HIGH RISK NEWBORN-2.pptx HIGHRISK CONDITIONS OF NEWBORN

presentation related to conditions of newborn

1. NEONATAL RESPIRATORY DISORDERS

2. Birth asphyxia ( ASPHYXIA NEONATORUM)

3. Incidence Birth asphyxia in underdeveloped countries 10% of newborns suffer mild to moderate birth asphyxia 1% of newborns suffer severe birth asphyxia

4. Risk factors Antepartum : Maternal diabetes post-term gestation Pregnancy induced hypertension multiple gestation Chronic hypertension Previous Rh sensitization maternal drug abuse Previous stillbirth maternal age >35 or<16 Bleeding in second or third trimester no prenatal care Maternal infection Polyhydramnios or oligohydramnios

5. Risk factors Intrapartum : Elective or emergency c/s Precipitous labour , prolonged labour Prolonged second stage of labour Premature labour Abnormal presentation Rupture of membranes > 24 hours Foul-smelling amniotic fluid Non reassuring fetal heart rate patterns Use of general anesthesia Prolapsed cord

6. CLINICAL FEATURES These depend upon the cause, duration of oxygen lack. Some common clinical features are, Cyanosis Bradycardia Stiff or limp limbs (Hypotonia) Poor response to stimuli Hypoxia Metabolic acidosis Shock (Asphyxia pallida)

7. CLINICAL CONSEQUENCES (PATHOLOGICAL CHANGES) HYPOXIA OR LOW APGAR SCORE HYPERPNEA & HYPER TENSION PRIMARY APNOEA GASPING ATTEMPT TO BREATH (IF IT UNRESOLVED) SECONDARY APNOEA BRADY CARDIA & SHOCK DIMINISHED CEREBRAL BLOOD FLOW CEREBRAL HAEMORRHAGE HYPOXIC ISHAEMIC ENCEPHALOPATHY (IF SEVERE) DEATH OR HANDICAP

8. DIAGNOSIS CHECK FOR APGAR SCORE at 1, 5 and 15 mts. Assessment Fetal heart rate slows Electronic fetal monitoring • persistent late deceleration of any magnitude • persistent severe variable deceleration • prolonged bradycardia • decreased or absent beat-to-beat variability Thick meconium-stained amniotic fluid Fetal scalp blood analysis show pH less than 7.2

9. Neonatal Evaluation of birth asphyxia APGAR Scoring A Appearance P Pulse G Grimace A Activity R Respirations

10. APGAR Score

11. Apgar Score Total Score = 10 score 7-10 normal score 5-6 mild birth asphyxia score 3-4 moderate birth asphyxia score 0-2 severe birth asphyxia

12. Effects of Asphyxia Central nervous system • infarction, intracranial hemorrhage, cerebral edema, seizure, hypoxic- ischemic encephalopathy Cardiovascular • bradycardia, ventricular hypertrophy, arrhythmia, hypotension, myocardial ischemia

13. Effects of Asphyxia Respiratory system • apnea, respiratory distress syndrome cyanosis Kidney & Urinary Bladder • acute tubular necrosis, bladder paralysis Gastrointestinal tract • necrotizing enterocolitis , stress ulcer

14. Effects of Asphyxia Hematology • Disseminated intravascular coagulation Metabolic • hypoglycemia, hyperglycemia, hypocalcemia, hyponatremia Integument • subcutaneous fat necrosis

15. MANAGEMENT It is of 2 types. PROPHYLACTIC DEFINITIVE PROPHYLACTIC MANAGEMENT Antenatal detection of high risk patients Early detection of fetal distress and timely termination Intra-partum use of electronic fetal monitoring Scalp blood ph assessment Careful administration of anaesthesia

16. DEFINITIVE Neonatal Resuscitation

17. Newborn Resuscitation Guidelines Meconium -stained amniotic fluid: endotracheal suctioning of the depressed - not the vigorous child Hyperthermia should be avoided 100% oxygen is still recommended, however if supplemental oxygen is unavailable room air should be used Chest compression: Initiated if heart rate is absent or remains < 60 bpm despite adequate ventilation for 30 sec Medications: Epinephrine 0.01-0.03 mg/kg if heart rate < 60 bpm in spite of 30 seconds adequate ventilation and chest compression Volume: Isotonic crystalloid solution or o-negative blood

18. Facts About Newborn Resuscitation The most important is to get air into the lungs

19. Prognosis Apgar score < 5 at 10 minutes : nearly 50 % death or disability No spontaneous respiration after 20 min : 60 % disability in survivors . No spontaneous respiration after 30 minutes : nearly 100 % disability in survivors

20. RESPIRATORY DISTRESS SYNDROME A neonate is said to be suffering from respiratory distress, When he has tachypnea with a respiratory rate of 60/ mt or more. In each and every infant with respiratory distress, it becomes mandatory to assess the situation and to determine the factors underlying the problem. Based on the below scoring system, the severity of respiratory distress can be assessed.

21. D efinit i on Respiratory distress s y nd r ome is define d as persistence of arterial the O 2 t e nsio n < 5 mmh g an d cen tral cyanosis in room air D . C . D UTTA

22. INCIDENCE It ranges from 75% at around 28 weeks to 52% at 30 weeks of gestation. Use of surfactant has significantly reduced the risk of neonatal death by >10 %

23. CLINICAL CAUSES PULMONARY Hyaline membrane disease Meconium aspiration Pulmonary hypoplasia Broncho pneumonia Airway obstruction

24. CLINICAL CAUSES CARDIOVASCULAR Congenital heart disease Heart failure Pulmonary hypertension

25. CLINICAL CAUSES NON-CARDIOPULMONARY Metabolic acidosis Hypo or hyperthermia Hypoglycemia Asphyxia Birth trauma Drugs Intracranial injury

26. PATHOPHYSIOLOGY Risk factors deficient surfactant production Unequal inflation of alveoli Increased efforts to keep unstable alveoli open Pulmonary vascular resistance increases Hypo perfusion of lungs

27. Hypo perfusion of lungs Right to left shunt Hypoxemia , hypercapnia ,acidosis Hyaline membrane formed Inhibition of gas exchange Decreased lung compliance Respiratory distress syndrome

28. CLINCAL MANIFESTATIONS (4-6 HOURS AFTER BIRTH) Tachycardia Tachypnea Chest retractions Fine crackles Expiratory grunting Nasal flaring Central cyanosis Ventilator failure Extremities puffy or swollen Apnea

29. Diagnostic evaluation 2 or more features if found at examination , more than an hour apart are enough to diagnose RDS Respiratory rate more than 60 breaths/min Nasal flaring Rib retraction Expiratory grunting Central cyanosis

30. Other investigations ABG analysis Shake test Chest x ray –ground glass mott l ing due to extensive atelectasis Assessment of severity of RDS Downe’s score Silverman-Anderson score

31. SHAKE’S TEST It can be done on the gastric aspirate to determine lung maturity. Mix 0.5 ml of gastric aspirate with 0.5 ml of absolute alcohol in a test tube and shake for 15 sec. Formation of bubbles indicate adequate surfactant and less chance of RDS.

