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CITW 15: The Red Ear

Welcome back to another Clinical Image of the Week from the case files of the Brown EM Residency!

HPI/ROS: 5 year old female with a history of recurrent otitis media who presents to the ED with right ear pain. Per the parents, she developed acute onset right ear pain and “redness” one week ago that was associated with fevers (Tm 103.2). She saw her pediatrician who started a course of Augmentin for otitis media, however, after three days of no improvement, she received IM antibiotics (unknown type) with only minimal improvement in symptoms. On the day of ED presentation, her ear redness had worsened and she had developed limited range of motion of the head and neck. Associated symptoms included headache, hearing loss, and sore throat. No congestion, runny nose, conjunctivitis, visual changes, numbness, weakness, discoordination, cough, dyspnea, wheezing, abdominal pain, vomiting, diarrhea, or rash. No sick contacts or recent travel. Shots are up to date.

Vital Signs: T 102.3, HR 156, RR 22, BP 118/72, SpO2 99% on RA

Pertinent physical exam: Patient found sitting on her mother’s lap, not playful or interactive. Right TM is erythematous and bulging. There is edema and erythema noted behind the right auricle with tenderness to palpation. Shotty cervical chain adenopathy appreciated. No ear discharge. Left TM is clear. Oropharynx is clear with moist mucous membranes. No focal or gross neurological deficits. No meningismus. Neck is supple. Heart is tachycardic. Abdomen soft, non-tender. Lungs clear to auscultation. No rashes. No other pertinent exam findings.

CT imaging was obtained:

Mastoiditis 1
Image 1: CT brain, axial cuts in bone window.
Mastoiditis 2
Image 2: CT brain, coronal cuts in bone window.

What’s the diagnosis?

Continue reading

Atrial Fibrillation, You’re a Heart Breaker, Dream Maker, Love Taker:

But At Least There is Low Risk for Thromboembolic Events With Speedy Conversion to Sinus Rhythm…

This post reviews the article from Weigner, Marilyn et al. “Risk for Clinical Thromboembolism Associated with Conversion to Sinus Rhythm in Patients with Atrial Fibrillation Lasting Less Than 48 Hours,” from the Annals of Internal Medicine in 1997 as part of the ongoing 52 article series.

Main Points:

  1. This article reveals only a 0.8% risk of clinical thromboembolic event for patients who were clinically estimated to be in atrial fibrillation for less than 48 hours.
  1. This trial data supports the recommendation for early cardioversion, either pharmacologic or through electric cardioversion, in patients with recent onset of symptoms without the need for prior diagnostic imaging to evaluate for clot burden.


Atrial fibrillation is a common arrhythmia and responsible for over 250,000 hospital admissions annually. Patients often feel the effects of depressed cardiac output from the loss of atrial systole and seek medical attention in hopes of improved quality of life. Patients may describe a range of symptoms including palpitations, dyspnea, dizziness, angina and fatigue. Studies have demonstrated that patients with atrial fibrillation for more than two days may have a greater than five percent risk of clinical thromboembolism and often require weeks of anticoagulation or screening with transesophageal echocardiography prior to cardioversion. This study sought to answer the question of whether or not patients who experienced only a short duration of symptoms were low risk for thromboembolic disease.


