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Orthostatic Hypotension in an Elderly Patient

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Orthostatic Hypotension in an Elderly Patient Self-assessment corner 685 the first 4-5 years of life. However, early severe insulin resistance states. Metformin and closure ofthe epiphyses leads to a reduced final thiazolidinedione have been tried with variable height. Hyperlipidaemia may result in pancrea- results in some patients with Type B insulin Postgrad Med J: first published as 10.1136/pgmj.74.877.685 on 1 November 1998. Downloaded from titis. Polycystic ovarian syndrome with hyper- resistance syndrome.5 Insulin-like growth androgenism and irregular menses has been factor-i, a member ofthe proinsulin family, also reported.' 2 The syndromes of partial lipodys- seems to hold promise in the treatment ofsevere trophy include face-sparing lipodystrophy and insulin-resistant states.6 Topical application of cephalothoracic lipodystrophy (box 1). tretinoin cream or gel has been found to be use- The pathophysiology of these disorders is ful in controlling acanthosis nigricans.7 Virilisa- poorly understood. The currently debated theo- tion features may require spironolactone, or ries are listed in box 2. The other insulin- resist- low-dose cyproterone or oral contraceptive pills. ant states are tabulated in box 3. No therapeutic agent has been shown to be uniformly effective Final diagnosis in treating insulin resistance. The diabetic state requires high dosages (sometimes thousands of Adult-onset acquired generalised lipodystro- units per day) of insulin. When very high doses phy with insulin resistance. are needed U500 preparations may help cut down the volume ofinjection. Insulin-sensitizing Keywords: lipodystrophy syndromes; wasting; diabetes agents may have a role in the treatment of the mellitus 1 Braimon JC, Moller DE. Hereditary and acquired syn- 5 Di Paolo S. Metformin ameliorates extreme insulin dromes of severe insulin resistance. In: Pickup J, William G, resistance in a patient with anti-insulin receptor antibodies: eds. Textbook ofdiabetes. Oxford: Blackwell Science, 1997; pp description of insulin receptor and post receptor effects in 26.1-15. vivo and in vitro. Acta Endocrinol 1992;126:1473-90. 2 Flier JS. Syndromes of insulin resistance and mutant 6 Morrow LA, O'Brien MB, Moller DE, Flier JS, Moses insulin. In: de Groot U, Besser M, Burger HG, et al, eds, AC. Endocrinology. Philadelphia: WB Saunders Company, 1995; Recombinant human insulin-like growth factor-I therapy pp 1592-604. improves glycemic control and insulin action in the Type A 3 Lawrence RD. Lipodystrophy and hepatomegaly with syndrome of insulin resistance. J Clin Endocrinol Metab diabetes, lipidaemia, and other metabolic disturbances. A case 1994;79:205-10. throwing new light on the action of insulin. Lancet 7 Moses AC, Abrahamson MJ. Therapeutic approaches to 1946;1:724. insulin resistance. In: Moller DE, ed. Insulin resistance. 4 Seip M. Lipodystrophy and gigantism with associated endo- Chichester: John Wiley and Sons, 1993; pp 385-410. crine manifestations: a new diencephalic syndrome? Acta Paediatr 1959;48:555-74. Orthostatic hypotension in an elderly patient L Allcock, C Polack, D O'Shea, P McKenna, D O'Shea http://pmj.bmj.com/ Department of An 81-year-old woman was admitted following a collapse. She described feeling progressively Medicine, North dizzy and faint for several weeks prior to admission. Five years previously she had undergone Tyneside Health Care oophorectomy and pelvic clearance for ovarian carcinoma. She had a history ofhypertension and NHS Trust, North ischaemic heart Tyneside General disease. Medications on admission were: isosorbide mononitrate 10 mg bid, on September 26, 2021 by guest. Protected copyright. Hospital, North methotrimeprazine 25 mg bid, fluoxetine 20 mg od, amitriptyline 50 mg nocte, aspirin 150 mg Shields, Tyne & Wear od, amiodarone 100 mg od, frusemide 80 mg od, and megestrol 160 mg od. NE29 8NH, UK Examination was unremarkable other than an orthostatic drop in blood pressure from 113/69 L Allcock mmHg lying to 83/50 mmHg on standing with postural-related dizziness. Her full blood count, C Polack electrolytes, urea, creatinine and glucose were all normal. A baseline cortisol (09.00 h) was < 50 D O'Shea nmol/l, with an P McKenna adrenocorticotropin (ACTH) level of 16 ng/l (reference range < 47). A short syn- acthen test confirmed adrenal insufficiency with a baseline cortisol of < 50 nmol/l and a peak of Department of 220 nmol/l at 30 minutes. Pituitary hormone profile showed gonadotropin levels to be suppressed Endocrinology, with luteinising hormone 0.1 IU/1, and follicle-stimulating hormone 0.7 IU/1, while her prolactin Charing Cross was 220 mU/l (60-600). Thyroid function tests showed a free thyroxine of 16.8 pmol/l (9.8-23.1) Hospital, and a thyroid-stimulating