Signs/ Symptoms Differentiating Peripheral and Central Vertigo22

Peripheral Central
Onset Sudden or Insidious Sudden
Severity of Vertigo Intense Spinning Ill-defined, may be severe or less intense
Prodromal Dizziness Occurs in up to 25%, often single episode Occurs in up to 25%, recurrent episodes suggest TIA’s
Intolerant of head movements/Dix-Hallpike Maneuver Yes Varies, but often intolerant
Associated Nausea/Diaphoresis Frequent Variable, but often frequent
Auditory Symptoms Points to peripheral causes May be present
Proportionality of Symptoms Usually proportional Often disproportionate
Headache/Neck Pain Unusual More likely
CNS signs/symptoms Absent Usually present
Head Impulse Test Abnormal Often normal
Nystagmus Horizontal Vertical/direction-changing
HINTS Testing Negative Abnormal in at least 1 out of 3 tests

Physical Exam

A focused neurological exam, including gait assessment, speech, and cranial nerves, in patients presenting with AVS is needed. Focal neurological deficits are consistent with a central cause of AVS. However, the absence of neurological deficits does not exclude a central cause. One review of AVS secondary to strokes found focal neurological deficits were present in 80% of cases.24 Additionally, Dix-Hallpike testing, while effective in diagnosing BPPV (a cause of triggered episodic vestibular syndrome), provides no diagnostic utility in the assessment of AVS.14 A potential tool for the Emergency Physician in evaluating patients with AVS is the HINTS examination.

HINTS Testing

HINTS testing is a three-part examination that consists of head impulse testing, nystagmus assessment, and test of skew. This test is the gold standard for diagnosis of posterior circulation strokes, as its sensitivity is higher than any imaging modality in the first 24-48 hours after symptom onset.  The HINTS test should  be used in patient complaining of continuous feelings of vertigo or dizziness, where concern for AVS is present.  It is not useful in patients with momentary position-related vertigo or patients with TIAs who are not dizzy when examined.25 For a great overview, see EMCrit at

The first component of the HINTS test is head impulse testing.  Head impulse testing consists of having the patient visually fixate on a target followed by a rapid 40 degree head turn. This process is then repeated in the other direction. A unilateral abnormal finding (saccade) is consistent with a peripheral process and a normal response (no saccade) to this testing is consistent with a central process (Kattah, Edlow).14,20  This test is depicted in Figure 2 and an abnormal response is shown in Video 1.

Video 1: Abnormal Head Impulse Test

Screen Shot 2017-03-10 at 5.14.10 PM

The second component of the HINTS test is assessment of nystagmus, which analyzes the characteristics of nystagmus during lateral gaze at 45-60 degrees, not at end-gaze. Direction changing nystagmus is consistent with a central cause of AVS and unidirectional horizontal nystagmus is more consistent with a peripheral cause. Assessment of nystagmus is specific but not sensitive for a central cause of AVS.22 Vertical or torsional nystagmus in a patient with AVS is a sign of a central etiology.  However, strokes presenting with AVS may have a normal (horizontal) finding of nystagmus.20 A study by Lee et al. found that approximately half of pseudolabyrinthine strokes present with unilateral, horizontal findings of nystagmus.26

The final component of the HINTS test is the test of skew, which assesses ocular misalignment. This is determined using the alternating cover test, which consists of covering one eye and then assessing for any movement/re-fixation when the eye is uncovered. Any realignment is consistent with a central process. An abnormal test of skew is shown in Video 2. This test is also specific but not sensitive for central causes of AVS.22

Video 2: Abnormal Test of Skew

A helpful mnemonic for the HINTS testing results that are consistent with central causes is INFARCT (Impulse Normal, Fast-phase Alternating, Refixation on Cover Test).20

Table 5.  INFARCT mnemonic for HINTS findings suggestive of central cause of vertigo.20

INFARCT mnemonic
Impulse Normal
Fast-phase Alternating
Refixation on Cover Test

Buyers Beware…

Many of the studies evaluating the HINTS exam utilized neuro-ophthalmologists with specialized equipment and training, often in patients not in the ED. Thus, translating this to regular ED practice must be done with caution. A slow-motion camera (there are several apps available for phone use) can assist in detecting subtle ocular findings. More studies are needed evaluating the HINTS exam conducted by emergency physicians on ED patients. For more potential pitfalls in the ED, please see EMCrit at


