case 2

Published on 24/06/2015 by admin

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Last modified 24/06/2015

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KG presented to a rural base hospital 2 months ago with severe recurrent epistaxis associated with easy bruising of 3 weeks’ duration. He denied any other mucosal bleeding or symptoms of anaemia. On investigation, he was diagnosed with idiopathic thrombocytopenic purpura (ITP) and initially treated with high-dose oral corticosteroids for 2 weeks. Despite treatment, his platelet count failed to recover and his symptoms persisted. He denied any steroid-associated side effects such as weight gain, insomnia, mood swings or oral candidiasis during this period. He had further investigations, including a bone marrow biopsy, and the diagnosis was not altered. He was then transferred to a hospital in the city for further treatment with intravenous normal immunoglobulin and plasmapheresis. The response to this treatment was suboptimal. At this point it was decided to carry out therapeutic splenectomy, which he is currently awaiting. Meanwhile he is managed on prednisolone 35 mg daily. He still experiences occasional epistaxis and skin bruising, but it is less severe than at presentation.
He had an acute myocardial infarction 3 months ago, from which he has made an uneventful recovery. Follow-up coronary angiography revealed the existence of double-vessel coronary disease and he is managed on medical anti-ischaemia therapy. He denies any ongoing angina or dyspnoea. He is currently on atenolol 50 mg daily, enalapril 10 mg mane and topical nitrate 25 mg 8 am to 8 pm daily. He denies any side effects associated with this therapy. He has the following risk factors for ischaemic heart disease: male sex, a past smoking history of 40 pack-years (he gave up smoking 4 weeks ago) and hypertension.
He was diagnosed with hypertension 9 years ago and has been managed on different medications. He is currently on amlodipine 5 mg twice daily and denies having any side effects associated with this medication. His general practitioner monitors his blood pressure, but not regularly. He has been told that his blood pressure is well controlled.
He denies any risk-prone behaviour for HIV infection.
His current medications in summary are atenolol, enalapril, nitrate patch, amlodipine and prednisolone. He is not on any therapeutic agent that is known to cause thrombocytopenia. He has no known allergies.
KG’s family history is unremarkable for any significant medical condition. His father died at the age of 87 and mother at the age of 84, and he is not aware of the causes of their deaths. His brother, aged 57, is well.
He worked as a clerk and is currently retired on an age pension, which is barely adequate to meet his and his wife’s needs.
KG is from a rural town more than 1000 km from the city, where he lives with his wife, aged 60. His wife is well. They have been married for 40 years and have two daughters, aged 37 and 40, both well, married, and living separately but still in the same town.
He is independent with his activities of daily living. He sees his GP only rarely. He lives in a house with two steps at the entrance and has no difficulty negotiating these.
The dietary history reveals satisfactory nutrition and he denies any problems with sleep. He consumes alcohol only on social occasions (less than 40 g per week).
While in hospital in the city for the past 2 weeks, only his wife has been visiting him. His wife stays at the accommodation facility provided by the hospital.
He has satisfactory insight into his condition.


KG is a moderately obese man. He was alert and cooperative. He was receiving normal saline through an intravenous cannula in his right forearm, the entry site of which appeared inflamed with surrounding erythema, warmth and tenderness.
His respiratory rate was 12 at rest, pulse rate 90 per minute. His blood pressure was 130/85 mmHg and he was afebrile. His estimated body mass index was 30 kg/m3.
He had diffuse non-palpable purpura over the dorsal and ventral aspects of his lower limbs distally and proximally, bilaterally. There were several ecchymoses in the dorsal aspect of his thorax. There was no evidence of mucosal bleeding or conjunctival pallor. His per rectum examination showed no evidence of gastrointestinal bleeding. There was no lymphadenopathy or splenomegaly.
In the cardiovascular examination, the jugular venous pressure was not elevated. His apex beat was palpable in the fifth intercostal space in the mid-clavicular line. The heart sounds were dual and normal. All his peripheral pulses were clearly palpable.
The examination of the respiratory and neurological systems were unremarkable. Surprisingly, there was no proximal muscle weakness.
His abdomen was soft and non-tender and there were no organomegaly or masses. There was moderate abdominal obesity but no purple striae.
Musculoskeletal examination was unremarkable and there was no bony tenderness, including in the vertebral column.
In summary, my impression is of a 64-year-old man presenting with symptomatic idiopathic thrombocytopenic purpura resistant to steroid therapy and necessitating splenectomy. He also has a history of hypertension and his situation is complicated by a recent myocardial infarction.
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