Modern Resident - The newsletter of AAEM/RSA
December/January 2014
Volume 5: Issue 4  |  FacebookTwitterLinkedIn


Your 2013-2014 Leaders:

President
Meaghan Mercer, DO

Vice President
Rachel Engle, DO

Secretary-Treasurer
S. Terez Malka, MD

Immediate Past President
Leana Wen, MD MSc

At-Large Board Members
Michael Gottlieb, MD
Calvin Hwang, MD
Sean Kivlehan, MD
Nicole Piela, MD
Edward Siegel, MD
Victoria Weston, MD

Medical Student Council President
Mary Calderone

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

Modern Resident Contributors

Copy Editor: Victoria Weston, MD
Managing Editor: Lauren Johnson, AAEM/RSA Staff

Special thanks to this issue's contributors:
Karina Bartlett, MSIV; Nicole Battaglioli, MD; Shawna Bellew, MD; Thomas Doran, MSIV; Jenna Erickson, MSIII; Kaitlin Fries, MSIII; Anand Gopalsami, MD MBA; Ashley Grigsby, MSIV; Nathan Haas, MSIV; Elise Heeringa, MSIV; Maite Huis in 't Veld, MD; Geoff Jara-Almonte, MD; Natalie Kirilichin, MD; Sean Kivlehan, MD MPH; James Lloyd, MSII; Alexander Simakov, MPH MSIV; and Julian Villar, MD

Interested in writing?

Email submissions to: info@aaemrsa.org

Please submit articles by January 28th for the February/March 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 mey 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 the AAEM/RSA, 555 East Wells Street, Suite 1100, Milwaukee, WI 53202, Tel (800) 884-2236; Fax: (414) 276-3349, Email: info@aaemrsa.org.

Hypokalemic Periodic Paralysis
Nathan Haas, MSIV
Loyola University Chicago Stritch School of Medicine

A 22-year-old male presents to the ED with a complaint of "not being able to move." He reports he was resting and watching television this evening, when he began experiencing rapidly progressive, painless weakness of his lower extremities. He has never experienced symptoms previously. He denies recent illness, travel, gastrointestinal disturbances or urinary symptoms. He has no past medical history, is on no medications and denies drug use. He believes his father experienced something similar many years ago. Upon further questioning, the patient states that he had vigorously worked out earlier in the afternoon.

The patient is afebrile and has normal vital signs. A thorough physical exam reveals symmetric 1/5 weakness in the lower extremities, 2+ reflexes throughout and a normal sensory exam. The patient is unable to stand or walk. Routine labs are pertinent for potassium of 1.4mM/L, and the patient's EKG is pictured below. What diagnoses must be considered, and what are your first steps in management?

This patient is profoundly hypokalemic, has had no recent illnesses and his reflexes are preserved; all of which support hypokalemia as the cause of his lower extremity weakness as opposed to Guillain-Barré syndrome. The EKG demonstrates classic manifestations of hypokalemia, including prominent U-waves (best seen here in lead V2), prolonged QT interval and ST depression. The differential diagnosis for symptomatic hypokalemia is broad and includes GI losses, urinary losses (including diuretic abuse), excessive sweating, decreased dietary intake or intracellular shifting of potassium (insulin, adrenergic activity, alkalotic states).

After excluding many of the above-mentioned causes and considering the patient's family history of similar events, Hypokalemic Periodic Paralysis (HPP) is the most likely diagnosis. HPP is a neuromuscular disorder that involves defective muscle ion channels, and is often familial. Acute attacks of paralysis are most commonly precipitated by strenuous exercise followed by rest (as in this patient), or by ingestion of a carbohydrate-rich meal. Definitive diagnosis is often established with genetic testing, muscle biopsy and/or EMG. HPP closely mimics Thyrotoxic Periodic Paralysis in presentation, and thyroid studies should be included in the evaluation of patients with acute onset paralysis to help differentiate. Patients with HPP typically have normal levels of potassium between attacks but present profoundly hypokalemic during provoked attacks, such as this one.

Acute management of HPP consists of judicious repletion of potassium and any other electrolyte disturbances with continuous cardiac monitoring. Patients typically are not truly potassium-depleted and thus, small increments of potassium are all that is needed to abort the acute attack. Rebound hyperkalemia is common following repletion and thus, some experts advocate slow repletion with 30meq of KCl every 30 minutes until serum levels normalize. Attacks can be prevented with potassium-sparing diuretics or topiramate.

Acute onset of ascending paralysis is often caused by Guillain-Barré syndrome, but several other causes exist including Hypokalemic Periodic Paralysis and Thyrotoxic Periodic Paralysis. In HPP, it is essential to avoid overzealous repletion of hypokalemia, as rebound hyperkalemia is a common complication.

References:

  1. Gutmann L, Conwit R. Hypokalemic Periodic Paralysis. UpToDate. N.p., 6 Feb. 2012. Web. 20 Nov. 2013.
  2. Venance, SL. The Primary Periodic Paralyses: Diagnosis, Pathogenesis and Treatment. Brain. 129.1 (2005): 8-17. Online.


Bringing Home Zebras: A Chance to Practice International EM in the U.S.
Elise Heeringa, MSIV
Loyola University Chicago

Case Presentation
A 35-year-old previously healthy Honduran man presents after a witnessed first-time, generalized tonic-clonic seizure. It resolved after EMS administered 10mg IM midazolam en route to the hospital. Family denies head injury or substance use, and the patient takes no medications. He has had two days of headache but no fever, sweats, nausea/vomiting, focal neurologic symptoms or weight loss.

Vital signs are within normal limits, and the patient is sleepy but arousable. He has no nuchal rigidity or focal neurologic deficits, and exam is otherwise unremarkable. Routine laboratory testing is also unremarkable including electrolytes, blood glucose, urine drug screen and alcohol level. However, CT head reveals an approximately 1cm cystic brain lesion with surrounding edema, as well as several scattered calcified lesions.

What zebra should you keep on your differential?

Discussion
Neurocysticercosis (NCC) is the most common parasitic CNS infection, and in the U.S. upwards of 2,000 people are diagnosed with it annually. The disease has a slight male predominance, and most patients are immigrants from endemic areas, namely Latin and South America, sub-Saharan Africa, India and Asia. Worldwide, cysticercosis affects some 50 million people, largely in rural parts of developing countries.

The disease is transmitted when a person ingests Taenia solium eggs shed in human feces. Infection with the adult tapeworms (taeniasis) is typically acquired by eating undercooked pork containing the immature larval cysts, called cysticerci. Pigs themselves acquire the cysticerci by consuming human feces infected by T. solium eggs.

