Modern Resident - The newsletter of AAEM/RSA
June/July 2013
Volume 5: Issue 1  |  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:
Kevin Bajer, PharmD; Michael Gottlieb, MD; Ashley Grigsby, MSIV; Nathan Haas, MSIII; Shannon O. McNamara, MD; Lauren Myers, MSIV; Randy Orr, MD; Matthew Pirotte, MD; Sierra Read, MSIV; Trent Reed, DO; Athena Kostidis Reed, MD; Giles Simpson, MD; Jennifer Stancati, MSII; Victoria Weston, MD; and Jason Zeller, MD.

Interested in writing?

Email submissions to: info@aaemrsa.org

Please submit articles by July 30th for the August/September edition.

Critical Care Pearl
Metabolic Acidosis: Bicarbonate Drips and Alternative Options
Victoria Weston, MD
Kevin Bajer, PharmD
Randy Orr, MD
Northwestern University

The focus of this critical care pearl is to discuss the use of bicarbonate drips for severe metabolic acidosis, as well as alternative options, which are available. Given the current nature of medication shortages, it is valuable to learn about the alternative options available for use in some of our most critically ill patients.

When approaching a patient with metabolic acidosis, it is important to consider the cause of their acidosis (e.g., increased generation of acids as in lactic acidosis, ketoacidosis and ingestions vs. loss of bicarbonate or decreased acid excretion). As this is a relatively broad topic, this critical care pearl will focus on the treatment of lactic acidosis, as treatment of ingestions may vary with the substance ingested.

Bicarbonate infusion is appropriate for use in severe metabolic acidosis as a temporizing measure while concurrently treating the underlying cause, which is most commonly septic shock in the medical intensive care unit. The threshold for initiating treatment remains debatable but typically is pH<7.1.

There are several methods to calculate the bicarbonate deficit to guide infusion rate for repletion; two methods are shown below:

Method 1:
Bicarbonate volume of distribution (HCO3 Vd) =
(0.4 + 2.6/measured HCO3) - ideal body weight

Ideal body weight: Males: 50 + 2.3 (height (in) - 60) OR Females: 45.5 + 2.3 (height (in) - 60)

HCO3 deficit (mEq) = HCO3 Vd x (desired HCO3* - measured HCO3)
*typically 10-15

Method 2:
HCO3 deficit (mEq) =
0.6 x wt (kg) x (15* - measured HCO3)
*Here, 15 is chosen as the end-point goal

To choose a rate, the bicarbonate deficit should be divided with half of the deficit repleted within the first 4 hours. Bicarbonate drips are provided as sodium bicarbonate 150mEq Dextrose 5% 1000mL. In a pinch, some physicians will choose an initial infusion rate of 150mEq run over 6 hours since this will provide an adequate replacement rate for most patients. Titration of further replacement should be guided by subsequent ABGs.

Of note, use of bicarbonate to correct metabolic acidosis requires adequate ventilation to release the CO2 generated. Potential risks and consequences of use include paradoxical CSF acidosis, hypernatremia, local tissue acidosis in cases of poor circulatory perfusion and diminished ionized calcium.

Given the current national sodium bicarbonate shortage, sodium acetate has been utilized more frequently as a therapeutic substitution. Acetate is metabolized systemically to bicarbonate on an equimolar basis when the body's acid-base balance is altered as a result of bicarbonate deficiency (metabolic acidosis). To form bicarbonate, acetate is slowly hydrolyzed to carbon dioxide and water, which are then converted to bicarbonate by the addition of a hydrogen ion. These conversions take place primarily in the liver. Thus, the actions of sodium acetate mimic those of sodium bicarbonate in patients with intact hepatic function but should NOT be given as an IV push. Sodium acetate is not an appropriate choice for patients without a bicarbonate deficit (i.e., patients requiring urinary alkalinization). There are other alternative options such as carbicarb and THAM; however, these have been less frequently used at our institution.

The following indications should always receive sodium bicarbonate:

  1. High dose methotrexate patients
  2. Liver transplant patients
  3. Cardiac surgery patients
  4. Salicylate overdose patients

References:

  1. Forsythe SM, Schmidt GA. Sodium bicarbonate for the treatment of lactic acidosis. Chest. 2000;117(1):260.
  2. Kurtz I. Acid-Base Case Studies. 2nd Ed. Trafford Publishing (2004); 68:150
  3. Marino PL. ICU book. 3rd Ed. Philadelphia:Lippincott, Williams, and Wilkins (2007); 551-553.

