Modern Resident - The newsletter of AAEM/RSA
August/September 2014
Volume 6: Issue 2 | Facebook  Twitter  LinkedIn

Inside This Issue

Deep Neck Space Infections
Alexandra Murray, OMSIV
Ohio University Heritage College of Osteopathic Medicine

Since the advent of modern antibiotic use, deep neck space infections have decreased in occurrence; however, when these infections take place, the complications can be life threatening.1-4 Because of the unique compartments of the cervical fascia, deep neck space infections can range in severity and have the potential to extend into the mediastinum. Based on how the infection propagates, these infections have the potential to cause upper airway edema, airway obstruction, mediastinitis, internal jugular vein septic thrombophlebitis, sepsis and septic embolization.1,2

Common Sources
Deep neck space infections can develop from infections of the teeth, salivary glands, nasal cavity, paranasal sinuses, pharynx and adenotonsillar tissues.1,2 In children, adenoids and tonsillar infections are the most common source as they create a drainage pathway through the retropharyngeal lymph nodes resulting in retropharyngeal, parapharyngeal and peritonisllar space infections.1 In adults, dentoalveolar infections are the most common source of infection. In particular, infections of the lower second and third molars are dangerous because their roots spread directly into the submandibular space.1 Other causes of deep neck space infections in adults include: pharyngitis, tonsillitis, sialoadenitis, trauma, foreing body ingestion, sinusitis, cervical lymphadenitis, middle ear infections, mastoid infections, and IV drug use.2

Diagnosis
Clinical presentations of deep neck space infections are widely variable and the complexity of the deep neck spaces can mask the severity of the infection.1 Emergent signs and symptoms that require airway protection are neck swelling, neck stiffness, trismus, "hot potato voice", dyphagia and dyspnea.1 Plain film X-rays are useful for initial screening and for quick assessment of airway compromise, whereas ultrasound can be used to differentiate between cellulitis and abscess. CT is the gold standard for diagnosis of deep neck space infection and can localize which compartments are affected. MRI takes more time to acquire than CT, but is a more specific for determining the extent of inflammation and edema.1

Treatment
The most serious complications of deep neck space infections are airway obstruction and spread of the infection to the mediastinum. For this reason, when deep neck space infections are suspected it is crucial that the airway be secured.1-4 Patients with cellulitis and small abscesses can respond to antibiotics alone, but surgical drainage should be performed in patients with larger abscesses, Ludwig's angina, anterior visceral space involvement and in those who do not respond to antibiotic treatment.3,4 Deep neck space infections are generally polymicrobial but recent reports suggest a high prevelance of staphyloccal species in the pediatric population.1 In addition, Klebsiella pneumoniae and Streptococcus species are found to be more prevalent in diabetics.1-4 Ultimately, choosing appropriate antibioitics based upon the likely microbiology of the infection is essentail for a successful outcome.

References:

  1. Maroldi R et al. Emergency imaging assessment of deep neck space infections. Semin Ultrasound CT MR. 2012 Oct; 33(5):432-42.
  2. Wang LF, Kuo WR, Tsai SM, Huang KJ. Characterizations of life-threatening deep cervical space infections: a review of one hundred ninety-six cases. Am J Otolaryngol. 2003 Mar-Apr;24(2):111-7.
  3. Boscolo-Rizzo P et al. Deep neck infections: a constant challenge. ORL J Otorhinolaryngol Relat Spec. 2006;68(5):259-65.
  4. Boscolo-Rizzo P, Da Mosto MC. Submandibular space infection: A potentially lethal infection. Int J Infect Dis. 2009 May;13(3):327-33.

Increasing the Paper Speed in Narrow-Complex Tachycardia
Destinee DeLemos, MD
Nathan Haas, MD
University of Michigan Department of Emergency Medicine

Narrow complex tachycardia often presents a diagnostic and therapeutic dilemma, and one simple trick can help in the correct identification of the underlying rhythm. With increasing heart rates, it becomes quite challenging for the emergency physician to distinguish between sinus tachycardia, paroxysmal supraventricular tachycardia (pSVT), atrial fibrillation and atrial flutter. If the underlying rhythm is not pSVT, an unnecessary adenosine trial can prove quite unpleasant for both the patient and physician.