After ingested eggs hatch and the larvae invade the intestinal wall, they preferentially form cysticerci in several sites including striated muscle and the CNS, with CNS involvement being termed neurocysticercosis. NCC most frequently involves the brain parenchyma itself, but it can also be extraparenchymal including meningeal, intraventricular, spinal or ocular sites.

Parenchymal lesions may be single or multiple and are usually located at the border of the gray and white matter. They may cause headache, seizure, altered mental status or focal neurologic deficits, and in rare cases may cause mass effect. Seizure is the most common manifestation, seen in 70-90% of symptomatic patients, and NCC is the leading cause of acquired epilepsy in the developing world.

Intraventricular and meningeal lesions may obstruct CSF flow, leading to hydrocephalus, with subarachnoid lesions also carrying a risk of vasculitis and stroke. Ocular cysticerci may be visible on fundoscopic exam and must be ruled out if NCC is diagnosed, as inflammation of degenerating subretinal cysticerci may damage vision.

Neurocysticeri typically do not provoke a host response while encased, but once a larva dies its disintegration releases antigens that lead to the inflammation that produces symptoms. As necrotic cysts are resorbed, calcifications may form.

Diagnosing NCC can be difficult, but usually involves a combination of history and neuroimaging. Lesions may be ring-enhancing, and a scolex (larval “head”) may be visualized, more often with MRI. The enzyme-linked immunoelectrotransfer blot (EITB) assay is the preferred serologic test, although its sensitivity may be limited depending on parasitic burden and the test may remain positive long after parasites are dead.

Seizures due to NCC can be managed and prevented with standard antiepileptic agents. In cases of hydrocephalus, treatment may require neurosurgical intervention. Recommendations regarding the use of anti-helminth treatments (e.g., albendazole or praziquantel) vary depending on disease extent, location and activity, because the inflammatory reaction provoked by dying larvae may lead to an initial worsening of symptoms. In many cases corticosteroids may be used in conjunction with anti-parasitic agents to reduce this effect. Antiepileptic treatment alone may be considered for single enhancing lesions, which tend to resolve spontaneously within six months.

References:

  1. Bruno E, Bartoloni A, Zammarchi L, Strohmeyer M, Bartalesi F, Bustos JA, et al. Epilepsy and Neurocysticercosis in Latin America: A Systematic Review and Meta-Analysis. PLOS Neglected Trop Dis. 2013; 7: 1-11.
  2. CDC, 2012. Parasites – Cysticercosis. Centers for Disease Control and Prevention. www.cdc.gov/parasites/cysticercosis/. (November 18, 2013).
  3. Del Brutto OH. Diagnosis criteria for neurocysticercosis, revisited. Patho Glob Health. 2012; 106: 299-304.
  4. Garg RK, Sinha MK. Multiple ring-enhancing lesions of the brain. J Postgrad Med. 2010; 54: 307-316.
  5. White Jr., AC. Epidemiology, transmission and prevention of cysticercosis. In: UpToDate. Baron, EL (Ed), Waltham, MA, 2013.
  6. White Jr., AC. Clinical manifestations and diagnosis of cysticercosis. In: UpToDate. Baron, EL (Ed), Waltham, MA, 2013.
  7. White Jr., AC. Treatment of cysticercosis. In: UpToDate. Baron, EL (Ed), Waltham, MA, 2013.

Advocacy Day Recap
Sean Kivlehan, MD MPH
AAEM/RSA Advocacy Committee Chair
University of California - San Francisco

Emergency physicians work at the front line of health care. As a consequence, we face challenges unique to our profession. We see patients who cannot afford their medications and return repeatedly for untreated chronic conditions, and we see patients who cannot obtain proper follow-up due to lack of adequate insurance coverage. We deal with the realities of a broken system that many providers can avoid: our door is clearly lit and always open, regardless of patient insurance status.

Advocacy Day
On October 9th, 2013, resident and medical student members of AAEM/RSA from across the country converged on Washington, D.C., for the second annual AAEM/RSA Advocacy Day. Building on the successes of last year, we were able to hold over 15 targeted meetings with members of Congress and their staff.

Lobbying 101
Our lobbyists at Williams & Jensen, a Washington, D.C., lobbying firm, hosted an informative educational session and guided us throughout our day in the capital. Learning the anatomy of a congressional office was an important first step; members of Congress maintain offices and staff both in the capital as well as their home region. Each has a chief of staff, legislative director, assistants and correspondents. While we were often able to meet directly with members of Congress, other times we would meet with their staff. We learned quickly that looks can be deceiving; although staffers can at times be young, they are the eyes and ears of the representatives and their senior staff.

The “Ask”
There is always a purpose to meeting a representative; frequently, it is to influence their opinion on legislation or increase their awareness of issues important to you and your industry. This is called the “ask.” Conveying this message can be difficult since congressional representatives may meet with dozens of people every day lobbying for issues across many industries. It is important to have a clear request, and to convey why they should act upon and remember your issue.

Do’s & Don’ts
An effective “ask” consists of four components: a personal anecdote, the facts illustrating that anecdote as part of a larger problem, how this problem affects the member of Congress and his or her constituents, and a proposed solution. Lists of facts and statistics can be lost in the inundation of information passing through these offices everyday. Focus your message and use your real life experience as a physician to make the facts personal. Getting the member of congress to contemplate your issues is the first step, which needs to be followed by drawing a connection to his or her constituency. Finally, deliver the punch line — the solution. Your solution could be a request for a vote for or against pending legislation, a new proposal, or revisiting an existing one.

Be a Decision Maker
Representative Raul Ruiz (D-CA), a residency trained emergency physician, hosted us for lunch at the National Democratic Convention Club. He discussed his remarkable journey from adolescence in the Coachella Valley, through medical training in Boston and Pittsburgh, to employment as an emergency physician in California, with election to the House of Representatives in 2012. He stressed the importance of having a seat at the table where decisions are made about our specialty and health care. He noted that while we may not all become congressional representatives; we can have our voices heard by getting involved. If you cannot be the decision maker, get as close to possible to one — which is what we did on Advocacy Day.

Make a Difference
If you think the system could be better than it is now, then get involved and make that change. Advocating allows us to give our patients a voice in the legislative process, and by advocating their interest, we are advocating ours. There are many opportunities to get involved on the national, state and local level. Remember that advocacy starts at home: most hospitals and medical schools have committees that can provide you with a platform for your message.