This was a prospective study of consecutive patients at two academic medical centers, Beth Israel Deaconess Medical Center in Boston, MA and the John Dempsey Hospital and University of Connecticut Health Center in Farmington, CT. 1822 adult patients with a diagnosis of atrial fibrillation were screened and 375 patients who were clinically estimated to have symptoms for less than 48 hours were enrolled. Those patients whose duration of symptoms were unclear or had already initiated long term anticoagulation with warfarin were excluded. Patients with a previous history of thromboembolic events were not excluded, but one patient who had an acute thromboembolism was not enrolled in the trial. Clinical and transthoracic echocardiography data and outcomes were collected from review of the medical records. Clinical embolic events were considered if they occurred during the index hospitalization or within one month after conversion to sinus rhythm. Conditions that may have predisposed patients to atrial fibrillation included: previous history of atrial fibrillation (181 patients, 48.3%), hypertension (156, 41.7%), coronary artery disease (114, 30.4%), infection (25, 6.7%), history of thromboembolism (23, 6.1%), excessive alcohol use (22, 5.9%), rheumatic heart disease (7, 1.9%). Patients were noted to have left atrial dimensions of 4.2 +/- 0.7cm (normal ≤ 4.0cm) and a left atrial length of 5.7 +/- 0.7cm (normal ≤ 5.2cm) based on transthoracic echocardiogram data. 218 out of 280 patients who had echocardiograms performed were noted to have at least some evidence of mitral valve regurgitation with 61 patients noted to have either moderate or severe regurgitation.

Patients converted back to a normal sinus rhythm either spontaneously or through pharmacologic or electric cardioversion methods. Conversion was considered spontaneous if it occurred without the use of medications or electricity or in the setting of use of ventricular rate-controlling agents (digoxin, beta-blockers, and calcium channel blockers).

Three patients (0.8%, 95% CI 0.2-2.4) were noted to have a clinically significant thromboembolism and surprisingly all converted spontaneously. The cases included a left parietal embolic stroked in an 86 year old female with history of hypertension; a right proximal brachial artery embolus in an 83 year old female with coronary artery disease; and a transient ischemic attack in an 89 year old female with a recent diagnosis of pneumonia.

This study was a consecutive series that relied on both real time data gathering as well as retrospective chart review.

Level of Evidence:

This study was graded a level II based on the ACEP Clinical Policy Grading Scheme for prognostic questions and had only minimal methodological flaws.


The three patients in this trial were identified as having increased risk for thromboembolism based of the Stroke Prevention and Atrial Fibrillation Study I and II, however, how best to achieve post conversion anticoagulation in the era of direct oral anticoagulants remains a hot topic for further study and debate.

Relevant articles:

Mookadam, M. Shamoun FE. Mookadam, F. “Novel Anticoagulants in Atrial Fibrillation: A Primer for the Primary Physician.” J Am Board Fam Med, 2015, 28(4):510-22

Source Articles:

Weigner, M. Caulfield, T. Danias, P. et al. “Risk for Clinical Thromboembolism Associated with Conversion to Sinus Rhythm in Patients with Atrial Fibrillation Lasting Less Than 48 Hours.” Annals of Internal Medicine, 1997, (126):615-20.

Faculty Reviewer: Dr. Siket

Hold the Fluids: Rethinking Early Crystalloid Resuscitation in Penetrating Trauma

By: Dr. Maddie Boyle

This is part of a recurring series examining landmark articles in Emergency Medicine, in the style of ALiEM’s 52 Articles.

This blog post reviews the article by: Bickell WH, et al. Immediate Versus Delayed Fluid Resuscitation for Hypotensive Patients with Penetrating Torso Injuries. NEJM. 1994; 331 (17): 1105 – 1109.

Main Points:

  1. Early, large volume crystalloid resuscitation in the trauma patient with penetrating wounds and hypotension may lead to hydraulic disruption of a formed clot and a dilutional coagulopathy, thereby exacerbating hemorrhage and decreasing survival.
  1. Restricting isotonic fluids in the penetrating trauma patient with hypotension prior to operative intervention (where definitive hemorrhage control can be achieved) lead to higher survival rates when compared to those individuals treated with early, aggressive isotonic fluid resuscitation (70% vs 62%, p=0.04). This paper suggests a potential adverse effect from aggressive crystalloid administration and emphasizes the importance of prioritizing surgical management in the patient with hemorrhagic shock from penetrating trauma.