Standard 12-lead EKGs are printed at 25mm/second. By simply doubling the paper speed to 50mm/second, the printed rhythm strip appears widened and exaggerated, which can aid in identifying finer details of the EKG. The images below demonstrate previously hidden flutter waves becoming more apparent at an increased paper speed.

Normal paper speed (25mm/s)

Increased paper speed (50mm/s)

Images Courtesy of Amal Mattu, MD FAAEM

A 2002 study evaluated the impact of increased paper speed on emergency physicians' abilities to correctly identify and treat narrow-complex tachycardias.1 Correct diagnosis improved from 63% to 71% using this simple maneuver, and the incorrect use of adenosine was decreased from 18% to 13%. Before jumping to adenosine for a narrow-complex tachycardia, consider this quick and easy trick to help determine the correct rhythm and prevent your patient from experiencing an unnecessary "impending sense of doom."

References:

  1. Accardi AJ, Miller R, Holmes JF. Enhanced Diagnosis of Narrow Complex Tachycardias with Increased Electrocardiograph Speed. The Journal of Emergency Medicine. 22.2(2002):123-26. Web. 14 July 2014.
  2. Lin M. Trick of the Trade: Speed up ECG Paper Rate to Differentiate Tachycardias. ALiEM. Academic Life in Emergency Medicine. 11 Dec. 2012. Web. 14 July 2014. http://www.academiclifeinem.com/trick-of-the-trade-speed-up-ecg-paper-rate-to-differentiate-tachycardias/.
  3. Mattu A. Mattu ECG Case: Sept 11 2011. YouTube. N.p., 9 Apr. 2012. Web. 14 July 2014. https://www.youtube.com/watch?v=EULaKVctVuA.


Ring Preservation: String Technique
Kaitlin Fries, OMSIV
Ohio University Heritage College of Osteopathic Medicine

It is not uncommon for a patient to present with ring tourniquet syndrome. Ring tourniquet syndrome is defined as a patient being unable to remove their ring due to distal phalanx swelling. The first step in ring removal is to determine the severity of the situation. Begin by assessing two-point discrimination and capillary refill to determine the significance of the constriction.1 If either of these are diminished, or a fracture is present, then rapid ring removal using ring cutters is the procedure of choice.1 However, if sensation and perfusion are intact, it is reasonable to attempt to preserve the ring.

In preparation, minimize the swelling by wrapping the affected finger with an elastic band and elevating it for a few minutes.1 It is also important to provide the patient with some form of regional anesthesia, such as a digital nerve block. Obtain a piece of string, umbilical tape or 0-gauge silk suture.1 Pass one end of the string from distal to proximal underneath the ring. Once this is accomplished, pick up the other end of the string and wrap the finger all the way to the distal tip. It is important that the loops of string contact one another and cover the underlying skin completely. Next, using the proximal end of the string, begin unwinding and advancing the ring. Passing over the proximal interphanalgeal (PIP) joint tends to be the most challenging part of the procedure, and abrasions may occur depending on the material used.1

References:

  1. Tintinalli JE. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. McGraw Hill; 2011:328-9.

Tox Talks: Drug Induced Noncardiogenic Pulmonary Edema
Ashley Grigsby, DO
Indiana University

Noncardiogenic pulmonary edema (NCPE) is a clinical entity consisting of alveolar fluid accumulation without evidence of cardiac cause.1 Although there are many non-toxicologic causes of NCPE, both opiate overdose and salicylate toxicity are known to cause NCPE and should be part of one's differential diagnoses.

Opiate overdose induced NCPE was first recognized by William Osler in 1880.2 It can occur with any opioid, including heroin and methadone. Although the pathophysiology of this phenomenon is not yet completely understood, it is believed that both direct drug toxicity and hypoxia induced alveolar permeability play a role in the development of pulmonary edema.1,2 New users and males are more at risk to develop NCPE than other opiate users. Symptoms become clinically apparent within 24 hours of use, but usually manifest within four hours.2,3 Treatment for NCPE in these patients is mostly supportive. In one case series, approximately 33% of patients required mechanical ventilation; fortunately, most are able to be extubated within 24 hours as the effects are short lasting.1 Naloxone may be beneficial in these patients to reverse the opioid toxicity. Patients who present with respiratory failure from opiate overdose should be observed for development of pulmonary edema, even if reversed with naloxone.2

