HIGH RISK NEWBORN- Part-I Mrs. U SREEVIDYA Msc . NURSING, Associate Professor, Apollo college of nursing, CHITTOOR
INTRODUCTION A newborn, regardless of gestational age or birth weight, who has a greater than average chance of morbidity or mortality because of conditions or circumstances superimposed on the normal course of events associated with birth and the adjustment to extra uterine existence … is termed as High-risk Newborn .
FACTORS –TO DEFINE HIGH RISK NEWBORN A) Demographic social factors B) Past medical history C) Previous pregnancy D) Present Pregnancy E)Labor and delivery F)Neonate
A) Demographic social factors Maternal age <16 or >40yr Poverty Unmarried Emotional or physical stress Illicit drug, alcohol, cigarette use
B) Past medical history Genetic disorders Diabetes mellitus Hypertension Asymptomatic bacteriuria Rheumatologic illness Immune –mediated disease Long-term medication
C) Previous pregnancy Intrauterine fetal demise Neonatal death Prematurity Intrauterine growth restriction Congenital malformation Incompetent cervix Blood group sensitization Neonatal thrombocytopenia Hydrops fetalis
D) Present Pregnancy Vaginal bleeding Sexually transmitted infections Multiple gestation Preeclampsia PROM Short interpregnancy time Poly-/ oligohydramnios Acute medical or surgical illness Inadequate prenatal care Familial or acquired hypercoagulable states Abnormal fetal USG findings Treatment of infertility
E)Labor: and delivery Premature labor (<37wk) Postdates pregnancy(≥42wk) Fetal distress Immature lecithin: spingomylin ratio; absence of phosphatidyleglycerol Breech presentation Meconium –stained fluid Nuchal cord abnormalities Cesarean section delivery Forceps delivery Apgar score <4 at 1 min
F)Neonate: Birth weight ≤2500 or ≥4000g Birth <37 or ≥42wk of gestation Small or large for gestational age Respiratory distress, cyanosis Congenital malformation Pallor, plethora, petechiae
Causes of Neonatal Mortality
DEFINITIO N S Low Birth Weight Baby : Live born baby weighing 2500 gram or less at birth. (VLBW: <1500 gm, ELBW:<1000 gm). ‐ Preterm baby : When the baby is born before term. i.e.: before 38 weeks of gestation. Premature baby : When the baby is born before 37 weeks of gestation.
Full term Newborn : When the baby is born between 38 – 42 weeks of gestation. Post term baby : When the baby is born after 42 weeks of gestation. DEFINITIONS
POST TERM NEWBORN CHARACTERISTICS Newborn emaciated Meconium stained Hair and nails long dry peeling skin Creases cover soles L imited vernix & lanugo
Major problems in preterm babies and those with IUGR PRETERM Hypothermia Perinatal asphyxia Respiratory distress syndrome Bacterial sepsis Apnea of prematurity Metabolic problems Hematologic problems feeding problems and Poor wt gain IUGR Perinatal asphyxia Meconium aspiration Hypothermia Hypoglycemia Feed intolerance Polycythemia Poor wt gain
Low birth weight baby
DEFINITION LOW BIRTH WEIGHT: LBW infant is defined as one whose birth weight is less than 2500gms irrespective of the gestational age. WHO/D.C.Dutta
LBW Very low birth weight infants weigh s 1500gms or less and extremely low birth weight infants weighs 1000gms or less.
CLASSIFICATION OF LBW INFANTS Low birth weight babies are again classified after correlating both the birth weight and gestational age into two groups. Preterm Small for gestation age(SGA)
Cont.. Preterm -The growth potential is normal and is appropriate for the gestational period (10 to 90 th percentile) Small for gestational age(SGA)- The term is to designate the newborn with birth weight less than 10 th percentile or less than gestational age.
Preterm infant DEFINITION: A baby born before 37 completed weeks of gestation calculating from the first day of last menstrual period is arbitrarily defined as preterm baby Babies born before 37 completed weeks usually weighing 2500gms or less.
