Fluoroacetic acid (1080) is frequently used to poison the introduced red fox
(Vulpes vulpes) in Australia. The symptoms of 1080
poisoning in dogs appear extremely distressing to observers as manic running,
yelping and convulsing are readily interpreted as being indicative of pain and
distress. Assessment of pain perceived by animals poisoned by 1080 is
difficult, as severe CNS disruptions alter behaviour and EEG patterns that may
otherwise be useful in such assessments. This study compared three drug agents
combined with 1080 to address the possibility of pain and distress that may be
experienced by foxes during 1080 toxicosis. A mixed-sex group of 15 foxes was
used in the trial of each of the three drugs: an analgesic (carprofen; 10 mg
kg–1), an anxiolytic/sedative (diazepam; 10 mg
kg–1) or an analgesic/sedative (clonidine;
0.75 mg kg–1). Each group of 15 foxes was randomly
allocated between three treatments of either 0.5 mg
kg–1 of 1080, 0.5 mg
kg–1 of 1080 and a dose of the trial drug, and a
dose of the trial drug alone. A telemetry collar was used on each fox to
monitor the duration and intensity of activity, and behaviour from dosage to
death was recorded using daylight/infra-red video cameras. In foxes dosed
with 1080 alone, a mean of 4.05 (0.86, P < 0.05) h
was observed from dosage to symptoms and 1.57 (0.46, P
< 0.05) h from symptoms to death. Diazepam reduced the overall intensity of
activity from dosage to death (P < 0.002) and from
first symptoms to death (P < 0.05). Diazepam also
extended the time until death (P < 0.01) and time
taken from dosage to first symptoms (P < 0.01). In
the dosages used, clonidine was not as effective as diazepam in reducing
activity associated with symptoms of poisoning, although it prolonged the time
taken from dosing to first symptoms (P < 0.05).
Carprofen did not significantly alter the progression of 1080 toxicosis or the
intensity of activity of foxes compared with the group that received 1080
alone. The initial symptoms of 1080 toxicosis include retching and manic
running and foxes may be more capable of suffering at this stage than after
collapse, where behaviour is likely to be associated with CNS disruption.
Diazepam may be effective in minimising any anxiety experienced by foxes
especially during the first symptoms of 1080 toxicosis.
UPBEAT appears to accelerate the transition from inpatient to outpatient care for acute nonpsychiatric admissions. Care coordination and increased access to ambulatory psychiatric services produces similar improvement in mental health and general health status as usual care.
Inhalation induction with sevoflurane was compared with propofol or sevoflurane/propofol in 60 unpremedicated adults. Target concentrations for the three groups (with 60% nitrous oxide) were 3% end-tidal sevoflurane, 12 mg/l propofol and 1.5% sevoflurane/6 mg/l propofol respectively, prior to insertion of a laryngeal mask airway (LMA) at 10 minutes. Induction of anaesthesia was satisfactory in each group, but movement response to LMA insertion was observed in 20 patients (least in the sevoflurane group). Cardiovascular responses were similar except for a lower heart rate in the sevoflurane group. EEG bispectral index suggested a greater depth of anaesthesia in the inhalation induction group. A bispectral index of 60 separated patients responding to LMA insertion from nonresponders (P=0.006), and had a sensitivity of 68% and specificity 70%. Movement response was not predicted by cardiovascular changes.
The compatibility of ketamine and morphine mixture was studied. In addition, pH adjustment to minimise local tissue irritation led to no change in stability of the mixture up to pH 5.9. It appears that ketamine and morphine mixtures are stable over a 24 h period.
The cardiovascular effects of intravenous sedation were studied in fifty patients after spinal anaesthesia for lower limb or pelvic surgery. Twenty patients received propofol (mean dosage 74 (SD 4) jiglkglminfor 0-20 minutes and 51 (SD 7) jiglkglminfor 20-40 minutes), twenty received midazolam (35 jiglkg+ 2.54 (SD 0.2) jiglkglminfor 0-20 minutes and 1.35 (SD 0.2) jiglkglmin for 20-40 minutes) and ten patients received saline infusion only. The forearm vasoconstriction in response to the spinal anaesthesia was measured by strain gauge plethysmography. Spinal anaesthesia lowered systolic and diastolic blood pressure by 18 (SED 4) mmHg and 9 (SED 2) mmHg respectively. (SED = standard error of the difference.) This was associated with a 32% decrease in mean forearm blood flow. Propofol and midazolam caused similar additional reductions in systolic and diastolic blood pressure (10 (SED 4) mmHg and 4 (SED 2) mmHg) and a decrease in heart rate (P < 0.005), but forearm vasoconstriction was not altered. In the control group, however, forearm vasoconstriction increased during 40 minutes in theatre (P < 0.05). Recovery from propofol was far more rapid than after midazolam and was virtually complete in ten minutes. This was reflected by an increase in blood pressure and in forearm vasoconstriction in the recovery period.
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