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The Newborn final THE PREMATURE INFANT Premature Birth

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The Newborn final THE PREMATURE INFANT Premature Birth

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									                                                   FOETAL PHYSIOLOGY

Placental Function:                                           Foetal Function:

   Transport:                                                   Liver – produces albumin, coagulation factors and red
        o Transport of nutrients from mother to foetus            blood cells
            as well as waste products in other direction
        o Also acts as “lung” – responsible for gaseous          Kidney – excretes urine (contributes to amniotic fluid)
            exchange of oxygen and carbon dioxide as
            well as maintenance of acid-base status              Endocrine organs – produce thyroid hormones,
                                                                  corticosteroids, mineralocorticoids, parathormone and
   Metabolism:                                                   insulin from 12 weeks’ gestation
        o Produces hormones, including human
            chorionic gonadotrophin (HCG), human                 Immunoglobulins – some produced from end of first
            placental lactogen (HPL) and human                    trimester
            chorionic thyrotropin (HCT)
        o Detoxifies drugs and metabolites                       Foetus breathes from about 11 weeks’ gestation, but
        o Has very high energy demands and                        this is irregular until ~20 weeks; at 36 weeks foetus
            consumes over 50% of the total oxygen and             breathes regularly
            glucose transported across it

Foetal Circulation:

   Consists of 2 umbilical arteries bringing
    deoxygenated blood to the placenta and
    a single umbilical vein carrying
    oxygenated blood back to the heart

   Aorta divides into the common iliac
    arteries and then the internal and
    external iliac arteries – the umbilical
    arteries are branches of the internal iliacs

   The umbilical vein drains into the portal
    sinus and thence bypasses the liver via
    the ductus venosus to reach the IVC

   Deoxygenated blood is carried by the 2
    UAs to the placenta where it is
    oxygenated as it comes into close
    apposition with maternal blood in
    intervillous spaces

   Oxygenated foetal blood is carried in the
    UV, where it bypasses the liver via
    ductus venosus  IVC and right atrium

   Much of the blood here is shunted across
    the foramen ovale from the RA to left

   Oxygenated blood is pumped by the RV
    into the pulmonary artery, but the majority
    bypasses the lungs via the ductus
    arteriosus to flow into the aorta

   Summary of shunts in foetal circulation:

        1.   Ductus venosus bypasses blood
             away from the liver
        2.   Foramen ovale shunts blood
             from RA to LA, bypassing lungs
        3.   Ductus arteriosus shunts blood
             from pulmonary artery to the
                                             ADAPTATION TO EXTRAUTERINE LIFE

Respiratory Adaptation:                                           Cardiovascular Adaptation:

   While the foetus is breathing in utero, the lungs are             With the first few breaths, arterial oxygen tension
    filled with fluid                                                  increases

   At the time of birth, the baby generates enormous                 This relative hyperoxia results in closure of the ductus
    negative pressures and fills the lungs with air                    arteriosus – functionally closed by 10 – 15 hours, but
                                                                       not anatomically closed until 4 – 7 days
   With the first 2 – 3 breaths, much of the foetal lung fluid
    is expelled; the remainder is absorbed into pulmonary             Marked fall in pulmonary vascular resistance shortly
    lymphatics and capillaries over first 6 – 12 hours                 after birth  pulmonary blood flow increases

   Stimulus for first breath is not known with certainty, but        Drop in pulmonary blood pressure  drop in pressure
    it’s probably due to the bombardment of physical                   on right side of heart  no longer shunting from RA to
    stimuli e.g. cutaneous and thermal changes; and                    LA across FO; takes some time to close and remains
    emptying of the lungs of fluid                                     patent in 10%

                                                                      After birth there is a marked decrease in blood flow in
                                                                       the IVC and the ductus venosus closes in response to
                                                                       this  remains as a vestigial remnant (ligamentum
                                                                       teres) throughout life

                                                                      Umbilical vessels take longer to obliterate and may still
                                                                       be cannulated for up to 10 days after birth

      Assessment of Infant at Birth:

          The APGAR score – performed at 1 minute, 5 minutes and 10 minutes:

                   Sign                             0                        1                             2
      Heart rate                                Absent                  < 100 / min                   > 100 / min
      Respiratory effort                        Absent                    Weak cry                     Strong cry
      Muscle tone                                Limp                  Some flexion                   Good flexion
      Reflex irritability (suction)          No response               Some motion                        Cry
      Colour                                     Pale;                 Centrally pink;                    Pink
                                            overall cyanosis          peripherally blue

                o    Score at one minute:
                         -    7 – 10  normal
                         -    4 – 6  moderately depressed
                         -    0 – 3  severely depressed

      Routine Resuscitation of Non-Asphyxiated Infant:                Resuscitation in Infant with Depression:

          Pharyngeal suction as head delivers                            Bag and mask ventilation:
                                                                               o Jaw should be held forward as operator
          Placing baby with head lower than baby                                  squeezes the bag at rate of 35 / min
                                                                               o Watch chest for adequate inflation and
          Keep baby warm by radiant heater or wrapped in                          auscultate for air entry
           warm blankets                                                       o Continuously assess heart rate and
          Gently suction pharynx and nares
                                                                          Intubation and positive-pressure ventilation:
          Auscultate heart and calculate APGAR                                 o Babies with Apgar score 0 – 3 at 1 min
                                                                                o If baby still blue following bag and mask
          Administer oxygen by face mask at rate of 1 – 2                      o If Apgar < 6 at 5 mins
           L/min if baby still blue                                             o Intubation may be orotracheal or
          Vitamin K (1mg) given IM or orally
                                                    EXAMINATION OF THE NEWBORN

1. General Appearance:                                                6. Neck:

   Facies:                                                               Full range of movement
         o      Chromosomal disorders e.g. 21, 18, 13                     Redundant skin at back = Turners’ or Down syndrome
         o      Foetal alcohol syndrome                                   Goitre
         o      Other syndromes
   Colour:                                                           7. Chest:
         o      Should be uniformly pink
         o      Generalised cyanosis, pallor, jaundice, plethora,         Shape and size
                bruises, petechial haemorrhages                           Signs of respiratory distress – recession
   Posture:                                                              Stridor – upper airways obstruction
         o   Normal position = hips abducted and partially flexed;        Breath sounds – symmetry, air entry and adventitial sounds
             knees flexed; arms adducted and flexed at elbow
         o   Limited movements, exaggerated or asymmetrical           8. Cardiovascular system:
             movements, hypotonia, stiffness
   Cry:                                                                  Pulses – radial and femoral
         o   Should be vigorous and sustained after stimulation           Apex beat
         o   Weak, high-pitched or hoarse is abnormal                     Auscultation
   Skin appearance:
         o   Mild peeling on mature babies is not abnormal            9. Abdomen:
         o   Abnormal appearances, pigmentation and naevi
   Head shape:                                                           Distension
         o   Moulding and caput succedaneum (oedematous                   Soft, non-tender
             thickening of scalp due to passage through vagina) is        Liver – normally palpable up to 1cm below right CM
             normal in newly born infants and disappears within 2 –       Spleen – tip can be palpated in 25% of normal infants
             3 days                                                       Kidney – may be palpable normally
         o   Plagiocephaly = flattening of occipital region on one        Anus – should be patent and normally situated
             side; no pathological significance
         o   Scaphocephaly = long head with flattened                 10. Umbilicus:
             temporoparietal regions = common in premature
             infants                                                      Vessels – normally 2 thick-walled arteries and a thin-walled vein
         o   Head size should be measured                                 Colour – normally translucent
         o   Fontanelles – normally soft and flat; bulging may be         Stump – cord usually separates by day 10 leaving a yellowish or
             due to raised ICP and is always abnormal                      greenish eschar
         o   Craniosynostosis = premature fusion of one or more           Umbilical hernia common in premmies
             skull bones; sagittal suture most common
                                                                      11. Genitalia:
2. Eyes:
                                                                          Testes
   Site:                                                                 Penis and urethra
            o Distance apart; too far = hypertelorism; too close =        Scrotum
              hypotelorism                                                Inguinal hernia
   Conjunctiva:                                                          Hymen – skin tags common
        o     Usually clear; but subconjunctival haemorrhages are         Vagina and vulva
              not uncommon
        o     Conjunctivitis                                          12. Extremities:
        o     Excessive lacrimation
   Cornea and iris:                                                      Feet – talipes equinovarus
        o     Cornea should be clear and red reflex elicited              Hips – dislocation
        o     Pupils should constrict to light directly and               Arms – range of normal movements
              consensually                                                Simian crease – may be present in Down syndrome

