Tuesday, June 4, 2019
Survival Outcome Neonates Early Sepsis Health And Social Care Essay
Survival Outcome Neonates Early Sepsis Health And Social C be EssayA Retrospective Comparative Study on the Survival Outcome of Neoates with Early - oncoming Sepsis with Sclerema Given Fresh Frozen Plasma at Davao aesculapian Centern Nursery-A One course of instruction ReviewObjectives To determine and compargon the option outcome of patients with earlier onset neonatal sepsis with sclerema given tonic fixed plasma plus threadbare therapy of neonatal sepsis to those who were just given standard therapy alone. Fresh Frozen plasma contains immunologic instruments which is insufficient in a neonate. This study would help us validate the government agency of FFP transfusion in a sick neonate with sclerema.De home age bracket Study designSetting Tertiary anguish hospitalParticipantsAll neonates presenting with clinical signs of neonatal sepsis with sclerema admitteded at Davao Medical Center glasshouse for the year 2008.Results and ConclusionINTRODUCTIONneonatal sepsis is a cl inical syndrome of bacteremia characterized by general signs and symptoms of transmission in the first month of life1. It has taken so many lives of newborn babies. The mortality rate continuously increases especi e really last(predicate)y in the third world countries standardised the Philippines so that primordial recognition, diagnosis and manipulation of infection is important because it is largely a preventable disease.neonatal Sepsis can be divided into two chief(prenominal) classes depending on the onset of symptoms related to sepsis- early-onset and late-onset neonatal sepsis2. Early onset is mainly due to antepartum infections vertically transfer while late-onset is the combination of the former and nosocomial infection.The incidence of neonatal sepsis varies from one institution to another with high grade in developing countries. In the United States , the incidence of a culture-proven sepsis is approximately 2 per 1000 livebirths and increases to 25 per 1000 liveb irths in babes with birthweight less than 1500 grams3. It is considered to be a major cause of richality during the first month of life contri besidesing to 13-15% of all neonatal expirations with highest rates seen in premature infants and in small for gestational age infants. The mortality rate in neonatal sepsis whitethorn be as high as 50% for infants who are not treated3. A local study conducted at MCU-FDTMF Hospital nursery found the incidence of neonatal septicaemia to be 9.6 %4 as compared to other studies at UP PGH which is 5.5%. At Davao Medical Center the incidence and the outcome fatality rate of neonatal sepsis for the year 2008 are about 5/1000 livebirths and 1.3% respectively5.Considering the nonspecificity of the early clinical signs of neonatal sepsis and the neonates relative state of immunosuppression, early diagnosis and treatment is of utmost important. The main freeze of treatment is antibiotic. Supportive management is geared towards therto a greater exte ntgulation to prevent hypothermia or hyperthermia, ensuring good ventilation/oxygenation to vital tissues, provision of optimal nutrition preferably with enteral feeding or TPN, prevention of hypoglycemia and electrolyte imbalance by administ symmetryn of parenteral fluids and vasopressors for hypotension. Adjunctive therapy includes fresh frozen plasma transfusion, exchange transfusion, immunoglobulin therapy, granulocyte-macrophage colony stimulating factor, and granulocyte transfusion.Sclerema is the ordered hardening of the skin and subcutaneous tissues to the extent that the skin could not be pitted nor picked up or pinched into a fold6.It is considered as a sign of a potentially fatal cardinal disease process like neonatal sepsis especially gram- negative sepsis. neonatal septicemia is invariably fatal when associated with sclerema7. Its inform mortality rates range from 67-88% with death occurring hours to days later on onset8.Although literature about the benefits of Fre sh Frozen Plasma transfusion in septic neonates with sclerema is scarce, our go through at SPMC nursery suggests improved outcome from neonatal sepsis with sclerema when given FFP. We do not give FFP to septic neonates without sclerema. We are doing this study to validate if indeed our apprehension is correct and if this practice is valid.The study will be limited to comparison of septic patients with sclerema only. This preselects the most seriously ill patients. By limiting the study to early onset neonatal sepsis, opportunistic infections from less virulent pathogens like candida and staphylococcus epidermides are