Introduction

Left Ventricular Assist Devices (LVADs) were initially developed as bridge therapy until transplantation but are now increasingly used as destination therapy for patients who are unable to undergo transplantation (1-4). As the number of patients receiving LVADs for destination therapy rises, general anesthesiologists are likely to encounter these complex cases more frequently, particularly in the context of non-cardiac surgeries (1-4). This case report discusses the perioperative management of an LVAD-dependent patient with acromegaly undergoing transsphenoidal resection of a pituitary macroadenoma.

Preoperative Assessment

Our patient, a 68-year-old male with acromegaly, was scheduled for pituitary adenoma resection. His medical history included non-ischemic dilated cardiomyopathy, which necessitated the implantation of an AICD/Pacemaker and HeartMate II LVAD, as well as suture closure of the aortic valve (AV) due to moderate aortic regurgitation (AR) five years ago. Other relevant medical conditions included hypertension (HTN), a smoking history of 42 pack-years, chronic obstructive pulmonary disease (COPD), obstructive sleep apnea (OSA) managed with continuous positive airway pressure (CPAP), type 2 diabetes, secondary adrenal insufficiency, secondary hypothyroidism, and a pituitary macroadenoma (GH-secreting) with acromegaly.

Notably, after starting treatment for acromegaly with lanreotide, the patient’s ejection fraction improved to 65%. However, the LVAD could not be explanted due to the suture closure of the aortic valve. The patient was scheduled for transsphenoidal resection of the pituitary macroadenoma as a potential means to discontinue the costly acromegaly medications.

Home medications included carvedilol, lisinopril, spironolactone, hydrocortisone, lanreotide, cabergoline, levothyroxine, and warfarin. A preoperative CT scan revealed a sellar mass encasing the left and right internal carotid arteries. The patient was evaluated in the cardiology clinic, where a plan was made to stop warfarin and bridge with a heparin drip as an inpatient three days prior to surgery, aiming for a normal INR.

Preoperative transthoracic echocardiography showed normal left ventricular inflow and outflow, an ejection fraction of 60-65%, mild dilation of the right and left ventricles, mild mitral and tricuspid regurgitation, and a pulmonary artery systolic pressure of 22 mmHg. On the morning of surgery, the complete blood count (CBC) and basic metabolic profile (BMP) were unremarkable. Although his coagulation profile was not available before induction, since warfarin had been stopped three days prior and his last INR before discontinuation was 1.9, we proceeded without waiting for the morning lab report.

During preoperative evaluation, the patient endorsed greater than 4 METs. The airway examination revealed a Mallampati grade III airway with limited mouth opening, a short/thick neck, and macroglossia.

Intraoperative Management

In the operating room, standard ASA monitors were placed, along with a pre-induction arterial line. General anesthesia was induced with propofol, ketamine, lidocaine, fentanyl, and rocuronium. Intubation with a video laryngoscope revealed a large, floppy epiglottis but intubation was successful on the first attempt.

The AICD/Pacemaker was reprogrammed to asynchronous mode at 80 BPM, as the patient was 50% pacer-dependent, and the defibrillator function was deactivated. Defibrillation pads were placed on the patient.

An LVAD coordinator was present in the operating room to monitor LVAD settings. Mean arterial pressure (MAP) was maintained between 60 and 80 mmHg using a low-dose phenylephrine infusion. Balanced anesthesia was maintained with sevoflurane and infusions of remifentanil, ketamine, and dexmedetomidine. Paralysis was maintained with rocuronium.

The patient was closely monitored for the development of Diabetes Insipidus (DI), and stress dose steroids were administered. Intravenous magnesium and acetaminophen were provided as part of multimodal pain control. The Neurosurgery team reported difficulty achieving hemostasis. The INR sent on the morning of surgery had come back as 2.1.  To help with hemostasis, Desmopressin 0.3 mcg/kg and 2 units of FFP were administered. The surgery was otherwise uncomplicated, with an estimated blood loss (EBL) of 400 mL. The patient was smoothly extubated while on remifentanil infusion. The postoperative course was uneventful, and he was discharged home after four days.

Case Discussion

Preoperative Management

LVAD patients scheduled for elective surgery, thorough preoperative evaluation and optimization should address any coexisting end-organ dysfunction, medications, anticoagulation status, and right ventricular dysfunction. Ideally, these patients should undergo noncardiac surgery at centers with personnel familiar with LVADs (1-4), including cardiac surgeons, LVAD nurses, and perfusionists.

Hemodynamic Considerations

Key monitored variables for the LVAD include speed (RPM), power (watts), flow (L/min), and pulsatility index (PI). Blood flow through the LVAD is primarily determined by the pump’s speed, with higher RPMs generating increased flow. Higher speeds increase power and flow but reduce pulsatility. While pump flow is a useful metric, it can vary by up to 20% from actual cardiac output, especially with native circulation through the aortic valve (AV). Pump flow should be used as a trend only. Pulsatility can vary with changes in the physiological environment and is inversely related to the extent of volume offloading by the LVAD from the native ventricle. A significant increase in pulsatility may indicate volume overload in the LV. As pump speed and flow increase, pulsatility decreases, which can elevate the risk of AV thrombosis, aortic regurgitation (AR), and arteriovenous malformations (AVMs). Increased power usage at stable RPMs may indicate pump thrombosis (1-4).

