A 55 year old Female patient was posted for Lap Cholecystectomy.
She was healthy 72 kg. Slightly over weight. No known problem with Diabetes, Hypertension or bronchial asthma. She was hypothyroid which was controlled with 5 years. Her ASA status was ASA-I with clear airway and Mallampaty score I
She was premedicated with Midazolam 3 mg and Pentazocine 30 mg.The induction of anaesthesia that was done with Atropine, Propofol, Scholine sequence with easy intubation.
Anaesthesia was maintained with N2O :O2 at 66:33 ratio Vecuronium and Isoflorane 0.8-1 %.
There was mild fluctuation of blood pressure during gas insufflation . The operation was uneventful duration of operation was less than 30 mins . At the end of surgery and when some resp effort was noticed she was revered with usual 2,5 mg prostigmine and 1,2mg atropine.
She was extubated after suction of mouth and airway. With in 10 mins she was alert and responding. Her breathing resp effort was normal with good forceful breathing on command. After some Oxygen inhalation 100% with mask for 2-3 mins she was sent to recovery room, where she was given Oxxygen by mask she appeared to be comfortable with no indication of pain or discomfort in abdomen / operated area.
After some time her Oxygen saturation slowly came down to 91-95 % in spite of oxygenation and her flow was increased to 6 litres. She was propped up in bed to 45 degree. She appeared to be alert not in distress or sedated. On command she could increase the tidal volume and obey command with respect to movement of limbs and over the next 20-30 mins her SpO2 remained unchanged at around 90~92% with Oxygen supplementation.
On enquiry she revealed no discomfort or distress. Resp rate was around 18~ 22/min with good tidal volume. She said she is more comfortable in sitting up position with head up tilt of more than 60 degree and she often sat up in bed. This indicated some airway obstruction. She neither had any broncho spasm wheeze or stridor. An injection of hydro cortisone 100 mg was given I V.emperically.
She was left in recovery for ne with close observation of vital parametres.
About 1 hrs later she suddenly had a bout of vigorous cough and a thick sputum block was coughed out. Lo her Oxygen saturation was back to 100 % in minutes.
The sptum that was causing if any obstruction was not detectable by clinical means with auscultation , nor the patient could feel the sputum causing any discomfort.
At the end of the day I will feel like blaming injection atropine that makes the sputum thick and can make a disaster at times like this.
Sunday, April 16, 2017
My publications and presentation
| PUBLICATIONS & Presentations | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Impact factor ( PIF):3.109 | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Presentations | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| An Unusual Foreign body in trachea | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| LMA Whats new | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Did I Make a Mistake | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Acid baseBalance - Management of Resp Acidosis | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Do you have a choice in Volatile Anaesthetic agents | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Newer Management of Pain | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Anaesthetic implication of prone
position in elderly. Prof Parmanik oration - OSIACON 2016-PURI: TOPIC: Pains and pleasures in Anaesthesia" |
||||||||||||||||||||||||||||||||||||||||||||||||||||
|
||||||||||||||||||||||||||||||||||||||||||||||||||||
| PK Mishra | ||||||||||||||||||||||||||||||||||||||||||||||||||||
| Signature | ||||||||||||||||||||||||||||||||||||||||||||||||||||
Saturday, July 30, 2016
Premature Reversal of musclerelaxation leads to complecation
A female patient 60 years of age was posted for Lap Cholecystectomy.
On evaluation the patient had GI problem 2 weeks back with
acute cholecystitis, distention , vomiting etc for which she was treated
conservatively and was seent back home with advice for early surgery of Gall
bladder.
She
was slightly plum with big tummy weighing 68kg. No h/o HTN, but DM type II with
blood sugar at 130 mg% was given glucose
and 5 units of Insulin. Her Hb was 11.2gm% TLC 12400, Amylase, LFT, Urea
and creatinine , Sodium and Pottasium were within normal limits. During PAC she
had more complain about back ache and sciatica type pain than Gall bladder
discomfort or pain. Her ECG and cardiac
reserve appeared to be OK clinically with good air entry to both lungs.
