FLUIDS & ELECTROLYTES 2INTERNAL MEDICINE.pdf

INTERNAL MEDICINE

1. Fluids and Electrolytes
(Part 2: Electrolytes)
Janice F. Bacani-Carandang, MD, DPPS

2. ELECTROLYTE COMPOSITION
nExtra-cellular fluid (ECF):
nSodium (Na+)
nChloride (Cl-)
nIntra-cellular fluid (ICF):
nPotassium (K+)
nProteins, organic anions and phosphorus
nThe difference in electrolyte compositions are
important in the evaluation and treatment of
electrolyte disorders.

3. SODIUM (Na+)
nThe dominant cation in the ECF
nNormal values: 135-145 mEq/L
nIntake:
nDetermined by the child’s diet
nReadily absorbed by the GIT
nCo-transport system with Glucose
nExcretion:
nThrough stool and sweat
nThrough the kidney-RAS

4. Hypernatremia
nSodium concentration of > 145 mEq/L
n3 Basic mechanisms:
nExcessive sodium
Iatrogenic, intentional salt poisoning, hyperaldosteronism
nWater deficit
Diarrhea, emesis, lactulose, burns
nWater and sodium deficits
GI losses, renal losses, cutaneous losses

5. Hypernatremia
nClinical manifestations:
nSigns of dehydration
nIrritable, restless, weak and lethargic
nVery thirsty, even with nausea
nBrain hemorrhage-most devastating
consequence; decrease in brain volume causes
tearing of blood vessels → seizures and coma
nThrombotic complications due to hypercoagulability:
strokes, peripheral thrombosis, RVT

6. Hypernatremia
nDiagnosis:
nHistory and PE
nUrine osmolality
nTreatment:
nImportant NOTto correct too rapidly.
nRate: <12 mEq/L in 24 hrs, or 0.5 mEq/L per
hour
nRestoration of intravascular volume with isotonic
fluid

7. Review of the Tonicity of IV Fluids
and their respective actions:
HYPOTONIC
(Pullsfluid out of the
intravascular space)
ISOTONIC
(Primarily remains in the
intravascular space)
HYPERTONIC
(Returnsfluid to the
intravascular space)
D5NM D5LR D10W
D5IMB PLR D50W
D5W D5NSS
D5 0.3NaCl PNSS

8. Hyponatremia
nSodium concentration of < 135 mEq/L
nClassification of Hyponatremia:
* Based on the patient’s volume status
nHypovolemic hyponatremia
Excess hypotonic IV, child abuse, diluted formula
nEuvolemichyponatremia
SIADH, water intoxication
nHypervolemichyponatremia
CHF, cirrhosis, Nephrotic syndrome, renal failure

9. Hyponatremia
nTreatment:
Important to avoid “overly rapid”
correction → leads to CPM(Central Pontine
Myelinolysis) → neurologic symptoms like
confusion, agitation, flaccid or spastic
quadriparesis, death
nBased on the pathophysiology of the specific
etiology

10. Computation of Sodium Deficit
nEg. 2.5 kg child with Na+ of 123
nDeficit: (Desired-Actual) X Weight X 0.6
(135-123) X 2.5 X 0.6
= 18 mEqs
nMaintenance: 2-4 mEq/kg
2 mEqX 2.5 kg = 5 mEqs
nTotal: 18 mEqs+ 5 mEqs= 23 mEqs

11. Composition of IV Solutions
Na K Cl
D5 LR 130 4 109
D5 0.3NaCl 51 51
D5 0.45NaCl 77 77
D5 0.9NaCl (NSS)154 154
D5 NR 140 5 98
D5NM 40 13 40
D5 IMB 25 20 23
* mEqs per liter of solution
*Choose the IV Fluid with the highest Na content to correct the deficit

12. Computation of Sodium Deficit
nHaving chosen NSS with Na of 154 meqs/L,
compute using ratio and proportion.
154 mEqs= X(X is the mEqsgiven during initial hydration)
1000 cc 100 cc (volume given during initial hydration)
where did this come from?

13. 2.5 kg child with Na+ of 123
1. Restore intravascular
volume (20 mL/kg)
20 ml X 2.5 kg= 50 ml over 20 mins
2. Rapid volume
repletion (20 mL/kg)
20 ml X 2.5 kg= 50 ml over 2 hours
3. Calculate 24-hr water
needs
(Maintenance + Deficit)
Maintenance: 100 (2.5 kg)= 250 ml
Deficit: 10% X 2.5 kg= 0.25L or 250 ml
TOTAL: 500 ml
4.Calculate 24-hr
electrolyte needs
5. Select an appropriate
fluid
(Give half in 8 hrs, less
the bolus given; then
give remaining in 16 hrs
500 ml divided by 2= 250 ml
250ml-100 ml= 150 ml in 8 hrs(18.75ml/hr)
The remaining 250 ml will be given in 16 hrs
(9.3 ml/hr)

14. Computation of Sodium Deficit
nUse NSS (154 mEqs/L), using ratio and
proportion:
154 mEqs= X (mEqsgiven during initial hydration)
1000 cc 100 cc (volume given during initial hydration)
nThen, cross-multiply:
X= 154(100) divided by 1000 = 15.4 mEqs
nBUT.. remember that your total computed Na
deficit is 23 mEqs…. How do you give the
remaining deficit?