Three Issues We Addressed at Advocacy Day in Washington, D.C.:

  • Medical Student Debt Reform: Rising tuition costs, increased interest rates on loans and a decrease in programs aimed at containing debt (grants and scholarships) have all contributed to the ever-increasing debt burden for medical students. As such, AAEM/RSA recommended capped tuition for medical students, access to affordable loans that are not dictated by fluctuations in the bond market, guaranteed existence of the Public Service Loan Forgiveness Program for those already making payments, and inclusion of emergency physicians in the National Health Service Corps.
  • Supporting GME: The American Association of Medical Colleges predicts an upcoming physician shortage of 62,900 doctors by the year 2015. This is expected to increase to 130,600 by the year 2025. In 2015, it is projected that the number of American medical school graduates will exceed the number of available GME positions in the country. AAEM/RSA recognizes the important role of GME funding to address challenges to our health care system, including improvement of quality of care, adapting to rapid improvements in medical technology and helping meet the increasing demand for physicians, and recommended increases to its funding.
  • Protecting Board Certification: Completion of a residency in emergency medicine should be a prerequisite to board eligibility; however, alternate pathways exist. AAEM/RSA believes giving non-residency trained physicians the title of “board certified” is disingenuous, and undermines the academic integrity of emergency medicine and those who have spent years specializing in the field.

AAEM Scientific Assembly Career Fair


Medical Student Debt Reform
Anand Gopalsami MD MBA
Natalie Kirlichin MD
Julian Villar MD
James Lloyd, MSII
AAEM/RSA Advocacy Committee

Introduction
This year, AAEM/RSA’s Advocacy Committee will focus its efforts on your behalf on four critical areas affecting emergency medicine residents and medical students interested in our specialty: medical education debt reform, the funding of graduate medical education/resident salaries, tort reform and protecting EM board certification. These issues were addressed during AAEM/RSA’s Advocacy Day in Washington, D.C., on October 9, 2013. We will keep you apprised of the committee's work through a series of articles in Modern Resident on each of these topics. Our first installment addresses debt reform.

The cost and debt burden of medical education is a critical and ever-increasing problem for all specialties, including our own. Medical school tuition and the subsequent debt burden required to pay for it, has increased dramatically over the last two decades and threatens to cripple future generations of physicians. Recently, new programs have been developed in an attempt to curtail the costs and to mitigate the effects of debt, but with little impact on the rate of expansion of the problem. More needs to be done. This year, the AAEM/RSA Advocacy Committee will lobby law-makers in Congress to adopt new and more aggressive policies to put a halt to this disaster in the making.

Student Debt Burden
In 2006, the AAMC estimated the median debt burden for graduates of public and private medical schools to be $119,000 and $150,000, respectively. In the last 30 years, the medical education debt has increased by a factor of 4.5, far outpacing inflation. This massive increase has been driven in large part, especially since the most recent economic downturn, by increased tuition costs and reduced availability of scholarships as a consequence of widespread budget cuts.

However, the above figures do not take into account the opportunity cost of attending medical school. By adding up lost wages, potential interest from debt obtained, and calculating the net present value of future lost revenue adjusted for inflation, the opportunity cost of attending medical school is far greater. The real cost is estimated to be $347,535.*

Recent Federal Loan Reforms
Since 2006, students taking out federal loans, including Stafford and Grad PLUS loans, have enjoyed fixed interest rates of 6.80 and 7.90%, respectively.2 These fixed loans have served as comparably inexpensive alternatives to many other private loans and functioned to temper overall fluctuations in interest rates on student loans as a whole. In the face of multiple budget crises and spiraling government debt, however, federal loans for graduate and professional students have taken numerous hits. The first of these hits came in the form of the Budget Control Act (BCA) of 2011, which eliminated the subsidization of Stafford loans for professional students.3 The AAMC predicts that this change alone will increase loan repayments by $10,000 to $20,000.4

Temporarily buffering the BCA is the recently passed Student Loan Certainty Act of 2013. The act eliminated the once fixed interest rates of Stafford and Grad PLUS loans and replaced them with rates based on interest rates of Treasury notes, effectively making them market-dependent. With current interest rates on Treasury notes the lowest they have been in years, the change is an appealing boon to students everywhere.1 However, as the market improves and interest rates on treasury bonds rise, so too will interest rates on student loans. Here’s how things will play out; initially, rates on Stafford loans for professional students will drop from 6.80 to 5.41%, while those of Grad PLUS loans will fall from 7.90 to 6.41%.1,5 As the economy recovers, this trend will reverse. Interest rates will be revised (i.e., raised) yearly for new Stafford and Grad PLUS loans and capped ultimately at maximum rates of 9.50 and 10.50% respectively.

Analysis of interest rates by the Congressional Research Service conservatively suggests that by 2016 the interest rates on Stafford and Grad PLUS loans for professional students will exceed their previously fixed rates of 6.80 and 7.90% respectively, and will approach their maximum rates a few years after.6 In essence, the Student Loan Certainty Act will transiently provide medical students with welcomed relief. Interest rates subject to the state of the market, however, are on course to return to and exceed their previous levels, thereby compounding student debt burden.

This trend is simply not sustainable.

Tuition Caps and Debt Forgiveness Programs
Currently, the AMA and AAMC have endorsed policies aimed at reducing tuition (tuition caps), increasing ways of paying for medical school (more grants and scholarships), and making it easier to repay debt (tax deductions on loan payments, advocating for a cap on interest rates, debt forgiveness, etc.).

A few different debt forgiveness programs have gained some attention recently. The National Health Service Corp (NHSC) provides debt repayment assistance to primary care providers working in underserved communities. Though emergency physicians are our nation’s primary safety net providers, we are ironically not eligible for the NHSC.

The Public Service Loan Forgiveness Program, authorized by the College Cost Reduction and Access Act of 2007, provides a potential source of debt reduction. Physicians in any specialty are eligible after 10 years of loan repayment and employment in a public service job. These include non-profit organizations, public health agencies, emergency management agencies, and residency and faculty positions at university medical centers and public hospitals. After 10 years, eligible physicians may have the remainder of their debt forgiven. Though this program appears promising, it is not guaranteed. Congress may choose to defund the program at any point, and physicians who have served for nine years and 364 days may no longer be eligible.

Summary
Rising tuition costs, increased interest rates on loans and a decrease in programs aimed at containing debt (grants and scholarships), have all contributed to the ever-increasing debt burden. As such, action should be taken on each of the following factors:

  1. Tuition should be capped.
  2. Interest rates on student loans should not be tied to fluctuations in the bond market.
  3. The Public Service Loan Forgiveness Program should become guaranteed for those already making payments.
  4. An effort should be made to increase available grants and scholarships.

*Assuming median salary for undergraduates is $45,000 and average medical school debt per year is $42,000, four years in medical school, 3% inflation rate, no debt from undergrad, and 12.75% median 25-year annualized return for the S&P 500.

