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

F4.large

  • 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.

POCUS FOCUS: Lung Ultrasound for Pneumonia

BY: MAX RUBINSTEIN, MD

The Case: A 5 year old previously healthy boy presents to the ED with three days of fever and progressive shortness of breath. His exam is notable for course rhonchi and decreased aeration in the right anterior lung. There was no personal or family history of asthma, eczema, or food allergies. He received an albuterol nebulizer with no effect.

The Diagnostic Intervention: Lung Ultrasound

Point of Care Lung Ultrasound:

Point of care lung ultrasound is highly useful in detecting pulmonary pathology commonly encountered in the emergency department, most notably pneumothorax, pulmonary edema, and pneumonia.  The basic technique of lung ultrasound in children is the same no matter what underlying process is suspected. The linear probe is used and oriented perpendicular to the rib in the longitudinal axis. This allows detailed visualization of the pleural line. This is perhaps the most important aspect of lung ultrasonography as 90% of respiratory dysfunction attributable to the lungs affects the pleura.1 Differences in the appearance of the pleural line help the clinician distinguish between causes of respiratory distress. There are several techniques described to adequately assess the lungs by ultrasound, the simplest of which is to image at three interspaces in the midclavicular, mid-axillary, and posterior lung fields.1,2

Figure 1.  Normal Lung Anatomy on Ultrasound

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Pneumonia on Ultrasound:

Pneumonia on lung ultrasound has a characteristic appearance. One can see “hepatization” of the lung as this normally echogenic and artifact filled tissue (see Figure 1) becomes echo-poor and increasingly tissue-like, resembling the liver on ultrasound (see Figure 2).  This is accompanied by “dynamic air bronchograms,” a branching lesion that courses through affected lung and moves with breathing. 3 This mobility helps distinguish pneumonia from atelectasis. A recent study found that dynamic air bronchograms have a 97% positive predictive value for pneumonia.4

How good is lung ultrasound for detecting pneumonia?

  • Sensitivity & Specificity in children > 90%5
  • When performed by emergency medicine physicians who have received a 1 hour training session, sensitivity drops to 86% but specificity is 97%.6
  • Ultrasound may also be better at detecting small pneumonias than standard chest x-ray.6 However, the clinical significance of this finding has yet to be determined.

Continue reading

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.

Background:

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.

Details:

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

A True Orthopedic and Vascular Emergency

Case: A 76-year-old male presents after falling down a long flight of stairs. On exam the patient has multiple obvious external injuries, including a grossly deformed right shoulder with a large overlying hematoma. His chest x-ray and shoulder x-ray demonstrate a superiorly and laterally displaced right scapula, as well as a comminuted right scapular fracture and clavicle fracture. On further CT imaging, the patient has subtle widening of the scapulothoracic articulation.

OneQuestion: What potentially devastating injury should be considered in this patient?

Continue reading

CITW 12: The Extra Weight

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

HPI: 27 year old male presents to the ED with left chest wall pain. He states he was bench pressing at the gym when he felt a “sudden twinge of pain and popping sensation” in his left upper arm and shoulder. He was unable to lift weights following this injury without experiencing excruciating pain. He subsequently noticed swelling and bruising on his left upper arm. He denies any other injuries, numbness, or weakness.

VS: HR 54, BP 112/64, RR 11, SpO2 100%, T 98.7

PE: Patient is noted to have weakness of the left arm with internal rotation and shoulder adduction. No other deficits appreciated. Neurovascularly intact.

Exam

What’s the diagnosis?

Continue reading

Coming Down the Pike: Zika Virus

8x11-ZikaENG
From the Pan American Health Organization Zika virus website: http://www.paho.org/zikavirus

What is Zika Virus?
A single-stranded RNA virus of the Flavivirdae family, genus Flavivirus. The virus was first identified in 1947 in a rhesus monkey in the Zika Forest, Uganda.

What are the signs and symptoms?
Only about 1 in 4 people infected with Zika develop signs or symptoms, which include fever, maculopapular rash, arthralgias and conjunctivitis. Additionally, Zika causes headaches, myalgias, retro-orbital pain and vomiting.

