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Paediatrics (Y4) > 14- Neonatology > Flashcards

14- Neonatology Flashcards

1
Q

Neonate definitions

A

– Term (> 37 weeks)
– Late preterm (34 – 36 weeks)
– Moderate preterm (32 – 34 weeks)
– Very preterm (28 – 32 weeks)
– Extremely preterm (< 28 weeks)
– Post term (> 42 weeks)

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2
Q

Birth weight classification

A
  • Low birth weight (< 2.5kg)
  • Very low birth weight (< 1.5kg)
  • Extremely low birth weight (< 1kg)
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3
Q

Problems of term babies

A

1) Hypoxic ischaemic encephalopathy
2) Respiratory distress
- Meconium aspiration syndrome
- Congenital pneumonia
- Persistent pulmonary hypertension
3) Sepsis
- Group B strep
- E.coli
4) Congenital abnormalities
- Gastroschisis
- Congenital heart problems

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4
Q

NIPE must be carried out within

A

72 hours
- screens for congenital abnormalities
- reassures parents
- to make referrals for further tests

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5
Q

NIPE procedure

A
  1. Weigh
  2. general inspection
  3. head
  4. skin
  5. face
  6. eyes
  7. ears
  8. mouth and palate
  9. neck and clavicles
  10. upper limbs
  11. chest
  12. abdomen
  13. genitalia
  14. lower limbs
  15. hips
  16. back and spine
  17. anus
  18. reflexes
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6
Q

reflexes

A

o Palmar grasp reflex
o Sucking reflex
o Rooting reflex
o Stepping reflex
o Moro reflex- drop

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7
Q

history taking format for neonates

A

PC
HPC
PMH
- birth history
- pregnancy
- maternal health
- resus history
Dx
FH
SH
Systemic review

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8
Q

presenting complaints in neonates

A
  • Prematurity <37 weeks
  • Respiratory distress e.g. grunting
  • Jaundice
  • Cyanosis
  • Poor feeding
  • Weight loss
  • Known congenital anomaly
  • Fractures/ skull swelling
  • Concerns about sepsis
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9
Q

HPC

A
  • Duration
  • Progression
  • Associated symptoms
  • Aggravating and relieving factors
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10
Q

Birth history

A
  • Gestation
  • Method of delivery
  • Complications at birth
  • Birth trauma
  • Delivery details: spontaneous, induced,
    instrumental, c-section
  • Resuscitation at birth
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11
Q

pregnancy history

A
  • Any notable history
  • Attended the scans
  • Vaccinations- whooping cough, influenza
  • Screening
    o Infections (TORCH, HIV)
    o Genetics
  • Smoking, alcohol and drugs
  • Any new diagnoses during pregnancy
    o Diabetes
    o Polyhydramnios/ oligo
  • Any DV
  • Any extra appointments or scan
  • Where sat on the growth chart
  • Fetal movements
  • Consanguineous parents
  • Anomaly scans
  • Antenatal steroids
  • Magnesium sulphate
  • Previous pregnancies and problems
  • Multiple or singleton
  • Maternal health
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12
Q

maternal history

A

o Medications
o Alcohol and drug use
o Maternal smoking
o Conditions e.g. lupus

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13
Q

family history

A
  • Siblings
  • Any inheritable disease e.g. CF
  • Congenital heart disease
  • Age pf parents
  • Consanguinity
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14
Q

social history

A
  • Child protection risks
  • Alcohol
  • Drugs
  • Learning difficulties
  • Mental illness
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15
Q

Systems review (neonatal course)

A
  • Ventilation
    o Number of days
    o Modality
    o FiO2
    o Max pressure
  • CVS- inotropes, PDA, CHD
  • Fluids/ feeds- days to full feeds, electrolyte disturbances, jaundice
  • Sepsis – source, Abx, cultures
  • Neurological- IVH, HIE, neuromuscular issue
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16
Q

Resuscitation history

A
  • Condition immediately after birth: colour, tone, HR, respiratory status
  • When 1st gaps
  • When 1st HR >100
  • Interventions with timing
    o Mask ventilation
    o Chest compressions
    o Surfactant
    o Intubation
    o UVS
    o Drugs (bicarbonate, adrenaline)
    o Special interventions e,g. chest drain
  • Apgar score
    o HR
    o respiratory effort
    o muscle tone
    o reflex irritability
    o colour
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17
Q

