To clot or not to clot: are there predictors of clinically significant thrombus formation in patients with gastroparesis and prolonged IV access?

Some patients with gastroparesis (GP) require sustained central intravenous access for hydration, medication and/or nutrition, leaving them at risk for venous thrombosis. We studied a group of 53 patients with gastroparesis for identifiable risk factors of clinically significant thrombosis. Patients requiring prolonged central IV access fell into two groups: those who had clinical incidence of IV catheter-related thrombosis confirmed radiologically (CLOT, n = 14), and those who did not form IV catheter thrombosis (NOCLOT, n = 39). We analyzed and compared clinical symptoms, serum/plasma coagulation studies, and autoimmune antibodies in the CLOT and NOCLOT groups. Patients in the CLOT group had statistically more Scl 70 antibodies than did the NOCLOT group, and another autoantibody, Ku 66, was found in higher titers in the NOCLOT group than the CLOT group. Other autoimmune and coagulation factors were not statistically different between the two groups, although a subgroup of CLOT patients had lower plasma Protein S levels. We conclude that the presence of Scl 70 autoantibodies is associated with increased clotting risk in this group of GP patients, and that the Ku 66 antibody may be associated with decreased risk of thrombosis in patients with GP. These findings, coupled with lower Protein S levels in some CLOT patients, suggests that autoimmune factors may be associated with GP patients who thrombose IV access versus patients who do not.

Assessing thrombosis risk in patients with idiopathic, diabetic, and postsurgical gastroparesis.

Patients with severe gastrointestinal motility disorders are often found to have intravenous access clots or deep venous thrombosis. It has previously been reported that many patients who have intravenous access thrombosis have concomitant thrombotic risk factors. In this study, the goal was to determine the underlying prevalence of hypercoagulable risk in a series of patients with documented gastroparesis. Investigators studied 62 consecutive patients (52 female; mean age, 42 y) who had symptoms of gastroparesis. All patients were evaluated for placement of a gastric neural stimulation device, or they had had one placed previously. Patients underwent a hematologic interview and standardized coagulation measures of thrombotic risk. Laboratory studies measured acquired elevations of Factor VII, Factor VIII, fibrinogen, lupus anticoagulant panel, antiphospholipid antibody panel, homocysteine (in the setting of kidney disease), and activated protein resistance. Investigators also measured congenital factors: Factor VIII (with C-reactive protein levels), antithrombin III, protein C, protein S (total and free), Factor II mutation, Factor V Leiden, methylenetetrahydrofolate reductase, and homocysteine. Fifty-five patients (89%) were found to have detectable hypercoagulable risk factors. Twenty-five of the 62 patients (40%) had a documented history of abnormal clotting, including deep venous thrombosis, intravenous access thrombosis, and pulmonary embolism. All patients with a previous history of thrombosis had detectable clotting abnormalities. Of 56 patients, 40 (71%) had hypercoagulability and did not have diabetes (P=.036), and 20 (36%) had hypercoagulability and no known history of infection. However, this value was not statistically significant when infection and hypercoagulability were compared (P=.408). A high prevalence of acquired and congenital hypercoagulable defects has been observed in patients with gastroparesis, which may predispose them to arterial and venous clots. This unique finding warrants consideration of coagulation evaluation in patients with severe gastroparesis, especially when these patients are placed in high-risk thrombophilic situations, such as hospitalization, prolonged intravenous access, and surgery.