3. Ears:                                                              13. Neurological screening:

   Preauricular skin tags or sinuses common                              Primitive Reflexes:
   Position = top of pinna should be above a horizontal line from              o     Moro
    inner and outer canthi; low set ears seen in a variety of                   o     Sucking
    conditions                                                                  o     Rooting
                                                                                o     Grasping
4. Nose:                                                                        o     Tonic neck reflex
                                                                          Spontaneous movements
   Exclude choanal atresia by passing catheter through                   Posture
                                                                          Tone
5. Mouth:                                                                 Deep tendon reflexes

   Lips – cleft lip
   Palate – cleft palate, bifid uvula, high arched palate
   Tongue – size and positioning
                                                  THE NORMAL NEONATE

Features of the Normal Neonate:

   Term baby > 37 weeks
   At birth, average = 3.5kg, 50cm long, head circumference 35cm
   HR 100 – 160; RR 40 – 60; Systolic BP 50 – 75
   Acrocyanosis normal (hands persistently cold and blue)
   2 fontanelles – anterior (1 – 4cm) and posterior (< 1cm)
   Freely mobile sutures (metopic, sagittal, coronal, lambdoid)
   Primitive reflexes – rooting, Moro, grasping, stepping, Babinski
   Suck reflex develops at ~ 34 weeks
   Obligate nose breathers until 5 months of age
   Liver palpable 2cm below costal margin
   Splenic tip palpable
   Bladder palpable just prior to voiding
   Innocent murmur normal
   Lose up to 5 – 10% weight in first 5 days; regained at 10 days
   Urinate soon after birth, then every 3 – 4 hours
   95% pass meconium by 24 hours
   40 – 50% have physiological jaundice
   Small occasional vomits
   Sleep for 18 hours / day
   Cry for 4 hours / day
                                                 JAUNDICE OF THE NEONATE

Physiology of Bilirubin Metabolism:

   Foetus:
        o Placenta and maternal liver metabolise the
            bilirubin from worn-out RBCs
        o If excessive foetal haemolysis e.g. in rhesus
            haemolytic disease  placenta and maternal
            liver may not be able to deal with excessive
            bilirubin load and umbilical cord and amniotic
            fluid with be stained yellow
        o Foetus will become anaemic as bone marrow
            and extramedullary organs fail to keep up
        o Foetus is capable of conjugating bilirubin in
            small amounts and when haemolysis occurs in
            utero this increases

   Newborn:
       o Bilirubin production:
               -   Most comes from senescent RBCs
               -   RBCs are destroyed in RE system and
                   haem is converted to unconjugated
       o Transport and liver uptake:
               -   Most unconjugated bilirubin in blood is
                   bound to serum albumin and
                   transported as a bound complex to the
                   liver (renders it non-toxic)
               -   Free, unbound bilirubin is fat soluble
                   and can cross the BBB and be
                   deposited in neurons  kernicterus
               -   Unconjugated bilirubin is extracted
                   from blood by hepatocytes
       o Conjugation and excretion:
               -   Unconjugated bilirubin is conjugated in
                   the liver with glucuronic acid
               -   Conjugated bilirubin is then excreted
                   into the bile then into the duodenum
                   and small intestine
               -   In the newborn (relatively sterile bowel
                   and poor peristalsis) much of
                   conjugated bilirubin is hydrolysed to
                   unconjugated bilirubin  enters
                   enterohepatic circulation for further
                   liver metabolism

Clinical Assessment of the Jaundiced Infant:                    Kramer’s Rule:

   Can be detected in the newborn when serum level is ~
    100 µmol / L
                                                                                 Zone 1 SBR = 100
   Kramer’s rule = blanching of infant’s skin with finger at
    standard zones and observe colour in blanched areas;                         Zone 2 = 150
    zones of jaundice reflect the downward progression of
    dermal icterus                                                               Zone 3 = 200
   Indications for investigations of jaundice:                                  Zone 4 = 250
         o Any infant visibly jaundiced in 1 24 hours of life
         o Any infant whose mother has rhesus Abs                                Zone 5 = > 250
         o A preterm infant w serum bilirubin > 150µmol / L
         o Term infant w serum bilirubin > 200 µmol / L
         o Any infant w signs of obstructive jaundice
         o Prolonged hyperbilirubinaemia > 1 week in term
             infants and > 2 weeks in preterms
                                         JAUNDICE OF THE NEONATE (CONTINUED)

Unconjugated Hyperbilirubinaemia:                                       Physiological Jaundice:

   Causes:                                                                Describes jaundice which is not severe enough to
       o      Rhesus and ABO incompatibility                                warrant treatment
       o      Hereditary spherocytosis
       o      G6PD deficiency                                              Presumed to be due to a temporary immaturity of
       o      Septicaemia and TORCH infection                               glucuronyl transferase and other factors in
       o      Extravasated blood and excessive bruising                     bilirubin metabolism
       o      Twin-to-twin transfusion
       o      Prematurity                                                  Should not fulfil any of the following criteria:
       o      Dehydration
       o      Hypothyroidism                                                    o    Clinical jaundice in 1 24 hours of life
       o      Breast milk jaundice                                              o    Total serum bilirubin > 300µmol / L in
       o      Delayed passage of meconium                                            term infant or 255 µmol / L in preterm
                                                                                o    Clinical jaundice persisting for > 10 days
   Investigations:                                                                  in term infant or > 2 weeks in preterm
        o Prolonged jaundice requires investigation when                             infant
             present for > 10 days in a term infant and > 14 days in            o    An “ill” infant
             a premature one
        o Haemoglobin
        o Blood film for RBC morphology                                 Others Causes of Unconjugated HB:
        o Maternal and infant blood grouping
        o Direct Coombs’ test                                              Infection:
        o Maternal haemolysis if ABO mismatch                                    o Bacterial infections, esp. septicaemia
        o Infection screen                                                            and UTIs may  unconjugated
        o Serum T4 and TSH                                                            hyperbilirubinaemia