Hypoxic ischaemic encephalopathy background

A

Occurs in neonates as a result of hypoxia during birth

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18
Q

Pathophysiology HIE

A
  • Hypoxia is a lack of oxygen, ischaemia refers to a restriction in blood flow to the brain and encephalopathy refers to malfunctioning of the brain.
  • Some hypoxia is normal during birth, however prolonged or severe hypoxia leads to ischaemic brain damage.
  • HIE can lead to permanent damage to the brain, causing cerebral palsy.
  • Severe HIE can result in death.
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19
Q

causes of HIE

A
  • Maternal shock
  • Intrapartum haemorrhage
  • Prolapsed cord, causing compression of the cord during birth
  • Nuchal cord, where the cord is wrapped around the neck of the baby
  • Macrosomina – baby gets stuck
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20
Q

long term effects of HIE

A

Long term effects
- Developmental delay
- Cerebral palsy
- Epilepsy
- Severe hearing impairment

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21
Q

Presentation of HIE

A

Suspected HIE in neonates when there are events that could lead to hypoxia during the perinatal or intrapartum period
- acidosis (pH < 7) on the umbilical artery
- blood gas
- poor Apgar scores
- features of mild, moderate or severe HIE (see below) or evidence of multi organ failure.

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22
Q

Management of HIE

A
  • Specialist
  • Supportive care with
    o neonatal resuscitation and ongoing optimal ventilation
    o circulatory support
    o nutrition
    o acid base balance
    o treatment of seizures
  • Therapeutic hypothermia-> can help protect the brain from hypoxic injury
  • follow up with paediatrician and MDT to ass development and lasting disability
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23
Q

therapeutic hypothermia

A

Aim: reduce inflammation and neurone loss after the acute hypoxic injury.
Protocol
- Involves cooling core temp of baby
- Baby transferred to neonatal ICU and actively cooled using cooling blankets and cooling hats
- Target between 33-34 degree measured using a rectal probe
- Continued for 72 hours, after which baby is gradually warmed to normal temperature over 6 hours
Reduces risk of:
- Cerebral palsy
- Developmental delay
- Learning disability
- Blindness
- Death

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24
Q

Necrotising enterocolitis background

A
  • Most common neonatal surgical emergency
  • Characterised by variable injury to the intestine, ranging from mucosal damage to necrosis and perforation
  • Mortality rate associated with NEC is between 20-30%
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25
Q

Pathophysiology of necrotising enterocolitis

A
  • Not quite understood
  • Likely to be due to an innate immune response to the microbiota of the premature infants gut causing inflammation and injury
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26
Q

risk factors for NEC

A

Risk factors
- Very low birth weight
- Formula feeding
- Intrauterine growth restriction (IUGR)
- Polycythaemia
- Hypoxia
- Preterm infants

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27
Q

Protective factors for NEC

A
  • Breastfed infants (reduces 6 fold)
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28
Q

presentation of nec

A

Presentation
- Feeding intolerance
- Vomiting (may be bile or blood-stained)
- Abdominal distention
- Haematochezia
- Abdominal tenderness
- Oedema
- Erythema
- Palpable bile
- Systemic features
o Apnoea
o Lethargy
o Bradycardia
o Decreased peripheral perfusion

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29
Q

scoring system for NEC

A
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30
Q

complications of NEC

A

Complications
- Intestinal perforation
- Sepsis
- Death
- Complication: intestinal stricture and short-bowel syndrome, neurodevelopment disorders

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31
Q

investigations for NEC

A

Bloods: FBC, UEs, blood gas, blood culture
- Full blood count- anaemia, thrombocytopenia and leukocytosis/leukopenia are often present.
- U & Es- hyponatraemia
- Blood gas- metabolic acidosis
- Blood culture- to rule out sepsis

X-ray
- distended bowel loops
- thcikened bwoel wall
- intramural gas
- gas in portal tract
- pneumoperitoneum

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32
Q

management of NEC: prophylaxis

A

o Antenatal steroids if premature delivery is anticipated
o Breastfeeding
o Probiotics

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33
Q

medical management of NEC (Bell stage I and II)

A
  • Without oral feeds for 10-14 days and replace with parenteral nutrition
  • IV antibiotics for 10-14 days

Systemic support
- Ventilatory support
- Fluid resus
- Inotropic support
- Correction of acid-base balance, coagulopathy and thrombocytopenia

34
Q

surgical management of NEC

A

Indication
- Intestinal perforation
- GI obstruction secondary to stricture formation
- Deterioration despite medical management