In addition, NCPE is a well-recognized manifestation of acute and chronic salicylate toxicity, occurring in 35% of cases.4 Several theories on the mechanism behind this toxicity exist. It is believed that salicylates directly act on the central nervous system and cause a massive catecholamine surge that shifts blood to the pulmonary circulation.4 Young patients with pulmonary edema should have a serum salicylate level to rule out toxic levels. Furthermore, patients presenting with pulmonary edema in the presence of a mixed respiratory alkalosis and anion-gap metabolic acidosis should have you consider salicylate toxicity as a potential cause.4 There are reported cases of normal gap acidosis in the setting of severe toxicity and a salicylate level would be reasonable in these patients as well.4 Treatment consists of supportive respiratory care and serum alkalization with intravenous sodium bicarbonate.5 Additionally, salicylate induced pulmonary edema is an absolute indication for hemodialysis.1 Because of the high morbidity and mortality associated with salicylate toxicity, it is important to consider it in your differential diagnoses.

NCPE as a clinical entity has many causes, but opiate and salicylate toxicity should be considered to prevent delay in diagnosis. It is especially important to consider it due to the lack of other clinical symptoms. If salicylate toxicity is confirmed, treatment with sodium bicarbonate and hemodialysis should occur promptly.

References:

  1. Givertz M. Noncardiogenic Pulmonary Edema. Up to Date. 2014. Accessed on 12 July 2014. Available from: http://www.uptodate.com/contents/noncardiogenic-pulmonary-edema?source=search_result&search=ncpe&selectedTitle=1~73
  2. Sterrett C, Brownfield J, Korn CS, Hollinger M, Henderson SO. Patterns of presentation in heroin overdose resulting in pulmonary edema. The American Journal of Emergency Medicine. 2003. 21(1), 32-4.
  3. Sporer K, Dorn E. Heroin-Related Noncardiogenic Pulmonary Edema. Chest [serial online]. November 2001;120(5):1628. Available from: Academic Search Premier, Ipswich, MA. Accessed July 12, 2014.
  4. Yuklyaeva N, Chaudhary A, Gorantla R, Bischof E. Salicylate-induced pulmonary edema - a near miss diagnosis. The American Journal of Emergency Medicine. 2004. 32(5), 490.
  5. Glisson JK, Vesa TS, Bowling MR. Current management of salicylate-induced pulmonary edema. Southern Medical Journal. 2011.104(3); 225-32.

Age-Based Cut Off in D-dimer Testing
Jimmy Tam Huy Pham, MHS MA MS IV
Jonathan P. Zygowiec, MPH MA MS IV
Arizona College of Osteopathic Medicine

Both deep vein thrombosis (DVT) and pulmonary embolism (PE) are forms of a disease called venous thromboembolism (VTE). In the United States alone, there are over 600,000 cases of DVT and PE every year.1 The incidence in the younger population increases from 1:1000 to 8:1000 in the older population, with a mortality rate reported as high as 30% in recent years. The diagnostic gold standards to confirm the blood clot have been venography and pulmonary angiography. More recently, they have been replaced by duplex ultrasound and computed tomography pulmonary angiogram (CTPA) for DVT and PE, respectively. However, an initial, much less expensive D-dimer test is often used to rule out VTE in patients presenting to the emergency department.

D-dimer testing is sensitive for thrombus formation; and in patients who are not high, risk this test is used to rule out venous thromboembolism. D-dimer has been shown to increase with age, which can cause a lower specificity in older patients. Specificity can range from 49-67% in patients ≤50 years of age, but in older patients (i.e., ≥80 years of age) the specificity is in range of 0-18%. Thus, although the initial D-dimer test is simple and inexpensive, it is less useful in the older patients. Recently, there have been numerous studies and meta-analyses indicating that an aged-based D-dimer cut off should be used to improve the diagnostic accuracy of D-dimer screening. However, a higher cut off may lead to increased false negative cases (i.e., missed VTE) and may make this approach less safe. Several studies have aimed to explore whether age-adjusted D-dimer can increase specificity without negatively affecting sensitivity.

