Modern Resident - The newsletter of AAEM/RSA
April/May 2013
Volume 4: Issue 6  |  FacebookTwitterLinkedIn

Your 2012-2013 Leaders:

Leana S. Wen, MD MSc

Vice President
Stephanie Gardner, MD

Taylor McCormick, MD

Immediate Past President
Teresa M. Ross, MD

At-Large Board Members
Rachael Engle, DO
Ali Farzad, MD
Megan Healy, MD
Sarah Terez Malka, MD
Meaghan Mercer, DO

Medical Student Council President
Mary Calderone

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

Modern Resident Contributors

Copy Editor: Rachael Engle, DO
Managing Editor: Lauren Johnson, AAEM/RSA Staff

Special thanks to this issue's contributors:
Thomas Damiano, MD; Manish Garg, MD; Michael Gottlieb, MD; Ashley Grigsby, MSIII; Casey Grover, MD; Christopher Helman, DO; Dylan Hendy, MSIV; Ryan Hodnik, DO; Geoff Jara-Almonte, MD; Christine Knettel, MD; Shannon McNamara, MD; Sean Nardi, MSIV; Aaron Pannier, MD; Sierra Read, MSIV; Victoria Weston, MD; and Jason Zeller, MSIV.

Interested in writing?

Email submissions to:

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

Photo of the Month
ENS Dylan Hendy, MSIV
Arizona College of Osteopathic Medicine
LT Christopher D. Helman, DO
Naval Medical Center Portsmouth

Patient Vignette:
Twenty-nine-year-old male was sent to the ED by a community clinic for a syncopal episode. The patient originally visited the clinic for a headache that resulted from a shelf falling on the back of his head while working in his garage two days earlier. The patient denies losing consciousness, amnesia, disorientation or N/V. However, upon further questioning the patient described an unwitnessed episode of “blacking out” while sitting in his car today. He states this episode may have lasted for 30-60 minutes. The clinic subsequently sent the patient to the ED for further workup. In the ED the patient explained that he has a history of chronic headaches and that his headache at present is similar with regards to onset, location and duration. However, to the best of his knowledge, today’s unwitnessed syncopal episode was a first time occurrence. Further ROS were negative. The patient has no other pertinent PMH and is taking no medications. Complete physical exam was unremarkable. A workup for a closed head injury and syncopal episode was performed. Laboratory data was WNL. Non-contrast CT head and CXR were both unremarkable. The following ECG was obtained:

What is the most likely diagnosis?

  1. ST elevation myocardial infarction
  2. Right bundle branch block
  3. Brugada’s Syndrome (BS)
  4. Wolff-Parkinson-White Syndrome

(C) Brugada's Syndrome (BS). The patient was referred to the emergency department (ED) for an unexplained syncopal episode. In the ED, BS is often diagnosed in patients presenting with unexplained syncope and abnormal ECG findings including ST elevations in V1-2 with an incomplete RBBB pattern.

Brugada's Syndrome results from a genetic defect in sodium channels and is more common in males and the Asian population. The most worrisome clinical manifestations of BS are ventricular arrhythmias or sudden cardiac death. There is a familial occurrence in up to half of the patients presenting with BS, however, patients who lack a family history should not be assumed low risk.

There are three types of Brugada patterns found on ECGs and these can be differentiated by observing the ST changes in leads V1-V3.

  • Classic Type 1 Brugada Pattern: referred to as the “coved type,” with ST elevation >2mm that gradually descends into a negative T wave.

  • Type 2 and Type 3 Brugada Pattern: referred to as "saddle back," with ST elevation >2mm and a biphasic T wave creating the "saddle back." If the terminal portion of the ST segment is >1mm then it is a Type 2 pattern, and if the terminal portion of the ST segment is <1mm then it is Type 3 pattern.

Our patient most likely has a Type 2 Brugada pattern. Refer to the images in your emergency medicine text to assist in further differentiating the three types of Brugada patterns. It is important to note that the Brugada pattern is often transient and episodic.

Patients who have findings concerning for BS require admission and further evaluation with electrophysiology testing. Pharmacologic therapy has been unsuccessful in preventing sudden cardiac death. Insertion of an implantable cardioverter-defibrillator is the current consensus for long-term care.


  1. Mattu, A. (2012). Brugada Syndrome [Online video]. Retrieved January 15, 2013, from
  2. Frackelton, M. Chapter 77. Dysrhythmias. In: Marx: Rosen's Emergency Medicine, 7th ed. Philadelphia, PA: Mosby Elsevier; 2010.
  3. Walker RA, Adhikari S. Chapter 22. Cardiac Rhythm Disturbances. In: Tintinalli JE, Stapczynski JS, Cline DM, Ma OJ, Cydulka RK, Meckler GD, eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. 7th ed. New York: McGraw-Hill; 2011
  4. Wylie, J. V., Pinto, D. S., & Josephson, M. E. (2012, August 29). Brugada Syndrome. In UpToDate. Retrieved January 15, 2013, from UpToDate.

AAEM Journal Club - Review of the Major Literature on Minor Head Trauma
Shannon McNamara, MD
Temple University Hospital

Minor traumatic head injury is a common presenting complaint to the emergency department. Emergency physicians must frequently decide which of these patients should undergo neuroimaging with CT to rule out significant intracranial injury. Two major clinical decision rules exist to try to identify patients who are high risk for injury and require imaging, but also those patients at low risk that do not. These decision rules must be very sensitive in order to identify all patients with significant intracranial injury. They should also be specific enough to identify low-risk patients who do not require imaging in order to both avoid unnecessary radiation exposure for such patients, and also improve clinical efficiency by decreasing the overall rate of imaging. This article will review the Canadian CT Head Rule, the New Orleans Criteria, two validation studies and resulting clinical guidelines based on the evidence.

The Canadian CT Head Rule
The Canadian CT Head Rule (Stiell 2001) was derived in a prospective, multicenter cohort study with 3,121 patients. Patients included in the study were 16 or older and had GCS 13-15. These patients experienced minor head trauma associated with loss of consciousness, amnesia or disorientation. Outcomes measured were needed for neurosurgical intervention and clinically important brain injury on CT. Sixty-seven percent of patients were examined by CT at the discretion of the treating physician, while 33% of patients did not undergo CT. Those patients not imaged were instead followed up in a telephone survey two weeks later to evaluate for signs and symptoms of clinically important brain injury. This served as a proxy outcome measure. A total of 8% of patients had clinically important brain injury on CT, and 1% of all patients required neurological intervention.

