An unusual cause of acute abdominal pain – A case presentation
Department of Colorectal Surgery, Royal Shrewsbury Hospital, Mytton Oak Road, Shrewsbury, UK
BMC Blood Disorders 2006, 6:1 doi:10.1186/1471-2326-6-1Published: 7 April 2006
In 1983, Graham Hughes described a condition of Antiphospholipid Syndrome in which there was a danger of thrombosis. The condition is readily detectable by blood tests and, once diagnosed; the risk of further thrombosis can be significantly reduced by anticoagulation treatments. Affected groups of patients can be distinguished by a specific blood test – the detection of antiphospholipid antibody (Ref-1). Patients with Hughes syndrome have hypercoaguable state with a markedly increased risk of both arterial and venous thrombosis and there is temporal persistence of antibody positivity.
A 44-year-old woman was admitted under the acute surgical "take" with left sided abdominal pain radiating to her back. She had a history of borderline thyrotoxicosis in the early 1990s. She was on etonogestrel-releasing implants for contraception and there was no history of previous deep venous thrombosis. She was very tender, locally, over the left side of the abdomen. Investigations showed haemoglobin of 13.2 g/dl, white cell count of 19.9 10*9/L, and platelets 214 10*9/L with neutrophilia. Amylase and renal function tests were found to be normal. Liver function tests were deranged with Gamma GT 244 u/l (twice normal). An abdominal Ultrasound Scan suggested a possible splenic infarction, which was confirmed by a CT scan of her abdomen. Tests were carried out to investigate the possibility of a post thrombotic state. Coagulation risk factors for thrombosis were within the normal limits; Protein S 67 %(60–140), Protein C 103 % (72–146), Antithrombin 3 110 %(80–120) and Activated P C Resistance was 1.9(2.0–4.3). The Hams test was negative but the Anticardiolipin antibody test was positive. IgM level was 52 (normal is up to 10) and IgG was 18.8 (normal is up to 10). She also had border line APC Sensitivity 1.9 (2 to 4.3). Kaolin time 49 sec (70–120) Ktmix 64 sec (70–120), thyroid function test revealed TSH 0.32 mu/L, fT4 20.2 pmol/L (10–25). Subsequent determination of Anticardiolipin antibody was negative. Her symptoms were settled with the use of simple analgesia and she was discharged home with long-term anticoagulation medication. The INR target for long-term anticoagulation was aimed at >3.
This case presented to us as an acute abdominal pain. Subsequent investigations revealed the presence of splenic infarction. Coagulation risk factors for thrombosis proved negative. Haematological investigations revealed the presence of anticardiolipin antibodies at the first instance but subsequent determinations were negative. Hence, it mimicked Hughes syndrome initially but the criteria for temporal persistence of anticardiolipin antibody was not fulfilled. Unusual surgical presentation of a thrombotic abnormality as abdominal pain due to splenic infarction.