Regarding pulmonary embolism, Douma et al. reported in a large study in 2010 that age-adjusted D-dimer combined with clinical probability greatly increased the proportion of older patients in which PE could safely be excluded.2 Van Es et al. reported in a 2012 validation study ithat irrespective of which clinical decision rule is used, age-adjusted D-dimer increases the number of patients >50 years in which PE can be safely excluded.3 Furthermore in 2012, Penaloza et al. concluded that age-adjusted cut off increased clinical usefulness of D-dimer in older patients.4 In a 2014 prospective validation study of 19 centers, Righini et al. reported that the combination of pretest probability assessment with age-adjusted D-dimer, compared to a fixed D-dimer cut off of 500µg/L, is associated with a large number of patients in which PE can be ruled out without an increase in missed pulmonary embolism.5

Regarding deep vein thrombosis, in 2012 Schouten et al. stated that the combination of low clinical probability of DVT and use of an age-dependent D-dimer cut off value for patients >50 years can safely exclude DVT, as compared to the conventional cut off value of 500µg/L. In a DVT validation study in 2012, Douma et al. report that age-adjusted D-dimer in combination with clinical probability greatly increases the proportion of older patients in which DVT can be safely excluded.6,7

Most recently, an article published in Chest Journal by Woller et al. reported that using an age-adjusted D-dimer threshold could enhance the efficiency for the work-up of suspected PE by decreasing the number of patients exposed to the risk and expense of CTPA. However, the authors caution that a prospective study with subgroup analyses should be done to assure the safety of adopting an age-adjusted D-dimer threshold among the older patients before clinical care implementation.8

Age-adjusted D-dimer testing increases specificity without modifying sensitivity in patients >50 years of age. In patients >50 years of age, using a clinical probability assessment plus an age-adjusted D-dimer cutoff increases the number of patients that can be safely ruled out for PE or DVT. These findings may lead to changes in practice that can save costs associated with unnecessary testing, and avoid the potential harm of exposing patients to unnecessary radiation. There is agreement that further prospective studies need to be conducted to validate these findings. It is important to note that different hospitals will use different assays of D-dimer and so the age-adjusted cutoff used in the above studies may not be universally applied at all institutions.

References:

  1. Schouten HJ, Geersing GJ, Koek HL et al. Diagnostic accuracy of conventional or age-adjusted D-dimer cut-off values in older patients with suspected venous thromboembolism: systematic review and meta-analysis. BMJ. 2013;346:f2492. doi: 10.1136/bmj.f2492.
  2. Douma RA, le Gal G, Söhne M et al. Potential of an age-adjusted D-dimer cut-off value to improve the exclusion of pulmonary embolism in older patients: a retrospective analysis of three large cohorts. BMJ. 2010;340:c1475. doi:10.1136/bmj.c1475.
  3. van Es J, Mos I, Douma R et al. The combination of four different clinical decision rules and an age-adjusted D-dimer cut-off increases the number of patients in whom acute pulmonary embolism can safely be excluded. Thromb Haemost. 2012 Jan;107(1):167-71. doi:10.1160/TH11-08-0587.
  4. Penaloza, A, Roy PM, Kline J et al. Performance of age-adjusted D-dimer cut-off to rule out pulmonary embolism. J Thromb Haemost. 2012;10(7):1291-6. doi:10.1111/j.1538-7836.2012.04769.x.
  5. Righini M, Van Es J, Den Exter PL et al. Age-adjusted D-dimer cutoff levels to rule out pulmonary embolism: the ADJUST-PE study. JAMA. 2014 Mar 19;311(11):1117-24. doi: 10.1001/jama.2014.2135.
  6. Schouten HJ, Koek HL, Oudega R et al. Validation of two age dependent D-dimer cut-off values for exclusion of deep vein thrombosis in suspected elderly patients in primary care: retrospective, cross sectional, diagnostic analysis. BMJ. 2012;344:e2985. DOI:10.1136/bmj.e2985.
  7. Douma RA, Tan M, Schutgens RE et al. Using an age-dependent D-dimer cut-off value increases the number of older patients in whom deep vein thrombosis can be safely excluded. Haematologica. 2012;97(10):1507-13 DOI:10.3324/haematol.2011.060657.
  8. Woller SC, Stevens SM, Adams DM et al. Assessment of the safety and efficiency of using an age-adjusted D-dimer threshold to exclude suspected pulmonary embolism. Chest. 2014 May 15 [Epub ahead of print] DOI: 10.1378/chest.13-2386.


