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Paediatrics > Neonatal Medicine > Flashcards

Neonatal Medicine Flashcards

1
Q

What are the classifications for a term, pre-term and post-term baby?

A 
Term = gestation 37-41w
Pre-term = <37w 
Post-term = >42w
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2
Q

What are the classifications for birthweight (low, v low, extremely low vs normal)?

A

normal = 3.5kg
low = <2.5kg
v low = <1.5kg
extremely low = <1kg

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3
Q

How to classify SGA vs LGA?

A

weight either <10th centile (SGA) or >90th centile (LGA)

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4
Q

State the features of the following maternal infections or pregnancy consumptions:

  • Alcohol (FAS)
  • Smoking
  • Rubella
  • Varicella
  • Syphillis
A

FAS:

  • absent philtrum, small upper lip
  • microcephaly
  • cardiac abnormalities
  • reduced IQ/LD
  • IUGR

Smoking:

  • stillbirth (foetus born with no signs of life>24w) or miscarriage
  • IUGR

Rubella (triad of):

  • cataracts
  • deafness
  • cardiac abnormalities

note: most risk <16w

Varicella:

  • skin scarring and limb hypoplasia
  • chorioretinitis/cataracts and small eyes
  • neurological defects (low IQ, microcephaly)

Syphillis:

  • rhinitis
  • saddle-nose
  • sensorineural deafness
  • hepatosplenomegaly, jaundice
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5
Q

What is positional talipes? How is it managed?

A

Where feet remain in their in-utero position; caused by intrauterine compression.
Normal sized foot which CAN be fully dorsiflexed to touch front of lower leg –> Mx = physiotherapy

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6
Q

What is Talipes Equinovarus and what are some causes/RFs? How is it treated?

A

‘club foot’ - inverted and supinated feet \ / (1:1000, M»F 2:1)

Idiopathic, may be secondary to oligohydramnios, also associated with DDH

Here the foot cannot be fully dorsiflexed to lower leg like positional talipes. Affected foot also is shorter and thinner calf muscles.

Mx = Ponsetti method (if mild-moderate; plaster casting and bracing) OR if severe, surgery

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7
Q

What is HIE? What are the causes?

A

Hypoxic Ischaemic Encephalopathy (HIE) is the neonatal condition which occurs when there has been perinatal asphyxia –> cardiorespiratory depression (0.05-1 in 1000 births)
(CP is the post neonatal condition - HIE which hasn’t been treated)

Causes of HIE:

  • Failed gas exchange over placenta (placental abruption)
  • Interruption of umbilical blood flow (e.g. shoulder dystocia –> cord compression)
  • Inadequate placental perfusion e.g. maternal hypotension
  • Compromised foetus (IUGR)
  • Failure to breathe at birth
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8
Q

How is HIE categorised?

A

The response within the first 48h is how the HIE is graded:

Mild:
- irritable infant
- responds excessively to stimulation
- staring eyes
- hyperventilation, 
-  hypertonia 
(complete recovery can be expected)
Moderate:
- abnormal movement
- hypotonic
- cannot feed
- seizures
(if fully resolved by 2w then good prognosis, otherwise bad)

Severe:
- no normal movements or response to pain
- limb tone fluctuates from hypo- to hypertonic
- seizures
(30-40% mortality, 80% have neurodisability if not cooled, which –> CP)

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9
Q

How do you manage neonates with HIE?

A

Supportive:

  • respiratory support
  • anticonvulsants
  • fluid restriction (transient renal impairment)
  • inotropes (for hypotension)
  • electrolytes and glucose (treat hypoglycaemia and electrolyte imbalances)

Therapeutic Hypothermia (>36w) - mild hypothermia can reduce the morbidity from HIE, requires NICU

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10
Q

What is Cerebral Palsy (CP)?

A

Non-progressive disturbances in the brain in the developing foetal or infant brain causing abnormalities in movement and posture which limits activity.

1/400 births - most common cause of motor impairment

(if 2y+ it is not CP but Dx as acquired brain injury)

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11
Q

What are the RF for CP?