32. SLIVERMAN-ANDERSON SCORE

33. Preventive measures Betametehosone-12mg Q24H*2doses- lung maturity before 34 weeks Assessment of lung maturity before premature induction of labour Prevent fetal hypoxia in GDM mothers Avoid hypothermia in the neonate

34. COMPLICATIONS Metabolic disorders Patent ductus arteriosus Low blood pressure Chronic lung diseases Intra cranial haemorrage

35. Treatment principles To prevent hypoxia and acidosis Maintain fluid balance Prevent atelectasis and pulmonary edema Avoid lung injury and infection

36. treatment NICU admission Baby placed in incubator Clear the airway Adequate warmth and humidified oxygen therapy Correction of hypothermia Correction of anemia , electrolyte imbalance Prevention of infection Frequent monitoring of ABG

37. Cont.. Surfactant therapy Preterm infants <28 weeks are administered within 15-20 minutes of life Commercially available surfactant Survanta Curosurf Neosurf

38. Nursing care Providing effective ventilation Providing optimal environment temperature Adequate nutrition by parenteral nutrition Oxygen therapy Minimal handling Position facilitating open airway with head supported by small sheet Encourage bonding Skin care –frequent position change Psychological support to the family

39. HYPOXIC ISCHAEMIC ENCEPHALOPATHY (HIE) HIE or hypoxic ischemic brain damage is brain injury due to hypoxemia and ischemia with decreased tissue perfusion. Incidence Perinatal asphyxia 1 to 1.5% in developed countries In India HIE is, 1.4% Incidence of cerebral palsy due to perinatal asphyxia - 10% in developed countries

40. Causes Main cause for HIE is oxygen deprivation to the brain. Some common causes of oxygen deprivation are, injury or complications during birth respiratory failure blocked or ruptured blood vessels in the brain lack of oxygen compression or injury to the trachea that reduces or stops breathing.

41. Risk factors Perinatal asphyxia is due to - abruptio placenta Prematurity PIH or Preeclampsia post maturity growth retardation prolapsed cord respiratory distress of the mother Hypotension

42. Pathogenesis pathogenesis of HIE depends upon, gestational age of the baby the timing and duration of insult the severity of insult maturity of the brain Based on the above, asphyxia results in loss of homeostatic mechanism and systemic hypotension results in impaired cerebral perfusion. Clinical features perinatal asphyxia leads to multi system organic damage. Other systems are affected well before the central nervous system.

43. Clinical stages 3 stages of HIE stage 1 –mild stage 2 –moderate stage 3 –severe In mild, neonate maybe asymptomatic at birth. But develops symptoms within first 12 hours and progresses till 72 hours to 5 days Investigations EEG, MRI, CT scan, Neuro sonography, spectroscopy

44. Management Initially neonatal resuscitation with supply of 100% oxygen by noting the apgar score. Supportive management once oxygen is established the supportive management is to be maintained. monitor blood gases , glucose , urea and electrolytes , creatinine and fluid balance. Mechanical ventilatory support is needed to maintain the blood gases and acid base balance, Status and to prevent hypoxia, hyperoxia, hypercapnia and hypocapnia. Hypotension should be promptly treated. Dopamine can be used to achieve adequate cardiac output. Fluid and electrolyte management is very important. Neonatal seizures can be treated by administration of available therapies with phenobarbitone, phenytoin and benzodiazepines. surgical care is needed with surgical drainage, in case of posterior cranial fossa hematoma. Infant must be referred to a paediatric neurologist in management of seizures and interpretation of EEG.

45. Follow up care The goal is to detect impairments and promote early interventions. Growth parameters should be clearly and closely monitored. Neurological examination and ophthalmic examination should be periodically done to detect impairments. Prevention Identify the risk factors and foetal distress in the antenatal period and provide appropriate treatment.

46. MECONIUM ASPIRATION SYNDROME (MAS). This respiratory disorder is caused by meconium aspiration by the fetus in utero or by the newborn during labor and delivery. MAS is often a sign that the neonate has suffered asphyxia before or during birth. The mortality rate can be as high as 50% and survivors may suffer long‐term sequelae related to neurological damage

47. CAUSES AND PATHOPHYSIOLOGY: Fetal hypoxia; e.g. cord prolapse that comes around the neck of the fetus many days before delivery. Babies born breech presentation. In both cases; intrauterine hypoxia Or breech presentation vagal nerve stimulation relaxation of the sphincter muscle releasing of the first stool (meconium) in the intrauterine life and becomes mixed with the amniotic fluid, with the first breath the baby can inhale meconium .

48. MAN A GEMENT Suctioning of the oropharynx by obstetricians before delivery of the shoulders. Immediate insertion of an ET tube and tracheal suctioning before ambu bagging (Maintain a neutral thermal environment). Gastric lavage, and emptying of the stomach contents to avoid further aspiration

49. MANAGEMENT Postural drainage and chest vibration followed by frequent suctioning. Pulmonary toilet to remove residual meconium if intubated. Antibiotic coverage (Ampicillin & Gentamicin). Oxygenation ( maintain a high saturation > 95%) Mechanical ventilation to avoid hypercapnia & respiratory acidosis

50. TRANSIENT TACHYPNEA OF THE NEWBORN (TTN) TTN is a benign disease of near‐term or term infants who display respiratory distress shortly after delivery. It occurs when the infant fails to clear the airway of lung fluid or mucus or has excess fluid in the lungs, this limit the amount of alveolar surface available for gas exchange, leading to increased respiratory rate and depth to better use of the surface available.

