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  • Book
    [edited by] Dr. Victoria Lynn Handa, Dr. Linda Van Le.
    Contents:
    Section I Preparing for Surgery: Surgical anatomy of the female pelvis
    Preoperative care of the gynecologic patient
    Section II Principles of Gynecologic Surgery: Anesthesia primer for the gynecologist
    Patient positioning for pelvic surgery
    Surgical techniques, instruments, and suture
    Incisions for gynecologic surgery
    Surgical control of pelvic hemorrhage
    Principles of laparoscopy
    Principles of robotic surgery
    Section III Perioperative and Postoperative Care of the Gynecologic Patient: Postoperative care of the gynecologic patient
    Section IV Contemporary Gynecologic Surgical Procedures
    Dilation and curettage
    Hysteroscopy
    Surgical management of abortion and its complications
    Surgery for benign vulvar conditions
    Tubal sterilization
    Surgery of the ovary and fallopian tube
    Myomectomy
    Vaginal hysterectomy
    Abdominal hysterectomy
    Laparoscopic and robotic-assisted hysterectomy
    Section V: Gynecologic Oncology
    Section VI: Surgery for Pelvic Floor Disorders
    Section VII: Management of Selected Gynecologic Conditions
    Section VIII: Surgery for Obstetrical Complications.
    Digital Access Ovid 2020
  • Article
    Holaday DA.
    Environ Health Perspect. 1977 Dec;21:165-9.
    Current knowledge of the quantitative aspects of biotransformation of halothane and the fate of its metabolites are reviewed. Absorbed quantities of the inhalation anesthetic average 12.7 and 18 g during 1 and 2 hr, respectively, of anesthesia. Reported fractions of halothane recovered as urinary metabolites range from 10 to 25%. An analysis of reports of bromide ion accumulation in plasma during and following anesthesia suggests that metabolism of halothane continues for 20-40 hr after exposure and that 22-24% of absorbed halothane is metabolized following 8 hr of anesthesia. Half-times for excretion of trifluoroacetic acid (TFA), a principal urinary metabolite of halothane, tend to confirm that biotransformation proceeds for 2 to 3 days following exposure. Other urinary metabolites which occur in small amounts include a dehydrofluorinated metabolite of halothane conjugated with L-cysteine and N-trifluoroacetyl-n-ethanolamine, both of which are evidence of the occurrence of reactive intermediates during the metabolism of halothane. Support for free radical formation has come from in vivo and in vitro demonstrations of stimulation of lipoperoxidation of polyenoic fatty acids by halothane. Irreversible binding of halothane metabolites to microsomal proteins and phospholipids has been shown to depend on the microsomal P-450 cytochrome system. Irreversible binding is increased by microsomal enzyme induction and by anaerobic conditions. Hypoxia increases irreversible binding to phospholipids, augments the release of inorganic fluoride and is followed by centrilobular hepatic necrosis. It is concluded that one-fourth to one-half of halothane undergoes biotransformation in man. One fraction is excreted as trifluoroacetic acid, chloride and bromide. A second fraction is irreversibly bound to hepatic proteins and lipids. Under anaerobic conditions fluoride is released, binding to phospholipids is increased, and hepatic necrosis may occur.
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