likely to be excluded and infection is most likely vertically transmitted and not nosocomial. This is to limit the varaiables due to etiologic agents that may affect outcome and interpretation of the result.Review of Related LiteratureThe defense system of the human torso consists of three components physical , cellular and humoral. Neonates are particularly deficien t in all three so that a more aggressive management is mandate to improve survival outcome when neonates develop septicemia.The physical and chemical barriers to infection in the human body are present in the newborn but are functionally deficient. The skin of a preterm infant is only a few cell-layers thick and is poorly cornified hence can easily be discredited paving the way for infection. The protective fatty acid production is withal low making them more undefended.At 23 weeks gestational age the foetus possesses T and B lymphocytes, macrophages, monocytes, polymorphonuclear cells and the capacity to synthesize all known immune factors.The ability of the T and B lymphocytes to produce cytokines is less in comparison to adults, moreover neonates are capable of generating appropriate adaptive immune responses. Langerhans cells are important in local infection and are present in the neonate at 18 weeks gestation.Phagocytes from preterm neonates show traffic pattern activity w hen suspended in frequent adult blood serum, however neonatal serum is deficient in immunoglobulin and co-occurrence so there is a mark reduction in adherence and chemotaxis. The neonatal neutrophil or polymorphonuclear (PMN) cell, which is vital for effective killing of bacteria is deficient in chemotaxis and killing capacity. Also neonatal PMNs are less deformable therefore they are less able to move through the extracellular matrix of tissues to puddle the site of inflammation and infection. The limited ability of neonate for phagocytosis and killing of bacteria is gain impaired when the infant is clinically ill. Lastly neutrophil reserves are easily depleted because of the diminished response of the bone marrow especially in the premature infant.The neonate is capable of synthesizing immunoglobulin M in utero at 10 weeks gestation, however IgM levels are generally low at birth unless the infant was exposed to an infectious agent during the pregnancy, thereby stimulating in creased IgM production. During pregnancy IgG is transported actively and passively across the placenta from about the 20th week of gestation and at full term the neonates IgG levels are higher than his mothers levels. The IgG in an infants plasma has a half-life of about three weeks.Until the infant is able to generate his own IgG, IgM and IgA there is a period of postnatal hypogammaglobulinemia. In a preterm neonate of 26 weeks gestation the plasma IgG levels are markedly lower and diminish to ineffective levels very quickly, increasing the risk of infection.Complement protein production can be detected as early as 6 weeks gestation however the concentration of the different components of the complement system widely varies among individual neonates. While some infants have had complement levels comparable with those in adults, deficiencies appear to be greater in the utility(a) pathway than in the classic pathway. The terminal cytotoxic components of the complement cascade that leads to killing of organisms, especially gram-negative bacteria are deficient. The deficiency is more marked in preterm infants. Mature complement activity is not reached until infants are aged 6-10 months. Neonatal sera have reduced opsonic deficiency against GBS, E. coli, and S pneumoniae because of decreased levels of fibronectin, a serum protein that assists with neutrophil adherence and has opsonic properties.Most common organisms causing early- onset neonatal sepsis include group B streptococci, gram -negative enteric organisms like E. coli. Listeria monocytogenes and Klebsiella are also a common isolates. Less common organisms include staphylococcus, other streptococci, anaerobes, and Haemophilus influenza9.The host-defence mechanism of neonates are immature. They have a markedly decrease levels of C3, Cy properdin and factor B which are very important in the alternative pathway of complement. Levels of IgM and IgA are also low at birth. Although IgG levels may be normal in term neonates, it is low in preterm infants. These relative deficiency of the neonates immune system complicated by low birthweight and decreasing age of gestation makes them more susceptible to life threatening infections10.Sadana,et al mentioned that the incomplete development of the host defense system of the neonate is largely