15. Computation of Sodium Deficit
nGive remaining as D5IMB (the usual IV fluids used
in the ward)with 25 mEqs/L of Na:
25 mEqs= X (mEqsNa given during 24 hrcorrection)
1000 400 cc(volume given during 24 hrcorrection)
nThen, cross-multiply:
X= 25 (400) divided by 1000 = 10 mEqs
nTotal: 15.4 mEqs+ 10 mEqs= 25.4 mEqs
(which is close to total deficit of 23 mEqs)

16. POTASSIUM (K+)
nThe dominant cation in the ICF
nNormal values: 3.5-5.1 mEqs/L
nMajority is in the muscle
nMaintained by the Na+K+ATPasesystem
nNecessary for the electrical responsiveness of
nerve and muscle cells, and for the contractility
of cardiac, skeletal and smooth muscles

17. Hyperkalemia
nPotassium concentration of > 5.1 mEq/L
nOne of the most alarming electrolyte abnormalities
because of the potential for lethal arrythmias
nBasic mechanisms:
nSpurious hyperkalemia (pseudohyperkalemia)
nIncreased intake
nTranscellular shifts
nDecreased excretion

18. Hyperkalemia
nClinical manifestations:
Most important effects are on membrane
polarization, espin the cardiac conduction system
-ECG changes: peaking of T waves
-ventricular fibrillation, asystole
-paresthesias, weakness, tingling

19. Hyperkalemia
nTreatment has two basic goals:
(1)to stabilize the heart to prevent life-threatening
arrhythmias and,
(2)to remove potassium from the body.
nHyperkalemic regimen: (to remove K from the body)
nCalcium gluconate-stabilizes the cell membrane
nSalbutamol/ Albuterol nebulizations
nSodium polystyrene gluconate (Kayexalate)-
exchange resin
nInsulin
nDialysis

20. Hypokalemia
nPotassium concentration of < 3.5 mEqs/L
nCommon in children, most cases related to
gastroenteritis
nBasic mechanisms:
nSpurious
nTranscellular shifts
nDecreased intake
nExtra-renal losses
nRenal losses

21. Hypokalemia
nClinical manifestations:
ECG changes: flattening of T-waves,
depressed ST segment, appearance of a u-wave
Muscle weakness and cramps, paralysis
Chronic: kidney damage
nTreatment:
nOral or IV potassium

22. Computation of Potassium Deficit
* E.g. 10 kg child with K+ of 2.44
nDeficit: (Desired-actual) X weight X 0.4
( 4.5 –2.44) X 10 X 0.4
= 8.4 mEq
nMaintenance: weight X 3
10 kg X 3 = 30 mEq
nTotal: 8.4 mEqs+ 30 mEq= 38.4 mEq

23. Composition of IV Solutions
Na K Cl
D5 LR 130 4 109
D5 0.3NaCl 51 51
D5 0.45NaCl 77 77
D5 0.9NaCl 154 154
D5 NR 140 5 98
D5NM 40 13 40
D5 IMB 25 20 23
* mEqs per liter of solution
*Choose the IV Fluid with the highest K content to correct the deficit

24. Computation of Potassium Deficit
nObserve the table of IV Solutions (previous slide)
nNotice that some fluids do not contain K
nThese are the fluids used for resuscitation-why do
they not have K?
nBecause you don’t know yet if the kidney is
functioning or not. If not, excess K cannot be
eliminated from the body → hyperkalemia →
DEATH!
nTherefore, IV fluids for resuscitation are non-K
containing.

25. Computation of Potassium Deficit
* D5 IMB has 20 mEq/L
nEx: Child is already up at the ward, hooked to
D5IMB at a given rate of 45 cc/hr:
45 cc/hrX 24 hrs= 1080 cc
nThen, multiply total fluid with mEqsK in IVF:
1080 cc X 20 mEqs/L = 21.6 mEq
nBut remember: TOTAL DEFICIT is 38.4 mEq
-21.6 mEq = 16.8 mEq
nTherefore, you still need 16.8 mEqsto correct the
total deficit.. WHAT WILL YOU DO NEXT?

