The Anesthesiologist’s Story: New Details Emerge In the Joan Rivers Case

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New York Post reporter Susan Edelman revealed on January 4 the name of the unfortunate anesthesiologist allegedly present on August 28 at Yorkville Endoscopy, during the throat procedure that led to the death of comedian Joan Rivers. She is reported to be Renuka Reddy Bankulla, MD, 47, a board-certified anesthesiologist from New Rochelle, NY.

Having her name made public will be a nightmare for Dr. Bankulla, as investigators will certainly target her role in Ms. Rivers’ sedation and the management — or mismanagement — of her resuscitation.

When the news of Ms. Rivers’ cardiac arrest and transfer to Mt. Sinai Hospital became public, many of us guessed that there might have been no qualified anesthesia practitioner — either anesthesiologist or nurse anesthetist — present during the case. The gastroenterologist and then medical director of the clinic, Dr. Lawrence Cohen, argued famously that the sedative propofol, which Ms. Rivers received, could be safely given by a registered nurse under his supervision, and that no anesthesiologist is necessary.

However, with the publication of the Centers for Medicare & Medicaid Services (CMS) report of September 5, it became clear that an anesthesiologist was definitely present. The anesthesiologist was identified only as “Staff #2″ in the report. She was interviewed by the CMS surveyors four days after the event, but said she was “advised by her legal representative not to discuss the case.”

Key pieces of information about what happened still haven’t been made public. Nonetheless, the surveyors gathered enough information to reach this conclusion:  “The physicians in charge of the care of the patient failed to identify deteriorating vital signs and provide timely intervention during the procedure.”

By any standard of care, the anesthesiologist clearly would be one of the physicians in charge.

What happened, and when?

It’s known from the CMS report that Ms. Rivers had normal vital signs on August 28 at 8:44 a.m., with an oxygen saturation (SPO2) of 100% while breathing room air. This number means that she had a satisfactory level of oxygen in her bloodstream. At 9:12 a.m., the SPO2 had decreased to 92%, a low-normal reading, but rose again to a healthy 97% by 9:21 a.m.

In a hand-written note later in the day, the anesthesiologist explained that she used a combination of “jaw thrust and increase in oxygen flow” to maintain oxygen levels in Ms. Rivers’ blood. These are standard maneuvers designed to open a patient’s airway and make it easier to breathe adequately. It is very common for a patient to experience some degree of airway obstruction when a fiberoptic scope is inserted into the mouth and the patient must breathe around it.

Ms. Rivers apparently underwent a total of three procedures to evaluate why her voice was raspy and getting worse:

1.  A nasal laryngoscopy by her ENT physician, Dr. Gwen Korovin, to look at her vocal cords;

2. An EGD (esophagoduodenoscopy) by Dr. Cohen to evaluate the severity of her GI reflux;

3. A repeat nasal laryngoscopy by Dr. Korovin immediately following the EGD.

It isn’t clear why the second look at the vocal cords was necessary. Sources have speculated that Ms. Rivers’ may have developed laryngospasm, or sudden closure of her vocal cords, but there is no documentation in the CMS report that this occurred. If laryngospasm did happen, the anesthesiologist and the ENT surgeon were well qualified to recognize and reverse it, and it would be rare for laryngospasm to cause permanent harm.

There are conflicting statements in the CMS report about the sequence of events immediately during and following the second laryngoscopy by Dr. Korovin.

An endoscopy technician is quoted as saying that Dr. Korovin withdrew the nasal scope at 9:30 a.m. The “Cardiac Arrest Record” states that Ms. Rivers went into cardiac arrest at 9:28 a.m. and cardiopulmonary resuscitation (CPR) was initiated at 9:30 a.m. A separate code record, called the “Endoscopy Code Blue Record”, noted that Ms. Rivers developed ventricular tachycardia with a pulse at 9:28 a.m., and that “assisted ventilation and chest compression” were initiated at the same time.

Both records indicate that epinephrine 1 mg and atropine 1 mg were administered, but the times differ. The first record documents that these medications were given at 9:38, while the second record states they were given at 9:28.

The last vital signs recorded on Ms. Rivers show that both her blood pressure and heart rate were decreasing, though the SPO2 was documented at a low-normal 92% at 9:26 a.m. and again at 9:30 a.m.  No respiratory rate is recorded at 9:26.  Neither a respiratory rate nor a pulse rate is recorded at 9:30 a.m., which is the approximate time that cardiac arrest appears to have been recognized and CPR begun.

