HIGH RISK NEWBORN.pptx

High risk newborn is a chapter under OBG for 4 th yr BSc nursing students. this helps them to understand about the classification of high risk newborn, KMC, problems associated with LBW babies, management of LBW babies.

1. HIGH RISK NEWBORN

2. High risk neonate is a newborn, regardless of GA or BW, who has a greater than average chance of morbidity, mortality because of conditions or circumstances associated with birth & adjustments to extrauterine existence. LBW <2.5kg SGA, weight <10th percentile ( IUGR) LGA, weight >90th percentile PRETERM, delivered before 37 weeks

3. LOW BIRTH WEIGHT BABY LBW babies are those weighing below 2500 g at birth VERY LOW BIRTHWEIGHT (VLBW) babies are those weighing below 1500 g at birth EXTREMELY LOW BIRTHWEIGHT (ELBW) babies are those who weigh below 1000 g at birth The definitions of LBW is based upon weight alone & do not consider the gestational age.

4. PHYSICAL ASSESSMENT SKIN Pallor Plethora - beetroot appearance in babies due to polycythemia Cyanosis Jaundice Skin rashes Milia Miliaria Petechiae or purpura rash

5. Bruising Erythema toxicum Infectious lesions - thrush, herpes simplex virus, umbilical sepsis, staphylococcal infection GENERAL ASSESSMENT WARNING SIGNS pallor Central cyanosis Apnoea lasting longer than 20 s HR<110 or >180 Beats/mn

6. RR<30 or >60 breaths/mn Skin T <36.2C or >37.2C Lack of spontaneous movement & responsiveness Abnormal lying position either hypotonic or hypertonic Lack of interest in surroundings jaundice

7. Infant is small & limp Thin skin, blood vessels beneath the epidermis Wrinkled skin with lanugo, little or no vernix caseosa No subcutaneous fat Head larger than the body ( cephalocaudal growth ) Prominent eyes Male genitalia - few scrotal rage,

8. Undescended testes Female genitalia - labia & clitoris are prominent Protruded abdomen Thin muscles Minimal creases on palm & soles Regurgitation Cyanosis, pallor, plethora Inactive, extended arms & legs

9. Poor reflexes Absence of sucking reflex Barrel or concave shaped chest Hypothermia, hypotonia, apnea, poor colour Nasal flaring, suprasternarnal , substernal retractions Grieving , stridor breath sound.

10. NURSING MANAGEMENT Maintenance of controlled thermal environment Monitoring HR,RR, & BP Collection of specimen ( blood glucose, haematocrit,Calcium,bilirubin, ABG)

11. Thermo regulation Infection & injury prevention Nutrition & hydration Prevention of Cx Respiratory support Skin care Energy conservation

12. KANGAROO MOTHER CARE

13. Kangaroo mother care (KMC) is used to promote closeness between a baby & mother & involves placing the nappy-clad baby upright between the maternal breasts for Skin to skin contact

14. COMPONENTS OF KMC Skin to skin contact Exclusive breastfeeding Support to mother & baby Discharge of baby

15. BENEFITS OF KMC Better adaptation to the environment Helps baby to sleep better Aids better mental development Makes breastfeeding convenient Promote healthy weight gain Reduces baby’s stress level Promotes increased lactation Helps mother to fight postpartum depression

16. Helps in bonding with father & mother It endorses the notion of togetherness Promotion of early tactile, audio visual & emotional contact for both, & the baby is given the opportunity to further his familiarity with the mother’s voice, smell & heart beat It provides a sense of containment & closeness that is reminiscent of the uterus

17. RESPIRATORY PROBLEMS

18. Neonates are susceptible to respiratory compromise, for a reasons like lack of maturation in other body systems & as a result of their stage of lung development, diseases like Hyaline Membrane Disease (HMD), where surfactant production is inhibited.

