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Infant Transport Team > Neonatal Neurology > Flashcards

Neonatal Neurology Flashcards

1
Q

Etiology of Neonatal Encephalopathy

A 
HIE 
Perinatal stroke
Metabolic Abnormalities 
Structure Brain
Maternal Toxins
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2
Q

SENTINEL events include

A

consider perinatal history when suspecting HIE:

-abruption, cord prolapse, non-reassuring FHR

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3
Q

Clinical Presentation of Neonatal Encephalopathy

A
  • abnormal LOC (hyperalert, obtunded, irritable++)
  • diminished movements
  • apneas
  • feeding difficulties
  • poor tone
  • abnormal posturing
  • absent primitive reflexes
  • seizures
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4
Q

Markers of acute HIE, no definition for cooling but signs suggestive of HIE

A
  • APGAR <5 at 5 and 10
  • cord pH <7.0
  • acute HIBI on MRI
  • presence of multi organ failure consistent with HIE
  • no gold standard, just a clinical case for NE
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5
Q

Indications for HIE cooling and HIE criteria

A

Criteria A:

  • ≥36 weeks GA within 6 hours
  • cord pH ≤7.0 or BD ≥-16

Criteria B:
>36 weeks
-pH 7.01-7.15 OR
BD -10 to -15.9 on cord gas within 1 hour

plus

hx of Acute perinatal event.

  • APGAR score < 5 at 5 and 10
  • or at least 10 minutes of PPV
  • evidence of mod-severe NE on exam
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6
Q

Complications of HIE treatment

A
  • arrythmias
  • hypotension
  • PHTN
  • coagulopathy
  • glycemic issues
  • lyte disturbance
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7
Q

Neuro exam tips for HIE

A
  • serial exams important (neuro status can fluctuate)
  • level of alertness/states of consciousness
  • medication effect
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8
Q

HIE tx and mgmt

A
  1. immediate mgmt:
    - ABC, passive cooling (turn off radiant warmer)
    - prevent secondary injury by massive cooling
  2. Therapeutic Hypothermia:
    ~33.5 rectal
    (active/passive NNT 6-7)
  3. Investigations (labs, imaging, CORD GAS)
  4. 50ml/kg/d TFI
  5. glucose goal: 3.3 - 6
  6. Morphine for analgesia
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9
Q

Risk Factors for IVH

A
  • Prematurity is greatest RF (≤32 weeks)
  • birth weight <1500g
  • HIE insult
  • vacuum or forceps assisted delivery
  • rapid shifts in BP
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10
Q

Why does prematurity have increased risk of IVH

A

premature neonates have undeveloped myelin sheath, meaning the neurons are at higher risk of injury.

The germinal matrix at 28 -32 weeks begins to involute and is generally absent after 32 weeks GA

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11
Q

Grading I-V IVH

A
  1. Hemorrhage limited to subspendymal matrix
    1. Hemorrhage extending into ventricular system
    2. Hemorrhage extending into ventricular system, with acute dilation because of flooding of 50% or more of one or both of the lateral ventricles
      4.
      Hemorrhage grade 1-3 with extension into brain parenchyma
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12
Q

IVH mgmt

A
  1. supportive (ICP bundle, Normo-everything)
  2. seizure mgmt
  3. Neuroprotection of newborn (Mg/antenatal steroids, cord clamping)
  4. serial monitoring via cranial U/S
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13
Q

Extra-cranial Birth related injuries

A
  • subgaleal hemorrhage
  • cephalohematoma
  • caput succedaneum
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14
Q

Subgaleal Hemorrhage and mgmt

A

Hemorrhage above the periosteum but beneath the epicranial aponeurosis.
-can have boggy heads

mgmt:

  1. supportive care for coags/blood volume
  2. monitor fontanelle size and head circumference
  3. standard investigations for labs
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15
Q

