Neonates Flashcards
1
Q
ADEPT trial
A
No difference in NEC in early vs late oral feeds in <35 weeks IUGR abnormal dopplers
2
Q
What things increase the risk of NEC (6)
A
PDA (indomethacin makes no difference)
Blood transfusions
H2 blockers
Antenatal augmentin
IVABs for >4 days (also increase death from NEC)
Targeting O2 sats 85-89% in extreme prems
3
Q
What things do not increase the risk of NEC (5)
A
Indomethacin for PDA Trophic feeds Early vs late feeds Increasing feeds by 30mL/kg/day Fortifier
4
Q
What things decrease the risk of NEC (3)
A
Antenatal steroids
Donor breast milk compared to formula
Probiotics (reduce incidence of severe NEC)
5
Q
Things that are protective against IVH (3)
A
Antenatal steroids
Indomethacin
Surfactant
6
Q
Reduce the risk of RDS (2)
A
Antenatal steroids
Caffeine (decrease assisted ventilation time)
7
Q
Reduce the risk of CNLD (1)
A
Caffeine (also decreased assisted ventilation time)
8
Q
Reduces the need for PDA ligation (1)
A
Caffeine
9
Q
Benefits of caffeine (CAP trial) (8) + 1 other finding of CAP
A
Decreased assisted ventilation time Decreased CNLD Decreased need for PDA ligation Increased disability free survival Decreased risk CP Decreased cognitive delay Reduced functional impairment and motor impairment at 11 years Decreased severe ROP
No significant different in mortality or developmental indices at 5 years
10
Q
Benefits of antenatal steroids (5)
A
Protective against NEC
Protective against IVH- decreased mortality, decreased grade 3 & 4, decreased PVL
Reduced RDS
Reduced mortality
Reduced risk systemic infections in the first 48 hours
11
Q
Things that reduce the risk of mortality (4)
A
Probiotics
Antenatal steroids
Resus in air vs O2
Targeting 90-95% in extreme prems (vs 85-89%
12
Q
Resus in air vs O2 (2)
A
Reduced severity HIE
Reduced mortality
13
Q
Worse developmental outcomes (4)
A
Hypoglycaemia- slightly worse
Hyperglycaemia- risk neurosensory issues
Low O2 85-89%- increased CP prems
Late preterm compared to term- worse dev 24 months, 3x incidence CP compared to term
14
Q
Indomethacin (3)
A
No difference in neurodevelopmental outcomes
Protective against IVH
No difference to NEC risk
15
Q
Sepsis (2)
A
Probiotics = reduced risk late onset sepsis
Antenatal steroids = reduced risk systemic infections in the first 48 hours
16
Q
ROP (2)
A
Caffeine = decreased severe ROP Oxygen = increased
17
Q
Probiotics
A
Reduced risk late onset sepsis
Reduced risk overall mortality
Reduced incidence severe NEC
18
Q
Components of breast milk not found in formula (7)
A
Secretory IgA
Lactoferrin- immunomodulation, iron chelation, antimicrobial action, trophic for intestinal growth
K-Casein
Oligosacccarides- prevention of bacterial attachment
Cytokines
Growth factors
Enzymes
19
Q
Conditions for which human milk has been suggested to have a protective effect (5)
A
Infections- diarrhoea, OM, UIT, NEC, sepsis
GI- coeliac disease, Crohns
Malignancy- all childhood cancer, lymphoma, leukaemia
Allergy
Obesity
Hospitalisations
20
Q
Complications of TPN (9)
A
Line complications eg. infection, thrombosis Hypoglycaemia Azotemia Nephrocalcinosis Hypoglycaemia if feeds suddenly stopped Hyperlipidaemia and hypoxia from lipid infusion Hyperammonaemia Metabolic bone disease (long term) Cholestatic jaundice/liver disease
21
Q
Cephalohaematoma
A
1-2%
Reabsorbed within 2/52-3/12
Can remain as a bony prominence of cyst-like defect
Assoc with underlying skull fracture 10-25%
22
Q
Subgaleal haemorrhage
A
Rupture of the emissary veins connecting the dural sinus to the superficial veins of the scalp
Resolves in 2-3 weeks
Risk of consumptive coagulopathy
23
Q
Predisposing factors to IVH (7)
A
Prem (unable to regulate cerebral blood flow), RDS, HIE, pneumothorax, hypovolaemia, hypertension, bleeding disorders (DIC, alloimmune thrombocytopenia, vit K deficiency eg. maternal phenytoin/phenobarbitone)
24
Q
Incidence IVH <1.5kg
Incidence PVL<1kg
A
30% <1.5kg
3% <1kg
25
Germinal matrix
o Gelatinous supependymal germinal matrix- site of origin for embryonal neurons and fetal glial cells, which migrate outwardly to cortex
