Common Complications in the Neonate

Transcription

1 Common Complications in the Neonate Loy Maslen, MSN, RN, NNP-BC, CPHM Perinatal CNS UW/Valley Medical Center March

2 Learning Objectives Define neonatal hypo/hyperthermia and recognize symptoms Discuss importance of preventing hypo/hyperthermia List interventions to maintain thermoneutrality Recognize risk factors for hypoglycemia Discuss physiology of hypoglycemia Review interventions for prevention and treatment of hypoglycemia List risk assessments in the late preterm and term infant Review hyperbilirubinemia causes and risk Discuss common treatments of jaundice in the newborn 2

3 Thermoregulation 3

4 Why Worry About Thermoregulation? Body temperature is one of the primary vital signs. In terms of ABC s think: A - Airway B - Breathing C - Circulation D - Degrees 4

5 Goal of Thermoregulation Maintain correct body temperature range in order to: maximize metabolic efficiency reduce oxygen use protect enzyme function reduce calorie expenditure 5**

6 Challenges of Thermoregulation in Neonatal Care Prior to delivery infants do not maintain temperature independently Infant s in-utero temp is generally 0.5 C higher than mother s temp Rapid cooling occurs after delivery 6

7 Transitional Adaptation: Thermoregulation Maintenance of body temp is a major task Skin is thin & blood vessels are close to the surface Have little subcutaneous fat to serve as barrier to heat loss Term infants have 3x the surface to body mass of an adult Preterm infants, SGA and IUGR infants have 4x the surface mass to body mass of an adult Preterm infants are especially susceptible to heat loss due to poor tone, fat and thinner skin than term infants 7

8 Heat Production The hypothalamus is the central regulating mechanism The hypothalamus can alter heat production and respond to temp changes by altering metabolism, motor tone, activity, vasomotor activity, and sweating to produce heat loss or gain 8

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10 Thermogenesis The sympathetic nervous system activates heat production in response to cold stress The process of non-shivering thermogenesis, or brown fat metabolism is the most important means of heat production in the neonate 10

11 Brown Fat Located around the great vessels, kidneys, adrenals, axilla, nape of the neck, and between the scapula 2-7% of the total body wt. in the term newborn Present at wks. gestation, stores will cont. to increase until 3-5 wks. post-delivery unless depleted Reduced supply in VLBW (less than 1500 g) and ELBW (less than 1000 g) and IUGR infants Cannot be replaced if used Metabolically very active due to cell size, cell number, and the internal mitochondrial structure 11

12 Brown Fat Metabolism Initiated by stimulation of thermal receptors, primarily in the face Controlled by the sympathetic nervous system norepinephrine stimulates the burning of brown fat triglycerides nonesterified free fatty acids and glycerol Thermogenic process of hydrolysis of the brown fat will require O2 and glucose O2 demand may result in hypoxia, acidosis, pulmonary vasoconstriction, and death Hypoglycemia can occur secondary to rapid consumption of CHO stores Heat will reach the skin by direct conduction through the body tissues or blood vessels 12

13 Heat Generation by Oxidative metabolism Glucose Fats Protein Cold Stress Metabolic Energy Needed Brain Heart Adrenal Gland 13

14 What Happens Next? Conversion of brown fat uses: Oxygen and glucose Infant will become hypoxic Infant will become hypoglycemic Infant will become acidotic Growth is affected Weight loss Diminished growth 14

15 Definitions To understand thermoregulation, we need to know some definitions 15

16 Neutral Thermal Temperature A neutral thermal temperature is the body temperature at which an individual's oxygen use and energy expenditure are minimized Minimal metabolic rate Minimal oxygen consumption 16

17 Temperature in the Newborn Infant Classification of hypothermia is based on core temperature NORMAL 36.5 to 37.5 C ( F) Cold Stress 36.0 to 36.4 C ( F) Cause for concern Moderate hypothermia C ( F) Danger, warm infant Severe hypothermia below 32 C (89.6 F) Outlook grave, skilled care urgently needed 17**

18 Thermoneutrality When the air temperature is in the correct range and the infant s body maintains a neutral thermal temperature, we have achieved thermoneutrality 18

