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My Phase 3a Revision > PAEDS - NEONATAL > Flashcards

PAEDS - NEONATAL Flashcards

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 are some GI complications of prematurity?

A
  • Necrotising enterocolitis,
  • neonatal jaundice,
  • feeding issues
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14
Q

PREMATURITY
What are some neuro complications of prematurity?

A
  • Cerebral palsy,
  • hearing/visual impairment,
  • intraventricular haemorrhage
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15
Q

PREMATURITY
What are some metabolic complications of prematurity?

A
  • Hypoglycaemia,
  • hypocalcaemia,
  • electrolyte imbalance,
  • fluid imbalance
  • hypothermia
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16
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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17
Q

PREMATURITY
What causes hypoglycaemia?

A

Lack of glycogen stores

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18
Q

PREMATURITY
What causes hypocalcaemia?

A

Kidneys + parathyroid not fully developed

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19
Q

PREMATURITY
What causes electrolyte, fluid imbalance + hypothermia?

A

Excess losses through skin

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20
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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21
Q

RDS
What are some risk factors of RDS?

A
  • Prematurity #1
  • Maternal DM
  • 2nd premature twin
  • C-section
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22
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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23
Q

RDS
What is the investigation for RDS?

A

CXR –

  • Reticular “ground-glass” changes
  • Heart borders indistinct
  • Air bronchograms
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24
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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25
Q

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

A
  • Antenatal dexamethasone
  • Increases surfactant production
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26
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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27
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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28
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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29
Q

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

A
  • Bilious vomiting
  • Intolerance to feeds
  • Distended, tender abdo with absent bowel sounds
  • Bloody stools
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30
Q

NEC. ENTEROCOLITIS
What are some investigations for necrotising enterocolitis?

A
  • Blood culture (sepsis)
  • CRP
  • Capillary blood gas = metabolic acidosis
  • AXR is diagnostic
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31
Q

NEC. ENTEROCOLITIS
What would an AXR show in necrotising enterocolitis?

A
  • 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
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32
Q

NEC. ENTEROCOLITIS
What are some complications of necrotising enterocolitis?

A
  • Dead bowel > perforation + peritonitis > sepsis + shock
  • Stricture formation
  • Short bowel syndrome (malabsorption) if extensive resection required
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33
Q

NEC. ENTEROCOLITIS
What is the management of necrotising enterocolitis?

A
  • A–E if shocked, ?artificial ventilation, ?circulatory support
  • Broad spec Abx 1st, NBM with IV fluids + total parenteral nutrition (NG to drain gas + fluid from stomach + intestines)
  • Surgical emergency > laparotomy for perforation
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34
Q

JAUNDICE
What is jaundice?

A
  • Abnormally high levels of bilirubin in the blood
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35
Q

JAUNDICE
What is the physiology relating to jaundice?

A

RBCs contain unconjugated bilirubin, they breakdown + release it into blood, conjugated in liver + excreted via biliary system (GI tract) or urine

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36
Q

JAUNDICE
What are some risk factors for jaundice?

A
  • LBW
  • Breastfeeding
  • Prematurity
  • FHx
  • Maternal diabetes
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37
Q

JAUNDICE
Jaundice can be split into 3 aetiological time categories.
What are these?

A
  • <24h = always pathological, usually haemolytic disease
  • 24h–2w = common
  • > 2w = also bad
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38
Q

JAUNDICE
What are some causes of jaundice <24h after birth?

A
  • Haemolytic diseases #1 = rhesus or ABO incompatibility, G6PD, spherocytosis
  • Congenital infection (TORCH), sepsis
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39
Q

JAUNDICE
What are some causes of jaundice 24h–2w after birth?

A
  • Physiological + breast milk jaundice (common)
  • Infection (UTI, sepsis)
  • Haemolysis, polycythaemia, bruising
  • Crigler-Najjar syndrome (rare inherited disorder with no UGT enzyme)
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40
Q

JAUNDICE
What are some causes of jaundice >2w after birth?

A
  • Unconjugated = physiological or breast milk, UTI, hypothyroid, high GI obstruction (pyloric stenosis), Gilbert syndrome
  • Conjugated (>25umol/L) = bile duct obstruction (biliary atresia), neonatal hepatitis
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41
Q

JAUNDICE
How does jaundice present?
When would you worry about jaundice persisting?

A
  • Yellow skin/sclera (may be more visible when outside in sunlight)
  • Persistent or prolonged jaundice worrying (>2w full term, >3w preterm)
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42
Q

JAUNDICE
What is physiological jaundice?

A
  • 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
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43
Q

JAUNDICE
How is physiological jaundice diagnosed?
How is physiological jaundice managed?

