Just got face to face with a moral dilemma and was wondering what the anaesthetic community would decide largely on this

called into see a 92 year old man who had fallen this morning and fractured his tibia
No previous surgery or allergy or major hospitalisation. Currently he is not receiving and drugs. He may have been on some in the past but progressively discontinued all of them.

Pale looking man , surprisingly had reasonable nutritional status.
He was drowsy, semi-conscious responding to minimal painful stimuli
History of hearing loss - could be the reason for failure to respond to verbal commands
respiration , airway control and pupils were all normal
CVS parameters were stable
He had a pansystolic murmur over the praecordium
RS showed a few scattered creps

Hb was 6.5
Urea was 84 and creatinine was 4.2
Electrolytes were unremarkable with potassium at 5.0
ECG shows old IWMI

Awaiting CT scan, my guess is that it will show nothing significant except for the atrophic changes associated with aging and dementia.

Has a compound fracture of Tibia and there is a steady ooze from the wound

Prior to the fall he was restricted to his room but could move by himself

The family asks if the surgery will set him back to normal

What would you think, say and do

I am awaiting the CT  and ECHO reports but am strongly inclined to advice not to subject this gentleman for anaesthesia and surgery. The risk is high and i am not sure that it will improve the quality of life

regs

GCS < 8 requires intubation as below this patient will not be able to protect his airway.

If the patient is unresponsive you dont need anything to intubate .
He will not resist or fight your attempts. But keep all emergency drugs ready and use xylocard to decrease rises in ICP

If he resists then he may need relaxants, usually suxa is used or you could use rocuronium
We do give some form of anaesthesia before giving relaxants

if hemodynamically stable use thiopentone
if unstable use Midazolam + fentanyl or Etomidate

You could try conscious sedation with remifentanyl infusion or dexmedetomidine infusion too.

In emergency intubation one usually does not have time to titrate doses so eyelash reflex may not be mandatory.
Eye lash reflex loss just shows that the patient is just about under, at this level his tracheal and carinal reflexes will still exist and chances of awareness are high

RECOMMENDED READING
miller - intubating the head injured patient in trauma

regs

with a little bit of effort preservative free morphine can be accessed.
Brand name VERMOR
i can send u the company details if interested
I have used 250 to 300 mcg of morphine in spinals but am very judicious about the patient population. Usually healthy, fit, robust patients.
It is my standard practice to use buprenorphine in all my spinals. I use about 150 mcg. I have had only 1 case where the respiratory rate was 8/min but the patient maintained adequate minute ventilation and CO2 removal. No respiratory problems otherwise. About 10% of these patients suffer from PONV and it can be quite distressing in a select few, requiring multiple doses of ondansetron and multimodal therapy.
I also use buprenorphine epidurally in a dose of 300 mcg.
I find that buprenorphine intrathecal produces good to excellent analgesia, lasting 24 to 72 hours, in majority of the patients.

I theorotically disagree with the learned Dr. Bhatt's opinion regarding the use of Naloxone, although in his vast experience his observation may be absolutely valid.
So the theory is
Naloxone is an opiod antagonist and is most effective against pure opiods that are agonistic at the MU receptors. So works well with morphine, fentanyl and all phenopiperidines
Buprenorphine is a partial agonist - antagonist drug. Its agonist action is at the KAPPA receptor and anatgonist action at the MU receptor.
So since buprenorphine is already antagonsit at the MU receptor I wonder how adding another antagonsit is going to reverse action especially since naloxone is ineffective at the KAPPA receptor

The other worrying point about buprenorphine is the fact that this highly lipid soluble drug has a FAST IN - SLOW OUT action. SO it binds fast but has a very slow dissociation constant . Hence if you get into undesirable trouble it may be very hard to reverse it.

Hence i use buprenorphine with extreme caution in the
extremes of age &
patients who have compromised respiratory function

regs

A 60 year old male is scheduled for emergency exploration of a AV fistula blow out at his left wrist. Bleeding has been arrested with a compression bandage
He is currently drowsy, arousable and disoriented
His BP is 170 / 100
His CVS and RS examination reveals nothing of significance
ECG shows LVH with strain
CXR - mild cardiomegaly
His HB is 8.5
urea is 86
creatinine is 6.6
Na is 129
K is 5.5

BT/ CT has not been done

The surgeons want to explore the site at the wrist and will use a tourniquet

Am i justified in using a regional block or is GA the way to go
If sedation is necessary what drugs would you choose

Hi all

Have a 65 year old lady posted for fractional curettage and proceed
She is a case of CML, treated and now in remission and is currently on on IMATINIB MESYLATE ( Gleevec)

THe side effects of this drug is quite exhaustive
This pt has an Effort tolerance < 4 METS and is a diabetic with reasonable control

Her history related to coagulation, renal and hepatic function is largely insignificant

Surgery may last 30 mins
I am planning to slip in a LMA under Propofol and Fentanyl
and maintain her under Spontaneous Ventilation with Sevoflurane