19 Neutral Thermal Environment An environment created by any method or apparatus to maintain the normal body temperature to minimize oxygen consumption and caloric expenditure Isolette/Versolette/Giraffe/Omnibed Radiant warmer 19

20 Insensible Water Loss Amount of fluid lost on a daily basis from the lungs, skin, respiratory tract, and water excreted in the feces Transepidermal water loss (TEWL)-quantity of water that passes from inside a body through epidermal layer (skin) to the surrounding atmosphere via diffusion and evaporation 20**

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23 Why Are Infants At Greater Risk for Thermoregulation Problems? 23

24 Mechanisms of Heat Loss Convection. The loss of heat from the newborn's skin to the surrounding air. Newborns lose a lot of heat by convection when exposed to cold air or draughts Conduction. The loss of heat when the newborn lies on a cold surface. Newborns lose heat by conduction when placed naked on a cold table, weighing scale or are wrapped in a cold blanket or towel Evaporation. The loss of heat from a newborn's wet skin to the surrounding air. Newborns lose heat by evaporation after delivery or after a bath. Even a newborn in a wet diaper can lose heat by evaporation Radiation. The loss of heat from a newborn s skin to distant objects, such as a cold window or wall 24**

25 Thermoregulation Risk Factors Preterm SGA/IUGR Neurologic problems Endocrine issues Cardiac /Respiratory problems Large open areas in the skin Sedated Infants Drug exposure Asphyxia Hypoglycemia 25**

26 Risk Factors for Preterm/SGA/IUGR Infants Less brown fat and glycogen stores Decreased ability to maintain flexion Increased body surface area compared to weight Frequent respiratory distress Increased IWL 26

27 Hypothermia Signs/symptoms Cool to touch Central cyanosis Acrocyanosis Poor feeding Abd Distention Apnea Increased gastric residual Bradycardia Tachypnea Restlessness Shallow and irregular resp rate Mottling Decreased activity Lethargy Irritability Diminished or absent reflexes Hypotonia Feeble cry Weak suck CNS depression Hypoglycemia Edema 27**

28 Prevention of Hypothermia Reduction of heat loss Consider the four ways by which the neonate experiences heat loss and intervene appropriately 28

29 Strategies to Prevent Heat Loss: CONVECTIVE HEAT LOSS can be prevented by: Providing warm ambient air temperature Placing infants less than 1500 grams in temperature controlled beds Keeping portholes of the isolette closed Warming all inspired oxygen On open warmers keeping sides up and covering infant if possible (Giraffe Omnibed) Using Infant Servo Temperature Control 29

30 Strategies to Prevent Heat Loss: RADIANT HEAT LOSS can be prevented by: Avoiding placement of beds near cold windows, walls, air conditioners, etc. Placing a knit hat on the infant s head Wrapping tiny babies in saran or bubble wrap Clothing the infant Developmental position devices Increase humidity environmental temperature 30

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33 Strategies to Prevent Heat Loss: CONDUCTIVE HEAT LOSS can be prevented by: Placing a warm diaper or blanket between the neonate and cold surfaces Placing infant on bed at time of delivery Warming all objects that come in contact with the neonate Admitting infant to a pre-warmed bed Skin-to-skin contact Bair Paws warming gown for mom and skin-to-skin in surgical delivery room 33

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35 Strategies to Prevent Heat Loss: EVAPORATIVE HEAT LOSS can be prevented by: Keeping the neonate and his/her environment dry Drying the baby immediately after delivery Placing preterm or SGA infant in occlusive wrap/bag at delivery/pass through windows Delay bath (unless maternal positivity for blood borne illness) 35**

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37 Interventions for at Risk Infants Pre-warmed bed/scales Do not leave bed on manual mode Servo mode allows the baby to control the heat output of the warmer units Chemical warming mattress Warm and humidify inspired gases Occlusive wrap/bag at delivery/pass through windows Minimal handling Developmental positioning 37

38 Interventions for at Risk Infants Open isolette portholes and doors only when necessary Blanket over bed Cluster care Use servo control Monitor closely when using warming lights 38

39 Avoidance of Hypothermia Avoid stressing the baby Monitor skin temperature carefully and when it normalizes remove the external heat sources one at a time to prevent rebound hypothermia 39

