66 year old female presented to the ED on January 13, 2023 with sharp lower abdominal pain, nausea, and vomiting similar to when she had a small bowel obstruction in 2019. There were no relieving factors. She had a history of diabetes, poorly controlled hypertension, hyperlipidemia, history of smoking, cardiovascular atherosclerotic disease, prior anteroseptal heart attack, ulcerative colitis, a prior cholecystectomy, prior bowel obstruction surgery, and hysterectomy. She was on mesalamine. She was admitted for small bowel obstruction and started on NG tube fluids.
January 14 chest X ray reports left lung collapse (atelectasis), opacity (density/mass) or infiltrate (lung infection).
X ray taken of the abdomen on January 14, showed persistent obstruction and she was scheduled for a diagnostic laparoscopy on January 15.
On January 15, noted in the records that the Patient stated she could not stop shaking, glucose check 243, sbp 130's. patient found to be sensitive to morphine.
EKG revealed a likely prior anteroseptal heart attack. No further evaluation or testing was performed as to her heart and lungs, nor was a cardiologist or pulmonologist consulted.
The patient was brought to the operating room at 1705. Decedent was intubated at 1723. The tube was secured, and the ventilator was activated with oxygen and air and low dose sevoflurane turned on. At approximately 1731, versed (1 mg), fentanyl (100 mcg), lidocaine (100 mg), propofol (150 mg) and rocuronium (50 mg) were administered while cricoid pressure was held. Dexamethasone (4 mg), metoclopramide (10 mg), and ondansetron (4 mg) were then administered. A few doses of phenylephrine (200 mcg) were administered prior to the incision to maintain resting blood pressure. Two grams of cefazolin were requested by the surgeon and given at 17:43.
The surgeon then made a five-millimeter incision in the right lateral abdomen, a five-millimeter port was then introduced into the abdomen under direct visualization with the help of a five-millimeter laparoscope. The surgeon then attempted to insufflate the peritoneum. However, the pressure was very high, and this was not successful. The surgeon requested a longer five-millimeter port. In the interim, the surgeon decided to insert a Veress needle to insufflate the abdomen. The surgeon made a two-millimeter stab incision in the left upper quadrant two-centimeters below the costal margin at the midclavicular line. The surgeon then inserted a Veress needle into the peritoneum. At that point, the anesthesiologist informed the surgeon that Decedent had a sudden decrease in her end tidal co2, and Decedent was unstable. Shortly thereafter, she became bradycardic. The surgeon withdrew the Veress needle and began chest compressions. At approximately 17:49, the ventilator alarmed to a sudden decrease in end-tidal carbon dioxide on the capnograph. The surgical team was alerted and attempts at insufflation were halted. Within a few seconds, Decedent's heart rate began to decrease. Epinephrine was given to Decedent. Chest compressions were started as the bradycardia had converted into ventricular fibrillation.
Code blue called at 17:50. The anesthesiologist switched the ventilator to manual mode and began to ventilate the decedent by manually squeezing the anesthesia circuit reservoir bag. end-tidal carbon dioxide level remained low. Compressions and ventilation continued with another dose of epinephrine given at approximately 17:55 by another anesthesiologist, who had been called to assist. The anesthesiologist continued to ventilate Decedent throughout the code, and Decedent had bilateral breath sounds as heard with a stethoscope. A second fluid bag was attached to a preexisting IV, and both fluid bags were placed on pressure for volume. Throughout the code, multiple doses of epinephrine, bicarbonate, and calcium were given. Pads were attached early in the code, but no shockable rhythm was ever seen after the initial shock at 17:52. Advanced cardiovascular life support was continued until 18:30 with no improvement in the patient’s condition. Decedent was pronounced dead at 18:30.