A
  • Only when all other causes excluded
  • Usually completely resolves by 10d, most babies otherwise healthy
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44
Q

JAUNDICE
What might cause breast milk jaundice?

A
  • Components of breast milk inhibiting liver to process bilirubin
  • Increased bilirubin absorption
  • Inadequate feeds > slow passage of stools
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45
Q

JAUNDICE
What is Gilbert’s syndrome?
How does it present?

A
  • AR deficiency of UDP-glucuronyltransferase = defective bilirubin conjugation
  • Unconjugated hyperbilirubinaemia (not in urine), jaundice may only be present if ill, exercising or fasting
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46
Q

JAUNDICE
What investigations would you perform in neonatal jaundice?

A
  • 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
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47
Q

JAUNDICE
When measuring bilirubin levels what are you looking for?
How would you measure bilirubin levels depending on age?

A
  • 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
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48
Q

JAUNDICE
What is the main complication of jaundice?
What is it?

A
  • Kernicterus
  • Bilirubin-induced encephalopathy caused by unconjugated bilirubin deposition in brain (basal ganglia + brainstem nuclei) as baby’s BBB are not well developed
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49
Q

JAUNDICE
What increases the risk of kernicterus?

A
  • Prematurity as immature liver
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50
Q

JAUNDICE
How does kernicterus present?
What are the outcomes?

A
  • Lethargy, poor feeding > hypertonia, seizures + coma
  • Permanent damage = dyskinetic cerebral palsy, LD + deafness
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51
Q

JAUNDICE
What is the management of jaundice?

A
  • 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
52
Q

JAUNDICE
What is phototherapy?

A
  • Converts unconjugated bilirubin > water-soluble pigment that can be excreted in urine, cover infant’s eyes
53
Q

JAUNDICE
What are some side effects of phototherapy?

A
  • Temp instability,
  • macular rash,
  • bronze discolouration
54
Q

HIE
What is hypoxic ischaemic encephalopathy (HIE)?

A
  • In perinatal asphyxia, gas exchange, either placental or pulmonary is compromised or ceases resulting in cardiorespiratory depression
55
Q

HIE
What happens as a result of cardiorespiratory depression?

A
  • Hypoxia, hypercarbia + metabolic acidosis
  • Compromised cardiac output reduces tissue perfusion > hypoxic ischaemic injury to brain
56
Q

HIE
What are the causes of HIE?

A

Anything leading to asphyxia =
- maternal shock,
- intrapartum haemorrhage,
- prolapsed or nuchal cord,
- placental abruption

57
Q

HIE
What is used to stage the severity of HIE?
What are the stages?

A

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
58
Q

HIE
What is the main complication of HIE?
How common is it?

A
  • Permanent brain damage > cerebral palsy
  • Moderate = 40%,
  • severe = 90%
59
Q

HIE
What is the acute management of HIE?

A

MDT resus –

  • Dry baby, APGAR, resp support
  • Treat seizures, EEG
  • Treat hypotension by volume + inotropes
  • Monitor + treat electrolytes
60
Q

HIE
What is the main therapeutic management of HIE?

A
  • Therapeutic hypothermia to protect brain from hypoxic injury
  • Cooled to PR temp 33–34 for 72h to reduce brain damage
61
Q

NEONATAL HYPOGLYCAEMIA
What is neonatal hypoglycaemia?

A
  • No agreed definition but <2.6mmol/L often used
62
Q

NEONATAL HYPOGLYCAEMIA
What are some risk factors for neonatal hypoglycaemia?

A
  • 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
63
Q

NEONATAL HYPOGLYCAEMIA
How does neonatal hypoglycaemia present?

A
  • Jitteriness, irritability, apnoea
  • Lethargy, drowsiness + Seizures
  • Long-term may cause permanent neuro disability
64
Q

NEONATAL HYPOGLYCAEMIA
What is the management of neonatal hypoglycaemia?

A
  • Regular bedside BM
  • Prevent by early + frequent feeding
  • IVI 10% dextrose (central venous catheter if higher concentration of dextrose to prevent skin necrosis) to maintain glucose >2.6mmol/L
65
Q

TORCH
What are the TORCH conditions?

A

Main congenital conditions
- Toxoplasmosis,
- Other (HIV),
- Rubella,
- CMV,
- Herpes + Syphilis

66
Q

TORCH
What are the characteristic features of toxoplasmosis?

A
  • Cerebral calcification, chorioretinitis + hydrocephalus
67
Q

TORCH
What is CMV?
How is it contracted?

A
  • Most common congenital infection
  • Herpes simplex virus via personal contact
68
Q

TORCH
How is CMV managed?

A

No therapy so no screening

69
Q

TORCH
What is the clinical presentation of CMV?

A
  • 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
70
Q

TORCH
How does herpes simplex virus present?

