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NEONATAL PHYSIOLOGY AND TRANSITION 
PERIOD 
Under guidence of Dr neelam dogra ma’am 
Presented by anuradha pandey
LEARNING OBJECTIVE 
physiological changes which take place following 
birth and appreciate the unique aspects of 
neonatal...
INTRODUCTION 
NEWBORN-first 24 hrs of life 
NEONATE-from birth to under four weeks(<28 days) 
TERM NEONATE-between 37 to <...
FETAL CIRCULATION
FETAL CIRCULATION 
AIM 
Oxygenated placental blood is preferentially delivered to the brain,myocardium and 
upper torso 
...
FETAL CIRCULATION 
(PARALLEL CIRCULATION) 
 Oxygenated blood via umbilical vein either through the liver or via the ductu...
PHYSIOLOGICAL CHANGES AT BIRTH 
UMBILICAL VESSELS- IMMEDIATELY AFTER CLAMPING: 
 constrict in response to stretching and ...
TRANSITION AT BIRTH 
Successful transition from fetal to postnatal circulation requires 
 clamping of umbilical cord and ...
RESPIRATORY CHANGES 
What part do each of these factors 
play in initiation of respirations in the 
Mechanical 
Chemical 
...
CHANGES AT BIRTH….MECHANICAL 
Compression of fluid from the fetal lung during vaginal delivery 
establishes the lung volum...
CHEMICAL EVENTS 
1. With cutting of the cord, remove oxygen supply 
2. Asphyxia occurs 
3. CO2 and O2 and pH = ACIDOSIS 
4...
SENSORY / THERMAL EVENTS 
Thermal--the decrease in 
environmental temperature after 
delivery is a major stimulus of breat...
BIOPHYSICAL CHANGE CONTINUED 
1)Alveolar distension, cortisol and epinephrine further stimulate type II 
pneumocytes to pr...
SHUNT CLOSURE 
physiological reverse shunt from left to right commonly occurs. 
FORAMEN OVALE 
 completely closed in 50% ...
CARDIOVASCULAR CHANGES 
1. Pressure 
in RA decreases 
2. Blood flows 
to the lungs 
4. Pressure in the 
LA increases RT 
F...
SHUNT CLOSURE 
IMPORTANT-stimulus 
such as hypoxia, acidaemia or structural anomaly can increase 
pulmonary vascular resis...
NEONATAL MYOCARDIAL FUNCTION 
term neonatal cardiac output is approximately 200 ml/kg/minute 
fewer myofibrils in a diso...
Ventricular maturation and associated 
ECG changes 
The fetal heart - right-side dominant, with the right ventricle 
respo...
LOW CARDIAC RESERVE-Left 
ventricle has high tone has limited contractile 
reserve due to;- 
Reduced no of alpha receptor...
MYOCARDIAL METABOLISM 
neonates can tolerate hypoxia better due to 
High concentration of glycogen 
More effective utili...
CARDIAC VALUES
FETAL RESPIRATORY SYSTEM 
ALVEOLAR DEVELOPMENT 
Continues even after birth 
At birth 24 million alveoli 
increases five...
FETAL RESPIRATORY SYSTEM 
SURFACTANT 
 type I and II pneumocytes are distinguishable only by 20-22 weeks 
present only af...
RESPIRATORY SYSTEM 
Diaphragm-two types of fibres 
Type 1-slow twitch, highly 
oxidative ,sustained contraction 
,less fat...
NEONATAL AIRWAY
NEONATAL AIRWAY 
 Larynx is funnel shaped 
 narrowest portion is cricoid –uncuffed tube 
preferred(micro cuff useful ,co...
DEVELOPMENTAL CHANGES OF 
RIB CAGE 
Chest wall development 
 Ribs oriented parallel and 
unable to increase the 
thoracic...
NEONATAL LUNG MECHANICS 
imbalance exists between chest wall rigidity and elastic recoil of 
neonatal lungs. (CONTAIN IMMA...
Neonatal lung mechanics-gas exchange 
 immature in neonates, 
 total shunt estimate of 24% of the cardiac output at birt...
Control of ventilation 
Peripheral chemoreceptors 
functional at birth but are initially silent because of high post deli...