26. Correction of Potassium Deficit
nTwo choices: give IV or oral Potassium
nComputation is via TRIAL and ERROR
nIf through IV: Just remember to keep the Potassium
Infusion Rate (KIR) at 0.1-0.3 mEq/kg/hr
So, incorporate pure K to D5IMB as follows:
20 mEq+ 16.8 mEqsX 45 cc/hr÷weight
1000
= 0.16 mEq/kg/hrKIR
Therefore, your K+ correction is within limits.

27. Correction of Potassium Deficit
nFor trial and error, you may adjust either the
amount of K (eg. 20 mEq) that you will
incorporate (comes in a vial from which you
extract K and inject to the IV fluid), or the IV
running rate (eg. 45 cc/hr)so that you fall
within the KIR.

28. Correction of Potassium Deficit
nOR you may opt to give oral supplementation of
KCl(10 mEqsper tab) at a dose of 2-4 meqs/
kg/day BID-QID, provided patient is able to take
in oral prep and will not vomit it, or fully conscious
and will not aspirate. In this case, you may give
1 tablet BID.

29. Magnesium (Mg+)
n4
th
most common cation in the body;
n3
rd
most common intracellular cation
n50-60% is in bone (serves as a reservoir)
nNormal values: 1.5-2.3 mg/dL
nA necessary co-factor for hundreds of enzymes
nImportant for membrane stabilization and nerve
conduction
nNeeded by ATP and GTP

30. Magnesium
nIntake
nGreen vegetables, cereals, nuts, meats, milk (30-50%
is absorbed)
nHuman milk (35 mg/L) < formula milk (40-70 mg/L)
nSmall intestine-major site of absorption (passive)
nExcretion
nRenal excretion-principal regulator of Mg balance;
70% in the TAL of the Loop of Henle

31. Hypomagnesemia
nRelatively common in hospitalized patients, but
mostly asymptomatic.
nCauses:
nGI Disorders
nDiarrhea: 200 mg/L Mg; Gastric contents: 15 mg/L
nNGT suctioning, IBD, Celiac disease
nRenal disorders
nMeds: Loop diuretics, mannitol, aminoglycosides
nDiabetes, ATN, chronic kidney diseases
nMiscellaneous causes
nIUGR, infants of diabetic mothers, exchange transfusion

32. Hypomagnesemia
nClinical manifestations:
nSecondary hypocalcemia (impaired release of PTH
by the parathyroid gland; blunting the tissue
response to PTH)
nTetany, seizures
nTreatment:
nParenteral Mg (Mg sulfate: 25-50 mg/kg slow IV)
nOral Mg (long-term therapy)

33. Hypermagnesemia
nAlmost always secondary to excessive intake
nMg present in high amounts in certain laxatives,
enemas, cathartics used in drug overdose
nUsually asymptomatic unless > 4.5 mg/dL
nInhibits acetylcholine release at the NMJ →
hypotonia, hyporeflexiaand weakness, paralysis
nOther S/S: lethargy, sleepiness, poor suck
nECG changes will also be present

34. Hypermagnesemia
nTreatment:
nIV hydration and loop diuretics
nDialysis, exchange transfusion in severe cases
nExcess Mg rapidly cleared if renal function is intact.
nAcute emergencies: IV calcium gluconate

35. Phosphorus
nMost phosphorus is in bone or is intracellular
nPhosphate is the most plentiful intracellular anion,
although the majority is part of a larger
compound (ATP)
n↑ in childhood: facilitate growth
nDiurnal variation: peak during sleep
nWith ATP: Critical for cellular energy metabolism
nWith calcium: for skeletal mineralization

36. Phosphorus
nIntake
nMilk and milk products (best sources); meat, fish
nVegetables > fruits and grains
nSmall intestine: site of absorption
nExcretion
nKidneys-regulate phosphorus balance (proximal
tubules)

37. Hypophosphatemia
nAge-dependent
nCauses of hypophosphatemia:
nTrans-cellular shifts-insulin, refeeding, tumor
growth
nDecreased intake-nutritional, preterms
nRenal losses-kidney transplant, hyperparathyroidism
nMulti-factorial-alcoholism, sepsis, dialysis

38. Hypophosphatemia
nClinical manifestations:
nRickets, muscle weakness & atrophy, rhabdomyolysis
nDiagnosis
nInvestigate nutrition, medications, familial disease
nTreatment:
nOral or IV phosphorus
nIncreasing dietary phosphorus

39. Hyperphosphatemia
nRenal insufficiency-most common cause
nCauses:
nTrans-cellular shifts
ntumor lysis syndrome, DKA
nIncreased intake
nenemas, laxatives, treatment of hypophosphatemia
nDecreased excretion
nrenal failure

40. Hyperphosphatemia
nClinical manifestations:
nHypocalcemia, systemic calcification
nDiagnosis:
nPlasma creatinine and BUN
nHx: intake of phosphorus, chronic diseases
nTreatment:
nPhosphorus binders

41. STUDY HARD!
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