Was exhaled carbon dioxide monitored?

One key question in all of this, it seems to me, is this:  why wasn’t monitoring of exhaled carbon dioxide (CO2) recorded along with the other vital signs?  Exhaled CO2 is the gold standard for effective exchange of air. A patient breathes in air and supplemental oxygen, and then breathes CO2 out. A patient who isn’t breathing at all won’t exhale any CO2. This can be the quickest way to determine that a patient isn’t breathing. Equipment for recording exhaled CO2 is widely available, and oxygen can easily be given during endoscopy via nasal prongs that are capable of transmitting exhaled CO2 for measurement.

It’s possible that CO2 was monitored but not recorded at Yorkville Endoscopy, but it seems unlikely. Standard monitors would record all the vital sign numbers, including the level of exhaled CO2.

In the absence of CO2 monitoring, it is possible that the team failed to realize that Ms. Rivers at some point wasn’t breathing effectively, and then stopped breathing altogether. This would explain why she went into cardiac arrest. Slowing of the heart rate may be an indicator of impending cardiac arrest, and the last heart rate recorded for Ms. Rivers had slowed to 47 beats per minute.

Why was the SPO2 still above 90%?

One puzzling piece of data is that the pulse oximetry reading was still 92% at 9:30 a.m., the time when cardiac arrest apparently had already occurred. Could the SPO2 be incorrect, or does this mean that the oxygen level in Ms. Rivers’ bloodstream was adequate and therefore not the primary problem?

Pulse oximetry readings depend on measuring the difference in light absorption between blood that carries oxygen and blood that doesn’t. The relative light absorption is processed by the device, and a level is reported. But the pulse oximeter isn’t completely reliable.

Above all, the pulse oximeter depends on pulse and blood flow. If a patient has low blood flow, low blood pressure, or is cold, the monitor may not be able to pick up accurate signals. Also, there can be a significant delay in the monitor’s ability to detect a drop in blood oxygen.  Studies have shown that it may take a pulse oximeter finger probe as long as two minutes to register a significant drop in blood oxygen levels, and even longer if the patient is cold or has poor circulation. Either of these factors could have affected the readings in Ms. Rivers’ case.

The final autopsy report determined that the cause of Ms. Rivers’ death was anoxic encephalopathy due to hypoxic cardiac arrest. This means that her brain was deprived of oxygen long enough to cause permanent, irreversible damage, regardless of what the pulse oximeter reading may have recorded some time earlier.

Airway, breathing, circulation

The ABC’s of resuscitation:

First, make sure the airway is open.

Second, make sure the patient is breathing or else take control of breathing for the patient.

Third, make sure the heart is beating effectively and circulating oxygen to the brain.

It’s impossible to tell from the CMS report if these goals were accomplished as quickly as they should have been. Standard practice is to insert a breathing tube immediately if the patient isn’t capable of breathing. There is no record in the CMS report of whether a breathing tube was inserted by the team at Yorkville Endoscopy, although news reports have stated that a breathing tube was in place by the time that emergency personnel arrived in response to the 911 call.

Drugs including epinephrine and atropine were given during the code, according to the clinic records. However, one record indicates that Ms. Rivers’ heart rhythm was ventricular tachycardia with a pulse. Epinephrine and atropine would not be the appropriate treatment for ventricular tachycardia according to standard ACLS protocol. So there is an unexplained discrepancy between the documented heart rhythm and the treatment given.

What should the anesthesiologist have done?

Anesthesiologists (and other qualified anesthesia practitioners) multi-task, by definition. We administer anesthesia drugs and sedatives appropriate to the type of surgery or diagnostic procedure. We monitor the patient’s vital signs continuously. We maintain the patient’s airway and ventilation, whether the patient is spontaneously breathing under sedation, or on a ventilator for surgery under general anesthesia.

Critically important — we intervene promptly to manage any change in the patient’s condition that occurs as a response to anesthetic drugs, to the surgery itself, or to any underlying medical problem that the patient might have such as heart disease or lung disease.

During the nasal laryngoscopy done by Dr. Korovin, and the EGD done by Dr. Cohen, the lights in the room were probably dimmed. The endoscopy views typically are displayed on a video monitor, and dimming the room lights improves the contrast.

