Neonatology At A Glance

Front 1

Maternal medical conditions

Back 1

Maternal medical conditions

Front 2

Fetal mortality and morbidity are increased with

Back 2

maternal insulin-dependent diabetes (type 1), mainly from congenital malformationsand intrauterine death

Front 3

how do you decrease congenital malformations and intrauterine death in type 1 diabetic mothers

Back 3

good diabetic control

this requires a multidisciplinary management and close prenatal surveillance

Front 4

what are the fetal problems associated with maternal diabetes

Back 4

congenital malformations

macrosomia

IUGR

Polyhydramnios

Preterm labor

Intrauterine death

Front 5

the risk of congenital malformations is 6% for a diabetic mother this is how much greater than normal babies from non diabetic mothers

Back 5

4 times normal

specific increased risk of cardiac malformations and caudal regression syndrome (sacral agenesis)

Front 6

macrosomia is due to

Back 6

maternal hyperglycemia resulting in fetal hyperinsulinemia, which promotes growth

Front 7

what % of diabetic mothers have macrosomic babies compared to non diabetic mothers

Back 7

25% diabetic mothers have macrosomic babies

versus 8% of infants of non diabetic mothers.

Front 8

Macrosomia predisposes to

Back 8

cephalopelvic disproportion andincreased risk of delivery-related complications, both to the mother(cesarean section and forceps delivery) and the fetus; includingbirth injuries.

Front 9

diabetic mothers have an increased risk of intrauterine growth restriction, how much

Back 9

3 fold increase

usually associated with maternal vascular disease

Front 10

diabetic mothers have a 10% risk of preterm labour

Back 10

true

Front 11

intrauterine death in diabetic mothers typically occurs

Back 11

suddenly in third trimester

Less commonwith good diabetic control and induction at 38 weeks.

Front 12

what neonatal complications do diabetic mothers get

Back 12

malformations and birth injuries

hypoglycemia

polycythemia

hyperbilirubinemia

respiratory distress syndrome

hypertrophic cardiomyopathy

renal vein thrombosis

Front 13

features of type 2 diabetes and gestational diabetes in pregnancy

Back 13

associated with perinatal coplications

glucose intolerance from gestational diabetes complicates 1-2% of pregs and may require dietary or insulin treatment

may cause neonatal macrosomia, hypoglycemia and polycythemia

Front 14

maternal medical conditions in pregnancy - broad groups

Back 14

diabetes mellitus type 1

type 2 diabetes and gestational diabetes

maternal red blood cell alloimmunization

- rhesus hemolytic disease - maternal antibodies to fetal red blood cell antigens

- other maternal antibody conditions to fetal red blood cell antigens - anti-Kell and anti-c

perinatal alloimmune thrombocytopenia

- analogus to rhesus hemolytic disease but maternal antibodies to fetal platelets instead

others

maternal hyperthyroidism

maternal hypothyroidism

autoimmune thrombocytopenic purpura

Front 15

define fetal hydrops aka hydrops fetalis

Back 15

fluid accumulation in at least 2 fetal fluid compartments e.g. ascites and pleural or pericardial effusion

Front 16

what sort of presentation would you have with rhesus hemolytic disease

Back 16

antibodies found at antenatal screens

previous pregnancy affected with hemolytic disease

fetal hydrops on ultrasound

detection of fetal anemia using ultrasound (middle cerebral artery blood flow increased for gestational age)

Maternal polyhydramnios.

Infant – jaundice, anemia, hydrops, hepatosplenomegaly.

Front 17

how rhesus hemolytic disease managed prenatally

Back 17

refer to specialist center if needed - due to increasing antibody levels on maternal blood screen

fetal rhesus genotyping can be done non invasively through free fetal DNA detection in maternal plasma

monitor with serial ultrasound for fetal anemia and signs of hydrops

doppler blood flow - checking for fetal anemia

measure fetal hematocrit (from cordocentesis)

intrauterine blood transfusion

deliver preterm if necessary

Front 18

how do you monitor fetal anemia

Back 18

usually by middle cerebral artery blood flow

Front 19

how is rhesus hemolytic disease managed postnatally

Back 19

check cord blood for blood type, hemoglobin, bilirubin and direct antibody test

monitor bilirubin closely as level may increase rapidly and cause high frequency deafness or kernicterus

start intensive phototherapy, adequate fluid balance and give IVIG (immunoglobulin) and perform an exchange transfusion if severe anemia or rapidly rising bilirubin concentration

May need ‘top up’ blood transfusion for anemia within first threemonths of age until endogenous hemopoiesis is normal.

Front 20

how is rhesus hemolytic disease managed postnatally - summart

Back 20

check cord blood for blood type, hemoglobin, bilirubin and direct antibody test

monitor bilirubin

start phototherapy and give IVIG +/- exchange transfusion if severe anemia

+- top up blood transfusion

Front 21

what is used in the prevention of rhesus hemolytic disease

Back 21

Anti D gammaglobulin

given to rhesus-negative mothers during pregnancy, after potentially sensitizing events, and after delivery.

Front 22

when do you give rhesus negative mothers Anti D gammaglobulin to prevent rhesus hemolytic disease

Back 22

during pregnancy, after potentially sensitizing events, and after delivery.

nb Neonatology at a Glance Fifteen percent of white women are rhesus-negative; less than2% of them become sensitized from inadequate or failedprophylaxis.

Front 23

whats the significance of maternal hyperthyroidism to the infant

Back 23

If mother is controlled on treatment, fetus and infant are usually unaffected.

Rarely causes:

Transient hyperthyroidism – fetal tachycardia, and neonatal hyperthyroidism (1–3%) – tachycardia, heart failure, vomiting, diarrhea and failure to thrive (despite good intake), jitteriness, goiter and exophthalmos (protuberant eyes). Treated for 2–3 months

Transient hypothyroidism – from maternal drug therapy

Front 24

whats the significance of maternal hypothyroidism to the infant

Back 24

Important cause of congenital hypothyroidism, leading to short stature and severe learning difficulties.

Front 25

whats the most common cause of maternal hypothyroidism worldwide

Back 25

commonest cause is iodine deficiency.

Front 26

whats the significance of Autoimmune thrombocytopenicpurpura (AITP) to the infant

Back 26

Maternal autoantibodies against platelet surface antigens cross the placenta and cause fetal thrombocytopenia.

Most fetuses unaffected.

Rarely requires treatment in utero with repeated intravenous platelet transfusions.If severe, may cause cerebral hemorrhage before birth or from birth trauma, but this is rare. Infants withsevere thrombocytopenia or petechiae at birth should be given intravenous immunoglobulin. Platelettransfusions are reserved for platelet count <20000mm3 (20 × 109/L) or active bleeding because of theanti-platelet antibodies. The platelet count declines over the first few days before increasing

Front 27

Maternal drugs affecting the fetus and newborn infant

Back 27

Maternal drugs affecting the fetus and newborn infant

Front 28

what are some of the maternal drugs affecting the fetus and newborn infant

Back 28

maternal smoking

alcohol

narcotics - cocaine, heroin,

thalidomide

anticonvulsants

antithyroid drugs

Androgens

Aspirin/non steroidal anti inflammatory drugs

opiates

folic acid inhibitors

warfarin

tetracyclines

BB and hypoglycemic agents

Front 29

In the fetus, maternal cigarette smoking is associated with:

Back 29

• increased risk of miscarriage, abruption and stillbirth

• reduction in birthweight, with increase in intrauterine growthrestriction (IUGR) related to number cigarettes smoked perday, with average birth weight reduction of 170 g at term.

Front 30

in a neonatal infant, maternal cigarette smoking is associated with

Back 30

• increased risk of sudden infant death syndrome (SIDS)

• increased wheezing in childhood.

Front 31

Severe prolonged maternal alcohol ingestion is associated with

Back 31

fetal alcohol syndrome (FAS)

Front 32

Advice to pregnantwomen from the American Academy of Pediatrics and theDepartment of Health in the UK is to

Back 32

avoid alcohol whilstpregnant although the effect of occasional, mild alcohol inges-tion or occasional binge drinking is not known

Front 33

whats Neonatal withdrawal (abstinence) syndrome

Back 33

Serious problem because of widespread use of narcotics andother drugs of dependency.

basically withdrawal symptoms associated with stopping narcotics or other dependent drugs

Situation often complicated by multiple drug use

Front 34

mothers on heroin are usually encouraged to change to

Back 34

methadone to mitigate neonatal withdrawal syndrome

Front 35

drug users are at increased risk of

Back 35

hepatitis B and C and HIV infection if intra-venous drug user.

Front 36

when does the onset of withdrawals start

Back 36

– heroin <2 days

– methadone <2 days but can be delayed up to 2 weeks.

Front 37

Cocaine does not cause problems from withdrawal but fromdirect transfer of the drug causing what fetal complications

Back 37

– placental infarction which may lead IUGR or placental abruption and antepartum hemorrhage or fetal death

– rarely, cerebral infarction in utero and neonatal seizures.

Front 38

Clinical features of opiate withdrawal.

Back 38

Irritability

Scratching

Wakefulness

Shrill cry

Tremors

Hypertonicity

Seizures

Unexplained pyrexia >38°C

Tachypnea (rate >60/min)

Vomiting

Diarrhea

Yawning

Hiccoughs

Salivation

Stuffy nose

Sneezing

Sweating

Dehydration

Front 39

when assessing someone with neonatal withdrawal syndrome what should you do

Back 39

assess them 6 hourly

also use a scoring system e.g. Finnegan's scoring system to determine whether therapy is required

Front 40

treatment for neonatal withdrawal syndrome

Back 40

Usually with oral morphine sulfate, aiming to wean by titration ofdose with score.

Medical and social services discharge planning meetings areoften required during pregnancy and after birth as the lifestyle ofmany drug users is not conducive to the care of babies andchildren

Front 41

medicines can also affect the

Back 41

fetus and newborn infants

Front 42

diethylstilbestrol (DES) given for threatened miscarriage in themother and subsequent association with

Back 42

clear-cell adenocarcinomaof the vagina and cervix in female offspring, evident only duringadolescence or early adult life.

Front 43

Pregnant women should avoid taking both prescribed and over-the-counter medications whenever possible

Back 43

true

Front 44

For prescribed drugs,the benefits must outweigh the risks and appropriate maternal andfetal surveillance should be undertaken.

Back 44

true

Front 45

Severe limb shortening (phocomelia, ‘like a seal’) frommaternal thalidomide therapy, which was widely marketed (not in US)for morning sickness from 1957. Teratogenic effects only recognizedseveral years later.

