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GENERAL PAST OBSTETRIC HISTORY ANTENATAL CARE OBSTETRIC/MEDICAL COMPLICATIONS LABOR DELIVERY IMMEDIATE CARE AT BIRTH FEEDING HISTORY POSTNATAL PROBLEMS FAMILY HISTORY PAST MEDICAL PROBLEMS PERSONAL/SOCIAL HISTORY
Least disturbing examination should be done first
Assess the state,posture, spontaneous activity, colour, any obvious respiratory distress or malformations
5 states of an infant are: Deep sleep Light sleep Awake & quiet Awake & active Awake & crying
Temperature Measured in the apex of the axilla—3min
Cold stress Assessed by touching the abdomen,
palms/soles In cold stress palms and soles are colder to
touch than the abdomen
Respiratory rate
40-60 breaths/min
Heart rate
Faster in preterms compared to term Normal range : 110-160 beats/min Bradycardia(<100/min) – heart disease Tachycardia(>160/min) – sepsis , anaemia,
fever or CCF
BP Flush method Doppler monitoring Direct intravascular measurement
Capillary refill time Estimated by applying firm pressure on the
sternum area for 5 sec Refill time is prolonged in case of
hypothermia and shock
LOW BIRTH WT : <2.5KG
VERY LOW BIRTH WT :<1.5KG
EXTREMELY LOW BIRTH WT : <1KG
Aberrant growth pattern is assessed by plotting the wt against the GA on a standard intrauterine growth curve
Appropriate for gestational age (AGA) Wt between 10th and 90th percentile
Small for gestational age (SGA) Wt falls below 10th percentile
Large for gestational age (LGA) Wt falls above 90th percentile for GA
Length : abt 50cmsHead circumference : 33-37cms at birthChest circumference : 3cm less than head circumference If the difference is more than 3cm -- IUGR
Ponderal Index Wt(gm)/length(cm3) x 100 <2 – asymmetrical growth retardation ≥2 – normal or symmetrical growth
retardation
PRE-TERM INFANTS Deep sole creases are absent or limited to
anterior 1/3rd
Breast nodule is <5mm Ear cartilage has poor elastic recoil Hair is fuzzy Testes are at the external ring and
scrotum has few rugosities Labia majora are widely separated
exposing labia minora and clitoris
SKIN AND HAIR Skin looked for scaliness , elasticity,
thickness , edema,rashes, lesions like hemangioma
Jaundice By compressing on the skin Colour imparted by the Hb in the blood
vessels is eliminated and the yellow colour due to bilirubin is high-lighted
Ecchymoses, petechiae—birth trauma
Lanugo hair - fine hair of fetal period that is shed at 28wks and later at term
Nails – hypoplastic finger nails indicate inutero exposure to valproate
HEAD AND FONTANELLESMolding – Gives the impression of a cliff with rise on
one side and a sharp fall on the other sideSynostosis - Feels like a mountain range with rise on both
sides of elevation
Craniotabes – Skull feel soft like a ping pong ball Due to delayed ossification and resorption of
bones Benign condition in neonates that resolves
spontaneously
Common Located in the
subcutaneous plane
Maximum size and firmness at birth
Softens progressively from birth & resolves within 2 or 3 days
Diffuse , crosses suture lines
Less common Located over parietal
bone,bw skull & periosteum
Increasing in size for 12-24hrs and then stable
Takes 3-6wks to resolve
Does not cross suture line ,has distinct margins
CAPUT SUCCEDANEUM CEPHALOHEMATOMA
Associated with linear fracture of skull bone in 5 – 25% ; hyperbilirubinaemia
Large fontanelles and split sutures : Raised ICP Certain chromosomal abnormalities Hypothyroidism Impaired bone growth like osteogenesis
imperfecta
NECK, FACE ,nose, EYES & EARS Neck masses-enlarged thyroid,scm
tumor,cystoid hygroma. Facial nerve paresis-birth injury. Absence of depressor anguli oris Nose – size,shape,patency,secretions , flaring Bilateral chaonal atresia
Natal teeth , retention cysts-disappear in few weeks.