   Management:                                                            Breastfeeding associated jaundice:
       o Prevention:                                                            o Increased bilirubin levels seen in first 2
               -  Early feeding reduces incidence of jaundice                       weeks of life in 60% of infants who are
                  by preventing dehydration and elevation of                        breastfed
                  free fatty acids                                              o Can be reduced by increased frequency
               -  Maintenance of adequate fluid intake =                            of breastfeeding in first few days of life
                  essential part of management                                  o May rarely cause kernicterus if untreated
               -  Breast-feeding associated jaundice is
                  minimised by frequent, early breastfeeding in            Breast milk jaundice:
                  first 3 days of life                                          o Prolonged jaundice that extends up until
                                                                                    the first 3 months of life
        o     Phototherapy:                                                     o Diagnosed by exclusion of other
                  -   Resulted in a decline in number of exchange                   aetiologies in a thriving infant
                      transfusions required
                  -   Phototherapy units of wavelength 450nm               Delayed passage of meconium:
                      used to degrade and isomerise                             o Jaundice due to increased enterohepatic
                      unconjugated bilirubin in the skin to non-toxic               absorption of bilirubin
                      bilirubin products
                  -   Complications of phototherapy:                       Gilbert’s syndrome:
                               Temperature instability                         o Autosomal dominant condition
                               Fluid disturbance                                     associated with a mild unconjugated
                               Retinal damage                                        hyperbilirubinaemia (< 85µmol / L)
                               Diarrhoea
                               Bronze baby
                                                                        Complications of Jaundice:
        o     Exchange transfusion:
                  -  May be required in conjunction with                   Kernicterus and bilirubin encephalopathy:
                     phototherapy for infants with severe jaundice
                  -  Allows:                                                    o    Classic presentation = progressive
                             Removal of unconjugated bilirubin                      development of lethargy, rigidity,
                             Removal of immune antibody if                          opisthotonos, high-pitched cry, fever and
                              present                                                convulsions over a period of 24 hours
                             Replacement of sensitised RBCs                    o    Followed by death in 50% of infants
                              with cells that cannot be                         o    Autopsy shows bilirubin staining and
                              haemolysed as easily                                   necrosis of neurons, especially in basal
                             Restoration of blood vol and                           ganglia and hippocampus
                              correction of anaemia                             o    Levels at which unconjugated bilirubin
                             Provision of free albumin for                          causes brain damage are unknown, and
                              bilirubin binding                                      it’s probably only free (non-protein
                  -                                                                  bound) bilirubin that is dangerous
                                          JAUNDICE OF THE NEONATE (CONTINUED

Conjugated Hyperbilirubinaemia:

   Much less common than unconjugated HB but much more
    serious prognosis

   Due to intra or extrahepatic obstruction / cholestasis

   Clinical features:
         o Usually presents in 2 week of life or later
         o Greenish skin discolouration
         o Dark bile-stained urine
         o Pale acholuric stools
         o Hepatosplenomegaly common
         o Failure to thrive

   Occasionally present at birth as a result of TORCH
    infection or rhesus isoimmunisation

   Causes:

        o     Neonatal hepatitis:
                   -    TORCH infection
                   -    Metabolic causes
                   -    α-1 antitrypsin deficiency
        o     Biliary atresia (intra or extrahepatic)
        o     Inspissated bile
        o     Choledochal cyst
        o     Hepatic necrosis
        o     CF
        o     Complication of parenteral nutrition

                                                             Classification of Jaundice According to Onset:

                                                                Early (days 1 – 2) – uncommon:

                                                                     o    Haemolytic jaundice (Rhesus, ABO)

                                                                Normal (days 3 – 10) – very common:

                                                                     o    Uncomplicated
                                                                     o    Complicated

                                                                Late (days 14+) :

                                                                     o    Breast milk – common
                                                                     o    Conjugated jaundice – uncommon
                                                                     o    Inherited deficiency of glucuronyl transferase –
                                                                          very rare
                                                        BIRTH TRAUMA

Introduction:                                                    Soft Tissue Injury:

   Definition = injuries to the infant resulting from                Erythema, abrasions and lacerations:
    mechanical forces (e.g. compression, traction) during
    the process of birth                                                   o   Seen following forceps and vacuum delivery,
                                                                               episiotomy, uterine incision at C-section
   Accounts for fewer than 2% of neonatal deaths
                                                                      Traumatic cyanosis / petechiae:
   Larger infants are more susceptible
                                                                           o   Occur over head, neck and upper chest
   Most are self-limiting and have a favourable outcome                       following a difficult delivery
                                                                           o   Usually fade within 2 – 3 days
   Risk factors:
        o Large-for-date infants                                      Ecchymoses:
        o Instrumental deliveries esp. forceps or
             vacuum                                                        o   Seen with traumatic deliveries, precipitate
        o Vaginal breech delivery                                              labour, preterm infants, poorly controlled
        o Abnormal / excessive traction during delivery                        deliveries or abnormal presentations

Injuries to the Head:

   Cephalohaematoma:
       o Subperiosteal collection of blood secondary to
           rupture of blood vessels between the skull
           and periosteum
       o Never crosses sutures
       o Linear skull fractures may underlie
       o Resolution occurs over a few weeks
       o Management = observation only

   Caput succedaneum:
       o A          serosanguineous,         subcutaneous,
            extraperiosteal fluid collection with poorly
            defined margins
       o Caused by pressure of the presenting part
            against the dilating cervix
                                                                Peripheral Nerve Injury:
       o Extends across the midline and over suture
                                                                    Brachial plexus injury:
       o Does not usually cause complications and
                                                                         o Occurs most commonly in large babies,
            usually resolves over first few days
                                                                              frequently with shoulder dystocia or breech
       o Management = observation only
                                                                         o Most are Erb palsy (C5-C6 paralysis of
   Skull fractures:
                                                                              muscles of upper arm and shoulder girdle)
        o Generally linear fractures require no specific
                                                                         o Associated traumatic lesions = fractured
                                                                              clavicle, fractured humerus, cervical cord
                                                                              injury, facial palsy
                                                                         o Most cases will resolve in first 4 months
                                                                         o Management = prevention of contractures
Bone Injury:
                                                                    Cranial nerve and spinal cord injury:
   Fractures:                                                           o Result from hyperextension, traction, and
        o Most often observed following breech delivery                       overstretching with simultaneous rotation
             +/- shoulder dystopia                                       o Facial nerve palsy most common
        o Clavicle = most frequently fractured bone;                     o Usually resolves or improves
             healing usually within 7 – 10 days

Intra-Abdominal Injury:

   Relatively uncommon
   Most serious acute complication = haemorrhage
   Liver = most commonly damaged internal organ
   Management = rapid identification and stabilisation with
    blood transfusion
                                                THE PREMATURE INFANT


                                         Gestation:
                                              o Term ≥ 37 weeks
                                              o Preterm < 37 wks
                                              o Post-term > 42 wks

                                         Birth weight:
                                               o Low birth weight < 2500g
                                               o Very low birth weight < 1500g
                                               o Extremely low birth weight < 1000g

                                         Weight for gestational age:
                                             o Appropriate for gestation (AGA) =
                                                                           th     th
                                                   birth weight between 10 and 90
                                             o Small for gestational age (SGA) =
                                                   birth weight < 10 centile
                                             o Large for gestational age (LGA) =
                                                   birth weight > 90 centile

    Risk Factors for Prematurity:           Short-Term Complications of Prematurity:

      Maternal:                                Respiratory:
           o Extremes of age                        o Respiratory distress syndrome
           o High gravidity                         o Periodic breathing, apnoea of newborn:
           o Low weight
           o Acute abdomen                      Cardiac:
           o Pyelonephritis                          o Patent ductus arteriosus (PDA)
           o Uterine anomalies
           o Pre-eclampsia                      Neurological:
           o Prior termination                      o Periventricular / intraventricular haemorrhage:
           o History of infertility
           o Genital infection                  Hepatic:
                                                    o Hypoglycaemia
      Foetal:                                      o Hyperglycaemia
           o     Multiple gestation                 o Hyperbilirubinaemia
           o     Foetal anomalies
           o     Polyhydramnios                 Renal:
           o     Foetal demise                      o       Dehydration, hyper/hyponatraemia, hyperkalaemia, metabolic
      Placenta & membranes:
           o Placenta previa                    GIT:
           o Abruptio placentae                         o   Necrotising enterocolitis
           o Premature rupture                          o   Feeding problems

      Social:                                  Haematological:
           o     Low SES                            o Anaemia
           o     Smoking
           o     Alcohol abuse                  Immunological:
           o     Illicit drug abuse                 o Infection
           o     Fatigue and stress
                                                Thermoregulation problems
      Idiopathic:
            o Previous preterm

                                            Late Onset Complications of Prematurity:

                                                Retinopathy of prematurity (ROP)

                                                Chronic lung disease

                                                Growth failure

                                                Neurodevelopmental impairments e.g. cerebral palsy, deafness
                                      SUPPORTIVE CARE OF THE PRETERM INFANT

Oxygen Therapy:                                             Thermoregulation:

   Oxygen is a toxic substance in the preterm infant and      Body temperature must be maintained in the normal
    may cause ROP                                               range (36.5 – 37)

   Arterial oxygen tension should be maintained between       Achieved by nursing preterm infant under an open
    50 and 80 mmHg                                              radiant heat source or in a closed incubator

   Methods of administration:
        o Directly into incubator
        o Nasal prongs
        o CPAP
        o Endotracheal tube                                    Premature infants require frequent feeding via NG
   Should be warmed to 35 – 37ºC and humidified
                                                               Should be started on 1 – 2 ml/kg increasing as
   Monitor via pulse oximetry                                  tolerated

                                                               Gastric aspirates must be checked before the next
Parenteral Fluids:

   Sick babies and infants < 1750g may need parenteral
    feeding with 10% dextrose infusion into umbilical or
                                                            Other Considerations:
    peripheral vein
                                                               Exogenous surfactant should be administered via ET
   Electrolyte requirements of preterm infants is
                                                                tube prior to 2 hours of age
    increased due to poor conservation by immature
                                                               Single IM dose of vitamin K should be administered at
   Close monitoring of serum electrolytes is necessary
                                             INFANT FEEDING AND NUTRITION

Specific Nutritional Requirements:                             Breastfeeding:

   Water:                                                        Advantages to the baby:
       o     A healthy breastfed infant will consume as                o Nutritional – provides baby with a source of
             much fluid as is required; and healthy bottle-                nutrition that changes with the baby’s
             fed infants will know how much they need and                  changing metabolic needs
             should be allowed to consume milk when they               o Confers an advantage in intellectual
             want it                                                       attainment
        o    Infants who have suffered IUGR should be                  o Anti-infective
             fed to an expected weight as if they had                  o Antiallergic – reduces risk of asthma and
             grown normally in utero                                       eczema in prone infants
        o    Ill premature infants will tolerate less than             o Protection against various illnesses e.g.
             their recommended volume                                      gastroenteritis; apparent protection against
   Energy:
        o Requirements depend on baby’s birthweight,              Advantages to the mother:
            gestational age and state of health                        o Sense of pride and achievement
        o Carbohydrate – lactose is sole carb in human                 o Promotion of close mother-baby relationship
            milk; provides 40% of infant’s total energy                o Weight loss
            requirement in milk                                        o Convenience
        o Fat in milk provides approx. half infant’s                   o Contraception – delays return to ovulation
            energy requirements                                        o Contraction of uterus  involution
        o Protein – 10% of infants requirements                        o Financial benefit
                                                                       o Health advantages – protection against
                                                                           ovarian and premenopausal breast cancer
                                                                           and osteoporosis
Feeding the VLBW Infant:
                                                                  Anti-infective properties:
   Some ill VLBW infants will not tolerate milk feeds and              o Breastfed infants are less likely to develop
    require total parenteral nutrition                                       gastroenteritis, NEC, OM and other serious
                                                                             infections e.g. septicaemia, meningitis
   For those in whom milk may be safely given, there is a              o Immunoglobulins – IgA = most important Ig
    choice between breast milk or formula feed                               secreted in breast milk; in very high
                                                                             concentrations in colostrum
   Breast milk:                                                        o Cells – macrophages, polymorphs and both T
        o Human milk is not nutritionally adequate for                       and B lymphocytes
            very immature infants                                       o Lysozyme – acts to lyse the E. coli cell
        o But has some advantages e.g. reduced risk of                       membrane
            infection, reduced risk of NEC, growth factors,             o Lactoferrin – binds iron (inhibits multiplication
            cognitive development                                            of some bacteria)
                                                                        o Antiviral properties – secretory IgA or
   Low birth weight formula:                                                interferon production by lymphocytes
        o Often contain more sodium, potassium,
             protein and carbohydrate than breast milk and        Contraindications to breastfeeding:
             regular artificial feeds                                  o In the mother:
        o Continue until infant is 35 weeks                                     -    Acute illness (relative)
             postconceptual age and then change to                              -    Chronic illness – neoplasms, mental
             regular formula feed                                                    illness, TB
                                                                                -    Breast infection / abscess
   Enteral vs. parenteral feeds:                                               -    HIV infection
        o Early exposure of baby’s gut to enteral feeds                o In the infant:
             has been shown to mature gut function                              -    Acute illness
        o Low-volume hypocaloric feeds (20ml/kg)                                -    Mechanical problems e.g. cleft lip
             reduce the time to reach full feeding                              -    Metabolic problems e.g.
                                                                                     galactosemia, lactose intolerance
   Principles of management:                                                   -    Breast milk jaundice
        o Early introduction of breast milk is beneficial,
             even if given in small volumes                       Supplements to breastfeeding:
        o Avoid milk feeding in the first 5 – 7 days in               o Full term infant:
             babies at high risk of NEC                                        -    Babies receive sufficient iron in
        o Nasogastric route is preferred                                            breast milk alone at least until 6/12
        o No advantage of continuous feeding over                              -    At ~6/12 some iron containing foods
             bolus feeding                                                          should be slowly introduced
        o TPN should only be used when milk feeding is                o Preterm infant:
             contraindication; use for the shortest                            -    Needs supplemental iron whether
             acceptable period of time                                              breastfed or not
                                    COMMON FEEDING DISORDERS IN THE NEONATE

                                                              Infant Colic:

                                                                 Some apparently healthy infants cry at certain
Vomiting:                                                         times during the day, especially in evening
                                                                  around 6pm
   Common problem in the newborn
                                                                 Tends to disappear spontaneously at around 3
   Non-organic causes:                                           months
       o Overfeeding
       o Incorrect preparation of feeds                          Often no obvious cause
       o Overstimulation or excessive handling
       o Crying                                                  Treatment:
       o Air swallowing                                               o Attention to feeding techniques
                                                                      o Posture feeding
   Organic causes:                                                   o Warmth to abdomen e.g. baths
        o Infection (UTI, GE, meningitis, OM)                         o Removal of milk from maternal diet
        o GOR
        o Gastritis (meconium, blood)
        o Hiatus hernia
        o Organic bowel obstruction                           Constipation:
        o Pyloric stenosis
        o Small bowel obstruction                                Aetiological factors:
        o Large bowel obstruction                                     o Inadequate / improper feeding e.g. too
        o Food allergy                                                     concentrated milk formula
                                                                      o Anatomical abnormalities e.g. anal
                                                                           stenosis, Hirschsprung’s, fissure in ano