Any advices on how to do it better
Any areas i need to focus on

regs

Sir
Many such instances have been encountered in teaching institutes where sometimes PGs on the learning curve end up with
My mind recalls this case
Young ASA 1 patient posted for uro-gynecological repair for complication after delivery
Assessment revealed a Mallampati score of 3 with IID, MTD and neck movements being normal. She had no other markers to predict a DA scenario.
I cant recollect why a GA was planned on her but i guess in those days with a paucity of epidural catheters and considering the length of surgery a GA might have been planned
That was the Pre-GEB era
After induction intubation failed
so a metal ETT introducer or stilette was used to mould the tube and I think intubation was  successful in the 2nd or 3rd pass
Rest of intra-op period went uneventfully
1st POD was unremarkable except for fever.
Oral fluids were started on day 2 and patient developed cough, wheeze, desaturation and progressive deterioration needing intubation and ventilation
A diagnosis of possible TE Fistula due to injury during intubation was diagnosed.
We lost the patient on day 5.
I am certain that a large number of such cases may have gone unreported

But the introduction of Sialastic GEB have certainly helped to overcome trauma that our old metal stillettes produced

regs

when you connect it to a column of liquid it measures the pressure in cm of H2O and at best this method of measuring is not very accurate
I have never measured these pressures
but i am sure that we can connect the system to a low pressure transducer and connect it to a monitor used for invasive pressure monitoring and then we can get more accurate results in mmof Hg. the principle is much the same as used to measure the CVP

I am also wondering if a indwelling catheter can be used. Maybe stick in a 22G IV cannula and put the catheter into the subarachnoid space and connect that to a pressure transducer system

I am uncertain whether a slow flush with heparin that we use to prevent from the catheter clotting has any role or is safe in CSF pressure monitoring

Actually even the best centres in India do not routinely monitor CSF pressures, because it is obviosly difficult and the information it yields is at best suspect

Beware the risk of infection spreading via the catheter inwards

regs

"A card" is the trade name for INTRA- ARTERIAL ECG GUIDANCE for proper positioning of CVC catheter tip at the confluence of SVC with the RA
You can google the Braun products and the catalogue should show up
Proper positioning of catheter tip is of paramount importance when there is a likelihood of air embolism. Aspiration of the embolised air will be possible only if the catheter tip is optimally placed

But Xray chest shows you pneumothorax which a ACARD cannot show. Pneumothorax can occur when the advancing needle touches the apical pleura or the lung itself. This has an incidence of 10% with SCL vein and about 3 -5 % with IJV insertion. Is more common in COPD patients.
Needle touching the pleura followed by IPPV during anaesthesia can produce significant pneumothorax or rarely potentially fatal tension Pneumothorax.
ACARD cannot detect this and this undoubtedly will require a Xray chest in the post op period although it can be delayed by a bit


regs

The only way for air to get in is if we put it there
Direct subcutaneous emphysema would have been a possibility if the fascial planes were breached by something like high pressure jet ventilation or gas insuffalation into tissue spaces like creating a pneumoperitoneum
In most other cases it usually occurs as an extension of air in the pleural space under pressure. The tracheal mucosal breach could just have facilitated this traversing of gas
With regards to a negative Xray finding, I wonder what position the Xray was taken in. Lying posture may have caused poor quality or artefactual problems. The pneumothorax needs to be more 150ml air to be picked up radiologically. Suppose there was a significant pneu,otorax and then through the tracheal mucosal injury it ran away into the mediastinum and then the lung expanded back, we could be missing the xray finding
This is only a hypothetical explanation and i am sure that what is confounding you could be correct
In anaesthesia it is prudent to think of common things first and always. So I am just applying these principles to your case

regs

The subcutaneous emphysema seems to be an extension of a pneumothorax that could have easily developed in this patient
1. Pneumothorax due to Volutrauma / Barotrauma to to aggressive IPPV. This could have lead to tension pneumothorax which itself is a well documented cause of bradyarrythmias and asystole.
2. Pneumothorax due to Cardiac compression due to rib fracture and pleural / pulmonary injury
3. In difficult airway instrumentation of airway with stilette and GEB can produce tracheal mucosal tear and hence could lead on to pneumothorax and massive mediastinal and subcutaneous airleak.
I have seen or encountered all the three causes of pneumothorax in my clinical practice

regs

Mace
your practice is consistent with recommended scientific evidence
I dont think the process can be made any safer
USG guidance, measured catheter length and aspiration should suffice
I wonder how an CXR is going to further aid confirmation of placement. CXR may reveal a pneumothorax if it develops secondary to pleural injury, which is why we use a USG to minimize it.
CXR in post-op period will suffice, unless you are going to IPPV the patient with large volume controlled ventilation and you want to avoid any chance of tension pneumothorax

a piece of advice
if your boss wants it that way and the facility is available why not get it done
it may not be necessary but it can do no harm
the only thing you will lose is a few minutes and a bit of scientific ego

regs

An ASA 1 patient undergoing GA
Glycopyrrolate 0.2 + Fentanyl 100mcg + IV paracetamol 1 gm
Xylocard 50 mg + Propofol 120 mg +Rocuronium 35 mg
Intubated with 7.5 mmHg oral ETT
N2O 2L + O2 1 L + Sevoflurane 1.5%
Pt on anaesthesia ventilator with TV of 500 ml and rate of 12.
The above picture is the ETCO2 tracing. All other monitored parameters were within normal limits.
After about 15 mins of continuing same line of management the ETCO2 tracing became normal

