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The Curious Events Surrounding
A Case of Acute Respiratory Failure following Interscalene Block
November 1, 2008
I write about this case because the scenario that precedes it is quite common and most of the time events never align to arrive at the rather dramatic point that was reached in this case. But the potential exists in every interscalene brachial plexus block done on a patient with COPD. I suspect you can go along through an entire career without encountering this, or see it tomorrow, but the opportunity is not rare.
The patient came to the operating room for acromioplasty and rotator cuff repair of the left shoulder. He was in his 50’s, his height and weight were average and had no known allergies. He had a 40 year smoking history of 1-2 packs per day and was recognized as having COPD but had not been on home oxygen therapy and only recently been started on inhaled steroids and bronchodilators. Preoperative chest x-ray showed hyperinflation. The assigned anesthesiologist reviewed his charts, interviewed him and formed a plan consisting of a general anesthetic supplemented for postoperative analgesia with an interscalene brachial plexus nerve block.
The Block
The patient agreed and while in the pre-operative unit, monitors were applied and the patient was sedated with 2 mg of the midazolam and 50 mcg of fentanyl. The left neck was prepped with chlorhexidine and sterile gel was applied. A shallow (8-10 mHz) ultrasound probe was placed against the neck and the brachial plexus was identified, first in the supraclavicular space, then followed cephalad into the interscalene space.
A lidocaine skin wheal was place and 22 gauge short bevel needle was inserted into the interscalene space in an out-of-plane approach and the block was performed using a total of 30 mls bupivacaine 0.375% with epinephrine 1:400,000. During the block there were repeated aspirations of the syringe to ensure that no vascular structures were entered and the needle was repositioned several times in order to optimally place the local anesthetic boluses. Sedative effect was light and the patient was speaking and answering questions throughout the procedure. He reported nothing unexpected and only a light amount of discomfort. The block was uneventful, The needle was removed and effects of the block were seen immediately in the inability of the patient to use his shoulder muscles to raise his left arm. The patient was counseled for what to expect from the block over the next 24 hours and was observed for approximately 5 to 6 minutes if there were any acute effects from the injected local anesthetic.
An Unexpected Result
Approximately 10 minutes later patient was wheeled to the operating room and the gurney was placed next to the operating table and the patient was in the process of moving across to the table when he suddenly sat up, clutched his chest, and said "I can't breath". He then collapsed back onto the bed pulling out his intravenous catheter in the process.
The anesthesiologist immediately began ventilating with a bag and mask while the circulating nurse pushed the "Code Blue" button for help. Personnel assembled, the code cart arrived. a second anesthesiologist restarted the IV. As soon as the IV was running, intralipid solution 20% was begun and eventually ran in to the amount of 150 mL (even though the EKG showed a regular rhythm, normal intervals and a rated of around 105 bpm). Simultaneously a muscle relaxant was given and the patient's trachea was intubated and ventilated with 100% oxygen. Non-invasive blood pressure revealed hypotension with the lowest pressure seen was 65 systolic prior to the IV restart and intubation.
The patient had become markedly cyanotic after his initial collapse with the lowest pulse oximetry showing saturations in the 50's. His saturations rose immediately with intubation and ventilations. Auscultations revealed no wheezing or rales. The scheduled surgery was abandoned and the patient was transferred to the postoperative care unit and placed on a ventilator assist-control . An arterial line was started in left radial artery and arterial blood gases done. The differential diagnosis of the time of the patient's collapse was pulmonary embolism, myocardial infarction, pneumothorax, and hemidiaphragmatic paresis.
A chest x-ray was taken in PACU to rule out pneumothorax, and a 12 lead EKG was done to rule out MI, both were negative for an explanation for the collapse. Troponins, and CPK were negative for indication of MI. The arterial blood gases after his resuscitation revealed a pH of 7.30, a pCO2 of 65, pO2 of 443, a base excess of -2.9 and a bicarbonate of 31 on an FiO2 of 0.8.
One possible explanation was the patient having had a pre-existing, unrecognized paresis or paralysis of the contralateral hemidiaphragm. If the interscalene block paralyzed the hemidiaphragm on the operative side, acute hypoventilation would ensue. After arrival in the postoperative care unit, when the patient was more aware and able to follow instructions, an ultrasound survey of the diaphragm was performed using a low frequency (2-4 mHz) curved array probe in M-Mode ultrasound. We found that the contralateral diaphragm was not paralyzed and the hemidiaphragm on the operative side was paralyzed as expected presumably from the block. Images from the ultrasound surveys of the hemidiaphragms are shown below.
