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
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:
As interpreted by your radiologist at Canadian Janus:
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):
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.
- 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.
- 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):
- lFB in airway may present atypically
- It’s all in the history (somewhere, even if obtained the next day!)
- Reassess, 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.
- Enderson et al. J Trauma. (1993) 35(5): 726-729
- Hitter et al. Int J of Ped Otorhinolaryngol (2007) 71: 1897—1903
- Kirkpatrick et al. J Trauma Acute Care Surg. (2013) 74(3):747-54
- Litmanovitz and Carlo. Pediatrics. (2008) 122(5) e975-979
- Shlizerman et al. Amer. J. Otol-Head and Neck Med and Surg (2010). 31:320-342
- Silva et al. Annals of Otol Rhinol Laryngol. (1998) 107:1998
- Stack. Chapter 15 “Cyanosis”. Textbook of Pediatric Emergency Medicine. (2010)
- Zerella et al. J Ped Surg. (1998) 33:1651-1658
- Zur and Litman. Ped Anesth. (2009) 19 (supp.1): 109-117