Procedures
- Intestinal resection with stoma formation
- Resection with primary anastomosis
- Stoma formation without resection
- Clip and drop resection (increase 28 day mort)
- Open and close laparotomy

35
Q

respiratory distress syndrome background

A
  • RDS affects premature neonates – born before lungs produce enough surfactant
  • <32 weeks
36
Q

pathophysiology of RDS

A
  • Inadequate surfactant leads to HIGH SURFACE TENSION WITHIN ALVEOLI
  • Leads to atelectasis – more difficult for alveoli and lungs to expand
  • Leads to inadequate gaseous exchange-> hypoxia, hypercapnia (high CO2) and respiratory distress
37
Q

presentation of RDS

A

apnea, cyanosis, grunting, inspiratory stridor, nasal flaring, poor feeding, and tachypnea (more than 60 breaths per minute). There may also be retractions in the intercostal, subcostal, or supracostal spaces

38
Q

investigations for RDS

A
  • CXR- ‘ground glass appearance’
39
Q

management of RDS: mother

A

Dexamethasone injection given to mother with suspected preterm labour
-> Increases production of surfactant and reduces incidence and severity of RDS

40
Q

management RDS: neonates

A
  • Intubation and ventilation to fully assist breathing if the respiratory distress is severe
    –>Support with breathing is gradually stepped down as the baby develops and is able to maintain their breathing, until they can support themselves in air.
  • Endotracheal surfactant, which is artificial surfactant delivered into the lungs via an endotracheal tube
  • Continuous positive airway pressure (CPAP) via a nasal mask to help keep the lungs inflated whilst breathing
  • Supplementary oxygen to maintain oxygen saturations between 91 and 95% in preterm neonates
41
Q

complications of RDS

A

Short term complications:
* Pneumothorax
* Infection
* Apnoea
* Intraventricular haemorrhage
* Pulmonary haemorrhage
* Necrotising enterocolitis

Long term complications:
* Chronic lung disease of prematurity
* Retinopathy of prematurity occurs more often and more severely in neonates with RDS
* Neurological, hearing and visual impairment

42
Q

Transient tachypnoea of the newborn

A
  • This is a tachypnoea present in the newborn infant, which usually resolves after 24hr without any intervention.
  • Neither hypoxia nor cyanosis are usually seen, but the child might need support on a neonatal unit if they are symptomatic.
  • Blood gases should be within normal value
43
Q

Meconium aspiration syndrome background

A
  • Spectrum of disorders marked by various degrees of RDS in newborns
  • Follows aspiration of meconium stained amniotic fluid (MSAD)
    o Antenatally
    o During birth
  • Can exacerbate other conditions such as sepsis and ischaemic insults
44
Q

Risk factors for meconium aspiration syndrome

A
  • Post term babies >42 weeks
  • Thick meconium at birth
  • Suffered birth asphyxia
  • Oligohydramnios
  • Maternal hypertension, diabetes, pre-eclampsia, smoking, drug use
45
Q

pathophysiology of meconium aspiration syndrome

A
  • After-effect of in-utero peristalsis-> meconium passage
  • Due to
    o Foetal hypoxic stress
    o Vagal stimulation due to cord compression
    o Chronic hypoxia
  • These factors can lead to fetal gasping which results in MAS
  • Once aspirated meconium stimulates the release of vasoactive and cytokine substances which activate inflammatory pathways -> vasculature change -> inhibit effects of surfactant
46
Q

Presentation of meconium aspiration syndrome

A
  • Tachypnoea >60 and tachycardia >160
  • Cyanosis
  • Grunting
  • Nasal flaring
  • Recessions
  • Hypotension systolic <70 mmHg
47
Q

complications of meconium aspiration syndrome

A

Complications
- Partial or total airway obstruction
- Foetal hypoxia
- Pulmonary inflammation infection
- Surfactant inactivation
- Persistent pulmonary hypertension

48
Q

investigations for MAS

A

Bloods
- FBC
- CRP- neonatal sepsis
- Blood culture
- ABG
- Dual pulse oximetry
- Echocardiography
- Cranial US
-
CXR
- Increased lung volumes (due to obstruction)
- Asymmetrical patchy pulmonary opacities
- Pleural effusions
- Pneumothorax
- Multifocal consolidation due to chemical pneumonitis