Autopsy Report stated:
“Post mortem examination, limited to chest and abdominal cavities, shows marked adhesion related changes involving bilateral lungs, liver, spleen and large and small intestines. No thrombosis or thromboemboli are seen. The left anterior descending exhibit significant calcific stenosis, 30% patent and the .left circumflex artery shows mild stenosis. No acute myocardial infarct is identified. No acute pneumonia or saddle emboli is noted. The liver shows mild steatosis and mild congestion. The kidney demonstrates acute kidney injury. The proximal small bowel shows focal dilation with fecal content. No marked acute inflammatory changes are noted within large and small Intestines.
Overall, the immediate cause of death is unclear. Speculation includes metabolic and hemodynamic instability from underlying small bowel obstruction. The presence of small bowel obstruction and dilation Is most likely secondary to pronounced adhesion, involving multiple organs, including the mesentery and small bowel. There is no histologic evidence of active ulcerative colitis. There is no bowel perforation or bowel injury identified from the latest attempt of laparoscopic procedure.”
Files:
Q: When was epinephrine injected (how long after end tidal C02 drop)?
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Q: Was the patient placed in Trendelenburg with the right side up to open the outflow tract from the right ventricle?
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Q: What were her lab studies immediately prior to her operation?
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Q: did they comment about capsular violation of the liver on autopsy? Was it specifically mentioned or looked at?
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Q: What were the initial insufflation pressures?
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Q: What was the flow rate set at when the Veress needle or the optiview trocar were first inserted?
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Q: How did they verify placement of the two trocars>
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Q: Did the autopsy note any injury to the liver or subcutaneous gas in the tissue?
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Do you believe there might have been medical error?
More detailed review of the operative and anesthesia record is needed, but my concern is for the veress needle to have caused a left sided tension pneumothorax that led to decreased end tidal CO2. That brings up the question of why an emergent chest tube was not placed in the left chest when the patient coded.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
If the veress needle did indeed cause a tension pneumothorax, this is a iatrogenic injury. More importantly, the surgical team should have placed a left sided chest tube, even if the diagnosis is not clear, in the setting of a patient coding.
What makes you a good expert for this case?
I am trauma and acute care surgeon with a total of 22 years of experience (counting surgical training years). I work in one of the busiest, largest and most reputable academic medical centers in the country. I am also a patient safety and quality expert and in charge of root cause analyses and M&M with many years of experience of evaluating mortalities and complications to identify errors, system issues and accountability issues.
How often do you encounter cases similar to this one in your practice?
Weekly between my two roles, clinical and administrative
Do you believe there might have been medical error?
The documentation is difficult to interpret. It reports that the endotracheal tube was inserted at 1723 but then the documentation of intubation drugs and cricoid pressure was at 1731. The documentation also states that there was a "sensitivity" to morphine. It is not clear how this was determined or manifested. Morphine and fentanyl cross reactivity is uncommon but still possible. It is also possible that there was hemodynamic collapse related to an Ancef allergy that was not recognized. There is also the possibility that an air embolus from the Veres needle caused the hemodynamic collapse, although there were no findings of that on the autopsy.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
It appears that there was no steroid treatment for an allergy to Ancef. Also, given the temporal relationship to the Veres needle and the hemodynamic collapse, it is possible that the needle contributed to the patient's demise.
What makes you a good expert for this case?
I am professor of surgery at a busy verified level one trauma center, where I have worked for over 16 years. I serve as the medical director of the scute care surgery section for the hospital. I am board certified in general surgery and critical care.
How often do you encounter cases similar to this one in your practice?
I do a lot of laparoscopic and robotic surgery using various methods of peritoneal access (Veres needle, optiview, Hasan port), and I am familiar with the complications and management of those complications for each approach
Do you believe there might have been medical error?
