Tag Archives: #FOAM

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.

Takeaways:

  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.

    References:

    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.”

EM Mindset: Longevity

Author: Loice A. Swisher, MD (EM Attending Physician, Mercy Philadelphia Hospital, Drexel University, College of Medicine) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

It was the waning few hours of my 3rd year resident’s sixth twelve hour shift.  There were a handful of drunken men sleeping on stretchers, likely to metabolize to freedom by the time the sun rose.  A couple asthmatics were sitting on chairs getting a breathing treatment, as they had run out of their inhalers.  A patient with knee pain for two years was just registering.  Then the ambulance doors opened letting forth sounds that would put screaming banshees to shame.  The accompanying officers in blue yelled, “running in and out of traffic naked; probably PCP.”  The resident, who had been doing admirably, sputtered “How have you been doing this for a quarter of a century?  How does this not get to you? “Her eyes silently pleaded, “What is the secret?”

Sure, the question regarding burnout was frequently bantered about thirty years ago when I was a 3rd year medical student considering this new specialty as my career.  The ‘party line’ so to speak was that few in emergency medicine at that time actually chose and trained for this field.  It was likely many, if not most, came to EM after ‘burning out’ in their chosen specialty.  Thus, they were already essentially behind the 8-ball when they moved their job to the emergency department.  We wouldn’t be at such risk.  We were going into this with eyes wide open.  We were trained for exactly the situations we would encounter.  We would know all the pitfalls, plateaus, and rewards.  We would be able to deftly negotiate the punishment of shiftwork, chaos, and lack of control to be able to leave the hospital enjoying life without being on call.  We got this.

Burnout has increasingly entered conversation, ever since the landmark 2012 article by Shanafelt showing nearly half of physicians at that time suffered from at least one symptom of burnout [1].  Since that time emergency medicine has consistently taken either the first or second spot within the house of medicine [2,3,4,5].  I was wrong.  We don’t ‘got this’.

The resident’s question was a fair one.  How does one have longevity and sustain passion in this line of work?  How do we avoid burnout from the systemic pressures piled on us?  How do we combat compassion fatigue or PTSD from constant flow of people being seen on the worst days of their lives?

At that moment, I desperately wished I had an answer.  Given the luxury of time for reflection, I came up with my top three.

  1. Find a passion: This is true both within and outside of work. I love to travel.  It gives me something to plan and dream about.  It is an identity outside the hospital.  What matters most is that it is something that brings you satisfaction and a sense of joy or worth.
  1. Identify someone to talk to: There is tough stuff in what we do. Sharing stories can decrease the intensity of emotions.  Knowing one is not alone is key to human existence.
  1. Carefully craft your mantras: A mantra is generally thought to be a repeated word or phrase that is a ‘sacred utterance’ which one tells themselves. It comes from “man” for mind and “tra’ for transport.  Thus, these words transport the mind to a vantage point with which we view the world.  The words we tell ourselves can change the way we see the world.

Returning to that resident, I wanted to say there are several things that keep me doing this, but in those moments the strongest one is the soundtrack in my mind.  You can create phrases that make patients seem like enemies, or you can develop others that reorient the world.

When those ambulance doors open unleashing ungodly sounds, my first thought is, “sounds like one of my kids.”  When I get out of my car for my shift I tell myself, “Tonight I have the opportunity to relieve pain and suffering. What could be better than that?”  Throughout the shift I tell myself “Emergency medicine is the last best place in medicine.”  And I mean every single one of them.

References / Further Reading:

[1] Shanafelt TD, Boone S, Tan L, et al.   Burnout and satisfaction with work-life balance among US physicians related to the general US populations. Arch Intern Med. 2012 Oct:172(18)1377-1385.

[2]http://www.medscape.com/features/slideshow/lifestyle/2017/overview accessed March 8, 2017.

[3]http://www.medscape.com/features/slideshow/lifestyle/2016/public/overview#page=2 accessed March 8, 2017.

[4]http://www.medscape.com/features/slideshow/lifestyle/2015/public/overview#2 accessed March 8, 2017.

[5]http://www.medscape.com/features/slideshow/lifestyle/2013/public#2 accessed March 8, 2017.

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) 

toxcard

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.

Question:

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

Pearl:

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:

HYPERTHERM

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.

References:

  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.