Historically, the standard approach for the trauma patient with hypotension has been aggressive volume resuscitation with crystalloid fluids in order to restore circulating volume and maintain organ perfusion. More recent studies suggest that aggressive crystalloid fluid administration prior to definitive hemorrhage control may be detrimental. Aggressive fluids in the bleeding patient may be deleterious for multiple reasons, most notably the risk of dislodging a softly form clot at the injury site with restoration of blood pressure and the risk of increased bleeding secondary to dilution of clotting factors when large volumes of crystalloid fluids are infused. Recent literature such as the PROPPR trial has investigated colloid based transfusion strategies, however, this study predates the data gathered from the recent Iraq and Afghanistan Wars.

The goal of this study was to evaluate fluid administration in hypotensive patients with penetrating torso trauma and determine whether delayed fluid-resuscitation (after operative intervention), compared to an early fluid administration conferred a survival benefit. Researchers performed a prospective, single center trial comparing immediate fluid resuscitation vs. delayed fluid resuscitation in patients with penetrating torso trauma with a pre-hospital systolic BP <90 mmHg requiring operative intervention for hemorrhage control. The study found a mortality benefit favoring delayed resuscitation: 70% of patients enrolled in the delayed-resuscitation group survived vs. 62% of patients in the immediate-resuscitation group (p=0.04). This study highlights numerous important questions regarding fluid strategy in the trauma patients, including the type of resuscitative fluid, the volume and timing of fluid administration. The results of this investigation continued to be queried today as research examines permissive hypotension and damage control resuscitation strategies in the trauma patient.


1: Adequate power.
2: Intention-to-treat analysis.


1: Semi-randomized, non-blinded.
2: Generalizability: Study population was largely young, healthy adult males.
3: Feasibility: The average time elapsed from ambulance call to operative intervention was approximately 2-hours for each study group. This type of rapid response and expedited time to operative intervention may not be attainable by many hospitals.
4: External validity: study cannot be applied to patients with blunt trauma, traumatic brain injury (where fluid resuscitation to achieve blood pressure control is paramount) or in those penetrating trauma patients with delayed presentation.
5: No mention of neurologic outcome with regards to survival benefit.


Prospective, single-center trial.

Population: Adults or adolescents (age ≥16 years) with gunshot or stab wounds to the torso who had a SBP ≤ 90 mm Hg in the field, including those patients with no blood pressure at the time of initial paramedic evaluation.

Patients were separated into two treatment groups based on the day of the month. Patients injured on even-numbered days were assigned to the immediate-resuscitation group, whereas those injured on odd-numbered days were treated in the delayed-resuscitation group. Patients in the immediate-resuscitation group received isotonic crystalloid (ringer’s acetate) en route, and those with SBP <100 mm Hg upon arrival in the ED received continuous infusion of crystalloid or pRBCs when necessary as determined by standards established by the American College of Surgeons Committee on Trauma. The delayed-resuscitation group did not receive fluids, regardless of clinical condition, outside of those small infusions required to keep lines patent. Otherwise, the two treatment groups were treated identically in terms of pre-hospital and trauma care. The average time from emergency dispatch to surgical intervention was approximately 130 minutes in both groups.

Surgical interventions were dictated by the injury and included thoracotomy within the ED, thoracotomy in the OR, laparotomy, neck exploration, and groin exploration. During surgical intervention, IV crystalloid and pRBCs were given as needed, independent of study group assignment in order to maintain SBP of 100 mm Hg, hematocrit ≥ 25% and urinary output ≥ 50 cc/hr in both treatment groups. The total volume of crystalloid and colloid fluids provided in the OR was not statistically different between the two study arms, however, the rate of intraoperative fluid administration was noted to be 117 +/- 126 for the immediate resuscitation group and 91+/- 88 for the delayed resuscitation group with a p value of 0.008.

The primary outcome measure was survival, defined as patients who did not die during hospitalization. Secondary outcome measures included six prospectively identified post-operative complications including: sepsis, coagulopathy, acute renal failure, ARDS, pneumonia and wound infection.