Canadian CT Head Rule
for minor head trauma in patients with witnessed LOC, amnesia or disorientation.
GCS 13- 15. Must Be ≥ 16 with no coagulopathy.

HIGH RISK FEATURES for neurosurgical intervention. If present, CT is indicated.
  1. GCS less than 15 at two hours after injury.
  2. Suspected open or depressed skull fracture.
  3. Signs of basal skull fracture (hemotympanum, ‘raccoon’ eyes, cerebrospinal fluid otorrhoea/rhinorrhoea, Battle’s sign)
  4. Two or more episodes of vomiting.
  5. Age 65 years or greater.
MEDIUM RISK FEATURES for clinically significant brain injury on CT. If present, CT or close observation indicated.
  1. Amnesia before impact of ≥30 minutes
  2. Dangerous mechanism (pedestrian vs. auto, an occupant ejected from a motor vehicle or a fall from a height of ≥3 feet or five stairs)

A significant limitation of this study is the definition of the outcome of clinically important brain injury. These were defined as lesions which "require neither admission nor specialised follow-up and are not correlated with longer term problems such as post-concussion syndrome," (Stiell 1395). Examples of the type of injuries detected in this study included focal subarachnoid hemorrhage, cerebral contusion <5mm in diameter, subdural hematoma <4mm thick, isolated pneumocephalus and some depressed skull fractures. Some physicians disagree with this definition and argue that many of these patients would require admission and follow-up in different settings.

The New Orleans Criteria
The New Orleans Criteria (Haydel) was published after a two-phase, single center, prospective cohort study. In phase one, 520 patients ages 3 years and older with GCS 15 after minor head trauma featuring loss of consciousness or amnesia were evaluated to determine which clinical findings correlated with positive head CT. The measured outcome was any acute traumatic intracranial lesion on the CT. In phase two, the predictive value of that set of clinical findings was evaluated on a separate group of 909 patients to determine the sensitivity and specificity of the criteria. They found that the criteria was 100% sensitive and 24% specific for intracranial injury. The study was limited by the relatively small size of the derivation sample and the fact that patients were not followed after discharge.

New Orleans CT Head Criteria
For minor head trauma with LOC, GCS 15 and normal neurological exam.

If any criteria are met, CT of head is indicated.
Age >60
Alcohol or drug intoxication
Persistent anterograde amnesia (short term memory deficits)
Visible trauma above the clavicles

Validation Studies
Both the Canadian CT Head Rule (CCHR) and the New Orleans Criteria (NOC) were validated by two major studies. These studies showed that the CCHR was consistently more specific than the NOC, but also sometimes less sensitive, depending on which outcomes were measured. The methods of these studies highlight the limitations based on the how clinically important injuries are defined. Smits et al.,evaluated sensitivity for any intracranial injuries on CT, while in 2005 Stiell et al., measured sensitivity only for clinically important injuries and for those requiring neurosurgical intervention.

Validation Studies Stiell Smits
Design Prospective cohort
1822 patients
Prospective cohort
3138 patients
CCHC Sensitivity
for any intracranial traumatic findings
- 83.4%
CCHC Sensitivity
for clinically important injury
100% -
CCHC Sensitivity
for neurosurgical intervention
100% 100%
CCHC Specificity 50.6% 37.2-38.9%
NOC Sensitivity
for any intracranial traumatic findings
- 98.3%
NOC Sensitivity
for clinically important injury
100% -
NOC Sensitivity
for neurosurgical intervention
100% 100%
NOC Specificity 12.7% 5.3-5.6%

In 2008, Jagoda et al., proposed a clinical policy adopted by ACEP for neuroimaging in acute mild traumatic brain injury that synthesized the evidence from the studies mentioned above and from several others. Their recommendations include features from both decision rules, but mainly follow the NOC due to the controversy surrounding the definition of clinically important injuries by the CCHR.

A brief summary in PDF form of these two decision rules and several validation studies can be found on Academic Life in Emergency Medicine at

Clinical Policy: Neuroimaging and Decision Making in Adult Mild Traumatic Brain Injury in the Acute Setting

Which patients with mild TBI should have a noncontrast head CT scan in the ED?

Level A recommendations: A noncontrast head CT is indicated in head trauma patients with LOC or posttraumatic amnesia only if one or more of the following is present: headache, vomiting, age greater than 60 years, drug or alcohol intoxication, deficits in short-term memory, physical evidence of trauma above the clavicle, posttraumatic seizure, GCS score less than 15, focal neurologic deficit or coagulopathy.

Level B recommendations. A non-contrast head CT should be considered in head trauma patients with no loss of consciousness or posttraumatic amnesia if there is a focal neurologic deficit, vomiting, severe headache, age 65 years or greater, physical signs of a basilar skull fracture, GCS score less than 15, coagulopathy or a dangerous mechanism of injury.* *Dangerous mechanism of injury includes ejection from a motor vehicle, a pedestrian struck and a fall from a height of more than three feet or five stairs.


  1. Haydel MJ, Preston CA, Mills TJ, et al., Indications for computed tomography in patients with minor head injury. N Engl J Med. 2000;343:100-105.
  2. Jagoda AS, Bazarian JJ, et al., Clinical Policy: Neuroimaging and Decision making in Adult Mild Traumatic Brain Injury in the Acute Setting. Annals of Emergency Medicine. 2008;52(6): 714-748.
  3. Lin M. Paucis Verbis: Head CT clinical decision rules in trauma. Academic Life in EM. 2012. Available from:
  4. Stiell IG, Wells GA, Vandemheen K, et al., The Canadian CT Head Rule for patients with minor head injury. Lancet. 2001;357:1391- 1396.
  5. Stiell IG, Clement CM, Rowe BH, et al., Comparison of the Canadian CT Head Rule and the New Orleans Criteria in patients with minor head injury. JAMA. 2005;294:1511-1518.
  6. Smits M, Dippel DW, de Haan GG, et al., External validation of the Canadian CT Head Rule and the New Orleans Criteria for CT scanning in patients with minor head injury. JAMA. 2005;294: 1519-1525.

Photo Case: Not All that Blisters is Burned
Aaron Pannier, MD
Naval Medical Center San Diego

Case presentation:
An 18-year-old male presents with a chief complaint of "blisters on his armpit" with mild itching. He states that he first noticed lesions that developed into blisters over the course of the last two days. He is concerned because his "bunkmate" has similar symptoms on his arm.

The patient's vital signs are within normal limits. Physical exam is unremarkable except for the skin exam of his right axilla. His medical and family histories are unremarkable. He is taking no medications and has no known drug allergies.

