Neonatal Congenital Heart Disease

Brief H&P

An 8-day old male infant, ex-full term, born by normal spontaneous vaginal delivery and discharged home 2 days after birth without identified complications or maternal infections presents with parents to the emergency department due to decreased activity. Starting on day-of-life six, the family noted that feeding appeared to be taking longer and the mother felt her infant was breathing faster.

On presentation, the patient was pale, dusky, lethargic and with mottled skin. Temperature 36.3°C (rectal), HR 170, RR 60, BP 62/35, SpO2 70%. Physical examination demonstrated flat fontanelle, coarse breath sounds, regular rate and rhythm without additional heart sounds or murmurs, and hepatomegaly with liver edge 3cm below costal margin. Capillary refill was delayed at 5-6 seconds. Supplemental oxygen was applied without effect.

Algorithm for the Evaluation and Management of Suspected Congenital Heart Disease in Neonates

Algorithm for the Evaluation of Neonatal Congenital Heart Disease

Neonates with undiagnosed congenital heart disease may present to the emergency department with nonspecific symptoms, and may be considerably unstable requiring immediate life-saving interventions.

Key Historical Features

  • Respiratory difficulty
  • Feeding difficulty (small quantities, diaphoresis during feeding)
  • Poor weight gain
  • Chromosomal abnormalities, syndromes
  • Maternal risk factors: diabetes, teratogen exposure, substance use
  • Sibling of affected child

Key Examination Findings

  • Vital signs: tachycardia, tachypnea, hypotension
  • Blood pressure differential (RUE vs. LE >8mmHg difference)
  • Pulse oximetry differential (RUE vs. LE >4% difference, <95%)
  • Cardiac examination: murmur, thrill, pulse differential, capillary refill, hepatomegaly

Workup

  • CXR: Evaluate for cardiomegaly, pulmonary vascular congestion
  • ECG: Evaluate for axis deviation (right axis deviation is normal for neonate)
  • ABG with co-oximetry

References

  1. Special thanks to Dr. Kelly Young, MD, MS, FAAP. Director, Pediatric Emergency Medicine Fellowship. Harbor-UCLA Medical Center Department of Emergency Medicine.
  2. Association AAOPAAH. Textbook of Neonatal Resuscitation. 2016.
  3. Lissauer T, Fanaroff AA, Miall L, Fanaroff J. Neonatology at a Glance. John Wiley & Sons; 2015.
  4. Steinhorn RH. Evaluation and Management of the Cyanotic Neonate. Clinical Pediatric Emergency Medicine. 2008;9(3):169-175. doi:10.1016/j.cpem.2008.06.006.
  5. MD MR. Chapter 7 – Cardiology. Twenty First Edition. Elsevier Inc.; 2018:156-202. doi:10.1016/B978-0-323-39955-5.00007-7.
  6. Gomella T, Cunningham M. Neonatology 7/E. McGraw-Hill Prof Med/Tech; 2013.
  7. Yee L. Cardiac emergencies in the first year of life. Emergency Medicine Clinics of NA. 2007;25(4):981–1008–vi. doi:10.1016/j.emc.2007.08.001.
  8. Yates MC, Rao PS. Pediatric cardiac emergencies. Emerg Med. 2013. doi:10.4172/2165-7548.1000164.
  9. Silberbach M, Hannon D. Presentation of congenital heart disease in the neonate and young infant. Pediatr Rev. 2007;28(4):123-131.
  10. Mastropietro CW, Tourner SP, Sarnaik AP. Emergency presentation of congenital heart disease in children. Pediatric Emergency …. 2008.
  11. Brousseau T, Sharieff GQ. Newborn Emergencies: The First 30 Days of Life. Pediatric Clinics of North America. 2006;53(1):69-84. doi:10.1016/j.pcl.2005.09.011.

Hyperthermia

Brief H&P

A young male with unknown medical history is brought in by ambulance with altered mental status. EMS reports that the patient was agitated, requiring restraints for transportation. On arrival, the patient is agitated, uncooperative and unable to provide history. Vital signs are notable for tachycardia, tachypnea and hypertension. Physical examination demonstrates diaphoresis and mydriasis, as well as increased muscle tone – particularly in the lower extremities with ankle clonus. A core temperature is obtained and noted to be elevated at 41.5°C. Point-of-care glucose is normal.

Rapid external cooling measures were instituted and several doses of intravenous benzodiazepines were administered with improvement in agitation. Laboratory studies were notable for a modest leukocytosis (WBC 18.4 without immature forms), serum sodium was 135 without osmolar gap, creatine kinase was slightly elevated without renal dysfunction, and thyroid function tests were normal. Toxicology screen was negative. ECG revealed sinus tachycardia but was otherwise normal and non-contrast computed tomography of the head was normal.

After a brief admission in the intensive care unit, the patient’s mental status improved and he reported MDMA use on the evening of presentation, he also described a history of major depression and was taking paroxetine.

Evaluation of Elevated Temperature

The designation of 38°C as “suspicious” for fever dates to 1868 and the analysis of over one million (axillary) temperature measurements by Carl Wunderlich1. Any cutoff is arbitrary and requires recognition of the clinical context and normal daily variations (with nadir in the morning and peak in evening) 2,3. What is clear is that peripheral thermometry (unless demonstrating fever) is unreliable and a core temperature should be sought4.

Thermoregulation

Temperature homeostasis is a balance between heat production and dissipation maintained by the anterior hypothalamus. Heat production is a byproduct of normal metabolic processes and skeletal muscle activity. Conservation, maintenance or dissipation of heat is aided by cutaneous vasodilation, sweating, or behavioral responses.

Fever is caused by endogenous or exogenous pyrogens which alter the homeostatic set-point, inducing thermogenesis and elevating the body temperature. Precipitants of fever are usually infectious, however non-infectious processes (ex. malignancy, tissue ischemia/infarction, auto-immune disease) resulting in inflammation can provoke a similar response 5-7.

There is no explicit temperature distinction to diagnose hyperthermia, instead the physiologic mechanism is different. In hyperthermia, the body’s homeostatic mechanisms are dysfunctional or overwhelmed due to heat exposure, excess production, ineffective dissipation or hypothalamic malfunction 8.

Algorithm for the Evaluation of Hyperthermia 8-15

Algorithm for the Evaluation of Hyperthermia

Implicated Agents in Drug-Induced Hyperthermic Syndromes 9,10

Serotonin Syndrome

Class Examples
SSRI sertraline, fluoxetine, paroxetine
Other anti-depressants trazodone, venlafaxine, lithium
MAOI phenelzine, isocarboxazid
Anti-epileptic drugs valproate
Analgesics meperidine, fentanyl, tramadol
Anti-emetic ondansetron, metoclopramide
Anti-migraine sumatriptan
Antimicrobial linezolid, ritonavir
Illicit substances MDMA, LSD

Neuroleptic Malignant Syndrome (NMS)

Class Examples
Typical anti-psychotic haloperidol, prochlorperazine
Atypical anti-psychotic risperidone, olanzapine, quetiapine, aripiprazole
Anti-dopaminergic metoclopramide, droperidol

References:

  1. Wunderlich CA. Das Verhalten Der Eigenwärme in Krankheiten. 1870.
  2. Mackowiak PA, Wasserman SS, Levine MM. A critical appraisal of 98.6 degrees F, the upper limit of the normal body temperature, and other legacies of Carl Reinhold August Wunderlich. JAMA. 1992;268(12):1578-1580.
  3. Lee-Chiong TL, Stitt JT. Disorders of temperature regulation. Compr Ther. 1995;21(12):697-704.
  4. Niven DJ, Gaudet JE, Laupland KB, Mrklas KJ, Roberts DJ, Stelfox HT. Accuracy of peripheral thermometers for estimating temperature: a systematic review and meta-analysis. Ann Intern Med. 2015;163(10):768-777. doi:10.7326/M15-1150.
  5. Dinarello CA. Infection, fever, and exogenous and endogenous pyrogens: some concepts have changed. J Endotoxin Res. 2004;10(4):201-222. doi:10.1179/096805104225006129.
  6. Greisman LA, Mackowiak PA. Fever: beneficial and detrimental effects of antipyretics. Curr Opin Infect Dis. 2002;15(3):241-245.
  7. Dinarello CA. Thermoregulation and the pathogenesis of fever. Infect Dis Clin North Am. 1996;10(2):433-449.
  8. Simon HB. Hyperthermia. N Engl J Med. 1993;329(7):483-487. doi:10.1056/NEJM199308123290708.
  9. Boyer EW, Shannon M. The serotonin syndrome. N Engl J Med. 2005;352(11):1112-1120. doi:10.1056/NEJMra041867.
  10. Berman BD. Neuroleptic malignant syndrome: a review for neurohospitalists. Neurohospitalist. 2011;1(1):41-47. doi:10.1177/1941875210386491.
  11. Hayes BD, Martinez JP, Barrueto F. Drug-induced hyperthermic syndromes: part I. Hyperthermia in overdose. Emerg Med Clin North Am. 2013;31(4):1019-1033. doi:10.1016/j.emc.2013.07.004.
  12. Oruch R, Pryme IF, Engelsen BA, Lund A. Neuroleptic malignant syndrome: an easily overlooked neurologic emergency. Neuropsychiatr Dis Treat. 2017;13:161-175. doi:10.2147/NDT.S118438.
  13. Musselman ME, Saely S. Diagnosis and treatment of drug-induced hyperthermia. Am J Health Syst Pharm. 2013;70(1):34-42. doi:10.2146/ajhp110543.
  14. Ahuja N, Cole AJ. Hyperthermia syndromes in psychiatry. Adv psychiatr treat (Print). 2018;15(03):181-191. doi:10.1192/apt.bp.107.005090.
  15. Tomarken JL, Britt BA. Malignant hyperthermia. Ann Emerg Med. 1987;16(11):1253-1265. doi:10.1016/S0196-0644(87)80235-4.

Wide-complex Tachycardia

Several algorithms exist for the electrocardigraphic evaluation of regular, wide-complex tachycardias with the objective of distinguishing ventricular tachycardia (VT) from a supraventricular tachycardia (SVT) with aberrant conduction. The algorithm detailed below, developed by Dr. James Niemann, presents an ED-centric approach favoring the diagnosis of the more life-threatening dysrhythmia. This approach recognizes that SVT with aberrancy is rare, particularly in patients with a history of cardiac disease where the likelihood of ventricular tachycardia exceeds 90%. The algorithm requires the use of only the most simple and easily-recalled criteria, and any point of failure along the algorithm lends to the universally-appropriate management as ventricular tachycardia.

