At the beginning let me confess that although recommended we seldom seem to follow the MODIFIED ALLEN'S TEST before we start A-lines on radial arteries of patient

Now the case scenario

A 32 year old lady was taken over by us in the surgical ICU after a major laprotomy for catecholamine secreting tumour. Her pre-operative co-morbities included hypertension, LVH and severe anaemia. All of them were corrected to optimal levels
Anaesthesia consisted of GA/ CV supplemented by a thoracic epidural. Intra-operatively she had her IJV cannulated but was maintained on ANIBP for lack of transducing facilities.
Intra-op problems included need for vasodilators initially and later vasopressors/ inotropes including Noradrenaline and Dopamine. She also received massive blood transfusion to replace her loss
Post-operatively she was put on elective ventilation.
Day 2 when we took her over, she had signs of septicaemia, myocardial dysfunction and a host of multisystem problems and was still on the ventilator.

All standard treatment protocols were inititated and to permit repeated ABG analysis and also to monitor CO and other variables including Systolic Pressure Variation, it was decided to put the patient on VIGLEO the PICCO monitor of Edward Lifesciences.
As per requirement, her left Radial artery was cannulated using a 18G cannula using the regular tranfixation technique. ALLENS TEST NOT DONE. Procedure was uneventful and tracings on the A-line were good.

24 hours later patient's left hand distal to the A-line became discoloured, cold and clammy. A diagnosis of vascular insufficiency was made. Causes seem to be multiple, but definitely also included suspected insufficiency of the palmar arch, which was not tested..
A-line was removed. Vascular opinion confirmed vascular insufficiency and patient was put on Heparin

We eventually lost the patient to MOFS,  but the blood flow to the affected limb did not improve.

NOW THE DILEMMA
A large number of papers are available that question the specificity and sensitivity of MODIFIED ALLEN"S TEST. All our Cardiothoracic surgery patients also do not have this test prior to their arterial cannulation
So do we need to perform it mandatorily

Although I did search I never found this out
What is the difference between ALLEN'S TEST and MODIFIED ALLEN'S TEST

Should this test be done only for arterial cannulation or also before we prick the artery for taking an ABG sample
Would leaving out this test and ending up with a very rare complication like this amount to negligence

Keenly looking forward to your inputs and experiences

regs

Epidural Needle placement
12 hrs after last dose of LMWH
first postoperative dose 4-12 hours after needle placement
catheters removed 10-12 hours  after LMWH and 4 hours prior to next dose;
postpone LMWH  by 24 hours if traumatic


The above mentioned are the ASRA guidelines for Anticoagulatns and Neuraxial blocks

There is a little difference if you follow the other  guidelines like spanish or German

regs

Crystalloids get out of central circulation within 20 mins in normal circulation. that is normal physiology and not leaky circulation. Leaky circulation is when edema occurs inspite of PCWP being normal like as in sepsis.

We are not debating colloids. But if you look at the Cochrane review there is no statistical difference between use of colloids and crystalloids

Simple - dont give huge neuraxial blocks to patients with renal and CVS disorders who will not tolerate the degree of sympathetic block induced by spinal

Sure ephedrine has alpha and beta effect but it is very short lived. Also increasingly phenylephrine is being recommended to tackle hypotension that requires vasoconstriction

High spinals can block cardioacelarator fibres. The name it self suggests that these fibres will decrease the heart rate and hence cardiac output. In such a scenario anticholinergics may play a better role in restoring rate and CO than inotropes

One man's food can be another man's poison
i wonder if your pudding or my pie is backed by adequate scientific evidence

at the end of the day you and me should be united by the science we practice and not  merely  by our personel experiences, preferences, likes and dislikes........................

These are the days of EVIDENCE BASED MEDICINE

regs

"giving fluids is an inferior way of treating a vasodilated circulation which is a leaky one. giving colloids makes a little more sense." - anaesami

I wonder why do you think that a otherwise normal system vasodilated by sympathetic blocakde of SAB is leaky.
Physiology is not so fragile. I wonder if there is any reference to support that arguement.


