Analgesics and anti-inflammatories
Aspirin, non-selective nonsteroidal anti-inflammatory drugs (NSAIDs) and the cyclooxygenase-2 (COX-2) inhibitor celecoxib have two main oedema-causing effects. The first is to inhibit the prostaglandin PGI2 arteriole vasodilatation effects. The second is interfering with prostaglandin E2 (PGE2) activity in the kidney meaning sodium and water is reabsorbed, rather than excreted.15
Corticosteroids promote sodium retention due to mineralocorticoid effects. Ordinarily, corticosteroids can be useful for controlling oedema and inflammation, such as with cerebral oedema, with anti-inflammatory and immunosuppressant activity. For some, however, oedema side effects will start to emerge above a specific threshold dose level.4,15,20
Mineralocorticoids increase sodium and fluid retention even though healthy kidneys can spontaneously increase diuresis to rebalance fluid level, relieving oedema. Fludrocortisone has the most mineralocorticoid activity, while dexamethasone, betamethasone and methylprednisolone have minimal mineralocorticoid activity.4,21,22
The muscle relaxant baclofen can increase oedema likelihood through several actions. It can increase capillary permeability (especially alongside alcohol), and GABA receptor activity can promote vasodilatation and reduce the vascular reflex to pressure changes.15
Oedema due to opioids can arise due to increased capillary effects.15