Case presentation 1:
A 40-year-old female who was 10 days s/p uneventful laparoscopic tubal ligation with lysis of adhesions presented with presumed sepsis and necrotizing fasciitis (fever, severe abdominal pain, odiferous fluid leak from the abdominal wall, elevated WBC and lactate, anemia, CT: free air in the abdomen, gas in the tissues). In the ED, she received fluid resuscitation (2 L) and antibiotics and was scheduled for emergent surgical exploration at 0940. Vital signs were 144/69, HR 114, respiratory rate 16, oxygen saturation 98%, temp 102.2F, and VAS 8/10 abdominal pain. She was designated an ASA PS 3E by the anesthesiologist and CRNA.
The induction and intubation at 1056 were uneventful. A radial arterial line and left subclavian double-lumen central venous line were placed and verified at 1104 by blood return from both lumens and pressure monitoring. Surgery began at 1105. At 1112, the assigned CRNA was given lunch relief by another CRNA. At 1113 (one minute later), there was an abrupt decline in EtCO2, and the endotracheal tube position was “verified.” The anesthesiologist was immediately called and arrived by 1116. The patient then became severely hypotensive, and a code was called for pulseless electrical activity (PEA) that progressed to asystole. According to the anesthesia record, the code began at 1113, while the code sheet began at 1120. During discovery, this time discrepancy led to confusion about when the first doses of epinephrine, atropine, and vasopressin had been given. The code (directed by the anesthesiologist and the surgeon both) followed ACLS protocol for medications and CPR. The primary working diagnosis during the code was a large pulmonary embolism, but not cardiac tamponade despite the proximity to the central line placement and the symptoms. The anesthesiologist noted in deposition that “none of the resuscitative measures had any effect” and that he considered tamponade, mentioning it to the surgeon during the code, but the surgeon’s testimony and other witnesses conflicted with this claim. No other studies (CXR, etc.) were done until afterward. The patient never recovered cardiac activity. The anesthesiologist stopped the code after 11 minutes at 1131.
A posthumous chest X-ray showed the subclavian central line ending at the superior vena cava/atrial junction “via a slightly atypical course,” a large heart and no pneumothorax. The autopsy showed two 1-2 mm acute perforations of the superior vena cava causing tamponade of over 500 ml. Experts opined that the primary liability was for failure to consider other causes besides pulmonary embolism and not to get a CXR; the code followed the appropriate treatment algorithm otherwise. The defense filed a Consent to Settle early on, but also proceeded with trial prep. The settlement was reached at the jury selection phase in the amount of the anesthesiologist’s insurance coverage and none for the CRNA or the anesthesia corporation.
Case presentation 2:
A 61-year-old male presented for retrieval of a removable IVC filter placed for a back surgery two weeks previously. The cardiovascular anesthesiologist had not done this exact procedure before, and the vascular surgeon requested monitored anesthesia care (MAC) for a “simple” retrieval.
The MAC consisted of midazolam and fentanyl with nasal cannula oxygen with EtCO2 monitoring. The surgeon planned to use a retrieval kit through a RIJ introducer with a “snare” to retrieve the filter. The patient was hemodynamically stable and “snoring” throughout this time. The surgeon had difficulty with the snare and consulted an interventional radiologist; they decided to retrieve the snare and filter through a femoral cutdown through the IVC, which was successful. The physician assistant (PA) started to close the groin. The anesthesiologist then placed an 18 ga peripheral I.V. because “he wanted to be able to push fluids as quickly as possible.” During the I.V. placement (<1 minute by report), the patient went into a wide complex heart rhythm followed rapidly by bradycardia. The blood pressure cuff was unable to get any reading, and there were no pulses palpable.
The PA began CPR and called for help. The anesthesiologist intubated uneventfully without any medications and administered epinephrine following the ACLS protocol for pulseless electrical activity. CPR were essentially ineffective by palpation; a radial arterial line, “a swan-ganz introducer, and CVP introducer” were placed. The anesthesiologist suspected a cardiac tamponade and performed a transesophageal echocardiogram, which revealed “a lot of fluid around the heart.” All the while, the ACLS protocol was followed (CPR, bolus epinephrine, norepinephrine infusions, and a “bunch of blood”). A cardiothoracic surgeon was consulted immediately for a subxiphoid pericardiectomy at 20 minutes into the code; he found “a lot of clot, including fresh blood.” He then performed a full sternotomy and secured the “3 cm rent in the junction of the right atrium and the vena cava” but did not attempt repair immediately to allow the anesthesiologist “to catch up with blood products.” Meanwhile, they were using partial (“sucker”) bypass, and the blood pressure was fully restored by 34 minutes into the code. He then undertook full repair with cardiopulmonary bypass, which was uneventful. The patient was taken to the ICU on minimal blood pressure support, but he never woke up from an anoxic brain injury verified by CT. He eventually was taken off life support. The determined cause of death was hypoxic encephalopathy following hemorrhage from a tear in the superior vena cava.
The defendants’ motion for summary judgment was upheld – stressing that nothing else could have been done to diagnose and treat the tamponade more promptly; it simply took time that the patient did not have, but there was no deviation in the standard of care.