2013 AAEM/RSA Midwest Medical Student Symposium


Hypertensive Emergency Board Review
Shannon O. McNamara, MD
Temple University Hospital

1. Which of the following acute clinical scenarios in the setting of markedly elevated blood pressure is NOT a likely sign of hypertensive emergency?

  1. Shortness of breath with rales on exam
  2. Elevated creatinine with proteinuria
  3. Headache with non-focal neurologic exam, no papilledema
  4. EKG changes with elevated cardiac enzymes
  5. Change in mental status with confusion

Answer:
C is correct.
Hypertensive emergency or hypertensive crisis is defined as acute end organ dysfunction related to markedly elevated blood pressure. Examples of organ dysfunction that define hypertensive emergency are listed below:

End Organ Damage in Hypertensive Emergency
Myocardial Infarction or Unstable Angina
Aortic Dissection
Life-threatening Bleeding
Pulmonary Edema or LV failure
Acute Renal Failure
Encephalopathy
Cerebral Vascular Accident: Ischemic or Hemorrhagic
Eclampsia/Preeclampsia

Hypertensive urgency is an outdated term that was previously used to describe the presence of significant hypertension with nonspecific symptoms. This term is no longer used and patients are instead described as having poorly controlled hypertension. (Rosen's, page 1079)

2. Which is a first line agent for treating hypertensive emergency in the setting of acute hypertensive encephalopathy?

  1. Hydralazine
  2. Clonidine
  3. Nitroglycerin
  4. Nitroprusside
  5. Enalapril

Answer:
D is correct.
Nitroprusside is first line for treatment of hypertensive encephalopathy. This potent vasodilator is rapid onset with a short half-life and can be administered as a titrated infusion. Adverse effects include accumulation of cyanide, an intermediate metabolic of nitroprusside, usually in the setting of renal failure or prolonged therapy.

Alternative agents used to treat hypertensive encephalopathy include fenoldopam, labetalol and nicardipine.

The chart below outlines common antihypertensives used in hypertensive emergencies with a brief explanation of their mechanism and specific indications.

Agent Mechanism Indications
Nitroprusside Vasodilation - smooth muscle Encephalopathy, pulmonary edema, aortic dissection, renal insufficiency.
Nicardipine Dihydropyridine calcium channel blocker Alternative agent in eclampsia, intracranial hemorrhage.
Nitroglycerin Vasodilation - venous Pulmonary edema, cardiac ischemia.
Labetalol α1, β Adrenergic blocker Intracranial hemorrhage, eclampsia. Alternative agent in encephalopathy, aortic dissection, renal insufficiency.
Esmolol β1 Adrenergic blocker Control tachycardia in aortic dissection or reflex tachycardia from other antihypertensive agents.
Phentolamine α-blocker Adrenergic storm: pheochromocytoma, MAOI crisis, cocaine overdose.
Fenoldopam Dopaminergic Receptor agonist Alternative agent in pulmonary edema.
Hydralazine Arteriolar vasodilation Not first line. Can be used in eclampsia.
Enalapril ACE inhibitor Alternative agent in pulmonary edema.

3. The patient from Question 2 has a blood pressure of 200/140. They report severe headache with vomiting and are drowsy and confused on exam. Papilledema is present. CT head shows no acute hemorrhage or infarct. Neurologic exam is otherwise non-focal. The patient is afebrile.

You decide to start antihypertensive therapy. What is your goal blood pressure for this patient in one hour?

  1. 140/90
  2. 160/100
  3. 180/120
  4. 200/115

Answer:
B is correct. BP 160/100 corresponds to MAP 120, or 25% of the initial MAP of 160. This patient appears to have hypertensive encephalopathy, a result of failed cerebrovascular autoregulation due to abruptly elevated blood pressure. Unlike CVA, when acute correction of elevated blood pressure may increase ischemia by decreasing cerebral perfusion, hypertensive encephalopathy is potentially reversible with adequate blood pressure control. In this clinical setting, the goal is to reduce the MAP by 25% or the diastolic pressure to 100-110 in the first hour of treatment. MAP is calculated: 1/3 x [(2 x diastolic) + systolic].