Case: Urinary Retention in a Young Female with Genital Herpes
Mary Calderone, MD
University of Michigan/St. Joseph Mercy Hospital

Case:
A 26-year-old female presents with one week of urinary retention following a diagnosis of genital herpes. The patient was recently diagnosed with genital herpes when she presented to her primary care provider (PCP) with vesicular genital lesions, myalgias, fever and general malaise with a confirmatory HSV-2 PCR test. She completed a full course of acyclovir and her vaginal lesions had resolved. Gradually over the subsequent three days, she developed symptoms including straining to urinate and the feeling of incomplete emptying of the bladder. She denied dysuria, flank pain, hematuria, fevers, chills, nausea or vomiting. Review of systems is notable for bilateral paresthesias and constipation. Her symptoms eventually progressed to acute urinary retention necessitating a previous ED visit at another hospital, during which urinalysis was negative for urinary tract infection and she was sent home with an indwelling catheter and a leg bag and instructed to follow-up with her PCP. On the day prior to presentation, she went to a follow-up appointment with her PCP, who removed the catheter. She returns to the ED again today complaining of continued urinary retention. Urinalysis is normal. A urine culture ordered by her PCP on the day prior is negative. A basic metabolic panel and complete blood count from the day prior are also unremarkable. Her physical exam is notable for normal vital signs, no costovertebral angle tenderness and mild suprapubic tenderness with a palpable bladder, but an otherwise benign abdomen. Her neurologic exam is unremarkable. She has normal rectal tone without saddle anesthesia. An ultrasound of the bladder confirms acute urinary retention and catheterization yields 1300cc of clear, yellow urine.

Discussion:
The diagnosis is herpes simplex virus type 2 (HSV-2) sacral radiculitis, often referred to as "Elsberg syndrome." Elsberg syndrome is characterized by acute urinary retention in combination with other signs of lumbosacral radicular dysfunction, such as constipation, erectile dysfunction, anogenital pain, parasthesias, sensory loss or flaccid paralysis of the leg muscles.1 This presentation can be caused by either reactivation of HSV-2 lying dormant in the sacral dorsal root ganglia or HSV-2 causing a primary genital infection.2 Cerebrospinal fluid studies in these patients may reveal lymphocytic pleocytosis, elevated albumin and positive HSV-2 PCR.3 MRI may be necessary to exclude other diagnoses in the differential such as demyelinating disease or cauda equina syndrome. Elsberg syndrome tends to be self-limiting, but the rare complication of ascending myelitis can occur and can cause death within weeks.4 Patients with diabetes, HIV infection or malignancy are at greater risk for this serious complication. Most cases of Elsberg syndrome resolve within one to four weeks.2 Management primarily involves intermittent self-catheterization.2 Administration of acyclovir may shorten the symptomatic period.2

References:

  1. Solbrig MV, Johnson, RT. Genital herpes: neurologic complications. Neurology Med Link. https://www.medlink.com/medlinkcontent.asp. Published June 27, 1995. Updated September 9, 2013. Accessed July 15, 2014.
  2. Haanpaa M, Paavonen J. Transient urinary retention and chronic neuropathic pain associated with genital herpes simplex virus infection. Acta Obstetrica et Gynceologica Scandinavica. 2004; 83(10): 946-949.
  3. Eberhardt O, Kuker W, Dichgans J, Weller M. HSV-2 sacral radiculitis (Elsberg syndrome). Neurology. 2004; 63(4): 758-759.
  4. Wiley CA, VanPatten PD, Carpenter PM, Powell HC, Thal LJ. Acute ascending necrotizing myelopathy caused by herpes simplex virus type 2. Neurology. 1987; 37(11):1791-1794.