What is the role of imaging in the ED evaluation of patients with vertigo?  Patients with physical exam findings concerning for a central process require urgent imaging to assess for hemorrhage, infarction, or tumor.22 In regards to the type of imaging, MRI in addition to CT is preferred due to poor visualization of the posterior fossa with CT.27 The sensitivity of brain CT for posterior circulation infarcts is only 7-42%.28-31 However, even a negative MRI does not rule out a posterior circulation stroke in patients with a high clinical suspicion for a central cause.  MRI with DWI within the first 48 hours of infarction may miss up to 10-20% of posterior circulation strokes.32

The most important tool to evaluate for a central cause in patients with AVS is the HINTS exam performed by an experienced physician.  In the evaluation of posterior circulation stroke, Kattah et al. examined the various methods for diagnosis, shown in Figure 3.20 An abnormal HINTS test has been shown to be 100% sensitive and 96% specific for the detection of central causes of AVS, making it more sensitive than even MRI in the first 24-48 hours.20  Furthermore, a brain MRI takes at least 5-10 minutes to conduct not considering wait time, in addition to thousands of dollars in cost.  The HINTS test can be done in minutes at no additional cost.

Figure 3.  Diagnostic Modalities for Posterior Circulation Stroke20

Screen Shot 2017-03-10 at 5.14.30 PM


In considering the disposition of these patients, Edlow et al. in 2015 recommended disposition criteria.14 They recommended a patient presenting with AVS is likely safe to go home if:

  • Patient is able to sit and stand independently
  • Patient has no cranial or cerebellar signs
  • Patient has HINTS testing suggestive of a peripheral process

 HINTS exam results indicative of peripheral vertigo are unidirectional, horizontal nystagmus, unilaterally abnormal head impulse test, and normal vertical eye alignment (no skew).  Together, these findings reduce the odds of a stroke by at least 50 fold.24

Pearls and Pitfalls


  • Clarify what the patient means by dizziness regarding timing and triggers of the onset of symptoms. Distinguish dizziness from syncope or other mimicking conditions, as these will require a different work-up.
  • Suspect a central etiology in patients with acute vestibular syndrome. Evaluate with the HINTS exam.
  • Use the HINTS test in patients presenting with Acute Vestibular Syndrome, as this is more sensitive than both CT and MRI for posterior circulation strokes.
  • Nystagmus is assessed during lateral gaze at 45-60 degrees, not at end-gaze. An abnormal response in a patient with AVS is vertical or torsional nystagmus. 
  • The HINTS exam should only be used in patients presenting with Acute Vestibular Syndrome, not patients with Triggered or Spontaneous Episodic Vertigo Syndrome.


  • Symptoms that worsen with movement do not confirm a peripheral process. Symptoms with movement may also exacerbate symptoms from a central process.
  • A normal head CT is not sufficient in excluding ischemic stroke.
  • MRI should not be relied upon in the initial 24-48 hours after symptom onset to rule out a posterior circulation stroke, as it may miss up to 10-20% of posterior circulation strokes.
  • Younger age does not exclude central causes of Acute Vestibular Syndrome. A stroke should still be suspected in patients younger than 50 if the physical exam is concerning for a central process.
  • Many of the classic distinguishing features of peripheral lesions are also found in central lesions.

Case Resolution

You return to the room of the 38 y/o female with dizziness to gather a more detailed history and physical.  You determine that the patient’s dizziness began yesterday morning after she awoke, was constant all day yesterday, and has not resolved today.  She has experienced difficulty walking since yesterday and is still feeling dizzy currently.  Astutely categorizing this patient as exhibiting AVS, you conduct a HINTS exam in addition to a neurologic exam.  The HINTS exam is notable for direction-changing nystagmus and a positive test of skew.  Concerned for a central etiology of this patient’s vertigo, you order a brain MRI in addition to consulting neurology for further workup and management.


This post is sponsored by, a supporter of FOAM and medical education, who with their sponsorship are making FOAM material more accessible to ER physicians around the world.

