- Email: [email protected]
Neonatal Hypoglycemia
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d
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Principles and practice Neonatal Hypoglycemia DOUGLAS FANTAZIA, RNC, BSN The pathophysiologic status of the neonate contributing to susceptibility for hypoglycemia is reviewed as a knowledge base for specific nursing practice. Three independent nursing actions are identified: assessment of risk factors, manipulation of factors promoting energy homeostasis, and validation of nursing practice.
T h e fetus receives a continuous supply of glucose throughout gestation via maternal-placental exchange by facilitated diffusion. This abundant supply is used as the main energy fuel of the fetus and is hoarded away in tissue glycogen stores to provide metabolic fuel for when the infant is separated from its placental source at birth. 1-4 T h e tremendous anabolism of the fetus accounts for its continuous energy needs even though many homeostatic functions are fulfilled by maternal metabolism. Gluconeogenesis, the manufacture of glucose from nonglucose precursors, may occur in utero from lactate and possibly other substrates to supplement the continuous placental supply. Gluconeogenesis is definitely active immediately after birth, primarily by hepatic cells when placental supply is no longer available. Conversion of amino acids to glucose is unlikely in the fetus as proteins are used mainly for growth rather than energy sources. Experimental evidence in neonatal animals suggests that protein utilization for fuel energy is possible, although much slower and less efficient than in Submitted: March 1983. Accepted with revisions: June 1983.
September/October 1984 JOCN Nursing
adults. Furthermore, neither fatty acids nor ketones appear to be significant energy sources in utero. Glucose is stored as glycogen beginning very early in gestation. The early storage site is within placental tissue; the primary site is then switched at approximately 20 to 24 weeks to hepatic storage. T h e fetal cardiac and skeletal muscle tissue also gradually accumulate glycogen as pregnancy progresses. At term, fetal glycogen stores in the liver are approximately twice those of an adult and almost ten times those of an adult in cardiac tissue. These large energy reserves are accumulated to sustain the infant through the transitional period following birth when the continuous placental supply of glucose ceases and metabolic pathways switch to fat as their principal fuel s o ~ r c e . l - ~ ’ ~ Birth initiates a major change in the infant’s energy metabolism as well as the more familiar cardio-respiratory transition. T h e work of establishing respirations, increased muscular activity, and the need to maintain thermoregulation in an all too often adverse environment contribute to a sudden demand for high metabolic energy. At the same time, the placental glucose infusion 1335.-7
has been cut off abruptly. These demands are great enough that, even in a healthy, full-term infant, up to 90% of the hepatic glycogen stores may be consumed by the end of the third hour following birth. Characteristically, blood sugar falls rapidly during the first few hours of life, stabilizing at about six hours of A controversy exists in the literature regarding the normal nadir value for blood sugar during these early hours of life.1*2,5,s-’1 Unanimously, there is agreement that too low blood sugar may compromise central nervous system function. Arguments for defining neonatal hypoglycemia as below 40 mg per 100 ml are eloquently outlined by Klaus and Fanaroff.‘ T h e human brain holds the dubious distinction of being the primary organ with limited capability of deriving energy from free fatty acids, and, thus, has a n obligatory glucose requirement.’ Immediately after birth, this glucose supply must come from glycogen stores. In healthy newborns, the glycogenolysis from hepatic stores proceeds at a production rate of 5 to 8 mg glucose per kg of body weight per minute. This rate of production has, in fact, been shown to correlate directly with brain eight.',^-^
297
Table 1. Etiologic Classification of Neonatal Hypoglycemia
Condition
Probable Biochemical Mechanism Inadequate glycogen stores
1. Premature AGA infants 2. SGA or intrauterine growth retardation 3. Perinatal stresslasphyxia
1. Decreased glycogen stores 2. Decreased glycogen stores and increased utilization 3. Increased utilization and inefficient (anaerobic) utilization 4. Elevation of free fatty acids 5. Increased metabolic consumption 6. Specific enzymatic deficiency
4. Cold-stressed infants 5. Sepsis
6. Glycogen storage disease
Hyperinsulinism 1. Infant of diabetic mother
1. Prolonged intrauterine islet cell
2. RH incompatibility
3. After exchange transfusion with acid citrate dextrose or citrate phosphate dextrose preserved blood 4. Beckwith-Wiedemann syndrome 5. Nesidioblastosis and islet cell adenomas 6. Maternal chlomropamide therapy
The etiology of hypoglycemia is reasonably discussed in terms of two general categories of inadequate stores or hyperinsulinism (Table After birth, the blood sugar reflects principally two balancing processes: the rate of endogenous hepatic release of glucose for gly-
stimulation 2. Increased glutathione released from hemolysis may stimulate insulin release 3. High glucose load results in hyperreactive insulin response
4. Islet cell hyperplasia
5. Adenoma or adenomatosis 6. Fetal betacell stimulation
cogenolysis and the rate of glucose ' Although an increased rate of glucose disposal or removal from the blood may exist without hyperinsulinemia, insulin represents the major factor influencing glucose utilization. Insulin production appears in the fetus at
induced
fuel source
\ \Neonatal
5-
J.
hypoglycemia
Figure 1. Stress as contributor toward neonatal hypoglycemia.
