Flashcards in Birth Deck (215)
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1
still birth
an infant born after the 24th week of pregnancy who does not, at any time show any other sign of life.
2
perinatal mortality
still births plus deaths in first week of life.
3
infant mortality
deaths from birth to 1yr.
4
post natal mortality
deaths from 4wks of age to 1yr.
5
gestational age
Age measured from the first day of the last menstrual period before conception and expressed in complete weeks or days.
6
chronological / postnatal age
Time elapsed from birth
7
Corrected age
Chronological age minus the number of weeks born before 40wks gestation.
8
Spontaneous abortion (miscarriage)
A conceptus born after spontaneous labour without any signs of life before 24 completed weeks gestation.
9
Live birth
A baby that displays any sign of life (i.e. breathing, heart beat, cord pulsation, or voluntary movement) after complete delivery from the mother, irrespective of gestation.
10
Stillbirth (late foetal death)
Foetal death prior to complete delivery from the mother after 24 completed weeks gestation.
11
Perinatal mortality
Includes all stillbirths and neonatal deaths in the first week.
12
Neonatal mortality
Death amongst live births before 28 days of age (whatever the gestation at birth).
13
Neonatal period
from birth to 28 postnatal days in term infants.
14
Preterm Birth
before 37 completed weeks gestation. 78% of births.
15
term birth
Between 37 and 42 completed weeks gestation.
16
Post-term (post-mature)
Birth after 42 completed weeks gestation. <5% of births.
17
Low birth weight (LBW)
Birth weight <2500g. 7% of births.
18
Very low birth weight (VLBW)
Birth weight <1500g. 1.2% of births.
19
Small for gestational age (SGA)
Birth weight <10th centile for gestational age.
20
what are the key differences between children and adults?
size
anatomy - short, soft neck, obstruct in overextenstion during resuscitation
physiology - pulse, resp rate, bp change with age
21
describe how the weight of an infant changes in the first year?
average birth weight = 3kg which increases to 10kg by 1 year
22
how can weight be predicted in children between the ages of 1-10?
weight (kg) = 2 (age in yrs + 4)
23
perinatal mortality risk factors?
• birth weight
• Cesarean delivery
• multiple delivery
• fetal distress
• meconium aspiration
• patent ductus arteriosus (PDA)
• maternal chorioamnionitis
• hypertension (pregestational and gestational, including preeclampsia)
• diabetes (pregestational and gestational)
24
REDUCING PERINATAL MORTALITY
preconception
early screening and intervention of risk factors/optimisation of patient for conception
25
REDUCING PERINATAL MORTALITY
antenatal care
early booking and screening
26
REDUCING PERINATAL MORTALITY
intrapartum
active management of 3rd stage of labour / magnesium sulphate
27
REDUCING PERINATAL MORTALITY
postpartum
effective review and follow up of child and mother after delivery
28
PRETERM LABOUR
1. what is it
2. what percentage of deliveries are preterm
3. what percentage occur <34 weeks
1. Labour occurring at <37 completed weeks gestation
2. 6%
3. 2%
29
PRETERM LABOUR
what factors impact on prognosis
• Availability of neonatal intensive care unit
• Gestational age and birh weight
• Baby condition at birth (aasphyxited infants more likely to die from respiratory distress syndrome)
• Immediate neonatal management
• Antenatal steroids
30
causes of preterm labour
• Previous pre term labour
• Premature rupture of the membranes
• Multiple pregnancy
• Polyhydranios
• Antepartum haemorrhage
• Fetal death
• Bacterial vaginosis
• Maternal pyrexia (UTI, infections)
• Uterine abnormalities
• Cervical incompetence
31
PRETERM LABOUR
what are the important aspects of examination
maternal pulse, temp, resp rate, uterine tenderness, foetal presentation, speculum, gentle VE
32
PRETERM LABOUR
what investigations are important
FBC, CRP, swabs, MSU, USS for foetal presentation and estimated weight, foetal fibronectin/transvaginal USS
33
management of preterm labour
• Is there threatened or real preterm labour (transvaginal cervical length scan (>15mm unlikely to be labour / fibronectin assay – if -ve unlikely to be labour)
• Admit if high risk
• Inform neonatal unit
• Check foetal presentation with USS
• Steroids (12mg betamethasone IM – 2 doses 24h apart) – reduce rate of respiratory distress, intraventricular haemorrhage and neontal death
• Consider tocolysis (nifedipine and atosiban iv)– drug treatment to prevent labour and delivery
• Aim to improve perinatal morbidity and morality
34
preventing preterm labour
•Treat bacterial vaginosis with clindamycin to reduce preterm prelabour rupture of membranes and low birth weight in women with previous preterm birth
• Progesterone – in high risk women reduces recurrence / in low risk womn with short cervix reduces preterm birth by 50% / cream or pessaries used
• Cervical sutures (cerclage) – elective in women with previous loss from cervical weakness / ultrasound indicated for those with short cervix / rescue in response to cervical dilatation
• Cervical pessary
• Reduction of pregnancy number – selective reduction of triplet or higher pregnancies to 2 reduces risk of preterm labour but also slightly increases risk of early miscarriage
• Methods for prediction of preterm labour – transvaginal USS of cervix, fetal fibronectin
35
describe preterm prelabour rupture of membranes?
1. how often it occurs and what is it often associated with
2. investigations
3. management
4. risks to fetus
1. 1/3 of preterm deliveries. 1/3 associated with overt infection
2. Ask about vaginal loss
Investigations: FBC, CRP, swabs, MSU, USS
3. If chorioamnionitis – betamethasone 12mg IM, deliver, broad spectrum antibiotics
If no chorioamnionitis – manage conservatively – admit, SCBU, 12mg betamethasone IM, antibiotics (erythromycin)
4. Risks to fetus: prematurity, infection, pulmonary hypoplasia, limb contractures
36
LOW BIRTH WEIGHT
1. how common is it
2. weight
3. why is it useful?
