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
 

Spinal Anaesthesia contributing death due to Propofol in patients with Cardiac diseased

                       70 year old female patient had a trochanteric fracture femure Lt side with fracture Radial of left radiun lower end. The old lady was bedridden for several days before taken up for surgery.
                     On evaluation she was weak , thin built, but conscious and well oriented.
Her blood reports of CBC, Sugar, Urea, Creatinine Electrolytes were within normal limit. But for several years she was suffering from CAD ( coronary artery disease ) and Valvular disease.
she was evaluated with 2D echo and the findings were low EF 42%. MS, and MR( Moderate). HR 100/min with NSR and BP 110/65 mmHg. The old lady was bed ridden for some time and there was no way to asses effort tolerance.

                         A small dose 1 mg of Midazolam and 10 mg of Ketamine was injected IV so that patginet could be positioned to Lateral to facilitate lumber puncture. With all aseptic measures and  with a 25G needle Lumber puncure was performed at L3-4 interspace and 1.7 ml of Sensorcaine was injected.  The patient was positioned appropriately . Oxygen was administered with face mask. The vital parametres were stable  and 500 ml of Ringers Lactate was loaded rapidly to the patinent.

For next 1 1/2 hours the  the surgery was continued eventless.Blood pressure was maintained at 90-96/ 55-60 mmHg. No ephedrine injection was gicven.

                          After the femur nailing was done uneventfully the surgeon removed the posterior slab from the hand. The patient felt pain and her blood pressure was above the pre op level.

                     The surgeon wanted to close manipulation of Radius  lower end under C Arm guidance.

Again An injection of Propofol 100 mg and  15 mg of Ketamine was mixed in the syringe and was administered  IV. Simultaneously Oxygen & N2O mixture was administered through aface mask. With in a few minutes the close manipulation was was over and during one sucg stage the patint reacted to pain of manipulation but settled. It was noted her hert rate was going down from 70 to 50 in 2 mins and was going down further. An atropine was ordered and by that time the HR was around 40 / min. Injection of atropine did not produce any tachy and the HR remained at 40 min. A second dose of atropine had no effect . so Injection adrenaline 1 mg diluted to 10 ml was prepared and 2 ml was injected. There was  a feel for radial arterial pulse with a blood pressure of 90/50 mmHg. But the Heart  did not sustain and again became bradycardic. A second dose of adrenaline followed by  Full intubation and artificial ventilation was done. It appeared that patint probably needed a pace maker as there was no P wave in the ECG monitor.

Now the patients relatives were counselled for possible complications of resistant brady cardia and the patient was shifted to ICU with ET tube and adrenaline. In the ICU an injection of Isoprenaline  and Nor adrenaline started  but the effect was short lived  . Later thye heart did not respond to adrenaline injection too. And in next 1/2 hour  the patient expired.

                 ANALYSIS of the case: The patient had a valvular problem. In these patients Spinal anaesthesia probably had some effect of low cardiac out put and possibly there was a compromised cardiac output. On the top of it propofol had some hypotensive effect and there was a further compromise in coronary filling . When the first cardiac problem was detected it was in the form of bradycardia which was noticed somewhat late.  The patient did not respond to injection of two ampules of atropine. But responded to to injection of adrenaline. But it was not sustained even to injection of Isoprenaline. So an injection of propofol combined with Spinal anaesthesia in a patient of cardiac disease is very very innapropriate.

 

 

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.