49
Q

management of MAS

A
  • Place in infant warmed as hypothermia inhibits surfactant production
  • Continuous oxygen sats
  • Ventilation/ oxygen therapy
    o Nasal cannula -aim for 92-97%
    o CPAP (beware of air trapping)
    o If above doesn’t work- invasive ventilation via intubation
  • Antibiotics e.g. ampicillin and gentamicin IV
    o Can be stopped at 48 hrs if cultures and clinical examination findings are negative
  • Surfactant
    o Endotracheal surfactant
  • If pulmonary hypertension – inhaled nitric oxide
  • Corticosteroids
    o Reduce inflammation on the lungs
50
Q

Retinopathy of prematurity background

A
  • A condition which affects preterm and low birth weight babies
  • Born <32 weeks usually
  • Scarring, retinal detachment and blindness caused by abnormal development of blood vessels in the retina
  • Treatment can prevent blindness -> screening very important
51
Q

pathophysiology of retinopathy of prematurity

A
  • Retina development is between 16 weeks to 37-40 weeks gestation
  • Blood vessels grow from the middle of the retina to the outer area
    o Development is stimulated by hypoxia -> normal condition in the retina during pregnancy
  • HOWEVER the retina is exposed to higher oxygen concentration in preterm babies -> particularly with supplementary oxygen during medical care -> therefore the stimulant (hypoxia) for normal vessel development is removed
  • When hypoxic environment recurs, retina responds by producing excessive blood vessels (neovascularisation), as well as scar tissue
  • Abnormal blood vessels may regress and leave retina without blood supply -> retinal detachment
52
Q

assessment of retinopathy of prematutiy

A

The retina is divided into three zones:
* Zone 1 includes the optic nerve and the macula
* Zone 2 is from the edge of zone 1 to the ora serrata, the pigmented border between the retina and ciliary body
* Zone 3 is outside the ora serrata
The retinal areas are described as a clock face, for example “there is disease from 3 to 5 o’clock”. The areas of disease are described from stage 1 (slightly abnormal vessel growth) to stage 5 (complete retinal detachment).

  • “Plus disease” describes additional findings, such as tortuous vessels and hazy vitreous humour.
53
Q

retinopathy of prematurity screening

A

Screening
- Babies born before 32 weeks or under 1.5kg are screen for ROP
- Performed by ophthalmologist
o 30 – 31 weeks gestational age in babies born before 27 weeks
o 4 – 5 weeks of age in babies born after 27 weeks
- Screening should happen every 2 weeks and can cease once retinal vessels enter zone 3- usually around 36 weeks

54
Q

management of retinopathy of prematurity

A

Management
- Treatment involves systematically targeting areas of the retina to stop new blood vessels developing.
- First line is transpupillary laser photocoagulation to halt and reverse neovascularisation.
- Other options are cryotherapy and injections of intravitreal VEGF inhibitors.
- Surgery may be required if retinal detachment occurs.

55
Q

neonatal sepsis backgroun

A
  • Causes by infection in the neonatal periods
  • Can result in signif morbidity and mortality esp if treatment delayed
  • Non specific presentation- requires high degree of suspicion and low threshold for starting broad spec abx treatment
  • Early onset : first 28-72 hours of life
56
Q

pathophysiology of neontal sepsis

A

Group B streptococcus (GBS)
o Commonly found in vagina (25%)
o Does not cause problem for mother
o Can be transferred to baby during labour and cause sepsis
o Prophylactic antibiotics are given during labour to reduce risk of transfer if the mother is found to have GBS in their vagina

  • Escherichia coli (e. coli)
  • Listeria
  • Klebsiella
  • Staphylococcus aureus
57
Q

Risk factors for neonatal sepsis

A
  • Vaginal GBS colonisation
  • GBS sepsis in a previous baby
  • Maternal sepsis, chorioamnionitis or fever > 38ºC
  • Prematurity (less than 37 weeks)
  • Early (premature) rupture of membrane
  • Prolonged rupture of membranes (PROM)
57
Q

Risk factors for neonatal sepsis

A
  • Vaginal GBS colonisation
  • GBS sepsis in a previous baby
  • Maternal sepsis, chorioamnionitis or fever > 38ºC
  • Prematurity (less than 37 weeks)
  • Early (premature) rupture of membrane
  • Prolonged rupture of membranes (PROM)
58
Q

Presentation of neonatal sepsis

A
  • Fever
  • Reduced tone and activity
  • Poor feeding
  • Respiratory distress or apnoea
  • Vomiting
  • Tachycardia or bradycardia
  • Hypoxia
  • Jaundice within 24 hours
  • Seizures
  • Hypoglycaemia
59
Q

