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a Paediatrics by themes > Neonatal Medicine > Flashcards

Neonatal Medicine Flashcards

1
Q

Define Stillbirth.

A

Foetus born with no signs of life ≥24 weeks of pregnancy.

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2
Q

Define Perinatal Mortality Rate.

A

Stillbirths + deaths within the 1st week per 1000 live births and stillbirths.

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3
Q

Define Neonatal Mortality Rate.

A

Deaths of live-born infants within the first 4 weeks after birth per 1000 live births.

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4
Q

Define Neonate.

A

Infant ≤28 days old.

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5
Q

What is the routine examination of the newborn?

A
  • Birthweight and BW centile - gestational age noted
  • General observation
    • Appearance, posture, movements, plethoric or pale, jaundice, rashes
  • Head circumference, fontanelle, face, red eye reflex, palate, clavicles
    • Cephalohematoma = benign - margins of skull sutures → resolve over few months
    • Caput Succedaneum = crosses Suture lines, resolve over few days, start at birth
    • Subaponeurotic/subgaleal haemorrhage = diffuse, boggy swellings with hypovolaemia and shock
    • Tense fontanelle = raised ICP, caput succedaneum, cephalohematoma, chignon → cranial USS
    • Depressed fontanelle = dehydrated
  • Hearing test
  • Breathing, chest wall movement, HR, abdomen, cord, hernias, pectus
    • Fall off by 40 days
  • Femoral pulses, genetalia, anus
  • Muscle tone, whole of back and spine, DDH, hands and feet
    • Fully dorsiflex the foot to touch lower leg to see if true talipes equinovarus
  • Primitive reflexes
    • Moro, stepping, asymmetric tonic, palmar, Babinskis, etc.
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6
Q

What biochemical screening is done at 7 days old?

A
  • Congenital hypothyroidism
  • SCD
  • CF - if +ve = check 4 DNA mutation panels
  • 6 inherited metabolic diseases
    • PKU
    • MCADD
  • Glutaric Aciduria T1*
    • Isovaleric Acidaemia
    • Homocystinuria
    • Maple Syrup Urine Disease
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7
Q

Describe hearing tests given to neonates?

A
  • 1st line: Evoked Otoacoustic Emission (EOAE) Testing – all babies receive this test!
    • Sound emitted into earphone to evoke an echo or emission from the ear if cochlear function is normal
  • 2nd line: Automated Auditory Brainstem Response (AABR) Audiometry
    • A computer will analyse the EEG waveforms evoked in response to a series of clicks
    • Indications
      • Fails EOAE
      • Too young for a regular test
      • Severe learning difficulty
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8
Q

What are the indications for Automated Auditory Brainstem Response (AABR) Audiometry?

A
  • Fails EOAE
  • Too young for a regular test
  • Severe learning difficulty
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9
Q

What test should be performed if a neonate misses their EOAE?

A

Distraction testing

  • Make sounds and observe infant’s behaviour to sound
  • Carried out at 7-9 months
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10
Q

What is Visual Reinforcement Audiometry?

A
  1. Condition child to respond to sound and once they are trained
  2. Reduce the volume until no longer respond as expected from conditioning
  • Carried out between 6m and 3 years - best 10-18 months
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11
Q

What audiometry tests can be carried out on toddlers?

A
  • Visual reinforcement audiometry
  • Performance and speech discrimination testing
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12
Q

What is Pure Tone Audiometry?

A
  • Child wears headphones and responds when they hear a sound.
  • ≥4 year old
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13
Q

What are the 3 main components of the neonatal and infant physical examination?

A
  • Observation
    • Sex determination
    • Cleft palate or foot
    • Respiratory effort
    • Skin colour
  • Body measurements and Vitals
    • Weight
    • Length
    • Head
    • Vitals
      • RR 35-60
      • HR 120-160
  • Exam of body and organs
    • Head to toe
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14
Q

What is Positional talipes?

A

Feet remain in their in-utero position

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15
Q

What is the management of positional talipes?

