Allegation
Plaintiff alleged the defendant anesthesiologist failed to appropriately monitor and treat respiratory symptoms, ultimately leading to the patient's death.
Case Details
A 46 YOF (5’4”, 227 lbs.) had an uncomplicated endoscopic septoplasty, submucous resection of the inferior turbinates, and bilateral maxillary sinusotomy. The patient's medical history was significant for chronic sinusitis, deviated nasal septum, nasal obstruction, hypercholesterolemia, HTN, migraine headaches, tonsillectomy, adenoidectomy, diagnostic laparotomy, and pubovaginal sling. Preoperative studies including a chest x-ray, were all within normal limits.
Under the direction of the defendant anesthesiologist, a CRNA intubated the patient for the procedure and placed her under general anesthesia. The procedure lasted approximately 1.5 hours and included drainage and removal of two large cysts. Sufenta 50 mcg, an opioid, was used. The procedure was without incident.
The patient was extubated in the OR and transferred to the PACU in stable condition. While in the PACU, her vitals were BP 191/86, P 87, and R 24. She was in a chin lift airway position with an SaO2 of 88% on 10L of O2 at 98% via face tent. A nasal packing was in place and caused the patient to be anxious. BP increased to 213/97, P 84, R 24, and SaO2 was 98% on 98% oxygen. An oral airway was placed since the patient was experiencing slight breathing difficulties.
Approximately 20 minutes later, the patient’s breathing improved. The oral airway was removed, and the patient's SaO2 was in the 94%-98% range on 40% oxygen. Her BP was down to 111/60. A nurse notified the defendant anesthesiologist that the patient's SaO2 had dropped to the low 90s. The defendant ordered albuterol and supplemental O2, as well as Demerol for pain.
The patient was having difficulty maintaining saturations in the 90% range, so the defendant anesthesiologist ordered a chest x-ray. The radiologist's impression was bilateral infiltrate more pronounced on the right than the left, which represented a dramatic change compared to the preoperative x-ray. The defendant anesthesiologist suspected non-cardiogenic pulmonary edema and ordered Lasix. Vital signs were BP 151/70, P 140, R 36, shallow and regular, and SaO2 66% on 98% oxygen. The PACU nursing notes documented the patient's SaO2 fluctuated in the 70%-80% range.
The patient received additional Lasix. The ABGs indicated a critical low pH of 7.27 (7.35-7.45), critical low PaO2 39.5 (80-100), critical low SaO2 64.5% (95%-100%), critical low HCO3 19.8 (22-26), and a PaCO2 44.1 (35-45). Almost two hours after an SaO2 of 66%, the patient was reintubated. One hundred milliliters of bloody drainage was suctioned from the endotracheal tube. The patient was transferred to the ICU. Abnormal laboratory results included a low critical potassium 2.8 (3.5-5.2), glucose 292 (70-110), CK-MB 4.8 (0-3.6), and high critical troponin 1.63 (.0-.6).
Initially, the patient improved overnight; however, her blood pressure dropped and her temperature spiked to 106°F. A chest CT scan revealed no evidence of pulmonary emboli. The cause of the fever could not be identified. A CNS disturbance was thought to be the possible cause, and a neurology consult was obtained. A head CT scan was unremarkable, and a lumbar puncture produced clear fluid and negative cultures. Cardiology and pulmonology were also consulted.
The patient continued to deteriorate. The following day, she became bradycardic and had an arrhythmia. A code was called and resuscitation efforts were unsuccessful; the patient was pronounced dead. An autopsy was performed, and according to the pathologist, the major pathological finding was an acute, relatively diffuse, lung injury, which developed into full-blown Acute Respiratory Distress Syndrome (ARDS). He indicated the cause was unclear and that there was some degree of myocardial injury as evidenced by the troponin level. In summary, the pathologist believed it was primarily a pulmonary death of uncertain cause.
The plaintiff alleged the defendant anesthesiologist failed to both monitor the withdrawal of anesthesia appropriately, and to identify and treat respiratory distress and upper airway obstruction. The failure to reintubate the patient until almost two hours after an SaO2 of 66% caused a lung injury that progressed to hypoxemia, pulmonary edema, ARDS, and ultimately death.
Expert Testimony
An expert for the plaintiff, a board-certified anesthesiologist, contended that giving Sufenta was below the standard of care. He testified that if fentanyl had been used it was more likely than not that the patient would have had a different result. The expert witness also criticized the use of Demerol. In addition, the plaintiff alleged the patient was extubated prematurely, and ABGs should have been obtained sooner. The expert witness said the patient experienced a laryngospasm after she had been in the PACU and developed noncardiogenic pulmonary edema caused by aspiration. He stated that the patient also developed negative pressure pulmonary edema (NPPE), and Lasix was not the correct treatment for NPPE.
The defense expert testified Sufenta was the appropriate medication. The reintubation was timely and within the standard of care. The patient developed ARDS, and an infectious process caused the patient’s death.
Resolution
This case was tried and resulted in a plaintiff’s verdict. However, it was reversed on appeal and a judgment as a matter of law was entered for the defense as the plaintiff’s expert did not meet the requirements of a similarly situated health-care provider.
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