Cleft palate Eyes;-subconj.hge.pupils,reactive to light Visual tracking assessment of the examiners
face Globe – 70% of adult size Cornea – 80% of adult size
Gross hearing – look for blink on response to noise
Accessory auricles & pre-auricular skin tags are a common finding that may be associated with renal anomalies
UMBILICUS , ANUS & SPINE Inspect no.of vessels in the cord, Single umbilical artery – renal and GI
anomalies. IUGR babies – long and thin cord with very
little Wharton jelly Palpate base of cord for presence of hernia
Spine – spina bifida . Masses and scoliosis Anal opening – for patency and position
GENITALIA (MALE & FEMALE) Examined by hips abducted in the supine
position Urethra- patency Clitoris - clitoromegaly
EXTREMITIES Make sure that arms and limbs are fully
movable Nail hypoplasia , syndactyly , polydactyly ,
oligodactyly , unequal limbs CTEV – calcaneovalgus / equinovarus
deformity
SYSTEMIC EXAMINATION
CHEST CVS ABDOMEN MUSCULOSKELETAL SYSTEM NUEROLOGICAL EXAMINATION
CRANIAL NERVES MOTOR EXAMINATION PRIMARY NEONATAL REFLEXES SENSORY EXAMINATION
APdia ≈ transverse dia Respiratory distress
Nasal flaring Grunting Tachypnea Intercostal & subcostal retraction
May indicate: Pneumonia RDS Delayed reabsorption of lung fluid Any other cardiorespiratory cause
Auscultation Absent respiratory sounds and presence of
bowel sounds– r/o diaphragmatic hernia
Heart disease: Tacypnea , cyanosis or both
Position of apex beat Congenital diaphragmatic hernia Pneumothorax
Unusual flatness/scaphoid shape of abdomen – congenital diaphragmatic hernia
Visible gastric / bowel patterns indicating ileus or other obstructions
Tenderness of abdomen – necrotising enterocolitis
Developmental dysplasia of hips (DDH) 1 in 800 live births Family history Breech delivery 2 tests Ortolani’s test Barlow maneuver
CRANIAL NERVES MOTOR EXAMINATION PRIMARY NEONATAL REFLEXES SENSORY EXAMINATION
CRANIAL NERVES Responds to soaked peppermint -32wks of gestatn. By 26wks blinks in response to light,at term fixation
and following is well established. Colour vision – 2 months Startles / blinks to loud sound – 28wks. Suck swallow co-ordination -32wks. Suck swallow breathing -34wks.
MOTOR EXAMINATION Minimal resistance to passive manipulation in
all limbs – by 28wks Distinct flexor tone in lower limbs – by 32wks
Differential hypotonia Selective hypotonia in the upper and the
proximal muscle group compared to the lower and distal group
Seen in early phase of hypoxic ischaemic encephalopathy
Ankle clonus Upto 5-10 beats accepted as normal in a
newborn Clonus of more than a few beats beyond 3
months of age is abnormalPlantar response If elicited by thumb nail- flexion response If elicited by pin drag- extension response
MORO REFLEX Best elicited by sudden dropping of baby’s
head in relation to trunk Response consists of opening of the hands
and the extension and abduction af the upper extremities ; followed by anterior flexion (embracing) of upper extremities with an audible cry
Hand opening present by 28wks Extension & abduction by 32wks Anterior flexion by 37wks Audicle cry appears by 32wks Moro reflex disappears by 3-6months in
normal infants
Most common cause of depressed / absent Moro reflex – generalised disturbance of CNS
Most useful abnormality of the Moro reflex to elicit is distinct asymmetry– feature of root plexus or nerve disease
Palmar grasp present by 28wks and strong by 32 wks This allows lifting of baby by 37wks . This
becomes less consistent on development of voluntary grasping at 2months
Elicited by stroking the palmar aspect of the hand taking care that the childs dorsum of hand should not touch examination cot.child grasps the finger.