Board Review: Methanol and Ethylene Glycol Ingestion
Sophia Johnson, DO
Shane Sergent, DO
Conemaugh Memorial Medical Center Emergency Medicine Residency

Ethylene glycol is found in antifreeze and methanol in windshield wiper fluid and other products.1 These substances are not directly toxic, but toxic metabolites are formed by their metabolism in the liver. They are metabolized sequentially by alcohol dehydrogenase (ADH) and aldehyde dehydrogenase. Methanol to formic acid and ethylene glycol to glycolic acid, glyoxylic acid, and oxalic acid.2

Both are rapidly absorbed and patients may initially appear intoxicated from the direct effect of the compounds.1,2 Ingestion with ethanol, a competitive inhibitor of ADH, can prolong or prevent presentation of symptoms.1 Methanol ingestion presents with CNS depression, visual complaints including photophobia, blurred vision or "snow field" vision, decreased visual acuity, and metabolic acidosis.2,3 Patients may have nausea, vomiting, abdominal pain, tachycardia, hypotension, dizziness or headache.2,4 Formic acid from methanol is toxic to the retina and patients might have optic disc hyperemia or papilledema on physical exam.1,2

Ethylene glycol ingestion causes CNS depression, renal failure and metabolic acidosis.2 Toxicity includes three stages. The first starts within 30 minutes to 12 hours and is neurologic. Patients may appear intoxicated and may progress to seizures. They can experience nausea, vomiting or abdominal pain.2 The second stage is cardiopulmonary and starts in 12-24 hours and may involve tachycardia, hypertension, arrhythmias, shortness of breath or CHF.2,3 The third stage is renal and is seen in 24-72 hours; it involves renal failure, flank pain and hematuria.2,4

Serum levels are ideal for diagnosis, but are often send-out labs that are not immediately available.1,2 ABG, glucose, chemistry panel (including electrolytes, BUN, creatinine, serum calcium), serum osmolarity, acetaminophen, salicylate, lactate, and serum ethanol levels should be ordered.1,2 Anion gap and osmolal gap should be calculated. In severe poisoning, osmolal gap is elevated soon after ingestion.1 Oxalate crystals in the urine are a late finding.1 Urinary fluorescence cannot exclude ethylene glycol ingestion if absent.2

Sodium bicarbonate is used to correct metabolic acidosis with a goal pH above 7.2.4 Fomepizole inhibits ADH. It also has less side effects and is easier to titrate than ethanol, a less-favored, treatment.4 Dosing involves a loading dose of 15mg/kg followed by doses of 10mg/kg every 12 hours.1,4 Hemodialysis is the best method to reduce serum alcohol levels and remove toxic metabolites, but is only indicated for severe metabolic acidosis, renal failure, ethylene glycol or methanol levels >50mg/dl, or evidence of end organ damage including visual abnormalities (methanol) or seizures.3,4

References:

  1. Sivilotti MLA, Winchester JF. Methanol and ethylene glycol poisoning. In: UpToDate, Traub SJ, Burns MM, Grayzel J(Ed), UpToDate, Waltham, MA. (Accessed on July 15, 2014).
  2. Smith JC, Quan D. Alcohols. In: Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, T. eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill; 2011. http://accessemergencymedicine.mhmedical.com/content.aspx?bookid+693&Sectionid=45915525. Accessed July 15, 2014.
  3. Kraut JA, Kurtz I. Toxic Alcohol Ingestions: Clinical Features, Diagnosis, and Management. Clinical Journal of the American Society of Nephrology. 2008; 3:208-225.
  4. Morgan DL, Borys DJ. Chapter 47. Poisoning. In: Stone C, Humphries RL. Eds. Current Diagnosis & Treatment Emergency Medicine. 7e. New York, NY: McGraw-Hill; 2011. https://accessemergecymedicine.mhmedical.com/content.aspx?bookid=385&Sectionid=40357263. Accessed July 15, 2014.


