We present a 71-year-old self-employed, non-smoking German female patient scheduled to undergo a right TKA. Relevant past medical history included type 2 diabetes mellitus treated with insulin (HbA1c 43 mmol/mol), BMI 35.5 kg/m2 (176cm/110kg), arterial hypertension (usual value 140/60 mmHg right arm) and restless leg syndrome. Important self-medications were metformin, valsartan, hydrochlorothiazide, nebivolol, aspirin, lercanidipine hydrochloride, levodopa and benserazide hydrochloride. The patient's history included a TKA on the right side in 2000, a traumatic dislocation in 2011 and a revision arthroplasty in 2012 caused by instability. These operations were performed under general anesthesia without complications.
In February 2018 the patient presented to our orthopedic outpatient department because of increasing pain in the right knee joint. Examinations showed implant loosening and a Staphylococcus epidermidis infection. Therefore, the patient was scheduled for two stage revision with implant removal and antibiotic loaded spacer implantation. Until the day of operation the patient got no antibiotic therapy. For pain management she got a prescription for celecoxib and metamizole PO as well as subcutaneous antithrombotic prophylaxis with enoxaparin sodium and the recommendation to cool, protect and store up the leg.
In the premedication visit the patient was classified as ASA III (according to the American Society of Anaesthesiologists) with a metabolic equivalent of ≥ 4. An electrocardiogram and current lab values (erythrocytes 7.0 mmol/l; Hb 7.0 mmol/l; Hk 0.32 l/l; CRP 5.7 mg/l; all others without abnormalities) were already done. The patient showed no signs of cardiopulmonary decompensation like dyspnea, edema or auscultatory abnormalities at this time. For the day of surgery 5mg oxazepam PO and usual medication except metformin, valsartan and hydrochlorothiazide was prescribed. The patient has been informed that she can eat until 6 hours before surgery and drink clear liquids until 2 hours before surgery. The procedure was performed under general anesthesia with endotracheal intubation. The initial vital parameters were a blood pressure (BP) of 160/80 mmHg and a heart rate (HR) of 65 bpm. The induction of anesthesia was performed under standard monitoring (non-invasive BP, HR and pulse oximetry) in the following order: propofol (180mg) intravenous (IV), sufentanil (20μg) IV and rocuronium (50mg) IV. Sevoflurane (target value of minimal alveolar concentration of 0,8-0,9) and sufentanil (10μg as single IV bolus at point of incision) were used to maintain anesthesia. Furthermore, 1g tranexamic acid IV and balanced electrolyte solution (jonosteril 2l for the hole surgery) was given. After induction BP was 95/55 mmHg, measurement was done every three minutes and documented every five minutes. The patient received norepinephrine (20ml/h »3μg/min over IV perfusion) for 20 minutes, directly after induction of anesthesia until surgically incision (28 minutes after induction), which was stopped at a mean arterial pressure of 65 mmHg. Thereafter, the patient was stable without catecholamines.
Surgeon saw intraoperative pronounced synovitis and intramedullary femoral and tibial periprosthetic infection membranes. They took a smear and the patient received cefuroxime 1,5g IV. During the tibial component spontaneously resolving episodes of asystole were observed on 3-lead-ECG. They were seen two times over maximum of two seconds and depended on the surgical manipulation. Before any intervention they ended spontaneously with complete removal and no hemodynamic changes were seen. Forty-five minutes after incision when the surgeon began the intramedullary reaming, there was a seven-second asystole again. This vanished after stopping the reaming. However, now asystole was associated with a fast fall in BP (42/18 mmHg), oxygen saturation (68%) and end-tidal CO2 (21 mmHg). The patient received 0.5 mg of atropine IV to prevent reproducible asystole for the rest of the procedure. Epinephrine was prepared but not injected because of the complete recovery of hemodynamic parameters after end of manipulation. Other reasons for asystole were checked without any indication of a reversible cause.
Around these events the patient had no signs of pain like hypertension or tachycardia. From the event of asystole until the end of the surgery, depth of anesthesia was monitored by the bispectral index (BIS), with no evidence of low anesthesia (BIS score of 42) after the last event. According to our standard operation procedure BIS was not indicated for this surgery but we wanted to exclude pain as a reason for another asystole (because of low anesthesia) until the end of operation.
Extubating was done without any problems. The patient got metamizole (1g) at the end of surgery to prevent postoperative pain. In the recovery room the patient got a 12-channel-EKG, laboratory tests to exclude ischemia, blood gas analysis and a transthoracic echocardiography without any abnormalities. Noninvasive cardiovascular investigations like repeated 12-channel-EKG, 24-hour Holter monitoring and ultrasound of extracranial vessels were done. These investigations revealed a couple of supraventricular ectopic but were otherwise unremarkable. The cardiologist assumed that the patient had a vagal reaction when bone manipulations were done by surgeon and advised atropine IV for following operations.
Six weeks later the patient underwent scheduled spacer removal and TKA. The patient got atropine IV after induction of anesthesia, to reach a higher HR and received invasive BP measurement and BIS-monitoring. As the surgeon manipulated the medullary cavity, the patient developed a self-limiting episode of bradycardia (40 bpm) lasting only three seconds. No other events were recorded during surgery or hospital stay.