Hypothyroidism should not be under estimated

Two cases of hypothyroidism is describedhaving different outcome
CASE-1
          Mrs N D, 67 yrs female was posted for rt sided knee replacement.. She was somewhat hefty 75 kg. No h/o hypertension, asthma. allergy, She was diabetic which is wel controlled.She was hypothyroid on medication for long time. All routine investigations were within normal limits and had a stable cardio Vascular status. There was a small rise in TSH 9.8. A repeat test showed TSH .6.7 Such a trivial thyroid dysfunction was taken very seriously. As planned she was given an epidural injection.
 The operation went on well. Pt was resting well without any complaints with repeated doses of epidural. By 24 hours she had a renal suppression with very low urine output inspite of normal if fluid. She had not any episodes of unusual hypotension.
       Whilre re evaluating the case she was found to be unusually more sedated with a single dose of tramadol.and from other clinical features like edema, lethergy,weakness etc. was noticed. With addition of thyroxin 150mcg by oral route her condition very quickly improved.

CASE-II

        

Delayed onset of Local Anaesthesia.

This young person of 30 years undergone dental treatment sometime back and had complained of unbearable  pain during the procedure.
When another dental treatment was needed , it was referred to me for possible anaesthesia support with adminstration of Gen Anaesthetic during dental treatment ( root canaling )
Before that the patient was called to the hospital  anaesthesia department.
He was adminstered local anaesthetic subcutaneously in various concentrations of  Lignocaine 1 %, Lignocaine 2 % , Sesorcaine 0.5%  in the forearm of both hands they were marked. After an interval of  of 5 mins  touch and pin prick test  and thermal response with ice cube was done on all injection sites and compared to non injection sites. There was hardly no change in  perception of above sensations.
The  tests were repeated after 15 mins and 20 mins and 30 mins when about 20-25 % pain
differentiation was observed. Thinking that most probably he will need Gen Anaesth for the procedure later, I let him go home.
As he was an educated person,  he was sent home and was asked to do the test on himself with a needle  Lo... the person called from home after  4 hours to say that after about 1 and 1/2 hrrs from the injectiopn,   he felt obliteration of touch sensation and no pain  on needle prick . So the onset was very very delayed.
With counselling and assurance and discussion with dental surgeon. the procedure was done under local anaesthesia using 1 % lignocaine  but after an waiting period of about more 1 hour. He felt no pain and  the procedure was uneventful. Other routine investigations were within normal limit.
Later on we had suggested a nerve conduction test but he did not report.

BURN from Defibrillator

A young patient of 28 years had some kind of dysrythmia and was on a pace maker. The earlier pacemakers were not intelligent enough to detect a VF and deliveer  DC shocks. After oseveral syncopal attacks he was admitted to ICU and was waiting for a new pacemaker with defibrillator./ In the CCU he suffered  repeated attacks of VF and arrested several times. While in ICU received DCshock several times.( 18 occasions )
The sisters in ICU gets panic while the patient goes to VF. In the process of application of jelly correct placement of PADS were not meticulously followed . In the process he had several burn injury to the chest wall. The author was witnessed one such event.
The patient finally placed a pacemaker with defibrillator with medication.( Ameodartone).  he was discharged. But he survived the ordeal.

Also

Also published
J of Evolution Med. Dent Sci./ Vol 5 /Issue 83 /Oct.17,2017

Vassopresin in Spinal Anaesthesia.. dangerous ???

When my  surgeon does a myomectomy an open one and if the tumor is large they used to tie the uterus with a infant feeding tube and the bleeding is less. So at the end of surgery when the tie is opened everything is fine in most cases.

                  Then came an era when he started to use Vasopressin diluted ( 20 IU diluted to 50 ml ). He injects the solution to uterus around the tumor. The parts become visibly white meaning severe vasoconstriction only around the tumour not the whole uterus. When vasopressin is ad ministered there is some cardio vascular disturbances in the form of various types of arrhythmia.

Mostly sinus Brady cardia, dropped heart beats. Extra systole, heart block with mild to severe hypotension in many patients.There we found a difference when the patient is under General Anaesthesia and spinal anaesthesia.   Of about nearly 75 cases in Spinal Anaesthesia and about 30 in General anaesthesia. the cardio Vascular effect were remarkable under spinal Anaesthesia. In most cases there was severe brady cardia coupled with hypotension of varying degree and needed an injection of Atropine ( 1 to 2 amps ) in almost all cases. Where as  under General anaesthesia hardly 5-6 cases needed any supportive treatment.
                 Now adays my surgeon after procuring a mercillator hardly going for open surgery. All cases ( single, multiple tumour ) and tumour size varying from 2 cm to 20 cm are removed Laparoscopicaaly and he uses an injection of Vassopressin to reduce vascularity of the tumour and freduced bleeding. The uterus is stiched with a suture that automatically tightens and needs no tying.
                 And I am  very releived as most cases are done under GA. Though there are case reports that Cardiac arrest has occured during use of Vassopressin under Lap surgery and removal of Myoma. What is important is watchfullness.



Note this is going to be published

Nitous Oxide Cylinder.. pressure gaudge..

