A Response to the “How a SHPOS is Born” article in The National Post

You may have read the article “How a SHPOS is born: What doctors call their very worst patients”, which was written by Anne Skomorowsky and published in The National Post (originally appearing on the Slate Magazine website) on November 10, 2014. Many people in the social media universe had very strong emotional responses to the article. If you haven’t read it, I encourage you to do so. I collaborated with several other individuals (Eve Purdy @eve_purdy, Teresa Chan @tchanMD, Swapnil Hiremath @hswapnil, Heather Murray @heatherm211, Ross Morton @signindoc) to produce a letter to the editor, which was submitted but was not published by The National Post. Thus, we decided to publish our letter on three FOAM websites (TheChartReview.org, manuetcorde.org, BoringEM.org) to share our response with the medical community online. Read below. Feel free to share your thoughts on the comments or on Twitter.

Dear Editor,

We read with horror the recent article “How a SHPOS is born: What doctors call their very worst patients” by Anne Skomorowsky dated November 10, 2014.

We were appalled that the author conveyed the impression that this offensive term, SHPOS, is common and used by the general medical community. The opening line “A medical acronym, SHPOS, helps a doctor summarize a patient’s history in just five letters” implies that the term “a doctor” would include a large number of practicing physicians.

This is false.

This article has sparked discussions over several social media platforms and in the hallways of our hospitals. The consensus from our investigation is that the majority have never used, nor heard of this disgraceful and offensive term. Physicians and learners spanning many generations (medical students to experienced physicians of greater than 20 years) and specialties (emergency medicine, internist, surgeons) agree that that the SHPOS term is completely foreign. The term is as uncomfortable to us as it is the intended readership. On digging a bit deeper (as a result of this article), it seems this term may have been used in the past, in the early 80s or before but given the unfamiliarity of currently practicing physicians, it is unlikely that it is used with any frequency today (1,2). Thus, to taint all current doctors with this archaic and unused term is a reckless overreach at best and slanderous at worst. In fact, the journalistic ethics of reintroducing such a horrible term back into the current lexicon is both irresponsible and dangerous. Language evolves over time, and most of the time with good cause, because terms like SHPOS are eliminated because of their inherent problems.

As a community we do recognize that the language physicians choose is important and appreciate that in many instances we might do better. We have explored issues around language in medicine through an international and open-access case study that can be accessed at one of the world’s pre-eminent medical education blogs (3). We would encourage readers interested in the use of slang by medical professionals to read this much more up to date, balanced and thoughtful exploration of the important topic. This document incorporated patient, allied health, and physician voices all together to generate a very robust discussion and handout for young physicians to read and better understand the importance of words in clinical practice.

Sadly, the information in this article was likely not verified among the health care professionals to whom it refers. Unfortunately, the message conveyed to the readership of the National Post and general public is that terms like “SHPOS” are commonplace and accepted among the medical community, and this supposition is largely unverified in Canada too – especially since it is merely a repurposing of a previously featured article from an American magazine. Acknowledging that slang and language are contextual, and cultural, the National Post might have been better served to do their own, contextually relevant, investigation into this issue, rather than simply feature the article of an American author.

We do not use the term SHPOS. The thesis of the article is simply untrue. This article potentially biases and inflicts pre-arrival damage to future doctor-patient encounters, creating barriers and potentially interferes with the relationship developed by current health care staff and the people they wish to help.

We urge your newspaper to consider the ramifications of posting such inaccurate and potentially damaging materials in the future.

Elisha Targonsky, MD CCFP-EM
Eve Purdy BHSc MD Candidate
Teresa Chan MD FRCPC
Swapnil Hiremath, MD MPH
Heather Murray MD MSc FRCPC
Ross Morton MD FRCP FRCPC FACP

 

The post A Response to the “How a SHPOS is Born” article in The National Post appeared first on The Chart Review.

Herpes Simplex in Disguise: Don’t I&D That Paronychia!

This post was kindly reviewed by Dr Mark Crislip (@MarkCrislip), an ID doc who runs a great ID FOAM site called edgydoc.com.

