PAEDS NEONATAL Flashcards

(145 cards)

1
Q

PAEDIATRIC LIFE SUPPORT
What is the first step of neonatal resuscitation?
How does it differ if the baby is <28w?

A
  • Warm + dry baby ASAP by vigorous drying (may stimulate breathing)
  • Heat lamp
  • Babies <28w in plastic bag while still wet + manage under heat lamp
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2
Q

PAEDIATRIC LIFE SUPPORT
What should be calculated whilst neonatal resuscitation occurs?
What is the next stage?

A
  • APGAR at 1, 5 + 10m
  • Stimulate breathing with vigorous drying
  • Place baby’s head in neutral position to keep airway open (towel under shoulder can help)
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3
Q

PAEDIATRIC LIFE SUPPORT
If breathing stimulation fails what is the next stage of neonatal resuscitation?

A

Inflation breaths if gasping or not breathing –

  • 2 cycles of 5 inflation breaths
  • No response + HR low = 30s of ventilation breaths
  • No response, HR <60bpm = chest compressions (3:1 with ventilation breaths)
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4
Q

PAEDIATRIC LIFE SUPPORT
You come across an unconscious child.
What are the first steps you would perform?

A
  • Danger = ensure safety
  • Unresponsive = shout for help
  • Open airway = head tilt + chin lift or jaw thrust
  • Look, listen + feel for breathing (noisy gasps do not count)
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5
Q

PAEDIATRIC LIFE SUPPORT
It appears that this child is not breathing.
What is your next step and explain how this would differ depending on the child’s age?

A
  • 5 rescue breaths
  • Infants = neutral position, cover mouth + nose with whole mouth
  • > 1y = head tilt chin lift, pinch soft part of nose + seal mouths
  • Ensure chest rise/fall for effectiveness (if not ?obstruction or try jaw thrust)
  • Note any gag or cough response to actions as sign of life
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6
Q

PAEDIATRIC LIFE SUPPORT
You have performed your 5 rescue breaths but there was no coughing or response to your efforts
What should be done next?

A

Check circulation –

  • Infant = brachial or femoral
  • Child = femoral or carotid
  • If pulse felt = continue rescue breathing until child takes over
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7
Q

PAEDIATRIC LIFE SUPPORT
You do not feel a pulse.
What should you do now?

A
  • Chest compressions 15:2 rescue breaths
  • Depress sternum by one-third depth of chest
  • Rate of 100-120bpm
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8
Q

PAEDIATRIC LIFE SUPPORT
How will your CPR technique depend on the child?

A
  • Infant = tips of two fingertips or encircle with thumbs
  • > 1y = heel of 1 hand on lower sternum
  • Larger = 2 hands interlocked as for adults
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9
Q

PAEDIATRIC LIFE SUPPORT
You are at a restaurant and notice a situation at the table next to you and offer support. A child appears to be choking.
What would indicate an effective cough and how would you manage this?

A
  • Loud, responsive, able to breathe, verbal
  • Encourage cough + continue to observe for deterioration or until obstruction relieved
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10
Q

PAEDIATRIC LIFE SUPPORT
What would indicate an ineffective cough and how would you manage this?

A
  • Unable to vocalise/breathe, cyanosis, silent/quiet cough
  • Conscious = 5 back blows, 5 thrusts
  • Unconscious = open airway, 5 breaths, CPR
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11
Q

PAEDIATRIC LIFE SUPPORT
How do the choking techniques differ for age?

A
  • Chest thrusts for infant, abdominal if >1y
  • Infants head down prone for back blows, supine for thrusts
  • Back blows more effective if child’s head down
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12
Q

PREMATURITY
What are some respiratory complications of prematurity?

A
  • Apnoea,
  • RDS,
  • bronchopulmonary dysplasia,
  • infections
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13
Q

PREMATURITY
What causes feeding problems in prematures babies?
How quickly should you build up feeds and why?

A
  • Unable to suck + swallow until 33–34w so will need NG
    • Build feeds up slowly to reduce risk of NEC
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14
Q

PREMATURITY
What causes hypoglycaemia?

A

Lack of glycogen stores

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15
Q

RDS
What is the pathophysiology respiratory distress syndrome (RDS)?

