STABLE Course Notes

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STABLE Course Notes 1. Sugar & Safe Care Aim for 2.8-6.0 mmol/L Avoid enteral feeding – insert IVC or UVC Risks for hypoglycaemia: 1. Prem (<37/40 gestation) 2. SGA 3. LGA 4. IDM 5. Stressed/sick 6. Some meds given to mother a. β -symps b. β -blockers c. Chlorpropamide d. Benzthiazides e. TCAs during 3 rd trimester Foetal glucose is approx 70-80% of maternal value 3 rd trimester = ↑ glycogen storage in liver Factors affecting BGL after birth: 1. ↓ glycogen stores 2. Hyperinsulinaemia 3. ↑ glucose utilisation Affecting: 1. Prem, SGA (@ term = 25% risk, prem SGA = ↑ risk) stressed/sick 2. IDM (insulin does not cross placenta. Foetus creates own insulin in response to mother glucose level. Cutting cord glucose stopped. May result in ↑insulin ↓ BGL), LGA (↑ insulin can be cause of LGA) 3. Prem, SGA, infection/shock/hypothermia/hypoxia (anaerobic metabolism; ↑ glucose consumption for ↓ ATP output)/cardiac or respiratory disease Screening: 15-30 min intervals until > 2.8mmol/L on at least 2 consecutive tests S&S of Hypoglycaemia: ASYMPTOMATIC Twitching Jitteriness Irritability Hypotonia Lethargy 1 | Page Rate x conc x 0.167 = mg/kg/min Weight OR 100ml/kg/day = 10g/kg/day 10g / 1.44 = mg/kg/min

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Personal notes taken during STABLE course

Transcript of STABLE Course Notes

Page 1: STABLE Course Notes

STABLE Course Notes

1. Sugar & Safe Care

Aim for 2.8-6.0 mmol/L

Avoid enteral feeding – insert IVC or UVC

Risks for hypoglycaemia:

1. Prem (<37/40 gestation)2. SGA3. LGA4. IDM5. Stressed/sick6. Some meds given to mother

a. β -sympsb. β -blockersc. Chlorpropamided. Benzthiazidese. TCAs during 3rd trimester

Foetal glucose is approx 70-80% of maternal value

3rd trimester = ↑ glycogen storage in liver

Factors affecting BGL after birth:

1. ↓ glycogen stores2. Hyperinsulinaemia3. ↑ glucose utilisation

Affecting:

1. Prem, SGA (@ term = 25% risk, prem SGA = ↑ risk) stressed/sick2. IDM (insulin does not cross placenta. Foetus creates own insulin in response to mother glucose level.

Cutting cord glucose stopped. May result in ↑insulin ↓ BGL), LGA (↑ insulin can be cause of LGA)

3. Prem, SGA, infection/shock/hypothermia/hypoxia (anaerobic metabolism; ↑ glucose consumption for ↓ ATP output)/cardiac or respiratory disease

Screening:

15-30 min intervals until > 2.8mmol/L on at least 2 consecutive tests

S&S of Hypoglycaemia:

ASYMPTOMATIC Twitching Jitteriness Irritability Hypotonia Lethargy High pitched cry Tachypnoea Cyanosis Poor suck Hypothermia Apnoea/irregular resps

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Rate x conc x 0.167 = mg/kg/min

Weight

OR

100ml/kg/day = 10g/kg/day

10g / 1.44 =

mg/kg/min

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Seizures

Treatment

1. D10W @ 80ml/kg/day via infusion pump (approx 5.5mg/kg/min)a. Central line for D15W and aboveb. Weight x 80ml / 24 = ml/hr

2. Bolus of 2ml/kg of D10W @ 1ml/min3. Rpt if no improvement4. Repeat & increase to 100ml/120ml/kg/day (or increase glucose concentration if pt not candidate for

↑ fluids)

NB prem may need ↑ fluids due to loss through thinner skin, radiant warmer, phototherapy lights etc.

Watch for ↑ BGL due to immature endocrine sys (i.e. may need ↑ fluids but ↓ glucose concentration)

UVC/UAC

UVC

Rapid IV access Difficulty gaining Peripheral IV More than 1 IVC needed CVC access for D12.5W+ Tip @ RA/IVC junction Preterm never more than 5cm; term never more than 7cm. Emergency placement – 3cm you’re in!

UAC

Continuous ABGs ABP monitoring NO MEDS – NaCl only to maintain patency AP CXR – T6-T9 (high line - preferred); L3-L4 (low line) Monitor for arterial spasm/emboli (discolouration of feet/abdo/buttocks/legs/groin)

NB In life threatening emergency – IO access (tibial) 18G

Heparin

0.5-1.0 unit/ml of fluid IV. CUMH – 0.5u/ml

NB Comes in different concentrations! Check packaging first!

Volvulus

Green coloured emesis. Never assume to be normal! Rule out malrotation.