hormone of 2.6 mU/l (0.35-5.5). An autoantibody screen was negative. Hammersmith CA-125 levels of 7 kU/l Hospitals NHS Trust, (0-35) and 171-OH-oestradiol below the working range ofthe assay sug- London W6 8RF, UK gested that she did not have recurrence of an oestrogen-secreting, epithelial ovarian carcinoma. D O'Shea Computed tomography (CT) scan of the brain and pituitary was normal and a CT scan of the abdomen and pelvis demonstrated normal adrenal glands, with no evidence of recurrence of the Correspondence to ovarian tumour. Dr D O'Shea, Department of Medicine, Royal Victoria Infirmary c/o Ward 15 Questions Offices, Queen Victoria Road, Newcastle 1 What are the Upon-Tyne, NE 1 4LP, UK potential causes of this patient's orthostatic hypotension? 2 What is the most likely cause ofher impaired hypothalamic-pituitary-adrenal (HPA) function? Accepted 23 April 1998 3 What treatment would you advise for her orthostatic hypotension? 686 Self-assessment corner Answers not necessary for the electrolytes to be disturbed or the random cortisol to be below normal for Postgrad Med J: first published as 10.1136/pgmj.74.877.685 on 1 November 1998. Downloaded from QUESTION 1 significant adrenal insufficiency to be present. Orthostatic hypotension has many causes (box 1), however, in this woman, the major contrib- QUESTION 3 uting factor is likely to be her medication. Iso- Initial therapy should revolve around omitting sorbide mononitrate, methotrimeprazine, ami- culprit medications and a trial of non- triptyline or frusemide may each cause pharmacological methods, including instruct- orthostatic hypotension directly. Megesterol, a ing the patient to get up in stages from lying synthetic progesterone, can also cause suppres- supine, exercises involving dorsiflexion of the sion ofthe HPA axis and, in the face of a physi- feet prior to standing which may enhance cal challenge, hypoadrenalism with orthostatic venous return, increase the heart rate and hypotension. As in this case, identifying the increase blood pressure. In the absence of a precipitating event in an elderly patient is not history of cardiac failure, salt intake could be always possible. increased. Elastic/support stockings may help, and elevating the head of the bed 5 to 20 degrees may prevent nocturnal diuresis. On the assumption that the orthostatic hypotension in this patient was drug related, the methotrime- Causes oforthostatic hypotension prazine and isosorbide mononitrate were stopped, and the doses of frusemide and Primary amitriptyline halved. Her symptoms and pos- * pure autonomic failure - idiopathic * Shy-Drager syndrome: with parkinsonian tural hypotension persisted. features, with cerebellar and pyramidal features, Following the result of the short synacthen or with multiple system atrophy (combination of test the patient was commenced on hydrocorti- above) sone 5 mg tid. At follow-up, her orthostatic Secondary hypotension and dizziness had resolved and her * general medical disorders, eg, diabetes, amyloid, weakness and fatigue had improved. The meg- alcoholism esterol was stopped and 6 weeks later she was * autoimmune disease, eg, systemic lupus symptom free with a subsequent baseline erythematosus, rheumatoid arthritis, cortisol of 519 nmol/l off the hydrocortisone. Guillian-Barre In view of the symptomatic improvement * carcinomatous autonomic neuropathy and * metabolic disease, eg, porphyria, B,2-deficiency recovery in baseline cortisol a further syn- * hereditary sensory neuropathies acthen test was not considered necessary. * central nervous system infectious disease, eg, herpes zoster, syphilis Discussion * central brain lesions, eg, vascular, tumours, multiple sclerosis, Wernicke's encephalopathy Megestrol is a * spinal cord lesions synthetic progesterone most fre- * renal failure quently used as a second-line agent in the * aging treatment ofbreast cancer, endometrial cancer, hypernephromas and prostatic carcinoma. http://pmj.bmj.com/ Drugs, including representatives from Synthetic progestagens have * selective neurotoxic drugs, eg, alcohol may beneficial * tranquilizers, eg, phenothiazines, barbiturates effects on survival' and increase appetite in * antidepressants, eg, tricyclics, monoamine patients with anorexia and advanced malig- oxdase inhibitors nancies. In the UK over 100 000 prescriptions * vasodilator hypotensive drugs, eg, prazosin, were written for megesterol in 1996 and it is hydralazine estimated that 12 500 new patients begin treat- * centrally acting hypotensive drugs, eg, ment each on September 26, 2021 by guest. Protected copyright. methyldopa, clonidine year. These numbers are likely to * adrenergic neurone blockers, eg, guanethidine increase with its evolving use in patients with * adrenergic blockers, eg, phenoxybenzamine, AIDS-associated cachexia.' labetalol While side-effects of high-dose
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