598 patients were ultimately considered for the study. 309 were enrolled in the immediate-resuscitation group and 289 in the delayed-resuscitation group. The patients were similar in their baseline demographics and clinical condition. Of the 598 patients, 70 died before operative intervention. The remaining 528 had an operative intervention: 260 patients in the delayed-resuscitation group and 268 patients in the immediate-resuscitation group.

The mean fluid administration prior to operative intervention in the immediate-resuscitation group was 2611 ml. The mean fluid administration prior to operative intervention in the delayed-resuscitation group was 386 ml.

The overall rate of survival was higher in the delayed-resuscitation group vs. immediate-resuscitation (70% vs 62%, p-0.04). The immediate-resuscitation group trended towards more intraoperative fluid loss (p=0.11) and required a higher rate of intraoperative fluid delivery in order to maintain SBP >100 (117 cc/hr vs. 91 cc/hr, p=0.008). There was a trend towards more complications (ARDs, pneumonia, etc.) in the immediate-resuscitation group compared to the delayed-resuscitation group (p-0.08), however, no definitive explanation for why this may have occurred was discussed.

The authors of this study propose that their results suggest that aggressive fluid administration in the patient with penetrating trauma should be delayed until the time of operative intervention. They suggest a risk for greater bleeding, hemodilution and coagulopathy with aggressive fluid administration. The authors acknowledge the limitations of their study, most importantly its inapplicability to blunt trauma patients and patients with severe head injuries, but advise similar studies in these groups in the future.

Level of Evidence:

Class II utilizing the ACEP grading scheme for therapeutic questions

Relevant articles:

Timing and volume of fluid administration for patients with bleeding
Hypotensive resuscitation strategy reduces transfusion requirements and severe postoperative coagulopathy in trauma patients with hemorrhagic shock: preliminary results of a randomized controlled trial.
PROPPR trial

Source Article:

Bickell WH, et al. Immediate Versus Delayed Fluid Resuscitation for Hypotensive Patients with Penetrating Torso Injuries. NEJM 1994; 331 (17): 1105 – 1109.


Resident Reviewer: Dr. Anatoly Kazakin
Faculty Reviewer: Dr. Matt Siket

CITW 14: The Blue Man

Welcome back to another Clinical Image of the Week from the case files of the Brown EM Residency!

HPI/ROS: 57 year old male with a history of bacterial endocarditis and hypertension presents to the ED for watery diarrhea. He reports gradually worsening diarrhea over the past three weeks after starting HIV post-exposure prophylaxis medications. He does not recall the names of the medications. He’s tried Imodium without relief. Associated symptoms include shortness of breath, nausea, and dizziness. Denies fevers, chills, chest pain, vomiting, abdominal pain, urinary symptoms, rashes, or swelling. He endorses recent antibiotic use for a sinus infection, but denies recent hospitalizations and other recent medication changes. He also endorses recent ETOH use, but denies illicit drug use.

Vital Signs: T 97.1, HR 114, RR 18, BP 121/75, SpO2 89% on RA

Pertinent physical exam: Ill appearing and diaphoretic. There is perioral and digital cyanosis (see below). 3/4 systolic heart murmur (chronic). Abdomen soft, non-tender. Lungs clear to auscultation. No other pertinent exam findings.

Cyanosis Pre
mage 1: Provider’s hand on the left, patient’s hand on the right. 

The patient was put on 100% O2 by non-rebreather and his SpO2 improved to only 90%.

What’s the diagnosis?

Continue reading

Time to Abandon Epinephrine for OHCA?

This is part of a recurring series examining landmark articles in Emergency Medicine, in the style of ALiEM’s 52 Articles.

Discussing: Wenzel, K. et al. A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med 2004;350(2):105-113.

Main Points:

  1. For out-of-hospital cardiac arrest (OHCA), vasopressin was similar to epinephrine in patients with ventricular fibrillation or pulseless electrical activity, with regards to survival to hospital admission and survival to hospital discharge. Vasopressin was noted to be superior, in both outcomes, for patients with asystole.
  1. In patients with refractory cardiac arrest and no ROSC, vasopressin followed by epinephrine may be more effective than epinephrine alone.