You are working a busy shift in the “Green Zone” of your emergency department. The next patient you see is a healthy 18yM with a complaint of a painful left index finger.

You review his vital signs:
Temp 36.1, pulse 82, BP 112/65, RR 16, O2 saturation 100%

The patient shows you his finger, which looks a lot like a paronychia:

WhitlowAs you examine him, you ask for elaboration on the history. He tells you his finger has been painful for 10 days. It began 2 days after cutting it in the yard while repairing his fence. Several days later it became immensely painful and red with a blister-like area. He went to a walk-in clinic where he was prescribed Cephalexin to treat a “finger infection.” He has since not improved.

He also mentions to you that his left armpit and elbow feel sore and tender to touch. You look at the elbow and see an erythematous area over the medial aspect. His is tender with palpable lymphadenopathy in the axilla.

Are there any other questions you would like to ask him?

 

You ask if there are any other other lumps he has felt, and he mentions two lumps in his groin. When you examine him, there is palpable lymphadenopathy in the groin and a few small ulcers at the base of his penis.

Further questioning reveals that he had an encounter with a new sexual partner 2 days after the incident in his backyard. This included non-vaginal intercourse.

You connect the dots and realize this is no paronychia. This is Herpetic Whitlow!

A bit on Herpetic Whitlow:

  • HSV 1 > HSV 2
  • Involves 1 or more fingers
  • Incubation period or 2-20 days
  • Symptoms include: burning/pain, redness, low grade temp and then a cluster of vesicles
  • May get recurrences like other herpes infections of the mouth and genitalia

Who is at risk for Herpetic Whitlow?

gingivostom

Children with herpetic gingivostomatitis.

genital

Adults/adolescents with genital herpetic infection.

Who else? Health care workers/dentists/hygienists

Diagnosis:

  • Mostly a clinical diagnosis
  • Easier to identify when presents as cluster of vesicles
  • Finger infection + axillary/elbow lymphadenopathy = Whitlow
  • Confirmation can be done by gently unroofing an ulcer and performing viral culture or PCR

nodes

Pitfalls:

  • Not always straight forward diagnosis; Whitlow can mimic a paronychia: small, clear vesicles may coalesce as fluid opacifies
  • Don’t perform and incision and drainage (I&D) on Herpetic Whitlow!
  • Risks of I&D include superimposed bacterial infection or, rarely, disseminated herpes or encephalitis
  • Wear gloves!

Treatment:

  • If caught early, offer oral or topical antivirals such as acyclovir or valacyclovir. Benefit is limited thereafter.
  • Screen, if appropriate, for other STIs.
  • Oral antiobiotics only if evidence of secondary bacterial infection.
  • Advise the patient to keep the infected finger away from the eyes to avoid HSV keratitis.

antivirals

Case Resolution:

You tell the patient that you believe his painful finger is due to an infection by the herpes virus that seeded the abrasion sustained while working in the yard. Unfortunately, the benefit of antiviral medications is minimal at this point. As well, you don’t expect him derive benefit from the oral antibiotic he has been taking (since there is no evidence of superimposed bacterial skin infection). You advise keeping the finger covered to avoid spread and offer testing for other STIs. One of the genital lesions is unroofed and swabbed. Several days later the culture returns positive for HSV-2.

References:

This post underwent minor revisions on Nov 18, 2014. Originally posted on Nov 17, 2014.

The post Herpes Simplex in Disguise: Don’t I&D That Paronychia! appeared first on The Chart Review.

Dramatic ECG Evolution of a STEMI

You have recently begun your daytime shift at the emergency department in Canadian Janus General Hospital. You are seeing a patient when you receive a call on your companion phone from an ECG technician to urgently read an ECG on a gentleman with chest pain at triage. Before you even get to triage, the tech meets you along the way and she hands you this ECG:

10:10 am

 pre-arrest

Interpretation: SCARY!
More specifically, the patient is in normal sinus rhythm at a rate of 60 bpm, with a normal axis and normal PR and QT intervals. The QRS complexes are narrow. You appreciate the obvious impressive down sloping ST segment depressions in multiple leads, including II, III, aVF and V3-V6. Furthermore, you suspect a hint of ST elevation in V1 and possibly aVR. The T wave in V1 is upright (often inverted in V1), which in this setting is also highly associated with ischemia. Findings of ST segment down sloping and ST depression >2mm (substantial) and >2 leads (widespread) are associated with poor prognosis and extensive coronary disease.