4. very low birth weight
5. extremely low birth weight
1. 42% stillbirths and 25% neonatal deaths were <10th birth weight centile
2. <2500g
3. Useful on a worldwide basis where gestational age at delivery is often unknown
4. 1500g
5. <1000g
37
what is intrauterine growth restriction
presence of pathology that is slowing foetal growth which if it could be removed would allow resumption of normal foetal growth. No tests available
IUGR is failure of growth in utero that may or may not result in SGA
38
LOW BIRTH WEIGHT
what is symmetric SGA?
all growth parameters symmetrically small- suggest foetus affected from early pregnancy
39
LOW BIRTH WEIGHT
what is asymmetric SGA?
weight centile < length and head circumference. Usually due to IUGR due to insult in late pregnancy eg pre-eclampsia
40
LOW BIRTH WEIGHT
causes of SGA
small parents
restricted foetal oxygen, glucose supply
placental dysfunction
maternal hypertension
multiple pregnancy, maternal illness
foetal abnormality
maternal substance exposure
41
LOW BIRTH WEIGHT
complications
increased risk of death and asphyxia, congenital infection, hypoglycaemia, polycythaemia, necrotising enterocolitis, thrombocytopenia, meconium aspiration syndrome
42
LOW BIRTH WEIGHT
management
routine postnantal care, clinical evaluation for underlying cause, thermal care and blood glucose monitoring, temp, pulse, resp monitor, admit to neonatal unit if birth weight <1800g
43
LOW BIRTH WEIGHT
small for gestational age
statistical definition used if birth weight below standard for gestational age.(<10th centile) Used antenatally when growth or size of fetus falls below statistically determined limits
44
LOW BIRTH WEIGHT
SGA risk factors
1. minor
2. major
1. maternal age >35, smoker 1-10 day, nulliparity, BMI <20 or 25-34.9, IVF singleton, previous pre-eclampsia, pregnancy interval <6 or >60 months, low fruit intake pre-pregnancy
2. maternal age >40, smoker >11 day, previous SGA, maternal/paternal SGA, previous stillbirth, cocaine use, daily vigorous exercise, maternal disease, heavy bleeding, low PAPP-A
45
LOW BIRTH WEIGHT
SGA neonatal complications
birth asphyxia
meconium aspiration
hypothermia
hypo-hyperglycaemia
polycytheamia
retinopathy of prematurity
persistent pulmonary hypertension
pulmonary haemorrhage
necrotising enterocloitis
46
LOW BIRTH WEIGHT
SGA long term complications
cerebral palsy
T2DM
obesity
hypertension
precocious puberty
behavioural problems
depression
alzheimers disease
cancer (breast, ovarian, colon, lung, blood)
47
POST NATAL TRANSITION
describe infant size and growth
Average infant = 3500g
Boys weight 250g more
During first 3-5 days upto 10% birth weight is lost which is regained by 7-10 days
First month average weight gain per week = 200g
48
POST NATAL TRANSITION
skin
Thin epithelial layer, incompletely developed sweat ad sebaceous glands
Prone to heat and water losses
Skin covered with greasy protective layer- vernix caseosa
49
POST NATAL TRANSITION
head
Average occipitofrontal head circumference is 35cm
Anterior fontanelle closes between 9 and 18 months
Posterior fontanelle closes by 6-8 weeks
50
POST NATAL TRANSITION
respiratory system
Changes at birth to convert from dependence on placenta to breathing air
In utero – airways filled with fluid containing surfactant in later stages of pregnancy. Oligohydramnios can lead to pulmonary hypoplasia
Lung fluid removed by squeezing of thorax during vaginal delivery, reduced secretion, increased absorption mediated by fetal catecholamines during labour and after birth
Surfactant lines the air – fluid interface of alveoli and reduce surface tension lung expansion and fall in pulmonary vascular resistance
Newborns mainly breath with diaphragm – 30-50 breaths/min
Brief self limiting apnoeic spells might occur during sleep
Respiratory distress syndrome more common in premature babies <32 weeks gestation (surfactant deficiency)
51
POST NATAL TRANSITION
cardiovascular system
in fetal circulation
- right sided (pulmonary) pressure exceeds left sided (systemic)pressure
- Blood flows from right to left through foramen ovale and ductus arteriosis.
52
POST NATAL TRANSITION
cardiovascular system
at birth
- Left sided pressure rises when umbilical vessels clamped
- Right sided pressure falls as lungs expand and rising PO2 triggers prostaglandin mediated vasodilatation
- Foramen ovale and ductus arteriosus close functionally shortly after birth. Ductus closes due to muscular contraction in response to rising oxygen tension
- Some congenital heart disease are ‘duct dependent’ ie flow through duct necessary for oxygen delivery and closure of duct precipitates deterioration
53
POST NATAL TRANSITION
ductus arteriosis
PGE1 and PGE2 keep the ductus arteriosus open via involvement of specific PGE-sensitive receptors (such as EP4 and EP2). ... Immediately after birth, the levels of both PGE2 and the EP4 receptors reduce significantly, allowing for closure of the DA and establishment of normal postnatal circulation.