responsible for the high mortality in neonatal sepsis11.In his study an increase in the levels of IgG, IgM, IgA andC3 was noted after exchange transfusion.Exchange transfusion offers removal of bacteria and toxins, improves oxygenation and perfusion as well as decreases haemorrhagic complications. The relative immunodeficiency state and susceptibility to sepsis and complications is the impetus for exploring treatment modalities other than antibiotics.There was an increase in the levels of IgG antibodies in septicemia patients with coagulase negative staphylococcus after FFP administration in the study made by Krediet, et al12The neonate being deficient in both humoral and cellular immunity is more vulnerable to infection. There are literature that suggests the usage of Fresh Frozen Plasma in patients with neonatal sepsis to compensate for the immunologic deficiencies. FFP improves neonatal chemotaxis, provides humoral or cellular factors13 and increases the levels of immunoglobulin such as IgG, IgA and IgM. FFP remains the only approved source of factors V,XI, protein C, protein S and plasminogen14 and basically all the clotting factors. Others would say that FFP transfusion in neonatal sepsis is good because it increases levels of IgG, IgA and IgM15 that will increase chances of survival.FFP contains immunoglobulins anc complement factors16.Fresh frozen plasma, the plasma separated from a unit of whole blood and frozen at -18 oC at bottom 8 hours of collection. It is a platelet-poor plasma17.Each bag has a volume of 175 to 250 ml and contains between 1 and 2 units of each coagulation factor per ml and 400 to 800 mg fibrinogen. It contains fibrinolytic and complement factors. It carries the same risks of viral transmission as other blood components and can cause allergic reactions and fluid overload.Indications for fresh frozen plasma, once used routinely in the support of critically ill-infants and children, have become more specific as evolving evidence has con faithfuled or disproved the efficacy of plasma in various circumstances. Fresh frozen plasma is currently indicated to treat the coagulopathies of massive hemorrhage, liver failure, disseminated intravascular coagulation and sepsis18.In an infant the fat has a higher saturated- to-unsaturated fatty acid ratio compared to adult fat and thus a higher melting point. Prematurity, hypothermia and shock and anatomic abnormalities have been postulated to further increase this ratio,possibly as a result of enzymatic alteration allowing precipitation of fatty acid crystals within the lipocytes. This condition has been suggested to result in the dramatic clini cal findings in the affected skin. Xray diffraction techniques have confirmed that infants with sclerema have an increase in saturated fats and that the crystals within the fat cells are composed of triglycerides.The exact incidence of sclerema neonatorum is noncitizen . All studies describe SN as extremely rare. The number of reported case in recent years have declined, probably as a result of a better neonatal care.Because sclerema neonatorum invariably is associated with serious rudimentary disease process, the mortality rate is high. In different series, the reported mortality rates range from 67-88%, with death occuring hours to days after onset. If the underlying disease is treated successfuly, the skin softens and returns to normal.Sclerema neonatorum shows a slight male preponderance, with an estimated male-to-female ratio of 1.51.Sclerema neonatorum is a disease check to the newborn period. It can present at birth, but onset within the first week of life is more common. The oldest reported infant presented with Pseudomonas septicemia is 106 days old.According to literature one half of the affected infants are premature, , and the others are full term but have a serious underlying disease. They are often of low birth weight and have cyanosis and low apgar scores.In one series, 75% of the mothers were healthy, while 25% had preeclampsia, placenta previa, or infection. Labor is usually normal and the delivery is spontaneous and nontraumatic.Physical findings appear perfectly, first on the thighs and on the buttocks and then spreading rapidly often affecting all separate of the body except the palms and the soles and the genitalia. The involved skin is pale, waxy, and firm to palpation. The skin cannot be pitted or pinched up because it is bound to the underlying tissues. The affected infant often dispalys flexion contractures at the elbows, knees and hips, temperature instability, restricted respiration, difficulty in feeding and decrease in spontane ous movement.17Recognition and the