Tonic neck response Elicited by rotation of the head Causes extension of the upper extremity on
the side to which face is rotatedand flexion of upper extremity on the side of the occiput
This disappears by 6-7 months
Even a neonate of 28wks has the ability to discriminate touch & pain
Pain results in alerting & slight motor activity and then later withdrawal and cry
Jaundice is an important problem in the first week of life
High bilirubin levels may be toxic to the developing CNS and may cause neurological impairment
60 % of term newborn will become visibly jaundiced in the first week of life
Most cases –benign ,no intervention needed
5-10%-clinically significant jaundice
Normal phenomenon in new borns Due to accumulation of unconjugated
bilirubin Appears beyond 1st day of life Peaks in 3-4 days Disappears by 7-10 days in a normal new
born Max. level of bilirubin is less than 12 mg/dl Preterm –it may go upto 14 mg/dl and
duration also will be prolonged(10-14 days)
Appearance of icterus on 1st day of life indicates a highly accelerated production of bilirubin starting from intrauerine life
Commonest cause-Rh or ABO Incompatibility
Aetiology1)The increased bilirubin production due to
break down of fetal RBC’s
2)The immaturity of hepatic conjugating mechanisms to handle bilirubin load
3)Delayed establishment of effective feeding which contribute to increased enterohepatic circulation
4)Defective uptake and excretion of bilirubin by the immature hepatocyte
Most common causes of jaundice depending o its day of appearance:
day 1:blood group incompatibility,usually Rh incompatibility, HS, G6PD
day 2-3:physiological jaundice, crigler najjar
later:sepsis,breast milk jaundice,neonatal cholestasis due to neonatal hepatitis or extra hepatic biliary atresia
Cong. Inf- CMV,rubella,toxo
Icterus in face only:approximately serum bilirubin is 4-6mg%
Icterus up to upper trunk:apprxm serum bilirubin is6- 8 mg%
Icterus upto lower trunk and thighs:8-12 mg%
Icterus upto lower legs and arms:12-14 mg%
Icterus of palms and soles:>15 mg%
Referred to as an elevation of TSB levels to the extent where treatment of jaundice is very likely to result into benefit than harm.
STB levels have been arbitarily defined as pathological if it exceeds 5 mg/dl on first day,10 mg/dl on 2nd day or 15 mg/dl thereafter in term babies
Appearance of jaundice within 24 hrs,TSB levels above expected normal range,presence of clinical jaundice beyond 3 wks and conjugated bilirubin
Due to decreased or delayed feeding ORDue to low volume of milk produced in first
2-3 days appears between 24-72 hrs of age,peaks by
5-15 days of life and disappears by the third week of life
Commonest cause of physiological jaundice
Milk of certain mothers contain some inhibitors of conjugation ( pregnanediol, non esterified long chain fatty acids etc)
So their babies may develop a mild unconjugated hyperbilirubinemia by 2nd or 3rd week of life
Unlikely in the first few days of life as breast milk secretion takes time to establish
These babies must be investigated for prolonged jaundice
A diagnosis should be considered if it is unconjugated(not staining the nappies)
And other causes for prolongation like continuing hemolysis,extravasated blood,G6PD Deficiency and hypothyroidism
Needs no treatment
Very rarely phototherapy may be required
If the breast milk is with held for 48 hrs,the jaundice comes down dramatically
Newborns detected to have yellow discoloration of skin beyond the legs
OR
when their clinically assessed TsB levels approach phototherapy range, should have lab confirmation of TSB
Important causes of jaundice in neoates include:
1)hemolytic:Rh compatibility,ABO incompatibility,G6PD Deficiency,thalassemias,heriditary spherocytosis
2)non hemolytic:prematurity,extravasated blood,inadequate feeding,polycythemia,idiopathic,breast milk jaundice
Is the newborn term or preterm? basic pathophysiology of jaundice is same in term and preterm neonates but babies at lower gestation are at a high risk of dvp brain damage at lower levels Is there any hemolysis? setting of Rh or ABO
Incompatibility,onset of jaundice within 24hrs, presence of pallor, hepatosplenomegaly, presence of haemolysis on the peripheral blood smear, raised reticulocyte count ( more than 8%), rapid rise of bilirubin ( more than 5mg/dl in 24hrs or more than .5mg/dl/hr should raise a suspicion of haemolytic jaundice
Is the baby otherwise sick( sepsis, asphyxia) or healthy?