A
  • Inadequate surfactant > high surface tension within alveoli
  • Leads to atelectasis (lung collapse) as more difficult for alveoli + lungs to expand so there’s inadequate gas exchange > hypoxia, hypercapnia + respiratory distress
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16
Q

RDS
What are some risk factors of RDS?

A
  • Prematurity #1
  • Maternal DM
  • 2nd premature twin
  • C-section
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17
Q

RDS
What is the clinical presentation of RDS?

A
  • Tachypnoea >60bpm
  • Increasing oxygen need
  • Laboured breathing = sternal + subcostal indrawing, nasal flaring, grunting
  • Cyanosis if severe
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18
Q

RDS
What is the investigation for RDS?

A

CXR –

  • Reticular “ground-glass” changes
  • Heart borders indistinct
  • Air bronchograms
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19
Q

RDS
What are the short and long term complications of RDS?

A
  • Short = pneumothorax, infection, apnoea, necrotising enterocolitis
  • Long = bronchopulmonary dysplasia, retinopathy of prematurity
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20
Q

RDS
What emergency treatment is required before the delivery of any preterm infant?

A
  • Antenatal dexamethasone
  • Increases surfactant production
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21
Q

RDS
What is the management of RDS?

A
  • Assisted ventilation by CPAP keeping lungs inflated or intubation if severe
  • Endotracheal surfactant via endotracheal tube
  • Supplementary oxygen for SpO2 91–95%
  • Breathing support gradually stepped down as baby develops
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22
Q

NEC. ENTEROCOLITIS
What is necrotising enterocolitis?

A
  • Disorder affecting premature neonates where part of bowel becomes necrotic
  • Associated with bacterial invasion of ischaemic bowel wall
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23
Q

NEC. ENTEROCOLITIS
What are some risk factors for necrotising enterocolitis?

A
  • Very LBW + premature
  • Formula feeds (breast milk protective)
  • RDS + assisted ventilation
  • Sepsis
  • PDA + other CHD
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24
Q

NEC. ENTEROCOLITIS
What is the clinical presentation of necrotising enterocolitis?

A

SYMPTOMS
- non-specific
- bilious vomiting
- altered stool pattern

SIGNS
- neonate in first few weeks of life
- abdominal distention
- bloody mucoid stool
- decreased bowel sounds
- palpable abdominal mass
- ascites
- bradycardia
- shock (lethargy, respiratory distress, temperature instability)