Pain Bloody stool Ischaemia Shock & metabolic acidosis

Peripheral IVC

24G or 28G scalp needle

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STABLE Course Notes

2. Temperature

Maintain whether patient well or unwell

1. EARLY Prem & SGA at ↑ risk of hypothermiaa. ↑ surface area v body massb. Less insulating fatc. Thinner immature skind. Little if any brown fat (5% of mass – back/spine/shoulder)

2. SMALL BW <1500g – problem accentuated3. SICK Infants who require resuscitation or are acutely unwell

a. Hypoxicb. Hypotonic (unable to flex/↓ activity ↓ heat generation)

NB Core temp = 36.5°C – 37.5°C

Mild 36-36.4°C

Moderate 32-35.9°C Grades of hypothermia

Severe <32°C

NB Hypothermia is an independent risk factor for mortality

Normal response to cold stress

Peripheral vasoconstriction, ↑ flexion & activity, metabolism of brown fat ↑ metabolic rate ↑ utilisation of O2 & glucose

Prem, SGA & hypoglycaemia are at increased risk of hypothermia

Decreasing heat loss

1. Pre-warm objects before contact (mattress, hands, steth, XR plates, blankets)2. Insulation between baby & surfaces3. Clothing, hats (not always practical)4. Chemical thermal mattress with cover5. Pre-heat room to 25-28°C6. Cover chin-to-feet with polyethylene covering (may not be useful >1500g BW)7. Closed, pre-warmed incubator8. Heat O2 & humidify9. Radiant warmer – do not obstruct during resus10. Quickly dry infant11. Do not bathe unstable infants – PPHN12. Minimise air turbulence13. Warm any IV solutions14. Thermal shades over windows15. Move infant away from windows & walls16. Radiant bed – SERVO-CONTROL MODE!

a. Temp sensor on RUQ

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Physiological response to hypothermia (term infants)

Cold stress

Hypothalamus stimulated

Norepinephrine released Pulmonary vasoconstriction

Brown fat

metabolism ↑ activity, flexion R-L shunting (aerobic) ↑ O2 consumption

↑ glucose utilisation

HYPOGLYCAEMIA HYPOXIA HYPOXAEMIA

Physiological response to hypothermia (pre-term infants)

Cold stress

Hypothalamus stimulated

Norepinephrine released Pulmonary vasoconstriction

Brown fat

metabolism ↑ activity & flexion↑ O2 consumption

Limited glucose stores

HYPOGLYCAEMIA HYPOXIA

Right – left shunting hypoxemia

Hypoxemia Hypoxia Anaerobic metabolism ↑ lactic acid ↓pH

Hypothermia

S&S of worsening Hypoglycaemia due to Hypothermia

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Respiratory distress ↓ LOC ↓ resp rate ↑ sepsis risk DIC ARF

NB For re-warming, incubator is best choice. Set to air temperature mode. Set 1-1.5°C above core temp.

Closely monitor – avoid sudden vasodilation & hypotension

Core temperature HR ECG BP Continuously monitor Resp rate & effort SpO2 > 90% ABB BGL

NB Baby can lose 150ml/day in non-sensible, uncontrolled fluid loss through evaporative heat loss. 1ml of fluid loss = 4 cal energy loss

Prolonged resus – turn off radiant warmer. Possible candidate for therapeutic hypothermia / passive cooling (33-34°C)

Rewarming – ½°C/hour

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STABLE Course Notes

3. Airway

Arterial Blood Gases (CUMH)

pH 7.30-7.45 (7.26 acceptable)

pCO2 35-45mmHg (4.5-6 kPa)

pO2 50-80mmHg (6.5-10 kPa)

HCO3- 19-26 mEq/L (18-24)

BE -4 to +4 (-6 to +6)

NB Temperature when taken should be input in order to give accurate results!

Respiratory Distress

Mild - ↑RR Moderate - ↑RR, cyanosis, abnormal ABG Severe – central cyanosis, struggling, abnormal ABG

NB N = 30-60 r/min; < 30 = laboured; gasping = pre-arrest (BVM/tube/PPV)

Tachypnoea & ↓ pCO2 (non-respiratory cause)

Congenital heart disease Metabolic acidosis Cerebral disorder (meningitis, oedema, haemorrhage)

Tachypnoea & ↑ pCO2 (respiratory cause)

RDS (surfactant deficiency in immature infant) Pneumonia (give ABx until proven otherwise!) TTN (retained foetal lung fluid) (↑risk in pre-labour section) Aspiration Pulmonary haemorrhage Airway obstruction Chest mass, diaphragmatic hernia, pneumothorax (CXR for definitive Dx) Penicillin is cheap, safe & effective – use it!

Gas exchange

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Resp Breathe in pO2 in alveoli ↑ O2 diffuses into plasma Diffuses into RBC O2 binds to Hb Hb saturated with O2 Heart pumped to body releases O2 to cells O2 diffuses into cells CO2 diffuses from cells into plasma lungs CO2 removed

High Low gradient

pO2 blood > pO2 tissues

100mmHg > 23mmHg

↑ HCO3- = compensating respiratory acidosis

↓pCO2 = compensating metabolic acidosis

Metabolic Acidosis (lactic)

Shock Poor perfusion Anaerobic metabolism Sepsis Hypothermia Congenital heart disease TRAUMA – accidental & intentional

Treatment of Metabolic Acidosis

Treat the cause! ↑ O2

Respiratory Acidosis

Lung disease Pneumothorax Airway obstruction ↓ resp effort Neurological injury Apnoea Mechanical interference

Treatment of Respiratory Acidosis

CPAP PPV

NB Deterioration with PPV in neonate – consider diaphragmatic hernia.