Algorithm for the Evaluation of Regular, Wide-Complex Tachycardia

Algorithm for the Evaluation of Wide-Complex Tachycardia

  1. aVR: Is the initial deflection in aVR positive? If yes, then VT.
  2. Concordance: Is there concordance (monophasic with same polarity) in all of the precordial leads? If yes, then VT.
  3. AV Dissociation: Is there evidence of AV dissociation (fusion or capture beats)? If yes, then VT.
  4. Bundle-branch morphology: Is the QRS morphology in V1 and V6 consistent with either LBBB or RBBB? If no, then VT.

References

  1. Neimann J. Wide QRS Complex Tachycardias. Lecture. Harbor-UCLA Department of Emergency Medicine. 2014:1-19.
  2. Vereckei A, Duray G, Szénási G, Altemose GT, Miller JM. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia. Heart Rhythm. 2008;5(1):89-98. doi:10.1016/j.hrthm.2007.09.020.
  3. Szelényi Z, Duray G, Katona G, et al. Comparison of the “real-life” diagnostic value of two recently published electrocardiogram methods for the differential diagnosis of wide QRS complex tachycardias. Acad Emerg Med. 2013;20(11):1121-1130. doi:10.1111/acem.12247.
  4. Brugada P, Brugada J, Mont L, Smeets J, Andries EW. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation. 1991;83(5):1649-1659.
  5. Lau EW, Pathamanathan RK, Ng GA, Cooper J, Skehan JD, Griffith MJ. The Bayesian approach improves the electrocardiographic diagnosis of broad complex tachycardia. Pacing Clin Electrophysiol. 2000;23(10 Pt 1):1519-1526.
  6. B Garner J, M Miller J. Wide Complex Tachycardia – Ventricular Tachycardia or Not Ventricular Tachycardia, That Remains the Question. Arrhythm Electrophysiol Rev. 2013;2(1):23-29. doi:10.15420/aer.2013.2.1.23.
  7. Vereckei A. Current algorithms for the diagnosis of wide QRS complex tachycardias. Curr Cardiol Rev. 2014;10(3):262-276.
  8. Garmel GM. Wide Complex Tachycardias: Understanding this Complex Condition: Part 1 – Epidemiology and Electrophysiology. West J Emerg Med. 2008;9(1):28-39.
  9. Garmel GM. Wide Complex Tachycardias: Understanding this Complex Condition Part 2 – Management, Miscellaneous Causes, and Pitfalls. West J Emerg Med. 2008;9(2):97-103.
  10. Griffith MJ, Garratt CJ, Mounsey P, Camm AJ. Ventricular tachycardia as default diagnosis in broad complex tachycardia. The Lancet. 1994;343(8894):386-388.

Ultrasound in Ectopic Pregnancy

Brief HPI:

A 27 year-old female is brought in by ambulance with syncope. Pre-hospital providers report that the patient developed pelvic pain, vaginal bleeding and lost consciousness. On their arrival, her blood pressure was 80mmHg systolic, point-of-care glucose was normal – a peripheral IV was started, fluids were administered and the patient was transported to the emergency department. On arrival, vital signs were notable for tachycardia and hypotension. The patient was lethargic, maintaining arousal only with constant verbal or noxious stimulation. Her abdomen was markedly tender throughout with rebound and involuntary guarding. Her last menstrual period was 5 weeks ago and she suspected that she was pregnant. Peripheral venous access was expanded and uncrossmatched blood products were rapidly transfused. Whole blood on a point-of-care pregnancy test was positive1, and a bedside FAST demonstrated free intraperitoneal fluid in the hepatorenal recess with large free pelvic fluid. Gynecology was consulted for emergent operative management of suspected ruptured ectopic pregnancy with hemorrhagic shock and the patient was taken to the operating room.

Algorithm for the Evaluation of Suspected Ectopic Pregnancy

Algorithm for the evaluation of ectopic pregnancy

Gallery

The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.
The POCUS Atlas

Ruptured Cornual Ectopic

Tubal Ectopic Pregnancy

Tubal Ectopic Pregnancy

Ectopic Pregnancy

Ectopic Pregnancy

Positive FAST in Ruptured Ectopic

Positive FAST in Ruptured Ectopic

The evaluation of suspected ectopic pregnancy, as with all complaints in the emergency department, begins with an assessment of patient stability: airway, breathing and circulation. The unstable patient requires immediate interventions to secure each critical component, all temporizing measures until the patient can be taken to the operating room for definitive management.

The evaluation and management algorithm for stable patients is dependent on findings of transabdominal & transvaginal ultrasonography, quantitative hCG level (relative to the institution-dependent discriminatory zone), and the identification of high risk historical and examination features that would prompt specialist consultation despite otherwise benign diagnostic tests.

If ultrasonography demonstrates a definite ectopic pregnancy (extrauterine live embryo,  adnexal mass containing yolk sac), gynecology consultation is warranted – the table below details candidates for attempts at pharmacologic therapy.

Requirements for methotrexate administration2,3

Absolute
Hemodynamic stability
Ultrasound findings consistent with an ectopic pregnancy
Willingness of the patient to adhere to close follow-up
No existing organ dysfunction: hepatic, renal, pulmonary, hematologic, immune
Relative
Unruptured ectopic mass <3.5cm
No fetal cardiac activity detected
hCG <5000 mIU/L

If an intrauterine pregnancy is identified such as a live embryo or yolk sac, barring the presence of risk factors for heterotopic pregnancy (namely, the use of assisted fertilization methods 2, 4-6), then an alternative cause for the patient’s symptoms should be sought.

If the ultrasound is non-diagnostic, patients should be stratified according to risk based on historical features, examination findings and quantitative hCG. If the hCG is above the institutional discriminatory zone, the absence of a definitive IUP is concerning, elevating suspicion for a non-visualized ectopic and warrants gynecology consultation. If the hCG is below the discriminatory zone, then certain features such as the presence of abdominal, adnexal or cervical motion tenderness, or high-risk ultrasonographic features including greater-than-moderate free pelvic fluid, complex fluid, or complex adnexal masses may be secondary features of ectopic pregnancy – again warranting consultation. If no high-risk features are present, close follow-up with repeat hCG and ultrasonography is reasonable.

Risk factors for ectopic pregnancy3

Risk factor OR
Previous tubal surgery 21
Sterilization 9.3
Previous ectopic 8.3
In utero exposure to diethylstilbestrol 5.6
Current IUD 5.0
History of PID 3.4
Infertility 2.7
Advanced maternal age 1.4-2.9
Smoking 1.5-3.9

Examination Findings in Ectopic Pregnancy6

Finding LR+
Cervical motion tenderness 4.9
Peritoneal irritation 4.2
Adnexal mass 2.4
Adnexal tenderness 1.9

Ultrasound Findings in Ectopic Pregnancy 7

Finding LR+
Ectopic cardiac activity >100
Ectopic gestational sac 23
Ectopic mass and fluid in Pouch of Douglas 9.9
Fluid in Pouch of Douglas 4.4
Ectopic mass 3.6
No IUP 2.2
Normal adnexa 0.55

Algorithm for the Evaluation of Vaginal Bleeding

Algorithm for the evaluation of vaginal bleeding

References:

  1. Fromm C, Likourezos A, Haines L, Khan ANGA, Williams J, Berezow J. Substituting whole blood for urine in a bedside pregnancy test. J Emerg Med. 2012;43(3):478-482. doi:10.1016/j.jemermed.2011.05.028.
  2. Bhatt S, Ghazale H, Dogra VS. Sonographic Evaluation of Ectopic Pregnancy. Radiol Clin North Am. 2007;45(3):549-560. doi:10.1016/j.rcl.2007.04.009.
  3. Barash JH, Buchanan EM, Hillson C. Diagnosis and management of ectopic pregnancy. Am Fam Physician. 2014;90(1):34-40.
  4. Lin EP, Bhatt S, Dogra VS. Diagnostic Clues to Ectopic Pregnancy. Radiographics. 2008;28(6):1661-1671. doi:10.1148/rg.286085506.
  5. Winder S, Reid S, Condous G. Ultrasound diagnosis of ectopic pregnancy. Australas J Ultrasound Med. 2011;14(2):29-33. doi:10.1002/j.2205-0140.2011.tb00192.x.
  6. Crochet JR, Bastian LA, Chireau MV. Does this woman have an ectopic pregnancy?: the rational clinical examination systematic review. JAMA. 2013;309(16):1722-1729. doi:10.1001/jama.2013.3914.
  7. Mol BW, van Der Veen F, Bossuyt PM. Implementation of probabilistic decision rules improves the predictive values of algorithms in the diagnostic management of ectopic pregnancy. Hum Reprod. 1999;14(11):2855-2862.
  8. First-Trimester Emergencies: A Practical Approach To Abdominal Pain And Vaginal Bleeding In Early Pregnancy. October 2003:1-20.
  9. Paspulati RM, Bhatt S, Nour S. Sonographic evaluation of first-trimester bleeding. Radiol Clin North Am. 2004;42(2):297-314. doi:10.1016/j.rcl.2004.01.005.
  10. Anderson FWJ, Hogan JG, Ansbacher R. Sudden Death: Ectopic Pregnancy Mortality. Obstet Gynecol. 2004;103(6):1218-1223. doi:10.1097/01.AOG.0000127595.54974.0c.
  11. Lozeau A-M, Potter B. Diagnosis and management of ectopic pregnancy. Am Fam Physician. 2005;72(9):1707-1714.
  12. Stone MB. Emergency Ultrasound Diagnosis of Ruptured Ectopic Pregnancy. Academic Emergency Medicine. 2009;16(12):1378-1378. doi:10.1111/j.1553-2712.2009.00538.x.
  13. Stein JC, Wang R, Adler N, et al. Emergency Physician Ultrasonography for Evaluating Patients at Risk for Ectopic Pregnancy: A Meta-Analysis. Ann Emerg Med. 2010;56(6):674-683. doi:10.1016/j.annemergmed.2010.06.563.
  14. Fromm C, Likourezos A, Haines L, Khan ANGA, Williams J, Berezow J. Substituting whole blood for urine in a bedside pregnancy test. J Emerg Med. 2012;43(3):478-482. doi:10.1016/j.jemermed.2011.05.028.
  15. Alkatout I, Honemeyer U, Strauss A, et al. Clinical diagnosis and treatment of ectopic pregnancy. Obstet Gynecol Surv. 2013;68(8):571-581. doi:10.1097/OGX.0b013e31829cdbeb.
  16. Arleo EK, DeFilippis EM. Cornual, interstitial, and angular pregnancies: clarifying the terms and a review of the literature. Clinical Imaging. 2014;38(6):763-770. doi:10.1016/j.clinimag.2014.04.002.
  17. Rodgers SK, Chang C, DeBardeleben JT, Horrow MM. Normal and Abnormal US Findings in Early First-Trimester Pregnancy: Review of the Society of Radiologists in Ultrasound 2012 Consensus Panel Recommendations. Radiographics. 2015;35(7):2135-2148. doi:10.1148/rg.2015150092.
  18. Diagnosis and Management of Ectopic Pregnancy: Green-top Guideline No. 21. BJOG. 2016;123(13):e15-e55. doi:10.1111/1471-0528.14189.
  19. Hahn SA, Promes SB, Brown MD, et al. Clinical Policy: Critical Issues in the Initial Evaluation and Management of Patients Presenting to the Emergency Department in Early Pregnancy. Ann Emerg Med. 2017;69(2):241–250.e20. doi:10.1016/j.annemergmed.2016.11.002.
  20. Lee R, Dupuis C, Chen B, Smith A, Kim YH. Diagnosing ectopic pregnancy in the emergency setting. Ultrasonography. 2018;37(1):78-87. doi:10.14366/usg.17044.