A

Antenatal: pre-term birth, chorioamnionitis, maternal infection

Perinatal: LBW, HIE, neonatal sepsis

Post-natal: meningitis

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12
Q

What are the causes of CP and their prevalence?

A

80% antenatal - vascular occlusion, structural maldevelopment, congenital infection, genetic syndromes, cortical migration disorders

10% due to HIE in delivery (e.g. cord compression –> dyskinetic CP)

10% post-natal –> PVL - periventricular leukomalacia secondary to ischaemia (+severe intraventricular haemorrhage)

Increased CP incidence when there is increased survival of very premature babies

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13
Q

How may someone with CP present?

A
  • Delayed developmental milestones (e.g. not sitting by 8m, not walking by 18m) +/- persistent primitive reflexes
    (non-progressive so no loss of previously attained milestones)
  • abnormal limb or trunk posture and tone in infancy –> stiffness and scissoring of legs, unable to weight bear, hypotonia (floppy) or spasticity (stiff), unable to lift head, rounded back when sitting, fisted hands)
  • feeding difficulties (slow, gagging, vomit), promoter miscoordination
  • abnormal gait if walking
  • hand preference BEFORE 1y (particularly spastic unilateral CP)

(Gross motor function classified by GMFCS) - level 1 is walking with no limitations - level 5 is with wheelchair)

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14
Q

How can you categorise CP and how common are each of these?

A 
Spastic CP (90%)
- damage to UMN pathway (pyramidal/corticospinal tracts)
Dyskinetic CP (6%)
- damage to basal ganglia

Ataxic (hypotonic) CP (4%)
- damage to cerebellum

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15
Q

Describe Spastic CP? What are the 3 main types and their presentation? What causes are these associated with?

A

Spastic CP (90%)

  • damage to UMN pathway (pyramidal/corticospinal tracts) –> increased tone - spasticity, brisk reflexes, ‘clasp knife’ rigidity (increased tone then gives under pressure)
  • presents early, even neonatally as hypotonia

3 main types of spastic CP:

  1. Unilateral/Hemiplegia -unilateral arm and leg, face-sparing
    - Presents at 4-12 months
    - [think Egyptian] fisting of affected hand and symmetric hand function, flexed pronated arm + tip-toe walk on affected side
    - initially flaccid but then increased tone
    - likely normal PMH and unremarkable birth Hx (unknown antenatal cause)
  2. Bilateral/Quadriplegia - all 4 limbs, often severe
    - involves trunk
    - opisthotonos
    - poor head control
    - low central tone (associated seizures, microcephaly, moderate-severe LD, (history of HIE!)
  3. Diplegia - legs affected to greater extent but all 4 limbs affected
    - abnormal walking
    - difficulty with functional hand use
    (associated with pre-term birth damage and PVL)
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16
Q

Describe dyskinetic CP? What is it caused by?

A

Dyskinetic CP (6%)

  • damage to basal ganglia
  • causes include HIE or kernicterus
  • involuntary uncontrolled movements
  • variable muscle tone predominated by primitive motor reflexes:
  • -> chorea (irregular, sudden, brief non-repetitive movements)
  • -> athetosis –> slow, writhing movements distally e.g. fanning fingers
  • -> dystonia –> simultaneous contraction of agonist/antagonist muscles i.e. twisted appearance
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17
Q

Describe ataxic (hypotonic) CP?

A

Ataxic (hypotonic) CP (4%)

  • damage to cerebellum
  • hypotonic CP, most genetically determined
  • hypotonia, ataxia, mal-coordination, delayed motor development +/- intention tremor
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18
Q

How would you investigate CP?

A

Ix:

  • MRI (offer if cause is not clear from Hx, developmental progress, clinical examination and cranial USS) - GA/sedation usually needed
  • Follow-up MDT (for 2y if RFs)
  • Screen for red flags of other neurological conditions (e.g. progressive disease)
19
Q

How would you manage a child with CP?