Screen Shot 2017-03-12 at 5.28.13 PM

References/Further Reading

  1. Lozano R, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010.
    Lancet. 2012 Dec;380(9859):2095-128.
  2. Mozaffarian D et al.  Heart Disease and Stroke Statistics-2016 Update: A Report From the American Heart Association
  3. Savitz S, Caplan L. Vertebrobasilar Disease. N Engl J Med 2005;352:2618-26
  4. Ferro JM, Pinto AN, Falcao I, et al. Diagnosis of stroke by the nonneurologist: a validation study. Stroke 1998;29:1106-9.
  5. Kerber KA, Brown DL, Lisabeth LD, Smith MA, Morgenstern LB. Stroke among patients with dizziness, vertigo, and imbalance in the emergency department: a population-based study. Stroke. 2006;37: 2484–2487.
  6. Caplan LR, Wityk RJ, Glass TA, et al. New England Medical Center Posterior Circulation Registry. Ann Neurol 2004;56:389-98.
  7. Bogousslavsky J, Van Melle G, Regli F. The Lausanne Stroke Registry: analysis of 1,000 consecutive patients with first stroke. Stroke 1988;19:1083-92.
  8. Moulin T, Tatu L, Vuillier F, Berger E, Chavot D, Rumbach L. Role of a stroke data bank in evaluating cerebral infarction subtypes: patterns and outcome of 1,776 consecutive patients from the Besancon Stroke Registry. Cerebrovasc Dis 2000;10:261-71.
  9. Vemmos K, Takis C, Georgilis K, et al. The Athens Stroke Registry: results of a five-year hospital-based study. Cerebrovasc Dis 2000;10:133-41.
  10. Crocco T, Goldstein J. Stroke. In Marx J, Hockberger R, Walls R. Rosen’s Emergency Medicine. 2014; 8: 1363-1374.
  11. Go S, Worman D. Stroke Syndromes. In: Tintinalli JE, Stapczynski J, Ma O, Yealy DM, Meckler GD, Cline DM. eds. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e. New York, NY: McGraw-Hill; 2016.
  12. Searls  DE, Pazdera  L, Korbel  E, Vysata  O, Caplan  LR: Symptoms and signs of posterior circulation ischemia in the New England Medical Center Posterior Circulation Registry. Arch Neurol. 2012; 69: 346.
  13. Bradley  WG, Daroff  RB, Fenichel  GM, Marsden  CD (eds): Neurology in Clinical Practice, 4th ed. Philadelphia, PA: Butterworth-Heinemann; 2004.
  14. Edlow JA, Newman-Toker D.  Using the Physical Exam to Diagnose Patients with Acute Dizziness and Vertigo.  J Emerg Med.  2016 Apr 50(4):  617-28.
  15. Drachman DA, and Hart CW: An approach to the dizzy patient. Neurology 1972; 22: pp. 323-334
  16. Kerber KA, Newman-Toker DE. Misdiagnosing dizzy patients: common pitfalls in clinical practice. Neurol Clin 2015;33:564–76
  17. Newman-Toker DE, Edlow JA. TiTrATE: a novel approach to diagnosing acute dizziness and vertigo. Neurol Clin 2015;33:577–99.
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Toxcard: DigiFab for Digoxin Toxicity

Author: Adriana Garcia, MD (Fidel Velázquez Sánchez Hospital) // Edited by: Cynthia Santos, MD (Senior Medical Toxicology Fellow, Emory University School of Medicine), Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)


 A 73 y/o female with PMH of dementia, CHF, and atrial fibrillation presents with confusion, abdominal pain, nausea and vomiting. She is unable to provide a history due to her dementia and AMS. Vitals: BP 160/80 mmHg HR 60 T 36° RR 18. Her EKG demonstrates AV block. Na 140 K 5.3 Cl 105 CO2 20 BUN 40 Cr 2.1. Her digoxin level is 5ng/mL and she weighs 50 kg.


What dose of Digoxin-specific antibody fragments (DsFab) should you use? How do you administer it?


The dose of DsFab can be estimated in three ways 1) a formula if the dose is known 2) a formula if a serum digoxin level is known or 3) use of an empiric dose. 

