C.

INTRODUCTION

The Baguio General Hospital & Medical Center (BGHMC) is a 109-year old general tertiary medical & training center with medical ancillary services under the national government. It was also declared as one heritage site in Baguio City in 2010. The hospital has been operating from 1902 until the present and is located along Governor Pack Road near Marcos Highway (presently Ben Palispis Highway) Rotunda, Baguio City. The hospital was also approved for 500 bed capacity through R.A 8634 of 1998 but due to manpower deficiencies the actual implementing is 400. BGHMC offers a wide range of services in 15 departments: their Pediatrics Department covers General Pediatrics, Hematology/ Oncology, Nephrology, Neurology, Newborn Medicine, Pediatric Intensive Care, and Paleontology. Group 1 under the supervision of Mrs.Ervina Luisa Delias Campus were assigned at the pediatric ward from July 17-18, 2012 (7:00 am - 3:00 pm shift). The group had 9 members namely: Aizel Buenaventura, Joanne Modesty Dela Cruz, Amabel Rina Estira, Henry Kierulf Hafalla, Blessing Mabborang, Charlene Patricia Nunez, Camille Joy Punsalan, Pamela Sayana, Charlemagne Suyat.

Neonatal Sepsis is an infection in the blood that spreads throughout the body and occurs in a neonate. Neonatal Sepsis is also termed as Neonatal Septicemia and Sepsis Neonatorum. Neonatal Sepsis has 2 types: The one that is seen in the first week of life is termed as Early- onset sepsis and most often appears in the first 24 hours of life. The infection is often acquired from the mother. This can be cause by a bacteria or

infection acquired by the mother during her pregnancy, a Preterm delivery, Rupture of membranes (placenta tissue) that lasts longer than 24hours, Infection of the placenta tissues and amniotic fluid (chorioamnionitis) and frequent vaginal examinations during labor. The second type or the Late-onset Sepsis is acquired after delivery. This can be cause by contaminated hospital equipment, exposure to medicines that lead to antibiotic resistance, having a catheter in a blood vessel for a longtime, staying in the hospital for an extended period of time. Signs and symptoms of Neonatal Sepsis includes but is not limited to: body temperature changes, breathing problems, diarrhea, low blood sugar, reduced movements, reduced sucking, seizures, slow heart rate, swollen belly area, vomiting, yellow skin and whites of the eyes(jaundice). Possible complications are disability and worst is death of the neonate.

The reported incidence of neonatal sepsis varies from 7.1 to 38 per 1000 live births in Asia, from 6.5 to 23 per 1000 live births in Africa, and from 3.5 to 8.9 per 1000 live births in South America and the Caribbean. By comparison rates reported in the United States and Australasia range from 1.5 to 3.5 per 1000 for EOS sepsis and up to 6 per 1000 live births for LOS sepsis, a total of 6-9 per 1000 for neonatal sepsis.

According to the Philippine Mortality Fact Sheet 2006 of the World Health Organization, in 1000 live births of neonates 17% of it died due to severe infection that includes deaths from pneumonia, meningitis, sepsis/septicemia, and other infections

during the neonatal period. According to world health statistics done in the year 2 0 0 4 N e o n a t a l I n f e c t i o n r a n k as no 11 as a leading cause of death it was f u r t h e r compared to the mortality statistics of the year 2030. In the year 2030 it was projected that in the year 2030 Neonatal Infection will be lower down to rank 21 as a leading cause of death. Updated mortality projections are based on historically observed relationships between trends in economic and social development and cause-specific mortality.

