Pediatrics & Therapeutics
Open Access

Impact of Hepatopathy after Heart Surgery in Pediatrics

Nancy Smith Searle^{* *}Correspondence: Nancy Smith Searle, Department of Pediatrics, Baylor College of Medicine, Houston, USA, Email:

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Description

The majority of congenital defects, 1% of all live infants have Congenital Heart Disease (CHD), which is the most prevalent (excluding bicuspid aortic valve disease). With Grown-Up Congenital Heart (GUCH) patients now outnumbering children with CHD in terms of overall survival, CHD patients have experienced a tremendous improvement in recent decades. The vastly increased chances of survival as a result of novel surgical methods, hybrid approaches, catheter procedures, and improvements in the management of intensive care units have drawn attention to and research on potential issues with the treatment of CHD patients. Patients with complicated CHD anomalies, and in particular those who require significant heart surgery in infancy, are still at high risk for higher postoperative morbidity and mortality rates.

The risk for secondary organ dysfunction can be triggered by postoperative decreased cardiac output, which can impact up to 25% of newborns and young infants after cardiac surgery, as well as the accompanying Systemic Inflammatory Response Syndrome (SIRS) after Cardiopulmonary Bypass (CPB) surgery. There are numerous descriptions of neurological dysfunction and mental retardation in CHD patients. It is also well described how renal failure necessitates temporary dialysis (either peritoneal dialysis or hemofiltration) to support and enhance postoperative renal function. The liver is susceptible to perioperative acute and chronic problems, possibly more than is typical given its lack of focus over a prolonged period of time. It is well known that liver dysfunction occurs when the Fontan circulation fails. Hepatic dysfunction is likely caused by a number of different factors. It can be the outcome of tissue hypoxemia brought on by congested central veins and poor cardiac output. These mechanisms work in both chronic and sudden cardiac failure. In addition, Secondary Sclerosing Cholangitis (SSC), which was recently discovered following cardiothoracic surgery and was originally noticed in critically ill patients with burns or polytrauma, is characterised by biliary obstruction, cholestasis, and bile duct necrosis that progresses quickly to cirrhosis. The biliary epithelium is substantially more sensitive to ischemia than hepatocytes with a dual blood supply, making it a potential primary pathomechanism of SSC. This is due to the prolonged postoperative low cardiac output that prevents adequate oxygen delivery to this tissue.

Cardiac hepatopathy was characterised as persistent postoperative cholestasis with an increase in specific laboratory cholestasis parameters (bilirubin, gamma-Glutamyltransferase (gGT)), impaired liver synthesis (reduced production of albumin and/or coagulation factors), with or without changes in the liver's sonography and histopathology in the course of the postoperative course. The STS-EACTS mortality categories (1–5) were used to calculate the surgical risk associated with the individual heart abnormalities and the planned surgical technique for them. Repeated evaluations of the right ventricle's performance utilizing the Tricuspid Annular Plane Systolic Excursion (TAPSE) on serial postoperative echocardiography were used to establish right heart dysfunction. Right heart dysfunction that appeared within the first seven days following the index procedure was divided into four stages: 0, 1, 2, and 3 correspond to mild, moderate, and severe right heart dysfunction, respectively. Repeated measures of the left ventricle's function were made on serial postoperative echocardiography utilizing the Fractional Shortening (FS), Simpson uni/biplane approaches, and Mitral Annular Plane Systolic Excursion (MAPSE) techniques. Repeated echocardiograms were used to monitor and manage left ventricular function in the event that the postoperative acoustic window was insufficient. In line with the classification of right heart dysfunction, the left heart dysfunction was likewise divided into four stages: 0—no, 1—mild, 2—moderate, and 3—severe. The necessity for medical and mechanical circulation support in the postoperative period was divided into four stages according to the degree of postoperative hypotension: 0—no, 1—mild, 2 — moderate, and 3—severe postoperative hypotension. The continuous infusion of inotropes (epinephrine, norepinephrine, and milrinone) throughout a 24-hour period postoperatively was referred to as their usage. Erythrocytes, fresh frozen plasma, and thrombocytes were administered during the entire perioperative course (during the intraoperative period and the full postoperative Intensive Care Unit (ICU) stay). The most significant postoperative side effects, such as pleural effusion, chylothorax, or arrhythmias, were examined. Pleural effusion, chylothorax, diaphragmatic paresis, and thrombosis were categorized as procedure-related variables, and arrhythmias needing permanent or temporary therapy (cooling and/or amiodarone medication, a transient or permanent pacemaker) were compiled. The treatment of an anatomical residue following the index surgery that is necessary in the postoperative course and prevents normal recompensation and recovery was classified as an unscheduled re-operation or re-intervention.

A postoperative infection was defined as a worsening of the clinical condition along with an increase in laboratory markers of inflammation (leukocytosis with or without (w/-) neutrophilia along with an increase in procalcitonin and an increase in Creactive protein), in addition to blood or wound cultures that were positive for pathogens and the requirement for escalating the antibiotic therapy (using broad-spectrum antibiotics). Total parenteral nutrition was described as the administration of nutrients (carbohydrates, proteins, and lipids) mostly intravenously more than 24 hours after surgery.