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Fellowship revision > Paediatrics > Flashcards

Paediatrics Flashcards

1
Q

What is the most cephalad intervertebral space @ which a spinal can be sited in a neonate where the risk of damage to the SC is minimal?

A

L3-4. 3rd foetal month the SC extends length of vertebral canal. Newborn/neonate: cord terminates @ L3. Adult: cord terminates @ L1-2 space.

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2
Q

Whats the TNZ in a neonate in deg c?

A

32-34 naked, 24-27degC clothed. TNZ= ambient temp range over which maintenance of core temp requires minimal energy expenditure. Neonate is a child in the first 28 days of life. Under 3/12 children can’t shiver. premiering (30wks gestation) has TNZ 34-35deg naked & 28-30 deg clothed. Adult TNZ is 27-37deg C.

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3
Q

what is the dose for defibrillator in paeds?

A

4J/kg

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4
Q

dose for Adr in paeds arrest?

A

10microg/kg

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5
Q

dose for atropine in paeds arrest?

A

20microg/kg

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6
Q

dose for fluid in paeds arrest?

A

20mL/kg

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7
Q

What’s the ETT size <1kg?

A

2.5

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8
Q

ETT size 1-3kg?

A

3

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9
Q

ETT size 3.5kg?

A

3.5

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10
Q

ETT size 10kg 1yo?

A

4

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11
Q

size of an ETT >1yo?

A

age/4 + 4

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12
Q

main cause of arrest in paeds?

A

hypoxia from airway obstruction

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13
Q

what’s the CPR ratio for infants & children?

A

15:2

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14
Q

dose of amiodarone for paeds arrest?

A

5mg/kg, after 3rd shock

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15
Q

Is paracetamol dosing based on actual or ideal body weight? What’s the dosing in <32 wks? <1/12? >1/12 (and loading)? When should loading not be given?

A

ideal, 10kg/kg (BUT 8-hourly so max 30mg/kg/24hrs), 10mg/kg (max 40mg/kg/24hrs), 15mg/kg (max 60mg/kg/24hrs), 20mg/kg loading dose >1/12 BUT the total 24hr dosing must not be exceeded. Don’t do a loading dose if the pt has received a paracetamol-containing product within the preceding 24hrs.

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16
Q

What’s a newborn vs neonate vs infant?

A

First mins to hrs of birth vs within first 28/7 of birth vs combined neonatal period up to 12/12 of life

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17
Q

When should paediatric vs newborn ALS techniques be used?

A

Use paeds techniques for any arrest beyond the first hours of birth up particularly if known cardiac etiology to arrest

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18
Q

At what temp should non-asphyxiated newborns of all gestations be maintained? Other considerations?

A

36.5-37.5. Dried, warm (skin to skin)

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19
Q

At what temp should infants at risk of, or who develop, hypoxic ischaemic encephalopathy be maintained?

A

normothermia, initiate induced hypothermia (& have admitted to NICU) if HIE confirmed

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19
Q

At what temp should infants at risk of, or who develop, hypoxic ischaemic encephalopathy be maintained?

A

normothermia, initiate induced hypothermia (& have admitted to NICU) if HIE confirmed

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20
Q

For term or late preterm infants >=34/40 deemed not to require immediate resus, what does ANZCOR suggest wrt cord clamping? How about preterm if don’t need immediate resus? And if need immediate resus?

A

Late (>=60 secs) vs immediate if >=34/40 but if <34/40, defer cord clamping at least 30 seconds. Infants who need immediate resus @ any gestation, no sufficient evidence to make recommendation wrt cord management

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21
Q

What are some equipment considerations for neonatal resus?

A

Practitioners should all be aware of assembly processes & alert to any errors- if unexplained hypoxia, change the gas supply & circuits or remove pts from ventilators by using self-inflating bag w RA- consider analysis of delivered gases & use an oxygen analyser in these situations.

