A 74-year-old man with cardiomyopathy, prior implantable defibrillator placement for ventricular tachycardia, hypertension, coronary artery disease, and type 2 diabetes presented on 12/26/2024 for planned laser extraction of a failed right ventricular defibrillator lead, with an abandoned right atrial lead also present. The records state he was not pacemaker-dependent. A transesophageal echocardiogram at the start of the procedure showed a dilated left ventricle with an ejection fraction of approximately 25–30%, a dilated right ventricle with mild hypokinesis, and trace-to-mild valvular regurgitation.
*Please see attached redacted OP note for reference*
According to the operative note, the procedure involved generator explant, preparation of the leads for extraction, and placement of a Bridge balloon through the femoral vein under fluoroscopic guidance. The note describes significant calcification along the leads. During extraction of the right ventricular lead, after approximately two-thirds of the lead had been removed, persistent hypotension developed. The Bridge balloon was deployed while emergency sternotomy was performed. The pericardium was described as full of blood, and brisk bleeding was identified from an approximately 1.5 cm defect on the anteromedial surface of the inferior vena cava. That injury was controlled and repaired with pledgeted suture. The operative note further states that the patient remained hemodynamically compromised and acidotic, cardiopulmonary bypass was instituted, the remaining right ventricular lead and abandoned right atrial lead were removed, and additional bleeding at the superior vena cava/innominate region was oversewn. The patient was then weaned from bypass, treated for coagulopathy, and closed with mediastinal and Blake drains left in place. The reviewed chronology reflects prolonged intraoperative hypotension and hypoxemia, along with substantial transfusion support.
Postoperatively, the patient was transferred intubated to the cardiovascular ICU. The reviewed records state that post-procedure transesophageal echocardiogram showed moderate right ventricular hypokinesis and moderate tricuspid regurgitation, without evidence of aortic dissection, and postoperative chest imaging reportedly showed satisfactory tube placement without pleural effusion or focal infiltrate. He required vasoactive and supportive infusions, including epinephrine, vasopressin, milrinone, and tranexamic acid. Early postoperative examination documented spontaneous respirations off sedation but failure to follow commands, minimal motor activity, sluggishly reactive pupils, preserved corneal reflexes, and absent vestibulo-ocular reflexes. Later that evening, he developed a tonic-clonic seizure and was treated with Ativan and levetiracetam. Head CT obtained afterward reportedly showed chronic/remote infarcts and chronic microangiopathic change without acute intracranial findings.
Over the next several days, the records describe persistent neurologic impairment with additional seizures and/or myoclonus requiring continued sedation and escalating antiepileptic therapy. EEG reportedly showed generalized periodic epileptiform discharges and later nonconvulsive status epilepticus evolving into a discontinuous or burst-suppression background. Neurologic examination remained poor, and MRI of the brain reportedly showed chronic cerebral and cerebellar infarcts without acute infarct or MRI evidence of hypoxic injury. During this period, he also continued to require critical care management for hemodynamic instability, anemia, thrombocytopenia, and volume-related issues. On 12/30/2024, the records state there was no apparent neurologic recovery, vasopressor support was again required, and he was compassionately extubated and pronounced dead later that day.
Appreciate insight into intraoperative or postoperative treatment.
Questions welcome.
Files:
Q: is it possible to see the anesthesia case record of the patients vitals and the perfusionist records
A: —
Do you believe there might have been medical error?
Interesting and unfortunate case. Tearing of venae cavae during procedures of lead extraction is a well known complication (with elevated mortality), although rare with current extraction devices and occlusion balloon devices. Two interesting aspects: 1) The site of injury was on the anteromedial aspect of the IVC (most common site of injury during lead extraction is the SVC). The IVC should not be on the path of the ventricular lead. This case possibly suggest that either a sharp edge of the lead approached the IVC during extraction and was dragged upward retraction, or was rather redundant and partially adhesed to the IVC. A relatively recent study (Arora Y et al. Ann Thorac Surg 2022; 113:1165-71) remarks the importance of repairing these tears on cardiopulmonary bypass (CBP). As the authors state "CPB initiation allows for a systematic, controlled response and the opportunity to induce controlled hypothermia. It buys the surgeon precious time to assess the extent of injuries methodically and calmly repair the injured vessel". It appears that the surgeons performed repair of the IVC injury while not on CPB, following a likely significant blood loss and while exposing a difficult anatomic target. Visualization of the IVC indeed requires a non negligible retraction of the right ventricle. If the latter is already not very functional, the patient's hemodynamics may become even further compromised an lead to end organ (brain, in this case) malperfusion. 2) After controlling the IVC bleeding, the team proceeded with the remaining portion of the lead extraction while on CPB. This possibly resulted in an additional injury now to the SVC. An option could have been to cannulate the patient in a bicaval fashion for CPB, open the right atrium and cut the distal aspect of the lead (likely sharp and calcified) under direct visualization. Post-operative care appears unfortunately was already affected by the perioperative events and appears unremarkable.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
Hard to establish causation without knowing hemodynamic parameters during the events and the time extent of hypotension. There are also insufficient data in regards whether there was any cerebral monitoring during the procedure, timing of resuscitation, etc. Effective surgical repair was achieved. It appears less clear whether the strategy of attempting lead extraction, without direct control of the lead causing the injury, was proper.