51. CLINICAL FEATURES The infant is usually near‐term or term. Exhibits tachypnea (> 80 breaths/min) shortly after delivery. The infant may also display mild grunting, nasal flaring, intercostal retraction, and cyanosis. Spontaneous improvement of the neonate, which considered as the most important marker of TTN

52. MANAGEMENT Usually, this condition resolves over 24–72 hours. Treatment is supportive and may include supplemental  oxygen  and  antibiotics .  Oxygenation. Start feeding as tachypnea improves. Outcome and prognosis: Peaks intensity reached at 36 hours of infant ’ s life. The disease is self‐limited (respiratory symptoms improve as intrapulmonary fluid is naturally absorbed or artificially mobilized using diuresis).

53. NEONATAL APNEA

54. DEFINITION AND CLASSIFICATION Apnea is the cessation of respiration accompanied by bradycardia and/or cyanosis for more than 20 second s . Types Pathological apnea: Apnea within 24 hours of delivery is usually pathological in origin. Physiological apnea: Apnea developing after the first three days of life and not associated with other pathologies, may be classified as apnea of prematurity

55. MANAGEMENT Monitor at‐risk neonates of less than 32 weeks of gestation Begin with tactile stimulation; gentle shaking or prick the sole of the foot often stimulate the infant to breath again If no response to tactile stimulation, bag and mask ventilation should be used during the spell. CPAP or ventilatory support in recurrent and prolonged apnea Pharmacological therapy: Theophylline. Treat the cause, if identified, e.g., Sepsis, Hypoglycemia, Anemia

56. Birth Injur ies

57. DEFINITION  In ju ri e s t o th e i n f a nt mechanical forces r e s u l ti ng during f r o m b ir t h (compression, traction)

58. INCIDENCE In 1970 ~ 64 deaths/100 000 births related to birth trauma In 1985 ~ 7.5 deaths/100 000 births related to birth trauma -- 88% decline Birth trauma causes < 2% of neonatal deaths Average ~ 6 - 8 injuries/1000 births

59. PREDISPOSING FACTORS Primigravida C ephalopelvic disproportion Small maternal stature maternal pelvic anomalies Prolonged or rapid labor Arrest of descent of presenting fetal part Oligohydramnios Resuscitation with CPR Abnormal presentation (breech/face) Use of forceps or vacuum extraction VLBW infant or extreme prematurity Macrosomia Large fetal head Fetal anomalies Fetal neuromuscular disease

60. CLASSIFICATION OF BIRTH INJURIES Soft Tissue Injuries (Abrasions, Bruising, Fat Necrosis, Lacerations) Extracranial Bleeding (Caput succedaneum, Cephalhematoma, Subgaleal Hematoma) Intracranial Bleeding (Subarachnoid, Epidural, Subdural, Cerebral, Cerebellar) Nerve Injuries (Facial and Cervical Nerve Roots, Horner Syndrome, Recurrent Laryngeal Nerve) Fractures (Clavicle, Humerus, Femur, Skull) Dislocations Eye Injuries (Subconjunctival and Retinal Hemorrhage) Solid Organ Injury (liver, spleen, kidney, adrenal glands)

61. CEPHALHAEMATOMA  It is swelling on infants skull, in which collection of blood occur between the pericranium & flat bones of skull. It is usually unilateral. Most of times it occurs over parietal bone. Predisposing factors: - - - CPD Precipitate labour forceps delivery

62.  Characteristics: - - - - N eve r p r e s e n t a t b i r t h , gr a du a l l y d e v e l o p s a ft e r 1 2 - 24 hours. Limited by suture line, never cross a suture. It is soft, circumscribed, fluctuant & in compressible. It persists for week.  Treatment : - N o t r ea t m e nt i s r e qu i r ed , a s b l oo d i s ab s o r be d i n course of time i.e. 6 to 8 weeks and swelling subside.

63. CAPUT SUCCEDANEUM  It is an oedematous swelling on the fetal skull in which serosanguinous infilteration occur into scalp tissue. Characteristics: - - - - - It is present at birth. It can cross suture line. It tends to grow less. It usually disappear within 36hours. It is diffuse type & pits occur when pressure is given with finger.

64. CAPUT SUCCEDANEUM

65. S U B A PONE U R OT I C HAEMORRHAGE  It is a condition, in which bleeding occurs below the epicranial aponeurosis. It is usually associated with vaccum extraction.

66.  Characteristics: - It is present at birth. - - - - It crosses suture line. It increases in size. A firm, fluctuent mass is seen. It can extend upto subcutaneous tissue of neck & eyelids. - It resolve over 2-3 weeks.

67.  Treatment: - It is absorbed, so no treatement but the baby should be observed for signs of;  hyperbilirubinemia.  A nea m i a .

68. Scalp Swellings in Newborns

69. F R A C T U R ES skull fracture - Fracture s of skull are rare. Fractures, occasionally associated with intra – cranial haemorrhages, seizures & death as contusion of the underlying brain m a y have occurred . Fractures may be fissures or depressed type . X- ray is required to diagnose skull fractures. Treatment: Uncomplicated fractures are usually symptomless. Pressure effect may be seen occasionally. Treatment is, depressed bone has to be elevated/ subdural haematoma may have to be aspirated/ excised surgically. Antibiotic s to prevent infection.

70. Clavicle fracture - Asymptomatic , associated with br a chial plexus dam a ge . Diagnosed: a crack may be heard during delivery, by feeling the distortion at the break, presence of crepitus and in late phase , callus formation . Treatment: A figure of eight bandage Union of bre a k can occur in 7- 10 days.

71. Humerus fracture - - It occur during bringing down of an extended arm in a breech presentation. A cr a ck m a y b e hea r d a t de l i ve r y . D i a gno s i s i s confirmed by x- ray. Treatment : . Splint to the upper arm by applying a crepe bandage. . A stable union takes place in 2- 3 m on t h s.

72. Femur fracture - - It can occur during delivery of extende d leg in a breech presentation. A crack is heard or felt at the time delivery. Diagnosed : It is confirmed by x- ray. Treatment : be i n g f i r m l y . S i m p l e sp l i nt i ng , a cr e pe b a nda ge applied to upper leg for 2- 3 weeks.