Gastro-Oesophageal Reflux:                                       Treatment:
                                                                      o Local anaesthetics for fissure in ano
   Common cause of vomiting                                          o Alteration of feeds may be indicated
   Caused by incompetent LOS                                            e.g. giving prune juice, extra water
   Prevalent in preterm infants
   Clinical features:
         o Vomiting at end of feed
         o Gradual improvement with growth                    Diarrhoea:
         o Cessation usually by end of 1 year
   Complications:                                               Stools initially change from dark green-black
         o Persistent vomiting  FTT                              (meconium), through a greenish-yellow
         o Oesophagitis, hiatus hernia, stricture                 transitional stage, and attain typical yellow
         o Obstructive apnoea, SIDS                               colour by 4 – 5 days
         o Recurrent aspiration of milk
   Investigations:                                              May be very frequent initially, especially in
         o Barium swallow                                         breastfed babies
         o Technetium milk scan
         o pH probe                                              Causes of diarrhoea:
   Treatment:                                                       o Maternal diet in a breastfed infant e.g.
         o Prone position with 30 - 40º head-up                           excessive chocolate, coca-cola etc
              tilt                                                   o Incorrect formula preparation, over-
         o Nurse infant in more upright position                          feeding
         o Thickening of feeds                                       o Infection (bacterial, viral, protozoal)
         o Drugs e.g. infant Gaviscon                                o Sugar intolerance – transient or
                                                                     o Steatorrhoea e.g. CF

Pyloric Stenosis:                                                Management:
                                                                     o Attention to fluid balance
   Usually presents after first month of life                       o Anti-diarrhoeal drugs NOT used

   Clinical features:
         o Projectile vomiting
         o More common in boys                                Failure to Thrive:
         o Visible peristalsis
         o Palpable “tumour”                                     Babies at least double birth-weight by 5/12 and
         o Often family history                                   treble it by 1 year
                                                                 Manifests as fall-off in wt gain & linear growth
   Treatment:                                                   A fall in growth curve when gluten is introduced
        o Surgical – muscle-splitting operation of                is suspicious of coeliac disease
           the pylorus                                           Normal head growth may continue despite poor
                                                                  weight gain, as brain growth is last to fail
                                        RESPIRATORY DISORDERS IN THE NEWBORN

                                              Respiratory Distress:

                                                  Following signs for > 4 hours:
                                                        o Tachypnoea > 60 / min
                                                        o Chest recession
                                                        o Cyanosis
                                                        o Nasal flaring
                                                        o Expiratory grunt
                                                        o Tracheal tug

                                                  Investigations:
                                                       o CXR
                                                       o Bacteriology – blood, urine,
                                                       o Virology – NPA, blood
                                                       o Haematocrit & FBC

Transient Tachypnoea of Newborn:          Respiratory Distress Syndrome:                    Other Causes of Respiratory Distress

   Benign disorder of 2 – 3% of                 Introduction:                                Pneumonia:
    newborns                                           o AKA Hyaline membrane                      o Presents with early or late
                                                           disease                                    onset respiratory distress
   Predisposing factors – retained                    o Specific entity in preterm                o Non-specific with lethargy,
    lung fluid:                                            infants                                    apnoea, bradycardia
        o Term / near term infant                      o Caused by lack of surfactant              o Ex = ↓ air entry,
        o Heavy maternal analgesia                                                                    crepitations, consolidation,
        o Birth asphyxia                         Epidemiology:                                       effusions
        o Caesarian section                           o Common condition – 1%                      o CXR = lobar pneumonia
        o Breech delivery                             o Predisposing factors:                         rarely occurs; widespread
        o Male sex                                            - Maternal DM                           diffuse / patchy coarse
                                                              - Antepartum haem                       changes
   Clinical features:                                        - Second twin                        o Organisms:
         o Tachypnoea                                         - Hypoxia at birth                           -    Gram –ve e.g. E.
         o Cyanosis                                           - Male                                            Coli, Klebsiella,
         o Grunt                                              - Caesarian                                       pseudomonas
         o Onset in first 1 – 3 hours                         - Family history                             -    Group B
         o Usually lasts < 24 hours                                                                             haemolytic strep
                                                 Clinical features:                                       -    Staph aureus
   Chest x-ray:                                       o Diagnosed at birth or first hrs                   -    Candida
       o Hyperinflation                                o Signs of respiratory distress                     -    Viral (rare)
       o Cardiomegaly                                  o Oedema
       o ↑ perihilar markings                          o Apnoea                                Meconium aspiration syndrome:
       o Perihilar cuffing                             o Course = ↑ for 24 – 72 hours              o Meconium staining of
       o Fluid in fissures                                  then diuresis and recovery 48              liquor occurs in 10 – 15%
       o Coarse streaking in lungs                          – 96 hours                                 of births, esp. breech,
                                                                                                       post-term, foetal distress
   Management:                                  Radiological signs:                              o Aspiration into lungs
       o 30 – 40% oxygen                              o Hypoinflation                                  occurs within a few
       o IV fluids                                    o Diffuse granuloreticular                       breaths of birth
       o No oral feeds                                    pattern (“ground glass”)                 o CXR  hyperinflated
                                                      o Air bronchograms                               lungs; widespread course
                                                      o Severe – diffuse white-out                     pulmonary infiltrate and
                                                 Management:
                                                     o Assisted ventilation                    Pulmonary hypoplasia:
                                                     o Exogenous surfactant                         o Bilateral hypoplasia occurs
                                                                                                       secondary to:
                                                 Prognosis:                                                -   Oligohydramnios
                                                      o Relates to severity and                             -   ↓ intrathoracic
                                                          gestational age                                       space e.g.
                                                      o Complications include                                   hydrops
                                                          neurosensory disabilities e.g.                    -   Chest wall
                                                          spasticity, deafness                                  deformities

Introduction:                                              Why is the newborn prone to heat loss?

   Central / core temperature should be maintained           Large surface area to body weight ratio
    between 36.7 and 37.3ºC
                                                              Limited ability to shiver
   Mechanisms of heat loss:
                                                              Deficiency of subcutaneous fat tissue
        o   Evaporation – when a moist baby is
            exposed to room temp there is conversion          Relative deficiency of brown fat and glycogen
            of liquid to vapour with subsequent loss of
            heat                                              Often born covered in liquor, vernix, meconium or
                                                               blood  moisture predisposes to loss of heat and
        o   Radiation – heat is dissipated down a              fluid by evaporation
            concentration gradient via the surrounding

        o   Conduction – direct heat loss from the skin
            to cooler objects e.g. wet nappies

        o   Convection – heat loss occurs via a
            current of moving air

   Mechanisms to conserve heat:
                                                           Prevention of Excessive Heat Loss:
        o   Peripheral vasoconstriction
                                                              Labour ward:
        o   Increased heat production:                             o Provision of warmth is first essential in
                 -  Increased basal metabolism with                    resuscitation of newborn
                    increased oxygen consumption                   o Overhead radiant heat warmer may be
                 -  Increased voluntary muscular                       useful
                 -  Involuntary muscular activity –           Nursery:
                    shivering (non-existent in preterm             o VLBW infants – no superficial layer of
                    infant)                                             keratin  ambient humidity in incubator
                                                                        will prevent losses
        o   Non-shivering thermogenesis – full-term                o Reduce radiant and convective heat loss
            infants are born with layer of brown fat                    by dressing infant whenever possible
            around the neck, between scapula and                   o Avoid positioning infant near cold window
            along aorta  can be rapidly metabolised               o Avoid placing infants in draughts
            to generate heat (under control of                     o Never place infant on cold surface or in
            sympathetic nervous system)                                 cold cot
                                                    THE FITTING NEONATE