What makes you a good expert for this case?
Cardiac surgical back for lead extraction is part of my practice.
How often do you encounter cases similar to this one in your practice?
I cover 2 of this cases every 4-6 weeks per year. Emergent repair of injury caused by lead extraction represents less than 1% of the cases.
Do you believe there might have been medical error?
I have read the provided material in detail several times and have familiarized myself with the case very well. Without summarizing the case again as has already been done above, I submit the following: The operative note details hypotension developing during the attempt to complete the removal of the RV ICD lead of a cardioverter defibrillator pacemaker that had been placed about 10 years ago. The lead removal was attempted with laser extraction. The lead seems to be about 10 years old with the last discharge about 10 years ago, and the patient being non pace maker dependent, based on the records and also the description of severe calcification on the leads as described, once they were removed. It is unclear if the lead was nonfunctioning and /or recalled or infected. The operative note describes placement of a bridge balloon in the SVC and innominate regions as usual and its position being marked and then withdrawn down to the IVC to be ready to deploy in case of an SVC laceration. Once the hypotension developed during the extraction attempt of the ICD lead, the bridge balloon was deployed but its unclear whether it was advanced back to the SVC-innominate region where usual ruptures would happen during extractions. The ICD lead in RV would not be expected to be in the IVC, so its unclear why there was a 1.5 cms laceration or tear in the antero-medial IVC and as to what was speculated as the cause of that IVC tear? The laser extractor would not have needed to be advanced into the IVC in an attempt to extract an RV lead. Once the patient's hemodynamics persisted to be poor with ongoing hypotension and hypoxemia, the patient was placed on cardiopulmonary bypass and the remaining lead extractions were completed, which then seem to have led to another site of bleeding at the SVC-innominate junction. That is not entirely unexpected, and was controlled. The period of time that the patient remained hypotensive and hypoxic is not detailed in the operative report but likely is a part of the anesthesia record. I substantial, that could explain the post-operative neurologic dysfunction. The total operative time on cardiopulmonary bypass is not readily discerned from the operative note hence it is hard to determine whether a prolonged pump run, and use of blood and plasma products added to the coagulopathy that further derailed a rocky post operative course in a patient with compromised left and right ventricular dysfunction. While post operative neurologic studies including a CT scan and subsequent MRI do not show any acute events, they do show chronic ischemic changes, and with the patients history of coronary artery disease and cardiomyopathy, it is possible and likely probable that the cerebral circulation was suboptimal at baseline at best and further exacerbated by poor cardiac output as gleaned from the moderate RV dysfunction and need for extensive hemodynamic support with inotropes and vasopressor agents.
Do you believe there might have been causation (i.e. the medical error resulted in an injury)?
Based on what I have read from the case, I can not determine a clear reason for the location of the tear in the IVC which is rarely ever the location of a tear during RV laser lead extraction. The Bridge Balloon is specifically designed to be used in the SVC at the junction close to the innominate vein to tamponade bleeding from an inadvertent tear while the patient is prepped for an emergent sternotomy. While the incidence of tears in SVC during lead extraction can be up to 1-3 % they are extremely rare in the IVC. There is no clear piece of document that leads to this conclusion but enough to speculate if the bridge balloon was inflated in the IVC instead of the SVC, or if the laser lead extractor travelled inadvertently to the IVC past the RV and tricuspid valve.
What makes you a good expert for this case?
I have experience with providing coverage for laser lead extractions and have had to salvage several patients who experienced hemorrhage during similar procedures (line placements) with lacerations of the SVC, innominate vein, common carotid artery, Right atrium and right ventricle, requiring emergent sternotomies and open repair.
How often do you encounter cases similar to this one in your practice?
Mishaps during wire manipulations of the central venous system are very common at our institution, both in the context of the EP lab and the several intensive care units where such procedures are routinely performed on a daily basis. we are a large tertiary care hospital.
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