Epidemiology

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

History
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

Nerves
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: https://www.dartmouth.edu/~humananatomy/about/credits.html
Figure 1. Cutaneous Nerve Supply of the Hand
O’Rahilly R. Basic Human Anatomy: Chapter 10: The Hand. 2008. Available from: https://www.dartmouth.edu/~humananatomy/about/credits.html

Vascularity

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

Alignment

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: http://www.seattlechildrens.org/healthcare-professionals/resources/case-studies/finger-fractures-dont-forget-rotation/
Figure 2. Assessment of Malrotation
Steinman S. Seattle Children’s Hospital Finger Fractures: Don’t Forget the Malrotation. 2017. Available from: http://www.seattlechildrens.org/healthcare-professionals/resources/case-studies/finger-fractures-dont-forget-rotation/

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: http://www.orthobullets.com/hand/6008/physical-exam-of-the-hand#
Figure 3. Froment’s Test
Ujash S. Physical Exam of the Hand. 2017. Available from: http://www.orthobullets.com/hand/6008/physical-exam-of-the-hand
Figure 4. Positive Jeanne's Test Ujesh, S. Physical Exam of the Hand. 2017. Available from: http://www.orthobullets.com/hand/6008/physical-exam-of-the-hand
Figure 4. Positive Jeanne’s Test
Ujesh, S. Physical Exam of the Hand. 2017. Available from: http://www.orthobullets.com/hand/6008/physical-exam-of-the-hand

Imaging

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: https://www.aliem.com/2011/tricks-of-trade-underwater/
Figure 5. Water Bath for Hand US
Lin, Michelle. Tricks of the Trade: Underwater Ultrasonography. 2011. Available from: https://www.aliem.com/2011/tricks-of-trade-underwater/

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

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

Pearls:

  • 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: http://www.orthobullets.com/hand/6008/physical-exam-of-the-hand#
  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 

References:

  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:
http://www.emdocs.net/leftmainstemi/
http://www.emdocs.net/hyperacute-t-waves/
http://www.emdocs.net/ber-vs-anterior-stemi/

ST Elevation in aVR:
http://www.emdocs.net/r-e-b-e-l-em-st-segment-elevation-lead-avr-getting-much-respect-amal-mattu/

Risk Stratification:
http://www.emdocs.net/chest-pain-controversies-risk-stratification-stress-test-utility-part-1/
http://www.emdocs.net/chest-pain-controversies-coronary-cta-use-part-2/

Management of Low-Risk Chest Pain:
http://www.emdocs.net/r-e-b-e-l-em-management-and-disposition-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


References:

  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

EM Mindset: Reading My Mind

Author: Judith E. Tintinalli, MD MS (Professor of EM / Chair Emeritus, Department of EM, University of North Carolina) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UT Southwestern Medical Center / Parkland Memorial Hospital) and Brit Long, MD (@long_brit)

A style of working, teaching, and learning in Emergency Medicine takes time to develop.   We don’t get much opportunity to see how our colleagues operate, except perhaps on change-over rounds, which are always pressed for time, and which don’t allow for discussions about why different attendings do things differently.  I’ve always thought of myself as a middle-of-the roader in our group: middle in terms of times, patients/hr, decisions to admit versus discharge. But I’m pretty good at documentation, work generally on the careful and compassionate side, can work at the speed of light when necessary, and have learned from the past so hopefully current mistakes are few and far between.

So, step into my office and I’ll share with you some of my habits, behaviors, and opinions that I’ve developed over the years.

Supervising Learners

Working in an academic medical center has great rewards.  Being surrounded by shadowers, medical students, and residents of all specialties keeps you on your toes. Medicine has moved from time-lapse to fast-forward, and residents who have recently completed inpatient rotations are terrific sources of changes in specialty practice patterns.  But the growing number of learners you are responsible for on a shift can be intellectually overwhelming and certainly slows down the process of patient care.  A different approach is needed for each level, so that one can loosen (but never eliminate) the level of supervision for the most senior learners.

I start my shifts explaining how to structure presentations. The goal is to get a good mental picture of the patient – ill-appearing, obese, amputee, in pain, blind or deaf, angry, demanding.  Then a concise statement of the triage note and patient’s problem, but with a listing of key meds/conditions that will affect the ED workup.  ‘This is a 65 year old patient with atrial fibrillation on Xarelto with 2 hrs of acute abdominal pain’.  Key meds for me are antithrombotics, immunosuppressives, steroids, insulin.  I’ll never forget a ‘routine’ intern presentation of a 65 year old woman who fell at home, and now had a femur fracture. When I went to evaluate her, I was aghast at not being told she had a heart transplant and had severe COPD requiring home oxygen.  How many times have I been told confidently that vital signs were ‘rock stable’, only to find a pulse rate of 120 or a BP of 230/170.