A history of the ddxof: mobile application

I’ve wanted a mobile companion application for ddxof for a while. I’m not entirely sure that anyone else feels strongly about it, but I use the content regularly on shift and trying to load even the mobile-optimized website on my phone was cumbersome. Dropbox worked for a while but it didn’t maintain the taxonomy I’d assigned on the website and text content wasn’t included.

While I have some experience with web development, a quick peek at Objective C and native app development suggested I would be in over my head. So, I sought some funding, designed a few basic screens in Sketch, and waited to see what the development team came up with.

Sketches of different screens on the app

Version 1.0

The app hung on this screen for 20 seconds on launch

When it loaded, things looked pretty good

It even had working favorites

In November, I saw the final product and it was a bit of a fixer-upper. Much of the functionality was present (including adding Favorites). Unfortunately, less attention seemed to have been paid to certain usability aspects and the visual style I’d developed in the design compositions.

Most glaring was the lack of any representation of a loading state. It pained me to watch coworkers download the app and see a blank screen that ignored their interaction attempts for a solid 20 seconds on the app’s initial launch.

Luckily, I got access to the source code and found that it was built with something called React Native. As I sifted through the code, I realized that I recognized and (mostly) understood what was happening. It was basically JavaScript, I know JavaScript! The display and styling portions were also easy to grasp as they’re similar to HTML and CSS respectively.

I tried to work backwards from the code I’d received but it was just too hard to grasp. The extent of my JavaScript experience prior to this was rudimentary so after going back and forth a few times between attempting to improve upon the existing app and just starting from scratch, I decided to dive in and begin anew.

Version 2.0

A real loading indicator

I lost a few things, no multiple algorithms, no categories/tags

By version 2.3, we had post categories/tags and a gallery view for multiple algorithms

Exactly 1 month later, I released version 2.0 of the ddxof: mobile application. Since it was built from scratch, I had to remove some of the features that were too complex for me to develop. Removing the option to save favorites was a tough choice but I was excited to have a version of the application that at least wouldn’t make me cringe when I saw it in use.

The only reason I was even able to get that far was the truly impressive community surrounding React Native. I thought of them a bit like plugins, and using a few components really simplified the process of interacting with the website’s API and storing content for offline use.

In landscape mode, the header occupied pretty much the entire screen

Version 2.4.2 shrunk the header down

Over the next two months, I worked on iterative functional and visual improvements including better server- and client-side caching, and the ability to see all of post’s algorithms (with an image gallery “plugin”). Things settled down by version 2.4.2, it worked, was mostly bug free, and I took a break.

Version 3.0

As I used the app more, a few things kept bugging me. I really missed being able to save favorites and I was often annoyed that the app didn’t allow interaction during attempts at refreshing content (even though usable cached content was available).

Version 3.0 with a more subdued color scheme

Favorites are back

Cached content remains accessible if a network error occurs

I knew favorites was going to be a problem, I’d tried tackling it earlier when I started working on version 2.0 but had given up. The problem is that an article marked as a favorite needs to be recognized across all parts of the application. This notion of state management in React Native seemed to commonly be handled by a library called Redux. However, despite my best efforts I simply could not wrap my head around the logic. After all, I’m still not a developer and I found myself getting lost in descriptions of “actions” and “reducers”. I was thrilled when I found Mobx which accomplished everything I needed in a much more understandable fashion. My favorites list became an observable that I could access and remained alive wherever I needed it and making the information persist on the user’s device was laughably easy with another plugin.

Using Mobx also meant that I could check for content updates in the background without interrupting the user’s ability to interact with cached content. The small indicator area lets users refresh the content, notify them of a refresh attempt and even connection errors.

The uncollapsed header in landscape mode

The header animates down when scrolling

I also took the opportunity to touch up a few interface issues. The header shrinks with a hopefully-subtle animation when scrolling to provide more space for content. I was also finding the red a bit overwhelming, the muted grays are much more my style.

I’m happy to announce that version 3.0 is now available on the App Store and Google Play Store. Please try it out and let me know what you think!

Sinus Tachycardia

Brief History and Physical:

A young female with a history of schizophrenia presents to the emergency department reporting hallucinations. She had been diagnosed with schizophrenia one year previously and was briefly admitted to a psychiatric hospital. She discontinued her anti-psychotic (risperidone) two months ago, and over the past week she reports increasingly prominent auditory and visual hallucinations.

She denies recent illness, vomiting/diarrhea, changes in urinary habits, new medications, alcohol or illicit substance use. She also denies chest pain, palpitations or shortness of breath.

Vital signs are notable for a heart rate of 148bpm and are otherwise normal (including core temperature). Detailed physical examination is normal except for a rapid, regular heart rate. Mental status examination demonstrated normal level of alertness and orientation, linear and cogent responses and occasional response to internal stimuli during which she appeared anxious.

Initial evaluation and management included a 12-lead ECG which showed sinus tachycardia. Multiple boluses of normal saline were initiated while awaiting laboratory workup.

ECG: Sinus Tachycardia

Presentation ECG demonstrates sinus tachycardia.

Update:

Laboratory studies were reviewed and unremarkable. Normal hemoglobin, normal chemistry panel, negative hCG, and negative toxicology screen. The patient remained persistently tachycardic with a heart rate ranging from 140-160bpm (again sinus tachycardia on 12-lead ECG). An atypical antipsychotic and anxiolytic were administered and additional studies were obtained. Serum TSH, troponin and D-dimer were normal and bedside ultrasound did not identify a pericardial effusion. The patient remained asymptomatic, reporting subjective improvement in anxiety and hallucinations. Psychiatry was consulted and the patient was placed in observation for monitoring of sinus tachycardia. Observation course was uneventful as the patient remained asymptomatic. Transthoracic echocardiography was normal. Psychiatry consultation recommended resumption of home anti-psychotic and outpatient follow-up. Tachycardia had improved but not resolved at the time of discharge (heart rate 109bpm) and the patient was instructed to follow-up with her primary care provider.


Algorithm for the Evaluation of Sinus Tachycardia

Algorithm for the Evaluation of Sinus Tachycardia

Any vital sign derangement is concerning and tachycardia may be associated with unanticipated death after discharge home1. The presence of tachycardia suggests one of several categories of hemodynamic, autonomic, or endocrine/metabolic derangement.

Demand for increased cardiac output

A perceived demand for increased cardiac output will prompt chronotropic (and inotropic) amplification before hypotension develops. Causative etiologies include: volume depletion (from hemorrhage, gastrointestinal or renal losses), distributive processes (such as infection), obstruction (pulmonary embolus, or pericardial effusion with impending tamponade), or tissue hypoxia (anemia or lung disease).

Autonomic nervous system

Autonomic nervous system disturbances induced by stimulant, sympathomimetic or anti-cholinergic use, or withdrawal of certain agents such as ethanol or beta-blockers may be at fault.

Endocrine and other causes

Hyperthyroidism and pheochromocytoma should be considered, and as diagnoses of exclusion: anxiety, pain, or inappropriate sinus tachycardia2.

Evaluation:
Core temperature
CBC
Troponin
D-dimer
Bedside cardiac ultrasound
Urine toxicology screen
Ethanol level
TSH/T4

Algorithm for the Evaluation of Narrow-Complex Tachycardia3,4,5,6

Algorithm for the Evaluation of Narrow-Complex Tachycardia

References:

  1. Sklar DP, Crandall CS, Loeliger E, Edmunds K, Paul I, Helitzer DL. Unanticipated Death After Discharge Home From the Emergency Department. Ann Emerg Med. 2007;49(6):735-745. doi:10.1016/j.annemergmed.2006.11.018.
  2. Olshansky B, Sullivan RM. Inappropriate sinus tachycardia. J Am Coll Cardiol. 2013;61(8):793-801. doi:10.1016/j.jacc.2012.07.074.
  3. Yusuf S, Camm AJ. Deciphering the sinus tachycardias. Clin Cardiol. 2005;28(6):267-276.
  4. Katritsis DG, Josephson ME. Differential diagnosis of regular, narrow-QRS tachycardias. Heart Rhythm. 2015;12(7):1667-1676. doi:10.1016/j.hrthm.2015.03.046.
  5. Bibas L, Levi M, Essebag V. Diagnosis and management of supraventricular tachycardias. CMAJ. 2016;188(17-18):E466-E473. doi:10.1503/cmaj.160079.
  6. Link MS. Clinical practice. Evaluation and initial treatment of supraventricular tachycardia. N Engl J Med. 2012;367(15):1438-1448. doi:10.1056/NEJMcp1111259.

Tetanus Prophylaxis

An Algorithm for Tetanus Prophylaxis in Adults1

Algorithm for Tetanus Prophylaxis in Adults

References:

  1. Diphtheria, tetanus, and pertussis: recommendations for vaccine use and other preventive measures. Recommendations of the Immunization Practices Advisory committee (ACIP). MMWR Recomm Rep. 1991;40(RR-10):1-28.