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25
NEC. ENTEROCOLITIS What are some investigations for necrotising enterocolitis?
- FBC = thrombocytopaenia and neutropenia - U&Es = deranged electrolytes - CRP = raised - blood gas = acidosis, raised lactate - abdominal x-ray = bowel wall thickening, gas filled loops, gaseous distention to consider - bowel USS = increased bowel wall thickness + echogenicity, free fluid collection, loss of bowel wall perfusion
26
NEC. ENTEROCOLITIS What would an AXR show in necrotising enterocolitis?
- Dilated loops of bowel - Bowel wall oedema (thickened bowel walls) - Pneumatosis intestinalis (intramural gas) - Pneumoperitoneum (free gas in peritoneum = perf) - Football sign = air outlining falciform ligament - Rigler's sign = air both inside/outside bowel wall - Gas in portal veins
27
NEC. ENTEROCOLITIS What are some complications of necrotising enterocolitis?
- Dead bowel > perforation + peritonitis > sepsis + shock - Stricture formation - Short bowel syndrome (malabsorption) if extensive resection required
28
NEC. ENTEROCOLITIS What is the management of necrotising enterocolitis?
STAGE 1 - conservative = NG tube, IV fluids, parenteral nutrition - medical = IV antibiotics (triple therapy), paracetamol +/- morphine STAGE 2 & 3 - conservative = NG tube, discuss with surgical team - medical = correct electrolytes, IV morphine, IV antibiotics (triple therapy) - surgical = laparotomy +/- bowel resection
29
JAUNDICE What is jaundice?
- Abnormally high levels of bilirubin in the blood
30
JAUNDICE What are some risk factors for jaundice?
- LBW - Breastfeeding - Prematurity - FHx - Maternal diabetes
31
JAUNDICE Jaundice can be split into 3 aetiological time categories. What are these?
- <24h = always pathological, usually haemolytic disease - 24h–2w = common - >2w = also bad
32
JAUNDICE What are some causes of jaundice <24h after birth?
- Haemolytic diseases #1 = rhesus or ABO incompatibility, G6PD, spherocytosis - Congenital infection (TORCH), sepsis
33
JAUNDICE What are some causes of jaundice 24h–2w after birth?
- Physiological + breast milk jaundice (common) - Infection (UTI, sepsis) - Haemolysis, polycythaemia, bruising - Crigler-Najjar syndrome (rare inherited disorder with no UGT enzyme)
34
JAUNDICE What are some causes of jaundice >2w after birth?
- Unconjugated = physiological or breast milk, UTI, hypothyroid, high GI obstruction (pyloric stenosis), Gilbert syndrome - Conjugated (>25umol/L) = bile duct obstruction (biliary atresia), neonatal hepatitis
35
JAUNDICE How does jaundice present? When would you worry about jaundice persisting?
- Yellow skin/sclera (may be more visible when outside in sunlight) - Persistent or prolonged jaundice worrying (>2w full term, >3w preterm)
36
JAUNDICE What is physiological jaundice?
- High concentration of RBCs in neonate which are more fragile with shorter life - Less developed liver - Foetal RBCs breakdown more rapidly releasing lots of bilirubin > normal rise in bilirubin = mild jaundice from 2–7d
37
JAUNDICE How is physiological jaundice diagnosed? How is physiological jaundice managed?
- Only when all other causes excluded - Usually completely resolves by 10d, most babies otherwise healthy
38
JAUNDICE What might cause breast milk jaundice?
- Components of breast milk inhibiting liver to process bilirubin - Increased bilirubin absorption - Inadequate feeds > slow passage of stools
39
JAUNDICE What is Gilbert's syndrome? How does it present?
- AR deficiency of UDP-glucuronyltransferase = defective bilirubin conjugation - Unconjugated hyperbilirubinaemia (not in urine), jaundice may only be present if ill, exercising or fasting
40
JAUNDICE What investigations would you perform in neonatal jaundice?
- FBC + blood film (polycythaemia, G6PD, spherocytosis) - Bilirubin levels - Blood type testing of mother + baby for ABO/Rh incompatibility - Direct Coombs (antiglobulin) test for haemolysis - TFTs, LFTs + urine MC&S
41
JAUNDICE When measuring bilirubin levels what are you looking for? How would you measure bilirubin levels depending on age?
- Split bilirubin = unconjugated (extra-hepatic) or conjugated (hepatobiliary) - >24h old = transcutaneous bilirubin meter if high, serum to confirm within 6h - <24h old = serum bilirubin within 2h
42
JAUNDICE What is the main complication of jaundice? What is it?
- Kernicterus - Bilirubin-induced encephalopathy caused by unconjugated bilirubin deposition in brain (basal ganglia + brainstem nuclei) as baby's BBB are not well developed
43
JAUNDICE What increases the risk of kernicterus?
- Prematurity as immature liver
44
JAUNDICE What is the management of jaundice?
- Bilirubin Tx threshold charts, plot age of baby against total bilirubin level + treat once at threshold - Phototherapy (450mm wavelength blue-green band) - Exchange transfusion if severe