This patient's MAP is 160. The goal MAP in 1 hour is 120, a 25% reduction. BP 160/100 = MAP 120.

References:

  1. Gray RO. Hypertension. In: Marx JA, Hockberger RS, Walls RM, et al., eds. Rosen's Emergency Medicine: Concepts and Clinical Practice. Philadelphia, PA: Mosby/Elsevier; 2010: 1076-1087.
  2. Wu MM. Chanmugam A. Hypertension. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Tintinalli's Emergency Medicine. 6th ed. New York, New York: McGraw-Hill Companies; 2004: 394-404.
  3. Walker G. MD Calc. Available at: http://www.mdcalc.com. Accessibility verified. May 22, 2013.

Image of the Month: The Brugada Syndrome
Matthew Pirotte, MD
Nathan Haas, MSIII
Loyola University Chicago Stritch School of Medicine

A 31-year-old Chinese man with no past medical history presented to the ED after a syncopal episode. He had no complaints and had been doing housework when syncope occurred. He denied any previous chest pain or shortness of breath, and was on no medications. His uncle died suddenly in his 50s of an unknown cause.

Upon examination, he was afebrile and his vital signs were within normal limits. He appeared well, and a thorough physical examination was unremarkable. CBC, BMP, cardiac enzymes, BNP and coagulation studies were unremarkable. His EKG is shown below.

What is your diagnosis, and what is your next step in management?

EKG

Image courtesy of Dr. Matthew Pirotte

Answer:
The Brugada Syndrome is critical for any emergency medicine physician to recognize, as it often is associated with ventricular fibrillation or sudden cardiac death. The syndrome was first characterized in 1992 as right bundle branch block, persistent ST-elevation in leads V1-V3 and sudden death in a patient with a structurally normal heart.1 The syndrome is likely related to a mutation in the SCN5A gene, which encodes a sodium ion channel in cardiac myocytes. Genetic testing is now available for diagnostic confirmation.

Affected patients often have family histories of sudden cardiac death, and the syndrome is most common in Asian men. The mean age of sudden death is 40 years, although ages at time of diagnosis range from 2 days to 85 years.2 Several pharmacological agents and conditions are thought to "unmask" the characteristic EKG findings of the Brugada Syndrome, including lithium, beta-blockers, antidepressants, neuroleptics, propafenone, fever, hypokalemia, hyperkalemia, hypercalcemia, alcohol and cocaine.3

Urgent referral to an electrophysiologist for evaluation is appropriate, and placement of an ICD is often warranted. Recognition of the pathognomonic EKG findings of the Brugada Syndrome is essential in any setting to prevent the progression to sudden cardiac death, as 4% of all sudden deaths and 20% of sudden deaths in patients with structurally normal hearts can be attributed to the syndrome.4

EKG EKG
Type I Brugada Changes: "coved" ST-elevation with inverted T-wave Type II Brugada Changes: "saddleback" pattern

References:

  1. Brugada P, Brugada J. Right Bundle Branch Block, Persistent ST Segment Elevation and Sudden Cardiac Death: A Distinct Clinical and Electrocardiographic Syndrome. Journal of the American College of Cardiology. 20.6 (1992):1391-396. Online.
  2. Brugada et al. Brugada Syndrome. GeneReviews. (2005). Online.
  3. Pirotte, M., J. Mueller, and T. Poprawski. "A Case Report of Brugada-type Electrocardiographic Changes in a Patient Taking Lithium." The American Journal of Emergency Medicine. 26.1 (2008): 113.e1-13.e3. Online.
  4. Delise, Pietro, Marras, Bocchino. Brugada-like Electrocardiogram Pattern: How to Stratify the Risk for Sudden Cardiac Death. Is Sports Activity Contraindicated? Journal of Cardiovascular Medicine. 7.4 (2006):239-45. Online.

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Toxicology Board Review Questions
Michael Gottlieb, MD
Cook County Emergency Medicine Residency

Which of the following chelating agents is recommended for acute lead poisoning with signs of encephalopathy?

