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Phase 3a > Paeds Neonatal medicine > Flashcards

Paeds Neonatal medicine Flashcards

1
Q

what are some causes of SGA?

A
  • constitutional - small parents
  • restricted foetal oxygen or glucose supple
  • fetal abnormality
  • maternal substance exposure
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2
Q

what are the complications of SGA?

A

increased risk of fetal death and asphyxia
hypoglycaemia
hypothermia
polycythaemia
NEC
thrombocytopenia/neutropenia/coagulopathy
meconium aspiration syndrome

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3
Q

what are the causes of LGA

A 
most frequently constitutional - large parents
mother has DM
fetal hyperinsulinemia
pancreatic islet cell hyperplasia 
hydrops fetalis 
Beckwith-Wiedemann syndrome
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4
Q

what are the complications of LGA?

A 
perinatal asphyxia 
nerve palsies 
shoulder dystocia 
fractures 
hypoglycaemia
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5
Q

what are some predisposing factors for prematurity?

A 
idiopathic 
previous preterm birth 
multiple pregnancy 
maternal illness 
PROM
uterine malformation 
cervical incompetence 
placental disease
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6
Q

what are the problems associated with prematurity?

A

Resp problems : surfactant deficiency causing resp distress syndrome, apnoea of prematurity, chronic lung disease

CNS: intraventricular haemorrhage, periventricular leukomalacia , retinopathy of prematurity

GI: NEC, inability to suck, poor milk intolerance

Hypothermia, immuno-compromised, impaired fluid/electrolyte homeostasis, PDA, anaemia of prematurity, jaundice, perinatal hypoxia

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7
Q

why are steroids given to mother if prematurity is suspected?
what steroids should be given?

A

dexamethasone

reduces severity of respiratory distress syndrome, NEC and periventricular haemorrhage.

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8
Q

what are different types of birth trauma?

A

head: caput succedaneum (oedema presenting on the scalp), Cephalohematoma, Subaponeurotic haematoma

Skin: traumatic cyanosis, lacerations

Nevre palsies: brachial plexus (Erb’s palsy), facial nerve palsy

Fractures - clavicle, long bone, skull. treatment = analgesia, limb immobilisation

soft tissue trauma - sternocleidomastoid tumour - overstretching of the muscles leads to haematoma, fat necrosis

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9
Q

what are some causes of the non-specifically ill neonate?

A 
infection 
hypothermia 
metabolic - inborn errors of metabolism 
cardiac
GI
CNS
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10
Q

how might the ill neonate present?

A

Skin: pallor, mottling, peripheral cyanosis, cool peripheries, cap refil>2seconds, rash, jaundice

Temp - up or down

CNS: lethargy, weak, unusual cry, hypotonia, irritability, jittery, seizures

Resp: apnoea, expiratory grunting, flaring nostrils, tachypnoea, intercostal or subcostal recession, tracheal tug

CVS: tachycardia, weak or absent pulses or hypotension should be considered late/pre-terminal signs

GI: vomiting, distended abdomen (ileus), diarrhoea, bloody stools, abdo tenderness, bilious vomit or aspirate

Metabolic - increased or decreased BG

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11
Q

how do you manage an non-specifically ill neonate?

A

assess ABC
secure airway - give O2 and provide ventilatory support if needed
transfer to neonatal unit
obtain vascular access and give bolus 0.9% saline 10-20mls/kg if circulatory compromise
monitor breathing
measure BP, blood glucose, U&E, FBC, blood gas
full septic screen (blood cultures, CXR/AXR, LP, C&S,
consider cranial USS if preterm/at risk
start a broad spectrum antibiotic (e.g. gentamycin)
if meningitis suspected give cefotaxime
if listeria infection give benzylpenicillin

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12
Q

what is physiological jaundice?

A

it is common and appear after 24 hours and peaks around day 3-4 and usually resolves by day 14
it is due to immaturity of hepatic bilirubin conjugation, but poor feeding can also contribute.

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13
Q

how do you treat elevated serum bilirubin above the gestation and age cut offs?

A
  • you need to stop it rising to the level that might cause kernicterus
  • treat the underlying cause
  • start blue light phototherapy (makes it so bilirubin can be excreted in urine)
  • use age/gestation charts to determine when to start phototherapy
  • measure SBR frequently
  • ensure adequate hydration
  • cover eyes during phototherapy
  • IVIG can be added
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14
Q

what is the presumption if jaundice occurs in the first 24 hours of life?

