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


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?

Children with herpetic gingivostomatitis.
Adults/adolescents with genital herpetic infection.

Who else? Health care workers/dentists/hygienists


  • 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



  • 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!


  • 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.


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.


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

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


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


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:



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:


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.


Channer K and Morris F. ABC of clinical electrocardiography: Myocardial ischaemia. BMJ. Apr 27, 2002; 324(7344): 1023–1026.

Life in the Fast Lane – T waves on ECG:

Life in the Fast Lane – Lateral STEMI on ECG:

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/

A Knee Out of Place

A 30yM presents to the Canadian Janus General ED at 11:30 pm with acute onset knee pain immediately after stopping awkwardly on his motorcycle. He had placed his left foot down while the vehicle was in motion, causing his leg to lock and hyperextend during a pivot-type movement. He denies any other injuries.

On exam he is in a lot of discomfort. Vital signs are all normal. His left knee is swollen and obviously deformed. Pedal pulses (DP and PT) are intact and equal quality bilaterally. You cannot appreciate a popliteal hematoma or a bruit/thrill. The colour of his lower limb is normal There is normal sensation in the lower leg and foot. Moving his knee/ankle/foot however, is very uncomfortable. There are no other injuries.

You suspect a knee dislocation. You give him a dose of fentanyl 1 mcg/kg while awaiting some portable X-rays. Fifteen minutes later you have your films. X-rays are shown below:


As suspected there is an anterior left knee dislocation. You plan to reduce the knee. As you think about your drug of choice, the nurse tells you that the patient consumed a sandwich and soft drink approximately 90 minutes ago. “Should we wait a few hours? I’ll make him NPO?”

You recall reading the recent clinical policy on ED procedural sedation from Ann Emerg Med “Clinical policy: procedural sedation and analgesia in the emergency department.”

To answer the question “In patients undergoing procedural sedation and analgesia in the emergency department, does preprocedural fasting demonstrate a reduction in the risk of emesis or aspiration?

Level B recommendations. Do not delay procedural sedation in adults or pediatrics in the ED based on fasting time. Preprocedural fasting for any duration has not demonstrated areduction in the risk of emesis or aspiration when administering procedural sedation and analgesia.”

You decide to proceed with the sedation and reduction.

Then the nurse says to you, “I will page RT, but which other ED doc will assist you with the sedation? Don’t you need two docs?”

You look at the ED tracker and see that all sections of the department are busy, with 2-3 hour wait times and a waiting room full of patients. You then recall that the “Clinical policy: procedural sedation and analgesia in the emergency department” paper also addressed this issue.

To answer the question “In patients undergoing procedural sedation and analgesia in the emergency department, what is the minimum number of personnel necessary to manage complications?

“Level C recommendations. During procedural sedation and analgesia, a nurse or other qualified individual should be present for continuous monitoring of the patient, in addition to the provider performing the procedure. Physicians who are working or consulting in the ED should coordinate procedures requiring procedural sedation and analgesia with the ED staff.”

You take this to mean that having an ED nurse and respiratory therapist in the room to monitor the patient is safe and efficient while you perform the reduction and keep an eye on the patient during sedation as well. Your nursing and RT colleagues agree with this plan. You proceed.

The nurse then asks, “So fentanyl and propofol? That’s what Dr Smith usually uses.”

You kindly reply and suggest that ketamine and propofol is a better option. It is associated with fewer adverse events (Messenger et al) and is very effective (Andolfatto et al). You have the nurse draw up 100 mg of propofol and 100 mg of ketamine for this 85 kg patient.

ketamine Propofol

After 50 mg of ketamine followed by 40 mg of propofol, you successfully reduce the knee by longitudinal traction and splint the joint in a Zimmer knee immobilizer. The sedation goes uncomplicated. His neurovascular exam is still normal.

Repeat X-ray is below:


The reduction is satisfactory, and you can now appreciate an associated fracture of the medial femoral condyle. You page your on-call orthopedic surgeon and while you order a post-reduction film. Pulses are still normal and the patient, now awake, has intact motor and sensory function in the lower extremity. You know that knee dislocations are associated with popliteal artery injury, with reported rates of 7-64% (E-medicine). Your orthopod calls back and you ask whether your patient needs angiography to rule out vascular injury. He says that serial (normal) exams overnight followed by admission and observation for 1-2 days would be sufficient enough to rule out a significant vascular injury. Just to be sure you call your vascular surgeon and they agree.

Is this a safe practice?