However, dimming the lights reduces the ability of the anesthesiologist to see the patient:  to observe skin color, and to see the rise and fall of the chest during breathing. It may be that the anesthesiologist wasn’t able to determine quickly enough that Ms. Rivers’ attempts to breathe were failing.

If a patient is in trouble, ultimately it is the anesthesiologist’s responsibility to determine that a procedure should be halted in order to rescue the patient from impending harm. Certainly in the case of upper endoscopy, it may be necessary to cut the procedure short if the patient is unable to breathe around an endoscope in the nose or mouth. It is unclear from the CMS report if the anesthesiologist identified the severity of Ms. Rivers’ deterioration, and whether or not she attempted to intervene prior to the onset of cardiac arrest.

The problem of the VIP patient

While I have no inside information as to what happened at Yorkville Endoscopy on August 28, it’s easy for me to imagine that this was an impossible situation for the anesthesiologist.

She was presented with a celebrity patient who was well known both to Dr. Cohen and to Dr. Korovin. She provided sedation with propofol, though it’s unclear exactly how much propofol was given. The medication administration record states that a total of 300 mg of propofol was given at 9:21 a.m., which would be a very large dose for a small, 81 year old patient. However, the anesthesiologist told the CMS surveyors that she actually gave only 120 mg of propofol.

Upper GI endoscopy and nasal laryngoscopy are stimulating procedures, and it may have been that Ms. Rivers reacted to the stimulation with coughing or movement, thus prompting the anesthesiologist to give more sedation.  With propofol, though, there is a very fine line between achieving an appropriate level of sedation, and producing sedation deep enough that breathing stops altogether.

If Ms. Rivers stopped breathing, it may not have been immediately obvious. In a dark room, with other physicians at the head of the table manipulating scopes in the patient’s nose and mouth, the anesthesiologist may have had very limited access to her patient. Even if she recognized that the patient was in distress, the other physicians may have refused to step aside and allow her to take control of the airway.

Once the severity of the problem was recognized, the physicians may have been reluctant to summon emergency personnel immediately, believing that they could manage the situation themselves. They may also have feared the inevitable publicity that would result.

Tragic outcome

At the end of the day, Ms. Rivers was resuscitated from cardiac arrest, but she had sustained irreversible brain damage from lack of oxygen. The tragedy of that outcome has a ripple effect. Inevitably, the lives of the physicians who were responsible for her care will never be the same.

As more information surfaces about the events of August 28, we can only hope that lessons will be learned that will benefit other patients in the future. There are minor surgeries and procedures, but there are no minor anesthetics.

Karen Sibert practices anethesiology in Los Angeles.

31 replies »

  1. My husband passed away on March 1st due to very similar situation and the Ambulance was responsible for the cause of my love dying, they failed at intubation and let him aspirate into his lungs. They let him be without oxygen for more than half hour and then drop off the patient at hospital brain dead. What made matters worse, the hospital played it off like they were doing “all they could” when they knew he was brain dead. I need help to make the people who are in volved held accountable for their actions and inactions.pleasr forward my story. I am I. California. Thank u

  2. At Bryan – CHWC when I was there, I do remember one case, where during the day, they called a code in the OR. I was working ED at the time, I ran up there to find the 17 year old, I had just admitted for appendicitis in trouble. I asked the c RNA what happened? He was working alone. No anesthesiologists work at Bryan. I would be it, and I was not privileged as such and I was working as an ER doctor. The c-RNA did not know I was an anesthesiologist. He said …. They put the trochar thru the iliac artery.

    BP was very low, and heart rate was in the 160’s. The c-RNA had turned off all the anesthetics.

    I set about placing a central line, and getting O negative blood up, and asked what had been given for the pressure, now 65/40 with hr 165. I asked if he had a level I. He chuckled …. Where do you think you are!!! This is Bryan, Ohio. They don’t even know what a level I is!!! What do you do when something like this happens? We call a Code!!!! I thought about if we ever called a code in the OR in Chicago, even when doing compressions, it would be unheard of.

    I asked if he had given any pressors. He said he had given ephedrine. I wondered if he knew this kid was in jail for cocaine issues. I asked if he had any neo, and he handed me a 10 mg vial. I said I needed a tb syringe. I mixed up .1 cc or 1000 mcg in 25 ml to get me to 4000 mcg/100ml or 40 mcg/cc, and gave the boy 120 mcg, or 3 cc’s which immediately got the pressure up. This took less than 30 seconds. The c-RNA was quite happy, and chortled, we are back in business, and turned his anesthetics back on. I said to him, you know that pressure is up from that neo we just gave. We had also started O neg blood and fluids. He asked when I had given it. I said about 5 minutes ago. Oh, it’s already wore off, he said. Not to damp his enthusiasm, I didn’t say anything, as I knew he would be ok.