A

that it is pathological

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15
Q

what is considered prolonged jaundice

A

> 14 days in term infants

>21 days in preterm infants

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16
Q

what are some causes of prolonged jaundice

A 
breastfeeding (usually resolves by 12 weeks)
enclosed bleeding (cephalhaematoma) 
prematurity 
haemolysis 
sepsis
hypothyroidism 
conjugated jaundice
hepatic enzyme disorders
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17
Q

what initial investigations would you perform for prolonged jaundice?

A 
SBR (total and conjugated)
U&E
FBC
direct coombs test
blood group 
TFTs
LFTs
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18
Q

what is kernicterus?

A

Kernicterus is diagnosed pathologically by gross yellow staining and necroses of neurons in the basal ganglia, hippocampal area, and cerebellum. It occurs secondary to the entry of bilirubin into the brain, which causes a disruption of cellular energy metabolism in the basal ganglia, hippocampal area, and cerebellum.

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19
Q

if the neonate survives what are the clinical features of kernicterus?

A

Cerebral cortex is usually spared. If the neonate survives, the clinical features include chorio-athetoid cerebral palsy, paralysis of upward gaze, sensorineural hearing loss, dental dysplasia, and intellectual deficits (less often in the mental retardation range)

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20
Q

what are some causes of neonatal hypoglycaemia?

A

reduced glucose stores: preterm, UUGR, LBW, inborn errors of metabolism

Increased glucose consumption: sepsis, hypothermia, perinatal hypoxia, polycythaemia, haemolytic disease, seizures

hyperinsulinemia: maternal DM, BWS, pancreatic islet cell hyperplasia

maternal beta blockers, tissued or malfunctioning IV infuxion

other rare causes - fetal alcohol syndrome, pituitary insufficiency, adrenal insufficiency

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21
Q

how might neonatal hypoglycaemia present?

A 
commonly asymptomatic 
jitteriness
apnoea
poor feeding
drowsy 
seizures 
cerebral irritability 
hypotonia 
macrosomia
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22
Q

how do you manage severe/symptomatic hypoglycaemia in neonates?

A

IV bolus 3-5mL/kg of glucose 10%

follow with 10% glucose infusion IV (4-6mg/kg/min)

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23
Q

what are some causes of neonatal seizures?

A

brain injury
CNS infection
cerebral malformation
metabolic causes (hypoglycaemia, hypo/hypernatremia , hypocalcaemia, hypomagnesia)
neonatal withdrawal from maternal substance abuse
kernicterus

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24
Q

how should you manage neonatal seizures?

A

give oxygen, maintain airway, insert IV, treat underlying cause
first line anticonvulsant - IV phenobarbital, second line IV clonazepam