Introduction:                                Clinical Assessment:                        Causes:

   Most neonatal seizures occur                 History:                                  Hypoxic-ischaemic encephalopathy
    over only a few days                              o Family history of
                                                           neonatal convulsions             Intracranial haemorrhage
   < 50% develops seizures later                     o Detailed pregnancy
    in life                                                history - ? TORCH                Metabolic:
                                                      o Delivery history –                       o Hypoglycaemia
   Most frequent during first 10                          type and APGAR                        o Hypocalcaemia
    days of life                                      o Postnatal history                        o Hypomagnesemia

                                                 Examination:                              Intracranial infections:
                                                     o Lethargy between                           o Meningitis
                                                         seizures                                 o Encephalitis
                                                     o Neurological exam                          o Toxoplasmosis
                                                                                                  o CMV
                                                                                                  o Bacterial – E. coli, strep

                                                                                            Cerebral malformations:
                                                                                                 o Lissencephaly
    Investigations:                                                                              o Polymicrogyria
                                                                                                 o Pachygyria
        Lab studies:
             o Serum glucose and electrolytes                                               Benign neonatal seizure syndromes:
             o CSF analysis                                                                      o Occur in first 48 – 72 hours
             o TORCH studies                                                                     o Disappear by 2 – 6 months
             o Urine acids                                                                       o Family history of seizures
             o Renal function                                                                    o Development normal

        Imaging:
             o Cranial ultrasound
             o Cranial CT
             o MRI

        Others:
             o EEG
             o Echocardiography

          Management:                                                         Follow-Up:

               Should be treated aggressively                                   Discontinue seizure medications between
                                                                                  3 and 6 months if further seizures have
               Correction of electrolyte abnormalities                           not occurred
                through central venous site
                                                                                 General recommendation is to use AEDs
               Obtain EEG to differentiate whether                               for 3 months then taper gradually
                events are epileptic or non-epileptic
                                                                                 Devlopmental evaluation for identification
               If inborn error of metabolism suspected,                          of physical / cognitive deficits
                discontinue feeding and institute IV
                solutions                                                        Complications:
                                                                                     o Cerebral palsy
               Consider antiepileptic drug therapy:                                 o Hydrocephalus
                                                                                     o Epilepsy
                    o    Phenobarbitol = initial drug of                             o Spasticity
                         choice                                                      o Feeding difficulties
                    o    If seizures continue, consider
                         phenytoin                                               Prognosis:
                                                                                      o If EEG normal, prognosis
                                                                                          excellent  seizures resolve
                                                                                          and normal development likely

Introduction:                                                      Symptoms:

   Term infants = blood glucose concentration of                     Major = apnoea, convulsions and coma
    2.2 – 2.5 mmol / L and in preterm infants = < 1.1
    mmol/L after the first 24 hours of life                           Minor = jitteriness, irritability, tremors, apathy,
                                                                       cyanotic spells and temperature instability
   Normoglycaemia in newborn = blood sugar levels
    of 2.6 mmol / L and above                                         Symptoms are non-specific and similar to those of
   Therefore recommendations = maintain preterm
    and term infants at risk of hypoglycamemia above                  May be asymptomatic
    2.5 mmol / L

Causes:                                                            Management:

   Decreased substrate availability:                                 Prevention:
        o SGA infants                                                      o Frequent heel-stick examination tests in
        o Premature infants                                                     at-risk infants e.g. IDM, SGA and
        o Second twin                                                           preterm infants
                                                                           o Early feeding  at risk infants should be
   Increased glucose utilisation:                                              fed within 2 hours of birth with high
         o Hyperinsulinaemia:                                                   glucose containing solutions
                 -   IDM
                 -   Rhesus isoimmunisation                           Treatment of established hypoglycaemia:
                 -   Islet cell tumour                                     o If asymptomatic hypoglycaemia fails to
         o Polycythaemia                                                      be corrected by early, frequent feeds, an
                                                                              infusion with 10% dextrose will be
   Inability to utilise glucose:                                             necessary
        o Glycogen storage disease type I                                  o Symptomatic will require a dextrose
        o Galactosemia                                                        infusion
        o Fructose intolerance                                             o Where possible, oral feeding should be
        o Inborn errors of amino acid metabolism                              continued

   Iatrogenic:                                                       Resistant hypoglycaemia:
         o Inappropriate infusion of glucose                               o Hydrocortisone
                                                                           o Glucagon
   Miscellaneous:                                                         o Diazoxide
        o Birth asphyxia                                                   o Investigation for insulinoma
        o Endocrine deficiencies
        o Hypopituitarism


                                   Severe symptomatic hypoglycaemia  very poor
                                    prognosis – 50% will die and 50% of survivors will
                                    have severe neurodevelopmental abnormalities
                                    e.g. mental retardation, convulsions, spasticity,

                                   Asymptomatic  infants are not at risk of abnormal
                                    neurodevelopmental outcome?

                                   Repeated low blood sugar levels may have a
                                    cumulative adverse effect on neural function
                                   INFANTS OF DIABETIC MOTHERS (IDM)

    Classification of Maternal Diabetes:              Effect on Foetus and Baby:

       Pregestational                                   The 2 main factors determining whether
                                                          maternal diabetes will have an effect on the
       Type 1 = due to beta cell destruction             foetus and baby are the vascular
                                                          complications that the diabetes causes the
       Type 2 = due to insulin resistance                mother, and the blood glucose control during
       Gestational diabetes
                                                         Vascular disease:
                                                              o Mothers with vascular complications
                                                                  are much more likely to develop
                                                                  hypertension in pregnancy  may
                                                                  affect foetal growth and well-being
Clinical Features of IDM:
                                                         Glucose control:
   Congenital malformations:                                 o Blood sugar should be maintained
       o Congenital heart disease, especially                     below 8mmol / L and hypoglycaemia
            VSD, transposition of great vessels                   avoided
            and coarctation of aorta
       o Renal vein thrombosis
       o Sacral / coccygeal agenesis
       o Left microcolon
       o Hypertrophic cardiomyopathy
   Stillbirth:
          o Increased risk of intrauterine foetal
                                                         Careful control of diabetes during pregnancy
                death during pregnancy
                                                          decreased many of the complications
   Small for gestational age (SGA)
                                                         Management involves:
                                                             o Obsessional diabetic control
   Macrosomia:
                                                             o Planned delivery in a suitably
       o Insulin = major trophic growth factor                  equipped hospital
           influencing foetal growth
                                                             o Examination for congenital
       o Infants are plethoric, obese, and
           Cushingoid in appearance
                                                             o Screening for expected
       o Enlarged liver, heart and spleen                       complications, especially
       o Increased body length and birth                        hypoglycaemia
       o Head circumference and brain
           weight are appropriate for
           gestational age
       o Excessive fat stores and inhibition of
                                                          Prognosis for IDM:
       o Larger size predisposes to other
           problems, e.g:
                -    Birth trauma                            Perinatal mortality rates = 30 /
                -    Birth asphyxia                           1000

