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Biomedical subjects

L Tarkkanen

Publications and source records attributed to L Tarkkanen.

At least 19 recordsLinked to original sources

Blood levels and half-life of methylmethacrylate after tourniquet release during knee arthroplasty.

The blood levels and the half-life of monomeric methylmethacrylate after tourniquet release were studied in nine patients with osteoarthrosis or rheumatoid arthritis of the knee joint, treated with the Townley prosthesis under spinal anesthesia. Several ventricular extrasystoles were monitored in one patient with high blood levels of monomeric methylmethacrylate (119.80 micrograms/ml). The blood levels of monomeric methylmethacrylate ranged between 0.10 and 1.44 microgram/ml in the rest of the patients. The half-life of monomeric methylmethacrylate in vivo was 47-55 min.

Aged↗

The effect of anaesthesia on changes in blood pressure and plasma cortisol levels induced by cementation with methylmethacrylate.

The effects of cementation on arterial blood pressure, arterial oxygen tension and plasma levels of cortisol were studied in 30 patients with femoral neck fracture treated with the Thompson prosthesis in spinal (n = 15) or general (n = 15) anaesthesia. In spinal anaesthesia hypotension of clinical importance was observed coincidentally with the use of methylmethacrylate, while the levels of plasma cortisol remained unchanged. A significant rise was noted in arterial blood pressure and plasma levels of cortisol after cementation in general anaesthesia. Arterial oxygen tension fell in both groups. These findings indicate that the hypotension frequently reported in connection with cementation is triggered by a complex mechanism which can be modified by the anaesthetic technique.

Aged↗

Methylmethacrylate blood levels in patients with femoral neck fracture.

The blood levels of monomeric methylmethacrylate were measured in 20 patients with fracture of the femoral neck, treated with a Thompson prosthesis under spinal anesthesia. Monomeric methylmethacrylate was detected in the blood stream in all patients; the maximum levels (mean 6.44 micrograms/ml, range 0.05-31.89 micrograms/ml) were measured 30 s after insertion of the Thompson prosthesis. A moderate drop in systolic blood pressure and a marked reduction of arterial oxygen tension was noted after cementation and insertion of the prosthesis; the mean maximum drops were 10.1 mm Hg (range 0-32 mm Hg) and 6.1 mm Hg (range 0-13.5 mm Hg) No dose-dependent correlation could be established between the levels of monomeric methylmethacrylate and the drop in arterial blood pressure or arterial oxygen tension.

Aged↗

Ventricular fluid pressure in neurosurgical patients receiving intravenous lorazepam for premedication.

The effect of 0.05 and 0.03 mg/kg of intravenously administered lorazepam on the ventricular fluid pressure (VFP) was recorded continuously for 45-90 minutes in 13 wakeful spontaneously breathing unanaesthetized patients with hydrocephalus. The initial VFP was low in 11 patients with low-pressure hydrocephalus, and at the upper level of normal in 2 who had stenosis of the aqueduct. Lorazepam caused minute changes in VFP. The largest transient increased (7 and 16 torr) occurred in the two patients with the highest initial VFP. Blood acid-base balance, blood pressure, and heart rate remained unaltered. However, lorazepam caused such drowsiness that it was difficult to check the patients' level of consciousness. For this reason, intravenously administered lorazepam in a dosage of 0.03 mg/kg or more seems unsuitable for premedication in neurosurgical patients with brain disease.

Adult↗

Unpredictable central nervous system effects after lorazepam premedication for neurosurgery.

Administration of lorazepam for preanaesthetic medication is generally expected to produce amnesic action. We conducted two studies to evaluate the relationship of plasma levels of lorazepam with its clinical effects. Forty patients, receiving 0.03 or 0.05 mg/kg lorazepam i.m. as preanaesthetic medication for various neurosurgical procedures, were asked 24 h after anaesthesia whether they could recall the insertion of the i.v. needle and a picture shown to them before induction of anaesthesia. Another 11 patients were given 0.03 mg/kg lorazepam i.v. and their degree of drowsiness was rated immediately before induction of anaesthesia. Plasma levels of lorazepam were measured by gas chromatography from samples drawn before induction of anaesthesia. No relationship between either the dose of lorazepam used or the plasma levels of lorazepam and the incidence of amnesia or the degree of drowsiness was observed. Three patients receiving 0.05 mg/kg of lorazepam i.m. had prolonged drowsiness, which made it difficult to check the patients' neurological condition after the operation. It is postulated that the unpredictable and variable central nervous system effects of lorazepam in neurosurgical patients may be due to differences in the capacity of lorazepam to penetrate the blood brain barrier.

