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Management of Hypoglycemia& Electrolyte Imbalance in newborns
Dr. Sunil Rao
Asistt. Professor
Department of Peadiatrics
Hypoglycemia
• Fetal period
• Transitional period
Fetal glucose homeostasis
• Fetus gets glucose by facilitated diffusion across placenta.
• GLUT 1 & 3 are present in placenta and fetal membrane
• Factors affecting glucose transport:
(a) Maternal glucose concentration
(b) Materno fetal glucose gradient
(c) Fetal endocrine milieu
(d) Degree of placental metabolism of glucose
Fetal glucose conc. is significantly lower than that of maternal BS.(20-30%)
• Linear relationship exists between prevailing maternal BS andfetal BS.
After delivery
• Harmones
• Receptors
• Key enzymes
Hormonal changes
Term healthy baby : increases hepatic glucoseproduction & generates alternate fuels (FFA andketone bodies) by suppressing insulin and increasingsecretion of counter regulatory hormones (glucagon,cortisol, and catecholamine)
This response is absent in Preterm, SGA, IDM,smaller of twins, infants of erythroblastosis fetalis.
• Confirming a diagnosis of clinically significant hypoglycemia requires, that one interpret the blood glucose level within the clinical context.
Alteration in hormones & metabolic fuels following births
Glucagon
Insulin
Glucose
Glycogen
FFA
Catecholamine
• Persistent hypoglycemia is associated with endocrine abnormalities and possible neurologic sequalae.
• The absence of overt symptom at low glucose levels does not rule out CNS injury.
Outcome
Abnormal neurodevelopmental assessment• Asymptomatic –6%
• Symptomatic with no seizure-12%
• Symptomatic with seizure-50%
In recurrent & persistent hypoglycemia• >3days-29%
• >5-7 days-42%
Hypoglycemic brain injuryDeterminants-
1.clinical presentation2.severity of hypoglycemia3.duration of hypoglycemia4.concomitant disorders
Areas involved-1.cerebral cortex (parieto-occipital)2.hippocampus (dentate gyrus)3.basal ganglia (caudatoputamen)
less involved-cerebellum,brain stem,s.cord
Anticipation and Monitoring
IDM
SFD
Preterms
Rh isoimmunization
Asphyxia, hypothermia, polycythemia, septicemia or any sickness
Any baby on IV fluids or TPN
Primigravida with cesarean
Frequency of monitoring
• IDM – cord bld, 1,2,3,6 hrs, then 6 hrly x 48 hrs
• Preterms/SFD – 1,2,3,6 hrs, then 6 hrly x 72 hrs
• On IV fluids, TPN or other sick babies – 6 hrly
• 2 hours after exchange transfusion
Management
Same management for Asymptomatic and Symptomatic
Consider & treat secondary causes Minibolus - 200 mg/kg glucose as 2 ml/kg of 10%
dextrose over1 minute. Infusion of 10%dextrose @ 6 mg/kg/min (3.6
ml/kg/hour) Do not bolus without increasing the infusion rate Check blood glucose after 15 minutes Use infusion pumps If no contraindication, start feeds simultaneously
Management Algorithm
Blood glucose (BG) < 40 mg/dl by strip
-------->Evaluate causes
Start IV lineMinibolus –2 ml/kg 10% dextrose IV over 1 minStart 10% dextrose infusion @ 6 mg/kg/min
EBM/formula feeds if no contraindication -------->
Check BG after 15 min
BG > 40 mg/dl ----->continuesame infusion and monitorblood glucose
BG < 40 mg/dlIncrease infusion rate by 2 mg/kg/min every 15 mintill euglycemia*. Use 2 IV lines at high infusion rates. Max: 12-14 mg/kg/min (12.5% dextrose)
Intractable HypoglycemiaCheck insulin : glucose ratioCentral venous lineHydrocortisone, Glucagon, Diazoxide
*Giving boluses of dextrose without increasing the infusion rate is of no use
Step 1: Estimation of concentration of stock solution
6 8 10 12 14 16
40 22 29 36 43 50 58
50 17 23 29 35 40 46
60 14 19 24 29 34 38
70 12 16 21 25 29 33
80 11 14 18 22 25 29
90 10 13 16 19 22 26
100 10 12 14 17 20 23
110 . 10 13 16 18 21
120 . . 12 14 17 19
130 . . 11 13 16 18
140 . . 10 12 14 16
150 . . . 12 13 15
160 . . . 11 13 14
170 . . . 10 12 14
180 . . . . 11 13
Glucose infusion rate (mg/kg/min)
Step 2: Preparation of 100ml of stock solution
Concentration of
Stock solution25%dextrose(ml) 10%dextrose(ml)
10% 0.0 100.0
11% 6.7 93.3
12% 13.3 86.7
13% 20.0 80.0
14% 26.7 73.3
15% 33.3 66.7
16% 40.0 60.0
17% 46.7 53.3
18% 53.3 46.7
19% 60.0 40.0
20% 66.7 33.3
21% 73.3 26.7
22% 80.0 20.0
23% 86.7 13.3
24% 93.3 6.7
25% 100 0
25% dextrose (ml) 50% dextrose (ml)
30% 80 20
35% 60 40
40% 40 60
45% 20 80
Tapering of dextrose infusion
When blood glucose has remained normal for 12 hours or if blood glucose exceeds 100 mg/dl, decrease the infusion by 2 mg/kg/min every 4-6 hours while checking blood glucose.
