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PubMed1989

Detection of antibodies to a halothane metabolite hapten in sera from patients with halothane-associated hepatitis.

Sera from 40 patients with a clinical diagnosis of halothane-associated hepatitis were tested for the presence of antibodies to the trifluoroacetate (TFA) halothane metabolite hapten using an ELISA assay, with TFA-albumin as the antigen. Positive results were obtained in 30% of cases of which 3/4 with encephalopathy were positive and 9/36 non-fulminant cases were positive. Antibody specificity to the TFA hapten was confirmed in each positive result by a 'hapten inhibition' experiment in which TFA albumin binding was blocked by preincubation of serum with TFA-lysine. Most probably this assay detects a relatively low affinity cross-reaction with the TFA hapten of antibodies in the patients' sera which are directed against specific TFA-labelled liver proteins. Anti-TFA-albumin antibodies were not detected in 28 normal subjects, 5 subjects with fulminant hepatic failure secondary to other causes, 6 subjects with a history of 2 or more exposures to halothane but with no evidence of liver disease and 28 patients with a variety of chronic liver diseases. It is concluded that ELISA testing using trifluoroacetylated rabbit serum albumin (TFA-RSA) as antigen is a quick and convenient assay for the confirmation of halothane-associated hepatitis in fulminant hepatic failure secondary to halothane, but is less sensitive when the illness follows a milder course.

Adolescent↗
PubMed1991

The role of the liver in the production of free radicals during halothane anaesthesia in the rat. Quantification of N-tert-butyl-alpha-(4- nitrophenyl)nitrone (PBN)-trapped adducts in bile from halothane as compared with carbon tetrachloride.

Halothane or CCl4 was co-administered with the spin trap N-tert-butyl-alpha-(4-nitrophenyl)nitrone (PBN) to rats fitted with bile duct cannuli or to isolated perfused liver preparations. Rats maintained under halothane anaesthesia generated significant amounts of free radicals, and 5-9 nmol was excreted in bile over 1 h. No adducts were detected in urine or plasma. The hepatic origin of these free radicals was confirmed by studies on isolated perfused livers where the addition of halothane to the perfusate resulted in the biliary elimination of the same PBN-trapped radical adducts. Similarly, following CCl4 administration, the same radical species were eliminated in bile in the whole animal and the perfused liver preparation. In the perfused liver, over 3 h the total biliary elimination of radicals derived from halothane or CCl4 (administered at equimolar concentrations) was approximately the same (5-7 nmol); however, the elimination of halothane-derived radicals was more rapid over the first 1 h.

Animals↗
PubMed1997

Deep halothane anaesthesia compared with halothane-suxamethonium anaesthesia for tracheal intubation in young children.

A double-blind and randomized study design was used to investigate 100 healthy children, aged 1-5 years. Intubating conditions and cardiovascular changes during deep halothane anaesthesia, defined as an end-tidal concentration of 2%, were compared with those changes during 1% halothane and suxamethonium relaxation. Intubating conditions were graded according to the ease of laryngoscopy, vocal cord position, coughing and jaw relaxation. In each group 96% of the children demonstrated acceptable intubating conditions. Jaw relaxation was worse in the 1% halothane/-suxamethonium group (P < 0.01). When anaesthesia with 2% or 1% halothane was compared there was a more pronounced decrease in systolic blood pressure (18 vs. 8%, P < 0.001). Junctional rhythm occurred more frequently during deep halothane anaesthesia (46 vs. 18%, P < 0.01). Intravenously (i.v.) administered atropine attenuated blood pressure depression significantly and reinstituted sinus rhythm in most cases.

Anesthesia, Inhalation↗
PubMed1998

Recovery after halothane anaesthesia induced with thiopental, propofol-alfentanil or halothane for day-case adenoidectomy in small children.