   Neonatal hypoglycaemia:                                  1% incidence of overt DM in
       o Due to hyperplasia of islet B-cells in               childhood
            foetal pancreas with foetal
                                                             10% have abnormal glucose
            hyperinsulinism from chronically
            elevated maternal glucose levels                  tolerance when tested in
       o Lasts for several days

   Respiratory distress:
       o Insulin has antagonistic effect on
            surfactant development
       o Even at full term
                                       HAEMOLYTIC DISEASE OF THE NEWBORN


   Rhesus antibody is the most common cause of
    severe HDN

   Rh antigens are expressed on RBCs only

   After initial exposure to foreign antigen,
    maternal immune system produces antibodies                  Clinical Assessment:
    (IgM) that do not cross placenta
                                                                    History:
   Later produces IgG that traverses placental                          o Women at risk for alloimmunisation
    barrier = primary response                                                should undergo Coomb’s test at first
                                                                              prenatal visit
   After sensitisation, maternal anti-D antibodies
    cross the placenta and attach to Rh antigen on                  Examination:
    foetal RBCs  lysed by lysosomal enzymes                            o Jaundice (at birth or < 24 hours)
                                                                        o Pallor (anaemia)
   Prolonged haemolysis  severe anaemia                              o Hepatosplenomegaly
    extramedullary haematopoiesis in liver, spleen,                     o Hydrops foetalis (severe)
    skin, placenta

   Unconjugated hyperbilirubinaemia after delivery
    only as placenta effectively metabolises bilirubin

   HDN associated with ABO incompatibility is
    limited to type O mothers with foetuses who
    have type A or B blood

    Comparison of Rh and ABO Incompatibility:

                        Characteristics                            Rh                         ABO
                                First born               5%                         50%
                                Later pregnancies        More severe                No increased severity
         Clinical aspects       Stillborn / hydrops      Frequent                   Rare
                                Severe anaemia           Frequent                   Rare
                                Jaundice                 Moderate – severe, freq    Mild
                                Late anaemia             Frequent                   Rare
                                DAT                      Positive                   Weakly positive
          Lab findings          Indirect Coombs test     Positive                   Usually positive
                                Spherocytosis            Rare                       Frequent

Management:                                                      Prevention:

   Monitor serial maternal antibody titres                         Rh immunoglobulin prevents Rh
                                                                     alloimmunisation when administered to mother
   In severely affected foetus  perform in-utero                   within 72 hours of delivery
    intravenous transfusion until 35 weeks gestation
                                                                    Administer RhIG to all unsensitised Rh-negative
   Phototherapy for hyperbilirubinaemia post-                       women at 28 weeks gestation

   Exchange transfusion to remove circulating
    bilirubin and antibody-coated RBCs                           Complications:

                                                                    Bilirubin encephalopathy (kernicterus)

                                                                    Late anaemia of infancy
                                                        INFECTION IN THE NEONATE

    The Immature Immune System:                                                   Susceptibility of the Neonate to Infection:

         Immune system is not functionally fully integrated                          Endogenous factors:
          until ~1 year of age                                                            o Low levels of Igs, especially IgM and IgA
                                                                                          o Premature infants fail to receive normal
         Specific immunity:                                                                  passive IgG transfer during last trimester
                                                                                          o Phagocytic action is less effective in the
               o     Mediated through lymphocytes (T and B                                    newborn
                     cells)                                                               o Opsonic activity is impaired, and
                                                                                              complement levels are low
               o     B cells:                                                             o IUGR infants appear more susceptible
                         -    IgM is first immunoglobulin to be
                              produced at 15 weeks gestation                          Exogenous factors:
                         -    IgG first produced at 20 weeks                               o Baby is born bacteriologically sterile, with
                         -    The 3 major Ig types are at                                     little competition from existing bacterial
                              minimal levels in the foetus and                                flora when exposed to potential pathogens
                              remain very low at birth                                         babies exposed to very early antibiotic
                         -    Adult levels of IgM by 1 year and                               use may be predisposed to colonisation
                              of IgG by 5 years                                               with pathogens
                         -    IgG is the only Ig that crosses the                          o Drugs may further impair immune function,
                              placenta  gives foetus effective                               especially corticosteroids
                              passive immunity but levels fall in                          o Fat emulsions – e.g. Intralipid impairs
                              months after birth                                              phagocytic function of WBCs
                                                                                           o Hyperbilirubinaemia reduces immune
               o     T cells:                                                                 function in several ways
                         -    Produced in the foetal bone
                              marrow and migrate to the thymus

         Non-specific immunity:
             o White blood cells especially granulocyte –
                 phagocytic function of engulfing bacteria

               o     Attracted to sites of inflammation by
                     chemotactic chemicals e.g. complement

               o     Impaired opsonic activity in the neonate
                     (complement and fibronectin)

                                                                    Origins of Infection

Intrauterine:                                             Intrapartum:                                     Acquired:

       Transplacental:                                        Colonisation of infant during                 Nosocomial:
            o    First trimester = TORCH                        passage through birth canal (only                  o   Bacteria:
                 infections                                     cause infection in small proportion)                        -      Staph. Aureus
            o    2nd trimester = syphilis                      Risk factor = prolonged rupture of                          -      GBHS
            o    3rd trimester and labour:                      membranes                                                   -      Coliforms
                        -   Viral = varicella, HBV,            Pathogens:                                                  -      Salmonella
                            Coxsackie, HIV                           o    Herpes simplex 2                                  -      Shigella
                        -   Bacterial = group B                      o    Neisseria gonorrhoeae                             -      Pseudomonas
                            haemolytic strep,                        o    HBV                                      o   Viruses:
                            listeria, H. influenzae,                 o    GBHS                                              -      Coxsackie
                            pneumococcus                             o    Chlamydia trachomatis                             -      Rotavirus
                        -   Protozoan = malaria                      o    Candida albicans                                  -      RSV
                                                                     o    ? HIV                                             -      Adenovirus
       Ascending infections:                                                                                               -      Echovirus
            o    Occur after rupture of                                                                            o   Fungal:
                 membranes                                                                                                  -      Candida
            o    Most common pathogens = bowel                                                                                     albicans
                 organisms e.g. E. coli, klebsiella,
                 proteus, pseudomonas; GBHS,
                 staph. aureus (rare)
                                          INFECTIONS IN THE FOETUS AND NEONATE

Pathogenesis of Intrauterine Infection:                                Pathogenesis of Ascending Bacterial Infection:

   Results from clinical or subclinical maternal infection               In most cases, foetus is not exposed to bacteria until
    with a variety of agents and haematogenous                             the membranes rupture and the infant passes through
    transplacental transmission                                            the birth canal and enters the extrauterine environment