References:

  1. H.R. 1911, 113th Cong. (2013) (enacted). Print.
  2. Fresne J, Youngclaus J. Medical Student Education: Debt, Costs, and Loan Repayment Fact Card. AAMC.org. AAMC, n.d. Web. 16 Sept. 2013.
  3. S. 365, 112th Cong. (2011) (enacted). Print.
  4. Youngclaus J, Fresne J. Physician Education Debt and the Cost to Attend Medical School - 2012 Update. AAMC.org. AAMC, Feb. 2013. Web. 15 Sept. 2013.
  5. Bidwell A. Obama Signs Student Loan Interest Rate Deal. US News. US News & World Report, 09 Aug. 2013. Web. 17 Sept. 2013.
  6. Smole DP. An Examination of Student Loan Interest Rate Proposals in the 113th Congress. 26 July 2013. R43094. Federation of American Scientists. Web. 15 Sept. 2013.


Crash Deliveries
Ashley Grigsby, MSIV
Arizona College of Osteopathic Medicine

It’s every EM physician’s worst nightmare — cardiopulmonary arrest in a pregnant patient. Although some EM doctors will go their entire careers without having a pregnant arresting patient, like all things in emergency medicine, we must be prepared for the worst. Cardiac arrest occurs in about 1 in 30,000 pregnancies. According to one review, the most common causes of arrest are cited as pulmonary embolism (29%), hemorrhage (17%), sepsis (13%), followed by peripartum cardiomyopathy, stroke, preeclampsia, amniotic fluid embolism, MI, and other cardiac diseases accounting for the remainder of cases.1

Initial resuscitation starts with ACLS protocol. However, there are pregnancy specific modifications required during initial resuscitation. If fundal height is at or above the umbilicus, the uterus should be displaced to the left to decrease compression of the inferior vena cava.1 This can be done by placing a wedge or rolled up towels under the patient's right side. As always, airway management is a priority, especially because pregnant women have a higher risk of hypoxemia due to physiologic changes associated with pregnancy. Bag mask ventilation and intubation can be more difficult, and the provider should prepare for a difficult airway.1 Intravenous access in the upper extremities is also important. Medications given through femoral lines may not reach the heart due to obstruction from the gravid uterus.1

Fetal monitoring, initially, is not required and resuscitation efforts should initially be focused on the mother. If the mother has return of spontaneous circulation, fetal distress can then be assessed. Gestational age can be assessed by fundal height; the level of the umbilicus corresponds to 20 weeks and the xiphoid process corresponds to 36 weeks.2 If you consider 24 weeks as fetal viability, about 3 to 4cm above the umbilicus can indicate possible viability. 2

According to the American Heart Association, the decision to deliver the fetus as part of the resuscitation process needs to occur within four minutes of unsuccessful maternal resuscitation. This is coined the “Five Minute Rule,” which states that the baby should be delivered within five minutes of maternal arrest. Delivery can relieve aortocaval compression and can increase maternal survival.1 Delivery in this time frame also improves the chances of normal neonatal neurological outcome.1

If perimortem cesarean delivery is performed, the exact technique should be well known to the provider. The procedure involves a midline incision from 2 to 3cm above the pubic symphysis extending to 1cm below the umbilicus.3 Extend the incision through the subcutaneous tissue, until exposure of the uterus is achieved.3 A 2 to 4cm midline vertical incision is then made to the uterus, taking care to protect the fetus.3 Delivery of the fetus involves inserting a hand between the head and the pubic symphysis, flexing the head and applying anterior and superior traction, while fundal pressure is applied by an assistant.3 Again, providers should be familiar with this technique before attempting.

When caring for a pregnant arresting patient, it is important to remember to take care of the mother first and foremost. ACLS protocol should be initiated with the proper pregnancy modifications. It’s important to involve obstetrics and neonatology early on in the resuscitation in the chance perimortem cesarean will be attempted. If resuscitation efforts are unsuccessful at four minutes, and fundal height is 3 to 4cm above the umbilicus, delivery should occur.

References:

  1. Zelop CM. Management of cardiopulmonary arrest in pregnancy. Up to Date. [Internet] 2013 [cited 2013 November 11]. http://0-www.uptodate.com.millennium.midwestern.edu/contents/management-of-cardiopulmonary-arrest-in-pregnancy?source=see_link&anchor=H2349341435#H2349341435.
  2. Campbell TA, Sanson TG. Cardiac arrest and pregnancy. J Emerg Trauma Shock. 2009; 2(1):34-42.
  3. Hendricks SK, Flippin A. Chapter 115. Perimortem Cesarean Section. In: Reichman EF, Simon RR, eds. Emergency Medicine Procedures. New York: McGraw-Hill; 2004. http://0-www.accessemergencymedicine.com.millennium.midwestern.edu/content.aspx?aID=43085. Accessed November 18, 2013.

Incidental Hyperglycemia in the Emergency Department
Shawna Bellew, MD
Mayo Clinic Emergency Medicine Residency

A 55-year-old female presented with headache. ED evaluation was unremarkable, with the exception of a blood glucose level of 250mg/dL. The patient had no history of diabetes mellitus, polyuria or polydipsia. Her last meal was the night prior. The patient was ultimately discharged with primary care follow-up. Shortly thereafter, the patient was admitted to an outside hospital due to hyperglycemia and elevated hemoglobin A1c. She had submitted a complaint to the department indicating that she felt she should have been admitted upon her original presentation for hyperglycemia.

The emergency department is increasingly becoming the safety net for those without primary care. According to the May 2012 report by the Centers for Disease Control and Prevention, almost 80% of adult ED visits were related to a lack of access to health care providers. Though there is no official consensus about the precise blood glucose level that would justify referral for an official HbA1c, fasting glucose or OGTT, a conservative recommendation would be that non-diabetic patients with random blood glucose levels above 200mg/dL are at increased risk of impaired glucose tolerance.1-2 An argument could be made that emergency department glucose values are invalid secondary to physiologic stress. However, studies suggest that any random blood glucose value above 200mg/dL is indicative of an elevated underlying HbA1c, regardless of the setting or fasting status. These patients should, at minimum, be informed of that they are at risk and instructed to follow-up with their primary care physician. A good resource for patient education is the website of the American Diabetes Association (www.diabetes.org), which contains patient friendly information in both English and Spanish.