ECG Guide: Pediatrics

ECG Standard

  • Full standard: no adjustment
  • Half-standard: commensurate reduction in amplitude (usually 50%)
  • Mixed: reduction in amplitude of precordial leads

Atrial Abnormalities

Right Atrial Abnormality (P pulmonale)
Peaked P-wave in II (>3mm from 0-6mo or >2.5mm >6mo)
Causes: right atrial volume overload, ASD, Ebstein, Fontan
Left Atrial Abnormality (P mitrale)
Wide, notched P-wave in II or biphasic in V1
Causes: MS, MR

Axis

  • Anatomical dominance of right ventricle until approximately 6mo
  • RAD normal
  • eRAD suggests AV canal defect

T-waves

  • 1st week of life: Upright
  • Adolescent: Inverted
  • Adult: Upright

Ventricular Hypertrophy

Right Ventricular Hypertrophy
R-wave height >98% for age in lead V1
S-wave depth >98% for age in lead V6
T-wave abnormality (ex. upright in childhood)
Causes: pHTN, PS, ToF
Left Ventricular Hypertrophy
R-wave height >98% for age in lead V6
S-wave depth >98% for age in lead V1
Adult-pattern R-wave progression in newborn (no large R-waves and small S-waves in right precordial leads)
Left-axis deviation
Causes: AS, coarctation, VSD, PDA

Examples


Normal Neonatal ECG

  • 2mo old
  • RAD
  • Inverted T-waves (normal)
  • Tall R-waves in V1-V3


Extreme Axis Deviation

  • Neonate with Down syndrome
  • Isoelectric in I, Negative in aVF negative in II  mean QRS vector -87°
  • Extreme RAD suggestive of AV canal defect


LVH:

  • Unrepaired Coarctation
  • Deep S-wave in V1 (>98%)
  • Tall R-wave in V6 (>98%)


RVH:

  • 10 year-old boy with pulmonary Hypertension
  • RAD after expected age for normal RAD
  • Tall R-waves in V1 (>98%)
  • Deep S-wave in V6 (>98%)


STEMI

  • ALCAPA (anomalous origin of the left coronary artery from the pulmonary artery): coronary artery arises anomalously from the pulmonary artery; as pulmonary arterial pressure falls during the first 6 months of infancy, prograde flow through the left coronary artery ceases and may even reverse.
  • HLHS (hypoplastic left heart syndrome): coronary arteries are perfused from a hypoplastic, narrow aorta that is susceptible to flow disruption
  • Orthotopic heart transplant with allograft vasculopathy
  • Kawasaki: coronary artery aneurysm with subsequent thrombosis


Benign early repolarization

  • 14 year-old male
  • Concave ST-segment elevation


Left Atrial Abnormality:

  • 9mo female with mitral insufficiency
  • Broad biphasic P-wave in V1
  • Tall, notched P-wave in II


Prolonged QT interval

  • 18-year-old female
  • Familial long QT syndrome and a history of cardiac arrest


WPW:

  • Delta wave, shortened PR interval

References

  1. O’Connor M, McDaniel N, Brady WJ. The pediatric electrocardiogram. Part I: Age-related interpretation. Am J Emerg Med. 2008;26(2):221-228. doi:10.1016/j.ajem.2007.08.003.
  2. Goodacre S, McLeod K. ABC of clinical electrocardiography: Paediatric electrocardiography. BMJ. 2002;324(7350):1382-1385.
  3. O’Connor M, McDaniel N, Brady WJ. The pediatric electrocardiogram Part II: Dysrhythmias. Am J Emerg Med. 2008;26(3):348-358. doi:10.1016/j.ajem.2007.07.034.
  4. O’Connor M, McDaniel N, Brady WJ. The pediatric electrocardiogram Part III: Congenital heart disease and other cardiac syndromes. Am J Emerg Med. 2008;26(4):497-503. doi:10.1016/j.ajem.2007.08.004.
  5. Schwartz P. Guidelines for the interpretation of the neonatal electrocardiogram. Eur Heart J. 2002;23(17):1329-1344. doi:10.1053/euhj.2002.3274.

Ultrasound in Dyspnea

Brief H&P:

A 68 year-old male with a history of hypertension, diabetes, hyperlipidemia, chronic obstructive pulmonary disease and congestive heart failure (CHF) with depressed ejection fraction presents via ambulance with a chief complaint of shortness of breath. EMS reports that the patient was tachypneic and saturating 80% on ambient air on their arrival. En route, he received nebulized albuterol, nitroglycerin and was started on non-invasive positive pressure ventilation (NI-PPV).

On arrival, he remains uncomfortable-appearing with a respiratory rate of 35 breaths/min and accessory muscle use. His heart rate is 136bpm, blood pressure is 118/85mmHg, and he is saturating 95% on an FiO2 of 100%. Attempts to obtain a history are limited due to difficulty comprehending his responses with the PPV mask on, and prompt desaturation with it off. Lung auscultation is similarly challenging due to ambient and transmitted sounds, although basilar crackles and diffuse expiratory wheezing are appreciated. Cardiovascular examination reveals a rapid and irregularly irregular rhythm. Assessment of jugular venous distension is limited due to the patient’s body habitus and the presence of mask straps around the patient’s neck. Lower extremities demonstrate 2+ pitting edema, symmetric bilaterally. Intravenous access is established and laboratory tests are sent. The ECG technician and portable chest x-ray are called.

The case presentation above demonstrates a common emergency department scenario: a critically-ill patient with undifferentiated dyspnea. Specifically, the scenario reveals a situation where the physical examination is either obfuscated by technical challenges or otherwise indeterminate. The patient is at risk for deterioration and targeted intervention is mandatory. If a COPD exacerbation is assumed, additional nebulized breathing treatments are indicated – a potentially costly jolt of beta agonists if the patient’s atrial fibrillation and rapid ventricular response are the consequence of decompensated systolic heart failure. Take the route of decompensated CHF and prompt afterload reduction with diuresis would be next – if incorrect, not only would the primary cause go untreated, but his tenuously-maintained blood pressure may suffer.

Algorithm for the Use of Ultrasound in the Evaluation of Dyspnea

Algorithm for the Use of Ultrasound in the Evaluation of Dyspnea

1. Lung Ultrasound

An approach incorporating point-of-care ultrasonography may be useful. First, a thoracic ultrasound is performed where certain causative etiologies might be identified immediately – for example absent lung sliding suggesting pneumothorax, or signs of generalized or subpleural consolidation.

The POCUS Atlas
The ultrasound images and videos used in this post come from The POCUS Atlas, a collaborative collection focusing on rare, exotic and perfectly captured ultrasound images.
The POCUS Atlas

Pneumothorax

Hepatization

Shred Sign

Pleural Effusion

2. Cardiac Ultrasound

Other findings on lung ultrasound may point to causes that are not primarily pulmonary. For example, if diffuse B-lines are encountered a focused cardiac ultrasound can be performed to grossly evaluate ejection fraction and estimate right atrial pressure.

B-Lines

Depressed EF

Dilated IVC

3. Venous Ultrasound

Finally, if the lung ultrasound is largely unremarkable (A-lines), a sequence of ultrasonographic findings including right ventricular dilation and the presence of a deep venous thrombosis would point to pulmonary embolism as the diagnosis.

DVT

RV Dilation

All ultrasound graphics from the algorithm are available for free, licensed (along with all content on this site) under Creative Commons Attribution-ShareAlike 4.0 International Public License.

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References

  1. Lichtenstein DA, Mezière GA, Lagoueyte J-F, Biderman P, Goldstein I, Gepner A. A-lines and B-lines: lung ultrasound as a bedside tool for predicting pulmonary artery occlusion pressure in the critically ill. Chest. 2009;136(4):1014-1020. doi:10.1378/chest.09-0001.
  2. Copetti R, Soldati G, Copetti P. Chest sonography: a useful tool to differentiate acute cardiogenic pulmonary edema from acute respiratory distress syndrome. Cardiovasc Ultrasound. 2008;6(1):16. doi:10.1186/1476-7120-6-16.
  3. Gallard E, Redonnet J-P, Bourcier J-E, et al. Diagnostic performance of cardiopulmonary ultrasound performed by the emergency physician in the management of acute dyspnea. Am J Emerg Med. 2015;33(3):352-358. doi:10.1016/j.ajem.2014.12.003.
  4. Lichtenstein DA. Lung ultrasound in the critically ill. Ann Intensive Care. 2014;4(1):1. doi:10.1186/2110-5820-4-1.
  5. Zanobetti M, Scorpiniti M, Gigli C, et al. Point-of-Care Ultrasonography for Evaluation of Acute Dyspnea in the ED. Chest. 2017;151(6):1295-1301. doi:10.1016/j.chest.2017.02.003.
  6. Lichtenstein DA, Mezière GA. Relevance of lung ultrasound in the diagnosis of acute respiratory failure: the BLUE protocol. Chest. 2008;134(1):117-125. doi:10.1378/chest.07-2800.
  7. Images from The POCUS Atlas
  8. Special thanks to Dr. Timothy Jang, Director Emergency Ultrasound Program, Director Emergency Ultrasound Fellowship, Associate Professor of Clinical Emergency Medicine, Department of Emergency Medicine at Harbor-UCLA

Technique for Video Laryngoscopy

Overview

Laryngoscopy had until recently remained relatively unchanged since the introduction of the Macintosh and Miller blades in the 1940’s. Advancements in fiberoptic technology have led to the development of multiple novel devices obviating line-of-sight requirements for direct laryngoscopy which may aid with endotracheal intubation in some populations. While there is no evidence to suggest that video laryngoscopy improves patient-centered outcomes, familiarity with the technique of video laryngoscopy is a critical educational objective for trainees who should be comfortable in the use of this and other rescue airway management adjuncts.

The image above shows a comparison of the curvature of straight (Miller), curved (Macintosh) and hyperangulated blades relative to the oral, pharyngeal and laryngeal axes. The hyperangulated blade easily positions a fiberoptic camera over the glottic opening, allowing easy visualization of the vocal cords. Passing the endotracheal tube without direct line-of-sight becomes the challenge of intubation.

The purpose of this guide is to explore the differences in technique for performing video laryngoscopy compared to direct laryngoscopy. Specifically, the guide is focused on video laryngoscopes with hyper-angulated blades (Verathon Glidescope, Storz C-MAC D-Blade) as these devices pose more challenges for appropriate use while potentially offering the greatest advantages for glottic visualization in challenging airway management.


Advantages and Disadvantages

Advantages1

  • Improved glottic visualization especially in scenarios with limited neck mobility as there is no need to align the oral-pharyngeal-laryngeal axes.
  • Allows others to view the screen and facilitate endotracheal intubation.

Disadvantages1

  • Difficulty passing endotracheal tube despite improved glottic visualization.
  • Obscured view by fogging or contaminated airway (blood, secretions, vomit).
  • Possibility for deterioration of skills in direct laryngoscopy.

Technique

Blade Insertion

Because of it’s unique shape, special care should be taken when inserting a hyperangulated blade to avoid dental/oropharyngeal injury. The handle of the blade may need to be angled towards the patient’s chest and turned slightly to facilitate atraumatic insertion.