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22
Q

What is the most sensitive indicator of resuscitation efficacy of the newborn?

A

Prompt increase in HR

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23
Q

What should the initial & subsequent assessment of the newborn address?

A

Tone, HR, breathing.. then subsequent assessment: HR, breathing, tone & oxygenation

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24
Q

What to do if the infant has low tone, isn’t breathing or can’t maintain HR >100bpm?

A

gentle positive pressure ventilation

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24
Q

What to do if the infant has low tone, isn’t breathing or can’t maintain HR >100bpm?

A

gentle positive pressure ventilation

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25
Q

What should be done if the newborn has regular respiratory effort but recession/retraction of lower ribs/sternum or persistent expiratory grunting?

A

gentle CPAP

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26
Q

Why pulse ox on R) hand in newborn?

A

know it’s pre-ductal

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27
Q

What goal HR should newborns achieve?

A

100 within 2 mins of birth

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28
Q

What interventions should occur if a newborns HR is <100bpm?

A

CPAP or positive pressure ventilation

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29
Q

When should pulse ox be used & what extra checks applied during it’s use?

A

use whenever need for resus is anticipated, CPAP or PPV or supplemental O2 used or if persistent cyanosis. Useful for HR & oxygenation, check HR intermittently with a stethoscope or ecg.

30
Q

What are some considerations for positioning of a newborn needing resus?

A

place on back, head neutral or slightly extended (sniffing), particularly if the bub’s head moulded during birth, causing a prominent occiput.
2cm thick blanket or towel under shoulders can help positioning.

31
Q

What steps should be taken if resp efforts occurring ventilation not effective (not achieving HR >100bpm)?

A

ensure airway patent eg. support of lower jaw, mouth opening or suction (latter only if very obvious signs of obstruction & only very briefly/carefully)

32
Q

What are the implications of meconium-stained fluid?

A

Bub may have meconium aspiration syndrome

33
Q

Steps to do if little/no chest movement with ventilation?

A

Improve technique of mask seal, correct head/jaw position, 2 people, increasing the inflating pressure until chest wall movement & HR increase. Suctioning may be required or an oropharyngeal or NP airway.

34
Q

What size self-inflating bag should always be available in case of failure of pressurised gas delivery devices during newborn resus?

A

240mL

35
Q

What initial pressures should be used for IPPV in newborns?

A

30cmH2O term, 20-25cmH2O in newborns, PEEP of 5cmH2O (but care with lung over expansion esp if preterm. Higher pressures may initially be required to aerate the lungs adequately for newborns yet to make a resp effort (use the minimum pressure to achieve visible chest wall movement & an increase in HR then decr once it’s apparent the newborn is responding to ventilation))

36
Q

what rate of ventilation for newborn?

A

40-60/min, insp time 0.3-0.5secs

37
Q

what are the risks of high (>8cm H2O) PEEP in newborn?

A

PTx, decr pulm blood flow

38
Q

What gas should be used when applying CPAP or PPV?

A

If term or near-term, air (first priority is to ensure adequate inflation). If SpO2 not meeting lower end of target, incr FiO2, once SpO2 90%, decr O2 []

39
Q

What’s the goal for timing of establishment of effective spontaneous or assisted ventilation?

A

1 minute

40
Q

Should routine direct laryngoscopy +/- tracheal suctioning be done routinely for newborns with mic-stained liquor?

A

No, ANZCOR suggests against it

41
Q

What’s the first step in newborn resus? then what?

A

drying & stimulation. If no response or effective rests or HR is <100 by 1 minute & not increasing, CPAP or PPV (if non-breathing) is the next step

42
Q

What’s the primary measure of effectiveness of ventilation in a newborn?

A

prompt improvement in HR which is sustained

43
Q

Which resuscitator device recommended by ANZCOR?

A

T-piece, as less mortality, bronchopulmonary dysplasia or rates of intubation for resuscitation
Must always have self-inflating bag avail for back-up in case of failure of pressurised gas delivery

44
Q

What are some benefits of PEEP in preterm neonates with RDS?