45
JAUNDICE What is phototherapy?
- Converts unconjugated bilirubin > water-soluble pigment that can be excreted in urine, cover infant's eyes
46
HIE What is hypoxic ischaemic encephalopathy (HIE)?
occurs when there is a reduction in oxygen supply and/or blood flow to the neonates brain, leading to neuronal damage and dysfunction
47
HIE What happens as a result of cardiorespiratory depression?
- Hypoxia, hypercarbia + metabolic acidosis - Compromised cardiac output reduces tissue perfusion > hypoxic ischaemic injury to brain
48
HIE what are the risk factors?
MATERNAL - HTN - diabetes - substance abuse - infection OBSTETRIC - prolonged labour - meconium-stained amniotic fluid - placental abruption - umbilical cord prolapse INFANT - prematurity - low birth weight - congenital abnormalities
49
HIE What are the causes of HIE?
Anything leading to asphyxia = - maternal shock, - intrapartum haemorrhage, - prolapsed or nuchal cord, - placental abruption
50
HIE what are the clinical features?
SYMPTOMS - poor feeding - irritability - lethargy - seizures SIGNS - altered level of consciousness - hypotonia - weak or absent reflexes - apnoea or irregular breathing
51
HIE what are the investigations?
- blood gas - blood tests - cranial USS to consider - MRI - EEG
52
HIE What is used to stage the severity of HIE? What are the stages?
Sarnat staging – - Mild = poor feeding, generally irritable + hyperalert, resolves in 24h - Moderate = poor feeding, lethargic, hypotonic, seizures, can take weeks to resolve - Severe = reduced GCS, apnoeas, flaccid + reduced/absent reflexes, half die
53
HIE What is the main complication of HIE? How common is it?
- Permanent brain damage > cerebral palsy - cognitive impairment - epilepsy - visual and hearing impairment - developmental delay - death
54
HIE What is the acute management of HIE?
- oxygen therapy - fluid + electrolyte management - antiepileptic drugs - therapeutic hypothermia - supportive care (temperature maintenance, adequate nutrition)
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HIE What is the main therapeutic management of HIE?
- Therapeutic hypothermia to protect brain from hypoxic injury - Cooled to PR temp 33–34 for 72h to reduce brain damage
56
NEONATAL HYPOGLYCAEMIA What is neonatal hypoglycaemia?
- No agreed definition but <2.6mmol/L often used
57
NEONATAL HYPOGLYCAEMIA How does neonatal hypoglycaemia present?
- may be asymptomatic AUTONOMIC - jittery - irritable - tachypnoea - pallor NEUROGLYCOPAENIC - poor feeding/sucking - weak cry - drowsy - hypotonia - seizures OTHER FEATURES - apnoea - hypothermia
58
NEONATAL HYPOGLYCAEMIA What is the management of neonatal hypoglycaemia?
ASYMPTOMATIC - encourage normal feeding (breast or bottle) - monitor blood glucose SYMPTOMATIC or VERY LOW BLOOD GLUCOSE - admit to neonatal unit - IV 10% dextrose
59
TORCH What are the TORCH conditions?
Main congenital conditions - Toxoplasmosis, - Other (HIV), - Rubella, - CMV, - Herpes + Syphilis
60
TORCH What are the characteristic features of toxoplasmosis?
- Cerebral calcification, chorioretinitis + hydrocephalus
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TORCH What is CMV? How is it contracted?
- Most common congenital infection - Herpes simplex virus via personal contact
62
TORCH What is the clinical presentation of CMV?
- 90% normal at birth - 5% = hepatosplenomegaly, petechiae at birth, growth issues, neurodevelopmental disabilities (cerebral palsy, epilepsy, microcephaly) - 5% = problems later in life, mainly sensorineural hearing loss
63
TORCH How does herpes simplex virus present?
- Herpetic lesions on skin or eye, encephalitis or disseminated disease
64
TORCH How does syphilis present?
- Rash on soles of feet + hands - Hutchinson's triad = keratitis, deafness, small + pointed teeth
65
MECONIUM ASPIRATION What is meconium aspiration?
- Meconium may be passed due to foetal hypoxia + at birth these infants may inhale it - Lung irritant resulting in mechanical obstruction + chemical pneumonitis + predisposing to infection
66
MECONIUM ASPIRATION What are some risk factors for meconium aspiration?
- Post-term deliveries at 42w - Maternal HTN or pre-eclampsia - Smoking or substance abuse - Chorioamnionitis
67
MECONIUM ASPIRATION What is the clinical presentation of meconium aspiration?
- Presence of meconium or dark green staining of amniotic fluid - Respiratory distress
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MECONIUM ASPIRATION What investigation would you do in meconium aspiration?
- CXR = hyperinflation, accompanied by patches of collapse + consolidation - High incidence of air leak > pneumothorax
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MECONIUM ASPIRATION What is a complication of meconium aspiration? What are some other risk factors for that complication?