INCIDENCE Preterm baby constitutes 2/3 rd of low birth weight babies. The incidence of low birth weight baby is about 30-40% in the developing countries as such the incidence of preterm baby is about 20-25%.
ETIOLOGY Spontaneous Induced
SPON T AN E OUS Health status of the mother Multiple pregnancy Advanced parental age Placental problems Preterm labour and premature rupture of membrane Low maternal weight Chronic and acute systemic maternal disease Ante partum haemorrhage Cervical incompetence Maternal genital colonization and infections Cigarette smoking during pregnancy Acute emotional stress Physical exertion Sexual activity Trauma Bicornuate uterus Congenital malformations
INDUCED Maternal diabetes mellitus Placental dysfunction as indicated by unsatisfactory fetal growth Eclampsia Fetal hypoxia Severe rhesus iso immunization
CLINICAL FEATURES Measurements: Size is small with relatively large head Crown- heel length is less than 47cm Head circumference is less than 33 cm But exceeds the chest circumference by more than 3 cm (normally 1.5cm)
Activity and posture: General activity is poor Automatic reflex response such as , Moro response, sucking and swallowing are sluggish or incomplete Baby assumes an extended posture due to poor tone
Face and head: Face appears small large head size Sutures are widely separated Fontanels are large Small chin Protruding eyes Optic nerve is usually unmyelinated Ear cartilage is deficient or absent with poor recoil Hair appears woolly, and fuzzy and individual hair fibres can be seen separately
Skin and subcutaneous tissues: Skin is thin, gelatinous, Shiny and excessively pink Abundant lanugo Plentiful vernix caseosa Edema may be present Subcutaneous fat is deficient Breast nodule is small or absent
CHARACTERISTICS OF PRETERM INFANTS Skin Bright pink, often translucent, depending on the degree of maturity Smooth and shiny ( may be oedematous) Small blood vessels clearly visible underneath the thin epidermis Fine lanugo hair is abundant
Ear cartilage Soft and pliable Soles and palms Minimal creases Smooth appearance Scarf sign Elbow may be easily brought across the chest with little or no resistance
Male genitalia Male infant’s scrotum is undeveloped and not pendulous Minimal rugae are present Testes may be in the inguinal canal or in the abdominal wall Female genitalia Clitoris is prominent Labia majora are poorly developed and gaping
COMPLICATIONS OF PRETERM BIRTH Central nervous system: Immaturity of central nervous system Poor cough reflex Un coordinated sucking and swallowing Retrolental fibroplasias Intra ventricular and periventricular haemorrhage
Respiratory system Resuscitation difficulties at birth Hyaline membrane disease Breathing is periodic and associated with intercostal recessions due to soft rib Pulmonary aspiration Atelectasis Broncho pulmonary dysplasia
Cardio vascular system The closure of ductus arteriosus is delayed among preterm infants G I system Regurgitations and aspirations Abdominal distension and functional intestinal obstruction Enter colitis Hyperbilirubinemia Hypoglycaemia
Thermo-regulation Excess heat loss Infections Renal immaturity The blood urea nitrogen is high Acidosis Edema Toxicity of drug Nutritional problems anemia Deficiencies of folic acid and Vit E osteopenia and rickets Biochemical disturbance hypoglycaemia, hypocalcemia, hypoxia
MANAG E MENT Care of preterm infant Intensive care protocol
IMMEDIATE CARE OF NEWBORN Cord is clamped immediately to prevent hypovolemi a . Cord length is kept 10-12 cms in case of exchange transfusion Airway is cleared Adequate oxygen is given Baby is wrapped including head with sterile towel Administer inj .vitamin k
Intensive care protocol Special care is needed incase of Inability to suckle the breast and to swallow Incapacity to regulate the temperature within limited range from 96-99F Inability to control the cardio- respiratory function without cyanotic attacks
PRINCIPLES OF SPECIAL CARE To maintain body temperature Adequate humidification to counter balance increased water loss Oxygen therapy and adequate ventilation To prevent infection To maintain nutrition and adequate nursing care