RESPONSE TO HYPOXIA 
characterized by 
1)an initial increase in ventilation followed by a decrease in ventilation; 
2).muc...
PERSISTENT PULMONARY HYPERTENSION OF 
THE NEW BORN/PERSISTENT FETAL 
CIRCULATION 
PATHOPHYSIOLOGY 
hypoxia, acidosis and i...
PERSISTENT FETAL CIRCULATION 
Goal- 
PaCO2-50 TO 55mmhg and Pao2-50-70 mmhg 
MANAGEMENT:- 
1)treat precipitating condition...
MECONIUM ASPIRATION 
 Marker for chronic hypoxia in utero in third trimester due to 
interferance in maternal circulation...
GUIDELINES FOR MANAGEMENT FOR 
MECONIUM ASPIRATION 
“If the baby is not vigorous (Apgar 1-3): Suction the 
trachea soon af...
Thermogregulation 
2.5-3.0 times higher surface area BW 
limited insulating capacity from subcutaneous fat and 
the ina...
R a d ia t io n 
C o ld R o o m T e m p . 
C o ld W a lls 
C o ld Ite m s o n B ed 
C o n d u c t io n 
C o ld S c a le 
C...
BROWN FAT 
6% of term bodyweight (dec in preterm) 
found in the interscapular region, mediastinum, axillae, vessels of t...
HEAT CONSERVATION 
heat loss minimized by 
 increasing the temperature of the surrounding environment. 
CAREFUL;- the env...
Haematology 
contains both adult (HbA) and fetal haemoglobin 
HbF 
70-80% upto 90% in preterm 
four globin chains alpha2...
HAEMATOPOIESIS 
occurs in the liver in utero 
but is restricted to bone marrow from 6 weeks post delivery, 
thus limiting ...
Hepatic 
Most enzymatic pathways are present 
inactive at birth 
become fully active at 3 months 
Albumin level low-mo...
Clotting factors 
1) do not cross the placenta; 
2)factors V, VIII and XIII are at adult concentrations before birth. 
3)v...
Renal 
EXCRETORY FUNCTION 
1 million nephrons is present by 34 weeks ’gestation. 
The glomeruli and nephrons are immatur...
BODY FLUID COMPOSITION 
75% of TBW,80-85% IN PRETERM 
Reduced to 60-65% BY one year 
ECF:ICF IS 2:1, 
The diuresis red...
FLUID THERAPY 
MAINTAINENCE FLUID- 
70,80,90,120 ml/kg on day 1/3/5/7 
Rest period-150ml/kg/24hr 
Fluid choice 
FIRST 48 h...
NERVOUS SYSTEM 
 precocious in development , 
continues to develop to achieve a full complement of cortical and brainste...
NERVOUS SYSTEM 
 Cerebral autoregulation is fully developed at term, maintaining cerebral perfusion 
down to a mean arter...
NOCICEPTION 
 pathways are developed by 24-28 weeks’ gestation, 
 The concept of neonatal nociception is now widely acce...
IMMUNOLOGIC ADAPTATION 
Active acquired immunity 
 Pregnant woman forms antibodies herself 
Passive acquired immunity 
 ...
KEY POINTS
KEY POINTS
THANK YOU
neonatal physiology and transition period
neonatal physiology and transition period
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neonatal physiology and transition period

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the presentation gives a brief idea about the basic physiology of neonates and the changes that occur during birth and neonatal period.