40 Baby Radiation Conduction Convection Evaporation Cold Room Temp. Cold Scale Bed Near Air Vent Wet Diaper Cold Walls Cold X-ray plates Oxygen left on Bath Cold Items on Bed Cold Blankets Passing Traffic Tachypnea 40

41 Hyperthermia 41

42 Hyperthermia HYPERTHERMIA also has negative consequences for the neonate Defined as a rectal/axillary temperature greater than 37.5⁰C (99.5⁰F) 42

43 Risk factors for Hyperthermia Excessive environmental temp Sepsis Dehydration Alterations in the hypothalamic control mechanism Birth Trauma Hypoxemia Anomalies Drugs 43

44 Signs of Hyperthermia Apnea Tachycardia Flushing Hypotension Tachypnea Irritability Poor Feeding Skin Temp > Core Temp 44

45 Consequences of Hyperthermia in Metabolic rate oxygen consumption Dehydration from insensible water loss Peripheral vasodilatation/ hypotension Fluid, electrolyte abnormalities Seizures 45

46 Skin Servo Control If the temperature probe is placed over brown fat deposit areas, the probe will be reading a core body temperature and not a skin temperature As the core temperature will be higher than the skin temp., the warming device will cool the environment The infant will then need to burn fat and calories to stay warm 46

47 Temperature Probe Placement Secure the temperature probe at/or about the costal margin of the chest, midway between the xiphoid and the navel. This placement should assure accurate skin temperature measurement Never lay infants on the probe, as this will also cause a falsely high temperature to be registered 47

48 Skin Temperature Probes Do Not lay infant on skin probe Do not place over: Bony prominences Areas of brown fat deposits Poorly vascularized areas Excoriated areas Keep probe exposed to heat source Keep probe securely attached Change position frequently to prevent skin breakdown 48

49 Post Prandial Coma K_5bT8z0 49

50 HYPOGLYCEMIA 50

51 Definition The S.T.A.B.L.E. Program defines hypoglycemia as: Glucose delivery or availability is inadequate to meet glucose demand 51

52 Normal Blood Glucose Defining a normal glucose level remains controversial mg/dl (Karlsen, 2006 and CCQCI 2011) > 40 mg/dl (Verklan & Walden, 2011) > 30 term, > 20 preterm (Kenner & Lott, 2004) > 45 mg/dl (AAP 2009) 52

53 Growth Charts Lubchenko vs. Olsen Chart 42% of SGA infants actually normal 27% of LGA infants actually normal We have been risking our babies based on faulty data This problem has also skewed our blood glucose data 53

54 AAP Position Statement There has been no substantial evidence-based progress in defining what constitutes clinically important [neonatal hypoglycemia (NH)], particularly regarding how it relates to brain injury, and that monitoring for, preventing, and treating NH remain largely empirical Blood glucose concentrations often dip to 30 mg/dl within 1 to 2 hours after birth in healthy neonates, but they typically return to more than 45 mg/dl with normal feeding within 12 hours 54

55 Incidence of Hypoglycemia Overall Incidence = 1-5/1000 live births Normal newborns 10% if feeding is delayed for 3-6 hours after birth At-Risk Infants LGA 8% Preterm 15% SGA 15% IDM 20% 55

56 Why is Hypoglycemia a Problem? Glucose is the primary fuel for the brain The brain needs a steady supply of glucose to function normally Glucose is the fetus only source of carbohydrate 56

57 Glucose Utilization in Neonates Compared with adults, infants have a higher brain to body weight ratio, resulting in higher glucose demand in relation to glucose production capacity Cerebral glucose utilization accounts for 90% of the neonate s glucose consumption 57

58 Glycogen Storage Fetal plasma glucose is 60 80% of the maternal glucose level The fetus stores glucose in the form of glycogen (liver, heart, lung, and skeletal muscle) Most of the glycogen is made and stored in the last month of the 3rd trimester 58

59 Glucose Transition to Extrauterine Life The fetus has limited ability to convert glycogen to glucose and must rely upon placental transfer of glucose to meet energy needs When the infant is born, the cord is cut and so is the major supply of glucose! 59

60 Being Born is Hard Work! The transition from fetus to newborn creates a significant energy drain on the newborn The newborn is now required to meet increased metabolic demands while changing the energy source from a placenta-supplied source to an external food source 60