We studied recovery from halothane anaesthesia in 93 children, aged 1-3 yr, undergoing day-case adenoidectomy. Children were allocated randomly to receive thiopental 5 mg kg-1 (group TH), alfentanil 10 micrograms kg-1 and propofol 3 mg kg-1 (group PAH) or 5% halothane (group HH) for induction of anaesthesia. In group TH, tracheal intubation was facilitated with succinylcholine (suxamethonium) 1.5 mg kg-1. In groups PAH and HH, tracheal intubation was performed without neuromuscular block, and succinylcholine was used only if required. Anaesthesia was maintained with 1-3% halothane during spontaneous respiration. Times to achieving predetermined recovery end-points were recorded. Quality of recovery was assessed using a score of 1-9 (best to worst) for sedation, crying, restlessness and agitation. A postoperative questionnaire was used to determine the well-being of the child at home, 24 h after operation. Emergence from anaesthesia (response to non-painful stimuli) occurred earlier in group HH (mean 9 (SD 6) min) than in groups PAH (13 (6) min, P < 0.01) and TH (18 (14) min, P < 0.01). Sitting up, walking and home readiness were achieved earlier in groups PAH and HH than in group TH (P < 0.05 for each variable). Children in group TH were more sedated during the first 30 min after anaesthesia than those in the two other groups (P < 0.05) while emergence-related delirium was more common in group HH than in group TH (P < 0.01). Well-being at home was similar in all groups. We conclude that induction of halothane anaesthesia with propofol-alfentanil or halothane provided more rapid recovery and earlier discharge than that with thiopental.

Adenoidectomy↗
PubMed1981

Halothane uptake and nitrous oxide concentration. Arterial halothane levels during Caesarean section.

The effect on halothane uptake of changing the nitrous oxide concentration during the first few minutes of a general anaesthetic for Caesarean section was investigated. In 10 mothers anaesthesia was maintained with halothane 0.4%, nitrous oxide 33% and oxygen 66%. In 10 others the sole difference in anaesthetic technique was that the ratio of nitrous oxide to oxygen was reversed for the first 3 minutes only. Serial maternal arterial blood samples showed a significant increase in halothane levels in the group where the nitrous oxide was increased, with p less than 0.02 at 1 and 2 minutes and p less than 0.05 at 3.4 and 5 minutes. After 5 minutes there was no significant difference between the two groups. Cord blood concentrations between the two groups were comparable. The difference in halothane levels is a demonstration of the influence of the concentration effect of nitrous oxide on the uptake of halothane, the second gas effect. The relevance of anaesthetic uptake to obstetric anaesthesia and awareness is discussed.

Anesthesia, Inhalation↗
PubMed1986

Distribution of halothane and the metabolites trifluoroacetic acid and bromide in the conceptus after halothane inhalation by pregnant mice.

Mice in late stage of gestation were exposed to halothane at various concentrations for 1 hr, and were killed at different time intervals after discontinuance of inhalation. The concentration of halothane in maternal plasma decreased rapidly, and in the amniotic fluid the halothane never reached more than 20% of maternal plasma levels. Trifluoroacetic acid (TFA) and bromide, formed mainly by maternal metabolism of halothane, accumulated in foetus and amniotic fluid with time, and reached plateau levels in amniotic fluid between 4 and 24 hrs. TFA infused intravenously to the mother reached higher levels in amniotic fluid after long survival times, than in maternal plasma. Equilibrium dialysis experiments showed that TFA and trichloroacetic acid (TCA) (previously shown to accumulate in amniotic fluid) were bound to amniotic fluid macromolecules only to approximately 20-30 percent. This was at the same magnitude (or lower) as compared to binding in maternal plasma, suggesting that such binding did not contribute to the observed retention in the amniotic fluid. Other possible explanations for the slow accumulation and long-term retention in amniotic fluid are transport by bulk flow via foetus, excretion via foetal urine, or paraplacentally through endometrium and foetal membranes, followed by trapping in the amniotic fluid. The significance of this accumulation of metabolites of halogenated organic solvents and halothane for their foetotoxicity is not clear.

Amniotic Fluid↗
PubMed1971

Post-halothane jaundice in relation to previous administration of halothane.