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neonatal physiology and transition period

  1. 1. NEONATAL PHYSIOLOGY AND TRANSITION PERIOD Under guidence of Dr neelam dogra ma’am Presented by anuradha pandey
  2. 2. LEARNING OBJECTIVE physiological changes which take place following birth and appreciate the unique aspects of neonatal physiology including: 1) limited reserve capacity for temperature control, cardiovascular and respiratory function 2)variable and individualized fluid requirements 3) implications of hepatic and renal immaturity
  3. 3. INTRODUCTION NEWBORN-first 24 hrs of life NEONATE-from birth to under four weeks(<28 days) TERM NEONATE-between 37 to < 42 gestational week PRETERM NEONATE-<37 gestational week irrespective ofBW POST TERM NEONATE-> or egual to 42 gestational week LOW BIRTH WEIGHT(LBW)<2500 GRAM irrespective of birth weight VERY LOW BIRTH WEIGHT(VLBW)<150O GRAM EXTREMELY LOW BIRTH WEIGHT(ELBW)< 1000 GRAM
  4. 4. FETAL CIRCULATION
  5. 5. FETAL CIRCULATION AIM Oxygenated placental blood is preferentially delivered to the brain,myocardium and upper torso lower oxygen tension blood distributed to the lower body and placenta  Preferential splitting is achieved via intra- and extracardiac shunts that direct blood into two parallel circulations (the left ventricle providing 35% and the right 65% of cardiac output. ) Fetal cardiacoutput is therefore measured as a combined ventricular output closure of the intracardiac (foramen ovale) and extracardiac shunts (ductus venosus and ductus arteriosus)
  6. 6. FETAL CIRCULATION (PARALLEL CIRCULATION)  Oxygenated blood via umbilical vein either through the liver or via the ductus venosus to reach IVC  blood remains on the posterior wall of the inferior vena cava, allowing it to be directed across the foramenovale into the left atrium by the Eustachian valve  blood passes left ventricle and aorta to supply the head and upper torso.  deoxygenated blood returning from the SUPERIOR vena cava and myocardium via the coronary sinus is directed through the right ventricle and into the pulmonary artery.  Most of this blood is returned to the descending aorta via the ductus arteriosus; ( 8-10%of total cardiac output passes through the high-resistance pulmonary circulation.)  Blood in the descending aorta either supplies the umbilical artery to be reoxygenated at the placenta or continues to supply the lower limbs.
  7. 7. PHYSIOLOGICAL CHANGES AT BIRTH UMBILICAL VESSELS- IMMEDIATELY AFTER CLAMPING:  constrict in response to stretching and increased oxygen content at delivery  large low-resistance placental vascular bed removed from the circulation increase SVR Reduction of blood flow along ductus venosus (passive closure over the following 3-7 days),reduced blood flow in IVC Lung expansion drops pulmonary vascular resistance  increase in blood returning to the LA These two changes reduce right atrial and increase left atrial pressures, functionally closing the foramen ovale within the first few breaths of life
  8. 8. TRANSITION AT BIRTH Successful transition from fetal to postnatal circulation requires  clamping of umbilical cord and removal of the placenta  increased pulmonary blood flow, Shunt closure
  9. 9. RESPIRATORY CHANGES What part do each of these factors play in initiation of respirations in the Mechanical Chemical Sensory/ Thermal IInniittiiaattiioonn ooff BBrreeaatthhiinngg neonate?
  10. 10. CHANGES AT BIRTH….MECHANICAL Compression of fluid from the fetal lung during vaginal delivery establishes the lung volume As the chest passes through the birth canal the lungs are compressed Subsequent recoil of the chest wall produces passive inspiration of air into the lungs Negative inspiratory pressures of up to 70-100 cm H2O are initially required to expand the alveoli (LaPlace’s relationships) which facilitate lung expansion by overcoming: airways resistance inertia of fluid in the airways surface tension of the air/fluid interface in the alveolus
  11. 11. CHEMICAL EVENTS 1. With cutting of the cord, remove oxygen supply 2. Asphyxia occurs 3. CO2 and O2 and pH = ACIDOSIS 4. Acidotic state-- stimulates the respiratory center in the medulla and the chemoreceptors in carotid artery to initiate breathing
  12. 12. SENSORY / THERMAL EVENTS Thermal--the decrease in environmental temperature after delivery is a major stimulus of breathing Tactile--nerve endings in the skin are stimulated Visual--change from a dark world to one of light Auditory--sound in the extrauterine environment stimulates the infant
  13. 13. BIOPHYSICAL CHANGE CONTINUED 1)Alveolar distension, cortisol and epinephrine further stimulate type II pneumocytes to produce surfactant 2)Expiration  initially active, pressures of 18-115 cm H2O generated amniotic fluid forced out from the bronchi. PHYSIOLOGICAL CHANGES LEAD TO- increasing blood flow and initiating the cardiovascular changes .