A

Physiotherapy

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16
Q

What is Talipes equinovarus?

A

Inverted and supinated feet - Club Foot

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17
Q

What are the risk factors for talipes equinovarus?

A
  • Oligohydramnios
  • Associated with DDH
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18
Q

What are the signs and symptoms of talipes equinovarus?

A
  • Foot cannot be fully dorsi-flexed to touch front of lower leg
  • Inverted and supinated feet
  • Affected foot is shorter and calf muscles are thinner
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19
Q

What is the management of talipes equinovarus?

A
  • Mild-moderate = Ponsetti method - plaster casting and bracing
  • Severe = Surgery
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20
Q

What is Hypoxic Ischaemic Encephalopathy (HIE)?

A

Ischaemic brain injury as a consequence of perinatal asphyxia.

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21
Q

What is the consequence of untreated severe HIE?

A

Cerebral palsy

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22
Q

What are the causes of HIE?

A
  • Failure of gas exchange across placenta
  • Interruption of umbilical blood flow - i.e. shoulder dystociia
  • Inadequate maternal placental perfusion
  • Compromised foetus - i.e. IUGR
  • Failure to breathe at birth
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23
Q

What are the signs and symptoms of mild HIE?

A
  • Irritable infant
  • Responds excessively to stimulation
  • Staring eyes
  • Hyperventilation
  • Hypertonia
  • Complete recovery can be expected
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24
Q

How is HIE graded?

A

Response within first 48 hours

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25
Q

What are the signs and symptoms of moderate HIE?

A
  • Abnormalities of movement
  • Hypotonic
  • Cannot feed
  • Seizures
  • Fully resolved by 2 weeks of age = good long-term prognosis
  • Persistent past 2 weeks = bad prognosis
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26
Q

What are the signs and symptoms of severe HIE?

A
  • No normal movements or response to pain
  • Tone in limbs fluctuates hypo- to hyper-tonic
  • Seizures - prolonged and refractory to treatment
  • Multi-organ failure may be present
  • 30-40% mortality
    • 80+% have neuro-disability (if not cooled) → cerebral palsy
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27
Q

What is the management of HIE?

A
  • Supportive
    • Respiratory support
    • Anticonvulsants - treat seizures
    • Fluid restriction
    • Inotropes - treatment of hypotension
    • Electrolytes and glucose - treat hypoglycaemia and electrolyte imbalances
  • Therapeutic Hypothermia
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28
Q

What is Cerebral Palsy?

A

Abnormality of movement and posture, causing activity limitation attributed to non-progressive disturbances that occurred in the developing foetal or infant brain.

  • Clinical features can emerge over time
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29
Q

What is the diagnosis of a brain injury after 2 years old?

A

Acquired Brain Injury

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30
Q

What are the risk factors for cerebral palsy?

A
  • Antenatal
    • Preterm birth
    • Chorioamnionitis
    • Maternal infection
  • Perinatal
    • LBW
    • HIE
    • Neonatal sepsis
  • Postnatal
    • Meningitis
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31
Q

What are the causes of cerebral palsy?

A
  • Antenatal - 80%
    • Vascular occlusion
    • Cortical migration disorders
    • Structural maldevelopment
    • Genetic syndromes
    • Congenital infection
  • HIE during delivery - 10%
  • Postnatal - 10%
    • PVL 2nd to ischemia ± severe intraventricular haemorrhage
      • ↑ survival of very premature babies = ↑CP incidence
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32
Q

What are the signs and symptoms of cerebral palsy?

A
  • Delayed milestones
    • Non-progressive condition so NO LOSS of previously attainted milestones
  • Persistent primitive reflexes
  • Abnormal limb or trunk posture and tone in infancy
    • Stiff legs, scissoring of legs
    • Unable to lift head
    • Unable to weight bear
    • Rounded back when sitting
    • Hypotonia (floppy)
    • Spasticity (stiff)
    • Fisted hands
  • Feeding difficulties - slow, gagging, vomit
  • Oro-motor miscoordination
  • Abnormal gait once walking
  • Hand preference before 1 year old → esp. spastic unilateral CP
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33
Q

How is gross motor function classified in cerebral palsy?