According to a prospective cohort study by Stannard et al, of 138 patients with knee dislocation, 116 had normal physical exams. Of these, 17 had angiography, in whom 1 had an intimal tear that was observed without consequence. Thus all 138 patients with normal vascular exams had good outcomes. Of note, all were admitted for a minimum of 48 hours for observation.

Similarly, a prospective study by Miranda et al of 35 patients with knee dislocations found that all 27 patients with a negative exam for hard findings* (see below) of vascular injury, none developed ischemia during their hospitalization. Of note, only 12 of these were available for long-term followup.

A bit more about knee dislocation:

  • Often due to a significant trauma mechanism such as MVC, auto-ped collision, fall from height or sporting injuries (Seroyer et al)
  • There is a high spontaneous reduction rate, which may account for missing this injury unless a thorough physical exam is performed. (EM Cases Ep 1)
  • At least 3 major ligaments usually rupture in order for the usually-stable knee joint to dislocate, thus any knee exam with multiplanar/multiligamentous instability should be a suspected dislocation that spontaneously reduced prior to ED arrival. (EM Cases Ep 1)
  • About 50-60% of dislocations are associated with fractures as well (Stannard et al).
  • *Hard signs of vascular injury include absence of distal pulses, active bleeding from an open injury, expanding haematoma, bruit or thrill in the popliteal fossa and distal ischemia (Seroyer et al)
  • Presence of hard signs of vascular injury requires prompt reduction even before pre-reduction images are obtained (Seroyer et al)
  • Many institutions and surgeons still recommend more advanced vascular imaging for all knee dislocations, including duplex ultrasonography, CT angiography or direct arteriography. (E-Medicine)
  • Ankle-brachial index (ABI) can be used with a sensitivity and specificity of 95% and 97% respectively to rule out clinically significant arterial injury. (E-Medicine)
  • How is ABI done? According to Khan et al, ABI is performed by measuring the two upper extremity blood pressures and recording the higher systolic BP number, followed by the two ankle pressures and recording the lower systolic BP. In the case of acute vascular injury, one would only record the systolic BP of the limb in question. Use the ankle pressure as your numerator and the arm pressure as your denominator. If your value is <0.9 should prompt vascular imaging.

Case Resolution:

The patient and ED staff were satisfied with the sedation and prompt reduction, even though he didn’t have an empty stomach. Your department flow wasn’t compromised. His pain resolved with reduction and immobilization and he had normal serial vascular exams. After a brief admission he was discharged with outpatient followup. MRI of the knee demonstrated the following injuries:

  • complete tears of ACL, PCL, MCL, LCL, biceps femoris and popliteus tendons
  • partial tears of the medial and lateral patellar retinacula
  • partial tearing of adductor magnus and the adductor tubercle insertion
  • partial tears of the medial and lateral gastrocnemius tendons and biceps femoris at myotendinous junction
  • displaced fracture fragments of the medial aspect of medial femoral condyle
  •  increased signal of the common peroneal nerve compatible with injury

How would you have managed a similar case?

  • Do you wait before performing procedural sedation for patients who aren’t fasted?
  • What is your preferred cocktail of sedation medications?
  • How does your institution manage knee dislocations with negative vascular exams? Vascular imaging for all, or serial exams?

Leave your comments below or tweet me at @ETtube

Thanks to Dr Paul Koblic for review and suggestions.


Andolfatto G, Willman E. A prospective case series of single-syringe ketamine-propofol (ketofol) for emergency department procedural sedation and analgesia in adults. Acad Emerg Med. 2011;18:237-245.

Godwin et al. Clinical Policy: Procedural Sedation and Analgesia in the Emergency Department. Ann Emerg Med. 2014;63:247-258.

Kelleher B and Brenner B. Emedicine: Knee Dislocation Clinical Presentation Accessed Aug 14, 2014.

Khan et al. Critical Review of the Ankle Brachial Index. Curr Cardiol Rev. 2008. 4(2) 101-106

Messenger DW, Murray HE, Dungey PE, et al. Subdissociative-dose ketamine versus fentanyl for analgesia during propofol procedural sedation: a randomized clinical trial. Acad Emerg Med. 2008;15:877-886.

Miranda FE et al. Confirmation of the safety and accuracy of physical examination in the evaluation of knee dislocation for injury of the popliteal artery: a prospective study. J Trauma. 2002 Feb;52(2):247-51; discussion 251-2.

Seroyer ST et al. Management of the acute knee dislocation: the Pittsburgh experience. Injury. 2008 Jul;39(7):710-8.

Stannard JP et al. Vascular injuries in knee dislocations: the role of physical examination in determining the need for arteriography. J Bone Joint Surg Am. 2004 May;86-A(5):910-5.