www.who.com An in-depth study about Neonatal Sepsis is so important for a nurse most especially if the nurse is working in a Neonatal Intensive Care Unit or the NICU department. A nurse should be properly educated regarding the cause of the neonatal sepsis, how it is acquired and prevented, and its complications. After the completion of the study, a nurse shall be able to: identify and differentiate the types of Neonatal Sepsis, be updated with the latest trends in the treatment of Neonatal Sepsis, perform a comprehensive assessment of Neonatal Sepsis, enumerate the different signs and symptoms of Neonatal Sepsis, list down the different diagnostic procedures that would help in the diagnosis of Neonatal Sepsis, identify and understand different types of medical treatment necessary for the treatment of Neonatal Sepsis, formulate nursing care plans utilizing the nursing process. Nursing centered objectives include: have critical thinking skills necessary for providing safe and effective nursing care, have a comprehensive assessment and implement care base on our knowledge and skills

of the condition, familiarize ourselves with effective inter-personal skills to emphasize health promotion and illness prevention, impart the learning experience from direct patient care.

CHAPTER I NURSING ASSESSMENT I. Patients Profile

Angel Balajo was born last May 31, 2012 at Ifugao Provincial Hospital. They reside somewhere in Lagawe, Ifugao. Based on his ballard score of maturational assessment of his gestational age, she is in between 30 to 31 weeks of age.

II. History of Present Illness Prior to delivery, her mother had a vaginal bleeding and early contraction, reason why her mother was brought early in the hospital. Initially after birth she was placed in the nursery unit of the hospital for observation. Patient was initially given antibiotics (Ampicillin & Cefuroxime) for 10 days. She was doing well but has marked jaundice for 1 month now. Mothers attempt of breastfeeding caused cyanosis, patient was fed through OGT. Persistence of cyanosis prompted referral to BGH for admission.

Obstetrical History

Ms. Ofelia Guihom is not married to the father of her child yet and has no plan of getting married as of the moment. She gave

birth to her first baby at the age of 18. She had given birth to Angel Balajo last May 31, 2012. Due to early contraction and vaginal bleeding, she was brought to Ifugao Regional Hospital and eventually delivered via NSD on the same day.

Pre-natal Preparation

According to her mother, she had a regular prenatal check-up. She cannot remember any immunizations. Based from our theory, we can conclude that the pregnancy was unexpected due to the young age, she is unemployed, and she is from the rural area where sometimes health facilities (RHU) are not as accessible as the ones we have in the city III. Physical Assessment July 11, 2012 Vital Signs: RR-55 bpm CR-137 bpm Temp- 36.7oC Measurements: Length- 34 cm Head Circumference- 29.5 cm Chest Circumference- 27 cm Abdominal Circumference- 25.5 cm Weight- 2,5 kgs Skin (+) jaundice Head: soft, firm and flat fontanels Eyes: (+) PERRLA, with pale palpebral conjunctiva Chest: no retraction

Abdomen: globular, soft, no palpable mass Extremities: symmetrical, full range of motion, no edema

July 18, 2012 Vital Signs: RR-44 bpm CR-154 bpm Temp- 36.6oC Measurements: Length- 34 cm Head Circumference- 29.5 cm Chest Circumference- 27 cm Abdominal Circumference- 26 cm Weight-2.4 kgs. Arm Circumference 7 cm General Appearance: The baby was born prematurely; small in size, skinny in built as compared to a full term baby, yellowish in color. Baby is less active and is afebrile. She has good cry and good suck and regularly demands feeding. Skin: With good turgor, no cyanosis, skin warm to touch, with jaundice sclera, face, and plantar surface keratinized skin Head: Diamond-shaped anterior fontanel, with triangular-shaped posterior fontanel, fontanels soft, firm and flat Eyes: no tears when crying, with pupils equal round reactive to light and accommodation , with blink reflex Ears: Symmetrical, no discharge or lesions, well curved pinna;

soft but ready recoil Nose: Bilateral patent nostrils, no nasal discharges, no nasal flaring Mouth: mucosa moist, tongue moves freely and does not protrude, with sucking and rooting reflex Neck: short and thin Chest: with evident xiphoid process, with symmetrical nipples, with symmetrical chest movements, no retractions, no murmur Abdomen: with abdominal respirations, soft, with bowel sounds, with passage of stool, no mass, globular Extremities: symmetrical, full range of motion, no edema, no abnormalities present.

