NICU Flashcards

1
Q

prematurity and the NICU

A

complex subspecialty of pediatric PT

knowledge beyond entry level- advanced education- fellowship programs

most fragile patients that PT will treat!

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2
Q

CA=

A

chronological age

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3
Q

AA=

A

age adjusted

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4
Q

viability=

A

23-24 weeks

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5
Q

SGA=

A

small for gestational age

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6
Q

AGA=

A

average for gestational age

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7
Q

LGA=

A

larger for gestational age

gestational diabetes

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8
Q

LBW=

A

low body weight

1501-2500 g= 3.5-5.5 lbs

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9
Q

VLBW=

A

very? low body weight

1001-1500 g= 2.2-3.5 lbs

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10
Q

ELBW=

A

extreme? low body weight

<2.2 lbs

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11
Q

micropremies=

A

<800g

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12
Q

what is average baby weight?

A

~7 lbs (3.25 kg)

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13
Q

500g=

A
  1. 5 kg

1. 1 lb

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14
Q

1000g=

A
  1. 0 kg

2. 2 lbs

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15
Q

1500g=

A
  1. 5kg

3. 5 lbs

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16
Q

2500g=

A
  1. 5 kg

5. 5 lbs

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17
Q

what are the 5 components of APGAR scores?

A
heart rate
resp rate
muscle tone
reflex irritability
color
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18
Q

what are the APGAR scores for heart rate?

A
0= absent
1= 100
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19
Q

what are the APGAR scores for resp rate?

A
0= absent
1= slow and irregular
2= good, crying
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20
Q

what are the APGAR scores for muscle tone?

A
0= limp
1= some flexion and ext
2= active movement
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21
Q

what are the APGAR scores for reflex irritability?

A
0= no response
1= grimace
2= cough or sneeze
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22
Q

what are the APGAR scores for color?

A
0= blue
1= pink, blue extremities
2= pink
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23
Q

neonatal care began in..

A

1880 in France with development of the incubator

increase in survival 1988-2002 for VLBW and ELBW due to antenatal steroids, aggressive resuscitation, surfactant therapy

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24
Q

what are the main principles of neonatal care?

A

support body temp
control infection
minimal handling
special care nursing

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25
Q

what are the nursery levels?

A

level 1: basic care
level 2: specialty care
level 3: subspecialty care

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26
Q

what is nursery level 1?

A

Basic care
35-37 weeks GA

stabilize infants less than 35 weeks until transfer

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27
Q

what is nursery level 2?

A

Specialty care (moderately ill)

2a: >32 weeks
2b: mechanical ventilation for brief period

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28
Q

what is nursery level 3?

A

Subspecialty care

3a: >28 weeks, minor procedures
3b: <28 weeks, high frequency ventilation/ pedi surgical specialists
3c: ECMO and complex cardiac surgery; cardiopulm bypass

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29
Q

what are the 6 environmental changes from in utero to NICU?

A
visual
auditory
gravity
tactile
proprioception
thermo-reg
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30
Q

what is the environmental change from utero to NICU for visual?

A

in utero: dim red glow

NICU: bright lights

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31
Q

what is the environmental change from utero to NICU for auditory?

A

in utero: rhythmic heart beats, respiratory sounds, muted voices

NICU: constant offensive noise-equipment alarms, voices, etc
drugs commonly used in the NICU increase risk for hearing loss

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32
Q

what is the environmental change from utero to NICU for gravity?

A

in utero: amniotic fluid= gravity eliminated, random movements

NICU: gravity makes movement into flexion difficult for hypotonic neonate

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33
Q

what is the environmental change from utero to NICU for tactile?

A

in utero: N/A

NICU: adverse tactile input from necessary medical interventions

causes sustained arousal causing a physiological toll on the child. In utero- sleeps 80% of the time vs. being on avg disturbed 23x in 24 hours– begins to respond negatively to touch b/c unable to discern medical necessity

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34
Q

what is the environmental change from utero to NICU for proprioception?

A

in utero: deep proprio input by uterine wall as moves

NICU: decreased proprio feedback

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35
Q

what is the environmental change from utero to NICU for thermo-reg?