  1. Succimer
  2. Penicillamine
  3. Dimercaprol
  4. Calcium EDTA
  5. Dimercaprol + Calcium EDTA

Answer:
E is correct.
Succimer is the agent of choice for asymptomatic, mild lead poisoning (45-70mcg/dL in children, 70-100mcg/dL in adults) because it is available PO and has a low side effect profile. Penicillamine is used predominately for the treatment of Wilson's Disease (copper chelation) and is no longer used in lead toxicity due to its significant side effect profile. For severe toxicity with signs of encephalopathy, Dimercaprol (previously known as BAL; British Anti-Lewisite) is given IM followed by calcium EDTA via continuous infusion to combine to chelate lead from the brain and body, respectively.

Dosages are as follows:
Succimer: 10mg/kg PO Q 8H x 5 days, followed by 10mg/kg Q 12H for 14 days
Dimercaprol: 4mg/kg IM Q 4H x 5 days
Calcium EDTA: 1500mg/m2 IV Q 24H via continuous infusion x 5 days (started 4 hours after Dimercaprol)

References:

  1. Gracia RC, Snodgrass WR. Lead toxicity and chelation therapy. Am J Health Syst Pharm. 2007 Jan 1; 64(1):45-53.
  2. Mann KV, Travers JD. Succimer, an oral lead chelator. Clin Pharm. 1991 Dec; 10(12):914-22.
  3. Patrick L. Lead toxicity, a review of the literature. Part 1: Exposure, evaluation, and treatment. Altern Med Rev. 2006 Mar; 11(1):2-22.

Tox Talks: But the Urine's Negative?!
Recognition and Management of Urine Tox Screen Negative Drug Intoxications, Part 2
Ashley Grigsby, MSIV
Arizona College of Osteopathic Medicine

As discussed in Part 1 of this article, the five panel drug screen commonly used in suspected drug intoxications can miss many dangerous drugs. It is important to recognize different toxidromes associated with these drugs to better manage and treat these patients. Here we will be discussing three more common urine negative drug intoxications.

Case 1: Fourteen-year-old male is brought in by EMS. His mother reports he is confused and she thinks he's hallucinating. Vital signs show tachycardia and hypertension. Physical exam reveals nystagmus.1

Dextromethorphan
Also known as "Robotripping," dextromethorphan (Robitussin) abuse, used for its hallucination effects, is a growing concern especially in adolescents. Nonmedical dextromethorphan use results in 6,000 emergency department visits each year in the United States.2 The medication is available OTC, and although many states have outlawed the sale to minors, many adolescents can still find it in their home drug cabinets. For completeness, it is possible for dextromethorphan to cause a false positive drug screen for PCP, but this is not always present.

  • Signs and symptoms: hallucinations, euphoria, tachycardia, mydriasis, ataxic gait, nystagmus may be seen.
  • Toxic dose: symptoms are dose dependent and range from mild stimulation and hallucinations to complete dissociation and unresponsiveness. The later occurs at doses ≥15mg/kg.2
  • Life-threatening effects: serotonin syndrome, respiratory depression in very young children, rhabdomyolysis, hyperthermia.
  • Possible co-ingestants: acetaminophen, pseudoephedrine and antihistamines.2
  • Treatment:
    • Benzodiazepines!
    • If ingestion within 1 hour, activated charcoal if airway is secure
    • Naloxone: can reverse respiratory depression in some patients
    • Active cooling measures if hyperthermic
    • If rhabdomyolysis: IV fluid repletion with normal saline with urine output goal of 4ml/kg per hour and monitor serum electrolytes
    • If serotonin syndrome: aggressive sedation with benzodiazepines and possible cyproheptadine in severe cases3

Case 2: Seventeen-year-old male brought in after attempting to stab his younger sister to rid her of the devil. He is aggressive, tachycardic and hypertensive.1

Bath Salts
Bath salts have been getting a lot of media attention lately and you have most likely heard of these substances. They were once legal, sold as bath salts or plant food under the "not for human consumption" label, but are now illegal in most places. They have both amphetamine-like properties and serotonin properties.4 In 2010, 41% of night club attendees had admitted to using bath salts.

