Jonas Åkeson

Acupuncture relieves pelvic and low‐back pain in late pregnancy

Background.  The study was designed to evaluate the analgesic effect and possible adverse effects of acupuncture for pelvic and low‐back pain during the last trimester of pregnancy.

Complications associated with peripheral or central routes for central venous cannulation.

We undertook a review of studies comparing complications of centrally or peripherally inserted central venous catheters. Twelve studies were included. Catheter tip malpositioning (9.3% vs 3.4%, p = 0.0007), thrombophlebitis (78 vs 7.5 per 10 000 indwelling days, p = 0.0001) and catheter dysfunction (78 vs 14 per 10 000 indwelling days, p = 0.04) were more common with peripherally inserted catheters than with central catheter placement, respectively. There was no difference in infection rates. We found that the risks of tip malpositioning, thrombophlebitis and catheter dysfunction favour clinical use of centrally placed catheters instead of peripherally inserted central catheters, and that the two catheter types do not differ with respect to catheter‐related infection rates.

Preoperative rectal diclofenac versus paracetamol for tonsillectomy: effects on pain and blood loss

Background: Diclofenac is widely used for postoperative analgesia but the perioperative safety of this drug is controversial because of its effect on platelet aggregation, which might increase blood loss. In a prospective investigator‐blinded study the effects of diclofenac and paracetamol on pain and blood loss were compared in patients undergoing tonsillectomy.

Clinical guidelines on central venous catheterisation

Safe and reliable venous access is mandatory in modern health care, but central venous catheters (CVCs) are associated with significant morbidity and mortality, This paper describes current Swedish guidelines for clinical management of CVCs The guidelines supply updated recommendations that may be useful in other countries as well. Literature retrieval in the Cochrane and Pubmed databases, of papers written in English or Swedish and pertaining to CVC management, was done by members of a task force of the Swedish Society of Anaesthesiology and Intensive Care Medicine. Consensus meetings were held throughout the review process to allow all parts of the guidelines to be embraced by all contributors. All of the content was carefully scored according to criteria by the Oxford Centre for Evidence‐Based Medicine. We aimed at producing useful and reliable guidelines on bleeding diathesis, vascular approach, ultrasonic guidance, catheter tip positioning, prevention and management of associated trauma and infection, and specific training and follow‐up. A structured patient history focused on bleeding should be taken prior to insertion of a CVCs. The right internal jugular vein should primarily be chosen for insertion of a wide‐bore CVC. Catheter tip positioning in the right atrium or lower third of the superior caval vein should be verified for long‐term use. Ultrasonic guidance should be used for catheterisation by the internal jugular or femoral veins and may also be used for insertion via the subclavian veins or the veins of the upper limb. The operator inserting a CVC should wear cap, mask, and sterile gown and gloves. For long‐term intravenous access, tunnelled CVC or subcutaneous venous ports are preferred. Intravenous position of the catheter tip should be verified by clinical or radiological methods after insertion and before each use. Simulator‐assisted training of CVC insertion should precede bedside training in patients. Units inserting and managing CVC should have quality assertion programmes for implementation and follow‐up of routines, teaching, training and clinical outcome. Clinical guidelines on a wide range of relevant topics have been introduced, based on extensive literature retrieval, to facilitate effective and safe management of CVCs.

Management of inadvertent arterial catheterisation associated with central venous access procedures.

OBJECTIVE This study aims to describe the clinical management of inadvertent arterial catheterisation after attempted central venous catheterisation. METHODS Patients referred for surgical or endovascular management for inadvertent arterial catheterisation during a 5-year period were identified from an endovascular database, providing prospective information on techniques and outcome. The corresponding patient records and radiographic reports were analysed retrospectively. RESULTS Eleven inadvertent arterial (four common carotid, six subclavian and one femoral) catheterisations had been carried out in 10 patients. Risk factors were obesity (n=2), short neck (n=1) and emergency procedure (n=4). All central venous access procedures but one had been made using external landmark techniques. The techniques used were stent-graft placement (n=6), percutaneous suture device (n=2), external compression after angiography (n=1), balloon occlusion and open repair (n=1) and open repair after failure of percutaneous suture device (n=1). There were no procedure-related complications within a median follow-up period of 16 months. CONCLUSIONS Inadvertent arterial catheterisation during central venous cannulation is associated with obesity, emergency puncture and lack of ultrasonic guidance and should be suspected on retrograde/pulsatile catheter flow or local haematoma. If arterial catheterisation is recognised, the catheter should be left in place and the patient be referred for percutaneous/endovascular or surgical management.

Cerebral pharmacodynamics of anaesthetic and subanaesthetic doses of ketamine in the normoventilated pig

There are still divergent opinions regarding the pharmacodynamic effects of ketamine on the brain. In this study, the cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRo2) and electroencephalogra‐phic (EEG) activity were sequentially assessed over 80 min in 17 normoventilated pigs following rapid i.v. infusions of anaesthetic (10.0 mg‐kg‐1; n = 7) or subanaesthetic (2.0 mg‐kg‐1; n = 7) doses of ketamine or of its major metabolite norketamine (10.0 mg‐kg‐1; n = 3). The animals were continuously anaesthetized with fentanyl, nitrous oxide and pancuronium. CBF was determined by the intra‐arterial mXe technique. Ketamine (10.0 mg‐kg‐1) induced an instant, gradually reverting decrease in CBF, amounting to ‐26% (P<0.01) at 1 min and ‐13% (P<0.05) at 10 min, a delayed increase in CMRo2 by 42% (P<0.01) at 10 min and a sustained rise in low‐ and intermediate‐frequency EEG voltage by 87% at 1 and 97% at 10 min (P<0.0001). It is concluded that metabolically formed norketamine does not contribute to these effects. Considering the dissociation of CBF from CMRo2 found 10–20 min after ketamine (10.0 mg‐kg‐1) administration, it is suggested that ketamine should be used with caution for anaesthesia in patients with suspected cerebral ischaemia in order not to increase the vulnerability of brain tissue to hypoxic injury. Ketamine (2.0 mg‐kg‐1) had no significant effects on CBF, CMRo2 or EEG. It therefore seems that up to one fifth of the minimal anaesthetic i.v. dose can be used safely for analgesia, provided that normocapnaemia is preserved.