A

Gross Motor Function Classification System

  • Level 1 = Walks no limitations
  • Level 2 = Walks some limitations
  • Level 3 = Walks with handheld mobility device
  • Level 4 = Self-mobility with limitations - may use powered mobility
  • Level 5 = Manual wheelchair
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34
Q

What are the types of cerebral palsy?

A
  • Spastic - 90%
    • Unilateral/Hemiplegia
    • Bilateral/Quadriplegia
    • Diplegia
  • Dyskinetic - 6%
  • Ataxic/Hypotonic - 4%
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35
Q

What is spastic cerebral palsy?

A
  • Damage to UMN (pyramidal tracts) pathway → increased tone (spasticity), brisk reflexes, extensor plantar, ‘clasp knife’ rigidity
    • Clasp knife = increased tone suddenly gives under pressure
    • Dynamic catch → faster the muscle stretched, greater the resistance, “velocity dependent”
  • Presents early, even neonatally as hypotonia
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36
Q

What are the features of unilateral/hemiplegia cerebral palsy?

A

Unilateral arm and leg - face spared

  • Presents 4-12 months with:
    • Fisting of affected hand and asymmetric hand function
    • Flexed pronated arm
    • With a tiptoe walk on affected side
    • Initially flaccid but then ↑↑ tone
    • Likely normal PMHx and unremarkable birth Hx
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37
Q

What are the features of bilateral/quadriplegia cerebral palsy?

A

All 4 limb - often severe

  • Involves the trunk
  • Opisthotonos (extensor positioning)
  • Poor head control
  • Low central tone
    • Associated seizures
    • Microencephaly
    • Moderate to severe learning disability
  • History of hypoxic-ischemic encephalopathy (HIE)
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38
Q

What are the features of diplegia cerebral palsy?

A

Legs affected to a greater degree - but all 4 limbs affected

  • Abnormal walking
  • Difficulties with functional use of hands
  • Associated with preterm birth damage and PVL
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39
Q

What is dyskinetic cerebral palsy?

A
  • Involuntary, uncontrolled movements
  • Caused due to damage to basal ganglia
    • HIE
    • Kernicterus
  • Variable muscle tone predominated by primitive motor reflexes
    • Chorea → irregular, sudden, brief non-repetitive movements
    • Athetosis → slow, writhing movements distally → fanning fingers
    • Dystonia → simultaneous contraction of agonist/antagonist muscles → twisted appearance
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40
Q

What is ataxic cerebral palsy?

A
  • Damage to cerebellum → causes hypotonia, ataxia, mal-coordination, delayed motor development ± intention tremor
  • Genetically determined
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41
Q

What are the appropriate investigations for suspected cerebral palsy?

A
  • MRI → can determine cause if not clear from history, developmental progress, clinical examination and cranial ultrasound
  • Follow-up MDT → if child has risk factors for CP, offer MDT follow-up for 2 years
  • Referral of all children with persistent toe walking
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42
Q

What are the early signs and symptoms of cerebral palsy?

A
  • Unusual fidgety movements or abnormal movement
  • Abnormalities of tone → includes hypotonia, spasticity or dystonia
  • Abnormal motor developing
  • Feeding difficulties
  • Delayed motor milestones
    • Not sitting by 8 months
    • Not walking by 18 months
    • Hand preference before 1 year
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43
Q

What are the red flag features for neurological conditions that aren’t cerebral palsy?

A
  • Absence of risk factors
  • Family history of progressive neurological disorder
  • Loss of already attained cognitive or developmental abilities
  • Development of unexpected focal neurological signs
  • MRI findings suggestive of progressive neurological disorder
  • MRI findings not in keeping with CP
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44
Q

What is the management of cerebral palsy?