Back 45

true

Front 46

Thalidomide during Organogenesis (<8 weeks ’ gestation) results in

Back 46

Short limbs (Fig. 9.2)Absent auricles, deafness

Front 47

Anticonvulsants:• carbamazepine• valproic acid (sodium valproate)• hydantoins (phenytoin)

during Organogenesis (<8 weeks ’ gestation) results in

Back 47

Fetal carbamazepine/valproate/hydantoinsyndrome – midfacialhypoplasia, CNS, limb andcardiac malformations

Developmental delay

Front 48

Antithyroid drugs (iodides,propylthiouracil) after 8 weeks gestation results in

Back 48

goitre

congenital hypothyroidism

Front 49

androgen medication after 8 weeks gestation results in

Back 49

masculinization of female

Front 50

aspirin or non steroidal anti inflammatory drugs after 8 weeks gestation results in

Back 50

closure of ductus arteriosus in fetus

Front 51

folic acid inhibitors (methotrexate) as cytotoxic therapy during organogenesis at <8 weeks gestation results in

Back 51

Fetal syndrome –

microcephaly,

neural tube defects,

shortlimbs

Front 52

warfarin (coumarin) during organogenesis at <8 weeks gestation results in

Back 52

Fetal coumarin (warfarin)syndrome –

nasal hypoplasia,

microcephaly,

hydrocephalus,

optic atrophy,

congenital heart defects,

stippled epiphyses,

purpuricrash

Front 53

tetracyclines during pregnancy at >8 weeks gestation results in

Back 53

Hypoplasia of tooth enamel,yellow–brown staining ofteeth

Front 54

beta blockers and hypoglycemic agents during pregnancy at >8 weeks gestation results in

Back 54

Neonatal hypoglycemia

Poor fetal growth

Front 55

during labor and delivery what drugs cause respiratory depression of the neonatal infant at birth

Back 55

opiate analgesia

Front 56

define kernicterus

Back 56

bilirubin induced brain dysfunction

Bilirubin is a highly neurotoxic substance that may become elevated in the serum, a condition known as hyperbilirubinemia

serious complication related to very high levels of bilirubin. It can lead to permanent brain damage, hearing loss and death. Signs and symptoms of acute encephalopathy include: hypotonia, lethargy, poor feeding, irritability, high-pitched cry, seizures, apnoea and hypertonia.

Front 57

jaundice in neonates is mostly

Back 57

physiological

Front 58

small neonate

Back 58

Low birth weight (LBW): <2500g

Very low birth weight (VLBW): <1500g

Extremely low birth weight (ELBW): <1000g

Appropriate for gestational age (AGA) infants weigh between the 10th and 90th percentile for gestational age.

Small for gestational age (SGA) infants weigh less than the 10th percentile for gestational age.

Large for gestational age (LGA) infants weigh above the 90th percentile for gestational age.

IUGR: Growth restricted infants are not achieving their growth potential. Growth restriction can cause an infant to be small for gestational age.

Front 59

Approximately 60% of infants born at 24 weeks gestation will survive to discharge. Chances of survival improve with gestational age and 97% of infants born at 30 weeks are expected to survive.

Back 59

true

Front 60

Preterm babies are however at risk of disability in the long term. This includes cerebral palsy, developmental delay and visual and hearing impairment.

Back 60

true

Front 61

Antenatal corticosteroid administration to women at risk of premature delivery results in a significant decrease in the mortality rate of preterm infants. It has also shown to decrease the morbidity associated with prematurity, including respiratory distress syndrome, intraventricular haemorrhage and necrotising enterocolitis.

Back 61

true

Front 62

Prolonged hypoglycaemia can cause permanent neurlogic damage. At risk infants need to be monitored and managed appropriately to prevent this serious complication.

Back 62

true

Front 63

Risk factors for hypoglycaemia are:

Back 63

Intrauterine growth restriction

Diabetic mothers

Large for gestational age

Prematurity

Hypothermia

Hypoxic ischemic encephalopathy

Sepsis

Haemolytic disease

Front 64

Birth asphyxia is defined as

Back 64

the failure to establish breathing at birth. Birth asphyxia is one of the major causes of early neonatal mortality.

Improved neonatal resuscitation skills improve neonatal survival.

Front 65

Hypoxic-ischaemic injury is the most common cause of

Back 65

neonatal encephalopathy.

use APGAR score to assess neuro function

Front 66

The VACTERL association consists of:

Back 66

Vertebral anomalies, anal atresia, cardiac defects, tracheoesophageal fistula, renal anomalies and limb anomalies

Front 67

There are two antiglobin (Coombs) tests

Back 67

Direct antiglobin test

Indirect antiglobin test

Front 68

Direct antiglobin test is used for

Back 68

used to detect antibodies on the red cell surface where sensitization has occured in vivo.

Front 69

a positive direct antiglobin test occurs in what conditions

Back 69

Haemolytic disease of the newborn

Autoimmune haemolytic anaemia

Haemolytic transfusion reactions

Front 70

Indirect antiglobin test is used for

Back 70

used to detect antibodies that have coated the red cells in vitro.

Front 71

the indirect antiglobin test is used in

Back 71

Routine cross-matching

Detecting blood group antibodies in pregnant woman

Front 72

Glucose-6-phosphate dehydrogenase (G6PD) is

Back 72

an enzyme that plays an important role in red blood cell metabolism. G6PD deficiency is an X-linked recessive hereditary disease that can manifest in neonates as prolonged jaundice. The jaundice occurs secondary to red blood cell haemolysis. African, Middle Eastern and Southeast Asian people are most commonly affected. A Coombs test will be negative because the haemolysis is not immune mediated.

Front 73

The normal temperature range for a neonate is 36.5°C to 37.2°C. If not adequately attended to a newborn infant may experience hypothermia and cold stress.

Back 73

true

Front 74

Infants lose heat through:

Back 74

Conduction - heat is lost through direct contact with a surface with a different temperature

Convection - air currents carry heat away from the body surface

Radiation - heat loss via electromagnetic waves from the skin to surrounding surfaces

Evaporation - heat loss when water evaporates from the skin or breath

Front 75

ward stuff

Back 75

ward stuff

Front 76

what respiratory condition in pediatric patients result in a focal or distributed sound across the chest on auscultation or what you can just hear

Back 76

asthma, bronchiolitis and croup result in wide spread or distributed sound

pneumonia and foreign object typically focal sound

Front 77

if you hear any focal sound then the patient needs a

Back 77

chest x ray

Front 78

management for mild to moderate and severe croup

Back 78

mild to moderate = steroids

severe = nebulised adrenaline

Front 79

brief pathophys of asthma

Back 79

allergen causes allergic response = mast cell release of histamines = bronchoconstriction and bronchospasms resulting in wheeze

Front 80

brief pathophys of bronchiolitis

Back 80

usually viral infection resulting in hypersecretion resulting in wheeze

Front 81

according to steve, children under 1 and maybe under 2 do not have asthma because they can't have an allergic reaction

Back 81

ok

Front 82

according to steve you treat asthma with beta agonist which will cause bronchodilation but it won't have the same effect on young infants with bronchiolitis, although as the children get older they develop more smooth muscle within their bronchioles which means that if you treat them with beta agonist for that bronchiolitis it will cause some bronchodilation and thus help to open up the airways (despite still having hypersecretion) reducing a wheeze

Back 82

ok

Front 83

Routine examination of the newborn infant

Back 83

Routine examination of the newborn infant

Front 84

A comprehensive medical examination within 24hours of birth, the ‘routine examination of the newborn infant’,should be performed. The purpose is to:

Back 84

detect any abnormalities

confirm and or consider the further management of any abnormalities detected antenatally

consider potential problems related to maternal pregnancy history or familial disorders

allow the parents to ask any questions and raise any concerns about their baby

determine whether there is concern by caregivers about the care of the baby following discharge

provide health promotion, especially prevention of SIDS

Front 85

A comprehensive medical examination within 24 hours of birth, the ‘routine examination of the newborn infant’, should be performed. The purpose is to: (summary)

Back 85

detect abnormalities

aid management decisions

id probs with maternal preg hx or familial probs

parents can ask questions about concerns

concern after discharge

health promotion esp prevent SIDS

Front 86

in preparing for a routine examination of the newborn infant what do you need to prpare

Back 86

Maternal charts (records)

Equipment

Environment

Front 87

Maternal charts (records):

Back 87

• Check maternal antenatal, labor and delivery charts.

Front 88

what equipment do you need for the routine exam of newborn infant

Back 88

• Tape measure.

• Stethoscope.

• Ophthalmoscope.

Front 89

what should you consider about the environment in which to carry out the routine examination of the newborn infant

Back 89

• Warm room free from drafts.

• Privacy, suitably lit.

• Examine on firm mattress in crib.

• Both parents present if possible.

• Always wash hands and clean stethoscope before eachexamination.

Front 90

regarding the infant what are important aspects to consider in the routine examination of the newborn infant

Back 90

baby must be completely undressed during the course ofthe examination so that all the body is observed

needs to be relaxed = successful exam

opportunitistic exam but must be done

Front 91

what does opportunitistic exam relate to

Back 91

i.e. check eyes whenopen, heart when quiet, hips left until last. However, the examina-tion must be complete.

Front 92

routine examination of newborn infants should include

Back 92

looking for any congenital abnormalities

general appearance, posture, movements

fontanel and skull structures - Look, feel

check for dysmorphic facies

check red reflex

pale/red face

check ears

look and feel for cleft palate

check tongue for central cyanosis

check breathing (RR, WOB, resp distress) and chest movement

check hands - digits, palmar crease

check for jaundice

auscultate chest

check back and spine

check abdomen - look, liver, spleen, kidney, masses, tender (whince)

check femoral pulses

check hips - DDH

check muscle tone

check genitalia - testis in scrotum, normal penis and anatomy for girls

check anus - look for patency

check feet for talipes

do measurements for weight, head circumference and length (crown-rump)

Front 93

Significant congenital abnormalities which may be identifiedon routine examination

Back 93

Dysmorphic infant (see Chapter 8)

Cataracts (see Chapter 61)

Cleft lip and palate (see Chapter 39)

Heart murmurs (see Chapter 48)

Urogenital – hypospadias, undescended testes (see Chapter 51)

DDH (developmental dysplasia of the hip)

Imperforate anus (see Chapter 47)

Spinal anomalies (see Chapter 58)

Front 94

Checking for red reflex. If absent, i.e. the pupil iswhite (cataracts, glaucoma, retinoblastoma), refer directly to

Back 94

an ophthalmologist

Front 95

what are the signs of respiratory distress

Back 95

increased respiratory rate

flaring of nostrils

grunting

chest retractions (sternal and intercostal)

Front 96

the normal live can be palpated below the costal margin

Back 96

yes, normal liver 1–2cm below costal margin, spleen tip and left kidney may be palpable

Front 97

whats the normal newborn heart rate

Back 97

110 to 160 beats/min

but may drop to 80 during sleep

Front 98

when examining the back and spine what are you looking for

Back 98

sacral dimples

hair

swelling

nevus

other lesions over the spine - e.g. spina bifida occulta ortethered cord

nb if these found do ultrasound and then maybe MRI

Front 99

in coarctation what difference in blood pressure is significant

Back 99

greater than 15mmHg

Front 100

how do you assess muscle tone in neonate

Back 100

observe for normal movements of limbs

feel when handling the baby (support the head when picking up baby)

on holding prone, term babies will lift their head to horizontal position

Front 101

Back and spine: check from top to bottom.Sacral dimples below the line of the natalcleft – common and benign. If proximal tonatal cleft, ultrasound to identify if there is a track to the spinal cord, though rare

Back 101

true

Front 102

neurologic examination of the newborn

Back 102

states of alertness

visual fixing and following

hearing

consolability

head circumference

face movements - cranial nerves, blinking, sucking strong

posture and spontaneous motor activity

Front 103

a detailed neurological exam is done if any concerns about

Back 103

neurological abnormality

Front 104

A normal neurologicexam is helpful prognostically, e.g. following hypoxic–ischemicencephalopathy, a normal neurologic examination and normalfeeding by 2 weeks of age are associated with

Back 104

a good prognosis

Front 105

in the infant examination of alertness it is classified using the

Back 105

prechtl scale

Front 106

using the prechtl scale for classifying the level of alertness of infant, describe it

Back 106

1: eyes closed, regular respiration, no movements state

2: eyes closed, irregular respiration, no gross movements state

3: eyes open, no gross movements state

4: eyes open, gross movements, no crying state

5: eyes open or closed, crying.

Front 107

for a satisfactory level of alertness using the Prechtl scale, the level must be

Back 107

state 3

Inability todo this may occur because the infant is abnormally lethargic orhyperexcitable (or deeply asleep or hungry!). An abnormal crymay also indicate abnormal neurology.