  • Signs and symptoms: aggression, tachycardia, hypertension, diaphoresis, bruxism, psychosis, seizures and murder have been reported.1
  • Life-threatening effects: hyperthermia, rhabdomyolysis, acute tubular necrosis, cardiac toxicity and suicide.4,5
  • Treatment:
    • Supportive
    • Aggressive cooling for hyperthermia
    • Benzodiazepines for agitation and seizures
    • Management of complications (e.g., check CK for rhabdomyolysis and renal function for tubular necrosis)
  • Pediatrics: young children in homes where bath salts are abused may present with symptoms from accidental ingestion. Symptoms include: crying, tachycardia, agitation, abnormal eye movements and ataxia.5 Consider intoxication if drug abuse is confirmed or suspected in the family.

Case 3: Thirteen-year-old female presents with acute psychosis. She has no known psychiatric history. She vomits during exam and is tachycardic.1

Spice
Much like bath salts, spice was once legal and sold as "incense" under the "not for human consumption" label. It is no longer legal. It is a synthetic cannabinoid but has a much higher affinity for the receptor used by other cannabinoids.1 Use of synthetic cannabinoids is increasing; in 2012, 11% of high school students in the United States reported use of these drugs.6

  • Slang terms: K2, yacatan fire, incense, Genie
  • Signs and symptoms: nausea/vomiting, tachycardia, red eyes, rarely seizures, dystonia paranoid psychosis.6
  • Can be found on specific drug screens, but not seen on five panel screen
  • Treatment: mainly supportive, long acting benzodiazepines, diphenhydramine for dystonia.6
  • Toxicity usually lasts less than 24 hours.6

In the next issue, the final part of this three part series will discuss the many different hallucinogens and their clinical management.

References:

  1. Claudius, I. The Legal High. In: American Academy of Emergency Medicine Conference, Children are Not Little Adults!. 2013 9 February. Las Vegas, Nevada. P 73-82.
  2. Rosenbaum C, Boyer EW. Dextromethorphan poisoning: Epidemiology, pharmacology and clinical features. Up to date. [Internet]. 2013 [cited 2013 26 May]. http://0-www.uptodate.com.millennium.midwestern.edu/contents/dextromethorphan-poisoning-epidemiology-pharmacology-and-clinical-features?source=search_result&search=dextromethorphan+overdose&selectedTitle=1~3.
  3. Rosenbaum, C, Boyer, EW. Dextromethorphan poisoning: Treatment. Up to date. [Internet]. 2013 [cited 2013 26 May]. http://0-www.uptodate.com.millennium.midwestern.edu/contents/dextromethorphan-poisoning-treatment?source=search_result&search=dextromethorphan+overdose&selectedTitle=2~3
  4. Prosser JM, and Nelson LS. The toxicology of bath salts: a review of synthetic cathinones. J Med Toxicol. 2012;8(1):33.
  5. Arnold TC, Ryan ML. Acute amphetamine and synthetic cathionon("bath salt") intoxication. Up to Date. [Internet] 2013 [cited 2013 26 May] http://0-www.uptodate.com.millennium.midwestern.edu/contents/acute-amphetamine-and-synthetic-cathinone-bath-salt-intoxication?source=search_result&search=bath+salts&selectedTitle=1~4#H350266282.
  6. Hoecker CC. Designer drugs of abuse. Up to Date. [Internet] 2013 [cited 2013 26 May]. http://0-www.uptodate.com.millennium.midwestern.edu/contents/designer-drugs-of-abuse?source=search_result&search=spice&selectedTitle=1~80#H21.

Emergency Medicine in Peru: Lessons for Compassionate Practice at Home
Sierra Read, MSIV
University of Washington School of Medicine

Research about emergency department utilization can be eye opening. A study in the October 2012 issue of Pediatric Emergency Care evaluated why pediatric patients who were triaged as non-urgent were brought to the ED. The majority of the responders were Latino and foreign-born. Though their child had a non-urgent condition, the majority of caregivers sought care because they perceived the child's condition as very urgent or extremely urgent. Participants also listed a desire to better understand basic childhood illnesses and dissatisfaction with primary care as reasons. I myself took my daughter to the ED once for a non-urgent issue. Despite being in medical school at the time and having the trust of the medical system that comes from having a physician father, I was still worried and seeking reassurance.

My last medical school rotation, an international elective in Peru, has given me some perspective on increased utilization among immigrants. I spent one month in the emergency department of El Hospital de Emergencias Jose Casimiro Ulloa. The health care system is set up very differently there. While recounting these stories, I hope to share some perspective.

