Study Of Treatment Strategies Of Severe OSAHS Patients Undergoing UPPP In Postanesthesia Care Unit

PARTⅠStudy of treatment strategies for severe OSAHS patients undergoing UPPP in postanesthesia care unitBackgroud: Obstructive sleep apnea and hypopnea syndrome (OSAHS) is a common chronic illness that affects 2% to 4% of middleaged adults. It is now seen as one end of a spectrum of sleep-related breathing disorders and is associated with hypertension, cardiovascular diseases, daytime sleepiness, impairment of quality of life. UPPP is the most commonly surgical treatment of obstructive sleep apnea syndrome. But there are high risk during the general ansthesia of the operation. Acute airway obstruction during anesthesia induction and after extubation as well as perioperative cardiac events is the main causes of death.The problem of airway obstruction during induction can be avoided by keeping spontaneously breathing, nasal endotracheal intubation blindly or directed by the fibreoptic bronchoscope. But there are even more risks in the postoperative period, because of the anatomy abnormality of the patients with severe OSAHS, as well as the severe edema in the pharyngeal mucosa. They seem to have more risks of acute airway obstruction and apnea even death after extubation. The restlessness and violent changes in hemodynamics can bring about cardiac events, strokes and bleeding. However, the study of postoperative treatment is seldom reported, and no systemical guidelines are available. At present, the postoperative management for the patients undergoing UPPP is to keep the endotracheal tube and monitor in postanesthesia care unit after the patients awakened. The administration of sedative-analgesia drugs seems to be limited because of the patients'hypersensitivity to these drugs, so that the patients are more discomfortable, and the occurrence of hypertention and tachycardia increases obviously. We investigate the therapeutic effect of midazolam-sulfentanyl sedative-analgesia and mechanical ventilation surport to the postoperative patients. Furthermore,α2 adrenoreceptor clonidine was added to above midazolam-sulfentanyl sedative-analgesia treatment for postoperative patients with severe OSAHS. A randomly comparative study was performed to investigate the efficacy ofα2 adrenoreceptor clonidine on postoperative stress and inflammatory response.Objective:1. To observe the effect and safety of midazolam sulfentanyl sedative-analgesia on postoperative patients undergoing UPPP or UPPP+hard palate plastic surgery suffered from severe OSAHS, and study the postoperative management strategies and reasonable drug therapy of the patents in PACU.2. To observe the therapeutic effect of clonidine for postoperative patients with severe OSAHS undergoing UPPP or UPPP+hard palate plastic surgery, and the efficacy on postoperative stress and inflammatory response.Methods:1. 40 patients suffered from severe OSAHS undergoing UPPP or UPPP+hard palate plastic surgery, and monitored in postanesthesia care unit(PACU) were enrolled in our study. All patients received midazolam sulfentanyl sedative-analgesia and ventilation support. The efficacy of sedative-analgesia was observed. Their changes of hemadynamics and the complications such as restlessness, nausea, vomit were recorded to evaluate the effect of the therapy.2. Sixty patients who suffered from severe OSAHS undergoing UPPP surgery and monitored in PACU overnight were divided randomly into two groups: control group (n=30) and clonidine group(n=30). All patients received the same anesthesia and the same midazolam sulfentanyl sedative-analgesia in PACU. The operative procedures were performed by the same groiup of surgeons. Clonidine3μg/kg(diluted to 5ml) intravenous injected slowly(in 3 minutes) were administered to patients in clonidine group, and normal saline in same volume were administered to the patients in control group. The blood pressure, heart rate, SPO2 were recorded at the time point as follows: entering PACU, 2hs, 4hs, 8hs in PACU respectively, and 3hs, 1hs, as well as the moment prior to extubation. The occurrence of agitation, nausea, vomiting was recorded. Blood samples were taken from artery for determination of plasma adrenline, noradrenaline, ACTH, IL-6, TNF-α.Results1. All patients were quiet and analgesia, no bismatch with the ventilator, and no remember of any events before stopping midazolam. There was no postoperative bleeding, acute airway obstruction, angina pectoris and myocardial infarction during PACU. But the hemadynamics changed significantly, esmolol and nitroglycerin have to be administered to keep the blood pressure stable and heart rate in the limited level.2. There were no statistical difference in VAS and SAS score between clonidine group and control group(P>0.05). There were no statistical difference in BP and HR between the two groups(P>0.05), but the administration of vasoactive agents in clonidine group was less than that in control group(P<0.01). The