61 Infants at Greatest Risk < 37 weeks gestation Infant of a diabetic mother Small for gestational age Large for gestational age IUGR and Post Term Exposure to certain medications Beta-sympathomimetics Beta-Blockers Chlorpropamide-used in diabetic mothers Benzothiazide diuretics Tricyclic antidepressents in the 3 rd trimester Stressed/ill infants 61**

62 Negative Glucose Effects Inadequate Glycogen Increased Utilization of Glucose Excessive Insulin 62

63 Inadequate Glycogen Glycogen stores increase rapidly in the last month of the 3 rd trimester Preterm infants are born before this occurs. What little glycogen is available is used up rapidly and their supply is depleted 63

64 Glycogen Depletion SGA: Birth weight < 10 percentile. Chronically stressed infants have higher metabolic demands and use up available glucose for growth and survival Markedly post-mature infants are at increased risk due to increased metabolic demand 64

65 Increased Glucose Utilization Sick/Stressed infants Causes increase in metabolic demand Uses up glucose quickly These include all sick, premature and SGA and IUGR infants 65

66 Excessive Insulin Levels Infants of Diabetic Mothers Many consequences for the neonate Single most important factor in determining the outcome for the infant is maternal glucose control 66

67 Birth injury is doubled C/S is tripled IDM Risks NICU admission is quadrupled Stillbirth is x 5 greater Congenital anomalies are x 2 5 greater Diabetes incidence is rapidly increasing due to obesity epidemic 67

68 Symptoms of Hypoglycemia Jitteriness Irritability Hypotonia Lethargy High-pitched cry Hypothermia Poor peripheral Perfusion CHF Poor suck/poor feeding Tachypnea Cyanosis Apnea Seizures Cardiac arrest Vomiting Pallor 68

69 Nursing Management Complete evaluation and review of systems Early breast feeding within minutes of birth Glucose monitoring within 2 hours Monitor pre-feeding glucose levels Hypoglycemia in the first few days after birth is defined as blood glucose <40 mg/dl (currently) Decrease infant metabolic needs Skin-to-skin Maintain thermostability 69

70 Persistent Hypoglycemia or Unable to Feed Establish IV access quickly Peripheral IV UVC Provide glucose: (5-8 mg/kg/minute) (100 ml/kg/day=7mg/kg/minute) Note: Less for LBW/ELBW Primary fuel Infant brain needs a steady supply to function Target glucose to at least 50 mg/dl is ideal 70

71 Prevention Increase awareness of conditions that predispose an infant to hypoglycemia Early screening of at-risk infants Early and frequent feedings Maintain temperature Monitor infant for signs and symptoms 71

72 Term and Late Preterm Preterm: <37 completed weeks Late preterm: 34 to 36 weeks 72

73 Concerns With Early Delivery Hypothermia Hypoglycemia Jaundice Respiratory distress Airleak TTNB RDS Sepsis Increased morbidity and mortality Disrupted parental bonding Increased LOS Increased cost 73

74 Rehospitalization During the first month after birth, latepreterm infants are more likely than term infants to be re-hospitalized for: Jaundice Feeding difficulties Dehydration Failure to thrive Suspected sepsis 74**

75 Quality Intervention Hard stop on non-medically indicated elective inductions Bishop s score greater than or equal to 9 Decrease C-Sect rate Decrease deliveries of convenience 75**

76 Medical Indications for Early Delivery Preeclampsia, eclampsia, gestational hypertension, or complicated chronic hypertension Oligohydramnios Prior classical cesarean delivery/prior myomectomy Placenta previa/ accreta Multiple gestations Fetal growth restriction controlled Placental abruption Chorioamnionitis P-PROM Pregestational diabetes with vascular disease Pregestational/gestational diabetes poorly controlled Cholestasis of pregnancy Alloimmunization of pregnancy with known or suspected fetal effects Fetal congenital malformation 76**

77 Jaundice 77

78 Big Yellow Picture Most newborn infants experience some degree of jaundice Most jaundice is benign, but because of the potential for bilirubin toxicity, newborn infants must be monitored to identify those at risk for excessive hyperbilirubinemia, treated appropriately and followed-up by experienced perinatal health care professionals 78