A

improved lung volumes, less apnoeas, lower O2 requirement

45
Q

What 3 findings confirm the effectiveness of ventilation of the neonate?

A

rise in HR >100bpm
improvement in oxygenation
slight rise of chest & upper abdo w each inflation

46
Q

How to calculate ETT diameter for infants?

A

GA in wks / 10
Typically, a 2.5 mm tube is appropriate for infants <1kg weight, a 3.0 mm tube for infants weighing 1 to 2 kg, a 3.5 mm tube for infants weighing 2 to 3 kg, and a 3.5 or 4.0 mm tube for infants over 3 kg

47
Q

What laryngoscope sizes used for newborns?

A

straight blade. Term or large preterm size 1 (10cm), small preterm <32/40 size 0 (7.5cm) very preterm size 00 (6cm)

48
Q

How calculate tube depth @ centre of lips?

A

weight in kg + 6 cm

49
Q

What’s the most reliable method to confirm ETT placement in resus of newborns w spont circulation?

A

calorimetric CO2 detector in neonates w spont circulation but it may have false -ve in pts w low pulm blood flow so look @ chest movement

50
Q

When could a SGA be considered in newborn resus? what size?

A

if facemask vent or ETT unsuccessful, in a term or near-term (>34/40, approx 2000g) newborn
Size 1 in newborns up to 5kg

51
Q

Along with checking for chest wall movement, improvement in SpO2 & improvement in HR, what else should be checked when SGA placed?

A

auscultation lungs

52
Q

What are some indications for endotracheal intubation in a newborn?

A

if despite facemask vent or SGA, persistent low HR, SpO2 lower than expected or falling or if facemask ventilation has been prolonged
specific conditions (eg. congenital diaphragmatic hernia, extremely low birth weight)
if no detectable HR consider early

53
Q

What equipment is needed to prepare for neonatal intubation?

A

T-piece resuscitator (or flow-inflating bag) and self-inflating bag (approximately 240 mL)
• neonatal facemasks (range of sizes suitable for premature and term newborn infants)
• Medical gases:
o a source of medical oxygen (reticulated and/or cylinder, allowing flow rate of up to 10 L/min) with flow meter and tubing
o a source of medical air plus air/oxygen blender
Suction apparatus and suction catheters (6Fr, 8Fr, and either 10Fr or 12Fr)
• Laryngoscopes with neonatal blades (size 00, 0, 1) plus spare bulbs and batteries. Ensure end
light is bright
• Endotracheal tubes (sizes 2.5, 3,3.5, and 4mm internal diameter). Important characteristics
of the tube include:
o uniform diameter, without a shoulder
o noeye
o uncuffed
o standard curve
o clear or translucent
o radio-opaque
o centimetre markings along the length to indicate depth of insertion
• Endotracheal stylet or introducer (optional for oral intubation, not used for nasal intubation)
• Supplies for securing endotracheal tubes (e.g., scissors, tape)
• Neonatal stethoscope
• Exhaled CO2 detector
• Magill neonatal forceps (optional)

54
Q

Which substances may create false +ve for calorimetric CO2 detectors?

A

Adr, surfactant

55
Q

What does the FLACC scale stand for? What age used for? rating scale?

A

Face
Legs
Activity
Crying
Consolability

2/12-7yo

0-10

56
Q

For what age is the CRIES pain scale used for?
What does it comprise of?
Valid & reliable?

A

0-6 months

5 behavioural & physiological variables shown to be associated with neonatal pain:

Crying
Requires increased O2 administration
Increased vital signs
Expression
Sleeplessness

Yes- valid & reliable

57
Q

When are most duct-dependent cardiac lesions diagnosed?

A

antenatal screening or postnatally at newborn pulse oximetry screening- some may present hours to days later as ductus arterioles starts to close

58
Q

How are the duct dependent lesions categorised?

