High risk neonate s & Complication

1. High risk neonates& Complication Dr. S Ghaemi, MD

2. High risk pregananciesHigh risk infants • Why high risk infants? • Neonatal morbidity • Long term morbidity and disability • Neonatal death • Why high risk pregnancies? • 75%Physiological pregnancies 5% ill neonates • 25% abnormal pregnancies 15-25% ill neonates

3. The goal • Screening risk factors • Prevention • Early management and therapy of ongoing complications

4. Risk factors • Preconception • Postconception • Delivery

5. Risk factors • Preconception • Economic, social • Cultural – behavioral • Biologic – genetic • Reproductive • Previous pregnancies and delivery • Chromosomal abnormalities • Mother desease • Diabetes, epilepsy, alergy, Fenylketonuria, endocrine disorders, congenital desease • Drug, alcohol abuse • Uterus anomaly • Mother age, weight

6. Risk factors • Postconception • Mother desease • Mother infections, gestosis • Chorioamnionitis • Diabetes, epilepsy, alergy, Fenylketonuria, endocrine disorders, congenital desease • Drug, alcohol abuse • Rh incompatibily • Hydramnios • Multiple pregnancies • Intrauterine growth retardation • Post-term infants

7. Risk factors • Delivery • Cephalopelvic disproportion • Dystocia • Prolonged labor • Abruptio placentae • Intrapartal hypoxia • Forceps (breus)

8. Risk factors • Hypoxia • HIE, IVH, PVL • Severe infection • Meningitis, TORCH, • Metabolic complications • Hypoglycemia, hypocalcemia, acidosis • Intrauterine drug exposure • Heroin, methadon, cocaine, alcohol

9. Term Post term SGA Preterm High RiskNeonates

11. Postmature Infant Post mature infants are prone to develop • asphyxia during labor secondary to placental insufficiency • meconium aspiration syndrome which may be unusually severe because post term, amniotic fluid volume is decreased and the aspirated meconium is less diluted; • neonatal hypoglycemia due to insufficient glycogen stores at birth. Because anaerobic metabolism rapidly uses the last of the glycogen stores, hypoglycemia is exaggerated if perinatal asphyxia has occurred.

12. SGA Small for gestational age infantor(IUGR)  Intrauterine growth restriction

13. Mortality and morbidity are increased in SGA infants compared to those who are appropriate for gestational age (AGA).

15. Approximately 10 percent of term infants in developed countries are SGA compared to 23 percent of term infants in developing countries.

16. CLASSIFICATION SGA infants have either symmetric or asymmetricIUGR. Infants with symmetric IUGR have reductions in both body and head growth. Symmetric IUGR begins in early gestation.

17. Asymmetric • Infants with asymmetric IUGR have reduced body weight and relatively normal length and head growth. • Abnormal growth typically begins in the late second or third trimesters

18. CLINICAL FEATURES SGA infants appear thin with loose, peeling skin and decreased skeletal muscle mass and subcutaneous fat tissue. The face has a typical shrunken or "wizened" appearance, and the umbilical cord often is thin (picture 1

20. Meconium staining may be present (picture 2). In newborns with asymmetric IUGR, the head appears relatively large compared to the size of the trunk and extremities.

22. Prematurity Short term disability • Intracranial pathology • IVH, PVL, brain atrophy, ventriculomegaly • Retinopathy • Chronic lung disease • Necrotising enterocolitis • Early and late onset sepsis

23. Long term disability • Cerebral palsy • Visual impairment • Sensorineural hearing loss • Epilepsy • Mental retardation • Growth retardation, failure to thrive

25. A term used broadly to describe a number of motor disorders characterized by impaired voluntary movement resulting from prenatal developmental abnormalities or perinatal or postnatal CNS damage occurring before age 5 yr. The term cerebral palsy (CP) is not a diagnosis but identifies children with nonprogressive spasticity, ataxia, or involuntary movements. Between 0.1 and 0.2% of children have CP syndromes; up to 1% of premature newborns or those small for gestational age are affected. Cerebral Palsy Syndrome

26. Etiology The cause often is hard to establish, but prematurity, in utero disorders, neonatal jaundice, birth trauma, and perinatal asphyxia play important roles. Birth trauma and perinatal asphyxia probably cause <= 15% of cases. Spastic paraplegia is especially common after premature birth, spastic quadriparesis after perinatal asphyxia, and athetoid and dystonic forms after perinatal asphyxia or kernicterus. CNS trauma or severe systemic disease during early childhood (eg, meningitis, sepsis, dehydration) may also cause a CP syndrome. Cerebral Palsy Syndrome

27. Mental Retardation Significantly subaverage intellectual quotient (IQ < 70 to 75) with related limitations in two or more of the following: communication, self-care, home living, social skills, community use, self-direction, health and safety, functional academics, leisure, and work.

