Intraoperative death during right laparoscopic nephrectomy of a polycystic kidney
Case Summary:
A 59-year-old male with polycystic kidney disease underwent a semi-elective hand-assisted laparoscopic right nephrectomy for recent recurrent bleeds into cysts. Twelve months prior, the patient had a myocardial infarct and was stented and placed on clopidogrel. The patient had a functioning renal transplant and was immunosuppressed. He was appropriately consented and clopidogrel ceased preoperatively.
It was clearly documented that the patient had a very large right kidney with resultant limited laparoscopic access, requiring cysts to be punctured to improve surgical access. During the (difficult) attempted hand-assisted laparoscopic procedure, the inferior vena cava (IVC) was torn at the confluence of the right renal vein. Immediate pressure to the IVC to control bleeding was applied, along with rapid conversion to an open flank procedure. Blood loss of 1.5–2.0 L was documented. It was noted that 5 runs of staples were fired across cysts abutting the IVC, resulting in the bleeding and conversion to open surgery. It would appear that these were applied in and around the hilum of the kidney; however, there was no mention of formal dissection/visualisation of the renal vessels. The patient was appropriately resuscitated with 2 units of packed cells and, during the open procedure, a vascular surgeon urgently attended the case and repaired the IVC.
Following the removal of the kidney, a full inspection of the renal bed and surrounding area excluded ongoing bleeding. With the patient on metaraminol and haemodynamically stable, the wound was closed. Within seconds of transferring the patient supine onto a bed bound for the intensive care unit, the patient became profoundly hypotensive, arrested, and had no filling of the cardiac chambers (as determined by ultrasound). Cardiopulmonary resuscitation commenced. A massive transfusion protocol was initiated, and the abdominal cavity was opened. A large volume of intra-abdominal blood was noted. Despite all attempts, the patient could not be saved. Bleeding was coming from the subhepatic venous drainage system. The repaired IVC appeared to be intact and not bleeding. The patient was profoundly acidotic just prior to arrest, was hypocapnic and on imaging (via ultrasound) was found to have empty ventricles.
Discussion:
This patient had a recent bleed into one of his renal cysts while on clopidogrel for a cardiac stent that had been placed more than 12 months earlier. It could be argued that in consultation with his cardiologist, before embarking on surgery, clopidogrel could have been permanently stopped and this may have prevented recurrent bleeds and therefore obviated the need for surgery.
Polycystic kidneys are very large and often encroach at the hilum across the vascular structures, making surgery and anatomical identification very difficult. While the literature lacks absolute clarity on when open rather than laparoscopic nephrectomy should be performed, kidneys with a diameter of greater than 16 cm are most commonly managed open. Clearly that depends on the experience of the surgeon and the theatre staff. The dimensions of this patient’s right kidney were 24x16x18 cm. In addition to the preoperative parameters, the initial operative findings of significant adherence to the duodenum and IVC, and the need to decompress cysts for access, were indicators to convert to open surgery.
Five vascular staple loads were used. The principles of laparoscopic nephrectomy mandates that hilar vessels are dissected free of surrounding tissue and identified for individual stapling. Arguably, only 2 vascular staple loads should have been used. It is unclear from the operative report where those vascular staple loads ran. An important aspect of the coroner's findings would be ensuring that the staple runs had not transected the IVC or compromised its calibre, impeding venous return and resulting in inadequate or complete loss of cardiac filling, acidosis and subsequent increased venous pressure in the IVC below that level, producing widespread venous bleeding.
The venous injury was identified promptly, bleeding controlled quickly with pressure and the operation converted to an open procedure. Appropriate expert assistance was sought and a consultant vascular surgeon scrubbed in with minimal delay, repairing an obvious defect in the infrahepatic IVC at the confluence of the right renal vein. Further inspection for ongoing bleeding was performed by both the primary and vascular surgeons, failing to identify further bleeding source(s). Within minutes of the patient having his wound closed, reopening was necessary and there was a very large volume of blood in the peritoneal cavity coming from the subhepatic venous drainage region.
Based on the information provided, the resuscitation status of the patient indicated a haemoglobin of 99 g/L just prior to transfer to the trolley on which the arrest occurred. Two units of blood had been given with pressures maintained on metaraminol. Within seconds, the patient arrested and had empty ventricles on ultrasound. Causes for a complete loss of venous return include massive loss of intravascular volume, anaphylaxis, tension pneumothorax, air embolus and obstruction to venous return. A pneumothorax was excluded. Assessment for anaphylaxis may have been performed but it is not clear from the notes. Although there was a large volume of blood when the abdomen was immediately reopened, it is unclear how this resulted in a seemingly sudden and complete loss of circulating volume such that there was no filling of the heart, thus the concern regarding an unrecognised CO2 embolus, IVC obstruction and anaphylaxis.
As mentioned, it is essential to follow up on the coroner’s assessment of the patient’s IVC to exclude significant occlusion due to the vascular stapling and/or the IVC repair, as that could account for empty cardiac chambers on ultrasound. If that is not apparent, then a failure to keep up with blood loss will have been a major contributing factor in the patient’s outcome.
Clinical Lesson:
In this case, a tear in the IVC was the adverse event that set off a cascade of vascular incidents resulting in death. Bleeding was associated with laparoscopic stapling and could have been avoided with an open approach. Preoperative scans, difficult initial access, lack of hilar vessel identification prior to stapling and incomplete exposure of the infra- and suprarenal IVC were all indications for conversion to open surgery before the vascular injury. Approaching this case laparoscopically is an area of concern contributing to the outcome.
Inadequate replacement of intravascular circulating volume is another consideration that may have contributed to death; however, as mentioned, the patency of venous return to the heart needs to be ascertained during the coroner’s examination.
Disclaimer:
Please note that these cases are edited from ANZASM first- or second-line assessments that have been generated by expert surgeons in the field. Any recommendations relate to these cases as they were presented.
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