incidence of restlessness, nausea, vomiting in clonidine group was less than that in control group(P<0.05). At 2hs after entering PACU, the plasma adrenaline, noradranaline, ACTH, IL-6, TNF-αlevels of clonidine group was much lower than that of control group(P<0.05).Conclusions1. Remaining nasal endotracheal tube and giving midazolam sulfentanyl sedative-analgesia could ensure the safty, reduce the complications, relieve the distress and improve the life quality of patients. However, the patients hemadynamics was still unstable.2. Although low dose clonidine could not improve the VAS,SAS score, the patients'tolerance to harmful stimulus increased, and the complications such as restlessness, nausea, vomiting reduced. Low dose clonidine could stabilize the hemadynamics, and attenuate the postoperative hypertention, tachycardia significantly. Clonidine could inhibit the postoperative stress and inflammatory response of the severe OSAHS patients undergoing UPPP, and relieve the postoperative pain and improve the patients recovery. PartⅡThe effect of clonidine on inflammatory response in hypoxia and trauma ratsObjective To set up a pharyngeal trauma model on rats suffered from hypoxia, and to study the effect of clonidine on inflammatory response post trauma and on the damage of the lung and kidney.Methods 40 male SD rat were divided into five groups randomly as follows: trauma control group(n=8), hypoxia control group(n=8), hypoxia trauma group(n=8), hypoxia trama clonidine pre-treatment group(n=8), hypoxia trama clonidine post-treatment group(n=8). The rats in trauma control group were placed in a sealed hypoxia chamber for 6 hours everyday for 6days, flowed with fresh air. The rats in hypoxia groups were placed in a sealed hypoxia chamber with 9.5-10.5% O2 6 hours everyday for 6 days. Then all the rats were anesthesized, intubated for mechanical ventilation (Vt 3ml,f=60bpm), femorale artery canulation for invasive blood pressure monitoring and femorale vein canulation for transfusion. The rats in hypoxia control group didn't receive any operation. The rats in trauma control group and in hyoxia trauma group received pharyngeal trauma that simulating the operation of UPPP. The rats in hypoxia trauma clonidine pre-treatment group and clonidine post-treatment group received clonidine 30μg/kg iv slowly (in 5 minutes) before and right after the pharyngeal trauma respectively. Mean artery pressure(MAP), HR were recorded at the time point as follows: before, on the instant and 1 hour after the trauma procedure in all groups. Blood samples were taken from artery to test serum TNF-α, IL-6 level. Specimens of lung and were examined, To explore the effect and kidney., and clonidine on the inflammatory response of the body..Results Hyperplasia of interstitium cell, the widen of the alveolar septum, the thicken wall of small vessels could be found under the light microscope in the lung of the rats in hypoxia control group. There are few inflammatory cells in the lung interstitium in trauma control goup. Hyperplasia of interstitium cells, widen of the alveolar septum, inflammatory cells are found in hypoxia control group. Few inflammatory cells in the lung institium in both hypoxia trauma clonidine pre-treatment group and hypoxia trauma clonidine post-treatment group except the hypoxia changes in the lung. The edema of the epithelial cells of renal tubule was found in rats kidney in all the hypoxia group, and there were no obvious difference among the hypoxia groups. The MAP and HR in all groups (except clonidine pre-treatment group and hypoxia control group) rose obviously at the trauma point(P<0.05), but no statistical defference among these groups(P>0.05). There were no significant changes of MAP and HR of the rats in clonidine pre-treatment group and hypoxia control group. MAP and HR of the rats in clonidine pre-treatment group, post-treatment group and hypoxia control group were much lower than that of trauma control group and hypoxia trauma group(P<0.05). There were no statistical difference of the MAP and HR among clonidine pre-treatment group, post-treatment group and hypoxia control group 1 hour after trauma(P>0.05). The concentration of serum TNF-α,IL-6 of the rats in hypoxia trauma group rose significantly 1 hour after the trauma, and was much higher than that of other groups(P<0.05). The concentration of serum TNF-α,IL-6 of clonidine pre-treatment group and clonidine post-treatment group was much lower than that of hypoxia trauma group(P<0.05). There was no difference in concentration of serum TNF-αand IL-6 between clonidine pre-treatment group and clonidine post-treatment group(P>0.05).Conclusions Continuous hypoxia could result in mild pathological changes of the rats lung and kidney. The inflammatory response resulted from pharyngeal trauma in hypoxia rats was more severe than that in the trauma control group. Clonidine could attenuate the inflammatory response after trauma, and protect the lung from injury.