The most likely scenario here is a carbon dioxide embolism from insufflation. This usually occurs if the verses needle or port were placed in the liver and commonly occurs in patients with significant adhesive disease. This is a known complication of laparoscopy, especially with a closed abdominal access (Veress needle or Optiview). This clearly was a component of this case, given that the surgeon had multiple attempts at entering the abdomen. When you develop a carbon dioxide embolism, the first thing that happens is a rapid drop in the end-tidal CO2, followed by a decrease in heart rate and blood pressure, which is the exact sequence of events. This complication in itself is well-known. The management here becomes critical. When was epinephrine injected (how long after end tidal C02 drop)? Was the patient placed in Trendelenburg with the right side up to open the outflow tract from the right ventricle? Why did they not comment about capsular violation of the liver on autopsy- it can be so small as a needle prick? What were the initial insufflation pressures? What was the flow rate set at when the Veress needle or the optiview trocar were first inserted?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
A carbon dioxide embolism at the time of surgery, if not managed appropriately, will cause death. This case will come down to the timing of recognizing the problem and the interventions. Actions in the 2 minutes immediately after the embolism will determine if the patient lives or dies. If everything was done appropriately, then maybe this can all be attributed to a bad outcome.
What makes you a good expert for this case?
I deal with C02 emboli on almost a monthly basis since I do robotic liver surgery (100% rate of occurrence). I understand how to manage them, and I educate my anesthesia team about them prior to every laparoscopic or robotic liver resection.
How often do you encounter cases similar to this one in your practice?
I encounter CO2 embolism almost monthly in the context of liver surgery. However, I encounter it as a complication of abdominal access during laparoscopy less than once every 2 years and none resulted in a death. Usually, if managed appropriately, patients have a 100% recovery rate. You only need to support the heart for a few minutes, and the C02 usually dissolves in the blood. Unless a large amount of CO2 was injected at high pressure, and it was not recognized in time.
Do you believe there might have been medical error?
Given the patient’s multiple medical co-morbidities and prior surgery for obstruction, she would have benefited from a more in depth pre operative risk stratification work up. Additionally, the likelihood that this surgery would have been performed successfully laparoscopically is quite low, as her post mortem evaluation demonstrated severe adhesive disease. When the optiview port did not work initially, a blind entry with a veress needle should have been avoided. With better pre operative evaluation, it may have become more evident that this patient would not tolerate pneumoinsufflation and an open procedure would have been preferable.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
This patient appears to be a high risk patient for both general anesthesia and surgery. With her co-morbid conditions, she warranted a more extensive pre-operative evaluation and risk stratification.
What makes you a good expert for this case?
I am double boarded in both general surgery and complex surgical oncology. I have been in practice for over 10 years with thousands of gastrointestinal cases completed while currently practicing at a high volume academic medical center.
How often do you encounter cases similar to this one in your practice?
Quite often. We tend to operate on many high risk patients, which greatly increases the risks of surgery. Thorough evaluation and discussion of risks with the patient prior to operative intervention is paramount.
Do you believe there might have been medical error?
My biggest concern with this case is that the patient was likely under resuscitated just prior to taking the patient to the operating room. Induction of anesthesia likely caused a further reduction in cardiac output, resulting in hypotension and a subsequent decreased end-tidal CO2 production. I would be curious to know what her urine output was the 12 hours prior to surgery as well as her electrolytes and creatinine/creatinine clearrance since the medical examiner identified acute kidney injury on their autopsy.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
Hypovolemic shock secondary to nasal gastric tube losses and dehydration, could have been made worse by induction of anesthesia.
What makes you a good expert for this case?
I am an associate professor of surgery, complex general surgical oncologist and board certified general surgeon who cares for patients with bowel obstructions frequently.
How often do you encounter cases similar to this one in your practice?
Many times in a given year I manage patients with acute and/or acute on chronic bowel obstructions.
Do you believe there might have been medical error?