Adult↗

Changes in the requirements for blood transfusion in brain surgery.

The amount of blood used in transfusions during certain neurosurgical operations was less in 1978-79 than in 1971-72 and in 1965-66. The operations investigated were for gliomas and meningiomas of the brain, pituitary adenomas, acoustic neurinomas, arteriovenous malformations, and arterial aneurysms. The major change in anaesthetic techniques between 1965-66 and 1971-72 was the introduction of hypocapnia by controlled artificial hyperventilation. We suggest that this was the main factor responsible for the reduction in the need for blood transfusions. The avoidance of halothane, the use of induced hypotension, and microsurgical technique may have been responsible for the smaller drop between 1971-72 and 1978-79. Good neurosurgical anaesthesia demands anaesthetic expertise, reliable apparatus, and instant laboratory service, but may also reduce costs by reducing the need for blood transfusions.

Anesthesia↗

Comparison of laryngotracheal and ultrasonic nebulizer administration of lidocaine in local anaesthesia for bronchoscopy.

Inhalation of nebulized minute lidocaine droplets has been suggested to be a very safe and pleasant method to produce topical anaesthesia for bronchoscopy. We produced topical anaesthesia of the respiratory tract either by laryngotracheal spraying (LS) of lidocaine (439 +/- 85mg) or ultrasonic nebulizer administration (UNA) of lidocaine (462 +/- 81 mg) in 40 patients undergoing bronchoscopy. All patients also received an average of 15 mg of diazepam intravenously. Both modes of lidocaine administration produced adequate anaesthesia and were safe, but when rated on the visual analogue scale, both the efficacy of local anaesthesia and the cooperation of patients during bronchoscopy were better (P less than 0.05) after LS than those after UNA. The peak plasma concentrations of lidocaine (means +/- s.d.) were lower and occurred earlier after UNA (0.53 +/- 0.34 micrograms/ml at 5-15 min after administration) than those after LS (0.89 +/- 0.63 micrograms/ml at 15-25 min after spraying). The highest individual values measured (2.54 micrograms/ml after LS and 1.17 micrograms/ml after UNA) were much less than those reported toxic lidocaine plasma concentrations. It is concluded that bronchoscopy can be conducted under local anaesthesia as successfully and safely using inhalation of lidocaine droplets from an ultrasonic nebulizer as when using laryngotracheal spraying of lidocaine.

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The influence of intramuscularly administered pethidine on the amnesic effects of intravenous diazepam during intravenous regional anaesthesia.

Patients undergoing surgery under regional anaesthesia often receive narcotic analgesics for premedication which may modify the sedative and amnesic effects of intravenously administered diazepam. Sixty-two patients scheduled for upper extremity surgery under intravenous regional anaesthesia received 0.15 mg/kg of diazepam intravenously to supplement the local anaesthesia. Thirty-two of the patients received 0.01 mg/kg of atropine plus 1 mg/kg of pethidine and 30 patients only atropine intramuscularly approximately 1 h before injection of diazepam. Another 30 patients received the same atropine-pethidine premedication and saline intravenously, and served as a reference group. Atropine-pethidine premedication followed by saline did not produce any amnesic effects. Sixty-nine and 38% of patients receiving atropine-pethidine premedication followed by diazepam did not remember a picture shown to them 15 min after diazepam injection or the performance of operation, respectively, the respective figures for patients given atropine premedication followed by diazepam being only 23% and 0% (P less than 0.01 - 0.001 between groups). The anti-recall of painful stimulus (exanguination) was significantly (P less than 0.01) more common when diazepam was given after pethidine premedication (31%) when compared to its injection after atropine alone (7%). The drowsiness produced by the drugs was greatest and the overall patient acceptability of the technique used most satisfactory when pethidine was used for premedication and diazepam for sedation. It is concluded that intramuscularly administered pethidine potentiates the amnesic action of intravenous diazepam for painful stimuli, prolongs the amnesic action of diazepam for visual stimuli and improves the patients' acceptability of intravenous regional anesthesia supplemented by intravenous diazepam.

Adult↗