With more than 600,000 sudden death in North America and Europe annually, optimization of CPR is crucial to improve a patient’s chance of survival. Epinephrine use has become controversial as it induces increased myocardial consumption and ventricular arrhythmias post-resuscitation. Endogenous vasopressin levels have been known to be elevated in successfully resuscitated patients. In small prior studies, vasopressin has been associated with higher rate of short term survival and improved blood flow to vital organs when compared to epinephrine. Current guidelines recommend the use of epinephrine during cardiac resuscitation, with vasopressin as a secondary alternative.


This study was a double-blind, prospective randomized clinical trial, conducted in 44 Emergency Medical Service units in three European countries, including those with OHCA unresponsive to defibrillation. 1186/1219 patients with OHCA were included in the trial with randomization to two injections of either 40 IU of vasopressin or 1 mg epinephrine, followed by additional treatment with epinephrine at the discretion of the emergency physician managing the resuscitation. Average age 66 years, 70% men, 61% attributed to cardiac causes, 78% arrests witnessed. 33 patients were excluded due to a missing study drug code. The rates of hospital admission were similar between the two treatment groups for patients with ventricular fibrillation (46.2 vs 43%, p=0.48) and pulseless electrical activity (33.7 vs 30.5%, p=0.65). Patients with asystole treated with vasopressin were more likely to survive to hospital admission (29.0 vs 20.3%, p=0.02) and hospital discharge (4.7 vs 1.5%, p=0.04). Among 732 patients without ROSC, additional treatment with epinephrine resulted in improvement in rates of survival to hospital admission (25.7 vs 16.4%, p=0.002) and discharge (6.2 vs 1.7%, p=0.002) in the vasopressin group, but not the epinephrine group. Continue reading

Should We Reconsider Antipyretics For Fever?

What is Fever?

Although often used interchangeably, the terms fever and hyperthermia refer to different processes, and the distinction is key. In fever the thermoregulatory set-point is elevated, and the body actively raises its temperature with chills and rigors to reach the new set-point. In hyperthermia the body’s temperature exceeds the set-point, due to increased heat production (eg hypermetabolic state) or decreased dissipation (eg high humidity or ambient temperature).1

Fever is generally defined as temperature ≥38°C (100.4°F) and results from a complex mechanism. The body produces pyrogens (specific cytokines) that act on the thermoregulatory center in the hypothalamus to increase the set-point. This is thought to occur by increased prostaglandin synthesis, and antipyretic drugs lower the set-point likely by inhibiting prostaglandin synthesis.2 There are also numerous endogenous antipyretics (cryogens).

Increased temperatures enhance immune function in many ways, including improved neutrophil migration and secretion of antibacterial substances, increased interferon, and increased T cell proliferation.1


Fever Anxiety

A 1980 study titled “Fever phobia: misconceptions of parents about fever” surveyed parents, and found 94% thought fever may have harmful effects, 18% thought brain damage or serious harm could result from fever <38.9°C (102°F), and 16% thought fever could rise up to 48.9°C (120°F) if untreated.3 A 2001 study re-examined similar questions, and found 76% believed serious harm could occur at ≤40°C (104°F).3

This phobia also exists among healthcare workers. A 1992 survey by the American Academy of Pediatrics in Massachusetts showed 65% of pediatricians thought fever alone is potentially dangerous, 72% “always or often” prescribed antipyretics for fever, and 89% recommended antipyretics for fever of 101-102°F.4 A 2000 study of pediatric emergency department nurses, with a median experience of 8 years, found 11% were unsure what temperature constituted fever, 29% thought permanent brain injury or death could occur from high fever, and 18% believed it is dangerous for children to be discharged from the emergency department if still febrile.5

Is Fever Harmful?