Is there an abnormality in the tracing or is it nothing to be worried about

regs

A 72 year old hypertensive & COPD patient with a trochanteric fracture was worked up for DHS
HT was controlled with Atenolol 50 mg OD
He had a smoking history of 50 pack years and had bad lungs at admission. The chest physician started him on Nebulized beta2 agonists, steroids and ipratropium.  As no improvement was seen he added IV Methylprednisolone 125 mg tds.
On day3 at assessment,  lungs still had bilateral wheeze and scattered crepitations and his ECHO was normal but for the concentric LVH. ECG was within normal limits and CXR showed tubular heart with hyperinflated lung fields.
Since conversion to GA if necessary would be risky, a CSE ( 2 needle, 2 interspace sequential technique) was planned so that post-op analgesia could be provided with an elastomeric pump infusion. LMWH dose was withdrawn 24 hours before needle placement.
After all the initial set up in OT as per scientific protocol, with the patient sitting Epidural attempted at L34 ISS with 16G Tuohy needle using LORT air technique. Inadvertent dural puncture ensued and the needle was withdrawn. Repeat epidural was done in T12L1 ISS, space identified and the catheter was passed caudad upto 4 cms in space to tip it probably at L23 level. When the catheter was aspirated CSF was noted. Uncertain about catheter position, epidural test dose was abandoned but the catheter was secured in place.
As per original plan, SAB was done in L34 ISS with 25G Quincke needle without experiencing any technical difficulty. 3 ml of 0.5% hyperbaric bupivacaine was given after free flow of CSF to aspiration.
Patient during  positioning on the fracture table was pain free but patient complained of pain to incision.
Epidural catheter reaspiration showed CSF. Hence hyperbaric 5% lignocaine was injected into the catheter to try and attempt a continuous spinal. 0.5 ml produced no improvement in analgesia or no decrease in BP. Every 5 mins a dose of 0.5ml ( total 3 doses)  was repeated but did not produce any effect.
Then 2% lignocaine with 1 in 200000 adrenaline was injected into the epidural catheter 2 ml / every 10 mins. After injection of about 6 ml, analgesia was complete and adequate and from then on surgery proceeded uneventfully. Intraoperatively 2 other epidural  top ups of 4 ml each were used without any untoward effect on block characteristics or hemodynamics.
UP FOR DISCUSSION
1.   How better could this case have been managed
2.   What is the management protocol  followed by majority in event of dural tap and / or CSF in the catheter
3.   Why did the spinal become patchy.  Although the most likely cause is placement of drug in the wrong space ( partially atleast because there was a block) Just wondering that if the lingo injected in L34 could have  spilled out of the subarachnoid space along with CSF from the dural puncture in the L23 space. Is that a possibility. Has anybody experienced it
4.   CSF in the catheter – was it from the catheter being in the subarachnoid space or the CSF leaked out of the dural puncture site and lying in epidural space. How to differentiate between the two scenarios.
Regs

There is nothing called as better anaesthesia
there is only safe and scientific anaesthesia or otherwise
extensive studies are available that show that the choice of anaesthetic does not change outcomes in ASA 1 to 3 patients
ASA 4 patients do well with controlled, titrated GA

All peripheral  limb surgeries are better done under RA.

Most of the centres do abdominal hysterectomies under SAB and the surgery is completed in 90 mins

What i do

IF extremely obese or has contraindication for surgery give a GA

In other cases SAB at L3L4 ISS - 3.5 ml of hyperbarIc bupivacaine + 150 mcg of buprenorphine
Adequate in 95 % of cases
In the remaining 5%,  if surgery gets prolonged pt experiences discomfort during start of closure. Also poses problems for the surgeon.
I induce with propofol 2 mg/kg + Suxa 1 mg / kg and put in a LMA. Once patient recovers -  leave her on spontaneous  ventilation with o2 + n2o and sevo

Rarely in cases that are likely to be prolonged I might opt for a combined spinal epidural (CSE) 2 needle 2 interspace sequential technique
start with SAb - same dose as mentioned without bupre
After 90 mins top up the epidural catheter with fractionated 5 ml doses of 0.5% bupivacaine

regs

There are several ways to approach a case
each with its own pro and con
if my opinion differs with my boss, I would state my view point to him and discuss.
I would document the advice given by boss and proceed as he advices

I am not certain if the ACLS guidelines recommend Digoxin as the primary drug to manage Vtach
If hemodynamically unstable - cardiovert
If stable - Amiodarone are probabaly the drugs of choice

That is just my viewpoint and since I am not your boss, you dont necessarily have to take it

reg