19. STAGES OF LUNG DEVELOPMENT EMBRYONIC PHASE - this lasts until 5th week of gestation, in this stage the proximal airways develop PSEUDOGLANDULAR PHASE - this lasts from 5th to the 16th week of gestation. During this phase there is development of the lower conducting airways, bronchi & large bronchioles

20. 3. CANALICULAR PHASE - lasts from 17th to the 24th week of gestation. It’s the period for the development of the gas exchanging bronchioles 4 . TERMINAL SAC PHASE - this takes place between the 24th week & 36th week of gestation. Surfactant production begins with increasing efficiency as the alveolar ducts develop. 5. ALVEOLAR PHASE -this is ongoing from the 37th week of gestation until the 8th year of age

21. During this phase alveoli increase in number & there is maturation of the surfactant production. SIGNS OF RESPIRATORY COMPROMISE GRUNTING - audible sound heard on expiration RETRACTIONS - occurs due to an increase in the need to create higher inspiratory pressure ASYNCHRONY - breathing has a SEE- SAW pattern as the abdominal & diaphragm

22. movements works out of unison 4. TACHYPNOEA - RR above 60 breaths/mn, & aims to remove hypercarbia & prevent hypoxia 5. NASAL FLARING 6. APNOEA - absence of breathing for more than 20 seconds, occurs due to increasing respiratory fatigue in baby

23. COMMON RESPIRATORY PROBLEMS Pneumothorax Transient tachypnoea of the newborn (TTN) Infection/Pneumonia Meconium Aspiration Syndrome Respiratory Distress Syndrome (RDS) Cardiac disease

24. MECONIUM ASPIRATION SYNDROME

25. Fetal asphyxia causes the passage of meconium into the liquor. This meconium is unproblematic unless the baby gasps or breathes in amniotic fluid, potentially inhaling meconium simultaneously The passage of meconium into the liquor is rarely seen prior to 34 weeks, which suggests this is due to immaturity of the pre-term GI The baby may present with initial respiratory distress with cyanosis, increased work of

26. Breathing & a barrel shaped chest The meconium becomes trapped in the airways & causes a ball- valve effect, the meconium then blocks the airway during expiration so that air accumulates behind the blockage. This can leads to rupture of alveoli & cause the baby to develop a pneumothorax & causes pneumonitis too

27. The concentration of meconium is directly related to the volume of AF. Assessment of AF by doing meconium crit, hematocrit readings <4gm/dl ml = thin = dilute brownish fluid 4 - 9gm/dl ml = moderate, yellowish brown fluid,not clear >9gm/dl ml = thick = pea soup consistency

28. These babies need full intensive care & ventilation to prevent further deterioration Use of EXTRACORPOREAL MEMBRANE OXYGENATION (ECMO) where prolonged cardiac & respiratory support is given. This system provides heart lung bypass support outside of the baby. Symptomatic treatment

29. RDS or Hyaline Membrane Disease The diagnosis of HMD is derived from the presence of hyaline membranes in the airways resulting from the damaged epithelium. This occurs as a result of the insufficient production of surfactant & is more commonly seen in preterm babies, maternal diabetes also can inhibit surfactant production The introduction of surfactant therapy into neonatal care has significantly decreased the

30. Mortality & morbidity associated with RDS. Surfactant consists of several different types of proteins & phospholipids, which also help to prevent infection & produce further surfactant The X-ray has a ground glass appearance across the lung fields, while severe distress is represented by a “ white out”, the greater the density of white out, that much severe the

31. Disease. The infant has an increasing respiratory distress & work of breathing Baby requires NICU care for weeks

32. NEONATAL INFECTION

33. MODES OF ACQUIRING INFECTION Transplacental infection From amniotic fluid After birth from health care providers Contaminated objects or droplet infection INFECTIONS ACQUIRED BEFORE or DURING BIRTH rubella

34. Varicella zoster Toxoplasmosis Candida - oral candidiasis, cutaneous candidiasis, disseminated candidiasis Ophthalmia neonatorum Meningitis Eye, skin, respiratory & GI infections Umbilical infection UTI

35. MANAGEMENT OF INFECTION Prevention of infections in the mother Prevention of infection in the newborn Provide a safe environment Handwashing Promote exclusive breastfeeding Maintaining skin integrity & pH balance to increase immune function, avoiding irritation or trauma of the baby’s skin

36. Restrict visitors Early diagnosis & Rx of infection Use individual equipment for each baby Isolate infected baby Adequate spacing of cots in hospital Health education infection control 3. Prevention of infection in midwife Follow universal precautions Use of PPE

37. Covering all skin lesions Changing gloves between patients & washing hands after gloves are changed Disinfecting all blood splashes & spillage Follow safe biomedical waste Mx Appropriate vaccination. Eg; Hepatitis B DIAGNOSIS OF INFECTION Physical assessment may include observation of :