Front 108

one of the neurological assessments of infant is visual fixing and following, what does this mean

Back 108

normal term infant should fix and follow a face or target of concentric black and white circles or a red ball moving from side to side

Front 109

when do you expect a neonate to be able to have visual fixing and following

Back 109

at about 32 weeks gestation

The infantshould make eye-to-eye contact when held about 30cm from theobserver.

Front 110

in a normal neurological examination of hearing how should an infant respond

Back 110

Infants respond to noise with a facial grimace, turning of the heador startle

Front 111

another aspect of neurological exam is consolability, what is this

Back 111

baby stops crying to voice or soothing movements or gestures such as rocking from side to side. It indicates communication between the infant and caregiver.

Front 112

why is it important to measure head circumference in a neurological exam of an infant

Back 112

This is a surrogate measure of brain volume and subsequently ofbrain growth.

Front 113

Face (cranial nerves)

Back 113

There should be normal facial movements, blinking of the eyesand ability to suck strongly.

Front 114

what is the posture of a term baby

Back 114

flexed of all four limbs

Movements are smooth, sym-metric and varied. The infant can move the fingers and can abductthe thumbs.

Front 115

in neonatal neurological exam its key to assess Posture and spontaneous motor activity

Back 115

Posture flexed

Passive tone in limbs and trunk

Active tone in limbs and trunk

Primary reflexes

Deep tendon reflexes

Plantar responses

Front 116

passive tone in limbs and trunk are key parts of the posture and spontaneous motor activity in assessing neurology of neonate

Back 116

Develops from hypotonia at 24 weeks of gestation to strong flexortone at 40 weeks, initially in the lower then upper limbs

Front 117

Posture

Back 117

32 weeks

Arms extendedSome flexion ofthe legs

40 weeks

Full flexion ofall four limbs

Front 118

Passive tone in limbs and trunks looks at 3 key areas

Back 118

popliteal angle

foot dorsiflexion

scarf sign

Front 119

Passive tone in limbs and trunk

Popliteal angle

Back 119

Popliteal angle - With thigh beside abdomen,extend knee as far aspossible

32 weeks

110 to 120 degrees

Term

90 degrees or less

Front 120

Passive tone in limbs and trunk

Foot dorsiflexion

Back 120

With knee flexed, ankle isdorsiflexedMeasure angle betweendorsum of foot and anteriorof leg

32 weeks

30 to 40 degrees

Term

0 degress

Front 121

Passive tone in limbs and trunk

Scarf sign

Back 121

Hand pulled across chesttowards opposite shoulderPosition of elbow noted

32 weeks

very weak resistance

Term

Does not reach midline (i.e. strong resistance)

Front 122

Active tone in limbs and trunk looks at 3 main things

Back 122

righting reaction

neck flexor tone

ventral suspension

Front 123

Righting reaction involves

Back 123

Holding infant uprightunder axillae

32 Weeks

Brief supportof lowerlimbs only

40 weeks

Upright andtakes weightfor few secs

Front 124

neck flexor tone (raise to sit) involves

Back 124

Holding infant's shoulders,pull from lying to sitting

32 weeks

No movementof headforwards

40 weeks

Minimal headlag. Similarlyfor neckextensor tone(back to lying)

Front 125

ventral suspension involves (holding baby with back to ceiling and chest to floor)

Back 125

32 weeks

Someextension ofhead andback

40 weeks

Head extendedabove body,back extendedand limbs fully flexed

Front 126

what are the primary reflexes that are assessed as a part of the motor part of the neurological exam

Back 126

Placing reflex

Palmar grasp

Plantar grasp

Asymmetric tonic neck reflex

Motor reflex

Front 127

describe the placing reflex

Back 127

When dorsum of foot isstimulated by edge of bed,places foot on the surface

Front 128

describe the palmar grasp

Back 128

flexion of fingers when object placed in the palm of the hand

Front 129

describe the plantar grasp

Back 129

toes curl on stroking the ball of the foot

Front 130

describe the asymmetric tonic neck reflex

Back 130

fencing posture on turning head to one side

Front 131

describe the moro reflex

Back 131

On sudden head extension (butsupport the infant’s head in yourhand), symmetrical abduction andextension followed by flexion andadduction of the arms

Front 132

if the primary reflexes cannot be elicited what does that indicate

Back 132

central nervous system depression

Moreimportant, their persistence suggests damage to upper corticalcontrol

Front 133

deep tendon reflexes may be decreased or increased in

Back 133

depressed in LMN lesions

occassionally increased with UMN lesions

check also for assymetry

Front 134

one deep tendon reflex is ankle clonus - what about it

Back 134

Ankle clonus is common and usually of no pathologicsignificance.

Front 135

plantar responses can be elicited but so what

Back 135

Elicited by stroking the lateral part of the foot from heel to toe.Unhelpful at this age as normal response may be flexor (toe down)or extensor (toe up).

Front 136

minor abnormalities in the first few days

Back 136

minor abnormalities in the first few days

Front 137

what are some of the minor abnormalities in the first few days

Back 137

distortion of the shape of the head (molding from delivery)

caput succedaneum, cephalhematoma, chignon

swollen eyelids

subconjunctival hemorrhages from delivery

small white cysts along the midline of the palate

breast enlargement

traumatic cyanosis

peripheral cyanosis

lanugo

vernix

umbilical hernia

vaginal discharge

cracking and peeling of skin

positional talipes

Front 138

how can you tell the difference between true talipes equinovarus (club foot) and positional talipes

Back 138

The foot can be fullydorsiflexed to touch the front of the lower leg. In true talipes equinovarus this is notpossible.

Front 139

minor abnormalities in the first few days

skin lesions

Back 139

stork bites

milia

miliaria

erythema toxicum

mongolian blue spots

transient pustular melanosis aka transient neonatal pustolosis

harlequin color change

sucking blisters

Front 140

other minor abnormalities

Back 140

natal teeth - front lower incisors present at birth, remove if loose to avoid risk of aspiration

extra digits - consult plastics; if thin skin tag, just tie off with silk thread

ear tags - consult plastics; has increased risk of renal abn.

Front 141

define lesion

Back 141

A lesion is any single area of altered skin. It may be solitary or multiple

Front 142

define rash

Back 142

A rash is a widespread eruption of lesions.

Front 143

define dermatosis

Back 143

Dermatosis is another name for skin disease.

Front 144

description of skin lesion

http://www.dermnetnz.org/terminology.html

Back 144

superficial/deep

distribution

configuration

colour

morphology

skin surface

secondary skin changes

Front 145

define macule

Back 145

A macule is an area of colour change less than 1.5 cm diameter.The surface is smooth.

if its greater = patch

Front 146

define papule

Back 146

Papules are small palpable lesions.

The usual definition is that they are less than 0.5 cm diameter, although some authors allow up to 1.5 cm.

They are raised above the skin surface, and may be solitary or multiple.

it may be:

Acuminate (pointed)

Dome-shaped (rounded)

Filiform (thread-like)

Flat-topped

Oval or round

Pedunculated (with a stalk)

Sessile (without a stalk)

Umbilicated (with a central depression)

Verrucous (warty)

Front 147

enlargement of a papule in three dimensions (height, width, length) is known as

Back 147

nodule

It is a solid lesion.

Front 148

define a cyst

Back 148

A cyst is a papule or nodule that contains fluid so is fluctuant.

Front 149

define plaque

Back 149

A plaque is a palpable flat lesion greater than 0.5 cm diameter. Most plaques are elevated, but a plaque can also be a thickened area without being visibly raised above the skin surface. They may have well-defined or ill-defined borders.

Front 150

what this

Back 150

Stork bites

Pink macules on upper eyelids, mid-forehead (also called salmonpatch) and nape of the neck (Fig. 20.4). Common. Dilated super-ficial capillaries. Those on the eyelids and forehead fade over thefirst year. Those on the neck persist but are covered with hair.

Front 151

whats this

Back 151

stork bite

Front 152

whats this

Back 152

Miliaria

Pin-sized vesicles, particularly over the neck and chest. Usuallydevelop at 2–3 weeks. Caused by sweat that is retained due toobstructed eccrine glands. Avoid excessive clothing and heating.

Front 153

whats this

Back 153

milia

White, pinhead-sized pimples on the nose and cheeks and fore-head. Resolve during first month of life. Are from retention ofkeratin and sebaceous material in the pilosebaceous follicles.

Front 154

whats this

Back 154

erythema toxicum

Small, firm, white or yellow pustules on erythematous base (Fig.20.5). It is the most common transient lesion, usually appears at1–3 days but up to 2 weeks of age; primarily on trunk, extremities and perineum. Moves to different sites within hours. Containseosinophils. May be present at birth.

Front 155

whats this

Back 155

erythema toxicum

arises over the first few days, spares the palms and soles. It does not bother the baby. It resolves spontaneously over one to two days.

Front 156

whats this

Back 156

erythema toxicum

affects 50% of full-term neonates but is uncommon in premature babies.

Front 157

mongolian blue spots

Back 157

Blue–black macular discoloration at base of the spine and on thebuttocks (Fig. 20.6). Usually but not invariably in black or Asianinfants. Sometimes also on the legs and other parts of the body.Fade slowly over the first few years. Of no significance unlessmisdiagnosed as bruises.

Front 158

Transient pustular melanosis(transient neonatal pustulosis)

Back 158

Resembles miliaria, but present at birth and may continue toappear for several weeks. Superficial vesiculo-pustular lesionsrupture within 48 hours to leave small pigmented macules withwhite surround. More common in black infants, in whom thelesions are often hyperpigmented.

Front 159

Harlequin color change

Back 159

Sharply demarcated blanching down one half of the body – oneside of the body red while the other is pale. Lasts a few minutes.Thought to be due to vasomotor instability. It is benign.

Front 160

sucking blisters

Back 160

Vesicles on hand, fingers or lips, from vigorous sucking in utero.

Front 161

whats the vernix

Back 161

greasy, yellow-white coating presentat birth, a mixture of desquamating cells andsebum which protects fetus from macerationin utero

Front 162

traumatic cyanosis

Back 162

skin discolorationand petechiae over the head and neck orpresenting part from cord around the baby'sneck or from a face or brow presentation.The tongue is pink

Front 163

small white cysts along the mid-line of the palate (Epstein pearls).Cysts of the gums (epulis) or floor ofthe mouth (ranula)

Back 163

true

Front 164

can it be normal to have swollen eyelids (without discharge) and vaginal discharge and cracking and peeling of the skin esp feet and hands at birth

Back 164

yes, don't worry it will go away

Front 165

what are some common or important birth injuries

Back 165

caput, chignon, cephalhematoma, subgaleal (subaponeurotic) hemorrhage, skull fractures

minor injuries = forcep marks; scalpel lacerations

Front 166

what are some common or important birth injuries to the face

Back 166

facial palsy

asymmetric crying facies

Front 167

what are some common or important birth injuries to the neck and shoulders

Back 167

fractured clavicle

brachial palsy - erb palsy

Front 168

what are some other common or important birth injuries

Back 168

extremety fracture

spinal cord injury

intraabdominal organ rupture, injury or bleed

genitalia bruising

Front 169

whats this

Back 169

chignon

Front 170

what are the anatomic locations of the different injuries to the head during birth

Back 170

Front 171

whats this

Back 171

Cephalhematoma

Front 172

whats this

Back 172

Subgaleal(subaponeurotic)hemorrhage

Front 173

which part of the skull is usually fracture in birth

Back 173

usually parietal

occipital in breech deliveries

Front 174

genital disorders

Back 174

genital disorders

Front 175

what genital disorders should you look out for in birth

Back 175

inguinal hernia

hydrocele

undescended testis

torsion of the testis

hypospadias

circumcision

Front 176

whats the classification of hypospadias

Back 176

Front 177

Infants with hypospadias must not be circumcised as the fore-skin may be needed at surgery.