There are credible arguments that the standard of care was breached in the areas of (1) pre-operative cardiopulmonary optimization and (2) choice of access/management of a suspected CO₂ gas embolism. Whether those deviations were the proximate cause of death will depend on the likelihood that better optimization or open access would have averted the arrest.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
Diminished Physiologic Reserve – During the 48-hour window before surgery, the team skipped low-burden cardiac, pulmonary, and glycemic optimization (ACC/AHA risk stratification, assessment of the abnormal chest X-ray, insulin correction). This left a patient with known coronary disease and possible infection far less able to tolerate hemodynamic stress. High-Risk Abdominal Entry – Instead of switching to an open (Hasson) approach once adhesions produced high insufflation pressures, the surgeon introduced a blind Veress needle. That maneuver in a “hostile” re-operative abdomen is well-documented to carry a markedly higher incidence of carbon-dioxide gas embolism. Incomplete Rescue – When the classic indicators of massive CO₂ embolism appeared (sudden drop in end-tidal CO₂ followed by bradycardia), the team halted insufflation but did not perform the guideline-endorsed Durant position, PEEP reduction, or right-atrial aspiration—actions that significantly improve return-of-spontaneous-circulation rates. Because (a) each step above is independently recognized in peer-reviewed guidelines as lowering the risk of peri-operative arrest, and (b) massive CO₂ embolism leaves no histologic footprint, it is more likely than not that the combined departures created—and then failed to reverse—the embolic event that caused the patient’s death. Thus, duty, breach, and proximate causation are satisfied.
What makes you a good expert for this case?
I am uniquely qualified to opine on this case because I am a board-certified colorectal and general surgeon who has spent more than three decades in active operative practice, managing over 400 small-bowel obstructions—including many “hostile” re-operative abdomens where laparoscopy, access choice, and carbon-dioxide embolism risks are daily realities—and teaching residents how to navigate those challenges safely. My familiarity with the very guidelines at issue (ACC/AHA peri-operative cardiac evaluation, ASA pre-anesthesia advisories, and SAGES small-bowel-obstruction and access standards) allows me to pinpoint and translate published expectations into plain language for judges and juries. Coupled with a robust medical-legal track record on both plaintiff and defense matters, peer-reviewed publications, and national teaching experience, I bring the rare blend of hands-on procedural expertise, scholarly credibility, and courtroom-tested communication skills needed to persuasively explain how the deviations in this case more likely than not caused the patient’s death.
How often do you encounter cases similar to this one in your practice?
In more than three decades as a colorectal and general surgeon I have treated well over 400 small-bowel obstructions—roughly a dozen each year between my clinical practice, call coverage, and tertiary referral work. About 15-20 % of those cases involve ‘hostile’ re-operative abdomens with dense adhesions, just like the scenario we’re discussing, and a smaller subset (~5 %) require urgent conversion from attempted laparoscopy to open surgery because of access or physiologic concerns. That experience, combined with reviewing several dozen similar cases in my medical-legal consulting role, gives me a solid benchmark for what constitutes prudent peri-operative preparation, safe entry technique, and appropriate rescue when complications arise
Do you believe there might have been medical error?
Complex case. Patient with ongoing bowel obstruction unclear volume status but had fall in BP on induction so some element of hypovolemia which would not be unexpected given her diagnosis and treated with a bolus of pressor. The surgeon was unable to place the 5 mm port successfully but it cause no injury based on the post mortem and then attempted to place a veress needle and also without injury based on the post morten. So why did the end tidal CO2 drop - it would have nothing to do with the surgeon. The cause was some event from induction- as a drop in end tidal CO2 would be from a drop in cardiac output. Now post mortem did not show a PE or MI to explain this sudden drop in end tidal CO2 and therefore cardiac output. But again the surgeon had no role in this. Unsure what was happening just based on the brief summary what was happening on the anesthesia side in terms of tracings and vitals and whether there was somehow anesthesia could have intervened but I am not an anesthesiologist. Sudden deaths are usually PE or MI which the post says was not the case here --- reaction to anesthesia in an already hypovolemic patient?
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
Again the surgeon's maneuvers did not cause this patients change in status but the induction of anesthesia may have played a role. Again event likely related to anesthesia induction and nothing to do with surgery. Post mortem not helpful. Maybe critical aortic stenosis was missed which would drop cardiac output and end tidal CO2 in a hypovolemic patient and can lead to cardiac arrest. Otherwise one would need to look at this from anesthesia standpoint with review of flowsheet but by an anesthesiologist not a surgeon.