Intractable hypoglycemia
• Uncorrected hypoglycemia despite a glucose infusion rate of 10-12 mg/kg/min or lasting more than 5-7 days
• Blood samples for glucose, insulin & C-peptide levels, other hormones and serum ammonia
• A central line to infuse higher concentration and higher rate of glucose.
• Glucagon 300 μg/kg IV or SC, or as infusion • Diazoxide 10-15 mg/kg/day P.O. or IV in 3 or 4
divided doses along with Chlorthiazide , Octreotide and Nifedipine
Key Messages
Both hypo and hyperglycemia are bad.
Checking BG is the only way to diagnose-anticipate and monitor.
Titrate glucose infusion rate to maintain euglycemia
Electrolyte Abnormality
• Hypernatremia
• Hyponatremia
• Hyperkalemia
• Hypokalemia
Electrolyte Requirements (meq/kg/d)
Term Preterm
------------------------------------------------------
Days Na K Cl Na K Cl
1 - - - - - -
2- 3. 3 3 3 2 3 2
4 -15 3 3 3 3-5 5 3
-------------------------------------------------------------
Na Requirements in PT mEq/kg/d
upto 5 < 30 wks
4 31-35 wks
3 if stable water balance
Compensate for increasing IWL
IV Fluid ml/kg/d :Pre Term Initial Orders
Day < 1Kgm 1-1.49kg =/>1.5kgm
(7.5% Dx) (10%Dx) (10%Dx)
1 100 90 80
2 * 110 100 90
3 120 110 100
4 125 150 120 110
5 125 150 125-150 125-150
* Add electrolytes. FT : Start with 60
I W L
IWL - Skin
• Depends on keratinization of skin
• Higher in PT
• Higher in first 3-5days
Measurement of IWL
Values in ml/kg/hr & (ml/kg/d)
Wt (Kg) Incubator Radiant Warmer
< 1 3.0 (72) 4.0 (96)
1 – 1.5 2.0 (48) 3.0 (72)
1.5 – 2 1.0 (24) 2.0 (48)
Hypernatremia >150 mEq/l in PT
Incidence ? 10 - 40 % , Higher in < 28 wks
Hyperosmolality increases CNS morbidity
Cause :
Insufficient water intake,
Excessive IWL
Excessive sodium intake in VLBW
Treatment of Hypernatremia
Correction Rate : 0.5 mEq per hour
Sudden changes in plasma osmolality:
Brain edema, Exacerbation of any ICH.
For shock use N Saline
Clinical Example:• 3 kg Neonate with poor feeding & lactation failure),
weighing 2.1 kgs on d 20 . S.Na is 175 meq/L.
Step 1 Assess water loss :
• Water Deficit = expected lean weight - current weight.
• Baby with poor feeding will loose lean body mass
• 0.5 to 1% mass every day.
• At loss of 0.5%/ d for 20d = 0.5% X 20 d of 3Kg
=3 kg minus 300 gm = 2700 Gms.
• As the baby weighs 2.1 kg at admission,
• Water deficit will be 2700 – 2100 = 600 gms or ml
Example • 2.7 kg baby wt 2.1 kg ,Na 175,
• Fluid deficit 2700 – 2100 = 600 ml
• Free Water Deficit = ( Actual Na – Desired Na/actual Na) X O.6 X Weight (kg)
• Or = (175 – 145/175) X 0.6 X 2.7 ie 0.277 L.
Calculate Na Deficit (meq) =
• Fluid Deficit (L) – Free water def (L) X 0.6 X actual Na
• = 0.6 – 0.277 x 0.6 x 175 = 33.9meq.
• Calculate final fluid composition
Example : final fluid composition
• Goal : correct water deficit 600 ml and Na deficit of 33.9 meq over 3 days.
• (Not more than 10 meq Na/ d). i.e. 200 ml of fluid deficit and 11.3 meq of Na deficit per day.
• Total fluid for D 1 = Maintenance fluid + deficit (200 ml)
• Maintenance Fluid = insensible losses (30ml/kg) + urine output
• Total Na on D1 = Maintenance Na(3/kg) + Deficit (11.3 meq)
• Similarly fluid is calculated for next 2 days.