A

cyanotic: eg; TGA, pulmonary atresia/stenosis, tricuspid atresia, severe ToF
left heart obstructive lesions (generally present with poor peripheral perfusion, difficult to feel pulses, lactic/metabolic acidosis which becomes more pronounced as ductus arteriosus closes: hypo plastic left heart syndrome, coarctation if the aorta, interrupted aortic arch, critical AS

59
Q

What’s normal SpO2 in newborns?

A

> =95% SpO2 & difference btwn R) hand & LL <=3%

60
Q

anaesthesia management for button battery ingestion?

A

to OT asap, don’t delay for honey/sucralfate or due to nbm status

confirm position in oesophagus with XR- note position of negative pole (direction @ risk of erosion), if in oesophagus, must be removed within 2hrs to avoid serious complications-
endoscopic removal
should have general +/- thoracic surgery +/- interventional cardiology or radiology.

anticipate need for massive transfusion- banked blood immediately available, large-bore IVC, consider art line & CVC & rapid infusion device. If had a sentinel bleed, at risk for subsequent bleeding.

RSI (un-fasted) & ETT (for safe foreign body removal)

If uncomplicated removal & oesophageal damage minimal + oesophageal pH neutralised with acetic acid, may extubate & observe as inpatient. If complication, ICU +/- intubated.

61
Q

Considerations for approach to sleep-disordered breathing in paeds?

A

preoperative snoring assessment, if they have OSA Dx, severity & level of control (eg. CPAP settings)
examination:
micrognatia, macroglossia, and midface hypoplasia. Syndromes associated with these anatomical abnormalities include Pierre Robin sequence
mouth breathing, elongated facies, chest retractions, obesity, failure to thrive, and inspection of tonsil size (adenotonsillar hypertrophy most common cause of OSA but tonsil size not correlated with OSA severity)
Ix: may have comp metabolic alkalosis suggesting chronic hypercapnia
If preop PSG, evaluate severity w AHI & nadir and duration of oxyhaemoglobin desaturation, and also the peak end-tidal carbon dioxide. If nadir O2 desat to 70% during sleep, may develop chronic hypercarbia and subsequently increased pulmonary pressures, cor pulmonale. These patients should have an electrocardiogram, echocardiogram, and evaluation by a cardiologist before proceeding with elective surgery. Cardiopulmonary issues less commonly in children cf adults

main intraop concern is risk of UA obstruction
NO sedative premed ideally
ideally IVC pre-induction
have a variety of airways

Opioid sparing strategy, titrate short-acting agents; these pts have upregulation of opioid receptors, more sensitive, reduce dose by 50%.
Remi good, non-opioid adjuncts paracetamol, dexamethasone, ketamine & single intraop dexmed 0.5microg/kg may improve pain scores & reduce emergence delirium for adenotonsillectomy

Extubate awake after full recovery of neuromuscular function

close respiratory observation and monitoring (abnorm vent responses to hypoxaemia & hypercapnoea)- their CPAP used

opioid-sparing anaesthetic and analgesic approaches- NSAIDS NOT contraindicated for bleeding risk (aside from ketorolac)

ADMIT for monitoring if:
<3yo
severe OSA on PSG
FTT
obesity
cardiac involvement (RVH)
downs syndrome
Hx craniofacial abnormalities
Hx prematurity
neuromuscular, chronic lung or sickle cell disease

62
Q

Signs of sleep-disordered breathing in children?

A

FHx OSA/SIDs
snoring, daytime sleepiness, mouth breathing, nighttime sweating, sleeping in unusual positions, parasomnias
extremes of body habitus
neurobehavioural disturbances
poor school performance
headaches
increased parental vigilance
eneuresis
CV sequelae (systemic or pulm HTN)
Accuracy of clin evaluation in predicting +ve sleep studies poor (30-85%)
PSG “gold standard” but costly, time consuming, not readily available, lack of standardised interpretation/diagnostic criteria, unclear if predictive of improved outcome so reserved for chn w FTT, craniofacial abnormalities, neuromuscular disorders, morbid obesity, polycythaemia or CV manifestations of unknown cause

63
Q

what’s central sleep apnoea?