54
POST NATAL TRANSITION
GI system
Most infants over 35 weeks have coordination to latch on to feed
At term – secretory and absorbing surfaces are well developed, and digestive enzymes (except pancreatic amylase)
Meconium within 6 hours (abnormal ifmore than 24 hours)
With normal feeding meconium replaced by yellow stool by day 3 or 4
Immaturity of liver enzymes responsible for conjugation of bilirubin responsible for physiological jaundice
55
POST NATAL TRANSITION
genitourinary system
Urine production during second half of gestation and makes up much of amniotic fluid
Infant may micturate during delivery and should void within 24 hours of life
Renal concentrating ability diminished in neonates
56
POST NATAL TRANSITION
haematopoietic and immune system
Newborn red cell contain fetal haemaglobin with a higher affinity for oxygen
Hb conc of cord blood range from 15-20g/dL, A large volume of blood is present in placenta and late clamping causes this blood to enter baby and can lead to polycythaemia
Impaired neutrophil reserves
Diminished phagocytosis and intracellular killing capacity
Decreased complement components
Low IgG2, leading to infections with encapsulated organisms
57
POST NATAL TRANSITION
thermal and metabolic
Core temp of fetus abou 0.5 degrees above mother (uses no energy staying warm)
After birth the ability to maintain temp comtrol is determined by environment and internal physiological processes
Newborns attempt to stay warm by increasing muscle activity and burning brown fat increasing metabolic rate. Newborns don’t shiver. Peripheral vasoconstricton also decreases heat loss to skin surface
Heat production requires oxygen and glucose and produces lactic acid, so persistent hypothermia may result in metabolic acidosis, hypoglucaemia, decreased surfactant production and poor growth
Maternal glucose readily crosses placenta and supplies fetus with energy for growth and to store glycogen inliver for use after birth
Release of catecholamines during labour and birth mobilises glycogen yet blood glucose levels decline after birth and lowest at 1 hour of age
58
NEWBORN BABY ASSESSMENT (NIPE)
1. when should it be done
2. why
1. Must be perfomed within 72 hours. Second examination at 6-8 weeks (usually GP)
2. screen for congenital abnormalities, make referrals for tests, provide reassurance for parents
59
NEWBORN BABY ASSESSMENT (NIPE)
introduction
Confirm infant name and DOB
Explain ‘examine head to toe’
Consent
Wash hands
Expose child
Ask questions during the check
60
NEWBORN BABY ASSESSMENT (NIPE)
questions
Pregnancy details (time, date, type, complications, screening results)
Breech presentation – if yes after 36 weeks USS of hips for dysplasia
Risk factors for infection
Family history
Feeding pattern, urination, passing meconium, parental concerns
61
NEWBORN BABY ASSESSMENT (NIPE)
what are the components?
introduction
questions
weight
inspection
tone
head
skin
face
eyes
ears
mouth and palate
neck and clavicles
upper limbs
chest
abdomen
genitalia
lower limbs
back and spine
anus
reflexes
62
NEWBORN BABY ASSESSMENT
weight
Check against weight chart
If small – head circumference and length to determine symmetrical growth restriction (fetal factors) or asymmetrical growth restriction (placental insufficiency)
63
NEWBORN BABY ASSESSMENT
inspection
Pallor – anaemia, haemorrhage, congestive cardiac failure
Cyanosis – peripheral vasoconstriction secondary to hypovolaemia / right to left cardiac shunting
Jaundice – high bilirubin
Posture – hemiparesis / erb’s palsy
64
NEWBORN BABY ASSESSMNENT
tone
Gently move limbs passively
Hypotonic infants – feel like a rag doll, difficulty feeding (common in downs syndrome)
65
NEWBORN BABY ASSESSMENT
head
Circumference (microcephaly/macrocephaly)
Shape – cranial sutures (closely applied, widely separated, normal
fontanelle – flat? Sunken? Bulging? (bulging – raised ICP eg hydrocephalus / sunken – dehydration)
66
NEWBORN BABY ASSESSMENT
skin
Birthmarks, bruising, lacerations
Body maps in red book
Colour- pallor, cyanosis, erythema, jaundice
Bruising/lacerations – location and size
Facial birthmarks – salmon patch, haemangiomas, port wine stain
Vernix – waxy white substance coating skin – normal
67
NEWBORN BABY ASSESSMENT
face
Dysmorphic features
Asymmetry
Trauma
Nose – patency of nasal passage
68
NEWBORN BABY ASSESSMENT
eyes
Erythema or discharge
Sclera
Position and shape of eyes
Red reflex (absence – congenital cataracts, retinal detachment, vitreous haemorrhage and retinoblastoma
69
NEWBORN BABY ASSESSMENT
ears
Pinna – asymmetry, skin tage, accessory auricles
Hearing screening test prior to discharge
70
NEWBORN BABY ASSESSMENT
mouth and palate
Clefts of the hard or soft palate- tongue depressor and torch
Tongue and gums – tongue tie
71
NEWBORN BABY ASSESSMENT
neck and clavicles
Length of neck, webbing
Neck lumps
Clavicular fracture
Cystic hygroma
72
NEWBORN BABY ASSESSMENT
upper limbs
Symmetry
Fingers – count/abnormal morphology
Palms – check for 2 palmar creases
Brachial pulse – asymmetry suggest vascular abnormality (coarctation of aorta
73
NEWBORN BABY ASSESSMENT
chest
Inspect
Resp rate (40-60)
Assess for increased work of breathing
Pectus excavatum / pectus carinatum/ asymmetrical chest wall expansion
Auscultate
Heart – auscultate (120-150bpm)
Pulse oximetry
74
NEWBORN BABY ASSESSMENT
abdomen
Inspect – distension, umbilicus, inguinal hernia in groin
Palpation – liver (No more than 2cm below costal margin), spleen (may be palpable at costal margin), kidneys (if easily palpable – polycystic kidney disease), bladder (dhouldnt be palpable)
75
NEWBORN BABY ASSESSMENT
genitalia
Male – position of urethral meatus, size (2cm at least), testicular swelling, palpate scrotum
Female – inspect labia (ensure not fused), clitoris (normal size), vaginal discharge (white discharge normal due to maternal oestrogens
76
NEWBORN BABY ASSESSMENT
lower limbs
Asymmetry,
Oedema
Ankle deformities
Missing digits
Tone
Movement
Range of knee joint movement
Palpate femoral pulses
Hips – barlowsand ortolanis tests-hip joint instability and dislocation
- Barlows – adduct hip and apply pressure on knee, if dislocate – positive
- Ortolani – flex hips and knees of supine infant to 90 degrees, pressure on trochanters and adduct, positive if clunk can be heard
77
NEWBORN BABY ASSESSMENT
back and spine
Inspect for scoliosis, hair tufts, naevi, brithmarks, sacral pits
78
NEWBORN BABY ASSESSMENT
anus
Patency
Meconium should be passed in first 24 hours
79
NEWBORN BABY ASSESSMENT
reflexes
Palmar grasp
Sucking
Rooting reflex
Stepping reflex
80
NEWBORN BABY ASSESSMENT
blood spot screening
Tests for 9 congenital conditions taken on day 5, heel prick test which requires 4 separate drops, results take 6-8 weeks to come back
• Sickle cell disease
•Cystic fibrosis
• Congenital hypothyroidism
• Phenylketonuria
• Medium-chain acyl-CoA dehydrogenase deficiency (MCADD)
• Maple syrup urine disease (MSUD)
• Isovaleric acidaemia (IVA)
• Glutaric aciduria type 1 (GA1)
• Homocystin
81
NEWBORN BABY ASSESSMENT
hearing screening
Otoacoustic emission-OAE within first 4 weeks of life, automatic auditory brainstem response testing is carried out if any uncertainty in OAE response
82
what is developmental hip dysplasia?