- Persistent pulmonary HTN of the newborn due to high pulmonary vascular resistance - RDS, sepsis, congenital diaphragmatic hernia, maternal SSRI use, maternal NSAID use in 3rd trimester (early closure of DA)
70
MECONIUM ASPIRATION | What is the management of meconium aspiration?
- Artificial (positive pressure) ventilation with oxygenation - Suction if no breathing
71
CLEFT LIP AND PALATE What is a cleft lip?
- Split or open section in upper lip, can go up to the nose
72
CLEFT LIP AND PALATE What is a cleft palate?
- Defect in hard or soft palate at roof of mouth which leaves an opening between the mouth + nasal cavity
73
CLEFT LIP AND PALATE What are some causes of cleft lip + palate?
- Chromosomal disorder or maternal AED therapy
74
CLEFT LIP AND PALATE What is the management of cleft lip + palate?
- MDT = plastic + ENT surgeons, paeds, orthodontist, SALT - Cleft lip repair ≤3m - Cleft palate repair 6-12m
75
OESOPHAGEAL ATRESIA What is oesophageal atresia?
- Upper + lower oesophagus in 2 sections + does not connect
76
OESOPHAGEAL ATRESIA What is the clinical presentation of oesophageal atresia?
- Persistent salivation + drooling from mouth after birth - May cough + choke when fed + have cyanotic aspiration - Some have other congenital malformations (VACTERL association)
77
OESOPHAGEAL ATRESIA What is the management of oesophageal atresia?
- Wide calibre feeding tube passed + checked by XR if reaches stomach - Continuous suction applied to tube passed into oesophageal pouch to reduce aspiration of saliva + secretions > neonatal surgical unit
78
GASTROSCHISIS What is gastroschisis?
- Bowel protrudes through congenital defect in anterior abdominal wall, adjacent to umbilicus but with no covering sac
79
GASTROSCHISIS What is gastroschisis associated with?
- Socioeconomic deprivation (smoking, mum <20y)
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GASTROSCHISIS What is a complication of gastroschisis?
Higher risk of dehydration + protein loss – - Wrap infants in several layers of clingfilm to minimise fluid + heat loss - NG tube passed + aspirated frequently - IVI dextrose + colloid support for protein loss
81
GASTROSCHISIS What is the management of gastroschisis?
- May attempt vaginal delivery - Urgent repair (theatre within 4h)
82
BRONCHOPULMONARY DYSPLASIA What is chronic lung disease of prematurity, or bronchopulmonary dysplasia?
- Premature babies often <28w diagnosed when infant requires oxygen therapy after they reach 36w gestation
83
BRONCHOPULMONARY DYSPLASIA What is the pathophysiology of bronchopulmonary dysplasia?
- Reduced lung volume + reduced alveolar surface area > diffusion defect
84
BRONCHOPULMONARY DYSPLASIA What is the clinical presentation of bronchopulmonary dysplasia?
- Increased work of breathing (tachypnoea, nasal flaring, recessions, low SpO2) - Crackles + wheezes on auscultation - Poor feeding + weight gain - Increased susceptibility to infection
85
BRONCHOPULMONARY DYSPLASIA What investigations would you do for bronchopulmonary dysplasia?
- CXR = widespread areas of opacification, cystic changes, fibrosis - Formal sleep study to assess SpO2 during sleep supports Dx + guides Mx
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BRONCHOPULMONARY DYSPLASIA How can bronchopulmonary dysplasia be prevented?
- Corticosteroids to mothers in premature labour <34w - CPAP rather than intubation where possible - Use caffeine to stimulate resp effort - Do not over oxygenate
87
BRONCHOPULMONARY DYSPLASIA What is the management of bronchopulmonary dysplasia?
- Some babies go home with low dose oxygen, weaned over first year - Monthly IM palivizumab for RSV (+ bronchiolitis) protection
88
DUODENAL ATRESIA What is duodenal atresia?
- Congenital absence or complete closure of duodenum This causes intestinal obstruction
89
EXOMPHALOS What is exomphalos, or omphalocele?
- Abdominal contents protrude through umbilical ring, covered with a transparent sac formed by the amniotic membrane + peritoneum
90
EXOMPHALOS What is exomphalos associated with?
- Other major congenital abnormalities, antenatal Dx
91
DUODENAL ATRESIA What can confirm it?
- AXR shows 'double bubble' from distension of stomach + duodenal cap
92
DUODENAL ATRESIA What is it associated with?
- Third have Down's
93
DUODENAL ATRESIA What is the management?
- Correct fluid + electrolyte depletion - surgical management is required to remove the narrowed part of bowel and reattach the ends.
94
DUODENAL ATRESIA What is the clinical presentation?
- most appear well at birth - when they atart to feed they are sick (vomit is green) - jaundice - not pass meconium in first day
95
GROUP B STREP INFECTION how do babies become infected?
- it can be passed on from the mother during pregnancy - it can be passed from the mother's genital tract during birth