298
Ineffective mobilization of glycogen stores
approximately 12 weeks gestation. Its release, however, does not appear to be in response to glucose but rather, perhaps, to amino acid levels.1*3*4In response to stress, the neonate and adult alike increase their catecholamine secretion. In the adult, this can lead to el'evation of the blood sugar by inducing glycogenolysis, the sequential degradation of glycogen to glucose. The neonate's catecholamines differ from the adult's in their great preponderance of norepinephrine. Norepinephrine minimally induces glycogenolysis and catecholamine secretion leads to elevation of serum-free fatty acids (FFA). Elevation of free fatty acids causes a fall in serum glucose as a result of the reciprocal relationship between these two s ~ b s t a n c e s . ' ~ ~ ~ ~ ~ ' ~ ~ ~ " This chain of events renders the neonate less tolerant of any stress since catecholamines may increase energy needs while decreasing the most efficient energy sourceplasma glucose (Figure 1). After two to three days, most of the neonate's tissues probably switch to fat as their primary energy fuel. Accordingly, in the first few days of life the majority of neonates are most susceptible to hypoglycemia. Infants subjected to perinatal stress may exceed their stored capacity to maintain blood glucoses. Intrauterine growth-retarded and premature infants may also prove to have inadequate glycogen stores. In these and other situations, hepatic glucose production appears incapable of equaling glucose utilization. Infants of diabetic mothers and erythroblastotic newborns are two examples of hypoglycemia caused from hyperinsulinism. Here, hypoglycemia results from excessive glucose disposal. Manifestations of neonatal hypoglycemia include a host of nonspecific signs, making the differential diagnosis extremely difficult and requiring laboratory confirmation (Table 2). Signs include ab-
September/October 1984 JOGN Nursing
normal or weak cry, apnea, cyanosis, hypothermia, jitteryness, lethargy, poor feeding, and tremors.
Table 2. Appearance of Neonatal Hypoglycemia Cause 1. Infant of diabetic mother
Nursing Implications T h e nurse’s role in the neonatal intensive care unit (NICU) includes responsibility for using the nursing process to formulate a patient care plan providing direction and coordination of maternal-neonatal care. This patient care plan is constructed through synthesis of the nursing goals and all other disciplinary care objectives into a systematic delivery of care. T h e purpose of the NICU nurse is to promote optimum restorative care for the improvement of the outcome of the neonate’s immediate or longterm transition and adaptation to extrauterine life. As an integral part of nursing, the patient care plan assists in attaining this purpose by assuring continuity and integration of all therapeutic measures and by establishing the priority that attention is given to the patient’s nonemergent need^.^*"-'^ Other health-care practitioners, such as respiratory care and social workers, supply the nurse with invaluable data and goals pertinent to their particular specialty area. The nurse then uses this information concomitantly with her broadbased, multisystems education background and assessment skills for the synthesis of a patient care plan. Traditionally, it has been the responsibility of the nurse to evaluate the newborn following birth. Supervision of the infant through the period of autonomic neurologic adjustment and recovery from the delivery process until the infant has stabilized has also been recognized as the responsibility of the nurse. l4-16 These combined responsibilities of assessing and supervising the care of the newborn are most appropriate for the nurse
September/October 1984 JOGN Nursing
2. 3. 4. 5. 6. 7. 8. 9. 10.