Some providers have concerns that the increased temperature or metabolic demand from fever will harm patients. Humans generally tolerate temperatures below 41°C (105.8F) without harm. In contrast to hyperthermia, it is extremely rare for fever as a host defense against infection to reach dangerous temperatures in neurologically normal patients, since the body is actively adjusting both the set-point and actual temperature.3 A 2011 American Academy of Pediatrics policy paper states “There is no evidence that fever itself worsens the course of an illness or that it causes long-term neurologic complications.” 6 Continue reading

CITW 13: Itch, itch, itch

Welcome back to another Clinical Image of the Week from the case files of the Brown EM Residency!

HPI/ROS: 37 year old male with no significant past medical history presents to the ED with a rash. He states that it began one month ago and has been getting worse. Associated symptom is intense pruritus. It is not painful and nothing of note has made it better or worse. He’s never had a rash like this before. He denies any fevers, chills, shortness of breath, chest pain, myalgia/arthralgias, abdominal pain, nausea, vomiting, diarrhea, or urinary symptoms. He denies any recent exposures (environmental or chemical), medication changes, recent infections, or sick contacts.

Vital Signs: T 98.6, HR 88, RR 14, BP 156/72, SpO2 99% on RA

Pertinent physical exam: Diffuse, papular rash along upper and lower extremities including trunk and back. The neck and face are spared. It is non-blanching, non-weeping, and there are no open sores. It spares the face, lower back, and calves. Patient appears well otherwise. No other pertinent exam findings.


TwoWhat’s the diagnosis?

Continue reading

You make me dizzy, Miss Lizzy: HINTS for assessing acute dizziness

The evaluation of the dizzy patient in the Emergency Department can be very complicated. The differential diagnosis is broad and misdiagnosis carries with it the potential for a high degree of morbidity and mortality. This summary will focus on patients with acute vestibular syndrome—patients with acute onset, continuous dizziness—and differentiating peripheral and central causes. We are not going to discuss vertigo or other causes of dizziness (see Table 1).

Screen Shot 2016-01-29 at 11.22.23 PM

Table 1: Timing and Trigger Approach to dizziness (from TiTrATE Approach to Dizziness, David E. Newman-Toker, MD, PhD)

One of the simplest ways to approach the dizzy patient is to categorize them based on the timing (episodic vs acute/continuous) and trigger (positional vs spontaneous; post-exposure vs spontaneous). Dizziness is difficult for patients to describe, so thinking of it in this way will minimize problems posed by vague and alternating histories to help narrow your differential and inform a targeted exam (Table 1).

A minority but significant percent of patients with acute vestibular syndrome have a stroke (population estimates range from 10-40%).1 Peripheral and benign causes includes cerumen impaction and benign positional vertigo. Symptoms are localized to the inner ear or CN8, are acute, benign, self-limited and often viral or post-viral. Vertigo with stroke is often abrupt, with maximum intensity at time of onset. Severe ataxia is common, but not always seen. Larger cerebellar strokes will produce symptoms localizing to the brainstem, like diplopia, dysarthria, limb ataxia, dysphagia, weakness or numbness, but 10% will have isolated vertigo without other symptoms.2

So, how can you tell the difference between central and peripheral causes?

Great reviews of vertigo can be found here, here, and here. While there are a number of articles in the Emergency Medicine literature, the most notable exam tool that is currently most broadly discussed is the HINTS exam.

The HINTS exam is an acronym for the three exam tools that help differentiate a non-hemorrhagic posterior cerebrovascular accident from other peripheral causes of acute vestibular syndrome. It stands for Head Impulse, Nystagmus, and Test of Skew. A number of derivation and validation studies, many of which were led by Dr. David Newman-Toker, have been published in recent years.

Kattah, et al6 found the HINTS. exam to be 100% sensitive and 96% specific for stroke in their 2009 publication in Stroke. In 2013, Newman-Toker, et al4 compared HINTS to the ABCD2 score in predicting ischemia in a prospective study among ED patients with one hour of dizziness at least one risk factor for stroke. They found HINTS to be superior to ABCD2 (ABCD2, SE61%, SP 62% vs HINTS SE 96.5% SP 84.4%), but both of these studies are limited by the fact that exams involved evaluations by specialists, primarily neuroophthalmologists, however Newman-Toker’s study included a vascular stroke trained emergency physician.