Back 177

true

Front 178

Neural tube defects and hydrocephalus

Back 178

Neural tube defects and hydrocephalus

Front 179

neural tube in embryo

Back 179

In the embryo, the flat neural plate folds to become the brain andspinal cord.

Front 180

Neural tube defects arise from a deficiency in thisprocess:

Back 180

• anencephaly – from failure of cranial development of most ofthe cranium and brain

• spina bifida – from failure of caudal development of thevertebral bodies and spinal cord

• midline defects – from failure of fusion, e.g. of the skull as anencephalocele.

Front 181

most neural tube defects are diagnosed how

Back 181

Most are now diagnosed antenatally, by ultrasound or α-fetoprotein measurement in maternal serum

Front 182

describe Anencephaly

Back 182

The condition is lethal; most are stillborn

most are diagnosed antena- tally and parents opt for termination of pregnancy.

Front 183

describe encephalocele

Back 183

Herniation of sac, which may contain brain, through a midlineskull defect. Most are occipital (Fig. 58.1). Developmental impairment is likely if brain tissue is in the sac or there are other cerebralmalformations.

Front 184

spina bifida types

Back 184

There are several types, of increasing severity:

• spina bifida occulta

• meningocele

• myelomeningocele

Front 185

spina bifida work up

Back 185

need ultrasound or MRI scan

Front 186

meningocele has a good prognosis when

Back 186

following surgery

Front 187

myelomeningocele has a number of complications what

Back 187

associated with chiari malformation (herniation of the cerebellar vermis through the foramen magnum)

kyphoscoliosis, DDH, talipes equinovarus

neuropathic bladder - dribbling, predisposes to UTIs and vesicoureteric reflux, HTN, chronic RF

neuropathic bowel - patulous anus

paralysis of the legs

sensory deficity over the legs = skin damage from trauma

Front 188

whats the management of myelomeningocele

Back 188

MDT

surgical closure to reduce infection risk and monitoring for hydrocephalus

Front 189

hydrocephalus

Back 189

This is from an excessive volume of cerebrospinal fluid (CSF).It is usually from blockage of CSF flow or a defect in CSFreabsorption.

Front 190

what are the congenital causes of hydrocephalus

Back 190

• Aqueduct stenosis.

• Chiari malformation.

• Atresia of outflow foramina of fourth ventricle (Dandy–Walkersyndrome).

• Congenital infection.

Front 191

what are the acquired causes of hydrocephalus

Back 191

• Post-intrventricular hemorrhage in preterm infants.

• Post-intracranial infection.

• Post-subdural/subarachnoid hemorrhage.

Front 192

what are the clinical features of hydrocephalus

Back 192

• Ventricular dilatation on imaging precedes symptoms or signs

• Increasing head circumference.

• Separation of sutures.

• Vomiting.

• Apnea, abnormal muscle tone, seizures, depressed con-sciousness.

• Dilatation of head veins.

• Setting-sun sign (eyes deviate downwards).

• Full then bulging fontanelle.

Front 193

management of hydrocephalus

Back 193

monitor with serial cranial ultrasound measurements for ventricular size and head circumference

if severe and progressive or symptomatic = ventricular shunt surgically inserted

Front 194

Hydrocephalus in preterm infants

Back 194

usually secondary to intraventricular hemorrhage, whichmay cause obstruction but mainly interferes with CSF reabsorp-tion. The ventricular dilatation may regress, but if it progresses aventricular shunt will be required. Ventricular shunt insertion insmall infants may have to be delayed because of the risk of skinbreakdown, or shunt blockage if the CSF protein is high. If theinfant becomes symptomatic but a shunt cannot be inserted, CSFmay need to be removed by lumbar or ventricular puncture. A largerandomized trial showed no difference in long-term outcomebetween repeated lumbar/ventricular taps compared with removalof CSF only when symptomatic. Drug treatment with acetazola-mide, which reduces CSF production, is not used as it has beenshown to be ineffective and carries a risk of electrolyte imbalance.Therapy with fibrinolytic agents is under investigation.

Front 195

bone and joint disorders

Back 195

bone and joint disorders

Front 196

what are congenital abnormalities of the hip and feet

Back 196

DDH and talipes equinovarus (club foot)

Front 197

management for club foot

Back 197

• Refer to orthopedic surgeon.

• Neonatal treatment – stretching, strapping or serial plaster castsstarted in first few days

• Maximal correction is by 3 months of age.

• Corrective surgery may be required at 6–12 months.

Front 198

bone and joint problems

Back 198

congenital = ddh and club foot

infection = septic arthritis, osteomyelitis

skeletal dysplasias = achondroplasia, osteogenesis imperfecta

Front 199

signs of septic arthritis

Back 199

• Decreased joint movement.

• Joint is swollen, warm, red (Fig. 60.4).

• Effusion may be present.

Front 200

is septic arthritis common in newborns

Back 200

no

• Usually from extension from underlying bone infection, ratherthan primary infection of the joint or from hematogenous spread.

Front 201

septic arthritis diagnosis by

Back 201

joint aspiration suggesting infection

Front 202

what imaging options do you have for septic arthritis

Back 202

Ultrasound – fluid in joint space.

Radionuclide bone scan, if indicated – hot spot.

MRI scan of bone if necessary.

Plain X-ray is of limited value – may show widened joint space.

Front 203

treatment for septic arthritis

Back 203

single or repeated needle aspiration

surgical drainage of hip joint if no improvement

antibiotics - for 3 to 6 weeks

Front 204

what are the long term complications of septic arthritis

Back 204

erosion of articular surface

joint ankylosis

Front 205

osteomyelitis in newborns

Back 205

• Rare in newborn.

• Most are hematogenous in origin, in metaphysis.

• Usually presents within first 2 weeks of life. Pathogens Commonest are Staphylococcus aureus and streptococci.

Signs

• No movement (pseudoparalysis) of limb.

• Red, warm, swollen, painful limb.

Diagnosis

• Blood culture positive.

• Bone aspiration for cultures if indicated. Imaging

• Ultrasound – periosteal elevation and soft tissue swelling.

• Radionuclide bone scan, if indicated – hot spot (needle aspira-tion does not produce positive bone scan).

• Plain X-ray – limited use at this stage, as only shows periostealelevation and soft tissue swelling.

• MRI scan of bone if necessary.

Treatment

Antibiotics – prolonged course for 3–6 weeks. Continue for 2–3weeks after symptoms resolve and ESR (erythrocyte sedimentationrate) or CRP (C-reactive protein) normalizes.

Front 206

Achondroplasia

Back 206

• Short bowed limbs, normal trunk, large head.

• Midface hypoplasia, frontal bossing.

• Trident hand (short and broad), protuberant abdomen.

Front 207

Osteogenesis imperfecta

Back 207

• Inherited disorder of type 1 collagen formation.

• Rare – 1 in 20 000 live births.

Clinical features

• Increased bone fragility, susceptibility to fracture (Fig. 60.5).

• Blue sclerae, defective tooth formation in some patients.

• Hearing loss.

• Scoliosis, kyphosis.

Front 208

feeding

Back 208

feeding

Front 209

Human milk is recommended as the exclusive food for all terminfants for the first

Back 209

6 months of life. Human milk is also recom-mended for preterm infants but may need fortification.

Front 210

All mothersshould be encouraged and supported to breast-feed. Counselingshould commence early in pregnancy and mothers should beassisted by nursing or lactation specialists.

Back 210

true

Front 211

The choice to breast- or bottle-feed is personal and formulafeeding should not be criticized

Back 211

true

Front 212

Nutritional characteristics of human milk comparedwith unmodified cow’s milk

Back 212

Protein

breast milk = 60% whey and 40 % casein, which is easily digestable and has high free aa and urea; glutamine the predominant aa, stimulates enterotropic hormones, enhancing feeding tolerance

Fat

breast milk has unsaturated fat

contains long chain polyunsat FA needed for nervous system development

Carb

high in lactose

minerals

low renal solute load

reduced phosphate: calcium ration

vitamin

supplementation required to breast milk to meet daily requirements

Front 213

does formula contain anti infective properties like breast milk

Back 213

no

Front 214

unmodified cow's, goat's and sheep's milk are unsuitable for infants

Back 214

true

Front 215

soy formula is sometimes used to prevent allergic disorders such as

Back 215

eczema and asthma

although evidence for this is lacking

about 10-30% of infants with cow's milk protein intolerance become sensitive to soy

Front 216

Immediate advantages of breast-feeding for the infant

Back 216

• Promotes mother–infant bonding.

• Ideal nutritional composition (see below).

• Contains immune factors (e.g. secretory IgA).

• Reduces gastroenteritis, possibly other infections.

• Less feeding intolerance.

• Reduces incidence of necrotizing enterocolitis in preterminfants.

• Promotes ketone production as an alternative energy substrateto glucose in first few days of life.

Front 217

long term advantages of breast feeding for the infant

Back 217

May reduce risk of SIDS (sudden infant death syndrome).

May decrease incidence and severity of eczema and asthma.

Less obesity, insulin-dependent diabetes mellitus (type 1) andinflammatory bowel diseases (Crohn disease and ulcerativecolitis).

Front 218

Advantages of breast-feeding for the mother

Back 218

• Enhances mother–infant bonding.

• More rapid postpartum weight loss.

• Decreased risk of osteoporosis.

• Decreased risk of breast and ovarian cancer.

• Increases time between pregnancies, which is important indeveloping countries.

Front 219

Potential complications of breast-feeding for the infant

Back 219

Cannot tell how much milk the baby has taken.

- This is monitored by checking baby’s weight.

Dehydration may occur if:

– inadequate milk supply/poor feeding technique

– hot weather.

Jaundice associated with breast milk:

– common

– exacerbated by dehydration

– even if requiring phototherapy, breast-feeding should becontinued

– is prolonged (>2 weeks of age) in 15%

– will require investigations to be performed.

Multiple births:

– twins can often be breast-fed, but rarely higher order births.

Vitamin K:

– low level in breast milk may predispose to hemorrhagicdisease of the newborn

– prophylaxis is required.

Front 220

Potential complications of breast-feeding for the infant

Back 220

can't tell how much milk they had

dehydration

jaundice

multiple births = twins ok, 1 teet each, but three = one misses out

vitamin K deficiency

Front 221

Potential complications of breast-feeding for the mother

Back 221

• Maternal feeling of inadequacy/upset if unsuccessful.

• Breast engorgement, cracked nipples – may be helped bymanual expression or breast pump.

• Mastitis

–requires maternal treatment and may disrupt feeding.

Front 222

Neonatology at a Glance Contraindications to breast-feeding

Back 222

Maternal HIV

Maternal TB (active infection)

inborn errors of metabolism - galactosemia, phenylketonuria

Front 223

drugs in breast milk

Back 223

• Most drugs are excreted in breast milk in such small quantitiesthey do not affect the infant.

• Where possible, all drugs, including self-medication, shouldbe avoided during breast-feeding. Most mothers who need medi-cations can continue breast-feeding, but a few drugs precludebreast-feeding.

Front 224

‘Breast is best’ for feeding newborn infants.