Mana g eme n t Prepare for high risk of need for resucsitation Gentle resu sc itation using small bags for PPV (Positive pressure ventilation) , use of CPAP (Continuous positive airway pressure) Take extra care to avoid hypothermia Special attention to maint ain of warm chain KMC Strict adherence to asepsis, hand hygiene Management of metabolic, hematologic abnormality Management of immature organ systems in preterm
Choosing initial methods of feeding >34 weeks Initiate breast feeding Observe if, positioning & Attachment are good, able to suck Effectiv e ly and long enough (10-15min) y es Breast feeding Start feeds by spoon Or paladai no Yes,spoon/ Paladai feeding No, start feeds by OG or NG tube No vomiting/abd distension Gastric tube feeding 3 2-34 w e e k s 28-31 weeks Observe if accepting well Without spilling/coughing <28wks Vomiting/abd distension Start IV fluid
Progression of oral feeding in preterm , LBW neonates & Infant on IV fluids Start trophic feeding by OGT And monitor for feed intolerence If accepting well Newborn with OGT feeds Gradually increase the feed volume Taper & stop IV fluids Try spoon feeds once or twice a day Put on mother’s breast and allow non nutritive suck Gradually ↑ the frequency & amount ↓OGT feeds Put the baby on mother’s breast before each feed, if good attachment and effective suckin g Taper and stop spoon feeds Once the mother is confident
Nutritional supplements for infants with birth wt between 1500-2499g Nutrition Method of supplementation Dose Duration Vitamin D Multivitamin drops 400IU/day 2wks to 1yr Iron Iron drops 2mg/kg/day 6-8wks to 1yr
Supplementation in VLBW neonates Calcium & phosphorus (140-160mg/kg /D ay & 70 - 80mg/kg/D ay for infants on EBM -Expressed breast milk ) Vitamin D, B complex, Zinc Folate (50 µg/kg/D) Iron - Supplementation should be added at different times in the day to avoid abnormal ↑ in osmola r ity
Management of inadequate wt gain Proper counselling of mothers, assessment of positioning/attachment & managing sore ,flat nipple s. Frequency & timing of both breast feeding and spoon or paladai feeding EBM by spoon or paladai feeding (preterm) Initiating fortification of breast milk when indicated
NURSING CARE Cushioned bed Avoid excessive light ,sound ,rough handling and painful procedures Use effective analgesia and sedation for procedures Provide warmth Ensure strict asepsis Cover the baby approximately
CONT… Provide effective and safe oxygenation Nutrition Tactile and kinesthetic stimulation Prone position or side lying with head lifted Phototherapy if needed Prevention of nosocomial infection Weight record daily Immunizations Family support
HYPOTHERMIA
DEFINITION AND CLASSIFICATION It is a condition characterized by lowering of body temperature than 36 ° C. Types of Hypothermia: Could be classified according to Causes and according to Severity .
CLASSIFICATION BASED ON CAUSE Primary Hypothermia: Seen immediately after delivery Normal term infant delivered into a warm environment may drop its rectal temperature by 1 – 2 ° C shortly after birth and may not achieve a normal stable body temperature until the age of 4 – 8 hours. In low birth weight infants , the decrease of body temperature may be much greater and more rapid unless special precautions are taken immediately after birth. (loss at least 0.25 ° C/ min.)
Secondary Hypothermia: This occurs due to factors other than those immediately associated with delivery. Important contributory factors are: e.g.: Acute infection especially Septicemia. CLASSIFICATION BASED ON CAUSE
CLASSIFICATION BASED ON SEVERITY II) According to Severity: Mild Hypothermia: < 36 ° C Moderate Hypothermia: < 35.5 ° C. Severe Hypothermia: < 35 ° C .
CLINICAL FEATURES Decrease in body temperature Cold skin on trunk and extremities Poor feeding in the form of poor suckling Shallow respiration Cyanosis Decrease activity, e.g. Weak cry
FOUR MODALITIES OF HEAT LOSS IN NEONATES Evaporation : Heat loss that resulted from expenditure of internal thermal energy to convert liquid on an exposed surface to gases, e.g.: amniotic fluid, sweat. Prevention: Carefully dry the infant after delivery or after bathing. 2. Conduction: Heat loss occurred from direct contact between body surface and cooler solid object. Prevention: Warm all objects before the infant comes into contact with them.