A

absence of both airflow & resp effort on PSG

64
Q

How do RDI & AHI vary?

A

the AHI counts apnoeas or hypopnoeas related to obstructive events, so is useful for the severity of OSA
RDI includes all events so may also account for central sleep apnoea

In paeds, apnoea for PSG is >90% decr airflow signal lasting >=90% of duration of at least 2 normal breaths (determined from the baseline breathing pattern)
hypopnoea is a >=30% decr airflow, lasting >=90% of the duration of @ least 2 normal breaths, ass’d w arousal or at least 30% desat. sleep-related hypovent is EtCO2 >50mmHg for >25% total sleap time. RERA incr effort, snoring, elev PCO2 that leads to arousal but isn’t apnoea or hypopnoea.

In children, concern for OSA if AHI or RDI is >1.
RDI >5 used as threshold abnormal in adults but not sensitive for chn.

65
Q

rate of post-tonsillar bleed?

A

5-10%, 1% of these to OT

66
Q

Approach to anaesthetising paed FB?

A

gas induce with IVC
ensure deep enough
GREAT topicalisation 7mg/kg (lasts 30 mins)
if v young, prop only (10mg/kg/hr, reduce RR to 2/3)
older prop + remi (0.05mcg/kg/min titrate) BUT no opioid if imminent obstruction

67
Q

aim MAP & cerebral SpO2 neonate?

A

MAP within 10% of baseline
cerebral SpO2 (NIRS) >=70% (validated in cardiac neonates)

68
Q

considerations for paeds DS?

A

diff airway, a-a instability, cardiac
vagotonic- atropine drawn up
co-induction with N2O, mac 6 then down quickly (vagotonic)

69
Q

caffeine load neonate

A

10/kg

70
Q

dehydration Ax neonates?

A

Hx- feeding, wet nappies
exam: weight change
Ix: Hct up, Na+ up, Cl up, lactate up, K+ down (classic dehydration pattern with pyloric stenosis low K+, high Na+, high lactate, hyperchloraemia- correct acid:base, replace K+ if making urine)

71
Q

approach to pyloric stenosis on e-board?

A

fluid & electrolyte resus
warm OT
4-quadrant NGT aspiration

72
Q

Transition from foetal to neonatal circulation & establishment of ventilation

A

RV pumps blood to lungs (high PVR, low flow) & lower body. LV (systemic circn, low resistance & low SVR) pumps blood to coronaries/brain/upper body.
Circulations in parallel due to shungs (FO & DA)
Foetal RV & LV equal size & wall thickness.
CO is dependent on HR so foetal distress is indicated by brady (FHR <100), risking hypoxaemia. FHR >180 may occur w foetal skull pressure.
single umbi vein has PO2 28, PCO2 35, pH 7.32, SO2 80%), 60% of this blood bypasses the liver in the ductus venosus, shunted directly to IVC whihc maintains relatively high SpO2 of IVC (67%)
40% of this moves via portal venous circ to liver then IVC
60% of the IVC blood is shunted via FO to the LA (relately well-oxygenated stream, directed by crista terminalis), SaO2 65% to supply coronaries & brain
40% mixes with poorly-O2 blood from head/neck via SVC (SaO2 32)
SaO2 in RV 50%. 10% of the RV output goes to lungs (w incr PVR due to HPV), 90% goes via ductus arteriosus in PA to the lower body (SaO2 60%)–> interinal iliac aa–> umbi aa–> placenta (PO2 18, PCO2 55, SaO2 45%, pH 7.21)

At birth, transition from foetal circulation w RV & LV in parallel to adult system in series, initiated by changes in resistance of neonatal circulation–> haemodynamic changes causing shunt closure