Transient neonatal hypoglycemia IUGR/SGA Perinatal stress Prematurity RH incompatibility Glycogen storage disease Maternal antidiabetic therapy Beckwith-Wiedemann syndrome Exchange transfusion Acid citrate dextrose or citrate phosphate dextrose preserved blood Heparin preserved blood
in light of the profound influence that care disturbances and other environmental factors have on neonatal survival and well-being. Some practical implications of this role regarding neonatal hypoglycemia entail at least three identifiable components: 1) T h e nurse should command an adequate knowledge of neonatal glucose metabolism with which to assess an individual infant’s risk of developing hypoglycemia; 2) This assessment provides a foundation for constructing a care plan promoting optimum health development and restoration; 3) Nursing practice must be validated by factual evaluation. T h e degree of monitoring needed to validate one’s assessment and intervention is a judgment that may vary from nurse to nurse for any given patient condition and situation. T h e frequency of monitoring must be consistent with the patient’s assessed risk and community standards for nursing practice. This decision should be made in collaboration with fellow nursing personnel. Assessment of an infant’s risk for developing hypoglycemia should include consideration of the following factors. 1) Perinatal history. Maternal diabetes, maternal chloropropamide therapy, birth asphyxia, cold stress,
Aae of Common Onset
1-4 hours Anytime within first 72 hours 24-72 hours Within 6 hours Variable Within first 24 hours First days or weeks First hours Within 24 hours or up to third day Up to 2-3 hours after completion
During the exchange
maternal fever, and/or chorioamnionitis are historic factors prompting one to anticipate neonatal hypoglycemia. 2) Gestational age. Determination of fetal development is prerequisite to assessing glycogen storage capacity. 3) Hematologac status. Maternalfetal blood incompatibility, polycythemia, and severe neonatal jaundice requiring exchange transfusion may potentiate risk of hypoglycemia. 4) Endocrine1 metabolic status. Conditions increasing metabolic demands, such as increased work of breathing, stress, or sepsis, as well as hyperinsulinemia conditions may deplete glycogen stores rapidly. 5 ) Nutritional status. Any infant whose condition prevents adequate caloric intake is at risk for developing hypoglycemia. Assessment of these and other risk factors should provide a n adequate basis for anticipation of hypoglycemia. However, because hypoglycemia may be asymptomatic and prophylactic, medical measures are often instituted early in highrisk infants and detection may be missed. Considerable variance exists in the literature regarding recommendations for routine screening by Dextrostix.@19295*10 Policy delineating routine Dextrostix
299
screening should be established by nursing and medical directors of each nursery and should allow latitude for checking individual infants when judged prudent by the nurse. Manipulating delivery of care and environmental factors present a very exciting challenge to nurses in the NICU. Therapeutic measures that reduce energy needs may prove to be the most efficacious mode of therapy for transient neonatal hypoglycemia and might even prevent its occurrence.’.’ Many questions remain unanswered in this area, but recent investigations are demonstrating profound effects on maintaining and restoring health in premature infants through simple nursing therapies. T h e use of nonnutritive sucking during gavage feedings, for example, has been reported to increase the neonate’s daily weight gain and lead to earlier bottlefeeding and earlier discharge. ”*l Nonnutritive sucking may also facilitate greater restfulness or lower activity levels, which would enable infants to conserve their energy stores.” Activity can dramatically increase energy requirements, especially in small infants; crying alone can double the infant’s metabolic rate.Ig Establishment and maintenance of a neutral thermal environment also has potent influence on the neonate’s metabo]ism. 1,5J 1,16 careful attention to environmental conditions, physical activity, and organization of care are all integrated in the patient care plan. With few exceptions, high-risk infants should be moved into an incubator. Although most incubators currently used are single wall types in which radiant heat loss cannot be completely controlled, nursing personnel can still effectively manipulate environmental factors, such as location of the incubator in relationship to windows and temperature of oxygen delivered to the baby’s environment. These consid-
300
erations, in concert with planned efforts to minimize disruption of rest and sleep, can significantly influence the infant’s calculated energy requirements. In addition, discrepancies between the infant’s required and received calories should be monitored. Validating the effectiveness of nursing therapeutics poses problems similar to those discussed for routine detection of hypoglycemia. Again, neonatal hypoglycemia may be asymptomatic, and how much monitoring an individual needs in order to make an assessment will vary from person to person and situation to situation. Here, also, recommendations from the literature are almost absent. Since the majority of authors are physicians, most attention has been paid to establishing routine screening for the initial diagnosis of neonatal hypoglycemia rather than data collection evaluating nursing interventions.’’2p’0 Some specific guides written by nurses are found in Avery’s Neonatology. Noteworthy here is the recommendation of obtaining a Dextrostix at least once per shift in infants exhibiting apnea. This recommendation should probably be expanded to include doing a Dextrostix immediately following an episode of apnea at least once in the nurse’s assessment. As pointed out by the American Academy of Pediatrics, keeping an environmental log of events or incidents that could affect the health of the infant is the nurse’s responsibility.I6Nursing assessment of the infant’s environment should in-
Proper function of warmers/isolettes; Degree of humidity and temperature of oxygen delivered either by hood or endotracheal tube; Attention to nursing measures aimed at reducing heat loss, such as immedi-
ate changing of wet diapers to avoid evaporative cooling (also required to ensure an accurate intake and output record); 4) Performing daily weights at consistent times, preferably before a feeding. Only then can monitoring unusual losses or gains as well as the pattern of weight gain be reliable. Complementary to the physician’s search for specific pathology, the nurse must search for and rule out environmental causes of suboptimal recovery or health maintenance. By working in concert, both can achieve a more accurate diagnosis. Conclusion T h e recognition and understanding of neonatal hypoglycemia have presented new challenges to the discipline of nursing. Though a great many questions remain unanswered, nursing interventions and therapeutics can facilitate the infant’s maintenance and recovery of health. More research is needed to define accurately the efficacy of specific nursing manipulations in preventing neonatal hypoglycemia. References 1. Klaus M, Fanaroff A. Care of the high-risk neonate. Philadelphia: WB Saunders, 1979:94-112,22442. 2. Kornes SB. High-risk newborn infants. St. Louis: CV Mosby, 1972:179-86. 3. Dawes GS. Foetal and neonatal physiology: a comparative study of the changes at birth. Chicago: Year Book Medical Publishers, 1968:210-20. 4. Fisher DA. Perinatal insulin, glucagon and carbohydrate metabolism. In: Perinatal endocrinology, a monograph of the eighth Mead Johnson Symposium on Perinatal and Developmental Medicine, 1975:30-8. 5. Avery GB, ed. Neonatology: pathophysiology and management of the newborn. Philadelphia: JB Lippincott, 1981 :48-88, 583-99.
