Background: To access the clinical effect of clonidine on reduction of myocardial ischemia events in patients with history of coronary artery disease undergoing noncardiac surgeries.
Methods: Sixty ASA class III patients with coronary artery disease were allotted at random to two groups in a prospective, double-blind study to receive either clonidine (3 micrograms/kg) or placebo (control group) 90 minutes before arrival at the operating room. Continuous EKG monitoring (Holter monitor) was performed to analyze the ST segment in lead II, V2 and V5 during the preoperative (since late hours the night before operation), intraoperative and early postoperative periods (total monitoring time = 24 hours). The episode of myocardial ischemia defined as the magnitude of ST segment depression of at least 1 mm, occurring 60 ms after the J point and persisting for three minutes or more was recorded. Perioperative hemodynamic data were analyzed with two-way ANOVA with repeated measures. Student's t-test for unpaired data was used for analysis of demographics. Chi-square test was used for ST segment changes. Results are expressed as mean +/- SD and P < 0.05 was considered to be statistically significant.
Results: In the control group, 9 patients (30%) were noted to have episodes of ischemia preoperatively, 7 patients (23.3%) intraoperatively, and 12 patients (40%) postoperatively. The occurrence of myocardial ischemia peaked in the early postoperative period (P < 0.05). On the contrary, in the clonidine group, 10 patients (33.3%) saw ischemic episodes preoperatively, 3 patients (10%) intraoperatively and 5 patients (16.7%) postoperatively. The incidence of myocardial ischemia in clonidine group was significantly lower than that in placebo group in intraoperative and postoperative periods. The mean arterial pressure was significantly lower in some clonidine-treated patients during perioperative periods (P < 0.05). A number of patients in clonidine group suffered from drowsiness (66.7%) after operation (P < 0.05), but they could be easily aroused. In regard to dryness of mouth, nausea and vomiting clonidine and control groups did not differ much (P > 0.05). Demerol consumption was significantly lower in clonidine group (43.7 +/- 4.6 mg) than in control group (76.3 +/- 3.7 mg, P < 0.05).
Conclusions: We conclude that premedication with oral clonidine can significantly reduce the incidence of perioperative myocardial ischemia in patients with CAD undergoing noncardiac surgeries. The incidence of myocardial ischemia in these patients is rather high during perioperative period, which deserves our exceptional caution.
Metastatic hepatocellular carcinoma (HCC) to the right atrium occurs rarely and may lead to lethal perioperative complications. A 61-year-old female who was about to undergo operation for resection of a right intraatrial tumor thought possibly to be metastatic hepatocellular carcinoma met with sudden protrusion of the tumor from the right atrial wall that sank into the right ventricle during induction of anesthesia. Right ventricular outflow tract obstruction developed and was quickly diagnosed by transesophageal echocardiography. Emergent cardiopulmonary bypass was rushed on the spot and the surgery was completed smoothly. Here we discuss the possible causes of the event and we recommend that special attention should be paid to the anesthetic techniques and proper precaution should be taken in the face of such a risky surgery.
Endotracheal intubation using a laryngoscope is the most rapid and usually the easiest means to ensure a patent airway. It has therefore earned its popularity in anesthesia and other acute health care practices. However, intubation by conventional technique is not always successful as at times direct vision of the glottis/vocal cords is impossible during laryngoscopy. Thus, acute airway obstruction remains a constant problem in all acute health care practices. To deal with this challenge, we have developed a new technique incorporating a modified Satin-Slip intubating stylet (Mallinckrodt Medical, St. Louis, MO, USA). First, cut the plastic sheath of the stylet at its distal end and push the sheath forward about one and a half inches. The soft plastic tip of the malleable stylet is then allowed to protrude from the endotracheal tube (ETT). When visualization of the glottic aperture is not possible, one simply places the soft plastic tip of the stylet under the epiglottis and advances it forward, and the tip will eventually enter the larynx. The ETT is then advanced off the stylet into the trachea. This new technique works very well in our experiences. It can be performed quickly with readily available inexpensive equipment. Our favorable experience leads us to believe it is one of the most promising additions to the current recommended alternatives.
Background: Hemorrhagic shock upregulates inducible nitric oxide (NO) synthase (iNOS) expression and the resultant NO overproduction. Liver is one of the major organs that is responsible for increased NO production after trauma-hemorrhage and resuscitation. Guanosine triphosphate cyclohydrolase I (GTPCH) is the rate-limiting enzyme for the synthesis of tetrahydrobiopterin (BH4), a necessary co-factor for iNOS activity. Very little is known about the effects of hemorrhagic shock on hepatic GTPCH expression.
Methods: Fifteen male Sprague-Dawley rats were randomly assigned to one of three groups, i.e. a sham instrumented (Sham) group, a sustained hemorrhagic shock (HS) group, and a hemorrhagic shock with resuscitation (HS/RES) group (n = 5 in each group). Controlled hemorrhagic shock was induced and the mean arterial pressure (MAP) was kept between 40-45 mmHg for sixty minutes in both HS and HS/RES groups. Then resuscitation with infusion of shed autologous blood and normal saline was performed in HS/RES group. Microdialysis probes were put in the liver and the right atrium for collection of serial samples. NO concentrations in dialysate samples were measured using chemiluminescence. Hepatic iNOS and GTPCH mRNA concentrations were analyzed using semiquantitative reverse transcription and polymerase chain reaction (RT-PCR).
Results: Hemorrhagic shock induced both the hepatic and circulating NO biosynthesis as well as hepatic iNOS mRNA expression. Resuscitation with shed blood/normal saline normalized this upregulation. However, no difference was found in mean hepatic GTPCH mRNA concentrations between groups in this experiment.
Conclusions: We provide the evidence that hemorrhagic shock-induced NO biosynthesis involves upregulation of iNOS transcription in liver tissue and GTPCH transcription is unaffected by either hemorrhagic shock or resuscitation. Furthermore, microdialysis is an ideal technique for serial sampling and that events can be followed.
Background: Anesthetic techniques are known to affect blood hemostasis, which may be responsible for the pathogenesis of postoperative venous thromboembolism. The purpose of this study was to evaluate the effect of general and spinal anesthesias on blood hemostasis using thromboelastography.
Methods: Forty patients undergoing arthroscopic knee surgery were enrolled for study and randomly allocated to one of two groups, to receive either general (GA; n = 20) or spinal anesthesia (SA; n = 20). In addition to thromboelastography, prothrombin and activated partial-thromboplastin time, and haematocrit and platelet count were also examined concurrently. Blood was sampled and examined before anesthesia to provide the baseline data (Time 1). Three more evaluations were performed at different time, i.e., twenty minutes after induction of anesthesia and just prior to skin incision (Time 2), thirty minutes after skin incision (Time 3), and three hours after surgery (Time 4).
Results: There were no intra- or inter-group differences noted as comparing the measured parameters obtained prior to, during, or three hours after surgery.
Conclusions: From the present study, we do not find any individual anesthetic technique which would have effect on the hemostasis of patients who received diagnostic arthroscopic surgery.