Back 224

true

Front 225

growth and nutrition

Back 225

growth and nutrition

Front 226

Between 24 and 36 weeks’ gestation, a fetus growing along the50th centile gains

Back 226

15 g/kg/day

Infants who are fed enterally require120–140 kcal/kg/day to maintain this rate of growth

Front 227

the weight of extremelypreterm infants is often initially static or may decline, and theinfant may take up to 21 days to regain birthweight. Thereafter,their growth improves but is often suboptimal. The reason for thisgrowth failure includes:

Back 227

• the infant is unable to tolerate high volumes of nutrients

• fluids may be restricted, e.g. patent ductus arteriosus

• intercurrent illness, e.g. infection.

Front 228

Nutrition for infant includes

Back 228

breast milk

donor human milk

formulas

supplements - iron, multivitamins, vitamin K

feeding

Front 229

what are the advantages of breast milk over formula feeds

Back 229

• better tolerated

• associated with a lower incidence of necrotizing enterocolitisand provides some protection against infection

• contains hormones and growth factors

• has better absorption of fats and improved bioavailability oftrace minerals

• promotes mother–infant bonding

• it is associated with improved cognitive development later inchildhood.

Front 230

what are the disadvantages of breast milk over formula feeds

Back 230

• depends on the mother being able to express sufficient milk overa prolonged period

• growth of the preterm infant may be suboptimal. Breast milkmay need to be enhanced with human milk fortifier to increase itsenergy, protein and mineral content. Human milk fortifiers containcow’s milk protein. Fortification is usually stopped once the infantis entirely breast-fed or weighs more than 2 kg.

Front 231

whats donor human milk and what is it used for

Back 231

its donor breast milk

its given to extremely preterm infants or infants at increased risk of necrotizing enterocolitis

The efficacy of donorhuman milk in improving outcome has not been determined.

Front 232

Low birthweight infant formulas

Back 232

supply the increased energy (24 kcal/oz, 80kcal/100mL), protein, sodium, calcium and phosphaterequired by low birthweight infants

Front 233

what supplements can be given to babies

Back 233

iron

multivitamins - A, B12, C, D, E

Vitamin K

Front 234

at what gestation would you expect a neonate to be able to suck and swallow

Back 234

34 to 35 weeks gestation

Front 235

for a term baby, they can be breast fed straight away, but extremely preterm infants cannot feed for themselves why

Back 235

are unable to suck and swallow until about 34–35 weeks ofgestation

also initially unable to tolerate milk in sufficient quantity to meet their nutritional requirements

Front 236

methods of feeding

Back 236

Minimal enteral (non-nutritive) feeding

Gavage (tube) feeding

Total parenteral nutrition (TPN)

Front 237

Minimal enteral (non-nutritive) feeding

Back 237

A small volume (e.g. 10–20 mL/kg/day), preferably with expressedbreast milk, is given during the first few days to stimulate guthormone production even when the infant is too unwell or unstableto tolerate the expected volume of feeds.

This helps intestinalmaturation, motility and gallbladder function, decreasing the timetaken to establish full enteral feeding; it also lowers serum bilirubinconcentrations

Front 238

Gavage (tube) feeding

The tube may be orogastric or nasogastric.

Back 238

Used when infants are too immature (<34 weeks’ gestational age)or ill to feed for themselves but are able to tolerate enteral feeds

The volume of milk is gradually increased. Feeds are withheldif aspirates are more than half the volume given or if biliouswith abdominal distension, blood in the stool or other featuressuggesting necrotizing enterocolitis. Reduced gut motility invery low birthweight infants may necessitate suppositories forconstipation. The tube may be orogastric or nasogastric. As nasogastric tubeslie in the narrowest part of the upper airway, just behind the nose,a size 5 French gauge tube increases airway resistance by 30–50%in preterm infants. This increases the work of breathing and mayincrease the frequency of apnea. Some units avoid nasogastrictubes if less than 35 weeks’ gestation, but orogastric tubes are moredifficult to fix securely. There is conflicting evidence regarding continuous versus bolusfeeding in relation to weight gain and the incidence of apnea andbradycardia. The infant’s oxygen tension falls with feeds in bothpreterm and term infants. It has been argued that continuousfeeding is more physiologic for preterm infants because it is acloser approximation to the way a fetus is fed in utero. However,bolus feeds are preferred as the response of gut hormones is morephysiologic.

Front 239

Total parenteral nutrition (TPN)

Back 239

feeding via central line usually or peripherally

Front 240

TPN is associated with a number of complications what

Back 240

• line-related infection

• conjugated hyperbilirubinemia

• electrolyte disorders

• hyperglycemia

• chemical burns from extravasation

• pleural or pericardial effusion – if tip of the central line becomesdisplaced and lies in the heart.

Front 241

fluid intake is markedly affected by

Back 241

gestational age

thermal environment (radiant warmer and isolette)

evaporative water loss (reduced by humidity etc)

Front 242

fluid intake for infants use the

Back 242

4 2 1 rule

4 ml/kg/hour for the first hour

2 ml/kg/hour for the next hour

1 ml/kg/hour for subsequent hours

Front 243

example of the 4 2 1 rule

you have a 2.7 kg baby and you need to give 70% of what ever fluid you plan to give as continuous infusion over an hour

Back 243

2.7 x 4 = 10.8

10.8 x 70% = 7.56

round up 7.56 = 8 ml/kg/hour

Front 244

you give 8 ml/kg/hour for the first hour, and you decide to start some feeding via tube/TPN, how much should you give

Back 244

the amount that was quoted in the hospital was Q2 hourly,

so you give the same as the fluid i.e. 8ml/kg/hour but this is a Q 2 hourly amount, i.e. like giving 8ml/kg/30min but you want to give a continuous infusion over an hour, so what do you do

you times 8 x 2 = 16ml/kg/hour of feeding

Front 245

lung development and surfactant

Back 245

fetal lung passes through 4 main stages of lung development during gestation

1) embryonic phase (3-5 weeks) - resp bud arises from ventral surface of foregut (esophagus)

2) pseudoglandular phase (6 - 16 weeks) - lobe branches develop

3) canalicular phase (17 - 24 weeks) distal airway develops

4) saccular phase (24 weeks to term) everything else

Front 246

Physiology and composition of surfactant

Back 246

It is hard to blow up a balloonthat is collapsed, i.e. has a small radius.Surfactant-deficient lungs are like this. (b) Itis easier to blow up once the balloon ispartially filled with air, i.e. has a larger radius.Lungs with surfactant are like this.

In the absence of surfactant, thepressure at the surface of the alveolus isgreater in the smaller than the larger alveolus,so the small alveoli collapse and the largeones expand. Surfactant lowers the surfacetension (T) and prevents alveolar collapse.

Front 247

surfactant is

Back 247

90% lipids

10% proteins

made by type 2 pneumocytes

reduces surface tension thus helps to prevent alveolar collapse (atelectasis) and improves lung compliance, reducing the work of breathing

Front 248

deficiency in surfactant causes

Back 248

respiratory distress syndrome

In surfactant deficiency, as the lung has low compliance (i.e. it isstiff), the change in lung volume for a given change in airwaypressure is much less than in the normal healthy newborn lung(Fig. 27.5). The pressure required to initiate lung inflation (‘openingpressure’) is also higher. Without surfactant the lung alveoli col-lapse to zero volume during expiration and the next breath startsfrom a low lung volume. These changes result in increased workof breathing and hypoxemia

Front 249

in suspected preterm babies you can give antenatal corticosteroids for lung maturation and surfactant production but what if the preterm baby is already born

Back 249

surfactant therapy can be given down a tracheal tube:

- natural surfactant

Preterm babies are given surfactant to either prevent or treatRDS. The strategies used are:• prophylactic surfactant – elective intubation and surfactantgiven in the first few minutes after birth• early selective surfactant – intubation and surfactant if infantneeds artificial ventilation after birth• rescue surfactant therapy – once the baby develops RDS.

Front 250

Effect of surfactant deficiency and lung immaturity in preterm infants.

Back 250

surfactant deficiency and structural lung immaturity leads to atelectasis which leads to

- hypoventilation (this then also leads to hypoxemia)

- hypoxemia + hypercarbia + acidosis

- ventilation/perfusion mismatch (this then also leads to hypoxemia)

hypoxemia + hypercarbia + acidosis leads to:

pulmonary vasoconstriction

+ right to left shunting of blood (within lung, ductus arteriosus, foramen ovale)

+ proteinaceous exudate in alveoli (hyaline membrane)

this leads to respiratory distress syndrome

Front 251

Respiratory distress syndrome (RDS) is also known as

Back 251

hyaline membrane disease (HMD) or

surfactant deficient lung disease (SDLD)

Front 252

whats the commonest respiratory disorder affecting preterms

Back 252

respiratory distress syndrome

nb a major cause of morbidity and mortality in preterm infants,although this has decreased markedly in recent years.

Front 253

the main risk factors for respiratory distress syndrome are

Back 253

prematurity

Front 254

surfactant is only produced towardsthe end of the second trimester and early third trimester

Back 254

true

Front 255

what are other risk factors for respiratory distress syndrome

Back 255

maternal diabetes mellitus

sepsis

hypoxemia and acidemia

hypothermia

Front 256

Characteristic histopathologic features of RDS include:

Back 256

• collapsed terminal air saccules

• overdistended terminal airways

• influx of inflammatory cells into the airway lumen

• interstitial edema and protein leak onto the surface of the airwaysand air saccules

• hyaline membrane formation in distal and terminal airways

• necrotic damage to airway epithelial cells.

Front 257

pathogenesis of RDS

Back 257

Caused by a deficiency in surfactant production or function. Thisresults in poor lung compliance (i.e. stiff lungs), which in turn leads to alveolar collapse and impaired gas exchange. Lung imma-turity may also contribute

Front 258

Antenatal corticosteroids markedly reduce:

Back 258

• incidence of respiratory distress syndrome

• mortality.

Front 259

Onset within 4 hours of birth of respiratory distress:

Back 259

• tachypnea (>60 breaths/minute)

• chest retractions (sternal and intercostal retractions)

• nasal flaring

• expiratory grunting

• cyanosis (if severe).

Front 260

how is RDS diagnosed

Back 260

based on history, physical signs, characteristic chestX-ray (Fig. 28.4) and clinical course

Front 261

Chest X-ray (after 4 hours of age) in RDS showing:

Back 261

• diffuse, uniform granular (ground glass) appearance of the lungs fromatelectasis

• air bronchogram – outline of air-filled large airways against opaquelungs

• reduced lung volume

• indistinct heart border as the lung fields are opaque (‘white-out’).

Front 262

Common causes of respiratory distress in preterm infants.

Back 262

Respiratory distress syndrome (surfactant deficiency)

Pneumonia/sepsis

Transient tachypnea of the newborn

Front 263

uncommon causes of respiratory distress in preterm infants

Back 263

Pulmonary hypoplasia

Pneumothorax

Congenital heart disease

Front 264

Rare causes of respiratory distress in preterm infants

Back 264

Diaphragmatic hernia

Non-respiratory – anemia, hypothermia, metabolic acidosis

Front 265

other causes of respiratory distress in preterm infants

Back 265

refer chap 38

Front 266

natural course of RDS

Back 266

is for the illness to become worse over the first24–72 hours and then improve over the next few days.

There isinitially tissue edema from transudation of fluid into alveoli andsubcutaneous tissues, which resolves with improvement of lungdisease.

These clinical features are markedly ameliorated by ante-natal corticosteroids and postnatal surfactant therapy.