Presence of lethargy, poor feeding, failure to thrive, hepatosplenomegaly, temp instability or apnoea may be a marker of underlying serious disease
Does the infant have cholestatic jaundice? Presence of dark yellow
urine( staining clothes) or pale coloured stools will suggest cholestatic jaundice
Does the baby have any bilirubin induced brain disfunction( kernicterus) ?
These include presence of lethargy, poor feeding and hypotonia. Advanced signs include seizures, retrocollis, paralysis of upward gaze, and shrill cry
Deposition of free unconjugated bilirubin in basal ganglia and subthalamic nuclei of brain
PHASE1 Poor suck, lethargy, hypotonia, depressed
sensorium, loss of morro,decreased tendon reflexes
PHASE 2 Hypertonia of
extensors,fever,retrocoloitis,opisthotonus,bulging AF,spasm,twitching
PHASE3 High pitched cry, convulsion , death
Choreoathetoid CP Upward gaze palsy SNHL MR Delayed motor skills
Hypoproteinemia
Sulfonamides Acidosis FFA
Asphyxia Prematurity Inf.
Risk factors for development of severe hyperbilirubinemia
2. Jaundice observed in the first 24hr 3. Blood group incompatability with positive
direct antiglobulin test( DCT), other known haemolytic disease( G6PD deficiency)
4. Gestational age- 35-36wks 5. Previous sibling received phototherapy 6. Cephalhaematoma or significant bruising 7. If breast feeding is inadequate with
excessive weight loss
INVESTIGATION1. Serum total bilirubin2. Blood group of mother and baby: detects any
incompatability3. Direct Coombs test: detects presence of
antibody coating on fetal RBCs 4. Indirect Coombs test: detects the presence
of antibodies against fetal RBC in maternal serum
5. Haematocrit decreasd in haemolysis 6. Reticulocyte count: increased in
haemolysis 7. Peripheral smear: evidence of
haemolysis 8. G6PD levels in RBC 9. Others: sepsis screen, thyroid fn tests,
urine for reducing substances to rule out galactosemia, specific enzyme or genetic studies for Crigglar Najjar, Gilbert and other genetic enzyme deficiencies
The parents should be explained about the benign nature of jaundice
The mother should be encouraged to breast feed frequently
The new born should be exclusively breastfed with no top feeds, water or dextrose water
Mother should be told to bring the baby to the hospital if the baby looks deep yellow or palms and soles also have yellow staining
Any new born discharged prior to 72hrs of life should be evaluated again in the next 48hrs for assessment of adequacy of breast feeding and progression of jaundice
PROLONGED JAUNDICE BEYOND 3 WEEKS This is defined as persistence of
significant jaundice( 10mg/dl) beyond 3 weeks in a term baby
The common causes include breastmilk jaundice, extravasated blood, ongoing haemolytic disease, G6PD deficiency and hypothyroidism
INTRAHEPATIC
METABOLIC
Tyrosinemia Galactosemia Gauchers Neiman pick CF Hypothyroidism
HBV,HCV, TORCH
IDIOPATHIC—NENONATAL HEPATITIS
Injury hypoplasia
EHBA Choledochal cyst Bile duct stenosis
Rule out cholestasis by noting the urine and stool colour and checking the level of direct bilirubin
DIAGNOSIS1. Investigations to rule out cholestasis( stool
colour, urine colour, direct and indirect bilirubin levels
2. 2. Investigations to rule out ongoing haemolysis, G6PD screen
3. Investigations to rule out hypothyroidism
4. Investigations to rule out UTI
HEALTHY BABY
BIRTH WEIGHT PHOTOTHERAPY EXCHANGE TRANSFUSION
<1000 gm 5-7 11-13
1001-1500 gm 7-10 13-15
1501-2000gm 10-12 15-18
2001-2500 gm 12-15 18-20
SICK BABY
Gestation PHOTOTHERAPY EXCHANGE TRANSFUSION
<28 5-6 11-14
28-29 6-8 12-14
30-31 8-10 13-16
32-33 10-12 15-18
PHOTOTHERAPY
Phototherapy is the primary treatment in neonates with unconjugated hyperbilirubinemia.
This therapeutic principle was discovered rather serendipitously in England in the 1950s and is now arguably the most widespread therapy of any kind (excluding prophylactic treatments) used in newborns.