28. Retinopathy of Prematurity(Retrolental Fibroplasia) A bilateral ocular disorder of abnormal retinal vascularization in premature infants, especially those of lowest birth weight, with outcomes ranging from normal vision to blindness.

29. Causes fo exogenouscongenital sensorineural hearing loss • Anoxia during birth • Congential infections • Rubella, CMV, HSV, Toxo, Siphilis • Rh incompatibility • Ototoxic drugs given to the mother

32. Failure To Thrive • Weight consistently below the 3rd percentile for age • Progressive decrease in weight to below the 3rd percentile • Weight < 80% of ideal weight for height-age • or a decrease in expected rate of growth based on the child's previously defined growth curve, irrespective of whether below the 3rd percentile.

33. Risks of multiple pregnancies  risk of fetal death  risk of neonatal death  risk of serious neonatal morbidity and long term diasbility The causes of risks Prematurity T T T S (twin to twin transfusion syndrome) Monochoriati

34. Preterm delivery in multiple pregnancies(weeks) • Singletons 39 • Twins 35,8 • Triplets 32,5 Alexander GR, Clin Obstetr and Gynecol 1998;41: 115-125 Orlebeke JF, Eur J Obstet Gynecol Reprod Biol 1993; 50:87-93

35. CNS impairment • M retardation and CP as a results of CNS impairment. • During intrauterinne life • Results of prematurity • Learning impairments are more common in twins. • Epilepsy is more often diagnosed in twins, mostly in monozygotic twins.

36. Long term morbidity in VLBW Infants (BW < 1500 g, age 2 years) (%)

37. CP and Mental retardation(BW < 1500 g, age 2 years) % CP Mental retardation

38. Epilepsie(BW < 1500 g, age 2 years) %

39. (BW < 1500 g) Sensorinural Hearing lossBlindness BW<1500 % ROP+Blindness Senzorineural deafness

40. Follow up • Early identification of developmental disability • Early identification a treatment of medical complications • Multidiscioplinary cooperation • Parents counseling regarding • Positioning, handling and feeding infants

42. دكتر ماسارو ايموتو محقق ژاپني با انتشار يافته‌هاي تحقيقات خود مدعي شد كه مولكول‌هاي آب نسبت به مفاهيم انساني تأثيرپذيرند.نظريه اين محقق ژاپني كه تاكنون از سوي مؤسسات علمي فيزيكي و زيست‌شناسي مورد تأييد قرار گرفته است، مبتني بر بررسي نمونه‌هاي فراواني از كريستال‌هاي منجمدشده آب و مقايسه آن با يكديگر است. Masaru imoto

43. كتاب ايشان با عنوان هاي مختلفي چون در چندين جلد منتشر شده است.ايشان در اغلب كشور هاي دنيا سمينار هاوكنفرانس هايي با اين پيام داشته ودارند. The messages from water

44. دكتر ايموتو معتقد است كه همانطور كه شكل ظاهري آب نسبت به ظرف ها ومكان هايي كه در آن قرار مي گيرد تغييرمي كند . شكل مولكولي آب هم نسبت به محيط و شرايط پيراموني خودش تغيير مي كند. آب هايي كه راكد هستند مانند آب پشت سد ها وآب درياچه ها بدليل عدم پويايي وحركت از لحاظ نماي مولكولي زشت وكريه هستندهمچنين آب هايي مانند آب رودخانه ها باوجود جاري بودن وسيلان داشتند بدليل اينكه از ميان شهر ها مي گذارند واكثر مردم داراي افكار منفي هستند نماي زشتي پيدا مي كنند.

45. بزرگترين در ياچه در مركز ژاپن .چون آب درياچه راكد است وايستاده ، همين سكون وايستادن باعث مي شود مولكولهاي آب زشت شوند. درياچه بيو ا كو

46. هر گونه سكون باعث زشتي آب مي شود. آب سد فوجي وارا

47. چون آب اين رودخانه از ميان شهر ها مي گذرد وبدليل طيف غالب منفي آدم ها نماي مولكولي آب به اين شكل در آمده است. رودخانه يودو

48. آب هايي كه تازه از دل كوه بيرون مي آيند بدليل اينكه در معرض افكار منفي قرار نگرفته اند نماي مولكولي خود را حفظ كرده اند.اين عكس دقيقا مربوط به زماني است كه چشمه از دل كوه بيرون مي آيد. چشمه سانبو ائجي (رودخانه سانبو ائجي)

49. چشمه ساي چو (رودخانه ساي چو) چشمه شيمانتو (رودخانه شيمانتو)

50. دكتر ايموتوآزمايشهاي خود را به مكانهاي خاصي محدود نكرده وآنها را با آب هاي مختلف ،در كشور هاي مختلف انجام دادند .اين عكس مربوط به رودخانه لوردز در فرانسه مي باشد. چشمه لوردز (رودخانه لوردز)