73. NERVE INJUR IES Facial nerve injury. Brachial plexus injury.

74. Facial nerve injury ra m us o f It is associated with forceps delivery. Fa c i a l n er v e i s c o m p r e ss e d a g a i n st mandible. It results in; . Unilateral facial weakness. . Eyelid of affected side remain open.

75.  Treatment : No treatment is required. Only cellulose eye drops in case eyelids open. Spontaneous improvement occur in 7- 10 days .

76. BRACHIAL PLEXUS INJURIES  It result from stretching or disruption of nerve of brachial plexus. Injuries result from; - Excessive lateral flexion of head & neck in case of shoulder dystocia or breech presentation. Diagnosed: x- ray of clavicle, arm, cervical spine & chest.

77. TY PES Erb’s palsy. Klumpk e ’s palsy. Erb’s palsy: . Arm rotated inwardly. . Arm lies limply by his side. . Unable to flex his elbow & lift his arm. . Half closed hand outwardly turned. Klumpk e ’s palsy: . Wrist drop and lim p fingers. . Involves lower arm, wrist and hand.

78. Treatment : Treatment for Erb’s palsy is, use of splint to hold the arm abducted to a right angle and externally rotated. The forearm is flexed at right angle & supinated and the hand is dorsiflexed. Treatment for Klumpke’s palsy is, splinting the arm with the forearm pronated and the fingers extended. Resting of arm for 7- 10 days. Massage & Full range of passive movements for shoulder, elbow & wrist.

79. PHRENIC NERVE INJURY It occurs with brachial plexus injury. It can affect one or both sides of diaphargm .

80.  Treatment: - simple o x y ge n t h er a py t o i nt e r m i t t en t po s i t i v e pressure ventilation. Complication: - Hypostatic pneumonia .

81. HO R NE R ’ S SYND R OME It is associated with klumpke’s paralysis. It results form damage to cervical sympathetic nerves. Symptoms - - - P tosis . E xop ht ha l m u s. Absence of sweating from affected side. Treatment: Spontaneous resolution may occur in 3 months.

82. SOFT TISSUE INJURY Injury to superficial tissues - - Bruising & excoriation. Eyelids & lips oedematous. Treatment: . No treatment unless complications. . Reassurance to mother .

83. Injury to liver & spleen injury to liver subscapular haematoma decreased hematocrit & haemaglobulin Treatment : - - Immediate resuscitative measures. Restoration of circulatory volume.

84. Renal injury - It leads to massive haemorrhage – lead to circulatory collapse. Diagnosed: by ultrsound Treatment : Supportive treatment. If required , blood transfusion.

85. Intestinal injury Result s in coagulopathy. Bleeding per rectum. Anaemia & feeding difficulties. Treatment : . I / V fluids. . Nasogastric suction. . Hematoma usually resolves.

86. MUSCLE INJURY Injury to sternomastoid muscle - Results in torticollis . It occurs during delivery of anterior shoulder in a vertex presentation or while rotating the shoulder in breech presentation.

87. TYPES : Tearing of muscle. Impaired blood supply. Treatment : . Swelling resolves over several weeks. . Muscle stretching exercises. . Sleep on opposite side of injury.

88. S K I N INJURY Bruising or subcutaneous fat necrosis- usually on face. In case of abscess – incision & antibiotics.

89. Prevention of injury in newborn Provide comprehensive antenatal & intrnatal care. Screen out the high risk babies who are likely to get injur ies during delivery. Continuously do fetal monitoring to find out cerebral anoxia. Give episiotomy carefully. Do not unduly stretch the neck.

90. Administer vitamin k . Prefer caserean, if difficult delivery is to be done i.e., by forceps. Never apply traction, till the blades are over biparietal plane. Avoid ventouse delivery for preterm babies. Take precautions while delivering after coming head in breech delivery.

91. HAEMORRHAGIC DISEASE OF THE NEWBORN

92. DEFINITION Hem o rrhagic diseas e of n e wborn which i s also known as vitamin K bleeding(VKDB ) i s a d e fic i en c y c oag u l a tion disturbance in newborn due to vitamin K deficiency.

93. CLASSIFICATION OF VITAMIN K DEFICIENCY (depending on onset of disease) Early onset Classic onset Late onset

94. Early onset-within first 24 hours. Classic onset-after 24 hours till 1 week Late onset-2-12 weeks

95. INCIDENCE Early onset-very rare Classic onset-2% Late onset-depending on disease

96. CAUSES OF VITAMIN K DEFICIENCY OF NEWBORN A moderate decrease of factors II, VII, IX and X may cause bleeding by 48-72 hours after birth .

97. CAUSES OF EARLY ONSET Maternal drugs (phenobarbitone , phenytoin , warfarin , rifampin, isoniazid) Inherited coagulopathy

98. CAUSES OF CLASSIC ONSET Vitamin k deficiency Breast feeding

99. CAUSES OF LATE ONSET Cholelithiasis – mal-absorption of vitamin k (biliary atresia , cystic fibrosis , hepatitis ) Warfarin ingestion Idiopathic in Asian breast fed infants.

100. COMMON CAUSES OF HDN Abnormalities of clotting factors DIC – due to infection, anoxia and shock Platelet dysfunction – thromboasthenia or thrombocytopenia Inherited abnormalities of blood coagulation – haemophilia Obstetric trauma

101. RISK FACTORS Babies who do not receive the preventative vitamin – K at birth. Exclusively breast fed babies – mostly in Asian countries (breast milk contains less vit-K than cow’s milk.) Babies, whose mothers have seizures and taken anti convulsant treatment.

