Regular tramadol use does not affect the propofol dose requirement for induction of anaesthesia.

BACKGROUND AND OBJECTIVES: An increased risk of awareness during general anaesthesia in patients receiving tramadol has been reported. We studied whether tramadol affects the amount of propofol required for induction of anaesthesia. METHODS: In this prospective controlled study, we evaluated 46 patients, half of whom used tramadol regularly. Entropy indices, state entropy and response entropy, were used to assess the level of hypnosis. Patients were anaesthetized with a propofol infusion (1 mg kg(-1) min(-1)) until they first became unconscious, and further until they developed a burst suppression pattern in the electroencephalogram. The doses of propofol needed to reach these end-points were recorded. RESULTS: The amount (median, (range)) of propofol required for loss of consciousness was 2.0 (1.0-5.5) mg kg(-1) and 2.4 (0.9-8.3) mg kg(-1) (P=0.95) in the tramadol users and controls, respectively. The amount of propofol required for burst suppression was 5.8 (3.9-12.7) mg kg(-1) and 6.4 (2.9-15.1) mg kg(-1) (P=0.89) in the tramadol users and controls. There was no difference between the groups in state entropy and response entropy during different stages of induction of anaesthesia. CONCLUSIONS: Tramadol did not affect the dose of propofol required to achieve loss of consciousness or burst suppression pattern in electroencephalogram during induction of general anaesthesia. However, there was a ninefold inter-individual variation in propofol dose requirement for loss of consciousness and a fivefold variation for reaching burst suppression. Due to extensive inter-individual variability, monitoring the level of hypnosis during general anaesthesia using propofol may enhance the correct dosage.

Effects of cigarette smoking on serum fluoride concentrations and renal function integrity after 1 MAC-h sevoflurane anaesthesia.

BACKGROUND: Tobacco smoke contains various chemicals which may affect drug metabolism. Sevoflurane is metabolized to inorganic fluoride, and elevated serum fluoride concentrations (S-F(-)) may cause deterioration of renal function. Whether smokers develop high S-F(-) and associated disturbances in renal function is not known. METHODS: We investigated sevoflurane metabolism in 25 non-smoking and 25 smoking (> 10 cigarettes/day) generally healthy women, aged 19-68 years, undergoing gynaecological elective surgery under one minimum alveolar concentration-hour (1 MAC-h) standardized sevoflurane anaesthesia. S-F(-) was measured for 24 h. Glomerular and tubular function was assessed by measuring serum and urine tumour-associated trypsin inhibitor (TATI), beta(2)-microglobulin and serum creatinine for 48 h after sevoflurane inhalation. RESULTS: There were no differences between the two study groups with regard to S-F(-). It increased significantly in both groups: in non-smokers, from a baseline between 1.0 and 11 micromol/l (median, 1.6 micromol/l) to a maximum between 8.2 and 40 micromol/l (26 micromol/l) (P < 0.001) and, in smokers, from a baseline between 0.5 and 5.2 micromol/l (1.7 micromol/l) to a maximum between 19 and 71 micromol/l (25 micromol/l) (P < 0.001). In both groups, S-F(-) remained elevated for the entire sampling period (P < 0.001). In all five women (one non-smoker and four smokers) with a maximum S-F(-) of 40 micromol/l or higher and an area under the serum fluoride concentration-time curve (AUC(F0-24)) of 500 micromol/h/l or higher, serum TATI increased above the pathological concentration of 3.0 nmol/l, whereas only six of the 45 patients with S-F(-) below 40 micromol/l had serum TATI above 3.0 nmol/l (P < 0.001). Beta(2)-Microglobulin increased significantly (> 1 mg/l) in two patients with high S-F(-) relative to two of the 45 patients with S-F(-) below 40 micromol/l (P= 0.005). None of the patients developed clinically detectable renal dysfunction. CONCLUSION: Smoking did not affect S-F(-) after sevoflurane anaesthesia. Glomerular dysfunction, seen as increased serum TATI, was noted in five women with S-F(-) above 40 micromol/l. Our results suggest that the renal toxic threshold of S-F(-) seems to be lower than the earlier reported value of 50 micromol/l.

