Blurred vision
BMJ 2006; 332 doi: https://doi.org/10.1136/sbmj.0605196 (Published 01 May 2006) Cite this as: BMJ 2006;332:0605196
A 76 year old right handed man presented to the accident and emergency department with blurred vision. It had developed 24 hours previously and was first noticed while he was watching television. The previous morning he had woken with a frontal headache, which was still present. He did not have any neck stiffness, other neurological symptoms, or loss of consciousness. The patient's medical history included a hernia repair, mild hypertension, and atrial fibrillation. He was taking warfarin 5 mg and amlodipine 5 mg for mild hypertension. At presentation, the patient was not in atrial fibrillation and was alert and conscious. Results of neurological and other examinations were normal apart from the presence of left contralateral homonymous hemianopia. Pupillary responses were preserved with no loss of visual acuity. Blood pressure was 160/100 mmHg and the international normalised ratio (INR) was 5.8. Results of other investigations were normal. Computed tomography of the head was requested.
Questions
What abnormalities are seen on the computed tomogram of the head?
What are the differential diagnoses and the sites of possible lesions for his visual field abnormality?
What is the diagnosis in this patient?
Why was he taking warfarin ?
What is the line of management in this patient?
Answers
The computed tomogram shows a bright (hyperdense) area—that is, an area of high attenuation—consistent with fresh blood in the right occipital lobe with no associated mass effect and a normal ventricular system. Diffuse whitematter changes suggest pre-existing cerebrovascular disease.
The differential diagnoses for left contralateral homonymous hemianopia include haemorrhagic or ischaemic stroke in the right occipital lobe supplied by the posterior cerebral artery, a parapituitary lesion affecting the right optic tract, or destruction of the whole right optic radiation. 1 Glioma, meningioma, abscess, arteriovenous malformation, and drugs (for example, ciclosporin) can all affect the visual cortex and cause field defects.
The patient has an intracerebral haemorrhage in the right occipital lobe associated with a moderately raised INR secondary to warfarin treatment for atrial fibrillation. The INR is the ratio of a patient's prothrombin time to that of a normal control. It is used to monitor the level of anticoagulation and to determine the dosage of anticoagulant required to attain a target INR, as recommended by the British Society for Haematology, for a specific indication.2
Thromboembolic stroke is associated with atrial fibrillation and is due to atrial thrombus formation resulting from ineffective atrial contraction.3 Oral anticoagulant treatment with warfarin reduces the risk of ischaemic stroke in patients with atrial fibrillation, and this treatment is therefore recommended for these patients. 3 The aim is to achieve an INR between 2 and 3.3 Oral warfarin is preferable to heparin for long term anticoagulation treatment because heparin can be given only intravenously or subcutaneously and it can have side effects such as thrombocytopenia, hypersensitivity reactions (urticaria, angioedema, and anaphylaxis), and osteoporosis after prolonged use.4 Heparin, like warfarin, is also associated with the risk of haemorrhage.4
Warfarin treatment was stopped and the patient was given vitamin K1 5 mg by slow intravenous infusion to correct his INR. Vitamin K is necessary for the effective production of blood clotting factors. Warfarin acts by interfering with the metabolism of vitamin K in the hepatic cells. The effect of warfarin is therefore antagonised by vitamin K. 4 The INR fell from 5.8 to 1.6 two days later. The patient was monitored for any deterioration in his clinical state, particularly neurological change, and was discharged in a stable condition.
Discussion
The patient's blurred vision was the result of a visual field abnormality following an intracerebral haemorrhage in the right occipital lobe. Blurred vision is a non-specific presenting complaint, and neurological examination and a detailed examination of the eye must be done to ascertain the exact nature of the visual deficit—that is, field loss, loss of acuity, or both. A detailed history, especially medical history and current drug history, give clues towards the diagnosis of intracerebral haemorrhage.
Warfarin and intracerebral bleeding
Warfarin is associated with an increased incidence of intracerebral haemorrhage, with most cases having an INR within therapeutic levels. 56 Increasing the intensity of anticoagulation increases the risk of warfarin related intracerebral haemorrhage.7 Warfarin also increases the risk of death after intracerebral haemorrhage, even at the commonly used therapeutic levels of anticoagulation—that is, INRs between 2 and 3.89 This mortality risk increases with increasing INR.8 Therefore, stringent control of the INR will reduce the risk of warfarin related intracerebral haemorrhage and may also reduce the mortality associated with intracerebral haemorrhage.8
Risk prediction for warfarin related intracerebral bleeding
Warfarin related intracerebral haemorrhage is associated with advancing age (especially over 75 years), cerebrovascular disease, and the intensity of anticoagulation.610 The presence and severity of hypertension may also contribute to the risk. 7 The importance of white matter abnormalities on the computed tomogram, known as leukoaraiosis (rarified white matter), has been highlighted by results from the EAFT and SPIRIT study groups. 11 It appears as increased hypodensity of the white matter on the scan. Leukoaraiosis is often found in elderly people and results from structural changes in small cerebral arteries and arterioles. 11 The fragility of small arteries after these changes predisposes to development of microhaemorrhages, which may then enlarge to clinically manifest haematomas when patients are given oral anticoagulants. 11 Leukoaraiosis is an independent and strong risk factor for major bleeding complications, particularly intracranial, in patients taking anticoagulants because of cerebral ischaemia of presumed arterial origin. 11
Our patient showed diffuse white matter changes on computed tomogram consistent with the presence of pre-existing cerebrovascular disease. Other factors used for risk prediction, as discussed above, applied in his case and led to his increased risk of warfarin related intracerebral haemorrhage and its subsequent occurrence.
Notes
Originally published as: Student BMJ 2006;14:196