102. COMMON SITES OF BLEEDING UMBILICUS MUCUS MEMBRANES GI TRACT VENI PUNCTURES CIRCUMCISION AREAS

103. SYMPTOMS OF VITAMIN K DEFICIENCY Early onset Cephal-hematoma Intra cranial hematoma Gastro intestinal bleeding Umbilical bleeding Intra abdominal

104. Classic onset - GI bleeding ENT bleeding Intra cranial bleeding Bleeding from circumcision Cutaneous bleeding Bleeding from injection sites

105. Late onset GI bleeding Cutaneous bleeding ENT bleeding Bleeding from injection sites Thoracic bleeding

106. DIAGNOSIS History collection Physical examination Assess for signs of bleeding

107. CONT.. Blood tests – CBC, BT, CT Coagulation profile Prothrombin time(PT) Partial thromboblastin time(PTT) Fibrinogen level Platelet count Reticulocyte count USG (locating bleeding) MRI (rare)

108. TREATMENT Treatment is depending upon, The underlying cause Maturity of the baby Overall health status Tolerance capacity Gestational age Severity and onset of the disease

109. TREATMENT Administration of vitamin K shot at birth-IM or IV(dosage vitamin K 0.5 to 1 mcg) Subcutaneous administration of vitamin K is given in symptomatic infants than IM If the bleeding is persistent , immediate blood transfusion is given –whole blood/fresh plasma until prothrombin level is increased . Parenteral supplement is given in case of late onset of vitamin K deficiency

110. PREVENTIVE MEASURES Vitamin k shot at birth Vitamin k administration for pregnant women who takes anti seizure medications

111. Forms of vitamin K – Vitamin K1-Phylloquinone – Vitamin K2-Menaquinone – Vitamin K3-Menodione

112. PROGNOSIS Prognosis is good, if blood loss is less and the treatment is promptly initiated. Prognosis is very poor in case of late onset of vitamin k deficiency .

113. COMPLICATIONS Intra cranial hemorrhage Retro peritoneal hemorrhage Death

114. Cong e nital Malformations

115. DEFINITION INCIDENCE CAUSES DIAGNOSIS Cong e nital Malformations

116. Congenital Malformations: Anenceplhaly Microcephaly Megalencephaly Septo-Optic Dysplasia Diast e matomyelia Polymycrogyria Encephalocele Spina bifida

117. Anencephaly A nencephaly is a cephalic disorder that results from a neural tube defect that occur when the cephalic(head) end of the neural tube fails to close, usually between 23 rd and 26thday of pregnancy, resulting in the absence of a major portion of brain, skull, and scalp.

118. Clinical Presentati o n: The National Institute of Neurological Disorders and Stroke (NINDS) describe d the presentation of this condition as follows - A baby born with anencephaly is usually blind, deaf, unconscious and unable to feel pain.

119. Symptoms: Absence of the skull Absence of the brain ( cerebral hemisphere and cerebellum) Facial features abnormalities. Cleft palate Congenital heart defects.

120. Diagnostic Evaluations : Pregnancy Ultrasound Amniocentesis Alpha- fetoprotein level. urine estriol level Pre-Pregnancy serum folic acid test.

121. Ma n ageme n t: There is no treatment for anencephaly. Treatment is support. Folic acid can help reduce the risk of certain birth defects. It is important for women who became pregnant to get enough folic acid. Multivitamin with folic acid should be taken every day by pregnant women's or women's planning for pregnancy. Getting enough folic acid can reduce the chance of neural tube defects by 50%.

122. Microcephaly.

123. Microcephaly. The term MiCROCEPHALY means small head . Microcephaly is a rare neurological condition in which an infant has a significantly smaller than normal head size because the brain has not developed properly or has stopped growing.

124. Causes and Risk factors:- Microcephaly can be caused by the exposure of harmful substances during the fetal development. The following may predispose a fet us to problem affecting it’s development of the head during pregnancy: Exposure to hazardous chemicals Methyl mercury Poisoning Lack of proper vitamins and nutrients in mothers diet.

125. Con t … Cytomegalovirus, rubella or varicella-zoster virus infection. Illegal drugs and alcohol consumptions Untreated phenylketonuria(PKU) Chromosomal Abnormalities such as Down syndrome.

126. Clinical Manifestations : Depending on the severity of the syndrome; baby’s head is very small Mental retardation’ Delayed motor function and speech Increased movement of arms and legs Facial distortion Hyperactivity Seizures Difficulty with coordination and balance Other brain and neurological abnormalities. Poor feeding developmental delays Intellectual disabilities.

127. Diagnostic evaluation: o Birth and family history o Physical exam ination o Prenatal ultrasound o Head CT or MRI o Blood and Urine test.

128. Management: T here is no treatment that will enlarge Childs head or reverse complications. Treatment is symptomatic and supportive. Treatment focuses on ways to manage child condition. Physical, speech, and occupational therapist helps to maximize abilities and minimize dysfunction. Medications also used to control seizures, hyperactivity and neuromuscular symptoms. Genetic counseling may help families to understand the risk for microcephaly in subsequent pregnancies.

129. Megalencephaly

130. Megalencephaly: M egalencephaly also called macrencephaly is a condition in which there is abnormally large , heavy and usually malfunctioning brain. T he brain weight is greater than the average for the age and gender of the individual. I t may be visible at birth or the head may become abnormally large in early years of life.

131. Causes: Genetic and non-genetic factors megalencephaly may occur as an autosomal dominanat (more common) or autosomal reccessive condition. Sotos syndrome( overgrowth syndrome) Alexander disease ( Leukodystrophy) chromosomal abnormality such as Klinefelter syndrome. non- Genetic Factors: transient disorder of cerebro spinal fluid. also it can be idiopathic.

132. Clinical Manifestations : developmental delays S eizures / convulsive disorder an abnormal brain cortex and spinal cord Mental retardation is common with megalencephaly. some neurological symptoms: delay of motor milestone such as holding up head, rolling over. Speech delay Poor muscle tone Body asymmetry Paralysis of more or both sides of body. Poor coordination Involuntary movements Visual disturbances

133. Diagnostic Evaluation : Medical history or family History physical exam ination and developmental and neurological exam. CT scan or MRI Laboratory testing for Genetic or Chromosomal Disorders.

134. Management: There is no specific cure for megelencephaly; routine Health care Maintenance including Periodic Head Measurements for Patients with neurological or Physical problems anti-epileptic drugs for seizures. Treatment of medical complications Rehabilitation for neurological problems such as speech delay , poor muscle tone.

135. Septo-Optic Dysplasia: S epto - optic dysplasia is a rare disorder characterize d by abnormal development of optic disc, pituitary deficiencies and often agenesis of the septum pellucidum .