A
  • Herpetic lesions on skin or eye, encephalitis or disseminated disease
71
Q

TORCH
How is herpes simplex virus managed?

A

Aciclovir, high mortality in disseminated

72
Q

TORCH
How does syphilis present?

A
  • Rash on soles of feet + hands
  • Hutchinson’s triad = keratitis, deafness, small + pointed teeth
73
Q

TORCH
How is syphillis managed?

A
  • If fully treated ≥1m before delivery = no treatment
  • Any doubts = benzylpenicillin
74
Q

MECONIUM ASPIRATION
What is meconium aspiration?

A
  • 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
75
Q

MECONIUM ASPIRATION
What are some risk factors for meconium aspiration?

A
  • Post-term deliveries at 42w
  • Maternal HTN or pre-eclampsia
  • Smoking or substance abuse
  • Chorioamnionitis
76
Q

MECONIUM ASPIRATION
What is the clinical presentation of meconium aspiration?

A
  • Presence of meconium or dark green staining of amniotic fluid
  • Respiratory distress
77
Q

MECONIUM ASPIRATION
What investigation would you do in meconium aspiration?

A
  • CXR = hyperinflation, accompanied by patches of collapse + consolidation
  • High incidence of air leak > pneumothorax
78
Q

MECONIUM ASPIRATION
What is a complication of meconium aspiration?
What are some other risk factors for that complication?

A
  • 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)
79
Q

MECONIUM ASPIRATION

What is the management of meconium aspiration?

A
  • Artificial (positive pressure) ventilation with oxygenation
  • Suction if no breathing
80
Q

CLEFT LIP AND PALATE
What is a cleft lip?

A
  • Split or open section in upper lip, can go up to the nose
81
Q

CLEFT LIP AND PALATE
What causes a cleft lip?

A

Failure of fusion of the frontonasal + maxillary processes

82
Q

CLEFT LIP AND PALATE
What is a cleft palate?

A
  • Defect in hard or soft palate at roof of mouth which leaves an opening between the mouth + nasal cavity
83
Q

CLEFT LIP AND PALATE
What causes it?

A

Failure of the palatine processes + nasal septum to fuse

84
Q

CLEFT LIP AND PALATE
What are some causes of cleft lip + palate?

A
  • Chromosomal disorder or maternal AED therapy
85
Q

CLEFT LIP AND PALATE
What are some complications?

A

Issues feeding, milk aspiration, speech delay + conductive hearing loss, recurrent otitis media (cleft palate)

86
Q

CLEFT LIP AND PALATE
What is the management of cleft lip + palate?

A
  • MDT = plastic + ENT surgeons, paeds, orthodontist, SALT
  • Cleft lip repair ≤3m
  • Cleft palate repair 6-12m
87
Q

OESOPHAGEAL ATRESIA
What is oesophageal atresia?

A
  • Upper + lower oesophagus in 2 sections + does not connect
88
Q

OESOPHAGEAL ATRESIA
What is it associated with?

A
  • Tracheo-oesophageal fistula + polyhydramnios
89
Q

OESOPHAGEAL ATRESIA
What is the clinical presentation of oesophageal atresia?

A
  • Persistent salivation + drooling from mouth after birth
  • May cough + choke when fed + have cyanotic aspiration
  • Some have other congenital malformations (VACTERL association)
90
Q

OESOPHAGEAL ATRESIA
What is the management of oesophageal atresia?

A
  • 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
91
Q

GASTROSCHISIS
What is gastroschisis?

A
  • Bowel protrudes through congenital defect in anterior abdominal wall, adjacent to umbilicus but with no covering sac
92
Q

GASTROSCHISIS
What is gastroschisis associated with?

A
  • Socioeconomic deprivation (smoking, mum <20y)
93
Q

GASTROSCHISIS
What is an investigation for gastroschisis?

A
  • USS shows free loops of bowel in amniotic fluid antenatally
94
Q

GASTROSCHISIS
What is a complication of gastroschisis?

A

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
95
Q

GASTROSCHISIS
What is the management of gastroschisis?

A
  • May attempt vaginal delivery
  • Urgent repair (theatre within 4h)
96
Q

BRONCHOPULMONARY DYSPLASIA
What is chronic lung disease of prematurity, or bronchopulmonary dysplasia?

A
  • Premature babies often <28w diagnosed when infant requires oxygen therapy after they reach 36w gestation
97
Q

BRONCHOPULMONARY DYSPLASIA
What is the pathophysiology of bronchopulmonary dysplasia?

A
  • Reduced lung volume + reduced alveolar surface area > diffusion defect
98
Q

BRONCHOPULMONARY DYSPLASIA
What happens to babies with bronchopulmonary dysplasia at birth?