3. Radiation: It occurred from body surface to relatively distant objects that are cooler than skin temperature. Convection: Heat loss is resulted from exposure of an infant to direct source of air draft. Prevention: Keep infant out of drafts. Close one end of heat shield in incubator to reduce velocity of air.
MANAGEMENT Infant should be warmed quickly by wrapping in a warm towel. Use extra clothes or blankets to keep the baby warm. If the infant is in incubator, increase the incubator ’ s temperature. Avoid exposure to direct source of air drafts. Check body temperature frequently. Give antibiotic s if infection is present .
HYPERTHERMIA
DEFINITION It is a condition characterized by an elevation in body temperature more than 37.5 ° C. Causes: Disturbance in Heat Regulating Center caused by intracranial hemorrhage. Incubator temperature is set too high .
MANAGEMENT Undress the infant. If at home; keep light cloth e s, cover that containing light sheet, Or only a diaper if the infant is inside an incubator. Reduction of incubator temperature. Provide Tepid sponge bath. If available; fill the water mattress with cold water, and keep it in contact with the infant ’ s skin. Increase fluid intake in the form of 5cc of Glucose 5% between feeds to prevent dehydration.
IQ Question
The first letters are in alphabetical order with a letter skipped in between each segment: C, E, G, I, K. The second and third letters are repeated; they are also in order with a skipped letter: M, O, Q, S, U.
HYPOGLYCEMIA
DEFINITION: Neonatal hypoglycemia is usually defined as a serum glucose value of < 40‐45 mg/dl. For the preterm infant a value of < 30 mg/dl is considered abnormal (hypoglycemia).
1- The main cause may be maternal malnutrition during pregnancy which leads to fetal malnutrition and of course a low birth weight. 2‐ Those infants , who are Small for gestational age (SGA), manifested by decrease in their birth weight and subcutaneous fat and hepatic glycogen. 3‐ Those infants ’ of diabetic mothers (IDM) or those named as large for gestational age (LGA). NEONATES AT RISK FOR DEVELOPING HYPOGLYCEMIA :
4‐ Those whom placentas were abnormal, e.g. placenta Previa. 5‐ Those whom their mothers had toxemia during pregnancy, e.g. eclampsia or pre‐eclampsia induction of labor preterm infant. 6‐ Those very ill or stressed neonates whom their metabolic needs were increased due to hypothermia, infection, respiratory distress syndrome, or cardiac failure.
Fetus receives glucose from the mother Cord cut Glucose level falls from 70 – 80 mg/dl to 50 mg/dl Hepatic glucose is released into the blood Cold extra‐uterine one, Beginning the respiratory cycles, Muscular activity Suckling effort High risk infant Risk for developing hypoglycemia . PATHOPHYSIOLOGY
CLINICAL MANIFESTATIONS CONTD : 7‐ Hypothermia. 8‐ Irregular respiratory pattern (Apnea). 9‐ Irritability. 10‐ High pitched cry followed by weak cry. 11‐ poor reflexes, especially sucking reflex .
Infants who develop hypoglycemia should immediately be given 2 cc/kg of 10% dextrose over 1 minute, repeated as needed . MANAGEMENT OF THE NEONATE WITH HYPOGLYCEMIA:
A continuous infusion of 10% glucose at a rate of 8 -10 mg/kg/min should be started to keep glucose values normal ( NOTE: 10 mg/kg/min of 10 % dextrose = 144 cc/kg/day). Frequent bedside glucose monitoring is necessary. When feedings are tolerated and frequent bedside glucose monitoring values are normal, the infusion can be tapered gradually.