Blade Advancement

Transition to viewing the screen once the tip of the blade is past the visualized posterior portion of the tongue. Advance the blade along the base of the tongue while monitoring the view on screen. Identify the epiglottis and guide the tip of the blade into the vallecula, the objective is to center the glottic aperture in the upper 2/3 of the screen.

Optimal View

The optimal view shows the vocal cords centered in the upper 2/3 of the screen. This provides adequate screen “real estate” to show the endotracheal tube entering the screen and provide more visual feedback as the tube position is manipulated.

Blade Adjustment

The shape of the hyperangulated blade means that visualizing the airway is less dependent on the lifting motion applied with direct laryngoscopy. Instead, angulating the tip of the blade upward by gently rocking the handle back (taking great care to avoid dental/oropharyngeal trauma) will dramatically improve the view.

Endotracheal Tube Insertion

Directly visualize the insertion of the endotracheal tube into the oral cavity. The endotracheal tube should be loaded with an appropriately angulated rigid stylet. Follow the curvature of the laryngoscope blade entering from the right corner of the mouth. When the endotracheal tube is passed along the edge of the laryngoscope blade, few adjustments will be required for successful endotracheal intubation.

Endotracheal Tube Position Adjustments

If the view is optimized but the endotracheal tube is off-center and does not directly pass the vocal cords into the trachea, subtle adjustments to the endotracheal tube can help guide it into position. Hold the endotracheal tube like a pencil, turning it slightly clockwise or counter-clockwise between your index finger and thumb to manipulate the distal tip left or right above the laryngeal opening.

Stylet Removal

Once past the vocal cords, the hyperangulated rigid stylet will limit continued passage of the endotracheal tube into the trachea as it will get stuck on the anterior surface of the trachea. To facilitate easy passage into the trachea, the stylet should be pulled back slightly to allow passage into the trachea before being fully removed and the tube secured in position.


Review of Evidence

Emergency Department:

  • C-MAC associated with higher rate of successful intubation and greater proportion of grade I-II Cormack-Lehane views compared to direct laryngoscopy.5
  • Glidescope associated with higher rate of successful intubation (and fewer esophageal complications) compared to direct laryngoscopy. 6
  • Glidescope associated with higher rate of successful intubation compared to direct laryngoscopy. 7

Adjustments to Challenging Tube Placement:

  • Combination of flexible-tipped endotracheal tube with rigid stylet (Verathon GlideRight stylet) may increase intubation success.8
  • No apparent benefit to “reverse camber” loading of stylet into endotracheal tube. Reverse camber loading references placing the angled stylet 180° opposite to the natural curvature of the endotracheal tube.9
  • If a malleable stylet is used, 90° angulation was associated with higher rates of successful intubation. 10

Recent Data:

  • Propensity score-matched analysis of multicenter emergency department airway registry – no significant difference in rates of successful intubation comparing Glidescope to direct laryngoscopy. 11
  • Randomized trial comparing direct and video laryngoscopy using C-MAC showed no difference in rates of successful intubation, duration of intubation attempt, aspiration events or length of hospitalization. For interventions randomized to direct laryngoscopy, the video laryngoscope screen was covered. 12

Meta-Analyses:

  • Meta-analysis (predominantly for intubations in the operating room) suggests video laryngoscopy associated with fewer failed intubations, particularly among patients with anticipated difficult airway. Insufficient evidence to analyze effects on incidence of hypoxia, respiratory complications, time to intubation, or mortality.13

References

  1. Maldini B, Hodžović I, Goranović T, Mesarić J. CHALLENGES IN THE USE OF VIDEO LARYNGOSCOPES. Acta Clin Croat. 2016;55 Suppl 1:41-50. doi:10.20471/acc.2016.55.s1.05.
  2. Levitan RM, Heitz JW, Sweeney M, Cooper RM. The complexities of tracheal intubation with direct laryngoscopy and alternative intubation devices. Ann Emerg Med. 2011;57(3):240-247. doi:10.1016/j.annemergmed.2010.05.035.
  3. Hurford WE. The video revolution: a new view of laryngoscopy. Respir Care. 2010;55(8):1036-1045.
  4. Cheyne DR, Doyle P. Advances in laryngoscopy: rigid indirect laryngoscopy. F1000 Med Rep. 2010;2:61. doi:10.3410/M2-61.
  5. Sakles JC, Mosier J, Chiu S, Cosentino M, Kalin L. A Comparison of the C-MAC Video Laryngoscope to the Macintosh Direct Laryngoscope for Intubation in the Emergency Department. Ann Emerg Med. 2012;60(6):739-748. doi:10.1016/j.annemergmed.2012.03.031.
  6. Sakles JC, Mosier JM, Chiu S, Keim SM. Tracheal Intubation in the Emergency Department: A Comparison of GlideScope® Video Laryngoscopy to Direct Laryngoscopy in 822 Intubations. J Emerg Med. 2012;42(4):400-405. doi:10.1016/j.jemermed.2011.05.019.
  7. MD JMM, MPH USP, BA SC, MD JCS. Difficult Airway Management in the Emergency Department: GlideScope Videolaryngoscopy Compared to Direct Laryngoscopy. J Emerg Med. 2012;42(6):629-634. doi:10.1016/j.jemermed.2011.06.007.
  8. Radesic BP, Winkelman C, Einsporn R, Kless J. Ease of intubation with the Parker Flex-Tip or a standard Mallinckrodt endotracheal tube using a video laryngoscope (GlideScope). AANA J. 2012;80(5):363-372.
  9. Jones PM, Turkstra TP, Armstrong KP, et al. Effect of stylet angulation and endotracheal tube camber on time to intubation with the GlideScope. Can J Anesth/J Can Anesth. 2007;54(1):21-27.
  10. Turkstra TP, Harle CC, Armstrong KP, et al. The GlideScope-specific rigid stylet and standard malleable stylet are equally effective for GlideScope use. Can J Anesth/J Can Anesth. 2007;54(11):891-896.
  11. Choi HJ, Kim Y-M, Oh YM, et al. GlideScope video laryngoscopy versus direct laryngoscopy in the emergency department: a propensity score-matched analysis. BMJ Open. 2015;5(5):e007884-e007884. doi:10.1136/bmjopen-2015-007884.
  12. Driver BE, Prekker ME, Moore JC, Schick AL, Reardon RF, Miner JR. Direct Versus Video Laryngoscopy Using the C-MAC for Tracheal Intubation in the Emergency Department, a Randomized Controlled Trial. Acad Emerg Med. 2016;23(4):433-439. doi:10.1111/acem.12933.
  13. Lewis SR, Butler AR, Parker J, Cook TM, Smith AF. Videolaryngoscopy versus direct laryngoscopy for adult patients requiring tracheal intubation. Cochrane Database Syst Rev. 2016;11:CD011136. doi:10.1002/14651858.CD011136.pub2.

ECG Guide: Part II

STEMI

STEMI

  • ST-segment elevation ≥ 1mm in two contiguous leads
  • : ≥ 2mm V2-V3
  • : ≥ 1.5mm V2-V3

Posterior STEMI

  • ST-segment depression V1-V3 Posterior ECG
  • ST-segment elevation ≥ 0.5mm in V7-V9

Sgarbossa Criteria

  • Evaluation for STEMI in LBBB or paced rhythm
  • Normal: ST-segment discordant with QRS

    • QRS associated with ST-segment depression
    • QRS associated with (commensurate) ST-segment elevation
  • Score ≥ 3 98% specific for MI

Elevation

  • Concordant ST-segment elevation ≥ 1mm in any lead (5 points)

Depression

  • Concordant ST-segment depression ≥ 1mm in V1-V3 (3 points)

Discordant Elevation

  • Discordant ST-segment elevation ≥ 5mm in any lead (2 points)

Modified Sgarbossa Criteria

  • ST:S ratio ≥ 0.25 in any lead
  • Presence of any criterion is positive

Other Causes of ST-segment Elevation

Benign Early Repolarization

  • Concave ST-segment elevation
  • Notch at J-point
  • Asymmetric T-waves (steeper descent)

Pericarditis

  • Diffuse ST-segment elevation (except aVR)
  • PR-segment depression
  • Ratio: ST-elevation to T-wave amplitude ≥ 0.25 in V6 suggests pericarditis

LVH Strain

  • ST-segment elevation in V1-V3 in the setting of LVH

LV Aneurysm

  • Q-waves with ST-segment elevation in precordial leads

Ischemia and Prior Infarcts

Wellens: Type A

Wellens: Type B

Q-waves

  • ≥ 40ms duration
  • Depth ≥ 25% of R-wave height

Syncope

ARVD

  • Epsilon wave

Brugada Syndrome: Type 1

  • Type 1: Coved ST-segment elevation

Brugada Syndrome: Type 2

  • Type 2: Saddle-back ST-segment elevation

HCM

  • Deep, narrow Q-waves

Wolff-Parkinson-White

  • Shortened PR-interval
  • Delta-wave

Other

Atrial Abnormalities

  1. Normal
  2. RAA: P-wave amplitude > 2.5mm in inferior leads
  3. LAA: P-wave duration increased (terminal negative portion >0.04s), amplitude of terminal negative component >1mm below isoelectric line in V1

Left Bundle Branch Block


  • QRS duration > 0.12s (3 boxes)
  • Broad or notched R-wave with prolonged upstroke in I, aVL, V5, V6
  • Associated ST-segment depression and T-wave inversion
  • Reciprocal changes in V1, V2 (deep S-wave)
  • Possible LAD

Right Bundle Branch Block


  • QRS duration > 0.12s (3 boxes)
  • RSR’ in V1, V2
  • Reciprocal changes in I, aVL, V5, V6 (deep S-wave)

Axes

All ECG tracings are available for free, licensed (along with all content on this site) under Creative Commons Attribution-ShareAlike 4.0 International Public License.

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CT Interpretation: Head

The emergency physician should be adept at the interpretation of computed tomography of the head, particularly for life-threatening processes where awaiting a radiologist interpretation may unnecessarily delay care.

As with the approach detailed previously for imaging of the abdomen and pelvis, a similar structured method for interpretation of head imaging exists and follows the mnemonic “Blood Can Be Very Bad”.