  1. loss of low resistance placental circulation (55% of CO) with clamp/closure of umbi vessels (vasoconstriction w exposure to air, cut)–> incr SVR (afterload for LV), incr LVEP & LA pressure
    reduces venous return via IVC reduces RAP
  2. closure of ductus venosus 1-3hrs post delivery (further reduces VR via IVC)
  3. Significant reduction in PVR with -ve Pit of 1st breaths, expansion lung parenchyma & opening of extra-alv vessels, loss of HPV w incr PAO2, endogenous NO will incr PAP, reduce LVEDP, reduce RA pressure, incr pulm Q incr LA pressure & LV preload
  4. when LA pressure > RA pressure, flap closure (mechanical) of FO, fusion septum secundum 4-6wks, in 10-30% anatomically patent for life; usually functionally closed if LAP > RAP but risk paradoxial embolism/CVA if RAP>LAP.
  5. DA closes within 15hrs of delivery (smooth m contraction w incr PAO2 of 1st breath, reduced concentration of circulating PGsE1&E2, permanent closure by thrombosis/fibrosisby 2-3/52 (ligamentum arteriosum); hypoxia & PGs (-) dA closure

over wks, LV thickness incr cf R)

Bronchial tree fully developed @ 16/40
surfactant produced from 24/40
arteries/vv formed w capillaries in alveolar wall by 28/40
foetal resp movements initially irreg then later reg & rapid (60/min)
@ term, foetal lung has 20mL/kg fluid, 35mL is squeezed & reabs into pulm circn w VD (chest wall compliant), post delivery the remaining fluid is absorbed w incr pulm BF w initiation of ventn (first breath -ve Pinsp 70-100mmHg to overcome surface tension & open alveoli for first time, subsequent breaths less -ve pressure needed as establishement of air-liquid interface, surfactant reduces surface tension). Get adult-like pressure-vol loop from 40mins. FRC established to 30mL/kg within 1hr.
newborn TV 5-8mL/kg, RR 30/min, MV 150mL/kg/min
“transitional” circulation target Sp2 70-90@ 3 mins, 85-90@ 10 mins
environmental sensory stimuli stimulate initiation of ventilation (stimulate reticular system), incr perfusion through chemoreceptors which also respond to hypercapnia/hypox/acidaemia w loss placental gas exchange (closure/clamp umbi vessels)

In-utero HbF 90%, reduces to 75% @ birth, replaced by HbA by 6/12

73
Q

Utero-placental circulation, regulation of flow & principles of placental gas exchange

A

Placenta= interface of maternal & foetal circulation, exchange of O2/CO2/glucose/lipid/H2O/electrolytes/drugs without immuno rejection; IgG=only Ab class crossing placenta so rhesus Abs can cross but ABO (IgM) can’t
endocrine organ (hCG, HPL, oest, prog)
synthesises glycogen, FAs, cholesterol, ALP MAO, COMT

uterine arteries–> spiral arteries penetrating myometrium, eject blood into intervillous spaces that bathe chorionic villi–> pass through the chorion (2 layers trophoblasts), foetal CT & endothelium–> foetal circulation
via the umbilical arteries, form umbi capillaries flowing to chorionic villi, drain to uterine vv.
The uterine blood flow has minimal autoregulation; essentially fully dilated during normal pregnancy (except for the 10% supplying myometrium from basal arteries which is autoregulated)