Hypotension in CNB is primarily due to a decrease in preload , due to decreased venous return to the right side of the heart. This occurs due to the relative hypovolumia due to the sympathetic blockade. The venous capacitance vessels in the lower limbs retain a large amount of blood in them. When preload decreases the CO is also decreased. Decreases in CO produce decrease in Diastolic BP and hence possibly decreases in coronary blood flow. Hence theorotically the myocardial O2 supply can be decreased.

Management must include fluids ( crystalloids or colloids) and vasopressors that produce alpha stimulation and hence increase SVR and BP.
Vasopressors of choice would be phenylephrine, mephentramine, ephedrine, metraminol and nor-adrenaline

Now there is a slight difference between vasopresoors and inotropes.
Vasopresssors increase the SVR without increasing myocardial contractility too much and hence are not arrythmogenic and do not increase myocardial oxygen demand very much.

Inotropes like Dopamine actually increase rate and myocardial contractility and hence increase myocardial O2 consumption

So in a CNB scenario where myocardial O2 supply is low , using dopamine increases myocardial O2 demand and hence worsens the imbalance

Also in sympathetic block of CNB, the myocardial contractility in largely unaffected. So why do  we need to increase contractility, we only need a vasoconstrictor like an alpha agonist.

Dopamine can produce alpha stimulation, but in high doses of > 15mcg/ kg/min. Such high doses can produce severe tachycardia. I wonder if you really used Dopamine in such high doses.

Using dopamine in lower doses primarily acts through
DA2 receptors(< 3 mcg/kg/min) where it will produce splanchnic vasodilatation and hence decrease in MAP
or
BETA recetors ( 15mcg/kg/min) where it will produce tachycardia and vasodilatation and hence decrease in MAP

If you so want an inotrope with alpha action I think adrenaline makes a better choice than dopamine

Dopamine is NOT A PANACEA for hypotension of any cause.
You should google the side effects of Dopamine and see the results

with this arguement i rest my case aganst the routine use of adrenaline to manage hypotension produced by extensive CNB blocks

I  think if after a CNB block a patient needs Inotrope to maintain his BP then the choice of CNB in such a patient itself may be questionable.

Regional anaesthesia has no parallels if used on the right patient for the right indication
But i think we are guilty of abusing RA in certain situations

regs

The incidence of sore throat after

ETT intubation is 1 in 2  - 50%
LMA is 1 in 5 - 20%
Facemask is  1 in 7 - 16%

so everything has been tried and nothing works effectively

best thing to do is warn the patient pre-op to expect the throat discomfort

regs

I agree with Dr. Bhatt's observations

Current evidence suggests that 5% Lignocaine hyperbaric should not be used for SAB
We have given up the drug totally pending further evaluation into 2% hyperbaric lignocaine

Vomiting in SAB is a hallmark of cerebral hypoperfusion and requires emergent intervention.

PE is a possibility
Also could the patient have had occult CAD not picked up on resting ECG. Younger onset coronary ischemia is quite common these days. The patient has developed crepitations indicating probably pulmonary edema probably due to LVF.

In PE, PVR increases and that produces pressure overload on the RV leading to usually RV failure.
ofcourse this could lead to decreased CO and coronary perfusion and finally LVF too

Prevention
all patients having any risk factor for developing PE ( this patient was obese) must receive LMWH ASAP, probably pre-op itself

Having said it let me record the truth
in my centre LMWH is not a routine.
multiple factors including
non-compliant surgeons, drug non-availability, avoidance to perform CNB

regs

2nd trimester is the safest period to give anaesthesia
GA/CV is the best  & most relaiable option
Goals to include
1.Anti aspiration prophylaxis
2.RSI intubation
3.Tocolytics to avoid premature labour
4.Avoid aortocaval compression with wedge
5.Ensure adequate uteroplacental blood flow by limiting Intra-abdominal pressure and haemodynamics
6.Fetal tococardiographic monitoring

I do not agree with Epidural and IV sedation with fentanyl /propofol in these pateints
reasons being
1.Airway protection under sedation is not assured
2.Ventilatory sufficieny in the presence of hypercarbia and sedation is not assured
3.With sedation risk of aspiration is increased
4.Epidural already produces hypotension, add on propofol and it may lead to significant decrease in uteroplacental blood flow
5.Patient already has decreased DO2 as a result of physiological dilutional anemia. Add hypoventilation due to sedation and hypotension and then you may be in and around critical DO2.

