Demystifying ED Consultations!!

One of the most crucial things that we do everyday at work is “asking for a consult/referral”. ED Consultations can be really difficult at times revolving around self-respect – diverse values – bonding - interests and interpersonal relationships. But “How to ask for a consult” is something that is rarely taught to EM residents, at least I was never taught this as a junior trainee in EM. Lets find out what’s the best way to get a consultation:

As Emergency Physicians deal with multiple other subspecialists, 24X7. It is our responsibility to take care of the sickest and simultaneously pass on the information and arrange for definitive care. To do this, we must have a thorough subject knowledge about General Emergency Medicine and also the competency to pass the information appropriately. There is not much of literature out there on this particular topic. Trainees screw up time and again; learning this skill gradually with their own goof ups gauging them as per the requirements of various consultants.

Whether this info is passed on to the specialty consultants/Attendings or Specialty Registrars/Residents depends on the institutional protocols. Here we are going to set some general rules that should probably work for everyone.

1)    Why/ When do you need a consult – Lead with a headline
You must have a succinct idea about this – Clarify the purpose and urgency of your consult. Do not start your medical school kind of presentation with a detailed history. They are too busy for that. Cut it short and come to the point ASAP, have your thoughts organized and the data that supports your thinking. Don’t ask for a consult just because the consultant is available; ask for it only if it is required.

2)    Gather your ingredients
Get all the data with you before you call them – history – old blood reports – meds – previous procedures - imaging etc. Another way of doing this is, by thinking, if you were in their shoes, then “what would you want”? When you do your rotations with them, understand their perspective to smoothen your consultations when you get back to the ED.

For instance - Few important specialty-specific questions that they love to know are:
(Note: This by no means is a complete list)

·      Neurosurgery: GCS, Na, Pupillary Response
·      Cardiology: ECG, Troponin, Previous Stress tests
·      Nephrology: Urine Output, K, Urea/Creat
·      OGYN: GPLA, LMP

And if you don't have an answer to something – never cook up a story or numbers – Be blunt and let them know that you DON’T KNOW.

3)    Negotiate
Whenever there is a difference of opinion, try to negotiate and settle down the differences. For instance, if the neuro consultant is too busy for a suspected epidural abscess and wants ED to get some sort of imaging first, ask him to send at least someone from neurology services (may be a resident/registrar) to evaluate the patient as you arrange for the imaging.

4)    Be Nice
Don't have a prejudice and avoid judging them if you have had a bad experience with them. Anyone will get upset if you call and tell them to come to the ED right away – This is human nature. Be nice and soft, but never compromise patient care.

All this can be summarized in the “5C” model of consultation:

5C Model

ü  Contact - Introduction of consulting and consultant physicians. Building of relationship.
ü  Communicate - Give a concise story (30-60seconds) and ask focused questions. DONT START MEDICAL SCHOOL CASE PRESENTATION – They don't have the time for that.
ü  Core Question - Have a specific questionor request of the consultant. Decide on reasonable timeframe for consultation. Come to the point ASAP.
ü  Collaboration - A result of the discussion between the emergency physician and the consultant, including any alteration of management – BARGAIN/ NEGOTIATE.
ü  Closing the Loop- Tell them what is the plan and whatever you understood

Document your conversation (better to record all telephonic conversations)

+ Don't forget the kindergarten basics

Ø  Greet & Introduce yourself
Ø  Confirm their name (Occasionally, some of them might get upset if you ask their name!)
Ø  Permission: Do you have a moment to discuss a case?
Ø  Be confident and pleasant
Ø  Listen to them and show respect for their opinion
Ø  Thank them
Ø  Also, practice a few times with your supervisor before you actually call them

Difficult Consults:
We all have seen nasty consultants who come to the ED and start throwing things around. 
Consultants are like "guests in your house". Treat them the way you treat your guests. This is going to turn things in your favour often getting them to do stuff you wanted to be done (procedure, admission etc.)

Use Key phrases: Often required to make people feel valued:

Ø  We need your expertise/help….
Ø  Your opinion is really going to make a difference….
Ø  I am concerned because….
Ø  I think this is best for the patient….
Ø  I would really appreciate if you could come down and see him once.…
Ø  I know you guys are really busy abut I cannot miss this diagnosis….
Ø  I don't want to waste your time but no one else can do it….
Ø  I know, It was a really busy day for you – but I need your help..