I was sorting through piles of papers looking for a lab result one day when I saw a mother running down the hallway with a bundle in her arms. Her baby was six weeks old and two weeks prior had been hospitalized for dehydration. He had two days of rhinorrhea, then stopped nursing. He was pale with a distended abdomen. She lived far away. He was tachycardic and hypotensive with peritoneal signs. The X-ray showed distended bowel, paucity of air in the pelvis and pneumoperitoneum under the diaphragm. The surgeon was called to consult while the pediatric attending guided the resident in placing a central line in a 6-week-old. There was no ultrasound in the ED and several attempts failed. After an hour, the line was placed and fluid resuscitation was intiated. The surgeon decided that the baby was too unstable to operate and admitted him to the ICU where he died two days later. This baby was sick and may have died anyway, but I can't help but wonder what would have happened if the hospital had an ultrasound available to help place the central line, or the supplies/practice to give intraosseous fluids. I asked the pediatrician what happened. He looked at me and said matter of factly that she [the mother] is from the hills and she doesn't understand.

One of the first patients I saw taught me about what it is like to be a patient in Peru. She presented with intense diffuse abdominal pain and hypotension. Since she was of childbearing age, she was evaluated on the OB floor with ultrasound to rule out ectopic pregnancy. She had positive-free fluid in her abdomen but no visible pregnancy. She was no longer considered an emergency and had to pay for medical care prior to receiving it. Her loved one went to the register and paid eight soles (about $3 dollars) for the medical consult and ultrasound. The intern stapled the receipt to the chart and headed over to take the history. After diagnosing possible pancreatitis, the intern wrote another bill for two needles, a syringe, IV tubing, 1L saline, a vacu-taner and tubes for the labs. The family member rushed to the pharmacy to buy the supplies and the register to pay for the labs. A few more receipts joined the first. The nurse drew the labs. Once the labs were back, the intern cut out the results and glued them to the chart. The results were consistent with pancreatitis. After three hours the patient requested some pain medications. The intern had been caring for 10 patients alone all morning while her supervising resident was busy with other patients a wall away. She hurried and wrote another prescription, sending the family member running off to the pharmacy once more.

I have only seen a handful of cardiac arrests so far in my training. Half of them have been in Peru. Unfortunately, most of them have had the same outcome, but there was one big difference between those I saw in Peru and in Seattle. All of the cardiac arrests that presented to the ED at my medical school teaching hospital were brought in by paramedics. The cases I saw in Peru were all brought in by their families. In Peru, there are ambulances; but most of the people don't use them. Most people don't even heed them on the street. I took an informal survey of taxi drivers while I was in Peru. I asked each taxi driver I met what they would do if they had an emergency. Would they try to get an ambulance? No. What would you do? Drive myself or call a friend to drive me. Why not? Too expensive, I don't have that much money. I saw a daughter and son carry their lifeless father out of their little car once and I followed him into the shock/trauma room. The code didn't last long. He had already been down for over 30 minutes. As we left, the daughter frantically asked the attending if there was more that could be done. Gruffly he said, "No, mi hijita. No. It has been too long."

I am not trying to criticize the efforts of the Peruvian physicians. By and large, they are great clinicians with huge hearts and are operating within a system with very different challenges than our own. However, these medical experiences are not unique and everyone I spoke with had a similar story either from their own experience or secondhand. As we care for patients, it is important to remember that those from different countries not only have different cultures but different health care systems as well, and they bring their expectations and assumptions about health care with them. Reflecting on these stories helps us better understand how past experiences color attitudes towards health care and the ways they advocate for their loved ones; regardless of if they are interacting with our medical system appropriately or not.

Reference:

  1. Kubicek, K et al. Pediatr Emerg Care. 2012 Oct;28(10):977-84.

Image of the Month: Two-year-old Female with Unilateral Clavicular Swelling
Jennifer Stancati, MSII
Giles Simpson, MD
Loyola University Chicago Stritch School of Medicine

Unilateral Clavicular Swelling

A 2-year-old female presents to the emergency department (ED) with her parents for "pain and swelling over her left collar bone." They say she was running in the hallway earlier today when she tripped over some laundry and fell to the floor, landing on her left shoulder. She immediately cried and complained of pain over her forehead, but not of shoulder pain. They gave her Tylenol and then she napped for several hours. When she woke up, her older sister noticed that "the top of her chest was swollen," so her parents brought her to the ED. Since the time of the fall, she has not lost consciousness and has been acting like herself. She did vomit from crying heavily, but her parents say this is not uncommon for her. She complains of pain over her head, but points to a different spot every time she is asked where it hurts. The child denies blurry vision, shortness of breath, weakness, numbness and tingling. She has no significant past medical, surgical or family history.

