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Abstract Summary: Neonatal sepsis is a clinical syndrome characterized by systemic signs of circulatory compromise caused by invasion of the blood stream by bacteria in the first four weeks of life. Cardiac dysfunction is a well-recognized complication of severe sepsis and septic shock is a major contributor to morbidity and mortality in patients with sepsis .The role of functional echocardiography in the neonatal intensive care unit for the evaluation of infant cardiovascular well-being has significantly expanded over the last 10 years. This study was conducted in NICU; Beni-Suef university Hospital. It included 75 neonates, 50 infected neonates (cases) and 25 apparently healthy neonates (acting as the control group). Cases and controls were subjected to full history taking, clinical and echocardiographic examination in addition to laboratory studies (CBC, CRP and blood culture). On clinical evaluation of the patients, Dyspnea and poor suckling were the commonest clinical presentation. Total leucocytic count (TLC) was not much informative for the diagnosis of neonatal sepsis (10% showed leukopenia and 18% showed leukocytosis) and thrombocytopenia was reported in 18%. C - reactive protein (CRP) was positive in 94% of the sepsis group ranging between 6 and 160 mg/dl (median =24 mg/dl). In our study mortality was 38% of affected cases, and coagulase negative staphylococci (CONS) were the most common organism. In our study, we found that candidal infection especially UTI shows increasing prevalence in cases of neonatal sepsis. Echocardiography is an essential part of modern neonatal intensive care. Its use should not be limited to cardiologists in the diagnosis and assessment of CHD but should be extended to the routine care of critically ill neonates. As with any investigative tool, echocardiography should be used in combination with clinical assessment and not as a replacement. In our study, it showed: Significant increase in pulmonary artery pressure in the septic neonates. This can be a complication of sepsis secondary to bacterial endotoxin causing pulmonary hypertension from several mechanisms, including the release of thromboxane, endothelin, and several cytokines. Sepsis also leads to hypothermia, acidosis, and hypoglycemia. This in turn lead to acute pulmonary vasoconstriction and increased pulmonary vascular resistance None of the other cardiac parameters had a significant difference between septic and non-septic neonates. We should follow up cases of neonatal sepsis by Echocardiography to assess systolic and diastolic functions in different stages of sepsis. |