fluid and electrolye balance

1. Caroline Straatmann,MD

2. 0.6 xweight
¼ Plasma
(Intravascular)
1/3ECF
¾ Interstitial
Fluid
2/3
ICF

3. Intracellular
(mEq/L)
Extracellular
(mEq/L)
Na 20 135-145
K 150 3-5
Cl 98-110
HCO₃ 10 20-25
PO₄ 110-115 5
Protein 75 10

4. A 12 year old boy with chronic renal
insufficiency secondary to
obstructive uropathy is admitted
for pancreatitis.
He cannot tolerate enteral
feeds and is on TPN.
He complains of his legs
feeling weak.
Labs show
144 120 60

5. What do you dofirst?
EKG
EKG shows peaked T
waves
What do you donext?
Give calcium gluconate
Stop his TPN, which has K
in it!

6. In addition to this treatment, which
one of the following would be the
most effective therapy for his
hyperkalemia?
 Subcutaneous insulin and slow
infusion of glucose
 Intravenous beta – 2 agonist
 Intravenous insulin
 Intravenous sodium bicarbonate
 Oral sodium polystyrene sulfonate

7. Growing child requires 1-2
mEq/kg/day
 Avoidpotassium deficiency
 Cellular growth
Serum potassium concentration
doesnot reflect total body
potassium content
 Ex: Diabetic ketoacidosis
Disturbance in serum K⁺ can
affect cell membrane resting
potential
 Muscle paralysis
 Ventricular arrhythmias

8. Serum K >5 mmol/L (5 meq/L)
Kidney failure is the leading
cause
Can be life-threatening due to
risk of ventricular arrhythmias
Normal renal response to
hyperkalemia
 Stimulate aldosterone secretion
which then stimulates urinary
potassium excretion

9. Sympto
ms
 Skeletal muscle
weakness
 Paralysis
 Parasthesias
 Respiratory failure

10. Decreased renal
excretion
 Reduced GFR
 Reduced tubular
secretion
Increased intake
Transcellular shifts
 Metabolic acidosis
 Tumor Lysis Syndrome
 Rhabdomyolysis
Aldosterone
deficiency or
resistance
Common Drugs
 Amiloride
 Spironolactone
 Cyclosporine/Tacroli
mus
 Heparin
 ACE inhibitors/ARBs
 Pentamidine
 Trimethoprim-
Sulfamethoxaz
ole

11. ICF
Na= 10 mmol/L
K=140 mmol/L
Na= 150
mmol/L
K=4 mmol/L
3Na
EC
F
2
K

12. Reason for K to have shifted outside the cells?
K shift to outside the cell after the blood was
collected?
 Hemolysis
 Tissue hypoxia distal to tourniquet
 Heel stick
Are the kidneys excreting K appropriately?
 GFR
 Drugs
 Aldosterone
Excessive dietary K intake contributing to the
problem?
 IVFs and TPN!!!

13. Repeat serum
K
EKG stat
If EKG shows changes, start
treatment immediately
 Progression of changes
 Peaked T waves-Prolonged PR
interval-ST depression-Widened
QRS-Ventricular fibrillation

14.  Peaked T waves
 Loss of P wave
 Widening of QRS
 ST depression
 Prolonged PR
interval
 Ventricular
dysrhythmi
as
 Cardiac arrest

15. Eliminate source of potassium
intake or offending drugs
K⁺ < 6 mEq/L
 Low potassium diet
 Diuretics
K⁺ > 6 mEq/L
 Cation exchange resin:
SPS

16. EKG changes =
EMERGENCY
Stabilize myocardium
 IV calcium chloride or calcium gluconate
(10%)
Shift potassium into cells
 Beta agonists, insulin/glucose,
sodium bicarbonate
Remove excess potassium from the
body
 Sodium polystyrene sulfonate (SPS)
 Furosemide

17. Weakness or
paralysis
Ileus
Cardiac
dysrhythmias
 Delayed
depolarization
 Flat/absent T waves
 U waves

18. U
WAVES BMP
 Hypernatrem
ia
 Alkalosis
 Bartter’s
Renin
Aldosterone
Cortisol

19. If > 2.0 mEq/L and no EKG changes, treat
orally with KCl, minimum 2mEq/kg/day
If < 2.0 and/or EKG changes, treat
intravenously, with KCl 40 mEq/L into
IV fluids
“Potassium runs”: not recommended
unless cardiac/ICU patient
Monitor potassium values until normal
valueis established

20. A 7 yo male with cystic fibrosis and
obstructive lung disease is admitted
for a 2 week h/o progressive lethargy.
He is obtunded.
Labs: Na=105, K=4, Cl=72, HCO3=21
Plasma osmolality= 222mOsm/kg H20
Urine osmolality= 604 mOsm/kg H20
Urine Na= 78 mEq/L

21. What is the most likely
diagnosis?
 Pseudohyponatremia
 SIADH
 Psychogenic polydipsia
 Hypoaldosteronism
How would you raise the plasma
sodium concentration?

