Sir, a long-standing patient of our practice, a 77-year-old Afro-Caribbean male who suffered from type II diabetes and hypertension, was undergoing a composite filling, when a slow but progressive swelling started developing around the lips, tongue and buccal mucosa (Fig. 1).

Figure 1
figure 1

Swelling developing around the lips, tongue and buccal mucosa

All treatment was immediately stopped, extra assistance was called and the emergency trolley was deployed. The patient was continually monitored and reassured. We administered chloropheniramine 20 mg and closely monitored him. The medical history was rechecked and he reported no known allergies or history of any other similar swellings. The medication list comprised of Metformin, Amlodipine, Atenolol, Ramipril and Allopurinol. Apart from this the medical history was unremarkable.

The patient was taken to A&E where he was kept on corticosteroids for a further two hours as the swelling started to subside. He was diagnosed as having angiodema secondary to ACE inhibitors. A report was immediately sent back to his general medical practitioner, asking them to change his ACE inhibitor medication. Following on from this there have been no further swellings.

Angiodema secondary to ACE inhibitors is a serious complication and some deaths have even been reported. This type of angiodema is becoming increasingly common for two reasons. The first being that ACE inhibitors are incredibly successful in the treatment of hypertension and congestive heart failure, and secondly due to the rise of life expectancy in Western societies, which has led to more patients with hypertension and congestive heart failure that have been prescribed these drugs. The swelling can be severe and therefore these drugs must always be considered in the medical history, as well as when investigating swellings around the lips, mouth and tongue as quite often they can mimic anaphylaxis type reactions or food allergies.

The angiotensin converting enzyme metabolises bradykinin, a potent vasodilating substance and converts angiotensin I to angiotensin II. Angiotensin II causes vasoconstriction and increases smooth muscle hypertrophy, both of which can lead to an increase in blood pressure. The ACE inhibitor therefore prevents conversion of angiotensin I to angiotensin II thereby lowering arteriolar resistance and increasing venous capacity. This causes extravasation of fluid into the subcutaneous tissues, which produces angiodema. For an unknown reason people of Afro-Caribbean origin are more at risk.

The acute management in these cases involves securing the patency of the upper airway. The next step, depending on the severity, can be the use of medications such as antihistamines, corticosteroids and if needed, adrenaline. In the secondary care setting intubation and surgical intervention may also be required in extreme cases. Long-term management includes changing medication.

Angiodema of the head and neck is potentially a life threatening condition that could quite easily present to the general dental practitioner and needs urgent attention and treatment.