Structural abnormality in hips due to abnormal development of fetal bones during pregnancy which leads to instability in the hips and a tendancy or potential for subluxation or dislocation. These can persist into adulthood. It is either be picked up during newborn examinations or later when child present with hip asymmetry and reduced range of movement
83
what are the risk factors for developmental hip dysplasia?
first degree family history, breech presentation, multiple pregnancy
84
describe the screening for developmental hip dysplasia?
• Newborn examination and at 6-8 weeks
Findings suggestive of DDH
• Different leg lengths
• Restricted hip abduction on one side
• Significant bilateral restriction in abduction
• Difference in the knee level when the hips are flexed
• Clunking of the hips on special test
• Ortolani test
• Barlow test
• Clicking on examination Is common
85
describe how a diagnosis of developmental hip dysplasia is made?
ultrasound of hips if child is suspected of having DDH, X-ray can be helpful
86
describe the management of developmental hip dysplasia?
Pavlik harness (if less than 6 months) – keeps hips flexed and abducted / surgery if harness fails of older than 6 months
87
ROUTINE CARE OF NEWBORN
weight?
routine measurements of weight (mean of 3.5 kg at term), head circumference (mean 35 cm), body length (mean 50 cm).
It is normal to lose up to 10 % of birth weight in the first few days
88
ROUTINE CARE OF NEWBORN
what is the role of giving vitamin K
prevent the haemorrhagic disease of the newborn.
routinely offered to all babies (orally or IM)
breast fed babies require 3 oral doses because breast milk contains less vit K than formula
89
ROUTINE CARE OF NEWBORN
cord
The cord is clamped, the umbilicus is kept clean and dry.
The cord usually detaches after a week.
90
ROUTINE CARE OF NEWBORN
delivery of the baby
Babies should be delivered in a warm room, rapidly dried with a warm towel, and then immediately wrapped or placed skin to skin on the mother’s front and then covered with a warm towel and a hat.
91
ROUTINE CARE OF NEWBORN
what routine observations are done daily
pulse, RR and temperature
92
What is vernix?
white waxy substance often present especially in preterm infants.
thought to provide insulation and lubrication
93
DEFINE
1. stillbirth
2. perinatal mortality rate
3. infant mortality rate
1. baby >24 weeks gestation showing no signs of life after delivery
2. stillbirths and deaths within first week of life per 1000 births (about 7/1000 in UK)
3. number of deaths in 1st year of life per 1000 live born infants (about 5/1000 in UK)
94
importance of the umbilical cord
2 arteries and 1 vein
after clamping it dries up and seperates within first week
can be site of infection
95
what is meconium?
green-black stool passed by babies in first days after birth
fresh meconium -stained liqor can be sign of fetal distress but can be normal in full term infants
asphyxiated gasping baby can aspirate meconium into lungs causing respiratory distress
96
NEWBORN BABY
first breath
interuption to umbilical blood flow and response to cold stimulates baby to take first breath within a minute of birth
lung fluid is actively reabsored as well as being expelled during delivery
surfactant in alveoli helps them to expand and fill with air
most babies can be dried, covered and given straight to the mother
occasionally the onset of breathing may be delayed and baby require resuscitation
97
describe the Agpar score
describes the condition of infant after birth. Severly compromised babies will require intubation, cardiac massage, IV drugs such as adrenaline and bicarbonate
used to describe the infants condition at birth
score 0-10 recorded at 1 min and 5 min of birth
scored between 0-10
normal score at 1 min is 7-10
babies with a score of 0-3 at 1 min require rapid resuscitation or they will die
98
what is assessed in the agpar score?
heart rate
respiration
tone
reflex to suction
colour
99
NEWBORN
in what situation may resuscitation be needed?
prematurity, foetal distress, thick meconium staining of the liquor, emergency caesarean section, instrumental delivery, known congenital abnormality, multiple births
100
hypoxic-ischaemic encephalopathy
Infants in poor condition at birth may have suffered hypoxic or ischaemic insult during pregnancy/labour. An already compromised fetus may decompensate with build up of lactic acid which could lead to organ damage.
Severe hypoxia = Umbilica l cord blood gas samples assessed (severe asphyxia pH<7, agpar <5 at 10 mins, delay in spontaneous respiration beyond 10 mins, development of characteristic encephalopathy with abnormal neurological findings
101
causes of intrauterine growth retardatiion
multiple pregnancy, placental insufficiency, maternal smoking, congenital infections, genetic syndromes.
102
TORCH infection
toxoplasmosis, other (syphilis), rubella, cytometalovirus, hepatitis, HIV
103
vitamin K deficiency
Vitamin k deficiency can lead to obstructive jaundice leading to poor synthesis of vitamin K dependent clotting factors and bleeding resulting in bruising. Breast milk is low in vitamin K. vitamin K should be given routinely to all newborns as a single IM injection or by mouth at birth, 1 and 6 weeks
104
NEONATAL SEPSIS
how can neonatal infection be acquired?
transplacentally, by ascent from the vagina, during birth, or postnatally.
105
NEONATAL SEPSIS
how can infections be categorised?
Infections are categorized as early-onset (first 48 hours) or late-onset (>48 hours).
106
NEONATAL SEPSIS
what are the risk factors for early onset infection
prolonged rupture of membranes (>18 h), signs of maternal infection, preterm labour, previous delivery has Group B Streptococcus(GBS). 20-30% women colonised by GBS, 1% chance baby developing sepsis
Infection prior to birth usually due to ascending infection with chorioamnionitis.