What is the diagnosis?

Diagnosis: Bullous Impetigo

Bullous Impetigo is a form of impetigo caused by S. aureus, most commonly seen in infants and young children. It occurs when vesicles of impetigo enlarge rapidly, forming bullae. The bullae are due to an epidermolytic toxin at the infection site produced by S. aureus targeting desmoglein 1. This causes intraepidermal cleavage at or below the stratum granulosum. The pathophysiology is similar to pemphigus with autoantibodies directed against desmoglein 1.

Lesions range from few at a local site to wide distribution. The fluid contents of the bullae turn from clear-yellow to turbid fluid. Usually the center of the thin bullae will collapse with fluid remaining in the periphery, which can continue for many days. Honey-colored crust may appear at the center of the lesion with an inflamed, red, serum-oozing base if the crust is unroofed. It may also dry to a red base with a scaly edge. Usually, the fluid-filled rim is replaced by a scaling border when round lesions enlarge and become contiguous with crust forming at the border. Lesions have little to no surrounding erythema.

Impetigo (bullous and nonbullous) has high infection rates for patients in close physical contact, and usually develops on intact skin surfaces. It is self-limiting, but lasts weeks to months if left untreated. Post-streptococcal glomerulonephritis can follow impetigo, but is uncommon in the bullous entity as it is usually purely staphylococcal. Regional lymphadenitis is uncommon. In infants, serious secondary infections like osteomyelitis, septic arthritis and pneumonia can evolve.

Treatment is important to reduce infectious spread, and to improve discomfort and cosmetic appearance. Oral antibiotics should be used if bullae are present, and should have activity against S. aureus and beta-hemolytic streptococci.


  1. Habif, TP. Clinical Dermatology: A Color Guide to Diagnosis and Therapy, 5th ed. Maryland Heights, MO: Mosby; 2010:335-337.
  2. Baddour, LM. Impetigo. UpToDate. Topic 7655 Version 9.0. Accessed via the web at on March 13, 2013.

Toxicology Board Review Questions
Michael Gottlieb, MD
Cook County Hospital

1. Which of the following dermatologic findings and potential causes is INCORRECT?

  1. Cyanosis – Methemoglobinemia
  2. Erythroderma – Boric Acid
  3. Pallor – Carbon Monoxide
  4. Jaundice – Hypercarotinemia (excess carrot intake)
  5. Brightly flushed skin – Niacin

Answer: C.

Methemoglobinemia causes cyanosis due to the oxidation of the iron molecule in hemoglobin, thereby reducing its oxygen carrying capacity. Boric acid (commonly found in a variety of products, but classically, pesticides) is well known to cause a "boiled lobster" skin rash. Carbon monoxide causes normal appearing or pink-colored skin due to its ability to increase hemoglobin’s affinity for oxygen, resulting in hyper-oxygenated red blood cells. Hypercarotinemia, classically seen among anorexic and bulimic teenagers replacing high calorie foods with low calorie carrots, results in excessive beta-carotene, a yellow-pigmented vitamin which mimics jaundice. Note: Hypercarotinemia, as opposed to hyperbilirubinemia, does not result in scleral icterus. Niacin (occasionally used to increase HDL in hypercholesterolemia) is well known to cause prostaglandin-mediated flushing, which may be mitigated by pretreating with aspirin before each dose.

2. All of the following symptoms can occur with Ciguatera poisoning EXCEPT ...

  1. Myalgias
  2. Flushing
  3. Metallic taste
  4. Reversal of temperature sensation
  5. Sensation of loose, painful teeth

Answer: B.

Ciguatoxin (found on warm-water, bottom-dwelling fish — including barracudas, sea bass, red snappers, grouper and sturgeons, among others) binds to sodium channels and increases sodium channel permeability. This results in a variety of symptoms, such as diaphoresis, bradycardia, hypotension, abdominal pain, nausea, vomiting, diarrhea, metallic taste, myalgias, arthralgias, weakness, headache, ataxia, vertigo, sensation of loose and painful teeth, reversal of temperature sensation, peripheral and peri-oral paresthesias and visual disturbances.

Flushing is a classic symptom of scombroid toxicity. Recall that scombroid poisoning is caused by histamine-producing bacteria on the surface of improperly stored dark, tropical fish (e.g. tuna, mackerel, mahi-mahi, etc.). Symptoms include headache, abdominal pain, nausea, vomiting, diarrhea, peri-oral and peripheral paresthesias, dizziness, palpitations and diffuse flushing of the skin.


  1. Wright RO et al. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med. 1999 Nov;34(5):646-56.
  2. Schillinger BM et al. Boric Acid Poisoning. J Am Acad Dermatol. 1982 Nov;7(5):667-73.
  3. Piantadosi CA. Carbon monoxide poisoning. N Engl J Med. 2002 Oct 3;347(14):1054-5
  4. Mazzone A, Dal Canton A. Image in clinical medicine. Hypercarotenemia. N Engl J Med. 2002 Mar 14;346(11):821.
  5. Hochholzer W. The facts behind niacin. Ther Adv Cardiovasc Dis. 2011 Oct;5(5):227-40.
  6. Lawrence DT, et al. Food Poisoning. Emerg Med Clin North Am. 2007 May;25(2):357-73
  7. Isbister GK and Kiernan MC. Neurotoxic marine poisoning. Lancet Neurol. 2005 Apr;4(4):219-28.

Image of the Month
Christine Knettel, MD
Manish Garg, MD
Temple University Hospital

A 48-year-old female with past medical history of hypertension presented with acute onset of headache and clear drainage from her right nostril. The patient reported a one-year history of persistent headaches and chronic clear drainage from the left nostril. She had no history of trauma, fever or visual changes, and had no prior surgical procedures of the head or neck. Exam was significant for clear drainage from bilateral nares, intact cranial nerves 2-12, a nonfocal neurologic exam and no evidence of meningismus or papilledema. Computed tomography (CT) of the brain was performed (Figure 1).

Figure 1: Axial and coronal views of the patient’s initial head CT.