You quickly go see the patient, and find a man in his 50’s, who is laying supine and appears unwell. He is talking to his wife and he is still connected to the ECG machine. Suddenly, the patient loses consciousness and you look at the ECG reading while checking his pulse and you see this (as the tech, by your side, hits the print button):

10:12 am

Vfib

Interpretation: SCARIER!
More specifically, the ECG shows ventricular fibrillation.

You immediately start chest compressions and call for a code blue. The stretcher is quickly mobilized from the triage area and you climb on, continuing compressions as your nurses wheel you both to a resuscitation room. The patient stiffens up beneath your hands and turns bluer and bluer. Once you arrive in the room, defibrillation pads are placed on the patient’s chest and someone else takes over compressions. In the meantime, you charge the biphasic defibrillator to 120 joules in case the patient is still in VF. Compressions are paused momentarily while you perform a rhythm & pulse check.

Pulse – none
Rhythm on the monitor – ventricular fibrillation

You immediately shock the patient and quickly resume CPR. Before 30 seconds pass, the patient begins to stir and move his limbs. Compressions stop and the patient has a pulse back. He is alert, coherent and able to tell you the following:

Name, date, place
PHx – smoking, HTN
Meds – ramipril

His chest pain started last night and abated, but recurred since early in the morning. He describes it as retrosternal pressure radiating to his shoulders bilaterally, worse on exertion. He was in a town nearby (2 hours away!) and decided to drive to your hospital. He still has chest pain now and looks unwell. You repeat the ECG. Your newest post-arrest ECG shows the following:

10:25am

postarrest

Interpretation: STILL SCARY
More specifically, you have an ST-elevation MI, with anterior leads V2-V3 showing significant ST segment elevation, as well as leads I and aVL. There is still ST depression in the inferior leads and V4-V6. The findings of ST elevation in precordial leads as well as I and aVL (high lateral leads) is highly associated (87%) with proximal LAD occlusion.

You give the patient ASA immediately and the cath lab at a nearby facility is contacted. He receives 60 mg of prasugrel and a 60 unit/kg IV blus of heparin and is sent to the receiving hospital with advanced paramedics and a fellow physician. Fortunately, the patient has no more episodes of malignant arrhythmias and he arrives to the cath lab in good condition. His procedure reveals a 99% occlusion of the proximal LAD, which is stented open. His troponin peaks at 54 (normal <0.12). Three days later, his ECG is as follows:

evolved

Interpretation: NSR around 55 bpm. The now evolved MI demonstrates poor R-wave progression and T-wave inversion in the precordial and lateral leads. ST depressions (and elevations) have disappeared.

Fortunately this gentleman had an excellent outcome. Had he presented to hospital 5 minutes later there would have been an out-of-hospital arrest, which would have let to delayed CPR and defibrillation.

References:

Channer K and Morris F. ABC of clinical electrocardiography: Myocardial ischaemia. BMJ. Apr 27, 2002; 324(7344): 1023–1026.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1122957/?report=classic

Life in the Fast Lane – T waves on ECG:
http://lifeinthefastlane.com/ecg-library/basics/t-wave/

Life in the Fast Lane – Lateral STEMI on ECG:
http://lifeinthefastlane.com/ecg-library/lateral-stemi/

For more on ECG’s, please check out my two favourite ECG websites:

Amal Mattu’s EKG of the week video series: http://ekgumem.tumblr.com/

Dr Stephen Smith’s ECG blog: http://hqmeded-ecg.blogspot.ca/

The post Dramatic ECG Evolution of a STEMI appeared first on The Chart Review.