The time interval since previous anaesthesia was compared in a surgical population in South Wales and in patients who developed jaundice after halothane. There was a significant difference in the pattern of time interval since previous general anaesthetics in the surgical population and in those patients who developed jaundice after halothane. In the group who developed jaundice there was an "excess" of patients who had had a previous halothane anaesthetic within four weeks. Halothane should if possible be avoided in patients who have had it before, particularly if this was within the previous four weeks. In the case of repeat halothane anaesthetics within four weeks, the risk seems to lie between 1 in 6,000 and 1 in 22,000.

Adult↗
PubMed1992

In vivo muscle 31P nuclear magnetic resonance spectroscopy during treatment of halothane-sensitive and halothane-nonsensitive pigs.

In vivo muscle 31P nuclear magnetic resonance spectroscopy was performed on 10 female pigs originating from a homozygous halothane-sensitive line and on 10 female pigs from a homozygous halothane-nonsensitive line. The mean concentration of phosphocreatine in the biceps femoris muscle of the anesthetized pigs decreased to 86% of the initial value after 11 minutes of halothane exposure (3%, oxygen flow 3 L/min). After the next 5.6 minutes, phosphocreatine concentration reached a minimal value of 52%, followed by a mean recovery to 76% of the initial value during the ensuing 11 minutes. Response was not observed in anesthetized homozygous halothane-nonsensitive pigs. Thus, a decrease to 86% of the initial value of phosphocreatine was 100% predictive for homozygous halothane-sensitive pigs with body weight ranging from 10 to 18 kg.

Adenosine Triphosphate↗
PubMed1991

Comparison of the hemodynamic effects of halothane alone and halothane combined with epidurally administered morphine for anesthesia in ventilated dogs.

The hemodynamic effects of 1.5 minimal alveolar concentration of halothane alone (1.6% end-tidal) and 1.5 minimal alveolar concentration of halothane (1.1% end-tidal concentration) combined with epidurally administered morphine were compared during controlled ventilation in 10 dogs used on 2 occasions and randomly allocated to 2 groups. Arterial blood pressure, cardiac index, stroke volume, left ventricular work, and pulmonary arterial pressure were significantly (P less than 0.05) higher in dogs of the morphine-treated group before administration of morphine. After epidural administration of morphine (0.1 mg/kg of body weight diluted in 0.26 ml of saline solution/kg), hemodynamic changes were not observed, and the aforementioned variables remained significantly (P less than 0.05) higher than values in dogs of the halothane only group. Compared with halothane (1.6%) alone, the reduction in halothane end-tidal concentration (1.1%) associated with epidurally administered morphine is beneficial in maintaining hemodynamic function.

Anesthesia↗
PubMed1987

Stimulatory effects of halothane and isoflurane on fluoride release and cytochrome P-450 loss caused by metabolism of 2-chloro-1,1-difluoroethene, a halothane metabolite.

The structural similarity of the halothane metabolite, 2-chloro-1,1-difluoroethene (CDE), to haloethenes that are metabolized by and inactivate cytochrome P-450, suggests that CDE may undergo secondary metabolism and degrade these isozymes. This possibility was examined in hepatic microsomes by determining fluoride release and cytochrome P-450 loss due to CDE metabolism in the presence of several anesthetics. CDE alone decreased cytochrome P-450 from phenobarbital-treated rats by as much as 37%, but the addition of isoflurane or halothane to incubations containing CDE increased the loss of cytochrome P-450 nearly twofold. Fluoride release was enhanced approximately 2.5 to 3 times by halothane or isoflurane; however, fluroxene inhibited fluoride release and did not enhance the loss of cytochrome P-450. Extrapolation of these results to the clinical situation suggests that the metabolism of CDE produced during halothane anesthesia and the accompanying cytochrome P-450 loss may contribute to the inhibition of drug metabolism produced by halothane.

Animals↗
PubMed1980

Lymphocyte cytotoxicity to halothane altered hepatocytes in patients with severe hepatic necrosis following halothane anaesthesia.

