Stage 1 and stage 2 necrotizing entercolittis ( nec ) A CLINICAL Case study

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STAGE 1 AND STAGE 2 NECROTIZING ENTERCOLITTIS (NEC) A CLINICAL CASE STUDY Presented by Ashley Robson, BSN, RNC-NIC, SNNP NNP II GNRS:6532

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Stage 1 and stage 2 necrotizing entercolittis ( nec ) A CLINICAL Case study. Presented by Ashley Robson, BSN, RNC-NIC, SNNP NNP II GNRS:6532. Objectives. -Maternal History -Maternal and Fetal risks and complications -Delivery and Stablization -Admission Assessment and diagnostics - PowerPoint PPT Presentation

Transcript of Stage 1 and stage 2 necrotizing entercolittis ( nec ) A CLINICAL Case study

Page 1: Stage 1 and stage 2 necrotizing  entercolittis  ( nec ) A CLINICAL Case study

STAGE 1 AND STAGE 2 NECROTIZING ENTERCOLITTIS (NEC) A CLINICAL CASE STUDY

Presented by Ashley Robson, BSN, RNC-NIC, SNNP

NNP II GNRS:6532

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Objectives

-Maternal History -Maternal and Fetal risks and complications -Delivery and Stablization -Admission Assessment and diagnostics -Primary admission diagnoses -Etiology and pathophysiology of primary admission

diagnses -Initial Plan of Care -Hospital Course by system -Medications -Theories and Evidence based practice -Family interactions -Discharge plan and follow-up

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Maternal History

-This is a 21 year old Hispanic mother G2P2 -Mother received prenatal care for a total of 4

visits -Blood Type: B Pos -RPR: Non-reactive -Hep B: Negative -HIV: Negative -Rubella: Immune -GBS: not done, negative on previous

pregnancy

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Maternal and Fetal risks and complications

Pregnancy complication included: -Premature labor at 25 weeks gestation -Premature rupture of membranes -Chorioamniomitis Maternal feverFetal Risks of prematurity: -Hypothermia -Infection -Respiratory distress and surfactant deficiency Electrolyte imbalances Patent ductus arteriosus Hyperbilirubinemia Pain Social Problems Developmental IssuesGomella, Cunninham, &Eyal, 2013

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Delivery Room and Stabilization Labor:-Membranes ruptured spontaneously 14 hours prior to delivery, copious amount with no odor-Infant was delivered vaginally with cephallic presentation. Infant:The infant was initially non-vigorous, warmth, drying, and stimulation provided. PPV initiated with Neopuff. Heart rate was 110 at 1 min of life, with no respiratory effort, PPV continued. Infant intubated at 3 minutes of life for poor respiratory effort with improvement in color and oxygen saturations. Good color change noted to the pedi-cap. Infant transferred to the NICU for further evaluation and stablization and delivery of surfactant.American Heart Association, 2011.

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Admission Assessment and diagnostics

Admission Physical Assessment:Activity/Neuro: active upon examColor/Skin: pink, no lesion, with brusing noted to the right and left armHead/Scalp: sutures separated, fontanels flat, brusing noted to scalp and forehead areaEENT: bilateral red reflex, orally intuabtedClavicles: intact, no crepitus Heart: pulses symmetrical and rhythm, regularLungs: subcostal and intercostal retractions, clear to auscultateAbdomen/ Umbilical cord: abdomen soft and non-distended, 3 vessel cordGenitalia: preterm female genitaliaExtremities: moves all extremities

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Admission diagnostics

Chest/ Abdomen xray: Lungs 8-9 rigs expanded with ETT at T3 and bilateral granular appearance, gavage tube in the stomach

Arterial Blood gas sampling: ph: 7.3, Pco2: 37, PO2: 49, hco3: 19, be: -8

Glucose: 83 CBC, blood culture, type and cross

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Primary admission diagoses

25 week female, 790 gram Preterm Infant VLBW Respiratory Distress of the Newborn Neonatal Sepsis

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Etiology and pathophysiology of primary admission diagnoses

Premature rupture of membranes occurs in 3% of pregnancies and premature contractions occurs in 10%.