38. Temperature instability Lethargy or poor feeding, dehydration, starvation Acidosis or hypoxia Bradycardia or tachycardia or any apnoea Reduced urine output & any vomiting CNS signs Lab investigations include - AF, placental tissue & cord blood for specific organisms

39. 2. CBC 3. Specimens of urine & meconium for specific organisms 4.swabs from nose, throat, umbilicus,skin rashes, pustules or vesicles 5. MRI, CT scan, US & chest X ray 6. Comprehensive neurodevelopmental examination

40. LP for CSF examination TREATMENT OF INFECTION Caring of the baby in a warm thermoneutral environment Good hydration & correction of electrolyte imbalance, with demand feeding if possible & intravenous fluids as required Maintaining skin integrity to increase thermoregulation & to prevent fluid loss

41. Prompt systemic antibiotics or other drug therapy & local Rx of infection Ongoing monitoring of neurobehavioural status Reducing separation of mother & baby Encouraging breastfeeding Providing evidence based information, support & reassurance to parents

42. HAEMOLYTIC DISORDERS

43. Life span of RBC is 120 days Breakdown of RBC takes place in LIVER,SPLEEN & MACROPHAGES Normal bilirubin level in neonates - 5 mg/dL For adults - 0.1 to 1.2 mg/dL

44. HAEMOGLOBIN HAEM GLOBIN IRON BILIVERDIN UNCONJUGATED BILIRUBIN AMINO ACIDS PROTEIN FORMATION RBC FORMATION

45. BILIRUBIN UNCONJUGATED BILIRUBIN Fat soluble Can’t excrete through urine & faeces Deposits in fatty tissues CONJUGATED BILIRUBIN Water soluble Excreted in faeces & urine Jaundice occurs as a result of obstruction in excretion

46. JAUNDICE Jaundice is caused by bilirubin deposits in the skin. In term neonates it appears when serum bilirubin concentrations reach 5-7 mg/dl Types : Physiological jaundice Pathological jaundice Haemolytic jaundice`

47. PHYSIOLOGICAL JAUNDICE It occurs when unconjugated (fat soluble ) bilirubin is deposited in the skin instead of being taken to the liver . It is a normal transition occurring in 50% of term & 80% of preterm babies.

48. Jaundice usually appears on 2nd & 3rd day & never before 24 hrs of life. Bilirubin level never exceed 200-215 micromol/L (12-13 mg/dL) For a preterm baby,bilirubin level is 165 micromol/L (10 mg/dL) Fades usually by 1 week of age.

49. CAUSES Increased RBC destruction due to shorter life span of excess RBC, the neonatal had acquired due to relative anoxia state during intrauterine life. Decreased albumin binding capacity - hypoxia,acidosis & hypothermia can interfere with this.

50. Deficiency of UDP-GT enzyme. The level of enzyme is low during first 24hrs of life causing reduced bilirubin conjugation in liver. Increased enterohepatic reabsorption -This process is increased as the newborn bowel lacks the normal enteric bacteria that break down conjugated bilirubin to urobilinogen.

51. Mx Initiate breastfeeding within half an hour from birth, & continue exclusive breastfeeding for the neonate. Check for serum bilirubin level Provide phototherapy Monitor for pale stools & dark urine, this may indicate cholestatic liver disease

52. PATHOLOGICAL JAUNDICE It appears within 24 hrs of birth,characterized by rapid rise in serum bilirubin. Criteria for diagnosing are: Jaundice within the first 24 hrs of life Rapid increase in total serum bilirubin >85 micromol/L (5 mg/dL) per day Total serum bilirubin >200 micromol/L (12 mg/dL)

53. Conjugated bilirubin >25-35 micromol/L (1.5-2 mg/dL) Persistence of clinical jaundice for 7-10 days in term or 2 weeks in preterm babies. CAUSES Interference in bilirubin production,transport,conjugation or excretion

54. Production : Increased RBC destruction or haemolysis causes increased bilirubin levels. Causes of increased haemolysis are: Blood type/group incompatibility Extravasated blood - from cephalhematoma Sepsis Polycythemia Spherocytosis - fragile red cell membranes

55. f . Haemoglobinopathies - sickle cell disease or thalassaemia g . Enzyme deficiencies - glucose-6-phosphate dehydrogenase maintains the integrity of red cell membrane. 2. Transport Factors that lower blood albumin levels or decrease albumin binding capacity include;