A
  • Info about prognosis to parents / parental education
    • Walking - children who can sit by age 2 years are likely to be able to walk unaided by 6 years old
    • Speech - 50% have difficulties with communication with 33% have difficulties with speech and language
    • Life Expectancy - more severe the CP the greater the likelihood of reduced life expectancy
  • Support Groups → SCOPE disability charity
  • Medication
    • Stiffness = 1st : diazepam → 2nd: baclofen
    • Sleeping = melatonin
    • Constipation = Movicol
    • Drooling = anticholinergic
  • Paediatrician - management of medical problems
    • 33% have epilepsy
  • Physiotherapy - encourage movement, improve strength and stop muscles from losing range of motion
  • Speech therapy
  • Occupation therapy - identify everyday tasks that may be difficult and help make these tasks more accessible
45
Q

What counselling should be given to parents with a child with cerebral palsy?

A
  • Explain the diagnosis → damage to the brain that would have occurred early in development
  • The damage to the brain doesn’t get worse, but the way it manifests will change as the child gets older
  • Refer to MDT and especially a paediatrician specialising in developmental disorders
  • Long-term management will include physiotherapy, speech and language therapy and special educational needs
  • Medications can also be given to help with symptoms
46
Q

What is Necrotising Enterocolitis?

A

Serious intestinal injury after a combination vascular, mucosal, toxic and other insults to an immature gut → exact cause is unknown

47
Q

What is the most common cause of surgical emergency in newborn babies?

A

Necrotising enterocolitis → 20% morbidity and mortality rate

48
Q

What are the risk factors for necrotising enterocolitis?

A
  • Prematurity - 7% of premature babies get NEC
  • LBW
  • PDA - or other serious cardiac deformity
49
Q

What are the signs and symptoms of necrotising enterocolitis?

A
  • Early signs
    • Biliary vomiting
    • Feed intolerance
    • Begins after starting enteral feeding
  • Abdomen distension
  • Blood-stained stool
  • Rapid deterioration and shock
50
Q

What are the appropriate investigations for suspected necrotising enterocolitis?

A
  • AXR – ‘gas cysts’ in bowel wall
  • Blood cultures
51
Q

What is the management of necrotising enterocolitis?

A
  • ‘Bell’ staging to decide on management
    • Bowel rest - stop oral feed and switch to parenteral nutrition
    • Broad-spectrum antibiotics - cefotaxime/tazocin and vancomycin
      • Stage IA/IB = 3 days
      • Stage IIA = 7-10 days
      • Stage IIB/III =14 days
    • Laparotomy - if perforated
52
Q

What are the complications of necrotising enterocolitis?

A
  • 20% mortality/morbidity in the acute scenario
  • Development of strictures
  • Malabsorption - if extensive bowel resection is necessary
53
Q

What percentage of newborns become visible jaundiced?

What are the causes of this?

A
  • >50%
  • Physiological Hb release from RBC - high Hb at birth
  • Breast milk jaundice - only >24hrs
  • RBC lifespan of 70 days rather than 120 days in adults
  • BR metabolism less efficient in 1st few days of life
54
Q

What may jaundice in a neonate <24hrs be a sign of?

A
  • Kernicterus
  • Haemolytic anaemia
    • G6PDD
    • PK deficiency
    • Hereditary spherocytosis
  • Infection/sepsis
  • Rhesus disease
  • Liver/metabolic disease
    • Gilbert’s
    • Crigler-Najjar
    • Dubin-Johnson
55
Q

What is kernicterus?

A

A form of encephalopathy due to deposits of unconjugated bilirubin in basal ganglia.

56
Q

What are the signs and symptoms of kernicterus?

A

Spectrum from severe damage → death

  • Lethargy
  • Poor feeding
  • Irritability
  • Increased muscle tone (arched back)
  • Seizures
  • Coma
  • Monitor closely with Rhesus disease
57
Q

What is the prognosis of kernicterus?

A
  • May develop into
    • Cerebral palsy
    • Learning difficulties
    • Sensorineural deafness
58
Q

What may jaundice in a neonate between 2 days to 2 weeks be a sign of?