How is it transmitted?
Zika Virus is primarily transmitted through the Aedes mosquito, which also transmits Dengue and Chikungunya. Transmission is also believed to take place vertically between mother and child, and through sexual contact.

Where has it been found?
As of the January 9, 2016, the following Pan American countries have seen confirmed cases of Zika virus: Brazil, Chile, Colombia, El Salvador, French Guiana, Guatemala, Honduras, Martinique, Mexico, Panama, Puerto Rico, Paraguay, Suriname, and Venezuela. 

Countries with confirmed Zika virus outside of the Americas include: Central African Republic, Egypt, French Polynesia, Gabon, India, Indonesia, Malaysia, Nigeria, The Philippines, Sierra Leone, Tanzania, Thailand, Uganda, and Vietnam

Why is it in the news?
Zika virus made national headlines in the United States in late December 2015 when Brazillian health officials advised would-be parents to delay pregnancy over concerns that Zika virus is contributing to a spike in microcephaly. The Brazil Ministry of Health reports a twenty-fold increase in the incidence of microcephaly over the past year in areas that have had confirmed Zika virus transmission (2,782 cases in 2015 versus 147 cases in 2014). The connection was made in November 2015 when Brazilian health officials found traces of Zika virus in a deceased newborn born with microcephaly.
zika_microcephaly
From the Pan American Health Organization Zika virus website, Epidemiological Alert, December 1, 2015

Additionally, Brazil has reported an increase in neurological syndromes in patients infected with Zika virus, most notably Guillain-Barré syndrome.

What is the treatment?
Supportive care: rest, fluids, antipyretics, and analgesics. Hold aspirin or NSAIDs until Dengue has been ruled out to reduce the risk of hemorrhage.

Sources:
Pan American Health Organization Zika virus website: http://www.paho.org/zikavirus

Brazil warns against pregnancy due to spreading virus, CNN, December 23, 2015
http://www.cnn.com/2015/12/23/health/brazil-zika-pregnancy-warning/

Foy BD, Kobylinski KC, Foy JLC, Blitvich BJ, Travassos da Rosa A, Haddow AD, et al. Probable non–vector-borne transmission of Zika virus, Colorado, USA. Emerg Infect Dis. 2011 May; http://www.ncbi.nlm.nih.gov/pubmed/21529401

Pan American Health Organization Epidemiological Alert: Neurological syndrome, congenital malformations, and Zika virus infection. Implications for public health in the Americas; December 1, 2015. PDF Direct Link

A new mosquito-borne threat to pregnancy women in Brazil, The Lancet, published online December 23, 2015. http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(15)00548-4/abstract

Hit Them Hard: The Use of H1 and H2 Antagonists for Acute Allergic Symptoms

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 Lin, R. Curry, A. Pesola, G. et al. “Improved Outcomes in Patients With Acute Allergic Syndromes Who Are Treated With Combined H1 and H2 Antagonists.” Annals of Emergency Medicine, November 2000; 36(5):462-8.

Main Points:

  1. In this randomized, double blinded, placebo controlled trial of 91 patients presenting with acute allergic symptoms fewer patients in the active arm (ranitidine + diphenhydramine) had signs of cutaneous involvement such as urticaria at 2 hours compared to the placebo group (placebo + diphenhydramine).
  1. There was no significant difference, however, between the placebo group and active group with regards to the absence of erythema or angioedema at two hours.

Background:

Many patients present to the emergency department with acute allergic syndromes. Anti-histamines, primarily diphenhydramine, are the mainstay therapy in most mild cases and are both safe and cost effective. The addition of H2 antagonists such as ranitidine to diphenhydramine may help improve clinical outcomes and expedite management in the emergency department. The primary goals of this study were to look for resolution of urticaria and angioedema at two hours from presentation. This study was well balanced in its patient recruitment and overall provides insight into real-world application of a second agent for management of allergic symptoms.