According to the 2011 National Diabetes Fact Sheet, there are approximately 7 million undiagnosed people with diabetes melitus (DM) in the United States, as well as 79 million with pre-diabetes. Patients may suffer from the vascular complications of pre-diabetes for almost a decade prior to being diagnosed with type 2 DM. With lifestyle modification, up to half of these patients may be able to delay or prevent progression from prediabetes to type 2 DM. Surveys suggest that up to 95% of ED patients would prefer to be informed of elevated glucose levels and would be willing to follow-up.3 Despite this, in a recent cross-sectional study of 106 non-diabetic patients who were discharged with hyperglycemia of greater than 150mg/dL from two San-Diego emergency departments, only one patient had discharge instructions or any documentation that mentioned hyperglycemia. Given the sheer number of patients at risk for diabetes and the volume of electrolyte panels ordered, this presents an opportunity to avoid comorbidity in these patients with little increased burden to the ED provider.

References:

  1. Ginde AA, Delaney KE, Pallin DJ, Cmargo, Jr., CA. Multicenter survey of emergency physician management and referral for hyperglycemia. J Emerg Med. 2010;38:264-70.
  2. Rouse MD, Shoukry CL. Elevated blood glucose levels in the emergency department: missed opportunities. J Emerg Nurs. 2013; epub ahead of print.
  3. Ginde AA, Delaney KE, Lieberman RM, Vanderweil SG, Camargo, Jr., CA. Estimated risk of undiagnosed diabetes in the emergency department: a multicenter survey. Acad Emerg Med. 2007;14:492-5.

Oncologic Emergencies
Maite Huis in 't Veld, MD
University of Maryland

In the United States, cancer is the second leading cause of death.1 For some patients, an oncologic emergency may be the initial manifestation of their illness. It is pertinent that the emergency physician is able to recognize and effectively treat conditions such as acute tumor lysis syndrome, malignant pericardial disease, superior vena cava syndrome and malignant spinal cord compression.

Acute Tumor Lysis Syndrome
Tumor lysis syndrome results from tumor cells that release their contents into the bloodstream, including the release of potassium, phosphorus, cytokines and nucleic acids.2 This can occur spontaneously or can be precipitated by therapy. The release of the tumor cell content can lead to significant hyperuricemia, hyperkalemia, hyperphosphatemia and hypocalcemia. At least two of these abnormalities are required for diagnosis.2 The electrolyte abnormalities subsequently may lead to renal insufficiency, cardiac arrhythmias and seizures. The release of cytokines can lead to a systemic inflammatory response, with possible multi-organ failure. The main stem of treatment is to reduce the risk of renal impairment and arrhythmias. The initial step in treatment should consist of fluid resuscitation and correction of electrolyte abnormalities. Recombinant urate oxidase can be used to correct uric acid levels.1 Renal replacement therapy can be considered in severe cases.

Malignant Pericardial Disease
Pericardial effusion is very common in cancer patients, with up to 34% of oncologic patients having a pericardial effusion.1 Most malignant pericardial disease is caused by metastasis, most frequently from lung, breast and hematologic sources. Patients present with exertional dyspnea and chest pain. ECG findings may include a low amplitude tracing and electrical alternans. Chest X-ray may reveal an enlarged cardiac silhouette. Echocardiography is the diagnostic imaging technique of choice. Echocardiography can clarify the hemodynamic significance of the effusion and guide pericardiocentesis.1 If the patient is hypovolemic, an initial volume bolus may be given, but this is of no additional value and potentially harmful if the patient is eu- or hypervolemic. Patients who are in shock require immediate bedside pericardiocentesis. Ultrasound can be used to guide the needle to help prevent laceration of the myocardium. If the patient is hemodynamically stable, the placement of an indwelling drainage catheter can be considered at time of pericardiocentesis, as there is a high rate of recurrence. Other options for treatment of chronic pericardial effusion include sclerosing therapy, balloon pericardiotomy or surgical window.1

Superior Vena Cava Syndrome
Superior vena cava syndrome (SVCS) is due to an occlusion of the SVC. SVCS in the setting of a malignancy is caused by extrinsic compression on the SVC by a mass in the middle or anterior mediastinum. The resulting increased venous pressure leads to facial edema, upper extremity edema, dyspnea, coughing, chest pain, shoulder pain, hoarseness and, rarely, cerebral edema.1,3 SVCS is frequently a clinical diagnosis, but can be confirmed by CT chest with contrast in the venous phase or MRI phlebocavography. The cornerstone of treatment is treatment of the underlying etiology, frequently necessitating a biopsy for histological and cytological examination. If there are signs of a threatened airway or hypotension, urgent stenting or thrombolysis may be considered after initial resuscitation of the patient.3 In the absence of the aforementioned acute symptoms, biopsy and staging should be performed to develop a tumor-and stage-specific treatment plan, often including radiation and chemotherapy.

Malignant Spinal Cord Compression
The spine is a frequent site of metastatic disease. Within the last two years of life, approximately 5% of patients experience spinal cord compression.1 Most patients will present with back pain, decreased motor control, sensory deficit, or bowel or bladder dysfunction. MRI of the entire spinal cord is the gold standard, with CT myelography as an alternative if MRI is not readily available. Treatment is aimed at pain control and prevention of paralysis. Radiotherapy can be initiated for radiosensitive tumors. High dose steroids can be used in patients with an abnormal neurologic exam. For some patients, surgical decompression can be considered.1

References:

  1. McCurdy, MT, Shanholtz, CB. Oncologic emergencies. Crit Care Med. 2012 Jul;40(7):2212-22.
  2. Howard SC, Jones DP, Pui CH. The tumor lysis syndrome. N Engl J Med. 2011 May 12;364(19):1844-54.
  3. Lepper PM, et al. Superior vena cava syndrome in thoracic malignancies. Respir Care. 2011 May;56(5):653-66.

ED Dental Visits
Kaitlin Fries, MSIII
Ohio University College of Osteopathic Medicine

Lack of access to preventative dental care is contributing to a nationwide increase in ED visits for dental complaints.1 In 2009, the Agency for Healthcare Research and Quality reported over 900,000 emergency department visits and close to 13,000 inpatient stays due to dental conditions. The most common dental-related ED diagnosis was dental caries (cavities), which made up 42% of the 900,000 visits, while 63% of the inpatient stays were due to dental abscesses. Forty-two percent of these patients were uninsured and much of the remaining 58% were on Medicaid.2 In 2009, the Government Accountability Office reported that finding a dentist that accepts Medicaid is an obstacle to providing children’s dental care nationwide, as only 10% of dentists participate in Medicaid.

The Agency for Healthcare Research and Quality found the following dental related diagnoses to be most prevalent in the ED: dental caries, abscesses, periodontitis and gingivitis. Data from the National Hospital Ambulatory Medical Survey revealed that a majority of these dental visits result in prescribed antibiotics and analgesics as well as patient referral to a clinic for definitive treatment.