Neonatal seizures mgmt

A
  1. Phenobarbital (loading 20mg/kg/dose over 20 minutes
  2. Phenobarbital 10mg/kg/dose
  3. phenobarbital 10mg/kg/dose
  4. Phenytoin (20mg/kg/dose over 20 minutes)
  5. Keppra (40-60mg/kg loading dose
  6. Midaz infusion (0.15-0.2mg/kg bolus + infusion 0.1-0.2mg/kg/hr)
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16
Q

What are some of the primitive reflexes

A

Suck, gag, grasp, pupillary and moro

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17
Q

How to assess central tone

A
  1. head lag
  2. vertical suspension
  3. ventral suspension
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18
Q

What to look for during posture assessment

A

arm/hip/knee

-extension,flexision or decorticate/decerebrate posturing

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19
Q

What are TORCH infections

A 
Toxoplasma
Other "covid"
Rubella
CMV
Herpes
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20
Q

What are TORCH infection

A

They are a group of congenital infections that are passed from mother to child at some point during pregnancy, during delivery or after birth

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21
Q

What are some metabolic abnormalities that can cause neonatal encephalopathy

A

Hypoglycemia

Inborn errors of metabolism

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22
Q

HUS days in high risk case

A

day 3, day 10-14 and day 48

23
Q

Clinical presentation of neonatal encephalopathy

A

-Abnormal LOC (hyperalert, obtunded, irritable, lethargic)

  • diminished movements
  • respiratory distress/apnea
  • feeding difficulties
  • poor tone
  • abnormal posturing
  • absent primitive reflexes
  • seizures
24
Q

Laboratory investigations and other diagnostic test needed for HIE

A

CBC, Chem 7, coags, Liver, cord gas

OTHERS:
EEG, HUS, Brain MRI, metabolic panel, LP

25
Q

Whats the treatment window for starting therapeutic hypothermia? And how long is cooling sustained?

A

Initiated within 6 hours after delivery, sustained for 72 hours at 33.5 +/- half degree

26
Q

What is the only proven therapy in HIE to prevent secondary injury. And whats the NNT?

A

cooling at 33.5 for GA of ≥35 weeks. NNT 6-7

27
Q

What is the purpose of sedation in HIE

A

Initially to prevent shivering, decreasing demand

28
Q

What are the abx coverage for HIE typically

A

amp and gent

29
Q

What would be some causes of term babies having IVH

A

Trauma during delivery, HIE, coagulopathy, therapeutic hypothermia, genetic abnormalities - not GM injuries cause its gone by 32 weeks.

30
Q

What’s the percentage of IVH that present “silent”

A

25-50% of cases are silent but are detected on routine ultrasound screening

31
Q

What are some causes of benign movements

A
  • jitteriness
  • sleep myoclonus (rapid jerk in sleep, more prone for these movements)
  • unlike seizures, these are always suppressible with firm pressure
32
Q

Benzodiazepine in status seizures

A

Ativan .1mg/kg over 30s-1minute

Midazolam .1mg/kg over 2-3 minutes

33
Q

Phenytoin classificaation

A

sodium channel blocker

34
Q

Loading dose of Phenytoin

A

20mg/kg over 20 minutes

35
Q

Special consideration with phenytoin

A
  • use .22micron filter because of risk of precipitation
  • not very soluble (incompatible with D5W)
  • negative inotrope
  • max rate of administration 1mg/kg/min to prevent hypotension/arrythmias
  • lots of drug reactions
36
Q

Phenobarbital classification and dose

A

barbiturate , which increases gaba efect

dose 20mg/kg iv over 20min

37
Q

Keppra loading dose and moa

A

MOA: unclear, but likely CCB

Loading dose: 60mg/kg

38
Q

Differentiate periodic breathing from AOP

A 
AOP = >20s
periodic = <20s
39
Q

The three types of AOP

A

central
obstructive
and mixed

40
Q

AOP is thought to be produced by

A

a blunted peripheral and central chemoreceptors. Normally the peripheral chemoreceptors response to variations in PCO2/PaO2. In preterms, the chemoreceptors are less responsive to these changes.

