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Green Bile Vomiting Guide for Neonatal Stabilization
- 1. STABLE NOTES Sugars Bowel Obstruction Vomiting of green colored bile emesis -never assume to be normal -should prompt rapid evaluation by neonatal experts Rule out Intestinal obstruction Malrotation with or w/o midgut volvulus Causes: Espohageal atresia Duodenal atresia Jejunoileal atresia Midgut volvulus Meconium ileus Colonic atresia Imperforate anus Esophageal Atresia/ Tracheoesophageal Fistula Signs: -Choking, coughing, cynosis with feeding Excessive saliation=if esophageal atresia Respiratiory distress secondary to aspiration Abdominal distension=fistula from trachea to stomach=air cannot escape stomach Maternal history Polyhydramnios suggest esophageal atresia or bowel obstruction STABILIZATION NPO Assess oxygenation and ventilation Instert suction catheter(replogle tube) into proximal esophageal pouch and connect to continuous suction to remove secretions Position prone= elevate head of bed to reduce refkux from stomach into trachea . *if contrast study needed – perform at tertiary care center* MALROTATION – MIDGUT VOLVULUS -REVIEW Presentation Abdomen -soft or tender -may or may not be distended With progressive vascular compromise of intestine, ischemia causes:
- 2. -significant pain -bloody stools -Shock and metabolic acidosis Volvulus Diagnosis and Stablilization -make NPO -gastric decompression with low intermittent suction -30-40 cm h2o -abdominal xray - may be normal=helpful only If abdominal - upper gastrointestinal UGI study - defines small bowel anatomy and if malrotation is present -pre DUODENAL ATRESIA “double bubble sign” Distended gas filled stomach Mildly distended gas filled duodenal bulb No Bowel gas remainder of bowel JEJUNOILEAL ATRESIA Atresia may be in ileum, jejunum or both Small bowel is dialated with gas prior to area of atresia MECONIUM ILEUS Inspissated meconium obstructs the terminal ileum Pellets of hard meconium prevent passing of gas or stool Can be associated with lack of pancreatic enzymes COLONIC ATRESIA Note dialated small intestine and colon up to the area of atresia IMPERFORATED ANUS Infant with gass filled bowel loops abdominal distention “loopy looking” FEMALE Meconium from a fistula external to hymen but not on perineal skin indicates rectobestibular fistula – most common type of imperforate anus in females Surgery 1-2 years old MALE May have low or high lesion Watch for meconium from fistula Immediate surgery – colostomy til 1-2 then it will be removed
- 3. SUGAR GUIDELINES If infant sick- avoid enternal feedings Peripheral iv 24 gauge iv cath. 23-25 gauge butterfly needle Back of hand Start distal to proximal IV INFILTRATION Monitor site closely for swelling and redness-infiltration, phlebitis Document hourly -appearance of iv -amount of fluid infused Preparation of Extrauterine life -In utero, fetus relies primarily on placental transfer of glucose and nutrients from mother to meet energy demands -fetal glucose values are approximate 70-80% of maternal value After birth -Gycogen stores Ezymes activate breakdown of glycogen back into glucose moleculres Inadequate Glycogen Stores High Risk Infants -preterm -small for gestational age with asymmetric and symmetric growth -risk for hypogycemia in term SGA infants - Markedly risk for preterm SGA infants Late Preterm Infant 34-36 completed weeks gestation Metabolically and physiologically immature Increased risk fo r: Hypoglycemia Feeding problems Temperature Respiratiory distress, apnea Hyperbilirubinemia Increased hospital readmission 3 fold higher mortality rate SGA
- 4. Birthweight <10 percentile for gestational age Causes of SGA or intrauterine growth restriction -Fetal factors chromosomal genetic, syndromes, metabolic disorders, intrauterine viral infections(CMV, Herpes) Maternal factors -nutrition, chronic illness, uterine, placental, drug/ toxin abuse, prescribed medications, genetic/familial, chronic stress A chronically stressed fetus uses most of all of placentally transferred glucose for growth and survival HYPERINSULINEMIA Infant of diabetic mother (IDM) Eleveated maternal glucose levels- glucose crosses placenta- increased fetal insuline production and release After umbilical cord cut-insulin level remains elevated-bood Macrosomic infants-increased risk for birth complications -shoulder dystocia Brachial plexus injury -arm and clavicle factures -organ injury -perinatal asphyxia INCREASED GLUOCSE UTILIZATION SICK INFANTS -infection -birht stress Hypoxia-anaerobic glycolysis Shock-anaerobic glycolysis Respiratory disease Cardiac disease Hypothermia Limited stores are rapidly depleted -preterm -SGA GLUCOSE MONITORING Gold standard for monitoring levels are bedside testing Whole blood glucose bedside test-estimates plasma glucose level May be 10-18%lower than plasma level Signs/symptoms General findings Abnormal cryin