  14. 14. SHUNT CLOSURE physiological reverse shunt from left to right commonly occurs. FORAMEN OVALE  completely closed in 50% of children by 5 years  remains probe patent in 30% of adults,  can facilitate paradoxical embolus and potential stroke. DUCTUS ARTERISUS-  drop in pulmonary artery pressure and increase in SVR reverses flow across the ductus arteriosus from L TO R  affected by blood oxygen content  circulating prostaglandins. E2  Functional closure occurs by 60 hours in 93% of term infants.,4-8 weeks permanent structural closure occurs via endothelial destruction and subintimal proliferation.
  15. 15. CARDIOVASCULAR CHANGES 1. Pressure in RA decreases 2. Blood flows to the lungs 4. Pressure in the LA increases RT Flow of blood from the lungs 3. Ductus Arteriosus begins to constrict 5. Increase pressure in the LA forces the foramen ovale to close
  16. 16. SHUNT CLOSURE IMPORTANT-stimulus such as hypoxia, acidaemia or structural anomaly can increase pulmonary vascular resistance and potentially re-open the ductus arteriosus or foramen ovale. which allows a right-to-left shunt, which worsens hypoxia . Eg seen in persistent pulmonary hypertension of the newborn.
  17. 17. NEONATAL MYOCARDIAL FUNCTION term neonatal cardiac output is approximately 200 ml/kg/minute fewer myofibrils in a disordered pattern, Less mature sarcoplasmic reticulum and transtubular system -nt dec CA-ATP ACTIVITY,dependent on exogenous ionized calcium follows the Franke Starling relationship of filling pressure to stroke volume, but on a much flatter section of the curve compared with adults. i.e limited increase in stroke volume for a given increase in ventricular filling volume. dependent on heart rate to increase cardiac output and cardiac output can respond to increased ventricular filling. 3 month parasympathetic vervous system effect more developed than sympathetiv Baroreceptors not well developed compared to chemoreceptorsfurther depressed under anaesthesia-bradycardia
  18. 18. Ventricular maturation and associated ECG changes The fetal heart - right-side dominant, with the right ventricle responsible for 65% of cardiac output in utero. The neonatal ECG reflects  RAD R wave dominance in lead V1 S wave dominance in lead V6. At 3-6 months the classical LAD pattern established as ventricular hypertrophy occurs in response to increased systemic vascular resistance
  19. 19. LOW CARDIAC RESERVE-Left ventricle has high tone has limited contractile reserve due to;- Reduced no of alpha receptors High level of circulating cathecholamines Limited recruitable stroke volume Immature calcium transport system Dec ventricular compliance effect of parasympathetic nervous system is more predominent Beta adrenergic receptors are more developed than alpha thus respond better to dobutamine and isiproterenol
  20. 20. MYOCARDIAL METABOLISM neonates can tolerate hypoxia better due to High concentration of glycogen More effective utilisation of anaerobic metabolism Hence can be resusitated easily if oxygenation and perfusion are reestablished Oxygen consumption increases after birth(at neutral temperature ) Full term child At birth-6ml/kg/min 10 days-7 ml/kg/min 4 week-8 ml/kg/min
  21. 21. CARDIAC VALUES
  22. 22. FETAL RESPIRATORY SYSTEM ALVEOLAR DEVELOPMENT Continues even after birth At birth 24 million alveoli increases fivefold in -300 million by 8 years of age Initally increases in no ,further increase by inc in size and airway development Lungs develop from the third week of gestation with completion of the terminal bronchioles by week 16
  23. 23. FETAL RESPIRATORY SYSTEM SURFACTANT  type I and II pneumocytes are distinguishable only by 20-22 weeks present only after 24 weeks,  the watershed time for pulmonary gas exchange and therefore extra-uterine survival production can be increased after 24 weeks by giving betamethasone to the mother, thereby improving neonatal lung function if premature delivery is anticipated APPLIED seen preterm babies  decreases the compliance – risk for respiratory distress syndrome , bronchopulmonary dysplasia and pulmonary hypertension
  24. 24. RESPIRATORY SYSTEM Diaphragm-two types of fibres Type 1-slow twitch, highly oxidative ,sustained contraction ,less fatigue Type 2-fast twitch, low oxidative ,quick contraction and easily fatigued New born have 25% TYPE-1, (PRETERM 10%),BY AGE OF TWO YRS 55% APPLIED-risk of diaphragmatic fatigue during hyperventilation
  25. 25. NEONATAL AIRWAY