Diagnosis: Dehiscence of cribriform plate with pneumocephalus.
The cribriform plate of the ethmoid bone creates a porous, fragile barrier between the intracranial and extracranial space. Dehiscence causing primary nontraumatic CSF rhinorrhea, as in this patient, may be caused by a persistent embryonic olfactory lumen, focal atrophy, or ruptured arachnoid projects of the olfactory nerve.1 Secondary causes include injury from surgical manipulation or craniomaxillofacial trauma. Common presenting symptoms of dehiscence include headache, visual changes, CSF rhinorrhea and anosmia.2

ED management includes conservative measures (bed rest with elevation of the head of the bed, strict sinus/CSF precautions), monitoring for signs of increased intracranial pressure and consultation with neurosurgery and otolaryngology. Lumbar drain placement and observation for spontaneous closure may obviate surgical intervention, however long-term data suggests that up to 29% of these cases subsequently develop bacterial meningitis.1,3 Routine administration of prophylactic antibiotics by ED physicians is not generally recommended.


  1. LaCour JB and Senior BA. Diagnosis, Evaluation and Management of CSF Rhinorrhea. In: Stucker F, De Souza C, Kenyon G, Lian T, Draf W, Schik B, editors. Rhinology and Facial Plastic Surgery. New York: Springer; 2009. p. 477-484.
  2. Ramsden JD, Corbridge R, Bates G. Bilateral cerebrospinal fluid rhinorrhea. Journal of Laryngology and Otology. 2000; 114: 137-138.
  3. Wax MK, Ramadan HH, Ortiz O, Wetmore SJ. Contemporary management of cerebrospinal fluid rhinorrhea. Otolaryngology – Head and Neck Surgery. 1997; 116 (4): 442-449.

Intussusception: Another Reason Why Ultrasound is Cool
Sierra Read, MSIV
University of Washington

Intussusception scares me. Probably because I first learned about it during my second year gastrointestinal course, when my perfect new baby was just turning six months old. She definitely had bouts of inconsolable crying but luckily her ileocecum was fine. During my ultrasound month I learned a few wonderful clinical pearls that have eased my fears a bit. I'd like to try to pass some of that knowledge along.

Brief Review of the Facts
Intussusception is the acquired invagination of a proximal segment of bowel (the intussusceptum) into a distal segment (the intussuscipiens). The mesentery of the intussusceptum is compressed leading to venous and lymphatic congestion and possibly ischemia, perforation and peritonitis. Most cases are ideopathic and without a clearly associated disease or pathological lead point. The majority of cases are in infants six months to 36 months of age. However, children with intussusception who are outside the most common age range are more likely to have an identifiable lead point. Intussusception is most common near the ileocecal junction but can occur in exclusively small bowel or large bowel too. The classic clinical presentation includes pain, a palpable sausage-shaped abdominal mass and currant-jelly stool; but is only actually seen 15% of the time!1 Other classic elements of the history include sudden onset of severe, intermittent abdominal pain interposed with pain-free periods. But as symptoms progress, patients can become lethargic, highlighting the importance of keeping intussusception in mind when evaluating a patient with altered mental status.

Why We Should All Use Ultrasound
Ultrasound (US) is the preferred method for screening children for intussusception. In fact, it can reach almost 100% sensitivity and specificity with an experienced ultrasonographer.2 When viewed in cross-section, the intussusception appears as a "bull's eye" (Image 1). It's important to remember to view the intussusception with color doppler as well to evaluate for ischemia (Image 2). Ultrasound is able to identify a lead point in two-thirds of cases of non-ideopathic intussusception.3 Also, US enables diagnosis of small bowel intussusception.4 Lesions <3cm or located paraumbilical or in the left abdomen increase suspicion for a small bowel intussusception.3

But What If I'm Not An Experienced Ultrasonographer?
This past September, Rivera et al. published a paper answering this question, "what if I'm not an experienced sonographer?"5 They developed a bedside US protocol to test the ability of novice sonographers with basic US training to identify intussusception. Using a linear transducer, the sonographers started in the RLQ with the indicator towards the patients right side. They identified the psoas muscle and swept the transducer superiorly towards the RUQ. Once the liver/gallbladder were identified, the transducer head was rotated with the indicator cephalad and swept to the LUQ. The head was rotated again returning the indicator to the patient's right and swept towards the LLQ (Image 3). They found that even with minimal training, their novice

sonographer’s sensitivity and specificity reached 85% and 97% respectively with bedside ultrasound. Those numbers are pretty good! However, practice makes perfect, so the next time you have a child with abdominal pain, don’t forget your probe!

For some wonderful images of intussusception, go to

Image 1: From; a classic target lesions seen in intussusception.

Image 2: Also taken from ultrasound cases; a target lesion of intussuception with color duplex applied, showing good perfusion of intussusceptum.

Image 3: Directions of probe movement in bedside ultrasound for intussusception.5 (Reprinted from Annals of Emergency Medicine, 60, Rivera A, Hsiao A, Langhan M, et al., Diagnosis of intussusception by physician novice sonographers in the emergency department, 264-268, Copyright 2012, with permission from Elsevier. Reprinted from The Lancet, Vol. 60, Rivera A, Hsiao A, Langhan M, et al., Diagnosis of intussusception by physician novice sonographers in the emergency department, Pages 264-268, Copyright 2012, with permission from Elsevier.)


  1. Yamamoto LG, Morita SY, Boychuk RB, et al. Stool appearance in intussusception" assessing the value of the term currant jelly." Am J Emerg Med. 1997; 15:293.
  2. Hryhorczuk AL, Strouse PJ. Validation of US as a first-line diagnostic test for assessment of pediatric ileocolic intussusception. Pediatr Radiol. 2009; 39:1075.
  3. Navarro O, Dugougeat F, Kornecki A, et al. The impact of imaging in the management of intussusception owing to pathologic lead points in children. A review of 43 cases. Pediatr Radiol. 2000; 30.594.
  4. Applegate KE: Intussusception in children: imaging choices. Semin Roentgenol. 2008 Jan;43(1):15-21.
  5. Rivera A, Hsiao A, Langhan M, et al. Diagnosis of intussusception by physician novice sonographers in the emergency department. Ann Emerg Med. 2012:60;264-268.

Tox Talks: But the Urine’s Negative?!
Recognition and Management of Urine Tox Screen Negative Drug Intoxications, Part 1
Ashley Grigsby, MSIII
Arizona College of Osteopathic Medicine

Drug intoxication is a common reason for emergency room visits. In 2009, there were 4.6 million ED visits for misuse or abuse of drugs, and about 1 million of those were due to illicit substances.1 The urine toxicology screen is the only screening tool emergency physicians have to detect the use of illicit drugs currently. However, the commonly used five panel drug screen can miss many dangerous drugs. Clinical suspicion and recognition of associated toxidromes are needed for appropriate management of these patients. This is the first of a three part series discussing common drugs that do not reliably show up on the five panel drug screen.