Finally, fresh off the presses is a new study just published in Neurology5 which used a combination of the ABCD2 score and HINTS exam to risk stratify patients into low, moderate, and high risk groups. The study was limited in that they used the HINTS exam in all patients, some who did not have nystagmus.   In the end, few patients with nystagmus who had a negative HINTS exam had a stroke.

Can EM physicians do it?

Obviously more studies remain to be done, but initial research is promising. Studies in EDs in Italy and Australia, for example, have shown high inter-evaluator reliability between emergency physicians and specialists7, 8 when assessing for stroke using exam findings of nystagmus, head impulse testing, and ability to ambulate.

What is the HINTS exam?

HINTS is a three part exam:

  1. Head Impulse
  2. Nystagmus
  3. Test of Skew
  • Head Impulse. This test relies on the vestibular-ocular reflex, which is a peripheral reflex that allows your eyes to focus while moving your head. When this is interrupted, your eyes lag. A POSITIVE test is consistent with peripheral vertigo. To

    Vestibulo-ocular Reflex

    say it another way, a positive head impulse test is reassuring.

    1. How to do it:
      1. Have patient fix eyes on your nose. And rapidly turn their head 20 degrees to one direction and back to center, then to other side.
        1. Eyes will stay fixed on your nose (if central)
        2. Eyes will first move to direction you moved their head, and then re-fixate on your nose. It is called “catch up” saccades. Eyes have to re-orient to your nose. = peripheral lesion


  • Nystagmus
    1. Peripheral vertigo should have fast beating nystagmus in only one direction.
    2. If it is direction changing = central
    3. Vertical nystagmus = central

  • Test of Skew
    1. You are looking for vertically disconjungate gaze (aka one eye is higher than other).
    2. This can be overcome by fixation, but can be ‘uncovered’ by the alternating cover test. Have them look at nose, cover one eye, will prevent covered eye from fixating. Then rapidly remove hand and see if eye misaligned will come back into alignment. Seeing realignment as eye is fixating on your nose. You are looking for that re-alignment.

To help guide your evaluation of the patient with acute vestibular syndrome, check out this new, handy guideline put together by Dr. Napoli and Dr. Siket:

Posterior stroke visio. AN 12#2

Guideline for the Acute Dizzy Patient in the Emergency Department, 2015

Try out the exam on your next dizzy patient and see how it goes. The best way to get comfortable with this exam is to practice!


Looking for more info?

Another EM overview of acute vestibular syndrome can be found on EMCrit.

Thank you to my Faculty Editors: Anthony Napoli, MD and Matt Siket, MD, MS

References/Further Reading:

  1. Tarnutzer AA, Berkowitz AL, Robinson KA, Hsieh Y, Newman-Toker DE. Does my dizzy patient have a stroke? A systematic review of bedside diagnosis in acute vestibular syndrome. CMAJ, June 14, 2011, 183(9).
  2. Nelson JA, Viirre K. Review: The Clinical Differentiation of Cerebellar Infarction from Common Vertigo Syndromes. West J Emerg Med. 2009;10(4):273-277.
  3. Newman-Toker DE, Kerber KA, Hsieh YH, et al. HINTS outperforms ABCD2 to screen for stroke in acute continuous vertigo and dizziness. Acad Emerg Med 2013;20:986–996.
  4. Seemungal BM, Bronstein AM. Review: A practical approach to acute vertigo. Pract Neurol 2008; 8: 211–221.
  5. Kerber KA, Meurer WJ, Brown DL, Burke JF, Hofer TP, Tsodikov A, Hoeffner EG, Fendrick AM, Adelman EE, Morgenstern LB. Stroke risk stratification in acute dizziness presentations: A prospective imaging-based study. Neurology 2015;85:1869–1878.
  6. Kattah, JC, Talkad AV, Wang DZ, Hsieh Y, Newman-Toker DE. 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;3504-3510.
  7. Vanni S, Pecci R, Casati C, Moroni F, Risso M, Ottaviani M, Nazerian P, Grifoni S, Vannucchi P. STANDING, a four-step bedside algorithm for differential diagnosis of acute vertigo in the Emergency Department. Acta Otorhinolaryngol Ital 2014;34:419-426.
  8. Vanni S, Nazerian P, Casati C, Moroni F, Risso M, Ottaviani M, Pecci R, Pepe G, Vannucchi P, Grifoni S. Can emergency physicians accurately and reliably assess acute vertigo in the emergency department? Emerg Med Australas. 2015 Apr;27(2):126-31.