96
GROUP B STREP INFECTION which babies are at more risk of becoming infected with group B strep?
- preterm labour - premature rupture of membranes - a long time between rupture of membranes and birth - internal foetal monitor - fever - past pregnancy with baby who had strep B - african-american/hispanic - group B strep in urine during pregnancy
97
GROUP B STREP INFECTION what are the symptoms of group B strep infection in newborns?
- respiratory distress (grunting, nasal flaring, tachypnoea, accessory muscle use) - tachycardia - apnoea - apparent change in mental status/lethargy - jaundice - seizures - poor/reduced feeding - abdominal distention - vomiting
98
GROUP B STREP INFECTION what are the symptoms of group B strep infection in babies are a week old?
- decreased movement in arm or leg - pain with movement of arm or leg - breathing problems - fever - red area on face or other part of the body
99
GROUP B STREP INFECTION what are the symptoms of group B strep infection in pregnant women?
- having to urinate often - having a sudden urge to urinate - pain when urinating - fever - nausea and vomiting - pain in side or back - uterus or belly is sore - fast heart rate
100
GROUP B STREP INFECTION what are the investigations?
- blood cultures - FBC, CRP - blood gas - urine microscopy - lumbar puncture - sputum culture
101
GROUP B STREP INFECTION? what is the management?
- IV antibiotics (IV benzylpenicillin with gentamicin) - NICU admission
102
GROUP B STREP INFECTION what are the possible complications in pregnancy?
- chorioamnionitis - infection of the amniotic fluid, sac and placenta - endometritis - postpartum infection - preterm labour
103
GROUP B STREP INFECTION what are the possible complications in newborns?
- meningitis - pneumonia - sepsis
104
GROUP B STREP INFECTION? how can newborn infection be prevented?
- test for group B strep at 35-37 weeks of pregnancy (vaginal + rectal swab, urine sample) - if test is positive, have IV antibiotics during labour - may be given antibiotics for certain risk factors - previous pregnancy with strep B infection - premature rupture of membranes/premature labour - fever during labour - rupture of membranes >18hrs before delivery
105
LISTERIA INFECTION How do babies become infected?
- It can be acquired in the womb or during/after delivery - pregnant women can become infected by eating contaminated food - soft cheese, seafood, unpasteurised dairy etc
106
PREMATURITY What are some GI complications of prematurity?
- Necrotising enterocolitis, - neonatal jaundice, - feeding issues
107
PREMATURITY What are some neuro complications of prematurity?
- Cerebral palsy, - hearing/visual impairment, - intraventricular haemorrhage
108
PREMATURITY What are some metabolic complications of prematurity?
- Hypoglycaemia, - hypocalcaemia, - electrolyte imbalance, - fluid imbalance - hypothermia
109
PREMATURITY What causes hypocalcaemia?
Kidneys + parathyroid not fully developed
110
PREMATURITY What causes electrolyte, fluid imbalance + hypothermia?
Excess losses through skin
111
JAUNDICE What is the physiology relating to jaundice?
RBCs contain unconjugated bilirubin, they breakdown + release it into blood, conjugated in liver + excreted via biliary system (GI tract) or urine
112
JAUNDICE How does kernicterus present? What are the outcomes?
- Lethargy, poor feeding > hypertonia, seizures + coma - Permanent damage = dyskinetic cerebral palsy, LD + deafness
113
JAUNDICE What are some side effects of phototherapy?
- Temp instability, - macular rash, - bronze discolouration
114
NEONATAL HYPOGLYCAEMIA What are some risk factors for neonatal hypoglycaemia?
- Preterm + intrauterine growth restriction (IUGR) = lack of glycogen stores - Maternal DM = infantile hyperinsulinaemia - LGA, polycythaemia or ill - Transient hypoglycaemia common in first hours after birth
115
TORCH How is herpes simplex virus managed?
Aciclovir, high mortality in disseminated
116
TORCH How is CMV managed?
No therapy so no screening
117
TORCH How is syphillis managed?
- If fully treated ≥1m before delivery = no treatment - Any doubts = benzylpenicillin
118
CLEFT LIP AND PALATE What causes a cleft lip?
Failure of fusion of the frontonasal + maxillary processes
119
CLEFT LIP AND PALATE What causes it?
Failure of the palatine processes + nasal septum to fuse
120
CLEFT LIP AND PALATE What are some complications?
Issues feeding, milk aspiration, speech delay + conductive hearing loss, recurrent otitis media (cleft palate)
121
OESOPHAGEAL ATRESIA What is it associated with?
- Tracheo-oesophageal fistula + polyhydramnios
122
GASTROSCHISIS What is an investigation for gastroschisis?
- USS shows free loops of bowel in amniotic fluid antenatally
123
BRONCHOPULMONARY DYSPLASIA What happens to babies with bronchopulmonary dysplasia at birth?