Dental Caries and Pulpitis: A new carious lesion is typically described as a soft to rubbery textured discoloration on the coronal or root surface of the affected tooth. Caries are most often caused by Streptococcus mutans or Streptococci sobrinus.3 Initially, pulpitis presents as a severe toothache with tenderness to palpation and pain exacerbated by hot or cold temperature exposure.3 Management typically includes oral analgesia, warm saline rinses, and, occasionally, narcotics.4 Patients can also be given a long-acting dental block until they are able to see the dentist for follow-up care.4

Periodontal Abscesses: These abscesses are treated the same as any oral abscess. Consider I&D, provide antibiotics effective against mouth flora, analgesics and instruct the patient to use warm saline rinses.4 Recommend close follow up.

Periodontal Disease (Gingivitis and Periodontitis): Gingivitis presents with swelling, bluish purple discoloration, and a tendency to bleed after eating or brushing; these symptoms can range from mild to severe.3 Patients normally do not complain of pain but typically complain of halitosis. Chronic gingivitis can lead to periodontitis, which is defined as “gingival inflammation with accompanying loss of supportive connective tissues.”3 Plaques and calculi will be present and frank pus may be seen in periodontal pockets.3 The most common complication of periodontal disease is tooth loss. Other complications include local or systemic spread, periodontal abscess and orofacial space infections.3

References:

  1. McKenna M. The Root of the Problem: Emergency Physicians Struggle To Provide Dental Care When No One Else Will. Annals of Emergency Medicine. Volume 55, Issue 6. June 2010. Pages A17-A19.
  2. Seu K , Hall K, Moy E. Emergency Department Visits for Dental-Related Conditions, 2009. HCUP Statistical Brief #143. November 2012. Agency for Healthcare Research and Quality, Rockville, MD.
  3. Chow A. Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections. UpToDate. May 13, 2013.
  4. Cline DM, Ma OJ. Tintinallis Emergency Medicine: Just the Facts. Third Edition; 2013. Section 17; Chapter 154: 546.

Neonatal Fever
Karina Bartlett, MSIV
University of Texas Health Science Center at San Antonio

The goal of emergency department evaluation of febrile neonates is to determine the etiology of any serious bacterial infection and provide appropriate treatment, indicating the need for empiric antibiotics and hospital admission. Fever in the neonate is >100.4°F (38°C). Rectal temperatures are more reliable than temporal and tympanic (infrared) thermometers.1 Once fever has been verified, treatment with acetaminophen 15mg/kg/dose is recommended either orally or by rectum.2

There are three clinical decision rules for febrile infants: the Rochester Criteria, Philadelphia Protocol, and Boston Low-Risk Criteria. Of these, only the Rochester Criteria includes decision rules for neonates <28 days old. The Rochester criteria state that, for a term infant <60 days old, with no history of antibiotic use, no treatment for jaundice, no chronic illness and an unremarkable physical exam, evaluation can consist of urinalysis, CBC and stool studies. With appropriate lab values (see table below), the infant can be considered low risk for serious bacterial infection.3

Urinalysis WBC<10 per hpf
CBC WBC>5000 and <15000/mm3
Absolute bands <1500/mm3
Stool WBC<5 per hpf

Unfortunately, the Rochester Criteria does not include a chest X-ray or a lumbar puncture. This has been shown to lead to approximately 1% of SBI cases missed using this criteria.4 It is, therefore, recommended that any febrile infant <30 days old undergo a full sepsis workup, receive empiric antibiotics and be admitted to the hospital.2 Sepsis workup should include CBC, urinalysis with culture, blood culture, lumbar puncture with CSF cell count and culture. Antibiotic therapy should be directed towards local susceptibilities of group B Streptococcus, E. coli, or Y. monocytogenes. One frequently-used regimen utilizes ampicillin and cefotaxime.2

References:

  1. Petersen-Smith A, Barber N, Coody D, et al. Comparison of aural infrared with traditional rectal temperatures in children from birth to age three years. J Pediatr. 125: 83, 1994.
  2. Wang VJ. Chapter 113. Fever and Serious Bacterial Illness. In: Cydulka RK, Meckler GD, eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill; 2011. 
  3. Ferrera PC, Bartfield JM, Snyder HS. Neonatal fever: utility of the Rochester criteria in determining low risk for serious bacterial infections. Am J Emerg Med. 1997;15:299–302.
  4. Jaskiewicz JA, McCarthy CA, Richardson AC, et al: Febrile infants at low risk for serious bacterial infection — an appraisal of the Rochester criteria and implications for management. Pediatrics, 94: 390, 1994.

Dive Injuries
Nicole Battaglioli, MD
York Hospital

Dive injuries may seem like rarities for the typical emergency department. However, the increase in the number of recreational divers and the use of local lakes and quarries increase the likelihood that a diver will present to your emergency department seeking medical treatment for a dive injury. Injuries are typically related to the compression and expansion of gases during a dive, or the presence of dissolved gasses in the bloodstream and tissues.

Ear and Sinus Injury
During a dive, air in the sinuses, inner and middle ear compresses due to the increase in ambient pressure. If air is blocked from filling the ear, negative pressure in the middle ear may cause the tympanic membrane to rupture. Inability to adequately equalize the ears may result in more mild injection or effusion of the inner ear causing vertigo and hearing loss. Additionally, if the sinuses are unable equalize, this can result in mucosal edema, facial pain and epistaxis. Treatment for ear and sinus barotrauma is mainly supportive, using decongestants and analgesics. Inner ear effusions and resultant hearing loss can last up to six weeks. Those with a ruptured tympanic membrane should be put on prophylactic antibiotics. Inner ear damage can be more serious — damage can be caused by valsalva attempts to equalize the ears that are too vigorous. This can result in rupture of the round or oval windows in the inner ear leading to endolymph leakage. This can cause sensorineural, rather than conductive, hearing loss as well as tinnitus and vertigo. Inner ear damage should be treated with bed rest, head elevation and referral to an ENT.

Pulmonary Injury
Just as air compresses when a diver descends, air re-expands when a diver ascends. If a diver holds their breath during an ascent, the air in their lungs will expand causing their alveoli to rupture. The greatest pressure difference occurs between the surface of the water and the first 10 meters, meaning that divers don’t have to be deep in the water to experience these kinds of injuries. Escaped air from alveoli can result in mediastinal or subcutaneous emphysema and pneumothorax. This air can also form an arterial gas embolism, resulting in neurological deficits such as; motor and sensory changes, visual disturbances, vertigo or convulsions. These more serious conditions must be treated with ACLS, 100% oxygen and recompression (hyperbaric treatment).