Red Flags for neonatal sepsis

A
  • Confirmed or suspected sepsis in the mother
  • Signs of shock
  • Seizures
  • Term baby needing mechanical ventilation
  • Respiratory distress starting more than 4 hours after birth
  • Presumed sepsis in another baby in a multiple pregnancy
60
Q

investigations for neonatal sepsis

A
  • FBC
  • CRP
  • Blood cultures
  • Relevant swabs and cultures
  • Urine culture if relevant
  • Lumbar puncture
    o If thought to be safe to do so
    o Strong clinical suspicion of infection
    o Clinical symptoms or signs suggesting meningitis
61
Q

Management of neonatal sepsis

A

Treatment for presumed sepsis
- If one risk factor or clinical feature - observation for 12 hours
- If two or more risk factors or clinical features start antibiotics
- If one single red flag start antibiotics
- Should be given within 1 hour of making decision to start them
- Take blood cultures before antibiotics given
- Check baseline FBC and CRP
- If suggestive of meningitis – lumbar puncture

Antibiotics of choice: benzylpenicillin and gentamycin (cefotaxime in lower risk babies)

Ongoing management
- Check CRP at 24 hours
- Check blood culture results at 36 hours
- Consider stopping abx if baby is
o Clinically well
o Blood culture negative
o CRP below 10
- Check CRP at 5 days if still on treatment
- If CRP >10 - LP

62
Q

intraventricular haemorrhage cause

A

occurs when fragile and immature blood vessels of premature neonates tear because of changes in blood flow through your baby’s brain after birth e.g. large changes in blood pressure

63
Q

intraventricular haemorrhage presentation

A
  • Within 72 hours of birth
  • Up to 50% asymptomatic
  • Larger bleeds may present as sudden catastrophic systemic collapse, bulging fontanelle, neurological dysfunction (e.g. seizures or anormal movements), anaemia and jaundice
64
Q

investigations for intraventricular haemorrhage

A
  • Cranial US
  • At risk groups of preterm infants <32 wks should be screen by cranial US (at 1wk, and at 1 month and or after sudden deterioration
65
Q

grading of intraventricular haemorrhage

A
  • Subependymal only
  • IVH +- ventricular dilation
  • IVH _- parenchymal involvement
66
Q

prevention of intraventricular haemorrhage

A

o Antenatal steroids
o Prophylactic neonatal indomethacin reduces incidence

67
Q

management of intraventricular haemorrhage

A

o supportive
o irrigation of lateral ventricles following surgical drain insertion is experiment

68
Q

complications of IVH

A
  • post haemorrhagic ventricular dilatation
  • haemorrhagic periventricular infarction
    o causes ischaemia- brain tissue death
69
Q

IVH prognosis

A

Prognosis
- subependymal of uncomplicated IVH does not affect neurodevelopment
- cerebral palsy is common in either PHVD present and treatment is required (50%) or parenchymal extension (80%)

70
Q

Neonatal jaundice background

A
  • Describes yellow colouring of skin and sclera due to high levels of bilirubin in the blood
  • Neonatal jaundice can be caused by unconjugated (physiological or pathological) or conjugated (always pathological)
71
Q

pathophysiology of neonatal jaundice

A
  • Bilirubin is released from RBCs when they break down in an unconjugated form
  • Unconjugated bilirubin is then conjugated by the liver and excreted via the biliary system into the:
    -> GI tract
    -> Via the urine
  • Long term damage such as Kernicterus can be caused by high levels of unconjugated bilirubin
72
Q

Clinical presentation of jaundice in neonates

A
  • Colour: All babies should be checked for jaundice with the naked eye in bright, natural light (if possible). Examine the sclera, gums and blanche the skin. Do not rely on your visual inspection to estimate bilirubin levels, only to determine the presence or absence of jaundice.
  • Drowsy: difficult to rouse, not waking for feeds, very short feeds
  • Neurologically: altered muscle tone, seizures-needs immediate attention
  • Other: signs of infection, poor urine output, abdominal mass/organomegaly, stool remains black/not changing colour
73
Q

Physiological jaundice (unconjugated)

A
  • There is a high conc of maternal RBC in the fetus and neonate – these RBC are more fragile than normal RBC
  • Neonate also have less developed liver function
  • Therefore neonatal RBC break down more rapidly than normal RBC, releasing lots of bilirubin
  • Normally this bilirubin is excreted via the placenta in fetus’
  • However after birth the neonate no longer has access to the placenta
  • Therefore a normal rise in bilirubin occurs shortly after birth: mild yellowing of the skin and sclera from 2-7 days of age -> usually resolves by 10 days and babies remain otherwise healthy
74
Q

Pathological causes of neonatal jaundice

A

Can be split into increased production or decreased clearance.