This region prone to bleeding due to being highly vascular + poor tissue support
Involutes as infant approaches term gestation
26
PVL
Focal necrotic lesions in the periventricular white matter- causing cerebral white matter injury resulting in motor abnormalities
27
Timing of IVH
75% dx within first 3 days
Small percentate late(day 14-30)
Rare after day 30
28
Clinical features IVH
Mostly asymptomatic
Severe- acute deterioration on day 2-3 of life- hypotension, pallor, apnoea, cyanosis, neurological signs, metabolic acidosis, anaemia
29
IVH grading
Grade 1: bleeding isolated to the GM
Grade 2: bleeding within the ventricle, no ventricle dilatation
Grade 3: IVH with ventricular dilatation
Grade 4: IVH and parenchymal haemorrhage
Ventriculomegaly: mild = 0.5cm-1cm, moderate = 1-1.5cm, severe >1.5cm
30
US features PVL
| Clinical features PVL
```
Usually present day 3-10 as early echodense phase, followed by echolucent (cystic) phase day 14-20
Spastic diplegia (lower motor extremity tracts)
```
31
Incidence post-haemorrhagic hydrocephalus
3-5% all VLBW
| 10-15% all LBW with IVH
32
Clinical signs hydrocephalus, prognosis
Enlarging head circ, bulging fontanelle, widely split sutures, lethargy, apnoea, bradys
Signs may be delayed by 2-4 weeks
3-5% require VP shunt, may have spontaneous regression
33
IVH prognosis- percent with Bayley Scales <70 in mental development, psychomotor development CP, blindness or deafness
```
Grade 1: no sig different
Grade 2: 50%
Grade 3: 55%
Grade 4: 70%
Prognosis worse in PVL, cystic PVL and hydrocephalus
Worse again with VP shunt insertion
```
34
Risks of high dose corticosteroids in VLBW (postnatal)
Week 1: metabolic derangements, poor growth, sepsis, bowel perf
After week 1: CP and neurodevelopmental delay, impaired growth
Risk worse with >6 weeks course
35
Pathophysiology of HIE
Neuronal necrosis of the cortex = cortical atrophy = cognitive delay, CP, dystonia, epilepsy, ataxia, bulbar and pseudobulbar palsy
Parasagittal injury = Spastic quadriparesis, cognitive delay, visual and auditory processing difficulty
More likely to have focal or multifocal cortical infarcts leading to focal seizures and hemiplegia
36
HIE stage 1
Hyperalert, normal tone/posture, hyperreflexia, myoclonus, strong moro reflex, mydriasis
No seizures and normal EEG
37
HIE stage 2
Lethargic, hypotonic
Flexion posture, hyperreflexia, mycoclonus, weak moro, myosis
Seizures common (~24 hrs due to cerebral oedema), low voltage EEG + seizure activity
Lasts 1-14 days
Variable outcome
38
HIE stage 3
Coma, flaccid tone, decerebrate posturing
Absent reflexes, no myoclonus, absent moro
Pupils unequal with poor light reflex
Decerebrate posturing rather than seizures
EEG- burst supression to isoelectric
Lasts days - weeks, results in death or severe deficits
39
Ix in HIE
Gold standard is diffusion-weighed MRI- increased sensitivity and specificity early
CT can be used to identify focal haemorrhagic lesions, diffusion cortical injury and damage to basal ganglia
US prefered in pre-term infants
Ampliture-intergrated EEG (aEEG)- PPV 85%, NPV 91-96% for adverse neurological outcomes
40
Therapeutic cooling in HIE
Reduces mortality and major neurodevelopmental impairment in term and near-term infants
Decreased apoptpsis, supresses production of neurotoxic mediators (glutamate, free radicals, NO, lactate)
Keep rectal temp 33.5
Start within 6 hours of birth, continue for 72 hours
41
Complications of therapeutic cooling
Thrombocytopenia
Bradycardia
Subcutaneous fat necrosis with hypercalcaemia
Cold injury syndrome
42
Prognosis of HIE
20-30% die in the neonatal period
| 33-50% of survivors have permanent neurodevelopmental abnormalities
43
Risk factors for death/severe impairment in HIE (10)
pH <6.7 on initial gas (90% death/impairment)
BE >25 (72% mortality)
Apgar 0-3 at 5 mins
Decerebrate posturing
Severe basal ganglia-thalamic lesions
Persistent of signs of severe HIE at 72 hours
Lack of spontaneous activity
Low apgar at 20 mins
Absence of spontaneous resps at 20 mins
Persistent of abnormal neurology at 2 weeks