If nothing is working to get them down to the ED, Remember:

  • Not to raise your Voice or Swear – Bad for you and for the patient as well
  • Don’t threaten them

Occasionally, despite doing your best, things are not going to turn out well. Then, just be polite and tell them you are going to speak to your consultant/supervisor/attending and get back


Tell them respectfully : “This discussion is not going anywhere, I think we both need to think over it and I shall get back in sometime”.

These methods may not always work but definitely provide us with a good framework for asking a consultation from the ED. Factors like your rapport, previous interactions with them also play an important role when you ask for a consultation.

Take Home Points
1)   5 Cs Contact, Communicate, Core Question, Collaborate & Close the loop
2)    Never raise your voice or swear at them
3)    Don't forget the Kindergarten Basics
4)    Know the key statements to get them down!


For further reading:
  1. Salerno, Stephen M., et al. "Principles of effective consultation: an update for the 21st-century consultant." Archives of internal medicine 167.3 (2007): 271-275.
  2. Kessler, Chad S., et al. "A prospective, randomized, controlled study demonstrating a novel, effective model of transfer of care between physicians: the 5 Cs of consultation." Academic Emergency Medicine 19.8 (2012): 968-974.
  3. EMRAP - Feb 2011 Episode Summary
  4. EMRAP - Sep 2013 Episode Summary

What Are Common Inherited Thrombophilias?

Patient Presentation
A 6-month-old female came to clinic for her health maintenance visit. She was growing well physically. Her mother had several questions regarding her normal development which were easily answered. The mother was most concerned because the family history was now positive for her sister (patient’s maternal aunt) having a recent deep venous thrombosis during pregnancy. The aunt’s evaluation showed Factor V Leiden and the mother was in the process of being tested. She wanted to know if the patient should also be tested. The past medical history showed no abnormal bruising/bleeding or other problems with the patient or other family members.

The pertinent physical exam showed a smiling infant with growth parameters in the 75-95% for age. Her examination was normal. The diagnosis of a healthy infant was made. The pediatrician recommended that first the mother finish her own evaluation and re-iterated that there were several things the mother could already do to decrease her own risk of blood clots including being active and a non-smoker. The physician said, “Being pregnant like your sister is also a risk, and one you need to discuss with your doctor and your husband about. Once we know if you have Factor V Leiden then we can talk about the baby’s risks. Usually we wait until the child is older to discuss testing, but we can have you talk with the genetic counselor if you would like to. The good news is that infants and children are at low risk for getting blood clots.”

Thrombophilia is the increased risk of thromboembolic disease due to a disorder. Thrombophilia can be inherited or acquired (such as antiphospholipid syndrome). The risk of thromboembolic events is much lower in children than adults.

At-risk patients should avoid:

  • Dehydration
  • Sitting for prolonged time periods during travel
  • Obesity
  • Smoking
  • Estrogen containing oral contraceptives

Common inherited thrombophilias include:

  • Prothrombin (Factor II mutation)
    • Second most common
    • Genetics: 1-2% prevalence is variable depending on location and ethnic background.
    • Cause: Abnormal point mutation of the prothrombin gene that causes increased levels of prothrombin, the precursor of thrombin.
  • Protein C
    • Relatively common
    • Genetics and epidemiology – 0.2% prevalence of general population. Heterozygous state is most common. Can occur in homozygous state but has severe thromboembolic events mainly in neonatal period.
    • Cause: Protein C becomes activated (activated Protein C = APC) and combines with Protein S. This complex then normally inactivates Factors Va and VIIIa. Protein C is Vitamin K dependent.
    • Two types:
      • Type 1 – antigen and activity levels are low (quantitative deficiency, 85% of cases)
      • Type 2 – antigen levels are normal and activity levels are low (qualitative deficiency, 15% of cases)
  • Protein S
    • Relatively uncommon
    • Genetics and epidemiology – 0.03-.13% prevalence of general population. Heterozygous state is most common. Can occur in homozygous state but has severe thromboembolic events mainly in neonatal period.
    • Cause: Free Protein S combines with Protein C. This complex then normally inactivates Factors Va and VIIIa. Protein S is Vitamin K dependent. Protein S is 60% protein bound.
    • Three types:
      • Type 1 – free antigen and total antigen is low (quantitative deficiency)
      • Type 3 – free antigen is low but total antigen is normal (quantitative deficiency)
      • Type 2 – normal free and total antigen levels but activity is low (qualitative deficiency)
  • Antithrombin
    • Least common
    • Genetics and epidemiology: 0.02% prevalence of Caucasian population, Autosomal dominant so heterozygous state is most common. Homozygous Type 1 is incompatible with life.
    • Cause: Acts to inhibit several coagulation factors including IIa, IXa, Xa, XIa, and XIIa.
    • Two types:
      • Type I – low antigen and activity levels (quantitative deficiency)
      • Type II – normal antigen but low activity levels (qualitative deficiency)