136. Causes: Idiopathic Young maternal age Familiar recurrence of at least one genetic form Risk factors: maternal smoking, alcohol consumption, use of addictive drugs during early gestation.

137. Clinical manifestations: optic nerve dysplasia Nystagmus inward and outward deviation of the eyes Pituitary deficiency Hypoglycemia Jaundice Severe mental retardation Seizures Brain impairment Hypotonia.

138. Management: Hormone Replacement:- all pituitary hormones can be replace d in pituitary deficiency V ision , physical and occupational therapies may be required. If brain impairment is significant , it cannot be made normal by any treatment.

139. Diast e matomyelia

140. Diast e matomyelia : It is a congenital disorder in which a part of spinal cord is split, usually at the level of upper lumbar vertebra . The particular malformation is a complete or partial separation of the spinal cord into two separate “hemi cords”. The separation usually occurs in the middle of the spinal cord and the hemi cords reunite below it. When the split do not reunite distally to the spur the condition is refer to as diplomyelia .

141. Clinical Manifestation: The sign s and symptoms may appear at any time of life: C u taneous Lesions: such has hairy patch, dimple, Hemangioma, subcutaneous mass, lipoma or teratoma override the affected area of spine is found. Neurological Symptoms: are nonspecifics , the symptoms are caused by tissue attachm e nts that limits the movements of the spinal cord within the spinal column.

142. These attachments causes an abnormal stretching of spinal cord. foot and spinal deformities. Weakness in the l egs Low back pain Scoliosis incontinence In adulthood: sign s and symptoms often includes progressive sensory and motor problems and loss of bladder and bowel control.

143. Diagnostic Evaluation : X-ray CT scan MRI Ultrasound in 3 rd trimester Management: symptomatic treatment Surgical Management: includes decompression of neural elements and removal of bony spur.

144. Polymicrogyria PMG is a disorder of neural migration resulting in structural malformation of the human brain characterized by an excessive number of small convolutions (gyri) on the surface of the brain . Either the whole surface or part of the surface can be affected. The cause is unknown in many case s . Other responsible factors are , infection during pregnancy , lack of oxygen , genetic causes. Sign and symptoms : developmental delays, feeding problems, respiratory problems , cerebral palsy, mental retardation.

145. Treatment:   Polymicrogyria  (PMG) malformation cannot be reversed, but the symptoms can be  treated . The removal of affected areas through hemispherectomy has been used in some cases to reduce the amount a seizure activity. 

146. Encephalocele (Cranium Bifidum):-

147. Encephalocele (Cranium Bifidum):- It is a neural tube defect characterized by sac- like protrusion of the brain and the membranes that cover it through the openings in the skull. These defects are caused by the failure of the neural tube to close completely during fetal development.

148. Classifications: Nasofrontal: present in the nose and forehead. Nasoethmoidal; present in the nose and ethmoid sinus Naso-orbit: present in the nose and the eye. Encephalomeningocele : if brain tissue is also involved. Meningocele: If bulging portion contains only CSF and overlying membrane.

149. Clinical Manifestation : Neurologic Problems Hydrocephalus Spastic quadriplegia Microcephaly Ataxia Developmental delay. Vision problems Mental and growth retardation Seizures.

150. Surgical Mangement: Surgery is performed to place the protruding tissues back into the skull , remove the sac and correct the associated craniofacial abnormalities.

151. Spina Bifida Spina bifida is a neural tube defect caused by the failure of the fetus spine to close properly during the first month of pregnancy.

152. Spina Bifida Occulta Closed Neural tube defects Spina Bifida Manifesta Spina bifida M en i ng o c e l e M y e l omen i ngoc ele Spina Bifida

153. 1) Spina bifida occulta : it is one of the most comon form in which one or more vertebrae are malformed. Occulta means hidden , indicates that the malformation or opening is covered by layer of skin. Symptoms: bladder and bowel problems or scoliosis. 2) Closed Neural tube defect: It is th e second type of spina bifida in w hich the spinal cord is marke d by a malformation of fat bone or membranous. S ymptoms : urinary or bowel dysfunction.

154. 3)Spina bifida manifesta: It is associated with nerve damage that can result in problem like walking, bladder control, and coordination. It can be seperated in to two classes: a) Spina Bifida meningocele: It is a rare type of spina bifida. In this type the meninges are pushed out between the openings in the vertebrae. The membranes can be usually removed during surgery. S ymptoms : S ymptoms are similar to closed neural tube defect, the nervous system is undamaged but may have other problems like bladder and bowel problems .

155. b) Myelomeningocele : - It is the most serious type of spina bifida. The spinal cord remains open along several vertebrae resulting in partial or complete paralysis of the parts of the body below the spinal opening. The membrane and spinal cord create , a sac in the baby's back. The sac is covered with meninges although it remains open leaving it vulnerable to infection leading to fatal .

156. Cause s and risk factors: Folic acid deficiency Previous pregnancy with neural tube defects Family history Use of anti-seizure medication s Diabetes Obesity High temperature in early pregnancy Excessive use of alcohol.

157. Clinical Manifestation s : Dimple Depression Birthmarks Hairy patch over the affected area Abnormal tuft of hair Loss of bladder or bowel control Partial or complete lack of sensation Weakness of legs , hip , feet of newborn

158. Buildup of fluid inside the skull Hair at the back part of pelvis Learning disabilities. Diagnostic Evaluation: Quadruple screen Maternal serum alpha fetoprotein test (MSAFP) Neurologic Examination X-ray, Ultrasound, MRI .

159. Management: Treatment depends on the type and severity of disorder: Surgery is usually helpful to close the spinal gap and prevent infection. Physical therapies, crutches and braces may be necessary to help problems resulting from nerve damage. if infant has hydrocephalus , ventricular peritoneal shunt can help drain any extra fluid from the head.

160. Catheter should be put to help regulate bladder function. Pharmacologic Management: Antibiotics to prevent infections like meningitis. Folic acid supplement to pregnant women Oxybutynin to prevent incontinence Physical therapy is also one of method s to prevent muscles from weakening.

161. Down's Syndrome... Down’s Syndrome is a genetic disorder caused by an extra 21 st chromosome. The egg carries 23 chromosomes; the sperm carries 23 chromosomes; the developing embryo should have 23 PAIRS of chromosomes…with no spares! Down’s Syndrome results in mental retardation. It was once known as Mongolism.