107
NEONATAL SEPSIS
what are the risk factors for late onset sepsis?
central lines, congenital malformation. Early-onset neonatal infection (3/1000 live births) usually caused by GBS or E.Coli.
108
NEONATAL SEPSIS
1. how does it present
2. investigation
1. as temperature instability, lethargy, poor feeding, collapse.
2. blood culture, CSF to exclude meningitis, FBC, CXR
109
NEONATAL SEPSIS
management
with antibiotics, which is commenced promptly, can be stopped if the results come back negative. For example, it can take up to 5 days for PCR on the CSF sample to come back.
110
NEONATAL HYPOGLYCAEMIA
blood glucose after birth
blood glucose drops naturally in the first hours of lie after birth before normalizing – newborns have the ability to utilize ketones/lactate for energy
All infant should be encouraged to feed in first hour if well enough.
111
NEONATAL HYPOGLYCAEMIA
what groups are at risk of hypoglycaemia?
infant of a diabetic mother, less than <2500 g; <37/70 gestation; birth asphyxia
112
NEONATAL HYPOGLYCAEMIA
when should glucose be checked?
Always check glucose in all infants who are unwell/lethargic/jittery.
113
NEONATAL HYPOGLYCAEMIA
what can hypoglycaemia be suggestive of?
hypoglycaemia can be a symptom of sepsis, hypothermia as well as anything that causes a baby to have reduced glucose stores, for example, intrauterine growth restriction or being preterm.
114
NEONATAL HYPOGLYCAEMIA
how does it present?
Most often hypoglycaemia is asymptomatic, but can present as jitteriness, poor feeding, drowsiness, cerebral irritability.
115
MATERNAL OPIATE WITHDRAWAL IN NEONATE
Infants at risk of maternal opiate withdrawal should be observed for signs of withdrawal several days after birth, and supportive measures should be offered such as frequent low volume feeding, dark quiet environment. Only if significantly symptomatic, start on low dose oral morphine with an aim of weaning off over days.
116
MATERNAL OPIATE WITHDRAWAL IN NEONATE
signs and symptoms
high pitch cry
hyperirritability
seizures
sleep deprivation
sleep fragmntation
tachypnoea
hypertension
tachycardia
diarhhoea
excessive weight loss
vomiting
sneezing
excessive suck
poor or excessive feeding
yawning
sweating
hyperthermia
hypertonia
tremors
117
RESPIRATORY DISTRESS IN NEONATES
causes
prematurity, meconium aspiration, pneumothorax, congenital lung malformations, congenital lung malformations, congenital pneumonia, transient tachypnoea of newborn, aspiration of milk or airway obstruction
118
WEIGHT LOSS AND FEEDING IN NEONATES
Support mothers to breastfeed
Normal for babies to lose 5-10% birthweight after birth – if excessive can be due to failure of maternal lactation, can lead to hypernatraemic dehydration. Treat with giving additional milk via nasogastric tube
Feeding difficulties can also be of infant origin – down syndrome, micrognathia, tongue tie, cleft palate
119
CLEFT LIP AND PALATE
Cleft lip alone 35% / cleft lip and palate 25% / cleft palate alone 40%
Polygenic
Some drugs teratogenic: anticonvulsants, methotrexate
Cleft lip – diagnosed at 18-20 week scan
Isolated clept palate difficult to diagnose antenatally
Some can be breast fed, others need feeding devices, surgical repair at 6-12 months
120
PIERRE ROBIN ANOMALY
Association of micrognathia, posterior displacement of the tongue and midline cleft of the soft palate
Prone positioning maintains airway patency until growth of mabdible established
Cleft is surgically repaired
121
OESOPHAGEAL ATRESIA
Trachea-oesophageal fistula usually present
Fetus is unable to swallow during intrauterine life, associated polyhydramnios
Diagnose before first feed by attempting to pass feeding tube intostomach and checking location by x-ray
40% have associated abnormalities (VACTERL: vertebral, anorectal, cardiac, trache-oesophageal, renal, limb)
122
GASTROSCHISIS
Bowel protrudes without any covering sac through a defect in anterior abdominal wall adjacent to umbilicus
Usually isolated anomaly
123
EXOMPHALOS
Abdominal contents herniate through umbilical ring and are covered with a sac formed by peritoneum and amniotic membrane
Associated with other major congenital abnormalities
124
NEURAL TUBE DEFECTS
Due to failure of fusion of neural plate in first 28 days after conception
Incidence fallen since 70s due to maternal nutrition, folic acid supplementation, better antenatal screening
125
what are the 3 main types of neural tube defects
spina bifida occulta, meningocele, myelomeningocele
Usually in lumbosacral region
126
NEURAL TUBE DEFECTS
1. encephalocoele
2. anencephaly
1. extrusion of brain and meninges through midline skull defect
2. cranium and brain fail to develop
127
NEURAL TUBE DEFECTS
spina bifida occulta
dorsal vertebral arch fails to fuse, may be overlying skin lesion such as tuft of hair or small dermal sinus. Tethering of the cord can cause neurological deficits with growth
128
NEURAL TUBE DEFECTS
meningocele
uncommon. Smooth, intact,skin covered cystic swelling filled with CSF. No neurological deficit or hydrocephalus and excision and closure of defect undertaken after 3 months
129
NEURAL TUBE DEFECTS
myelomeningocele
90% of overt spina bifida. Open with herniation of both the cord and meninges, commonly leaking of CSF. Neurological deficits are always present and can include: motor and sensory loss in lower limb, neuropathic bladder and bowel. There is often scoliosis and associated hydrocephalus due to Arnold chiari malformation. Surgery prevents infection but doesn’t restore neurological function
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CONGENITAL TALIPES EQUNOVARUS
club foot
Entire foot is fixed in inverted and supinated position
Should be distinguished from ‘ positional talipes’ in which deformity is mild and can be corrected with passive manipulation
Refer to orthopaedic surgeons and physiotherapy early because treatment including serial casting is needed to prevent disability
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DOWNS SYNDROME
dysmorphic features
trisomy 21
hypotonia, brachycephaly, short neck, short stature, flattened face and nose, prominent epicanthic folds, upward sloping palpable fissures, single palmar crease
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DOWNS SYNDROME
complications
learning disability, recurrent otitis media, deafness, visual problems, hypothyroidism, cardiac defects (ASD, VSD, patent ductus arteriosus, tetralogy of fallot), atlantoaxial instability, leukaemia, dementia
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DOWNS SYNDROME
antenatal screening
- combined test (11-14 weeks gestation) – combines ultrasound (nuchal translucency) and maternal blood tests (beta HCG / A PAPPA)
- triple test – 14-20 weeks gestation – maternal blood tests (beta-HCG, alpha fetoprotein, serum oestriol – low indicates greater risk)
- quadruple test – 14-20 weeks gestation, same as triple test but also includes inhibin A maternal blood.