The picture is self explanatory One Nitrous Oxide cylinder when connected to anaesthesia machine showed the pressure to be 100kPa, where as the other cilder fitted to the other port showed 50kPa. When the cylinders were interchanged the pressure  in the gauge also changed.
So it was presumed this cylinder is mixed with some other gas which is exerting this additional pressure.
As there was noscope to examine this gas. , the gases from the cylinder was discharged to open atmosphere slowly  in an open space.
So all are cautioned that  a very high pressure in N2O cylinder should be looked at. There were some discussion that there is no need for Pressure gaudge in N20 side as the pressure is always  the same as long as  the last  drop of liquid N2O is present. But here is a scenario where the pressure gaudge  could help us to avoid a possible critical incident in Anaesthesia.

50 Joules for successful defibrillation

Introduction:

            Definite protocol for resuscitation after Cardiac arrest  exists and practiced all over the world. But the success lies in early detection and early defibrillation .

It is also seen  after 10 mins of resuscitation if the activity does not return  there it is likely that the patient has residual neurological deficit because of ischaemic encephalopathy.

            We describe here with 1 cases of Cardiac arrest  lasting 21 minutes  and 28  minutes, which was successfully revived with no neurological deficit

Case 1.  A middle aged patient of 48 years undergoing open  Cholicystectomy. The patient  was of ASA- ! with no known abonormality of any parameter. The patient was premedicated with Midazolam 2mg , Pentazocine 30 mg and  induced with Thiopentone 200 mg and intubated with Vecuronium 6mg . The anaesthesia was maintained with Oxygen 33%N2O 66%  , Halothane 0.5- 0.7 % and IPPV Manually. About 45 mins after induction of Anaesthesia the operation was over there was no undue Hemodynamic changes  intraoperatively.  After the end of surgery about 40- 45 mins from the start, limited bagging was done so that  respiratory activity can be noticed , some CO2 accumulation was allowed so as to stimulate the respiration.. Within a short time respiratory activity appeared and the  the patient was allowed to breath spontaneously with 100 % Oxygen  with intermittent support..Then Injection of Neostigmine  and atropine mixture was given slow IV over 3 minutes. Before completion of  all the prostigmine  there was alarm in monitor with bizarre waves, thinking that the lead has come off, it was readjusted and  the same pattern continued, When the radial pulse was examined , there was no pulse. Immidiately it was  thought that the patient has gone  to Ventricular fibrillation which was confirmed with another monitor. Immidiately a defibrillator was called for, Artificial ventilation continued with 100 % Oxygen and external Cardiac massage  commenced . There was  panic in OR ,I started a good and forceful cardiac massage and  the assistants were encouraged to do the same  where pulsatile plethysmographic waves were detected in Pulse Oxymeter  with Saturation of 60 – 75 %. When a BPL defibrillator arrived it did not start because the battery was almost totally discharged The  failed to charge 200 joules even when connected to electricity supply.  The BPL supplier was contacted who advised  to  charge the battery before  charging the defibrillator. With no other option  the external Cardiac massage continued  with full  vigor.   When somebody was fiddling with the defibrillator , it changed to  the Pediatric mode.  By this time more than 18 mins had elapsed  . With the pediatric mode the defibrillator was charged with 50 joules, that was the upper limit  in pediatric setting . Initially it also failed. Again after 3 mins it clicked. With intruption of External cardia c massage. 50 joules were delivered.

Alash ! It worked The rythm was convereted to sinus  witha HR of 60 which increased to 90. The peripheral pulse was plabale and the NIBP recorded was 105/60 mmHg. and SpO2 99-100 %. There was no facility to do an ABG analysis or adminster any Sodi bicarb. The patient was hyperventilated for next 15 mins when ts respiratory effort returned and was vey normal. Consciousness returned too. Post op recovery was totally uneventful. When we checked with the monitor trend graph we found  that the period of fibrillation was around 21 mins. 

Discussion: what could be the cause ?

24 Hrs after surgery with no damage, no memory of any incident

Rapid & severe hypotension

A look at these photographs from the trend graph shows  the following. When there is a slipped arterial blood vessel the result is devastatting.....
Pic1 : Time 13 :07 
 HR 111, BP:  125/74

Pic 2 shows : Time 13:08 
HR ...   BP : 54 / 39 ( Mean BP - 45 )

Pic 3 shows Time 13.09

HR  110 , BP 26/ 19 ( Mean 22 )

PIC : 4  Time  13.10

HR 71 , BP 20 / 13 ( Mean 13 )

PIC : 5  Time 13.11

HR 52 , BP 28/ 13 ( Mean 15 )

PIC 5  shows Time 13.12
HR 55 , BP 55/39

 PIC 6  shows Time 13.13
HR 93 BP 28/ 19

What you have to do is push and push the blood  through the canula by a 20 ml syringe , push and push & push

Theere was no use of ionotrops, no ephedrine, no mephenteramine.......
And after



PIC 7 : Time 13.49

HR 108 BP 72 / 47 ( Mean 58 )

The patient had a remarkable recovery after another 6 hours of  continued surgery under epidural anaesthesia, sedation, 10. 5 Lits of I/V fluid  including 6 Inits of blood transfusion, 2 units of Hesta starch, and an Injection of Lasix.  As the graph shows the Blood pressure  next few hours were around 80 mmhg systolic  and 45 -50 mm Diastolic

Post operatively ,there was no renal shutdown or dysfunction.

This was possible because the hypotension was of short duration ........ and  the mean blood pressure was around 50~60 mmHg.  intraoperatively .