A 79-year-old Caucasian man with initial diagnosis of vascular dementia was admitted to the old age psychiatric unit on 3rd November 2009. He experienced several falls, developed vivid visual hallucinations, increase paranoia and fluctuating mental/cognitive state, he was extremely sensitive to antipsychotic medication and the possibility of Lewybody dementia was also considered. He was already taking Quetiapine 25 mg due to visual and auditory hallucinations and behavioural problems with little effect and wasn't able to tolerate increase dose. His medical history included ischaemic heart disease, atrial fibrillation, congestive heart failure, coronary artery bypass in 2001, pacemaker in 2004, stroke in 2006 and eczema. He was receiving the following long-term medications, simvastatin, lansoprazole, furosemide, aspirin, warfarin, bisoprolol, candesartan and quetiapine.
His pretreatment blood tests showed stable INR within target range (2–2.5). Other blood tests were also non-significant.
As the patient remained unsettled and became increasingly paranoid and distressed using antidementia drug to alleviate his symptoms as well as tapering of antipsychotics in longer term was considered. Rivastigmine transdermal patch 4.6 mg was commenced on 11th November 2009. It was noted that he developed mild subconjunctival haemorrhage on 17th November 2009 with no bleeding from any other parts of the body. He didn't sustain any fall and his blood pressure remained stable so it was felt that subconjunctival haemorrhage could be spontaneous occurrence and bloods were checked next morning for INR. On 18th November 2009 blood test revealed slight increase of INR upto 3.2. Based on the INR results he was given relatively lower doses of Warfarin. On 20th November 2009 it was noted that the degree of subconjunctival haemorrhage had increased and was covering whole conjunctiva of left eye, INR was checked on the same day and showed increase upto 4.4.
At this stage we liaised with haematologist, ophthalmologist and cardiologist. We with held Aspirin and Warfarin. Rivastigmine transdermal patch was the only recent additional medication and was therefore discontinued. Three days later INR was 2.4 within target range and Warfarin was recommenced. Subconjunctival haemorrhage also resolved within 10 days.
Findings of high INR and subconjunctival haemorrhage appeared to be unrelated to other causes because of the following reasons:
- Patient was taking combination of Warfarin and Aspirin since 2006 with stable INR within target range, on the particular regimen of Warfarin dosage prior to the commencement of rivastigmine transdermal patch.
- There are certain drugs which are known to potentiate the Warfarin's anticoagulant effect, but our patient didn't have any changes apart from rivastigmine transdermal patch and he didn't use any alcohol either.
- There are other causes of increase INR but we excluded other causes such as liver disease, haemodilution, transfusion, disseminated intravascular coagulation, heparin.
- It was the subconjunctival haemorrhage that led our attention towards clotting profile, although subconjunctival haemorrhage can occur spontaneously, more common in older people, can occur with bouts of sneezing and coughing, due to head injury or injury to eye, high blood pressure, blood dyscrasias or if taking Warfarin.
- But we believe in our patient subconjunctival haemorrhage could be the manifestation of high INR. It could be merely due to drug therapy (Warfarin) or spontaneous as patient didn't have any head or eye injury, his blood pressure remained stable on frequent checks and he didn't have any bouts of coughing or sneezing.