we attempted a study on SAB for lower abdominal laproscopic surgeries.
Surgeries included were lap appendicectomy, lap hernia and lap varicocoelectomy
we ensured neutral position only and kept intra-abdominal pressures limited to 12mmHg.
SAB level was T4 - T5. Sedation included Midazolam 50mcg/kg and ketamine 0.5mg/kg

We had to abandon study  since all patients needed conversion to GA except one who was managed with unacceptably high doses of ketamine.

Primary complaint was severe pain in shoulder area and some patients expressed discomfort during breathing although SaO2 and ETCO2 were within acceptable limits.

Although there is plenty of literature our experience did not support the findings

Is there any stadardization regarding the diameter of Adult and Paediatric T pieces at their FGF, patient and machine end.
Is there any reference that details about its ID and the length of the expiratory limb.

I find that different makes seem to have different connector sizes and the Diameter of the FGF tube and length of expiratory limb is also inconsistent.
I also read an article that utilizes a 20 ml syringe with plunger removed and a hole in the middle of it into which the O2 supply is attached. One end of the syringe attaches to the ETT and the other end is open to atmosphere to act as expiratory port.
What FGF will it supply at say  flow of 5 or 1o lpm.
Want it increase resistance to expiration thus increasing WOB

SHO's are arbitrarily using 10 and 5 ml syringes to prepare such T pieces and I wonder about their effectivity

Is there as easy equipment to actually measure the FiO2 being delivered with such contraptions

Thanks for the info

Dextrose containing IV fluids have no role in anaesthesia unless you are dealing with
1. Diabetic patient and Dextrose as part of intra-op regime
2. Proven Hypoglycaemia esp in Neonates

Why is dextrose not used?
1. Anaesthesia perse increases glucose levels even in normal under influence of released stress hormones
2. Anaesthesia leads to decreased quantity and quality of insulin
3. Adverse incidents have poor outcomes in the presence of Hyperglycaemia
4. Intra-op hyperglycaemia produces atleast 8 - 10 undesirable effects on the physiology( any decent literature will give you the details)

What is ideal fluid ?
One that stays in the intravascular compartment longest , is iso-osmotic  and iso- tonic
Crystalloids - RL & NS
Colloids - pick your choice (My choice Hetastarch)

Dextrose containing fluids - owe their osmolality to dextose. Once infused Dex is taken into cell leaving behind hypo-osmotic free water whcih moves intracellular. It does not stay in IV compartment( where youneed it most after SAB) and can produce cellular edema

My recommendation

preload with 20 ml/kg of Rl or NS ( 20% remains in the IV compartment about 20 mins later)
Same dose for colloids produces better and longer lasting effect.
Individual choices for patient or a combination of both carefully weighing the risk- benefit ratio is the best approach

Current ASA advisory on obstetric Anaes Apr 2007

Preloading strongly recommended before CNB.
Does not abolish hypotension but minimizes the severity and duration of hypotension

40 years - No comorbid factors can tolerate fall in Hb to 7 mg ( HCT 25%)
currently her HCt is 30% ( Hb of 10)

She must be 60 kg
Her estimated Blood volume is 4200 ml

Her allowable blood loss to reach a Hct of 25% is about 650 ml.
Should try and restrict the blood loss to that level.

Waitng to improve Hb using Iron could take too long and may lead to dissemination of malignancy
Iron supplemented with Erythropoetin, both parenterally may improve Hb faster.

After discussion with the surgeon I will proceed with surgery and use techniques to mininmize blood loss using intraoperative Normovolemic hypotension within lowest acceptable limits.

Since she is an ASA 1 patient I would maintain MAP between 50 to 55 mm Hg.

Oral premed - Oral Benzodiazepine + oral clonidne 2mcg/kg

Fent 2 mcg/kg + Lignocard 1.5 mg /kg
Propofol 2 mg/kg + Vecuronium 0.1 mg/kg
N20 66% + O2 33% + Isoflurane 1%
Vec + Fent as needed

Restrictive fluid protocol to maintain Uo of 0.5 ml/kg/hr

Hypertension

beta blockers ( if HR >70) + Ntg titrated to maintain MAp to desired levels.

Reverse and extubate whn fully awake

Intraop hypo to be managed with crystalloids, colloids and vasopressors

What more is the haematologist going to do on this case

regs

Figured this one out
the N2 comes from the air that got embolised

Normally ET N2 is 0
Even a increase of 1 to 3 mm of N2 is extremely sensitive

It is more sensitive than decrease in ETCO2 because several other factors can decrease ETCO2 like
hypothermia
hyperventilation
hypotension

ofcourse you need to be using a multigas monitor

Amongst the myraid of techniques recommended to detect air embolism during neurosurgery the top few based on sensitivity are
Trans-oesophageal echo
Doppler Ultrasound
Decrease in End Tidal CO2
Increase in End Tidal N2.