A

in utero: well controlled

NICU: at risk for problems

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36
Q

premie vs. full term:

A

hypotonia

extremities: ext and ABD

decreased midline and flexor activity

decreased spontaneous movements

reflexes: absent, decreased or variable

medical concerns:

  • respiratory issues
  • cardiopulm issues
  • feeding problems
  • temp regulation
  • BP instability
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37
Q

what are other medical categories associated with motor risk?

A

neurological

IVH: intraventricular hemorrhage

respiratory

metabolic

congenital heart disease

viral/infection

substance exposure

other

orthopedic

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38
Q

neurological conditions:

A

HIE: hypoxic ischemic encephalopathy

PVL: periventricular leukomalacia

PVHI: hemorrhagic infarct necrosis

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39
Q

what is HIE?

A

hypoxic ischemic encephalopathy: episode of asphyxia on neonate’s brain (can occur concurrently or serially)

  • cerebral ischemia
  • hypoxemia

interference with umbilical BF (ischemia) resultant systemic hypotension and decreased cardiac output.

and poor gas exchange (hypoxemia) from the mother’s circulation through the placenta to the fetus, recurrent apnea, or severe respiratory disease. Hypoxemia also decreases myocardium causing bradycardia and hypotension which leads to further ischemia.

after severe HIE, stupor or coma requiring mechanical vent. 12-14 hours- seizures and apnea, then out of stupor/coma and increased seizure activity. May re-enter stupor/coma state at 24-72 hours of life. moderate HIE may improve arousal level in 2-3 days and are at much less risk for mortality and longterm neuo problems than severe. Mild-asphyxia immediately before birth and usually recover well requiring minimal resuscitation. Initially lethargic then hyper alertness, irritability, exaggerated moro and DTR.

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40
Q

what is PVL?

A

periventricular leukomalacia

  • symmetrical, non-hemorrhagic, bilateral lesion
  • spastic diplegia
  • most common

ischemic lesion to the brain of the premature infant

motor tracts involving the LEs are closest to the ventricles.

may be transient or may reduce to cystic cavities that are highly correlated with CP. SDI-because of proximity of the ventricular system of descending motor fibers that innervate the LEs (if more lateral can involve UEs also)

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41
Q

what is PVHI?

A

periventricular hemorrhagic infarct necrosis

spastic/hemi/asymmetrical quad

key: prevent fluctuating BP

42
Q

what is IVH?

A

intraventricular hemorrhage

most common brain lesion in <32 weeks

occurs in approximately 40% of premies

there is an inverse relationship b/w gestational age and incidence of IVH

most occur w/in the first 2 postnatal days, 90% by 72 hours

subependymal germinal matrix which is a gelatinous area that contains a rich vascular network. the matrix is prominent from 26-34 weeks of gestation and is usually gone by term.

43
Q

what are the grades for IVH?

A

I: isolated germinal matrix

II: IVH w/ normal vent. size

III: IVH w/ vent dilation

IV: IVH w/ parenchymal hemorrhage (into the periventricular white matter)

I & II: minimal risk for LT neuro deficit

III & IV: sign higher incidence- hydrocephalus, CP and MR, cystic formations

44
Q

respiratory conditions:

A

RDS: respiratory distress syndrome

BPD: bronchopulmonary dysplasia

MA: meconium aspiration

45
Q

what is RDS?

A

respiratory distress syndrome

characterized by: chest wall retraction, cyanosis, expiratory grunt, nasal flaring and tachypnea

<37 weeks

leading cause of death in premature neonates which has reduced lately

due to pulmonary immaturity and a decrease of surfactant associated with RDS and thus introduction of exogenous surfactant has sign decreased morbidity and mortality. Steroids to increase lung development also prior to the preterm birth

46
Q

what is BPD?

A

bronchopulmonary dysplasia:

chronic lung disease of infancy

believed due to iatrogenic factors (caused by Dr.)

trauma with mechanical vent, elevated concentrations of administered O2, endotracheal integration. Ciliary destruction followed by necrosis of respiratory cells. Recovery from damage >= 1 year. Chronic lack of O2 impairs neuromotor development

47
Q

what is mechanical aspiration?

