Subject(s)
Arrhythmias, Cardiac/etiology , Lithotripsy/adverse effects , Urinary Calculi/therapy , Adolescent , Child , Child, Preschool , Humans , InfantABSTRACT
BACKGROUND: Thromboprophylaxis is commonly required following caesarean section. However the effect of thromboprophylactic dosages of subcutaneous heparin on coagulation is unknown because conventional laboratory tests are largely unaffected. The aim of this study was to determine if thromboelastography could detect and quantify the effect of unfractionated heparin on coagulation profile when given at the time of surgery. METHODS: Nineteen women undergoing elective caesarean section were recruited. Blood samples collected before and after administration of subcutaneous unfractionated heparin 7500 IU underwent thromboelastography using both plain and heparinase cuvettes. Anti-factor Xa levels were also measured. RESULTS: There was a significant difference in R times between plain and heparinase samples (-10.6%, P=0.0072) indicating that thromboelastography could detect an effect of unfractionated heparin. Compared to baseline there were significant decreases of R times in plain (-20.4%, P=0.033) and heparinase (-28.8%, P=0.0001) samples despite the administration of unfractionated heparin. Anti-factor Xa levels were virtually undetectable (mean 0.01 U/mL). CONCLUSION: Thromboelastography was able to detect and quantify the effect of unfractionated heparin on blood coagulability, an effect not detected by conventional laboratory tests. Thromboelastography demonstrated a pro-coagulant effect of surgery that was only partially mitigated by the use of unfractionated heparin. In this study, at a dose of 7500 IU subcutaneous unfractionated heparin appears to have little anticoagulant effect.
Subject(s)
Cesarean Section , Postoperative Complications/diagnosis , Postoperative Complications/prevention & control , Thrombelastography , Thrombosis/diagnosis , Thrombosis/prevention & control , Adult , Anesthesia, Epidural , Anesthesia, Obstetrical , Anesthesia, Spinal , Anticoagulants/administration & dosage , Anticoagulants/therapeutic use , Factor Xa Inhibitors , Female , Heparin/administration & dosage , Heparin/therapeutic use , Heparin Lyase/chemistry , Humans , Pregnancy , Sample SizeABSTRACT
A 29-year-old patient presented with dysphonia, dysphagia and a progressive history of stridor over 6 weeks. His past medical history included childhood nasolabial rhabdomyosarcoma treated by surgery, chemotherapy and radiotherapy. This had resulted in marked abnormalities of the facial skeleton, limited neck extension and restricted mouth opening of 1 cm, in part due to dental implants. After careful discussion and planning within a multidisciplinary team, the airway was optimised by temporary removal of the dental implants. This enabled a suspension laryngoscope to be passed, permitting carbon dioxide laser treatment to an obstruction at the laryngeal inlet and eliminating the need for a tracheostomy.
Subject(s)
Airway Obstruction/surgery , Dental Implants , Laryngoscopy/methods , Laser Therapy/methods , Adult , Airway Obstruction/etiology , Combined Modality Therapy , Device Removal , Head and Neck Neoplasms/therapy , Humans , Male , Patient Care Team , Rhabdomyosarcoma/therapyABSTRACT
Halothane hepatitis occurs because susceptible patients mount immune responses to trifluoroacetylated protein antigens, formed following cytochrome P450-mediated bioactivation of halothane to trifluoroacetyl chloride. In the present study, an in vitro approach has been used to investigate the cytochrome P450 isozyme(s) which catalyze neoantigen formation and to explore the protective role of non-protein thiols (cysteine and reduced glutathione). Significant levels of trifluoroacetyl protein antigens were generated when human liver microsomes, and also microsomes from livers of rats pre-treated with isoniazid, phenobarbital or beta-naphtoflavone, were incubated with halothane plus a nicotinamide adenine dinucleotidephosphate (NADPH) generating system. Immunoblotting studies revealed that the major trifluoroacetyl antigens expressed in vitro exhibited molecular masses of 50-55 kDa and included 60 and 80 kDa neoantigens recognized by antibodies from patients with halothane hepatitis. Much lower concentrations of halothane were required to produce maximal antigen generation in isoniazid-induced rat microsomes, as compared with phenobarbital or isosafrole-induced microsomes (0.5 vs 12.5 microl/ml). In isoniazid-induced microsomes, antigen generation was inhibited > 90% by the nucleophiles cysteine and glutathione and by the CYP2E1-selective inhibitors diallylsulfide and p-nitrophenol, but was unaffected by inhibitors of other P450 isozymes (furafylline, sulfaphenazole or triacetyloleandomycin). Neoantigen formation in six human liver microsomal preparations was inhibited in the presence of diallylsulfide, but not by furafylline, sulfaphenazole or triacetyloleandomycin, and exhibited marked variability which correlated with CYP2E1 levels. These results suggest that the balance between metabolic bioactivation by CYP2E1 and detoxication of reactive metabolites by cellular nucleophiles could be an important metabolic risk factor in halothane hepatitis.