Intubation

Weight (in kg) + 6 = tube mark @ lips

Ventilation

Time-cycled mode

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Start low, work up

VLBW LBW TermRate 30-60 30-60 20-50Insp time ≥0.25 Match GA < 0.45PIP 14-22 18-24 20-28PEEP 3-4 4-5 4-5

↑ PIP = ↑ TV = ↓ pCO2

↑ PEEP = ↓TV (unless ↑ PIP) = ↑pCO2

NB Adjust PEEP first, then PIP, then insp. time

Analgesia

Morphine – ref NEOPAIN study

0.05-0.1mg/kg per dose IV/IM/SC 15-30 min admin time

Fentanyl

1-2mg/kg per dose IV 15-30 min admin time

Sucrose

12-24% solution Term – 0.5-2.0ml Pre-term – 0.1-0.4ml

NB Sedatives ≠ Analgesia

Needle Aspiration of Pneumothorax

1. Turn 45°, pneumo side up2. 4th/5th IC space3. Mid-axillary or anterior axillary

CDH

8/40 gestation – diaphragm develops. Mortality 40-60% with CDH Recognition

o Cyanosiso Resp distresso Scaphoid/sunken abdomen

Risk of pneumothorax with PPV

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NB DO NOT PPV if CDH – intubate!

Stabilisation of CDH

Blow-by O2 10F OG tube CXR Pre & post-ductal SpO2% - observe for PPHN. Greater than 10% difference = R-L shunting Vitals Volume boluses Dopamine Observe for pneumothorax Analgesia

PPHN

PDA &/ FO remain open

3 main causes

1. ↑ muscularisation2. Vasospasm – acidosis, hypoxia, hypothermia, sepsis3. ↓ lung size – pulm hypoplasia, CDH

CPAP

Indications

1. Needs support but not intubation2. ↑ severity/frequency of apnoea3. ↑ work of breathing4. ↑ O2 requirement5. CO2 retention, acidosis (mild)6. Atelectasis7. Tracheobronchomalacia (flaccidity of tracheal cartilage)

Contra-indications

1. Progressive respiratory failure2. ↑pCO23. ↑ acidosis4. Hypoxemia5. CDH, TEF, choanal atresia, cleft palate, cardiovascular instability, ↓ resp drive

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STABLE Course Notes

4. Blood Pressure

Hypovolemic, cardiogenic & septic shock

HR x SV = CO

Fluids

10ml/kg/dose over 15-30 mins (NaCl or Ringers)

Whole blood – over 30mins-2hrs

Sodium Bicarbonate

4.2% solution For tx of severe metabolic acidosis (pH < 7.15) 1-2mEq/kg/dose over 30-60 mins IV

Dopamine

5-20mcg/kg/min IV

Group B Strep – risk factors

Temp > 38.5°C Labour > 18hrs UTI / Previous delivery

Double penicillin to treat meningitis.

Ref HIP trial

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STABLE Course Notes

5. Lab Work

Blood count

Blood culture The 4 B’s

Blood glucose

Blood gas

Risk of infection

PROM POL Chorioamnionitis (inflammation of foetal membranes) Increased risk of infection with

o Maternal infectiono Maternal fevero Maternal GU tract infectiono ROM > 18hrso Instrumentation useo Intubation/cannulation etc.

Neutrophils

Mature – Poly, Seg, Neut, PMNs

Immature – Metas, Bands, Stabs

Immature-to-total (I/T) ratio is important Absolute Neutrophil Count (ANC) in important (↓ ANC = ↑ RIP risk in presence of sepsis)

NB ANC ≤ 1800 in term / pre-term is abnormal!

ANC = Segs + Bands + Metas

I/T > 0.25 (25%) – suspect that the infant is fighting infection.

(Meta +band) Immature = I/T Ratio

(Segs + meta + band) Total

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NB I/T > 0.8 = ↑ risk of death from sepsis

Platelets

100-150k Abnormal

<100k Definitely abnormal, investigate for bleeding

<25k Dangerously low

VLBW (<1.5kg) 275k +/- 60k

LBW (<2.5kg) 290k +/- 70k Normal platelet values

Term 310k +/- 68k

NB NEVER withhold antibiotic therapy on basis of N FBC!

Time between onset of infection & FBC changes can be 4-12 hours!

Antibiotics

Ampicillin

100mg/kg/dose Give over 3-5 mins Every 12 hours

Gentamicin

2.5mg/kg/dose Give over 30 mins Every 12-24 hours

APGAR

<3 critical

4-6 low

7-10 normal

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How Ready Is This Child?

HR, RR, Irritability, Tone, Colour

APGAR

Appearance, Pulse, Grimace, Activity, Respiration

IVC & SVC

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AORTA

PA

PDA

PFO

RT Subclavian (pre-ductal)