Ketamine and midazolam decrease cerebral blood flow and consequently their own rate of transport to the brain: An application of mass balance pharmacokinetics with a changing regional blood flow

Mass balance pharmacokinetics, with simultaneous blood sampling from an artery and the internal jugular vein, was used to characterize the cerebral uptake of ketamine, norketamine, and midazolam in normoventilated pigs. Intravenous injections of ketamine or midazolam decreased the cerebral blood flow (CBF)by one third, as measured by intermittent133Xewashout. By means of pharmacodynamic models, the effects on the CBFcould be predicted from the arterial drug concentrations. The high-resolution CBFvs. time curves thus generated allowed the calculation of cerebral drug levels from arteriovenous concentration gradients in spite of a continuously changing regional blood flow. By their effects on the CBF,ketamine and midazolam decreasetheir own rateof transport to the brain, the immediate 30-35% drops in CBFgiving similar reductions in initial net influx of drug. Physiological pharmacokinetic models assuming a constant regional blood flow are therefore not appropriate. Under clinical conditions, the CBFis determined mainly by the effects of the anesthetics and by the arterial CO2tension. CBFchanges in either direction influence the transport of drugs to the brain and may consequently result in impaired or exaggerated drug effects.

Desflurane induces more cerebral vasodilation than isoflurane at the same A‐line® autoregressive index level

Background:  Clinical use of desflurane in neuroanesthesia remains under debate. Comparison of dose‐dependent vasodilatory properties between desflurane and isoflurane, the more traditional volatile agent for clinical neuroanesthesia, requires equianesthetic dosing of the agents. Reproducible neurophysiological measurements of the level of anesthesia in an individual, e.g. the A‐line® autoregressive index (AAI), can be used for an equipotent dosage of two volatile agents in the same individual.

Desflurane increases intracranial pressure more and sevoflurane less than isoflurane in pigs subjected to intracranial hypertension.

Summary: Desflurane and sevoflurane may have advantages over isoflurane in neuroanesthesia, but this is still under debate. A porcine model with experimental intracranial hypertension was used for paired comparison of desflurane, sevoflurane, and isoflurane with respect to the effects on cerebral blood flow (CBF), cerebrovascular resistance (CVR), and intracranial pressure (ICP). The agents, given in sequence to each of six pigs, were compared at 0.5 and 1.0 minimal alveolar concentrations (MAC) and three mean arterial blood pressure (MAP) levels (50, 70, and 90 mm Hg) at normocapnia and one MAP level (70 mm Hg) at hypocapnia. MAC for each agent had been previously determined in a standardized manner for comparison reliability. CBF was measured with 133Xe. MAP was lowered by inflation of a balloon catheter in the inferior caval vein and raised by inflation of a balloon catheter in the descending aorta. ICP was measured intraparenchymally. Two Fogarty catheters positioned extradurally were inflated to a baseline ICP of 20 to 22 mm Hg at 0.2 MAC of each agent. CBF and ICP with the three agents at normocapnia and MAP 70 and 90 mm Hg at both 0.5 and 1.0 MAC were as follows (P < 0.05): desflurane > isoflurane > sevoflurane. None of the agents abolished CO2 reactivity. High-dose desflurane resulted in a higher CBF at hypocapnia than corresponding doses of sevoflurane or isoflurane, but there were no significant differences between the agents in ICP at hypocapnia. The present study showed that desflurane increased ICP more and sevoflurane less than isoflurane during normoventilation, but the differences disappeared with hyperventilation.

Cerebral blood flow at 0.5 and 1.0 minimal alveolar concentrations of desflurane or sevoflurane compared with isoflurane in normoventilated pigs.

Whether desflurane and sevoflurane have clinical advantages over isoflurane in neuroanesthesia is much debated. A porcine model was used for comparison of desflurane and sevoflurane with isoflurane with respect to their cerebrovascular effects. The minimal alveolar concentration (MAC) of each of the three agents was first determined in a standardized manner in six domestic juvenile pigs to enhance comparison reliability. Six other pigs were then anesthetized with isoflurane, desflurane, and sevoflurane, given in sequence to each pig in an even crosswise order with the first agent also used to maintain anesthesia during surgical preparation. Cerebral blood flow (CBF) was calculated from the clearance curve of intraarterially injected 133Xe. The mean arterial pressure (MAP) was invasively monitored. The estimated cerebrovascular resistance (CVRe) was calculated by dividing MAP with CBF, thereby approximating the cerebral perfusion pressure with MAP. For both MAC levels, the trend for CBF was desflurane > isoflurane > sevoflurane, and the trend for MAP and CVRe was sevoflurane > isoflurane > desflurane. Statistical comparison of desflurane and sevoflurane with isoflurane with respect to CBF and MAP revealed two statistically significant differences—namely, that CBF at 1.0 MAC desflurane was 17% higher than CBF at 1.0 MAC isoflurane (P = .0025) and that MAP at 1.0 MAC sevoflurane was 16% higher than MAP at 1.0 MAC isoflurane (P = .011). Consequently, in this study at normocapnia, these agents did not seem to differ much in their cerebral vasodilating effects at lower doses. At higher doses, however, desflurane, in contrast to sevoflurane, was found to induce more cerebral vasodilation than isoflurane.