Front 267

Management of RDS

Back 267

• antenatal corticosteroids

• surfactant therapy – prophylaxis/rescue via tracheal tube

• oxygen therapy

• prevention of lung collapse – by applying CPAP (continuouspositive airway pressure) or PEEP (positive end-expiratory pressure) on a mechanical ventilator

• lung expansion – by applying a peak inspiratory pressure witha mechanical ventilator, if necessary

• provision of intensive care

Front 268

The main complications are:

Back 268

• infection/lung collapse

• air leaks

• patent ductus arteriosus

• pulmonary hemorrhage

• intraventricular hemorrhage

• bronchopulmonary dysplasia (chronic lung disease).

Front 269

air leaks which is a complication of RDS - what does it include

Back 269

Pulmonary interstitial emphysema (PIE)

pneumothorax

Front 270

Pulmonary interstitial emphysema (PIE)

Back 270

There is tracking of air from the overdistended terminal airwaysinto the interstitium. Increases risk of pneumothorax and bronchopulmonary dysplasia (chronic lung disease).

thus terminal a/ws overdistended = air gets into interstitium

Front 271

Pneumothorax occurs in about 10% of infants ventilated for RDS. Presents with:

Back 271

increased oxygen requirement reduced breath sounds and chest movement on the affected side hypoxemia, hypercarbia and acidosis on blood gases shock.

Confirmed by transillumination of the chest or chest X-ray

tension or spontaneous pneumothorax can occur

Front 272

A tension pneumothorax is treated by urgent aspiration followed by insertion of a chest tube.

Back 272

true

Front 273

Pulmonary hemorrhage

Back 273

This is hemorrhagic pulmonary edema.

In preterm infants it isusually associated with left heart failure from a patent ductusarteriosus (left-to-right shunting) with respiratory distress syndrome requiring mechanical ventilation.

Causes blood staining of tracheal aspirate with or without shock. Incidence is about 3% of infants with respiratory distress syndrome requiring mechanical ventilation. Most of these infants willhave received surfactant, but this is no longer considered to be arisk factor.

Coagulation may be deranged.

Front 274

pulmonary hemorrhage is usually associated with

Back 274

left heart failure from a patent ductus arteriosus (left to right shunting) with respiratory distress syndrome requiring mechanical ventilation

Front 275

whats the treatment of pulmonary ventilation

Back 275

• increase ventilation

• surfactant

• if necessary, replace blood/volume and clotting factors, butavoid fluid overload

• close patent ductus arteriosus. Massive pulmonary hemorrhage has a high mortality.

Front 276

respiratory distress in term infants

Back 276

respiratory distress in term infants

Front 277

signs of respiratory distress

Back 277

Tachypnea (RR > 60/min)

+Nasal flaring

+Grunting (prolongedexpiration againstclosed glottis)

+Chest retraction

– suprasternal

– intercostal

– subcostal

cyanosis if severe

Front 278

how do you monitor respiratory distress in term infants

Back 278

• Oxygen saturation (maintain >95% in term infants).

• Respiratory rate, heart rate, BP, temperature.

• Arterial blood gases if needing oxygen >30%

Front 279

what investigations should you do in addition to monitoring in respiratory distress in term infants

Back 279

• Chest X-ray – confirms respiratory disease, excludes pneumothorax, diaphragmatic hernia, lung malformations.

• Complete blood count,blood cultures,C-reactive protein,consider lumbar puncture.

Front 280

management of respiratory distress

ABC + ABs

Back 280

• Airway and breathing – oxygen/CPAP/mechanical ventilationas required.

• Circulatory support if necessary.

• Intravenous fluids or frequent nasogastric feeds.

• Intravenous antibiotics – broad-spectrum coverage

Front 281

Common causes of respiratory distress in term infants

Back 281

transient tachypnea of the newborn

Front 282

less common causes of respiratory distress in term infants

Back 282

Pneumonia/sepsis

Meconium aspiration

Pneumothorax

Congenital heart disease/heartfailure

Persistent pulmonary hypertensionof the newborn (PPHN)

Hypoxic–ischemic encephalopathy

Front 283

Rare causes of respiratory distress in term infants

Back 283

Surfactant deficiency

Diaphragmatic hernia

Tracheo-esophageal fistula

Pulmonary hypoplasia

Pleural effusion(chylothorax)

Milk aspiration

Airway obstruction e.g. choanal atresia

Lung anomalies (cystic congenitaladenomatoid malformation (CCAM),lobar emphysema, pulmonarysequestration)

Neuromuscular disorders

Severe anemia

Metabolic acidosis (inborn error ofmetabolism)

Front 284

Transient tachypnea of the newborn (TTNB)

Back 284

This is by far the most common cause of respiratory distress interm infants.

Caused by delay in the absorption of lung liquid especially following elective cesarean section.

Usually settles within first day or two of life, but may have mildoxygen requirement and take several days to resolve.

Front 285

pneumonia is a less common cause of respiratory distress in a term infant, but what are the risk factors for pneumonia in this case

Back 285

prolonged rupture of the membranes (PROM),

maternal fever,

chorioamnionitis,

preterm

Front 286

less common causes of respiratory distress in a term baby caused by pneumonia

All infants with respiratory distress should be started on broad-spectrum antibiotics until the results of the blood culture, C-reactiveprotein (CRP), complete blood count (CBC), lumbar puncture (ifperformed) are known.

Back 286

true, why? to rule out pneumonia causing the respiratory distress

Group B strep is the most common cause

Front 287

Meconium aspiration

Back 287

The proportion of infants who pass meconium at birth increaseswith gestational age, affecting 20–25% at 42 weeks.

Front 288

Meconium aspiration

Back 288

Asphyxiatedinfants may start gasping and aspirate meconium before delivery.At birth infants may inhale thick meconium which results in mechanical obstruction, chemical pneumonitisand inactivation of surfactant .

There is a high incidenceof air leak.

Surfactant therapy may be beneficial.

Mechanical ventilation is often required.

Accompanying persistent pulmonaryhypertension (PPHN) may require nitric oxide or sildenafil and sometimes ECMO (extracorporeal membrane oxygenation), i.e.cardiopulmonary bypass.

Front 289

pneumothorax at term causing respiratory distress is most commonly a complication of

Back 289

mechanical ventilation or CPAP

less common spontaneous

Front 290

heart failure

Back 290

Check for evidence of heart failure

– including active precordium,enlarged heart, gallop rhythm, heart murmurs and enlarged liver.and that femoral pulses are palpable (reduced in coarctation of theaorta, hypoplastic left heart syndrome).

Front 291

Persistent pulmonary hypertension of the newborn(PPHN)

Back 291

Pulmonary hypertension leads to right-to-left shunting of blood:

• across the patent foramen ovale

• across the patent ductus arteriosus

• intrapulmonary.

Front 292

Persistent pulmonary hypertension of the newborn (PPHN) is usually secondary to

Back 292

birth asphyxia

meconium aspiration

sepsis

diaphragmatic hernia.Occasionally it is the primary disorder.

Front 293

Persistent pulmonary hypertension of the newborn (PPHN) usually presents as

Back 293

cyanosis or difficulty in oxygenation

Front 294

specific investigations for PPHN

Back 294

CXR

echo

Front 295

management of PPHN

Back 295

• Oxygen.

• Optimize mechanical ventilation.

• Circulatory support as required.

• Consider surfactant therapy.

• Pulmonary vasodilator – nitric oxide (NO). Sildenafil (Viagra)also appears to be effective.

• Consider high-frequency oscillatory ventilation (HFOV).

• Extracorporeal membrane oxygenation (ECMO) as rescuetherapy for severe respiratory failure.

Front 296

rare causes of respiratory distress in a term baby

Back 296

surfactant deficiency

diaphragmatic hernia

Front 297

Surfactant deficiency

Back 297

Rare in term infants. May occur in infants of maternal diabetes orwith surfactant protein B deficiency, a rare genetic disorder.

Front 298

Diaphragmatic hernia

Main problems

Back 298

• Pulmonary hypoplasia, as herniated bowel reduces lung development in the fetus.

• Lung compression by the bowel, which increases in size as airenters it.

• Pulmonaryhypertension(PPHN) –pulmonary arterioles reducedin number and size, and smooth muscle is hypertrophied.

• Other anomalies – present in 15–25%.

Incidence 1 in 4000 births.

Front 299

the most common site for a diaphragmatic hernia is

Back 299

Left-sided hernia of bowel through the posterolateral foramen ofthe diaphragm (Bochdalek).

Front 300

whats the presentation for diaphragmatic hernia

Back 300

• Prenatal – on ultrasound screening, polyhydramnios. Mostidentified antenatally. For antenatal management

• Resuscitation – failure to respond; deteriorates with bag andmask ventilation.

• Respiratory distress – but onset may be delayed if underlyinglung well developed.

Front 301

Physical signs of diaphragmatic hernia

Back 301

• Reduced air entry on affected side.

• Apex beat displaced.

• Scaphoid abdomen – from reduced content of bowel.

Front 302

how is diaphragmatic hernia diagnosed

Back 302

chest abdo xray

Front 303

how do you manage diaphragmatic hernia

Back 303

• Intubate and ventilate from birth. Gentle ventilation, allowingpermissive hypercapnia, i.e. PaCO2 > 60 mmHg (8 kPa) but main-taining pH > 7.25. Avoid mask ventilation.

• Pass large nasogastric tube and apply suction.

• Stabilize and support circulation.

• Early TPN (total parenteral nutrition).

• Surgical repair – delay until stable and PPHN is resolving.

• Nitric oxide or sildenafil (Viagra) for PPHN.

• Extracorporeal membrane oxygenation (ECMO) – pre- andpost-surgery in selected cases.

Front 304

how many people die of diaphragmatic hernias

Back 304

20-30%

Front 305

Milk aspiration

Back 305

Risk of aspiration if infant has cleft palate, neurologic disorderaffecting sucking and swallowing or has respiratory distress.

Infants with bronchopulmonary dysplasia (chronic lung disease)often have gastroesophageal reflux, which predisposes toaspiration.

Front 306

respiratory support

Back 306

respiratory support

Front 307

what are the different types of respiratory support

Back 307

supplemental oxygen

CPAP – continuous positive airway pressure

positive pressure ventilation

HFOV – high-frequency oscillatory ventilation

NO – nitric oxide

ECMO – extracorporeal membrane oxygenation.

Front 308

when to give supplemental oxygen

Back 308

to avoid hypoxemia

Hyperoxemia should also be avoided asit may increase the risk of ROP (retinopathy of prematurity) inpreterm infants and of tissue damage from release of free radicals

In preterm infants, arterial oxygen tension is maintained at 45–80 mmHg (6.0–10.5 kPa) and oxygen saturation at 90–95%

Term infants – maintain oxygen saturation at >95%.

Front 309

CPAP aims to prevent alveolar collapse at endexpiration and stabilize the chest wall. It also allows supplementaloxygen to be delivered continuously.

Back 309

true

Front 310

CPAP is used for

Back 310

infants withmoderate respiratory distress and for recurrent apnea.

respiratory support after birth even in preterms

help wean someone off mechanical ventilation

Front 311

CPAP may be delivered as:

Back 311

• bubble CPAP – the pressure is determined using a watermanometer

• flow-driver CPAP – the flow driver provides a constant streamof oxygen; special nasal prongs maintain a constant pressurethroughout the infant’s respiratory cycle by changing the directionof flow during expiration (fluidic flip).

Front 312

Complications of CPAP are:

Back 312

• pneumothorax

• feeding difficulties due to gaseous distension of the stomach

• often poorly tolerated by term infants.

Front 313

If respiratory failure develops, mechanical ventilation is required. Some infants with bronchopulmonary dysplasia (chronic lungdisease) require nasal CPAP for many weeks. Prolonged use ofnasal prongs may cause nasal trauma, long-term damage to thenasal septum and deformity of the nose. Correct fixation willminimize this.