prompt institution of therapy specific to the underlying disease process are mandatory such as antibiotics, steroids, exchange transfusions and FFP transfusion.Definition of TermsNeonatal sepsis-It is a clinical syndrome of bacteremia characterized by systemic signs and symptoms of infection in the first month of life. Neonatal sepsis encompasses systemic infections of the newborn including septicemia, meningitis, pneumonia, arthritis, osteomyelitis and urinary tract infection of the newborn19.Associated factors for early onset neonatal sepsis include lowbirthweight, PROM, back up smelling liquor, multiple vaginal examinations and maternalistic fever20Early onset neonatal sepsis-It usually presents within the first 48 hours of life. In severe cases, the neonate may be symptomatic in utero, (fetal tachycardia, poor beat to beat variability) or within the first few hours after birth. The source of the infection is generally in the maternal genital, gastrointestinal, urinary tract . Clinically neonates usually present with respiratory distress and pneumonia. Presence of some perinatal risk factors has been associated with an increased risk of early onset sepsis.Frozen Frozen Plasma It is the plasma removed from a unit of whole blood and frozen at or below 55 degrees Fahrenheit within 8 hours of collection. It contains all the coagulation factors in normal amounts and is free of red cells, leukocytes and platelets. It is not a concentrate of clotting factors.Sclerema Neonatorum-It is derived from the Greek password sclerosmeaning hard. It is considered best as a sign of a potentially fatal underlying disease process in the newborn period. Physical findings appear suddenly first on the thighs and buttocks and then spreading rapidly, often affecting all parts of the body except the palms, soles and genitalia. The involved skin is pale, waxy and firm to palpation. The skin cannot be pitted or pinched up because it is bound to the underlying tissues.It can present at birth but onset within the first week of life is more common. Associated underlying conditions include septicemia, pneumonia, hypothermia, metabolic acidosis, respiratory distress syndrome, congenital heart defects, gastroenteritis and intestinal obstruction.Clinical Signs of Neonatal Sepsis(At least 2 clinical signs supported by laboratory findings)1.sclerema2.hypoglycemia/hyperglycemia3.temperature instability4.tachypnea/respiratory distress5.Apnea6.Poor perfusionLaboratory findings1..I/T ratio 0.22.leukopenia 3.Neutropenia 4.Thrombocytopenia Research Question allow for FFP transfusion improves the survival outcome of the sick neonates with early onset neonatal sepsis with sclerema given the standard therapy plus FFP?Is the use of FFP justifiable in the treatment of neonatal sepsis with sclerema in terms of cost and survival outcome?Significance of the studyMany studies have been done to improve the survival outcome of neonates with septicemia . The progress in terms of the available adjuctive therapies in the treatment of neonatal sepsis entail a higher cost which is an issue to our marginalized patients who cannot afford such expensive add on treatment hence inspired the researcher to study fresh frozen plasma transfusion which is much more affordable and readily available to the neonates with septicemia particularly with sclerema. FFP contains immunologic factors helping the immunologically deficient neonate in fighting serious infections.This study aims to evaluate the effects of FFP transfusion in the subset of neonates with high case fatality rate. They are the candidates that would benefit from the terminal cytotoxic complement with the coagulation cascade that FFP may provide.OBJECTIVES OF THE STUDYGeneral ObjectiveTo determine and compare the survival outcome of patients with early- onset neonatal sepsis with sclerema given the standard therapy (antibiotic + supportive care ) plus fresh frozen plasma to those wit h early -onset neonatal sepsis given only the standard therapy (antibiotic + supportive care ) at Southern Philippines Medical Center- Nursery for the year 2008 .Specific ObjectivesDetermine the incidence of sclerema in early onset neonatal sepsis in SPMC.Determine the rate of early onset neonatal sepsis with sclerema in SPMC.Determine the mortality rate of neonates with early onset sepsis with sclerema.Identify the possible the maternal fetal/neonatal factors related to early neonatal sepsis with scleremaCompare the outcome1.resolution of scleremaChapter 2METHODOLOGYStudy DesignThis paper will be an empirical descriptive and comparative study on the survival outcome of patients with neonatal sepsis with sclerema admitted