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DOWNS SYNDROME
antenatal testing
- screening gives risk score, when risk is greater than 1 in 150 women are offered amniocentesis or chorionic villus sampling
- chorionic villus sampling – ultrasound guided biopsy of placental tissue (before 15 weeks)
- amniocentesis – ultrasound guided aspiration of some amniotic fluid using needle and syringe, later in pregnancy
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DOWNS SYNDROME
non invasive prenatal testing
simple maternal blood tests
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DI GEORGE
Caused by microdeletion on chromosome 22q11.2
Most children have de novo microdeletion (15% inherited)
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DI GEORGE
features
cardiac defects (aortic arch), subtle dysmorphism (wide and prominent nasal bridge, down slanting eyes, small mouth), parathyroid aplasia/hypoplasia, thymus aplasia, short stature
Consider in children diagnosed with TOF or aortic arch abnormalities or those with CHD eg VSD who has hypernasal speech,cleft palate, submucous cleft palate, hypocalcaemia, asymmetric crying facies, recurrent infections, learning difficulties, speech and language delay
Diagnosis missed on routine chromosome analysis -need FISH study
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TURNER SYNDROME
When a female has a single X chromosome making them 45 XO
Life expectancy close to normal
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what are the features of turner syndrome
short stature, webbed neck, high arching palate, downward sloping eyes with ptosis, broad chest with widely spaced nipples, cubitus valgus, underdeveloped ovaries, late or incomplete puberty, most infertile
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TURNER SYNDROME
associated conditions
recurrent otitis media, recurrent UTI, coarctation of aorta, hypothyroidism, hypertension, obesity, diabetes, osteoporosis, various specific learning disabilities
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TURNER SYNDROME
management
growth hormone therapy, oestrogen and progesterone, fertility treatment
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NEONATAL JAUNDICE
1. how often is it?
2. what type is it usually>
3. what may significant jaundice indicate
4. what are the issues with high serum unconjugated free bilirubin
1. 60% term / 80% preterm
2. unconjugated
3. may indicate underlying disease
4. neurotoxic and cause kernicterus
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NEONATAL JAUNDICE
what can the causes be classified into/
due to increased production of bilirubin or decreased clearance of bilirubin
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NEONATAL JAUNDICE
describe the causes of increased bilirubin production
• Haemolytic disease of the newborn
• ABO incompatibility
• Haemorrhage
• Intraventricular haemorrhage
• Cephalo-haematoma
• Polycythaemia
• Sepsis and disseminated intravascular coagulation
• G6PD deficiency
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NEONATAL JAUNDICE
describe the causes of decreased clearance of bilirubin?
• Prematurity
• Breast milk jaundice
• Neonatal cholestasis
• Extrahepatic biliary atresia
• Endocrine disorders (hypothyroid and hypopituitary)
• Gilbert syndrome
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NEONATAL JAUNDICE
describe physiological jaundice
There is a high concentration of red blood cells in the fetus and neonate. These red blood cells are more fragile than normal red blood cells. The fetus and neonate also have less developed liver function. Fetal red blood cells break down more rapidly than normal red blood cells, releasing lots of bilirubin. Normally this bilirubin is excreted via the placenta, however at birth the foetus no longer has access to a placenta to excrete bilirubin. This leads to a normal rise in bilirubin shortly after birth, causing a mild yellowing of skin and sclera from 2 – 7 days of age. This usually resolves completely by 10 days. Most babies remain otherwise healthy and well.
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NEONATAL JAUNDICE
1. when does it occur
2. cause
3. how does it progress
1. Common and appears after 24 hrs, peaks around day 3-4 and usually resolves by 14 days
2. Due to immaturity of hepatic bilirubin conjugation, but poor feeding can also contribute
3. Jaundice progresses in cephalic-caudal direction
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NEONATAL JAUNDICE
1. when does action need to be taken in physiological jaundice?
Action needed when serum bilirubin is above gestation and age cut offs (>300umol/l in term infant at 72 hours
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NEONATAL JAUNDICE
treatment of physiological jaundice
stop bilirubin rising to level that may cause kernicterus
• Treat underlying cause eg sepsis
• Start ‘blue light’ phototherapy
• Use age/gestation specific charts to determine level to start phototherapy
• Measure SBR frequently
• Ensure adequate hydration
• Cover eyes for phototherapy
• Exchange transfusion with or without IV immunoglobulin if very high
• If within 24 hours assume pathological and start phototherapy, check SBR, FBC, direct coombs test and blood group, consider septic screen/TORCH
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NEONATAL JAUNDICE
what are the causes of jaundice within first 24 hours?
haemolysis, red cell enzyme defects, red cell membrane defects, sepsis, severe bruising
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NEONATAL JAUNDICE
what is prolonged jaundice and its causes?
(>14 days in term infant/ >21 days preterm)
• Causes: breastfeeding, enclosed bleeding, prematurity, haemolysis, sepsis, hypothryidism, conjugated jaundice, hepatic enzyme disorders
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NEONATAL JAUNDICE
investigations and treatment of prolonged jaundice
• Initial investigations: SBR, U&E, FBC, DCT, blood group, TFT, LFT, glucose
• Treatment: depends on cause, rarely phototherapy is beneficial eg crigler Najjar syndrome
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NEONATAL JAUNDICE
description and causes of conjugated jaundice
• Stools may be clay coloured in obstructive jaundice
• Causes – sepsis, TPN, biliary tract obstruction, viral hepatitis, TORCH, alpha antrypsin deficiency, cystic fibrosis, inspissated bile syndrome after haemolytic disease, galactosaemia, other inherited metabolic disease, idiopathic giant cell hepatitis
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NEONATAL JAUNDICE
investigations and treatment of conjugated jaundice
• Initial investigations: same as for prolonged jaundice, and radiology, enzyme testing, viral serology, liver biopsy, histology
• Treatment depends on cause
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NEONATAL JAUNDICE
describe jaundice in premature neonates?
