A support carer requested a home visit on behalf of her client, who is a-82-year Caucasian lady living alone. Three days previously, in the presence of the support carer, she had had acute symptoms last 15 minutes during which she was alert but disorientated, could not express her speech, and afterwards found that writing had become difficult. There was no loss of consciousness and neither was there any weakness or paraesthesia in any of her limbs. She improved over a few hours, and on the day of the visit, she felt as if she was back to normal. She diagnosed herself as having had a transient ischaemic attack.
On closer questioning, she explained that for several years she had been on prednisolone for her eye problems (temporal arteritis) and 2 weeks previously this drug had been stopped after a period of reduction in the dose under GP supervision. She had been keen to come off them as she had suffered from dyspeptic symptoms.
On the day of the visit, her clinical examination was unremarkable, with the exception of a blood pressure measurement of 160/80. However her home BP recordings were in normal range. She is right handed, was alert and orientated, and her specific cardiac (e.g. sinus rhythm, no murmurs or carotid bruits) and neurological system (e.g. speech, power, writing) examinations were normal. There was no temporal artery tenderness.
Past medical history from her clinical records showed that she had been diagnosed in October 2005 with ischaemic heart disease (IHD) on the basis of atypical chest symptoms and an abnormal ECG showing inferior ischaemic changes. Her initial treatment for this was nitrolingual spray and aspirin, but she had refused a statin. In November 2006, she presented with visual symptoms and pain in her jaw and an ESR of 36, and was commenced on oral steroid with a provisional diagnosis of temporal arteritis. She responded well with resolution of her symptoms to this initial treatment, but in early 2007 wanted to reduce her dose of prednisolone because of dyspeptic symptoms. However some of symptoms returned and she was referred to the ophthalmology service for further confirmation of the diagnosis. Her temporal artery biopsy result came back as showing 'inflammatory changes' and together with her symptoms including the partial loss of vision in her left eye; she was given a formal diagnosis of TA and recommended to continue the prednisolone. To this treatment, she was given a proton inhibitor, and by now she had stopped using her nitrolingual spray.
She was married but had no children, never smoked and always been tea-total. She retired as a book-keeper many years ago and has carer support because of mobility problems, but she was ambulant around her house.
Based on her clinical history a diagnosis of transient ischaemic attack secondary to withdrawl of treatment for temporal arteritis was made, and with her agreement prednisolone 30 mg daily was re-commenced. Follow up at 1 week was arranged to consider referral for TIA clinic depending on her symptoms and blood results. During the home visit, routine blood samples were collected, which were later reported as an ESR of 27 and random cholesterol of 5.4.
Her clinical records were reviewed 2 weeks after the first visit, and showed that she had had no further symptoms, a referral to TIA clinic and simvastatin treatment had been offered, but both options were refused. Her prednisolone dose was now down to a maintenance dose of 7.5 mg daily.