PHOTOTHERAPY Unconjugated bilirubin in skin gets
converted into water soluble isomers on exposure to light of a particular wavelength(460-490mm)
These isomers are water soluble, nontoxic and excreted in intestine and urine
For phototherapy to be effective, bilirubin needs to be present in the skin
Phototherapy acts by several ways1. Configurational isomerisation: The z
isomer of bilirubin are converted into E isomers
The reaction is instantaneous upon exposure to light
Reversible as bilirubin reaches the bile duct
After exposure of 8-12hrs of phototherapy this constitutes about 25% of STB which is nontoxic.
As it is excreted slowly it is not a major mechanism for decrease in TSB.
2. Stuctural isomerisation: Its irreversible intramolecular
cyclization where bilirubin is converted into lumirubin
This is directly proportional to the dose of phototherapy
This product forms 2-6% of TSB which is rapidly excreted from the body
This mainly responsible for phototherapy induced decline in TSB
3. Photo oxidation: This is a minor reaction
Bilirubin converted into small polar products that are excreted in urine
although bilirubin is bleached through the action of light, the process is slow
TYPES OF LIGHTSpecial blue lamps with a peak output at 460-490nm are the most efficient.
In India CFL phototherapy is most commonly used.
Nowadays blue LED are using instead of CFL as it has long life and is capable of delivering high irradiance.
Efficacy of phototherapy depends upon irradiance, surface area exposed, distance from phototherapy unit, initial TSB level and adequacy of breast feeding.
Sunlight is relatively ineffective because of low blue content of light.
Hyperpyrexia and skinburns occur in prolonged sunlight exposure
Procedure for providing phototherapyRoom temp should be 25-28c
Undress the baby compltly except the diaperCover the eyes with a patch that should not block the eyes.Keep baby at a distance 30-45cm from the light source
Ensure adequate breast feeding. Turn the baby after each feed to expose
maximum surface area of the baby to light Monitor temp every 2-4hrs. Measure TSB level every 12-24hrs. Record body weight daily Ensure that the baby passes adequate amnt
of urine(6-8 times/day).
Phototherapy should be provided continuously except during breast feeding sessions
Discontinue phototherapy when STB falls below age specific phototherapy cut off
Monitor for rebound STB rise after 24hrs of stopping phototherapy for babies with haemolytic disorders
SIDE EFFECTS: Rash, over heating, dehydration and
diarrhoea,hyperthermia,bronze baby,retinal damage,DNA breaks.
HIGH DOSE INTRAVENOUS IMMUNOGLOBULIN:
reduces need for exchange transfusion in hemolytic jaundice such as in Rh or ABO Incompatibility
blocks Fc receptor and inhibit hemolysis The 2004 AAP guidelines suggest a dose-500-
1000 mg/kg as slow infusion over 2 hrs
Double volume exchange transfusion (DVET)should be performed if the TSB levels reach to age specific cutoff for exchange transfusion or if infant has signs of bilirubin encephalopathy.
It is performed by pull and push technique using umbilical venous route.
Indication for DVET at birth in infants with Rh isoimmunisation
-cord bilirubin is 5mg/dl or more -cord Hb is 10g/dl or less.
-Reticulocyte >15% -previous sibling history
PHENOBARBITONE: INDUCES GLUCORONYL TRANSFERASE
ENZYME
THUS IMPROVES CONJUGATION AS WELL AS UPTAKE AND EXCRETION OF BILIRUBIN BY LIVER CELLS
TIN ZINC
Decrease formation of bilirubin by inhibiting heme oxygenase
Babies with serum bilirubin ≥20 mg/dl Those who req.exchange transfusion BERA-3 mnths
Antenatal investigation should include maternal blood grouping. Rh positive baby born to a Rh negative mother is at ahigh risk for hyperbilirubinemia and requires greater monitoring. Anti D injection after first obstetrical event ensures decreased risk of sensitisation in future pregnancies
Ensuring adequate breast feeding Parent education
Parent education regarding danger signs should include yellowish discolouration below knees and elbows or persistent jaundice beyond 15days as reason for immediate check up by health personnel.
High risk babies such as with large cephalhematoma or family history of jaundice should be asked to come for follow up after 3 days of discharge and reassessed
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