Case 27 by Lawrie Kidd

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A 38 year old man is admitted for drainage of a symptomatic malignant right sided pleural effusion. Using ultrasound guidance, 2.5 litres are drained. The drain is removed and the patient left the radiology suite for the ward with a plan for subsequent discharge.

An Intensive Care review is requested because over the next few hours he becomes increasingly tachycardic and short of breath.

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One examination:

A – Patent

B – Tachypnoeic (25/min).

Increased work of breathing.

Talking in short sentences.

Saturations 94% on 6L/min (Hudson mask).

Symmetrical chest movement.

Crepitations audible at right lower/mid zone.

Right slightly dull to percussion.

C – Tachycardic (100 bpm). Clinically regular pulse. Peripherally cool. JVP not elevated. BP 95/65.

D – Orientated. Feels scared and struggling with breathing.

What is going on?

[/toggle] [toggle title=”1st CXR” id=”tgl-3″] [az_lightbox_image_sh image_url=”https://intensivecarenetwork.com/wp-content/uploads/2016/01/XRAY-CHEST-0001.jpg” thumb_width=”” title=”” gallery_name=”” class=””]With permission from the patient[/toggle] [toggle title=”2nd CXR” id=”tgl-4″] [az_lightbox_image_sh image_url=”https://intensivecarenetwork.com/wp-content/uploads/2016/01/XRAY-CHEST-0002-B.jpg” thumb_width=”” title=”” gallery_name=”” class=””]With permission from the patient[/toggle] [toggle title=”Answer” id=”tgl-5″]

The patient had developed re-expansion pulmonary oedema. He was treated with non-invasive ventilation and intravenous diuretics. Over the next 24 hours he improved significantly and was subsequently discharged out of ICU.[/toggle] [toggle title=”More Info” id=”tgl-6″]

Re-expansion pulmonary oedema (RPO) is a condition that occurs when a collapsed lung re-expands, typically after treatment for pneumothorax or pleural effusion (1). Clinically it presents in a manner typical of this patient i.e. rapid onset tachypnoea and dyspnoea. Hypotension and cardiovascular collapse can also occur, with a mortality estimated to be as high as 20% in one case series (2).

It was first described following drainage of a large volume pleural effusion in 1853 (3). Incidence of RPO may be as high as 14% (4) although more recent estimates place the incidence at less than 0.1% (5). Radiological incidence, in the absence of clinical signs may be considerably higher (6).

Risk factors for RPO are felt to include the volume drained (7)although some discrepancy exists within the literature (8). Nonetheless, BTS Guidelines err on the side of caution and suggest an upper limit of 1.5L (9). Other risk factors include younger age (2) and speed of re-expansion (10). As such, it is recommended that intercostal drains are not placed on suction, at least not initially (9).

The treatment of RPO is largely supportive, using positive-pressure ventilation, which if required can be invasive. This is felt to reduce shunting, re-expand collapsed alveoli and increase functional residual capacity (1). Other mainstream treatment modalities described include the use of diuretics and steroids (4,8). The use of differential lung ventilation has been described in a case where traditional methods had proved unsuccessful (11).

The pathophysiology of RPO is unclear. The endpoint is a re-expansion of the lung and the reversal of hypoxic pulmonary vasoconstriction, followed by an increase in the permeability of endovascular cells which in turn leads to pulmonary oedema (12). The return of reactive oxygen species and lipid and polypeptide mediators may lead to endothelial damage (12). Other pro-inflammatory cytokines including IL-8 and monocyte chemoattractant protein 1 have also been implicated (1).

A direction of future research may be the role of xanthine oxidase inhibitors (e.g. Allopurinol) that have been shown to prevent the xanthine oxidase-induced endothelial damage demonstrated to be associated with lung re-expansion (13).

References

Neustein, SM. (2007). Reexpansion pulmonary edema. J Cardiothorac Vasc Anesth, 21(6), 887-891.
Mahfood S., Hix WR., Aaron BL, Blaes P, Watson DC. (1988). Reexpansion pulmonary edema. Ann Thorac Surg, 45(3), 340-345.
H. Pinault. Considérations cliniques sur la thoracentèse. (1853) [doctoral thesis]. Paris.
Matsuura Y, Nomimura T, Murakami H, Matsushima T, Kakehashi M, Kajihara H. (1991). Clinical analysis of reexpansion pulmonary edema. Chest Journal, 100(6), 1562-1566.
Ault MJ, Rosen BT, Scher J, Feinglass J, Barsuk JH. (2015). Thoracentesis outcomes: a 12-year experience. Thorax, 70(2), 127-132.
Taira N, Kawabata T, Ichi T, Yohena T, Kawasaki H, Ishikawa, K. (2014). An analysis of and new risk factors for reexpansion pulmonary edema following spontaneous pneumothorax. J Thorac Dis, 6(9), 1187.
Josephson T, Nordenskjold CA, Larsson J, Rosenberg LU, Kaijser M. (2009). Amount drained at ultrasound-guided thoracentesis and risk of pneumothorax. Acta Radiologica, 50(1), 42-47.
Feller-Kopman D, Berkowitz D, Boiselle P, Ernst A. (2007). Large-volume thoracentesis and the risk of reexpansion pulmonary edema. Ann Thorac Surg, 84(5), 1656-1661.
Roberts ME, Neville E, Berrisford RG, Antunes G, Ali NJ. (2010). Management of a malignant pleural effusion: British Thoracic Society pleural disease guideline 2010. Thorax, 65(Suppl 2), ii32-ii40.
Sherman SC. (2003). Reexpansion pulmonary edema: a case report and review of the current literature. J Emerg Med, 24(1), 23-27.
Cho SR, Lee JS, Kim. (2005). New treatment method for reexpansion pulmonary edema: differential lung ventilation. Ann Thorac Surg, 80(5), 1933-1934.
Sivrikoz MC, Tunçözgür B, Bakir K, Meram İ, Koçer E, Cengiz B, Elbeyli L. (2002). The role of tissue reperfusion in the reexpansion injury of the lungs. Eur J Cardiothorac Surg, 22(5), 721-727.
Saito S, Ogawa J, Minamiya Y (2005). Pulmonary reexpansion causes xanthine oxidase-induced apoptosis in rat lung. Am J Physiol Lung Cell Mol Physiol, 289, L400–L406.