Normal Neuroanatomy

Brainstem
Posterior Fossa
High Pons
Cisterns
Ventricles

Blood: Blood

Density
Acute: hyperdense (50-100HU)
1-2wks: isodense with brain
2-3wks: hypodense with brain

Types/Locations

Intraparenchymal Hemorrhage/Contusions
Sudden deceleration of the head causes the brain to impact on bony prominences (e.g., temporal, frontal, occipital poles).
Non-traumatic hemorrhagic lesions seen more frequently in elderly and located in basal ganglia.
Intraventricular Hemorrhage
White density in otherwise black ventricular spaces, can lead to obstructive hydrocephalus and elevated ICP.
Associated with worse prognosis in trauma.
Subarachnoid Hemorrhage
Hemorrhage into subarachnoid space usually filled with CSF (cistern, brain convexity).
Extracranial Hemorrhage
Presence of significant extracranial blood or soft-tissue swelling should point examiner to evaluation of underlying brain parenchyma, opposing brain parenchyma (for contrecoup injuries) and underlying bone for identification of fractures.

Can: Cisterns


Evaluating the cisterns is important for the identification of increased intracranial pressures (assessed by effacement of spaces) and presence of subarachnoid blood.

  • Circummesencephalic: CSF ring around midbrain and most sensitive marker for elevated ICP
  • Suprasellar: Star-shaped space above the sella
  • Quadrigeminal: W-shaped space at the top of the midbrain
  • Sylvian: Bilateral space between temporal/frontal lobes

Be: Brain

Evaluate the brain parenchyma, including an assessment of symmetry of the gyri/sulci pattern, midline shift, and a clear gray-white differentiation.

Very: Ventricles

Evaluate the ventricles for dilation or compression. Compare the ventricle size to the size of cisterns, large ventricles with normal/compressed cisterns and sulcal spaces suggests obstruction.

Bad: Bone

Switch to bone windows to evaluate for fracture. The identification of small, linear, non-depressed skull fractures may be difficult to identify as they are often confused with sutures – surrogates include pneumocephalus, and abnormal aeration of mastoid air cells and sinuses. The Presence of fractures increases the suspicion for intracranial injury, search adjacent and opposing parenchyma and extra-axial spaces.

Example #1

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CT Head Interpretation

  • Ill-defined lesion in right parietal white matter with a large amount of surrounding vasogenic edema with midline shift and right uncal herniation.
  • Acute on subacute right extra-axial subdural hematoma.
  • Effacement of basilar cisterns.

Example #2

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CT Head Interpretation

  • Bilateral subacute subdural hematomas, left larger than right and associated with rightward midline shift.
  • Left lateral ventricle is partially effaced.

Example #3

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CT Head Interpretation

Subdural hematoma with significant herniation

References

  1. Perron A. How to read a head CT scan. Emergency Medicine. 2008.
  2. Arhami Dolatabadi A, Baratloo A, Rouhipour A, et al. Interpretation of Computed Tomography of the Head: Emergency Physicians versus Radiologists. Trauma Mon. 2013;18(2):86–89. doi:10.5812/traumamon.12023.

Sickle Cell Crises

Brief H&P

A 27 year-old male with sickle cell disease (HbSC) on hydroxurea and with a history of 2-3 hospitalizations per year for vaso-occlusive pain crises manifested by arthralgias and back pain presents to the emergency department with 3 days of worsening joint pain affecting his entire body but predominantly his knees and lower back. He is familiar with this pain and attempted therapy at home with ibuprofen, then hydrocodone-acetaminophen, and finally hydromorphone without improvement and presented to the emergency department.

On review of systems, he denied chest pain, cough, or shortness of breath. He has some periumbilical abdominal pain but tolerated normal oral intake on the day of presentation without vomiting nor changes in bowel habits. He otherwise denied fevers, peripheral numbness/weakness, urinary or fecal incontinence or retention. He similarly denies trauma, weight loss, night sweats, or intravenous drug use.

Objectively, the patient’s vital signs were normal and he was well-appearing. Mucous membranes were moist and skin turgor was normal. There were no appreciable joint effusions, warmth, nor limitation to active/passive range of motion of any joints. His back had no midline tenderness to palpation or percussion, normal range of motion in all axes and extremity sensation and strength testing were normal. Abdominal and genitourinary examinations were normal. The patient had preserved perineal sensation to light touch and normal rectal tone – a core temperature was obtained which was also normal.

Peripheral access was established and a parenteral dose of hydromorphone equivalent to his home oral dose was administered (0.015mg/kg). Repeat dosing was required at 15 minutes due to persistent pain scale of 10. Diphenhydramine and acetaminophen were also administered, for potential opioid-sparing effects, recognizing the limited evidence to support these relatively benign adjuncts.

Laboratory studies were notable for anemia (though stable compared to baseline measures), appropriate reticulocyte count, no evidence of hemolysis and with normal electrolytes and renal function.

A thorough history and examination did not identify a critical precipitant for the patient’s symptoms which were presumed to be secondary to a vaso-occlusive pain crisis. On reassessment, the patient’s pain was improved and an oral dose of hydromorphone was administered with continued observation and serial reassessments for two hours thereafter. The patient’s hematologist was available for follow-up the subsequent morning and the patient was discharged home.

Pharmacokinetics of Commonly-Used Opiate Analgesics1-3

Medication Route Onset Peak Duration
Morphine IV 5-10min 20min 3-5h
IM 15-30min 30-60min
PO 30min 1h
Oxycodone PO 10-15min 30-60min 3-6h
Hydrocodone PO 10-20min 4-8h
Fentanyl IV <1min 2-5min 30-60min
Hydromorphone IV 5min 10-20min 3-4h
PO 15-30min 30-60min
Codeine PO 30-60min 60-90min 4-6h

Spectrum of Sickle Cell Trait and Disease4

Algorithm for the Evaluation and Management of Sickle Cell Crises4-10

Algorithm for the Management of Sickle Cell Crises

References:

  1. Lexicomp Online®, Adult Drug Information, Hudson, Ohio: Lexi-Comp, Inc.; November 4, 2017.
  2. Trescot AM, Datta S, Lee M, Hansen H. Opioid pharmacology. Pain Physician. 2008;11(2 Suppl):S133-S153.
  3. Vieweg WVR, Lipps WFC, Fernandez A. Opioids and methadone equivalents for clinicians. Prim Care Companion J Clin Psychiatry. 2005;7(3):86-88.
  4. Glassberg J. Evidence-based management of sickle cell disease in the emergency department. Emergency Medicine Practice. 2011;13(8):1–20–quiz20.
  5. Raam R, Mallemat H, Jhun P, Herbert M. Sickle Cell Crisis and You: A How-to Guide. Ann Emerg Med. 2016;67(6):787-790. doi:10.1016/j.annemergmed.2016.04.016.
  6. Piel FB, Steinberg MH, Rees DC. Sickle Cell Disease. N Engl J Med. 2017;376(16):1561-1573. doi:10.1056/NEJMra1510865.
  7. Lovett PB, Sule HP, Lopez BL. Sickle cell disease in the emergency department. Emerg Med Clin North Am. 2014;32(3):629-647. doi:10.1016/j.emc.2014.04.011.
  8. Yawn BP, John-Sowah J. Management of Sickle Cell Disease: Recommendations From the 2014 Expert Panel Report. Vol 92. 2015:1069-1076.
  9. Zempsky WT. Evaluation and Treatment of Sickle Cell Pain in the Emergency Department: Paths to a Better Future. Clinical Pediatric Emergency Medicine. 2010;11(4):265-273. doi:10.1016/j.cpem.2010.09.002.
  10. Aliyu ZY, Tumblin AR, Kato GJ. Current therapy of sickle cell disease. Haematologica. 2006;91(1):7-10.

CT Interpretation: Abdomen/Pelvis

As with the systematic approach preferred for the evaluation and management of other processes explored on this site, a similarly structured method for the interpretation of imaging commonly obtained in the emergency department may afford the same benefits – namely, the timely identification of pathology while avoiding costly missed diagnoses. In this post, I propose an approach to the interpretation of computed tomography of the abdomen and pelvis.

Aorta Down

Thoracic Aorta

Thoracic Aorta

Start with the descending thoracic aorta

Abdominal Aorta

Abdominal Aorta

Follow the abdominal aorta down including its branches (celiac, SMA, paired renal arteries, IMA)

Aortic Bifurcation

Aortic Bifurcation

Continue to the bifurcation of the abdominal aorta to the left and right common iliac arteries

Veins Up

Femoral Veins

Femoral Veins

Start with the left and right femoral veins

Inferior Vena Cava

Inferior Vena Cava

Follow the inferior vena cava up

Infrahepatic IVC

Infrahepatic IVC

The inferior vena cava gains contrast from the renal veins

Right Atrium

Right Atrium

The inferior vena cava empties into the right atrium

Solid Organs Down

Heart and Pericardium

Heart and Pericardium

Evaluate for the presence of a pericardial effusion or cardiomegaly

Spleen

Spleen

Heterogenous contrast-enhancement is normal

Pancreas

Pancreas

The tail of the pancreas lies in the hilum of the spleen

Liver

Liver

Evaluate the intrahepatic bile ducts for dilation or pneumobilia, portal venous system for gas, and liver parenchyma for vascular abnormalities or abscesses

Gallbladder

Gallbladder

Evaluate for radioopaque stones, pericholecystic fluid or surrounding fat stranding

Adrenal

Adrenal

A wishbone-shaped structure superior to the kidneys

Kidney and Ureter

Kidney and Ureter

Evaluate for hydronephrosis or hydroureter

Bladder

Bladder

Continue down into the pelvis; in a female patient the evaluation should include the uterus and adnexa

Rectum Up

Rectum

Rectum

Having reached the inferior-most portion of the image following solid organs, move upward again from the rectum

Sigmoid

Sigmoid

Evaluate the sigmoid colon for diverticulitis

Transverse

Transverse

Continue following the sigmoid colon up the descending colon to the transverse colon and the hepatic flexure

Cecum

Cecum

Continue down the ascending colon to the cecum

Appendix

Appendix

At the cecum, attempt to identify a small tubular structure (the appendix) - evaluate for periappendiceal fat stranding, perforation or abscess

Esophagus Down

Esophagus

Esophagus

Start at the esophagus, evaluate for perforation or hernia

Stomach

Stomach

Continue to the stomach and duodenum

Small Bowel

Small Bowel

Evaluate the small bowel for obstruction (dilation, air-fluid levels)

Tissue-specific Windows

Lung Window

Lung Window

Switch to lung window to evaluate the lung parenchyma and continue through the abdomen to identify intraperitoneal free air

Bone Window

Bone Window

Use the bone window to identify fractures or lytic lesions

Try It Yourself

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CT Abdomen/Pelvis Interpretation

  • Cystic lesion in the inferior right lobe of the liver most consistent with hepatic abscess.
  • Multiple calcified gallstones in the gallbladder.