  26. 26. NEONATAL AIRWAY  Larynx is funnel shaped  narrowest portion is cricoid –uncuffed tube preferred(micro cuff useful ,costly)  Large size of the tongue-increases chances of obstruction and difficult laryngoscopy  Higher level of larynx(c3 in preterm,c4 in term and c5-c6 in adults)-straight blade more useful  Epiglottids- short,stubby,omega shaped, angled over laryngeal inlet-control with laryngeal blade more difficult  Tip of epiglottids lies at c1,with close apposition with soft palate-allows simultaneously sucking and breathing  Vocal cords angled-blind intubation ,tube may lodge at anterior commisure  Large occiput-more flexion may lead to obstruction
  27. 27. DEVELOPMENTAL CHANGES OF RIB CAGE Chest wall development  Ribs oriented parallel and unable to increase the thoracic volume during inspiration  At 2 yrs old associated with standing and walking, ribs are oriented oblique  Cartilaginous structure with inward movement during inspiration
  28. 28. NEONATAL LUNG MECHANICS imbalance exists between chest wall rigidity and elastic recoil of neonatal lungs. (CONTAIN IMMATURE ELASTIC FIBRES,thus tendency to recoil)  increase closing capacity to the point of exceeding functional residual capacity (FRC) until the age of 6. To counteract this, neonates produce positive end expiratory pressure(PEEP) via high resistance nasal airways and partial closure of the vocal cords Limited Inspiratory reserve volume Minute volume is maintained by high respiratory rate Respiratory fatigue common
  29. 29. Neonatal lung mechanics-gas exchange  immature in neonates,  total shunt estimate of 24% of the cardiac output at birth, reducing to 10% of cardiac output at 1 week.  rapid reduction in shunt fraction improves arterial oxygenation and reduces the effort of breathing. implications during anaesthesia.  effective FRC is reduced( physiological PEEP and intercostal muscle tone is lost)  along with an increased shunt fraction and High metabolic rate (6-8ml ofO2/kg/minute), These factors contribute to a potential rapid desaturation in neonates under anaesthesia.
  30. 30. Control of ventilation Peripheral chemoreceptors functional at birth but are initially silent because of high post delivery blood oxygen content. Receptor adaptation occurs over 48 hours, APNOEA OF PREMATURITY neonates exhibit periodic breathing pattern defined as an apnoea of less than 5 seconds often followed by tachypnoea., Premature neonates exhibit apnoeic episodes of more than 15 seconds or a shorter period a/w fall in heart rate  due to loss of central respiratory drive  improves with maturity  may persist up to 60 weeks postconceptual age Anaemia i.e. haematocrit<30% is any independent risk factor
  31. 31. RESPONSE TO HYPOXIA characterized by 1)an initial increase in ventilation followed by a decrease in ventilation; 2).much rapid than adults due to low resting carbon dioxide Response Varies with  temperature, level of arousal and maturity .
  32. 32. PERSISTENT PULMONARY HYPERTENSION OF THE NEW BORN/PERSISTENT FETAL CIRCULATION PATHOPHYSIOLOGY hypoxia, acidosis and inflammatory mediators l/t persistent increase in pulmonary artery pressure persistent fetal circulation Ppt condition- birth asphyxia, meconium aspiration sepsis, CDH, maternal use of nsaids, GDM,,casearen delivery Leads to R TO L shunt resulting in profound hypoxia,with elevated PCO2
  33. 33. PERSISTENT FETAL CIRCULATION Goal- PaCO2-50 TO 55mmhg and Pao2-50-70 mmhg MANAGEMENT:- 1)treat precipitating condition eg hypoxia,hypoglycemia 2)Inhaled nitric oxide 3)Mechanical ventilation 4)high frequency ventilation 5)exogenous steroids 6)inhaled steroid 7)ECMO 8)experimental-slidnafil
  34. 34. MECONIUM ASPIRATION  Marker for chronic hypoxia in utero in third trimester due to interferance in maternal circulation  passage of meconium in utero-fetus breathes in meconium mixed amniotic fluid enters in pulmonary circulation  Leads to varying degree of respiratory distress  Increase in amount of amount of musle in blood vessels of distal respiratory units
  35. 35. GUIDELINES FOR MANAGEMENT FOR MECONIUM ASPIRATION “If the baby is not vigorous (Apgar 1-3): Suction the trachea soon after delivery (before many respirations have occurred) for ≤ 5 seconds. If no meconium retrieved, do not repeat intubation and suction. If meconium is retrieved and no bradycardia present, reintubate and suction. If the heart rate is low, administer PPV and consider repeat suctioning. “ “If the baby is vigorous (Apgar >5): Clear secretions and meconium from the mouth/nose with a bulb syringe or a large-bore suction catheter. In either case, the remainder of the initial resuscitation: dry, stimulate, reposition, and administer oxygen as necessary.”