September/October 1984 JOGN Nursing
6. Toew CJ: Metabolic fuel metabolism: metabolic differences between prenatal and postnatal life. In: Fuel metabolism in the fetus and newborn, a monograph of the third Mead Johnson Symposium on Perinatal and Developmental Medicine, 197 3 :3- 12. 7. Drash AL. Carbohydrate and energy metabolism. In: Developmental nutrition. Columbus: Ross Laboratories, 1979: 19-24. 8. Cloherty JP, Stark AR, eds. Manual of neonatal care. Boston: Little, Brown & Co., 1980:257-9. 9. Behrman RE, ed. Neonatal-perinatal medicine. St. Louis: CV Mosby, 1977~712-35. 10. Schreiner RL, ed. Care of the newborn. New York: Raven Press, 1981~69-75. 1 1. Greenberg RE. Glucose homeostasis in the newborn. In: Fuel metabolism in the fetus and newborn, a monograph of the third Mead Johnson Symposium on Perinatal and Developmental Medicine, 1973~9-60.
12. Statement on the scope of highrisk perinatal nursing practice. Kansas City: American Nurses’ Association publication, 1973. 13. Maternal-child health nursing practice. Kansas City: American Nurses’ Association publication, 1973. 14. Toward improving the outcome of pregnancy. Committee on Perinatal Health Recommendations. White Plains: T h e National Foundation-March of Dimes, 1977. 15. Bellig LL. T h e expanded nursing role in the neonatal intensive care unit. Clin Perinatol 1980;7(1): 15972. 16. Standards and recommendations for hospital care of newborn infants. Evanston, IL: American Academy of Pediatrics, the Committee on Fetus and Newborn, 1977. 17. Field T, et al. Nonnutritive sucking during tube feedings: effects on preterm neonates in an intensive care unit. Pediatrics 1982: 70(3):38 1-4.
PRIMARY CARE NURSE PRACTITIONER
18. Measel CP, Anderson GC. Nonnutritive sucking during tube feedings: effect upon clinical course in premature infants. JOGN Nurs 1979;8:265. 19. Czajka-Narins DM, Weil WB. Calories. In: Oliver K, Cox B, Johnson T , Moore W. Developmental nutrition. Columbus: Ross Laboratories. 1979:9-18.
Address for correspondence: Douglas Fantazia, RN, St. Mary’s Hospital, c / o NICU, 235 West 6th Street, Reno, NV 89520.
Mr. Fantazia is a neonatal nurse practitioner at St. Mary’s Hospital in Reno, Nevada. Mr. Fantaziais NCCcertified as a neonatal intensive care nurse and also certified as a respiratory therapy technician.
MEETING
“Practice, Politics and Power,” a national conference sponsored by the Primary Care Nurse Practitioner Interest Group of the California Nurses’ Association, Region 12, is scheduled November 2-3,1984, at the Miyako Westin Hotel in San Francisco, California. Sessions during the conference will include information on nurse practitioner collegiality, third-party reimbursement,aging issues, nutrition, sports injuries, eating disorders, osteoporosis, arthritis, acne, hypertension, working with the disabled, clinical research for the nurse practitioner, and more. Twelve contact hours will be offered. Cost for CNA/ANA members is $135 and indudes two lunches and syllabus materials. For copiesof the conference prospectus and additional information, contact: Golden Gate Nurses’ Association, CNA Region 12, 2601 Mission St., 9th fl., San Francisco, CA 941 10, (415)821-7400.