She
was given an Injection Diclofenac aqua before surgery so that sciatica pain
will diminish and her anxiety will be resolved. She was premedicated with Midazolam 3 mg. Nalbuphine 20 mg after 10 mins induced withPropofol 100 mg and
intubated with ease with 7.5 mmET tube after succynyl chiline injection of
100mg. Connected to ventilator with low tidal volume of 375mg and resp rate of
20 /min . Injection of Vecuronium initially 3 mg . As a routine pre incision
procedure takes about 15 mins so another
2mg Vecuronium was added at this time a total of 5mg. And Halothane 0.8 % was
added. To the FGFlow mixture of O2 nd N2O going at 1.5l to 3.0 L/min
The procedure was uneventful
with minimal fluctuation of Vital
parameters of HR, BP, and SpO2. The skin to skin procedure lasted 22 mins. As
displayed on the timer clock on the wall of the OT.
As the surgery was over so soon
we were waiting for the muscle elaxant to wear off. With O2 and N2O mixture
running at 50:50. There was no respiratory effort till next 15 mins. We tried
to stimulate the resp with under ventilation and accumulation of CO2 to some
extent but not more tham 50 mmHg as shown in ETCO2 monitor. There was no CO2 in expired gas.
At this stage the surgeon wanted
to take up another case and finish his OT list and go to OPD.
But all my effort to stop N2O and stop ventilation for sometime did not help. With much hesitation
half of the mixture of Prostigmine 2.5mg and atropine1.2 mg ( diluted to 10 ml)
was given IV. Slowly. In next 5 mins there was a flicker of resp movement in
Bag and small CO2 curve appeared and being encouraged with that the rest of the
mixture was injected. By this time the next patient was standing by the OT for
spinal anaesthesia . More movement of resp
was noticed but still with a high expired CO2 of 60mm. But the coughed
on the tube and there was fall in Spo2 even with 100 % oxygen. So the patient
was extubated assuming that her respiration will be quiet and will improve over
next 5-10 mins. As soon as she was extubated the patient was shifted to trolley
and taken to Recovery room to accommodate the next surgical case.
In the recovery room the
patients breathing appeared to be inadequate with SpO2 less than 90%. An air
way was given respiration was watched . It was found that the patient was
showing signs of incomplete reversal
with jerky muscular movement of limbs and
inadequate respiratory movement. A second dose of Neostigmine atropine mixture
was given IV . Still there was no improvement. The big abdomen caused more embarrassment to respiratory
function. It was intermittently supported with Ambu bag and mask ventilation.
When ever there was some fall in Spo2 a little ambu bagging helped to regain
Spo2 to 100 %. In the process it was suspected that there is a stomach is
inflated with air and we tried to remove
the air introducuing a feeding tube
and were not sure how much was removed. The presence of feeding tube
made the bag mask ventilation difficult and therefore the patient was intubated
with a 7.5 mm tube on the recovery trolley as such with out any drug or
additional muscle relaxant. As such she resisted a little and intubation was
completed with ease .
As we tried several times with a
T –piece connection to maintain resp
,But the respiratory drive and
ventilation did not improve more Ambu
bagging support was needed to main Oxygen saturation and avoid CO2 retention
and sweating. Some secretion appeared in
the Et tube at this time it was felt probably the patient has aspirated with
some Gastric content during Ambu and
mask ventilation. So the patient was shifted to ICU for full and controlled
ventilation.
The patient was initially put on
Pressure control with SIMV FiO2 0.5 Pr
20cm Peep of 5 and SIMV rate of 12. IE ratio of 1:2 but spO2 was still low and
Ambu ventilation showed better SpO2. So the setting was changed to Pure pressure control Pr of 20cmH2O PEEP of
10 . f=15 I;E ratio of 1:1.5 FiO2 =0.6.
Over the next 15-20 mins patient was stabilized for SpO2, HR. BP was low
because of high Intrathoracic pressure and a rapid fluid and a small dose of
nor adrenaline helped. A small dose of
Lasix. Change of Antibiotics wasdone. By
next 4 hrs the pt was better with stable vitals and patient looking up.