22. 2.
8
1
8
Normal=280-295 mOsm/kg
Osmotic equilibrium tightly
regulated between ECF and ICF
compartments
Water moves between
compartments in response to
alterations in osmolality of either
compartment
2 [Na⁺] + [BUN] + [Glucose]

23. • Serum osmolality is tightly regulated
• Sodium is the major determinant of
serum osmolality
• Sodium balance is regulated by the
kidney
• Serum sodium does not reflect total
body sodium content
• Na requirements in growing child
• 2-3 mEq/kg/day

24. Drawn from an indwelling
catheter
Hyperlipidemia
 Normal plasma Osm
Hyperglycemia
 Drives water into extracellular space,
diluting the Na concentration
▪ Plasma osm will behigh
▪ Na decreases 1.6 mEq/L for each 100 mg/dL
rise in glucose

25. Serum Na <130
mEq/L
Loss of sodium
Gain of water
Most common cause is
intravascular volume depletion
from gastroenteritis
 After volume expansion, will be able to
regulate free water excretion

26. Lose more salt relative to water
but still hypovolemic
Hyponatremic dehydration
GI losses (prolonged AGE/hypotonic
intake)
Renal losses
 Chronic diuretic therapy
 Salt wasting nephropathy
 Adrenal insufficiency
Skin losses
 Cystic fibrosis
(hyponatremic/hypochloremic)

27. Hypervolem
ia
Fluid
overload
 Congestive heart
failure
Water intoxication
 Diluted formula
 Hypotonic fluids
SIADH

28. History and
Physical
 Determine volume status
 Estimate sodium intake and
output
If hypovolemic:
 Renal or Extrarenal losses?
 Urine Na⁺
 Does kidney respond
appropriately to hypovolemia?
 Urine specific gravity
 Urine osmolality

29. Correct underlying
cause
 Hyponatremic dehydration
 SIADH
▪ Fluid restriction (insensible water losses) until Na levels
normalize
Rate of correction depends on how quickly it
developed
Acute hyponatremia is more dangerous
Increased risk of herniation or apnea from increased ICP from
rapid,
unbalanced water movement into brain cells
In general, correction with hypertonic
salinein unnecessary unless there are
neurological manifestations of

30. Sodium deficit (mEq) = Fluid
deficit (L) X
0.6 X [Na⁺] in ECF
(mEq/L)
Excess sodium deficit
=
PLU
S
(Desired Na⁺ - Actual Na⁺) X (0.6 L/kg) X
Wt (kg)
 Desired Na⁺ is 135mEq/L
Maintenance and ongoing losses
Replace over 24 hours

31. As sOsm falls, water moves into cells, and
risk of cerebral edema
If severe (<120 mEq/L), may observe
seizures, altered mental status,
vomiting
For Na⁺ < 120 mEq/L, raise Na⁺ to 125
mEq/L by giving 3% saline
Rapid correction of hyponatremia :
central pontine myelinolysis

32. EARL
Y
Headache
Nausea andvomiting
Lethargy
Weakness
Confusion
Altered consciousness
Agitation
Gait disturbances
ADVANC
ED
Seizures
Coma
Apnea
Pulmonary edema
Decorticate posturing
Dilated pupils
Anisocoria
Papilledema
Cardiac arrhythmias
Central diabetesinsipidus

33. 2 ml/kg bolus of 3% NaCl, max 100 ml
over 10 min
Repeat 1-2 times until symptoms
improve
Goal of correction is 5-6 mEq/L in
first 1-2 hours
Recheck sNa q2 hours
Moritz et al. Pediatr Nephrol
(2010) 25: 1225-1238

34. Insufficient
Correction
Cerebral
Edema
Too aggressive
Correction
Demyelinati
on
•Acute hyponatremia=Most dangerous
•Symptomatic hyponatremia = Medical
Emergency

35. A 9 yr old boy who has cerebral palsy is
admitted to CHNOLA following 4 days of
diarrhea. His initial serum
Na level is 174mEq/L. Once circulatory
volume is restored, the primary focus of the
fluid management must be to provide
appropriate amounts of:
 Chloride
 Free water
 Glucose
 Phosphate
 Potassium

36. Serum sodium >150 mEq/L
Always abnormal and should be
evaluated
Free water deficit
Increased sodium intake/retention
Increased serum Osm
Does not imply total body sodium
overload

37. Rarely develops in those who have
access to free water
Most often from inability to access
free water
At risk
 Ineffective
breastfeeding
 Critically ill patients
 Infants
 Neurologically

38. Children who have
hypernatremic dehydration
often appear minimally
dehydrated on exam.This is
due to maintenance of:
 Extracellular fluid volume
 Intracellular fluid volume
 Total body glucose
 Total body sodium
concentration
 Total body water balance

39. Water
Deficit
Renal loss
 Diuretic use
 Nephropathy with renal concentrating
defect
 Diabetes insipidus
Extrarenal loss
 Vomiting/Diarrhea
 Skin losses