Emergency Medicine Cases, Episode 1: Occult Fractures & Dislocations


Scareway Case #3: A Hypoxic Toddler

You’ve just started your evening ED shift at Canadian Janus General Hospital when you are called STAT to resuscitation room #1. The nurse says there is a child with an oxygen saturation of 50%!

You rush to the room to find a 20 month old boy, crying inconsolably. He appears dusky and greyish around the lips. While nurses are applying an NRB mask, you peek at his pulse oxymetry which shows 47%. The child continues to cry, and your quick ABC exam reveals the following:

A: A patent airway, with no tongue/uvula swelling, drooling, stridor or FB in the oropharynx.
B: You cannot appreciate any increased work of breathing (tracheal tug/indrawing/nasal flaring) and grossly there is equal air entry bilaterally without any audible wheeze or crackles. The child is, however crying incessantly.
C: HR is 160. Pulses are equal in all limbs. Capillary refill is < 2 seconds.

As you wait for a better reading on the pulse oxymeter, you quickly review the triage note…


  • CC: unwell
  • Family visiting from Phillipines
  • Brought to ED because child “felt unwell” as per mom (with a substantial language barrier)
  • Persistent crying/irritability since morning
  • Mild coughing today; previously well
  • PHx: none
  • Meds: none
  • Allergies: none


  • Temperature 36.6
  • Pulse 162
  • BP 96/40
  • RR 30
  • O2 Sat: 50%

You stand and watch the pulse-ox. There is a good reliable waveform and it has reached a plateau at 63% on NRB mask! You quickly run and change your scrubs and regain your composure. This child is sick!

Clearly more data is needed here from history and physical. You call for a portable CXR, get some labs and an IV and consider your DDx for a cyanotic child (adapted from Textbook of Pediatric Emergency Medicine – Table 15.3):

– parenchymal lung disease ie. pneumonia
– upper airway obstruction: aspiration of FB, epiglottitis/croup, anaphylaxis
– lower airway obstruction: asthma, bronchiolitis, anaphylaxis
– tension pneumothorax or massive hemothorax
– Cardiac: congenital heart disease, CHF, cardiogenic shock
– Pulmonary: pulmonary embolism, pulmonary hemorrhage, pulmonary hypertension
– Peripheral vascular: septic shock
– chest wall/poor inspiratory effort
– methemoglobinemia

More history is collected from mom at the bedside, though the language barrier makes this a struggle of sorts:

  • PHx – none
  • Meds – none
  • Allergies – none
  • No fever, or recent URI (mild cough today)
  • No known congenital or acquired cardiac disease
  • No witnessed/suspected coughing or choking episode/aspiration
  • No new meds or suspected toxic exposures

You attempt a more detailed exam. The child is alert and continues to cry but when he settles temporarily, you notice that the O2 sats actually creep up to 70%. It is still difficult to appreciate any increased work of breathing, stridor, wheeze or discrepancy in air entry. Heart sounds are normal with no murmurs. BP readings are equal in all limbs.

Surprisingly, your labs come back before your portable CXR:

  • ECG – sinus tachycardia, otherwise normal
  • VBG: 7.23/45/35/19/-9
  • Normal MethHb
  • Lactate 4.9
  • WBC 20.8, Hb 140, Plts 492
  • Normal lytes/chemistry

Finally your CXR is taken:

What is your interpretation? Abnormal, yes. Before scrolling ahead, reconsider your DDx and whether this image helps narrow things down.

As interpreted by your radiologist at Canadian Janus:

click to enlarge

Given the findings on your CXR and labs you’ve narrowed down your DDx to lung parenchymal disease (Out of the equation are cardiac and metabolic/metHb). Still on the table: FB aspiration, pneumonia +/- effusion. It’s difficult to account for the pneumothorax (PTX), though.

You go back to the family and ask again about any prior choking/coughing spells or illness/fever. The answer again is “no”. Your patient continues to maintain oxygen saturations in the 60’s, so the decision is made to intubate. ETI goes smoothly and actually O2 sats come up to 90%.

You’re feeling better about the stability of the patient and feel confident that the most likely explanation for this degree of hypoxia and associated X-ray (with severe atelectasis and tracheal shift to the right) is aspirated airway FB. You arrange transfer to a tertiary care centre with pediatric ICU capabilities and readily available bronchoscopy. In the meantime you cover your patient with antibiotics in case of pneumonia. However, as the patient is transferred from stretcher to stretcher, the oxygenation saturation reading drops to the 68% and BP drops from 102/70 to 80/62. Instead of panicking, you quickly recall your approach to the patient with dropping O2 sats on a ventilator: DOPES (for more on DOPES, visit EmCrit.org Episode 16).