Learning Point
Factor V Leiden

  • Most common thrombophilia, named for the city of Leiden, Netherlands where it was discovered.
  • Genetics and epidemiology – Prevalence is variable depending on location and ethnic background. 1% in African American population, 2% in Hispanic population and 5% in European background. Mainly occurs in heterozygous state. Homogygotes have a high risk with thrombosis in up to 80/1000.
  • Cause: Factor V Leiden is an abnormal activated Protein C (APC) caused by a point mutation replacing arginine with glutamine at position 1691 which changes the amino acid at position 506 of the protein. Normally APC inactivates coagulation Factor V which then slows down the clotting process and prevents the clots from becoming too large. Is usually inactivated by activated protein C. Factor V Leiden doesn’t allow the APC to work, so the coagulation Factor V continues to allow the clot to grow.
  • Screening is controversial – Prior to a known thrombotic event, many people recommend to wait until children are adolescent age for screening so patients can make informed choices particularly as epidemiology in children is much different than adults. Screening after a thromboembolic event is less clear and most people would evaluate the patient and screen for thrombophilias as this will also help with treatment decisions.

Questions for Further Discussion
1. What are the Vitamin K dependent coagulation factors?
2. What is the role of imaging in evaluation and treatment of thromboembolic events?
3. What is the role of genetic counseling in thromboembolic events?

Related Cases

To Learn More
To view pediatric review articles on this topic from the past year check PubMed.

Evidence-based medicine information on this topic can be found at, the National Guideline Clearinghouse and the Cochrane Database of Systematic Reviews.

Information prescriptions for patients can be found at MedlinePlus for these topics: Blood Clots and Bleeding Disorders.

To view current news articles on this topic check Google News.

To view images related to this topic check Google Images.

To view videos related to this topic check YouTube Videos.

Varga EA, Moll S. Prothrombin 20210 Mutation (Factor II Mutation). Circulation. 2004; 110: e15-e18.

Haywood S, Liesner R, Pindora S, Ganesan V. Thrombophilia and first arterial ischaemic stroke: a systematic review. Arch Dis Child. 2005 Apr;90(4):402-5.

Kenet G, Nowak-Gottl U. Venous thromboembolism in neonates and children. Best Pract Res Clin Haematol. 2012 Sep;25(3):333-44.

Heleen van Ommen C, Middeldorp S. Thrombophilia in childhood: to test or not to test. Semin Thromb Hemost. 2011 Oct;37(7):794-801.

Kalpatthi, RV, Kirkland KR, Tarantino CA. Screening for Factor V Leiden Mutation. The Link – Kansas City Mercy Infectious Disease. 2015; April 7(4).


Donna M. D’Alessandro, MD
Professor of Pediatrics, University of Iowa Children’s Hospital

LITFL Review 183

LITFL review

Welcome to the 183rd LITFL Review. Your regular and reliable source for the highest highlights, sneakiest sneak peeks and loudest shout-outs from the webbed world of emergency medicine and critical care. Each week the LITFL team casts the spotlight on the blogosphere’s best and brightest and deliver a bite-sized chuck of FOAM.

The Most Fair Dinkum Ripper Beauts of the Week

resizer The Emergency Medicine Educator’s Conference (EMEC) posted the first of its conference videos. Dan Boden shares Derby’s ideas and success on teaching the whole department. Plenty of food for thought….. [SL]


The Best of #FOAMed Emergency Medicine

  • Bryan Hayes reviews the literature supporting the use of ketamine for rapid sedation of the agitated patient on ALiEM. [AS]
  • The utility of medical expulsive therapy in renal colic has been questioned many times. Ryan Radecki highlights a recent large RDCT that may put the topic to rest once and for all. [AS]
  • The PHARM featured a talk by our own Mat Goebel on “Killer EKGs (other than STEMI)” geared toward prehospital providers. [ML]
  • In case you missed it last week, the May edition of the Annals of Emergency Medicine audio summary is available! [MG]