Details:

The methodology within this study was rigorous, though the sample size was small. This trial was a randomized, double blinded, placebo controlled trial that enrolled 91 patients at an academic emergency department in New York, NY. Enrollment was based on a convenience sampling associated with the study physicians’ scheduling. Patients were enrolled in this study if they were adults who presented with acute urticaria, acute angioedema, acute unexplained stridor or acute pruritic rash following an exposure to a food, drug or contact with latex. Patients underwent vital sign monitoring, examination for physical findings such as: presence and extent of urticaria and erythema, presence of angioedema, wheezing, stridor, abdominal distention or tenderness, as well as symptom scoring. This data collection occurred at presentation, at 1 hour and 2 hours.

This study demonstrated a statistically significant difference, p=0.03, in the resolution of urticaria in the active group compared to the placebo group at two hours. One significant limitation in this study is that the treating physician was able to administer supplemental medications such as epinephrine, corticosteroids, bronchodilators and additional doses of antihistamine at their discretion with significantly more participants in the ranitidine arm receiving epinephrine, 17, compared to 9 in the placebo arm. The placebo arm had more use of additional antihistamine, 10, compared to 2 in the ranitidine arm. These additional therapies are documented in table 3; however, it is unclear if the severity of illness was equal between the two groups. The authors do note in their discussion that there was no observed covariate effect for epinephrine administration with respect to urticaria resolution.

Level of Evidence:

This study was graded a level I based on the ACEP Clinical Policy Grading Scheme

Surprises:

Within the sample groups there was significant history of asthma as well as other nonasthmatic atopic conditions which supports the theory that certain individuals are genetically predisposed to allergic syndromes.

Source Articles:

Lin, R. Curry, A. Pesola, G. et al. “Improved Outcomes in Patients With Acute Allergic Syndromes Who Are Treated With Combined H1 and H2 Antagonists.” Annals of Emergency Medicine, November 2000; 36(5):462-8.

Faculty Reviewer: Dr. Siket

Perusing the Literature (PTL): Steroids for Anaphylaxis?

This month we continue our Perusing of the Literature. Once again, this section consists of recent articles that residents and attendings have stumbled across that have raised an eyebrow. These posts are meant to spark a discussion and do not represent a change in the standard of care (unless otherwise noted).

January 2016:

The Article: Grunau BE, et al. Emergency Department Corticosteroid Use for Allergy or Anaphylaxis Is Not Associated With Decreased Relapses. Ann Emerg Med. 2015;66:381-389.

The One-Liner: Corticosteroid use does not appear to be associated with a decrease in allergy-related ED revisits in patients presenting with allergic reactions or anaphylaxis.

Background: Allergy-related ED visits account for approximately 1.0% of all visits. Aside from antihistamines, corticosteroids use in allergic reactions has increased from 22% to 50% from 1993-2004. The anti-inflammatory effect of steroid therapy intends to reduce risk of biphasic reactions, decrease the severity of reactions, and decrease ED return visits.

Methods: This was a retrospective cohort study in 2 urban EDs during a 5-year period, assessing patient encounters classified as ‘anaphylaxis’ or ‘allergic reaction’. The primary aim of this study was to determine if steroid administration in ED allergy patients decreased relapses to additional care within 7-days. Authors also aimed to identify potential benefits of steroids in decreasing death, clinically important biphasic reactions, or all-cause repeated ED visits. There were no defined protocols for allergic reactions and physicians managed the patients in an individualized manner. The patient’s health number was used to identify all patients who returned to any regional ED or died within the province during a 7-day follow-up period.
Anaphylaxis was defined as meeting 1 of the following 3 criteria:
• Skin or mucosal involvement AND respiratory compromise or SBP • Two of the following after exposure to ‘likely allergen’: 1) Skin or mucosal involvement, 2) respiratory compromise, 3) SBP • SBP An allergic reaction was defined as a clinical presentation in which criteria for anaphylaxis were not met, but provider deemed the cause of signs/symptoms to be result of allergic process.