Gas exchange influenced by:
1. placental blood flow
Uterine & placental blood flow therefore dependent on maternal CO, directly related to uterine perfusion pressure which:
-reduces with maternal hypotension (hypovolaemia, GA agents or neuraxial, A-C compression), incr uterine venous pressure (IVC compression, prolonged uterine contraction), incr uterine arterial resistance (catecholamines, alpha agonists, PET, extreme hypocapnia)

ie UBF= (UAP-UVP)/UVR

  1. PaO2 gradient
    Oxygen transfer from Mum–> foetus across placental barrier= “simple passive diffusion”;
    PaO2 gradient (Mo uterine art 105–> umbi vein 28), PaCO2 umbi art 55–> maternal uterine vein 45mmHg.
    both small, hydrophobic.
    CO2 20x more diffusible than O2 so more influenced by maternal-ofetal blood flow rates.
  2. diffusion capacity placenta
    Ficks: rate= ((diffusional SA x solubility x concn gradient)/(sq root MW x membrane thickness))
    placenta less efficient (1/10th O2 exchanged) cf lung
    less permeable, SA 15m2 vs 80m2, thickness 3.5microm vs 0.5
    uterine art & vein Q 600mL/min, umbi 300mL/min (ie. there’s shunting attenuating efficency)
  3. Maternal & foetal []Hb & O2 affinities
    HbF promotes L)-shift OHDC (it lacks B chains so doesn’t interact w 2,3 DPB, promotes relaxed Hb conformation with 500x > affinity for O2 vs T conformation.
    foetal Hb 190g/L (incr O2 carrying capacity) cf maternal 120g/L
  4. acid base status: double Bohr effect in trans-placental gas exchange: as CO2 offloaded from umbi arteries to placenta, less CO2 & H+ in foetal circulation promotes L) shift foetal OHDC & incr O2 affinity & uptake as move from umbi art to vein. at maternal side, incr CO2 & H+ promote “taut” conformiation of Hb & less O2 affinity/carriage (R)-shift OHDC as move from uterine art to vein.
    Haldane: deoxyHb higher affinity for CO2 than oxyHb so better CO2 carriage, 70% of the haldane is due to CO2 binding terminal amine groups of proteins, 30% is due to H+ being better buffered by imidazole moieties on histidine of Hb. On foetal side, reverse haldane; O2 upload reduces affinity for CO2 & enhances CO2 offloading. double haldane therefore facilitates trans-placental CO2 movement, further enhanced by maternal hyperventilation.
  5. placental O2 consumption (30% of the O2 transferred)
74
Q

Neonatal fluids:

A

extreme preterm neonate TBW is 90% of body wt
Term neonate TBW 75%
Abrupt reduction of TBW occurs approx 48-72hrs after birth, closely related to cardiopulm adaptation
Incr insensible water loss in preterm babies (evaporation through immature epithelial layer)
phototherapy incr IWL so need to incr fluid intake 10-20mL/kg/day
Newborns undergo a diuresis in the days following birth (reduction of TBW)
Body weight reduces 10-15% in preterm & 5-10% in term due to contraction of TBW

physical examination re: fluid status; can be unreliable, observe within context of body wt, haemodynamic monitoring, Hct, serum chemistries, acid-base & UO. Ax hydration status:
-oedema
-skin turgur
-mucous membranes
-periorbital tissue
-ant fontanelle
-consciousness

-HR= an early indicator of CV compromise
-BP= important indicator of IV volume but usually a late sign of depletion
-pulse volumes
-tachypnoea (met acidosis)
-CRT >3 secs may indicate poor tissue perfusion

-Na+ & K+ requirement 2-4mmol/kg/24hrs

-for neonates, glucose [] >12.5% require central venous access

Standard maintenance fluid for neonates:
First 24hrs of age: 10% glucose (500mL)
>24hrs age:
10% glucose 500mL + 10mmol KCl + 0.225% NaCl

day 1 of life, 60mL/kg/day
day 2: 80mL/kg/day
3 100mL/kg/day
4 120mL/kg/day
5 120mL/kg/day
basal requirement is 6-8mg/kg/min glucose for newborns, 10% glucose @ 60mL/kg/day gives 4.2mg/kg/min glucose

GI losses: if more than 20mL/kg, replace mL for mL w 0.9% NaCl + 10mmoL KCl

resus: 10-20mL/kg 0.9% saline as rapidly as possible

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