Neonates Have Risk Factors or Manifestations of Sepsis Clinical Trial
Official title:
An Audit Study on Management of Neonates With Neonatal Sepsis Admitted to Asyut University Children Hospital
The present study aims to evaluate management of neonates with neonatal sepsis admitted to
the Neonatology Unit, Assiut University Children Hospital according to the guidelines of the
American Academy of Pediatrics, 2018,[25] searching for defects, obstacles, or needs to
improve the management of such cases.
We consider that this critical appraisal of our own performance, is a crucial step before any
further corrections or developments of that performance could take place.
Definition:
Neonatal sepsis is a systemic response to infection documented by positive blood culture in
the first month of life. [1]
Classification:
It may be categorized as early-onset or late-onset.
Early-onset sepsis is associated with acquisition of microorganisms from the mother.
Transplacental infection or an ascending infection from the cervix may be caused by organisms
that colonize the mother's genitourinary (GU) tract; the neonate acquires the microorganisms
as it passes through the colonized birth canal at delivery. Of newborns with early-onset
sepsis, 85% present within 24 hours, 5% present at 24-48 hours, and a smaller percentage
present within 48-72 hours. Onset is most rapid in premature neonates. [2]
Late-onset sepsis occurs after 3 days of life and is acquired from the caregiving
environment.[3] Pathophysiology:[10] Neonates are particularly vulnerable to infection as a
result of lower non-specific immunity (inflammation) and specific (humeral), such as low
phagocytosis, chemotaxis response delay, minimal or absence of immunoglobulin A and
immunoglobulin M (IgA and IgM), and low levels of complement.
Sepsis in the neonatal period can be obtained before birth through the placenta from the
maternal blood stream or during labor for ingestion or aspiration of infected amniotic fluid.
Sepsis early (less than 3 days) obtained in the perinatal period, infection can occur from
direct contact with the organism from the gastrointestinal or genitourinary tract maternal.
The most frequent infecting organism is group B streptococcus (GBS) and Escherichia coli,
which is present in the vagina. GBS emerged as a highly virulent microorganisms in the
neonate, with a high mortality rate (50%) in infants exposed to Haemophilus influenzae and
Staphylococcus negative coagulation are also often seen in early-onset sepsis in infants with
very low birth weight.
Advanced Sepsis (1 to 3 weeks after birth) primarily nosocomial, and organisms that attack is
usually staphylococci, Klebsiella, enterococcus and pseudomonas. Coagulation negative
staphylococci, commonly found as the cause of septicemia in infants of low birth weight and
very low birth weight. Bacterial invasion can occur through such Gated umbilical stump, skin,
mucous membranes of eyes, nose, pharynx, and ear, and internal systems such as the
respiratory system, nervous, urinary, and gastrointestinal.
Postnatal infection, derived from cross-contamination with other babies, personnel, or
objects in the environment. Bacteria commonly found in water sources, a humidifier, sink
pipes, suction machines, most equipment respiration, and arterial and venous catheters
inserted used for infusion, blood sampling, monitoring of vital signs.
The process begins with the invasion of the pathophysiology of bacterial sepsis and systemic
contamination. The release of endotoxin by bacteria cause changes in the function of the
myocardium, changes in uptake and utilization of oxygen inhibition of mitochondrial function,
and progressive metabolic chaos. In sepsis sudden and severe, complemen cascade caused much
death and damage cells. The result is a decrease in tissue perfusion, metabolic acidosis, and
shock, disseminated intravascular coagulation resulting (DIC) and death.[11]
Patients with immune disorders have an increased risk for serious nosocomial sepsis.
Cardiopulmonary manifestations of gram-negative sepsis can be replicated by injection of
endotoxin or Tumor Necrosis Factor (TNF). Barriers to employment TNF by anti-TNF monoclonal
antibody greatly weakens manifestation of septic shock. When the bacterialcell wall
components are released in the bloodstream, cytokine-activated, and can further lead to more
physiological mess. Either alone or in combination, bacterial products and pro-inflammatory
cytokines trigger a physiological response to stop the invaders (invader) microbes. TNF and
other inflammatory mediators increase vascular permeability and vascular tone imbalance, and
the imbalance between perfusion and increased metabolic needs of the network.[12]
Shock is defined as a systolic pressure below the 5th percentile for age or defined with cold
extremities. Capillary refilling the late (more than 2 seconds) is seen as a reliable
indicator of a decrease in peripheral perfusion. Peripheral vascular pressure in septic shock
(heat) but be very up on a further shock (cold). In septic shock tissue oxygen consumption
exceeds oxygen supply. This imbalance is caused by peripheral vasodilatation in the
beginning, during further vasoconstriction, myocardial depression, hypotension, ventilator
insufficiency, and anemia.[13]
Septicemia shows the emergence of a systemic infection of the blood caused by the rapid
multiplication of microorganisms or toxic substances, which can cause huge psychological
change. These substances can be pathogenic bacteria, fungi, viruses, and rickets. The most
common cause of septicemia is a gram-negative organisms. If the protection of the body is not
effective in controlling the invasion of microorganisms, septic shock may occur, which is
characterized by hemodynamic changes, imbalance of cellular functions, and multiple system
failures.
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