Gradually Fi)2, PEEP and Pressure was reduced after overnight ventilation the
patient was extubated and transferred to
Ward with out any hassle.
Analysis:
1.
Fundamentally the process of reversal
should have been initiated after some respiratory activity is seen.
2.
The patient should not have been extubated just because started bucking on the
tube.
3.
Re intubation should have been planned earlier
4.
What ever way one ventilate with Ambu bag and mask. There is always chance of
air going to stomach.
5.
Chance of Aspiration regurgitation is
highest during this period and can not be ruled out.
6.
Persistent Hypoxic episode could lead to
pulmonary edema.
7. In this case development of pulm
edema could be either of the factors as mentioned above.
 |
| Lady who suffered |
Unusual Cardiac complication in a case of Diagnostic Hystero Laparoscopy.
Unusual Cardiac complication:
NM 28 yrs olf female patient was presented for Diagnostic and Therapeutic Hystero Laparoscopy under General Anaesthesia for primary infertility and possible tubal block.
A preoperative evaluation revealed that she was having RBBB and Left Anerior hemiblock ( Bifacicular block). a 2D Echo cardiography by the cardiologist no other problem with Good LV function and a mild Diastolic dysfunction. She was healthy . Blood reports including Sodium and Pottasium was normal. Airway Normal, She was planned GA with LMA/iGEl intubation. with Scholine and Non depolarising muscle relaxant to be added if the procedure is prolonged
She was induced with Midazolam 2 mg, Nalbuphoine 15 mg followed by propofol 100mg and Sucynyl choline100mg and was intubated with a size 3 iGEL and was ventilated She was monitored with EKG, SpO2, NIBP, EtCO2. Simultaneously Hysteroscopy and CO2 inflation was done and 10 mins through the procedure without any apparent defect the surgeon was about finishing when we noticed suddenly the Cardiac rate jumping to 192 / min. At that stage the complexes looked like VT but on close observation it was felt that there is clear ventricular complex and regular rhythm. Diagnosis of Supra ventricular Tachycardia ( SVT ) was done. A carotid sinus massage yielded no result. A 120 mg of Xylocard was pushed after which the heart rate dropped to below 165/min but was not sustained. ( See picture )
Her blood pressure was 140/90, Radial pulse was feeble but palpable. In the meantime surgical procedure was over CO2 removed . But the tachycardia continued. An injection of Ameodarone 150 mg started in a syringe pump as a loading dose. The heart rate came down to 160-170 / min with stable blood presuure. In the mean time the patient recovered from Anaesthesia . and we decided to shift to HDU and continue therapy and monitor the pt closely . Injection of Ameodarone loading dose had no effect. Thinking it might cause a precipitation of block the dose was reduced for sometime.Addition of some more Xylocard brought down Heart rate to 140 but reverted back to 160-170
By this time pt was fully awake and did not seem to have any discomfort or complain. We also consulted the Cardiologist who advised to continue Ameodarone therapy after the loading dose. So initially 30mg / hour follwoerd by 60 mg / hour. After one more hour the patient had a bout of vomiting and suddenly the heart rate dropped to 88 /min. and continued to remain so.,
Next a repeat ECG showed the same ECG pattern as it was before surgery.( picture)
The patient was discharged next day.
it is very difficult to comprehend why the rhythm was converted to a different kind . As you can see the picture above the atrial focus caused the pattern possibly.
There was no Hypoxia,or Acidosis, or electrolyte disturbance to make a dramatic change.
How ever Ameodarone remains the drug of choice and very effective.
NM 28 yrs olf female patient was presented for Diagnostic and Therapeutic Hystero Laparoscopy under General Anaesthesia for primary infertility and possible tubal block.