September/October 1984 JOCN Nursing
30 1
d
*
Principles and practice Neonatal Hypoglycemia DOUGLAS FANTAZIA, RNC, BSN The pathophysiologic status of the neonate contributing to susceptibility for hypoglycemia is reviewed as a knowledge base for specific nursing practice. Three independent nursing actions are identified: assessment of risk factors, manipulation of factors promoting energy homeostasis, and validation of nursing practice.
T h e fetus receives a continuous supply of glucose throughout gestation via maternal-placental exchange by facilitated diffusion. This abundant supply is used as the main energy fuel of the fetus and is hoarded away in tissue glycogen stores to provide metabolic fuel for when the infant is separated from its placental source at birth. 1-4 T h e tremendous anabolism of the fetus accounts for its continuous energy needs even though many homeostatic functions are fulfilled by maternal metabolism. Gluconeogenesis, the manufacture of glucose from nonglucose precursors, may occur in utero from lactate and possibly other substrates to supplement the continuous placental supply. Gluconeogenesis is definitely active immediately after birth, primarily by hepatic cells when placental supply is no longer available. Conversion of amino acids to glucose is unlikely in the fetus as proteins are used mainly for growth rather than energy sources. Experimental evidence in neonatal animals suggests that protein utilization for fuel energy is possible, although much slower and less efficient than in Submitted: March 1983. Accepted with revisions: June 1983.
September/October 1984 JOCN Nursing
adults. Furthermore, neither fatty acids nor ketones appear to be significant energy sources in utero. Glucose is stored as glycogen beginning very early in gestation. The early storage site is within placental tissue; the primary site is then switched at approximately 20 to 24 weeks to hepatic storage. T h e fetal cardiac and skeletal muscle tissue also gradually accumulate glycogen as pregnancy progresses. At term, fetal glycogen stores in the liver are approximately twice those of an adult and almost ten times those of an adult in cardiac tissue. These large energy reserves are accumulated to sustain the infant through the transitional period following birth when the continuous placental supply of glucose ceases and metabolic pathways switch to fat as their principal fuel s o ~ r c e . l - ~ ’ ~ Birth initiates a major change in the infant’s energy metabolism as well as the more familiar cardio-respiratory transition. T h e work of establishing respirations, increased muscular activity, and the need to maintain thermoregulation in an all too often adverse environment contribute to a sudden demand for high metabolic energy. At the same time, the placental glucose infusion 1335.-7
has been cut off abruptly. These demands are great enough that, even in a healthy, full-term infant, up to 90% of the hepatic glycogen stores may be consumed by the end of the third hour following birth. Characteristically, blood sugar falls rapidly during the first few hours of life, stabilizing at about six hours of A controversy exists in the literature regarding the normal nadir value for blood sugar during these early hours of life.1*2,5,s-’1 Unanimously, there is agreement that too low blood sugar may compromise central nervous system function. Arguments for defining neonatal hypoglycemia as below 40 mg per 100 ml are eloquently outlined by Klaus and Fanaroff.‘ T h e human brain holds the dubious distinction of being the primary organ with limited capability of deriving energy from free fatty acids, and, thus, has a n obligatory glucose requirement.’ Immediately after birth, this glucose supply must come from glycogen stores. In healthy newborns, the glycogenolysis from hepatic stores proceeds at a production rate of 5 to 8 mg glucose per kg of body weight per minute. This rate of production has, in fact, been shown to correlate directly with brain eight.',^-^
297
Table 1. Etiologic Classification of Neonatal Hypoglycemia
Condition
Probable Biochemical Mechanism Inadequate glycogen stores
1. Premature AGA infants 2. SGA or intrauterine growth retardation 3. Perinatal stresslasphyxia
1. Decreased glycogen stores 2. Decreased glycogen stores and increased utilization 3. Increased utilization and inefficient (anaerobic) utilization 4. Elevation of free fatty acids 5. Increased metabolic consumption 6. Specific enzymatic deficiency
4. Cold-stressed infants 5. Sepsis
6. Glycogen storage disease
Hyperinsulinism 1. Infant of diabetic mother
1. Prolonged intrauterine islet cell
2. RH incompatibility
3. After exchange transfusion with acid citrate dextrose or citrate phosphate dextrose preserved blood 4. Beckwith-Wiedemann syndrome 5. Nesidioblastosis and islet cell adenomas 6. Maternal chlomropamide therapy
The etiology of hypoglycemia is reasonably discussed in terms of two general categories of inadequate stores or hyperinsulinism (Table After birth, the blood sugar reflects principally two balancing processes: the rate of endogenous hepatic release of glucose for gly-
stimulation 2. Increased glutathione released from hemolysis may stimulate insulin release 3. High glucose load results in hyperreactive insulin response
4. Islet cell hyperplasia
5. Adenoma or adenomatosis 6. Fetal betacell stimulation
cogenolysis and the rate of glucose ' Although an increased rate of glucose disposal or removal from the blood may exist without hyperinsulinemia, insulin represents the major factor influencing glucose utilization. Insulin production appears in the fetus at
induced
fuel source
\ \Neonatal
5-
J.
hypoglycemia
Figure 1. Stress as contributor toward neonatal hypoglycemia.