I think we as anesthetists continue to be enamoured with techniques rather than goals.
I can tell for sure that there is no evidence that EA is safer or superior to GA in pregnancy or in lap surgeries.

regs

A samll puncture wound into lung during fall sets up the source of pneumothorax.
Since patient is spontaneously breathing the intra-pleural pressures are negative and they are driving the ventilation, so no leak of air or pneumothorax occurs.
As soon as you started anaesthesia and initiated IPPV the  positive pressure now drives the ventilation. With each IPPV breath a small amount of air leaks into the pleural space. This small leak is repeated every breath and can eventually lead to pneumothorax and tension pneumothorax.
So that is why it can still take 2 hours of IPPV before the incident occured

ofcourse just thinking aloud

regs

Obviously air has got into the fascial planes and has been driven in by high pressure and hence the extensive distribution of subcutaneous emphysema
We just need to figure out the route

The patient had hypotension, increased airway pressure, desaturation and asystole and was revived - so there was a correctable cause for that scenario of events that is why he survived

The commonest cause that fits into this clinical picture is a major pneumothorax progressing probably to tension pneumothorax.

So where did the pneumothorax occur from?
That is open to speculation!
During the fall he had a puncture wound into his lungs. Was asymptomatic till he was on spontaneous ventilation, the moment IPPV was initiated under anaesthesia patient developed slowly progressive pneumothorax progressing to the situation cited.

Alternatively operation around T11, the surgeons were very close to the posterior reflection of the pleura. They could have produced an inadvertent damage to the pleura during dissection or drilling which progressed to tension pneumothorax and arrest.

Air embolism can occur in spinal surgeries and can produce hypotension, increased airway pressure and asystole, but however it cannot produce such severe subcutaneous emphysema. So that kind of rules it out. Also massive air embolism producing arrest has a poor response to treatment.

Tracheal rent, although a possibility, seems far fetched and unlikely. There seems to be no airway instrumentation and intubation seems to have proceeded quite uneventfully.

Whatever be the cause of this catastrophe the anaesthetic team needs to appreciated for monitoring the patient effectively, picking up the life threatening complication in time, intervening appropriately and saving themselves and the patient from disastrous consequences. Commendation to all involved.

Finally inspite of our best intentions and attempts so many things seem to remain beyond our control in anaesthesia. Complications - expected or unexpected, are going to continue to occur and we just have to make sure that our monitoring and record keeping is as fool proof as possible, all necessary and practicable protocols are in place and above all Providence continues to shower his blessings on us

keep the good show going.

regs

We activate the epidural component of CSE intra-operatively depending upon the need of the surgery.
If motor paralysis is necessary to proceed with surgery we go with 0.5% bupivacaine + 2 - 5 mcg/ ml of fentanyl. We usually use fractionated doses of 3 - 5 ml at a time. We monitor the level and add on the drug as necessary to get the desired block level.

IF we need only sensory block we prefer 0.25% bupivacaine with the same strength of Fentanyl and in the same dosaging schedule.

Need to remember that using 0.5% solution tends to produce more hypotension than diluter solutions.

We repeat all top up every 60 to 90 mins depending upon patient needs, haemodynamic stability and progress of surgery

reg

Propofol is non-teratogenic
Although safely used in Obstetric Anaesthesia, the product insert says that enough studies are not available for recommending its use. So use at your own caution.

Propofol is not approved for RSI also. It can cause more hypotension than Thio in a rapidly administered large dose scenario.
Also there is work that seems to suggest that the peak effect of Thiopentone is better matched to the peak effect of Suxamethonium. I  dont remember if propofol peaks earlier or a wee bit later. Will post about it after rechecking the original article.

Yes. standard GA can increase the risk of both premature labour and IUD. So need to monitor fetal wellbeing and also use tocolytics as necessary. Avoid N2O if possible

regs

You would find that answer  in any standard anaesthesia text book
The key points are
1. Risk of Aspiration - prevent it
2. Avoid Aorto-caval compression. - wedge
3. Prevent decrease in utero-placental blood flow -  maintain MAP
4. Monitor fetal tococardiography
5. Prevent premature labour , fetal death - tocolysis, Avoid N2O
6. AVOID TERATOGENIC AGENTS.