INFANT OF DIABETIC MOTHER
INFANT OF DIABETIC MOTHER
INFANT OF DIABETIC MOTHER
Maternal hyperglycemia Fetal hyperglycemia in‐utero Fetal hyperinsulinemia‐ increased fat and glycogen synthesis‐ Macrosomic infant Cord clamped Interrupts the transplacental glucose supply Inspite of which Hyperinsulinemia persists, this leads to hypoglycemia PATHOPHYSIOLOGY
DISORDERS IN INFANTS OF DIABETIC MOTHERS Hypoglycemia. Hypocalcemia. Hypomagnesemia. Cardio‐respiratory disorders Hyperbilirubinemia (Unconjugated)
MANAGEMENT: For the mother: Good antenatal care for proper control of maternal diabetes For an infant: All IDMs should receive continuous observation and intensive care. Serum glucose levels should be checked at birth and at half an hour, 1, 2, 4, 8, 12, 24, 36 and 48 hours of age
If clinically well and normoglycemia; oral or gavage feeding should be started and continued with 2 hours intervals. If hypoglycemic; give 2 – 4 ml/kg of 10% dextrose over 5 minutes, repeated as needed. A continuous infusion of 10% glucose at a rate of 8‐10 mg/kg/min. Start enteral feeding as soon as possible. Give Corticosteroids in persistent hypoglycemia. Oxygen therapy for RDS, Calcium gluconate 10% for hypocalcemia, phototherapy for hyperbilirubinemia MANAGEMENT cont :
NEONATAL INFECTIONS
NEONATAL INFECTIONS Infection is still one of the leading causes of neonatal death in developing countries. The neonates are more susceptible to infection as they are deficient in natural immunity and acquired immunity. Preterm infants are at high risk for perinatal infections. Neonates that survive from sepsis often suffer from severe neurological as well as severe parenchymal lung diseases. NEONATAL SEPSIS INTRODUCTION
The newborn infant is uniquely susceptible to acquire infection, whether bacterial, viral or fungal. Bacterial sepsis and meningitis continue to be major causes of morbidity and mortality in the newborn. The mortality rate due to sepsis ranges from 20% to as high as 80% among neonates. Surviving infants can have significant neurologic squeal because of CNS involvement .
DEFINITION Neonatal sepsis is a disease of neonates (who are younger than 1 month) in which they are clinically ill and have a positive blood culture.
RISK FACTORS FOR NEONATAL INFECTION Rupture of membrane s > 18 hours Maternal intrapartum fever > 100.4˚F Low birth weight infant (< 2500 g) Prematurity (< 37 weeks) Chorioamnionitis Mother with (G roup - B S treptococcus ) infection Repeated vaginal examination s in labour Invasive procedures of monitoring
MOST COMMON RISK FACTORS Maternal risk factors: e.g.: Premature /prolonged rupture of membrane s . Neonatal risk factors: e.g.: Prematurity (less immunologic ability to resist infection + more liable to penetrate their defensive barriers).
MODE OF INFECTION Antenatal Transplacental : maternal infection that can affect the fetus through transplacental route are predominantely the viruses, they are rubella, cytomegalovirus, herpes virus, HIV, chicken pox and hepatitis – B virus. Other infections are syphilis, toxoplasmosis and tuberculosis. Aminonitis : Following premature rupture of the membranes can affect the baby following aspiration or ingestion of infected amniotic fluid.
INTRANATAL Aspiration of infected liquor or meconium following early rupture of the membranes or repeated internal examination. This may lead to neonatal sepsis, pneumonia and meningitis. while the fetus is passing through the infected vagina – eyes are infected – opthalmia neonatorum or oral thrush with candid albican Improper asepsis while caring the umbilical cord.
POSTNATAL – NOSOCOMIAL INFECTIONS Transmission due to human contact – infected mother, relative s or staff of the nursery. Cross infection from an infected baby in the nursery. Infection through feeding, bathing, clothing or air-borne. Infection in environment of neonatal intensive care (NICU) or invasive monitoring.
COMMON ROUTES OF TRANSMISSION Through the maternal blood , through placenta as rubella, toxoplasma, and syphilis. From the vagina or cervix, as groups B streptococci. The newborn may be , come in contact as it passes through the birth canal with gram negative organisms. The newborn may come in contact in its environment after birth (Coagulate positive or negative staphylococci). When a susceptible host acquires the pathogenic organism, and the organism proliferates and overcomes the host defense, infection results.