  36. 36. Thermogregulation 2.5-3.0 times higher surface area BW limited insulating capacity from subcutaneous fat and the inability of neonates to generate heat by shivering until 3 months of age. Heat loss 1) radiation(39%) 2)convection (34%) 3)evaporation (24%) and 4)conduction(3%). THERMOGENESIS 1)by limb movement and 2) by stimulationof brown fat (non-shivering thermogenesis).
  37. 37. R a d ia t io n C o ld R o o m T e m p . C o ld W a lls C o ld Ite m s o n B ed C o n d u c t io n C o ld S c a le C o ld X -ra y p la tes C o ld B la n k e ts C o n v e c t io n B e d N e a r A ir V e n t O x y g e n le ft o n P a s s in g T ra ffic E v a p o r a t io n W e t D ia p e r B a t h T a c h y p n e a B a b y
  38. 38. BROWN FAT 6% of term bodyweight (dec in preterm) found in the interscapular region, mediastinum, axillae, vessels of the neck and perinephric fat highly vascular with sympathetic innervation high mitochondrial content to facilitate heat generation Non-shivering thermogenesis .1. Skin receptors perceive a drop in environmental temperataure 2. Transmit impulses to the central nervous system 3. Which stimulates the sympathetic nervous system 4. Norepinephrine is released at local nerve endings in the brown 5. Metabolism of brown fat 6. Release of fatty acids
  39. 39. HEAT CONSERVATION heat loss minimized by  increasing the temperature of the surrounding environment. CAREFUL;- the environmental temperature exceeds neonatal temperature then heat will be gained, which can be harmful as the ability to sweat is present only after 36 weeks postconceptual age.) by warming surrounding air and minimizing air speed across the baby’s skin,  increasing ambient humidity and reducing air speed across the neonate. Insensible water loss through the skin can be minimized by putting the preterm neonate in a plastic bag or covering the body,and especially the head
  40. 40. Haematology contains both adult (HbA) and fetal haemoglobin HbF 70-80% upto 90% in preterm four globin chains alpha2delta2 greater affinity for oxygen and helps maintain the molecular structure and function in a more acidic environment facilitates oxygen transfer across the placenta from maternal HbA.  replaced with HbA at approximately 6 month of age. Postdelivery, increase in 2,3-diphosphoglycerate levels, shifting the oxygen dissociation curve to the right,
  41. 41. HAEMATOPOIESIS occurs in the liver in utero but is restricted to bone marrow from 6 weeks post delivery, thus limiting potential sites for haemoglobin synthesis. PHYSIOLOGICAL ANAEMIA OF INFANCY Occcurs around 8-10 week of age HbF is lost faster than HbA is synthesized.  low levels of erythropoietin due to improved tissue oxygenation after birth decreased lifespan of HbF-laden red blood cells  relative increase in the blood volume, These factors contributes to the shrinking cellmass
  42. 42. Hepatic Most enzymatic pathways are present inactive at birth become fully active at 3 months Albumin level low-more free drug in circulation Risk of hypoglycemia-low glycogen stores and dec synthetic function UNCONJUGATED HYPERBILIRUBINEMIA Unconjugated bilirubin levels rise during the first 48 hours  rapid breakdown of HbF poor conjugating abilities of the immature liver. exacerbated in presence of haemolysis, sepsis, dehydration or excessive bruising;  can cross the blood brain barrier kernicterus and subsequent developmental delay. Bilirubin levels gradually fall over the first 2weeks,  jaundice in term infants being rare beyond this period