Pneumobilia: Hepatic Gas Applied

Brief HPI

A 45 year-old female with a history of pre-diabetes and gastroesophageal reflux disease presents with 3 days of epigastric abdominal pain. She describes constant, burning abdominal pain which worsened on the day of presentation associated with two episodes of non-bloody and non-bilious emesis. The patient was tender to palpation in the epigastrium and right upper quadrant.

Right upper quadrant ultrasound

Laboratory studies were largely normal. A complete blood count demonstrated minimal leukocytosis (11.6 with normal differential), and liver function tests were normal.

A right-upper quadrant ultrasound was obtained which demonstrated “strongly shadowing structures in the gallbladder fossa which might represent a wall-echo-shadow, calcified gallbladder wall, or air within the gallbladder”.

The patient underwent contrast-enhanced computed tomography of the abdomen and pelvis which is shown below.

Imaging

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CT Abdomen/Pelvis with Contrast

Pneumobilia, intra- and extra-hepatic biliary duct dilation, pericholecystic fat stranding, and an air-fluid level within a contracted gallbladder. Mildly dilated loops of ileal bowel with a possible transition point in the right lower quadrant. Findings suggestive of possible gallstone ileus.

The patient was taken to the operating room for exploratory laparotomy, possible cholecystectomy and possible small bowel resection for presumed gallstone ileus. Intra-operative findings were notable for a cholecystogastric fistula which was repaired.

Differentiation between Portal Venous Gas and Pneumobilia

The patient’s CT demonstrated mostly central hepatic gas. This finding combined with the presence of an air-fluid level in the gallbladder was most consistent with pneumobilia. This case demonstrates an application of the previously-developed algorithm for the evaluation of hepatic gas in a relatively unique pathologic process.
Hepatic Gas: Pneumobilia  vs. Portal Venous Gas

Dermatologic Emergencies

Brief H&P

A 68 year-old male with hypertension and gout presents with rash for 2-3 weeks. He note some subjective fevers but is otherwise asymptomatic. He denies recent travel or sick contacts. When asked about his medications, he reports that his primary care provider started him on allopurinol approximately two months ago.

He first noted the rash on his face, characterizing it as “pimples” which were slightly pruritic. The lesions subsequently spread to his trunk and extremities and have been growing in size.

Objectively, vital signs were notable for fever (38.2°C) and tachycardia (108bpm). Examination demonstrated diffuse blanching erythema most prominent on the trunk and extremities. The remainder of the physical examination was normal. Laboratory studies were obtained and notable for a complete blood count (CBC) with peripheral eosinophilia, as well as mildly elevated serum transaminases.

The patient was diagnosed with Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS), likely owing to the initiation of a xanthine oxidase inhibitor. He improved after withdrawal of the drug and a brief course of systemic corticosteroids.


Principles of Dermatologic Emergencies

Critical dermatologic processes can be broadly divided into two categories:

1. Cutaneous manifestation of critical illness

The presence of a dermatologic abnormality does not itself represent a life-threat. Instead, the skin lesion is a signal suggestive of the presence of an underlying critical process. The prototypical example would be the petechiae/purpura in meningococcemia.

2. Acute Skin Failure

As with any other organ system failure, Acute Skin Failure carries significant morbidity and mortality and is characterized by derangements in normal skin function.

Critical functions of skin
Temperature regulation
Protection against excess fluid loss
Mechanical barrier to prevent penetration of foreign materials
Important pathophysiologic changes in ASF
Increased peripheral vasodilation (dramatic increase in cardiac output to low-resistance circuits) and increased vascular permeability resulting in relative hypovolemia and shock.
Increased blood flow and dysfunction of eccrine sweat glands results in altered temperature regulation (usually hypothermia)
Fluid imbalances occur, similar to burns (transepidermal water loss) which varies in quality somewhat between “dry” (erythroderma) and “wet” (vesiculobullous) diseases
Electrolytes: increased basal metabolic rate, hyperglycemia (insulin resistance), hypophosphatemia, protein depletion
Barrier dysfunction: increased risk of infection
Management
Intensive Care Unit: Dermatologic (DICU) or Burn Center preferred
Treatment: Temperature management, early enteral nutrition, fluid/electrolyte management, local wound care, disease-specific management
Complications: Sepsis/shock, ARDS, high-output CHF, known complications of critical illness (multi-organ failure, GI ulcers, VTE)
Long-term complications: occular (ectropion, keratitis, ulcer), esophageal (stricture), GU (urethral stricture, phimosis, vaginal stenosis), Integumentary (scarring, alopecia)

Skin Lesions and their Pathophysiology

The objective of this algorithm is to develop a systematic approach to the evaluation of dermatologic processes with a focus on the identification of dermatologic emergencies. The foundation of this approach is an understanding of the underlying pathophysiologic mechanisms for each of four broad categories of dermatologic processes which guide the resultant differential diagnosis.

Erythroderma

Pathophysiology
Extensive cutaneous capillary dilation, results in widespread exfoliation of the epidermis
Inflammatory mediators result in dramatic increase of epidermal turnover rate, accelerated mitotic rate, increased number of germinative skin cells.
Causes
Exfoliative toxin
Eosinophils
Basophils/Histamine
Skin-homing T-cells

View Erythroderma Algorithm

Petechiae/Purpura

Pathophysiology
Represent the passage of erythrocytes from the intravascular to extravascular compartment
May be the result of disruption of vascular integrity (trauma, infection, vasculitis) or disorders of primary or secondary hemostasis
Palpable
If lesions are palpable, this may suggest a more prominent underlying inflammatory process such as vasculiitis.
When cutaneous manifestations are identified, other small vessels may be affected (commonly renal and pulmonary

View Petechiae/Purpura Algorithm

Fluid-filled

Pustule
Pustules more commonly suggest an infectious process (bacterial, fungal)
Vesiculobullous
Vesiculobullous lesions are generally more concerning
Loss of basic structural elements maintaining cohesion between keratinocytes in the epidermis, or between the epidermal layer and the dermis (near basement membrane zone).
Intraepidermal blisters tend to be flaccid, fragile and thin-roofed.
Subepidermal blisters have a thick roof and can remain intact when compressed
Often due to autoantibodies targeting structural proteins in the skin.

View Fluid-filled Algorithm

Maculopapular

Pathophysiology
Catch-all term with a wide range of potential pathophysiologic mechanisms and causative etiologies.
Any process that results in erythroderma, petechiae, or fluid-filled lesions may start as a macule or papule.
Pathophysiology is of little guidance in this category where we must instead rely on the patient’s history and identification of red-flags to exclude dermatologic emergencies.
High-risk Features (Identified by dermatologists to stratify urgency of inpatient consultations):
Ill-appearing, vital sign instability
New-onset fever with rash
Mucocutaneous or ocular lesions
Recent introduction of anti-convulsant or sulfa-drug
Skin pain
Immunocompromised

View Maculopapular Algorithm

Algorithm for the Evaluation of Dermatologic Processes

Algorithm for the Evaluation of Dermatologic Processes
An algorithm for the evaluation of dermatologic processes was developed initially by Lynch in 1984. Since then, several modified Lynch algorithms have emerged. The concept of an algorithmic approach to dermatologic diagnosis was further expanded with the development of VisualDx, a decision-support application. There is evidence to suggest that the use of algorithms and decision support tools like VisualDx (and by extension this algorithm) may aid with the development of more thorough differential diagnoses and improve diagnostic accuracy.


References

Reviews

  1. Wolf R, Parish LC, Parish JL. Emergency Dermatology, Second Edition. August 2017:1-369.
  2. Usatine RP, Sandy N. Dermatologic emergencies. Am Fam Physician. 2010;82(7):773-780.
  3. Shilpi Khetarpal MD, Anthony Fernandez MP. Dermatological Emergencies. Cleveland Clinic. http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/dermatology/dermatological-emergencies/. Published August 2014. Accessed August 5, 2017.
  4. McQueen A, Martin SA, Lio PA. Derm emergencies: detecting early signs of trouble. J Fam Pract. 2012;61(2):71-78.
  5. Browne BJ, Edwards B, Rogers RL. Dermatologic emergencies. Prim Care. 2006;33(3):685–95–vi. doi:10.1016/j.pop.2006.06.002.
  6. Drage LA. Life-threatening rashes: dermatologic signs of four infectious diseases. Mayo Clinic Proceedings. 1999;74(1):68-72. doi:10.4065/74.1.68.
  7. Baibergenova A, Shear NH. Skin conditions that bring patients to emergency departments. Arch Dermatol. 2011;147(1):118-120. doi:10.1001/archdermatol.2010.246.

Erythroderma

  1. Tan TL, Chung WM. A case series of dermatological emergencies – Erythroderma. Med J Malaysia. 2017;72(2):141-143.
  2. Karakayli G, Beckham G, Orengo I, Rosen T. Exfoliative dermatitis. Am Fam Physician. 1999;59(3):625-630.

Petechiae/Purpura

  1. Stevens GL, Adelman HM, Wallach PM. Palpable purpura: an algorithmic approach. Am Fam Physician. 1995;52(5):1355-1362.

Algorithms

  1. Lynch PJ, Edminster SC. Dermatology for the nondermatologist: a problem-oriented system. YMEM. 1984;13(8):603-606.
  2. Nguyen T, Freedman J. Dermatologic Emergencies: Diagnosing And Managing Life-Threatening Rashes. Emergency Medicine Practice. 2002;4(9):1-28.
  3. Murphy-Lavoie H, LeGros TL. Emergent Diagnosis of the Unknown Rash: an Algorithmic Approach-Rash Is Among the Top 20 Reasons for ED Visits in the United States. Certain Rashes …. Emergency Medicine; 2010.
  4. Dean S. Emergency Medicine Dermatology. 2017:1-20. doi:10.21980/J8DW21.
  5. Talley NJ, O’Connor S. Clinical Examination. Elsevier Health Sciences; 2013.
  6. Jack AR, Spence AA, Nichols BJ, Peng DH. A simple algorithm for evaluating dermatologic disease in critically ill patients: a study based on retrospective review of medical intensive care unit consults. J Am Acad Dermatol. 2009;61(4):728-730. doi:10.1016/j.jaad.2008.12.025.

DRESS

  1. McQueen A, Martin SA, Lio PA. Derm emergencies: detecting early signs of trouble. J Fam Pract. 2012;61(2):71-78.
  2. Cardoso CS, Vieira AM, Oliveira AP. DRESS syndrome: a case report and literature review. BMJ Case Rep. 2011;2011. doi:10.1136/bcr.02.2011.3898.

