Anesthesia and analgesia
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Anesthesia and analgesia · Dec 1999
Randomized Controlled Trial Clinical TrialThe failure of negative pressure rewarming (Thermostat) to accelerate recovery from mild hypothermia in postoperative surgical patients.
The Thermostat device (Aquarius Medical Corp., Phoenix, AZ) is used in a new technique to accelerate recovery from hypothermia by mechanically distending blood vessels in the hand, thereby increasing transfer of exogenous heat to the body core. We evaluated the use of the Thermostat device in patients with mild postoperative hypothermia (< 36 degrees C). We studied adult patients undergoing elective surgery, general anesthesia, and neuromuscular blockade. Patients with an initial postoperative tympanic membrane temperature < 36 degrees C were randomized into two groups: 1) Thermostat, which consisted of a hypothermia warming mitt/seal and thermal exchange chamber for 60 min, and 2) conventional treatment, which consisted of warm blankets and/or radiant heat. Of the 191 patients enrolled, 60 (31%) developed hypothermia and were randomized to receive the Thermostat (n = 30) or conventional methods (n = 30). Fourteen patients in the Thermostat group and 17 patients in the conventional group rewarmed to 36 degrees C before discharge from the recovery room (P is not significant). There were no differences in vital signs, rewarming time, time to discharge from the recovery room, or postoperative temperature between groups. We conclude that patients with mild postoperative hypothermia rewarmed in a similar fashion, regardless of whether the Thermostat or conventional methods were used. ⋯ We found that a commercially available negative pressure rewarming device (Thermostat; Aquarius Medical Corp., Phoenix, AZ) was not effective in accelerating rewarming in postoperative hypothermic surgical patients after general anesthesia.
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Anesthesia and analgesia · Dec 1999
Randomized Controlled Trial Comparative Study Clinical TrialA comparative study of the postoperative allogeneic blood-sparing effect of tranexamic acid versus acute normovolemic hemodilution after total knee replacement.
Both acute normovolemic hemodilution (NVHD) and tranexamic acid (TA) are potentially useful allogeneic blood conservation strategies after total knee replacement. However, the relative efficacy of these blood-sparing techniques is unknown. Therefore, to compare the postoperative allogeneic blood sparing of NVHD and TA after total knee replacement, we investigated 40 patients in a prospective, single-blinded study protocol. In Group TA, 30 min before deflating the limb tourniquet, an IV infusion of TA, 15 mg/kg, was administered over a 30-min period. Thereafter, a constant IV infusion of 10 mg x kg(-1) x hr(-1) was administered until 12 h after deflation of the limb tourniquet. Before induction of anesthesia, NVHD patients were bled to a target hematocrit of approximately 28%. Intravascular blood volume was maintained with lactated Ringer's solution. All autologous blood was transfused at the end of the surgery. Postoperatively, hematocrit was measured daily. In all cases, a hematocrit <27% was the postoperative transfusion trigger. Before discharge, deep vein thrombosis was excluded by Echo Doppler. Three months after surgery, the incidence of delayed thromboembolic events was assessed. The two groups were demographically comparable. In Group NVHD, 843 mL+/-289 of autologous blood was removed. Despite autologous blood transfusion, during the early postoperative period and until the third postoperative day, the NVHD group had significantly (P < 0.01) lower mean hematocrits when compared with the TA group. Thereafter, because of a significantly (P < 0.0008) greater allogeneic blood requirement in the NVHD group, no statistically significant difference in mean hematocrit recordings was noted among the groups. Blood accumulation in the surgical drain 12 h postoperatively, was significantly (P < 0.0008) higher in the NVHD group (259 mL+/-156) when compared with the TA group (110 mL+/-62). Significantly (P < 0.0008) more allogeneic blood was transfused in the NVHD group (19 U/13 patients) when compared with the TA group (2 U/2 patients). No abnormal Echo Doppler studies were reported. During the 3-mo follow-up period, a deep vein thrombosis and pulmonary embolus were documented in one patient in the NVHD group. We conclude that perioperative hemodynamic stability and allogeneic blood sparing is superior after tranexamic acid administration when compared with normovolemic hemodilution. ⋯ For total knee replacement, when compared with normovolemic hemodilution, tranexamic acid administration is associated with superior perioperative hemodynamic stability and allogeneic blood sparing.
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Anesthesia and analgesia · Dec 1999
Assessing platelet and fibrinogen contribution to clot strength using modified thromboelastography in pregnant women.
The monoclonal antibody fragment c7E3 Fab (ReoPro), by binding to platelet surface fibrinogen receptors (glycoprotein, GPIIb/IIIa), inhibits platelet aggregation and its interaction with fibrinogen. In this study, we used thromboelastography with ReoPro to evaluate the independent contribution of fibrinogen and platelets to clot strength. Thromboelastography was performed in 21 healthy, term parturients scheduled for elective cesarean delivery with 360 microL of celite-activated whole blood and with 5 microL of (2 mg/mL) ReoPro added to 355 microL of celite-activated whole blood. The contribution of platelets to clot strength (MAplt) was derived by subtracting MAfib (maximal amplitude with ReoPro) from MAwb (maximal amplitude with whole blood). Thus, MAwb - MAfib = MAplt. The value for MAwb (mean +/- SD) was 73+/-4 mm, for MAfib it was 33+/-5 mm, and for MAplt it was 40+/-3 mm. The contribution of fibrinogen and platelets to the MAplt was 45% and 55%, respectively. Modified thromboelastography using ReoPro in healthy parturients can be used to determine the contribution of fibrinogen and platelets to blood clot strength. ⋯ Determining the independent contribution of platelets and fibrinogen to the maximal amplitude of thromboelastography using c7E3 Fab may further improve the use of thromboelastography in detecting and treating coagulation defects.
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Anesthesia and analgesia · Dec 1999
Clinical TrialThe hemodynamic effects of propofol in children with congenital heart disease.
We studied the hemodynamic effects of propofol during elective cardiac catheterization in 30 children with congenital heart disease. Sixteen patients were without cardiac shunt (Group I), six had left-to-right cardiac shunt (Group II), and eight had right-to-left cardiac shunt (Group III). The mean (+/-SD) ages were 3.8+/-3.1 yr (Group I), 3.2+/-3.7 yr (Group II), and 1.0+/-0.6 yr (Group III). After sedation and cardiac catheter insertion, hemodynamic data and oxygen consumption were measured before and after the administration of propofol (2-mg/kg bolus, 50- to 200-microg x kg(-1) x min(-1) infusion), and values were compared by using a paired t-test (significance: P < 0.05). After the propofol administration, systemic mean arterial pressure and systemic vascular resistance decreased significantly and systemic blood flow increased significantly in all patient groups; heart rate, pulmonary mean arterial pressure, and pulmonary vascular resistance were unchanged. Pulmonary to systemic resistance ratio increased (Group I, P = 0.005; Group II, P = 0.03; Group III, P = 0.10). In patients with cardiac shunt, propofol resulted in decreased left-to-right flow and increased right-to-left flow; the pulmonary to systemic flow ratio decreased significantly (Group II, P = 0.005; Group III, P = 0.01). Clinically relevant decreases in Pao2 (P = 0.008) and Sao2 (P = 0.01) occurred in Group III patients. We conclude that propofol can result in clinically important changes in cardiac shunt direction and flow. ⋯ The principal hemodynamic effect of propofol in children with congenital heart defects is a decrease in systemic vascular resistance. In children with cardiac shunt, this results in a decrease in the ratio of pulmonary to systemic blood flow, and it can lead to arterial desaturation in patients with cyanotic heart disease.