44
Erb palsy
C5, C6
Waiter-tip arm
Good prognostic sign if retains hand power
Can have associated phrenic nerve injury (C345)
45
Klumpe paralysis
C7, C8, T1
| Paralysed hand and ipsilateral horner syndrome
46
Physiology of transition to pulmonary respiration
Increased maternal catecholamine, vasopression, prolactin, glucocorticoids = change lung epithelia from a chloride secretory mode to Na reabsorptive mode = liquid from the lungs is driven into the interstitum
With first breath, surfactant decreased surface tension of the alveoli
With first breath decreased hydrostatic pressure in the pulmonary vasculature increases pulmonary blood flow = better removal of pulmonary fluid
Rising pCO2, declining pH and PO2 = trigger for first breath
47
Treatment apnoea of prematurity
Caffeine or theophylline
- Increase central resp drive by lowering threshold of response to hypercapnia, enhancing contractility of the diaphragm and reducing diaphragmatic fatigue
SIde effects of caffeine- tachycardia, feed intolerance
Doxapram as a second line
HFNP/CPAP if mixed or obstructive picture
48
Idiopathic apnoea of prematurity- onset, pathophysiology, prognosis
Onset first 1-2 weeks of life (may be later with RDS)- needs Ix if onset later than this, or term infant
Usually mixed apnoea- obstructive apnoea leads to paradoxical response- hypoxia results in central apnoea
Usually resolve by 37/40, longer if <28/40
Not an independent risk factor for SUDI
49
Incidence RDS
<28/40 60-80%
| 32-36 15-30%
50
Risk factors RDS (7)
```
Maternal DM
Multiple births
LSCS
Precipitous labour
Asphyxia
Cold stress
Affected sibling
```
Asphyxia, hypocoa, pulmonary ischaemia, cold stress - suppress surfactant production
51
Protective factors RDS
Maternal hypertension, maternal heroin use, PROM, antenatal corticosteroids
52
Constituents of surfactant (4)
Lecithin
Phosphhatidylglycerol
Apoproteins (surfactant proteins A, B, C, D)
Cholesterol
53
Pathophysiology of RDS
Surfactant deficiency --> failure to obtain FRC --> lungs become atelectatic
Prem lungs more compliant - more prone to atelectasis
Atelectasis = VQ mismatch = hypercapnia
Hypercapnia + hypoxia + acidosis = pulmonary arterial vasoconstriction = R to L shunt
54
Surfactant comes from
Type II alveolar cels
55
Natural course of RDS
Worsening for 3 days, then improvement
56
CXR RDS
Fine reticular granularity of the parenchyma and air bronchograms
Typical pattern develops during the first day
57
Indications for surfactant (4)
pH <7.2
pCO2 >60
O2 satd <90% at FiO2 40-70% on CPAP
Persistent apnoea
58
Pharmacological treatment for RDS
Systemic corticosteroids- mortality and CNLD at 36 weeks sig reduced, but side effects significant
Inhaled corticosteroids- reduced death/CNLD at 36 weeks, no increase in adverse events
Caffeine reduced extubation failure
59
Adverse effects UAC (7)
Serious complications 2-5%
Thrombosis- clots on tip 95%, signs of thrombosis include narrowing of the pulse pressure, disappearance of the dicrotic notch
Spasm- treat with topical GTN, remove line
Vascular perforation
Ischaemic/chemical necrosis of abdominal organs
Impairment of circulation to the leg
Infection
Renovascular HTN weeks later
60
Adverse effects UVC (5)
```
Thrombosis
Vascular perforation
Infection
Cardiac perforation
Portal vein thrombosis --> portal hypertension
```
61
Pathophysiology CNLD
Volutrauma
Free radicals from O2 (immature lungs cannot metabolise free radicals)
Worsened with infection, chorio, PDA, malnutrition
?FHx asthma or atopy
62
Histology CNLD (3)
Alveolar hypoplasia
Variable saccular wall fibrosis
Minimal airway disease
63
4 stages of CNLD
Acute lung injury
Exudative bronchiolitis
Proliferative bronchiolitis
Obliterative fibroproliferative bronchiolitis
64
Classification of CNLD
For infants <32 weeks who had O2 >=28 days, assess at 36 weeks/discharge home (whichever earliest)
For infants >32 weeks who had O2 at least 28 days, assess at 28-56 days postnatal or DC home (earliest)
Mild: now on RA
Moderate: FiO2 <30%
Severe: >30% FiO2 or PPV
65
Prevention of CNLD (2)
| Makes no difference (1)