A

aspirates meconium with initial breath

causes airway obstruction that can cause respiratory distress

FT or post term at greater risk with 5-15% of live births

endotracheal suctioning required. MAS is defined as resp distress in an infant through meconium stained amniotic fluid whose symptoms can’t be otherwise explained

48
Q

what are metabolic conditions?

A

metabolic acidosis

hyperbilirubinemia

49
Q

what is metabolic acidosis?

A

reduced body pH

increase hydrogen forming acid or increase loss of basic material

increased production or inadequate excretion of hydrogen or loss of bicarbonate ions in the urine or stools- causes reduction in pH of the body

50
Q

what is hyperbilirubinemia?

A

accumulation of bilirubin in the blood

blood incompatibility, physiological jaundice, reabsorption of blood and infection

kernicterus- yellow staining of the brain -high incidence of mortality and LT neurological sequelae

51
Q

what are congenital heart disease conditions?

A

PDA: patent ductus arteriosus

ASD: atrial septal defect

VSD: ventricular septal defect

tetralogy of fallot

52
Q

what is PDA?

A

shunts blood from pulmonary artery to the descending aorta

normal in utero, closes shortly after birth

thus shunts blood away from lungs which do not participate in gas exchange during fetal life. Typically closes shortly after birth but failure to close can vary from large (congestive heart failure with pulmonary vascular obstructive disease) to small insignificant PDA

53
Q

what is ASD?

A

left to right shunting of blood

majority close spontaneously in first 3 years

lead to pulmonary vascular obstructive disease and associated pulmonary HTN.

if does not close, surgical closing at 4-5 years with suturing or insertion of a patch

54
Q

what is VSD?

A

ventricular septal defect

most common structural cardiac defect

left to right shunting of the ventricles

range from small to large w/ pulmonary HTN and R ventricular hypertrophy. If this hypertrophy becomes great, shunting can reverse as R vent pressure overcomes the L.

In R to L- see cyanosis.

can close spontaneously but if large and symptomatic, will close surgically

55
Q

what is tetralogy of fallot?

A

VSD, PAS, R vent hypertrophy AND an aorta that overrides the interventricular septum

56
Q

what is PAS?

A

pulmonary artery stenosis

narrowing at or just below the pulmonary valve last- aorta being positioned over the ventricular septal defect instead of the L ventricle

57
Q

what are viral/infection conditions?

A

toxoplasmosis

rubella

cytomeglaovirus

herpes

HIV

58
Q

infection:

A

developing brain is highly susceptible to injury from infection in utero or neonatal period

59
Q

what is toxoplasmosis?

A

carried by cat feces- avoid while pregnant

60
Q

what is cytomeglaovirus?

A

herpes virus that usually acts as an opportunistic virus to AIDS

61
Q

80% of children with HIV get it via?

A

via transplacental transmission

62
Q

90% of children with HIV show signs of?

A

encephalopathy (static or progressive)

63
Q

what are conditions of substance exposure?

A

FAS: fetal alcohol syndrome

  • facial features
  • motor coordination difficulties
  • learning difficulties

Cocaine exposure

  • LBW, IUGR, preemies
  • withdrawal

narcotics
-withdrawal from heroine first 4 days; methadone slightly later

64
Q

what is necrotizing enterocolitis?

A

first 6 weeks

<2000g w/ prenatal insults

intestinal ulcers and hemorrhage w/ possible intestinal perforation

65
Q

what is ROP?

A

retinopathy of prematurity: lesion caused by an ischemic event that interfere w/ the development of retinal blood vessels.

high levels of O2 causes vascular proliferation towards the hypoxic area

main cause of childhood blindness w/ abnormal growth of blood vessels occurs in the immature part of the retina

first year- heal themselves; leave nearsightness/strabismus; or continue w/ abnormal growth

66
Q

what are orthopedic conditions?

A

BPI: brachial plexus injury

Clubfoot

metatarsus varus

tibial torsion

CDH: congenital diaphragmatic hernia

67
Q

what is BPI?