162. Physical Characteristics: Muscle hypotonia, low muscle tone Flat facial features, a somewhat depressed nasal bridge and a small nose Upward slanted eyes, small skin folds on the inner corner of the eyes Short neck Misshaped ears White spots on the colored part of the eye Single skin crease in the palm of the hand Excess flexibility in joints Heart defects Sight and hearing problems Large and protruding tongue Fifth finger has one flexion furrow instead of two Excessive space between large and second toe Down's Syndrome...

163. A risk factor is something that increases chance of getting a disease or condition. Genetics: If either parent is a carrier of a specific type of Down's syndrome there is an increased risk of giving birth to a child with this type of Down's syndrome. Age: The chance of having a child with Down's syndrome increases after a woman reaches age 35. Sex: More boys are born with Down's syndrome. Down's Syndrome...

164. CONGINITALMALFORMATIONS IN NEWBORN AND THE SURGICAL EMERGENCIES

165. MECONEUM ILEUS

166. FOLLOW UP OF HIGH RISK NEONATES

167. Introduction Steady improvement in the quality of perinatal care in India more VLBW and ELBW babies are surviving. But the incidence of chronic morbidities like cerebral palsy(incidence 4.5-10%)etc. has increased. Timely and appropriate intervention.

168. Need For Follow Up Potential disconnect between perinatal outcomes and longterm outcomes To assess efficacy and safety of therapies- Short term outcomes , not sufficient. Understanding of association between risk factors, therapies and survival. No database of outcomes of at risk neonates available in India.

169. Candidates requiring Follow Up Mild Risk: 1. preterm, Weight 1500 g - 2500g 2. HIE grade I 3. Transient hypoglycemia 4. Suspect sepsis 5. Neonatal jaundice needing PT 6. IVH grade 1

170. Moderate Risk: 1. Babies with weight – 1000 g- 1500 g or gestation < 33 weeks 2. Twins/triplets 3. Moderate Neonatal HIE 4. Hypoglycemia, Blood sugar<25 mg/dl 5. Neonatal sepsis 6. Hyperbilirubinemia > 20mg/dL or requirement of exchange transfusion 7. IVH grade 2 8. Suboptimal home environment

171. High Risk: 1. Babies with <1000g birth weight and/or gestation <28 weeks 2. Major morbidities such as chronic lung disease, intraventricular hemorrhage, and periventricular leucomalacia 3. Perinatal asphyxia - Apgar score 3 or less at 5 min and/or hypoxic ischemic encephalopathy 4. Surgical conditions like Diaphragmatic hernia, Tracheo-oesophageal fistula 5. Small for date (<3rd centile) and large for date (>97th centile) 6. Mechanical ventilation for more than 24 hours 7. Persistent prolonged hypoglycemia and hypocalcemia 8 . Seizures

172. 9. Meningitis 10. Shock requiring inotropic/vasopressor support 11. Infants born to HIV-positive mothers 12. Twin to twin transfusion 13. Neonatal bilirubin encephalopathy 14. Major malformations 15. Inborn errors of metabolism / other genetic disorders 16. Abnormal neurological examination at discharge

173. Place and Personnel for Follow Up Place of Follow Up should be- 1.easily accessible 2.directions should be made known. LOW RISK BABIES :- PLACE-at a well baby clinic . Follow up with paediatrician/primary care provider OBJECTIVE -to screen for deviation in growth and development.

174. MODERATE RISK :- PLACE -in or near to a facility providing level 2 or level 3 NICU care . Follow up with neonatologist and developmental paediatrician. OBJECTIVE -to screen for developmental delay , manage intercurrent illnesses . FOLLOW UP TEAM SHOULD CONSIST OF :- Developmental paediatrician Developmental Therapist Radiologist Ophthalmologist Audiologist Physiotherapist Social worker & Dietician

175. HIGH RISK BABIES : - PLACE - same as for Moderate risk Follow up with Neonatologist . OBJECTIVE - to supervise and screen for developmental delay FOLLOW UP TEAM SHOULD CONSIST OF :- Team as for moderate risk PLUS Paediatric neurologist Geneticist Occupational Therapist Speech therapist Endocrinologist Paediatric surgeon Orthopaedician

176. Predischarge Preparation before discharge plus Active surveillance required in follow up To be done/planned before discharge :- 1.Medical examination. 2.Neurobehavioural and Neurological examination 3.Neuroimaging. 4.ROP screening 5.Hearing screening 6.Screening for congenital Hypothyroidism. 7.Screening for metabolic disorders. 8.Assessment of parent coping and developmental environment

177. Discharge Summary has to be provided. It must contain:- 1. Gestation, 2. Birth weight, 3. Discharge weight 4. Discharge head circumference, 5. Feeding method and dietary details, 6. Diagnosis (medical problems list), 7. Medications 8. References to other departments

178. 9. Days on oxygen and gestation when baby went off oxygen, 10. Findings of last hematological assessment, 11. Metabolic screen, 12. ROP screen, 13. Hearing screen, 14. Thyroid screen, 15. Ultrasound cranium, 16. Immunization status, 17. Assessment of family

179. Follow up protocol Following are to be done at follow up:- Medical Examination- Nutrition and growth, Immunization Neurological examination Development assessment Ophthalmologic assessment- squint and refraction Hearing and Language and speech 6.Gross Motor Function 7.Behavioural, Cognitive and intelligence status.

180. Schedule for Follow Up Frequency and type of tests used depends on “intensity or level of follow up” assigned. Initial weekly follow up to ascertain adjustment to home environment and weight gain. Neuromotor exam at discharge and at 1,3 ,6,9 and 12 months of age. Squint and Refraction-at 9 months to 1 year of age. Other visual problems at 1 year and yearly till school age.

181. Language and speech assessment – newborn hearing test AND repeat hearing test at 1 year. Development Assessment –At least once in:- 1. first 6 months, 2. next 6 months , 3.every year till 5 years . Formal Developmental assessment - within 2 months of parental concern/abnormal screening test. AT :- 2 years -severity of disability 3-4 years – intelligence and later prediction of IQ scores 6 years – School achievement 8 years - IQ, , neurophysiological functions and school performance HOW LONG TO FOLLOW UP?- Till late adolescence, or at least till school.