    I asked him if he still needed me, as I had an ED full of patients downstairs. He said oh, we’re fine. I said, well, here’s the phenylephrine, it’s 40 mcg/cc, I would give 3 cc at a time to support his pressure, and they should have crossmatched blood up here soon. I thought just for a sec about telling him I was also an anesthesiologist. He had already dismissed me as just a helpful ED doc. I didn’t even consider telling him ephedrine doesn’t work in someone who uses cocaine, and it wasn’t my place to tell him as an ED doc. On the way out, there was a worried couple. I stopped to say, they just had a little trouble with his blood pressure, but he’s fine now.

    They ended up flying an vascular surgeon with anesthesiologist from Fort Wayne by helicopter to finish the case. The boy did fine. The next day, the CEO thanked everyone involved. I wasn’t even mentioned, and I thanked the Lord, as I wasn’t at the time privileged at that hospital for anesthesia, but working as an ER doc.

    As far as working full time in anesthesia, I am a new grad in anesthesia, with limited experience. I would be a newbie without years of anesthesia experience, but willing to work. It might take a week to get me up to speed. I am however a seasoned ED doc with no problems with intubation, lines, critical care management, able to handle things at a level II trauma center. One time with a boy that got hit by a train, cut in two, I had to place 3 central lines to keep him alive. They didn’t have a level 1 there either.

  3. Laryngospasm can CAUSE an airway issue within seconds, which is a challenge for anyone, c-RNA or MDA. I had a case during residency, post removal of an LMA, and had to ram a ET tube down. Had no time to give a paralytic. Had negative pressure pulmonary edema. Pulse oxy went down to 60’s. Patient did fine, but was admitted overnight. We have this saying, in our program, if you haven’t run across a difficult airway issue, you haven’t done enough cases. And I was an ED doc, before I went into anesthesia, and thought I was hot stuff. So far, I haven’t been sued, but statements like yours are stupid. It brings the entire profession down. so quit it.


  4. “Possibly unbeknownst to the medical team, as the CO2 increased it caused the oxygen-hemoglobin dissociation curve to shift to the right. A right shift means that oxygen has a higher affinity, binds more tightly, to hemoglobin. Thus, making it difficult for hemoglobin to release the oxygen molecule to the tissues.”

    Not bad, BUT.

    Acidosis causes a left shift of the Bohr curve, which increases release of oxygen to the tissues, Hgb binds less tightly, and making it easier for oxygen to be released to the tissues. But this didn’t help, since she was unable to get oxygen to the lungs to begin with d/t to apnea, and/or laryngospasm from manipulation of the vocal cords, preventing egress of CO2 and inhalation of O2. Each change in the pH by 0.1 causes elevation of K by 0.5, causing hyperkalemic arrest of the heart, preceded by VT. As far as Epine not working well in low pH pts, you need to review your ACLS, or at least quote me an article proving this.

    Reply from an oral examiner for MDA’s

  5. When someone stops breathing, the CO2 level climbs immediately, causing CO2 narcosis, further making it harder to overcome the apnea that has occurred compounded by the propofol that is on board. It takes almost 2 minutes for the pulse oxy levels to drop, indicating severe hypoxia. The acidosis that occurs from the CO2 accumulation, is almost immediate, and won’t be indicated by the pulse oximeter. There’s no way any anesthesiologist would administer propofol without an ETCO2 monitor, indicating apnea. Otherwise, he must play very close attention to the breathing rate of the patient, at least every 10 seconds, and monitor continually for airway obstruction. This was inattention by the anesthesiologist or cRNA, and below standard of care.

  6. I would really like to know if Sux was even available at this GI center. Many outpatient stand alone GI outpatient centers do not want to stock sux (the standard muscle relaxation drug to break a spams). The reason is obvious why they don’t stock sux. It’s because if you have any malignant hyperthermia triggering agent (like sux and anesthesia inhalation gases). You would need to have a MH cart and it’s drugs. Since MH is a rare (but potentially deadly complication). The best ans cheapest way to save on the estimated $3000 to maintain an MH cart and it’s meds is to avoid having any MH triggering agents (sux and an an anesthesia ventilation machine). So did the facility have sux available? Lawyers for facility will counter argue they stock Roc available to break a spasm. But the reality is the common sense thing to do besides basic maneuvers to break spams is to use sux to break the spams as a last resort.

