Is there any effect of Dexmedetomidine induced hypotension on hemostatic markers?

Induced hypotension is the planned and regulated decrease of arterial blood pressure with the goal of reducing blood loss and enhancing operating area visibility. Various pharmacological and nonpharmacological approaches may be used to produce induced hypotension. In this study, researchers conducted an evaluation and comparison of the alterations in platelet aggregation, coagulation, and fibrinolysis status in patients having spine surgery under normotensive and dexmedetomidine-induced hypotensive anesthesia.

A total of sixty patients who were scheduled to have spine surgery were assigned randomly to two distinct groups: the normotensive group and the dexmedetomidine-induced hypotensive group. The evaluation of platelet aggregation was conducted at several time points: before the surgical procedure, 15 minutes after the initiation of anesthesia, 60 minutes and 120 minutes after the incision was made, at the conclusion of the surgery, and 2 hours and 24 hours after the operation. The preoperative, 2-hour postoperative, and 24-hour postoperative measurements included prothrombin time (PT), activated partial thromboplastin time (aPTT), platelet count, antithrombin III, fibrinogen, and D-dimer levels.

The preoperative platelet aggregation percentages were similar in both groups. The study observed a significant increase in platelet aggregation at 120 minutes after skin incision and during the postoperative period in the normotensive group, compared to the preoperative value (P < 0.05). However, there was no significant decrease in platelet aggregation during the intraoperative induced hypotensive period in the dexmedetomidine-induced hypotensive group (P > 0.05). In the normotensive group, there was a substantial rise in postoperative PT and aPTT, as well as a significant drop in platelet count and antithrombin III, when compared to the preoperative values (P < 0.05). However, in the hypotensive group, these parameters did not show significant changes (P > 0.05). The postoperative D-dimer levels exhibited a substantial rise in both groups when compared to the preoperative baseline (P < 0.05).

The study found that there was a significant increase in collagen-induced platelet aggregation in the normotensive group at 120 minutes after skin incision, at the conclusion of the surgery, and during the postoperative period. However, in the hypotensive group, platelet aggregation decreased insignificantly during the induced hypotensive period and remained statistically insignificant until the end of surgery and during the first 24 hours after the operation. With respect to the alterations in coagulation and fibrinolytic state after surgery, it was seen that the normotensive group exhibited a statistically significant drop in platelet count, fibrinogen, and antithrombin III levels two hours postoperatively. However, the decrease in these parameters was not found to be statistically significant in the hypotensive group. The postoperative D-dimer level exhibited a significant rise in both groups; however, the increase was more pronounced in the normotensive group as compared to the hypotensive group.

In the hypotensive group, there was a negligible drop in platelet aggregation throughout the induced hypotensive phase. This decrease remained statistically insignificant throughout the duration of the operation and during the first 24 hours after the surgery. The implementation of induced hypotension effectively inhibited the rise in platelet aggregation and mitigated the observed disruption of the hemostatic system seen in the normotensive cohort. The observed reduction in platelet aggregation resulting from induced hypotension may be attributed to the vasodilatory effects and the consequent decrease in vessel wall shear stress. There was a notable increase in platelet aggregation throughout both the intraoperative and postoperative periods in the normotensive group, accompanied by substantial changes in coagulation markers. The administration of dexmedetomidine-induced hypotensive anesthesia resulted in the prevention of heightened platelet aggregation seen in the normotensive group. This approach also demonstrated superior preservation of platelet and coagulation factors.

Reference –

Eid, Gehan M.; Mostafa, Shaimaa F.; Abu Elyazed, Mohamed M.. Dexmedetomidine induced hypotension and hemostatic markers. Journal of Anaesthesiology Clinical Pharmacology 39(1):p 18-24, Jan–Mar 2023. | DOI: 10.4103/joacp.JOACP_111_21