40. Increased Sodium
Intake/Retention
Salt poisoning
Exogenous sodium
 Hypertonic
feeding/saline
 NaHCO3
administration
Mineralcorticoid
excess
Hyperaldosteronism

41. Determine volume
status
Blood pressure
Renal water loss
 Kidney does not appropriately respond to
hypovolemia
 Low urine s.g andosmolality
 High urine Na⁺
Extrarenal water loss
 Kidney responds appropriately to hypovolemia
 High urine s.g.
 Low urine Na⁺

42. Treat cause
Correct volume disturbance if
present
Replace free water deficit
 4mL/kg x (desired change in serum Na
(mEq/L))
Risk of cerebral edema from
rapid correction

43. Stone
s
 Renal
calculi
Bones
 Bone pain
Moans
 Depressio
n
Groans
 Constipati

44. Sympto
ms
 Weakness, irritability, abdominal
cramping, n/v, polyuria, polydipsia, renal
stones, pancreatitis, shortened QT
interval
Differential diagnosis
 Hyperparathyroidism, excessive calcium
intake, malignancy, thiazides, prolonged
immobilization, sarcoidosis

45. Most hypercalcemic patients are also
volume depleted
Hydration to increase UOP and Ca
excretion
 NS with potassium at 2-3x maintenance if
renal function and BP allow
Forced diuresis
 Furosemide
Calcitonin
Bisphosphonates
Dialysis

46. A 18 month old with ESRD secondary to
renal dysplasia on chronic peritoneal
dialysis has a serum Mg of 3.2. He is
asymptomatic. All other values are
normal except his BUN/Cr.
What is your next step in management?
 Change to hemodialysis
 Increase phosphate
binders
 Increase vitamin D
 Continue peritoneal
dialysis

47. Etiologi
es
 Renal failure
▪ Common in CKD due to
decreased excretion
▪ Levels in AKI parallel potassium
and are derived from the
intracellular pool
▪ Rapid cell lysis
 Excessive administration

48. Sympto
ms
 Decreased DTRs, lethargy, confusion
 Hypocalcemia (hypermagnesemia
suppresses PTH)
Rarely of clinical significance
Treatment
 Stop supplemental Mg
 Diuresis
 Dialysis

50. You are called to the floor at 2 am to
see a 16 yo orthopedic post-op
patient because his BP is160/100
What do you do?
A 5 yo boy is brought to the ER
because of new-onset generalized
seizure which has subsided by the
time he arrives. He is
postictal with BP of 160/100.
What do you do?
Is this HTN urgency or emergency?

51. HTN Emergency is elevated SBP
and DBP with acute end-organ
damage
 Stroke (ischemic/hemorrhagic)
 Pulmonary edema
 HTN encephalopathy
HTN urgency does not have end
organ damage.
 HA, Nausea, Blurred vision

52. In children, 75% of cases of HTN
emergency will be secondary to renal
or renovascular causes
What do you need to do before
treatment?
Rule out increased ICP as etiology of
HTN
Get plasma renin activity level
If the patient is bleeding or
coagulopathic, treat the elevated
BP urgently

53. ICU
Don’t lower BP too
rapidly
 Lower no more than 20-25% in 1st 8
hours
 Preserve cerebral perfusion
Acute goal is a mildly elevated
BP

54. A 5 yo boy is brought to the ER
because of new-onset generalized
seizure which has subsided by the
time he arrives. He is
postictal with BP of 160/100.
What would you start?
What would be your immediate BP
goal?
Goal around 130/85 (20% reduction)

55. Nitroprussi
de
 Arterial and venous
vasodilator
 Very short-acting
 Easily titrated
 Cyanide toxicity
 Don’t use in renal or liver
failure
IV Calcium channel
blockers
 Nicardipine

56. IV
Labetalol
 Alpha and beta blocker: decreases
peripheral vascular resistance
 Continuous or intermittent dosing
 Do not use in asthmatics, lung
disease, CHF, diabetics
IV Enalapril (Enalaprilat)
IV hydralazine
 Potent arterial vasodilator
 Infants

57. You are called to the floor for a 8 yo
child with PIGN who is seizing.
His BP is 155/98
What do you do for immediate
treatment?
IV labetalol bolus dose
Transfer to PICU for nicardipine or
labetalol infusion
Goal is to decrease his BP by 20-25%
in first
8 hours

58. Severe asymptomatic
HTN
 May have headache
Most commonly due to non-
adherence or ingestion of large
amounts of salt
Reduce BP over several hours to
days
Oral medications

59. Oral
medications
 Nifedipine
▪ Short-acting- see effectsin 15-
20 min
▪ 0.25 mg/kg initial dose
▪ 10 mg capsules
 Isradipine
▪ Short-acting: effects within one
hour
▪ 0.05-1 mg/kg/dose
 Labetalol
▪ Heart rate is dose limiting factor