Pericardial effusions (>15-50 ml) and cardiac tamponade cause varying degrees of circulatory compromise and are readily diagnosed with echocardiography (J Am Soc Echocardiogr 2013;26:965-1012.e15). The Closed Claims Project has published that 16 (14.5%) of 110 cases related to central venous catheters were associated with tamponade (Anesthesiology 2004;100:1411-8). Iatrogenic cardiac tamponade (ICT), often from perforation of the vena cava or the heart itself, is commonly associated with hemodynamic collapse; ICT is about 3%-35% of all tamponade etiologies. Tamponade can be caused by as little as 100-150 ml of pericardial fluid. The typical findings or symptoms include tachycardia, hypotension, elevated venous pressures, and jugular venous distension (Am J Emerg Med 2022;58:159-74). In hemodynamic collapse from tamponade, CPR will be largely ineffective because of lack of cardiac filling (J Trauma 2002;53:1183-4). The incidence of complications from central venous catheterization is 10%-20%, but ICT is fortunately rare (0.14%-1.4%), though often catastrophic (mortality rates from 37.5% up to 100% if untreated or with ventricle perforation) (Cureus 2023;15:e37695; Cardiol J 2016;23:57-63). It is a known but uncommon complication of IVC filter procedures as well. Absolute mortality and morbidity risks for ICT are at least 10% (Am J Emerg Med 2022;58:159-74). It is known that if the initial presentation is successfully treated, the long-term outcome can be good (J Am Soc Echocardiogr 2013;26:965-1012.e15).
Treatment of ICT can involve removal of the fluid (needle pericardiocentesis) as well as repair of the primary cause with open intrathoracic or cardiac surgery. Pericardiectomy (window) is usually reserved for chronic or more hemodynamically stable pericardial effusions. Removing even a small amount of pericardial fluid through pericardiocentesis in an unstable tamponade patient can rapidly improve hemodynamics, but unless the primary cause is not also resolved, the fluid will reaccumulate (Am J Emerg Med 2022;58:159-74). Pericardiocentesis has a morbidity rate of 1%-3% and mortality rate from procedural injuries of <1% (Cardiovasc Diagn Ther 2011;1:11-36). Early pericardiocentesis in the ED for tamponade that presents prior to full arrest has been shown to decrease survival at one year significantly, but little is known for OR presentation (Am J Emerg Med 2022;58:159-74). Pericardiocentesis can confirm the diagnosis and can be lifesaving if the tamponade does not immediately recur; but with ICT, recurrence is very likely, if not guaranteed (Cureus 2023;15:e37695).
Thus, the choice of pericardiocentesis versus open thoracotomy repair is a surgical judgment. The definitive treatment of ICT is surgical repair of the injury via either thoracotomy or sternotomy, but that requires more time (than pericardiocentesis), general anesthesia, and possibly cardiopulmonary bypass or even hypothermic circulatory arrest, all of which are associated with increased risks. Both of these cases had full hemodynamic compromise with noted ineffectiveness of CPR, which is the likely cause of the catastrophic outcomes. Arguments can be made that a needle pericardiocentesis might temporarily improve perfusion and lessen the injury, perhaps even changing the outcome, but ICT would rapidly recur. Case 2 shows the choice to proceed to definitive repair, but it also shows the risk of a bad outcome.
The first difficulty in treating tamponade is considering it as a diagnosis; this was apparently the failure of Case 1. The advanced cardiac life support (ACLS) protocols include the “6Hs and 6Ts” for evaluating the etiology of PEA or asystole for just this reason (2020 guidelines; cpr.heart.org). In the absence of echocardiography, Case 1 could have used traditional, nonguided pericardiocentesis as a last-ditch effort, thereby also confirming the diagnosis (but first the diagnosis would need to be considered). In one series of ICT during hiatal hernia surgeries, 23% of cases were only identified at autopsy, and overall mortality was 33.3%, even when the complication was expected (Heliyon 2019;5:e01537).
These cases demonstrate several useful lessons regarding malpractice and the law. First, despite very similar anesthesia care following accepted (i.e., ACLS) standards and similar clinical outcomes, very different litigation outcomes were achieved in part because of clinical judgment, but also due to differences in communication and documentation. In cases with severe neurologic injury and/or death, even when the care is deemed appropriate, outcome bias means that there is always a risk that a trial verdict could be in opposition to the appropriate care, perhaps even excessively (beyond liability policy limits). Therefore, settlement or summary judgment (a decision based on specific points of the case in general without going to trial) is often preferred. The value of clear and thorough communication during and after the event and clear and complete documentation (without time discrepancies and “chart battles”) cannot be overstated.
In one case, the treatment protocols were followed, the use of clinical judgment defined by ACLS to diagnose the etiology was performed systematically, and the definitive treatment was accomplished – but not before irreversible brain damage had occurred. There were no documentation deficits or time discrepancies (that could not be defended), and communication during and after the event between the primaries was also appropriate and respectful. Because the expert witnesses generally agreed with the care and thought there was nothing further that could have been done, the defense asked for summary judgment, which found for the defendants with no liability.
In the other case, the treatment protocols were followed, but the clinical judgment piece was not. Care was stopped before diagnosis was made (via CXR or echocardiography) or therapeutic interventions were tried (pericardiocentesis, etc.). In fact, the etiology was not determined until the autopsy. There were significant time discrepancies and documentation questions that had to be defended in deposition. Communication was respectful but incomplete or conflicting. The defense chose to settle to avoid the risk of damages beyond the coverage limits.