THE COMMON PATHOGENS Group b streptococcus (GBS), Staphylococcus aureus, E. Coli, Klebsiella and pseudomonas, Fungus(candida) and anaerobes.
THE PRIMARY SITES OF INFECTION Skin, Nasopharynx, Oropharynx, Conjunctiva and Umbilical cord.
COMMON SITES OF INFECTION Eyes – opthalmia neonatorum Skin Umbilicus Oral thrush Severe systematic : Respiratory tract Septicaemia Meningitis Intra – abdominal infections
CLASSIFICATION OF NEONATAL SEPSIS Early onset Sepsis Late onset Sepsis Newborns with early‐onset infection present within 24 hours till 72 hours. Early‐onset sepsis is associated with acquisition of microorganisms from the mother during pregnancy (transplacental infection), or during labor (an ascending infection from the cervix). Late‐onset sepsis occurs beyond the first 72 hours of life (most common after the 3 rd day till the 7 th day after birth) and is acquired from the care giving environment (Nosocomial infection).
CLINICAL FEATURES Decreased activity Excessive crying Apnea Jaundice Hypo /Hyper thermia Bulging or full fontanel Seizures Hypoton i a
LA BORATORY FINDINGS Raised Total leukocyte count (WBC count) Raised C – reactive Protein (CRP) Increased Erythrocyte Sedimentation Rate (ESR) Cultures positive
MANAGEMENT Prevention: through proper application to infection control practices. Early onset sepsis; give intrapartum antimicrobial prophylaxis (IAP) to the mother.
PREVENTION Demonstrate the effect of hand washing upon the prevention of the nosocomial infections. Standard precautions should be applied in the nursery for infection prevention. Instillation of antibiotics into newborn ’ s eye 1‐2 hours after birth is done to prevent the infection. Skin care should be done using w a rm water & may use mild so a p for removal of blood or meconium . Cord care should be given regularly using alcohol or an antimicrobial agent .
MANAGEMENT (CONT..) Neonates with clinically suspected sepsis: Culture should be obtained first. The recommended antibiotics are ampicillin and gentamicin. Third generation cephalosporins (Cefotaxime) may replace gentamicin if meningitis is clinically suspected Late onset neonatal sepsis: Vancomycin in combination with either gentamicin or cephalosporins should be considered in penicillin resistant cases.
A n tibiotic the r a p y – b r oa d spec t rum are given to cover the germ positive and anaerobes. Inj. Ampicillin ne g a ti v e o r g anis m s as w ell as the 150 m g /k g / e v ery 1 2 hou r s , g e n t a m y cin 3 - 4 mg/kg/every 2 4 ho u r s , usu a l l y a r e s t a r t e d . I n a s e v e r ely ill p a t ie n t, cefotaxime or ceftazidime is also added.
C ONT… Supportive therapy and management of complications as needed. E.g. mechanical ventilation for RDS, dopamine for hypotension, ant i convulsion therpy for seizure s, sodium bicarbonate for metabolic acidosis and Immunotherapy with hyper immune globulins.
GENERAL AND NURSING MANAGEMENT cont.. Encourage breast feeding from the mother. Adequate fluid and caloric intake should be administered by gavage feeding or intravenous fluid as ordered. Extra‐measure s for hypothermia or hyperthermia that may be take n to the newborn. Administering medications as doctor order. Follow the isolation precautions. Monitoring intravenous infusion rate and antibiotics are the N urses responsibility .
Administer the medication in the prescribed dose, route, and time within hour after it is prepared to avoid the loss of drug stability. Care must be taken in suctioning secretions from the newborn as it may be infected. Isolation procedures are implemented according to the isolation protocols of the hospital. Observe for the complication s e.g. meningitis and septic shock . Encourage in‐service programs and continuing education of nurse s regardin g th e in f I e A P c t T e i o a c n hi n c g o Sl i n d e t s r 2 o 1 l 5 p - 2 r e 1 6 cautio n 4 s Cont …
HEMO L YTIC DISEASES OF NEWBORN
Hemolytic Disease The term hemolytic disease is limited to conditions in which the rate of RBCs destruction is accelerated and the ability of bone marrow to respond is unimpaired.