Results:
• Total of 2701 ED patient encounters
• Corticosteroids administered to 1181 (44%) patients; 469 (17%) received parenteral, 786 (29%) received oral formulation; prescription for oral steroid at ED discharge in 819 (30%) encounters
• During the 7-day follow-up period, there were 170 (6.3%) allergy-related revisits – 75 (5.8%) patients in the steroid group and 95 (6.7%) in the nonsteroid group (95% CI 0.63 to 1.17).
• Anaphylaxis patients (n=473); there were 15/348 (4.3%) allergy-related re-visit in the steroid group, and 7/125 (5.6%) in the non-steroid group (95% CI 0.41 to 3.27)
• Allergic reaction patients (n=2228); there were 60/940 (6.4%) allergy-related revisits in the steroid group, and 88/1288 (6.8%) in the non-steroid group (95% CI 0.63 to 1.31)
• NNT with steroids to prevent 1 additional ED revisit was 176
• No deaths during any of index visits or within follow-up period for any patient (2698/2715; 99.4% patients able to be have provincial data linkage established)
• 5 clinically important biphasic reactions. 4 in steroid group, 1 in non-steroid group.

Limitations:
• Clinical impression was the basis for the diagnosis of allergic reaction
• Cannot confirm filling of prescriptions or tolerance of steroid course
• Physicians on index visit may have instructed patients to return for reassessment
• Patients with biphasic reactions may have represented out of the region

Author: Cameron Gettel, MD PGY1
Resident Section Editor: Adam Janicki, MD PGY4
Reviewed by Gita Pensa, MD, Clinical Assistant Professor, Department of Emergency Medicine

52 Articles: Lysis vs Transfer for PCI (NEJM 2003)

ST segments:
fear
a lytic in my hand,
or transfer?

-Unknown, 2015

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

Discussing:

Andersen et al., NEJM 2003.  A Comparison of Coronary Angioplasty with Fibrinolytic Therapy in Acute Myocardial Infarction.

Main Points:

  1. This prospective randomly-controlled trial investigated whether patients with STEMIs who presented to community hospitals would benefit from transport to specialized centers for percutaneous coronary intervention (PCI) rather than remaining at the local hospital for fibrinolysis. The authors demonstrated an almost 5% reduction in reinfarction rate at 30 days between the two groups.
  1.  STEMI patients that presented to community centers and received aspirin+metoprolol+heparin+PCI within 2 hours, including transfer time, had statistically significantly fewer reinfarctions at 30 days than the STEMI patients who remained at the initial facility andon alteplase+aspirin+metoprolol+heparin.  Ultimately, PCI was shown to be superior to fibrinolytic if available in a timely fashion.

Background:

It is now an established tenet that timely PCI in an experienced center by experienced interventionalists is the best treatment for STEMI.  Historically, with no PCI available at the presenting facility, STEMI patients received anticoagulation and fibrinolytics.  But there were obvious and dangerous concerns in applying a “PCI-or-bust” policy universally, as there are only so many PCI centers to drive patients to, and “time is myocardium.”  So the best treatment for the patient with a STEMI in the middle of the proverbial forest was unknown.  Lyse or transfer?  This study made significant progress towards helping us answer this question.

Methods:

1572 patients were enrolled, 1129 from 24 referral hospitals and 443 from 5 PCI centers.  All of these patients were randomly assigned to receive lysis & anticoagulation (LA) or anticoagulation & PCI (APCI), with the patients from the referral hospitals therefore being transferred for their PCI.  And yes, patients who presented to PCI centers and were assigned LA therefore did not receive PCI.  Risk characteristics of all the patients were similar.  LA patients received 300mg aspirin PO, 20mg metoprolol IV, an “accelerated” alteplase treatment (15mg bolus + 0.75mg/kg over 30min + 0.5mg/kg over the next 60min), and unfractionated heparin for 48h (5000U bolus + infusion titrated to aPTT 70-90sec).  APCI patients received 300mg aspirin IV, 20mg metoprolol IV, unfractionated heparin (10,000U bolus + infusion during procedure to activated clotting time 350-450s).  In patients receiving PCI, GPIIb/IIIa blockers were given at discretion of proceduralist, arteries were treated only if stenosed >30% or if TIMI “flow grade” was <3, non-infarct-related arteries were NOT intervened on, and all patient received Ticlodipine (500mg) or Clopidogrel (75mg) for 1 month afterwards.  The primary endpoint was a composite of death from any cause, clinical reinfarction, or disabling stroke at 30 days follow up.