Getting Skinny in the ED by Implementing Lean Process Improvement
Nick Pettit, PhD OMSIII
Ohio University Heritage College of Osteopathic Medicine

Emergency departments (EDs) and hospitals alike are facing problems such as overcrowding, increasing costs and delays all of which arise from inefficiencies, inadequacies or deficiencies within the entire medical process. Within the last several years there has been an emergence of research that is aimed at quality improvement. Hospitals have begun to utilize an approach developed by Toyota termed the "Lean processes," which seeks quality improvement by examining (and improving) every step of the medical process.1

Implementation of Lean methodologies are finding success within various EDs across the country. One example is the adoption of Lean process in identifying bottlenecks within the ED. By identifying bottlenecks within the ED, such as delays in radiology, hospitals can optimize protocols and medical resources to ultimately improve patient care.2 Other examples of successful Lean processes implemented within the ED setting are the expedition of time-dependent stroke care and reducing dwell times in a trauma resuscitation unit.3, 4

Lean methodology offers significant opportunities within the ED as demonstrated by a review article in the Annals of Emergency Medicine.5 However, the current successes are at large academic institutions and the observed results may not be directly applicable at smaller or community based EDs. Smaller EDs likely do not have the resources, personnel or time to implement similar investigations. Thus, it would be beneficial to identify generalizable improvement strategies that are applicable irrespective of both the ED size and volume. Some of the many areas that may warrant investigation include: ED wait times, reduction in time of psychiatric consults, improved discharge processes, improved handoffs/sign-outs, improved radiology times, less hassle in the admitting process, etc.6 While every patient is certainly unique, there seems to be a lack of organization when it comes to certain procedures, such as physician handoffs and discharges. By reducing variability and introducing more standardized protocols among the aforementioned processes, patient care and satisfaction will likely benefit. There are many hurdles yet to overcome, but the implementation of Lean processes has great potential for improving both efficiency and patient care.

References:

  1. Gershengorn HB, Kocher R, Factor P. Management strategies to effect change in intensive care units: lessons from the world of business. Part II. Quality-improvement strategies. Ann Am Thorac Soc. 2014;11:444-453 doi:10.1513/annalsats.201311-392AS.
  2. Ryan A, Hunter K, Cunningham K et al. STEPS: Lean thinking, theory of constraints and identifying bottlenecks in the emergency department. Ir Med J. 2013;106:105-107.
  3. Ford AL, Williams JA, Spencer M et al. Reducing door-to-needle times using Toyota's lean manufacturing principles and value stream analysis. Stroke. 2012;43:3395-3398 doi:10.1161/strokeaha.112.670687.
  4. Parks JK, Klein J, Frankel HL et al. Dissecting delays in trauma care using corporate Lean six sigma methodology. J Trauma. 2008;65:1098-1104 doi:10.1097/TA.0b013e318188e8ad.
  5. Holden RJ. Lean thinking in emergency departments: a critical review. Ann Emerg Med. 2011;57:265-278 doi: 10.1016/j.annalemergmed.2010.08.001.
  6. Woods RW, Reintjes S, Nagy P. Quality improvement projects based in the emergency department. Radiology. 2014;4:423-424 doi:10.1016/j.jacr.2014.01.002.


Holiday Heart Syndrome
Dylan Hendy, DO
Arrowhead Regional Medical Center
Michael Flores, MSIII
Western University of Health Sciences

Patient Vignette:
A 29-year-old male presents to the emergency department with the chief complaint of a “rapid heart rate with palpitations,” which began 2.5 hours ago following heavy alcohol consumption the night before. Further history reveals the patient had a similar episode of these symptoms “years ago” after binge drinking. He states he was placed on an unknown medication to control his heart rate, which he no longer takes regularly. Patient denies recent upper respiratory tract infection, fever, chills, shortness of breath, chest pain, nausea, vomiting, dizziness or syncope. Patient also denies any illicit drug usage. Basic laboratory tests, including thyroid stimulating hormone and urine drug screen, are all within normal limits.

Question:
What is the diagnosis?

  1. Brugada syndrome
  2. Atrial flutter
  3. Holiday heart syndrome
  4. Multifocal atrial tachycardia

Answer:
C is correct. The answer is holiday heart syndrome. This patient presents with new-onset atrial fibrillation with rapid ventricular response after a night of excessive alcohol ingestion, or “binge drinking.” The pattern of cardiac arrhythmias following acute alcohol ingestion was first recognized in the early 1970’s by Phillip Ettinger. He termed this association “holiday heart syndrome” due to the increased frequency of occurrences around the holidays or after weekends. Up to 60% of these binge drinkers will develop a transient atrial fibrillation or supraventricular tachycardia without the presence of any structural heart disease. Generally, this condition spontaneously resolves over a 24-hour period of abstinence from alcohol.

