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Case Report | Volume 7 Issue 1 (Jan - Jun, 2025) | Pages 39 - 43
Anaesthesia considerations: Active Prosthetic Valve Endocarditis with cardiogenic shock
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1
Cardiac Anesthesia resident, Asian Heart Institute and Research Centre, BKC
2
Senior Cardiac Anesthesia Consultant, Asian Heart Institute and Research Centre, BKC
3
Cardiac Anesthesia consultant, Asian Heart Institute and Research Centre, BKC
Under a Creative Commons license
Open Access
Received
Jan. 11, 2025
Revised
Jan. 30, 2025
Accepted
Feb. 13, 2025
Published
Feb. 23, 2025
Abstract

Prosthetic valve endocarditis (PVE) is an infection of the endocardial surface that occurs on parts of the prosthetic valve due to microbial infestation. It is the most severe form of IE with an incidence of 1 – 6% of patients with valve prosthesis (Delgado V et al, 2023). According to 2023 European Society of Cardiologists (ESC) guidelines for management of endocarditis early PVE (within 6 months of valve surgery) is class I indication of surgery with new valve replacement and complete debridement (Delgado V et al, 2023). Surgery is also an indication in patients presenting with cardiogenic shock and heart failure secondary to PVE. Despite early use of surgical approaches, the nature of redo procedures increase the rate of morbidity and mortality with an inhospital mortality rate of about 20 – 40% (Delgado V et al, 2023). According to the 2023 ESC statistics, eventhough surgery is the best treatment option for PVE, it is performed in only 70% of the indicated cases due to the complexities and extensive postoperative care associated with the same. This article presents management of a patient presenting with cardiogenic shock and heart failure secondary to prosthetic valve endocarditis.

INTRODUCTION

Prosthetic valve endocarditis (PVE) is an infection of the endocardial surface that occurs on parts of the prosthetic valve due to microbial infestation. It is one of the most dreaded and lethal complication of valve replacement. It occurs in 1-6% of patients with valve prosthesis, with an incidence of 0.3 – 1.2% per patient per year (Delgado V et al, 2023) and accounts for 20% of all infective endocarditis (Glaser N et al, 2017). A higher risk of PVE is reported in patients with biological compared with mechanical valves (Glaser N et al, 2017). Patients with PVE present with symptoms similar to other types of infectious endocarditis (IE), including fever and chills, shortness of breath, pleuritic chest pains, anorexia, and weight loss (Khalil H et al, 2022). The medical management involves maximum non-toxic dose of empirical higher antibiotic therapy for atleast 6 weeks. However, a surgical intervention is indicated in case patient develops heart failure, severe prosthetic valve dysfunction, intracardiac fistula, presence of bacteremia even after appropriate antibiotic regime, development of abscess or fungal/highly resistant bacterial organism causing PVE. Despite the appropriate diagnosis and use of surgical treatment in PVE, morbidity and mortality remain high (Khalil H et al, 2022). Redo surgeries in addition to PVE with cardiogenic shock greatly increase the perioperative morbidity and mortality. Age, CPB time, IABP use, postoperative cerebrovascular accident and MREDO are identified as independent risk factors for 30-day mortality post redo cardiac surgeries (Norton EL et al, 2023).

PVE carries the highest mortality rates compared to other types of IE (Khalil H et al, 2022). Hence, multidisciplinary action with interdepartmental coordination is required to successfully manage such a case.

This case report describes successful anaesthetic, surgical and intensive care management of prosthetic aortic valve endocarditis requiring redo aortic valve replacement with a preoperative Euroscorell of 76.73%.

 