A

brachial plexus injury

contractures and atrophy

positioning and ROM

following breech or forceps delivery

spontaneous recovery seen in first few days/weeks. IF delayed contractors at shoulder and elbow, weakness in ER, /, ABD, elbow flex, supination, and wrist /. Positioning to prevent further damage to plexus- 2 week recovery prior to rehab

68
Q

what is clubfoot?

A

plantarflexion, inversion and supination

hereditary

associated w/ other disorders

69
Q

what is metatarsus varus?

A

adduction of the forefoot

flexible-PROM

rigid- serial casting

70
Q

what is tibial torsion?

A

typically self corrects by 8y/o

tibial torsion night brace

medial torsion improves w/ time.

lateral torsion often worsens bc the natural progression is toward increasing external torsion (as seen w/ CP). May be due to lax ligaments at knee.

71
Q

what is CDH?

A

congenital diaphragmatic hernia

dynamic splinting

surgically when discovered later

barlow: supine w/ hips and knees flexed to 90. grasp the thigh medially over the lesser trochanter w/ the other hand stabilizing the pelvis. Apply gentle downward pressure w/ abd hip. As fem head slips over ace tabular rim a subtle clunk is felt.

72
Q

what are common NICU goals?

A

1- state regulation: autonomic, motor, state, attention, interactive

2- parent-infant interaction

3-increased self-regulation behavior through environmental modification

4- postural alignment- therapeutic handling/positioning

5- enhance oral-motor feeding

6- inc. visual & auditory reaction

7- prevent secondary muscle contracture

8-address orthopedic issues

9- developmental assessment

10- positive transition from NICU to home

11- parent education

73
Q

what are goals of therapeutic handling/positioning?

A

facilitate midline orientation/symmetry

promote newborn flexion

enhance self-quieting skills and behavioral organization

encourage relaxation and improve digestion

prevent bony deformities and skin breakdown

increase awareness of body in space

facilitate visual and auditory skill development

facilitate development of head control

decrease hyperextension of neck and trunk

reduce elevation of the shoulders

decrease retraction of the scapula

reduce extension of the LEs

activation of flexor muscles

74
Q

state regulation:

A

5 states to assess in the premie

FT: function smoothly w/ all supporting and enhancing one another

Premie: do not develop simultaneously and demonstrates signs of distress

75
Q

what are 5 states to assess in the premie?

A

autonomic or physiological response

motor development

state control

attention and interaction behaviors

self-regulation

76
Q

understanding signs:

what are signs of stress?

A

happy signs
self-regulatory behaviors

Signs of stress:

  • physiological indicators
  • motor indicators
  • behavioral indicators/state
  • attention/interaction
77
Q

what are happy signs?

A

smooth respiration

pink, stable color

animated facial expressions

brightening of the eyes

“oh” face

cooing

smiling

well-regulated muscle tone

78
Q

what are self-regulatory behaviors?

A

smooth body movements/postural changes

visual locking

hand to mouth activity

sucking

hand clasping

grasping

79
Q

physiological indicators of stress:

A

change in vitals: resp rate/rhythm, HR, BP

color changes

cough, sneeze, yawn

visceral responses (vomiting, bowel movements, hiccups, gagging)

80
Q

what are motor indicators of stress?

A

sudden change in muscle tone

flaccidity

stiffness

changes in quality of movement

81
Q

what are behavioral/state indicators of stress?

A

irritability

staring/gaze aversion

hyper alertness/sleeplessness and restlessness

roving eye movements/ gazed eye appearance

82
Q

what are attention/interaction signs of stress?

A

demonstrate physiological, motor and behavioral indicators

unable to integrate social interaction w/ other sensory input

83
Q

what is congenital muscular torticollis?

A

CMT is defined as the shortening of the SCM causing the neck to laterally flex to the affected side and rotate to the opposite side.

CMT is the most common type of torticollic and the 3rd most common congenital MS anomaly.

CMT is estimated to occur in 1/300 live births.

84
Q

what causes CMT?

A

damage to or shortening of the SCM

exact etiology is unknown

  • in utero positioning
  • lack of space in utero
  • traumatic birth
  • multiple birth
  • increased incidence w/ breech presentation
  • low amniotic fluid
85
Q

what are clinical features of CMT?