41
Q

When is apnea considered significant

A

When its associated with bradycardia or desats

42
Q

HIE criteria A

A

≥36 weeks and ≤6 hours of age

Cord gas <7.0 or BE ≥ -16

43
Q

HIE criteria B

A
  • pH 7.01 to 7.15 or BD -10 to -16 on card gas within one hour
  • Hx of sentinel event with APGARS <5 at 10 or 10 min PPV
  • Evidence of moderate to severe encephalopathy on clinical exam
44
Q

Define Neonatal encephalopathy

A

Neonatal encephalopathy is a heterogenous, clinical defined syndrome characterized by disturbed neurologic function in the easiest days of life in an infant born at or beyond 35 weeks gestation, manifested by a reduced LOC, seizures, often accompanied by difficulty with imitating and maintaining respiration, and by depression of tone and reflexes

45
Q

Clinical presentation of neonatal encephalopathy

A

The neonate who is encephalopathy may have an abnormal state of consciousness and present with:

  • hyperalert
  • irritability
  • lethargic
  • obtunded
  • diminished spontaneous movements
  • respiratory or feeding difficulities
  • poor tone
  • abnormal posture
  • absent primitive reflexees
  • seizure activity
  • low Apgars
46
Q

What are some important functions to think of outside of neurology with encephalopathy patients

A

when thinking about encephalopathy, think about the autonomic function affecting other systems (cardiovascular tone, respiratory function, metabolism of glucose)

47
Q

Neuroassessment :

LOC neonate

A

LOC

  • alert, lethargic, or comatose
  • AVPU
  • Sleeping vs awake
  • if the baby is approached with a sound they should startle
  • the baby shouldn’t be hyperexcitable
47
Q

Neuroassessment :

LOC neonate

A

LOC

  • alert, lethargic, or comatose
  • AVPU
  • Sleeping vs awake
  • if the baby is approached with a sound they should startle
  • they baby shouldn’t be hyperexcitable
48
Q

Neuro assessment Neonatal:

posture

A
  • Normal posture is flexed hip and knees (fetal position)
  • Immature babies have extension of the legs normally
  • “arms/hip/knee extension/flexison.. decorticate or decerebrate posturing”
49
Q

Neonatal neuro assessment: Central tone (axial tone)

A
  • “normal, hypotonic or flaccid”
  • head lag
  • head lag assesses axial tone. When assessing, lift the baby from the bed by their arms but support their head to assess
50
Q

Neonatal neuro assessment peripheral tone

A

normal, hypotonic, flaccid,

Limb tone:

  • ability of the provider to stretch or flex the limbs and the passive resistance seen. Passive tone is assessed when the baby is not fighting manipulations.
  • Hypertonia of the limbs is seen as inability to stretch.
51
Q

Pathogenesis of IVH in premature neonates

A

Premature neonates have an underdeveloped myelin sheath, meaning thee neutrons are at higher risk of injury.

Germinal matrix fragility from lack of structural support due to immaturity. In preterm infants GMH-IVH generally originates within the GM; Which is the highly cellular and vascularized layer in thee subtendymal and sub ventricular zone that gives rise to neutrons and glia during fetal development

At 28 weeks GA, the GM beings to involute as it cellularity and vascularity decreases by term, its generally absent. This is why we dont see IH beyond 28-32 weeks

Consider IVH to the significant form of brain injury in preterm infants, where as HIE is the significant form of brain injury in term infants.

52
Q

Why dont we see IVH in neonates >28 weeks

A

At 28 weeks GA, the GM beings to involute as it cellularity and vascularity decreases and by term, its generally absent. This is why we don’t see IVH beyond 28-32 weeks

Infant Transport Team (14 decks)

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