High success rate and low incidence of headache and neurological symptoms with two spinal needle designs in children.

BACKGROUND: In children, only a few trials have evaluated the use of spinal needles with special tip designs. In this study, we compared the success rate and incidence of post-dural puncture complaints of two small-gauge spinal needle designs used in children undergoing spinal anaesthesia (SA). METHODS: Three hundred and three children aged 9 months to 17 years presenting for subumbilical surgery were randomly assigned to have a 26G Atraucan (n = 156) or 27G Whitacre (n = 147) spinal needle for SA. The number of attempts to obtain successful cerebrospinal fluid (CSF) return and the success rate of SA were recorded. The first week of recovery was recorded by a diary. RESULTS: Both groups had a similar one-attempt success rate: 80% in the Atraucan group and 81% in the Whitacre group. Failure to obtain CSF occurred in one patient in the Atraucan group and in two patients in the Whitacre group. Paraesthesia was observed more commonly in the Whitacre group (10%) than in the Atraucan group (2%) (P = 0.004). The success rate of SA was 96%, with no differences between the two needles; one child was given general anaesthesia and 11 children (3%) a single dose of supplemental analgesia for the skin incision. Forty-one children (15%) developed a headache, 13 of which were classified as post-dural puncture headache (PDPH), seven cases (5%) in the Atraucan group and six (4%) in the Whitacre group; none of the children required a blood patch. Fifteen children (10%) in the Atraucan group and nine (7%) in the Whitacre group developed low back pain. Two children (1%) in the Atraucan group and four (3%) in the Whitacre group developed transient neurological symptoms (TNSs). CONCLUSION: Both needles were associated with a high success rate and a low incidence of complaints.

Fluoride metabolism in smokers and non-smokers following enflurane anaesthesia.

BACKGROUND: Inorganic fluoride is released by the metabolism of enflurane and the increased serum fluoride concentrations may impair renal function. Tobacco smoke consists of numerous reactive compounds that can either induce or inhibit drug metabolism. Studies on the interaction of smoking with anaesthetic drug metabolism and possible toxicity are warranted. METHODS: Sixteen non-smoking and 17 smoking (>10 cigarettes day(-1)) generally healthy women undergoing elective gynaecological surgery were given 1 MAC (minimum alveolar concentration)-hour standardized anaesthesia with enflurane in oxygen-air mixture. The serum inorganic fluoride and renal function markers beta(2)-microglobulin, tumour-associated trypsin inhibitor (TATI) and serum creatinine were measured for 48 h. RESULTS: The greatest inorganic fluoride concentration was between 8.4 and 21.0 (mean 13.8 (SD 3.4)) micromol litre(-1) in the non-smokers and between 8.6 and 38.0 (18.7 (7.0)) micromol litre(-1) in the smokers; the mean difference was 4.9 micromol litre(-1) (95% confidence interval (CI) 1.0-8.8, P<0.05). Serum beta(2)-microglobulin, TATI and creatinine were not increased. Serum inorganic fluoride concentrations were significantly greater in the smokers compared with the non- smokers 1, 2, 3 and 6 h after 1 MAC-hour inhalation with enflurane (P<0.05). Inorganic fluoride concentrations were still increased 24 h after anaesthesia in both groups. Urine beta(2)-microglobulin and TATI creatinine ratio remained at low values during the whole 48-h period in both groups. CONCLUSIONS: Regular smoking is associated with an increase in serum inorganic fluoride concentration after anaesthesia with enflurane, but there are no signs of renal damage.

Clonidine provides opioid-sparing effect, stable hemodynamics, and renal integrity during laparoscopic cholecystectomy.

BACKGROUND: Carbon dioxide pneumoperitoneum causes a hemodynamic stress response and decreases urine output because of an activated renin-angiotensin-aldosterone system (RAAS). Clonidine is a potent antihypertensive drug that suppresses RAAS. METHODS: The effects of clonidine 4.5 mg/kg or saline on hemodynamics, neuroendocrine response, and renal parameters were compared in 30 healthy patients undergoing laparoscopic cholecystectomy. RESULTS: Heart rate, arterial blood pressures, and plasma renin activity were lower during and after pneumoperitoneum in patients with clonidine. There were no differences in urine output, urine oxygen tension (reflecting medullary perfusion), or antidiuretic hormone between the groups. N-acetyl-b-D-glucosaminidase, a marker of proximal tubular damage, was minimally elevated after clonidine. CONCLUSIONS: Clonidine enabled stable hemodynamics and prevented activation of RAAS seen as unchanged plasma renin activity. Clonidine may be beneficial during laparoscopy in patients with hypertension, cardiovascular, and/or renal diseases.