Slow it or Fix it? Long-term Management Strategy for Atrial Fibrillation

This is part of a recurring series examining landmark articles in Emergency Medicine, in the style of ALiEM’s 52 Articles.

Main Points:

  1. This 2002 randomized multicenter trial found that the use of rate control drugs demonstrated similar mortality at five years (primary outcome) to antiarrhythmic strategy.
  2. Rate control strategy also demonstrated decreased hospitalization and decreased adverse drug effects (secondary outcome) compared to antiarrhythmic drugs.


At the time of the publication of this article, the initial management of atrial fibrillation remained unclear. The risk of stroke and increased mortality of atrial fibrillation were well recognized, but the relative risks and benefits of the different management approaches was widely contested. The AFFIRM (Atrial Fibrillation Follow-up Investigation of Rhythm Management) trial aimed to determine whether rate control or rhythm control was superior in long-term outcomes in patients with atrial fibrillation. The trial was a randomized multicenter trial enrolling a total of 4060 patients with a fib who were randomized to either rhythm control or rate control strategies. Both strategies had equal mortality, while the rate control strategy showed decreased hospitalization and adverse drug effects. The strengths of this study were its robust size, the generalizability and the study design. However there was significant cross over and cross back in this study as it was an intention to treat study.


This was a multicenter RCT that enrolled 4060 patients over the age of 65 with atrial fibrillation. The patients were randomized at each of the sties to either rhythm control or rate control strategy. Both groups had similar demographic and baseline characteristics including rates of CHF, duration of a fib, and ejection fraction. The rhythm control strategy allowed treating physicians to use cardioversion as necessary and treat with any of 9 options of antiarrhythmics. The rate control strategy allowed physicians to decide between beta blockers, calcium channel blockers or digoxin. The rate control group was required to be on Coumadin, while the rhythm group was encouraged to be on anticoagulation especially during the initial month to 12 weeks after rhythm control.

This was an intention-to-treat study. There was significant cross over and cross back observed during the study in both arms, though significantly greater cross over in the antiarrhythmic group. These patients were followed for an average of 3.5 years.

The primary outcome of the study was mortality. There was no significant difference in mortality between the rate control and rhythm control groups (p=.08). The authors state there is a trend towards lower mortality in rate controlled group at 3.5 years. Graphically they depict a divergence of mortality as time passes with rate control group trending towards lower mortality. They did find that it was significantly more likely for patients in rhythm control group to be hospitalized and experience adverse drug effect. p (p<.001).

Limitations to the study include the amount of cross over present, the variety in medications used in the rhythm treatment strategy. In addition this study is only applicable to those aged 65 or greater, and cannot be generalized to all patients with atrial fibrillation.

Level of Evidence:

Level II based on ACEP grading scheme for therapeutic questions.

Source Articles:

Wyse, D G et al. “A Comparison of Rate Control and Rhythm Control in Patients With Atrial Fibrillation.” The New England Journal of Medicine 2002; 347.23: 1825-1833.

Resident Reviewer: Dr. Kazakin
Faculty Reviewer: Dr. Siket