A preoperative evaluation revealed that she was having RBBB and Left Anerior hemiblock ( Bifacicular block). a 2D Echo cardiography by the cardiologist no other problem with Good LV function and a mild Diastolic dysfunction. She was healthy . Blood reports including Sodium and Pottasium was normal. Airway Normal, She was planned GA with LMA/iGEl intubation. with Scholine and Non depolarising muscle relaxant to be added if the procedure is prolonged
Her blood pressure was 140/90, Radial pulse was feeble but palpable. In the meantime surgical procedure was over CO2 removed . But the tachycardia continued. An injection of Ameodarone 150 mg started in a syringe pump as a loading dose. The heart rate came down to 160-170 / min with stable blood presuure. In the mean time the patient recovered from Anaesthesia . and we decided to shift to HDU and continue therapy and monitor the pt closely . Injection of Ameodarone loading dose had no effect. Thinking it might cause a precipitation of block the dose was reduced for sometime.Addition of some more Xylocard brought down Heart rate to 140 but reverted back to 160-170
By this time pt was fully awake and did not seem to have any discomfort or complain. We also consulted the Cardiologist who advised to continue Ameodarone therapy after the loading dose. So initially 30mg / hour follwoerd by 60 mg / hour. After one more hour the patient had a bout of vomiting and suddenly the heart rate dropped to 88 /min. and continued to remain so.,
Next a repeat ECG showed the same ECG pattern as it was before surgery.( picture)
The patient was discharged next day.
it is very difficult to comprehend why the rhythm was converted to a different kind . As you can see the picture above the atrial focus caused the pattern possibly.
There was no Hypoxia,or Acidosis, or electrolyte disturbance to make a dramatic change.
How ever Ameodarone remains the drug of choice and very effective.
Wednesday, June 17, 2015
Saturday, June 13, 2015
Diabetes a nightmàre for anaesthesiologists
Type II DM is quite common in patients undergoing surgical procedure. Some times in quite a sizable no of patients it is detected at the time of screeing for operation. However insignificant it may be , it can cause havoc even death . Here are some case reports.
CASE 1
In earlier years of my anaesthesia practice, A relative young man of 35 yrs old was posted for Laparotomy and proceed for suspected peptic perforation. An emergency proicedure. There was no History of Diabetes from clinical examination. He was induced with Thiopentone , Scholine sequence of intubation followed by N2O+ O2 and ether anaesthesia with spontaneous respiratiobn with a boyles machine and Maggils semi open circuit was used.Additional Intra operative relaxation was provided with small doses of scholine and a deeper levels of ether anaesthesia.The intra operative monitors were BP, Pulse,Resp, Pupil and reflexes. At the end of surgery patient was extubated and sent to ward to recover slowly .The patient had gradually deeper levels of Comma and died finally. A blood sample taken and sent while comatose for blood sugar. The report received after death showed to be more than 600 mg%.
CASE 2.
A 62 yr old man underwent TURP under Spinal anaesthesia. He was mildly diabetic and received 6-4-6 units of insulin pre operatively. At the end of surgery it was observed on the table that there was still bleeding from the prostatic fossa. Surgeon wanted to inspect it again. As the effect of anaesthesia was still there , the surgeon proceeded and started to look for the bleed. And tried to remove some more prostatic t8ssue. As it took some time the pt started to be restless, So a GA was instituted with thio-Pentazocin-Midazolam and Vecuronium combination. After about 1 hr of GA there was delay in return of resp activity and fluctuations of BP, tachycardia . The patient was put on ionotropic support and ventilator. There was no facility to do bed side blood sugar estimation but with each dextrose containing solution 5 units of insulin was given. By next 4 hours pts condition detoriated , unresponsive , hypotensive and died. A blood sample collected before death for blood sugar showed the value to be 368.
CASE 3.
A 58 yr old lady relative of a doctor was posted for Lap Cholecystectomy. During preop screening she was found to be diabetic witha a random blood sugar of 230mg.
She was put on an insulin subcutaneoußly at a titrating doses of insulin by evening her blood sugar was 98. As planned she underwent Lap Chol with pre op blood sugar of 135. The operation was uneventful so also recovery. Normal protocol for fluid therapy analgesic was followed. Post op blood sugar control was not veŕy rigid. 8 hrs post operative the patient became restless then tachycardia and hypotension. All support was given by the doctor relative . By next 6 hrs the pt became unresponsive , slowly collapsed and died at mid night.
CASE 4.