Case 1: Twenty-one-year-old male presents to the ED after being picked up outside of a night club. He believes that he has incredible mental powers. He's euphoric and trying to hug everyone. Vital signs reveal hypertension, a temperature of 39.6°C and a pulse of 156 bpm.


  • "X," "Molly," "E," "Rolls," "Beans"
  • Often mixed toxidromic symptoms due to co-ingestion of other substances including GHB, ketamine, heroin and cocaine.2
  • Minor adverse reactions include bruxism, ataxia, hypertension, tachycardia.
  • Severe Complications
    • Malignant HTN
    • Aortic dissection
    • Seizure
    • Severe Hyponatremia
    • Intracranial hemorrhage
    • DIC
    • Serotonin Syndrome
    • Myocardial Infarction
    • Rhabdomyolysis
    • Hepatotoxicity

Management of ecstasy intoxication first includes the ABCs. Airway may be compromised in severe hyponatremia with neurological symptoms, and often necessitates endotracheal intubation.3 If oxygenation is poor, you should consider an alternative diagnosis as this is very unlikely with ecstasy intoxication. Severe hypertension is common and it has both a central and peripheral component. Benzodiazepines can be used as initial management of the central component of their hypertension, lorazepam 1-2mg IV push repeated as necessary.3 Beta blockers should be avoided in ecstasy due to the unopposed alpha affect that may worsen their hypertension. Electrocardiogram should be done to evaluate for cardiac ischemia. Severe hyperthermia, >41°C, should be managed with an ice bath, milder hyperthermia can be treated with ice packs and cooling blankets. Severe hyponatremia can cause cerebral edema, brain herniation or death, and should be managed based on clinical presentation and severity of hyponatremia.3 UpToDate recommends hypertonic saline in patients with marked neurologic symptoms from their hyponatremia; whereas, mild hyponatremia can be treated with fluid resuscitation alone.3 Seizures may occur in the presence or absence of hyponatremia and should be treated with benzodiazepines and correction of hyponatremia if necessary.3 Phenytoin should be avoided in ecstasy-induced seizures.3

Case 2: Fourteen-year-old female is brought in by EMS after sudden cardiac death at her home. EMS reports v tach rhythm with successful defibrillation and return of ROSC.4

Inhalants abuse is common in the adolescent population due to the low cost and availability of these agents. The average household has 30-50 products with abuse potential. Eleven percent of high school students report using inhalants at some point in their life, and the incidence of use is gradually increasing across the country. The actual chemical compounds differ widely based on the products but the majorities are hydrocarbons (benzene, toluene, etc.), nitrites or nitrous oxide.4 Inhalants can have both acute and chronic complications; only acute management will be discussed here.

  • Slang terms: "huffing," "sniffing," "dusting," "bagging"
  • Death is most commonly from: asphyxia, suffocation, choking on vomitus or careless and dangerous behavior after intoxication.5
  • Sudden Sniffing Death: cardiovascular collapse after inhalation due to sensitization of the myocardium to catecholamines.5
  • Other dangerous complications
    • Hypoxia from displacement of oxygen
    • Hepatotoxicity
    • Metabolic acidosis with potassium and phosphate wasting
    • Burns from inhalant ignition
    • Lead toxicity
    • Methemoglobin from nitrites
  • Initial workup of inhalant toxicity should include: pulse oximetry, electrocardiogram and cardiac monitoring, complete blood count, complete metabolic panel, urinalysis and methemoglobin (nitrites only).5
  • Treatment
    • Management of the ABCs and supportive care based on clinical presentation
    • Symptomatic methemoglobinemia: treatment with high dose oxygen and IV methylene blue.5
    • Psychiatric screening for depression and suicidal ideations
  • Patients who are asymptomatic in the ED may be discharged home with adequate follow-up; other patients often require admission based on clinical severity.5


  1. Center for Behavioral Statistics and Quality, Substance Abuse and Mental Health Services Administration. DAWN Report: Highlights of the 2009 Drug Abuse Warning Network Findings on Drug-Related Emergency Department Visits. Rockville, MD. 2010 Dec. Available from:
  2. Hahn, IH. MDMA Toxicity. Medscape Reference. [Internet]. 2013 [cited 2013 9 April].
  3. Hoffman, RJ. MDMA intoxication. UpToDate. [Internet]. 2013 [cited 2013 9 April].
  4. Claudius, I. The Legal High. In: American Academy of Emergency Medicine Conference, Children are Not Little Adults!. 2013 9 February. Las Vegas, Nevada. 73-82.
  5. Endom, EE, and Perry, H. Inhalent abuse in children and adolescents. UpToDate. [Internet]. 2012 [cited 2013 10 April].

Image of the Month
Victoria Weston, MD
Northwestern University

A 79-year-old male with a past medical history significant for hypertension and gout presented with a swollen, inflamed knee. His symptoms were present for three days, and he had difficulty bearing weight on the affected knee due to pain. He denied fevers, chills, trauma or falls. He had no prior surgeries or injuries to the affected knee, and had no hip pain. He was taking allopurinol and colchicine, but had run out of his medications the week prior to presentation.

On exam, he had large gouty tophi over both hands and feet. His knee was warm to touch and exquisitely tender to palpation. However, he had full range of motion. He also acknowledged picking his skin overlying his knee. Although other possibilities were considered in our differential including septic arthritis and possible overlying cellulitis, this image was chosen for the accompanying X-ray, which described a mass consistent with a “massive” gouty tophus of his knee. Of note, uric acid levels are often normal in acute gout flares and this test is thought to be of limited utility in the emergency department.


  1. Ruder S, and Lewiss, R.E. Arthritis in the ED: detecting high risk etiologies and providing effective pain management. Emergency Medicine Practice. 2004; 6(10):1-24.

Board Review Questions: Wilderness Medicine Topics
Sean Nardi, MSIV
Dylan Hendy, MSIV
Arizona College of Osteopathic Medicine
Ryan Hodnik, DO
University of Nevada School of Medicine-Las Vegas

1) A 64-year-old male in cardiopulmonary arrest is brought into your emergency department by EMS. The patient was found unresponsive at a nearby park and bystander CPR was started immediately. Which of the following causes of adult cardiopulmonary arrest has the best prognosis?