Back 313

true

Front 314

Is it better to commence nasal CPAP or intubate and givesurfactant in extremely preterm infants at birth?

Back 314

Trials (SUPPORT and COIN) have shown no significant difference in BPD (bronchopulmonary dysplasia) or mortality butnasal CPAP infants need fewer days of ventilation. Nasal CPAP has the attraction of being less invasive thoughmany subsequently require mechanical ventilation.

Front 315

Positive pressure ventilationIndications

Back 315

• Increasing oxygen requirement or work of breathing or increasing PaCO2 while on nasal CPAP.

• Respiratory failure – defect in oxygenation (hypoxemia) and/orcarbon dioxide elimination (hypercarbia).

• Respiratory support of the extremely preterm infant for first fewdays of life to prevent respiratory failure – depends on unit policy

• Apnea – prolonged/recurrent.

• Upper airway obstruction.

• Congenital diaphragmatic hernia.

• Circulatory failure.

Front 316

Intermittent positive pressure ventilation (IPPV)

Back 316

Ventilatory support is administered using a mechanical ventilatorthrough a tracheal tube. With conventional ventilation, intermittentpositive pressure ventilator breaths are given on a background ofcontinuous distending pressure (positive end expiratory pressure,PEEP) (Fig. 25.4). Alveolar ventilation is determined by the dif-ference between peak inspiratory pressure (PIP) and PEEP, theinspiratory time and respiratory rate. Most conventional neonatal ventilators are pressure-limited andtime-cycled. They are used as tracheal tubes are not cuffed and sothere is an air leak.

Front 317

In the presence of marked chest retractions, provide respiratorysupport, including mechanical ventilation if necessary, even ifthe blood gases are normal. Evidence of respiratory failure on blood gases is a latefeature.

Back 317

true

Front 318

Patient-triggered (assist/control) ventilation andsynchronous intermittent mandatory ventilation

Back 318

Two forms of synchronized mechanical ventilation are availableto promote synchrony between the ventilator and a baby’s ownrespiratory efforts – patient-triggered ventilation (PTV) and syn-chronous intermittent mandatory ventilation (SIMV). Bothmethods use a baby’s own spontaneous respiration to trigger theventilator to deliver a breath, usually from the change in airwaypressure or flow measured in the ventilator circuit; or from arecording of the infant’s respiration. In PTV each breath triggersthe ventilator; in SIMV only a preset number of breaths in a giventime are triggered. In both, there is a backup ventilation rate if theinfant does not breathe. Multicenter studies have failed to show any advantages of PTVor SIMV over conventional ventilation for preterm infants withrespiratory distress syndrome, although these forms of ventilationmay decrease the need for sedation. There is also increasing use of combining nasal CPAP with IMV(intermittent mandatory ventilation), i.e. additional positive pres-sure ventilation or SIMV.

Front 319

What are the causes of deterioration of a ventilated infant?

Back 319

Sudden deterioration:

• Tracheal tube blocked/displaced.

• Ventilator/circuit disconnected or malfunction.• Air leak – tension pneumothorax or pneumomediastinum.

• Pulmonary hemorrhage.

• Hemorrhage – intraventricular or other sites.

Slow deterioration:

• Increased lung secretions.

• Infection.

• Patent ductus arteriosus.

• Anemia.

• Developing bronchopulmonary dysplasia (chronic lungdisease).

Front 320

not finished still page 66 and 67

Back 320

...but i think unimportant

Front 321

adaptation to extrauterine life

Back 321

adaptation to extrauterine life

Front 322

The transition from intrauterine to extrauterine life involves acomplex sequence of physiologic changes that begin before birth.Remarkably, although infants experience some degree of intermit-tent hypoxemia during labor, most undergo this transition smoothlyand uneventfully. If not, cardiorespiratory depression requiresprompt and appropriate resuscitation.

Back 322

true

Front 323

summary of physiological changes in fetal to neonatal transition

Back 323

fetal circulation

- blood flow across the ductus arteriosus

- blood flow across the foramen ovale

- lungs - are filled with lung liquid

newborn circulation

- closed ductus arteriosus

- lungs - become aerated

Front 324

when they refer to liquor in hospital what are they referring to

Back 324

amniotic fluid

Front 325

physiological changes in fetal to neonatal transition

Back 325

before birth :

- lungs filled with fluid, oxygen supplied by placenta, goes to RA, some goes via patient foramen ovale to LA thus into aorta and circulation

- blood vessels that supply and drain the lungs are constricted due to high pulmonary pressures (due to the fluid), so most blood flows from the right side of heart through the ductus arteriosus to the aorta

- shortly before and during labor, lung liquid production reduces

- during descent through the birth canal, infants chest is squeezed and some lung liquid exudes from the trachea

- Multiple stimuli (thermal, chemical, tactile) initiate breathing.Serum cortisol, ADH (antidiuretic hormone), TSH (thyroid-stimulating hormone) and catecholamines dramatically increase.

- The first gasp is usually within a few seconds of birth. A negativeintrathoracic pressure is generated to achieve this. Most lung liquid is absorbed into the bloodstream or lymphatics within the first fewminutes of birth.

• Aeration of the lungs is accompanied by increased arterialoxygen tension; the pulmonary artery blood flow increases and thepulmonary vascular resistance falls.

• Contraction of the umbilical arteries restricts access to the lowresistance placental circulation. This results in increased peripheralvascular resistance and an increase in systemic blood pressure.

• The fall in pulmonary vascular resistance and the rise in systemic vascular resistance result in near equalization of pressuresacross the duct and virtual cessation of ductal flow

Front 326

Conditions associated with abnormal neonatal adaptation to extrauterine life.

Fetal, maternal and placental causes

Back 326

Fetal causes

Preterm/post-dates

Multiple birth

Forceps or vacuum-assisted delivery

Breech or abnormal presentation

Shoulder dystocia

Emergency cesarean section

Intrauterine growth restriction (IUGR)Meconium-stained amniotic fluid

Abnormal fetal heart rate trace

Congenital malformations

AnemiaInfection

Front 327

Conditions associated with abnormal neonatal adaptation to extrauterine life.

Fetal, maternal and placental causes

Back 327

Maternal causes

General anesthetic

Maternal drug therapy

Pregnancy-induced hypertension

Chronic hypertension

Maternal infection

Maternal diabetes mellitus

Polyhydramnios

Oligohydramnios

Front 328

Placental conditions associated with abnormal neonatal adaptation to extrauterine life

Back 328

Chorioamnionitis

Placenta previa

Placental abruption

Cord prolapse

Front 329

what are some of the consequences of abnormal transition from fetal to extrauterine life

Back 329

hypoxic ischemic encephalopathy, persistent pulmonary hypertension andmulti-organ system failure.

Front 330

the APGAR score named after Virginia Apgar, an anesthesiologist,is used to describe an infant’s condition during the first few minutesof life

Back 330

true

Front 331

whose Ignaz Semmelweis

Back 331

hungarian guy

first guy to wash his hands before surgery

Front 332

when should you do an apgar score

Back 332

assigned at 1 and 5 minutes of life

If thescore is still below 7 or the infant is requiring resuscitation, it iscontinued every 5 minutes until normal or 20 minutes of age

Front 333

Although often assigned, few babies truly attain a score of 10,because it is uncommon for the baby to be pink all over. The Apgarscore is useful as a guide in rapidly assessing respiration, circula-tion and the nervous system, and as a record of the infant’s condi-tion shortly after birth

Back 333

true

Front 334

APGAR score includes

Back 334

Activity (muscle tone)

Pulse

Grimace

Appearance (colour)

RR

Front 335

The Apgar score is not used to determine the need forresuscitation.

Evaluation for resuscitation is made second by second and isbased on the three most important signs:

Back 335

RR

HR

colour

Front 336

How does resuscitation affect the Apgar score?

Back 336

The Apgar score is assigned irrespective of resuscitationbeing performed.

Front 337

Can one determine Apgar scores in preterm infants?

Back 337

Yes. However, the extremely preterm infant’s maximumscore is reduced by poor muscle tone and weaker response tostimulation than term infants.

Front 338

Sustained, severe asphyxia (Fig. 11.2) in utero or during laborresults in

nb sustained, severe asphxia in utero or during labor = increased WOB, then first apnea, HR falls but BP maintained

if continuing asphyxia = infants gasps, HR falls more, BP falls, over several minutes after last gasp, theres a secondary apnea

- to recover give positive pressure ventilation, +/- chest compressions

Back 338

the infant making increased respiratory effort, followedby a period of apnea (primary apnea). During primary apnea theheart rate falls to about half its normal rate but the blood pressureis initially maintained.

With continuing asphyxia, the infant starts to gasp, the heart rateslowly falls, as does the blood pressure. After several minutes, aftera last gasp, there is secondary apnea. To recover, positive pressureventilation, if necessary accompanied by cardiac compressions, isrequired

Front 339

What is the long-term significance of a low Apgar score (3or less)?

Back 339

An infant with a low Apgar score at 1 minute but respondingrapidly to resuscitation has an excellent prognosis. An infant with a low Apgar score beyond 10 minutes of agein spite of adequate resuscitation is at increasing risk of neuro-logic injury resulting in cerebral palsy the longer the scoreremains low.

Front 340

Cardiac disorders

Back 340

cardiac disorders

Front 341

Congenital heart disease:

Back 341

• is the most common group of structural malformations

• affects 6–8 per 1000 live births• accounts for 30% of all congenital abnormalities.

Front 342

what are the risk factors cardiac disorders

Back 342

• Chromosomal disorders and syndromes, e.g. trisomy 21 (Downsyndrome), microdeletion chromosome 22 abnormalities (foraortic arch abnormalities and Di George sequence), Turner,Noonan, Williams, syndromes and many others.

• Maternal – diabetes mellitus, teratogenic drugs, e.g. anticonvul-sants, fetal alcohol syndrome.

• Congenital infection, e.g. rubella.

• Siblings of affected child – only slight increase in risk.

Front 343

microdeletion chromosome 22 abnormalities (for aortic arch abnormalities and Di George sequence)

Back 343

ok

Front 344

clinical presentation of neonatal cardiac disorders

Back 344

• Antenatal detection on ultrasound screening.

• Detection of a heart murmur.

• Heart failure – respiratory distress/shock.

• Cyanosis

Front 345

antenatal diagnosis of especially severe cardiac lesions done

Back 345

via antenatal ultrasound

e.g. hypoplastic left heart

Lesions such as transposition of the great arteries and coarctationof the aorta are difficult to identify.

Front 346

what do you do if you find a cardiac abnormality of neonate at increased risk of one during antenatal ultrasound

Back 346

refer to perinatal cardiac specialist

Antenatal detection allowsparents to be counseled and postnatal management planned

Front 347

About a quarter of infants with congenital heart disease presentin the neonatal period and usually have severe lesions

Back 347

true

Front 348

Classification of cardiac disorders.

Back 348

Acyanotic or cyanotic

Front 349

acyanotic cardiac disorders include - shunts, obstruction and pump failure

Back 349

Shunts (‘holes’)

VSD (ventricular septal defect) 32%

PDA (patent ductus arteriosus) 12%

ASD (atrial septal defect) 6%

Obstruction (‘narrowing’)

Pulmonary stenosis 8%

Aortic stenosis 5%

Coarctation of the aorta 6%

Hypoplastic left heart

Pump failure

Supraventricular tachycardia (SVT)

Cardiomyopathy

Front 350

cyanotic cardiac disorders include

Back 350

Transposition of the greatarteries 5%

Reduced pulmonary bloodflow

Tetralogy of Fallot 6% (most common)

Pulmonary atresia

Tricuspid atresia

Total anomalous pulmonary venousconnection (TAPVC)

Front 351

In infants with congenital heart disease:

Back 351

• 10–15% have complex heart disease with multiple lesions

• 10–15% of children with congenital heart disease haveabnormalities of other systems.