  43. 43. Clotting factors 1) do not cross the placenta; 2)factors V, VIII and XIII are at adult concentrations before birth. 3)vitaminK-dependent clotting factors (II, VII, IX, X, protein C and S) are initially low # because of a lack of vitamin K stores and # immaturehepatocyte function causing a prolongation in prothrombin time .4)Platelet function diminished due to low levels of serotonin and adenine nucleotides, despite platelet counts in the adult range VITAMIN K PROPHYLAXIS #Breast milk is a poor source of vitamin K #Endogenous synthesis by the gut flora is not established for the first few weeks after birth. #protect against haemorrhagic disease of thenewborn
  44. 44. Renal EXCRETORY FUNCTION 1 million nephrons is present by 34 weeks ’gestation. The glomeruli and nephrons are immature at birth Low GFR and limited concentrating ability.  Suseptible to both dehydration and volume overload Lack of renal medulla osmotic gradient and absence of medullary tubules limit urinary concentrating ability,half that of the adult (1200-1400 mOsm/kg) Glycosuria and aminoaciduria are commonly detected because of immature active transport pumps in the proximal tubule. ENDOCRINOLOGY Renal immaturity affects vitamin D formation and calcium homeostasis. The fetus and neonate have a high calcium and phosphate requirement for bone formation and growth.
  45. 45. BODY FLUID COMPOSITION 75% of TBW,80-85% IN PRETERM Reduced to 60-65% BY one year ECF:ICF IS 2:1, The diuresis reduces the extracellular water (30% of TBW) and ICF increases due to growth of cellls- reaches adult value by 1 yr Blood volume Full term-85 ml /kg Preterm90-100 ml /kg(50 ml/kg is plasma) important postnatal adaptation to facilitate lung function and reduces the risks of symptomatic patent ductus arteriosus, necrotizing enterocolitis and bronchopulmonary dysplasia
  46. 46. FLUID THERAPY MAINTAINENCE FLUID- 70,80,90,120 ml/kg on day 1/3/5/7 Rest period-150ml/kg/24hr Fluid choice FIRST 48 hrs-10% glucose Higher in pre term Na and k 2-3 meq/100 ml Beyond that-5% glucose(preterm higher glucose requirement) IMPORTANT-newborn of diabetic mother, small for gestational age, glucose monitoring must
  47. 47. NERVOUS SYSTEM  precocious in development , continues to develop to achieve a full complement of cortical and brainstem cells by 1 year. neonatal cerebral circulation receiving one-third of cardiac output compared with one-sixth of cardiac output in adults The blood brain barrier is immature in the neonatal period  increased permeability to fat-soluble molecules potentially increasing the sensitivity to certain anaesthetic drugs(
  48. 48. NERVOUS SYSTEM  Cerebral autoregulation is fully developed at term, maintaining cerebral perfusion down to a mean arterial pressure of 30 mmHg, reflecting the lower blood pressures found in neonates.  ANS better developed to protect against hypertension than hypotension because the parasympathetic system predominates., reflected in the propensity of neonates to bradycardia and relative vasodilation.  Delayed myelination-easier intraneural penetration of LA,short time of onset and diluted conc as effective as concentrated
  49. 49. NOCICEPTION  pathways are developed by 24-28 weeks’ gestation,  The concept of neonatal nociception is now widely accepted, with adultlike physiological stress and behavioural responses to a noxious Stimulus  Neonates undergoing awake nasal intubation increase mean arterial pressure by 57% and intracranial pressure by a similar amount.  Noxious stimulus exposure in the neonatal period can also affect behavioural patterns in later childhood, suggesting adaptive behaviour and memory for previous experience
  50. 50. IMMUNOLOGIC ADAPTATION Active acquired immunity  Pregnant woman forms antibodies herself Passive acquired immunity  Mom passes antibodies to the fetus  Lasts for 4-8 months  Newborn begins to produce own immunity about 4 weeks of age
  51. 51. KEY POINTS
  52. 52. KEY POINTS
  53. 53. THANK YOU

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