A

Suffer with RDS, need oxygen therapy or ventilation + intubation at birth

99
Q

BRONCHOPULMONARY DYSPLASIA
What is the clinical presentation of bronchopulmonary dysplasia?

A
  • Increased work of breathing (tachypnoea, nasal flaring, recessions, low SpO2)
  • Crackles + wheezes on auscultation
  • Poor feeding + weight gain
  • Increased susceptibility to infection
100
Q

BRONCHOPULMONARY DYSPLASIA
What investigations would you do for bronchopulmonary dysplasia?

A
  • CXR = widespread areas of opacification, cystic changes, fibrosis
  • Formal sleep study to assess SpO2 during sleep supports Dx + guides Mx
101
Q

BRONCHOPULMONARY DYSPLASIA
How can bronchopulmonary dysplasia be prevented?

A
  • Corticosteroids to mothers in premature labour <34w
  • CPAP rather than intubation where possible
  • Use caffeine to stimulate resp effort
  • Do not over oxygenate
102
Q

BRONCHOPULMONARY DYSPLASIA
What is the management of bronchopulmonary dysplasia?

A
  • Some babies go home with low dose oxygen, weaned over first year
  • Monthly IM palivizumab for RSV (+ bronchiolitis) protection
103
Q

DUODENAL ATRESIA
What is duodenal atresia?

A
  • Congenital absence or complete closure of duodenum This causes intestinal obstruction
104
Q

DUODENAL ATRESIA
What is the clinical presentation?

A
  • most appear well at birth
  • when they atart to feed they are sick (vomit is green)
  • jaundice
  • not pass meconium in first day
105
Q

DUODENAL ATRESIA
What can confirm it?

A
  • AXR shows ‘double bubble’ from distension of stomach + duodenal cap
106
Q

DUODENAL ATRESIA
What is it associated with?

A
  • Third have Down’s
107
Q

DUODENAL ATRESIA
What is the management?

A
  • Correct fluid + electrolyte depletion
  • surgical management is required to remove the narrowed part of bowel and reattach the ends.
108
Q

EXOMPHALOS
What is exomphalos, or omphalocele?

A
  • Abdominal contents protrude through umbilical ring, covered with a transparent sac formed by the amniotic membrane + peritoneum
109
Q

EXOMPHALOS
What is exomphalos associated with?

A
  • Other major congenital abnormalities, antenatal Dx
110
Q

EXOMPHALOS
What is the management?

A

C-section at 37w, staged repair as primary closure difficult

111
Q

GROUP B STREP INFECTION
how do babies become infected?

A
  • it can be passed on from the mother during pregnancy
  • it can be passed from the mother’s genital tract during birth
112
Q

GROUP B STREP INFECTION
which babies are at more risk of becoming infected with group B strep?

A
  • 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
113
Q

GROUP B STREP INFECTION
what are the symptoms of group B strep infection in newborns?

A
  • being fussy, sleepy + having breathing problems (signs of sepsis)
  • breathing fast + making grunting noises (signs of pneumonia)
  • breathing problems + periods not breathing
  • change in BP
  • convulsions
114
Q

GROUP B STREP INFECTION
what are the symptoms of group B strep infection in babies are a week old?

A
  • 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
115
Q

GROUP B STREP INFECTION
what are the symptoms of group B strep infection in pregnant women?

A
  • 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
116
Q

GROUP B STREP INFECTION
what are the investigations?

A
  • blood cultures
  • lumbar puncture
  • sputum culture
117
Q

GROUP B STREP INFECTION?
what is the management?

A
  • IV antibiotics
  • NICU admission
118
Q

GROUP B STREP INFECTION
what are the possible complications in pregnancy?

A
  • chorioamnionitis - infection of the amniotic fluid, sac and placenta
  • endometritis - postpartum infection
  • preterm labour
119
Q

GROUP B STREP INFECTION
what are the possible complications in newborns?

A
  • meningitis
  • pneumonia
  • sepsis
120
Q

GROUP B STREP INFECTION?
how can newborn infection be prevented?

A
  • 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
121
Q

LISTERIA INFECTION
How do babies become infected?

A
  • 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
122
Q

LISTERIA INFECTION
what is the clinical presentation?

A

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

123
Q

LISTERIA INFECTION
what is the prognosis?

A
  • 10-50% of newborns with listeria infection die
  • the death rate is higher in those with early onset listeriosis
124
Q

LISTERIA INFECTION
what is the prevention?

A
  • pregnant women should avoid eating unpasteurised dairy, soft cheeses, raw veg, deli meats, meat spreads and smoked seafood
125
Q

LISTERIA INFECTION
what is the management?

A

ampicillin + aminoglycoside (gentamycin)

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