56. Hypothermia,acidosis or hypoxia can interfere with albumin binding capacity Drugs that compete with bilirubin for albumin binding sites (eg : aspirin,sulphonamides & ampicillin) 3. Conjugation Immaturity of the neonate’s enzyme system interferes with bilirubin conjugation in the liver.other factors are ;

57. a)Dehydration,starvation,hypoxia & sepsis. (O2 & glucose are required for conjugation) b) TORCH infections (toxoplasmosis,others,rubella,cytomegalovirus,herpes) c) Other viral infections (eg; neonatal viral hepatitis) d) Other bacterial infections,particularly caused by E.coli

58. e) Metabolic & endocrine disorders that alter UDP-GT enzyme activity( eg; Crigler- Najjar disease & Gilbert’s syndrome) f) Other metabolic disorders such as hypothyroidism & galactosaemia. 4. Excretion Hepatic obstruction caused by congenital anomalies such as extrahepatic biliary atresia

59. Obstruction by bile plugs from increased bile viscosity (eg: cystic fibrosis,TPN,haemolytic disorders & dehydration) Infection,other congenital disorders & idiopathic neonatal hepatitis,which can also cause an excess of conjugated bilirubin Saturation of protein carriers needed to excrete conjugated bilirubin into the biliary system.

60. KERNICTERUS

61. Kernicterus ( bilirubin toxicity ) is an encephalopathy caused by deposits of unconjugated bilirubin in the basal ganglia of the brain,where bilirubin levels can be >340 micromol/L (20mg/dL) Signs : Lethargy Changes in muscle tone High pitched cry irritability

62. RISK FACTORS Hypoxia Acidosis Infection Hypothermia Dehydration Preterm & sick babies

63. HAEMOLYTIC JAUNDICE

64. Reason for increased Hb destruction in the fetus are Rhesus (RhD) isoimmunization or ABO incompatibility RhD INCOMPATIBILITY This occurs when a Rhesus positive baby enter a Rhesus negative mother’s blood stream. Mother’s blood treats the D antigen on positive blood cells as a foreign substance

65. & produces antibodies Patterns of Rhesus factor inheritance MOTHER FATHER BABY dd DD (HOMOZYGOUS) DD dd Dd (HETEROZYGOUS) Dd,dd dd dd dd

66. Causes Fetomaternal haemorrhage - small amounts of fetal Rh positive blood cross the placenta & enter the Rh negative mother’s blood. Any procedure or incident where +ve blood leaks across the placenta During any blood or platelet transfusion or drug use

67. Prevention of RhD isoimmunization Anti D Ig Administer Anti D Ig within 72 hrs of birth Anti D Ig is a human plasma based product that is used to prevent women producing anti D antibodies. It is not used when anti D antibodies are already present in the maternal blood

68. It does not protect against the development of other antibodies that cause haemolytic disease of the newborn Antenatal Prophylaxis Following Sensitizing Events Anti D Ig should be administered within 72 hrs of birth to all non sensitized Rh -ve mother inn the following cases:

69. Spontaneous miscarriage before 12 weeks requiring Sx intervention Any threatened,complete,incomplete or missed abortion after 12 weeks of pregnancy Termination of pregnancy by surgical or medical methods regardless of gestational age Ectopic pregnancy Amniocentesis,cordocentesis,chorionic villi sampling,fetal blood sampling or other invasive intrauterine procedure such as

70. shunt insertion ECV Fetal death in utero or stillbirth Abdominal trauma or antepartum haemorrhage Transfusion of Rh +ve blood or platelets or drug use

71. Administration of Anti D Ig ABO grouping & Rh type, Rh -ve mother are screened or Rh antibodies test (indirect Coomb test). A negative test shows absence of antibodies or sensitization Blood is retested at 28 weeks of pregnancy,if antenatal prophylaxis is routine, the first dose of anti D Ig is given Blood is retested at 34 weeks of GA, where

72. antenatal prophylaxis is not in place When anti D Ig prophylaxis is given at 28 weeks of GA,blood is not retested at 34 weeks of GA as it is difficult to distinguish passive anti D Ig from immune anti D. 2nd routine dose is given at 34 weeks of GA Following the birth cord blood is taken for the confirmation of Rh type ,ABO grouping,Hb,serum bilirubin & presence of

73. maternal antibodies A Kleihauer acid elution test is carried out on an anticoagulated maternal blood sample within 2 hrs of time to detect fetal Hb & estimates the no. of fetal cells in a sample of blood Anti D Ig is given into the deltoid muscle,where absorption is optimal.