Early CPAP and rapid extubation
Vitamin A supplementation in first 4 weeks
Surfactant makes no difference
66
Prognosis CNLD
Mortality 10-25% (cor pulmonale or infection esp RSV)
Asthma later in life
Frequent readmissions with pulmonary infections (improve with age)
67
MAS incidence
5% of infants with med liquor
30% require mechanical ventilation
3-5% mortality
68
MAS pathophysiology
Complete peripheral airway obstruction leads to atelectasis and VQ mismatch
Partial airway obstruction leads to ball-valve effects and therefore air trapping = air leak
Proximal airway obstruction
Inflammation and chemical pneumonitis
69
MAS natural Hx
Usually improves within 72 hours
| Tachypnoea may persist for days-weeks
70
MAS CXR
patchy infiltrates, coarse streaking of both lung fields, increased AP diameter, flattening of the diaphragm
71
Predisposing factors for PPHN
```
Any respiratory pathology (eg. MAS, TTN)
Being generally unwell
Polycythaemia
Maternal NSAID use (in utero constriction of DA)
Maternal late trimester SSRI use
Amniotic leak/oligohydramnios
```
72
Clinical features PPHN
Presents in the first 12 hours of life
Severe cyanosis with tachypnoea, minimal resp distress
Hypoxia is labile and out of proportion to CXR findings
Hypoxia intermittently unresponsive to O2
73
Treatment PPHN
Oxygenation
Ensure adequate BP- ionotropes if required
NO- relaxes vascular smooth muscle (side effects methaemoglobinaemia, nitrous dioxide acting as a pulmonary irritant, rapid wean leading to rebound pulmonary HTN)
ECMO in 5-10%
74
Morgagni diaphragmatic hernia
Retrosternal hernation- failure of the sternal and crural portion of the diaphragm to fuse
2-6% of CDH
Often diagnosed incidentally as mass behind heart on CXR
Can have recurrent resp infections, cough, vomiting, GORD, strangulation
75
Bockdaleck diaphragmatic hernia- epidemiology, associations
Females 2x more common
90% of CHD
85% L sided, <5% bilateral
Associated abnormalities in 30%- CNS lesions, oesophageal atresia, omphalocele, cardiovascular lesions, T21, T13, T18, Cornelia de Lange, Turner
76
Bockdaleck diaphragmatic hernia diagnosis
Antenatal US >50%- polyhydramnios, chest mass, mediastinal shift, gastric bubble/liver in thoracic cavity, fetal hydrops
Best prognostic factor fetal lung:head size on 24-26week US: lung:head < 1 = no survival
77
Bockdaleck diaphragmatic hernia clinical presentation
Can have a "honeymoon" period of up to 48 hours
Scaphoid abdo
Resp distress
BS in chest
78
Bockdaleck diaphragmatic hernia prognosis and ongoing issues:
67% survival (limited by pulmonary hypoplasia)
Often develop BPD and have ongoing pulmonary issues later in life
GORD 50% - more common in hiatal hernia
Intestinal obstruction 20%
Recurrent hernia 5-20%
FTT in the first few years
Neurocognitive defects – 67% of ECMO, 24% without ECMO
Pectus excavatum and scoliosis
79
Pulmonary haemorrhage and surfactant use
Rate increased- 1-5% of patients who receive surfactant
80
Progress of air through the GIT as seen on AXR
Air in the jejunum by 15-60 mins
Air in the ileum by 2-3 Air in the colon by 3 hours
No air in rectum at 24 hours is abnormal
81
Things associated with meconium plugs (5)
```
Small L colon syndrome in infants of diabetic mothers
CF
Rectal agangliosis
Maternal opiate use
Maternal MgSO4 for PET
```
82
Incidence of NEC
1-5% of NICU patients
| Incidence and fatality inversely related to gestation and BW
83
Pathogenesis of NEC
Mucosal or transmucosal necrosis of the intestine
Most common distal ileum and proximal colon
Triad of intestinal ischaemia, enteral nutrition (metabolic substrate for bacteria) and bacterial
translocation
Clusters of cases suggest an infectious component
84
Modified Bell's staging for NEC- Stage I
Clinical signs: lethargy, temperature instability, apnoea, bradycardia, vomiting, abdominal distension, haematochezia
AXR: intestinal dilatation
Treatment: NBM, TPN, NG suctioning, ABs
85
Modified Bell's staging for NEC- Stage II
Clinical signs: (as per stage I: lethargy, temperature instability, apnoea, bradycardia, vomiting, abdominal distension, haematochezia)