LVAD function is closely linked to cardiac hemodynamics. The pump flow adjusts with hemodynamic changes throughout each cardiac cycle, affecting pump power, pulsatility index, and flow. Effective management requires understanding these variables and their impacts. Volume status and right ventricular (RV) function significantly affect LVAD flow and, consequently, cardiac output. Patients with concurrent right ventricular failure might require pulmonary vasodilators or ionotropic support to improve RV stroke volume. Additionally, afterload plays a crucial role in LVAD function, as it directly affects LVAD flow. Increased systemic vascular resistance can adversely impact the device’s output (1-4).

Intraoperative goals include ensuring adequate preload, maintaining afterload, avoiding abrupt changes in systemic vascular resistance (SVR), and preventing iatrogenic right ventricular (RV) strain (5-6).  In our patient, moderate AR reduced LVAD efficacy, necessitating AV closure to prevent backflow but making the patient entirely dependent on the LVAD for cardiac output.

These patients may have a palpable pulse, no pulse, or a weak and intermittently palpable pulse depending on the pump speed, native left ventricular function, and left ventricular preload. The lack of pulsatility seen with LVAD patients can complicate monitoring of pulse oximetry and non-invasive blood pressure (NIBP), which depend on pulsatile flow. If blood pressure cannot be obtained via Doppler ultrasound or manual measurements, invasive hemodynamic monitoring via an arterial line should be considered (3, 5-6).

Attention must be given to the device’s electrical power requirements, including battery backup during transport. Careful placement of the grounding pad from the electrosurgical unit is essential to ensure that the electrical current does not pass through the LVAD. Many patients also have automated internal cardioverter-defibrillators, which should be deactivated during surgery to prevent interference with the electrocautery unit; external defibrillator pads should be applied instead. Strict aseptic techniques must be observed for all invasive procedures, and antibiotic prophylaxis should be administered perioperatively (3,5,6).

Management of Anticoagulation

LVAD patients are usually anticoagulated with warfarin and aspirin, with a goal INR of 2.0 – 3.0 (7). Hemorrhagic events are ten times more common than thrombotic events. LVAD patients are thought to develop an acquired type 2A von Willebrand disease due to the high-shear environment created by the LVAD. (8) There is limited literature regarding LVAD patients undergoing neurosurgical procedures, which tend to have a higher risk of hemorrhagic complications. The most common neurosurgical procedure performed on LVAD patients is emergency evacuation of intracranial hemorrhage, which often has a poor outcome (3). Intracranial hemorrhage has been reported to occur in up to 23% of patients with LVADs (9). Perioperative anticoagulation should be personalized to each patient’s risk factors for hemorrhage versus thrombosis. Chronic anticoagulation is required due to the risk of thrombus in the pump motor, and reversal for surgery must be done cautiously (10). In one review of 405 LVAD patients, intracranial hemorrhage (ICH) occurred in 10% (11). Of the patients who received antithrombotic reversal, 30% had inadequate reversal, and 4% had thrombotic complications, such as deep vein thrombosis.

For elective surgeries, patients can be bridged from warfarin to intravenous heparin preoperatively. In emergent situations, FFP can be used to reverse the effect of warfarin; however, complete reversal of anticoagulation should not be the goal (3-6). Previous case studies have confirmed the rarity of LVAD failure despite correction of anticoagulation.

Anesthetic Considerations for Acromegaly and Transsphenoidal Pituitary Resection

Patients with acromegaly are at increased risk of difficult airway, hypertension, cardiomyopathy, atherosclerosis, obstructive sleep apnea (OSA), sodium dysregulation, and insulin resistance. Endoscopic transsphenoidal pituitary resections carry a high risk of Diabetes Insipidus (DI) and bleeding, which can affect preload (12). Intraoperative CSF leak has been identified as a risk factor for developing long-term postoperative DI.

Airway management can be challenging in these patients due to macroglossia, prognathic jaws, excess soft tissue, and small glottic openings (13-14). Preoperative assessment and preparation should include a detailed airway evaluation and readiness for a difficult airway. Although these patients are at increased risk for OSA, non-invasive positive pressure ventilation is avoided to prevent disruption of surgical closure and to minimize the risk of disturbing the skull base repair (15).

Minimizing opioid use through multimodal pain management and prophylaxis for postoperative nausea and vomiting is crucial (17). Emergence and extubation should be smooth to reduce the risk of bleeding, pneumocephalus, and CSF leak. Remifentanil has been shown to suppress the cough reflex during emergence (16).

Conclusion

Anesthetizing patients with LVADs can be challenging; however, with meticulous preparation, monitoring, and vigilance, these patients can safely undergo complex neurosurgical procedures.

 

Figure 1: Internal mechanism of The HeartMate II: an axial-flow CF LVAD propels blood parallel to the axis of rotation of the rotor (Chung et al).

References

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