Front 352

heart mumurs - Detected in 1–2% of normal infants on routine examination. The cause may be:

Back 352

A transient flow murmur

Pulmonary artery branch stenosis

Congenital heart disease

Front 353

whats a transient flow murmur

Back 353

related to circulatory changes following birth.

The murmur is soft, systolic, at the left sternal edgeor pulmonary area in a well infant whose examination, includingfour limb blood pressure measurements, is otherwise normal.

Front 354

whats a murmur associated with Pulmonary artery branch stenosis.

Back 354

The murmur is best heardin the pulmonary area and radiates to the axilla and back. Resolvesin a few weeks.

Front 355

Congenital heart disease murmurs

Back 355

Though uncommon, the most worrying of these are duct-dependent lesions, which may result incirculatory failure or cyanosis when the ductus arteriosus closes

The femoral pulses may be palpable even in coarctation of theaorta shortly after birth as the ductus arteriosus is still patent.

definitive diagnosis = echo

pulse oximeter useful

if theres an innocent flow murmur, reassess infant in a few days to check murmur gone with worsening sxs to parents

if worsening sxs develop = refer to peds cardiologist and echo

Front 356

does the absence of a murmur exclude congenital heart disease

Back 356

no

Front 357

Causes of heart failure in the neonatal period.

Back 357

Left-to-right shunting (high-output failure) Patent ductus arteriosus

Atrioventricular septal defect (AVSD)/large ventricular septal defect (VSD)

Left ventricular outflow obstruction (duct-dependent systemic circulation)

Severe coarctation of the aorta

Critical aortic valve stenosis

Hypoplastic left heart syndrome

Myocarditis/cardiomyopathy

Arrhythmias

Supraventricular tachycardia (SVT)

Non-cardiac

Severe anemia, polycythemia, arteriovenous malformation, e.g. vein of Galen malformation

Front 358

whats this

Back 358

a hypoplastic left heart

Front 359

whats this

Back 359

SVT

Front 360

Atrioventricular septal defect (AV canal defect)

Back 360

• Common (40%) in trisomy 21 (Down syndrome).

• Surgery at 2–4 months.

Front 361

Large ventricular septal defect

Back 361

• Only presents at about 1–3 months, when pulmonary vascularresistance is low and left-to-right shunt maximal.

• Surgery if medical therapy fails.

Front 362

Left ventricular outflow obstruction (low-output heartfailure/shock when duct closes) causes

Back 362

Severe coarctation of the aorta/interruption of the aortic arch

Hypoplastic left heart

Supraventricular tachycardia

Front 363

Severe coarctation of the aorta/interruption of the aortic arch - key features

Back 363

Key clinical sign is weak or absent femoral pulses.

Blood pressurein the arms is markedly higher than in the legs (>20mmHg).

Surgery is required.

Less severe lesions may present as hypertension in adults.

Front 364

Hypoplastic left heart

Back 364

Presents with signs of low cardiac output when ductus arteriosuscloses.

Pulses are weak at presentation, and there is severe meta-bolic acidosis.

Fatal without treatment – requires a series of palliative operations (Norwood procedure) or heart transplantation.

Front 365

Supraventricular tachycardia

Back 365

Heart rate 220–300 beats/min

• Heart is usually structurally normal, but accessory pathway(Wolff–Parkinson–White syndrome) is present in 40%.

• If no response to placing ice pack on face, give the drug adenosine, or DC cardioversion

Front 366

Central cyanosis

Back 366

• is clinically detectable if there is over 5g/dL of reducedhemoglobin

• is best detected in tongue/mucous membranes

• in the absence of respiratory distress is usually due to cyanoticcongenital heart disease (Table 48.1).

If there is respiratory distress, the cause may be:

congenital heart disease

pulmonary disease

PPHN (persistent pulmonary hypertension of the newborn) polycythemia.

Front 367

Peripheral cyanosis (acrocyanosis)

Back 367

Hands and feet are blue. Common in infants in the first couple ofdays of life and in children of any age when cold.

The tongue andmucous membranes are pink. It is of no clinical significance in theabsence of hypovolemia or shock.

Front 368

‘Traumatic’ cyanosis

Back 368

Cyanosis of the head, often with petechiae from venous congestion, e.g. caused by umbilical cord around baby’s neck or facepresentation. Tongue is pink. Resolves spontaneously.

Front 369

transposition of the great arteries

Back 369

aorta comes out of right ventricle and pulmonary artery from the left ventricle

to survive, blood needs to mix via the foramen ovale or ductus arterious, less mixing = severe cyanosis

Front 370

with transposition of the great arteries, profound cyanosis occurs in the

Back 370

first day or two of life when the duct closes, but may be delayed if an ASD cause sufficient mixing

Front 371

whats the management of transposition of the great arteries

Back 371

give prostaglandin infusion to keep duct open

balloon atrial septostomy to enlarge the foramen ovale (= promote mixing circulations)

switch operation needed - where pulmonary artery and aorta switched over, coronary arteries also have to be transferred to the new aorta, which is technically demanding

Front 372

Total anomalous pulmonary venous connection (TAPVC)

Back 372

The pulmonary veins, instead of connecting into the left atrium,connect into the right side of the circulation, sometimes below thediaphragm.

If the connection is narrow (obstructed) they present with cyanosis, respiratory distress and poor cardiac output. This may bedifficult to distinguish from surfactant deficiency. Treatment issurgical, sometimes in an emergency

Front 373

regarding cardiac anomalies what investigations should you do

Back 373

first you need to distinguish between, respiratory disorder, congenital heart disease and persistent hypertension of the newborn

CXR - for lung diseases, enlarged heart (outflow obstruction or volume overload), abnormal shapes

ECG - arrythmias, AVSD, tricuspid atresia

Hyperoxia test

echo and doppler

cardiac catheterisation

Front 374

on chest x ray what are you looking for

Back 374

enlarged heart

abnormal shapes (boot strap = ToF; egg on side with TGA)

prominent pulmonary vascular markings from excess blood flow to lungs e.g. left to right shunt from patent ductus arteriosus

reduced pulmonary vascular markings (oligemic) from reduced blood flow to the lungs e.g. tetralogy of fallot

Front 375

whats the hyperoxia test

Back 375

its just an arterial blood gas

measuring partial pressure of oxygen at the radial artery

If PaO2 >110mmHg (15kPa):

– unlikely to be cyanotic heart disease

– usually lung disease or PPHN (persistent pulmonary hypertension of the newborn).

If PaO2 <110mmHg (15kPa):

– likely to be cyanotic heart disease, but can be severe lungdisease or PPHN.

Front 376

management for cardiac anomalies

Back 376

ABC

correct metabolic acidosis, hypoglycemia and hypocalcemia

give IV prostaglandin to keep ductus arteriosus patent (unless ASD then its already open)

if in heart failure:

- high output failure (after first weeks of life) - fluid restrict (acute only), diuretics, ACE inhibitors e.g. captopril

- low output failure/shock - inotropes, volume support, arrhythmias require specific treatment

refer to pediatric cardiac center

Front 377

Why may giving prostaglandin be life-saving?

Back 377

By keeping the ductus arteriosus patent when the circulationis duct-dependent. This occurs:

• with obstruction to outflow of the left ventricle, when thesystemic circulation is maintained by blood flowing right to leftacross the patent ductus, e.g. severe coarctation of the aorta(Fig. 48.8)

• with reduced pulmonary blood flow, when the pulmonarycirculation is maintained by blood flowing from left to rightthrough the duct, e.g. pulmonary atresia (Fig. 48.9).

Front 378

Ductus arteriosus – connects the pulmonary artery with thedescending aorta

Back 378

true

Front 379

ongoing patent ductus arteriosus is beneficial in patients with

Back 379

pulmonary hypertension

some forms of congenital heart disease

Front 380

In utero – ductal patency:

Back 380

dependent on low PaO2 and high concentrations of vasodilatingprostaglandins (PGE2 and PGI2)

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Postnatal – ductal constriction is promoted by:

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• the rise in oxygen tension with the first breaths

• the increase in pulmonary blood flow, which enhances clearanceof the local vasodilating prostaglandins.

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Ductal closure takes place in two stages:

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• functional closure – 24–48 hours after birth

• anatomic closure – may take 2–3 weeks.

In preterm infants, there may be delay in anatomic closure.

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with preterm infants a patent ductus arteriosus will eventually

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close spontaneously

but unlikely for a term baby with a patent ductus arteriosus defect

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what are the risk factors for patent ductus arteriosus

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• Prematurity – incidence increases with decreasing gestationalage; most are less than 32 weeks’ gestational age.

• Respiratory distress syndrome.

• Sepsis

• Pulmonary hypertension.

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clinical features of PDA patent ductus arteriosus

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Excessive pulmonary blood flow:

• Tachypnea.

• Increase in oxygen requirement.

• Carbon dioxide retention, difficulty weaning from mechanicalventilation.

• Apnea and bradycardia.

Reduced systemic perfusion:

• Tachycardia

• Widened pulse pressure, causing bounding pulses

• Active precordium

• Heart murmur (see below)

• Hepatomegaly (from right-sided heart failure).

• Systemic hypotension; low diastolic arterial pressure in all.

Heart murmur (Fig. 32.3):

systolic

best heard at left sternal border. If heart failure is present:

gallop rhythm (extra third heart sound)

may be loud pulmonic component (P2) of second heart sound. Silent PDA, i.e. no murmur but PDA present – common, usuallylarge shunt.

The classic continuous murmur, systole extending into diastole,heard in older infants is rarely present in preterm infants.

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what is the typical murmur heard for a PDA

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classic continuous murmur, systole extending into diastole, heard in older infants is rarely present in preterm infants.

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clinical features of PDA with excessive pulmonary blood flow

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• Tachypnea.

• Increase in oxygen requirement.

• Carbon dioxide retention, difficulty weaning from mechanical ventilation.

• Apnea and bradycardia.

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clinical features for PDA with reduced systemic perfusion

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• Tachycardia

• Widened pulse pressure, causing bounding pulses

• Active precordium

• Heart murmur (see below)

• Hepatomegaly (from right-sided heart failure).

• Systemic hypotension; low diastolic arterial pressure in all.

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what investigations do you have for a PDA

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chest x ray

echo with pulsed color doppler

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management for PDA

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medical management

surgical closure

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medical management of PDA

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fluid management - fluid restrict esp if tx with indomethacin or ibuprofen (as they cause fluid retention) but reconsider if renal output normal

diuretics - furosemide which leads to increased prostaglandin renal production to keep PDA, only use if medical tx failed/CI and waiting for surgery

prostaglandin synthase inhibitors aka cyclooxygenase inhibitors (COXi)

- indomethacin

- ibuprofen

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surgical closure of PDA

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done if medical tx fails

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what are some of the complications of surgery for PDA

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• post-ligation cardiac syndrome – low systolic arterial pressure,need for cardiotropes and difficulty with oxygenation secondary toimpaired left ventricular function

• recurrent laryngeal nerve damage, common, causing vocal cordparalysis

• chylothorax from damage to thoracic duct

• pneumothorax

• ligation of pulmonary artery by mistake

• mortality (<1%) but surgical closure is associated with worselong-term neurological outcome.

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What are the associated mobidities of PDA

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• Pulmonary hemorrhage

• Cranial hemorrhage

• Necrotizing enterocolitis

• Bronchopulmonary dysplasia (chronic lung disease).