Always pathological if starts in first 24 hours.

**
Increased production of bilirubin:**
* Haemolytic disease of the newborn
* ABO incompatibility
* Haemorrhage
* Intraventricular haemorrhage
* Cephalo-haematoma
* Polycythaemia
* Sepsis and disseminated intravascular coagulation
* G6PD deficiency

Decreased clearance of bilirubin:
* Prematurity
* Breast milk jaundice
* Neonatal cholestasis
* Extrahepatic biliary atresia
* Endocrine disorders (hypothyroid and hypopituitary)
* Gilbert syndrome

75
Q

Prolonged jaundice

A

Jaundice for >14 days in term infants and 21 days in preterm. Consider:
- Infection
- Metabolic: hypothyroid/ pituitism, galactosaemic
- Breast milk jaundice: well baby, resolves between 1.5-4 months
- GI: biliary atresia, choledochal cyst

76
Q

Investigations for neonatal jaundice

A

Bilirubin
* Transcutaneous bilirubinometer (TCB) can be used in >35/40 gestation and >24 hours old for first measurement. TCB can be used for all subsequent measurements, providing the level remains <250 µmol/L and the child has not required treatment
* Serum bilirubin to be measured if <35/40 gestation, <24 hours old or TCB >250 µmol/L
* Infants that are not jaundice to the naked eye do not need routine bilirubin checking.
* Total and Conjugated Bilirubin is important if suspected; liver or biliary disorder, metabolic disorder, congenital infection or prolonged jaundice. Do not subtract conjugated from total to make management decisions for hyperbilirubinemia.

Further investigations
- Blood group (mother and baby) and DCT
- FBC for haemoglobin and haematocrit

As needed
- U&Es if excessive weight loss/dehydration
- Infection screen if unwell or <24 hours including cultures: blood, urine, CSF
o TORICH screen
- Glucose-6-phosphate dehydrogenase
- LFTs if suspected hepatobiliary disorder

77
Q

Kernicterus

A
  • Brain caused by excessive bilirubin levels
  • It is the main reason that neonatal jaundice is treated to keep bilirubin levels below certain thresholds
  • Bilirubin can cross the BBB and cause direct damage to the CNS

- Presentation
o Less responsive
o Floppy
o Drowsy baby
o Poor feeding

- Prognosis
o Cerebral palsy
o LD
o Deafness

78
Q

interpretation of treatment threshold graph for babies with neonatal jaundice

A
  • Above the line for phototherapy
    o Commence phototherapy and bilirubin monitored
    o During phototherapy repeat bilirubin 4-6 hours post initiation to ensure not still rising, 6-12 hourly once level is stable or reducing
  • Below the line for phototherapy
    o >50µmol/L below, clinically well with no risk factors for neonatal jaundice do not routinely repeat level
    o <50µmol/L below, clinically well repeat level within 18 hours (risk factors present) to 24 hours (no risk factors present)
  • Stopping phototherapy
    o Once >50 umol/l below treatment line on the threshold graphs
    o Check for rebound hyperbilirubinaemia 12-18 hours after stopping phototherapy
79
Q

Phototherapy

A
  • Interpret bilirubin levels using treatment threshold graphs that are gestation specific
    o The more premature the infant the lower the level of bilirubin tolerate before neurological impairment
  • Remember: eye protection, breaks for breastfeeding/ nappy changes/ cuddles
80
Q

if phototherapy not working

A

Exchange Transfusion
This is the simultaneous exchange of the baby’s blood (hyperbilirubinaemic) with donated blood or plasma (normal levels of bilirubin) to prevent further bilirubin increase and decrease circulating levels of bilirubin.
Performed via umbilical artery or vein and is indicated when there are clinical features and signs of acute bilirubin encephalopathy or the level/rate of rise (>8.5µmol/L/hour) of bilirubin indicates necessity based on threshold graphs. This will require admission to an intensive care bed.

81
Q

TORCH infections

A

Paediatrics (Y4) (42 decks)

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