Dr David McCreary
Emergency Physician
Peer review:
Dr Mike Khoury

The Case
A 60-year-old female presents to the Emergency Department with progressive shortness of breath over several months. On assessment in the emergency department, she had marked shortness of breath at rest and oxygen saturations of 90% on room air. A portable erect chest X-Ray was performed.



How would you describe this X-ray?
What has caused these changes?
- An uncommon complication following draining of a pneumothorax or pleural effusion
- Incidence is reported between 0.2-14% (according to the British Thoracic Society), though most reports seem to be <1%
Let’s level-up on Re-Expansion Pulmonary Oedema (RPO)…
Pathophysiology
The pathophysiology of RPO is multifactorial and poorly understood (a great caveat when writing about any condition).
The primary (or at least the easiest) theory is:
- Ventilation and perfusion of collapsed lung
- Leads to a dramatic inflammatory response
- Causes increased permeability of pulmonary capillaries
One can think of this as a type of reperfusion lung injury.
Risk Factors
- Age 20-40 years
- Duration of lung collapse >72 hours
- Application of negative pressures (>20cmH2O) during drainage
- Rapid, large-volume drainage (>1.5L fluid)
You can’t do much about their age, but you can take the other factors into consideration when draining.
Clinical Features
Pretty much all the symptoms of severe/flash pulmonary oedema, but <24 hours post pleural drainage
- Chest discomfort
- Cough
- Frothy sputum
- Dyspnoea
- Hypoxia
- Marked work of breathing
OK, pulmonary oedema management – that’s nitrates and diuretics, right?
Well, no, not in this case. I’ll spare you my rant (for now) about diuretics in flash pulmonary oedema – in the meantime Swami over at EMDocs.net has a pretty concise explanation here. Generally speaking, flash APO patients haven’t been sat at home being given litres of fluid by medical staff so are unlikely to be truly fluid overloaded – their fluid is just in the wrong place. Their problem is with afterload. Oh there I go, and I said I was going to spare the rant…
Nitrates then? Well, as per the above partial-rant ordinarily they are the mainstay of APO treatment. But with RPO there is no evidence for them and they are unlikely to work as we aren’t dealing with afterload physiology here.
So, what does that leave us?
Supportive care:
- The severe cases are likely to need NIV or invasive ventilation (as did the patient from this case)
- Lie the patient with the unaffected side down – this will encourage dependent blood flow to the good lung
- Fluids – rather than diuresis, if anything these patients may need some filling
Prevention is, as they say, better than cure:
- Suction: if you are using negative pressure, keep it below 20cmH2O
- Avoid that completionist temptation and limit draining to 1-1.5L
- If patient reports vague chest pressure this may a sign of precipitous drop in intrapleural pressure so thoracocentesis should be stopped
Any guidelines on this?
Why yes, the BTS 2010 guideline says thoracocentesis should be stopped when:
- No more fluid or air can be aspirated (that’s a given, no?)
- The patient develops cough or chest discomfort
- 5L has been withdrawn
There are descriptions of 3-6.5L being drained without issue, but the guidelines are more conservative due to the reportedly terrible mortality of RPO (up to 20%).
This best-evidence review does suggest that patients with no respiratory symptoms could drain larger volumes to dryness, with caution to avoid negative intrathoracic pressures. I’d say that’s something for a risk/benefit, case-by-case decision.
But wait, my patient clearly has a lot more than 1.5L fluid – what do I do with the rest?
The BTS guideline briefly comments that in the case of pleural effusions, the amount drained in the first hour should be a maximum of 1.5L. After an hour the remaining fluid can be drained off slowly.
If in doubt, contact your friendly neighbourhood respiratory team for advice.
And while we’re talking pleural fluid – particularly for the exam-sitters out there…
How do you categorise the causes of pleural effusion?
- Think: heart failure / atelectasis / hepatic hydrothorax / hypoalbuminaemia / nephrotic syndrome
Exudate: an alteration of local factors precipitating fluid collection
- Think: malignancy / ARDS / Pancreatitis / Empyema / Sarcoidosis
- Exudate = Excess Protein
What criteria do we use to determine if fluid is exudate?
- Pleural fluid protein / Serum protein >0.5
- Pleural fluid LDH / Serum LDH >0.6
- Pleural fluid LDH > 2/3 of the upper limit of normal for serum LDH
Yes, it’s worth memorising those if you are sitting exams. For everyone else, there’s always MDCalc.
Remember, this post isn’t to discourage you from draining symptomatic effusions – but let it give you pause for thought and hopefully have you prepared in case RPO happens on your watch. That’s all for now.
– Dave
References / Further Reading:
- The 2010 BTS Thoracocentesis Guideline
- This best evidence topic: Does re-expansion pulmonary oedema exist? (Spoiler: they conclude yes, but rarely).
- This case report with brief review of RPO
- MDCalc’s Light’s Criteria calculator
- Anand Swaminathan’s discussion of furosemide for APO on emDocs.net – read this and save yourself my rants

David McCreary
Emergency Fellow, Alfred Health