74. Dose of Anti D Ig IM dose of 500 IU of anti D Ig will suppress the immunization that could occur following a FMH of 4-5 ml of RhD positive red cells. 500 IU of anti D Ig at 28 & 34 weeks of GA for women in their first pregnancy 250 IU following sensitizing events up to 20 weeks gestation.

75. Effects of RhD isoimmunization Anaemia Hypoxia Edema CCF Increased bilirubin levels in brain causes neurological damage Haemolytic anaemia leads to hydrops fetalis & death

76. fgyfyfuygfuyfuygy tftyyf Babies are pale, have edema & ascites & may be stillborn

77. Postnatal Rx of Isoimmunization Prevent further haemolysis Reduce bilirubin levels Remove maternal RhD antibodies from the baby’s circulation Combat anaemia

78. ABO INCOMPATIBILITY Occurs when mother’s blood group is O & the baby is group A or less often group B

79. Physical Assessment of a Baby with Jaundice Extent of changes in skin & scleral colour Head to toe progression of jaundice Lethargy & decreased eagerness to feed Dark urine or light stools Dehydration,starvation,hypothermia,acidosis or hypoxia Vomiting,irritability or high pitched cry

80. Rx Modalities PHOTOTHERAPY 1

81. Phototherapy or Light therapy is referred to as Heliotherapy, where patient is exposed to daylight or to a specific wavelength of light using polychromatic polarised light,fluorescent lamps,light emitting diodes & fibreoptic mattresses. Phototherapy converts fat soluble unconjugated bilirubin into water soluble bilirubin & decreases the likelihood of neurotoxicity or kernicterus

82. INDICATIONS FOR PHOTOTHERAPY For preterm infants <1500 g - between 85 & 140 micromol/L (5&8 mg/dL) For preterm infants >1500 g, sick infants & those with haemolysis -

83. Between 140&165 micromol/L (8&10mg/dL) For healthy term infants jaundiced after 48hrs - between 280 & 365 micromol/L ( 17 & 22 mg/dL) TYPES OF PHOTOTHERAPY Conventional phototherapy systems Uses high intensity light from conventional white & more recently blue,blue-green

84. & turquoise fluorescent lamps 2. Fibre optic light systems These uses a woven fibre optic pad that delivers high intensity light with no ultraviolet or infrared radiation. SIDE EFFECTS OF PHOTOTHERAPY Side effects of conventional white & blue fluorescent phototherapy are ;

85. Hyperthermia,increased fluid loss & dehydration Damage to the retina from the high intensity light Lethargy or irritability,decreased eagerness to feed,loose stools Skin rashes & skin burns Alterations in a baby’s state & neurobehavioral organization

86. Isolation & lack of usual sensory experiences,including visual deprivation A decrease in calcium level leading to hypocalcemia Low platelet counts & increased red cell osmotic fragility BRONZE BABY SYNDROME,riboflavin deficiency & DNA damage

87. CARE OF BABY UNDER PHOTOTHERAPY TEMPERATURE - maintain warm thermoneutral environment,monitor for hypo/hyperthermia EYES - eye shields or patches must cover the eyes without occluding the nose,& not be too tight or cause eye discharge or weeping SKIN - skin is cleaned with warm water & observed for rashes,dryness & excoriation

88. HYDRATION- monitor I/O chart,demand feeding is continued,extra fluids may require for ill & dehydrated babies NEUROBEHAVIOURAL STATUS- includes sleep & wake status,feeding behaviours,responsiveness,response to stress & interaction with parents & other carers CALCIUM LEVELS- monitor for hypocalcemia(7 mg/dL or <1.7 micromol/L

89. BILIRUBIN LEVELS - reducrd bilirubin level appesrsto be greatest in the first 24hrs of phototherapy PARENT SUPPORT

90. EXCHANGE TRANSFUSION 2

91. Assisting in withdrawing baby’s blood,which contains high bilirubin & replacing with fresh blood through umbilical vein. With HDN, sensitized erythrocytes are replaced with blood compatible with both the mother’s & the infant’s serum Helps to increase Hb level