  7. Good Article! and the punch line is so true “There are minor surgeries and procedures, but there are no minor anesthetics”…

  8. Dr. Karen makes several observations; I will extract some of her points.
    Introduction(as alleged)
    1. The procedure was performed in a surgical center.
    2. An anesthesiologist is quoted as “being in the area.”
    3. Where was the succinylcholine? Was it used?
    4. If the patient’s ETCO2 was not monitored, we now have a plausible pathway for the series of events that would ultimately lead to her passing.
    Facts in Surgery(as alleged)
    A. The patient is 80-year plus VIP (rumored to have ischemic heart disease) was taken into the operative suite for a series of upper GI procedures.
    B. The patient was deeply sedated(not a general anesthetic) with propofol, and her vitals were monitored.
    C. During the procedure, it has been alleged that the endoscopist tried to remove a lesion on her vocal cord.
    D. Allegedly, as soon as the endoscopist touched the lesion the vocal cords(closed) adducted.
    E. Without an emergency critical intervention nothing, good would come out of this.
    *Plausible Mechanism of Mortality
    -Removing the lesion from the vocal cord, while the patient was sedated, caused the vocal cords to adduct.
    – With the vocal cord closed the patient is now inhaling against a closed glottis: Negative Pressure Pulmonary Edema
    -With the vocal cords adducted there was no exchange of respiratory gasses.
    -We perform non-invasive measurement of oxygenation with a pulse oximetry[Do this experiment: attach a pulse oximeter to your finger and note the oxygen percentage. Take two breaths and hold it in. As you begin to grasp for air you should note that the pulse oximeter is usually over 90%]
    -The real danger was the bill up of CO2. CO2 is used as an indice to help access the patient’s ventilatory effort.
    -Possibly unbeknownst to the medical team, as the CO2 increased it caused the oxygen-hemoglobin dissociation curve to shift to the right. A right shift means that oxygen has a higher affinity, binds more tightly, to hemoglobin. Thus, making it difficult for hemoglobin to release the oxygen molecule to the tissues.
    -As the CO2 increased, the patient would become more acidiotic.
    -The normal pH is 7.4. It is thought that for catecholamines to work optimally the pH should be greater than 7.2. Thus, if the pH is below 7.2, we could potentially lose some of the potency of catecholamines such as epinephrine(EPI), norepinephrine(NE).
    -These medications, NE and EPI, increase the body’s blood pressure and performance of the heart.(increased heart rate, stronger contraction, elevated cardiac output)
    -With an elevated CO2 level, and decreased oxygenation can lead to a reflex tachycardia.
    -It is alleged that the patient suffered from some degree of ischemic heart disease?
    -If the heart is working hard(increased heart rate, stronger contraction, elevated cardiac output, increased oxygen consumption). With the patient body being incapable of transporting an adequate oxygen supply through their “stenosed” coronary vessels; a myocardial infarction and subsequent mortality are conceivable.

  9. The use of a wireless Bluetooth connected precordial stethscope would have given the anesthesiologist the earliest warning of impending hypoxia setting up.The combination of this often ignored “”powerful sense ” of breath sounds coupled with pulse oximetry and ETCO2 would have proved effective even in a darkened room.Perhaps it’s time to consider what many anesthesia practitioners both CRNA and MD have given up or perhaps never have taken up…listening for that vital life sound..breathing.

  10. There are no “VIP” patients, only alive ones and dead corpses. Failure to recognise the difference can be a problem

  11. Gi/Ent team dominated airway over anesthesiologist. Good lesson for all of us anesthesia to protect our field (read airway)and NOT to be intimidated by those esos.

  12. 1. Rather than loss of the airway, is it possible that the initial event was v tach triggered by epi or cocaine, administered as part of the nasal prep, in the setting of hypercarbia?

    2. I also wonder if the EMR itself was a factor – it can be a major distraction in an unfamiliar setting with a lot of other stuff going on. Perhaps this anesthesiologist did not work in this location regularly.