Upon examination, she is in no apparent distress, is cooperative, interactive and using her left arm. Her skin is warm and capillary refill is less than 3 seconds. There is an area of round swelling 4cm x 2cm in the left supraclavicular region the size of an egg that is tender but not erythematous. She has normal range of motion, and equal strength bilaterally. Vitals are within normal limits.

An X-ray of the chest is ordered, which indicates no fractures or dislocations. A second X-ray is ordered of the clavicle, which reports soft tissue swelling overlying the left clavicle but no fractures.

After the X-ray came back showing no fractures or dislocations, what would you do next?

An ultrasound would provide a noninvasive assessment with quick results and would therefore be favored over a CT or MRI in this situation.

The ultrasound showed an irregular heterogeneous 3.9cm x 3.9cm x 2.1cm multiseptated nonvascular mass in the left supraclavicular region consistent with an abscess or conglomerate of enlarged lymph nodes.

Labs were ordered:
BMP: within normal limits
CBC: all normal except for:
WBC: 14.2 K/UL
Diff: SEG = 33%, LYMPH = 52%, REACTIVE LYMPH= 6%, MONO = 5%, EO = 4%
PLT 431 K/UL
PTT and INR within normal limits.

After consulting orthopedics and pediatric surgery, there is discussion about the etiology of the mass (e.g., swollen lymph node, confluence of the lymphatic system, lymphocytic mass). The emergency physician advised the parents to keep the child in the hospital for further evaluation of the mass and to observe any skin changes due to increasing size, but the parents opted to take the child home. Two months later, the mass has gone away and the child appears to be back to normal. Follow-up appointments have not been able to determine a definitive diagnosis.

Reference:

  1. Lin D, Deschler DG. Evaulation of a neck mass. UpToDate. Basow, DS (Ed), UpToDate. Waltham, MA, 2013.

Neurological Emergencies: A Neuroanatomical Review
Lauren Myers, MSIV
Trent Reed, DO
Athena Kostidis Reed, MD
Loyola University Chicago Stritch School of Medicine

The Case:
A 59-year-old male presents to the emergency department with 2 hours of dizziness and falling secondary to unsteadiness. He has vomited three times since the dizziness began. When asked to further clarify his dizziness the patient does note that the "room is spinning." His wife noticed his voice is a bit more hoarse than usual, and his words are harder to understand. The patient also notes difficulty signing his name when registering in the ED.

Physical Exam Findings:

  • General: no acute distress, speaking full sentences though hoarse voice and dysarthric speech noted
  • Eyes: left pupil 2mm and reactive with mild ptosis on that side, right pupil 4mm and reactive, EOMI, mild horizontal and rotary nystagmus, fast component to the right
  • Throat: moist mucus membranes, left soft palate paralysis noted
  • Heart: RRR no m/r
  • Lungs: clear to auscultation
  • Extremities: no edema and 2+ pulses throughout
  • Neuro:
    • CN: 2-12 intact aside from loss of pinprick and temperature sensation in left face involving all three divisions of the trigeminal nerve, asymmetric soft palate and hoarse voice as noted above, and asymmetric pupils, ptosis, and nystagmus as noted above
    • Sensation: loss of pinprick and temperature sensation in right hemibody below the chin, normal vibration and position sense throughout
    • Strength: 5/5 throughout upper and lower extremities bilaterally
    • Reflexes: 2/4 throughout upper and lower extremities bilaterally
    • Cerebellar: dysmetric finger to nose on left, unsteady heel to shin on left, dysdiadochokinesia on the left
    • Gait: ataxic and appeared to be stumbling to the left
    • Romberg: negative

Discussion
The patient presents to the emergency department with the classic symptoms of Wallenberg Syndrome, also known as Lateral Medullary Syndrome. These include vertigo, nausea/vomiting, ataxia, hoarseness, numbness and clumsiness. The most common cause is from occlusion of the posterior inferior cerebellar artery (PICA). It can also occur from occlusion of the vertebral artery. Our patient suffered an occlusion of the left PICA.