182. Follow Up Schedule (AIIMS) Birth wt below 1500g or GA below 32 wk. Other C o n diti o ns After 3-7 days of discharge 2 weeks after discharge Every 2 wks until 3 kg 6, 10, 14 wks of postnatal age At 3, 6, 9, 12,15 and 18months of age and then for every 6 months until age of 8years

183. MANAGEMENT OF THE NEONATE AT RISK : Prevention First of all, providing a warm environment. Early enteral feeding is the single most important E nteral feeding is to be started, if the infant is able to tolerate nipple or nasogastric tube feeding.

184. These infants should have glucose values monitored until they are taking full feedings and have three normal pre‐feeding readings above 40‐45 mg/dl. Car e must be taken to ensure that breastfeeding mothers are providing an adequate i n ta k e . If the infant at risk for hypoglycemia is unable to tolerate nipple or tube feeding, maintenance of IV therapy with 10% glucose should be initiated and glucose levels monitored. MANAGEMENT (CONT…)

185. Take home message All new born s are precious Extra effort, extra care Communicat e as early as possible Early referral prevention

186. Nursing Interventions Rationale Monitor neonate’s condition. To determine the need for intervention and the effectiveness of therapy. Monitor vital signs To have a baseline data Provide TSB Helps in lowering down the temperature Ensure that all equipment used for infant is sterile, scrupulously clean. Do not share equipment with other infants Prevents the spread of pathogens to the infant from equipment Administer antipyretics as ordered Aids in lowering down temperature Nursing Diagnosis Hyperthermia related to inflammatory process/ hypermetabolic state as evidenced by an increase in body temperature, warm skin and tachycardia Outcomes Patient will maintain normal core temperature as evidenced by vital signs within normal limits and normal WBC level Patient will still maintain normal core temperature as evidenced by normal vital signs and normal laboratory results.

187. Nursing Interventions Rationale Monitor and record vital signs To note for the alterations in V/S (decreased BP, Increased in PR and temp) Note for the causative factors that contribute to fluid volume deficit To assess what factor contributes to fluid volume deficit that may be given prompt intervention. Provide TSB if patient has fever To decrease temperature and provide comfort Provide oral care by moistening lips & skin care by providing daily bath To prevent injury from dryness Administer IV fluid replacement as ordered Replaces fluid losses Administer antipyretic drugs if patient has fever as ordered To reduce body temperature Nursing Diagnosis Fluid volume deficit related to failure of regulatory mechanism Outcomes Patient will be able to maintain fluid volume at a functional level as evidenced by individually adequate urinary output with normal specific gravity, stable vital signs, moist mucous membranes, good skin turgor and prompt capillary refill and resolution of edema.

188. Nursing Diagnosis Ineffective tissue perfusion related to impaired transport of oxygen across alveolar and on capillary membrane Outcomes Patient will demonstrate increased perfusion as evidenced by warm and dry skin, strong peripheral pulses, normal vital signs, adequate urine output and absence of edema. Nursing Interventions Rationale Note quality and strength of peripheral pulses To asses pulse that may become weak or thready, because of sustained hypoxemia Assess respiratory rate, depth, and quality To note for an increased respiration that occurs in response to direct effects of endotoxins on the respiratory center in the brain, as well as developing hypoxia, stress. Respirations can become shallow as respiratory insufficiency develops creating risk of acute respiratory failure. Assess respiratory rate, depth, and quality To assess for compensatory mechanisms of vasodilation Assess skin for changes in color, temperature and moisture To promote circulation /venous drainage Elevate affected extremities with edema once in a while Conserves energy and lowers O2 demand Provide a quiet, restful atmosphere To maximize O2availability for cellular uptake

189. Nursing Diagnosis Interrupted breastfeeding related to neonate’s present illness as evidenced by separation of mother to infant Outcomes The mother will identify and demonstrate techniques to sustain lactation until breastfeeding is initiated The mother shall still be able to identify and demonstrate techniques to sustain lactation and identify techniques on how to provide the newborn with breast milk. Nursing Interventions Rationale Assess mother’s perception and knowledge about breastfeeding and extent of instruction that has been given. To know what the mother already knows and needed to know. Give emotional support to mother and accept decision regarding cessation/ continuation of breast feeding. To assist mother to maintain breastfeeding as desired. Demonstrate use of manual piston-type breast pump. Aid in feeding the neonate with breast milk without the mother breastfeeding the infant. Review techniques for storage/use of expressed breast milk To provide optimal nutrition and promote continuation of breastfeeding process Determine if a routine visiting schedule or advance warning can be provided So that infant will be hungry/ ready to feed Provide privacy, calm surroundings when mother breast feeds. To promote successful infant feeding Recommend for infant sucking on a regular basis Reinforces that feeding time is pleasurable and enhances digestion. Encourage mother to obtain adequate rest, maintain fluid and nutritional intake, and schedule breast pumping every 3 hours while awake To sustain adequate milk production and breast feeding process

190. Nursing Diagnosis Risk for Impaired parent/neonates Attachment related to neonates physical illness and hospitalization. Outcomes The mother will identify and demonstrate techniques to enhance behavioral organization of the neonate After discharge the parents will be able to have a mutually satisfying interactions with their newborn. Nursing Interventions Rationale Interview parents, noting their perception of situational and individual concerns To know what the parents feelings about the situation. Educate parents regarding child growth and development, addressing parental perceptions Helps clarify realistic expectations Involve parents in activities with the newborn that they can accomplish successfully Enhances self-concept Recognize and provide positive feedback for nurturing  and protective parenting behaviors Reinforces continuation of desired behaviors

191. THANK YOU

192. TRUE/ FALSE ? A SNEEZE IS FASTER THAN AN EYE BLINK. FINGERNAILS GROW FASTER THAN HAIR. RIGHT LUNG IS SLIGHTLY SMALLER THAN LEFT LUNG. A BABY HAS MORE BONES THAN AN ADULT. A SHARK CAN BLINK IT’S EYES. FROZEN VEGETABLES ARE LESS NUTRITIOUS THAN FRESH VEGEBLES. YOU MUST DRINK “8 GLASSES” OF WATER PER DAY. YOU CAN DISINFECT A WOUND WITH HONEY.