298
Ineffective mobilization of glycogen stores
approximately 12 weeks gestation. Its release, however, does not appear to be in response to glucose but rather, perhaps, to amino acid levels.1*3*4In response to stress, the neonate and adult alike increase their catecholamine secretion. In the adult, this can lead to el'evation of the blood sugar by inducing glycogenolysis, the sequential degradation of glycogen to glucose. The neonate's catecholamines differ from the adult's in their great preponderance of norepinephrine. Norepinephrine minimally induces glycogenolysis and catecholamine secretion leads to elevation of serum-free fatty acids (FFA). Elevation of free fatty acids causes a fall in serum glucose as a result of the reciprocal relationship between these two s ~ b s t a n c e s . ' ~ ~ ~ ~ ~ ' ~ ~ ~ " This chain of events renders the neonate less tolerant of any stress since catecholamines may increase energy needs while decreasing the most efficient energy sourceplasma glucose (Figure 1). After two to three days, most of the neonate's tissues probably switch to fat as their primary energy fuel. Accordingly, in the first few days of life the majority of neonates are most susceptible to hypoglycemia. Infants subjected to perinatal stress may exceed their stored capacity to maintain blood glucoses. Intrauterine growth-retarded and premature infants may also prove to have inadequate glycogen stores. In these and other situations, hepatic glucose production appears incapable of equaling glucose utilization. Infants of diabetic mothers and erythroblastotic newborns are two examples of hypoglycemia caused from hyperinsulinism. Here, hypoglycemia results from excessive glucose disposal. Manifestations of neonatal hypoglycemia include a host of nonspecific signs, making the differential diagnosis extremely difficult and requiring laboratory confirmation (Table 2). Signs include ab-
September/October 1984 JOGN Nursing
normal or weak cry, apnea, cyanosis, hypothermia, jitteryness, lethargy, poor feeding, and tremors.
Table 2. Appearance of Neonatal Hypoglycemia Cause 1. Infant of diabetic mother
Nursing Implications T h e nurse’s role in the neonatal intensive care unit (NICU) includes responsibility for using the nursing process to formulate a patient care plan providing direction and coordination of maternal-neonatal care. This patient care plan is constructed through synthesis of the nursing goals and all other disciplinary care objectives into a systematic delivery of care. T h e purpose of the NICU nurse is to promote optimum restorative care for the improvement of the outcome of the neonate’s immediate or longterm transition and adaptation to extrauterine life. As an integral part of nursing, the patient care plan assists in attaining this purpose by assuring continuity and integration of all therapeutic measures and by establishing the priority that attention is given to the patient’s nonemergent need^.^*"-'^ Other health-care practitioners, such as respiratory care and social workers, supply the nurse with invaluable data and goals pertinent to their particular specialty area. The nurse then uses this information concomitantly with her broadbased, multisystems education background and assessment skills for the synthesis of a patient care plan. Traditionally, it has been the responsibility of the nurse to evaluate the newborn following birth. Supervision of the infant through the period of autonomic neurologic adjustment and recovery from the delivery process until the infant has stabilized has also been recognized as the responsibility of the nurse. l4-16 These combined responsibilities of assessing and supervising the care of the newborn are most appropriate for the nurse
September/October 1984 JOGN Nursing
2. 3. 4. 5. 6. 7. 8. 9. 10.