A

Mx:
[V. MDT ORIENTATED]

  • -> Patient education + information about condition and prognosis
  • walking: children who can sit by 2y likely to walk unaided by 6y
  • speech: 50% have communicating difficulties, 33% have SAL difficulties
  • life expectancy likelihood varies on severity of CP
  • support = SCOPE charity and www.cerebralpalsy.org.uk
  • -> MDT approach (main members = nurse, paediatrician, physio, OT, SALT, dietician, psychologist; supplementary = visual/hearing, orthotics, orthopaedics)
  • Paediatrician - 33% have epilepsy so give anticonvulsants (1/5 affected)
  • Physio - encourage movement and improve strength and prevent loss of muscle ROM
  • SALT - improve language abilities
  • OT - identify everyday tasks that may require help/assistance
  • Good nutritional intake and supplements (VitD, Ca)
  • Refer for hearing or visual impairment issues

Medication:

  • Stiffness - 1st line Diazepam, 2nd Baclofen
  • Sleeping - melatonin
  • Constipation (3/5 affected) - Movicol
  • Drooling - anticholinergic
20
Q

How would you explain the CP Dx in PACES?

A
  1. Explain Dx - damage to the brain which has happened early in the child’s development ,the damage does not get worse but may show itself in different ways as they get older
    - Refer to MDT + paediatrician specialist - this will be long term care and involve many members including physiotherapists etc and what they do
    - medicines can also be given for symptoms such as seizures, stiffness, sleeping problems etc
    - support groups etc
21
Q

What is necrotising enterocolitis and who does it affect?

A

Most common surgical emergency in newborns with a 20% morbidity and mortality

Tends to affect PREMATURE (7% of prems) and LBW babies (PDA is also a RF)

Occurs due to immature/fragile bowels causing serious intestinal injury (thought to be due to combined factors including ischaemia + infection as often begins after starting enteral feeding)

22
Q

How may a baby with NEC present?

A

early signs = biliary vomiting, feed intolerance

  • abdomen distension
  • blood stained stool
  • rapid deterioration + shock
23
Q

How would you manage (Ix + Mx) a baby with NEC

A

Ix:

  • -> Exam, Obs
  • -> Blood cultures to exclude sepsi, FBC, electrolytes (hyponatremia)
  • -> AXR (‘gas cysts’ in bowel wall, distended loops of bowel, portal venous gas, intramural air)

Mx:
Bell staging is used to decide management
- Bowel rest (NBM and switch to parental feeding)
- NG tube on free drain, monitor aspirates
- BS Abx (cefotaxime/tazocin and vancomycin) for either 3 days (Stage IA/IB), 7-10 days (IIA) or 14 days (IIB)
- Respiratory support, fluids +/- inotropes
- Laparotomy if perforated on AXR or failed response to other treatment

long term consequences (bar mortality) include development of strictures and malabsorption if bowel resection required

24
Q

What is TTN, cause, how does it present and how is it managed?

A

Transient tachypnoea of the neonate is the commonest cause of respiratory distress in term infants (more common in C-section deliveries)
Cause: delay in resorption of lung fluid

Babies will present with cyanosis, high RR (>60)

Ix: CXR shows fluid in horizontal fissure
[Dx after exclusion of other causes]

Mx: Additional O2 if needed but settles within 1st day of life

25
Q

What is persistent pulmonary hypertension in a newborn, it’s associations and how is it Ix + managed?

A

Life-threatening occurrence in neonates due to high pulmonary vascular resistance (R->L shunting within lungs and atrial+ductal levels)
–> Associated with birth asphyxia, meconium aspiration, septicaemia and RDS

S/S: Presents with cyanosis after birth - absent heart murmurs and signs of HF

Ix:

  • -> CXR (normal heart but pulmonary oligaemia - increased dark/translucent areas)
  • -> Urgent Echo to ensure no cardiac defect

Mx:

  • Oxygen (+/- inhaled NO)
  • Ventilation and intubation; if unsuccessful could use HFOV (high-frequency oscillatory ventilation) or even ECMO (extracorporeal membrane oxygenation)
  • Consider surfactant, and suction of secretions
  • Fluids and inotropes

mortality <10%, 25% expected to have some hearing/learning impairment

26
Q

What is RDS and who does it affect?