A
  • Physiological jaundice
  • Breastfeeding jaundice
  • Metabolic
    • Gilbert’s
    • Crigler-Najjar
    • Dubin-Johnson
  • Haemolysis
    • G6PDD
    • PK deficiency
    • Hereditary spherocytosis
  • Infection/Sepsis
  • Congenital hypothyroidism
  • Dehydration/Bruising/Polycythaemia
59
Q

What may jaundice in a neonate >2 weeks be a sign of?

A
  • Physiological jaundice
  • Breastfeeding jaundice
  • Pyloric stenosis
  • Congenital hypothyroidism
  • Biliary atresia
  • Inherited metabolic conditions
    • Gal-1 PUT deficiency
    • A1AT deficiency
    • Tyrosinaemia Type 1
    • Peroxisomal disease
  • Ascending cholangitis
  • Cystic fibrosis
  • Idiopathic neonatal hepatitis
60
Q

Which of the causes of neonatal jaundice are due to cBR opposed to uBR?

A
  • Congenital hypothyroidism - also uBR
  • Biliary atresia
  • Inherited metabolic conditions
  • Ascending cholangitis
  • Cystic fibrosis
  • Idiopathic neonatal hepatitis
61
Q

What are the appropriate investigations for neonatal jaundice?

A
  • Measure Bilirubin
    • <24 hours = Serum BR
      • Direct = total BR : Indirect = uBR → can assume tBR = uBR
    • 24 hours to 2 weeks = Transcutaneous BR
      • Spectroscopy to measure light reflection from the skin → if result is >250 μmol/L → check the result by measuring serum bilirubin
    • >2 weeks = Split serum BR
  • Assess risk of developing kernicterus
  • Investigations of Underlying Cause
    • Haematocrit
    • Blood group of mother and baby
    • DAT test - Coombs if <24hrs
    • FBC / blood film
    • G6PDD levels
    • MC&S of blood, urine and/or CSF - if suspected infection
    • TSH
    • LFTs
    • Osmotic fragility - hereditary spherocytosis
62
Q

What are the risk factors for developing kernicterus?

A
  • Serum bilirubin >340 μmol/L in babies >37 weeks’ gestation
  • Rapidly rising bilirubin of >8.5 μmol/L per hour
  • Clinical features of kernicterus
    • Poor feeding
    • Extreme lethargy
    • Hypotonia
    • High-pitched cry
63
Q

What is the management of neonatal jaundice?

A
  • No treatment needed
  • Phototherapy ± IVIG → converts uBR to water-soluble cBR
    • Repeat BR measurement every 4-6 hours until drops below threshold or stable
      • Ensure short breaks for breastfeeding
      • Protect eyes
      • Monitor temperature
    • Stop once BR >50umol/L below threshold for treatment
    • Check for rebound hyperbilirubinaemia with serum BR measurement 12-18 hours after
    • Intensive phototherapy given if
      • Rapidly rising serum BR
      • Serum BR within 50umol/L of exchange transfusion threshold (after 72hrs of life)
      • BR level fails to respond after 6 hours of therapy
  • Exchange transfusion + Phototherapy ± IVIG + Folic acid after (to prevent anaemia)
64
Q

When is IVIG used in cases of neonatal jaundice?

A
  • Rhesus disease
  • Lower albumin → lower ability to bind BR
  • ABO incompatibility
  • Leaky BBB
65
Q

What counselling should be given to parents with a child with neonatal jaundice?

A
  • Explain that neonatal jaundice is common and usually harmless
    • If <1 day, >14 days or >7 days of first presentation of jaundice = explain you will investigate the cause
    • If physiological explain why it happens
  • Explain treatment - light therapy
  • Reassure that the light therapy is not harmful - but eyes will be protected, and blood samples will need to be taken quite regularly
  • Encourage frequent breastfeeding (e.g. every 3 hours) and to wake the baby up to feed
  • Explain need to stay in after phototherapy has stopped to check rebound hyperbilirubinaemia
  • Refer to resources:
    • NHS Choices Neonatal Jaundice Factsheet
    • The Breastfeeding Network
    • Bliss - for premature and sick babies
66
Q

What are the signs of respiratory distress in a neonate?