  13. Excellent analysis Dr Sibert. It seems to me that the anesthesiologist involved was culpable by virtue of:
    1. Not ensuring that she had all equipment and drugs to deal with try not-unexpected emergency. If succinylcholine was not available she should NEVER have agreed to participate. No excuses
    2. Being too timid to intervene and stop the procedure ( which was not agreed to by the patient ). Again this is inexcusable
    3. If end tidal CO2 monitoring was not available age should never have elected to be part of the assault team. This was clearly assault.

  14. I disagree. The nasal/oral prongs give us good evidence that CO2 is present and along with vigilance we can confirm respiratory effort. Combine this waveform with the saturatilon and you get very useful information. At our institution, such a waveform is referred to as “moguls”, like the humps in skiing, and a saturation of 100% is called “triple blue” since the 3-digit readout is blue in color. A patient with “moguls” and a “triple blue” is considered “Bueno- Bueno” and we all know what that means!! Hence, no lack of communication among staff.

    When we experience declining saturation and ventilatory effort, everyone knows at the same time. Likewise, when all is well the spirit of “Bueno-Bueno” prevails!


  15. Just a few comments:

    I think that talking about the management of anesthesia under these circumstances if very useful; however, in light of the fact that much of the information referred to is has not been vetted and incomplete, references to the alleged specifics of the case are probably ill advised. Why??

    1) “Having her name made public will be a nightmare for Dr. Bankulla, as investigators will certainly target her role in Ms. Rivers’ sedation and the management — or mismanagement — of her resuscitation.”

    It appears that mentioning the alleged person’s name seems to that nightmare along regardless of who made the name public in the first place.

    2)” The anesthesiologist was identified only as “Staff #2″”

    I can see why it is referred to in this way and for good reason.

    3) ““advised by her legal representative not to discuss the case.”

    Meaning, that we are not only presented with incomplete and non-vetted information but, in addition, we only have one side of the situation presented.

    4) ““surveyors gathered enough information to reach this conclusion: “The physicians in charge of the care of the patient failed to identify deteriorating vital signs and provide timely intervention during the procedure.”

    First of all, the blog does not identify exactly who these “surveyors” are. This is a luxury or protection that the alleged does not enjoy.

    5) “The physicians in charge of the care of the patient failed to identify deteriorating vital signs and provide timely intervention during the procedure.”

    This is a conclusion that was reportedly reached by the “surveyors”. This does not make it fact.

    Again, while the discussion of anesthetic management in these circumstances has merit, this piece contains a lot of speculation regarding the specific case cited. If I am reading too much into this or I am commenting without all the facts, I apologize. This is my take on this and only the information presented here.

  16. It is unwise to place much emphasis on recorded times and report fragments, especially those that are in news or legal reports. Our studies of the process of reconstructing causal chains after major events show that the accounts generated are plausible, reasonable, and usually wrong. Immediate, independent, technically-grounded investigation — a common practice in major transportation accidents — will give a quite different picture. Accidents are not produced by linear causal chains but by the concatenation of multiple, individually minor flaws that align to create a trajectory to failure. What is surprising is not that a patient sometimes dies during airway procedures. What is surprising is that it doesn’t happen more often.

  17. Analyzing CO2 through nasal prongs lacks specificity as well as sensitivity, making us complacent when used as an estimation of ventilation. Respiratory gas at the nares is often diluted to an unknown degree by room air and/or supplemental O2. The patient can be breathing adequately through the mouth while a minimal amount of CO2 appears at the nares, or much worse, a normal value of CO2 can be detected, but if this has been diluted, severe hypoventilation could be present. Manufacturers of sampling catheters have exploited clinicians’ poor understanding of the difficulty of monitoring true END-TIDAL CO2 and have made a killing, in more ways than one.

  18. Bottom line is most of us have been there. Usually we get away with it but when stuff hits the fan we can only rest easy if we know we had everything in place and did not compromise our values to save the owner a buck!

    My company, Preops, Inc, spent a lot of time years ago reviewing ASU and office based operating rooms to guarantee compliance with state regulations and patient safety. We would be happy to provide this assistance again as needed.

  19. Thank you Dr. Sibert for keeping us well informed of the facts. I agree with your conclusions and also feel for Dr. Bankulla. The main problem may have been best stated by Frank; this is BIG BUSINESS!! Since the CMS (appropriately) pays more for anesthesia services, as documented in last years WSJ articles, everyone wants a piece. The bureaucRATs who own these centers will cut costs anywhere. I recently polled our local ASUs and found none of them permit succinylcholine because it requires them to spend the $3k on Dantrolene! The lesson to anesthesiologists is clear; proceed with extreme caution as you enter these 3rd party agreements. Make sure you have what you need either on their cart or in your pocket, and maintain control of YOUR airway, even when you share.