+ metabolic acidosis, thrombocytopenia, abdominal tenderness, absent bowel signs
IIa: mildly ill
IIb: moderately ill
AXR: intestinal dilatation, pneumatosis intestinalis, portal venous gas
Treatment: NBM, TPN, NG suctioning, ABs
86
Modified Bell's staging for NEC- Stage III
IIIa: shock
Can also have ascites
Medical Mx
IIIb: perforation
AXR: pneumoperitoneum
Surgery
87
Indications for surgery for NEC
```
Perforation
Positive result from abdominal paracentesis culture
Failure of medical Mx
Single fixed bowel loop on XR
Abdominal wall erythema
Palpable mass
```
88
NEC prognosis
Medical Mx fails in 20-40%
Failed medical Mx= 10-30% mortality
Early complications:
- Dehiscence
- Infection
- Complicaions with stoma
Late complications:
- Strictures 10%
- Short bowel syndrome
- Cholestatic jaundice
- Adverse neurodevelopmental outcomes
89
Cause of 10% weight loss after birth
Diuresis driven by ANP release
| Increased urinary sodium excretion
90
UVC line placement
```
Should be at the level of the diaphragm (T8-9)- IVC just outside R atrium
UVC length (cm) = (1.5 x birthweight (kg)) + 5.5
```
91
UAC line placement
High- T6-T9
Low- L3/L4
106% shoulder-to-umbilicus distance (+2cm),
UAC distance (cm) = (birthweight (kg) x4) + 7
92
Ventilation of pre-term infant
Rate 60-80
I time 0.5-0.38sec
Volume guarantee- 4mL/kg
PaCO2 45-55mmHg
93
CPAP benefits
Reduced need for IPPV
Decreased rate and severity of apnoea
Increased chance of successful extubation
Decreased resp acidosis and O2 requirements post extubation
94
CPAP risks
Increased incidence IVH
Nasal trauma
Increased incidence pneumothorax
95
To improve oxygenation
Increase FiO2
Increase PIP
Increase PEEP
Increase IT
96
To improve carbon dioxide clearance
Decrease PIP
Decrease PEEP
Increase ET
Increase rate
97
Oxygenation index (a measure of how much mean airway pressure is being used to acheive the current arterial oxygen tension- higher = worse lung disease)
OI = (MAP/FiO2)/PaO2
98
SIMV
Ventilator delivers a mandatory number of breaths at a set PIP and IT, but will attempt to synchronise with the baby's respirations
If apnoeic- just the back up rate
If breathing- will get the mandatory no of breaths, and baby can take additional breaths
+/- VG
99
SIPPV
AKA Patient triggered ventilation (PTV)
AKA Assist control (A/C)
Each spontaneous breath triggers a ventilator breath at a set PIP and IT
If apnoeic/hypopnoeic a backup rate will be delivered
If breathing above the rate, the baby will receive each breath assisted
+/- VG
100
Pressure support ventilation (PSV)
Each spontaneous breath delivers a set PIP, but the IT is determined by the baby
+/- VG
101
HFV
Background continuous distending pressure = MAP (analagous to PEEP)- determines oxygenation
Oscillation of the airway pressure around the MAP at high frequencies = amplitude - determines CO2 removal (determined by chest wiggle)
Decreased frequency improves CO2 clearance
Frequency = 10-15Hz
102
Criteria for cooling HIE
Criteria for acidosis:
- Apgar =<5 at 10 mins
- pH <7.00 or BE =10 mins
And either of:
- Evidence of mod-severe encephalopathy 1-6 hours of age
- Seizures
And no absolute contraindications:
- Uncontrolled critical bleeding
- Uncontrolled hypoxia due to PPHN
- Imminent withdrawal of life supports planned
And meets all of the following:
- >=35 weeks
- BW >= 1800g
- Able to begin cooling by 6 hours of age
103
Stimulus and timing of PDA closure
Functional closure 15-48 hours, anatomical closure by 3 weeks in term babies (longer in prems)
Main stimulus is increased PaO2
104
How much glucose should be given in hypoglycaemia (mg/kg/min)
7.5-8 mg/kg/min of glucose
105
Formula for calculating glucose infusion rate (mg/kg/min)
(Glucose % x mL/kg/day)/144
106
Threshold for hypoglycaemia screen
Requiring >= 10mg/kg/min glucose
| Persistent/recurrent after 72 hours
107
How much glucose does the neonatal liver produce
6-8mg/kg/min
108
Fractional excretion of Na- calculation, what the results mean
FE Na = Urine Na x Serum Cr / Serum Na x Urine CR
FE Na+≥2.5% in term infants suggests renal failure.