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25
what is given to neonates to prevent haemorrhagic disease of the newborn??
vitamin K
26
what are the advantages of breast feeding?
decrease maternal post partum haemorrhage mild maternal contraceptive effect increased bonding decreased maternal breast cancer risk cheap decreased infant mortality decreased GI and resp infection rate dcreased later autoimmune disease incidence
27
what are the contraindication to breastfeeding?
positive maternal HIV status certain maternal medications (amiodarone) maternal herpes zoster over breast infantile galactosaemic or phenylketonuria primary lactose intolerance
28
what is respiratory distress syndrome ?
it refers to lung disease caused by surfactant deficiency - largely seen in pre-term infants. It is rare in >32 weeks gestation
29
what are the risks/causes for RDS?
``` CS delivery hypothermia perinatal hypoxia meconium aspiration congenital pneumonia maternal diabetes past fam history ```
30
what is the presentation of RDS?
cyanosis tachypnoea chest in drawing grunting within 4 hours of birth
31
what investigations would you perform for RDS?
CXR - bilateral, round glass appearance, airway bronchograms, reduced lung volume and indistinct heart border SpO2 monitoring and blood gasses
32
how do you manage RDS?
prevention during pregnancy: maternal corticosteroids to induce fetal lung maturation oxygen assisted ventilation exogenous surfactant given via endotracheal tube - should be considered if extremely preterm antibiotics e.g. penicillin and gentamycin until congenital pneumonia has been excluded as it can mimic RDS nutrition - iv fluids
33
what is bronchopulmonary dysplasia?
a form of chronic lung disease that affects infants who have been born preterm. Now BPD is a condition of impaired alveolar development - mechanical, oxidative and inflammatory factors all contribute to lung injury
34
what are the risk factors for Broncho-pulmonary dysplasia?
``` gestational immaturity low birth weight males Caucasian heritage IUGR family history of asthma history of chorioamnionitis ```
35
what are the symptoms of bronchopulmonary dysplasia?
``` breathlessness difficulty feeding cough wheeze poor growth hyperinflated chest increased work on breathing abnormal breath sounds evidence of pulmonary hypertension ```
36
what is chronic lung disease of prematurity defined as?
the need for supplemental oxygen at or beyond 36 weeks post-menstrual age
37
what is old BPD?
when long periods of mechanical ventilation for RDS leading to lung damage
38
what is hypoxic-ischaemic encephalopathy?
clinical syndrome of brain injury secondary to a hypoxic-ischaemic insult
39
what are the causes of hypoxic-ischaemic encephalopathy?
decreased umbilical blood flow e.g. cord prolapse decreased placental gas exchange e.g. placental abruption decreased placental perfusion maternal hypoxia inadequate postnatal cardiopulmonary circulation
40
how does hypoxic-ischaemic encephalopathy present?
it varies depending on the severity of cerebral hypoxia there may be a range of symptoms and signs affecting: - level of consciousness, muscle tone, posture tendon reflexes, suck, heart rate, and CNS homeostasis
41
how should you manage hypoxic-ischaemic encephalopathy?
- resuscitation at birth; insert IV +/- arterial lines - avoid hyperthermia - assess eligibility for therapeutic hypothermia - start cerebral function analysis monitoring - assess for features of dysmorphism and birth trauma - assess neurological features - exclude other causes of encephalopathy (e.g. meningitis, metabolic disturbances, maternal drugs, CNS malformation and haemorrhage. - expect and manage multi-organ failure - monitor and maintain homeostasis
42
what is the gold standard treatment for hypoxic-ischaemic encephalopathy?
therapeutic hypothermia lower temperature to 33-34 within 6 hours of the insult hypothermia is maintained for 72 hours before gradual rewarming
43
what is necrotising enterocolitis ?
Necrotising enterocolitis is one of the leading causes of death among premature infants. Initial symptoms can include feeding intolerance, abdominal distension and bloody stools, which can quickly progress to abdominal discolouration, perforation and peritonitis.
44
what are the causes of NEC?
multifactorial - severe intestinal necrosis is end result of an exaggerated immune response within the immature bowel leading to inflammation and tissue injury. It rarely occurs before milk feeding commences but the timing of the first feed appears not to be relevant predisposing factors: prematurity, IUGR, hypoxia, polycythaemia, exchange transfusion , hyperosmolar milk feeds
45
how does NEC present ?
it usually presents in the second week after birth early signs: non specific illness, vomiting/bilious aspirate from gastric tube, poor feed toleration, abdo distension Late: additional abdominal tenderness, blood/mucus/tissue in stools, bowel perforation, shock, DIC, pneumatosis intestinalis, hepatic portal venous gas, signs of intestinal perforation
46
what would you see on an abdominal XR with a neonate with NEC?
dilated bowel loops (often asymmetrical in distribution) bowel wall oedema pneumatosis intestinalis (intramural gas) portal venous gas pneumoperitoneum resulting from perforation air both inside and outside of the bowel wall (Rigler sign) air outlining the falciform ligament (football sign)
47
what is the management of NEC?
Prophylaxis: antenatal steroids and breast milk are protective IV Abx for 10-14 days (benzylpenicillin, gentamycin and metronidazole) systemic support - assisted ventilation, correct BP and DIC, parenteral nutrition Surgical opinion - indications for surgery and GOI perforations, deterioration despite medical intervention (necrotic bowel likely), GI obstruction