  20. The monitoring of CO2 is a significant point that you brought up. Sure, the SaO2 can read 92%; not unexpected if you have high rate cannula O2 being infused into the airway. But if she is not adequately exchanging, it is entirely possible that the CO2 is high, at some critical value. Given the limited release of data, we can all be arm chair quarterbacks (those of us who are anesthesiologists or anesthetists) but only when all of the facts are known can we truly estimate what happened. We’ve all been there and we were able to prevent the tragic outcome, hopefully. And, yes, in the meantime i feel for this practitioner as her life has probably been severely disrupted since this happened.

  21. Dr. Silbert’s discussion is the best I have seen on the scenario – celebrity patient, special treatment, unconsented procedure, dim lighting. And no one speaking up. Cascading errors, starting with anyone allowing any procedure on vocal cords without a secured airway and appropriate emergency drugs. Very curious, though, that there are only 7 responses to this discussion and 60-something responses to Dr. Silbert’s previous well-done article, now that the identity of the anesthesia provider has come out. And no vitriol or professional slander. Very curious.

  22. I can definitely see the obstacles posed by dealing with a celebrity patient pointed out by Dr Sibert. I had some of the same concern that she raises. In regards to recognition of failing SAO2 and inadequate ventilation, when doing these cases in a poorly lit room I will make sure I have the volume turned up on the pulse Ox and that I am monitoring Etco2. It would concern me if I did not have access to key medications such as succinylcholine to facilitate a rapid resolution to the laryngospasm. If, perhaps, the other physicians using the flixible scopes would not relinquish control of the head of the table to the airway expert the case would become untenable to manage.

  23. I have to hope that SOMETHING more than jaw thrust was used to re establish a patent airway in Ms. Rivers….

  24. A wrongful death lawsuit is highly likely. Like Dr. Vader, I feel very much for Dr. Bankulla too, as I hope my concluding paragraphs above make clear. This is a horrible situation for anyone involved to face.

    Some sources have mentioned that Dr. Bankulla was working for Somnia at the time of the incident, but I don’t have any official verification of that.

    More information will certainly be available as details of any lawsuit are made public.

  25. “These stories are rarely as clear cut as they sound.”

    Very true. Unfortunately there will be some major consequences as below.

    “I have to wonder if this is the precursor to a lawsuit .”

    Most definitely.

  26. Kinda interesting that the Post broke the story ..

    “The Post has learned …”

    I have to wonder if this is the precursor to a lawsuit

    Wouldn’t be the first time that a plaintiff has fired the opening rounds of a suit through the media and there’s no better outlet for that than the Post ..

    Also interesting in my opinion :

    From the Post report. This is likely to be an issue —

    “Reddy told probers only that she gave Rivers 120 milligrams of the powerful anesthetic Propofol — not the 300 stated in medical records. She explained that she had mistakenly “double-clicked” on computerized records”.

    No details available on what EMR Yorkville Endoscopy uses ..

  27. I feel for Dr. Bankulla.

    If you’re out there reading this – hang in there ..

    These stories are rarely as clear cut as they sound

  28. There are a couple of issues with this center doing outpatient GI.
    1. The center I do not believed had succinycholine available (the most common drug to break a largynospasm. Why is that important? Because it’s a for profit center. They did not want to have a malignant hyperthermia cart and replace expired medicines every 12-18 months (costs around $3000 to maintain MH cart). That just shows you the greed involved in some of these GI center. Since succinycholine can “trigger MH (rare)”. But that is the main reason they do not have sux at these center.

    2. The anesthesiologist was “employed” by a “third party company”. I don’t know who exactly the “third party” is. But many times the third party is a shell company owned or has significant ties to the GI physician owners. The Office of Inspector General has already frown on these type of arrangement as break Stark laws (physican self referral). Look up OIG opinion 12-06.

    GI is big business. Anesthesia for private insurance patients are big business. Often times the anesthesiologist bill is greater than the GI procedure bill. That’s why everyone wants a “cut” of the anesthesia profit. Including the for profit GI physician owners. They will sometimes have an arrangement where they literally collect 49% of the anesthesia profits from shell company.