So, focused and concise presentations help a busy attending prioritize which patients need to be seen as soon as possible. They also teach learners how to present to consultants.

Teaching in the ED

There’s a growing body of EM literature that focuses on clinical teaching in the busy ED.  Each of us has to develop our own style.  I like to ask for the main, and then major differential diagnoses, before the learner spews out the orders, so the learner can demonstrate why each order is needed. I keep trying to minimize laboratory orders, but one of our jobs is to let each learner order stuff, and with experience, to be able to gain confidence in clinical judgement and stop ordering unnecessary labs and imaging. That is a trial and error process. One good tool is to ask the resident ‘If this patient came into your office, would you send them to the ED to get these lab tests or imaging?’

One of the best teaching tools I use is to ask a question that I myself cannot answer.  Like – ‘OK this person with prior DVT and PE is on Xarelto, and now we’re concerned about another PE. What’s the failure rate for Xarelto and does this patient have any risk factors for failure?’  Another tool is to come armed with a recent article you’ve read, ready to whip it out when needed.   For example, our residents like to order stress tests out of the ED for patients with low probability chest pain, because we have a protocol, but ask them ‘why’, ‘how’, or ‘what does it cost the patient’ and you’re met with silence.  So for a while I kept a copy of Long and Koyfman’s article  ‘Current Controversies in the Evaluation of Low Risk Chest Pain (JEM Dec 2016)’ in my doctor bag,  let them see the current data on the topic, and then give the opportunity to re-evaluate their decision.   Another one I kept with me recently was the recent study on single-dose decadron 12 mg po for adults with mild-moderate asthma.  As residents don’t read journals anymore, it gives them the opportunity to at least read a journal abstract.

Procedures and Consultations

In emergency medicine, we’ve structured our residency programs so the majority of learning and teaching is in tertiary care centers.  Consider the disadvantages: where specialty consultants are available 24/7, it can be a lot easier to call ortho to reduce a hip, evaluate a fracture or tap a joint, to call GU to place a difficult Coude catheter, or to have neurology decide who gets tPA for possible stroke.  The community EM practices that most of our residents will select after graduation will typically have a very limited menu of emergency consultants, and I’m not sure we are training them well for these environments.  I always have residents think through their treatment plans before calling the consultant, as this is their future reality.  I remember during the early days of EM training, moonlighting was really frowned upon.  The philosophy was that the only time anybody cared about resident learning was during residency, so every minute should be spent reading, seeing patients, and learning.  The medical environment has changed, and our senior residents get invaluable experience moonlighting that we cannot give them in a tertiary care environment.

Disposition and Follow-Up

This is where I think attendings and residents diverge.  I explain that everyone, learner or attending, has his or her own inherent ability to tolerate uncertainty.  If a resident strongly wants to admit a patient that I feel can be safely discharged, I challenge him or her to present the case to the admitting team. This gives a chance to practice skills needed in a community ED setting.  Another area of divergence is how far to go to exclude specific diagnoses in the ED. In our current medical care system, where so many patients have no insurance, giving them a clean bill of health in the ED means a lot. So ultrasounds, MRIs, and CT scans, and sometimes consultations in the ED to provide a clear follow-up plan, are more and more part of routine management.  Disposition requires a lot of stepped-thinking. Recently I took over a shift where a young Spanish-speaking woman came into the ED with a disc of a head CT identifying a brain tumor. Imaging had been done at an outside community hospital without neurosurgeons, and the patient was told to make an appointment with a neurosurgeon.  Mystified, she came into the ED.  Her discharge had already been written by the previous shift team, and the phone number of neurosurgery clinic was provided.  We held the discharge and consulted neurosurgery.  The CT was reviewed, an MRI was then done, decadron and Keppra were recommended by the neurosurgeon, and a clear follow-up was arranged in 3 days in neurosurgery clinic.  These steps would be very difficult to manage as an outpatient, where waits for an MRI can be weeks; payment is required before testing; the clinic appointment team may or may not speak Spanish; and it can take weeks to get an appointment in an overburdened neurosurgery clinic.  Another important principle I try to teach is ‘we cannot predict the future’.  Residents will sometimes say, oh, why get this specialized imaging; why call the consultant, they won’t do anything; why try for admission – there’s an easy answer.  I cannot predict the future – can you?