PATHOPHYSIOLOGY (SCHEMATIC DIAGRAM)

SEPSIS VS APNEA OF PREMATURITY

A Clinical Paper Presented to the Faculty of the School of Nursing University of Baguio

In Partial Fulfillment of the Requirements for the Subject NCENL01

Presented by:

BSN II NBB

GROUP I

Presented to: Mrs. Ervina Luisa D. Campus Clinical Instructor

July 2012

Sepsis is a serious medical condition caused by the bodys response to infection. Infection is a microbial phenomenon characterized by an inflammatory response to the presence of microorganisms. Systemic inflammatory response syndrome (SIRS) is a systemic or whole body response to an infection. Sepsis can now be more accurately defined as a systemic inflammatory response syndrome (SIRS) resulting from infection. Infection + SIRS = SEPSIS Precipitating factors in the early onset include: Maternal Pyrexia Infection Bacteria (S. aureus, E. coli) Virus (enterovirus, adenovirus) Maternal UTI Chorioamionitis Poor prenatal care Precipitating factors in the late phase include: Prolonged hospitalization Presence of foreign body Cross infection Low birth weight Meconium staining Hazardous uterine environment Predisposing factors include: Gender Race AOG <35 wks When a microbe infects tissues, a cascade of pro-inflammatory mediators are released. But these are counter balanced by the release of Anti-inflammatory agents. It is this balance that enables the mobilization of defense and microbe killing mediators while allowing blood tissue repair and healing. Example of the pro-inflammatory agents is the cytokine TNF (tumor necrosis factor) which promotes the inflammatory response. So, pro-inflammatory agents are the ones responsible for the inflammation response. Example of an anti-inflammatory response include the cytokine IL-10 inhibits the production of multiple, diverse inflammatory mediators from activated macrophages and dendritic cells. So, anti-inflammatory response works to reduce inflammation and promote healing (anti-inflammatory). In sepsis, this equilibrium is disturbed and the pro-inflammatory mediators dominate to elicit endothelial damage. SIRS (increased pro-inflammatory response gave rise to SIRS) response is balanced by the CARS (complementary anti-inflammatory response syndrome). When there is an excess pro-inflammation, there is an increased propensity to develop MODS (multiple Organ Dysfunction Syndrome. When there is an excess of anti-inflammatory inflammation, the patient is at risk for opportunistic or secondary infections. The subsequent balance between the proinflammatory (SIRS) and anti-inflammatory (CARS) response has been referred to as the mixed antagonistic response syndrome or MARS. Studies of the extent of coagulation and fibrinolysis abnormalities in sepsis have shown

that endothelial damage promotes coagulation. Normally, modulators promotes fibrinolysis to counter-act the thrombosis. In sepsis, however, the endothelial damage is proposed to suppress fibrinolysis, further contributing to the loss of control. As the body tries to return to a normal state the endogenous modulators of homeostasis are consumed and their levels become low. In parallel, the endothelial damage promotes further inflammation, thereby, endothelial damage accumulates and in turn so does coagulation. Uncontrolled cascade of inflammation and coagulation fuels the progression of sepsis. The initial phase (ebb phase) that last 1-3 days only is how a neonates body compensate for losses that occur during sepsis. The body slows thing down in order to let the body recover. The Ebb phase consists of many clinical manifestations, including: Hypometabolism Decreased energy expenditure Decreased cardiac output Lowered oxygen consumption Vasoconstriction The late phase that occurs after the initial Ebb phase doesnt recover, it goes to hyperdrive. This is partly due to the exaggerated inflammatory response. The flow phase consists of several clinical manifestations: Hypermetabolism Increased energy expenditure Increased cardiac output High oxygen consumption Sepsis, also known as the sepsis syndrome or SIRS, is the combination of inflammation throughout the body; problems with the blood's clotting mechanism In its most severe form, sepsis can drastically reduce blood flow to the major organs, leading eventually to septic shock, widespread organ failure and death. At the end of the hyperdrive (compensary mechanism), negative feedback occurs: Sudden decrease BP Diminished PR Decreased body temperature That leads to poor perfusion