Signs include:

  • Central nystagmus due to involvement of the vestibular nuclei.
  • Ipsilateral limb dysmetria due to involvement of spinocerebellar tract or cerebellar hemisphere.
  • Ipsilateral Horner's Syndrome due to interruption of descending sympathetic pathway.
  • Dysphagia, dysarthria, dysphonia and ipsilateral palate and vocal cord paralysis due to involvement of CN IX, X or the nucleus ambiguus.
  • Impaired pain and temperature sensation over the ipsilateral face and contralateral body due to involvement of the spinal trigeminal nucleus and spinothalamic tract, respectively.
  • Nausea, vomiting, vertigo and hiccupping due to involvement of the reticular formation and vestibular nuclei.

Wallenberg Syndrome

Photo Courtesy of Wikimedia Commons: By John S. To, M.D. (Own work) [Public domain], via Wikimedia Commons from Wikimedia Commons

We believe the discussion of Wallenberg Syndrome in the emergency department is important since it should be considered in cases of central vertigo. While we do not discuss the treatment modalities in detail, it is most important for emergency physicians to recognize the syndrome and quickly activate the stroke protocol for treatment of this difficult to diagnose syndrome.

References:

  1. Castro, Merchut, Neafsey. Neuroscience, An Outline Approach. Mosby Press, St. Louis, MO. 2002.
  2. Tintinalli et al. Tintinalli's Emergency Medicine, 7th Edition. 2012.
  3. UpToDate, Lateral Medullary Syndrome. 2012.

Suspected Abuse?
Jason Zeller, MD
Drexel University College of Medicine

My patient with suspected abuse was a young girl with a continuous second-degree road rash burn in the shape of an upside down U surrounding her buttocks. The questions in my mind as I walked into the room were: 1) How do you manage to get a second-degree burn of that shape in that specific location?; 2) Is the explanation provided plausible? In this case, the story was that the patient had fallen off the back of her sister's bike.

Looking at this child and her mom, it did not seem like an abuse picture, clinically. Ultimately, the patient told a consistent story and had seen her PCP earlier that day, who was able to confirm the story. However, making determinations like these can be challenging. Cases like these present in many different ways, and we are mandated to be reporters of child abuse.

A Netherlands study from 2012 provides us with a very general checklist for use in evaluating pediatric patients for child abuse:

  1. Is the history consistent?
  2. Was there unnecessary delay in seeking medical help?
  3. Does the onset of the injury fit with the developmental level of the child?
  4. Is the behavior of the child/caregivers and the interaction appropriate?
  5. Are the findings of the top-to-toe examination in accordance with the history?
  6. Are there any other signals that make you doubt the safety of the child or other family members?

My suggestions are as follows:

  • Obtain a clear description of the mechanism of injury.
  • Be non-confrontational in attempting to obtain this information.
  • Avoid providing leading explanations of how you believe the injury may have occurred to the patient or family.
  • Interview the child separately from the parents.
  • Use open-ended questions.

In cases of concern for abuse, you may notice:

  • Injuries that are either poorly explained or do not go along with the history.
  • A history with minor changes over time or between different family members.
  • Delay in seeking treatment.
  • An explanation that is not consistent with the pattern, age or severity of the injuries.
  • Injuries reported as accidental in covered areas such as the back or buttocks.

It is important to observe the child. Are they acting normal for their age? Are they lethargic? How are they interacting with the others in the room, especially the caregivers? Are there any signs of head injury or other obvious injuries? What other odd or unexplainable symptoms do they present with?

It is imperative to document your history and physical appropriately and to remember that physicians are mandatory reporters of child abuse. This is just a general overview of how to approach a family or young child who you may or may not suspect for abuse. Whether your pediatric exposure is low or high, this necessary topic deserves a closer look.

References:

  1. Kellogg, N. D. (2007). Evaluation of suspected child physical abuse. Pediatrics. 119(6), 1232-1241.
  2. Ricci, L. (2011). Child Abuse Clinical Presentation. Medscape. Retrieved 6/2/2013.