A

Respiratory distress syndrome is a deficiency of lung surfactant
Common in those born <28w gestation (50% born 26-28w, 25% born 30-31w)

RF: male, DM mothers due to delayed lung maturation, CS births and 2nd born of premature twin

27
Q

How may a child with RDS present and how would you Ix + manage it vs prevention?

A

PC: high RR (>60), increased work of breathing and grunting, cyanosis if severe

Ix:

  • clinical diagnosis
  • SpO2
  • CXR has characteristic ‘ground glass’ appearance, may show pneumothorax due to RDS/ventilation, indistinct heart border

Mx:
[Antenatal]
- Steroid therapy (delivery<34w)
- Tocolytic therapy so steroids have at least 24h to work (delays labour)

[Post natal]

  • O2/OptiFlow and ventilation (CPAP or articifical, mechanical)
  • +/- exogenous surfactant
28
Q

What is CLD in neonates and who does it affect?

A

Chronic lung disease of prematurity is often defined as O2 dependence beyond 36w gestational age. Occurs when infection, barotrauma or iatrogenic injury causes chronic lung problems [BPD is one type/also CLD].
Increased risk in premature infants, LBW or low GA

29
Q

How would CLD present and how would you manage it (Ix+Mx)?

A

PC:

  • 23-26w progressing from ventilation –> wean to CPAP –> supplementary O2
  • Signs of respiratory distress, poor feeding, poor weight gain

Ix:

  • CXR - widespread opacification
  • CBG or VBG - acidosis, hypercapnia, hypoxia

Mx:

  • Respiratory support of high flow humidified oxygen/ CPAP/ventilation + surfactant
  • Corticosteroid therapy (dexamethasone if 8/+d old for short-term clinical improvement - however use limited due to neurodevelopment SE)
  • Caffeine citrate if 30/+w corrected GA, starting within 3d birth
  • NO: only if pulmonary hypoplasia/HTN

Important to reduce ventilation/intubation if not needed due to injury.
Also note: babies on long-term O2 are at risk of ROP (screening for this)

30
Q

How may a pneumothorax occur in a neonate? How is it managed?

A

May occur from RDS, or the ventilation used as therapy for RDS –> pulmonary interstitial emphysema
(as prevention, infants should be ventilated with the lowest pressures to provide adequate chest movement and blood gases)

Mx:

  • Immediate decompression
  • O2 therapy
  • Chest drain if tension pneumothorax
31
Q

What is meconium aspiration? What are some RFs?

A

Respiratory distress in a newborn due to presence of meconium in the trachea (causing mechanical obstruction or/and chemical pneumonitis)

  • > 8-20% pass meconium before birth giving a chance of aspiration
  • > Rare in preterm - greater risk the greater the gestational age
  • > RFs = GA>42w, Fetal disress/hypoxia, meconium stained amniotic fluid, oligohydramnios, chorioamnionitis and maternal Hx of HTN/smoking or substance abuse
32
Q

How does meconium aspiration present and how would you Ix it?

A

Sx:
- Respiratory distress - increased RR, chest retraction and hypoxia

Ix:

  • CXR (diagnostic) = over inflated lungs, patches of collapse and consolidation, may see pneumothorax/pneumomediastinum from air leak
  • FBC/CRP/Cultures
33
Q

How would you manage meconium aspiration?

A

Mx:

  • Observe if normal term infant with meconium stained fluid but no history of GBS
  • Features of infection then give IV ampicillin and gentamicin
  • If severe - give O2 and NIV (CPAP)
34
Q

What is meconium ileus and what is it associated with? How is it managed?