The pathogenesis is not completely understood. However, several mechanisms have been proposed to explain the arrhythmogenic properties of acute alcohol ingestion. First, studies have found that alcohol intoxication stimulates the secretion of epinephrine and norepinephrine, which results in slightly increased sympathetic output leading to an increase in heart rate and an increase in the risk of arrhythmias. A second mechanism involves the alcohol metabolite acetaldehyde acting on the cardiac cells, which leads to a decrease in the sodium current and ultimately interferes with cardiac conduction. It is believed that these two mechanisms may work synergistically. It is well known that continued excess alcohol consumption can lead to alcoholic dilated cardiomyopathy, which results in permanent structural changes along with permanent atrial and ventricular arrhythmias. However, for simple cases of holiday heart syndrome occurring in young individuals without a history of cardiac disease, the prognosis is good and the atrial arrhythmias should resolve within 24 hours. If the ventricular rate is excessive as in the case described above, an AV nodal blocking agent such as a beta-blocker or calcium channel blocker (verapamil or diltiazem) may be used temporarily for rate control. Cardioversion may be considered for patients with atrial fibrillation approaching a duration of 48 hours in order to prevent the need for anticoagulation. Once arrhythmias resolve, healthy, young patients can usually be safely discharged from the emergency department with precautions to avoid excessive alcohol consumption in the future.

References:

  1. Budzikowski A. Holiday Heart Syndrome. Medscape, 4 Jan. 2012. Web. 19 June 2014.
  2. Ettinger PO, Wu CF, De La Cruz Jr. C, Weisse AB, Ahmed SS, Regan TJ. Arrhythmias and the "Holiday Heart": alcohol-associated cardiac rhythm disorders. Am Heart J. 1978;95(5):555–562.
  3. Leonard G. Epidemiology of and Risk Factors for Atrial Fibrillation. UpToDate. 06 May 2014. Web. 19 June 2014.
  4. Tonelo D, Providencia R et al. Holiday Heart Syndrome Revisited after 34 Years. Arq Bras Cadiol. 2013, 101(2): 183-189.

Your 2014-2015 Leaders:

President
Meaghan Mercer, DO

Vice President
Victoria Weston, MD

Secretary-Treasurer
Edward Siegel, MD

Immediate Past President
Leana Wen, MD MSc

At-Large Board Members
Nicole Battaglioli, MD
Mary Calderone, MD
Michael Gottlieb, MD
Sean Kivlehan, MD
Amrita Lalvani, MD
Andrew Phillips, MD

Medical Student Council President
Michael Wilk

Publications Advisor - Ex-Officio Board Member
Joel Schofer, MD MBA RDMS FAAEM

Copy Editor: Mary Calderone, MD
Managing Editor: Lauren Johnson, AAEM/RSA Staff

Modern Resident Contributors

Special thanks to this issue's contributors:
Mary Calderone, MD; Destinee DeLemos, MD; Kaitlyn Fries, OMSIII; Ashley Grigsby, MSIV; Nate Haas, MD; Sophia Johnson, DO; Alexandra Murray, OMSIII; Nicholas Pettit, PhD OMSIII; Jimmy Tam Huy Pham, MHS MA MSIV; Shane Sergent, DO; Joseph Zygowiec, MPH MA MSIV

Interested in writing?

Email submissions to: info@aaemrsa.org

Please submit articles by September 15th for the October/November edition.

Articles appearing in Modern Resident are intended for the individual use of AAEM members. Opinions expressed are those of the authors and do not necessarily represent the official views of AAEM/RSA. Articles may not be duplicated or distributed without the explicit permission of AAEM/RSA. Permission is granted in some instances in the interest of public education. Requests for reprints should be directed to AAEM/RSA, 555 East Wells Street, Suite 1100, Milwaukee, WI 53202, Tel (800) 884-2236; Fax: (414) 276-3349, Email: info@aaemrsa.org.

 

AAEM/RSA  |  555 East Wells Street, Suite 1100  |  Milwaukee, WI 53202
Tel: (800) 884-2236  |  Fax: (414) 276-3349  |  Email: info@aaemrsa.org

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