CASE REPORT

A 51year old, male (height: 185cms, weight: 100kgs), known case of rheumatic heart disease and bicuspid aortic valve underwent bioprosthetic aortic valve replacement with aortic root replacement 2 years back, presented with multiple episodes of highgrade fever in past 2 months, which were insidious in onset and relieved with antibiotics prescribed by family physician.About 3 weeks back he developed breathlessness of NYHA grade III, associated with orthopnea and feeling of chest tightness for which he was taken to nearby hospital. He was diagnosed with heart failure associated with prosthetic valve endocarditis and acute kidney injury and was medically managed for the same. However, the patient condition deteriorated and he was transferred via cardiac ambulance to our institute for further evaluation and management. On examination his heart rate was 80/min and regular, blood pressure was 80/60 mm Hg, saturation of 100% on room air, bilateral pedal edema and crepitations were present in bilateral lung fields. He also gave history of undergoing dental procedure 6 months back without an adequate antibiotic cover which was thought to be the cause for PVE. The inotrope and vasopressor support wasescalated and intraaortic balloon pump (IABP) was inserted percutaneously via right femoral artery to maintain hemodynamics. Bedside 2D Echocardiography showed an echogenic structure of 18mm X 20mm moving to and fro and was attached to aortic valve, suggestive of aortic valve vegetation; severe Aortic stenosis with max/mean gradient of 82/46 mm Hg; Aortic annulus of 0.5cm2; severe Left Ventricle systolic dysfunction with ejection fraction of 20% and global LV hypokinesia. Based on the given scenario it was decided to post the patient for Redo Prosthetic Aortic Valve replacement with aortoplasty after preoperative optimization. The left radial artery and right internal jugular central venous access was secured in ICU. Foleys catheter was inserted and hourly urine output was noted. Preoperative blood investigations stated hemoglobin 10.8gm%, serum creatinine 3.1mg/dL, blood urea nitrogen 44mg/dL, INR 1.7 and serum potassium 3.9mEq/L. Four units of fresh frozen plasma was transfused a day prior to surgery in view of deranged INR. On the day of surgery, patient was shifted from ICU to operation theatre with hemodynamic monitoring and IABP support with arterial blood pressure of 90/56 mm Hg at 1:1 IABP support and augmentation of 106 along with infusion Inj. Noradrenaline @ 0.13 mcg/kg/min and Inj. Vasopressin 0.08 units/min. The standard ASA monitors including ECG, saturation probe were applied. Left radial artery cannula was transduced to determine invasive arterial pressure. He was induced with Inj. Etomidate and Inj. Rocuronium.Pulmonary artery catheter with CCO-SvO2 monitoring was inserted via a 8.5Fr sheath through right internal jugular venous access. Pre procedure baseline cardiac index was 1.2ml/min/m2, cardiac output 2.9L/min and opening Pulmonary artery pressure was 65/42 mm Hg. Transesophageal echocardiography was also used intraoperatively and findings were confirmed (fig 1 and 2). Balanced anaesthesia was maintained with Isoflurane, Inj. Atracurium infusion and Inj. Midazolam + Buprenorphine infusion. Inotrope and vasopressor infusions of Inj. Noradrenaline, Vasopressin and Dopamine were titrated to maintain a mean arterial pressure of more than 65mmHg. Right Innominate artery using a 10mm graft and right atrium was used for arterial and 29Fr three stage single venous cannulation respectively. LV vent was inserted in the right superior pulmonary vein and a retrograde cardioplegia cannula was inserted in coronary sinus. Cannulation was done after heparinization with 4mg/kg of intravenous Heparin and ACT of 511seconds. Del Neido cardiolplegia solution was used to arrest the heart and start cardioplulmonary bypass and it was repeated every 45 minutes. The prosthetic aortic valve sutures were cut and it was removed along with the vegetation. The annular tissue was scooped and debrided. After a thorough wash the instrument set and trolley were changed. A new tissue bioprosthetic valve of 25 mm was inserted and ascending aortoplasty was done. On pump the ACT was maintained above 500 seconds. Hemofilter was used for hemoconcentration and ultrafilterationduring CPB. Aortotomy was closed and after a hot shot of warm cardioplegia and adequate deairing the arortic cross clamp was removed. The total cross clamp time was 2 hours 30 minutes. After a reperfusion time of 45 minutes the patient was gradually weaned off bypass. The total cardiopulmonary bypass time was 4 hours 9 minutes. Decannulation was done and adequate hemostasis was achieved after an adequate dose of Inj.Protamine for heparin reversal and to achieve and ACT of 138seconds post bypass. Post procedure Transeesophageal study showed no paravalvular leak and a maximum/mean gradient of 6.6/3.3 mm Hg across the neo aortic valve (Fig 3). The CCO-SvO2 monitor showed an improved cardiac output of 6.3L/min and cardiac index of 3.1 ml/min/m2(Fig 4) with high dose inotrope and intraaortic balloon pump. Massive blood transfusion including 3150ml of PRBC, 1600ml of fresh frozen plasma and 300ml of cryoprecipitate were transfused intraoperatively. A right ventricular epicardial pacing wire and two pericardial drains were inserted prior to sternum closure. Post procedure patient was shifted to surgical intensive care sedated, intubated and on maximum augmentation of intraaortic balloon pump, Inj Noradrenaline at 0.13mcg/kg/hrinfusion, Inj. Dopamineat 0.06mcg/kg/min infusion, Inj. Vasopressin at0.08 units/minand Inj. Adrenalineat 0.05mcg/kg/min infusion to maintain a mean arterial pressure of 65 to 80 mm Hg.

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