Transient neonatal hypoglycemia IUGR/SGA Perinatal stress Prematurity RH incompatibility Glycogen storage disease Maternal antidiabetic therapy Beckwith-Wiedemann syndrome Exchange transfusion Acid citrate dextrose or citrate phosphate dextrose preserved blood Heparin preserved blood
in light of the profound influence that care disturbances and other environmental factors have on neonatal survival and well-being. Some practical implications of this role regarding neonatal hypoglycemia entail at least three identifiable components: 1) T h e nurse should command an adequate knowledge of neonatal glucose metabolism with which to assess an individual infant’s risk of developing hypoglycemia; 2) This assessment provides a foundation for constructing a care plan promoting optimum health development and restoration; 3) Nursing practice must be validated by factual evaluation. T h e degree of monitoring needed to validate one’s assessment and intervention is a judgment that may vary from nurse to nurse for any given patient condition and situation. T h e frequency of monitoring must be consistent with the patient’s assessed risk and community standards for nursing practice. This decision should be made in collaboration with fellow nursing personnel. Assessment of an infant’s risk for developing hypoglycemia should include consideration of the following factors. 1) Perinatal history. Maternal diabetes, maternal chloropropamide therapy, birth asphyxia, cold stress,
Aae of Common Onset
1-4 hours Anytime within first 72 hours 24-72 hours Within 6 hours Variable Within first 24 hours First days or weeks First hours Within 24 hours or up to third day Up to 2-3 hours after completion
During the exchange
maternal fever, and/or chorioamnionitis are historic factors prompting one to anticipate neonatal hypoglycemia. 2) Gestational age. Determination of fetal development is prerequisite to assessing glycogen storage capacity. 3) Hematologac status. Maternalfetal blood incompatibility, polycythemia, and severe neonatal jaundice requiring exchange transfusion may potentiate risk of hypoglycemia. 4) Endocrine1 metabolic status. Conditions increasing metabolic demands, such as increased work of breathing, stress, or sepsis, as well as hyperinsulinemia conditions may deplete glycogen stores rapidly. 5 ) Nutritional status. Any infant whose condition prevents adequate caloric intake is at risk for developing hypoglycemia. Assessment of these and other risk factors should provide a n adequate basis for anticipation of hypoglycemia. However, because hypoglycemia may be asymptomatic and prophylactic, medical measures are often instituted early in highrisk infants and detection may be missed. Considerable variance exists in the literature regarding recommendations for routine screening by Dextrostix.@19295*10 Policy delineating routine Dextrostix
299
screening should be established by nursing and medical directors of each nursery and should allow latitude for checking individual infants when judged prudent by the nurse. Manipulating delivery of care and environmental factors present a very exciting challenge to nurses in the NICU. Therapeutic measures that reduce energy needs may prove to be the most efficacious mode of therapy for transient neonatal hypoglycemia and might even prevent its occurrence.’.’ Many questions remain unanswered in this area, but recent investigations are demonstrating profound effects on maintaining and restoring health in premature infants through simple nursing therapies. T h e use of nonnutritive sucking during gavage feedings, for example, has been reported to increase the neonate’s daily weight gain and lead to earlier bottlefeeding and earlier discharge. ”*l Nonnutritive sucking may also facilitate greater restfulness or lower activity levels, which would enable infants to conserve their energy stores.” Activity can dramatically increase energy requirements, especially in small infants; crying alone can double the infant’s metabolic rate.Ig Establishment and maintenance of a neutral thermal environment also has potent influence on the neonate’s metabo]ism. 1,5J 1,16 careful attention to environmental conditions, physical activity, and organization of care are all integrated in the patient care plan. With few exceptions, high-risk infants should be moved into an incubator. Although most incubators currently used are single wall types in which radiant heat loss cannot be completely controlled, nursing personnel can still effectively manipulate environmental factors, such as location of the incubator in relationship to windows and temperature of oxygen delivered to the baby’s environment. These consid-
300
erations, in concert with planned efforts to minimize disruption of rest and sleep, can significantly influence the infant’s calculated energy requirements. In addition, discrepancies between the infant’s required and received calories should be monitored. Validating the effectiveness of nursing therapeutics poses problems similar to those discussed for routine detection of hypoglycemia. Again, neonatal hypoglycemia may be asymptomatic, and how much monitoring an individual needs in order to make an assessment will vary from person to person and situation to situation. Here, also, recommendations from the literature are almost absent. Since the majority of authors are physicians, most attention has been paid to establishing routine screening for the initial diagnosis of neonatal hypoglycemia rather than data collection evaluating nursing interventions.’’2p’0 Some specific guides written by nurses are found in Avery’s Neonatology. Noteworthy here is the recommendation of obtaining a Dextrostix at least once per shift in infants exhibiting apnea. This recommendation should probably be expanded to include doing a Dextrostix immediately following an episode of apnea at least once in the nurse’s assessment. As pointed out by the American Academy of Pediatrics, keeping an environmental log of events or incidents that could affect the health of the infant is the nurse’s responsibility.I6Nursing assessment of the infant’s environment should in-
Proper function of warmers/isolettes; Degree of humidity and temperature of oxygen delivered either by hood or endotracheal tube; Attention to nursing measures aimed at reducing heat loss, such as immedi-
ate changing of wet diapers to avoid evaporative cooling (also required to ensure an accurate intake and output record); 4) Performing daily weights at consistent times, preferably before a feeding. Only then can monitoring unusual losses or gains as well as the pattern of weight gain be reliable. Complementary to the physician’s search for specific pathology, the nurse must search for and rule out environmental causes of suboptimal recovery or health maintenance. By working in concert, both can achieve a more accurate diagnosis. Conclusion T h e recognition and understanding of neonatal hypoglycemia have presented new challenges to the discipline of nursing. Though a great many questions remain unanswered, nursing interventions and therapeutics can facilitate the infant’s maintenance and recovery of health. More research is needed to define accurately the efficacy of specific nursing manipulations in preventing neonatal hypoglycemia. References 1. Klaus M, Fanaroff A. Care of the high-risk neonate. Philadelphia: WB Saunders, 1979:94-112,22442. 2. Kornes SB. High-risk newborn infants. St. Louis: CV Mosby, 1972:179-86. 3. Dawes GS. Foetal and neonatal physiology: a comparative study of the changes at birth. Chicago: Year Book Medical Publishers, 1968:210-20. 4. Fisher DA. Perinatal insulin, glucagon and carbohydrate metabolism. In: Perinatal endocrinology, a monograph of the eighth Mead Johnson Symposium on Perinatal and Developmental Medicine, 1975:30-8. 5. Avery GB, ed. Neonatology: pathophysiology and management of the newborn. Philadelphia: JB Lippincott, 1981 :48-88, 583-99.