  1. Traumatic
  2. Lightning Strike
  3. Myocardial Infarction
  4. Hyperkalemia

(B) Lightning Strike. Lightning strikes are fatal in one out of 10 strikes and typically kill more people in the United States than any other natural disaster except floods. Although cardiopulmonary arrest is the major cause of death in lightning injuries, victims frequently survive cardiopulmonary arrest with intact neurological function if resuscitation is started early. The mechanism of cardiopulmonary arrest is due to simultaneous depolarization of myocardial cells as well as cells in the medullary respiratory center. It is important to note that while respiratory arrest due to central nervous system injury often persists, intrinsic cardiac automaticity may ensue after initial injury leading to return of spontaneous circulation (ROSC). Therefore, the traditional rules of out-of-hospital mass casualty incidents do not apply to lightning victims. Victims who appear to be in cardiopulmonary arrest should be triaged as highest priority and it is imperative to promptly perform CPR, or at the minimum, ventilation to provide oxygen for perfusion during the lag between recovery of cardiac and respiratory function. Choices A, C and D all have a poorer prognosis than that of cardiopulmonary arrest due to a lightning strike, with traumatic arrest having the worst prognosis.

2) You are a physician at the Mount Everest base camp when a climber presents to your clinic with a 7cm linear laceration to his right forearm. You determine that the wound will need sutures to close and you wish to anesthetize the area locally. However, the patient states he is allergic to lidocaine. Which of the following is a safe alternative to lidocaine and will provide adequate anesthesia?

  1. Eutectic mixture of local anesthetic (EMLA)
  2. Tetracaine gel
  3. Diphenhydramine
  4. Bupivicaine

(C) Diphenhydramine. Although rare, true allergies to amides and esters do exist. In this case, diphenhydramine may be used to provide local anesthesia. When injected subcutaneously or subdermally, diphenhydramine works as a sodium channel blocker and will provide up to 25 minutes of anesthesia. It is usually prepared in a solution comprised of 4:1 normal saline and 5% diphenhydramine. Important side effects to be aware of include pain at the site of injection and the potential development of vesical formation and tissue necrosis. In addition to its anesthetic properties, diphenydramine is a great drug to carry in the field for other ailments as well. It can be used for its antihistamininic properties in allergic reactions, for patients with insomnia, motion sickness, symptomatic relief of upper respiratory infections and may also be applied topically for minor burns, sunburns and abrasions. Choices A, B and D all have amides or esters and may cross react and produce an allergic reaction.

3) During an EMS rotation you are first on scene to a drowning victim. The patient is a 20-year-old female without vital signs, who was submerged for an unknown amount of time. Which of the following accurately describes the course of action to be taken?

  1. Extricate the patient and perform five initial Heimlich maneuvers to remove fluid from the lungs.
  2. Pronounce the patient as she is: without vital signs and has been submerged for an unknown amount of time.
  3. Immediately begin mouth-to-mouth resuscitation and start chest compressions as soon as the patient is on a solid surface.
  4. Extricate the patient and perform continuous chest compressions until you arrive at the emergency department.

(C) Immediately begin mouth-to-mouth resuscitation and start chest compressions as soon as the patient is on a solid surface. In a drowning victim that is without vital signs, outcome is dependent on the interval preceding CPR. These patients represent a divergence from thinking traditionally seen in current ACLS protocol due to the cause of arrest being hypoxia rather than heart disease. Therefore, mouth-to-mouth assisted ventilation should begin immediately, even before the victim is extricated from the water. Chest compressions are impractical prior to removal from the water but should be initiated once the victim is on a solid surface. The Heimlich maneuver is ineffective when there is no reason to believe a foreign body is obstructing the airway and may be dangerous in a victim at risk for aspiration. Pronouncing the patient at the scene is also unwise as there are case reports of functional recovery for individuals submerged up to 66 minutes, and furthermore, bystander accounts of time submerged are usually inaccurate.


  1. Auerbach, Paul S. and Ramin Jamshidi. Wilderness Medicine. 6th ed. Philadelphia: Mosby, 2012. 438.
  2. Davis, Chris, MD, Anna Engeln, MD, Eric Johnson, MD, Scott McIntosh, MD, Ken Zafren, MD, Arthur Islas, MD, Christopher McStay, MD, William Smith, MD, and Tracy Cushing, MD. "Wilderness Medical Society Practice Guidelines for the Prevention and Treatment of Lightning Injuries." Wilderness & Environmental Medicine. 23 (2012): 260-69.
  3. Gibbs, Michael and Douglas C. Dillon Local and Regional Anesthesia. Tintinalli's Emergency Medicine. 7th ed. New York: McGraw Hill, 2011.
  4. Green SM, Rothrock SG, Gorchynski J: Validation of diphenhydramine as a dermal local anesthetic. Annals of Emergency Medicine. 23:1284, 1994.
  5. Knaut, Andrew and David Richards. Drowning. Rosen's Emergency Medicine. 7th ed. Philadelphia: Mosby, 2010. 1929-932.
  6. Timothy G. Price and Cooper, Mary A. Electrical and Lightning Injuries. Rosen's Emergency Medicine. 7th ed. Philadelphia: Mosby, 2010. 1893-902

Thrombolytic Usage in ST-Segment Elevation Myocardial Infarction
Thomas Damiano, MD
Christiana Care Hospital

Lean, Mean, ED Resident Machine: Resident Application of Lean Tools

Many of us train at tertiary care centers with 24/7 catheterization labs where fibrinolytic therapy for STEMI is infrequently used. The reality is that the shops we work in after residency, or even EDs that we train in other than our main hospitals, may be capable of getting STEMI patients to percutaneous coronary intervention (PCI) within a prescribed goal 90 minute door, or recently 120 minute first medical contact to PCI. Therefore, it is important to know how to use fibrinolytic agents for treatment of STEMI, the data behind their usage, pitfalls and contraindications.

The rapid decision to use fibrinolytic therapy in STEMI patients should be pre-determined by institution-specific protocols. The decision to use fibrinolytic therapy can be complicated, especially when patients present within three hours of symptom onset. There is level 1A recommendation to transfer the patient with STEMI to an institution capable of PCI if the patient can be transferred with less than 120 minutes of time to first medical contact to PCI. In a meta-analysis, delay to PCI greater than 62 minutes, provided no survival advantage versus fibrinolysis (Nallamothu, 2003).1 In additional studies, mortality rates were similar between PCI and fibrinolysis groups if delay was greater than 90 minutes, and no different if greater than 120 minutes. Most recently, the STREAM trial showed similar rates in endpoints between fibrinolysis with delayed PCI and primary PCI in STEMI patients with time to first medical contact within three hours of symptom onset, but anticipated delay to PCI greater than one hour (Armstrong, 2013).2 The ACCF/AHA guidelines state that patients with STEMI presenting up to 12 hours from symptom onset, barring certain high risk or those with contraindications, should be treated with immediate reperfusion therapy if it is anticipated that primary PCI cannot be performed within 120 minutes of first medical contact (ACCF/AHA, 2013).3

Once the decision to use fibrinolytic therapy is made and the patient consented, one must choose the appropriate dose for bolus and re-bolus and/or drip. One must know which fibrinolytic his institution’s formulary stocks, as the dosing differs between streptokinase, t-PA, r-PA and TNK. Some protocols recommend reduction of dose based on various age cutoffs. A prudent emergency physician would also, at least, be aware of the trials testing his institution’s fibrinolytic of choice (GUSTO, ASSENT, etc.). Except in the case of allergy, patients should also be administered antiplatelet (aspirin and clopidogrel) and antithrombin (heparin or heparinoid).4 Although there is less evidence for transfer of lower risk patients who receive fibrinolysis at a hospital that does not offer PCI, it is generally recommended the patient should be transferred to a PCI-capable hospital.