D: displacement of the ETT
O: obstruction of ETT
P: pneumothorax (tension)
E: equipment failure
S: stacking of breaths (ie in asthmatic)

Suction provides modest but transient improvement of oxygenation, up to 78% – no mucous plugs come up. You check your ETT again, which is in the same position and you don’t have time for a CXR to demonstrate if it’s migrated to the right mainstem. Given the PTX present on the CXR and use of positive pressure ventilation (PPV), you suspect this child may have a tension PTX (though you recognize that the initial CXR shows tracheal shift toward the PTX). You consider whether this child would likely need a tube thoracostomy.

Few rigorous studies explore whether chest tubes are needed in patients with PTX on PPV, none of which are representative of your hypoxic toddler without preceding trauma:

  • Enderson et al conducted a prospective study in 1993 on blunt trauma adult patients with occult PTX (seen on CT, but not CXR). They found 8 of 21 patients with occult PTX on PPV randomized to observation had either progression, 3 of whom had tension pneumothorax.
  • Kirkpatrick et al (2013) studied adult trauma patients with occult PTX on PPV and found observation was a safe strategy though risk of need for pleural drainage increased with time on PPV.
  • Litmanovitz and Carlo looked at neonates with PTX and PPV, and suggest that those with lower ventilator pressure settings and better blood gases could be safely observed without immediate placement of a chest tube.

Despite some evidence in various settings (occult PTX in neonates on PPV, PTX in blunt trauma on PPV, see references above) that PTX can be managed conservatively on PPV, you feel that this child’s 20% PTX can only get worse on a ventilator, and you decide to place a chest tube in the ED to ensure a safe and stable transfer. You perform an emergent needle decompression (with minimal air output) followed by placement of a chest tube in the right side of the chest. There is some improvement in O2 sats (85%) and systolic BP come back up to 95. You repeat a CXR (findings shown):

click to enlarge
click to enlarge

The PTX is gone with a chest tube in situ. The ETT is in satisfactory position. There is persistent atelectasis, mediastinal shift away toward the atelectatic lung, and an opacified right mainstem. You are sure this is compatible with an aspirated airway FB. Transfer to the receiving hospital is arranged.

Transfer goes well and the patient undergoes immediate bronchoscopy in the OR upon arrival. Two pieces of peanut are found in the right mainstem bronchus. Following the procedure the patient does extremely well. When asked about recent choking on peanuts, the parents recall that the prior evening (!) he indeed had a coughing spell while eating some nuts.

A bit on FB aspiration (Hitter et al, Shlizerman et al, Silva et al):

  • Peak age 10-24 months
  • Often misdiagnosed as croup, asthma, pneumonia, bronchiolitis
  • Younger age usually associated with organic matter
  • In absence of choking event, diagnostic delay can be months
  • Most frequent presenting complaint = witnessed choking episode! (initially absent in the case presented here)
  • Complete triad of  (1) cough, (2) wheeze, (3) decreased breath sounds – present in minority of patients
  • Stridor present if FB is in trachea
  • Exam only 56-86% sensitive, 26-72% specific

So what was the delay or confusion in this case for making the diagnosis? Shouldn’t this have been readily apparent when the child was initially assessed? The table below, adapted from Shlizerman et al, demonstrates how poorly history and physical perform in making the diagnosis of an aspirated airway FB.

click to enlarge

Chest X-ray in FB aspiration (Hitter et al, Silva et al, Zerella et al):

  • Sensitivity 62-85%,  Specificity 30-97%
  • FB radio-opaque in <20% of cases
  • Most common finding: air-trapping
  • May also see atelectasis if complete obstruction (Atelectasis present in 12-40% of CXR)
  • Occasionally pneumothorax or pneumomediastinum if bronchi or alveoli perforate/rupture

Depending on the type of obstruction, the findings and CXR features can differ. See the table below (reference Zur and Litman):

click to enlarge


  • lFB in airway may present atypically
  • lIt’s all in the history (somewhere, even if obtained the next day!)
  • lReassess, repeat tests/findings that don’t make sense, and reconsider your diagnosis
  • Traditionally taught that CXR will often lie (not show findings in FB) when history/physical very suggestive
  • This case is an example when the history and physical lie and CXR is your biggest clue

Special thanks to Dr Paul Koblic for his peer review and contributions.


Related links: Scareway Case: What went wrong here?, Scareway Case #2 with Yen and Minh