The causes of premature rupture of membranes are unknown, but risk factors are: previous pregnancy affect my PROM, black race, smoking, infections, and severe polyhydraminos (Sadler, 2012).

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Etiology and pathophysiology of primary admission diagnoses

Respiratory Distress of the Newborn: Incidence of respiratory distress syndrome is 91% at 23-25 weeks gestation. Severity of RDS is thought to decrease with the use of antenatal steroids. Characteristic chest radiography findings are: uniform reticulogranular pattern to lung fields. Surfactant deficiency is the primary cause of RDS. The lack of surfactant leads to atelectasis. Risk factors for RDS include: prematurity, male sex, familial predisposition, Cesarean delivery without labor, maternal diabetes, ect. ( Gomella, Cunningham, & Eyal, 2013). The infant with RDS exhibits tachypnea, grunting, nasal flaring, and retractions of the chest wall.

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Etiology and pathophysiology of primary admission diagnoses

Chorioaminionitis is a major risk factor for sepsis. Risk for chorioaminionitis include: spontaneous labor, multiple digital vaginal exams, meconium stained fluid, long length of labor and membranes rupture, and internal fetal or uterine monitoring (Gomella, Cunningham & Eyal, 2013).

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Stage 1 and Stage 2 NEC

Necrotizing entercolitis (NEC) is characterized by intestinal tract damage, onset usually in the first several weeks after birth

Initial symptoms can include: Vomiting Diarrhea Delayed gastric emptying Abdominal distention, tenderness Ileus Apnea Lethargy Decreased perfusion Shock

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Stage 1 and Stage 2 NEC

This is normal versus necrotic bowel

Surgical intervention would be necessary

Infant needs to be NPO, IV fluids, and antibiotics

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Stage 1 and Stage 2 NEC

Stage 1A and IB- (Suspected disease)-NPO diet and antibiotics for 3 days-IV fluids, including TPN

Stage 2A and 2B-(Definite disease)-Consider respiratory support and cardiovascular support-NP0 and antibiotics for 14 days-Consider surgery consult

Springer, 2014

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Initial Plan of Care

Place infant in a preheated bed Continuous cardio-pulmonary monitoring NPO SIMV R-40, PIP-18, PEEP-5 Adjust fio2 to maintain saturations 85-92 Arterial Blood gas upon admission and as needed Insert Umbilical Arterial Catheter, Umbilical Venous Catheter. Chest/Abdomen Xray CBC, blood culture, type and cross, glucose Lytes every 12 hours Dextrose 7.5% with 2 grams AA and 25 units of heparin running

though the UVC at 65ml/kg/day 1/4 NS+ 25 units of heparin running though UAC at 15ml/kg/day

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Initial Plan of Care

Ampicillin 50mg/kg every 12 hours IV Gentamicin 4.5mg/kg every 24 hours IV Gentamicin levels if on for 4 days Follow Blood culture for 5 days Caffeine 20mg/kg loading dose (Young, 2009). Place 8FR gavage tube Neuro sonogram on day of life 7 1st Newborn screen at 24 hours of life T/D bilirubin every 12 hours Monitor for PDA and consider ECHO

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Hospital course by system

Resp: 3/25-3/28 intubated on SIMV, 3/28-5/15 CPAP, 5/15-present HFNC

1 dose of surfactant given upon admission Cardio: 4/1 large PDA, Left to Right shunt after 1 round of

indomethocin, 4/21: Moderate PDA, Left to Right shunt, 5/19: no PDA, left to right shunt, and PFO

Heme: last transfused on 5/19 for hematocrit of 26. 15ml/kg PRBC given.

GI: History of Stage 2 NEC, recently Stage 1 NEC on 5/12 and NPO until 5/19th and feeds restarted after PRBC transfusion. 5/22: not tolerating feeds with increased emesis and residuals. Plan to have a barium swallow and UGI

GU: unremarkable

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Hospital course by system

CNS: HUS #1,2,3- no IVH, HUS #4- no IVH, persistent thalamic vasculopathy.