Unsuccessful fibrinolytic therapy can be signaled by worsening chest pain or ST segment elevation, worsening hemodynamic stability or ventricular tachydysrrhythmias (Heper, 2008).5 Conversely, so-called reperfusion dysrhythmias, namely sinus bradycardia and accelerated idioventricular rhythms, tend to signal successful reperfusion as well as improvement in chest pain, hemodynamics and decrease in ST-segment elevation.

Finally, it is important to know what are and are not contraindications to fibrinolytic therapy for STEMI patients. Obvious risks for major bleeding are also obvious contraindications. While patients over 75 do have a higher incidence of hemorrhagic stroke, age alone is not a contraindication. A significant decrease in mortality after 12 hours has not been shown, with the exception of those with a stuttering history over that time period. A blood pressure greater than 200/120 is generally an absolute contraindication. CPR is not a contraindication unless greater than 10 minutes. Prior ischemic stroke is a relative contraindication and prior hemorrhagic stroke absolute. Prior MI or even CABG are not contraindications.4

Although fibrinolytic therapy for STEMI is used infrequently by medical students and residents, it is important to understand its use in order to offer this potentially life-saving therapy in this high risk patient population.


  1. Nallamothu, BK. Percutaneous coronary intervention versus fibrinolytic therapy in acute myocardial infarction: is timing (almost) everything? Am J Cardiol. 2003 92 (7): 824
  2. Armstrong, PW. Fibrinolysis or Primary PCI in ST-Segment Elevation MI. N Engl J Med. 2013; 368:1379-1388.
  3. 2013 ACCF/AHA Guideline for the Management of ST-segment Elevation MI
  4. Rosen’s Emergency Medicine. 7th edition Chapter 76, p977-979.
  5. Heper, G. Association of impaired thrombolysis in myocardial infarction myocardial perfusion grade with ventricular tachycardia and ventricular fibrillation following fibrinolytic therapy for ST-segment elevation myocardial infarction. Journal of the American College of Cardiology. 51(5):546-51, 2008 Feb 5.

Health Policy Corner: Prescription Drug Monitoring Programs
Casey Grover, MD
Stanford/Kaiser EM Residency

Nonmedical use of prescription medications has reached epidemic proportions in the United States. Over 7 million Americans over the age of 12 use prescription medications for non-therapeutic reasons each year — which unfortunately results in a large number of emergency department (ED) visits.1,2 As much as we try to identify patients that present to the ED in an attempt to obtain prescription medications for nonmedical reasons, research in this area has predominantly consisted of small studies that are difficult to apply to the general ED population.3-7

What are we to do with this difficult situation? A recent study in Annals of Emergency Medicine demonstrated that having access to a patient’s prescription history of controlled substances changes the way in which emergency physicians prescribe pain medication.7 And this makes intuitive sense — being able to obtain objective information as to the amount of narcotics or benzodiazepines a patient has been using prior to showing up in your ED is a powerful tool. Consider a hypothetical patient who is asking for a refill of his Vicodin for chronic back pain because he claims that his primary care physician is out of town. In reviewing his prescription record, you might find that he has received 200 tablets of Vicodin within the past two weeks. Armed with this information, it would be easy to let the patient know that he probably has enough Vicodin at home to treat his pain, that you are concerned he has a problem with prescription medication and that you don’t feel comfortable giving him any refills.

Physicians are finally getting access to such prescription histories through the use of Prescription Drug Monitoring Programs (PDMPs). These programs are run state by state, and usually consist of web-based software that allow physicians to search for and review a patient’s recent use of controlled substances that are available by prescription (such as opiates, muscle relaxants and benzodiazepines). Nearly all states have such programs in place. Visit the Alliance of States with Prescription Monitoring Programs’ website ( to see how to get access to the PDMP in your state.


  1. Substance Abuse and Mental Health Services Administration. (2010). Results from the 2009 National Survey on Drug Use and Health: Volume I. Summary of National Findings (Office of Applied Studies, NSDUH Series H-38A, HHS Publication No. SMA 10-4586Findings). Rockville, MD.
  2. Substance Abuse and Mental Health Services Administration, Office of Applied Studies. Drug Abuse Warning Network, 2006: National Estimates of Drug-Related Emergency Department Visits. DAWN SeriesD-30, DHHS Publication No. (SMA) 08-4339, Rockville, MD, 2008.
  3. Zechnich AD, Hedges JR. Community-wide emergency department visits by patients suspected of drug-seeking behavior. Acad Emerg Med. 1996 Apr;3(4):312-7.
  4. McNabb C, Foot C, Ting J, Breeze K, Stickley M. Diagnosing drug-seeking behavior in an adult emergency department. Emerg Med Australas. 2006 Apr;18(2):138-42.
  5. Chan L, Winegard B. Attributes and behaviors associated with opioid seeking in the emergency department. J Opioid Manag. 2007 Sep-Oct;3(5):244-8.
  6. Ossipov MH, Lai J, Vanderah TW, Porreca F. Induction of pain facilitation by sustained opioid exposure: relationship to opioid antinociceptive tolerance. Life Sci. 2003 Jun 27;73(6):783-800.
  7. Baehren DF, Marco CA, Droz DE, et al. A statewide prescription monitoring program affects emergency department prescribing behaviors. Ann Emerg Med. 2010; 56: 19-23. e1-3.

Innovations in Emergency Medical Care Update
Jason S. Zeller, MSIV
Drexel University College of Medicine

You may remember the Infrascanner™ 1000 from my previous article. The Infrascanner™ is a portable device that allows for immediate screening of intracranial bleeding. The scanner allows for knowledge of a brain bleed prior to CT and neurosurgical intervention — further leading ER docs to evaluation within the "golden hour." It is especially helpful in the triage of patients with possible bleeds using Near Infrared Spectroscopy (NIRS).