The effect of ketorolac and sevoflurane anesthesia on renal glomerular and tubular function.

UNLABELLED: We assessed the renal effects of the combination of ketorolac and sevoflurane anesthesia by using sensitive and specific markers of renal proximal and distal tubular and glomerular function. Thirty women (ASA physical status I and II) undergoing breast surgery received either ketorolac 30 mg IM or saline at premedication, at the end, and 6 h after anesthesia maintained with sevoflurane. Peak levels of serum fluoride at 2 h after the end of anesthesia were 30.1 micromol/L (21.0-50.0 micromol/L) in the Ketorolac group and 33.3 micromol/L (13.0-38.0 micromol/L) in the Control group (mean and range, not significant). Urine alpha1-microglobulin indexed to urine creatinine was increased from 2 h after the start of anesthesia until the first postoperative day in the Ketorolac group (peak level, 0.8 +/- 0.4 mg/mmol; upper limit of normal, 0.7 mg/mmol) but did not change in the Control group. Urine glutathione-S-transferase (GST)-alpha indexed to urine creatinine (GST-alpha/creatinine) and GST-pi/creatinine were increased 2 h after anesthesia and returned to baseline values thereafter in both groups. There were no changes in serum cystatin C and urine kallikrein or urine output per hour between groups. The perioperative administration of ketorolac to healthy, well hydrated patients anesthetized with sevoflurane did not produce renal glomerular or tubular dysfunction. IMPLICATIONS: Ketorolac 90 mg IM, given in divided doses over approximately 10 h to patients anesthetized with sevoflurane with a fresh gas flow rate of 4-6 L/min, did not result in clinically significant changes in renal glomerular or tubular function.

Ketorolac is not nephrotoxic in connection with sevoflurane anesthesia in patients undergoing breast surgery.

UNLABELLED: Ketorolac, which may cause renal vasoconstriction by cyclooxygenase inhibition, is often administered to patients anesthetized with sevoflurane that is metabolized to inorganic fluoride (F(-)), another potential nephrotoxin. We assessed this possible interaction using urine N-acetyl-beta-D-glucosaminidase indexed to urinary creatinine (U-NAG/crea) as a marker of proximal tubular, beta2-microglobulin as a tubular, urine oxygen tension (P(u)O(2)) as a medullary, and erythropoietin as a marker of tubulointerstitial damage. Thirty women (ASA physical status I-II) undergoing breast surgery were included in our double-blinded study. They were allocated into two groups receiving either ketorolac 30 mg IM (Group K) or saline (Group C) at the time of premedication, at the end of, and 6 h after anesthesia maintained with sevoflurane. Urine output, U-NAG/crea, P(u)O(2,) serum creatinine, urea, and F(-) were assessed. Blood loss was larger in Group K (465 +/- 286 mL vs 240 +/- 149 mL, mean +/- SD, P < 0.05). The MAC-doses of sevoflurane were similar. U-NAG/crea increased during the first 2 h of anesthesia and serum F(-) peaked 2 h after the anesthesia without differences between the groups. There were no statistically significant changes in P(u)O(2), erythropoietin, beta2-microglobulin, serum creatinine, urea, or urine output during anesthesia or the recovery period in either group. Our results indicate that the kidneys are not affected by ketorolac administered in connection with sevoflurane anesthesia. IMPLICATIONS: The different kinetics of N-acetyl-beta-D-glucosaminidase indexed to urinary creatinine and serum inorganic fluoride during and after sevoflurane anesthesia suggest that the observed mild renal tubular function deterioration is not caused by inorganic fluoride. Administration of ketorolac IM is therefore considered safe in adequately hydrated healthy adult patients given sevoflurane anesthesia.