92. Done for babies with: 255 micromol/L(15 mg/dL) for preterm babies, <1500 g 300-400 micromol/L(17-23 mg/dL) for sick & pre term babies > 1500 g, & with haemolysis 400-500 micromol/L (23-29 mg/dL) for healthy term babies

93. DRUG Rx Metalloporphyrins to reduce the level of unconjugated bilirubin 3

94. BIRTH INJURIES

95. Trauma during birth includes: Trauma to skin & superficial tissues Muscle trauma Nerve trauma Fractures

96. TRAUMA TO SKIN & SUPERFICIAL TISSUES Skin - scalp abrasions,bruising or superficial fat necrosis,puncture wound,lacerations resulting from forceps blades, vacuum extractor cups,scalp electrodes & scalpels Superficial tissues - includes oedematous swelling or bruising. Caput succedaneum is the diffuse oedematous swelling under the scalp & above the periosteum.

97. In face presentation, cervical os may restrict venous return & becomes congested & causes bruising of eyes & edematous lips In breech - bruised & edematous genitalia & buttocks

98. MUSCLE TRAUMA Injuries to muscle result from tearing or when the blood supply is disrupted. TORTICOLLIS The most commonly damaged muscle is the sternocleidomastoid muscles Excessive traction or twisting causing tearing to these muscles can occur during birth of the anterior shoulder of a fetus with a cephalic

99. presentation or during rotation of the shoulders when the fetus is being born by vaginal breech or C section 1-3 cm, apparently painless,hard lump of blood & fibrous tissue is felt on the affected muscle,the muscle length is shortened,therefore the neck is twisted to the affected side; a torticollis or wry neck. Mx - passive muscle stretching exercise

100. NERVE TRAUMA FACIAL NERVE On the affected side,has no nasolabial fold The eyelid remain open Mouth is drawn over to the unaffected side Excessive drooling Difficulty in feeding & swallowing Rx : if the eye is opened ,regular instillation of methyl cellulose eye drops which can

101. lubricate the eyeball Cosmetic Sx interventions can be done

102. 2. Brachial plexus

103. Nerve roots exiting from the spine at the fifth to eight cervical & the first thoracic vertebrae form a matrix of nerves in the neck & shoulder. Brachial plexus trauma results from excessive laceration,rotation or traction of the head & neck during vaginal breech birth or when shoulder dystocia occurs. There are three main injuries;Erb’s palsy,Klumpke’s palsy & total brachial plexus injury

104. ERB’S PALSY Paralysis of shoulder & the arm (not the hands) due to damage of 5th & 6th cranial nerves Baby’s affected arm is inwardly rotated,the elbow extended,the wrist pronated & flexed & the hand partially closed ( the waiter’s tip position) Baby’s hand is limp

105. KLUMPKE’S PALSY The shoulder & upper arm are unaffected Lower arm,wrist & hand are paralyzed resulting in wrist drop & no gasp reflex Occurs due to damage to the lower brachial plexus involving the 7th & 8th cervical & 1st thoracic nerve roots.

106. Total brachial plexus palsy There is complete paralysis of shoulder,arm & hand,lack of sensation & circulatory problems due to damage of all brachial plexus nerve roots INVESTIGATIONS X-ray US,MRI

107. FRACTURES Clavicular # - occurs with shoulder dystocia,vaginal breech birth or a macrosomic baby Humerus # - midshaft # occur with shoulder dystocia,vaginal breech birth Femur # - midshaft # due to vaginal breech birth Skull #

108. HAEMORRHAGE Blood volume in term baby = 80-100 ml/kg For a preterm = 90-105 ml/kg Haemorrhage can be due to : Trauma Disruptions in blood flow Or can be due to related to: Coagulopathies 2. Other causes

109. Haemorrhage due to trauma Cephalhematoma Subaponeurotic haemorrhage Subdural haemorrhage Haemorrhage due to disruptions in blood flow Subarachnoid haemorrhage Germinal matrix/intraventricular haemorrhage & intraparenchymal lesions

110. Haemorrhage related to coagulopathies Vitamin K deficiency bleeding (VKDB) This occur up to 12 months of age Commonly occurs between birth & 8 weeks of life Forms of VKDB : EARLY (0-24 hrs) CLASSICAL (1-7 days)