- 5. Poor feeding( poor suck and coordination Hypothermia Neurologic sings Tremors Jitteriness Irritability Hypotonia Lethargy Seizures Cardiorespiratory signs Tachypnea Respiratory distress Apnea Cyanosis Glucose levels 50-110 INITIAL IV FLUID and Rate Glucose utilization rate in fasting healthy term infant=4-6 mg/kg/min D10w w/o electorlytes 80ml/kg/day delivers a glucoses dose of 5.5 mg kg/ min D10W 80 ml/kg/day 5.5 mg/kg/min D10W 60 ml/kg/day 4.2 mg/kg/min D12.5W 60 ml/kg/day BSG <50 mg/dl Establish IV access begin D10 infusion at 80 ml/kg/day Give IV bolus 2ml/kg D10W 1 ml/min Recheck blood glucose 15-30 minutes after bolus Do not give D25 and D 50 bolus Repeat IV bolus- 2ml/kg d10w Increase infusion to 100ml /kg/day Repeat iv bolus – 2ml/kg UVC Indications Emergency IV access for resuscitation fluids and medications
- 6. Unable to establish peripheral IV within reasonable times or attempts When more than one IV line is required To administer glucose concentrations > D12.5W Exchanges transfusion CONTRAINDICATIONS Omphalitis, peritonitis, omphaleocele, necrotizing IO If unable to establish IV access, consider IO route. Inserted into medical aspect of tibial bone, just below tibial tuberosity Needle positioned into bone marrow access to central circulation May be used in an emergency for : Medications, blood products and fluids UVC Cath size 1.5 kg 3.5 fr Over 1.5-5 fr UAC Indications Continuously monitoring arterial blood pressure Monitor arterial blood gases Contraindications Medications via. UC UVC If tip is proper position can use for all medications, includining vasopressors and blood admin. UAC Avoid using or medication for blood administration Never infuse VP through arterial line UVC location Tip in inferior vena cava Above diaphragm- at right atrial (RA) junction- variable thoratic locatin for each baby Low placement For emergency use only Insert 2-4 cm until blood return Non pulsatibel flow in low position-flush after medications Tip IN HEART
- 7. Risk for arrhythmias, thrombus formation, perforation, tamponade, emboli, endocarditis TIP in liver Risk for necrosis, portal hypertension, peritoneal perforation, intestinal HEPARINE SAFETY Added to central line to help prevent thrombus formation Use commercially prepared fluid containing heparin whenever possible Dose= 0.5 to 1 unit of heparin ‘ UAC SAFETY Use caution with speed of drawing and returning and flushing fluid Use transducer to evaluate wave form from blood pressure monitoring SUGAR KEY POINTS Avoid enternal feedings (PO or NG) in sick infants TEMPERATURE Maintenance of normal body temperature is a priority for ALL infants Routine care activities which conserve infants body heat include Removing wet linens Bundling in warm blankets Placing skin to skin on mothers chest Covering head with a hat Dressing in clothes In sick preterm infants , aim at resuscitation and stabilization can place an infant at risk for hypothermia Being undressed Wet kin , linens Cool room temperature Invasive procedures Cold bed, hands, equipment Normal core temp. 97.7-99.5 Definitions of hypothermia Mild- 96.6-96.8 Moderate- 96.6-89.6
- 8. Severe- 89.6 <95 if less than 1000 g Most at risk Preterm /LBW SGA Prolonged resuscitation Acutely ill-spesis Open abdominal and body defects Hypotonia from sedatives, analgesics, paralytics or anestetics COLD STRESS Cold receptors in skin transmit signals to hypothalamus Norepinephrine released Vasoconstriction and brown fat metabolism Brown fat metabolism Purpose heat production Brown fat 2-7% of total body weigh at term Norepinephrine- triggers brown fat metabolism Generates heat when burned or metabolized Term infants muscles activity and flexion Flexion of arms and legs surface area for heat loss increased risk for hypothermia preterm infants most at risk HEAT LOSS Occurs on a gradient from a warmer to cooler Babys warm body to cooler air or surgaces Heat loss accentuated when there is more than one mechanism of heat loss present Prevention Chemical mattress- Transradiate warmer (4 hour timeframe) Cold O2 blown at face Cold O2 inhalved Use warm humidified oxygen HEAT GAIN Secure temp probe on right upper quadrant of abdomen Therapeutic/ neuroprotective hypothermia for treatment of hypoic ischemic encephalopathy
- 9. Unitentional / accidental hypothermia and rewarming guidelines ACUTE PERINATAL EVENTS Impaired placental – fetal perfusion Causes- PA, uterine rupture, prolapsed/ cord ruptured maternal collapse, CPR Results in decreased fetal cardiac output HYPOXIC ISCHEMIC ENCEPHALOPATHY 3-5 per 1000 births Neurologic impacts : cerebral palsey , cognative development delay Canidates Start within 6 hours of birth >36 weeks of gestation >1800 grams ABG ph<7.0 or base deficit >16 Abnormal neurological exam AIRWAY Respiratory distress- most common reason for referral to intensive care nursery Deciding best method to support breathing and when to support is often challenging Determining reason for respiratory distress begins with information gathering -maternal and infant history Presenting signs and timing Physical exam Lab and xray evaluation Respiratory failure can occur rapidly Prevention- provide an appropriate level of support Support ranges from nasal cannula to positive pressure ventilation