Physiological jaundice is exaggerated due to immature liver increasing risk of complications such as kernicterus (brain damage due to high bilirubin levels)
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what is haemolytic disease of the newborn and its causes?
• Cause of haemolysis and jaundice in the neonate
• Causes by incompatablity between rhesus antigens on surface of RBC of mother and fetus
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BREASTFEEDING
when should breastfeeding be attempted
as soon as possible and within 2-3 days
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BREASTFEEDING
what is the difference shown on growth charts in breast fed babies?
Breastfed babies will weigh less than bottle fed on growth charts
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BREASTFEEDING
what is the correct position
babys chin touching breast but nose not touching. Slow, rhythmic jaw movements and suckling noises (first few sucks may be short and not draw milk)
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BREASTFEEDING
describe expressing milk?
practicality reasons, relieve painful breast engorgement, air nutrition (if baby poor suckler, taught by midwife, can be performed manually
Milk should be used within 48 hours if refrigerated, 3 months if frozen
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what are the benefits of breastfeeding?
• Reduce allergy risk (not long term risk)
• Macrophages, lymphocytes, IgA
• To get all benefits – don’t begin weaning until 6 months old, avoid cows milk until 1 yrs, avoid egg until 2 yrs, avoid nuts and fish until 3yrs
• Contains LCPs – involved with nervous development - increase IQ
• Reduced risk of obesity, insulin resistance, diabete
• Acid in milk promotes ‘friendly’ bacteria growth in bowel
• Reduces infant mortality, pneumonia and diarrhoea
• Bonding
• Reeuce necrotisng entercolitis
• Cheap
• Health benefits to mother - weight loss, ovarian and breastcancer risk reduction, promote uterine contractions (reduce risk of PPH if breast feeding occurs within minutes, promote oxytocin release (reduce anxiety)
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what are the contraindications to breastfeeding?
• HIV +ve
• Amiodarone
• Antithyroid drugs
• Opiates
• Antimetabolites
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what are the potential complications of breastfeeding?
• Breast engorgement
• Breast abscess
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BOTTLE FEEDING
• Not many contraindications
• Advertising formula milk is banned for <6 months
• Cost
• Advantages – others can take active role in feeding, some mothers like reassurance knowing the exact volume of feeds
• Measure correcty – underfed = reduced growth / overfed = hypernatraemia, constipation, obesity
• 150ml/kg/24hr in 4-6 feeds
• Younger – require more feeds
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what are the types of formula?
birth-1 year
follow on formula
soya milk
hydrolysed formula
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describe birth - 1 year formula?
• Altered cows milk with solute concentrations reduced and protein, fat and vitamin content altered
• Added LCPs, omega 3 +6
• Protein is in form of whey or casein
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describe follow on formula?
• High casein content
• 6 months onwards to 24 months
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describe formula soya milks?
• Strongly discouraged
• High levels of oestrogen like products which can cause hormonal problems in boys and thyroid problems and reduced immunity
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when is hydrolysed formula used?
Used when allergy to cows milk
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WEANING
1. why?
2. when?
1. iron stores low by 6 months, encourages oral motor skill, nutritional requirements not met by milk alone
2. no sooner than 6 months
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WEANING
what are the issues with late weaning?
• Increased risk of furture feeding problems
• New food textures needed to prevent fussy eating
• Risk of iron deficiency anaemia
• Risk of rickets
• Poor weight gain/growth
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what weight gain is expected per week for the following age groups
1. 0-3 months
2. 4-6 months
3. 7-9 months
4. 9-12 months
1. 200g
2. 150g
3. 100g
4. 50-75g
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VACCINATION SCHEDULE
8 weeks
1st 6 in 1
1st pneumococcal
1st rotavirus (oral)
1st Men B
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VACCINATION SCHEDULE
what is in the 6 in 1 vaccine
diptheria
tetanus
pertussis
polio
Hib
Hep B
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VACCINATION SCHEDULE
12 weeks
2nd 6 in 1
2nd rotavirus (oral
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VACCINATION SCHEDULE
16 weeks
3rd 6 in 1
2nd pneumococcal
2nd Men B
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VACCINATION SCHEDULE
12-13 months
Hib, men C
1st MMR
booster - pneumococcal
booster - Men B
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VACCINATION SCHEDULE
2 - 9 years
annual childrens flu vaccine
nasal spray
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VACCINATION SCHEDULE
3 years 4 months
booster 4 in 1
2nd MMR
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VACCINATION SCHEDULE
what is included in the 4 in 1
diptheria
tetanus
pertussis
polio
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VACCINATION SCHEDULE
12-13 yrs
HPV
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VACCINATION SCHEDULE
13-18 years
booster - 3 in 1
men ACWY
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VACCINATION SCHEDULE
what is in the 3 in 1
diptheria
tetanus
polio
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what is sudden infant death syndrome?
the sudden and unexpected death of a child under 1 for which no adequate case is found after a thorough post morten and case report
Causes 40% of death in infants under a week old
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SIDS
what is the triple risk model
-environmental factors
-infants at higher risk of other medical problems (preterm)
-many physiological changes happen between 2-4 months
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SIDS
child related risk factors
• 1-6 months (peak at 12 weeks)
• Preterm or very low birth weight
• M>F
• Multiple births
• Family history
• Maternal age (increased risk if under 20)
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SIDS
environmental risk factors
• Low SES
• Single parents
• Smoking
• Co-sleeping
• Winter
• Sleeping on front (8x)
• Sleeping on side (2x)
• Coexistant illness
• Baby overheats at night
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SIDS
what is the back to sleep campaign?