A

PHYSICAL EXAM:

  • restriction of neck ROM
  • head tilted toward the shortened SCM and the chin rotated to the opp side
  • characteristic mass palpable in the affected SCM (usually resolves spontaneously by 2-6 months of age)
  • plagiocephaly
  • facial asymmetry

during delivery, if the SCM muscle is stretched or pulled, it may tear, causing bleeding and bruising w/in the ms. the injured ms. develops fibrosis (scar tissue) which causes the ms. to shorten and tighten, pulling the infant’s head to 1 side. The fibrosis forms a mass or lump that sometimes can be felt on the side of the neck.

86
Q

what are associated anomalies w/ CMT?

A

hip dysplasia

foot deformities

plagiocephaly

facial asymmetry

GERD

87
Q

diagnosis of CMT:

A

typically made by the infant’s pediatrician based on physical exam and hx

ant-post and lat radiographs of the cervical spine

ultrasound of the affected SCM

88
Q

differential diagnosis of CMT:

A

alternate diagnoses should be considered in infants in whom CMT is suspected but who lack of hx consistent w/ the typical presentation of CMT

  • skeletal abnormalities
  • Klippel-Feil syndrome
  • benign paroxysmal torticollis
  • ophthalmologic disorders
  • brachial plexus palsy
  • Sandifer’s syndrome/gastroesophageal reflux
89
Q

what are red flags for CMT?

A

poor visual tracking

abnormal muscle tone

extramuscular masses

asymmetries inconsistent w/ CMT

remember medical red flags (vomiting, weight loss, etc)

acute or late onset

suspected hip dysplasia or scoliosis

90
Q

what is positional torticollis?

A

back to sleep campaign

car seats and other baby equipment

little to no tummy time

91
Q

PT eval/hx/intake for CMT:

A

standard intake form

birth history:

  • age of onset of sx
  • pregnancy hx
  • presentation at delivery
  • delivery (forceps, vacuum)
  • head posture and preference
  • tolerance to tummy time and time in “containment” devices
  • milestones
92
Q

objective tests for CMT:

A

posture

ROM (active and passive)

strength (righting reactions)

cranial measurements

pain

skin integrity and symmetry of skin folds

93
Q

PT intervention for CMT:

A

neck PROM

neck and trunk AROM

development of symmetrical movement patterns

environmental adaptations

parent/caregiver education

94
Q

how is torticollis treated?

A

first 12 months: conservative

  • PROM to SCM, upper traps, hyoids
  • positioning and handling
  • AROM/strengthening
  • neck righting reactions
  • environmental adaptions

surgical intervention:

  • > 12 months old; no response to PT
  • referred >12 months w/ cervical rotation >30 degrees and facial asymmetries

untreated:
- facial/cranial asymmetries
- cervical scoliosis w/ compensatory T curve
- occular and vestibular impairment

95
Q

stretching of the tight SCM

A

lateral flexion

cervical rotation

96
Q

strengthening of the contralateral muscles;:

A

lateral neck flexion via head righting

  • side carry
  • ball exercises
97
Q

positioning:

A

position infant w/ head in midline

prop head to discourage lateral neck flexion to side of tight SCM

encourage active rotation to non-preferred side

encourage supervised tummy time

98
Q

what are additional methods used to treat CMT?

A

taping

cervical orthoses

  • tubular orthosis for torticollis (TOT collar)
  • torticollis orthosis (post-op)

massage

botox injections

surgery

craniosacral therapy

myofascial release

chiropractor

99
Q

what is deformational plagiocephaly?

A

caused by external forces applied to the soft infant skull

common in babies w/ CMT since they almost always have the same area of their head in contact with the surface

100
Q

what is plagiocephaly?

A

flattening on one side of the occiput

prominent forehead on same side

may see facial asymmetry w/ flattening on one side of the face and/or misaligned ear, eye or mouth

101
Q

treatment for deformational plagiocephaly:

A

positioning

orthotics

  • DOC band
  • STAR band
102
Q

what are factors influencing CMT outcomes?

A

compliance w/ home program

severity of torticollis

pt’s age at onset of tx

pt’s tolerance for handling