September/October 1984 JOGN Nursing
6. Toew CJ: Metabolic fuel metabolism: metabolic differences between prenatal and postnatal life. In: Fuel metabolism in the fetus and newborn, a monograph of the third Mead Johnson Symposium on Perinatal and Developmental Medicine, 197 3 :3- 12. 7. Drash AL. Carbohydrate and energy metabolism. In: Developmental nutrition. Columbus: Ross Laboratories, 1979: 19-24. 8. Cloherty JP, Stark AR, eds. Manual of neonatal care. Boston: Little, Brown & Co., 1980:257-9. 9. Behrman RE, ed. Neonatal-perinatal medicine. St. Louis: CV Mosby, 1977~712-35. 10. Schreiner RL, ed. Care of the newborn. New York: Raven Press, 1981~69-75. 1 1. Greenberg RE. Glucose homeostasis in the newborn. In: Fuel metabolism in the fetus and newborn, a monograph of the third Mead Johnson Symposium on Perinatal and Developmental Medicine, 1973~9-60.
12. Statement on the scope of highrisk perinatal nursing practice. Kansas City: American Nurses’ Association publication, 1973. 13. Maternal-child health nursing practice. Kansas City: American Nurses’ Association publication, 1973. 14. Toward improving the outcome of pregnancy. Committee on Perinatal Health Recommendations. White Plains: T h e National Foundation-March of Dimes, 1977. 15. Bellig LL. T h e expanded nursing role in the neonatal intensive care unit. Clin Perinatol 1980;7(1): 15972. 16. Standards and recommendations for hospital care of newborn infants. Evanston, IL: American Academy of Pediatrics, the Committee on Fetus and Newborn, 1977. 17. Field T, et al. Nonnutritive sucking during tube feedings: effects on preterm neonates in an intensive care unit. Pediatrics 1982: 70(3):38 1-4.
PRIMARY CARE NURSE PRACTITIONER
18. Measel CP, Anderson GC. Nonnutritive sucking during tube feedings: effect upon clinical course in premature infants. JOGN Nurs 1979;8:265. 19. Czajka-Narins DM, Weil WB. Calories. In: Oliver K, Cox B, Johnson T , Moore W. Developmental nutrition. Columbus: Ross Laboratories. 1979:9-18.
Address for correspondence: Douglas Fantazia, RN, St. Mary’s Hospital, c / o NICU, 235 West 6th Street, Reno, NV 89520.
Mr. Fantazia is a neonatal nurse practitioner at St. Mary’s Hospital in Reno, Nevada. Mr. Fantaziais NCCcertified as a neonatal intensive care nurse and also certified as a respiratory therapy technician.
MEETING
“Practice, Politics and Power,” a national conference sponsored by the Primary Care Nurse Practitioner Interest Group of the California Nurses’ Association, Region 12, is scheduled November 2-3,1984, at the Miyako Westin Hotel in San Francisco, California. Sessions during the conference will include information on nurse practitioner collegiality, third-party reimbursement,aging issues, nutrition, sports injuries, eating disorders, osteoporosis, arthritis, acne, hypertension, working with the disabled, clinical research for the nurse practitioner, and more. Twelve contact hours will be offered. Cost for CNA/ANA members is $135 and indudes two lunches and syllabus materials. For copiesof the conference prospectus and additional information, contact: Golden Gate Nurses’ Association, CNA Region 12, 2601 Mission St., 9th fl., San Francisco, CA 941 10, (415)821-7400.
September/October 1984 JOCN Nursing
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