79 Definitions Hyperbilirubinemia is an increase in the serum bilirubin characterized by jaundice Bilirubin Unconjugated (indirect acting) Conjugated (direct acting) Jaundice is a yellowish discoloration of the skin, sclera and mucous membranes Rarely perceptible until the serum bilirubin level exceeds 7.0 mg/dl Acute Bilirubin Encephalopathy: Clinical nervous system findings caused by bilirubin toxicity Kernicterus: Chronic, permanent clinical sequelae of bilirubin toxicity 79

80 Incidence Term babies: 50%-60% Preterm babies: 80% Physiologic Most Common Pathologic Requires investigation Prevent bilirubin encepholopathy 80

81 Physiologic Jaundice Occurs in newborns due to: Higher concentration of RBCs Shorter life span of RBCs Exacerbated by decreased intake Not associated with underlying disease Breast milk jaundice is benign Relatively low conversion of bilirubin to urobilinogen by the intestinal flora, resulting in relatively high absorption of bilirubin back into the circulation Bilirubin level 15 mg/dl or less 81

82 Investigate: Pathologic Jaundice Jaundice occurring within first 24 hours of life Rapidly increasing greater than 5 mg/dl in 24 hours Clay colored stools Total bilirubin more than 19.5 mg/dl Direct bilirubin more than 2.0 mg/dl Persisting Greater than 2 weeks in full term Greater than 3 weeks in preterm 82

83 Transcutaneous Bilirubin The early discharge of neonates from hospitals makes transcutaneous measurement of total bilirubin concentration a useful tool to monitor neonatal jaundice High degree of correlation between cutaneous bilirubin and TSB is the basis of transcutaneous bilirubinometry 83

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85 Direct Serum Bilirubin Before reaching the liver, bilirubin is called unconjugated Bilirubin combines with certain sugars to create a water-soluble form called conjugated bilirubin (direct/conjugated) bilirubin Conjugated bilirubin passes out of the liver, and into the colon, it is converted back into the unconjugated form en route to being excreted from the body 85

86 Indirect Bilirubin Most laboratories use a test that detects conjugated bilirubin, which is called direct By subtracting the direct bilirubin from the amount of total bilirubin, an estimate of unconjugated bilirubin, called indirect, is obtained. 86

87 Bilirubin Metabolism As red blood cells are lysed, they release hemoglobin Heme molecules (from hemoglobin) are converted to bilirubin Bilirubin (unconjugated or indirect) is bound to serum albumin Transferred to the liver where it is conjugated to glucuronate by glucuronyl transferase Conjugated (direct) bilirubin is excreted into bile A fraction of bilirubin from the stool is reabsorbed into the blood via the portal circulation (enterohepatic circulation) 87

88 Risk Factors Maternal Blood type ABO or Rh incompatibility Breastfeeding Drugs: diazepam or oxytocin Ethnicity: Asian, Native American Maternal illness: Diabetes Neonatal Birth trauma Drugs Excessive weight loss Infections: TORCH Infrequent feedings Male Polycythemia Prematurity Sibling with bili 88**

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90 CAUSES OF INDIRECT (UNCONJUGATED) HYPERBILIRUBINEMIA 90

91 Increased Lysis of RBCs Isoimmunization (blood group incompatibility: Rh, ABO and minor blood groups) RBC enzyme defects (e.g., G6PD deficiency, pyruvate kinase deficiency) Infection (sepsis, urinary tract infections) RBC structural abnormalities (hereditary spherocytosis, elliptocytosis) Sequestered blood (e.g., cephalohematoma, bruising, intracranial hemorrhage) Polycythemia Shortened life span of fetal RBCs (80 vs. 120 d) 91

92 Decreased Hepatic Uptake Immature glucuronyl transferase activity in all newborns Gilbert Syndrome Crigler Najjar Syndrome Pyloric stenosis Hypothyroidism Infants of Diabetic Mothers Breastmilk Jaundice (pregnanediol inhibits glucuronyl transferase activity) Increased Enterohepatic Reabsorption Breast feeding jaundice (due to dehydration from inadequate milk supply) Bowel obstruction No enteric feedings 92**