A

Meconium ileus is a thick, sticky meconium that has a prolonged passing time

  • Usually passed within 24h of delivery but if not, then may be ileus
  • Child may vomit instead of stool passage
  • Associated with CF (90%) and billiary atresia

Mx:

  • 1st line = Gastrograffin enema (or NAC)
  • 2nd line = surgery
35
Q

What are some differentials for billious vomiting in neonates?

A

DDx:

  • > NEC - in premature infants
  • > Duodenal atresia - <6h after birth, associated with Down’s
  • > Jejunal/ileal atresia - <24h after birth
  • > Meconium ileus - 24-48h after birth
  • > Malrotation volvulus - 3-7d after birth
36
Q

What is neonatal hypoglycaemia? What are some RFs for it? How do babies present?

A

Glucose <2.2 mol/L

RFs = Maternal diabetes/GDM, IUGR, maternal beta-blocker use

May be asymptomatic or:

  • -> Jittery
  • -> Feeding difficulties
  • -> Cyanosis/blue tinge + breathing difficulties
37
Q

How is neonatal hypoglycaemia managed? How is it prevented?

A

Prevented by:

  • Feeding baby within 30 mins of birth
  • Frequent subsequent feeding with milk every 2-3h

Mx:

  • IF sugar 1.5-2.5mmol/L
  • -> Feed immediately
  • -> Recheck glucose after 30 mins; if stilll low then consider admission and starting IV glucose
  • If sugar <1.5 mmol/L or symptomatic
  • -> Admit to neonatal unit
  • -> Confirm hypoglycaemia with lab blood glucose assay
  • -> IV 10% glucose 2ml/kg bolus
  • -> Followed by infusion of 3.6ml/kg/hr of 10% glucose
  • -> Frequently recheck glucose until stable: aim for 3-4mmol/L (e.g. every 15min)
38
Q

If the neonatal hypoglycaemia is due to hyperinsulinism, what can you give? [3]

A

Glucagon infusion

Diazoxide (stops insulin release) + chlorthiazide

Somatostatin analogue

39
Q

What is billiary atresia and a future risk of it? How does it present?

A

Rare - progressive fibrosis and obliteration of extra and intra hepatic trees
–> Chronic liver failure in 2y

S/S:

  • Persistent neonatal jaundice - obstructive mild jaundice
  • No vomiting
  • Pale stools, dark urine
  • Normal birthweight but then faltering growth
  • Hepatosplenomegaly
40
Q

How would you Ix biliary atresia? What is the gold standard, and confirmatory test? What would these results show?

A

Ix:

  • cBR is raised after 14d
  • USS 1st line –> shows triangular cord sign
  • LFTs, PT/INR, FBC, GGT raised
  • Gold = TIBIDA isotope scan (cholescintegraphy - nucelar scan)
  • ERCP + biopsy for confirmation
41
Q

How would you treat biliary atresia?

A

Mx:

  • 1st line = Kasai hepatoportoenterostomy
  • Transplant if unsuccessful
  • Mx of complications, e.g. in first year:
  • -> Fat soluble vitamins (ADEK)
  • -> Urseodeoxycholic acid t promote bile flow
  • -> Prophylactic antibiotics (cotrimoxazole) to prevent cholangitis
42
Q

What is Potter’s sequence and 2 causes of it?

A

Potters = typical physical appearance of a baby due to oligohydramnios experienced when in the uterus: e.g. club foot + pulmonary hypoplasia

  1. Bilateral renal genesis –> low UO
  2. AR PKD (autosomal domiannt form in adults) –> low UO

Do genetic karyotyping (+/- renal USS)

43
Q

What is CAKUT and its mutated gene?

A

Congenital anomalies of kidney and urinary tract (CAKUT) = group of abnormalities affecting the kidneys or other structures of the urinary tract

PAX2 mutation

44
Q

What is the difference between a low rectal anomaly and a high rectal anomaly?

A

Low anorectal anomaly – anus closed over, in a different position or narrower than usual + fistula to skin

High anorectal anomaly – bowel has closed end at high level, does not connect with anus, usually associated with bladder/urethral/vaginal fistula

Paediatrics (14 decks)

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