Decompression Sickness
During a dive, inert gases like nitrogen dissolve into the tissues. If ascent is attempted too quickly or a diver neglects to perform a safety stop, the gas can form bubbles in the tissues and joints causing tissue damage — this is commonly referred to as “the bends.” Symptoms can include poorly localized joint pain, skin rash and pruritis — these symptoms will usually resolve with recompression therapy. Type II decompression sickness (DCS) is more serious and presents with neurological symptoms such as dizziness, numbness and gait abnormality. A pulmonary variant of DCS is caused by a large pulmonary gas embolism — patients will present with substernal chest pain, cough and potentially cardiovascular compromise. The treatment for DCS involves 100% oxygen and emergent hyperbaric treatment.

The diagnosis and treatment of dive related injuries can be challenging. Despite the variations in presentation, the first line treatment for any dive accident is hydration and 100% oxygen. The Divers Alert Network (DAN) can be used as a resource during the treatment of a patient with a diver injury. This organization has a support staff 24 hours a day to assist providers with care coordination and evacuation of a patient.


Septic Bursitis Review
Geoff Jara-Almonte, MD
Hennepin County Medical Center

Septic bursitis is inflammation of the bursa caused by an infectious process. The olecranon and prepatellar bursae are the most commonly affected owing to their superficial locations. Infection may be the result of repetitive minor trauma, direct inoculation due to penetrating trauma, or local or hematogenous spread. S. Aureus is the most common causative organism (identified in 80% of fluid positive cultures in some studies), followed by beta hemolytic streptococci. Treatment varies with severity and can range from oral antibiotics alone to operative debridement and bursectomy with prolonged IV antibiotics.

The greatest challenge for the emergency physician is differentiating septic bursitis from other inflammatory, non-septic causes. Historical and physical findings including fever, chills, local cellulitis, preceding trauma and serum inflammatory markers may help clarify the diagnosis, but none are sufficiently sensitive or specific to be relied upon exclusively. If not contraindicated, bursa aspiration can be performed to further evaluate for septic bursitis. A bursal fluid WBC count less than 1,000/mL is thought to be inconsistent with infection, while counts greater than 10,000/mL should be considered positive. Other fluid analyses including gram stain, glucose, crystal identification and culture.

For treatment, empiric antibiotic administration is recommended, and should include coverage for MRSA if there is a high community prevalence. In patients who are immuno-suppressed, anti-pseudomonal agents can be added. Some studies have shown good success with oral antibiotics alone, especially in patients with milder disease and minimal systemic involvement.

References:

  1. Smith DL, et al.Septic and nonseptic olecranon bursitis. Utility of the surface temperature probe in the early differentiation of septic and nonseptic cases. Arch Intern Med. 1989 Jul;149(7):1581-5.
  2. Wasserman AR, et al. Septic bursitis: a case report and primer for the emergency clinician. J Emerg Med. 2009 Oct;37(3):269-72. Epub 2007 Jul 20.
  3. Stell IM. Management of acute bursitis: outcome study of a structured approach. J R Soc Med. 1999 Oct;92(10):516-21.
  4. Stell IM. Septic and non-septic olecranon bursitis in the accident and emergency department--an approach to management. J Accid Emerg Med. 1996 Sep;13(5):351-3.
  5. Ho G Jr. Comparison of nonseptic and septic bursitis. Further observations on the treatment of septic bursitis. Arch Intern Med. 1979 Nov;139(11):1269-73.
  6. Zimmermann B 3rd, Et al. Septic bursitis. Semin Arthritis Rheum. 1995 Jun;24(6):391-410. (Abstract Only)
  7. Marx, et al Eds. Rosen's Emergency Medicine: Clinical Concepts and Practice 7th ed. Elsevier, 2010. pp 564-5

Factor V Leiden
Alexander Simakov, MPH MSIV
AAEM/RSA Medical Student Council
University of Sint Eustatius

Case Presentation
Twenty-six-year-old male presents with sudden onset right-sided substernal chest pain and dyspnea. Pain is pleuritic in nature. Patient was previously healthy, but did note intermittent bilateral calf pain for several months prior. Patient was tachycardic and tachypneic but satting 99% on room air. Exam was notable for decreased air movement over the right hemithorax. EKG showed sinus tachycardia. CXR revealed a right sided infiltrate with associated pleural effusion. Notable labs were as follows: troponin <0.04, CK-MB=0.0, PT=13.6, INR=1.22, PTT=26.7, WBC=8.45, HGB=13.4g/dL, HCT=39.3, PLT=235, D-dimer=1456. A spiral CT scan confirmed the presence of a pulmonary embolus, and the patient is started on Lovenox. During his inpatient stay, pleural thoracocentesis culture is negative, but hematology tests confirm high levels of Factor V Leiden and low levels of Protein S; and Factor V homozygosity is later confirmed.

Discussion
Factor V Leiden, which causes resistance to activated protein C (APC), accounts for 40 to 50% of all cases of inherited thrombophilia.1,2 Mutation of Factor V can be observed as both aspects of genetic predisposition and as acquired causes.3 Populations at risk include Caucasians of European descent, Jewish, Israeli, Arab, Canadian and Indian populations.4,5 The highest prevalence is seen in Greece, Sweden and Lebanon, where it has been reported to be as high as 15% in some areas.6,7 Acquired sources of the mutation have been attributed to elevated levels of Factor VIII, pregnancy, use of contraceptives, the presence of phospholipid antibodies, as well as unknown causes, and has been known to increase the incidence of confirmed Factor V Leiden in some categories as much as thirty-fold.8-10

Diagnosis can be achieved through direct PCR with various markers or, more commonly, through a second-generation APC resistance assay that is reported to have specificities and sensitivities nearing the 100% range.11-14 Although ECGs have poor utility in the diagnosis, the D-dimer blood test can also be utilized, as well as CT angiography.15-17 Treatment of venous thromboembolism in these patients typically involves anticoagulation with heparin with bridging to Coumadin. 18-19

References:

  1. Mateo, J, Oliver, A, Borrell, M, et al. Laboratory evaluation and clinical characteristics of 2,132 consecutive unselected patients with venous thromboembolism — results of the Spanish Multicentric Study on Thrombophilia (EMET-Study). Thromb Haemost. 1997; 77:444.
  2. Margaglione, M, Brancaccio, V, Giuliani, N, et al. Increased risk for venous thrombosis in carriers of the prothrombin G G20210A gene variant. Ann Intern Med. 1998; 129:89.
  3. Nicolaes, GA, Dahlback, B. Factor V and thrombotic disease: description of a janus-faced protein. Arterioscler Thromb Vasc Biol. 2002; 22:530.1
  4. Rees, DC, Cox, M, Clegg, JB. World distribution of factor V Leiden. Lancet. 1995; 346:1133.
  5. Lee, DH, Henderson, PA, Blajchman, MA. Prevalence of factor V Leiden in a Canadian blood donor population. CMAJ. 1996; 155:285.
  6. Awidi, A, Shannak, M, Bseiso, A, et al. High prevalence of factor V Leiden in healthy Jordanian Arabs. Thromb Haemost. 1999; 81:582.
  7. Irani-Hakime, N, Tamim, H, Kreidy, R, Almawi, WY. The prevalence of factor V R506Q mutation-Leiden among apparently healthy Lebanese. Am J Hematol. 2000; 65:45.71
  8. Zöller, B, Svensson, PJ, He, X, et al. Identification of the same factor V gene mutation in 47 out of 50 thrombosis-prone families with inherited resistance to activated protein C. J Clin Invest. 1994; 94:2521.
  9. de Visser, MCH, Rosendaal, FR, Bertina, RM. A reduced sensitivity for activated protein C in the absence of factor V Leiden increases the risk of venous thrombosis. Blood. 1999; 93:1271.
  10. Vandenbroucke, JP, Koster, T, Briet, E, et al. Increased risk of venous thrombosis in oral-contraceptive users who are carriers of factor V Leiden mutation. Lancet. 1994; 344:1453.
  11. Le, DZ, Griffin, JH, Greengard, JS, et al. Use of a generally applicable tissue factor-dependent factor V assay to detect activated protein C-resistant factor Va in patients receiving warfarin and in patients with a lupus anticoagulant. Blood. 1995; 85:1704.
  12. Dahlback, B. Resistance to activate protein C, the Arg506 to Gln mutation in the factor V gene, and venous thrombosis. Functional tests and DNA-based assays, pros and cons. Thromb Haemost. 1995; 73:739.
  13. Zehnder, J, Benson, R, Cheng, S. A microplate allele-specific oligonucleotide hybridization assay for detection of factor V Leiden. Diagn Mol Pathol. 1997; 6:347.
  14. Zehnder, J, Van Atta, R, Jones, C, Sussman, H, et al. Cross-linking hybridization assay for direct detection of factor V Leiden. Clin Chem. 1997; 43:1703.
  15. Rodger, M, et al. Diagnostic value of the electrocardiogram in suspected pulmonary embolism. Am J Cardiol. 2000; 86:807.
  16. Kruip, MJ, Slob, MJ, Schijen, JH, et al. Use of a clinical decision rule in combination with D-dimer concentration in diagnostic workup of patients with suspected pulmonary embolism: a prospective management study. Arch Intern Med. 2002; 162:1631.
  17. Kline, JA, Wells, PS. Methodology for a rapid protocol to rule out pulmonary embolism in the emergency department. Ann Emerg Med. 2003; 42:266.
  18. Wells PS, Anderson DR, Rodger MA, et al. A randomized trial comparing 2 low-molecular-weight heparins for the outpatient treatment of deep vein thrombosis and pulmonary embolism. Arch Intern Med. 2005;165(7):733-738.
  19. Kearon, C, Kahn SR, Agnelli G, et al. Antithrombotic Therapy for Venous Thromboembolic Disease: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines (8th Edition). Chest. 2008;133; 454S-545S.

Utility of the EKG in Hyperkalemia
Thomas Doran, MSIV
Lake Erie College of Osteopathic Medicine

The classic “peaked T-wave” EKG is frequently referred to as the pathognomonic appearance of hyperkalemia. With further increases in serum K+ concentration, we might expect the EKG to have widening QRS complexes and diminished or disappearing P-waves. In severe hyperkalemia an ominous sine-wave pattern may eventually develop.1 But how reliable are these appearances when gauging the clinical significance of an elevated K+ from the lab? Can we use the EKG to guide treatment of hyperkalemia? Consider this:

  1. A retrospective 2008 study of 90 patients with primarily mild to moderate elevations of potassium (mean was 7.1mmol/L) demonstrated that only half of subjects had any EKG changes at all. Their conclusion was that EKG is very poor in both sensitivity and specificity and that “there is no support for [its] use in guiding treatment of stable patient.”2
  2. Although severe hyperkalemia generally produces EKG changes, two case reports from 1986 showed that severely elevated potassium (>9.0mmol/L) can manifest without any changes whatsoever.3

While decidedly not definitive, these observations show up in commonly referenced practice guidelines.4 EKGs should be interpreted with caution for gauging the success of emergent reversal of this life-threatening electrolyte abnormality.

References:

  1. Goldberger: Clinical Electrocardiography: A Simplified Approach, 8th ed., Chapter 10, Electrolyte Disturbances.
  2. Montague BT, Ouellette JR, Buller GK. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol. 2008;3(2):324.
  3. Szerlip HM, Weiss J, Singer I. Profound hyperkalemia without electrocardiographic manifestations. Am J Kidney Dis. 1986;7(6):461.
  4. Mount DB, Sterns RH, Forman, JP. Clinical manifestations of hyperkalemia in adults. http://www.uptodate.com/contents/clinical-manifestations-of-hyperkalemia-in-adults?source=see_link&anchor=H8#H8.

Critical Care Pearl: 'Tis the Season for Frostbite
Jenna Erickson, MSIII
Chicago Medical School

Frostbite can occur in exposed skin at temperatures below 28 degrees Fahrenheit, with rapid onset in windy conditions. Cellular damage occurs when extracellular fluid freezes, forming ice crystals that both drive fluid out of cells and directly puncture the membrane. Exposure due to inadequate clothing most commonly occurs in the homeless and those with vehicular breakdown. Skin exposure causes increased risk for those employed in mail delivery, law enforcement and farming industries. Medical conditions such as Raynaud's phenomenon, diabetes, peripheral vascular disease and smoking place individuals at higher risk despite adequate skin coverage.

There are four clinical stages of damage in frostbite: 1) superficial color changes; 2) blistering with clear fluid; 3) hemorrhagic blisters; and 4) full-thickness necrosis. Traditional management of frostbite involves heating, hydrating and treating wounds to preserve tissue and prevent infection. The effected area is immersed in a warm water bath (40 degrees Celsius) for a minimum of 30 minutes. Nerve reactivation during reheating can be extremely painful, and pain medications may be necessary. After reheating, blisters should be treated according to degree of damage, and antibiotic ointment applied as needed. Patients are then monitored for improvement or eventual amputation.

References:

  1. Flatt, AE. Frostbite. Proc (Bayl Univ Med Cent). 2010 July; 23(3): 261–262.