hypoxia /hypoxia/ (hi-pokse-ah) reduction of oxygen supply to a tissue below physiological levels Septic shock A sepsis induced state of severe hypotension despite aggressive fluid therapy. Multiple Organ Dysfunction Syndrome (MODS) A progressive dysfunction in two or more organs of the body after the onset of sepsis where intervention is needed to sustain life. The main clinical manifestation of DIC is bleeding which is due to depletion of coagulation factors and platelets, fibrinolysis, and the anticoagulant effect of FDPs. Fibrinolysis is a normal body process that keeps naturally occurring blood clots from growing and causing problems. Primary fibrinolysis refers to the normal breakdown of clots. Coagulation is the process by which blood forms clots. Coagulopathy may also occur as a result of dysfunction or reduced levels of platelets. Excessive coagulation leads to the formation of a thrombus, potentially obstructing blood flow. Disseminated intravascular coagulation (DIC), also known as disseminated intravascular coagulopathy or consumptive coagulopathy, is a pathological activation of coagulation (blood clotting) mechanisms that happens in response to a variety of

diseases. DIC leads to the formation of small blood clots inside the blood vessels throughout the body.[1] As the small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin (e.g. from sites where blood samples were taken), the gastrointestinal tract, the respiratory tract and surgical wounds. The small clots also disrupt normal blood flow to organs (such as the kidneys), which may malfunction as a result. Lactic acid is produced when oxygen levels in the body drop In medicine, metabolic acidosis is a condition that occurs when the body produces too much acid or when the kidneys are not removing enough acid from the body http://www.slideshare.net/jstyle4u/sepsis-1154107 http://www.slideshare.net/crisbertc/neonatal-sepsis-presentation http://www.slideshare.net/jstyle4u/sepsis-1154107 http://cellular-immunity.blogspot.com/2007/12/inflammatory-response.html http://www.slideshare.net/changezkn/sepsis-5552949 http://www.slideshare.net/sothep/severe-sepsis-and-septic-shock http://www.scribd.com/doc/20266496/The-Pathophysiology-of-Sepsis http://www.scribd.com/doc/25259851/Neonatal-Sepsis http://www.scribd.com/doc/26468315/Pathophysiology-of-Neonatal-Sepsis-secondaryto-Neonatal-Pneumonia Neonatal neutrophils are deficient in their ability to adhere to vessel walls at site of infection Neonatal neutrophils have decreased chemotaxis due to decreased chemoattractant Production. Chemoattractants attract neutrophils to the site of infection. Neonatal neutrophils therefore cannot reach the site of infection because of the chemotaxis deficiency caused by decreased chemoattractant production. Opsonization is the coating of a pathogen with antibodies that makes it susceptible to phagocytosis Phagocytosis is the process of cells (phagocytes) engulfing, ingesting, & destroying pathogens There are 3 integrated responses to sepsis Activation of Inflammation Activation of Coagulation Impairment of Fibrinolysis Inflammation is the bodys response to infection.When this occurs white blood cells (WBCs) generate and release cytokines or mediators of inflammation. The enhanced clotting continues making tiny clots or microthrombi in the vascular system which impairs blood flow and organ perfusion. Fibrinolysis, or the breakdown of clots, is the bodys response to the increased clotting and inflammation. In sepsis this breakdown is inhibited. The increase levels of these two inhibitors, Plasminogen Activator Inhibitor-1(PAI-1) and Thrombin Activatable Fibrinolysis Inhibitor (TAFI), suppress fibrinolysis even more creating a state of coagulopathy.