Why I love Emergency Medicine

A recent JAMA article reported that emergency medicine has the highest burn-out and fatigue rate of any other specialty.  If that is so, why are medical students flocking to our residency programs? Not every shift is wonderful – some are exhausting, filled with contentious problems or patients. Most times I look forward to a shift, but sometimes it is hard to put one foot in front of the other as I walk to my desk.  But I think all of us would rather be emergency physicians rather than anything else.  We have the unique ability to help patients when they are most vulnerable.  We have to establish rapport within minutes, not weeks or months.  We work in a terrific team environment.  We learn to be flexible, can calm down irritable consultants, and like to make fast decisions.  We can work a lot of shifts or fewer shifts. We don’t carry our patient burdens home with us. Life is good.

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?

Background

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 https://emcrit.org/podcasts/posterior-stroke/.

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 https://emcrit.org/emnerd/adventure-veiled-lodger/.

Imaging

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

Disposition

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

Pearls

  • 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.

Pitfalls

  • 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 www.ERdocFinder.com, a supporter of FOAM and medical education, who with their sponsorship are making FOAM material more accessible to ER physicians around the world.

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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.
  18. Newman-Toker DE, Cannon LM, Stofferahn ME, Rothman RE, Hsieh YH, Zee DS. Imprecision in patient reports of dizziness symptom quality: a cross-sectional study conducted in an acute care setting. Mayo Clin Proc 2007;82:1329–40.
  19. Bisdorff A, Staab J, Newman-Toker D. Overview of the international classification of vestibular disorders. Neurol Clin 2015;33: 541–50.
  20. Kattah  JC, Talkad  AV, Wang  DZ, et al.: HINTS to diagnose stroke in the acute vestibular syndrome: three-step bedside oculomotor examination more sensitive than early MRI diffusion-weighted imaging. Stroke. 2009; 40: 3504.
  21. Lee  H, Kim  JS, Chung  EJ, et al.: Infarction in the territory of anterior inferior cerebellar artery: spectrum of audiovestibular loss. Stroke. 2009; 40: 3745.
  22. Goldman B. Vertigo. 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.
  23. Savitz  SI, Caplan  LR, Edlow  JA: Pitfalls in the diagnosis of cerebellar infarction. Acad Emerg Med. 2007; 14: 63.
  24. Tarnutzer  AA, Berkowitz  AL, Robinson  KA, et al.: Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome. CMAJ. 2011; 183: E571.
  25. Caplan LR. Posterior circulation cerebrovascular syndromes. https://www.uptodate.com/contents/posterior-circulation-cerebrovascular-syndromes. Accessed February 22, 2017.
  26. Lee H, Sohn SI, Cho YW, et al. Cerebellar infarction presenting isolated vertigo: frequency and vascular topographical patterns. Neurology 2006;67:1178–1183.
  27. Kerber  KA, Schweigler  L, West  BT, et al.: Value of computed tomography scans in ED dizziness: analysis from a nationwide representative sample. Am J Emerg Med. 2010; 28: 1030.
  28. Chalela JA, Kidwell CS, Nentwich LM, et al. Magnetic resonance imaging and computed tomography in emergency assessment of patients with suspected acute stroke: a prospective comparison. Lancet 2007;369:293–8.
  29. Hwang DY, Silva GS, Furie KL, Greer DM. Comparative sensitivity of computed tomography vs. magnetic resonance imaging for detecting acute posterior fossa infarct. J Emerg Med 2012;42:559–65.
  30. Kabra R, Robbie H, Connor SE. Diagnostic yield and impact of MRI for acute ischaemic stroke in patients presenting with dizziness and vertigo. Clin Radiol 2015;70:736–42.
  31. Ozono Y, Kitahara T, Fukushima M, et al. Differential diagnosis of vertigo and dizziness in the emergency department. Acta Otolaryngol 2014;134:140–5.
  32. Saber Tehrani AS, Kattah JC, Mantokoudis G, et al. Small strokes causing severe vertigo: frequency of false-negative MRIs and nonlacunar mechanisms. Neurology 2014;83:169–73.