A
  • High RR (>60)
  • Laboured breathing
  • Chest wall recessions
  • Nasal flaring
  • Expiratory grunting
  • Cyanosis
67
Q

What is a consequence of high O2 level treatment in a neonate?

A

Retinopathy of prematurity

68
Q

What is Transient Tachypnoea of the Neonate?

A

Delay in resorption of lung fluid resulting in respiratory distress.

69
Q

What is the commonest cause of respiratory distress in term infants?

A

Transient Tachypnoea of the Neonate

  • More common in C-Section deliveries
70
Q

What are the appropriate investigations for suspected transient tachypnoea of the neonate?

A
  • Obs → cyanosis, high RR
  • CXR → fluid in horizontal fissure
  • Diagnosis made after exclusion of other causes
71
Q

What is the management of transient tachypnoea of the neonate?

A
  • Usually settles within first day of life
  • Additional O2 if required
72
Q

What is Persistent Pulmonary Hypertension?

A

High pulmonary vascular resistance → right to left shunting within lungs and at atrial and ductal levels.

73
Q

What is associated with persistent pulmonary hypertension in a neonate?

A
  • Birth asphyxia
  • Meconium aspiration
  • Septicaemia
  • RDS
74
Q

What are the signs and symptoms of persistent pulmonary hypertension?

A
  • Cyanosis after birth
  • Absent heart murmurs with signs of HF
75
Q

What are the appropriate investigations for suspected persistent pulmonary hypertension?

A
  • CXR → normal sized heart but some pulmonary hypovolaemia
  • Echocardiogram → ensure no cardiac defect
76
Q

What is the management of persistent pulmonary hypertension?

A
  • Medications:
    • O2
    • Inhaled NO
    • Sildenafil
  • Ventilation:
    • Mechanical ventilation / Circulatory support
      • High-frequency ventilation
    • If Severe = ECMO ± heart and lung bypass
77
Q

What is the prognosis of persistent pulmonary hypertension?

A
  • Mortality = <10%
  • 25% likely to have some impairment such as learning difficulties or deafness
78
Q

What is Chronic Lung Disease of Prematurity?

A

Lung damage due to pressure and volume trauma from artificial ventilation, O2 toxicity, and infection.

  • Often defined by an O2 dependence at 36w corrected GA
79
Q

What are the risk factors for chronic lung disease of prematurity?

A
  • Premature infants
  • LBW
  • Low GA
80
Q

What are the signs and symptoms of chronic lung disease of prematurity?

A
  • Respiratory distress
  • Increasing O2 requirements
  • Poor feeding
  • Poor weight gain
81
Q

What are the appropriate investigations for suspected chronic lung disease of prematurity?

A
  • CXR → widespread opacification
  • VBG or CBG
    • Acidosis
    • Hypercapnia
    • Hypoxia
82
Q

What is the management of chronic lung disease of prematurity?

A
  • Respiratory support
    • Prolonged artificial ventilation → wean to CPAP → wean to additional O2
  • Corticosteroid therapy
    • Dexamethasone for short term clinical improvement
      • Limit use due to concern about abnormal neuro development and other adverse effects
83
Q

How can chronic lung disease of prematurity be prevented?

A
  • Minimise ventilation-associated lung injury using strict monitoring and maintaining of tidal volume
84
Q

What is Respiratory Distress Syndrome in a Neonate?

A

Deficiency of surfactant - phospholipids and proteins produced by type II pneumocytes

85
Q

What are the risk factors for respiratory distress syndrome in a neonate?

A
  • Prematurity
    • Decreases with increasing gestation
      • 50% of 26-28w
      • 25% of 30-31w
  • Male
  • DM mothers - due to delayed lung maturation
  • CS
  • 2nd born of premature twin
86
Q

What are the signs and symptoms of respiratory distress syndrome in a neonate?