• Sleep on back with feet at foot of bed
• Don’t use pillows and avoid blankets/hats
• Sleep in parents room for 6 months
• Don’t smoke
• Don’t bring baby into bed with you
• Don’t sleep with infant in chair
• Prompt health if infant is unwell
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SIDS
what steps should be taken after SIDS?
• Document everything, notify relevant people, do bloods, sample infants clothing and bedding, autopsy and coroners inquest, reassure family that its no-ones fault, non accidental injury?, suppression of lactation
CONI – care of next infant
• Supports patients who’ve previously have a child die from SUID giving extra support, home visits, resuscitation training, equipment such as movement monitors
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FAIURE TO THRIVE
what is it?
• Failure to grow at expected rate (growth falls away from standardised weight or height centile)
• Weight is the most sensitive indicator in infants and young children, height better in older children
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causes of failure of thrive
• 95% due to not enough food offered or taken
• In developing countries – poverty is main cause
• Uk- socioeconomic difficulties, emotional deprivation,unskilled feding or belief systems regarding appropriatenutrition
• Organic causes
• Decreased appetite
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organic causes of failure to thrive?
• Decreased appetite
• Inability to ingest
• Excessive food loss (gastro-oesophageal reflux,pyloric stenosis, dysmotility, DM)
• Malabsorption
• Increased energy requirements (congenital heart disease, cystic fibrosis, malignancy, sepsis)
• Impaired utilisation (IEM, endocrinopathies)
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management of failure to thrive
• History: age of onset of FTT, timing of weaning, dietary history
• Full examination – accurate growth measurement
• If organic disease possible: FBR, ESR/CRP, U&E, creatinine, total protein and albumin, calcium, PO4 3-, LFT, immunoglobulins, coeliac antibody screens, urinalysis
• Further investigation is suggestive symptoms or the faltering growth is severe: IEM screen, karyotype, serum lead (pica), sweat test, upper endoscopy, small intestinal biopsy, CXR, bone age, skeletal survey, abdominal US, head CT/MRI, oesophageal pH monitoring, ECG, faecal occult blood
• If non organic disease – seek dietary advice
• If resolves in few weeks give positive reinforcement and supervise as outpatient
• If persists- admit for investigation and observe response to superised dietary input (adequate growth in hospital suggests non organic cause)
• If FTT continues at home after improvement in hospital refer to social services
• If FTT continues in hospital, organic disease most likely
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clinical features of gastro-oesophageal reflux
• Mild symptoms
• Regurgitation/posseting
• In a minority symptoms can be severe and cause problems such as failure to thrive, oesophagitis or recurrent aspiration pneumonia
• Recurrent regurgitation or vomiting
• Oesophagitis might be manifested by irritability, features of pain after feeding
• Blood in vomit
• Iron deficiency anaemia
• Can cause recurrent aspiration pneumonia, FTT, cough, bronchospasm (with wheezing) and bronchiectasis
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risk factors for gastro-oesophageal reflux?
At risk: preterm (especially with chronic lung disease), children with cerebral palsy, infants with congenital oesophageal anomalies eg after repair of trachea-oesophageal fistula
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diagnosis of gastro-oesophageal reflux?
• Clinical diagnosis
• 24 hr oesophageal pH monitoring in older children or impedance studies in infants
• Barium studies – exclude underlying anatomical abnormalities
• Endoscopy – indicated in patients with suspected oesophagitis
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management of mild gastro-oesophageal reflux?
For most mildly affected infants, reassurance is required and 95% resolve by 18 months
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what might more troublesome gastro-oesophageal reflux respond to?
More troublesome reflux may respond to thickening the feed with inert carob-based agents
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what drugs can be used to manage severe gastro-oesophageal reflux?
• Prokinetics such as domperidone – speed gastric emptying and increase lower oesophageal sphincter pressure
• Drugs to reduce gastric acid secretion (H2 antagonists or PPIs)
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what surgery can be considered for severe gastro-oesophageal reflux with complications?
Nissen fundoplication (fundus of stomach is wrapped around lower oesophagus
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presentation of cleft lip and palate?
Split or open section of the upper lip, cleft palate is where a defect exists in hard or soft palate leaving an opening between mouth and nasal cavity
Occur randomly
Not life threatening but can cause issues with feeding, swallowing and speech
Psycho-social implications
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management of cleft lip and palate
Refered to local cleft lip services
MDT
Nurses,
Plastic, maxillofacial and ENT surgeons, dentist, speech and language therapists, psychologists, GP
Ensure able to eat and drink – special shaped bottes and teats
Surgery to correct usually at 3 months for lip or 6-12 months for cleft palate
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Hirschprung's disease
presentation
Absence of ganglions in a segment of the bowel
Failure to pass meconium, abdominal distension, pain and vomiting, poor weight gain, can lead to enterocolitis
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Hirscchprungs disease management
Surgical resection of abnormal bowel followed by reanastomosis
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oesophageal atresia presentation
Oesophagus ends in a blind ended pouch rather than connect to stomach
Attempt at feeding could cause aspiration pneumonia, stomach acid could flow into lungs
Can coexist with other birth defects VACTERL
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oesophageal atreasia
management
Close fistula surgically and connect the 2 ends of oesophagus
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trachea-oesophageal fistula presentation
Abnormal connection between oesophaus and trachea
Copious salivation, choking, coughing, vomiting, cyanosis
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trachea-oesophageal fistula management
Resection of any fistula and anastomosis of any discontinuous segments
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hypospadias presentation
Urethra doesn’t open in usual location in head of penis
Characteristic appearance, meatus lower, foreskin only partially developed
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hypospadias
management
Not serious condition
Delay surgery until child old enouth to consent
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inguinal hernia presentation
Bulge in groin or scrotum
Severe pain, vomiting, no appetite, redness, bruising
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inguinal hernia management
All are repaired
Surgical (laparoscopic)
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undescended testis
management
If haven’t descended by 6 months unlikely to do so
Orchidopexy to move testicles into correct position
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hydrocele
presentation
Accumulation of serous fluid in body cavity
No pain
Testicle appears swollen
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