1) If amount ingested is known:
  • In an acute overdose the # of vials can be calculated based on the ingested dose. Each vial neutralizes approximately 0.5mg of digoxin.[1,2]

Number of vials=   [(amount ingested in mg) x (0.8 bioavailability)]/(0.5 mg/vial)                                                                    

  • Note: The bioavailability for digoxin tablets is 0.8 and for digoxin capsules it is 1.[1]
  • The table below can also be used as a quick reference to calculate # of vials.
dig table
 Table source:
2) If serum digoxin level is known:

Number of vials=    [(serum digoxin level in ng/ml) x (weight in kg)]/100                                                                            

For our case, # of vials = 5 ng/ml x 50 kg/ 100 = 2.5

3) Emergent situations:

  • In an emergent situation involving an acute ingestion of unknown amount, 10 vials can be given initially for both adults and children. Observe for a response and can repeat with another 10 vials as needed. Monitor for volume overload in children.
  • In an emergent situation involving a chronic ingestion of unknown amount, 3-6 vials can be given for adults and 1-2 vials can be given for children.[1,2]

Indications for DsFab:

  • life-threatening dysrhythmia,
  • hyperkalemia: K+ > 5.0 mEq/L,
  • [digoxin] > 15 ng/ml at any time or > 10 ng/ml 6 hours post ingestion, regardless of clinical effects,
  • chronic elevation of [digoxin] associated with dysrhythmias, significant GI symptoms, or AMS,
  • acute ingestion of 10 mg in an adult or 4 mg in a child,
  • poisoning by non-digoxin cardiac glycoside. [2]

Note: In chronic poisoning, both the potassium and digoxin level may be NORMAL. In fact, it chronic overdoses the potassium level is often decreased.

Administrating DsFab:

  • Each 40mg vial of DigiFab (which binds 0.5 mg digoxin) should be reconstituted with 4 mL sterile water to yield an isosmotic solution with a concentration of 10 mg/mL.
  • The reconstituted solution can be diluted in normal saline to an appropriate volume for administration.
  • Infuse over at least 30 minutes.
  • If cardiac arrest is imminent a bolus injection can be given.
  • The reconstituted solution should be used immediately, if not it can be refrigerated and used within 4 hours.
  • Adverse effects of DigiFab include hypokalemia (K should be monitored frequently) and worsening atrial fibrillation or congestive heart failure. Anaphylaxis is rare.[1,3]
  • Measuring total serum digoxin concentration after DsFab will not be useful since it represents the free plus bound digoxin. Free digoxin concentrations are more clinically useful but they are more difficult to perform, sometimes erroneous  and are not readily available. The patient’s cardiac status should be monitored for signs of recurrent toxicity.[3]

Note: DsFab is only available in the U.S. as DigiFab since 2011. Previously, Digibind was available and used successfully but was discontinued in 2011 when DigiFab came on the market. They are both very similar except that DigiFab is prepared using the digoxin derivative as the hapten.[3]

Main point:

The # of vials of DsFab can be calculated based on the amount ingested for acute overdoses or the digoxin serum concentration in chronic overdoses. In emergent situations where the ingested dose or the serum level is unknown 10 – 20 vials is the recommended for acute ingestions and 3-6 vials for chronic ingestions. Each vial of Digoxin Fab should be reconstituted in 4 mL of sterile water and given slowly over at least 30 minutes. Unless in cardiac arrest, in which a bolus injection can be given. Watch out for hypokalemia and worsening a fib or CHF with Digoxin Fab administration. Don’t rely on measuring digoxin levels after giving DigiFab; the patient’s cardiac status should be monitored for signs of recurrent toxicity.

  1. Micromedex Drug Information, Digoxin Immune Fab. Available at:
  2. Hack J. Cardioactive steroids (Chapter). In Goldfrank’s Toxicological Emergencies, 11th edition (2015). Editors: Hoffman R, Howland M, Lewin N, Nelson L, Goldfrank L. McGraw Hill; New York.
  3. Howland M. Antidotes in depth: Digoxin-Specific Antibody Fragments (Chapter). In Goldfrank’s Toxicological Emergencies, 11th edition (2015). Editors: Hoffman R, Howland M, Lewin N, Nelson L, Goldfrank L. McGraw Hill; New York.