48
what investigations would you perform for NEC?
``` FBC U&E creatinine coagulation screen albumin blood gas blood culture AXR ```
49
what staging can be used to grade severity of NEC?
Bells staging of NEC stage 1: suspected NEC stage 2: definite NEC stage 3: advanced NEC
50
what are the causes of orofacial clefts?
multifactorial and includes genetic and environmental factors environmental factors: maternal folic acid deficiency, maternal exposure to alcohol, tobacco, steroids, anticonvulsants and retinoic acid 30% ore syndromic e.g. Pierre-Robin syndrome
51
how do treat orofacial clefts?
refer to specialist cleft lip and palate MDT surgical repair of lip is usually at 3 months, palate is at 6-12 months later on speech therapy and dental input may be needed.
52
what are the problems of orofacial clefts?
feeding: orthodontic devices may be helpful speech: with speech therapy 75% of children develop normal speech increased risk of otitis media for cleft palate babies
53
what are the commonest variants of orofacial clefts?
isolated cleft lip (15%) isolated cleft palate (40%) combined cleft lip and palate (45%)
54
what is meconium aspiration syndrome?
Meconium aspiration syndrome refers to respiratory distress in the newborn as a result of meconium in the trachea. It occurs in the immediate neonatal period. It is more common in post-term deliveries, with rates of up to 44% reported in babies born after 42 weeks. It causes respiratory distress, which can be severe. Higher rates occur where there is a history of maternal hypertension, pre-eclampsia, chorioamnionitis, smoking or substance abuse.
55
what would a CXR show in an infant with meconium aspiration syndrome?
generalised lung over inflation with patchy collapse/consolidation +/- air leaks
56
how should meconium aspiration syndrome be managed?
supplemental oxygen intermittent positive pressure ventilation or high frequency oscillatory ventilation if ventilation required give surfactant and antibiotics
57
what is meconium ileus?
Usually delayed passage of meconium and abdominal distension The majority have cystic fibrosis X-Rays will not show a fluid level as the meconium is viscid, PR contrast studies may dislodge meconium plugs and be therapeutic Infants who do not respond to PR contrast and NG N-acetyl cysteine will require surgery to remove the plugs
58
how is meconium ileus managed?
Gastograffin enema | Laparotomy for unsuccessful enema
59
what can cause bilious vomiting in neonates?
``` Duodenal atresia Malrotation with volvulus Jejunal/ileal atresia Meconium ileus NEC ```
60
``` what is duodenal atresia? who is it common in? How will it present? what will XR show? how is it treated? ```
Duodenal atresia is the congenital absence or complete closure of a portion of the lumen of the duodenum. It causes increased levels of amniotic fluid during pregnancy ( polyhydramnios) and intestinal obstruction in newborn babies common in trisomy 21 it will present with bile-stained vomiting AXR will show double bubble sign of gas in the stomach and proximal duodenum surgical treatment: side to side duodenoduodenostomy the prognosis is excellent
61
what is small bowel atresia? what are the clinical features? what would you see on an XR? was is the treatment?
a type of intestinal atresia where there is a gap in the bowel causing complete blockage/obstruction of the bowel - usually caused by vascular insufficiency in utero Clinical features - bile stained vomit and abdo distension shortly after birth AXR will show air-fluid levels treated with laparotomy - end to end anastomosis - the prognosis depends on the length of the remaining bowel
62
what is oesophageal atresia
Associated with tracheo-oesophageal fistula and polyhydramnios May present with choking and cyanotic spells following aspiration VACTERL associations
63
what is VACTERL association
``` vertebral anomalies Anorectal anomalies cardiac anomalies TOF renal abnormalities Limb abnormalities ```
64
how is oesophageal atresia diagnosed?
passage of 10F NGT CXR - the tube stops in the upper thorax. Air in the stomach indicated a fistula between the trachea and the distal oesophagus (TOF)
65
how should oesophageal atresia be managed?
- the baby should be kept warm and disturbed as little as possible - the upper oesophageal pouch should be aspirated regularly by oropharygneal suction or a Replogle tube standard IV fluids started preoperative antibiotics are not required unless there is evidence of aspiration pneumonia babies who require mechanical ventilation must be referred urgently for surgery because gas will escape down the TOF and produce progressive gastric distension, which impairs ventilation further, ultimately leading to gastric perforation.
66
what is Gastroschisis?
Gastroschisis is a birth defect of the abdominal (belly) wall. The baby's intestines are found outside of the baby's body, exiting through a hole beside the belly button. The hole can be small or large and sometimes other organs, such as the stomach and liver, can also be found outside of the baby's body.
67
how is Gastroschisis managed?
Immediate - cover the exposed bowel with clingfilm keep the baby warm and hydrated AXR is NOT necessary Surgery: the defects require surgical closure as rapidly as possible. Often this has to be staged using a silo because the abdomen is too small to accommodate the intestine. The silo is reduced serially over a period of 1-2 weeks and then secondary closure of the defect is performed Nutritional - total parenteral nutrition may be required for many weeks because the intestinal function is slow to resume after the abdominal wall is closed. However, the long-term outcome is excellent.

Phase 3a (41 decks)

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