A
  • At delivery or within 4 hours of birth
    • High RR (>60)
    • Laboured breathing with recessions and nasal flaring
    • Expiratory grunting - trying to make +ve airway pressure
    • Cyanosis
87
Q

What are the appropriate investigations for suspected respiratory distress syndrome in a neonate?

A
  • Clinical diagnosis
  • Pulse oximetry
  • CXR
    • Ground-glass appearance
    • Pneumothorax (from ventilation)
    • Indistinct heart border
88
Q

What is the management of respiratory distress syndrome in a neonate?

A
  • Antenatal:
    • Steroid therapy (delivery <34w)
    • Tocolytic therapy
  • Postnatal:
    • O2 and ventilation
89
Q

How can ventilation-associated pneumothoraces be prevented in neonates?

A
  • Ventilated with the lowest pressures that provide adequate chest movement and blood gasses
90
Q

What is the management of a pneumothorax in a neonate?

A
  • Immediate decompression
  • O2 therapy
  • Chest drain if tension pneumothorax
91
Q

What is Meconium Aspiration?

A

Respiratory distress in the newborn due to presence of meconium in trachea.

  • Causes mechanical obstruction and/or chemical pneumonitis → pneumonia/infection
  • Occurs exclusively in immediate neonatal period
92
Q

What percentage of babies pass maconium before birth?

A

8-20%

93
Q

What are the risk factors for meconium aspiration?

A
  • GA >42 weeks - rare in pre-term
  • Maternal history of HTN/PET/smoking/substance abuse
  • Foetal distress/hypoxia
  • Oligohydramnios
  • Meconium stained amniotic fluid
  • Chorioamnionitis
94
Q

What are the signs and symptoms of meconium aspiration?

A
  • Respiratory distress
    • Increased RR
    • Chest retraction
    • Hypoxia
95
Q

What are the appropriate investigations for suspected meconium aspiration?

A
  • CXR (diagnostic)
    • Overinflated lungs
    • Patches of collapse and onsolidation
    • Pneumothorax (from air leak)
    • Pneumomediastinum (from air leak)
  • Bloods
    • FBC
    • CRP
    • Culture
96
Q

What is the management of meconium aspiration?

A
  • Obs
  • Antibiotics → IV ampicillin and IV gentamicin
  • O2 and NIV (i.e. CPAP) - in severe cases
97
Q

What is Meconium Ileus?

A

Thick, sticky meconium that has a prolonged passing time

  • Meconium usually passes within 24hrs of delivery → if it doesn’t there may be ileus
98
Q

What are the signs and symptoms of meconium ileus?

A
  • No passing of meconium stool in first 24hrs
  • Vomiting of meconium instead of passing it as stool
99
Q

What is meconium ileus associated with?

A
  • Cystic fibrosis - 90%
  • Biliary atresia
100
Q

What is the management of meconium ileus?

A
  • 1st line = Gastrograffin enema - N-acetylcysteine can be used
  • 2nd line = Decompressive surgery
101
Q

What are the causes of bilious vomiting in the neonate?

A
  • NEC
  • Duodenal atresia
  • Jejunal/Ileal atresia
  • Meconium ileus
  • Malrotation volvulus
102
Q

At what age does bilious vomiting present in NEC?

A

Prematurity

103
Q

At what age does bilious vomiting present in duodenal atresia?

A

<6hrs after birth

104
Q

At what age does bilious vomiting present in jejunal/ileal atresia?

A

<24hrs after birth

105
Q

At what age does bilious vomiting present in meconium ileus?

A

24-48hrs after birth

106
Q

At what age does bilious vomiting present in malrotation volvulus?

A

3-7 days after birth

107
Q

What is the management of duodenal atresia?

A

Duodenoduodenostomy - anastomosis between two duodena to bypass an obstructed segment of the duodenum

108
Q

What is the management of jejunal/ileal atresia?

A

Laparotomy

a Paediatrics by themes (26 decks)

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