4 Austin JL, Preis LK, Crampton RS, et al. Analysis of pacemaker malfunction and complications of temporary pacing in the coronary care unit. Am J Cardiol 1982;49:301-6.

5 Winner S, Boon N. Clinical problems with temporary pacemakers prior to permanent pacing. J R Coll Physicians Lond 1989;23:161-3.

6 Hynes JK, Holmes DR Jr, Harrison CE. Five-year experience with temporary pacemaker therapy in the coronary care unit. Mayo Clin Proc 1983;58:122-6.

7 Jowett NI, Thompson DR, Pohl JE. Temporary transvenous cardiac pacing: 6 years experience in one coronary care unit. Postgrad Med J 1989;65:211-5.

8 ACP/ACC/AHA Task Force on Clinical Privileges in Cardiology. Clinical competence in insertion of a temporary transvenous ventricular pacemaker. J Am Coll Cardiol 1994;23:1254-7.

9 Medical Practice Committee and Council of the British Cardiac Society. Choice of route for insertion of temporary pacing wires: recommendations of the Medical Practice Committee and Council of the British Cardiac Society. Br Heart J 1993;70:592.

10 Hildick-Smith DJ, Petch MC. Temporary pacing before permanent pacing should be avoided unless essential. BM/ 1998;317:79-80.

11 Madsen JK, Meibom J, Videbak R, et al. Transcutaneous pacing: experience with the Zoll noninvasive temporary pacemaker. Am Heart J 1988;116:7-10.

12 Ferguson JD, Banning AP, Bashir Y. Randomised trial of temporary cardiac pacing with semirigid and balloon-flotation electrode catheters. Lancet 1997;349:1883.

13 Petch MC. Temporary cardiac pacing. Postgrad Med J 1999;75:577-8.

IMAGES IN MEDICINE

Cushing’s syndrome due to an adrenocortical carcinoma

Figure 1 Abdominal computed tomography showing left adrenal tumour.

A 46 year old woman presented with a short history of hirsutism, facial plethora, amenorrhoea, progressive weight gain, and hypertension. Cushing’s syndrome was suspected and confirmed biochemically. Urine free cortisol concentrations measured as cortisol/creatinine ratios on two successive 24 hour urine collections were raised at 80 and 169 nmol/mmol respectively (reference range 5-55).

High dose dexamethasone suppression test was done (dexamethasone 2 mg orally every six hours for 48 hours). Basal serum cortisol was 599 nmol/l and failed to suppress after 48 hours, remaining raised at 555 nmol/l. This was suggestive of primary adrenal disease as cortisol levels normally suppress to less than 50% of basal levels in pituitary driven Cushing’s disease. Serum testosterone was raised at 7.2 nmol/l (0.5-2.6). Urinary catecholamine levels were normal. The short history and raised testosterone level was suggestive of an adrenal carcinoma. Abdominal computed tomography showed a large left adrenal tumour with central necrosis and no evidence of metastases (see fig 1). An adrenal carcinoma was subsequently completely resected.

Primary adrenal tumours are responsible for about 10% of cases of Cushing’s syndrome. Adrenocortical carcinomas are uncommon with an incidence of 2 per million per year and occur more commonly in women. Raised androgen levels in Cushing’s syndrome are suggestive of malignant adrenal tumours.

Adrenal carcinomas are rapidly progressive and have usually metastasised to the lungs and liver at diagnosis. Mitotane, an isomer of the insecticide DDT, has been used as adjunctive therapy to treat metastatic disease.

S Nag, A McCulloch

Department of Endocrinology, Bishop Auckland General Hospital, Cockton Hill Road, Bishop Auckland, Co Durham DL 14 6AD, UK; s.nag@btopenworld.com