How did N2 come into the picture since during preoxygenation we had denitrogenated the patient and we are now ventilating with a gas mixture containing only N2O and O2.
What monitoring device are we using routinely that would pick up N2 in the expired gas - ?? multigas monitor working on Mass spectrometry or Raman effect

I have just lost the picture..............

3 degrees under my belt and so much more unlearnt in anaesthesia

Ondansetron - prolonged QT interval and cost effectiveness
Does it worry you
we use buprenorphine in all our CNB for post-op analgesia.
In the few rare cases that end up with PONV even Ondansetron 8mg IV tds is of no use
Droperidol might be a rescue antiemetic in such situations but have no expereince working with that drug

no experience
but i presume scientifically speaking
you could use the shortest acting mu opioid receptor pure agonist - remifentanyl or fentanyl
Risk of foetal depression is expected and can be managed with paediatrician on standby with naloxone and airway access devices if necessary

But why not consider an inhalational alternative
Entonox is touted to be an excellent alternative to CLEA

we are happier with the known devil(Halothane) than the unknown

Miller 5th ed clearly states that HALOTHANE MUST NOT BE USED IN NORMAL ADULT PATIENTS UNLESS YOU HAVE A DEFINITIVE (hardly any) INDICATION.

I do use halothane extensively too. But even if 1 patient develops fulminant hepatic failure it will be difficult to defend it.
Iso flurane, Sevo and Des also have there own problems

But current scientific evidence would support a move away from Halo to Iso/ Sevo

We swore by Gallamine, we dropped for Pancuronium and now we are into Vec, Atra and Roc

Move where the scientific evidence takes you and thats the basic essence of evidence based medicine

Regs

I and the lawyers advising us anaesthesiologists would agree with you
On the other hand i just saw a case of tracheal stenosis today after an uncomplicated ETGA.
really sad and scary
I wonder why we never pay attention to the volume of air we use in our ETT cuffs esp since we use N2O in our balanced anaesthetic technique

a wee bit but not much
but there is alot of protocols in anaes that sound like rules in mathematics
Maybe research into some aspects of anaesthesiology like pharmacokinetics may be based on mathematical models
Statistics is another branch of maths that has application in all the research work we do
hope this feedback is useful to you

In India ketamine is practically used for every possible procedure. Starting from sub-anaesthetic doses to provide analgesia down to being the sole anaesthetic agent for diagnostic laproscopies of the pelvis.
Some use it along with narcotics
Along with Propofol called the PK regime it si gaining worldwide attention.
Need to remember that ketamine is not the answer to all anaesthetic troubles - it does not protect the airway, it is a mocardial depressant in catecholamine depleted patients and emergence delirium can cause problems.
The other worry is its abuse and addiction. In recent times it is the most smuggled drug from India for pleasure puposes. I fear that very soon it may be banned or difficult to procure owing to its abuse potential

Not totally wrong but a wee bit lucky too.
I ended up doing a radical mastectomy under LMA /CV
No ETCO2
Somewhere along the anaesthetic the LMA must have partially malpositioned
Net result - a hypercarbic patient with delayed recovery
Ofcourse got her out safely
The point is if everything goes well with LMA its OK
but if something goes wrong like minimal aspiration, inadequate ventilation or intra-op laryngospasm then it will be extremely difficult to defend.
We could have intubated the patient which is a definitive airway

we dont use infusions
we stay with 1 ml of 0.5% hyperbaric bupivacaine, repeated at the earliest evidence of discomfort
The original 24G catheters approved for continuous spinals are associated with a possibility of cauda equina syndrome.
Threading in a 16 or 18G epidural catheter must definitely increase that risk.
Also moving pt to Post-op with catheter in SA space may increase the risk of direct infection transmission to meninges
I am in favour of removing the catheter ASAP.
Use it for intra-op anaes but remove the catheter before shifting him from OT
For post op analgesia just prior to catheter removal you may want to inject a long acting intrathecal narcotic like Morphine or Buprenorphine

rarely epidural spaces maybe separated by spta much like the caudal space in adults
What is more common is the sparing of the L5 segemnt.
This nerve root is extremely large in some individuals and is difficult to block by epidural drugs in teh ususal concentration.
This may produce sparing of the segmental distribution producing breakthrough pain