I wanted to give you all an update and introduce the Infrascanner™ 2000. This is a new version of the device, using the same Infrared technology to detect hemoglobin in the brain. This new Infrascanner model differs in that it integrates what was once a separate PDA into a single, rugged, streamlined device. The Infrascanner™ 2000 was developed in partnership with the U.S. Navy and Marine Corps and may be an important device in the future of military, emergency triage and EMS to reduce time and quickly triage head trauma patients. The device is even marketed for use on the sidelines of sports playing fields where head injuries are common.

From Product Brochure:
How does it work?
"Extra-vascular blood absorbs NIR light more than intra-vascular blood since there is a greater concentration of hemoglobin (usually 10 fold) in an acute hematoma than in the brain tissue where blood is contained within vessels. The Infrascanner™ measures the difference in NIR light absorption at corresponding locations on the left and right sides of the head. The detection depth is superficial (within 3.5cm of the skin surface), where blood migrates in most cases of bleeding."

Infrascanner Detection Abilities:

  • Patient measurement is completed within 2-3 minutes.
  • Can detect hematomas greater than 3.5cc in volume.
  • Detects hematomas up to 2.5cm deep from the surface of the brain (or 3.5cm from the skin surface).
  • Accuracy: In patients with epidural, subdural and intracerebral hematomas: Sensitivity = 88% / Specificity = 90.7%.

The Infrascanner™ 2000 is now FDA approved.
Again, I would like to reiterate that this device is simply a screening tool. It does not replace a CT, however it can be used as a way to quickly assess need for further studies or immediate transfer to neurosurgical facility. It is up to you to see if there is need for this in your practice, or prehospital care service.

AccuVein™ AV400

Ever spend an hour getting line access in the ED? Need to get difficult peripheral access even in the dark? This new device may be the solution.

The AccuVein™ AV400 is an FDA approved vein illumination device. The device is a great solution for those hard to find veins in the ED and in the prehospital environment. The AccuVein™ AV400 is a portable device that is held above the skin, creating a real time map of the veins directly onto the skin. The device allows health care professionals to "verify vein patency and avoid valves or bifurcations." The AccuVein™ AV400 can detect veins up to 10mm deep with "accuracy to the width of a human hair." To make things easier in difficult situations, the device can be held at any angle of visualization and also has an inverse option for ease of viewing smaller veins.

From the product news site:

"Weighing less than 10 ounces, the hand-held portable device uses point-and-click technology. With a range of hands-free options, it can quickly switch between a hand-held and hands-free mode, freeing the practitioner’s hands to perform the procedure."

As we think of new ways to better patient care and satisfaction in the ED, new devices which may reduce patient discomfort need to be explored.

All information obtained directly from the Accuvein product page:

Central Line Infections
Geoff Jara-Almonte, MD
Hennepin County Medical Center

Central line infections are a common, costly and morbid complication of intensive care. In 2006, a study published in the New England Journal of Medicine detailed how simple interventions to improve placement and care of central lines in the ICU could reduce infection rates to zero. Since then, other studies in critical care literature have shown significant improvement in infection rates when those same interventions were adopted.

Comparatively, little is known about the infection risk of central lines placed in the ED. A 2010 review article found only a few studies looking at infection rates of ED placed lines. They identified central line associated bloodstream infection (CLABSI) rates ranging from 0-24.1 per 1000 line days, but due to limitations in the data, were unable to compare this to rates of infection in ICU placed lines.

A core set of best practices identified from ICU studies has been compiled by the Institute for Healthcare Improvement (IHI) into a central line bundle, and has trickled down into most ED’s as standard practice. These include: using chlorhexidine prep, avoiding the femoral site, using maximal sterile precautions (cap, mask, gown, large sheet, gloves) and placing a sterile dressing.

Despite widespread adoption of the bundle, we do know that ED staff are less than perfect at following sterile techniques. A study from an academic trauma center retrospectively analyzed video recordings of central line insertions and found adherence to sterile precautions ranging from 88-32% depending on patient acuity. Senior residents, fellows and faculty were less likely to follow sterile precautions than more junior residents.

Interventions that have been used successfully in the ICU to increase adherence of IHI bundle practices include use of a pre-procedure checklist and dedicated procedural observers, who are empowered to stop a procedure if deviations from best practices are noted. Based on survey data, we know these practices are fairly common in ICU’s (92% for checklist and 78% for procedural observer in one study), however much less frequent in ED’s (52% and 33% respectively). Despite their documented efficacy in the ICU, no published studies looking at implementation of either checklists or procedural observers in the ED were found.

Central line infections are an avoidable and unacceptable complication. Despite our knowledge of best practices in the ICU environment, it is unknown whether or not these are transferrable to the emergency department. This is an area in which more research is needed.


  1. Pronovost P, Needham D, Berenholtz S, Sinopoli D, Chu H, Cosgrove S, Sexton B, Hyzy R, Welsh R, Roth G, Bander J, Kepros J, Goeschel C. An intervention to decrease catheter-related bloodstream infections in the ICU.  N Engl J Med. 2006 Dec 28;355(26):2725-32.
  2. Lemaster CH, Agrawal AT, Hou P, Schuur JD. Systematic review of emergency department central venous and arterial catheter infection. Int J Emerg Med. 2010 Nov 5;3(4):409-23. doi: 10.1007/s12245-010-0225-5.
  3. Guzzo JL, Seagull FJ, Bochicchio GV, Sisley A, Mackenzie CF, Dutton RP, Scalea T, Xiao Y.  Mentors decrease compliance with best sterile practices during central venous catheter placement in the trauma resuscitation unit. Surg Infect (Larchmt). 2006 Feb;7(1):15-20.
  4. Berenholtz SM, Pronovost PJ, Lipsett PA, Hobson D, Earsing K, Farley JE, Milanovich S, Garrett-Mayer E, Winters BD, Rubin HR, Dorman T, Perl TM. Eliminating catheter-related bloodstream infections in the intensive care unit. Crit Care Med. 2004 Oct;32(10):2014-20.
  5. Schuur JD, Hou PC, Pallin DJ, Yokoe DS, Espinola JA, Camargo Jr CA. Central Venous Catheter Infection Practices in US Emergency Departments and Intensive Care Units. Annals of Emergency Medicine Research Forum Abscracts. Vol 60, No 4s Oct 2012.