at Southern Philippines Medical Center for the year 2008 using a Cohort study design.PopulationThis study will include all neonates with early-onset neonatal sepsis with sclerema admitted at Southern Philippines Medical Center -Nursery for the year 2008.Inclusion criteriaAll neonates admitted at Southern Philippines Medical Center -Nursery who presents with the clinical signs of early- onset neonatal sepsis with sclerema.Exclusion criteria1.All neonates presenting with clinical signs of neonatal sepsis with sclerema occurring beyond 48 hours of life.2. All non-institutional deliveries presenting with early onset neonatal sepsis with sclerema.3. All neonates admitted at the NICU with obvious congenital anomalies like syndromic features, cleft lip and palate etc.Data CollectionData will be collected by the researcher through a retrospective chart review. The researcher will scan and evaluate each chart of the patient with neonatal sepsis for the presence of sclerema in the progress notes. A data sheet will be use for each patient.Research consultant will be asked for validation of diagnosis. strong-minded variable -Fresh Frozen Plasma transfusionDependent variable- survival outcome of neonates with early onset sepsis with scleremaSample SizeAl l neonates admitted at Southern Philippines Medical Center-Nursery who fulfilled the inclusion criteria for the year 2008 will be used as a sample in this study.Data Analysis correlation coefficient and odds ratio will be used to summarize the data for the comparative part. Means and standard deviation for the descriptive part and percentage and rates as per standard definition.Ethical ConsiderationThe approval of the hospital research committee and the ethics committee will be sought before the conduct of the study. no. acknowledgment data or marks will be placed in each patient included in the study. The data will be unploughed by the researcher for 5 years. control panel 1.Patient clinical profileName AGA___SGA___LGA___AgeWeightAOGSexMedical record numberlength of stay in the hospital Date of admission Date of dischargeDiagnosis upon admissionFinal diagnosisOUTCOME died survived HAMA transferred transout to blue areaCause of deathAge at onset of sepsis(hours)Age at ons et of sclerema(hours)AntibioticsAmpicillin/GentamycinCefotaxime/AmikacinPiperacillin + Tazobactam/AmikacinMeropenemCefepimeNeonatal risk factorsBirthweight1.VLBW2.LBW 3.normal weight4.LGAAPGAR SCORE (5 minute)0-34-67-10Ballard Scoring34-3737ComorbiditiesNeonatal pneumoniaMeconium aspirationIntubationPulmonary hypertensionPneumothoraxOthers (specify)MATERNAL RISK FACTORSPremature labor and deliveryProlong Rupture of membraneAntenatal SteroidChorioamnionitis artful Operative DeliveryMaternal infection within 2 weeks of deliveryUTIRTIPreeclampsia/eclampsiaPlacenta previa/ abruptioOthers (specify)SCLEREMAHours first notedFFP transfusionYes /hours before transfusionNo event of sclerema post FFPYes- number of hours first noted resolutionNo-OUTCOMEDiedSurvivedCOMPLICATIONS NOTEDTable 2. ANTIBIOTICSStandard care+FFPStandard care congeriesNo.%No.%No.%Ampicillin+GentamycinCefotaxime +AmikacinPiptazo+AmikacinMeropenemCefepimeTotalTable 2.BIRTHWEIGHTStandard care+FFPStandard careTotalNo.%No.%No .%VLBW LBW AGALGATotalTable 3. APGAR SCORE(5 MINUTE)Standard care+FFPStandard careTotalNo.%No.%No.%0-34-67-10TotalTable 4. BALLARDS SCOREStandard care+FFPStandard careTotalNo.%No.%No.%34-37 weeks37 weeksTotalTable 5. ComorbiditiesStandard care+FFPStandard careTotalNo.%No.%No.%Neonatal pneumoniaMeconium aspirationIntubationPulmonary hypertensionPneumothoraxOthers (specify)TotalTable 6. Maternal Risk FactorsAntibiotic+Standard care+ FFPAntibiotic +Standard careTotalNo.%No.%No.%Preterm labor/deliveryRBOWAntenatal SteroidChorioamnionitisOperative DeliveryMaternal infectionUTIRTIPreeclampsia/eclampsiaPlacenta previa /abruptioOthers (specify)TotalTable 7. Onset and Resolution of ScleremaAntibiotic+Standard care+ FFPAntibiotic +Standard care onlyOnsetresolutionTotal time of scleremaTable 8. OutcomeSurvived drainedTotalNo.%No.%No.%Antibiotic+Standard care+ FFPAntibiotic +Standard careTotalConceptual frameworkBabies admitted at DMC nursery 2008No sepsisCompare resultsSepsis with scleremaAnti biotic+Standard care+ FFPAntibiotic +Standard careSepsis without scleremaEarly-onset neonatal sepsisCOST/BUDGETCOUPON BOND.P.400.00PRINTINGP700.00RESEARCH MATERIALS ..1,000.00______________________P 2,100.00 date TABLE (May 2009- December 2010)MayPRESENTATION TO RESEARCH COMMITTEEAND ETHICSJune -OctoberDATA GATHERINGNovemberPRESENTATION OF RESULTSDecemberSUBMISSION OF HARD COPIES
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