Rh incompatibility: Rh incompatibility is a condition which develops when an Rh negative mother conceives a fetus which is Rh positive. Isoimmunization: When the mother produces A nti b odie s directed against fetus RBC surface Ag.
THE MOST COMMON…. Cause of Maternal Isoimmunization Feto- maternal Bleed Risk Factors of Feto-maternal Bleed: Amniocentesis Ectopic pregnancy
RBC Rh Antigen : Rh “ D ’’ Ag Mother produces: Anti Rh (D) Abs THE MOST COMMON….
Rh Incompatibilty Rh (-) woman + Rh (+) man = Rh (+) children Rh positive fetus cross the placental barrier and enter into Rh negative mother’s blood stream. mother’s immue system reacts fetal Rh antigen stimulus by producing a large number of anti-Rh antibodies. mother’s antibodies + feotus RBCs=hemolysis
Mother must be Rh - Dad must be Rh + Coombs test must be positive Abs must be assoc i a t e d with Hemolysis Ab titer must be above 1:8 Is the baby at risk? Anti Lewis Abs No n -He m ol y tic ABS Anti KELL Abs Anti RH(D) Abs Hemol y t ic ABS
Erythroblastosis Fetalis Hemolytic anemia and it occurs during transplacental transmission of maternal antibodies to fetal RBCs. The disorder usually results from incompatibility between maternal and fetal blood groups.
Mother’s antibodies destroy baby's RBCs and the baby develops anemia. The baby's body tries to compensate for the anemia by releasing immature RBCs called erythroblasts from the bone marrow. Liver and spleen to become enlarged potentially causing liver damage or a ruptured spleen.
Jaun d ice (Icterus gravis neonatorum) Infants have high levels of bilirubin in their blood , which leads to jaundice. (hyperbillirubinemia) Shorter life span of RBCs Unconjugated billirubin binds to albumin and travels to liver. Increase d reabsorption of conjugated billirubin from GI tract.
Kernicterus Free bilirubin is lipid soluble. Deposited in brain. It causes a condition known as Kernicterus.
Diagnostic features of Hydrops fetalis- Mother is rh – ve Serological examination reveals presence of rh antibodies May be presence of poly hydramnios sonography- to detect oedema in the skin, scalp and pleural/pericardial effusion. Straight X-Ray abdomen showing ‘ Budha ’ position of the fetus . The baby at birth looks pale and oedematous with an enlarged abdomen due to ascites. There is enlargement of liver and spleen. Placenta is large, pale , oedematous with fluid oozing from it. Fetal death occurs sooner or later due to cardiac failure. The baby is either stillborn or macerated and even if born alive, dies soon after.
Diagnosis of Haemolytic diseases Routine blood Test Fetus Blood Test Indirect Coombs Test Direct Coombs Test
Direct Coombs test or DAT RBCs wash to remove plasma RBCs are incubated with anti- hemoglobulin. Antihemoglobulin binds to patient’s antibodies that are attached with RBCs Agglutation indicates positive DAT.
Indirect coombs test or IDT The IDT deals with extracted plasma. Unbound antibodies remains in blood Plasma is then incubated with reagent RBCs. Antibodies binds to reagent RBCs. Positivr IDT indicates presence of antibodies in blood.
Treatment Rho-Gamma Globulin Administe re d at 28 th week of pregnancy After 72 hours of Delivery .
RhoGam vaccination Contains antibodies to RH (+) But not harmfull enough Mother’s body react to these antibodies and never reacts to fetal anti gen s.
Intrauterine blood transfusion Given to replace fetal RBCs that are being destroyed by mother’s allo antibodies. Keep the fetus healthy until he or she is mature enough to be delivered.