FE Na+<2.5% in term infants suggests pre-renal failure
FE Na+ is high in preterm infants because of tubular immaturity.
109
Electrolyte requirements in neonates
Na 3 mmol/kg/day
K 2 mmol/kg/day
Ca 1 mmol/kg/day
110
Causes of hyponatremia in prem baby (8)
High FE Na due to prematurity (renal tubular immaturity)
Inadequate Na+ intake.
Excessive water intake- Excessive maternal fluid intake during labour/delivery can lead to neonatal hyponatraemia.
Diuretic therapy, especially loop diuretics (e.g. furosemide).
Acute tubular necrosis (tubular Na+ loss) and other causes of renal failure.
Indomethacin- Reduces free water clearance and fractional excretion of sodium, with the lower free water clearance leading to hyponatraemia.
SIADH- ADH has a limited ability to concentrate the urine in the newborn, and acts primarily as a vasopressor.
Excess Na+ loss- Diarrhoea, Gastric, pleural, CSF, 17OH progesterone deficiency.
111
PVL- areas of the brain affected, clinical features
Periventricular leucomalacia most commonly involves the optic radiations adjacent to the trigone of the lateral ventricle, and the anterior corticospinal fibres adjacent to the intraventricular foramen
Clinically, it can produce decreased visual acuity, inferior visual field constriction, visual cognitive impairment, ocular motility disturbances, and spastic diplegia.
112
Congenital lobar emphysema
Usually becomes apparent in neonatal period
Many diagnosed prenatally
Clinical features: range from mild tachypnoea and wheeze to severe dyspnoea and cyanosis
Affects upper and middle lobes, LUL most common
Affected lobe is nonfunctional due to overdistension which may cause atelectasis of the ipsilateral normal lung
Mediastinal shift due is to overdistension
113
Blood group factors associated with haemolytic disease of the newborn
90% D (Rh)
| Mostly big C and big E otherwise
114
Amount of Rh positive blood required to enter maternal circulation to mount a response
>1mL
115
Why is ABO incompatibility protective against Rh incompatibility
Rh positive cells are rapidly removed from the maternal circulation by pre-existing Anti-A or Anti-B antibodies
116
What metabolic complication is common in babies with haemolytic disease of the newborn
Hypoglycaemia- hepatosplenomegaly + large pancreas in utero due to anaemia
117
Kernicterus- pathology
Deposition of unconjugated bilirubin in the basal ganglia and brainstem nuclei
At risk babies eg. disease, asphyxia- disruption of the blood-brain barrier leading to earlier kernicterus
118
Kernicterus - clinical features
2-5 days after birth
Lethargy, poor feeding, absent moro initially
Opisthotonos
Convulsions and spasms
By 3 years of age: bilateral choreoathetosis, seizures, intellectual impairment, high-frequency hearing loss
119
Impact of Na on growth
| Ix to determine if total body Na stores are adequate
Sodium is an important growth factor, stimulating cell proliferation and protein synthesis and increasing cell mass
Maintaining urinary Na+ higher than K+ assures that Na+ intake is adequate
120
Changing from CMV to HVF
Baseline CXR, ensure large enough ETT with no leaks
Leave FiO2 the same
Set Hz 10-15 (low term, high prem)
MAP ~2-4cmH20 higher than on CMV
Set amplitude required for discernible chest wiggle
121
Outcome ELBW
40% mortality
16% no impairment
22% mild impairment
22% mod-severe impairment