Hyponatremia <130 mEq per litre
• More common than hypernatremia in PT.
• Cause : high urinary Na loss -VLBW on diuretic
• SIADH as in asphyxia, RDS, pneumnia
• Renal disease : high urinary Na loss
Therapy options :
Fluid restriction
Sodium chloride.
Hyponatremia <130 mEq per litre
• More common than hypernatremia in PT.
• Cause : high urinary Na loss -VLBW on diuretic
• SIADH as in asphyxia, RDS, pneumnia
• Renal disease : high urinary Na loss
Therapy options :
Fluid restriction
Sodium chloride.
Hypotonic Hyponatremia Osm <280 mosm/l
• Hypovolemic
• Euvolemic
• Hypervolemic
Hypovolemic Hyponatremia
• Renal losses:
• VLBW on diuretics
• Adrenal insufficiency,
• Proximal RTA,
• Metabolic alkalosis,
• pseudohypoaldost’ism
UNa >20 mEq/1
Treat withSaline
• Extrarenal losses:
• Gastrointestinal vomiting, Diarrhea, tubes/fistula
• Sweat
• Third space
UNa <20 mEq/1
Treat with Saline
Na Content of Body Fluids meq/l
Sources Na Cl
Stomach 50-80 100-150
Small int / Bile 100-140 90-120
Ileostomy 45 – 135 20-120
Diarrhea 10 - 90 10-110
Euvolemic Hyponatremia
• SIADH
• (Asphyxia, ICH, RDS, Pneumonia)
• Water intoxication, IV therapy
• UNa>20 mEq/1
• Water restrict
Hypervolemic Hyponatremia
• Edema-forming states
• Congestive hrt failure
• BPD
• UNa<20 mEq/1
• Water restrict
• Renal failure
• Acute
• Chronic
• UNa>40 mEq/1
• Water restrict
Therapy of Hyponatremia
• mEq Na required =
(desired Na - present Na) X 0.6 X wt
If seizure, coma, Na<120meq/l, Correct to 125 mEq/l within 4 hrs
• Use 3% NaCl = 513 mEq/L (0.5meq/mL)Dose:125-Actual XwtX0.6 in 4 Hrs
• Delay in correction may cause death
• Rest of correction : +maintainance over 48 Hrs
Example: Fast correction
• S. Na = 115meq/L in a 2 kg baby
• Desired Na = 125meq/L
• Na Deficit = (125-115) X2 Kg X0.6 = 12meq in 4 h.
• Vol of 3% NaCl (0.5meq/mL) = 24 ml in 4 h
• Rest of correction upto 135 meq (=10meq) + maintainance3/kg in 48 hrs
Example:Slow correction • S. Na = 122meq/L on Day 7 in a 1.5 kg baby
• Desired Na = 135meq/L
• Na Deficit = (135-122)X1.5X0.6 = 11.7meq.
• To be corrected over 48 h.
• Maintenance Na (3meq/kg/day) = 3 X 1.5 X 2 = 9 meq.
• Total Na for 48 h = 11.7 + 9 = 20.7meq.
• Fluid requirement for 48 h = 150 X 1.5 X 2 = 450 ml.
• Hence 21 meq Na in 450 ml of fluids over 48 hours
• i.e. around 5 meq Na in 100 ml OR N/3 solution,
Late hyponatremia in PT 1-5wk
• Etiology: Poor Na conservation by kidneys
• Negative Na balance and excess ECF.
• Adding NaCl to the formula
normalizes Na, increases blood volume &
inhibits ADH secretion.
Hyperkalemia Diagnosis
• Asymptomatic, ,Brady/tachy rhythm,collapse
• ECG:Incr rate of repolarisation: tall T
• Red conduction :
Atrial - Flat P,Prolonged PR
• Ventricular -wide QRS,slur
ECG: Hyper K
Peaked T wavesFlattened P waves, increasing PR (suppression of atrial activity ) QRS widening and slurring. ( conduction delay in ventricular tissue )
Hyperkalemia Treatment
Stop exogenous K
• Normalize Conduction: Ca gluc 1-2ml (100-200 mg)/kg
• Lasix 1mg/kg :renal loss
• Cellular shift of K:
Alkalemia HCO3 ,hyperventilate PH>0.1 : K<0.6
Insulin Bolus = 10% Dx 2ml + 0.5U Insulin /kgWt
Infusion 10% Dx 2-4ml/kg/hr, Insulin10u/dl
• Peritoneal dialysis/ET, Kayexalate 1g/kg in 2ml NS rectally 4 Hrly
Hypokalemia
ECG-conduction defects (prolonged QT, U)
ECG changes: Hypo K
Prominent U waves, bifid T waves, flattened T, QTc prolongation