Musculoskeletal-unremarkable. Ophthalmology: 1st exam on 5/25 FEN: feedings started at 20ml/kg/day at day 2 of life, fluids

running through UVC/UAC for 7 days, PICC placed in the left leg on 4/15, history of Stage 1&2 NEC, currently NPO for barium enema and UGI

Infectious Disease: history of chorioaminitis, CBC, blood culture sent upon admission, antibiotics started, antibiotics resumed for 7 days on 5/12-5/19. Urine CMV sent on 4/12-negative

Immunizations: 2 month immunization consent singed Health Maintanence: #1 NBS-WNL, #2 NBS- abnormal thyroid,

labs WNL.

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Medications

Ampicillin 50ml/kg IV every 12 hours Gentamicin 4.5mg/kg IV every 24 hours Erythromycin eye ointment upon admission 0.5mg Vitamin K given IM on admission 2ml/kg Surfactant given via ETT upon admission Caffeine loading dose 20mg/kg (Young, 2009).IV accessUAC/UVC placed 3/25PICC placed in left left on 4/15Multiple PIV sites

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Probiotics for prevention of NEC in preterm neonates

An interesting evidence based article that I found and have never heard of is the use of probiotics for the prevention of NEC in preterm neonates. It is suggested that this might provide an

increased barrier to migration bacteria, exclusion of pathogens, have a different response to microbial products, augment IGA.

AlFaleh & Anabrees, 2014

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Providing a facility that promotes family centered care

The evidence behind providing family centered care suggests advantages are: Decrease stress levels of the parents Encouraging family to family support and

networking Providing families with emotional and

financial support Providing culturally competent care

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Family interactions

-We need to keep the family involved in their babies care providing family-centered care.-This particular family speaks Spanish and the language line is available to update parents, answer questions, and obtain consents. -Parents should not be considered visitors and should be treated like an essential component of the infants care-Keep a multi-disciplinary approach to the care-The environment in the hospital should be conducive to provide the needs of the parents including privacy(Martin, Fanaroff, and Walsh, 2011).

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Discharge plan and Follow-upThe discharge process needs to start upon admission, which gives the family adequate time to process information, practice skills and ask questions. There are some helpful ideas when preparing families to go home; especially when they might be going home with hospital equipment including oxygen. Making a binder for the family with all discharge instructions and follow up appointments is helpful (Hynes & Andrews, 2012) Hearing screen needs to be performed prior to discharge This premature infant will follow-up with ophthalmology on

a routine basis Immunizations need to be administered based off the AAP

guidelines This infant meets criteria for a car seat trial

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References

AHA/AAP. (2011).Textbook of Neonatal Resuscitation, 6th Edition. AlFaleh , K., Anabrees, J., (2014). Probiotics for prevention of necrotizing enterocolitis in preterm

infants. Cochrane Database of Systematic Reviews.Issue 4. Art. No.: CD005496. DOI: 10.1002/14651858.CD005496.pub4

Blackburn, S. (2007). Maternal, Fetal, & Neonatal Physiology (3rd edition). St. Louis, Missouri: Saunders Elsevier.

Gomella, T. L. (2013). Neonatology management, procedures, on-call problems, diseases, and drugs (7th ed.). McGraw Hill Medical

Hynes, R.A., Andrews, T.M., (2012). Discharge Planning In J. P. Cloherty, E. C. Eichenwald, A. R. Hansen, & A. R. Stark (Eds.), Manual of neonatal care (7th ed.). (pp. 203-218). Philadelphia, PA: Lippincott Williams & Wilkins.

Martin, R.J., Fanaroff, A.A., Walsh, M.C. (2011). Neonatal-perinatal medicine: diseases of the fetus and infant (9th ed.). Volume 2. St. Louis, Missouri: Elsevier Mosby

Sadler, T.W. , (2012). Medical Embryology (12th ed.). Baltimore, Maryland: Lippincott Williams & Wilkin

Shields , L.., Zhou , H., Pratt, J., Taylor, T., (2012), Family-centred care for hospitalised children aged 0-12 years. Cochrane Database of Systematic Reviews .Issue 10. Art. No.: CD004811. DOI: 10.1002/14651858.CD004811.pub3

Springer, S.C., (2014). Necrotizing Enterocolitis. Retrievedf from http://emedicine.medscape.com/article/977956- overview.

Young, T.E., & Mangum, B. (2009). Neofax. Thomson Reuters.