   E.g. CMV, treponema, rubella, varicella                               Human birth canal is colonised with aerobic and
                                                                           anaerobic organisms that may  ascending amniotic
   Transplacental infection may occur at any time during                  infection and colonisation of neonate at birth
    gestation, and signs and symptoms may be present at
    birth or delayed for months or years                                  Vertical transmission may occur in utero or more
                                                                           commonly during labour and / or delivery
   Consequences of infection:
       o Spontaneous abortion                                             In most cases, bacterial colonisation does not result in
       o Congenital malformation                                           disease
       o Intrauterine growth retardation
       o Premature birth                                                  Factors influencing which infant develops disease:
       o Stillbirth                                                            o Prematurity
       o Acute disease in neonatal period                                      o Underlying illness
       o Asymptomatic persistent infection                                     o Invasive procedures
                                                                               o Inoculum size
   Timing of infection is important:                                          o Virulence of infecting organism
        o 1 trimester  alter embryogenesis                                   o Transplacental maternal antibodies
             congenital malformations e.g. rubella
        o 3 trimester  active infection at delivery e.g.
                                                                       Pathways of Ascending / Intrapartum Infection:
   For some etiologic agents, maternal immunity is
    effective and antibody is protective for foetus (e.g.
    rubella); for others, maternal antibody may ameliorate
    the outcome of infection or have no effect (CMV)

Pathogenesis of Late Onset Post-Partum Infection:

   Post-natal infections may be transmitted by:
        o Direct contact with hospital staff, the mother
            or other family members
        o Breast milk (HIV, CMV)
        o Inanimate sources e.g. contaminated

   Most common source = hand contamination of health
    care personnel

   Most cases of meningitis from haematogenous

                                           Aetiology of Foetal and Neonatal Infection:

        Intrauterine transplacental                 Vertical transmission:                 Nosocomial infection:
         infections:                                       o HIV                                 o Coag-neg staph
              o Syphilis                                   o HSV                                 o Gram neg bacilli e.g.
              o Rubella                                    o CMV                                     E. coli, Klebsiella
              o CMV                                        o Group B haemolytic                  o Enterococci
              o Toxoplasmosis                                   streptococcus                    o S. aureus
              o Parvovirus B19                             o Enteric organisms                   o Candida
              o Varicella                                  o Gonococci and                       o Enteroviruses
                                                                Chlamydiae                       o CMV, RSV, HSV

                                                                      Initial Signs and Symptoms of Infection
                                                                                 in Newborn Infants:

                                                                       General:
        Clinical Manifestations of Transplacental
                                                                           o Fever, temperature instability
                  Intrauterine Infections:
                                                                           o “Not doing well”
                                                                           o Poor feeding
           Present from birth:
                                                                           o Oedema
                o Intrauterine growth restriction
                o Microcephaly / hydrocephalus
                                                                       Gastrointestinal system:
                o Intracranial calcifications
                                                                            o Abdominal distension
                o Chorioretinitis
                                                                            o Vomiting
                o Cataracts
                                                                            o Diarrhoea
                o Myocarditis
                                                                            o Hepatomegaly
                o Pneumonia
                o Hepatosplenomegaly
                                                                       Respiratory system:
                o Anaemia
                                                                           o Apnoea, dyspnoea
                o Hydrops foetalis
                                                                           o Tachypnoea, retractions
                o Skin manifestations including
                                                                           o Flaring, grunting
                     petechiae, purpura, vesicles
                                                                           o Cyanosis
           Late sequelae:
                                                                       Renal system:
                o Sensorineural hearing loss
                                                                           o Oliguria
                o Visual disturbances
                o Seizures
                                                                       CVS:
                o Neurodevelopmental
                                                                           o     Pallor, mottling, cold, clammy
                                                                           o     Tachycardia
                                                                           o     Hypotension
                                                                           o     Bradycardia

                                                                       CNS:
                                                                           o     Irritability, lethargy
Evaluation of a Newborn for Infection or Sepsis:                           o     Tremors, seizures
                                                                           o     Hyporeflexia, hypotonia
   History (specific risk factors):                                       o     Abnormal Moro reflex
        o Maternal infection during gestation or at                        o     Irregular respirations
              parturition (type and duration of Ab therapy)                o     Full fontanel
                             -    UTI                                      o     High-pitched cry
                             -    Chorioamnionitis
        o Maternal colonisation with GBS, gonorrhoea,                  Haematologic system:
              HSV                                                          o Jaundice
        o Gestational age / birthweight                                    o Splenomegaly
        o Multiple birth                                                   o Pallor
        o Duration of membrane rupture                                     o Petechiae, purpura
        o Complication delivery                                            o Bleeding
        o Foetal tachycardia (distress)
        o Age at onset
        o Location at onset (hospital, community)
        o Medical intervention:
                                                              Suspected Intrauterine Infection:
                             -    Vascular access
                             -    Endotracheal intubation
                                                                 TORCH:
                             -    Parenteral nutrition
                                                                     o Toxoplasmosis
                             -    Surgery
                                                                     o Other agents (syphilis etc)
                                                                     o Rubella
   Evidence of other diseases:
                                                                     o CMV
        o Congenital malformations (heart disease, NTD)
                                                                     o HSV
        o Respiratory tract disease (RDS, aspiration)
        o Necrotising enterocolitis
                                                                 Features supporting diagnosis:
        o Metabolic disease e.g. galactosemia
                                                                      o IUGR
                                                                      o Hematologic involvement
   Evidence of focal / systemic disease:
                                                                      o Ocular signs
        o General appearance, neurological status
                                                                      o CNS signs
        o Organ system diseases
                                                                      o Other organ system involvement
        o Feeding, stools, urine output, extremity
                                                                      o Nonimmune hydrops
                                         CONGENITAL DISLOCATION OF THE HIP

Introduction:                                                 Aetiology:

   Should be detectable during routine screening                19 in 1000 births
    examination at birth
                                                                 Left > right due to foetal positioning causing left hip
   Examination of the hip should start with observation          to be more adducted than the right
    for signs of established dislocation e.g. unequal leg
    length and asymmetry of thighs                               Following associations with CDH:

   Examination should be conducted in 2 parts:                         o     Polygenic / multifactorial condition – recurs
                                                                              in families at rate of 1 / 30
        o    Ortolani’s (reduction) test:
                 -     Assesses whether hip is already                  o     Presentation – breech / vertex ratio of 10:1
                 -     Flex hip and knees to 90º                        o     Females > males 6 : 1
                 -     Grasp baby’s thigh with middle
                       finger over greater trochanter and               o     Race – increased incidence in some
                       lift it to bring the femoral head                      countries e.g. Italy
                       from its dislocated position
                       posterior to opposite the                        o     Abnormalities producing muscular
                       acetabulum                                             imbalance around the joint e.g. spina bifida,
                 -     Simultaneously the thigh is gently                     hypertonia
                       abducted, reducing the femoral
                       head over the posterior lip of the               o     Syndromes e.g. trisomy 13, trisomy 18
                 -     Positive finding = reduction                     o     Multiple congenital abnormalities
                       sensed by feeling a clunk, and
                       movement forward of the head of
                       the femur

        o    Barlow’s (dislocation) test:
                 -    With one hand fixing the pelvis               Management:
                      with the thumb anteriorly over
                      symphysis pubis and the other                        Keep hip immobilised in an abducted
                      fingers posteriorly over coccygeal                    position for 2 – 3 months to allow
                      region                                                acetabular rim to develop and hip
                 -    Other hand grasps baby’s thigh                        ligaments to strengthen
                      and adducts it gently downwards
                 -    Dislocation is palpable as the                       After 3 months, splint can be removed
                      femoral head slips over the                           and check x-rays are taken at 6 and 23
                      posterior lip of the acetabulum                       months of age
   Infants may have normal hips at birth which may                        Fixed dislocations of the hip, failure to
    subsequently dislocate  examine hips at 6-week                         respond to treatment and late
    assessment                                                              diagnosed dislocated hips will require
                                                                            individual orthopaedic consideration
   Failure to abduct a hip is a very significant sign

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