111. c) LATE (1-12 months, although the peak onset is before 8 weeks) 2. Thrombocytopenia Platelet count <1,50,000/ microlitre Severe thrombocytopenia <50,000/microlitre Babies at risk are : A severe congenital or acquired infection ( eg: syphilis,cytomegalovirus,rubella,toxoplasmosis,bacterial infection)

112. b) isoimmune thrombocytopenia c) inherited thrombocytopenia Or whose mother : Has idiopathic thrombocytopenia,purpura,SLE or thyrotoxicosis Takes thiazide diuretics 3. Disseminated intravascular coagulation

113. Haemorrhage related to other causes Umbilical haemorrhage Vaginal bleeding Haematemesis & melaena Haematuria Bleeding associated with IV access

114. CONVULSIONS

115. A convulsion is a sign of neurological disturbance not a disease & its a medical emergency Convulsive movements tend to be slower,less equal,are not necessarily stimulated by disturbance, cannot be stopped by restraint & are always pathological

116. CAUSES OF CONVULSIONS IN NEWBORN ARE : CATEGORY SELECTED CAUSES CNS Intracranial haemorrhage,intracerebral haemorrhage,hypoxic-ischemic encephalopathy,kernicterus,congenital abnormalities M etabolic Acquired disorders of metabolism,hypo & hyperglycaemia,hypo & hypercalcaemia,hypo & hypernatraemia,inborn errors of metabolism O ther Hypoxia,congenital infections,severe postnatally acquired infections,neonatal abstinence syndrome,hyperthermia I diopathic unknown

117. TYPES ARE : Subtle convulsions Focal tonic convulsions Clonic convulsions Myoclonic convulsions

118. Treatment Clear airway Provide adequate ventilation Semi prone position,with the head in neutral position Suctioning Administer O2 if required Active resuscitation Temperature regulation

119. Drug therapy - phenobarbitone & phenytoin,topiramate,levetiracetam

120. CONGENITAL MALFORMATIONS

121. A congenital abnormality is any defect in form,structure or function CAUSES OF CONGENITAL MALFORMATIONS CHROMOSOMAL ABNORMALITIES SINGLE GENE DEFECT MITOCHONDRIAL DNA DISORDERS MULTIFACTORIAL DISEASES TERATOGENS

122. WHO IS AT RISK ?? Women over 35 yrs Family history of neural tube defect or previous history of NTD Previous child born with chromosomal anomaly Parent carriers of sex linked or autosomal traits History of recurrent abortion

123. DIAGNOSIS US Clinical evaluation at birth MRI Radiography

124. IMPERFORATED ANUS A condition in which partial or complete obstruction of the anus,discovered at birth due to failure of the anus to develop normally in the embryo. More prevalent in males TYPES: High imperforated anus : it is a condition where rectum ends above the puborectalis

125. Sling.can be associated with rectourinary fistula in males or recto vaginal fistula in females 2. Low imperforated anus : it is a condition where rectum has transversed the rectalis sling DIAGNOSIS Absence of meconium passage Failure to pass a rubber catheter Radiology to detect atresia

126. MANAGEMENT Perineal anoplasty Colostomy for high imperforated anus MECONIUM ILEUS It is a manifestation of fibrocystic disease of the pancreas.

127. Pathophysiology Deficiency of pancreatic enzyme Causes meconium in the intestine inspissated This obstructs the lumen of lower ileum

128. DIAGNOSIS Obstruction of small gut Sweat test X ray Rectal mucosal biopsy to exclude Hirschsprung’s disease

129. MANAGEMENT Transaction of gut containing inspissated meconium anastomosis

130. FETAL ALCOHOL SYNDROME IUGR A growth restricted infant with microcephaly,flat facies,close-set eyes,epicanthic folds,small upturned nose,thin upper lip & low set ears Child can have learning difficulties Experiences acute withdrawal symptoms

131. Mx : Supportive therapy Counselling for the mother

132. FEEDING OF HIGH RISK NEONATE

133. EARLY FEEDING - initiate breastfeeding within half an hour after birth BREASTFEEDING - exclusive breastfeeding CUP/ KATORI/PALADAI FEEDING NASO/ ORAL GASTRIC TUBE FEEDING FORMULA FEEDING( complementary feeding/top-ups) SUPPLEMENTARY FEEDING

134. PALADAI/KATORI FEEDING

135. INFECTION CONTROL IN NICU