Procedure position of placenta through ultrasound image. Antiseptic solution to clean mother’s abdomen Anesthetic injection to make abdominal region insensitive Needle is inserted
From mother's abdomen into the fetus's abdomen or an umbilical cord vein. A compatible blood type is delivered into the fetus's umbilical cord vessel.
Management after delivery : Phototherapy for neonate with mild jaundice Exchange transfusion in Severe cases
HYPERBILIRUBINEMIA (NEONATAL JAUNDICE)
DEFINITION Hyperbilirubinemia is an elevation in the neonatal serum bilirubin ≥ 12.9 mg/dl in F ull‐term, F ormula feed infant OR ≥ 15 mg/dl in P reterm, B reast feed infant Characterized by JAUNDICE, which is defined as “yellowish discoloration of skin and mucous membranes”. In the neonate , clinical jaundice is diagnosed if the total serum bilirubin is ≥ 7 mg/dl.
The following are possible causes of hyperbilirubinemia in the newly born infants: Over production of bilirubin. Under excretion of bilirubin. Combined over production and under excretion. Physiological jaundice. Breast milk associated jaundice . CAUSES
CAUSE
PHOTOTHERAPY: PRINCIPLES Cover the infant ’ s eyes and genital organs. The infant must be turned frequently to expose all body surface areas to the light. Continued until the Serum bilirubin level must be 10mg% . In e ach shift, eyes are checked for evidence of discharge or excessive pressure on the lids and eye care should be done using warm water, then apply eye drops or ointment.
Eye cover should be removed during feeding, and this opportunity is taken to provide visual and sensory stimuli. Avoid oily lubricants or lotion on the infant ’ s exposed skin, because this can act as a barrier that prevent penetration of light through the skin. Increase feeds in volume and calories. Add 20% additional fluid volume to compensate for insensible and intestinal water loss. 8. Maintain Intake and output chart. PHOTOTHERAPY cont.. :
OBJECTIVES: To correct anaemia. To remove the circulatory antibodies. To eliminate the circulatory bilirubin. PROCEDURE: The route of transfusion should preferably be through the umbilical vein. A plastic catheter of 1 mm diameter is passed about 7 cm beyond the umbilicus, so as to place it in the inferior vena cava. Blood should be warmed to 37 C. 15 ml of fetal blood is withdrawn first followed by 10 ml to be pushed in- return slowly. (PUSH-PULL METHOD) For every 100ml of blood transfused, 1meq of sodium bicarbonate is given to combat metabolic acidosis and 1 ml of 10% calcium gluconate to prevent tetany due to transfusion of citrated blood.
COMPLICATION S OF HYPERBILIRUBINAEMIA The most common complication of hyperbilirubinemia is Kernicterus (Bilirubin Encephalopathy), which usually occurs when the unconjugated serum bilirubin level exceeds than 20 mg/dl. In small, sick preterm infants, even a bilirubin level in a low range may cause Kernicterus.
Clinical Presentation: Kernicterus progresses through 4 stages: Stage I: Poor Moro reflex, poor feeding, vomiting, high‐pitched cry, decreased tone and lethargy. Stage II: Spasticity, seizures, fever. Neonatal mortality is high at this stage (80%). Stage III: A symptomatic (Spasticity decreases and all remaining clinical signs and symptoms may disappear). Stage IV: Appears after the neonatal period. Long‐term sequelae can include: spasticity quadriplegia, deafness and mental retardation (for the 20%).
Hypoxia, acidosis, hypoglycaemia, hypothermia or sepsis enhance the pathogenesis, so that affection may occur even at a low levels of bilirubin. It is clinically characterised by lethargy, hypotonia, poor feeding and loss of moro reflex. Gradually, hypertonia, severe illness is manifested by respiratory distress and opisthotonous , hyperpyrexia, convulsions, enlarged liver and spleen. PREVENTION & MANAGEMENT: Regular and periodic estimation of blood bilirubin level. In susceptible cases, treat with exchange transfusion. Use of barbiturates and photherapy also treat the condition.
Neonates with overt neurologic features usually die (75%). Those who survive often suffer from MR and cerebral palsy.