Lymphocytes from three of four patients with severe unexplained hepatitis following halothane anaesthesia were cytotoxic in vitro for liver cells isolated from rabbits following halothane anaesthesia, and less so for control hepatocytes. While the latter reaction could be blocked by addition of a purified liver membrane lipoprotein (LSP), this had no effect on the cytotoxicity to "halothane" hepatocytes. These results provide evidence that patients with severe halothane-associated hepatitis are sensitised to a liver cell antigen distinct from LSP, which arises as a result of halothane anaesthesia.

Adult↗
PubMed1980

Antibodies to the surface of halothane-altered rabbit hepatocytes in patients with severe halothane-associated hepatitis.

Circulating antibodies reacting specifically with the cell membrane of hepatocytes isolated from halothane-anesthetized rabbits were detected in nine of 11 patients with fulminant hepatic failure after helothane-induced anesthesia. The immunoglobulin deposition, as revealed by immunofluorescence, showed a granular pattern on the hepatocyte surface membrane. Preincubation of halothane-pretreated, but not of control, hepatocytes with serum containing this antibody rendered them susceptible to cytotoxic effects of normal lymphocytes in vitro. Control studies using serum from subjects repeatedly exposed to halothane without the development of liver damage, and from patients with viral and toxic liver injury have confirmed the specificity of these findings to serve halothane-associated liver injury. These results provide further evidence of an immunologic component in this condition.

Adult↗
PubMed1984

Effects of hypersensitivity to a halothane metabolite on halothane-induced liver damage.

The effect of immunologic hypersensitivity to a metabolite of halothane (trifluoroacetate) on the halothane-hypoxia-induction model was tested in mice and rats. Male Fisher 344 rats (200 g) were immunized with ovalbumin-trifluoroacetate (OVA-TFA) and the time course of the delayed hypersensitivity response determined. The animals had a peak response between 4 and 6 weeks after immunization. Rats were immunized with OVA-TFA, OVA, or saline 5 weeks before being anesthetized. Ten days before anesthesia, the animals were started on 0.1% phenobarbital in the drinking water. The animals were anesthetized with 1% halothane and 14% oxygen for 2 h. Hypersensitivity to TFA had no effect on the liver damage in either the mouse or the rat. These results do not rule out an immunologic vector in halothane hepatitis but make the involvement of TFA unlikely.

Animals↗
PubMed1992

Thermoregulatory thresholds for vasoconstriction in pediatric patients anesthetized with halothane or halothane and caudal bupivacaine.

The thermoregulatory threshold for vasoconstriction has been studied in infants and children given isoflurane, but not in those given halothane anesthesia. More importantly, the effect of vasoconstriction on central temperature in pediatric patients remains unknown. Also unknown is the effect of caudal analgesia on vasoconstriction thresholds. Accordingly, in the first portion of this study, we determined the central thermoregulatory threshold in 23 infants and children given approximately 0.6% halothane and caudal anesthesia for abdominal surgery. Patients were prospectively assigned to one of four weight groups: 5-10, 10-20, 20-30, and 30-50 kg. The threshold was considered the central temperature triggering peripheral vasoconstriction, and significant vasoconstriction was defined as a forearm-fingertip skin-surface temperature gradient exceeding 4 degrees C. Thresholds were similar (approximately 35.7 degrees C) in each study group, suggesting that thermoregulatory responses to halothane anesthesia are similar in infants and children of differing weights. However, they were higher than expected based on the previously reported thresholds in pediatric patients given isoflurane anesthesia. After peripheral vasoconstriction, central temperature continued to decrease in patients weighing more than 30 kg but remained constant or increased slightly in the others. These data suggest that thermoregulatory responses are more effective in infants and small children than in bigger children or adults. In the second part of this study we evaluated the effect of caudal analgesia on the thermoregulatory threshold for vasoconstriction. Children undergoing hypospadias repair were anesthetized with halothane (0.9%) and oxygen. Following induction, they were randomly assigned to caudal analgesia (n = 7) or penile nerve block (n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Caudal↗
PubMed1977

Adiposity and the pharmacokinetics of halothane. The effect of adiposity on the maintenance of and recovery from halothane anaesthesia.