Results:

  • For patients presenting to PCI centers, there was a 45% reduction in composite outcome with PCI, from 12.3% in the LA group to 6.7% in the APCI group (P = 0.05).
  • For patients presenting to referral hospitals, there was a 40% reduction in the composite outcome with PCI, from 14.2% in the LA group to 8.5% in the APCI group (P = 0.002)
  • Driving the difference within the composite outcome was clinical reinfarction: 1.6% in all APCI vs 6.3% in all LA (P =  0.001).  Differences in death and stroke rates at 30 days were not statistically significantly different between all APCI and all LA patients, whether they were transferred to a PCI center or were already there.
  • The median distance from referral site to PCI center was 50 km
  • Transfer was highly protocolized, with emphasis on shaving-off every precious second of ischemic time.  This cooperation and efficiency resulted in 96% of referral patients landing on the nearest participating PCI table in 2 hours or less.
  • The study was stopped after the 1129 patients, when the third interim analysis showed referral APCIs were reinfarcting less than the referral LAs; this was built into the design as a study cutoff as it implies that APCI is better in both settings.

Discussion:

  • The bottom line is the balance between the proven benefits of PCI and the ischemic time on the myocardium.  There are many variables at play in the “lyse vs transfer (vs both)” decision (see below). These variables include: location and severity of the ischemia, comorbidities and stability of the patient, EMS capabilities, distance, receiving PCI center experience, available medications, etc.  The decision may not always be clear, every patient is probably different, and there is an overwhelming amount of research on this topic.  Do your best.
  • Implementing the airtight transfer logistics they executed here is an obstacle, science aside.
  • In hindsight, your heart has to go out (no pun intended) to the 12.3% of LA patients who presented to a PCI center, got heparin & alteplase, and had a poor outcome.  Their willingness to participate has certainly saved lives.
  • Did you notice that the referred APCI patients did not receive fibrinolysis, only asa, metoprolol, and UFH?  The older research on immediate PCI after fibrinolysis showed no benefit and increased adverse effects.  New and ongoing research on “facilitated PCI,” or PCI after fibrinolysis, using ever-advancing interventional equipment and techniques, may be changing this for some high risk patients for whom PCI is not available within 90 minutes.  For further reading, see these:

Herrmann HC, et al.  Benefit of facilitated percutaneous coronary intervention in high-risk ST-segment elevation myocardial infarction patients presenting to nonpercutaneous coronary intervention hospitals.  JACC Cardiovac Interv.  2009 Oct;2(10):917-24.

Ellis SG, et al.  Facilitated PCI in patients with ST-elevation myocardial infarction.  N Engl J Med. 2008 Maay 22;358(21):2205-17.

Ellis SG, et al. Facilitated percutaneous coronary intervention versus primary percutaneous coronary intervention: design and rationale of the Facilitated Intervention with Enhanced Reperfusion Speed to Stop Events (FINESSE) trial. Am Heart J. 2004; 147: E16.

Level of Evidence:

Based on the ACEP grading system for therapeutic questions this study was graded level I.

Surprises:

The study inclusion criteria was defined as the symptoms for greater than 30 minutes, but less than 12 hours with associated cumulative ST-segment elevation of at least 4mm in at least two contiguous leads.

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

CITW 11: The Bouncing Baby

Aside

CITW 11: The Bouncing Baby

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

HPI: A 2-year old boy presents after being “bounced” by his 12-year old brother in a “bouncyhouse” at a birthday party.  He had the immediate onset of knee pain and refused to weight bear on his right leg.  He has never had an injury before and has no prior medical problems.

VS: HR 140 (crying), BP 94/50, RR 40, SpO2 98%, T 98.8

PE: Agitated and screaming whenever you enter the room.  Apparent right knee effusion, but no erythema.  He will not tolerate ROM well, but you note that he flexes his right hip when his parents lower his feet to the floor to avoid putting his right foot down.  It is difficult to assess for point tenderness due to patient agitation.

X-rays are obtained of the right hip, femur, knee and tib/fib:

Screen Shot 2015-11-28 at 11.43.26 AM Screen Shot 2015-11-28 at 11.43.41 AM Screen Shot 2015-11-28 at 11.43.55 AM

What’s the Diagnosis?

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