What makes you a good expert for this case?
Have been performing expert review for many years and on a number of cases including writing reports and participating in depositions (as an expert). Have been involved in surgical quality at a major urban hospital since 2008 and perform in house malpractice review. I am currently on the faculty of a major medical school, Chief of Surgery of the hospital I have worked in for 2+ decades and have the title of Surgical Quality Officer.
How often do you encounter cases similar to this one in your practice?
Again this case in unique and hopefully no surgeon ever has a patient arrest during surgery (except maybe an unstable trauma patient or ruptured AAA). Most surgeons will never have a case where a patient who was stable arrests during surgery. I unfortunately am not so lucky and did have a patient arrest on me in the operating room and miraculously survive. My one time and hopefully only time in my 25 years. It really should never happen. But if you are asking how many laparoscopies I perform a year its probably 200-250 - but again in this case the surgery itself had nothing to do with this patient arresting (at least from the surgeons side of the table/drape).
Do you believe there might have been medical error?
18 years as Board Certified General Surgeon and Oral General Surgeon Examiner
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
The case has two concerning events that went unnoticed by the attending surgeon and the Anesthesiologist. 1. A 5mm port was placed under direct vision in the right upper quadrant. The surgeon was unable to insufflate the abdomen. This raises the question as to the location of the trocar. It was either in the liver itself (No documentation on the limited autopsy provided) or in the subcutaneous tissue. The veress needle was then placed in the left upper quadrant. I would have anticipate that the C02 was attached and no verification test was performed. I do not appreciate a record of a "saline drop" test before the insufflation began. The outcome was the tip of the veress needle entered into a vessel or fatty tissue. As a result, the patient "threw" a C02 emboli to the right atrium which occluded the blood flow tot the right ventricle and ultimately to the lungs. It is a rare event (0.1%) of case. If the Surgeon and Anesthesiologist would have been alert they could have place the patient in the LEFT lateral decubitus, trendelenburg position to "trap" the C02 bubble in the right atrium and hopefully allow it to absorb. A classic murmur can be heard on these patients, "water-wheel." In addition, an echo in the OR would have been helpful with a right internal jugular central venous catheter or swan ganz to try an aspirate the C02. However, the mortality is very high and success rate of saving these patients is very low.
What makes you a good expert for this case?
18 years as Board Certified General Surgeon and Oral General Surgeon Examiner This is a classic board question.
How often do you encounter cases similar to this one in your practice?
I have done 1000s of laparoscopic cases and i have one C02 emboli.
Do you believe there might have been medical error?
This patient is in a cardiovascular compromised position, and most likely under-resuscitated as bowel obstruction patients usually are. The veress needle insertion either caused a gas embolism by penetrating a vein, or caused a vagal response precipitating arrest. There was no mention of blood in the retroperitoneum so I would think it is less likely there was Veress needle misplacement into a large vein. Thus leaving the vagal response to a CV compromised patient. I guess the question then becomes do you do a laparoscopic approach on this patient first, or go straight to laparotomy. And I would say there is no evidence pre-op that she would react in this way to anesthesia and peritoneal insufflation.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
I don't think there was an error in management. I think this patient had underlying unknown CV risk that could not be appreciated pre-op. If there was Veress needle penetration of a vein causing gas embolism I would think there would be some evidence on autopsy. If there was a gas embolism I would think it would be the inferior mesenteric vein, or a tributary or splenic vein. These areas seem to be checked on the autopsy and there is no mention of injury there.
What makes you a good expert for this case?
General, Emergency & Trauma surgeon for over 10 years. Have done thousands of laparoscopic cases. 100s w Veresss needles.
How often do you encounter cases similar to this one in your practice?
I have not had a patient die in this manner, I have had patients become unstable with insufflation of the peritoneum. I have done 100s of laparoscopic cases (at lease started) for bowel obstruction.
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