Pericardial effusion and tamponade complicating treated graves' thyrotoxocosis.

Editor,

Pericardial effusion has been reported in Graves disease. We report a case where symptoms of cardiac failure and the development of a symptomatic pericardial effusion were the predominant manifestations of thyrotoxicosis undergoing treatment.

Case report

A 42 year old lady was admitted with a six-week history of increasing shortness of breath. She described pleuritic chest pain and had recently noticed ankle oedema. She had no symptoms typical of thyrotoxicosis. There was no relevant past medical history. One week before hospitalisation she was found to have markedly elevated thyroid function tests with Free T4 >100 pmol/L (NR 11–21) and TSH <0.02 mU/L (NR 0.3–4.5) and had commenced treatment with Carbimazole (40 mgs od) and Propanolol (80 mgs b.d.).

On admission she was dyspnoeic at rest with a sinus tachycardia. BP was 118/62. Bilateral pitting leg oedema, a small goitre and a right pleural effusion confirmed on chest X-Ray were noted. Biochemically there was continued evidence of hyperthyroidism - FT4 34.9 and TSH <0.02 with positive anti-thyroid peroxidase antibodies; 215 IU/ml (NR 0–135). C-reactive protein (CRP) was raised at 109. An echocardiogram revealed normal left ventricular function and evidence of a small localised pericardial effusion. There was no pericardial tamponade at this time. Following continued treatment with beta-blockers and an increased dose of Carbimazole (60 mgs o.d.) and diuretics the patient's clinical condition improved and she was discharged.

Two weeks later she presented with further respiratory distress and was noted to have a raised venous pressure and a BP of 84/60. Thyroid function tests showed continued improvement. Repeat CXR revealed cardiomegaly (Figure 1). Repeat echocardiogram demonstrated a large pericardial effusion (Figure 2). The patient was transferred to the regional cardiology centre where 275mls of blood stained fluid was drained from the pericardial space with immediate improvement in dyspnoea and blood pressure. Biochemically the fluid was an exudate; culture and cytology were negative. Following this she remained well.

Fig 1

CXR on admission (left) showing a small pleural effusion and normal cardiac shlhouette. Repeat film 2 weeks later (right) showing appearances in keeping with a pericardial effusion

Fig 2

Repeat echocardiogram confirming large pericardial effusion (arrowed).

Conclusions

This case shows that pericardial effusion resulting in tamponade can develop in Graves thyrotoxicosis even during anti-thyroid treatment and with improving thyroid function tests.

A Medline search over the last twenty years uncovered two other reports of similar cases in English journals with a further report in a Japanese journal1–4. Authors from Oxford described a series of four patients all presenting with chest pain and effusions as the predominant manifestation of otherwise occult Graves' thyrotoxocosis.2 The most recent case report from Israel3 describes a patient who developed a pericardial effusion despite treatment of hyperthyroidism. In this case tamponade did not develop and pericardiocentesis was not required. The aetiology of these complications is unclear although the blood stained nature of the pericardial effusion and the preceding pain and raised CRP suggests an inflammatory pericarditis. We therefore suggest it would be prudent to exclude Graves' thyrotoxicosis in any patient presenting with an unexplained pericardial effusion despite the absence of classical symptoms of thyrotoxicosis. Furthermore, in a patient with active Graves' disease, symptoms such as chest pain and dyspnoea need to be considered as potentially heralding the development of cardiac tamponade. While this complication is rare it may be rapidly fatal and thus go unrecognised and unreported.