NEC Sepsis (Final 4) PDF

PROBLEMS RELATED TO INFECTIOUS PROCESS NEC SEPSIS Necrotizing - enterocolitis NEC  DEFINITION NEC is an acute inflammatory disease of the bowel with increased incidence in preterm and other high-risk infants; it is most common in preterm infant...

PROBLEMS RELATED TO INFECTIOUS PROCESS NEC SEPSIS Necrotizing - enterocolitis NEC  DEFINITION NEC is an acute inflammatory disease of the bowel with increased incidence in preterm and other high-risk infants; it is most common in preterm infants  PATHOPHYSIOLOGY The precise cause of NEC is still uncertain, but it appears to occur in infants whose GI tract has suffered vascular compromise. Contributory factors for NEC include the following: intestional immaturity, such as gastrointestional dysmotility; impaired digestive capacity; altered regulation of intestinal blood blow; barrier dysfunction; altered antiinflammatory control; and impaired host defense. Frequent use of antibiotic therapy and antiacid medications, followed by enteral feeding, are believed to increase the risk of NEC. Prematurity remains the greatest risk factor in this disease  NECROTIZING ENTEROCOLITIS Bacterial Proliferation Immature GI host defense Feeding Substrate Intestinal ischemia Damage of GI mucosal cell lining ↓ Mucosal cells edema &ulceration ↓ Death of these cells Unable to synthesize Stop secreting protective Protective IGM mucus ↓ Unprotected thin bowel wall is attacked by proteolytic enzymes ↓ Mucosa is permeable to macromolecules(eg. Exotoxines) ↓ Gas forming bacteria invade the damaged area to produce peumatosis Intestinalis  Clinical Manifestations The prominent clinical signs of NEC are a distended abdomen, gastric residuals, and blood in the stools. Because NEC closely resembles septicemia, the infant may “not look well.” Nonspecific signs include lethargy, poor feeding, hypotension, apnea, vomiting (often bile-stained), decreased urinary output, and hypothermia. The onset is usually between 4 and 10 days after the initiation of feedings, but signs may be evident as early as 4 hours of age and as late as 30 days. NEC in full-term infants almost always occurs in the first 10 days of life. The early clinical signs of NEC are subtle and nonspecific and may often be overlooked for other conditions; the earliest clinical signs include lethargy, abdominal distention, and high gastric residuals. Late-onset NEC is confined primarily to preterm infants and coincides with the onset of feedings after they have passed through the acute phase of an illness such as RDS.  Diagnostic Evaluation 1. ABD XR: Radiographic studies show a sausage-shaped dilation of the intestine that progresses to marked distention and the characteristic intestinal pneumatosis— “soapsuds,” or the bubbly appearance of thickened bowel wall and ultralumina. Air may be present in the portal circulation or free air observed in the abdomen, indicating perforation. 2. Laboratory findings may include anemia, leukopenia, leukocytosis, metabolic acidosis, and electrolyte imbalance. In severe cases, coagulopathy (disseminated intravascular coagulation) or thrombocytopenia may be evident. 3.Blood culture: Organisms may be cultured from blood, although bacteremia or septicemia may not be prominent early in the course of the disease.  Therapeutic Management Treatment of NEC begins with prevention. : 1.Oral feedings may be withheld for 24 to 48 hours from infants who are believed to have suffered birth asphyxia. 2.Breast milk is the preferred enteral nutrient because it confers some passive immunity (IgA), macrophages, and lysozymes. There is evidence that human milk may have a protective effect against the development of NEC. 3. Minimal enteral feedings (trophic feeding, GI priming) in VLBW infants have gained acceptance. Some studies have shown that such feedings may be protective against NEC in nonasphyxiated preterm infants. 4. The administration of maternal antenatal steroids may prevent NEC in some infants by promoting early gut closure and maturation of the gut barrier mucosa.  …….prevention…. 5.oral probiotics effectively prevent NEC when given within the first 7 days and continued for 14 days in preterm infants (≤34 weeks of gestation) and/or those of a birth weight ≤1500 g 6. Lactoferrin, the major whey protein in human milk, in combination with lysozyme, which is also found in human milk, may have a significant role in the prevention of NEC and neonatal sepsis in high- risk preterm infants; both act in the intestine to kill harmful bacteria and enhance intestinal immune properties  Medical treatment of confirmed NEC consists OF *** With early recognition and treatment, medical management is increasingly successful) 1)discontinuation of all oral feedings; 2) institution of abdominal decompression via nasogastric suction; NGT FD 3) administration of IV antibiotics; and 4) correction of extravascular volume depletion, electrolyte abnormalities, acid-base imbalances, and hypoxia. 5) Replacing oral feedings with parenteral fluids decreases the need for oxygen and circulation to the bowel. 6)Serial abdominal radiograph films (every 4 to 6 hours in the acute phase) are taken to monitor for possible progression of the disease to intestinal perforation. 7) If there is progressive deterioration under medical management or evidence of perforation, surgical resection and anastomosis are performed.  Extensive involvement may necessitate surgical intervention and establishment of an ileostomy, jejunostomy, or colostomy.  Sequelae in surviving infants short-bowel syndrome colonic stricture with obstruction fat malabsorption failure to thrive secondary to intestinal dysfunction.  