A 42 yr old man suffer3d from pelcic fracture. He was type II mildly diabetic . Was converted to insulin before surgery with a dose of 8-8-10 units. The surgery 2as supposed to last for 6 to 8 hrs. An combined spi al epidural was planned and adminstered. During the course of surgery bedside blood sugar was monitored and insulin was being given into the i v drip which varied from 6 to 10 units. The patient was sedàt2d with Midazolam of 5 mg1Inspite of insulin the blood sugar remained above 200mg. It was also observed the patient is developing tachycardia and mild hypotension around 90~100 mmHg. There was no significant blood loss. A combination of RL, DNS , Ns was being aďminstered. It was a matter of concern when the heart rate increased beyond 160. At this point an ABG (arterial blood gas) analysis was done It showed metabolic acidosis with a pH of 7.24 and a blood sugar of 285 and K 3.1. Now the patient was tretaed in line with diabetic keto acidosis. With 1.5 litres of NS. 40 mEq K and 50 ml of Sodi bicarbonate and 30 u its of insulin over the nexþ hour brought things under contŕol. The patient slowly revovered with reďuced heart rate and stable CVStatus IN NEXT 8 HRS TIME.
CASE 5
A 50 yeaŕ old man was undergoing lumber disecþomy/ root decompression for radicular pain in left limb. He was hefty with a body wt of 95 kg . Had a slightly raised blood sugar which is detected during screeing. He was converted to insulin therapy before opn and received 8-6-10 units of insulin regular and mixtard combination. Pre op blood sugar on the morning od surgery was 112 mg. The patient was induced with Midazolam 5mg Propofol 130 mg Pentazocin 30 mg and intubated with scholine and veron 6 mg aded to continue ventilation. Pt was positioned prone and operation started. Abour 20 mins through operation pt started sweating. There was no apparent reason. No hypoxia, Sodalime canister was warn. There was not much tachycardia. Hypoglycemia was thought of and a 5% DNS started . A blood sample for HGT showed to be 168. The blood was taken when the Glucose containing solution was on. There fore the next bottle was added with 8 units of soluble insulin . An injecgtion of atropine was given I/v. In next 20 mins or so the sweating decreased slowly and the patient was continued to be given NS 1000 ml to compensate for profuse sweating estimated to be not less than 1.5 lit.
The procedure was completed with release of pr on root and the patient was repositioned and reversed with prostigmine and atropine. The pt recovered completely.
CASE 6
A 68 YR OLD MAN WAS POSTED FOR cabg FOR DIFFUSE CORONARY ARTERY DISEASE .
He was diabetic but mild with daily insulin requirement of 16 units on;y
Immidiate post op period was stormy with diabetic keto acidosis and was treated accordingly. The cardio vascular instability during that period was finally diagnosed when an ABG was done and metabolic acidosis detected , which was treated accordingly wirth 1500 ml of NS, Sodi bicarb, Pottasium.and insulin infusion.
CASE 1
In earlier years of my anaesthesia practice, A relative young man of 35 yrs old was posted for Laparotomy and proceed for suspected peptic perforation. An emergency proicedure. There was no History of Diabetes from clinical examination. He was induced with Thiopentone , Scholine sequence of intubation followed by N2O+ O2 and ether anaesthesia with spontaneous respiratiobn with a boyles machine and Maggils semi open circuit was used.Additional Intra operative relaxation was provided with small doses of scholine and a deeper levels of ether anaesthesia.The intra operative monitors were BP, Pulse,Resp, Pupil and reflexes. At the end of surgery patient was extubated and sent to ward to recover slowly .The patient had gradually deeper levels of Comma and died finally. A blood sample taken and sent while comatose for blood sugar. The report received after death showed to be more than 600 mg%.
CASE 2.