Thirty fit patients (15-70 years, 46-98 kg) undergoing body-surface operations were selected to include a wide range of adiposity (12-45% of total body weight estimated from measurements of skinfold thickness). They were anaesthetized with halothane and 70% N2O in O2. From measurements of total ventilation (ml min-1 kg-1) and of halothane concentrations in inspired (F1) end-tidal (FE') and 'mixed-spill' (FS) gases, the following parameters were calculated for 5-min intervals from 20 to 40 min after induction; the rate of uptake of halothane per percent inspired concentration (Vha1 ml min-1%-1) and the degree of equilibrium achieved with the inspired concentration, calculated as FE'/F1 expressed as a percentage. Multiple-regression analysis of the results for 19 patients, taking account of the effects of body fat, ventilation, age, and the blood-gas partition coefficient lambda of halothane for the individual patient, showed that Vha1 increased with adiposity (b=0-375, P=0-0019), and with ventilation (b=0-054, P=0-09) but decreased with increasing age (b=-0-258, P=0-006). The time intervals between the end of the anaesthetic and the achievement of four defined levels of recovery (response to painful stimulus obedience to a simple command, response to a question, orientation in time and space), were recorded. Multiple-regression analysis showed that recovery time increased with addiposity, duration of administration and end-tidal concentration at the end of the administration, and decreased with increasing age. All four effects were statistically non-significant at the first levels of recovery but all increased at the later levels and all eventually became significant.

Adolescent↗
PubMed1981

Oxidative metabolism of halothane in the production of altered hepatocyte membrane antigens in acute halothane-induced hepatic necrosis.

Previous investigations have shown that patients with fulminant hepatic failure after halothane anaesthesia have a circulating antibody which reacts with an antigen present on the surface of halothane-altered hepatocytes. In the present study, it has been shown that the expression of the antigen is associated with the oxidative metabolism of halothane, in contrast with results of other groups which have shown that the reductive route is involved in the direct hepatotoxic reaction attributed to halothane.

Animals↗
PubMed1987

Metabolism of halothane in children having repeated halothane anaesthetics.

Metabolism of halothane was studied in nine children receiving daily halothane anaesthetics (from 10 up to a maximum of 31) over periods of two to seven weeks. Serum bromide concentrations never exceeded 3.5 mmol/l, a concentration below the toxic threshold. Repeated halothane anaesthetics at short intervals did not induce the reductive metabolism of halothane as assessed by 2-chloro-1,1,1-trifluoroethane (CTF) in the expired breath. One patient developed viral hepatitis A during the course of anaesthetic administration; this patient was the only one whose serum bromide concentrations fell substantially and whose exhaled CTF concentration increased as more anaesthetics were administered.

Adult↗
PubMed1975

Circulatory effects of halothane and halothane-nitrous oxide anesthesia in the dog: spontaneous ventilation.

The cardiovascular effects of equipotent (minimum alveolar concentration; MAC) doses of halothane versus halothane plus 25% N2O (H25N2O) in spontaneously breathing dogs do not differe except that nitrous oxide increased mean arterial pressure (AP) and decreased arterial oxygen partial pressure (PAO2). When 75% nitrous oxide was added to halothane anesthesia, AP, mean pulmonary artery pressure (PAP), heart rate (HR), cardiac output (CO), stroke volume (SV), total peripheral resistance (TPR), and left ventricular work (LVW) increased and PAO2 and hemoglobin saturation decreased. Arterial oxygen tensions below 80 torr were common at moderate and deep anesthetic levels of halothane plus 75% N2O (H75N2O). The specific contribution of N2O, hypoxemia, hypercapnia, or temporal recovery (or a combination of these) in producing cardiovascular stimulation were not determined.

Anesthesia, Inhalation↗