Is Iso passé?

I'm 42 tomorrow. A number which Douglas Adams said was the answer to something. Not that old, I think, but old enough to be seen as an old dog with old tricks. In the teaching hospitals I am often quizzed by trainees as to why I am using thiopentone (see a previous blog fro one expanation) or isoflurane. (Not that I use them all the time!) Isoflurane used to be kept in directors' offices, only to be used for special indication. Now its going the way of halothane. The flight of time! But it's such a nice drug: no metabolites or fluoride, no compound A, no arrythmias. I revisted comparative pharmacology today when I provided anaesthesia for free flap surgery. The literature indicates that isoflurane leads to better graft survival than sevoflurane and the older agents, probably because it is a better vasodilator without causing too much cardiac depression. So there is more to volatile agent choice than the faster offset that the drug companies emphasise. One difference that is not well known is the greater bleeding with sevoflurane compared to isoflurane. Workers from the Department of Anesthesia, Kitano Hospital, Osaka, Japan have produce several papers which conclude that sevoflurane has a significant bleeding tendency effect, most likely by inhibition of platelet aggregation. So in addition to old fashioned thipentone induction for the bleeding patient (so to avoid excessive hypotension of propofol), isoflurane should be used for maintenance (so to avoid the anti-platelet action of sevoflurane). And perhaps it should remain the agent of choice for surgery with a tendency to bleeding, such as cesarean section?

Adelaide Frolics

The Adelaide ANZCA ASM played like the regional anaesthesia empire strikes back. The regional enthusiasts gave some acknowledgment that RA contributes little to reducing serious adverse outcomes and they dismissed the significance of one in a few thousand chance of bad sequelae. However they derided "naffing confidence intervals", showed a picture of a satisfied fat American after a sciatic nerve block and one of the speakers made the alarming revelation that she was turned on by a successful peripheral block- well if that's what it takes to bed an anaesthetist....

Therese Horlocker continued her message about anticoagulants and regional anaesthesia. My impression of her view is that it is mostly a matter of careful timing, but this month's (June 06) BJA reveals that ceasing antiplatelet therapy perioperatively greatly increases the risk of a perioperative cardiac event. And with more diabetes, more coronary stenting and more use of clopidogrel for secondary prevention I think we will be increasingly presented with patients on antiplatelet therapy. It is hard to see how ceasing this therapy to allow neuraxial blocks will increase the overall benefit, particularly if the surgery can be reasonably attempted with the antiplatelet drugs on-board.

She also gave a bit about preexisting neurological disease and RA. The “double-crush phenomenon” occurs when an insult (such as lignocaine or a needle contact) to an already affected nerve has a synergistic negative effect. Multiple sclerosis is well known as disease that may be susceptible to the effects of local anaesthetics and the possible direct nerve trauma of a needle. Despite the hypothetical, Therese's Mayo Clinic has a reassuring case series of RA and MS. But if you don't need to do it, do you need to do it? Perhaps so in obstetric cases; should we consider that for MS cases we only use dilute bupivacaine for labour, concentrated epidural ropivacaine for CS, and avoid spinal doses (at least large doses) and epidural lignocaine and adrenaline?

Intravenous paracetamol for cesarean caesarean analgesia-elixir or lolly water?

Intravenous paracetamol bottles have appeared on the shelves of the obstetric theatre operating room like stubbies in the cricket club change shed. Are they just another expense to the economy and another stress on the environment, or does IV paracetamol actually do some good? A pubmed search finds little that recommends the use of paracetamol by any route for caesarean. For other surgery, a metaanalysis in Anesthesiology Dec 2005 by Elia et al concludes that only NSAIDs are analgesic. At most, paracetamol is opioid sparing, but it offers little more over an NSAID that has already been given. But until recently it has been a very cheap drug, with few side-effects. (The potential for liver necrosis is always possible though, and there have been iatrogenic perioperative cases.) So it has been commonly given in recent times: a cheap, harmless and probably useless effort which at least comes with good intentions. But now it comes in a big jar, which needs venting. In dental surgery IV proparaectamol's onset of action is very rapid, but ultimately is less effective than the oral route 2-3 hours later (Moller, BJA 94 5) because it presumably redistributes. So why give IV paracetamol to a patient who is blocked with regional anaesthesia, and will be for another hour or two? Its peak effect (which is little anyway) will have peaked and waned by the time the regional anaesthesia has resolved. So if paracetamol must be given why not give it in its oral form? Oral medication is usually well absorbed and tolerated after caesarean section. Oral paracetamol is cheap and palatable, and its onset time will more likely correspond to the time of anaesthesia's end . But for all the good it does, you may as well stick it up an arse.