 
The patient was placed in the intensive care unit overnight while the block dissipated and he was extubated without incident the next morning. The sensory effects of the interscalene brachial plexus block lasted until approximately 3 am the next day, for a block of 20 hours in duration. The patient was discharged soon after extubation with no other problems noted.
So How did We Get Here?
A probable explanation for this scenario, considering the results of the tests, is that the patient had fairly significant COPD and was a carbon dioxide retainer prior to surgery. Prior to the block the patient was sedated with IV midazolam and fentanyl which probably caused more hypoventilation in turn increasing the patient’s carbon dioxide and decreasing the patient’s already blunted sensitivity to the rising CO2 level. Finally as a side effect of the interscalene block, the local solution (bupivacaine) spread around the front of the anterior scalene muscle and came into contact with the phrenic nerve, creating a conduction block and a paresis or paralysis of the hemidiaphragm on the side of the block. This lack of movement in the hemidiaphragm further reduces the tidal volume and causes another increase in the amount of CO2 remaining in the venous blood. Eventually the spiralling levels of carbon dioxide and the accompanying acidosis reaches a level that causes widespread vasodilatation and syncope.
The pulling out of the intravenous line was just a happy coincidence.
What can we do about this?
It has long been recognized that an increased risk exists for respiratory complications in patients with pre-existing pulmonary disease following interscalene block. This procedure is commonly performed because the risk benefit balance is in favor of the block over the use of narcotics in the patient with obstructive pulmonary disease. So what are our options in terms of the care of the patient with obstructive pulmonary disease undergoing shoulder arms surgery needing an interscalene block? It doesn't seem prudent to deny patients with COPD the benefits of regional block but there must be a way to minimize or manage the inherent risk in the block.
A provisional plan may be to perform incentive spirometry prior to interscalene block in patients whose history indicates they are at risk for problems related to loss of function of a hemidiaphrgam. After the block the patient can use the spirometer again to compare their ability to move air. This may give the clinician a "heads-up" in time to provide enough ventilatory support to avoid a more dramatic course.
In addition, it is probably a good idea to modify the usual interscalene technique in favor of a low-volume technique (as discussed on the Neuraxiom pages "Low Volume Interscalene" and the "PSIB Project"). Some time in the past it became dogma that hemidiaphragmatic paralysis inevitably follows interscalene block just as gravy follows pork-chops, but early last year the "Phrenic Sparing Interscalene Block" (PSIB) project conducted here on the Neuraxiom site showed that a simple low volume technique could avoid this complication in the majority of cases. This axiomatic finding was once again "discovered" in a paper in a major professional journal . (During the work on this project a friend, Dr. Andre Ceccoli in France carried out a wonderfully simple series of surveys mapping the variation in position of the phrenic nerve in relation to the brachial plexus usng ultrasond and a nerve stimulator. The results of this series are quite worth looking at and can be found at http://www.usra.ca/UIA/GetPublicAbstract.php?UserID=18&AbsID=b3f0860f6ebed0db84cfb2302740f1a7).
In the low volume modification we use between 5 and 10 mls and control the injected local so that it stays within the brachial plexus sheath as much as is possible. By using a lower volume and avoiding overflow of the local solution across the anterior side of the anterior scalene we can, in the majority of cases, avoid local anesthetic contact with the phrenic nerve, and thereby avoid the hemidiaphragmatic paralysis. There will be cases where contact is unavoidable because in a small percentage of anatomical variations the phrenic actually travels with the brachial plexus between the scalenes, but according to our small sampling in the PSIB project the hemidiaphragm will remain functioning in about 75% of blocks done with 10 mls or less (without taking the time to map the position of the phrenic using a nerve stimulator).
Why not use the low volume technique all of the time then? Because we sacrifice duration the the low volume. The low volume technique yields a solid block with good coverage that lasts between 8 and 10 hours usually. It's possible that this block may be lengthened a bit by using some local cooling at the site of the block but probably not more than a couple hours at best.
Still these steps may be enough to avoid or mitigate the loss of additional respiratory function caused by sedation and the occasional loss of a hemidiaphragm.
Summary
To some extent this particular event probably unfolded as it did as a fault of just bad timing, and to that degree the clinical situation is probably much more common than is recognized. If the patient had reached the operating room a few minutes earlier he may have been asleep and mechanically ventilated. If this had happened before the patient reached the point hypoventilation that pushed his carbon dioxide level to the critical level, the respiratory acidosis would never have occurred. At the end of the case, the weakened respiratory effort would have been recognized and the patient would have remained on a ventilator until he recovered enough to be extubated (a much more common scenario).
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