93 CONJUGATED (DIRECT) HYPERBILIRUBINEMIA (CHOLESTASIS) 93

94 Hepatitis: Hepatocellular Disease Neonatal idiopathic hepatitis Viral (Hepatitis B, C, TORCH infections) Bacterial (E. coli, urinary tract infections) TPN Hepatic ischemia Erythroblastosis fetalis (late, Inspissated Bile Syndrome ) **

95 Most Common Metabolic Disorders Alpha-1 antitrypsin deficiency Galactosemia Tyrosinemia Fructosemia Glycogen storage disorders Cerebrohepatorenal disease (Zellweger) Cystic fibrosis Hypopituitarism 95**

96 Biliary Tree Abnormalities Extrahepatic biliary atresia: In first 2 weeks, unconjugated bilirubin Paucity of bile ducts (Alagille s vs. nonsyndromic) Choleduchal cyst Bile plug syndrome 96**

97 BILIRUBIN ENCEPHALOPATHY Mildest form causes sensorineural hearing loss due to damage to the cochlear nuclei Severe encephalopathy causes kernicterus When bilirubin concentration exceeds the binding capacity of serum albumin Displacement of bilirubin from albumin by acidosis or certain drugs (e.g.,sulfonamides, ceftriaxone) Sepsis Preterm infants at risk due lower serum albumin concentrations and risk for acidosis and sepsis 97

98 Kernicterus Early stage: Extreme jaundice, diminished or absent startle reflex, poor feeding, profound sleepiness and lethargy Moderate stage: High pitched cry, arched back with neck hyperextended backwards, bulging fontanels and seizures Late stage: (full neurological syndrome): High frequency hearing loss, intellectual disability, muscle rigidity, speech difficulties, seizures and movement disorders 98

99 Phototherapy Phototherapy employs blue wavelengths of light to alter unconjugated bilirubin in the skin The bilirubin is converted to less toxic watersoluble photoisomers Excreted in the bile and urine without conjugation Decision to initiate phototherapy is based on the newborn's age and total serum bili level 99**

100 Bili Lights neoblue lights: Low setting=single phototherapy, High setting=double phototherapy Bilibed: Low setting=single phototherapy, High setting=double phototherapy Biliblanket: Good to use with breastfeeding rooming in mothers as it is less disturbing to families if only single phototherapy is ordered Spotlight: Least preferred therapy, use only if other methods are unavailable, as lights do get hot, so temperature monitoring and measured distance from infant is very important. Low setting=single phototherapy, high setting=double phototherapy 100

101 Bili Lights Low intensity irradiance - Light from conventional or single phototherapy. High intensity irradiance Light from intensive or double phototherapy with an irradiance of at least 30 µw/cm²/nm. It is acceptable to use any combination of lights or a bili bed to achieve triple or quadruple therapy if ordered Consult your LIP if you are unsure what would work best for your patient 101

102 Nursing Care Mitigate water loss Cover infants eyes and genital area Maximal skin exposure Monitor temperature Parent education Inspect eyes with care Protect and monitor skin Positioning 102

103 Equipment Overhead Phototherapy light-spot light, or neoblue lights Isolette, radiant warmer, or crib Eye patch kit Skin barrier prep Phototherapy light meter Tape Measure 103

104 Conclusions Hypothermia in the newborn is due more to a lack of knowledge than to lack of equipment. Hypothermia is a preventable condition that has well documented impact on morbidity and mortality. Therefore, assisting the infant to maintain a normal body temperature and preventing hypothermia during stabilization is critical 104

105 Conclusions Maternal and birth history is useful in determining infants at risk for hypoglycemia Monitor baby for signs and symptoms of hypoglycemia Know your hospital s policy for screening and timing of interventions 105

106 Conclusions Move toward minimizing elective inductions of late preterm infants Follow quality guidelines for medical indications for delivery Review the infant s risk factors and assess for rapidly changing conditions Recognize signs and symptoms of distress in the newborn 106

107 Conclusions Review maternal and birth history for risk factors for jaundice Observe infant for signs and symptoms of jaundice Use TcB to assist with monitoring bili levels Discover your hospital s equipment and hyperbilirubin procedures 107

108 Questions? Thank You THE END 108