A 62 yr old man underwent TURP under Spinal anaesthesia. He was mildly diabetic and received 6-4-6 units of insulin pre operatively. At the end of surgery it was observed on the table that there was still bleeding from the prostatic fossa. Surgeon wanted to inspect it again. As the effect of anaesthesia was still there , the surgeon proceeded and started to look for the bleed. And tried to remove some more prostatic t8ssue. As it took some time the pt started to be restless, So a GA was instituted with thio-Pentazocin-Midazolam and Vecuronium combination. After about 1 hr of GA there was delay in return of resp activity and fluctuations of BP, tachycardia . The patient was put on ionotropic support and ventilator. There was no facility to do bed side blood sugar estimation but with each dextrose containing solution 5 units of insulin was given. By next 4 hours pts condition detoriated , unresponsive , hypotensive and died. A blood sample collected before death for blood sugar showed the value to be 368.
CASE 3.
A 58 yr old lady relative of a doctor was posted for Lap Cholecystectomy. During preop screening she was found to be diabetic witha a random blood sugar of 230mg.
She was put on an insulin subcutaneoußly at a titrating doses of insulin by evening her blood sugar was 98. As planned she underwent Lap Chol with pre op blood sugar of 135. The operation was uneventful so also recovery. Normal protocol for fluid therapy analgesic was followed. Post op blood sugar control was not veŕy rigid. 8 hrs post operative the patient became restless then tachycardia and hypotension. All support was given by the doctor relative . By next 6 hrs the pt became unresponsive , slowly collapsed and died at mid night.
CASE 4.
A 42 yr old man suffer3d from pelcic fracture. He was type II mildly diabetic . Was converted to insulin before surgery with a dose of 8-8-10 units. The surgery 2as supposed to last for 6 to 8 hrs. An combined spi al epidural was planned and adminstered. During the course of surgery bedside blood sugar was monitored and insulin was being given into the i v drip which varied from 6 to 10 units. The patient was sedàt2d with Midazolam of 5 mg1Inspite of insulin the blood sugar remained above 200mg. It was also observed the patient is developing tachycardia and mild hypotension around 90~100 mmHg. There was no significant blood loss. A combination of RL, DNS , Ns was being aďminstered. It was a matter of concern when the heart rate increased beyond 160. At this point an ABG (arterial blood gas) analysis was done It showed metabolic acidosis with a pH of 7.24 and a blood sugar of 285 and K 3.1. Now the patient was tretaed in line with diabetic keto acidosis. With 1.5 litres of NS. 40 mEq K and 50 ml of Sodi bicarbonate and 30 u its of insulin over the nexþ hour brought things under contŕol. The patient slowly revovered with reďuced heart rate and stable CVStatus IN NEXT 8 HRS TIME.
CASE 5
A 50 yeaŕ old man was undergoing lumber disecþomy/ root decompression for radicular pain in left limb. He was hefty with a body wt of 95 kg . Had a slightly raised blood sugar which is detected during screeing. He was converted to insulin therapy before opn and received 8-6-10 units of insulin regular and mixtard combination. Pre op blood sugar on the morning od surgery was 112 mg. The patient was induced with Midazolam 5mg Propofol 130 mg Pentazocin 30 mg and intubated with scholine and veron 6 mg aded to continue ventilation. Pt was positioned prone and operation started. Abour 20 mins through operation pt started sweating. There was no apparent reason. No hypoxia, Sodalime canister was warn. There was not much tachycardia. Hypoglycemia was thought of and a 5% DNS started . A blood sample for HGT showed to be 168. The blood was taken when the Glucose containing solution was on. There fore the next bottle was added with 8 units of soluble insulin . An injecgtion of atropine was given I/v. In next 20 mins or so the sweating decreased slowly and the patient was continued to be given NS 1000 ml to compensate for profuse sweating estimated to be not less than 1.5 lit.
The procedure was completed with release of pr on root and the patient was repositioned and reversed with prostigmine and atropine. The pt recovered completely.
CASE 6
A 68 YR OLD MAN WAS POSTED FOR cabg FOR DIFFUSE CORONARY ARTERY DISEASE .
He was diabetic but mild with daily insulin requirement of 16 units on;y
Immidiate post op period was stormy with diabetic keto acidosis and was treated accordingly. The cardio vascular instability during that period was finally diagnosed when an ABG was done and metabolic acidosis detected , which was treated accordingly wirth 1500 ml of NS, Sodi bicarb, Pottasium.and insulin infusion.
Subscribe to:
Posts (Atom)