You have not stated the kind and site of surgery.
If CNB is possible that is the best choice. You could choose SAB or Continuous epidural or any other regional procedure as appropriate.

If GA is needed for surgery then go with full fledged GA including RSI and Prokineitcs, H2 antagonists and all the protocol that goes with GA for LSCS.
Ritodrine, terbutaline have been used as tocolytics

Dont forget to get a Obgyn consult before and after surgery

Quite a few anaes drugs need to be avoided - N2O, Benzodiazepines

Inhalationals, IV anesthetics, Muscle relaxants and Narcotics are all safe

regs

Ofcourse you decide when and how to activate the epidural component of CSE

IF  we are using CSE for say a long ortho case - we usually give the intial SAB of 3.5 ml of 0.5% bupivacaine and we try to run the case entirely on spinal. we use the epicath for post-op analgesia as needed. In such a case, before shifting the patient out we give an epi topup of 6 to 10 ml of .0625 or .1 % bupi with the desired narcotic ( fentanyl or preservative free morphine or buprenorphine or tramadol)  added.

If we use CSE for a very sick patient or Obgyn we give a small dose SAB like 1 to 1.5 ml of 0.5% bupi and after checking the level we immediately start extending the block slowly with titrated doses of 2% ligno given in the epicatheter. We keep giving about 3 - 5 ml and keep checking level. This gives us time to titrate the level slowly upwards and hence time also to adequately  treat the slowly developing hypotension. If surgery gets prolonged we switch to 0.25 or 0.125% bupi along with desired narcotics as the need may be.

regds

I was just wondering what ETT size you used. Most of us make the mistake of trying to push in a much larger ETT. It is recommended that the ETT be atleast less in dia by 1 mm than the correct oral ETT. Adult males should get only a 7 mm and female adults 6mm. Appropriate size adjustments to be made acoording to age

Other wise there is very little you can do in the face of profuse bleeding due to injury to the Little's area.
Good powerful working suction - Yaunkers in mouth
Another suction with soft catheter through the other nostril
and intubate at the earliest

regs

Dr. Mishra
I am teaching anaesthesia for the last 20 years
I do agree that Indian doctors or anaesthesiologists are neither inferior nor less trained than the rest.
But do you really think that we follow protocols.
No need to look far, just look at how the national family planning programme of this country works.
Have you any idea about the conditions in which we anaesthetize people . if they die they contribute to MMR. They have practically no monitoring even for laproscopic sterilization.
Also now MBBS doctors are trained for 6 months in anaesthesia and are allowed to perform anaesthesia for LSCS. It is a national programme headed by an anaesthesia chief. Soon these guys gravitate to giving anaesthesia to all cases. So are they trained enough.
Have you, me or our brethern viewed this with any seriousness. Will we permit our kith and kin to be anaesthetized by these govt certified people.

I have passed 4 degrees in anaesthesia and even now we all practice things that if said in the exams I would not have got any degrees. We dont practice it because we have no protocol in place and no rigid rules to see that we adhere to them. Why then ask questions in the exam, fail them if they dont answer but dont follow them in clinical practice
IV Ranitidine and Metoclopramide is adviced for all OB coming for LSCS. the evidence is there. Do you think all of us follow it.
Is our pre-oxygenation and intubating positions standardized. Do we use ETCO2 and temperature monitoring for all our cases. DO we have a PACU . Do we record discharge criteria and scores.
Are all of us aware the Intra-cardiac adrenaline got stopped in 1999. Do we have defibrillators at every anaesthetic spot.
Dont blame the administration, if we followed protocol the entire anaesthesia community would have risen together and made it happen.
Dr. Bhatt has stated the obvious and I am in full agreement with him.
I think we are all improving all the time but still very far away from Utopia.
Let us also stop using the untrue scenario of our country being poor. Look at our cars, our shopping malls and how rich our politicos are. So lets stop kidding ourselves.
We need protocols in place and we need accountability to these protocols and we need more original research so that the Indian anaesthesiologist can set the guidelines for the world

regs