Clinical hemorheology and microcirculation · 2021
The effect of diabetic ketoacidosis (DKA) and its treatment on clot microstructure: Are they thrombogenic?
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Pillai Suresh, Davies Gareth, Lawrence Matthew, Whitley Janet, Stephens Jeffrey, Williams Phylip Rhodri, Morris Keith, Evans Phillip Adrian
Аннотация
BACKGROUND: Diabetic ketoacidosis (DKA) is a medical emergency with a high mortality rate and is associated with severe metabolic acidosis and dehydration. DKA patients have an increased risk of arterial and venous thromboembolism, however little is known about this metabolic derangement in the first 24 hours of admission and to assess its effect on coagulation. We therefore utilised a novel functional marker of clot microstructure (fractal dimension - df) to assess these changes within the first 24 hours.
METHODS: Prospective single centre observational study to demonstrate whether the tendency of blood clot formation differs in DKA patients.
RESULTS: 15 DKA patients and 15 healthy matched controls were recruited. Mean df in the healthy control group was 1.74±0.03. An elevated df of 1.78±0.07 was observed in patients with DKA on admission. The mean pH on admission was 7.14±0.13 and the lactate was 3.6±2.0. df changed significantly in response to standard treatment and was significantly reduced to 1.68±0.09 (2-6& h) and to 1.66±0.08 at 24& h (p < 0.01 One-way ANOVA). df also correlated significantly with lactate and pH (Pearson correlation coefficient 0.479 and -0.675 respectively, p < 0.05).
CONCLUSIONS: DKA patients at presentation have a densely organising less permeable thrombogenic clot microstructure as evidenced by high df. These structural changes are due to a combination of dehydration and a profound metabolic acidosis, which was reversed with treatment. These changes were not mirrored in standard clinical markers of thromboge-nicity.
METHODS: Prospective single centre observational study to demonstrate whether the tendency of blood clot formation differs in DKA patients.
RESULTS: 15 DKA patients and 15 healthy matched controls were recruited. Mean df in the healthy control group was 1.74±0.03. An elevated df of 1.78±0.07 was observed in patients with DKA on admission. The mean pH on admission was 7.14±0.13 and the lactate was 3.6±2.0. df changed significantly in response to standard treatment and was significantly reduced to 1.68±0.09 (2-6& h) and to 1.66±0.08 at 24& h (p < 0.01 One-way ANOVA). df also correlated significantly with lactate and pH (Pearson correlation coefficient 0.479 and -0.675 respectively, p < 0.05).
CONCLUSIONS: DKA patients at presentation have a densely organising less permeable thrombogenic clot microstructure as evidenced by high df. These structural changes are due to a combination of dehydration and a profound metabolic acidosis, which was reversed with treatment. These changes were not mirrored in standard clinical markers of thromboge-nicity.