Nursing Care Management Astute nursing care is a key factor in the prompt recognition of the early warning signs of NEC. When the disease is suspected, the nurse assists with diagnostic procedures and implements the therapeutic regimen. Vital signs, including blood pressure, are monitored for changes that might indicate bowel perforation, septicemia, or cardiovascular shock. Measures are instituted to prevent possible transmission to other infants. ENTERIC PRECAUTIONS It is especially important to avoid rectal temperatures because of the increased danger of perforation. To avoid pressure on the distended abdomen and to facilitate continuous observation, infants are often left undiapered and positioned supine or on the side.  NSG……… Conscientious attention to nutrition and hydration needs is essential antibiotics are administered as prescribed. The time at which oral feedings are reinstituted varies considerably but is usually at least 7 to 10 days after diagnosis and treatment. Because NEC is an infectious disease, one of the most important nursing functions is control of infection. Strict hand washing is the primary barrier to spread, and confirmed multiple cases are isolated. COHORT Persons with symptoms of a GI infection should not care for these or any other infants.  NSG……… The infant undergoing surgery requires the same careful attention and observation as any infant with abdominal surgery, including ostomy care (as applicable). the nurse is continually alert for signs of complications, such as: 1. septicemia, 2. disseminated intravascular coagulation, 3. hypoglycemia, and 4. other metabolic derangements eg met.acidosis  NURSING ALERT Observe for indications of early development of NEC by : 1. checking the abdomen frequently for distention (measuring abdominal girth, measuring residual gastric contents before feedings, and listening for the presence of bowel sounds) and 2. performing all routine assessments for high-risk neonates.  SEPSIS SEPTICEMIA  Sepsis, or septicemia refers to a generalized bacterial infection in the bloodstream. Neonates are highly susceptible to infection because of diminished: 1. nonspecific (inflammatory) 2. specific (humoral) immunity, such as impaired phagocytosis, delayed chemotactic response, minimum or absent IgA and immunoglobulin M (IgM), and decreased complement levels. Because of the infant’s poor response to pathogenic agents: 1. there is usually no local inflammatory reaction at the portal of entry to signal an infection 2. the resulting symptoms tend to be vague and nonspecific. →→→Consequently, diagnosis and treatment may be delayed  RISK FACTORS 1. high-risk infant has a four-times greater chance of developing septicemia than does the normal neonate. 2. The frequency of infection is almost twice as great in male infants as in females and also carries a higher mortality for males. 3. Other risk factors are prematurity, congenital anomalies or acquired injuries that disrupt the skin or mucous membranes, 4. invasive procedures such as placement of IV lines and ET tubes, 5. administration of total parenteral nutrition, and 6. nosocomial exposure to pathogens in the NICU..  PREVENTION 1. Thorough hand washing is the single most important infection control measure in the NICU. 2. Proper handling of formula and supplies such as syringes and gavage tubes is also vital to prevent infection. 3. Breastfeeding has a protective effect against infection and should be promoted for all newborns. It is of particular benefit to the high-risk neonate : a. Colostrum contains agglutinins that are effective against gram-negative bacteria. b. Human milk contains large quantities of IgA and iron-binding protein that exert a bacteriostatic effect on Escherichia coli. c. Human milk also contains macrophages and lymphocytes that promote a local inflammatory reaction  Pathophysiology The premature withdrawal of the placental barrier leaves infants vulnerable to most common viral, bacterial, fungal, and parasitic infections.  Immune substances, primarily immunoglobulin G (IgG), are normally acquired from the maternal system and stored in fetal tissues during the final weeks of gestation to provide newborns with passive immunity to a variety of infectious agents. Early birth interrupts this transplacental transmission; thus preterm infants have a low level of circulating IgG. The concentrations of immune substances directly relate to the length of gestation.  IgA, which plays a role in defense against viral infections, and IgM, with properties that are most efficient in dealing with gram negative organisms, are not transferred to the fetus, leaving the infant highly vulnerable to invasion by these organisms.  ,,,,,,,,,,,,  Defense mechanisms of neonates are further hampered by a low level of complement, diminished opsonization ability, monocyte dysfunction, and a reduced number and inefficient function of circulating leukocytes.  Furthermore, leukocytes with diminished motility and phagocytic capacity are unable to concentrate their limited numbers selectively at the site of infection.  In addition, a hypofunctioning adrenal gland contributes only a meager antiinflammatory response. These deficiencies permit rapid invasion, spread, and multiplication of organisms.  An immature gut mucosal barrier further predisposes the preterm infant to bacteria, which may easily cross the mucosa into the bloodstream.  Sources of Infection Sepsis in the neonatal period can be acquired: 1. prenatally across the placenta from the maternal bloodstream 2. or during labor from ingestion or aspiration of infected amniotic fluid. 3. Prolonged rupture of the membranes always presents a risk for maternal-fetal transfer of pathogenic organisms. In utero transplacental transfer can occur with a variety of organisms and viruses such as cytomegalovirus, toxoplasmosis, and Treponema pallidum (syphilis), which cross the placental barrier during the latter half of pregnancy  Early-onset sepsis (EOS)  (