Suffer with RDS, need oxygen therapy or ventilation + intubation at birth
124
EXOMPHALOS What is the management?
C-section at 37w, staged repair as primary closure difficult
125
LISTERIA INFECTION what is the clinical presentation?
symptoms are similar to sepsis - listlessness, irritable, poor feeding - Early onset = low birth weight, obstetric complications, evidence of sepsis soon after birth - late onset = usually full-term, previously healthy neonates, present with meningitis/sepsis
126
LISTERIA INFECTION what is the prognosis?
- 10-50% of newborns with listeria infection die - the death rate is higher in those with early onset listeriosis
127
LISTERIA INFECTION what is the prevention?
- pregnant women should avoid eating unpasteurised dairy, soft cheeses, raw veg, deli meats, meat spreads and smoked seafood
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LISTERIA INFECTION what is the management?
ampicillin + aminoglycoside (gentamycin)
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SIDS what is sudden infant death syndrome (SIDS)?
it is sudden unexplained death in an infant. it usually occurs in first 6 months.
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SIDS what are the risk factors?
- not prone sleeping - parental smoking - prematurity - bed sharing - hyperthermia - head covering other risk factors - LBW - male sex - maternal drug use - multiple births - incidence increases in winter
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SIDS what are protective factors?
- breastfeeding - room sharing - use of dummies
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SIDS what measures can be taken to reduce the risk of SIDS?
- put baby on their back when not directly supervised - keep head uncovered - place feet at foot of the bed to prevent them sliding down under blanket - keep cot clear of toys and blankets - maintain a comfortable room temperature (16-20 degrees) - avoid smoking (avoid handling baby after smoking) - avoid co-sleeping (particularly on sofa or chair) - if co-sleeping avoid drugs, alcohol, sleeping tablets or deep sleepers
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SIDS where can you direct people for support?
lullaby trust - charity to support families affected bereavement services
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HSV ENCEPHALITIS what is it?
inflammation of the brain caused by herpes simplex virus (HSV)
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HSV ENCEPHALITIS what is the cause?
- neonates = HSV-2 (genital herpes) - older children = HSV-1 (cold sores)
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HSV ENCEPHALITIS what is the clinical presentation?
- altered consciousness - altered cognition - unusual behaviour - acute onset focal neurological symptoms - acute onset focal seizures - fever
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HSV ENCEPHALITIS what are the investigations?
- lumbar puncture - CT scan (if lumbar puncture is contraindicated) - MRI - EEG - swabs - HIV testing
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HSV ENCEPHALITIS what is the management?
IV acyclovir repeat LP to ensure successful treatment before stopping antivirals
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HSV ENCEPHALITIS what are the complications?
- lasting fatigue + prolonged recovery - changes to personality or mood - changes to memory and cognition - learning disability - headaches - chronic pain - movement disorder - sensory disturbance - seizures - hormonal imbalance
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CONGENITAL HYPOTHYROIDISM what is it?
one of the most common preventable causes of intellectual disability
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CONGENITAL HYPOTHYROIDISM what are the causes?
- primary congenital hypothyroidism - thyroid dysgenesis - dyshormonogenesis - secondary or central congenital hypothyroidism
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CONGENITAL HYPOTHYROIDISM what are the risk factors?
- medication use during pregnancy - maternal advanced age - family history of thyroid disease - low birth weight - preterm birth - multiple pregnancies
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CONGENITAL HYPOTHYROIDISM what are the clinical features?
- prolonged neonatal jaundice - poor feeding + weight gain - hypothermia - macroglossia - large fontanelle - distended abdomen with umbilical hernia - dry skin - hoarse cry - myxoedema - bradycardia
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CONGENITAL HYPOTHYROIDISM what are the investigations?
- newborn screening = TSH>20 - TFTs - thyroid USS - hearing assessment
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CONGENITAL HYPOTHYROIDISM what is the management?
levothyroxine