The Best of #FOAMcc Critical Care

The Best of #FOAMus Ultrasound

  • Ultrasound to diagnose the cause of AMS? Great case from ALiEM highlighting the role of US in the undifferentiated hypotensive patient. [AS]
  • In light of recent discussion on 2-point vs whole leg ultrasound for DVT, the Ultrasound Podcast demonstrates the whole upper leg approach. [MG]
  • Essential case from Ultrasound of the Week. Everyone memorise these images from a common scenario of acute shortness of breath. [SO]

The Best of #FOAMPed Pediatrics

  • REBEL EM ventures into pediatrics with a post on 7 pediatric hacks for your ED. [AS]

The Best of #FOAMim Internal Medicine

  • Louisville invites you inside the brain of a cardiologist in Bradyarrythmias with Dr Brown. [ML]

The Best of Medical Education and Social Media

News from the Fast Lane

Reference Sources and Reading List

Brought to you by:

The post LITFL Review 183 appeared first on LITFL: Life in the Fast Lane Medical Blog.

Alarming alarms

Labs and Lytes 022

Author: Sarah Yong
Reviewer: Chris Nickson

You have just arrived at a MET call for a 73 year-old lady admitted overnight with recurrent falls and collapse for investigation. At first glance the patient is alert and looks comfortable. You hear the monitor alarming constantly as the nurse passes you the following rhythm strips:

Click to enlarge

Click to enlarge

Q1. What is your interpretation of these rhythm strips?

Sinus bradycardia HR ~60 bpm with intermittent sinus arrest / sinus exit block, shown by 2 missing p waves followed by 2 ventricular escape beats at a rate just under 40 bpm

Q2. What would you like to do next?

  1. Assess the patient
  2. Decide if they’re stable or unstable
  3. Look for underlying cause

Assess the patient

  • Assess ABCDE
  • Simultaneously apply monitoring (SpO2, ECG, NIBP) and O2 if required

Are they stable, unstable or have high-risk features?

  • This will help determine your next steps in management
  • Patients are considered “unstable” if there are features of myocardial ischaemia, shock, acute heart failure or hypotension
  • Patients are high risk for asystole if they have had recent asystole, complete heart block with broad QRS, Mobitz II AV block or ventricular pauses > 3 seconds
  • If they’re unstable or have high risk features, give atropine 500-600mcg IV and prepare for pacing (see below)

Look for an underlying cause (see the LITFL Bradycardia DDX page for the differentials)

  • 12 lead ECG: myocardial ischaemia, myocarditis, cardiomyopathy
  • Transthoracic echo: structural dysfunction
  • Bloods: FBE, UEC, CMP, thyroid function
  • Rule out infection: septic screen if indicated
  • Exclude hypothermia, medications, toxins

On further assessment, the patient remains alert and asymptomatic with no chest pain, shortness of breath or presyncope. HR remains 59 with ongoing pauses of up to 4 seconds and episodes of bradycardia down to 30 bpm. BP was 96/, improving to 127/75 when the rate spontaneously picks up to 60 bpm.

Q3. What management options are available for this condition?

Management includes pacing via pharmacological, transcutaneous, transvenous or epicardial routes.


  • Atropine 500 – 600mcg boluses, repeat to max 3mg
  • Adrenaline infusion up to 10mcg/min
  • Isoprenaline infusion 0.5 – 5mcg/min


  • Temporary cardiac pacing via defibrillator using pads or paddles placed externally on chest


  • Temporary: bipolar pacing lead (II guidance), paceport PA catheter, or balloon flotation leads
  • Permanent: single chamber, dual chamber, bi-ventricular (resynchronisation), pacemaker-defibrillator


  • Used in the post-cardiac surgery patient with temporary epicardial AV pacing wires in situ (inserted by surgeon prior to closure)

Q4. The patient is commenced on an isoprenaline infusion at 0.5mcg/min, with improvement in his rhythm. Briefly describe the mechanism of action and potential adverse effects of this drug

Isoprenaline is a synthetic sympathomimetic drug with almost exclusive beta agonist effects. Isoprenaline is called isoproterenol in North America.

It can be administered via a proximal peripheral line in the short term, so it is worthwhile preparing it before the patient becomes unstable. Low-dose isoprenaline infusion can be run on the cardiac wards at The Alfred.

Potential adverse effects include:

  • Worsening cardiac function: by increasing myocardial oxygen demand while decreasing effective coronary perfusion
  • Ventricular arrhythmias
  • Worsening of heart block
  • Contains sulfite moiety: potential allergic / anaphylactic reaction

References and links

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