Evidence-Based Algorithms

  1. David CV, Chira S, Eells SJ, et al. Diagnostic accuracy in patients admitted to hospitals with cellulitis. Dermatol Online J. 2011;17(3):1.
  2. Chou W-Y, Tien P-T, Lin F-Y, Chiu P-C. Application of visually based, computerised diagnostic decision support system in dermatological medical education: a pilot study. Postgrad Med J. 2017;93(1099):256-259. doi:10.1136/postgradmedj-2016-134328.

Pediatric Foreign Body Ingestion

Brief H&P

XR Chest: Circular radioopaque foreign body likely in the antrum of the stomach.

A healthy 5 year-old boy is brought to the pediatric emergency department after he informed his parents that he accidentally swallowed a coin just prior to presentation. He has no complaints and on evaluation appears to be breathing comfortably and is tolerating secretions normally. A plain radiograph was obtained and is shown below.

The patient remained well-appearing and was discharged with primary care follow-up.


Indications for Emergent Endoscopy

  • Esophageal button battery
  • Severe symptoms
  • Sharp foreign body in esophagus
  • Multiple magnets in esophagus or stomach

Radiographic Findings


Esophageal foreign bodies typically orient coronally. For example, a coin will appear as a circle on an anteroposterior projection.

Tracheal foreign bodies typically orient sagitally. For example a coin will appear as a line on an anteroposterior projection.

Algorithm for the Evaluation and Management of Pediatric Foreign Body Aspiration

Algorithm for the Management of Pediatric Foreign Body Ingestion

References

  1. Sahn, B, et al. Foreign Body Ingestion Clinical Pathway. 1 Aug. 2016, www.chop.edu/clinical-pathway/foreign-body-ingestion-clinical-pathway. Accessed 26 Aug. 2017.
  2. Wyllie R. Foreign bodies in the gastrointestinal tract. Current Opinion in Pediatrics. 2006;18 N2 -(5).
  3. Uyemura MC. Foreign body ingestion in children. Am Fam Physician. 2005;72(2):287-291.
  4. Chung S, Forte V, Campisi P. A Review of Pediatric Foreign Body Ingestion and Management. Vol 11. 2010:225-230.
  5. Louie MC, Bradin S. Foreign Body Ingestion and Aspiration. Pediatrics in Review. 2009;30(8):295-301. doi:10.1542/pir.30-8-295.
  6. Green SS. Ingested and Aspirated Foreign Bodies. Pediatrics in Review. 2015;36(10):430-437. doi:10.1542/pir.36-10-430.

Penetrating Neck Trauma

Brief H&P

A young male presents to the emergency department after a self-inflicted stab wound to the neck. Examination revealed a knife handle protruding from the left lateral neck. A plain radiograph is shown below.

CXR: Radiopaque foreign body in left neck.

The patient was initially stable but developed shortness of breath upon attempting to lie flat for advanced imaging and was taken emergently to the operating room. Neck exploration showed no obvious neurovascular injuries, and the course of the 6cm blade was posterior to the trachea and esophagus. The knife was removed with “considerable force” as it was likely lodged within a portion of vertebral bone. The patient underwent esophagoscopy and bronchoscopy without identified tracheoesophageal injuries. The patient did well post-operatively and was discharged home.

Zones of Injury1-3

Previously, the evaluation and management of hemodynamically stable patients with penetrating neck injury was guided by the anatomic “zone” of injury. The affected zone guided the performance of additional diagnostic procedures including potentially morbid neck explorations.

Neck Zones of Injury

Understanding zone definitions remains important for the emergency physician to appreciate potentially implicated underlying structures. However, the advent of modern imaging modalities, specifically computed tomography with angiography, provides appropriate sensitivity for vascular and tracheoesophageal injuries when combined with detailed physical examination and maintenance of an appropriate threshold for the performance of additional studies if warranted by the clinical presentation (suboptimal imaging, concerning projectile trajectory, etc).

Zone Definition
I Clavicles/sternum to cricoid cartilage
II Cricoid cartilage to the angle of mandible
III Superior to the angle of mandible to the skull base

 

Algorithm for the Evaluation of Penetrating Neck Trauma

 

References

  1. Sperry JL, Moore EE, Coimbra R, et al. Western Trauma Association critical decisions in trauma: penetrating neck trauma. J Trauma Acute Care Surg. 2013;75(6):936-940. doi:10.1097/TA.0b013e31829e20e3.
  2. Brywczynski JJ, Barrett TW, Lyon JA, Cotton BA. Management of penetrating neck injury in the emergency department: a structured literature review. Emerg Med J. 2008;25(11):711-715. doi:10.1136/emj.2008.058792.
  3. Shiroff AM, Gale SC, Martin ND, et al. Penetrating neck trauma: a review of management strategies and discussion of the “No Zone” approach. Am Surg. 2013;79(1):23-29. doi:10.1007/978-3-662-49859-0_29.

 

Principles of Neonatal Resuscitation

The following resource for neonatal resuscitation and neonatal critical care was developed with the guidance of Dr. Agrawal (Neonatology) while on rotation at the White Memorial Medical Center Neonatal Intensive Care Unit.

Endotracheal Tube Size1-3

Simplified Formula
Estimated gestational age in weeks ÷ 10 = round to nearest half-size uncuffed tube

NRP Recommendation

Gestation age (weeks) Weight (kg) ETT Size (ID, mm) Depth (cm from lip)
<28 <1.0 2.5 6-7
28-34 1.0-2.0 3.0 7-8
34-38 2.0-3.0 3.5 8-9
>38 >3.0 3.5-4.0 9-10

Laryngoscope Blade Size

Age Blade
Preterm 0
Term 1

Umbilical Vein Catheter Placement4

ED Indications
Unstable neonate
Contraindications
Omphalocele
Gastroschisis
Necrotizing enterocolitis
Depth
4-5cm or until blood return (for emergent placement)

Umbilical artery/vein catheter position on plain radiograph.

Umbilical catheter size

Weight (kg) Size (F)
<1.5 3.5
1.5-3.5 5
>3.5 8

Umbilical catheter positioning on plain radiographs

Umbilical venous catheter position can be verified with a plain radiograph. Positioning within the umbilical vein can be confirmed by tracing a cephalad trajectory from the insertion point at the umbilicus. An umbilical artery catheter will first pass caudally into the internal iliac artery before travelling cephalad into a common iliac artery and the abdominal aorta.

Medications5

Medication Dose
Epinephrine 0.1mL/kg (1:10,000) IV, 0.01mg/kg
Volume Expansion 10mL/kg (normal saline, blood)
Naloxone 0.1-0.2mg/kg
Dopamine 5-20mcg/kg/min IV infusion

Neonatal Physiology and Transition to Extrauterine Life6

An important principle in neonatal resuscitation is supporting the appropriate transition from intra- to extra-uterine life which is dependent on several key anatomic and physiologic changes occurring in an optimal environment.

Anatomy7

Fetal Circulation
Neonatal Circulation

Fetal Circulation

In the fetal circulatory system, oxygenated blood is delivered via the umbilical vein, entering the inferior vena cava via the ductus venosus. The majority of this oxygenated blood passes through the right atrium and into the left atrium through the foramen ovale to enter the systemic circulation.

Meanwhile, high pulmonary pulmonary vascular resistance (due to hypoxic vasoconstriction in fluid-filled alveoli) means that most of the deoxygenated right ventricular output is routed through the ductus arteriosus and enters into the systemic circulation – mixing with oxygenated blood distal to the highest priority end-organs (brain and heart), to be reoxygenated at the placenta.

Post-transition Circulation

The transition to extra-uterine life involves several key steps detailed below and is supported by appropriate ventilation, oxygenation and temperature regulation.

  1. Alveolar Fluid Clearance
    Catecholamine and hormone changes (predominantly corticosteroids) during the process of labor induce changes in enzymatic expression that result in the resorption of alveolar fluid into the interstitial space. At the time of delivery, negative intra-thoracic pressure from inspiration further promotes the resorption of alveolar fluid. Mechanical thoracic compression from delivery may also contribute.
  2. Respiration and Breathing
    Disconnection from the placenta ceases the transfer of placenta-derived factors including prostaglandins. The withdrawal of tonic inhibition of central respiratory drive from prostaglandins with cord clamping stimulates rhythmic breathing. The infant’s initial breaths and resultant lung expansion promotes alveolar expansion and stimulates surfactant production – this decreases alveolar surface tension, increases lung compliance and further facilitates breathing.
  3. Circulatory Changes
    At delivery, clamping the umbilical cord removes a large bed of low-resistance circulation, increasing systemic vascular resistance and systemic blood pressure. At the same time, lung expansion and alveolar aeration decreases pulmonary vascular resistance and pulmonary arterial pressures. At the ductus arteriosus, increased systemic vascular resistance combined with decreased pulmonary vascular resistance decreases shunting and contributes to closure. Similarly, as left atrial pressure approaches and exceeds right atrial pressure, right-to-left flow across the foramen ovale ceases. Collectively, these changes serve to effectively separate the left- and right-sided circulations.

NRP Resuscitation Algorithm5,8

Neonatal Resuscitation Algorithm

References

  1. Luten R, Kahn N, Wears R, Kissoon N. Predicting Endotracheal Tube Size by Length in Newborns. J Emerg Med. 2007;32(4):343-347. doi:10.1016/j.jemermed.2007.02.035.
  2. Peterson J, Johnson N, Deakins K, Wilson-Costello D, Jelovsek JE, Chatburn R. Accuracy of the 7-8-9 Rule for endotracheal tube placement in the neonate. J Perinatol. 2006;26(6):333-336. doi:10.1038/sj.jp.7211503.
  3. Kempley ST, Moreiras JW, Petrone FL. Endotracheal tube length for neonatal intubation. Resuscitation. 2008;77(3):369-373. doi:10.1016/j.resuscitation.2008.02.002.
  4. Anderson J, Leonard D, Braner DAV, Lai S, Tegtmeyer K. Videos in Clinical Medicine. Umbilical Vascular Catheterization. Vol 359. 2008:e18. doi:10.1056/NEJMvcm0800666.
  5. Association AAOPAAH. Textbook of Neonatal Resuscitation. 2016.
  6. Caraciolo J Fernandes MD. Physiologic transition from intrauterine to extrauterine life. UpToDate.
  7. Sadler TW. Langman’s Medical Embryology. Lippincott Williams & Wilkins; 2011.
  8. Perlman JM, Wyllie J, Kattwinkel J, et al. Part 7: Neonatal Resuscitation: 2015 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations. In: Vol 132. American Heart Association, Inc.; 2015:S204-S241. doi:10.1161/CIR.0000000000000276.